This document discusses various types of ocular trauma including classification, symptoms, assessment, diagnostics, and treatment. It covers closed and open globe injuries, corneal abrasions, extraocular foreign bodies, orbital fractures, hyphema, eyelid lacerations, globe ruptures, and chemical burns. Common injuries from blunt trauma include commotio retinae, retinal hemorrhages, choroidal ruptures, and vitreous hemorrhage or detachment. Assessment examines mechanism of injury and complications involving iris, lens, vitreous, choroid, and retina. Treatment priorities are irrigation, antibiotics, patching, referral to ophthalmologist, and surgery if needed to repair damage and prevent complications.

1. Ocular Trauma

2. Ocular Trauma Classification
Mechanical
Eye injuries
Closed Globe
Contusion Lamellar
laceration
Superficial
Foreign body
Open Globe
Laceration
Penetrating
Intra ocular
Foreign Body
Perforating
Rupture
4/25/2023
(Kuhn F., et al, A standardized classification of ocular trauma. Ophthalmology 1996,
103:240-243).
2

3. Closed globe Vs Open globe
Closed Globe ( Penetration
into the cornea)
Open Globe ( Penetration
through the cornea)
Kuhn F., et al, The Birmingham Eye Trauma Terminology system (BETT): J Fr
Ophtalmol. 2004 Feb;27(2):206-10.
4/25/2023 3

4. TYPE OF INJURY
• Refers to the mechanism of injury.
A. Rupture
B. Penetrating
C. Intraocular foreign body
D. Perforating
E. Mixed
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5. Complications
• Common anterior segment complications were
– iris prolapse (43%)
– cataract (36% )
– hyphema (17%).
– glaucoma
• Common posterior segment complications were
– Vitreous haemorrhage (31%),
– Berlin’s oedema (15%),
– retinal detachment (9%) and
– RAPD (7%).
– Signs of infection at presentation 11%
– IOFB (9%) –
• 4% in anterior segment
• 5% in posterior segment
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6. Corneal Abrasion
• Partial or complete removal of an area of
epithelium of the cornea
• Most common eye injury seen in the ER
• Common causes: FB, contact lenses, exposure
to UV light

7. Corneal Abrasion
Symptoms/Assessment
Mild to severe pain
Foreign body sensation
Photophobia
Normal to slightly decreased
visual acuity
Injected conjunctiva
Tearing
Abnormal Fluorescein stain

8. Corneal Abrasion
Treatment
– Topical analgesic
– Topical ophthalmic
antibiotic
– Tight patch to affected
eye for 12-24 hours
Education
– Follow-up care
– Proper patching
techniques
– Instillation of meds
– S/S of infection
– Use extra precaution
with activities requiring
depth perception

9. Extraocular Foreign Body
• Can enter as a result from hammering,
grinding, working under cars, or working
above the head
• “Something going into my eye”
• Metal, sawdust, dust particles
• Metal can form a rust ring on the cornea

10. Extraocular Foreign Body
Symptoms/Assessment
– Pain
– Foreign body sensation
– Tearing
– Redness
– Normal to slightly abnormal
visual acuity
– Fluorscein stain abnormal
– FB visualized
Diagnostics
– Magnifying lens
– Fluorescein stain
– Slit-lamp

11. Extraocular Foreign Body
Treatment
–Topical anesthetic
• Topical anesthetic inhibit
wound healing and are
toxic to corneal
epithelium
–Gentle irrigation with NS
– FB removal with moist
cotton swab, needle, eye
spud if irrigation
– Patch both eyes to
reduce unsuccessful
consensual movement
– Possible admission

12. Orbital fracture
• Fracture of the orbit without a fracture of the
orbital rim
• Common cause: blunt trauma from fist, ball,
or nonpenetrating object
• These fractures are associated with
entrapment and ischemia of nerves or
penetration into
a sinus

13. Orbital fracture
Symptoms/Assessment
Hx of blunt trauma
Diplopia
Facial anesthesia
Pain
Sunken appearance of the
eye
Limited vertical eye movement
EOM abnormal
Crepitus
Periorbital edema,
hematoma, ecchymosis
Subconjunctival
hemorrhage
Look for other injuries

14. Orbital fracture
Diagnostics
– Visual acuity
– Fundoscopy
– CT scan
– X-rays
• Orbits
• Facial
• Waters’
Treatment/Education
– Ophthalmological consult
– Analgesics
– Antibiotics
– Ice pack
– Refrain from blowing nose
– Follow-up care
– Possible admission or
surgery

15. Hyphema
• Blood in the anterior chamber from the iris
bleeding
• Usually result of blunt trauma
• Significant risk of secondary bleeding in 3-5
days with outcomes poor

16. Hyphema
Symptoms/Assessment
– Blurred vision
– Blood tinged vision
– Pain
– Visualized blood in
anterior chamber at
bottom of iris
– Assess for other
associated injuries

17. Hyphema
Treatment/Education
– Have patient sit upright or
bedrest with HOB 30°
– Patch or shield both eyes
– Diuretics to decrease
intraocular pressure
– Refrain from taking aspirin
– Refer to ophthalmologist
– Admission

18. Eyelid Laceration
Symptoms/Assessment
– MOI
– Visual disturbance
– Laceration
– Protrusion of fat
– Upper lid does not raise
– Assess for ocular injuries
– Bleeding
Treatment/Education
– Stop bleeding: Avoid
direct pressure on the
eye
– Surgical repair
– Topical analgesic
– Td
– Wound care
– S/S of infection
– Follow-up

19. Globe Rupture
• Ocular Emergency
• Penetrating or perforating injury

20. Globe Rupture
Symptoms/Assessment
– MOI
• Blunt
• Penetrating
– Sudden visual impairment or
loss
– Pain
– Asymmetry of globe
– Extrusion of aqueous or
vitreous humor
– Direct visualization of FB
– Irregularities in pupillary
borders
– Diagnostics
• CT scan
• MRI
• Orbit films
• Slit-lamp exam

21. Globe Rupture
Treatment
– Ophthalmological referral
– Do not open eye
– Keep patient in Semi-
Fowlers position
– Patch/shield affected both
eyes
– IV analgesics
– IV antibiotics
– Calm, supportive
environment
– Admission/Surgery
– If impaled object: Secure
it.
Do Not
Remove IT!

22. CHEMICAL BURNS
• Caused due to external contact by acids or
alkalis.
• Only ocular injury, requiring immediate
treatment.
• It is an ophthalmic emergency.

23. MODE OF INJURY
• These usually occur with external contact with
chemical under following circumstance
• Domestic accidents ex: with ammonia,solvents
detergents & cosmetics
• Chemical laboratory accidents with alkali ,acids
• Chemical warfare injuries
• Self inflicted chemical injuries seen in
malingerers & psychopaths

24. ACID BURNS
• These are comparatively
lesser dangerous than
alkali burns

25. CAUSES
• Inorganic acids –
hydrochloric acid,
sulphuric acid, nitric
acid
• Glacial acetic acid
• Acetic acid
• Chromic acid
H2SO4
HCL

26. MECHANISM
• Forms a precipitate of tissue proteins which
coagulate thus causing tissue damage & scar
formation.
• The coagulation forms a barrier that prevents
deep penetration.

27. OCULAR SIDE EFFECTS
• Restricted to lids,
conjunctiva & cornea.
• Conjunctival –
necrosis &
symblepheron.
• Corneal – necrosis &
staphyloma.

28. ALKALI BURNS
• These are much
more dangerous
than acid burns.

29. CAUSES
• Caustic potash
• Lime
• Liquid ammonia or ammonium hydroxide
• Caustic soda

30. MECHANISM
• The hydroxyl group causes saponification of fats
& proteins & also causes release of proteolytic
enzymes like collagenase, elastase.
• Thus severe melting of the tissues occur.
• The pH of tissues correlates with tissue damage.
• Irreversible damage is seen with pH of 11.5

31. • Alkalis dissociate the fatty acids of cell membrane &
therefore destroy the tissue.
• In hydroscopic- they extract water from cells causing
necrosis.
• Combines with lipids of cells to form soluble
compounds thus causing softening of tissue.
• This all increases in increased penetration of the
alkali in the tissue.
• Alkali burn therefore spreads widely & the action
continues for some days

32. MANAGEMENT
• To minimize the damage
• Avoidance of complication
• Control of acute inflammation
• Support regeneration of epithelium &
reparative process

33. GRADES OF CHEMICAL
BURNS
good
a) Corneal
haze
b) Iris details
visible
a) Congestion
b) Chemosis
c) Ischemic(< 1/3
)
II
good
epithelial
damage only
a) Chemosis
b) No ischaemia
I
VISUAL
PROGNOSIS
CORNEA
CONJUNCTIVA
GRAD
E

34. doubtful
a)Total
epithelial loss
b)Stromal haze
c)Iris details not
visible
a) Ischemia (1/3-
½)
III
poor
a) Total corneal
opacity
b) No view of
iris & pupil
a) Ischaemia > ½
IV
VISUAL
PROGNOSIS
CORNEA
CONJUNCTIVA
GRADE

35. TREATMENT
• Immediate & thorough
wash with available
clean water or saline
• chemical neutralization
• Mechanical removal of
contaminant
• Removal of
contaminated & necrotic
tissue

36. TREATMENT
• Prevention of
symblepharon
• Antibiotic drops,topical
steroids ,antiglaucoma
therapy
• Lubricants
• Therapeutic bandage
contact lens for
persistent epithelial
defect

37. SURGICAL REHABILITATION
• Conjunctival grafting
• Penetrating or preparatory lamellar
keratoplasty may be done
• Optical penetrating keratoplasty may be
done after one year of complete healing

38. ROLE OF OPTOMETRIST
• Irrigation
• History taking
• Visual assessment
• Therapeutic contact lens
• Referring to ophthalmologist
• Prosthetic contact lens

39. Mechanics of blunt trauma to eyeball: A, direct impact;B,
compression wave force; C, reflected compressionwave;
D,rebound compression wave.

40. Mechanics of blunt trauma to
eyeball
Blunt trauma of eyeball produces damage by
different forces as described below:
1. Direct impact on the globe. It produces
maximum damage at the point where the blow is
received Fig A
2. Compression wave force. It is transmitted
through the fluid contents in all the directions and
strikes the angle of anterior chamber, pushes the
iris lens diaphragm posteriorly, and also strikes the
retina and choroid. This may cause considerable
damage.

41. Sometimes the compression wave may be so explosive, that
maximum damage may be produced at a point distant from the
actual place of impact. This is called contre-coup damage.(Fig-B)
3. Reflected compression wave force. After striking the outer
coats the compression waves are reflected towards the posterior
pole and may cause foveal damage (Fig-C).
4. Rebound compression wave force. After striking the posterior
wall of the globe, the compression waves rebound back
anteriorly. This force damages the retina and choroid by forward
pull and lens-iris diaphragm by forward thrust from the back .(Fig
D)

42. 5. Indirect force. Ocular damage may also be
caused by the indirect forces from the bony
walls and elastic contents of the orbit, when
globe suddenly strikes against these structures.

43. Iris, pupil and ciliary body
1. Traumatic miosis. It occurs initially due to
irritation of ciliary nerves. It may be associated
with spasm of accommodation.
2. Traumatic mydriasis (Iridoplegia). It is usually
permanent and may be associated with
traumatic cycloplegia.
3. Rupture of the pupillary margin is a
commonoccurrence in closed-globe injury.

44. 4. Radiating tears in the iris stroma, sometimes
reaching up to ciliary body, may occur
occasionally.
5. Iridodialysis i.e., detachment of iris from its
root at the ciliary body occurs frequently. It
results in a D-shaped pupil and a black biconvex
area seen at the periphery.
6. Antiflexion of the iris. It refers to rotation of
the detached portion of iris, in which its
posterior surface faces anteriorly

45. 7. Retroflexion of the iris. This term is used when
whole of the iris is doubled back into the ciliary
region and becomes invisible.
8. Traumatic aniridia or iridremia. In this
condition, the completely torn iris (from ciliary
body) sinks to the bottom of anterior chamber
in the form of a minute ball.

46. 9. Angle recession refers to the tear between
longitudinal and circular muscle fibres of the
ciliary body. It is characterized by deepening of
the anterior chamber and widening of the ciliary
body band on gonioscopy. Later on it is
complicated by glaucoma.

47. 10. Inflammatory changes. These include
traumatic iridocyclitis, haemophthalmitis, post-
traumatic iris atrophy and pigmentary changes.
Treatment. It consists of atropine, antibiotics
and steroids. In the presence of ruptures of
pupillary margins and subluxation of lens,
atropine is contraindicated

48. Lens It may show following
changes:
1. Vossius ring. It is a circular ring of brown
pigment seen on the anterior capsule. It occurs
due to striking of the contracted pupillary
margin against the crystalline lens. It is always
smaller than the size of the pupil.
2. Concussion cataract. It occurs mainly due to
imbibition of aqueous and partly due to direct
mechanical effects of the injury on lens fibres.

49. Traumatic absorption of the lens. It may occur
sometimes in young children resulting in
aphakia.
4. Subluxation of the lens. It may occur due to
partial tear of zonules. The subluxated lens is
slightly displaced but still present in the
pupillary area. On dilatation of the pupil its edge
may be seen.

50. Depending upon the site of zonular tear
subluxation may be vertical (upward or
downward), or lateral (nasal or temporal).
5. Dislocation of the lens. It occurs when rupture
of the zonules is complete. It may be intraocular
(commonly) or extraocular (sometimes).

51. Intraocular dislocation may be anterior into the
anterior chamber, or posterior into the vitreous.
Extraocular dislocation may be in the
subconjunctival space (phakocele) or it may fall
outside the eye.

52. Vitreous
1. Liquefaction and appearance of clouds of fine
pigmentary opacities (a most common change).
2. Detachment of the vitreous either anterior or
posterior.
3. Vitreous haemorrhage. It is of common
occurrence .
4. Vitreous herniation in the anterior chamber may
occur with subluxation or dislocation of the lens.

53. Choroid
• 1. Rupture of the choroid. The rupture of
choroid is concentric to the optic disc and
situated temporal to it. Rupture may be single
or multiple. On fundus examination, the
choroidal rupture looks like a whitish crescent
(due to underlying sclera) with fine
pigmentation at its margins. Retinal vessels
pass over it.

54. 2. Choroidal haemorrhage may occur under the
retina (subretinal) or may even enter the
vitreous if retina is also torn.
3. Choroidal detachment is also known occur
following blunt trauma. Traumatic choroiditis
may be seen on fundus examination as patches
of pigmentation and discoloration after the eye
becomes silent.

55. Retina
1. Commotio retinae (Berlin’s oedema). It is of
common occurrence following a blow on the
eye. It manifests as milky white cloudiness
involving a considerable area of the posterior
pole with a ‘cherry-red spot’ in the foveal region.
It may disappear after some days or may be
followed by pigmentary changes.

56. 2. Retinal haemorrhages. These are quite common
following concussion trauma. Multiple haemorrhages
including flame-shaped and preretinal (subhyaloid) D-
shaped haemorrhage may be associated with traumatic
retinopathy.
3. Retinal tears. These may follow a contusion,
particularly in the peripheral region, especially ineyes
already suffering from myopia or senile
degenerations.

57. 4. Traumatic proliferative retinopathy (Retinitis
proliferans). It may occur secondary to vitreous
haemorrhage, forming tractional bands.
5. Retinal detachment. It may follow retinal tears or
vitreo-retinal tractional bands.
6. Concussion changes at macula. Traumatic
macular oedema is usually followed by pigmentary
degeneration. Sometimes, a macular cyst is formed,
which on rupture may be converted into a lamellar or
full thickness macular hole.

58. Intraocular pressure changes in closed-globe
injury
1. Traumatic glaucoma. It may occur due to
multiple factors.
2. Traumatic hypotony. It may follow damage to
the ciliary body and may even result in phthisis
bulbi.

59. Traumatic changes in the refraction
1. Myopia may follow ciliary spasm or rupture of
zonules or anterior shift of the lens.
2. Hypermetropia and loss of accommodation
may result from damage to the ciliary body

60. INTRAOCULAR FOREIGN BODIES
Penetrating injuries with foreign bodies are not
infrequent. Seriousness of such injuries is
compounded by the retention of intraocular
foreign bodies (IOFB).
• Common foreign bodies responsible for such
injuries include: chips of iron and steel (90%)
particles of glass, stone, lead pellets, copper
percussion caps, aluminium, plastic and wood.

61. Mechanical effects of IOFB
Mechanical effects depend upon the size,
velocity and type of the foreign body. Foreign
bodies greater than 2 mm in size cause
extensive damage. The lesions caused also
depend upon the route of entry and the site up
to which a foreign body has travelled. In general
these include: Corneal or/and scleral
perforation, hyphaema, iris hole; Rupture of the
lens and traumatic cataract;

62. • Vitreous haemorrhage and/or degeneration;
• Choroidal perforation, haemorrhage and
inflammation;
• Retinal hole, haemorrhages, oedema and
detachment

63. Locations of IOFB
Having entered the eye through the cornea or
sclera a foreign body may be retained at
any of the following sites
1. Anterior chamber. In the anterior chamber,
the IOFB usually sinks at the bottom. A tiny
foreign body may be concealed in the angle of
anterior chamber, and visualised only on
gonioscopy.

64. 2. Iris. Here the foreign body is usually entangledin the
stroma.
3. Posterior chamber. Rarely a foreign body may
sink behind the iris after entering through pupil or after
making a hole in the iris.
4. Lens. Foreign body may be present on the anterior
surface or inside the lens. Either an opaque track may be
seen in the lens or the lens may become completely
cataractous.
5. Vitreous cavity. A foreign body may reach here through
various routes .

65. Common sites for retention of an
intraocular foreign body: 1, anterior
chamber; 2, iris; 3, lens; 4, vitreous;
5, retina; 6, choroid; 7, sclera; 8,
orbital cavity
diagrammatic depiction of routes of access
of a foreign body in the vitreous,
through: A, cornea, pupil, lens; B, cornea,
iris, lens; C, cornea, iris, zonules; D, sclera,
choroid, retina.

66. Reactions of the foreign body,
Inorganic foreign body
Depending upon its chemical nature following 4
types of reactions are noted in the ocular tissues
1. No reaction is produced by the inert
substances which include glass, plastic,
porcelain, gold silver and platinum.
2. Local irritative reaction leading to
encapsulation of the foreign body occurs with
lead and aluminium particles.

67. 3. Suppurative reaction is excited by pure
copper, zinc, nickel and mercury particles.
4. Specific reactions are produced by iron
(Siderosis bulbi) and copper alloys (Chalcosis):

68. • Siderosis bulbi It refers to the degenerative
changes produced by an iron foreign body.
Sidesosis bulbi usually occurs after 2 months
to 2 years of the injury. However, earliest
changes have been reported after 9 days of
trauma.

69. Mechanism
The iron particle undergoes electrolytic
dissociation by the current of rest and its ions
are disseminated throughout the eye. These
ions combine with the intracellular proteins and
produce degenerative changes. In this process,
the epithelial structures of the eye are most
affected.

70. Clinical manifestations
1. The anterior epithelium and capsule of the lens are
involved first of all. Here, the rusty deposits are
arranged radially in a ring. Eventually, the lens becomes
cataractous.
2. Iris It is first stained greenish and later on turns
reddish brown.
3. Retina develops pigmentary degeneration which
resembles retinitis pigmentosa.
4. Secondary open angle type of glaucoma occurs due
to degenerative changes in the trabecular meshwork.

71. Chalcosis
It refers to the specific changes produced by the
alloy of copper in the eye.
Mechanism. Copper ions from the alloy are
dissociated electrolytically and deposited under
the membranous structures of the eye. Unlike
iron ions these do not enter into a chemical
combination with the proteins of the cells and
thus produce no degenerative changes.

72. Clinical manifestations
1. Kayser-Fleischer ring. It is a golden brown ring which
occurs due to deposition of copper under peripheral
parts of the Descemet’s membrane of the cornea.
2. Sunflower cataract. It is produced by deposition of
copper under the posterior capsule of the lens. It is
brilliant golden green in colour and arrangedlike the
petals of a sun flower.
3. Retina. It may show deposition of golden plaques at
the posterior pole which reflect the light with a metallic
sheen

73. Reaction of organic foreign bodies
• The organic foreign bodies such as wood and other
vegetative materials produce a proliferative reaction
characterised by the formation of giant cells.
• Caterpillar hair produces ophthalmia nodosum,
which is characterised by a severe granulomatous
iridocyclitis with nodule formation.