Dog Eats Horse - An Unusual Cause of Intestinal Perforations

What happens when a dog eats a horse? In this case summary, Ashley Magee, DVM, DACVS, discusses how the surgical team and ICU worked together to save this patient.

Views: 2921 - Comments: 3

You are here

An eight-month-old, intact male Rottweiler presented to DoveLewis for weakness and vomiting of an uncertain length of time. The owners had been out of town for four days and the pet sitters did not notice signs of illness. He had no interest in food. No diarrhea was noted. On presentation he was depressed, tachycardic, markedly dehydrated with injected mucus membranes and sunken eyes, and exhibited pain on cranial abdominal palpation. He was weak and unsteady while standing with no evidence of orthopedic or neurologic disease. VD radiograph of abdominal foreign bodyRectal temperature at presentation was 102.7F, and his respiratory rate was elevated. Blood pressure was within normal limits.

Initial diagnostics included a CBC and serum chemistry panel. Results included a moderate leukocytosis with a neutrophilia and hemoconcentration. Urine collection was unsuccessful.
Right lateral abdominal radiograph of foreign body
Abdominal radiographs were performed (figure 1). A cylindrical metallic density was identified within the stomach. Mineralized material was present in both the stomach and the colon. Decreased abdominal detail suggestive of abdominal effusion was identified. Several small gas bubbles in the cranial abdomen were visible on one projection, suggesting pneumoperitoneum.

Due to the decreased abdominal detail on radiographs, a full abdominal ultrasound was performed. The ultrasound was suspicious for a pancreatic abscess and/or gastrointestinal perforation due to the presence of a thickened irregular pancreas, a fluid pocket at the caudal aspect of the stomach, multiple foci of peritoneal gas and an atonic GI tract.

Abdominocentesis was performed and fluid cytology found occasional degenerate neutrophils and occasional extracellular cocci with rare short rods, an elevated total protein and a low fluid glucose level. Surgical measurement of foreign body before removal from intestine.Surgical view into abdomen during procedure with suction being applied to cavity.Foreign body magnets post surgical removal, on paper towel.Due to the indications of septic peritonitis and possible GI perforation, preparations were made for an exploratory ceilotomy.

An abdominal exploratory revealed extensive adhesions involving a full thickness colonic perforation, the duodenum, omentum and an associated omental abscess in addition to a moderate amount of abdominal effusion. A similar gastric perforation was noted in the dorsal gastric wall 3cm from the greater curvature (Figure 2). Exploration of the gastric perforation found a foreign body containing 4 small (5mm x 7mm) round magnets covered with cloth material wedged within the thickened gastric wall (Figure 3). The omental abscess was intimately associated with the splenic vasculature, so a splenectomy was required for adequate debridement of the abscessed tissues. Aerobic and anaerobic cultures of the omental abscess were obtained.Pateitn post-op, wearing vest and t-shirt carrying feeding tubes, etc. The colonic and gastric perforations were debrided and closed with an omental patch placed over the site of the colonic perforation. Two Jackson-Pratt drains were placed in the abdomen, one in the cranial aspect and one in the caudal aspect, for drainage, cytologic monitoring and quantification of abdominal effusion (figure 4). A nasogastric tube was placed to the level of the gastric fundus during surgery for post-op removal of gastric reflux, as well as to allow enteral feeding in the post-op period.

The patient was continued on a fentanyl, lidocaine and ketamine CRI for analgesia post-operatively. He received two plasma transfusions to correct hypoalbuminemia that had become apparent with fluid resuscitation, to help with operative and ongoing losses, and to treat a mild prolongation in PT and PTT that developed post-operatively. Fluid therapy included Plasmalyte with 2.5% dextrose, since the patient had become hypoglycemic, and hetastarch for additional oncotic support. Enrofloxacin,  ampicillin sulbactam and metronidazole therapy were continued for broad spectrum antibiotic coverage. An indwelling Foley urinary catheter was placed to monitor urine output and to maintain cleanliness.  The patient continued to vomit post-operatively.  Total parenteral nutrition was instituted in order to further support the patient.

Despite aggressive debridement of abscessed tissues and intraoperative lavage with >10 L fluids, the initial abdominal drain cytology  24 hours after surgery showed a moderate amount of extracellular rods in addition to neutrophils with intracellular rods.   Enrofloxacin was discontinued and amikacin was added to the antibiotic regime, and abdominal lavage was instituted every eight hours via the drains to combat ongoing septic peritonitis. Due to recurrent hypoglycemia, 2.5% dextrose supplementation was continued.  

Over the second and third days of hospitalization, the patient improved, demonstrating decreased nausea and vomiting, improved urine output, and decreasing PT and PTT values.  On the fourth day of hospitalization, the patient began to eat small amounts of soft food. Blood glucose levels remained within the normal range and dextrose supplementation was discontinued. The rate of crystalloid administration was reduced. Due to static but continued hypoalbuminemia hetastarch was continued for oncotic support. JP drain fluid production decreased, and cytology showed only occasional degenerate neutrophils with scant intracellular bacteria. Abdominal lavage was discontinued due to the improved cytology. Due to the administration of amikacin, urine sediment was evaluated for possible casts. None were noted.

On the fifth day of hospitalization, the patient was bright and alert. He continued to eat well, despite occasional regurgitation. Abdominal drain cytology found no evidence of extracellular or intracellular bacteria.  Later that evening, the abdominal drains and NG tube were removed and he was weaned off all IV fluids including the parenteral nutrition.

The patient was discharged home on the morning of the sixth day of hospitalization on amoxicillin/clavulinate, cefpodoxine, metronidazole, famotidine and tramadol. Amikacin therapy was discontinued due to the injectable nature of the drug and possible nephrotoxic effects.  Foreign body horse plush toy on paper towel, post surgical removal.Culture results were reported two days after discharge from the hospital. The anaerobic culture was overgrown with swarming Proteus mirabilis. The aerobic culture grew two strains of Escheria coli, Proteus mirabilis, and an Enterococcus species. All bacterial species were susceptible to amoxicillin or amoxicillin/clavulinic acid. Antibiotics were adjusted accordingly. The patient continued to regurgitate a small amount at home. His appetite and energy level remained high. The Clavamox was continued for 42 days. The clients determined the source of the magnets to be a plush horse toy (figure 5).

Gastrointestinal tract necrosis and subsequent perforation from ingested foreign material is a relatively common occurrence in canines.  This case is unusual in that the cause was ingested magnets that presumably traveled separately though the intestinal tract until they were positioned in adjacent intestinal lumens, in this case, the body of the stomach and colon. Once in close proximity to each other, the magnets were attracted to each other though the bowel walls, came together and compressed the interposed intestinal walls until intestinal necrosis, then perforation, occurred that resulted in septic peritonitis and abscess formation.   This is a well documented cause of intestinal perforations, intestinal fistula formation, and septic peritonitis  in children, often with devastating outcomes.  

In this case, the magnets were still within the lumen of the gastric perforation at the time of surgery, effectively occluding it and limiting widespread gross contamination of the abdominal cavity with gastric contents.  The colonic perforation was walled off by omentum and splenic mesentery forming a localized abscess in the region of the spleen, pancreas, stomach and proximal colon, limiting gross fecal contamination.  It is interesting that overt signs of sepsis (prolongation in clotting times, hypoglycemia) did not become apparent until during and after surgery, likely due to the localization and containment of the abscess until debridement of the abscess was undertaken. Debridement, although necessary for the successful outcome of the case, inevitably exposed bacteria, toxins and inflammatory mediators more directly into the patient’s system where they could exert a more dramatic systemic effect. Wide debridement of the abscess, repair of the perforations, copious abdominal lavage, then aggressive post-operative management of the patient’s signs of sepsis and early nutritional support was integral to this dog’s timely recovery and discharge from the hospital.

Septic peritonitis can be treated with intraoperative lavage and debridement alone, debridement and lavage coupled with open abdominal drainage or with closed suction drainage. We chose closed suction drainage via Jackson Pratt drains due to the ability to close the abdomen but continue to remove accumulating fluid, bacteria and inflammatory by products from the abdomen continuously via the drains. The ease of fluid collection also allows for daily cytologic analysis which is quite helpful to gauge the patient’s progress in resolving the infection.  In this case, identifying a septic cytology detected within 24 hours after surgery allowed us to institute lavage and  a change in antibiotic therapy which ultimately helped us to resolve the septic peritonitis without the need for multiple anesthetic procedures (as would be needed for lavage with open abdominal drainage) or a second surgery.

In veterinary patients with signs of septic peritonitis with small circular metallic foreign bodies, the index of suspicion of a magnet foreign body should be high.  In these cases, or in patients known to have ingested magnets, we would strongly recommend the pieces should be removed immediately whether or not they are currently causing an obstruction, due to the potential for severe intestinal damage.

Alzahem A, Soundappan S, Jefferies H, Cass D. Ingested magnets and gastrointestinal complications. J Pediatr Child Health 2007; 43: 497-498.
Cauchi J, Shawis R. Multiple magnet ingestion and gastrointestinal morbidity. Arch Dis Child 2002; 87: 539-540.
Dutta S, Barzin A. Multiple magnet ingestion as a source of severe gastrointestinal complications requiring surgical intervention. Arch Pediatr Adolesc Med 2008; 162(2): 123-125.
Kircher M, Milla S, Callahan M. Ingestion of magnetic foreign bodies causing multiple bowel perforations. Pediatr Radiol 2007; 37: 933-936.
Oestreich A. Worldwide survey of damage from swallowing multiple magnets. Pediatr Radiol 2009; 39: 142-147.
Uchida K, Otake K, Iwata T, Watanabe H, Inoue M, Hatada T, Kusunoki M. Ingestion of multiple magnets: hazardous foreign bodies for children. Pediatr Radiol 2006; 36: 263-264.

Acknowledgements:  We would like to thank Dr. Bullard and staff of Cornelius Veterinary Clinic for the referral of this case, the owners of the patient for permission to present the case for teaching purposes and Dr. Mara Hickey, former DoveLewis intern, for her work on the case report.

Add To Training Plan


Content Assignment