Figure 13-3 Severe, grade IV alkali burn with epithelial loss and stromal necrosis. (Courtesy of James J. Reidy, MD.)

Acid Burns

Acids denature and precipitate proteins in the tissues they contact. Acidic solutions tend to cause less severe tissue damage than do alkaline solutions because of the buffering capacity of tissues as well as the barrier to penetration formed by precipitated protein. The exception to this is hydrofluoric acid, which can cause significant anterior segment destruction. Acids do not directly cause loss of the proteoglycan ground substance in the cornea, although they too can incite severe inflammation and damage to the corneal matrix.

Management of Chemical Injuries

Many of the current recommendations for management are based on animal models of acute alkaline injury.

The most important step in the management of chemical injuries is immediate and copious irrigation of the ocular surface with water or balanced saline solution. If these liquids are not available, any other generally nontoxic and unpolluted solutions can also be used to avoid delaying treatment. Commercially available eyewash solutions such as Cederroth Eye Wash (Cederroth, Upplands Väsby, Sweden) may have some advantages over plain saline solutions. If possible, irrigation should be initiated at the site of the chemical injury and continued until an ophthalmologist evaluates the patient. The eyelid should be immobilized with a retractor or eyelid speculum, and topical anesthetic should be instilled. Irrigation may be accomplished using handheld intravenous tubing, an irrigating eyelid speculum, or a Morgan medi-FLOW Lens (MorTan, Missoula, MT), a special scleral contact lens that connects to intravenous tubing. Irrigation should continue until the pH of the conjunctival sac normalizes. The conjunctival pH can be checked easily with a urinary pH strip. If this is not available, it is better to “overtreat” for prolonged periods of irrigation than to “guess” that the pH has normalized.

Because they can continue to release the toxic chemical, particulate chemicals should be removed from the ocular surface with cotton-​tipped applicators and forceps. Eversion of the upper eyelid should be performed to search for material in the upper fornix (Fig 13-4), and the fornices should be swept with an applicator to ensure that no particulate matter remains in the eye.

Figure 13-4 A, B, C, and D show steps in fashioning an eyelid retractor from a paper clip. E, Using the retractor for double eversion reveals a foreign body on upper eyelid. (Courtesy of John E. Sutphin, MD.)

The next phase of management should be directed at decreasing inflammation, monitoring intraocular pressure (IOP), limiting matrix degradation, and promoting reepithelialization of the cornea. An intense polymorphonuclear (PMN) leukocyte infiltration of the corneal stroma has been known to occur in acute alkali burns. PMNs may be a major source of proteolytic enzymes capable of dissolving corneal stromal collagen and ground substance. Corticosteroids are excellent inhibitors of PMN function, and intensive topical corticosteroid administration is recommended for the acute

phase (first 10–14 days) following chemical injuries. The dosage should be markedly reduced after 10–14 days, because corticosteroids can inhibit wound healing and possibly exacerbate sterile stromal melting. Corticosteroids also increase the risk of secondary infection by means of inhibition of normal ocular surface immune mechanisms; thus, their untoward side effects in the chronic phase may exceed their beneficial effects.

A deficiency of calcium in the plasma membrane of PMNs inhibits their ability to degranulate, and both tetracycline and citric acid are potent chelators of extracellular calcium. Therefore, oral tetracyclines and topical 10% sodium citrate have theoretical benefits for inhibiting PMN-induced collagenolysis. In addition, topical 1% medroxyprogesterone may be effective in suppressing collagen breakdown and is used in some centers.

Topical cycloplegics are recommended for patients with significant anterior chamber reaction. In the early stage of the injury, there may be a rise in IOP, which can be controlled by use of oral carbonic anhydrase inhibitors in order to avoid toxicity from topical glaucoma medications. However, if the corneal epithelium is healing normally, topical therapies may be used as well. BCSC Section 10, Glaucoma, discusses medications for IOP control in depth.

Measures to promote wound healing and inhibit collagenolytic activity may help prevent stromal ulceration. Severe alkali burns in rabbit eyes have been found to reduce aqueous humor ascorbate levels to one-third of normal levels. Reduced aqueous humor ascorbate has been correlated with corneal stromal ulceration and perforation. Systemic administration of ascorbic acid to rabbits with acute corneal alkaline injuries has restored the aqueous humor ascorbate level to normal and significantly reduced the incidence of ulceration. High-dose ascorbic acid is believed to promote collagen synthesis in the alkali-burned eye because ascorbic acid is required as a cofactor for this synthesis. There is currently no widely accepted standard for administration of ascorbic acid to corneas after chemical injury, but one recommendation is for patients to receive 1–2 g of vitamin C per day. However, because this therapy is potentially toxic to the kidneys, patients with compromised renal function are not good candidates for this approach.

There are certain key practices that facilitate epithelial healing in acute and chronic chemical injury. Patients should be treated initially with intensive nonpreserved lubricants. Necrotic corneal epithelium should be debrided to minimize the release of inflammatory mediators produced by damaged epithelial cells and to promote reepithelialization. A bandage contact lens or temporary tarsorrhaphy may be beneficial for protecting ocular surface epithelium once it has begun to move onto the peripheral cornea. Sometimes, the bandage contact lens is not retained easily because of the swelling and inflammatory response. A tarsorrhaphy has the advantage of not increasing the risk of corneal infection, which is a concern with contact lens use in eyes with poor epithelium. Avascular sclera will usually not epithelialize until revascularization occurs. If scleral melting occurs, then a rotational tarsoconjunctival graft from the adjacent eyelid can be performed to promote revascularization.

Autologous conjunctival or limbal transplants from a patient’s uninvolved fellow eye may restore the integrity of the damaged corneal epithelium. Amniotic membrane transplantation may be helpful in suppressing inflammation and promoting reepithelialization and prevention of symblepharon formation, and it should be considered in the early postinjury phase. Limbal stem cell transplantation may be performed as soon as 2 weeks after chemical injury if no signs of corneal epithelialization have appeared. However, in general, the prognosis of limbal grafts is better when the eye is not very inflamed; thus, waiting until the acute inflammation has subsided is helpful. Similarly, the prognosis for corneal transplantation is improved if the ocular surface inflammation has resolved either through the passage of time (months to years) or after limbal stem cell grafting (ocular surface reconstruction), if necessary. Even when there is no active ocular surface inflammation, stromal