Dalia G. Said

BASICS

DESCRIPTION

Injury that follows exposure of the ocular surface or adnexa to solid, liquid, or gaseous form of corrosive substances such as acids and alkalis or irritants such as oxidants, solvents, reducing agents, and alkylating agents.

EPIDEMIOLOGY

Incidence

• Chemical burn to the eye represents 7–10% of eye injuries.

• Burns to the face are reported to involve at least 1 eye in 15–20% of cases.

• Chemical burns are largely accidental, 73.9% being work related. In a smaller proportion they result from an assault.

• It is more common in men than women, related to increased occupational and industrial exposure in men.

• The incidence ratio of acid burn to alkali burn ranges from 1:1 to 1:4.

RISK FACTORS

• Certain occupations: Ocular chemical burn is reported to account for 3–4% of occupational injuries.

• Noncompliance with health and safety regulations, e.g., inadequate or inappropriate use of protective eye wear and clothing

GENERAL PREVENTION

Safety goggles with side shields should be worn when working with chemicals or caustics or helmets with safety goggles for workers with occupational exposure to chemicals. Appropriate masks or breathing apparatus should be used when working with noxious fumes or gases.

PATHOPHYSIOLOGY

• The severity of the burn depends on the nature of the substance and the duration of exposure. Alkalis cause more damage than acids.

• Tissue damage occurs through denaturation and coagulation of the cellular proteins as well as vascular ischemia.

• The high pH (hydroxyl ion content) of alkaline agents causes saponification of the fatty elements of cell membranes with cell disruption and death. Cations react with carboxyl groups of stromal collagen and the interfibrillary glycosaminoglycans resulting in hydration with thickening and shortening of stromal collagen and hydrolysis of glycosaminoglycans. Loss of glycosaminoglycans renders the collagen susceptible to enzymatic digestion and degradation. Alkalis, especially ammonia and sodium hydroxide, penetrate tissue rapidly and are more likely to damage deeper structures within the anterior chamber.

• Acids penetrate tissue less readily (except hydrofluoric acid). The hydrogen ion causes damage by pH change and the anion causes protein precipitation and denaturation, which in turn retards penetration of acid.

• Chemical penetration into the anterior chamber lowers aqueous ascorbate and glucose. Low ascorbate concentrations are related to subsequent retarded collagen synthesis.

ETIOLOGY

Chemical burns can be caused by acids, bases, oxidants, solvents, reducing agents, and alkylating agents. They can also be caused by chemical weapons such as mustard gas or urticants such as phosgene oxide.

DIAGNOSIS

HISTORY

• History is the key to diagnosis. Nature of the chemical can be ascertained if a sample is available.

– pH testing of the conjunctival sac using a pH paper strip will help differentiate acids from alkalis.

• Symptoms: Pain, photophobia, lacrimation, and visual impairment. Blepharospasm may supervene.

PHYSICAL EXAM

• Besides the eye(s), the surrounding skin of the face and scalp or further afield may also be involved and occasionally injury to the oral mucosa and respiratory and gastrointestinal tracts related to inhalation or ingestion of chemicals can threaten life.

• Clinical manifestations are described in three stages (1): Immediate effects of the injury, extending from onset to 1 week postinjury; Intermediate, representing the host healing response from the end of week 1 to week 3; and Late, representing changes associated with repair, regeneration, or lack thereof.

– Ocular surface epithelium: There may a central corneal abrasion with an intact limbus or the limbus may be partially or totally involved. Varying areas of the conjunctiva too may be involved. Limbal and conjunctival involvement is more common in the inferior half. Fluorescein staining is helpful in determining the extent of abrasion.

– Limbus ischemia: Presents as sectors of blanched or pale limbus with associated necrosis and hemorrhage. Injured blood vessels appear as dark columns of blood with no visible flow.

– Corneal stroma: May be hazy or opaque and thick with folds or striae secondary to endothelial involvement. Corneal sensations may be impaired.

– Anterior chamber: The iris may show injection, hemorrhage, necrosis, and pigment dispersion. The pupil response may be sluggish or absent. The lens may be intumescent and ciliary body damage can manifest as hypotony. Clogging of the trabecular meshwork with inflammatory debris can result in raised pressure.

• In the intermediate stage, if some limbal or conjunctival epithelium survives, re-epithelization commences. The cornea may be covered by corneal or conjunctival epithelium. If no epithelium survives, the ocular surface is covered by a centripetally advancing fibrovascular pannus. Recanalization of some of the damaged blood vessels may lead to further hemorrhages. Inflammatory cell infiltration occurs and can later lead to stromal melts and ulceration.

• In the late stage of moderate to severe burns, the cornea is covered by a fibrovascular pannus. Superficial and deep vascularization, stromal ulceration, persistent epithelial defects can lead to a descemetocele and perforation. Loss of nerves may lead to a neurotrophic state with repeated healing and breakdown of the surface.

– Conjunctival repair may lead to symblepharon, subepithelial fibrosis with progressive contracture leading to forniceal shortening and lid margin deformities such entropion, trichiasis, and lagophthalmos with exposure. Tear film abnormalities due to loss of goblet cells (mucin) and obstruction of orifices of the lacrimal or accessory lacrimal ductules (aqueous) may manifest. This can lead to keratinization of the cornea and conjunctiva. Cicatricial stenosis or occlusion of the lacrimal puncta may occur and offset a “dry eye” state.

– Retrocorneal or cyclitic membranes and fibrosis of the ciliary body can lead to persistent hypotony and phthisis. On the other hand, scarring in the drainage angle and peripheral anterior synechiae can lead to intractable glaucoma.

• Secondary infection can occur at any stage.

DIAGNOSTIC TESTS & INTERPRETATION

Diagnostic Procedures/Other

• Eyes with chemical burns must be graded at the first opportunity. Dua’s classification indicating the number of clock hours of limbal involvement and percentage of conjunctival involvement is recommended (2).

• Clinical appearances can be deceiving and change rapidly.

– Total corneal and limbal epithelial loss can be associated with a clear cornea.

– A clear cornea with a good view of the iris can rapidly become hazy or opaque.

– An initially “stable” cornea may develop stromal thinning or melting within hours, especially after the first week.

– Intraocular pressure (IOP) can be difficult to measure with the Goldman tonometer or Tonopen. An irregular and thick cornea can produce erratic readings. Digital palpation may be the only reliable method in some cases.

– Secondary infection may have an atypical presentation.

TREATMENT

MEDICATION

First Line

• Check pH of conjunctival sac with a pH filter paper strip. Instill a topical anesthetic agent. Keep eye(s) open with a speculum, keep room lights dim, and perform copious irrigation with normal saline, balanced salt solution, or Ringer’s lactate. Use approximately 1–2 L over 30–40 min delivered through an intravenous tube with free flow.

– Recheck pH. If around 7, stop irrigation and examine conjunctival sac right up to fornices by double everting the upper lid. Remove any particulate matter and excise devitalized tissue.

– Recheck pH after a 20-min interval. Chemicals may leach out of tissues and alter pH. If less or greater than 7, recommence irrigation.

Second Line

• Lubrication: Preservative-free artificial tear drops and ointment

• Anti-inflammatory: Steroid drops. Be wary of steroid use in the presence of melting.

• Antibiotics: drops or ointment

• Ascorbate: 10% drops 2–4 times a day. Can cause pronounced stinging and may not be tolerated. Oral tablets 2 g q.i.d.

• Sodium citrate: a potent inhibitor of polymorphonuclear proteases. 10% drops, 4–6 times a day. Oral doxycycline (protease inhibitor) 50 mg twice a day

• Atropine 1% or cyclopentolate 1% b.i.d. Avoid phenylephrine as it can exacerbate ischemia by vasoconstriction.

• IOP lowering: drops, e.g., timolol 0.25% twice a day if needed. Oral acetazolamide tablets 250 mg q.i.d. may be preferable especially if there is marked pigment dispersion and AC inflammation.

• Pain management: according to severity

ADDITIONAL TREATMENT

General Measures

• Punctal plugs: if tear film is inadequate

• Lid taping: to reduce exposure and in the presence of stromal melts

• Conformer ring: to limit or avoid symblepharon formation

Issues for Referral

• Most chemical burns are mild and can be managed in the primary care setting.

• Severe burns with extensive limbal and anterior chamber involvement should be referred to a specialist center.

Additional Therapies

• Autologous serum drops: 20–100%, 4 to 6 times a day

• Acetylcysteine 20%, fibronectin, epidermal growth factor, sodium or calcium EDTA (0.2 mol) subconjunctival heparin and others have been tried

SURGERY/OTHER PROCEDURES

• Valve shunts or cycloablation to control pressure. The latter can increase intraocular inflammation

• Lens extraction if lens is swollen and causing pupil block

• Mucus membrane and amniotic membrane graft to cornea and conjunctiva

• Lid surgery to address entropion, ectropion, trichiasis, or lagophthalmos

• Sequential sector conjunctival epitheliectomy (SSCE) to prevent conjunctival epithelium from migrating on to the cornea in partial corneal burns or to remove conjunctival epithelium that has already encroached on to the cornea

• Auto or allo limbal transplants (in cases with total stem cell deficiency). Avoid use of autolimbal or living related donor tissue in the early to intermediate stages as the risk of losing the transplanted tissue in the ongoing inflammatory reaction is high.

• Transplant of ex vivo expanded sheets of limbal or oral mucosal cells

• Corneal graft procedures should be considered only after the cornea is repopulated with limbus derived epithelial cells. Some form of immunosuppression is usually required postoperatively.

ONGOING CARE

PROGNOSIS

• The more superficial the burn, the better the prognosis.

• 12 clock hours of limbus involvement with 100% conjunctival involvement (grade VI) [Dua’s classification] has the worst prognosis.

COMPLICATIONS

• Lid deformities

• Dry eyes

• Extensive symblepharon

• Limbal stem cell deficiency

• Corneal vascularization and scarring

• Secondary infection

• Glaucoma or phthisis

• Cataract

• Disorganization of anterior segment

• Severe visual impairment including loss of eye

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