Residency · Residency · Ophthalmology
Chemical Burns of the Eye: Emergency Management and Reconstruction
Introduction
Chemical burns of the eye constitute a true ophthalmic emergency. Alkali injuries are generally more severe than acid injuries due to their ability to penetrate deep ocular tissues rapidly. Immediate and copious irrigation is the single most important intervention, taking priority over all other assessments. Long-term outcomes depend on the extent of limbal stem cell damage and the resultant cicatricial changes.
Pathophysiology
Alkali Burns
Saponification of cell membrane fatty acids allows rapid penetration. Alkali agents (lye, ammonia, lime, cement) can reach the anterior chamber within seconds to minutes. Causes liquefactive necrosis: progressive destruction of collagen and ground substance. Damages limbal stem cells, conjunctival goblet cells, trabecular meshwork, lens epithelium. Common agents: sodium hydroxide (NaOH), calcium hydroxite (Ca(OH)2), ammonia (NH3)
Acid Burns
Cause coagulative necrosis: protein precipitation creates a barrier limiting further penetration. Exception: hydrofluoric acid penetrates deeply like alkali due to fluoride ion. Generally better prognosis than alkali burns of equivalent severity. Common agents: sulfuric acid (battery acid), hydrochloric acid, acetic acid.
Phases of Healing
Immediate (0-7 days): acute inflammation, epithelial defect, stromal edema, limbal ischemia. Early repair (7-21 days): re-epithelialization, collagenase activity, risk of sterile corneal melting. Late repair (3 weeks - months): vascularization, scarring, symblepharon formation, stem cell failure.
Emergency Management
Immediate Irrigation
Begin irrigation immediately at the scene; do not wait for transport or assessment. Use any available non-toxic fluid: water, saline, lactated Ringer solution, balanced salt solution. Continue irrigation for a minimum of 30 minutes (2-3 liters of fluid) Use a Morgan lens or IV tubing for continuous irrigation in the emergency department. Check pH after irrigation; continue until pH is neutral (7.0-7.4) for at least 30 minutes. Sweep fornices with a moistened cotton-tipped applicator to remove particulate matter (especially lime/cement)
Double evert upper lids to inspect and irrigate the superior fornix.
Clinical Assessment (After Irrigation)
Visual Acuity
Document best corrected visual acuity; even light perception is prognostically important.
Slit-Lamp Examination
Corneal epithelial defect: size and location; fluorescein staining. Corneal clarity: mild haze vs. dense opacification (indicates stromal damage) Limbal ischemia: blanching of limbal vessels; assessed in clock hours (most important prognostic factor) Conjunctival involvement: chemosis, blanching, necrosis. Anterior chamber reaction: cells and flare; IOP assessment (may be elevated or low) Lens: acute cataract from alkali penetration.
Classification
Roper-Hall Classification (Modified Hughes)
| Grade | Cornea | Limbal Ischemia | Prognosis |
|---|---|---|---|
| I | Clear | None | Excellent |
| II | Hazy, iris details visible | < 1/3 (< 4 clock hours) | Good |
| III | Opaque, iris details obscured | 1/3 - 1/2 (4-6 clock hours) | Guarded |
| IV | Opaque, iris/pupil not visible | > 1/2 (> 6 clock hours) | Poor |
Dua Classification
Six-grade system incorporating percentage of conjunctival involvement in addition to limbal ischemia. More granular assessment of moderate-to-severe injuries (grades III and IV subdivided) Better predictive value for surgical outcomes.
Medical Management
Acute Phase (First 7-14 Days)
Topical antibiotics: fluoroquinolone drops to prevent secondary infection. Cycloplegic agents: cyclopentolate or atropine for ciliary spasm and to prevent posterior synechiae. Topical corticosteroids: aggressive use in the first 7-10 days to reduce inflammation. Taper or discontinue between days 10-14 to avoid inhibition of collagen synthesis during the repair phase. Ascorbate: topical (10% sodium ascorbate) and oral (1-2 g daily); promotes collagen synthesis by fibroblasts. Citrate (10% topical): chelates calcium, inhibits polymorphonuclear cell migration and collagenase activity.
Preservative-free artificial tears: frequent lubrication. IOP management: topical beta-blockers, alpha-agonists, or oral acetazolamide if elevated. Amniotic membrane transplantation: early application in moderate-to-severe burns promotes re-epithelialization and reduces inflammation.
Anti-Collagenase Strategies
Medroxyprogesterone (1%): inhibits collagenolysis. Tetracyclines (doxycycline 100 mg PO BID): matrix metalloproteinase inhibition. N-acetylcysteine (10-20% topical): mucolytic with anti-collagenase properties. Tissue adhesive (cyanoacrylate) for impending or actual corneal perforation.
Surgical Management
Acute Surgical Interventions
Debridement: necrotic tissue removal to promote re-epithelialization. Amniotic membrane transplant (AMT): sutured or as a ProKera ring device. Tenon advancement or conjunctival flap: provides vascular supply to ischemic areas. Tarsorrhaphy: temporary closure to protect epithelium. Corneal gluing for perforation or significant thinning.
Chronic Phase Reconstruction
Limbal Stem Cell Transplantation
Required when limbal stem cell deficiency (LSCD) develops: conjunctivalization of cornea, persistent epithelial defects, neovascularization. Autograft (from fellow eye): for unilateral LSCD; keratolimbal autograft (KLAU) or conjunctival-limbal autograft (CLAU) Allograft (cadaveric or living related donor): for bilateral LSCD; requires systemic immunosuppression. Cultivated limbal epithelial transplantation (CLET): ex vivo expansion of limbal stem cells on amniotic membrane; allows smaller biopsy. Simple limbal epithelial transplantation (SLET): small limbal biopsy from fellow eye, fragmented and distributed on amniotic membrane over the recipient eye.
Keratoplasty
Indicated after limbal stem cell restoration when corneal scarring persists. Penetrating or lamellar keratoplasty. Poor prognosis without prior stem cell reconstitution (graft failure from conjunctivalization)
Ocular Surface Reconstruction
Symblepharon lysis with AMT or mucous membrane grafting. Forniceal reconstruction for motility restriction. Keratoprosthesis (Boston KPro type I or II) for end-stage disease after multiple graft failures.
Complications
Persistent epithelial defects, corneal melting, and perforation. Limbal stem cell deficiency and conjunctivalization of the cornea. Symblepharon, ankyloblepharon, and cicatricial entropion. Secondary glaucoma (from trabecular meshwork damage or synechiae) Corneal neovascularization and scarring. Dry eye from goblet cell loss and lacrimal gland duct obstruction.
Cataract, phthisis bulbi.
Key Clinical Pearls
Irrigation is the most important intervention and must begin immediately; do not delay for visual acuity testing or other assessments. Limbal ischemia measured in clock hours is the most important prognostic indicator in chemical burns. Topical corticosteroids should be used aggressively in the first 7-10 days but tapered after day 10-14 to avoid inhibiting corneal collagen repair. Limbal stem cell transplantation must precede keratoplasty in eyes with limbal stem cell deficiency to prevent graft failure.
References
- Roper-Hall MJ. Thermal and chemical burns. Trans Ophthalmol Soc U K. 1965;85:631-653.
- Dua HS, King AJ, Joseph A. A new classification of ocular surface burns. Br J Ophthalmol. 2001;85(11):1379-1383.
- Sangwan VS, Basu S, MacNeil S, Balasubramanian D. Simple limbal epithelial transplantation (SLET): a novel surgical technique for the treatment of unilateral limbal stem cell deficiency. Br J Ophthalmol. 2012;96(7):931-934.
- Fish R, Davidson RS. Management of ocular thermal and chemical injuries, including amniotic membrane therapy. Curr Opin Ophthalmol. 2010;21(4):317-321.