Case Presentation: A 79-year-old male with a history of coronary artery disease status post coronary artery bypass surgery, atrial fibrillation, osteoporosis with vertebral compression fractures presented to the ED for severe right flank spasms. He was recently admitted and discharged just 3 days prior for similar complaints which were attributed to thoracolumbar compression fractures. He reported right upper quadrant abdominal pain but denied fever, chills, loss of appetite, nausea, emesis, dyspnea, chest pain, and alcohol consumption. He was afebrile (36.8℃), without tachycardia (87 bpm), but was mildly hypotensive (102/54 mmHg). He had a normal respiratory rate (18) and O2 saturation (94%). On exam, he appeared slightly jaundiced, and his mentation was appropriate; however, on the subsequent day, his mentation worsened. Abdominal exam revealed right upper and lower quadrant abdominal pain without guarding or rebound tenderness. Murphy’s sign was negative. Labs revealed significant leukocytosis with a WBC count of 20.7, which was 9.8 during his prior admission. Lipase was normal. LFTs were significant for an elevated total bilirubin (2.2; 1.1 direct component), alkaline phosphatase (279), ALT (93) and AST (69). His LFTs were also elevated at his prior admission including a total bilirubin of 2.5, alkaline phosphatase of 255, and an ALT and AST of 84 and 63, respectively. The patient was found to have Klebsiella Oxytoca bacteremia. CT abdomen and pelvis showed an obstructing calculus in the neck of the gallbladder and was consistent with acute cholecystitis (Figure 1). Ultrasound was consistent with acute cholecystitis with possible small, contained perforation at the gallbladder fundus.After antibiotic initiation, general surgery was consulted and recommended a cholecystostomy tube. Subsequent biliary fluid grew Klebsiella Oxytoca identifying the source of the bacteremia. Post-cholecystostomy tube labs showed overall improvement in the leukocytosis and cholestatic labs, however, the hepatocellular markers including ALT (128) and AST (120) continued to elevate which was concerning Mirizzi Syndrome (MS). He subsequently underwent ERCP with stenting and calculus removal.
Discussion: MS, a rare condition, complicates only 0.1% of cases of cholelithiasis. MS is defined as extrinsic compression of the common hepatic duct (CHD) or the common bile duct (CBD) due to an impacted stone and associated inflammation in the neck/infundibulum of the gallbladder, or the cystic duct. Due to obstruction and inflammation, complications include cholangitis and fistula formation with the CHD/CBD, respectively. Indeed, MS is classified based on the presence of a fistula, where the absence is considered Type I MS which was seen in our case. While this condition can present similarly to other biliary tree/gallbladder disorders, in our case, MS was suspected given the prominent elevation of hepatocellular markers post-cholecystostomy tube and worsening mention concerning for obstruction and cholangitis. Management typically requires surgical intervention. However, ERCP can be definitive treatment in patients, like ours, who are deemed a poor surgical candidate.
Conclusions: Here we present a rare case of cholelithiasis complicated by MS and gallbladder perforation. In cases where acute cholecystitis is managed with cholecystostomy tube placement, a subsequent rise in hepatocellular markers should prompt MS in the differential diagnosis.
