Alkali: Examples include sodium hydroxide (lye), calcium hydroxide (lime, cement, plaster), and ammonia.

Acids: sulfuric acid (battery fluid)

Mace (chloroacetophenone) and teargas

Organic solvents

Detergents

Symptoms

Pain, redness, tearing, decreased vision

Signs

Mild to moderate

Burns and edema of the eyelid

Conjunctival injection, chemosis, abrasion

Punctate or large epithelial defects on cornea (Fig. 11-1A)

Mild anterior chamber activity

Severe

Severe burns of the skin of the eyelids

Severe chemosis, conjunctival necrosis, conjunctival ischemia (sludging or absence of blood flow through conjunctival vessels) (Fig. 11-1B–E)

Scleral/limbal ischemia

Significant anterior chamber activity

Corneal epithelial defects, edema, or melting (Fig. 11-1F)

Poor or no view of the anterior chamber because of corneal haze (Fig. 11-1G)

Intraocular pressure may be low, normal, or elevated in acute stages.

The degree of limbal ischemia and corneal haziness carries prognostic importance.

Treatment

Mild cases may be treated on an outpatient basis. Severe injuries may require hospitalization.

Copious irrigation with normal saline through an IV infusion set for at least 30 minutes and repeated every 30 minutes until neutral pH is reached.

Mechanical removal of foreign particles and debridement of necrotic tissues should be performed with a cotton-tipped applicator or jeweler’s forceps under topical anesthesia.

Frequent instillation of preservative-free tear drops (q1h)

Cycloplegics (e.g., scopolamine 0.25% or atropine 1% t.i.d.)

Topical antibiotic ointment (e.g., erythromycin, bacitracin, or tetracycline) q2h if an eye patch is not used. Pressure patching may aid in reepithelialization.

Control intraocular pressure if it is elevated, either with topical drops or oral carbonic anhydrase inhibitors

For injuries with significant inflammation and without risk of corneal melting, topical corticosteroid (e.g., dexamethasone 0.1% or prednisolone 1%) q1–2h may be used during the first week, tapered during the second week, and increased after epithelial healing if necessary. A combination antibiotic–corticosteroid (e.g., tobramycin 0.3%–dexamethasone 0.1% ointment) q1–2h can also be used.

Topical acetylcysteine 10% drops q.i.d. may help control collagenase activity and corneal melting.

High-dose vitamin C 1 g PO t.i.d. and topical ascorbate 10% drops q1–6h may be helpful in severe alkali burns.

Doxycycline 100 mg PO b.i.d. can be used to decrease collagenase activity.

Early amniotic membrane graft or amniotic membrane on a scleral ring (e.g., Pro-Kera) may be beneficial in severe cases.

If there is symblepharon formation, daily sweeping of the fornices with a cotton-tipped applicator or glass rod can be performed under topical anesthesia to break the adhesions. Alternatively, a scleral shell may be used.

For progressive corneal melting or perforation, tissue adhesive, amniotic membrane graft, limbal stem cell graft, lamellar patch graft, or penetrating keratoplasty may be necessary.

Complications

Corneal haze or scarring

Infectious keratitis

Dry eyes

Symblepharon

Cicatricial entropion or ectropion

Trichiasis or distichiasis

Punctal stenosis or occlusion

Limbal stem cell deficiency

Pannus formation

Cataract

Glaucoma

Prognosis

Dismal to excellent, depending on the severity of the injury (Fig. 11-1H). In general, alkaline substances cause the most severe injuries, because they penetrate ocular tissues easily.

Figure 11-1. Chemical burn. A. A mild acid injury caused a large corneal abrasion, which has been stained with yellow fluorescein dye. There is minimal to no conjunctival blanching, and the cornea is essentially clear. Mild chemical burns generally resolve without serious consequences. B. A sulfuric acid injury occurred to this patient’s right eye. There is a large central and inferior corneal epithelial defect and mild inferior conjunctival blanching. Chemical burn. C. This eye withstood a battery acid (sulfuric acid) injury. There is moderate conjunctival blanching and mucus adherent to the conjunctiva and cornea. D. The left eye of the patient seen in B has a much more extensive sulfuric acid injury. The epithelium is necrotic and has already sloughed off of the superior cornea. There is extensive conjunctival and scleral blanching inferiorly and nasally. Chemical burn. E. High-magnification view of the eye seen in D demonstrates ischemia of the conjunctiva and sclera. There is segmentation of the red blood cells, indicating lack of blood flow. The greater the degree of ischemia, the worse is the prognosis. F. A severe lye (sodium hydroxide) injury caused extensive ischemic damage in the lower two-thirds of the eye. The cornea has undergone necrosis centrally, leading to a perforation requiring an emergency corneal transplant. This alkali injury eventually resulted in enucleation. Chemical burn. G. Twelve days after a severe alkali injury, the conjunctiva and sclera remain blanched and the cornea is opaque. There has been no reepithelialization of the damaged cornea or conjunctiva. H. Many years after a severe chemical burn, the cornea remains totally scarred and vascularized.

THERMAL AND ELECTRICAL BURNS

THERMAL BURNS

Thermal burns can be mild to severe and can occur at any age. Cigarette burns are not uncommon in small children, whose eyes may be at hand level of a person holding a cigarette.

Etiology

Curling irons

Cigarettes, especially children

Flames

Hot liquids

Molten metals