Vascular complications in percutaneous biliary interventions

Abstract

Percutaneous biliary interventions are indicated for both benign or malignant biliary strictures to treat obstructive jaundice and/or biliary leak. Major vascular complications include active bleeding or more frequently pseudoaneurysm formation, bilio-portal, bilio-venous or arterio-biliary fistulae and intra- or peri-hepatic hematoma. Such adverse events can occur during the procedure itself or, more often, several days to weeks after the initial procedure. Major vascular complications frequently manifest with symptoms of hemobilia (jaundice, pain, melena or hemochezia and reduced serum hemoglobin levels), which in some cases lead to life-threatening hemodynamic compromise. Computed tomography angiography is mandatory to diagnose the cause and site of bleeding, while simultaneously depicting the anatomy, in order to plan the treatment. Covered stents, liquid embolic agents and coils are the commonest devices used, depending on the underlying pathology. Although such complications are rare, they are frequently life-threatening, and require prompt treatment. Therefore, interventional radiologists must be proficient in their management. This narrative minireview aims to outline management strategies of the most frequent intra- or post-procedural vascular complications following biliary interventions.

Key Words: Biliary intervention; Percutaneous transhepatic biliary drainage; Biliary stent; Vascular complications; Pseudoaneurysm; Bilio-portal fistula; Bilio-venous fistula; Arterio-biliary fistula; Hemobilia

Core Tip: Vascular complications after percutaneous biliary interventions, though rare, are potentially life-threatening and require prompt diagnosis and management. These may include pseudoaneurysms, vascular fistulas, and hematomas, which can present with hemobilia, pain, or hemodynamic instability. Computed tomography angiography is essential for diagnosis and treatment planning. Common treatments include covered stents, coils, and liquid embolics. This narrative minireview outlines the recognition and management of such complications during or after biliary drainage or stenting.

INTRODUCTION

Percutaneous biliary interventions comprise a group of critical interventional radiological techniques employed primarily for decompressing both benign or malignant obstructed biliary system, to treat biliary leak and/or obstructive jaundice, particularly in patients for whom endoscopic access is not feasible. Percutaneous transhepatic cholangiography with biliary drainage/stent placement is a common interventional radiology procedure performed under combined ultrasonographic and fluoroscopic guidance that includes percutaneous transhepatic puncture with cannulation of a peripheral biliary radicle followed by contrast material injection and imaging-guided wire and catheter manipulation in order to place a tube or stent to provide external or preferably internal drainage of bile.

Percutaneous transhepatic biliary drainage (PTBD) placement is indicated to decompress obstructed biliary tree diverting bile out or channeling it into the duodenum, beyond the obstructed tract. Providing direct access to the biliary tract is mandatory for many therapeutic purposes that include: Dilate biliary strictures, remove bile duct stones, stent malignant lesions, brachytherapy/phototherapy, radiofrequency ablation, endoluminal tissue sampling and foreign body retrieval[1]. Despite its technical maturity and broad therapeutic application, percutaneous biliary intervention remains associated with a spectrum of complications, most notably hemorrhagic events.

Before any percutaneous biliary intervention, a careful assessment of several factors is mandatory as to evaluate the risk of procedure-associated bleeding, such as anticoagulation and chemotherapeutic agents or patient conditions like hematologic disorders and hemorrhagic diathesis[2]. Complications during PTBD placement occur in about 10% of cases and can be classified in minor (such as pain or catheter dislodgment) and major complications, which can result in death of the patient[3]. All complications can happen during the procedure or, more frequently, days or weeks after the initial procedure (Figure 1). This narrative minireview aims to outline management strategies of the most frequent intra- or post-procedural vascular complications following biliary interventions, including PTBD or stent placement, endoluminal tissue sampling.

Figure 1 A 55-year-old male with malignant biliary obstruction (cholangiocarcinoma Klatskin 4). The “pull-back cholangiogram” depicts an arterio-biliary fistula (orange circle).

VASCULAR COMPLICATIONS

Vascular complications are clinically evident by bleedings and could be moderate and transitory or severe, in relation to arterial pseudoaneurysms, portobiliary/arterio-biliary fistulas, or intrahepatic hematomas[4]. The incidence of hemorrhage after percutaneous biliary interventions varies from 1.1% to 9.9%[5]. Major vascular complications usually arise with hemobilia, pain, reduced serum hemoglobin levels, in some cases leading to hemodynamic instability.

Assessing the hemodynamic status by measuring vital signs, stabilizing by administration of i.v. fluids, oxygenation and blood transfusion, if necessary, is the first step. The blood investigations needed to be performed include hemoglobin level, hematocrit, international normalized ratio (INR) and platelet count[6]. The most relevant risk factors for hemorrhagic complications after PTBD placement have been grouped by Pulappadi et al[6] in patient related and technique related factors and are shown in Table 1.

Table 1 Risk factors for hemorrhagic complications after percutaneous transhepatic biliary drainage[6].

Patient related factors	Technique related factors
Advanced age (≥ 73 years)	Large bore puncture needle (18G)
Chronic kidney disease	Central duct puncture
Cirrhosis	Minimally/non-dilated biliary system
Deranged coagulation parameters	Multiple number of punctures and catheters
Ongoing use of antithrombotic agents	Presence of ascites

MANAGEMENT

Cholangiography through the percutaneously placed catheter, also using the “pull-back cholangiogram” technique, is usually the first investigation of choice in a hemodynamically stable patient[1], often combined with ultrasonography looking for hemoperitoneum, subcapsular hematoma or pseudoaneurysms. If no cause is evident, computed tomography angiography (CTA) is mandatory to diagnose the cause of the bleeding and better depict the anatomy, in order to plan the treatment. In certain cases of delayed bleeding noted even months after the initial procedures, a 4-phases, contrast-enhanced computed tomography (CT) imaging (non-contrast, arterial, portal-venous and delayed phases), is advised as the initial diagnostic step, to allow a more comprehensive evaluation of the whole abdomen. If CTA fails to detect the bleeding site with persistent deranged hematocrit, an intra-arterial selective digital subtraction angiography (DSA) is necessary. Covered stents, liquid embolic agents and coils are the commonest materials used, depending on the underlying cause.

HAEMOBILIA DUE TO ARTERIO-BILIARY FISTULAS

Haemobilia is a life-threatening complication of PTBD and refers to bleeding into the biliary system, consequently draining into the duodenum causing gastrointestinal (GI) bleeding. It should be distinguished from bilhemia, which describes a bile leak from the biliary system into the bloodstream due to a fistulous communication with the hepatic venous system.

The pathophysiology of haemobilia following PTBD primarily involves the iatrogenic injury of the intrahepatic branches of the hepatic arteries, during the transhepatic passage of either the access needle or the catheters, or both. While minor vascular trauma auto resolves, larger injuries can lead to the formation of direct arterio-biliary fistulas causing GI bleeding or pseudoaneurysms causing intermittent GI bleedings, with or without concomitant arterioportal communication. Additionally to the arterial pressure effect which directs the blood to the biliary system, bile contributes to the continuous erosion of the injured arteries, preserving the fistula and preventing from clot formation leading to persistent haemorrhage. The reported incidence of PTBD complicated by haemobilia varies in the literature between 1% to 15%. However, more recent reports indicate a 2.6% risk of hepatic artery injury with PTBD[7].

Clinical presentation

The classic Quincke’s triad of haemobilia, is present in only 25%-30% of cases[8] and includes: GI bleeding. This is the most common manifestation, ranging from occult bleeding to melena and even hematemesis or haematochezia, depending on the volume and degree of bleeding (high- or low-flow communications). It is typically presented in the early post-procedural period, but can be also present several weeks or months following the procedure especially in cases of pseudoaneurysms formation that could rupture at any time. Notably, biliary catheter dislodgement or exchange could cause the rupture of a previously formed pseudoaneurysm or incite bleeding of an injured arterial branch that was previously tamponaded by the catheter, causing late haemobilia[9]. Biliary colic: Right upper quadrant or epigastric pain caused by the passage of blood clots through the biliary tree, leading to transient obstruction and pain. Jaundice: Bile stasis and hyperbilirubinemia again occurring due to obstruction of the bile duct from blood clots. In cases in which a drainage biliary catheter is in place, blood into the external draining bag is a typical sign of haemobilia. Other symptoms may include nausea, vomiting, as well as typical signs of haemorrhage ranging from hemoglobin drop to hypovolemic shock.

Risk factors

Several factors of haemobilia have been identified including advanced age, comorbidities such as coagulopathy, malignancy, cirrhosis and renal insufficiency, as well as technical aspects such as multiple punctures/passes for access, a non-dilated biliary system, larger access needle size, left-sided access and central biliary access[10].

Diagnosis and treatment

The recognition of the above symptoms should incite the suspicion of haemobilia and immediate complete blood count, liver biochemical, coagulation profile and 4-phases contrast enhanced CT should be obtained to verify the diagnosis (Figure 2). Abnormal leucocytosis and liver biochemistry is also expected. Antibiotics, hydration and transfusions are generally required. Coagulation disorders should be immediately corrected. Intermittent, chronic bleeding is indicative of pseudoaneurysm formation. The management steps for vascular complications are outlined in Table 2.

Figure 2 A 59-year-old female patient with obstructive jaundice due to three colorectal liver metastasis (max diameter of largest lesion 7 cm) underwent biliary drainage as to enable radioembolization therapy. A: Access was obtained from the left lobe due to extensive right lobe metastatic disease. Selective Internal Radiation Therapy was successfully performed. However, 10 weeks after Selective Internal Radiation Therapy the patient reported blood within the percutaneous transhepatic biliary drainage collective bag. Following urgent admission hemobilia was diagnosed (right quadrant pain and melena); B and C: Computed tomography angiography depicted a pseudoaneurysm in proximity to the percutaneous biliary catheter (arrows), as well as good response to the radioembolization (treated lesions with significantly decreased perfusion and size); D and E: Selective digital subtraction angiography of the celiac axis verified the pseudoaneurysm which was arising from a left hepatic artery branch (arrow). Selective “back to front door” embolization was using a 1.98Fr microcatheter and detachable microcoils. F: At 48 hours bile in the collecting bag was clear of blood, blood tests normalized and the patient was discharged asymptomatic.

Table 2 Steps and management of arterial and venous haemobilia.

Step	Arterial haemobilia (high-flow)	Venous haemobilia (low-flow/bilio-venous)
Clinical presentation	Hemodynamic instability, hematemesis, rapid hemoglobin drop, pulsatile blood in bag	Dark blood-tinged bile, melena, insidious hemoglobin drop, often stable vitals
Initial action	Emergency stabilization: IV fluids, blood transfusion, urgent interventional radiology consult	Conservative: Saline flush of catheter, monitor vitals and hemoglobin
Diagnostics	Mandatory computed tomography angiography followed by urgent digital subtraction angiography	“Pull-back” cholangiogram; computed tomography angiography to identify the tract; percutaneous
Primary treatment	Selective transcatheter arterial embolization	Catheter upsizing: Replace with a larger bore drain for tamponade
Technical strategy	“Back to front door” (sandwich)	Portal covered stenting (in high flux fistulas)
Alternative	Covered stents if main hepatic artery branches are involved	Temporary clamping (24-48 hours) or percutaneous tract embolization
Resolution	Confirm cessation of bleeding via digital subtraction angiography and clinical monitoring	Maturation/scarring of the tract; resolution of “haemobilia”

CT diagnosis of a small pseudoaneurysm can be challenging especially in the presence of a biliary catheter and therefore one should focus in the access track or the area around the draining catheter. The diagnosis of active bleeding or pseudoaneurysm, or arterio-portal fistula is an indication for minimal invasive treatment with percutaneous, trans arterial embolization (TAE). When CT fails to detect the bleeding site due to the presence of a biliary draining catheter, an intra-arterial selective DSA is necessary. During this procedure, the biliary catheter should be removed (over the wire) to unmask the pathology and confirm bleeding or pseudoaneurysm. If present, same session embolization should be performed. Selective TAE is the gold standard treatment for haemobilia as it is minimally invasive, with a high success rate in controlling bleeding while preserving liver parenchyma[2]. Selective catheterization of the bleeding branch using a microcatheter is suggested for a successful and uncomplicated embolization. Various materials can be used, but the largest experienced has been reported using mainly coils, or glue, or both. When coils are used the “back to front door” (also known as the “sandwich” technique), is advised to avoid retrograde collateral supply (Figure 2). Intralesional coiling, additional to the “back to front door” technique can also be used as to more effectively seal the communication with the biliary system which is preserved by the presence of bile. Supplementary glue within the aneurysm or the fistula can also be used with caution and in low dilutions (up to 1:1), as to avoid non targeted occlusion of major biliary branches. Previous reports have shown the success rate of TAE to range between 80%-100%[11].

Failure of TAE treatment has been reported due to inability to identify the bleeding vessel or due to incomplete occlusion of the lesion. Nonetheless, other methods such as successful embolization of the lesion via the biliary access have also been reported[12] (Figure 3). Moreover, in cases of incomplete embolization or recurrence, repeat embolization is always an option and can be easily performed. Endoscopic methods have been also reported to be effective in the treatment of haemobilia however in the ambit of intrahepatic arterial branches their efficacy remains uncertain, given the fact that most of these cases where initially treated for malignancies not accessible by endoscopy. Surgical intervention is reserved for cases where TAE is not technically feasible (e.g., altered vascular anatomy due to previous surgery or significant stenosis or occlusion of the superior mesenteric artery and celiac axis) or has repeatedly failed, and in the presence of massive, life-threatening hemorrhage that cannot be controlled by other means. Of note, successful TAE has been reported even in the absence of direct arterial access via the percutaneous approach using combined ultrasound and fluoroscopy-guidance to occlude the pseudoaneurysm with N-butyl cyanoacrylate (NBCN) glue[13].

Figure 3 A 53-year-old female patient with colorectal liver hilar metastasis and right lobe endoscopic plastic stent underwent left lobe percutaneous transhepatic biliary drainage. A: Computed tomography angiography revealed a pseudoaneurysm in proximity to the percutaneous biliary catheter (arrow); B: Selective digital subtraction angiography from the common hepatic artery confirmed the presence of the pseudoaneurysm arising from the left hepatic artery (arrow); C and D: The left hepatic artery was selectively catheterized with a 1.98Fr microcatheter and proximately embolized with pushable microcoils; as the back to front door” technique was not feasible (microcatheter was not advancing distal to the lesion) the catheter was removed over a 0.035’ guide wire (arrow), E and F: An 8Fr sheath was placed and using a 5Fr angled catheter (arrow) and the same microcatheter via the 5Fr catheter (arrowhead), the sack of the pseudoaneurysm was embolized using pushable microcoils (arrow). Note that during removal of the biliary catheter arterial blood was noted, confirming the necessity of further embolization from the biliary access; G: Check computed tomography angiography at 7 days, prior to discharge, confirmed the occlusion of the pseudoaneurysm. The patient was discharged asymptomatic.

Relative contraindications include cases of liver allografts and portal vein thrombosis, in which extensive arterial occlusion can result in severe hepatic ischemia. However, this can also be avoided by super selective embolization of the bleeding branch or of solely the pseudoaneurysm using the percutaneous or biliary approach. Additionally, small-diameter stent grafts or flow-diverting stents could be also considered to occlude the lesion while preserving vessel patency[14]. Following embolization, the existing PTBD catheter should be patent and properly positioned (or re-positioned) to facilitate drainage of blood clots and bile, thereby preventing biliary obstruction and cholangitis. Flushing the catheter with saline is imperative to clear clots. In cases where a draining biliary catheter is not in place (e.g., in cases of biliary stenting and late haemobilia), the placement of a draining catheter should be considered once the patient’s condition has stabilized.

Cholangitis is a rare complication following haemobilia[15]. Correct antibiotic therapy and long-term drainage following TAE are the keystones of prevention against this life-threatening event[16]. Pseudoaneurysms can form during PTBD, even without haemobilia, if puncture trauma affects an intercostal artery, an intrahepatic branch (from access attempts without catheter insertion), or the extrahepatic arterial network[17,18]. Haemobilia is a life-threatening complication of PTBD and while conservative management may suffice for minor bleedings, endovascular embolization has revolutionized the treatment of significant haemobilia, offering a safe and effective minimally invasive approach. Surgical intervention should be reserved only for refractory cases.

BILHEMIA DUE TO BILIO-PORTAL FISTULAS

Bilio-portal fistulas in biliary interventions are generally caused by the transhepatic passage of the needle or by balloon catheter dilatation of bile ducts. Their management is based on the clinical assessment of the patient, as well as the experience of the interventional radiology team. Patients typically present with intermittent dark blood in the drainage bag or melena. A mild haemobilia due to a low-flux fistula generally regress spontaneously without interventions or by injection of cold physiological solution through the PTBD, but can also be treated by placing - through a guidewire - a larger caliber catheter for biliary drainage with the holes tract located distal to the fistula point: This will lead to the progressive maturation and scarring of the fistulotic tract. Alternative therapeutic methods are tamponing with a balloon catheter in order to obtain hemostasis or placing a biliary stent covering the fistula point[19]. In some cases, portal branch covered stenting could be performed (Figure 4). Fistulas embolization is less common in literature: It is generally used in cases of large or high flux fistulas. Embolization could be performed by the pre-existing biliary access using microcoils or plugs[20-22]. NBCN glue is also a good option to embolize the portal branch involved (Figure 5).

Figure 4 Large perihilar portobiliary fistula in patient with percutaneous transhepatic biliary drainage. A: Percutaneous transhepatic biliary drainage with evidence of portobiliary fistula; B: A covered stent was inserted in the portal branch to treat the fistula.

Figure 5 Protobiliary fistula following external biliary drainage insertion. A and B: Cholangiography via multipurpose catheter shows an iatrogenic bilio-portal fistula (orange circle) occurred during percutaneous transhepatic cholangiography; C: It was treated by N-butyl cyanoacrylate glue embolization of the portal branch; D: Computed tomography scan revealed glue deposition and complete embolization of the fistula.

BILIO-VENOUS FISTULAS AND OTHER HEPATIC VENOUS COMPLICATIONS FOLLOWING PTBD

While considerable attention has been devoted to injuries involving the hepatic artery and portal venous system, complications related to the hepatic venous outflow are less frequently reported and often underrecognized in clinical practice. Hepatic venous injuries during PTBD occur due to the anatomical course of the hepatic veins, particularly in the right lobe of the liver, where segment VI bile ducts may lie in close proximity to the right hepatic vein. In these scenarios, an inadvertent transgression of the vein during catheter insertion or manipulation can lead to the development of a bilio-venous fistula or frank venous bleeding. The rarity of this complication, combined with often nonspecific or delayed clinical manifestations, contributes to diagnostic challenges and a potential underestimation of its true incidence[1,6].

Venous bleeding is characteristically low-pressure in nature, and thus, initial presentations may be subtle, manifesting as dark red or blood-tinged bile draining through the catheter. In the absence of overt hemodynamic instability, such signs can be erroneously attributed to minor parenchymal injury or procedural trauma. Nevertheless, persistent or delayed bleeding, melena, hematemesis, or an unexplained drop in hematocrit following PTBD should prompt a detailed investigation. When venous channels are involved, particularly the hepatic or large caliber portal venous branches, bleeding may continue insidiously, eventually leading to significant blood loss or secondary complications such as hemoperitoneum[6,23].

The diagnosis of hepatic venous injury relies on a combination of imaging techniques. Initial cholangiography may reveal vascular opacification suggestive of communication between the biliary system and the venous vasculature. A more sensitive approach is the use of the “pull-back” cholangiogram, where a vascular sheath is inserted over a guidewire following catheter removal. During contrast injection, visualization of the hepatic vein or early filling of the inferior vena cava indicates a biliovenous fistula. Additionally, ultrasound and CT, particularly in the portal venous phase, can aid in identifying associated hematomas, active extravasation, or displacement of the catheter into vascular structures[3,6].

Management strategies for hepatic venous injury following PTBD are dictated by the extent of bleeding and the caliber of the injured vessel. In cases of minor venous transgressions involving small peripheral tributaries, conservative management is often sufficient. This may include repositioning the catheter to exclude side holes from the site of injury, upsizing the catheter to increase tamponade effect, or clamping the catheter for 24-48 hours. These approaches promote hemostasis through direct compression of the injury site. In cases of suspected catheter instability or poor tract maturation, additional skin fixation using purse-string sutures may be necessary to prevent displacement[1,6].

When major bleeding occurs due to injury to central hepatic veins or when conservative measures fail, interventional techniques become essential. Percutaneous embolization of the transhepatic tract using gelfoam, coils, or NBCN glue has been successfully employed in such scenarios (Figure 6)[6]. This approach is particularly beneficial in patients who are poor surgical candidates or in whom bleeding persists despite catheter-related adjustments. Rarely, when a bilio-venous fistula is large or centrally located, placement of a covered stent in the hepatic vein or bile duct may be considered to isolate the communication, although this carries risks of hepatic infarction or cholangitis due to side branch occlusion[6].

Figure 6 A 73-year-oid patient with cholangiocarcinoma and bile leak. A: Magnetic resonance cholangiopancreatography demonstrates a filling defect in the distal common bile duct (arrow), later diagnosed as cholangiocarcimona. The patient subsequently underwent surgical resection with biliodigestive anastomosis; B: Bile leakage was observed from the surgical drain, prompting percutaneous transhepatic cholangiography. In the days following the percutaneous transhepatic cholangiography, the patient developed sepsis; C: Computed tomography was performed and revealed a marked angulation of the percutaneous drain in close proximity to vascular structures (arrow); D: Along with thrombosis and the presence of gas bubbles in the right suprahepatic vein (arrow); E: A repeat interventional radiology procedure was carried out, which confirmed the presence of a biliovenous leak (arrow) and a new drain was placed in a different right bile duct (arrowhead); F: Subsequently, the biliovenous fistula tract was embolized using N-butyl cyanoacrylate glue (arrowhead); G: Finally, the previously positioned access route was removed, with continued embolization of the entire access tract (arrowhead); H: On follow-up computed tomography after removal of the biliary drain and resolution of the patient’s clinical condition, faint remnants of the embolic material are still visible (arrowheads).

A specific form of venous complication is bilhemia, wherein bile enters the systemic circulation via a biliovenous fistula, especially when biliary pressures exceed venous pressures in the setting of distal biliary obstruction. Clinically, this is reflected in disproportionately high serum bilirubin levels without corresponding biliary dilation. Although typically self-limiting upon biliary decompression, recognition of this phenomenon is crucial to avoid unnecessary interventions[6].

Prevention remains a cornerstone in reducing the incidence of venous complications during PTBD. Procedural planning should include cross-sectional imaging to delineate vascular and biliary anatomy, with a preference for targeting peripheral ducts over centrally located ducts that are more likely to be accompanied by large vessels[1,23]. Ultrasound-guided access should be employed whenever feasible, using color Doppler to avoid vascular structures. The choice of access needle is also important; smaller gauge needles (21-22G) are associated with lower bleeding risk compared to larger bore needles (e.g., 18G), particularly in non-dilated systems. Operator experience, attention to technical detail, and adherence to standardized protocols such as those proposed by Cardiovascular and Interventional Radiological Society of Europe (CIRSE) are all vital in minimizing iatrogenic injury[23].

Coagulopathy correction prior to the procedure is imperative. According to both CIRSE and Society of Interventional Radiology guidelines, PTBD is classified as a high-risk procedure for bleeding, warranting careful assessment of coagulation parameters. Recommended thresholds include an INR of ≤ 1.8 and a platelet count ≥ 50000/mm³. However, in life-threatening conditions, biliary interventions could be performed even in patients not meeting the specific coagulation criteria, providing that all actions to correct coagulopathy - even temporary - have been made. The use of antiplatelet or anticoagulant medications should be managed in consultation with the treating physician, balancing thrombotic and hemorrhagic risks[6,23].

In summary, while hepatic venous complications following PTBD are infrequent, their clinical significance warrants heightened awareness. A comprehensive understanding of liver vascular anatomy, diligent procedural planning, and timely use of advanced imaging techniques are essential for diagnosis. Most cases can be managed conservatively; however, when necessary, interventional embolization or stenting should be employed with due caution. As the field of interventional radiology continues to evolve, further prospective data and multicenter registries are needed to better characterize these complications and refine therapeutic algorithms.

INTRAHEPATIC AND PERIHEPATIC HEMATOMAS AFTER PERCUTANEOUS BILIARY DRAINAGE

Hepatic hematomas are primarily caused by vascular injury during biliary access, particularly with multiple puncture attempts or in patients with coagulopathy or non-dilated ducts. While exact incidence is difficult to determine, hepatic hematomas are among the most common bleeding complications of PTBD, contributing to the overall bleeding rate of 10.8%-23% reported in large series[3,6]. Subcapsular hematomas typically result from small-caliber venous injuries or parenchymal lacerations. These may present with right upper quadrant or epigastric pain and are often incidentally discovered on postprocedural imaging. Extension of bleeding beyond the liver capsule can lead to perihepatic or intraperitoneal collections, which may result in hemodynamic instability or hemoperitoneum[3]. Vascular injuries associated with intrahepatic hematoma include active contrast extravasation, pseudoaneurysm, and arterio-biliary or arterio-portal fistulas.

Contrast-enhanced CT is the modality of choice for identifying and characterizing hematomas. Intrahepatic hematomas appear as lenticular collections beneath the liver capsule, while perihepatic hematomas may demonstrate active contrast extravasation if bleeding is ongoing. On ultrasound, hematomas may mimic bilomas or abscesses, highlighting the importance of cross-sectional imaging for accurate diagnosis[3,23]. If the vascular injury lies adjacent to the catheter, pseudoaneurysm or contrast extravasation may not be evident unless the catheter is withdrawn over a guidewire and an angiogram is performed.

Management depends on the hematoma’s size, hemodynamic impact, and progression. Small, stable hematomas are typically managed conservatively with close monitoring, analgesia, and supportive care. Blood transfusion may be necessary in the event of significant hemoglobin drop. Larger or expanding hematomas, especially those accompanied by signs of arterial bleeding or hemodynamic instability, require more aggressive intervention. Selective embolization via endovascular approach is often warranted when an injured arterial branch is identified (Figure 7)[3]. To prevent reperfusion via intrahepatic collateral vessels, the injured artery should be occluded using the “back to front door” technique. Placement of covered stent grafts should be considered for main branches of the left or right hepatic arteries, where embolization could compromise a substantial portion of the liver. Glue is a commonly used liquid embolic agent in this setting and may also be delivered percutaneously following image-guided access.

Figure 7 Patient with recurrent cholangiocarcinoma involving segment IV, approximately 18 months after prior right hepatectomy. A: Computed tomography scan showing a large mass (arrow) in the right liver lobe, in keeping with cholangiocarcinoma; B: The patient underwent percutaneous transhepatic cholangiography for hyperbilirubinemia. An initial attempt at percutaneous biliary access to segment III was unsuccessful; residual contrast medium can be seen in segment III (arrowhead); C: Due to the onset of severe epigastric pain, computed tomography was performed, revealing a large hematoma in the left hepatic lobe (arrowhead); D: With evidence of arterial blush from a branch supplying segment III (arrowhead); E: Angiographic evaluation confirmed this finding, both on common hepatic artery catheterization (arrowhead); F: And during selective angiography (arrowhead); G: Embolization of the arterial lesion was performed using coils (arrowhead); H: The final proximal angiographic control demonstrated successful exclusion of the treated branch from arterial flow, with no further contrast extravasation.

Preventive strategies, as outlined in CIRSE and Radiological Society of North America guidelines, include meticulous preprocedural planning, correction of coagulopathy (targeting INR < 1.5 and platelet count > 50000/μL), use of fine needles (21-22G), preference for peripheral duct access, and avoidance of multiple puncture attempts. Real-time ultrasound guidance is strongly recommended to minimize the risk of vascular injury and hematomas formation[3,23].

CONCLUSION

Vascular major complications after biliary procedures are rare and most of the times life-threatening, venous injuries, instead, are more common and usually self-limiting; arterial injuries result in greater blood loss and often require active management. Careful assessment of risk factors that could increase the chance of bleeding and taking necessary pre-procedure precautions are fundamental to reduce the occurrence of such complications. Most of the times the patient is stable, with transient haemobilia; in these cases, cholangiography and ultrasonography can usually identify the cause of bleeding and repositioning of a larger catheter can sometimes tampon the bleeding. In cases of arterial injury CTA and a prompt interventional approach is required in the vast majority of the cases. Managing vascular complications is a requisite for every interventional radiologist who performs biliary interventions.