Percutaneous transhepatic biliary drainage (PTBD) is a common interventional radiology (IR) procedure typically used in the treatment of biliary obstruction when an endoscopic approach has failed or is not technically feasible. PTBD has a low overall complication rate with the Society of Interventional Radiology suggesting adverse event thresholds of 10% for major complications, 5.7% for hemorrhage, 2% for hemobilia, and 3.3% for death, with the average reported rates of each of these being significantly lower. However, in rare instances serious complications such as vascular injury occur. The present report describes a case of a 62-year-old woman with Non-Alcoholic Steatohepatitis (NASH) cirrhosis and remote Whipple procedure who developed symptomatic choledocholithiasis with failed Endoscopic Retrograde Cholangiopancreatography (ERCP). Interventional radiology was consulted for PTBD, which was complicated by an iatrogenic portobiliary fistula (PBF). Diagnosis required sequential imaging and procedural evaluation, as initial non-invasive computed tomography (CT) and initial portal venography failed to clearly demonstrate the connection due to catheter occlusion of the fistula. This case report focuses on the management of this complication, which was successfully treated with balloon-expandable covered stent placement in the biliary system and dual-tract coil embolization.

Aneurysms of the pancreaticoduodenal arcade are uncommon visceral artery aneurysms that are strongly associated with stenosis or occlusion of the celiac axis and that may rupture irrespective of size. Rupture produces a peripancreatic or retroperitoneal hematoma, and duodenal stenosis is a recognized sequela; biliary complications have rarely been reported. An 84-year-old man admitted with an acute Stanford type B aortic dissection with a thrombosed false lumen was managed conservatively with strict blood pressure control. Surveillance non-contrast computed tomography (CT) on day 7 incidentally showed a periduodenal hematoma, absent on day 5, in a patient who had no abdominal pain. Contrast-enhanced CT on day 8 demonstrated a 5-mm aneurysm of the anterior inferior pancreaticoduodenal artery (AIPDA) adjacent to the hematoma, together with severe celiac origin stenosis. The same narrowing was present on the day 0 study, as demonstrated on retrospective review. Coil embolization on day 12 occluded the aneurysm, and the arcade remained patent, maintaining collateral blood flow to the liver; the celiac origin stenosis was not treated. Postprandial vomiting began on day 16, and imaging on day 19 confirmed high-grade stenosis at the distal descending duodenum. He was managed with nasogastric decompression and parenteral nutrition, and endoscopy showed a short, tight stenosis of extrinsic appearance with normal mucosa. On day 37, he developed septic shock with direct-predominant hyperbilirubinemia, and CT showed a dilated biliary tree with severe narrowing of the common bile duct at the level of the coils. According to the Tokyo Guidelines 2018, grade III acute cholangitis was diagnosed, and an endoscopic nasobiliary drainage catheter was placed without sphincterotomy; blood and bile grew extended-spectrum beta-lactamase-producing Escherichia coli. The duodenal stenosis improved sufficiently for an oral elemental diet on day 45 and a full oral diet on day 47, and he was discharged home walking unaided on day 60. Rupture of an AIPDA aneurysm may be painless, although this is not the usual presentation, and may be detected only on surveillance imaging; severe cholangitis may follow in a patient with a persistent periduodenal hematoma and duodenal obstruction. Both complications were managed nonoperatively.

BACKGROUND Thyrotoxicosis is associated with well-recognized and clinically significant complications, including congestive heart failure and cardiac arrhythmias. The relationship between hyperthyroidism and hepatic dysfunction is complex, with several proposed pathophysiological mechanisms; however, direct cholestatic injury is frequently overlooked. Although mild liver enzyme elevation is common in hyperthyroidism, clinically overt jaundice is rare. Nevertheless, increasing evidence from case reports and case series suggests that thyrotoxicosis, especially Graves disease, can result in cholestatic-pattern jaundice. This temporal association is supported by substantial improvements in jaundice and liver biochemistry after antithyroid therapy. CASE REPORT A 62-year-old woman presented with a 1-month history of right upper quadrant abdominal pain, unintentional weight loss, and jaundice. Laboratory evaluation demonstrated cholestatic-pattern liver injury, and abdominal ultrasound revealed a solitary gallstone without evidence of acute or chronic cholecystitis. Abdominal computed tomography demonstrated right-sided heart failure with pericardial and bilateral pleural effusions and congestive hepatopathy. Endoscopic retrograde cholangiopancreatography showed no filling defects, excluding biliary obstruction. Because the patient had persistent sinus tachycardia, thyroid function tests were performed. The findings were consistent with primary hyperthyroidism and elevated thyroid-stimulating hormone receptor antibodies); thyroid ultrasound and scintigraphy results supported toxic multinodular goiter. Treatment with methimazole led to dramatic improvement of the jaundice. Given the possibility of competing etiologies, thyrotoxicosis was considered the most likely contributing factor to cholestatic jaundice onset. CONCLUSIONS This case highlights the importance of considering hyperthyroidism in the differential diagnosis of jaundice, particularly in diagnostically challenging cases.

A 91-year-old Chinese man with a 30-year history of diabetes and 5-year history of hypertension presented in January 2026 with acute epigastric pain and obstructive jaundice. Unenhanced CT showed dilated bile ducts with multiple linear hyperattenuating structures mimicking biliary stones. ERCP after sphincterotomy yielded abundant blood clots but no calculi, with persistent active bleeding; cholangioscopy revealed an irregular friable bleeding lesion at the left hepatic duct/hilar confluence. Fully covered metal and plastic stents were placed, with marked reduction of bleeding. Follow-up CT two weeks later showed a 5.5×3.6 cm segment-VI mass with wash-in/wash-out enhancement, consistent with hepatocellular carcinoma. Intraductal blood clots can mimic biliary stones; cholangioscopy localized the bleeding source during ERCP and redirected management.

A 37-year-old man presented with epigastric pain, nausea, vomiting, and diarrhoea. Ultrasound demonstrated cholelithiasis with a stone impacted at the gallbladder neck. During laparoscopic cholecystectomy, the gallbladder was found to the left of the falciform ligament and was attached to an accessory liver lobe by a peritoneal fold containing vascular structures. Meticulous dissection and achievement of the critical view of safety allowed safe completion of the procedure without biliary or vascular injury. Postoperative magnetic resonance imaging with magnetic resonance cholangiopancreatography demonstrated a pedunculated accessory liver lobe arising from segment IV and a trifurcation-type portal vein anomaly without biliary obstruction. This case illustrates how coexisting congenital hepatobiliary and vascular variants can alter intraoperative orientation and highlights the importance of anatomy-based dissection when unexpected anatomy is encountered during laparoscopic cholecystectomy.

Cholecystoduodenal fistula and cholecystocolonic fistula are rare complications of gallstone pathology. A 62-year-old female presented to our surgical assessment unit with abdominal pain and vomiting. A computed tomographic scan revealed complex biliary-enteric fistulas. The fistulas involved the gallbladder, duodenum, and colon, with evidence of partial gastric outlet obstruction secondary to a gallstone in the proximal duodenum. Furthermore, imaging revealed a large gallstone impacted proximal to the diverticular stricture in the sigmoid colon. A minimally invasive approach to resolve the fistula was unsuccessful; endoscopic retrograde cholangiopancreatography and sigmoidoscopy to dislodge the gallstones failed. This led to a laparotomy with jejunal enterotomy for stone removal and a Hartmann's procedure to address the impacted gallstone and the sigmoid diverticular stricture. Furthermore, the repair of both fistulae was performed during the index operation at the second operation, while dealing with unexpected colostomy necrosis.

Saw palmetto (SP) is a widely used herbal supplement for benign prostatic hyperplasia (BPH) and is generally considered safe. However, rare cases of SP-associated drug-induced liver injury (DILI) have been reported. We describe a case of cholestatic hepatitis attributed to SP, highlighting the diagnostic challenges associated with herbal supplement use and polypharmacy. A 70-year-old male with a history of BPH, hypertension, chronic obstructive pulmonary disease, atrial fibrillation, and cholecystectomy presented with one month of jaundice, pruritus, and pale stools. Physical examination demonstrated scleral icterus without abdominal tenderness. Laboratory evaluation revealed an alkaline phosphatase level of 215 U/L, total bilirubin of 7.3 mg/dL (direct bilirubin = 5.0 mg/dL), alanine aminotransferase of 305 U/L, aspartate aminotransferase of 133 U/L, and an international normalized ratio of 3.8 while receiving warfarin therapy for atrial fibrillation. Viral hepatitis serologies were negative. Right upper quadrant ultrasonography demonstrated mild biliary ductal prominence, and magnetic resonance cholangiopancreatography excluded biliary obstruction. Liver injury was initially attributed to congestive hepatopathy because of newly reduced left ventricular ejection fraction (34%-40%). However, the patient remained clinically euvolemic, liver biochemistries failed to improve, and progressive hyperbilirubinemia prompted further evaluation. A detailed medication history revealed over-the-counter SP use for approximately four months, discontinued two months before presentation, and a recent one-week course of trimethoprim-sulfamethoxazole for a urinary tract infection. Transjugular liver biopsy with measurement of the hepatic venous pressure gradient (6 mmHg) demonstrated cholestatic hepatitis with portal and lobular inflammation, eosinophilic infiltration, and bile duct proliferation, consistent with DILI. Right and left heart catheterization demonstrated normal filling pressures and the absence of obstructive coronary artery disease, making congestive hepatopathy unlikely. Warfarin was reversed with vitamin K and transitioned to apixaban because of concern for potential hepatotoxicity. The patient was treated with ursodiol and cholestyramine, resulting in gradual improvement in liver enzymes and bilirubin, and was discharged with close hepatology and cardiology follow-up. This case highlights SP as a rare but important suspected cause of cholestatic DILI. Although causality cannot be definitively established because of concomitant exposure to other drugs, SP was considered the most likely implicated agent based on the temporal relationship with exposure, exclusion of alternative etiologies, compatible histopathologic findings, and clinical improvement after its discontinuation. Clinicians should routinely inquire about over-the-counter and herbal supplement use when evaluating unexplained liver injury. Increased awareness, comprehensive medication reconciliation, and improved regulation of dietary supplements may facilitate earlier recognition and reduce preventable hepatotoxicity.