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Can Vet J. 2010 January; 51(1): 85–88.
PMCID: PMC2797356

Language: English | French

Chronic mesenteric volvulus in a dog

Abstract

A chronic, partial mesenteric volvulus was found on laparotomy of an adult Bernese mountain dog with a 4-month history of intermittent vomiting, diarrhea, and weight loss. The dog had elevated cholestatic and hepatocellular leakage enzymes, increased bile acids, azotemia, isosthenuria, and a hypokalemic, hypochloremic, metabolic alkalosis. The dog recovered fully following reduction of the volvulus.

Résumé

Volvulus mésentérique chronique chez un chien. Un volvulus mésentérique partiel chronique a été trouvé lors d’une laparatomie sur un Bouvier bernois adulte présentant de manière intermittente depuis 4 mois des vomissements, de la diarrhée et une perte de poids. Le chien présentait des enzymes cholestatiques et hépatocellulaires élevés, des acides biliaires accrus, de l’azotémie, de l’isothénurie et une alcalose hypokaliémique, hypochlorémique et métabolique. Le chien s’est complètement rétabli après la réduction du volvulus.

(Traduit par Isabelle Vallières)

A 29.4 kg, 4-year-old, castrated male, Bernese mountain dog was presented to the veterinary teaching hospital at the Western College of Veterinary Medicine with a 4-month history of intermittent vomiting, diarrhea, and weight loss. Symptomatic treatment with ranitidine (Zantac, Nu-Pharm, Richmond Hill, Ontario), metoclopramide (Reglan, Sandoz Canada, Boucherville, Quebec), and sucralfate (Sulcrate, Nu-Pharm, Richmond Hill, Ontario) and intermittent hospitalization with intravenous fluid therapy achieved partial response with firmer feces and less frequent vomiting. However, within 1 to 2 wk of discontinuing therapy, clinical signs relapsed. The dog was on intravenous fluid therapy 24 h prior to referral to the teaching hospital. Dietary trials, using commercial gastroenteric diets had been attempted with no long-term improvement and the dog had since been maintained on a commercial raw food diet. Three years prior to presentation, the dog had an intestinal foreign body removed surgically via a single enterotomy in the proximal duodenum. Distemper, canine adenovirus 2, parainfluenza, parvovirus, and rabies vaccinations were current.

Case description

On presentation, physical examination revealed a thin body condition (body condition score 2/5), 10% dehydration, and lethargy. There was mild intestinal thickening on abdominal palpation, but there was no pain response.

A complete blood (cell) count (CBC) lacked a stress leukogram and was within normal limits except for a mild monocytosis (1.972 × 109/L; reference range: 0.08 to 1.0 × 109/L). A serum biochemistry profile indicated hyponatremia (135 mmol/L; reference range: 145 to158 mmol/L); hypokalemia (2.9 mmol/L; reference range: 3.8 to 5.6 mmol/L); hypochloremia (85 mmol/L; reference range: 103 to 118 mmol/L); mild azotemia (urea 16.2 mmol/L; reference range: 3.5 to 11.4 mmol/L); and creatinine (140 μmol/L; reference range: 41 to 121 μmol/L); severe alanine aminotransferase (ALT) elevation (1301 U/L; reference range: 19 to 59 U/L) and moderate alkaline phosphatase (ALP) elevation (533 U/L; reference range: 9 to 90 U/L); moderate gamma-glutamyltransferase (GGT) elevation (37 U/L; reference range: 0 to 8 U/L); and a mild hyperbilirubinemia (total bilirubin 8.0 μmol/L; reference range: 1.0 to 4.0 μmol/L). Amylase and lipase were within the reference ranges. Urine specific gravity (1.018) was approaching isosthenuria and the pH was 6.5. The urine sediment was inactive.

On blood gas analysis, a metabolic alkalosis was noted (pH 7.5, bicarbonate 30 mmol/L; reference range: 15 to 25 mmol/L). Fasting and post-prandial serum bile acids were moderately elevated (fasting serum bile acids 85 μmol/L; reference range: 0 to 10 μmol/L and post-prandial serum bile acids 43 μmol/L; reference range: 0 to 20 μmol/L). Given the lack of a stress leukogram, an ACTH stimulation test was performed and the results were normal. Fecal culture was negative for common pathogens and fecal flotation was negative for parasitic ova and oocysts. Leptospira titers were assayed, given the abnormalities of both renal and liver parameters. Titers for L. pomona, L. icterohaemorrhagiae, L. canicola, L. bratislava, L. grippotyphosa were negative (< 1:40). The titer for L. autumnalis (1:80) was suspicious.

Abdominal radiographs on presentation revealed 2 large bone fragments in the stomach and marked gas distension of the small intestine suggestive of gastrointestinal obstruction. Abdominal radiographs taken 24 h later showed that the bone fragments had passed into the caudal colon, and the obstructive gas pattern had resolved. No abnormalities were noted on thoracic radiographs or abdominal ultrasonography.

Intravenous fluid therapy (Normosol-R) was initiated at 1.5 times maintenance [80 mL/kg body weight (BW), q24h] plus the calculated deficit (10% dehydration) of 2.6 L (50% of the deficit replaced in the first 8 h and the remainder over the next 16 h). Potassium chloride (KCL) was supplemented based on serial blood gas electrolyte measurement (Hospira, Montreal, Quebec). The dog was treated with ampicillin (Novopharm, Toronto, Ontario), 22 mg/kg BW, TID, IV, and enrofloxacin (Baytril, Bayer, Toronto, Ontario), 2.5 mg/kg BW BID, PO. No vomiting was noted after hospitalization, so food was reintroduced 24 h after admission.

After 2 d of intravenous fluid therapy, ALT (590 U/L), ALP (331 U/L), GGT (26 U/L), and total bilirubin (5 mmol/L) were still elevated; azotemia, however, had resolved. Mild hypoalbuminemia had developed (27 g/L; reference range: 28 to 38 g/L).

Exploratory laparotomy was recommended based on multiple organ involvement. An exploratory surgery would help to rule out a portosystemic shunt and to evaluate and obtain biopsies of the liver, kidneys, and intestines. A coagulation panel was found to be normal.

The dog was pre-medicated with hydromorphone hydrochloride (Sandoz Canada), 0.1 mg/kg IM, and induced with propofol (Rapinovet 10 mg/mL, Schering Plough, Pointe-Claire, Quebec), 4.0 mg/kg IV, and diazepam (Sandoz Canada), 0.2 mg/kg IV, to allow endotracheal intubation. Anesthesia was maintained with inhaled gas anesthetic, isoflorane (IsoFlo, Abbott Animal Health, St. Laurent, Quebec). A morphine epidural was administered. Dextrans (10 mL/kg) were administered intraoperatively, in response to hypotension. Exploratory surgery via a midline celiotomy approach revealed numerous omental and mesenteric adhesions. A chronic mesenteric volvulus was present that involved the distal jejunum, ileum, and ileoceco-colic junction with associated fibrous mesenteric adhesions. The volvulus was in a clockwise direction and involved the jejunum wrapped around the ileocolic root. The volvulus was not tight and all portions of the intestine involved appeared viable with minimal evidence of venous congestion. The adhesions were sharply dissected to allow reduction of the volvulus. A splenic vein portogram was performed using iohexol (Omnipaque; Amersham Health, Oakville, Ontario), 0.33 mL/kg, and intra-operative fluoroscopy. Results were viewed with fluoroscopy. There was no evidence of a portosystemic shunt. Bile was aspirated for cytology and culture. Liver was biopsied and submitted for aerobic and anaerobic culture. Biopsies of liver, left renal cortex, duodenum, jejunum, and the antrum of the stomach were submitted for histopathology. Cefazolin (Sandoz Canada), 22 mg/kg q2h, was administered twice during surgery.

Recovery was routine, and the dog was maintained on IV fluids (Normosol-R) at 1.5 times maintenance fluid rate with KCl added (20 mEq/L) for 2 d post surgery. Analgesia was provided with hydromorphone, 0.05 mg/kg, SQ, q6h, for 12 h post surgery.

Histopathology results were as follows: terminal hepatic perivenular fibrosis and zone 3 granular hepatopathy, mild mixed inflammatory cell enteritis with lacteal dilation involving the duodenum and jejunum, and mild small mononuclear gastritis. No renal lesions were noted in the kidney biopsies. Liver biopsy and bile aspirate cultures were negative for aerobes and anaerobes.

The dog was discharged from the hospital 2 d later after eating and drinking well with no signs of vomiting or diarrhea. Tramadol (compounded at WCVM, PCCA, London, Ontario), 100 mg BID, enrofloxacin (Baytril; Bayer, Toronto, Ontario), 75 mg BID, and amoxicillin (Amoxil, Pfizer Canada, Kirkland, Quebec); 400 mg BID, were prescribed for at home administration PO for 7 d.

One week after surgery, the dog was doing well clinically with good appetite (cooked homemade diet and commercial bland diet) and no vomiting. Fecal consistency had continued to improve but was still slightly soft. Hepatocellular enzyme concentrations had decreased but continued to be mildly elevated: ALT 98 U/L, Alk Phos 154 U/L, GGT 12 U/L. Urine specific gravity was 1.014 but no azotemia was present. Fasting and post-prandial bile acids were normal. Two weeks after surgery hepatocellular enzyme concentrations had normalized.

Acute titers for L. autumnalis had been suspicious for leptospirosis (1:80) but convalescent titers were negative. The dog gained 14 kg over the next several months and has remained clinically normal for 18 mo since surgery.

Discussion

Mesenteric volvulus is a rare, acute, and often fatal condition in dogs (1,2). It occurs when there is a twisting of the bowel on its mesenteric axis, which is different from intestinal torsion where the bowel twists on itself (3). Mesenteric volvulus usually results in occlusion of the cranial mesenteric artery and vein and their branches, leading to vascular obstruction and venous congestion in the distal duodenum, jejunum, ileum, cecum, ascending colon, and proximal descending colon (1). Death is usually due to shock and endotoxemia, secondary to intestinal necrosis, euthanasia, or surgery (2,4).

Most cases of mesenteric volvulus have no identifiable cause. Abnormalities in gastrointestinal motility secondary to disorders such as exocrine pancreatic insufficiency (particularly in German shepherd dogs), inflammatory bowel disease, ileocolic intussusception, gastric dilatation volvulus, and gastrointestinal foreign bodies may predispose a dog to mesenteric volvulus (3). In adult humans, intestinal volvulus is rare and may be primary or secondary to an anatomic abnormality such as a neoplasm or adhesion (5). Mesenteric volvulus in dogs can be either partial or complete, which presumably can be the case with intestinal volvulus (4).

Mesenteric volvulus has no pathognomonic clinical signs, although the presentation often includes weakness, recumbency, and shock in acute cases (3). There may also be a history of vomiting, diarrhea, hematemesis, or hematochezia (4,6). Abdominal pain and distension may also be noted (2). Abdominal radiographs often show distension of the small intestines and decreased abdominal detail (4,7). In humans, transabdominal ultrasonography may reveal a whirlpool sign created by the mesenteric artery and vein malposition with mid-gut intestinal volvulus (8). This whirlpool sign may also be visualized using computed tomography (8). Clinicopathological results are variable and may be within normal limits or include hypoalbuminemia, hypoproteinemia, and hypokalemia (1,3).

The dog in this case had a history of chronic intermittent vomiting and diarrhea. Although vomiting and diarrhea are not unusual findings in mesenteric volvulus, the chronic course is unreported in the literature to our knowledge. The long duration of signs allowed significant weight loss to occur. He was not in shock, and did not present with abdominal distension or pain. The gas pattern on abdominal radiographs could have suggested an obstructive pattern or a functional ileus but the clinical presentation was not consistent with an acute obstruction or volvulus. The volvulus was not tight enough to cause marked impedance of blood flow and may have caused either a motility disorder or intermittent mild ischemia. Clinicopathological findings indicated an upper gastrointestinal obstruction and multi-organ involvement. Hypokalemia can occur with mesenteric volvulus and was likely due in this case to vomiting and diarrhea. Obligate kaliuresis due to diuresis at the referring clinic or related to the metabolic alkalosis may have also played a role in development of hypokalemia. In metabolic alkalosis, potassium can shift to the intracellular compartment and there is increased secretion of potassium at the distal renal tubules. Decreased dietary intake alone would not be sufficient to cause hypokalemia, but these other factors may have exacerbated it (9).

As previously noted, foreign bodies, enteritis, and abdominal adhesions may be associated with volvulus. The dog had a history of all these conditions. He had a previous history of having had a foreign body. The omental and mesenteric adhesions noted on exploratory surgery for the volvulus, could have been related to his previous foreign body surgery. It may be possible that when “running the bowel” during the initial exploratory surgery, a displacement or mesenteric twist may have occurred. This displacement or twist could have subsequently become permanent as adhesions formed. Adhesions in dogs generally result from ischemia, inflammation, or infection. An intestinal leak or area of ischemia may have been present in association with the previous foreign body. Alternatively, these adhesions could have been related to the chronic course of the volvulus. On intestinal biopsy, inflammatory bowel disease with a cellular infiltrate comprised primarily of lymphocytes and plasma cells was found. However, whether any of these conditions was a cause or effect of the volvulus is unknown.

The hepatic histopathology finding of zone 3 granular hepatopathy and perivenular fibrosis is indicative of altered blood flow or chronic obstruction of hepatic venous outflow (10). There was no indication of inflammation. The association between ischemic hepatopathy and mesenteric volvulus has not previously been reported in dogs but portal hypoperfusion with resultant ischemic hepatopathy could be anticipated with a mesenteric volvulus just as it occurs in gastric dilatation-volvulus (10). This claim is further supported by a case report in a human of ischemic hepatitis and mesenteric volvulus (11). However, in the human case report, concurrent chronic pulmonary disease likely induced hypoxic hepatic injury in addition to portal hypoperfusion. Chronic alteration of hepatic blood flow such as would be anticipated in the present case, could then lead to fibrosis.

An alternative or additional explanation for the reactive hepatopathy observed in this case is hepatopathy induced by endogenous toxins and/or nutritional changes related to the mild inflammatory bowel disease (IBD) noted on histopathology (12). In humans, there is a relationship between IBD and hepatobiliary disease with nearly 1/3 of human IBD patients having concurrent abnormal hepatic enzyme activity (13). It has been suggested that dogs with IBD can have mildly elevated ALT and ALP activities, and occasionally an increase in serum bile acids (as seen in this case) but there does not seem to be any peer-reviewed literature to support this claim (14). It is postulated that IBD could instigate a release of inflammatory mediators, as well as increase intestinal permeability to endo-toxins and bacteria which enter the portal system leading to extrahepatic bacterial infections or inflammation and resultant hepatic cholestasis (12). It is speculated that this dog, which had been fed a raw food diet, may have had a high bacterial load in the gastrointestinal tract (15). In addition to direct bacterial or endotoxic insult to hepatocytes, the subsequent release of inflammatory mediators from Kupffer cells can cause hepatocellular damage (13). One would anticipate seeing periportal inflammatory cells on histopathology if IBD were the cause of a reactive hepatopathy, but no hepatitic inflammatory cell population was noted on histopathology, arguing against IBD as a cause of the reactive hepatopathy.

Kidney biopsy revealed no abnormal findings, despite the history of azotemia in the presence of inadequate urine concentration. Hypokalemia was one of a number of electrolyte abnormalities. Hypokalemia is a common finding in dogs with mesenteric volvulus, or dogs with vomiting and diarrhea (3). Depletion in potassium can result in the loss of renal concentrating ability (9). The dog had also been treated with intravenous fluid therapy as recently as 24 h prior to the urinalysis. Fluid therapy can decrease urine specific gravity even before fluid deficits have been replaced. The isosthenuria may have resulted from the prior fluid therapy together with hypokalemia. Given these potential explanations and the resolution of the azotemia with fluid therapy, the azotemia was considered pre-renal in origin. The normal renal biopsies supported this assumption.

This case report shows that mesenteric volvulus may present as a chronic gastroenteritis with evidence of multi-organ involvement. Mesenteric volvulus requires laparotomy for diagnosis and correction. Successful treatment requires both supportive care and resolution of the volvulus. CVJ

Footnotes

Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office ( gro.vmca-amvc@nothguorbh) for additional copies or permission to use this material elsewhere.

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