Two days after ERCP the patient complained of abdominal pain

Two days after ERCP, the patient complained of abdominal pain and bloody stools. Bloody drainage from the PTGBD catheter was also noted. After conservative treatment, the condition showed no improvement, with persistent mild bloody stool passage and a progressively falling smad inhibitor level down to 8.7 g/dL. Upper gastrointestinal endoscopy revealed a normal stomach, but fresh oozing and blood clots at the ampullary orifice (Fig. 2). After active resuscitation with tranexamic acid, vitamin K1, and fresh frozen plasma infusion, hemobilia was improved gradually without further bloody or tarry stool passage. Then he was discharged temporarily with total bilirubin and Hb levels at 4.8 mg/dL and 10.1 g/dL, respectively. Five days after discharge, he visited our emergency room due to abdominal pain, fever, and progressive amount of bloody stool. Serum biochemical studies revealed a total bilirubin level of 7.7 mg/dL, a hemoglobin concentration of 8.0 g/dL, a white blood count of 15,600/μL, and a C-reactive protein level of 47 mg/L. Under the preliminary diagnosis of cholangitis with recurrent hemobilia, parenteral ceftriaxone and blood components were given. Hemodynamic instability was followed by a rapid deterioration for which an emergent angiographic study was performed, but it showed no active bleeder. After active resuscitation, gastrointestinal bleeding persisted with recurrent bloody stool passage and hypotension (BP: 84/53 mmHg; Hb: 6.5 g/dL). A repeated emergent angiogram again demonstrated no identifiable bleeding source. Upper gastrointestinal endoscopy merely showed several shallow gastric ulcers without active bleeding. Despite intermittent bloody stool passage, hemodynamic stability was resumed after aggressive fluid resuscitation. A plain abdominal film later showed abnormal location of the stent in the right iliac fossa (Fig. 3), which gave the impression of stent migration. Subsequent abdominal computed tomography (CT) revealed stent impaction at the ascending colon without any evidence of abnormal peritoneal fluid or gas accumulation suggestive of perforation of the colon or other hollow organs (Fig. 4). Conservative treatment strategy with intravenous fluid and transfusion was adopted because of the CT finding and the absence of peritoneal signs typical of peritonitis. However, after 3 days of observation and a daily packed red blood cell transfusion of 500 mL to maintain an Hb concentration above 9 g/dL, bloody stool passage persisted. As a result, colonoscopy was performed, which showed embedding of the tip of stent in the wall of ascending colon at the hepatic flexure, resulting in wall erosion and bleeding. No sign of diverticulum or other source of bleeding was evident. After prompt removal of the stent together with administration of intravenous tranexamic acid and fresh frozen plasma, the patient\'s bloody stool subsided with overall improvement in clinical condition. Subsequently, he underwent conventional cholecystectomy and choledocholithotomy 5 days later, and made an uneventful recovery.
Discussion The etiology of hemobilia changes with an increase in incidence from accidental trauma to iatrogenic hemorrhage due to the widespread use of invasive hepatobiliary procedures. In reviewing 222 patients of hemobilia from 1996 to 1999, we find that 147 were iatrogenic following hepatobiliary intervention while accidental trauma accounted for only 5%. Early diagnosis of hemobilia depends on the level of clinical suspicion. Typical manifestations of the triad of abdominal pain (52–70%), gastrointestinal bleeding (83–93%), and jaundice (30–60%) may be present in only 22–28% of patients. As a result, our patient was suspected to have “recurrent hemobilia” as he visited our emergency room the second time presenting with the typical triad. Hemobilia is not usually considered a clinically significant entity as it is a rare cause of gastrointestinal bleeding. The management of hemobilia aims at hemostasis and relieving biliary obstruction. Active intervention is indicated for severe or recurrent bleeding. Angiography is considered the diagnostic tool of choice. In our patient, the initial hemobilia could be due to a combination of initial uncontrolled sepsis and procedure-related trauma. Then hemobilia would be self-limited after sepsis control with decompression of the infected bile and the use of broad-spectrum antibiotics. Despite untreated choledocholithiasis under the initial critical condition, biliary stenting apparently relieved the jaundice of the patient through dislodgment of the impacted stones at the sphincter of Oddi through which free flow of the infected bile into the duodenum was possible.