Pathophysiology Of Caustic Injuries Alkali

Alkali injuries can induce deep tissue injury from liquefaction necrosis. After caustic alkali exposures, proteins are rapidly denatured and lipids undergo saponification. Initially, there is direct cellular destruction from contact with the alkali. This is followed by thrombosis of local microvasculature that leads to further tissue necrosis. Solid or granular alkali caustics often injure the oropharynx and proximal esophagus. Liquid alkali ingestions are characterized by esophageal injuries. Severe intentional alkali ingestion may cause multisystem organ injuries, including gastric perforation, and necrosis of abdominal viscera. Severe injuries to the pancreas, gallbladder, and small intestine after intentional ingestion have been reported. 2

The most common household alkali is bleach, a 3% to 6% sodium hypochlorite solution with a pH of approximately 11. Household liquid bleach is not corrosive to the esophagus, but ingestion may cause emesis secondary to gastric irritation or pulmonary irritation related to chlorine gas production in the stomach or when mixed with other substances.3 Other injuries reported with bleach include pneumonitis after aspiration and sight-limiting ocular injuries. Industrial strength bleach may contain much higher concentrations of sodium hypochlorite, and ingestion may result in esophageal necrosis.

Solid alkali ingestions may have greater potential for proximal esophageal tract injury and less for distal injury.

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