Introduction

Gallbladder torsion is defined as an axial rotation of the gallbladder at the cystic duct and can result in compromised bile and blood flow, leading to infarction, necrosis, and perforation of the gallbladder or cystic duct. With early surgical intervention, the risk of perforation and bile peritonitis is reduced.^1,2

In human medicine, gallbladder torsion is a rare but important differential diagnosis when patients present with an acute abdomen. Knowledge has been collected through ∼500 case reports.¹ Most involve the relaxation and atrophy of a previously normal mesentery in the elderly, leading to a floating gallbladder attached to the liver by an elongated mesentery.^1,3 But there are also congenital types in which the mesentery covers only the cystic duct and artery.^4,5 Alternatively, the gallbladder is attached to the biliary system solely by the cystic duct, with no attachment to the liver. This is called a wandering gallbladder.³ These congenital malformations are thought to be exacerbated following liver atrophy in the elderly patient, thus leading to a higher incidence of torsion late in life.⁶ However, torsion has been reported in all age groups, the youngest being 2 yr old.⁷

Currently described differential causes for extrahepatic biliary diseases in dogs include cholecystitis, necrotizing or emphysematous cholecystitis, pancreatitis with associated periductal fibrosis, abscesses, neoplasia, trauma, cholelithiasis, and gallbladder mucocele.^8–10 Gallbladder torsion is a rare condition in dogs. The anatomic variation “wandering gallbladder” that may predispose for gallbladder torsion has not been previously described as an incidental finding in dogs. Based on a complete literature review, this is the first report of a torsion of a wandering gallbladder leading to secondary bile leakage in an otherwise healthy juvenile dog presenting with an acute abdomen.

Case Report

An 11 mo old intact female German shepherd dog weighing 29 kg was presented with a history of acute-onset of cascade vomiting over 24 hr. The owner described the dog as previously healthy, although she did have concerns about the dog being slightly underweight. Upon presentation, the dog had a moderately depressed demeanor; the mucous membranes were pink but tacky, and a 5% dehydration was estimated. The dog was tense and painful upon cranial abdominal palpation. A body condition score of 3/9 was estimated. The remainder of the physical examination did not reveal any abnormalities.

The complete blood count was within reference range (RR). Abnormal findings on the serum chemistry profile included potassium slightly below RR at 3.8 (RR 4–5.1 mg/dL) and alanine-amino-transferase slightly elevated at 1.79 (RR <1.4 μkat/L).

Right lateral and ventrodorsal abdominal radiographs showed a slight loss of serosal detail in the central ventral abdomen and a few small gas-distended intestinal loops. An abbreviated ultrasound revealed a slightly increased amount of peritoneal effusion in the right-cranial quadrant and gas- and fluid-distended bowel loops.

The dog received two intravenous crystalloid fluid boluses of ringer acetate^a at a rate of 20 mL/kg over 20 min and was placed on a continuous rate infusion of 5 mL/kg/hr after initial stabilization as well as being given a maropitant citrate^b 1 mL/kg subcutaneous injection and esomeprazole^c 1 mg/kg IV. Upon clinical reevaluation, the dog was normovolemic, and the vital signs remained within normal range despite a persistent dolent abdomen and vomitus.

Because of the continuation of signs and the ultrasonography findings of increased peritoneal fluid in the cranial abdomen and the gas-/fluid-filled and distended bowel loops, a surgical exploratory laparotomy was recommended.

The dog was premedicated with methadone^d 0.2 mg/kg intramuscularly and diazepam^e 0.2 mg/kg IV; and anesthesia was induced with IV propofol^f 0.5 mg/kg to effect. The dog was intubated and maintained with inhaled sevoflurane^g in 100% oxygen. Ringer acetate at a dose of 10 mL/kg/hr IV was given during anesthesia.

Surgical exploration of the abdomen was performed via a ventral midline celiotomy. Upon inspection of the liver, the gallbladder was seen to be in an intraperitoneal position rotated 7–10 times counterclockwise around the axis of the cystic duct and artery, and a clear demarcation of nonviable and viable duct was visible. Leakage of bile was noted at this border. The gallbladder appeared normal in size (8 × 4 × 4 cm) but was without the normal peritoneal attachments to the quadrate and right middle liver lobes (Figure 1). Because of the multiple times the gallbladder had rotated, it had started to entrap the distal part of the right pancreatic limb (Figure 2). The gallbladder was derotated to release the pancreas and was then resected using hemoclips^h and a circumferential ligature of polyglactin 2-0ⁱ placed proximal to the demarcation on the cystic duct and artery. No adhesions were found, and the bile contamination in the abdomen was minimal. The abdomen was lavaged with warm isotonic saline. Once released from the entrapment with the gallbladder, the pancreas appeared to have no further trauma. No other concurrent abnormalities or malformations were noted. The abdomen was closed routinely, and the gallbladder was submitted for histopathologic evaluation.

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The dog recovered well from anesthesia, and vital signs remained within normal limits overnight. Postoperative pain was relieved with methadone 0.2 mg/kg q 4 hr, and fluids were continued at 5 mL/kg/hr overnight until the dog was able to feed on a low-fat diet. After surgery, there were no further episodes of vomiting, and the abdomen was soft on palpation the next day. The dog was discharged from the hospital with robenacoxib^j 1.4 mg/kg per os q 24 hr for 5 days. Recovery was uneventful. At suture removal and at 1 yr follow-up, the dog was asymptomatic, active, and alert and maintained a body weight of 30 kg.

Histopathology revealed no inflammatory changes and no signs of neoplasia; most of the sample showed extensive necrosis of the wall with islands of normal gallbladder epithelium, consistent with ischemic necrosis secondary to torsion.

Discussion

Gallbladder torsion has been reported in a middle-aged German shepherd dog having adhesions from previous peritoneal-pericardial hernia surgery and an abdominal foreign body. In this case, the complete absence of normal anatomic attachments to the hepatic fossa was also recognized as a predisposing factor.¹¹ The case presented here describes a similar congenital malformation with a complete absence of peritoneal and connective tissue attachments to the liver, a wandering gallbladder according to human terminology, as the only predisposing factor allowing for the torsion to occur in this juvenile dog.³

A different etiology for the torsion of the cystic duct was described in two case reports involving German shepherd dogs with a previous history of surgery, in whom the gallbladder twisted together with the quadrate and right middle liver lobes. In both cases, the anatomy was normal, with the normal connective tissue attachment between the liver and the gallbladder.^12,13 Table 1 summarizes these four published cases.

TABLE 1 Currently Published Cases of Gall Bladder Torsion in Dogs

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Gallbladder torsion can be classified as either incomplete, in which rotation is ≤180°, or complete, in which rotation is >180°. Both clockwise and counterclockwise rotation has been described in humans.⁶

With 7–10 times of 360° twisting in a counterclockwise fashion, this torsion was complete and illustrates that when excessive twisting occurs, there is also a risk for damage to or strangulation of nearby organs such as the pancreas.

Volvulus of abdominal organs most commonly involves the stomach, mesentery, colon, or spleen. It is interesting that all four cases involving torsion of the gallbladder have occurred in German shepherd dogs because in studies involving splenic torsion and mesenteric torsion, the German shepherd dog breed has also been found to be at increased risk.^14,15

The actual torsion is thought to be initiated from violent peristaltic movements of neighboring organs, sudden body movements, or abdominal trauma.¹⁰ All three of the previously reported canine cases involving torsion of the cystic duct had multiple disorders associated including previous surgery, an abdominal cavity foreign body, adhesions, lymphoma, gastric dilation and volvulus, splenectomy, and pericardioperitoneal hernia. Preexisting or concurrent gastrointestinal tract diseases such as exocrine pancreatic insufficiency and lymphoplasmacytic enteritis have been associated with colonic torsions and mesenteric torsions.^16,17 In this case, however, there were neither concurrent pathologies or malformations nor symptoms involving the gastrointestinal tract before presentation or developing during the follow-up period.

Both cases of gallbladder torsion, with >360° of torsion, were presented with a sudden onset of symptoms of 1–2 days duration and characterized by abdominal pain and vomitus. This is a clinical presentation similar to what is seen in humans with complete torsion rather than the incomplete torsion of the gallbladder, often mimicking biliary colic.⁴

Hematological abnormalities in these two cases were nonspecific; in humans, liver function tests are usually normal, the bilirubin may be elevated, and only with the onset of gangrenous cholecystitis are increases in c-reactive protein and white blood cell count noted.⁴ The peripheral bilirubin was not elevated in our case as a result of the common bile duct remaining patent, as only the cystic duct was acutely obstructed with the torsion. Also, the amount of bile leakage to the abdomen was minimal because of early detection and surgery.

Gallbladder torsion has traditionally only been diagnosed intraoperatively in human medicine as a result of often unremarkable blood values and radiographic changes.¹ However, since 1991, 25% of human patients have been diagnosed preoperatively.⁶ This has been made possible by an increased awareness of the condition as well as by the recognition of specific ultrasound features such as a thickened gallbladder wall with pericholecystic fluid located below its normal anatomic fossa (the sign of the floating gallbladder). Furthermore, the duct can have an echogenic conical structure (representing the twisted pedicle) at the gallbladder neck, and both gross gallbladder distention and no distention occur.^5,18 The ultrasonographic examination and the preoperative radiographs in this case showed unspecific findings, indicating free fluid locally in the right-cranial abdominal quadrant, and there was no gross gallbladder distention. The final diagnosis was made during the exploratory laparotomy. There was no sign of previous trauma, but because this pathology has never been observed at surgery or at postmortem and reported, this remains a suspected case of a wandering gallbladder. A high index of suspicion is needed to diagnose this rare clinical finding preoperatively, avoiding the complication of bile peritonitis.

Conclusion

Based on a complete literature review, this is the first report of a gallbladder torsion in a juvenile dog presenting with an acute abdomen. Prompt intervention contributed to a favorable outcome, avoiding severe bile peritonitis, with the patient alive and happy at recheck 1 yr later. This case report further supports listing this uncommon clinical finding as a differential diagnosis for extrahepatic biliary disease, potentially leading to bile peritonitis and presenting as an acute abdomen. More case reports on gallbladder torsion as well as descriptions of diagnostic imaging are necessary to obtain a better understanding of the prevalence, predisposing factors, and variations in presentation.