You are on page 1of 46

TOXICITY, CAUSTIC

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

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.
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.
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.
History
The physician should try to identify the specific agent ingested, as
well as the concentration, pH, and amount of substance ingested. The
time, nature of exposure, duration of contact, and any immediate on-
scene treatment are important in determining management of toxicity.
The presence or absence of the following symptoms should be
determined since the presence of any of these symptoms suggests the
possibility of significant internal injury. However, their absence does
not preclude significant injury.
Dyspnea
Dysphagia
Oral pain and odynophagia
Chest pain
Abdominal pain
Nausea and vomiting
Rapidly obtaining reliable information on the
particular agent involved is vital. This is particularly true of
uncommon caustic agents, some of which have important
toxic concerns beyond those of a simple caustic ingestion.
A good example of this is the potential for abrupt, life-
threatening hypocalcemia following ingestion of hydrogen
fluoride, even in a relatively dilute form such as that found
in some rust removers. Case reports of patients surviving
such suicidal ingestions underline the value of being able to
anticipate and aggressively manage the systemic
hypocalcemia, which is unique to hydrogen fluoride, with
intravenous calcium. Other examples of caustic agents with
unique toxicities include phenol, zinc chloride, and mercuric
chloride, all of which can cause significant systemic toxicity
and which may require significant changes in management.
Physical
As with the history, physical examination
findings 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:
Stridor
Hoarseness
Dysphonia or aphonia
Respiratory distress, tachypnea, hyperpnea
Cough
Other signs of injury may include the
following:
Tachycardia
Oropharyngeal burns - These are important when
identified; however, significant esophageal
involvement may occur in the absence of
oropharyngeal lesions.
Drooling
Subcutaneous air
Acute peritonitis - Abdominal guarding, rebound
tenderness, and diminished bowel sounds
Hematemesis
Indications of severe injury - Altered mental
status, peritoneal signs, evidence of viscous
perforation, stridor, hypotension, and shock
Causes
Common acid-containing Common alkaline-
sources containing sources
Toilet bowl cleaning Drain cleaning products
products Ammonia-containing
Automotive battery liquid products
Rust removal products Oven cleaning products
Metal cleaning products Swimming pool cleaning
Cement cleaning products
products Automatic dishwasher
Drain cleaning products detergent
Soldering flux containing Hair relaxers
zinc chloride Clinitest tablets
Bleaches
Cement
Differential Diagnoses
Burns, Chemical Pneumonia, Toxicity, Chlorine Gas
Gastrointestinal Aspiration Munchausen
Bleeding Gastroesophageal Syndrome
Burns, Thermal Reflux Disease Toxicity, Iron
Pertussis Pneumonia, Bacterial Anaphylaxis
Dysphagia Hemolysis Toxicity, Mercury
Perforated Peptic Renal failure Bronchiolitis
Ulcer Hydrofluoric acid Vomiting
Epiglottitis, Adult Shock (many Croup or
Phenol potential causes) Laryngotracheobronc
Esophageal Hypocalcemia hitis
Perforation, Rupture Strictures, especially Zinc chloride
and Tears gastric Epiglottitis
Plant Poisoning, Mercury chloride Gastroenteritis
Oxalates Stridor
Esophagitis Metabolic Acidosis
Other Problems
Airway obstruction may occur secondary to edema,
bleeding, and the presence of necrotic material.
Because this can develop rapidly, airway protection
is paramount following caustic ingestions. Delays in
securing a definitive airway can result in increased
difficulty due to progressive airway edema.
Esophageal gastric, bowel, airway, or vascular
perforation may occur.
Fluid losses from vomiting, third spacing, and
gastrointestinal bleeding may lead to hypovolemia
and shock. This is particularly true after ingestion of
metallic chlorides.
After significant acidic ingestions, the patient
may develop metabolic acidosis, hemolysis,
and multiorgan failure including acute renal
failure.
Hypocalcemia develops precipitously after
ingestion of significant amounts of hydrogen
fluoride.
In patients who survive the initial phases of
injury, late-developing problems include
strictures, fistula, hypomotility disorders, and
an increased risk of gastrointestinal cancers.
Laboratory Studies
pH testing of product
A pH less than 2 or greater than 12.5 indicates greater
potential for severe tissue damage.5
A pH outside of this range does not preclude significant
injury.
pH testing of saliva: Unexpected high or low values may
confirm ingestion in questionable cases; however, a
neutral pH cannot rule out a caustic ingestion.
Complete blood count (CBC), electrolyte levels, BUN
(blood urea nitrogen)levels, creatinine level, and ABG (Arterial
Blood Gas) levels may all be helpful as baseline values and
as indications of systemic toxicity.
Liver function tests and DIC panel may also be helpful to
establish baselines or, if abnormal, confirm severe injury
following acid ingestions.
Urinalysis and urine output may help guide fluid
replacement.
Type and cross are indicated for any potential
surgical candidates or those with the potential
for gastrointestinal bleeding.
Obtain aspirin and acetaminophen levels as well
as an ECG in any patient whose intent may have
been suicidal.
In cases of hydrofluoric acid (HF) ingestion,
precipitous falls in calcium level may lead to
sudden cardiac arrest. Although ionized calcium
levels are likely to have too long a turnaround to
be clinically useful, cardiac monitoring and serial
ECGs may help anticipate this event.
Imaging Studies
Chest radiography: Obtain an upright chest radiograph in
all cases of caustic ingestion. Findings may include
pneumomediastinum or other findings suggestive of
mediastinitis, pleural effusions, pneumoperitoneum,
aspiration pneumonitis, or a button battery (metallic
foreign body). However, the absence of findings does not
preclude perforation or other significant injury.
Abdominal radiography: Findings may include
pneumoperitoneum, ascites, or an ingested button battery
(metallic foreign body).
If contrast studies are obtained, water-soluble contrast
agents are recommended because they are less irritating to
the tissues in cases of perforation.
CT (X-ray computed tomography) will often be able to
delineate small amounts of extraluminal air, not seen on
plain radiographs.
Procedures
Airway protection is critical following caustic ingestion if
there is any indication of airway compromise. This can develop
rapidly and be complicated by multiple factors.
Cardiac monitoring is indicated for any patient with a caustic
ingestion.
Large-bore intravenous access allows administration of fluids
and medications as needed.
Endoscopy is generally inicated for the following patients:
Small children
Symptomatic older children and adults
Patients with altered mental status
Patients with intentional ingestions
Others with a potential for significant injury (eg, ingestion
or large volumes or concentrated products)
However, because of the risk of increased injury,
esophagoscopy should not be performed in patients with
evidence of esophageal or gastrointestinal perforation,
significant airway edema, or necrosis and in those who
are hemodynamically unstable.
Obtaining meaningful information from endoscopy after
treatment with activated charcoal is very difficult.
Routine use of activated charcoal is not recommended in
caustic ingestions.
Endoscopic ultrasonography has been shown to more
accurately show the depth of lesions than endoscopy
alone. Further studies will be necessary to determine the
utility of this procedure in aiding in diagnosis and
treatment.
Treatment
Prehospital Care
Attempt to identify the specific product,
concentration of active ingredients, and estimated
volume and amount ingested. Obtain MSDS
(Material Safety Data Sheet) 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, although controversial,
may be beneficial if administered as soon as
possible after a solid or granular alkaline ingestion,
to remove any adhering particles 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.
Some authors discourage 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.
Emergency Department Care
In the treatment area, patients suspected of ingesting
a caustic substance should be triaged to a high priority
for prompt evaluation and treatment. This includes
prompt evaluation of airway and vital signs as well as
immediate cardiac monitoring and intravenous access.
Airway control
Because of the risk of rapidly developing airway edema,
immediate assessment of the patients airway and mental
status should be performed and continually monitored.
Equipment for endotracheal intubation and
cricothyrotomy should be readily available. Gentle
orotracheal intubation or fiberoptic-assisted intubation is
preferred. Blind nasotracheal intubation should be avoided
due to the increased risk of soft-tissue perforation.
If possible, it is best to avoid inducing paralysis
for intubation because of the risk of anatomical
distortion from bleeding and necrosis. If a
difficult airway is anticipated, IV ketamine can
be used to provide enough sedation to obtain a
direct look at the airway.
Cricothyrotomy or percutaneous needle
cricothyrotomy may be necessary in the
presence of extreme tissue friability or
significant edema.
Gastric emptying and
decontamination
Do not administer emetics because of risks of
re-exposure of the vulnerable mucosa to the
caustic agent. This may result in further injury or
perforation.
Gastric lavage by traditional methods using
large-bore orogastric Ewald tubes are
contraindicated in both acidic and alkaline
ingestions because of risk of esophageal
perforation and tracheal aspiration of stomach
contents.
Large-volume liquid acid ingestions may benefit
from nasogastric tube (NGT) suction if performed
rapidly after ingestion. Pyloric sphincter spasm may
prolong contact time of the agent to the gastric
mucosa for up to 90 minutes. NGT suction may
prevent small intestine exposure. Esophageal
perforation is rare. NGT suction may be of particular
value following ingestion of zinc chloride, mercuric
chloride, or hydrogen fluoride, unless signs of
perforation are present. This should be done after
consulting with a regional poison control center.
Activated charcoal is relatively contraindicated in
caustic ingestions because of poor adsorption and
endoscopic interference.
Dilution: Dilution may be beneficial for ingestion of solid or
granular alkaline material if performed within 30 minutes
after ingestion using small volumes of water. Because of
the risk of emesis, carefully consider the risks versus
benefits of dilution.
Do not dilute acids with water because of excessive heat
production.
Neutralization: Do not administer a weak acid in alkaline
ingestions or a weak alkaline agent in acid ingestions. There
is a risk of heat production resulting from this exothermic
reaction. In addition, the risk of emesis makes this a
hazardous intervention.
Intravenous fluids and blood products may be required in
the event of significant bleeding, vomiting, or third spacing.
Consultations

Airway management can be a


multifaceted problem and may be best
approached with the availability of a wide array
of visualization techniques, and, if time allows,
a team of experts. However, the rapid
development of airway edema may prompt the
need for rapid airway management with the
best immediately available visualization
approach.
Obtain a surgical consultation when the
following are expected or observed:
Perforation
Mediastinitis
Peritonitis
Obtain an endoscopic consultation for the
following patients:
Small children
Symptomatic older children and adults
Patients with altered mental status
Patients with intentional ingestions
Others with a potential for significant injury (eg,
ingestion or large volumes or concentrated
products)
Consultation with the local poison control
center may be helpful, particularly if unfamiliar
or unique agents are involved. These may
include industrial strength detergents, button
batteries, zinc chloride, mercuric chloride,
hydrogen fluoride, phenol, and Clinitest
tablets.
Once a patient is stabilized, obtain a
psychiatric consultation for any patients with a
history of an intentional ingestion.
Medication
Supportive care, rather than specific antidotes, is
the mainstay of management following caustic
ingestions. A significant exception to this would be the
aggressive administration of intravenous calcium for
dysrhythmias precipitated by hypocalcemia from
hydrogen fluoride ingestion. Such therapy is best
performed with the guidance of the toxicologist at the
local poison center.
The use of corticosteroids, previously proposed to
be beneficial, should be discouraged. Studies have
shown that stricture formation is based on the depth
of the tissue damage.
The following agents may be of value in supportive
care.
Antibiotic, Cephalosporin (Third
Generation)
These agents should be administered if evidence of
perforation exists. A third-generation cephalosporin or
ampicillin/sulbactam may be considered.
Proton Pump Inhibitor
Proton pump inhibitors reduce exposure of injured
esophagus to gastric acid, which may result in decreased
stricture formation.
Analgesic, Narcotic
Narcotic analgesics should be used to reduce the pain
associated with these ingestions.
Deterrence/Prevention
Caustic substances should be kept in their
original labeled containers to avoid accidental
ingestion. They should be stored out of reach
of toddler-aged children.
Workplace policies and procedures need to be
developed and disseminated, so that
employee exposures can be treated quickly
and effectively.
Complications
Airway edema or obstruction may occur
immediately or up to 48 hours following an
alkaline exposure.
Gastroesophageal perforation may occur acutely.
Secondary complications include mediastinitis,
pericarditis, pleuritis, tracheoesophageal fistula
formation, esophageal-aortic fistula formation, and
peritonitis.
Delayed perforation may occur as many as 4 days after
an acid exposure.
Deep circumferential or deep focal burns may result in
strictures in more than 70% of patients; these
strictures typically develop 2-4 weeks postingestion.
Gastric outlet obstruction may develop 3-4 weeks after an acid
exposure.
Upper gastrointestinal hemorrhage may occur acutely in caustic
exposures.
Delayed upper GI bleeding may occur in acid burns 3-4 days after
exposure as the eschar sloughs.
Though many button batteries may pass through the GI tract
without causing damage, they can result in perforation at any
time during their course through the gastrointestinal system,
particularly if they are damaged.
Zinc chloride, mercuric chloride, and phenol can all cause
significant systemic toxicity.
Cardiac arrest from sudden hypocalcemia may occur in patients
who have ingested hydrogen fluoridecontaining substances.
Patients have been successfully resuscitated with aggressive use
of intravenous CaCl2.
Long-term risks include squamous cell carcinoma, which
occurs in 1-4% of all significant exposures and may occur
as late as 40 years after exposure.
Prognosis
The prognosis is directly proportional to the degree
of tissue damage, which is primarily a function of
the duration of exposure and the physical
properties of the agent involved. These include the
pH, the volume, and concentration of the agent; its
ability to penetrate tissues; and its titratable
reserve. The titratable reserve is a term that reflects
the amount tissue required to neutralize a given
amount of agent.
Some agents have the ability to cause systemic
toxicity that affects the prognosis in addition to
their caustic properties. These include phenol, zinc
chloride, mercuric chloride, and hydrogen fluoride.