Emergency Medicine · Ocular and Dermal Chemical Injuries
The facts most likely to be tested
Immediate copious irrigation with water or saline is the definitive first-line treatment for all chemical ocular and dermal exposures.
Alkali burns cause liquefactive necrosis, allowing for deeper tissue penetration and more severe damage than acidic exposures.
Acidic burns typically result in coagulation necrosis, which creates an eschar that limits further penetration of the chemical.
Ocular pH testing must be performed after irrigation to ensure the pH has returned to a neutral range of 7.0 to 7.2.
Hydrofluoric acid exposure requires immediate application of calcium gluconate gel to neutralize fluoride ions and prevent systemic hypocalcemia.
Dry chemical agents, such as lime or phenol, must be brushed off the skin prior to irrigation to prevent an exothermic reaction.
Morgan lens placement is the preferred method for continuous, high-volume irrigation in patients with ocular chemical burns.
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A 34-year-old laboratory technician presents to the emergency department after accidentally splashing a clear liquid into his right eye. He reports immediate intense burning pain, photophobia, and blurred vision. On physical examination, the patient has conjunctival injection and corneal epithelial defects. The pH of the affected eye is measured at 11.5.
What is the most appropriate next step in management?
Immediate copious irrigation with normal saline or lactated Ringer's solution.
The patient has an alkali ocular burn, which causes liquefactive necrosis; immediate irrigation is the most critical step to prevent permanent vision loss, as tested by the first bet.
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High yield triage
Etiology / Epidemiology
Occurs via alkali or acid exposure. Alkali burns are more severe due to liquefactive necrosis.
Clinical Manifestations
Pain, erythema, and corneal opacification. Immediate irrigation is the priority.
Diagnosis
Clinical diagnosis based on history. pH testing of the conjunctival sac is the gold standard.
Treatment
Copious irrigation with water or saline until pH 7.0-7.2 is achieved. Do not neutralize.
Prognosis
Severity depends on depth. Full-thickness burns carry high risk of symblepharon and permanent vision loss.
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Epidemiology & Etiology
Chemical burns are common in industrial and household settings involving cleaning agents. Alkali substances (e.g., lye, ammonia) penetrate deeper than acids. Acid exposure typically causes coagulative necrosis, which limits tissue penetration.
Pertinent Anatomy
The eye is the most critical site for chemical injury. The corneal epithelium acts as a barrier, but rapid penetration leads to permanent damage of the limbal stem cells.
Pathophysiology
Alkali agents cause liquefactive necrosis, saponifying fats and denaturing proteins, allowing deep ocular penetration. Acids cause coagulative necrosis, creating a protein coagulum that acts as a physical barrier to further injury. Systemic toxicity may occur with large surface area exposures.
Clinical Manifestations
Patients present with intense pain, blepharospasm, and decreased visual acuity. Corneal haze or limbal ischemia (blanching) are red flag signs of severe injury. Look for conjunctival injection and potential secondary glaucoma.
Diagnosis
Diagnosis is primarily clinical. The gold standard is pH testing of the inferior fornix using litmus paper. A normal ocular pH is 7.0–7.2; irrigation must continue until this range is restored.
Treatment
Immediate copious irrigation with isotonic saline or water is the first-line intervention. Do not attempt chemical neutralization as the exothermic reaction causes further thermal damage. Use a Morgan lens for sustained delivery. Follow with topical antibiotics and cycloplegics for pain.
Prognosis
Prognosis is dictated by the extent of limbal ischemia. Complications include corneal scarring, symblepharon (adhesion of eyelid to globe), and secondary cataracts. Long-term monitoring by ophthalmology is mandatory.
Differential Diagnosis
Thermal burn: history of heat source exposure
Corneal abrasion: history of trauma without chemical exposure
Ultraviolet keratitis: history of welding or sun exposure
Foreign body: localized sensation relieved by removal
Infectious keratitis: presence of discharge and infiltrates