Ingesta-associated choledocholithiasis in horses: 2 cases and literature review.

Equine ingesta-associated choledocholithiasis is a rare cause of morbidity and mortality. We describe here the clinical, gross, histologic, and microbiologic features of this condition in 2 horses and compare the features to 2 previous cases. Case 1 was a 4-y-old Thoroughbred mare with colic. Case 2 was an 18-y-old American Paint Horse mare with colic, chronic weight loss, and inappropriate mentation. Both had elevated biochemical markers of hepatocellular injury and cholestasis and were euthanized given a poor prognosis. Case 1 had a well-formed 5-cm choledocholith surrounding a piece of hay, and had chronic neutrophilic cholangiohepatitis, bridging fibrosis, and extrahepatic obstruction. Case 2 had an ill-formed choledocholith with occasional hay fragments, wood stick, and twigs, and had regionally extensive hepatocellular necrosis with mild neutrophilic cholangiohepatitis and bridging fibrosis. Enterococcus casseliflavus and Escherichia coli were isolated in both cases; Clostridium spp. were also isolated from case 2. All 4 reported cases had increased activity of cholestatic enzymes, hyperbilirubinemia, portal inflammation, and bridging fibrosis. Colic, pyrexia, leukocytosis with neutrophilia, and elevated hepatocellular enzyme activity were documented in 3 cases. Foreign material in all 4 cases was plant origin (choledochophytolithiasis), including hay (n = 2), sticks/twigs (n = 2), and grass awns (n = 1). Ingesta-associated choledocholithiasis may be considered as a cause of colic, pyrexia, and elevated cholestatic biomarkers in horses.

Choledochotomy and primary repair of extrahepatic biliary duct rupture in seven dogs and two cats.

OBJECTIVE: To report clinical findings and outcome in dogs and cats undergoing choledochotomy or primary repair of extrahepatic biliary duct rupture. METHODS: Retrospective study of dogs (n=7) and cats (n=2) that had choledochotomy or primary bile duct repair. RESULTS: Extrahepatic biliary obstruction was confirmed at surgery in all cases. The underlying cause in four dogs and both cats was choledocholithiasis, two dogs had gall bladder mucocoeles with associated bile duct rupture, and one dog had inspissated bile obstructing the bile duct secondary to gall bladder carcinoid tumour. Three dogs and both cats had choledochotomies performed to relieve extrahepatic biliary obstruction, and four dogs with bile duct rupture underwent primary repair of the defect. One dog with a bile duct rupture was re-explored four days postoperatively and had suffered dehiscence of the repair; this rupture was re-repaired. All animals were discharged from the hospital, and did not have clinical recurrence of extrahepatic biliary obstruction. CLINICAL SIGNIFICANCE: Choledochotomy and primary repair of extrahepatic biliary duct rupture were associated with low perioperative morbidity and no mortality in this small cohort of cases. These techniques are reasonable options either alone or in conjunction with other procedures when bile duct patency cannot be re-established by catheterisation or bile duct discontinuity exists.

Duplex gall bladder associated with choledocholithiasis, cholecystitis, gall bladder rupture and septic peritonitis in a cat.

A 10-year-old cat was presented with a history of inappetence, pyrexia and weight loss. Clinical investigations showed anaemia, hyperbilirubinaemia, septic peritonitis and a double gall bladder with choleliths in an extrahepatic duct. Initial medical stabilisation was performed. At laparotomy, a duplex gall bladder with two separate cystic ducts was identified. The left gall bladder was thickened and had ruptured at the apex. Multiple choleliths were identified in the left cystic duct. The right gall bladder and cystic duct were grossly normal. The ruptured gall bladder was repaired, the gallstones were removed via a choledochotomy of the left cystic duct and a choledochoduodenostomy was created from the dilated left cystic duct. The cat remained depressed and anorexic, and it was euthanased 72 hours postoperatively at the owners' request. This is the first ante-mortem investigation of extrahepatic biliary disease associated with gall bladder duplication in the cat.