Chemical and thermal injuries of the eyes. Surgical and medical treatment based on clinical and pathophysiological findings

Abstract

Light burns heal well within a few days. Severe chemical and thermal injuries of the eyes destroy surface epithelia and cause ischemic necroses of conjunctiva, cornea, sclera, iris, ciliary body, and lids. An inflammatory response follows with leucocyte infiltration and release of inflammatory mediators. Prostaglandins, lipoxygenase products, cytokines, superoxide radicals and Iysosomal enzymes are known to be active in eye burn disease. Their activities result in corneal, scleral and conjunctival ulceration, tissue proliferation and scarification, which develop within weeks, months and even years after the accident. Pathophysiological events produce defined clinical pictures. Some agents take special actions, e.g. alkali penetrates within seconds into the anterior chamber, sulfuric acid burns as well as quick lime burns forming slaked lime produce considerable heat. Hydrofluoric acid is highly toxic and induces early necroses. Heat causes deep ischemic necroses and lateron strongly shrinking scars. Onset and intensity of first aid decided on the outcome. Immediate rinsing is essential. Cool water, saline, Ringers lactate solution and BSS are good rinsing media. For first aid, buffered Previn seems suitable. Major chemical and thermal injuries need a variety of medical and surgical treatments: Necroses must be excised surgically. Tenon plasty is performed to reconstruct conjunctiva. Amnion-, limbus- and early keratoplasty or artificial epithelium are applied, initially to save the cornea from melting, and later to restore vision. Conjunctical, lid and intraocular surgery may be necessary. The aim of medical treatment is to suppress the inflammatory response and to prevent infection. Corticosteroids, antibiotics, ascorbate and inhibitors of proteolytic enzymes are used. Secondary glaucoma must not be forgotten. Extensive therapy is sometimes rewarding, results are presented.