LIQUEFACTIVE AND

COAGULATIVE
NECROSIS
PROCEDURE:
Place a strip of pig mesentery or

01 intestine measuring 4 x 4 cm on
each of three evaporating dishes.

Dish 1 = instill 1 mL HCl.

Dish 2 = instill 1 mL NaOH.

02
Dish 3 = instill 1 mL HCl. After 1 minute,
instill NaOH on the same tissue.
Dish 4 = instill 1 mL NaOH. After 1
minute, instill HCl on the same tissue.

Observe the effects of each

03 chemical on the tissues by giving the

grade based on the scoring system
below.
SCORING SYSTEM:
CAUSTICS AND CORROSIVES
• Can cause tissue injury by a chemical reaction.

• The vast majority of caustic chemicals are acidic or alkaline

substances.
➢ damage tissue by:
accepting a proton (alkaline substance)
donating a proton (acidic substance) in an aqueous
solution.
CAUSTICS AND CORROSIVES
• The pH of a chemical
➢ measures of how easily the chemical accepts or donates a
proton.

➢ This relates to the strength of the acidic or alkaline

substance,

➢ provides some, but not precise correlation with the

likelihood of injury.
CAUSTICS AND CORROSIVES
• 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.
CAUSTICS AND CORROSIVES
• 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) of the substance
involved;
3. the substance's physical properties
a. pH
b. concentration
c. ability to penetrate tissue
d. titratable reserve.
 PATHOPHYSIOLOGY
OF ALKALINE AND
ACIDIC INGESTION

• 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
• Cause tissue injury by liquefactive necrosis.
➢ a process that involves:
▪ Saponification of fats
▪ solubilization of proteins.

➢ Cell death occurs from:

▪ emulsification
▪ disruption of cellular membranes
➢ allowing the alkaline substance to diffuse into deeper
layers of the mucosa.
ALKALINE INGESTIONS
• 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.

ALKALINE INGESTIONS
• 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
1. oropharynx,
2. hypopharynx,
3. esophagus.
is the most commonly involved organ with the stomach
much less frequently involved after alkaline ingestions.
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.
ALKALINE INGESTIONS
• 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,

➢ Full-thickness burns result in strictures in nearly 100% of cases.
• The most severe burns also may be associated
with esophageal perforation.
COMMON ALKALINE-CONTAINING SOURCES
• Drain-cleaning products
• Ammonia-containing products
• Oven-cleaning products
• Swimming pool – cleaning products
• Automatic dishwasher detergent
• Hair relaxers
• Clinitest tablets
• Bleaches
• Cement
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.
ACID INGESTIONS
• 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.

COMMON ACID-CONTAINING SOURCES
• Toilet bowl – cleaning products
• Automotive battery liquid
• Rust-removal products
• Metal-cleaning products
• Cement-cleaning products
• Drain-cleaning products
• Soldering flux containing zinc
chloride
HISTORY TAKING
• To determine the management of toxicity, the physician
should try to identify
1. the specific agent ingested
2. concentration
3. pH
4. amount of substance ingested
5. time
6. nature of exposure
7. duration of contact
8. any immediate on-scene treatment
HISTORY TAKING
• The presence or absence of the following symptoms should be
determined
• Dyspnea
• Dysphagia
• Oral pain and odynophagia
• Chest pain
• Abdominal pain
• Nausea and vomiting
PHYSICAL EXAMINATION
➢May be deceptively unremarkable after a significant caustic
ingestion, despite the presence of significant tissue necrosis.

➢ Signs of impending airway obstruction may include the

following:
1. Stridor
2. Hoarseness
3. Dysphonia or aphonia
4. Respiratory distress, tachypnea, hyperpnea
5. Cough
PHYSICAL EXAMINATION
Other signs of injury may include the following:
1. Tachycardia
2. Oropharyngeal burns
These are important when identified; however, significant
esophageal involvement may occur in the absence of
oropharyngeal lesions
3. Drooling
4. Subcutaneous air
5. Acute peritonitis
Abdominal guarding, rebound tenderness, and diminished
bowel sounds
6. Hematemesis
PHYSICAL EXAMINATION
Indications of severe injury include the following:
1. Altered mental status
2. Peritoneal signs
3. Evidence of viscus perforation
4. Stridor
5. Hypotension
6. Shock
INITIAL EVALUATIONS
• NPO status with IV fluids

• Labs: CBC, BMP, and ABG levels as well as urinalysis to provide

baseline values and as indications of systemic toxicity.

• In the case of hydrofluoric acid ingestion (found in some rust

removers), calcium levels should be monitored closely.

• Chest and abdominal X-rays are taken to look for

pneumomediastinum, pleural effusions, aspiration pneumonitis,
pneumoperitoneum, and/or a disk battery.

In the case of disk batteries lodged in the esophagus, immediate

removal is required.
INITIAL EVALUATIONS
• Endoscopy should be performed within the first 12-48 hours
following ingestion.

• Tissue damage is graded on a scale of 0 to 3 with 0 being

normal mucosa.
INITIAL EVALUATIONS
• Grade 1 involves injury limited to edema and erythema of the
mucosa.

• Grade 2A burns are transmucosal, linear ulcerations and

necrotic tissue with whitish plaques and/or hemorrhages.

• Grade 2B burns have Grade 2A findings but are

circumferential.

• Grade 3 burns are transmural and involve ulceration and

necrosis and even perforation.
• Circumferential burns are most likely to lead to stricture formation.
INITIAL EVALUATIONS
For any burn grade 2B or 3

• it is recommended to place a nasogastric (NG) tube under

direct endoscopic visualization.
➢ This helps stent open the injured area
➢ A means to provide nutrition during the healing phase.
➢ Additionally, NG tube suction may be beneficial in
treating large volume liquid acid ingestions to help
minimize damage to the stomach and small intestine.
INITIAL EVALUATIONS
• Do not induce emesis as vomiting may lead to additional
esophageal injury and even perforation.

• Gastric lavage is also contraindicated due to risk of

esophageal perforation and tracheal aspiration of stomach
contents.

• Neutralization should never be attempted because it is

exothermic, potentially further exacerbating tissue damage.
INITIAL EVALUATIONS
• It is also not recommended to attempt dilution of ingested
material.
➢ Any attempts greater than 30 minutes after ingestion are
• unlikely to be beneficial
• and there is a risk of inducing emesis with this technique.
INITIAL EVALUATIONS
• Steroids do not protect against the development of
esophageal strictures and may even be harmful.

• Third-generation cephalosporin or ampicillin/sulbactam

if there is evidence of perforation.

• Narcotics are beneficial in reducing pain associated with

caustic ingestions.