Acute periocular signs of injury include periorbital edema and erythema, deepithelialized skin, and loss of eyelashes and eyebrows. A spectrum of clinical manifestations after a chemical injury could be described, which may vary substantially over time. It is essential to make sure that no foreign bodies are embedded in any part of the ocular structures. The initial examination (after thorough irrigation as described below) includes a complete eye examination. Conjunctival inflammation and loss of goblet cells can leave the ocular surface prone to dryness, scarring, and contracture of the fornices. Long-term rises of intraocular pressure can occur from fibrotic damage to the trabecular meshwork as well as the inflammatory debris trapping within the meshwork. Shrinkage and contraction of the cornea and sclera may lead to acute rise of intraocular pressure. Acids cause protein coagulation in the epithelium, which limits further penetration into the deeper layers of the eye (hydrofluoric acid is an exception among acid since it can rapidly pass through cell membranes). Due to the rapidity of this process, patients may experience irreversible intraocular damage in as little as 5–15 minutes. They may also find their way to the anterior chamber damaging the trabecular meshwork, ciliary body, and the lens. Basic substances are lipophilic and penetrate the eye more rapidly compared to acidic chemicals. The typical presentation after a chemical injury is a sudden onset of severe pain, epiphora, and blepharospasm. The goal of treatment is to minimize further damage to ocular surface and ultimately restore a normal ocular surface anatomy and visual function. Given their younger age, the long-term disabilities that follow ocular burns could dramatically affect the patients’ lives. This type of injury is most common among men 20 to 40 years of age that typically work in industrial chemical laboratories or factories. Chemical burn is considered a true ocular emergency and requires immediate and intensive evaluation and care. IntroductionĪ chemical ocular burn usually occurs when a corrosive substance is accidentally introduced to the eye and/or periocular tissues. Limbal stem cell transplantation, amniotic membrane transplantation, and ultimately keratoprosthesis may be indicated depending on the patients’ needs. The goal of treatment is to restore the normal ocular surface anatomy and function. The treatment starts with simple but vision saving steps and is continued with complicated surgical procedures later in the course of the disease. The degree of limbal, corneal, and conjunctival involvement at the time of injury is critically associated with prognosis. The clinical course can be divided into immediate, acute, early, and late reparative phases. The victims of such incidents are usually young, and therefore loss of vision and disfigurement could dramatically affect their lives. Ocular chemical burns are common and serious ocular emergencies that require immediate and intensive evaluation and care.
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