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  • Systematic Review
  • Open Access

5 March 2025

Cystic Artery Bleeding: Imaging Insights and Systematic Review of Endovascular Management

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1
Radiology Unit 1, Department of Medical Surgical Sciences and Advanced Technologies “GF Ingrassia”, University Hospital Policlinico “G. Rodolico-San Marco”, 95123 Catania, Italy
2
Department of Radiology, Ospedale del Mare, ASL NA1 Centro, 80147 Naples, Italy
3
Unità Operativa Semplice Dipartimentale di Imaging Polmonare e Tecniche Radiologiche Avanzate (UOSD IPTRA), Department of Medical Surgical Sciences and Advanced Technologies “GF Ingrassia”, University Hospital Policlinico “G.Rodolico-San Marco”, University of Catania, 95123 Catania, Italy
4
Department of Radiology, Fondazione IRCCS Policlinico San Matteo, 27100 Pavia, Italy
Gastrointest. Disord.2025, 7(1), 20;https://doi.org/10.3390/gidisord7010020
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Abstract

Background: Cystic artery bleeding (CAB) is a rare but potentially life-threatening condition. Its etiologies span iatrogenic trauma, inflammatory diseases, and trauma, often presenting variably as hemoperitoneum, upper gastrointestinal bleeding, or hemorrhagic shock. The clinical heterogeneity of CAB complicates its diagnosis, necessitating a high index of suspicion and reliance on imaging modalities, particularly computed tomography (CT), for accurate identification of bleeding sources and differentiation from other causes of abdominal pain. Methods: This pictorial essay highlights key imaging findings in CAB and pseudoaneurysms, emphasizing the role of ultrasound, CT, and digital subtraction angiography (DSA) in diagnosis and management planning. Additionally, a systematic review of transcatheter arterial embolization (TAE) is presented, consolidating data from 64 studies encompassing 90 patients. Results: The review evaluates patient demographics, etiologies, clinical presentations, and procedural outcomes, underscoring TAE’s high efficacy and safety as a first-line treatment. Conclusions: The findings reinforce the importance of early diagnosis and tailored intervention strategies to optimize outcomes in CAB management.

1. Introduction

Cystic artery bleeding (CAB) is an exceedingly rare occurrence, with fewer than one hundred cases reported in non-traumatic settings and only a handful associated with traumatic conditions [1,2]. This rarity poses a significant challenge for including CAB in the differential diagnosis of acute abdominal or gastrointestinal presentations.
The etiology of CAB encompasses a spectrum of factors, including iatrogenic trauma (notably during cholecystectomy), inflammatory conditions such as acute cholecystitis or pancreatitis, and post-traumatic injuries [1,3]. Its clinical presentation is highly heterogeneous, primarily influenced by the underlying cause and the severity of the hemorrhage. Symptoms can range from intraperitoneal bleeding to upper gastrointestinal hemorrhage, including hemobilia (defined as blood within the biliary tree) and, in severe cases, hemorrhagic shock [1].
Due to its diverse manifestations, CAB often eludes prompt recognition, necessitating high clinical suspicion. Imaging, particularly computed tomography (CT), plays a pivotal role in identifying the bleeding source, characterizing the hemorrhage, and differentiating CAB from other potential causes of abdominal pain or gastrointestinal bleeding [1].
Management strategies for CAB vary depending on the clinical context and the etiology of the bleeding. Surgical intervention and conservative therapy remain important options; however, transcatheter arterial embolization (TAE) has emerged as a cornerstone in the treatment of CAB, especially in cases arising from blunt trauma, laparoscopic cholecystectomy complications, duodenal ulcers, cholecystitis, gallstone erosion, or idiopathic origins [1,2].
This paper aims to comprehensively review the imaging findings associated with cystic artery bleeding and pseudoaneurysms, and to conduct a systematic analysis of the existing literature on interventional treatment strategies for these conditions.

1.1. Cystic Artery Vascular Anatomy

Anatomical variations, reported in 31.9% of individuals, include anomalous courses, variable lengths, and multiple cystic arteries, highlighting the complexity of this vascular anatomy.
The cystic artery typically arises from the right hepatic artery, traversing from the posterior to the cystic duct within the hepatobiliary triangle (Calot’s triangle). This region, bordered by the liver, common hepatic duct, and cystic duct, contains the cystic artery, lymphatics, and connective tissue [4,5].
In 79% to 89% of individuals, the cystic artery arises from the right hepatic artery. However, it may also originate from other branches of the celiac axis, including a replaced or accessory right hepatic artery, the gastroduodenal artery, the left hepatic artery, or the superior mesenteric artery (Figure 1) [5,6,7]. As the cystic artery approaches the gallbladder, it typically divides into two branches: a larger anterior superficial branch that courses beneath the serosal layer on the left side of the gallbladder, and a smaller posterior deep branch that runs between the gallbladder and the gallbladder fossa, forming a vascular network around the gallbladder [5,8].
Figure 1. Illustration of the most common variations of the cystic artery. Cystic artery (CA), right hepatic artery (RHA), left hepatic artery (LHA), proper hepatic artery (PHA), common hepatic artery (CHA), gastro-duodenal artery (GDA), superior mesenteric artery (SMA), celiac trunk (CT), inferior pancreatic-duodenal artery (IPDA), right gastric artery (RGA).
Anatomical variations, reported in 31.9% of individuals, include anomalous courses anterior to the common hepatic or bile ducts or inferior to the cystic duct. Additional variations include differences in the length of the cystic artery, with short or elongated courses, and the presence of multiple cystic arteries [5,9].

1.2. Etiology and Pathophysiology

CAB, including pseudoaneurysms (CAP), is a rare but clinically significant condition with multifactorial etiologies, including inflammatory, traumatic, and iatrogenic causes [10,11]. CAP results from localized arterial wall disruption, leading to rupture contained by the surrounding tissues [12].
Inflammatory processes, such as acute cholecystitis, weaken the arterial wall through erosion and thrombosis of the vasa vasorum, promoting pseudoaneurysm formation [12]. Chronic conditions, including gallstone-induced cholecystitis, exacerbate this damage, increasing the risk of rupture [8,10].
The cystic artery’s proximity to the gallbladder wall makes it particularly vulnerable in inflammatory states, often resulting in late-stage diagnosis [13].
Traumatic causes, accounting for 2% of blunt abdominal injuries, include shear forces that cause avulsion or laceration of the artery. Penetrating trauma, although less common, results in direct arterial damage and is often accompanied by liver or gallbladder injury (Figure 2, Figure 3 and Figure 4) [6].
Figure 2. Hemodynamically stable 78-year-old male who suffered motor vehicle accident (MVA) trauma (Hb 8 g/dL, n.v. 13–18; PCR 2.04 mg/dL, n.v. 0.0–0.5; WBC 7.66 103/mm3 n.v. 4.2–10.5). He underwent a CT with IV contrast ((a) non-contrast, (b) arterial, (c) venous, (d) delayed phase) that showed hepatic contusion and a conspicuous perihepatic and pericholecystic hematoma with cystic artery laceration and active bleeding ((c), white arrow), detected on the anterior gallbladder profile that increases in the portal (c) and delayed phases (d) particularly evident adjacent to a subcapsular (pre-existing) cyst. The patient underwent TAE successfully with super selective embolization of the anterior branch of the cystic artery (coils and PVA particles). The hepatic contusion was treated conservatively. Postoperatively, the patient was stable.
Figure 3. Hemodynamically stable 30-year-old male who suffered MVA trauma (Hb 11.9 g/dL, n.v. 13–18; PCR 0.43 mg/dL, n.v. 0.0–0.5; WBC 15.19 103/mm3 n.v. 4.2–10.5). He underwent CT with IV contrast ((a) non-contrast, (b) arterial, (c) venous, (d) delayed phase) that showed subcapsular and pericholecystic hematoma, laceration with non-active bleeding of the fourth hepatic segment and cystic artery active bleeding ((b), white arrow) along the anterior gallbladder profile with conspicuous increase of contrast extravasation in portal (c) and delayed (d) phases.
Figure 4. Arterial phase coronal MPR CT images (a) and Digital Subtraction Angiography (DSA) (b) both showing cystic artery conspicuous bleeding. (b) DSA demonstrates the entity of the bleeding (black arrow). The patient underwent TAE successfully with super-selective embolization of the anterior branch of the cystic artery (coils and Gelfoam).
Iatrogenic injury, primarily from laparoscopic cholecystectomy, is the leading cause of CAB. Vascular damage during hepatobiliary triangle dissection, often due to diathermy, compounded by bile duct injury, delays healing and predisposes to CAP formation [14]. Histological studies reveal extensive loss of elastic and muscular fibers in CAPs, which increases susceptibility to rupture and life-threatening hemorrhagic events [15,16].

1.3. Clinical Manifestations

CAB presents with a wide range of symptoms, influenced by its etiology and the extent of the hemorrhage. Symptoms vary from mild abdominal discomfort to severe hemorrhagic shock, posing diagnostic challenges [11,17].
In traumatic cases, CAB often manifests as hemoperitoneum with abdominal pain, distension, and tenderness. Severe hemorrhage may lead to hypotension, tachycardia, and altered mental status, reflecting hemodynamic instability. Active intraperitoneal bleeding in blunt trauma frequently progresses rapidly to shock [6].
Non-traumatic and iatrogenic CAB, commonly associated with CAP, typically presents after pseudoaneurysm rupture. While Quincke’s triad—right upper quadrant pain, jaundice, and gastrointestinal bleeding—is observed in less than one-third of cases, abdominal pain (77.9%) and upper gastrointestinal bleeding (64.4%) are more frequent [10,18].
Severe CAP rupture may result in hemorrhagic shock, with 19.4% requiring emergency care [18]. Imaging often reveals biliary obstruction or hemoperitoneum, emphasizing the need for timely recognition and intervention [2,16,19].

2. Imaging

Imaging plays a pivotal role in diagnosing and managing cystic artery bleeding and pseudoaneurysms. Early and accurate identification of the bleeding source is critical for timely intervention. Modalities such as ultrasound (US), computed tomography (CT), and digital subtraction angiography (DSA) are employed based on clinical suspicion and resource availability [10,20].
FAST-US accurately detect hemoperitoneum in unstable polytraumatized patients [21,22]. In non-traumatic CAB, an ultrasound may detect hemoperitoneum [23] and cystic artery pseudoaneurysm, although few cases are reported in the literature in which the US detected the presence of macroaneurysms [24]. At B-Mode, cystic artery pseudoaneurysm appears as an anechoic cavitary lesion within the gallbladder wall. Color Doppler is mandatory to detect an arterial flow within the lesion suggestive of a pseudoaneurysm. In macroaneurysm, color Doppler US has the potential to visualize the characteristic “Yin-Yang” flow pattern and the “To and Fro” flow pattern in the spectral analysis within the pseudoaneurysm itself [24].
The pseudoaneurysm’s size and neck can be measured, but the communication between the sac and the originating artery is not easily visualized [25]. The gallbladder may appear distended and exhibit hyperechoic fluid for intraluminal blood accumulation. It is important to emphasize that although cystic artery pseudoaneurysms are rare, the low frequency with which they are incidentally detected by US, before their rupture and bleeding, may also be related to the lack of knowledge of this pathological entity [26].
Oesophagogastroduodenoscopy can detect hemorrhage in 60% of patients, and ERCP may detect hemobilia but cannot locate the source of bleeding [1].
For these reasons, multiphase CT represents the cornerstone modality for evaluating suspected cystic artery bleeding and the presence of pseudoaneurysm with high sensitivity, and provides additional insight into the underlying etiology. CT also plays a critical role in the planning of percutaneous treatment by enabling the identification of aberrant vasculature and anatomical variations [27].
In a non-enhanced CT, characteristically, one key finding is the presence of hyperdense fluid that embraces the gallbladder; this typical anatomical disposition of the hemoperitoneum should alert radiologists [28]. Following intravenous (IV) contrast administration, in the arterial phase, extravasation of contrast material may be evident within the gallbladder fossa, potentially along the course of the cystic artery’s anterior or posterior branches.
A CAP can be identified as a hyper-enhancing focus during the arterial phase along the cystic artery branches (Figure 5, Figure 6, Figure 7 and Figure 8). This finding demonstrates a change in attenuation but not morphology in the venous and delayed phases (Figure 9 and Figure 10). Because of the possible presence of pre-existing gallbladder stones or surgical clips from a previous cholecystectomy, images should be examined carefully in different CT phases to differentiate hyperdense material appearing in an angiographic phase that should not be present at the same location in non-contrast images. Delayed images can be useful in differentiating between active extravasation or CAP and relatively benign processes [1,28,29,30].
Figure 5. 82-year-old man hospitalized for pneumonia who suddenly complained of jaundice, right upper quadrant pain and sudden decline of Hb 7.1 g/dL (PRO B NP 39,473 pg/mL, n.v. < 375; PCR 9.9 mg/dL, n.v. 0.0–0.5; WBC 23.78 103/mm3 n.v. 4.2–10.5). He underwent an abdominal CT with IV contrast ((a) non-contrast, (b) arterial, (c) venous, (d) delayed phase), that showed subcapsular and pericholecystic hematoma with endoluminal active bleeding originating from a cystic artery pseudoaneurysm (CAP) ((b), white arrow). The patient underwent TAE successfully (coils).
Figure 6. Coronal CT image in arterial phase that clearly shows CAP with irregular margins (white arrow).
Figure 7. 58-year-old man who was hospitalized and underwent more than one ERCP for choledocholithiasis. He complained of severe right upper quadrant pain and sudden decline of Hb 7.3 g/dL (PCR 10.82 mg/dL, n.v. 0.0–0.5; WBC 18.76 103/mm3 n.v. 4.2–10.5). He underwent an abdominal CT with IV contrast (a) non-contrast, (b) arterial, (c) venous, (d) delayed phase), which showed dilated intrahepatic bile ducts and a markedly dilated common bile duct that present inhomogeneous content and air bubbles from a previous procedure and sphincterotomy. Within the common bile duct a cystic artery pseudoaneurysm was detected with active extravasation (white arrow). The patient underwent TAE successfully.
Figure 8. MPR coronal (a) and sagittal (b) clearly demonstrate cystic branch pseudoaneurysm bleeding (arrow).
Figure 9. 74-year-old male hospitalized for hip fracture who underwent arthroplasty (Hb 8 g/dL, n.v. 13–18; PRO B NP 39,473 pg/mL, n.v. < 375; PCR 5.04 mg/dL, n.v. 0.0–0.5; WBC 7.25 103/mm3 n.v. 4.2–10.5), who suddenly complained of jaundice, right upper quadrant pain and melena. He underwent an abdominal CT with IV contrast ((a) non-contrast, (b) arterial, (c) venous, (d) delayed phase), which showed a distended gallbladder with slightly hyperdense content and a rounded hyperattenuating focus (white arrow) that did not change form and was isodense to a blood pool in the venous and delayed phases. Diagnosis: CAP with no active bleeding. The patient underwent cholecystectomy and was discharged.
Figure 10. 80-y.o. woman with lung infection (candidiasis) with worsening of inflammatory markers. (a) Non-contrast axial CT imaging demonstration of perihepatic and perisplenic fluid collections, and the presence of fluid in the gallbladder bed. The gallbladder appears increased in size. (b) Axial CT image shows the presence of globular enhancing vascular image (yellow arrow) along the gallbladder wall in arterial phase. The globular vascular image did not change form and was isodense to a blood pool in the venous and delayed phases (c,d). Diagnosis: CAP with no active bleeding.
DSA allows real-time visualization of vascular dynamics, identifying active extravasation, pseudoaneurysms, or arteriovenous fistulas with unparalleled accuracy (Figure 4). DSA is particularly invaluable in cases where non-invasive imaging is inconclusive or when immediate therapeutic intervention is warranted [3,19].
DSA also plays a pivotal role in assessing collateral blood flow. This evaluation is essential when embolizing major hepatic vessels, as it prevents ischemic complications in the liver parenchyma. For instance, significant collateral flow from the left hepatic artery can obviate concerns about right hepatic artery occlusion during embolization [15,17].

3. Treatment

CAB, whether related or not to CAP, is a rare event, and the therapeutic approach relies on the patient’s general condition and the risk from the anaesthesiologist.
Surgery with cholecystectomy and proximal ligation or clipping of the cystic artery is considered the gold standard, but an emergency cholecystectomy can present challenges for surgeons who must manage the hemorrhage [1].
Although there are no established guidelines, transarterial embolization (TAE) nowadays represents the preferred therapeutic approach to restore hemodynamic stability [31,32].
Given the increasing role of interventional treatment as the preferred strategy in these conditions, we conducted a comprehensive systematic review of the literature on percutaneous embolization for cystic artery bleeding, including cases related to CAP and non-CAP etiologies.

3.1. Results

3.1.1. Study Selection and Characteristics

This systematic review identified 462 articles for initial screening based on predefined inclusion and exclusion criteria. After removing duplicate records, 97 articles remained. Screening of titles and abstracts excluded 365 articles for lack of relevance. Following a full-text review and application of inclusion criteria, 64 articles were included in the final analysis [2,3,10,13,14,15,16,17,19,20,25,26,29,30,31,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81]. The selection process was summarized in a PRISMA flow diagram (Figure 11).
Figure 11. PRISMA flow diagram for study selection.

3.1.2. Patient Demographics and Clinical Presentation

Data from 64 studies encompassing 90 patients were analyzed (Table A1). The median age was 64.5 years (±16.45), with a median of 67.5 years (95% CI, 63.2–71.0) and a range of 16 to 91 years. A predominance of males was observed, with 59 males (65.5%) and 31 females (34.5%).
The most common etiology was acute cholecystitis (52 cases, 58%), including two cases of cholecystocolic fistula [29,48]. Other etiologies included iatrogenic injury (15 cases, 17%), primarily post-cholecystectomy (nine cases, 10%); tumor bleeding (four cases, 4.5%); and chronic cholecystitis (four cases, 4.5%). Less frequent causes were duodenal ulcer (3%, three cases, [41]), Mirizzi syndrome (three cases, 3%, [15,43,47]), acute pancreatitis (two cases, 2%, [61,80]), and trauma (two cases, 2% [3,41]). Singular cases included arteriovenous malformation [77], Bouveret syndrome [33], spontaneous rupture of the cystic artery [16], cystic artery–gallbladder fistula [17], and xanthogranulomatous cholecystitis [76].
Presenting symptoms included right upper quadrant pain (57 cases, 63%), melena (29 cases, 32%), hematemesis (24 cases, 27%), and jaundice (18 cases, 20%). Hemodynamic instability was noted in 9% of patients (eight cases). A minority of patients (three cases, 3%) presented with nonspecific symptoms, such as nausea, anorexia, or incidental imaging findings [3,38,77].

3.1.3. Imaging and Diagnostic Findings

Contrast-enhanced computed tomography (CECT) was the diagnostic modality of choice in all cases except one, where US alone was performed before digital DSA. Imaging modality was not specified in the studies by Liu B et al. [64] and Kim HC et al. [41].
Endoscopy was performed in 43 patients, revealing active bleeding or blood oozing in 22 cases. DSA identified pseudoaneurysms in 64 cases (64/70 91%), with rupture and active bleeding in 30 cases (43%). Bleeding from the cystic artery was documented in five cases, including two with cystic artery–gallbladder fistulas [17,51]. A single case of arteriovenous malformation of the gallbladder fed by two dilated cystic arteries was reported [77]. DSA findings were not specified in the study by Kim HC et al. [41].

3.1.4. Management and Outcomes

TAE was performed in all patients except two, where percutaneous embolization was used [34,66].
Coils were the most frequently used embolic agents in TAE, applied alone in 49 cases (49/88 56%) or combined with gelfoam (three cases), thrombin (one case), or stent placement (one case).
N-butyl cyanoacrylate (NBCA) was used in 18 cases (18/88 20.5%), either alone or combined with coils (two cases), lipiodol (two cases), or a combination of lipiodol, coils, and gelfoam (two cases). Other agents included gelfoam alone (four cases, 4/88 4.5%) and PVA particles (500–700 µm) in three cases, either alone or with gelfoam or coils. Rarely used materials included blood clot [41] and Onyx. In percutaneous embolization cases, NBCA and thrombin were utilized, respectively.
Complications were reported in eight patients. Ischemic cholecystitis occurred in four patients [16,41], hepatic ischemia in two cases [2,53], and one case each of liver abscess treated with antibiotics [20] and peritonism with worsening abdominal pain post-embolization [78].
Cholecystectomy was performed in 29 patients. Additionally, one patient underwent ligation of the right hepatic artery, and another required an extended right hepatectomy.
Most patients achieved complete recovery. However, nine patients died, seven of whom died postoperatively or of multiorgan failure secondary to sepsis.

3.2. Materials and Methods

This review was conducted following the “PICO” method and “Preferred Reporting Items for Systematic Review and Meta-Analysis” (PRISMA) statement guidelines. The study did not directly involve humans, and did not require the Institutional Review Board approval of our department.
The systematic review was performed using PubMed, Scopus, and Embase databases, using the following medical subject headings (MeSH), keywords and EMBASE Subject Headings (EMTREE): “cystic artery”, “bleeding”, “hemorrhage”, “pseudoaneurysm”, “rupture” and “embolization”.
The study was carried out utilizing the specified headings in combination with the following Boolean operators: (bleeding OR hemorrhage OR haemorrhage OR pseudoaneurysm OR rupture) AND (cystic artery) AND (embolization OR embolisation). The titles, abstracts, and reference lists of the retrieved publications were screened based on predefined inclusion and exclusion criteria. Full-text articles were then reviewed in detail to assess their eligibility for inclusion.
The initial search period was arbitrarily set to begin in 1990, with screening conducted between September 2024 and October 2024 by two independent authors (F.T. and R.C.). Discrepancies were resolved through consensus or a third reviewer (S.T.).
The inclusion criteria were studies, including case reports and case series, reporting cystic artery vascular bleeding or vascular injury (pseudoaneurysm or fistula) treated with embolization (transarterial and/or percutaneous).
The exclusion criteria were recurring articles from the same authors, duplicate articles, articles not written in English, publications before the year 1990, editorials and commentaries, review articles without new case data, studies infrom which the exact origin of the bleeding (e.g., hepatic artery) could not be determined, studies that use angiography but not embolization, and studies in which embolizing treatment was not specified.
In doubtful cases, articles were included in this stage were named “uncertain” and required the evaluation of the full text to make the final decision.
Data extracted from the publications included the first author, year of publication, study design, sample size, patient demographics (age and sex), underlying etiology, presenting symptoms, initial imaging modality (ultrasound, CTA, MRI, or DSA), use of endoscopy, DSA findings, and type of interventional procedure performed. Technical details of the embolization procedure, including the embolic material used and complications, were also collected. Additionally, the need for subsequent surgery or intervention and clinical outcomes, when reported, were documented.

4. Discussion

Percutaneous selective cystic artery embolization (CAE) has emerged as an efficacious treatment strategy in the acute setting for patients with CAP or CAB, and it can be performed with high success rates and cessation of bleeding in up to 90% of patients [1,29,40,41].
CAE offers advantages such as reduced mortality and morbidity, improved identification of the bleeding vessel, and higher rates of achieving hemorrhage control.
This systematic review consolidates data from 90 cases, providing comprehensive insights into its etiology, presentation, diagnostic strategies, treatment modalities, and outcomes.
Acute cholecystitis, identified in 58% of cases, leads to local vascular damage due to prolonged inflammation and enzymatic degradation of the arterial wall. Iatrogenic causes, particularly from laparoscopic cholecystectomy, accounted for 17% of cases, emphasizing the need for meticulous surgical techniques to avoid inadvertent vascular injury. Malignancy-associated CAP, though less common (4.5%), underscores the importance of considering vascular complications in advanced gallbladder carcinoma or HCC [37,41,49].
The clinical spectrum of CAB is broad, with gastrointestinal bleeding as the most common presentation. Hematemesis (27%) and melena (32%) were predominant, accompanied by hemodynamic instability in severe cases (9%). Right upper quadrant pain, present in 63% of cases, reflects the inflammatory or ischemic component of the gallbladder pathology [1,82].
CT angiography represents the diagnostic modality of choice, utilized in 99% of cases. DSA, although invasive, confirmed pseudoaneurysm and active extravasation in all cases where performed, guiding therapeutic embolization. Endoscopic findings, while variable, reveal active bleeding or blood oozing in 50% of cases, providing critical clues in hemobilia cases.
Transarterial embolization represents the preferred approach for managing cystic artery bleeding, particularly in urgent hemodynamic stabilization cases. This minimally invasive technique achieves rapid hemostasis, demonstrating high technical success and minimal procedural risks [31].
The choice of embolic agent varied, with coils being the most frequently used (56%), followed by N-butyl cyanoacrylate (20.5%), each offering specific advantages and limitations [13,19].
Coil embolization is the preferred method due to its versatility in treating vessels of varying sizes and its ability to be introduced without the risk of increased pressure within the vascular lesion [71]. Coils provide durable occlusion, making them ideal for pseudoaneurysms with well-defined arterial feeders.
Minor complications, such as coil migration, were reported in isolated cases [25]. However, their utility is limited in high-flow bleeding or complex vascular anatomies, where alternative agents may be more appropriate [20].
Liquid embolic agents such as N-butyl cyanoacrylate (NBCA) provide an effective solution for high-flow bleeding or tortuous vasculature. NBCA polymerizes rapidly upon contact with blood, forming a permanent occlusion [83]. Its efficacy in patients with coagulopathies is particularly noteworthy, as its action is independent of coagulation status. Despite its advantages, NBCA requires technical expertise due to risks of non-target embolization and catheter adhesion [83].
Combining agents, such as NBCA with Lipiodol or gelfoam, have been described in cases requiring additional hemostatic efficacy [20,35].
Temporary agents like gelfoam offer a temporary occlusion, achieving hemostasis through mechanical obstruction and are particularly effective in low-flow conditions.
However, the temporary nature of gelfoam may result in recurrent bleeding, necessitating repeat embolization [16,84].
The selection of embolic material should be tailored to the patient’s specific clinical scenario. For high-flow bleeding or complex vascular anatomy, NBCA or a combination of coils and NBCA may be preferred. Coils remain optimal for localized lesions with well-defined anatomy, while gelfoam may be considered for temporary hemostasis in select cases. Adjunctive agents such as thrombin or lipiodol can further enhance the efficacy of embolization when used judiciously [20,35].
Thrombin direct injection into the pseudoaneurysm under Ultrasound and Doppler guidance has also been reported, but it is considered a non-selective procedure with potential collateral effects such as bowel and liver infarcts [34,66].
Although TAE is generally safe, complications can arise, typically related to ischemic injury or non-target embolization. Ischemic cholecystitis, occurring in approximately 4.5% of cases, is among the most frequently reported complications [16,41]. This condition necessitates prompt diagnosis with imaging and early intervention, such as cholecystectomy or drainage, to prevent sepsis [16,41].
Hepatic ischemia, though rare, is more likely with extensive embolization involving the hepatic artery [2,53]. Conservative management, including hydration and close monitoring, is often sufficient; however, severe cases may require surgical revascularization [20]. Non-target embolization, associated primarily with liquid agents like NBCA, underscores the importance of meticulous technique and selective catheterization. Infections and abscess formation have also been observed, particularly in patients with pre-existing biliary infections [20]. These complications are typically managed with antibiotics and abscess drainage [20].
Post-procedural monitoring is crucial for identifying these potential complications, and super selective embolization of the anterior or posterior branch of the cystic artery, when possible, reduces the risk of post-procedural complications thanks to the anastomotic network [8].
The need for cholecystectomy after embolization remains a point of debate. In this review, 32% of patients underwent cholecystectomy, primarily to address the underlying pathology, such as gallbladder gangrene, or to prevent recurrence. Early cholecystectomy, particularly in patients with gallbladder necrosis or severe inflammation, was associated with favorable outcomes. Conversely, a conservative approach with observation was effective in patients without persistent symptoms or high-risk features. The timing of cholecystectomy should be individualized based on the patient’s clinical stability and the resolution of acute inflammation [71,80].
The outcomes of TAE for cystic artery bleeding are generally favorable. Most patients achieve complete recovery [83]. Complications are infrequent, and the mortality rate remains low. These results underscore the efficacy and safety of TAE as a first-line treatment in this setting.

5. Conclusions

Isolated CAB is rare, occurring in traumatic, non-traumatic, or idiopathic cases. CT is crucial for diagnosing trauma-related CAB, and for identifying hemoperitoneum near the gallbladder with active extravasation. Non-operative trauma management often involves transarterial embolization. In non-traumatic or iatrogenic cases, prior cholecystectomy or inflammation should prompt suspicion of CAP. Even in unrelated exams, early CT detection of CAPs can enable timely intervention, preventing rupture and life-threatening complications while improving patient outcomes.
Despite advancements in diagnostic and therapeutic techniques, CAP remains a diagnostic challenge due to its rarity and nonspecific presentation. Future research should focus on developing standardized diagnostic protocols and exploring novel therapeutic agents to enhance clinical outcomes. Additionally, long-term follow-up studies are needed to assess the durability of embolization and the risk of recurrence.

Author Contributions

Conceptualization S.T., F.T., D.G.C. and R.C.; Methodology F.T. and R.C.; Formal Analysis F.T., D.G.C. and R.C.; Investigation F.T. and R.C.; Data Curation S.T., F.T., D.G.C. and R.C.; Writing—Original Draft Preparation F.T., D.G.C. and R.C.; Writing—Review & Editing F.T., R.C. and C.B.; Visualization S.P., F.D.S., F.P., G.F., G.S., P.R. and M.S.; Supervision, A.B. and S.T.; Project Administration S.T. All authors meet the ICMJE Recommendations for authorship credit. All authors have read and approved the manuscript and agree to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All authors have contributed equally. The authors had full access to the data and take full responsibility for its integrity. All authors have read and agree to the manuscript as written. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

For this retrospective analysis, it was not necessary to request authorization from the ethics committee. The contents of this paper are consistent with the principles of the Declaration of Helsinki in the latest version.

Data Availability Statement

No new data were created or analyzed in this study. Data sharing is not applicable to this article.

Acknowledgments

The author(s) received no financial support for the research, authorship and/or publication of this article.

Conflicts of Interest

The authors declare no conflict of interest.

Appendix A

Table A1. Summary of characteristics of the selected study.
Table A1. Summary of characteristics of the selected study.
Authors/YearType of the StudyNumber of PatientsSexAgeEtiologyMain SymptomsType of LesionInterventional TreatmentEmbolic AgentsProcedure-Related ComplicationsProcedures After TreatmentOutcome
Sarmento Costa M et al., 2024 [33]case report1M88Bouveret syndrome (bilioenteric fistula)HematemesisPseudoaneurysmTAECoilsN/RNoRecovered
Giurazza F et al., 2024 [34]technical report1M71Acute cholecystitisN/RPseudoaneurysmPENBCAN/RNoRecovered
Heidari A et al., 2024 [35]case report1F64Acute cholecystitisAbdominal pain, hematemesisPseudoaneurysmTAEPVA (500–700 µm) + gelfoamN/RCholecystectomyRecovered
Khawjah A et al., 2024 [2]case report1M54Acute cholecystitisAbdominal pain, hematemesis, jaundicePseudoaneurysm ruptureTAECoils + gelfoamHepatic ischemiaCholecystectomyRecovered
Anns MK et al., 2024 [36]case report1M64Iatrogenic (laparoscopic cholecistectomy)Hematemesis, melenaPseudoaneurysmTAECoilsN/RNoRecovered
Okamoto S et al., 2024 [37]case report1M80Neoplastic (HCC)Abdominal pain, melena, jaundicePseudoaneurysm ruptureTAENBCA + Lipiodol + gelfoam + coilsN/RNoRecovered
Rais A et al., 2024 [13]case report1F71Acute cholecystitisAbdominal painPseudoaneurysmTAENBCA + LipiodolN/RCholecystectomyRecovered
Robbie R et al., 2024 [25]case report1M83Acute cholecystitisBleeding per rectumPseudoaneurysmTAECoilsN/RNoRecovered
Saha B et al., 2024 [38]case report1M70Acute cholecystitisAbdominal painPseudoaneurysmTAECoilsN/RCholecistectomyRecovered
Sibria D et al., 2024 [19]case report1F38Iatrogenic (laparoscopic cholecistectomy)Abdominal pain, jaundice, bleeding per rectum, melenaPseudoaneurysmTAECoilsN/RNoRecovered
Mie T et al., 2024 [39]case report1F78Acute cholecystitisAbdominal pain, jaundicePseudoaneurysm ruptureTAENBCA + LipiodolN/RNoRecovered
Khan H et al., 2023 [40]case report1M88Acute cholecystitisAbdominal pain, jaundicePseudoaneurysm ruptureTAECoilsN/RCholecystectomyRecovered
Kim HC et al., 2023 [41]retrospective study1M43Acute cholecystitisMelenaN/RTAEblood clotN/RCholecystectomyRecovered
retrospective study1F34Iatrogenic (cholecystostomy)HemoperitoneumN/RTAEGelfoamN/RN/RRecovered
retrospective study1F54NeoplasticMelenaN/RTAENBCAN/RN/RRecovered
retrospective study1F49Acute cholecystitisHematemesisN/RTAENBCAIschemic cholecystitisN/RDeath from MOF, sepsis
retrospective study1M75Acute cholecystitisHematocheziaN/RTAENBCAN/RN/RRecovered
retrospective study1F52Iatrogenic (RFA)HemoperitoneumN/RTAENBCAN/RN/RRecovered
retrospective study1F71NeoplasticJaundiceN/RTAENBCAN/RN/RRecovered
retrospective study1M74Acute cholecystitisBlood in cholecystostomy tubeN/RTAENBCAN/RN/RDeath from MOF, sepsis
retrospective study1M48TraumaHemoperitoneumN/RTAENBCAIschemic cholecystitisN/RRecovered
retrospective study1M48Acute cholecystitisBlood in cholecystostomy tubeN/RTAENBCAIschemic cholecystitisN/RDeath from MOF, sepsis
retrospective study1M80Acute cholecystitisHematemesisN/RTAENBCAN/RN/RRecovered
retrospective study1F78Acute cholecystitisHematemesisN/RTAENBCAN/RN/RDeath from pneumonia
retrospective study1F78Duodenal ulcerHematemesisN/RTAECoilsN/RCholecystectomyRecovered
retrospective study1M67Duodenal ulcerMelenaN/RTAENBCAN/RN/RRecovered
retrospective study1F56Duodenal ulcerMelenaN/RTAEGelfoamN/RN/RDeath from MOF, sepsis
retrospective study1M78Acute cholecystitisAbdominal painN/RTAENBCAN/RCholecystectomyRecovered
retrospective study1M64Acute cholecystitisBlood in cholecystostomy tubeN/RTAENBCAN/RN/RRecovered
retrospective study1M80Acute cholecystitisHemoperitoneumN/RTAENBCAN/RN/RDeath from MOF, sepsis
retrospective study1M85Iatrogenic (cholecystostomy)Blood in cholecystostomy tubeN/RTAENBCAN/RN/RRecovered
retrospective study1M70Iatrogenic (cholecystostomy)Abdominal painN/RTAENBCAN/RN/RRecovered
Liu YL et al., 2023 [42]case report1M81Acute cholecystitisAbdominal pain, melena, hemobiliaPseudoaneurysm with active bleedingTAECoilsN/RCholecystostomyRecovered
Shrivastava A et al., 2023 [26]case report1M41Acute cholecystitisAbdominal pain, melenaPseudoaneurysmTAECoilsN/RCholecystostomy + cholecystectomyRecovered
Williams T et al., 2023 [43]case report1M61Mirizzi syndromeAbdominal painPseudoaneurysmTAECoilsN/RCholecystostomyRecovered
Zainab R et al., 2023 [44]case report1M55Acute cholecystitisAbdominal pain, hematemesis, melenaPseudoaneurysmTAECoilsN/RN/RRecovered
Itagaki Y et al., 2023 [45]case report1F70Acute cholecystitisJaundicePseudoaneurysmTAECoilsN/RCholecystectomyRecovered
Christodoulou P et al., 2022 [46]case report1M67Iatrogenic (laparoscopic cholecistectomy)Abdominal painPseudoaneurysm ruptureTAECoilsN/RCholecystectomyRecovered
Fukushima R et al., 2022 [47]case report1F73Mirizzi syndromeAbdominal pain, jaundicePseudoaneurysm ruptureTAECoilsN/RCholecystectomyRecovered
Amakye DO et al., 2021 [48]case report1M66Acute cholecystitis (cholecystocolic fistula)Abdominal painPseudoaneurysm ruptureTAECoilsN/RNoRecovered
Mahalingam S et al., 2021 [49]case report1M52Neoplastic (carcinoma gallbladder)Abdominal pain, hematemesis, melenaPseudoaneurysm ruptureTAENBCAN/RCholecystostomyRecovered
Nguyen D et al., 2021 [50]case report1M74Acute cholecystitisAbdominal pain, hematemesis, melenaPseudoaneurysm with active bleedingTAECoilsN/RCholecystectomyRecovered
case report1M74Acute cholecystitisN/RPseudoaneurysm with active bleedingTAEPVA (500–700) + coilsN/RCholecystectomyRecovered
Acharya S et al., 2020 [51]case report1F62Chronic cholecystitis Abdominal pain, bleeding per rectumCystic artery-gallbladder fistula with bleedingTAECoilsN/RNoRecovered
Carey F et al., 2020 [29]case report1M47Acute cholecystitis (cholecystocolic fistula)Abdominal pain, bleeding per rectumPseudoaneurysm with active bleedingTAECoilsN/RNoRecovered
Leshen M et al., 2020 [52]case report1M16Acute cholecystitisAbdominal pain, hematemesisPseudoaneurysm with active bleedingTAECoilsN/RCholecystectomyRecovered
Proença AL et al., 2020 [53]case report1F73Iatrogenic (ERCP)Abdominal pain, hematemesis, melenaPseudoaneurysm with active bleedingTAENBCAHepatic ischemiaCholecystectomyRecovered
Yam MKH et al., 2020 [54]case report1F51Acute cholecystitisAbdominal pain, hematemesis, melenaPseudoaneurysm with active bleedingTAEPVA + CoilsN/RCholecystostomy + cholecystectomyRecovered
Rossini M et al., 2019 [55]case report1M66Iatrogenic (laparoscopic cholecistectomy)Abdominal pain, hematemesis, melenaPseudoaneurysm with active bleedingTAECoilsN/RNoRecovered
Sada DM et al., 2019 [56]case report1M69Iatrogenic (cholecystostomy)Abdominal painPseudoaneurysm with active bleedingTAEOnyxN/RNoPostoperative death
Tanaka T et al., 2019 [57]case report1F80Acute cholecystitisAbdominal pain, melenaPseudoaneurysm ruptureTAECoilsN/REndoscopic biliary drainageRecovered
Kuzman MS et al., 2018 [58]case report1F25Acute cholecystitisAbdominal painPseudoaneurysmTAENBCA + CoilsN/RCholecystostomy + cholecystectomyRecovered
Sunkara PRV et al., 2018 [14]case report1M56Acute cholecystitisAbdominal painPseudoaneurysm ruptureTAECoilsN/RCholecystectomyRecovered
Machado NO et al., 2017 [10]case report1F70Iatrogenic (laparoscopic cholecistectomy)Abdominal painPseudoaneurysm with active bleedingTAECoilsN/RNoRecovered
Maddineni S et al., 2017 [59]case report1F54Acute cholecystitisAbdominal pain, melenaPseudoaneurysm with active bleedingTAEThrombin + CoilsN/RCholecystostomyDeath due to non-procedure-related complications
Tapnio RH et al., 2017 [60]case report1F91Acute cholecystitisAbdominal painPseudoaneurysm with active bleedingTAECoilsN/RCholecystectomyRecovered
case report1M61Acute cholecystitisAbdominal painPseudoaneurysm with active bleedingTAECoils + gelfoamN/RCholecystectomyRecovered
case report1M91Acute cholecystitisAbdominal painPseudoaneurysmTAECoilsN/RCholecystostomyRecovered
Thillai M et al., 2017 [61]case report1M33Acute pancreatitisMelenaPseudoaneurysm with active bleedingTAEGelfoamN/RCholecystostomyRecovered
Trombatore C et al., 2017 [62]case report1M64Acute cholecystitisAbdominal pain, jaundicePseudoaneurysm with active bleedingTAECoilsN/RCholecystectomyRecovered
Hall TC et al., 2016 [63]case report1M88Acute cholecystitisAbdominal pain, melenaPseudoaneurysm with active bleedingTAENBCA + Lipiodol + gelfoam + coilsN/RNoRecovered
Liu B et al., 2016 [64]case report1M82Iatrogenic (laparoscopic cholecistectomy)HemobiliaPseudoaneurysm with active bleedingTAECoils + stentN/RNoRecovered
Shelmerdine SC et al., 2015 [31]case report1M72Acute cholecystitisAbdominal pain, hematemesis, melenaPseudoaneurysm with active bleedingTAECoilsN/RNoRecovered
Aljiffry MM et al., 2014 [65]case report1M57Acute cholecystitisAbdominal painActive bleeding from cystic arteryTAEGelfoamN/RCholecystectomyRecovered
Kulkarni V et al., 2014 [15]case report1M55Mirizzi syndromeAbdominal pain, jaundice, melenaPseudoaneurysmTAECoilsN/RCholecystectomyRecovered
Kumar A et al., 2014 [66]case report1F45Iatrogenic (laparoscopic cholecistectomy)HemobiliaPseudoaneurysm with active bleedingPEThrombin (400 units)N/RNoRecovered
Mokrane FZ et al., 2013 [67]case report1M67Acute cholecystitisHematemesisPseudoaneurysm with active bleedingTAECoilsN/RNoRecovered
Nana GR et al., 2013 [68]case report1M74Acute cholecystitisAbdominal pain, hematemesis, jaundicePseudoaneurysmTAECoilsN/RCholecystostomyRecovered
case report1F79Acute cholecystitisAbdominal pain, melena, jaundicePseudoaneurysmTAECoilsN/RNoRecovered
Priya H et al., 2013 [17]case report1M22SpontaneousAbdominal pain, hematemesis, melena, jaundiceFistula (cystic artery-gallbladder)TAECoilsN/RCholecystectomyRecovered
Chong JJR et al., 2012 [69]case report1M56Acute cholecystitisAbdominal pain, hematemesisPseudoaneurysmTAECoilsN/RCholecystectomyRecovered
Petrou A et al., 2012 [70]case report1F34Iatrogenic (laparoscopic cholecistectomy)Abdominal pain, hematemesisPseudoaneurysmTAECoilsN/RLigation of right hepatic arteryRecovered
Siddiqui NA et al., 2011 [30]case report1M58Acute cholecystitisAbdominal pain, jaundicePseudoaneurysmTAECoilsN/RCholecystectomyRecovered
Desai AU et al., 2010 [71]case report1F78Chronic cholecystitis Abdominal pain, melena, jaundicePseudoaneurysmTAECoilsN/RNoRecovered
Hague J et al., 2010 [72]case series1M83Acute cholecystitisAbdominal pain, hemoperitoneumPseudoaneurysmTAECoilsN/RNoRecovered
case series1M79Acute cholecystitisAbdominal pain, hemobiliaPseudoaneurysmTAECoilsN/RNoRecovered
case series1M83Acute cholecystitisAbdominal pain, melenaPseudoaneurysmTAECoilsN/RNoDeath from esophageal carcinoma within 2 months
Nkwam N et al., 2010 [73]case report1M71Acute cholecystitisAbdominal painPseudoaneurysmTAECoilsN/RCholecystostomyRecovered
Osada H et al., 2010 [3]case report1M62TraumaAsymptomatic PseudoaneurysmTAECoilsN/RNoRecovered
Contini S et al., 2009 [74]case report1M58Chronic cholecystitis Abdominal pain, melena, jaundiceActive bleedingTAECoilsN/RCholecystectomyRecovered
Mullen R et al., 2009 [75]case series1F75Chronic cholecystitis Abdominal pain, hematemesis, melenaPseudoaneurysmTAECoilsN/RNoRecovered
case series1M82Acute cholecystitisAbdominal painPseudoaneurysmTAECoilsN/RNoRecovered
Ouazzani A et al., 2009 [16]case report1M74SpontaneousAbdominal painActive bleeding (rupture)TAEParticles (500–700 µm)Ischemic cholecystitisCholecystectomyRecovered
Nakase Y et al., 2008 [20]case report1F63Iatrogenic (laparoscopic cholecistectomy)Abdominal pain, melena, hematemesisPseudoaneurysmTAENBCA + CoilsLiver abscess treated with antibioticsNoRecovered
Shimada K et al., 2008 [76]case report1M68Xanthogranulomatous cholecystitisJaundice, hemobiliaPseudoaneurysmTAECoilsN/RExtended right hepatectomyRecovered
Osada H et al., 2007 [77]case report1F78Arteriovenous malformationAsymptomatic Arteriovenous malformationTAECoilsN/RNoBlood flow in AVM persisted; patient developed HCC recurrence after 4 years
Saluja SS et al., 2007 [78]case report1F43Acute cholecystitisHematemesis, melenaPseudoaneurysmTAECoils + gelfoamA day later the patient had increasing abdominal pain and appearance of peritoneal signs localized to the RUQ of the abdomenCholecystectomyRecovered
Maeda A et al., 2002 [79]case report1M62Acute cholecystitisAbdominal pain, jaundicePseudoaneurysmTAECoilsN/RCholecystectomyRecovered
Delgadillo X et al., 1999 [80]case report1M28Acute pancreatitisAbdominal pain, hematemesisPseudoaneurysmTAECoilsN/RNoRecovered
England RE et al., 1998 [81]case report1F71Acute cholecystitisAbdominal pain, jaundicePseudoaneurysmTAECoilsN/RNoDeath from MOF, sepsis

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