Chemical injuries to the external eye can range in severity from mild irritation to complete destruction of the ocular surface and adnexa (eyelids), resulting in corneal opacification, loss of vision, and even loss of the eye. Chemical injuries may occur in the home or workplace. Some of the most severe ocular chemical injuries are caused by strong alkalis (eg, lye) or acids used for assault. Table 14-1 lists some common caustic chemicals that can cause ocular injury.
Whenever possible, the offending chemical agent should be identified. The severity of a chemical injury depends on the pH (acid or alkali), the volume and duration of contact, and the inherent toxicity of the chemical. Frequently, the container of the toxic agent offers instructions for treatment or a phone number to call for detailed assistance.
Alkali Burns
The most severe chemical injuries occur with alkaline (high pH) solutions because they cause saponification of fatty acids in cell membranes and ultimately cellular disruption. Once the surface epithelium is damaged, alkaline solutions readily penetrate the corneal stroma, where they rapidly destroy the proteoglycan ground substance and collagen fibers of the stromal matrix. Strong alkaline substances may also penetrate through the endothelium into the anterior chamber, causing severe tissue damage and intense inflammation.
Table 14-1 Common Alkalis and Acids Causing Eye Injuries
The visual prognosis is often determined by the extent of ocular surface injury and the effect of skin burns on eyelid function. There are multiple classification and grading schemes for chemical injuries. The Hughes classification scheme (as modified by Thoft) divides chemical injuries of the cornea into 4 categories (Table 14-2) based on clinical findings. The scheme shown in Table 14-3 establishes the grade of injury based on clinical signs, symptoms, and expected outcomes. The most unfavorable visual prognosis is associated with extensive limbal epithelial damage. The limbus contains corneal epithelial stem cells; damage to this region can lead to disruption in the cells repopulating the corneal epithelium. Blanching occurs when the vascular supply to this critical area is disrupted via death of vascular endothelial cells in the conjunctiva. The resultant limbal and anterior segment ischemia is a poor prognostic feature for eyes thus affected (Figs 14-1 through 14-4). If the conjunctiva recovers, vascularization may occur (Fig 14-5). Repopulation of the corneal surface epithelium with undifferentiated conjunctival cells leads to poor epithelial adhesion and recurrent breakdown, and possibly chronic inflammation if the original trauma is severe. Intraocular chemical penetration may result in cataract formation and secondary glaucoma; the latter is thought to result from damage to the trabecular meshwork, which can affect outflow facility.
Table 14-2 Prognostic Features of Chemical Injury of the Eye
Table 14-3 Classification Scheme for Chemical Injury to the Human Eye Based on Clinical Findings
Patients with severe alkali burns are fortunate if the conjunctival and corneal surface vascularize and stabilize. Patients with alkali burns may not be candidates for penetrating keratoplasty because the loss of goblet cells impairs graft survival, but they may be candidates for limbal stem cell transplantation followed by keratoplasty or keratoprosthesis. In the most severe cases, phthisis of the globe may occur or, in the absence of vascularization, melting may lead to enucleation.
Bagley DM, Casterton PL, Dressler WE, et al. Proposed new classification scheme for chemical injury to the human eye. Regul Toxicol Pharmacol. 2006;45(2):206–213.
Colby KA. Chemical injuries of the cornea. Focal Points: Clinical Modules for Ophthalmologists. San Francisco: American Academy of Ophthalmology; 2010, module 1.
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.