Clinical Diagnosis and Management of Ocular Trauma

Clinical Diagnosis and Management of
OCULAR TRAUMA
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Clinical Diagnosis and Management of
OCULAR TRAUMA
JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

New Delhi Ahmedabad Bengaluru Chennai Hyderabad Kochi Kolkata
Lucknow Mumbai Nagpur St Louis (USA)
Ashok Garg MS PhD FIAO (Bel) FRSM FAIMS ADM FICA
International and National Gold Medalist
Chairman and Medical Director
Garg Eye Institute and Research Centre
235-Model Town, Dabra Chowk
Hisar-125005, India
B Shukla MS PhD MAMS FICS
Director of Research
RJN Institute of Ophthalmology
Chandra Bhawan, 1, Jhansi Road
Gwalior-474002, India
Jerome Jean Bovet MD
Consultant Ophthalmic Surgeon FMH
Clinique de Loeil
15, Avenue Du Bois-de-law-Chapelle
CH-1213, Onex, Switzerland
Mahipal S Sachdev MD
Centre for Sight, B-5/24, Safdarjung Enclave
New Delhi-110029, India
CS Dhull MS PhD FIAO
Professor and Head
Regional Eye Institute of Ophthalmology
Pt. BD PGIMS, Rohtak-124001, India
Editors
Jose M Ruiz-Moreno MD PhD
Professor of Ophthalmology
Albacete Medical School, University of
Castilla La Mancha
Avendia de Almansa, 14 02006, ALBACETE
Spain
T Mark Johnson MD FRCS
Consultant Vitreo Retinal Surgeon
National Retina Institute
Suite 101, 5530 Wisconsin Ave
Chevy Chase 20815, USA
Keiki R Mehta MS DO FRSH FIOS
Mehta International Eye Institute and
Colaba Eye Hospital
Seaside, 147, Shahid Bhagat Singh Road,
Mumbai-400005
India
Bojan Pajic MD
Chief of the Cornea and Refractive
Surgery Department
Klinik Pallas Louis Giroud-
Str. 20 4600, Olten
Switzerland
Belquiz A Nassaralla MD PhD
Consultant Ophthalmic Surgeon
Department of Cornea and Refractive Surgery
Goiania Eye Institute, Goiania
GO, Brazil
Cyres K Mehta MS FSVH FAGE
Director and Consultant
Mehta International Eye Institute and Colaba Eye Hospital
Seaside, 147, Sahid Bhagat Singh Road, Mumbai-400005, India
Foreword
Bruce Wallace
Published by
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Clinical Diagnosis and Management of Ocular Trauma
2009, Editors
All rights reserved. No part of this publication and DVD ROM should be reproduced, stored in a retrieval system, or transmitted
in any form or by any means: electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission
of the editors and the publisher.
This book has been published in good faith that the material provided by Contributors is original. Every effort is made to
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First Edition: 2009
ISBN 978-81-8448-470-0
Typeset at JPBMP typesetting unit
Printed at Ajanta Offset
Dedicated to
- My Respected Param Pujya Guru Sant Gurmeet Ram Rahim Singh Ji for his
blessings and motivation.
- My Respected Parents, teachers, my wife Dr Aruna Garg, son Abhishek and
daughter Anshul for their constant support and patience during all these days
of hard work.
- My dear friend Dr Amar Agarwal, a renowned International Ophthalmologist for
his constant support, guidance and expertise.
Ashok Garg
My family (Magali, my wife and Jorge, Guillermo and Magali my children) for the
time, comprehension and patience that they have had with me during all these years
of hard work.
Jose M Ruiz-Moreno
Sir Stewart Duke-Elder, my ideal and inspiration for ophthalmology.
B Shukla
My wife Joanne and my son Connor for providing me with their love, wisdom and
support throughout the years.
T Mark Johnson
- Yveric, Luc and Fanny Laure.
- Silvio Korol, who was not only a teacher but also an intellectual guide and a
friend.
Jerome Jean Bovet
Zena the light of my life.
Keiki R Mehta
My family without whose help it would not have been possible to do book.
Mahipal S Sachdev
To my son Valentin Aleksandar.
Bojan Pajic
My dear wife Dr Indira Dhull and my children Tushar and Chirag.
CS Dhull
To my parents Lucia and Justino, for their blessings and motivation. To my husband
Joao, a great partner at home and at work. To my children Arthur, Joao Neto
and Anna Paula, who have been giving me constant support and love.
Belquiz A Nassaralla
- My parents for everything.
- To Vini my Best friend.
Cyres K Mehta
Contributors
Ajay Aurora MS
Divector
Retina-Clinic
Dr. Chaudhary Eye Centre and
Laser Vision, 4802 Bharat Ram Road
24, Daryaganj,
New Delhi
India
Amar Agarwal MS FRCS FRC Ophth
Consultant
Dr. Agarwals Eye Hospital
19, Cathedral Road
Chennai-600086,
India
Amol Mhatre MS
Aditya Jyot Eye Hospital Pvt. Ltd
Plot No. 153, Road No.9
Major Parmeshwaran Road
Opp. SIWS College, Gate No.3
Wadala, Mumbai-400031
India
Arturo Perez-Arteaga MD
Medical Director
Centro Oftalmologico Tlalnepantla
Dr Perez - Arteaga Vallarta No. 42
Tlalnepantla, Centro,
Estado de Mexico
54000, Mexico
Ashok Garg MS PhD FIAO (Bel)
FRSM FAIMS ADM FICA
International and National Gold Medalist
Garg Eye Institute and Research Centre
235-Model Town,
Dabra Chowk
Hisar-125005
India
Ashok Sharma MS
Director
Dr. Ashok Sharmas Corneal Centre
SCO 833-834 (2nd Floor)
Sector 22-A,
Chandigarh-160022
India
Athiya Agarwal MD DO FRSH
Consultant
19, Cathedral Road
Chennai-600086, India
Belquiz A Nassaralla MD PhD
Consultant Ophthalmic Surgeon
Department of Cornea and
Refractive Surgery
Goiania Eye Institute, Goiania
GO, Brazil
B Shukla MS PhD MAMS FICS
Director of Research
RJN Institute of Ophthalmology
Chandra Bhawan, 1, Jhansi Road
Gwalior-474002, India
Binoo Nayer DOMS
Consultant Ophthalmologist
Hindu Rao Hospital
New Delhi, India
Bojan Pajic MD
Chief of the Cornea and Refractive
Surgery Department
Klinik Pallas Louis Giroud-
Str.20 4600, Olten
Switzerland
Boris Malyugin MD Phd
Chief of Department of Cataract and
Implant Surgery
Dy. Director General
S. Fyodorov Eye Microsurgery
Complex State Institution,
127486 Moscow
Beskudnikovsky blvd 59A
Russia
Brigitte Pajic-Eggspuhler MD
AugenZentrumPajic (AZP)
Research Institute
Titlisstrasse 44, 5734
Reinach, Switzerland
CS Dhull MS PhD FIAO
Professor and Head
Regional Eye Institute of
Ophthalmology
Pt. BD PGIMS, Rohtak-124001
India
Chandresh Baid MS
19, Cathedral Road
Chitra Ramamurthy MS
Director
The Eye Foundation
DB Road, Coimbatore-641002
India
Cristina Masini MD
Institute of Ophthalmology
University of Modena and Reggio Emilia
via del Pozzo 71-41100, Modena
Italy
Cyres K Mehta MS FSVH FAGE
Director and Consultant
Colaba Eye Hospital
Seaside, 147, Sahid Bhagat Singh
Road, Mumbai-400005
India
Daljit Singh MS DSC
Director
Dr Daljit Singhs Eye Hospital
57-Joshi Colony
Amritsar-143001, India
David F Chang MD
Clinical Professor of Ophthalmology
University of California
762, Altos Oaks Drive, Suite-1
Los Altos, CA 94024,
USA
Dhivya A MS
19, Cathedral Road
Chennai-600086,
India
Douglas W Morck MD
Department of Ophthalmology
The Eye Care Centre
2550, Willow St., Section G
Vancouver, BC V5Z3N9
Canada
viii
D Ramamurthy MS
Medical Director
The Eye Foundation
D.B. Road
Coimbatore-641002
India
D Shukla MS MAMS
Consultant
Vitreo Retina Unit
Aravind Eye Care System
Madurai (Tamil Nadu)
India
Earl Crouch MD
Eastern Virginia Medical School
880, Kemphsville Road
Suite 2500, Norflock, Virginia-23502
USA
Eric D Crouch MD
Assistant Professor of Pediatric
Ophthalmology
880, Kemphsville Road
Suite 2500, Norflock, Virginia-23502
USA
Eric D Donnenfeld MD FACS
Ophthalmic Consultants of Long Island
Suit 402
2000 North Village Ave.
Rockville Centre, NY 11570
USA
Essam El Toukhy MD FRCOPH
Assistant Professor of Ophthalmology
Cairo University
Debuty Director, National Eye Center,
Egypt
Gaurav Luthra MS
Director, Drishti Eye Centre
Dehradun, Uttrakhand
India
Gian Maria Cavallini MD
Director
Italy
Gina Chavez MD
Director
The Eye Care Centre
Canada
GK Das MD
UCMS and GTB Hospital
Shahdara, New Delhi
India
Harmit Kaur MS
Daljit Singh Eye Hospital
57, Joshi Colony
Amritsar-143001
India
Henry D Perry MD FACS
Chief of Corneal Services
Nassau University Medical Center
East Meadow, New York
2000 North Village Ave
Rockville Centre, NY 11570
USA
Hsi-Kung Kuo MD
Department of Ophthamology
Chang Gung Memorial Hospital
Kaohsiung Medical Center
123, Ta-PEi Road, Niao-Sung
Hsien, Kaohsiung, Hsien, 883
Taiwan, ROC
Ian Bell MD
NY Eye Institute, New York
USA
Indu R Singh MS
57, Joshi Colony
Amritsar-143001
India
Jaroslaw Kulinski MD
Department of Pediatric
Ophthalmology, Hertza 9, 04-603
Warsaw
Poland
Jasna Ljubic MD
General Hospital
Department of Physical Medicine &
Rehabilitation, 16000 Leskovac
Serbia
Javier A Montero MD
Pio del Rio Hortega University
Hospital, Ophthalmology Unit
C/Rondilla de Sta Teresa 9, Valladolid
47010,
Spain
Jerome Jean Bovet MD
Consultant Ophthalmic Surgeon FMH
Clinique de Loeil
15, Avenue Du Bois-de-law-Chapelle
CH-1213, Onex, Switzerland
Joo J Nassaralla Jr MD PhD
Rua L n
o
53 # 12
o
andar, Setro Oeste
Goiania, Goias
Brazil, ZC : 74.120-050
John D Sheppard MD MMSc
Associate Professor of Ophthalmology
Microbiology and Immunology
Clinical Director, Thomas R. Lee
Centre for Ocular Pharmacology
Norfolk, Virginia 23501
USA
Jose M Ruiz-Moreno MD PhD
Albacete Medical School, University of
Castilla La Mancha
Avendia de Almansa, 14 02006,
ALBACETE
Spain
Kanupriya Mhatre MS
India
Karol Stasiak MS
Department of Pediatric
Ophthalmology, Hertza 9, 04-603
Warsaw, Poland
Keiki R Mehta MS DO FRSH FIOS
Colaba Eye Hospital
Seaside, 147, Shahid Bhagat Singh
Road,
Mumbai-400005
India
Kiranjit Singh MS
57, Joshi Colony
Amritsar-143001
India
KK Bhalla MS
57, Joshi Colony
ix
Leonardo Toledo Netto MD
Medical Director
Olho.com Eye Clinic
Department of Cornea and Cataract
Surgery, Aparecida de Goiania
GO, Brazil
Luca Campi MD
Italy
M Edward Wilson MD
Storm Eye Institute
Miles Center for Pediatric
Ophthalmology
Medical University of South Carolina
Charleston, SC 29425
USA
Mahipal S Sachdev MD
Centre for Sight, B-5/24, Safdarjung
Enclave
Marek E Prost MD
Professor of Ophthalmology and
Director Center for Pediatric
Ophthalmology Hertza 9, 04-603
Warsaw, Poland
Matteo Piovella MD
Director
CMA Centro Microchirurgia
Ambulatoriale
Via Donizetti 24-20052
Monza, Italy
Neeraj Sanduja MD
Director
Delhi Retina Centre,
4802 Bharat Ram Road
24, Daryaganj, New Delhi
India
NR Biswas MD DM
Professor of Ocular Pharmacology
Dr. RP Center for Ophthalmic Sciences
AIIMS, Ansari Nagar
New Delhi, India
P Bhasin MS
Director
RJN Ophthalmic Institute
Gwalior
India
P Dutta MS
Director
Dutta Eye Clinic, Gwalior
India
Pei-Chang Wu MD
Chang Gung Memorial Hospita-
Kaohsiung Medical Center
123, Ta-PEi Road, Niao-Sung
Hsien, Kaohsiung, Hsein, 883
Taiwan, ROC
Quresh B Maskati MD
Maskati Eye Clinic
Mumbai, India
Rajni Sharma MD
Ex-Senior Resident
Department of Pediatrics
AIIMS, Ansari Nagar
Rajpal Vohra MD
Dr Rajendra Prasad for Ophthalmology
All India Institute of Medical Sciences
New Delhi, India
Rania Abdel Salam MD
Lecturer of Ophthalmology
Cairo University,
National Eye Center, Egypt
Ranjit Singh MS
Director
57, Joshi Colony
Ritesh Gupta MD
Senior Resident
Vitreo-Retina,
Trauma and ROP Service
Dr. RP Centre for Ophthalmic Sciences
AIIMS, New Delhi-110029, India
Rene Cano-Hidalgo MD
Chairman
Conde De Valenciana
Vitreous and Retina Department
Professor of Ophthamology
National Institute of Mexico (UNAM)
Mexico
Richard Mathias MD
The Eye Care Centre
2550, Willow St, Section G
Canada
Ritika Sachdev MS
Sr. Resident
Dr. RP Centre for Ophthalmic Sciences
AIIMS, Ansari Nagar
Rupal H Trivedi MD MSCR
MUSC - Storm Eye Institute
167 Ashley Ave
Charleston, SC 29425, USA
Rupesh V Agrawal MD
Consultant
Comprehensive Ophthalmology
Uveitis and Ocular Trauma
LV Prasad Eye Institute
Kallam Anjil Reddy Campus
Banjara Hills, Hyderabad-500034
India
S Natarajan MS
India
Satish Desai MS
Shri Ganapati Netralaya
Jalna (India)
Saumil Sheth MS
Plot No. 153, Road No. 9
Opp. SIWS College, Gate No. 3
India
Shui Lee MD FRCS
Central Square Unit
255-4231 Hazelbridge
Way Richmond
BC, V6X-3L7
Canada
Simon P Holland MB FRCSC FRCOph
Clinical Professor
The Eye Care Centre
Canada
Simone Pelloni MD
Italy
x
Soosan Jacob MS
19, Cathedral Road
Chennai-600086,
India
Sumit Sachdeva MS
Assistant Professor of Ophthalmology
RIO, PGIMS
Rohtak, India
Sunil Vasani MS
Eye-r-Us Clinic
Gowalia tank, Mumbai-400036
India
Sunita Agarwal MS DO PSVH
19, Cathedral Road
Supriya Dabir MS
India
Syed Asghar Hussain MS
India
T Mark Johnson MD FRCS
Consultant Vitreo Retinal Surgeon
National Retina Institute
Suite 101, 5530 Wisconsin Ave
Chevy Chase 20815, USA
Tracy L Lee MD
The Eye Care Centre
Vancouver, BC V5Z3N9, Canada
Vandana Jain MD
Plot No. 153, Road No. 9
Opp. SIWS College, Gate No. 3
India
Viney Gupta MD
Assistant Professor of Ophthamology
Dr RP Center for Ophthalmic Sciences
AIIMS, Ansari Nagar
Yog Raj Sharma MD
Dr. R.P. Center for Ophthalmic Sciences
AIIMS, Ansari Nagar
New Delhi -110029, India
Yumi G Ohashi B.Sc
The Eye Care Centre
Vancouver, BC V5Z3N9, Canada
Yuri Flores MD
Consultant
Vitreoretina Surgeon
Centro Oftalmologico Tlalnepantla
Dr. Perez - Arteaga Vallarta no.42
Tlalnepantla, Centro,
Estado de Mexico 54000,
Mexico
Foreword
I was called to examine a man in the hospital emergency room who had been injured
in a motor vehicle accident. I was told the patient had an eye that was red and swollen.
There was urgency in the voice of the consulting doctor, so I hurried to the hospital to
examine this patient. After I arrived, I found the patient to have no evidence of a sight
threatening problem. But, this man had definite signs of a skull fracture, open fracture
of the right femur and probable rib fractures. And I was the first specialist called to see
this patient.
This experience reminded me of how serious ocular trauma can be to patients, their
families and even our medical colleagues outside of Ophthalmology. The impact of an
accident that could lead to loss of visual function is frightening.
Fortunately, the evaluation and treatment of ocular injuries has improved significantly. Newer imaging systems
and other diagnostic equipment provide better methods for detecting the extent of damage to the eye and
adnexa. Advancements in microsurgical technology give us new equipment needed to repair a wide variety
of ocular injuries.
This important textbook, edited by Professor Garg, offers a step by step update to modern evaluation
and treatment of ocular and adnexal trauma. Since all injury cases are unpredictable by nature,
having a reliable reference to access information on the latest in diagnostic and surgical repair
is valuable to all medical care professionals involved in the care of patients who are suddenly
afflicted with traumatic eye disease.
Congratulations to Professor Garg and his contributing editors who have provided us with a
well organized, thorough and practical guide to handle traumatic ocular conditions.
Prof. Bruce Wallace MD
Medical Director
Wallace Eye Surgery
4110 Parliament Drive
Alexandria, LA 71303 (USA)
Tel.: 318-448-4488
www.wallaceeyesurgery.com
Preface
Ocular Trauma is an important and vast subject and has assumed greater significance in this present era of
Modern Technology when greater industrial and vehicular revolution have taken place. As a result of this incidence,
ocular trauma has increased sharply and now it is one of the leading causes of monocular blindness specially
in children and in young generation. Early and effective treatment of ocular trauma is mandatory to achieve
best possible outcome thus decreasing blindness. With latest technologies, equipment and techniques, it is
possible to manage traumatized eyes in a better way. Very few International quality books are available on
this important subject for the Ophthalmologists.
Present book has been conceived and written to provide latest uptodate information on this vast subject.
56 chapters of this book have been written by International experts on this field covering both anterior and
posterior segment ocular trauma. We have tried to cover all clinical aspects of ocular trauma in both segments.
Accompanying video DVD ROM shows surgical skills by International Masters for Ocular Trauma Management.
We are grateful to Shri Jitendar P Vij (CEO), Mr. Tarun Duneja (Director Publishing) and all staff members
of M/s Jaypee Brothers Medical Publishers Pvt. Ltd. who took extraordinary efforts in the preparation of this
book.
We are sure that present book shall provide deep insight into state of art ocular trauma management in
a simplified and comprehensive manner. This book shall be an integral part of shelf of every Ophthalmologist
clinical chamber who have to encounter ocular trauma cases in their professional practice.
Editors
Contents
SECTION I
PRELIMINARY AND BASIC CONSIDERATIONS
IN OCULAR TRAUMA
1. Epidemiology and New Classification of Ocular Trauma ............................................................. 3
Joo J Nassaralla Jr, Belquiz A Nassaralla (Brazil)
2. New Classification of Ocular Trauma.......................................................................................... 7
B Shukla, D Shukla (India)
3. Clinical Evaluation of Ocular Trauma....................................................................................... 10
B Shukla (India)
4. Evaluation and Initial Management of a Patient with Ocular Trauma ....................................... 13
Rupesh V Agrawal (India)
SECTION II
ANTERIOR SEGMENT OCULAR TRAUMA
5. Role of Ultrasound Biomicroscopy in Evaluation of the Anterior
Segment in Closed Globe Injuries ........................................................................................... 25
Ritika Sachdev, Mahipal S Sachdev, (India)
6. Management of Eyelid Inju0ries ............................................................................................... 28
Rania Abdel Salam, Essam El Toukhy (Egypt)
7. Management of Lacrimal Injuries ............................................................................................. 33
8. Hyphema ................................................................................................................................. 35
Earl Crouch, Eric Crouch (USA)
9. Management of Corneal Injuries .............................................................................................. 41
Ashok Sharma (India)
10. Chemical Injuries of the Eye ................................................................................................... 50
Quresh B Maskati (India)
11. Injuries of the Eye due to Physical Agents (Thermal, Ultrasonic and Electrical Injuries) .......... 55
12. Radiational Injuries to the Eye ................................................................................................ 59
13. Traumatic Angle Recession GlaucomaL An Overview............................................................... 64
Cyres K Mehta, Keiki R Mehta (India)
14. Management of Blunt Trauma of Anterior Segment ................................................................. 67
15. Management of Traumatic Cataract .......................................................................................... 74
Rupesh V Agrawal, Satish Desai (India)
16. Management of Traumatic Luxation of the Crystalline Lens ..................................................... 80
Arturo Prez-Arteaga, Yuri Flores (Mexico)
xvi
17. Traumatic Cataract in Children ................................................................................................ 86
Rupal H Trivedi, M Edward Wilson (USA)
18. Scleral Fixated IOL in Trauma ................................................................................................. 94
19. Iris Trauma ............................................................................................................................ 100
20. Post-traumatic Strabismus ...................................................................................................... 106
B Shukla, P Bhasin (India)
21. Management of Orbital Trauma and Fractures ........................................................................ 108
22. Management of Anterior Segment Trauma: An Update........................................................... 125
CS Dhull, Sumit Sachdeva (India)
23. Glued IOL ............................................................................................................................. 132
Amar Agarwal, Dhivya A, Soosan Jacob, Athiya Agarwal, Chandresh Baid, Ashok Garg (India)
SECTION III
POSTERIOR SEGMENT OCULAR TRAUMA
24. Management of Traumatic Hemorrhages to the Posterior Segment ......................................... 139
Javier A Montero, Jose M Ruiz-Moreno (Spain)
25. Traumatic Retinal Detachments ............................................................................................. 149
Neeraj Sanduja, Ajay Aurora, Gaurav Luthra (India)
26. Retained IOFB....................................................................................................................... 155
27. Penetrating Posterior Segment Trauma ................................................................................... 160
T Mark Johnson (USA)
28. Traumatic Retinopathies......................................................................................................... 167
Scott Pfahler, T Mark Johnson (USA)
29. Management of Endophthalmitis ............................................................................................ 174
Pei-Chang Wu, Hsi-Kung Kuo (Taiwan)
30. Management of Pediatric Ocular Trauma ................................................................................ 181
Yog Raj Sharma, Ritesh Gupta, Rajni Sharma (India)
31. Management of Blunt Retinal Trauma .................................................................................... 189
32. Applications of Stem Cell Therapy in Ophthalmology............................................................ 200
Rajpal Vohra (India)
33. Primary Globe Repair ............................................................................................................ 214
SECTION IV
IATROGENIC OCULAR TRAUMA AND ITS
COMPLICATIONS MANAGEMENT
34. Management of Iatrogenic Inflammation of the Eye ............................................................... 223
NR Biswas, GK Das, Viney Gupta (India)
35. Management of Postrefractive Keratitis ................................................................................... 229
Eric D Donnenfeld (USA)
xvii
36. Optimized NSAIDs and Antibacterial Prophylaxis in Cataract Surgery ................................... 232
Ashok Garg (India), Ian Bell (USA)
37. Optimizing Visual Outcomes with NSAIDs Therapy in Cataract and Refractive Surgery ......... 235
Eric D Donnenfeld, Henry D Perry (USA)
38. Management of Cystoid Macular Edema ................................................................................ 242
Arturo Prez-Arteaga, Ren Cano-Hidalgo (Mexico)
39. Managing Intraoperative Floppy Iris Syndrome ...................................................................... 250
David F Chang (USA)
40. Toxic Anterior Segment Syndrome......................................................................................... 254
Simon P Holland, Douglas W Morck, Richard Mathias,
Tracy L Lee, Gina Chavez, Yumi G Ohashi (Canada)
41. Small Pupil Phaco: An Innovative Technique ......................................................................... 259
Boris Malyugin (USA)
SECTION V
CURRENT CONCEPTS AND RECENT ADVANCES IN
MANAGEMENT OF OCULAR TRAUMA
42. Trauma after Refractive Surgery ............................................................................................. 269
D Ramamurthy, Chitra Ramamurthy (India)
43. Complication and Contusion after Phakic IOL ....................................................................... 273
Jerome Jean Bovet (Switzerland)
44. Management of Corneal Lacerations....................................................................................... 279
Shui Lee (Canada)
45. Sports Injuries in Eye ............................................................................................................ 283
B Shukla, Binoo Nayar (India)
46. Management of Travel Eye Injuries ........................................................................................ 286
Leonardo Toledo Netto, Belquiz A Nassaralla (Brazil)
47. Ocular Injuries after Vehicular Accident and Possible Prevention........................................... 290
Bojan Pajic, Brigitte Pajic-Eggspuehler, Jasna Ljubic (Switzerland)
48. Bottle Cork Injury to the Eye................................................................................................ 296
Gian Maria Cavallini, Matteo Forlini, Cristina Masini, Luca Campi, Simone Pelloni (Italy)
49. Ocular War Injuries................................................................................................................ 300
Jaroslaw Kulinski, Karol Stasiak, Marek E Prost (Poland)
50. Trauma of Anterior Eye Segment: An Update ........................................................................ 311
Boris Malyugin (Russia)
51. Management of Ocular Trauma with Plasma (Fugo) Knife ...................................................... 319
Ranjit Singh, Indu R Singh, Kiranjit Singh, Harmit Kaur, KK Bhalla, Daljit Singh (India)
52. Chandelier Illumination and Bimanual Vitrectomy Used to Remove a Dislocated IOL ........... 328
Amar Agarwal, Soosan Jacob, Athiya Agarwal, Sunita Agarwal, Ashok Garg (India)
53. Principles and Management of Ocular Trauma........................................................................ 331
Syed Asghar Hussain, Amol Mhatre, Kanupriya Mhatre, Supriya Dabir,
Saumil Sheth, Vandana Jain, S Natarajan (India)
54. Eyelid Injuries and Reconstruction: An Update...................................................................... 345
Quresh Maskati, Sunil Vasani (India)
55. Prevention of Ocular Trauma ................................................................................................. 349
B Shukla, P Dutta (India)
56. Endophthalmitis Preventiion Strategies .................................................................................. 352
John D Sheppard (USA)
Index ................................................................................................................................................. 355
Preliminary and
Basic Considerations in
Ocular Trauma
C H A P T E R
1
Epidemiology and
New Classification of
Ocular Trauma
Joo J Nassaralla Jr, Belquiz A Nassaralla (Brazil)
Introduction
An injury to the eye or its surrounding tissues is the
most common cause for attendance at an eye hospital
emergency department. The extent of trauma may
range from simple superficial injuries to devastating
penetrating injuries of the eyelids, lacrimal system, and
globe. The surgical management of such injuries is
directed primarily at the restoration of normal ocular
anatomy; the ultimate goal is to prevent secondary
complications and maximize the patients visual
prognosis. Dramatic improvements in the surgical
management of ocular trauma have evolved over the
past two decades. However, persistent inadequacy in
the standardized documentation of eye injury morbi-
dity and treatment outcome limits the development
and widespread introduction of techniques for preven-
ting and improving the prognosis of serious eye
trauma.
Professional associations like the International
Society of Ocular Trauma (ISOT), and the United
States Eye Injury Registry (USEIR), have been formed
to promote research, elaborate epidemiologic
investigations, highlighting preventable sources of
injury, emerging patterns of trauma, treatment
outcomes and disseminate its results. The USEIR is
presently working with the ISOT to establish the World
Eye Injury Registry (WEIR). International registries
have been established or are in start-up phase in Brazil,
British Armed Forces, Bolivia, Canada, China,
Colombia, Croatia, Finland, India, Italy, Germany,
Greece, Hungary, Israel, Kenya, Korea, Lithuania,
Mexico, New Zealand, Portugal, Romania, Saudi
Arabia, Singapore, Slovakia, Slovenia, South Africa,
Spain, Switzerl and, Turkey, Venezuel a, West
Indies(Trinidad), Yugoslavia, Zimbabwe with assistance
from the United States Eye Injury Registry.
1
Unfortunately, the lack of an unambiguous
common language remains a major limiting factor in
effectively sharing eye injury information. Without a
standardized terminology of eye injury types, it is
impossible to design projects like the USEIR or the
WEIR; clinical trials in the field of ocular trauma cannot
be planned; and the communication between
ophthalmologists remains ambiguous.
1,2
So, a
standardized terminology for eye injury has been
developed by the USEIR based on extensive
experience and repeated reviews by international
ophthalmic audiences. By always using the entire globe
as the tissue of reference, classification is unambiguous,
consistent, and simple. It provides definitions for the
commonly used eye trauma terms within the
framework of a comprehensive system.
1
Epidemiology
Eye injuries are a major and under recognized cause
of disabling

ocular morbidity that especially affect the
young. The public

health importance of such ocular
trauma is undeniable. Injuries

generate a significant
and often unnecessary toll in terms of

medical care,
human suffering, long-term disability, productivity

loss,
rehabilitation services, and socioeconomic cost.
1-3
Globally, more than 500.000 blinding injuries
occur every

year. Approximately 1.6 million people
are blind owing to ocular

trauma, 2.3 million are
bilaterally visually impaired, and 19

million have
unilateral visual loss.
3,4
Every year, approximately 2
million eye injuries occur in the United States, of which,
more than 40 thousand results in permanent visual
impairment.
6,7
Prior studies in which the incidence of
eye injury has been examined have produced varied
results, in part because of study design differences.
8-
13
When considering eye injuries requiring hospital
admission, rates have ranged from 8 to 57 per
100.000.
8-13
Despite the heterogeneity of results, these
studies provide important information regarding the
burden of eye injury. However, they have all been
limited to a single year or narrow time frame making
it difficult to determine trends in injury rates over time.
In the United States, a population-based study
reported a prevalence rate of 19.8% and an average
annual incidence rate of 3.1 per 1000 population.
14
4
In a more recent study from 1992 through 2002, the
incidence of eye injury declined overall and the
estimated rate of eye injury ranged from 8.2 to 13.0
per 1000 population.
5
Worldwide, ocular trauma is a leading cause of no
congenital monocular blindness among

children.
16-20
Children are disproportionately affected by ocular
injuries. In the United States, a population-based study
reported

an annual incidence of ocular trauma in
children of 15.2 per 100.000.
18
In general, males are
more frequently reported to have eye injuries

than
females.
17-24
Results varied across studies regarding

the
age-specific frequency of eye injuries
17-26
with some
reporting

a higher incidence in older children and others
in younger children.

A study conducted among
Brazilian children found that the group

aged 0 to 5
years was at greatest risk, regardless of sex, and

that
among those older than 5 years, eye injuries were
more

frequent in boys.
26
Although the overall

financial cost derived from
ocular injuries can only be estimated,

direct and indirect
costs combined run into hundreds of millions

of dollars
per year. Developing countries carry the heaviest
burden, and they are the least able to afford the costs.
8
Domestic accidents (40%), industrials (13%), and
street/highway accidents (13%) are the most common
circumstances in which ocular injury occurs, (Fig. 1.1).
Eye injuries incurred during athletic activity (13%) are
becoming more common with the increasing popularity
of indoor court games. A recent survey found
racquetball to exceed other sports in generating ocular
injuries, followed by tennis, baseball, basketball, and
soccer.
1
Fig. 1.1: Places of eye injury
1
The most common sources of eye injuries are blunt
object (31%), sharp object (18%), and motor vehicle
crash (9%), (Fig. 1.2).
While the incidence of ocular trauma has been
described in the United States,
6,8,12,15
United Kingdom,
10
Sweden,
27
and Greece,
28
it has not been well studied
in other industrialized countries, like Italy, where clinical
research on ocular trauma is limited to the pediatric
population and sportsmen.
22,29,30
Available information
regarding the distribution and magnitude

of ocular
trauma in developing countries is very scarce, and

the
existing data are difficult to interpret because reporting
is extremely poor and especially because of the
completely different

settings of the occurrence of ocular
trauma.
3
Among other factors,

underreporting and lack
of standardized forms and national integrated

databases
make assessment of the current picture and compari-
sons

within and across countries practically impossible.
2
In addition,

developing countries often lack adequate
infrastructure for

persons with eye injuries to reach a
primary care center, when

one exists, and the lack of
awareness of preventive measures

and/or immediate
actions increases the risk for complications

and
consequent visual disability and blindness.
8
From a
public health and injury prevention perspective, current
information on eye injuries rates is needed to develop
effective plans for disseminating eye injury prevention
materials to the public and to earmark adequate
funding for these initiatives.
1,2
New Classification
The new classification of ocular trauma has been
endorsed by the Board of Directors of the International
Society of Ocular Trauma, the United States Eye Injury
Registry, the Hungarian Eye Injury Registry, the Vitreous
Society, the Retina Society, and the American Academy
of Ophthal mol ogy. This cl assification system
categorizes ocular injuries at the time of initial
examination. It is designed to promote the use of
standard terminology and assessment, with applications
to clinical management and research studies regarding
eye injuries (Fig. 1.3).
1,2,32
Fig. 1.2: Sources of eye injury
1
5
Epidemiology and New Classification of Ocular Trauma
Fig. 1.3: The proposed new ocular traumatology system.
1
The green boxes show the diagnoses that are used in
clinical practice
The new ocular trauma terminology system.
1,2,31,32
provides definitions for the commonly used eye trauma
terms as follows:
1. EyewallFor clinical and practical purposes, the
term eyewall must be restricted to the rigid
structures of the sclera and cornea.
2. Closed-globe injuryThe eyewall does not have
a full-thickness wound. Either there is no corneal
or scleral wound at all (contusion) or is it only partial
thickness (lamellar laceration).
3. Open-globe injuryThe eyewall has a full-thickness
wound. The cornea and/or sclera sustained a
through-through injury; depending on the inciting
objects characteristics and the injurys circum-
stances, ruptures and lacerations are distinguished;
the choroid and the retina may be intact, prolapsed
or damaged.
4. RuptureFull-thickness wound of the eyewall,
caused by a blunt object; the impact results in
momentary increase of the intraocular pressure.
The eyewall gives way at its weakest point (at the
impact site or elsewhere; example: an old cataract
wound dehisces even though the impact occurred
elsewhere); the actual wound is produced by an
inside-out mechanism.
5. LacerationFull-thickness wound of the eyewall,
usually caused by a sharp object; the wound occurs
at the impact site by an outside-in mechanism.
6. Penetrating injurySingle laceration of the eyewall,
usually caused by a sharp object. No exit wound
has occurred; if more than one entrance wound
is present, each must have been caused by a
different agent.
7. Intraocular foreign body injury (IOFB)Retained
foreign object(s) causing entrance laceration(s). An
IOFB is technically a penetrating injury but is
grouped separately because of different clinical
impl ications (treatment modal ity, timing,
endophthalmitis rate, etc.).
8. Perforating injuryTwo full-thickness lacerations
(entrance and exit) of the eyewall, usually caused
by a sharp object or missile. The two wounds must
have been caused by the same agent.
Participation of individual treating ophthalmologists
is critical to the development of comprehensive
epidemiologic eye injury data. Documentation of each
serious eye injury is important work, and, through this
cooperative effort, will ultimately benefit all patients
and physicians. It is expected that this system eventually
will become the standardized international language
of ocular trauma terminology, improving accuracy in
both clinical practice and research, irrespective of
geographic origin.
References
1. United States Eye Injury Registry. Eye trauma
epidemiology and prevention. Available at: http://
www.useironline.org/prevention.htm. Accessed July 6,
2008.
2. Worl d Eye Injury Registry. Avail abl e at: http://
www.weironline.org/prevention.htm. Accessed July 6,
2008.
3. Serrano JC, Chalela P, Arias JD: Epidemiology of
Childhood Ocular Trauma in a Northeastern Colombian
Region. Arch Ophthalmol 2003;121:1439-1445.
4. Pizzarello LD. Ocular trauma: time for action. Ophthalmic
Epidemiol 1998;5:115-116.
5. Negrel AD, Thylefors B. The global impact of eye injuries.
Ophthalmic Epidemiol 1998;5:143-169.
6. McGwin G, Xie A, Owsley C: The rate of eye injury in
the United States. Arch Ophthalmol 2005;123:970-976.
7. Mieler W: Overview of ocular trauma. In Principles and
Practice of Ophthalmology. 2nd edition. Edited by: Albert
D, Jakobiec F. Phil adel phia, WB Saunders Co.
2001;5179.
8. Tielsch JM, Parver L, Shankar B: Time trends in the
incidence of hospital ized ocul ar trauma. Arch
Ophthalmol 1989; 107:519-523.
9. McCarty CA, Fu CL, Taylor HR: Epidemiology of ocular
trauma in Australia. Ophthalmology 1999; 106:1847-
1852.
10. Desai P, MacEwen CJ, Baines P, Minassian DC: Incidence
of cases of ocular trauma admitted to hospital and
incidence of blinding outcome. Br J Ophthalmol 1996;
80:592-596.
11. Klopfer J, Tielsch JM, Vitale S, See LC, Canner JK: Ocular
trauma in the United States: eye injuries resulting in
6
hospitalization, 1984 through 1987. Arch Ophthalmol
1992; 110:838-842.
12. Karlson TA, Klein BE: The incidence of acute hospital-
treated eye injuries. Arch Ophthalmol 1986; 104:1473-
1476.
13. Wong TY, Tielsch JM: A population-based study on the
incidence of severe ocular trauma in Singapore. Am J
Ophthalmol 1999; 128:345-351.
14. Wong TY, Klein BE, Klein R: The prevalence and 5-year
incidence of ocular trauma. The Beaver Dam Eye Study.
Ophthalmology 2000; 107:2196-2202.
15. McGwin GJr, Hall TA, Xie A, Owsley C: Trends in Eye
Injury in the United States, 19922001.
16. MacEwen CJ, Baines PS, Desai P. Eye injuries in children:
the current picture. Br J Ophthalmol 1999;83:933-936.
17. Jandeck C, Kellner U, Bornfeld N, Foerster MH. Open
globe injuries in children. Graefes Arch Clin Exp
Ophthalmol 2000;238:420-426.
18. Strahlman E, Elman M, Daub E, Baker S. Cause of
pediatric eye injuries: a population-based study. Arch
Ophthalmol 1990;108:603-606.
19. Takvam JA, Midelfart A. Survey of eye injuries in
Norwegian children. Acta Ophthalmol (Copenh) 1993;
71:500-505.
20. Cascairo MA, Mazow ML, Prager TC. Pediatric ocular
trauma: a retrospective survey. J Pediatr Ophthalmol
Strabismus 1994;31:312-317.
21. MacEwen CJ. Ocular injuries. J R Coll Surg Edinb.
1999;44:317-323. Invest Ophthalmol Vis Sci 2006;
47:521-527.
22. Cillino S, Casuccio A, Di Pace F, Pillitteri F, Cillino G: A
five-year retrospective study of the epidemiological
characteristics and visual outcomes of patients
hospitalized for ocular trauma in a Mediterranean area.
BMC Ophthalmology 2008; 8:6
23. May DR, Kuhn FP, Morris RW, et al. The epidemiology
of serious eye injuries from the United States Eye Injury
Registry. Graefes Arch Cl in Exp Ophthal mol
2000;238:153-157.
24. Nelson LB, Wilson TW, Jeffers JB. Eye injuries in
childhood: demography, etiology, and prevention.
Pediatrics 1989;84:438-441.
25. Rapoport I, Romem M, Kinek M, et al. Eye injuries in
children in Israel: a nationwide collaborative study. Arch
Ophthalmol 1990;108:376-379.
26. Moreira CA Jr, Debert-Ribeiro M, Bel for t R Jr.
Epidemiological study of eye injuries in Brazilian children.
Arch Ophthalmol 1988;106:781-784.
27. Blomdahl S, Norell S: Perforating eye injury in the
Stockholm population. Acta Ophthalmologica 1984;
62:378-390.
28. Mela EK, Dvorak GJ, Mantzouranis GA, Giakoumis AP,
Blatsios G, Andrikopoulos GK, Gartaganis SP: Ocular
trauma in a Greek population: review of 899 cases
resulting in hospitalization. Ophthalmic Epidemiol 2005;
12:185-190.
29. Capoferri C, Martorina M, Menga M, Sirianni P: Eye
injuries from traditional sports in Aosta Val l ey.
Ophthalmologica 1994; 208:15-16.
30. Bianco M, Vaiano AS, Colella F, Coccimiglio F, Moscetti
M, Palmieri V, Focosi F, Zeppilli P, Vinger PF: Ocular
complications of boxing. Br J Sports Med 2005; 39:70-
74.
31. International Society of Ocular Trauma at: http://
www.isotonline.org. Accessed July 6, 2008.
32. Kuhn

F, Morris R, Witherspoon CD, Heimann K, Jeffers
JB and Treister G. A standardized classification of ocular
trauma. Ophthalmology 1996;103(2):240-243.
C H A P T E R
2
New Classification of
Ocular Trauma
B Shukla, D Shukla (India)
Introduction
Classification is the basis of understanding a subject.
Duke-Elder has broadly divided ocular trauma
(Injuries) into mechanical and non-mechanical.
1
He
has also divided them into several types depending
on the environment such as industrial, agricultural,
travel, etc.
2
Several other authors have also classified
ocular trauma is different ways.
3,4
However, one
problem with all these classification has been the
variability of terminology which has been used by
different authors in different ways like laceration,
penetration, perforation, blunt, sharp, etc. In absence
of standardization of terminology the literature has
become confusing and non-comparable. In a
l andmark paper Kuhn et al standardized the
terminology in ocular trauma and gave a standardized
classification of ocular trauma which has been
universally accepted.
5
Other authors have further
elaborated this and gave more details which are useful
for prognosis.
6,7
Kuhn et al have basically divided eye injuries into
closed globe and open globe types, the tissue of
reference being the cornea and sclera which they
termed as eyewall.
5
Closed globe injuries include
contusion in which there is no wound of cornea or
sclera. In lamellar laceration there is a partial thickness
wound in cornea or scleara. In either case there is
no full thickness wound. In open globe injury there
is always a full thickness wound. This can occur from
a blunt object with an inside out mechanism and is
termed rupture. It can also occur by sharp objects
by an outside in mechanism and is termed laceration.
Laceration includes penetration (single laceration with
one wound of entry), perforation (double laceration
with one wound of entry and one wound of exit)
and intra-ocular foreign bodies with single entrance
laceration. Figure 2.1 explains this classification.
The above classification is ideal for mechanical
injuries. However, ocular trauma includes many non-
mechanical injuries like chemical, thermal, traditional,
and others. These injuries can not be classified by the
above classification. For them better classification are
available, e.g. Duas classification for ocular surface
burns.
8
Secondly the ocular adnexa including the lids,
lacrimal apparatus, conjunctiva and orbit are parts of
ocular trauma. The above classification has not taken
account of this category.
Lastly it may be mentioned that any subject can
be viewed from many angles and thus can have more
than one classifications on the parameter chosen as
the basis of classification and each of the classifications
has its val idity. Thus uveitis can be divided
anatomically into anterior, intermediate, posterior,
and pan uveitis. From pathological point of view it
could be granulomatous or non-granulomatous;
clinically it could be acute, chronic or recurrent and
etiologically it could be infective, allergic, toxic or
traumatic.
9
Similarly keratoplasty can be lamellar or
penetrating or mushroom from depth consideration.
It can be partial, sub-total or total from diameter
consideration. From objective point of view it could
be optical, therapeutic, cosmetic or preparatory.
10
Considering the above points it was thought to
develop a more comprehensive type of classification
of ocul ar trauma which is being presented in
Fig. 2.2.
Fig. 2.1: Classification of ocular trauma after Kuhn et al
8
Fig. 2.2: General classification of ocular trauma
Ocular trauma is first divided into local, associational
and environmental. In local the injury is limited to
eyeball and ocular adnexa; in associational it is
associated with head injury (affecting visual pathway)
or face as in blast injuries or with many organs of the
body known as polytrauma. Here the life of the patient
assumes primary importance. As the name suggests
the environmental injuries depend on the environment
and could be congenital, industrial, agricultural, travel
(RTA*) criminal or casual (usually domestic). The local
injuries are further divided into mechanical and non-
mechanical types. The latter includes the chemical,
thermal, radiational, electrical, ultrasonic and
barometric. The mechanical injuries are divided into
adnexal and global. The former include the lids,
lacrimal apparatus, orbit and conjunctiva. Globe
injuries are again divided into structural (anatomical)
and pathological. The former include the anterior
segment and posterior segment injuries with the details
of structures included in each group. The pathological
group represents the current classification suggested
by Kuhn et al.
5
Though open globe injury includes
IOFB (intra-ocular foreign bodies) but the closed globe
group does not include EOFB (extra-ocular foreign
bodies) in Kuhns classification. The author has
included them firstly because they are extremely
common: they are extremely painful and lastly if they
are in center they can cause extreme loss of vision.
In this group the author has also included IMFB
(intra-mural foreign bodies). If the tissues of reference
is cornea and sclera (eyewall) what is within it will be
intra-ocular and what is outside it will be extra-ocular.
But whatever is within the coats of eyewall is neither
intra-ocular nor extra-ocular. The author has coined
this word EMFB quite some time back and it has
been used at other places. This group also includes
dislocations which may be anterior, posterior, and
inferior (rarely they could be superior). In the
pathological group in addition to closed and open globe
there can also be destructive globe injuries which
includes traumatic enucleation, evisceration and a full
thickness laceration which covers one third of globe
circumference or more. In these cases chances of
functional recovery are absent.
The subject of ocular trauma is very wide and
variable and perhaps no classification can adequately
encompass all the entities included in ocular trauma.
Nevertheless in our present state of knowledge it
address some of points lacking in the existing classi-
fication and is fairly comprehensive. It may be stated
that this classification is not totally exclusive and different
combination of different categories are possible.
Acknowledgement: I wish to express may gratitude to
the Ocular Trauma Society of India to encourage me
in formulating this classification and accepting it after
giving useful suggestions.
* Road Traffic Accident.
9
New Classification of Ocular Trauma
References
1. Duke-Elder S. System of Ophthalmology, Vol XIV,
Injuries, Part 1, Henry Kimpton, London, 1972, P. ix.
2. Ibid. p.7-60.
3. Lambah P : Trans Ophthal Soc, Adult eye injuries at
Wolverhampton, 1968; 88:66173.
4. Roper Hall M : Brit J Ophthal, 1954;38:65
5. Kuhn F, Morris R, Witherspoon CD et al : Ophthalmology,
1996;103:240-43.
6. Pieramici DJ, Sternberg P, Aaberg TM et al : Amer J
Ophthal, 1997;123:820-31.
7. Raja SC, Pieramici DJ : Classification of Ocular Trauma,
In : Kuhn F, Pieramici DJ, Editor. Ocular Trauma,
Principles & Practice, Thieme Publication, New York,
2002. P. 6-8.
8. Dua HS, King AJ, Joseph A: A new classification of
surface burns, Br J Ophthalmol 2001;85:1379-83.
9. Duke-Elder S, Perkins ES: System of Ophthalmology, Vol.
IX Diseases of the uveal tract, Henry Kimpton, London,
1990;41-130.
10. Dhanda RP, Kalevar V: Corneal Surgery, Chapter 9,
Classification, RK Publications, Indore, 1994, P. 95-101.
C H A P T E R
3
Clinical Evaluation
of Ocular Trauma
B Shukla (India)
Introduction
A disease can be managed adequately only when it
is properly evaluated. Evaluation can either be clinical,
done by the clinician himself or investigational done
by sophisticated machines usually by other specialists
like pathologists, radiologists, etc. Clinical evaluation
includes a careful history and a thorough clinical
examination of the patient.
Before taking a detailed history two conditions
have to be ruled out. If with ocular trauma there is
a life threatening situation; respiratory, cardiovascular
or neurological, the patient should be immediately
referred to appropriate physician or surgeon after a
quick preliminary examination.
1
Secondly if there is
an acute ocular emergency like chemical burn, severe
bleeding or central retinal artery occlusion treatment
has to be started before or during evaluation.
Injuries are very common in children.
2-6
In clinical
evaluation the approach to child has to be a little
different from that in adults. Pain may cause severe
blepharospasm, watering and in an unfamiliar situation
the child is bound to be most unwilling to be examined
or even questioned. The approach has to be very
gentle and indirect. It is better not to touch the patient
initially and let him remain comfortable in mothers
lap. After some time it may be possible to examine
the eye with fine retractors along with assurance and
coaxing. Should these tricks fail the child has to be
examined under sedation or general anesthesia. In
some cases it may be feasible to treat also once he
is under anesthesia.
In older patients one should begin with a careful
detailed history. History may be taken from the
patient, a relative or a witness. In rural areas there
is more risk of infection. The exact circumstances of
the injury has to be ascertained first. This includes the
location, object of injury along with its shape, size,
and velocity. Its chemical nature and whether its is
solid, fluid, or gaseous has also to noted. Exact time
of injury and the various symptoms along with their
severity should be recorded. It is important to know
pre-trauma vision in both eyes and the time when
food/ drink was taken last. Medical and/or surgical
treatment received should be noted in details and
tetanus immunization should be ascertained. In past
history diseases like diabetes mellitus, hypertension,
bleeding disorders, HIV/AIDS, and allergy to drugs
should be noted. It is important to know alcohol
consumption and use of other drugs. All previous eye
surgeries done should be recorded especially cataract,
keratoplasty, and radial keratotomy.
After a careful history, examination of the eye is
very important for clinical evaluaiton. This includes
general, structural and functional examination.
Structural examination would include adnexal,
anterior segment and posterior segment examination.
General Examination
In all serious injuries pulse, respiration, temperature,
and blood pressure should be recorded first to decide
whether the case should be first seen by an ophthalmo-
logist or to be referred to a physician or surgeon. The
general behavior of the patient and level of concious-
ness should also be noted. Any evidence of injury in
the neighboring area or organs should also be observed.
Structural Examination
OCULAR ADNEXA
Orbit
The position of globe in orbit should be noted. There
may be exophthalmoso, enophthalmos, downwards
dislocation (hypophthalmos) or upward dislocation
(hyperophthalmos) which is rate. Orbital rim should
be palpated for any local irregularity or tenderness
indicating fracture. Emphysema in the surrounding
area would be additional proof. Compressibility of
globe into orbit should be noted. More resistance
indicates orbital hemorrhage or hematoma besides
tumor mass.
11
Clinical Evaluation of Ocular Trauma
Conjunctiva
Conjunctiva should be examined for congestion, sub-
conjunctival hemorrhage and foreign bodies
particularly in the lower fornix and sulcus subtarsalis
small areas of chemosis, hemorrhage or pigmentation
may some times be indicative of globe laceration.
8
Conjuctival abrasions can be stained by rose bengal.
Lids
Lids are meant to protect the globe, hence, they bear
the brunt of trauma quite often. In injuries the lids
may show edema, contusion, partial and rarely
complete laceration. In blast injuries they may be
studded with multiple foreign bodies. It is desirable
to evert the upper lid only after ensuring that there
is no open globe injury. Singeing of cilia is a typical
sign of flame burn.
9
In late cases entropion, ectropion,
or ptosis may be seen.
Lacrimal Apparatus
Lower lid injuries with sharp objects is commonly
associated with division of the lower canaliculus. It must
be looked for at the earliest under microscope and
confirmed by syringing with any colored fluid. Later
treatment becomes very difficult. Rarely there may be
dislocation of the lacrimal gland.
10
FUNCTIONAL EXAMINATION
Visual Acuity
It is by far the most important part of eye examination
which is usually done first. In trauma cases it may be
slightly delayed till the patient settles down. Ideally
vision should be recorded in each eye with a standard
chart (Snellen/ ETDRS). In many serious injuries the
vision is often too low and may be recorded by finger
counting, hand movements or perception of light (PL).
The last one has to be done very carefully and
repeatedly by a strong light (indirect ophthalmoscope).
Projection of rays (PR) should also be tested with a
pen torch. Visual acuity has great importance in work
related injuries, medico-legal cases and in assessing the
effect of treatment. In some conditions the vision tends
to fluctuate.
11
If correcting glasses are not available pin
hole vision may be taken. Knowledge of pre-trauma
vision is important in assessing the loss.
RAPD
It is important to assess afferent pupillary defect by
swinging light test. It is affected by optic nerve lesion,
gross retinal lesion but rarely by anterior segment
lesions.
12
IOP
Intra-ocular pressure is important and may be
attempted by non-contact tonometer. By no means
pressure should be exerted on the globe in an open
globe injury as intra-ocular content may prolapse. A
low IOP is indicative of open globe injury, a ciliary
shock or retinal detachment. Raised IOP is suggestive
of severe hyphema, angle recession or severe uveitis.
However, it does not rule out an occult laceration of
globe.
13,14
Ocular Motility
Ocular motility like IOP it is important but has to
avoided in an open globe injury for the risk of extrusion
of intra-ocular contents.
15
It is important in cranial nerve
injuries (III,IV,VI). However, pseudo-squint due
mechanical reasons must be ruled out. For this a forced
duction test can be done after some time if there is
no full thickness laceration of globe.
16
Field Testing
Central field by Amslers chart and peripheral fields
by confrontation test can be done at initial examination.
Visual field loss usually indicate visual pathway lesion.
More sophisticated tests can be done later if indicated.
Malingering
This is not very uncommon in some trauma patients
particularly those who want to avoid their duties or
who can get some advantage by compensation. These
tests are not very easy and there is a battle of wits
between the patient and doctor. However a few tests
done carefully can prove malingering.
By following a definite routine in clinical evaluation
much information is gained and future strategy for
treatment can be chalked out with confidence. The
following assessments can be made after a proper
clinical evaluation:
a. Open globe or closed globe injury
b. Immediate treatment or reference
c. Prognosis.
It may be added that a properly drawn diagram
is much more useful than written words, hence a few
labeled diagram of injury must be drawn.
References
1. Harlan JB, Ng EWM, Pieramici DJ. In Kuhn F Pieramici
DJ (Eds): Ocular Trauma, chapter 9, p. 52. Thieme
Publication: NY, 2002.
2. Shukla B: Epidemiology of Ocular Trauma, Chapter 3,
Observation and analysis. Jaypee Brothers Medical
Publishers: New Delhi, 2002;32-36.
12
3. Canavan YM, OFlaherty MJ et al. A 10 year survey of
eye injuries in Northern Ireland. Brit J Ophthal 1980;
64:61825.
4. Rapoport I, Romem M, Kinek M et al. Eye injuries in
children in Israel. Arch Ophthal 1990;108:376-79.
5. Gothwal K, Adolph S, Jalali S et al. Demography and
prognostic factors of ocular injuries in Southern India,
Aus NZ J Ophthalmol 1999;27:318-25.
6. Niiranen M, Raivio I. Eye injuries in children. Brit J
Ophthalmol 1981;65:43638.
7. Boldt HC, Pulido JS, Blodi CF et al. Rural Endo-
phthalmitis. Ophthalmology 1989;96:172226.
8. Hamil, MB. Clinical Evaluation. In Shingleton BJ, Hersh
PS, Kenyon KR (Eds): Eye Trauma, Chapt. 1, p. 9, Mosby
Year Book: St. Louis, 1991.
9. Duke Elder S. System of Ophthalmology, Vol XIV
Injuries, Part 2, p. 758, Henry KImpton, London, 1972.
10. Ibid. Part 1, p. 307.
11. Anderson RL, Panje WR, Gross EE: Optic Nerve
blindness following blunt forehead trauma. Ophthal-
mology 1982;89:44555.
12. Sharma YR, Singh, DV. Clinical Evaluation in ocular
trauma. In Shukla B, Natarajan S (Eds): Management of
Ocular Trauma, Section 1, Chapter 4, p. 16, CBS
Publishers, New Delhi, 2005.
13. Cherry PMH. Rupture of globe. Arch Ophthalmol 1972;
88:498507.
14. Rusell SR, Olsen KR, Folk JC. Predictors of scleral rupture
and the role of vitrectomy in severe blunt ocular trauma,
Amer J Ophthal 1988;105:253-57.
15. Fackler ML. Wound Ballistics, a review of common
misconceptions. JAMA 1988;259:2730-36.
16. Long JA, Mann TM. Orbital Trauma. In Ocular Trauma,
Edit. Kuhn F Pieramici DJ, Chapter 36, p. 385. Thieme
Publication: NY 2002.
C H A P T E R
4
Evaluation and Initial Management
of a Patient with Ocular Trauma
Rupesh Vijay Agrawal (India)
Introduction
Fact is much different from fiction, fact is reality of
life while fiction is hope of life and today the fact is
that the rate of incidence of ocular trauma has
increased tremendously in this world of modernization
due to road traffic accident and many other day-to-
day mishaps.
No one starts a day believing that he will sustain
trauma to his organ of vision, yet thousands of people
are injured each day. The sudden realization that what
had been taken for granted is lost and life may be
changed forever leads to extreme anxiety for the
patient as well for the patients family.
The human eye is a delicate, vital organ and
repairing damage to it can often challenge the limits
of medical science. Ophthalmologists those
surgeons who specialize in treatment of eye injuries
must constantly stay abreast of new developments
and techniques to keep their skills finely honed.
The significance of eye injuries is obvious to
everyone even though the eyes represent only 0.1% of
the total body surface, it is through this organ that
most of the information reaches the human animal,
whether living in a big city or in the wind. A person
with ocular trauma has to go through severe initial
anxiety, changes in career and lifestyle, impaired
quality of life, economical setbacks and occasionally
permanent physical disfigurement. Ocular trauma has
therefore had a significant socioeconomic impact on
both the involved family and on society in general.
In the present era of specialization and super-
specialization where many of us deal with only a certain
group of disease; most patients who present with
complaints of other segment of the eye are not treated
but, referred to a colleague. A patient with ocular
trauma however need immediate attention and
referral is an option only after certain diagnostic or
primary first aid therapeutic procedures have been
performed.
Ocular trauma cuts across specialities and for that
matter a medico either a physician or a surgeon should
have the basic understanding about the initial
evaluation, diagnosis and primary management before
referring to a qualified ophthalmologist for further
management.
A standardized terminology of eye injury is
important to fulfill a very basic requirement in
medicine to prevent unambiguous communication.
An ideal ocular trauma terminology system was
introduced by Birmingham Eye. Trauma Terminology
(BETT) and satisfies all elements requested by an ideal
system.
When confronted with the ocular trauma patient,
the initial evaluation always begins with the assessment
of the patient. As ophthalmologist in evaluating the
eye trauma patient, one should always assess the whole
patient, keeping in mind that the person may have
sustained non-ocular injuries which may be life
threatening and must be addressed first. In such
situations, the ophthalmologist should not hesitate to
refer the injured patient to trauma center for initial
triage. Once it has been determined that the patient
is stable, and other serious nonocular injuries have
been addressed, a thorough medical/surgical history
is taken followed by a more focused ocular history.
Key elements include prior surgery, vision prior to
the trauma and detailed history of the traumatic
incident.
A full examination is carried out in a methodical
and rational fashion, beginning with gross external
inspection. Visual acuity is measured in each eye
separately. Optic nerve function is assessed by testing
for relative afferent pupillary defect. Ocular exami-
nation is done with help of torch light and followed
by detailed slit lamp evaluation without much
manipulation of the injured globe. Obvious open
globe injury can often be appreciated with a simple
pen light examination. Fundus examination should
be carried out at the initial setting if the view of the
fundus is not precluded secondary to media opacity.
Presence or absence of any obvious infection is
documented.
Uncooperative and pediatric patients should be
examined under anesthesia in a controlled setting
involving experienced critical care personnel.
14
Additional information in cases of suspected retained
intraocular foreign bodies can be obtained by perfor-
ming radiological investigations. Photodocumentation
is recommended whenever feasible.
Approach to a Patient with
Ocular Trauma
THE GOALS OF THE INITIAL EVALUATION
I. Complete evaluation of the eye and ocular adnexa
A. Recognition of emergent conditions
1. Life-threatening injuries
a. Respiratory distress
b. Cardiovascular compromise
c. Massive bleeding and shock
d. Major trauma to any organ system
2. Emergent ocular conditions (appropriate
emergency treatment can be started)
a. Chemical injuries
b. Central retinal artery occlusion (CRAO)
B. Recognition of the complete extent of ocular
involvement
II. Identification of confounding factors
A. Other associated non-life threatening
injuries:
1. Bleeding
2. CNS trauma
3. Other injuries
B. Concurrent medical conditions
1. Diabetes mellitus
2. Atherosclerotic cardiovascular disease
3. Sickle cell hemoglobinopathy
4. Bleeding disorders
5. Infectious diseases:
a. Hepatitis
b. AIDS
C. Foreign bodies
III. Need for further testing
A. Radiologic
B. Ultrasonographic
C. Electrophysiologic
D. Hematologic/serologic
IV. Development of initial therapeutic plan
Approach in Emergency
HISTORY
History of the event
Once emergent life or sight threatening conditions are
ruled out, complete description of the events sur-
rounding the injury should be elicited from the patient,
family members, and witnesses to know:
Activity at the time of injury
Involved parties
Where the incident occurred
What happened, and
How events progressed following injury
History of contact lenses, spectacles, or protective
eyewear at the time of injury.
From this, one can assess potential severity of the
injury and the risk for occult ocular damageretained
foreign bodies, posterior globe rupture and orbital
fracture.
Pastocular and Medical History
Previous ophthalmic surgery,
Non penetrating procedures: radial keratotomy
(ed vulnerability of traumatic damage)
Presence of periocular appliances (e.g. scleral buckle
or orbital implant) or
Intraocular lenses (may become dislodged or
dislocated and complicate injury)
Prior ophthalmic medical conditions: e.g. glaucoma
patiented risk for visual field compromise even
after short duration of elevation of intraocular
pressure
Preinjury visual acuity
Amblyopia or other ophthalmic conditions asso-
ciated with ed visual acuity important in cases of
litigation
General Medical History Regarding
Hematological condition
Bleeding disorder
Anticoagulant medications
Sickle cell anemia (inpatients with hyphema)
Possibility of pregnancy in females of childbearing
age (may influence the choice or use of medications
or other types of therapy)
Alcohol or drug abuse
Neurologic disorders e.g. epilepsy
All medications currently being taken by the patient
Allergies
Tetanus immunization status (patients with
lacerating or penetrating injuries ay require tetanus
prophylaxis)
History of Prior Treatment
Previous treatment for the injury
Any self-treatment (e.g. use of eye irrigants,
compresses, and ocular medications)
Dosage and duration of therapy (may confound
the results of microbiologic culture tests)
15
Evaluation and Initial Management of a Patient with Ocular Trauma
Name and location of physician from whom
treatment is taken
Amount and time of recent food intake (affect
decisions about anesthesia, if surgery is required)
History of Specific Injuries
Chemical injury:
Can cause extremely rapid and serious tissue
destruction
Treatment (irrigation) should begin simul-
taneously with the examination.
Detailed history should be obtained following the
institution of emergency treatment.
All chemical injuries should be presumed initially
to be alkali injuries until proven otherwise.
History:
Type of agent (can take help of local poison control
center)
Characteristics of the exposure
Amount of material in contact with the eye
Duration of contact, and
Physical character of the material (i.e. fluid, paste,
gel, or particulate).
Any prior treatment, such as lavage or irrigation
Examination of facial structures and airway
Evaluate for possible presence of a foreign body
Foreign-Body Injury
Foreign-Body Injury Checklist
1. Source material
Composition: determines ocular toxicity (eg.
iron or copper versus glass or plastic)
Associated activity at time of injury
2. Origin:
Size and shape
Energy
Temperature
3. Probable trajectory
4. Risk of microbiologic contamination
Blunt trauma
History to determine:
1. The amount of energy transferred to the globe and
orbit: involvesvector and quantity of the force
generated by the impact and size of the impact
area.
2. Physical characteristics of the object: include density,
size, and presence of sharp or cutting edges.
3. Location of the impact
Thermal burn
Unusual type:
1. The amount of thermal energy transferred depends
on temperature of the agent,
2. Duration of contact,
3. Character of the agent
Electrical burns
Amount of electrical energy involved (i.e., amperage
and voltage of the current) and location of entrance
and exit points is important
Animal Bites
Identify the type of animal and circumstances.
Attack was spontaneous or provoked?
Location of the animal to test for the presence of
transmissible disease
EXAMINATION
Goal
Complete evaluation of the injured eye and determi-
nation of the absolute and relative position, stability,
and integrity of each ocular and intraocular structure
and need for further testing and treatment.
Examination Technique
Look for the presence of occult or unsuspected
injury
To prevent further damage and avoid inappropriate
examination techniques.
Eye shield protectionin open globe injury
In children or uncooperative adultsexamination
under sedation or general anesthesia is preferred.
No drops or ointments should be instilled, until
rupture is ruled out.
If transportation of patient is not possible,
emergency examination kit should be available.
Appropriate culture equipment and materials
should be available for.
External Examination
Face and Lids (Fig. 4.1)
Points to be recorded:
Any abnormal position of the globe relative to other
bony structures
Presence of subcutaneous emphysema (indicate #
of sinuses)
Presence of any foreign bodies
Depth and extent of skin lacerations
Visualization of orbital fat
Associated injuries to the face, head, and neck .
Small puncture wounds
Lacrimal drainage system or lid margin involvement
Ptosis, levator function and lid fissure size
In canthal structures abnormality,
Medial canthal distances should be measured, and
Sketch of the observed dimensions is made.
Bleeding should be controlled with tamponade and
tissue cleaned gently with a gauze sponge and sterile
saline or hydrogen peroxide.
16
Note:
Periorbital and lid ecchymosis or hemorrhage
(Location and character)
(In #of orbital roofupper lid hemorrhage and
lateral bulbar SCH is +
In basal skull fracturesperiocular ecchymosis may
be present)
Inspect orbital and facial bones and palpate for
areas of step-off, or discontinuity and note any
asymmetry.
Injuries to the midfaceocclusion of the teeth.
Areas of skin anesthesia (s/o underlying #)
In patients with a history of trauma and sudden
onset of a red eye,
- auscultate the closed lids and temporal area for
the presence of a bruit
- may indicate a carotid-cavernous fistula.
Conjunctiva
Note:
Areas of subconjunctival hemorrhage
Abnormal pigmentation of the bulbar conjunctiva
(+ in globe rupture)
Lacerations or breaks in the bulbar conjunctiva
Presence of contact lenses, especially in the
unconscious patient.
Cornea:
Evaluate the epithelial surface and light reflex and any
visible abnormalities of the anterior segment.
Visual Acuity
Establish a baseline visual acuity.
No light perception (NLP) should be carefully
confirmed and documented with help of indirect
ophthalmoloscopy light (have a profound impact
on subsequent surgical decisions).
If visual acuity recording is not possible for some
reasons, one should specify the reasons for inability
to check the vision.
Pupil
Pupillary findings can indicate intracranial pathology
and lesions responsible for diminished vision.
In an unconscious patient, the pupillary reflexes
may be the only indicator of visual system function
that can be evaluated.
Note
Shape
Location
Light reaction and
Eccentricity or irregularity.
Dilated pupil in head injury:
May indicate increasing intracranial pressure with
associated neurologic problems.
Iris sphincter damage and
Pharmacologic mydriasis,
Preexisting pupillary abnormalities unrelated to the
injury should be looked.
Eccentric or peaked pupils: s/o intraocular damage
or scleral or corneal rupture
Always look for the consensual light reflex of the
fellow eye in case of distorted pupil in the injured eye
(Fig. 4.2).
RAPD is s/o:
Injury in the afferent pathway: may be due to:
Optic nerve injuries such as: contusion, avulsion
and transection
Retinal injuries: commotio retinae (Berlins edema)
and retinal detachment
Profound vitreous hemorrhage.
Extraocular Motility
First rule out the presence of a ruptured globe
Post-traumatic orbital congestion may affect ocular
motility.
Note:
All defects in ductions and versions and grade it
for later comparison
Fig. 4.1: Lid laceration
Fig. 4.2: Consensual light reflex
17
Diplopia or
Restriction of movement of the globe and identify
any paretic or underacting muscles
Restriction of movement may be due to:
Orbital floor # (hyesthesia of the cheek and
enophthalmos may be +)
Secondary to injury to motor innervation
Direct muscle trauma or
Intraorbital injury from foreign bodies or
penetrating wound
Forced duction test may be in intact globe
Visual Fields
Confrontation technique - appropriate in the
emergency setting.
Slit Lamp Examination of Anterior Segment
Step-by-step examination from the lid margins to the
palpebral, bulbar, and tarsal conjunctiva, followed by
the cornea, anterior chamber, iris, lens, and vitreous
is performed.
Gonioscopy may be performed if globe is intact
and if there is no hyphema.
Conjunctiva:
1. Subconjunctival hemorrhage record the area and
extent
2. Conjunctival chemosis nonspecific or may have
underlying injury
3. Conjunctival abrasions staining with fluorescein
or rose bengal highlights abrasion
4. Inspect embedded foreign material.
5. Conjunctival lacerations isolated or multiple
Cornea
Examine all the layers using variety of slit-lamp lighting
and inspection techniques (Fig. 4.3).
Any foreign body size, shape and location
Corneal opacities.
Corneal discontinuity or laceration
Depth of a laceration or perforating injury
Seidels test
Edema and suppuration
Generalized after some toxic or chemical insults
or severe concussive injury.
Localized common,
secondary to regional endothelial dysfunction
seen following concussive injuries
with lacerating injuries of the stroma
Infection of the corneaIf a microbial keratitis
scraping done
The endotheliuminspected for discontinuities,
guttata, enlarged endothelial cells, and pseudo-
guttata. (overlying stromal edema may indicate a
concussive endotheliopathy, resolves without
sequelae)
Anterior Chamber
Note
1. Depth and contour of anterior chamber across its
entire height and width.
Irregular Eg.
Choroidal detachment or hemorrhage,
Foreign bodies in or behind the iris,
Localized intumescence of the lens following
rupture of the lens capsule,
Iridocorneal adhesion with leakage of aqueous
secondary to corneal perforation.
Shallow anterior chamber
In loss or misdirection of aqueous humor
Posterior pressure from a suprachoroidal hemor-
rhage.
Deep anterior chamberrupture of the posterior
sclera and vitreous loss.
2. Contents of the anterior chamber:
Cells and flare reaction
seen in traumatic iritis (sequelae of blunt
trauma).
Note the degree of inflammatory response and
grade (important for future comparison)
Blood (hyphema) (Fig. 4.4).
confirmed or ruled out in all cases of blunt or
penetrating injury bleeding source identified if
possible.
Others (Fig. 4.5): Hypopyon, lens fragments,
vitreous, or foreign bodies
Iris (Fig. 4.6)
Note:
Contour and geometry if abnormal- indicate local
damage to the iris or to structures located behind
it (e.g. rupture of the lens capsule, lenticular foreign
bodies, or ciliary body hemorrhage or detachment).
Irregularities in the iris
Direct illumination, retroillumination of the iris
to detect small holes or perforations. Fig. 4.3: Corneal laceration
18
Fig. 4.4: Hypahaema
Fig. 4.5: Hypopyon in anterior chamber
Fig. 4.6: Traumatic cataract with iridodialysis
Fig. 4.7: Ruptured traumatic cataract
with intraocular foreign body
Fig. 4.8: Subluxated lens
Pupil shape:
irregular or elliptical pupilan occult scleral
perforation with peripheral iris,
peaked pupilvitreous prolapse in anterior
chamber,
Sphincter tears and bleeding sites.
Lens (Figs 4.7 and 4.8)
Note: Lens position, stability, clarity, and capsular
integrity, (Examine both before and after dilatation)
Sclera (Figs 4.9 and 4.10)
Note: The presence or absence of scleral laceration
with or without vitreous prolapse and presence of
associated intraocular foreign body.
Intraocular Pressure
Have direct prognostic and diagnostic significance
Should not be checked in cases with open globe
injury
19
Vitreous Body and Retina
Inspect the vitreous body, posterior pole, and
peripheral retina
Document
posterior scleral ruptures or discontinuities
foreign bodies,
retinal tears or detachments,
edema,
hemorrhage, and
vitreous opacities
Scleral depression is attempted only when globe
rupture is ruled out.
Fundus examination is done in all trauma patients
(except exempt for neurosurgical or other reasons)
after bilateral pupillary dilation.
Dilation should be performed cautiously in uncons-
cious patients ,with significant head trauma or
contusion (after neurologist opinion).
Document in the chart the time, dose, and identity
of the dilating agents in confused or unconscious
patients.
Fig. 4.9: Scleral laceration with vitreous prolapse
Fig. 4.10: Foreign body
Fig. 4.11: Berlins edema
Character of vitreous opacity or irregularity -
localized or diffuse.
A complete inspection of the retina and choroid
should be performed in all trauma patients, from the
ora to the posterior pole in all quadrants.
Edema of the retina (Fig. 4.11)
Commotio retinae, Berlins edema- response of the
retina to concussive injury characterized by pale swelling
and obscuration of choroidal detail. May be associated
with a significant loss of vision.
Retinal hemorrhage
Note:
Location and character
Hemorrhage of the nerve fiber layerflame shaped
Intraretinal hemorrhages - blotches with irreregular
border
Subinternal limiting membrane hemorrhages may
stream into vitreous cavity
Tears or breaks in the retina
Can follow concussive or penetrating injury
Most common in superonasal quadrant, followed
by inferotemporal quadrant
Retinal holes should be noted
Retinal detachments10-15% of retinal detach-
ments are secondary to trauma
Retained intraocular foreign bodiesfrequently
surrounded by halo of edema with central plume
of blood. Use of a magnet to test for ferrous
composition of foreign body is contraindicated can
lead to further retinal damage or detachment.
Scleral ruptures
Choroidal injuries:
Rupture appears as a hemorrhagic linear zone
with overlying retinal edema may be obscured
by vitreous hemorrhage white in colour
20
0ptic Nerve
It is the third most frequently damaged cranial nerve
by indirect injury.
Note:
Edema,
Loss of margin clarity,
Hemorrhages in nerve fiber layer.
Spontaneous venous pulsations of the central retinal
vein-suggests normal IOP
Cup disc ratio- if increased - possibility of previous
glaucomatous
The optic nerve trauma
Direct:
In penetrating injuries to the orbit
Severe trauma can lead to avulsion either
partially or completely
Leads to hole in the posterior sclera at the site
of optic nerve through which retinal vessels pass
posteriorly.
Blunt trauma to the forehead or brow - contusion
of the intracanalicular portion of the optic nerve.
Special Studies: ERG and VEP in the Acute Setting
ERGa valuable prognostic test in injuries
complicated by opaque media.
Hirosee and coworkers found that:
Recordable ERG and VEP not always indicate good
prognosis.
But non-recordable ERG indicate a poor visual
outcome.
Hutton found normal VEP as a single predictor for
good postoperative visual acuity in trauma patients
ERG in the acute setting has little value in predicting
eventual visual outcome nonrecordable ERG may
indicate poor prognostic sign.
Visual Evoked Potential (VEP)
Main benefit is to support for clinical decision to proceed
with enucleation in cases with nonrecordable VEP.
Initial Management of Ocular
Trauma Patient
The initial management of a traumatized patient
comprises of the steps to minimize further trauma,
minimize infectious risks, minimize psychological trauma
and most importantly minimize legal problems. The
designing of subsequent management plan is then
individualized for the particular patient and injury. The
surgeon must not act on a trial and error basis but
Pearls
I. Trauma Patient in emergency
Ophthalmologist must take a step back
Rule out life threatening injuries
Emergency
Brief history
Clinical examination
Initial management
Patient counseling
Diagnostic tests
Surgical or conservative management
II. Predictors of scleral rupture:
Predictors of Scleral rupture
Bullous subconjunctival hemorrhage
Decreased digital tension
Abnormally deep/shallow AC
Subconjunctival pigmentation
III. Predictors of RIOFB:
Clinical indicators of RIOFB
History and mode of ocular trauma
Entry wound in sclera/limbus/cornea/iris
Localised traumatic cataract
Direct visualisation
according to the strategic plan, he or she must make
adjustments as demanded by additional findings on
the operation table based on the scientific literature
and personal experience.
Compared with only few years ago, we are in a
much better position to actually help people with ocular
trauma. Not only do we have a better understanding
of the postinjury processes occurring inside the eye
but the expertise of the surgeon and the equipment
at our disposal to actually improve the outcome is
constantly improving. There are organizations that
have ocular trauma as one of their missions in terms
of its prevention, treatment and rehabilitation.
It is the responsibility of physician, surgeon and
the ophthalmologist to reduce the incidence of ocular
trauma by taking into consideration the preventive
aspects of ocular trauma and to decrease the morbidity
caused by same to the extent possible.
Last but not the least, every effort should be made
for a visually handicapped person to achieve a positive
attitude about his or her capabilities to successfully use
residual vision and live a full and enjoyable life as a
visually impaired person.
21
IV. Factors indicating significant ocular injury:
Factors indicating a significant ocular injury
Markedly reduced visual acuity
A relative afferent pupillary defect
Relative shallowing of the anterior chamber
Irregularity of the pupil
Conjunctival chemosis
Hyphema and vitreous hemorrhage
Markedly reduced intraocular pressure
V. Four pronged initial management:
Initial management
To minimize possibility of further trauma
Bibliography
1. AK Gupta. Current topics in ophthalmology-VII, page No.
435-86.
2. Bradford J. Shingelton, Eye Trauma; Clinical evaluation:
3-24.
3. Hung Cheng. Emergency ophthalmology, chapter 6-
Trauma 130-58.
Minimize risk of infection
Minimize psychological trauma
Minimize legal problems
Anterior Segment
Ocular Trauma
C H A P T E R
5
Role of Ultrasound Biomicroscopy
in Evaluation of the Anterior
Segment in Closed Globe Injuries
Ritika Sachdev, Mahipal S Sachdev (India)
Ultrasound Biomicroscopy
The original ultrasound biomicroscope developed by
Pavlin, Sherar and Foster is based on 50 to 100 MHz
transducers, incorporated into the B-mode clinical
scanner. Higher frequency transducers permit
increased resolution, but only at the expense of
decreased tissue penetration depth. The commercially
available UBM is most often configured with a
50 megahertz transducer, which provides a tissue
resolution of approximately 50 microns and a
penetration depth of 4-5 mm. This permits
visualization of the anterior segment. At 60 MHz the
zonular apparatus is slightly better visualized.
Increasing the transducer frequency to 100 MHz
increases the tissue resolution to approximately
20 microns, but the decreased penetration depth limits
scanning to the cornea and has been used in refractive
surgery. The increased penetration depth afforded with
a 42 MHz transducer permits visualization of the entire
ciliary body and may be useful in studies of
accommodation.
The clinical use of this instrument is no more difficult
than the conventional immersion ultrasonography.
The technique is similar to the traditional immersion
B-scan.
The ultrasound probe is suspended from an
articulated arm to diminish motion artifacts. Lateral
displacement is minimized by the linear scan format.
Scanning is performed in the supine position.
Following instillation of topical anesthetic, a 20 mm
eye cup is inserted between the lids The purpose of
the cup is to hold the methylcellulose or other coupling
medium. After insertion of the probe in the coupling
medium, the real time image is displayed on the video
monitor and can be stored for later analysis.
The plane of the section, distance from the center
of the anterior chamber, and the orientation of the
probe with respect to the perpendicular may affect
the apparent structural configuration of the anterior
segment.
Pathology behind anterior segment opacities can
be imaged in detail and the ability to image angle
structures in cross-section allows a new quantitative
method of gonioscopy. The ability to define the
relationship of the iris, posterior chamber, zonules,
ciliary body and lens is potentially helpful in
understanding the mechanisms of glaucoma. Anterior
segment tumors difficult to define with conventional
can be measured and the extent of invasion
determined. Differentiation of the tissue on the basis
of internal acoustic characteristics is aided by very fine
backscatter speckle patterns at these frequencies.
Clinical ultrasound biomicroscopy has shown
significant potential as an aid in diagnosis of ocular
disease. However, the extent of associated injuries and
the open nature of ocular injuries precludes the time
and manipulation necessary for such an examination.
Ultrasound Biomicroscopy in
Ocular Trauma
Berinstein et al described ultrasound biomicroscopy
as a safe and effective adjunctive tool for the clinical
assessment and management of ocular trauma,
especially when visualization is limited and multiple
traumatic injuries are involved.
1,2
Ocular trauma may result in diverse anterior
segment pathologies such as hyphema, cyclodialysis
and angle recession. Many of these anatomical
disturbances can be detected and differentiated with
UBM.
In angle recession, blunt trauma to the anterior
segment forces the iris against the anterior lens capsule,
trapping the aqueous within the anterior chamber and
displacing it towards the angle recess (Figs 5.1A to
C). The increased pressure within the angle recess
may result in a tear in the face of the ciliary body,
resulting in the gonioscopic appearance of an
abnormally wide ciliary body band or angle recession.
On the other hand, if the ciliary body is avulsed
from its normal attachment from the scleral spur, a
cyclodialysis cleft, creating a direct communication from
the anterior chamber to the suprachoroidal space may
26
Figs 5.1A to C: UBM examination of the angle and the iris
be formed. Gonioscopy shows a dehiscence between
the ciliary muscle and the sclera, beginning at the scleral
spur and continuing to the ciliochoroidal space.
Although cyclodialysis clefts may be visualized by
direct visualization during gonioscopy, the attempt may
be unrewarding in post-operative and traumatized eyes
because of the presence of hazy media, disturbed
anatomy and hypotony. When hazy media or
abnormal anterior segment architecture prevent or limit
adequate visualization during gonioscopy, UBM can
be used to differentiate cyclodialysis, angle recession
and ciliary body detachment. In addition, the presence
of supraciliary fluid and visualization of a connection
from the anterior chamber to the supraciliary space
confirms the diagnosis of cyclodialysis. Early diagnosis
and appropriate management of cyclodiaysis clefts are
Figs 5.2A and B: Zonular assessment- Role of UBM
examination. Direct visualization of zonules- Detailed 360
o
scanning
important because visual recovery may occur with
resolution of hypotony and is dependent on its extent
and duration.
Disinsertion of the iris root from its insertion into
the ciliary body (iridodialysis), pupillary block,
peripheral anterior synechiae in the presence of
complete hyphema preventing visualization of the
anterior chamber, and vitreous prolapse into the
anterior segment can also be identified with UBM.
Zonular damage after closed globe injury is not
uncommon and its significance is well known to the
anterior segment surgeon. The loss of zonular fibres,
in association with a traumatic cataract, might result
in an unstable lens and with an increased probability
of vitreous presentation and in the worst case scenario,
loss of lens into the vitreous cavity.
Visualization of zonules requires a careful 360 degree
scanning with the long axis of the transducer
perpendicular to the zonules and has a significant
learning curve. Zonular defects, when present, are seen
as abrupt cessation of the bright reflective lines of
zonular fibres associated with blunting of the ciliary
processes (Figs 5.2A and B).
UBM can also detect small foreign bodies of various
compositions, including those missed by computed
tomography (CT) or B-scan ultrasound. It is particularly
valuable in the detection of small, non-metallic foreign
bodies.
Ozdal et al reviewed the indications for performing
ultrasound biomicsroscopic examination in 109
patients.
3
UBM examinations were preformed for the
evaluation of zonules before cataract surgery (49.5%),
examination of the anterior segment in the presence
27
Role of Ultrasound Biomicroscopy in Evaluation of the Anterior Segment in Closed Globe Injuries
of media opacity such as total hyphema or corneal
scar (32.1%), detection of suspected ocular foreign
bodies (10.1%) and the evaluation of ocular hypotony
(8.3%).The time course of imaging after trauma was
variable and ranged from one day to 55 years.
In all 61.5% eyes had a closed globe injuries
whereas 38.5% had open globe injuries.
The most common UBM findings in closed globe
injuries were zonular deficiency (64.2%), angle recession
(43.3%), iridodialysis (17.9%), dislocated lens (16.4%),
hyphema in 13.4%, peripheral anterior synechiae
(8.9%).
The most UBM common findings in open globe
injuries were zonular deficiency (54.8%), iridodialysis
(26.2%), peripheral anterior synechiae (26.2%), angle
recession (14.3%) and ruptured anterior capsule
(14.3%).
ASSESSMENT OF ZONULES
Pavlin and Foster were the first to describe the imaging
of zonular fibres using UBM.
The role of ultrasound biomicroscopy in pre-
operative assessment of zonular status after trauma was
evaluated by McWhae et al
4
. 59 cases with no clinically
visible zonular damage were examined by ultrasound
biomicroscopy with a 50 MHz probe. Occult zonular
loss was identified in 42.9% of the patients. Referring
surgeons found the information helpful in surgical
planning and anticipating complications in these cases.
This study concluded that UBM is an effective method
for identifying occult zonular damage in patients in
patients with anterior segment trauma. There is however
a significant learning curve in the examination techni-
que. A similar study by Liu Y Z et al also established
the the role of ultrasound biomicroscopy in delineating
the presence and extent of zonular loss in subluxated
lenses.
5
FOREIGN BODIES
Foreign body detection rates were 36.5% by
ultrasound, 88.9% by CT scan and 99.4% with UBM.
The diagnosis of foreign body on UBM was based on
high refl ective echoes causing shadowing or
reverberations.
6
UBM was particularly valuable in picking up
nonmetallic foreign body. In cases with intracorneal
and intrascleral foreign bodies, UBM was used to
determine the depth of the visible foreign body.
7
IRIS AND CILIARY BODY STATUS
Total traumatic aniridia after blunt trauma in a
psuedophakic patient was detected using UBM as the
near total hyphema precluded a detailed slit lamp
examination of the iris structures. UBM revealed iris
root remnants, a normal ciliary body, an in the
bagacrylic intraocular lens, and descemet membrane
dehiscence at the corneal tunnel through which the
iris had extruded.
8
Ultrasound biomicroscopy has been described as
a safe, accurate and non-invasive diagnostic tool in
the diagnosis of cyclodialysis clefts and is of particular
use when other conventional methods of diagnosis
are inconclusive.
9
The pathogenesis of transient high myopia after
traumatic myopia was evaluated in two patients using
ultrasound biomicroscopy by Ikeda et al.
10
UBM
showed annular ciliochoroidal effusion with the ciliary
body edema, anterior rotation of the ciliary processes,
and disappearance of the ciliary sulcus and a myopia
of 9.75 dioptres was noted. The myopia and the UBM
findings normalized in eleven days. In the second
patient UBM revealed a partial cyclodialysis, shallowing
of the anterior chamber and thickening of the
crystalline lens. The resolution of these UBM findings
and the normalization of the myopia was seen
seventeen days after trauma.
UBM thus has a well-established yet only partly
explored role in evaluating cases of ocular trauma and
providing an insight to the pathology of the various
manifestations of concussional injuries.
References
1. Berinstein DM, Gentile RC, Sidoti PA, Stegman Z, Tello
C et al. Ultrasound biomicroscopy in anterior segment
trauma. Ophthalmic Surg Lasers, 1997; 28: 201-07.
2. Genovesi F, Rizzo S, Chiellini S, Romani A, Gabbriellini
et al. Ultrasound Biomicroscopy in the assessment of
penetrating or bl unt anterior chamber trauma.
Ophthalmologica. 1998; 212 Suppl 1:6-7.
3. Ozdal MP, Mansour M, Deschenes J. Ul trasound
biomicroscopic evaluation of traumatized eye. Eye. 2003;
17(4): 467-77.
4. Mcwhae JA, Crichton AC, Rinke M. Ul trasound
biomicroscopy for assessment of zonules after blunt
trauma. Ophthalmology.2003 ;110(7): 1340-3.
5. Liu Y Z et al. Zhonqua Yanke Za Zhi. 2004; 40(3):
186-88.
6. Guha S, Bhende M, Baskaran M, Sharma. Role of UBM
in detection and localization of anterior segment
foreign bodies. T Ann Acad Med Singapore.
2006;35(8):536-45.
7. Vincent A. Dermano et al. Ultrasound biomicroscopy as
a tool for detecting and localizing occult foreign bodies
after ocular trauma. Ophthalmology.1999;106:301-05.
8. Doro D, Deliqianni V. Ultrasound biomicroscopy in
traumatic aniridia 2 years after phacoemulsification.
Journal of cataract and refractive surgery. 2006 ;32(10):
1753-55.
9. Bhende et al. UBM in the diag UBM in diagnosis and
management of cyclodialysis cleft. Indian Journal of
Ophthalmology. 1999;47(1):19-23.
10. Ikeda N, Ideka T, Nagata M, Mimura O. Pathogenisis of
transient high myopa al ter bl unt eye trauma.
Ophthalmology. 2002; 109(3): 501-07.
C H A P T E R
6
Management of Eyelid Injuries
Introduction
Eyelid and adnexal injuries can be a part of
multisystem trauma. The basic ABCs of the trauma
management should be considered and applied in
every trauma patient. This includes securing a patent
airway and stabilization of the circulation. Ophthalmic
evaluation and management are deferred until more
serious problems are addressed.
Once the patient is stable, attention could be
directed to the eyelid injuries. The patient should be
evaluated for any globe or optic nerve injuries. This
may be difficult especially in patients who are
unconscious or uncooperative. The eyelid may be
swollen and difficult to open, so care should be taken
to avoid forceful opening of the eyelid as this may
worsen the already traumatized globe.
Evaluation of Lid Injury
HISTORY
Circumstances of the injury can help determine the
type and extent of the trauma. The mechanism of
injury can give an idea about the depth of the wound
as well as the possibility of foreign body presence.
Falling to the grounds or in contaminated places
especially of the patient is young to report should raise
a high index of suspicion for the presence of foreign
bodies especially of organic nature.
Some symptoms can also give a clue about the
extent of damage. Drop of vision suggests globe or
optic nerve injuries. Presence of diplopia or hypothesia
suggests orbital wall fracture. History of any ocular
diseases or surgeries should be documented. Any
medical problems, topical or systemic medications,
drug allergy as well as problems from anesthesia
should be known. History of tetanus immunization
is essential. If the patient had not tetanus immunization
within 5 years, tetanus toxoid 0.5 ml should be
administered. If the patient had never been
immunized, 250 units of tetanus immunoglobulins are
administered.
In case of animal bite, the rabies immunization of
the animal and if the animal has been quarantined
should be cleared.
EXAMINATION
This should include evaluation of the globe, adnexal
tissue, orbit and face. If the patient is conscious and
cooperative, visual acuity, pupillary responses,
intraocular pressure measurement as well as dilated
fundus examination should be performed. Sometimes
examination under anesthesia can be done to avoid
further globe injuries during manipulation of the
eyelid.
The eyelid is examined for the extent of the wound
and if it involves the septum, the muscle, lid margin
or canaliculus. Canalicular injury is suspected when
the injury lies medial to the punctum which is usually
laterally displaced compared to the other side or the
opposite one. Medial or lateral canthal injuries as well
as tissue loss should be ruled out
Evaluation of the orbit includes searching for ocular
motility deficit, surgical emphysema, hyposthesia of
the check, nose or upper lip in addition to palpable
orbital rim fractures. Orbital imaging with CT is
requested when orbital wall fracture or presence of
foreign body is suspected.
The lid injuries can be associated with face and
neck injuries. A thorough examination of head and
neck should be carried out and other specialties may
be involved in the repair process. All findings should
be documented and photographed.
Principles of Wound Repair
The wound should be closed as soon as possible. Yet
the repair can be delayed if the patient is systemically
not stable or there are more life-threatening injuries.
Any globe injuries should be addressed first. Lid wound
repair could still be delayed up to 48 hours following
trauma without jeopardizing the outcome.
29
During the repair, the wound should be properly
inspected for the presence of any retained foreign
bodies, deep orbital injuries or occult globe injuries.
The extent of the wound should be established. Foreign
bodies should be removed as they may be missed and
cause chronic infection, abscess or sinus formation, or
granuloma. The lid tissue is highly vascular and minimal
debridement is required. Gentle handling of lid thin
skin is necessary to minimize further trauma.
It should be remembered to re-establish the
integrity of the basic lid parts; anterior lamella, posterior
lamella, the lid retractors mainly the levator, the
canaliculi and the canthal tendons. The wound
landmarks are identified and reattached first. These
include the wound angles, apex of skin flaps and brow
hair line. The orbital septum should not be incorpora-
ted in the repair as it may lead to lid retraction and
lagophthalmos.
Most lid wounds could be repaired under local
anesthesia using lidocaine1% with epinephrine
1:100.000. This can be done in the emergency room
if minor or in the operative theater in most injuries.
General anesthesia is reserved for extensive injuries,
associated canalicular injuries or poorly cooperative
patients. The skin is usually closed by non-absorbable
sutures, e.g. 6-0 polyprolene, nylon or silk. Some
surgeons use 6-0 polyglycolic acid (Vicryl) for repair
in young children. Interrupted sutures are usually used,
however, linear parts of the skin wounds could be closed
by running sutures. Skin sutures are usually removed
after 5-7 days.
Major lid reconstructions should be delayed unless
the cornea is seriously at risk. It is advisable to defer
interference for 3-6 months before repairing a defect
such as lid retraction, unsightly scars or ptosis unless
the patient develops signs of corneal exposure that
cannot be controlled conservatively by local lubricants.
WOUNDS WITH NO OR MINIMAL TISSUE LOSS
Superficial Lacerations
They involve the skin and underlying muscle. It should
be emphasized that proper examination of the wound
extent is very important as an innocent superficial
wound may have a significant underlying injury. Simple
wound closure is done with no tension. This could be
facilitated by undermining the edges.
Horizontal muscle lacerations will approximate
themselves without suturing yet vertical muscle
lacerations should be closed with 6-0 Vicryl sutures.
In more complex wounds such as stellate injuries,
care should be taken to follow the skin lines as much
as possible and avoid shortening of the anterior lamella
that may lead to lid retraction. Closure of these wounds
is individualized and depends on the site and extent
of the wound. Any wound extension or further incisions
taken should be fashioned so as to be parallel to the
lid margin. For example, lacerations of V type shape
could be closed and transformed into Y shape.
Deep Lacerations Involving the Levator Complex
If the upper lid septum is involved in the injury, the
orbital pre-aponeurotic fat becomes exposed and the
levator muscle may be violated. So in such situation,
the muscle should be identified while the wound is
repaired. If it is found dehiscent, it should be primarily
reattached to the tarsal plate at its normal attachment
level. Care should be taken to avoid incorporating or
suturing the opened orbital septum.
Marginal Wounds
It is crucial to cl ose the marginal l id wounds
meticulously to achieve a proper anatomic repair thus
reducing postoperative complications. Bad wound
repair will lead to lid notching, lagophthalmos and
corneal exposure. If there is no or minimal tissue loss,
primary repair of the wound can be done. It should
be in two layers. The wound edges are approximated
by 6/0 silk suture passing through the tarsal palate and
exiting at the meibomian gland orifices 1.5-2 mm from
the wound edge. It is approximated to make sure that
the wound edges are coapted and slightly everted.
Other two sutures are taken at the lash line and the
grey line. None of them is secured until the tarsal wound
is closed with 6/0 Vicryl sutures that involve 90% of
the tarsus thickness so as to avoid rubbing against the
cornea (Fig. 6.1). The marginal sutures arms are left
long and tied beneath a skin suture so as to keep them
away from the cornea. The skin wound is closed. The
margin sutures are removed after 10 days as earlier
Fig. 6.1: Lower l i d margi nal wound wi th margi nal
approximating sutures and a suture that involves 90% of
the tarsal thickness
30
removal may lead to wound separation and notching.
In children the marginal sutures can be taken using
6/0 Vicryl and left to dissolve spontaneously (Figs 6.2A
and B).
WOUNDS WITH SIGNIFICANT TISSUE LOSS
Tissue loss may be in anterior lamella or it can be full
thickness involving the lid margin. In such conditions,
it should be remembered to avoid undue tension on
the wound margins. This situation can be dealt with
in a manner similar to lid reconstruction after tumor
excision. Lateral canthotomy and graded cantholysis
of the corresponding crus of the lateral canthal ligament
can be helpful in a lot of conditions. If more anterior
lamellar tissue is needed a Tenzel flap techniques could
Figs 6.2A and B: Lower lid full thickness wound involving
the margin in a 5 years child (A). Same eye 10 days after
the repair with remnants of the vicrly sutures (B)
Figs 6.3A and B: A 24 years old male with upper lid wound
with tissue defect (A). Same eye 3 weeks after repair using
Tenzel flap (B)
be used (Figs 6.3A and B). Care should be taken
to place the lateral canthal angle at a higher position
as it usually descends in few months. Posterior lamella
could be formed using periosteal flaps of free
tarsoconjunctival grafts form the other eye (in case
of upper lid) or even from the same eye (in case of
the lower lid injury). Mustarde flaps as well as lid sharing
procedures could be considered in defects > 50% of
the lid length.
WOUNDS ASSOCIATED WITH
CANALICULAR INJURIES
They can result from direct trauma to medial canthal
area or indirectly by avulsive forces caused by trauma
31
to the orbit. They are common with dog bites and
midface injuries. Early repair of the canalicular injury
is much easier and more successful than late repair
or conjunctivo-dacryocystorhinostomy with Jones
tube.
Canalicular lesions may be missed. They should
be suspected in injuries medial to the punctum that
may be and may be laterally displacement. The
diagnosis is confirmed by direct visualization of the cut
edge or passing a probe into the canaliculus.
Repair of canalicular injuries is done under general
anesthesia. A stent should be placed through the
transected canaliculus. Bicanalicular silicone tube is
commonly used, however, some surgeons use
monocanalicular tubes. In case of bicanalicular tube
use, the severed canaliculus is intubated first. Both are
retrieved from the nose. The marginal wound is then
repaired and canthal tendon wound is also repaired
before tying the silastic tube (Fig. 6.4). After the
wound is approximated, the tube is secured by three
square knots and left in place for 6 months (Figs 6.5A
and B).
The medial cut end of the canaliculs could be identi-
fied under the microscope with high magnification. It
can also be identified using injection of a fluorescein
dye or vescoelastic material into the sac through the
intact canaliculus. Pooling saline in the medial canthal
area with injecting air into the intact canaliculus will
point at the site of cut canaliculus where the air bubbles.
If the wound is ragged freshening of the edges may
be helpful. Retrograde intubation using Pigtail probes
is better avoided as it can cause a false passage.
If the punctum is lacerated, the medial canaliculus
could be marsupialized or opened to the conjunctival
sac and the lid woundis repaired ignoring the injured
punctum and canaliculus.
Figs 6.5A and B: Lower lid marginal wound involving the
lower canaliculus (A). After inserting the tube and repair
of the wound (B)
Fig. 6.4: Lower canalicular injury with a bicanalicular tube
inserted first before the repair of the marginal wound
WOUNDS ASSOCIATED WITH CANTHAL
TENDON INJURIES
Medial Canthal Tendon
Their injuries are usually associated with canalicular
injuries that should be repaired before repairing the
severed tendon. The injury may involve any part of
tendon. Repair of the cut posterior limb of the tendon
is crucial as if not repaired, the lid globe apposition
is markedly affected and traumatic telecanthus usually
results (Fig. 6.6). It should be put in mind that repair
of medial canthal tendon should provide a posterior
pull on the medial canthus thus keeping the lid globe
apposition and gives a good cosmetic appearance.
By the time of injury repair, either:
i. The two ends of the cut tendon could be identified:
In this condition, the tendon is repaired using non-
32
of the tendon could not be identified, the sutures are
passed through the intact periorbital at the region of
the posterior lacrimal crest.
The tendon is totally avulsed from the bone: This may
be associated with medial orbital wall fractures. If the
bone is and the periorbita are intact, suturing into the
periorbita at the posterior lacrimal crest using non-
absorbable suture may be a solution (Fig. 6.7B). Y
shaped microplate could also be used. In case of bone
fracture, the bone should be stabilized then a microplate
is placed. In case of unstable or absent bone fragment,
transnasal wiring of the medial canthal tendons should
be done.
Lateral Canthal Tendon
i. The two cut ends of tendon could be identified:
A horizontal mattress suture is used across the cut ends
using non-absorbable material. If the lateral end could
not be identified, the tendon is fixated to the
periostium, if intact, at a higher position than its normal
as wound contracture and the effect of gravity will pull
the lateral canthus slightly inferior.
ii. The tendon is avulsed from the bone: A small drill
hole could be done in the lateral orbital rim just above
the lateral orbital tubercle. A non-absorbable suture
attached to the remnants of the lateral canthal tendon
is passed through the hole and tied.
Lid Burns
Burns of the eyelid are rare. They can be due to
thermal, chemical or electric current injuries. They
usually occur in patients who have suffered significant
burns over a large surface area of the body. The first
priority is to establish and maintain a patent airway.
Once stable, the globe should be properly examined.
If the globe is injured, topical antibiotics and
cycloplegics are administered. Topical steroids should
not be used as they can cause corneoscleral melting.
An amniotic membrane scleral shell could be also
applied. The lid skin should be covered with a broad
spectrum antibiotic ointment Most of these patients
are semiconscious or heavily sedated and need proper
corneal protection using lubricants. The lids may be
swollen and form a protection to the cornea. If this
is not the case especially with marked exposure, a large
temporary tarsorrhaphy could be performed.
Once cicatricial changes start to develop usually
associated with deterioration of the ocular surface
condition, early intervention should occur. Early use
of full thickness skin grafts or variable types of flaps
had been suggested to reduce the ocular morbidity
in selected cases.
Fig. 6.6: A 3-year-old child who had a dog bite with badly
repaired medial canthal tendon injury showing medial
ectropion and traumatic telecanthus
Figs 6.7A and B: Repair of the medial canthal tendon injury
with reattachment to its remnants (A). Reattachment of the
avulsed tendon to the intact periorbita (B)
absorbable or wire suture. A horizontal mattress suture
is placed in the distal end of the tendon. The two
needles are brought from posterior to anterior through
the proximal part (Fig. 6.7A). If the proximal part
C H A P T E R
7
Management of Lacrimal Injuries
Introduction
Lacrimal injuries are usually not isolated. They are
almost always associated with lid injuries or orbital or
nasal fractures. Eyelid, orbital and adnexal injuries
can be a part of multisystem trauma. The basic ABCs
of the trauma management should be considered and
once the patient is stable, it is possible to properly
examine the eyelid with the upper lacrimal passages,
orbital injuries as well as the associated globe or optic
nerve affection. It should be remembered that upper
lacrimal drainage system can be involved in chemical
or thermal injuries.
Evaluation of Lacrimal Injuries
HISTORY
The conditions of trauma can give an idea about the
nature and the extent of injury. Being usually
associated with lid or orbital injuries, high index of
suspicion should exist to be able to detect lacrimal
passage injuries. Lacrimal gland injury is usually rare
and may be associated with orbital roof fractures or
deep upper lid wound.
Review of medical history is essential as well as
drug allergy history of tetanus immunization and
problems encountered with anesthesia.
EXAMINATION
Routine systematic examination of the eyelid, globe
and orbit should be performed. Canalicular injury is
suspected when the injury lies medial to the punctum
which is usually laterally displaced compared to the
other side or the opposite one. Medial or lateral canthal
injuries as well as tissue loss should be ruled out
Lacrimal passage injuries associated with orbital
or nasal fractures may be overlooked especially with
the edema or ecchymosis. However, associated nasal
bone fractures as well as traumatic telecanthus should
raise the index of suspicion.
In case of late presentation of lacrimal drainage
system injuries, systematic evaluation should be
adopted. This includes, evaluation of the conjunctiva
for presence of adhesions as well as assessment of
the punctual position, direction and patency. Positive
regurge test is a sure sign of nasolacrimal duct
obstruction. Dye disappearance test show delay as
compared to the other side. Probing may show
strictures of the canaliculi or fibrosis of the lacrimal
sac that usually felt as a soft stop. Irrigation test can
show the extent of NLD obstruction. Nasal
examination is very important is such cases as a
deviated septum resulting from the original trauma
may be the reason of the lacrimal passage problems.
Orbital CT whither conventional cuts or in three
dimensions can show the fractures sites and their extent
as well as associated nasal deformities.. Dacryocysto-
graphy can show nasolacrimal duct obstructions site
and extent.
Proper lacrimal system evaluation is necessary for
choosing the treatment protocol.
Wounds Associated with Canalicular Injuries
They can result from direct trauma to medial canthal
area or indirectly by avulsive forces caused by trauma
to the orbit. They are common with dog bites and
midface injuries. Early repair of the canalicular injury
is much easier and more successful than late repair
or conjunctivo-dacryocystorhinostomy with Jones
tube.
Canalicular lesions may be missed. They should
be suspected in injuries medial to the punctum that
may be and may be laterally displacement. The
diagnosis is confirmed by direct visualization of the
cut edge or passing a probe into the canaliculus.
Repair of canalicular injuries is done under general
anesthesia. A stent should be placed through the
transected canaliculus. Bicanalicular silicone tube is
commonly used. However, some surgeons use
monocanalicular tubes. In case of bicanalicular tube
use, the severed canaliculus is intubated first. Both
34
are retrieved from the nose. The marginal wound is
then repaired and canthal tendon wound is also
repaired before tying the silastic tube (Fig. 7.1). After
the wound is approximated, the tube is secured by
three square knots and left in place for 6 months
(Figs 7.2A and B).
The medial cut end of the canaliculs could be iden-
tified under the microscope with high magnification.
It can also be identified using injection of a fluorescein
dye or vescoelastic material into the sac through the
intact canaliculus. Pooling saline in the medial canthal
area with injecting air into the intact canaliculus will
point at the site of cut canaliculus where the air bubbles.
If the wound is ragged freshening of the edges may
be helpful. Retrograde intubation using Pigtail probes
is better avoided as it can cause a false passage.
If the punctum is lacerated, the medial canaliculus
could be marsuplized opened to the conjunctival sac
and the lid woundis repaired ignoring the injured
punctum and canaliculus.
Lacrimal Sac and Nasolacrimal Duct Injuries
These lesions may be missed as these parts are included
in a protective bony structure. A high index of suspicion
should be present to anticipate these problems. They
are usually associated with nasoethmoidal fractures,
sometimes with blow out fractures of the orbit and
types II and III Le Fort fractures.
A nasoethmoidal fracture usually results from a
force delivered across the nasal bridge and its very
common in automobile accidents in which the face
strikes the dashboard. The nasal bones become
fractured and displaced. The lacrimal and sphenoidal
bones are usually crushed. They are associated with
surgical emphysema. Traumatic telecanthus is usually
present in association with lacrimal passage injury.
Fig. 7.1: Lower canalicular injury with a bicanalicular tube
inserted first before the repair of the marginal wound
Figs 7.2A and B: Lower lid marginal wound involving the
lower canaliculus (A) After inserting the tube and repair of
the wound (B)
If the fracture is detected and repaired, irrigation of
the lacrimal system by the end of the repair should be
done. If there is a free system irrigation, nothing more
is needed to be done. If there is some minor resistance
exists, probing and bicanalicular silicone intubation
where the tube is left for 3-6 months may be of use.
If these fractures are not detected and corrected,
chronic dacryocystitis can occur and needs dacryo-
cystorhinostomy (DCR). It is sometimes associated with
excess bone formation in the area of the nasal and
lacrimal bone that accentuates the possibly present
traumatic telecanthus. This bone can be debulked
while performing the DCR. The surgery can be
associated with repair of the present telecanthus.
Old Traumatic Lacrimal Passage Injuries
Management of such injuries varies according to the
site and extent of obstruction and addressed in a similar
way as non-traumatic cases. For example, destruction
of the upper lacrimal system especially with chemical
injuries and obliteration of the canaliculi usually
necessitates conjunctivo-dacryocystorhinostomy
(CDCR) with insertion of Lister Johns tube. Chronic
dacryocystitis or complete NLD obstruction are treated
by conventional DCR.
C H A P T E R
8
Hyphema
Earl Crouch, Eric Crouch (USA)
Introduction
Blunt trauma to the eye may result in injury to the
iris, angle structures, and other intraocular structures.
Hemorrhage into the anterior chamber, or hyphema,
is common in children. Generally, a projectile that
strikes the eyeball produces the hyphema. A great
variety of projectile missiles and objects have been
commonly found to cause hyphema including balls,
rocks, projectile toys, air gun, paint balls, bungee
cords, and the human fist. With the increase of child
abuse, fists and belts have started to play a prominent
role. Boys are involved in three-fourths of cases.
Rarely, spontaneous hyphemas occur and may be
confused with traumatic hyphemas. Spontaneous
hyphemas are secondary to neovascularization, ocular
neoplasms (retinoblastoma), and vascular anomalies
(juvenile xanthogranuloma). Vascular tufts that exist at
the pupil l ary border have been impl icated in
spontaneous hyphema. A traumatic hyphema may be
graded by measuring the height of the layered hyphema
in the anterior chamber in millimeters. A hyphema is
an ocular emergency and should be referred imme-
diately.
History
An exact history of the trauma should be obtained
to assess the velocity involved, which in turn may
indicate the extent of ocular damage that may have
occurred. Inquiry must be made to determine if visual
acuity changes occurred immediately after the injury.
Flashing lights are often seen at the instant of injury
and indicate irritation of the retina, as any message
to the brain from the retina is perceived as light.
Persistent blurred vision is indicative of a more serious
injury. It may indicate blood in the anterior chamber
that is suspended in the aqueous humor. Free-floating
blood in the anterior chamber can generally not be
appreciated by direct ophthalmoscopy. A slit-lamp is
necessary to observe the suspended red blood cells
in the anterior chamber.
Examination
A hyphema may be graded by the following system:
grade 1layered blood occupying less than 1/3 the
anterior chamber, grade 2blood filling 1/3 to 1/2
of the anterior chamber, grade 3blood filling more
than 1/2 but less than the total anterior chamber, and
grade 4total clotted hyphema filling the anterior
chamber, often referred to as an blackball or eight
ball hyphema. Alternatively, hyphemas may be
graded by measuring the height of the hyphema in
millimeters from the inferior limbus. These grading
systems enable the ophthalmologist to monitor the
progress of the hyphema resolution.
Secondary hemorrhage associated with traumatic
hyphema results in a markedly worse prognosis.
Eventual visual recovery to an acuity of 20/50
(6/15) or better occurs in approximately 64% of
patients with secondary hemorrhage compared with
79.5% of those in whom no rebleeding occurred. True
secondary bleeding into the anterior chamber is
indicated by an obvious increase in the amount of
bl ood in the anterior chamber. Secondar y
hemorrhage occurs in approximately 22% of all
hyphema patients (range 7 to 38%). The rate of
secondary hemorrhage is Caucasians is between 8-
10%. The incidence of secondary hemorrhage is
higher in hyphemas that occupy 50% or more of the
anterior chamber.
There are specific complications of traumatic
hyphema. They are directly attributed to the retention
of blood in the anterior chamber and include posterior
synechiae, peripheral anterior synechiae, corneal
blood staining, and optic atrophy. Optic atrophy may
result from either acute, transiently elevated intraocular
pressure or chronically elevated intraocular pressure.
Posterior synechiae may form in patients with traumatic
hyphema. They are secondary to iritis or iridocyclitis.
Posterior synechiae are uncommon in patients treated
medically but occur more frequently in patients who
have had surgical evacuation of the hyphema.
Peripheral anterior synechiae occur frequently in
36
medically treated patients in whom the hyphema has
remained in the anterior chamber for a prolonged
period (9 days or more).
Corneal blood staining occurs primarily in patients
who have a total hyphema and associated elevation
of intraocular pressure. Factors that may increase the
likelihood of corneal blood staining are: (1) initial state
of the corneal endothelium (decreased viability
resulting from trauma or advanced age, e.g. cornea
guttata); (2) surgical trauma to the endothelium; (3)
a large amount of formed clot in contact with the
endothel ium; and (4) prol onged el evation of
intraocular pressure. Each of these factors affects
endothelial integrity. Corneal blood staining may occur
with low or normal intraocular pressures; it may also
occur in hyphemas that are less than total. Corneal
blood staining has a larger potential for occurrence
in patients who have a total hyphema that remains
for at least 6 days with concomitant, continuous
intraocular pressures above 25 mm Hg. Corneal blood
staining may require several months or more to clear.
Non-glaucomatous optic atrophy in hyphema
patients may be due either to the initial trauma or to
transient periods of markedly elevated intraocular
pressure. Diffuse optic nerve pallor is the result of
transient periods of markedly elevated intraocular
pressure; it occurs with constant pressure of 50 mm
Hg or higher for 5 days or 35 mm Hg or higher for
7 days. We have observed a number of patients with
sickle cell trait who developed a non-glaucomatous
optic atrophy with relatively small elevations of
intraocular pressure (35 to 39 mm Hg) that lasted 2 to
4 days. Despite maximum medical therapy, final visual
acuity was less than 20/400 in all patients. We continue
to observe optic atrophy in sickle cell trait patients
referred to our institution that have not had vigorous
control of intraocular pressure and/or delay in
paracentesis. Other studies indicate that patients with
sickle cell hemoglobinopathies and anterior chamber
hyphemas have more sickled erythrocytes in their
anterior chambers than in their circulating venous
blood. The sickled erythrocytes obstruct the trabecular
meshwork more effectively than normal cells, and there
is a concomitant elevation of intraocular pressure to
higher levels with lesser amounts of hyphema.
Moderate elevation of intraocular pressure in patients
with sickle cell hemoglobinopathy may produce rapid
deterioration of visual function due to profound
reduction of central retinal artery and posterior ciliary
artery perfusion.
Associated Exam Findings
There are a variety of complications associated with
hyphema and blunt globe trauma. External exami-
nation may reveal a contusion of the lids and periorbital
tissues. A black eye may be serious or relatively minor.
If accompanied by severe pain, bleeding, or constant
blurred vision, more serious eye trauma must be
considered. An orbital CT scan and ophthalmologic
consultation should be considered to rule out a
ruptured globe. Depending on the mechanism of
injury, corneal and scleral lacerations may also occur.
Frequently, signs of corneal and scleral lacerations
include unequal pupils, decreased intraocular pressure,
iris prolapse, or hyphema. Frequently, a corneal
laceration also involves the lens. Almost all ocular
trauma cases include bleeding or dilation of blood
vessels on the surface of the eye resulting in the
formation of subconjunctival hemorrhages. This sign
may be observed with any degree of eye injury. For
instance, a subconjunctival hemorrhage may be
spontaneous and often indicates minor injury. In the
presence of a hyphema, a subconjunctival hemorrhage
suggests more serious injury and necessitates the
evaluation for a possible occult ruptured globe.
Hyphema may result in lacerations of the sphincter
muscle of the pupil. They are manifested by traumatic
mydriasis. Unlike the unequal pupils seen with
congenital anisocoria, traumatic mydriasis is
characterized by recent onset of unequal pupils and
by the irregularity of the dilated pupil. Although
traumatic mydriasis by itself is not harmful, it suggests
severe blunt trauma and is an indication for a careful
assessment of other ocular structures, including the
vitreous and retinal periphery.
Ophthalmologists should consider posterior injuries
to the globe may be present, including retinal
detachment, retinal tear, and vitreous hemorrhage.
An increase in previous floaters or the onset of new
floaters may occur with hyphema. In such cases, a
complete eye exam including either dilation should
be performed to evaluate for a retinal detachment.
In cases of hyphemas that obscure direct visualization
of the posterior segment B-scan ultrasonography
should be completed. Additional evaluations may
include orbital CT imaging to evaluate for associated
orbital fracture. Traumatic detachment of the retina
can be observed after blunt eye injury, especially in
older individuals. The patient may complain of reduced
overall brightness in the involved eye or may have
continuous light flashes, indicating retinal traction. After
eye trauma it is imperative to inspect not just the central
portions of the retina but the peripheral portions as
well. Other serious post-traumatic injuries are traumatic
tears of the iris, subluxation or dislocation of the lens
that occasionally displaces into the anterior chamber,
and blowout fracture of the orbit that present with
impaired eye movement in the upward direction
37
Hyphema
because of entrapment of the inferior rectus muscle.
These serious injuries are generally readily identified.
Patients presenting with hyphema should also have
evaluations to rule out penetrating injuries of the globe,
acute angle-closure glaucoma, pupillary block, corneal
foreign body, and acute iritis. Blunt trauma may also
result in vitreous hemorrhage, posterior vitreous
detachments, and commotio retinae.
Prognosis and Treatment of
Hyphema
Cataract, choroidal rupture, vitreous hemorrhage,
angle recession glaucoma, and retinal detachment are
commonly associated with traumatic hyphema,
compromising the final visual acuity. It is important
to recognize that the prognosis for visual recovery from
traumatic hyphema is directly related to three factors:
1. Amount of associated damage to other ocular
structures (i.e. choroidal rupture or macular
scarring)
2. Whether secondary hemorrhage occurs
3. Whether complications of glaucoma, corneal blood
staining, or optic atrophy occur.
Treatment modalities should be directed at
reducing the incidence of secondary hemorrhage and
the risk of corneal blood staining and optic atrophy.
The success of hyphema treatment, as judged by
recovery of visual acuity, is good in approximately 75%
of patients. Approximately 80% of hyphema patients
with less than one-third filling of the anterior chamber
regain visual acuity of 20/40 (6/12) or better.
Approximately 60% of those with more than half but
less than total hyphema regain 20/40 or better, whereas
only approximately 35% of those with initially total
hyphema have good visual results. Approximately
60% of hyphema patients below age 6 years have
good visual results; older age groups have progressively
higher percentages of good visual recovery.
Hyphema should be carefully managed with bed
rest, shielding the injured eye, and appropriate treat-
ment either pharmacologically or surgically in order
to minimize potential complications. Patients with sickle
cell disease or sickle cell trait should be closely
monitored for possible elevated intraocular pressure
and rebleeding events. Some ophthalmologists use
aminocaproic acid or oral steroids in addition to topical
treatment with steroids and mydriatics. Some studies
have demonstrated a lower incidence of secondary
hemorrhage with aminocaproic acid treatment. Patients
with hyphema and angle recession require life-long
evaluation for possible glaucoma. Common treatment
plans include atropine sulfate 1% 3 times a day for
Fig. 8.1: Traumatic hyphema
Fig. 8.2: Traumatic hyphemaGrade II
Fig. 8.3: Traumatic hyphemaGrade IV
7 days and topical dexamethasone 0.1% 4 times a
day. Additionally, treatment includes a protective shield
for the involved eye.
In general, hyphemas are best managed with
medical treatment followed by surgical treatment as
indicated. Surgical management can be difficult and
is associated with a series of potential complications.
Surgery is best reserved for severe hyphemas or thus
unresponsive to medical management. Surgery is often
unnecessary when less than 50% of the anterior
chamber is involved. In general, corneal staining with
blood resolves, but may take several weeks. Even total
38
Fig. 8.4: Optic atrophy secondary hyphema-induced
glaucoma
Fig. 8.5: Commotio retinae associated with hyphema
Fig. 8.6: Retinal detachment with subretinal hemorrhage
Fig. 8.7A: Angle resection
Fig. 8.7B: BB ball relative size
Fig. 8.8: Choroidal rupture with macular scar and
retinal hemorrhage
39
Hyphema
Fig. 8.9: Choroidal rupture involving macula
hyphemas should be conservatively managed for
4 days before considering surgery. Spontaneous
resolution often occurs rapidly during this period. After
Surgical intervention is usually indicated on or after
the fourth day for total hyphemas. Surgical indications
also include: intraocular pressure of 50 mm Hg or
greater for 4 days, Grade III hyphemas lasting 6 days
or with pressures of 25 mm Hg, or Grade II hyphemas
lasting longer than 8 days. Also, special attention should
be given to sick cell trait and sickle cell disease patients.
In these patients, an intraocular pressure great than
35 mm Hg for more than 24 hours increases the need
for surgical evacuation.
Complications of hyphema surgery include damage
to the corneal endothelium, lens, or iris; prolapse of
the intraocular contents; rebleeding; and increased
synechiae formation. The preferred technique is eva-
cuation of the hyphema with vitrectomy instrumen-
tation. The initial clear corneal incision is fashioned
and a vitrectomy hand piece is gently placed into the
anterior chamber. Extreme care is required to avoid
any contact with the iris, the lens, or the corneal
endothelium. Intraoperative secondary hemorrhage
may occur. Raising the infusion bottle to approximately
70 cm above the eye for several minutes provides
tamponade in most cases. At the end of the surgical
procedure, filling the anterior chamber with an air
bubble is helpful. Standard closure is created with
10-0 nylon corneal sutures.
In patients with total hyphema, some surgeons
advocate trabeculectomy with peripheral iridectomy.
The trabeculectomy is performed through a partial thick-
ness sclera incision. Peripheral iridectomy is performed
with the trabeculectomy. Two 10-0 nylon scleral flap
sutures are used to close the trabeculectomy site.
Because these surgical procedures have a variety of
associated complications, the surgeon should approach
each case with a patient-specific treatment plan.
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C H A P T E R
9
Management of Corneal Injuries
Introduction
Incidence of eye injuries requiring hospitalization has
been reported 15.2 per 100000 population/year.
Open globe injuries occur four times more often than
close globe injuries. Accidental injuries may occur while
at work, during sports activities and in vehicular
accidents. Children usually get accidental injuries while
playing or as a result of accidental fall. Rarely children
may present with self inflicted injuries, which are
usually mild. A case of bilateral self infiltrated
penetrating needle injury been reported. Majority
(95%) of occupational injuries occur in the workers
who are negligent of using protective measures as per
norms. Injuries due to assaults mostly occur in males
and are more severe in nature. The worst eye injury
occurs during the war or terror attacks.
Terminology in Ocular Trauma
Penetrating eye injury, perforating eye injury, globe
rupture and corneal laceration are commonly used
t erms t o descri be ant eri or segment t rauma.
Penetrating injury is defined as full thickness wound
of eye-ball coat caused by sharp object. Penetrating
injury may have an associated retained intraocular
foreign body. Perforating injury has both entry and
exit wounds caused by the same object. Globe
rupture is the term used to describe open globe
injury with a blunt object. Laceration wound of the
eyeball coat caused by a sharp object. It can be
part i al t hi ckness (l amel l ar) or f ul l t hi ckness
(penetrating).
Classification
The ocular trauma classification group has developed
a classification system for mechanical injuries of the
eye.
1
Open globe injury classification has been
described as under (Table 9.1).
TABLE 9.1: Open-globe injury classification
Type
Rupture
Penetrating
Intraocular foreign body
Perforating
Mixed
Grade
> 20/40
20/50 to 20/100
19/100 to 5/200
4/200 to light perception
No light perception
Pupil
Positive: Relative afferent papillary defect present in
affected eye
Negative: Relative afferent papillary defect absent in
affected eye
Zone
Isolated to cornea (including the corneoscleral limbus)
Corneoscleral limbus to a point 5 mm posterior into
the sclera
Posterior to the anterior 5 mm of sclera
In this chapter the discussion will be centered on
the management of corneal injuries and complications.
Management of Acute
Corneal Injury
Open gl obe injury (OGI) needs emergency
management. Brief history including mode of injury,
causative agent and prior treatment should be
recorded. Infants and children may not allow eye
examination to assess the severity of injury. One
should not force examination as it may aggravate eye
injury. Ophthalmic examination should aim at
ascertaining whether or not the patient requires
surgical intervention. In case the patient requires
surgical intervention he should be prepared for general
anesthesia. Tetanus prophyl axis shoul d be
administered. In case there is suspicion of retained
42
intraocular foreign body, an X-ray orbit (AP) and lateral
view should be done. Primary repair of the corneal
injury should be performed as early as possible. In
case a preliminary examination reveals that no surgical
intervention is required and the patient is co-operative
then patient may be examined in detail. In case child
is unco-operative for examination and it is not possible
to decide whether he needs surgical intervention the
child should be examined under general anesthesia.
Children and apprehensive patients should be
examined using simple pen light or flashlight. Slit-lamp
biomicroscopy and indirect ophthalmoscopy are
preferred and ideal methods of examination and
should be performed on all the co-oprerative patients.
SLIT-LAMP BIOMICROSCOPY
Conjunctiva
Conjunctiva should be examined to rule out any foreign
body, and conjunctival tear. One should specifically
look for scleral laceration.
Cornea
Detailed examination of cornea on slit lamp should
be performed to detect, corneal abrasion, corneal
foreign body, corneal opacity and corneal ulceration.
Corneal perforation if detected should be confirmed
on Seidels test. Schematic corneal drawing should be
prepared to record width, depth of corneal laceration.
Sclera
Sclera laceration may go undetected due to overlying
intact conjunctiva. It is better to suspect scleral wound
in case of conjunctival chemosis, discoloration of con-
junctiva and extensive sub-conjunctival hemorrhage.
Scleral perforation should also be suspected in case
of unexpl ained hypotony. Corneal l aceration
extending to the limbus may be extending to the sclera.
In all such situation it is better to expose the sclera
after peritomy and rule out scleral wound.
Anterior Chamber
Anterior chamber examination should include
examination of pupil, iris, and angle of the anterior
chamber. Deep anterior chamber may indicate angle
recession and subluxated lens. The shallow anterior
chamber suggests choroidal detachment, anterior
dislocation of lens and leaking corneoscleral wound.
Detailed examination of the iris to detect sphincter
tears, iridodialysis and iridodonesis should be done.
Gonioscopy should be performed to detect angle
recession. In case of acute injury, if open globe injury
is not there gonioscopy may be performed after a week
or 10 days. In acute injury patient may be
apprehensive and may not be co-operative due to
pain. Anterior chamber examination should also rule
out uveitis (flare, cells and keratic precipitates) and
hyphema.
Lens
Crystalline lens may be clear or cataractous. In case
lens is clear look for phacodonesis, an indication of
subluxation or irregular anterior chamber suggestive
of dislocation of the lens. Vitreous into the anterior
chamber defects may present. In case of cataractous
lens rupture of anterior capsule should be ruled out.
The findings of the clinical examination should be
recorded in detail. Clinical signs on slit-lamp biomicro-
scopy may be recorded by drawing schematic color
coded diagrams. Photographic documentation of the
clinical findings should also be done (Figs 9.1 and
9.2).
Parents counseling is the most important, as they
may be anxious and have lot of questions to ask. Parents
and child should be explained the nature of injury.
The prime importance of primary repair should be
Fig. 9.1: Full thickness corneal laceration
Fig. 9.2: Corneal laceration repair followed by cataract
extraction and PCIOL implantation
43
emphasized. Visual prognosis may be explained after
primary repair. In case patient is having lens damage
or posterior segment injury necessity of future
surgeries may be explained.
Anesthesia
Primary repair in cases with open globe injuries is always
performed under general anesthesia. Use of succinyl-
choline during anesthesia is avoided as it increases the
intraocular pressure.
2
Inhalational agents including
halothane, more recently isoflurane and sevoflurane
do not raise the intraocular pressure and are safer for
day care surgery. Patient should be kept at a deeper
plane of anesthesia and recovery should be uneventful.
Under local anesthesia there is always danger of
worsening of injury due positive intraocular pressure.
In a recent study regional anesthesia with monitored
anesthesia care has been found a reasonable alternative
to general anesthesia for selected patients with open
globe injuries.
3
The patients treated with this option
had corneal/limbal laceration, smaller length of
laceration (<6.5 mm), formed anterior chamber and
no afferent pupillary defect. The operating time in the
local anesthesia/sedation group is reported to be shorter
mean than in the general anesthesia group.
PRINCIPLES OF REPAIR: PRINCIPLES OF
SURGICAL REPAIR
Extent of corneal injury should be measured and
possible extension to the sclera should be ruled out.
In case, the corneal laceration is extending up to the
limbus, peritomy should be performed and the end of
the corneal laceration should be identified. The extent
of scleral laceration from the limbus should be
measured. Wound should be thoroughly cleaned off
the debris. Corneal lacerations should be carefully
examined for the present of eyelash. Eyelash presence
in the corneal wound or intracorneal may lead to cyst
formation. Cilia may also get implanted into the anterior
chamber and even the traumatic cataractous lens.
Patient in whom multiple cilia impacted in the capsular
bag and their removal before intraocular lens
implantation has been reported.
4
Irrigation of the wound
and removal of corneal foreign bodies is performed.
Recent iris prolapse presenting within few hours should
be reposited. Old iris prolapse, torn iris and iris with
possible focus of infection should be abscised. In case
of ciliary body prolapse, it should not be abscised. Ciliary
body can be reposited. Light cautry may be applied
to small portion if required. Anterior chamber fluid
should be sent for microbial cultures.
5
It is good practice to divide the corneal scleral
laceration into the smaller segments. One should put
a suture at limbus and divide it into corneal and scleral
laceration. Even scleral or corneal laceration can be
further subdivided by putting sutures in between at
certain landmarks such as pigmentary lines on the
corneal epithelium. Corneal sutures should be deep
upto 80-90% of corneal thickness. Corneal sutures
with shallow bites cause posterior wound gap. Corneal
surgeons use adequate number of sutures in the
peripheral cornea and less number of sutures near
the visual axis. Corneal sutures produce compression
of the corneal wound on either side of the corneal
suture.
6
The length of the wound compression is equal
to half of the suture length. Corneal sutures should
be placed in such a way so that the compression zone
around the corneal sutures just overlap each other.
Corneal sutures with longer bites induce larger corneal
astigmatism. The depth of the corneal sutures on either
side should be equal. The unequal depth of the corneal
sutures may produce corneal step. The bites of the
sutures should be at right angle to the corneal wound.
The oblique placement of the sutures may cause
horizontal displacement of the corneal wound edges.
To close clean incised wound without any tissue
incarceration continuous suture may be used. Any
corneal suture causes flattening of the overlying cornea
surface. Corneal sutures cause steepening of the 180
meridian and flattening of the meridian 90 to the
suture. The tension across the sutures used in repairing
corneal laceration should be adequate. The tighter
sutures cause more steepening. Intraoperative
keratometer is useful to be adjust the tension across
the sutures to reduce postoperative corneal
astigmatism. At the end of the repair of the corneal
laceration anterior chamber should be reformed. A
separate stab incision should be used to infect air into
the anterior chamber. In the repair of corneal laceration
air has advantage over Ringers lactate. In case child
has an associated lid laceration, corneal repair is
performed first and lid repair later. Canalicular injuries
should be meticulously repaired. Continuity of the
canaliculus should be ensured.
CORNEAL LACERATION WITH TISSUE LOSS
Approximation of corneal laceration with tissue loss
is extremely difficult. Conventional sutures fail to
achieve the water tight closure and in addition distort
cornea grossly. Special measures may be needed to
close these lacerations.
1. Purse string suture: Radial linear limbs of the corneal
laceration should be closed with conventional
interrupted sutures. The central defect may be
closed with the 360 continuous purse string suture.
Purse string suture will generate centripetal
compression force and aid in achieving firm closure.
44
2. Cyanoacrylate tissue adhesive: Another option to
obtain water tight closure in corneal laceration with
tissue loss is to apply cyanoacrylate tissue adhesive
(CTA). CTA application in this situation may be
combined with either interrupted sutures or with
purse string suture. Any tissue iris or anterior capsule
incarcerated in the corneal wound should be
disengaged before CTA application. Area around
the tissue loss should be de-epithelialized. A
minimum quantity of CTA should be applied. This
will provide a firmly adherent adhesive plug that
will seal the perforation. Bandage contact lens
shoul d be pl aced to prevent irritation and
dislodgment of the adhesive plug.
3. Penetrating keratoplasty: In extensive loss of corneal
tissue even purse string suture may not work. These
cases may not be amenable to either purse string
suture or CTA application. Larger loss of the corneal
tissue may be better managed with penetrating
keratoplasty. Penetrating keratoplasty takes care of
the tissue loss and provides better and secured
anterior chamber.
All corneal perforations should be considered
infective unless proved otherwise and should be treated
accordingly (Fig. 9.3). Infective corneal laceration may
also be treated with application of cyanoacrylate tissue
adhesive application in addition to topical antibiotics
(Figs 9.4A to D). Lamellar corneal injuries with tissue
loss may be treated with cyanoacrylate tissue adhesive
application, deep lamellar keratoplasty and multi
layered amniotic membrane transplant (Figs 9.5
and 9.6).
VISCOELASTIC MATERIALS
Viscoelastic substance should be used to deepen the
anterior chamber and protect corneal endothelium.
Fig. 9.3: Corneal perforation with infection with
traumatic cataract
Figs 9.4A and B: Infective corneal perforation in patient
with prior RK
In addition one can always use air in the anterior
chamber. Air gives clear view of the tissue incarcenated
in the corneal wound. Mobility of the air bubble and
extent of the air bubble give useful information that
the anterior chamber is deep. Multiple small air bubbles
indicate that there may be vitreous in the anterior
chamber.
MANAGEMENT OF INJURY TO LENS
In general lens extraction is avoided at the time of
primary repair of corneal laceration. There is always
a risk of aggravation of sub-clinical infection and
developing endophthalmitis. However, if there is gross
laceration of capsule and lose lens matter in the anterior
chamber, one should aspirate the lens matter. In case
there is lens matter mixed with vitreous one can perform
anterior vitrectomy with lensectomy. In the exceptional
case with clean incised corneal wound lens capsule
laceration may be present. In since a patient one can
perform aspiration of the lens matter and perform
posterior chamber intraocular lens implantation. Small
corneal laceration (1-2 mm) self-sealing may be left
45
there is tissue incarcerations iris or capsule, corneal
wound should repaired even if it is already sealed.
The incarcerated tissue must be disengaged to avoid
fibrous in growth and avoid fistula formation. Iris
incarceration may also pre-dispose to sympathetic
ophthalmia.
TYPE OF SUTURES
Corneal laceration is repaired using 10 0 monofila-
ment nylon (Alcon or Ethicon) suture. Scleral ruptures
are repaired using polypropylene sutures. Iridoplasty
and pupiloplasty is also performed using 10(0)
polypropylene sutures. Conjunctival tear should be
sutured using polyglactin (vicryl 8 (0) sutures. Lid repair
is done using 6 (0) silk sutures.
POSTOPERATIVE TREATMENT
Following corneal injury repair child is put on systemic
antibiotic, systemic steroids and systemic anti-
inflammatory drugs. In addition the child should be
put on frequent topical antibiotic, topical steroids and
cycloplegics. In the postoperative period one should
monitor intraocular pressure and postoperative
inflammation. Once postoperative inflammation has
subsided one should perform posterior segment
evaluation. In case adequate view of the retina is not
obtained because of corneal edema, corneal scar or
cataractous l ens one shoul d get B-scan
ultrasonography, to make suture that there is no retinal
detachment, endophthalmitis or vitreous hemorrhage.
Delayed post traumatic propionibacterium acnes
endophthalmitis has been reported.

Children may
recover good vision after surgery for traumatic cataract
despite corneal scar. In some cases of adequate
posterior capsular support is not available they may
need scleral fixated PCIOL.
Fig. 9.4D: Healing of infective corneal perforation with
glue application and bandage contact lens
Fig. 9.4C: Glue application in infective corneal
perforation
Fig. 9.5: Large corneal injury with tissue loss
unsutured if the wound is stable and there is no tissue
incarceration. Shelving wound is more stable than
vertical edges of the wound. Bandage contact lens may
be considered making the wound more stable. In case
Fig. 9.6: Deep anterior lamellar keratoplasty for corneal
scarring and multiple stromal foreign bodies
46
TRAUMATIC WOUND DEHISCENCE
FOLLOWING PENETRATING KERATOPLASTY
Penetrating keratoplasty requires long-term follow-up.
Major potential complications include graft reaction,
suture related problems, infective keratitis, recurrence
of disease and cataract. Wound dehiscence is a rare
complication occurring in an otherwise normal graft.
Traumatic wound dehiscence may occur any time after
penetrating keratoplasty. Cases of traumatic wound
dehiscence have been reported many years after
successful keratoplasty. In various series incidence
ranging from 1.3 to 2.5% has been reported. Young
male patients are most often affected.
Keratoconus, pseudophakic corneal edema, graft
failure, endothelial dystrophy and viral keratitis have
been reported as indications of keratoplasty in cases
of wound dehiscence. The indication of the original
graft is not thought to influence the risk wound
dehiscence. Grafts on avascular corneas heal without
vascularization. The vascularization of the corneal
wound strengthen the corneal scar. Larger grafts have
longer scars and are theoretically at higher risk of
dehiscence. Corneal wounds closer to the limbus heal
better. Post-penetratng keratoplasty corneal scars never
regain the normal corneal strength even after years.
Therefore corneal graft remains at risk of wound
dehiscence even after years. Bilateral wound dehiscence
has been reported. Bilateral poor visual acuity, alcohol
abuse and use of non-inflammatory sutures are
predisposing factors.
Immediate wound repair of the original graft is
needed. Even if the original graft is opaque or
edematous immediate primary repair is warranted.
Delay in primary wound repair enhances the risk of
infective karatitis, suprachoroidal hemorrhage and
endophthalmitis. Advanced age is another risk factor
for development of suprachoroidal hemorrhage.
Prognosis
Older patients record poor visual outcome after
treatment of traumatic wound dehiscence.
Complications of Corneal Injury
The objective of repair of anterior segment injury is
to repair the damage, prevent the complications and
provide effective visual rehabilitation to the patient.
Following successful repair of the injury, the patient
should be monitored for development of following
complication. Traumatic cataracts were the most
common vision-limiting factor in all categories of open-
globe injuries. Injuries in zones II and III. Blunt-force
ruptures were associated with increased rates of retinal
detachments, phthisis, and enucleation, contributing
to the poorer visual prognosis in these patients.
Although extremely rare systemic complication of
venous air embolism has been reported during repair
of penetrating injury in a child.
TRAUMATIC CATARACT
Significant open globe injury is frequently associated
with development of cataract. Details of management
options will be discussed in a separate chapter.
CORNEAL INFECTION
During examination and surgery patient should be
specifically looked for presence of any infiltrate. Patient
with history of injury with dental wires may get
polymicrobial keratitis. Patient suffering corneal injury
with wooden splinter or with retained intracorneal
wooden foreign bodies may develop fungal infection.
Corneal foreign body shoul d be removed on
emergency basis. In case such a patient develops an
infiltrate corneal scraping should be performed. The
material obtained on corneal scraping should be
subjected to direct microscopy and cultures (bacteria
and fungus). Intensive topical antibacterial/antifungal
treatment should be initiated in these patients. In case
of fungal keratitis systemic antifungal treatment should
be given in moderate and severe keratomycosis.
IRIS/CAPSULAR INCARCERATION
Any tissue iris or capsule tags incarceration in the corneal
wound should be prevented. In case incarceration of
the tissue is there it should be removed. In case it is
persisting after primary repair, it should be treated
during the second operation. Tissue incarceration may
lead to wound leak, corneal fistula, inadvertent blebs,
endophthalmitis, fibrous ingrowth or epithelial
downgrowth. The corneal fistula should be detected
using Seidels test and should be treated immediately.
Fibrous ingrowth or epithelial down growth should be
avoided as it may later lead to intractable glaucoma.
Traumatic iris cyst is a rare complication of full thickness
corneal laceration (Fig. 9.7).
SECONDARY GLAUCOMA
Patients undergoing repair of eye injury should be
closely mentioned for development of secondary
glaucoma. Intraocular pressure should be recorded
on every visit. In case of corneal scarring non-contact
tonometer may be used to record IOP. In case IOP is
high it should be controlled medically. Surgical option
may be desirable once it is not controllable with medical
47
POST-TRAUMATIC ENDOPHTHALMITIS
Endophthalmitis following OGI is a serious complica-
tion. Microbial contamination is an important risk
factor for development of endophthalmitis. Despite
high frequency of microbial contamination, it develops
only in few cases. Systemic antibiotics, virulence of
organisms and host factors play role in the development
of endophthalmitis. Poor vision at presentation,
isolation of virulent organism, longer length of
corneoscleral laceration (>8.0 mm), delayed primary
repair (>72 hours) and uveal tissue and vitreous
prolapse have been identified as risk factors favoring
development of endophthalmitis.
7
The incidence of
endophthalmitis can be reduced by early referral of
trauma cases.
8
Prophylactic intravitreal broad spectrum
antibiotic injection has been found to decrease the risk
of post-traumatic endophthalmitis.
9
In a recent series endophthalmitis due to Bacillus
species has been reported. Bacillus isolates have been
found to be sensitive vancomycin, gentamycin and
fluoroquinolones.
10
The organism was not found to be
sensitive to penicllin or cefalosporins. Endophthalmitis
caused by Bacillus cerus results in poor visual outcome.
10
SYMPATHETIC OPHTHALMIA
Sympathetic ophthalmia is defined as bilateral, granu-
lomatous, pan-uveitis generally occuring following
open globe injury or rarely following intraocular
surgery. Incidence between 0.2% and 1% has been
reported follwing open globe injury and 0.001%
following surgery has been reported.
11
Risk is more
if the injury extends into the ciliary body region. Uveal
tissue/iris incarceration into the corneal or scleral wound
also enhances the risk of sympathetic ophthalmia.
Patient should be educated that difficulty in reading
may be the earliest sign of the disease. In the early
stage the disease present as granulomatous uveitis.
Once clinical diagnosis is established, the patient should
be put on topical and systemic steroids.
POSTERIOR SEGMENT COMPLICATIONS
Every patient suffering penetrating eye injury should
be subjected to the detailed retina evaluation even if
there is not obvious injury to the posterior segment.
These patients should be kept under follow-up. The
retina should be examined with scleral depression at
least 2 times a year. Patients who need penetrating
grafts or secondary scleral fixated PCIOL should be
critically examined for any retina problem before
undertaking surgery. These patients may develop
retinal detachment months to years after the primary
repair. In case the media is not clear patient should
undergo ultrasonography to rule out posterior segment
Fig. 9.7: Iris cyst following repair of corneal laceration
Fig. 9.8A: Clear graft in a patient with corneal traumatic
corneal scar
Fig. 9.8B: Ahmed gluaucoma valve for post-PK
glaucoma
treatment. Glaucoma may occur after penetrating
keratoplasty done for visual rehabilitation. These cases
may need glaucoma surgery, Ahmed valve to control
intraocular pressure (Figs 9.8A and B).
48
problem before performing cataract surgery or
penetrating keratoplasty.
ASTIGMATISM
Patients with less than 3 mm corneal laceration usually
have corneal astigmatism (<3.00D) where as 4 mm
or longer incision has higher corneal astigmatism. Low
or moderate astigmatism (<3.00 D) is common and
can be easily managed with prescription of glasses.
High astigmatism (>3.00D) requires different set of
evaluation and management. High astigmatism may
occur despite meticulous primary repair.
12
High
astigmatism with sutures still in place may decrease
with selective suture removal. Once all the corneal
sutures are out, accurate refraction should be done.
In case of a child it should done as cycloplegic refraction.
Best corrected visual acuity with spectacle correction
should be noted. In case visual acuity with pin hole
is better than spectacle correction, it means that there
is significant irregular astigmatism. Corneal topography
should be performed and surface regularity index may
be high in these cases. Such a patient should under
go rigid gas permeable contact lens trial. In addition
to irregular astigmatism, problems such as ametropia
following aphakia, high astigmatism or aniridia can be
solved with good visual results, good tolerance and
less complications.
14
High astigmatism can be managed
with astigmatic keratotomy. LASIK, epi-LASIK and
photo-astigmaic keratotomy may be performed to treat
corneal ametropia and corneal astigmatism.
12
Visual Rehabilitation
In case visual acuity with spectacle correction does not
improve RGP contact lenses should be considered.
Reverse geometry RGP contact lens, with large
diameters, could be another alternative in irregular
corneal surface with corneal scar.
13
Fluorescein pattern
analysis could be better fitting technique in these cases.
This fitting could involve less time and fewer visits.
Computer-aided fitting was of limited value in these
cases.
14
In case patient does not want rigid gas
permeable contact lens, the patient may be considered
for alternate surgical options.
Patents intolerant to RGP may be considered for
astigmatic keratotomy or laser vision correction. In case
of child with poor compliance for contact lenses,
secondary intraocular lens implantation may be useful
in preventing amblyopia (Fig. 9.9).
15
Patients who have corneal scar passing through the
visual axis may need deep anterior lamellar keratoplasty
or penetrating keratoplasty (Figs 9.10A and B).
Secondary intraocular lens implantation if required may
Fig. 9.9: Secondary scleral fixated intraocular lens
implant in patient with corneal injury
Fig. 9.10A: Traumatic corneal scar involving visual axis
Fig. 9.10B: Clear graft in patient with traumatic corneal scar
be performed at the same sitting. In case the iris has
been damaged iridoplasty may be performed. If the
longer sector of the iris is missing the special intraocular
lenses with opaque periphery may be implanted to avoid
glass and improve cosmetic appearance.
49
WAR RELATED INJURIES
The most common cause of the eye injuries during
the war are explosions with fragmentation injury. Open
globe injuries, are more common and usually bilateral.
OGIs received during war are for more serious and
devastating. It is difficult to salvage the eye. A large
number of eyes (30 to 35%) may need to be removed
(enucleation, evisceration, or exenteration). Some of
the patients may even require bilateral enucleation.
Injuries to other body systems are common. In
Operation Iraqi Freedom 797 severe eye injuries
including 483 OGIs (49 bilateral) were treated by
United States Army ophthalmologists.These injuries
were most commonly caused by explosion trauma.
16
OGIs may also occur in survivors of terror attacks
victims that involve the use of explosive materials.
These explosives are commonly of a high explosive
type (HE) and may be fashioned into improvised
explosive devices (IED) that incorporate additional
materials to maximize trauma and injuries. Serial IED
explosions have occurred in commuter trains in several
cities including London, Madrid and Mumbai. In a
report 16 of 28 patients (57.1%) had ocular injuries
whereas 12 (42.8%) were found to be normal. Injuries
were seen in 22 eyes, 10 unilateral and six bilateral.
The common injuries were periorbital hemorrhages
(09 eyes, 40%); first or second degree burns to the
upper or lower lids (seen in 07 eyes, 31.8 %) and
corneal injuries (seen in 08 eyes, 36.3%). Open globe
injuries were seen in two eyes of two patients (09%).
One patient (4.5%) had a traumatic optic neuropathy.
17
Ophthalmologists should be aware of this pattern
of ocular injuries. Protocols should include the
screening of patients in a short time, diagnostic tests
including B-scan, visual evoked potential (VEP), etc
and performing early surgery at the time of injury.
Most of the severe eye injuries are missed and are not
treated at an initial assessment.
Prevention of Eye Injuries
Occupational open globe injuries are usually severe
and are associated with a poor visual outcome.
Mandatory use of protective eyewear and alcohol-free
environment at the work place is likely to reduce the
incidence of severe occupational open globe injuries.
Educating parents and children about the potential
for eye injuries at home and during hazardous activities
should be an important public health goal.
18
In
addition, promoting the use of appropriate protective
eyewear by children during activities with a high risk
of ocular trauma will help prevent future eye injuries.
Although the path is long and arduous but with
the current advancements in microsurgical techniques
it is possible to rehabilitate eyes with corneal injuries
to near normal.
References
1. Pieramici DJ, Sternberg P Jr, Aaberg TM Sr, et al. A
system for classifying mechanical injuries of the eye
(globe). The Ocular Trauma Classification Group. Am J
Ophthalmol 1997;123820-31.
2. Chidiac EJ, Raiskin AO Succinylcholine and the open
eye.Ophthalmol Clin North Am 2006;19:279-85.
3. Scott IU, Gayer S, Voo I, Flynn HW Jr, Diniz JR,
Venkatraman A. Regional anesthesia with monitored
anesthesia care for surgical repair of selected open globe
injuries. Ophthalmic Surg Lasers Imaging 2005;36:122-28.
4. Ram J, Sharma A. Traumatic implanation of cilia into the
capsular bag. Afro Asian J Ophthalmol 1992;Vol
XI(2):194-95.
5. Gupta A, Srinivasan R, Kaliaperumal S, Setia S. Microbial
cultures in open globe injuries in southern India. Clin
Experiment Ophthalmol. 2007;35:432-38.
6. Hamill MB. Corneal and Scleral trauma. Ophthamol Clin
N Am 2002;15:185-94.
7. Gupta A, Srinivasan R, Gulnar D, Sankar K, Mahalakshmi
T. Risk factors for post-traumatic endophthalmitis in
patients with positive intraocul ar cul tures Eur J
Ophthalmol 2007;17(4):642-47.
8. Narang S, Gupta V, Simalandhi P, Gupta A, Raj S, Dogra
MR. Paediatric open globe injuries. Visual outcome and
risk factors for endophthalmitis. Indian J Ophthalmol
2004;52:29-34.
9. Narang S, Gupta V, Gupta A, Dogra MR, Pandav SS, Das
S. Role of prophylactic intravitreal antibiotics in open
globe injuries. Indian J Ophthalmol 2003;51:39-44.
10. Miller JJ, Scott IU, FlynnHW Jr, et al. Endophthalmitis
caused by Bacil l us species. Am J Ophthal mol
2008;145:883-88.
11. Marak GE. Recent advances in sympathetic ophthalmia.
Surv Ophthalmol 1979;24:141-56.
12. Jain S, Azar DT, Pineda RP. Management of astigmatism
after corneal trauma. Int Ophthalmol Clin 1986;47-55.
13. Martin R, de Juan V. Reverse geometry contact lens fitting
in corneal scar caused by perforating corneal injuries.
Cont Lens Anterior Eye 2007;30:67-70.
14. Grnauer-Kloevekorn C, Habermann A, Wilhelm F,
Duncker GI, Hammer T. Contact lens fitting as a possibility
for visual rehabilitation in patients after open globe
injuries Klin Monatsbl Augenheilkd 2004;221:652-7.
15. Sharma A, Basti S, Gupta S. Secondary IOL implantation
in children. J Cataract Refract Surg 1997;23:675-680.
16. Thach AB, Johnson AJ, Carroll RB, Severe eye injuries
in the war in Iraq, 2003-2005 Ophthal mol ogy
2008;115:377-82.
17. Mehta S, Agarwal V, Jiandani P. Ocular injuries in
survivors of improvised explosive devices (IED) in
commuter Trains BMC-Emerg Med 2007;27;7:16.
18. Brophy M, Sinclair SA, Hostetler SG, Xiang H. Pediatric
eye injury-related hospitalizations in the United States.
Pediatrics 2006;117:1263-71.
C H A P T E R
10
Chemical Injuries of the Eye
Quresh B Maskati (India)
Introduction
Among the ocular hazards that modern day humans
face, the incidence of chemical injuries has been
forever on the rise. Causes range from industrial and
agricultural accidents, domestic accidents, assaults and
chemical warfare. Uncommon causes are self inflicted
injuries and improper use of drugs.
1,2
The eye is exposed to a wide variety of chemicals
of diverse nature, either by accident or design. The
injuries so caused vary considerably, from the most
trivial causing transient irritation to the most severe,
causing complete loss of integrity of the visual apparatus.
The protective mechanisms of the eye are generally
of not much help in these types of injuries. The bony
orbit protects against large size objects, but offers no
barrier to liquids and gases. The eyelids may suffer
extensive damage themselves in cases of chemical
injury. Liquids mix with tears and spread rapidly,
extending the area of contact. Reflex lid closure and
blepharospasm may trap solid particles, especially lime,
beneath the lids, leading to prolonged contact.
1,2
Pathogenesis
The commonest types of chemicals are acids and
alkalis. Most chemical injuries have a striking similarity
in their pathogenesis, following the pattern of acid
or alkali burns.
ACIDS
They cause their damage within the first few hours. They
produce a coagulation of the surface proteins into
insoluble acid albuminates, which form a barrier to
further penetration. Therefore the damage is restricted
and the lesions are sharply demarcated and non-
progressive.
ALKALIS
These cause a saponification of cellular barriers,
denaturation of mucoids, swelling of collagen and
severe disruption of stromal mucopolysaccharides.
Thus they are able to progressively penetrate deeper
into the stroma. Alkali injuries are hence considered to
have a poorer prognosis as compared to acid injuries.
3
Classification
Several classifications have been in vogue in the past.
a. Hughes classification: Mild, moderate and severe.
This depended on the visibility of anterior chamber
details and the blanching of the surrounding
conjunctiva. However, it did not assess the area
of surface involvement.
b. Thofts classification: 4 grades of severity from
grade1 to grade 4 based on area of perilimbal
conjunctival necrosis and amount of corneal
epithelial loss.
4
However, in those days, the concept of limbal stem
cells and their role in regeneration of the conjunctival
and corneal epithelium was not well understood.
Modern classifications such as that proposed by Dr.
Harminder Dua of Nottingham, UK (Table 10.1) fill
in that lacuna and hence give the reviewer a better
idea of the prognosis of such cases.
7
Management
GENERAL PRINCIPLES
First Aid
This consists of immediate and thorough removal of the
chemical to the extent possible. Ideally the antidote of
the chemical can be used. Practically this is usually not
feasiblethe easiest way is a liberal washing of the eye
with Ringers lactate or Normal saline or even tap water,
if nothing else is available, for 30 to 60 minutes.
Examination
A thorough examination of the involved structures
is then carried out with a good illumination (slit lamp,
51
TABLE 10.1: Dua classification of chemical burns
Grade Prognosis Clinical findings Conj.involvement Analogue scale
I Very good 0 clock hours of limbal involvement 0% 0/0%
II Good < 3 clock hours of limbal involvement <30% 0.1-3/1-29.9%
III Good >3-6 hours of limbal involvement >30-50% 3.1-6/31-50%
IV Good to guarded >6-9 hours of limbal involvement >50-75% 6.1-9/51-75%
V Guarded to poor >9-<12 hours of limbal involvement >75-<100% 9.1-11.9/75.1-99.9%
VI Very Poor Total limbus (12 hours) Involved Total conj (100%) 12/100%
The analogue scale records accurately the limbal involvement in clock hours of affected limbus/percentage of conj.
Involvement. While calculating percentage of conj. Involvement, only involvement of bulbar conjunctiva, up to and including
the conjunctival fornices is considered.
if possible) and the extent of damage assessed. Any
particles, especially in cases of lime are picked up with
a forceps or a cotton bud. The fornices must be
searched well, with double eversion of the lids, which
will reveal trapped lime particles. If the patient is a
child this may require examination under general
anesthesia as soon as the general condition of the patient
permits. The author has discovered lime particles deep
in the fornix even months after the injury, which have
been missed by others because the child was not
examined under general anesthesia with double
eversion. Special attention is paid to examination of
the adnexa, as their involvement will considerably
worsen prognosis. Also, the lesions are graded
according to Duas or any other classification.
Medication
Topical anesthetics should be sparingly used, as they
tend to retard epithelial healing. Systemic analgesics
can be administered. A cycloplegic like atropine should
be instilled to reduce the pain and discomfort of
Cyclitis. Topical antibiotics should be used to prevent
infection. Acetazolamide should be started in cases with
moderate to severe burns to prevent secondary
glaucoma. This is a wise precaution, as intraocular
pressure cannot be taken in the early stages of chemical
injuries.
Surgical Maneuvers
Early paracentesis has been recommended, especially
in cases of alkali burns, though its advantages have
not been proved. Mechanical removal of
contaminated, necrotic tissue will promote faster
healing. According to a study done at L.V. Prasad Eye
Institute, use of amniotic membrane grafts in the early
stages significantly reduced overall morbidity of
chemical burns lesions.
6
Sweeping of a glass rod around
the fornices is done daily, especially in the areas where
symblepharon is threatening to develop. A conformer
or moulded scleral contact lens can also be inserted
to prevent symblepharon.
Role of Vitamin C
Topical ascorbic acid has been advocated to promote
corneal regeneration as it has been found that the
aqueous in most cases of chemical injuries, especially
alkali are markedly scorbutic (very low to unrecordable
levels of vitamin C). Ascorbic acid is very necessary
for fibroblasts to lay down healthy collagen.
4
This
reparative process starts soon after the injury occurs.
This is a cheap and freely available drug. It is sold
as ampoules of 500 mg in 5 cc or as 1000 mg in
10 cc. This is the exact concentration that is required
of topical vitamin C, i.e. 10%. It does not need any
further dilution. All you have to do is break an ampoule
of vitamin C injection, pour into a sterile glass bottle,
put an eyedropper on the mouth of the bottle and
dispense. In case ampoules of vitamin C are not
available, tablets of Vitamin C, 500 mg can be dissolved
in distilled water (5 cc) and dispensed. The drops
should be used frequently every few minutes for
the first 2 hours and then hourly for the first 48 hours.
They can be continued 4-6 times a day for the first
couple of weeks. Studies have shown this significantly
reduces the risks of perforations and cornel melts.
Autohemotherapy
Many researchers have tried the use of blood and blood
products in the treatment of chemical injuries and some
of the earliest results of this technique were reported
by Dubrovina (1951). In fact it is even mentioned in
the early Duke-Elder (2) volumes on ophthalmology,
now sadly no longer looked at by most postgraduates!
In this technique, 0.5 to 1.5 ml of the patients own
venous blood drawn from the ante-cubital vein is
injected under the conjunctiva in the perilimbal region
and in the fornices. This is repeated every other day
or as required. The aim of this therapy is manifold.
Blood acts as a buffer, ensures more intimate contact
with the diffusing chemical, than that achieved by
surface irrigation. It thus causes a dilution of the
chemical, besides ensuring separation of the tissues
52
and acting as a barrier against deeper penetration. This
is of great advantage, especially in severe alkali burns.
Also, its fibrinolytic action tends to inhibit the formation
of symblepharon and it acts as a cushion in between
the superficial and deeper tissues. Platelets fill the gaps
on the denuded surface. They also adhere to collagen
by changing their shape from the usual oval to an
amoeboid shape. Antiproteases in the blood inhibit
collagenases, preventing the breakdown of newly
formed collagen.
Newer Drugs
There is increasing research on the use of citrates,
progesterone, epidermal growth factors and some
other medications to promote healing. It may be a
few years before they attain mainstream status for use
in all cases.
RECENT ADVANCES IN THERAPY
Stem Cells
It is now well established that stem cells for the cornea
as well as conjunctival epithelium are located in the
limbal palisades of Vogt. In chemical injuries one or
more clock hours of the limbus may be affected,
causing destruction of these cells. These stem cells, in
normal circumstances, divide into daughter cells, which
undergo transformation into transient amplifying cells
then into terminally differentiated cells as they move
into the cornea, finally forming healthy corneal
epithelial cells. If the stem cells are destroyed, healthy
corneal epithelium will not fill the surface defects. This
causes persistent epithelial defects. These invite
vascularization and conjunctivalization or growth of
cells of conjunctival phenotype on the corneal surface.
Penetrating keratoplasties in cases with stem cell
deficiency are doomed to failure for cast off corneal
epithelium cannot be replaced from the depleted stem
cell reservoir. Diagnosis of stem cell deficiency can be
made by direct observation of loss of the limbal
palisades and limbal ischemia and by indirect evidence
such as persistent epithelial defects, conjunctivalization
and vascularization of the cornea in cases of chemical
burns.
If there is a partial stem cell deficiency, it can be
treated by scraping of the conjunctivalised area of the
cornea and amniotic membrane grafting. This gives
a chance for the distal, unaffected stem cells to grow
down and populate the areas of stem cell loss. This
process may have to be repeated several times.
7
If however, there is a total or near total stem cell
deficiency, the stem cells need to be transplanted to
the affected eye. The donor stem cells can be taken
from the other eye in unilateral burns (ideal). In bilateral
burns, there are several options. If there is an
unaffected area, a small piece of limbal tissue can be
cultured in vitro and the cultured stem cells can be
transplanted to one or both eyes. The other option
is use of stem cells donated by living related donors.
If these are not possible, one can use cadaveric stem
cells from eye bank eyes. In all these cases however,
it is mandatory to give prol onged systemic
immunosuppressive therapy for a period of at least
6 months. Several authors are in favor of much longer
dosage regimens, over years. Stem cell transplant is
usually always done in association with amniotic
membrane transplantation.
Amniotic Membrane Transplant
As said earlier, in partial stem cell deficiency, it may
be sufficient to repeatedly scrape the diseased
epithelium and place a large piece of amniotic
membrane tissue (AMT) over the cornea. Amniotic
membrane is the innermost lining of the foetus and
is obtained from healthy donors who are HIV free,
delivered by cesarean section. Ideally, the membrane
is preserved in liquid nitrogen after mounting on
specially treated nitrocellulose paper for 6 months. The
mother is then retested for HIV to eliminate the window
period effect. If negative, the AMT can be used in the
manner described above. AMT has several properties,
which make it an ideal tissue it down regulates
inflammatory processes and up regulates healing
processes. It also provides an ideal substrate for
epithelial cells to grow over it and populate the areas
of epithelial defects. AMT has 2 sides a smooth side,
which is the epithelial side and a sticky side, which is
the stromal side. It has increasingly wider applications
in anterior segment surgeries, such as in pterygium
repair, which are outside the scope of this chapter. It
is occasional l y used in acute chemical burns
management for its antiinflammatory properties. The
greater the inflammation, the faster the AMT gets
absorbed, but not before down regulating the existing
inflammation. However, it is more commonly used in
cold cases, in partial stem cell deficiency and in total
stem cell loss (in combination with stem cell transplants).
It handles fairly easily and can be sutured using either
8/0 polyglycolic acid sutures or 10/0 nylon. It can be
sutured directly on the cornea. It can also be used
for symblephara release and fornix reconstruction.
Here, after release of the symblephara, the AMT is
pushed deep into the fornices. Sutures passed through
the AMT are brought out through the eyelid and
sutured over small cut pieces of rubber tubing on the
outside. Results are amazing patients with moving
body vision can regain 6/6 vision with a combination
of stem cells and AMT!
53
Keratoprosthesis
In cases where there is total stem cell loss and bilateral
blindness with disfigured anterior segments and gross
tear deficiency, the above 2 treatments will not help.
These are the cases where Keratoprosthesis surgery
(KP) has a role. This surgery is reserved for those who
have good perception of light with accurate projection
in the better eye and a B-scan showing attached retina.
There are several types of KPs available in the world.
The commonly used ones are the Dohlmanns, the
Pintucci and the OOKP (osteo-odonto-KP). The largest
number of KPs implanted is the Singh-Worst KPs. The
author has till date (2008) done 75 Pintucci KPs with
a 11-year follow-up. 65% of operated patients
regained useful vision i.e. they were able to carry out
activities of daily living independently. This is the largest
series of KPs in Asia outside Amritsar.
Fig. 10.2: Acid burns
Fig. 10.1: Acid burns with pseudopterygium
Fig. 10.3: Post-alkali burns pseduopterygium
Fig. 10.4: Chemical burn treated with subconjunctival
venous blood
Conclusion
Chemical injuries are increasing in the modern world.
Acids and alkalis are the main chemicals implicated.
Emergency treatment if reported early may make all
the difference between saving the eye and irreversible
blindness. Early use of cheaply and freely available
treatments such as topical vitamin C and auto-
hemotherapy can reduce morbidity in these cases
Modern methods of managing post-burns corneal
problems such as AMT, stem cell transplant and finally
54
Keratoprosthesis have considerably improved overall
prognosis in these unfortunate patients.
References
1. Duke Elder, Sir Stewart. Diseases of the Outer Eye. Henry
Kimpton Publishers 1965;8(2):604-31,995-1002.
2. Duke Elder, Sir Stewart. Non-Mechanical Injuries. Henry
Kimpton Publishers; 1972;Vol. XIV, Part 2:011-1088.
3. Henriquez AS. Scanning El ectron Microscope in
Experimental Alkali Burnt Corneas. Abstracts of VI Congress
of European society of Ophthalmology 1980;240.
4. Sfalangakos L, Tranos, Mitsonis J, Kouroubetsis J. The
management of chemical burns of the cornea. The cornea
in health and disease. Abstracts of VI Congress of
European Society of Ophthalmology 1980;245.
5. Thoft RA, Friend J Kenyon KR. Ocular Surface response
to trauma. International Ophthalmology Clinics. Summer
1979;19(2).
6. Sridhar MS, Sridhar MS, Bansal AK, Sangwan VS, Rao
GN. Amniotic Membrane Transplantation in Acute
Chemical and Thermal Injury. American Journal of
Ophthalmology July 2000;130:134-36.
7. Dua HS, King AJ, Joseph A. A New classification of
Ocular Surface Burns. Br J Ophthalmol 2001;85:
1379-83.
C H A P T E R
11
Injuries of the Eye due to
Physical Agents
(Thermal, Ultrasonic and Electrical Injuries)
Introduction
The injuries to the eye due to physical agents can
result from thermal, ultrasonic or electrical agents in
addition to radiation injuries of the eye. In the present
chapter, we will highlight:
I. Thermal injuries to the eye.
II. Ultrasonic injuries to the eye.
III. Electrical injuries to the eye.
Non-mechanical Eye Injuries
Radiational injuries
Thermal injuries
Ultrasonioc injuries
Electrical injuries
Thermal Injuries
The injuries of the eye and the adnexa can be caused
by both extremes of temperature and are hence
associated with thermal burns and freezing or exposure
to cold.
HYPERTHERMAL INJURIES
Flame Burns
It can occur secondary to explosion of stove/Gas
heater, industrial cases from high temperatures and
inflammable fluids, gases, Ovens, Furnaces, petrol
stores, burning building wherein people are trapped,
accidents in travel, in automobiles, trains, ships,
airplanes, in war-the flame thrower, the napalm bomb,
explosive fire in the confiance of tank on land, burning
plane in the air, explosion of gun-turret of a ship,
tragedy of swimming through boiling or burning oil
floating on the sea.
Clinical lesions: Eyes themselves are rarely involved
in a flame burn unless the heat is intense and
prolonged, lashes and brows may be scorched, skin
of the lids deeply burned, lids may be destroyed,
however the tarsal plates remain intact, cornea
shrivelled, ocular tissues damaged in varying degrees,
in worst cases whole eye and the orbital contents
incinerated, areas of black eschar may appear which
as they fall off leave raw islands, extensive loss of tissue
on forehead, cheeks, eyelids leads to black and
shapeless mask, infection can occur and can spread
inwards causing orbital cellulitis and infective
dacryoadenitis. Healing is slow and can leads to
inexorable contraction distorting the face.
Contact Burns
It can occur secondary to contact of the eye and the
adnexa with lighted ends of cigars or cigarettes, shreds
of tobacco from pipes, head of lighted match or a
firework, glowing coal or hot cinders from a fire,
industry-flying pieces of glowing metal, slag, solder,
lead or glass or with solid bodies such as slag, molten
metal with high melting point such as iron, molten
glass, very hot bodies above 1000C.
Clinical lesions: In the conjuntiva, hyperemia,
violent chemosis, greyish white coagulated plaque. In
the cornea superficial or deeper burns, superficial
burns will be grey or yellowish clouding of the epithelium
which develops into erosion whereas in deeper burns
cornea become grey and opaque like ground glass
or white like procelain, a line of demarcation eventually
forms and the slough is cast off, leaving an ulcer which
if deep becomes infected and may perforate. Healing
is by formation of fibrous tissue, resultant leucoma
is permanent.The other complications of contact burns
can be bullous keratitis, ectasia, corneal staphyloma,
pseudopterygium, symblepharon and on the other
hand deeply penetrating lesion involves the sclera which
may be perforated resulting in prolapse of uvea and
vitreous, purulent uveitis, panophthalmitis.
Scalds
It occurs secondary to burns by hot fluids affecting
the lids, can lead to conjunctival swelling and chemosis
and symblepharon in chronic cases.
56
Treatment
Treatment of the lid burn:
The best emergency measure is to cover the face
with sterile dressing or handkerchief.
In early stage the affected area thoroughly cleansed
with saline and surrounding area with soap and
water
All the aseptic measures to be taken while treating
this patients
Blisters to be fully opened, loose epidermis cut away,
remnants of signed lashes removed
Antibiotic cream applied over the denuded area.
Sofratulle dressing applied
For full thickness burns of the lids, the only effective
treatment is graft
Full thickness skin graft should be carried out as
an emergency measure.
Treatment of the burns of the eye:
Local analgesics avoided owing to their deleritious
effect on epithelialization.
Topical cycloplegics Atropine eye drops
Systemic NSAIDs/Sedatives to achieve comfort
Antibiotics to prevent secondary infection
Ocular lubrication for corneal burns
Glass rod to be passed in the fornices to prevent
the risk of symblepharon or use of symblepharon
ring
Conjunctival transposition flap
Corneal leucomatous opacity at later stage can be
replaced by corneal graft-PK or LK
Amniotic membrane graft or Limbal cell transplant
also has a role to play
Topical corticosteroids also can be used judiciously
in case to case basis.
HYPOTHERMAL INJURIES
Surgical Hypothermia
It occurs in cardiovascular surgery and in neurosurgery
or by immersing the patient in ice packs and cold baths,
supplemented by injection of lytic cock-tail.
Clinical lesions: At temperatures far under the
therapeutic range opacities developed in the cornea
and lens associated with widespread cellular and
hemorrhagic changes in the ocular tissues, particularly
in the ciliary body and retina. Retinal arteries and veins
become indistinct and show a fine stippling of the blood
column and the retina becomes pale and optic disc
white, however, within two seconds of restoration of
the circulation the fundus assumes its normal
appearance.
Accidental Hypothermia
It occurs on exposures at high altitudes in snow-storm.
Aviators in open aircraft, in a damaged cockpit or while
bailing out from an aircraft in difficulties can also suffer
from hypothermia.
Clinical lesions: Clinical cases are rare because of
the protection afforded by the richly vascular lids and
the care usually taken of them even in conditions of
severe stress and even the temperature of cornea is
3 to 5 degrees less than the other tissues of the body.
There can be varying degrees of conjunctival
hyperemia, corneal erosion or opacity which may
disappear without any ill effects. Severe bilateral
ulceration of the cornea leading to permanent opacity
of the cornea.
Cryosurgery
It is used as a therapeutic modality in different cases
with varying indications. The effects of the freezing on
the various ocular tissues and intraocular fluids depends
on the temperature used, the area involved, the length
of application and the type of cell principally
concerned.
Clinical lesions:
Conjunctiva: Congestion, edema.
Muscles and tendons: Edema and hemorrhage
Sclera: Swelling and separation of scleral fibers seen
microscopically, no clinically evident change
Ciliary body: Freezing of ciliary body resulting in
reduce aqueous humor formation
Lens: Freezing of the lens utilised in cryoextraction
of the lens
Retina and choroid: Adhesive chorioretinal reaction
Vitreous: Vitreous ice balls.
Ultrasonic Injuries
Sound waves (sonic or acoustic energy) which are
audible to the human ear produce no recognizable
ocular injury. Ultrasonic vibrations above the limits of
hearing may produce characteristic biological reactions.
Besides its diagnostic and therapeutic applications,
ultrasonic energy can produce the following injuries
to the eye.
CLINICAL LESIONS
Eyelidsepilation, ulceration of the skin edema.
Corneaslight and transient turbidity and swelling
in superficial corneal layers, earlier changes are
reversible but the later are irreversible and lead to
necrosis. High intensities of radiation cause necrosis
and ulceration of the epithelium, a general
57
Injuries of the Eye due to Physical Agents (Thermal, Ultrasonic and Electrical Injuries)
thickening of the stroma with the formation of dense
leucomatous opacities.
LensTwo types of cataractCavitation and
Thermal. In cavitation cataract a zone of frothy,
spume like turbidity of the deeper layers of the
cortex around the nucleus. In thermal cataract there
is densely white permanent opacity and it develops
after radiation of high frequency and greater
intensity.
Vitreousliquefied irreversibly by a few seconds
exposure.
Retina and choroidadhesive chorioretinal
adhesion with less damage to the sclera than caused
by diathermy or by ultrasonic energy of megahertz
frequencies, retinal edema within 12-24 hours
followed by proliferative and pigmentary changes.
Electrical Injuries
Electrical injuries are due to passage of an electric
current through the body and the commonest cause
being direct double contact between two live electric
conductors or a single contact either direct or by short
circuit, between a conductor and the earth so that the
circuit is completed. The similar effect result on being
stuck by lightning. There is a point of entry and often
of exit of the elctric current causing an electrical burn,
the passage of current usually produces violent tetanic
spasms of the muscles, low voltage currents cause
auricular fibrillation and high voltage currents affects
the central nervous system and lead to loss of
consciousness or death from respiratory failure or
cardiac arrest and shock. The high resistance offered
by the non-nervous tissue accounts for the thermal
effects of electric injuries, which may result in immediate
coagulation of the proteins of the cells.
CLINICAL LESIONS
Lesions of the lidsTypical electrical burn at the
point of entry imprint as a sharply defined necrotic
mark without surrounding hyperemia. Lid burns
differs from heat burns in that the former are
painless, dry and aseptic and usually circumscribed,
mainly due to the very high temperatures and short
duration. Electrical gangrene may supervene in the
subsequent days or weeks due to circulatory
impairment.
Lesions of the conj unctivaThere can be
substantial damage to the eye in both electrical as
wel l as l ightning injuries. Minor degree of
conjunctival hyperemia and ciliary injection will
invariably occur in each and every case of electrical
burn. There can be subconjuctival effusion of blood
which is transient and which disappears in few days
time.
Corneal lesionsThe commonest lesions are
interstitial opacities which can be punctate, striate
or diffuse. This type of generalised corneal
cloudiness usually clears up in few days. However,
if destructive electrical burn is formed the epithelium
may become necrotic and exfoliate and sensation
may be impaired or lost so that serious ulceration
may devel op and become recurrent and
permanent scar may form. In some cases there can
be purulent infiltration of entire cornea, extensive
necrosis, perforation or phthisis of the globe.
Lesions of the iris and ciliary bodyIris and ciliary
body show irritative changes in any type of electrical
injury. There can be mild and transient iritis,
sometimes widespread synechiae formation with
heavy aqueous flare and occasionally hyphema.
Lesions of the pupilUnilateral or bilateral extreme
miosis with sluggish or absent reactions, spasm of
accomodation.
Electric cataractLenticular opacities form
sometime after the accident and is sometimes the
only finding in cases with electrical injury. Main
changes are localized in the capsule itself and in
the immediate cortex underneath the capsule. It
involves both anterior and posterior surface of lens.
There is formation of vacuoles underneath the
capsule. The type of opacification varies from slight
indefinite haze to densely crowded punctate
opacities. There can be evident polychromatic
lusture seen on the lens.
Lesions of the retina and choroidRetinal edema,
papilledema, hemorrhages, traumatic chorioretinitis
in the periphery, detachment of the retina, vitreous
opacities. Most dramatic changes are at the posterior
pole which can be combination of the electric
current and radiation resulting in macular edema,
punctate pigmentary degeneration, cystoid changes.
Optic nerveOptic neuritis.
Functional disabilitesPhotophobia, blepharo-
spasm, transient blindness to permanent bilateral
visual loss, concentric contraction of the field, ring
scotoma, absolute central scotoma, disturbance of
binocular fusion.
LIGHTNING INJURY
Even in fatal cases the body may be unmarked,
In some a deep necrotic burn is formed at the point
of entry,
In others an arborescent tracery of linear burns
appears (lightning prints).
Mydriasis, partial internal ophthalmoplegia,
blindness from optic atrophy, deafness, loss of
memory, nervous damage.
58
Injury to the retina caused by brilliance of flash
plays an inconspicuous part in the total damage,
retinal damage in the macular area, rupture of the
choroid.
TREATMENT
First and foremost is saving of life.
Local burns of the skin of the lids or in the vicinity
is treated as in case of thermal burns.
Treatment of ocular lesions is on the general
principles: Rest, atropine, local heat.
Bibliography
1. Ophthalmology Clinics of North America by Ferenc Kuhn
et al. volume 15, Non mechanical injuries.
2. System of ophthalmology by Sir Stewart Duke Elder, Vol.
XIV, Injuries, Part 2, Non Mechanical Injuries.
3. Work and the Eye, 2nd edition of Rachel V North,
Woburn MA, Butterworth Heinemann, 2001;51-74.
C H A P T E R
12
Radiational Injuries to the Eye
Introduction
Radio and television signals, radar, heat, infrared,
ultraviolet, sunlight, starlight, cosmic rays, gamma rays,
and X-rays all belong to the electromagnetic spectrum
and differ only in their relative energy, frequency, and
wavelength. These waves all travel at the speed of
light, and unlike sound they can all travel through
empty space. The frequencies above visible light have
enough energy to penetrate and cause damage to
living tissue, damage that can be as minor as a sunburn
caused by ultraviolet light or as extreme as the
incineration of Hiroshima, Japan, during World War
II. Lower frequencies do not penetrate, but can cause
eye and skin damage, primarily due to the heat they
transmit. The energy of electromagnetic radiation is
a direct function of its frequency. The high-energy,
high-frequency waves, which can penetrate solids to
various depths, cause damage by separating molecules
into electrically charged pieces, a process known as
ionization. Atomic particles, cosmic rays, gamma rays,
X-rays, and some ultraviolet are called ionizing
radiation. The pieces they generate are called free
radicals. They act like acid, but they last only fractions
of a second before they revert to harmless forms.
Adjusting the energy of therapeutic radiation can select
a depth at which it will do the most damage. Ionizing
radiation also does damage to chromosomes by
breaking strands of DNA. DNA is so good at repairing
itself that both strands of the double helix must be
broken to produce genetic damage. Because radiation
is energy, it can be measured. There are a number
of units used to quantify radiation energy. Some refer
to effects on air, others to effects on living tissue. The
roentgen, named after Wilhelm Conrad Roentgen,
who discovered X-rays in 1895, measures ionizing
energy in air. A rad expresses the energy transferred
to tissue. The rem measures tissue response. A
roentgen generates about a rad of effect and produces
about a rem of response. The gray and the sievert
are international units equivalent to 100 rads and
rems, respectively. A curie, named after French
physicists who experimented with radiation, is a
measure of actual radioactivity given off by a
radioactive element, not a measure of its effect. The
average annual human exposure to natural
background radiation is roughly 3 milliSieverts (mSv).
It is reasonable to presume that any amount of
ionizing radiation will produce some damage.
However, there is radiation everywhere, from the sun
(cosmic rays) and from traces of radioactive elements
in the air (radon) and the ground (uranium, radium,
carbon-14, potassium-40 and many others). Earths
atmosphere protects us from most of the suns
radiation. Living at 5,000 feet altitude in Denver,
Colorado, doubles exposure to radiation, and flight
in a commercial airliner increases it 150-fold by lifting
us above 80% of that atmosphere. Because no
amount of radiation is perfectly safe and because
radiation isever present, arbitrary limits have been
established to provide some measure of safety for
those exposed to unusual amounts. Less than 1% of
them reach the current annual permissible maximum
of 50 mSv.
It is therapeutic, accidental, and deliberate radiation
that does the obvious damage. There has not been
much in the way of deliberate radiation damage since
Nagasaki, but accidental radiation exposure happens
periodically. Between1945 and 1987, there were 285
nuclear reactor accidents, injuring over 1,550 people
and killing 64. The most striking example, and the
only one to endanger the public, was the meltdown
of the graphite core nuclear reactor at Chernobyl in
1986, which spread a cloud of radioactive particles
across the entirecontinent of Europe. Information
about radiation effects is still being gathered from that
disaster. There have also been a few accidents with
medical and industrial radioactivity.
Nevertheless, it is believed that radiation is
responsible for less than 1% of all human disease and
for about 3% of all cancers. This figure does not include
lung cancer from environmental radon, because that
information is unknown. The figure could be
significant, but it is greatly confounded by the similar
effects of tobacco.
60
Radiation can damage every tissue in the body.
The particular manifestation will depend upon the
amount of radiation, the time over which it is
absorbed,and the susceptibility of the tissue. The fastest
growing tissues are the most vulnerable, because
radiation as much as triples its effects during the growth
phase. Bone marrow cells that make blood are the
fastest growing cells in the body. A fetus in the womb
is equally sensitive. The germinal cells in the testes and
ovaries are only slightly less sensitive. Both can be
rendered useless with very small doses of radiation.
More resistant are the lining cells of the bodyskin
and intestines. Most resistant are the brain cells, because
they grow the slowest.
The relative sensitivity of various tissues gives a good
idea of the wide range that presents itself. The numbers
represent the minimum damaging doses; a gray and
a sievert represent roughly the same amount of
radiation:
Fetus 2 grays (Gy).
Bone marrow 2 Gy.
Ovary 2-3 Gy
Testes 5-15 Gy.
Lens of the eye 5 Gy.
Child cartilage 10 Gy.
Adult cartilage 60 Gy.
Child bone 20 Gy.
Adult bone 60 Gy.
Kidney 23 Gy.
Child muscle 20-30 Gy.
Adult muscle 100+ Gy.
Intestines 45-55 Gy.
Brain 50 Gy.
Notice that the least of these doses is a thousand
times greater than the background exposure and nearly
50 times greater than the maximum permissible annual
dosage. The length of exposure makes a big difference
in what happens. Over time the accumulating damage,
if not enough to kill cells outright, distorts their growth
and causes scarring and/or cancers. In addition to
leukemias, cancers of the thyroid, brain, bone, breast,
skin, stomach, and lung all arise after radiation. Damage
depends, too, on the ability of the tissue to repair itself.
Some tissues and some types of damage produce
much greater consequences than others.
Immediately after sudden irradiation, the fate of
the patient depends mostly on the total dose absorbed.
This information comes mostly from survivors of the
atomic bomb blasts over Japan in 1945. Massive doses
incinerate immediately and are not distinguishable
from the heat of the source. A sudden whole body
dose over 50 Sv produces such profound neurological,
heart,and circulatory damage that patients die within
the first two days. Doses in the 10-20 Sv range affect
the intestines, stripping their lining and leading to death
within three months from vomiting, diarrhea,
starvation, and infection. Victims receiving 6-10 Sv all
at once usually escape anintestinal death, facing
instead bone marrow failure and death within two
months from loss of blood coagulation factors and the
protection against infection provided by white blood
cells. Between 2-6 Sv gives a fighting chance for survival
if victims are supported with blood transfusions and
antibiotics. One or two Sv produces a brief, non-lethal
sickness with vomiting, loss of appetite, and generalized
discomfort.It is clearly important to have some idea
of the dose received as early as possible, so that
attention can be directed to those victims in the 2-
10 Sv range that might survive with treatment. Blood
transfusions, protection from infection in damaged
organs, and possibly the use of newer stimulants to
blood formation can save many victims in this category.
Local radiation exposures usually damage the skin and
require careful wound care, removal of dead tissue,
and skin grafting if the area is large. Again infection
control is imperative.
Injuries of the Eye due to
Ionizing Radiation
X-rays, beta rays, and other radiation sources in
adequate doses can cause ocular injury.
LIDS
The eyelid is particularly vulnerable to X-ray damage
because of the thinness of its skin. Loss of lashes and
scarring can lead to inversion or eversion (entropion
or ectropion) of the lid margins and prevent adequate
closure.
CONJUNCTIVA
Scarring of the conjunctiva can impair the production
of mucus and the function of the lacrymal gland ducts,
thereby causing dryness of the eyes.
LENS
X-ray radiation in a dose of 500-800 R. directed toward
the lens surface can cause cataract, sometimes with
a delay of several months to a year before the opacities
appear.
Injuries due to Ultraviolet
Radiation
CORNEA
Ultraviolet radiation of wave lengths shorter than 300
nm (actinic rays) can damage the corneal epithelium.
61
This is most commonly the result of exposure to the
sun at high altitude and in areas where shorter wave
lengths are readily reflected from bright surfaces such
as snow, water, and sand.
Exposure to radiation generated by a welding arc
can cause welding flash burn, a form of keratitis.
LENS
Wavelengths of 300-400 nm. are transmitted through
the cornea, and 80% are absorbed by the lens, where
they can cause cataractous changes.
Epidemiologic studies suggest that exposure to solar
radiation in these wavelengths near the equator is
correlated with a higher incidence of cataracts.
They also indicate that workers exposed to bright
sunlight in occupations such as farming, truck driving
and construction work appear to have a higher
incidence of cataract than those who work primarily
indoors.
Experimental studies have shown that these wave-
lengths cause changes in the lens protein, which lead
to cataract formation in animals.
Injuries due to Visible Radiation
(Light)
Visible light has a spectrum of 400-750 nm. If the
wavelengths of this spectrum penetrate fully to the
retina, they can cause thermal, mechanical, or photic
injuries.
THERMAL INJURIES
They are produced by light intense enough to increase
the temperature in the retina by 10-20C.
Lasers used in therapy can cause this type of injury.
The light is absorbed by the retinal pigment epithelium,
where its energy is converted to heat, and the heat
causes photocoagulation of retinal tissue.
MECHANICAL INJURIES
They can be produced by exposure to laser energy
from a Q-switched or mode-locked laser, which
produces sonic shock waves that disrupt retinal tissue.
PHOTIC INJURIES
They are caused by prolonged exposure to intense
light, which produces varying degrees of cellular
damage in the retinal macula without a significant
increase in the temperature of the tissue.
Sun gazing is the most common cause of this type
of injury, but prolonged unprotected exposure to a
welding arc can also damage the the retinal macula.
There may be permanent decrease in visual acuity.
The intensity of light, lenght of exposure, and age
are all important factors. The older ones are more
sensitive, also those who have had cataract surgery
because filtration of light by the lens is impaired.
Injuries due to Infrared Radiation
Potters may be exposed to this type of radiation.
Wavelengths greater than 750 nm. in the infrared
spectrum can produce lens changes.
La cataracte des verriers(glassblowers cataract)
is an example of a heat injury that damages the anterior
lens capsule among unprotected artists. Denser
cataractous changes can occur in unprotected workers
who observe glowing masses of glass or iron for many
hours a day.
Another important factor is the distance between
the worker and the source of radiation. In the case
of arc welding, infrared radiation decreases rapidly as
a function of distance, so that farther than 3 feet away
from where welding takes place, it does not pose an
ocular hazard anymore but, ultraviolet radiation still
does. That is why welders wear tinted glasses and
surrounding workers only have to wear clear ones.
When we speak of type of exposure, potters look
at their cone packs for very short periods of time in
a repeated way, more often nearing the end of firing;
and also according to the use of other methods for
measuring temperature, like the concomitant use of
a thermocouple and a reading device.
So, these short-term exposures are spaced by
quite longer exposure-free periods and the sum of
the former does not correlate with the concept of many
hours a day.
We have searched the literature pertaining to
Occupational Health and Safety and have not found
a single case of presumed ceramicists or potters
cataract, even if the trade of potter is quite older than
the one of glassblower.
Therefore, I do not think that any of the above
types of radiation present a threat to potters.
It is a good thing, mainly at high temperature, to
wear lightly tinted industrial grade safety glasses to
better visualize cones (ocular ergonomics) and also to
reassure those who are more worried.
These glasses also offer a better protection than
typical sun-glasses in case of projection of hot dust
particles from a gas kiln when looking through the
peephole in a soft brick door.
By the way with ageing, most if not all of us, will
suffer from cataracts of the senile type.
62
The progress or change and the related reduction in
vision is usually quite slow.
Nuclear sclerosis-an increasing density in the central
mass of protein-causes a myopic change than can be
corrected by changing glasses for some years-in many
instances restoring vision to near normal.
Welding Arc Injuries
Eye injuries account for one-quarter of all welding
injuries, making them by far the most common injury
for welders, according to research from the Liberty
Mutual Research Institute for Safety. Those most at
risk for welding-related eye injuries are workers in
industries that produce industrial and commercial
machinery, computer equipment, and fabricated metal
products.
The best way to control eye injuries is also the most
simple: proper selection and use of eye protection.
Helmets alone do not offer enough protection. Welders
should wear goggles or safety glasses with sideshields.
Goggles provide better protection than safety glasses
from impact, dust, and radiation hazards.
Unfortunately, workers dont always wear goggles
or safety glasses because of low perception of risk,
poorly maintained lenses, discomfort, having to wear
prescription lenses underneath, and vanity. It is
important to stress to workers that welding-related eye
injuries come from a number of sources, including:
mechanical damage from being struck by flying
particles and chipped slag; radiation and
photochemical burns from ultraviolet radiation
(UVR), infrared radiation, and intense blue light;
and irritation and chemical burns from fumes
and chemicals.
To help in reducing eye injuries, you should educate
workers about all of the dangers they face and should
implement an eye protection plan that outlines proper
welding behavior.
Cumulative Damage Risks
All of the most common types of welding (shielded
metal-arc or stick welding, gas metal-arc welding, and
oxyacetylene welding) produce potentially harmful
ultraviolet, infrared, and visible spectrum radiation.
Damage from ultraviolet light can occur very quickly.
Normally absorbed in the cornea and lens of the eye,
ultraviolet radiation (UVR) often causes arc eye or arc
flash, a very painful but seldom permanent injury that
is characterized by eye swelling, tearing, and pain.
While most welding-related eye injuries are
reversible, with more than half of injured workers
returning to work in less than two days and 95 percent
in less than seven days, some eye injuries are
irreversible and permanent visual impairment occurs.
This is especially true with infrared and visible spectrum
(bright light) radiation. Both can penetrate through
to the retina andalthough this is rarecan cause
permanent retinal damage, including cataracts,
diminished visual acuity, and higher sensitivity to light
and glare.
And welders are not the only workers at risk. While
the welding arc is the principal source of UVR, other
workers in the area can sustain eye damage from the
radiation as far as 50 feet away from UVR reflecting
off shiny surfaces, concrete, or unpainted metals. To
counteract this reflection, you should install shielding
curtains where practical or require that all workers in
the area wear appropriate eye protection.
Yet, despite the insidious damage radiation can
cause, molten and cold metal particles striking the eye
are still the most common sources of eye injuries.
Eye Protection Goes Beyond
the Helmet
Helmets and protective clothing shield welders from
sunburn and welders flash, but with the majority
of their work performed with the helmet up, welders
also need to wear goggles or safety glasses with
sideshields. These will protect them from particles sent
flying during pre-job grinding, hammering, and
power chipping that make it past the helmets
protective front.
Some guidelines and safety warnings for welding
suggest workers should not wear contact lenses, even
though there does not appear to be any research that
would support such a recommendation. In fact, the
National Safety Council, the American Welding Society,
and the FDA all acknowledge that wearing contact
lenses while welding is safe and even can provide UV
protection. The only caveat is that contact lenses should
not be used as eye protection in place of safety glasses
or goggles.
Once the proper goggles/shields are in hand, you
can turn your attention to the type of helmet best suited
for the job. Published tables are available through the
welding helmet vendor or the Internet, which can help
you determine the most appropriate lens shade based
on the type of welding and the amperage of the
welding unit. It is a common misconception that a
darker shade provides more protection against UV.
Properly maintained welding helmets, regardless of
shade, provide 100 percent protection against UV,
according to the manufacturers.
63
Arc welding helmets can be fixed shade or variable
shade. Typically, fixed shade helmets are best for daily
jobs that require the same type of welding at the same
current levels, and variable helmets are best for workers
with variable welding tasks. Helmet shades come in
a range of darkness levels, rated from 9 to 14 with
14 being darkest, which adjust manual l y or
automatically, depending on the helmet. To determine
the best helmet for the job, select a lens shade that
provides comfortable and accurate viewing of the
puddle to ensure a quality weld.
Now that your workers have the right eye protection
for the job, it is time to implement an ongoing eye
protection plan that ensures they use the equipment
properly.
Bibliography
1. Occupational and Environmental Medicine. Joseph
Ladoue and al, last edition.
2. Occupational Medicine, Zenz C, 2003.
3. Oshline and Nioshtic database, 2004.
4. Precis de Medecine du Travail, Desoille H, Scherrer J,
Truhaut R, last edition.
C H A P T E R
13
Traumatic Angle Recession
Glaucoma: An Overview
Cyres K Mehta, Keiki Mehta (India)
This chapter deals with blunt trauma to the eyeball
leading to angle recession glaucoma.
Synonyms: Angle-recession glaucoma, post-
traumatic angle recession glaucoma, contusion angle
recession glaucoma, contusion angle deformity.
History
Treacher Collins described the micropathology of angle
recession glaucoma as a split into the ciliary muscles
in its entire circumference so that angle of the chamber
was prolonged out. In 1945 DOmbrain postulated
that angle recession led to increased intraocular tension.
Angle recession may be associated with many other
conditions associated with the ocular trauma sustained
such as, such as dislocation or subluxation of the lens,
traumatic cataract, iridodialysis, cyclodialysis, hyphema
and retinal detachment, extraocul ar muscl e
avulsion,orbital trauma and globe rupture in extreme
cases.
When Blunt (non-penetrating) injury is sustained
by the eye by an object moving parallel to the visual
axis,the cornea and anterior sclera is displaced
backwards. This leads to a compensatory equatorial
expansion. Aqueous and vitreous are relatively
incompressible and transmit the force so that the ocular
tissues undergo sudden expansion and possibly tearing.
The General features of non-penetrating trauma
are (Campbells classification of the 7 tissue rings).
1. Pupillary sphincter tears.
2. Iridodialysis.
3. Anterior ciliary body tearWe can have a angle
recession or a tear in the face of the ciliary body.
The rupture of the ciliary body between its
longitudinal and circular fibers shows that this is
the weakest portion of the ciliary body.This leads
to deepening of the Anterior chamber also known
as angle recession.
4. Cyclodialysis, or a separation of the ciliary body
from the sclera.
5. Trabecular dialysis or a tear through the trabecular
meshwork.
6. Tearing of the l ens zonul es l eading to
phacodonesis, iridodonesis, subluxation or total
dislocation of the lens backwards.
7. Retinal dialysis at the ora or a giant retinal tear.
After blunt trauma to the globe we can divide
pressure fluctuation into EARLY (few days to few
weeks) and LATE (few weeks and later). Intraocular
pressure (IOP) may be reduced because of 2 reasons.
Firstly due to to trauma to the ciliary body the
amount of aqueous secretion is reduced and secondly
due to a total tear of the trabecular meshwork into
Schlemms canal the aqueous outflow is greatly
exaggerated, or, due to a cylodialysis developing
the aqueous is been drained out via uveoscleral
ouflow.
Alternatively in the short-term the pressure can
rise up for several weeks.This is due to increased
resistance to the outflow of aqueous due to trabeculitis
(swelling of the meshwork) due to circulating cytokines
and prostaglandins.Treatment with corticosteroid is
advocated here.
Late Post-traumatic Glaucoma:
Angle Recession Glaucoma
INTERNATIONAL INCIDENCE
In 60-94% of cases of patients with blunt ocular injury
in Africa angle recession was noted.
In Africa angle recession glaucoma was frequently
bilateral.
The presence of angle recession does not neces-
sarily mean the onset of raised IOP and nerve head
pathology.
Other studies have indicated that 6-20% of all
individuals with angle recession went on to develop
late onset glaucoma.
Again another study showed a 5-8% conversion
to glaucoma after angle recession.
A 3:1 to 4:1 male preponderance was noted by
some studies.
65
Traumatic Angle Recession Glaucoma: An Overview
INDIAN INCIDENCE (ACCORDING TO
SIHOTA AND SOOD)
Of all traumatic glaucoma patients, 71% were below
30 years of age. There was a 90% male preponderance
Blunt trauma was the mode of injury in 85% of cases.
The cricket ball, tennis ball, gilli-danda (a small flying
stick), hockey stick, bamboo stick and stone were
responsible for 30% cases; fire cracker injury in 20%
cases and 50% were work-related, assaults or accidental
injury. In eyes having angle recession, two or more
quadrants were involved in 87% cases. Other features
of trauma like sphincter tear, hyphema, iridodialysis,
subluxation, dislocation, vitreous hemorrhage, retinal
detachment, and cataract could be seen in various
combinations in about 95% cases. Fifty percent of
traumatic glaucomas had an IOP of =30 mm Hg and
56% had a vision =20/200.
SLITLAMP FINDINGS
The chamber appears deeper than the other eye.Other
features of blunt trauma such as phacodonesis,
iridodialysis and hyphema might be seen.
GONIOSCOPIC FINDINGS
Gonioscopically angle recession is characterized by
widening of the ciliary body and prominence of the
cilary spur. Sometimes trabecular meshwork tears are
seen along with iridodialysis and cyclodialysis.
After the injury scar tissue may fill the angle
recession cleft confounding the diagnosis at later follow
ups, so, as soon as blunt trauma is noted and the cornea
is clear enough and the patient cooperative enough
a gonioscopy should be carried out.
FURTHER INVESTIGATIONS
Ultrasound Biomicroscopic Study and or
Anterior Segment OCT
Ultrasound biomicroscopy produces high-resolution
images of the anterior segment, providing cross-
sectional views of the angle in vivo similar to those
of a histologic section.
This noninvasive procedure is readily performed
in a clinical setting in an intact globe.
High-resolution images of angle recession, irido-
dialysis, and cyclodialysis have been described.
Anterior segment OCT is another modern diagnostic
tool which can study the angle (Ziess Visante and
others).
Pathology
After the initial injury to the ciliary body and or trabe-
cular meshwork, scarring occurs, causing obstruction.
Also a descemets like membrane is seen growing from
the cornea over the angle similar to the membrane
seen in iridocorneal endothelial syndrome.
Chandl er cl aimed that gl aucoma is due to
impairment of the action of ciliary muscles,due to the
tear in its body, which open the pore of the trabecular
meshwork
Cases with involvement of lesser area of angle
showed no rise of intraocular pressure during the follow
up period. This agrees with the findings of Alter who
observed glaucoma to be associated more commonly
in cases having 240 degrees or more of angle
involvement.
It is usually agreed that more than 180 degrees
of angle involvement are required for pressure
elevation in most cases.
Its interesting to note that that the other eye in
unilateral angle recession glaucoma are more likely to
have elevated IOP as well as be steroid responders.
Its safe to conclude that eyes with a tendency to
develop higher IOP have a greater tendency to develop
glaucoma after blunt trauma.
Figs 13.1A and B: Traumatic glaucoma
66
Management of Angle
Recession
In Angle Recession Glaucoma beta blockers like
Levobunolol, alpha agonists like Brimonidine, prostag-
landin analogues like Latanoprost and carbonic
anhydrase inhibitors like Dorzolamide all can help
lower intraocular pressure.
However, Pilocarpine and other miotics are contra-
indicated as they decrease uveoscleral outflow.Once
the meshwork is scarred uveoscoleral outflow is the
predominant pathway for aqueous egress.
Nd:Yag Laser trabeculopuncture as well as laser
trabeculoplasty have proved to be ineffective in the
long term and mildly effective in the short-term at best.
Non-Penetrating Deep Sclerectomy has no role to
play in these cases as trabecular meshwork is scarred
in its entirety usually.
Filtering surgery is less effective in angle recession
glaucoma eyes than in eyes with chronic simple
glaucoma.Mitomycin C application increases the
success rate in some studies to beyond 50% for 5 years.
Valve implants such as the Molteno and Ahmed
have proved to be successful with certain studies
showing 57% survaival rate at 5 years.
Continual follow-up with effective medical and
surgical management is the key to long-term glaucoma
management in these cases.
Bibliography
1. Alper MG. Contusion angle deformity and glaucoma.
Arch Ophthal (Chicago) 1963;69:455.
2. Campbell DG. Traumatic Glaucoma. In Shingleton BJ,
Hersh PS, Kenyon KR (Eds): Eye Trauma, St
Louis,1991,Mosby.
3. Chandler, P. A. Secondary glaucoma. Tr. Ophthal. Soc.
Australia 1960;20:17.
4. d' Ombrain, A. Traumatic or ' Concussion' chronic
glaucoma. Brit. J. Ophthal 1949;33:495.
5. Ellong A, Ebana MC, Nyouma ME, Bella HA, Ngosso A,
Njoh LC. Post-traumatic glaucoma with irido-corneal
angle injuries in Cameroon. Bull Soc Belge Ophtalmol
2005;298:21-28.
6. Girkin CA, McGwin G Jr, Long C, Morris R, Kuhn F.
Glaucoma after ocular contusion: A cohort study of the
United States eye injury registry. J Glaucoma 2005;14:
470-73.
7. Pettit, T. H. and Keates, E. U. Traumatic cleavage of the
chamber angle. Arch. Ophthal, (Chicago) 1963;69:438.
8. Sihota R, Sood NN, Agarwal HC. Traumatic glaucoma.
Acta Ophthalmol Scand 1995;73:252-54.
9. Treacher-Collins, E. T. On Pathological examination of
three eyes lost from Contusion. Tr. Ophthal. Soc. U.K.
1962;12:180
10. Wolff, S. M. and Zimmerman, L. E. Chronic Secondary
glaucoma. Amer. J. Ophth 1962;54:547.
Figs 13.2A and B: Cyclodialysis
Fig. 13.3: Angle recession (wide CBB)
Fig. 13.4: Iridodialysis
C H A P T E R
14
Management of Blunt Trauma
of Anterior Segment
Introduction
Blunt ocular trauma usually causes closed globe injury
resulting several vision threatening complications.
Injuries to the posterior segment structures causes
poorer visual outcome compared to the anterior
segment lesions. In this chapter the injuries to the
anterior segment lesions will be discussed. Injuries to
the crystalline lens also will be discussed in detail in
a separate chapter. Ocular trauma classification group
has developed a classification system for mechanical
injuries of the eye. Closed globe injury classification
is described in detail. Open globe injury classification
will be included in the chapter on open globe injury.
Specific variable including vitreous hemorrhage,
retinal detachment and hyphema have not been
included in the classification of closed globe injuries.
Study on identification of prognostic factors affecting
visual outcome in all types of closed globe injures in
lacking. Patients suffering from closed globe injuries
and presenting with hyphema have been studied in
detail. In these patients visual acuity at presentation
has been shown to predict final visual acuity. In a
retrospective study on pediatric ocular trauma,
patients with only anterior segment involvement had
82% chance of getting final visual acuity of 20/30 or
better, in comparison to combined anterior and
posterior segment involvement with 47% chance of
achieving 20/20 or better visual acuity.
Closed-globe Injury:
Classification
1
TYPE
A. Contusion
B. Lamellar laceration
C. Superficial foreign body
D. Mixed.
GRADE
Visual acuity
1. > 20/40
2. 20/50 to 20/100
3. 19/100 to 5/200
4. 4/200 to light perception
5. No light perception.
PUPIL
Positive: Relative afferent papillary defect present in
affected eye.
Flow chart 14.1: Classification of ocular trauma
68
Negative: Relative afferent papillary defect absent in
affected eye.
ZONE
I. External (limited to bulbar conjunctiva, sclera,
cornea)
II. Anterior segment (involving structures in anterior
segment internal to the cornea and including the
posterior lens capsule; also includes pars plicate
but not pars plana)
III. Posterior segment (all internal structures posterior
to the posterior lens capsule).
Birth Trauma
It is rare and has been reported to occur during parturi-
tion. Trauma usually results from faulty application of
forceps during child birth. This may result in vertical
Descemets membrane tear, resulting in severe corneal
edema.
2, 3
It may take 8-12 weeks for corneal edema
to resolve. Once corneal edema subsides, the child
has very high astigmatism (8-12 D). High astigmatism
is due to flattening of meridian 90 to the Descemets
membrane tear and corresponding steeping of
meridian parallel to the Descemets membrane tear.
At the time of presentation with corneal edema it
should be differentiated from other causes of
congenital corneal clouding. Congenital Hereditary
Endothelial Dystrophy is bilateral and corneal edema
in buphthalmos has associated high intraocular
pressure. In the acute stage mild topical steroids,
hyperosmotic agent and anti-glaucoma drug to keep
the intraocular pressure low should be given. In the
later stage when edema has subsided astigmatism may
be treated with either glasses or RGP contact lens. RGP
filling may be difficult in neonates. Astigmatic
keratotomy and compression sutures may be tried.
In case the astigmatism is higher the astigmatic
keratotomy and compression sutures may be
combined. One should aim for higher correction as
regression is bound to occur. In case astigmatism is
not manageable astigmatic keratotomy and compres-
sion sutures, deep anterior lamellar keratoplasty may
be the ideal option. In non-resolving cases optical PKP
may be considered.
Hyphema
The occurrence of blood in the anterior chamber
following blunt trauma signifies severe intraocular
trauma associated damage to intraocular tissues.
Traumatic hyphema may cause significant visual
reduction, particularly if secondary hemorrhage occurs.
Raised intraocular pressure (IOP) occurs in 24 to 32%
of all traumatic hyphemas.
4
Treatment options should
aim at controlling the IOP, reducing the incidence of
secondary hemorrhage, decreasing intraocular
inflammation and reducing the associated vision
threatening complications including corneal blood
staining and optic nerve damage (Figs 14.1 and
14.2).
OPHTHALMIC EXAMINATION
The patient with traumatic hyphema should undergo
a complete ophthalmologic evaluation. The time of
onset and type of injury should be recorded accurately
and in detail. The object producing the injury and the
method by which it produced the injury give additional
information to assess the extent intraocular damage.
The ocular examination should be in detail. Hypersthesia
or anesthesia on periorbital skin may indicate blowout
fracture. Examination of the ocular adenexa, the eyelids
Fig. 14.1: Total corneal blood staining following
blunt trauma
Fig. 14.2: Spontaneous resorption (Partial) of corneal
blood staining
69
Management of Blunt Trauma of Anterior Segment
and the conjunctiva should be done for any laceration.
Proptosis may indicate retrobulbar hemorrhage;
enophthalmos and/or restrictions in extraocular muscle
rotations suggest a blowout fracture. Visual acuity with
best optical correction should be recorded. In case the
visual acuity is markedly reduced, perception and
projection of the light should be tested. Response to
consensual reaction of the pupil of the normal eye
should be recorded. Extremely poor visual acuity
suggests optic nerve or macular damage.
The cornea should be examined for presence of
preexisting disease. The cornea with compromised
endothelium is prone to develop blood staining.
Record the amount and character of the hyphema.
Careful drawing of the shape of the clot or of the level
of free cells aids in evaluation of secondary hemorrhage
or resolution of the hyphema. One should note the
iris and the lens details that are visible beyond the
hyphema.The pupil should be dilated if one suspects
intraocular foreign body, rupture or perforation of the
globe, or retinal tears or detachment. In most instances,
a detailed fundus examination may only be possible
later, following resolution of the hyphema. In such cases
B-scan ultrasonography should be performed.
Ultrasound biomicroscopy is provides accurate details
of the angle structures including zonular status, angle
recession, cyclodialysis, and the detection of small
superficial and intraocular foreign bodies. IOP should
be recorded by applanation tonometry. Avoid
gonioscopy until a week or 10 days as it may be painful
and the patient may not be able to co-operate.
SEVERITY GRADES OF HYPHEMA
Grade 1: Hyphema less than one-third of the anterior
chamber. Grade 2: Hyphema one-third to one-half
of the anterior chamber. Grade 3: Hyphema one-half
to less than total. Grade 4: Hyphema total clotted
hyphemas. Total clotted hyphema is often referred to
as black-ball or eight-ball hyphema.
The source of blood into the anterior chamber is
a tear at the iris or ciliary body, usually at the angle
structures. A tear at the anterior aspect of the ciliary
body is the most common site of bleeding. The
resolution of hyphema occurs through trabecular
meshwork and Schlemms canal or the juxtacanalicular
tissue.
Raised Intraocular Pressure
Raised IOPs (above 21 mm Hg) may accompany
hyphemas of any grade. Severe and persistent
elevations of IOP are associated with near total or total
hyphemas. The initial period of elevated IOP within
24 hours is often followed by a period of either normal
or below normal pressure during the second to the
sixth day. The initial raised IOP is probably the result
of trabecular clogging by erythrocytes. This is followed
by a period of reduced pressure due to decreased
aqueous production. Subsequently with the recovery
of the ciliary body function the intraocular pressure
rises. Significant number of patients may present with
persistent raised intraocular pressure.
Secondary Hemorrhage
Secondary bleed into the anterior chamber results in
a markedly increased incidence of complications and
worse prognosis. Secondary hemorrhage may occur
in nearly 20% of all patients with hyphema.
4
The
incidence of secondary hemorrhage is higher in
hyphemas of grades 3 and 4. Secondary bleed usually
occurs on the third or fourth day, but may occur
anytime from the second to the seventh day .
4
Several
studies documented that secondary hemorrhage occurs
more frequently in African American patients.
5
In a
study four (40%) of the 10 patients with secondary
hemorrhage had positive sickle cell trait or SA
hemoglobin. Secondary bleed is attributed to lysis and
retraction of the clot that has occluded the injured
vessel.
4
The secondary bleeding may result in raised
IOP and corneal blood staining. Secondary bleed is
associated with a poorer visual prognosis.
COMPLICATIONS OF HYPHEMA
Complications from traumatic microhyphema treated
with standard measures are few.
6
Hyphema may cause
posterior synechiae, peripheral anterior synechiae,
corneal blood staining, and optic atrophy. Optic
atrophy may result from acute rise of IOP or persistent
high IOP. Posterior synechiae may secondary to iritis
or iridocyclitis. Peripheral anterior synechia occur more
frequently in patients who had under gone surgical
intervention. Cl oseness of fol l ow-up may be
determined by IOP on presentation.
Medical Management
Standard protocol for traumatic microhyphema
includes atropinization, bed rest, shield and restriction
of antiplatelet medications. Bilateral patching, complete
bed rest and sedation are not recommended. Patient
remains ambulatory and mild sedation can be given
to apprehensive patients. Patient should be advised
to keep the head elevated at 30-45

as

it allows the
hyphema to settle inferiorly. Superior angle remains
free for the aqueous drainage. This also allows proper
monitoring of the progress and also allows early
recognition of rebleed. The antiplatelet effect of aspirin
tends to increase the incidence of rebleeding in
70
traumatic hyphema and shoul d be avoided.
Nonsteroidal anti-inflammatory drugs such as
mefenamic acid, also share this antiplatelet effect.
Various topical medications including cycloplegics for
the traumatic iridocyclitis and miotics to increase the
surface area of the iris to enhance resorption of the
hyphema have been recomended. Topical atropine
sulfate 1% is indicated for iritis and to break the
pupillary block. Topical use of steroids after the fourth
or fifth day of persistant hyphema may be
advantageous to decrease iridocyclitis and to prevent
the formation of PAS or posterior synechiae. Secondary
hemorrhage seems to be unaffected by the use of
topical corticosteroids. In one of the studies the systemic
administration of ACA has been found effective in the
prevention of recurrent bleed.
7
The antifibrinolytic
activity of ACA given systemically has been demons-
trated to decrease the incidence of secondary
hemorrhage in other areas of the body.
ACA retards clot lysis by preventing plasmin from
binding to lysine molecules in the fibrin clot. ACA, a
lysine analogue, competitively inactivates plasmin by
occupying the lysine-binding site on plasmin that would
normally bind to fibrin. In addition, ACA binds to
plasminogen, so that when activated to plasmin, it
cannot attach to fibrin. These effects stabilize the clot-
vessel-wall interface, decreasing the potential for
secondary hemorrhage.

When ACA was administered
in a dosage of 100 mg/kg every 4 hours, orally, for
5 full days, a statistically significant reduction in the
incidence of rebleeding of traumatic hyphemas was
observed.

Systemic ACA should be used in patients
with hyphemas that occupy 75% or less of the anterior
chamber since the clot may persist in the anterior
chamber for an increased period during administration
of the drug. The continued retention of the clot in
the anterior chamber would be a disadvantage with
larger, grade 4 hyphemas.
Topical ACA appears to be a safe, effective
treatment to prevent secondary hemorrhage in
traumatic hyphema. It is as effective as systemic ACA
in reducing secondary hemorrhage. No systemic side
effects were observed with topical use. Topical ACA
provides an effective outpatient treatment for traumatic
hyphemas. In a study topical ACA group had a final
visual acuity of 20/40 or better in 86% of patients,
compared with 69% of patients in the systemic group.
Some studies have investigated the application of
intracameral tissue plasminogen activator (t-PA) in the
management of traumatic hyphema.
8
A potential risk
with t-PA is the associated risk of developing rebleeding
of the initial wound. The application has been
considered in resolving hyphemas that either fail to
clear spontaneously or are associated with malignant
IOP.
Surgical Intervention
Most hyphemas, including total hyphema, should be
treated medically for the first 4 days. Spontaneous
resolution of the hyphema occurs rapidly during this
period. In general the patients with grade1 and 2
respond to the medical treatment favorably. Immediate
surgical intervention is indicated in case the IOP remains
elevated at 50 mm Hg or higher for 4 days. In case
the surgical intervention is delayed optic atrophy may
occur in 50% and corneal blood staining in 43% of
patients with total hyphemas.
9
Surgery for hyphema
should be carefully planned. Risks of surgery include
damage to corneal endothelium, lens, and/or iris,
prolapse of intraocular contents, rebleeding, and
increased synechia formation.
PARACENTESIS
Paracentesis causes little surgical trauma and reduces
the elevated IOP. Paracentesis is especially beneficial
in patients with sickle-cell trait or disease. However,
the decrease in IOP may be transient, and there may
be no appreciable reduction in the amount of the
formed clot.
IRRIGATION
Irrigation by a single- or double-needle technique has
the advantage of a small incision. We prefer entry at
the 1 oclock position in the right eye and at the 11
oclock position in the left eye with a diamond blade.
The entry should be through clear cornea. The
irrigating needle should then extend just through the
corneal endothelium and a slow push-pull maneuver
with the single-needle technique washes out the
erythrocytes from the anterior chamber clot, often
leaving the fibrin matrix. To reduce the likelihood of
rebleeding during the operative procedure, care
shoul d be undertaken not to produce viol ent
alterations in the anterior chamber pressure. If
rebleeding does occur, sodium hyaluronate can be
effectively introduced for tamponade. After a 5-minute
wait, irrigation maneuvers can be resumed.
Using a one- or two-needle technique, the surgeon
must be particularly careful to have direct visualization
of the anterior chamber, but this technique has some
disadvantages. Maintaining the position of the needle
tip in the anterior chamber may be difficult during the
procedure. A hazardous situation is created when the
collar-button type of formed clot occupies both the
anterior and posterior chambers. This produces
pupillary block with anterior displacement of the iris-
lens diaphragm.
71
ANTERIOR CHAMBER MAINTAINER
Anterior chamber maintainer has been found useful
in the surgical management of traumatic hyphema.
10
Two paracentesis are made as in standard technique
of evacuation of hyphema. The first one is made in
the lower temporal quadrant and accommodates a
20-gauge anterior chamber maintainer (ACM) that is
connected to a bottle of Balanced Salt Solution. The
second paracentesis is made in an upper quadrant and
serves to evacuate liquefied blood and blood clots.
With an ACM in place, the fluctuations of intraoperative
IOP are minimized and the AC depth is stabilized
throughout the operation. The risk of renewed
bleeding is reduced because of the continuous positive
intraoperative IOP. The ACM is an important tool in
the surgical management of traumatic hyphemas
because it facilitates AC washout and reduces iatrogenic
damage to the iris and corneal endothelium.
REMOVAL OF HYPHEMA WITH VITRECTOMY
The evacuation of the hyphema can be performed
with vitrectomy. The initial clear corneal incision is
made with a diamond blade. To avoid the iris and
lens, the blade is oriented and pushed into the anterior
chamber in such a manner that it is parallel to the
plane of the iris. With the vitrectomy cutting port half
open and the infusion line in place, it is possible to
irrigate and aspirate free blood from the formed clot.
The aspiration mode is initially set at 200 mm Hg
vacuum and the cutting speed set at 200 cycles per
minute for the procedure. Aspiration mode is
increased to 400 mm Hg as needed. Extreme care
is required to avoid contact with any iris, lens, or
corneal endothelium. This operative procedure is used
to remove the central portion of the clot. It is not
necessary to remove the entire clot in the periphery
of the anterior chamber.
Bleeding during the surgical procedure can be
controlled by elevation of the infusion bottle to
approximately 70 cm above the eye for several
minutes. In case the bleeding persists the anterior
chamber may be filled with sodium hyaluronate to
tamponade the bleeding site. At the completion of the
surgical procedure, an air bubble may be left in the
anterior chamber. This will help to control any
secondary bleeding during the post-operative period.
Visual outcome in these cases depends upon the
extent of posterior segment injuries. Poor visual
outcome in patients with posterior segment injuries
has been observed. In contrast patients with occurrence
of secondary hemorrhage may have better outcome
in absence of posterior segment injury.
CORNEAL BLOOD STAINING
Corneal blood staining usually occurs following trau-
matic hyphema. Hyphema combined with secondary
glaucoma are most common risk factors for developing
corneal blood staining.
11
Cornea blood staining may
rarely occur following non-traumatic hyphema. Coneal
blood staining has been reported following hyphema
due proliferative diabetic retinopathy.
12
Severe corneal
blood staining in the left eye secondary to a sponta-
neous total hyphema and raised intraocular pressure
in an eye with iris neovascularization has been reported
in a 54-year-old man with severe proliferative diabetic
retinopathy. Despite anterior chamber washout, the
cornea remained virtually opaque and thickened. The
patient subsequently underwent pars plana vitrectomy
with endolaser using a temporary keratoprosthesis,
insertion of a Morcher iris-surround intraocular lens and
penetrating keratoplasty. Histopathology of the excised
corneal button revealed fine eosinophilic granules
composed of aggregations of hemoglobin and its
breakdown products dispersed throughout the stroma,
with occasional foci of weakly positive Perl staining for
intracellular hemosiderin. Fluorescence confocal
microscopy revealed a marked increase in fluorescence
throughout the corneal stroma and the basal epithelial
layer.
A case of corneal bl ood staining due to a
hemorrhagic descemet membrane detachment has
been reported. A 72-year-old man had an anterior-
chamber intraocular lens removed for presumed
uveitis-glaucoma-hyphema syndrome, developed an
intraoperative hemorrhagic detachment of the
Descemet membrane attributed to peripheral corneal
neovascularization. Corneal blood staining rapidly
developed, and a partial-thickness paracentesis was
required to evacuate the lamellar hematoma and
allow reattachment of the Descemet membrane:
Hemorrhage from posterior corneal vessels can result
in a hemorrhagic detachment of the Descemet
membrane. Corneal blood staining can develop
rapidly in an intracorneal or retrocorneal hemorrhage.
The blood can be removed without incising the
Descemet membrane by making a partial-thickness
paracentesis
13
.
Corneal blood staining mostly occurs in patients
who have a total hyphema and associated raised IOP.
Predisposing factors for development of corneal blood
staining include compromised endothelium, grade
hyphema, raised IOP and surgical trauma in removing
large clot. Rarely corneal blood staining may occur
with low or normal IOPs, this occurs in cases in whom
the endothelium is already compromised. However,
these latter two instances can probably be anticipated
only in eyes with a severely damaged or compromised
endothelium. Risk of developing corneal blood staining
72
is more in patients with full chamber hypema and
persistently raised IOP of more than 25 mm Hg.
Spontaneous clearing of corneal blood staining is
known and may require 8 months to 2 years.
14
IRIS AND ANGLE CHANGES
The classical sign suggestive of close globe injury is the
presence of ring of pigment clumps over the anterior
capsule. The ring is known as Vossius ring. The size
of the ring is smaller than the size of the pupil.
Iridoschisis is lamellar separation of anterior and
posterior iris. The blunt force compresses the globe
in the anterior - posterior direction and thus stretches
the equatorial diameter. Sudden increase in the
pressure in the anterior chamber puts stress on the
iris sphincter, root of the iris circular and longitudinal
cilliary muscle fibers, resulting angle recession. Iris is
torn at thinnest portion and the thinnest portion of
the iris is at root, iris insertion at anterior ciliary body.
Clinically the condition is described as iridodialysis.
Blunt trauma may cause separation of longitudinal
fibers from the scleral spur creating a cyclodialysis cleft.
A technique for repair of traumatic iridodialysis that
avoids the need for iris sutures has been described.
15
Following a limbal peritomy, sclerostomy sites level with
the iris base are created at each clock hour of the irido-
dialysis using a microvitreoretinal blade. Vitreoretinal
forceps passed through these ports are used to
incarcerate the peripheral iris. No suture material is
used to secure the iris. The conjunctiva is closed with
absorbable sutures. The technique has been reported
successful in simple iridodialysis repair and in
conjunction with intraocular procedures.
SECONDARY GLAUCOMA
Glaucoma in hyphema may develop due to variety
of mechanisms. These mechanisms include trabecular
blockage with erythrocytes, pupillary block due to full
chamber clotted blood, angle recession and peripheral
anterior synechia. Clinically, the presence of increased
pigmentation at the angle, elevated baseline IOP,
hyphema, lens displacement, and angle recession of
more than 180 degrees have been significantly
associated with the occurrence of chronic glaucoma
after closed globe injury.
16
On UBM findings such as
a wider angle and the absence of cyclodialysis were
significant predictors for the subsequent development
of traumatic glaucoma. Less than 10% of patients
having angle recession develop glaucoma. The
mechanism of glaucoma is outflow obstruction due
to scarring or a hyaline membrane covering the angle.
Patients presenting with hyphema and associated
vitreous hemorrhage may have raised intraocular
pressure 2 weeks to 3 months later. The erythrocytes
after losing hemoglobin, become ghost cells in the
vitreous cavity. The ghost cells may pass forward into
the anterior chamber, with resultant elevation of IOP.
The condition is described as Ghost Cell glaucoma.
The treatment of secondary post-traumatic open
angle glaucoma is disappointing. The patients are
young, the disease is advanced, and the compliance
to the treatment and follow-up are poor. The
prevention of post-traumatic glaucoma is based on
the control of ocular trauma and the periodic follow-
up of patients with and history of non-perforating injury
of the eye. In another study several independent
predictive factors including poor initial visual acuity,
advancing age, lens injury, angle recession, and
hyphema were found to be significantly associated with
the development of posttraumatic glaucoma.
MISCELLANEOUS CHANGES
Changes in the refractive status of the eye have been
reported following blunt trauma. Ultrasound biomicro-
scopy (UBM) and ultrasonography of the anterior
segment in the eye may be helpful to diagnose and
confirm these changes.
17
Blunt trauma can dislocate
angle-supported pIOLs. Implantation of these IOLs
should be discouraged in patients who perform
activities that put them at risk for eye trauma.
18
Tube
extension using angiocatheter material is used in
glaucoma flitering surgery. This surgery is a viable, cost-
effective option in difficult cases. Following blunt
trauma intrusion of the tube into the anterior chamber
has been reported.
19
Placing a securing suture in patients
prone to eye trauma can be considered The c-fos and
c-jun mRNAs have been observed to transiently express
in corneal and lens epithelial cells after blunt trauma.
20
Ocular blunt trauma activates corneal and lens
epithelial cells without apparent corneal ablation or
direct injury in the lens epithelium. Such activation in
lens epithelium has been postulated to be involved
in cataractogenesis..
Eyes with scleral rupture after blunt trauma may
rarely get complicated by proliferative vitreo-
retinopathy. In certain cases, retinal detatchment or
proliferative vitreoretinopathy may not develop
following extensive scleral rupture. A 56-year-old man
sustained blunt trauma to his left eye. Visual acuity was
light perception. The fundus was obscured by hyphema.
Computed tomography imaging and the presence of
extensive subconjunctival hemorrhage suggested scleral
rupture. Prompt primary surgery to repair a 25-mm
scleral rupture was performed under general anesthesia.
No retinal detachment developed. Two years
postoperatively, visual acuity increased to 12/20. This
case shows that retinal detachment and proliferative
73
vitreoretinopathy may not complicate extensive scleral
ruptures in certain patients.
21
Sympathetic ophthalmia
has been reported to occur following nonpenetrating
ocular trauma.
22
Prevention of blunt ocular trauma is of paramount
importance in decreasing the incidence of these injuries.
Use of preventive measures while at work or during
high risk sports should be strictly complied. Public
education on the use of protective glasses and other
protective measures should be given at regular
intervals. In case blunt trauma occurs prompt
examination and urgent treatment may limit the ocular
morbidity.
References
1. Pieramici DJ, Sternberg P Jr, Aaberg TM Sr, et al. A
system for classifying mechanical injuries of the eye
Ophthalmol 1997;123820-31.
2. Al-Amry M, Khan AO. Descemets membrane breaks
following forceps delivery. J Pediatr Ophthalmol
Strabismus 2007;44:192.
3. Regis A, Dureau P, Uteza Y, Roche O, Dufier JL. [Ocular
injuries and childbirth] J Fr Ophtalmol 2004;27:987-93.
4. Crouch ER Jr, Williams PB. Trauma: Ruptures and
bleeding. In: Tasman W, Jaeger EM, eds. Duanes Clinical
Ophthal mol ogy. Phil adel phia, Pa: JB Lippincott
1993;4:1-18.
5. Pal mer DJ, Gol dberg MF, Frenkel M, Fiscel l a R,
Anderson, RJ. A comparison of the two dose regimens
of epsilon aminocaproic acid in the prevention and
management of secondary traumatic hyphemas.
Ophthalmology 1986;93:102-108.
6. Recchia FM, Sal uja RK, Hammel K, Jeffers JB.
Outpatient management of traumatic microhyphema.
7. Crouch ER Jr, Frenkel M. Aminocaproic acid in the
treatment of traumatic hyphema. Am J Ophthalmol
1976;81:355-60.
8. Laatikainen L, Mattila J. The use of tissue plasminogen
activator in post-traumatic total hyphaema. Graefes Arch
Clin Exp Ophthalmol 1996:234:67-68.
9. Weiss JS, Parrish RK, Anderson DR. Surgical therapy of
traumatic hyphema. Ophthalmic Surg 1983;14:343-345.
10. Yu T, Dahan E, Yin ZQ, Levitz LM. Use of an anterior
chamber maintainer in the surgical management of
traumatic hyphaemas. Clin Experiment Ophthalmol
2008;36:206-08.
11. Kloek C, Brauner S, Chen TC. Corneal blood staining
after traumatic hyphema J Pediatr Ophthalmol Strabismus
2007; 44: 256.
12. Patel H, Patel DV, Brookes NH, McGhee CN. Clinico-
pathological features of severe corneal blood staining
associated with proliferative diabetic retinopathy. Clin
Experiment Ophthalmol 2006 ;34:272-74.
13. Sharma PS, Stone DU. Corneal blood staining secondary
to hemorrhagic descemet membrane detachment. Cornea
2007;26:1273-74.
14. Fraser C, Liew S, Fitzsimmons R, Arnold J. Spontaneous
resolution of corneal blood staining. Clin Experiment
Ophthalmol 2006;34:279-80.
15. Richards JC, Kennedy CJ. Sutureless technique for repair
of traumatic iridodialysis. Ophthalmic Surg Lasers
Imaging 2006;37:508-10.
16. Sihota R, Kumar S, Gupta V, Dada T, Kashyap S, Insan
R, Srinivasan G. Early predictors of traumatic glaucoma
after closed globe injury: trabecular pigmentation,
widened angle recess, and higher baseline intraocular
pressure. Arch Ophthalmol 2008;126:921-26.
17. Kim SI, Cha YJ, Park SE. A case report on the change
of the refractive power after a blunt trauma. Korean J
Ophthalmol 2008;22:53-57.
18. Leccisotti A Traumatic pupillary capture of the haptic of
an angle-supported phakic intraocular lens. J Cataract
Refract Surg 2006;32:2133-34.
19. Sheets CW, Ramjattan TK, Smith MF, Doyle JW Migration
of glaucoma drainage device extender into anterior
chamber after trauma. J Glaucoma 2006;15:559-61.
20. Shirai K, Saika S, Okada Y, Miyamoto T, Ueyama T,
Ohnishi Y. Transcriptional activation in lens epithelial cells
following an ocular blunt trauma. J Cataract Refract Surg
2005 ;31:1226-30.
21. Takayama K, Yasukawa T, Okada M, Sumida A, Watanabe
N, Uchida S. Large blunt scleral rupture without retinal
detachment. Ophthalmic Surg Lasers Imaging 2008;39:
242-45.
22. Bakri SJ, Peters GB 3rd. Sympathetic ophthalmia after
a hyphema due to nonpenetrating trauma. Ocul Immunol
Inflamm 2005;13:85-86.
C H A P T E R
15
Management of Traumatic Cataract
Rupesh V Agrawal, Satish Desai (India)
Introduction
Cataract is by far the commonest complication causing
loss of vision following any type of ocular injury. The
management of such cases is an important problem
in ophthalmology and prognosis is variable. Extent
of associated damage to anterior and posterior segment,
time of intervention, operative and postoperative
complications go a long way in determining the ultimate
prognosis. The type of trauma, extent of lenticular
involvement and associated secondary rise of
intraocular pressure are factors of paramount
importance which could dictate the exact time of
management of traumatic cataract. Cataracts caused
by blunt trauma classically form stellate or rosette
shaped posterior axial opacities that may be stable
or progressive, whereas penetrating trauma with
disruption of lens capsule forms cortical changes that
may remain focal if small or may progress rapidly to
total cortical opacification. Lens dislocation and
subluxation are found commonly in conjunction with
traumatic cataract.
Pathophysiology
Blunt trauma is responsible for coup and contrecoup
ocular injury. Coup is the mechanism of direct impact.
It is responsible for Vossius ring (imprinted iris pigment)
sometimes found on the anterior lens capsule following
blunt injury.
When the anterior surface of the eye is struck
bluntly, there is a rapid anterior-posterior shortening
accompanied by equatorial expansion. This equatorial
stretching can disrupt the lens capsule, zonules, or
both. Combination of coup, contrecoup, and
equatorial expansion is responsible for formation of
traumatic cataract following blunt ocular injury.
Penetrating trauma that directly compromises the
lens capsule leads to cortical opacification at the site
of injury. If the rent is sufficiently large, the entire lens
rapidly opacifies, but when small, cortical cataract can
seal itself off and remain localized.
SEX
Male-to-female ratio in cases of ocular trauma is 4:1.
AGE
Work- and sports-related eye injuries most commonly
occur in young adults and children.
HISTORY
Mechanism of injurySharp versus blunt
Past-ocular historyPrevious eye surgery, glau-
coma, retinal detachment, diabetic eye disease
Past medical historyDiabetes, sickle cell, Marfan
syndrome, homocystinuria, hyperlysinemia, sulfate
oxidase deficiency
Visual complaints
Decreased visionCataract, lens subluxation,
lens dislocation, ruptured globe, traumatic optic
neuropathy, vitreous hemorrhage, retinal
detachment
Monocular diplopiaLens subluxation with
partial phakic and aphakic vision
Binocular diplopiaTraumatic nerve palsy,
orbital fracture
PainGlaucoma secondary to hyphema,
pupillary block, or lens particles; retrobulbar
hemorrhage; iritis.
Physical Examination
Complete ophthalmic examination (tailored in
cases of globe compromise)
Vision and pupilsPresence of afferent pupi-
llary defect (APD) indicative of traumatic optic
neuropathy
Extraocular motilityOrbital fractures or
traumatic nerve palsy
Intraocular pressureSecondary glaucoma,
retrobulbar hemorrhage
Anterior chamberHyphema, iritis, shallow
chamber, iridodonesis, angle recession
75
LensSubluxation, dislocation, capsular inte-
grity (anterior and posterior), cataract (extent
and type), swelling, phacodonesis
VitreousPresence or absence of hemorrhage,
posterior vitreous detachment
FundusRetinal detachment, choroidal
rupture, commotio retinae, preretinal hemorr-
hage, intraretinal hemorrhage, subretinal
hemorrhage, optic nerve pallor, optic nerve
avulsion.
Traumatic Cataract (Types)
Penetrating
Concussion (Rosette cataract)
Infrared irradiation (Glass Blowers cataract)
Electrocution
Ionizing radiation.
Causes
Traumatic cataracts occur secondary to blunt or
penetrating ocular trauma.
Other Problems to be
Considered
Globe rupture
Orbital fractures
Retinal detachment
Secondary glaucoma
Traumatic optic neuropathy.
Factors to be Analyzed
Corneal involvement
Preoperative and postoperative BCVA
Visual axis involvement
Breach in anterior capsule
Lens matter in anterior capsule
Pre-existing posterior capsular rent on ultrasound
Subluxation of the traumatic cataractous lens
Associated iridodialysis.
Imaging Studies
B-scanIf posterior pole cannot be visualized
A-scanPrior to cataract extraction
CT scan orbitsFractures and foreign bodies.
Causes of Postoperative
Non-improvement of BCVA
in Traumatic Cataract
Amblyopia
Corneal scar involving visual axis
Cortex in papillary area
Subluxation of IOL
IOL tilt
CME
Traumatic optic neuropathy
Pupillary capture.
Medical Care
If glaucoma is a problem, control intraocular pres-
sure with standard medications; add corticosteroids
if lens particles are the cause or if iritis is present.
Focal cataract:
Observation if cataract is outside the visual axis
Miotic therapy may be of benefit if the cataract
is close to the visual axis.
In some cases of lens subluxation, miotics may
correct monocular diplopia; mydriatics may allow
for vision around the lens with aphakic correction.
PRACTICAL POINTS IN MANAGEMENT OF
TRAUMATIC CATARACT
Corneoscleral integrity
Meticulous restoration of normal relationships
Sufficient release of posterior synechiae
Capsular and zonular integrity
Vitreoretinal changes.
Surgery
Depending on the clinical situation, the surgical
management of a traumatic cataract is performed
either a standard anterior limbal or posterior pars plana
approach. An anterior approach is best for a traumatic
cataract unless there is complete lens dislocation or
capsular rupture with significant lens material
incarcerated in the vitreous.
PRACTICAL TIPS WHILE PERFORMING
TRAUMATIC CATARACT SURGERY
Planning surgical approach is of utmost importance
in cases of traumatic cataract.
Preoperative capsular integrity and zonular stability
should be surmised.
76
In cases of posterior dislocation without glaucoma,
inflammation, or visual obstruction, surgery may
be avoided.
Indications for surgery include the following:
Unacceptable decreased vision
Obstructed view of posterior pathology
Lens-induced inflammation or glaucoma
Capsular rupture with lens swelling
Other trauma-induced ocul ar pathol ogy
necessitating surgery.
Standard phacoemulsification or manual small
incision cataract surgery may be performed if lens
capsule is intact and sufficient zonular support
remains.
Intracapsular cataract extraction is required in cases
of anterior dislocation or extreme zonular instability.
Anterior dislocation of the lens into the anterior
chamber requires emergency surgery for its
removal, as it can cause pupillary block glaucoma.
Pars plana lensectomy and vitrectomy may be best
in cases of posterior capsular rupture, posterior
dislocation, or extreme zonular instability.
Automated irrigation/aspiration can be used in
patients younger than 35 years. Look for the
posterior capsular support preoperatively, should
be careful while performing automated irrigation
aspiration and while switching the anterior chamber
maintainer on as the fluid flow inside the eye can
enl arge the pre-existing posterior capsul ar
dehiscence and can result in lens matter drop or
nucleus drop.
Lens implantation:
Capsular fixation is the preferred placement if
lens capsule and zonular support are intact. In
the case of surgery to remove a traumatic
cataract, the CTR may be implanted before or
after phacoemulsification. Although early inser-
tion provides support during phacoemulsifi-
cation, it may create additional zonular trauma.
The use of iris or capsule retractors at the
capsulorhexis edge or the use of a capsular
tension segment (CTS; Morcher GmbH,
Stuttgart, Germany (not currently approved by
the FDA]) during phacoemulsification are other
alternatives that do not induce significant
capsular torque during insertion. The CTS is a
partial PMMA ring segment containing an
anteriorly offset eyelet through which an iris
retractor or suture may be placed.
Capsular tension ring should never be implanted
in cases with broken capsulorrhexis and in eyes
with pre existing posterior capsular rent.
Polymethyl methacrylate (PMMA) capsular
tension rings allow capsular fixation in cases of
zonular dialysis less than 180 degrees.
Sulcus fixation is safe if posterior capsule is
compromised but zonular support is maintained.
Suture fixation is chosen if both capsular and
zonular supports are insufficient and the angle
is damaged minimally.
Anterior chamber placement is an option if no
posterior support remains and iris or ciliary body
trauma prevents suture fixation.
Aphakia may be a better choice in young
children and patients with highly inflamed eyes;
they may experience better outcomes if lens
implantation is deferred.
COMPLICATIONS
Surgery for traumatic cataract is associated with high
incidence of complications and surgeon should
anticipate and be prepared for complications during
the surgery. The different complications during
traumatic cataract surgery can be:
Posterior capsular rent
Zonular dialysis
Fig. 15.1: CTR in bag
Fig. 15.2: Traumatic cataract with torn anterior capsule
77
Fig. 15.3: Deposits on IOL
Fig. 15.4: Partial lens abscess
Fig. 15.5: Postcataract surgery with partially
repaired iris
Fig. 15.6: Traumatic cataract with breached AC
Fig. 15.7: Traumatic cataract with foreign body
Fig. 15.8: Traumatic cataract with haem
78
Fig. 15.9: Traumatic cataract with IOL in torn bag
Fig. 15.10: Traumatic cataract with iris hole
Fig. 15.11: Traumatic cataract with loose lens mattter in AC
Fig. 15.12: Traumatic cataract with subluxation of lens
Fig. 15.13: Early Rosete cataract
Nucleus or lens matter drop
Postoperative unusual inflammation
Posterior capsular opacification
Pupillary capture of IOL
Postoperative refractive surprise.
Bibliography
1. Benezra D, Cohen E, Rose L. Traumatic cataract in
children: correction of aphakia by contact lens or
intraocular lens. Am J Ophthalmol. 1997;123(6):773-82.
79
2. Eckstein M, Vijayalakshmi P, killedar M, Gilbert C, Foster
A. Use of intraocular lenses in children with traumatic
cataract in south India. Br J Ophthalmol 1998;82(8):
911-15.
3. Gain P, Thuret G, Maugery J. Management of traumatic
cataracts. J Fr Ophtal mol . Review French 2003;
26(5):512-20.
4. Jacob S, Agrawal A, Agrawal A, Agrawal S, Patel N, Lal
V. Efficacy of a capsular tension ring for phaco-
emulsification in eyes with zonular dialysis. J Cataract
Refract Surg 2003;29(2):315-21.
5. Kazem MA, Behbehbani JH, Uboweja AK, Parmasivam
MB. Traumatic cataract surgery assisted by trypan blue.
Ophthalmic Surg Lasers Imaging 2007;38(2):160-63.
6. Krishnamachary M, Rathi V, Gupta S. Management of
traumatic cataract in children. J Cataract Refract Surg
1997;23(Suppl 1):681-87.
7. Mian SI, Azar DT, Colby K. Management of traumatic
cataracts. Int Ophthalmol Clin Review 2002 Summer;
42(3):23-31.
8. Moreno J, Sainz C, Maldonado MJ. Intraoperative and
postoperative complications of Cionni endocapsular ring
implantation. J Cataract Refract Surg 2003;29(3):492-97.
9. Panda A, Kumar S, Das H, Badhu BP. Striving for the
perfect surgery in traumatic cataract following penetrating
trauma in a tertiary care hospital at eastern Nepal.JNMA
J Nepal Med Assoc 2007;46(167):119-25.
10. Praveen MR, Vasavada AR, Singh R. Phacoemulsification
in subluxated cataract. Indian J Ophthalmol 2003;
51(2):147-54.
C H A P T E R
16
Management of Traumatic Luxation
of the Crystalline Lens
Introduction
This chapter will cover different criteria regarding the
management of the Traumatic Luxation of the Lens.
Many authors have spoke about this topic worldwide
and the clinical and surgical concepts are not uniform.
These differences might be in some cases because the
blunt eye trauma is different from one patient to
another, and so the degree of zonular damage can
be different, and also some associated lesions-, but
furthermore, as new technologies are arising in the
ophthalmic field (e.g. iris claw IOLs, iris fixation IOL
techniques), some ophthalmic surgeons developed
more experience in some particular technique or
device, and so the management can be complete
different from one surgeon to another.
We will try to review different approaches
according the current literature and our personal
experience, but the reader must consider that science
is always working ahead in benefit of the patients,
so some criteria might be out of site after a short
period of time.
Blunt Eye Trauma
As the reader has noticed viewing this book, the
possibilities of damage (going from mild, to moderate
and severe) to the eye structures during a blunt trauma
are enormous; no one particular case is exactly the
same than another, and distinctive considerations must
be taken in count in each clinical evaluation and
approach. It is also known that the clinical condition
of the eye can have variations according the time of
evolution of the lesion, clinical management, pre-
existent eye diseases (e.g. high myopia, pseudo-
exfoliation), and many other possibilities that can
influence the clinical course and so the management
of the case, and finally the outcome.
We will describe the condition in which the
crystalline lens has been moved from its anatomical
position because of a blunt eye trauma, either
associated or not, to some other damage to the eye
structures; if well not all the possibilities of damage
can be review (even in the whole textbook), a didactic
classification has been done in this chapter, trying this
way to cover as much alternative lesions as possible,
in order to obtain a didactic scheme useful during
the clinical evaluation, the plan of a surgical approach,
the intraoperative management, the eventual
postoperative complications and the clinical prognosis.
Luxation and Subluxation of the
Crystalline Lens
(Figs 16.1 and 16.2)
In many circumstances these conditions are not easy
even to distinguish between them, since the finding
of a proper definition; for some authors when some
zonular attachments still exist the condition is defined
as subluxation, and the complete crystalline lens
luxation is defined by the whole loose of zonular
attachments. Even so, sometimes the clinical
evaluation of these two forms of crystalline lens
dislocation can be difficult to perform; if well this might
be difficult in a non-traumatized eye (e.g. Marfan
syndrome), you can now imagine an evaluation of
this condition in a traumatized eye, when sometimes
some other lesions can decrease the visualization of
the examinator (e.g. hyphema, suprachoroid
hemorrhage), not only at the clinical approach, but
furthermore, at the paraclinical evaluation (e.g. eye
ultrasound, eye scan). Because of this, sometimes the
final definitions are performed at the intraoperative
period, and so the clinical evaluation and trans-
operative decisions are the rule. So, we think that for
the starting point of evaluation of these cases of
dislocated crystalline lens because of a traumatic
condition, the surgeon must think from the start, that
all the zonular attachments have been lost, and only
during the intraoperative period the real dimension
81
Management of Traumatic Luxation of the Crystalline Lens
of the zonular damage can be seen. Even so, sometimes
after and accurate evaluation and management of a
subdislocated crystalline lens, with cataract surgery and
in-the-bag IOL implantation, a late IOL dislocation
can be seen; it means that a long term complication
is still changing our first clinical impression.
CLINICAL EVALUATION
A complete preoperative evaluation of the condition
and situation of the crystalline lens, is of crucial
importance for the design of the management of these
lesions. Situations like position, movement, degree of
opacity, integrity of the capsular bag and degree of
hydration, are maybe the most important features to
appraise, in order to establish an adequate medical
criteria of management. Keep always in mind during
the diagnostic period, the proper evaluation of damage
to the rest of the structures of the eye and the evolution
that the lesions might have, by their own, during a
certain period of time.
Previous Medical Conditions
The medical history of some previous conditions of
the particular patient, have great importance. Systemic
conditions like diabetes, connective tissues diseases,
coagulation pathologies between others, enhance our
multidisciplinary point of view of the case; systemic
medication like aspirin or other anticoagulants are
mandatory to know.
Previous eye diseases and/or ocular surgeries and
trauma, are of course mandatory to ask to the patient;
but furthermore, and of particular importance for the
evaluation of the crystalline lens feature, some particular
eye conditions like diseases associated with progressive
zonular weakening and capsular contraction (e.g.
pseudoexfoliation syndrome, uveitis, myopia, Marfan
syndrome); the possibility of a previous zonular weak,
can change by complete our point of view, and so
our surgical approach; with some previous condition
of zonular weakening, even a minor ocular trauma,
can dislocate by complete the crystalline lens.
Also alternative treatments (prescribed or not) that
the patient had has, in an attempt to solve the traumatic
condition of the eye before our first contact with him,
are very value to appraise; some of them are able to
affect the initial lesion and even convert it into a worst
scenario; keep in mind and ask for them.
Sometimes because the anxiety experienced by the
patient, relatives and medical personal, a complete
clinical history is not properly taken; the surgeon must
be aware of the previous medical conditions of the
patient, because some factors of the medical history
might be decisive in the decision taking process.
Trauma Mechanism
The evaluation of the trauma mechanism is of critical
importance in the possibility of a zonular weakening;
because of the transmission of forces into the ocular
globe, sometimes the surgeon can see an eye almost
free of damage during the first clinical evaluation
(maybe some low degree of traumatic uveitis), but
the eye might have severe zonular damage (even
without cataract formation); so the proper history
taking about the trauma mechanism is mandatory. As
you might see in different parts of this book, there
are currently types of trauma mechanism that cause
a particular kind of damage in the eye; they are well
known.
Fig. 16.1: Traumatic lens dislocation with
cataract formation
Fig. 16.2: Traumatic lens subluxation
82
Associated Lesions to the Lens Luxation
It is difficult to find a traumatic lesion of the ocular
globe capable to cause only zonular weakening and
a luxation or subluxation of the crystalline lens as an
unique lesion; if well it can happen, it is almost a rule
that the crystalline damage is accompanied by injury
to some other ocular and extraocular (e.g. orbital)
structure, that must be complete addressed during a
clinical and paraclinical approach. Also, the surgeon
must keep in mind that some conditions might change
with the running of time; sometimes the initial clinical
features are not related to the crystalline lens lesion
itself (e.g. increase in the intraocular bleeding,
presentation of retinal detachment, increase in the
intraocular pressure because an angular recession), but
within the evolution, a non-primary lens-related
situation, can become an indication of lens removal
(e.g. evolution from a subluxation to a complete
luxation, development of phacomorphic, phacolitic or
narrow-angle glaucoma). So, the critical observation
of associated lesions in the first and ulterior evaluations,
are of critical importance.
Zonular evaluation (dynamic evaluation,
clinical and with ultrasound)
Is mandatory to consider the possibility of zonular
damage in all cases of ocular trauma; the condition
of the crystalline lens attachments conforms an
important part of the design of further activities in the
management of these patients.
The first clinical evaluation is the observation;
despite the complete clinical view of the anterior and
posterior segments of the eye, a particular focus must
be pointed into the crystalline lens. Integrity of it,
presence of opacities, integrity of the capsular bag and
possible clinical visualization of the zonules under
maximum pupil dil ation, are between others,
mandatory points that must be seen during the
ophthalmic exploration of a traumatized eye; a
dynamic clinical evaluation of the lens, is also
obligatory; it means to ask the patient to move the
eye in slow and rapid movements, in order to achieve
phacodonesis.
Sometimes the degree of subluxation is easy to
observe, but even so the dynamic evaluation is very
useful to achieve a clinical approach to the degree of
zonular weakening. If a complete luxation is present,
a complete clinical indication in the ocular fundus is
mandatory, with the objective to plan the surgical
approach.
In some cases, because of media opacities and
inflammatory process, it is not easy to evaluate the
real condition of the zonular attachments; this
conforms for many surgeons the indication of an
ultrasonic evaluation of the globe (eye echography);
I do believe, that echograhy must be performed in
all cases of eye trauma, not only because it helps
evaluate the integrity of the globe and some other
associated features in presence of not-clear media, but
also because it helps demonstrate the weakening of
the zonula in cases of suspected lens subluxation, and
furthermore, in cases of complete luxation helps
achieve the location of the crystalline lens within the
eye.
So, thinking in performing echography in all cases
of ocular trauma (even in the presence of clear media),
not only some subclinical conditions can be discovered
by this way, moreover the weak of the zonula is very
easy to evaluate with this method; remember to have
a good communication with your echographist, and
even think that you must be present during the study,
because the dynamic ultrasonography (echography
under ocular movement) is very helpful to achieve
some subclinical zonular damage. Finally, in cases of
complete luxation, echography helps the surgeon
achieve integrity of the capsular bag and movement
capacity of the crystalline lens inside the vitreous cavity
(dynamic echography with changes in the patient
position), of particular importance for planning the
surgical strategies.
Some other studies can be very helpful in the
evaluation of the traumatized (and maybe dislocated)
lens (e.g. Computed Tomography), but the dynamic
ultrasonic evaluation conforms a nice approach to
obtain a mostly complete information regarding the
crystalline lens conditions and associated features.
Surgical Approach
Despite the whole evaluation of the complete damage
to the intra- and extraocular structures caused by the
trauma, the management of the dislocated crystalline
lens will be pointed here. The management includes
a broad spectrums of actions, going from doing
nothing in case of a moderate dislocation without
cataract formation, until a complete cataract extraction
from the vitreous cavity and an IOL implantation
without capsular support.
The surgical approach must take in count also as
a very important concept, the correct time to act;
it means that sometimes the surgeon has to wait and
not to plan a surgical approach until some particular
features have been solved (e.g. bleeding resolution,
decrease in inflammation), but in some other occasions
the urgent surgery indication must be the rule to follow
(e.g. development of phacolitic or phacomorphic
glaucoma, high intraocular pressure because of
83
hydrated cataract, incomplete dislocation with weak
zonulas and possibility to develop a drop nucleus into
the vitreous cavity). This is why the management of
this type of conditions requires knowledge but also
a good dose of common sense; sometimes to share
the case with some colleagues can be useful.
The concept of the touch of the crystalline as the
first step in case of a surgical approach, is still alive;
it is a very objective method to evaluate the integrity
and the weakness of the zonula and can corroborate
or change by complete the tentative surgical plan; it
must be carefully performed in order to avoid cause
more zonular damage; it is a useful maneuver that
helps obtain more information about the case.
Anyhow, during the entire time of a surgical approach,
the surgeon must be aware to experience surprises
because it is a traumatized eye; these precautions must
be in the mind even in the postoperative period,
because unexpected complications are the rule.
Now we will describe some different possibilities of
surgical approaches, depending upon the complete
diagnostic, trying to cover diagnostic and technique
of choice.
PHACOEMULSIFICATION
AND IOL PLACEMENT IN SUBLUXATED
CRYSTALLINE LENS
The indication should be subluxated cataractous lens,
or subluxated non-cataractous lens that compromises
the vision. Remember that sometimes, is better not
to perform surgery, and this possibility must be
discussed with the patient according the particular case.
For the special purpose of lens extraction in
subluxation, helpful maneuvers and devices can be
used; some examples are wide capsulorhexis to avoid
pressure over the capsular bag, capsulectomy instead
to capsulotomy to avoid pull the capsule, iris retractors
inserted in the capsular bag to center it during phaco,
capsular tension rings for subluxated lens, ultra-small
incision technology, phacoemulsification out of the
bag (phaco at the iris plane to avoid force applied
to the capsular bag), positive intraocular pressure
during the entire procedure, bi-axial irrigation/
aspiration, continuous viscoelastic injection inside the
capsular bag and transscleral bag fixation with sutures
(with or without capsular rings) between others. When
performing these techniques, the objective is to
maintain the integrity and the center position of the
capsular bag with the main objective of an IOL
implantation, in the bag and, as much as possible,
in the center of the pupil.
Remember wait for surprises any time during the
surgery and at the postoperative period, because it
is a traumatized eye.
INTRACAPSULAR EXTRACTION
Intracapsular extraction means to take outside the
eye the entire crystalline lens contained in its capsular
bag. It is a maneuver that even in our times should
be considered in some special cases, for example
complete lens luxation to the anterior chamber, or
furthermore into the subconjuntival space, as we saw
in some occasion, in which a simple conjunctival
incision was enough to remove he entire dislocated
lens. If well, the entire lens removal through a wide
incision is not frequently seen in the ophthalmic surgery
in our days, it is something that must be keep inside
the surgeons mind for some particular cases of
complete lens luxation after severe eye trauma.
PARSPLANA VITRECTOMY PLUS
PHACOEMULSIFICATION IN
THE VITREOUS CAVITY
It is indicated in cases of complete lens luxation into
the vitreous cavity; should be performed after a
complete study that allows the surgeon to obtain
information about the position of the crystalline lens
and the additional damage caused by the eye trauma;
the medical indication for this technique increases when
there is a suggestion of inflammatory process or some
structural damage caused by the subluxated lens.
A complete pars plana vitrectomy must be
performed prior to remove the lens from inside the
vitreous cavity; it helps increase visualization inside the
globe (remove of vitreous opacities), but also helps
decrease the retinal traction during the lens removal.
After the vitrectomy, many techniques have been
described to remove the lens like phacoemulsification
in the vitreous cavity, chopstick, FAVIT, phacoemulsi-
fication in the anterior segment and for soft lenses the
lensectomy during the vitrectomy by itself, between
others. The goal is to remove the complete lens
material just after a complete vitrectomy has been
performed; after that a complete review of the
retina, periphery and optic nerve is done, and some
other maneuvers if needed like endophotocoagulation,
subretinal fluid drainage or silicon oil insertion if
required; remember that al ways the surgeon
must be aware of surprises because of the traumatized
eye.
PERFORMING A COMPLETE PLACEMENT OF
CRYSTALLINE LENS INTO THE VITREOUS
CAVITY
Just like in the old times of cataract surgery, the
complete luxation to the crystalline lens (with cataract
or not), or the non-surgical approach in case of a
complete lens dislocation into the vitreous cavity, is
84
also an option that must be inside the mind of the
attending surgeon of these traumatized eyes.
It was demonstrated, since the early days of cataract
surgery, that in presence of integrity of the capsular
bag, the crystalline lens must remain inside the vitreous
cavity for many years without consequences. So,
depending upon the case, the surgeon has the option
of leave it for years inside the vitreous cavity, if it is
already there, and there is not inflammatory response
or mechanical damage; sometimes the principle better
not to damage applies very well; if the case has an
almost complete luxation, sometimes the surgical
technique to follow can be to convert it to a complete
vitreous luxation, with particular careful of not to
damage the capsular bag; if this occurs, a complete
lens extraction is mandatory.
If the surgeon choose this option talking with the
patient, both must be aware that when a reaction
occurs inside the eye any time during the life (e.g.
inflammatory process), the lens extraction must be
performed; a good communication is mandatory;
anyhow, the IOL implantation can be performed even
with the lens inside the vitreous cavity.
IOL PLACEMENT CONSIDERATIONS
If well some particular patients because of the
conditions of the eye should not be implanted and
must be managed with contact lens, in most of the
cases the rule to follow is to obtain the maximum of
visual rehabilitation by replacing the crystalline lens
with a IOL; even so, sometimes because of the
particular lesions caused by the eye trauma, some
individual considerations must be done.
We can divide this topic in two big fields:
1. With capsular support: If during the surgery the
capsular bag was conserved (with or without
capsular tension ring), an in the bag IOL
implantation is feasible. Just think about the
possibilities between one piece or three pieces
IOL`s according your particular case and needs.
Never forget that a IOL placed in the capsular bag
with a zonular lesion, can lead to long term
complications; you are not safe forever
2. Without capsular support: We can divide this point
between anterior chamber and posterior chamber
lens.
An anterior chamber lens is still an option for many
surgeons; some others try not to use them because
of the endothelial cells consequences; some surgeons
feel more frightened to use them in traumatized eyes,
because of some potential lesions in the anterior
chamber structures, like iris lesions, trabecular lesions,
and angle structure lesions, between others. Some
surgeons are using iris claw IOLs (e.g. Artisan) to achieve
emmetropia in eyes without capsular support;
controversies still are in the field, because if well they
have not angle complications, they still have the corneal
features, with the consequent need to long-term
follow-up. Anterior chamber lenses, angle supported
or iris supported, are a good option for correction of
aphakia in traumatized eyes according the needs of
the case.
Posterior chamber lenses are preferred because they
are far away from the corneal endothelium and it has
been demonstrated the less incidence of corneal
edema. Many techniques have been described for the
implantation of a posterior chamber lens without the
posterior capsule support; scleral fixation, iris suture
and scleral glue between others; the technique of
choice will depend upon the particular features of the
traumatized eyes and the preferences of the surgeon.
It has been demonstrated the long-term safety of the
posterior chamber IOLs, so it can be described as the
method of choice for correction of aphakia in
traumatized eyes, any time that it can be possible and
the surgeon has the experience enough to implant
this mode.
Prognosis and Long-term
Considerations
The luxation of the crystalline lens, after a traumatic
lesion of the eye is a severe medical condition that
much of the times is not coming alone, if well
accompanied by some other severe injuries if the eye
that can lead to potential bad visual recovery. A perfect
evaluation of the conditions associated to the luxation
are mandatory in order to establish the priorities of
action to solve the injuries; sometimes other lesions,
like retinal detachment or acute glaucoma, have
priority of action; sometimes during a single surgical
procedure, many features can be corrected, including
the luxation or subluxation of the lens; in some other
traumatic lesions is better not to do nothing; the criteria
will depend upon the severity of the lesions, a perfect
evaluation of all of them, the experience of the surgeon,
the surgical findings and the possible postoperative
complications. It is not an easy thing to do, and
sometimes long-life follow-up is needed.
A particular condition will be mentioned at the end
of this chapter as a remainder that a traumatic lesion
of the lens can lead to long term complications; it is
the late in-the-bag IOL dislocation, condition that has
been studied for many authors and that if well it is
not exclusive of the traumatic lesions of the eye (e.g.
pseudoexfoliation, high myopia, Marfan syndrome),
it is a severe condition that allows us to keep in mind
85
that a good communication with our patients and
medical service according to ethic principles through
the years is mandatory.
As a final point do not forget in these cases, to
perform an individualized informed consent, with the
enumeration of each and every preoperative diagnosis
and possible short and long term complications; never
give a definitive prognosis to these patients.
Bibliography
1. Amar Agarwal, Athiya Agarwal, Soosan Jacob, Sugandha
Sinha. Chopstick technique aids IOL implantation in
broken posterior capsule cases. Ocular Surgery News,
US edn, December 1, 2007.
2. Amar Agarwal, Swati Agarwal. Technique helps remove
lens fragments that have fallen into the vitreous. Ocular
Surgery News Eudope/Asia-Pacific Edition, December
2006.
3. Amar Agarwal. Technique helps remove lens fragments
that have fallen into the vitreous. Ocular Surgery News,
US edn, May 1, 2006.
4. Gimbel HV, Condon GP, Kohnen T, Olson RJ. Late in-
the-bag intraocular lens dislocation: Incidence, prevention
and management. Journal of Cataract and Refractive
Surgery. Nov. 2005;Vol 31; issue 11, 2193-2204.
5. Gundula Bading, Jost Hillenkamp, Helmut G. Sachs,
Veit-Peter Gabel, Carsten Framme. Long-term Safety and
Functional Outcome of Combined Pars Plana Vitrectomy
and Scleral-Fixated Sutured Posterior Chamber Lens
Implantation, 18 June 2007. American Journal of
Ophthalmology. September 2007;144(3);371-7.
6. F Hakan Oner, Nilufer Kocak, A. Osman Saatci.
Dislocation of capsular bag with intraocular lens and
capsular tension ring. Journal of Cataract and Refractive
Surgery. 2006;32(10):1756-8.
7. Khalid Hasanee, Iqbal Ike K. Ahmed. Capsular tension
rings: update on endocapsul ar support devices.
Ophthalmology Clinics of North America December
2006;19(4):507-19.
8. Manuel Monteiro, Antonio Marinho, Salgado Borges,
Lucas Ribeiro, Castro Correia. Scleral fixation in eyes with
loss of capsule or zonule support. Journal of Cataract
and Refractive Surgery April 2007;33(4):573-6.
9. Marije L Sminia, Monica Th.P. Odenthal, Nitza Gortzak-
Moorstein, Liesbeth JJM. Wenniger-Prick, Hennie J
Vlker-Dieben. Implantation of the Artisan iris
reconstruction intraocular lens in 5 children with aphakia
and partial aniridia caused by perforating ocular trauma,
10 March 2008. Journal of AAPOS. 2008;12(3):268-72.
10. Sharon P Bord, Judith Linden. Trauma to the Globe and
Orbit. Emergency Medicine Clinics of North America
2008(26)1:97-123.
11. Sunil K Rao, Paul B Greenberg, Theodoros
Filippopoulos, Ingrid U. Scott, Nickolas P. Katsoulakis,
Yoash R. Potential impact of seatbelt use on the spectrum
of ocular injuries and visual acuity outcomes after motor
vehicle accidents with airbag deployment, 31 August
2007. Enzer Ophthalmology 2008;115(3):573-6.
12. Sleyman Kaynak, Zeynep Ozbek, Eser Pasa, F Hakan
Oner, Gray Cingil. Transscleral fixation of foldable
intraocular lenses. Journal of Cataract and Refractive
Surgery April 2004(30)4:854-57.
13. Wojciech Omulecki, Katarzyna Stolarska, Aleksandra
Synder. Phacofragmentation with perfluorocarbon liquid
and anterior chamber or scleral-fixated intraocular lens
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lenses. Journal of Cataract and Refractive Surgery 2005;
31(11):2147-52.
C H A P T E R
17
Traumatic Cataract in Children
Rupal H Trivedi, M Edward Wilson (USA)
Introduction
Children are highly vulnerable to ocular injury,
especially sports-related ocular injury. Traumatic
cataracts can be an immediate, early or late sequel
of any ocular trauma. Management of traumatic
cataract remains a challenge, in part because each
case is unique. Surgical techniques need to be
customized case by case based on associated ocular
injuries. Pediatric cataract surgery is challenging and
a traumatic etiology simply adds more challenges.
Such surgery in children should draw from both the
principles of pediatric non-traumatic cataract removal
techniques and the advancements in adult traumatic
cataract removal techniques. Optimum timing of
cataract surgery (duration between development of
cataract and removal of cataract) is debatable. The
timing of lens removal surgery is important in children
not only to achieve better anatomical outcome but
also to achieve better visual outcome. Surgery too
earl y may resul t in excessive postoperative
infl ammation and many cel l deposits on the
intraocular lens (IOL). Surgery too late may result in
deprivational amblyopia.
Epidemiology
Cataract formation after traumatic injury is a common
cause of ocular morbidity and visual loss. While no
segment of society escapes the risk of eye injury, the
victims primarily at risk are the young (median age
26 years).
1
The majority of all eye injuries occur in
persons under thirty years of age (57%).
1
The toll of
injury in terms of human suffering, as well as long-
term disabilities, loss of productivity, and economic
impact, can only be imagined.
1
Trauma has been reported to be responsible for
up to 29% of all childhood cataracts.
2
At the Storm
Eye Institute, our database includes 103/866 eyes
(11.9%) with traumatic cataract (unpublished data).
Boys are more frequently affected than girls (68%
versus 32%
3
). The majority of traumatic cataract cases
occur in children while playing or when they are invol-
ved in sport-related activities. Commonly implicated
objects include knives, BB guns, firecrackers, sticks,
thorns, rocks, pencils, arrows, airbags, paintballs, and
toys. Prevention of eye injuries is of utmost importance
and is the team responsibility of parents, teachers,
coaches, ophthalmologists, pediatricians, and
optometrists.
4
The American Academy of Pediatrics
and the American Academy of Ophthalmology pub-
lished a statement recommending types of protective
lenses and frames for specific sports.
4
In addition, soft-
core baseballs have been recommended for youth
league games. However, a case report of 7-year old
boy is published who was struck in his left eye by
a soft core baseball, which was lobbed to him from
a short distance by his father, an ophthalmologist.
5
Pathophysiology
Blunt trauma is responsible for coup and countercoup
ocular injury.
6
Coup is the mechanism of direct impact.
It is responsible for the Vossius ring (imprinted iris
pigment) sometimes found on the anterior lens capsule
following blunt injury. Countercoup refers to distant
injury caused by shockwaves traveling along the line
of concussion. When the anterior surface of the eye
is struck bluntly, there is a rapid anterior posterior
shortening accompanied by equatorial expansion.
This equatorial stretching can disrupt the lens capsule,
zonules, or both. Combinations of coup, countercoup,
and equatorial expansion are responsible for the
formation of traumatic cataract following blunt ocular
injury. Penetrating trauma that directly compromises
the lens capsule often leads to cortical opacification
at the site of injury. If the rent is sufficiently large, the
entire lens rapidly opacifies (Fig. 17.1). When the
capsular rent is small, however, the capsule may seal
and the cortical cataract may remain localized.
Cataracts caused by blunt trauma classically form
stellateor rosette-shaped posterior axial opacities
87
that may be stable or progressive, whereas penetrating
trauma with disruption of the lens capsule forms cortical
changes that may remain focal if small or may progress
rapidly to total cortical opacification. Anterior and/or
posterior capsule defect, intralenticular foreign body,
partial/total zonular loss, and dislocation and
subluxation of the lens are often found in combination
with traumatic cataract. Other less common associated
complications include glaucoma (usually related to
hyphema and angle recession), retinal detachment,
choroidal rupture, intraocular hemorrhage, retrobulbar
hemorrhage, traumatic optic neuropathy, and globe
rupture. Anterior capsule rupture (with flocculent lens
matter in the anterior chamber) may be associated
with an increased intraocular pressure. However,
flocculent lens material in the anterior chamber is much
better tolerated in children than in adults. This may
allow the surgeon to delay surgery for 1-3 weeks until
the inflammation from the original injury (or injury
repair) subsides.
Preoperative Evaluation
In the setting of traumatic cataract, the ophthalmologist
must first take a step back and examine other ocular
injuries in detail.
7
The surgeon doing cataract surgery
should be suspicious of injury to other ocular structures.
Management depends on the degree and type of
injury. Localized traumatic cataracts (especially if not
in the visual axis) may be managed conservatively,
while more significant lens opacities generally require
cataract extraction. Similarly, capsular perforation may
be managed with observation if small and not centrally
located. Frequently, such injuries will develop only very
localized opacification of the underlying cortex without
progression to generalized cataract.
The initial patient evaluation is one of the most
important critical steps in the management of any
traumatic cataract. Data gathered during this exami-
nation, to a large extent, direct further investigations
and establish immediate priorities. One of the most
important aspects of this first examination is the
description of the exact circumstances of the injury.
This facilitates the development of risk estimates for
occult injuries, such as intraocular foreign body (IOFB),
chemical exposure, and posterior rupture of the globe.
Examination
BEFORE DILATION
1. Best-corrected visual acuity (BCVA).
2. Fixation preference.
3. Pupillary reflex: Presence of afferent pupillary defect
may be indicative of traumatic optic neuropathy.
4. Intraocular pressure (if there is no evidence of ocular
rupture).
5. Iris: Multiple small ruptures of the pupillary
sphincters are common and result in a permanent
traumatic mydriasis (Fig. 17.2). The clinical evalua-
tion should also include a careful predilatation
examination of the iris for trans-illumination defects.
If present, it should be documented and following
dilatation, the underlying lens surface should also
be inspected for anterior capsular defect that
indicate a penetrating injury or IOFB.
6. Zonule: Although detection of zonular loss is not
always possible prior to pupil dilation, suggestive
findings include phacodonesis, an increase in
myopic refractive error, abnormal peripheral lens
curvature in one or more quadrants, an abnormal
light reflex on retinoscopy, a visible lens equator,
or vitreous in the anterior chamber.
Fig. 17.1: Total cataract in an eye with ruptured
anterior capsule
Fig. 17.2: Postoperative follow-up of a child operated at
14 years of age for traumatic cataract showing traumatic
mydriasis
88
AFTER DILATION
1. Slitlamp examination (after pupillary dilation) is
recommended if feasible. This helps identify and
document the type of cataract, the position and
stability of the lens, integrity of the lens capsule and
the overall status of the anterior segment. When
slitlamp examination is not possible in the awake
state, it can be done using a portable instrument
in the operating room in conjunction with the
examination using the operating microscope.
2. A posterior segment examination, including
examination of the retinal periphery, should be
carried out in detail if the view through the lens
allows. Greven and colleagues
8
found that only
30% of eyes that suffered from contusion injuries
had normal preoperative posterior segments;
emphasizing need for B-scan if the posterior pole
cannot be visualized.
3. Gonioscopy may be helpful to evaluate the angle
structures and for recognizing vitreous at the lens
equator or areas of loss of zonular support.
4. If planning for IOL implantation, keratometry and
immersion A-scan ultrasound for globe axial length
measurement should be attempted. Even when
corneal scarring is present, keratometry of the
injured eye should be attempted. Changes in
corneal curvature as the result of an injury will
change the IOL power needed to achieve the
refractive goal. At times the keratometry readings
of the fellow eye need to be used but this will
further compromise the accuracy of the
postoperative refraction in rel ation to the
postoperative goal. Cohen
9
reported a 4 D of IOL
power surprise in a adult patient when the IOL
power was calculated using the K and AL of the
fellow eye.
A Guarded prognosis for anatomical and
functional outcome is to be thoroughly explained
to the patient and patients relatives. The full extent
of the eye injuries are not always known prior to
cataract surgery. It is also important to explain about
the possibl e need for additional surgeries
depending on the type of injury (retinal
detachment, keratoplasty for dense corneal scar
obstructing visual axis, etc).
Timing of Surgery
The timing of traumatic cataract surgery in children
is important. Some authors have reported cataract
surgery at the time of primary repair.
10
While the
development of amblyopia in children necessitates
prompt removal of a cataract when it develops, cataract
surgery is not necessarily required at the time of initial
repair even when anterior capsular rupture is present.
Cataract surgery can be deferred whil e the
inflammatory response is treated with topical steroids.
Advantages of secondary cataract removal are better
visibility, better IOL power calculation, anterior segment
reconstruction, and stabilization of a hemato-ocular
barrier. Ten of our patients (43.4%) had anterior
capsule rupture and crystalline lens involvement at the
time of injury and had their cataract surgery deferred
for times ranging between 2 days and 6 months
(average 20 days).
11
Cataract surgery is usually not
performed concurrent with the primary repair of an
open globe. The exception to this rule would be a
small eyewall laceration that can be closed securely
prior to cataract surgery and that doesnt significantly
interfere with visualization of the cataract. If cataract
surgery is delayed for several weeks, it can be
combined with the removal of the sutures used to close
the corneal laceration thereby minimizing the number
of times the child has to be anesthetized. If it is unclear
if the cataract is visually significant, cataract surgery
should be delayed until the cornea is fully healed and
the childs vision can be tested with an optical
correction. If the cataract is visually significant, its
removal should not be delayed too long because of
the potential for the child to develop amblyopia and
lose binocularity. The median interval between the
injury and cataract was 8 weeks in a series by Gardin
and Yorston.
3
Authors noted that children older than
7 years at the time of surgery were more likely to have
a delay of 1 year or more (P=0.016).
Surgical Details
General principles of pediatric cataract surgery should
be followed. Specific differences have been described
herein.
Anesthesia: In anticipation of difficult surgery,
general anesthesia is preferable even in older
children who might otherwise be cooperative for
local anesthesia.
Anterior capsule management: Performing the
capsulorhexis may be difficult in pediatric traumatic
cataract. Besides higher elasticity of pediatric
anterior capsule, traumatic cataracts are often
associated with ruptured anterior lens capsule or
fibrosis of the anterior capsule. In addition,
performing the capsulorhexis may be difficult in
a case of traumatic cataract due to a lack of the
usual zonular counter traction forces. To address
this situation, initiate the capsular tear in the location
of the greatest zonular stability and complete it in
the direction of the zonular dialysis. Very dense
fibrous capsule can be removed with intraocular
89
scissors, radiofrequency diathermy or Fugo plasma
blade. Staining of the anterior lens capsule may
be helpful to enhance visibility in these eyes with
a torn anterior capsule or white cataract.
Anterior capsule staining can be

successfully done
using nontoxic capsular dyes such as indocyanine
green 0.5% or trypan blue 0.1%. Typically, these
cataracts may be white in many instances, and
indocyanine green or trypan blue can be very
helpful. An intact capsulorhexis is also mandatory
for a capsular tension ring (CTR) placement. After
the capsulorhexis is complete, in cases of zonular
dialysis, capsular retractors can aid in visualization
of the lens and in its removal.
Avoid doing hydrodissection if the integrity of the
posterior capsule is in question.
Posterior capsule and vitreous management:
Management of the posterior capsule depends on
the age of the patient and the status of the posterior
capsule (intact v/s torn). In young patients with
complex trauma, staged approach (leaving behind
intact posterior capsule at the time of initial cataract
surgery and planning a secondary surgery to
remove the center of the posterior capsule after
the IOL is properly fixed into the lens capsule) may
help proper placement of the IOL. This staged
approach may not be necessary for the surgeon
who operates on children frequently. However, it
may be better for surgeons unaccustomed to
operating on chil dren. Posterior capsul e
opacification occurs quickly in most cases of
complex traumatic cataract surgery. Therefore,
prepare the family that the best vision will likely
come after this planned second surgery. Repair of
iris defects or other more el ective surgical
maneuvers can also be done during this secondary
procedure, which is often done 4-8 weeks after
the initial cataract removal. Kenalog can be used
to identify residual vitreous (Fig. 17.3).
Intraocular lens implantation: Intraocular lens
implantation offers a constant optical correction
and, as such, helps in the prevention of amblyopia.
Children often have difficulty wearing contact lenses
due to poor comfort, and poor motivation to wear
the lens. In addition, aphakic contact lenses are
not suitable for the developing world because of
their high cost and the need for meticulous hygiene.
The use of IOLs has been studied in children with
traumatic cataract since Choyce first reported the
use of an anterior chamber lens in a child after
trauma in 1958.

BenEzra and associates
12
had
reported a better visual acuity and less strabismus
in children with traumatic cataract after implanting
an IOL, when compared to those wearing contact
lenses. Continued advances in IOL design,
biomaterial and power calculations are making it
the preferred option.
In young children, it is generally best to under-
correct an eye in anticipation of a myopic shift as
the child becomes older. In-the-bag fixation is
believed by most to be the best site for IOL
implantation as it sequesters the implant from uveal
structures, reduces the chance of lens decentration,
and delays PCO formation.
13
In-the-bag placement
of the IOL haptics improves implant stability and
minimizes uveitis and pupillary capture.
14
Fifteen
of our 21 eyes with primary implantation had the
IOL placed in the capsular bag.
11
Traumatic cataract
cases often present unique challenges, as it is not
always possible to fixate the IOL haptics in the
capsular bag due to anterior and/or posterior
capsule tears from trauma or the difficult surgical
procedure. If the IOL must be placed in the ciliary
sulcus, as with extensive traumatic posterior capsule
rupture, try to capture the IOL optic through the
anterior capsulotomy. Gardin and Yorston noted
that they could implant an IOL in the capsular bag
in 32% of eyes, in the sul cus in 28% and
asymmetrical (bag/sulcus) in 5.6% of eyes (34%
unknown).
3
Care should be taken to position the
haptics of the IOL on the most stable remnants
of the lens capsule. Malplacement of the IOL is
more common, however, in traumatic cataracts
since damage to the capsular bag, zonules and iris
may predispose to decentration and pupil capture.
Using ciliary sulcus-fixated IOLs in children following
traumatic cataract removal resulted in visual
outcomes similar to those for capsular bag IOLs
but with more complications, in particular uveitis
and pupillary capture. The use of multifocal capsular
bag IOLs following removal of a traumatic cataract
has also been explored. In comparison with
Fig. 17.3: Use of kenalog in identifying residual
vitreous in anterior chamber
90
standard, monofocal, capsular bag IOLs, the
multifocal lenses resulted in improved uncorrected
near visual acuity and stereopsis, as well as
decreased spectacle dependency. However,
multifocal IOLs reply on centration of the IOL and
the pupil. Neither are achievable in all cases of
trauma. Since traumatic cataracts are most often
unilateral, the child will rely mostly on the natural
accommodation of the uninjured eye for near
viewing. Multifocal IOLs are best when used
bilaterally. For these reasons, the use of multifocal
IOLs in pediatric trauma has remained low.
Several reports on groups of patients with angle-
supported anterior chamber IOLs in traumatic
pediatric aphakia have been published. Due to the
high incidence of secondary glaucoma, progressive
pupil distortion, endothelial loss, and the limited
experience with these IOLs in children, angle-
supported IOLs have not gained widespread
acceptance. Scleral-fixated IOLs are considered a
more acceptable alternative for the bag or ciliary
sulcus implantation of posterior chamber IOLs, in
the absence of capsular support in children.
However, concerns have been raised about the risk
of conjunctival and scleral erosion of scleral sutures
leading to infection, IOL tilt, dislocation of the lens
in the vitreous cavity, vitreous or ciliary body
hemorrhage, and secondary glaucoma. Recently,
Sminia ML and colleagues
15
described the long-
term follow-up of Artisan aphakia IOL implantation
in five aphakic eyes without capsular support, after
cataract extraction following penetrating ocular
trauma. The authors noted that the Artisan aphakic
IOL offers a useful alternative for correction of
traumatic childhood aphakia. Although results were
from a smal l series, the authors feel that
implantation of the Artisan aphakic IOL can be
considered a treatment option in aphakic eyes of
children that lack capsular support due to trauma.
Zonular loss: Zonular dialysis may also exist in other
conditions that are not traumatic, such as pseudo-
exfoliation or Marfans syndrome. The difference
is that these conditions involve diffuse, progressive
zonular disease as opposed to a one-time focal
disturbance that occurs upon trauma. Although the
surgical approach to cataract surgery may be similar
in both scenarios, long-term capsular stability is
better in traumatic cases. The degree of zonular
dehiscence dictates the management approach. The
choice and positioning of the IOL depends on the
degree and location of zonular disruption. In eyes
with no zonular disruption and an intact posterior
capsule, a standard capsular bag-fixated IOL may
be used. With a small area of zonular incompetence,
a capsular bag IOL may also be used, but the
haptics should be oriented toward the area of
incompetence in order to expand and stabilize the
capsular bag fully. With more significant zonular
disruption, IOL implantation should be combined
with CTR. They are not recommended when the
integrity of the posterior capsule has been breeched.
For zonular dialysis of up to 150 degrees, the use
of a conventional CTR followed by standard
cataract removed and IOL implantation is often
successful. The CTR can be implanted before or
after the cataract is removed. Although early
insertion provides support during cataract removal,
it may create additional zonular trauma. The use
of iris or capsule retractors at the capsulorhexis edge
or the use of capsular tension segments (CTS)
during cataract removal are other alternative that
do not induce significant capsular torque during
insertion. For more significant or progressive zonular
dialysis the Cionni-modified CTR is useful
alternative to the conventional CTR. It can be
sutured to the sclera without compromising the
capsular bag, thus allowing the CTR and capsule
to be held in place even in the presence of significant
zonular incompetence. Otherwise one or two CTS
devices may be used and may also be placed in
cases of an anterior capsular tear, incomplete
capsulorhexis, or posterior capsular rupture.
Iris damage: Occasionally the iris may require
suturing. Iridodialysis defects are usually repaired at
the time of IOL implantation using a series of double-
armed10.0 prolene sutures (Figs 17.4A to C) on
a long straight STC-6 needle. A small paracentesis
is made 180 degrees away from the iridodialysis.
Both needles of the double-armed prolene are
passed through the paracentesis (one at a time)
and across the anterior chamber. The needle is
allowed to pick-up the peripheral detached edge
of the iris base and then exits the sclera as close
to where that iris segment should naturally attach
as possible. Each double-armed prolene is passed
in a mattress fashion and is tied external to the
sclera. Rather than using a scleral flap, we simply
leave the suture ends long and tuck then under
the conjunctiva and Tenon fascia. This seems to
prevent suture ends from gradually eroding
through the conjunctiva. Cuts and tears in the pupil
margin are also often closed with the same type
of suture material. This can be done at the initial
surgery but is often easier when done as a
secondary procedure in a well-healed pseudo-
phakic eye. The use of aniridia implant devices such
as iris diaphragm rings and iris section shields may
be appropriate in cases of a significant loss of iris
tissue. These devises are not yet FDA approved
for use in the USA. Pupilloplasty and/or repair of
iridodialysis may also be required.
91
Figs 17.4A to C: Iris sutured for traumatic iris tear
Removal of corneal suture: If corneal suture from
original trauma is present and wound healing has
been completed, corneal suture can be removed
at the time of cataract surgery (Fig. 17.5).
Postoperative Medication
Depending on the case, we may sometimes increase
the frequency of steroid drops. Also, a short course of
systemic steroids may be indicated. If IOP control had
been a problem after the original trauma, perhaps during
hyphema resolution, it is likely that elevated IOP will
be seen transiently after cataract surgery. Prophylactic
oral Diamox is recommended during the early healing
phase in such cases.
Postoperative Complications
Gardin and Yorston noted that the most frequent early
complications was severe anterior uveitis with fibrin
formation in the anterior chamber, which occurred in
51.2%.
3
Fibrinous uveitis was common in recently
injured eyes, occurring in 60% of eyes injured 6 weeks
or less before surgery and 44% if injured more than
6 weeks before cataract surgery (P=0.02). Eckstein
and colleagues however did not find an association
between postoperative fibrinous uveitis and recent
trauma.
16
Other sequel include posterior capsular
opacification (PCO) and/or secondary membrane
formation, pupillary capture, IOL precipitates
(Fig. 17.6), and decentration/dislocation of the
implant. Complications in our series included visually
significant PCO in 5 cases (21.7%), pupillary capture
in 2 cases (8.6%) and IOL dislocation in 1 case
(4.34%).
11
We continue to recommend planned
primary posterior capsulectomy in children too young
to undergo an awake Nd: YAG laser capsulotomy.
Occurrence of pupillary capture can be reduced after
a precise fixation of the IOL within the capsular bag
or the use of optic capture into the anterior or posterior
capsulorhexis. Decentration/dislocation of an IOL can
occur because of traumatic zonular loss and/or
inadequate capsular support. Posterior capture of the
IOL optic may be useful, at times, to obtain better
centration of the implanted IOL. Asymmetric IOL
fixation, with one of the haptics in the capsular bag
and the other in the ciliary sulcus can also lead to
Fig. 17.5: Corneal suture removal can be done at the
time of cataract surgery if wound appears to be healed
92
decentration and should, therefore, be avoided.
Explantation or repositioning of the IOL may be
necessary in some cases presenting with significant
decentration/dislocation. Fracture of an implanted
posterior chamber IOL after trivial trauma in a child
operated originally for traumatic cataract has been
reported. Such spontaneous fracture of IOL may be
because of mechanical weakening, commonly
attributed to a defective lens production or repetitive
movements of the IOL during psuedoaccomodative
effort. Moreover, in children extensive fibrosis around
the IOL can induce torsion at the optic haptic junction.
Perhaps a sudden anterior movement of the vitreous
due to a rapid head movement induced by trauma,
in the setting of a relatively fixed pupillary captured
IOL, may break the IOL at its already stressed optic-
haptic junction, resulting in optic lying in the anterior
chamber. The possibility of this complication can be
explained while explaining while discussing a guarded
prognosis to the parents.
17
Visual Outcome
The prognosis for retention of good vision in pediatric
eyes suffering traumatic cataracts has greatly improved
over the last few decades. Primary IOL implantation
has a greatly improved visual outcome. Several
surgeons from countries with high traumatic cataract
rates and conditions prohibitive of contact lens wear,
have recently reported successful IOL implantation in
injured children.
10, 12-14, 18-21
Compliance with amblyopia
therapy is necessary in younger children to get
maximum visual outcome, even following an excellent
surgical result. Binkhorst and Gobin
22
, reviewed a case
series originally published by Mc Kimura in 1961.
Twenty-six children with unilateral traumatic cataract
had been treated at McGill University Hospital and
the University of California Medical Center in San
Francisco. Despite treatment, most of the patients had
visual acuity in the range of counting fingers; only one
child retained visual acuity better than 20/200.
Binkhorst and Gobin
22
recommended the use of IOLs
in this situation and suggested this treatment would
improve the visual outcomes in children with lenticular
opacity.
Our results (as well as the experience of several
other authors) confirm that good visual outcome is
frequently possible following IOL implantation in
children. In our patients, 78% achieved a best-
corrected visual acuity of 20/40 or better after a mean
follow-up of 2.3 years. Koenig et al
20
reported 20/40
or better visual acuity in 87% (7 out of 8) of eyes
undergoing IOL implantation for pediatric traumatic
cataracts. The average follow-up in their series was 10
months. Gupta et al
19
reported that 9 (50%) of 18
children with unilateral traumatic cataract achieved 20/
40 (or greater) visual acuity after IOL implantation,
with an average follow-up of 12 months. In many cases
corneal l eucomata contributed to decreased
postoperative visual acuity. Similarly, Anwar et al,
10
BenEzra et al,
12
Eckstein et al
16,
Pandey et al,
14
and Brar
et al,
13
reported visual acuity of 20/40 or better in
73.3%, 79.0%, 65.2%, 67.0%, 85% and 62% of cases,
respectively, after traumatic cataract surgery with IOL
implantation in children. Gardin and Yorston
3
noted
that amblyopia was found in 42 of 108 children
(38.9%) 8 years or younger at the time of injury with
a minimum follow-up of 1 month. The risk of
amblyopia significantly increased when there was a
long interval between trauma and cataract surgery.
Fourteen of 23 eyes (60.9%) in children 8 years or
younger at the time of injury who had surgery at least
1 year after the trauma were amblyopic. Of the 85
who had surgery less than 1 year after their injury,
28 (32.8%) were amblyopic (P=0.015). The authors
further noted that of the 21 eyes with unfavorable
visual outcome (worse than 20/200), amblyopia was
the most common cause (9 eyes, 42.8%), followed
by retinal detachment (5 eyes, 23.8%).
Summary
Cataract formation is a well-recognized consequence
of blunt and penetrating ocular trauma. It results from
direct lens injury, contusive ocular damage, or lens
dislocation and is often associated with traumatic injury
to the cornea, iris, and vitreous. Traumatic cataract
can present many challenges to the ophthalmologist.
It adds the challenges presented by childhood cataract.
Fig. 17.6: Deposits on IOL optic
93
Comprehensive examinations, careful planning for
surgical management and a close follow-up are
necessary for a favorable outcome in these cases.
Further prospective studies are probably needed to
specifically address the optimum timing of cataract
surgery in cases of pediatric traumatic cataract.
However, based on our experience, we suggest primary
repair of the injury first, and cataract surgery after a
2-4 weeks of topical steroid and atropine treatment.
This delay may be helpful in achieving the optimum
surgical outcome by reducing the postoperative
inflammation in these eyes and allowing healing to
occur. Long delays before cataract removal must be
avoided during the amblyopia prone years, which
extend to approximate the age of 8 years. Successful
surgery requires a wide variety of techniques to the
particular occasion and case. These factors include the
history and circumstances of the ocular trauma,
hypotony or the elevation of IOP, inflammation, and
the extent of associated anterior segment trauma. We
support the continued use of IOLs in children in eyes
with traumatic cataract.
References
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A. Aetiology of childhood cataract in south India. Br J
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4. Protective eye wear for young athletes. A joint statement
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ophthalmology. Philadelphia: Lippincott Williams and
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2002;22:575-80.
9. Cohen KL. Inaccuracy of intraocular lens power
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J Cataract Refract Surg 2001;27:1519-22.
10. Anwar M, Bleik JH, von Noorden GK, el-Maghraby AA,
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children. J Pediatr Ophthalmol Strabismus 1994;31:
157-61.
11. Wilson ME, Trived RH, Pandey SK. Traumatic cataracts
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(editors). Pediatric Cataract Surgery: Techniques,
Complications, and Management Ahmedabad: Lippincott
Williams and Wilkins, 2005.
12. BenEzra D, Cohen E, Rose L. Traumatic cataract in
children: correction of aphakia by contact lens or
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13. Brar GS, Ram J, Pandav SS, Reddy GS, Singh U, Gupta
A. Postoperative complications and visual results in
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14. Pandey SK, Ram J, Werner L, et al. Visual results and
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1999;25:1576-84.
15. Sminia ML, Odenthal MT, Wenniger-Prick LJ, Gortzak-
Moorstein N, Volker-Dieben HJ. Traumatic pediatric
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intraocular lens implantation. J Aapos 2007;11:555-8.
16. Eckstein M, Vijayalakshmi P, Killedar M, Gilbert C, Foster
A. Use of intraocular lenses in children with traumatic
cataract in south India. Br J Ophthalmol 1998;82:
911-5.
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Devilee M. Intraocular lens implantation in children with
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20. Koenig SB, Ruttum MS, Lewandowski MF, Schultz RO.
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C H A P T E R
18
Scleral Fixated IOL in Trauma
Introduction
Ocular trauma is one of the leading common problems
that ophthalmologists dealing with. The incidence of
ocular trauma is going up day-by-day with increasing
population and varied occupations. It is very common
occupational hazard with certain occupations such as
building construction workers, carpenters, and also
very commonly seen during road traffic accidents and
in children. With the advances in surgical techniques
and availability of facilities, the prognosis of traumatic
cases is improving significantly and the management
and the visual prognosis of ocular trauma has changed
significantly over the past few days.
Lens injury during ocular trauma is one of the
commonest associations and traumatic cataract is one
of the commonest finding in any ocular trauma.
Mode of Lens Injury in Ocular
Trauma and its Presentation
The lens can be injured by various ways during ocular
trauma. There can be direct trauma to the lens leading
to its rupture and cataract. In other cases there can
be an indirect trauma as during blunt trauma without
causing a direct injury but leading to a cataract due
to altered lens metabolism more commonly known
as the rosette-shaped cataract. The exact mechanism
is not known but postulated mechanism include
microtrauma to the lens fibers and the capsule leading
to influx of aqueous in the lens and hydration of the
lens fibers and cataract.
Traumatic cataracts can be associated with
subluxtaion or zonular dialysis and/or intralentiular
foreign bodies. It is not uncommon to find posterior
segment complications associated with the cataract.
Many times the lens is dislocated out of the wound
and can be absent or can even lay subconjunctivaly.
More often than not it can get dislocated into the
vitreous posteriorly. Hence careful evaluation is
important in every trauma case. Also there can be
posterior segment complications such as retinal
detachment or a retained intraocular foreign body
in the posterior chamber, vitreous hemorrhage and
choroidal rupture and scar. This is important as the
prognosis of the outcome depends on the associated
damage as the cause of vision loss can be due to these
additional injuries than due to the anterior segment
injury. Patient counselling and prognostication, hence
becomes a very important aspect of treating ocular
trauma.
Aphakia is one of the common probl ems
encountered in patients with trauma. It can be a result
of complete loss of the lens and capsular support
during the trauma itself or it can be as a result of
zonular dialysis or lens subluxation beyond a few clock
hours in which case capsular support for implantation
of a posterior chamber lens can be inadequate. In
some cases, doing an ICCE or performing pars plana
lensectomy is required for managing the cataract. In
these circumstances the options that remain are an
implantation of an anterior chamber IOL or a
secondary scleral fixated IOL in the sulcus.
Scleral Fixated IOL vs Anterior
Chamber IOL
With the advances in the techniques in the surgery
and availability of vitrectomy machines in most of the
centers and availability of scleral fixated lenses more
readily in the market, the trend is shifting towards
inserting a scleral fixated IOL, whenever possible.
A traumatised eye is very commonly associated
with additional complications such as posterior
segment complications and corneal tears which need
to be dealt with. In addition there can be damage
to the anterior chamber angle structures. Hence, a
patient with traumatized eye need routine follow-up
and detailed evalution of the angle by gonioscopy,
intraocular pressure and posterior segment. Also there
95
can be additional damage to the iris structures such
as iridodialysis or damage to the iris sphincter leading
to a dilated pupil. In other circumstances, the iris may
have been abscised during the primary wound repair,
leading to inadequate iris support. Hence, an ACIOL
implantation may not always be possible.
In some circumstances, an ACIOL is best avoided
such as when the patient will need detailed posterior
segment evaluation with fully dilated pupils which is
not possible with an ACIOL in situ. This is important
as patients with ocular trauma are prone for retinal
detachments and need detailed fundus evaluation with
indentation. It is also avoided in patients who may
otherwise have normal posterior segment in the eye
in question but may have a history of retinal
detachment in the other eye or in the family, in which
case routine examination is necessary. ACIOLs are also
contraindicated in patients with glaucoma and in
patients with narrow angles, in whom frequent
gonioscopy is required which can be difficult with the
haptics of an ACIOL in the angle. There can be
associated angle recession in traumatized eyes and an
ACIOL can further aggravate the damage. ACIOLs
are also not advisable in patients with corneas with
low endothelial counts as the ACIOL can lead to
corneal decompensation and bullous keratopathy.
Moreover, the advantage of SFIOL over ACIOL
is its placement in the anatomical location with a
placement closest to the nodal point of the eye giving
better optical properties.
Indications of SFIOL
1. Monocular aphakia in patients with contact lens
intolerance.
2. Ol d and disabl ed persons with tremors,
Parkinsonism or other physical disabilities which
makes handling and using spectacles and contact
lenses difficult.
3. Children in whom maintaining contact lenses can
be a problem and contact lens wear may be
difficult. Also, non-compliance with the contact
lenses can lead to amblyopia.
4. Young patients who find the prospect of using a
contact lens lifelong, unacceptable.
5. In patients undergoing penetrating keratoplasty for
corneal scars involving visual axis.
6. Contralateral pseudophakia.
Preoperative Workup
1. Detailed history with previous surgical notes, if
available should be procured.
2. Detailed slitlamp examination of the anterior
segment should be carried out. It involves checking
for the status of the cornea including corneal scars,
astigmatism, and endothelial status. Anterior
chamber depth and anterior chamber cells and flare
should be checked for. Zonular dialysis, lens
capsular rupture and intralenticular foreign bodies
should be noted. A careful examination should be
made to look for vitreous prolapse into the anterior
chamber in which case cataract extraction needs
to be carried out more carefully to avoid further
damage and inadvertent traction on the vitreous.
3. Detailed fundus examination is a must in all cases
of ocular trauma; to rule out traumatic endoph-
thalmitis, retinal dialysis and detachments and any
foreign body in the posterior segment. Choroidal
rupture should be looked for. A choroidal rupture
involving the macular area is associated with poor
visual outcomes. Careful examination of the
macular are should be done to rule out Berlins
edema and cystoid macular edema or a traumatic
macular hole which may need to be tackled during
the surgery. Optic nerve should be also examined
for traumatic optic neuritis or atrophy or in some
cases traumatic optic nerve avulsion.
4. In cases where the fundus view is not there an
ultrasonography B-scan needs to be done to rule
out any posterior segment complications.
5. Biometry and A-scan for axial length should be
done.
Technique of Insertion of SFIOL
Can be classified as:
A. 2 point fixation
B. 4 point fixation
Can also be classified depending on the technique of
passing the sutures as:
A. Ab-interno procedure where the suture is passed
from inside out (i.e. from the anterior chamber to
the exterior)
B. Ab-externo procedure where the suture is passed
from outside in (i.e. from the exterior into the
anterior chamber.
Can also be classified as:
A. Anterior approachmore commonly followed by
anterior segment surgeons and easy to perform.
B. Posterior approachmore commonly performed
by posterior segment surgeons. Requires greater
surgical skill and more advanced vitrectomy
setup.
96
2 POINT FIXATION
In this technique, the IOL is fixed to the sclera at 2
points with 2 10-0 prolene sutures. This is a faster
technique and less cumbersome. Hence, it is easier
to perform and good for beginners. However, the
stability of the IOL is lesser as compared to 4 point
fixation and the chances of decentration or tilts are
higher.
4 POINT FIXATION
In this technique, the IOL is fixed to the sclera at 4
points with 10-0 prolene sutures. However, it requires
more skill and is more time consuming. The sutures
can get entangled and a mix-up of sutures can cause
improper fixation of the IOL. Hence this procedure
can become cumbersome and difficult to perform.
AB-INTERNO TECHNIQUE
This is a blind technique wherein after making 3 mm
3 mm scleral flaps at the limbus, the 10-0 prolene
needle is passed through the eyelet of the haptic and
then the needle is passed through the AC and brought
out about 1 mm from the limbus under the scleral
flaps. This technique requires lot of skill and experience
as while passing the needle underneath the iris, it can
damage the iris itself or the ciliary body or in some
cases if the needle goes more posteriorly it can cause
breaks in the retina and can cause a retinal detachment.
Also the most important factor which makes it a non-
preferred technique by many is that the placement
of IOL is more posterior with this technique rather
than in the ciliary sulcus as has been found in many
studies. Hence, this technique although fast may not
be suitable for beginners and who are inexperienced.
AB-EXTERNO TECHNIQUE
This technique is easier to perform and requires little
experience and the learning curve is faster. Also, the
procedure is done under direct view and hence more
accurate as to the placement of the IOL perfectly in
the sulcus. In this procedure after making scleral flaps
or grooves, a 27G needle is passed 1mm from the
limbus into the eye behind the iris and held in place
in the pupillary axis. From the opposite side, a
10-0 prolene suture with a straight needle is passed
into the eye and passed into the bore of the 27G needle
under observation and the 27G needle is pulled out
bringing with it the needle. A superior 7 mm wound
is then created and the loops brought out, cut and tied
to the eyelets of the haptics of an SFIOL and the IOL
is then inserted in sulcus and the sutures pulled out and
fixed to the sclera in the bed. The flaps are then sutured
back with 7-0 vicryl covering the prolene knot.
ANTERIOR APPROACH
In the anterior approach, the SFIOL is inserted after
doing only anterior and core vitrectomy from the
anterior approach with making the par plana
sclerotomies. The advantage of this approach is that
it is simpler and easier to perform. The technique is
also faster. However, the chances of postoperative
complications are higher as the removal of vitreous
is incomplete and this can be a constant source of
irritation resulting in chronic cystoid macular edema,
secondary glaucoma or uveitis.
POSTERIOR APPROACH
In this approach, conventional 3 port pars plana
vitrectomy is performed completely with an induction
of posterior vitreous detachment. Limited base excision
is also performed in the area where the SFIOL will
be placed. The SFIOL is then inserted either with the
ab-externo or the ab-interno technique by 2 point or
4 point fixation.
We preferably perform ab-externo 4 point fixation
of SFIOL by the posterior approach in traumatized
eyes and it will be described in detail.
After doing routine surgical asepsis, the eye to be
operated is painted and draped.
270 degree conjunctival peritomy is performed.
2 partial thickness square shaped limbal based
scleral flaps of 3 3 mm are made at 3 and
9 O clock.
A self sealing trilaminar 7 mm scleral tunnel is made
at 12 O clock.
3 sclerotomies are made at 3 mm from the limbus.
If a cataract is present, then lensectomy is done
with a vitrectomy cutter. In cases where the cataract
is dense, it is either delivered out through the tunnel
or by phacoemulsification.
Complete par plana vitrectomy is done. In cases
where the posterior vitreous is not detached, PVD
is induced with either by suction or by an
intraocular forceps. In traumatized eyes this step
is very important as the chances of a cystoid
macular edema are very high. Also if the PVD gets
induced in the postoperative period it can lead to
retinal break formation in the already compromised
eye and cause retinal detachment.
Then limited base excision is done in the region
where the SFIOL haptics will be placed; in this case
at 3 Oclock and 9 O clock position. This has
2 advantages. It prevents the constant irritation of
the vitreous by the haptics on movement of the
eye and also prevents traction on the vitreous by
the haptics preventing retinal breaks.
97
A detailed fundus examination is then carried out
with indirect ophthalmoscope with scleral inden-
tation.
Any breaks in the retina or dialysis or suspicious
areas are treated with cryopexy.
A double armed 10-0 prolene suture with straight
needle is used for the procedure. The suture is cut
in the center.
A 27G or 28G needle is passed from the inferior
end of one of the scleral grooves into the eye behind
the iris and help in place in the pupillary area. The
needle of the 10-0 prolene suture is then passed
from the opposite side and passed into the bore
of the 27G needle and the needle is withdrawn
pulling the suture along with it. The procedure is
repeated on the superior end of the grooves. So,
now there are 2 10-0 prolene sutures passing across
the anterior chamber behind the iris with the ends
of the sutures on the outside.
The loops of the sutures are then brought out from
the scleral tunnel and cut in the center and the
ends secured.
The sutures on the left side are then to the eyelet
of the haptic of an SFIOL. The procedure is
repeated on the other side.
The IOL is then inserted in the sulcus and the
sutures are pulled out on either side taking care
that the IOL does not flip.
The left side sutures are then tied to each other
and the procedure is repeated on the other side.
The ends of the knots are left long, about 1 mm,
and are covered by the scleral flaps and the flaps
are sutured back by 7-0 or 8-0 prolene sutures.
The sclerotomies are then closed by 7-0 vicryl and
conjunctiva is closed.
Advantages of Posterior Approach in
Traumatized Eyes
More often than not, there is some amount of posterior
segment involvement due to the primary trauma. There
can be posterior dislocation of the lens or IOL into the
vitreous which needs to be removed. In other cases,
there can be incarceration of the vitreous into the wound
which can be a source of traction on the retina and
hence needs treatment. There may be associated
vitreous hemorrhage which needs vitrectomy if present
since a long time. Also, retinal breaks and dialysis are
fairly common after closed globe injuries which may
not be always be possible to see during the preoperative
period due to either vitreous hemorrhage or due to
a non-dilating pupil due to posterior synechiae or due
to a corneal scar. These can be better visualized and
treated by the posterior approach. Posterior vitreous
detachment is almost universal in traumatised eyes.
This can induce fresh breaks in some instances and
can cause retinal detachment. Also, the trauma can
cause macular involvement by way of a traumatic
chronic cystoid macular edema or an epiretinal
membrane formation or, in some cases, full-thickness
macular holes. These can also be managed during the
IOL implantation itself by combining it with total
vitrectomy with internal limiting membrane peeling.
Complications of SFIOL
CYSTOID MACULAR EDEMA
It is the most common complication seen after ant IOL
implantation. The incidence increases whenever it is
associated with complications. In the absence of the
posterior capsule this more common due to the antero-
posterior vitreous traction on the macul a. In
traumatised eyes, the trauma itself may cause CME,
more often chronic and non-responding. This can be
reduced with good vitrectomy releasing all traction on
the macula and preferably with an induction of PVD.
GLAUCOMA
This is also fairly common with SFIOL. This can be
due to incomplete vitrectomy or due to viscoelastic
device induced. It can also be secondary to entangled
vitreous in the vitreous which can cause uveitic
glaucoma. Rarely, the SFIOL can cause a pupillary
block and lead to rise in IOP. In same cases glaucoma
can be unrelated to the SFIOL itself and can be due
to damage to the trabecular meshwork during the
primary trauma.
LENS DECENTRATION AND LENS TILT
There can occur some amount of lens decentration and
tilt during the placement of the SFIOL in the sulcus and
while tying the sutures to the sclera. Sometimes, the
sutures can be loose causing an inferior subluxation of
the IOL. This can cause significant glare or diplopia. The
lens can also get tilted during the tying of the sutures or
due to passage of sutures at different levels in the sclera
on the two sides. The incidence of this complication is
lesser in SFIOLs fixed to sclera by the 4 point fixation
technique and by the ab-externo technique. However,
some amount of lens tilt is very well tolerated by the
patients with glasses and in clinical practice does not pose
a big problem. However, lens subluxation needs
treatment if the patient is symptomatic.
RETINAL DETACHMENT
It is a rare complication than can occur in any
complicated cataract surgery including SFIOL. This can
98
be prevented by doing a good preoperative evaluation
and a good intraoperative fundus examination to
identify any breaks and treat them.
CHOROIDAL DETACHMENT
It a very rare complication but can occur. There can
be a leak from the site of entry of the 27G needle
or from a leaking sclerotomy leading to hypotony. This
can be managed by countering the hypotony by
injecting intraocular air or saline and by a course of
oral steroids.
UVEITIS
It is more commonly seen in SFIOLs operated from
the anterior route in which vitrectomy is incomplete
and this leads to constant irritation of the vitreous
leading to uveitis. Trauma itself can lead to some
amount of uveitis. This can be managed by adequate
vitrectomy ensuring the lens is free of vitreous and
by using topical steroids in the postoperative period.
ENDOPHTHALMITIS
The 10-0 prolene suture forms a tract for the micro
organisms to gain entry into the posterior segment
leading to endophthalmitis. The knot of the suture also
provides a nidus for the proliferation of organisms.
There can occur delayed endophthalmitis or in some
cases even acute endophthalmitis. This can be
prevented by adequately rotating the knot in the scleral
bed or by covering it with a scleral flap. In established
cases, intravitreal antibiotics and topical antibiotics can
be started.
SUTURE EROSION
This is again a rare complication but possible. The
knot can erode through the scleral bed and can be
constant source of irritation leading to foreign body
sensation, pain, watering, and discomfort. The knot
can provide a nidus for micro-organisms and cause
an endophthalmitis. If there complete erosion of
Fig. 18.1: Applied anatomy for SFIOL
Fig. 18.2: Site of scleral tunnel for insertion of SFIOL and
partial thickness scleral grooves for 100 prolene sutures
Fig. 18.3: Technique of passing 100 Prolene suture: 10
0 prolene passed through one end of scleral groove,
engaged out through another scleral groove with help of
27 G, 1 inch needle bent at the tip
Fig. 18.4: Passing of suture through IOL islet in SFIOL haptics
suture, it can break and the lens can dislocate in which
case the procedure may have be repeated. Suture
erosion can be prevented by burying the knot in the
sclera and/or covering it with scleral flap. This should
99
be in turn covered by the conjunctiva. In case suture
erosion still occurs, a scleral patch graft should be used
to cover the exposed suture
Conclusion
IOL implantation has come a long way in the recent
years. With the advances in techniques, the options
that will be available will increase. With the growth
of industries and population, the number of ocular
trauma will increase. Hence, the management will of
ocular trauma and post-trauma rehabilitation will also
need to change with changing times and increasing
patient demands and expectations. Traumatic cataracts
being complicated on most occasions, the need for
a scleral fixated IOL will always be there. Hence the
need to learn the technique and implement it is the
need of the hour for ophthalmologists today. However,
patient counseling and regarding the risks and benefits
should be discussed in detail with the patients. Patients
should be well informed about the intra-operative and
post-operative complications and the availability of
alternatives. Only highly motivated patients are ideal
candidates for an implantation of SFIOL. In such
patients, SFIOL is a boon and will be a very good
and viable option vis--vis contact lenses.
Bibliography
1. Ab externo scleral suture loop fixation for posterior chamber
intraocular lens decentration: clinical results. J Cataract
Refract Surg. Chan CC, Crandal l AS, Ahmed II.
2006;32(1):121-28.
2. Anterior chamber and sutured posterior chamber
intraocular lenses in eyes with poor capsular support.
Cataract Refract Surg. Donaldson KE, Gorscak JJ, Budenz
DL, Feuer WJ, Benz MS, Forster RK 2005;31(5):903-09.
3. Asadi R, Kheirkhah A. Long-term results of scleral fixation
of posterior chamber intraocular lenses in children.
Ophthalmology. 2008 Jan;115(1):67-72. Epub 2007;3.
4. Comparison of outcomes of primary and secondary
implantation of scleral fixated posterior chamber intraocular
lens. Br J Ophthalmol Lee VY, Yuen HK, Kwok AK
2003;87(12):1459-62.
5. Comparison of Outcomes of Primary Scleral-Fixated versus
Primary Anterior Chamber Intraocular Lens Implantation
in Complicated Cataract Surgeries. Ophthalmology, Kwong,
H. Yuen, R Lam, V Lee, S Rao, D Lam.Volume 114, Issue
1, Pages 80-85 Y.
6. Comparison of secondary implantation of flexible open-
loop anterior chamber and scleral-fixated posterior chamber
intraocular lenses. J Cataract Refract Surg. Evereklioglu C,
Er H, Bekir NA, Borazan M, Zorlu F 2003;29(2):301-08.
7. Long-term safety and functional outcome of combined pars
plana vitrectomy and scleral-fixated sutured posterior
chamber lens implantation. Am J Ophthalmol. Bading G,
Hil l enkamp J, Sachs HG, Gabel VP, Framme C
2007;144(3):371-377.
8. Scleral-fixated intraocular lens implantation in unilateral
aphakic children. Ophthalmology. Kumar M, Arora R, Sanga
L, Sota LD 1999;106(11):2184-89.
9. Scleral-fixated posterior chamber intraocular lenses in non-
vitrectomized eyes. Eye. Yang YF, Bunce C, Dart JK, Johnston
RL, Charteris DG. 2006;20(1):64-70.
10. Secondary intraocular lens (IOL) implantation: anterior
chamber versus scleral fixation long-term comparative
evaluation. Eur J Ophthalmol. Dadeya S, Kamlesh, Kumari
Sodhi P. 2003;13(7):627-33.
Fig. 18.5: Scleral tunnel
Fig. 18.6: SFIOL in situ
Fig. 18.7: Traumatic cataract with posterior
capsular dehiscence
C H A P T E R
19
Iris Trauma
Iris Prolapse
INTRODUCTION
The iris is a thin, colored diaphragm that is situated
anterior to the lens. Although the root of the iris is
attached to the ciliary body, the rest of the iris is
unsupported. In the event of a corneal wound, the
iris tends to prolapse out. Iris prolapse occurs when
the iris tissue is observed outside of the wound; iris
incarceration occurs when the iris tissue reaches the
wound without prolapsing outside the eye. Iris prolapse
can occur secondary to cataract surgery also.
PATHOPHYSIOLOGY
Iris prolapse can occur when the cornea is perforated
due to any cause. In 1995, using flow mechanics and
the Bernoulli principle, Allan provided a theoretical
explanation of iris prolapse. With a corneal perforation,
the aqueous humor rapidly escapes, and a relative
vacuum is created in front of the iris, thus leading to
iris prolapse. Prolapsed iris tissue can be healthy or
inflamed or infected or epithelialized with inflammatory
membrane or with conjunctival tissue. Depending on
the status of the prolapsed iris tissue, the iris is either
reposited or abscessed or left untouched.
MORTALITY/MORBIDITY
Iris prolapse is a serious condition and, if left
untreated, can result in infection and loss of the eye.
It acts as nidus for infection and route of entry for
microorganisms to enter into the eye. If the prolapsed
iris is exposed (e.g. corneal laceration), immediate
surgical intervention is needed because infection can
spread through the iris and into the eye. If the prolapsed
iris is covered by the overlying conjunctiva (e.g. surgical
wound), immediate surgical intervention is usually not
needed.
CLINICAL PROFILE OF A PATIENT WITH
IRIS PROLAPSE
History
The iris is a sensitive tissue in the eye. At the time
of an iris prolapse, patients often experience pain.
Patients with a perforated corneal ulcer frequently
provide a history of severe pain that has since
subsided.
The iris can prolapse after surgery (e.g. cataract,
corneal transplant), following trauma (e.g. corneal
laceration, scleral laceration), through a perforated
corneal ulcer, or through a corneal melt associated
with rheumatoid arthritis.
However, the commonest cause by and large of
iris prolapse is the ocular trauma.
Signs
In peripheral iris prolapse, the iris appears as a knuckle
of colored tissue, resulting in a partial peripheral
synechia. When the prolapse is central, the entire
pupillary margin may prolapse, resulting in a total
anterior synechia. In patients with a perforated cornea,
the prolapsed iris is exposed.
Depending on the duration of prolapse, the
appearance of the iris may vary. In cases of recent
prolapse, the iris appears viable. With time, the iris
appears dry and nonviable. In patients who have
undergone corneal transplant surgery or cataract
surgery with a clear corneal incision, the appearance
of the iris is the same as in a perforated cornea. When
the iris prolapses through a scleral wound, it appears
as a colored mass beneath the overlying conjunctiva.
In this case, the iris remains viable for a long time.
The pupil appears peaked in the region of the iris
prolapse. The anterior chamber is formed as the
prolapsed iris seals the wound. Minimal or no wound
leakage occurs. Wound leak is verified using the Seidel
test. A drop of 2% fluorescein sodium is instilled in
the conjunctival sac. The wound is examined under
the slit lamp with cobalt blue light. The fluorescein
101
Iris Trauma
appears greenish. Wound leak can be easily identified
when the fluorescein is diluted by the aqueous humor.
Gentle pressure on the eye may be needed to induce
leakage.
However, whenever the iris tissue is plugging the
internal lip of corneoscleral wound, the Siedels test is
of no significance, as it will be false negative mainly
because of the iris and inflammatory membrane pluging
the internal lip of corneal or corneoscleral wound.
Intraocular pressure is lower than normal, but
hypotony is uncommon after iris prolapse.
In long-standing iris prolapse, chronic iridocyclitis,
cystoid macular edema, or glaucoma may be seen.
The prolapsed iris may act as a scaffold for infection,
epithelial downgrowth, or fibrous ingrowth. Rarely,
sympathetic ophthal mia may occur. Careful l y
examining the fellow eye for flare and cells is important
to rule out sympathetic ophthalmia.
Lab Studies
Iris prolapse is a clinical diagnosis.
Imaging Studies
In long-standing iris prolapse, if cystoid macular
edema is suspected, fluorescein angiography may
be performed. Cystoid macula edema appears as
a flower petal in the late stages of the angiogram.
CT scan of the orbits is indicated with traumatic
iris prolapse to aid in diagnosing other ocular and
orbital trauma and especially if the history is
suggestive of intraocular foreign bodies.
In traumatic iris prolapse, ocular ultrasound may
be gently performed by experienced personnel.
This imaging modal ity may hel p to l ocate
intraocular foreign bodies and to assess the status
of the posterior segment of the eye. Care should
be taken while performing the ocular ultrasound
because undue pressure can cause prolapse of the
intraocular contents.
TREATMENT
Conservative Treatment
Iris prolapse is a serious condition that requires prompt
medical management. As soon as the diagnosis is made,
an eye shield should be applied to prevent further
damage. One should try and avoid pressure patch over
the traumatized eye as the pressure patch by itself can
act as nidus for infection and with the eye being closed,
the organisms can flourish inside the closed eye.
Medical treatment is only indicated when the
prolapse is small, is covered by the conjunctiva, and
is without any other complications. In these cases, the
eye may be observed.
No eye drops or ointment should be applied in
open eyes with prolapse iris. Intravenous antibiotics
should be considered because infection from an iris
prolapse can spread to the intraocular contents. Broad
spectrum antibiotics are recommended. Tetanus toxoid
may be considered depending on the immunization
status and the wound type.
Surgical Care
Prompt surgical management is necessary when
conjunctival coverage is not present or in the presence
of complications. The primary goal of surgery is to
restore the anatomical integrity of the eye. Visual
restoration is only a secondary goal.
General anesthesia should be used during surgery.
Retrobulbar anesthesia and peribulbar anesthesia are
not recommended because they increase both
intraorbital pressure and loss of additional intraocular
tissue; however, they may be used if general anesthesia
is contraindicated.
Through a paracentesis incision, a viscoelastic agent
is injected into the anterior chamber in the region of
the iris prolapse. This mechanical force may be enough
to release the prolapse and to reposition the iris.
If the viscoelastic method is unsuccessful, then a
cyclodialysis spatula with the longer end is introduced
through the paracentesis incision. The spatula is swept
from the center to the periphery of the prolapse to
avoid unnecessary tension on the iris root. The corneal
wound may be sutured depending on its length and
integrity.
If the prolapse occurred within the previous 24-
36 hours and if the iris is viable, the iris is reposited.
The sings of viable iris tissue are glistening iris tissue
with no inflammatory membranes on surface of iris
tissue. The texture and glow of iris tissue are the
important indicators for viability of iris tissue.
If the iris does not appear viable, then it is abscised.
The iris should be abscised if signs of epithelialization
are present. The abscission involves pulling of the iris
tissue and cutting some part of normal healthy iris tissue
along with non-viable iris tissue which is prolapsed out.
The excision involves just cutting the prolapsed iris tissue
flushing through the corneal surface.
If the iris prolapse occurs after surgery, the same
principle is used. The wound must be revised, or
additional sutures should be applied to make the wound
watertight.
When the iris prolapse occurs after a corneal
perforation, the iris can be reposited. Cyanoacrylate
glue and a bandage contact lens may be used to seal
the perforation. If unsuccessful or if the perforation
is large, an emergency corneal patch graft or corneal
transplant is necessary.
102
Holistic Approach
In patients with a corneal melt due to medical causes
(e.g. rheumatoid arthritis), appropriate consultations
must be obtained.
Iridodialysis
INTRODUCTION AND CAUSES
Iridodialyses, sometimes known as a coredialysis, is a
localized separation or tearing away of the iris from
its attachment to the ciliary body, are usually caused
by blunt trauma to the eye,

but may also be caused
by penetrating eye injuries. An iridodialysis may be
an iatrogenic complication of any intraocular surgery
and at one time they were created intentionally as part
of intracapsular cataract extraction. Iridodialyses have
been reported to have occurred from boxing, airbag
deployments, high-pressure water jets,

elastic bungee
cords, bottle caps opened under pressure, water
balloons, fireworks, and various types of balls.
SYMPTOMS AND SIGNS
Abnormal pupils affect patients in several ways,
including photophobia and glare. These patients often
describe discomfort or difficulty in brightly lit areas,
such as supermarkets, or on sunny days. Typically, they
report that sunglasses do not alleviate their symptoms
either outside or indoors. Edge glare from an exposed
intraocular lens optic margin can elicit similar complaints
and may induce disturbing crescents, arcs of light, tails
on lights and other optical aberrations.
Rarely, an irregular pupil may induce an undesired
refractive effect. Since the visual axis usually goes
through the geometric center of the pupil, the visual
axis-corneal intercept may be abnormally placed
through an area of irregular corneal topography.
Those with small iridodialyses may be asymptomatic
and require no treatment, but those with larger dialyses
may have corectopia or polycoria and experience
monocular diplopia, glare, or photophobia. Iridodia-
lyses often accompany angle recession and may cause
glaucoma or hyphema. Hypotony may also occur.
An abnormal pupil may also have deleterious
psychosocial effects. As a society, we place a psychic
premium on the appearance of the eyes. It is common
for people to make instant judgments about others
based on how their eyes look. A shifty gaze, for
example, may be interpreted as dishonest. If people
are uncomfortable looking into the eyes of a person
with an abnormal iris, that can play an important role
in that individuals interpersonal interactions and,
perhaps, affect his self-esteem.
TREATMENT AND MANAGEMENT
In our enlightened age of small incision, closed-system
anterior segment surgery, we have increased surgical
control over the intraocular environment and have
developed the skills for more sophisticated iris repair.
Simultaneously, we are more attentive to glare and
photophobic complaints from our cataract and
refractive surgery patients. The confluence of increased
awareness and surgical abilities set the stage for the
new epoch in iris surgery.
Iridodialysis causing an associated hyphema has to
be carefully managed, and recurrent bleeds should
be prevented by strict avoidance of all sporting
activities. Management typically involves observation
and bed rest. Red blood cells may decrease the outflow
of aqueous humor, therefore the eye should be kept
soft by giving oral acetazolamide. Accidental trauma
during sleep should be prevented by patching with
an eye shield during night time. Avoid giving aspirin,
heparin/warfarin and observe daily for resolution or
progression. A large hyphema may require careful
anterior chamber washout. Rebleeds may require
additional intervention and therapy.
Later, surgical repair may be considered for larger
avulsions causing significant double vision, cosmesis
or glare symptoms.

Surgical repair is usually done by
10-0 prolene suture taking the base of iris avulsion
and suturing it to the scleral spur and ciliary body
junction.
SURGICAL PLANNING
Like most intraocular procedures, repairing a damaged
iris requires preoperative planning and meticulous
technique. With careful attention to detail and basic
principles, you can master the art of iris repair.
Preoperatively, you must determine whether there
is sufficient iris tissue remaining to achieve the desired
goals. It is often difficult to assess how much tissue is
present because the iris stroma may be contracted or
rolled over. Careful examination and review of prior
operative notes are helpful in determining whether
tissue has been removed. Typically, there is more iris
present than you might think based on slit-lamp
examination.
Furthermore, iris tissue is usually very stretchable
and can cover larger areas than you might initially
anticipate. Usually, if the patient retains two-thirds or
more of normal iris tissue, surgical repair can produce
a good functional and anatomic result. For cases in
which large amounts of iris tissue is absent, artificial
iris diaphragms, overlapping rings or sectoral implants
may be a more appropriate option to augment the
remaining native iris tissue.
103
Iris Trauma
PRINCIPLES OF IRIS REPAIR
The basic principles of iris repair are fairly straight-
forward. First, instillation of a miotic agent such as
pilocarpine, puts the iris stroma on maximal stretch,
increasing the surface area. Intracameral manipulations
should be performed under viscoelastic agents to
prevent chamber volatility, iris stretching and corneal
endothelial damage. When choosing your viscoelastic
agent, remember that you may be removing it
manually through a small incision. Highly retentive
agents may be difficult to remove without automated
irrigation and aspiration, while retained bits of overly
viscous materials can cause a significant postoperative
intraocular pressure rise. The very soft and friable
consistency of the iris demands an atraumatic
technique. Often, posterior or peripheral anterior
synechiae prevent proper mobilization of the iris
leaflets. Therefore, gentle blunt or sharp synechiolysis
may be the first step in repair. When the sphincter
is involved in the injury or damage, reapposing the
severed pupil margin establishes a central pupil and
creates a more taut iris diaphragm, facilitating further
steps.
Because patients may develop glare symptoms
when the optic margin of an implant lens is exposed,
the repaired iris leaflets should cover all IOL edges.
When an implant placement or exchange is performed
coincident with iris repair, a larger optic implant may
facilitate this task.
Suture Placement
Suture and needle choices are up to the surgeons
preference. With a long track record in the anterior
segment, the prolene suture appears resistant to
hydrolysis in the anterior chamber and, therefore, may
be a better choice than nylon.
The needle enters the anterior chamber via a
conveniently placed paracentesis site. The paracentesis
should be large enough to allow easy ingress of a
Kuglen hook. Take special care to avoid catching any
corneal fibers as the needle passes through the
paracentesis tract. The sharp-tipped needle passes
through the iris with a minimum of countertraction
and minimal iris tearing. The long, curved shape
permits passage of the needle in a closed-chamber
fashion through a paracentesis. The proximal iris leaflet
is engaged by the needle tip, then the distal iris leaflet.
The needle is then passed out through the peripheral
cornea.
Suture Tying
Tying the suture with the sliding knot technique
(introduced to ophthalmology by Steven Seipser, MD)
minimizes iris traction. This technique allows the knot
to slide into the anterior chamber without pulling iris
tissue to the wound margin and without cumbersome
intracameral knot-tying maneuvers. Once the suture
has been passed, place a Kuglen hook through the
initial paracentesis tract, engage the suture just beyond
the distal iris pass and draw a loop of suture out through
the paracentesis site. Maintaining proper orientation
of the sutures is of utmost importance in creating a
knot. The orientation should be:
1. Trailing suture strand;
2. Part of loop from distal iris pass and;
3. Part of loop exiting peripheral cornea.
If the loop folds over and changes the relative
position of 2 and 3, a twist occurs instead of the
intended knot. Pass the trailing suture around the
middle arm of the loop twice. Then gently draw
together the trailing strand and the exited strand on
the opposite side of the eye, pulling the two iris leaflets
together and creating the first throw of a knot. Retrieve
the suture loop a second time for a single locking throw
and trim the knot.
Repair of Iridodialysis
Iridodialysis and iris repair share similar principles and
some similar techniques, with a few caveats. Use a
double-armed suture. In a similar closed-chamber
approach, I engage the peripheral iris margin with the
first needle tip and pass the suture through the scleral
wall at the level of the iris root. I pass the second needle
through the same paracentesis and engage the
peripheral iris root about one to two clock hours away.
The second needle is similarly passed out the sclera
and the suture is tightened and tied externally, drawing
the peripheral iris to the scleral wall. The knot is
trimmed and rotated internally.
Iris Implants
When significant amounts of iris tissue are damaged
or missing, iris repair may be impossible. In these eyes,
artificial iris implants can augment the iris diaphragm,
thereby reducing photophobia and glare. A variety
of artificial implant designs are available in Europe and
elsewhere, though currently none are Food and Drug
Administration approved for use in the United States.
The currently manufactured iris implants come in five
categories:
1. Large diameter, rigid iris diaphragms with or
without a central optic (Morcher GMBH, Germany
and Ophtec, The Netherlands).
2. Overlapping, interdigitating iris rings (Morcher).
3. Capsular tension rings with opaque iris segments
(Morcher).
104
Fig. 19.1: Sphincter tear
Fig. 19.2: Iridiodialysis with macerated iris
Fig. 19.3: Iridodialysis with traumatic cataract
Fig. 19.4: Iris and ciliary body prolapse
Fig. 19.5: Iris prolapse
Fig. 19.6: Postcataract surgery withh CTR
105
Iris Trauma
4. Intracapsular Hermeking iris prosthetic system
implants (Ophtec).
5. Custom iris implants with enclavation fixation
(Ophtec).
COMPLICATIONS
Those with traumatic iridodialyses particularly by blunt
trauma are at high risk for angle recession, thereby
causing increased intraocular pressure (IOP). This is
typically seen about 100 days or three months after
the injury, and is thereby called 100 day Glaucoma.
Medical or surgical treatment to control the IOP may
be required if glaucoma is present. Soft opaque contact
lenses may be used to improve cosmesis and reduce
the perception of double vision.
Bibliography
1. Arya SK, Malhotra S, Dhir SP, Sood S. Ocular fireworks
injuries. Clinical features and visual outcome. Indian J
Ophthalmol 2001;49(3):189-90. PMID 15887729.
2. Beetham WP. Cataract Extraction with Iridodialysis.
Trans Am Ophthalmol Soc 1941;39:104-15. PMID
16693243.
3. Behndig A. Results with a modified method for scleral
suturing of intraocular lenses. Acta Ophthalmologica
Scandinavica 2002;80(1),16-18.
4. Brown SM. A technique for repair of iridodialysis in
children. J AAPOS. 1998;2(6):380-2. PMID 10532731.
5. Cassin B, Solomon S. Dictionary of Eye Terminology.
Gainsville, Florida: Triad Publishing Company 1990.
6. Cline D, Hofstetter HW, Griffin JR. Dictionary of Visual
Science. 4th ed. Butterworth-Heinemann, Boston
1997;ISBN0-7506-9895-0.
7. Cornea and External Diseases: Trauma: Traumatic
Iridodialysis. Digital Reference of Ophthalmology.
Accessed 2006.
8. Kiel J, Chen S. Contusion injuries and their ocular
effects. Clin Exp Optom. 2001 Jan;84(1):19-25. PMID
12366340.
9. Ogawa GS. The iris circlage suture for permanent
mydriasis: a running suture technique. Ophthalmic Surg
Lasers 1998;29(12):1001-09.
10. Osher RH. Peripupillary membranectomy. Video J
Cataract Refract Surg. 1991;Volume VII, Issue 4.
11. Osher RH. Surgical repair of the fixed, dilated pupil.
Consultation Section. J Cat Refract Surg 1994;20(6):
665-66.
12. Sul l ivan BR. Gl aucoma, Angl e Recession.
eMedicine.com. August 16, 2006. Accessed October 11,
2006.
13. Viestenz A, Kuchle M. Eye contusions caused by a bottle
cap. A retrospective study based on the Erlangen Ocular
Contusion Register (EOCR) Ophthal mol oge
2002;99(2):105-08. German. PMID 11871070.
14. Walker NJ, Foster A, Apel AJ. Traumatic expulsive
iridodialysis after small-incision sutureless cataract
surgery. J Cataract Refract Surg 2004;30(10):2223-24.
PMID 15474840.
C H A P T E R
20
Post-traumatic Strabismus
B Shukla, P Bhasin (India)
Introduction
After ocular trauma strabismus is not a common
finding. Shukla
1
in a study of 1600 cases found cranial
nerve involvement in 57 cases. Of these there were
12 cases of VII N. Palsy. If these are excluded the
involvement of III, IV, VI N palsy would be in 45 cases
(2.8%) (Figs 20.1 to 20.3). Many studies have shown
the ocular cranial nerve involvement in head injuries.
Thus Rucker
2
found it in 13.9% cases and Rush
3
in
19.7% cases. It is quite possible that there might be
involvement of both as orbits and eye balls cannot
be strictly excluded from head injury.
Prakash
4
and Menon
5
have also reported the invol-
vement of head trauma as a cause of cranial nerve
palsies (III, IV, VI N). They have not mentioned as to
how many cases of cranial nerve palsies were due to
ocular trauma or whether ocular trauma was also a
part of head injury. After head trauma they found the
VI N to be commonly affected.
Distribution of ocular cranial nerve involvement
after ocular trauma was as follows (Table 20.1).
Fig. 20.1: III N palsy with ptosis LE
Fig. 20.2: Immobile on dextro-version with dilated and
fixed pupil
Fig. 20.3: VI nerve palsy after jeep accident
TABLE 20.1: Distribution of ocular cranial nerve
involvement after ocular trauma
Cranial N. Number Percent
IIIrd N 29 64.45
IVth N 05 11.11
VIth N 11 24.44
Total 45 100.00
107
Post-traumatic Strabismus
Thus the III cranial nerve was found to be most
commonly involved. For obvious reasons all cases of
post-traumatic strabismus are of paralytic nature.
In most cases the squint appeared shortly after injury.
However in flew cases it appeared late after develop-
ment of contracture in the muscles. Hence the
management in most cases in conservative up to
6-8 months. Surgery may be planned for residual
squint after this period.
Traumatic squint can result from:
1. Disintegration of extra-ocular muscles.
2. Intramuscular edema or hemorrhage.
3. Entrapment of muscles in bony fractures.
4. Direct injury to the extra-ocular muscles or their
nerve supply.
The management will also differ according to the
pathology involved.
Traumatic Disinsertion
This may be due to intra-orbital penetration of sharp
objects like a knife or after some surgical procedures
like excision of pterygium or limbal dermoid removal.
The muscles may be partially or totally disinserted from
its attachment on the globe. This can be diagnosed
by forced duction test (FDT), ultrasound, EMG or CT
scan. The disinserted muscle should be re-attached to
its original insertion.
Intramuscular Hemorrhage
This is usually caused by a blunt object to the orbit
or to the muscle. The muscle gets swollen due to blood
and is unable to contract or relax properly. The
treatment in conservative by anti-inflammatory and
anti-hemorrhagic drugs. Cold compression may be of
some help and rest to the movement of eye ball should
be given.
Entrapment of Muscle
This is the result of fracture of the orbital walls. It is
commonly seen in blow out fractures where the floor
of the orbit gives way and inferior rectus muscle gets
entrapped at the fracture site. If there is diploma in
the primary and down ward position surgical
intervention is indicated with release of muscle and
repair of floor of orbit by silastic plates.
Direct Trauma
This is usually do to blunt objects causing traumatic
inflammation to the muscles and their nerve supply.
Anti-inflammatory and steroids would be useful in such
cases. These injuries usually recover soon.
During the recovery period it may be useful to
occlude one eye to prevent intractable diploma or
prescribe prismatic glasses to minimize it. Alternate
occlusion should be done to prevent amblyopia. On
the whole prognosis is good in these cases and surgery
is rarely required.
References
1. Shukla B., Epidemiology of Ocular Trauma, Ist Ed., Jaypee
Brothers Medical Publishers, New Delhi 2002;82.
2. Recker C.W., Amer J. Ophthal 1996;61:1293-98.
3. Rush JA, Young B.R., Arch. Ophthal 1981;99:76.
4. Prakash P, Reddy S.K. Ind. J. of Orthopt and Pleoptics
1979;15:1.
5. Menon V., Singh J., Prakash P., Ind. J. Ophthal 1983;32:
447-53.
C H A P T E R
21
Management of Orbital Trauma
and Fractures
Orbital Injuries
Orbital injuries may be part of panfacial trauma that
range from mild even nonsignificant to severe and
debilitating, however, such injuries are of secondary
importance to securing airway, stabilizing the circulation
and protecting the cervical spine. Trauma to the orbit
can involve the globe, eyelid, sinuses and the brain.
The nature and severity of the injury depend on the
mechanism of trauma.
After securing the lifesaving measures, a team
approach incorporating a plastic surgeon, otolaryngo-
logist, a neurosurgeon in addition to the ophthalmolo-
gist is needed for the facial trauma patients evaluation.
A systematic ocular and orbital examination is necessary
to delineate any subtle injuries as delay in the diagnosis
of orbital and ocular problems may worsen the
prognosis.
ANATOMIC CONSIDERATIONS
The orbit is a four-sided conical structure with its base
directed forwards and apex projecting medially towards
the optic foramen. The base or the orbital rim is
outlined by thick strong bone: the supraorbital arch
of the frontal bone above, the zygoma and maxilla
inferiorly, the zygoma laterally and the frontal process
of the maxilla medially. The walls of the orbit consist
of relatively thin bone. The orbital volume is about
30 ml and the orbital depth is approximately 4.5 cm.
Consequently, slight change in the bony anatomy will
be reflected on soft tissue and globe position.
The medial wall is formed of the frontal process
of the maxilla and the lacrimal bone forming the
lacrimal fossa behind which is the extremely thin, less
than 0.5 mm, lamina paparycea of the ethmoids and
finally the lesser wing of the sphenoid and the optic
foramen (Fig. 21.1). Being exceptionally thin and
fragile, medial wall fractures are usually subtle and
accompany many orbital injuries. The medial wall
transmits the anterior and posterior ethmoidal arteries
and nerves at the junction between the ethmoidal bone
and the orbital plate of the frontal bone. Trauma to
this wall is frequently associated with orbital hemor-
rhage, epistaxis and surgical emphysema.
Fig. 21.1: Bones forming the medial wall
The roof is composed mainly of the orbital plate
of the frontal bone and posteriorly the lesser wing of
sphenoid separating the orbit from the frontal lobes
of the brain. It is thinnest anteriorly where it is related
to the frontal sinus.
The orbital floor is composed of the orbital plates
of the maxilla and zygomatic bones with a small
contribution from the palatine bone posteriorly. The
posterior limit of the floor is defined by the inferior
orbital fissure and a small vertical component of the
palatine bone posteromedially. Near the apex the
inferior orbital fissure transmits venous channels as well
as the infraorbital and zygomatic nerves. Contained
entirely in the maxilla, the infraorbital groove posteriorly
becomes the infraorbital canal as it gains a roof
(Fig. 21.2). It opens 4 mm below the orbital rim as
the infraorbital foramen that transmits the infraorbital
nerve and vessels. The floor is also thin, 0.5 to 1.0 mm
109
Management of Orbital Trauma and Fractures
thus it easily fractures especially medial to the
infraorbital canal.
The lateral wall is thick formed of the frontal process
of the zygomatic bone and the frontal bone anteriorly
and the greater wing of sphenoid posteriorly. It
transmits the zygomatic nerve and artery which often
splits into the zygomaticotemporal and zygomaticofacial
branches before entering the bone.
EVALUATION OF ACUTE ORBITAL AND
PERIORBITAL INJURIES
Initial evaluation starts with complete history to
determine the circumstances of the present injuries.
Low velocity impact such as a human punch usually
produces injury limited to the region of impact. High
velocity injury such as motor vehicle accidents is often
associated with soft tissues and skeletal injuries that
are more extensive and may be remote from the
impact. With projectile injuries such as with shattered
glass or missiles, intraocular, subcutaneous and orbital
foreign bodies should be ruled out.
It is better to remove blood and debris as well as
any superficial foreign bodies to do a careful and precise
examination of the injured area as well as the sur-
rounding areas. Blunt low velocity trauma usually cause
edema and contusions and the extent of the facial
fractures is often more than in cases associated with
extensive lacerations as the energy of the impacting
force in the former is dissipated by the skeleton rather
than soft tissue. Palpation of the orbital rims, malar
eminences, zygomatic arches and nose may show
fractures and surgical emphysema.
A complete ophthalmic examination is a must to
rule out globe injuries and present medicolegal
problems. If the patient is conscious, the visual acuity
and field by confrontation should be documented.
Pupil diameter and responses to light as well as swinging
flash light test should be also documented. Presence
of afferent papillary defect denotes optic nerve injury,
however if both optic nerves are equally damaged,
this sign may be absent. The lid, adnexa, conjunctiva,
cornea, anterior chamber, iris and lens should be
examined with magnification either by slit lamp or a
magnifying loupe for lacerations, tissue loss, hemor-
rhage, opened globe injuries, presence of foreign
bodies or lens displacement. When ocular rupture is
suspected, globe exploration should take place before
any fracture repair.
The retina and optic nerve should be examined
on both sides using the ophthalmoscope looking for
retinal edema or hemorrhages as well as optic nerve
pallor or edema. The caliber of the retinal vessels
comparing arteries to veins is also evaluated. Engorged
non-pulsatile veins may signify increased orbital
pressure, similarly central retinal artery pulsations
denotes increased ocular or orbital pressure. B scan
ultrasound can be performed if media opacity
precludes the visualization of the retina.
The position of the globe on the affected side in
comparison to contralateral one should be noted and
measured, if possible, by the exophalmometer. The
eye positions should be evaluated from the vertex
prospective; however, significant lid edema may cause
bias. Vertical globe displacement can be estimated by
putting a ruler across the medial canthi and noting
the point at which it crosses the globe at each side.
A depressed orbital floor fracture leads to globe ptosis.
Enophthalmos occurs with increased orbital volume
such as in wall fractures. While proptosis occurs due
to increased soft tissue contents such as hemorrhage
and/or reduction of orbital volume associated with
inward displacement of one or more of its walls. If
the condition is associated with reduced vision or
afferent papillary defect, computed tomography (CT)
examination is immediately done and intervention
should not be delayed. Presence of pulsatile proptosis
suggests abnormal vascular communications or
transmission of dural pulsations through a fractured
displaced orbital roof.
In a conscious cooperative patient with minimal lid
edema eye movements all directions of gaze should
be examined. The patient is asked to report any
diplopia at any direction of gaze. Gaze restriction can
be caused by nerve injury, soft tissue swelling, direct
muscle injury or entrapped muscle within a skeletal
fracture. Forced duction and diplopia fields are
performed when indicated.
Hyposthesia in areas around the orbit should be
looked for especially in the cheek which is supplied
by the commonly injured infraorbital nerve. Upper
Fig. 21.2: Orbital floor
110
lid position should be noted and documented as ptosis
may occur as a result of nerve injury, levator aponeu-
rosis laceration or dehiscence or later from fibrosis.
Soft tissue landmarks of the orbit such as canthal
angles may be displaced by fractures of the underlying
bone. For example, increased intercanthal distance
suggests nasoethmoidal fractures involving the
reflected part of the medial canthal tendon while
inferiorly placed lateral canthus suggests inferior
dislocation of the zygoma. If the medial wall is involved,
the lacrimal drainage system should be evaluated.
Radiological Evaluation
Radiological studies especially computed tomography
(CT) play an indispensable role in evaluating the orbital
trauma and detecting radio-opaque foreign bodies.
Both axial and coronal CT sequences are required.
Coronal images in 2 mm sections delineate the
orbital floor, roof, medial and lateral walls, the naso-
ethmoid region, the orbital rim and the face
surrounding the orbit. It helps delineate the size, shape
and location of fractures and associated soft tissue
injuries.
Axial scans permit evaluation of the lacrimal
drainage pathways, nasal and paranasal sinuses, medial
and lateral walls of the orbit, superior and inferior
orbital rims, zygomatic arch, pterygoid plates,
tempromandibular joint, base of the skull, superior
orbital fissures and optic canal. It allows to show globe
placement in comparison to the unaffected side.
The combination of axial and coronal scans can
give most of the needed information in trauma cases.
Three dimensional scans are helpful in obtaining a more
accurate evaluation and understanding of the situation,
hence help in deciding the best line for treatment. They
are generated from the reformatting 1.5 mm slices on
conventional CT scan using a special software computer
program. They are very helpful in old trauma cases
as they show the deformity, the site, size and
appearance of bony defects as well as bone fractures.
Problems associated with orbital trauma:
Orbital hemorrhages and emphysema
Traumatic optic neuropathy
Orbital fractures
Septic cavernous sinus thrombosis
Carotid cavernous fistula
Orbital foreign bodies
PROBLEMS ASSOCIATED WITH
ORBITAL TRAUMA
Orbital Hemorrhages
Bleeding is frequently associated with periorbital trauma
and fractures. Blood may be found in the eyelid
anterior to the orbital septum due to direct tissue injury.
These tissues afford extensive hemorrhage that may
extend to the lid margin and even cross the nasal bridge
to the uninvolved eyelid.
Mild to moderate orbital hemorrhage commonly
accompany orbital trauma. Both conditions can cause
variable degrees of proptosis, globe displacement and
motility disturbance. If severe, they may cause
increased intraocular pressure, central retinal artery
occlusion, marked proptosis with corneal exposure as
well as compressive optic neuropathy leading to vision
loss.
Blood may also accumulate in the subperiosteal
space. The extent of the blood is limited by bone suture
lines where periorbita becomes firmly adherent. If the
periotrbita is intact, the patient may present with mild
proptosis and globe displacement. If the periorbita is
disrupted the hemorrhage becomes extensive and
moves towards the orbital septum and bulbar
conjunctiva.
If there is mild proptosis with normal or minimally
elevated intraocular pressure with no visual compro-
mise, follow up can be safe and the hemorrhage will
gradually resolve over 1 to 3 weeks usually without
sequalae.
In sudden and extreme orbital hemorrhage threa-
tening vision, lateral canthotomy and cantholysis of
the superior or inferior crura should be performed.
If this is not effective, the hematoma should be drained
either through lid crease incision if placed superiorly
or though lower lid blepharoplasty incision if inferiorly
placed. In either condition, the orbital septum must
be opened to allow the egress of the blood from the
socket. The stab incisions and canthal tissue could be
repaired when swelling decreases.
Surgical Emphysema
This means accumulation of air in the subcutaneous
tissue (Fig. 21.3). This is a common finding in medial
wall and floor fractures as they involve walls of the
paranasal sinuses. The condition usually increases when
the patient blows his nose and there is a crepitus felt
on palpation. Reassurance of the patient and
instruction not to forcibly blow his nose are usually
enough till the symptoms are relieved provided there
are no associated orbital or ocular problems detected.
Traumatic Optic Neuropathy
Optic neuropathy may accompany orbital and head
injuries.This is diagnosed by presence of decreased
vision, afferent papillary defect with otherwise normal
eye in a patient with trauma history. The cause of this
problem is multifactorial including direct or indirect
mechanisms.
111
Direct optic neuropathy results from compression along
the course of the optic nerve by bone fragments
(Fig. 21.4), retrobulbar or subperiosteal hematoma,
and foreign body or by fractures that narrow the optic
canal. Rarely, the optic nerve may be avulsed. When
clinically suspected, CT evaluation of the orbit, optic
canal and sinuses can identify the cause.
Indirect optic neuropathy is diagnosed when there
are no radiologic findings of abnormalities damaging
the nerve. It may be caused by abrupt brain
deceleration with forwards movement causing
compression of the intracranial optic nerve. It can also
be due to contusion and edema resulting from
deformation of the optic canal. The small arterioles
in the intracanalicular optic nerve my rupture leading
to infarction or hematoma of the optic nerve or sheath.
Edema and vasospasm are thought to cause nerve
ischemia.
Patients may suffer from sudden complete loss of
vision after trauma which is usually caused by actual
tear or primary complete optic nerve necrosis. These
patients have poor prognosis in spite of treatment.
Other patients experience delayed visual loss (hours
to days) or partial visual loss usually due to partial
ischemic infarction or compression by edema or
hemorrhage however, these patients have better
prognosis.
Treatment remains controversial. High-dose
corticosteroids are used in treating indirect optic
neuropathy. Extracranial transethmoidal optic canal
decompression is an alternative treatment especially
if the vision drops while on steroid treatment. Direct
optic neuropathies attributable to mechanical nerve
compression usually require surgical treatment and
removal of the offending factor such as repair of floor
fracture, intracranial optic canal decompression, hema-
toma drainage and optic nerve sheath fenestration.
CAROTID CAVERNOUS FISTULA
It results from shearing of intracavernous carotid artery
during deceleration injuries, or direct artery injury by
foreign body or bone shrapnel. They develop shortly
after trauma but the onset of symptoms may be
delayed. They present with progressive proptosis usually
pulsatile with subjective and objective bruit. IOP is
usually elevated with engorged retinal veins. Brain CT
scans with contrast confirm the diagnosis. The fistula
can be closed using endovascular occlusion with coils
which is the preferred technique.
Septic Cavernous Sinus Thrombosis
Fracture of the posterior ethmoidal or sphenoidal
sinuses may allow concomitants with the paranasal
sinuses to reach the cavernous sinuses. They usually
have a rapid presentation and associated with low
grade fever, headache, orbital pain or diplopia. This
is followed by progressive proptosis, mydriasis,
ophthalmolplegia due to nerve palsy and eventually
visual loss due to compressive optic neuropathy. If not
treated, septic thrombosis may spread to the cerebral
veins leading to increased intracranial tension.
Fig. 21.3: Fracture in the medial wall associated with surgical
emphysema and air could be seen within the orbital cavity
Fig. 21.4: A case of a 7-year-old child with trauma to the
sinuses and fracture of the ethmoid and sphenoidal bones.
There is a bony fragment that is pressing the optic nerve
112
MRI may show a mass caused by thrombus in the
sinus compressing the intracavernous part of the
internal carotid. Cerebral arteiography and venography
may be used however MRA presents a good
alternative. Early diagnosis is of extreme importance
as it improves the prognosis. Systemic antibiotics are
the main line of treatment. Anticoagulant treatment
is used to prevent progressive thrombosis if not
controlled by antibiotics within 48-72 hours; however,
they should not be used if a fungal etiology is suspected
due to increased risk of mycotic aneurysm formation.
Orbital Foreign Bodies
A high index of suspicion may lead to discovery of
intraorbital foreign bodies. The patient usually reports
a history of trauma to the face with a foreign body
entering the eye or the orbit. In case of loss of
consciousness, or psychiatric illness, the patient may
fail to give a helpful history. Foreign bodies may be
found without any antecedent history of trauma where
the initial injury is thought to be insignificant and usually
forgotten. Such patients may remain asymptomatic
for long periods of time until the foreign body provokes
a reaction, forms an abscess or begins to extrude.
Some foreign bodies may inflict immediate,
sometimes irreversible, damage to the globe, extra-
ocular muscles, orbital bone, optic nerve as well as
cranial nerves. Infection and inflammation can result
secondary to contaminated foreign body entering the
globe or penetrating an adjacent sinus. The latter can
present with associated surgical subcutaneous
emphysema. The long term effects of the foreign body
can be due to chronic inflammation, migration and
scar tissue formation. Chronic inflammation causes
foreign body granuloma that can be of significant size
causing mechanical effects with globe displacement and
limitation of its motility. The latter can also result form
extraocular muscle fibrosis or soft tissue scarring.
A fistula to the skin or conjunctiva may be formed with
pus drainage or extrusion of the foreign body.
The anatomic structure of the orbit allows large
pieces of metal or organic material to be imbedded
without significant signs or symptoms unless one of
the orbital contents is involved. The location of the
foreign body within the orbit influences the presenting
picture as well as the management decision. Large
objects usually tend to enter the inner canthus injuring
the caruncle or the lacrimal drainage system and may
become deeply buried within the orbit and in some
cases tend to displace the globe.
The nature of the foreign body contributes to the
severity of the response and considerably affects the
decision of foreign body removal. Most metals are inert
and in the absence of infection, they cause no
disturbance to the eye and orbit. Copper is poorly
tolerated and can induce purulent inflammation. Glass,
stone, plastic, and bullets are often well-tolerated and
need no intervention unless they migrate to the surface
and become extruded or palpable so that they can
be easily removed. Organic foreign bodies are poorly
tolerated and are usually associated with chronic
inflammatory reaction and abscess formation.
CT is necessary to detect and localize the foreign
body (Fig. 21.5). It can estimate its size and the extent
of damage to the surrounding structures. The
combination of axial and coronal scans can give three
dimensional localization of the foreign body. CT
resolution of metal foreign bodies is approximately
0.05 mm; of wood, 2.0 mm and of glass 0.75 to
2.0 mm according to the lead content. One millimeter
sections in the scan are recommended to detect orbital
foreign bodies. Absence of foreign body in the scan
does not totally exclude its presence especially with
the suggestive history and presence of symptoms.
Although MRI has no established role in foreign
body detection, it should be remembered to avoid
its use in cases of suspected metallic foreign bodies
as they may be drawn out of their location with injury
to the globe or adjacent orbital structures.
Most of inert foreign bodies do not require inter-
vention, and the surgical removal decision should be
consider the risk benefit. If the foreign body is to be
removed, the surgical approach is planned according
to the site of the foreign body. The entrance wound
should be explored in a manner that wont cause
damage to orbital tissue. In case that such wound is
not present or healed, anterior, medial or lateral
orbitotomy can be used. If the foreign body is located
Fig. 21.5: Axial CT scan showing an intra-orbital
metallic foreign body near the lateral orbital margin
113
at the orbital apex, a neurosurgical anterior craniotomy
approach is required. If the foreign body is thought
to be metallic, a surgical magnet can be used. Metal
foreign body localizers can be used intraoperatively
to confirm the radiographic information about the
location of the foreign body.
Organic foreign bodies foreign bodies must be
removed with great care as they usually fragment. This
is followed by irrigation to remove the pus and small
fragments. Pus is sent for culture and sensitivity for
bacteria and fungi and appropriate treatment is given.
Complications associated with such procedure may
be due to the surgery or the foreign body itself. The
surgeon may fail to localize the foreign body, the
foreign body may become fragmented or it may cause
adjacent tissue damage, e.g. blood vessels, nerves and
muscles leading to hemorrhage, diplopia or loss of
vision.
Orbital Fracture
Orbital fractures can be generally divided to blow out
fractures and fractures that involve the orbital rim.
ORBITAL FLOOR AND BLOW OUT FRACTURES
Blow out fractures are the most common periorbital
fracture seen in ophthalmic plastic surgical practice.
A blow out fracture by definition does not involve the
inferior orbital rim. On the contrary, a floor fracture
should involve the orbital rim. However, the findings
and treatments are similar.
PATHOGENESIS
Two theories exist to explain the origin of orbital floor
blow out fractures. The hydraulic theory by Smith and
Regan postulated that when a blunt object (usually
spherical and larger than the orbital base) hits the orbit,
the globe and soft tissues are retropulsed suddenly
increasing the intraorbital pressure. To relieve this
pressure, the orbital floor blows out into the maxillary
sinus usually medial to the infraorbital canal where
the bone is thinnest (Figs 21.6A and B). Sometime
the medial wall gives way due to its fragility. This is
considered a safety mechanism for the globe.
Fujino proposed a buckling force theory. When a
blow strikes the inferior orbital rim, the rim is displaced
posteriorly and the force is transmitted to the thin
orbital floor that buckles and fractures into the maxillary
sinus, then the inferior rim returns back to its normal
position intact. In general, variable degrees of both
mechanisms are supposed to be present in a given
patient with a blow out fracture.
The fracture may be linear just parallel and medial
to the inferior orbital groove, trap door that transiently
Figs 21.6A and B: A. Shows a blunt trauma to the anterior
orbit. B. Shows that the contents are compressed with
increases intraorbital pressure so that the floor gives way
separate at the groove, close spontaneously entrapping
muscles and soft tissue and they are very common
in children, hinged fracture along the inferior border
of the ethmoid entering the maxil l ary sinus,
comminuted or combination of all of the above. Non-
displaced and trap door type are more associated with
diplopia while enophthalmos is more associated with
hinged and comminuted types.
Clinical Presentation
Diagnosis of such fracture depends on suggestible
history, periorbital ecchymosis and emphysema.
Palpation of the inferior orbital rim may reveal a step
off deformity, discontinuity or point tenderness. If the
infraorbital canal is involved in the fracture, anesthesia
may involve the ipsilateral cheek, upper lip, gums and
nose.
Enophthalmos can be due to orbital expansion due
to inferior displacement of the orbital floor. This could
be accentuated by soft tissue herniation into the
maxillary sinus mainly the periorbita, fat and
connective tissue, damage to the Lockwood suspensory
ligament as well as collapse of the fine fibrous septa
that support the orbital fat and muscles. Globe ptosis
114
is uncommon even with large floor fractures however,
it can results from significant diminution of Lockwoods
l igament support. Immediatel y after injury,
enophthalmos can be masked by orbital hemorrhage
and edema posterior and inferior to the globe. If
enophthalmos is severe, a prominent superior sulcus
deformity can be present.
Diplopia is a frequent finding in blow out fractures.
This was attributed to inferior rectus or inferior oblique
muscle entrapment in the fracture. Yet it was found
that actual muscle entrapment is rare. Orbital fat
entrapment is commoner and the fibrous septa that
connect the fat and the periostium with the inferior
rectus and oblique muscles tighten due to edema or
intraorbital hemorrhage thus restricting ocular motility
and felt as restriction on forced duction test. With time,
these septa may stretch and relax improving the ocular
motility and diplopia.
The patient usually suffers from vertical diplopia.
The patient may have limited supraduction, infraduc-
tion or both. If the inferior rectus restriction is anterior
to the equator, hypotropia results while if it is posterior
to it, hypertropia results.
Injuries to the extraocular muscle or the motor
nerves are additional causes for diplopia. Direct contu-
sion or laceration of the muscle can be worsened by
muscle hematoma. While the motor nerves can be
damaged by hemorrhage within their sheath, stretched
by orbital edema or hemorrhage or suffer from
concussion.
Radiologic studies are helpful in establishing the
diagnosis. Waters plain X-ray views provide an excellent
view of the orbital floor, showing any bone disruption
or herniation. Orbit CT especially the coronal cuts
delineates the fracture and the bone soft tissue
relationship (Figs 21.7 and 21.8). However, the
mere radiologic presence of a fracture is not an
indication for surgical repair.
Management
Repair of the orbital floor fractures is mainly indicated
in restricted ocular motility showing no improvement,
diplopia especially within the central 30 field, enoph-
thalmos of 3 mm or progressive, defects of more
than 50% of the orbital floor that are almost always
likely to cause enophthalmos as well as incarcerated
muscle causing oculocardiac reflex on ocular motility
and rare cases of globe ptosis.
Timing
No universally agreed guidelines exist for the repair
of blow out fracture. If in doubt, the patient should
be evaluated every 2-3 days during the first 2 weeks,
diplopia fields and forced ductions are followed carefully
Figs 21.7A and B: A. Shows coronal CT scan with fracture
floor and the tear drop appearance. There is a fluid level
in the maxilla. B. Shows a fractured mid floor with tissue
herniation
Fig. 21.8: A combined floor and medial wall fracture
115
for any change. During this time, hemorrhage and
edema will resolve during the first week allowing more
accurate assessment. As long as motility improves, the
patient should be followed up. On the other hand,
if surgery is to be done, the best time is not beyond
2 weeks. After this, adhesions between bone fragments,
sinus mucosa and the orbital tissues render the repair
quite difficult.
Procedure
Surgical repair of blow out fractures comprises good
exposure through incision, periosteal dissection and
exposure of the fracture, release of the entrapped
tissues as placement of an implant to prevent adhesions
between the orbital tissues and nasal mucosa. The
surgeon can proceed from an orbital (subciliary or
fornix) approach or an antral (Caldwell- Luc)
approach. The orbital approach is preferred as it is
safer and more effective. In selected cases with large
floor defects or with tenaciously herniated orbital
contents, a combined orbital and antral approach can
be used.
Implants
Many materials are available for repair of orbital wall
fractures. They include:
A. Autogenous bone
Cancellous bone grafts cannot be used due to high
absorption rate, 60-80% of the volume may be lost.
Split thickness calvarial or membranous bones such
as ribs, iliac crest or the cranium have less absorption
rate; 15-30%. This material needs a second surgical
site with incidence of morbidity such as hematoma,
infection. Harvesting them needs proper and formal
training. The graft is usually placed with the cortical
side towards the recipient bone and it may need to
be secured by micro or miniplates.
B. Alloplastic material
a. Porous polyethylene: It is porous integrated
biocompatible implant with average pore size
200-240 microns. It is easy to mold manually
or the help of heat yet it is structurally stable.
b. Silicone: A non porous material that is easy to
fashion, inert, safe and effective with low rate
of migration, infection and extrusion. It is pre-
ferred in cases of orbital volume augmentation.
c. Methyl methacrylate polymer (cranioplastic): It
is mixed with copolymer to form a mixture that
have a doughy consistency and can be placed
to augment orbital volume. This material
remains malleable for 3-5 minutes so that it can
be shaped. If it hardens before molding is com-
plete, a pneumatic drill is used to fashion it.
It is better to be avoided in patients with chronic
sinusitis due to the reported incidence of
systemic toxicity and late infection.
d. Microplates: They are used of there is no
enough bone to support the implant. They are
made of titanium alloy. There are less corrosive
than steel and produce less scatter on CT
studies. They are not magnetic and can be safely
imaged by MRI. They are used to reform the
orbital rim, medial and lateral canthal angles
as well as walls. The alloplastic implants are
placed over them to augment the orbital
volume.
e. Porous polyethylene implants with embedded
titanium provide a new alternative to alloplastic
implant materials for orbital reconstruction with
a profile that combines several advantages of
porous polyethylene and titanium implants.
f. Others like Supramid and Teflon
g. Experimental work was done on bone
morphogenetic protein (BMP) implant with and
without platelet-rich plasma (PRP), which is
supposed to promote fracture consolidation in
the orbit fracture treatment with scarce
inflammatory reaction, and may be a good
alternative in orbit fracture reconstruction.
Radiological studies suggested intramem-
branous and progressive cavitation and
ossification without a reduction in implant size
and with signs of calcium deposition; these
events were confirmed by histological analysis.
Surgical Procedures
All are done under general anesthesia and forced
duction test is performed initially to confirm the degree
of tissue entrapment.
Incision: Variable incisions can be used to expose the
inferior orbital rim as well as inferior part of the medial
wall.
a. Subciliary approach: It is similar to that used in
lower lid transcutaneous blepharoplasty. The lid is
infiltrated with 1% lidocaine with 1:100:000
epinephrine and a horizontal incision 2 mm below
the lid margin is made. It should not extend too
far laterally to avoid compromise of lymphatic
drainage. A skin muscle flap is created and retracted
inferiorly using Desmarres retractor. This approach
is more associated with postoperative lower lid
malpositions namely ectropion.
b. Lower transconjunctival approach: The inferior
fornix is incised 4 mm below the lower edge of
the tarsus. Lateral canthotomy and inferior
cantholysis can be done to widen the exposed field.
The conjunctiva, Ml l ers muscl e and the
116
capsulopaplepbral fascia are severed and the plane
between the orbicularis and the capsulopaplpebral
head is reached. Tissues are dissected till the inferior
orbital rim is reached. A 4-0 silk tractional suture
is passed through conjunctiva and lower lid
retractors. This approach is preferred as it is simple,
provides excellent exposure with no visible scar and
it has minimal risk for postoperative lid malpositions.
However, there is a rare risk of entropion due to
scarred posterior lamina.
c. Antral (Caldwell-Luc) approach: An incision is made
in the gingival margin of the canine fossa. Periostium
is elevated and separated from the anterior surface
of the exposed maxilla. A periosteal elevator is used
to create an osteotomy opening into the maxillary
sinus. Bone fragments and blood are then
evacuated from the sinus. In conjunction with orbital
approach, the herniated tissues are gently reposited
superior to the orbital floor. The maxillary sinus
may then be packed with either petroleum gauze
imbricated with antibiotic or a catheter balloon.
The other end of the gauze or catheter is brought
out through an antrostomy to facilitate its removal.
This approach has limited visualization, poor access
for placement and securing the floor implant, poor
hemostasis, higher infection rate, lack of permanent
globe support and hazards of forcing bony fragments
into the globe and optic nerve. That is why this
approach is seldom used for fracture floor repair unless
there is complete absence of orbital floor.
Exposure of the orbital floor
Dissection is carried out till the inferior orbital rim using
blunt and sharp dissection keeping the orbital septum
intact to avoid fat herniation. Then the periostium is
opened 1.5 mm below the orbital rim and elevated
from the orbital floor. With the help of periosteal
elevator, the periostium is separated from the floor
posteriorly; the fracture is localized and exposed, first
the lateral border then the medial and posterior limits.
The infraorbital bundle should be identified. Any
unattached bone fragments should be removed.
Incarcerated tissues are freed from the fracture using
hand on hand maneuver with the periosteal elevator
and the metal suction tip or malleable retractors. This
is easy in cases of recent fractures yet if the tissues are
swollen, the extraction becomes difficult and the bone
can be depressed into the maxillary antrum. In case
of hinged fractures or in some selected cases, the
fracture may be enlarged to achieve atraumatic release.
Care should be taken to avoid undue bleeding and
trauma to the nearby optic nerve.
Optic nerve should be checked every now and then
by detecting the pupillary light reaction or dilating the
pupil and noting the optic nerve perfusion by the
ophthalmoscope.
Forced duction should be repeated to ensure that
no more incarcerated tissues are present. Any bone
fragments or blood should be aspirated from the
maxillary antrum before the defect is covered.
A sterile alloplastic material is fashioned to cover
the defect completely and overlapping the surrounding
intact bone by 3-4 mm circumferentially. This sheet
should not be too large or too thick. The edges are
smoothened to avoid trauma to adjacent structures
or erosion through the covering periostium. The
alloplastic material should be soaked in antibiotic
before it is inserted. The thickness of the plate usually
range from 0.4-0.6 mm. Thicker implants are indicated
in cases of significant enophthal mos and
hypophthalmos yet they have the risk of limiting
extraocular muscles. The more posterior the implant
is placed, the more it reduces enophthalmos. The more
anterior it is, the more it reduced hypophthalmos. The
choice of the material depend on the nature of the
fracture as well as the surgeon preference and training,
When the defect is large or multiple walls are
involved, plates and screws are preferred; bone grafts
may be a good choice in experienced hands. Titanium
mesh may be used if the residual bone is not enough
to support an implant. It is not enough by itself and
it usually needs to be covered by bone or alloplastic
material.
The implant can be fixated by either placing it
behind the orbital rim and the mere periosteal closure
will keep it in place or two small fixation holes are
drilled in the infraorbital rim just anterior to the defect
as well as the anterior edge of the implant. Then the
implant is secured to the orbital floor anteriorly by
Supramid 2-0 sutures.
Forced duction test is repeated. Coexistent medial
wall fracture can be repaired at the same time.
Hemostasis is secured and the periostium is closed over
the implant. Lateral canthus is repaired in case of
cantholysis and canthotomy. The opened layers are
then closed anatomically.
Eye patch is better avoided and the patient should
be watched for bleeding, pupillary reaction and visual
acuity postoperatively. Systemic antibiotics, anti-
inflammatory drugs as well as cold foments are proven
useful.
Complications
Diplopia may persist or worsen after the surgery. This
can occur due to fibrosis of the muscle, orbital fat or
connective tissue septa either present prior to surgery
or secondary to inflammation induced by the surgery.
117
It can be due to unidentified nerve injury before
surgery. Diplopia may worsen due to improperly placed
implant or residual tissue entrapment. A muscle
procedure is better deferred 6-12 months after surgery
during which the diplopia may improve or the patient
can wear prisms. If a surgery is to be done it is better
to be with adjustable sutures.
Overcorrection may occur due to thick implant
augmented by postoperative edema that usually
resolves after a month. On the other hand, residual
enophthalmos may be present due to inadequate
restoration of orbital volume, bone graft absorption,
migrating implant or orbital fat atrophy. It can be mild
requiring no further intervention. In some cases,
minimal ipsilateral upper lid elevation using Fasenella
Servat procedure or contralateral upper lid blepharo-
plasty to deepen the superior sulcus can be enough
to camouflage the appearance. In more extensive
cases, the implant may be exchanged for a thicker
one.
The orbital implant may become infected. It may
be oversized and extruding. In both conditions the
implant should be removed and replaced with a proper
sized one. If fibrous tissue sufficient to cover the defect
has formed since the original surgery, the implant may
not require any replacement. Chronic lid swelling with
superior globe displacement may indicate the presence
of a fluid filled cyst formed around the implant. The
implant should be removed and the cyst excised.
Ectropion, lower lid retraction or chronic edema
may result when the skin approach is used. Retraction
can occur due to adhesions between the orbital septum
and the inferior orbital rim. This can be corrected by
recessing the lower lid retractors.
Persistent infraorbital nerve anesthesia may occur.
It may be injured or just compressed by the implant.
If the nerve is not cut, function usually returns within
1 year. Sometimes the implant can be exchanged with
widening the foramen decompressing the nerve.
In some cases, the patient may get tolerant to the
numbness in this area.
Blindness may occur in 1 : 1500 cases. It can be
secondary to compression of the optic nerve by the
implant, orbital edema or hemorrhage. This can be
prevented by avoiding undue pressure on the globe
during surgery, continuous optic nerve monitoring,
screening patients for cl otting abnormal ities
preoperatively, using intra and postoperative steroids,
complete hemostasis before wound closure, avoiding
compressive ocular dressing postoperatively and
continuous monitoring of the pupil and visual acuity.
It should be remembered that the optic nerve may
be damaged from the original injury with delayed visual
loss from edema and vascular occlusion and may
appear coincidently with surgery and mistakenly
blamed on the surgical procedure.
NASO-ORBITAL AND MEDIAL ORBITAL WALL
FRACTURES
These fractures result from a force delivered to the
nasal bridge or medial orbital rim. These are the
weakest in the midface bones and usually injured by
the dashboard in cases of automobile accidents. They
are commonly associated with fracture floor and
contribute to the presenting enophthalmos.
In mild cases, the injury is limited to the nasal bone
and the frontal process of the maxilla. In more severe
cases, the lacrimal and ethmoid bones (Fig. 21.9)
may crack and splay laterally causing traumatic
telecanthus, flattening and widening of the midface,
rounding of the medial canthus, epistaxis, periorbital
ecchymosis, subcutaneous emphysema (if the ethmoid
is fractured), with bony nasolacrimal duct injury
causing epiphora. The medial rectus is rarely entrapped
in the fracture with less common horizontal gaze
limitation.
CSF rhinorrhea suggests a cribriform plate fracture.
Most of cases are managed conservatively. The patient
is treated by bed rest, intravenous antibiotics and
instructed not to blow the nose or smoke. If the condi-
tion persists, neurosurgical interference is required.
Hemorrhage may be severe if the anterior and or
posterior ethmoidal arteries are injured. The bleeding
usually stops promptly. However, nasal packing or
direct ligation may be required. Any coexistent upper
airway obstruction should be relieved.
If the fracture extends to the lacrimal bone and
ethmoid, traumatic telecanthus may result (Figs
21.10A and B). This usually requires repositioning
of the bony fragments and transnasal wiring combined
with canthal Y-V plasty. If there is enough bone support
Y miniplate is inserted and used for the telecanthus
repair.
Fig. 21.9: Medial wall fracture
118
If dacryostenosis is present, dacryocystorhinostomy
may be required. Nasal bone fractures should be
repaired by otolaryngeologist or plastic surgery. If
associated with fracture floor, the floor should be
repaired first with the implant the usually forms a
platform for the medial wall implant
Transnasal Wiring: Surgical Technique
A. If the contralateral nasal bone is intact:
Under general anethesia, a vertical incision is made
nasal to the medial canthus. This may take a V-Y or
C-U configuration if skin muscle advancement is also
required in the reconstruction. The incision is carried
to the fracture site adjacent to medial canthal tendon
avoiding the lacrimal drainage system. The splayed
bone at the posterior lacrimal crest is thinned using
cutting burr. Either a 2-0 supramid suture or 27 gauge
stainless steel wire is used to engage the superficial head
of the tendon. If insufficient tendon remains, the
supramid or wire may be positioned in the medial
portion of the upper and lower tarsi.
On the intact side, a 15 mm vertical incision is made
into the skin and subcutaneous tissues just anterior to
the insertion of the superficial head of the medial
canthal tendon. The periostium is opened vertically
at the anterior lacrimal crest and reflected anteriorly.
A 5 mm opening is made by a drill through the bone
and nasal mucosa anterior to the attachment.
A Wright needle or 16 gauge trocar is passed from
the surgically drilled opening (normal side) through
the nasal septum, emerging at the fracture site. Some
pressure is needed to penetrate the septum. Care
should be taken to prevent momentum from carrying
the needle immediately through the fracture site with
the possibility of globe injury which lie in close proximity
to the medial wall. Malleable retractors are placed to
protect the globe.
The supramid or wire suture are placed within the
eyelet of the Wright needle or within the trocar after
removing the stylet and this material becomes properly
positioned as the needle/torcar is withdrawn. The two
ends are tightened around 8 mm metal bloster pin
on the sound side and the traumatized canthus is
quantitatively drawn medially as the Supramid or wire
is secured.
The deeper layers are closed with 5-0 Vicryl mattress
suture, followed by skin closure with running 7-0 silk
suture.If nasal pads are to be placed, this should be
done before the trocar is removed. A second loop of
wire is passed through the trocar after the transnasal
wiring is completed but before the skin closure, the
loop is cut leaving two free skin wires. The end of each
is passed through one of two silicone pads. The wires
from each side are twisted together over a dental roll
to compress the skin in the canthal region. The nose
pads and the skin sutures are left in place for 7-10
days, then the skin wires and pads are removed.
B. Bilateral naso-orbital fractures:
If bilateral naso-orbital fractures, the bone may be
insufficient on either side to support the reconstruction.
In this condition, standard transnasal wiring technique
takes place where two medial canthal incisions are
made; bone penetration should be done at the
posterior lacrimal crest level leaving intact bone anterior
to this site to avoid forwards migration of the wire.
The trocar is passed and two looped 32 gauge
stainless steel wires are passed; one loop with the ends
of the other are tagged with the hemostat and they
will become the skin wires, the other fixates the canthal
tendons bilaterally. The medial canthal tendon is
secured to the loop by 4-0 non-absorbable suture.
The two ends of the wire are twisted on themselves
forming a second loop that is also secured to the medial
canthal tendon on this side. The looped wire is
tightened pulling the medial canthal angles towards
the nasal septum. The skin wires are tied over nose
pads to restore the concavity of tissues at the medial
canthal area and removed in a similar time to the
above.
C. Lateral wall fractures:
The orbital plate of the zygoma is less able to absorb
the trauma impact. It often fractures with orbital fat
Figs 21.10A and B: Cases of traumatic telecanthus. There
is flattening of the nose, scar at the site of fracture. The case
on the left side was associated with severe ptosis while
both suffered from nasolacrimal duct obstruction
119
herniation into the temporal or malar regions. Lateral
wall fractures are usually associated with fractures of
the zygoma and corrected with replacement of the
zygoma. Large defects usually need split cranial grafts
with semi-rigid fixation to the orbital rim.
D. Trimalar (Tripod/Tripartite) fractures:
It results form a lateral blow to the cheek resulting in
a fracture of the zygomatic bone. Most commonly,
the zygoma is fractured at its sutural junction with the
frontal bone superiorly, the zygomatic arch laterally
and maxilla medially. This can happen in different
combinations. Trimalar fractures may present with
bone fragments either displaced or properly positioned.
Non-displaced zygoma fractures do not require surgery.
In cases of completely displaced fracture (Figs
21.11A and B), the bone fragment may be displaced
posteriorly. This causes a step like deformity of the
infraorbital rim at the zygomaticomaxillary suture, a
flattened malar process and depression of the
zygomaticofrontal suture superior to the lateral canthus.
Hypothesia over the infraorbital nerve distribution is
a common association. Difficulty to open the mouth
can be present due to displaced fragment impinging
on the temporalis muscle yet extraocular muscle
imbalance is usually absent.
The incompletely displaced zygoma is hinged either
at the frontal or maxillary attachment. If hinged to the
frontal bone, there is usually no canthal displacement
as the lateral canthal tendon and Lockwoods ligament
are still attached to the lateral orbital tuberculum. The
main displacement is at the zygomaticomaxillary suture
causing lower lid retraction inferolaterally and increased
scleral show while the globe remains in its place. There
is a step deformity at the inferior orbital rim and inferior
rectus may be entrapped in the fracture site resulting
in diplopia.
If the zygoma is hinged at the maxilla, the lateral
tubercle is usually displaced inferiorly associated with
outer canthus and globe displacement. There is a
palpable gap in the lateral orbital wall. Sometimes the
lateral orbital rim becomes displaced superiorly and
posteriorly causing malar flattening associated with a
bulge in the lateral orbital rim and the lateral canthal
angle may be displaced superiorly. In either condition,
there is no step deformity of the inferior orbital rim
nor diplopia as there is no muscle entrapment.
Management
The fracture is reduced under general anesthesia and
fixed in its place.
Surgical Technique
Closed reduction: that can be either done by:
a. Towel clip that grasps the central portion of the
fractured bone, elevating it into position until the
fragment is felt to pop into place.
b. An intraoral buccal sulcus incision where a blunt
instrument is placed beneath the zygoma then
upward and outward pressure is applied to restore
the bone in place (Fig. 21.12).
c. Gillis approach which is commonly used (Fig.
21.13). A 4 cm incision is placed at the temporal
fossa hairline and carried down through the
temporalis fascia and muscle to the periostium.
A periosteal elevator is inserted beneath the
temporalis fascia and gently passed downwards till
a point below the zygoma. Leverage is applied to
the elevator in an upward and outward direction
reducing the fracture. The fragment can be guided
by the surgeons other hand.
In fresh fractures, the zygomatic bone once in place,
it usually maintains its position. The temporalis fascia
is closed with 4-0 Vicryl while the subcutaneous layer
Figs 21.11A and B: Axial scans showing varieties of
zygoma complete fractures
120
Fig. 21.12: Lateral view for intraoral buccal approach
Fig. 21.13: Gillis approach
is approximated by 5-0 Vicryl in vertical mattress. The
skin is finally closed by 6-0 silk sutures. If the zygoma
is unstable, open and direct interosseus wiring is done.
Open reduction (Fig. 21.14)
A superolateral eye brow incision and a horizontal
incision directly over the inferior orbital rim fracture
site are fashioned. Dissection is carried to the fracture
sites then a periosteal elevator is inserted via the inferior
incision and the zygoma is rotated up into its position.
All tissues entrapped within the fracture line should
be released.
Specially designed miniplates and microplates are
used to approximate the fractured bones. Small drill
holes are placed on each side of the fractured zygoma-
Fig. 21.14: Incision and wiring in open reduction
ticofrontral and zygmoaticomaxillary sutures while
protecting orbital structures during drilling. The screws
are advanced until the head is firmly supporting the
plate.
Other methods of fixation include intramaxillary
inflatable balloon and direct interosseus wiring where
the bone fragments are united by 27-gauge wire that
is tightened by wire twister without excessive tightening.
It is effective in relatively stable fractures. The wire ends
are cut leaving nearly 5 mm long and reposited in
a drill hole or pressed flat against the bone to avoid
injury to overlying structure.
If sufficient periostium remains, it should be closed
by 5-0 interrupted Vicryl sutures. Muscles and sub-
cutaneous layers are also closed with 5-0 Vicryl. Skin
is closed by 6-0 silk sutures.
If the malar flattening persists after reduction which
usually occurs with comminuted fractures, the malar
eminence can be augmented by alloplast or bone graft
placed in a subperiosteal pocket via inferior fornix or
Caldwell-Luc incision.
Le Fort fractures (Fig. 21.15)
Le Fort fractures involve the maxilla and are usually
complex, asymmetric and incomplete. Pure Le Fort
fractures are uncommon. Le Fort I is a low transverse
maxillary fracture that does not extend to the orbit.
The fragment of the maxilla containing the teeth is
separated from the remainder of the facial bones.
In severe cases, it may be free floating.
Le Fort II fractures are pyramidal, involving the
maxilla, nasal bone and medial orbital floor. This
fracture begins at the lower portion on the nasal bones,
across the naso-orbital margin above the nasolacrimal
canal through the medial orbital floor (sometimes
associated with blow out fracture) over the infraorbital
rim through the inferior orbital canal involving the
121
anterior and posterior walls of the maxillary sinus. This
fracture crosses the posterior pillar of the upper jaw,
the pyramidal and pterygoid processes, and
pterygomandibular fissure ending at the medial orbital
margin and lateral wall of the nose. This fracture may
be partially displaced or free floating.
Le Fort III fractures create a craniofacial dysjunction
involving both orbits, separating the maxilla from the
skull; the facial skeleton is free floating attached to the
cranium by only soft tissue. This fracture extends from
the upper portion of the nasal bone, across the orbital
margin near the frontomaxillary suture through the
ethmoid bone passing posteriorly and inferiorly below
the optic foramina to the inferior orbital fissure. It then
separates into two segments; one extends upwards
along the zygomaticosphenoid suture between the
orbital roof and the lateral orbital wall crossing the
lateral orbital rim at the zygomaticofrontal suture. The
second portion extends inferiorly and posteriorly
crossing the pterygoid process. The zygomatic arch is
also involved.
Le Fort II and III may extend to the orbital apex
affecting the optic nerve and reducing vision.
Management of these fractures require open reduction
usually with arch bars. They may be associated with
skull fracture thus requiring conjoint work with
neurosurgery.
Orbital roof fractures (Fig. 21.16)
Isolated roof fractures are uncommon due to the
strength of the superior orbital rim. They can be seen
with wounds inflicted by sharp objects, gun shots or
in association with Le Fort III fractures.
It may be associated with brow and eyelid
ecchymosis, forehead hyposthesia, ptosis and diplopia.
The latter is secondary to superior rectus or oblique
affection as well as damage to the trochlea. Ptosis
Fig. 21.15: Le Fort fractures I, II and III respectively from left to right
Fig. 21.16: Coronal scan showing fracture roof of the orbit
results from third nerve affection, direct muscle injury
or muscle entrapment. The fracture may extend to
the superior orbital fissure and optic canal with resultant
damage to the optic, oculomotor, trochlear and
abducent nerves. In rare occasions with large or
depressed fracture it may present with gl obe
displacement, secondary menigeocele or encephalocele
with and pulsatile proptosis.
Superior orbital rim, frontal sinus and glabellar
fractures either remain extracranial or communicate
with the intracranial compartment. If air is detected
in the anterior cranial fossa in case of orbital roof
fracture, this signifies a dural tear. Unless a significant
displacement is found, superior orbital rim fractures
dont need surgical reduction, displaced fractures of
small size without involving the orbital roof and did
not violate the intracranial space can be repositioned
and wired under the microscope. All other superior
122
rim or roof fractures should be evaluated and managed
by a neurosurgeon.
Orbital blow-in fractures:
Any of the four walls may be fractured and displaced
towards the centre reducing the orbital volume and
causing edema, proptosis and optic nerve compression
either directly or by secondary increase of intraorbital
pressure. Diplopia and mechanical restriction of
extraocular muscle movements as well as globe injuries
can also be detected. The most common in fractured
walls are the roof and the lateral wall (Fig. 21.17).
Cases with optic neuropathy or marked proptosis
causing exposure should be managed as soon as
possible.
Fig. 21.17: Fractured zygoma incarcerated
behind the intact globe
Role of Endoscopy in Management of Orbital
Fractures
Endoscopic repair of orbital fractures could become
a predictable and efficient treatment alternative to
traditional method. It is can be used for repair of
isolated floor or medial wall fractures not associated
with orbital rim fractures. It has also been tested for
repair of delayed cases with promising results. It offers
a hidden incision, improved fracture visualization, and
avoidance of post-operative eyelid malposition,
however, specific knowledge of endoscopic anatomy
is required.
Via an endoscopic endonasal approach, a wide
middle meatal antrostomy in case of floor fractures
or intransal ethmoidectomy in case of medial wall
fracture is created. Adhesions between the protruded
periorbita and the paranasal sinus mucosa are dissected
and the bone fragments are removed. The orbital floor
is supported by a saline filled balloon, which is
connected with an infant feeding catheter and passed
through the middl e meatal antrostoma. After
confirming the reduction of the orbital floor by
postoperative CT, the catheter is ligated and cut in short
to keep it in the nasal cavity. A silastic or Medpore
implant sheet soaked in antibiotic solution can also be
used for the floor or medial wall fracture repair.
Temporary supporting of the orbital wall with a
detachable temporary balloon, or a silastic sheet and
Merocel packing was removed 4 weeks after surgery
in the out-patient clinic (Figs 21.18A and B).
Management of Old Standing Orbital Trauma
The patient is evaluated in a manner similar to acute
cases with more stress on the globe position, ocular
motility, forced duction testing as well as diplopia fields.
If globe reposition is indicated, it should be done before
muscle or eyelid surgeries. Bony orbit may be restored
by osteotomies and open reduction or volume
augmentation by placing an implant in the subperio-
steal space. Soft tissues incarcerated in the sinus should
be carefully removed however, fibrosis render this step
difficult with more possibility of tissue injury. Adjustable
suture technique is better used for muscle surgery in
such cases. Sometimes, glasses with plus lenses can
Figs 21.18A and B: Endoscopic view of floor fracture A: before surgery, B: after repair
123
be prescribed for blind eyes to reduce the apparent
enophthalmos.
Orbital contour deformity:
This may arise from old trauma that was not or poorly
repaired. If the defect is small, no further management
will be needed. In case of large defects, subperiosteal
custom made implants are used. The extent of the
deformity is defined by radiological studies and the
ocularist takes mold of the affected region incorporating
the defect. A positive impression is fashioned from the
mold using the desired alloplastic material. This can
be designed using special computer programs. Methyl
methacrylate and proplast implants are usually
effective.
Surgical technique: Under general anesthesia, one or
two small incisions are placed adjacent to but not
overlying the deformity in conformity with Langers
lines. The incision is carried down till the deformity
using sharp and blunt dissection. If the periostium is
intact, a periosteal pocket is created to receive the
implant. Alloplastic materials soaked in antibiotic
solution are mildly modified using scissors. The
surrounding bone may be modified using a drill with
fine burr head. The alloplastic material is placed within
the periosteal socket and secured in place using 2-0
Supramid sutures
The wound is closed in two or three layers with
interrupted sutures.
Late hypophthalmos or enophthalmos:
Implantation of various materials in the subperiosteal
space along the orbital floor can augment this area
thus raising the globe and moving it anteriorly. Materials
used for orbital floor fractures are used to correct globe
malpositions yet they are thicker especially posterior.
Beads and pellets forms of these materials can be used
and they require smaller incisions. The floor exposure
is very similar to the approaches described for orbital
floor fracture repair. The periostium is incised elevated
from the floor using periosteal elevator and malleable
retractors. The implant is placed in the created space
with the same precautions taken for floor fracture
implants, i.e. pupil and forced duction test. Some
authors inserted porous polyethylene (Medpor)
particles diced about 1 1 cm diameter through a
lateral canthal incision to orbital floor with successful
results. The advantages of this technique are limited
incision, decreased postoperative edema, volumetric
adjustability, and applicability under local anesthesia.
Soft tissue fillers have been tried to correct
enophthalmos, They include autologous fat, cross
linked collagen (Zyplast) and self inflating hydrogel
pellets. The latter should not be used in cases with
visual potential as they may induce high pressures.
Calcium hydroxyapatite gel (Radiesse) as well as
hyaluronic acid can be injected to augment the volume
in eyes with mild enophthalmos and intact vision.
Hyaluronic acid was described to be injected intraconal.
The surgeon should always compare to the sound
side for globe position, restoration of the supratarsal
sulcus as well as alignment with the sound side.
Correction of the condition may result in aggravating
existing ptosis that requires surgical intervention.
Late persistent handicapping diplopia:
Muscle surgery is advocated after the motility and
diplopia measurements are stabilized. Orbital floor
surgery can improve it when it is performed up to
5 weeks post trauma yet the extraocular muscle
motility rarely improves after that. The surgery is
individualized according to the degree of ocular
imbalance. Adjustable sutures are preferred
Most of patients suffer from diplopia on downgaze
interfering with reading. If the eye can move up
normally with normal forced duction test on upgaze,
A reverse Knapp procedure is performed in which the
medial and lateral recti are placed at or several
millimeters behind the original inferior rectus insertion.
If the eye cannot move upwards normally with
positive forced duction test, inferior rectus is recessed
till the eye can be normally moved upwards during
surgery. Then a modified reverse Knapp procedure
is performed 3-6 months later; thus avoiding working
on three muscles at the same time for fear of anterior
segment ischemia.
Fadom operation can be done attaching the
inferior rectus to the sclera in the sound eye. This
decreases diplopia in down-gaze yet it inhibits
downwards movement and makes the patient tilt his/
her head on reading.
Telecanthus
A Y shaped miniplates can be used to correct
telecanthus when there is enough bony support. In
case of bone destruction, transnasal wiring is the
procedure of choice.
Surgical Technique
A medial orbitotomy incision is made just medial to
the medial canthus and anterior to the lacrimal drainage
system. Soft tissue and scar are debulked, any
displaced bone fragments are either reduced or
removed. A Y shaped miniplate is attached to the nasal
bone or frontal bone with screws keeping the long
limb directed posteriorly.
The medial canthal tendon is engaged by a wire
on a free needl e then passed through the
corresponding hole of the plate mirroring the place
of the posterior lacrimal crest. One of the previously
placed screws is loosened and the wire is wrapped
around its head.
124
The wire is tightened while the assistant keeps
medial traction on the canthal tendon aiming at over
correction. Then the ends of the wire are cut, twisted
and bent back into the miniplate
The tissues are closed in anatomical layers and
finally the skin is closed using 6-0 silk sutures.
Summary
Orbital and globe injuries are common in maxillofacial
traumas. Proper and systematic assessment is
mandatory to detect any subtle lesion and should be
done as soon as life-saving measures are taken. Proper
understanding of the anatomy, possible problems and
their mechanisms is of utmost importance for proper
management. Early reconstruction is desirable yet late
repair is a challenge requiring many and staged
procedures. The treatment is individualized according
to the patients condition. Proper assessment and
planning is the key for obtaining good results.
Bibliography
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findings in patients with orbitozygomatic complex
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2008 May;66(5):888-92.
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new approach? Arch Facial Plast Surg 2007 Nov-
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6. Fernandes R, Fattahi T, Steinberg B, Schare H:
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C H A P T E R
22
Management of Anterior Segment
Trauma: An Update
CS Dhull, Sumit Sachdeva (India)
Conjunctival, Corneal, and
Scleral Injuries
Evaluating the anterior segment encompasses a very
important aspect in the proper diagnosis and manage-
ment of ocular trauma. By anterior segment trauma
we mean to evaluate the structures of the eye in front
of the crystalline lens (including the lens itself), but in
this chapter we will discuss only injuries related to
conjunctiva, cornea and sclera with special reference
to penetrating injuries.
CONJUNCTIVAL INJURIES
Conjunctiva is the most superficial layer of eye and
the inner eyelids. The role of conjunctiva though is
neither visual nor structural, but it does offer first line
of ocular defence against chemical agents and low
velocity foreign bodies. It is generally the first to be
involved in cases of blunt trauma to eye and orbit.
As it is highly vascularized, therefore, its wounds heal
rapidly. The injuries to conjunctiva are generally not
as painful as those of cornea.
Types of Injuries
Hemorrhage: Subconjunctival hemorrhage (Fig.
22.1) though alarming is generally of no intrinsic
consequence. It can be due to any of the following
reasons:
a. Idiopathic (spontaneous)
b. Minor trauma (finger nail injury)
c. Major trauma (scleral rupture)
d. Systemic conditions (hypertension, bleeding
dyscrasias, physical exertion, valsalva maneuvers
etc.)
The significance of the condition lies not in the
presence of blood, which generally absorbs sponta-
neously within 2 weeks and without adverse conse-
quences. The real danger is a thick layer of blood
concealing an underlying wound signifying occult scleral
rupture. The examiner must, therefore, obtain
complete history and perform complete examination
to rule out scleral rupture, foreign body or laceration.
The condition itself requires no specific treatment,
except reassurance to the patient.
Fig. 22.1: Subconjunctival hemorrhage
Erosion: Loss of the conjunctival epithelium is much
less painful than that of the cornea, and healing occurs
fast. When de-epithelialization occurs as a result of a
chemical injury and is accompanied by ischemia, the
condition should be considered very serious and
requires immediate treatment. Antibiotic ointment can
be applied as a lubricant and as an anti-infective agent.
Chemosis: Conjunctival edema is a pathology that may
accompany virtually any type of eye trauma. It is
basically due to dysfunction of its vascular endothelium.
While itself insignificant, it may point towards conditions
l ike chemical injury, endophthal mitis, orbital
hemorrhage, orbital fracture, insect bite, retained
intraocular foreign body, or more serious carotid-
cavernous fistula. The severity of the underlying
pathology and the degree of chemosis may not be
proportional. There is no specific treatment: the
causative condition must be addressed. Topical
corticosteroids may help reduce the edema.
126
Emphysema: It occurs when air gets entrapped in or
underneath the conjunctiva. More commonly, the
source is a paranasal sinus in the presence of an orbital
fracture. Blowing the nose or coughing exacerbates
the emphysema and should strongly be discouraged
until the etiology is treated. Removal of the air is not
necessary; once the resupply is cut off, the air quickly
absorbs.
Foreign body: Conjunctival bodies generally adhere
to the upper palpebral conjunctiva (most commonly
in the sulcus subtarsalis) and lower fornix. These
generally cause pain and discomfort due to continuous
rubbing of cornea with each blink. Superficial objects
are usually easy to recognize and remove. The FBs
embedded superficially may be removed with a cotton
tipped applicator while those embedded deeper require
some type of a sharp instrument like a 26 G disposable
needle and often topical anesthesia has to be given
before its removal. Glass foreign bodies (like from
broken spectacles) may be difficult to identify. Proper
slit lamp examination with dyes help in delineating the
FB.
Laceration: The conjunctiva is elastic and mobile and
therefore very resistant to trauma from blunt objects,
but a sharp object like broken glass can cause
conjunctival laceration as easily.
As with foreign bodies, a complete history has to
be taken and a detailed slit lamp examination must
be performed to rule out any retained foreign body
and ruptured globe. Fundus examination should also
be carried out to rule out deeper injury. Generally
lacerations less than 1 cm do not require any repair,
but more than that have to be repaired with an
absorbable suture like 8-0 vicryl. Care should be taken
not to incarcerate Tenons capsule into the wound.
Simple wounds generally heal within a week and no
treatment is required, except antibiotic ointment.
CORNEAL INJURIES
The cornea is frequently involved in facial and ocular
trauma. Corneal injuries comprise a very important
aspect of ocular trauma as they are directly responsible
for the visual outcome in the patient. Management
of corneal injuries requires great skills of observation,
diagnosis and planning, especially in children as they
are more susceptible to such injuries and have a larger
part of life lead with ocular morbidity.
Corneal trauma can be extremely painful: the
epithelium, only 50 m thick, has a large number of
unmyelinated nerve endings. Trauma deeper than the
epithelium, breaching the Bowmans membrane causes
scar formation, which:
a. Reduces the corneas transparency
b. Alters the corneas shape causing astigmatism and
halo formation
c. Makes the normally smooth surface uneven, so
leads on to symptoms of dry eye.
d. Leads to significant and permanent structural
weakness.
Evaluation of Corneal Injury
History: If the injury is caused by a chemical agent,
history-taking must be limited to asking a few crucial
questions before treatment is started: type of the agent;
time of the incident; and the therapy already applied.
In all other cases, history should be detailed, so as to
learn about the circumstances and consequences of
the injury, the risk factors, etc.
Inspection: Careful inspection should be performed
after the eyelids have been gently pulled apart to allow
viewing the cornea completely. Utilizing focal,
illumination may reveal erosions, blood vessels, scars,
edema, infiltration, foreign bodies, and lamellar or full-
thickness wounds. It is preferable to use some
magnification (like a loupe) while examining the cornea.
Changing the angle of illumination also increases the
chance of detecting the abnormality.
Slit lamp is the most appropriate equipment for
detecting pathologies of cornea. Magnification along
with different illumination techniques are invaluable
in reaching the correct diagnosis. Sometimes, a local
anesthetic agent (like proparacaine 0.5%) is required,
if the pain is intense and patient is squeezing the
eyelids. This is more so in patients with foreign bodies.
All topical anesthetics are toxic, however, and their
longer-term use is contraindicated.
Application of certain dyes like Fluorescein (Fig.
22.2) and Rose Bengal can help in identifying erosions
and the damaged epithelial tissue respectively.
Fig. 22.2: Corneal abrasion stained by fluorescein dye
127
Management of Anterior Segment Trauma: An Update
1. With direct illumination, the object is viewed
via light scattered from its anterior surface. But, due
to the complex optical nature of the cornea and the
multiple interactive surfaces, clear foreign bodies (e.g.
glass, plastic) and even lacerations may be difficult to
appreciate.
Under retroillumination, the object is illuminated
from behind; the light can be reflected from the
iris or the fundus, providing a light from back of
cornea, highlighting the opacities.
Sclerotic scatter is based on the principle of
internal reflection. Light entering the cornea from
the limbus is totally internally reflected from the
epithelial and endothelial surfaces; any interruption
in the light path results in light scattering. This is
very helpful in detecting corneal foreign bodies as
well as structural abnormalities.
2. In indirect illumination, the illuminating beam
is at 45, the biomicroscope is focused on cornea. The
area examined is lateral to the illuminated area and
receives illumination from the neighboring area. It is
helpful in detecting microcystic edema and infiltrates
in anterior cornea.
Specific Injuries
CORNEAL ABRASION (FIG. 22.3)
It accounts for nearly 10% of patients who present
with ocular injuries in the emergency.
In this only the epithelial layer is damaged. The
abrasion can be partial or full thickness, and as long
as Bowmans layer is not disturbed, healing generally
follows without scarring. Healing of the abraded
epithelium occurs in several stages:
1. Initially, there is a migration of peripheral cells onto
the area of denuded basement membrane;
2. This is followed by proliferation of the epithelial
cells to restore epithelial thickness;
3. And finally there is formation of hemidesmosomal
attachments to the underlying basement mem-
brane.
Limbal stem cells play an important role in the
process, and their injury can lead to significant healing
difficulties.
Symptoms
Intense pain
Lacrimation
Photophobia
Fig. 22.3: Corneal abrasion
Examination
Examination of patients with corneal abrasion is
generally difficult because of the pain, watering and
photophobia. A drop of topical anesthetic (e.g.
proparacaine 0.5%) can be of great benefit, permitting
proper evaluation.
Examine the face of the patient first to evaluate
any associated injuries and then specifically the cornea
is inspected.
Slit lamp examination is done followed by fluo-
rescein dye staining to delineate the abrasion. The
underlying stroma should be examined for any deeper
pathology.
Flow Chart 22.1: Various slit lamp examination techniques are helpful in examining the cornea completely
128
Treatment
Antibiotic ointment: To cover the sensitive surface
and to prevent infection. Once the integrity of a
healthy epithelial surface has been reestablished,
there is no further need for topical antibiotics.
Cycloplegic drops to alleviate the pain resulting
from reactive spasm of the sphincter muscle. The
drug should be short-acting (like cyclopentolate
0.5%)
Bandage soft contact lens may also be used; this
does not interfere with the external oxygen supply
or the patients ability to use the eye during the
healing process.
Note: The use of tight pressure-patching is not
recommended as it interferes with the external oxygen
supply to cornea, raises the surface temperature, and
prolongs healing. Risk of infection is also increased.
RECURRENT EROSION
Recurrent erosion occurs in 7 to 8% cases.
1
It occurs
probabl y due to abnormal adhesion compl ex
formation in the base of epithelial defect. This results
in delayed sloughing of the healed epithelial surface.
Recurrent erosions are especially common if the trauma
is caused by: finger nail, sheet or edge of paper and
vegetative matter.
History
The patient gives a typical history of intense lacrimation
and photophobia in eyes upon wakening up and the
symptoms improve by mid-day. Sometimes if the
erosion is large, the symptoms persist for days.
Treatment
The treatment is aimed at allowing the adhesion
complexes to form and allowing the hemidesmosomal
anchoring fibers to extend into the basement
membrane to secure the epithelium firmly in place.
Topical hyperosmotic agent (e.g. 5% sodium
chloride ointment) is applied at night, immediately
before retiring. In the majority of cases, a topical
hyperosmotic agent applied nightly for 8 weeks
results in resolution of the condition. This reduces
the epithelial edema and helps the epithelium to
adhere to Bowmans layer.
2
Extended-wear bandage contact lens, changed
every two weeks and worn day and night for up
to 8 weeks.
Surgical debridement to remove the loose epithe-
lium and scrubbing the basement membrane
without damaging the Bowmans layer. Remove
any hypertrophy using a cotton-tip applicator or
a surgical blade.
Stromal micropuncture:
3
The rationale behind this
treatment is that, due to inadequate adhesion, the
epithelium is not anchored to its basement
membrane. The micropunctures are aimed at
attaching the epithelium by taking advantage of
the normal scarring following injuries to Bowmans
layer.
Eximer laser ablation of basement membrane and
superficial Bowmans membrane.
4,5
YAG-laser treatment of Bowmans membrane.
FOREIGN BODIES
Corneal foreign bodies are second most common form
of eye trauma (Fig. 22.4). These can result from
minor trauma, like an insect wing falling into the eye,
or small iron foreign body from a grinder. These
generally embed superficially in corneal epithelium and
generally do not reach the Bowmans membrane,
while high velocity foreign bodies can embed deeply
into the stroma. Multiple foreign bodies should be
suspected if the etiology is explosion.
Fig. 22.4: Corneal foreign body (arrow)
Evaluation
The patient should be examined initially with a torch
light, looking for foreign material on the skin or
conjunctiva, which if present should alert the examiner
to the possibility of a corneal foreign body. The slit
lamp, however, remains the most effective method of
detection. All the different techniques of slit lamp
examination should be employed while examining the
patient as some transparent foreign bodies like glass
and plastic can be difficult to visualize in diffuse
illumination but stand out in retro-illumination.
The patient presents with symptoms of irritation
and pain, though the pain is not so much as in corneal
erosion.
129
Treatment
The cornea must be properly anesthetized with
drops (0.5% proparacaine).
Superficial FBs are best removed using a cotton-
tip applicator or a 26G needle. The foreign body
should be gently lifted so as to minimize the trauma
to neighboring tissue. Rust rings, which can develop
as early as within a few hours should also be
removed, using a sharp needle.
6
Once the FB has
been extracted, the condition should be treated
as an erosion.
Deep-seated FBs should be dealt with care. If the
depth of foreign body in stroma cannot be
ascertained then the removal should not be
attempted. The patient should then be taken to
operation theatre for proper evaluation and
removal. Special instruments like fine tipped forceps
should be used to remove any foreign body
protruding deep in stroma (e.g. splinter). Care
should be taken to remove it through the same
track that it had entered.
Unless there is tissue loss, most wounds resulting
from FBs are self-sealing, although occasionally the
utilization of bandage soft contact lenses or a
corneal glue can be required.
CORNEAL LACERATIONS AND RUPTURE
Corneal lacerations may be full or partial thickness
wound caused by a sharp object and typically involves
the stroma. Most of the lacerations are full thickness.
7
Evaluation
Proper history is must in such cases as it helps the
clinician in deciding not only the course of action to
be taken, but also if there is any deeper pathology
(like retained IOFB).
Signs of Global Perforation
Any one or combination of the following suggests
possible perforation of the globe:
Markedly decreased visual acuity.
Hypotony (decreased IOP).
Shallowing or flattening of the anterior chamber
or hyphema.
Alteration in pupil size, shape, or location..
Focal iris-corneal adhesion.
Corneal, lens, or vitreal track.
Acute onset lens opacity.
Marked conjunctival edema (chemosis) or
subconjunctival hemorrhage.
Inspection of the area is done first with a torch light
after carefully separating the lids. Care should be taken
not to apply deeper pressure on globe because if the
injury is deeper then the intraocular contents can
prolapse out upon slightest pressure on the globe. If
the lids are swollen then lid retractors can be used to
separate them.
Slit-lamp examination is mandatory to evaluate the
wound completely. All the different techniques of slit
lamp examination can be employed to come to a
proper diagnosis.
Partial thickness lacerations: Small, self-sealing, clean
wounds require no intervention other than
prophylactic antibiotics and mild cycloplegics for a few
days.
Larger flaps if displaced need suturing, while still
larger, self-sealing, clean wounds need a bandage
contact lens or glue.
Full-thickness wound (Fig. 22.5): When the diagnosis
is confirmed, unless the wound is tightly sealed, the
wound has to be repaired.
Fig. 22.5: Open globe injury: Full thickness wound at
limbus with iris prolapse
Corneal Tear Repair
Timing: The tear has to be repaired as early as possible
in the operation theatre so as to prevent any chances
of infection.
The basic principles of wound repairing are:
8
1. The wound should be sutured preferably under
general anesthesia under all aseptic conditions.
2. The wound should be made watertight.
3. Depth of sutures is very important in giving best
results. Ninety percent suture depth is recommen-
ded.
4. Suture bites should be equal on both sides, unless
the wound is oblique. Sutures should be equidistant
and should have equal tension in all of them.
5. If the limbus is involved, first suture is applied there,
then the cornea is sutured and then sclera. If the
wound is zig zag type, then sutures are applied at
angles first (Fig. 22.6A).
130
6. The suture arms in the optical area are kept smaller
than those at the periphery to minimize scarring in
that area (Fig. 22.6B). In the visual center no
sutures should be placed unless absolutely
necessary.
7. Knots should be buried so as to cause less
discomfort and less chances of vascularization if
knots cannot be buried for some reason then
bandage contact lens should be applied.
SCLERAL INJURIES
Scleral injuries account for about 30% of all ocular
injuries. Although unlike cornea, sclera does not play a
direct role in the visual process, but it accounts for most
of the globe stability and rigidity. The proximity of the
sclera to vital tissues such as the choroid, ciliary body,
and the retina gives it significant clinical implications.
Evaluation
Proper evaluation of sclera is must before proceeding
for management. The sclera is examined under slit-
lamp to identify the type of injury. Subconjunctival
hemorrhage and chemosis can make the visualization
difficult so imaging studies like ultrasonography and
CT scan should be ordered to rule out any occult
pathology and also to evaluate the condition
thoroughly.
Specific Conditions
Foreign bodies: If the FB is anterior then it has to be
removed by freeing the tissues around it. This is
relatively simple unless the object is partially inside the
globe. If that is the situation then it requires great skill
to free the FB from sclera. The depth of the FB has
to be identified and injury to adjacent structures has
to be taken into consideration.
If the foreign body is posterior, then a judicious
consideration is made that whether the foreign body
is accessible or not. If accessible the scleral cutdown
is advisable and if not then it should be left to VR
surgeon for taking the foreign body from inside.
Lacerations: The lacerations can be full thickness or
partial thickness.
I. Partial thickness lacerations: If small can be left as
such but if large may require suturing. The technique
of suturing is similar to the one for full thickness
wounds.
II. Full thickness lacerations: Full thickness lacerations
have to be sutured and suturing technique differs
according to the situation
First assess the general condition of patient to rule
out any life-threatening condition.
Always prefer general anesthesia to local or topical.
If the wound is corneoscleral, then first suture is
applied at the limbus and then cornea is sutured
followed by the sclera (Fig. 22.7).
If the wound is scleral only then firstly the conjunc-
tiva and Tenons capsule is separated and the full
Fig. 22.6B: Schematic representation of how sutures are
applied on cornea. Note that sutures at the periphery are
longer than those at center
Fig. 22.6A: Zig-zag tear repaired with sutures
applied at angle first
Fig. 22.7: Corneoscleral wound: First suture applied at
limbus then cornea and then sclera
131
length of the wound is exposed. Then 50% rule
is applied to close the wound. In this the initial suture
is placed at halfway mark of the wound (50%) and
next suture at 25% and the third at 75% mark and
so on. Alternatively closure can be started from
the proximal end to the distal, with close as you
go technique. This technique is helpful in those
tears too in which the distal end is not visualized
(Fig. 22.8).
Fig. 22.8: First suture at the limbus and then go from
anterior to posterior
If the wound goes beneath the muscle then, firstly
the assistant should try to move the muscle aside
with a retractor, but if it is not possible then the
muscle is first carefully secured and then cut at the
insertion, the scleral wound is then sutured and
the muscle reattached to its original place (Figs
22.9A and B).
8-0 nylon sutures are preferably used in closing
the sclera as they have a good tensile strength. The
depth of the bites can be upto 80% of the tissue
thickness.
Fig. 22.9A: Scleral wound extending below the muscle
Fig. 22.9B: Wound closed after disinserting the muscle
and securing it properly
Care should be taken that at no stage undue
pressure is applied on the globe as it will lead on
to tissue and vitreous prolapse. Also while closing
the wound care should be taken not to incarcerate
any tissue in the suture tract.
If the posterior limit of the tissue is not identified,
then the wound is closed as far as possible without
undue force, and the remaining wound is left as
such, to be healed by natural process of scarring
or should be left for VR surgeon to manage from
inside.
Conjunctiva is carefully closed over the repaired
sclera to avoid any chances of infection.
References
1. Weene LE. Recurrent corneal erosion after trauma: a
statistical study. Ann Ophthalmol 1985;17:52124.
2. Kenyon KR. Recurrent corneal erosion: pathogenesis and
therapy. Int Ophthalmol Clin 1979;19:16995.
3. McLean EN, MacRae SM, Rich LF. Recurrent erosion:
treatment by anterior stromal puncture. Ophthalmology
1986;93:78488.
4. Dausch D, Landesz M, Klein R, et al. Phototherapeutic
keratectomy in recurrent corneal epithelial erosion.
Refract Corneal Surg 1993;9:41924.
5. John ME, Van der Karr MA, Noblitt RL, et al. Excimer
laser phototherapeutic keratectomy for treatment of
recurrent corneal erosion. J Cataract Refract Surg 1994;
20:17981.
6. Zuckerman B, Lieberman TW. Corneal rust ring. Arch
Ophthalmol 1960;63:254-64.
7. Duke-Elder S, MacFaul PA. Lacerations of the cornea. In:
Duke-Elder S (Ed). System of Ophthalmology. Vol XIV.
Part 1. St. Louis: Mosby; 1972.
8. Beatty RF, Beatty RL. The repair of corneal and corneo-
scleral lacerations. Semin Ophthalmol 1994;9:16576.
9. Ferenc Kuhn. In Ocular Traumatology; 1st (edn). Springer
2008.
C H A P T E R
23
Glued IOL
Amar Agarwal, Dhivya A, Soosan Jacob, Athiya Agarwal
Chandresh Baid, Ashok Garg (India)
Introduction
We devised a new surgical technique for implantation
of a posterior chamber intraocular lens (IOL) in eyes
with deficient or absent posterior capsule with the use
of biological glue. We used a quick acting surgical fibrin
sealant derived from human blood plasma, with both
hemostatic and adhesive properties.
Scleral Fixated IOL
Intraocular lens implantation (IOL) in eyes that lack
posterior capsular support has been accomplished in
the past, by means of iris fixated IOL,
1,2
anterior
chamber intraocular lens and transscleral IOL
fixation
3-12
through the ciliary sulcus or pars plana.
Surgical expertise, prolonged surgical time, suture
induced inflammation, suture degradation, and
delayed IOL subluxation or dislocation due to broken
suture are some of the limitations in sutured scleral
fixated intraocular lenses (SFIOL). It is also difficult
and time consuming requiring minute and perfect
adjustment of suture length and tension to ensure good
centration of SFIOL.
Fibrin Glue
Fibrin glue
13-15
has been used previously in various
medical specialities as a hemostatic agent to arrest
bleeding, seal tissues and as an adjunct to wound
healing. The fibrin kit we used was ReliSeal (Reliseal,
Reliance Life Sciences, India). It is available in a sealed
pack, which contains freeze dried human fibrinogen
(20 mg/0.5 ml), freeze dried human thrombin (250
IU/0.5 ml), aprotinin solution (1500 kiu in 0.5 ml),
one ampoule of sterile water, four 21G needles, two
20G blunt application needles and an applicator with
two mixing chambers and one plunger guide.
Surgical Technique
After inserting the infusion cannula or anterior chamber
maintainer, localized peritomy is done. Two partial
thickness limbal based scleral flaps about 4 4 mm
are created exactly 180 degrees diagonally apart
(Fig. 23.1) and about 1.5 mm from the limbus. This
is followed by vitrectomy via pars plana or anterior
route to remove all vitreous traction. Two straight
sclerotomies with a 22G needle are made about
1.5 mm from the limbus under the existing scleral flaps.
The sclerotomies are positioned such a way that the
superior one lies close to the upper edge of the flap
and the inferior one close to the lower edge of the
flap. A scleral tunnel incision is then prepared about
2 mm from the limbus for introducing the IOL. While
the IOL is being introduced with the left hand of the
surgeon using a McPherson forceps, an end gripping
25G micro-rhexis forceps (Micro Surgical Technology,
USA) is passed through the inferior sclerotomy. The
tip of the leading haptic is then grasped with the micro
rhexis forceps, pulled through the inferior sclerotomy
Fig. 23.1: Scleral flaps prepared 180 degrees diagonally
apart. Note the infusion cannula fixed in and eye without
any capsule
133
Glued IOL
Fig. 23.2: Tip of the haptic grabbed by the 25 gauge mirco-
rhexi s forceps (MST, USA) and then that hapti c i s
externalized under the scleral flap
Fig. 23.3: Superior haptic grabbed by the 25 gauge micro
rhexis forceps (MST, USA) and then externalized under the
scleral flap
Fig. 23.4: Fibrin glue applied. Note the
haptic which is externalized
Fig. 23.5: PC IOL well positioned and centered
following the curve of the haptic (Fig. 23.2) and is
externalized under the inferior scleral flap. Similarly,
the trailing haptic is also externalized through the
superior sclerotomy under the scleral flap (Fig. 23.3).
Then, the reconstituted fibrin glue thus prepared is
injected through the cannula of the double syringe
delivery system under the superior (Fig. 23.4) and
inferior scleral flaps. Local pressure is given over the
flaps for about 10 to 20 seconds for the formation
of fibrin polypeptides (Fig. 23.5). The anterior
chamber maintainer or the infusion cannula is
removed. Conjunctiva is also closed with the same fibrin
glue.
In case of those patients who had a luxated IOL,
similar lamellar scleral flaps as described earlier were
made and the luxated IOL haptic was then grasped
with the 25 gauge rhexis forceps and exteriorized and
glued under the scleral flaps (Figs 23.6A to E). The
Fig. 23.6A: Subluxated IOL. Note the infusion cannula
fixed and scleral flaps prepared. Vitrectomy being done
134
Fig. 23.6B: Haptics externalized under the
scleral flaps and IOL well centered
Fig. 23.6C: Fibrin glue applied and scleral flaps seal
the haptic of the IOL
Fig. 23.6D: IOL haptic now glued by the fibrin glue
Fig. 23.6E: Fibrin glue seals the conjunctiva
haptic of the IOL if protruding beyond the scleral flap
can be tucked in a tunnel created in the sclera
(Fig. 23.7). Our follow-up anterior segment OCT
(Figs 23.8A and B) showed postoperative perfect
scleral flap adhesion as early as day 1 and continues to
remain well maintained at one week and one month.
Fig. 23.7: IOL haptic tucked through a scleral tunnel
Fig. 23.8A: Anterior segment OCT of scleral flap
Fig. 23.8B: Anterior segment OCT of the IOL.
Note IOL well centered
135
Glued IOL
Discussion
This fibrin glue assisted sutureless PCIOL implantation
technique as described by us would be useful in a
myriad of clinical situations where scleral fixated IOLs
are indicated, such as, luxated IOL, dislocated IOL,
zonulopathy or secondary IOL implantation. In
dislocated posterior chamber PMMA IOL, the same
IOL can be repositioned thereby reducing the need
for further manipulation. Externalization of the greater
part of the haptics along its curvature stabilizes the axial
positioning of the IOL and thereby prevents any IOL
tilt.
16
In the 12 eyes of our 12 patients, no complications
like postoperative inflammation, hyphema, decen-
teration, glaucoma or corneal edema were seen after
a regular follow-up till now. We expect less incidence
of UGH syndrome in fibrin glue assisted IOL
implantation as compared to sutured scleral fixated
IOL. This is because, in the former the IOL is well
stabilized and stuck onto the scleral bed and thereby,
has decreased intraocular mobility whereas in the latter,
there is increased possibilty of IOL movement or
persistent rub over the ciliary body. Visually significant
complications due to late subluxation
17
which has been
known to occur in sutured scleral fixated IOL may also
be prevented as sutures are totally avoided in this
technique. Moreover, the frequent complications
18
of
secondary IOL implantation like secondary glaucoma,
cystoid macular edema or bullous keratopathy were
not seen in any of our patients. Another important
advantage of this technique is the prevention of suture
related complications
19-21
like suture erosion, suture knot
exposure or dislocation of IOL after suture disintegration
or broken suture. Chances of scleral melt
22-24
and haptic
exposure is not increased by this technique except
possibly, in high risk patients like rheumatoid arthritis.
The other advantage of this technique is the rapidity
and ease of surgery. Since all the steps of tying the
difficult to handle 10-0 prolene suture to the IOL
haptic eyelets, the time required to ensure good
centration before tying down the knots as well as time
for suturing scleral flaps and closing conjunctiva are
done away with, the total surgical time is significantly
reduced. It is also easier and does not require much
surgical expertise to use the 25 gauge forceps to grasp
and exteriorize the haptic. Fibrin glue takes only 20
seconds to act in the scleral bed and it helps in adhesion
as well as hemostasis. Fibrin glue has been shown to
provide airtight closure and by the time the fibrin starts
degrading, surgical adhesions would have already
occurred in the scleral bed.
The commercially available fibrin glue that we used
is virus inactivated and is checked for viral antigen with
polymerase chain reaction, hence the chances of
transmission of infection is very low. But with tissue
derivatives, there is always a theoretical possibility of
transmission of viral infections,
25
therefore, it is
mandatory to get informed consent from the patient
before the procedure. Though the use of fibrin glue
in ophthalmology is considered off-label, it has been
successfully used in the eye since long. Its various uses
in the eye include repair of lacerated canaliculi
28
to
seal full thickness macular holes,
26,27
to seal cataract
incisions,
32-35
corneal perforations, and traumatic lens
capsule perforations,
29
It has also been used for
temporary closure of scleral flaps
31
after trabeculectomy
in eyes with hypotony, conjunctival fistula closure
30
,
conjunctival autografts,
31
and amniotic membrane
transplantation.
36,37
Gabor et al
38
have shown sutureless scleral IOL
fixation by placing the IOL haptic in a scleral tunnel.
Our technique differed from other suturel ess
methods,
38,39
by use of the fibrin glue which enhances
the rate of adhesion with hemostasis. We also used
scleral flaps as in conventional sutured SFIOLs and
this makes the learning curve very simple. There is
also no danger of intra-ocular infection gaining entry
through the tunnel as the fibrin glue hermetically seals
the flaps leaving behind no possible entry route for
microbes. There was no glue induced intraocular
inflammation in any of our patients and all 12 eyes
had clear media on the postoperative visits. Scleral
indentation performed in the operated eyes showed
no change in the axial positioning of the IOL. After
one month of fol l ow-up, we found no IOL
decentration or any other complications in any of the
operated 12 eyes.
Summary
Fibrin glue assisted sutureless PC IOL implantation is
appropriate for eyes with deficient or absent posterior
capsule and this can be performed easily with the
available IOL designs, instruments and with less surgical
time. However, a longer duration follow-up might be
necessary to judge the long-term functional and
anatomical results of the procedure.
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Ophthalmol 1993;111:1167-68.
32. Grewing R, Mester U. Radial suture stabilized by fibrin
glue to correct preoperative against-the-rule astigmatism
during cataract surgery. Ophthalmic Surg 1994;25:446-
48.
33. Mester U. Wound closure with fibrin adhesive in cataract
surgery. In: Schlag G, Ascher PW, Steinkogler FJ,
Stammberger H, eds, Fibrin Sealing in Surgical and
Nonsurgical Fields, vol 5: Neurosurgery, Ophthalmic
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34. Rauber M, Mester U, Zuche M. Fibrin adhesive for
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Schlag G, Ascher PW, Steinkogler FJ, Stammberger H,
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37. Duchesne B, Tahi H, Galand A. Use of human fibrin glue
and amniotic membrane transplant in corneal perfora-
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38. Gabor SG, Pavilidis MM. Sutureless intrascleral posterior
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39. Maggi R, Maggi C. Sutureless scleral fixation of intraocular
lenses. J Cataract Refract Surg 1997;23(9):1289-94.
Posterior Segment
Ocular Trauma
C H A P T E R
24
Management of Traumatic
Hemorrhages to the
Posterior Segment
Javier A Montero, Jose M Ruiz-Moreno (Spain)
Introduction
Ocular trauma is a significant cause of visual impairment
in the United States and the leading cause of unilateral
blindness worldwide. Ocular trauma is more frequent
among adult males mainly due to occupational reasons,
though females and children may also present ocular
damage secondary to trauma. Isolated damage to the
anterior segment occurs in more than half of the cases
and isolated damage to the posterior segment is
uncommon.
1
Approximately 2.5 million injuries occur annually,
40,000 of which cause serious visual loss. Vision is lost
because of primary mechanical damage of vital ocular
structures and secondary complications, such as
infectious endophthalmitis and retinal detachment due
to intraocular fibrous proliferation and contraction.
1
The presence of marked vitreous hemorrhage is
associated with poor visual prognosis in ocular trauma
involving the posterior segment. Poor prognostic factors
include presenting visual acuity of light perception or
lower, hyphema, and traumatic cataract. Severe
vitreous hemorrhages after closed-globe injury are
frequently associated with various anterior and
posterior segment pathologies, and early vitrectomy
is considered to improve early visual rehabilitation and
management of any potentially treatable posterior
pathology.
2
Ocular hemorrhage associated with trauma may
occur after blunt and penetrating injuries. A careful
and complete ophthalmic examination is required in
every case since injuries causing minimal signs of
damage to one part of the eye may cause a significant
injury in another part of the eye with severe
consequences for the patient and occasionally to the
ophthalmologist who has misdiagnosed the trauma.
Blunt injuries are more common and cause more
cases of visual impairment than penetrating injuries,
although the frequency of severe damage, blindness,
and loss of the globe itself is greater with ocular
penetration or rupture. Two types of injuries may
disrupt the continuity of the sclera: penetration by
relatively sharp objects, and rupture caused by massive
blunt trauma.
The visual prognosis is more favorable when the
primary mechanical damage caused by sharp
penetration is limited to the anterior segment of the
eye. Modern microsurgical techniques permit better
wound closure and reconstruction of the anterior
ocular structures. Penetrating injuries involving the
posterior segment carry a less favorable prognosis. The
primary mechanical damage of vital structures by such
injuries may be so great that useful vision is instantly
destroyed. However, the application of appropriate
vitreoretinal surgery to prevent or treat secondary
complications may result in the preservation of eyes
that would otherwise be lost.
Both eyes should always be examined. Visual acuity
determination should be performed in the first place;
if standardized charts are not available we should at
least be able to determine finger counting and reading
abilities and the distance of these exams should be
recorded. If none of these abilities can be reached,
the light perception and projection abilities should be
recorded. The evaluation of the direct and consensual
pupillary reflexes is of great prognostic value. Decreased
visual acuity is usually a sign of severity. Over 40%
of the cases report marked visual acuity loss (lower
than 20/200) associated with severe ocular trauma.
Anterior segment examination may disclose corneal
lacerations, traumatic iritis, hyphema, damage to lens
and vitreous opacities among others, which may limit
the examination of the posterior segment (Fig. 24.1).
Ocular examination should be extremely careful until
the absence of ocular perforation has been established,
avoiding pressure on the eye ball and administration
of drops or ointments (Fig. 24.2).
In the presence of hyphema posterior segment
examination should be gently performed in order to
prevent further bleeding and scleral indentation should
be avoided for 2-3 weeks.
140
Fig. 24.1: Subconjunctival hemorrhage after severe blunt
trauma masking scleral rupture. The patient presented
vitreous hemorrhage with choroidal rupture
Fig. 24.2: Retroequatorial intraocular foreign body
which penetrated through the lower lid
Fig. 24.3: Ultrasonography A and B scan reveals a
marked choroidal hemorrhage with vitreous blood
A careful examination of the vitreous, posterior pole
and peripheral retina under pharmacologic mydriasis
is mandatory, since anterior or posterior hemorrhage
may later mask damage to the posterior segment.
Indirect ophthalmoscopy is a useful tool to evaluate
damage to the posterior segment allowing a fast
binocular examination of the vitreous and the retina
and verification of the presence of intraocular foreign
bodies (IOFB). Posterior pole biomicroscopy using
contact and non contact lenses will improve the detailed
examination of the macula, though non contact lenses
are more useful reducing the risk of squeezing an injured
eye. Scleral depression may increase the risk of
intraocular bleeding and should only be performed
once ocular rupture has been discarded.
Anterior, central and posterior vitreous examination
should be performed and the presence of any
hemorrhage or vitreous opacity recorded. The location
and size of the opacities should be recorded, as well
as the presence of posterior vitreous detachment.
Pigment clusters may appear floating in the peripheral
or anterior vitreous following detachment of the
vitreous base from the pars plana.
Fig. 24.4: Grade I vitreous hemorrhage
The size, location and characteristics of hemorrhages
should be recorded. Vitreous hemorrhages may vary
in size, location and density. Initially they are usually
close to the damaged area, though they may later
spread and occupy the whole vitreous cavity precluding
examination of posterior segment structures. If
posterior segment examination is not satisfactory due
to the presence of anterior segment or vitreous hemor-
rhages contact A-scan and B-scan ultrasonography are
helpful for detecting posterior vitreous detachment and
differentiating it from retinal detachment (Fig. 24.3).
The symptoms associated with posterior hemor-
rhages will depend on the locations and size of the
hemorrhage. Peripheral retinal hemorrhages may be
asymptomatic; retinal, choroidal or retrohyaloidal
hemorrhages affecting the posterior pole will present
as central scotomata (Fig. 24.4); and patients with
vitreous hemorrhages will complain of floaters, blurred
vision or even light perception vision, depending on
the amount of blood present.
141
Management of Traumatic Hemorrhages to the Posterior Segment
Pathogenesis
Blunt trauma may cause damage to the eye by three
different mechanisms: coup, contrecoup and ocular
compression. Coup refers to local damage at the site
of impact, whereas contrecoup refers to injuries at the
opposite side of the eye caused by shock waves that
traverse the eyeball with foci of tissue damage along
the path of the shock waves, especially at interfaces
of tissues of different density.
The ocular compression mechanism is determined
by the inextensibil ity of the eyebal l and the
incompressibility of intraocular fluids so that when the
eye is compressed along its anterior-posterior axis, it
expands in its equatorial plane causing severe traction
at the vitreous base. Ocular compression may cause
scleral rupture even in eyes which have not undergone
previous surgery. In these cases the two most common
locations for scleral rupture are at the limbus and
parallel to the muscle insertions between the insertion
and the equator. The hallmarks of scleral rupture are
severe reduction in visual acuity, an afferent pupillary
defect, hypotony, abnormally deep anterior chamber,
decreased ocular ductions, severe subconjunctival
edema, hyphema, and vitreous hemorrhage. Scleral
rupture can rarely be confirmed by ophthalmoscopy
because severe vitreous hemorrhage and/or hyphema
nearly always accompany scleral rupture. Ultrasono-
graphy and computed tomographic scanning may
show a shrunken globe, retinal detachment, partial or
compl ete posterior vitreous detachment and
vitreoretinal adherences. The visual prognosis of
ruptured globes is usually very poor.
The aetiologies and the mechanisms of damage of
penetrating injuries are highly variable and cause a
wide spectrum of acute structural alterations and
secondary complications.
Penetration of the eye by relatively blunt objects
causes compression of the gl obe resul ting in
iridodialysis, subluxation and dislocation of the lens,
traumatic cataract, choroidal rupture, retinal breaks
at the vitreous base borders and vitreous detachment.
Ruptures of the uvea produce anterior chamber,
choroidal, subretinal, and vitreous hemorrhage.
Massive blunt trauma causes corneal and scleral
ruptures and may avulse the optic nerve.
Penetrating objects cause lacerations of the cornea,
iris, lens, sclera, ciliary body, choroid, retina, and optic
nerve, usually combined with anterior chamber,
choroidal, subretinal, and vitreous hemorrhages and
occasional prolapse and incarceration of the lens, uvea,
retina, and vitreous. Cleary and Ryan reported on the
increased frequency of retinal detachment following
penetrating ocular trauma associated with vitreous
hemorrhage.
3
The secondary complications of ocular
penetration may cause visual impairment. They include
the toxic effects of IOFB, such as copper and iron,
and the introduction of bacteria and fungi with
consequent infectious endophthalmitis. Retained lens
material and blood and the incarceration of vitreous
and uvea causes chronic inflammation that may play
an important role in the stimulation of intraocular
fibrocellular proliferation. At a later stage, blood and
lens material in the presence of large scleral wounds
may induce formation of fibrocellular proliferation
which, upon contraction may cause traction retinal
detachment, retinal breaks, rhegmatogenous retinal
detachments, proliferative vitreoretinopathy, cyclitic
membranes, ciliary body detachments, hypotony, and
phthisis bulbi.
Classification
Even though these lesions seldom appear isolated,
hemorrhages to the posterior segment may be classi-
fied for a didactic purpose as:
Vitreous hemorrhages
Retrohyaloidal hemorrhages
Retinal hemorrhages
Choroidal hemorrhages
Papillary and peripapillary hemorrhages
Hemorrhages associated with indirect trauma
VITREOUS HEMORRHAGES
The presence of vitreous hemorrhage has been
associated with retinal detachment and surgical removal
of the blood seems to reduce the frequency of retinal
detachment.
3
The role of the presence and manage-
ment of vitreous hemorrhage has been reported by
several series,
4, 5
as well as the role of the quantification
of the hemorrhage. Brinton et al reported functional
recovery in 48% of the eyes presenting moderate to
severe vitreous hemorrhage vs 67% of the eyes with
mild or no vitreous hemorrhage.
6
Blood proteins may be involved in vitreous proli-
feration mediated by hemorrhages. Fibronectin is a
high molecular weight glycoprotein with a chemotactic
action on retinal pigment epithelium (RPE), fibroblasts
and giant cells and mediates in the interaction between
collagen and the RPE. Fibronectin has been detected
in epiretinal membranes in human eyes following
retinal detachment repair after ocular trauma.
7, 8
Platelet
derived growth factor (PDGF), complement and
interleukins also induce intravitreal fibrosis.
It is necessary to quantify the amount of vitreous
hemorrhage. One accepted classification for this
quantification was proposed at the Vitrase for Vitreous
Hemorrhage study
9
as Grade I when retinal detail is
142
visible with some hemorrhage present and laser
photocoagulations is possible; Grade 2 with large retinal
vessels visible but central retinal is not visible enough
to perform adequate posterior laser treatment; Grade
3 with red reflex and no retinal vessels are seen behind
the equator; and Grade 4 with no red reflex.
The symptoms of vitreous hemorrhage are visual
acuity loss, perception of mobile dark spots in the visual
field. Associated signs are visualization of erythrocytes
floating in the anterior vitreous behind the lens with
dilated pupil. Intense vitreous hemorrhage may lead
to loss of pupillary reflex and blurring of retinal details
(Fig. 24.5). Retinal tear and detachment should be
disclosed in all cases of traumatic vitreous hemorrhage.
B scan ultrasonography is a useful tool to perform
examination of vitreoretinal adherences.
Vitreous hemorrhages may appear secondary to
blunt trauma following scleral rupture, vitreous
detachment, tears in the iris, ciliary body, choroid, or
retina. We should assume that a retinal break is present
until proved otherwise. Blood from choroidal ruptures
accumulates beneath the neurosensory retina passing
through the retina into the vitreous cavity.
Vitrectomy is indicated for vitreous hemorrhage
caused by ocular contusion when a retinal detachment
is suspected because of sudden additional loss of vision,
when a retinal detachment is detected through a
window in the hemorrhage, when a large retinal break
or retinal detachment is diagnosed by ultrasound, or
when there is no improvement after a reasonable
period of observation.
10-13
RETROHYALOIDAL HEMORRHAGES
Retrohyaloidal hemorrhages usually appear following
incomplete posterior vitreous detachment as a result
of vitreoretinal traction or transit of subretinal blood
(Fig. 24.6). Retrohyaloidal or preretinal hemorrhages
are usually thick, masking retinal vessels and may show
a characteristic boat-shape with a superior horizontal
level. Even though retrohyaloidal blood tends to
disappear spontaneously, treatment has been proposed
in order to reduce the contact of blood with the retina
and decrease its toxic effect.
14-16
INTRARETINAL HEMORRHAGES
Intraretinal hemorrhages may appear under different
circumstances associated with ocular or distant trauma.
The location of the blood will determine the presence
of symptoms. Extrafoveal bl ood is usual l y
asymptomatic. Juxtafoveal and subfoveal blood may
present as paracentral or central scotomata.
Subretinal blood is toxic for the retina and the RPE
17
and thick hemorrhages worsen visual prognosis.
Additionally, it is considered that the presence of
hemorrhage limits the closure of the retinal or
choroidal tear.
The image of retinal hemorrhages may vary
depending on how deep the retina is affected. Blood
affecting the retinal nerve fibre layer appears as flame
shaped hemorrhages, whereas hemorrhages affecting
the nuclear layers appear as irregular shaped spots
(Figs 24.7 to 24.9). Retinal hemorrhages usually do
not mask retinal vessels.
CHOROIDAL HEMORRHAGES
Posterior choroidal ruptures are probably caused by
anterior-posterior compression and equatorial
expansion. Blunt trauma may produce hemorrhage
into the choroid secondary to Bruchs membrane
rupture and tear of the overlying RPE and underlying
choriocapillaris. Patients with angioid streaks and other
conditions known to be associated with an inelastic
and fragile Bruchs membrane are especially vulnerable
to choroidal rupture.
Fig. 24.5: Grade 3 vitreous hemorrhage
Fig. 24.6: Retrohyaloidal hemorrhage
143
Fig. 24.7: Submacular hemorrhage
causing central scotoma
Fig. 24.8: Spontaneous resorption of
submacular hemorrhage
Fig. 24.9: Complete spontaneous resorption of macular
hemorrhage. Visual acuity was 20/20
Choroidal hemorrhages may vary in intensity from
small subretinal hemorrhages associated with Bruchs
membrane ruptures to huge suprachoroidal
hemorrhages that may complicate corneal or scleral
lacerations leading to expulsive hemorrhages.
Choroidal hemorrhages may be massive leading
to ocular hypotony and choroidal detachment, usually
associated with vitreous hemorrhage or mask subretinal
hemorrhages.
18
Direct choroidal ruptures are uncommon and
usually anterior and oriented parallel to the ora. Indirect
ruptures are more common and tend to occur away
from the site of impact. A choroidal rupture may be
initially obscured by a subretinal hemorrhage caused
by tearing of the choriocapillaris. Later, after the blood
has resorbed, a white curvilinear streak concentric to
the optic disc is seen. Only rarely is a rupture oriented
radially with respect to the optic disc. Most are temporal
to the disc and single, although nasal and multiple
ruptures can also occur (Fig. 24.10). Typical small
choroidal hemorrhages are rounded, dark red-blue
and frequently take many weeks to resorb and may
leave areas of pigment alteration.
Visual prognosis is generally good unless the
choroidal rupture is under the foveola, or an associated
subretinal hemorrhage extends under the foveola).
The overlying nerve fiber layer is almost never torn.
Therefore, a rupture can be located between the disc
and the macula and yet not affect the visual acuity.
Choroidal ruptures can, months to years later, be
complicated by the development of a choroidal
neovascular membrane, with serous or hemorrhagic
retinal detachment and loss of central vision.
19
In these
cases photodynamic therapy
20
and more recently
intravitreal antiangiogenic therapy may be useful.
PAPILLARY AND PERIPAPILLARY
HEMORRHAGES
Papillary and peripapillary hemorrhages may appear
following optic nerve damage by blunt trauma. Possible
Fig. 24.10: Choroidal ruptures
144
mechanisms include compression by intrasheath
hemorrhage and oedema and direct shock-wave
trauma to the nerve fibers. The management involves
high-dose intravenous steroids, especially if they can
be started within 8 hours, surgical decompression of
optic nerve sheath hematoma and neurosurgical
decompression of the optic canal. Avulsion of the optic
nerve may be accompanied by severe damage to other
ocular tissues or be the sole manifestation of apparently
minor direct trauma.
HEMORRHAGE ASSOCIATED WITH
INDIRECT TRAUMA
Shaken baby syndrome may be associated in one
third of the cases with ocular manifestations, above
all subconjunctival and retinal hemorrhages.
Intraocular hemorrhages are considered to be a
predictive of intracranial bleeding and the severity
of the latter is related to that of the neurological
lesion. Funduscopic examination usually reveals
retinal hemorrhages, perimacular folds, cotton
wool spots, optic disk edema, and venous stasis.
Less frequently, vitreous hemorrhages, retinal
detachment, retinoschisis and chorioretinal atrophy
are seen.
Terson syndrome is characterised by a preretinal
hemorrhage associated with subarachnoidal
hemorrhage. The intraocular hemorrhage has been
classically attributed to transit of blood through the
optic nerve sheaths. Presently, intraocular blood
is considered to be secondary to rupture of
peripapillary and epipapillary capillaries caused by
increased intracranial pressure. Ophthalmoscopy
usually reveals a preretinal hemorrhage in the
peripapillary and macular area located exterior to
the inner limiting membrane (ILM). However, blood
may go through the ILM and appear as a vitreous
hemorrhage. The most frequent complication of
Terson syndrome is the appearance of epiretinal
membranes.
Purtscher retinopathy is a haemorrhagic vasculo-
pathy characterized by mul tipl e retinal
hemorrhages, areas of retinal pallor around the
optic disk and decreased visual acuity. A serous
macular detachment may appear associated with
vascular dilation and tortuosity and optic disk
oedema. Purtscher retinopathy is secondary to
blunt head trauma and thoracic compression. This
syndrome is usually bilateral and the symptoms
usually appear 48 hours after the trauma. The
peripheral retina is commonly spared. Fluorescein
angiography can reveal focal areas of arteriolar
obstruction, capillary nonperfusion, disc edema,
and dye leakage from retinal arterioles, capillaries,
and venules. The aetiology of the white retinal
lesions resulted is controversial. Extravasated lymph
from retinal vessels, reflux venous shock waves,
arteriolar and fat emboli and blood product emboli
formed after complement activation have been
proposed. Clinically, the retinal lesions resolve over
a period of weeks to a few months followed
occasionally by pigment migration and optic
atrophy. Visual acuity may return to normal or near
normal.
Valsalva retinopathy is characterized by preretinal
(retrohyaloidal) hemorrhages in the macular area,
and is secondary to Valsalva manoeuvres associated
with vomiting, coughing. Visual function usually
returns to normal spontaneously. Hemorrhages
located on the macula may present as decreased
visual acuity, but the syndrome is usual l y
asymptomatic.
Retinitis sclopetaria is defined by the rupture of the
choroid or retina caused by shock waves generated
by passage of a high-velocity missile through the
orbit without directly striking the eye. Initial clinical
manifestations may be a subretinal or vitreous
hemorrhage with decreased visual acuity. As the
blood clears, breaks in the Bruchs membrane and
in the choriocapillaris are frequently seen as well
as fibrous tissue proliferation into the eye. Retinal
detachment rarely occurs because of fibrous tissue
proliferation binding the retina to the choroid.
Medical Management
Intravitreal ovine hyaluronidase has been used to
promote resorption of intravitreous blood. 1125
patients with vitreous hemorrhage and visual acuity
worse than 20/200 during more than one month were
randomized 55 IU or 75 IU ovine hyaluronidase or
saline. Clearance of blood was achieved at months
1, 2 and 3 in 13%, 26%, and 33% of patients injected
with 55 IU compared with 6%, 16%, and 26% of
saline-treated patients.
9
Tissueplasminogen activator has been used in
combination with surgery,
21
with intravitreal injection
of gas (in patients with traumatic choroidal rupture)
22
or as isolated therapy
23
with favorable results,
improving vision and occasionally deferring the need
for vitrectomy. These procedures have been used in
cases of subfoveal
21, 22, 24
and retrohyaloidal
23
thick
hemorrhages. After a mean follow-up of 10.5 months
final visual acuity improved by 2 lines or greater in
10 (67%) of 15 eyes and measured 20/80 or better
in 6 (40%) of 15 eyes in on series with complications
including breakthrough vitreous hemorrhage in three
eyes and endophthalmitis in one eye.
24
However the
145
reported series were short and randomized clinical trials
are missing.
Krypton, Argon and Nd-YAG laser treatment have
been performed in patients with intraocul ar
hemorrhages to improve visual acuity by removing
preretinal blood permitting its transit to the vitreous
cavity. Dellaporta reported on the use of argon laser
retinotomies to the posterior pole of one patient with
thick submacular hemorrhage permitting escape of
subretinal blood into the vitreous.
25
A less aggressive
approach using Nd-YAG laser was tried on patients
with retrohyaloidal hemorrhages.
14
Visual acuity in all
cases before laser treatment was hand movement.
After laser treatment, the hemorrhage instantly drained
into the vitreous cavity, resulting in rapid improvement
of vision. After a mean follow-up of 26.3 months no
retinal damage or rebleeding occurred due to the laser
treatment, and vitrectomy was not required in any
eye. However most of the reports lack long term
follow-up. Ulbig et al reported on the the effects of
drainage of premacular subhyaloid hemorrhage into
the vitreous with an Nd-YAG laser in a large series of
21 patients with a circumscribed premacular subhyaloid
hemorrhage of various causes with long-term follow-
up. Even though in 16 eyes visual acuity improved
within 1 month, four eyes had persistent, dense,
nonclearing vitreous opacity for at least 3 months and
finally required vitrectomy. One case with clotted
hemorrhage did not drain into the vitreous. Final visual
outcome was determined by the underlying diagnosis,
such as Valsalva retinopathy (7 eyes), diabetic
retinopathy (7 eyes), branch retinal vein occlusion (4
eyes), and retinal macroaneurysm, Terson syndrome,
or blood dyscrasia (1 eye each). Eyes with Valsalva
retinopathy fared the best. Complications included a
macular hole in 1 eye and a retinal detachment from
a retinal break in a myopic patient. The authors
concluded that drainage of premacular subhyaloid
hemorrhage into the vitreous with an Nd-YAG laser
is a viable treatment alternative for eyes with recent
bleeding, but the risks and benefits have to be weighed
in a randomized trial and compared with those of
deferral of treatment or primary vitrectomy.
Nd-YAG laser has been reported to complete
vitreous hemorrhages in order to achieve vitreolysis
and permit spontaneous resorption of the vitreous
blood.
26
SURGICAL MANAGEMENT
Vitreoretinal surgery is helpful in the management of
subluxation or dislocation of the lens, vitreous
hemorrhage, and retinal detachment caused by ocular
trauma, permitting identification and treatment of
retinal breaks created at the time of blunt injuries
because of the removal of nonclearing vitreous
hemorrhage. Vitreoretinal surgery is also of great value
in the repair of penetrating injuries with retained
nonmagnetic foreign bodies and selected cases of
magnetic IOFB that are difficult or dangerous to extract
with an electromagnet and in the management of eyes
with posttraumatic endophthalmitis. Secondary
complications, including traction and rhegmatogenous
retinal detachments, are minimized by the timely
removal of hemorrhage, disrupted lens, and damaged
vitreous.
Additionally, the presence of vitreous hemorrhage,
as well as delay in IOFB removal, preoperative retinal
detachment and primary surgical repair combined with
the IOFB removal have been significantly associated
with the postoperative retinal detachment and a poorer
visual outcome.
27
The aim of vitrectomy is to remove vitreous
opacities. A standard three-port 25 or 23 G vitrectomy
technique is preferred for nonclearing vitreous
hemorrhage. Initially, a central core of opaque vitreous
is removed, beginning sufficiently close to the lens that
the tips of the cutter and endoilluminator can be
visualized, while maintaining the cutting orifice of the
probe under visual control in order to be able to
examine the aspirated material. The excision is
progressively carried posteriorly until the anticipated
plane of the posterior hyaloid is approached. A small
opening is made in the detached posterior hyaloid,
through which unclotted blood is aspirated by use of
active suction from a soft-tipped cannula. Once the
retina has been visualized, it is best to remove as much
retrohyaloidal blood as possible to prevent dispersion
into the vitreous cavity with consequent loss of visual
control.
Recently opacified vitreous may be red, yellow or
mild green whereas old blood looks brown and dirty.
While removing dense haemorrhagic vitreous we may
find areas with old liquefied blood that may obscure
visualization of the retina. In such cases we should bring
the probe forward in order to be able to visualize its
tip until visualization of the vitreous cavity has become
clearer. Actively bleeding foci in the iris, ciliary body
or retina are treated by raising the intraocular pressure
and using endodiathermy if necessary. If visualization
of the bleeding foci is not possible, a fluid-air
interchange can be performed to permit
endodiathermy and the eye is refilled with liquid in
order to proceed with vitrectomy. Fresh blood tends
to clot and firmly adhere to the retina, whereas old
blood liquefies in a few days and is more easily
aspirated.
Significant vitreous hemorrhages occurring weeks
before surgery are usually associated with sponta-
146
neously detached posterior vitreous. In these cases the
posterior hyaloid is removed. Peripheral, adhered
opacified vitreous can be trimmed using the vitrectome
under scleral depression. This procedure is performed
with the cutting orifice of the probe aiming forward
and taking care to not to damage the pars plana.
If the posterior vitreous cortex is not detached, it
can be separated from the retina by gentle suction
with a soft-tipped cannula at the edge of the optic
disc. The elevated cortex is penetrated with a hooked
needle creating a window through which a pick is
introduced to enlarge the area of cleavage. With the
plane between hyaloid and retina established, the
surgeon attempts to remove the entire cortical vitreous
except for the firmly attached portion at the anterior
vitreous base. Cortex that does not separate with gentle
manipulation is isolated from surrounding vitreous to
eliminate traction on the retina. It is important to
remove the cortical vitreous from areas adjacent to
retinal breaks. Failure to do so may result in subsequent
tangential traction and retinal detachment. A scleral
buckle should be considered if retinal breaks cannot
be freed from surrounding vitreous cortex.
Blood remnants deposited behind the posterior
hyaloid are easily removed using an extrusion tip, even
though they may form whirlpools.
Sclerotomies placed close to the 3 oclock and
9 oclock positions facilitate maximal excision of the
hemorrhagic anterior vitreous skirt improving visuali-
zation of the peripheral retina and pars plana. With
use of coaxial illumination and scleral depression, the
peripheral vitreous on the temporal side of the globe
is trimmed with the cutter placed in the temporal
sclerotomy, reaching both the superior and inferior
quadrants, after which it is transferred to the nasal
sclerotomy, and the process is repeated.
The crystalline lens may be damaged if the fiberoptic
endoilluminator is used internally to illuminate the
peripheral vitreous on the opposite side of the globe.
This may be avoided by directing the cone of light
from the through the cornea to augment or replace
the coaxial light source.
Hemorrhagic retrolenticular vitreous can be
stripped from the posterior capsule of the lens by gentle
aspiration into the cutting port followed by withdrawal
of the probe and simultaneous activation of the cutting
mode, though this procedure may be dangerous in
young children because the retrolenticular vitreous is
adherent to the lens, and may lead to cataract
formation. It is usually preferable to preserve an intact
clear lens than to perform a complete removal of
peripheral and retrolenticular vitreous.
Removal of subretinal bl ood requires the
elimination of the vitreous surrounding the clot. An
extrusion cannula is placed through the retinal tear
towards the surface of the clot. In those cases where
not tear can be detected, endodiathermy is performed
to create a retinotomy in an area that does not affect
much visual function and suction is performed over
the clot. In those cases with organized hemorrhages,
the clot can be removed using an extrusion cannula
and moving the clot to and fro to release adherences
to the RPE, and the clot is carefully removed,
occasionally with the aid of intraocular forceps or the
vitrectomy probe. The retinotomy is later treated by
laser and a gas bubble is injected in order to flat the
retina.
It is necessary to expose as much peripheral retina
and vitreous base as possible in order to be able to
locate retinal breaks caused by ocular contusion. All
retinal breaks should be treated: endolaser is used for
posterior breaks, whereas peripheral breaks are treated
with indirect laser assisted by scleral depression or
transscleral cryoretinopexy. Cryotherapy is preferred
when residual opaque vitreous partially obscures the
targeted break.
Encircling scleral buckles are ususally not necessary
after vitrectomy for nonclearing vitreous hemorrhage
caused by ocular contusion when a clear view of the
fundus periphery reveals no peripheral retinal tears
or signs of traction, such as vitreous base avulsion. A
buckle is usually not needed for treated retinal breaks
without retinal detachment. A local scleral buckle
should be used when there is residual traction on a
posterior break. The peripheral retina should be
supported by an encircling scleral buckle when traction
on breaks in the oral zone persists or the periphery
is poorly visualized because of residual opaque
vitreous.
Patients with penetrating ocular trauma may present
with severe vitreous hemorrhage and associated retinal
detachment. Removing the hemorrhage and repairing
the retinal detachment can be a surgical problem.
Besides the l imited surgical view due to the
hemorrhage, an incomplete separation of the posterior
hyaloid membrane can allow the detached retina to
be drawn towards the port of the vitrectomy
instrument, producing an inadvertent retinal tear.
Perfluoroperhydrophenanthrene (Vitreon) has been
used to manage penetrating ocular trauma with
concurrent retinal detachment and a partial vitreous
detachment, either at the time of surgery or as noted
ultrasonographically. The perfluorocarbon liquid
helped to separate the partially detached posterior
hyaloid membrane and flatten the detached retina
simplifying removal of the vitreous hemorrhage and
management of the retinal detachment.
28
147
Prophylactic treatment of most traumatic retinal
breaks is indicated. Breaks at the point of impact are
one exception because they are frequently self-sealing
and the surrounding necrotic retina and choroid often
unite in a common scar. In those cases when scleral
depression reveals a slight elevation and movement
of their edges and the surrounding retina, prophylactic
treatment is advised. Traumatic macular holes also are
not treated to prevent additional loss of central vision.
They seldom cause retinal detachments when left
alone.
Despite the advanced surgical techniques the
prognosis of massive suprachoroidal hemorrhages
remains guarded and the visual outcome is poor.
29
Massive suprachoroidal hemorrhages following ocular
trauma have been managed by secondary surgical
intervention with radial sclerotomies combined with
vitrectomy, use of perfluorocarbon, and silicone oil.
30
Pre and post operative ophthalmoscopy and B-scan
ultrasonography, as well as visual acuity measurement
are required. In all cases, anatomic restoration of ocular
structures was achieved. Distance visual acuity
improved in all cases (preoperative Snellen visual acuity
ranged from light perception to hand motions;
postoperative Snellen visual acuity ranged from 20/
400 to 20/60) after a mean follow-up period of 17
months.
Another series reported the outcome of
hemorrhagic choroidal detachment with retinal and
adherence of the kissing retina, where surgery was
delayed one to three weeks to allow liquefaction of
the blood clot.
31
All eyes had complete ocular
evaluation including ultrasound, and were treated with
steroids before surgical treatment. The procedure
consisted of anterior chamber fluid infusion, posterior
drainage sclerotomies, and primary total pars plana
vitrectomy with posterior hyaloid removal. Mean
follow-up was 9.4 months. Visual acuity after surgery
improved in all eyes from light perception to 20/60.
One patient without light perception improved to 20/
200. Secondary surgical treatment with combined
radial scl erotomies and vitrectomy shoul d be
considered in order to minimize the damaging effect
and maximize the anatomic and functional restoration.
The natural history of traumatic posterior segment
hemorrhages depends on the underlying cause and
is generally more favorable in eyes without underlying
disease. Ocular hemorrhage may not resolve sponta-
neously and early vitrectomy surgery is necessary and
beneficial, especially in cases where other ocular
damage is involved.
32
New strategies for the treatment
of vitreous hemorrhage, such as pharmacologic
vitreous liquefaction, may be important in the future.
References
1. Fact Sheet. National Society to Prevent Blindness. New
York, 1980.
2. Yeung L, Chen TL, Kuo YH, et al. Severe vitreous
hemorrhage associated with closed-globe injury. Graefes
Arch Clin Exp Ophthalmol 2006;244:52-7.
3. Cleary PE, Ryan SJ. Method of production and natural
history of experimental posterior penetrating eye injury
in the rhesus monkey. Am J Ophthalmol 1979;88:
212-20.
4. Barr CC. Prognostic factors in corneoscleral lacerations.
5. de Juan E, Jr., Sternberg P, Jr., Michels RG. Timing of
vitrectomy after penetrating ocul ar injuries.
6. Brinton GS, Aaberg TM, Reeser FH, Topping TM,
Abrams GW. Surgical results in ocular trauma involving
the posterior segment. Am J Ophthalmol 1982;93:
271-8.
7. Weller M, Fischbach R, Heimann K, Wiedemann P.
[Significance of fibronectins in proliferative retinal
diseases]. Fortschr Ophthalmol 1988;85:263-6.
8. Xu H. [Pathogenesis of traumatic proliferative vitreoretino-
pathy]. Yan Ke Xue Bao 1992;8:80-2.
9. Kuppermann BD, Thomas EL, de Smet MD, Grillone LR.
Pool ed efficacy resul ts from two mul tinational
randomized control l ed cl inical trial s of a singl e
intravitreous injection of highl y purified ovine
hyaluronidase (Vitrase) for the management of vitreous
hemorrhage. Am J Ophthalmol 2005;140:573-84.
10. Wirth MG, Helbig H. Vitreous hemorrhage in children.
Klin Monatsbl Augenheilkd 2006;223:440-2.
11. Manuchehri K, Kirkby G. Vitreous hemorrhage in elderly
patients: management and prevention. Drugs Aging
2003;20:655-61.
12. Chiquet C, Zech JC, Gain P, Adeleine P, Trepsat C. Visual
outcome and prognostic factors after magnetic extraction
of posterior segment foreign bodies in 40 cases. Br J
13. Winthrop SR, Cleary PE, Minckler DS, Ryan SJ.
Penetrating eye injuries: a histopathological review. Br J
Ophthalmol 1980;64:809-17.
14. Celebi S, Kukner AS. Photodisruptive Nd:YAG laser in
the management of premacular subhyaloid hemorrhage.
Eur J Ophthalmol 2001;11:281-6.
15. Ulbig MW, Mangouritsas G, Rothbacher HH, Hamilton
AM, McHugh JD. Long-term results after drainage of
premacular subhyaloid hemorrhage into the vitreous with
a pulsed Nd:YAG laser. Arch Ophthalmol 1998;116:
1465-69.
16. Kroll P, Busse H. [Therapy of preretinal macular
hemorrhages]. Klin Monatsbl Augenheilkd 1986;188:
610-2.
17. Gl att H, Machmer R. Experimental subretinal
hemorrhage in rabbits. Am J Ophthalmol 1982;94:
762-73.
18. Weis A, Kodsi SR, Rubin SE, et al. Subretinal hemorrhage
masquerading as a hemorrhagic choroidal detachment
in a case of nonaccidental trauma. J Aapos 2007;11:
616-7.
148
19. Dolan BJ. Choroidal neovascularization not associated
with age-related macular degeneration. Optom Clin 1996;
5:55-76.
20. Harissi-Dagher M, Sebag M, Gauthier D, et al .
Photodynamic therapy in young patients with choroidal
neovascularization following traumatic choroidal rupture.
Am J Ophthalmol 2005;139:726-8.
21. Laatikainen L, Mattila J. Tissue plasminogen activator
(tPA) to facilitate removal of post-traumatic submacular
hemorrhage. Acta Ophthalmol Scand 1995;73:361-2.
22. Holland D, Wiechens B. Intravitreal r-TPA and gas
injection in traumatic submacul ar hemorrhage.
Ophthalmologica 2004;218:64-9.
23. Chung J, Kim MH, Chung SM, Chang KY. The effect of
tissue plasminogen activator on premacular hemorrhage.
24. Hassan AS, Johnson MW, Schneiderman TE, et al.
Management of submacular hemorrhage with intra-
vitreous tissue plasminogen activator injection and
pneumatic displacement. Ophthalmology 1999;106:
1900-6; discussion 1906-7.
25. Dellaporta AN. Evacuation of subretinal hemorrhage. Int
26. Ivanov AN, Degtiareva EM, Maliuta GD. [YAG-laser
treatment for traumatic hemophthalmia]. Vestn Oftalmol
2007;123:22-5.
27. Erakgun T, Egrilmez S. Prognostic factors in vitrectomy
for posterior segment intraocular foreign bodies. J
Trauma 2008;64:1034-7.
28. Desai UR, Peyman GA, Harper CA, 3rd. Perfluorocarbon
liquid in traumatic vitreous hemorrhage and retinal
detachment. Ophthalmic Surg 1993;24:537-41.
29. Dong X, Yuan G, Wang W. [Surgical treatment of
traumatic suprachoroidal hemorrhage]. Zhonghua Yan
Ke Za Zhi 2002;38:654-6.
30. Feretis E, Mourtzoukos S, Mangouritsas G, et al.
Secondary management and outcome of massive
suprachoroidal hemorrhage. Eur J Ophthalmol 2006;
16:835-40.
31. Quiroz-Mercado H, Garza-Karren CD, Roigmelo EA,
Jimenez-Sierra JM, Dalma-Weiszhausz J. Vitreous
management in massive suprachoroidal hemorrhage. Eur
J Ophthalmol 1997;7:101-4.
32. Simon J, Sood S, Yoon MK, et al. Vitrectomy for dense
vitreous hemorrhage in infancy. J Pediatr Ophthalmol
Strabismus 2005;42:18-22.
C H A P T E R
25
Traumatic Retinal Detachments
Introduction
Traumatic retinal detachment is assuming more and
more importance in present day era of rapid industria-
lization of our country. The role of trauma in the
causation of retinal detachment has been recognised
for long. Coopers (1859) first described traumatic
retinal detachment. Leber
1
in 1916 observed that
ocular contusions played an important role in the
etiology of retinal detachment in 16.18% of cases. All
types of injuries, i.e. ocular contusions, perforating
ocular injuries and concussion injuries to lead can cause
retinal detachment.
Traumatic retinal detachments have been classified
into two groups due to blunt trauma and due to per-
forating trauma. Bl unt trauma rel ated retinal
detachment is more common while the one due to
perforating injury is comparatively rare.
Blunt Trauma Related Retinal
Tears and Retinal Detachments
Traumatic retinal detachment constitute a special group
of retinal detachment on account of certain important
clinical features. Young males and small children are
more vulnerable to ocular trauma because of their
outdoor activities. The commonest type of trauma
responsible for the occurrence of retinal detachment
is in the form of blunt injuries to the eye which
commonly include sports injuries, fist blow injuries and
automobile injuries.
The force of the injury is an important factor in
determining the extent of vitreo-retinal damage and
subsequent formation of retinal breaks. A peripheral
retinal degeneration with associated vitreous traction
is likely to develop retinal break and retinal detachment
following a direct or indirect trauma to the eye. Cases
having risk factors like high myopia, aphakia or fellow
eyes of retinal detachment, are more prone to develop
retinal detachment following a traumatic injury to the
eye. Traumatic injuries to such eyes irrespective of the
nature of trauma needs a meticulous screening of the
peripheral retina to look for the presence of retinal
defects and retinal detachment. These eyes should be
periodically observed even if no vitreo-retinal
pathology is observed in the initial examination soon
after trauma, because there is a latent period between
the time of trauma and the development of retinal
detachment.
2-4.
Traumatic retinal tears development takes place
because of equatorial expansion of the globe. It is
uncommon for a patient to develop an acute
rhegmatogenous retinal detachment after blunt
trauma. Most trauma victims are young with solid
vitreous, providing internal tamponade to the retina
despite retinal tears or dialyses. However, with time
the vitreous liquefies, allowing fluid to form in the
vitreous cavity, which can pass through the retinal
breaks and detach the retinal. The incidence of
traumatic retinal detachments has been found to be
around 20%.Cox
5
studied 160 patients with traumatic
retinal detachments; 60% of these were found to have
oral types of retinal breaks. Another study on post-
traumatic retinal detachments found that 84% of these
were associated with retinal dialyses, 8% with giant
retinal tears, 3% with horseshoe tears, and 5% with
round holes.
Ross
6
evaluated 50 eyes with trauma related detach-
ments and found that myopia was present in 12.5%
of these eyes and 41% of the patients were first
diagnosed more than 1 year after their injury. He
attributed the higher risk of the inferotemporal dialysis
to lack of protection of the superotemporal globe, Bells
phenomenon, and being the weakest point of the
peripheral retina. The associated ocular abnormalities
were vitreous base avulsion, demarcation lines, pars
plana detachments, retinal cysts, vitreous hemorrhage,
angle recession, and traumatic cataracts.
Goffstein and Burton
7
noted that the most common
locations for posttraumatic retinal dialysis (in descen-
ding order) are inferotemporal (27-73%), superonasal
(2-46%), superotemporal, and inferonasal. Retinal
150
dialyses may have a slow progression and onset of
symptoms, as they often occur in young patients
without vitreous syneresis. Thus, the accumulation and
progression of the subretinal fluid is often very slow
and pigmented demarcation lines are often noted.
Goffstein and Burton
7
noted that pathognomonic
features of previous injury include retinal detachments
with superonasal dialyses, large necrotic retinal holes,
and fibrous growth. Cox
5
also noted avulsions of the
vitreous base (virtually pathognomonic for a contusion-
related retinal detachment)and equatorial holes 36%
cases in post trauma cases. Equatorial holes were either
small, round multiple retinal breaks, or were large,
irregular tears with ragged edges. Cox attributed
these larger holes to retinal hemorrhage and necrosis
that occurred at the time of impact.
The anatomic results after scleral buckling surgery
in these eyes are excellent; the overall reattachment
rate is approximately 95%, with 87 to 94% of the cases
reattached after one operation. Good visual outcome
is achieved in most of the cases, as one surgical series
reported a final visual acuity of 20/40 or better in 44%
of eyes, 20/50 to 20/100 in 24% and 20/200 or worse
in 32%.
Traumatic retinal breaks without detachment may
be treated with laser or cryoretinopexy alone. Most
traumatic retinal detachments can be treated with
conventional scleral buckling techniques. Because of
the potential for retinal damage 180 degrees from the
impact site, an encircling element is recommended as
this gives the entire vitreous base support and helps
relieve anteroposterior traction. Principles of scleral
buckling are same as in a nontraumatic detachments.
Johnston
8
reported 77 eyes with retinal breaks after
contusive injury; 65 developoed rhegmatogenous
detachment. Surgical intervention maintained retinal
apposition in 96% of the eyes.
Traumatic Giant Retinal
Tears (GRT)
A giant retinal tear is a tear that extends for 90 degrees
or more of the globe circumference. This tear may
be circumferential or may show radialization and
extension posteriorly. The differentiating feature
between retinal dialysis and giant retinal tears is that
there is a free, mobile posterior retinal flap that may
or may not become inverted posteriorly in the latter.
Preop
Postop
Fig. 25.1: A large HST at edge of a lattice with total retinal detachment produced by blunt trauma. Patient underwent
scleral buckling surgery with intraocular SF6 gas injection. Postoperatively retina is on with good buckle effect
151
Fig. 25.2: Blunt trauma induced macular hole with peripheral HSTs with retinal detachment
Fig. 25.3A: Post Blunt trauma Temporal GRT with posterior extension of GRT edge with bare choroid
Fig. 25.3B: Postop Attached retina with GRT edge covered with old laser marks
Fig. 25.3C: Post traumatic GRT in a high myopic young patient
152
Most cases of GRT are idiopathic and are associated
with a high incidence of myopia. Trauma is the second
most common cause of giant retinal tears (25% of
cases) and many of them have associated myopia. In
traumatic GRTs, there may not be an immediate
accumulation of subretinal fluid or a posterior
inversion of the flap as the vitreous remains solidified
and liquefied over days.
Scleral buckling alone does not suffice for the
management of GRTs as the detachment is large and
also vitreous needs to be removed so as to relieve any
traction on the anterior flap and edges of GRT.
Although these detachments have been repaired
successfully in the past with a variety of scleral buckling
techniques, modern vitreoretinal surgery has signifi-
cantly increased the rat of anatomic reattachment.
The surgical technique used in the repair of
traumatic giant retinal tears include a pars plana
vitrectomy with complete base excision and a low,
broad encircling scleral buckle to support the vitreous
base. A lensectomy may be needed depending on the
amount of cataractous changes or in cases of
subluxated lens or in cases of anterior peripheral GRT.
The perfluorocarbon liquids are an important
intraoperative tool for managing GRTs as it keeps the
posterior retina in place while working on anterior
retina and also allows unfolding of the inverted
posterior flap with the patient in a supine position.
After the core vitrectomy, approximately 0.5 ml of the
perfluorocarbon liquid is injected over the optic nerve
head to unfold and reposition the tear. All traction on
edges of GRT are removed befor putting more PFCL
so as to avoid subretinal migration of PFCL. The
anterior flap of the tear should be removed, as it may
retract anteriorly, causing traction on the ciliary body
or covering it with secondary hypotony or iris
neovascularization. More perfluorocarbon liquid is
injected slowly until the level of the liquid is just posterior
to the margin of the tear. The wide angle systems are
very helpful in giving a panormic view and managing
GRT cases. Indirect laser photocoagulation or
endolaser photocoagulation is done under perfluoro-
carbon l iquid to the margin of the tear. The
perfluorocarbon liquid and silicon oil direct exchange
is done at the end of the case. Aylward and associates
9
reported the results of 38 cases of traumatic giant retinal
tear; 37% were due to penetrating trauma and 63%
to nonpenetrating trauma. Reattachment was achieved
in 89% of the eyes at 12 months follow-up.
Penetrating Injuries-related
Retinal Incarcerations and
Retinal Detachments
There is a frequent failure in localisation of retinal
breaks following penetrating ocular injury on account
of poor visibility of retina due to associated lenticular
opacities, uveitis and/or fibrous tissue changes in the
vitreous. The morphological and functional results after
retinal surgery in traumatic retinal detachment are not
spectacular probably on account of a longer duration
of retinal detachment, frequent macular involvement
and a common occurence of proliferative vitreo-
retinopathy. It would thus be reasonable to understand
that an early diagnosis of traumatic retinal detachment
may have great bearing on the surgical results of these
cases.
Ultrasonography is an important diagnostic tool for
cases where the retinal details are not visible on first
examination, for assessment of the state of vitreous
and retina in such cases.The role of ultrasonography
in such cases is immense and can help design better
management of retinal detachment by indicating
emergency of the treatment of posterior segment
pathology. In cases with intraocular foreign body use
of ultrasonography can be made for detection of
intraocular foreign body and presence or absence of
retinal detachment besides vitreous changes.
PATHOPHYSIOLOGY
Penetrating injuries cause varying amount of initial
mechanical damage. The most important secondary
Fig. 25.3D: Postop fundus photograph showing attached retina with laser marks at edge of GRT
153
change is vitreous contraction and organization due
to nonvascularized intravitreal fibrocellular prolifera-
tion. These changes, in most cases, result from
intravitreal fibrovascular and fibroglial proliferation,
which leads to traction on the ciliary body and the
retina. This proliferation seems to occur more
commonly in injuries with lacerations of the ciliary body
and retina and in injuries with vitreous hemorrhage.
This causes both posterior-to-anterior and circum-
ferential traction on the adjacent peripheral retina.
10,11
The peripheral retina is dragged anteriorly and centrally
and may progress to total traction retinal detachment.
The pathoanatomic changes after penetrating
injuries are observed in both experimental animal
models and human eyes.
10,11
In the rhesus monkey,
a large pars plana wound involving the vitreous gel
and combined with intravitreal injection of blood was
often followed by a marked local inflammatory
response, fibrocellular proliferation, and then cyclitic
membrane formation with secondary tradition retinal
detachment due to contraction of cellular membranes
in the anteroperipheral part of the vitreous cavity.
Ultrastructural study of the fibrocellular membranes
demostrated myofibroblasts, perhaps accounting for
the contractile nature of the proliferative tissue.
12
Serum components fobronectin and platelet-
derived growth factor stimulate cell migration and
proliferation.
13,14
These factors are probably present in
high concentration when dense vitreous hemorrhage
occurs. The trauma may cause breakdown of the
blood-aqueous barrier, and serum components may
diffuse into the damaged viteous gel. Several authors
made these observations in the animal model (1)
occurrence of a posterior vitreous detachment 1 or
2 weeks after the injury and intravitreal blood injec-
tion,
10
(2) a substantial population of myofibroblasts
noted between 12 and 21 days after the injury,
15
and
(3) only minimal fibrous proliferation when the experi-
mental injury was repeated and combined with
intravitreal injection of emulsified lens material rather
than blood.
16
Cleary and Ryan
17
described an experimental
model for penetrating ocular injury with vitreous
hemorrhage. Invariably, a traction retinal detachment
seen clinically after penetrating ocular injuries. In
subsequent studies they demonstrated that vitrectomy
performed at either day 1 or day 14 after injury could
reduce the risk of traction retinal detachment at a
statistically significant level.
18,19
These observations
supported the clinical impression that by removing the
scaffold for intraocular proliferation, vitrectomy may
reduce the incidence of severe visual loss after
penetrating injuries.
SURGICAL PRINCIPLES FOR VITRECTOMY
Vitrectomy for penetrating ocular trauma was first
advocated by Coles and Haik in 1972. There is
considerable disagreement about the appropriate
timing of surgery. Some experienced surgeon favor
operating within the first 48 to 72 hours, and others
prefer delaying surgery for 4 to 10 days or 10 to 14
days after injury.
Delaying vitreous surgery beyond 72 hours after
the injury permits further diagnostic evaluation,
including utralsonography and electrophysiology. It also
permits the operation to be performed under
conditions more favorable than emergency circum-
stances. Occurrence of a posterior vitreous detachment
is important because this makes achievement of the
surgical objectives easier and safer.
In addition, several authors have noted the
problems of severe hemorrhage when attempting early
vitrectomy,
20
presumabl y secondary to uveal
congestion associated with acute penetrating injury.
Hemorrhagic choroidal detachment can accompany
a penetrating injury, which makes it difficult to insert
an infusion cannula or other vitrectomy instruments
properly without damaging the retina. Delaying surgery
may decrease the risk of uncontrollable intraoperative
hemorrhage, as well as allow choroidals to resolve and
making the drainage easier.
First of all, Iris tissue, vitreous gel, and lens material
incarcerated in an anterior segment wound are
reposited or excised by conventional methods, or by
using a vitrectomy probe through a limbal or pars plana
incision. The placement of scleral buckle offsets traction
forces in the anterior periphery that occur despite
vitrectomy and is intended to prevent peripheral
detachment from spreading to involve the posterior
retina. Secondary fibrous proliferation and traction in
the posterior half of the posterior segment are largely
prevented by removing the posterior cortical
vitreous.
21,22
Retinal detachment secondary to retinal incarcera-
tion requires complete relief of the traction at the incar-
certation site.The technique of relaxing retinotomies
was later described by Machemer and associates
23
and
was found to be extremely useful in relieving the
traction at the incarceration, freeing the retina and thus
allowing retinal reattachment. When performing a
relaxing retinotomy for traumatic incarceration, the
retinotomy should be extended onto normal,
nonincarcerated retina to ensure a complete relaxation.
The incarcerated retina, which lies anterior to the
retinotomy, should be completely excised if at all
possible, as this may be a future scaffold for
reproliferation and/or traction of the ciliary body.
Chang and associates
24
have described the use of the
perfluorocarbon liquids to reattach and stablize the
retina while performing the relaxing retinotomy for
anterior retinal incarcerations. The perfluorocarbon
154
liquid is slowly injected over the optic nerve head until
just posterior to the incarceration site, allowing
stabilization and reattachment of the retina. The
relaxing retinotomy is then performed just anterior to
the perfluorocarbon liquid bubble, taking care to avoid
any subretinal migration of the perfluorocarbon liquid.
After the mechanical objectives of vitrectomy have
been achieved, any remaining intraocular foreign
bodies are removed. Foreign bodies are first mobilized
by removing the surrounding vitreous get and lysing
any adhesions to the retina. If an inflammatory capsule
is present, it is incised with a hooked needle or MVR
blade. If the foreign body is small and magnetic, it
can be engaged with a magnet introduced into the
vitreous cavity. The foreign body may be grasped with
forceps in the vitreous cavity with hand shake
technique, after being elevated from the retina with
a magnet.Air fluid exchange is performed to flatten
the retina. Retinal breaks are treated by transscleral
cryotherapy or by endolaser photocoagulation/indirect
laser ophthalmoscope. Most cases require silicon oil
as an intraocular tamponade agent.
Summary
Early diagnosis of retinal detachment in a case of
perforating injury is not easy as these cases invariably
present with lot of anterior segment changes in the
form of corneal edema, hyphema and traumatic
cataract. Retinal detachment associated with per-
forating injuries revealed a younger age group, a
smaller latent period, a poor anatomical and functional
prognosis particularly if there has been gross vitreous
insult after the removal of intraocular foreign body.
Management of traumatized eyes has dramatically
changed over the years. Introduction of newer
microsurgical instruments and techniques has made
possible better care of previously unsalvaged eyes.
References
1. Leber Graife-Saemisch hb.d.ges Augenheilk, 15th ed.
Leipzig 1916;5:693.
2. Schepens CL, Marden D, Amer J. Ophthal mol
1966; 61: 213.
3. Schepens CL. Traumatic retinal detachments : Clinical and
experimental study. In Retina and Retinal Surgery. C.V.
Mosby Company: St Louis, 1969;302.
4. Shukla M, Ahuja OP, Bajaj RP. Proc All Ind Ophthalmol
Soc 1980;38:212.
5. Cox MS, Schepens CL, Freeman HM: Retinal detachment
due to ocular contusion. Arch Ophthalmol 1966;76:678.
6. Ross WH: Traumatic retinal dialyses. Arch Ophthalmol
1981;99:1371.
7. Goffstein R, Burton TC: Differentiating traumatic from
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1982;89:361.
8. Johnston PB: Traumatic retinal detachment, Br J
9. Aylaward GW, Cooling RJ, Leaver PK: Trauma-induced
retinal detachment associated with giant retinal tears,
Retina 1993;13:136.
10. Cleary PE, Ryan SJ: Method of productio and natural
history of experimental posterior penetrating eye injury
in the rhesus monkey, AM J Ophthalmol 1979;88:212.
11. Cleary PE, Ryan SJ: Histology of wound, vitreous, and
retina in experimental posterior penetrating eye injury
in the rhesus monkey, Am J Ophthamol 1979;88:221.
12. Cleary PE, Minckler DS, Ryan SJ: Ultrastructure of traction
retinal detachment in rhesus monkey eyes after a
posterior penetrating ocular injury, Am J Ophthalmol
1980;90:829.
13. Campochiaro PA, Jerdan JA, Glaser BM: Serum contains
chemo attractants for human retinal pigment epithelial
cells, Arch Ophthamol 1984;102:1830.
14. Campochiaro PA, Glaser BM: Platelet-derived growth
factor is chemotactic for human retinal pigment epithelial
cells, Arch Ophthalmol 1985;103:576.
15. Ussmann JH, Lazarides E, Ryan SJ: Traction retinal
detachment. A cell-mediated event, Arch Ophthamol
1981;99:869.
16. Cleary PE, Jarus G, Ryan SJ: Experimental posterior
penetrating eye injury in the rhesus monkey. Vitreous-
lens admixture, Br J Ophthamol 1980;64:801.
17. Cleary, PE, and Ryan, SJ: Method of production and
natural history of experimental posterior penetrating eye
injury in the rhesus monkey, AM J Ophthal mol
1979;88:212-220.
18. Cleary, PE, and Ryan, SJ: Vitrectomy in penetrating eye
injury: results of a controlled trial of Vitrectomy in an
experimental posterior penetrating eye injury in the
rhesus monkey, Arch Ophthalmol 1981;99:287-292.
19. Conway, BP, and Michels, RG: Vitrectomy techniques in
the management of selected penetrating ocular injuries,
20. Abram, GW, Topping, TM, and Machemer, R: Vitrectomy
for injury, Arch Ophthalmol 1979;97:743.
21. Topping TM, Abrams GW, Machemer R: Experimental
double-perforating injury of the posterior segment in
rabbit eyes. The natural history of intraocul ar
proliferation. Arch Ophthamol 1979;97:735.
22. Abrams GW, Topping TM, Machemer R: Vitrectomy for
injury. The effect on intraocular proliferation following
performation of the posterior segment of the rabbit eye,
Arch Ophthamol 1979;97-743.
23. Machemer R, Aaberg TM: Vitrectomy, ed 2, New York,
1979, Grune & Stratton.
24. Chang S, Reppucci V, Zimmerman NJ, et al :
Perfluorocarbon liquids in the management of traumatic
retinal detachments, Ophthamology 1989;96:785.
C H A P T E R
26
Retained IOFB
Introduction
Penetrating ocular trauma with a foreign body is a rare
but serious ophthalmic emergency. Intraocular foreign
bodies (IOFB) can be inert,
20
but often cause serious
damage inside the eye and must be removed promptly.
The final resting place of and damage caused by an
IOFB depend on several factors, including the size,
the shape, and the momentum of the object at the
time of impact, as well as the site of ocular penetration.
In addition to the initial damage caused at the time
of impact, the risk of endophthalmitis and subsequent
scarring play an important role in the planning of the
surgical intervention.
Mode of Injury
Hammering and using power tools are the most
important causes for retained IOFBs. In most of the
cases, tiny metal particles are seen as intraocular foreign
bodies, which often get chipped free while hammering
on metal.
1-3
In a retrospective study conducted on
patients of retained IOFBs,
4
protective safety goggles
were not worn by any of the 235 patients who sustained
intraocular foreign body injuries in this manner. This
study indicates the need to emphasize the value of
safety glasses in health education programs.
Williams and associates
5
compared penetrating
ocular injuries with retained foreign bodies in patients
aged 18 years or less and in adults. The most common
cause of intraocular foreign bodies was a projectile
weapon or explosion (60%) in the younger patients
versus hammering (84%) among the adults.
Clinical Manifestations
A complete examination of both eyes is necessary,
including the visual acuity.
The patient should be carefully questioned about
the circumstances of the injury. The source of the
foreign body, if known, should be considered to
determine the structure and magnetic properties
of the object.
A corneal or scleral entry wound and a hole in the
iris provide trajectory information.
The slit lamp findings may show chemical effects
related to metallic foreign body or exudation
suggestive of infection or hyphema.
The indirect ophthalmoscope through a dilated
pupil may allow direct visualization of the IOFB
and to look for presence of vitreous hemorrhage,
retinal breaks or retinal detachment. Direct obser-
vation of the foreign body is the best method of
localization.
Gonioscopy and scleral depression are not
recommended in an open globe.
Many factors influence ultimate visual recovery.
These include the size, material, and location of the
IOFB; the associated ocular injuries; and the develop-
ment and management of late complications after
IOFB removal.
6,7
Williams and associates
8
studied 105
eyes with retained intraocular foreign bodies and found
that the factors associated with a poor visual outcome
were a wound 4 mm or greater in length, regardless
of location, and an initial visual acuity of less than
5/200.
The most commonly encountered intraocular
foreign body material are iron and copper. Both are
reactive inside the eye and have the potential to cause
significant damage if not removed.
9
Iron can cause siderosis bulbi. Retinal pigment
epithelial cells take up iron and migrate perivascularly
producing a clinical picture resembling retinitis
pigmentosa. Iris becomes brownish resulting in
heterochromia. Iron is also deposited in the dilator
and sphincter muscles resulting in early mydriasis. In
the advanced stage the iris becomes atrophic. Deposi-
tion of iron in the lens occurs initially in the lens capsule
and imparts brownish spots on the anterior lens capsule.
Copper and copper-containing alloys, such as brass
and bronze, may cause chalcosis. Ocular changes are
caused by the affinity of the basement membrances
of ocular structure for copper. Involvement of
156
Descemets membrane results in a Kayser-Fleischer
ring, which appears as a peripheral greenish blue ring.
Deposition in the lens capsule forms greenish blue ring.
Deposition in the lens capsule causes a greenish brown
sunflower cataract. Deposits of copper have been
demonstrated in the internal limiting membrance of
the retina and intraretinal glial tissue.
Localization of IOFB
Thirty-two percent of all intraocular foreign bodies are
located in the anterior segment. Fifteen percent of
intraocular magentic foreign bodies are found in the
anterior chamber, 8% in the lens, 70% in the posterior
segment, and 7% in the orbit as a result of perforation.
When IOFBs are retained, their precise localisation
is important in surgical decision-making. For many
years, the standard technique of localizing of foreign
bodies involved special applications of conventional
radiographic imaging. These methods were inaccurate
and difficult, could cause iatrogenic damage to the
globe, and were not useful in detecting radioluscent
foreign bodies. Now a days, radiographic localization
of intraocular foreign bodies has been replaced by
ultrasonography and CT scan.
Ul trasound B scan can accuratel y l ocal ise
intraocular foreign bodies in majority of cases. The
examination often must be performed gently through
closed lids in open globe. The usefulness of echography
is limited by shadowing caused by highly reflective
surfaces such as air, reverberation artifacts creating by
some intraocular foreign bodies. Ultrasonography is
not accurate in determining whether a foreign body
is intraocular or extraocular or if it is embedded in
the eye wall when the foreign body is located within
1 mm of the sclera.
10
Ul trasound biomicroscopy (UBM), a high-
frequency (50 MHz), high-resolution imaging techni-
que, offers cross-sectional images of the anterior
segment to a depth of 5 mm and is helpful in localizing
aneriorly placed intraoular foreign bodies. However,
B-scan ultrasound cannot be used to assess anterior
segment structures as its resolution is not sufficiently
high.
11-13
CT scan has emerged as the imaging technique of
choice in the evaluation of IOFBs. CT scan can
demonstrate a perforation of the globe and localize
metallic and nonmetalic foreign bodies. The CT scan
also provides valuable information about intraocular
structural alterations, including the presence of a
dislocated lens or choroidal hemorrhage 2 mm sections
on CT scan are able to localize IOFB as small as 0.7 mm
in size. The CT scan is noninvasive and can be
performed on uncooperative patients and easily
identifies multiple foreign bodies.
14-16
It is a noninvasive
technique requiring minimal patient cooperation and
can be used to image radioluscent and radiopaque
foreign bodies. CT scanning does have limitations, in
that metallic IOFBs often create significant scattering
artifact that may obscure their precise location. This
can be particularly bothersome when attempting to
determine whether a foreign body is intraretinal or
intrascleral. In addition, identify some of the lower
density foreign bodies, such as wood, may be difficult
with CT scanning.
17
Magnetic resonance imaging (MRI) has proved
useful for imaging intraocular tumors and other lesions.
However, the magnetic fields and heat generated
during MRI scanning preclude examination of patients
with potential intraocular of intraorbital metallic foreign
bodies. MRIs main role is in accurately and safely
localizing wood and plastic intraocular foreign bodies.
Management
Patient should be put on frequent topical steroid
antibiotic combination drops with intravenous broad
spectrum antibiotics. The management of an
intraocular foreign body begins with primary repair
of the perforated globe. Primary surgery, when
appropriate, must include closure of entrance wounds
and repositioning or removal of incarcerated uvea to
prevent risk of endophthalmitis.
Removal of an IOFB is recommended at the time
of repair of the entry site or soon afterward as soon
as corneal clarity permits. IOFBs cause inflammation
and often are rapidly surrounded by a fibrous capsule
that can make delayed surgical removal more difficult.
Foreign bodies may contain copper, which can cause
immediate severe inflammatory changes, or iron, which
can cause chronic siderotic damage to the eye.
18
In
addition, traumatic endophthalmitis, particularly
associated with the Bacillus cereus, is more commonly
seen with IOFBs than with other forms of penetrating
injuries.
Vitreous hemorrhage associated with an intraocular
foreign body can result in the development of fibrotic
bands that may detach the retina. Tolentino and
colleagues demonstrated in rabbits that vitreous
hemorrhage in the presence of an intraocular foreign
body resulted in a proliferative fibroblastic reaction that
caused retinal detachment and phthisis bulbi. Animals
with intraocular foreign bodies but without vitreous
hemorrhage did not develop these changes. Early
vitrectomy in eyes with foreign bodies and vitreous
hemorrhage

can either prevent or eliminate these
changes before significant intraocular damage has
occurred. In a series by Percival
19
on late complications
157
Retained IOFB
from intraocular foreign bodies, retinal detachment
was present in 42% of patients with vitreous
hemorrhage but onl y 4% of those without
hemorrhage. The incidence of retinal detachment was
only slightly higher if the foreign body was embedded
in the retina rather than lying in the vitreous.
Foreign bodies in the anterior segment of the eye
are usually easy to remove. The pupil should be
constricted before removal is attempted. IOFBs located
in corneal stroma can be removed by cutting down
directly over the foreign body. Magnetic foreign bodies
located in the anterior chamber or on the iris can be
taken out through a limbal incision with a magnet or
foreign body forceps or a toothed forceps.
The posterior segment intraocular foreign bodies
whether magnetic or nonmagnetic should be removed
as their retention may severely damage the eye. Two
types of magnets are used to remove magnetic
intraocular foreign bodies. The Electromagnets are
heavy, bigger in size and exert a substantially stronger
force. These magnets can pull a foreign body at great
speeds, and when misaligned, the foreign body can
strike intraocular structures or the eye wall with
damaging effect. Other type of magnet commonly
used these days are Rare Earth magnets, and their
magnetic pole is located at the tip. The magnetic pull
of these instruments is coaxial with the tip. The pulling
force only affects the magnetic foreign body when the
instrument closely approaches it, which minimizes
unwanted movements of the foreign bodies. Different
tips sizes of rare earth magnets are available which can
be introduced through the 20 gauge sclerotomy
opening.
For posterior segment IOFBs, removal by external
approach may be adopted when a small magnetic IOFB
is present in region of pars plana.
Accurate localization is necessary to mark the
incision point. Conjunctival peritomy is performed and
if necessary, rectus muscles are isolated and looped
with sutures to allow adequate exposure. Either partial
thickness scleral flap or full thickness sclerotomy is
performed. IOFB is removed with help of magnet
(metallic IOFB) or toothed forceps. In most of the cases,
IOFB is difficult to remove with magnet because of
fibrotic strands or encapsulation of IOFB. Shock and
Adams reported good anatomic and visual results
following attempted pars plana external magnetic
extraction in 13 patients with retained intraocular
foreign bodies.
In most of the cases of posterior segment IOFBs,
a primary vitrectomy is indicated when a foreign body
is associated with media opacities, IOFB is in vitreous
cavity or adherent to the retina or vitreous strands or
located intraretinally.

A Standard 3 port vitrectomy is
done.
Figs 26.1A to D: Retained IOFB with traumatic endo-
phthalmitis (A) At presentation: PL +, (B) 1 week after
vitrectomy, IOFB removal and silicon iol injection, (C and D)
At 3 months after surgery
158
Figs 26.2A and B: (A) IOFB impacted superior to macula
in right eye, (B) Postop at 1 monthScar at FB impaction
site BCVA 6/18
Figs 26.3A to C: (A and B) Site of IOFB entry through
sclera, (C) PostopRetina on, Buckle effect
Clear all vitreous strands away from IOFB to reduce
risk of traction on the retina when IOFB is removed.
Retrieval of IOFB done with forceps or magnet. Using
shake hand technique. If IOFB is large then enlarge
sclerotomy circumferentially. Vitreous base should not
extrude through enlarged sclerotomy to reduce risk
of iatrogenic retinal tear formation.
The surgeon must have the foreign body grasped
firmly when removing it through the sclerotomy. If
the foreign body is dropped, it will likely strike the
macula and bring about poor visual consequences.
Injection of l iquid perfl uorocarbon has been
recommended as a means to protect the macula.
Very large IOFB (more than 3 mm size) should
be removed through a limbal incision. Lensectomy is
required in such cases.
IOFB is grasped with a magnet or IOFB forceps
and brought into the anterior chamber. Infusion line
is turned off to reduce iris prolapse.
Second forceps is introduced through limbal incision
to grasp IOFB and extract the IOFBt.Care is taken not
to increase retinal injury site or to create hemorrhage.
Retinal break treatment consists of removing all
vitreous traction, cryopexy or laser photocoagulation
and intraocular tamponade with silicon oil.
A prophyl actic encircl ing scl eral buckl e is
recommended in all eyes receiving vitrectomy for
management of penetrating injuries with IOFB.
Summary
Prognosis in cases of retained IOFBs is dependent on
the location and size of the injury as well as the substance
involved and the time of removal. Overall, patients
159
Retained IOFB
2. Armstrong MFJ: A review of intraocular foreign body
injuries and complications in N. Ireland from 1978-1986.
Int Ophthalmol 1988;12:113-17.
3. Khan D, Kundi N, Mohammed Z, et al: A 6 years survey
of intraocular and intraorbital foreign bodies in the North-
west Frontier Province, Pakistan. Br J Ophthalmol
1987;71:716-19.
4. Trevor-Roper PD: The later results of removal of intraocular
foreign bodies with the magnet. Br J Ophthalmol 1944;
28:361-65.
5. Williams DF, Mieler WF, Abrams GW: Intraocular foreign
bodies in young people. Retina 1990;10(suppl):S45-49.
6. ONeill E, Eagling EM: Intraocular foreign bodies: Indications
for lensectomy and vitrectomy. Trans 1954;38:727-33.
7. Bal l antyne JF: Siderosis bul bi. Br J Ophthal mol
1954;38:727-33.
8. Williams DF, Mieler WF, Abrams GW, et al: Results and
prognostic factors in penetrating ocular injuries with retained
intraocular foreign bodies. Ophthalmology 1988;85:
911-16.
9. Knave B: Electroretinography in eyes with retained
intraocular metallic foreign bodies: A clinical study. Acta
Ophthalmol 1969;100(suppl):1-63.
10. Loffredo A. Cennamo G. Sammartino A, et al: The value of
the association of radiological methods with echographic
examination in the study of intraocular foreign bodies,
Ophthalmologica 1979;179:18-24.
11. . Laroche D, Ishikawa H, Greenfield D, Liebmann J M, Ritch
R. Ultrasound biomicroscopic localization and evaluation
of intraocular foreign bodies. Acta Ophthalmology Scand
1998;76:491-95.
12. Barash D, Goldenberg-Cohen N, Tzadok D, Lifshitz T,
Yassur Y, Weinberger D. Ultrasound biomicroscopic
detection of anterior ocular segment foreign body after
trauma. Am J Ophthalmol 1998;126:197-202.
13. Berinstein DM, Gentile RC, Sidoti PA, Stegman Z, Tello C,
Liebmann JM, et al. Ultrasound biomicroscopy in anterior
ocular trauma. Ophthalmic Surg Lasers 1997; 28: 201-07.
14. Lobes LA Jr, Grand MG, Reece J, et al: Computerized axial
tomography in the detection of intraocular foreign bodies.
15. Gaster RN, Duda EE: Localization of intraocular foreign
bodies by computed tomography. Ophthalmic Surg
1980;25-29.
16. Leone CR Jr. Wilson FC: Computerized axial tomography
of theorbit. Ophthalmic Surg 1976;7(2):34-44.
17. Opilow, HW, Ackerman, AL, and Zimmerman, RD:
Limitations of computerized tomography in the localization
of intraocul ar foreign bodies, Arch Ophthal mol
1986;104:1477-82.
18. Neubauer, H: Ocular metallosis, Trans Ophthalmol Soc UK
1979;99:502-10.
19. Percival SPB: Late complications from posterior segment
intraocular foreign bodies: With particular reference to
retinal detachment. Br J Ophthalmol 1972;56:462-68.
20. De Juan, E, Sternberg, P, and Michels, RG: Penetrating
injuries: types of injuries and visual results, Ophthalmology
1983;90:1318-22.
Figs 26.4A to C: (A,B) Preop photo-red glass IOFBs with
subretinal altered hemorrhage, (C) 2 months postop
following vitrectomy and IOFBs removal vision-6/18
with IOFBs have an excellent prognosis, with 75%
regaining visual acuity of 5/200 or better in one series,
as opposed to only 58% for those patients having a
penetrating injury without an IOFB.
References
1. Behrens-Baumann W, Praetorius G: Intraocular foreign
bodies: 297 consecutive cases. Ophthal mol ogica
1989;198:84-88.
C H A P T E R
27
Penetrating Posterior
Segment Trauma
T Mark Johnson(USA)
Epidemiology
The incidence of open globe injury is estimated at
3/100 000 person years.
1
Open globe injuries have
a bimodal distribution with the highest rates in young
persons and the elderly. The National Eye Trauma
Registry in the US (1985-1991) reported that 83%
of penetrating trauma occurred in men with a median
age of 27 years.
2
The inciting event varies with the demographics of
the study. In a case series of penetrating injuries in
a single a tertiary care US hospital 33% of penetrating
traumas were the result of gunshot wounds and 21%
were secondary to motor vehicle accidents.
1
The
National Eye Trauma Registry in the US (1985-1991)
noted that penetrating eye trauma occurred at home
(28%), workplace (21%), recreational activities (11%)
and associated with transportation (8%).
2
Explosive injuries have a high rate of open trauma.
In a case series of 57 explosive injuries 96% of cases
had open globe injuries and 76% had intraocular
foreign body (IOFB).
3
In a case series of 797 severe
ocular injuries occurring during the war in Iraq (2003-
2005) 438 injuries were open globes including 49
bilateral injuries.
4
Many risk factors for occupational open globe injury
are modifiable. In a case series of work place open
globe injuries from 1994-1998 it was noted that 77%
of patients were not using recommended protective
eye wear and 14% of patients were under the influence
of alcohol.
5
The National Eye Trauma Registry noted
alcohol to be a factor in the injury in 24% of cases
and illicit drug use in 8%.
2
Pathophysiology
Several mechanisms of trauma have been described
in ocular trauma and lead to characteristic patterns
of injury. These include:
Blunt trauma: Blunt trauma leads to compression
of the globe.
6
Anterior posterior compression of
the globe is associated with equatorial stretching
during the initial deformation. This is followed by
recovery resulting in overshoot with anterior
posterior elongation and equatorial contraction.
Finally there is a rebound phase of repeated
oscillations. Globe rupture can result occur at
several points of anatomic weakness including the
limbus, previous surgical wounds and posterior to
the rectus muscle insertions.
Penetrating trauma: The compl ications of
penetrating trauma result from progressive
contraction of vitreous membranes leading to
secondary retinal detachment, ciliary body injury
and secondary hypotony. Vitreous membranes
develop within 2 to 3 weeks of initial trauma. The
membranes often radiate to the initial laceration
site. In a series of 74 eyes with retinal detachment
following penetrating injury showed that the
detachment resulted from contraction of vitreous
membrane at perforation site.
7
Animal models of
penetrating trauma describe the cellular events of
heal ing that l ead to secondary membrane
formation.
8
In the initial phase of healing (3 days)
is characterized by infiltration of the inner aspect
of the wound by leukocytes and macrophages.
Proliferation of fibroblasts from the episclera, uvea
and non pigmented ciliary epithelium follows at
day 6. The fibroblasts proliferate along vitreous
strands and form membranes l eading to
progressive retinal detachment at day 12.
Several factors that influence the healing response
to trauma include the presence of blood and foreign
bodies. Blood and its components contribute the
membrane formation and proliferation. In rabbit models
of trauma autologous blood injection, compared with
saline injections, seems to be critical to development
of secondary vitreous membranes and detachment.
9
Serum derived proteins such as fibronectin may play
161
Penetrating Posterior Segment Trauma
an important role in the stimulation of intravitreal
proliferation. The presence of foreign material also
complicates the nature of the trauma. Foreign bodies
contribute to trauma in the following ways: (1) direct
tissue injury; (2) increased risk of secondary infection
or inflammation and (3) secondary late ocular toxicity
including toxicity caused by oxidative reactions to some
reactive metals (iron, copper).
Classification
1996 OCULAR TRAUMA CLASSIFICATION
10
Term Definition
Eyewall Sclera and cornea
Closed globe No full thickness wound
Open globe Full thickness wound
Rupture Full thickness due to blunt trauma
Laceration Full thickness due to sharp trauma
Penetrating Single laceration
Perforating 2 full thickness lacerations
Intraocular foreign body Retained foreign body
LOCATION
Zone I
Cornea / corneoscleral
Zone II
Anterior 5 mm of sclera
Zone III
More than 5 mm posterior to limbus
Clinical Features
While obtaining history is often critical in the diagnosis
and management of patients it is often difficult to obtain
a clear history in the traumatized patient. This is often
related to factors such as secondary injuries and the
influence of alcohol. The mechanism of injury is impor-
tant to understanding the nature of the ocular injury,
especially the possibility of intraocular foreign body.
Important aspects of the clinical examination
include:
Visual acuity: Visual acuity is an important prognostic
factor
Presence of a relative afferent pupillary defect
Intraocular pressure: The IOP is often low but a
normal or elevated IOP does not rule out rupture
of the globe.
Anterior Segment examination: Occult globe
rupture results from scleral rupture posterior to the
limbus. Anterior segment features suggestive of
occult globe rupture include chemosis and an
asymmetrically deep anterior chamber in the
traumatized eye.
Investigations
Radiology investigations are important in the determi-
nation of the presence of an intraocular foreign body.
Various methods of evaluation include plain film
X-rays and CT scan. CT scan is currently considered the
preferred technique for evaluation of IOFB. It is useful
for imaging radiolucent and radiopaque foreign bodies.
The absorption characteristics of IOFB can be quantified
in Hounsfield units.
11
Wood appears least dense on CT
followed by plastic and then glass. Metallic foreign bodies
all have the same absorption and, therefore, CT scan
cannot differentiate the type of metal present.
Ultrasonography is also useful in evaluating the
traumatized globe. It allows visualization of posterior
segment through opaque media. It can be utilized in
the determination of the presence of posterior vitreous
detachment (PVD), retinal detachment or foreign body.
Management
Successful management of penetrating trauma requires
meeting several specific objectives of management. The
primary objectives are: (1) clear optical media; (2)
prevent future retinal tears and detachment by
removing the vitreous scaffold at the laceration site
and prevent formation of pre retinal membranes and
(3) remove foreign body.
There are several principles of management that
influence the ease of vitrectomy. Water tight primary
repair of globe during primary repair is crucial.
Secondary vitrectomy techniques require that the initial
traumatic wounds be watertight to maintain the
integrity of the globe. The timing of vitrectomy appears
to be important in outcome. Studies suggest that
surgery undertaken within 14 days of trauma reduces
the rate of retinal detachment in experimental
models.
12,13
Surgery at 14 days is technically easier due
to the development of posterior vitreous detachment.
3 port vitrectomy with wide field visualization is the
standard method of management of complex posterior
segment ocular trauma. There are several technical
considerations in surgical repair.
Infusion Port
Intraocular infusion is a key component of vitrectomy
as it is required for maintenance of intraocular pressure
during surgical manipulation. Port should be placed
in healthy sclera and well secured to the globe to
prevent it being disl odged during surgical
manipul ation. Infusion port must be free of
incarceration and able to free flowly in the vitreous
cavity to avoid secondary retinal or choroidal
detachment. Standard 4 mm cannulas are typically
162
adequate, however, longer 6 mm cannulas are
available for cases with anterior vitreous contraction
or choroidal detachments. In cases where the infusion
cannot be visualized initially an anterior infusion in the
anterior segment of limbus can be employed. A 20
gauge needle on a separate infusion line can often
be helpful as an alternate infusion until the pars plana
infusion can be visualized.
Visualization of the Posterior Segment is Essential
Anterior segment hemorrhage should be cleared using
passive washout techniques or cutting instruments.
Corneal management can be difficult in traumatized
eyes. In cases of severe corneal trauma a temporary
keratoprosthesis can be employed. Alternatively
endoscopic visualization systems allow posterior
segment manipulation without need for a clear anterior
segment media. Cataract or traumatic disruption of
the lens may prevent visualization. Lens material can
be removed using the vitrectomy instrument or the
pars plana ultrasonic fragmentation instrument
depending on the density of the lens material. The
decision to preserve the lens capsule for intraocular
lens placement will vary with the nature and complexity
of the trauma. In cases with high risk of vitreous
proliferation complete removal of the lens capsule is
often preferred to avoid leaving scaffolding for
membrane formation. Removal of the lens capsule
should be complete with scleral depression being of
assistance to visualize and remove the peripheral lens
material and capsule.
Vitrectomy
Vitrectomy is accomplished with high speed cutting
instruments. The vitreous of the traumatized eye is
typically blood stained. The appearance of the blood
will vary with the timing of surgery with acute blood
appearing red but older blood having an ochre
appearance. Older vitreous hemorrhage is often
associated with a denser, more congealed vitreous gel
than acute hemorrhages. The objectives during
vitrectomy include: (1) removal of blood to allow
visualization of the retina and (2) creation of a complete
posterior vitreous detachment. Constant visualization
of the vitrectomy port is key to avoiding secondary
trauma, particularly in cases where visualization is
difficult. The vitrectomy port should be anteriorly
oriented and constantly visualized. In cases of extensive
vitreous hemorrhage the surgeon should be constantly
looking for signs of retinal vessels to avoid inadvertent
retinal trauma. In dense hemorrhages exploration of
the vitreous cavity begins centrally and then progresses
peripherally. If the location of the retina is in question,
then posterior dissection is often initiated nasally so
that in case of retinal injury it occurs away from the
macula. PVD creation can be difficult in the eyes of
younger patients. The posterior hyaloid can be
engaged with active suction and elevated. In difficult
cases a bimanual technique employing suction and a
lighted membrane pick can be helpful. The posterior
hyaloid is elevated with the suction instrument and
the pick is used to engage the hyaloid and lift it from
the retinal surface. Vitreous skirt is peeled anteriorly
to the vitreous base and trimmed as much as safely
possible, avoiding anterior retinal injury.
Vitreous Bands
Vitreous bands may appear white and can be dense,
elastic membranes. Vitreous bands lead to secondary
traction on the retina. Vitreous bands can be divided
and truncated with the vitrectomy instrument or
intraocular scissors.
Pre-retinal Membranes
Various techniques of removal of pre-retinal
membranes have been described including vitreoretinal
picks, barbed MVR blades and intraocular forceps.
Subretinal membrane removal is typically only
necessary if the organized bands prevent complete
retinal flattening.
Retinal Incarceration
Retinal incarceration can produce traction on the retina
or prevent complete retinal flattening. Retinotomy is
often required in the management of incarceration.
14
Endodiathermy is placed around the incarceration site
and the retina is divided with intraocular scissors or
the high speed cutter.
Choroidectomy
Anecdotal evidence for removal of devitalized choroidal
tissue at the time of vitrectomy to reduce the rate of
secondary PVR and redetachment.
Foreign Body Removal
The objective of surgery is complete and atraumatic
removal of the IOFB. Methods for removal include
external magnets and direct removal. External magnets
have been used for over 100 years in ophthalmology
for the removal of foreign bodies, however, they have
been increasingly replaced by direct removal techni-
ques. Electromagnetic current is used to draw the
foreign body to the eye wall where it can be removed
via a prepared sclerotomy. Direct removal via direct
visualization is preferred method for IOFB removal,
thus avoiding secondary iatrogenic trauma. Foreign
bodies may be encased in an inflammatory capsule
163
that must be incised prior to removal. Intraocular
magnets and specialized forceps can be used to
manipulate the foreign body and allow extraction
through a limbal sclerotomy.
Retinal Detachment
Once al l traction from vitreous or pre-retinal
membranes is relieved the retina can be flattened. The
retina is flattened with air-fluid exchange or use of
perfluorocarbon liquids. Perfluorocarbon liquid is often
preferable in trauma cases due to easier visualization
of the retina during the application of retinopexy.
Endolaser or indirect laser retinopexy is applied to any
retinal breaks observed.
Scleral Buckle
Encircling scleral buckles support the vitreous base and
may be useful in preventing later retinal detachment.
Animal models of retinal injury with randomized
placement of episcleral buckle at the site of the
laceration suggested that the buckle reduced vitreous
traction and reduced the degree of fibrovascular
proliferation at the injury site.
15
Some studies suggest
that placement of a scleral buckle significantly reduces
the risk of later retinal detachment. A series of eyes
undergoing vitrectomy with and without scleral buckle
suggested that the encircling buckle reduced the rate
of subsequent detachment.
16
27% developed a detach-
ment without a prophylactic buckle compared with
8% that received a prophylactic buckle. Other series
have found that the detachment rate without a
prophylactic buckle was 23% compared to 13% with
a buckle.
17
In a prospective controlled clinical trial of
prophylactic scleral buckle with PPV in patients with
retained IOFB without retinal detachment 28 patients
underwent surgery.
18
Rate of secondary retinal
detachment was 6.6% with prophylactic scleral buckle
and 30.8% without scleral buckle. While suggesting
benefit to prophylactic scleral buckle the results did
not meet statistical significance. In a matched
retrospective series of patients undergoing prophylactic
scleral buckle placement at the time of open globe
repair.
19
19 patients with prophylactic scleral buckle
placement and 19 patients without scleral buckle were
matched by visual grade, zone of injury and
mechanism of injury. Patients with scleral buckle had
significantly better visual outcome (20/270 versus hand
motions). There was a trend towards lower retinal
detachment rate with prophylactic scleral buckle
placement (26% versus 53%) that did not meet
statistical significance. Some series do not suggest a
significant benefit to prophylactic scleral buckle. In a
series of 33 patients with retinal detachment and
vitreous hemorrhage after closed globe injury
underwent PPV/PPL.
20
In a non-randomized
comparative review of 15 patients with prophylactic
scleral buckle and 18 without. No difference in retinal
detachment rate (24% with scleral buckle and 17%
without) was observed.
Perfluorocarbon Liquid
Perfluorocarbon liquids can be useful for manipulation
and stabilization of detached retina. They may also
be useful in the manipulation of IOFB.
21
Silicone Oil
Tamponade is typically required for cases with retinal
detachment. Tamponade can be achieved with intra-
ocular gas or silicone oil. No comparative trials of gas
versus silicone oil in the context of penetrating ocular
trauma exist. the Silicone Oil study excluded patients
with retinal detachment in the setting of prior trauma.
Silicone oil tamponade may be useful in cases of severe
ocular trauma. A case series of 23 patients with IOFB
with placement of silicone oil at the time of initial repair
showed utility.
22
61 % had retinal detachment at the
time of initial surgery. 78% had silicone oil removed
after average of 9.1 months. Complete retinal reattach-
ment was achieved in 83% of eyes. Only 30% achieved
reattachment with one procedure with 70%
developing PVR. Visual acuity stabilized with an average
acuity of 20/640 and 55% achieving better than 20/
400. Another case series of 13 eyes undergoing PPV
after trauma examined the role of silicone oil
tamponade.
23
Cases had lacerations greater than 4 disc
diameters, primary RD greater than 2 quadrants or
persistent intrasurgical hemorrhage. 11 eyes underwent
silicone oil removal at average of 5.8 months with visual
acuity ranging from 20/25 to 20/200. 2 eyes developed
PVR.
Antibiotics
Endophthalmitis is a potentially devastating compli-
cation of penetrating trauma. Antibiotic prophylaxis
seems reasonable though there is little evidence that
clarifies the preferred route of administration or the
true efficacy of these measures.
Complications
ENDOPHTHALMITIS
Epidemiology
Two to seven percent of penetrating injuries result in
culture proven endophthalmitis.
24
164
Risk Factors
The presence of IOFB increases the risk of secondary
infection. A delayed primary repair increases risk of
infection significantly. A 24 hour delay in primary repair
increases the risk of infection from 3.5 to 13.4%.
25
Disruption of the lens also increases the risk of infection
15.8 times.
26
In a case series of 110 eyes in Southern
India with open globe injuries that underwent culture
of aqueous or prolapsed ocular tissue at the time of
injury 56 patients had contamination (42 bacterial and
14 fungal).
27
19 patients developed endophthalmitis
with 18 having initial contamination noted. Multivariate
analysis demonstrated that delayed surgical intervention
greater than 72 hours, uveal tissue prolapse and
corneoscleral laceration were associated with an
increased risk of positive culture.
Etiology
The spectrum of organisms causing post-trauma
endophthalmitis differs from those observed in post-
operative endophthalmitis. Bacillus cereus is often
observed in traumatic endophthalmitis, particularly in
cases of IOFB contaminated with soil. Organisms
observed in one series of post-traumatic endophthal-
mitis include:
28
Staph epidermidis 24%.
Bacillus cereus 22%
Strept 13%
Gram negative 11%
Staph aureus 8%
Fungi 8%
SIDEROSIS
Siderosis results from retention or iron containing IOFB
leading to oxidation and cellular damage. The clinical
features include: iris heterochromia with the affected
eye becoming brownish; a mid dilated, non-reactive
pupil; brown lens deposits; secondary open-angle
glaucoma and peripheral pigmentary degeneration of
the retina associated with vascular sclerosis. A decreased
b wave on ERG is frequently noted.
CHALICOSIS
Chalicosis results from retention of copper containing
foreign bodies. The clinical features include: Kayser
Fleischer ring; blue green peripheral corneal ring;
sunflower anterior subcapsular cataract; refractile metallic
aqueous particles and greenish iris discoloration.
Prognosis
Improvements in surgical management have resulted
in better visual outcomes in patients suffering posterior
segment trauma. Studies conducted between 1952
and 1970 showed that only 6 % of patients with
ruptured globes achieved better than 5/200 visual
acuity.
30
Later studies conducted between 1985 and
1993 found that 36% of patients achieved better than
20/40.
31
Several prognostic factors influence the outcome
of open globe injuries. Poorer initial visual acuity
predicts a poorer outcome. A case series of 453 patients
with penetrating injuries showed that chance of
regaining visual acuity better than 5/200 was 97% if
the initial acuity was better that 5/200 and only 36%
if the initial acuity was worse than 5/200.
31,32
The size
of laceration is also important prognostically with
lacerations greater than 10 mm carrying a poorer visual
prognosis.
31
The location of laceration has been
associated with outcome with more posterior lacerations
having a poorer prognosis, presumably due to more
Fig. 27.1: Right eye of young male following trauma from
a homemade projectile device. Visual acuity was no light
perception at presentation. He underwent primary repair.
Post day 1 acuity was light perception
Fig. 27.2: Left eye of the same patient was light perception
at presentation. The eye underwent primary repair. Day 1
acuity was no light perception. At day 3 the eye became
inflamed and phthsical and underwent enucleation
165
extensive retinal injury. In a series of 453 traumatized
eyes 60% of eyes with lacerations anterior to the muscle
insertions achieved functional vision in comparison to
28% where the lacerations extended posterior to the
muscles and only 4% where the laceration extended
posterior to the equator.
31
The prognostic effect of an
IOFB varies with the size and shape of the foreign body
and the location of injury. In general the presence of
an IOFB does not necessarily indicate a poor prognosis
with approximately 1/3 of eyes in most series achieve
20/40 or better acuity.
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right eye on day 4. Surgery involved vitrectomy, 360
reti notomy and peel i ng of membranes, temporary
keratoprosthesis and corneal transplantation with silicone
oil tamponade. Five years later visual acuity was 20/200
with aphakic spectacles
Fig. 27.4: Fundus photo of the right eye shows attached
posterior pole under silicone oil with extensive laser
166
plana vitrectomy with and without scleral buckling. Retina
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C H A P T E R
28
Traumatic Retinopathies
Scott Pfahler, T Mark Johnson (USA)
Commotio Retinae
The term commotio retinae (latin for retinal contusion)
was coined by Berlin in 1873.
1
ETIOLOGY AND PATHOLOGY
Commotio is primarily observed following blunt ocular
trauma (anterior contra-coup injury). Electrical injuries
have also been described with similar findings.
In both animal and human histological reports, the
areas of retinal whitening have been shown to be frag-
mented outer segment photoreceptors. Later changes
include swelling of photoreceptor inner segments and
breakdown of the outer blood-retinal barrier.
2
Other
pathologic findings include cystic spaces, disruption of
RPE plasma membranes and loss of RPE apical
processes.
3
Experimental models suggest that the outer
blood-retinal barrier is re-established 7 to 14 days post-
injury and that outer segments show evidence of
regeneration. Clinical methods of evaluation of the
foveal cone pigment has suggested impairment at the
time of the acute injury with resolution by 3 months
follow-up visits.
4
CLINICAL FEATURES
Ophthalmoscopic examination reveals an area of retinal
whitening which can be found in both peripheral retina
as well as the posterior pole. If the retinal whitening occurs
in the posterior pole, the term Berlins edema is used.
1
In
both animal and human histological reports, the areas of
retinal whitening have been shown to be fragmented
outer segment photoreceptors. Other pathologic findings
include cystic spaces, disruption of RPE plasma
membranes and loss of RPE apical processes.
3,5
DIAGNOSTIC TESTING
Fluorescein angiography often reveals early hypo-
fluorescence with late leakage, described by Gass as
acute pigment epithelial edema.
6
Recent reports
using OCT have described increased reflectivity at the
level of the photoreceptor outer segments in the area
of retinal whitening
7,8
(Fig. 28.1).
TREATMENT AND PROGNOSIS
The natural history of commotio retinae has shown
to resolve in about 2-3 days, usually with return of
visual acuity. If injury occurs in the macula, reports
of permanent visual loss has been reported.
Traumatic Macular Hole
The first report case of traumatic macular hole
secondary to blunt ocular trauma was reported by
Knapp in 1869.
9
ETIOLOGY AND PATHOLOGY
The mechanism of traumatic macular hole formation
has been thought to be the result of ocular deformation
of the posterior pole at the time of trauma. This appears
to lead to secondary retinal edema with cystoid
changes in the outer retina
10,11
(Fig. 28.2).
CLINICAL FEATURES
Macular holes in patients suffering blunt trauma often
have different features from the more common
Fig. 28.1: OCT of patient with commotio retinae with
increased reflectivity at the level of the photoreceptors
168
Fig. 28.2: OCT of patient with traumatic macular hole
idiopathic macular hole. Given that the pathogenesis
is related to ocular deformation at the time of trauma
rather than abnormal progression of posterior vitreous
detachment a PVD is rarely encountered in these
patients. In one series only 15% of cases had an
associated PVD at diagnosis.
12
Traumatic macular holes are more typically elliptical
with irregular edges. Traumatic holes tend to be larger
in size ranging from 0.2 to 0.5 DD.
12
At diagnosis the
holes are often associated with other features of trauma
including hyphema, commotion retina and vitreous
hemorrhage. Secondary retinal detachment may occur.
Spontaneous closure of traumatic macular holes is well
described. Studies of mERG in patients with spontaneous
closure of traumatic macular holes show improved func-
tion with closure though recovery is often incomplete.
13
In cases with persistent macular hole vitrectomy is
typically recommended. Creation of a posterior
vitreous detachment can be challenging in pediatric
patients. Autologous plasmin has been used as a
surgical adjunct to assist in creation of PVD.
14
Removal
of the internal limiting membrane may be useful to
improving the rate of hole closure though no
comparative studies exist in the context of traumatic
macular holes.
15,16
Surgical closure rates have been
reported to range from 87 to 100%.
14-17
Visual recovery
is variable and is influenced by the underlying ocular
injury. Approximately 50% of patients achieve better
than 20/50 acuity.
18
Choroidal Rupture
Choroidal ruptures can occur after blunt trauma
(compression/contusion injuries). The incidence of this
type of injury is between 5-10% of all blunt ocular
trauma.
19
ETIOLOGY AND PATHOGENESIS
Positioned between the elastic scleral and retina, the
inelastic Bruchs membrane/RPE/Choriocapillaris
complex is susceptible to rupture and tearing.
20-22
Direct trauma can result in contusion necrosis of
the choroid with a rupture oriented parallel to the ora
serrata. Indirect choroidal ruptures result in a posterior
rupture that is concentric to the optic nerve. This occurs
following a compressive force upon the posterior pole
combined with the anchoring effect of the optic nerve.
CLINICAL FEATURES
Typical findings include intrachoroidal, subretinal and
intraretinal hemorrhages. Commotio retinae is often
accompanied with the choroidal rupture.
20-22
Following
choroidal rupture the local area of injury undergoes
bleeding, fibrovascular tissue proliferation and then
RPE hyperplasia. Retinal tissue injury is variable and
can range from no direct injury to full thickness
fibrovascul ar prol iferation with vitreo retinal
proliferation
20
(Figs 28.3A and B).
The most common secondary complication of
choroidal rupture is development of choroidal neovas-
cularization. Reports of CNV following choroidal rupture
have been reported as early as one month post-injury
Fig. 28.3A: Post-blunt trauma patient has acute
subretinal hemorrhage
Fig. 28.3B: Two weeks later clearance of subretinal
blood shows evidence of choroidal rupture
169
to four years later.
23-26
A study of 111 patients with
choroidal rupture showed that older age and macular
choroidal rupture where strongly associated with CNV
formation.
27
Another study identified proximity to the
fovea and length of the rupture as risk factors for
developing CNV.
28
DIAGNOSTIC TESTING
Indocyanine green angiography and fluorescein
angiography may aid in the visualization of ruptures
not seen clinically.
23,24
Optical coherence tomography
may be a useful adjunct in following patients with
choroidal ruptures.
Current options for treatment of CNV associated with
choroidal rupture are thermal laser photocoagulation,
photodynamic therapy, photodynamic therapy with
adjuvant feeder vessel therapy, anti-VEGF intravitreal
injections, submacular surgery. No comparative trials
of therapy exist.
29-32
The visual prognosis associated with choroidal
rupture depends upon the location and the presence
of neovascularization. A long-term study (4 years, 32
eyes) of patients with choroidal ruptures secondary in
the foveal region, juxtafoveal, and extrafoveal regions
had final visual acuities of 20/68, 20/35, and 20/60
respectively over a period of 4.5, 3.5, and 4.4 years.
33
Chorioretinitis Sclopetaria
The term chorioretinitis sclopetaria has been used to
describe chorioretinal injury from high velocity vehicle,
typically a bullet or other high velocity projectile. This
phenomenon was first described by Goldzieher in
1901.
34
Classically these injuries occur following a high velocity
missle injury to the orbit. This has been attributed to
shock waves within the orbit resulting in ruptures of
choroidal and retinal layers with or without hemorrhage.
The projectile does not contact the globe structures.
The proximity to the globe, the size of the projectile
and its velocity may influence the nature of the injury.
Following the initial injury, observational and pathologic
accounts have described a fibrovascular and pigmentary
proliferation with loss of photoreceptors.
35
CLINICAL FEATURES
At the time of the acute injury there is extensive retinal
edema and hemorrhage. The borders of the injury
are often serrated. Due to the extensive fibrosis
associated with this injury, retinal detachment is a rare
occurrence associated with this condition
36
(Fig. 28.4).
No treatment has been described to date. Visual prog-
nosis is dependent upon the location of the injury, with
the worst visual prognosis involving the posterior pole.
Purtschers Retinopathy
The term Purtschers retinopathy was derived from
Otmar Purtschers original description of with multiple
retinal white spots scattered throughout the posterior
pole after trauma in 1912. He suspected that these
white spots were caused by lymphatic extravasations
associated with increased intracranial pressure
associated with head trauma.
37
Purtschers retinopathy arises following severe head
trauma or chest compression without direct globe
injury. It is generally considered to be a rare
phenomenon with the incidence of Purtschers
retinopathy estimated at 0.24 cases per million
population per year in the United Kingdom.
The pathogenesis of Purtscher retinopathy has been
widely debated, possible causes include fat emboli, air
embolization, venous reflux with endothelial swelling,
and severe angiospasm.
38-43,45
A common link between
many cases has been leukocyte aggregation by acti-
vated complement factor 5 (C5a) which can occur in
the conditions mentioned previously. Despite the wide
range of opinions regarding the etiology the apparent
occlusion of capillaries on IVFA suggest an emboli
nature.
40, 43,44
Fig. 28.4: Extensive subretinal hemorrhage and retinal
edema following blunt trauma with a paintball gun
170
CLINICAL FEATURES
Typically findings in Purtscher retinopathy are bilateral
but there have been reports of unilateral cases. Visual
acuity typical ranges from 20/200 to CF with possible
visual recovery to pre-event levels. Findings often
include inner retinal whitening polygonal in shape
which spare areas near the vasculature. Often upon
resolution of the retinal edema/cotton-wool spots, there
is nerve fiber layer dropout, mottling of the RPE in
the involved areas and possible optic atrophy.
45
DIAGNOSTIC TESTING
IVFA findings can vary from staining and leakage of
the vasculature early in the course of the disease to
capillary non-perfusion late in the disease. ICGA can
reveal choroidal hypofluorescent areas.
Some reports suggest high dose corticosteroids as
therapy for Purtshers retinopathy but there are no
randomized trials to evaluate this treatment.
45
Valsalva Retinopathy
Retinopathy caused by a sudden increase in venous
pressure in the retinal capillary network has been
reported. With the valveless nature of the venous
system in the head and neck, increases in abdominal
or intrathoracic pressure can be transmitted to the
head and neck resulting in a sudden increase in the
capillary venous pressure with subsequent retinal
hemorrhage.
46
Reports of this phenomenon have been
associated with the Valsalva maneuver, heavy lifting,
childbirth, motor-vehicle airbags, sexual activity,
choking, vigorous dancing, refractive surgery.
50-54
CLINICAL FEATURES
Visual loss can occur with hemorrhages in the macular
region. Peripheral hemorrhages are often asympto-
matic. More extensive hemorrhages can occur with
sub-internal limiting membrane hemorrhages and the
possibility of breaking through and becoming sub-
hyaloid or vitreous hemorrhages.
47
One published case
report using OCT showed that the anatomic location
was likely sub-ILM.
48, 49
Most Valsalva hemorrhages are minimally symptomatic
and do not require treatment. Many symptomatic
hemorrhages will resolve spontaneously. Treatments
have been described for large subhyaloid hemorrhages
that obscure the macula. Treatment options include
Nd:YAG laser hyaloidotomy, krypton laser membro-
tomy, or vitrectomy with membrane peel.
55,56
The
prognosis in this condition is good, with vision often
returning following resolution of the hemorrhage.
Shaken Baby Syndrome/
Child Abuse
The presence of retinal hemorrhages in a child is highly
suspicious for abuse and non accidental head trauma.
Retinal hemorrhages are a common finding in
childhood abuse cases and are the most common
ocular finding in children with manifestations of child
abuse occurring 11-23% of abused children and 50-
80% of shaken babies.
57
Conversely direct, accidental
head trauma in children rarely produces intraocular
hemorrhages.
58
In a series of 241 infants hospitalized
with subdural hematomas 77.5% of children with
shaken baby syndrome had intraocular hemorrhage
compared with 0% with a history of direct, accidental
trauma.
58
The likely cause of these hemorrhages are the
sudden, severe acceleration/deceleration head and
neck movementts. Children are usually age three or
younger in age.
60
Similar ophthalmic findings have been
described in abused children that are older.
61
Macular
retinoschisis is a characteristic autopsy finding that is
not observed with other forms of head trauma.
62
CLINICAL FEATURES
Involvement of ophthalmologists in the screening for
shaken baby syndrome is of paramount importance.
55 % of non-ophthalmologists involved in shaken baby
cases fail to examine the retina.
59
External signs of shaking
or child abuse may be absent with only retinal
hemorrhages and subdural/subarachnoid hemorrhages
present. In one case series of 75 cases of shaken baby
syndrome 93 % had subdural hematoma, 44 % cerebral
edema and 16 % subarachnoid hemorrhage.
63
Clinical
features include intraretinal, preretinal and sub ILM
hemorrhages (Fig. 28.5).
DIAGNOSTIC TESTING
All cases of suspected abuse need to be evaluated by
a multi-disciplinary team. Neuroimaging is important
due to the frequent association with intracranial
hemorrhage.
Recent studies involving optical coherence tomo-
graphy have shown evidence of vitreomacular traction
171
associated with preretinal blood. In addition evidence
of perimacular folds and hemorrhagic macular retino-
schisis were documented.
64
Management of this condition necessitates prompt noti-
fication of children services authorities in the community
and treatment of underlying retinal hemorrhagic and
neurologic sequelae. In one series of 241 infants 82%
of intraocular hemorrhages resolved within 4 weeks.
58
In cases of premacular hemorrhage that obscure the
visual axis vitrectomy should be considered to reduce
the risk of ambyopia.
Retinal Tears, Retinal Dialysis
and Detachments
In many case series, blunt force trauma causes the
majority of traumatic retinal detachments (70-86%)
The most common age and sex demographic is young
males, who overall account for the majority of trauma
cases.
65-67
A large case series consisting of 160 patients
with retinal detachment showed that signs of detach-
ment manifested within two years of injury in most
cases, however, a wide range exists. 12% of detach-
ments are noted within 24 hours. Some presentations
may be delayed by many years.
68
The pathological mechanism thought to cause
retinal tears and detachments is the rapid anterior-
posterior compression of the globe/vitreous structure
which causes a degree of vitreous base traction and
subsequent retinal tears. If the vitreous has not liquefied
the break may remain stable but if liquid vitreous
accumulates near the break, a future retinal detach-
ment is possible. Animal models of high velocity
projectiles suggest that direct corneal trauma tended to
produce tenting of the nasal retinal while peripheral
trauma produced direct retina effects.
69
High speed
cinematography describes four phases of globe
deformation from high velocity trauma: (1) compression
of the globe with decreased axial length and equatorial
expansion; (2) decompression with an increase in axial
length and a decrease in equatorial diameter; (3)
overshoot with a rebound in axial lengthening and
equatorial shortening and (4) oscillation of small
movement of the eye.
70
Retinal breaks appear to develop
via two mechanisms: (1) vitreous base contraction with
traction on the anterior retina or (2) contusion necrosis
of the retina secondary to direct trauma.
CLINICAL FEATURES
Traumatic retinal detachments differ from routine
rhegmatogenous detachments by the nature of the
pathologic retinal break. Traumatic detachments are
more likely to arise from dialyses (55% of traumatic
detachments versus 5% of rhegmatogenous detach-
ments) or giant retinal tears (16 % of traumatic detach-
ments versus 2 % of rhegmatogenous detachments).
71
Lattice degeneration is much less commonly observed
in traumatic retinal detachment series.
The preferred treatment of retinal breaks and detach-
ments secondary to trauma vary but include laser
retinopexy, cryopexy, pneumatic retinopexy, scleral
buckle, pars plana vitrectomy, or combinations of these
treatments. The prognosis depends up the extent and
duration of the retinal break or detachment.
68
Treatment
options for traumatic retinal dialysis can include laser
demarcation for small inferior temporal dialysis, while
scleral buckling has been shown to be successful in 96-
98% of eyes with trauma associated retinal dialysis .
72-75
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C H A P T E R
29
Management of Endophthalmitis
Pei-Chang Wu, Hsi-Kung Kuo (Taiwan)
Introduction
Endophthalmitis is defined by marked inflammation
of intraocular fluids and tissues. When caused by
microorganisms, endophthalmitis often results in severe
visual loss. The broad categories of endophthalmitis
include postoperative (acute-onset, chronic or delayed
onset, bleb-associated), post-traumatic, endogenous
and miscellaneous, such as intravitreous triamcinolone
associated endophthalmitis, microbial keratitis and
suture removal (Table 29.1). These categories are
important in predicting the causative organism and
guiding therapeutic decisions before microbiological
confirmation.
TABLE 29.1: Classification of endophthalmitis
and most frequent organisms
1. Postoperative
a. Acute-onset: coagulase (-) staphylococci (Staph.
Epidermidis), Staphylococcus aureus, Entero-
coccus species, Streptococcus species, gram-
negative bacteria (Pseudomonas)
b. Chronic: P. acnes, coagulase (-) staphylococci,
fungi
c. Bleb-associated: Streptococcus species, Hemo-
philus influenza, Staphylococcus species
2. Post-traumatic: Bacillus species, Staphylococci
3. Endogenous: Candi da speci es, gram-negati ve
bacteria (Klebsiella pneumoniae), S. aureus
4. Miscellaneous
a. Corneal ulcer perforation: Pseudomonas, Staphy-
lococcus species
b. Intravitreous triamcinolone associated
c. Suture removal associated.
Acute Postoperative
Endophthalmitis
Acute postoperative endophthalmitis is defined as the
occurrence of intraocular infection within 6 weeks after
surgery by the Endophthalmitis Vitrectomy Study
(EVS).
PROPHYLAXIS
In recent evidence-based literature, Cillua et al found
preoperative irrigation with povidone-iodine (PI) to
be a most strongly recommended technique based
on the current clinical evidence (Table 29.2).
1
PI is
a potent antiseptic with a wide spectrum of activity
against both gram-positive and gram-negative bacteria,
fungi and viruses. Antimicrobial activity contributes to
the 1% free iodine released that occurs after contact
with the skin for 30 seconds to 1 minute, and this
effect will last for 1 hour.
2, 3
Iodine penetrates the cell
wall and reacts with amino acids and nucleotides, which
ultimately disrupt the cells protein synthesis. Despite
the wide use of PI solutions as disinfectants in hospitals,
these solution have been reported to be susceptible
to contamination with Pseudomonas cepacia, which
could be passed on to the patient.
4
Preoperative preparation with 5% PI solution
dropped into the conjunctival sac followed by a skin
preparation of 10% PI solution has been recom-
mended.
5
Our retrospective, case-controlled study
found that patients who received 10% PI skin disinfec-
tion combined with 5% PI conjunctival disinfection had
significantly less risk of developing post-cataract surgery
endophthalmitis. However, a modified preparation
TABLE 29.2: Prophylactic methods to prevent bacterial
endophthalmitis after cataract surgery
1
Prophylacitic intervention Clinical
recommended
Postoperative subconjunctival antibiotics C
Preoperative lash trimming C
Preoperative saline irrigation C
Preoperative povidone-iodine antisepsis B
Preoperative topical antibiotic therapy C
Irrigating solutions containing antibiotics C
Intraoperative heparin C
Grade A is considered very important or crucial to clinical
outcome, grade B as moderately important, and grade C is
of questionable use
175
method of 5% PI on both the skin and conjunctiva
has been used in many institutes and for simple ocular
surgery, such as intravitreous injection.
6,7
Caution should
be taken to avoid touching the lid margin and lashes
when the needle is inserted into the eye.
INTRAOCULAR ANTIBIOTICS
Intravitreal antibiotic therapy could reach far greater
intraocular antibiotic concentration than any other
method of administration. It is the main stay of
treatment for infective endophthalmitis. In instances
of instant and prompt treatment required in order to
save the vision, inaccuracies of gram-staining results
and unavailable culture results, broad-spectrum
intravitreal antibiotics covering almost all the gram-
positive and gram-negative bacteria are necessary. A
few selected drugs are currently recommended,
including vancomycin, ceftazidime and amikacin. In
the EVS, the antimicrobial sensitivity profile of amikacin
and ceftazidime was similar at 89% against gram-
negative organism, and all gram-positive cocci were
sensitive to vancomycin.
8
Vancomycin
Vancomycin is the drug of choice for gram-positive
bacteria in acute postoperative endophthalmitis. It is
a bactericidal drug whose primary mode of action is
inhibiting synthesis and assembly of the bacterial cell
wall. It has a strong antimicrobial effect against gram-
positive bacteria, especially Staphylococcus aureus,
Staphylcoccus epidermidis and enterococcus, including
methicillin-resistant Staphylococcus aureus. In
intraocular use, concentrations of up to 2 mg/0.1 mL
have been demonstrated to be non-toxic to the retina.
9
The EVS recommended a dose of 1.0 mg/0.1 mL.
10
The half-life of the drug is reduced in inflamed eyes
and prolonged in normal vitreous.
11
Even in inflamed
eyes, therapeutic levels are still detected up to 72-84
hours after injection. Vancomycin is also cleared more
rapidly in aphakic, vitrectomized eyes.
9, 11
Ceftazidime
Ceftazidime is a third-generation cephalosporin that
has a bactericidal effect by disrupting cell wall synthesis.
Third-generation cephal osporins have strong
antibacterial effects against gram-negative bacilli. They
also have an added effect against Streptococcus
pneumonia, pyogenes and other streptococci.
Cephalosporins have little effect against Staphylococcus
aureus but a strong effect against Pseudomonas
aeruginosa. In contrast to the aminoglycosides,
ceftazidime carries a lower risk of retinal toxicity and
a broader therapeutic index. However, intravitreous
ceftazidime was not evaluated in the EVS and it has
been shown that in-vitro ceftazidime precipitates in
vitreous humor at body temperature, irrespective of
the presence of vancomycin.
12
In clinical studies,
ceftazidime has been demonstrated to precipitate in
inflamed eyes resulting in possible subtherapeutic
concentration. Reconstitution with normal saline as
opposed to balanced salt solution produced less
precipitation. Intravitreous ceftazidime is typically
injected at a concentration of 2.25 mg/0.1 mL.
13
Like
vancomycin, half-life is decreased in aphakic,
vitrectomized and inflamed eyes.
Aminoglycosides
Aminoglycosides have a bactericidal effect through
ionic interaction with the cell surface, energy
dependent uptake phases and binding to ribosomes.
Amikacin has a strong bactericidal effect against aerobic
and facultative gram-negative bacilli. It has a synergistic
effect with vancomycin and other cell wall active
antimicrobials (penicillins and cephalosporins).
Aminoglycosides such as amikacin and gentamicin
have been used for intravitreous injection. Gentamicin
has been reported to cause macular toxicity.
14
Aminoglycoside-induced macular infarction is thought
to result from an increased concentration by the
gravity-induced accumulation of drugs on the macula
in a supine patient. Although animal experiments
15
have shown that amikacin is safer than gentamicin,
a potential for macular toxicity might still exist. Amikacin
has been shown to cause macular infarction with loss
of macular capillaries and pre-retinal hemorrhage.
16-18
The standard intravitreous dose of amikacin is 0.4
mg/0.1 mL. This is the dose used in the EVS.
Pharmacokinetic studies in animals were similar to
vancomycin pharmacokinetics in the vitreous cavity.
However, levels measured 24 hours after injection were
equal to or less than the minimal inhibitory concen-
tration (MIC) for most organisms sensitive to
amikacin.
19
Lower concentrations in the vitreous may
necessitate the need for repeat injections of amikacin
if there is no response. No toxicity has been contributed
to a single injection but repeated injections should be
undertaken with caution due to the possible risk of
macular infarction.
18, 19
Nasal side recumbency for
about 30 minutes might be suggested after intravitreous
injection of amikacin.
Repeated vitreous tapping and injection of
antibiotics, together with pars plana vitrectomy, should
be consider if there is no clinical improvement or if
the condition deteriorates within 48 to 72 hours.
20
176
SYSTEMIC ANTIBIOTICS
The systemic antibiotics that cross the blood retinal
barrier include cefazolin, ceftazidime and cipro-
floxacin.
21-23
In the EVS, intravenous ceftazidime and
amikacin were evaluated, and it was concluded that
these antibiotics did not alter final visual acuity or media
clarity.
10
However, subsequent to the publication, this
conclusion has come under question. First, these two
drugs did not cover the most common micro-organisms
of gram-positive bacteria in postoperative endoph-
thalmitis. Second, intravenous amikacin has little
intraocular penetration. The recommendation against
intravenous antibiotic use was not warranted and might
be based on inadequate data.
Intravenous vancomycin has been suggested as an
alternative therapy to systemic ceftazidime and amika-
cin because of its superior gram-positive coverage.
However, vancomycin penetrates poorly into the
vitreous yielding an inadequate antibacterial effect.
24,25
Oral ciprofloxacin might be an effective drug against
many common infecting organisms causing endoph-
thalmitis.
26
However, older-generation fluoroquino-
lones (ciprofloxacin, ofloxacin and levofloxacin) are
increasingly ineffective against some of the pathogens
most commonly responsible for postoperative
endophthalmitis. In contrast, the newer-generation
fluoroquinolones (gatifloxacin and moxifloxacin) show
promising results; they not only display effective activity
against gram-negative bacteria, as do the older-
generation fluoroquinolones, but also demonstrate
enhanced potencies against gram-positive bacteria.
27
Orally administered gatifloxacin was able to penetrate
into the non-infl amed human eye, and reach
therapeutic levels in the aqueous and vitreous
humors.
28
Gatifloxacin has a broad spectrum of
coverage over the bacteria involved in endophthalmitis.
It also has a low MIC of 90, good tolerability and
excellent bioavailability after oral administration. Oral
gatifloxacin has the ability to achieve rapid, effective
levels in the aqueous and vitreous, with the notable
exceptions of not achieving effective levels against
Enterococcus or Pseudomonas. Gatifloxacin may thus
represent a good adjunctive treatment for certain types
of endophthalmitis.
SUBCONJUNCTIVAL AND TOPICAL
ANTIBIOTIC THERAPY
Subconjunctival and topical antibiotics are often used
to supplement intravitreal injections in attempt to
increase the concentration of antibiotics within the
anterior segment of the eye. Subconjunctival
administration can reach therapeutic concentrations
in the eye, especially in the aqueous humor. However,
conflicting data regarding the intravitreal penetration
after periocular antibiotic injection have been
reported.
29
In addition, subconjunctival injection is
more painful and coul d not be as frequentl y
administrated as topical antibiotics. A risk of macular
infarction when using gentamicin has also been
reported.
14
Of the currently used antibiotics, the third-
generation cephal osporins (ceftazidime and
ceftriaxone) achieve the highest vitreous levels.
Topical application is associated with very poor
vitreous penetration. However, significant intraocular
levels of antibiotics can be achieved with frequent
administration of highly concentrated solutions
30
,
especially if the corneal epithelium has been damaged.
For acute-onset postoperative endophthalmitis, topical
vancomycin (50 mg/mL) with amikacin (20 mg/mL)
or ceftazidime (50 mg/mL) administered hourly is
recommended. This regimen can then be adjusted for
the specific organism after culture and sensitivity results
are available.
STEROID TREATMENT
The early use of corticosteroids, in addition to antibiotics,
reduces inflammation and subsequent retinal damage
in endophthalmitis. Corticosteroid therapy may be
administered topically, intravitreally or systemically. In
the EVS, oral prednisone was used at a dose of 30 mg
orally twice a day for 5 to 10 days.
Intravitreous dexamethasone has been increasingly
employed as an alternative to systemic therapy.
Dexamethasone sodium phosphate is typically used
in an intravitreous concentration of 0.4 mg/0.1 mL.
This is equivalent to 40 mg of oral prednisone.
Experimental studies have shown that intravitreal
dexamethasone has a large safety window and that
it prolongs the half-life of intravitreal vancomycin.
31,32
Triamcinolone acetonide (4 mg/0.1 mL) is more potent
and equivalent to 50 mg of oral prednisone. Recently
it has been reported that intravitreal triamcinolone
combined with intravitreal antibiotics appear to have
TABLE 29.3: Recommended doses of initial management
of infective postoperative endophthalmitis
Route Drug Dose
Intravitreal Vancomycin 1 mg in 0.1mL
Ceftazidime 2.25 mg in 0.1mL
Amikacin 0.4 mg in 0.1mL
Dexamethasone 0.4 mg in 0.1mL
Subconjunctival Vancomycin 25 mg in 0.5mL
Ceftazidime 100 mg in 0.5mL
Topical Vancomycin 50 mg/mL drop q1h
Amikacin 20 mg/mL drops q1h
Systemic Fluoroquinolones 400 mg bid
(oral)
Gatifloxacin
177
a safety profile similar to current modalities, with a
favorable effect on visual recovery and function in acute
postoperative endophthalmitis.
33
VITRECTOMY
Vitrectomy debulks the vitreous cavity, reduces the load
of bacteria and toxins, and makes space for
intravitreous antibiotics. Only core vitrectomy is
recommended, due to fear of causing retinal break
as the vitrector is near to the fragile, inflamed retina
in a cloudy vitreous. In addition, it is always combined
with intravitreous antibiotic injection. The EVS
concluded that immediate vitrectomy was not beneficial
for patients with an initial visual acuity of hand
movement or better.
10
Among patients with initial light-
perception-only vision, it was three times more likely
that a visual acuity of 20/40 or better would be achieved
after vitrectomy. Compl ications of pars pl ana
vitrectomy include infection, bleeding, cataract,
glaucoma and retinal detachment.
In summary, the authors recommend the following
for management of acute postoperative endophthal-
mitis. Noting the patients unusual symptoms, carefully
examining signs associated with infection and a highly
alert mind in the physician are important in early
intervention, especially for immunocompromised and
diabetic patients. It is good to initiate topical antibiotics
and cycloplegics immediately during close follow-up
when there is suspicion of infection. The current choice
of drugs is ciprofloxacin 0.3% or ofloxacin 0.3%. If
infection is strongly suspected, the presenting vision
is important in deciding between a vitreous tap and
vitrectomy in conjunction with intraocular antibiotic
injection. Culture of vitreous fluid from a vitreous tap
or vitrectomy is essential for microbiology sensitivity
patterns. The flow-chart for management of acute
endophthalmitis is shown in Figure 29.1. For
intravitreous antibiotic injection, we prefer intravitreal
vancomycin (1 mg) and ceftazidime (2.25 mg) or
amikacin (0.4 mg) combined with intravitreal dexamet-
hasone (0.4 mg). The rationale and choice of systemic
antibiotics is best left to the treating physician. Systemic
fluoroquinolone is suggested (Tables 29.3 to 29.5).
Chronic Postoperative
Endophthalmitis
There are two different types of chronic postoperative
endophthalmitis, one is caused by Propionibacterium
acnes and the other is caused by fungus. These
microorganisms should be considered especially when
the initial culture result is negative. The culture plates
should be investigated for at least 2 weeks. However,
the culture rate is very low. Polymerase chain reaction
(PCR) detection of bacterial DNA with specific primers
from vitreous samples may prove a useful means of
diagnosing delayed postoperative endophthalmitis.
34
There are two important retrospective studies by
Aldave et al
35
and Clark et al
36
on P. acnes induced
postoperative endophthalmitis. The choice for
intravitreous antibiotic injection is vancomycin (1 mg
in 0.1 mL). However, intravitreous injection of
antibiotics alone is associated with a very high rate
recurrence. Pars plana vitrectomy, partial capsulectomy
TABLE 29.4: Antimicrobial agents: dosages for ophthalmic use
Drug Topical Subconj. Intravitreal Intravenous Oral dosage
(in 0.5ml) (in 0.1ml) dose
Aminoglycosides
Gentamicin 14 mg/ml 20 mg 0.1 mg 1.4 mg/kg q8-12hr
Tobramycin 14 mg/ml 20 mg 0.1 mg 1.4 mg/kg IV, IV, q8-12hr
Amikacin 20 mg/ml 25-50 mg 0.4 mg 7.5 mg/kg q12hr
Cephalosporins
Cefazolin 50 mg/ml 50 mg 2.0 mg 1 g q8h
Cefotetan 3.0 mg 1 g q12h
Ceftriaxone 2.0 mg 1-2 g q8h
Ceftazidime 50 mg/ml 100 mg 2.25 mg 1-2 g q8h
Penicillins
Oxacillin 50 mg/ml 0.5 mg 2 g q4h 500 mg qid
Miscellaneous
Clindamycin 20 mg/ml 15-40 mg 1 mg 600 mg q8h 150-450 mg qid
Ciprofloxacin 0.3% 0.1 mg 400 mg q12h 500-750 mg bid
Gatifloxacin 400 mg bid
Chloramphenicol 5 mg/ml 2 mg 750 mg q6h 250-750 mg qid
Erythromycin 10 mg/ml 0.5 mg 500-1000 mg q6h 250-500 mg qid
Vancomycin 50 mg/ml 25 mg 1-2 mg 1 g q12h
178
IOAB: Intraocular antibiotics
Fig. 29.1: Flow-chart for the manage of acute
postoperative endophthalmitis
TABLE 29.5: Antifungal dosages in ophthalmic use
Drug Topical Subconj Intravitreal Usual intravenous Oral dosage
(in 0.5 ml) (in 0.1 ml) dose
Polyenes
Amphotericin B 2.5-10 mg/ml 300 g 5-10 g/ml 1mg/kg/day
Natamycin 5%
Nystatin 100,000 U/g
ointment
Imidazoles
Fluconazole 2% 400 mg/day
Clotrimazole 1% 5-10 mg 60-150 mg/kg/day
Econazole 1% 30 mg/kg/day 200 mg tid
Ketoconazole 1-5% 200-400 mg/day
Miconazole 1% 5-10 mg 0.25 mg 25 mg/kg/day in
2-3 divided doses
Thiabendazole 4% 25 mg/kg/day
Pyrimidines
Flucytosine 1% 50-150 mg/kg/day
and intravitreous antibiotic injection without intraocular
lens (IOL) exchange are usually successful on long-
term follow-up. For patients with recurrent intraocular
inflammation, pars plana vitrectomy, total capsular bag
removal, intravitreous antibiotic injection and IOL
exchange or removal is a uniformly successful strategy.
Recommended treatment for chronic fungal
endophthalmitis is pars plana vitrectomy and intravitreal
injection of amphotericin B (5-10 g in 0.1 mL).
37
Effective systemic amphotericin concentration is still
unknown. In cases of yeast endophthalmitis (i.e.
Candida species), high doses of oral fluconazole (400-
600 mg/day) are recommended.
38
BLEB-ASSOCIATED ENDOPHTHALMITIS
It is important to distinguish between a localized bleb
infection (blebitis) and true bleb-associated endoph-
thalmitis. In cases of blebitis, topical antibiotics and
subconjunctival antibiotics, such as vancomycin and
ceftazidime, can usually be given in an out-patient
setting.
39
Bleb-associated endophthalmitis is typically
characterized by a delayed onset, more virulent
pathogens and poor visual prognosis. Due to the more
virulent microorganisms (Streptococcus species and
Haemophilus influenzae) and resulting poor visual
prognosis, immediate pars plana vitrectomy, and
intravitreal injection of vancomycin and ceftazidime
are recommended.
40
Topical and systemic antibiotics
(vancomycin and ceftazidime) should be used.
POST-TRAUMATIC ENDOPHTHALMITIS
Due to the initial injury, delay in primary wound repair
and more virulent organisms (Bacillus or Staphylo-
coccus species), post-traumatic endophthalmitis
generally has a worse visual outcome than other
categories. Endophthalmitis caused by Bacillus species
179
is characterized by a rapidly progressive course, ring
corneal infiltrates and, generally, a poor visual
outcome, even with prompt therapy.
41
Prophylactic
intravitreal broad spectrum antibiotic injection
decreases the risk of post-traumatic endophthalmitis.
42
In addition, systemic antibiotics are usual l y
administered.
43
Endogenous Endophthalmitis
Endogenous endophthalmitis is more commonly
diagnosed in immunocompromised and debilitated
patients. Once the diagnosis of endophthalmitis is
suspected, blood or urine cultures should be obtained
and other organ involvement must be sought by
consultation with an infectious disease specialist or
internist. The use of systemic antibiotics is also usually
undertaken.
Candida albicans is the most common organism
causing endogenous fungal endophthalmitis and
Aspergillus species is the second most common fungal
cause.
44
The management of endogenous Candida
endophthalmitis is generally tailored to the clinical
situation. When chorioretinal infiltrates are present with
no or minimal vitreous involvement, systemic therapy
alone is recommended. With moderate or severe vitritis,
or deterioration in spite of systemic therapy, vitrectomy
and intraocular amphotericin B are recommended.
Endogenous bacterial endophthalmitis often is an
initial finding leading to the diagnosis of bacterial
endocarditis, sepsis and liver abscess in Asians. In
patients with diabetes and liver abscess, endogenous
Klebsiella pneumoniae endophthalmitis is endemic in
the Chinese population.
45
It is a very fulminant infection
and often results in poor visual outcome. Prompt
diagnosis and vigorous treatment with intravitreous
injections of vancomycin, amikacin and dexametha-
sone within 24 hours can save the patients eyes and
vision.
46
Systemic antibiotics and intraocular antibiotics
are recommended. Early vitrectomy for endogenous
Klebsiella pneumoniae endophthalmitis might be
beneficial.
47
However, debilitation and confinement in
bed because of the sickness in these patients often
results in it being unlikely that anesthesia and surgery
can be performed in the operating room.
Intravitreous Triamcinolone-
associated Endophthalmitis
Triamcinolone injection has become popular for
treating macula edema in many diseases. Although
some patients appear to have an infectious endo-
phthalmitis, many reports detail a pseudoendo-
phthalmitis that resolves without invasive treatment,
which might be caused by triamcinolone crystal in the
anterior chamber or an inflammatory reaction to the
solvent toxin. Infectious endophthalmitis usually
manifests acutely or subacutely with pain. It was
concl uded that in certain eyes injected with
triamcinolone, the differential diagnosis should include
a sterile, toxic endophthalmitis and it may be
appropriate to observe the patient closely every 8 to
12 hours to determine if the inflammation is worsening
or improving. However, if new symptoms develop
more than several days after injection, infectious
endophthalmitis should be presumed and treatment
initiated immediately.
48
Conclusion
Early recognition of endophthalmitis, together with
appropriate and timely treatment, can often reduce
visual loss.
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C H A P T E R
30
Management of Pediatric
Ocular Trauma
Yog Raj Sharma, Ritesh Gupta, Rajni Sharma (India)
Introduction
Ocular trauma is a leading cause of unilateral blindness
in children. The American Academy of Pediatrics (AAP)
(1987) reported that 66% of all ocular injuries occur in
persons 16 years of age or younger, with the highest
frequency between 9 and 11 years of age. Virtually all
studies of pediatric ocular trauma show a male to female
predominance of approximately 4:1 attributed in part
to boys more frequently choices of sharp and pointed
play objects.
1-6
Sports equipment especially cricket ball,
stones, wooden sticks (Gilli danda),
1
fire-crackers,
2
bow
and arrow,
1
etc. are the items most often implicated.
Pediatric ocular trauma occurs most often during play
that is not supervised by an adult (AAP1987).
Other ocular disorders may be noticed first after
even subtle trauma. An injury may bring to light pre-
existing leukocoria, strabismus or proptosis. Therefore
one should always consider nontrauma etiologies in
the evaluation of injured child.
Caring for children with ocular trauma involves
several distinctive aspects such as:
The possibility of prenatal injuries
Diagnostic challenges due to limitations experienced
during history taking and examination
The developing visual system and the potential for
amblyopia
An orbit that is immature (cosmesis following
enucleation and evisceration)
Predisposition to certain types of trauma (e.g. fire-
crackers or toys related).
Evaluation
HISTORY
Evaluation of ocular trauma requires a thorough
history, preferably from the child. Keep in mind that
a child may fabricate a history if involved in a forbidden
activity when injured. Likewise, parents may withhold
information if they feel that their negligence contributed
to the accident. Some of the key information that needs
to be gathered is given below:
Mechanism of injury
Exact time and place of injury
Visual status before the trauma
Any history of strabismus, congenital abnormalities
ocular surgery, injury, patching or glasses
Childs general medical status before trauma
Childs tetanus immunization status
Loss of vision, floaters or flashes of light.
EXAMINATION
It is important to establish a routine to assure a complete
assessment. Examination of a child who has sustained
ocular trauma is often difficult and frightening for both
the child and the ophthalmologist. Patience, gentle
technique, careful preparation and attention to detail
provide the best outcome for everyone. Noncontact
parts of the examination should be performed first.
No external pressure should be exerted on the globe
at any time during the examination.
If an infant or toddler is extremely uncooperative,
restraining in a papoose board may become necessary.
A wire eyelid speculum may be needed to retract the
eyelids. It should be used only when it is certain that
the globe is not ruptured or lacerated.
Toddlers may be restrained in a position in which
parent and assistant hold the child and the ophthal-
mologist examines the child.
In cases where above measures do not allow
adequate examination, appropriate sedation (e.g.
Chloral hydrate 25-100 mg/kg, p.o.) should be used.
Sedation of the pediatric patient may be complicated
by vomiting, anaphylaxis, seizure, airway obstruction
or cardiorespiratory arrest. Sedation should only be
performed in a facility where the childs vital signs are
monitored and resuscitation and ventilatory equipment
are at hand. It is advisable that an anesthetist or a
pediatrician be present while sedating a child.
182
Visual Acuity
Determination of visual acuity is the single most
important aspect of the ocular examination. Measure
the visual acuity of each eye separately. With a co-
operative child, a Snellen chart, tumbling E , or illiterate
eye chart is used. In younger children, visual acuity
is assessed by fixation and ability to follow target.
Ocular Examination
Estimate visual fields by bringing an object into the
childs view from multiple angles.
Examine the eyelids and lacrimal drainage system
to detect possible injuries. Gently palpate the orbital
rim for any irregularities or crepitus. Examine and
record each pupils size, shape and reaction to light.
Examine the conjunctiva and sclera to identify
lacerations, perforations or foreign bodies.
If an open globe is suspected, examination should
be stopped at this point to prevent further injury to
the eye. A large eye shield or pad and bandage (not
pressure patch) should be applied over the eye. The
remainder of the examination should be performed
under general anesthesia.
Assess intraocular pressure with Goldmann
applanation tonometer, Perkins tonometer, tono-pen
or careful finger tip palpation. Stain the cornea with
fluorescein paper and examine with slit lamp to identify
abrasions. Examine anterior chamber fro hyphema,
hypopyon or other abnormalities. Evaluate the motility
of both eyes after excluding globe perforation. A
dilated fundus exam (with or without scleral depression,
as appropriate), is also essential during the trauma
examination.
Obtain radiologic evaluation for injuries consistent
with orbital fractures or retained foreign body.
Specific Eye Injuries
Common eye injuries in children are discussed below
in brief.
BIRTH TRAUMA
Delivery may be associated with ocular and periocular
injuries.
7
These include lid edema, subconjuctival hemor-
rhage, corneal edema, corneal abrasion, hyphema,
vitreous and retinal hemorrhage. The use of forceps
during delivery increases the chances of injury.
Periorbital Ecchymosis and Edema
Periorbital ecchymosis and edema are present after
birth. One needs to rule out other causes of lid closure
or swelling, e.g. congenital ptosis or conjunctivitis.
Managementin most cases the injury is self limited,
requiring no treatment. Persistent eyelid closure may
produce monocular amblyopia. The patient should
be followed periodically to assess visual development
and presence of astigmatism. Correction of refractive
error may be necessary to prevent amblyopia.
Corneal Damage (Breaks in Descemets Membrane)
Corneal trauma is usually caused by the use of forceps
during delivery. The resulting corneal edema is localized
to the area of the break and usually clears within weeks
without intervention. Although there generally is vision
loss with this condition caused by amblyopia and high
refractive errors,
8
corneal transplantation is usually not
necessary.
Retinal Hemorrhages
Retinal hemorrhages are seen in about 20% of
newborn infants within 24 hours of birth.
9
These
hemorrhages usually resolve quicklyand are seen
in fewer than 3% of infants by day 5 of life. These
are more likely to be seen after forceps or vacuum
extraction deliveries. And are seen in fewer than 1%
of cesarean deliveries.
These should be observed to assure resolution. This
usual l y occurs within a month. Diagnostic or
therapeutic intervention is usually not necessary. Child
abuse should be ruled out if its found after baby is
at home.
EYELID LACERATIONS
Lid lacerations may present with significant disfigure-
ment. Laceration involving medial side of the lid
(Figs 30.1A and B) may damage the lacrimal
drainage system. For superficial lacerations, clean the
wound and surrounding skin with povidone iodine
and irrigate thoroughly with saline, and remove any
foreign material that may still be present. Then apply
an antibacterial ointment and sterile dressing.
For deeper lacerations, suturing with 8-0 silk or
nylon is required. Complicated lacerations require an
oculoplastic surgeon consult. These are lacerations that
have extensive tissue loss or have damaged the lacrimal
drainage system, levator aponeurosis, and/or the
medial canthus tendon.
CORNEAL AND CONJUNCTIVAL FOREIGN
BODIES (FIGS 30.2 AND 30.3A AND B)
Patients can be completely asymptomatic, but generally
foreign bodies cause mild to moderate eye pain
depending on their composition, location, and the
patients pain tolerance. When examining a patient
with a possible foreign body, it is always important to
183
Management of Pediatric Ocular Trauma
Figs 30.1A and B: Lid laceration involving the medial canthal
area. Lacrimal drainage system was unaffected in this patient
Fig. 30.2: Corneal foreign body
inspect the fornices thoroughly and evert the eyelids
to look for occult palpebral conjunctival foreign bodies.
Before removing a corneal foreign body, always
attempt to localize its depth because a penetrating
Figs 30.3A and B: A large foreign body located medial to
limbus. It was found to be superficial and there was no
penetrating trauma
object should be considered an open-globe injury and
co-managed with an anterior segment or corneal sub-
specialist, when available. Superficial corneal foreign
bodies are removed with a moistened cotton-tipped
applicator or with the help of 26G needle after putting
a drop of topical anesthetic solution. Patients may
continue to report the sensation of a persistent foreign
body even after removal of foreign body. This is usually
because of small associated corneal epithelial defect.
After the foreign body is removed, patch the eye for
12 to 24 hours with a topical antibiotic to allow the
epithelium to heal.
SUBCONJUCTIVAL HEMORRHAGE
It can be caused by blunt trauma, forceful sneezing
or eye rubbing. It usually results from breakage of the
fragile conjunctival blood vessels. Whenever a trauma-
tic subconjunctival hemorrhage occurs, a more severe
underlying ocular injury, e.g. an occult scleral perfora-
tion or retained foreign body, etc. should be ruled out.
184
CORNEAL PENETRATION (FIGS 30.4A AND B)
The Seidel test can be crucial in determining whether
the patient has a full- or partial-thickness laceration.
When examining these patients, gentle digital pressure
may enhance the Seidel test and will allow a general
assessment of the IOP if the depth of the laceration
is uncertain.
Fig. 30.4A: Large corneoscleral penetrating wound with
hyphema and iris prolapse
Fig. 30.4B: Prolapsed iris excised and wound repaired
using 10-0 monofilament nylon
TRAUMATIC HYPHEMA
Blunt ocular trauma can disrupt the vessels of iris and
ciliary body resulting in hyphema (blood in the anterior
chamber, Fig. 30.5). Hyphema without history of
significant trauma should raise the suspicion of bleeding
diatheses, leukemia, juvenile xanthogranuloma, iris
neovascularization, retinoblastoma or fictitious history
by the child. During the slit-lamp examination, it is
of the utmost importance to grade the hyphema,
because this will dictate both the management and
follow-up of the condition.
Fig. 30.5: Hyphema
Grading of hyphema
Grade Percentage of anterior chamber filled
with blood
Microscopic Circulating red blood cells only
I < 1/3
II 1/3-1/2
III 1/2- near total
IV Total (eight-ball)
The main goals of treatment are to normalize
intraocular pressure and to minimize the likelihood of
rebreeding. Rebleeding of a hyphema occurs in
5-33% of untreated eyes with hyphema and it typically
occurs 2 to 5 days after the injury (when clot retraction
and lysis are occurring).
10, 11
Complications after
hyphema are more common after rebleeding which
may include corneal blood staining, optic atrophy,
central retinal artery occlusion and peripheral anterior
synechiae. The management of traumatic hyphema
is controversial. But generally hospitalization with
moderate restriction of physical activities is often
recommended. Topical steroids are started to decrease
anterior chamber inflammation. Atropine ointment1%
or eye drops hommatropine 2% is given to keep the
pupil in fixed and dilated position. (Short acting
cycloplegic such as tropicamide is avoided as it may
precipitate rebleeding.) Aminocaproic acid (antifibrino-
lytic agent) can stabilize clot formation at the site of
hemorrhage and thus reduce the incidence of
rebleed.
12,13
It is given as 50 mg/kg, p.o., every 4 hourly
for five days. Commonly encountered side effects are
nausea, vomiting and postural hypotension. It is
contraindicated in pregnant women.
185
Surgical drainage of hyphema is indicated if:
1. To prevent optic atrophy:
If IOP is more than 50 mm Hg for 5 days.
2. To prevent corneal blood staining I eyes with a large
hyphema:
If there is any indication of blood staining.
3. To prevent peripheral anterior synechiae.
If total hyphema persists for 5 days.
Various surgical techniques have been described
to remove the blood. These include paracentesis,
anterior chamber washout with one needle irrigation
or irrigation-aspiration technique and clot evacuation
with a forceps. Automated hyphemectomy
(Figs 30.6A to C) using vitrectomy instruments
inserted through limbal incisions permits controlled
removal of blood in the anterior chamber.
14, 15
TRAUMATIC CATARACT
It can be caused by both blunt and penetrating trauma.
Blunt ocular trauma typically leads to stellate or rosette-
shaped opacification which is usually axial in location
and involves the posterior capsule. In perforating
trauma, direct compromise of the lens capsule by
penetrating object leads to cortical opacfication at the
site of injury. If the perforation is small, then it may
get sealed off and cataract remains localized whereas
if the capsular tear is large, the entire lens can rapidly
opacify.
Primary cataract extraction is indicated if there is
obvious capsular rupture with lens matter in anterior
chamber (Fig. 30.7) or when there is posterior
segment injury (retinal detachment, endophthalmitis
or intraocular foreign body) and the cataract disallows
the proper management of these conditions. In all
other cases, cataract surgery is deferred so that
intraocular inflammation and hemorrhage subsides.
The anterior approach (scleral tunnel or limbal or
corneal incision) is the method of choice for cataract
surgery. It should preferably be done by phaco-
emulsification with or without IOL implantation. This
should be followed-up by rapid employment of optical
correction and occlusion therapy to prevent amblyopia
if the child is less than 8 years old.
VITREOUS AND RETINAL CONDITIONS
That can be caused by trauma are as follows:
Intraocular Foreign Body
Intraocular foreign body (IOFB) should be considered
for all high-velocity ocular injuries, particularly those
resulting from metal-on-metal activities.
Figs 30.6A to C: Hyphemectomy using vitrectomy
instruments
One should particularly look for a self-sealing
penetrating wound, iris hole, lens opacities, shallow
anterior chamber, or low IOP in suspected IOFB cases.
In many cases, IOFB can be identified by slit-lamp
biomicroscopy or indirect ophthal moscopy
(Fig. 30.8). However, if the media is hazy or if foreign
body is suspected but not visualized, imaging
186
Fig. 30.7: Traumatic cataract with rupture of anterior
capsule and lens matter in anterior chamber
modalities are necessary. CT scan has emerged as the
imaging modality of choice to rule out IOFB. Modern
spiral CT scanning with 1mm cuts is effective in
detecting a 0.5 mm metallic, glass or stone in 100%
of cases.
16
MRI is contraindicated if a metallic foreign
body is suspected.
Endophthalmitis occurs in up to 48% of eyes with
an IOFB injury and only the timing of surgery (>24
hours) and the type of FB (e.g. wood) are associated
with higher rates. The clinical findings include retinal
periphlebitis, marked anterior chamber reaction or
hypopyon, and severe vitreal inflammation.
Metallic IOFBs can cause toxic retinal metallosis,
but even inert IOFBs can cause proliferative vitreo-
retinopathy and/or debilitating ocular inflammation.
The treatment is prompt surgical removal via pars plana
vitrectomy (with or without lensectomy) involving
magnetic and/or forceps assisted IOFB removal.
Fig. 30.8: Foreign body impacted in retina temporal to fovea
Commotio Retinae
Commotio retinae is also known as Berlins edema or
concussion edema. It is caused by blunt trauma (a
contrecoup injury), with the force being transmitted
through the vitreous and finally onto the retina and
choroids. With this condition, there will be a confluent
area of retinal whitening due to outer photoreceptor
disruption and RPE damage, but not edema. Blood
vessels are seen distinctly and are undisturbed under
the retinal whitening. The retinal opacification gradually
subsides over several weeks and visual function usually
returns to its pretrauma level. However, a permanent
loss of vision is not unusual and can be associated with
changes in the retinal pigment epithelium.
Choroidal Rupture
Choroidal rupture is detectable as a yellow or white
crescent-shaped subretinal streak that is often
concentric with the optic nerve. The rupture can be
single (Fig. 30.9) or multiple and may be obscured
for several days to weeks by overlying pre- or sub-
retinal hemorrhage. Patients with this condition are at
a greater risk for developing a choroidal neovascular
membrane, so they should be followed every 3 to 6
months. They should also be instructed to monitor
their vision daily with an Amsler grid and to report
any significant changes.
Fig. 30.9: Post-traumatic choroidal rupture
with macular hole
Retinitis Sclopeteria
Retinitis sclopeteria or chorioretinitis sclopeteria is a
rare condition in which the patient sustains both a
choroidal and retinal rupture. It is a concussive injury
to the posterior segment and results from shock waves
produced by orbital penetration of a high-velocity
object. The object does not penetrate the sclera but
187
ruptures the choroid and retina in the area adjacent
to its path. The visual acuity is almost always poor.
This condition occurs when a high-velocity object grazes
the globe, but does not rupture the sclera. Patients
with retinitis sclopeteria require a prompt retinal consult
because surgical intervention may be necessary.
Traumatic Macular Hole
Traumatic macular hole (Fig. 30.10) is clinically similar
to the idiopathic variety in appearance. It can follow
commotio retinae, subretinal hemorrhages and cystoid
macular edema. Postcontusion necrosis may result in
macular edema and macular cyst formation. Over
months to years, rupture of cyst layer/s can lead to
formation of lamellar or full thickness macular hole.
Acute lamellar or full thickness macular hole is usually
caused by contrecoup vitreofoveal traction.
Fig. 30.10: Post-traumatic large macular hole
Pars plana vitrectomy with removal of internal limi-
ting membrane (ILM) and gas/ silicon oil tamponade
has been found to be successful (anatomical closure)
in more than 90% of cases.
17
Visual improvement has
been reported in 69-94% of cases.
17-19
Surgical adjuvant
such as autologus plasmin enzyme may improve the
rate of anatomic success
20
. However, because a
significant number of cases of traumatic macular hole
may close spontaneously, it may be wise to just follow
up these patients for initial 3 months or so.
Traumatic Retinal Detachment
Traumatic retinal detachment (RD) (Fig. 30.11) is a
rhegmatogenous detachment that can be caused by
retinal dialysis or a retinal tear. B-scan ultrasonography
is necessary to rule out an RD if media is hazy and
one is unable to visualize fundus. When appropriate,
utilize scleral depression after trauma to help rule out
retinal dialysis.
Fig. 30.11: Post-traumatic retinal detachment
with early macular pucker
A patient with a macula-on RD (i.e. the macular
region of the retina is intact) should receive a retinal
consultation and undergo surgery within 1 to 2 days
of diagnosis. These patients should be confined to bed
rest until surgery. A macula-off RD (i.e. the macular
region has detached) is less urgent and these patients
should have a retinal consultation and surgery within
approximately one week.
Childrens lack of cooperation with postoperative
positioning influences the surgeons decision during
retinal detachment surgery. Its very difficult to separate
the nondetached posterior hyaloid in pediatric eye;
nonetheless, vitreous removal should be as complete
as possible as leaving behind the posterior hyaloid
increases the risk of proliferative vitreoretinopathy.
Plasmin may have a future role in these cases. Silicon
oil is preferred over gases as tamponading agent as
former requires minimal positioning and immobility.
Child Abuse
Child abuse must always be considered in a child
younger than 3 years of age who presents with
intraocular hemorrhages, cataract or subluxated lens,
retinal detachment or retinischiasis, or periorbital
ecchymosis. The ocular findings in shaken baby
syndrome may occur without any obvious external
injury. Retinal hemorrhages have been described in
shaken baby syndrome in which repeated acceleration
and deceleration is supposed to damage intraocular
and intracranial blood vessels and thereby results in
intraocular and intracranial hemorrhage. Typically the
retinal hemorrhages are bilateral, but may be
asymmetric or even unilateral. Other causes of retinal
188
hemorrhage such as leukemia, accidental trauma,
leukemia, thrombocytopenia, anemia, etc. should be
ruled out. Severe visual morbidity with shaken baby
syndrome may be due to retinal detachment, optic
nerve atrophy or cortical blindness.
Eye Injury Prevention
The vast majority of eye injuries are preventable. Key
components of prevention incl ude parental
supervision, education of children and protective
eyewear. Ophthalmologists and parents must reinforce
the importance of not playing with objects like
gillidanda, fire-crackers and bow and arrow. Health
education on the preventive aspects of ocular trauma
in schools as well as through mass media like television
can help in achieving this goal.
Protective eyewear is the most important measure
to prevent eye injuries in children. Plano polycarbonate
goggl es with a 2-3 mm center thickness are
recommended for sports.
Summary
Ocular trauma is an important cause of monocular
blindness in children. Due to young age, inability to
cooperate with examination and the potential for
development of amblyopia, children presenting with
eye injuries are evaluated and treated slightly differently
from adults. Proper communication should be
maintained between the ophthalmologist and family
throughout the course of treatment.
References
1. Jaison SG, Silas SE, Daniel R, Chopra SK.A review of
childhood admission with perforating ocular injuries in
a hospital in north-west India. Indian journal of
ophthalmology 1994;42(4):199-201.
2. Sarda RP, Mehrotra AS, Ratnawat PS, et al. Ocular injuries
in childhood. Indian J Ophthalmol 1971;19:67-70.
3. Niiranen M, Raivio I. Eye injuries in children. Br J
Ophthalmol 1981;65:436-38.
4. Moreira CA Jr, Ribeiro MD, Belfort R Jr. Epidemiological
study of eye injuries in Brazil ian chil dren. Arch
Ophthalmol 1988;106:781-84.
5. Rapoport I, Romem M, Kinek M, et al. Eye injuries in
children in Israel. A National Collaborative Study. Arch
Ophthalmol 1990;108:376-79.
6. Canavan VM, OFlaherty MJ, Archer DB, et al. A ten year
survey of eye injuries in Northern Irel and. Br J
Ophthalmol 1980;64:618-25.
7. Holden R, Morsman DG, Davidek GMB, OConner GM.
External ocular trauma in instrumental and normal
deliveries. Br J Obstet Gynecol 1992;99:132.
8. Angell LK, Robb RM, Berson FG. Visual prognosis in
patients with ruptures in Descmets membrane due to
forceps injury. Arch Ophthalmol 1981;99:21-37.
9. Sezen F. Retinal hemorrhages in new born infants. Br J
Ophthal 1970;55:248.
10. Volpe NJ, Larrison WI, Hersh PS et al Secondary
hemorrhage in traumatic hyphema. Am J Ophthalmol
1991; 112: 507-13.
11. Thomas MA, Parrish RK, Feuer WJ. Rebleeding after
traumatic hyphema. Arch Ophthalmol 1986 Feb;
104(2):206-10.
12. McGetrick JJ, Jampol LM, Gol dberg MF, et al .
Aminocaproic acid decreases secondary hemorrhage
after traumatic hyphema. Arch Ophthalmol 1983 Jul;
101(7):1031-33.
13. Kutner B,Fourman S, Brein K Aminocaproic acid
reduces the risk of secondary hemorrhage in patients
with traumatic hyphema. Arch Ophthalmol 1987 Feb;
105(2):206-08.
14. Stern WH, Monclal KM. Vitrectomy instrumentation for
surgical evacuation of total anterior chamber hyphema
and control of recurrent anterior chamber hemorrhage.
Ophthalmol Surg 1979; 10: 34-37.
15. McCuen BW, Fung WE. The rol e of vitrectomy
instrumentation in the treatment of severe traumatic
hyphema. Am J Ophthalmol 1979;88:930-34.
16. Dass AB, Ferrone PJ, Chu RY etal. Senstivity of spiral
computed tomography scanning for detecting intraocular
foreign bodies. Ophthalmology 2001; 108: 2326-28.
17. Kuhn F, Morris R,Mester V, et al. Internal limiting
membrane removal for traumatic macular holes.
Ophthalmic Surg Lasers 2001 Jul-Aug;32(4):308-15.
18. Amari F, Ogino N, Matsumura M et al. Vitreous surgery
for traumatic macular holes. Retina. 1999; 19(5):410-13.
19. Chow DR, Williams GA, Trese MT et al. Successful closure
of traumatic macular holes. Retina 1999;19(5):405-09.
20. Margherio AR, Margherio RR, Hartzer M et al Plasmin
enzyme-assisted vitrectomy in traumatic pediatric macular
holes. Ophthalmology 1998 Sep;105(9):1617-20.
C H A P T E R
31
Management of Blunt
Retinal Trauma
Introduction
As part of the ocular traumatology, the damage caused
by an impact directly or indirectly to the retina, can
be smooth, and with total visual recovery, or in some
other cases, can cause a severe visual impairment, with
tremendous consequences for the life of the patient.
The visual prognosis after ocular trauma depends
on a number of factors; a large proportion of eyes
with severe and irreversible visual loss due to trauma
almost always exhibit posterior segment injuries. These
injuries lead to vitreoretinal complications that may
occur immediately, days, weeks, or even years after
the initial trauma. Recent advances in microsurgical
techniques, as well as an improved understanding of
the pathophysiol ogy of these vitreoretinal
complications, may minimize the visual loss, even in
the more severely affected eyes. Therefore, although
prevention remains the ultimate goal, the adequate
diagnosis and state of the art management of
posterior segment injuries are important factors in
reducing the magnitude of visual loss in injured eyes.
If well the traumatic lesions to the posterior segment
of the eye too often are not alone, it means that an
ocular trauma is able to cause damage in many other
structures of the globe, we will try in this chapter, to
establish didactic classifications in order to cover the
broad spectrum of possible lesions, and so improve
the clinical evaluation, allowing the physician, to decide
an adequate option of treatment for each particular
patient.
We have also to remember, that very often the
impact to the retina, in particular in cases of blunt,
trauma is not frequently a direct impact, it is a result
of the transmission of forces inside the eye, and the
wave of impact goes frequently from the anterior
segment, to the posterior segment of the eye; the
implications of this physical concept are that sometimes
the damage caused in the retina not always correlate
with the force of the impact and the mechanism of
trauma; this can lead to underestimate the damage
in cases of minor trauma. Maybe this is the first concept
that the attending surgeon must keep in mind when
observing and evaluating a traumatized eye.
In this order of ideas, the possibilities are enormous;
blunt ocular trauma, orbital trauma and systemic
trauma may cause a variety of posterior segment
abnormalities (our matter in this chapter); trauma may
cause damage to the retina (commotio retinae), retinal
pigment epithelium (retinal pigment epithelial edema),
choroid (choroidal rupture) and optic nerve (optic
nerve evulsion) alone or in combination; traumatic
macular holes and retinal detachment or dialysis;
trauma to the orbital tissues adjacent to the globe can
cause concussive forces with damage to multiple
structures within the eye (chorioretinitis sclopetaria);
systemic trauma may result in diffuse retinopathy
(Purtschers retinopathy, shaken baby syndrome) or
localized retinal abnormalities (whiplash retinopathy,
fat embolism syndrome). Alterations in intravascular
(Valsalva retinopathy) or intracranial pressure (Tersons
syndrome) due to a variety of causes may result in
preretinal or vitreous hemorrhage and associated visual
loss.
The purpose of this chapter is to review the
mechanism of posterior segment injury in blunt
trauma, the initial evaluation and a perspective of some
of the most important entities involved in the trauma
to the posterior segment.
Mechanism of Damage in
Blunt Trauma
The transfer of blunt forces to the globe is the
mechanism seen in the majority of ocular injuries. Even
in high-speed projectile injuries, in which the
mechanism of injury is primarily due to penetrating
or sharp forces, associated blunt forces are involved.
Blunt forces involve the posterior segment in several
ways:
190
First there is direct contusion tissue damage at the
site of impact. This is known as a coup injury, and
includes retinal edema, necrotic changes, and
choroidal hemorrhage at the site of impact.
Second, injury can occur distant from the impact
site as the force is transferred through the globe
to a contralateral site. This is called the contracoup
injury; examples of it include retinal edema and
choroidal contusions in the posterior pole; in these
lesions the posterior pole was not impacted directly,
but the transmission of forces affect it in different
degree.
Finally, there are injuries caused by the globe
deformation; some authors have documented by
high-speed cinematography, globe deformation
following the application of blunt forces to the
cornea. In these movies we can see initially how
the anteroposterior axis is compressed; then the
anteroposterior axis is decompresses and so a
rebound expansion occurs. Then the equatorial
axis begins to expand as the anteroposterior axis
compresses but doesnt reach maximum expansion
until after the anteroposterior axis begin its rebound
decompression. This tremendous change of intra-
ocular forces of compression and decompression
within different axis of the globe, creates shearing
forces within the eye at tissue interfaces that are
especially concentrated at the vitreous base.
Choroidal rupture, vitreous base avulsion, iris root
disinsertion, retinal dialysis and tears, and posterior
vitreous separation are examples of injuries caused
by these shearing forces.
After reading this, the clinical comprehends that
he must be aware of damage caused by ocular blunt
trauma at any site of the eye; so a complete evaluation
of all structures is mandatory, even in case of an
pretended minor trauma.
Initial Evaluation
Proper identification and management of patients with
posterior segment injury begin with a systematic
approach to obtaining a complete history and conduc-
ting a thorough ophthalmic examination. The reader
will be able to see more details in some other chapters
of this book, but some important points will be
featured regarding the posterior segment blunt trauma;
because open and closed globe injuries are approached
differently it is important for the ophthalmologist to
make this determination as soon as possible.
The circumstances surrounding the trauma are
important and should be obtained directly from the
patient and/or an eyewitness in particular if the patient
is unable to communicate. Even in cases in which the
globe status is obvious, careful documentation of these
circumstances, as well as the use and type of safety
glasses or other protective devices, has medical and
legal relevance. The history should determine the
preinjury ocular status and the possibility of extraocular
trauma; the ocular baseline should include preinjury
vision, refractive status (myopic eyes are affected with
more severity with minor traumas), preexisting ocular
diseases (e.g. retinal diseases, pseudoexfoliation,
glaucoma), and previous ocular surgery (e.g. cataract,
retinal surgery). The note of circumstances that should
raise suspicions of open globe injuries is mandatory,
high-speed projectile injuries, use of power tools, high-
speed grinding of metal, leak from high-pressure
hydraulic system, metal-on-metal impact, sharp
penetrating injuries and severe blunt injury (racquetball
or golf ball, stick or bat injury to orbit).
Individual Pathologies Description
COMMOTIO RETINAE
Definition and Clinical Findings
Commotio retinae is also known as Berlins edema, but
the latter term is not completely appropriate. The clinical
characteristic of this condition is a confluent area of
retinal whitening due to outer photoreceptor disruption
and RPE damage, but not edema. Blood vessels are seen
distinctly and are undisturbed under the retinal
whitening. Commotio retinae resul ts in retinal
opacification following blunt trauma. Mild commotio
retinae usually settles spontaneously with minimal
sequelae but more severe cases are associated with visual
loss. Commotio retinae can occur anywhere in the
retina, but it is usually maximal in the area opposite to
the blow (countracoup injury). So, explaining the
pathophysiology of the condition, the retinal changes
are caused by a contrecoup that is created by blunt
trauma, with the force being transmitted through the
vitreous and finally onto the retina and choroid
(Figs 31.1 and 31.2).
Histopathology
Immediately after injury, the only abnormality is
disruption of the receptor outer segments. From one
to six days after trauma, many receptor cells undergo
degeneration. The retinal pigment epithelium phago-
cytoses the degenerating outer segments, occasionally
migrating into the retina. There is no extracellular retinal
edema. The opacity of commotio retinae seems to
represent disrupted receptor cells. Visual loss may result
from permanent loss of receptors. The pigment
epithelial response to traumatic receptor damage is
191
Management of Blunt Retinal Trauma
Fig. 31.1: Commotio retinae
Fig. 31.2: Berlin`s edema
similar to that observed in experimental retinal
detachment and light-induced retinal damage.
Management
There is usually no treatment required because
commotio retinae tends to resolve without sequela.
The management consists of repairing the traumatic
collateral damage and emotionally supporting of the
patient, especially if vision is poor. Visual acuity
monitoring, Amsler grid testing, and measurement
of retinal thickness can provide data indicating the
progress of recovery; however, no known topical,
oral or surgical solution has been offered as a
treatment for the commotion it self. If patients initially
have decreased acuity, they should be informed that,
in the majority of cases, improvement takes place
spontaneously. However, they should also be adverted
that in some instances visual acuity remains disabled.
Concurrent treatment of any resultant uveitis should
include a topical cycloplegic and, when appropriate,
a topical corticosteroid. Cystoid macular edema (CME)
is a classical complication of ocular inflammation. CME
can result from a rupture of the inner or outer blood-
ocular barrier, and it responds poorly to topical and
surgical modalities. Topical nonsteroidal and steroidal
preparations along with oral carbonic anhydrase
inhibitors and injected steroidal depots have been used,
but with varied results; sometimes these medication
makes a placebo effect in the patient but also in the
physician.
TRAUMATIC MACULAR HOLE
Initial Concepts
The first macular holes reported by Knapp, in 1869,
and Noyes, in 1878, were traumatic in nature.
Traumatic macular holes are reported to occur in
about 6% of eyes with blunt trauma. The mechanism
of traumatic macular hole formation may not be
singular. Idiopathic macular holes are believed to be
caused by tangential vitreoretinal traction at the fovea;
so, traumatic macular holes may be caused by a similar
mechanism. In fact, surgical repair of traumatic
macular holes is identical to that for idiopathic macular
holes, with removal of the posterior hyaloid and
peeling of epiretinal or internal limiting membranes,
and yields similar anatomic and visual results. There
is no doubt that some of these traumatic macular
holes may be caused by cystoid degeneration
following postcontusion commotio and RPE edema.
Under these circumstances the visual prognosis would
be more guarded and surgical repair may not be as
effective.
Pathogenesis
Macular holes have become the focus of much interest
and controversy

in ophthalmology. Much of this
renewed interest stems from new

theories of
pathogenesis

and the development of a possible

surgical
treatment

for macular holes. Despite the numerous
proposed theories, the pathogenesis of these lesions
is still

not well understood. Most current investigators
believe that

tangential vitreous traction plays an
important role in their

pathogenesis, as we described
in the section of mechanism of blunt trauma. However,
there are several mechanisms by which

this tangential
traction may be produced. Gass

mentioned that
condensation and contraction of the prefoveal cortical
vitreous with glial cell proliferation in this condensed
vitreous

may generate tangential traction. Guyer and
192
Green suggested

that fluid movements of the liquefied
vitreous in an enlarged

premacular bursa can exert
traction on the remaining formed

cortical vitreous, with
that traction transmitted tangentially

to the fovea.
These finding suggests that the named mechanisms
are important in

the generation of tangential traction
leading to the macular hole

formation, and cellular
proliferation may not play a major role in their
pathogenesis. Studies also found that retinal fragments
are a rare feature

of the vitreous in these patients; they
are thus unlikely to

be a constituent of macular hole
opercula. Opercula are therefore

better termed
pseudo-opercula, as has been previously suggested.
A mild

chronic inflammatory infiltrate (lymphocytes)
is present in

some cases of macular holes. Inflammation
and cellular or fibrocellular

membrane fragments are
more frequent in traumatic holes than

in idiopathic
holes. The significance of this difference is

unclear, but
it is likely a direct result of the initial trauma.
Studies of Mechanical Forces
Evidence from animal studies and biomicroscopic and
surgical observations of patients with a traumatic
macular hole strongly suggest that vitreous traction is
important in their pathogenesis. Experimental
observation shows that sudden compression of the
globe produces an immediate stress on the retina at
points of vitreous attachment. High-speed photography
of blunt trauma reveals indentation of the cornea
followed by expansion of the globe at the equator.
This outward expansion of the equator is followed by
flattening of the posterior pole and then posterior
displacement of the posterior pole of the eye. It seems
likely that with this trampoline-like movement of the
posterior pole, traction forces may in fact be along
the surface of the retina, that is tangential, not unlike
what occurs in a more gradual manner with idiopathic
macular holes. This sudden traction exerted on the
anatomically thin fovea results in an immediate
formation of a macular hole in most cases (Fig. 31.3).
Treatment
Vitrectomy surgery for idiopathic macular holes has
been shown to improve vision in some eyes. Current
techniques include removal of the posterior hyaloids
and all epiretinal membranes from the macular area
and prolonged postoperative macular gas tamponade.
However, the role of vitrectomy surgery for a macular
hole caused by blunt ocular trauma is not still well
established.
The results of different series are encouraging.
Despite significant blunt trauma of different types,
vitrectomy surgery for macular holes can result in a
high likelihood of improved vision and a risk of comp-
lications, that seems no greater than with vitrectomy
surgery for idiopathic macular holes. Further, studies
of different approaches with posterior vitrectomy are
needed to establish a consistent result for this condition;
meanwhile different approaches are being performing
according the case, the criteria and the resources
worldwide.
TRAUMATIC RETINAL TEARS
(RETINAL BREAKS)
Despite the surgical management (enough material to
fill an entire book), we will describe in this stage some
features that can differentiate a Traumatic retinal Tear
from those Non-Traumatic and the clinical features to
evaluate during the initial examination.
Peripheral retinal breaks occur at sites of strong
vitreoretinal adhesions. During blunt trauma vitreo-
retinal traction may occur by the forceful displacement
or separation of the vitreous. Globe deformation also
causes various shearing forces that further amplify the
vitreoretinal traction (coup and countercoup).
Retinal breaks resulting from trauma can be
horseshoe-shaped flap tears or operculated holes.
Formed vitreous is often attached to the elevated flap
of a horseshoe tear and the free-floating operculum
of the hole. These tears can occur along the vitreous
base or at the edge of lattice degeneration or
chorioretinal adhesions. If a retinal vessel is involved
in the tear, a dense vitreous hemorrhage can occur;
the attending surgeon must always remember that a
vitreous hemorrhage can advice about a retinal rupture,
that sometimes is covered by the blood at the initial
examination.
Giant retinal tears are retinal breaks that extend
3 or more clock hours. They occur at the edge of the
vitreous base, which remains attached to the anterior Fig. 31.3: Traumatic macular hole
193
flap; their formation will depend upon the transmission
of forces inside the globe, but also upon some previous
retinal damage (e.g. high myopia).
A retinal dialysis is a discontinuity or separation
of the retina from the pars plana at the ora. It is most
frequently traumatic in nature and is characterized
by attachment of the vitreous to the posterior retinal
flap. This is in contradistinction to retinal tears, in
which the vitreous usually adheres to the anterior
flap; anyhow, vitreo-retinal traction is present in almost
all the times. Traumatic retinal dialysis occurs most
often in either the inferotemporal or superotemporal
quadrant. The ri sk of progressi on to reti nal
detachment is significant.
Therefore, all traumatic retinal tears and dialyses
are treated prophylactically with photocoagulation or
cryotherapy. Giant retinal tears that continue to tear
despite photocoagulation also can be treated with
scleral buckling.
TRAUMATIC RETINAL DETACHMENT
Like in the previous section, the retinal detachment
can include entire books; we will describe only some
features regarding the traumatic etiology of this
condition.
Mechanism of Pathology
Traumatic retinal detachments occur primarily as the
result of retinal changes at the vitreous base. Goffstein
and Burton, reported that 53% of traumatic retinal
detachments were caused by retinal dialyses, 16% by
giant retinal tears, 11% by horseshoe flap tears, and
8% by tears at the edge of lattice. Retinal detachments
can also happen secondary to traumatic tears of the
ciliary epithelium. Sometimes during the clinical evalua-
tion is difficult to identify the specific cause.
The majority of these traumatic tears and detach-
ments occur in younger individuals. The vitreous often
is quite well formed and has not yet undergone a
posterior vitreous detachment (PVD). This well-formed
vitreous often limits the progression of retinal detach-
ment, especially if it is caused by an inferior dialysis.
As time progresses and the vitreous becomes more
liquid or separates further, the detachment can then
progress more rapidly. This explains why many
traumatic detachments do not present until several
months or even years after the original trauma. At this
point the physician must remember that after an initial
trauma, the patient must be educated to follow
multiple evaluations, even without symptoms; this
condition can imply even some legal issues.
Detachments al so can be associated with
proliferative vitreoretinopathy (PVR). This is especially
true in traumatic detachments associated with
subretinal or vitreous hemorrhage, giant retinal tears,
or severe ocular contusions in which there has been
an opportunity for RPE and other fibroglial cells to
gain access to the vitreous cavity. Even a condition
like vitreitis can lead to retinal detachment because
of its inflammatory condition.
Some studies conducted to study phakic retinal
detachments have characterized some of the implied
features and have helped to establish improved
guidelines for medicolegal determinations. Myopes
typically developed giant tears and nasal dialyses;
emmetropes frequently developed inferotemporal
dialyses. It also has been noticed that lattice degene-
ration did not increase post-traumatic detachments risk.
Dialyses and giant tears caused 69% of traumatic
detachments in comparison with 6% of the cause of
nontraumatic detachments. Experience has shown that
the overwhelming majority of traumatic retinal
detachments are rhegmatogenous in origin. Retinal
breaks are predominantly located within the vitreous
base region but may occur at sites of focal scleral impact
or from posterior vitreous avulsion.
Management
Although the use of scleral buckling techniques alone
may be sufficient, closed microsurgery may be required
in some cases to relieve retinal traction and to facilitate
the identification and permanent closure of the retinal
breaks. Prophylactic measures including the use of
closed microsurgery, play a vital role in the manage-
ment of traumatic retinal breaks and prevention of
complex retinal detachment.
Traumatic retinal detachments are treated primarily
by scleral buckling. The results and visual outcomes
are quite favorable. As previously mentioned, most
of these patients (young patients) have well-formed
vitreous with posterior hyaloid attachment. Sometimes
during a pars plana vitrectomy a posterior vitreous
detachment may be difficult to create and the
morbidity associated with the vitrectomy may be
greater than that seen with scleral buckling.
Because of these reasons, some authors attempt
to avoid an intraocular approach in the repair of these
detachments. However, there are several well known
indications for a primary repair of retinal detachment
by pars plana vitrectomy; vitreous hemorrhage
obscuring visualization, posteriorly dislocated crystalline
lens, giant retinal tear with everted flap, proliferative
vitreoretinopathy, subretinal hemorrhage and a large
irregular posterior retinal tear.
In these traumatic cases it is useful sometimes to
combine the vitrectomy with an encircling element to
support the vitreous base on a broad, shallow buckle.
The final decisions must be taken by the attending
194
surgeon according the case, the experience and the
available resources.
VITREOUS HEMORRHAGE
Vitreous hemorrhage can occur through a variety of
different mechanisms and sometimes is not becoming
the main trouble; in fact many times it is only the advice
of some other disturbances occurring in the posterior
segment because of the blunt trauma. It can be the
clinical manifestation of iridodialysis, ciliary body
trauma, avulsion or tear of a retinal vessel, and
breakthrough of subretinal blood from a choroidal
rupture between the most important.
Visually significant vitreous hemorrhages should be
followed closely; within the days after the trauma, the
hemorrhage can change, but also can change the
circumstances of the posterior segment it self. There
may be peripheral retinal pathology and eyes with
VITREOUS BASE AVULSION
The vitreous base represents the region of strongest
adhesion between the retina and vitreous. The vitreous
bases strong adhesion continues anteriorly beyond
the ora into the pars plana and ciliary epithelium.These
adhesions are stronger in the young eye.
Avulsion of the vitreous base is characteristic of
blunt ocular trauma. It is the result of ocular
deformation and shearing forces caused by the blunt
trauma mentioned previously in this chapter.
Frequently the avulsed vitreous base may be
associated with a retinal dialysis or giant retinal tear
because the same shearing forces (coup and counter-
coup).Therefore, the presence of an avulsed vitreous
base should alert the examiner to the possibility of
associated retinal or ocular injuries. These injuries can
occur later in time than the initial trauma. In fact, some
studies reported that an avulsed vitreous base was
associated with a dialysis or giant tear in 26% of
traumatic retinal detachments, a particular high
percentage; this condition should aware the surgeon
to observe frequently the retina for days and weeks,
in particular in younger patients.
CHOROIDAL RUPTURE
Definition and Cinical Findings
Choroidal ruptures are breaks in the choroid, the
Bruch membrane, and the retinal pigment epithelium
(RPE) that result from blunt ocular trauma and can
be secondary to indirect or direct trauma. Cases
secondary to direct trauma tend to be located more
anteriorly and at the site of impact and parallel to the
ora serrata, whereas those secondary to indirect trauma
occur more posteriorly (countercoup). These ruptures
have a crescent shape and are concentric to the optic
disc. Indirect choroidal ruptures are almost 4 times
more common than direct ruptures.
Histopathology
After blunt trauma, the ocular globe undergoes mecha-
nical compression and then sudden hyperextension.
Because of its tensile strength, the sclera can resist this
insult; the retina is also protected because of its elasticity.
The Bruch membrane does not have enough elasticity
or tensile strength; therefore, it breaks! Concurrently,
the small capillaries in the choriocapillaris are damaged,
leading to subretinal or sub-RPE hemorrhage.
Hemorrhage in conjunction with retinal edema may
obscure the choroidal rupture during the acute phases,
so frequently observation of retinal hemorrhages is
mandatory.
As the blood clears, a white, curvilinear, crescent-
shaped streak concentric to the optic nerve is seen.
Fig. 31.4: Vitreous and pre-retinal hemorrhage
retinal tears and vitreous hemorrhage are at increased
risk for detachment due to fibroglial proliferation.
Sometimes the changes in the retina can not be seen
through the blood, so frequent ultrasonography is
recommended to rule out the development of retinal
detachment and to follow up the vitreous hemorrhage
it self (Fig. 31.4).
It is preferable to treat vitreous hemorrhages
expectantly; a conservative behavior should be the
initial rule. Delayed clearing of the vitreous hemorrhage
without the presence of other retinal abnormalities,
presence of retinal tears that cannot be adequately
visual ized for treatment (corroborated with
ultrasonography and sometimes even the clinical
suspect), development of retinal detachment, and
erythroclastic glaucoma are some indications for the
surgical removal of the vitreous hemorrhage.
195
Direct choroidal ruptures are characterized by a
complete absence of choroid and RPE. The overlying
retina is intact but atrophic because the lack of nutrition.
In indirect choroidal ruptures, choroidal neovasculari-
zation (CNV) is a common finding during the early
healing phases. Most CNV is in the subretinal space.
With time, most CNV involutes spontaneously. In a
small number of cases, a disciform scar or fibrous tissue
may grow into the retina and vitreous cavity. During
the healing phase, choroidal neovascularization
occurs, but in most cases, it involutes spontaneously;
a good, and long-term follow-up is mandatory in these
lesions.
Diagnosis
The physical findings are retinal edema (Berlins
disease), hemorrhagic detachment of the macula,
serous detachment of the macula, subretinal hemor-
rhage and a white curvilinear crescent-shaped streak
concentric to the optic nerve (Figs 31.5 and 31.6).
The imagines studies helping the diagnostic of
choroid hemorrhage and associated lesions; fluorescein
angiography may be a useful adjunct to detect CNV;
if CNV is absent, hypofluorescence occurs during the
early phase of the angiogram due to disruption of the
choriocapillaris. During later stages, hyperfluorescence
occurs from the adjacent healthy choriocapillaris; if
CNV is present, early hyperfluorescence followed by
late leakage is present on the angiogram.
Management
Conservative treatment is recommended for most
choroidal ruptures. During the healing phase of
virtually all choroidal ruptures, CNV is present, with
spontaneous resolution in the majority of the cases.
In 15-30% of patients, CNV may recur and lead to
a hemorrhagic or serous macular detachment with
concomitant visual loss.
The treatment of CNV will depend upon the locali-
zation; if CNV is extrafoveal, it may be treated success-
fully with laser photocoagulation; if CNV is subfoveal
or juxtafoveal, consider pars plana vitrectomy with
membrane extraction, with all the implicating risks
because of working near the fovea.
Most patients with choroidal ruptures do not reach
a final visual acuity of 20/40 or better; poor visual
acuity is associated with macular involvement. If the
rupture does not involve the fovea, good vision is
expected.
Most CNV occurs within the first year. However,
CNV has been reported to occur as late as 35 years
after the choroidal rupture. For legal reasons the
surgeon must always remember that choroidal
neovascularization can occur again, and so periodic
examinations are necessary.
Prognosis
If the rupture does not involve the fovea, good vision
is expected. In 15-30% of patients, CNV may arise
again and lead to a hemorrhagic or serous macular
detachment with concomitant visual loss. This usually
occurs during the first year but can also occur decades
later. Older age and macular rupture, the length of
the rupture, and the distance of the rupture to the
center of the fovea may be risk factors for CNV and
so important factors in the long term prognosis.
OPTIC NERVE AVULSION
Definition and Clinical Findings
Traumatic optic neuropathy (TON) refers to an acute
injury of the optic nerve secondary to trauma. The
optic nerve axons may be damaged either directly or
indirectly and the visual loss may be partial or complete.
An indirect injury to the optic nerve typically occurs
from the transmission of forces to the optic canal from
Fig. 31.5: Choroid fracture
Fig. 31.6: Choroidal rupture
196
blunt head trauma. This is in contrast to direct TON,
which results from an anatomical disruption of the optic
nerve fibers.
Patients can present with a variable degree of vision
loss (decreased visual acuity, visual field abnormalities,
or loss of color vision). Most cases (up to 60%) present
with severe vision loss of light perception (LP) or
worse.
In the acute phase, the optic nerve usually appears
normal on funduscopic examination, but optic nerve
atrophy is often seen 3-6 weeks after the injury; so
the clinical must be aware to perform periodical
revisions of the traumatized eye during a long period
of time.
Mechanisms of Injury
There are two known forms of optic nerve injury:
Indirect injury: In indirect TON cases, the injury to
the axons is thought to be induced by shearing forces
that are transmitted to the fibers or to the vascular
supply of the nerve. Studies have shown that forces
are transferred and concentrated in the area near
the optic canal. The tight adherence of the optic
nerves dural sheath to the periosteum within the optic
canal is also thought to contribute to this segment
of the nerve being extremely susceptible to the
deformative stresses of the skull bones. Such injury
leads to ischemic injury to the retinal ganglion
cells within the optic canal.
Direct injury: A secondary mechanism can result
in optic nerve swelling after the occurrence the acute
injury. The optic nerve swelling can exacerbate retinal
ganglion cell degeneration by further compromising
the vascular blood supply, either through a rise in
intraluminal pressure or reactive vasospasm. These
secondary mechanisms, in theory, form the rationale
for optic canal decompression via medical (e.g.steroids)
or surgical means (e.g. bony decompression).
Diagnosis
Even in an acute trauma setting, patients should have
a visual acuity assessment as soon as possible. If the
patient cannot read the top letter on the eye chart,
the visual acuity may be recorded with the following
nomenclature; counting fingers vision, hand motion
perception, light perception (LP), or no light perception
(NLP), sometimes are the obtained lectures.
The pupil examination assesses for a relative or
complete afferent pupillary defect. An eye with a
unilateral optic nerve injury will demonstrate an
afferent papillary defect, verifying the presence of TON,
but not excluding other diagnosis. In the rare cases
of a bilateral TON, both pupils may be dilated and
nonreactive to light if the injury is profound.
At the funduscopic, because the location of the
injury in most of the cases is within the posterior orbit
or the optic canal, the optic disc typically appears
normal on funduscopic examination on initial diagnosis.
Optic nerve atrophy usually appears 3-4 weeks after
the traumatic event, and the disc acquires a diffuse
pallor. Rarely, optic nerve changes can be seen with
direct injuries to the retrobulbar section of the optic
nerve, presenting as an avulsed optic nerve head or
optic disc swelling with surrounding hemorrhage
(Figs 31.7 and 31.8).
Computed Tomography of orbits, comparing both
optic nerves anatomy, are sometimes of great value,
but even so, sometimes even in the presence of severe
optic nerve damage, the funduscopic and the radiologic
findings can be normal.
Fig. 31.7: Optic nerve avulsion
Fig. 31.8: Optic nerve atrophy
197
Management
Steroids have been used in TON since the early 1980s;
they are thought to provide neuroprotection in
traumatic central nervous system injury through their
antioxidant properties and inhibition of free radical-
induced lipid peroxidation. Recent studies have
demonstrated that the therapeutic role for cortico-
steroids in the management of TON is unsubstantiated.
If steroids are considered to be used in cases with
concomitant traumatic brain injury, it must not be a
decision of the ophthalmologist by it self; dangerous
circumstances involving the central nervous system can
be mascared. The use high or lower doses of steroids
is also not clearly defined by the literature as useful
for optic nerve protection. May be, as has been seen
in other sections of this chapter, they can provide a
placebo effect in the patient, family, but also in the
physician.
The indication for surgical therapy in indirect optic
nerve trauma is to decompress it at the site of injury,
which is often the intracanalicular segment. Surgical
decompression is thought to help reduce optic nerve
compression and subsequent vascular compromise that
may occur as a result of the indirect injury. Another
probably benefit of surgery that has been postulated,
is to remove bone fragments that may be injuring on
the optic nerve within the optic canal. However, no
randomized, controlled studies have been performed
to evaluate the role of surgery in this disease.
Conclusions
Traumatic optic neuropathy (TON) can lead to pro-
found visual loss from either indirect or direct
mechanisms. The diagnosis can be made with
accurate history taking and clinical examination, based
on the presence of visual loss and an accompanying
relative afferent pupillary defect. The optimal treatment
for TON, however, remains debated among physicians.
Corticosteroids should not be used in cases with
concomitant traumatic brain injury or in patients who
present 8 hours or more after initial injury. Based on
the available evidence, surgical decompression of the
optic canal is not routinely recommended. If treatment
with either steroids, surgical intervention or both is
considered, appropriate information and informed
consent should be given to the patient and their family;
they should know (and sign) the potential benefits and
the risks.
CHORIORETINITIS SCLOPETARIA
Definition
It is a proliferation of fibrous tissue in the choroid and
retina as the result of contusion of the sclera by a high
velocity missile; it is the result of traumatic chorioretinal
rupture followed by marked fibrovascular proliferation
with variable replacement of the choroid and retina
with no retinal detachment.
Contusion force may lead to choroidal ruptures
with hyperplasia and migration of the retinal pigment
epithelium into the retina and choroid, epiretinal
membrane formation, loss of photoreceptors and
marked atrophy of the optic nerve.
Diagnosis
The diagnosis should be established only based on
clear objective findings, a relative afferent pupillary
defect or an evoked visual response. The most
important factor in determining the force of injury is
the velocity. As higher the speed of the projectile object,
the greater the tissue disruption at the impact zone
due to the delivered kinetic energy. The shock wave
energy released by the projectile object is considered
as the main cause of choroidal and subsequently retinal
injury (Fig. 31.9).
Treatment
Retained intraorbital metallic foreign bodies may
accompany chorioretinitis scleopetaria, commotio
retinae, vitreous hemorrhages, or some other times
this entity can be presented alone; treatment of
concomitant damage should be done. In the case of
bullets, gun pellets, the usual management is
conservative due to the inert nature of this type of
metallic foreign bodies. There are considerable
reported cases with chorioretinitis sclopetaria due to
bullet gun injuries; the characteristic pattern of
choroidal and retinal changes caused by a high
velocity projectile object passing through the orbit,
in close proximity to the globe is usually seen in this
condition.
Fig. 31.9: Retinitis sclopetaria
198
The role of steroids is also in debate with no demons-
tration of real benefit in their application.
PURTSCHER RETINOPATHY
Definition and Causes
Purtscher retinopathy is a hemorrhagic and vaso-
occlusive vasculopathy, which, in 1912, was first
described as a syndrome of sudden blindness associated
with severe head trauma. These patients had findings
of multiple white retinal patches and retinal hemor-
rhages that were associated with severe vision loss.
Since its original description, Purtscher retinopathy has
been associated with traumatic injury, primarily blunt
thoracic trauma and head trauma, but also with
numerous non-traumatic diseases; it is seen in diverse
conditions, including acute pancreatitis, fat emboli-
zation, amniotic fluid embolization, and vasculitic
diseases. Bilateral manifestations are seen most
commonly in systemic conditions, but unilateral
findings have been also reported. Decreased vision
occurs in the affected eyes, generally in the range of
20/200 to counting fingers. Vision can often improve
within several months to a range of 20/30 to 20/200,
depending on the severity of the retinal findings.
Hystopathology
The exact pathophysiology remains somewhat
controversial, and different mechanisms have been
described; the main mechanism purposed is vascular
occlusion. The characteristic white lesions are known
as cotton-wool spots, and correspond to retinal
microinfarcts at the level of the nerve fiber layer, caused
by the ischemic lesion. Fluorescein angiogram reveals
leakage, and it can suggests that an acute endothelial
cell injury is caused by trauma; possibly this is the
predisposing factor that lead the retinal vessels to
occlusion. Other possible sources of emboli include
fat emboli in cases of long bone fractures and perhaps
pancreatitis from enzymatic digestion of omental fat,
amniotic fluid embolization during childbirth and post-
partum, air emboli from traumatic chest compression,
and granul ocyte aggregation resul ting from
complement activation.
Diagnosis
In a funduscopic view, macular cotton-wool spots and
intraretinal hemorrhages in patients with this history
of trauma are diagnostic of the condition. Patients with
traumatic Purtscher retinopathy present with a recent
history of blunt chest trauma or head trauma. The
severity of chest trauma is not always correlated with
the incidence and/or severity of retinopathy, which is
observed in these patients. Some other findings can
include serous detachment of the macula, preretinal
hemorrhages, dilated vessels, and optic disc edema.
Confluent cotton-wool spots in the central macula may
simulate the cherry-red spot that is seen in central retinal
artery occlusion. Retinal microinfarcts that are observed
in patients with fat embolization are usually smaller
in size and located in the peripheral, not central, retina.
Pigment migration and optic atrophy have been
reported as late findings in the disease (Fig. 31.10).
Angiogram with fluoresceine is very useful to
corroborate the ischemic damage, but many times the
only characteristic clinical pattern, is enough to
determine the diagnosis. Without history of trauma,
physician should consider fat embolization, amniotic
fluid embolization, retinal vasculitis, system lupus
erythematosus, dermatomyositis, scleroderma and
radiation retinopathy, between others.
Management
No proven treatment exists for Purtscher retinopathy
that occurs after traumatic injury. In patients with
retinopathy due to systemic vasculitis, steroid therapy
is theoretically beneficial.
Visual prognosis is guarded, although initially
decreased vision may improve over a period of months.
The most important prognostic finding that is associated
with a poor visual prognosis is central macular
infarction, due to the ischemic condition.
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Fig. 31.10: Purtscher retinopathy
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C H A P T E R
32
Applications of Stem Cell
Therapy in Ophthalmology
Rajpal Vohra (India)
Introduction
In Ophthalmology, there are various conditions where
there is no treatment available like Retinal degene-
rations, and total deficiency of stem cells which occurs
in alkali burns in cornea. Stem cells are recent advances
in Ophthalmology, which has given newer therapeutic
modalities in the management of retinal diseases, which
were thought to be incurable. Stem cell therapy is an
upcoming new mode of treatment in present time.
Stem cell research offers hope to countless patients
whose conditions have here to fore been deemed
incurable. Better understanding of stem cell behaviors
and functions will lead to insights into biological
mysteries encompassing the fields of angiogenesis,
development, tissue homeostasis, wound healing, and
carcinogenesis.
The potential use of stem cells in the treatment of
a variety of human retinal disease remains
tremendously exciting. There is by ethical controversy
in use of fetal tissue so the actual potential use of such
approaches remains yet unexplored. Adult tissue is less
controversial and more readily available, holds promise
but the pluripotency and actual utility of stem cells
obtained from this source remains uncertain. Clearly,
populations of progenitor cells exist in the ciliary margin
and bone marrow and each may have significant utility
as we seek to repair and rebuild damaged retinas. Even
if such complex tissue reconstruction could be
successfully completed, re-establishing functional visual
pathways will be an even greater challenge.
Definition of Stem Cells
Stem cells are pluripotent cells capable of differentiating
into variety of cell types. There are two sources of stem
cells:
1. Stem cells from adult tissue
2. Stem cells from fetal material called embryonic
stem cells.
Embryonic stem cells are typically isolated from
blastocysts and have pluripotency.they can give rise
to virtually any adult tissue cell type under appropriate
conditions. Truly pluripotent embryonic stem cells have
been identified that can give rise to a multitude of
differentiated cell types. Stem cell is the origin of life.
Ultimate the stem cell, fertilized egg, is formed from
fusion of the haplid progeny of germinal stem cells.The
fertilized egg is totipotent.
Adult derived stem cells typically reside in adult tissue
in a quiescent, undifferentiated state and under
appropriate stimuli will divide and differentiate into
the cell types of tissue in which they reside or if
appropriately stimulated into other cell types. Normal
tissue renewal is accomplished by the differentiating
progeny of the stem cells, the so called transit-
amplifying cells.
During early embryonic development, each cell
divides and gives rise to two daughter cells with the
same potential:symmetric division. During normal tissue
renewal in the adult, each progenitor cell gives rise
to one daugther cell that remains a progenitor cell,
and one daugther cell that begins the process of
determination to a terminally differentiated cell leading
to termination- asymmetric division. During normal
tissue renewal in adult organs, tissue stem cells give
rise to progeny that differentiated into mature
functioning cells of that tissue. Stem cell with less than
totipotentiality are called Progenitor Cells.
The Ivanova et al are doing large scale genomic
analysis and Ramalho Santos M et al are doing
transcriptional profiling of stem cells.
At present there is a controversy whether adult
tissue containing pluripotent stem cells will serve as a
source of regenerative tissue.
Lee MS et al, has done recent clinical trial using
adult bone marrow (BM) derived stem cells to
regenerate infracted myocardium have reported
success in improving cardiac functions. Presuming on
the basis of bone marrow stem cells differentiating into
201
Applications of Stem Cell Therapy in Ophthalmology
myocardium is not supported by experimental data
by Murry CE et al.

According to Balasam LB et al
hematopoietic stem cells adopt mature hematopoietc
fates in ischemic myocardium. According to Anderson
DJ, et al these clinical observations cannot be
invalidated but raises many questions regarding
interpretation and emphasizes that there is a need to
establish rigorous standards by which such clinical
studies are evaluated.
Very limited work has been done regarding retinal
stem cells.There has been extensive literature work
done an stem cells giving rise to vascular, muscle
nervous hemopoietic tissue. Very limited work has
been done on the retinal stem cells.
There are four basic population of cells that may
contain dormant progenitor cells.
1. Retinal stem cel l s that can give rise to
photoreceptors
2. Muller/glial stem cells
3. Retinal pigment epithelial [RPE]; and endothelial
progenitor cells [EPC]
Recently adult bone marrow-derived HSCs
containing EPC is an intresting areas of research.
Role of Retinal Stem Cells and
Muller Glial Cells
Reh TA et al. has shown that regenerative capacity
exists in retina of amphibians and chicken embryos
after injury.

The vertebrate retina is derived from paired
evaginations from the neural tube in embryonic
development and is initially produced by progenitor
cells similar to those that generate the neurons and
glia of other areas of the central nervous system. In
some amphibians and fish, the retina continues to grow
along with the eye throughout the life of the animal.
The new retinal cells are added at the ciliary margin
of the eye from the mitotic activity of neural/glial stem
cells in a region known as the germinal zone and are
seamlessly incorporated into the existing retinal circuitry.
Little is known about the cell or molecular biology of
these stem cells; however, studies of retinal progenitor
cells in chick and mammalian embryos have led to
the identification of several factors that control their
proliferation. Moreover, studies of retinal regeneration
have shown that retinal stem cells can also be derived
from two or perhaps three additional sources after
retinal damage: (a) the retinal pigmented epithelium
(RPE) in amphibians and embryonic chicks and
mammals; (b) a specialized rod progenitor in fish; and
(c) the Muller glial cells. While there is currently no
evidence for a neural/glial stem cell in the adult
mammalian retina, and the retina of the mature
mammal does not show regenerative capacity after
damage, there is a possibility for the reinitiation of stem
cell potential at the peripheral retinal margin, from
the RPE or from the Muller glial cells. The application
of information derived from the studies of retinal
progenitor cells in developing organisms should soon
provide a test of these possibilities.
This regenerative capacity derives from quiescent
stem cells that reside in the adult retina of these species.
Similar regenerative capacity has been demonstrated
in mammalian retina. For a population of retinal stem
cells to exist in the adult retina, it would have been
necessary for such a population of progenitor cells to
remain quiescent after the retina has fully differentiated.
Livesey FJ et al has done large scale Genomic anlysis.
Blackshaw S et al has done Genomic analysis of mouse
retinal development.
The work of livesey and Blackshaw can serve as
the starting point for the evaluation of numerous genes
and their potential role in the regulation of retinal cell
developmental determination. How genes are
progressively switched on and off in an orderly fashion
during the generation of specific retinal cell types, and
how this overlaps with gene sets utilized during the
establishment of other, nonretinal neuronal cell types,
will contribute significantly to our understanding of
retinal progenitor biology. Dyer MA et al has done
study in regulation of cell proliferation in retinal
development.

Das AV et al has done identification of
c-KIT receptor as a regulator of adult neural stem cells
in the mammalian eye and the role of various
transcription factor and signaling molecules during this
process have provided insight into putative
mechanisms whereby the mammalian retina holds in
reserve a subset of progenitor cells that theoretically
could be used to regenerate damaged issued in the
in the adult.

Clearly, James J et al has studied the the
development state of the retina and the context in
which a specific cell finds itself will determine how a
particular retinal progenitor cell behaves: whether it
will terminally differentiate or maintain a quiescent state
from which it can letter emerge to give rise to cells
useful in repair of a damaged retina will depend not
only on its own developmental programme, but the
microenmorvironment in which it finds it self.
James J et al has done cellular and molecular
characterization of early and late retinal stem cells/
progenitors: differential regulation of proliferation and
context dependent roll of notch signaling.
James J et al has done transcriptional profiling
studies of retina at different states of development
coupled with in vitro studies of progenitor cell
populations should provide the information necessary
to begin such an analysis and determine what
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conditions help maintain quiescence and what
conditions stimulate proliferation and subsequent
differentiation of retinal progenitor cell populations.
Konobu T et al have shown that cells with
characteristics of retinal neuron have been obtained
from a number of embryonic tumor cell line, including
neuroblastoma, gliaoblastoma, but because of the
malignant potential of these cells they are not likely
to be useful.
Martinez-Serrano A et al, have cultured virally
transformed, immortalized neuronal precursors were
evaluated for their ability to differentiate into retinal
neurons after intraocular implantation.
Bain G et al have attempted at inducing in vitro
differentiation of embryonic stem cells into retinal
neuronal phenotypes were done using a variety of
factors, including retinoic acid.
Tropepe V, et al has identified Retinal progenitor
stem cells in the adult mammalian eye. Ahmad I, et al
have done Identification of neural progenitors in the
adult mammalian eye. Retinal progenitor cells have
been identified in ciliay margin. These cells were not
isolated from central or peripheral pigmented
epithelium. These cells are clonally expanded in culture
to give rise to a variety of retinal cells types, including
rod photoreceptors, bipolar neurons, and muller glia.
The differentiation of these cells from the ciliary margin
pigmented cel l progenitors is not due to
transdifferentiation of the ciliary margin cells, but rather,
clonal proliferation and defferentiation as observed in
a true stem cell.
Fischer AJ et al have shown that in chicken an adult
differentiated muller gila can serve as a source of stem
cells that will, in response to injury, or cytokinenes,
differentiate, proliferate and redifferentiate into
additional glial cells or neurons.
Turner DL, et al have identified common progenitor
cells that gives rise to both Muller glia and retinal
neurons.
Thus, the concept that Muller glia of the adult retina
can serve as potential source of retinal stem cells is
consistent with molecular profiling of developing
mammalian retinas that shown a high degree of
similarity between the gene expression profiles of Muller
glia and mitotic retinal progenitor cells in the mouse.
Since the Muller glia are the cells that commonly
proliferate in response to retinal injury, it would not
be surprising that these cells also retain the potential
to defferentiate along a number of pathways, some
of which may lead to retinal neuronal replacement.
Ooto S et al have done a recent study significantly
expanded this concept: amarcine, horizontal, and
photoreceptor phenotypes were mammalian retina in
the presence of extrinsic factors (e.g. retinoic acid) or
activation of intrinsic genes. These studies are most
provocative, could provide additional insight into
retinal regeneration in mammals, and provide a
rationale for the targeting of Muller glial in certain
inherited and acquired retinal degenerative disorders.
If we isolate retinal stem cells from the adult
mammalian eye and then using them to regenerate
diseased retina then it will have a great therapeutic
effect. There have been some reports suggesting that
if multipotent progenitor cells isolated from retina of
neonatal mice retina are used in the early, then some
level of visual function may be obtained in animal eyes
with retinal degeneration. At cellular level it is very
difficult to establish functional neuronal connection
between implanted progenitor cells or sheets of
photoreceptor and the hosts nerve fiber layer prior
to reestablishing visual pathways that would lead to
functional vision.
Role of Retinal Pigment
Epithelial Stem Cells
RPE cel l s and photoreceptors enjoy an cl ose
relationship both anatomically and functionally. Where
is the principal underlying defect in many inherited
retinal degenerations is stil l a question: the
photoreceptor or RPE cells ?. Although with the advent
of molecular genetics this confusion has become less,
but the interdependency between these two cells types
remains and there is often concomitant degeneration
of both cell types observed in a variety of inherited
and acquired degenerative disease of the retina. In
this regardRPE cell transplantation has been
evaluated both for its potential to replace diseased RPE
as well as to provide a source of cells whose phenotypic
differentiation may be manipulated by various
cytokines and trophic substances. Thus, RPE cell lines
have been developed for use as RPE cell transplants,
cell-based drug delivery platforms, and photoreceptor
stem cells.
Transplantable RPE cell lines may serve as stem
cells of sorts to replenish diseased RPE cells themselves.
In a number of macular and retinal degenerative
disorders there is atrophy of the RPE and associated
malfunctioning in the phototransducing cellular
machinery. Damaged RPE cells and associated atrophy
are hallmarks of age-related macular degeneration and
heroic surgical approaches have been considered to
provide photoreceptors in such individuals with
healthier, RPE-rich regions of the retina through retinal
translocation and the insertion of RPE sheets.
Human RPE cell lines enjoy an extended life span
after being stably transfected with a plasmid encoding
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the simian virus 40 large T antigen and many of the
factors expressed by functional RPE cells in vivo are
observed to be expressed by these transformed cell
lines. When these cells are transplanted subretinally
into a rat model of retinal degeneration (the RCS rat),
loss of visual function is attenuated and cortically
dependent visual function is preserved long-term.
These RPE cell lines can be transferred with plasmids
encoding a variety of trophic factors shown to have
protective effects on photoreceptors and then
encapsulated into polymer devices that permit diffusion
of cell products into the tissue into which they are
transplanted. When transformed RPE cell lines are
transfected with a plasmid encoding one such factor,
ciliary neurotrophic factor (CNTF), and transplanted
directl y into the vitreous of dogs with retinal
degeneration, photoreceptor degeneration is reduced.
Fur ther more, production of this factor and
implantation of the encapsulation device into the
vitreous of normal rabbits did not lead to toxic effects
on either the electroretinogram or retinal histology in
these animals at doses that protect photoreceptors in
dogs with retinal degeneration. Such cell-based
delivery devices may be used to provide trophic factors
for the treatment of a variety of retinal degenerative
diseases and, in fact have recently been used in a
human clinical trial evaluating the efficacy of CNTF
in the treatment of retinal degeneration. In this respect,
the implanted encapsulated cell devices function as a
stem cell, providing factors critical to the prevention
of, or recovery from, retinal degenerative disease.
Spontaneously differentiating human embryonic
stem cell lines having many molecular and functional
characteristics of RPE cells have been touted as a
potential source of transplantable RPE cells for
subretinal transplantation into human retinas. Large-
scale genomic analysis was used to compare these cells
to primary human RPE cell lines and they were found
to resemble more closely the molecular signature of
primary RPE cells than previously reported, established
human RPE cell lines. If these cell lines can be
maintained in cell banks and altered so as to facilitate
immune acceptance, they may represent a source of
transplantable tissue.
Studies done over a decade ago evaluated the
potential use of RPE cells as stem cells of sorts: when
RPE cells were injected subretinally into the eyes of
mice with inherited retinal degeneration, rescue of
photoreceptors was observed. It was found that
exogenously injected basic fibroblast growth factor
could mimic this rescue. This led to the concept that
RPE cells may, under appropriate conditions, serve
as a form of cell-based therapy and may, under certain
circumstances, provide a transplantable pool of cells
to rescue diseased photoreceptors and, as such, have
utility in the treatment of retinal degenerations.
Role of Bone Marrow: Derived
Stem Cells
BONE MARROW HEMATOPOIETIC
STEM CELLS
In 1917, Pappenhein postulated the existensce of an
undifferentiated stem cell for blood cells. The hema-
topoietic or blood forming cells are located in the bone
marrow. The lineage of blood cells extends from a
resting stem cell, to transit- amplifyilng precursor cells,
to mature circulting blood cells. Untill recently, most
primitive bone marrow progenitor cell was believed
to be pluripotent, giving rise to stromal cells and
lymphocytic cells, as well as RBCs, WBCs. In addition
to hematopoietic precursor, bone marrow also
contains a mesenchyamal progenitor cell can give rise
to many other cell types such as muscle cells, astrocytes,
and neurons,as well as stromal cells that support
hematopoiesis. However, the accumulating evidence
is that, not only does the bone marrow contain a pluri/
multipotent blood forming stem cell, but it also contains
a cell that has the capacity to circulate to other organs
and replace different nonhematopoietic tissues.
Although these bone marrow-derived cells have
markers of the hematopoietic stem cell [HSC], it has
not been ruled out that this multipotent cell may be
of stromal origin. Serial transplantation indicates that
a single bone marrow cell may give rise to many
different tissue types and suggest that a common
precursor must exist, not only for stromal and
hematopoietic lineages, but also other germ layer-
derived cell types. It is this putative totipotent bone
marrow cell that has stimulated the great revival of
interest in adult stem cells in the last few years. There
are still some caveats to the generally accepted
assumption of pluripotentiality of tissue stem cells
including HSCs.
Role of Adult Bone Marrow:
Derived Endothelial Progenitor
(Stem) Cells
Abnormalities in the retinal or choroidal vasculature:
macular edema, retinal and vitreous hemorrhage, and
fibrovascular scarring commonly contribute to visual
loss in diseases such as age retinal macular degene-
ration, diabetic retinopathy, retinopathy of prematurity,
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and neovascular glaucoma. Retinitis pigmentosa are
commonly thought of as neuronal degenerations, but
most also exhibit vascular abnormalities traditionally
attributed to loss of neuronal elements and accompan-
ying decreased metabolic demand leading to vascular
atrophy. Otoni A et al have describe a newly emerging
paradigms: the existence of trophic cross-talk
between local vascular networks and the tissues they
supply and such interactions almost certainly help to
maintain a functional differentiated state in a variety
of organ systems.

Shen Q et al have shown that,
endothelial cells are also now known to provide trophic
substance that greatly stimulate self-renewal and
expand neural differentiation of neural stem cells.

Given
such interdependency of vascular endothelial cells and
surrounding tissues, it may be possible to use one cell
type to rescue the other in the face of severe stress
such as hypoxia or genetically encoded cell-specific
degenerations. Under such conditions it would be
desirable to have available populations of progenitor
cells useful for such protection.
BONE MARROW: DERIVED STEM CELLS
CAN EXERT A NEUROTROPHIC RESCUE IN
RETINAL DEGENERATION
Humphries P et al has done molecular genetics of
retinitis pigmentos and has identified mutations in over
110 different genes, accounting for only a relatively
small percentage of the known affected individuals
many of these mutations are associated with enzymatic
and structural components of the phototransduction
machinery, including rhodopsin. Most inherited human
retinal digenerations
Otoni A et al have shown that bone marrow
derived stem cells exert vasculotrophic properties.
These cells have also recently been reported to
completely prevent retinal vascular degeneration
ordinarily observed in mouse models of retinal
degeneration, and the vascular rescue correlates with
neuronal rescue. The inner nuclear layer remains nearly
normal and the outer nuclear layer containing
photoreceptors is significantly preserved, with the
rescued mice being predominantly cones. Detectable,
albeit severely abnormal electroretinogram recordings
are observed in rescued mice at time when they are
never observed in control treated, or untreated, rd/
rd eyes. This rescue effect is also observed when human
bone marrow-derived Lin- HSCs are used to treat
severe combined imnunodeficient mice with retinal
degeneration. Large-scale genomic analysis of rescued
eyes revealed significant upregulation of antiapoptotic
gene. It is important to note that the injected bone
marow-derived progenitor cells are never observed
anywhere but in or near blood vessels since these cells
are derived from green fluorescent protein. How this
is going to be used in human is still in question?
Role of Bone Marrow: Derived
Stem Cells in Retinal and
Choroidal Neovascularization
It was Grant and colleague who has first directly
demonstrated that systemically administered HSC
(Hematic stem cell can function as Hemangioblast
during hypoxia stimulated retinal neovascularization).
Hematopoetic stem cells contains a pool of EPCs
(endothelial progenitor cells) capable of incorporating
into retinal vasculature has recently been demonstrated
by several groups. Grant and col l eague have
demonstrated that circulating, undifferentiated
precursor cells can be recruited to sites of retinal
neovascularization and, along with proliferation of local
endothelial cells, can contribute to new blood vessel
growth and development. The relative contribution
of circulating precursor cells and endogenous retinal
vascular endothelial cells to newly forming vasculature
in human disease remains unknown; the experiments
of Grant and colleagues demonstrate that circulating
cells can incorporate into laser-stimulated retinal
neovascularization, but the role of these cells in
nonirradiated hosts where the proliferation of local
inflammatory, precursor, and endothelial cells is not
impaired by lethal irradiation remains unclear. Studies
from several groups have demonstrated, using the
same irradiation/bone marrow reconstitution model
that circulating stem cells can also contribute to laser-
stimulated choroidal neovascularization.
Dorrell MI, et al have demonstrated a role for the
adhesion molecule, R-Cadherin, in the targeting of
HSC to the retinal vasculature when small molecule
antagonizes or function blocking antibodies to
R-Cadherin are used to pretreat Lin-HSC prior to
intravitreal injection, the cells no longer target sites of
angiogensis and participate in the formation of new
retinal blood vessels. Integrin alpha 4 beta 1, a
adhesion molecules may play a role in targeting
circulating EPCs to sites of abnormal angiogenesis
during vascularization of tumor, and that these integrin
may be potential therapeutic target if, indeed circulating
EPCs contribute to pathological ocular angiogenesis.
Interfering with the function of such targeting molecule
used by EPCs to target sites of pathol ogical
neovascularization in combination with cell based
therapies to produce angiostatic molecues locally could
significantly reduced abnormal angiogenesis.
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BONE MARROWDERIVED STEM CELLS CAN
EXERT A VASCULOTROPHIC RESCUE EFFECT
Otoni A at al have injected Lin- HSCs directly into
the eyes of newborn mice while they were forming
their retinal vasculature; in this environment, these cells
can target activated astrocytes, a hallmark of many
ocular vascular and degenerative diseases. Once
targeted to this template of activated astrocytes, the
Lin HsCs participate in normal developmental
angiogenesis in both neonatal mice or injury-induced
neovascularization in the adult.
The HSC fraction used in these studies not only
inhibited angiogenesis when engineered to express an
antiangiogenic, but also resued and stabilized
(e.g. matured) degenerating vessels. More surprisingly,
it was also observed that by preventing vascular
degenertion there is a trophic rescue effect on the
photoreceptors themselves, suggesting that autologuous
bone marrow grafts of HSC fractions containing EPC
may provide trophic effects on associated neural tissue
that goes beyond simple nutrition. Such observations
could provide a rationale for the use of HSC in the
treatment of a variety of inherited retinal degenerations
such as retinitis pigmentosa.
The use of stem cells are difficult and it is also very
difficult to transfer and, it will be necessary to improve
transfection efficiency. The use of human stem cell for
cell base therapy in the eye present a technical
challenge.
Another enigma in the circulating stem cell filled
is the issue of HSC Homing, R-Cadherin is clearly
involved, but all of the molecular signals have not yet
been identified. Identification of these signals would
be of immense benefit in terms of exploiting the
potential use of HSC in therapeutic angiogenesis as
well as directed cell therapy. Finally, which shall type
in adult bone marrow actually adheres to astrocytes
and incorporate into the developing vasculature.
Lund RD et al have shown cells isolated from
umbilical cord tissue rescue photoreceptors and visual
functions in a rodent model of retinal disease.
Progressive photoreceptor degeneration resulting from
genetic and other factors is a leading and largely
untreatable cause of blindness worldwide. The object
of this study was to find a cell type that is effective
in slowing the progress of such degeneration in an
animal model of human retinal disease, is safe and
could be generated in sufficient numbers for clinical
application. We have compared efficacy of four
human-derived cell types in preserving photoreceptor
integrity and visual functions after injection into the
subretinal space of the Royal College of Surgeons rat
early in the progress of degeneration. Umbilical tissue-
derived cells, placenta-derived cells, and mesenchymal
stem cells were studied; dermal fibroblasts served as
cell controls. At various ages up to 100 days,
electroretinogram responses, spatial acuity and
luminance threshold were measured. Both umbilical-
derived and mesenchymal cells significantly reduced
the degree of functional deterioration in each test. The
effect of placental cells was little better than controls.
Umbilical tissue-derived cells gave large areas of
photoreceptor rescue; mesenchymal stem cells gave
only localized rescue. Fibroblasts gave sham levels of
rescue. Donor cells were confined to the subretinal
space. There was no evidence of cell differentiation
into neurons, of tumor formation or other untoward
pathology. Since the umbilical tissue-derived cells
demonstrated the best photoreceptor rescue and
unlike mesenchymal stem cells were capable of
sustained population doublings without karyotypic
changes, it is proposed that they may provide utility
as a cell source for the treatment of retinal degenerative
diseases such as retinitis pigmentosa.
Recent Advances
Atmaca-Sonmez P et al have investigated whether
hematopoietic stem cells (HSC) given systemically can
home to the damaged subretinal space and express
markers of RPE lineage. They have shown that
systemically injected HSC homed to the subretinal
space in the presence of RPE damage and that FC
promoted survival of these cells. Furthermore, the RPE-
specific marker RPE-65 was expressed on adoptively
transferred HSC in the denuded areas.
Harris JR et al have shown that HSCs/HPCs can
migrate to the RPE layer after physical or chemical
injury and regenerate a portion of the damaged cell
layer. Bone marrow-derived cells home to and
regenerate retinal pigment epithelium after injury.
The wet form of ARMD is characterized by
choroidal neovascularization (CNV). A prior study has
shown that adult hematopoietic stem cells (HSCs)
contribute to approximately 50% of newly formed
vasculature in CN. Sengupta N et al have shown that
stromal-derived factor (SDF)-1 is involved with homing
of HSCs from bone marrow to target tissue. Vascular
endothelial cadherin (VE-cadherin, or CD144) is
involved in endothelial cell adhesion. Preventing
homing and/or adhesion of progenitor cells to
damaged choroid could reduce CNV.
METHODS: Adult C57BL/6J mice.
RESULTS: CNV lesions from eyes treated with anti-
CD144 showed significantly less incorporation of gfp+
206
cells compared with those treated with anti-SDF-1.
Antibody treatment generally reduced the degree of
gfp+ stem cell recruitment and incorporation into the
CNV lesions, compared with the control. Treatment with
either antibody also significantly reduced the size of the
CNV lesions. These results indicate that homing and
adhesion of progenitor cells to CNV may be targeted
differentially or in combination to prevent CNV.
Role of Corneal Stem Cell in
Pediatric
Stem cell research offers hope to countless patients
whose conditions have here to fore been deemed
incurable. Better understanding of stem cell behaviors
and functions will lead to insights into biological
mysteries encompassing the fields of angiogenesis,
development, tissue homeostasis, wound healing, and
carcinogenesis. Clarity of vision requires smooth ocular
surface on which the corneal epithelial cells undergo
continuous turnover every 3 to 10 days.Tragically,
many patients are blinded and devastated by severe
ocular surface diseases due to limbal stem cell
deficiency even though, besides opaque cornea, their
eyes are otherwise healthy. Corneal stem cell
transplantation offers hope by creating clear windows
for these eyes; unfortunately, the long-term successful
outcome remains limited. The nature of corneal
epithelial stem cell is poorly understood, but many
circumstantial evidences suggest the presence of
source cells in the limbal region of the eye.
Nonetheless, the precise biomarker of corneal stem
cell remains elusive. The stem cell puzzle can be solved
with application of the fundamental scientific method-
asking salient questions at the right time and finding
answers using keen observations and proper tools.
Readily accessibility and structural simplicity of the
cornea lend themselves to study of the stem cell biology.
The ability to identify and isolate corneal stem cell will
be a gateway to meaningful investigation into its
biology. This advance will also have direct impact on
improving the efficacy of promising stem-cell-based
therapies, including limbal stem cell transplantation.
Technical advances in the surgical reconstruction
of severely injured or diseased ocular surfaces have
improved the quality of the life for many of those
affected. An ever-present hurdle, however, is the
limited availability of suitable donor material, partly
because of this, the concept has emerged of fabricating
transplantable tissue constructs by expanding small
biopsies of corneal epithelial cells taken from the limbs.
Conjunctival stem cells represent a small quiescent
subpopulation of epithelial cells of ocular surface.
Corneal epithelial stem cells reside in the basal region
of the limbus, and are involved in renewal and
regeneration of corneal epithelium. Following injury,
basal stem cells are stimulated to divide and undergo
differentiation to form transient amplifying cells (TAC).
Subsequent cell divisions result in non-dividing post-
mitotic cells (PMC),which migrate towards the central
cornea and superficially forming terminal differentiated
cells (TDC).
The first step is the isolation of healthy corneal
epithelial cell, and these are collected from the
unaffected eye of the individual to be treated if the
problem is in one eye only, or from donor material
if the problem is bilateral. These cells are then cultivated
in the laboratory for a couple of weeks under carefully
monitored conditions, so that they grow into a nicely
stratified cellular multi-layer, which resembles corneal
epithelium, in situ. This can then be used for the surgical
repair of the ocular surface. One problem, however
is that cells grown in this way on regular cell culture
dishes are difficult to detach from the underlying plastic
without damaging them in some way. Now, however,
evolving research has provided a way to obtain intact,
isolated corneal epithelial cell sheets with minimal
harm. The secret lies in the use of a novel temperature-
responsive culture surface, which readily supports cell
growth, but also allows easy cell release.
OCULAR SURFACE STEM CELLS (FIG. 32.1)
More than two decades ago, Thoft and Friend described
the X,Y and Z hypothesis which explained how corneal
epithelial cells are continuously shed from the surface
and regenerated by cells from the periphery. The limbal
stem cell residing in the alisades of Vogt are now
believed to be the never-ending source of corneal
epithelial cells. Adult corneal and conjunctival stem cells
represent a small, quiescent subopulation of epithelial
cells of the ocular surface. The limbus is a 1.5 mm-
to-2 mm-wide area that straddles the cornea and
Fig. 32.1: Ocular surface stem cells
207
bulbar conjunctiva. Corneal epithelial stem cells reside
in the basal region of the limbus, and are involved
in the renewal and regeneration of the corneal
epithelium.

Following injury, these limbal basal stem
cel l s are stimul ated to divide and undergo
differentiation to form transient amplifying cells (TACs)
(Fig. 32.2). Subsequent cell divisions result in non-
dividing post-mitotic cells (PMCs), which then
terminally differentiate and migrate towards the central
cornea and superficially, taking on the final corneal
phenotype as terminal differentiated cells (TDCs). Their
presence al l ows continued repl acement and
regeneration of tissues following injury, thereby
maintaining a steady-state population of healthy cells.
Conjunctival and corneal epithelial cells have been
shown to belong to two separate, distinct lineages.
Unlike corneal epithelium, conjunctival epithelium
consists of both non-goblet epithelial cells as well as
mucin-secreting goblet cells. Wei et al showed that both
these populations of cells arise from a common
bipotent progenitor cell. The conjunctival forniceal
region appears to be the site that is enriched in
conjunctival stem cell, although stem cells are also likely
to be present in other regions of the conjunctiva.
Fig. 32.2: Limbal epithelial stem cell therapy
HOPE OF STEM CELLS FOR UNTREATABLE
EYE DISEASE
There are practical and ethical issues to the use of
embryonic stem cells and the alternative of using
somatic or adult stem cells has major advantage in
terms of immediate clinical application. The adult
human eye harbors stem cells in the limbal region,
in the conjunctiva, the pars plana and plicata of the
retinal ciliary margin and adult human retina.
IDENTIFICATION OF STEM CELLS
Several putative stem cells markers have been
proposed, although no single molecular marker that
is specific for stem cells has been identified.
Taking advantage of the slowcycling characteristic
of stem cells, an indirect method of labelling stem cells
was developed.
Another characteristic of stem cells is their capacity
to remain highly proliferative in vitro.

Cells that have
the highest proliferative capacity (holoclones-with less
than 5% of colonies being terminal) are considered
stem cells. Pelligrini et al showed by clonal analysis that
nuclear P63 was abundantly expressed by epidermal
and limbal holocolones, but were undetectable in
paraclones, suggesting that P63 might be a marker
of keratinocyte stem cells.
Disease Arising from Stem Cell Deficiency due to
Ocular Surface Causes
Ocular surface failure may be of two types according
to Tseng et al depending on the epithelial phenotype
as identified by impression cytology. Type 1 failure
characterized by squamous metaplasia where the non-
keratinized corneal epithelium is converted to a
keratinized epithelium. Type 2 failure is characterized
by limbal stem cell deficiency where the normal corneal
epithelial is replaced by conjunctival epithelium. Limbal
stem cell deficiency can be caused by the variety of
hereditary or acquired disorders. Inherited disorders
include aniridia keratitis and kratitis associated with
multiple endocrine deficiency, in which limbal stem
cells may be congenitally absent or dysfuntional.
Acquired conditions that may result in limbal stem cell
deficiency include Stevens-Johnson syndrome,
chemical injuries, ocular cicatricial pemphigoid, contact
lens-induced keratopathy, multiple surgeries or
cryotherapies to the limbal region, neurotrophic
keratopathy and peripheral ulcerative keratitis.
Acquired disorders from the majority of cases seen in
the clinical setting.
Limbal stem cell deficiency is characterized by
persistent or recurrent epithelial defects, ulceration,
corneal vascularization, chronic inflammation, scarring,
208
and conjunctivization (conjunctival epithelial ingrowth),
with resultant loss of the clear demarcation between
corneal and conjunctival epithelium at the limbal
region (Fig. 32.3).
The diagnosis of the presence of limbal deficiency
is crucial as these patients are poor candidates for
conventional corneal transplantation alone. Conven-
tional corneal transplantation alone. Conventional
corneal transplantation does not address the problem
of inadequate corneal epithelial replacement, and
subsequent conjunctival ingrowth, vascularization and
an inflammation ultimately results in grant rejection
and failure.
Chronic instability of the corneal epithelium and
ulceration may lead to progressive melting of the
cornea and subsequent perforation. The pathgnomic
feature is conjunctival epithelial ingrowth over the
cornea. Limbal stem cell deficiency may be localized
or generalized,

localized stem cell deficiency is
characterized by some sectors of normal and some
sectors showing conjunctivization in regions devoid of
healthy epithelium. Impression cytology confirms the
presence of conjunctival goblet cells.
Diagnosis of limbal stem cell deficiency is crucial
as these patients are poor candidates for conventional
corneal transplantation,

as conventional corneal
transplantation does not address the problem of
inadequate corneal epithelial replacement which leds
to subsequent conjunctival ingrowth, vascularization
and inflammation finally resulting in graft failure and
rejection.
Limbal autograft transplantation, first described in
detail by Kenyon and Tseng,

was limited to unilateral
cases or bilateral cases with localized limbal deficiency,
where sufficient healthy tissue was available for
harvesting.
Inpatients with bilateral diffuse disease, allogenic
limbal graft is required, which when obtained from
cadaveric donors, the entire 360

annulus of limbus
can be transplanted, either as intact annular ring or
in several contagious segments. Limbal allograft may
also be obtained from HLA matched living related
donors, to reduce risk of immunologic rejection
(Fig. 32.4).
Limbal stem cell transplant may be combined with
penetrating keratoplasty which may be in same setting
or in a staged manner. Severe ocular surface disorders
are often associated with conjunctival or lid pathology
which may require adjunctive surgical procedures in
reconstruction of ocular surface such as fornicela
reconstruction with symblepharon release, correction
of cicatrising lid disease.
The use of allogenic grafts is associated with risk
of graft rejection and there may be need for long-
term systemic immunosuppression with cyclosporin,
FK 506 or mycophenolate mofetil. Inspite of good
early success in several studies,subsequent reports
suggest that approximately 50% of these grafts fail with
in 3 to 5 years.
LIVE-RELATED VS CADAVERIC LIMBAL
TRANSPLANTATION (LT)
In the unilateral and bilateral cases of LSCD, fresh
donor tissue may be harvested either from the healthy
fellow eye in the former, or from a live-related donor
or corneo-scleral rim or enucleated eye of a cadaver
in case of the latter.
It is essential to screen the donor thoroughly prior
to surgery for evidence of limbal stem deficiency. Close
monitoring of the donor is advised after surgery, as
it is yet unknown how these eyes will respond to an
epithelial insult in the future and there may be stem
cell attrition due to inflammation and sub-clinical donor
disease. The other alternative in bilateral cases is
cadaveric limbal allo-transplantation.
Fig. 32.3: Limbol stem cell deficiency
Fig. 32.4
209
CULTIVATED VS DIRECT LIMBAL
TRANSPLANTATION
The potential problems with direct limbal trans-
plantation include harvesting a relatively large amount
of limbal tissue (upto 6 clock hours) from healthy
donor eyes. Pellegrini et al were the first to describe
culturing of limbal stem cells ex vivo thereby spear-
heading ophthalmology into the field of regenerative
medicine. Technically cultivated stem cells have the
disadvantages of the long procedure.
1. It takes 10 days to 2 weeks for the cells to grow.
2. A dedicated stem cell laboratory is required.
Bioengineered Ocular Surface Equalents for
Transplantation (Fig. 32.5)
Limbal autograft overcomes the problem of
immunologic rejection, but because large segments are
required this places the donor eye at the risk of surgically
induced donor stemcell deficiency. The use of
autologus cultivated limbal stemcell has overcome this
problem.

for this procedure only a small limbal biopsy
is needed (approximately 2mm
2
),which minimizes the
risk of damage to the donor eye. This is then cultivated
on various substrates, such as human amniotic
membrane or fibrin based substrates, which results in
a composite graft which is then transplanted on the
diseased eye. With this procedure reasonable success
upto one year of follow-up has been achieved.

More
recently Tan DT et al demonstrated the development
of serum-free derived conjunctival tissue- equalents.
The use of bioengineered tissue replacements
represents the future for replacement and regeneration
of various tissues and organs.
Hisatomi T et al have provided direct and novel
evidence for the migration of BM and HSC cells into
the sclera differentiating into macrophages and
dendritic cells.Vast infiltration of BM and HSC cells was
found to be part of inflammatory process in EAU.
Corneal epithelial stem cells are known to be
localized to the basal layer of the limbal epithelium,
providing a model system for epithelial stem cell
biology; however the mechanisms regarding the
maintenance of these stem cells in their specialized
niche remain poorly understood. N-cadherin is a
member of the classical cadherin family and has
previously been demonstrated to be expressed by
hematopoietic stem cells. In the present study Hayashi
R, et al have demonstrated that N-cadherin is expressed
by putative stem/progenitor cells as well as melanocytes
in the human limbal epithelial stem cell niche.
Additionally, they have demonstrated that upon in vitro
culture using 3T3 feeder layers, loss of N-cadherin
expression occurs with cell proliferation. These results
indicate that N-cadherin may be a critical cell-to-cell
adhesion molecule between corneal epithelial stem/
progenitor cells and their corresponding niche cells in
the limbal epithelium.
Sun CC demonstrated that intact human AM may
prevent cultured human limbal epithelial cells from
undergoing apoptosis. IL-1RA might be a candidate
mediator to exert as an anti-apoptotic molecule during
the interaction between human limbal epithelial cells
and intact human AM.
Li W et al after dissolution of original amniotic BM,
new BM formed by ex vivo expanded human limbal
corneal epithelial cells on iAM deposits much faster
and is more mature,resulting in regeneration of a limbal
epithelial phenotype. In contrast, BM deposition is
delayed and remains immature on dAM, resembling
wound healing by a corneal epithelial phenotype. Thus,
BM resynthesis may be used as another objective
readout for assessing the success of ex vivo expansion
of limbal epithelial progenitor cells on AM.
Recently, Prof Yuichi Mori, dr Hiroshi Yoshioka of
Waseda and Dr Samuel JK Abraham (Cardiac surgeon,
Yamanashi University Hospital, Japan) in collaboration
with M/S Nichi-In Biosciences (P) Ltd has started a
joint venture program in india with G Sitalakshmi from
Sankara Nethralaya and are in the process of
collaborating with dr Rajpal from RP Centre using non-
biological (Totally synthetic) material called
Mebiol Gel.
First time in the world:
This is the first time in the world that a nonbiological
(Totally synthetic) material has been used as a substrate
to grow (cultivate) corneal limbal stem cells thereby Fig. 32.5
210
paving a way for avoiding biological materials for this
purpose and avoiding viral and other dangerous
known and unknown contamination in such biological
materials as well as chances of rejections. The invention
has been proven with all the latest scientific parameters
that the cells are stem cells and upon confirmation of
the same by our co-researchers in Japan, a joint patent
through PCT (Patent Cooperation Treaty) has been
filed.
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C H A P T E R
33
Primary Globe Repair
Introduction
Trauma to the sclera and cornea are common. Review
of data of United States Eye Injury Registry and Indian
Eye Injury Registry revealed that approximately 10%
of all reported serious eye injuries involve cornea and
sclera. Males are predominantly affected and more
common in younger age. However, more than half
of the injuries occur at home.
It can occur secondary to penetrating injury or
blunt trauma. The open globe injury secondary to blunt
trauma is termed as globe rupture and those secondary
to penetrating injury is termed as lacerating injuries.
It can be partial thickness or full thickness laceration.
Regardless of the object and nature of injury, the
management algorithm is similar in all cases with open
globe injuries. The four pronged approach in manage-
ment of open globe injuries is:
a. Prevent further trauma to the eye
b. Minimize risk of infection
c. Prevent psychological trauma to the patient and
his family
d. Minimize legal problems to oneself and to his
institute.
Objectives of Globe Repair
PRIMARY
Restoration of structural integrity
Achieve watertight closure
Prevent infection
Smooth and optically effective refractive surface
Spherical cornea to minimize astigmatism and better
contact lens fitting
Reduce scarring
SECONDARY
Removal of disrupted lens and vitreous
Avoid uveal and vitreous incarceration
Removal of intraocular foreign bodies
The basic objective of globe repair should be DO
NOT HARM.
Strategic Planning for Primary
Globe Repair
No two ocular trauma cases are alike and irrespective
of the configuration or etiology of ocular trauma, the
following four pronged approach to ocular trauma
patient will help in optimizing anatomical and visual
results in ocular trauma patients. The four pronged
approach is:
Minimizing possibility of further trauma to the eye:
Further trauma to the eye can be minimized by
trying to operate at the earliest possible, protecting
the eye with rigid eye shield and avoiding
manipulation of the traumatized eye in emergency
out patient clinic.
Minimizing infectious risks: Infectious risks to the
eye can be prevented by operating the eye as early
as possibl e and by giving broad spectrum
intravenous antibiotics.
Minimizing psychological trauma to the victim and
victims family can be minimized by gentle but frank
counseling of trauma victim and his family. Guarded
visual prognosis should be explained to the patient
and all the consequences should be gently
explained. Need for prolonged postoperative
follow-up and compliance is warranted to the
patient at initial setting.
Minimizing legal problems to oneself and to selfs
institute by proper documentation and filling up
medicolegal forms as and when required.
Algorithm for Management of
Open Globe Injury
Complete evaluation of the eye and adnexa.
Ancillary testing as necessary.
215
Identification of any factors that could confound
the management.
Development and execution of the therapeutic
plan.
COMPLETE EVALUATION OF THE
EYE AND ADNEXA
Detailed history including details about the incidence
and objects causing the injury should be elucidated
from the patient or informant and documented in the
file. Relative afferent papillary defect or consensual
reflex of the light in fellow eye should be assessed for
optic nerve integrity. External examination and diffuse
slitlamp examination should be carried out to assess
the complete extent of damage to the eye without
causing further trauma to the eye and intraocular
structures. Fundus examination should be carried out
at the earliest sitting if fundus view is not precluded
because of media haze.
ANCILLARY TESTING AS NECESSARY
Ultrasound examination of the eye with gentle standoff
technique can be employed to assess the posterior
segment status and to rule out intraocular foreign body
in suspected cases. X-rays or CT scans can be employed
in selective cases to rule out intraocular foreign body
and/or bony status of the orbit/optic canal.
IDENTIFICATION OF ANY FACTORS THAT
COULD CONFOUND THE MANAGEMENT
To watch out for infection, intraocular foreign bodies
or other factors which can have impact on final visual
outcome.
DEVELOPMENT AND EXECUTION OF THE
THERAPEUTIC PLAN
The planning in cases of open globe injury could be
of broad spectrum comprises.
Surgical vs Nonsurgical
Management
NONSURGICAL MANAGEMENT
Nonsurgical management can be considered in cases
with self sealed corneal laceration or those which can
be sealed with help of tissue adhesives and small
conjunctival lacerations. Cyanoacrylate glue is the tissue
adhesive which can be of great help in providing
support lasting for several days to several weeks.
Cyanoacrylate glue on exposure to air starts getting
polymerized. Dry the surface of the cornea after
removing the loose or necrotic tissue and then apply
the thin layer of cyanoacrylate glue with help of cotton
tip applicator. The glue is allowed to get dry and if
required another thin layered film of glue is applied
on the previously layered glue. Bandage contact lens
needs to be applied on surface of glue and cornea
following tissue adhesive application.
SURGICAL MANAGEMENT
The different surgical options which can be contemp-
lated depending on the case to case basis:
Corneal laceration repair
Corneoscleral laceration repair
Scleral laceration repair
Limbal laceration repair
Patch grafts
With or without iris abscission or repositioning
With or without lens aspiration
With or without vitrectomy and intraocular
antibiotic injections
With complete pars plana vitrectomy with other
vitreoretinal procedures
The management of these injuries is thus a thought
out process, rather than a reflexive response to an
obvious injury. The present chapter will highlight on
the surgical principles for corneal and scleral laceration
repair.
Anesthesia
The recommended anesthesia in all open globe injuries
should be general anesthesia, but the cases with small
lacerations can be managed under local anesthesia.
The patient is prepared for surgery as soon as possible
and should be medically and neurosurgically cleared.
For general anesthesia, the time of the last meal or
drink determines when surgery is scheduled. To prevent
aspiration, at least 6 hours should have elapsed since
the last meal. Once the physician decides to repair the
laceration, the patient should be kept NPO. Anesthesia
should be achieved without any increase in intraocular
pressure, which can occur during intubation or because
of anesthetic agents. Depolarizing agents (e.g. succinyl-
choline) are not used. Although succinylcholine
possesses several advantages, it contracts extraocular
muscles and increases intraocular pressure. External
pressure from the mask can also increase intraocular
pressure.
Preparing the Eye
The eye should be prepared and draped with care.
Pressure should not be applied to the globe. The eye
is irrigated with a sterile balanced salt solution (BSS)
to remove any superficial foreign bodies. The eye is
216
gently examined to evaluate the extent of damage.
If the globe appears unstable, sutures are first applied
prior to exploration of the wound.
Most Corneal Lacerations
Most corneal lacerations require suture placement.
Prompt, secure wound closure is especially important in
children who are at greater risk of inadvertently rubbing
the eye with consequent reopening of a tissue adhesive
or contact lens supported wound. Large corneal
laceration, sclera laceration, corneoscleral laceration,
displaced wound, wounds with tissue incarceration such
as iris or lens or vitreous incarceration should be taken
up for primary wound repair at the earliest possible.
Small Corneal Laceration with Reasonably
Formed Anterior Chamber
Suture the corneal wound directly with 10-0 nylon
suture, need not enter into anterior chamber.
Less Stable Wound with Shallow or Flat Anterior
Chamber
Wound cleaning with normal saline, formation of
anterior chamber with help of viscoelastic. Viscoelastic
can be injected through side port made with help of
MVR blade, but in cases of collapsed globe it might be
difficult to make the side port and form the chamber
with viscoelastic and hence in such cases viscoelastic can
be injected directly through the corneal wound and
chamber can be completely or partly formed. The
eventual aim in corneal laceration repair is definitive
placement of corneal sutures to make the wound
watertight, minimize scarring, and reconstruct the native
nonastigmatic corneal contour. One can start by taking
superficial temporary sutures in order to approximate
the wound edges and subsequently those sutures can
be replaced with definite deep sutures at end of surgery.
Monofilament 10-0 Nylon Suture Material
Monofilament 10-0 nylon suture material on a fine
spatulated design microsurgical needle is used for
corneal suturing. Some surgeons even prefer use of
11-0 nylon sutures especially for wounds involving
visual axis. A number of strategies for corneal suturing
are available. The simplest involves progressively
halving the wound with simple interrupted sutures.
These definitve corneal sutures should be approximated
1.5 mm long, approximately 90% deep in the stroma,
and of equal depth on both sides of the wound.
Shallow sutures will cause internal wound gape; sutures
that are asymmetric or of unequal depth will result
in wound override. On the contrary, full thickness
sutures can act as conduit for microbial invasion. In
shelved wounds, the placement of sutures should be
equidistant with respect to internal aspect of the wound
and tied without undue tension to optimize tissue
apposition. On the other hand, wounds with
macerated or edematous edges require longer sutures
for security.
Suture Bites through the Visual Axis
Suture bites through the visual axis should be avoided.
If suture needs to be taken through the visual axis,
a number of techniques can be used to minimize
scarring. Sutures near to visual axis should be shorter,
superficial and relatively loose as against the peripheral
sutures which should be longer, deeper and tighter.
So, also the visual axis can be straddled by sutures
placed at each side of, but not directly through the
axis itself. More importantly, No Touch Technique
is employed wherein the globe is stabilized away from
the site of corneal wound and sutures are directly
passed through the corneal wound without holding
the corneal wound edges which will prevent tissue
damage in visual axis thereby preventing scarring at
visual axis.
Number of Suturing Techniques
Number of suturing techniques has been discussed and
described in the literature. In cases with straight
lacerations, a running shoestring closure may minimize
astigmatism and scarring, however at times the wound
integrity may not be achieved as perfectly as it could
have been with interrupted sutures. If a running suture
is used, the bites should be placed perpendicular and
equidistant to a best fit imaginary line through the
wound, irrespective of laceration itself. However, while
using an interrupted suture technique for curvilinear
or irregular lacerations, all sutures should be placed
perpendicular to the wound to avoid transverse shifting
of the wound margins.
Corneoscleral Laceration
In cases with corneoscleral laceration, first, a suture
is applied to the limbus, and the wound is tightly
secured. This suture helps to anatomically approximate
the wound. After the first suture is applied, an iris
prolapse or a vitreous prolapse is treated. In the
presence of an iris prolapsed depending on the viability
of iris tissue it is either repositioned or absiccised. In
the presence of a vitreous prolapse, a vitrectomy is
performed with cellulose sponges or an automated
vitrector. During the vitrectomy, traction on the vitreous
should be avoided. Any vitreous in the anterior
segment may be removed using a vitrectomy machine.
After the corneal wound is repaired, the scleral wound
217
is explored. This exploration is achieved by performing
a limbal peritomy at the site of the limbal wound. The
sclera wound is secured with help of interrupted or
continuous 7-0 vicryl suture or 8-0 vicryl suture.
Segments of scleral laceration are explored and
repaired. This method helps to stabilize the eye and
to prevent uveal or vitreous prolapse.
Scleral Laceration
Scleral laceration should be repaired as far posteriorly
as possible; far posterior scleral ruptures may be left
unsutured. While repairing scleral lacerations, care
must be taken to not exert pressure on the globe. In
the presence of uveal prolapse, the prolapsed tissue
is reposited. The preferred method of sclera wound
closure over prolapsed uveal tissue is a zippering
technique wherein the sclera wound is closed from
anterior end, i.e. limbal end with interrupted sutures
placed successively proceeding posteriorly. One should
never do excision of the prolapsed uveal tissue unless
it is necrotic because it causes excessive bleeding.
Vitreous prolapse is managed by performing a
vitrectomy with cellulose sponges and scissors or by
using an automated vitrector. At every step, care should
be taken to prevent iatrogenic damage. The sutures
are placed closely together and tied to achieve a
watertight closure. The conjunctiva is sutured using 8-
0 or 9-0 Vicryl.
Posterior Scleral Laceration
Scleral laceration without corneal involvement may
occur in a variety of settings. Posterior sclera dehiscence
or occult sclera dehiscence can be suspected based
on history and mode of ocular trauma, poor visual
acuity, conjunctival chemosis, deep or shallow anterior
chamber, low intraocular pressure, hyphema and/or
subconjunctival pigmentation. Lacerations extending
beyond equator of the globe can be left unsutured
if attempting suturing is causing more trauma to the
globe, this sclera perforations will be taken care by
delayed secondary healing.
Patch and a Shield
A patch and a shield are applied to the eye. Postopera-
tively, patients should be carefully monitored for signs
of infection. Pain, photophobia, redness, tearing, or
a deterioration of vision should alert the physician to
look for signs of endophthalmitis. Conjunctival
injection, chemosis, corneal edema, and elevated
intraocular pressure may be present but are not
diagnostic of infection. A more than expected anterior
chamber reaction and cells in the vitreous are most
suggestive of endophthalmitis.
Fig. 33.1: Corneal laceration operated elsewhere
Fig. 33.2: Corneal laceration repaired under
topical anesthesia
Fig. 33.3: Corneal laceration repaired with hypopyon
218
Fig. 33.4: Corneal laceration with eye lash in wound
Fig. 33.5: Corneal laceration with infection of
wound edges
Fig. 33.6: Corneal laceration with traumatic cataract
Fig. 33.7: Corneal wound revision done
Fig. 33.8: Open globe injury repaired
Fig. 33.9: Open globe injury with iris prolapse
219
Fig. 33.10: Post-corneal tear repaired with SFIOL
Summary
Corneal and sclera wounds commonly present to the
emergency clinic and management of this cases should
be prioritize to optimize visual potential in traumatized
eyes. Management of corneal and sclera laceration
requires careful evaluation and planning prior to closure.
The globe must be closed so that it is watertight with
the original anatomy restored and the original function
can be as approximated as possible. Closure of the
cornea and sclera is different from the typical skin
technique of halving the wound. Corneal wound is
closed based on the principles explained whereas sclera
wound should be carefully explored and should be
addressed by doing atraumatic sclera laceration repair.
Bibliography
1. Beatty RF, Beatty RL. The repair of corneal and sclera
lacerations. Semin Ophthalmol 1994;9(3):165-76.
2. Coumhaire-Poutchinian Y. Management of the repair of
scleral and corneal injuries. Bull Soc Belge Ophtalmol
1996;260:81-88. (Article in Ffrench)
3. Drews RC. Sodium Hyaluronate (Healon) in the repair
of perforating injuries to the eye. Ophthalmic surg
1986;17:23-29.
4. Eisner G: Eye surgery: an introduction to operative
technique, New York, 1980 Springer-Verlag.
5. Hamill BM. Corneal and Scleral trauma. Ophthalmol Clin
N Am 15(2002):185-94.
6. Hersh PS, Shingleton BJ, Kenyon KR. Management of
corneoscleral lacerations. Eye Trauma. 1991. Mosby's
Publications 143-58.
7. Lamkin JC, Azar DT. Simultaneous corneal laceration
repair, cataract removal and posterior chamber intraocular
lens implantation. Am J Ophthalmolo. 1992 Jun 15;
113(6):626-31.
8. Lin DT, Webster RG Jr, Abbott RL. Repair of corneal
lacerations and perforations. Int Ophthalmol Clinics.
1988 Spring 28(1):69-75.
9. Rowsey JJ, Hays JC, Refractive reconstruction for acute
eye injuries, Ophthalmic Surg 1984;15:569-74.
10. Russel SR, Olsen KR, Folk JC. predictors of sclera rupture
and the role of vitrectomy in severe blunt ocular trauma.
Am J Ophthalmol 1984;102:547-50.
Iatrogenic Ocular Trauma
and its Complications
Management
C H A P T E R
34
Management of Iatrogenic
Inflammation of the Eye
NR Biswas, GK Das, Viney Gupta (India)
Introduction
For the treatment of any type of inflammation
including iatrogenic, both the steroids and non-steroidal
anti-inflammatory drugs may be used.
The corticosteroids are essential drugs in ophthal-
mological diseases. It is a boon to the patients when
it is used with proper indications. It is a two-edged
sword, and can cause serious complications and side
effects if it is used unwisely. Are we using corticosteroids
judiciously? This question must always be kept in mind
and answered before instituting this therapy. Before
planning the corticosteroid therapy, we must keep in
mind its ocul ar hazards. In cl inical practice
corticosteroids are often used as shotgun therapy or
as a placebo when all is not going well. This practice
must be discouraged.
Topical Application
The route of administration of corticosteroids depends
primarily on the site of involvement. Topical therapy
is effective in anterior segment diseases, including
disorders of lids, conjunctiva, cornea, iris and ciliary
body. Ease of application, relatively low cost, and
absence of systemic complications strongly favor local
routes whenever they are effective.
The course of posterior segment disease (chorio-
retinitis, optic neuritis, and posterior scleritis) is not
appreciably affected by topical corticosteroids and
requires systemic therapy.
a. Are diluted corticosteroid drops effective in
controlling intraocular inflammation?
It was demonstrated that diluted corticosteroids have
therapeutic anti-inflammatory effect in strengths of
0.01 and 0.005 percent.
b. Corticosteroids in infective corneal diseases:
Local installation of corticosteroids in frank suppurative
conditions are generally considered as contraindications
to their use. In experimental studies the available 0.1
percent dexamethasone further diluted as 1:10 or 1:20
dilution had no virus or fungal replications enhancing
effect when instilled 10 times a day, while 1:5 dilution
or undiluted available dexamethasone drops (0.1%)
enhanced virus and fungal growth. Moreover,
adequately diluted corticosteroid does not increase the
risk of enhancing the collagenase effect.
c. Corticosteroid therapy in vernal conjuncti-
vitis and allergic disorders: The use of cortico-
steroids locally has a beneficial effect in vernal
conjunctivitis. But prolonged use is attended by
unwanted side effects like cataracts, glaucoma and
secondary keratoconus.
d. Use of corticosteroids in alkali burns of
cornea and conjunctiva: The use of corticosteroids
in alkali burns is obligatory and seems beneficial.
e. Use of corticosteroids in pseudophakic
bullous keratopathy (PBK): The effects of 5%
hypertonic sodium chloride drop and deturgescent
drops, prepared by mixing betamethasone eye drops
(0.1%) 1 ml; glycerin, 1 ml and artificial tear drops
8 ml, achieving 10% glycerin and 1:0 betamethasone
eye drops (0.1%), were compared in a controlled
clinical trial in 50 cases of PBK. These were instilled
10 times a day. The deturgescent drops were
significantly superior in subjective as well as objective
parameters like discomfort, foreign body sensation,
corneal clarity and improvement in vision, etc. as
compared to 5% hypertonic saline.
f. Ocular hypertensive effect of corticosteroids:
Surgical trauma causes inflammation which demands
the use of corticosteroids to prevent the trabecular
meshwork, corneal endothelium and other inner
structures of the eye from damage by inflammatory
response as well as its debris. But, ocular hypertension
inducing effects restrict their wide usage. In this regard,
1:10 or 1:20 diluted steroid did not have any ocular
hypertensive effect.
224
The use of 1:10 or 1:20 dexamethasone (0.1%)
for specified periods is safe to be used in glaucoma
patients after intraocular surgery or when there is an
associate uveitis, as there should be negligible risk of
producing hypertension.
Systemic Therapy
Prednisone has become a corticosteroid of choice
because it is inexpensive, short acting, and relatively
free from sodium retention. It may be used in divided
doses, a single daily dose, or a single alternate day
dose.
Single daily dose: For long-term low-dosage
maintenance (as for chronic uveitis), a single, morning,
daily dose of prednisone may be optimal.
Alternate day therapy: The undesirable side effects
of systemic corticosteroid therapy can be substantially
reduced by using alternate day therapy rather than
divided dosage. Briefly stated, the entire total dose of
corticosteroid that would have been given during a
2-day period is administered as a single dose every
other morning.
Repository Injection
The ophthalmologist who wishes to administer cortico-
steroids by subconjunctival injection should consider
use of the repository form of methyl-prednosolone
acetate (Depo-Medrol). Thus suspension form of pre-
dnisolone provides a constant source of corticosteroid
that lasts for 2 to 4 weeks.
Intravitreal Injection
Intravitreal 0.1 ml (Dose 50 mg/ml) is injected to
prevent proliferation of fibroblast. It seems helpful to
combat proliferative vitreoretinopathy.
Controlled Release Vehicles
Ocusert devices delivering 10 mg of hydrocortisone
acetate/hr were used to treat allergic conjunctivitis.
Pulse Therapy
Slow intravenous infusion of 100 mg Prednisolone daily
for consecutive three days shows good response in
Haradas disease. If needed, repeat dose can be given
after 14 days.
Indications
In general, corticosteroid therapy may be helpful for
all allergic ocular diseases, for most non-pyogenic
inflammations (episcleritis, scleritis, uveitis, interstitial
keratitis, optic neuritis and the like), and for the
reduction of immunologic responses.
USE IN OCULAR SURGERY
1. Cataract
2. Corneal graft rejection
3. Glaucoma surgery
4. Retinal detachment
5. Vitreous surgery
6. Strabismus
7. Intraocular foreign body.
Contraindications and
Complications
SYSTEMIC COMPLICATIONS
Peptic ulceration
Osteoporosis
Femoral head ischemia necrosis
Pseudotumor cerebri
Exophthalmos.
LOCAL CONTRAINDICATION AND
COMPLICATIONS
Superinfection
Activation of tuberculosis
Uveitis
Glaucoma
Corticosteroid mydriasis
Corticosteroid induced cataract.
The severe scleritis associated with rheumatoid
arthritis, an example of immunological disorder does
respond to corticosteroid treatment but the patient may
suffer structural loss of sclera upto more severe
scleromalacia as a result of treatment.
Sympathetic ophthalmia is a classic example of a
disease responsive to corticosteroid therapy, but
requires prolonged therapy.
Non-specific iridocyclitis and chorio-retinitis, as well
as herpetic keratitis do seem to benefit from cortico-
steroid therapy.
Posterior ocular effects require systemic adminis-
tration or retrobulbar injection.
225
Management of Iatrogenic Inflammation of the Eye
Responsive Diseases
BOECKS SARCOID UVEITIS
The response of Boecks sarcoi d uvei ti s to
corticosteroid therapy may be very gratifying. Topical
use of corticosteroids and mydriatics is often
insufficient to arrest the disease. Addition of systemic
corticosteroid therapy has frequently given prompt
subjective relief, followed within a few weeks by
considerable objective improvement. Upto 200 mg
daily was used and produced a consistently favorable
symptomatic effect.
ORBITAL MYOSITIS
Acute inflammation of one or more extraocular muscles
may be a sequel to upper respiratory infections. These
painful restrictions of movement may respond
promptly to corticosteroid therapy.
OCULAR PEMPHIGOID
Although pemphigoid is characteristically a slowly
progressive chronic subepithelial scarring process,
episodes of acute inflammation may occur. These
typically are nonresponsive to topical corticosteroid
therapy. Systemic corticosteroids in dosage of 60 to
100 mg/day have caused remission of the disease.
HERPES ZOSTER
In a small series of 11 patients with herpes zoster, very
favorable results were reported from the systemic
administration of cortisone or ACTH.
NEOPLASMS
Hemangiomas, intracranial plasmacytoma, medullo-
blastoma, ewings tumors respond well to corticosteroid
therapy.
TOLOSA-HUNT SYNDROME
Recurrent unilateral, painful, acute ophthalmoplegia
responds dramatically to corticosteroid therapy within
2 to 3 days. A daily dosage of 60 mg prednisone was
used.
ANTERIOR SEGMENT ISCHEMIA
Prednisolone 1% was used four times daily, with
gradual clearing of the corneal edema and anterior
chamber cellular reaction.
PSEUDOTUMOR CEREBRI
Dexamethasone 0.5 mg is prescribed three doses daily
for 3 weeks.
TOXOPLASMOSIS
It can be treated with high corticosteroid doses (upto
100 mg prednisone per day for a prolonged period
with specific antitoxoplasmic therapy).
OTHER INDICATIONS
Corticosteroid is found to be useful in cysticercosis.
Use of Nonsteroidal Anti-
inflammatory Drugs in
Inflammation
In the treatment of ocular inflammation, the appeal
of nonsteroidal anti-inflammatory drugs (NSAIDs)
hinges on the complications associated with the more
established therapy for ocular inflammation, i.e.
corticosteroids. Although an overlap exists between
the mechanisms of action of both, the use of NSAIDs
may be safer than the use of corticosteroids, as the
latter may produce adverse effects such as glaucoma,
opportunistic infections, and posterior subcapsular
cataracts. In sharp contrast, topical NSAIDs are known
to cause only minor adverse effects such as burning,
stinging and hyperemia of the conjunctiva.
OCULAR INFLAMMATION
A simple definition of ocular inflammation would be
inflammation of any part of the eye. Intraocular
inflammation can be subdivided into inflammation of
the anterior and posterior segments of the eye. The
cardinal signs of ocular inflammation are hyperemia,
increased vascular permeability, oedema, and cellular
(leukocytes, mast cell, platelets, etc.) infiltration into
ocular fluids and tissues. In experimental anterior
uveitis, miosis and a rise in intraocular pressure which
is usually due to the breakdown of the blood-aqueous
barrier with subsequent release of protein and fibrin
into the aqueous humor, but not of cellular infiltration,
is observed. Inflammation after paracentesis usually
disappears within 2-3 hrs.
To understand the history of NSAID use in
ophthalmology, one must appreciate the relevance of
prostaglandins in the eye. In 1971, Vane and Smith
established the connection between the clinical effect
of acetylsalicylate and inhibition of prostaglandin
systesis
1,2
. It is now well-known that aspirin and other
NSAIDs produce their clinical efficacy by inhibiting
cyclooxygenase and thus inhibiting prostaglandin
synthesis (Fig. 34.1). Specific drugs belonging to each
class are listed in Tables 34.1 and 34.2.
226
Fig. 34.1: Mechanism by which nonsteroidal anti-
inflammatory drugs produce their clinical effect
TABLE 34.1: Systemic nonsteroidal anti-inflammatory agents
Drug Drug name How supplied Typical adult daily dose
(mg) (mg)
Salicylates Aspirin 325-925 650 q4th
Diflunisal 250, 500 250-500 bid
Fenamates Mefenamate 250 250 qid
Meclofenamate 50, 100 50-100 qid
Indoles Indomethacin 25, 50, 75 25-50 tid-qid,
(slow release) 75 bid
Sulindac 150, 200 150-200 bid
Tolmetin 200, 400, 600 400 tid
Phenylacetic acids Diclofenac 35, 50, 75 35-75 bid
Pheynylalkanoic acids Fenoprofen 200, 300, 600 300-600 tid
Ketoprofen 25, 50, 75 75 tid, - 50 qid
Piroxicam 10, 20 10 bid, 20 daily
Flurbiprofen 50, 100 100 tid
Ketorolac 10 10 qid
Naproxen 250, 375, 500 250-500 bid
275-550 275-550 bid
200, 300, 400
Ibuprofen 600, 800 400-800 tid
Pyrazolones Phenylbutazone 100 100 tid-qid
Oxyphenylbutazone 100 100 tid-qid
Para-aminophenols Acetaminophen 80, 325, 500, 650 650 q4th
TABLE 34.2: Topical nonsteroidal anti-inflammatory agents
Name Strength Typical doses
Flurbiprofen 0.03% solution 1 drop every 30 minutes
for 2 hrs
Preoperatively (Total
dose: 4 drops)
Suprofen 1.0% solution 2 drops at 1.2 and 3hours
preoperatively or every
4 hours while awake
on the day of surgery.
Diclofenac 0.1% solution qid
Ketorolac 0.5% solution tid
Indomethacin 0.5%-1.0% qid
suspension
MECHANISM OF ACTION
NSAIDs act mainly as anti-inflammatory agents by
inhibiting cyclooxygense and lipo-oxygenase enzymes
which lead to inhibition of products like prostaglandins,
thromboxane and l eukotrienes which induce
inflammation. Ocular actions of prostaglandins include
an increase in vascular permeability, breakdown of the
blood-aqueous barrier and induction of miosis.
Cystoid Macular Edema (CME)
Topical NSAIDs are effective in preventing postsurgical
angiographic CME when topical or subtenons
corticosteroid injections are given concurrently. Only
one study (involving 50 patients) has demonstrated
similar effect with a topical NSAID in the absence of
concurrent corticosteroid therapy.
4
Several studies have
demonstrated that prophylactic treatment with a
topical NSAID has a beneficial effect on visual function.
In one study, this effect was shown even in the absence
227
Management of Iatrogenic Inflammation of the Eye
of concurrent corticosteroid therapy. Topical NSAIDs
also are effective in the treatment of angiographically
documented subclinical CME, and this can translate
into improved visual function. Oral NSAIDs have also
been shown to be effective in both the prevention
and treatment of CME after cataract surgery. However,
a study demonstrating a positive effect on visual
function with oral promote one NSAID still is lacking.
There is no strong evidence to promote one NSAID
over another.
Postoperative Inflammation
Fluorophotometric analysis has made available a
quantitative means of studying anterior chamber
inflammation. With this tool, it has been possible to
evaluate, in a reproducible fashion, the effect of
NSAIDs on postoperative inflammation. By using both
slit lamp and fluorophotometric analysis as a part of
randomized double-masked placebo-controlled
studies, several topical NSAIDs like indomethacin
1.0%,
5
flurbiprofen 0.03%,
6
ketorolac 0.5%
7,8
and
diclofenac 0.1%
9
have been shown to reduce
postoperative inflammation. The positive effect of
NSAIDs was seen in both intracapsul ar and
extracapsular cataract surgery. It is important to note
that whereas in most of the studies, corticosteroids were
given concurrently, two of these studies were
conducted without concurrent corticosteroid therapy
7,8
.
In these studies, topical ketorolac 0.05% proved to
be better than placebo in controlling inflammation
after cataract surgery.
In the treatment of postsurgical inflammation, the
superiority of NSAID over placebo has led to a
comparison of NSAIDs with corticosteroid. Ketorolac
0.5%
10
and dicl ofenac
11
were compared to
dexamethasone and prednisolone, respectively. In both
studies, there was no significant difference in the
reduction of postoperative inflammation by slit-lamp
examination between patients on NSAIDs and those
on corticosteroid topical therapy. However, it should
be noted that in the ketorolac study, a subtenon
injection of corticosteroid was given to all the patients
and this may have contributed to the lack of difference
between the two treatment groups. Concurrent
corticosteroid therapy was not a factor in the study
comparing diclofenac with prednisolone. When
fluorophotometry was used in both comparative
studies, it was found that control of inflammation in
the topical NSAID treatment group was better achieved
than in the corticosteroid groups.
Regardless of the preceding findings, it is a common
practice to use topical corticosteroid alone to control
post-cataract surgery inflammation. Nevertheless, the
US food and Drug Administration (FDA) has approved
the use of the diclofenac 0.1% four times daily, starting
24 hours after cataract surgery for this purpose. Thus,
it is possible to substitute a topical NSAID for a topical
corticosteroid to control postoperative inflammation,
especially in eyes with significant steroid responsive
glaucoma.
Uveitis
In contrast to post-surgical inflammation, many forms
of uveitis require prolonged steroid therapy to control
inflammation. At times, the therapeutic effort must be
escalated to the use of subtenon injections or oral
administration of corticosteroid. Of course, the risk of
iatrogenic glaucoma and cataract becomes substantial
in these situations. Therefore, NSAIDs are gaining a
more secure position in the treatment of certain forms
of uveitis.
Scleritis and Episcleritis
Topical NSAIDs have no proven efficacy in the
treatment of episcleritis. In fact, they appear to be
less effective than topical corticosteroids in reducing
epi scl eral i nj ecti on and pai n associ ated wi th
episcleritis
12
. In contrast, systemic NSAIDs are the
agents of choice in the treatment of non-necrotizing
simple, diffuse, and nodular scleritis.
13
One may have
to proceed sequentially through several different
NSAIDs unti l one fi nds the one that works.
Furthermore, when a steroid is needed, the duration
and dose of the steroidal may be reduced with the
adjunctive use of an NSAID.
Allergic and Giant Papillary Conjunctivitis
Vernal keratoconjunctivitis most commonly occurs in
children and young adults. It shares with contact lens-
associated giant papillary conjunctivitis (GPC) the
common finding of giant papillary conjunctivitis (GPC)
on the upper palpebral conjunctiva. The standard
treatment for both is topical steroids until a topical mast
cell stabilizer takes effect.
Side Effects of NSAIDs
Common adverse effects following instillation of topical
NSAIDs include burning, stinging, and hyperemia of
conjunctiva. Allergic and hypertensive reactions are
also reported following use of topical NSAIDs. Systemic
side effects following use of NSAIDs mainly include
gastritis, but are unlikely to occur with topical
administration.
228
Conclusion
NSAIDs have wide potential for use in various ocular
disorders, though the effects vary from one individual
to another and the effect is unpredictable. More
research is required to develop newer NSAIDs which
can be used for various inflammatory disorders of the
eye with more effective action with minimal ocular
toxicities.
Currently corticosteroids are still the drugs of choice
in the treatment of ocular inflammation. However,
because their prolonged use may result in severe ocular
side effects, it would be therapeutically beneficial to
develop nonsteroidal anti-inflammatory drugs that
have similar or greater efficacy than steroids but not
their ocular side effects.
References
1. Flck AJ: Cyclo-oxygense inhibitors in Ophthalmology.
Surv. Ophthalmol 1992;36:259-84.
2. Gil man AG, Ral l TC, Nies AS, Tayl or P: The
pharmacologic basis of therapeutics. Elmsford: Pergamon
1990:638-81.
3. Abramson SB, Weisman G: The mechanism of
nonsteroidal anti-inflammatory drugs. Arthritis Rheum
1989;32:1-9.
4. Flach AJ, Jampol LM, Weinberg D, et al: Improvement
in visual acuity in chronic aphakic and pseudophakic
cystoid macular edema after treatment with topical 0.5%
ketorolac tromethamine. Am. J. Ophthalmol 1991;
112:514-19.
5. Sanders DR, Kraff ML: Steroidal and nonsteroidal anti-
inflammatory agents. Effects on postsurgical inflammation
and bl ood-aqueous barrier breakdown. Arch.
Ophthalmol 1984;102:1453-56.
6. Sabiston MB, Tessler D, Summersk H, et al: Reduction
of inflammation following cataract surgery by flurbiprofen.
Ophthalmic Surg 1987;18:873-77.
7. Flach AJ, Graham J, Kruger LP, et al: Quantitative
assessment of postsurgical breakdown of the blood-
aqueous barrier following administration of ketorolack
tromethmine sol ution. A doubl e-masked, paired
comparison with vehicle-placebo solution study. Arch.
Ophthalmol 1988;106:344-47.
8. Flach AJ, Lavelle CJ, Olander KW, et al. The effect of
ketorolac 0.5% solution in reducing postsurgical
inflammation following ECCE with IOL. Double masked,
parallel comparison with vehicle. Ophthalmology.
1988;95:1277-84.
9. Vickers FF, McGuigan LJB, Ford C, et al. The effect of
diclofenac sodium ophthalmic drops on the treatment of
postoperative inflammation. Invest. Ophthalmol. Vis. Sci.
(ARVO suppl) 1991;32:793.
10. Flach AJ, Kraff MC, Sanders DR, et al. The quantitative
effect of 0.5% ketorolac tromethamine solution and 0.1%
dexamethasone sodium phosphate sol ution on
postsurgical blood aqueous barrier. Arch. Ophthalmol
1988;106:480-83.
11. Kraff MC, Sanders DR, McGuigan L, et al. Inhibition of
bl ood aqueous humour barrier breakdown with
diclofenac. A fluorophotometric study. Arch. Ophthalmol
1990;108:380-83.
12. Lyons CH, Hakin KN, Watson PG. Topical flurbiprofen:
an effective treatment for epoiscleritis? Eye 1990;4:
521-25.
13. Vitale A, Foster CS: Nonsteroidal anti-inflammatory
drugs. In: Zimmerman TJ, ed. Textbook of ocular
pharmacology, New York: Lippincott-Raven, 1995.
C H A P T E R
35
Management of
Postrefractive Keratitis
Eric D Donnenfeld (USA)
Introduction
Laser in situ keratomileusis (LASIK) is the most
commonly performed surgical procedure to correct
refractive errors and is the most common elective
procedure performed in the United States. LASIK
offers many benefits over photorefractive keratectomy,
including increased visual rehabilitation, decreased
stromal scarring, less postoperative pain, less irregular
astigmatism, minimal regression, and the ability to treat
a greater range of refractive disorders.
1,2
Compared
to other refractive procedures, LASIK preserves the
integrity of Bowmans membrane and the overlying
epithelium, thus decreasing the risk of microbial
keratitis. However, microbial keratitis following LASIK
has become an increasingly recognized, sight-
threatening complication of refractive surgery.
3-10
The incidence of infectious keratitis following LASIK
is unknown and can vary widely depending on the
study. One large, retrospective study investigating the
complications associated with LASIK surgery found an
incidence of two infections in 1,062 eyes,
7
and another
similar study found an incidence of one infection in
1,019 eyes.
8
A more recent case series of LASIK-
associated infections encountered at a single institution
quotes an estimated incidence between 1:1000 and
1:5000.
9
Based on a comprehensive review and
analysis of the published literature on infections
following LASIK, Chang and colleagues
5
also noted
that the incidence of infection after LASIK can vary
widely (0-1.5%). The American Society of Cataract
and Refractive Surgery (ASCRS) Cornea Clinical
Committee developed a post-LASIK infectious keratitis
survey and conducted a survey of the organizations
members in 2001 and again in 2004.
10
In the 2001
survey, there was an incidence of 1 infection for every
2919 procedures performed by physicians returning
the questionnaire (116 post-LASIK infections were
reported by 56 LASIK surgeons who had performed
an estimated 338,550 procedures). These results are
contrasted to 1 infection for every 2131 procedures
performed by physicians returning the questionnaire
in 2004. The increase in incidence of infections is
presumably due to an increase in gram-positive resistant
organisms, most likely due to methicillin resistant
Staphylococcus aureus. Culture results revealed
opportunistic infections and gram-positive bacteria as
the most common organisms in 2001 (Fig. 35.1A).
In contrast, as noted above, in 2004 gram-positive
bacteria have increased in incidence while opportunistic
infections, specifically atypical mycobacteria, have seen
a marked reduction (Fig. 35.1B).
Fig. 35.1B: ASCRS 2004 culture results of post-LASIK
infectious keratitis
Fig. 35.1A: ASCRS 2001 culture results of post-LASIK
infectious keratitis
230
In 2004, the epidemic of atypical mycobacteria that
was seen in 2001 (Fig. 35.1B) ended. Cases from
atypical mycobacteria decreased from 48 to 5%. This
decrease is presumably due to the use of fourth-
generation fluoroquinolones and improved sterile
technique. It was interesting to note that no patient
who received a 4th generation fluoroquinolone as
prophylaxis developed an atypical mycobacteria
infectious keratitis in the 2004 survey. However, the
overall incidence of infectious keratitis increased in
2004 from 2001.
The results of these surveys and an analysis of the
trends seen in the data can help to guide prophylaxis
and treatment of infections keratitis following LASIK.
Infectious keratitis is a potentially devastating
complication of LASIK. A high degree of suspicion
coupled with a rapid diagnosis and appropriate therapy
can result in visual recovery. For prophylaxis against
a post-LASIK infectious keratitis there are several steps
which can be implemented. Preoperatively, all patients
considering refractive surgery should have a thorough
examination of their eyelids and lacrimal apparatus.
Treatment of infectious lid disease prior to LASIK with
hot compresses and a topical antibiotic ointment applied
three times daily to the lid margin may decrease the
risk of a bacterial keratitis. A small minority of clinicians
recommend performing monocular surgery or the use
of separate instruments when performing bilateral
surgery.
11
Some clinicians recommend the use of sterile
drapes, gowns, gloves and masks by the treating
physician and assisting technician. A10% betadine
solution lid prior to cataract surgery has been shown
to decrease the incidence of endophthalmitis following
cataract surgery and is recommend by many clinicians
when performing LASIK.
12
Proper sterilization
techniques can prevent the use of contaminated
instruments. As several epidemics of atypical
mycobacteria have been associated with the use of
non-sterile water to clean instruments or the use of
ice during LASIK surgery,

all fluids applied to the eye
before, during and after LASIK should be sterile.
13
Antibiotic prophylaxis for LASIK should emphasize
the need to provide broad-based spectrum coverage
with gram-positive emphasis. The antibiotic should be
non-toxic to promote epithelial healing and should
provide coverage against atypical mycobacteria which
is the most common opportunistic organism responsible
for post-LASIK infections. Finally, the antibiotic should
penetrate effectively into the cornea and achieve
therapeutic levels in the mid stroma. Fourth generation
fluoroquinolones (gatifloxacin 0.3% and moxifloxacin
0.5%) for antibiotic prophylaxis of LASIK and PRK are
recommended as they best meet the criteria listed
above.
13
We begin topical therapy 1 hour prior to
surgery and at the conclusion of LASIK we dehydrate
the cornea for 1-2 minutes to improve flap adherence
and then apply antibiotic directly on the dehydrated
flap to improve antibiotic absorption into the cornea.
With PRK, we place the antibiotic directly onto the
stromal bed and soak the bandage contact lens in
antibiotic for 30 seconds prior to placing the contact
lens on the eye. Postoperatively, patients receive a
fourth generation fluoroquinolone four times a day
for 5 days with LASIK and for one day after the
epithelial defect has closed with PRK.
We divide infectious keratitis following LASIK into
rapid onset within the first two weeks of surgery and
late onset which can occur from 2 weeks to 3 months
following surgery.
13
The organisms seen in early onset
infectious keratitis within the first two weeks are
common bacterial pathogens such as staphylococcal
and streptococcal species. Gram-negative organisms
are rare. The organisms seen in late onset infectious
keratitis after two weeks are usually opportunistic such
as fungi, nocardia and atypical mycobacteria. The
published literature review of LASIK-associated
infections by Chang and colleagues supports this
classification of infection.
5
Based on their study, gram-
positive organisms were more likely to present within
7 days of surgery (p = 0.001) while mycobacterial
infections were more likely to present 10 or more days
after surgery (p < 0.001).
5
Since the organisms responsible for infectious
keratitis following LASIK often will not respond to
empiric therapy, as with the results from the previous
survey, we recommend lifting the flap, scraping, and
culturing all suspicious cases, and selecting appropriate
culture media including blood agar, chocolate agar,
Sabourauds agar and thioglycolate broth.
13
For
infectious keratitis after two weeks, we recommend a
growth media for atypical mycobacteria such as
Lowenstein-Jensen or Middlebrook 7H-9 media in
addition to the previous culture media. If these special
media are unavailable, we recommend using blood
agar as atypical mycobacteria grow quite well on these
plates. At the time of culture we also recommend
scraping the infiltrate and performing a Gram stain,
Gomori-methenamine silver stain, and Ziehl-Neelsen
stain to rule out unusual pathogens such as nocardia,
atypical mycobacteria, and fungi. In cases in which
cultures are negative and the infection continues to
a corneal biopsy or PCR should be considered.
For the treatment of both rapid-onset and delayed-
onset infectious keratitis, it is recommended to elevate
the flap and culture. Irrigation of the flap interface with
an appropriate antibiotic solution (fortified vancomycin
50 mg/ml for rapid-onset keratitis and fortified amikacin
20 mg/ml for delayed-onset keratitis) may be helpful.
For rapid - onset keratitis, we recommend a fourth-
generation topical fluoroquinolone such as gatifloxacin
231
Management of Postrefractive Keratitis
0.3% or moxifloxacin 0.5% be given in a loading dose
every 5 minutes for 3 doses and then every 30 minutes
alternating with an antimicrobial which is rapidly
bacteriocidal and has increased activity against gram-
positive organisms, such as cefazolin 50 mg/ml every
30 minutes.
13
In patients who work in a hospital
environment or have been exposed to a hospital
surgical setting or health care environment, there is
an added risk of methicillin-resistant Staphylococcus
aureus (Solomon R, Donnenfeld E, Perry H, et al.
methicillin resistant Staphylococcus aureus infectious
keratitis following refractive surgery. Presented as a
paper at the American Society of Cataract and
Refractive Surgery Symposium on Cataract, IOL, and
Refractive Surgery, San Diego, Calif, 2004). In those
patients who work in a hospital environment or have
had exposure to a health care environment, we
recommend the substitution of vancomycin 50 mg/ml
every 30 minutes instead of cefazolin to provide more
effective therapy against MRSA. In addition, we
advocate the use of oral doxycycline 100 mg twice
daily (to inhibit collagenase production) and also
recommend discontinuing corticosteroids.
For delayed-onset keratitis, which is commonly due
to atypical mycobacteria, nocardia and fungi, we
recommend beginning therapy with amikacin 35 mg/
ml every 30 minutes alternating with vancomycin
50 mg/ml every 30 minutes, starting oral doxycycline
100 mg BID, and discontinuing corticosteroids.
Alternative therapy for delayed-onset keratitis, which
woul d cover atypical Mycobacteria, incl udes
cl arithromycin and fourth-generation fl uoro-
quinolones. This treatment will not cover fungal
infections, and therefore, treatment for all cases of
infectious keratitis should be modified based on culture
and scraping results and response to therapy.
Infectious keratitis after LASIK frequently presents
with inflammation in the corneal interface, which can
mimic diffuse lamellar keratitis (DLK). DLK usually
occurs within the first few days following LASIK, unless
there is postoperative ocular trauma.
14
The appearance
of an interface inflammation more than one week
following LASIK should be presumed to be infectious
unless proven otherwise. Since DLK usually presents
with a diffuse appearance while infectious keratitis has
focal area of infiltration, any focal infiltrate surrounded
by inflammation following LASIK should be considered
infectious until proven otherwise.
In conclusion, infectious keratitis is a potentially
devastating complication following LASIK. Culture
results reveal gram-positive bacteria as the most
common organisms. Infectious keratitis may present
as late as months following LASIK, and its frequent
misdiagnosis at initial presentation may result in
significant vision loss. Antibiotic prophylaxis for LASIK
should emphasize the need to provide broad-based
spectrum coverage with gram-positive emphasis. For
treatment, we do not recommend empiric therapy as
most organisms are opportunistic and do not respond
to conventional therapy. A high degree of suspicion
with flap elevation and culturing should be performed
on all eyes suspected of infectious keratitis following
LASIK.
References
1. Hersh PS, Brint SF, Maloney RK, et al. Photorefractive
keratectomy versus laser in situ keratomileusis for
moderate to high myopia: A randomized prospective
study. Ophthalmology 1998;105:1512-23.
2. Azar DT, Farah SG. Laser in situ keratomileusis versus
photorefractive keratectomy: An update on indications
and safety. Ophthalmology 1998;105:1357-58.
3. Garg P, Bansal AK, Sharma S, Vemuganti GK. Bilateral
infectious keratitis after laser in situ keratomileusis: A case
report and review of the literature. Ophthalmology
2001;108:121-25.
4. Solomon A, Karp, CL, Miller D, et al. Mycobacterium
interface keratitis after laser in situ keratomileusis.
5. Perry HD, Doshi SJ, Donnenfeld ED, et al. Herpes
simplex reactivation following laser in situ keratomileusis
and subsequent corneal perforation. CLAO J
2002;28:69-71.
6. Chang MA, Jain S, Azar DT. Infections following laser in
situ keratomileusis: An integration of the published
literature. Surv Ophthalmol 2004;49:269-80.
7. Stulting RD, Carr JD, Thompson KP, et al. Complications
of laser in situ keratomileusis for the correction of myopia.
8. Lin RT, Maloney RK. Flap complications associated with
lamellar refractive surgery. Am J Ophthalmol 1999;
127:129-36.
9. Karp CL, Tuli SS, Yoo SH, et al. Infectious keratitis after
LASIK. Ophthalmology 2003;110:503-10.
10. Solomon R, Donnenfeld ED, Azar DT, Holland EJ,
Palmon FR, Pflugfelder SC, Rubenstein JB. Infectious
keratitis after laser in situ keratomileusis: Results of an
ASCRS survey. J Cataract Refract Surg 2003;29:
2001-06.
11. Kohnen T. Infections after corneal refractive surgery: Can
we do better? (editorial). J Cataract Refract Surg 2002;
28:569-70.
12. Speaker MG, Menikoff JA. Prophyl axis of
endophthal mitis with topical povidone-iodine.
13. Donnenfeld ED, Kim T, Holland E, et al. Management
of infectious keratitis following laser in situ keratomileusis.
14. Stulting RD, Randleman JB, Couser JM, Thompson KP.
The epidemiology of diffuse lamellar keratitis. Cornea
2004;23:680-88.
C H A P T E R
36
Optimized NSAIDs and
Antibacterial Prophylaxis in
Cataract Surgery
Ashok Garg (India), Ian Bell (USA)
Introduction
Cataract surgery is one of the most commonly
performed ocular surgery in the world. Given the ability
of ocular surface flora to enter the eye during surgery,
many of the prophylactic techniques aim is to suppress
their number and to limit the growth of those
organisms that do enter the eye during intraocular
surgery. Antimicrobial prophylaxis is an essential
component of both cataract and refractive surgeries.
Choosing an antibiotic for surgical prophylaxis in the
clinical setting can also be challenging.
The key surgical prophylaxis paradigm shift in recent
years for long practicing ophthalmologists is the
growing evidence for preoperative use of both topical
antibiotics and anti-inflammatory drops. The second
shift is the realization that we should discontinue
antibiotics more quickly and ensure use of anti-
inflammatory for the full course of therapy. These
changes are key for limiting post-cataract (iatrogenic)
inflammation and infection while they prevent the
development of antibiotic resistance in patients. In the
preoperative period a fourth-generation fluoroquino-
lone such as Moxifloxacin 0.5% solution, a non-
steroidal anti-inflammatory such as topical Nepafence
0.1%, suspension, and a topical steroid such as
prednisolone acetate 1% should all be administered.
Loading the eye with an antibiotic prior to the
surgical insult reduces the risk of endophthalmitis.
Fur thermore studies have shown that the
non-steroidal, anti-inflammatory drugs (NSAIDs) and
the steroids are synergistic and both work better if the
eye is loaded preoperative.
There are two basic ways to approach the
preoperative loading. One approach provides the
drops within the three-to-four dose delating resimen
in the surgical induction area. We can add
Neosynephrine 10% Cyclogyl solution (1% Cyclo-
pentolate HCl), an antibiotic, steroid, non-steroidal,
so actually they get loaded up with five different drops.
Our preoperative routine is three doses of drops starting
30 to 60 minutes before surgery.
Some surgeons prefer to start the drops 24 hours
preoperative while others start the drops three days
preoperative.
There are sel ect indications where anti-
inflammatory drug dosing should begin a week
preoperative including high-risk cases for inflammation
and secondary macular edema. Such patients includes
those with a long-term, history of chronic uveitis and
diabetes mellitus and patients with pigmentary
retinopathy and macular edema, and those who
developed macular edema in the first eye after cataract
surgery.
With high-risk patients such as those who are
immunocompromised or prone to infection, we can
start the antibiotic three days preoperative rather than
just on the table.
In our routine cases, I load the entire drop regimen
in the eye in the operating room, but the high-risk
cases you may start, three to seven days preoperative.
There is not yet a consensus, but you may want to
go a little longer and by more intense on the high-
risk patients.
The research evidence does not clearly identify
whether drug delivery shortly preoperative or several
days preoperative is better. However, as the patients
become higher risk, We tend to have a slightly longer
and more intense course of antibiotic and anti-
inflammatory drops.
Routine patients that never had a problem
generally start to receive the drug in the operating room
prior to surgery because it is easiler on the patient.
Postoperative Schedule for
Cataract Patients
The major changes in recent years from previous
antibiotic experience is the perioperative and short
233
Optimized NSAIDs and Antibacterial Prophylaxis in Cataract Surgery
postoperative course of the drugs. We now limit
antibiotic use because the risk of endophthalmitis drops
with in a week when the wound seals. It is the long-
term, low-dose use of these drugs that leads to resistant
organisms.
Our approach is to administer antibiotics and anti-
inflammatory drops (steroid and NSAID) at the end
of the case. My staff administer them agains in the
recovery area before the patient goes home.
We have patients use the antibiotic drops three
times a day for one week. Other surgeons have them
take the antibiotic for as few as five days.
However, the anti-inflammatory drug is required
for longer use. Evidence suggests the blood aqueous
barrier breakdown that occurs after cataract surgery
persists for four to eight weeks. Because the average
breakdown lasts about six weeks, we should treat with
anti-inflammatory drops for one to two months in
routine cases. This will prevent any rebound of
inflammation or other secondary issues.
We need to have patients use the anti-inflammatory
drops a big longer than some surgeons think is
necessary because often the eyes are quiet and
comfortable by two to three weeks after surgery, but
there is still some risk for cystoid macular edema up
to six weeks postoperative.
For example, for at-risk patients preoperative dosing
is recommended for one week and postoperative
dosing is recommended for four weeks to several
months.
Drug Dosages
The dosing regimen we use instillation of the topical
Nevanac, which is a TID drop, a three-times daily drop.
We use Moxifloxacin, Nepafenac, and a topical steroid,
which seems more than adequate, as these drugs have
demonstrated efficacy in contributing to good surgical
outcomes.
Ophthalmologists should be aware of adding
NSAID drug to their regimen. Most patients recover
without complications when surgeons only use an
antibiotic and a steroid. However, there are indications
that over 10% of patients will develop a very mild
macular edema without an NSAID. Thats a risk that
NSAIDs can eliminate.
We have pretty minimally invasive cataract surgery
today, and people work really hard at their surgical
technique, but probably the one thing that could have
the greatest impact on their outcomes would be to
add an NSAID to their regimen.
The incidence of very mild macular edema without
an NSAID, even in a good surgeons hands, is about
12% and adding as NSAID takes it down to less than
1% so you get a hug reduction in one of the most
common sight threatening complications of cataract
surgery just by adding an NSAID and using it properly.
Proper dosing of antibiotics, NSAIDs, and steroid
plays a very important role in preventing complications
such as infection or CME.
Minimizing these complications with effective agents
and proper therapeutic dosing regimens will improve
our surgical outcomes.
Surgeons can greatly improve their chances of a
successful surgical outcome if they keep in mind three
key criteria in selecting antibiotics: potency, penetration,
and safety. A good balance of these aspects especially
potency and penetration provides the best patient
protection.
An antibiotic that is highly potent and effective at
kiling infections at lower concentrations would lose
much of its efficacy if it was unable to penetrate the
tissue. Conversely, a medication that penetrates
extremely well but lacks potency also would not be
very functional.
Clinicians are best served by an effective combi-
nation of penetration and potency.
Although researchers are frequently asked whether
potency or penetration is more important, the only
clear answer is the most effective approach is to
combine these factors.
Measuring Potency
Identifying an antibiotics strength in penetration and
potency is important, but surgeons should be aware
that potency definitions vary. The most common
assessment of an antibiotics potency, the minimum
inhibitory concentration (MIC), traces whether
organisms growth has been stopped. However, the
definition still alows viable organisms to remain. This
most common term may not be the most important.
Another standard, minimum bactericidal concentration
(MBC), tracks whether 99.9% of the organism is killed
(MBC is approximately 4x the MIC). The final measure-
ment, mutant prevention concentration (MPC), gauges
whether the organism was killed with mutations
prevented (MPC is approximately 8x the MIC).
Drugs with the lowest potency numbers in MIC,
MBC or MPC are among the most potent. With
postoperative infections being potentially sight
threatening, it is ideal to exceed these levels with the
antibiotic concentrations in the target tissues.
234
Penetration Tracking
Antibiotic tissue penetration plays a key role in
protecting against infection.
This issue arises when examining the research on
various antibiotics; some may have good potency
statistics in vitro, but we fail to identify the in vivo
performance of the antibiotic. The latter will tell
ophthalmologists what levels of the drug our patients
actually will get in the cornea, the anterior chamber,
and the vitreous. Our research administering
fluoroquinolones to a cornea transplant model prior
to corneal transplant and then examining the antibiotic
levels in the cornea showed Moxifloxacin had three
times the concentration of Gatifloxacin.
Similar research at various International Research
Centres on aqueous concentrations of antibiotic
applied a series of drops preoperative and measured
aqueous concentration at the time of cataract surgery.
Those researchers identified the same three-fold
greater penetration of Moxifloxacin. Protection can be
defined by overlaying these concentrations with the
MICs for potential pathogens.
In vivo potency after tissue penetration is a better
measure of antibiotic efficacy than speed of kill in vitro.
The latter removes all of the factors that determine
how the antibiotic performs in human tissue. These
studies disrergard the reality of penetration of the
antibiotic through human tissue. For these reasons
in vivo potency and penetration studies will always
have more real-world resonance than in vitro speed
of kill research. The aqueous humor concentrations
achieved in the International Resarch Centres were
tested against a Staph. aureus ocular isolate using disk-
diffusion analysis. The moxifloxacin achieve a 24 mm
zone of inhibition, and Gatifloxacin had no zone of
inhibition. This surrogate model accounts for tissue
penetration and potency at the potential site of
infection, thus defining protection.
Safety Evaluation
In addition to potency and penetration, a solid
evaluation of antibiotics for surgical prophylaxis should
assess whether the drug is non-toxic. Efforts to prevent
the use of non-toxic medication should look for
epithelial problems or endothelial problems.
As a class of drugs, the Fluoroquinolones have
proven to by very safe and non-toxic.
Our experience with all fourth-generation Fluoro-
quinolones has found that they are very safe. Research
comparing corneal epithelial healing postoperative
when Moxifloxacin or Gatifloxacin are used have
found very similar would healing rates. In fact, an
independent well-controlled study evaluating wound
healing post-PRK for Moxifloxacin and Gatifloxacin
were conducted in USA. The conclusion was that both
the drugs are safe. Generally, they found that eyes
treated with Moxifloxacin healed faster and had smaller
defects than those treated with Gatifloxacin.
Rabbit model studies that created epithelial defects
and tracked healing when the two antibiotics are used
found similar results. Clinical trials looking at healing
after PRK also identified similar healing. Both
Fluoroquinolones are safe and non-toxic.
C H A P T E R
37
Optimizing Visual Outcomes with
NSAIDs Therapy in Cataract and
Refractive Surgery
Eric D Donnenfeld, Henry D Perry (USA)
Introduction
Ophthalmic nonsteroidal anti-inflammatory drugs
(NSAIDs) are becoming a cornerstone for the
management of ocular pain and inflammation. Their
well-characterized anti-inflammatory activity, analgesic
property, and established safety record have also made
NSAIDs an important tool to optimize surgical
outcomes. Ophthalmic NSAIDs currently play four
principle roles in ophthalmic surgery including the
prevention of intraoperative miosis during cataract
surgery, management of postoperative inflammation,
the reduction of pain and discomfort following cataract
and refractive surgery, and the prevention and
treatment of cystoid macular edema following cataract
surgery.
Ocular inflammation is characterized by redness,
swelling, and/or pain associated with irritation or
trauma to the eye. Common triggers of ocular
inflammation include allergies, meibomian gland
dysfunction, ocular diseases (traumatic iritis, peripheral
corneal inflammatory keratitis, episcleritis, and
unilateral nongranulomatous idiopathic iritis) and most
importantly ophthalmic surgical procedures.
The strict regulation of inflammatory reactions
within the eye

is vital in maintaining both anatomical
integrity and visual

function. Left unregulated,
inflammation within the eye may

lead to extensive
ocular damage, resulting in impaired vision.
Ocular inflammatory pathways commence with the
triggering of the arachidonic acid cascade. The cascade
is triggered either by mechanical stimuli (such as the
case of surgically-inflicted trauma) or by chemical
stimuli (such as foreign substances or allergens).
Prostaglandins are generated in most tissues by
activation of the arachidonic acid pathway.
Phospholipids in the cell membrane are the substrate
for the enzyme phospholipase A to cause generation
of arachidonic acid and, in turn, the enzymes cyclo-
oxygenases and lipoxygenases act on arachidonic acid
to produce a famil y of chemical l y distinct
prostaglandins, and leukotrienes (McColgin). Clinical
symptoms of prostaglandin production include
hyperemia miosis, poor vision, pain, and cystoid
macular edema (CME),
It is well accepted that inhibition of prostaglandin
synthesis and release reduces the inflammatory
response induced by surgery and allergies, thereby
reducing the clinical symptoms of prostaglandin
production (McColgin). Prostaglandin synthesis can be
suppressed by inhibiting phospholipase A2, which
inhibits the release of arachidonic acid from the
intracellular stores, or by inhibiting the conversion of
arachidonic acid to prostaglandin via the cyclooxy-
genase pathway. Multiple portions of this pathway can
be blocked and different classes of anti-inflammatory
medications have differing effects on this pathway.
For example, corticosteroids interfere with the
activity of phospholipase A2, thereby inhibiting the
release of arachidonic acid and the production of all
arachidonic acid metabolites including prostaglandins.
(Polansky and Weinreb, 1984).
In contrast, the nonsteroidal anti-inflammatory
agents (NSAIDS) specifically and irreversibly inhibit the
synthesis of prostaglandins by interfering with the
activity of cyclo-oxygenases (COX-1 and COX-2).
(Polansky and Weinreb, 1984).
Rationale for Treating Ocular
Inflammation
Reducing ocular inflammation is critical because failure
to do so may cause patients discomfort, pain, visual
loss, and increase the risk for the development of CME.
CME is potentially the most adverse ocular outcome
of prostaglandin production. CME is caused by cystic
accumulation of intraretinal fluid in the outer plexiform
and inner nuclear layers of the retina, as a result of
breakdown of the blood-retinal barrier. It is the most
common following intraocular surgery, and in patients
236
with venous occlusive disease, diabetic retinopathy, and
posterior segment inflammatory conditions (Quin).
However, CME can develop in surgeries with no
obvious complications. The condition is often asymp-
tomatic and may only be detected with fluorescein
angiography or optical coherence tomography (Quin,
Roberts). Although the exact incidence of CME is still
unclear, CME is a frequent cause of visual loss
following even uncomplicated cataract surgery. Studies
suggest that the rate of clinical CME ranges from 1-
2% (Ray), while the incidence of angiographic CME
may be as high as 9-19% (Ursell, Mentes). In a recent
study, patients using ketorolac tromethamine 0.4% pre-
operatively 1-3 days prior to surgery had no instances
of CME, whereas the steroid-only group and the
Fig. 37.1: Prostaglandin synthesis
group that got the NSAID just 1 hour prior for anti-
miosis had a rate of 12% CME as detected by OCT
(Donnenfeld). CME frequently has a late onset,
occurring 4-6 weeks postoperatively. CME often
presents with blurred or decreased central vision or
painless retinal inflammation or swelling. Visual loss is
usually temporary but may be irreversible in refractory
to conservative treatment. In high risk patients such
as diabetics the risk of CME and permanent vision loss
is even greater.
NSAIDs are also frequently used to inhibit
intraoperative miosis during cataract surgery. Miosis
may restrict the surgeons field of view during cataract
surgery, thereby hindering the progression of the
procedure, and increasing the risk of complications
and posterior capsule rupture (Guzek, Stewart). The
NSAIDs prevent miosis by limiting prostaglandin
synthesis within the tissues by inhibiting cyclooxygenase
and reducing inflammation. They also help to maintain
increased pupillary size during the surgical procedure
thereby helping to reduce complications.
Pharmacologic Therapy for
Ocular Inflammation
Ocular inflammation is currently treated with either
topical corticosteroids or NSAIDs. The corticosteroids,
considered the gold standard for the treatment of
ocular inflammation, are associated with an increased
incidence of adverse events that warrant their judicious
use. These adverse events include cataract formation,
a rise in intraocular pressure, increased susceptibility
Fig. 37.2: Background diabetic retinopathy
increases the risk of CME
237
Optimizing Visual Outcomes with NSAIDs Therapy in Cataract and Refractive Surgery
Fig. 27.3: Preoperative NSAIDs reduce pupil
constriction during cataract surgery (Donnenfeld)
to microbial infections due to a suppressed host
immune-response, retardation in corneal epithelial and
stromal wound healing. Steroids are not safe for
periods of extended use as prolonged use is associated
with development of glaucoma, visual acuity defects
and loss of visual field, and posterior subcapsular
cataract formation.
A safer alternative to corticosteroids for the
treatment of ocular inflammation are the NSAIDs.
There are four classes of NSAIDS available for topical
ophthalmic use: indoles, phenylacetic acids, an
arylacetic acid pro-drug, and phenylalkanoic acids.
Indomethacin 1% aqueous suspension is an indole
derivative that is available outside of the United States
(OBrien). Dicl ofenac 1% is a water-sol ubl e
phenylacetic derivative approved by the FDA as a
treatment to minimize inflammation related to cataract
surgery and as a therapeutic option for the reduction
of pain and photophobia after cataract surgery.
Bromfenac 0.09% is a recently approved twice-daily
topical phenylacetic compound indicated for the
treatment of postoperative cataract inflammation.
Originally available as a systemic medication, the
product was removed from the market in the United
States because of potentially fatal liver toxicity but has
been available as an ophthalmic agent in Japan for
several years. Nepafenac 0.1% is approved as a three
times a day treatment for pain and inflammation
associated with cataract surgery. This agent is an
arylacetic acid pro-drug. Flurbiprofen 0.03% and
suprofen 1% are water-soluble phenylalkanoic acids
approved by the FDA for intraoperative use during
cataract surgery for inhibition of excessive miosis during
cataract surgery. Ketorolac tromethamine 0.4% is also
a water-soluble phenylalknaoic acid and is approved
for the treatment of for the reduction of ocular pain
and burning/stinging following corneal refractive
surgery.
NSAIDs for Control of Pain
Following PRK
The recently reported pooled analysis of 2 multicenter,
randomized, double-masked, vehicle-controlled,
parallel-group studies of 313 patients with unilateral
photorefractive keratectomy (PRK) evaluated the safety
and analgesic efficacy of ketorolac tromethamine 0.4%
ophthal mic sol ution in postoperative patients
(Solomon). After surgery, patients were treated with
1 drop of ketorolac tromethamine 0.4% ophthalmic
solution (n = 156) or vehicle (n = 157) four times
daily for up to 4 days. Pain intensity, pain relief, use
of escape medication, and severity of ocular symptoms
were assessed and adverse events, epithelial healing,
and visual acuity recorded. Patients in the ketorolac
group reported significantly less pain intensity than
patients in the vehicle group (P<.001). During the
first 12 hours post PRK, 50% fewer patients in the
ketorolac group than in the vehicle group had severe
to intolerable pain [41.6% (64/154) and 84.5% (131/
155), respectively]. The median time to no pain was
30 hours in the ketorolac group and 54 hours in the
vehicle group (P<.001). Ketorolac patients reported
significantly greater pain relief than vehicle patients
throughout the study (P<.001) and used significantly
less escape medication than vehicle patients for 48
hours post-PRK (P<.008). The authors concluded that
ketorolac 0.4% ophthalmic solution is safe and effective
in reducing ocular pain when used 4 times daily for
up to 4 days post-PRK.
NSAIDs vs Steroids
A recent study compared the efficacy, safety and patient
comfort of two topical steroids (prednisolone 1% and
rimexolone 1%) with ketorolac tromethamine 0.5%
after extracapsular cataract extraction in a prospective,
randomized, double-masked study of 45 patients.
Patients were assigned to receive topical treatment with
prednisolone, rimexolone or ketorolac tromethamine
ophthalmic solution after phacoemulsification for
cataract extraction. Although there were no significant
between-group differences in inflammatory cell counts,
(P=0.165), flare readings in the anterior chamber were
lowest (P=0.008) in the ketorolac group. One patient
in the prednisolone group experienced elevated IOP
and had to be excluded. The authors concluded that
ketorolac tromethamine provides good control of
238
intraocular inflammation after cataract extraction
without the risk of a steroidal IOP increase (Herneiss).
Holzer and associates reported that ketorolac
tromethamine ophthalmic solution 0.5% was is
effective as loteprednol etabonate ophthalmic
suspension 0.5% in reducing inflammation after routine
phacoemulsi-fication and IOL implantation, suggesting
that ketorolac tromethamine 0.5% is a safe and
effective antiinflammatory alternative to steroids after
cataract extraction.
Similarly, Solomon and associates reported
ketorolac tromethamine 0.5% is a safe and effective
anti-inflammatory alternative to steroids after cataract
extraction. In that study, ketorolac tromethamine 0.5%
was as effective as rimexolone 1% in reducing
inflammation after cataract surgery. There were no
between-group differences in signs and symptoms of
inflammation, intraocular pressure, or Kowa cell and
flare measurements in this double-masked, prospective
evaluation of 36 patients (Solomon and Vroman
2001).
NSAIDs for the Inhibition of
Miosis
Srinivisin and associates reported that topical ketorolac
was a more effective inhibitor of miosis than topical
diclofenac during extracapsular cataract extraction and
IOL implantation. Ketorolac also provided a more
stable mydriatic effect throughout surgery. In a study
of 51 patients who were prospectively randomized to
receive ketorolac 0.5% or diclofenac 0.1% at 3
intervals preoperatively. In this study, the ketorolac
group showed a consistent trend toward larger pupil
diameters at subsequent surgical intervals as well as
greater inhibition of miosis in the ketorolac group.
Similarly, Snyder and associates reported that the
use of ketorolac as a single agent negated the need
for use of a combination of preoperative NSAID
(flurbiprofen) and postoperative cosrticosteroid for the
prevention of intraoperative miosis and postoperative
inflammation in cataract surgery. In their study of 26
patients, there were no statistically significant differences
in dilation (preoperative versus postoperative) or cell
and flare postoperatively. The authors concluded that
the use of ketorolac as a single agent could eliminate
the expense of using separate anti-inflammatory and
antimiotic preparations preoperatively and post-
operatively, thereby enhancing surgeon convenience
and patient convenience and compliance (Snyder).
Recently, a large study (n=118) compared the
effects of topical ketorolac with topical 0.03%
flurbiprofen on the inhibition of surgically induced
miosis during phacoemulsification cataract surgery.
Mean horizontal pupillary diameter measurements for
both medications were similar at the start of surgery.
However, a consistent trend of larger pupillary
diameter was seen in all subsequent surgical intervals
in the ketorolac-treated group. Changes from baseline
measurements also indicated a more significant
inhibition of miosis at all subsequent intervals, and a
more stable mydriasis throughout the procedure in
the ketorolac-treated group (Solomon 1997).
NSAIDs and Topical Steroids
It is well accepted that combination topical therapy
with a corticosteroid and a NSAID is more effective
than either agent dosed individually for treatment of
CME following cataract surgery, and a recent study
by Rho and associates supports this paradigm. The
authors compared combination therapies of diclofenac
sodium 0.1% and prednisolone acetate 1%, with
ketorolac tromethamine 0.5% and prednisolone
acetate 1%, for treatment of CME in 68 patients
following uncomplicated cataract surgery. Complete
resolution of CME was noted in 28% of diclofenac
patients and in 25% of ketorolac patients. Final vision
improved three or more lines in 58% and 53% of
patients, respectively. None of the patients showed signs
of corneal toxicity or significant intraocular pressure
rise during the treatment period. The authors
concluded that combination therapy with NSAIDs and
steroids was effective in reducing the severity of
pseudophakic CME and in improving final vision.
The findings of Rho and associates are supported
by another recent study by Heier and associates (Heier,
2000). That study evaluated the efficacy of ketorolac,
prednisolone acetate 1.0%, and ketorolac and
prednisolone combination therapy in the treatment
of acute, visually significant, clinical CME following
cataract extraction surgery in a randomized, double-
masked, prospective trial of 28 patients. Treatment was
continued until CME resolved or for 3 months,
whichever occurred first and then tapered over 3 weeks.
The average improvements in Snellen visual acuity
were 1.6 lines with ketorolac monotherapy, 1.1 lines
with steroid monotherapy, and 3.8 lines with
combination therapy. More patients in the combination
group achieved at least a two-line improvement (89%
of combination patients versus 67% of ketorolac and
50% of steroid patients). Moreover, these patients
improved faster with combination therapy than with
monotherapy with either agent (1.33 months for
combination therapy compared with 1.43 months for
ketorolac patients and 2.75 months for steroid
patients). Improvements in contrast sensitivity and
239
leakage on fluorescein angiography tended to mirror
improvements in Snellen acuity. The authors concluded
that treatment of acute, visual l y significant
pseudophakic CME with ketorolac and prednisolone
combination therapy appears to offer benefits over
monotherapy with either agent alone.
A study by Arshinoff et al evaluated postoperative
pain in 97 PRK patients using different topical NSAID
protocols. In their study, treatment with topical
homatropine hydrobromide, either diclofenac sodium
or ketorolac tromethamine, and a soft contact lens
was most effective in achieving post-PRK analgesia.
They also found that NSAIDs added to topical steroid
protocols had a significantly greater effect than steroids
alone on reducing myopic regression for one year
postoperatively (Arshinoff, 1994).
Prevention of CME
All available evidence demonstrates that ketorolac is
an effective treatment for acute and chronic CME.
Several studies, however, suggest that ketorolac is also
able to prevent CME in postoperative patients. A study
by Flach and associates (1990) suggested that ketorolac
prevents CME without the risks associated with
concomitant topical steroid treatment. In that study,
50 patients with bilateral cataracts were enrolled in a
placebo-controlled, paired-comparison, double-
masked study. Eleven patients had evidence of
angiographic (angiographic aphakic CME) ACME on
postoperative day 40. Two of these patients demons-
trated bilateral ACME, one patient had ACME in the
NSAID-treated eye, and eight patients had ACME in
the placebo-treated eye. This was a statistically
significant difference favoring drug treatment. In
addition, the signs of anterior ocular inflammation were
greater in the eyes with ACME.
Roberts presented data from a clinical study at the
2005 meeting of ASCRS that demonstrated that
patients using preoperative and postoperative NSAIDs
had less postoperative increase in macular thickness
than those who did not use NSAIDs. In that study,
200 patients undergoing phacoemulsification were
randomized to two pharmaceutical treatment
regimens, differing only by the inclusion/exclusion of
ketorolac 0.4% into the standard treatment regimen.
Outcome measures included macular thickness by OCT
at preoperative and 4 weeks postoperative, contrast
sensitivity by FACT, and Snellen visual acuity. After 4
weeks, the change in macul ar thickness was
substantially greater without NSAIDs than with
(10.4 m compared with 4.2 m, respectively). There
were no differences in visual acuity. The author
concluded that macular edema decreases the quality
of postoperative vision and that the use of pre-
operative and postoperative NSAIDs decreases the
amount of postoperative macular edema.
Many clinicians are hesitant to prescribe topical
NSAIDs for long-term use because of prior reports of
corneal melting associated with topical NSAIDs (Flach,
Gaynes).

However, analysis of NSAID-associated
corneal events implicates the now defunct generic
diclofenac product, diclofenac sodium ophthalmic
solution as the agent primarily responsible (Gaynes).
The demonstrated safety of ketorolac throughout
numerous studies, some as long as 6 weeks duration,
suggests that this drug is safe for extended use. If fact
ketorolac has actually been recommended for the
treatment of post-cataract inflammation in a patient
with systemic steroid treated rheumatoid arthritis post-
phacoemulsification. In this patient the fear of melting
led the physician to avoid topical NSAIDs. However,
the severe reaction postoperatively led him to using
it successfully in the second eye with excellent results
(Caronia).
The available evidence demonstrates that NSAIDs
are highly effective analgesics for pain associated with
cataract and refractive procedures. The ability to
provide relief of patient pain is critical because patients
have high expectations and expect almost no pain with
ophthalmic surgeries. Patients who experience ocular
pain or discomfort may therefore believe that their
surgeon may have substandard surgical skills and the
resulting patient dissatisfaction and potential for
negative word of mouth to the patients colleagues
and friends may have adverse consequences for a
surgical practice. Choosing the most effective topical
agent for relief of ocular inflammation and pain
postoperatively is therefore.
The adjunctive use of NSAIDs with steroids optimizes
surgical outcomes as numerous studies have
demonstrated that the combination of an NSAID and
steroid is more effective for the treatment of post-
operative inflammation, CME, and improving visual
acuity than either NSAID or steroid monotherapy.
Perhaps the most important effect to surgeons is
the increased amount of dilation preoperatively and
the tendency for the dilation to remain for the entire
procedure. Some surgeons have likened this effect as
like having a third hand during surgery. Other studies
point out the direct relationship between pupil size and
rate of surgical complications (Donnenfeld).
In recent years, there has been a substantially
amount of debate in the ophthalmic community
regarding the use of NSAIDs prior to surgery to prevent
the formation of CME. We understand and accept that
increased inflammation postoperatively is associated
240
with an increased risk of developing CME. In fact, a
study by Ursell and associates reported that patients
who had angiographic CME at day 60 were more likely
to have had more postoperative inflammation than
patients who did not develop CME. (Ursell) It follows,
therefore, that preventing inflammation with pro-
phylactic dosing would decrease the risk of developing
CME. A recent study by Donnenfeld and associates
(Donnenfel d) does provide us with evidence
supporting the use of ketorolac 0.4% as surgical
prophylaxis against CME. The study was a prospective
evaluation of 100 patients randomized in a double-
masked fashion prior to phacoemulsification into 4
groups: one group received preoperative ketorolac
tromethamine 0.4% four times daily for 3 days and
three doses every 15 minutes immediately surgery,
another received four doses on the day before surgery
ketorolac 0.4% and three doses every 15 minutes
immediately surgery, another received ketorolac only
3 times (every 15 minutes) in the hour immediately
surgery, and the fourth group was randomized to
control. In that study, use of ketorolac for 1 or 3 days
reduced the incidence of CME. No patients in these
groups had CME at week 2, compared with 12% (3/
25) of control patients and 4% (1/25) of patients in
the 1 hour group. This study suggests that three day
preoperative dosing with ketorolac effectively prevents
CME. Other findings of that study demonstrated that
ketorolac maintained pupil size, reduced discomfort,
limited reductions in epithelial cell counts, and reduced
patient need for additional anesthesia. Ketorolac also
provided substantial reductions in the amount of time
needed to perform surgery, making it a cost-effective
pharmaceutical for cataract surgery. Most of these data
followed a clear dose-response pattern, suggesting that
maximum prophylaxis can be expected with the three
days dosing regimen, though even 1 day of ketorolac
was consistently superior to 1 hour of ketorolac or to
control. Flach and Roberts that ketorolac is an effective
prophylaxis against CME.
If a 3-day dosing regimen of ketorolac is effective
surgical prophylaxis, what is the most appropriate
postoperative dosing regimen? In my experience, 4
weeks of QID dosing with ketorolac 0.4% is optimal
for most patients, in patients with diabetes mellitus we
use at least 6 weeks of therapy and most important
in patients with diabetic retinopathy we use ketorolac
0.4% for at least three months to help protect this
most susceptible group from developing CME.
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33. Solomon KD, Donnenfeld ED, Raizman M, et al. Safety
and efficacy of ketorolac tromethamine 0.4% ophthalmic
solution in post-photorefractive keratectomy patients. J
Cataract Refract Surg 2004 Aug;30(8):1653-60.
34. Solomon KD, Turkalj JW, Whiteside SB, Stewart JA,
Apple DJ. Topical 0.5% ketorolac vs 0.03% flurbiprofen
for inhibition of miosis during cataract surgery. Arch
Ophthalmol 1997 Sep;115(9):1119-22.
35. Solomon KD, Turkalj JW, Whiteside SB, Stewart JA,
Apple DJ. Topical 0.5% ketorolac vs 0.03% flurbiprofen
for inhibition of miosis during cataract surgery. Arch
Ophthalmol 1997;115:1119-22.
36. Solomon KD, Vroman DT, Barker D, Gehlken J.
Comparison of ketorolac tromethamine 0.5% and
rimexolone 1% to control inflammation after cataract
extraction. Prospective randomized double-masked
study. J Cataract Refract Surg 2001 Aug;27(8):1232-37.
37. Srinivasan R, Madhavaranga. Topical ketorol ac
tromethamine 0.5% versus diclofenac sodium 0.1% to
inhibit miosis during cataract surgery. J Cataract Refract
Surg 2002 Mar;28(3):517-20.
38. Stewart R, Grosserode R, Cheetham JK, et al. Efficacy and
safety profile of ketorolac 0.5% ophthalmic solution in
the prevention of surgically induced miosis during
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39. Ursell PG, Spalton DJ, Whitcup SM, Nussenblatt RB.
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1492-97.
40. Waterbury LD, Flach AJ. Efficacy of low concentrations
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C H A P T E R
38
Management of Cystoid
Macular Edema
Arturo Prez-Arteaga, Ren Cano-Hidalgo (Mexico)
Introduction
Cystoid macular edema (CME) is an inflammatory
condition of the central retina that can be produced
for many causes, since drugs for other ophthalmic
diseases until surgical intervention of the eye. If well
the initial descriptions of the disease can be found as
a surgical complication, now we know much more
conditions that can produce these clinical and para-
clinical findings, so that we can talk about a multi-
factorial disease.
Many drugs are involved in the treatment of this
condition. The choose of each one is according the
etiology of the inflammatory process, preference of the
physician, response of the patient, underlying disease,
severity of visual loss and anatomic findings. Even surgical
treatment has been described, and so the use of specifical
drugs during and after the procedure; so it is a very
good way to review the drugs involved in the treatment
of this pathologic condition according to the physioscopy
of this book, the use of anti-inflammatory drugs in
ophthalmology. In fact several proven treatment
modalities are available and so on new therapies are
continuing to expand our horizons.
First the reader will find in this chapter a brief
description of CME definition, etiology, clinical findings
and diagnostic strategies. Then the drugs that are
involved in the treatment of this condition, including
those used in the surgical treatment will be described.
Definition
CME is a pathologic condition of the macula with
swelling where multiple cyst-like (cystoid) areas of fluid
appear in the central retina, mostly in the outer
plexiform layer. It is a painless disorder that according
to the cause and severity can be fully reversed or can
cause permanent visual loss. Sometimes this condition
has clinical manifestations from low to severe, but also
can occur in the sub-clinic plane.
Etiology
POST-SURGICAL, PRIMARY OR SECONDARY
(CAPSULOTOMY)
It was first described as the Irving-Gass syndrome; a
pathologic condition where Irving in 1953 mentioned
a decrease in the visual acuity with vitreoretinal
alterations after the intracapsular surgery of the lens,
and Gass and Norton described the typical fluorangio-
graphic changes of this condition. At that time 77%
of the eyes operated with intracapsular cataract surgery
developed some degree of CME, even sometimes sub-
clinical.
During the days of the extracapsular cataract
extraction the incidence decreased because the
preservation of the posterior capsule and the decrease
of vitreous loss. Even so, this incidence increase when
there is posterior capsule rupture in an extracapsular
technique. With the entrance of phacoemulsification
techniques for cataract surgery the incidence was even
less, but again, it was demostrated that the main goal
to decrease this condition is the conservation of the
posterior capsule and to avoid the vitreous loss. It is
still to be proved that the newest technologies of
minimally invasive cataract surgery can produce a
statistical reduction of post-cataract surgery CME.
The posterior capsulotomy is also a very well-known
procedure that can lead to CME, and it is also related
to the rupture of the retinal and accuous barriers; so
in this field new technologies and evolution of
intraocular lenses that can reduce the incidence of
posterior capsule opacification are very important.
Any kind of intraocular surgery can produce
sometime some degree of CME. At the end the cascade
of events become from the rupture of the intraocular
barriers. The initial trauma (damage, surgery, etc.)
produce the liberation of the chemical mediators of
the inflammation to the accuous and vitreous; mainly
prostaglandins are produced by the damaged tissue
and the traumatized epithelial cells, but many other
243
Management of Cystoid Macular Edema
factors like the complement, the platelet activation
factor, lisozomal enzymes, cytoquines, nitric oxide,
endothelin and interleukin. We can conclude that any
factor that contributes to the rupture of the barriers
blood-accuous and blood-retinal is going to increase
the possibility to develope CME.
MICROVASCULAR DAMAGE
This is commonly found in diabetic retinopathy,
occlusive diseases like retinal vein occlusions, and other
less commonly diseases like idiopathic juxtafoveal
capillary telangiectasia. The main factor is again the
rupture of the intraocular barriers that this vascular
alterations produce and the liberation of the mentioned
mediators during the acute vascular event. Some other
factors like the VEGF and IGF-1 liberated by the
ischemic tissues, have been involved in the rupture
of the intraocular barriers and so in the production
of CME. Any syndrome associated with sub-retinal
neovascularization can have the same effect.
INFLAMMATORY DISEASES
The most well-known form of uveitis that can produce
CME is pars planitis; in fact CME is the main cause
of visual loss in this inflammatory process, but many
other forms of uveitis like Behets disease, Crohns
disease, rheumatoid arthritis, sarcoidosis and some
other forms of non-specifical uveitis can produce some
degree of CME. The cause is as mentioned before,
the liberation of the inflammatory mediators.
POST-MEDICATION (ANTIGLAUCOMA DRUGS
AND PRESERVATIVES)
The first reference about the relation between an anti-
glaucoma medication and the development of CME
was described by Becker in 1967 and was with the
use of epinephrine; was noted years after, that this
incidence was more in the aphakic patient. It is well
known at this time, that the topical epinephrine
increase the prostaglandins in the eye, in particular
in the aphakic one, and so the rupture of the
intraocular barriers.
Some other medications were described to
produce this effect like dipivalylepinephrine, timolol
and benzalconium chloride. Recently with the arise of
new pharmacologic groups of anti-glaucomatous
medication, in particular prostaglandins, the incidence
of post-medication CME has increase. A lot of studies
have been conducted in this field and what we know
currently is that latanoprost, travoprost, bimatoprost
and unoprostone can produce some degree of CME
and that this incidence can increase with the association
of risk factors like cataract surgery, uveitis, posterior
capsulotomy and diabetic retinopathy.
This concepts must be taken in count by the
physician at the time to prescribe this medications in
particular if some risk factors are present in some patient.
If the therapy can be done with another medication
it will be better, but if it must be continued for some
reason, the util ization of non-steroidal anti-
inflammatory drugs can avoid the development of
CME without loss of the hypotensor effect of the anti-
glaucoma drugs. Also a constant follow-up with the
explanation to the patient of specific symptoms of
macular disease and Amsler test in each visit for
glaucoma control, are mandatory.
PERIPHERAL RETINAL LESIONS
A peripheral lesion, can lead by itself, to the rupture
of the intraocular barriers and so the development of
CME. It is a good behavior to explorate the periphery
of the retina in a case when we find CME and we
are trying to know the cause.
TUMORAL DISEASES
Because of acummulation of leakage and rupture of
the barriers, many ocular tumors, like malignant
melanomas, peripheral capillary hemangiomas and
Coats disease can be also cause of CME.
EYE HYPOTONY
It can be post-traumatic, with or without rupture of
the globe, it can be followed cataract surgery, glaucoma
procedures or choroidal effussions of any cause. At
the end, the low intraocular pressure is the cause for
the rupture of the intraocular barriers and so the
liberation of mediators.
OPTIC NERVE DISEASES
Optic nerve inflammations like true papilledema,
neuropathy or some ischemic diseases can produce
CME.
RETINAL TRACTION
Peripheral traction, macular traction, epiretinal
membranes, and traction produced by diabetic
retinopathy (even without direct macular traction) are
common entities that can produce CME.
FINAL COMMON PATHWAY OF UNDERLYING
DISEASES
Ischemic, tractional, inflammatory, toxic and genetic.
244
Histopathology
The breakdown of the inner blood-retinal barrier due
to vasogenic and/or cytotoxic causes is the initial event
in CME. There is a leaking of the perifoveal capillaries
leading the formation of edema. The fluid collects in
the loosely arranged outer plexiform layer of Henle;
in this layer the fibers are arranged in an horizontal
pattern. This is the cause of the petalloid flower
appearance that is seen as characteristic of this disease
in the angiogram (cystic pattern) (Fig. 38.1).
Electronic microscopy has shown acummulation of
intracelullar fluid within expanded Mller cell processes.
Fig. 38.1: Cystic pattern
Clinical Findings
There is always an history of previous ocular disease,
surgery, medication, vitreous pathology or another
condition in the patient that developes CME.
Sometimes it can be very easy to obtain, like previous
cataract surgey or posterior capsulotomy, but in some
others, the physician must be very accurate like in
glaucoma medications, posterior vitreous detachment
or peripheral tears that may lead to the break of the
inner blood-retinal barrier.
The main symptom of CME is the reduction of
visual acuity, even so, here are many forms of CME
that goes free of visual symptoms. Many patients that
undergo a cataract surgery can develop some degree
of sub-clinical CME, and the only one evidence can
be found in a retinal fluorogram. The degree of the
disease and so the severity of symptoms frequently
correlates with the degree of complications during the
cataract surgery, if this is the case. So the reduction
of visual acuity may undergo from a minimal degree,
like 20/25 and be not notice by the patient, until very
poor visuality like 20/400 or less in severe cases. Like
some others macular diseases the patients can
experience some degree of metamorphopsia.
At the clinical examination the evidence of surgery,
trauma, vascular retinal diseases and others like
glaucoma diseases must be achieved. Of course the
main study is the fundoscopy where the macular
thickening and/or swelling can be found. It also can
be found in many degrees depending upon the severity
of the disease, and can go since a loss of foveolar reflex
with out clinical evidence of edema, to a characteristic
cystic appearance. This is the typical clinical finding in
the ophthalmoscopy, radiating cystic spaces emana-
ting from the macula. Of course, in these cases, there
is a complete loss of the red reflex. The red free light
examination is mandatory, where a honeycombed
appearance is seen, and it corresponds to the fluid
filled cyst (Fig. 38.2). In severe cases these cyst may
coalesce into a macular cyst and then form a hole.
Fig. 38.2: Loss of red reflex
PARACLINICAL APPROACH
No laboratory studies are necessary to establish the
diagnosis of CME. The main study in the establishment
of this diagnosis is the fluorescein angiogram (FA).
In the FA parafoveal retinal capillary leakage is seen
in the early and mid phases. These phases are not
characteristic of CME because the acummulation of
fluid in certain conditions is delayed, so the late phase
has a particular importance, and it is about 20 minutes
and sometimes can be more, to find the characteristic
petaloid pattern of leakage in the macula.
Another related conditions can be seen in the FA
according the underlying disease: If likeage micro-
aneurysms are present, diabetic retinopathy can be
the cause; vascular collaterals can be due to retinal
oclussion; optic nerve findings are also useful in the
final etiologic diagnosis establishment.
Optical coherence tomography (OCT) is a non-
invasive method also very useful in the final diagnosis
245
of CME because the fluid-filled spaces in the retina
are easily seen. This cross-sectional image of the retina
can also be helpful in the monitoring over time of the
disease by quantifying the amount of fluid inside the
retina in serial studies. A non-invasive study can be
the ideal modality in monitoring the response to
treatment.
In particular cases an electroretinogram can also
be helpful but not mandatory (Figs 38.3 to 38.5).
Fig. 38.3: Macular quistic edema
Fig. 38.4: CME plus epiretinal membrane
Fig. 38.5: Epiretinal membrane plus macular cystic edema
Treatment
The treatment of CME can be divided in two
approaches that finally in the practice are combined
but in the theory we are going to describe separately.
NON-SURGICAL APPROACH
Many drugs have been involved for the treatment of
CME during the time. Some of them are used as a
traditional fashion and some others are emerging as
new therapeutic resources.
Nonsteroidal Anti-inflammatory Drugs (NSAIDs)
The main effect of this group of drugs is to estabilize
the blood-retinal barrier. This effect is because they
inhibit the enzyme cyclo-oxygenase. They can be used
by systemic way and also in the form of eyedrops.
The main examples of this group of medications are:
1. Indomethacin
2. Ketorolac
3. Diclofenac
They inhibite the prostaglandin synthesis by
decreasing the activity of the enzyme cyclo-oxygenase.
These drugs in the topical form must be used as a
medication in the preoperative and postoperative
period of some intraocular procedures like cataract
surgery, posterior capsulotomy and peripheral
iridectomy for example, to reduce the incidence of
CME. This profilactic form also helps to reduce the
postoperative inflammatory process. As has been said
before, the development of CME in some way
correlates with the degree of manipulation during the
ocul ar surgery and some factors have been
demonstrated in the development of CME like the
time of light microscope exposure, posterior capsule
rupture and vitreous manipulation. Of course, a real
clean surgery can decrease the incidence of CME,
but anyway, the use of NSAIDs is mandatory. New
operative devices that avoid the use of direct light
exposure during the ocular surgery are promising in
the near future to decrease the incidence of CME in
uncomplicated surgery cases.
The use of systemic NSAIDs is only reserve for the
cases of complete diagnosis of CME; even so some
surgeons are using them as a profilactic medication.
There is not a recomended time for the use of systemic
NSAIDs for the treatment of CME; the time of use
will depend upon the response of each patient in
particular according the follow-up.
Because sometimes it is a long-term medication,
secondary effects of NSAIDs must be always taken in
count. In the systemic medication, gastric effects should
be monitoring during the visits of the patient. A history
of gastric diseases including ulcerative disease and
bleeding is mandatory when oral indomethacin is in
use. If some of these effects are present the
therapeutic must be suspended and replaced by other
medication.
Local NSAIDs have also some secondary effects;
long-term use may delay wound healing and has been
246
reported cases of corneal stromal thinning or melting
in some particular patients receiving diclophenac
eyedrops for extended period of time. If symptoms
like blurred or diminished vision and signs of corneal
deposits, retinal changes and scotoma are present, the
medication must be suspended.
Corticosteroids
Steroidal medication is very useful in the treatment
of CME and also in the prevention of it. The routine
use of steroids in the eyedrops form before and after
surgical procedures, has decrease the incidence of
postsurgical CME, even in complicated cases.
The most frequent form of steroid medication for
CME is topical, in the form of prednisolone acetate;
it is indicated in several conditions of steroid-responsive
intraocular inflammation. The presentation is at 1%
solution and can be used several times in a day
according the severity of the inflammation. The amount
and time of administration must be measured according
the response of the disease to the treatment.
Monitoring of the side effects of topical steroids like,
raise in the intraocular pressure and an increased risk
of secondary ocular infections, must be evaluating
during the time of therapy and this should be
discontinued if some of these effects are found. Not
all patients have the same response to steroids
according the rise in the intraocular pressure; some
patients can tolerate large periods of time without
changes in the pressure, but some others cannot
tolerate too much medication. If the topical steroid
therapy is really needed in these cases, the physician
can add some glaucoma therapy; medications that can
increase the CME should be avoided (e.g. latanoprost,
travoprost, epinephrine); the best adjunctive anti-
glaucoma medication is dorsolamide that also can have
some benefit effects in the macula. Other side effects
of long-term topical steroids like subcapsular cataract
formation must be addressed.
The use of injections of long acting depot-steroids
(e.g. triamcinolone) into the sub-Tenon space has also
a role in the treatment of CME. This external way of
administration that can have more penetration to the
retina; the drug delivery to the retina is superior by
this route in comparison to peribulbar. In some cases
of uveitic CME refractory to conventional treatment,
the triamcinolone has been used in intravitreous
injection alone or in combination with some other
drugs. Triamcinolone alone has been effectively in
reducing CME and improving vision; some studies are
currently underway in the combination of this steroidal
drug with other drugs, like bevacizumab (Avastin).
Oral steroids play also an important role in the
treatment of CME because the effect in the stabilization
of the blood-ocular barrier. They can be useful in some
forms of uveitic CME. Nevertheless the secondary
effects of systemic corticoid medication must be
avoided, and this is why recently the medication of
CME is trying to move to the ocular space instead the
systemic route.
Carbonic Anhydrase Inhibitors (CAIs)
Carbonic anhydrase is an enzyme present in the apical
and basal surfaces of the retinal pigment epithelium
cell membrane. Its action is to pump and produce a
change in the ion flux. CAIs enhance this pumping
action of these cells, and helps to improve this ion flux
that affects the cellular environment of the retina.
CAIs are commonly used in ophthalmology, in
particular in the glaucoma cases, where the topical
medication is not enough to control the intraocular
pressure, so it is a well-known resource. Also the
physician is close to side effects of the CAIs, like the
alteration in the ionic composition of blood, increase
in urine excretion, and in large doses hepatic and
metabolic problems. So it is known that it is not a
chronic medication, it has to be used according the
severity and response to treatment of CME and the
physician has to advice the patient the side effects, the
mode to contrarest them and the total communication
they both have to mantain in order to manage the
dose in good response, but also in good levels of side
effects. This medication should be suspended as soon
as possible according the evolution of CME.
The presentation of acetazolamide is in tablets of
250 mg and can be given until three to four times
a day. Close monitoring of antiinflammatory and side
effects is mandatory.
Intravitreal Medication
Recently new drugs are appearing in the retinal medi-
cation field for intravitreal injection, like Bevacizumab
(Avastin) and Pegaptinib, also called Macugen. These
drugs are promising results in many retinal vascular
disorders l ike occl usive diseases and diabetic
retinopathy. The side effects are not completely known,
and many trials around the world are in progress at
this time to achieve consistent results.
The apparently positive action seen in some vascular
disorders lead the possibility to use them in CME. Some
of them are including only diabetic patients, some
others only postoperative cataract patients and some
others are combining the avastin with triamcinolone.
During the middle of year 2007 these trials will be
finish and we will be able to know the safety, efficacy
and probably side effects of these drugs in the
treatment of CME.
247
SURGICAL APPROACH AND DRUGS RELATED
The surgical treatment is not the first choice in the
treatment of CME; nevertheless, some particular
situations can lead to the indication of pars plana
vitrectomy (PPV):
Cases of uveitis related CME.
Remove of vitreous strands that can cave an effect
of pull the retina, from anterior and posterior
segment structures.
Remove inflammatory mediators from the vitreous
(e.g. memory cells, cytoquines), that can be
mantaining an inflammatory response.
Remove of retained lens fragments.
Remove of epiretinal membrane.
Because the rupture of the blood-retinal barrier,
after the PPV there is an increase in the peneration
of topical and oral steroids. Also some surgeons are
happy with the use of triamcinolone during the surgical
approach, achieving so the benefit effect of both,
vitrectomy and intravitreal medication. We believe at
this time, that the PPV by itself is not enough for the
treatment of CME; we agree that it must be
accompanied by intravitreal medication.
The side effects of steroids in the vitreous cavity
must be addressed continuously because the possibility
of changes in IOP; in this particular case sometimes
it is very difficult to achieve a good IOP because the
deposit effect of the steroid. Even so, sometimes
without steroid medication in the vitreous cavity, PPV
it self, is able to produce an increase in IOP of difficult
control.
The final decision to perform a PPV must be carefully
evaluated and consented between the surgeon and
patient, because of the possible side effects.
Conclusion
At the end of the day a lot of factors are going to
influence the prognosis of a patient who develops CME.
The main factor of all is the inherent cause of the
disease; it will not be the same a patient who develops
CME because of a glaucoma treatment (in this case
the suspension of the prostaglandin and the medical
treatment with NSAIDs can be enough to reverse by
complete the disease without any permanent loss of
vision), that a CME caused by a chronic pars planitis
of difficult treatment (in this case a chronic CME can
lead to severe decrease of vision).
Patients who are going to be operated, in particular
anterior segment procedures, must be medicated since
the preoperative period, through the operation and
during the postoperative time, with drugs that can
decrease the development of CME, like steroids and
NSAIDs according the case. After all we know about
this disease, prevention and treatment we believe this
should be mandatory. Also in patients with glaucoma
control with prostaglandines, this therapy should be
avoided and the control must be followed with another
anti-glaucoma medication, during the pre, trans and
postoperative period. If it is not possible to eliminate
the prostaglandin and NSAIDs should be started in
addition. Of particular importance is the glaucoma
patient, who is receiving medication that can produce
CME; the physician must be alert to any kind of sign
that can advice the presentation of CME. The adjuntive
NSAIDs therapy can be helpful in cases where is
impossible to avoid prostaglandins.
New medications are promising good results, even
alone or in combination, for the treatment of refractory
CME. Like all new products, we are specting some
new non-reported adverse effects; the test of time,
like always, will lead us to the complete knowledge
of their specific indications.
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30. Miyake K, Mibu H, Horiguchi M, et al. Inflammatory
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31. Miyake K, Miyake Y, Kuratomi R. Long-term effects of
topically applied epinephrine on the blood-ocular barrier
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32. Miyake K, Miyake Y, Maekubo K et al. Incidence of
cystoid macular edema after retinal detachment surgery
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1985;100:510-9.
33. Miyake K, Ota I, Ibaraki N et al. Enhanced disruptionof
the blood-ocular barrier and the incident of angiographic
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Ophthalmol 2001;119:387-94.
34. Miyake K, Ota I, Maekubo K, Ichihashi S, Miyake S.
Latanoprost accelerates disruption of the blood-aqueous
barrier and the incidence of angiographic cystoid macular
edema in early postoperative pseudophakias. Arch
Ophthalmol 1999;117:34-40.
35. Miyake K, Shirasawa E, Hikita M, et al. Synthesis of
prostaglandin E in rabbit eyes with topically applied
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36. Miyake K, Sugiyama S, Norimatsu I et al. Prevention of
cystoid macular edema after lens extraction by topical
indomethacin. Albrecht von Graefes Arch Klin Exp
37. Miyake K. Prevention of cystoid macular edema after lens
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Albrecht Von Graefes Arch Klin Exp Ophthalmol 1977;
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38. Mondino BJ, Nagata S, Glovsky MM. Activation of the
alternative complement pathway by intraocular lenses.
39. Nishi O, Nishi K, Imanishi M. Synthesis of interleukin-
1 and prostaglandin E2 by lens epithelial cells of human
cataracts. Br J Ophthalmol 1992;76:338-41.
40. Ohrloff C, Schalnus R, Rothe R, et al. Role of the posterior
capsule in the aqueous-vitreous barrier in aphakic and
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198-201.
41. Ozaki H, Hayasi H, Vinores SA et al. Introvitreal sus-
tained release of VEGF causes retinal neovascularization
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42. Pollack A, Leiba H, Bukelman A, et al. Cystoid macula
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43. Rossetti L, Chaudhuri J, Diickersin K. Medical profilaxis
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44. Schumer RA, Camras CB, Mandahl AG. Putative side
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45. Schumer RA, Camras CB, Mandalh AK. Latanoprost and
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46. Sjoquist B, Al megard B, Khal il ef V, et al . The
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50. Vinores SA, Sen H, Campochiaro PA. An adenosine
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C H A P T E R
39
Managing Intraoperative
Floppy Iris Syndrome
David F Chang (USA)
Introduction
In 2005, John Campbell and I first described a new
small pupil syndrome associated with systemic
tamsulosin that we named intraoperative floppy iris
syndrome (IFIS).
1
In addition to a tendency for poor
pupil dilation, we identified a triad of intraoperative
signs that characterize IFISiris billowing and
floppiness, iris prolapse to the main and side incisions,
and progressive intraoperative miosis
1
(Fig. 39.1).
Particularly when such iris behavior is unexpected, the
rate of complications such as posterior capsule rupture,
vitreous loss, and iris trauma is increased with IFIS.
1,2
Tamsul osin (Fl omax), a systemic al pha-1
antagonist, is the most widely prescribed treatment
worldwide for benign prostatic hyperplasia (BPH),
which is characterized by increased urinary frequency.
Systemic alpha-1 antagonists improve the lower urinary
tract symptoms of BPH by relaxing the smooth muscle
in the prostate and lower bladder wall. By allowing
more complete emptying of the bladder, these
medications decrease night time urinary frequency.
Alpha-1 receptors also mediate contraction of the iris
dilator muscle, and we proposed that loss of dilator
muscle tone and rigidity was the cause of the floppy
iris. Furthermore, we postulated a semi-permanent
effect because of several cases of IFIS in patients who
had discontinued tamsulosin several years before
surgery. Indeed, in a prospective trial, stopping
tamsulosin preoperatively did not prevent or decrease
the severity of IFIS.
2
Since our initial report, it has become clear that
other systemic alpha-1 blockers such as doxazosin
(Cardura), terazosin (Hytrin), and alfuzosin (Uroxatral)
can also cause IFIS. However, the frequency and
severity of IFIS is much less with these non-specific
alpha-1 antagonists, as compared with tamsulosin.
3
This difference may relate to the much greater affinity
and specificity of tamsulosin for the alpha-1A receptor
sub-type that predominates in both the prostate and
the iris dilator muscle.
2,4
IFIS can be classified as being mild (good dilation;
some iris billowing without prolapse or constriction),
moderate (iris billowing with some constriction of a
moderately dilated pupil), or severe (classic triad and
poor preoperative dilation). In a prospective study of
167 eyes in patients taking tamsulosin, the distribution
of IFIS severity using this scale was as follows: 10%
no IFIS, 17% mild, 30% moderate, and 43% severe.
2
There can be significant variability in the severity of
IFIS between different patients, and even between two
eyes of the same patient. This makes it difficult to
determine whether one pupil management strategy
is superior to another. In fact, the various IFIS
techniques discussed in this chapter can be combined
and it is therefore hel pful to master several
complimentary approaches.
As general surgical principles for IFIS patients, one
should make a well-constructed shelved incision,
perform hydrodissection more gently than usual, and
reduce the irrigation and aspiration flow parameters
if possible. Bimanual microincisional cataract surgery
Fig. 39.1: Intraoperative floppy iris syndrome in a patient
taking tamsulosin. In addition to iris prolapse to the phaco
and side port incision, the pupils has constricted limiting
visibility
251
Managing Intraoperative Floppy Iris Syndrome
may be helpful, particularly for mild to moderate IFIS.
1
This technique utilizes water tight incisions and allows
the surgeon to dissociate the irrigation and aspiration
currents. Keeping the irrigation inflow anterior to the
iris can lessen the iris billowing and prolapse.
In our original report, we noted that mechanical
pupil stretching, performed with or without partial
sphincterotomies, did not prevent iris prolapse or pupil
constriction with IFIS.
1
Excessive iris manipulation may
in fact worsen the iris prolapse in IFIS. Instead, we
found that mechanical pupil expansion, such as with
iris retractors, was far more effective. Subsequently,
several other strategies for the surgical management
of IFIS have been suggested, and are outlined below.
Because IFIS results from alpha-1 receptor
blockade of the iris dilator muscle, a variety of
pharmacologic strategies for managing IFIS have been
proposed.
2, 4-10
As first suggested by Sam Masket,
preoperative atropine drops (e.g., 1% t.i.d. for 1-2
days preoperatively) can provide sufficient cycloplegia
to prevent intraoperative miosis
2,5,6
. However, as a
single strategy atropine alone is often ineffective for
more severe cases of IFIS.
2
Stopping tamsulosin
preoperatively is of unpredictable and questionable
value, and has the potential to cause acute urinary
retention in patients with severe BPH. This is particularly
true if preoperative atropine is used.
Direct intracameral injection of alpha agonist drugs
is an excellent pharmacologic strategy for preventing
or mitigating IFIS. Richard Packard first reported using
intracameral phenylephrine,
7, 8
and Joel Shugar
subsequently suggested using epinephrine for this
purpose.
9
By presumably saturating the alpha 1-A
receptors, these agents can further expand the pupil
(Figs 39.2A and B). Alpha agonists may also prevent
billowing and prolapse by increasing iris dilator smooth
muscle tone and maximizing iris rigidity. Preserved
solutions should be avoided and one should use a
diluted mixture (e.g., 1:1000 bisulfite-free epinephrine
(American Regent) mixed 1:3 with BSS or BSS+) in
order to buffer the acidic pH of the commercial
preparation. Finally, Sam Masket reported excellent
results with the synergistic combination of preoperative
topical atropine with intracameral epinephrine in a
small series patients taking tamsulosin.
6
As first described by Bob Osher and Doug Koch,
Healon 5 (Advanced medical optics) is a maximally
cohesive ophthalmic visco-surgical device that is
particularly well-suited for viscomydriasis and for
blocking iris prolapse in IFIS
2, 10
(Fig. 39.3). However,
to avoid immediately aspirating Healon 5 the surgeon
must employ low flow and vacuum parameters (e.g.
< 175-200 mmHg; < 26 ml/min). This strategy is
therefore less suitable if a surgeon wishes to use high
vacuum settings for denser nuclei. Wendell Scott has
Figs 39.2A and B: Pupil diameter in tamsulosin patient before
(A) and after (B) injection of 0.2 ml of intracameral epinephrine
solution (bisulfite-free 1:1000 mixed 1:3 with BSS)
Fig. 39.3: Healon 5 viscomydriasis in a patient with
IFIS following removal of the cortex
proposed injecting Healon 5 peripherally over the iris,
and then filling the central chamber with a dispersive
agent such as viscoat (Alcon) to create a Healon 5
donut. The viscoat will better resist aspiration and
delay the evacuation of Healon 5. For surgeons
252
the Milvella Perfect Pupil are disposable PMMA pupil
expansion rings whose grooved contours are threaded
alongside the pupillary margin using metal injectors
(Figs 39.4A to C). In contrast, a disposable plastic
injector is used to insert Eagle Visions Graether
disposable silicone pupil expansion ring. All of these
rings are more difficult to position if the pupil is less
than 4 mm wide or if the anterior chamber is shallow.
Iris retractors are a more popular mechanical
strategy for pupil expansion in IFIS. Placement of the
hooks in a diamond configuration has several significant
advantages
11
(Figs 39.5A and B). The subincisional
hook retracts the iris downward, and out of the path
of the phaco tip. This maximizes exposure in front of
the phaco tip while the nasal hook facilitates chopper
placement. One millimeter limbal paracenteses are
made in each quadrant, including a separate stab
incision made just posterior to the temporal clear corneal
incision. In this way, the subincisional hook and the
Figs 39.4A to C: Management of IFIS using a Morcher
PMMA pupil expansion ring. (A): Ring is inserted with an
injector. (B): Ring is threaded along pupil margin to maintain
a constant diameter. (C): Following removal of the ring, iris
prolapse and pupil constriction occur during removal of the
viscoelastic
favoring high vacuum and flow settings, DisCoVisc
(Alcon) has been advocated by Satish Modi.
A final set of strategies util izes devices to
mechanically expand and maintain the pupil diameter
during surgery. Both the Morcher 5S Pupil Ring and
Figs 39.5A and B: Management of IFIS using 4-0 prolene
iris retractors in a patient taking tamsulosin. (A): retractors
placed in a diamond configuration, with the sub-incisional
retractor placed directly behind the clear corneal phaco
incision. (B): Pupil constriction and iris prolapse occurring
after removal of the iris retractors
253
Managing Intraoperative Floppy Iris Syndrome
phaco tip access separate entry tracks. If the pupil is
fibrotic, overstretching it with iris retractors can cause
bleeding, sphincter tears, and permanent mydriasis.
This typically does not occur with the IFIS pupil, which
is so elastic that it readily springs back to physiologic
size despite being maximally stretched. Options include
6-0 nylon disposable retractors (Alcon) or reusable 4-
0 polypropylene retractors (Katena, FCI). Being of the
same size and rigidity as an IOL haptic, the latter are
easier to manipulate and can be repeatedly autoclaved
making them more cost effective to use.
It is much easier and safer to insert iris retractors
and pupil expansion rings prior to creation of the
capsulorhexis. If the pupil dilates very poorly or billows
during injection of intracameral lidocaine, one should
suspect severe IFIS and consider using these
mechanical devices. Often, the pupil dilates reasonably
wel l -preoperativel y, and it is not until after
hydrodissection or during phaco that the prolapse and
miosis occur. Healon 5 and intracameral epinephrine
are excellent rescue techniques in this situation where
it is difficult to visualize the capsulorhexis edge. If one
chooses to insert iris retractors at this point, one should
retract the pupil margin with a second instrument to
avoid hooking the capsulorhexis margin with the
retractors.
Eliciting a history of current or prior alpha-blocker
use should alert surgeons to anticipate IFIS and to
employ these alternative strategies either alone or in
combination. A prospective, multi-center prospective
trial using these techniques in 167 consecutive eyes
from patients on tamsulosin demonstrated excellent
outcomes and only a 0.6% posterior capsular rupture
rate.
2
Because of the variability in IFIS severity
associated with tamsulosin and other alpha-1 blockers,
surgeons may consider using a staged approach in
dealing with this condition.
8
Pharmacologic measures
alone are often adequate for managing the pupil in
mild to moderate IFIS cases. Even if they fail to expand
the pupil, intracameral alpha agonists can reduce or
prevent iris billowing and prolapse by increasing iris
dilator muscle tone. If the pupil diameter is still
inadequate, viscomydriasis with Healon 5 can further
expand it for performing the capsulorhexis. Finally,
mechanical expansion devices insure the most reliable
and optimal surgical exposure for severe IFIS, and
should be considered when other complicating risk
factors (e.g. dense nuclei, narrow angles, posterior
synechiae, weak zonules, pseudoexfoliation, etc.) are
present.
References
1. Chang DF, Campbell JR. Intraoperative floppy iris
syndrome associated with tamsulosin (Flomax). J Cataract
Refract Surg 2005;31:664-73.
2. Chang DF, Osher RH, Wang L, Koch DD. A prospective
multicenter evaluation of cataract surgery in patients
taking tamsulosin (Flomax). Ophthalmology 2007;114:
957-64.
3. Blouin M, Blouin J, Perreault S, et al. Intraoperative
fl oppy iris syndrome associated with Al pha-1
adrenoreceptors. Comparison of tamsul osin and
alfuzosin. J Cataract Refract Surg 2007;33:1227-34.
4. Chang DF. Chapter 10: Intraoperative floppy iris
syndrome. In Agarwal A, ed. Phaco Nightmares.
Conquering Cataract Catastrophies. Slack Publishing Inc.
2006.
5. Bendel RE, Phillips MB. Preoperative use of atropine to
prevent intraoperative floppy-iris syndrome in patients
taking tamsulosin. J Cataract Refract Surg 2006;
32:1603-5.
6. Masket S, Belani S. Combined preoperative topical
atropine sulphate 1% and intracameral nonpreserved
epinephrine hydrochloride 1:2500 for management of
intraoperative floppy iris syndrome. J Cataract Refract
Surg 2007;33:580-82.
7. Gurbaxani A, Packard R. Intracameral phenylephrine to
prevent floppy iris syndrome during cataract surgery in
patients on tamsulosin. Eye 2005: Nov 11; [Epub ahead
of print].
8. Manvikar S, Allen D. Cataract surgery management in
patients taking tamsulosin. J Cataract Refract Surg 2006;
32:1611-4.
9. Shugar, JK. Intracameral epinephrine for prophylaxis of
IFIS [letter]. J Cataract Refract Surg 2006; 32: 1074-5
10. Arshinoff SA. Modified SST-USST for tamsulosin-
associated intraocular floppy iris syndrome. J Cataract
Refract Surg 2006;32:559-61.
11. Oetting TA, Omphroy LC. Modified technique using
flexible iris retractors in clear corneal surgery. J Cataract
Refract Surg 2002;28:596-98.
C H A P T E R
40
Toxic Anterior Segment Syndrome
Simon P Holland, Douglas W Morck, Richard Mathias,
Tracy L Lee, Gina Chavez, Yumi G Ohashi (Canada)
Introduction
Toxic anterior segment syndrome (TASS) is increasingly
recognized and reported as an early complication of
cataract surgery.
1-9
Postoperative inflammation of
unknown cause was previously considered as a sterile
endophthalmitis although vitritis is uncommon. Multiple
outbreaks have recently been reported stimulating
extensive research and the creation of a task force.
The understanding of TASS is thus rapidly evolving
and will likely lead to improved prevention and
management of outbreaks.
Diagnosis and Clinical Features
TASS presents as early and severe postoperative
inflammation following anterior segment surgery.
Symptoms include fibrin formation, corneal edema,
minimal or no pain, and the absence of vitreous
involvement.
10
Differentiation from conditions such as
infectious endophthalmitis (IE) is critical. Table 40.1
summarizes the key differences between TASS and IE.
TASS usually presents on the day of surgery or the
first day postoperatively, whereas IE presents later,
usually day 3 to 7, accompanied by pain and vitreal
involvement.
10-13
Figure 40.1 shows a case of TASS
with characteristic features presenting on the day of
surgery, and Figure 40.2 shows a case of IE. Rarely
low grade vitritis may be seen in severe cases of TASS
probably from some spillover from the anterior
segment. In such cases the vitritis is a result of culture-
negative or sterile endophthalmitis rather than
infectious endophthalmitis.
10,11
Vitreous taps and more
recently PCR can be used to differentiate the two
conditions.
14
When the diagnosis is unclear the practi-
tioner should treat as IE due to the severity of its
sequelae.
15,16
DIAGNOSIS
Postoperative
Anterior segment inflammation
Unknown cause.
DIFFERENTIAL DIAGNOSIS
Pain and/or vitritis usually indicates infectious
endophthalmitis.
TABLE 40.1: Differential diagnosis TASS vs infectious endophthalmitis
Presentation TASS Infectious endophthalmitis
Onset (usual) 6 to 24 hours 3 to 7 days
postoperatively postoperatively
Symptoms Blurred vision Pain, blurred vision
Cornea Edema Edema
Anterior chamber Cells Cells
Fibrin, membranes Fibrin variable
Hypopyon Hypopyon
External findings None Variable: Lid swelling
Discharge Conjunctival
chemosis
Vitreous Clear, rarely vitritis Vitritis (primarily
Response to topical (culture negative) culture positive)
steroids Rapid improvement to No improvement
resolution within days
255
Fibrin/membranes
Corneal edema
No or minimal pain.
Pathology
Changes to the pH and osmolality or the inadvertent
introduction of an antigen can initiate a cellular
response. The histological examinations of corneal
buttons taken from patients with TASS showed an
almost absent endothelial cell layer, with the epithelium
thinned and the stroma diffusely thickened.
8
The
massive damage to the endothelial layer is a result of
its sensitivity to toxic agents.
11
Epidemiology and Etiology
The epidemic in the United States prompted the
American Society of Cataract and Refractive Surgery
(ASCRS) to assemble a special task force to deal with
the growing problem.
19
The task force reported that
over 100 centers experienced an outbreak of TASS
prior to May 2006 and this only included clinics that
chose to self report.
20
Many outbreaks may be
unreported given the potential for poor publicity, and
regulatory and liability issues. The increasing incidence
of TASS is likely due to an actual rise in numbers rather
than simply an increased awareness. Growing interest
in TASS is resulting in the rapid expansion of knowledge
regarding the cause and therefore the management
and prevention of the condition.
The etiology of TASS is speculative, although there
is increasing acceptance of its multifactorial causation.
The ASCRS task force, and several other researchers
have complied a list of possible risk factors and potential
causes of TASS.
3,5-8,20-23
These potential etiology factors
are listed in Table 40.2.
10
It is likely that individual
TASS cases not occurring in an outbreak are due to
complications during surgery such as iris stretching,
retained cortex and a prolonged surgery.
10
Multiple
factors have been associated with TASS outbreaks
ranging from inappropriate chemical composition of
irrigating solutions to the presence of endotoxins on
poorly sterilized instruments.
13
INTRAOCULAR MEDICATIONS, IRRIGATING
SOLUTIONS AND BALANCED SALT SOLUTION
Many TASS outbreaks have been attributed to
contaminants, endotoxins and preservatives gaining
access to the anterior chamber during or following
surgery.
5,7,12
Outbreaks have been linked to external
eye rinses, such as Eye Stream (Alcon, Ft. Worth, Texas)
due to the preservative content.
5
Ointments applied
Fig. 40.1: TASS on the first postoperative day
(Courtesy: SLACK Inc)
10
Fig. 40.2: Early endophthalmitis presenting on the day
of surgery (Courtesy: SLACK Inc)
10
Toxic Endothelial Cell Destruction Syndrome
(TECDS) is a related syndrome that specifically
indicates localized corneal endothelial damage and is
considered to be within the continuum of TASS.
2,5,7,17
The clinical features of TASS have been well
described in previous literature.
1,2,5,7,10,11
Most patients
are asymptomatic but may have blurred vision and
redness within 24 hours of surgery . Pain is almost
never a feature al though there may be mil d
discomfort. Characteristic clinical features include a
severe anterior chamber cellular response with fibrin,
membrane formation and the occasional hypopyon.
Corneal edema, described as limbus to limbus, is
frequently present.
10,11,18
When patients present
predominantly with corneal edema and less marked
anterior chamber inflammation the cause is more likely
to be toxic agents (e.g. preservatives, ointments).
FEATURES
Within 48 hours
Cellular reaction 2-4+
256
postoperatively also have the potential to gain access
to the anterior chamber. One study described a TASS
outbreak following the application of postoperative
ointments and tight eye patching.
8
The use of
contaminated balanced salt solution (BSS) has also
been associated with TASS outbreaks. Endotoxin was
discovered in balanced salt solution (BSS) manufac-
tured by Cytosol Laboratories (Lenoir, NC).
10,24
INSTRUMENT CONTAMINATION
Detergent residues left on reusable instruments have
the potential to cause corneal toxicity.
2,21
Prolonged
cycle sterilization is needed to deactivate enzymes and
other active ingredients in detergents.
11
TASS outbreaks
have been associated with the dried residue on reusable
cannulas.
10
Impurities can also be present in sterilizer steam.
9,22
An outbreak of TASS was associated with inadequate
maintenance of steam sterilizer systems with resulting
copper, zinc, nickel, sulfate and silica impurities.
9
Instruments can also become contaminated with
endotoxin following short cycle steam sterilization.
25
The sterilization process kills bacteria but does not
inactivate endotoxin, which can be a potent initiator
of an inflammatory immune response and has been
associated with TASS outbreaks.
10,11,22,26
Ultrasound baths may also be a source of contami-
nation. Klebsiella pneumonia and bacterial endotoxin
were identified in the ultrasonic cleaning bath during
one TASS outbreak.
3
TASS is often associated with IOL implantation, but
more recently has also been observed following
placement of phakic IOL.
18
It is important to consider
IOL polishing compounds, as well as the chemical
structure of the lens as possible causes of TASS.
6,23
Etiology
Edematoxic, e.g. preservatives
Inflammationendotoxin.
Causation
Sterilization issues most common
Beware of re-usable cannulas.
Treatment
Conventional treatment is focused on the suppression
of the inflammatory immune response and includes
topical steroids given every half hour to hour for the
first three days followed by gradual tapering.
10
During
this acute period the patient should be monitored
closely for anterior segment inflammation, corneal
edema, and intraocular pressure (IOP). In particular
monitor for an IOP increase several days following the
initial presentation due to damage to the trabecular
meshwork.
11
Improvements are generally seen within
the first 24 to 48 hours of steroid commencement.
Anterior chamber washout has been reported but
outcomes are uncertain and it is not generally recom-
mended.
10,11
When there is corneal and endothelial
toxicity a penetrating keratoplasty may be necessary.
Points
Rapid response to frequent steroid drops.
Outcomes
Early diagnosis and treatment usually result in an
excellent outcome. Most mild cases clear within several
days to weeks.
21
Glaucoma is a potential complication
due to either initial trabeculitis or fibrin membrane
formation.
10
Severe TASS can result in permanent
endothelial damage, cystoid macular edema and
permanently dilated pupil requiring corrective
surgery.
21
COMPLICATIONS
Misdiagnosis
Glaucoma
Corneal edema
Cystoid macular edema.
Investigation and Reporting
Outbreak investigation is difficult with the multifactorial
etiol ogy al though steril ization issues usual l y
predominate. Consequences to an affected clinic
may be severe with voluntary or mandated closure.
TABLE 40.2: Potential etiology factors associated
with TASS (previously published: SLACK Inc).
10
Intraocular causes
Incomplete cortex removal, pupil stretching, and possible
immunological differences (as with DLK in atopic
patients).
Intraocular medication
Dosing errors with antibiotics, preservatives, ointments
8
,
and pH imbalance.
Instrument contamination
Bacterial endotoxins, dried debris, e.g. inadequate
cleaning of cannulas, persistence of detergents, irrigating
solutions, endotoxins in irrigating fluids (Endosol),
10,24
incorrect pH or composition of irrigating fluids.
257
Proactive reporting to local regulatory authorities and
seeking support from colleagues, as well as academic
and public health resources is advisable.
10,27
CASE AND OUTBREAK DEFINITION
Postoperative anterior segment inflammation of
unknown cause occurring within 48 hours of surgery
with one or more of the following features: anterior
chamber response 2+ or greater, fibrin, membranes,
corneal edema without significant vitritis.
10
Criteria for
a TASS outbreak have not been established as they
have for conditions such as DLK.
28
However, any
occurrence of more than two affected patients should
raise concerns and merit investigation since this may
rapidly escalate.
DATA COLLECTION
Suggested data include; demographics, VA before and
after surgery, symptoms, clinical features, day of
surgery, day of onset and diagnosis, any associated
conditions, subsequent management and outcome. It
is important to record details of the surgical procedure
including instrument preparation and specifically any
staffing or procedural changes made prior to the onset.
Retrospective collection of data is difficult and it is
recommended to collect data and note changes as they
happen making the creation of an epidemic curve less
problematic.
MICROBIAL INVESTIGATIONS
Bacterial culturing, biofilm sampling and analysis of
steam distillate and BSS for endotoxin may help
determine the cause of the outbreak. The sterilizer
reservoir, internal tubing of the sterilizer, ultrasound
baths, cannulas and air and water supplies have proved
to be useful sampling areas.
10,12,13
TASS investigations are often difficult and require
careful planning. It is usually best to designate one
staff member to manage the outbreak, including data
collection and media consultation. Another important
issue to consider is the disclosure of TASS as a further
risk of cataract surgery, particularly during a TASS
outbreak.
Once an investigation has been concluded dissemi-
nation of the findings will help other practitioners solve
their TASS outbreaks or hopefully avoid them. The
TASS task force is one example of how this sharing
of knowledge has likely reduced the risk of further
outbreaks.
INVESTIGATION
Suspect everything.
Conclusion
TASS outbreaks have become of major concern in
the ophthalmology community. The assembly of the
TASS task force and the numerous recent studies on
the subject has assisted in controlling TASS outbreaks.
The final task force report concluded that there was
no one factor attributable to TASS outbreaks but rather
multiple potential etiological factors. It appeared that
cleaning and sterilization of instruments for cataract
surgery was the most important of the identified factors.
It is recommended that all reusable cannulas and
instruments be thoroughly flushed with sterile,
deionized/distilled water after cleaning at the conclusion
of each case.
29
Although TASS outbreak reports, at least in the
United States, now appear to be declining it is
important to constantly monitor and improve cleaning
and sterilization protocols. Growing awareness resulting
in early diagnosis and treatment, with prompt
dissemination of new information will hopefully
eliminate TASS as a significant complication of modern
cataract surgery.
References
1. Monson MC, Mamalis N, Olson RJ. Toxic anterior
segment inflammation following cataract surgery. J
2. Breebaart AC, Nuyts RMMA, Pels E, et al. Toxic
endothelial destruction of the cornea after routine
extracapsular cataract surgery. Arch Ophthalmol 1990;
108:1121-5.
3. Kreisler KR, Martin SS, Young CW, et al. Postoperative
inflammation following cataract extraction caused by
bacterial contamination of the cleaning bath detergent.
4. Nel son DB, Donnenfel d ED, Perry HD. Steril e
endophthalmitis after sutureless cataract surgery.
Ophthalmolgy 1992; 99:1655-7.
5. Liu H, Routley I, Teichmann KD. Toxic endothelial cell
destruction from intraocular benzalkonium chloride. J
Cataract Refract Surg 2001; 27:1746-50.
6. Jehan FS, Mamalis N, Spencer TS, et al. Postoperative
sterile endophthalmitis (TASS) with the MemoryLens. J
Cataract Refract Surg 2000; 26:1773-7.
7. Eleftheriadis H, Cheong M, Saneman S, et al. Corneal
toxicity secondary to inadvertent use of benzalkonium
chloride preserved viscoelastic material in cataract
surgery. Br J Ophthalmol 2002; 86:299-305.
8. Werner L, Sher JH, Taylor JR, et al. Toxic anterior
segment syndrome and possible association with
ointment in the anterior chamber following cataract
surgery. J Cataract Refract Surg 2006; 32:227-35.
9. Hellinger WC, Hasan SA, Bacalis LP, et al. Outbreak of
toxic anterior chamber syndrome following cataract
surgery associated with impurities of autoclave steam
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moisture. Infect Control Hosp Epidemiol 2006;
27(13):294-8.
10. Holland SP, Morck DW, Chavez G, Lee, TL. Toxic anterior
segment syndrome. In Agarwal A (Ed). Refractive Surgery
Nightmares: Conquering Refractive Surgery Catastrophes.
Thorofare, NJ: SLACK Incorporated. In press.
11. Mamalis N, Edelhauser HF, Dawson DG, et al. Toxic
anterior segment syndrome. Review/update. J Cataract
Refract Surg 2006; 32:324-33.
12. Holland SP, Chavex G, Morck D, Mathias. Toxic Anterior
Segment Syndrome After Cataract Surgery Associated
with Short-Cycle Sterilization presented at the ASCRS
Symposium on Cataract, IOL and Refractive Surgery, San
Francisco, USA , March 17-22, 2006. Available at
www.ascrs.org. Accessed June 12, 2006.
13. Holland SP, Morck D, Lee T. Update on toxic anterior
segment syndrome. Current Opinion in Ophthalmology.
In press.
14. Van Gelder RN. Applications of the polymerase chain
reaction to diagnosis of ophthalmic disease. Surv
Ophthalmol 2001; 45(3):248-58.
15. West ES, Behrens A, McDonnell PJ, et al. The incidence
of endophthalmitis after cataract surgery among the US
medicare population increased between 1994 and 2001.
Ophthalmology 2005; 112:1388-95.
16. Wallin T, Parker J, Jin Y, et al. Cohort study of 27 cases
of endophthalmitis at a single institution. J Cataract
Refract Surg 2005; 31:735-41.
17. Duffy RE, Brown SE, Caldwell KL, et al. An epidemic of
corneal destruction caused by plasma gas sterilization;
the toxic endothelial cell destruction syndrome team.
Arch Ophthalmology 2000;118:1167-76.
18. Moshirfar M, Whitehead G, Beutler BC, et al. Toxic
anterior segment syndrome after Verisyse iris-supported
phakic intraocular lens implantation. J Cataract Refract
Surg 2006; 32(7):1233-7.
19. The American Society of Cataract and Refractive Surgery
(ASCRS) (2005). Press release June 22, 2006: TASS task
force. Retrieved August 15, 2006, from http://
www.ascrs.org/press_releases/Toxic-Anterior-Segment-
Syndrome-Outbreak-Preliminary-Report.cfm.
(ASCRS) (2005). Press release May 22, 2006: TASS
Outbreak Update. Retrieved June 1, 2006, from http:/
/ www. as cr s . or g/ pres s _rel eas es / upl oad/ Updat e
Briefing.doc.
21. Parikh C, Sippy BD, Martin DF, Edelhauser HF. Effects
of enzymatic sterilization detergents on the corneal
endothelium. Arch Ophthalmol 2002; 120:165-72.
22. Whitby JL, Hitchins VM. Endotoxin levels in steam and
reservoirs of table-top steam sterilzers. J Cataract Refract
Surg 2002; 18:51-2.
23. Meltzer, DW. Sterile hypopyon following intraocular lens
surgery. Arch Ophthalmol 1980; 98:100-4.
24. US Food and Drug Administration. (2006). Patient
advisory Feb 13th 2006; FDA-Requested Recall - Cytosol
Laboratories, Inc. Product Contains Dangerous Levels of
Endotoxin. Retrieved Feb. 14, 2006, from http://
www.fda.gov/bbs/topics/news/2006/NEW01315.html.
25. Holland SP, Mathias RG, Morck DW, et al. Diffuse
lamellar keratitis related to endotoxins released from
sterilizer reservoir biofilms. Ophthalmol 2000; 107(7):
1227-33.
26. Rietschel ET, Brade H. Bacterial endotoxins. Sci Am 1992;
267:54-61.
27. Mamalis, N. TASS outbreaks: What should we do?
Cataract and Refractive Surgery Today, July 2006;53-5.
28. Bigham M, Enns CL, Holland SP, et al. Diffuse lamellar
keratitis complicating laser in situ keratomileusis;
postmarketing surveillance of an emerging disease in
British Columbia, Canada, 2000-2002. J Cataract Refract
Surg 2005; 31:2340-44.
(ASCRS). (2005). Press release September 22, 2006:
Toxic Anterior Segment Syndrome (TASS) Outbreak Final
Report. Retrieved September 22, 2006, from http://
www.ascrs.org/press_releases/Final-TASS-Report.cfm.
C H A P T E R
41
Small Pupil Phaco:
An Innovative Technique
Boris Malyugin (Russia)
Introduction
In spite of several recent innovations in cataract surgery
patients with small pupils are always challenging.
Poor pupil dilation we can be observed in cases
complicated by pseudoexfoliation syndrome, uveitis,
posterior synechiae, trauma or previous intraocular
surgery.
1-6
Significant amount of patients who present for
phacoemulsification cataract surgery have pupils that
do not respond adequatel y despite several
pharmacological attempts with different mydriatic
agents. Inadequate pupil dilation can decrease
visualization during all stages of the phacoemulsification
including capsulorhexis, hydrodissection, lens nucleus
disassembly and IOL insertion. This compromises the
surgery and increases the risk for complications.
Pharmacological therapy with the use of nonsteroi-
dal eyedrops or strong mydriatics such as phenylephrine
10% sometimes lead to unwanted ocular and systemic
side effects. Intracameral mydriatics is an effective, and
safe addition to topical mydriatics in phacoemulsifica-
tion.
7
In some cases their use can simplify preoperative
patients preparation and in certain high-risk groups,
may reduce the risk for cardiovascular side effects.
Unfortunately present pharmacological approaches
of managing a small pupil during cataract surgery have
limitations. Most surgeons decide to dilate the pupil
mechanically at the time of the surgery if pharmaco-
logical agents fail.
There is no general recommendation or solution
to the small pupil problem because the strategies for
pupil enlargement greatly depend on surgeon skill and
preferences, as well as on intraoperative situation.
There are four main dilation methods: the first is the
synechiolysis, the second is mechanical stretching, the
third is the cutting method and the fourth is the iris
retraction.
In the first methodthe surgeon separates the
adhesions between the iris, the lens capsule and/or
the cornea. The technique of pupillary membranec-
tomy with the forceps presented by R.Osher
6
is also
effective in some cases.
The second methodmechanical stretching of the
pupil was introduced by Miller and Keener.
8
It is usually
effective for small pupils with the rigid iris tissue which
is usually caused by prior miotic use, pseudoexfoliation,
or posterior synechiae. Stretching can be achieved with
the spatula, Sinskey hook or special instrument. Beehler
pupil dilator.
2
Usually a pair of hooks is introduced
through 2 stab incisions in the cornea engage the iris
sphincter. After that the hooks are pulled in opposite
directions. This maneuver creates microscopic sphincter
tears which enlarge the pupil aperture. The main
advantage of this procedure is that it is relatively simple
and requires no special instruments. Mechanical
stretching of the pupil usually provides sufficient access
to the l ens and maintains the pupil diameter
intraoperatively.
Sometimes iris stretching technique leads to instabi-
lity of its papillary margin, which can compromise
cataract surgery. In some eyes and stretching technique
fails to adequately expand the pupil.
9
The drawback
of this technique is that it is creating permanent damage
of the iris sphincter. The micro tears of the sphincter
muscle are usually clinically asymptomatic but
sometimes result in bleeding and pigment dispersion
postoperatively. In a study of stretch pupilloplasty by
Dinsmore
10
10% of 50 patients developed an enlarged
atonic pupil postoperatively. All patients had a history
of injury or inflammatory disease.
Partial-thickness iris sphincter cuts made with micro
scissors is a common pupil enlargement technique.
11
The cutting method is more controlled but requires
multiple maneuvers of the scissors inside the anterior
chamber which can result in corneal endothelial
damage. The disadvantages are the same as those with
the stretching method.
Suboptimal pupil dilation in response to the
preoperative mydriatic protocols and minimal efficacy
260
of pupil stretching techniques is a usual indication to
the intraoperative use of iris hooks or other mechanical
pupil dilation devices. For the iris retraction several
devices have been introduced in the clinical practice.
The main disadvantages of these devices include the
bulkiness and rigidity. They are difficult to insert,
remove, and manipulate through a small incision.
Graether
12
developed a pupil expander that
according to his data is superior to other methods of
pupil enlargement, causing less sphincter trauma and
fewer cases of permanent pupil size alteration. Pupil
dilation technique with the hydrogel ring reported by
Siepser
6
has a potential benefits but very limited clinical
use. The Perfect Pupil device (Milvella) is a disposable
polyurethane ring with the 0.24 mm flanged groove
throughout the length of the ring and an integrated
arm that allows insertion and removal from the anterior
chamber at the end of surgery.
11
Retracting the iris tissue rather than cutting it as
in a classic sector iridectomy is much simpler and results
in a much better postoperative pupil appearance.
Mackool
13
was the first one who described a 4-point
iris retractor configuration for phacoemulsification. He
developed metal iris retractors connected to small
blocks of titanium. The latter allows for stabilization
of the hooks during the retraction of the iris. This
method was enhanced with the introduction of the
flexible iris retractor by de Juan and Hickingbotham.
14
Traditionally, 4 evenly spaced retractors are placed
through limbal paracentheses 90 degrees apart from
one another. The corneal incision is centered on 1 of
the 4 sides of the square.
15
Some surgeons use iris
retractors in a triangular pattern decreasing the number
of additional corneal incisions. The use of the iris hooks
may lead to the damage of the pupillary margin
intraoperatively producing a semimydriatic non-
reacting pupil postoperatively.
Modification of the original square retractor
configuration is described by
16
the rotation of the square
improves lens access in clear corneal phacoemulsification
by orienting the phacoemulsification needle along the
diagonal. This was called by Dupps and Oetting
diamond configuration of retractors.
17
Advantages
of this technique include ease of conversion from
phacoemulsification, optimal orientation of the maxi-
mum pupil diameter nucleus expression or intracapsular
lens removal, and conservation of iris tissue.
Birhall
18
assessed the effect on pupil shape and
circumference of various flexible iris hook positions.
He confirmed that malpositioned iris hooks may
increase pupil stretching with possible deleterious effects
on postoperative pupil function. He recommends
using additional fifth hook to create a pentagonal pupil
that reduces pupil stretching by 17%.
Masket
19
and Yuguchi and coauthors
20
recommends
the pupil not be stretched by the hooks to larger than
a 5.0 mm square because overstretching produces
irregular atonic pupils postoperatively. Novak
21
suggests
the use of hooks with rigid pupils smaller than 3.0 mm
(4.0 mm with a hard nucleus) and smaller than 4.0
to 5.0 mm for an inexperienced surgeon. In extremely
small and rigid pupils he prefers combining the use
of hooks with a radial sphincterotomy.
During engagement of the pupillary edge with the
iris hook, it may catch and damage the capsule, leading
to an anterior capsule tear that may extend to the
periphery. To avoid this problem, a drop of viscoelastic
material should be injected between the iris and the
capsule before the hook is inserted. The other useful
technique is to keep the hook parallel to the iris plane
during the insertion and to tilt it slightly posterior right
near the pupillary edge to engage the iris only. The
iris hooks may become loosened during surgery. Their
tips may become dislocated, no longer holding the
pupillary edge. This can cause some problems including
iris aspiration and chafing from contact with the
phacoemulsification needle.
Small degrees of pupil dysfunction are common
place after cataract surgery with and without iris mani-
pulation but usually this causes no subjective
symptoms. Halpern and coauthors
22
found an
incidence of postoperative atonic pupil of 1.1% after
phacoemulsification, with pupil diameters ranging from
6.0 to 8.0 mm.
Most of the surgical maneuvers for enlarging the
pupil and preventing its intraoperative constriction are
not safe enough. They can lead to an increased risk
of iris sphincter tear, bleeding, iris damage, posterior
capsule tears, and loss of the vitreous body. The
postoperative complications can include an atonic pupil
of irregular shape with poor cosmetic result, and
photophobia.
The rate of occurrence of iris prolapse has been
reported between 0.3% and 1% in complicated cataract
cases.
23
Allan
24
described one of the critical factors of
iris prolapse during phaco which relates to fluid velocity.
Allans model considers the Bernoulli principle as the
most important because when the velocity of fluid
passing through the anterior chamber increases, the
force exerted on the iris increases by the square of
the velocity.
We calculated the speed of the emulsion in the
anterior chamber during the phaco procedure with the
Millenium CCS (Bausch and Lomb) for US handpiece
settings: 1.0 mm Microflow US needle, vacuum 300 mm
Hg, bottle height 85 cm, and I/A handpiece settings:
coaxial handpiece, 0.3 mm opening, vacuum 550 mm
Hg, bottle height 90 cm. For the calculation we utilized
261
Small Pupil Phaco: An Innovative Technique
Fig. 41.1: Fluid velocity distribution along the line connecting the opposite points of the anterior
chamber angle (X1X2) in case when the US handpiece location in the middle of the anterior
chamber at the iris plane
Fig. 41.2: Fluid velocity distribution along the line connecting the opposite points of the anterior
chamber angle (X1X2) in case when the US handpiece is location in the middle of the lens
nucleus
the equation of Navie-Stocks. The calculations were
performed for the two positions of the handpiece: in the
center of the anterior chamber at the iris plane
(Fig. 41.1) in the middl e of the capsul ar bag
(Fig. 41.2) and close to the center of the posterior
capsule (Fig. 41.3).
Figures 41.4 and 41.5 represent the color coded
map of fluid velocity distribution around the US and
irrigating-aspirating handpiece. The areas of the highest
currents are located in the angle of 40 to 60 degrees
with the apex at the end of the aspiration orifice. Three
zones of high (more than 120 cm/sec) medium (80-
120 cm/sec) and low (80 cm/sec) fluid velocities are
represented.
The pupil often dilates poorly in atrophic irises, with
significantly decreased iris tone unable to withstand
the fluidic currents in the anterior chamber and
maintain the correct position of the iris. These
calculations give us some conclusions. In small pupil
iris tissue is located closer to the zone of the high fluidic
currents that is why it is more likely to be aspirated
into the US or IA handpiece. Decreasing of flow
262
Fig. 41.3: Fluid velocity distribution along the line connecting the opposite points of the
anterior chamber angle (X1X2) in case of US handpiece location close to the center
of the posterior capsule
Fig. 41.4: Fluid velocity distribution around the
handpiece tip of the US
Fig. 41.5: Fluid velocity distribution around the tip of
irrigating-aspirating handpiece
parameters is an important factor of preventing iris
damage during phacoemulsification. Not only reducing
the flow can make an appreciable difference in these
cases, but also central positioning and minimal
movements of the handpiece are also important to
prevent iris damage. Endocapsular lens nucleus
fragmentation is much safer because the areas of the
highest fluidics currents are located inside the capsular
bag away from the corneal endothelium and iris.
Chang and Campbell
25
recently described the
intraoperative floppy-iris syndrome (IFIS) associated
with systemic administration of the -1A antagonist
tamsulosin (Flomax). The intraoperative diagnostic
triad of this symptom is fluttering and billowing of the
iris stroma, a tendency to iris prolapse through the
main and/or side-port incisions, and progressive
constriction of the pupil during surgery. Stretching of
the pupil is ineffective in IFIS because the iris pupil
margin remains elastic and the pupil immediately
snaps back to its original size following attempts at
stretching it.
Viscomydriasis with high viscosity OVDs such as
Healon5 are very useful in small pupil phaco cases.
S.Arshinoff
26
described a technique using ophthalmic
263
viscosurgical devices to perform cataract surgery in
patients taking tamsulosin. This method uses a
combination of the two OVDs. The lower-viscosity
dispersive OVD which is highly retentive despite the
presence of moderate fluid turbulence is injected in
the periphery of the anterior chamber and covers the
endothelial layer and the iris. The viscoadaptive central
layer of Healon5, according to S.Arshinoff adds a
relatively rigid OVD roof above the surgical space and
adds rigidity to the OVD structure to keep the iris from
moving and the Viscoat in place. The BSS layer just
over the pupillary space and below viscoadaptive central
layer provides working space for the phaco tip. The
surgeon is working in the endocapsular space and
Healon5 is not attracted into the phaco tip and the
OVD shell structure remains intact throughout the case.
This technique gives satisfactory iris stability and permits
uneventful surgery.
Cataract surgery in cases of iridoschisis may result
in aspiration of iris fibers flowing in the anterior
chamber.
5, 11
In these cases stretching the iris with various
instruments or dilating the pupil with iris retractors may
not prevent the danger contact of US needle with the
iris tissue and aspiration of fibers.
Intaoperative iris manipulations may lead to severe
postoperative fibrinoid reaction especially in eyes with
pseudoexfoliation syndrome, chronic uveitis, glaucoma
or diabetes. Tat is why cataract surgery in the presence
of a small pupil remains one of the most difficult and
challenging cases.
IQ-ring
To enhance phaco surgery in complicated small-pupil
cases we designed the new device which was called
IQ-ring (Fig. 41.6). It is used in cases of pupil miosis
refractory to dilation protocols. The device is a square,
O-shaped, temporary implant with four circular curls
that holds the iris at equidistant points. One-piece
design with the curls at each angle of the ring provides
balanced stretching and gentle holding of the iris tissue.
The main principle of iris pupillary margin fixation with
the curl is represented on Figure 41.7.
The insertion of IQ-ring is carried out through the
main incision. The pupil expander is positioned
centrally and gently pushed at each angle with the
help of a Sinskey hook to trap the iris in the four curls.
Once in place, the ring expands the pupillary opening
to 6.0 mm. The IQ-ring provides stable mydriasis with
no trauma to the iris tissue and no need for additional
paracentheses. It retracts the iris away from the flow
currents and thus helps to prevent its incarceration
into the US and I/A handpieces. As the result of the
IQ-ring implantation we obtain a square, 6 mm pupil
dilation that allows for safe and comfortable maneuvers
during phacoemulsification.
The ring is usually inserted at the beginning of the
phaco procedure through an unenlarged 2.8 mm clear
corneal incision into the pupillary aperture. The
surgeon can control the iris without significant changes
of his accustomed technique. The capsulorhexis,
hydrodissection, phacoemulsification, and injection of
the intraocular lens are performed through the
expanded pupil with the device in place. In case of
necessity the ring can be inserted at any stage of the
operation.
Cadaver eye study using scanning electronic micro-
scopy showed that much less damage to the pigmented
iris tissue was caused by the new instrument than by
conventional iris retractors (Figs 41.8 and 41.9).
Surgical Technique
Topical anesthesia is applied using 2% lidocain, and
the paracenthesis is done at 12 oclock. A 2.8 mm
temporal clear corneal incision is performed using the
disposable metal blade. A dispersive ophthalmic
viscosurgical device (OVD) is injected in the anterior
chamber to stabilize it and protect the corneal
endothelium. The IQ-ring is introduced into the AC
through the clear corneal phacoincision using forceps
and Sinskey hook (Fig. 41.10). The device is placed
in the AC and laid flat on the iris. It is then attached Fig. 41.6: The general view of IQ-ring
Fig. 41.7: The principle of iris pupillary margin fixation
with the curl of IQ-ring
264
Fig. 41.8: IQ-ring implantation in the cadaver eye
Fig. 41.9: Scanning electronic microscopy of the pupillary
margin of the cadaver eye after implantation of the IQ-ring
and conventional iris hooks
Fig. 41.10: IQ-ring is inserted through the main clear
corneal incision
Fig. 41.11: The iris is fixated in the loops of the device
Fig. 41.12: Phacoemulsification of the nucleus with the
IQ-ring in place
to the pupillary margin in a circular manner, resulting
in a pupillary opening approximately 6.0 mm wide
(Fig. 41.11). Capsulorhexis is performed using forceps
or a bent needle.
Hydrodissection and hydrodel ineation are
performed with BSS until the nucleus could be rotated
freely inside the capsular bag. Phacoemulsification is
done with the Millenium CCS phacoemulsifier (Bausch
and Lomb) using a modified quick-chop technique
(Microflow or Kelman US needle; 36% of linear US
power; pulse 10 pps, duty cycle 80%; vacuum settings
at 350 mm Hg; bottle height 85 cm). A deep but short
central trench is made in cases of the hard nucleus
cases. The step-by-step chop in situ and lateral
separation technique allows nucleus division with
minimal stress on the capsular bag (Fig. 41.12).
Coaxial or bimanual irrigation/aspiration is used to
clean residual cortical fibers from the capsular bag
(Fig. 41.13). The capsular bag is then filled with the
cohesive OVD and foldable intraocular lens (IOL) is
inserted using injector through unenlarged incision.
Forceps flexible IOL insertion usually requires incision
enlargement from 3.5 to 3.75 mm.
Then the device is loosened from the pupillary margin
using a Sinskey hook and laid on the iris (Fig. 41.12).
265
Fig. 41.13: Irrigation-aspiration after IOL implantation
and removal of the device
Fig. 41.14: The ring is cut with the Vannas scissors
Fig. 41.15: The ring is removed from the anterior chamber
through the clear corneal incision with the forceps
Fig. 41.16: Final situation after surgery
The ring is cut with the Vannas scissors and retracted from
the anterior chamber through the clear corneal incision
with the forceps (Figs 41.14 and 41.15). Aspiration
is performed to remove the residual OVD. After
viscoelastic removal, the clear corneal incision is hydrated
with balanced salt solution (BSS) (Fig. 41.16).
On the first postoperative day, the eyes presented
with minor cell and flare in the anterior chamber. The
pupillary margin was minimally disturbed or undama-
ged and the IOL well centered. We usually treat patients
with small pupils after the surgery more aggressively than
uncompl icated patients with topical steroids,
cycloplegics, and sometimes systemic steroids Patients
receive local antibiotic and steroid treatment for 4-6
weeks.
Conclusion
Adequate transpupillary access to the lens is essential
to the success of phaco procedures especially in cases
with zonular weakness and capsular inadequacy. We
believe that our iris retraction technique with IQ-ring
has several advantages.
First, the IQ-ring does not require additional inci-
sions. This instrument is inserted through main incision,
thus reducing surgical trauma and minimizing the risk
of contamination and postoperative inflammatory
reaction.
Second, the device is applying pressure to the
sphincter muscle over an area which is wider than in
cases of iris hooks. It is particularly useful in patients
in which cutting or tearing of the iris tissue should be
avoided. Especially in the presence of rubeosis, chronic
anterior uveitis, or systemic coagulopathy. Iris rim is
safely fixed in the loops of the ring and there is no
risk of iris aspiration during phacoemulsification.
Third, compared to other long-in-use iris retractors
IQ-ring has the advantage of being friendlier with the
eye, due to the well-distributed stretching and gentle
holding of the delicate iris tissue, and to the easier and
266
less traumatic implantation. It has no sharp or pointed
endings that can damage the eye.
Fourth, equidistant position of the loops that holds
the iris tissue ensure correct position of the iris and
prevents the effect of overstretching of the pupil
observed in incorrect iris hooks position.
Fifth, IQ-ring provides sufficient room for nucleus
fragmentation and removal. The device configuration
and plate design allows surgeon to work in the deep
lens layers below the iris plane and the square-shaped
pupil formed by the ring. This provides enough space
for grooving and cutting the nucleus and increased
peripheral visualization during the chopping phase of
the procedure.
In summary, different techniques of nucleus
disassembly in small-incision cataract surgery requires
wide and unobstructed view of the anterior portion of
the lens as well as the instruments inserted in the anterior
chamber. The other important factor is sufficient
manipulability of the instruments which is critical for the
successful completion the surgery. A pupil that fails to
dilate makes cataract removal more difficult with added
risk. The IQ-ring adequately dilates the pupil, prevents
iris sphincter damage. It is easy to insert and remove.
The ring expands the pupil to 6.0 mm, protects the iris
sphincter during surgery, and allows the pupil to return
to its normal shape, size, and function after the operation.
IQ-ring is an important tool in phacoemulsification
surgery. Careful intraoperative manipulation and inser-
tion of the IQ-ring with liberal use of OVD can help
prevent complications. After the surgery most of our
patients had pupils almost indistinguishable from the
appearance before surgery with the preserved func-
tional activity. We consider IQ-ring among the most
effective methods to increase the size of even very rigid
small pupils during phacoemulsification surgery. We use
it in cases with IFIS syndrome with a great success. The
use of this method is highly recommended as it is likely
to reduce postoperative abnormalities in pupil size and
function.
References
1. Drolsum L, Haaskjold E, Davanger M. Results and
complications after extracapsular cataract extraction in eyes
with pseudoexfoliation syndrome. Acta Ophthalmol
(Copenh) 1993; 71:77176.
2. Fine IH. Pupilloplasty for small pupil phacoemulsification.
J Cataract Refract Surg 1994; 20:19296.
3. Gimbel HV. Nucleofractis phacoemulsification through a
small pupil. Can J Ophthalmol 1992; 27:11519.
4. Kershner RM. Management of the small pupil for clear
corneal cataract surgery. J Cataract Refract Surg 2002;
28:182631.
5. Smith GT, Liu CSC. Flexible iris hooks for phacoemulsi-
fication in patients with iridoschisis. J Cataract Refract Surg
2000; 26:127780.
6. Vasavada A, Singh R. Phacoemulsification in eyes with a
small pupil. J Cataract Refract Surg 2000; 26:121018.
7. Lundberg B, Behndig A Intracameral mydriatics in
phacoemulsification cataract surgery J Cataract Refract Surg
2003; 29:236671.
8. Miller KM, Keener GT Jr. Stretch pupilloplasty for small pupil
phacoemulsification (letter). Am J Ophthalmol 1994;
117:10708.
9. Chang DF. Phaco strategies for complicated cataracts. In:
Chang DF, ed, Phaco Chop; Mastering Techniques,
Optimizing Technology, and Avoiding Complications.
Thorofare, NJ, Slack 2004;17398.
10. Dinsmore SC. Modified stretch technique for small pupil
phacoemulsification with topical anesthesia. J Cataract
Refract Surg 1996; 22: 2730.
11. Auffarth G, Reuland AJ., Heger T, Volcker HE, Cataract
surgery in eyes with iridoschisis using the Perfect Pupil iris
extension system J Cataract Refract Surg 2005; 31:1877
80.
12. Graether JM. Graether pupil expander for managing the
small pupil during surgery. J Cataract Refract Surg 1996;
22:53035.
13. Mackool RJ. Small pupil enlargement during cataract
extraction; a new method. J Cataract Refract Surg 1992;
18:52326.
14. de Juan E Jr, Hickingbotham D. Flexible iris retractor [letter].
Am J Ophthalmol 1991; 110:77677.
15. Nichamin LD. Enlarging the pupil for cataract extraction
using flexible nylon iris retractors. J Cataract Refract Surg
1993; 19:79396.
16. Oetting TA, Omphroy LC. Modified technique using flexible
iris retractors in clear corneal cataract surgery. J Cataract
Refract Surg 2002; 28:59698.
17. Dupps WJ., Oetting TA. Diamond iris retractor configuration
for small-pupil extracapsular or intracapsular cataract
surgery J Cataract Refract Surg 2004; 30:247375.
18. Birchall W, Spencer AF. Misalignment of flexible iris hook
retractors for small pupil cataract surgery: effects on pupil
circumference. J Cataract Refract Surg 2001; 27:2024.
19. Masket S. Avoiding complications associated with iris
retractor use in small pupil cataract extraction. J Cataract
Refract Surg 1996; 22:16871.
20. Yuguchi T, Oshika T, Sawaguchi S, Kaiya T. Pupillary functions
after cataract surgery using flexible iris retractor in patients
with small pupil. Jpn J Ophthalmol 1999; 43:20-24.
21. Novak J. Flexible iris hooks for phacoemulsification.
J Cataract Refract Surg 1997; 23:82831.
22. Halpern BL, Pavilack MA, Gallagher SP. The incidence of
atonic pupil following cataract surgery. Arch Ophthalmol
1995; 113:44850.
23. Rho DS, Kahn M, Obstbaum SA. Complications of cataract
surgery. In: Charlton JF, Weinstein GW, eds, Ophthalmic
Surgery Complications: Prevention and Management.
Philadelphia, JB Lippincott Co., 1995; 95116.
24. Allan BD. Mechanism of iris prolapse: a qualitative analysis
and implications for surgical technique. J Cataract Refract
Surg 1995; 21:18286.
25. Chang DF, Campbell JR. Intraoperative floppy iris syndrome
associated with tamsulosin. J Cataract Refract Surg 2005;
31:66473.
26. Arshinoff S. Modified SSTUSST for tamsulosin-associated
intraocular floppy-iris syndrome. J Cataract Refract Surg
2006; 32:55961.
Current Concepts and Recent
Advances in Management of
Ocular Trauma
C H A P T E R
42
Trauma after Refractive Surgery
D Ramamurthy, Chitra Ramamurthy (India)
Introduction
Refractive surgeries gained momentum from 1960s
with inception of RK followed a decade later by
evolution of excimer laser and PRK, had a crescendo
in 1990s with Lasik gaining footage and the revolution
has been ever on with increasing vigor and growing
understanding.
On an average, over 17 million have undergone
LASIK so far. More than 2 million LASIK procedures
have been performed each year. Over 22 % with a
refractive error of 5 D to 7 D have undergone LASIK
in US. A further revelation tells us that 19 % of the
US refractive surgeons have themselves undergone
refractive surgery.
If one reflects on the popularity and demand of
a surgical procedure on the human body, refractive
procedures claim the 2nd position, next only to cataract
surgery.
The primary concerns which needs reflection is
occurrence of trauma of the refractive surgery per se
and trauma after refractive surgery.
Trauma in LASIK could range from flap related
complications, rare instances of corneal perforations,
corneal infection, macular hemorrhage, interface
deposits, epithelial ingrowth and irregular astigmatism.
The increasing concern following LASIK is that the force
that the residual untreated cornea could resist
decreases as a result of a thinner stromal bed and can
lead to Iatrogenic Keratectasia. Trauma from RK
could range from perforation to residual refractive
error, would response unpredictability, hyperopic shifts,
starburst phenomenon and drop in BCVA. PRK could
complicate issues with its varying wound response
trends with incremental need for topical steroids,
residual nebular haze, residual refractive error, etc.
But the burgeoning problem is the propensity of
late onset trauma impact in any of these eyes and the
risk: benefit ratio.
If we look at the profile of refractive surgery
patients, its largely a young, active and working
population in the prime of their productive life.
US Eye Injury Registry in 1999
1
assessed closed
Vs open globe injury in 173 patients who had undergone
refractive surgery prior to injury. 165 of these eyes
developed traumatic wound dehiscence. Only 20.6
% recovered 20/200 or better vision. The primary
concern which arises from this study data is the effect
of trauma on ocular integrity. The other possibility is
the probability of closed globe injury getting converted
to an open globe injury, in a setting of post-refractive
surgery.
Trauma in Radial Keratotomy
Radial keratotomy (Fig. 42.1) was introduced in 60s
and 70s. It maintained its stand as a popular refractive
procedure till 90s.
Cassey et al
2
came up with the analysis of the tensile
strength of corneal wounds. The conclusion derived
was that the weakest point in the eye in a post incisional
surgery is the site of incision. After complete healing,
the tensile strength is only 50% of normal.
Fig. 42.1: Radial keratotomy
Pin heiro et al
3
further assessed corneal integrity
after refractive surgery. The analysis indicated that
following blunt injury in a normal eye, rupture
270
occurred at limbus or sclera. Post RK, rupture occurred
through the incision (Fig. 42.2). Deeper, larger or
more the incisions, higher the risk.
Fig. 42.2: Rupture through incision
Probably in this setting, mini RK gained acceptance.
Reducing incision length
4
appears to reduce the
likelihood of corneal rupture, a more advantageous
position in patients predisposed to ocular trauma.
Histological evidence on examination of corneal
buttons post RK shows that wound healing of incisions
is not completed several years after the procedure.
Epithelial plugs of various size still incompletely fill the
somewhat dehiscent wound margins. Fibroblastic
activity
5
in the surrounding stroma remains incomplete.
Mc Knight et als
6
report on corneal rupture following
RK in cats subjected to BB gun injury. They conclude
that for the same intensity of injury rupture occurs in
RK treated eyes with hyphema occurred in untreated
eyes.
We cannot however conclude that post RK eyes
are condemned to rupture. The risk ratio is higher in
all probability and demands for a continued usage of
protective eye wear in instances of exposure to trauma.
Slade SG et al report
7
on ocular integrity after
refractive procedures makes a comparative study on
RK, PRK, LASIK and normal eyes. The conclusions
derived are that RK eyes ruptures at significantly lower
stress levels. PRK and LASIK eyes are not significantly
different from normal eyes. The sites of rupture are
the same as normal eyes in PRK and LASIK.
Trauma in PRK
Burnstein et al report
8
on PRK ablations in human
cadaver eyes indicate that these eyes following PRK
ablations of 6.00 to 54 D were infused with nitrogen
gas to build high pressure in the eye and the ablation
zones responded to pressure trauma only after a
42 D treatment. There has been no reported cases
to date of rupture occurring in the cornea at the site
of ablation after PRK.
Trauma in LASIK
The stromal wound healing after LASIK occurs at the
flap edges and is minimal compared to the PRK group.
This may support in part our clinical observation that
less corneal haze was noted after LASIK then after PRK
as a result of less disorganized stromal collagen fibers
from wound healing process.
POSSIBLE MECHANISMS
Theoretically, the force that the cornea would resist
is directly proportional to the thickness of the residual
untreated stroma after lasik
9
, i.e. thinner the thickness,
the more vulnerable to blunt ocular injury it will be.
According to Munnerlyns formula:
Ablation depth in microns (m) =
Optical zone in mmdiopters of myopia
3
To prevent ectasia, a minimal residual stromal bed
thickness of at least 250 is advocated. Following injury
in a LASIK flap, there are 2 probable sites of injury.
A shearing force could act at the junction between the
flap and the corneal bed which separates the flap from
the bed. In addition, a perpendicular penetrating force
perforates the residual thinner cornea. Most complica-
tions associated with LASIK are flap related. They
include intra-operative flap complications like shifted
flap, button hole formation, free flap, wrinkled flap
and postoperative complication like micro and macro
striae and flap slippage and dislocation.
The mechanisms
10
postulated for early flap
adherence includes endothelial pumping, capillarity,
fiber interlacing, intra-corneal suction, intra-corneal
molecular attraction and ionic bonding and strength
of the epithelium. Whatever the mechanism, the
anecdotal ease with which a flap can be lifted years
after surgery for retreatments is a definite indication
that the flap actually never heals fully (Fig. 42.3).
Trauma to LASIK Flap
Early flap complications occur in the first 24 hours.
The sequence of events declines after one week. The
flap slippage and displacement most commonly occur
in the early postoperative period and presumably as
a result of mechanical disruption such as forceful
blinking, lid squeezing and eye rubbing (Fig. 42.4).
271
Trauma after Refractive Surgery
Fig. 42.3: Enhancement 5 years after LASIK Fig. 42.6: Late flap dislocation
The longer the time interval between occurrence
and intervention, probability of intractable micro and
macro striae (Fig. 42.7) drop in BCVA, irregular
astigmatism and even onset of DLK is likely.
Fig. 42.7: Macro striae in post-LASIK trauma
These flaps need to be lifted, both surfaces of the
flap hydrated thoroughly, stretched to the gutter and
ironed out in a direction perpendicular to the direction
of the striae. The interface also needs to be thoroughly
irrigated and if in an eventuality of a long wait to inter-
vention, possibility of epithelial ingrowth increases and
appropriate debridement is indicated. Recalcitrant
macrostriae demand removal of the overlying epithe-
lium, hydrate, stretch and ironing of the flap. Lin
et al report
11
on complications with lamellar refractive
surgery indicates flap adhesion and bonding occurs
between 5 to 100 days with peak strength between
and of the original strength.
Reports of late flap complications following LASIK
has been reported from 10 days to 5 years - playing
Fig. 42.4: Flap dislocation within 24 hours
Fig. 42.5: DLK after foreign body removal
A mere foreign body removal with a spud or a
needle on a LASIK flap acts like a shearing force, could
cause flap slippage or DLK (Fig. 42.5). Recent or late
dislocation of flap demand immediate attention
(Fig. 42.6).
272
with basket ball, dog, motor vehicle accident with
airbag injury, playing in snow, army field training, peck
by pet bird and multiple trivial injuries of this fashion.
Diffuse lamellar keratitis (DLK) can be precipitated
by the least of trauma and needs to be kept in mind
and be treated vigorously (Fig. 42.8).
Fig. 42.8: Diffuse lamellar keratitis
Trauma in Surface Treatments
Surface ablations are by and large more risk free
related to trauma although the refractive outcomes
would be compromised without adequate wound
modulators. The absence of the thick flap created in
LASIK makes surface treatment more bio-mechanically
stable and makes it less vulnerable to trauma.
Trauma in Phakic IOL Implants
Iris supported Phakic IOLs have multiple reports of
disenclavation of haptics and decentration of phakic IOL
(Fig. 42.9) which could lead to progressive endothelial
loss if immediate intervention is not forth coming.
Conclusion
The conclusive ideas which emerge from this chapter
is that one needs to practice abundant caution.
Wearing shatter proof protective glasses is a necessary
precaution. Literature reports are few, clinical
experience rare but awareness of such occurrences
and educating our patients would be preventive at
large.
Fig. 42.9: Phakic IOL disenclavated after trauma
References
1. US Eye Injury Registry in 1999.
2. A. R. Gasset; C. H. Dohlman The tensile strength of
corneal wounds. Arch Ophthalmol 1968;79:595-602.
3. MN Pinheiro, MR Bryant, R Tayyanipour. Corneal
integrity after refractive surgery: effects of radial keratomy
and mini-radial keratotomy Ophthalmology 1995;
102:297-301.
4. Casebeer JC, Shapiro DR , Phillips S. Severe ocular
trauma without corneal rupture after radial keratotomy:
case reports. J Refract Corneal Surg 1994; Jan-Feb: 10
(1): 31-33.
5. Pinheiro MN , Bryant MR, Tayyanipour R et al. Corneal
integrity after refractive surgery. Effects of radial
keratotomy and mini-radial keratotomy. Ophthalmology
1995 Feb; 102 (2): 297-301.
6. McKnight SJ, Fitz J, Giangiacomo J.et al .Report on
corneal rupture following RK. Ophthalmic Surgery 1988;
19:165-67.
7. Peacock LW, Slade SG, Martiz J, et al. Ocular integrity
after refractive procedures Ophthalmology 1997;104:
1079-83.
8. Burnstein Y, Klapper D, Hersh PS Experimental globe
rupture after excimer laser photorefractive keratectomy.
Arch ophthalmol 1995;113:1056-59.
9. Sun CC, Chang SW, Tsai RF. Traumatic Corneal
Perforation With Epithelial Ingrowth After Laser In Situ
Keratomileusis. Arch Ophthalmol 2001;119:907-09.
10. Cda RP, Narvaez J, King JA, et al. Late-onset traumatic
dislocation with central tissue loss of laser in situ
keratomileusis flap. Cornea 2006 Oct;25(9):1107-10.
11. Lin RT, Maloney RK. Flap complications associated with
lamellar refractive surgery Am. J Ophthalmology 1999;
127:129-136.
C H A P T E R
43
Complication and Contusion
after Phakic IOL
Jerome Bovet (Switzerland)
Introduction
The implantations of IOLs in the phakic eye (phakic
IOLs) is a relatively old technique to correct ametropia,
they have been used in clinical practice in refractive
surgery for 15 years.
The early problems are related to the design of
the lens and the meticulous details of surgery. The late
postoperative complications are related to the
interaction of the IOL and the intimate ocular tissues
during the lifetime of the patient. Lifelong, regular
follow-up care is essential in all cases.
Explantation of the lens may ameliorate some of
the complications. Later in life, if the patient develops
a cataract, it should be possible to do an atraumatic
explantation, followed by cataract extraction and
impl antation of another appropriate IOL.
Development of a newer, safer technology to correct
ametropia may necessitate explantation of the IOL.
However, the presence of the IOL inside the eye
has been associated with complications specific to the
type of phakic IOLs involved. Some of these compli-
cations have led to changes in design of some lenses
and to discontinuing of others.
9
Currently, only a few long-term studies are available
with phakic IOLs the complication spectrum appear
slowly and some lenses become forbidden to insert
in some European country.
8
We will describe the most frequent late complica-
tions and traumatisme associated with implantation of
phakic IOLs.
Anterior Chamber Phakic IOLs
(Fig. 43.1)
ENDOTHELIAL COMPLICATIONS AND
ANTERIOR CHAMBER DEPTH
The main concern about AC Phakic IOLs is loss or
damage to the endothelial integrity. An Exact
preoperative examination should exclude those
patients with low endothelial cell count or those with
shallow anterior chambers because the risk of cell loss
increases as the distance between phakic IOL and the
endothelium decreases.
We know today that a minimum of 1.5 mm
between the IOL and the corneal endothelium is
needed to long-term safety. This explains the damage
to the endothel ium, if not expl anted earl y to
endothelial decompensation.
3,11,12
Meticulous long-term follow-up of each patient is
at the moment necessary for any AC phakic IOL to
detect those individuals with significant damage to the
endothelium and to explant the phakic IOL before
clinically necessary.
PIGMENT DISPERSION AND LENS
DEPOSITS
Although no definite incidence for these conditions is
reported in the literature, these conditions are seen
in clinical practice. They normally do not negatively
affect visual acuity and thus no futher procedure
except for regular clinical observationis necessary.
Fig. 43.1: Eye care IOL (corneal)
274
CHRONIC INFLAMMATION AND UVEITIS
As the angle-supported AC phakic IOL is positioned
directly in front of the iris, chronic inflammation and
pigment dispersion are possible .
SIZE-RELATED COMPLICATIONS PUPIL
OVALIZATION AND IRIS RETRACTION (FIG. 43.2)
Angle supported anterior chamber phakic IOLs need
to have the same size of the anterior chamber in order
to fit there exactly without causing damage to the ocular
tissues.
Fig. 43.2: Anterior chamber aphakic IOL with
ovalisation of the pupilla
This is now possible with the visante OCT (Carl
Zeiss Meditec) or with the Pentacam (Oculus AG) which
give you the exact morphology and sizing of the
anterior chamber (Figs 43.3 and 43.4).
If an anterior chamber angle-supported phakic IOL
is too short, the IOL will rotate in the anterior chamber
causing important glare. Rotation of the angle-
supported phakic IOLs might occur due to undersizing.
In fact, 80% of eyes showed rotation greater than 15
degrees.
8
A more frequent and serious complication is the
pupil ovalisation. Ovalization of the pupil is a specific
complication of angle-AC phakic IOLs. The position
of haptics in the sclerocorneal angle and their size might
lead to mild deformation of the iridosclerocorneal
architecture, resulting in iris retraction and pupil
ovalization.
Pupil distortion starts after 12 to 18 months of
implantation, the pupil showing ovalisation, the longer
axis being always the axis of the IOL.
Iris retraction with oval pupil deformation remains
a concern of the angle-supported phakic IOLs. This
mater together with potential damage to endothelial
cells, is the major objection against the current lens
designs (Figs 43.5 and 43.6).
Fig. 43.3: The Visante OCT (Carl Zeiss Meditec)
Anterior chamber
Fig. 43.4: Pentacam Oculus AG. Anterior chamber and
pachymetry
Fig. 43.5: Anterior chamber Phakic IOL NuVita
Bausch and Lomb Permanent mydriasis
INDUCED ASTIGMATISM
Surgically induced astigmatism is of significance because
patients request acceptable unaided postoperative
visual acuity.
GLARE AND HALOS
One disadvantage of AC phakic IOLs is that they are
positioned in front of the pupil, with edge affects as
275
Complication and Contusion after Phakic IOL
Fig. 43.6: Pupillary bloc with anterior phakic IOL
a potential source of optical aberrations. Furthermore,
the relatioin of pupil size and center to the optic of
the lens is a crucial factor that should be evaluated
and discusses preoperatively.
GLAUCOMA
The risk of acute angle glaucoma is well known from
aphakic anterior chamber IOLs therefore a peripheral
iridectomy is recommended for this IOL.
CATARACT FORMATION
As the AC phakic IOL is positioned away from the
lens, cataract formation is of less significance when
compared to posterior chamber phakic IOLs.
Iris-fixated Anterior Chamber
Phakic Intraocular Lenses
(Fig. 43.7)
The iris-fixated IOL is marketed in Europe as the Artisan
has been used since 1978 for pseudophakic IOLs,
mainly for secondary implantation in aphakic eyes.
Since 1986, the Worst-Fechner IOL has been
implanted in phakic eyes for the correction of high
myopia and subsequently hyperopia. The original
design was modified in 1991 to assure a sufficient vault
between the IOL optic and the iris.
COMPLICATIONS OF IRIS-SUPPORTED
PHAKIC IOLS
5
One frequent complication is the loosing of the IOL
from the iris. This can occur spontaneously or after
Fig. 43.7: Iris fixated lens: iris claw
minor trauma. However, this complication is always
the consequence of the so called weak grasp, that
is insufficient amount iris tissue grasped in the claw
(Figs 43.8 and 43.9).
We will related an eye trauma with an artisan which
induce a intumescent cataract, retinal detachcment and
loss of vision.
There are in fact very few complications related
to Artisan/Artiflex.
Fig. 43.8: Decentration of the lens with not enough iris
tissue grasp: Iris claw Artisan
Fig. 43.9: Iris claw Artisan, decentration
276
ENDOTHELIAL CELL LOSS AND ANTERIOR
CHAMBER DEPTH
Damage to the endothelium can occur mostly because
of the IOLs direct contact with the inner surface of
the cornea, either during impl antation or by
postoperative changes in IOL position.
The height of the Artisan lens and the potential
closeness to the cornea increase with the dioptric
power. Therefore, a sufficient anterior chamber depth
(ACD) for the calculated IOL is necessary. The distance
between the implant and the corneal endothelium
should not be less than 1.5 mm. This may be a problem
more for the hyperopic than the myopic iris-claw
phakic IOL.
CHRONIC INFLAMMATION AND UVEITIS
The possiblility of chronic inflammation has always
been a major concern with the iris-claw lens, as this
IOL is fixated directly in the iris tissue and causes
pressure or shear forces when the eye is moving.
Careful postoperative monitoring of inflammatory
signs is necessary. If persistent intraocular inflammation
occurs that is not sufficiently treatable with drugs, the
removal of the implant must be considered.
PUPIL OVALIZATION AND DECENTRATION
Pupil ovalization or irregularity can occur if the fixation
of the haptics is perfomed asymmetrically. No
pregressive pupil ovalization has been reported so far.
This can lead to difficulties if the pupil itself is
decentered and if the optical axis is not in the middle of
the pupil. Postoperative decentration is possible if the
enclavation is not sufficient.
Postoperative dislocations due to blunt ocular trauma
have been described. In the authors experience, they
observed only case of possible phakic IOL dislocation
in a patient with very thin iris tissue (Fig. 43.10).
GLARE AND HALOS
Phakic IOLs are often implanted in eyes of compara-
tively young patients with a large scotopic pupil
diameter. This can result in glare phenomena if the
pupil is larger than the IOL optic.
GLAUCOMA
Because the anterior chamber angle is not affected
by the haptics of the iris-claw IOL, lens size-related
secondary glaucoma is not pratically possible. A
peripheral iridectomy or iridotomy is necessary for the
prevention of a papillary block.
CATARACT FORMATION
Cataract formation due to the iris-claw lens is very
unlikely with myopic eye because it is inserted over
a miotic pupil without contacting the crystalline lens.
Cataract formation has been reported in association
with the iris-claw lens and hypermetropia on a long-
term basis.
The increasing size of the crystalline lens with age
and the formation of cataract, especially of an
intumescent type, will greatly disturb the tissue
relations. An early management of cataract, including
the explantation of the implanted phakic lens, will be
needed.
Implantation of a phakic lens in a hyperopic eye
ought to be a small event for the operated eye;
unfortunately, it is not so. Therefore, lifelong regular
follow-up care is essential.
CASE REPORT (FIGS 43.11 AND 43.12)
A 41-year-old worker presented with a sudden loss
of vision in the left eye after trauma. He reportedly
had receive a cable on his left eye.
The patient had had uneventful bil ateral
implantation of Artisan toric phakic IOLs 1 year earlier
to correct RE S-19.5 C -2.5 respectively LE S-14.0
C-3.0 the vision after one week was VAWC 0.5/0.6
On presentation at the emergency room, the left
eye visus light perception. The globe presented no
open wound. Anterior chamber had an hyphema, The
Artisan phakic IOL were not found on examination.
An intumescent white cataract with ruptured capsule
and 180 degrees zonulolyse prolapsed inside the AC.
No vitreous prolapse in AC. Eye pressure on the left
eye was 38 mm Hg.
On the echo B the retina seem on place and the
iris-claw lens seem on the retina. Fig. 43.10: Dislocated iris claw
277
Complication and Contusion after Phakic IOL
Fig. 43.11: Schematic trauma and iris claw inside the
vitreous chamber
Fig. 43.12: Schematic trauma and iris claw inside the
vitreous chamber
In urgency the cataract was phacoemulsified and
an anterior vitrectomy under topical anesthesia with
propofol general anesthesia, was performed to remove
the hemorrhage and to diminish the pressure.
Four days later a 23 gauges 3 ports posterior
vitrectomy was done to remove the Artisan aphakic
lenses which was enclaved by the claw on the retina.
A retinal tears was found at the place of the claw of
the lens full vitrectomy, 180 degrees of endolaser and
exchange Dkline-air-silicone was done. A phakic artisan
lens was replace on the iris.
One week after the second operation the visus
BCVA was 3/10.
Two months postoperatively, he develloped a PVR
posterior and anterior a second 23 gauges 3 ports
posterior vitrectomy was performed with a full shawing,
360 degrees retinotomy and panphotocoagulation.
Silicone was injected at the end of procedure.
One year later, he developed a neovacularised
cornea and a ophthisic eye.
Discussion
This case show that the old initial corneal wound of
6 mm was strong enough and no dehiscence appear.
The iris claw give a rigidity to the anterior chamber
and prevent the natural elasticity of the globe, result
of the rupture of the zonule lens subluxation and
dislocation. The contusive injury was strong enough
to dislocate the artisan lens and to push the lens all
through the posterior chamber where a claw pinch
the retina and do a retina tears.
Traumatic dislocation of an Artisan IOL is a rare
complication, with only 5 reports in the clinical
literature.
1,2,4,6,7,13
Most dislocations resulted in the haptic
claw tearing free from the iris at one point, which could
be easily corrected by reenclavation. Based on the
reports, it seems probable that the enclavation force
of the haptic claw is insufficient or the iris tissue is not
strong enough to hold the Artisan IOL during ordinary
trauma.
This case stresses the need for protection in eyes
with previous eye surgery and may reduce the risk,
particularly when the patient is involved in activities
such as hard worker,contact sports, e.g. football, tennis,
squacrh. Despite five operations,when the eye develop
a proliferative vitreoretinopathy (PVR) under silicone
oil, it is very difficult not to finish with a phthisic eye.
4
Posterior Chamber Phakic
Intraocular Lenses
14
(Figs 43.13 and 43.14)
The specific complications of PC phakic IOLs are caused
by their position between the iris and the natural lens.
The most common complicationscataract formation,
papillary block, and glaucomaare dependent on the
lens position, material, and original design.
Fig. 43.13: Posterior phakic IOL ICL (Staar)
278
CATARACTS HAVE ALWAYS BEEN
THE MAIN CONCERN
Cataracts related to posterior chamber phakic IOLs
are anterior subcapsular opacities. The phakic IOLs
induced cataracts typically start between 12 and 18
months after surgery with some anterior subcapsular
opacities, progressing later causing sometimes the need
of cataract surgery.
The reason, why these cataracts develop, is not
well established, although it is widely believed that
depends mainly on the space (vault) between the IOL
and the natural lens.
PUPILLARY BLOCK, ACUTE GLAUCOMA AND
MALIGNANT GLAUCOMA
Because of the PC phakic IOLs the iris can be pushed
forward and narrow the anterior chamber angle, so
a pupillary block with acute glaucoma can appear,
especially in hyperopic eyes. This problem can be
prevented by creating an intraoperative surgical
iridectomy.
For hyperopic treatement, the preoperative
iridotomy is even more important in preventing early
pupillary block.
Conclusion
Good results are obtained as much by surgical skill
as by the lens design chosen. A regular detailed follow-
up examination is essential for all operated cases to
detect and treat any untoward problem early, so that
no damage occurs. The crystalline lens, IOP, and
endothelial cell status are important guides to the
continued good health of the eye.
The operated eye needs to be protected from
rubbing and trauma because they tend to upset the
delicate balance between the implanted IOL and the
adjacent ocular tissues.
Yearly eye examination is an essential ingredient
of Aphakic IOL follow-up, and as soon as a trauma
occurs.
References
1. Asano-Kato N, Toda I, Hori-Komai Y, et al. Experience
with the Artisan phakic intraocular lens in Asian eyes.
J Cataract Refract Surg 2005;31:91015.
2. Ball JL, McLeod BK. Traumatic wound dehiscence
following cataract surgery: a thing of the past? Eye 2001;
15:4244
3. Baikoff G, Arne JL, Bokobza Y, et al. Anglefixated Anterior
Chamber Phakic Intraocular Lens for Myopia of -7 to
-19 diopters. J Refract Surg 1998;14:282-93.
4. Banta JT, Cebulla CM, Quinn CD. Closed globe
Injuries:anterior segment. In Banta JT (Ed): Ocular trauma
Sauders Elsevier, 2007.
5. Benedetti S, Casamenti V, Marcaccio L, et al. Correction
of myopia of 7 to 24 diopters with the Artisan phakic
intraocular lens: two- year follow-up. J Refract Surg 2005;
21:11626
6. Ioannidis A, Nartey I, Little BC. Traumatic dislocation and
successful re-enclavation of an Artisan phakic IOL with
analysis of the endothelium. J Refract Surg 2006;
22:1023.
7. Lee JS. Traumatic aniridia and aphakia after Artisan
intraocular lens implantation. J Cataract Refract Surg
2007;33:134142.
8. Kohnen T, Mirshahi A, Bhren J, Kasper T, Baumeister
M. Complications of phakic Intraocular lenses (Chap 9).
In Hardten DR (Eds): Phakic Intraocular lenses. Slack Eds
2007.
9. Marinho A, Salgado R. Complications of phakic IOLs
(Chap 18). In Garg A (Ed): Mastering the Techniques of
Lens based Refractive Surgery (Phakic IOLs). Jaypee
Brothers, 2005.
10. Marinho A. New generation Phakic IOL implant for
myopia provides good vision quality. Euro Times
1998;3(6):26.
11. Mimouni F, Colin J, Koffi V, et al. Damage to the corneal
endothelium from anterior chamber intraocular lenses in
phakic eyes. Refract Corneal Surg 1991;7:277-81.
12. Saragoussi JJ, Cotinat J, Renard J, et al. Damage to the
corneal endothelium by minus power anterior chamber
intraocul ar l enses. Refractive Corneal Surgery
1991;7:282-85.
13. Yoon H, Macaluso DC, Moshirfar M, Lundergan M.
Traumatic dislocation of an Ophtec Artisan phakic
intraocular lens. J Refract Surg 2002;18:48183
14. Zaldivar R, Davidorf JM, Oscherow S. Posterior Chamber
phakic IOL for myopia of -8 to -19 diopters. J Refract
Surg 1998;14:294-305.
Fig. 43.14: Visian ICL (Staar)
C H A P T E R
44
Management of Corneal
Lacerations
SH Lee (Canada)
Introduction
Laceration of cornea is one of the leading causes of
ocular morbidity. The management of such injury,
whether medical or surgical, is directed primarily at
the restoration of normal ocular anatomy. The
ultimate goal is to prevent secondary complication and
maximize the patients visual prognosis.
Injury Assessment
A meticulous injury assessment is important in
determining the extent of injury.
This should include detection of presence or
absence of intraocular foreigner body, orbital bony
injury or adnexal tissues injury such as lacrimal duct
injury.
A quick history must be obtained, how it happened,
when it happened, past ocular history, past medical
history, including current topical and oral medications
and allergy.
A short but focused ocular examination should be
conducted. Visual acuity, ocular mobility, external
examination, anterior and posterior segment
examination, including intraocular pressure if possible
should be documented. Auxiliary tests such as X-rays,
CT scans will help to determine the extent of the injury.
All documented details should be neatly written on
patients chart not only for medical record, but for
medical legal purpose if required in the future.
Perforating or Nonperforating
Corneal Laceration
The primary goal is to determine whether it is a
perforating or nonperforating corneal laceration, as
the former type of injury is always surgically managed,
and the latter may be medical or surgically managed.
If in doubt, it is best to suture the wound especially
if the wound edge is not in good apposition.
It is a good principal to follow the Flow chart
44.1.
Medical Management
All suspected nonperforating corneal laceration must
be carefully examined to rule out perforation, such
as microscopic leak.
Seidel testing with 2% fluorescein will be helpful,
Gentle digital pressure may reveal it is indeed a self
sealing wound.
All self sealing corneal lacerations may be treated
with eye patch or bandage contact lens, with broad
spectrum antibiotic eye drop frequently. Patient has
to be monitored daily on outpatient basis. Any
Flow chart 44.1: Management of corneal laceration
280
symptom or sign of infection such as infectious keratitis
or endophthalmitis should admit the patient to the
hospital for more intense treatment. Any sign of
anterior chamber becomes progressively shallow, or
the corneal wound becomes unstable, suturing of the
wound must be considered. Every effort must be made
to minimize scarring and surface irregularity. The
bandage contact lens should not be removed until the
wound is stable, and complete re-epithelialization has
occurred.
Surgical Management
If the corneal laceration is perforating, it should be
determined whether it is: simple or complex laceration,
with or without uveal. Crystalline lens vitreous, retinal
or scleral involvement. It is important to detect any
corneal tissues loss, and whether it is irrepairable
severely damaged globe.
The primary goal in repairing corneal laceration
is to achieve a water tight globe with structural integrity.
Other secondary goals will be removal of any lens
fragments, vitreous incarceration, uveal tissue
incarceration or prolapse and intraocular foreigner
body if they are detected during the surgery. To restore
the normal or near normal anatomical relationship is
the final goal.
Simple Corneal Laceration
Stable wound, with watertight laceration, and formed
anterior chamber, 10-0 monofilament nylon may be
placed directly across the wound without entering the
anterior chamber, The suture has to be 90% depth
through the stroma, 1.5 mm in length, and equal
depth on each side of the wound (Fig. 44.1). Some
corneal surgeons would think 100% depth through
the stroma will be better, but at least in theory, such
suturing would provide a conduit for allowing micro
organism from external surface to enter the eye.
Fig. 44.1: After suturing of corneal laceration
Other incorrect corneal suturing should be avoided;
shallow suturing leads to internal wound gape, suture
with unequal depth will create wound override
(Fig. 44.2).
Fig. 44.2: Positions of corneal suturing.
(A) Correct. (B) Wrongsuturing too shallow and lead to
i nternal gape. (C) Wrongsuturi ng through and
through.100% depth, creating a conduit. (D) Wrong
unequal distant from each side of the wound lead to wound
distortion. (E) Wrongsuture with unequal depth and
distance will cause wound over ride. (F) Correct
Placement of sutures through the visual axis should
be avoided. If the laceration affecting the visual axis,
suturing should avoid the central cornea, by placing
it on either side of the wound but not through the
axis, and by making sure the suture bites close to the
visual axis short (Fig. 44.3).
Fig. 44.3: Placement of sutures. (A) Correct, central cornea
no suture, (B) wrong, as suturing run through the visual
axis
Unstable wound with shallow or no anterior
chamber. A viscoelastic is used to recreate the anterior
chamber through a newl y created side port
(Fig. 44.4). Any incarcerated ocular tissues into the
wound should be either excised or repositioned. At
281
Management of Corneal Lacerations
time that anterior chamber cannot be formed, because
of leaking, temporary suture to close the wound may
be required, and subsequent removal will be required
once the wound become stable. Once the wound
become stable, the accurate appositional way of correct
suturing should be carried out.
Fig. 44.4: Recreation of anterior chamber with viscoelastic.
Viscoelastic material is injected into anterior chamber
through the side port
Complex Corneal Laceration
Wound
The goal is to achieve good wound apposition with
minimal distortion.
An irregular wound is first subdivided into straight
segments with interrupted sutures. Long deep and
relatively tight peripheral sutures and short, shallow,
appositional sutures near the central corneal may
restore the normal corneal dome and surface corneal
topography.
Some of those complex corneal laceration wound
are shown in Figures 44.5 and 44.6:
Fig. 44.5: Complex corneal laceration. A T-or Y- shaped
laceration often leaks at the apex and may be difficult to
close. A purse string suture is generally effective in closing
such laceration
Corneal Laceration with
Tissue Loss
The wound can be divided into central, paracentral,
peripheral.
Central with tissue loss will be treated with corneal
graft (Fig. 44.7).
Paracentral with tissue loss will be treated with
suturing or tissue glue or combination of the two.
Peripheral with tissue loss will be treated with patch
graft (Fig. 44.8).
Use of Tissue Glue
In most cases of corneal laceration, use of tissue glue
is only for adjunct treatment to suturing.
Fig. 44.6: Stellate laceration close by (A) bridging sutures,
(B) purse string suture, and (C) multiple interrupted sutures
and tissue adhesive in the center
Figs 44.7A and B: Penetrating keratoplasty for central
corneal laceration with tissue loss, removal of lacerated
cornea. Curved scissor and supra sharp knife are used
instead of trephine
282
Fig. 44.8: Final appearance of cornea after patch graft
after peripheral corneal laceration with tissue loss
It is useful in small puncture wound with leaking,
selected small perforated laceration, and paracentral
laceration with suturing.
When deciding to use tissue adhesive, the corneal
surface is dried with a cellulose sponge and the epi-
thelium surrounding the perforation is debrided, tissue
adhesive (cyanoacrylate) is applied to the edge of the
perforation with 25-gauge needle on a tuberculum
syringe with least amount or in the form of a bead
(Fig. 44.9).
A bandage contact lens is placed for comfort and
to protect the adhesive from being lodged by the eyelids
Frequent following up is necessary to ensure the
perforation is sealed.
Corneal Laceration with
Involvement of Other Ocular
Structure
With lens involvement, depending upon the extent
of involvement, lensectomy may be required. Any lens
fragment has to been removed, and anterior
vitrectomy has to be performed.
With uveal tissue involvement, incarceration of
uveal tissues have to be repositioned or excised.
With vitreous or retinal tissue involvement, service
of retinal subspecialist will be required, and it will be
multispeciality approach.
With intraocular foreign body, it has to be removed
with any means possible.
Conclusion
It is important to manage corneal laceration according
to the fl ow chart for management of corneal
laceration; Use of appropriate surgical techniques of
Figs 44.9 A to C: (A) Puncture corneal wound with leaking.
(B) #25 gauge needle on tubercular syringe with tissue
glue in the form of bead. (C) Final appearance of corneal
wound after tissue glue, the bandage contact lens had been
removed and the corneal surface has been re-
epitheliumized
suturing to minimizing the corneal scarring, to stabilize
the wound and to re-establish normal or near normal
anatomical relationship is vital.
A clearer understanding of corneal laceration and
the use of appropriate surgical approaches may permit
the reduction the rate of ocular morbidity and enhance
visual rehabilitation after trauma.
Bibliography
1. Cowden JW, Hu BV. A new surgical technique for
posterior chamber lens fixation during penetrating
keratoplasty in the absence of capsular or zonular
support. Cornea 1988;7:231.
2. Hersh PS, Kenyon KR. Anterior segment reconstruction
following ocular trauma. Int Ophthalmol Clin 1988;
28:57.
3. Mackenson G, Faulborn J. Primary and secondary
reconstruction of the eyeball after extensive lacerations.
Ophthalmic Surg 1974;5:43.
4. Refojo MF, Dohlman CH, Ahmad B, et al. Evaluation of
adhesives for corneal surgery. Arch Opthalmol 1968;
80:645.
5. Smiddy WE, et al. Contact lenses for visual rehabilitation
after corneal laceration repair. Ophthalmology 1989;
96:293.
C H A P T E R
45
Sports Injuries in Eye
B Shukla, Binoo Nayar (India)
Introduction
The word Sports includes many entities. It includes
all types of game (indoor and outdoor) and all types
of athletic events. Some authors have used the word
Recreational instead of sports and that would include
many more diverse activities found in different parts
of the world and to account for all of them is no easy
job.
This problem can be looked at from various angles.
There can be age wise distribution, regionwise,
seasonwise and from the point of view of the agent
causing injury. In the present chapter sports injuries
will be considered from the last point of view with
passing reference to other modes of injury.
Since there has been no standardization in the
terminology of ocular trauma for a long time nor any
uniformity in study design it is by no means easy or
valid to make any comparison. In one study at Boston
34% ruptured globes were reported from trauma.
1
In
another study from Stockholm 23% of perforating
injuries were found due to sports.
2
The incidence of
paediatric injuries from Maryland was reported as 15.2
per 100,000.
3
Hyphaema has been mentioned as a
special feature of sports trauma
4
(Fig. 45.1). From
USA baseball and basket ball are reported as common
sports injuries.
5-6
US eye injury registry has reported
sports injury upto 12%.
7
The author in a study of 1744
eyes found 12.27% sports injuries.
8
Classification
Broadly speaking most of the sports injuries could be
classified on the basis of the source of injury as follows:
1. Ball injuries
2. Physical contact injuries
3. Miscellaneous injuries.
BALL INJURIES
Perhaps this is the commonest type of sports injury
as most of the children, youngsters or even adults play
with some type of ball. The main advantage here is
that as a ball is a rounded structure it is not likely to
cause very severe injury unless it hits with a great force.
From the formula E= mv
2
it can be reasoned that
harder balls will hit with greater force and are more
likely to cause greater damage. Cricket ball and hockey
ball can be included in this category. However a third
factor is also important and that is the curvature of
the ball. The greater is radius of curvature (bigger in
size) the less they would cause damage as the brunt
of the force will be taken up by the orbital rim and
less damage is likely to occur to the eyeball. On the
contrary balls with lesser radius of curvature (smaller
balls) can cause greater harm as that they can enter
the orbital cavity and directly hit the eyeball. Thus ball
injuries could be large, medium or small ball injuries.
a. Small balls like golf and squash balls can cause
severe eye injuries because of their curvature, some
mass and great velocity. Out of 29 cases of golf
ball injuries USEIR
9
has reported 12 (41%) as open
globe injury which has a very poor prognosis. Table Fig. 45.1: Traumatic hyphaema RE
284
PHYSICAL CONTACT INJURIES
In many sport there is close physical contact which
can lead to eye injuries. Boxing and wrestling are
common games in this group. In India Kabaddi is
a popular game in rural areas where also there is close
physical contact between players. In a report from New
York out of 74 boxers about two third had some
evidence of eye injury.
10
Black eye is commonly seen
in boxing. Free style wrestling is also a dangerous
game. In other games also like basketball, football and
soccer contact with hand or foot can cause either a
direct injury or after a fall. There are other types of
ball injuries also.
MISCELLANEOUS
There many other types of sports and games in
different parts of the world which can lead to ocular
trauma. Some of them include fishing, hunting, water
sports, motor sports, Bungee cord and fireworks. The
last one is quite common in many countries during
festivals and can cause a burn or blast injuries sometimes
to both the eye balls.
11
Air gun injuries are also
common in young boys. As in all types of injury males
are four times prone to sports injury and the incidence
is highest in 11-15 age group.
12
The incidence of sports trauma also depends on
the craze of a particular game in a particular country.
Thus cricket is very popular in South Asia (India,
Pakistan, Ceylone and Bangla Desh). In Europe football
and soccer are extremely popular. In USA boxing and
tennis are very common games apart from baseball
and basketball.
References
1. Schein OD, Hibbers PL, Shingleton BJ, et al. The
Spectrum and burden of ocular injury. Ophthalmology,
1988;95:300-05.
2. Blomdahi S, Norell S. Perforating eye injury in the
Stockolm population, An epidemiological study, Acta
Opthalmol 1984;62:378-90.
3. Strahlman E, Elman M, Baker S. The incidence and
causes of pediatric ocular trauma, a population based
study, Invest Opthalmol Vis Sci 29 (ARVO Suppl).
1988;63.
4. Kennedy RH, Brubaker RF. Traumatic hyphaema in a
defined population. Am J Ophthalmol 1988;106:
123-30.
5. Karloson T, Klein B. The incidence of acute hospital
treated eye injuries. Arch Ophthal 1986;104:1473-76.
6. White M, Morris R, Feist R, et al. Eye Injury, prevalence and
prognosis by setting. South Med J 1989;82:151-58.
7. Ference K, Mester V, Mann L, et al. Eye injury epidemilogy
and prevention of ophthalmic injuries. Kuhn F, Pieramici
DJ (Eds). In: Ocular Trauma, Tieme Publication,
New York 2002;19.
tennis ball can cause no injury because of its very
light weight.
b. Medium size balls like cricket and hockey balls can
also cause very severe injuries because of their
hardness and velocity. In cricket right handed
batsmen can get their left eye more affected and
vice versa (Fig. 45.2). In hockey the goal keeper
is at great risk (Fig. 45.3). However due to helmet
such injuries have become rare. Tennis ball though
of lesser weight also causes severe eye injury
because of high velocity. Thus a tennis ball weighs
only 58 grams but its velocity is 132/second.
10
c. Large size balls include football, volleyball,
basketball and others. Though these games are very
commonly played usually they do not cause a severe
injury. Thus in a report from USEIR out of the 13
cases of football and 24 cases of soccer none
received an open globe injury though in basketball
out of 66 cases 11 had open globe injury.

In
basketball physical contact with hand and fist can
also add to the severity of injury. So is true with
baseball.
Fig. 45.2: Cricket ball injury
Fig. 45.3: Hockey ball injury
285
Sports Injuries in Eye
8. Shukla B. Sports Injuries. Shukla B, Natarajan S (Eds).
In: Management of ocular Trauma, CBS Publishers, New
Delhi 2005;322.
9. Vinger PF. The need for standardization for protec-
tive eyewear in sports. Kuhn F, Pieramici DJ (Eds). In:
Ocul ar Trauma, Thieme Publ ication, New York
2002;456-57.
10. Giovinazzo VJ, et al. The ocular complications of boxing,
ophthalmology 1987;587-95.
11. Wilson RS. Fireworks blindness: A co-operative study.
South Med J 1980;73:728-31.
12. Laroche GR, McIntyre L, Schertzer RM. Epidemiology of
severe eye injuries in childhood. Opthalmology 1988;
95:1603-07.
C H A P T E R
46
Management of Travel
Eye Injuries
Leonardo Toledo Netto, Belquiz A Nassaralla (Brazil)
Introduction
There are approximately 2.4 million ocular and orbital
injuries in the US per year, 20,000 to 68,000 of which
are vision-threatening injuries, and some 40,000
persons sustain significant vision loss each year.
1
The
Eye Injury Registry of Alabama (EIRA) has published
a study with 514 serious eye injuries of which 5% have
resulted from travel accidents.
2
After an accident, the case history should be
directed particularly to details of the trauma, pre-injury
vision, previous ocular surgery, medical history, current
medications, and allergies. Since many periorbital and
eyelid injuries can also involve the globe, a history of
any change in visual acuity or severe ocular pain after
the injury should be obtained.
Visual acuity may be difficult to ascertain and topical
anesthesia may be necessary to facilitate this task.
Detailed history is fundamental to the selection of
appropriate investigative procedures and for the
planning of therapy. In addition, any serious ocular
trauma may invol ve medicol egal action, and
consequently the importance of taking and carefully
recording a detailed history cannot be overemphasized.
External examinations should always include
pupillary testing, extraocular motilities measurements,
and confrontation visual fields. If the patient has
sustained blunt ocular trauma, a cover test (or Maddox
rod testing) should be performed, the eyelids and
orbital margins should be palpated, and forehead and
cheek sensitivity should be evaluated.
Slit-lamp examination should include fluorescein
staining, which is necessary for Seidel testing and
applanation tonometry, but tonometry should be
deferred if there is a known open globe injury. A dilated
fundus exam (with or without sclera depression, as
appropriate) is also essential during the trauma
examination.
Travel eye injuries may be divided in non-contact
or direct traumatic injuries and most of them are
preventable.
Prevention and Management
NON-CONTACT EYE INJURIES
The use of spectacles, even those with impact-resistant
lenses, is not enough to protect your eyes during your
summer trip. In fact, they can increase the risk by
shattering under high impact. However, they are of
slight value in the presence of small splash hazards or
the flight of small insects.
On travels, it is common to have dirt or grit in the
eye. It can be harmless, but it can also scratch the
eyeball and cause infection. In this case, it is important
to take the time to flush the eye clean.
Other frequent condition on travels is sun super
exposition. High intensities of UVB light are hazardous
to the eyes, and exposure can cause welders flash
(photokeratitis or arc eye) and may lead to cataracts,
pterygium,

and pinguecula formation. Protective
eyewear is beneficial to those who are exposed to
ultraviolet radiation, particularly short wave UV. Given
that light may reach the eye from the sides, full coverage
eye protection is usually warranted if there is an increased
risk of exposure, as in high altitude mountaineering.
Mountaineers are exposed to higher than ordinary levels
of UV radiation, both because there is less atmospheric
filtering and because of reflection from snow and ice.
Exposition to new groups of allergens in different
countries, cities and hotel rooms may also affect
travelers.
3
When traveling by auto, bus or train, potential
irritants or allergens can include dust mites, indoor
molds, pollens and other substances. Common
allergens such as mites and molds can lurk in the
carpeting, upholstery and ventilation systems of
vehicles. Before beginning a lengthy auto trip, it is
important to turn on the air conditioner or heater and
open the windows for at least 10 minutes prior to
entering the car. This will help remove dust mites and/
or molds that may be in the system. Outdoor allergens,
such as pollens and molds, are also potential hazards,
especially when traveling with open windows.
287
Management of Travel Eye Injuries
Cigarette smoke or outdoor air pollution can
worsen allergy symptoms. To avoid excess air pollution
when traveling by automobile, it is better to travel in
early morning or late evening, when the air quality
is better and it is possible to avoid heavy traffic.
Air quality on planes can greatly affect the allergic
patient. While all domestic flights are now smoke free,
many international flights are not. If traveling abroad,
allergic patients should make sure they are seated as
far as possible from the smoking section when getting
a seat assignment.
Many travelers stay at hotels. Hotel rooms,
however, often contain large concentrations of dust
mites and molds in carpeting, mattresses and
uphol stered furniture that can worsen al l ergy
symptoms. Irritant fumes from cleaning products may
also cause problems. When making hotel reservations,
it is important to ask if there are allergy-proof rooms
available. If the patient is sensitive to molds, it is better
to request a sunny, dry room away from areas near
indoor pools. Also, for those who have allergies to any
animals, it is important to inquire about the hotels
pet policy, and request a room that has been pet-free.
According to Aslam et al
4
, at the emergency
department of the Chelsea and Westminster Hospital
in London, UK, 12% of the emergencies involving the
ocular surface are related to contact lens wearers. The
main environmental factor in pressurized cabins that
can affect eyes is low humidity.
3
The optimum humidity
range for comfort is between 40% and 60%. However,
cabin humidity may drop to 11% after takeoff. The
low cabin humidity during air travel increases aqueous
tear evaporation and can cause ocular discomfort such
as dryness, especially for contact lens wearers. The
presence of a contact lens in the eye can produce a
condition called contact lens-induced dry eye (CLDE),
in an otherwise normal individual. Contact lenses may
disrupt normal tear physiology through thinning and
breakup of the tear film, interrupt tear film reformation
and rupture the lipid layer with consequent increase
in tear film evaporation. The symptoms include
grittiness, scratchy eyes, lens intolerance, and blurred
vision. Therefore, contact lens wearers should know
preventive measures as follows:
1. Beverages containing alcohol or caffeine and certain
medications can exacerbate dryness. If lenses are
worn during air travel, avoid alcohol and coffee
consumption.
2. Lens deposits reduce lens wetting and increase tear
evaporation. Clean the lenses thoroughly before
the journey. If you are a disposable lens wearer,
insert new fresh lenses. If you are a yearly
replacement lens wearer, use a protein remover
in addition to your normal lens cleaning regime
before the journey.
3. If you are a frequent flyer, avoid using high water
contact lenses because this type of lens dries and
distorts easier. Materials such as silicone hydrogel
or rigid gas permeable lens may help.
4. Contact l ens care systems which contain
moisturizing agents as HPMC and Propylene Glycol
can create a shield of moisture between the lens
and the eye, to ensure prolonged lubrication. For
sensitive eyes, a hydrogen peroxide system may
help in reducing irritation.
5. Use lubrication drops during the flight. A lubricating
eye drop containing sodium hyaluronate, has been
proven to effectively reduce dry eye symptoms.
Use a preservative-free formula for sensitive or
allergy-prone eyes.
6. Carry a pair of spectacles with you. If dryness
persists, remove the lenses and wear the spectacles.
7. Under new flight security regulations, there are
limitations on carrying liquid over 100 ml per
container in hand baggage. In this case, you can
carry a contact lens case containing fresh multi-
purpose contact lens solution. If you experience
any discomfort, simply remove your lenses and
place them in the lens case.
8. In desert, beaches and tropical countries it is very
important to use sunglasses with U-V protection.
Make sure the label states that the lenses block 99
to 100 percent of both UVA and UVB rays. When
you are driving the sunlight can reflect from the
road pavement, or when you are shipping, the
water like the snow in skiing, can burn the eyes
surface.
DIRECT TRAUMATIC INJURIES
In a study published in 1998 by the Flight Safety
Foundation,
5
there are an estimated 4,500 incidents
of injuries from falling baggage each year in the U.S.
and about 10,000 such events worldwide. Baggage
can emerge uncontrol l ed from overhead
compartments if the contents shift in flight or if the
compartments were loaded beyond their capacity. This
study was based on a survey of 462 falling baggage
events on the 757 aircraft of an unnamed major U.S.
airline. Of these 462 events, which occurred during
the mid-1990s, a person was struck in 397 cases. In
those cases where a person was struck, there were 67
injuries involving bruising, 53 injuries involving
lacerations, and 277 cases resulting in no injuries. More
than 90 percent of the injury cases involved head
injuries to aisle seat passengers.
In automobile trips we have to consider the air bag,
an inflatable device designed to decrease the morbidity
associated with high speed vehicle collisions. Front air
bags, for the driver and right-front passenger, mainly
provide protection against head contact with the
288
steering wheel and dashboard. They are designed as
supplementary restraint systems (SRS), meaning that
the protection they provide is in addition to that offered
by the use of a regular lap-and-shoulder seat belt.
Because air bag deployment happens so rapidly,
it is extremely important that vehicle occupants should
not be too close to the air bag modules. These are
generally located in the steering wheel hub and the
upper right-front dashboard. There would be significant
risk of head, neck and chest injury if an occupant were
to be struck by the flaps of the air bag cover as they
open (punch out), or by the rapidly expanding fabric
of the bag as it is inflated (membrane loading). Most
agencies recommend that occupants should be at least
25 cm (10 inches) away from the air bag module.
Child passengers in the right-front seat of vehicles
equipped with air bags are of particular concern. Rear-
facing infant carriers should never be installed in the
right-front seat when there is an air bag. This would
place the childs head much too close to the passengers
air bag module. Many children have been killed or
seriously injured in this manner. Similarly, most agencies
recommend that children aged 12 and under should
be seated in the rear of the vehicle with an age-
appropriate restraint system (infant carrier, child seat,
booster cushion and seat belt). Children frequently dont
sit still in vehicles. They will often sit on the edge of
their seat, lean forward, and may even slip their body
out of the seat belt or child restraint harness. If a child
were to do this in the right-front passengers seat at
the very instant that a collision occurred, they would
be out of position and too close to the air bag, and
this could easily result in serious injury or fatality.
6
Corneal injuries have been frequently reported in
adults in association with air bag deployment.
7
This
type of corneal injuries may resul t from two
mechanisms. The first is a chemical keratitis resulting
from exposure to the alkaline sodium azide gas that
is used to inflate the air bag. The second mechanism
is blunt impact between the eye and the air bag.
8
Figure 46.1 shows a blunt eye trauma after air bag
deployment.
9
It is difficult to determine the true incidence and
range of severity of these ocular injuries for two reasons.
First, patients involved in motor vehicle accidents may
have multiple systemic injuries, and ocular trauma may
therefore not be recognized. Second, a bias of
ascertainment exists, in that severe ocular injuries are
more likely to be reported than the minor injuries.
Few case series of air bag-related ocular injuries have
been reported, and these also are biased towards severe
injury.
10
Such injuries range from relatively mild (e.g.
corneal abrasions, eyelid ecchymosis) to severe (e.g.,
hyphema, lens injury, retinal detachment and angle
recession).
11
Figure 46.2 shows a case of a man who
sustained an airbag-induced face and periorbital injury.
It highlights the potential harm that can be caused by
airbags.
9
Fig. 46.2: Airbag-induced face and periorbital injury
(From: Spoor TC)
Fukagawa et al
12
demonstrated corneal endothelial
cell damage in an animal model of blunt ocular air bag
injury. In this model, porcine eyes were placed in the
orbits of a crash-test dummy and exposed to deploying
air bags at different distances, air bag weights, and bag
inflation powers. Histopathologic examination of the
corneas after air bag inflation revealed damage to the
corneal endothelial cell membranes and exposure of
Descemets membrane, consistent with detachment of
Descemets membrane or endothelial cell loss.
Air bag associated ocular injuries have only rarely
been described in children.

In a retrospective study,
Lueder
10
reviewed the medical records of seven
children who were injured by air bags and concluded
Fig. 46.1: Airbag-related blunt eye trauma
(From: Spoor

TC)
289
Management of Travel Eye Injuries
that serious ocular injuries may result, although most
injuries heal without detrimental long-term effects.
However, there can be serious consequences if the
child is too close to the air bag when it deploys. The
most serious injuries in these children were cataracts
and glaucoma. Other injuries were blood in the front
chamber of the eye, alkali bum, temporary loss of
consciousness and visual acuity, eyelid laceration, black
eye, swelling and hemorrhaging of the blood vessels
under the outer surface of the eyeball, corneal lesions
and abrasions, and iris inflammation. Figure 46.3
shows the right eye of a 4-year-old boy seriously
injured after a vehicle (Fiat Uno) lateral crash. The
child was unbelted and seated in the rear of the car.
His eye was hit by fragments of glass from the broken
side window.
Chemical eye injuries may also affect travelers, and
they are potentially blinding injuries.

If chemicals are
splashed into the eye, the eye and the conjunctival
sacs (fornices) should be washed out immediately with
copious

amounts of water. Alkali injuries are more
common and can be more deleterious. Bilateral
chemical exposure is especially devastating, often
resulting in complete visual disability. Immediate,
prolonged irrigation, followed by aggressive early
management and close long-term monitoring, is
essential to promote ocular surface healing and to
provide the best opportunity for visual rehabilitation.
Fig. 46.3: Operating microscope view of a corneal laceration
in the right eye of a 4-year-old boy after a lateral car crash.
There was a significant hyphema (iris details are obscured),
soft globe, expulsion of the lens and iris extrusion
Conclusion
Eternal vigilance is the price of safety. The greatest
deterrent to ocular injury is educated awareness of
risk and careful avoidance procedures. Trauma, usually
needless, continues to be one of the major causes of
lost eyes. Automobile crashes continue to be one of
the most common causes of death from age 1 to 24
years. Males distinctly predominate in the statistics of
ocular injury and are increasingly represented in motor
vehicle crash. Proper and complete assessment of any
patient with ocular trauma is the basic prerequisite for
anatomical and visual rehabilitation of a patient with
ocular trauma.
References
1. Rappon JM. Ocular Trauma Management for the Primary
Care Provider. In: www.opt.pacificu.edu. Accessed June
15, 2008.
2. White MF Jr, Morris R, Feist RM, Witherspoon CD, Helms
HA Jr, John GR. Eye injury: Prevalence and prognosis
by setting. South Med J 1989;82(2):151-8.
3. Wong Gunter.In: Leaving on a Jet Plane- Tips for
contact l ens wearers who travel on a pl ane.
In:www.useronline.org. Accessed June 15, 2008.
4. Aslam SA, Sheth HG, Vaughan AJ. Emergency manage-
ment of corneal injuries. Injury 2007;38(5):594-7.
5. Rozmaryn L. Head Injury risks from overhead luggage.
The AirSafe J 1999;13.
6. Braver ER, Ferguson SA, Greene MA, Lund AK.
Reductions in deaths in frontal crashes among right front
passengers in vehicles equipped with passenger air bags.
JAMA 1997;278:1437-9.
7. Smally AJ, Binzer A, Dolin S, Viano D. Alkaline chemical
keratitis: eye injury from airbags. Ann Emerg Med
1992;21:1400-2.
8. Ingraham HJ, Perry HD, Donnenfeld ED. Airbag Keratitis.
N Engl J Med 1991;324:1599-600.
9. Spoor TC. An Atlas of Ophthalmic Trauma. Editora
Manole Ltda, Sao Paulo, Brasil, 1999;3:35-44.
10. Lueder GT. Airbag-associated ocular trauma In children.
11. Driver PJ,Cashwell LF,Yeatts RP. Air bag associated
bil ateral hyphemas and angl e recession. Am J
Ophthalmol 1994;118:250-51.
12. Fukagawa K, Tsubota K, Kimura C. Corneal endothelial
cell loss induced by air bags. Ophthalmology 1993;100:
1819-23.
C H A P T E R
47
Ocular Injuries after Vehicular
Accident and Possible Prevention
Bojan Pajic, Brigitte Pajic-Eggspuehler, Jasna Ljubic (Switzerland)
Introduction
Constructional improvement of passengers safety in
cars alone did not result in a significant decline of open
globe injuries in traffic accidents. Only after compulsory
seat belt legislation was introduced, a 60-70%
reduction in ocular injuries was observed. Emerging
statistics have revealed seat belts to be the primary
occupant safety system, and use of seat belts along
with airbags has provided a cumulative reduction in
adult accident injuries and fatalities. Airbags gained
widespread popularity as an effective means of
reducing severe injury and death during motor vehicle
accidents in the late 1980s. Airbags on both the driver
and passenger side are mandatory on all 1998 and
later-model cars and in 1999 and later light trucks.
With use of both airbags and seat belts, fatalities have
been reduced 50% in all types of crashes. Fatalities
have been attributed to the airbag deployment, many
occurring during slow-speed crashes. The purpose of
this investigation is to examine data reported in the
numerous case studies of ocular injuries attributed to
airbag depl oyment in order to gain a better
appreciation of the scope of ocular damage and to
identify individuals more susceptible to such injuries.
When travelling in the right front passenger seat during
frontal crashes, adults have a significantly lower
mortality risk when airbags are deployed, but children
have a substantially increased mortality risk.
1
Ocular
injuries associated with airbag deployment have been
reported in many adults.
2-19
The Airbag System
The airbag is a coated nylon bag housed within the
steering column on the driver side and within the
dashboard on the passenger side.
20
Sensors located
within the vehicle structure are activated when a crash
occurs at 19.3 km/h or faster and within a 60 frontal
arc. An electrical signal is sent to the airbag cartridge,
which contains a combustible solid-state powder,
usually sodium azide (NaN
3
), and an oxidizing agent.
21
The combustion of sodium azide produces mostly inert
nitrogen gas, but other byproducts include ammonia,
carbon dioxide, nitric oxide, carbon monoxide, an
alkaline aerosol containing sodium hydroxide, and
various metallic oxides. An inert talc powder used in
packaging also is discharged. Heat is an additional by-
product of the combustion process. The expanding
bag splits the plastic casing and is propelled out of the
storage compartment at 160 to 320 km/h, depending
on the manufacturer. The entire inflation sequence is
completed within 0.05 seconds (Table 47.1). The
airbag capacity varies widely, but most fully inflated
bags contain 60 L of gas on the drivers side and 140
L on the passengers side. The driver-side airbag
expands to a depth of 25 to 30 cm. The passenger-
side airbag expands to a greater depth. Some bags
are tethered, others are not. A tethered bag contains
one or more straps that limit its anterior-posterior
expansion. The airbag quickly begins to deflate through
vents directed away from the occupant. Systems vary
widely between vehicle models. The purpose of the
airbag is to cushion the occupant from the rigid
components of the vehicle interior. In order to provide
the desired cushion, the airbag should expand with
sufficient speed to be fully inflated before the occupant
moves forward following impact. Occupants who are
positioned too close to the wheel may be caught within
the envelope of the expanding airbag. Even when
TABLE 47.1: Airbag inflation sequence
Time (sec) Action
0 Frontal impact
0.015 Sensors signal to cartridge NaN3 ignited
Bag inflation begins
0.05 Bag fully deployed
0.06 Occupant strikes fully inflated bag
1-2 Bag deflates
291
Ocular Injuries after Vehicular Accident and Possible Prevention
properly belted, occupants will move forward, although
to a lesser degree. In any motor vehicle accident there
are at least 2 collisions: the vehicle with the object of
impact and the occupant with the airbag or car interior.
Usually a third, or rebound, collision also occurs.
Methods
The investigators performed an exhaustive review of
the literature of peer-reviewed papers published
between 1991 and 2008 that described ocular injuries
related to airbag inflation or car accident. Furthermore,
own experience are insert in this review study. Each
of the paper, inclusively the own data, that formed
the database for this study was reviewed, and
information pertaining to the following variables was
extracted from each article and recorded on a SPSS
spread sheet: patient age, sex, position in the vehicle
(driver or front-seat passenger), patient height, eye
wear (if any) worn by the patient at the time of the
accident, eyes injured, last reported visual acuity, seat-
belt use at the time of the accident, the object of impact,
speed of the vehicle at impact, and all ocular injuries
resulting from the accident. Heights reported in inches
were converted to centimeters, and speeds reported
in mph were converted to km/h.
Results
Review of the literature from 1991 to 2008 and own
data identified describing 518 patients with ocular
injuries accident deployment during a motor vehicle
accident.
1-51
PATIENT PROFILE
343 (66.2%) of the injured occupants were male, and
175 (33.8%) were female. The age of the patients
varied between 1 and 83 years, with a mean age of
25.5 years. 70.5% of patients were wearing three-point
seat belts, 29.5% were known to be not belted.
OCULAR INJURY PROFILE
55.3% of occupants sustained injuries limited to the
anterior segment of the eye, 31.7% to both anterior
and posterior segments and 13% to the posterior
segment.
ANTERIOR SEGMENT INJURIES
Corneal abrasion occurred in 163 of the total database
of 518 patients, and hyphema was reported in 105
of occupants (Table 47.2). A cataract was present
in 151, and the lens was dislocated or subluxated in
101 of patients. Angle recession was found in 21 and
chemical keratitis in 12. The integrity of the globe was
compromised in 63 of patients. Most of these ruptured
globes sustained significant damage to many ocular
structures with resultant poor vision. As might be
anticipated, injuries to the periorbital area (7.5%) were
common and included lacerations, burns, and
contusions. Some lacerations required skin grafting and
plastic repair. Other anterior segment injuries included
traumatic iritis (2.5%), iris tear (2.5%), orbital fracture
(2.9%), and facial nerve palsy (0.2%).
POSTERIOR SEGMENT INJURIES
Retinal or vitreous hemorrhage occurred in 15.5% of
injured occupants (Table 47.3). Retinal tear or
detachment (11%) and commotio retinae (3.1%) were
also common. Other traumatic injuries reported were
macular hole (0.8%), choroidal rupture (1%),
traumatic maculopathy (2.9%), and optik disc edema
(0.2%). Most likely, these patients also sustained
anterior segment injuries, but they were not docu-
mented.
VISUAL ACUITY
Best-corrected visual acuity at the last examination with
a mean follow-up time of 6.5 months was as follows.
In 9.19% a enucleation had to be performed. 13%
TABLE 47.2: Anterior segment injuries
No of patients % patients
Corneal Abrasio 163 31.5
Hyphema 105 20.3
Eyelid laceration, burn,
periorbitale contusion 39 7.5
Iritis 13 2.5
Iris tear 13 2.5
Cataract 151 29
Angle recession 21 4
Corneal/scleral laceration/
ruptured globe 63 12.2
Chemical keratitis 12 2.3
Lens dislocated/subluxated 101 19.5
Orbital fracture 15 2.9
Facial nerve palsy 1 0.2
TABLE 47.3: Posterior segment injuries
No of patients % patients
Vitreous/retina hemorrhage 80 15.4
Retina tear/detachment 57 11
Commotio 16 3.1
Macular hole 4 0.8
Choroidal rupture 5 1
Traumatic maculopathy 15 2.9
Optic disc edema 1 0.2
292
had no light perception. 4.81% there was light
perception. 7.79% of patients had a visual acuity of
less than 0.05. 2.41% had a final visual acuity of 0.01,
12.63% had a best-corrected visual acuity of less than
0.4, 24.32% had less than 0.7 and 25.85% had a
final visual acuity of less than 1.0 (Fig. 47.1).
In the age group of 18 to 22 years old has the
highest risk of injury. The most number of accidents
(85%) were during the night, it is said between 18.00
and 06.00 oclock and during winter time, from
October to March. 17.9% patients admitted that, at
the time of the accident, they were under the influence
of alcohol.
Discussion
A 58 to 73% reduction of penetrating ocular injuries
occurred when use of a car seat belt became obli-
gator.
54-56
The seat belt protects the eye from injury
as it prevents the forward movement of the body and
consequently the possible hit of the head against the
windshield of the car.
Airbags are most effective in preventing fatal driver
injury in pure frontal crashes but also are effective in
10 oclock to 2 oclock frontal arc crashes. They play
no role in side, rear, or rollover crashes. In crashes
of all types, the airbag and seat belt combination
reduced fatalities 50 compared with unbelted drivers
in a passenger car without an airbag (Table 47.4).
The airbag alone reduced driver fatality 13%, and the
seat belt alone, 45%.
20
NHTSA has calculated the
effectiveness of occupant protective systems in reducing
moderate and serious driver injury in frontal crashes
compared with unbelted drivers with no airbag
(Table 47.5). The airbag is less effective than a
combination of seat belt and airbag or the seat belt
alone.
NHTSA reported 113 fatalities attributed to airbag
deployment as of September 1,1998.
57
Forty-seven
were adults, only 13 of whom were properly restrained.
Fifteen infants in passenger-side rear-facing car seats
were killed. The infants head was too close to the
expanding bag. Fifty-one children aged 1 to 12 were
killed, none of whom were properly restrained.
Children should be in the back seat and belted! The
Insurance Institute for Highway Safety updates these
statistics periodically.
58
Spontaneous deployment of
airbags also has been reported.
59
Several large-scale
recalls have occurred because of the potential threat
of spontaneous airbag deployment. Occupants
positioned within 25 centimeters of the wheel or
dashboard cannot avoid being injured.
NHTSA has permitted manufacturers to depower
the airbag by 20 to 35%.
20
Depowering the bag should
reduce airbag-induced injuries in smaller and average-
sized occupants but may place larger individuals at
increased risk of injury, particularly during high-speed
crashes. Side airbags already have been placed in the
newer car models. Concern has been expressed for
passenger-side children as well as adults resting against
the door. So-called smart bags are being developed.
The next generation of sensors will enable the airbag
to deploy according to the severity of the impact, the
proximity of the occupant to the bag, and the weight
and height of the occupant. The development of this
technology is ongoing and will be phased in over the
next few years.
Seat-belt performance varies greatly between
manufacturers. The configuration of airbags and their
speed and pattern of deployment vary by model and
manufacturer. These factors, which are very important
to the safety engineer, could not be documented in
these cases. Although the airbag deployment and the
eye injury seem to be cause and effect in most cases,
other elements, such as collision with the rear-view
mirror, side window, or loose articles within the car
interior, may have played a role. These precautions
not withstanding, this investigation serves to increase
the awareness of the role of occupant safety systems
in motor vehicle accidents and to document air-bag-
Fig. 47.1: Visual acuity distribution after injuries
TABLE 47.4: Estimated effectiveness of occupant
protection system in reducing fatality risk for passengers
and drivers in all types of crashes
System used Fatality Reduction
Air bag+lap-shoulder belt 50%
Air bag alone 13%
Manual lap-shoulder belt 45%
TABLE 47.5: Estimated effectiveness of occupant
protective systems in reducing injury
Injury severity System used front damage
Moderate Air bag+lap-shoulder belt 61%
Air bag alone 6%
Serious Air bag+lap-shoulder belt 69%
Air bag alone 8%
293
related eye injuries and the factors associated with their
occurrence.
The majority of the ocular injuries in this series are
the result of blunt trauma between the occupant and
the airbag, in either its expanding phase or its fully
inflated status. Obviously, a greater impact force will
be generated when a forward-moving eye strikes an
expanding bag. Penetrating injuries and alkali burns
are exceptions to the blunt trauma mechanism.
27, 32,
47
Severe blunt trauma has been shown experimentally
to decrease the anterior-posterior diameter of the globe
by 41%.
60
Reduction of the anterior-posterior diameter
of the globe beyond 60% will result in rupture.
61
The
flattening of the anterior chamber may cause the
corneal endothelium to come in contact with the iris
and anterior surface of the lens. There is an expansion
of the equatorial diameter of the globe. Severe traction
on the vitreous base develops during the initial phase
following impact.
61
This has been demonstrated
experimentally with pellet guns and is believed to
explain much of the ocular damage sustained in
nonperforating BB gun injuries.
62
Most of the ocular
injuries to the iris, angle, lens, vitreous, retina, and
choroid documented in this study are compatible with
a blunt trauma injury mechanism.
63
It has been shown
that the airbag dramatically decreases brain injury in
motor vehicle accidents.
20, 24
The combination of airbag
plus a lap-shoulder belt reduces the risk of moderate
and serious head injury to drivers in frontal crashes
by 75%, compared with a 38% reduction for seat belts
alone. However, the brain is fully encased by rigid
bone. The eye has an open surface.
A great deal of publicity has been given to the
increased risk of airbag injury to individuals of small-
stature who, presumably, are positioned closer to the
steering wheel. Many of the reports reviewed in this
investigation mention this circumstance. NHTSAs
comprehensive report contains information suggesting
that occupants of small-stature are at greater risk of
injury.
20
While this sounds very reasonable, hard data
are lacking. Driver position in relation to the steering
wheel is more important than actual stature.
The corneal abrasions are the result of impact with
the airbag, either directly or in an abrasive slap
motion from an unfolding bag. Most of the corneal
surface often is involved. Generalized stromal edema
and folds in Descemets membrane frequently are
present. One investigator described the imprint of the
airbag on the cornea. The imprint of an open eye,
complete with eye shadow, mascara, and lashes has
been seen on the airbag. The airbag deploys quicker
than a blink. Fortunately, most corneal abrasions heal
without sequellae, although a decreased endothelial
cell count has been demonstrated experimentally and
clinically.
14, 29, 65
In one patient with irreversible bullous
keratopathy, a corneal transplant was required.
13
Burns
have been estimated to occur in 7.8% of all injuries
associated with airbag deployment.
25, 66
Burns may be
due to vented hot nitrogen gas or melting of clothing
or may be chemical in origin.
67
Chemical keratitis is
the result of corneal contact with the ammonia, sodium
hydroxide, and the alkaline aerosol that are emitted
as by-products of the combustion of sodium azide,
which is used to inflate the airbag.
2, 68
While the hot
nitrogen gas and the by-products are vented away
from the occupant, accident circumstances may bring
the alkali into contact with the eyes. Resulting burns
will depend on the amount and duration of corneal
exposure to the alkali.
Hyphema injury, along with angle recession, is the
result of the sudden increase in pressure created by
the flattening of the anterior chamber following. The
aqueous has nowhere to go and dissects the angle
and iris root.
63
Most hyphemas absorbed. The long-
term potential complication of angle recession
glaucoma should be discussed with patients.
The majority of developed cataract were described
as an opacification of the anterior capsule and cortex.
They are the result of contact between the corneal
endothelium and the anterior lens surface. The integrity
of the lens capsule was compromised in other cases,
leading to more severe opacification. Dislocation and
subluxation of the lens are the result of zonular rupture
secondary to deformation of the globe. Bilateral lens
dislocation occurred in one case.
38
The rapid horizontal expansion of the globe at the
vitreous base creates traction that results in retinal breaks
and dialysis in this area.
62, 64
Several clinical studies have
demonstrated the preponderance of retinal damage
associated with blunt trauma to occur at the ora serrata
and vitreous base.
69-71
The position of the retinal tears
and detachments in this study was not described in
sufficient detail to allow further speculation on an
airbag trauma pattern. All patients with air-bag-related
injuries should have a thorough indirect ophthalmo-
scopic examination when possible and ultrasound
examination in those cases in which vitreous hemor-
rhage or hyphema prevents adequate visualization.
Commotio retinae and macular holes injuries are the
result of a countercoup-type force commonly found
in blunt trauma to the globe.
63
Likewise, those patients who have undergone
refractive surgeries, including RK, PRK and LASIK, are
also more at risk for development of severe ocular
injuries, secondary to compromised corneal integrity.
72,73
The airbag is appropriately labeled SRS (Supple-
mental Restraint System). The best way to reduce the
294
risks of injury from the car interior or the airbag in
a motor vehicle accident is to wear a seat belt and
be properly positioned 25 centimeters or more from
the wheel. Children should be in the back seat and
belted.
References
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Reductions in deaths in frontal crashes among right front
passengers in vehicles equipped with passenger airbags.
JAMA 1997;278:1437-9.
2. Smally AJ, Binzer A, Dolin S, Viano D. Alkaline chemical
keratitis: eye injury from airbags. Ann Emerg Med
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C H A P T E R
48
Bottle Cork Injury to the Eye
Gian Maria Cavallini, Matteo Forlini, Cristina Masini
Luca Campi, Simone Pelloni (Italy)
Introduction
In the field of blunt ocular trauma the bottle cork injury
of the eye can cause severe damage to the globe with
secondary loss of visual function that can be permanent
as we observed in the literature and in the series we
report.
Various studies show the dangerous effect of
pressurized fluid, well-known even under normal
circumstances.
1,2
Sellar and Jonhston
3
highlight the
serious nature of these injuries in Britain pointing out
the danger of glass bottles containing carbonated
drinks, especially to young children. In his review of
the databases of the United States (USEIR), Hungarian
(HEIR), and Mexican (MEIR) eye injury registers,
Kuhn
4
reports that whilst most eye injuries caused by
bottles containing carbonated drinks improved, in 26%
of cases the patient remained legally blind. Another
work describes ocular injuries caused by bottle caps
in Israel.
5
Archer and Galloway
6
reviewed the medical records
of nine patients consecutively diagnosed with
champagne cork eye injuries over a 4-year period.
A cork ejected from an upright bottle can reach a
height of 12 meters and strikes the eye at a speed
of about 15 meters per second. When the diameter
of a blunt object is smaller than that of the orbital rime,
as in the case of a bottle cork, the full impact of the
shock wave is borne by the globe, without any of it
being absorbed by the orbital bony structures.
Shooting a bullet of 0.345 grams of weight against
a pig eye at a speed of 66.44 m/sec (chosen in order
to gain a kinetic energy lower than that able to rupture
the globe) the anteroposterior diameter can decrease
to 59% during the compression phase and simul-
taneously an expansion of the equatorial diameter can
reach 128% of the normal length and a flattening of
the posterior pole occurs (Delori and Pomerantzeff
experiments).
7
During this compression phase huge
tractional forces develop at the vitreous base, at the
periferic retina and at the macular region. Following
the compression phase, a decompression can be
observed and the antero-posterior diameter becomes
longer than the original one due to oscillatory forces
depending on various factors such as the intrinsic
elasticity of the tissues involved. In this phase, the eye
structures are stretched and if the elasticity is lower
than the oscillating forces the eye tissues may rupture.
An acute increases in vitreo-retinal traction is
produced from the expansion, which often results in
retinal dialysis. Traumatic retinal dialysis most
commonly occurs inferotemporally and superonasally.
It can occur at the anterior margin of the vitreous base
in the pars plana at the junction of the ciliary epithelium
and neural retina, or in the retina at the posterior
margin of the vitreous base.
8
In another situation a direct contusion injury to the
globe can lead to disruption of the retina and necrotic
breaks. One common finding with blunt injuries, which
may lead to acute visual loss is Berlins edema
(Commotio retinae).
9
The scleral spur is also involved
and intraocular pressure (IOP) is raised.
This type of domestic injury is considered as being
unusual and is often underestimated, however it can
be the cause of disabling functional sequelas.
The incidence seems to be higher in regions with
large-scale production and sale of sparkling wine. This
kind of wine induces fermentation inside the bottle,
resulting in a rise in pressure that can reach 4
atmospheres, high enough to release an expulsion
speed of at least 15 m/sec; this means that the cork
reaches the eye in less than 0.1 sec (faster than blinking
reflex), from an average distance of 40-50 cm with
a strength of impact of about 100 atmospheres.
6
A bottle cork can damage the ocular structures of
the anterior and posterior segments, both directly in
the impact area and also through a counterblow effect.
This particular type of eye injury is characterized
by a compression phase and rapid decompression with
lengthening of the antero-posterior axis beyond the
physiological range, causing sudden distortion of the
297
intraocular structures that can result in various different
lesions (Fig. 48.1).
From an analysis of different kinds of bottle corks,
the plastic ones were found to ensure good tightness
on account of their inherent tension, so that when the
bottle is opened a kind of explosive discharge of energy
is released. On the contrary, the natural cork expands
inside the bottle because of the inner damp ambient
and its discharge is consequently less violent.
A particular type of sparkling wine is manufactured
in the province of Modena, which ferments, generating
pressure inside the bottle that can cause the ejection
of the cork similar to that of a bottle of champagne.
In Modena University we collected a series of 34
consecutive cases of bottlecork eye injury admitted
to the Ophthalmology Institute of Modena in the last
8 years that needed hospitalization. We assessed the
anatomic and functional consequences of the injury
in a retrospective study.
10
Of the cases of eye injury admitted to our
department in this 8-years period, 11% were bottle
cork injuries, 13% were occupational accidents, 5%
were road accidents, 13% were sport injuries, 23%
were domestic accidents, and other types accounted
for 35%.
In all cases the bottle cork or cap hit the eye of
the person opening the bottle, did not involve
bystanders in any case. Sparkling wine was involved
in all cases: white in 71%, and red in 29%; 38% of
the bottles were homemade wine and 62% were
commercial. The types of cork were as follows: 38%
stoppers without wire, 32% corks and 30% metal
crown caps.
About seasonal distribution, theres a greater
incidence in January, on account of the holiday period,
and in October, due to wine fermentation which
infl uences the internal pressure of the bottl e
(Fig. 48.2). All cases are closedglobe injury according
to Kuhns classification.
11,12
Clinical Features
The clinical features more frequently observed are:
Hyphema (79%) (Figs 48.3 and 48.4)
Corneal edema (59%)
Periferic retinal edema (24%)
Subl uxation of the crystal l ine l ens (21%)
(Fig. 48.5)
Retinal hemorrhage (18%)
Iridodialysis (15%) (Fig. 48.6)
Retinal tear (9%)
Posterior pole retinal edema with macular involve-
ment causing a poor vision acuity (6%)
Retinal detachment (6%)
Complete displacement of the IOL (3%)
Traumatic cataract (3%)
Fig. 48.1: Compression > decompression > passing beyond primary position
Fig. 48.2: Month-by-month distribution of
bottle cork eye injuries
298
Fig. 48.3: Hyphema
Fig. 48.4: Hyphema
Fig. 48.5: Lens subluxation
Fig. 48.6: Iridodialysis
Sequelas are:
Pupil motility anomalies (21%)
Traumatic cataract (21%)
Post-traumatic ocular hypertension (6%)
Maculopathy (3%)
Optic neuropathy (3%)
Treatment
In most of the cases the treatment consists of general
medical practice and use of local anti-hemorragic and
anti-inflammatory medication.
In some cases it can be necessary to treat the ocular
hypertension with carbonic anhydrase inhibitors
administered generally and with beta-blockers
administered locally.
Surgical treatment is necessary in the most severe
cases:
If a lens luxation occurs it is necessary to perform
a complete Via Pars Plana Vitrectomy, preferably with
Posterior Hyaloid removal, and make a secondary IOL
scleral fixation. Recently, the approach can be done
with transconjunctival mini-invasive (25, 23G)
strategies. In these cases a Iris fixation secondary
implantation could be the gold standard, avoiding in
this way to open the conjunctiva.
In case of traumatic cataract, a phacoemulsification
coul d be difficul t depending on the grade of
subluxation. If vitreous is in anterior chamber, a
vitrectomy is necessary, via limbus or via pars plana,
using preferably a mini-invasive (25, 23G) approach.
In presence of retinal detachment, after an accurate
examination we can choose for an episcleral approach
or for internal approach with vitrectomy: in the last
situation the choice of the tamponade agent depends
on the retinal situation and the preferences of the
surgeon.
The iris injuries need adequate iris plastic surgery,
even if many cases of iridodialysis, usually well limited,
dont need surgical treatment.
Prevention
In most of the cases visual acuity on admission was
generally very low, and although most patients made
an almost complete recovery, very severe visual
impairment was observed in others.
299
These cases prove that bottle cork eye injury can
involve very severe traumas, although most patients re-
cover almost totally with appropriate medical treatment.
More information and prevention is needed,
particularly in certain periods of the year and in specific
areas of the country. It is advisable to fit bottles with
safety devices and/or include captions describing the
hazard posed by bottle caps/corks.
4
Moreover, the
introduction of a standardized type of screwable cork
could be effective in preventing ejection. Alternatively
the use of a contention system, connecting the cork
to the bottle neck with a wire, could represent another
preventive possibility.
References
1. Al Salem M, Sheriff SMM. Ocular injuries from carbonated
soft drink bottle explosions. Br J Ophthalmol 1984;
68:281-3.
2. Gupta AK, Nadiger M, Moraes O. Ocular injury from a
carbonated beverage bottle. J Pediatr Ophthalmol
Strabismus 1980;17:394-5.
3. Sellar PW, Johnston PB. Ocular injuries due to exploding
bottles of carbonated drinks. BMJ 1991;303:176-7.
4. Kuhn F, Mester V, Morris R, Dalma J. Serious eye injuries
caused by bottles containing carbonated drinks. Br J
5. Koval R, Teller J, Belkin M, Romem M, Yanko L, Savir
H. The Isaraeli ocular injuries study. A nationwide
collaborative study. Arch Ophthalmol 1988;106:776-80.
6. Archer D, Galloway NR. Champagne-cork injury to the
eye. Lancet 1967;2:487-9.
globe under high-speed impact: its relation to contusion
injuries. Invest Ophthalmol 1969;8:290-301.
8. Greven CM. Retinal Breaks. In: Yanoff M, Duker JS (eds)
Opthal mol ogy. Mosby, Phil adel phia, section 8,
1999;38.2.
9. Rubsamen PE. Posterior Segment Ocular Trauma. In:
Yanoff M, Duker JS (eds) Opthalmology. Mosby,
Philadelphia, section 8, 1999;43.2-3.
10. Cavallini GM, Lugli N, Campi L, Pagliani L, Saccarola P.
Bottle cork injury to the eye: a review of 13 cases. Eur
J Ophthalmol 2003;13(3):287-91.
11. Kuhn F, Morris R, Witherspoon CD, Heimann K, Jeffers
JB, Treister G. A standardized classification of ocular
trauma. Ophthalmology 1996;103(2):240-3.
12. Pieramici DJ, Sternberg P Jr, Aaberg TM Sr, Bridges WZ
Jr, Capone A Jr, Cardillo JA, de Juan E Jr, Kuhn F,
Meredith TA, Mieler WF, Olsen TW, Rubsamen P, Stout
T. A system for classifying mechanical injuries of the eye
Ophthalmol 1997;123(6):820-31.
C H A P T E R
49
Ocular War Injuries
Jaroslaw Kulinski, Karol Stasiak, Marek Prost (Poland)
Introduction
In our times of global terrorism the occurrence of
injuries caused by the explosives is not limited only
to the battlefields but also to the countries which do
not wage war. Very often civilians in seemingly peaceful
cities are more frequently victims of such a trauma
than military personnel on the modern battlefield. So
speaking about war injuries that this description
should be nowadays applied not only the soldiers but
also to the civilians.
Eyes occupy only 0.29% of the body surface and
4% of the face surface. However, ocular injuries are
extremely important health problem, because of their
predominating role in perception. Despite the fact that
eyeballs are relatively small organ, their direct injuries
are usually extensive and severe. It is due to the short
distance and proximity of the explosives. They are
mainly caused by the explosive wave and objects of
different size colliding with the human body with very
high speed and kinetic energy. Even with small
diameter such factors may produce severe ocular
damages. They results not only in extensive injuries
but also in severe functional outcomes (Fig. 49.1).
It is estimated that ocular injuries are bilateral in 15
to 25% of cases.
Fig. 49.1: Eye-bulb atrophy in a soldier after blunt
ocular trauma during Iraqi operation
Percentage of soldiers who experienced ocular
injuries is increasing with the consecutive wars and
military conflicts. Inaccurate data indicate that this
percentage accounted for about 1.5 to 2% during the
I World War, about 2 to 3.3% during the II World War,
3 to 8% during the Korean War, 5 to 9% of casualties
in Vietnam, about 10% in Arab-Israeli War and 13%
of Iraqis operations. (Ari 2006, Homblass 1981, Heier
et al, 1993, La Plana et al 1997, Mader et al 1993).
Various authors state that ocular injuries connected
with military operations (wars, terrorist actions,
landmine clearing) accounts for 16% of all injuries.
It is due to an increase in head trauma by about 40%
in 1982-2005, compared to an increase of all injuries
and wounds by 12% (Rustemeyer et al 2007).
One should bear in mind that the first specialist
ophthalmologic aid may be delayed during the war.
Despite usually efficient medical evacuation medical
help is not always possible immediately after trauma.
Moreover, war injuries frequently involve several
organs, additional l y del aying ophthal mol ogic
examination and treatment.
Field hospital should be equipped with basic
ophthalmologic devices, enabling examination of the
globe anterior segment and eye fundus in the slit lamp.
Physician-ophthalmologist, ophthalmologic technician
or optometrist should carry out examination of the
eyes. Very important is access to the split lamp in
examination room of the field hospital. This lamp
enables preliminary evaluation of the degree and
severity of trauma and decision on the further
diagnostic and therapeutic procedures. Some field
hospitals are also equipped in teleconsultaion system.
Help of specialists from other health care centers is
possible in some difficult cases.
Demographic characteristics of patients reporting
to the field hospital with eye diseases depend on the
type of military operations in the said region. Bancroft
and Lattimore saw only 48 (3%) patients with ocular
injuries out of 1471 patients who reported to the
301
Ocular War Injuries
ophthalmologic service in the transportation base
support hospital during 9 months in 1995 (Bancroft
et al 2001). Remaining 168 (11%) patients presented
with ocular diseases, requiring an intensive treatment.
Nine patients required evacuation from the military
operation region but not necessary surgical treatment
in other specialist centers. However, this hospital was
located some hours of drive from the front line.
Statistics cited by the authors working in vicinity
of the military operations are far worse. Thach et al
noted 797 severe ocular injuries, including as many
as 438 open globe injuries, in the war in Iraq during
34 months (from March 2003 to December 2005)
(Thach et al 2008). Enucleation was performed in 116
cases, including 6 patients with bilateral enucleation.
Heier reported 108 (14%) patients with ocular injuries
out of 767 wounded, including 20 patients had to be
evacuated for further specialist treatment, during
Operation Desert Storm (1990-1991) (Heier et al
1993). Retrospective study carried out by Muzaffar
et al. a total of 91 eyes of 51 men, clearing landmines
in the aftermath of the Russo-Afghan war, were
operated within 39 months (from November 1992
to January 1996) (Muzaffar et el 2000). Total blindness
(NPL) was seen in 37.5% of the eyes, and visual acuity
was below cfbe. in further 20.8%. Only 16.4% of
injuries were classified as mild with VA over 0.3. Eyelids
plasty (50% of eyes), evisceration (23.1%), and
vitrectomy (17.6%) predominated in the treatment.
It should be mentioned that all these patients
worked without any eye protection. Bajaire et al
published data on performed vitreo-retinal surgeries
during a 8-year follow-up period (from January 1995
to June 2003) (Bajaire et el 2006). As much as 40%
of injuries involved zone I to the corneal limbus, 44%
zone II from the corneal limbus to 5 mm behind
it, 16% of injuries were localized in zone III in the
posterior globe pole. Visual acuity in 98% eyes was
below 1/40. During vitrectomy, silicone oil was used
in 65% of cases, perfluorocarbons in 21%, lensectomy
in 82%, IOFB was removed in 72% of cases, and
endolaser was used in 81% of cases. Improvement
was seen in 43%, stabilization in 41%, and sight
worsening in 15% of cases. Factors of poor prognosis
included: lesions in zone III, retinal detachment,
intraocular inflammation, and perforating trauma.
From the above listed data, it results that ocular
injuries constitute serious problem, not only medical
but also social and economic. Americans estimated that
the cost of one soldier exclusion from the service due
to ocular injury for 5.9 days on average amounted
to $6295 (Buckingham et al 2001). Ocular injuries
may be classified as multiorgan, when the eye is only
one of many damaged organs, and uniorgan, involving
the eye and adnexa only.
Mechanical Ocular War Injuries
GLOBE AND ADNEXAL INJURIES
Global and adnexal injuries may be classified in several
ways. First of all, they may be classified by causative
factor as: incised, punctured, crushed, lacerated, and
contused injuries. Ocular injuries may also be classified
by anatomical structures involved. To unify the classi-
fication of mechanical ocular injuries the International
Trauma Classification was approved in 1996 (Table
49.1) (Fryczkowki et al 2003), Kuhn et al 1996,
Pieramici et al 1997).
TABLE 49.1: International ocular trauma classification
Open Closed
Type A Rupture A Contusion
B Penetrating B Laceration
C IOFB C Superficial FB
D Perforating D Mixed
E Mixed - -
Degree 1 >20/40 1 >20/40
by visual 2 20/5020/100 2 20/5020/100
acuity 3 19/10020/800 3 19/10020/800
4 19/800LP 4 19/800LP
5 NLP 5 NLP
Zone I Cornea to I External
corneoscleral
limbus
II Within 5 mm of II Anterior segment
the limbus
III Sclera more than III Posterior segment
5 mm from limbus
Marcus Positive Positive
Gunn Negative Negative
Below ocular injuries that may result from the
military operations are briefly discussed. However, the
authors focus on the specific ocular war injuries. Sequels
of the globe injuries by anatomical structures presents
Table 49.2.
Management varies in dependence on the type of
injury. As it is seen in the table, the treatment is
frequently surgical. Therefore, knowledge, experience,
proper equipment in the wards and OR are required.
Applied procedures do not differ from these used in
any ophthalmologic center.
Open Globe Injuries
Open globe injuries are one of the most severe ocular
injuries. They are most frequently produced by
landmine blasts or hand grenades. It is estimated that
such injuries constitute 50 to 80% of trauma in the
contemporary battlefields with penetrating and
perforating wounds with IOFB predominance, often
302
TABLE 49.2: Globe injuries by anatomical structures
Anatomical structure Type of injury Sequel Treatment Prognosis
Eyelids Abrasion, closed or open Upper lid ptosis, lacrimal tract S Good
global injury disruption, hemorrhage
Lacrimal apparatus Dislocation Edema S Good
Lacrimal ducts Disruption Lacrimation, inflammation S Good
Conjunctiva Abrasion, rupture Hemorrhage, defects S Good
Cornea Epithelial abrasion Recurrent defects C Good
Rupture of the Scars, keratoconus, C Poor
posterior limiting corneal edema,
membrane of the cornea anterior adhesions
Sclera Rupture Uveal prolapse, vitreous prolapse, C Poor
retinal impaction, hypotonia, loss of vision,
inflammation, retinal detachment, glaucoma
Abrasion Hemorrhage C Good
Anterior chamber Rupture of the iris sphincter Photophobia C/S Good
Iridodialysis Inflammation C/S Good
Iridoschisis Edema C Good
Angle recession Inflammation C
Hyphema Corneal incrustation, C/S Favorable
secondary glaucoma
Pupillary muscles paralysis Photophobia C Good
Traumatic iritis Adhesions, secondary glaucoma C Good
Refraction disorders Hypermetropia, myopia C Good
Vitreous hernia Vitreous base avulsion, retinal C Good
detachment
Lens Opacities (Vossius Cataract C, Good
rings, subcapsular, sometimes
disseminated, diffused) awaiting
Luxation Deterioration of sight C Poor
Subluxation Refraction disorders C/S Poor
Rupture of the Opacity cataract S Good
lenticular capsule
Vitreous Hemorrhage Opacities, sparkling floaters, C/S Poor
photoreceptors damage,
retinal pigmentation
Posterior vitreous C Good
detachment
Retina Tear, detachment Complete retinal detachment S Poor
from the limbus
Retinal detachment Worsening, loss of vision S Poor
Commotio retinae
(Berlins edema,
Terson syndrome,
Purtschers angiopathic
retinopathy, peripheral
retinal edema) Vision deterioration C Favorable
Hemorrhage Vision deterioration,
proliferations, retinal detachment C Poor
Macular hole Vision deterioration Laser Poor
therapy
Choroid Rupture Retinal detachment C Poor
Detachment of the Intraocular pressure drop papilledema, C Poor
ciliary body retinal edema, choroidal detachment
Post-traumatic inflammation Scotoma C Good
Lesions to the ciliary Accommodation disorders, lens dislocation,
muscles or nerves ciliary muscle spasm C Good
Orbit Hemorrhage Optic nerve and orbital structures compression S
Soft tissues edema Optic nerve and orbital structures compression S/C Poor
Fracture of the orbital walls Orbital structures and eyeball damage S Poor
Optic nerve Rupture of the optic Partial damage C Good
nerve II vessels
Detachment Vision loss C Poor
Legend: S surgical treatment ; C conservative treatment.
303
Ocular War Injuries
multiple (about 80%). Foreign bodies, both metallic
and non-metallic may penetrate to the ocular adnexa,
eyeball, orbit or even maxillary sinusal structures or
brain (Biehl et al 1999). Therefore, detailed diagnostic
procedures with possible ultrasound, X-ray and CT
are very important in the field hospital already. Open
globe injuries damage ocular adnexa (eyelids,
conjunctiva, cornea, and sclera) in nearly all instances.
Copious hemorrhage, edema, and pain are usually
seen. Plastic, gunpowder, sand, dust, and bacterial
pathogens are deposited in the eye following open
globe injuries. Each ocular war open injury is
considered infected and requires antibiotic therapy as
soon as possible. Therefore, an incidence of intraocular
inflammation after any injury is rare because an early
administration of antibacterial agents.
Fig. 49.2: Scar after corneoscleral wound caused by
landmine shrapnel in a soldier of Iraqi operation
The treatment is frequently two-staged. The firs stage
takes place as soon as possible after reporting to the
doctor. It comprises post-traumatic wounds care with
anatomical structures reconstruction and intensive anti-
inflammatory therapy with antibiotic therapy. Foreign
bodies are removed and eyelids, conjunctival, scleral,
and retinal wounds are sutured.
Then, the patient should be evacuated to the
centers, where the treatment aimed at proper sight
functioning reconstruction is possible. Timing plays an
important role in the treatment of the open globe
injuries. The majority of surgeries should be carried
out soon after injury, as remote outcome frequently
depend on the time of surgery. It is especially true in
case of retinal detachment, IOFB and intraorbital
foreign bodies removal, perforating eyeball wounds,
intraocul ar infl ammation, prophyl actic retinal
photocoagulation. Other injuries may (and sometimes
should) wait until partial healing of the post-traumatic
wound have been achieved. The treatment of some
open globe injuries (e.g. eyelids plasty, hemorrhagic
vitreous opacities, macular holes, orbital walls fractures,
post-traumatic cataract surgery, keratoplasty, anti-
glaucoma surgeries) may be delayed until partial healing
of the post-traumatic wound have been achieved or
make the decision on surgical operation time
dependent on the course of therapy (Gos et al 2001).
As it was already mentioned, the outcome of
treatment is sometimes unsatisfactory for the patient
but adequate visual acuity may be preserved. The
treatment is always surgical in such cases and should
be carried out in the specialist centers, following
medical evacuation from the regions of direct military
operations. It is always connected with the necessary
hospitalization, surgical treatment, and sometimes
discharge.
Closed Globe Injuries
It is different in case of the closed globe injuries. As
ocular wounds usually force the victim to seek medical
aid, contusions (especially mild) are often ignored.
Some authors estimate that contusions constitute about
50% of all ocular injuries (Kozuchowska 1986).
Symptomatology of these injuries varies from no
symptoms and signs to the immediate blindness of the
injured eye, depending on the severity of trauma. The
following symptoms usually accompany the contusion:
bl urred vision, reddening, hemorrhage, pain,
photophobia, sensation of veils, dots, curtains in the
front of eye, sight instability (Szaflik et al 1998). All
these symptoms are usually the reason of early
reporting to the ophthalmologic clinic, enabling an
early diagnosis and proper treatment which is often
less invasive (e.g. in retinal detachment) than that
del ayed. Post-traumatic sequel s may devel op
asymptomatically or the symptoms may be scare, slow
(e.g. retinal peripheral injuries), and may easily be
overlooked by the patient (Waclawiak-Dabrowska et
al 2007). It may be the case of peripheral retinal
detachment, which may lead to complete detachment
of retina (Fig. 49.3). Similar situation concerns sequels
of the peripheral hemorrhages into the retina.
Fibroproliferative changes leading to the secondary
retinal detachment may develop after months following
the injury (Bajaire et al 2006). Properly performed
laser therapy mainly protects the patient against such
complications. However, the patient should regularly
report to follow-up visits in order to not overlooking
preventable complications.
MULTIORGAN INJURIES
The firs group is usually related to multiorgan injuries,
mainly craniofacial. Ophthalmologists are participating
to the specialist team dealing with the treatment and
patients care. Prospective studies have shown that
304
Figs 49.3A and B: Choroi dal ruptures, subreti nal
hemorrhage and peripheral retinal dialysis (black arrows)
after blunt trauma of eyeball in soldier during service in Iraq.
Yellow arrows indicate barrage retinal laser coagulation
Fig. 49.4: Total retinal detachment with superior retinal
laceration after blunt trauma
craniocerebral trauma involved the damage of at least
one cranial nerves connected with the organ of vision
(cranial nerves IIVII). Risk factors of these nerves
damage include: severity of trauma (it should be noted
that these nerves damage occurred also in mild injuries
in about 10%), causative factor and its energy, skull
base fractures, and intracranial hematomas. An
incidence of post-traumatic nerve damage is shown
in the Table 49.3 (Mariak et al 2002).
TABLE 49.3: Post-traumatic nerve damage
Damaged nerve Percentage of injuries
Optic nerve II 1.2 to 16%
Oculomotor nerve III 2.4 to 15.8%
Trochlear nerve IV 0.15 to 20%
Trigeminal nerve V 1.3 to 4.2%
Abducent nerve VI 2 to 26%
Facial nerve VII 2.0 to 60%
Post-traumatic damage of these nerves, especially
partial, may be overlooked during patients hospita-
lization immediately after injury. Such patients are
usually hospitalized in emergency wards, their health
status is severe and there is no possibility to perform
complete ophthalmologic examination. These patients
frequently report to the ophthalmologist with some
delay. Delayed treatment of the ocular injuries poses
quite a problem. Treatment in such cases do not differ
from these used in any ophthalmologic center.
Fig. 49.6: Post-traumatic optic nerve atrophy
in a soldier of Iraqi operation
Fig. 49.5: Post-traumatic lens subluxation in a soldier
of Iraqi operation
305
Ocular War Injuries
PROPHYLAXIS OF THE OCULAR INJURIES IN
THE BATTLEFIELD
Prophylaxis is of utmost importance due to such
serious complications of the ocular injuries. It is,
however, quite limited in the battlefield. Nevertheless,
an incidence of ocular diseases may be partially reduced.
It is justified by the health and economic reasons.
The most important is eye protection (special
protective goggles) during all military operations, which
protect the eyes against dust and other contaminants
and all minor ocular injuries. Glasses of eye protective
devices should be made of polycarbons of 2.3 or
3 mm thick. They may protect against injuries of kinetic
energy up to 18 J or even higher, depending on the
direction of action. Eye protective devices should be
safe, comfortable, disperse an impact on the large
craniofacial surface, not limiting the field of vision, and
not to stem up. Sometimes such goggles are made
individually for every soldier, taking his sight defects,
needs, habits, craniofacial anatomy, and type of effected
operations into consideration (Chizh et al 1999).
Moreover, wearing of contact lenses should be
banned. Their proper cleaning and observation of rules
concerning the wear of these lenses are difficult during
military operations. Between military operations,
recommendations depend on the climatic conditions
and environment. Military operations in the deserts
require wearing sunglasses with side shield, protecting
not only against excessive insolation but also against
sand. It the tropics, special attention should be paid
to insects as their bites may produce not only diseases
but also allergic reactions.
Non-mechanical Ocular War
Injuries
OCULAR WAR INJURIES RESULTING FROM
THE USE OF MASS DESTRUCTION WEAPONS
Use of the mass destruction weapons aimsfrom the
tactic point of viewat attaining the best possible
military effect without engaging a lot of means and
number of soldiers. Unfortunately, such an effect is
related to not only maximum enemy loss but also civil
population and complete destruction of non-military
objects and environmental pollution in case of nuclear
weapon use. However, maximum effect on the eyes
has chemical warfare agents, out of all types of
weapons. These agents significantly decrease ability to
carry military actions due to visual disturbances and
accompanying ailments.
Presenting an effect of chemical warfare agents on
the organ of vision, we propose to use military and
not medical terminology. An action of chemical warfare
agents is determined by its localization, identity, and
neutralization. This action may be related to both
military and terrorist operations. In general, mass
destruction weapon is divided into chemical warfare,
biological warfare, and nuclear warfare. Mass destruc-
tion weapons may be transported by artillery shells,
ballistic missiles or bombs. Chemical and biological
warfare agents may additionally be thrown down in
containers or dispersed from aircrafts.
Chemical Warfare
History of sulphur fumes and hot pitch use is as old
as history of wars. These agents were used in Greece
(Peloponnesian Wars) and in China already in the 5th
century BC. Chemical warfare was extensively used
as battlefield weapons during the I World War. In 1914,
French and Germans use chlorine, and in 1915,
Germans used hydrogen cyanide (prussic acid) and
Yperite (mustard gas). Ever since, an international
community elaborated various agreements that aimed
at disarming under strict and effective control. In 1925,
chemical warfare was banned by the Geneva Protocol.
The Polish government put a motion on biological
warfare ban, which was added to this Protocol. In
1972, Biological and Toxic Weapons Convention was
agreed upon and ultimately signed by 108 countries
in 1975. In 1993, Chemical Weapons Convention on
the Prohibition of the Development, Production,
Stockpiling and Use of Chemical Weapons and on
Their Destruction came into force. Unfortunately, there
are cases of unobserving these agreements.
Chemical warfare agents can be grouped into
military toxic agents (military gases, volatile liquids
dispersed as aerosols), and military auxiliary agents
(incendiary agents, defoliants, tear gas). Toxic effect
of these agents always depends on the dose, i.e.
concentration and duration of action of the said
substance.
Military toxic agents
Depending on the effect, military toxic agents are
grouped into nervous system damaging agents (nerve
agents), blister agents, suffocating, choking, and
hallucinogenic compounds. Remaining agents may
produce only transient ocular irritation manifested by
reddening and lacrimation.
1. Phosphororganic compounds (nervous system
damaging agents, nerve agents): Phosphororganic
compounds are volatile liquids. They absorbed from
airways and conjunctiva as well as from the skin, if
contaminated clothes were not earlier removed. They
were primarily used as insecticides (pesticides), i.e. plant
protection agents. However, it was found that they
are highly toxic for humankind. As chemical warfare
306
the following compounds are used: tabun (GA), sarin
(GB), soman (GD), cyclosarin (GF), and X gases (VX
or AX). Recent reports on the use of these agents come
from Iran-Iraq conflict in 1987. These agents act by
blocking acetylcholinesterase (AchE). Accumulation of
acetylcholine in the parasympathetic nerves endings
produce muscarinic effect in the iris and ciliary body,
lacrimal gland and conjunctival blood vessels. Effects
of nerve agents are also visible in the bronchi, bladder,
gastrointestinal tract, and heart. Nicotine effect is
connected with acetylcholine accumulation in the
postsynaptic part of the myoneural junction and some
sympathetic ganglia. Laboratory confirmation of
intoxication is a decrease in erythrocyte AchE.
Ocular symptoms are the earliest and occur at the
lowest dose. They include: Maximum miosis (lasting
up to 14 days), sensation of pressure and weight in
the eyeballs, ocular pain, injection of the conjunctiva.
Miosis may be accompanied by sight disorders,
especially peripheral, whereas ciliary body stimulation
transient accommodation myopia. There may occur
intraocular pressure (IOP) disorders: decrease in IOP
related to the reduction in aqueous production or an
increase in IOP from the papillary block. Then, a
sequence of general symptoms follows, including: pain
of the frontal region, rhinorrhea, hypersalivation,
sweating, bradycardia, chest pain, bronchospasm and
dyspnea, nausea, vomiting, abdominal cramps,
involuntary miction, and defecation, somnolence,
speech disorders, muscular tremor, convulsions,
parestesis, pulmonary edema, blood pressure drop,
paralysis of the respiratory muscles, respiratory arrest,
and death. General symptoms may persist for some
days. High doses cause death within some minutes.
Medical management of intoxication with phos-
phororganic agents includes so-called pretreatment,
i.e. pyridostigmine administration. It reversibly binds
AChE for about 12 hours, blocking this way an entry
of phosphororganic agents. Pyridostigmine
administration should immediately be discontinued,
if contamination was detected. Protection against
chemical attack in the battlefield includes wearing a
facemask, which protects the eyes and airways for
about 30 minutes. Within aid procedures, prefilled
syringes with atropine should used (it has muscarinic
anticholinergic activity), oxime drug (nicotinic
chol inergic action), and benzodiazepine
(anticonvul sant). Drugs shoul d be injected
subcutaneously or intramuscularly. Atropine dose is
repeated every 5 to 15 minutes, depending on the
degree of poisoning and achievement of the general
atropinization. Next phase of management is victim
evacuation from the battlefield, removal of the
contaminated clothes, skin decontamination, airways
cleaning (suction), oxygen therapy, and transportation
to the medical station.
2. Blister agents: These agents serve to decrease
military capability by the local burning effects or forcing
wearing the protective clothes, which markedly reduce
mobility. Such agents include: sulphur mustard gas
(HD), nitrogen mustard gas (HN), lewisite (L),
phosgene oxime (CX). These agents produce chemical
ocular burns, burns of airways, skin, intestines, and
affect circulatory system.
i. Mustard gas (Yperite): Sulfur mustard (sulfur
Yperite) is one of the oldest and best-known chemical
weapons. It was used for the first time by Germans
near the city of Ypres (Belgium; it took its name after
the name of this city) in 1915. Later, it was used by
Italians in Ethiopia in 1936, Japanese during the war
with China in 1937, Iran-Iraq conflict in 1985-1988;
Iraq used it also against Kurdish minority in 1988.
Nitrogen mustard, manufactured for the first time in
1935, is a new generation of the burning chemical
warfare agents. One should remember that it might
be used in the contemporary battlefields.
Mustard gas is a liquid used in the form of an
aerosol. It easily penetrates through military uniforms,
ordinary clothes, skin, and mucous membranes. This
compound may also persist in humid soil and water
in the colloidal form for days. Mechanism of its action
on the tissues is not fully explained. However, it is
known that DNA, RNA, cellular membranes, enzymes
and proteins are damaged by the alkilation with
particular affinity to guanine. This leads to cytotoxic,
cytostatic, and mutagenic effects (Dabrowska et al
1994). Characteristic feature of mustard gas is latency,
lasting for several to dozens hours. Then, progressing
lesions develop, producing irreversible damage.
The eye is the organ most sensitive to mustard gas.
Threshold of its stimulation is 10-fold lower than that
for skin and airways. Even if characteristic odor of
Yperite (mustard) is not detectable, the first ocular
symptoms of contamination may appear within one
hour. These ocular symptoms occur most frequently
in about 4 to 6 hours in the form of burning sensation,
photophobia, blurred vision, and painful blepharo-
spasm. Simultaneously, mustard gas is penetrating the
skin, leading to the general poisoning.
In order of incidence, the following symptoms are
observed: mild conjunctivitis (75%), severe conjunc-
tivitis with superficial keratitis a symptom of orange
rind, edema and eyelids reddening (15%), superficial
corneal abrasions erosions, and inflammation with
injection in the corneal limbus, lesions to the eyelids
epithelium (10%), deep corneal injury with ulceration,
neovascularization, necrosis of conjunctiva, and deep
burns of eyelid skin (Solberg et al 1997). Ocular
response to the contamination may include also
adherence of the iris to the cornea, leading ultimately
307
Ocular War Injuries
to the secondary gl aucoma. Latent and rare
complication of mustard gas action may be irreversible
superficial corneal opacification, requiring keratoplasty,
and/or recurrent conjunctivitis, keratitis, and blepharitis
(AmedP-6). An effect on the cornea is tetraphasic:
loosening of the epithelial intercellular junctions,
damage of stromal collagen, stimulation of the stromal
neovascularizing factor, and apoptosis of endothelial
cells.
Ocular symptoms herald other consequences of
the contamination. They include: chemical skin burns
with blisters, rhinorrhea, vocal cords injury with
hoarseness or aphonia, increased mucus secretion in
the airways, bronchospasm, persisting cough, nausea
and vomiting, diarrhea. Other squeals include: skin
hyperpigmentation or discoloration, painful ulcerations
of the skin, aphonia or chronic hoarseness, chronic
obturative pulmonary disease (COPD), intestinal
hemorrhage and perforation, aplastic anemia,
leucopenia, depression, loss of libido, anxiety. It was
also found that mustard gas increases the risk of
pulmonary carcinoma in chemical causalities and
manufacturers (Norman 1975, Woda et al 1968). It
should be born in mind that general symptoms, such
as headache and abdominal pain, nausea and
vomiting, anemia, and leucopenia may be identical
with those in radiation sickness.
Basic medical management of chemical causalities
is careful washing of skin and irrigation of eyes as well
as removal of the contaminated clothes. Eyes and
mucous membranes are washed with water or normal
saline and sodium bicarbonate for at least 2 minutes,
immediately after contamination with mustard gas
(Wilems 1989). Delayed eye irrigation is useless as
mustard gas is already absorbed. Mustard gas is
removed from the skin wooden spatula, when
contaminated clothing was removed, and powdered
with anti-gas powder (calcium chloride or magnesium
oxide). Activated carbon and synthetic resins may also
be used for this purpose(Smith et al 1991). Then,
exposed skin is washed with water and soap and
normal saline. Treatment of ocular injuries include
appl ication of topical antibiotic ointments,
corticosteroids, and mydriatics for dozens weeks to
several months (Safarinejad et al 2001). Then, the
patients are followed-up for months to detect possible
corneal and anterior chamber symptoms. Wartime
practice indicates, however, that for the treatment
severity of injuries, depending on the dose and rapid
decontamination is more important than medical
procedures.
ii. Lewisite: Lewisite was synthesized in by WL Lewis
in USA in 1918 (it was named after him). Most
probably it was not used as chemical warfare agent
up-to-now. Pure lewisite is colorless and odorless liquid
and these features are its virtue from the military point
of view. Usually impurities give it brown coloring and
odor similar to that of geraniums. Which can be
undetectable in the battlefield. Lewisite, similarly to
mustard gas, penetrates clothes, mucous membranes,
and skin. As it contains arsenic atom, lewisite disturbs
cellular energetic processes, blocking SH groups in
pyruvate dehydrogenase and inhibiting acetylco-
enzyme A synthesis.
Lewisite produces severe ocular injuries. The first
sign of ocular injury is painful blepharospasm, followed
by: chemosis and blepharoedema, keratitis and iritis
with hypopyon within 1 hour after the contact.
Inflammation usually resolves but the necrosis of
conjunctiva, corneal opacification, corneal pannus,
secondary glaucoma, and cataract may persist after
severe injury.
Intensive pain of eyeballs, skin and blisters filled
with liquid toxic for not only surrounding tissue but
also for medical staff is characteristic for lewisite
contamination. It exerts a severe irritating effect on
the airways, forcing the immediate use of anti-gas
facemask. Lewisite absorbed to the circulating blood,
mainly through the respiratory tract, causes hemolytic
anemia, increased capillary permeability, pulmonary
edema, damage of both liver and kidneys, and
hypovolemic shock.
The treatment includes copious eye irrigation with
water and normal saline. Topical antibiotic ointments,
strong mydriatics (atropine solutions) are used. An
important element of the treatment is BAL British
Anti Lewisite (dimercaptol) chelating arsenic and
liberating SH groups of pyruvate dehydrogenase. It
is used topically in the form of ophthalmic ointment,
skin ointment, and systematically in intramuscular
injections.
iii.Phosgene oxime: Phosgene oxime, being
classified as blister agent (vesicant), has an irritating
action without producing the blisters. It is solid
compound dispersed in the form of aerosol for military
purposes. Mechanism of its action is not clearly
explained, but most probably it damage protein and
enzyme structures. Contact with the eyes causes edema
of the conjunctiva and keratitis, leading to its
opacification and marked decrease in visual acuity.
Typical for phosgene oxime action are skin lesions in
the form of reddening and urticaria progressing to the
skin necrosis with suprainfections. Medical management
includes decontamination with water and sodium
bicarbonate. Then, topical antibiotics and preparations
accelerating the healing of cornea and skin are applied.
3. Remaining military toxic agents: One should
remember that each case of the conjunctival irritation
manifested by reddening, burn sensation or lacrimation
308
requires facial mask wearing and detecting procedures.
Such symptoms may be the first sign of battlefield
contamination with deadl y substances. These
substances include: lung damage agents (phosgene,
diphosgene, chlorine, chlorpicrin), cyanide compounds
(hydrogen cyanide, cyanogen halides, cyanogens
chloride, cyanogens bromide). Every case of paralyzing
agents use both depressants, tranquillizers and
stimulants, hallucinogens (LSD, amphetamines)
papillary dilatation is seen together with typical
neurological symptoms.
Military auxiliary agents
To this group of agents belong: lacrimators, defoliants,
incendiary agents, and smoke screen. In general, these
agents do not cause direct irreversible immobilization
of the enemy and according to the international law
are approved for use, except defoliants, dioxan, and
incendiary bombs.
1. Lacrimators and smoke screens: Lacrimators
(tear gas, pepper gas) are military gases irritating the
eye and upper respiratory tract. They rapidly and
transiently cause stinging sensation and, tearing (for
about 15 minutes), and reddening (for about 30
minutes) of the eyes, reddening of the eyelids (for about
1 hour) without toxic consequences. Rarely, the
corneal epithelium is damaged. Ocular symptoms are
accompanied by the cough and rhinorrhea. Similar
but weaker effects are produced by the smoke screens,
used to mask location of the military troops or in shock
tactics. These agents serve not only as warfare agents
but also as riot control agents used by police forces.
Medical management includes: eye irrigation with water
and possible use of topical antibiotics. Chlorine
derivatives (calcium hypochlorite) are banned as their
chemical reactions with lacrimators may produce toxic
effects.
2. Dioxins and defoliants: Dioxins chemically
damage the skin, mainly on the face and hands,
manifested as chloracne, leaving deep, sometimes
disfigurating scars. As far as the eyes are concerned,
dioxins may produce deformity of the eyelids, leading
to the recurrent conjunctivitis and marginal blepharitis.
Skin lesions persist for years and may be accompanied
by the lesions to pancreas, liver, and immunological
system, anemia, and neurological diseases. The best-
known dioxin is TCDD. Its mechanism of action and
treatment of poisoning are unknown. Actually, cases
of Dixon poisoning are rare and are related only to
terrorist attacks or intelligence actions. During the wars
in Korea and Vietnam, several cases of poisoning with
dioxins being added to defoliants were noted in both
participants of the conflict. Defoliants are phytotoxic
chemicals used to remove plants in the battlefields.
These plants may serve as food or shelter in the natural
terrain configuration. The most toxic proved purple
agent and orange agent, containing high levels of
dioxins.
3. Incendiary agents: They serve to eliminate
mankind and damaging the equipment and objects
(flammable aluminum and phosphorous compounds,
hydrocarbon fuels: gasoline, refuel, fuel oil, kerosene).
These agents cause ocular, skin and mucous mem-
branes burns, and combustion gases are additionally
toxic for respiratory tract and central nervous system.
i. Thermal ocular burns: In wartime, thermal
ocular burns result from the use of incendiary agents,
incendiary bombs, flames of exploding shells and fire.
Military thermal burns do not differ from the typical
eye burns, described elsewhere, except the presence
of gunpowder remnants or foreign bodies connected
with the explosion. However, ocular burns with
phosphorus need separate discussion.
ii. Burns caused by phosphorus: White phos-
phorus is used in the phosphorus incendiary bombs.
It is self-ignition agent, which produces white fumes
in the air. White phosphorus is a cause of numerous
and deep burns of the skin and eyes. Therefore,
immediate decontamination is of utmost importance.
The particles of white phosphorus are mechanically
removed from the eyelids, conjunctiva and cornea.
The eye and exposed skin are abundantly washed with
1% copper sulfate solution or 5% sodium bicarbonate,
which neutralize phosphorus. Then, abundant irrigation
with water or normal saline is necessary. It not only
cleans and cools the tissue but also removes copper
compounds, preventing general intoxication. Medical
treatment involves topical antibiotic use, epidermization
preparations, mydriatics, and corticosteroids later.
Biological Warfare
Biological warfare agents consist of microorganisms and
their toxins. These agents serve for permanent elimina-
tion of the enemy, quite often with mortal effect.
International agreements concerning the ban of
biological weapons are similar to that concerning
chemical weapons and were agreed upon in 1925 and
1972. Despite of biological weapons ban, several
countries still experiment with biological weapon, which
is also within the interest of terrorist organizations (so-
called bioterrorism).
The following warfare agents are considered mortal:
botulin toxin (BTX), SEB toxin (staphylococcal entero-
toxin type B cadaveric poison), antrax, tularemia.
Brucellosis, Q fever, VEE fever incapacite the enemy.
Out of all types of the biological warfare agents,
characteristic ocular signs are produced by the botulin
309
Ocular War Injuries
toxin, produced by Clostridium botulinum. It inhibits
acetylcholine release in the myoneural endings and
parasympathetic nerves. Ocular symptoms include:
papillary dilatation, accommodation disorders and
double vision. The general symptoms include: mouth
dryness, peristalsis impairment, speech and swallowing
disorders, breathing muscles paralysis. Antitoxin is used
in the treatment. Mortality rate in untreated subjects
is about 65% in about 18 to 36 hours.
Nuclear Warfare
Nucl ear weapon is characterized by the most
destructive action, out of all types of weapons. Its effect
on the vision is connected with five elements of
explosion: blast, thermal radiation, shock wave,
penetrating radiation, and radioactive pollution. Data
on the nuclear warfare effects on the human body
come from the end of the II World War, when USA
dropped the atomic bombs on the Japanese cities
Hiroshima and Nagasaki (on the 6th and 9th August
1945). Other nuclear explosions were related to the
nuclear weapons testing carried out by several countries
during so-called Cold War. It should be assumed that
such tests did not involve experiments on human
beings. The Cold War arming was followed by the
period of nuclear disarmament. In 1963, United States,
Soviet Union, and Great Britain Kingdom signed an
agreement which banned testing in the atmosphere,
outer space, and under water. However, tests
underground tests were permissible. In 1968, an
agreement on nuclear weapons non-proliferation,
signed by 178 countries, and prolonged open-ended
in 1995. A comprehensive test ban was approved by
UN General Assembly in 1996; 170 nations have now
signed. Actually, China, France, Russia, United States,
Great Britain, India, and Pakistan have nuclear
weapons. Moreover, it is stored in post-Soviet regions:
Bielarus, Kazkhstan, and Ukraine. It is probable that
also Israel and Iran have nuclear weapons.
There are several typical ocular injuries in nuclear
explosion survivors. Intensive light during nuclear
explosion causes transient central vision disturbances.
Thermal radiation, related to the blast, produces eye
burns and lens opacification. This problem is discussed
in detail within the effects of explosion blast and laser
light. Shock wave means translocation of air with
supersonic speed and it is not produced in case of
neutron bomb explosion. Shock wave may cause
mechanical injuries related to the foreign bodies in the
eye and circulatory disorders due to the sudden change
of the air pressure (Flick 1948).
Nuclear explosion produces penetrating radiation
and radioactive pollution. Both may produce similar
disorders known as radiation sickness. Ocular and
systemic clinical effect will depend on the dose and
absorbed energy. Penetrating radiation is produced
during nuclear explosion, lasts for dozen seconds, and
is composed of electromagnetic gamma rays and
neutron radiation. Radioactive pollution is related to
the radioactive dust fallout after explosion and
radioactive substances formation by the neutron
radiation. It results in X, gamma, alpha, beta, and
proton rays emission, the most intense during a few
days but persisting for years.
Radiation sickness may develop within hours after
nuclear explosion. However, it should be born in mind
that now, when the nuclear weapons are banned,
symptoms of radiation sickness may result from
inappropriate storage of the radioactive substances,
leak of nuclear reactors cooling water, overheating or
explosion in the nuclear power plants. General
symptoms of the radiation sickness include: headache,
abdominal pain, nausea, vomiting, gastrointestinal
hemorrhage, skin burns. Later, anemia and leucopenia
develop. Ocular effects of the radiation sickness include
edema and reddening of eyelids with madarosis.
Blisters on the eye lids skin, necrotic conjunctival
ulceration, corneal erosion, and corneal stroma
infiltrations follow. Ultimately, eye lids scar deformities,
conjunctival adhesions, corneal defects with perforation
are observed. Typical sequel is postradiation cataract
that may develop from 3 months, already (Sinskey
1955). It begins with punctate dot opacification in the
front of the posterior lens capsule, progressing to the
subcapsular discoid changes, and finally involves the
whole lens (Ham et al 1953). Patients with general
symptoms of the radiation sickness manifested by
hematopoietic disorders but without visible ocular
problems require periodical eye fundus examination
to detect possibl e intraretinal and preretinal
hemorrhages, hemorrhages into vitreous.
OCULAR WAR INJURIES RELATED TO THE
LASER LIGHT AND EXPLOSION BLASTS
Accidental laser use and explosion blasts produce
electromagnetic wave of the visible light, similar to
infrared light harmful for the macula. It results in the
central vision disturbances, manifested by the visual
acuity decrease, central scotoma and color sensitivity
disorders. Mechanism of these pathologies involves
photochemical macular metabolism disorders with
accompanying small foci of the internal structures
edema and intraretinal blood extravasation. Listed
disorders may persist for about 1 to 3 months. Lesions
to the macular pigmentary epithelium and its outer
structures are also possible (Harris et al 2003). The
later occur, if the electromagnetic wave mainly consist
infrared light, being a component of laser light, falling
vertically on the eye. Laser light falling on the eye under
certain angle causes local skin, conjunctival and corneal
310
lesions. Explosion blast is accompanied by thermal
radiation which causes eyelids skin, conjunctival and
corneal burns as well as lens opacification (Harris
et al 2003, Pariselle et al 1988). Prophylactic measures
include wearing of goggles, first of all. In the treatment
topical anti-inflammatory agents are applied. One
should also consider the administration of anti-
edematous drugs, such as carbonic anhydrase
inhibitors. In more severe cases corticosteroids are
injected periorbitally. Periodical ophthalmologic follow-
up central vision examinations are also necessary,
including visual acuity, color and contrast sensitivity,
Amsler test, computer-assisted perimetry. Additional
tests and examinations should also be considered:
fl uorescein angiography, optical coherence
tomography, electrophysiological tests.
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C H A P T E R
50
Trauma of Anterior Eye
Segment: An Update
Boris Malyugin(Russia)
Introduction
The division of the eye trauma to anterior and posterior
is rather relative. Not infrequently anterior segment
trauma is associated with the damage of the posterior
eye structures including vitreous body, retina, choroid,
sclera and optic nerve. More over traumatic influence
l eading to the anterior segment damage can
compromise the eye but facial muscles, bones, brain,
and other structures as well. That is why all traumatic
cases require comprehensive examination of the eye
and surrounding structures. In many cases of the eye
injuries require urgent examination by physician and
therapy.
Injuries of the Lids
INTRODUCTION
Lid injuries of various etiologies can be isolated or
combined with traumatic changes of the eye and
surrounding tissues. Lid lacerations are usually caused
by bytes, or by sharp objects.
CLINICAL SIGNS AND SYMPTOMS
Direct blow to the eyelids cause blood infiltration of
the lid tissues, echymosis, and may be associated with
subconjunctival and orbital hemorrhages. In some
cases, blood moves with the gravity from the lid to the
check area.
In cases of laceration if it contains fat that means
that the orbital septum has been perforated. The
absence of the lid fold and blepharoptosis are the signs
of the levator muscle damage.
Special attention should be pointed to the diagnosis
of the orbital fractures. The latter is typically signaled
by ecchymosis, lid swelling, proptosis, an in some cases
ophthalmoplegia, subcutaneous emphysema from
fracturing of the sinuses causing crepitation during
palpation.
Orbital roof fractures can also be associated with
liquior-rhinorrhea. Clinical suspicion of a blowout
fracture is based on diagnosing one or more of the
following symptoms: anesthesia of the nose and the
skin of the lower lid, diplopia, pain at the upward gaze,
displacement of the globe (downward or inward).
INVESTIGATIONS
As a first step the physician has to collect the history.
Second step include the determining of the injury extent.
Particular attention should be drawn to the underlying
globe.
X-ray examination should be performed if the
fracture of the orbit is suspected.
Lid hemorrhages usually does not have serious
consequences but they can signal the injury of the
orbital content which can be much more serious, for
instance fracture of the roof of the orbit. Lid hematomas
can also be associated with contusion injuries of the
eye.
TREATMENT
Treatment is greatly depends of the extent of the injury.
In cases of lid hemorrhage without damaging of the
eye and other orbital structures optimal tactics will be
to wait a period of time necessary for the for the
spontaneous resorbtion of blood.
Bites (from humans or animals) should be cleared
of the debris and irrigated with antiseptics and then
allowed to heal with secondary tension. The use of
prophylactic antibiotics is strongly recommended. In
cases of animal bites (dogs, foxes, etc.) prophylaxis
against rabies must be considered.
For lid lacerations primary repair with suturing
should be performed. Careful reapproximation of all
ruptured tissue planes and reconstruction of defects will
ensure functional and cosmetic result.
312
Repair of the lid lacerations requires knowledge of
the anatomy. The lid is a triple-layered structure
composed of skin (anterior layer), orbicularis muscle
(middle layer) and tarsus and palpebral conjunctiva
(posterior layer). All three layers of the lids should be
closed separately.
During the lid reconstruction it is extremely
important to save as much of the natural lid margin
as possible. Special attention should be directed not
only to obtain the complete lid closure but also to repair
the functional passage of tears with blinking into the
lacrimal canaliculi and the lacrimal sac. In cases of
damaged medial parts of the lids canaliculi should be
carefully explored and reconstructed if necessary.
If medial or lateral tarsal tendons were cut at the
time of trauma they should be identified and repaired.
In the cases of conjunctival deficiency mucous
membrane grafts taken from the contralateral eye or
buccal cavity can be used with great success.
An orbital fracture in the absence of the physical
symptoms in many cases does not require operative
intervention. The most frequent indications for the
surgery are disabl ing dypl opia and severe
enophthalmos. Surgical intervention in orbital floor
fracture is not considered and emergency and usually
delayed for 2 or more weeks.
PROGNOSIS
Lids tissue is a richly vascularized that is why it heals
rapidly. Primary repair of lid lacerations will produce
a very good cosmetic result. The latter depends on the
extent and direction of the formed scar. On the other
hand in delayer repair, presence of necrotic tissue and
after bites can delay healing and result in compromised
cosmetic appearance. Secondary reconstructive surgery
can be considered if this clinical situation arises.
Abrasions of the Globe
INTRODUCTION
Corneal erosions are caused by eye scratching with
fingernails, hairbrushes, sand blowing in the air,
incorrect handling of the contact lenses, etc. The other
cause is the foreign body (FB) located under the upper
lid.
Right after injury there is sudden onset of pain,
lacrimation and blepharospasm. Eye motions as well
as blinking can aggravate pain syndrome. Even at the
absence of the FB, a foreign-body sensation is
produced.
INVESTIGATIONS
The examination can be performed with the penlight
or under the slit lamp. Fluorescein drops or paper strips
are very helpful in detecting the presence and extent
of epithelial defect.
A careful history must also be elucidated in order to
find out the possibility of the presence of foreign bodies
and perforations.
In corneal epithelial defects differential diagnosis
should be performed with recurrent erosion due to the
damage of the epithelial basement membrane, herpes
simplex keratitis, dry eyes, neurotrophic kertitis, atopic
disease, ocular surface inflammation, damage to the
limbal stem cells due to the chemical burns and limbal
ischemia.
TREATMENT
Patients should be treated with antibiotics and
cycloplegics. A broad-spectrum antibiotic ointment
should be placed in the eye followed by placement
of a semi-pressure patch on the eye. Use of ocular
surface lubricants in small erosions may be enough to
improve patient comfort and support the healing
process at the same time preventing infection. In eyes
with corneal abrasions corticosteroids are strictly
contraindicated.
In cases of foreign bodies located in the upper fornix
the patient is seated and a drop of anesthetic is instilled.
Then patient is asked to look down, the examiner
perform lid eversion and remove FB from the
conjunctival sac.
PROGNOSIS
In small corneal abrasions the prognosis is favorable.
Epithelization is usually achieved in 24 to 48 hours.
Blunt Injuries of the Globe
INTRODUCTION
Blunt injuries of the globe can be caused by a variety
of objects that strikes the eye and disrupts its content.
Conjunctival hemorrhage is the most common sign of
ocular trauma (Fig. 50.1). By itself it has no
consequences. In some cases severe bleeding can cause
ballooning of the conjunctiva.
313
Trauma of Anterior Eye Segment: An Update
Hyphema is the other characteristic sign of the blunt
eye trauma (Fig. 50.2). This term refers to blood
retained in the anterior chamber. Some hyphemas are
small and located in the inferiorly, while the others may
fill the entire anterior chamber.
The extent of visual loss depends on the level of
hyphema. In total hyphema when the entire anterior
chamber is filled intraocular pressure is invariably
elevated.
In the early post-traumatic period the aqueous
humor contains cells and protein. Mild inflammation
of uveal tissue may typically follow any trauma to the
eye.
Hard blows of the eye typically produce iris sphincter
rupture with traumatic mydriasis. The latter can be
transitory or permanent. Traumatic iridodialysis of
various extents may be one of the consequences of
the blunt trauma (Fig. 50.3). Not infrequently
iridodialysis is associated with traumatic cataract
(Fig. 50.4).
In blunt trauma pigment epithelium can be
imprinted in the anterior surface of the lens forming
a Vossius ring (Fig. 50.5). It is produced as the result
Fig. 50.1: Post-traumatic conjunctival hemorrhage
Fig. 50.2: Appearance of hyphema following blunt trauma
Fig. 50.3: Traumatic iridodialysis secondary to blunt injury
Fig. 50.4: Traumatic cataract and iridodialysis
secondary to blunt injury
of forceful impact of the iris against the anterior surface
of the lens. This sign is rather diagnostic and has no
clinical significance and it is usually gradually resolves
with time.
Blunt injury can cause acute or late cataract
formation. Contusion cataract may form even in the
absence of detectable damage of the capsule. Opacities
usually localized in the anterior and/or posterior
subcapsular region. Rosette-shaped cataract is often an
early manifestation of lens contusion. It is located axially,
involves posterior lens capsule, and can either improve
spontaneously or progress to opacification of entire lens.
Blunt injury of the eye can also cause lens dislocation
and subluxation (Fig. 50.6). The leading mechanism
of this is the compression of the globe in axial direction
with expansion in the equatorial plane leading to
zonular rupture. The lens may be dislocated in the
anterior chamber or in the vitreous cavity.
Location of the lens in the anterior chamber impedes
the aqueous humor outflow and causes pupillary block
glaucoma (Fig. 50.7). Iridodonesis is observed in cases
of lens posterior dislocation when the patient moves
the eye quickly.
314
In blunt injuries even in cases when conjunctiva
remains intact, rupture of sclera may occur. The most
common sites of the rupture are: limbal area, rectus
muscle insertion and equator of the globe.
In patients with previous surgery (corneal trans-
plantation, radial keratotomy, cataract extraction) after
blunt trauma postoperative wound dehiscence can
occur.
INVESTIGATIONS
Medical history is a very important issue. Specific
ophthalmic tests include: refraction, visual acuity,
keratometry, biometry, B-scan ultrasonography,
gonioscopy. Slit-lamp microscopy is a major method
of eye examination. During examination pupil should
be maximally dilated. In all cases of blunt trauma
particular attention should be paid to fundus
examination. Physician has to evaluate not only affected
eye but also the fellow eye when possible.
In blunt trauma scleral ruptures can be present without
being visible to the examiner. Rupture is being suspected
when the eye is soft.
TREATMENT
A medication in conjunctival hemorrhage does not
speed up blood resorption. The latter usually occurs
within several days or weeks depending on the amount
of blood. In conjunctival ballooning it has to be kept
lubricated with ointment until the swelling diminishes.
In hyphemas medications inducing mydriasis and
cycloplegia are indicated together with sedation and
patching of the traumatized eye. In severe hyphemas
systemic aminocapronic acid in a dose of 50 mg/kg
can sharply decrease the incidence of rebleeding. In
the hemorrhage does not resorb promptly, anterior
chamber lavage should be performed in order to
prevent blood staining of the cornea.
Careful monitoring of the intraocular pressure and
prompt treatment of ophthalmic hypertension are
mandatory. Beta-blockers, carbonic anhydrase
inhibitors and osmotic agents are widely used.
In cases of lens dislocation into the anterior chamber
leading to glaucoma emergency surgery is usually
indicated. Dislocation of the lens in the vitreous cavity
never requires emergency lens extraction. These
patients are managed surgically after inflammation
decrease.
The main treatment method of visually disabling
cataract is extraction. In general, traumatic cataracts
can be safely removed with phacoemulsification
followed by posterior chamber intraocular lens
implantation. Indications for the surgical tactics in each
particular case vary extensively.
Risks of the modern small incision cataract surgery
are few if technically performed well. So the main source
of complications is the ocular comorbidity. Special
surgical techniques (vitrectomy, capsular tension rings,
pupil expansion devices) and alternative methods of
IOL fixation (i.e. scleral and iris fixation) should be
considered since zonular dehiscence, loss of capsular
Fig. 50.5: Vossius ring on the anterior capsule of the
eye with history of blunt trauma
Fig. 50.6: Dislocated cataractous lens following blunt trauma
Fig. 50.7: Lens dislocated into anterior chamber
315
integrity, small pupils and some other clinical findings
and intraoperative events are not uncommon in
traumatic cataract cases.
In corneal wound dehiscence, urgent surgery is
indicated. Suture placement can be combined with iris
reposition, cataract extraction, and hyphema washout
if necessary.
PROGNOSIS
Hyphemas usually clear spontaneously. In some cases
of hyphemas rebleeding can occur. The highest
frequency of rebleeding is between 3 and 5 days after
initial trauma. In severe traumatic hyphemas glaucoma
and corneal blood staining are the matters of concern.
The latter can lead to persistent corneal opacity.
If total hyphema is the result of the secondary
hemorrhage the prognosis is unfavorable. In cases when
the lens is involved the prognosis of vision is reduced.
In surgical reconstruction final visual acuity depends
on the retinal function.
Cataract removal usual l y l eads to visual
rehabilitation. Nevertheless, ophthalmic co-morbidity
may prejudice good visual outcome. The final visual
acuity of patients with traumatic cataracts who undergo
surgery depends on a couple of factors including
amount of the initial eye damage, surgical trauma of
the ocular structures, and degree and duration of
postoperative infl ammation. Proper medical
management of operated patients is essential for a
successful outcome of treatment.
Perforating Injuries of the Globe
Intraocular Foreign Bodies
INTRODUCTION
The physician must suspect the presence of the retained
intraocular or intraorbital foreign body (FB) in all cases
when periorbital or ocular tissues are lacerated.
Patients usually complain on the pain, photophobia,
foreign body sensation, loss or decrease of vision. Lid
swelling, tearing, eye redness, tissue defects at the
wound entry site, corneal erosion, hyphema are the
most common but not the only symptoms physician
can observe. Local corneal defect and edema signals
the site of perforation. Small sharp particles may pass
through the cornea and sink inferiorly into the angle
of the anterior chamber.
Clinical symptoms greatly depend on the localization
of the FB. With the most common sites in the anterior
segment are: conjunctival fornix of the upper or lower
lid, corneal epithelium and stroma, anterior chamber
and lens.
Foreign body located on the corneal surface can
be single or multiple, clearly visible or detected only
with meticulous slit-lamp. Different biological or physical
objects can be found (fragments of glass or metal,
fragments of insects, etc.). From the metal foreign bodies
rust, pieces of metal from grinding wheel, etc. are one
of the most often discovered. In metal objects a rust
ring can surround the foreign body.
In perforating or penetrating injury aqueous humor
enters the lens through the capsular defect. This results
in lens swelling, local opacification rapidly progressing
to complete cataract formation (Fig. 50.8). If the
capsule defect is small it sometimes can heal
spontaneously or can be blocked by the iris. In this
cases localized lens opacity develops.
Perforating ocul ar injuries may l ead to
endophthalmitis (Fig. 50.9). Characteristic clinical
signs of this condition are: lid edema, corneal haze,
aqueous inflammation, vitreous opacification,
conjunctival hyperemia, edema and pain.
Fig. 50.8: An intralenticular metallic foreign body
Fig. 50.9: Bacterial endophthalmitis after ocular trauma
316
INVESTIGATIONS
Patients history and detailed description of the injury
should be obtained.
Single or double eversion of the lid is important
in the search and visualization of the FB located in the
upper lid fornix. Direct visualization is very useful in
determining the presence and location of the foreign
body. It is sometimes very difficult to visualize small
and transparent foreign bodies (for instance small
particles of glass or plastic) even with the slit lamp.
Iris defects due to perforation may be visible under
direct light or with transillumination. Examination of
the anterior chamber angle with the gonioscope can
be useful in detecting small FB lying in the angle.
Gonioscopy should be performed with caution not to
produce aqueous humor leak through the site of
penetration. Ophthalmoscopy after maximal pupil
dilation should be used in cases of suspected FB in
the vitreous or on the retina.
In cases of opaque ocular media (extensive corneal
edema, hyphema, cataract and vitreous hemorrhage)
A- and B-scans, X-ray examination, computerized
tomograms must be performed in suspected cases.
Some of these examinations can also determine
whether or not the FB is magnetic.
Main differential diagnosis relates to the fact whether
intraocular FB is present or not. Physician should keep
in mind that multiple foreign bodies are not uncommon.
The latter is characteristic to the explosions and blasting
injuries (multiple intracorneal rocks), shotgun blasts and
the like.
TREATMENT
In cases of perforating ocular injuries prompt
therapeutic intervention is justified. Local and systemic
wide spectrum antibiotics shoul d be given.
Corticosteroids are administered in order to limit the
destructive effect of inflammation that accompanies
infection.
In most cases of globe lacerations urgent surgery
with the suturing of the wound site should be
performed.
Clinical management in cases of FB largely depends
of the judgment of the following factors: localization
of the foreign body, its shape, size and composition,
extent of the trauma of surrounding tissues and the
decision of whether remove it or leave in place.
The ophthalmologist must decide for or against
removal of the foreign body after careful judgment of
all relevant factors. The risks of inflammation, toxic
chemical effects and fibrovascular proliferation should
be taken into consideration.
These effects largely depend on the chemical nature
of the FB. If the foreign body contains iron or
particularly copper treatment tactics should be
aggressive and early surgery is mandatory. The opposite
is true in small non-magnetic FB containing no or
minimal concentrations of aggressive substances.
FB located in the anterior segment is not difficult
to remove. In many cases anterior segment foreign
bodies can be removed through the wound of entry.
If the object is small (2-3 mm in diameter) extraction
with magnet through the entry route may be considered.
Larger object can be removed utilizing the limbal
approach.
Tears in the lens capsule of 2 mm in size can seal
without causing cataractous changes. Thus small foreign
bodies can be left in the lens. Bigger FB causing diffuse
cataracts should be managed during cataract extraction.
Intensive antibiotic treatment (topical, oral or IV)
should be administered in all cases of intraocular FB.
With metal FB in the superficial corneal layers, after
topical anesthesia is being applied, the patient is brought
under slit lamp and the metal fragment is lifted with
the 25G needle on a syringe or a special instrument.
Foreign body located in the deep corneal layers should
be removed under the operating microscope. In cases
of full thickness corneal penetrations suturing of the
wound should be done in order to achieve watertight
seal. Postoperatively patients should be treated with
antibiotics and cycloplegics.
PROGNOSIS
Once the presence of the FB in the eye has been
established, the prognosis depends on the variety of
factors. In the eye with the injury limited to the anterior
eye segment prognosis is favorable in most cases and
depends of the effectiveness of the surgical repair and
antibiotic treatment. In cases without good light
projection the prognosis is not infrequently poor. Foreign
bodies containing cooper or iron are particularly dange-
rous due to the chalcosis and siderosis development.
Traumatic perforations of the cornea lead to scar
formation (Figs 50.10 and 50.11).
Consideration of the potential development of
sympathetic ophthalmia in perforating globe injury is
absolutely necessary. Sympathetic ophthalmia is more
likely in severe globe injury with excessive damage
of the uveal tissue leading to eye globe atrophy (Fig.
50.12).
317
Fig. 50.10: Corneo-scleral scar involving iris and lens
Fig. 50.11: Complete cataract after perforating corneal
injury with iris and lens capsule damage
Fig. 50.12: Eye globe atrophy
Ultraviolet Corneal Burns
INTRODUCTION
Ultraviolet corneal burns can be caused by the use of
sunlamps or welding lamps without use of proper eye
protection.
In ultraviolet corneal burns there is typically a delay
in the onset of the symptoms. Interval after the exposure
can reach up to 5-8 hours. A patient complains of eye
irritation, photophobia, pain, and foreign body
sensation. These symptoms can progress to severe pain
and blepharospasm.
INVESTIGATIONS
Careful history and slit-lamp examination should be
performed. Topically applied fliorescein can reveal
punctuate corneal staining.
In ultraviolet corneal burns differential diagnosis should
be performed with ocular surface inflammation, dry
eye, chemical burns.
TREATMENT
Patients should be treated with antibiotics and ocular
surface lubricants.
PROGNOSIS
The prognosis is usually favorable. Rehabilitation is
usually achieved in 24 to 48 hours.
Chemical and Thermal Burns of
the Eye
INTRODUCTION
Burns of the eye are one of the most urgent ocular
emergencies. The extent and severity of damage are
determined by the nature and concentration of the
chemical agent as well as the time of contact with the
tissue.
The damage caused by acids is progressive but longs
only within the first few hours. Their buffering with tissue
proteins lead to the tendency of damage localization
at the area of the contact with the agent.
Alkali can penetrate rapidly into the tissue. This effect
is determined by their ability to damage cellular
membrane lipids, causing disruption of cells and melting
of tissue. Tissue penetration of alkali occurs quickly and
their effect may lasts for days.
Exposure to flame rarely affects the cornea and eye
globe, but more likely to cause the lid damage.
Patient complains on the severe pain and loss of vision.
Main symptoms include: necrosis of the skin, lids
318
swelling, blepharospasm, necrosis of conjunctiva,
corneal opacification (the severity is judged upon the
possibility to visualize the anterior chamber structures).
In the most severe cases corneal perforation may occur.
Strong alkalis cause ischemia and coagulative
necrosis of conjunctiva and sclera. The extent and
severity of damage is judged by the severity of corneal
opacification and degree of perilimbal ischemia.
In thermal burns marked edema and tissue necrosis
of the lids are usually present.
INVESTIGATIONS
In chemical burns steps in evaluation and treatment
include: anamnesis, identification of the nature of the
chemical agent, visual acuity evaluation. Determination
of the conjunctival pH should be done if the nature
of the chemical agent is unknown. For this matter pH
paper touched to the affected tissue will show whether
chemical is acidic or basic.
The examiner should be looking for the presence of
ocular perforating injuries and intraocular foreign
bodies. The nature of the chemical agent should be
differentiated.
TREATMENT
The eye should be irrigated immediately after injury
with minimum of 1.0 liter of water. The only very rare
exception is the chemicals that react violently with
water. The use of the neutralizing agents is feasible in
case they are available. Fornices of the conjunctival
sac should be washed thoughtfully. The latter can
require application of local anesthetic agents to prevent
patients squeezing.
Chemical matter and debris should be removed with
irrigation, cotton swabs, and forceps.
In moderate and severe alkali burns immediate
paracenthesis of the anterior chamber should be
performed. Aqueous humor drainage is done with the
purpose to lower aqueous pH.
Medications: topical antibiotics, cycloplegics,
corticosteroids, hypotensive medications if necessary.
Surgical treatment including mucous membrane or
conjunctival grafts can be used in cases of
symbleopharon and delayed epithelisation. Lamellar
or penetrating corneal transplantations in acute
chemical burns are limited to the cases of corneal
perforation. Limbal stem cells transplantation with or
without lamellar corneal grafting recently showed their
efficiency in restoration of the optical clarity of the media
in long-term period after corneal burns.
In thermal burns the treatment of shock and pain
as well as infection control are of primary importance.
In burns of lid antibiotic ointments are prescribed,
topical steroids remains controversial.
PROGNOSIS
Alkaline materials penetrate more rapidly into the
cornea and anterior chamber. That is why the results
of alkali burns are more severe then those of burns
caused by acids.
Moderate and severe chemical burns may lead to
scarring of conjunctiva with symblepharon formation.
Cataracts are common consequence of severe chemical
burns, especially alkali. Alkali penetration into the
anterior chamber and coagulation of the anterior
chamber angle structures can result in glaucoma.
Skin scarring of the lids can cause cosmetic defects
but also chronic epiphora, trichiasis, exposure keratitis,
corneal opacification. Damage of the tear ducts and
lacrimal glands may lead to severe dry eye.
C H A P T E R
51
Management of Ocular Trauma
with Plasma (Fugo) Knife
Ranjit Singh, Indu R Singh, Kiranjit Singh, Harmit Kaur,
KK Bhalla, Daljit Singh (India)
Introduction
Ocular trauma throws up interesting and varied clinical
situations, some of which really make us scratch our
brains and make us wish we had something more than
our regular instrumentation to deal with the problems
at hand.
In this chapter we are going to discuss the
management of some such peculiar situations as a result
of ocular trauma, which we feel are either difficult or
outrightly impossible to be tackled.
We are going to discuss the role of a new surgical
instrument known as the Plasma Knife in the
management of such problems.
While traditional definition of trauma brings to our
mind, accidents involving injuries to the eyes, we
strongly feel that iatrogenic reasons of ocular trauma
cannot be evaded while discussing this subject. So
badly operated eyes have also been included in this
textbook of ocular trauma.
What is Plasma (Fugo) Knife?
Before we go any further with this chapter, it is
imperative to understand the nature of the instrument
that is going to be referred to most frequently during
the course of this article, i.e., the Plasma Knife. Designed
by Dr.Richard Fugo, in USA, this device has been tuned
for ophthalmic use.
The plasma, which we refer to, is also known as
the fourth state of matter. Plasma is distinctly different
from, solids, liquids and gases. It is also the most
abundant phase of matter in the universe as both stars
and interstellar dust consist of plasma. Plasma is often
referred to as ionized gas. This is similar to normal
gas except that electrons have been stripped from their
respective nucleons and float freely within the plasma.
Pl asma is el ectrical l y conductive and can be
manipulated by magnetic fields.
Plasma can be found in a variety of everyday
contexts, including plasma displays, fluorescent lamps,
neon signs, plasma balls, photolithographic etching
machines, flames, lightning, aurora borealis and more.
The cutting abilities of plasma can be gauged from
the fact that Plasma cutters are used in the industry
for precision cutting of steel.
Fugos plasma knife is a surgical device that uses
plasma (focused electromagnetic energy) to perform
precision cutting of ocular tissues. In the Fugos plasma
knife, the plasma generating engine has been bundled
into a small unit, which creates enough energy to be
safely used for ophthalmological applications.
Plasma generation is done in a filament fixed to
a hand piece and connected to the plasma generating
engine. The filament is barely thicker than a human
hair (100 micron). The tip can be made in different
lengths and can be bent as required. Only the extreme
tip gets activated for cutting. An electronic charge pump
causes the upper layer of atoms in the filament (about
a micron deep) to transform from the solid state into
the activated plasma state. A focused electromagnetic
field is used to control, contour and shape these plasma
particles into a plasma cloud around the filament.
(Fugo, 1999).
The temperature at the tip as measured with a
thermocouple is as high as 4500 degrees centigrade,
though the amount of total heat produced is very little
because the surface area of the plasma produced is
very small. The atomic particles that make up this
plasma cloud are in such a high state of agitation that
they literally dissolve the molecular bonds of the
material they come in contact with. The tiny filament
doesnt bend, even when cutting through something
as strong as cow-hide, because it never touches the
material. The plasma cloud dissociates the material
faster than the hand can move the instrument. (Fugo,
1999).
Cutting with even the sharpest diamond knife needs
at least some counter pressure but the plasma knife
320
can cut through without any tactile feedback. This fact
has been tested by floating an enucleated eyeball(fixed
to piece of foam) in water and then trying a diamond
knife and the plasma knife to cut. The eyeball would
just float away when the diamond knife would touch
it and cutting was not possible at all. On the other
hand the activated plasma knife filament would
effortlessly pass through the eyeball with minimum
push. However, the characteristics of a cut created by
a diamond knife and a plasma knife are fundamentally
different because of obvious reasons.
Fig. 51.1A: Fugos plasma Knife Unit, including the
console, activation footswitch and the handpiece
The Fugos plasma knife unit essentially consists of
a console, a foot switch and a handpiece, to which
disposable plasma delivery tips are attached. The
machine runs on rechargeable batteries. A single charge
delivers up to one hour of continuous plasma energy.
There are two setting switches on the machine. One
knob adjusts between low medium and high energy
while the other knob selects the intensity of cutting
energy.
Fig. 51.1B: Low magnification picture of the Plasma knife
tip attached to the hand piece with a bayonet mount
Fig. 51.1C: Magnified view of the plasma knife tip. Plasma
generation takes place on the extreme tip of the exposed
filament
The plasma blade tip is essentially an electrically
conducting needle, which ends into a 100 micron fiber.
All except the extreme tip of the 100 micron fiber is
insulated and waterproofed. The tip can be made up
to any required length or bent into any desirable
shape.
Fig. 51.1D: Activated plasma knife filament seen under
magnification. The yellow part is the plasma and the orange
part is the photon cloud.It is the plasma which cuts, not the
photon cloud. If plasma is generated in a dark room,it emits
bright flashes of light
An uncharged plasma blade filament has no cutting
ability at all. It is the plasma that creates the incision.
The inactivated tip has difficulty even in abrading
corneal epithelium. (Fugo, 1999). The activated tip
easily cuts through a 50 micron stainless steel wire.
The Fugos Plasma Knife has been approved by
US FDA for performing capsulotomy and trans-ciliary
filteration for glaucoma. Already things are underway
for the introduction of this fundamental technology
in general surgery and dentistry.
321
Management of Ocular Trauma with Plasma (Fugo) Knife
Though originally designed capsulotomy device we
found limited usage of this for the said purpose, but
found it to be invaluable as a cutting instrument for
thick irido-capsular membranes, something which is
difficult/impossible to be cut with a capsulotomy needle,
a vannas scissor or a vitrectomy cutter. It is this ability
that finds this machine a place in the management
of tough cases of ocular trauma.
Key Properties of Plasma Knife
a. Cuts effortlessly.
b. There is no tissue drag.
c. Coagulates as it cuts.
d. Ease of use.
Fig. 51.2A: A 22-year-old male patient suffered injury in a
road accident 6 months ago. Left eye was lost and the right
eye suffered bad injuries. Cornea had been repaired. The
ruptured cataract had absorbed on its own, leaving behind
a thick membrane in the pupil formed by the fusion of the
anterior and the posterior capsule and imprisoned lens
material. It was planned to clear the visual axis with the
plasma knife and implant an Iris Claw Lens
Fig. 51.2E: An Iris Claw Lens implant is fixed to the
anterior surface of the iris
Fig. 51.2B: The plasma knife tip was introduced into the
anterior chamber through a 2.8m keratome incision while
a cannula was introduced from the left paracentecis to
deliver continuous methyl cellulose irrigation
Fig. 51.2C: The plasma blade was activated and a round circle
was traced in the optical axis in an effort to cut the dense
membrane. You can very well visualize the process of cutting
and the formation of cavitation bubbles in the figure above
Fig. 51.2D: The plasma knife membranectomy was
completed with the cut out part of the membrane resting
in the centre.This piece was removed with a forceps and
limited anterior vitrectomy done
322
Fig. 51.2F: A 10-month post operative picture of the patient
with corrected visual acuity of 6/18 Snellens. Patient had
to wear high cylindrical glasses because of corneal
scarring. As of now, the patient is mobile
Fig. 51.3A: Intraoperative picture of an encapsulated
metallic foreign body in the retina.During the pre-operative
evaluation, it was the B-scan and the CT scan which
confirmed the presence of the foreign body cocooned
inside the fibrous tissue.During vitrectomy the fibrosis was
found to be so thick that it could not be split open with the
tip of a vitrector or 24-gauge needle. We even tried using
a diamond blade, mounted on a 20-gauge tip to cut the
shell open but of no avail.So the services of the plasma
knife were sought. The endo-laser marks can be seen
applied to the retina all around the foreign body
Figs 51.3C to E: Showing the various stages of the
exposure of the foreign body while the fibrotic tissue is
being sliced with the plasma knife.There was no push
generated by the plasma knife during the cutting of the
fibrous tissue, unlike the needle and the diamond blade
Fig. 51.3B: A special plasma knife tip, long enough to reach
the retinal surface was utilized to expose the hidden foreign
body. You can see the tip of the foreign body getting
progressively exposed
Fig. 51.3F: This is a picture of the extracted foreign body
being held with an intraocular foreign body removal forceps,
which will be removed via pars plana
323
Fig. 51.4A: A 9-year-old female child suffering from
Iatrogenic trauma having been operated for congenital
cataract 4 years ago.The parents were unaware whether
lens implantation had been done or not. The pupil was slit
like and closed off with a layer of pigment.Patient was taken
up for exploratory surgery because of strongly positive
perception and projection and a normal B-Scan ultrasound
Fig. 51.4B: Iris hooks were used to keep the pupil
expanded after dissecting the adhesions of the posterior
surface of the entire iris to the tissues below.Below the iris,
we discover a intraocular lens encapsulated between a
thick anterior and posterior capsule
Fig. 51.4C: The plasma knife was first used to cut the anterior
capsule while the anterior chamber was continuously
irrigated with methyl cellulose.The plasma knife tip was
traced on the fibrotic anterior capsule and within no time
the thick capsule was inundated
Fig. 51.4D: A very thick membrane (posterior capsule) could
be visualized very clearly under the intraocular lens.A gap
was created between the posterior chamber intraocular
Lens and the posterior capsule so that the plasma knife
tip could be slipped into the gap
Fig. 51.4F: A perfect opening was created in the centre of
the thick posterior capsule. The cut out piece of the
posterior capsule was removed with a forceps and limited
anterior vitrectomy was performed
Fig. 51.4E: The plasma knife was pushed under the
intraocular lens. It was then activated and a circle was
traced on the fibrosed posterior capsule
324
Fig. 51.4G: Picture at the end of the procedure with a
clear visually axis
Fig. 51.4H: A 4-month post-operative picture of the same
eye showing a nicely created opening in the centre in the
visual axis.The immediate visual result was poor because
of amblyopia and pleoptics were started
Fig. 51.5: Picture of a posterior chamber IOL which went on
to progress to optic capture into the pupil, cheese wiring of the
haptics through the iris tissue and complete closure of the pupil
with irido - capsular tissue. Vain attempts to clear the pupil with
a yag laser are visible as pits on the optic of the lens. Since the
tissues were strongly fused to each other, the plasma knife was
used to cut through the stubborn tissue, which obliged by creating
a round pupil in the middle. The rest of the abnormalities continue
to exist but the patient can see now and has no other major
problem
Fig. 51.6A: Picture of a childs eye aged 6, post penetrating
ocular trauma, having been repaired elsewhere along with
i mpl antati on of a posteri or chamber l ens. A thi ck
vascularized membrane was visible in the pupil and the
intraocular lens formed a part of this complicated mess.
Perception and projection of light was strongly positive and
B-Scan ultrasound revealed a clear posterior segment,
therefore we decided to clear the visual axis
Fig. 51.6B: Since the implantation of the intraocular lens
was far from satisfactory, it was decided to explant the lens
after dissecting it carefully from its surrounding tissues.
Plasma knife was then used to slice through the membrane
after retracting the pupil. This one day post-operative
picture of the patient after membranectomy along with
limited anterior vitrectomy
Fig. 51.6C: Two months post-operative picture of the
same eye showing a clear visual axis
325
Fig. 51.7A: Intraoperative picture of an eye in an 11-year
old child after blunt trauma with a fire cracker.There was
mature traumatic cataract with fibrosed and thickened
anterior capsule and traumatic mydriasis. We decided to
do the capsulorrhexis with the plasma knife
Figs 51.7B and C: Pi ctures showi ng pl asma kni fe
capsulotomy in progress while the viscoelastic was being
injected through the side port
Fig. 51.7D: Implantation of the intraocular lens into the
capsular bag could be done. The capsulotomy performed
within the fibrosed capsule is clearly visible. It seems that
in the absence of the plasma knife, optimal surgical
outcome may not have been possible
Fig. 51.8A: A typical case of blunt trauma with add on
Iatrogenic ocular trauma in a 12-year-old girl operated for
traumatic cataract and lens implantation elsewhere. The
intraocular lens visible in the anterior chamber had
seemingly migrated from the posterior chamber into the
anterior chamber.While one haptic was still behind the iris,
the optic was in front of the iris and the second haptic was
seen missing, having broken off near the haptic-optic
junction.Whether this was accidentally broken while
implanting or deliberately done will never be known.In
addi ti on, there was an i nti mi dati ng vascul ari zed
iridocapsular membrane in the pupillary area. Since B-Scan
reveal ed a normal l ooki ng posteri or segment and
perception and projection of light was good,we decided to
explant the lens and perform pupilloplasty
326
Figs 51.8B and C: After explantation of the broken
intraocular lens, we tried to do pupilloplasty with a
vitrectomy cutter as well as with a capsulotomy needle.Both
of these instruments were not only ineffective but also led
to bleeding from the tissues
Figs 51.8D and E: Then we pressed the plasma knife into
service. A perfect pupilloplasty could be performed with the
plasma knife with minimal bleeding and fuss.Limited
anterior vitrectomy followed the pupilloplasty
Fig. 51.8F: Postoperative outcome of the surgery, 20 days later
shows a quiet eye with a clear visual axis. We can certify that
without the plasma knife, this case would have been
impossible to perform
327
Technique of Using the Plasma
Knife
Basically plasma knife cuts whatever tissue it comes
in contact with but for working in a closed anterior
chamber, the following technique has been evolved.
Whenever plasma knife tip is activated in a fluid
medium, cavitation bubbles are produced and these
bubbles can lead to poor visibility by sticking to the
endothelium. To counter this problem, we use a simple
device to continuously inject a viscoelastic material
(usually methyl cellulose)through the side port. The
surgeon inserts a 24 gauge cannula attached to a
syringe filled with a viscoelastic. The assistant is
responsible for injecting the viscoelastic while the
plasma knife is activated. This serves a dual purpose
of keeping the anterior chamber deep at all times as
well as pushes the cavitation bubbles away from the
working tip and out through the main incision. This
leads to precise cutting and minimum time spent inside
the anterior chamber.
Clinical Examples of
Management of Cases of
Trauma with the Plasma Knife
Case 1 (Figs 51.2A to F)
Case 3 (Figs 51.4A to H)
Case 4 (Figs 51.5)
Case 5 (Figs 51.6A to C)
Case 6 (Figs 51.7A to D)
Conclusion
The plasma knife is a capable cutting instrument which
has been approved as a device that can be safely used
inside the eye. Its impeccable cutting ability along with
property of hemostasis makes it a capable machine.
I will not be too off the mark in saying that this
machine deserves a place inside every ophthalmic
operating set-up. We may not come across cases like
the ones described here everyday, but the presence
of this device in the operating room provides us with
additional capabilities and allows us to undertake
surgeries which normally may be turned away from
the outpatient room itself.
As of now there are not too many users of this
machine, hence the experience is just very limited.
When one buys an expensive machine you expect
certain specific indications where it is supposed to be
used. While a couple of indications have been outlined
there is much more that is still to be figured out. What
you have just gone through are but just a few examples.
I am sure that with time, more indications are bound
to evolve.
Disclaimer: The authors have no financial interest in
the device(s) mentioned here.
C H A P T E R
52
Chandelier Illumination and
Bimanual Vitrectomy Used to
Remove a Dislocated IOL
Amar Agarwal, Soosan Jacob, Athiya Agarwal
Sunita Agarwal, Ashok Garg (India)
Introduction
Numerous advances in microsurgical techniques have
led to highly safe and effective cataract surgery. Two
of the current trends in the evolution of modern
cataract techniques include increasingly smaller surgical
incisions associated with phacoemulsification (e.g.
sub 1.4 mm incisions as in Phakonit with rollable IOL
implantation)
1
, as well as the movement from
retrobulbar and peribulbar anesthesia to topical
anesthesia, and even no anesthesia techniques.
2
Despite such advances, the malpositioning or
dislocation of an intraocular lens (IOL)
3-5
due to
capsular rupture or zonnular dehiscence remains an
infrequent but important sight-threatening
complication for contemporary cataract surgery. The
key to the prevention of poor visual outcome for this
complication is its proper management.
Management of a Malpositioned
IOL
Disturbing visual symptoms such as dipl opia,
metamorphopsia, and hazy images are associated with
a dislocated intraocular lens (IOL) (Fig. 52.1). If not
properly managed, a malpositioned IOL may also
induce sight-threatening ocular complications,
including persistent cystoid macular edema, intraocular
hemorrhage, retinal breaks, and retinal detachment.
Contemporaneous with advances in phakonit
microsurgical techniques for treating cataracts, a
number of highly effective surgical methods have been
developed for managing a dislocated IOL.
Chandelier Illumination
Visualization is done using a Chandelier illumination
in which xenon light is attached to the infusion cannula.
This gives excellent illumination and one can perform
Fig. 52.1: Dislocated IOL on the retina
Fig. 52.2: IOL lying over the macula. Notice the wide field
view of the retina. This is because of the wide field contact
lens being used and the Chandelier illumination which is
seen in the upper left hand corner
329
Chandelier Illumination and Bimanual Vitrectomy Used to Remove a Dislocated IOL
a proper bimanual vitrectomy as an endoilluminator
is not necessary for the surgeon to hold in the hand.
(Fig. 52.2). A Reinverter system has to be used if
one is using a wide field lens (Volk or Oculus). The
supermacula lens (Fig. 52.3) helps give better
steropsis so that one will not have any difficulty in
Fig. 52.3: View using the super macula lens. This gives
better steropsis
Fig. 52.4: Diamond tipped forceps lifting a looped IOL
lying on the retina after a vitrectomy
Fig. 52.5: Forceps holding the IOL and the vitrectomy probe
cutting the vitreous adhesions. This is bimanual vitrectomy
which is possible due to the Chandelier illumination
Fig. 52.6: Handshake technique. Using two forceps one
can hold the IOL comfortably and bring it anteriorly
Fig. 52.7: IOL brought out anteriorly through the limbal route.
Notice in the upper right and left corners infusion cannulas
fixed. One is for infusion and the other for the Chandelier
illumination. One can also have the same infusion cannula
with the Chandelier illumination
holding the IOL with a diamond tipped forceps
(Fig. 52.4). When one is using the Chandelier
illumination system one hand can hold the IOL with
the forceps and the other hand can hold a vitrectomy
probe to cut the adhesions of the vitreous thus doing
a bimanual vitrectomy (Fig. 52.5). One can also use
two forceps to hold the lens thus performing a hand
shake technique (Fig. 52.6). The lens is then brought
out anteriorly and removed through the limbal route
(Fig. 52.7).
Reinverter System
When we use the wide field indirect contact vitrectomy
lenses we have to use a reinverter as the image is seen
inverted. The reinverter again makes the image erect
so that the surgeon does not have difficulty in
operating. The one we use is the one from Zeiss
microscopes which has a foot switch connection. In
330
other words on pressing the footswitch button the
reinverter works.
The Volk Reinverting operating lens system is also
present. It has a unique single-element prism design.
This installs in the Zeiss and other microscopes. It offers
surgical visualization ranging from high magnification
of the macula to panoramic viewing upto and including
the ora serrata.
Wide Field Indirect Contact
Vitrectomy Lenses
These are essential for performing proper bimanual
vitrectomy. When one is doing vitrectomy for dropped
IOL we use the Mini Quad Volk lens or the Oculus
lens. These lenses give the view of the retian upto the
ora serrata. When one wants to pick up the IOL with
the diamond tipped forceps then we use the
Supermacula Volk lens. This lens gives very high
magnification. Another advantage of this lens is the
better steropsis so that you know exactly where the
IOL haptic is in relation to the retina. These lenses come
with a handle so that the assistant can hold the lens
comfortably.
Bimanual Vitrectomy
The advantage of the bimanual vitrectomy set-up is
that the hand which normally holds the endoilluminator
is free and so one can use two instruments to
manipulate the dropped IOL. The Chandelier
illumination system we used was from Synergetics
(USA) and the machine was the Photon. Sophisticated
filtering techniques within the Photon and its associated
fiberoptics are used to provide higher illumination
levels.
References
1. Agarwal A, Agarwal S, Agarwal A. Phakonit: Lens
removal through a 0.9 mm incision. In: Agarwal A
Phacoemulsification, Laser Cataract Surgery and Foldable
IOLs First edition. Jaypee Brothers 1998.
2. Agarwal A, Agarwal A, Agarwal S. No Anesthesia Cataract
surgery. In: Agarwal A Phacoemulsification, Laser
Cataract Surgery and Foldable IOLs Second edition.
Jaypee Brothers 2000.
3. Chang S. Perfluorocarbon liquids in Vitreo-retinal surgery.
International Ophthalmology Clinics-New approaches to
vitreo-retinal surgery: Vol32, No.2, Spring 92: 153-63.
4. Chan CK, An improved technique for management of
dislocated posterior chamber implants. Ophthalmol
1992; 99:51-57.
5. Chan CK, Agarwal A, Agarwal S, Agarwal A. Management
of dislocated intraocular implants. In: Ophthalmology
Cl inics of Nor th America, Posterior Segment
Complications of Cataract Surgery, December 2001;
editors: P.N. Nagpal, I. H. Fine; W. B. Saunders,
Philadelphia 681-93.
C H A P T E R
53
Principles and Management
of Ocular Trauma
Syed Asghar Hussain, Amol Mhatre, Kanupriya Mhatre
Supriya Dabir, Saumil Sheth, Vandana Jain, S Natarajan (India)
Introduction
Ocular trauma classification groups has classified
mechanical injuries to the eye into 2 categories.
1. Open globe: Full thickness defect in corneoscleral
coat of the eye and
2. Closed globe : Ocular injuries without full thickness
defect of the globe
Classification
Mechanical Eye injury can be classified

as follows
(Table 53.1).
TABLE 53.1: Classification of mechanical eye injuries
1. Open Globe Injury Classification
Type
A. Rupture
B. Penetrating
C. Intraocular foreign body
D. Perforating
E. Mixed
Grade
Visual Acuity
1. 20/40
2. 20/50-20/100
3. 19/100-5/200
5. No light perception
Pupil
Positive: relative afferent pupillary defect present in
affected eye.
Negative: relative afferent pupillary defect absent in
affected eye.
Zone
I. Isolated to cornea( including corneoscleral
limbus).
II. Corneoscleral limbus to a point 5 mm posterior
into the sclera.
III. Posterior to the anterior 5 mm of sclera.
2. Closed Globe Injuries Classification
Type
A. Contusion
B. Lamellar laceration
C. Superficial foreign body
D. Mixed
Grade
Visual acuity
1. 20/40
2. 20/50-20/100
3. 19/100-5/200
5. No light perception
Pupil
Positive: relative afferent pupillary defect present in
affected eye.
Negative: relative afferent pupillary defect absent in
affected eye.
Zone
I. External (limited to bulbar conjunctiva, sclera,
cornea)
II. Anterior segment (involving structures in anterior
segmentinternal to the cornea and including the
posterior lens capsule; also includes pars plicata
but not pars plana)
III. Posterior segment ( all internal structures posterior
to the posterior lens capsule)
DIFFERENT TERMS USED IN OCULAR TRAUMA
Closed globe: Eye wall does not have a full thickness
wound.
Open globe: Eye wall has a full thickness wound.
Laceration: Full thickness wound caused by a sharp
object.
Penetrating injury: Single full thickness wound
caused by a sharp object.
Intraocular foreign body (IOFB): Retained foreign
body causes a single entrance wound.
Perforating injury: Two full thickness wounds- entry
and exit wound.
Contusion: Closed globe injury resulting from a
blunt object.
332
Lamellar laceration: Closed globe injury of the eye
wall or bulbar conjunctiva caused by a sharp object.
EPIDEMIOLOGY OF OCULAR TRAUMA
The general incidence reported is variable both in India
and abroad. In India, the reported incidence varies
from 1-5%. In almost all studies, the incidence of
injuries is higher in males than females. Male
preponderance is understandable as they are more
exposed to outdoor activities. Maximum incidence of
injuries occur in 21-30 years of age. Shukla and Verma
have found 29.2% incidence as occupational.
PROGNOSTIC FACTORS
Despite of advances in ocular imaging, instrumentation,
materials, and surgical procedures, the management
of open globe injuries continue to pose difficult
management dilemmas. Prognosis depends on various
factors such as initial visual acuity, presence or absence
of relative afferent pupillary defect, type and zone of
injury, time elapsed between the injury and surgery,
cataract formation or dislocation of lens and also
presence or absence of retinal detachment or
endophthalmitis.
Closed Globe Injuries
ANTERIOR SEGMENT TRAUMA CORNEAL
INJURIES
This is one of the most common ophthalmic emer-
gencies.
The most common presentations are:
1. Corneal Foreign Bodies
2. Lamellar Corneal Lacerations
3. Vossius Ring
4. Traumatic Hyphema
5. Traumatic Cataract
Corneal Foreign Bodies
Clinical features
Foreign Body Sensation
Conjunctival Congestion
Watering of Eyes
Photophobia
Ocular examination may reveal edematous lids. Slit
Lamp examination shows foreign body embedded in
the corneal epithelium.
Management: After informing the patient about the
procedure, instill topical anaesthetic drops into the eye.
Also explain to the patient about infection and
sensation of foreign body in the affected eye.
Then, the cornea is scraped with the help of a 26
G needle and the foreign body is removed. Following
this, the eye is instilled with antibiotic ointment and
eye pad is applied.
The common complications encountered with are
corneal ulcer, corneal perforation and traumatic
cataract. Then, flurbiprofen should be added as an
anti-inflammatory. Vitamin C may be supplemented
to promote re-epithelisation. Regular follow up,
protective goggles for 24 hrs and review is advised.
A deep corneal foreign body may cause corneal
opacity abscess.
Lamellar Corneal Lacerations
History: The patient usually presents with history of
injury or unconsciousness, convulsions, bleeding from
nose, ears, etc.
Evaluation: The patient is subjected to a complete
general and ophthalmic examination, including Slit
Lamp Examination, which is a must. Determination
of visual, acuity and Siedels Test should be performed
in all cases of occult injury.
Siedel's Test: This test is performed to rule out occult
perforation of Descemet's Membrane. In positive cases,
there is a high risk of endophthalmitis and hypotony.
Traumatic hyphema
Traumatic hyphema generally occurs in young active
people, predominantly males, and also children,
accounting for nearly 50% of all eye injuries.
The mechanism could either be due to direct impact,
compressive wave force, reflected compressive wave
or rebound compressive wave. It is usually caused by
a high velocity projectile or an object which strikes the
exposed portion of the eyeball, the total extent of the
damage depending upon the nature, size, anatomical
location and force of impact.
The most common causative factors are balls, rocks,
toys, human fists and gun pellets, etc. The usual effect
of a blunt compressive force onto an eyeball results
in the sudden decrease in the antero posterior
dimensions of the eyeball, thus causing a compensatory
increase in the anterior equatorial circumference of
the globe. This leads to the posterior displacement of
the iris-lens diaphragm, with scleral expansion in the
equatorial zone. This, in turn leads to shearing and
disruption of the circulus arteriosus iridis major, arterial
branches of the ciliary body, and / or recurrent choroidal
arteries and veins, crossing between the ciliary body
and episcleral venous plexus, resulting in hyphema.
In cases where no layering of blood is visible in the
anterior chamber, but few red blood corpuscles are
333
Principles and Management of Ocular Trauma
seen, it is called as microhyphema. In later stages, this
has propensity to develop into a hyphema. If the whole
anterior chamber is filled with a massive organized
hyphema constituting clotted blood, it is called as "Eight
Ball Hyphema".
The anterior chamber bleed usually results from
tears or splits in the iris, ciliary body, trabecular
meshwork, zonule, lens and peripheral retina, in
response to blunt ocular trauma.
The anterior segment manifestations usually include
corneal abrasion, endothelial denudation, corneo-
scleral rupture, scleral rupture, iris sphincter tears,
iridodialysis, angle recession, cyclodialysis, iris
meshwork tears, vossius ring, zonular rupture, cataract,
lens subluxation, etc.
The posterior segment manifestations include
vitreous hemorrhage, retinal edema, retinal dialysis,
retinal hemorrhages, horseshoe tear, choroidal
rupture, sclopeteria retinitis, optic nerve avulsion, etc.
If left untreated, a total hyphema of over six days
with more than 25 mm Hg of intraocular pressure
tends to develop blood staining of the cornea. In
addition, the raised intraocular pressure over long
periods of time can cause optic nerve damage.
The line of management is medical and surgical.
The patient is advised hospitalisation, sedation, bed
rest, elevated head position to 30, eye shield, 1%
Atropine eye drops b.i.d. (controversial), topical cortic-
osteroids (1% prednisolone q.i.d.), oral prednisolone
(0.75mg/kg per day). Some surgeons recommend oral
Aminocaproic acid (50mg/kg q.i.d.) or tranexamic acid
which are both antifibrinolytic agents.
Associated secondary glaucoma (IOP>30 mmHg)
is treated aggressively with topical beta blockers (0.5%
timolol b.i.d.), alpha agonist (0.2% brimonidine t.i.d.),
carbonic anhydrase inhibitor (2% topical dorzolamide
t.i.d.) or 50 mg oral methazolamide t.i.d.) and 20%
IV mannitol (1 gm/kg to 2 gm/kg over 45 mins).
Surgical interventions have also been advocated
such as paracentesis, irrigation and aspiration, clot
expression, clot excision with automated vitrectomy
apparatus.
LENS AND TRAUMA
Trauma affects the human lens in different ways such
as vossius ring, discrete sub epithelial opacities, rosette
shaped opacities, zonular cataracts, concussion
cataracts, capsular tears, swelling, zonular dehiscence
without lens displacement, lens displacement and
dislocation.
Blunt trauma in an anterior-posterior direction
causes shortening in that meridian with stretching of
the equator which may cause zonular disruption with
resultant subluxation or dislocation of the lens. In this
event, the whole suspensory ligament apparatus is
drawn behind the iris. The lens may remain in the
patellar fossa, retained by its attachment to the vitreous
or the ligamentum hyaloideocapsularis. The lens
becomes tremulous, and its position is determined by
the traction of the intact zonulae and the effect of
gravity. The patient presents with myopia and
impairment of accommodation as well as astigmatism,
which is usually impossible to correct.
When the lens is completely dislocated from the
patellar fossa, it may be seen incarcerated in the pupil,
in the anterior chamber, in the vitreous (either free
floating - lens natans) or fixed - lens fixata, in the sub
conjunctival space - phacocele, in the sub scleral space
or sub retinal space or may be wandering forwards
into the AC and backwards into the vitreous, through
the pupil.
The usually associated complications include Lens
Particle Glaucoma, Phacolytic Glaucoma, Lens induced
angle closure, Rubeosis iridis, uveitis, keratitis, retinal
detachment and sensory deprivation amblyopia.
The investigations include Macular Function Tests,
IOP, Angle Study, B-Scan Ultrasonography and
el ectrophysiol ogical tests (ERG, VEP) and
Radiographic studies (X-ray, OCT, CT Scan and MRI).
The techniques of lens removal are Anterior Limbal
Route (Bimanual Lenticular aspiration, Epilenticular
IOL implantation, ECCE, Phacoemulsification and the
delamination technique). These may be followed by
IOL implantation (in the capsular bag, sulcus fixated,
iris fixated). The posterior route techniques are (Pars
Plana Lensectomy, Pars Plana recovery of a posteriorly
dislocated lens).
CLOSED GLOBE INJURY TO THE IRIS AND
CILIARY BODY
The uvea may be involved in both contusion and con-
cussion injuries. In rare instances the generated force
overcomes the resilience of the outer scleral coat and
causes a laceration or perforation with uveal incarcera-
tion.
The effects of blunt injury on the uvea are traumatic
miosis, traumatic mydriasis, vossius ring, hyphema, iris
sphincter tears, iris laceration, iridoschisis, iridodialysis,
anteflexion of the iris, iris avulsion, retroflexion of iris
and traumatic iridocyclitis.
Blunt trauma to the ciliary body results in ciliary
body laceration, iridodialysis, angle recession,
cyclodialysis and ciliochoroidal detachment.
Investigations
Ancillary Tests: Plain X-ray, Orbit, USG, OCT, CT Scan
and MRI, Electrophysiological Tests (VEP, ERG).
334
POSTERIOR SEGMENT TRAUMA
Blunt injuries to the ocular, periocular and cranial
regions can produce ocular damage by Contrecoup
mechanism where the injury is at a site opposite to
site of injury.
Anterioposterior compression results in horizontal
displacement of intra ocular structures.
COMMOTIO RETINAE (BERLIN'S EDEMA)
Commotio Retinae was first described by Berlin in
1873. It is seen as a greyish white Opacification of the
outer retina. It always typically occurs opposite to the
site of impact and may occur anywhere in the posterior
segment. Visual acuity is usually affected if macular
edema is involved. Histological examination shows that
there is edema in the outer retinal layers along with
some photoreceptor loss. Fluorescein Angiography
shows no breakdown in the Blood Retinal Barrier. Later
in the course, RPE mottling shows areas of hyper and
hypofluorescence. The prognosis is usually good with
the lesions resolving completely or with varying degrees
of RPE mottling.
CHOROIDAL RUPTURE

(FIG. 53.1)
Indirect choroidal ruptures result from compressive
injury to the posterior pole of the eye.
11
With the
horizontal expansion of the globe, the elastic retina
and tough sclera resist tearing, but the Bruch's
membrane is prone to rupture. Classically, the ruptures
at the site of trauma may also be seen, which tend
to be anterior and parallel to the ora. Choroidal
ruptures are typically singular, concentric to the disc
and temporal. Initially they may be obscured by
overlying hemorrhage and become visible later. The
visual acuity is affected if it passes through the fovea.
FFA may be of use to detect small ruptures and the
location in relation to the foveal centre. The ruptures
may allow secondary choroidal neovascularisation
which needs to be monitored.
The etiology of Commotio Retinae is unknown.
Sipperly, Quigley and Gass' experimental model
suggests that the visual outcome of an eye with
Commotio retinae is dependent on the number of
location of damaged photoreceptors.
TRAUMATIC MACULAR HOLE

(FIG. 53.2)
Trauma accounts for 9% of Full Thickness Macular
Holes. They may occur due to posterior contusion
necrosis, following subfoveal hemorrhage or due to
acute vitreo retinal traction. The size varies from 300
- 500 with a sharp irregular margin and a cuff of
neuro sensory detachment. It rarely leads to a retinal
detachment. OCT is the best method to demonstrate
a macular hole. Surgical anatomic closure is achieved
in 93% cases following vitrectomy with membrane
peeling and fluid gas exchange. They show good visual
recovery perhaps due to the younger age of the
patients and early diagnosis.
Fig. 53.2: Traumatic macular hole
PUTSCHER'S RETINOPATHY
Severe head trauma or chest compression in the absence
of direct trauma to the globe results in Putscher's
Retinopathy. Its frequency is unknown. It is characterised
by multiple patches of superficial retinal whitening and
retinal hemorrhage surrounding a hyperaemic Optic
Nerve Head. It is seen in subjects with head injury,
chest compression injury, acute pancreatitis, childbirth,
connective tissue disorders and retrobulbar anaesthesia.
Though the pathogenesis is not well understood, the
entire picture above has in common, the ability to
activate massive amounts of complement. The resultant
leukoemboli may be a source of retinal arteriolar
embolization. A similar picture is seen in the Fat Embolism
Syndrome in patients with fractured medullated bones. Fig. 53.1: Choroidal rupture
335
RETINAL TEARS AND TRAUMATIC RETINAL
DETACHMENT

(FIG. 53.3)
Blunt Trauma is the commonest cause of traumatic
retinal detachment, more common in young males
(78%-87%). Myopes are more likely to develop retinal
detachment after blunt trauma.
Fig. 53.3: Traumatic retinal detachment
Ocular contusion produces a forceful anteriopos-
terior compression of globe, with a resultant lateral
expansion of the equatorial region and disinsertion or
tearing of the retina. Blunt trauma is the cause of 70%-
80% of traumatic retinal detachment, 80% occurring
within two years of the injury. Retinal dialysis is the
most common retinal break produced by blunt trauma.
Other breaks seen are also usually anterior produced
by traction at the borders of the vitreous base.
Contusion results in retinal detachment which is
pathogenically due to vitreous base avulsion. Some
breaks are a result of tissue necrosis seen directly at
the site of trauma, especially in the inferotemporal
quadrant, which is the most exposed. Traumatic
syneresis of the vitreous gel then leads to a retinal
detachment. Myopes are more susceptible to develop
retinal detachment especially along with nasal dialysis
and giant tears.
CHORIORETINITIS SCLOPETERIA
Sclopeteria is a simultaneous full thickness rupture of
the retina and choroid when a highly velocity missile
penetrates the orbit and travels in close proximity to
the globe. Shock waves cause a rapid deformation of
the globe. The retina and choroid rupture exposing
the underlying sclera, once the overlying hemorrhages
clear. Retinal detachment is rarely seen due the
extensive scarring. A pars plana vitrectomy may be
required for non-clearing vitreous hemorrhage. The
site of involvement determines the final visual acuity.
Indirect choroidal ruptures result from compressive
injury to the posterior pole of the eye.
TERSON'S SYNDROME
It is a syndrome of vitreous hemorrhage in association
with any form of intra cranial hemorrhage. It is seen
in 3%-8% of individual s with subarachnoid
hemorrhage commonly due to a ruptured aneurysm.
Usually bilateral, there may be associated intra-
retinal, sub-retinal and pre retinal hemorrhages. A
peculiar dome shaped pre-retinal hemorrhage is
sometimes seen within the vascular arcades between
the internal limiting membrane (ILM) and Posterior
Hyaloid Face (PHF). Late sequelae may include
Epiretinal Membranes (ERMs) and macul ar
abnormalities.
The pathogenesis is unknown but may be due to
an acute rise in intracranial pressure which is transmitted
down the intra vaginal space of the optic nerve. The
venous stasis due to compression and stretching of
the intraorbital veins lead to a rapid increase in
intraocular venous pressure causing distension and
rupture of fine causing distension and rupture of fine
papillary and retinal capillaries.
Surgical management hastens visual rehabilitation
and may avoid potential complications of persistent
blood in the vitreous.
VALSALVA RETINOPATHY
Raised intra-thoracic pressure causes decreased venous
retina which may be associated with pre-retinal
hemorrhages. Visual loss occurs due to a hemorrhagic
detachment of the ILM, pre-retinal hemorrhage,
vitreous hemorrhage and dissection of blood under
the retina.
Part of the blood may turn yellow after several days.
Serous detachment may replace the resorbing blood.
Recovery of normal vision with spontaneous reattach-
ment is the rule.
OPTIC NERVE AVULSION

(FIG. 53.4)
It occurs typically when an object intrudes between
the orbital wall and globe and displaces the eye or
there is sudden rotation or abduction of the globe.
The optic nerve is disinserted from the retina, choroid
and vitreous. The lamina cribrosa is retracted from
the scleral rim. There is a total or partial visual loss
depending on the degree of avulsion. Initially, the optic
nerve is covered by hemorrhage. When the media
clears a striking cavity is seen where the optic nerve
has retraced into its dural sheath.
There is no known effective medical or surgical
treatment.
336
TRAUMATIC OPTIC NEUROPATHY
Damage to one or both nerves may occur with blunt
trauma to the head. Prognosis for recovery of vision
is poor. Treatment with high dose corticosteroids has
been advocated along with surgical decompression in
selected cases.
Corneoscleral Laceration
with Lens and Vitreous
Involvement
Large corneal lacerations or small penetrating injuries
caused by projectiles can cause significant lens damage.
The decision about lens removal depends on critical
pre and intra-operative assessment. If lens capsule is
ruptured and surgical visualization is adequate, it is
preferable to complete all operative interventions at
one session.

In cases with posterior capsular rupture
with vitreous involvement, lensectomy with pars plana
vitrectomy are advisable. Primary IOL insertion should
not be performed if there is vitreous in AC or surgical
visualization is poor. Wound should be watertight and
free of vitreous incarceration at the conclusion of
surgery.
Posterior Scleral Laceration
Scleral lacerations without corneal involvement may
be difficult to diagnose due to relatively formed eyeball
and anterior chamber. Signs of posterior rupture
include bullous sub-conjunctival hemorrhage, poor
vision, shallow or very deep anterior chamber, low
IOP, rarely high IOP due to choroidal hemorrhage,
hyphema and distorted pupil. Their management
requires a 360. Conjunctival peritomy, followed by
cautious exploration of the site and extent of wound.
It is preferable to repair tear as it is being uncovered
to prevent further uveal or vitreal prolapse; and then
explore further. Dilated fundoscopy followed by
intraoperative cryo-photocoagulation can be done to
prevent future retinal detachments.
Alternatively, corneo-scleral repair can be done in
two sittings. Initial repair of tear to close the globe and
volume replacement, followed by vitrectomy within
10 days if required for retinal tears, endo drainage
of subretinal blood or fluid, internal tamponade, scleral
buckle with encirclage and endolaser or external
cryotherapy.
Corneoscleral Laceration with
Tissue Loss
Small punctured wounds may simply be sutured tightly.
For large tissue loss, tissue replacement techniques such
as full thickness and lamellar patch graft are more
appropriate for restoration of structural integrity
without astigmatism inducing distortion. Primary
penetrating keratoplasty with anterior segment
reconstruction are the definitive treatment for complex
injuries with extensive tissue loss.
Irreparable Scleral Rupture
Badly ruptured eyes with extensive tissue loss and no
visual function should be enucleated in the interest
of the other eye.
Postoperative Management
Appropriate medical therapy comprising of systemic
and topical antimicrobials to control infection and
corticosteroids to minimize inflammation and scarring,
should be instituted. Anti-glaucoma therapy for IOP
control and lubricants or bandage contact lens for
ocular surface stabilization may be required.
Conclusion
The management of open globe injuries continues to
pose difficult management dilemmas. The standard
practice worldwide in these cases should be to
undertake a primary surgical repair to restore the
structural integrity of the globe at the earliest
opportunity regardless of the extent of the injury and
the presenting visual acuity. Despite microsurgical
improvements in management in this devastating
Fig. 53.4: Optic nerve avulsion
337
setting, there remain many eyes that cannot be
salvaged. A primary enucleation is usually only
considered in eyes that are beyond primary repair.
Delayed repair, lens disruption, extent of wound,
vitreous prolapse, posterior location of the wound,
foreign body and rural setting are the known risk
factors for poor visual outcome in ocular trauma. In
an Indian study by Narang et al incidence of open
globe injuries and the outcome in children, and the
risk factors for post-traumatic endophthalmitis was
studied. It was concluded from the study that delayed
repair, bow and arrow injuries and household injuries
were associated with significantly higher risk of
endophthalmitis. The incidence of endophthalmitis can
be reduced by early referral of trauma cases and
parental supervision.
To conclude, open globe injuries can be present
in varying severity and though the overall prognosis
is grave, prompt surgical intervention can result in
better visual outcome.
Intraocular Foreign Body
Intraocular foreign body represents a subset of open
globe injury that involves both anterior and posterior
segments of the eye. An intraocular foreign body may
traumatize the eye mechanically, introduce infection
or exert toxic effects intraocularly. Foreign body may
be lodged anywhere from anterior segment to retina
and choroid. Notable mechanical effects include
cataract formation, vitreous hemorrhage, retinal tears
and hemorrhage. Due to their high velocity, most of
the IOFB's come to lie in the posterior segment of the
eye.
Intraocular foreign bodies occur in 18 to 41% of
the open globe injuries. Most patients are young males
in 3rd and 4th decades. Commonest case is an occupa-
tional hazard involving hammering metal or stone.
Sharp particles require less energy to penetrate the
eye as compared to blunt particles resulting in lesser
degree of damage to ocular tissues. In contrast blunt
objects like gun pellets require much more energy to
penetrate the eye resulting in severe ocular tissue
destruction.
Smaller size is difficult to detect but easier to
remove. Proliferative vitreoretinopathy is common
with larger IOFB's.
COMPOSITION
IOFB's may be grouped into 3 types according to their
composition
1. Metallic: 80-90% of IOFBs' out of which 55-80%
are magnetic in nature.
A. Inert: Metals like gold, silver and platinum are
inert in nature and are tolerated well in the eye
for long periods.
B. Toxic: Metals like iron copper and lead are toxic
in nature and requires immediate removal.
Copper is the most injurious metal to the eye.
2. Inorganic non-metals: Stone, glass, porcelain
are relatively inert and may be tolerated by the
eye.
3. Organic: Wood and vegetable matter of foreign
bodies are commonly associated with agricultural
trauma and result in severe endophthalmitis and
poor visual outcome.
EVALUATION OF A PATIENT WITH IOFB
History
A few direct questions should be sufficient for the
ophthalmologist to suspect the presence of an IOFB
in eyes with an open globe injury. In case of doubt,
it is advisable to err on the side of an IOFB presence.
The most common cause for litigation against the
ophthalmologist in a trauma case is a missed IOFB.
It is important to remember that the patient may be
unaware of any object entering (even striking) the eye,
and the vision may be unaffected initially. Sometimes
the circumstances (e.g. polytrauma cases) divert
primary attention towards systemic evaluation and
management sidelining the ocular assessment, e.g.
road traffic accident, blast injuries, which commonly
result in multiple IOFBs' (Fig. 53.5).
Ocular Examination
A complete examination of both the eyes is necessary,
including the visual acuity and the presence of relative
afferent pupillary defect. When pupil in the traumatized
eye cannot be examined, a reverse RAPD in the fellow
Fig. 53.5: Fundus photograph showing Metallic IOFB
338
eye is a poor prognostic sign. A corneal entry wound
and a hole in the iris provide trajectory information.
Localized conjunctival chemosis strongly suggests
perforation. Most common site of entry for IOFB is
cornea (65%) followed by sclera (25%) and limbus
(10%). A corneal passage is usually accompanied by
iris hole and traumatic cataract which reduces the
velocity of IOFB and decreases the damage potential.
A scleral entry allows the foreign body to retain its
momentum which therefore causes more damage.
Most eyes have a single IOFB. Multiple IOFB's are
usually associated with firearm or blast injuries.

The
slit lamp is extremely useful in detailing all anterior
segment pathologies. The indirect ophthalmoscope
through a dilated pupil may allow direct visualization
of the IOFB, which gives the most useful information
for the surgeon. Gonioscopy and scleral depression
are not recommended unless the entry wound has
been surgically closed.
Lab Studies
Culture an IOFB or a sample of vitreous if an infection
is suspected. Remember that a positive result does not
mean that an infection is occurring and that a negative
result does not preclude the possibility of endophthal-
mitis.
Imaging Studies
They are useful to detect the presence and localization
of IOFBs' in presence of opaque media such as cataract
or vitreous hemorrhage.
Plain X-ray of orbit is the simplest and readily
available tool for IOFB detection. It is useful if a
metallic IOFB is present and a CT scan is unavailable.
However, it is difficult to ascertain the intra/extra
ocular location of foreign body.

Another dis-
advantage of plain X-ray is that small metallic and
nonmetallic IOFB are frequently missed.
CT scans are the test of choice for IOFB localiza-
tion.

It allows detection of IOFB 0.5 mm or more
in diameter.

Though 3 mm cuts allow rapid
detection of foreign bodies; wood plastic and small
metal l ic foreign bodies may be missed. A
consultation with the CT technician is helpful in
selecting the optimal section so as to reduce the
risk of a false-negative result. Helical CT scans have
a very high identification rate.

Limitations of CT-
scan are in detecting an inorganic IOFB and ocular
soft tissue damage.
MRI generally is not recommended for metallic
IOFB's as the strong magnetic fields may move
the IOFB causing intraocular damage
Ultrasound is a useful tool in localizing IOFB's, and
its careful use is possible even if the globe is still
open; alternatively, intraoperative use after wound
closure can be attempted. USG is very effective
in detecting radiolucent IOFB, assessing the status
of retina, vitreous, choroids and optic nerve and
detecting globe perforation. IOFB appears as high
density echo which persists at a low gain and
shadowing of the retina choroids sclera complex.
Ringing bell phenomenon may be seen. The ultra-
sound biomicroscope may help with IOFB's in the
anterior segment or angle of anterior chamber.
Other Tests
Electroretinography is useful if a chronic IOFB is found
and siderosis is either suspected or present. Four stages
are recognized: initially, a and b waves are normal or
supernormal. Later, a wave is larger and b wave
smaller. Still later, b wave becomes subnormal in
amplitude. Eventually, ERG becomes non-recordable.
These changes can be reversed by IOFB removal
before the b wave amplitude is significantly reduced.
PATHOPHYSIOLOGY
The final resting place of and the severity of damage
caused by an IOFB depend on several factors,
including the size, the shape, and the momentum of
the object at the time of impact, as well as the site
of ocular penetration.
IOFB primarily damages the ocular tissue mecha-
nically. The injuries include corneal/scleral perforation,
cataract formation, vitreous hemorrhage, retinal tears
and hemorrhage. In addition to the initial damage
caused at the time of impact, the risk of endophthalmitis
and subsequent scarring play an important role in the
planning of the surgical intervention. Retained metallic
IOFB additionally results in a delayed chemical injury,
metallosis bulbi, caused by electrolytic dissociation of
metal ions. These ions react with the tissues and cause
oxidative damage that interrupts cell function by
altering cell membrane permeability and lysosomal
breakdown. The common metals that dissociate in this
manner are iron and copper.
Siderosis
Iron is the most common intraocular foreign body.
It undergoes dissociation resulting in deposition of iron
intraocularly, notably the lens epithelium and the
retina. It results in toxic effects on cellular enzyme
systems resulting in cell death. Signs involve reddish
brown discolouration of iris, deposits on anterior
capsule, secondary glaucoma and pigmentary
339
retinopathy. Pigmentary retinopathy has most
profound effect on vision. ERG manifests progressive
attenuation of the b-wave over time.
Chalcosis
Severe ocular reaction occurs due to an intraocular
foreign body with high copper content, leading to an
endophthalmitis like presentation followed by phthisis
bulbi. When the copper content of intraocular foreign
body is low, it results in chalcosis. In these cases
electrolytically dissociated copper is deposited
intraocularly, forming a Kayser-Fleischer ring and
anterior sunflower cataract similar to those seen in
Wilson's disease.
MANAGEMENT
Primary Care Guidelines
Since most of FB's come to rest in the posterior segment,
the attending ophthalmologist should refer the case
for tertiary care, if the expertise and equipment
required for comprehensive globe reconstruction is not
available. Before referral, the primary ophthalmologist
should use systemic medications to control pain and
anxiety. The injured eye should be patched and
covered with a shield before referring the patient.

A
tetanus booster may also be appropriate.
Principles of Management
The timing of intervention is primarily determined by
whether the risk of endophthalmitis is high. If the risk
is high, immediate (emergency) surgery is indicated;
in most other cases, the surgeon has the option of
deferring intervention for a few days to reduce the
risk of intraoperative hemorrhage. If endophthalmitis
occurs, it is present at the time of patient presentation
in over 90% of the cases. Broad spectrum systemic
antibiotics can be started though their effectiveness is
not proven.

Intravitreal antibiotics may be useful in
high risk cases like IOFB of vegetable matter, rural
injury.
IOFBs in the anterior chamber are typically
removed through a paracentesis (not through the
original wound) performed at 90-180 from where
the IOFB is located. Viscoelastics should be used
to reduce the risk of iatrogenic damage to the
corneal endothelium and the lens.
An intralenticular IOFB does not necessarily cause
cataract. Unless there is a risk of siderosis or the
loss to follow-up is high, the IOFB and the lens
may be left in situ. Otherwise, usually, the IOFB is
extracted first, the lens is extracted second, and an
intraocular lens (IOL) is implanted simultaneously.
A posterior segment IOFB requires a pars plana
vitrectomy,

unless the tissue damage is minimal. The
posterior hyaloid should always be removed, and
any deep impact should be prophylactically treated.
For the actual removal, the best tool to extract a
ferrous IOFB is a strong intraocular magnet.

For
non-magnetic IOFBs; a proper forceps may be
used. External electromagnets should not be used
since they do not allow controlled extraction. Rarely,
a scleral cut-down is used. Corneo-scleral tear
repair and removal of traumatic cataract are
frequently required at the same sitting. As a rule-
all IOFB's should be removed except in certain
circumstances.
A chronic, inert, encapsulated or intralenticular
IOFB without clinical / electrophysiological evidence
of toxixcity in a quiet eye may be left alone, after
proper patient counseling. A periodic follow up with
ERG monitoring is necessary.
Large IOFB's in a phthisical irreparably damaged
eye with no perception of light are better left alone.
Once ERG is extinguished in an eye with established
metallosis, the ocular damage is almost irreversible
and IOFB removal is unlikely to improve the
outcome.
Surgical Techniques
The posterior segment intraocular foreign bodies are
removed by vitrectomy or via trans-scleral route.
Magnetic IOFB Extraction: This approach is non-
invasive but largely uncontrolled. External electro-
magnets like the permanent hand magnet and the
newer Broson Magnion instrument can be used to exert
powerful magnetic pull after scleral cut down. In case
of an anterior IOFB, magnet can be applied directly
over the IOFB. For a posterior intravitreal IOFB which
is away from the retina, magnet can be applied
indirectly through pars plana. The indirect approach
may damage the retina or crystalline lens by IOFB
movement. This technique is useful in small (< 3 mm),
anterior, visible, intravitreal, magnetic IOFB in a fresh
case.
Non-magnetic IOFB Extraction: Requires extraction
with intraocular forceps combined with vitrectomy and
if required lensectomy.
Pars Plana Vitrectomy (PPV)
Vitrectomy is indicated for large, posterior, invisible,
nonmagnetic, intra/subretinal or encapsulated IOFB's
or those associated with retinal detachment, endoph-
thalmitis or vitreous hemorrhage. PPV nowadays has
become the standard modality for foreign body
340
management due to greater control and less risk of
iatrogenic injury.

Induction of posterior vitreous
detachment, wherever possible, is now a standard step
in PPV to eliminate ERM and PVR. Endolaser
photocoagulation is done around site of FB impaction
to prevent future retinal detachment. Perflurocarbon
liquids (PFCL) can be used to float the IOFB and
prevent iatrogenic macular damage. PFCL may not
be able to support heavy metallic IOFB. The foreign
body is picked up from retina or vitreous after
removing its adhesions, with an intraocular magnet
or forceps depending upon its magnetic properties.
For medium sized IOFB, sclerotomy is enlarged for
removal. For large IOFB's (> 5 mm) limbal incision
or Open Sky Approach may be required. If corneal
damage is present, corneal button is removed and
temporary keratoprosthesis is used followed by corneal
grafting. Special forceps like Stroinko forceps or ureter
stone forceps can be used for large non-magnetic IOFB
(e.g. glass). Primary silicone oil tamponade is used in
patients with severe intraocular foreign body (IOFB)
injuries and high risk of proliferative vitreoretinopathy.
Primary silicone oil stabilizes the retina during the critical
period of active PVR and limits the visual loss in the
long term.

Prophylactic 360 degrees encircling scleral
buckle placed at the time of pars plana vitrectomy
reduces the risk of retinal detachment in future.
PROGNOSIS
Postoperative anatomic and visual outcome after IOFB
removal is limited by proliferative vitreoretinopathy,
RD and endophthalmitis. Endophthalmitis occurs in
16-45% of eyes with IOFB depending upon time delay
in removal of IOFB, type of IOFB (inorganic or organic
vegetative) or self contaminated injuries.

The main risk
factors for PVR and RD are the size of IOFB, retinal
injury and traumatic cataract. The recent advances in
surgical techniques have been associated with a
significant improvement in prognosis.
Post-traumatic Inflammation
TRAUMATIC ENDOPHTHALMITIS
Post-traumatic endophthalmitis is a rare but catastro-
phic event associated with open globe injuries.
Traumatic endophthalmitis, a type of exogenous
endophthalmitis, is unique in having a high incidence
of Bacillus species especially B.cereus.

These eyes have
more intense symptoms and signs than eyes with acute
postoperative endophthalmitis, perhaps due to more
virulent organisms and in addition trauma itself. The
diagnosis of traumatic endophthalmitis depends on a
high index of suspicion followed by vitreous biopsy
and culture techniques. Gram-negative bacilli (65.2%)
are found to be the predominant cause for fulminant
onset, Gram-positive bacillus (28.4%) for acute onset,
and fungi (52.3%) for chronic onset of infections.

The
incidence of post-traumatic endophthalmitis varies
from 3.3 to 16.5%. Several predisposing factors
increase the risk of endophthalmitis following ocular
trauma such as delayed primary repair, retained
intraocular foreign body, disruption of lens.

These eyes
require immediate surgical repair. Most of the
infections in post-traumatic endophthalmitis are
polymicrobial

with high culture positivity.

Bacillus
elaborates several enzymes and exotoxins leading to
rapid onset fulminant endophthalmitis with systemic
features like fever and leukocytosis. Vitreous biopsy
shows blood stained purulent material. B. cereus is
commonly found in cases with retained intraocular
foreign body.
CLINICAL FEATURES
Symptoms like pain, photophobia, redness, visual loss
are present both due to trauma itself and endophthal-
mitis also. It is of utmost importance to rule out endo-
phthalmitis if pain and visual loss is not proportionate
to clinical signs.
Clinical signs include lid edema, circumcorneal
congestion, corneal edema, hypopyon, vitritis, retinal
periphl ebitis or hazy view of fundus. Fungal
endophthalmitis though rare, can be present late after
initial trauma repair, presenting as persistent or
worsening vitritis and snow ball opacities in vitreous
(Figs 53.6 and 53.7).
Management of Post-traumatic Endophthalmitis
Prophylaxis: Prophylactic systemic antibiotics covering
the common causative organisms of traumatic
endophthalmitis (especially Staphylococcci and Bacillus
cereus) and good intraocular penetration should be
Fig. 53.6: Anterior segment photograph of post-traumatic
endophthalmitis showing corneal wound (white arrow) and
hypopyon
341
started in all cases of traumatic open globe injuries.
Oral Fl uroquinol ones have good intravitreal
penetration and are the drug of choice.

Tetanus
prophylaxis should be considered in all open globe
injuries especially the contaminated cases. The role of
prophylactic intravitreal antibiotics is controversial due
to their toxicity. Prophylactic intravitreal antibiotics
should be given in cases with high risk of infection
such as intraocular foreign body, lens disruption, soil
contamination and injuries in rural setting at the time
of primary repair.
Microbiology: In addition to complete clinical
examination, a complete microbiologic work up is
essential for confirmation of endophthalmitis and the
causative agents. The various specimens taken are
vitreous tap or biopsy, AC tap, corneal scraping,
vitrectomy cassette fluid or removed IOFB. Smears
of specimens are sent for staining( Gram, Giemsa and
fungal stains) and inoculated on various agar like
chocol ate agar, bl ood agar for bacteria and
Sabauroud's agar for fungi. Microbiologic work up
should include antibiotic susceptibility testing of isolates
which would help in any alteration of antibiotic therapy
in future.
B-scan Ultrasonography: It is useful in evaluating
posterior segment status in hazy media. USG will show
moderate density echoes in vitreous cavity suggestive
of exudation or membranes. We can detect any
associated retinal or choroidal detachment.USG also
detects related conditions such as IOFB and dropped
nucleus.
Medical Management: Mainstay of medical therapy
are systemic, intravitreal and topical antibiotic drops
with or without steroids. Steroids help in reducing the
inflammation associated damage to the intraocular
structures.
Systemic therapy is usually by intravenous route.
Intravenous ceftazidime and vancomycin (both 1 gm
12 hourly) are ideal for initial therapy.

The same
combination is preferred for intravitreal injections:
Vancomycin 1 mg in 0.1 ml and ceftazidime 2.25 mg
in 0.1 ml. Vancomycin covers the gram positive oraga-
nisms that usually cause post-traumatic endophthalmitis
whereas ceftazidime covers gram-negative organisms.
In case of suspicion of fungal etiology intravitreal
amphotericin B 0.005 mg in 0.1 ml can be given.
Topical therapy is started with hourly administration
of fortified antibiotic solutions (cefazolin, gentamicin)
or fluroquinolone (ciprofloxacin or gatifloxacin) eye
drops. Use of adjunctive steroids in the form of intra-
vitreal or topical dexamthasone or topical prednisolone
eye drops is important to decrease the tissue destructive
effects of the inflammation.
Surgical management: Vitrectomy is generally
required in cases of post-traumatic endophthalmitis,
due to severity of the infection and the associated
trauma. Essentially a core vitrectomy should be
performed to reduce the microbial load. Peripheral
vitreous is better left alone as the retina is very friable
and can lead to iatrogenic tears and detachment. A
lensectomy may be required in cases of traumatic
cataract or severe pars plana exudates sticking the back
of the lens leading to poor visualization of vitreous.
Any associated pathologies like IOFB or retinal
detachment can be tackled during vitrectomy.
Perflurocarbon liquid (PFCL) helps in removal of IOFB
and also protects the retina from damage.

The retinal
detachment is repaired with vitrectomy, fluid-air
exchange and endolaser followed by intravitreal gas
or silicon tamponade and intravitreal antibiotics and
steroids. Intravitreal injections are repeated after 48
to 72 hours of first injection depending on the response
to therapy or half life of the drugs.
Patient should be made aware of the guarded
nature of visual prognosis and need for repeat
procedures like intravitreal injections or vitrectomy in
view of worsening of the condition. Among eyes with
positive intraocular cultures after open globe injury,
the visual prognosis is guarded. Clinical features
associated with better visual acuity outcomes include
better presenting visual acuity, culture of a non-virulent
organism, lack of a retinal detachment, absence of
clinical endophthalmitis, and shorter wound length.
Prevention of infection by prompt primary repair of
the wound and detection of earliest signs of infection
is of utmost importance.
Sympathetic Ophthalmitis
It is a bilateral granulmatous panuveitis occurring
subsequent to penetrating trauma involving uveal tissue
prolapse or intraocular surgery. The traumatized eye
Fig. 53.7: Fundus photograph showing vitreous haze
342
is known as the exciting eye and the fellow eye which
also develops uveitis is known as the sympathizing eye.
Presentation is usually between two weeks to three
months, with 90% of cases occurring within first year of
injury. Injuries account for 47% of patients while ocular
surgery 44% of patients.

Patient may also have systemic
manifestations similar to VKH syndrome, like headache,
tinnitus, dysacousis, aloepecia, vitiligo and poliosis.
The exciting eye has signs of initial trauma, besides
being irritable. The fellow eye is also inflammed and
photophobic, and shows anterior granulmatous uveitis,
vitritis and multifocal choroidal infiltrates in the mid
periphery. Histology shows sub RPE infiltrates
corresponding to the Dalen Fuchs nodules. Severe
cases may show choroidal thickening or exudative
retinal detachment on ultrasonography.
FFA shows multifocal leaks at the RPE level, with
subretinal pooling in presence of exudative detach-
ment.Dark spots seen in ICG are suggestive of active
disease.
Enucleation of the traumatized eye, if severely and
irreversibly damaged with no visual potential, should
be performed within ten days of injury to prevent risk
of sympathetic ophthalmitis. Uveitis may require
treatment in the form of topical and systemic steroids
that should be continued for at least a year with gradual
tapering to reduce the risk of relapse. Immunosup-
pressive therapy with high dose systemic steroids such
as intravenous methylprednisolone and steroid-sparing
agents such as cyclosporin A and azathioprine have
improved the prognosis.
ENUCLEATION
Primary enucleation should be considered for severe
irreparable injuries with no visual potential. Secondarily,
enucleation can be attempted if the severely damaged
lost eye is unsightly or uncomfortable. This should be
performed within ten days of injury to prevent risk
of sympathetic ophthalmitis.
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C H A P T E R
54
Eyelid Injuries and Reconstruction:
An Update
Quresh Maskati, Sunil Vasani (India)
Introduction
Most eyelid defects, full thickness or otherwise, come
from cancers such as basal cell carcinoma or otherwise.
In traumatic defects, the defect may be partial or full
thickness and a simple inspection of the trauma site
often reveals that slowly piecing the remnants together
like a jigsaw puzzle will correct the defect. Most
ophthalmic or oculoplastic surgeons must know the
consistency and limitation of periorbital tissues to begin
eyelid reconstruction. The same knowledge can also
be applied for cosmetic surgery.
Eyelid Injuries
A careful history to evaluate the circumstances under
which the injury was caused is mandatory. Some injuries
are simple with only superficial lacerations of the lid
while other facial trauma may involve injuries to the
head and neck regions along with severe lid injury.
The latter should be dealt with immediately as they
may be life threatening. Hence it is imperative to establish
that the injury is localized only to the eyelid and
surrounding adnexa before beginning management.
CLASSIFICATION
The authors prefer to classify eyelid injuries into:
1. Simple lacerations
2. Complex injuries
3. Full thickness margin defects (a) with tissue loss (b)
without tissue loss
4. Damage to levator aponeurosis
5. Associated with eye/orbital injuries
6. Canalicular lacerations.
ANATOMY REVIEW
The upper eyelid can be broadly broken up into:
a. Anterior lamella
b. Posterior lamella.
The anterior lamella is broadly made up by skin
(thinnest in the body) and orbicularis oculi muscle.
The posterior lamella is broadly made up by the tarsal
plate, conjunctiva, Mullers muscle and the levator
aponeurosis in its posterior part.
An important surface anatomy landmark is the eyelid
crease in the upper eyelid, which is formed by the
attachment of a few fibres of the levator aponeurosis
to the skin. A recession of the eyelid crease with ptosis
and a good levator function may signify levator
dehiscence.
Also important are the medial and central pads of
fat that lie on and are important landmarks in finding
the levator aponeurosis. The palpebral portion of the
lacrimal gland replaces the lateral fat pad in the upper
eyelid.
EXAMINATION
All examination should begin with a thorough search
for any damage to the globe. In a conscious patient,
visual acuity, intra-ocular pressure check, slit lamp bio
microscopy and fundus examinations are mandatory.
It is important to include assessment of ocular motility
in the initial exam. Remember, even seemingly trivial
eyelid injuries may be associated with underlying globe
injuries. In patients with altered sensorium, a complete
eye examination should be still carried out.
Assessment of Adnexal Injuries
In conscious patients compl ete and thorough
evaluation of the eyelids and lacrimal system should
be carried out. The levator muscle can be assessed
by the eyelid crease, the margin reflex distance (MRD)
and the levator function test. Medial lacerations may
cause canalicular tears or canthal tendon disinsertion.
The punctum may be displaced laterally.
346
Evaluation of the Orbit
Sometimes severe injuries may cause significant eyelid
edema, which may hamper proper eye examination.
Manipulation of the eyelids in these cases may
exacerbate pre-existing globe damage. Such patients
should be examined under anesthesia. Orbital injuries
can be evaluated with CT scan with axial and coronal
cuts to rule out associated orbital fractures and foreign
bodies. CT scan may also help in assessing optic nerve
compression or damage. A further MRI examination,
after ruling out metallic foreign bodies in the orbit can
be carried out if necessary for further optic nerve /
muscle/adnexal studies.
If facial/nasal or head neck regions are affected,
additional help from the concerned specialists should
be sought.
MANAGEMENT
The aim of all management is to restore function, vision
and cosmesis to as close to normal as possible. If the
patient is intoxicated or unconscious and immediate
surgery cannot be performed, tissues should be washed
and repositioned as close to normal as possible. A light
dressing with topical antibiotics can be given. Intravenous
steroids and antibiotics or oral antibiotics should be
administered. Intra-muscular tetanus toxoid injection
should also be administered. The surgeon can safely
wait 24-48 hours before attempting surgical
intervention.
Anesthesia
Minor lacerations can be repaired in the outpatient
department itself under local anesthesia. 2% lidocaine
with epinephrine 1:100,000 can be infiltrated locally
before closure. General anesthesia should be adminis-
tered for complex or deeper injuries. However, sedation
with monitored care along with local infiltration with
or without a regional nerve block will suffice in most
cases.
Surgical Tips
Examine globe thoroughly for perforations and
injuries if necessary, explore.
Wash all wounds with saline and a solution of 1gm
cefazolin in 250 ml saline.
Prepping can be done with diluted solution of
povidone-iodine.
Remove al l foreign bodies after thorough
exploration of all affected tissues.
Check anterior and posterior lamella
Look for lid laxity, indicative of canthal tendon
injury
Examine upper and lower canaliculi, lacrimal gland
and levator muscle.
To avoid lid notching, try to close wounds
horizontally i.e. parallel to lid margin in the upper
eyel id and vertical l y in the l ower l id, i.e.
perpendicular to lid margin (Figs 54.1A and B).
Simple eyelid laceration can be closed directly with
slight margin eversion. Care should be taken to
avoid tension on wound edges. The authors prefer
to close vertical lacerations in layers with 6/0
polyglactin and skin with 6/0 polypropylene.
Horizontal lacerations spontaneously reapproxi-
mate themselves due to orbicularis sphincter
action.
Disfigurement of the anterior lamella can cause
complex lacerations. We try to undermine the edges
to mobilize the tissue to aid anatomically perfect
apposition. Debridement should be minimal. After
debridement, a V shaped laceration can be converted
to a Y shaped configuration after removal of the
devitalized apex (Figs 54.2A and B).
LID MARGIN REPAIR
Proper and immaculate closure of lid margin injuries
should be sought for rewarding results. Failure to do
so will cause lid disfigurement and notching and may
lead to corneal drying and complications.
Figs 54.1A and B: (A) Incorrect closure with lid notch,
(B) Correct closure
Figs 54.2A and B: (A) Devitalized apex,
(B) Y-shaped flap
347
Eyelid Injuries and Reconstruction: An Update
Figs 54.3A and B: (A) First silk suture through the tarsal
plate is tied first. Second through the grey line. Third and
fourth behind and in front of the lash lines. (B) Skin and
muscles closed in layers.
Fig. 54.4: Tenzel rotation flap
Fig. 54.5: Technique for lateral canthotomy and lid
closure
Evaluate lid tissue loss by trying to approximate the
cut edges of the margins and see if closure can be
achieved without tension. If this is possible, the marginal
defect has to be closed in layers separately, i.e. the anterior
and posterior lamellae (Figs 54.3A and B).
If there is tissue loss and the wound cannot be
closed without tension, a lateral cantholysis or
canthotomy (Fig. 54.4) in mild cases and a Tenzel
type rotational flap in moderate tissue loss can be
carried out (Fig. 5). For upper eyelid, the arc of the
circle is below the lateral canthus and for lower it is
above the canthus. For severe tissue or lid loss,
Mustarde type flaps or lid sharing procedures can be
used.
While attempting closure of small lid margin
lacerations, the wound has to be modified to avoid
formation of lid notch. The entire vertical portion of
the tarsus has to be removed corresponding to the
width of the deficit. The tarsal excision is carried out
perpendicular to the lid margin. A V shaped defect
is converted into a pentagon shaped defect before
closure.
LEVATOR MUSCLE DEHISCENCE
In levator muscle disinsertion cases, the patient may
present with mild to moderate ptosis with or without
the presence of a laceration. If the orbital fat is seen
in the wound, the same signifies damage to the orbital
septum. Exploration is sought in such cases. The orbital
septum is identified, exposed and fully opened and
the levator aponeurosis is explored. Tears in the muscle
can be repaired with 6/0 polyglactin sutures. The
disinserted aponeurosis can be sutured to the tarsal
plate with 3 6/0 polypropylene sutures. Care should
be taken to preserve the lid contour. All prolapsed
lacrimal gland tissue should be repositioned before
cl osure. There shoul d be no ectropion or
lagophthalmos after closure is complete.
CANALICULAR LACERATIONS
Commonly missed injuries.
Look carefully for the severed edges.
Fig. 54.6: Canlicular repair with stent
348
Fig. 54.7: Eyelid avulsion preoperative
Fig. 54.8: Eyelid injury with canalicular injury
Fig. 54.9: Eyelid injury with zygoma fracture 4
Fig. 54.10: Eyelid injury with zygoma fracture 7
Irrigation from the ipsilateral punctum with
fluoroscein stained saline or injection of air may
help identify the cut edge of the punctum.
Authors prefer to use bicanalicular stents, left in
place for 6 months for repair (Fig. 54.6).
The surrounding lid margin and adventitia can be
repaired as described earlier.
In our opinion the pigtail probe should be avoided.
Before repairing the canaliculi it is important to
determine the presence of any canthal tendon
avulsion.
Repair of the posterior horn of the medial canthal
tendon is necessary to maintain the lacrimal pump
function.
Approximation and suturing of the 2 cut edges of
the tendon with 6/0 polypropylene is sufficient to
maintain function.
The tendon can also be sutured directly to the
periosteum.
If both are absent micro-plating can be considered.
Care must be taken to avoid inadvertent damage
to the lacrimal sac during repair.
Conclusion
Though eyelid trauma has myriad manifestations,
general surgical principles are to be followed in repair.
Repair is to be attempted once the general condition
of the patient permits; meticulous cleaning of the
injured area, maintenance of asepsis is essential. In
most cases one can manage edge to edge apposition
as the lids are fairly forgiving of minor tissue loss.
However, in cases of major tissue loss or where there
is concurrent injury to canaliculi or canthal tendons,
plastic repair as outlined above will yield very
satisfactory results in terms of function andcosmesis.
Bibliography
1. Color Atlas of Ophthalmic Plastic Surgery: A.G.Tyers,
J.R.O.Collins.
2. Oculoplastic Surgery: William P Chen.
3. Ophthalmic Plastic and Reconstructive Surgery: Frank
A Nesi, Richard D Lisman, Mark Levine.
C H A P T E R
55
Prevention of Ocular Trauma
B Shukla, P Dutta (India)
Introduction
Prevention is better than cure is an often quoted
phrase. It can not be over-emphasised in ocular
trauma. However it has remained more of a precept
than practice. In ocular trauma it can be seen from
Table 55.1.
However this scarcity on prevention can be
defended in a way as primary prevention in ocular
trauma is not easy and secondary prevention can be
managed by early and efficient treatment which has
been discussed in detail in most of the books. Primary
prevention is a little difficult as it is basically a problem
of children and young adults many of whom are bound
to indulge in all types of sports, fight, fast driving, etc.
Secondary prevention depends on availability of good
hospitals and efficient doctors at a convenient distance
and cost. Tertiary prevention is basically rehabilitative
and ameliorative.
The subject of prevention of ocular trauma can be
looked at by several ways. Mention has already be
made about primary, secondary and tertiary preven-
tion.
5
It can also be considered from environmental
point of view whether occurring during the profession,
during sports, driving, in criminal assault, agricultural,
in war or at home. The third way would be to avoid
in specific risk groups and lastly educational and
legislative. All these views are not mutually exclusive
and combination is possible. We shall however deal
the subject mainly from the environment point of view.
It may also be stated that the subject of prevention
is linked to the epidemiology of ocular trauma in a
given population or region. This is bound to alter from
country to country and within a large country from
one region to another. This study on one hand will
give the magnitude of the problem and on the other
hand it would help in deciding the priority areas of
prevention. In one study on epidemiology on ocular
trauma in Northern India the incidence of avoidable
injuries is stated as 67%.
6
Although it is believed that
many eye injuries are preventable
7
actual data for the
same is scarce.
Occupational Injuries
In most of the Western studies work related or
occupational eye injuries are very common.
8-10
In a
report from MP, India 40.7% injuries were work related
including labourers, farmers, industrial and sedentary
workers.
11
In many factories the workers are at high
risk of getting eye injuries. In many cases flying splinters
and particles are a big hazard. Not only protective
glasses should be provided but the machines should
also be guarded from emitting particles. Ordinary
glasses or goggles usually do not provide much
protection and in some cases can cause damage after
breaking.
12
Toughened or laminated glasses are better.
However polycarbonate lenses with variable central
thickness depending on degree of safety required are
considered very satisfactory.
13
However, at many places
TABLE 55.1: Ocular trauma coverage in various books
No. Year Name of book Author Total pages On prevention % age
1. 1972 System of Oph. Vol. 14, Injuries Duke-Elder S
1
1350 0 0%
2. 1991 Eye Trauma Singhleton BJ et al
2
410 3 0.7%
3. 2002 Ocular Trauma Kuhn F et al
3
445 2 0.45%
4. 2005 Management of Ocular Trauma Shukla B et al
4
324 5 1.5%
350
APPENDIX: RECOMMENDATIONS OF INDIAN INSTITUTE OF STANDARDS.
16
Classification of hazards related to eye, face and ear protection equipment.
Hazards against which protection equipment for eyes, face and ear should be used are given in Table 1.
TABLE 1: Hazards against which protection equipment for eyes, face and ear should be used
Code No. Protection against hazard Typical Industrial operations
of Hazard
H-1 Impact Clipping, caulking, sealing, grinding of metals. Stone dressing, turning
of case iron and non-ferrous metals, etc.
H-2 Dust Sealing, grinding, handling of cement, clay, etc.
H-3 Splashes from metals Babbiting, pouring of lead in joints, die casting, dipping in hot metals,
pouring of molten metals and foundry work
H-4 Splashes of liquids Handling of acids, alkalis and other chemicals
H-5 Irritating gases and vapours -
H-6 Reflected light and glare Testing of lamps, sheet metal and lathe work
H-7 Injurious radiant energy Oxy-acetylene welding and cutting furnace work; electric arc welding;
open hearth, bessemer and crucible steel making
H-8 Noise -
Selection of equipment for different hazards
Different types of eye, face and ear protection equipment should be selected keeping in view the hazards they can
protect against. Guidance may be taken from the information given in Table 2.
TABLE 2: Selection of different types of eye, face and ear protection equipment keeping in
view the hazards they can protect against
Code No. Brief description of Recommended against Remarks
of equipment equipment hazard code number
E-1 Safety spectacles with side H-1, H-6 and H-7 Spectacles may be fitted with
shields, safety lenses mounted clear, tinned, blue or welding
in spectacle-type frame filter gas lenses.
E-2 Cup-type goggle. Two pieces H-1, H-3, H-6 and H-7 Goggle may be fitted with clear,
holding safety lenses and tinted, blue or welding filter
connected across the nose, glass lenses
and provided with head-band
or harness
E-3 Goggles
(a) With ventilation H-4 -
(b) Without ventilation H-4 and H-5 -
E-4 Dust goggles H-2 -
E-5 One piece eye protectors H-1, H-2, H-3, H-4, H-6 and H-7 Should be capable of being
(Monogoggles) used over prescription glasses
E-6 Face shields H-1, H-3, H-4, H-6 and H-7 -
E-7 Wire mesh goggles H-3 -
there is no quality control and the goggles or face masks
are cumbersome to wear. In a study it was found that
only 10% of those injured at work were wearing some
kind of protective device.
8
Wearing of safety devices
is not strictly enforced at many places.
Recreational Injuries
Various types of sports and games are common causes
of eye injuries. In Western countries boxing is a very
common cause of eye injury.
14
Damage is usually in
proportion to mass and velocity (E=1/2 mv
2
). Hence
hard balls like cricket and hockey balls can cause severe
injury. However in eye injuries the radius of curvature
of a ball is also important as smaller balls can enter
the orbit easily causing severe damage to eye ball like
the squash or golf balls. On the contrary larger balls
like basketball, volleyball and football are unlikely to
cause severe injury unless they strike with great force.
Various devices like pads, abdominal guards, wrist and
elbow guards are now available to minimize sport
injuries. Helmets by cricket players and hockey goal
351
Prevention of Ocular Trauma
keepers are very useful devices to minimize eye injuries.
In some countries like India bow and arrow are
common games and many eyes are lost due to sharp
arrow injury. Gilli danda is another such game
commonly played in rural areas. Children should be
advised and prevented from playing such dangerous
games. Even a passer-by can get hurt.
Travel Injuries
The quality and the width of roads are not increasing
in proportion with the alarming increase in cars and
two wheelers. In addition the fast life in cities and
indulgence in liquor and smoking are also factors
contributing to increasing number of road accidents.
Use of cell phone while driving is not yet prohibited
in many places which may also be a causative factor
in road accidents. Wearing of seat belts and helmets
can minimize such injuries. In some places animals are
also freely roaming adding to disaster. Strict regulations
should be enforced by the concerned authorities.
Other Injuries
Other eye injuries can occur during a difficult labour,
criminal assault and in domestic setting. Adequate
precautions, education and legislation can minimize
these injuries. Domestic or casual injuries are quite
common.
It has been seen that children are more at risk for
injuries hence they should never be given pointed toys
or any type of fire work. They should also be not left
alone. In a recent report it was found that all injuries
occurring in children below 16 years were unsuper-
vised.
15
Similarly though injuries decline with advance in
age there is again a rise in the very old. They are more
prone to fall due to weakness, walking difficulties or
poor sight. A one eyed person is also at great risk
because of restricted field of vision and needs special
protection. Those who have undergone previous eye
surgeries like cataract, keratoplasty and radial
keratotomy are at a greater risk as relatively minor
injuries can cause rupture of the globe due to
dehiscence at the operative site.
Proper education, awareness and strict
enforcement of traffic rules can go a long way to
prevent eye injuries. However as stated earlier
secondary prevention by early reporting and treatment
can also prevent a more severe damage.
References
1. Duke-Elder S : System of Ophthalmology, vol. IVX,
Injuries Henry Kimpton, London 1972.
2. Shingleton BJ, Hersh PS, Kenyon KR :Eye Trauma, Mosby
year Book, St.Louis 398-400.
3. Ocular Trauma : Kuhn F, Pieramici DJ : Ocular Trauma,
Thieme Publication, New York, 2002;19-20.
4. Shukla B, Natarajan S : Management of Ocular Trauma,
CBS Publishers, New Delhi, 2005;317-21
5. Park K : Parks Text Book of Preventive and Social
Medicine, 14th Ed., Banarsidas Bhanot Publishers,
Jabalpur 1995, 6.
6. Shukla, B : Epidemiology of Ocular Trauma, Jaypee
Brothers Medical Publishers, New Delhi, 2002;91.
7. Vinger PF : The eye in sports medicine. In : Duane TD,
Jaeger, EA, Edit.Clnical Ophthalmology, Vol. 5, Harper
and Row 1985.
8. Schein OD, Hibberd PL, Shingleton BJ et al :The
spectrum and burden of ocular injury, Ophthalmology
1988;95:300-05.
9. Glynn R, Seddon J, Berlin B : The incidence of eye
injuries in New England adults, Arch Ophthalmol, 1988;
106:78589.
10. Saari M, Parvi V : Occupational eye injuries in Finland,
Acta Ophthalmol Suppl. 1984;161:17-28.
11. Shukla, B : Epidemiology of Ocular Trauma, Jaypee
Brothers Medical Publishers, New Delhi 2002;33-34.
12. Keeney A, Fi ntel mann E, Renal do D : Cl i ni cal
mechanism of non industrial trauma, Am J Opthalmol
1972;74:662.
13. Schein OD, Vinger PF : Epidemiology and Prevention,
In : Eye Trauma, Edit. Shingleton BJ, Hersh PS, Kenyon
KR, Mosby Year Book, St. Louis 1991, Chapter 36, p.
399-401.
14. Giovinazzo VJ et al : The ocular complications of boxing,
15. Vats S, Murthy GVS, Chandra M et al :Epidemiological
study of ocular traumain an urban slum population
in Delhi, India, Indian J Ophthalmol 2008:56:313
16.
16. Shukla B, Dutta P. Prevention of ocular trauma. In :
Shukla B, Natarajan S Edit, Management of ocular
trauma, CBS Publishers, New Delhi 2005;320-21.
C H A P T E R
56
Endophthalmitis Prevention
Strategies
John D Sheppard (USA)
Introduction
Perfected treatment strategies depend on a surgeons
preferences and individual patient needs.
Infectious complications following routine cataract
surgery are the most feared of all ophthalmic infections,
due to the high expectations for cataract operations
in the 21st century. Endophthalmitis complicates
approximately one in every 1,000 cataract operations.
With clear corneal incisions, this rate may be rising.
Risk factors cited in the peer-reviewed literature include
extracapsular surgery, intracapsular surgery, clear
corneal incisions, diabetes mellitus, prolonged surgical
time, previous or concurrent trabeculectomy, repeated
instrument entry and exit, chronic blepharitis, chronic
conjunctivitis, keratitis sicca, ocular surface disease,
capsular rupture, vitreous prolapse, and vitrectomy
surgery. The potential for this risk may rise to one in
every 100 cases with vitreous loss. Although rapid
diagnosis and expeditious surgical intervention can
preserve excellent visual function in many patients with
endophthalmitis, preventive measures are the
cornerstone of any surgical management strategy.
New Concepts in
Endophthalmitis Treatment
The landmark Endophthalmitis Vitrectomy Study
(EVS), conceived by Dr Bernard Doft and completed
in 1995, found that 70% of endophthalmitis cases were
caused by coagulase-negative, Gram-positive micro-
cocci, overwhelmingly Staphylococcus epidermidis.
1
This study has revolutionized our treatment algorithm
for postcataract surgery endophthalmitis, recognizing
the essential aspects of vitreous-tap diagnosis and
expeditious injection of intravitreal antibiotics, while
surprisingly raising the threshold for pars plana vitrec-
tomy for patients with light perception or worse-quality
vision.
New data have extended our understanding of the
pathogenesis and prevention of postoperative
endophthalmitis since the completion of the EVS.
Postcataract infections originate by one of three routes:
(1) introduction through instrumentation at the time
of surgery; (2) inoculation through the wound after
cataract surgery; and (3) (although extremely rarely)
by endogenous spread from concurrently infected
extraocular tissues, such as a tooth abscess or infected
diverticulum. Material presented at the 2002 ARVO
meeting in Fort Lauderdale, Florida, in particular
offered insight into bacteriologic factors relevant to
cataract surgery.
Existing Literature
With experience and consideration of extensive
laboratory data, most surgeons now believe that
postcataract infections are introduced into the eye from
the ocular surface. This belief brings into question the
traditional use of topical perioperative aminoglycosides
for cataract patients, especially when most endoph-
thalmitides are Gram-positive and aminoglycosides are
so insoluble. In our analysis, Gram-positive isolates from
163 patients with bacterial conjunctivitis were only
85% sensitive to tobramycin, while 97% were sensitive
to levofloxacin, a third-generation fluoroquinolone,
83% to sulfasoxazole, 77% to ciprofloxacin, and only
75% to trimethoprim, commonly used in combination
with the Gram-negative agent, polymyxin B.
2
Franco Recchia of Vanderbilt University and
colleagues clearly showed that an increasingly higher
percentage of postcataract infections are due to Gram-
positive organisms.
3
In a study of 493 consecutive patients
with postcataract endophthalmitis, researchers cultured
an organism from the vitreous in 318 cases (65%).
During the last decade of the 20th century, gram-
positive isolates increased from 92 to 97%. Furthermore,
resistance rates to commonly used prophylactic
antibiotics increased; resistance among all isolates to
353
Endophthalmitis Prevention Strategies
ciprofloxacin rose significantly (23 to 38%), while
resistance to ciprofloxacin and cefazolin rose among
coagulase-negative staphylococci (18 to 38%).
In his new study from Stanford University,
Christopher Ta and associates compared the ability of
21 different antibiotics to cover coagulase-negative
Staphyl ococcus organisms.
4
Researchers took
preoperative conjunctival swabs from 66 patients prior
to applying antibiotics or antiseptic. Their analysis
concluded that, among the four fluoroquinolones
tested, levofloxacin had the highest antistaphylococcal
susceptibilty (91%) compared to norfloxacin (79%),
ofloxacin (75%), and ciprofloxacin (73%). Conversely,
resistance patterns also favored levofloxacin at only
5%, whereas norfloxacin was 18%, ciprofloxacin 20%,
and ofloxacin 23%.
Practical Clinical Practice
Revealing in vivo data from Frank Bucci, MD, in
Wil kes-Barre, Pennsyl vania, demonstrate that
l evofl oxacin reaches therapeutic aqueous
concentrations, therefore exceeding the mic90 for both
Staphylococcus and Streptococcus.
5
Dr Bucci found
that 0.5% levofloxacin reached four- to sevenfold
higher aqueous concentrations than 0.3% ciprofloxacin
when administered according to identical preoperative
regimens. The ciprofloxacin levels were below the
established NCCLS MIC90 for both Staphylococcus
and Streptococcus. Dr Bucci also noted that, higher
intracameral levofloxacin concentrations could be
achieved with a regimen of administering five drops
every 10 minutes immediately prior to surgery, when
compared to administering the drug four times per
day for 2 days preoperatively. He achieved an
additional 50% increase in aqueous levels by combining
the two regimens.
Starr, Jensen and Fiscella
6
showed that, of 24
endophthalmitis cases in 9,079 patients, eyes receiving
topical ofl oxacin postoperativel y devel oped
endophthalmitis significantly less often than those
receiving topical ciprofloxacin (P<.0009). According
to these investigators, this difference in endophthalmitis
rates may reflect differences in pharmacological and
bioavail abil ity properties that exist among
fluoroquinolone antibiotics. Ciprofloxacin, the least
soluble of available topical fluoroquinolones, achieves
the lowest intraocular levels. Levofloxacin, with 3.3
times more active drug per drop than ofloxacin, might
be the preferred choice at this time because of superior
Gram-positive coverage and solubility.
Even though some surgeons have popularized the
use of antibiotic infusion through balanced saline-
irrigating solutions during cataract surgery, a group of
researchers in Arizona, led by Robert Snyder, MD, do
not see the efficacy of this approach.
7
Dr Snyder and
his colleagues noted that antibiotics chosen for infusion
should be fast-acting, due to the limited time exposure
to purported intracameral bacterial contaminants. The
fluoroquinolones showed dose-dependent killing. On
the other hand, vancomycin killing did not correlate
with drug concentration relative to the MIC of
Staphylococcus species tested. Fluoroquinolones may
be more suitable for killing bacteria seeded into the
anterior chamber than vancomycin. Because
vancomycin concentration decreases rapidly in the
anterior chamber following surgery completion,
residual surviving organisms with exposure to this
antibiotic of last resort could have a high likelihood
of vancomycin resistance. Those who advocate
aminoglycoside antibiotic infusion during routine
surgery ignore both the severe potential retinal toxicity
of this class, and waning Gram-positive sensitivity.
Microbial Antibiotic Resistance
Careful clinical analysis customized to each prospective
cataract patient by a knowledgeable, conscientious
surgeon provides the best solution to endophthalmitis
risk. There is no single agent capable of killing every
microbe known to cause postoperative infections.
8
Even in this brief review of recent ARVO abstracts,
epidemiologic patterns differ between hospitals, cities,
and regions, a fact that renders each surgeon uniquely
capable of understanding the peculiarities of their own
bacteriologic environs. Although newer fourth-
generation fluoroquinolones, such as moxifloxacin and
gatifloxacin, may demonstrate increased potency for
Gram-positive bacteria over second- and third-
generation drugs, the fourth-generations demonstrated
no advantage for Gram-negative coverage in a keratitis
study conducted by Kowalski et al.
9
Gram-negative
resistance appears to cross all fluoroquinolone
generations. Thus, miniscule but significant holes have
appeared in the once-invincible fluoroquinolone
familys Gram-negative coverage spectrum. The best
protection of all may be a thorough povidone-iodine
preparation,
10
including the periorbital skin, lids, lashes,
and conjunctival cul-de-sac.
Consistent routines, meticulous iodine preparation
and reliable surgical technique, coupled with highly
effective and penetrating topical antibiotics given
frequently prior to surgery, provide our patients with
the best defense against infection.
354
References
1. Han DP, Wisniewski SR, Wilson LA, et al: Spectrum and
susceptibil ities of microbiol ogic isol ates in the
Endophthalmitis Vitrectomy Study. Am J Ophthalmol
1998;122:1-17.
2. Sheppard JD, Oefinger PE, Wegerhoff PE: Susceptibility
patterns of conjunctival isolates to newer and established
anti-infective agents. IOVS 2002 (abstr 1588) (suppl).
3. Recchia FM, Busbee BG, Pearlman RB, et al: Changing
trends in the microbiologic aspects of post-cataract
endophthalmitis. Arch Ophthalmol 2005;123:341-46.
4. Ta CN, Mino de Kaspar H, Chang RT, et al: Antibiotic
susceptibility pattern of coagulase-negative staphylococci
in patients undergoing intraocular surgery. IOVS 2002
(abstr 4444) (suppl).
5. Bucci FA: An in vivo comparison of the ocular absorption
of l evofl oxacin versus ciprofl oxacin prior to
phacoemulsification. IOVS 2002 (abstr 1579) (suppl).
6. Starr MB, Jensen MK, Fiscella RG: A retrospective study
of endophthalmitis rates comparing quinolone antibiotics,
Am J Ophthalmol 2005:140;769-71.
7. Snyder RW, Krueger T, Nix DE: Kill curves for vancomycin
versus 3rd generation quinolones. IOVS 2002 (abstr
4452) (suppl).
8. Benz MS, Scott IU, Flynn HW, et al: In vitro susceptibilities
to antimicrobials of pathogens isolated from the vitreous
cavity of patients with endophthalmitis. IOVS 2002 (abstr
4428) (suppl).
9. Kowalski RP, Karenchak LM, Romanowski EG, et al: An
in vitro comparison of 2nd, 3rd, and 4th generation
fluoroquinolones against bacterial keratitis isolates. IOVS
2002 (abstr 1585) (suppl).
10. Ciulla TA, Starr MB, Masket S: Bacterial endophthalmitis
prophylaxis for cataract surgery: an evidence-based
update. Ophthalmology 2002;109(1):13-24.
11. John D. Sheppard, MD, MMSc, serves as Professor of
Ophthalmology, Microbiology and Immunology, as well
as Program Director for Ophthalmology Residency
Training at the Eastern Virginia Medical School in
Norfolk, Virginia. He is also Clinical Director of the
Thomas R. Lee Center for Ocular Pharmacology. Dr.
Sheppard may be reached at (757) 622-2200;
docshep@hotmail.com
Index
A
Abrasions of the globe 312
clinical signs and symptoms 312
differential diagnosis 312
investigations 312
prognosis 312
treatment 312
Acute postoperative endophthalmitis
174
intraocular antibiotics 175
aminoglycosides 175
ceftazidime 175
vancomycin 175
prophylaxis 174
steroid treatment 176
subconjunctival and topical
antibiotic therapy 176
systemic antibiotics 176
vitrectomy 177
Algorithm for management of open
globe injury 214
B
Bimanual vitrectomy 330
Birth trauma 68
Blunt eye trauma 80
Blunt injuries of the globe 312
investigations 314
prognosis 314
treatment 314
Blunt retinal trauma 189
individual pathologies description
190
chorioretinitis sclopetaria 197
choroidal rupture 194
commotio retinae 190
purtscher retinopathy 198
traumatic macular hole 191
traumatic retinal detachment
193
traumatic retinal tears 192
vitreous base avulsion 194
vitreous hemorrhage 194
initial evaluation 190
mechanism of damage 189
Blunt trauma of anterior segment 67
Blunt trauma related retinal tears and
retinal detachments 149
Bottle cork injury to the eye 296
clinical features 297
prevention 298
treatment 298
C
Causes of postoperative non-
improvement of BCVA in
traumatic cataract 75
Chandelier illumination 328
Chemical and thermal burns of the
eye 317
investigations 318
prognosis 318
treatment 318
Chemical injuries of the eye 50
management 50
general principles 50
recent advances in therapy 52
pathogenesis 50
acids 50
alkalis 50
classification 50
Chorioretinitis sclopetaria 169
etiology and pathogenesis 169
treatment and prognosis 169
Choroidal rupture 168
diagnostic testing 169
Chronic postoperative endophthalmitis
177
bleb-associated endophthalmitis
178
post-traumatic endophthalmitis 178
Clinical evaluation of ocular trauma 10
general examination 10
structural examination 10
functional examination 11
ocular adnexa 10
Closed globe injuries 332
Commotio retinae 167
etiology and pathology 167
Complication and contusin after
phakic IOLs 273
anterior chamber phakic IOLs 273
cataract formation 275
chronic inflammation and
uveitis 274
glare and halos 274
glaucoma 275
induced astigmatism 274
pigment dispersion and lens
deposits 273
size-related complications
pupil ovalization and
retraction 274
iris-fixated anterior chamber
phakic intraocular lenses
275
cataract formation 276
chronic inflammation and
uveitis 276
complications of iris-supported
phakic IOLs 275
endothelial cell loss and anterior
chamber depth 276
glare and halos 276
glaucoma 276
pupil ovalization and
decentration 276
posterior chamber phakic
intraocular lenses 277
Complications of corneal injury 46
astigmatism 48
corneal infection 46
iris/capsular incarceration 46
posterior segment complications 47
post-traumatic endophthalmitis 47
secondary glaucoma 46
sympathetic ophthalmia 47
Complications of SFIOL 97
choroidal detachment 98
cystoid macular edema 97
endophthalmitis 98
glaucoma 97
lens decentration and lens tilt 97
retinal detachment 97
suture erosion 98
uveitis 98
Conjunctival injuries 125
types 125
Corneal injuries 126
evaluation 126
Corneal laceration 279
complex corneal laceration wound
281
corneal laceration with tissue loss
281
356
injury assessment 279
medical management 279
perforating or nonperforating
corneal laceration 279
simple corneal laceration 280
surgical management 280
use of tissue glue 281
Corneoscleral laceration with lens and
vitreous involvement 336
Corneoscleral laceration with tissue
loss 336
Cultivated vs direct limbal
transplantation 209
Cystoid macular edema 242
clinical findings 244
etiology 242
histopathology 244
treatment 245
E
Electrical injuries 57
clinical lesions 57
lighting injury 57
Endogenous endophthalmitis 179
Endophthalmitis prevention strategies
352
Evaluation of a patient with ocular
trauma 13
approach in emergency 14
examination 15
history 14
approach to a patient with ocular
trauma 14
Eye injury prevention in children
188
Eyelid injuries 345
anatomy review 345
canalicular lacerations 347
classification 345
examination 345
levator muscle dehiscence 347
lid margin repair 346
management 346
F
Fugos plasma knife 319
key properties 321
technique 327
G
Glued IOL 132
fibrin glue 132
scleral fixated IOL 132
surgical technique 132
H
Hyphema 35
associated exam findings 36
examination 35
history 35
prognosis 37
treatment 37
Hyphema 68
complications 69
ophthalmic examination 68
severity grades 69
raised intraocular pressure 69
secondary hemorrhage 69
I
Iatrogenic 223
complications 224
contraindications 224
controlled release vehicles 224
indications 224
intravitreal injection 224
pulse therapy 224
repository injection 224
responsive diseases 225
anterior segment ischemia 225
Boecks sarcoid uveitis 225
herpes zoster 225
neoplasms 225
ocular pemphigoid 225
orbital myositis 225
pseudotumor cerebri 225
Tolosa-Hunt syndrome 225
toxoplasmosis 225
systemic therapy 224
topical application 223
Indications of SFIOL 95
Initial management of ocular trauma
patient 20
pearls 20
Injuries of the lids 311
investigations 311
prognosis 312
treatment 311
Intraoperative floppy iris syndrome 250
Intravitreous triamcinolone associated
endophthalmitis 179
IOFB 155
clinical manifestations 155
localization 156
management 156
mode of injury 155
Iridodialysis 102
causes 102
complications 105
principles of iris repair 103
iris implants 103
repair of iridodialysis 103
suture placement 103
suture tying 103
signs 102
surgical planning 102
symptoms 102
treatment and management 102
Iris prolapse 100
clinical profile of a patient with
iris prolapse 100
mortality/morbidity 100
pathophysiology 100
treatment 101
conservative treatment 101
holistic approach 102
surgical care 101
Irreparable scleral rupture 336
L
Late post-traumatic glaucoma 64
international incidence 64
indian incidence 65
slit lamp findings 65
gonioscopic findings 65
pathology 65
Luxation and subluxation to the
crystalline lens 80
clinical evaluation 81
intracapsular extraction 83
IOL placement considerations 84
phacoemulsification and IOL
placement in subluxated
crystalline lens 83
prognosis and long-term
considerations 84
surgical approach 82
M
Management of a malpositioned 328
Management of acute corneal injury 41
corneal laceration with tissue loss
43
management of injury to lens 44
postoperative treatment 45
principles of repair 43
slit-lamp biomicroscopy 42
anesthesia 43
anterior chamber 42
conjunctiva 42
cornea 42
lens 42
sclera 42
traumatic wound dehiscence 46
type of sutures 45
viscoelastic materials 44
Management of corneal injuries 41
classification 41
terminology 41
Management of eyelid injuries 28
evaluation of lid injury 28
examination 28
history 28
principles of wound repair 28
wounds associated with canthal
tendon injuries 31
wounds with no or minimal
tissue loss 29
wounds with significant tissue
loss 30
Management of lacrimal injuries 33
evaluation of lacrimal injuries 33
examination 33
history 33
357
Index
Management of traumatic cataract 74
causes 75
complications 76
medical care 75
pathophysiology 74
physical examination 74
surgery 75
types 75
Medical management of blunt trauma
69
Mode of lens injury in ocular trauma
and its presentation 94
Muller glial cells 201
N
New classification of ocular trauma 7
New concept in endophthalmitis
treatment 352
NSAIDs and topical steroids 238
NSAIDs for the inhibition of miosis 238
NSAIDs vs steroids 237
O
Occupational injuries 349
Ocular injuries after vehicular accident
290
air bag system 290
methods 291
results 291
Ocular surface stem cells 206
Ocular trauma 3
epidemiology 3
new classification 4
Ocular war injuries 300
mechanical 301
non-mechanical 305
Optimized NSAIDs and antibacterial
prophylaxis in cataract
surgery 232
drug dosages 233
measuring potency 233
penetration tracking 234
postoperative schedule for cataract
patients 232
safety evaluation 234
Orbital fracture 113
naso-orbital and medial orbital
wall fractures 117
management 119
transnasal wiring 118
orbital floor and blow out
fractures 113
pathogenesis 113
clinical presentation 113
complications 116
implants 115
management 114
procedure 115
surgical procedure 115
timing 114
Orbital injuries 108
anatomic considerations 108
carotid cavernous fistula 111
orbital foreign bodies 112
septic cavernous sinus
thrombosis 111
evaluation of acute orbital and
periorbital injuries 109
problems associated with orbital
trauma 110
orbital hemorrhages 110
surgical emphysema 110
traumatic optic neuropathy 110
P
Pediatric ocular trauma 181
evaluation 181
examination 181
history 181
specific eye injuries 182
birth trauma 182
corneal and conjunctival
foreign bodies 182
corneal penetration 184
eyelid lacerations 182
subconjunctival hemorrhage
183
traumatic hyphema 184
vitreous and retinal conditions
185
Penetrating injuries related retinal
incarcerations and retinal
detachments 152
pathophysiology 152
surgical principles vitrectomy 153
Penetrating posterior segment trauma
160
classification 161
complications 163
chalicosis 164
endophthalmitis 163
siderosis 164
epidemiology 160
investigations 161
location 161
management 161
pathophysiology 160
prognosis 164
Perforating injuries of the globe
intraocular foreign bodies
315
investigations 315
prognosis 316
treatment 316
Pharmacologic therapy for ocular
inflammation 236
Posterior scleral laceration 336
Postrefractive keratitis 229
Post-traumatic strabismus 106
direct trauma 107
entrapment of muscle 107
intramuscular hemorrhage 107
traumatic disinsertion 107
Practical clinical practice 353
Prevention of CME 239
Primary globe repair 214
management 215
nonsurgical 215
surgical 215
objectives 214
strategic planning 214
Principles and management of ocular
trauma 331
Purtschers retinopathy 169
R
Radiational injuries to the eye 59
injuries due to infrared radiation 61
injuries due to ultraviolet radiation
60
cornea 60
lens 61
injuries due to visible radiation 61
mechanical injuries 61
photic injuries 61
thermal injuries 61
injuries of the eye due to ionizing
radiation 60
conjunctiva 60
lens 60
lids 60
Rationale for treating ocular
inflammation 235
Recreational injures 350
Reinverter system 329
Retinal tears, tetinal dialysis and
detachments 171
Role of adult bone marrow in
endothelial progenitor
(Stem) cells 203
Role of bone marrow in stem cells
203
Role of bone marrow in stem cells in
retinal and choroidal
neovascularization 204
Role of corneal stem cell in pediatric
206
Role of retinal pigment epithelial stem
cells 202
Role of retinal stem cells 201
S
Scleral fixated IOL vs anterior
chamber iol 94
358
Scleral injuries 130
evaluation 130
specific conditions 130
Shaken baby syndrome child abuse
170
Small pupil phaco 259
IQ-ring 263
Specific injuries 127
corneal abrasion 127
examination 127
symptoms 127
foreign bodies 128
evaluation 128
treatment 129
recurrent erosion 128
history 128
treatment 128
Sports injuries in eye 283
classification 283
ball injuries 283
physical contact injuries 284
Stem cell therapy in ophthalmology 200
T
Technique of insertion of SFIOL 95
Thermal injuries 55
hyperthermal injuries 55
contact burns 55
flame burns 55
scalds 55
hypothermal injuries 56
accidental hypothermia 56
cryosurgery 56
surgical hypothermia 56
Toxic anterior segment syndrome 254
diagnosis 254
epidemiology 255
etiology 255
investigation 256
pathology 255
treatment 256
Trauma in LASIK 270
Trauma in phakic iol lmplants 272
Trauma in PRK 270
Trauma in radial keratotomy 269
Trauma in surface treatments 272
Trauma to LASIK flap 270
Traumatic angle recession glaucoma 64
history 64
Traumatic cataract in children 86
epidemiology 86
examination 87
pathophysiology 86
postoperative complications 91
postoperative medication 91
preoperative evaluation 87
surgical details 88
timing of surgery 88
visual outcome 92
Traumatic giant retinal tears 150
Traumatic hemorrhages to the
posterior segment 139
classification 141
choroidal hemorrhages 142
hemorrhage associated with
indirect trauma 144
intraretinal hemorrhages 142
papillary and peripapillary
hemorrhages 143
retrohyaloidal hemorrhages 142
vitreous hemorrhages 141
management 144
medical 144
surgical 145
pathogenesis 141
Traumatic macular hole 167
etiology and pathology 167
Traumatic retinal detachments 149
Travel eye injuries 286
prevention and management 286
direct traumatic injuries 287
non-contact eye injuries 286
U
Ultrasonic injuries 56
clinical lesions 56
Ultrasound biomicroscopy in ocular
trauma 25
assessment of zonules 27
foreign bodies 27
iris and ciliary body status 27
Ultraviolet corneal burns 317
investigations 317
prognosis 317
treatment 317
Use of nonsteroidal anti-inflammatory
drugs in inflammation 225
mechanism of action 226
ocular inflammation 225
side effects of NSAIDs 227
V
Valsalva retinopathy 170
Visual rehabilitation 48
Vitrectomy lenses 330
W
Welding arc injuries 62

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