Toxicoses From Corrosive Agents in Animals

Corrosive agents can be acidic or alkaline:

• 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 super-chlorination agents (so-called pool shock treatments).

In general, alkaline products with pH > 11 pose a risk of notable corrosive injury.

In corrosive-agent toxicoses, extent of local tissue injury is related to the area affected and duration of contact.

Acids produce immediate coagulative necrosis of tissue and impart marked pain on contact, which can limit exposure. The extent of acid burns is usually evident shortly after contact.

Alkaline agents produce immediate, penetrating liquefactive necrosis of tissue. However, the lack of notable discomfort on contact with alkaline products can result in prolonged exposure, and burns from alkaline products tend to be deeper and more extensive than burns from acidic agents. Burns from alkaline agents can take up to 12 hours after exposure to become fully apparent. Esophageal burns are more common with alkaline agents, and the absence of notable oral burns does not necessarily indicate that no esophageal damage has developed.

Full-thickness ulceration of the esophagus can result in pleuritis or peritonitis because of the leakage of ingesta into body cavities. Esophageal burns can lead to stricture formation during healing, resulting in dysphagia, megaesophagus, and aspiration pneumonia. In addition, although the contents of the stomach can buffer and dilute corrosive agents, gastric ulceration and possibly perforation can occur in cases of extensive exposure.

Respiratory exposure to corrosive agents (especially acids) can result in respiratory distress, tracheobronchitis, or pneumonitis.

Dermal or ocular exposures can result in severe ulceration of the dermis or cornea.

Clinical signs of corrosive-agent toxicosis that can occur after ingestion include vocalization, hypersalivation, lethargy, polydipsia, vomiting (with or without blood), abdominal pain, dysphagia, pharyngeal edema, dyspnea, and oral, esophageal, and gastric ulceration. In severe cases, shock can develop rapidly after exposure.

Lesions are initially milky white to gray; however, they gradually turn black as eschar formation occurs. Necrotic tissue can slough within days of exposure.

Dyspnea, cyanosis, and pulmonary edema can occur secondary to inhalation of corrosive agents. Respiratory lesions can include tracheitis, bronchitis, pneumonitis, pulmonary edema, or aspiration pneumonia.

Dermal exposure can result in notable burns, with local pain, erythema, and tissue sloughing.

Ocular exposure can result in 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 can develop secondary to perforating esophageal or gastric ulcers.

• Decontamination by administration of neutral fluids

• Supportive care for corrosive injury to tissues

Because of the rapid action of corrosive agents, much of the damage from exposure occurs before treatment can be started. Stabilization of patients with dyspnea, shock, or severe electrolyte abnormalities is always a priority. Recent oral exposures should be treated by immediate dilution with water or milk.

Under no circumstances should emesis be attempted, because of the risk of further mucosal exposure to corrosive material. Similarly, gastric lavage is contraindicated because of the risk of perforation of weakened esophageal and 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 corrosive agents, and the presence of charcoal on damaged mucosa can impede wound healing.

Dilution should be followed by general supportive care, including monitoring for respiratory difficulty, managing pain, and administering antimicrobials (if ulcers are present) and anti-inflammatories as needed.

The esophagus and stomach should be endoscopically evaluated for ulceration approximately 12 hours after exposure; this time frame allows the full extent of tissue injury to become apparent.

Administration of corticosteroids in cases with extensive esophageal mucosal injury is controversial. Corticosteroids decrease inflammation and can help minimize stricture formation; however, they also suppress the immune system and can increase susceptibility to secondary infection. In patients with substantial oral or esophageal burns, gastrostomy tubes might be necessary to provide nutrition while affected tissues heal.

Dermal or ocular exposures should be managed by flushing with copious amounts of water or saline (0.9% NaCl) solution. Eyes should be flushed for a minimum of 20 minutes, and then the cornea should be stained with fluorescein to detect corneal injury. Standard topical treatments for dermal or ocular burns should be applied as needed.

Also see Principles of Therapy of Toxicosis in Animals.

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-ion batteries also tend to contain alkaline material.

The alkaline gel in batteries produces liquefactive necrosis of tissues on contact, resulting in burns that can penetrate deeply into tissue. Disk batteries (also known as button cell, coin, or watch batteries) can lodge in the esophagus and generate a current against the esophageal walls, resulting in circular ulcers that have the potential to perforate. Rare instances of oral thermal burns have been reported secondary to spontaneous combustion of lithium-ion batteries. Some battery casings can 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. In addition, small batteries (especially disk batteries) can be inhaled and pose a choking hazard.

Clinical signs of foreign body obstruction include vomiting, anorexia, abdominal discomfort, and tenesmus. Respiratory obstruction due to battery inhalation can be associated with acute onset of dyspnea and cyanosis. Mucosal burns can occur within the oral cavity, esophagus, and, less commonly, stomach. Esophageal perforation can lead to secondary pyothorax, and gastric perforation can result in acute blood loss and peritonitis.

• Clinical evaluation

• Radiographic evaluation

Radiographic evaluation can help to confirm a diagnosis of alkaline battery toxicosis 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 toxicosis due to other corrosive agents.

• Removal of the battery

• For ingestion of lithium-ion disk batteries, administration of tap water boluses

• For corrosive injuries, supportive care

For batteries swallowed intact without any chewing, induction of emesis can result in expulsion. Because alkaline gel can leak onto the 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, administration of boluses of tap water (20 mL, PO, every 15 minutes) will delay the development and decrease the severity of current-induced esophageal ulceration.

The decision of whether to remove a battery from the stomach depends on patient size, battery size, and evidence of battery puncture. Radiographic evaluation can help to determine the location of the battery casing; generally, batteries that have passed through the pylorus will pass through the intestinal tract uneventfully (addition of bulk to the diet in the form of psyllium or other fiber, as well as judicious administration of cathartic agents, can facilitate passage). Serial radiography to verify the battery's location is recommended until the battery is expelled.

Batteries that do not pass through the pylorus within 48 hours of ingestion are unlikely to pass on their own and can require surgical or endoscopic removal. Batteries that have obviously been punctured should be removed surgically to prevent gastric or intestinal ulceration due to the leakage of alkaline gel. Endoscopic removal is not recommended if the battery casing is suspected to have been punctured.

Treatment of cases with suspected oral, esophageal, or gastric ulceration is the same as for other alkaline corrosive-agent injuries. Dermal and ocular exposures to alkaline gels should be managed by copious rinsing of the skin with tap water or the eyes with saline (0.9% NaCl) solution. Affected areas should be monitored for the development of ulcers, and topical preparations should be administered as needed.

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.

Cationic detergents are locally corrosive agents that produce dermal, ocular, and mucosal injury. Although many cationic detergents are pH neutral, the pathogenesis of tissue injury from cationic detergents is similar to that of alkaline corrosive agents (ie, liquefactive necrosis with delayed onset of clinical signs). In addition, exposure to cationic detergents can result in systemic effects ranging from CNS depression to pulmonary edema. The mechanism for these systemic effects is not known.

Clinical signs of cationic-detergent toxicosis resulting from oral exposure arise within 6–12 hours of ingestion and include oral ulceration, stomatitis, pharyngitis, hypersalivation, lingual edema, lethargy, vomiting, abdominal discomfort, and increased upper respiratory noise. Affected animals frequently have substantial fever and elevated 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 can occur secondary to ocular exposure. Lesions can include GI, ocular, or dermal irritation or ulceration.

• Management of life-threatening clinical signs

• Supportive care of local corrosive injuries

Systemic clinical signs of cationic-detergent toxicosis should be treated as needed. Diazepam (0.5–2 mg/kg, slowly IV) can be administered for seizures. Fluid therapy can help ameliorate hypotension.

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 administered for dilution and the patient monitored for the development of oral or esophageal burns. Oral burns should be treated as other corrosive injuries. Dermal and ocular exposures should be managed by thorough flushing of the affected area with tepid water or saline (0.9% NaCl) solution, followed by monitoring for the development of dermal or ocular irritation or ulceration. Topical preparations should be applied to dermal or ocular burns as needed. In severe cases, analgesics can be indicated.