A 3-year-old 3.1-kg (6.8-lb) castrated male Yorkshire Terrier was referred to the emergency service of the Foster Hospital for Small Animals at Cummings School of Veterinary Medicine because of a 3-day history of vomiting, hyporexia, and lethargy. The dog had been seen playing with a set of neodymium desk toy magnetsa before the onset of clinical signs and was suspected to have ingested them.
Radiography performed at the local veterinarian's office approximately 24 hours before the referral examination revealed the presence of several round metallic objects in the dog's stomach. A laxative was administered orally and an enema performed to facilitate passage of the magnets through the gastrointestinal tract. The dog continued to vomit and developed signs of severe abdominal pain, and it was referred to the authors’ facility the following day.
Physical examination revealed signs of pain associated with the cranial portion of the abdomen and moderate tachypnea with abdominal effort. Initial clinicopathologic evaluation revealed mild metabolic acidosis (blood pH, 7.26; reference range, 7.337 to 7.467), hyperlactatemia (7.9 mmol/L; reference range, 0.0 to 2.0 mmol/L), mildly high BUN concentration (38.0 mmol/L; reference range, 12.0 to 28.0 mmol/L), hypoglycemia (41 mL/dL; reference range, 80 to 120 mL/dL), hyponatremia (135.9 mmol/L; reference range, 140.0 to 154.0 mmol/L), and hypochloremia (107 mmol/L; reference range, 109 to 120 mmol/L).
Initial stabilization including an IV bolus administration of lactated Ringer's solution and IV dextrose supplementation was initiated, and whole body radiography was performed. Radiographic views of the abdomen revealed 13 well-defined metal opacities arranged in a ring pattern in the abdominal portion of the esophagus and gastric cardia with extension into the gastric fundus (Figure 1). An increase in soft tissue opacity within the pleural space was also noted, with multiple pleural fissure lines and rounding of the left caudal lung lobe margins (radiographic signs consistent with pleural effusion).
The dog was anesthetized, and upper gastrointestinal endoscopy was performed to evaluate the integrity of the esophagus and stomach and to potentially retrieve the magnets. The magnets were embedded in the gastric and caudal esophageal mucosa. After passage of the endoscope through the lower esophageal sphincter, the dog became increasingly dyspneic, hypotensive, and bradycardic. Thoracocentesis was performed, and approximately 100 mL of septic exudate with a mixed population of cocci and rods was removed from the thoracic cavity. Because of the strong suspicion of esophageal perforation, the dog was administered broad-spectrum antimicrobial treatment with ampicillin (22 mg/kg [10 mg/lb], IV) and enrofloxacin (10 mg/kg [4.5 mg/lb], IV) and was prepared for exploratory surgery of the thorax and abdomen.
Routine ventral midline celiotomy was performed in conjunction with a median sternotomy. The diaphragm was incised at the esophageal hiatus to gain access to the abdominal portion of the esophagus. A gastrotomy was performed at the gastric cardia, and the magnets were removed from the gastric cardia and abdominal portion of the esophagus. Perforations of the stomach and esophagus were evident where adjacent magnets had attracted and become conjoined, subsequently causing pressure necrosis of the tissue. A focal region of tissue surrounding the esophageal perforation was severely inflamed and contained a thick discharge (consistent with the exudate). The authors believed that this region contained a localized abscess, which was ruptured by the manipulation of the esophagus during the endoscopic examination. The perforations were debrided and closed with 4–0 polydioxanone suture in a simple continuous pattern, and the thoracic and abdominal cavities were thoroughly lavaged with 1.5 L of sterile saline (0.9% NaCl) solution. A thoracostomy tubeb was placed as well as a low-profile gastrostomy tubec for nutrient and medication delivery.
The dog was treated with intensive supportive care over the next 48 hours. Although some clinical improvement was seen following surgery, the dog ultimately had acute cardiovascular arrest approximately 48 hours after surgery and was unable to be resuscitated. A necropsy was not performed, so the cause of death was unknown.
Bucky Balls, Maxfield & Oberton Holdings LLC, New York, NY.
Mila International Inc, Erlanger, Ky.
Low-profile gastrostomy tube, Cook Medical Inc, Winston-Salem, NC.
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