Meropenem

  • PDF / 174,457 Bytes
  • 1 Pages / 595.245 x 841.846 pts (A4) Page_size
  • 5 Downloads / 118 Views

DOWNLOAD

REPORT


1 S

Vanishing bile duct syndrome: case report A 79-year-old man developed vanishing bile duct syndrome (VBDS) during treatment with meropenem for Serratia marcescens infection [route and duration of treatment to reaction onset not stated]. The man brought to a hospital in 2019 by ambulance due to sudden-onset of abdominal pain and collapsed at a local shop. He was hypotensive and showed bradycardia. He was rushed to the operating room for open exploratory laparotomy, which showed a ruptured infrarenal abdominal aortic aneurysm. He successfully underwent open repair of the aneurysm. During the procedure he had a significant blood loss and treated with packed cells units, fresh-frozen plasma, cryoprecipitate, platelets and crystalloids. After the surgery, he was shifted to the ICU, intubated and treated with unspecified vasopressors. He showed a medical history of benign prostatic hypertrophy and hypertension. His pre-admission regular medications included atorvastatin, amlodipine and dutasteride/ tamsulosin. He also had a documented allergy to penicillin in the form of a rash. He remained unstable postoperatively. He showed acute kidney injury, mild abdominal hypertension required sedation and paralysis. On post-operative day 10, he was extubated. However, he was again intubated after few hours because of worsening respiratory failure. On the same day, he developed signs of sepsis including leukocytosis and fever and he later became unstable and which needed unspecified vasopressors. Because the source of infection was not clear, vancomycin and meropenem 1g every 8 hours were initiated, and Serratia marcescens was isolated in several consecutive blood cultures. The bacterium was sensitive to meropenem, ciprofloxacin and cotrimoxazole, whereas resistant to cephalosporins and penicillins. His haemodynamic and renal function were eventually improved. However, he remained ventilator-dependent and was encephalopathic. As a result, he underwent a tracheostomy on post-operative day 14. Thereafter, he developed hyperbilirubinemia and showed mildly deranged liver transaminase levels (including alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transferase and alkaline phosphatase) and biochemical markers of cholestasis. These abnormalities were attributed to bile duct obstruction although lack of evidence of cholelithiasis or dilation of biliary ducts during abdominal CT scan or ultrasound imaging. The bilirubin continued to increase rapidly to 200 µmol/L. Endoscopic retrograde cholangiopancreatography (ERCP) and transcutaneous hepatic cholangiography were carried out. The imaging and ERCP revealed widely patent right and left hepatic and common biliary ducts with smooth tapering toward the ampulla. The cystic duct was also patent. Nevertheless, the stent was inserted in the common bile duct during ERCP and an 8.5-French external biliary drain was also inserted under fluoroscopic guidance by an interventional radiologist. He did not show improvement after cholangiography and insertion of the external bilia