Results suggest that cholecystectomy is an effective treatment for gallbladder mucocele. Although perioperative mortality rate is high, prognosis after discharge from the hospital is excellent. Rupture of the gallbladder warrants emergency surgical intervention but does not preclude a positive outcome.

Fourteen dogs with enlarged gallbladders and immobile stellate or finely striated bile patterns on ultrasound are described. Smaller breeds and older dogs were overrepresented, with 4/14 Cocker Spaniels. Most dogs presented for nonspecific clinical signs such as vomiting, anorexia and lethargy. Abdominal pain, icterus and hyperthermia were the most common findings on physical examination. All dogs except one had serum elevation of total bilirubin and/or alkaline phosphatase, alanine aminotransferase and gamma glutamyl transferase. All dogs were diagnosed with a gallbladder mucocele upon histologic and/or macroscopic evaluation. Ultrasonographically, mucoceles are characterized by the appearance of the stellate or finely striated bile patterns and differ from biliary sludge by the absence of gravity dependent bile movement. On ultrasound, gallbladder wall thickness and wall appearance were variable and nonspecific. The cystic or common bile duct were normal sized in 5 dogs although all 5 had evidence of biliary obstruction at surgery or necropsy. Loss of gallbladder wall integrity and/or gallbladder rupture were present in 50% of the dogs, all located in the fundus. Gallbladder wall discontinuity on ultrasound indicated rupture whereas neither bile patterns predicted the likelihood of gallbladder rupture. Pericholecystic hyperechoic fat or fluid were suggestive of but not diagnostic for a gallbladder rupture. Cholecystectomy appears to be an appropriate treatment for mucoceles, if not to treat a gallbladder rupture, at least in most dogs to prevent it since gallbladder wall necrosis was identified by histology in 9 of 10 dogs. Mucosal hyperplasia was present in all gallbladders examined histologically. Positive aerobic bacterial culture was obtained from bile in 6 of 9 dogs. Cholecystitis was diagnosed histologically in 5 dogs and 4 dogs had signs of gallbladder infection solely upon bacterial bile culture. Gallbladder infection was not present with all the mucoceles suggesting that biliary stasis and mucosal hyperplasia may be the primary factors involved in mucocele formation. Based on the results of our study, we suggest two alternate courses of action in the presence of a distended gallbladder with an immobile ultrasonographic stellate or finely striated bile pattern: a cholecystectomy when clinical or biochemical signs of hepatobiliary disease are present or a medical treatment (antibiotics and choleretics) and patient monitoring by follow-up ultrasound examinations when the patient does not have clinical or biochemical abnormalities. An aerobic bile culture should be obtained in all patients, by ultrasound-guided fine needle aspirate or at surgery.

This consensus statement on chronic hepatitis (CH) in dogs is based on the expert opinion of 7 specialists with extensive experience in diagnosing, treating, and conducting clinical research in hepatology in dogs. It was generated from expert opinion and information gathered from searching of PubMed for manuscripts on CH, the Veterinary Information Network for abstracts and conference proceeding from annual meetings of the American College of Veterinary Medicine and the European College of Veterinary Medicine, and selected manuscripts from the human literature on CH. The panel recognizes that the diagnosis and treatment of CH in the dog is a complex process that requires integration of clinical presentation with clinical pathology, diagnostic imaging, and hepatic biopsy. Essential to this process is an index of suspicion for CH, knowledge of how to best collect tissue samples, access to a pathologist with experience in assessing hepatic histopathology, knowledge of reasonable medical interventions, and a strategy for monitoring treatment response and complications.

Background: Portal vein thrombosis (PVT) has been reported infrequently in dogs. Objectives: To characterize the presentation, associated disease conditions, and outcome in dogs with PVT. Animals: Client-owned dogs with a diagnosis of PVT and a complete medical record. Methods: Records were retrospectively analyzed for presentation, history, physical examination, clinicopathologic data, diagnostic imaging, treatment, and outcome.Results: Thirty-three dogs were included. Common clinical signs were vomiting, diarrhea, abdominal pain, ascites, and signs of hypovolemic shock. Associated disease conditions included hepatic (14/33), neoplastic (7/33), immune (5/33), and infectious (4/33) diseases, protein-losing nephropathy (3/33), hyperadrenocorticism (2/33), protein-losing enteropathy (1/33), and pancreatitis (1/33). Fourteen dogs were receiving glucocorticoids at the time of diagnosis. Twenty-nine dogs had at least 1 predisposing condition for venous thrombosis, and 11 had 2 or more. Thrombocytopenia (24/33), increased liver enzyme activity (23/33), and hypoalbuminemia (20/33) were common laboratory abnormalities. Clinical syndromes at the time of PVT diagnosis included shock (16/33), systemic inflammatory response syndrome (SIRS), (13/33) and disseminated intravascular coagulation (3/33). Twenty-four dogs had acute and 9 had chronic PVT. Multiple thrombi were found in 17/33 dogs. Nineteen dogs survived to discharge. Dogs treated with anticoagulant therapy were more likely, whereas those with acute PVT, multiple thromboses or SIRS were less likely to survive.Conclusions and Clinical Importance: Hepatic disease is a common pre-existing condition in dogs with PVT. PVT should be considered in dogs with risk factors for venous thrombosis presenting with abdominal pain, ascites, and thrombocytopenia. Studies evaluating anticoagulant therapy in the management of PVT are warranted.

One hundred and fifty dogs with histopathologically confirmed intestinal disease were evaluated retrospectively. Sixty-one dogs had enteritis and 89 dogs had intestinal neoplasia. Ultrasonographic findings including the thickness and distribution of the intestinal lesion, the integrity of intestinal wall layering, regional lymph node thickness, the location of the intestinal segment involved, and regional motility were evaluated. Dogs with intestinal tumor had wall thickness (1.5 cm) significantly greater than dogs with NSE lesions (0.6 cm; p < 0.001). Ninety-nine percent of dogs with intestinal tumor had loss of wall layering while 88% of dogs with NSE had normal or altered wall layering (p < 0.001). Dogs with NSE were significantly more likely to have diffuse lesion (72%) than dogs with intestinal tumor (2%; p < 0.001). Lymph node median thickness in 24/61 dogs with NSE was 1.00 cm. The median thickness of the lymph nodes in 56/89 dogs with intestinal tumors was 1.9 cm. A multivariate analysis showed that loss of wall layering alone was an excellent predictive factor in differentiating intestinal tumor from NSE. In our population, dogs with loss of intestinal wall layering were 50.9 times more likely to have a tumor than enteritis.