Duodenogastric Intussusception with Concurrent Gastric Foreign Body in a Dog: A Case Report and Literature Review

Introduction

The purpose of this article is to report the first known case of a duodenogastric intussusception with a concurrent foreign body and to review the literature surrounding this topic.

Case Report

A 3 yr old spayed female boxer weighing 22.8 kg presented to the Michigan State University Veterinary Teaching Hospital for severe, acute vomiting and tenesmus. The vomiting began the morning of presentation and > 10 episodes, some including hematemesis, occurred prior to presentation. There was no known dietary indiscretion associated with the episodes of severe vomiting. It was reported that for the last 1 yr the dog had a history of vomiting when in situations of high anxiety. Those situations occurred 2–3 times/mo and usually only involved one episode of vomiting.

On presentation, the dog’s temperature was 39.3°C, heart rate was 150 beats/min, respiratory rate was 60 breaths/min, and mucous membranes were tacky. The dog appeared uncomfortable, and the abdomen was painful upon palpation. Packed cell volume, total solids, venous blood gas, complete blood cell count, and serum biochemical panel were obtained prior to initiating fluid therapy. A 500 mL bolus of Normosol-R^a was administered IV followed by a constant rate infusion at 120 mL/kg/day. Hydromorphone^b (0.1 mg/kg) was administered IV.

Three-view abdominal radiographs showed a rounded, well-defined foreign object in the stomach, the rim of which had a mineral opacity. Cranial to that object (also in the body of the stomach), a larger, round, soft-tissue opacity was present (Figures 1A–C). On the left lateral projection, a distinct, gas-filled pylorus was not seen (Figure 1B). The small intestine was empty of both ingesta and air. Based on the history, physical examination, and radiographic findings, a diagnosis of gastric outflow obstruction secondary to a gastric foreign body and an undefined, round, soft-tissue opacity mass near the pyloric region was made. Differential diagnoses for the round, soft-tissue opacity were a second foreign body, neoplasia, polyp, and granuloma.

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Clinicopathologic abnormalities included a packed cell volume and total solid of 68% and 8.1 g/dL, respectively (references ranges, 41–55 and 6.0–7.4, respectively). Venous blood gas showed hyperglycemia (148 mg/dL; reference range, 66–115 mg/dL) and hyperlactatemia (6.2 mmol/L; reference range, 0.3–3.4 mmol/L). The complete blood cell count revealed a leukocytosis (18.12 × 10³/μL; reference range, 5.90–11.60 × 10³/μL) with a mature neutrophilia (16.49 × 10³/μL; reference range, 4.00–8.20 × 10³/μL). The serum biochemical panel revealed an increased creatinine (2.3 mg/dL; reference range, 0.7–2 mg/dL), hypochloremia (100 mmol/L; reference range, 107–116 mmol/L), hypercalcemia (11.4 mg/dL; reference range, 9.4–10.9 mg/dL), hyperphosphatemia (7.3 mg/dL; reference range, 2.1–4.6 mg/dL), hypermagnesemia (3.5 mg/dL; reference range, 1.5–2.4 mg/dL), hyperproteinemia (8.4 g/dL; reference range, 5.6–7.5 g/dL), and hyperalbuminemia (4.6 g/dL; reference range, 2.8–4 g/dL).

After adequate cardiovascular stabilization, the dog was anesthetized for endoscopic examination of the upper gastrointestinal tract, biopsy of the round, soft-tissue opacity mass, and possible foreign body removal using a 9.5 mm diameter flexible endoscope^c. A small amount of green ingesta was present in the stomach as well as a golf ball measuring 4 cm in diameter (Figure 2). Attempts to remove the golf ball failed due to its smooth, firm surface and size. Endoscopy showed that the round, soft-tissue opacity mass seen on radiographs was about 7 cm in diameter, firm, and deep purple in color. The pyloric sphincter could not be identified. Based on the need to correct the gastric outflow obstruction, remove the golf ball, and address the large, soft-tissue mass, the patient was taken to surgery.

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A routine ventral midline celiotomy was made from the xyphoid process to the pubis. Exploration of the abdomen revealed a duodenogastric intussusception involving the pylorus, proximal duodenum, and right limb of the pancreas (Figure 3A). The duodenogastric intussusception was the cause of the gastric outflow obstruction and was the round, soft-tissue mass seen on the radiographs and via endoscopy. Gentle yet firm traction was placed on the descending duodenum and the stomach was simultaneously squeezed to force the intussuscepted duodenum and pyloric sphincter aboral. With forceful steady traction and digital pressure (Figure 3A), the intussusception was reduced with minimal serosal tearing. After reduction of the intussusception, the pyloric and proximal duodenal walls were markedly edematous (~  2 cm thick), had mild serosal bruising, and almost no palpable lumen in the region of the pyloric antrum. The portion of the right limb of the pancreas that was involved in the intussusception was mildly edematous. A gastrotomy was performed in the body of the stomach, and the golf ball was removed. A two layer gastrotomy closure was performed with 3-0 polydioxanone^d. The mucosal layer was closed with a simple continuous pattern, and the seromuscular layer was closed with a continuous Lembert pattern. A routine, right-sided incisional gastropexy was performed in a minimally bruised region of the pylorus using 3-0 polydioxanone.¹ Following the gastropexy, the duodenum was placed in its correct anatomic position along the right dorsolateral body wall caudal to the last rib. Starting 10 cm aboral to the pyloric sphincter, a duodenopexy was performed by placing simple interrupted 3-0 polydioxanone sutures 1 cm apart in an aboral direction as shown in Figure 3B. An effort was made to leave enough distance between the pyloric sphincter and the start of the duodenopexy for peristalsis and the passage of large boluses of ingesta. The surgical sites were lavaged with warm, sterile saline, and the abdomen was closed routinely.

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Postoperatively, buprenorphine^e (0.01 mg/kg) was administered IV q 6 hr. Famotidine^f (0.5 mg/kg) was administered IV q 12 hr. Acepromazine^g (0.001 mg/kg) was administered IV pro re nata for sedation. Normosol-R was administered IV at a rate of 120 mL/kg/day until the dog ate a small amount of a bland canned dog food 14 hr after surgery. Fourteen hr after surgery, the IV fluid rate was decreased to 60 mL/kg/day, and treatment with buprenorphine and famotidine was continued until the dog was discharged from the hospital. Normal urination and defecation of soft stools were noted during the hospital recovery. The dog’s appetite continued to improve, and neither vomiting nor regurgitation occurred during recovery. The patient was discharged 38 hr after surgery and was prescribed tramadol^h (4.3 mg/kg per os q 8–12 hr pro re nata) for pain.

Two wk after surgery, the owner contacted the hospital by phone to report the dog had one episode of vomiting associated with eating the contents of a soiled baby diaper. The dog was otherwise bright, alert, and responsive. Instructions were given to monitor the dog closely and to return to the veterinarian if another episode of vomiting occurred. One month after surgery, the dog was re-examined at the Michigan State University Veterinary Teaching Hospital. No further episodes of vomiting were reported, and the physical exam was within normal limits. The owner was contacted by phone 1 yr postsurgically and reported that the dog was completely normal. The owner had no knowledge of any episodes of vomiting since the previously reported episode 2 wk after surgery.

Discussion

Intussusception is defined as the taking up or receiving of one part within another, especially the enfolding of one segment of intestine within another.² The segment of intestine that is displaced into the lumen of another is referred to as the intussusceptum. The receiving segment of the intestine is referred to as the intussuscipiens. Intussusceptions most commonly occur in the direction of normal peristalsis (normograde) but can occur in a reverse peristalsis direction (retrograde).¹

The exact etiology of intussusceptions is unknown, and an intussusception has not been reproduced experimentally. The pathophysiology of intussusceptions may involve either an inhomogeneity in a bowel segment or a mechanical linkage of nonadjacent bowel segments, leading to either a kink or fold in the bowel wall that is propagated circumferentially and longitudinally into an intussusception.^3,4 Examples of inhomogeneity include a flaccid or indurated segment of bowel or a region of the gastrointestinal tract that undergoes a sudden change in diameter. Examples of mechanical linkage include pedunculated polyps, linear foreign bodies, or extraluminal adhesions.⁵ Most intussusceptions occur in dogs < 1 yr of age and are considered idiopathic.^5–7 Other reported causes of intussusception include parasitism, viral enteritis, acute gastroenteritis, dietary indiscretion, foreign bodies, intestinal masses, renal transplants, anesthesia, and abdominal surgery.^5–9 More recently, case series have reported leptospirosis and methiocarb toxicity as causes of intussusceptions in dogs.^10,11

Intussusceptions are named by citing the intussusceptum followed by the intussuscipiens. For example, an ileocolic intussusception is a normograde intussusception in which the ileum has invaginated into the colon. Ileocolic intussusceptions are most common; however, intussusceptions can occur anywhere along the gastrointestinal tract. Dogs with intussusceptions in the lower gastrointestinal tract may present with a chronic history of clinical signs. In contrast, dogs with intussusceptions high in the gastrointestinal tract usually present with severe, acute clinical signs, and death can occur from hypovolemia, electrolyte disturbances, and acid-base imbalances.^5,8

The dog described in this report had a duodenogastric intussusception in which the pylorus and duodenum were invaginated into the stomach. Duodenogastric intussusceptions, being both high within the gastrointestinal tract and retrograde, are rare. The authors are aware of only five previously reported cases of pylorogastric/duodenogastric intussusceptions.^12–16 The mean age of the five previously described patients was 4 yr. The reported breeds consisted of an Old English sheepdog (case 1), a basset hound (case 2), a rottweiler (case 3), a Saint Bernard (case 4), and a Maltese (case 5).^12–16 Three out of the six cases of pylorogastric/duodenogastric intussusception (including the present case) had had a known history of dietary indiscretion associated with the onset of clinical signs.^12,13,15 All dogs presented for an acute onset of severe vomiting. Tachycardia, abdominal discomfort, dehydration, and electrolyte abnormalities were consistent findings. The diagnosis of pylorogastric/duodenogastric intussusception was made during surgery in all dogs except case 5. Case 1 acutely died postoperatively of suspected toxemia, and case 2 was euthanized due to extensive gastric necrosis.^12,13 Case 3 presented in acute renal failure, underwent surgical correction of the pylorogastric intussusception, and renal biopsies were taken. Mild glomerulonephritis with occasional hyaline cast was diagnosed based on the renal biopsies, and the dog survived >  20 mo. Case 4 also presented in acute renal failure, underwent a Y-U pyloroplasty during surgery to relieve the outflow obstruction caused by profound pyloric edema, and survived >  1 yr.^15,17 Likewise, case 5 presented in acute renal failure. In that case, the pylorogastric intussusception was diagnosed with ultrasound, the intussusception reduced spontaneously, but the dog was euthanized due to renal failure.¹⁶

The five previously reported cases and the case described in this report are similar in both history and clinical findings. Clinical signs and diagnostic test results were consistent with a pyloric outflow obstruction in all dogs. In each case, the differential diagnoses included foreign body, gastric neoplasia, and soft-tissue proliferation. The correct diagnosis of an intussusception was made intrasurgically. Abdominal ultrasonography of case 3 showed a large, echogenic mass that extended into the lumen of the gastric fundus, but the individual wall layers of the intussusception could not be seen.¹⁴ The case described in this report did not have an abdominal ultrasound performed due to the known indication for surgery (i.e., foreign body). Endoscopy was performed based on the potential for foreign body retrieval, mass identification, and obtaining biopsies. Due to edema and venous congestion, it was not possible to identify the mass as an intussusception with endoscopy in the dog described herein. The foreign body had no surface for grasping; thus, it was not removable via endoscopy. Despite the use of endoscopy in this case, the authors recommend abdominal ultrasonography as the diagnostic test of choice due to its reliability for diagnosing intussusceptions.^16,18

This is the first reported case of a pylorogastric/duodenogastric intussusception in conjunction with a foreign body. In most of the previously reported cases of pylorogastric/duodenogastric intussusception, a foreign body was suspected on preoperative abdominal radiographs, but no foreign object was found during surgery. The dog reported herein had a 1 yr history of vomiting (several times/mo), which resolved after surgery. Multiple possibilities exist to explain this resolution, including a chronic, spontaneously reducing, mild duodenogastric intussusception similar to case 5.¹⁶ Chronic foreign bodies have been described in the veterinary literature, and it is reasonable to theorize that the golf ball was the cause of this dog’s chronic vomiting.^6,19 Another possible explanation for the resolution of vomiting after surgery is fixation of the stomach in a new position by gastropexy, similar to the manner in which the left-sided gastropexy functions in the repair of hiatal hernias.²⁰

Significant pyloric wall edema has been described in all cases of pylorogastric/duodenogastric intussusception. The actual pyloric wall thickness was measured to be up to 2 cm in one case.¹³ In a previously reported case, a Y-U pyloroplasty was performed during surgery in attempt to increase the diameter of the pyloric outflow tract.¹⁵ In the case described herein, the pyloric wall edema was palpated and estimated to be about 2 cm thick after reduction of the intussusception. The surgeon chose not to intervene with a Y-U pyloroplasty based on its potential morbidity and the gastrointestinal tract’s ability to repair itself after removal of the insult. The patient described in this report ate well without vomiting 14 hr after surgery. Although severe pyloric wall edema is commonly encountered in cases of pylorogastric intussusception, the decision to perform a Y-U pyloroplasty should be made on a case-by-case basis until further information is available.

To reduce the possibility of intussusception recurrence, a gastropexy and duodenopexy were performed in this case. Given that most cases of high intussusceptions occur in large breed dogs, a right-sided gastropexy can also serve as a prophylactic procedure for the prevention of gastric dilatation-volvulus. The duodenopexy in this case was performed without either incision or abrasion of the seromuscular layer. This decision was based on multiple factors, including easy reversal if complications resulted, and stronger adhesions were not thought to be needed as the probable cause (i.e., the foreign body) was removed. The entire length of the intestinal tract was not plicated in this case (or in any other case of a high intussusception). Recurrence of a pylorogastric/duodenogastric intussusception has not been described; however, recurrence rates of up to 17% have been reported for other types of intussusceptions.⁸ Early publications promoted the use of routine enteroplication with surgical correction of intussusceptions.^5,21 Since that time, publications have shown no recurrence without enteroplication, and no significant difference in the need for a second surgical procedure between plicated and nonplicated groups was noted.^7–9 Complications of enteroplication, such as small intestinal obstruction from plant material or strangulation, have been described in up to 19% of cases.⁷ Randomized, multicenter, prospective clinical studies are needed to evaluate the role of enteroplication with both high and low intussusceptions. Until then, the authors advocate the use of gastropexy and duodenopexy for high intussusceptions, knowing that each individual surgeon must balance the potential benefits with the risk of complications.

Conclusion

Pylorogastric/duodenogastric intussusception is a rare problem in veterinary medicine. It appears to be more common in large breed dogs, but can occur in small breeds. All cases reported to date have presented with severe, acute vomiting. Dietary indiscretion, renal failure, and gastric foreign body are possible predisposing factors. The survival rate of the six reported cases of pylorogastric/duodenogastric intussusception is 50%. High intussusceptions are a surgical emergency, but preoperative stabilization of the patient’s cardiovascular needs, electrolyte imbalances, and underlying disease (such as renal failure) is important. Reduction of the intussusception may be difficult and require a gastrotomy. The use of a right-sided incisional gastropexy and duodenopexy has been proposed to help prevent recurrence.¹⁵ Increasing knowledge, improved diagnostics (e.g., ultrasonography), and early treatment seem to be improving the survival rates associated with high intussusceptions; however, more information is needed about this rare condition to guide further recommendations.