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CGI, HYPHAEMIA & CHEMICAL INJURIES OF THE EYEAyesha S Abdullah29.11.2013

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Learning outcomesBy the end of this lecture the students would be able to1. Correlate the effects of CGI on various parts of the eye

with the mechanism of close globe trauma2. Identify the complications of CGI3. Diagnose hyphaema and describe the principles of

management and complications of hyphaemia4. 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 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

 a) Surgical repair of the fracture through conjunctival incision

via the inferior fornixb) Surgical repair of the fracture with a plastic platec) Surgical repair via Caldwell Luc approachd) Surgical repair via skin incision over the inferior orbital rime) Wait for 02 weeks and provide symptomatic treatment

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Effects of close globe injury (CGI)

Mechanism AP compression Expansion in the equatorial plan Transient & excessive increase in IOP Impact is primarily absorbed by ??

Lens –Iris diaphragm & vitreous The damage can happen in any tissue commonly has long-term effects/ sequelae

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Close Globe Injuries Subconjunctival Haemorrhage Corneal abrasion Acute corneal oedema Traumatic iritis Traumatic Mydriasis / Miosis Hyphaema Iridodialysis Cyclodialysis / Angle recession Ciliary shock

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Close Globe Injuries Subluxation and dislocation of lens Cataract Posterior vitreous detachemet Vitreous haemorrhage Choroidal rupture Commotio retinae Retinal Breaks

Dialysis Equatorial tears Macular holes

Optic nerve avulsion

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Hyphaema Source of bleeding? Iris /ciliary body / both Immediate threat –

Secondary haemorrhage Can happen up to a week, mostly first 24 hrs The haemorrahge is larger than the original bleed Most common problem is raised intraocular

pressure

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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

Hyphaema

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Treatment of Hyphaema 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

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

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Sources 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)

Commonest alkalis causing chemical injury are ammonia, sodium hydroxide & lime

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Sources 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

Commonest acids are sulphuric, sulphurous, hydrofluoric, acetic , chromic and hydrochloric acid.

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Pathophysiology 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

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Pathophysiology 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 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

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Clinical presentation History

Ascertain 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

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

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Signs 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 0-5) 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 Treat Systemic injury Ocular involvement

removing the offending agent controlling inflammation promoting ocular surface healing preventing infection controlling IOP

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First AidRemove the chemical (irrigation)

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

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Promote ocular surface (epithelial) healing

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)

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Control inflammation 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.

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Prevent infection When the corneal epithelium is absent,

the eye is susceptible to infection. Prophylactic topical antibiotics during

the initial treatment stages

Control IOP

• Oral acetazolamide

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Control pain Severe chemical burns can be extremely

painful. Oral NSAIDS Ciliary spasm can be managed with the

use of cycloplegic agents

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Surgical Care Early

Debridement Temporary amniotic membrane Limbal stem cell transplant Lysis of conjunctival symblepharon

Late Surgery for conjunctival adhesions Keratoplasty Cataract extraction Keratoprosthesis Glaucoma surgery

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Follow up 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

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Complications Primary complications include the

following Conjunctival inflammation Corneal abrasions Corneal haze and edema Acute rise in IOP Corneal melting and perforations

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Complications 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 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

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Home work 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