Introduction

Corneal alkali wound is a potentially severe clinical problem. Despite many experimental investigations and clinical trials, it has long been recognized as a d a c u l t disorder to treat, having a long-standing protracted course and frequently resulting in various unsightly complications (Hughes 1946a,b; Duke-Elder & MacFaul 1972). According to recent epidemiological surveys on chemical trauma, the incidence of chemical injury constitutes 7 to 10% of all ocular trauma (Pfister 1983,1984a). Moreover, alkali burns of the eye still represent the major severe events among the chemical trauma (26%) (Morgan 1987). Most of the injuries from alkali occur in industrial and home accidents, and as the result of assault. Alkali injury of the eye is more likely to occur among the young, working, lower socioeconomical group (Klein & Lobes 1976; Morgan 1987). The common agents, involved in causing alkali injury, are plaster, various cleaning agents, fertilizer, cement etc., which contain agents as ammonia (NHJ, lye (NaOH), lime (Ca(OH),), and other hydroxides @OH, Mg(OH),) (Duke-Elder & MacFaul 1972; Lemp 1974; Mogan 1987). Ammonia gas forms ammonium hydroxide (NH,OH) which can cause major ocular damage. Ammonia is highly soluble in lipid and rapidly penetrates the eye, causing the most severe ocular damage. Lime penetrates the cornea relatively poorly because it reacts with the epithelial cell membrane, forming calcium soaps that precipitate and prevent further penetration (McCulley 1983). The main factors which govern the severity of the alkali wound are the character of the cation, volume and concentration of the alkali, duration of the exposure, pH of the solution, and speed of penetration in the tissue for different kinds of alkali solution (Hughes 1946a; Duke-Elder & MacFaul 1972). The main substantial difference between alkali and acid concerns their biological reaction in the tissue. Alkali dissociates and saponifies cell membranes, denaturates collagen, and thus penetrates deeply into the anterior chamber and damages the structures in the eye, including iris, lens, ciliary body, and even retina (Hughes 1946a,b; Girard et al. 1970; Smith & Conway 1976). Acid, in contrast, coagulates proteins in the superficial tissue, thus providing a barrier to prevent deep penetration into the eye, while diluting residual acid in the external eye (Duke-Elder & MacFaul 1972; Lemp 1974). Hughes (1946a,b) classified alkali wounds in three stages, i.e. A) mild: erosion of corneal epithelium, faint haziness of cornea, and no ischemic necrosis of conjunctiva and sclera, B) moderately severe: corneal opacity blurring iris details, and minimal ischemic necrosis of conjunctiva and sclera, and C) severe: blurring of pupillary outline, and blanching of conjunctiva and sclera. According to this classification he provided the clinical and pathological course of alkali wounds of the eye (Hughes 1946b). Later on, this classification was modified and devised to a four-step classification (Ballen 1964; Roper-Hall 1965). The assessment of severity involves three factors, 1) damage to the lids and adnexae, 2) degree of limbal ischemic necrosis, and 3) degree of initial stromal opacification (Roper-Hall 1965; Dohlman & Pfister 1972). The extent of damage in the surrounding tissue is an influencing factor to the prognosis. The clinical course of the alkali wounded eye can be generalized as an acute stage, a repair stage, and a late complication stage (Hughes 1946b; Lernp 1974). The general principles for clinical management of the alkali wounded eye constitute irrigation, removal of chemical particles, some recommend paracentesis of anterior chamber, and symptom relief with analgesics and sedatives combined with cycloplegics as immediate treatments. The treatment during the repair stage is to enhance and support the biological healing process by various medical (Dohlman & Pfister 1972; Lemp 1974;