S3442 No Stones to Overturn: An Unexpected Cause of Acute Pancreatitis

Introduction: Hemorrhagic cholecystitis, bleeding into the gallbladder wall or lumen, represents <4% of cholecystitis but can provoke pancreatitis when clot obstructs the cystic or common bile duct. Trauma, malignancy, anticoagulation, cirrhosis, and renal failure increase risk. Overlap with calculous disease delays recognition and raises mortality. Case Description/Methods: A 69-year-old man with atrial fibrillation on warfarin, coronary artery disease (CAD), Heart Failure with Reduced Ejection Fraction (HFrEF), and gout presented with sudden diffuse abdominal pain, nausea, and diaphoresis. Vitals: heart rate 132, Mean Arterial Pressure (MAP) 58 mmHg (on norepinephrine), temperature 38°C. Abdomen distended, diffusely tender, no Murphy sign. Labs: White Blood Cell (WBC) 17.4 × 10⁹/L, hemoglobin 11.2 g/dL, platelets 212 × 10⁹/L, International Normalized Ratio (INR) 3.4, total bilirubin 1.8 mg/dL, alanine aminotransferase 88 U/L, lipase >30 000 U/L; Bedside Index of Severity in Acute Pancreatitis (BISAP) 2, 48-h Ranson 6. Right upper quadrant ultrasound showed sludge, trace pericholecystic fluid, no stones. Computed tomography was deferred. Warfarin reversed with prothrombin complex concentrate (PCC) and vitamin K. A 10-F cholecystostomy tube drained sanguineous bile, confirming hemorrhagic cholecystitis. Despite drainage and broad antibiotics, he developed encephalopathy, hypoxemia, and refractory shock requiring intubation and additional vasopressors. Organ support was weaned; he left Intensive Care Unit (intensive care unit) on day 6 and rehab on day 10. Laparoscopic cholecystectomy at 6 weeks was uneventful; pathology showed chronic cholecystitis with organized clot. He was asymptomatic at 3 months and back on anticoagulation. Discussion: Hemorrhagic cholecystitis should be considered when acalculous cholecystitis occurs in anticoagulated or coagulopathic patients. Doppler ultrasound may show non-shadowing echoes; contrast computed tomography demonstrating high-attenuation content (HU >50) supports blood. Clot migration can trigger severe pancreatitis, explaining this patient’s extreme lipase and high severity scores. Mortality rises with necrosis or perforation, so rapid recognition and drainage are crucial. While laparoscopic cholecystectomy is definitive, unstable patients benefit from temporizing cholecystostomy, which decompresses the biliary tree and permits physiologic optimization before surgery. Prompt reversal of coagulopathy further improves safety.

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Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001141228.07724.7d
Primary Topic
Pancreatitis Pathology and Treatment
Type
article
Field-Weighted Citation Impact
0.00
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article

S3442 No Stones to Overturn: An Unexpected Cause of Acute Pancreatitis

Robert Ondracek, Olugbenga Oyesanmi, Faizan Ahmed, Patrick Stocker et al.
The American Journal of Gastroenterology
Pancreatitis Pathology and Treatment
article

S3442 No Stones to Overturn: An Unexpected Cause of Acute Pancreatitis

Robert Ondracek, Olugbenga Oyesanmi, Faizan Ahmed, Patrick Stocker, Rohan Shah, Andrew Ondracek
article en

Abstract

Introduction: Hemorrhagic cholecystitis, bleeding into the gallbladder wall or lumen, represents <4% of cholecystitis but can provoke pancreatitis when clot obstructs the cystic or common bile duct. Trauma, malignancy, anticoagulation, cirrhosis, and renal failure increase risk. Overlap with calculous disease delays recognition and raises mortality. Case Description/Methods: A 69-year-old man with atrial fibrillation on warfarin, coronary artery disease (CAD), Heart Failure with Reduced Ejection Fraction (HFrEF), and gout presented with sudden diffuse abdominal pain, nausea, and diaphoresis. Vitals: heart rate 132, Mean Arterial Pressure (MAP) 58 mmHg (on norepinephrine), temperature 38°C. Abdomen distended, diffusely tender, no Murphy sign. Labs: White Blood Cell (WBC) 17.4 × 10⁹/L, hemoglobin 11.2 g/dL, platelets 212 × 10⁹/L, International Normalized Ratio (INR) 3.4, total bilirubin 1.8 mg/dL, alanine aminotransferase 88 U/L, lipase >30 000 U/L; Bedside Index of Severity in Acute Pancreatitis (BISAP) 2, 48-h Ranson 6. Right upper quadrant ultrasound showed sludge, trace pericholecystic fluid, no stones. Computed tomography was deferred. Warfarin reversed with prothrombin complex concentrate (PCC) and vitamin K. A 10-F cholecystostomy tube drained sanguineous bile, confirming hemorrhagic cholecystitis. Despite drainage and broad antibiotics, he developed encephalopathy, hypoxemia, and refractory shock requiring intubation and additional vasopressors. Organ support was weaned; he left Intensive Care Unit (intensive care unit) on day 6 and rehab on day 10. Laparoscopic cholecystectomy at 6 weeks was uneventful; pathology showed chronic cholecystitis with organized clot. He was asymptomatic at 3 months and back on anticoagulation. Discussion: Hemorrhagic cholecystitis should be considered when acalculous cholecystitis occurs in anticoagulated or coagulopathic patients. Doppler ultrasound may show non-shadowing echoes; contrast computed tomography demonstrating high-attenuation content (HU >50) supports blood. Clot migration can trigger severe pancreatitis, explaining this patient’s extreme lipase and high severity scores. Mortality rises with necrosis or perforation, so rapid recognition and drainage are crucial. While laparoscopic cholecystectomy is definitive, unstable patients benefit from temporizing cholecystostomy, which decompresses the biliary tree and permits physiologic optimization before surgery. Prompt reversal of coagulopathy further improves safety.

The American Journal of GastroenterologyVol. 120(10S2)
Openalex Percentile: Top 52%
Pancreatitis Pathology and Treatment
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