Dig Dis Sci (2010) 55:2767–2769 DOI 10.1007/s10620-010-1319-x
STANFORD MULTIDISCIPLINARY SEMINARS
Endoscopic Management of a Spontaneous Gallbladder Perforation and Bile Leak Craig Munroe • Amie E. Padilla-Thornton • George Triadafilopoulos • Jacques Van Dam Glen Lutchman
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Received: 9 June 2010 / Accepted: 14 June 2010 / Published online: 15 July 2010 Springer Science+Business Media, LLC 2010
Case Presentation and Evolution A 53-year-old man with a past medical history of alcoholic liver disease complicated by esophageal varices, ascites, hepatic hydrothorax, and hepatic encephalopathy presented to a local community hospital with 10-day history of abdominal pain. His pain was 10/10 in intensity, constant, worse in the supine position, increasing on the dependant side of the abdomen (when lying on the left side, the pain worse on left and vice versa), and improved in the upright position. The pain was not worsened by food and was not associated with fevers, chills, nausea or chest pain. He also reported shortness of breath and diarrhea, but denied rectal bleeding. When he was admitted to the local hospital, his white blood cell (WBC) count was 15,000/mm3, predominantly bands and neutrophils. Because of concern for spontaneous bacterial peritonitis, empiric antibiotics were started and a nasogastric tube was placed. An abdominal ultrasound revealed a cirrhotic liver and a contracted gallbladder with mild gallbladder wall thickening. There was insufficient ascites to perform a diagnostic paracentesis. An abdominal radiograph series was negative for free air.
C. Munroe (&) G. Triadafilopoulos J. Van Dam G. Lutchman Division of Gastroenterology and Hepatology, Department of Medicine, Stanford University School of Medicine, Stanford University Medical Center, 300 Pasteur Drive, Always Building, Rm M211, Stanford, CA 94305-5187, USA e-mail:
[email protected] A. E. Padilla-Thornton Department of Radiology, Stanford University School of Medicine, Stanford University Medical Center, 300 Pasteur Drive, A149 MC 5202, Stanford, CA 94305, USA
Over the next 24 h, his pain continued to worsen and there was intermittent abdominal distention. A computed tomography (CT) of the abdomen and pelvis revealed a nodular liver capsule consistent with cirrhosis and large volume ascites (Fig. 1a). The gallbladder was contracted around dependent radio-opaque calculi (arrow, Fig. 1a). Two radio-opaque calcified structures in pelvis (arrow, Fig. 1b) consistent with gallstones with associated free fluid in pelvis were also seen. He was transferred to our institution. The patient’s past medical history was significant for alcoholic cirrhosis, and he had been on the liver transplant list. He also had a history of an incarcerated umbilical hernia that was repaired in 2008, as well as cholelithiasis. Upon transfer he was receiving piperacillin and tazobactam, vancomycin, ondansetron, pantoprazole, lactulose and hydromorphone as needed. He had no known drug allergies. He was single and did not smoke tobacco. The patient had discontinued alcohol use in 2008, and had no history of illicit drug use. Family history was negative. On physical examination, his vital signs were stable. The patient appeared to be in no acute distress with icteric conjunctiva and a nasogastric tube in place. There were decreased breath sounds bilaterally with a diffusely distended abdomen with tenderness to palpation in all quadrants. There was shifting dullness and a fluid wave consistent with ascites, but no guarding or rebound. The patient had scrotal and lower extremity edema but no asterixis. The patient had a WBC count of 10,300/mm3, hematocrit 27.2%, mean corpuscular volume 84.7, platelet count 86,000/ mm3, sodium 136 mmol/L, carbon dioxide 19 mmol/L, blood urea nitrogen 42 mg/dL, creatinine 1.5 mg/dL, albumin 3.1 g/dL, total bilirubin 8.3 mg/dL, alkaline phosphatase 130 U/L, aspartate aminotransferase 37 U/L, alanine aminotransferase 29 U/L, and international normalized ratio for
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Fig. 2 Cholescintigraphy: delayed supine image demonstrates hepatobiliary clearance of Tc-99m HIDA into the duodenum. Activity is seen layering along the right paracolic gutter (arrow), confirming the presence of a bile leak
Fig. 1 Non-enhanced CT abdomen and pelvis upon admission. a Nodular liver capsule, consistent with cirrhosis with large volume ascites is seen. Contracted gallbladder around dependent radioopaque calculi (arrow). b Two radio-opaque calcified structures in pelvis (arrow) consistent with gallstones with associated free fluid in pelvis
prothrombin time 1.8. A diagnostic paracentesis revealed bilious, turbid fluid, 3,200 nucleated cells (25,000 red blood cells), 15% neutrophils, 80% monocytes. Ascitic fluid albumin was less than 1.0 g/dL and the serum-ascites albumin gradient was 2.6. A hepatobiliary iminodiacetic acid (HIDA) scan showed radioactivity layering along the right paracolic gutter (arrow Fig. 2), confirming the presence of a bile leak. The patient remained on nothing by mouth, continued on antibiotics, and a surgical consultation was obtained. Given the patient’s significant peri-operative risk, a percutaneous drain was placed in the right upper quadrant in order to drain the bile that had accumulated, reduce the chances of a chemical peritonitis and hence defer surgery. An endoscopic retrograde cholangiopancreatography (ERCP) demonstrated clear contrast extravasation from the region of the cystic duct, diagnostic of a bile leak (Fig. 3). A stent was placed across the cystic duct into the common hepatic duct to promote trans-papillary bile flow. Over the next week, the patient’s abdominal pain improved and a followup paracentesis revealed a decrease in peritoneal bilirubin
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Fig. 3 Endoscopic retrograde cholangiopancreatography (ERCP). Pigtail loop from percutaneous drainage catheter in right upper quadrant (white arrow). The endoscope is seen cannulating the papilla. Retrograde contrast opacification of the biliary system demonstrates clear contrast extravasation from the region of the cystic duct (black arrow)
levels. A repeat HIDA scan showed no further bile leak 10 days into his hospital stay, and he was discharged home in stable condition.
Discussion Spontaneous gallbladder perforation is a rare complication of cholelithiasis and acute cholecystitis. The condition has
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been reported in 2–10.6% of cases of acute cholecystitis, with higher rates in patients who are managed conservatively, those with comorbid medical conditions, females, and the elderly [1]. Presenting symptoms typically mimic acute cholecystitis without gallbladder perforation. According to the Niemeier classification, type I perforations (16% of cases) are associated with acute free perforations and bile peritonitis and have the highest mortality rate; type II perforations (68%) are associated with subacute pericholecystic abscess formation; and type III perforations (16%) are associated with fistulous connections with adjacent organs or structures and are thought to be chronic [2, 3]. Indeed, cholecysto-enteric fistulas are relatively rare complications of gallstone disease with perforation, with cholecysto-duodenal fistula being the most common type (70%). Most fistulas form insidiously, and are usually not detected until surgery unless there is associated gallstone ileus [4]. A retrospective study in 2004 found that the incidence of gallbladder perforation in patients with acute cholecystitis was 5.9%. The condition was associated with significant morbidity (35%) and mortality (9.6%), particularly in patients with type 1 perforations [5]. In one study, 30 of 11,360 patients who underwent cholecystectomy had gallbladder perforations, and only 3% of these were diagnosed preoperatively. Nine of the perforations were contained, and 21 of them were free. Patients with gallbladder perforations were more likely to be Hispanic, men, older, have cardiovascular disease, require intensive care unit admission and have more postoperative complications. Cholecystectomy within 24 h improved patient outcomes [6]. Classically, type II perforations can be managed conservatively. Emergency surgery is traditionally required for type I, septic type II and type III perforations with gallstone ileus [1]. The case presented was a type I gallbladder perforation and successfully managed without surgery. The patient likely had undiagnosed cholecystitis and subsequent perforation in the setting of his advanced liver disease. During his inpatient stay, a repeat HIDA scan
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following ERCP and biliary stent placement revealed intestinal bile flow and no signs of bile leak. Larger studies with more patients are needed to evaluate the use of ERCP and stent placement as an alternative treatment of this condition in patients who are more suitable surgical candidates to minimize peri-operative complications.
Key Messages • •
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Spontaneous gallbladder perforation, a rare complication of cholelithiasis, mimics acute cholecystitis. Cholescintigraphy is essential for demonstration of a bile leak; CT imaging may reveal extravesicular gallstones. Combined radiologic and endoscopic management using percutaneous peritoneal drainage combined with cholecysto-duodenal stent placement may facilitate spontaneous closure and abort the need for surgery in patients with serious morbidity.
References 1. Chong VH, Lim KS, Mathew VV. Spontaneous gallbladder perforation, pericholecystic abscess and cholecysto-duodenal fistula as the first manifestations of gallstone disease. Hepatobiliary Pancreat Dis Int. 2009;8:212–214. 2. Swayne LC, Fillipone A. Gallbladder perforation: correlation of cholescintigraphic and sonographic findings with the Niemeier classification. J Nucl Med. 1990;31:1915–1920. 3. Neimeier DW. Acute free perforation of the gallbladder. Am Surg. 1934;99:922–944. 4. Hussein M, Gardiner K. Omental and extraperitoneal abscesses complicating cholecystocolic fistula. HPB (Oxford). 2003;5:194– 196. 5. Menakuru SR, Kaman L, Behera A, et al. Current management of gall bladder perforations. ANZ J Surg. 2004;74:843–846. 6. Stefanidis D, Sirinek KR, Bingener J. Gallbladder perforation: risk factors and outcome. J Surg Res. 2004;131:204–208.
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