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Although rare, ocular chemical burns have the poten-tial to cause devastating ophthalmic injuries that may have long-term sequelae and are thus classified as veritable ocular emergencies. Ocular burns account for 3 to 4% of occupational injuries and 7 to 18% of ocular trauma in the United States, the majority of these being chemical injuries.1,2 In a 7-year Austra-lian study, ocular burns comprised 5.5% of industrial burn accidents.3 Ocular burns are most commonly seen in young men, either at the workplace or in home environments.4 Alkali burns are more common than acid burns, with caustic agents being the most

common.5 Commonly encountered agents in alkali injury include ammonia, lye, potassium hydroxide, magnesium hydroxide, and lime.6 The most serious injuries are caused by ammonia (commonly found in fertilizers and cleaning agents) and lye (found in drain cleaners), whereas the most commonly reported inju-ries involve lime, a constituent of plaster.4

In general, alkalis are more damaging to the eye than acids as they possess both hydrophilic and lipo-philic properties. The interaction of hydroxyl ions with cell membranes causes saponification, which leads to disruption and cell death.7 Such liquefactive necrosis destroys barriers to penetration allowing the injurious agent to move rapidly to underlying tis-sues. This inherent ability of alkalis to penetrate the eye means that alkali injuries can damage not only the corneal endothelium, but also deeper structures of the anterior segment. The cations formed by alkali dissociation interact with the carboxyl groups of gly-cosaminoglycans to cause corneal opacification via hydration.8 Distortion of the collagen framework of

Copyright © 2013 by the American Burn Association 1559-047X/2014

DOI: 10.1097/BCR.0b013e31829b0037

J Burn Care Res

Alkali burns are known to possess high pathological potential because of their inherent ability to lyse cell membranes and penetrate intraocular structures with devastating results. The authors aimed to evaluate the most common cause of this presentation, the current treatment approaches to injury, and eventual outcome as related to severity. The authors performed a retrospective review of all patients who sustained chemical-related ocular injuries seen at the Concord Hospital Burns Unit, Australia between January 2005 and March 2012. Management was based on cooperation between ophthalmic staff and the burns unit, with emphasis on early aggressive intervention and rigorous follow-up. The records of 39 patients who presented with chemical-related injury were assessed, 12 of whom had confirmed alkali burns involving the cornea. The most commonly implicated agent was sodium hydroxide, usually in the context of otherwise trivial domestic accidents. Acute medical management included copious irrigation and the use of analgesics, cycloplegics, and topical antibiotics. In half the cases, steroid drops and oral vitamin C were also used. Ten of the 12 patients (83%) had return to premorbid visual acuity. Complications included cicatrical ectropion (n = 1), pseudoexfoliative syndrome (n = 1), and symblepharon (n = 1). Surgical correction was needed in the one patient with cicatrical ectropion. This case series shows that appropriate acute management minimizes the potentially devastating sequelae of ocular alkali burns. Emphasis should be placed on prevention of domestic and workplace injuries when using alkaline products. (J Burn Care Res 2014;35:261–268)

From the *Royal Prince Alfred Hospital, Camperdown, New South Wales, Australia; †Porter Eye Care, Mt. Gravatt, Queensland, Australia; and ‡Concord Repatriation General Hospital, Con-cord West, New South Wales, Australia.

Address correspondence to Robert J. George, MB, ChB, Royal Prince Alfred Hospital, Missenden Road, Camperdown, New South Wales, 2054, Australia.

Alkali-Related Ocular Burns: A Case Series and Review

Daniel J.L. Bunker, MBBS,* Robert J. George, MB, ChB,* Andrew Kleinschmidt, FRANZCO,† Rohit J. Kumar, MBBS,* Peter Maitz, FRACS‡

Journal of Burn Care & Research262 Bunker et al May/June 2014

the trabecular meshwork and release of prostaglan-dins increases intraocular pressures.7

As ocular chemical burns can result in devastat-ing injuries including permanent loss of vision, prompt recognition and adequate treatment is vital to optimize outcomes. We performed a retrospective review of alkali ocular injuries presenting at Concord Hospital, Sydney, Australia during a 7-year period. The Roper-Hall classification system was used to grade eye injuries and guide prognosis. An analysis was performed to determine common characteristics in presentation, management, and outcome. We dis-cuss the pathophysiology of alkali ocular burns and present general treatment principles to assist clini-cians in dealing with these important injuries.

METHODS

We performed a retrospective review of all patients with alkali ocular injuries seen at the Concord Hos-pital Burns Unit, Sydney between January 2005 and March 2012. Twelve patients were identified, and their management and outcomes are reported. Management was based on cooperation between ophthalmic staff and the burns unit with criteria including the following:

• Determining the injurious agent implicated • Initial ophthalmic evaluation with documen-tation of the severity of the injury as per the Roper-Hall Classification System and pretreat-ment visual acuity

• Early aggressive treatment • Rigorous follow-up • Assessment of posttreatment visual acuity

An analysis of the 12 patients was undertaken to determine common characteristics in presentation, treatment, and prognosis.

RESULTS

Twelve patients were found for inclusion in our review (Table 1). Age ranged from 21 to 66 years, with three women and nine men. Injuries occurred largely in the home (n = 9) and workplace (n = 2), with one isolated case of assault. The sites of injury included either the right eye alone (n = 2) or both eyes (n = 10). The injurious agents were caustic soda (n = 5), sodium hydroxide (n = 3), drain cleaner (n = 2), concrete (n = 1), and bicarbonate (n = 1). In this cohort of patients, ocular burns comprised Roper-Hall grade I (n = 5), grade II (n = 4), and grade III (n = 3).

All patients were initially treated according to emergency eye protocols consisting of copious eye

irrigation and urgent ophthalmic review. All patients received antibiotics, either topically or systemically: the most commonly used antibiotic was chloram-phenicol. Steroids were commonly prescribed (n = 6), as was vitamin C (n = 6). Artificial tears were seldom prescribed in this cohort of patients (n = 4). Atro-pine was used for two patients and citrate for one. Tetracyclines were given to three patients.

Visual acuity at presentation and after treatment is shown in Table 1. In 83% of cases (10 of 12 patients), vision was restored to baseline, and in the remaining two cases vision returned to near-baseline. The two patients with persisting visual impairment comprise a Roper-Hall grade I and grade III injuries. Complica-tions included cicatrical ectropion (n = 1), pseudo-exfoliative syndrome (n=1), and symblepharon (n = 1). Surgical correction was needed in the one patient with cicatrical ectropion.

DISCUSSION

The 12 patients we reviewed sustained ophthalmic alkali burns in the domestic or workplace settings. For most patients, initiation and maintenance of medi-cal treatment resulted in complete recovery. These results indicate the importance of initiating prompt treatment to salvage eye tissue in low-grade injuries. In a previous Australian study of 159 cases of ocular chemical burns, most were grade I to grade II inju-ries, which resulted in no permanent visual impair-ment.9 A recent large study from China revealed that alkali agents are the major cause of chemical-related eye injury. Mirroring our demographic findings, most cases were men with a median age of 35 years, how-ever, mostly within an industrial context. Here, prog-nosis was found to be much worse than in our study, with only 2% of eyes recovering an acuity greater than 6/60. The investigators found that education regard-ing workplace safety regulations as well as basic first aid measures accounted for the reported large incidence and poor prognosis associated with chemical eye inju-ries.10 Another study from India found that poor out-comes were associated with inappropriate and delayed emergent care, even within a tertiary setting.11

The management of each case depends on a num-ber of factors, including the severity of the injury, the type of offending substance, and ophthalmo-logical assessment. In general, the treatment of any ocular chemical injury should consist of immediate primary therapy followed by measures of supportive care to promote corneal healing, limit inflammation, and reduce ulceration while avoiding complications. More severe injuries often require additional inter-vention, including surgical treatment.

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Natural HistoryMcCulley identified four distinct pathophysiological and clinical phases with regard to chemical eye inju-ries: immediate, acute (0–7 days), early repair (7–21 days), and late repair (greater than 21 days).6 The immediate findings after a chemical injury to the eye are related to the relative toxicity of the substance, its depth of penetration, and the area of involvement.6 It has been recognized that certain findings on ini-tial clinical examination can be a valuable indicator of long-term prognosis. A commonly used classification scheme was developed by Hughes in 1946, later mod-ified by Ballen in 1963, and again adapted by Roper-Hall in 1965 to provide prognostic guidelines based on corneal appearance and the extent of limbal isch-emia (Table 2).12–16 The stems cells that are thought to reside in the palisades of Vogt, in the corneal

limbus, play an important role in reepithelialization and recovery. Limbal ischemia therefore provides an indirect means of assessing limbal stem cell injury.

We note that more recently a new classification scheme for ocular surface burns was proposed by Dua et al.49 Their major criticism is that the Roper-Hall classification has poorer prognostic power in severe ocular surface burns. According to the Roper-Hall classification, any injury with greater than 50% limbal ischemia is classified as most severe (grade IV). However, Dua et al49 have argued that even with 75% degree of limbal ischemia, outcome can be fair rather than the poor prognosis implied by a grade IV Roper-Hall classification. Although this might indeed be the case, we used the Roper-Hall classification in our present study, as it was the sys-tem used by our ophthalmic colleagues.

Table 1. Patients presenting with oculavar burns

Sex Age Eye Agent Visual Acuity Roper-Hall Treatment F/U Outcome

M 24 Right Caustic soda Right: 6/9 Grade II Topical: chloramphenicol, citrate, ascorbate, artificial tears

Oral: Vitamin C

Right: 6/6 Vision restored

M 44 Both Concrete Right: 6/5Left: 6/5-1

Grade II Topical: fusidate, chloramphenicol, artificial tears

Right: 6/6Left: 6/6

Vision restored

M 52 Both Caustic soda Right: 6/60Left: 6/18

Grade II Topical: dexamethasone, artificial tears, ciprofloxacin

Right: 6/9Left: 6/6

Vision restored

F 62 Both Sodium hydroxide

Right: 6/9 + 2Left: 6/9 + 1

Grade I Topical: chloramphenicol Right: 6/6Left: 6/6

Vision restored

M 21 Both Drain cleaner Right: 6/5 + 3Left: 6/6-2 L

Grade I Topical: chloramphenicol Right: 6/5Left: 6/5

Vision restored

M 52 Right Drain cleaner 6/60 Grade III Topical: chloramphenicolOral: Vitamin C, doxycycline

Right: 6/12 Diminished visual acuity

M 66 Both Caustic soda Right: 6/18Left: 6/18

Grade III Topical: chloramphenicol, prednisone, ascorbate

Oral: Vitamin C

Right: 6/6Left: 6/6

Vision restored

F 72 Both Sodium hydroxide

Right: 6/9Left: 6/9

Grade II Topical: chloramphenicol, prednisone, ascorbate, homatropine

Oral: Vitamin C

Right: 6/6Left: 6/6

Vision restored

M 51 Both Sodium hydroxide

Right: 6/6Left: 6/6

Grade I Topical: dexamethasone, artificial tears, chloramphenicol

Oral: Vitamin C, doxycycline

Right: 6/6Left: 6/6

Vision restoredCicatrical ectropion

needing surgical correction

M 66 Both Caustic soda Right: 6/6-1Left: 6/6-1

Grade I Topical: chloramphenicol, fusidate

Right: 6/6 Left: 6/9

Diminished visual acuity in left eye

Pseudoexfoliatve syndrome left eye

M 21 Both Caustic soda Right: 6/36Left: 6/60

Grade III Topical: chloramphenicol, prednisone, ascorbate, tetracycline

Right: 6/18Left: 6/18

Diminished visual acuity in both eyes

Symblepharon left lower conjunctiva

M 32 Both Bicarbonate Right: 6/6Left: 6/6

Grade I Topical: dexamethasone, chloramphenicol, atropine

Right: 6/6Left: 6/6

Vision restored

Journal of Burn Care & Research264 Bunker et al May/June 2014

During the first week (acute phase) there is a slow initiation of reepithelialization and keratocyte pro-liferation accompanied by progressive ocular surface inflammation. Some grade I injuries heal completely during this period.5 Grade II injuries display some evidence of reepithelialization and partial recovery of stromal clarity, whereas grade III and IV inju-ries display no or only minimal reepithelialization accompanied by a primary wave of inflammatory cell infiltrate.

In the early repair phase, grade II injuries show continued proliferation of keratocytes, corneal and conjunctival epithelium, which aids in restoring the ocular surface. In more severe injuries (grades III and IV), epithelialization is delayed or completely arrested.5 The second wave of inflammatory infil-trate begins in grade II and III injuries that have not been treated with anti-inflammatories and grade IV injuries that have not been debrided. Remain-ing necrotic tissue present in grade IV injuries con-tributes to leukocyte accumulation with the release of enzymatic mediators.16 Ulceration can occur in grade IV injuries as result of this inflammatory response, the compromised blood supply, and loss of collagenase inhibitors.17

In the late repair phase, we see four types of healing patterns corresponding to the grade of the injury. Grade I injuries show complete resolution of the epithelial defects via normal epithelial recov-ery, although transient clinical problems may arise from corneal anesthesia, goblet cell dysfunction, and mucin abnormalities.5 Grade II injuries display delayed differentiation, with reepithelialization in the regions where limbal stem cells were preserved and persisting epithelial defects in areas of complete stem cell loss. There may be superficial vascular pannus overgrowth in these areas, with symptoms of ocular lubrication dysfunction and superficial epitheliopathy for some months.5 Most grade III injuries showed delayed reepithelialization from the conjunctival epi-thelium with subsequent progressive fibrovascular pannus overgrowth. There can be progressive thin-ning of the cornea through proteolytic activity and reduced vascular-derived anticollagenases, creating

the potential for perforation. The pannus tissue, accompanied by corneal scarring, can impair visual function by obscuring the optical axis. Long-term sequelae include dry-eye disorders, cicatricial entro-pion, symblepharon, and trichias.5

With an absence of epithelium from the cornea and proximal conjunctiva, grade IV injuries usually display ongoing limbal ischemia and necrosis. Enzy-matic destruction leading to sterile ulceration can be expected if it has not already occurred in the early repair phase. It is imperative that surgical replace-ment of the ocular surface be attempted in all cases that have not reepithelialized by the late repair phase. Because of the widespread damage associated with such injuries, evidence of anterior segment necro-sis, anterior synechiae, cataract, glaucoma, phthi-sis bulbi, and hypotony may develop.18 Even with appropriate management, the prognosis for severe ocular injuries is poor.

ManagementThe treatment of ocular alkali burns can be divided into a number of broad principles. These include removing the offending substance, providing analge-sia, limiting inflammation and collagen degradation, controlling intraocular pressure, preventing infec-tion, and promoting healing (Table 3). Although the management of each ocular burn is treated on a case-by-case basis, these broad principles and correspond-ing treatment options provide the clinician with an armamentarium to tackle complex ocular injuries.

Table 3. Management of ocular burns4

Goals Management

Remove agent Copious irrigationAnalgesia Topical analgesics, cycloplegicsIntraocular pressure control Carbonic anhydrase inhibitors,

β-blockers, surgeryLimit inflammation Steroids, citratePrevent infection Antibiotics, tetanusPromote healing Ascorbate, artificial tears, soft

contacts, surgeryInhibit collagenase activity Tetracyclines

Table 2. The Roper-Hall classification system

Grade Cornea Limbus Prognosis Stem Cells

I Corneal epithelial damage No limbal ischemia Excellent Little or no lossII Corneal haze, iris details visible <1/3 limbus ischemic Good Subtotal lossIII Total epithelial loss, stromal

haze, iris details obscured1/3–1/2 limbus ischemic Guarded Complete loss, retention of some proximal

conjuctival epitheliumIV Cornea opaque, iris, and pupil

obscured>1/2 limbus ischemic Poor Complete loss and loss of proximal

conjunctival epithelium

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Emergency. The most important initial treat-ment for any chemical eye injury is irrigation. Delay of even a few minutes allows for a longer contact time between the ocular surface and the undiluted chemical, permitting further exposure and additional damage. Prompt initiation and adequate duration of irrigation for eye injuries has been shown to have positive correlation with both outcome and length of hospital stay.19–21 There has been concern using plain water for initial irrigation because it is hypo-tonic relative to the corneal stroma, which could facilitate corneal edema and hence transmission of the offending substance deeper into the delicate corneal matrix.22 A higher osmolarity substance is therefore recommended for initial irrigation, includ-ing amphoteric substances for neutralization. Pilot studies have shown that an amphoteric solution can reduce time to reepithelialization in grade I and II burns via capture of ions, acid/base chelation, and movement of water to the corneal surface, thereby restoring pH to normal more quickly.23,24 However, the emphasis remains on sufficient irrigation. Of note, it is not advisable to attempt to neutralize a chemical burn using a substance of opposite pH.22

Irrigation should be continued for at least 30 min-utes, after which the pH of the tears should be tested for neutrality, with further irrigation initiated if this has not been achieved. More effective irrigation may be facilitated by instillation of a topical local anes-thetic and lid speculum. As it is possible for particu-late chemical matter to remain sequestered under the eyelids, it is imperative to search the conjunctival for-nices using a moistened cotton-tipped applicator and eversion of the lids if required. Of crucial importance to establishing definitive care are initial history and examination and arranging for rigorous follow-up with an ophthalmologist. A visual acuity at or near baseline, as well as absence of limbal ischemia or cor-neal opacity, are predictive of a good outcome.5,21

Medical Therapies. Aggressive medical manage-ment to promote epithelial wound healing should be commenced as soon as feasible, particularly for grade I and II injuries. Tear substitutes are commonly pre-scribed, especially in the elderly or those patients with a history of dry-eye disorders. For long-term use, preservative-free preparations are preferred, to avoid toxicity to the already delicate epithelium. Their use is more beneficial if epithelialization is delayed or healing complicated by recurrent erosions. Epithelial wound healing is theoretically enhanced by occlu-sive therapies (soft contact lenses, tarsorrhaphy, or collagen shields), which protect the migrating epi-thelium from the repetitive abrasive action of the eyelids. However, in practice these modalities tend

to be poorly tolerated, especially in the acute stage when the eye is inflamed.

Further modalities have been proposed to aid in epithelial healing, including epidermal growth fac-tor, fibronectin, and retinoic acid. Epidermal growth factor is a polypeptide that can induce epithelial hyperplasia and has been shown to be beneficial in promoting epithelial migration after experimental alkali injuries.25 Fibronectin is a glycoprotein present in the extracellular matrix, which has been shown to facilitate cell-to-matrix and cell-to-cell adhesions.26 Given topically under experimental conditions, fibro-nectin has displayed promise in promoting reepithe-lialization.27 Retinoic acid is thought to aid in the transdifferentiation of conjunctival epithelium into corneal epithelium after chemical injury.28 It has dem-onstrated usefulness in the management of ocular sur-face disorders associated with abnormal keratinization as well as goblet cell disorders.29 Such therapies are yet to evolve in the clinical setting. Furthermore, topical autologous platelet-rich plasma might be a beneficial additive in promoting more rapid reepithelialization in more severe ocular burns.48

Medical therapy is also directed at limiting the inflammatory response. Corticosteroids beneficial in reducing tissue injury related to inflammation have been shown to enhance deep stromal healing.12,24 Studies have shown them to have no adverse effect on outcome in the early phases of injury (<10 days).30 In acutely chemically injured eyes, clinicians may be hesitant to use them because of their ability to pro-mote sterile corneal ulceration: corticosteroids are known to have deleterious effects on stromal repair by interfering with collagen synthesis and hindering keratocyte migration in the area of injury.31,32 These effects are possibly deleterious when the corneal repairs process begins in the early repair phase. Hence in the acute setting the use of steroids to control the inflammatory response warrants their use. Evidence suggests that prolonged treatment with topical ste-roids in conjunction with ascorbate (a cofactor in collagen formation) does not result in corneoscleral melting.33,34 The potential benefits of corticosteroids can by maximized by their intensive use in the first 7 to 10 days, followed by a tapered dose or replacement with less powerful anti-inflammatory medications.

Some degree of iridocyclitis frequently follows burns with significant epithelial loss and tissue necro-sis. Mydriatics are recommended to prevent posterior synechiae formation and to reduce the discomfort associated with ciliary spasm. Topical antibiotic cover in the form of either ointment or drops is used in the immediate postburn period to decrease the risk of secondary infection seeding in the compromised

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ocular surface. This should be continued until the ocular surface has reepithelialized. Tetanus prophy-laxis can be considered although there is divided opinion as to whether it is clinically indicated.35,36 Intraocular pressure can rise in the setting of chemi-cal eye burns from scleral contraction and damage to the trabecular meshwork, which interferes with drainage.21 In these cases, treatment with carbonic anhydrase inhibitors or β-blockers may be useful. Ophthalmological follow-up is vital as surgical relief of intraocular pressure may be necessary if medical therapies are ineffectual.

Therapy should also be directed toward minimiz-ing the risk of corneal ulceration while supporting repair. Collagenase inhibitors have been investigated in experimental alkali injuries, but only a limited number are available for clinical use. Of these, acet-ylcysteine has shown favorable effects in a number of studies.37,38 Its disadvantages are that it is an unstable compound requiring frequent application and can be toxic to the eye. Tetracyclines, given either topically or systemically, have been shown to inhibit collagen-olytic degradation of the cornea after moderate to severe ocular chemical injuries.39 Their action, which is independent of their antimicrobial properties, is primarily via inhibition of matrix metalloproteinase. Ascorbate is reduced in the aqueous humour after alkali injury, and supplementation may reduce the incidence of ulceration.40

Surgical Interventions. Surgical intervention may be applied initially in severe ocular burns to promote reepithelialization and transdifferentiation of the ocu-lar surface. Tenoplasty may be performed to approxi-mate epithelium to a denuded corneal surface or when limbal vascularity is compromised and requires immediate reestablishment.41 When limbal stem cell populations are depleted, limbal cell transplantation may be employed, acutely or in the later stages to maximize the probability of generating a pheno-typically normal corneal epithelial surface.42 Such transplantation has been shown to allow reepithe-lialization of the corneal surface in approximately 2 weeks, along with improvements in vision and symp-toms. Mucous membrane and conjunctival trans-plantation may also be employed in the later stages of recovery to assist in cases where lid–globe appo-sition is unfavorable and the conjunctival fornices require re-establishment. The latter is uncommonly performed unless in the context of an acute chemi-cal injury, where advancement of Tenon’s capsule to reestablish limbal vascularity is used in conjunction with limbal autograft transplantation.17 Amniotic membrane transplant has also been employed and

shown to reduce inflammation, vascularization, and scarring while promoting epithelialization.43,44

Surgical techniques may also assist to support repair and minimize ulceration if progression to cor-neal thinning and perforation occurs, usually seen after grade IV injuries in the early or late phases of repair. Successful limbal stem cell transplantation produces an intact epithelium that excludes poly-morphonuclear leukocytes from the corneal stroma and produces cytokines that inhibit fibroblast col-lagenase production, thus arresting further sterile corneal ulceration.45,46 Symblepharon is a potential outcome of severe scarring, for which the patient may undergo limbal transplantation.46 Tissue adhe-sives, where sterile ulceration of the corneal stroma has either already occurred or is imminent, can be used to provide immediate tectonic support and form an impenetrable barrier, which excludes PMN leukocytes from the site and induces fibrovascular scarring.45 However, where possible, tissue adhesive should be avoided or applied cautiously as subse-quent cicatrix can impair visual acuity. Where tissue adhesive is inadequate or inappropriate to manage an acute perforation, tectonic keratoplasty may be necessary. Transferring of corneal tissue, limbal stem cells, and tenoplasty combine to address issues of tectonic support, vascular deficiencies, and surface epithelial abnormalities.

If there is inadequate restoration of the ocular surface despite initial interventions, further surgical techniques may be used to attempt late rehabilita-tion. Limbal cell transplantation can be of benefit after chemical injury with complete limbal stem cell loss when used in conjunction with superficial kera-tectomy, provided that the majority of scarring and corneal opacification is confined to the superficial layers. Under such circumstances this procedure can result in dramatic improvement in visual acuity.47 Conjunctival transplantation can attempt to improve the mechanical function of the ocular surface. Where fornix obliteration or abnormal lid–globe relation-ships exist, normal anatomical reconstruction may be satisfactorily attained via mucosal membrane grafts. Additionally, keratoprosthesis, where artificial cor-neal material (eg, “osteo-Odonto-Keratoproshtesis” or “AlphaCor”) can be transplated. The prognosis is very bleak in the presence of intraocular abnormali-ties (glaucoma, hypotony, retinal detachment).

Overall, a better understanding of ocular surface regeneration has facilitated new developments in the treatment of ocular burns. However, reported recovery rates, especially for more severe injuries, remain highly variable between centers. This is likely

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to relate, in part, to inconsistencies in the reported severity classification of individual cases.11

CONCLUSION

Although ocular alkali burns are uncommon, failure to recognize and appropriately treat these injuries can lead to destruction of epithelium and ischemic necro-sis of lids and anterior chamber structures with cata-strophic sequelae. The great majority of alkali burns appear to be either workplace related or secondary to domestic accidents, with caustic soda being the most common causative agent. Acute management includes irrigation, examination, and coordination of care between a burns unit and ophthalmologist. Although numerous medical and surgical interventions are available, their appropriateness must be assessed on a case-by-case basis. Prognosis varies according to the severity of the ocular surface burn, specifically corneal epithelial damage and the extent of limbal ischemia. Our case study of 12 patients receiving specialist care showed return to previous visual acuity in most cases. Prevention of these injuries with workplace health and safety promotion remains the ultimate aim.

ACKNOWLEDGMENTSWe sincerely thank Dr. Allan Kruger and Professor Stuart P. Pegg at Royal Brisbane Hospital for providing the initial idea for the study.

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