Chemical and Thermal Injuries of the Eye

Key Concepts

Chemical injuries are true ophthalmic emergencies.
Treatment should commence immediately—detailed history can wait.
Copious irrigation with a neutral solution is primary treatment.
Delayed treatment may result in penetration of chemical to anterior chamber.
Remove particulate matter during irrigation.
pH should be checked regularly and continued after irrigation ceases.
Strong acids and alkalis are equally destructive.
Medical treatment should include antibiotics, corticosteroids, citrate, and ascorbate.
Long-term sequelae may lead to blindness.
Rehabilitative surgery should be delayed until inflammation subsides.
Eyelid and forniceal abnormalities should be addressed prior to rehabilitation of the ocular surface.
Remember to monitor for glaucoma.

Acknowledgments

We thank Dr. Jay J. Meyer, MD (University of Auckland) for his significant contribution to the previous version of this chapter. All clinical photographs are courtesy of the authors of this chapter, with the exception of Fig. 95.1 kindly provided by Dr. Sue L. Ormonde, MD, FRCOphth, and Fig. 95.6 kindly provided by Dr. Chi-Ying Chou, MBChB (University of Auckland Department of Ophthalmology, New Zealand).

Introduction

Ocular chemical injuries are true ophthalmic emergencies due to the potential for permanent visual impairment or even blindness. Where strong alkalis and acids are involved, significant exposure results in severe injury to the ocular surface, adnexa, and intraocular structures. In these cases, the visual prognosis is poor, and functional (or physical) loss of the eye is not uncommon. Insult to the limbal environment and resident stem cell population impairs the regenerative capacity of the cornea resulting in chronic ocular surface disease and portends a poor prognosis for visual rehabilitation with traditional keratoplasty. Cicatrization of the ocular adnexa, intractable glaucoma, cataract formation, and retinal and optic nerve damage may further limit visual potential. The visual rehabilitation of severe ocular chemical burns is complex and typically protracted over many years with multiple interdisciplinary surgeries.

Over the last two decades, the prognosis of these severe ocular burns has improved, partly due to emphasis on eye protection in the workplace, but also due to significant advances in our understanding of the corneal and ocular surface inflammatory and healing response, together with more targeted medical and surgical management. Although the final visual outcome is strongly related to the severity and nature of the initial chemical exposure, the prognosis is heavily influenced by the timing of appropriate treatment.

Epidemiology of Chemical Eye Injuries

Worldwide, an estimated 107,000 people are blinded each year by ocular chemical injury. The frequency and distribution vary by geographic region and are purported to be higher and more severe in developing countries compared with highly developed countries.

Fortunately, the majority of chemical eye injuries are classified as mild, and severe chemical injuries are relatively rare, with a reported incidence ranging between 0.02 and 1.58 per 100,000. ^, Bilateral injury occurs in about a quarter of victims. ^, The archetypical burn victim is classically a young male industrial worker ; however, a recent large epidemiologic survey from the United States reported that age-specific injuries were the highest among children aged 1–2 years. The same study also reported gender equivalency and identified individuals in the first and second lower income quartiles as being at the greatest risk of chemical injury.

Chemical burns can occur in a wide range of scenarios, including domestic, agricultural, industrial, and, much less commonly, assault. ^, ^, Ultimately, as many victims are young, working individuals, ocular burns can have a profound economic and psychologic impact on the injured and their families.

Etiology of Chemical Injury: Causative Agents

Acids and alkalis are the agents most commonly associated with significant chemical eye injuries. The severity of the injury depends on a number of factors including: (1) concentration and pH of the solution, (2) the extent of ocular surface exposure, and (3) the duration of ocular exposure before treatment is instigated. These injuries can be further compounded by foreign material, for example, concrete debris (high-power pumps; Fig. 95.1 ), metal fragments (fireworks and car batteries), or plant material (agricultural injuries). Therefore any history of high velocity or explosive events makes the exclusion of forniceal, subconjunctival, or intraocular foreign bodies mandatory. Further details of the acids and alkalis commonly associated with ocular injuries are highlighted in Tables 95.1 and 95.2 .

Fig. 95.1, A patient who sustained a severe chemical eye injury from a high-pressure concrete hose, leaving the whole anterior segment encased ( A ) in solidified concrete ( B ).

Table 95.1

Common Causes of Alkali Injury

Common Alkalis	pH of 0.1 M Solution	Sources/Uses	Comments
Ammonium hydroxide (NH ₃ )	11.1	Fertilizers, refrigerants, cleaning agents	Rapid penetration
Sodium Hydroxide (NaOH)—Lye	13	Caustic soda, drain cleaner, manufacture of pulp, paper, textiles and soaps	Rapid penetration
Potassium hydroxide (KOH)	12	Caustic potash	Dissolution in water strongly exothermic. Corrosive
Magnesium Hydroxide (Mg [OH] ₂ )	10.5	Fireworks	Combined chemical and thermal injury
Calcium hydroxide (Ca[OH] ₂ )—Lime	12.4	Cement, plaster, whitewash, industrial cleaners	Often found in composite mixtures. Poor penetration. Retained particulate matter provides sump for ongoing toxicity

Table 95.2

Common Causes of Acid Injury

Common Acids	pH of 0.1 M Solution	Sources/Uses	Comments
Sulfuric (H ₂ SO ₄ )	1.2	Battery acid, industrial cleaners	Diprotic acid
Sulfurous (H ₂ SO ₃ )	1.5	Fruit and vegetable preservatives, bleach, refrigerants	Good penetration
Hydrofluoric (HF)	2.1	Mineral refining and production, glass polishing and frosting, gasoline alkylation	Severe injury due to rapid penetration and chelation of calcium and magnesium ion
Acetic (CH ₃ COOH)	2.9	Vinegar	Classified as a weak acid but corrosive in concentrated form
Hydrochloric (HCL)	1.1	Gastric acid, household cleaning, plastics production	Stable on storage
Chromic (H ₂ CrO ₄ )	1	Chrome plating	Diprotic acid

Alkalis readily penetrate the eye as the hydroxyl ion (OH) saponifies plasma membranes resulting in cell disruption and death. Changes in aqueous humor pH are observed within a few seconds of contact with ammonium hydroxide and within 3–5 minutes after sodium hydroxide injury. ^, By contrast, the vitreous has been shown to maintain its physiologic pH, even in the presence of anterior chamber pH elevation; an ability attributed to the buffering capacity of the crystalline lens and the iris. Therefore the diffusion of proinflammatory cytokines is proposed as the mechanism of retinal damage rather than the direct effect of alkali on the retina.

In general, acids penetrate the corneal stroma much less readily than alkalis as they induce precipitation of the epithelial proteins, which then form a barrier against further chemical ingress. However, if an acid succeeds in penetrating the stroma, the damage to ocular structures is similar to that observed in alkali injury. Indeed, studies have shown no clinically significant differences in clinical course and prognosis between severe acid and alkali burns.

Sequelae

A summary of potential sequelae of ophthalmic chemical burns is provided in Table 95.3 . Figs. 95.2–95.4 highlight some of the complications of chemical burns.

Table 95.3

Potential Ophthalmic Sequelae of Chemical Burns

Lids	Posterior displacement of meibomian orifices Trichiasis Ectropion Entropion Lagophthalmos
Ocular surface	Dry eye Loss of goblet cells Damage to lacrimal system Corneal melt Corneal opacity/scarring Corneal neovascularization Intraocular inflammation Limbal stem cell deficiency Recurrent corneal erosions Nonhealing epithelial defects Symblepharon/ankyloblepharon Microbial keratitis
Elevated intraocular pressure	Secondary glaucoma
Intraocular structures	Iris ischemia Fixed dilated pupil Ciliary body shut down with secondary hypotony Cataract Retinal detachment Phthisis

Fig. 95.2, A severe microbial corneal stromal abscess complicating a chemical eye injury.

Fig. 95.3, Symblepharon (arrows) involving the superior forniceal conjunctiva.

Fig. 95.4, Trichiasis occurring as a sequela of a combined thermal and chemical injury.

Classification

Early assessment should include careful documentation of the extent and severity of corneal, limbal, and conjunctival involvement as it provides an important reference tool in formulation of subsequent evaluation and management plans.

Classification schemes for grading the severity of the initial injury are useful in guiding treatment and provide an estimation of prognosis. The Roper–Hall classification system ( Table 95.4 ) was introduced in the mid-1960s and is the most established and commonly applied system. It provides prognostic guidelines based on the degree of corneal haze and the amount of perilimbal ischemia. However, there have been changes in the understanding and management of ocular surface injuries in the years since the introduction of the Roper–Hall classification. In particular, there has been an enhanced understanding and appreciation of the role of the limbus in wound healing. In order to reflect these changes, Dua proposed a new classification scheme in 2001 ( Table 95.5 ) based upon clock hours of limbal involvement (as opposed to ischemia) as well as the percentage of conjunctival involvement. The Dua classification has been shown to have superior prognostic value over the Roper–Hall classification scheme in the context of severe ocular burns.

Table 95.4

Roper–Hall Classification 1965

Grade	Prognosis	Corneal Appearance	Limbal Ischemia
I	Good	Epithelial damage	None
II	Good	Haze but iris details visible	<1⁄3
III	Guarded	Total epithelial loss with haze that obscures iris detail	1⁄3–½
IV	Poor	Cornea opaque with iris and pupil obscured	>½

Table 95.5

Dua Classification 2001

Grade	Prognosis	Clock Hours of Limbal Involvement	Conjunctival Involvement (%)	Analog Scale ∗
I	Very good	0	0	0/0%
II	Good	≤3	<30	0.1–3/1%–29.9%
III	Good	>3–6	>30–50	3.1%–6%/31%–50%
IV	Good to guarded	>6–9	>50–75	6.1–9/51%–75%
V	Guarded to poor	>9–<12	75–<100	9.1–11.9/75.1%–99.9%
VI	Very poor	12	100	12/100%

∗ The analog scale records accurately the limbal involvement in clock hours of affected limbus/percentage of conjunctival involvement. While calculating percentage of conjunctival involvement, only involvement of bulbar conjunctiva, up to and including the conjunctival fornices, is considered.

Examples of mild, moderate, and severe chemical burns are highlighted in Figs. 95.5–95.7 , respectively.

Fig. 95.5, A mild chemical injury resulting in a focal corneal epithelial and conjunctival defect and conjunctival hyperemia ( A ). Fluorescein staining demonstrates epithelial defect ( B ).

Fig. 95.6, A moderate chemical injury resulting in three clock hours of limbal ischemia.

Fig. 95.7, A severe chemical injury with diffuse limbal and conjunctival ischemia and corneal edema.

Emergency Management

Irrigation

Initial emergency management involves prompt irrigation and the removal of residual chemical debris from the eye. The objectives are to minimize the ingress of the chemical agent into the anterior chamber and to remove a potential reservoir for ongoing injury. The most important intervention to reduce the severity of the injury is immediate copious irrigation. Irrigation should be continued until pH neutralization is achieved. The pH of both eyes should be tested, even in cases of apparent unilateral injury, to avoid unrecognized injury. External irrigation for 90 minutes reduces the pH by 1.5 units according to animal models. Although there may be an advantage to using amphoteric buffering solutions, urgency may necessitate the use of any available neutral irrigation fluid.

Eversion of the eyelids (sometimes double eversion) is required for complete inspection and cleaning of the fornices, which may harbor retained particles or foreign bodies. It is imperative to remove all particulate matter as it may continue to cause chemical injury after the initial insult. In some severe cases, sedation or general anesthesia may be necessary to examine the patient effectively and remove particulate matter.

Aqueous Humor Replacement

External irrigation is of limited value in eliminating chemicals once they have reached the intraocular chambers. Animal models of alkali injuries have shown that a paracentesis lowers the aqueous humor pH by 1.5 pH units, and subsequent anterior chamber reformation with buffered phosphate solution can lower the aqueous pH by a further 1.5 pH units. However, this approach is not part of contemporary routine practice, and the value of paracentesis and anterior chamber irrigation in chemical injury remains controversial.

Acute Management

The acute management of ocular chemical burns is targeted toward the control of inflammation, prevention of stromal breakdown, promotion of reepithelialization and repair, and prevention of complications.

A retrospective study of patients with alkali burns showed that intensive therapy with a combination of topical corticosteroids, antibiotics, ascorbate and citrate, atropine, and oral vitamin C was most effective in the treatment of patients with Roper–Hall Grade III injuries (with reference to time to reepithelialization and visual acuity). Conversely, intensive therapy delayed reepithelialization in the context of grade I and II injuries, presumably as a result of drug toxicity and inhibition of reepithelialization by corticosteroid.

Control of Inflammation

Topical Corticosteroids

There is a lingering controversy regarding the use and timing of topical corticosteroids in the treatment of chemical burns. While corticosteroids have the advantageous effects of inflammatory cell suppression and collagenase inhibition, they also suppress keratocyte migration and collagen production and therefore may cause corneal thinning.

Sterile ulceration occurs when there is an imbalance between collagen synthesis and proteolytic degradation. Consequently, the risk of sterile ulceration in the first week following a chemical injury is relatively modest but increases as the corneal repair process becomes established at about day 14 postinjury. Experimental models have demonstrated that the use of corticosteroids in the first 10 days postinjury does not appear to have an adverse effect on outcome. An early animal study by Donshik et al. observed that the prolonged use of topical corticosteroids was associated with an increase in the incidence and severity of corneal ulceration. More recent studies have suggested that the corneal ulceration observed in Donshik et al.’s study with longer duration topical corticosteroids may have actually been a product of the prolonged scorbutic state of the aqueous humor rather than a direct action of topical steroids per se . Subsequently, Davis et al. and Brodovsky et al. concluded that the prolonged use of topical steroids is not associated with corneoscleral melting when used in conjunction with topical ascorbate.

Prevention of Stromal Breakdown

Tetracyclines

The efficacy of tetracyclines in reducing collagenase activity and corneal ulceration has been demonstrated in experimental alkali injuries. ^, This action is independent of their antimicrobial properties and is thought to occur through multiple mechanisms, including inhibition of gene expression of neutrophil collagenase, inhibition of [α] ₁ -antitrypsin degradation, and scavenging of reactive oxygen species. An additional mechanism is through the chelation of zinc—an element indispensable to the activity of matrix metalloproteinases. ^, Animal studies have shown that topical treatment with doxycycline can also reduce the incidence and extent of corneal neovascularization if given prior to the appearance of this delayed pathology.

Oral tetracycline 250 mg four times per day; doxycycline 100 mg daily; or minocycline 100 mg twice per day can be given in combination with topical tetracycline preparations (1% suspension or 3% ointment).

Ascorbate

Following a chemical injury, ascorbate levels in the aqueous humor may fall as a result of damage to the ciliary body epithelium. This scorbutic state has the potential to compromise stromal repair because ascorbate is a key cofactor in collagen synthesis. Topical or systemic supplementation of depleted aqueous ascorbate levels has been demonstrated to reduce the incidence of corneal thinning and ulceration following experimental alkali injuries if an aqueous humor concentration of 15 mg/dL can be achieved. Therefore early supplementation is absolutely critical—because ascorbate has no demonstrable effect on the progression of ulceration once it has become established. Supplementation can be achieved through the hourly topical application of 10% sodium citrate eye drops and/or 1000 mg of oral ascorbic acid given four times a day. In severe injuries, topical administration is superior to systemic administration, presumably due to the reduced capacity of the ciliary body epithelium to concentrate ascorbate into the aqueous humor.

Citrate

In contrast to ascorbate, citrate is effective in both preventing and retarding the progression of corneal ulcers. Citrate chelates extracellular calcium and diminishes the activity of polymorphonuclear leucocytes by reducing membrane and intracellular calcium levels. Citrate has been shown to reduce neutrophil infiltration by 63% in the early phase and 92% in the late phase following chemical injury and also has an inhibitory effect on collagenase. As is the case with ascorbate, the topical application route is superior to the systemic route, and a 10% solution of citrate eye drops may be administered hourly.

Because citrate and ascorbate reduce corneal ulceration via different mechanisms, their combined use offers a decided therapeutic advantage over treatment with citrate alone. Typically, citrate has a greater effect than ascorbate on more severely injured eyes because of its inhibitory action on the inflammatory response. Severe chemical injuries may deplete collagen-producing fibroblast populations in the corneal stroma, thereby limiting the beneficial effect of ascorbate.

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