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.
Etiology:
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 algicides and “shock” agents. In general, alkaline products with pH >11 pose risk of significant corrosive injury.
Pathogenesis:
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.
Treatment:
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.
Alkaline Batteries
Ingestion of alkaline batteries poses a risk of GI tract corrosive injury and foreign body obstruction. Dogs are most commonly involved.
Etiology:
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.
Pathogenesis:
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.
Diagnosis:
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.
Treatment:
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 needed.
Cationic Detergents
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 habits.
Etiology:
Cationic detergents are present in a variety of algicides, 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.
Pathogenesis:
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.
Treatment:
Systemic signs should be treated symptomatically, eg, diazepam (0.5–2 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.
