Management of Chemical Injuries
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, the clinician may use any other pure, nontoxic solution to rinse the ocular surface and dilute the offending agent. Alkali burns are true emergencies, and irrigation should be initiated at the site of the chemical injury and continued until an ophthalmologist evaluates the patient.
The eyelid can be opened 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 special scleral contact lens that connects to intravenous tubing. Irrigation should continue until the pH of the conjunctival sac normalizes. The conjunctival pH should be checked with a urinary pH strip. If this strip is not available, it is better to overtreat with prolonged periods of irrigation than to assume that the pH has normalized and discontinue treatment too early.
Because prolonged exposure to toxic particles can exacerbate chemical damage to the ocular surface, 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 14-9), and the fornices should be swept with an applicator to ensure that no particulate matter remains in the eye.
Management over the next few days, the intermediate period, should aim to decrease inflammation, monitor intraocular pressure (IOP), limit matrix degradation, and promote reepithelialization of the cornea. Many of the following recommendations for management are based on animal models of acute alkaline injury.
A–D, Steps in fashioning an eyelid retractor from a paper clip. E, Use of the retractor for double eversion reveals a foreign body on the upper eyelid.
(Courtesy of John E. Sutphin, MD.)
An intense polymorphonucleocyte (PMN) infiltration of the corneal stroma can occur following acute alkali burns. PMNs deliver proteolytic enzymes that, in the absence of an intact epithelium, dissolve corneal stromal collagen and ground substance. Corticosteroids are excellent inhibitors of PMN function, and intensive treatment with a topical corticosteroid is recommended for 10–14 days following a chemical injury. Thereafter, the frequency of the corticosteroid drops should be markedly reduced to prevent inhibition of wound healing and exacerbation of stromal melting. Corticosteroids retard epithelial wound healing and increase the risk of secondary infection by inhibiting normal ocular surface immune defense mechanisms, so their adverse effects in the chronic phase probably exceed their beneficial effects.
A deficiency of calcium in the plasma membrane of PMNs inhibits their ability to degranulate. Both tetracycline and citric acid are potent chelators of extracellular calcium. Therefore, oral tetracyclines and topical sodium citrate 10% have theoretical benefits for inhibiting PMN-induced collagenolysis. Topical medroxyprogesterone 1% may be effective in suppressing collagen breakdown and is used at some centers. Use of topical cycloplegics should be initiated and may be continued for patients with discomfort or significant anterior chamber reaction.
In the early stage of a chemical 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. See BCSC Section 10, Glaucoma, for a detailed discussion of medications used to control IOP.
Measures that promote wound healing and inhibit collagenolytic activity prevent stromal ulceration. Severe alkali burns in rabbit eyes 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 restores the level of aqueous humor ascorbate to normal and significantly reduces the incidence of ulceration. High-dose ascorbic acid is believed to promote collagen synthesis in the alkali-burned eye, given that ascorbic acid is required as a cofactor for collagen synthesis. Currently, there is no widely accepted standard for administration of ascorbic acid after chemical injury, but some recommend that patients take 1–2 g of vitamin C per day. Because this therapy is potentially toxic to the kidneys, ascorbic acid should not be administered to patients with compromised renal function.
Frequent use of nonpreserved topical lubricants helps facilitate epithelial healing in the acute and chronic stages of chemical injury. Necrotic corneal epithelium should be debrided to minimize the release of inflammatory mediators from damaged epithelial cells and to promote reepithelialization. A bandage contact lens may be beneficial for protecting ocular surface epithelium once migration onto the peripheral cornea has begun; however, acute conjunctival swelling and inflammation or late symblepharon formation may prevent retention of the contact lens. A temporary or permanent tarsorrhaphy facilitates reepithelialization due to increased corneal coverage, but as with contact lens use, the drawback is the increased risk of infection in eyes with compromised defense mechanisms. Avascular sclera usually does not epithelialize until revascularization occurs. If scleral melting occurs, a rotational graft of tarsoconjunctival tissue from the adjacent eyelid can be performed to promote revascularization.
Autologous conjunctival or limbal stem cell transplantation using tissue from the patient’s uninjured eye may facilitate healing of the corneal epithelial defect. Amniotic membrane may be helpful in suppressing inflammation, promoting reepithelialization, and preventing symblepharon formation; this option should be considered 1–2 weeks after injury. Limbal stem cell transplantation may be performed as soon as 2 weeks after chemical injury if no signs of corneal epithelialization have appeared. However, the prognosis of limbal grafts is better when the eye is not very inflamed; therefore, it is preferable to wait until the acute inflammation has subsided. A new technique known as simple limbal epithelial transplantation (SLET) combines limbal stem cell transplantation with use of amniotic membrane (see Chapter 13). If there is damage to the conjunctiva of both eyes, then either amniotic membrane alone or oral mucosal grafts may be necessary.
The long-term prognosis for a corneal transplant is improved if the ocular surface inflammation has resolved either over 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 vascularization in the host bed is associated with a much higher risk of rejection in these keratoplasty cases. Keratoprosthesis is another surgical option for these patients, but again, the prognosis is best when the inflammation has been brought under control.
Chan CC, Biber JM, Holland EJ. The modified Cincinnati procedure: combined conjunctival limbal autografts and keratolimbal allografts for severe unilateral ocular surface failure. Cornea. 2012;31(11):1264–1272.
Tejwani S, Kolari RS, Sangwan VS, Rao GN. Role of amniotic membrane graft for ocular chemical and thermal injuries. Cornea. 2007;26(1):21–26.
Vazirani J, Basu S, Sangwan V. Successful simple limbal epithelial transplantation (SLET) in lime injury–induced limbal stem cell deficiency with ocular surface granuloma. BMJ Case Rep. 2013;bcr2013009405.
Excerpted from BCSC 2020-2021 series: Section 10 - Glaucoma. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.