Acute hemobilia following computed tomography-guided percutaneous liver biopsy: A case report

Abstract

BACKGROUND

Acute hemobilia is an uncommon complication of computed tomography (CT)-guided percutaneous liver biopsy.

CASE SUMMARY

We report a 57-year-old man with colorectal liver metastases. He underwent biopsy due to disease progression after multiple lines of anticancer therapy, including antiangiogenic agents and chimeric antigen receptor T-cell therapy. During stepwise withdrawal of the coaxial cannula, he suddenly developed severe right upper quadrant pain, diaphoresis, nausea, sinus tachycardia, and a positive Murphy’s sign. Immediate non-contrast CT revealed marked gallbladder distention and new hyperattenuating contents compared with preprocedural imaging. Acute hemobilia was diagnosed based on the timing of symptom onset, clinical findings, and CT features. His symptoms resolved with conservative management. Previous therapies may have contributed to the endothelial injury and microvascular fragility, while loss of the tamponade effect during cannula withdrawal may have allowed bleeding into an injured biliary structure.

CONCLUSION

Prophylactic gelatin sponge tract embolization warrants consideration when suspected microvascular fragility coexists with technically complex biopsy.

Key Words: Arteriobiliary fistula; Hemobilia; Mechanical tamponade effect; Percutaneous liver biopsy; Tract embolization; Case report

Core Tip: We report a case of a heavily pretreated patient who developed acute hemobilia during coaxial cannula withdrawal after computed tomography-guided liver biopsy. Immediate non-contrast computed tomography and physical signs enabled prompt diagnosis. Loss of mechanical tamponade and possible treatment-related vascular vulnerability were considered plausible, although they are unconfirmed contributing factors. In selected cases, prophylactic gelatin sponge tract embolization during coaxial cannula withdrawal may be considered a reasonable preventive option.

INTRODUCTION

Percutaneous liver biopsy is an established diagnostic modality for hepatic lesions, with overall bleeding rates below 2%[1]. Clinically significant hemobilia is rarely reported[2-4]. Preprocedural risk assessment has traditionally focused on coagulation parameters, platelet count, coagulation factors, antithrombotic use, and relevant medical history. Antiangiogenic agents, such as bevacizumab and regorafenib, may alter the structural integrity and repair dynamics of the hepatic microvasculature[5-7]. Chimeric antigen receptor T-cell (CAR-T) therapy is associated with endothelial dysfunction, particularly in the setting of cytokine release syndrome (CRS)[8]. However, the relevance of these effects to bleeding after percutaneous biopsy remains uncertain. In this report, we describe a case of acute hemobilia that developed during coaxial cannula withdrawal in a patient with colorectal liver metastases who had previously received chemotherapy, antiangiogenic agents, and CAR-T therapy. We also discuss the possible roles of mechanical tamponade and pressure-gradient redistribution in the development of hemobilia, as well as selective tract embolization in patients with suspected vascular fragility.

CASE PRESENTATION

Chief complaints

A 57-year-old man with colorectal liver metastases was admitted to the oncology department because of disease progression after multiple lines of anticancer therapy.

History of present illness

In May 2021, the patient underwent laparoscopic radical resection for sigmoid adenocarcinoma. Histopathological examination revealed serosal and lymphovascular invasion, with metastases in 8 of 22 regional lymph nodes. From February 2023 to September 2024, he received multiple lines of therapy, including cetuximab plus FOLFIRI, bevacizumab plus FOLFOX, and regorafenib plus trifluridine/tipiracil. In September 2024, during post-CAR-T infusion monitoring, he developed septic shock, immune-related myocarditis, severe pneumonia, and ileus, which together met the criteria for high-grade CRS. After 1 month of intensive care, he recovered and was discharged. Two months after the infusion, computed tomography (CT) revealed an increase in both the size and number of the pre-existing hepatic lesions. Because of disease progression after multiple lines of therapy, rebiopsy was performed to reassess the tumor histology, immune microenvironment, and molecular profile; the aim was to identify new mutations or other actionable alterations and to determine eligibility for clinical trials. CT guidance was selected to allow precise planning of the access route to the target lesion. An 18-gauge coaxial needle system was used and adjusted in multiple directions (cranial, caudal, dorsal, and ventral) to obtain five tissue cores. The sampling procedure was well tolerated. Only a small amount of dark blood was observed at the cannula hub, with no active external bleeding, severe pain, or hemodynamic instability. The cannula was then gradually withdrawn at a rate of approximately 1-2 cm per minute. During withdrawal, the patient suddenly developed severe right upper quadrant pain, rated 7/10 on the numeric rating scale, accompanied by diaphoresis, nausea, and sinus tachycardia.

History of past illness

The patient had no history of diabetes mellitus, hypertension, cardiovascular disease, tuberculosis, chronic hepatitis B or C virus infection, or known gallbladder disease.

Personal and family history

The patient reported a 40-year history of smoking 4-5 cigarettes per day and light alcohol consumption over a similar period. There was no relevant family history.

Physical examination

Physical examination revealed a positive Murphy’s sign without radiating pain or vomiting. Intramuscular dezocine (5 mg) was administered immediately for analgesia. The patient remained hemodynamically stable.

Laboratory examinations

The laboratory test results on admission, including prothrombin time, activated partial thromboplastin time, alanine aminotransferase, aspartate aminotransferase, total bilirubin, serum creatinine, and estimated glomerular filtration rate, were within acceptable ranges for biopsy.

Imaging examinations

Immediate CT demonstrated marked gallbladder enlargement compared with the preprocedural baseline. The gallbladder lumen contained diffuse hyperattenuating material, with a mean attenuation of 51 ± 6 Hounsfield units (Figure 1A).

Figure 1 Dynamic computed tomography progression of acute hemobilia following computed tomography-guided percutaneous liver biopsy. A: Acute phase of complication (immediately post-withdrawal). An axial unenhanced computed tomography (CT) scan demonstrates significant gallbladder distension compared to the preoperative baseline, filled with diffuse, homogeneous intraluminal hyperdensity (mean CT attenuation: 51 ± 6 Hounsfield units; arrow), consistent with acute intraluminal hemorrhage; B: Preoperative baseline comparison. The baseline CT image obtained prior to the biopsy shows a physiologically collapsed gallbladder with no evidence of intraluminal abnormalities or prior biliary disease; C: Stable observation phase (5 days post-procedure). A repeat CT scan reveals stabilized gallbladder dimensions and persistent intraluminal hyperdensity without further expansion, indicating a contained and non-progressive hemobilia; D: Follow-up absorption phase (1 month post-procedure). A follow-up CT scan demonstrates restoration of normal gallbladder morphology with complete absorption of the intraluminal hematoma.

FINAL DIAGNOSIS

Acute hemobilia was clinically diagnosed based on the sudden onset of right upper quadrant pain during cannula withdrawal and the presence of new hyperdense material within an enlarged gallbladder on CT. Preprocedural imaging showed a normal, nondistended gallbladder (Figure 1B). The pain resolved within 10 minutes, and repeat imaging showed no further increase in gallbladder size or intraluminal blood volume. A vascular-biliary communication was considered the most likely source of bleeding. However, neither the bleeding vessel nor the presence of an arteriobiliary fistula could be confirmed because angiography was not performed.

TREATMENT

The patient remained hemodynamically stable, and his pain subsided rapidly. As repeat CT showed no evidence of ongoing bleeding, conservative management was continued. He received intravenous fluids, prophylactic levofloxacin, hemocoagulase agkistrodon, and etamsylate. Neither angiographic embolization nor surgery was required. During observation, he was monitored for recurrent abdominal pain, gastrointestinal bleeding, jaundice, fever, worsening anemia, hemodynamic instability, and signs of biliary obstruction.

OUTCOME AND FOLLOW-UP

The patient experienced no recurrence of abdominal pain. His hemoglobin level decreased slightly, while bilirubin and liver enzyme levels remained stable. Follow-up CT showed marked resolution of the hematoma after 5 days and complete absorption at 1 month, with normalization of the gallbladder size (Figure 1C and D).

DISCUSSION

CT-guided percutaneous liver biopsy is associated with a low rate of serious complications[1]. Hemobilia is uncommon and has been rarely reported after percutaneous liver biopsy[2,9]. In this case, the timing of symptom onset, abrupt right upper quadrant pain, and appearance of new hyperattenuating material within an enlarged gallbladder strongly supported a diagnosis of procedure-related acute hemobilia. The normal appearance of the gallbladder before biopsy and the marked change after the procedure further supported acute bleeding rather than pre-existing sludge or concentrated bile. Nevertheless, because CT angiography, catheter angiography, and endoscopic evaluation were not performed, the exact bleeding vessel and the nature of the anatomical communication remain uncertain.

The timing of symptom onset was particularly informative. The patient remained stable during tissue sampling but developed abrupt right upper quadrant pain during withdrawal of the coaxial cannula. According to Sandblom’s model of hemobilia, a pressure gradient exists between the hepatic arterial and biliary systems[10]. When an artery and an adjacent bile duct are injured simultaneously, the higher arterial pressure may drive blood into the lower-pressure biliary tract. During tissue sampling, the indwelling coaxial cannula may temporarily compress injured microvessels and small bile ducts. This tamponade effect could explain the slight oozing at the cannula hub and the absence symptoms while the cores were collected. Once the cannula was withdrawn, this compression was lost, potentially allowing blood to pass through a vascular-biliary communication created by the needle injury[11]. The accumulation of blood within the gallbladder could then increase the intraluminal pressure and cause acute pain. However, this proposed sequence remains hypothetical because neither active contrast extravasation nor a vascular-biliary fistula was demonstrated.

The patient’s treatment history provided additional context for this case. Long-term antiangiogenic therapy with bevacizumab and regorafenib can impair endothelial repair, vascular remodeling, and wound healing[12]. CAR-T therapy, particularly when complicated by CRS, has been associated with endothelial activation and barrier dysfunction[9,13]. Although the CRS had resolved by the time of biopsy, the presence of residual endothelial dysfunction could not be assessed. The combined effects of antiangiogenic exposure and previous severe treatment-related endothelial activation may therefore have reduced local vascular resilience. In this fragile microenvironment, the contractile response and spontaneous thrombotic closure of transected microarteries may have been compromised. Following the loss of mechanical tamponade during stepwise cannula withdrawal, the injured vessels may have been unable to maintain hemostasis, allowing high-pressure arterial blood to extravasate into adjacent low-pressure bile ducts. However, endothelial biomarkers, such as von Willebrand factor and angiopoietin-2, were not measured. Therefore, a direct causal relationship between antiangiogenic or CAR-T therapy and post-biopsy hemobilia cannot be established. Instead, these exposures may act as contextual risk modifiers when biopsy is technically challenging.

Procedure-related factors may also have contributed. Although the specimens were obtained using a coaxial system, five cores were acquired with several intralesional directional adjustments. These adjustments may have increased the extent of tissue injury and the likelihood of simultaneous injury to small vessels and bile ducts. This possibility is consistent with reports linking the number of needle passes to the risk of hemorrhage[14].

Prophylactic biopsy-tract embolization may be considered in selected cases in which anticipated procedural complexity coexists with suspected vascular vulnerability. Removal of the coaxial cannula eliminates any residual tamponade effect, and spontaneous hemostasis may be insufficient. Tract embolization during cannula withdrawal has been reported to reduce post-biopsy bleeding[15]. However, the available evidence does not establish that tract embolization specifically prevents hemobilia or that it is routinely indicated after antiangiogenic or CAR-T therapy. Standard preprocedural assessment should continue to include platelet count, coagulation parameters, antithrombotic exposure, relevant liver disease, lesion characteristics, access route, and anticipated technical complexity. Previous anticancer treatment may be considered as part of the overall clinical assessment but should not be used alone to classify a patient as being at high risk. When tract embolization is considered appropriate, gelatin-sponge slurry or small pledgets can be delivered through the coaxial cannula during withdrawal to promote local hemostasis. Prospective studies are needed to identify the patients most likely to benefit and to determine the safest embolization technique.

This report has several limitations. First, a single case cannot establish a causal link between previous treatment and microvascular fragility. Endothelial injury markers, such as von Willebrand factor and angiopoietin-2, were not measured; therefore, the role of treatment-related endothelial dysfunction remains hypothetical. Second, angiography was not performed because the patient improved rapidly and repeat CT showed no evidence of ongoing bleeding. Consequently, neither an arterial source nor a vascular-biliary fistula was directly demonstrated. Finally, although the timing of symptom onset suggests that stepwise cannula withdrawal may have triggered the event, the respective contributions of needle injury, multiple core samples, directional adjustments, and loss of mechanical tamponade cannot be excluded. Prospective studies are required before this preventive strategy can be recommended for routine use in heavily pretreated patients.

CONCLUSION

Prophylactic gelatin sponge embolization of the biopsy tract may be considered when suspected microvascular fragility coexists with a technically complex biopsy. However, further prospective evaluation is required before its routine use can be recommended.