A 1-year-old 26-lb (11.8-kg) spayed female Australian shepherd was presented to a veterinary clinic for evaluation one hour after chewing on two AA alkaline batteries.
At home, the owner found two AA alkaline batteries with two small puncture holes in them. The owner noticed a red blotch on the dog’s tongue and brought the dog to the clinic.
On physical examination, the dog was bright, alert, and responsive. A mild superficial abrasion was noted along the left buccal surface of the tongue. No other significant changes were noted, and the physical examination was otherwise unremarkable.
Oral irritation was already present at the time of the initial examination, so the dog was administered medications to protect the gastrointestinal (GI) tract. These included sucralfate (500 mg mixed in water until a slurry forms and then given orally t.i.d. for five days) and famotidine (10 mg orally once daily for five days).
Since damage to the mucosa can be delayed and the full extent of the damage may not be recognizable until about 12 hours after the exposure,1 the owner was instructed to monitor the dog at home for worsening lesions in the mouth, hypersalivation, lethargy, anorexia, and vomiting.
About 18 hours after the exposure, the dog became lethargic, developed mild hypersalivation and anorexia, and was again presented to the veterinary clinic. The physical examination revealed moderate ulceration of the buccal mucosa and tongue. The dog’s temperature was normal, and abdominal palpation did not seem to elicit pain. Results from a complete blood count and serum chemistry profile were normal. Tramadol (50 mg orally t.i.d. for five days) and amoxicillin-clavulanic acid (125 mg orally b.i.d. for seven days) were administered.
The dog was hospitalized for monitoring. Within four hours of hospitalization, the patient began eating small amounts of critical care canned dog food.
The dog was discharged 12 hours after admittance. The owner was instructed to continue giving all medications (sucralfate, famotidine, tramadol, amoxicillin-clavulanic acid) for the labeled time frames and to only feed the dog canned food until the lesions in its mouth resolved. The dog was fully recovered seven days after the exposure.
Dry cell batteries contain an electrolyte solution or gel of either potassium hydroxide or sodium hydroxide, both of which are alkaline. Chemically, alkaline materials generate an aqueous solution in which there are more hydroxyl (OH-) ions than hydrogen (H+) ions.2 Alkaline materials can cause corrosive injury on contact with tissues through a process called liquefaction necrosis, which includes protein dissolution, collagen destruction, fat saponification, and cell membrane emulsification.
During liquefaction necrosis, the tissues soften and allow the alkali to penetrate deeply into the tissues.1 Exposure to an alkaline material causes little to no pain initially, unlike exposure to an acid. Thus, patients are not deterred from accidental exposure.
In cases in which a battery is chewed and punctured, the alkaline material may leak out and cause localized tissue damage. If the battery was not swallowed, the damage is most likely to occur in the mouth, but it is also possible that there will be damage in the esophagus and farther down the GI tract. The esophagus is most at risk since it does not produce protective secretions that dilute the toxin like the mouth and stomach do. Lesions in the esophagus may lead to perforation or, when healed, scar formation and contracture, leading to long-term esophageal stricture.1
If the battery has been ingested, in addition to the above concerns, it may also pose a foreign-body-obstruction threat, or if the battery remains in the stomach long enough for the casing to break down, heavy metals such as zinc or lead may be released and lead to toxicosis.
Clinical signs of irritation of the lips or tongue or in the mouth may occur within a few hours of exposure to a chewed battery, and ulceration may take up to 12 hours to fully develop.1 The patient may also exhibit the clinical signs of lethargy, hypersalivation, dysphagia, anorexia, vomiting (potentially with blood), abdominal discomfort, hyperthermia, and melena.1 Hyperthermia occurs, possibly because of corrosive tissue damage and inflammation from the alkali. Affected animals often show mild to moderate leukocytosis.
If the battery that was ingested is a button or disc battery, there are additional risks. Button batteries are found in many electronic devices including hearing aids, games, watches, calculators, and greeting cards. As described above, alkaline liquid can also seep from damaged disc batteries. In addition, there is the added risk of injury to adjacent tissues from the current flowing between the cathode and anode, which results in electrolysis of endogenous salt and the production of corrosive sodium hydroxide2 if the battery becomes lodged in the GI tract, particularly the esophagus. Thus, significant corrosive damage, including esophageal burns, necrosis, and perforation, can occur even if the button battery does not leak.1
Mucosal burns can also be caused by thermal or electrical injury or due to exposure to other corrosive materials, such as acids, disinfectants, cationic-containing detergents or potpourri, automatic dishwasher detergent, formaldehyde, concentrated bleach (sodium hypochlorite), and phenols.
Diagnosis is based on a history of exposure and the consequent development of any of the clinical signs listed above. Since batteries have metal casings, radiography can be helpful in determining if any portion of the battery was swallowed and, if so, the location of the battery in the GI tract. In cases of button battery ingestion, radiography is particularly helpful in determining if the battery has become lodged in the esophagus.
Endoscopic examination of the oropharynx, esophagus, and stomach by using a flexible endoscope is recommended to determine if ulceration has occurred (since esophageal ulceration may be present even if no ulcers are present in the mouth) and to determine the severity of ulceration.1 Diagnostic endoscopy is most useful if performed at least 12 hours after the exposure because the development of the ulceration may be delayed, but it should be performed within 24 hours of the exposure. If a battery is identified radiographically in the esophagus or stomach, therapeutic endoscopy to remove the battery may be indicated.
Patients that have ingested corrosive materials should be given a small amount of milk or water immediately to dilute the corrosive material. (In this case, the window of opportunity for dilution had passed by the time the patient was presented to the clinic.) The recommended dose is 2 to 6 ml/kg orally, which is about 3 to 9 tbsp in a 50-lb dog.3 If a button battery was ingested, giving serial doses of water (20 ml every 15 minutes) may delay and lessen the severity of the lesions.3
If the battery is leaking, emesis is contraindicated to prevent additional exposure of the esophagus to the alkaline corrosive material. Activated charcoal is also contraindicated since it is unlikely to bind to the corrosive material, may make visualization of ulceration difficult, and could be released into the abdominal cavity if GI perforation develops.3
Once a button battery has moved into the stomach, if it is not large compared with the size of the patient, it will likely continue to pass through the GI tract and be expelled in the feces. A button battery lodged in the esophagus should be removed through endoscopy immediately since marked esophageal mucosal necrosis was observed in dogs after as little as 15 minutes of contact with a 3-volt disc battery.1
Bulking agents, such as wheat bread, psyllium, or canned pumpkin, may be helpful in moving small button batteries or battery pieces through the GI tract.3 Sucralfate (0.5 to 1 g orally as a slurry t.i.d.) should be given to patients that develop mucosal irritation or ulceration, in addition to giving an H2 blocker (e.g. famotidine 0.5 to 1 mg/kg orally daily to b.i.d.) or a proton pump inhibitor (e.g. omeprazole 0.5 to 1 mg/kg orally once a day).4 These medications should be given until the clinical signs have resolved, often in seven to 10 days or longer. Patients with ulceration should also be given a broad-spectrum antibiotic to combat secondary infection.
Anorectic patients may need nutritional and fluid support. Opioid or opioid-like medications, such as tramadol (2 to 5 mg/kg orally two to four times a day), a fentanyl patch, or buprenorphine (0.005 to 0.02 mg/kg two to four times a day) can be given to lessen the pain of ulceration.4
Monitor patients for 24 hours for clinical signs of GI irritation or ulceration. If ulceration develops, monitor the patient’s complete blood count and body temperature. Perform endoscopy of the stomach or esophagus if needed to observe the extent of mucosal damage or to remove a battery seen on radiographs.
Alkaline battery exposure in dogs can cause corrosive injury and GI ulceration, especially in the mouth and esophagus. Esophageal ulceration can lead to perforation and stricture formation. Treatment measures may include immediate dilution with milk or water; the administration of GI protectants, pain medications, broad-spectrum antibiotics, liquid food, and supportive care; and the removal of the battery or pieces of the battery through endoscopy or surgery.
1. Gwaltney-Brant S. Batteries. In: Plumlee KH, ed. Clinical veterinary toxicology. St. Louis: Mosby Elsevier, 2004;140-142.
2. Litovitz T. Button batteries. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical toxicology. Philadelphia: WB Saunders Co, 2001;1027-1031.
3. DeClementi C. Prevention and treatment of poisoning. In: Gupta RC, ed. Veterinary toxicology: basic and clinical principles. London: Elsevier, 2012;1364-1368.
4. Plumb DC. Plumb’s veterinary drug handbook. 5th ed. Ames, Iowa: Blackwell Publishing, 2005; 321, 573, 722, 774.