Omental torsion in a guinea pig (Cavia porcellus)

Abstract

An adult intact male guinea pig (Cavia porcellus) was presented with gastrointestinal stasis. Radiographic findings demonstrated a gas- and fluid-filled cecum. Treatment was initiated but the animal died shortly after presentation. Gross postmortem revealed omental torsion with vascular thrombosis and necrosis. This is the first report of omental torsion with vascular thrombosis in a domestic animal.

A 3-year-old, intact male, guinea pig (Cavia porcellus) was presented on emergency to the Western College of Veterinary Medicine. The guinea pig had a 3-week history of decreased appetite. There was a marked decrease in water consumption, and a decrease in the production of feces. The diet consisted of fresh vegetables (mainly lettuce and tomatoes) and a commercial guinea pig diet (Hagen Guinea Pig Pellets; Rolf C. Hagen, Montreal, Quebec). Supplemental Vitamin C was not added to the diet; there had been no previous medical problems.

Case description

On physical examination, the guinea pig was depressed and dehydrated, with sunken eyes. The guinea pig had a thin body condition (body condition score 2/5) and weighed 900 g. The guinea pig was hypothermic, with a rectal temperature of 34.8°C (normal range: 37.2°C–39.5°C) (1), a heart rate within normal limits (240 beats/min; normal range: 230–380 beats/min) (1), and a normal respiration rate (90 breaths/min; normal range: 42–150 breaths/min) (1) with an increased respiratory effort. The mucous membranes were pink and there were no abnormalities noted on oral examination, using an otoscope. Dry and firm feces were produced at a decreased frequency. There was pain on abdominal palpation and the stomach was empty. Blood glucose was within normal limits (6.9 mmol/L; normal range: 3.33–10 mmol/L) (1). Further blood work was declined by the owner.

After physical examination, lactated Ringer’s solution (Abbott Laboratories, Saint-Laurent, Quebec) was administered subcutaneously at a dose of 20 mL/kg body weight (BW). Full body radiographs were taken. The cecum was enlarged and contained air and fluid. Based on the history and radiographs, the guinea pig was diagnosed with gastrointestinal bloat. A gastric volvulus was not detected on interpretation of the radiographs.

Treatment for gastrointestinal stasis was instituted, consisting of lactated Ringers solution (LRS) 120 mL/kg/d BW, SC, q8h; butorphanol tartrate (Torbugesic; Fort Dodge Animal Health & Animal Health Care Wyeth, Madison, New Jersey, USA) 2 mg/kg BW, SC, q8h; vitamin C (Life Brand, Toronto, Ontario) 100 mg/kg BW, PO, q24h, and simethicone (Ovol; Church & Dwight, Mississauga, Ontario) 20 mg/kg BW, PO, q8h. Force feeding was performed 4 times daily using critical care for herbivores (Critical Care for Herbivores; Oxbow Pet Products, Murdock, Nebraska, USA). The guinea pig was housed in a quiet and warm environment and placed on a heating pad for the remainder of the night.

The following morning, the guinea pig remained depressed and reluctant to move. The eyes remained sunken, and although feces continued to be produced, they remained dry. The guinea pig had eaten grass hay overnight. The body temperature had increased to 36.7°C, the heart rate was 290 beats/min and the respiration rate was 48 breaths/min. On percussion of the abdomen, a gas-filled stomach was elicited. The guinea pig decompensated as the day progressed, becoming less responsive and reluctant to move despite supportive treatment. The guinea pig was found dead in his cage the following morning; a postmortem was performed.

The gross morphological findings revealed 30 mL of yellow-brown turbid fluid in the abdominal cavity (a mixture of feed and fibrin); an omental torsion with a gastric displacement caudally into the abdomen, and a 90° partial gastric torsion with a 1-cm perforation on the greater curvature, approximately 5 cm cranial to the pylorus. The omental bursa was rope-like in appearance, congested, and had twisted upon its longitudinal axis at least 10 times. There was no evidence of attachment of the omental torsion to the gastric perforation. The gastric perforation could not be classified as ante- or postmortem. There was also a fibrinous peritonitis, hepatic lipidosis, and pulmonary congestion. Additional histologic findings included vascular thrombosis and glandular necrosis of the gastric mucosa with a multifocal suppurative histiocytic omental steatitis. The likely cause of death was the shock associated with an omental torsion and its associated vascular thrombosis and subsequent necrosis.

Discussion

The etiology of omental torsion in this case remains unknown. Omental torsion occurs when the omentum twists on its long axis, causing subsequent venous obstruction, edema, and vascular compromise leading to infarction and necrosis. Extravasation of fluid into the peritoneal cavity will cause an aseptic peritonitis, resulting in serosanguineous fluid (2). Common sequelae of omental torsions involve infarction, rupture of the torsed omental segment, intraperitoneal hemorrhage, adhesions, peritonitis, and abscess formation (3). In this case, it is possible that gastric perforation due to the torsion resulted in a fibrinous peritonitis, but it remains unknown as to whether the gastric perforation was antemortem.

Changes and irregularities in the omentum can increase the risk of primary omental torsions (4), in which a movable omental segment rotates around a pivot point. These torsions can occur as a result of inflammation and edema (4), anatomic abnormalities, and obesity (5,6). Coughing, straining, trauma, abrupt changes in body position, hyperperistalsis, and compression of the omentum by the liver and the abdominal wall (3) are all triggers. Secondary omental torsions differ, in that they have the free end of the omentum attached to a site with pre-existing pathology such as an adhesion, a cyst, a tumor, an external or internal hernia, a focal site of inflammation, or a congenital abnormality (7).

In humans, omental torsion can present clinically as acute abdomen (8), gastritis (8), acute appendicitis (9), pain in an iliac fossa (10), hip pain and a limp (11), acute abdominal distress (12), and duodenal ulcers (13).

The diagnosis of omental torsion is usually made intraoperatively in humans, as a result of the uncommon occurrence and nonspecific symptoms. Diagnosis requires confirmation via imaging techniques. Ultrasound and computed tomography (CT) have both been used to diagnose omental torsions preoperatively. The findings on ultrasound and CT are best described as an abdominal mass with a concentric distribution of fibrous and fatty folds that converge over the site of the torsion (14,15).

Spontaneous derotation can occur, but because of reported recurrent abdominal pain, conservative treatment is not recommended (16). The treatment for omental torsion consists of surgical omental resection. A simple manual detorsion is contraindicated because of the risk of necrosis and vessel thrombosis (16). Resection of the involved segment along with a segmental omentectomy is advised to reduce the risk of adhesion formations (2,17,18).

The greater omentum will often move to cover the stomach when there has been a gastric volvulus (19); however, the lack of omentum covering the stomach coupled with the severity of the omental torsion and its associated vascular thrombosis and necrosis indicated that the torsion was significant. The gastrointestinal ileus that occurred may have been instigated by dietary factors, underlying dental issues, infectious causes and/or stress. It is likely that the abdominal pain elicited in this guinea pig was secondary to the omental torsion, with the guinea pig subsequently becoming anorexic.

To the authors’ knowledge, omental torsion with vascular thrombosis and necrosis has not been reported in animals. It is thought that this guinea pig had a primary omental torsion and the underlying cause could not be found. Omental torsion around the right gastroepiploic artery, which supplies the greater curvature of the stomach, has been reported in humans (20). It is possible that a similar event occurred in this guinea pig, causing subsequent infarction and necrosis.

Hepatic lipidosis is a common sequela to anorexia in guinea pigs and can be seen as soon as 12 h after the start of anorexia. Pulmonary congestion may be evident with sepsis which may have occurred from the mucosal necrosis and ischemic damage in the stomach. The omental steatitis likely occurred from arterial occlusion, as torsion can cause fat necrosis (8), pressure necrosis, and peritonitis (3).

While the clinical signs of acute abdomen may be recognized clinically as pain on abdominal palpation and gastrointestinal stasis, omental torsion is difficult to diagnose without imaging modalities. Independent of the cause of the gastrointestinal ileus, guinea pigs decompensate rapidly and pain management is imperative. Exploratory laparotomies as a diagnostic tool in guinea pigs should be approached with caution as anesthetic management can be difficult in unstable patients. In this case, medical management did not resolve the condition and an exploratory laparotomy may have helped to avoid the deleterious effects of an omental torsion. Omental torsion with vascular thrombosis and necrosis should be considered as a differential diagnosis for abdominal pain and gastrointestinal stasis in guinea pigs. CVJ