Acid or alkaline corrosives produce significant local tissue
injury that can result in full-thickness burns of skin, cornea, and the mucosa of
the oral cavity, esophagus, and stomach. All species are susceptible. Heavy coats
may provide some protection from dermal exposure.
Corrosives are divided into acid and alkaline corrosives.
Acidic household products include anti-rust compounds, toilet bowl cleaners,
gun-cleaning fluids, automotive batteries, swimming pool cleaning agents, and
etching compounds. Alkaline corrosive agents include drain openers, automatic
dishwasher detergents, toilet bowl cleaners, radiator cleaning agents, and
swimming pool algaecides and “shock” agents. In general, alkaline products with
pH >11 pose risk of significant corrosive injury.
Acids produce immediate coagulative necrosis of tissue and
impart significant pain on contact, which may limit exposure. Alkaline agents
produce immediate, penetrating liquefactive necrosis of tissue; the lack of
significant discomfort on contact with alkaline products may result in prolonged
exposure. For these reasons, burns from alkaline products tend to be deeper and
more extensive than burns from acidic agents. Burns from alkaline agents may
take up to 12 hr after exposure to become fully apparent, whereas the extent of
acid burns is usually evident shortly after contact. Esophageal burns are more
common with alkaline agents, and the absence of significant oral burns does not
necessarily indicate that no esophageal damage has developed. Full thickness
ulceration of the esophagus may result in pleuritis or peritonitis due to
leakage of ingesta into body cavities. Esophageal burns may result in stricture
formation during healing, resulting in dysphagia, megaesophagus, and aspiration
pneumonia. Additionally, although the contents of the stomach may serve to
buffer and dilute corrosive agents, gastric ulceration and possibly perforation
may occur with significant exposures. Respiratory exposure to corrosives
(especially acids) may result in respiratory distress, tracheobronchitis, or
pneumonitis. Dermal or ocular exposures may result in severe ulceration of
dermis or cornea.
Clinical Findings and Lesions
Clinical signs that may occur after ingestion of corrosive
agents include vocalization, hypersalivation, lethargy, polydipsia, vomiting
(with or without blood), abdominal pain, dysphagia, pharyngeal edema, dyspnea,
and oral, esophageal, and/or gastric ulceration. In severe cases, shock may
develop rapidly after exposure. Lesions are initially milky white to gray but
gradually turn black as eschar formation occurs. Necrotic tissue may slough
within days of exposure. Dyspnea, cyanosis, and pulmonary edema may occur
secondary to inhaled corrosive agents. Dermal exposure may result in significant
burns, with local pain, erythema, and tissue sloughing. Ocular exposure may
cause blepharospasm, epiphora, eyelid edema, conjunctivitis, or corneal
ulceration. Burns of skin, cornea, and GI mucosa range from mild ulceration to
full-thickness necrosis with extensive tissue sloughing. Peritonitis or
pleuritis may develop secondary to perforating ulcers of esophagus or stomach.
Respiratory lesions may include tracheitis, bronchitis, pneumonitis, pulmonary
edema, or aspiration pneumonia.
Because of the rapid action of corrosive agents, much of
the damage from exposure occurs before treatment can be started. Stabilization
of animals presenting as dyspneic, in shock, or with severe electrolyte
abnormalities is always a priority. For recent oral exposures, immediate
dilution with water or milk should be done. Under no circumstances should emesis
be attempted because of the risk of further mucosal exposure to corrosive
material. Likewise, gastric lavage is contraindicated because of the risk of
perforation of weakened esophageal/gastric walls and the risk of further
exposure of mucosa to the corrosive material as it is removed. Attempts to
chemically neutralize an acid with weak alkali (or alkali with weak acid) are
also contraindicated because of the production of exothermic reactions that can
result in thermal burns. Activated charcoal is ineffective in cases involving
ingestion of corrosives, and the presence of charcoal on damaged mucosa may
impede wound healing.
After dilution, general supportive care should be
instituted, including monitoring for respiratory difficulty, pain management,
antibiotics (if ulcers are present), and anti-inflammatories as needed.
Endoscopic evaluation of the esophagus and stomach for ulceration should be
performed ~12 hr after exposure; this time frame will allow the full extent of
tissue injury to become apparent. The use of corticosteroids in cases with
significant esophageal mucosal injury is controversial. Corticosteroids decrease
inflammation and may aid in minimizing stricture formation, but they also
suppress the immune system and may enhance susceptibility to secondary
infection. In animals with significant oral and/or esophageal burns, gastrostomy
tubes may be necessary to provide nutrition while affected tissues heal.
Dermal or ocular exposures should be managed by flushing
with copious amounts of water or physiologic saline; eyes should be flushed for
a minimum of 20 min, followed by fluorescein staining. Standard topical
treatments for dermal or ocular burns should be instituted as needed.
Ingestion of alkaline batteries poses a risk of GI tract
corrosive injury and foreign body obstruction. Dogs are most commonly
Alkaline batteries are present in many household
electronic products, including remote controls, hearing aids, toys, watches,
computers, and calculators. Most alkaline dry cell batteries use potassium
hydroxide or sodium hydroxide to generate currents. Nickel-cadmium and
lithium batteries also tend to contain alkaline material.
The alkaline gel in batteries causes liquefactive
necrosis of tissues on contact, resulting in burns that can penetrate deeply
into tissue. Lithium disk or “button” batteries may lodge in the esophagus
and generate a current against the esophageal walls, resulting in circular
ulcers that have the potential to be perforating. Some battery casings may
contain metals such as zinc or mercury, posing hazards of foreign body
obstruction and metal toxicosis if they remain in the stomach for prolonged
periods. Additionally, small batteries (especially disk batteries) may be
inhaled and pose a choking hazard.
Clinical Findings and Lesions
For discussion of alkaline burns, see Corrosives. Foreign body obstruction may
present as vomiting, anorexia, abdominal discomfort, or tenesmus.
Respiratory obstruction due to battery inhalation may present with acute
onset of dyspnea and cyanosis. Mucosal burns may occur within the oral
cavity, esophagus, and less commonly, stomach. Perforation of the esophagus
may lead to secondary pyothorax, while gastric perforation may result in
acute blood loss and/or peritonitis.
Radiographs may help to confirm the diagnosis as well
as the location of the battery; however, some disk batteries do not show up
well on radiographs. Differential diagnoses include GI or respiratory
foreign bodies and other oral, dermal, or ocular corrosive agents.
For batteries swallowed intact without any chewing,
induction of emesis may result in expulsion. Because of the risk of leakage
of alkaline gel onto oral and esophageal mucosa during vomiting, emesis
should not be induced if there is any possibility that the battery casing
has been punctured. When disk batteries have been ingested, 20 mL boluses of
tap water every 15 min will decrease the severity and delay the development
of current-induced esophageal ulceration. The decision on whether to remove
a battery from the stomach depends on the size of the animal, battery size,
and evidence of battery puncture. Radiography may be performed to determine
the location of the battery casing; generally, batteries that have passed
through the pylorus will pass through the intestinal tract uneventfully
(adding bulk to the diet and judicious use of cathartics may facilitate
passage). Serial radiography to verify battery location is recommended until
the battery is expelled. Batteries that do not pass through the pylorus
within 48 hr of ingestion are unlikely to pass on their own and may require
surgical or endoscopic removal. Batteries that have obviously been punctured
should be removed surgically to prevent gastric or intestinal ulceration due
to leakage of alkaline gel. Endoscopic removal is not recommended in cases
in which it is suspected that the battery casing has been punctured.
Treatment of cases with suspected oral, esophageal, or gastric ulceration is
the same as for other alkaline corrosive injuries (see Corrosives). Dermal or ocular exposures to alkaline gels should
be managed by copious rinsing of the area with tap water (skin) or
physiologic saline solution (eyes). The affected areas should be monitored
for development of ulcers, and topical therapy administered as
Exposure to cationic detergents may result in local
corrosive tissue injury as well as severe systemic effects. All species are
susceptible. Cats are at increased risk of oral exposure because of grooming
Cationic detergents are present in a variety of
algaecides, germicides (including quaternary ammonium compounds),
sanitizers, fabric softeners (including dryer softener sheets), and liquid
potpourris. Concentrations of cationic detergents ≤2% have been associated
with oral mucosal ulcers in cats.
Cationic detergents are locally corrosive agents,
causing dermal, ocular, and mucosal injury similar to that of alkaline
corrosive agents. Additionally, exposure to cationic detergents may result
in systemic effects ranging from CNS depression to pulmonary edema. The
mechanism for these systemic effects is not known.
Clinical Findings and Lesions
Signs of oral exposure include oral ulceration,
stomatitis, pharyngitis, hypersalivation, swollen tongue, depression,
vomiting, abdominal discomfort, and increased upper respiratory noises
within 6–12 hr of ingestion. Affected animals frequently have significant
fever and increases in WBC counts. Systemic effects include metabolic
acidosis, CNS depression, hypotension, coma, seizures, muscular weakness and
fasciculation, collapse, and pulmonary edema. Dermal irritation, erythema,
ulceration, and pain are possible with dermal contact. Conjunctivitis,
blepharospasm, eyelid edema, lacrimation, and corneal ulceration may be seen
secondary to ocular exposure. Lesions can include GI, ocular, or dermal
irritation or ulceration.
Systemic signs should be treated symptomatically, eg,
diazepam (0.5–2.0 mg/kg, slow IV) for seizures, fluid therapy for
hypotension, etc. Because of the potential for corrosive mucosal injury,
induction of emesis and administration of activated charcoal are
contraindicated with cationic detergents. For recent oral exposures, milk or
water can be given for dilution, and the animal monitored for development of
oral or esophageal burns. Oral burns should be treated the same as other
corrosive injuries (see Corrosives). Dermal and
ocular exposures should be managed by thorough flushing of the affected area
with tepid water or physiologic saline, followed by monitoring for
development of dermal or ocular irritation or ulceration. Topical treatment
for dermal or ocular burns should be instituted as needed; in severe cases,
analgesics may be indicated.
Last full review/revision May 2013 by Sharon M. Gwaltney-Brant, DVM, PhD, DABVT, DABT