Management of obstructive jaundice secondary to hemorrhagic cholecystitis following a high-altitude fall: A case report

Abstract

Hemorrhagic cholecystitis is a rare cause of obstructive jaundice and presents diagnostic and therapeutic challenges. This case report describes a patient with obstructive jaundice secondary to hemorrhagic cholecystitis who was successfully treated with percutaneous transhepatic gallbladder drainage and endoscopic retrograde cholangiopancreatography. A 42-year-old woman sustained a high-altitude fall resulting in pulmonary contusion and pelvic and femoral fractures. After orthopedic surgery, she developed hemorrhagic cholecystitis. Although percutaneous transhepatic gallbladder drainage resolved the intragallbladder hemorrhage, obstructive jaundice persisted due to a blood clot in the common bile duct, caused by hemobilia, obstructed biliary outflow. Subsequent endoscopic retrograde cholangiopancreatography successfully removed the clot and restored biliary drainage. The patient achieved complete clinical recovery and was discharged without complications within 1 month. Obstructive jaundice due to hemorrhagic cholecystitis is uncommon and requires prompt diagnosis and intervention. To our knowledge, this report is among the few describing successful combined management with percutaneous transhepatic gallbladder drainage and endoscopic retrograde cholangiopancreatography using a fully covered metal stent and endoscopic nasobiliary drainage for obstructive jaundice secondary to hemorrhagic cholecystitis complicated by hemobilia.

Introduction

Hemorrhagic cholecystitis (HC) is a rare complication of acute cholecystitis, with an estimated incidence ranging from 0.2% to 2.0%. Traumatic events account for approximately 50% of cases. ¹ Diagnosis is challenging because clinical manifestations and imaging findings are often nonspecific. Timely diagnosis and intervention are essential to prevent complications such as cholangitis, pancreatitis, recurrent cholecystitis, and gallbladder rupture. Here, we report a rare case of obstructive jaundice (OJ) secondary to HC. OJ requires prompt treatment to prevent secondary liver failure and death. ²

In this report, we describe a case of OJ secondary to HC that was ultimately diagnosed by gallbladder puncture. The patient was managed with percutaneous transhepatic gallbladder drainage (PTGBD) and medical therapy, avoiding the need for cholecystectomy. Blood accumulation within the gallbladder lumen led to secondary OJ, which was successfully treated by endoscopic retrograde cholangiopancreatography (ERCP) with clot extraction, placement of a fully covered metal stent, and endoscopic nasobiliary drainage (ENBD). To our knowledge, this case represents a rare example of successful combined management using PTGBD and ERCP with a fully covered metal stent and ENBD for OJ secondary to HC.

Case presentation

A 42-year-old Chinese woman was admitted to the intensive care unit (ICU) with a 4-day history of left hip pain. Four days earlier, she had fallen from the third to the second floor while working at a construction site. On ICU admission, computed tomography (CT) revealed pulmonary contusion, a lumbar spine fracture, a femoral shaft fracture, and multiple pelvic fractures. She had no significant medical history and denied regular medication use, including anticoagulant or antiplatelet agents, as well as any family history of hepatobiliary disease. Coagulation parameters were within normal limits before and after the bleeding episode. After ICU admission, laboratory testing showed a markedly elevated D-dimer level (3072 ng/mL). Duplex ultrasonography (USG) of both lower extremities demonstrated bilateral intermuscular venous thrombosis, and anticoagulation therapy with low-molecular-weight heparin was initiated. Inferior vena cava venography with filter placement was subsequently performed. During the ICU stay, empiric antibiotic therapy with ceftazidime was started. After initial management, the patient was transferred to the Department of Trauma Surgery for internal fixation of the left proximal femoral fracture. On postoperative day 3 (9 days after the initial injury), she developed right upper quadrant abdominal pain, jaundice, nausea, and vomiting.

On physical examination, the patient was afebrile with stable vital signs. She had right upper quadrant abdominal tenderness, a positive Murphy sign, and percussion pain in the hepatic region. On admission, hemoglobin (HB) was 90 g/L and remained relatively stable after transfusion of 4 units of packed red blood cells. Liver function tests were normal except for hypoalbuminemia (29.3 g/L, reference range, 40–55 g/L). However, 9 days after admission, HB decreased to 77 g/L. Inflammatory markers were elevated, including a neutrophil percentage of 89.5% (40%–75%) and a C-reactive protein level of 42.87 mg/L. Liver biochemistry showed marked hepatic dysfunction: alanine aminotransferase 1036 U/L (normal range: 7–40 U/L), aspartate aminotransferase 1225 U/L (13–35 U/L), γ-glutamyl transpeptidase 339 U/L (7–45 U/L), alkaline phosphatase 819 U/L (35–135 U/L), total bilirubin 273.5 μmol/L (0–21 μmol/L), and direct bilirubin, 253.8 μmol/L (0–8 μmol/L). Coagulation studies showed a prothrombin time (PT) of 16 s (12.8 s), PT activity of 54%, and an international normalized ratio of 1.4. Other laboratory parameters, including platelet count and renal function, were within normal limits.

Initial transabdominal USG performed on post-injury days 9–10 showed heterogeneous bile within the gallbladder lumen, with bile layering and no posterior acoustic shadowing, suggesting cholestasis. On post-injury day 10, the patient was transferred to the Department of Gastroenterology because of progressive jaundice and worsening liver function. Given the presentation of OJ and liver dysfunction of unclear etiology, a repeat USG was performed. This examination demonstrated mixed echogenic material at the gallbladder base that did not shift with changes in body position, raising suspicion for a gallbladder hematoma (Figure 1). Subsequent abdominal CT confirmed a hyperdense lesion within the gallbladder lumen consistent with hematoma, without evidence of hepatic parenchymal injury or active contrast extravasation (Figure 2). Mild dilation of the extrahepatic bile duct was also noted; however, no definite intraductal calculi were identified, and this finding was not initially considered clinically significant (Supplemental Figure 1).

Figure 1.

Transabdominal ultrasonography (USG) image demonstrating mixed echogenicity (white arrow) within the dependent portion of the gallbladder. No movement of the contents was observed with changes in the patient’s position.

Figure 2.

Abdominal CT scan demonstrates a high-density material within the gallbladder lumen, which is consistent with a hematoma (white arrow).

To further clarify the etiology, gallbladder puncture was performed after discussion with the patient’s family. A total of 60 mL of dark red blood was aspirated (Supplemental Figure 2), and no additional bloody drainage was observed after catheter placement. Abdominal CT confirmed appropriate drain position and excluded bile duct disruption or ongoing hemorrhage (Supplemental Figure 3).

A multidisciplinary team comprising hepatobiliary surgeons, hematologists, and gastroenterologists reviewed the case. Given stable HB levels and vital signs, immediate surgery was not indicated. Therefore, we pursued conservative management with the option of duodenoscopy and ERCP if needed. During ERCP, the common bile duct (CBD) was mildly dilated (approximately 9.5 mm), and the gallbladder was not visualized (Supplemental Figure 4). A 2 mm endoscopic sphincterotomy (EST) was performed. A long-filling defect was observed within the CBD. A dark red blood clot was then extracted from the duodenal papilla using a balloon catheter, confirming that the biliary obstruction was due to intraductal blood clots rather than choledocholithiasis. A fully covered metal stent was placed in the CBD to maintain biliary drainage, and an ENBD tube was inserted (Supplemental Figure 5).

After the procedure, liver enzyme levels began to decrease on postoperative day 2 and returned to near-normal values within 1 month. The stent and the gallbladder drainage catheter were subsequently removed during an outpatient visit. From the patient’s perspective, jaundice and abdominal discomfort resolved completely after treatment, and she reported satisfaction with the clinical outcome.

The clinical course is summarized in Table 1.

Table 1.

Timeline of clinical events.

Time points	Clinical events
Day 0	The patient fell from the third to the second floor at a construction site, sustaining blunt trauma
Day 4	Admitted to ICU with left hip pain; CT revealed pulmonary contusion, lumbar spine fracture, femoral shaft fracture, and multiple pelvic fractures
Days 4–5	Elevated D-dimer (3072 ng/mL); duplex ultrasonography confirmed bilateral intermuscular venous thrombosis; anticoagulation with low-molecular-weight heparin initiated
Day 5	Inferior vena cava venography with filter placement performed
Day 6	Transferred to the Department of Trauma Surgery
Day 6	Internal fixation surgery for left proximal femoral fracture
Day 9 (postoperative day 3)	Transabdominal ultrasonography revealed cholestasis. Onset of right upper abdominal pain, jaundice, nausea, and vomiting
Days 9–10	Laboratory tests revealed marked liver dysfunction, hyperbilirubinemia, and an inflammatory response; hemoglobin decreased to 77 g/L
Day 10	Initial and repeat abdominal ultrasonography suggested gallbladder hematoma
Day 10	Abdominal CT confirmed an intragallbladder hematoma and mild extrahepatic bile duct dilatation
Day 10	Gallbladder puncture performed; 60 mL of dark red blood aspirated
Day 11	Multidisciplinary team discussion; conservative management adopted
Day 11	ERCP performed; blood clot removed from the common bile duct; EST, biliary stent, and ENBD placed
Day 13	Liver enzyme levels began to decline
~1 month	Liver function tests returned to near-normal levels
Follow-up	Removal of biliary stent and gallbladder drainage tube in an outpatient clinic; patient recovered without complications

CT: computed tomography; ICU: intensive care unit; ERCP: endoscopic retrograde cholangiopancreatography; EST: endoscopic sphincterotomy; ENBD: endoscopic nasobiliary drainage.

Discussion

HC is an uncommon presentation of hemobilia. While acalculous cholecystitis has been linked to a small number of hemobilia cases, ³ the classic triad of upper abdominal pain, gastrointestinal bleeding, and jaundice is present in only 22%–35% of patients. ⁴ Currently, iatrogenic injury is the leading cause of hemobilia, accounting for approximately 50% of cases.^1,5 Less frequent causes include trauma, liver biopsy, hepatobiliary procedures, biliary tumors, parasitic infestations, ruptured aneurysms involving the biliary ducts, anticoagulation therapy, and bleeding diathesis associated with conditions such as renal failure or cirrhosis. ⁴ Post-traumatic hemobilia has a reported incidence of approximately 3%, ⁶ typically arising from blunt abdominal trauma, unlike this case, where a high fall was the culprit. Although gallbladder hematomas observed on ultrasound (US) and CT scans can mimic gallbladder carcinoma or invasive hilar cholangiocarcinoma, definitive diagnosis remains challenging. ⁷ Additionally, the liver’s anatomic position provides some protection, reducing the likelihood of direct injury to the gallbladder. However, a large volume of blood within the gallbladder lumen can coagulate and migrate into the bile duct, causing obstruction and jaundice, as observed in our patient. In this case, ERCP provided definitive diagnostic confirmation.

Several factors may explain the delayed diagnosis. First, the onset of HC was insidious, and early intragallbladder bleeding was not detected on the initial abdominal CT scan, which showed no clear evidence of abdominal organ injury or liver laceration. Second, the progressive decline in HB was likely obscured by concomitant trauma-related bleeding, lowering clinical suspicion for biliary hemorrhage. In addition, bile has a ticoagulant property that may help prevent the rapid formation of a large, obstructing clot. Instead, small thrombi may gradually adhere to the bile duct wall and enlarge over time, ultimately leading to complete obstruction of the CBD.

Notably, the initial abdominal CT scan showed gallbladder wall thickening without evidence of hepatic contusion, laceration, or subcapsular hemorrhage. The initial intragallbladder bleeding was also overlooked. Hemobilia can present with a delayed onset. ⁴ In this case, hemobilia was not diagnosed until 16 days after the fall, when the patient presented with severe liver injury and jaundice. The preoperative HB level was 82 g/L. The first HB measurement after ERCP showed a slight decrease to 74 g/L, but increased to 87 g/L 4 days later. Throughout the patient’s stay in our department, vital signs remained stable, and there was no melena or hematemesis. No blood transfusion was required.

The patient recovered within 1 month, although she remained at risk for serious complications. The development of severe jaundice prompted emergency PTGBD to expedite diagnosis, which ultimately demonstrated gallbladder hemorrhage. Notably, the initial transabdominal US finding of biliary sludge resembled that reported in a similar case in the literature. ⁸

Further evaluation with contrast-enhanced abdominal CT was performed to exclude other potential causes of hemobilia; no arteriobiliary fistula, pseudoaneurysm, or other abnormalities were identified. ⁹ Magnetic Resonance Imaging was not performed because of the metallic hardware implanted during surgery for the femoral shaft fracture. Angiography is considered the gold standard for both the diagnosis and treatment of hemobilia because it enables precise localization of the bleeding source and allows for arterial embolization, which is the first-line intervention. ¹⁰ In this case, the patient’s blood counts remained stable after the gallbladder hemorrhage, and there was no hematemesis, melena, or a significant drop in blood pressure. Therefore, management consisted of bowel rest, fluid resuscitation, and antibiotic therapy.

Sandblom noted that in cases of slow or minor bleeding, blood and bile do not readily mix, leading to the formation of solid clots that may subsequently cause cholangitis, cholecystitis, or pancreatitis. ¹¹ However, in cases of significant bleeding, blood and bile can mix, and the resulting clot may obstruct the bile duct, causing OJ, as observed in our patient. This distinction is crucial for understanding the pathophysiology of HC and for guiding appropriate management strategies.

Esophagogastroduodenoscopy has limited sensitivity (12%–50%) for detecting hemobilia. ¹¹ Given the mildly dilated CBD observed on CT, we proceeded with ERCP to establish the diagnosis. During the procedure, a small papillary sphincterotomy was performed, followed by the extraction of a dark red blood clot using a balloon catheter. No active bleeding was identified. In addition, angiography did not reveal significant bile duct dilatation, likely because the filling defect in the distal bile duct was caused by a blood clot with an elongated oval configuration and soft, dense, elastic characteristics. ¹¹

Reportedly, earlier intervention is associated with faster recovery and a better prognosis. ¹² Rather than extracting the blood clot, Zhou et al. placed a plastic bile duct stent across the clot. ¹³ The patient’s delayed recovery in that report may have been due to inadequate drainage. In the present case, we selected a fully covered metal stent combined with ENBD, an approach that, to our knowledge, has not been previously reported. Compared with plastic stents, fully covered metal stents provide a larger luminal diameter, facilitating more effective clearance of biliary blood clots and reducing the risk of early stent occlusion by clots. ¹⁴ The addition of ENBD enables continuous external drainage and real-time monitoring for rebleeding, thereby enhancing procedural safety. ¹⁵ Given the patient’s recent trauma and surgical history, we favored a minimally invasive endoscopic approach over surgery, consistent with emerging reports on hemobilia management.^10,14 The patient’s liver function gradually improved by postoperative day 2. HC was managed through multidisciplinary consultation; however, a potential risk of nonoperative management includes delayed gallbladder rupture due to necrosis. ¹⁶

Conclusion

Management of this patient was particularly challenging because of the absence of specific clinical manifestations, which delayed the diagnosis of gallbladder hemorrhage. This case highlights the diagnostic value of PTGBD in patients presenting with severe jaundice of unclear etiology. Notably, the combination of a covered metal stent and ENBD after ERCP was an effective and innovative strategy for clearing biliary blood clots and achieving sustained, comprehensive biliary decompression. This approach may help guide clinical decision-making in similar complex hepatobiliary cases and may have implications for refining therapeutic strategies and guideline recommendations. Importantly, this case highlights the essential role of a multidisciplinary approach in optimizing outcomes for patients with complex hepatobiliary disorders.

Supplemental Material

sj-docx-1-sco-10.1177_2050313X261429634 – Supplemental material for Management of obstructive jaundice secondary to hemorrhagic cholecystitis following a high-altitude fall: A case report

Supplemental material, sj-docx-1-sco-10.1177_2050313X261429634 for Management of obstructive jaundice secondary to hemorrhagic cholecystitis following a high-altitude fall: A case report by Rui Meng, Wei-Hua Liu, Wen-Na Shi, Yu-Ping Bai and Hong-Bin Wang in SAGE Open Medical Case Reports