Christian A. Tomaszewski
Caustic exposures in the United States totaled more than 130,000 in 2008. They consist of three groups: (1) intentional ingestions in adolescents and adults; (2) unintentional exposures in children; and (3) accidental exposures, often occupational. Although a minority, intentional exposures caused the most morbidity.
Alkali exposures mainly result from cleaners, such as sodium hydroxide in drain openers and ammonium hydroxide in fertilizers. Acid exposures involve household and toilet cleaners, such as sulfuric and hydrochloric acid, and the more insidious rust remover, hydrofluoric acid, which is potentially lethal through dermal exposure.
The most common caustic exposure is household bleach, with approximately 37,000 annual exposures. Although potentially lethal in large intentional ingestions, it rarely results in any morbidity among the countless incidental pediatric exposures each year.
The strength of a caustic and duration of the exposure determine the extent of injury. As a rule of thumb, injuries can be expected at pH <3 or >11.
Alkalis penetrate deeply into tissue through liquefaction necrosis. Liquid alkali ingestions cause proximal damage to the esophagus, which may lead to stricture formation or perforation.
Strong acids produce coagulation necrosis, with early eschar formation, which usually protects against deeper esophageal injury. Regardless, both esophageal and gastric injury can occur with acid ingestion.
Hydrofluoric acid is a weak acid (pKa = 3.2) that can cause delayed morbidity from the fluoride component, which penetrates deeply into tissues, complexes with calcium and magnesium, and leads to cell death.
Caustics can cause injury at various levels. Laryngotracheal injury is suggested by dysphonia or stridor. Injury to the GI tract usually manifests as dysphagia, odynophagia, epigastric pain, or vomiting. Direct injury to the lungs can occur from aspiration or inhalation of acid fumes.
Esophageal injuries from caustic ingestion are classified by endoscopy as grades 1 to 3: (1) edema and hyperemia; (2) ulceration, blisters, and exudates (2A are non-circumferential and 2B circumferential or deeper); and (3) deep ulcerations and necrosis. Higher grades of injury are more likely to result in stricture or perforation in the first 1 to 2 weeks.
Intentional injuries can cause severe GI tract injury without clinically obvious signs.
Unintentional injuries, usually in children, may have esophageal injury even when asymptomatic, although stridor, drooling, or vomiting usually accompany serious esophageal injury (grade 2 or 3).
Complications of severe caustic injury include shock from GI bleeding or perforation. Chest discomfort may signify mediastinitis.
Dermal exposures usually produce local pain and irritation. However, hydrofluoric acid differs in its ability to cause deep and delayed tissue necrosis. At concentrations <20%, pain and erythema may not develop for 24 hours; at 20% to 50%, burns typically evolve within 8 hours. Burns from concentrations >50% can cause systemic toxicity with hypocalcemia, hypomagnesemia, and hyperkalemia, which can cause fatal ventricular dysrhythmias. Oral ingestions of hydrofluoric acid result in earlier mortality through similar mechanisms.
DIAGNOSIS AND DIFFERENTIAL
Accidental ingestions of household caustics in children usually require no workup if asymptomatic.
Intentional ingestions, or ingestions of strong caustics may require the following labs: blood gas, electrolyte panel, hepatic profile, CBC, coagulation profile, lactate, and serum type and screen.
Obtain serum calcium and magnesium levels and perform an ECG to evaluate for prolonged QT intervals or changes suggestive of hyperkalemia in cases of hydrofluoric acid exposure.
Upright chest radiograph can be used to detect peritoneal or mediastinal free air. CT is useful when GI perforation is suspected.
EMERGENCY DEPARTMENT CARE AND DISPOSITION
Administer 100% oxygen to any patient with respiratory symptoms. Strongly consider early intubation in patients with respiratory distress since rapid deterioration can develop and control of the airway can become difficult.
Gastric decontamination is contraindicated in caustic ingestions. In cases of large ingestions of strong acids, a nasogastric tube can be inserted for removal of stomach contents.
Dilution is only indicated if it can be performed within 30 minutes of ingestion in patients who can swallow without pain. Neutralization is not routinely recommended.
Early diagnostic endoscopy is indicated after intentional caustic ingestions. In unintentional ingestions, endoscopy is recommended only if the patient is symptomatic with stridor, significant oropharyngeal burns, vomiting, drooling, or food refusal. Endoscopy should be performed within 12 hours of ingestion to avoid iatrogenic perforation.
Steroids to decrease strictures are controversial and not routinely recommended.
Prophylactic antibiotics are not indicated.
Emergency laparotomy may be indicated for peritoneal signs or free air. Esophageal injuries with perforation may require surgery for mediastinitis. Delayed esophageal dilation or stenting may be necessary for strictures.
Systemic toxicity from acid ingestions such as acidosis, hemolysis, coagulopathy, and renal failure should be appropriately managed.
Treat ocular exposures, especially alkali, with copious irrigation and reassessment every 15 minutes. Conjunctival pH should be below 7.5 to 8.0 before irrigation is discontinued. Presence of corneal haziness or opacity, or limbal ischemia, requires ophthalmologic evaluation for possible anterior chamber irrigation.
Dermal exposures to caustics require copious irrigation with water. Exceptions include exposures to lime or caustic powders such as cement, which must be brushed off before irrigation.
Admit patients with symptomatic caustic ingestion. Grade 1 injuries of the esophagus can be discharged if tolerating oral intake. Grade 2A injuries require observation. Grade 2B and 3 injuries are at risk for perforation or bleeding and require admission to intensive care. Severe dermal burns may also require admission.
Hydrofluoric acid dermal exposures require additional treatment after irrigation. Treat small areas of exposed skin with topical calcium gluconate gel (commercially available or use 3.5 grams of powder mixed with five ounces of water-soluble surgical lubricant), applied to the area for 10 to 15 minutes until pain control is achieved and repeated every 4 to 8 hours as needed.
In non-digital areas, if relief is not obtained through topical application, or in cases of extensive exposure, consider intradermal calcium gluconate 5% (1:1 mix with NS) injected into the burn area with a maximum dose of 0.5 mL/cm2. In digits and hands, calcium gluconate (10 mL of 10% in 40 mL of NS or D5W) can be infused into the radial artery of the affected extremity over 4 hours.
Oral ingestions of hydrofluoric acid and severe dermal exposures (>20% concentration) require aggressive treatment: nasogastric aspiration of stomach contents within 60 minutes of ingestion followed by instillation of 300 mL of 10% calcium gluconate may be helpful; monitor serum calcium and magnesium levels closely and replace as needed; monitor and treat for hyperkalemia.
Suspected disc battery ingestions require a chest radiograph to exclude esophageal entrapment, which requires prompt endoscopic removal to prevent esophageal perforation from local pressure necrosis and alkaline release. Batteries in the stomach can be managed expectantly with a repeat radiograph in 24 to 48 hours to insure distal passage.
For further reading in Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed., see Chapter 194, “Caustics,” by Nicole C. Bouchard and Wallace A. Carter.