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CGI, HYPHAEMIA &
CHEMICAL INJURIES OF THE
EYE
Ayesha S Abdullah
29.11.2013
Learning outcomes
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By the end of this lecture the students would be able to
1. Correlate the effects of CGI on various parts of the eye
with the mechanism of close globe trauma
2. Identify the complications of CGI
3. Diagnose hyphaema and describe the principles of
management and complications of hyphaemia
4. Correlate the pathophysiology of chemical injury (with
acids and alkali) to the clinical presentation &
complications of chemical injuries of the eye
5. Describe the first aid measures and specific management
of a case with chemical injury
6. Identify the complications of chemical injury
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a)
b)
c)
d)
e)
A 20 year old man while fighting another young man had sustained
trauma to the right orbit 2 days back. He had minimal enophthalmos
and restricted upward movement of the right eye with double vision
in up-gaze only. The CT scan shows fracture of the floor of the orbit.
The most appropriate line of management is
Surgical repair of the fracture through conjunctival incision via the
inferior fornix
Surgical repair of the fracture with a plastic plate
Surgical repair via Caldwell Luc approach
Surgical repair via skin incision over the inferior orbital rim
Wait for 02 weeks and provide symptomatic treatment
Effects of close globe injury (CGI)
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Mechanism
 AP
compression
 Expansion in the equatorial plan
 Transient & excessive increase in IOP
 Impact is primarily absorbed by ??
 Lens
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–Iris diaphragm & vitreous
The damage can happen in any tissue
commonly has long-term effects/ sequelae
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Close Globe Injuries
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Subconjunctival Haemorrhage
Corneal abrasion
Acute corneal oedema
Traumatic iritis
Traumatic Mydriasis / Miosis
Hyphaema
Iridodialysis
Cyclodialysis / Angle recession
Ciliary shock
Close Globe Injuries
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Subluxation and dislocation of lens
Cataract
Posterior vitreous detachemet
Vitreous haemorrhage
Choroidal rupture
Commotio retinae
Retinal Breaks
Dialysis
 Equatorial tears
 Macular holes
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Optic nerve avulsion
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Hyphaema
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Source of bleeding?
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Iris /ciliary body / both
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Immediate threat –
 Secondary
 Can
 The
haemorrhage
happen up to a week, mostly first 24 hrs
haemorrahge is larger than the original bleed
 Most
common problem is raised intraocular pressure
Hyphaema
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Most hyphaemas resolve without complications but
complications can happen with long standing cases
The complications are, secondary glaucoma, optic
nerve damage and corneal staining
The greater the extent of hypahema greater the
chances of complications i.e blood filling more than
half of the AC
Treatment of Hyphaema
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Small (less than 1/3rd of the AC) can be managed
at home
Larger hyphaema requires hospitalization for closer
monitoring to avoid secondary bleed and
complications
For lowering the IOP; beta blockers, Alpha agonist ,
CA inhibitors
For associated traumatic uveitis; topical steroids
Immobilization of the iris in the dilated position to
avoid secondary haemorrhage; mydriatics
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Hyphaema
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Chemical Injuries of the Eye
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About 2/3rd of the chemical injuries happen at
workplace the rest at home
Almost any chemical can cause ocular irritation
Serious damage however happen with acids and
alkalis
Alkali injuries are more common because they are
used more frequently
Bilateral chemical exposure could be extremely
damaging resulting in blindness and disfigurement
Sources
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Common sources of alkali are
Cleaning products (eg, ammonia)
 Fertilizers (eg, ammonia)
 Drain cleaners (e.g, lye)
 Cement, plaster, mortar (e.g, lime)
 Airbag (automobile) rupture (e.g, sodium hydroxide)
 Fireworks (eg, magnesium hydroxide)
 Potash (eg, potassium hydroxide)
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Commonest alkalis causing chemical injury are
ammonia, sodium hydroxide & lime
Sources
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Common sources of acids are
Battery acid (eg, sulfuric acid)
 Bleach (eg, sulfurous acid)
 Glass polish (eg, hydrofluoric; behaves like an alkali)
 Vinegar (eg, acetic acid)
 Chromic acid (brown discoloration of conjunctiva)
 Nitric acid (yellow discoloration of conjunctiva)
 Hydrochloric acid
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Commonest acids are sulphuric, sulphurous, hydrofluoric,
acetic , chromic and hydrochloric acid.
Pathophysiology
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Severity depends upon
 The
nature/ properties & concentration of the chemical
 Area of the affected surface
 Length of exposure
 Associated damage e.g. thermal /electrical/ explosive
Pathophysiology
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Alakli burns are more damaging than acid burns
because it penetrates deeper1
Necrosis and shedding of the corneal and conjunctival
epithelium
Damage to the limbal vasculature
Limbal ischemia
 Persistent corneal epithelial defects
 Conjunctivaliztion & vascularization of the cornea
 Corneal ulceration and perforation
 Conjunctival and adnexal scarring
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Corneal healing
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Loss of epithelium
Migration of cell derived from the limbal stem cells
Phagocytosis of the necrosed collagen by the
keratocytes and new collagen is laid down
Clinical presentation
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History
 Ascertain
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the nature of the chemical and mode of injury
Complaints are
 Pain
(often extreme)
 Foreign body sensation
 Blurred vision
 Excessive tearing
 Photophobia
 Red eye(s)
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Physical examination
A thorough physical examination should be deferred
until the affected eye is irrigated copiously, and the pH
of the ocular surface is neutralized.
After irrigation, a thorough eye examination is
performed focusing on
clarity and integrity of the cornea
 degree of limbal ischemia
 Anterior chamber reaction
 Signs of deeper penetration of the chemical
 IOP.
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Signs
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Conjunctival inflammation
Particles in the conjunctival fornices
Perilimbal ischemia (LI-blanching) The most significant
prognostic indicator for corneal healing.
Greater the extent of blanching, the worse the
prognosis
LI is documented as number of clock hours
Signs
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Corneal epithelial defect: Corneal epithelial damage can
range from mild diffuse punctate epithelial keratitis (PEK) to a
complete epithelial defect.
Stromal haze: Haze can range from a clear cornea (grade 05) to a complete opacification
Corneal perforation
Anterior chamber inflammatory reaction: more common with
alkali injury
Increased IOP
Adnexal damage/scarring
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Principles of management
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Treat Systemic injury
Ocular involvement
 removing
the offending agent
 controlling inflammation
 promoting ocular surface healing
 preventing infection
 controlling IOP
First Aid
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Remove the chemical (irrigation)
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Immediate copious irrigation remains the single most
important therapy for treating chemical injuries
Immediate irrigation with even plain tap water is
preferred without waiting for the ideal fluid
The irrigation solution must contact the ocular
surface. Irrigation should be continued until the pH
of the ocular surface is neutralized, usually
requiring 1-2 liters of fluid
Promote ocular surface (epithelial)
healing
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Artificial tears
Bandage contact lens
Ascorbate plays a fundamental role in collagen
remodeling, leading to an improvement in corneal
healing.
Amniotic membrane transplant
topical Sodium Ascorabte 10% given 2 hourly and
1-2 g of vitamin C given orally ( not recommended
in renal disease)
Control inflammation
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Inflammatory mediators
Controlling inflammation with topical steroids can
help break this inflammatory cycle
Citrate both promotes corneal wound healing and
inhibits PMNs via calcium chelation.
Prevent infection
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When the corneal epithelium is absent, the eye is
susceptible to infection.
Prophylactic topical antibiotics during the initial
treatment stages
Control IOP
• Oral acetazolamide
Control pain
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Severe chemical burns can be extremely painful.
Oral NSAIDS
Ciliary spasm can be managed with the use of
cycloplegic agents
Surgical Care
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Early
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Debridement
Temporary amniotic membrane
Limbal stem cell transplant
Lysis of conjunctival symblepharon
Late
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Surgery for conjunctival adhesions
Keratoplasty
Cataract extraction
Keratoprosthesis
Glaucoma surgery
Follow up
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In patients with severe chemical injuries, short
hospitalization in an ophthalmic care unit to closely
monitor
In general, the prognosis of ocular chemical injuries
is directly correlated with the severity of insult to
the eye and adnexal structures.
Roper-Hall grading system
Complications
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Primary complications include the following
 Conjunctival
inflammation
 Corneal abrasions
 Corneal haze and edema
 Acute rise in IOP
 Corneal melting and perforations
Complications
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Secondary complications include the following:
Secondary glaucoma
 Secondary cataract
 Conjunctival scarring
 Corneal thinning and perforation
 Complete ocular surface disruption with corneal scarring
and vascularization
 Corneal ulceration (sterile or infectious)
 Complete globe atrophy (phthisis bulbi)
 Blindness
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Management summary
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Immediate, prolonged irrigation
Followed by referral to ophthalmologist for
aggressive early management
Close long-term monitoring
Essential to promote ocular surface healing and to
provide the best opportunity for visual
rehabilitation
Home work
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How can we grade the severity of chemical injury
of the eye?
Not more than 4 lines
By Thursday next week before the Friday class
Both homeworks