Escolar Documentos
Profissional Documentos
Cultura Documentos
OVERVIEW
Background
Chemical injuries to the eye represent one of the true ophthalmic emergencies, wherein time is truly
critical. While almost any chemical can cause ocular irritation, serious damage generally results from
either strongly basic (alkaline) compounds or strongly acidic compounds. Alkali injuries are more
common and can be more clinically challenging, with a significant potential for long-term morbidity.
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. [1, 2, 3] See the image below.
Pathophysiology
The severity of this injury is related to chemical composition, pH, volume, concentration, duration of
exposure, and degree of penetration of the chemical. The mechanism of injury differs slightly between
acids and alkali. [4]
Acid injury
Acids dissociate into hydrogen ions in the cornea. This usually occurs when a strong acid has a pH of
less than 4. The hydrogen molecule damages the ocular surface by altering the pH, while the anion
causes protein denaturation, precipitation, and coagulation. Protein coagulation creates a barrier and
http://emedicine.medscape.com/article/1215950-overview 1/6
8/28/2017 Ophthalmologic Approach to Chemical Burns: Background, Pathophysiology, Epidemiology
thus generally prevents deeper penetration of acids and is responsible for the ground glass
appearance of the corneal stroma following acid injury. Hydrofluoric acid is an exception; it behaves
like an alkaline substance because the fluoride ion has better penetrance through the stroma than
most acids, leading to more extensive anterior segment disruption. [4]
Alkali injury
Alkaline substances are lipophilic and can penetrate cell membranes. They dissociate into a hydroxyl
ion and a cation in the ocular surface. The hydroxyl ion saponifies cell membrane fatty acids, while the
cation interacts with stromal collagen and glycosaminoglycans. This interaction facilitates deeper
penetration into and through the cornea and into the anterior segment. Subsequent hydration of
glycosaminoglycans results in stromal haze. Collagen hydration causes fibril distortion and shortening,
leading to trabecular meshwork alterations that, in turn, result in increased intraocular pressure (IOP),
sometimes permanent. Additionally, the inflammatory mediators released during this process stimulate
the release of prostaglandins, which can further increase IOP. [5] See the image below.
Alkali burn. Note the severe conjunctival reaction and stromal opacification blurring iris details inferiorly.
View Media Gallery
Epidemiology
Frequency
United States
Chemical injuries are responsible for approximately 7% of work-related eye injuries treated at US
hospital emergency departments. [6] More than 60% of chemical injuries occur in workplace accidents,
30% occur at home, and 10% are the result of an assault. [7] Thus, 90% result from accidental
exposures. Safety glasses can help prevent injuries, but industrial accidents often involve chemicals
under high pressure. Safety glasses are not of much defense in this setting.
Mortality/Morbidity
As many as 20% of chemical injuries result in significant visual and cosmetic disability; only 15% of
patients with severe chemical injuries achieve functional visual rehabilitation.
Race
http://emedicine.medscape.com/article/1215950-overview 2/6
8/28/2017 Ophthalmologic Approach to Chemical Burns: Background, Pathophysiology, Epidemiology
No overall racial predilection exists; however, young black males are more likely to have high-
concentration, high-impact alkaline chemical injuries secondary to assault. [8]
Sex
Males are 3 times more likely to experience chemical injuries than females. [7]
Age
Chemical injuries can strike any population; however, most injuries occur in patients aged 16-45
years. [6, 7]
Clinical Presentation
References
2. Hodge C, Lawless M. Ocular emergencies. Aust Fam Physician. 2008 Jul. 37(7):506-9.
[Medline].
3. Spector J, Fernandez WG. Chemical, thermal, and biological ocular exposures. Emerg Med Clin
North Am. 2008 Feb. 26(1):125-36, vii. [Medline].
4. Pfister DA, Pfister RR. Acid injuries of the eye. Fundamentals of Cornea and External Disease.
Cornea. 2005. Vol 2.: 1277-84.
5. Pfister RR, Pfister DA. Alkali injuries of the eye. Fundamentals of Cornea and External Disease.
Cornea. 2005. Vol 2: 1285-93.
6. Xiang H, Stallones L, Chen G, Smith GA. Work-related eye injuries treated in hospital
emergency departments in the US. Am J Ind Med. 2005 Jul. 48(1):57-62. [Medline].
7. Morgan SJ. Chemical burns of the eye: causes and management. Br J Ophthalmol. 1987 Nov.
71(11):854-7. [Medline].
8. Klein R, Lobes LA Jr. Ocular alkali burns in a large urban area. Ann Ophthalmol. 1976 Oct.
8(10):1185-9. [Medline].
9. Wagoner MD, Kenyon KR. Chemical injuries of the eye. Clinical Practice. Albert, Jakobiec, eds.
Principles and Practice of Ophthalmology. 2000. Vol 2: 943-59.
10. Kheirkhah A, Johnson DA, Paranjpe DR, Raju VK, Casas V, Tseng SC. Temporary sutureless
amniotic membrane patch for acute alkaline burns. Arch Ophthalmol. 2008 Aug. 126(8):1059-66.
[Medline].
12. Kheirkhah A, Johnson DA, Paranjpe DR, Raju VK, Casas V, Tseng SC. Temporary sutureless
amniotic membrane patch for acute alkaline burns. Arch Ophthalmol. 2008 Aug. 126(8):1059-66.
[Medline].
http://emedicine.medscape.com/article/1215950-overview 3/6
8/28/2017 Ophthalmologic Approach to Chemical Burns: Background, Pathophysiology, Epidemiology
13. Jafarinasab MR, Feizi S, Javadi MA, Karimian F, Soroush MR. Lamellar keratoplasty and
keratolimbal allograft for mustard gas keratitis. Am J Ophthalmol. 2011 Dec. 152(6):925-932.e2.
[Medline].
15. Kawashima M, Kawakita T, Satake Y, Higa K, Shimazaki J. Phenotypic study after cultivated
limbal epithelial transplantation for limbal stem cell deficiency. Arch Ophthalmol. 2007 Oct.
125(10):1337-44. [Medline].
16. Clare G, Suleman H, Bunce C, Dua H. Amniotic membrane transplantation for acute ocular
burns. Cochrane Database Syst Rev. 2012 Sep 12. 9:CD009379. [Medline].
17. Tuft SJ, Shortt AJ. Surgical rehabilitation following severe ocular burns. Eye. 2009 Jan 23.
[Medline].
18. Dua HS, King AJ, Joseph A. A new classification of ocular surface burns. Br J Ophthalmol. 2001
Nov. 85(11):1379-83. [Medline].
19. Brodovsky SC, McCarty CA, Snibson G, et al. Management of alkali burns : an 11-year
retrospective review. Ophthalmology. 2000 Oct. 107(10):1829-35. [Medline].
20. Dohlman CH, Cade F, Pfister R. Chemical burns to the eye: paradigm shifts in treatment.
Cornea. 2011 Jun. 30(6):613-4. [Medline].
21. Hemmati H, Colby K. Treating Acute Chemical Injuries of the Cornea. EyeNet. October 2012.
[Full Text].
22. Stern G, Goins K, Pelton R. Focal points, Chemical Injuries of the Cornea. March 2010. 1-14.
23. Suri K, Kosker M, Raber IM, Hammersmith KM, Nagra PK, Ayres BD, et al. Sutureless amniotic
membrane ProKera for ocular surface disorders: short-term results. Eye Contact Lens. 2013
Sep. 39(5):341-7. [Medline].
Media Gallery
Alkali burn. Note the severe conjunctival reaction and stromal opacification blurring iris details
inferiorly.
Severe chemical injury with early corneal neovascularization.
Complete cicatrization of the corneal surface following chemical injury.
of 3
Tables
Back to List
http://emedicine.medscape.com/article/1215950-overview 4/6
8/28/2017 Ophthalmologic Approach to Chemical Burns: Background, Pathophysiology, Epidemiology
Author
Mark Ventocilla, OD, FAAO Adjunct Clinical Professor, Michigan College of Optometry; Editor,
American Optometric Association Ocular Surface Society Newsletter; Chief Executive Officer, Elder
Eye Care Group, PLC; Chief Executive Officer, Mark Ventocilla, OD, Inc; President, California Eye
Wear, Oakwood Optical
Mark Ventocilla, OD, FAAO is a member of the following medical societies: American Academy of
Optometry, American Optometric Association
Simon K Law, MD, PharmD Clinical Professor of Health Sciences, Department of Ophthalmology,
Jules Stein Eye Institute, University of California, Los Angeles, David Geffen School of Medicine
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of
Ophthalmology, Association for Research in Vision and Ophthalmology, American Glaucoma Society
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: Cornea
Society, AAO, OMIC, Aerie, Bausch & Lomb, Bio-Tissue, Shire, TearLab<br/>Serve(d) as a speaker or
a member of a speakers bureau for: Allergan, Bausch & Lomb, Bio-Tissue.
Chief Editor
Andrew A Dahl, MD, FACS Assistant Professor of Surgery (Ophthalmology), New York College of
Medicine (NYCOM); Director of Residency Ophthalmology Training, The Institute for Family Health
and Mid-Hudson Family Practice Residency Program; Staff Ophthalmologist, Telluride Medical Center
Andrew A Dahl, MD, FACS is a member of the following medical societies: American Academy of
Ophthalmology, American College of Surgeons, American Intraocular Lens Society, American Medical
Association, American Society of Cataract and Refractive Surgery, Contact Lens Association of
Ophthalmologists, Medical Society of the State of New York, New York State Ophthalmological
Society, Outpatient Ophthalmic Surgery Society
Additional Contributors
Acknowledgements
Geoffrey Broocker, MD, FACS is a member of the following medical societies: American College of
Surgeons
Evan S Loft is a member of the following medical societies: American Academy of Ophthalmology,
American Medical Association, American Society of Cataract and Refractive Surgery, Association for
Research in Vision and Ophthalmology, and Phi Beta Kappa
J Bradley Randleman, MD is a member of the following medical societies: Alpha Omega Alpha,
American Academy of Ophthalmology, American Society of Cataract and Refractive Surgery, Cornea
Society, and International Society of Refractive Surgery
http://emedicine.medscape.com/article/1215950-overview 6/6