Caustic ingestions

Yousef Al-Khadher

• Caustic ingestion is a serious

medical problem with a variety of

clinical presentations and a complicated clinical course.

General characteristics

General characteristics• 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 ) or donating a proton

(acidic) 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.

General characteristics

• 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

1. the duration of contact;

2. the amount and state (liquid, solid)

3. the substance’s physical properties, such as its

pH, concentration, ability to penetrate tissue,

4. and its titratble reserve.

General characteristics

Epidemiology & mood of toxicity

• An estimated 5000 to 15000 caustic ingestions occur

per year. The age of occurrence of these ingestions

shows a bimodal pattern. The 1st peak is seen in

children aged 1 to 5 years, with most of these

ingestions being accidental, though reports of child

abuse have been reported . This problem in

children is spreading in developing countries

because these agents become more available.

• The other peak age is seen among adults aged 21

years and older, most of them are intentional

suicide attempts.

• In children, 18% to 46% of all caustic

ingestions are associated with

esophageal burns. This number may

be higher in adults who often consume

larger amounts of the caustic

substance as part of a suicide

attempt.

Mechanism • 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 ingestion 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.

Liquefactive necrosis

• 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.

Mechanism

• 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.

Mechanism

• 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.

Mechanism

• 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.

Mechanism

• Unlike alkaline, 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.

Mechanism

• 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.

Mechanism

• Significant exposures may also

result in gastrointestinal

absorption of the acidic

substances leading to

significant metabolic

acidosis, hemolysis, acute

renal failure, and death.

Mechanism