Erwin Dipraja

TRAUMA MATA
LASERASI PALPEBRA
Lid laceration

• Any lid defect should be repaired by direct closure whenever

possible, even under tension, since this affords the best functional
and comestic result
Management

• Superficial lacerations parael to the lid margin without gaping 

sutured with 6-0 black silk or nylon  sutures are removed after 5-6
days
• Lid margin lacerations invariably gape without careful closure and
prevent notching must be sutured with optimal alignment:
5-0 silk vertical mattress suture is inserted in line with the meibomian gland
orifices, about 2 mm from the wound edges and 2 mm deep, and left untied
Tarsal plate edges are apposed with partial-thickness lamellar 5-0 absorbable
(e.g. polyglactin) sutures, which are tied anteriorly
The lid margin silk suture is then tied so that the cut edges slightly pucker the
wound; the ends are left fairly long, e.g. 2 cm
The overlying skin is closed with interrupted 6-0 or 7-0 nylon or absorbable
sutures, securing the ends of the silk suture to direct these and its knot away
from the cornea.
• Lacerations with mild tissue loss just sufficient to prevent direct
primary closure  lateral cantholysis in order to increase lateral
mobility
• Lacerations with extensive tissue loss  require major
reconstructive procedures similar to those used following resection
of malignant tumours
• Canalicular lacerations should be repaired within 24 hours  the
laceration is bridged by silicone tubing (Crawford tube), which is
threaded down the lacrimal system and tied in the nose, following
which the laceration is sutured
• Alternatively, repair of a single canaliculus can be performed using
a monocanalicular stent and, if necessary, suturing its footplate to
the lid using 8-0 material
• Tetanus status  It is critical to ensure that the patient’s tetanus
immunization status is satisfactory after any injury:
without any prior immunization  250 units of human tetanus
immunoglobulin (IM)
If previously immunized but a booster has not been administered within
the last 10 years  IM or subcutaneous tetanus toxoid
HIFEMA
Hyphema

• Contusive forces  tear the iris vessels and damage the anterior
chamber angle  Blood in the aqueous may settle out in a visible
layer
• Acute glaucoma occurs if the trabecular meshwork is blocked by fibrin and
cells or if clot formation produces pupillary block
Treatment

• Rest
• Steroid drops should be started; aspirin & NSAID avoided
• eye should be examined frequently for secondary bleeding, glaucoma, or
corneal blood staining from iron pigment
• oral aminocaproic acid (100 mg/kg every 4 hours up to a maximum of 30 g/d
for 5 days)
• stabilize clot formation reduces the risk of rebleeding
• surgically evacuated if intraocular pressure remains elevated (> 35 mm Hg
for 7 days or 50 mm Hg for 5 days)
• Vitrectomy instruments
•  remove the central clot and lavage the anterior chamber
• viscoelastic evacuation
•  small limbal incision is made to inject the viscoelastic  clearing the anterior
chamber
EROSI KORNEA
Erosi Kornea

• Terkelupasnya epitel kornea diakibatkan oleh gesekan keras

dalam waktu singkat epitel di sekitarnya dapat bermigrasi dengan
cepat dan menutupi defek tersebut.
• Tanda dan gejala :
 Terasa sangat sakit
 Mata berair
 Lakrimasi
 Fotofobia
 Penglihatan terganggu
 Kemerahan
 Blefarospasme dan mata berair biasanya membangunkan pasien
pada malam hari / terjadi pada saat terbangun
 Biasanya ada riwayat abrasi kornea
• Pemeriksaan: Fotofluoresensi  kornea berwarna hijau
Kanski JJ, Bowling B. Clinical ophthalmology: a systemic approach. 8th
ed. UK: Saunders Elsevier. Page 211
Tatalaksana

• Gejala akut :
Cyclopentolate 1% dua kali sehari
Debridemen dengan spon selulosa steril / cotton bud
Diklofenak topikal 0,1% mengurangi rasa sakit
Hipertonik natrium klorida 5% tetes empat kali sehari dan salep pada waktu
tidur dapat meningkatkan adhesi epitel
• Gejala berulang :
gel topikal pelumas atau salep, atau salin hipertonik salep  saat tidur 
bisa untuk jangka panjang
Debridement sederhana dari epitel di daerah yang terlibat  menghaluskan
lapisan Bowman dengan laser excimer
Bandage contact lenses
DISLOKASI LENSA
Traumatic lens dislocation

• Partial or complete traumatic

lens dislocation may occur
following a contusion injury

• Classification
• Partial  no symptoms
• Lens floating in vitreous 
• blurred vision and usually a red eye
• Iridodonesis  quivering of the iris
when the patient moves the eye
Complications Treatment
• Uveitis and glaucoma • no complications  left
untreated
• uveitis or uncontrollable
glaucoma occurs 
• lens extraction must be done
despite the poor results
possible from this operation
• technique of choice is limbal or
pars plana lensectomy using a
motor-driven lens and vitreous
cutter
PERDARAHAN SUBKONJUNGTIVA
 Perdarahan Subkonjungtiva

• Pecahnya pembuluh darah yang • Etiologi : spontan

ada di bawah lapisan • Batuk/bersin yang terlalu kuat
konjungtiva • Mengejan
• Muntah
• Mengangkat beban berat
• Trauma (benda asing, infeksi,
menggosok mata)

http://www.allaboutvision.com/conditions/hemorrhage.htm
http://www.mayoclinic.org/diseases-conditions/subconjunctival-hemorrhage/basics/causes/con-20029242
Perdarahan Subkonjungtiva

• Faktor resiko: • Tatalaksana :

• Hipertensi • Kompres hangat.
• Kelainan pembuluh / pembekuan
darah
• Prognosis :
• Sembuh sendiri dalam 1-2 minggu
• Tanda dan gejala: tanpa pengobatan
• Bercak merah
• Terasa mengganjal dan tidak nyeri
Kelainan Mata Merah Penglihatan Menurun

1. Keratitis
2. Glaukoma Akut
3. Uveitis
4. Iridosistitis
5. Keratokonjungtivis
6. Xeropthalmia
LUKA BAKAR KARENA TRAUMA KIMIA
Chemical burns

• treated as ophthalmic emergencies

• Treatments
• Immediate tap-water lavage
• obvious foreign bodies should also be irrigated away if possible
• Sterile isotonic saline (several liters per injured eye) is instilled with standard
intravenous tubing
• lid speculum and local anesthetic infiltration of the lids may be necessary to
overcome blepharospasm
• Analgesics and topical anesthetic and cycloplegic agents are nearly always
indicated
• moistened cotton-tipped applicator and jeweler's forceps to remove particulate
matter from the fornices
• Watch for respiratory distress due to soft-tissue swelling of the upper airways
• pH of the ocular surface is checked by placing a strip of indicator paper in the
fornix
• resume irrigation if the pH is not between 7.3 and 7.7
• apply an antibiotic ointment and a pressure dressing after lavage
Alkali burns

• cause an immediate rise in intraocular pressure owing to contraction

of the sclera and trabecular meshwork damage
• secondary pressure rise occurs 2-4 hours later from the release of
prostaglandins, which potentiate an intense uveitis
• Treatment
• topical steroids, antiglaucoma agents, and cycloplegics during the first 2
weeks
• Ascorbate (vitamin C) and citrate drops
• trial with collagenase inhibitors (acetylcysteine) may prove beneficial
• Corneal exposure and persistent epithelial defects  artificial lubricants,
tarsorrhaphy, or a bandage contact lens

• Long terms complications

• glaucoma, corneal scarring, symblepharon, entropion, and keratitis sicca
Thermal burns

• Etiologi:
• Ultraviolet irradiation, even in moderate doses  painful superficial keratitis
(6-12 hour after exposure)
• Other e/ electric welding arc without the protection of a filter, short circuits in high-
voltage lines, or exposure to the reflections from snow without protective sunglasses
("snow blindness“)
• severe cases of "flash burn“
• pressure patching with an antibiotic ointment
• mydriatic is instilled if there is iritis
• Excessive exposure to radiation (x-ray) produces cataractous changes that
may not appear for many months after the exposure
Treatment

• topical antibiotics and sterile dressings

• corneal damage is sustained  extensive lid swelling initially makes
pressure patching unnecessary
• Tarsorrhaphies and moisture chambers fashioned from plastic wrap
then protect the cornea
• Full-thickness skin grafts are delayed until skin contraction is no
longer progressing
BENDA ASING KORNEA
Corneal foreign bodies

• Sign & symptoms

• pain and irritation that can be felt
during eye and lid movement
• Fluorescein 
• exposed basement membrane of an
epithelial defect
• highlight aqueous leakage from
penetrating wounds (positive Seidel
test)
• pattern of vertical scratch marks
on the cornea  foreign bodies
embedded on the tarsal
conjunctival surface of the upper
lid
• Contact lens overwear  corneal
edema
Treatment

• Simple corneal epithelial defects  antibiotic ointment and a

pressure patch to immobilize the lids
• removal of foreign matter
• anesthetic can be given
• a spud or fine-gauge needle used to remove the material during slit lamp
examination
• Examples
• Metallic rings surrounding copper or iron fragments  battery-operated drill with a burr
tip
• Deeply embedded inert materials (eg, glass, carbon)  may be allowed to remain in the
cornea
• aqueous leak requiring sutures or cyanoacrylate glue  microsurgical technique

• antibiotic ointment should be instilled and the eye patched

• wound should be examined daily for evidence of infection
• NOTE !!
• Never give a topical anesthetic solution to the patient for repeated use after a
corneal injury
• delays healing, masks further damage, and can lead to permanent corneal scarring
• Steroids should be avoided while an epithelial defect exists
• Recurrent epithelial erosions sometimes follow corneal injuries 
• patching, bandage contact lens, corneal micropuncture, or excimer laser
phototherapeutic keratectomy (PTK)
BENDA ASING KONJUNGTIVA
LASERASI DUKTUS LAKRIMALIS
Canallicular laceration

• Often occur in the setting of trauma

• Canalicular trauma refers to sudden physical injury  damage to the
lacrimal drainage system of the eye
• The canaculi are the mucosal ducts through which tears drain from
the eye
• The lacrimal canalliculi are located within the medial aspect of the
eyelid. This area area is unlike the rest of the eyelid because it does
not contain a tarsal substructure
• Injuries to the canalicular portion of the tear drainage system can
occur as isolated injuries or as one component of more extensive
injuries, including multiple marginal lidlacerations, orbital fractures,
and globe injuries
• An injury to the lacrimal drainage system leads to scarring and
stenosis  epiphora
Etiology

• A force which displaces the eyelid from its strong attachment at

the medial canthal tendon, lacrimal, and maxillary bone, tend to
cause avulsion in the medial aspect of the eyelid
• Result from direct or indirect trauma
• Direct trauma: severing the lacrimal portion of the lid with objects,
such as glass,coat hangers, knives, dog bites, cat claws, fingernails, or
other sharp objects
• Indirect trauma: blunt injury to the ocular adnexa from such
mechanisms as blows to the face, blunt weapons, or falls onto blunt
objects
• Because of its superficial location in the medial lid  vulnerable to
trauma
Management

• Canalicular lacerations should be repaired within 24 hours  the

laceration is bridged by silicone tubing (Crawford tube), which is
threaded down the lacrimal system and tied in the nose, following
which the laceration is sutured
• Alternatively, repair of a single canaliculus can be performed using a
monocanalicular stent and, if necessary, suturing its footplate to the
lid using 8-0 material
TRAUMA TELINGA
TRAUMA AURIS
Haematoma auris
• Haematoma auris is a collection of blood between the auricular cartilage and
perichondrium

ETIOLOGY:
• Usually produced by trauma, although occasionally the spontaneous rupture
and blood vessel may be the cause

PATHOGENESIS AND PATOLOGY:

• While subcutaneous heametomas resorb without consequence,
subperichondria serosangiunous fluid stimulates the proliferation of
mesenchymal cells in the overlying perichondrium  chondroblasts forming
new cartilage in 7-10 days  ‘cauliflower ear’ deformity
• This occurs almost exclusively on the anterior surface of the auricle where the
skin is tightly adherent to the underlying perichondrium  shearing forces
applied tothe ear separate the perichondrium from the cartilage
• On the posterior surface, intervening areolar tissue allows the skin to glide
over the perichondrium
• Rarely, a tear through the cartilage can allow haematomas to colect under the
perichondrium on both sides of the cartilage
Clinical pictures

• History of trauma, often sport-related (wrestling and rugby

scrumming classicaly producing there shearing ijuries )
• Haematoma  painless and inflammation is minimal
Treatment

• Requires evacuation observing strict asepsis

• This is achieved through either aspiration with a thick bore needle, or if this is
inadequate, in incision
• Such an incision can be hidden on the anterior surface by placement parallel to
natural contours
• Posterior incision with removal of a small ‘window’ of cartilage has been
advocated
• Aspiration alone, however, results in a very high incidence of re-collection until
the perichondrium is again firmly adherent (about 7 days)  to prevent this:
 The use of moulded pressure bandages or splints applied on both sides of the pinna
 A drain left in the incision site
 A posterior incision, with excision of a disc of cartilage and placement of a suction drain
 Through-and-through ‘mattress’ or ‘quilting’ sutures to apply compression, with or without
materials to distribute the compression more evenly
• After 7-10 days, aspiration is ineffective and most authors state that surgery for
removal of the organizing haematoma and newly formed cartilage with/withoug
overlying perichondrium is necessary
Outcome

• If left untreated  the natural outcome is thought to be deformity of

the pinna and the classic ‘cauliflower’ or ‘wrestler’s’ ear
• Supervening infection  perichondritis and cartilage necrosis
TRAUMA TULANG TEMPORAL
Temporal bone trauma

•  physical insult of the temporal bone induced by impact with a

blunt surface or penetrating missile

• Classification
• By etiologies
• By site of any resulting fracture
• Reference to the long axis of the petrosus temporal bone
 longitudinal & transverse; often mixed

• Epidemiology
• 8.5/100 members of population (U.S.)
Clinical features

• History
• Elevated hearing threshold at frequencies of 4kHz & higher in patients who
sustained a temporal bone fracture
• Loss all hearing on the affected ear (17%)
• Conductive hearing loss of greater than 20 dB HL
• Clinical signs
• Evidence of penetrating injury to the temporal region of the skull
• Otorrhoea
• Bruising of the mastoid process (Battle’s sign)
• Otoscopy
• fresh blood in the external auditory meatus
• Haemotympanum alone has highest positive predictive value
Investigations
• Radiology
• Coronal & axial high resolution CT (gold standard)
• MRI  identify number of cases of temporal bone contusion
• Hearing assessment
• Pure tone audiometry
• Air-bone gap because of incus dislocation & fracture of stapes
• Tympanometry
• Electric response audiometry  assess thresholds
• Vestibular asessment
• Nystagmus  should be checked; provide vestibular involvement
• Acute vestibular failure  horizontal beating nystagmus away from the affected ear
• Electronystagmography caloric testing (after recovery)
• Facial nerve function
• Observing active & passive facial movements
• Electroneurography
• Facial nerve exploration
• Cerebrospinal fluid leak
• CSF otorrhoea / CSF rhinorrhoea should be tested
Management

• Prophylactic antibiotics
•  similar incidence of meningitis in patients treated & untreated with
antibiotics
• Laceration of the external auditory meatus
• Conservative management
• AWARE!! If the impressive haemorrhage is happening  laceration of jugular bulb
• Tympanic membrane perforation
• Avoidance of water/other contaminants
• Surgical closure (if the perforation persist for >= 3 mo)
• Haemotympanum
•  blue appearance on the drum
• Th/  spontaneous resolution within 3-6 weeks
• Ossicular disruption
• Tympanoplasty, most freuently by repositioning the incus
• Labyrinth injury/fracture
• Bed rest & vestibular sedative
• Overview
• Isolated sensorinerual hearing loss  no active treatment
• Presence of vertigo & tinnitus  bed rest, head elevation, avoidance of
straining
• Vertiginous symptoms not settle with above regime, in the presence of
persisting/fluctuating sensorineural hearing loss  exclude other causes (ex:
retrocochlear lesion) by MRI
• Facial palsy
• Argued  but patients with complete immediate palsies not operated on 
50% recovered better
• CSF leak
• Spontaneous resolution within 5 days
• If not  lumbar drainage
TRAUMA MEMBRAN TIMPANI
 TRAUMA MEMBRAN TIMPANI
TYMPANIC MEMBRAN PERFORATION
ETIOLOGI blows to the ear, severe atmospheric overpressure, exposure to excessive
water pressure (eg, in scuba divers), and improper attempts at wax removal
or ear cleaning, Insertion of objects into the ear canal purposely (eg, cotton
swabs) or accidentally, concussion caused by an explosion or open-handed
slap across the ear, head trauma (with or without basilar fracture)

S O A P
audible whistling Otoskopi : perforasi Perforasi membran -Cleaning of the
sounds during membran timpani timpani affected ear if
sneezing and nose necessary
blowing, hearing loss, Audiometri : tuli -Myringoplasty (if fail
tinnitus, sudden pain konduktif to heal
(due to middle ear spontaneously)
barotrauma), bleeding Timpanometri -Antibiotic (if there is
secondary infection)

1. Scott Brown 7th Ed. ( Vol 3; Page 3504-3505)

2.http://emedicine.medscape.com/article/858684-overview (updated on July 14,2015)
3. http://www.msdmanuals.com/professional/ear-nose-and-throat-disorders/middle-ear-and-tympanic-membrane-
disorders/traumatic-perforation-of-the-tympanic-membrane (updated on December 2012)
BAROTRAUMA (AEROTITIS MEDIA)
Otitic barotrauma

•  pathological conditions of the ear induced by pressure changes

• Barotrauma: injury produced by mechanical forces caused by a
change of pressure in a gas filled space
• Mild cases: airline passangers
• Severe cases: slap injuries typically sustained during an assault, water skiing,
high board diving, blast injuries
• Pressure/volume relationship
• Ambient pressure
• Pressure is equally applied to all body structures  no differential pressure
across any membranes or systems
• The exception, if there is an air-filled cavity within the body
•  like the middle ear which is bony cavity  no distention or expansion
• The vasculature within the wall of middle ear is in continuity with that the
rest of the body  intraluminal vascular pressure reflect the ambient
pressure
• If there is a relative negative middle ear pressure due to a failure to equalize via the tube
 increasing difference between the intraluminal vascular pressure & the middle ear air
pressure  sufficient gradient exist  oedema & even the rupture of those vessels
within the mucosal lining
Pathoetiology of inner ear barotrauma
(compression/descent)
Physiological consequences of
decompression (ascent)
• During middle ear pressure exceeds that of the ambient pressure 
passive ventilation of air through the eustachian tube into pharynx
• Occurs every 13.25 m of ascent/flying regardless of the speed of
decompression
•  suboptimal tube function  oedema & haemorrhage
• To continue ascending
•  relatively positive middle ear pressure compared to ambient pressure 
outward bulging of the tympanic membrane + traction force applied to the
oval window via the ossicles + inward force of the round window
•  pressure gradient is increased = ambient pressure has decreased
Clinical features of otitic barotrauma

• Compresion injuries
• Injuries at stable pressure
• Decompression injuries
Compression injuries

• External ear barotrauma

(external ear squeeze, reversed ear, reverse eae squeeze)
• e/  earplugs, cerumen foreign bodies, exostoses, tight fitting diving hood
• Signs & symptoms
• Pain, increasing with depth
• Canal skin & tympanic membrane  injected, petechial hemorrhage, bleeding
• Treatment
• Immediate decompress by ascending
• Meatus should be kept dry
• Diving avoided until the skin appears normal
• Occlusive ear plugs avoided (diving > 1,5 m & when flying)
• Middle ear barotrauma
(barotitis media, middle ear squeeze)
• Sign & symptoms
• Blocked ear with strong desire to equalize
• Otalgia  worsens with increased compression & the inability to equalize the middle
ear pressure
• Sudden severe pain  perforation
• Conductive hearing lose because ossicular damage
• Tympanic membrane  normal appearance to free hemorrhage + perforation
• Treatment
• Symptoms but no sign  no treatment
• Symptoms & sign, no perforation  oral/topical nasal decongestan
• Perforation  initial observation + cleaning of the affected ear
• Prevention  oral decongestan, nasal baloon inflation, myringotomies
• Inner ear barotrauma
• Inner ear hemorrhage
• Transient or minimal vestibular symptoms
• Mild to moderate sensorineural hearing loss
• Good recovery

• Labyrinthine membrane tears

• Vertigo, tinnitus, hearing loss often at 1-2kHz which is permanent
• Temporal bone studies  reissner’s membrane rupture
• Inner ear damage 
• Hemorrhage around reissner’s & the round window membrane
• Rupture of the utricle & saccule
• Perilymphatic fistula
• Sign & symptoms
• Transient dysequilibrium & dizziness
• Difficulty equalizing the middle ear pressure
• Sudden onset of vertigo, sensorineural hearing loss, tinnitus
• Acute symptoms resolve quickly, mild dysequlibrium, mild persistent nausea & motion
intolerance, subtle senses of ‘not coping’  chronic perilymphatic fistula
• Dysequilibrium which worsen / changes to momentary vertigo when performing manoeuvres
which increase the intracranial pressure
• Suspected in an otherwise healthy ear if there is sensorineural hearing loss of rapid onset,
constant dysequilibrium, positional nystagmus, tulio phenomenon (momentary vertigo with
exposure to sudden loud noise), tinnitus
• Tympanic membrane  signs of middle ear barotrauma
• Nystagmus usually towards the opposite side
• Other examination
• Tympanometry in conjunction electronystagmography
• Electrocochleography with tone-burst stimuli
• High definiton MRI & CT  promising investigations
• Treatment
• Bed rest for minimum 5 days
• Exploration by surgical, indications
• Those with progressive hearing deterioration observed on daily or more frequent,
audiometry
• If the vestibular symptoms fail to imrove after days
• Failure of complete resolution after 1 mo
Injuries at stable depth

• High pressure nervous (neurological) syndrome

isobaric gas counterdiffusion
•  when divers are exposed to extremely high pressures
• Sign & symptoms
• Tiredness, general dizziness, tremors that progress with increasing pressure, ataxia,
myoclonus
• Sudden onset of vertigo & nausea with nystagmus
• Skin eruption occur where gas bubbles are found in deeper skin layers
• Symptoms may occur at a stable depth, characteristically soon after changing the
inspired gas mixture (helium-oxygen) to one that includes a second inert gas
• Treatment
• Risk <<  slow descents & avoiding inert gas changes at depth
• recompress back
Decompression (ascent) injuries

• Alternobaric vertigo
•  asymmetrical middle ear overpressure stimulation
• e/  unilateral equalization problems
• Minor middle ear congestion & oedema or unilateral eustachian dysfunction
• Characteristics
• Occurs on ascent within 2 minutes of surfacing
• Short lived, maximum duration of 10 min
• Tumbling sensation / tilting rather than rotating
• Examinations
• Electronystagmography  true vestibular nystagmus when middle ear overpressure was
present in only one ear during controlled decompression in compression chamber
• Barotraumatic facial palsy
(facial baroparesis, alternobaric facial palsy)
• Most widely accepted explanation  induced neuropraxia
•  vasa nervora of the facial nerve < when middle ear pressure >
• Blood flow rapidly return to normal when the middle ear pressure is relieved
• Sign & symptoms
• Rapid onset, relieved after a few minutes
• Treatment
• Persistent palsy & painful bulging membrane  myringotomy
• Rapid resolution does not occur  oral steroid
• Decompression illness suspected / uncertatinty as to the true diagnosis persists 
myringotomy with grommet inserted