Background
Caustics and corrosives cause tissue injury by a chemical reaction. The vast majority of caustic chemicals are acidic or alkaline substances that damage tissue by accepting a proton (alkaline substance) or donating a proton (acidic substance) in an aqueous solution.
The pH of a chemical is a measure of how easily the chemical accepts or donates a proton. This relates to the strength of the acidic or alkaline substance, and provides some, but not precise correlation with the likelihood of injury. Substances with a pH less than 2 are considered to be strong acids; those with a pH greater than 12 are considered to be strong bases. The severity of tissue injury from acidic and alkaline substances is determined by the duration of contact; the amount and state (liquid, solid) of the substance involved; and the substance's physical properties, such as its pH, concentration, ability to penetrate tissue, and its titratable reserve. The latter reflects the amount of tissue required to neutralize a given amount of the involved substance and is particularly useful for measuring the amount of damage that can be caused by caustics, such as phenol, which have a near-neutral pH.
Pathophysiology
Caustic chemicals produce tissue injury by altering the ionized state and structure of molecules and disrupting covalent bonds. In aqueous solutions, the hydrogen ion (H+) produces the principle toxic effects for the majority of acids, whereas the hydroxide ion (OH-) produces such effects for alkaline substances.
Alkaline ingestions
Alkaline ingestions cause tissue injury by liquefactive necrosis, a process that involves saponification of fats and solubilization of proteins. Cell death occurs from emulsification and disruption of cellular membranes. The hydroxide ion of the alkaline agent reacts with tissue collagen and causes it to swell and shorten. Small vessel thrombosis and heat production occurs.
Severe injury occurs rapidly after alkaline ingestion, within minutes of contact. The most severely injured tissues are those that first contact the alkali, which is the squamous epithelial cells of the oropharynx, hypopharynx, and esophagus. The esophagus is the most commonly involved organ with the stomach much less frequently involved after alkaline ingestions. Tissue edema occurs immediately, may persist for 48 hours, and may eventually progress sufficiently to create airway obstruction. Over time, if the injury was severe enough, granulation tissue starts to replace necrotic tissue.
Over the next 2-4 weeks, any scar tissue formed initially remodels and may thicken and contract enough to form strictures. The likelihood of stricture formation primarily depends upon burn depth. Superficial burns result in strictures in fewer than 1% of cases, whereas full-thickness burns result in strictures in nearly 100% of cases. The most severe burns also may be associated with esophageal perforation.
Acid ingestions
Acid ingestions cause tissue injury by coagulation necrosis, which causes desiccation or denaturation of superficial tissue proteins, often resulting in the formation of an eschar or coagulum. This eschar may protect the underlying tissue from further damage. Unlike alkali ingestions, the stomach is the most commonly involved organ following an acid ingestion. This may due to some natural protection of the esophageal squamous epithelium. Small bowel exposure also occurs in about 20% of cases. Emesis may be induced by pyloric and antral spasm.
The eschar sloughs in 3-4 days and granulation tissue fills the defect. Perforation may occur at this time. A gastric outlet obstruction may develop as the scar tissue contracts over a 2- to 4-week period. Acute complications include gastric and intestinal perforation and upper gastrointestinal hemorrhage.
Endoscopic view of the esophagus after ingestion of an acid is shown in the images below.
Toxicity, caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the extensive thrombosis of the esophageal submucosal vessels giving the appearance similar to chicken wire. Courtesy of Ferdinando L. Mirarchi, DO, Fred P. Harchelroad Jr, MD, Sangeeta Gulati, MD, and George J. Brodmerkel Jr, MD.
Toxicity, caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the appearance of the thrombosed esophageal submucosal vessels giving the appearance of chicken wire. Courtesy of Ferdinando L. Mirarchi, DO, Fred P. Harchelroad Jr, MD, Sangeeta Gulati, MD, and George J. Brodmerkel Jr, MD.
Toxicity, caustic ingestions. Endoscopic view of the esophagus in a patient who ingested hydrochloric acid (Lime-a-way). Note the extensive burn and thrombosis of the submucosal esophageal vessels, which gives the appearance of chicken wire. Courtesy of Ferdinando L. Mirarchi, DO, Fred P. Harchelroad Jr, MD, Sangeeta Gulati, MD, and George J. Brodmerkel Jr, MD. Significant exposures may also result in gastrointestinal absorption of the acidic substances leading to significant metabolic acidosis, hemolysis, acute renal failure, and death.
Epidemiology
Frequency
United States
Ingestions of caustic substances accounted for more toxic exposures than any other class of agents. Cleaning substances, many of which contain potentially caustic agents, account for more than 200,000 exposures per year reported to US poison control centers.[1, 2, 3, 4]
Mortality/Morbidity
The alkali drain cleaners and acidic toilet bowl cleaners are responsible for the most fatalities from corrosive agents.
- Approximately 10% of caustic ingestions result in severe injury requiring treatment.
- Between 1% and 2% of caustic ingestions results in stricture formation.
Race
No race predilection exists.
Sex
No sex predilection exists.
Age
Childhood ingestions: Approximately 80% of caustic ingestions occur in children younger than 5 years. Critical solid ingestions are rare because children generally do not swallow the burning particles that adhere to their oropharynx. Liquid ingestions, however, can be quite serious.
Adult ingestions: Most intentional ingestions occur in adults. Adult exposures have increased morbidity than childhood exposures because of the often higher volume of the exposure and the presence of possible co-ingestants. Occupational exposures often are more severe than other exposures because industrial products are more concentrated than those found in the home.
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