A 5-year-old neutered Somali cat weighing 4.3 kg presented with a 2-week history of icterus with severe anorexia, lethargy and vomiting. On presentation, severe icterus, fever (39.8°C) and weight loss (11%) were observed.

The complete blood count (Procyte DX; IDEXX) result was within the reference interval (RI). A blood chemistry panel (FUJI DRI-CHEM 7000V; Fujifilm) revealed elevated liver enzymes and hyperbilirubinemia. The serum amyloid A (SAA) concentration (FUJI DRI-CHEM IMMUNO AU10V; Fujifilm) was also increased (Table 1).

Thoracic and abdominal radiographs were unremarkable. Abdominal ultrasonography (ARIETTA 70; Hitachi) revealed an 11 mm long oval hyperechoic mass within the distal aspect of the dilated CBD. Intrahepatic bile ducts were also dilated. No ascites or gastrointestinal perforation was identified. EHBO appeared to be caused by intraluminal obstruction by the mass (Figure 1).

After intravenous therapy with maropitant citrate and metoclopramide in the hospital, exploratory laparotomy was performed under general anaesthesia on day 4. Epidural anaesthesia was delivered using ropivacaine hydrochloride and medetomidine hydrochloride (2 mg/kg and 2 μg/kg, respectively). Fentanyl and ketamine (1 μg/kg/h and 0.2 mg/kg/h, respectively, as a continuous infusion) were continued until the day after surgery.

With the cat in dorsal recumbency, a ventral midline incision was made from the xiphoid process to the umbilicus. Highly viscous ascitic fluid was noted on abdominal entry, which was collected for cytological analysis and bacterial culture. The mass was palpable within the distal portion of the CBD. The proximal CBD was approximately 20 mm dilated and adherent to the duodenum (Figure 2a). When the adhesion was dissected using bipolar forceps, a 15 mm long duodenal perforation was found at the adhesion site, and multiple ulcerative lesions were recognised in the mucosa around the site. The mass and perforation site were resected, followed by a choledochoduodenostomy with the Billroth II procedure (Figure 2b,c). First, the distal CBD was dissected from the portal vein and pancreas using bipolar forceps or sterilised cotton swabs, ligated twice with hemoclips and cut with Metzenbaum scissors proximal to the confluence point of the pancreatic duct. Then, it was decided that the gastrointestinal tract from the pyloric antrum to the duodenum rostral to the major duodenal papilla would be resected. Branches of the right gastric and gastroepiploic arteries and veins in this area were ligated using bipolar forceps. The pyloric antrum was cut with a stapling device (Endo GIA Tri-Staple 2.0 mm × 60 mm; Medtronic) and the duodenum was occluded with Doyen forceps and cut with Metzenbaum scissors. The CBD proximal to the mass was cut using Metzenbaum scissors, and all resected tissues were examined histopathologically. A bile sample was also collected for bacterial examination.

Biliary and intestinal tract reconstruction started with end-to-end choledochoduodenostomy, which was closed with 5-0 polydioxanone monofilament suture material in a Gambee’s continuous pattern. Subsequently, a side-to-side jejunal anastomosis (Braun anastomosis) was performed as follows: the jejunum 10 cm distal to the caudal duodenal flexure was juxtaposed 20 cm distal to the site. Occluding with a Doyen forceps, 4 cm long full-thickness incisions were made in the antimesenteric border of the sites using a scalpel and Metzenbaum scissors. The anastomosis was completed using a simple continuous pattern of 4-0 polydioxanone monofilament suture material. Finally, the middle of the loop was anastomosed to the ventral aspect of the stomach (side-to-side gastrojejunostomy) in an isoperistaltic fashion, using the same material (Figures 2 and 3). There was no tension at either of the anastomosis sites. Liver biopsy, peritoneal lavage and abdominal drainage tube placement were also performed. The abdomen was closed routinely, and a feeding tube was placed through the oesophagus into the stomach. The tube was not removed until the cat died.

The cat recovered uneventfully from the surgery and received intravenous nutrition for 2 days after surgery. Enteral nutrition was started on day 7. A small amount of gastric juice (<10 ml) was occasionally withdrawn through the feeding tube. Icterus and anorexia improved almost completely during hospitalisation without nausea and vomiting. The abdominal drainage tube was removed on day 9. Bacterial cultures of both the ascitic fluid and bile samples were negative. Cefmetazole sodium and clindamycin phosphate were continued for 1 week postoperatively. Supportive medications including maropitant citrate, lansoprazole, metoclopramide, mosapride citrate, prednisolone, albumin tannate and probiotics were administered at the usual doses and continued until death. The cat was discharged on day 15.

Based on histological and immunohistochemical findings, the mass was diagnosed as a neuroendocrine carcinoma with gastrin-producing cell differentiation (Figure 4), and the liver sample was diagnosed as chronic cholangiohepatitis. No tumour cells were observed in the stomach, duodenum or liver.

Serum gastrin concentrations were measured retrospectively and were elevated on days 1 and 15 (970 and 740 pg/ml, respectively; RI ⩽200 pg/ml in humans; Hoken Kagaku).

Four days after discharge (day 19), the cat revisited with severe anorexia, lethargy and pyrexia. Only the SAA concentration was markedly increased. As the gallbladder wall appeared to be thickened on abdominal ultrasonography, bacterial cholecystitis was suspected. The cat was treated with enrofloxacin and supportive care. Eight days later, anorexia and lethargy improved almost completely and the body temperature was normal. The SAA concentration was decreased to the RI. Enrofloxacin was continued until the patient’s death.

On day 55 (40 days after discharge), the cat returned with occasional vomiting. No anorexia or lethargy was observed. Liver enzymes and SAA concentration were increased without hyperbilirubinaemia. Abdominal ultrasonography showed multiple mixed-pattern hepatic nodules (up to 10 mm) and swelling of the left hepatic lymph node. Exacerbation of cholangiohepatitis or tumour metastases was suspected. The owner declined further examination. There was no subsequent anorexia or lethargy, but occasional vomiting and weight loss persisted. The increase in liver enzymes and SAA concentration worsened gradually, with mild anaemia, and the cat died on day 103. A postmortem examination was not performed.