1) Caustic ingestions can cause serious damage through chemical reactions that alter tissue structure. Strong acids and bases pose the highest risk. 2) Ingestions most commonly affect children accidentally and adults intentionally, with thousands of cases annually resulting in esophageal burns. 3) Alkalis cause "liquefactive necrosis" through fat saponification and protein solubilization. Acids induce "coagulation necrosis" through protein denaturation, forming a protective eschar.

1. Caustic
ingestions
Yousef Al-Khadher

4. • Caustic ingestion is a serious
medical problem with a variety of
clinical presentations and a
complicated clinical course.
General characteristics

5. 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.

6. • 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

7. • 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

9. 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.

10. • 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.

11. 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.

12. • 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.

13. Liquefactive necrosis

14. • 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

15. • 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

16. • 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

18. • 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

19. • 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

20. • 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

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