Acid and alkali poisoning

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.
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.
 Significant exposures may also result in gastrointestinal absorption of the acidic
substances leading to significant metabolic acidosis, hemolysis, acute renal failure, and death.

Treatment
 Attempt to identify the specific product, concentration of active ingredients, and
estimated volume and amount ingested. Obtain MSDS sheets when possible for
workplace exposures. The product container or labels may be available. Avoid
exposure to health care workers.
 Do not induce emesis or attempt to neutralize the substance by using a weak acid or
base. This induces an exothermic reaction, which can compound the chemical injury
with a thermal injury. It may also induce emesis, re-exposing tissue to the caustic
agent.
 Small amounts of a diluent may be beneficial if administered as soon as possible after
a solid or granular alkaline ingestion, to remove any particles that are adhering to the
oral or esophageal mucosa. Water or milk may be administered in small amounts. It is
very unlikely to be of any benefit after more than 30 minutes.
 This practice is controversial: Some of the literature available on this topic
discourages the use of diluents because of the concern of inducing emesis resulting in
re-exposure of tissue to caustic agent.
 Diluents should not be used with any acid ingestion or liquid alkaline
ingestion. The risk of vomiting with re-exposure of the oral or esophageal mucosa to
the offending substance can result in worsening injury or perforation.