A 66-year-old man with a history of severe peripheral vascular disease and left iliac artery stent placement was seen in his primary care doctor's clinic for acute onset of jaundice, malaise and dark urine over 3–4 days. He had a dull, aching epigastric and right upper abdominal pain for 2 weeks prior to presentation. He could not relate worsening pain to meals and could not identify any inciting factors for the pain. Pain lasted from a few minutes to an hour once it occurred and it happened approximately 3–4 times daily. He had no history of nausea or vomiting. Jaundice developed rapidly in the 3–4 days prior to presentation, which made him visit his primary care doctor. He had been feeling tired most of the day for the past 2–3 weeks. Physical exam demonstrated scleral and skin icterus and minimal epigastric tenderness on deep palpation. Laboratory testing showed elevated liver enzymes: AST 92 U/l (normal 7–40 U/l), ALT 145 U/l (normal 7–56 U/l), ALP 443 U/l (normal 25–110 U/l) and total bilirubin 25.3 mg/dl (normal 0.3–1.2 mg/dl), direct bilirubin 18.9 mg/dl. Complete blood count was normal. CT scan of the abdomen revealed intrahepatic biliary ductal dilation, a 1.5 cm CBD above the pancreas and rounded radiopaque densities (possibly stones ranging from 3 to 4 mm) in the CBD within the pancreas. The pancreatic duct was normal. No masses or enlarged lymph nodes were noted. His primary care provider referred him to a community gastroenterologist who performed ERCP. During ERCP, the CBD could not be cannulated or opacified and the pancreatic duct was normal. The patient was referred to the University Gastroenterology Center for repeat ERCP. He arrived 2 days later for a repeat attempt. Labs were repeated prior to the procedure and showed AST 150 U/l, ALT 159 U/l, ALP 1,024 U/l, total bilirubin 33.7 mg/dl, WBC 18,100/μl (normal 4,500–11,000/μl) and INR 1.3 (range 0.8–1.2). EUS was performed prior to ERCP to evaluate the bile ducts and pancreas further and to determine the cause of biliary obstruction. Type 1 Mirizzi syndrome was noted on EUS (fig. 1), showing proximal CBD dilation, narrowing of the CBD due to extrinsic compression from cystic duct stone, acoustic shadow from cystic duct stone, stone in the cystic duct and distal CBD stone. Repeat ERCP was performed and the CBD was cannulated over the pancreatic duct wire. A mid CBD narrowing, distal CBD stones, proximal CBD and extrahepatic duct dilation were noted, and biliary sphincterotomy was performed. An extraction balloon was used to remove the small stone from the distal CBD. Cholangiography (fig. 2a) showed a dilated cystic duct and a dilated CBD, proximal to the obstructing stone in the cystic duct. Figure 2b depicts a stone in the cystic duct which moved slightly with catheter use during ERCP, causing relief of obstruction in the CBD. The cystic duct stone was moved to the CBD with a biliary balloon. Then, a mechanical basket lithotripter (fig. 3a) was used to crush the stone, which was now lying in the CBD. Stone fragments were delivered out with a large extraction balloon. A dilated cystic duct and CBD were noted at the end of the procedure after complete stone extraction (fig. 3b). The patient was clinically stable after the procedure and had an uneventful recovery. He was seen 7 weeks later in the clinic. His skin and scleral icterus had resolved completely. Epigastric pain did not recur after the procedure. He is scheduled for an elective cholecystectomy.