Development of Spontaneous Bacterial Peritonitis after Extended Hepatic Resection in a Patient without Evidence of Liver Cirrhosis
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Hilar cholangiocarcinomas are often treated with liver resections. Hepatic dysfunction and infection are common postoperative complications. Although secondary bacterial peritonitis due to abdominal abscess or perforation is common, we report herein the first case of spontaneous bacterial peritonitis after hepatic resection. A 61-year-old male patient without underlying liver disease was diagnosed as having a Klatskin tumor,and a right trisectionectomy with caudate lobectomy was performed. From postoperative days 18-28, the patient gained 4.1 kg as ascites developed, and showed evidence of hepatic insufficiency with prolonged prothrombin time and jaundice. Computed tomography,performed at postoperative day 28 when fever had developed, showed only ascites without bowel perforation or abscess. When paracentesis was performed, the serum-ascites albumin gradient was 2.3 g/dL, indicating portal hypertension, and the ascites’polymorphonuclear cell count was 1,156/mm3. Since the clinical, laboratory, and image findings were compatible with spontaneous bacterial peritonitis, we started empirical antibiotics without additional intervention. Follow-up analysis of the ascites after 48 hours revealed that the polymorphonuclear cell count had decreased markedly to 108/mm3; the fever and leukocytosis had also improved. After 2 weeks of antibiotic treatment, the patient recovered well, and was discharged without any problem.
Abstract
Hilar cholangiocarcinomas are often treated with liver resections. Hepatic dysfunction and infection are common postoperative complications. Although secondary bacterial peritonitis due to abdominal abscess or perforation is common, we report herein the first case of spontaneous bacterial peritonitis after hepatic resection. A 61-year-old male patient without underlying liver disease was diagnosed as having a Klatskin tumor,and a right trisectionectomy with caudate lobectomy was performed. From postoperative days 18-28, the patient gained 4.1 kg as ascites developed, and showed evidence of hepatic insufficiency with prolonged prothrombin time and jaundice. Computed tomography,performed at postoperative day 28 when fever had developed, showed only ascites without bowel perforation or abscess. When paracentesis was performed, the serum-ascites albumin gradient was 2.3 g/dL, indicating portal hypertension, and the ascites’polymorphonuclear cell count was 1,156/mm3. Since the clinical, laboratory, and image findings were compatible with spontaneous bacterial peritonitis, we started empirical antibiotics without additional intervention. Follow-up analysis of the ascites after 48 hours revealed that the polymorphonuclear cell count had decreased markedly to 108/mm3; the fever and leukocytosis had also improved. After 2 weeks of antibiotic treatment, the patient recovered well, and was discharged without any problem.
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