Cystic artery embolism after transarterial chemoembolization for hepatocellular carcinoma: A case report and review of the literature

Abstract

BACKGROUND

Acute cholecystitis due to unintended cystic artery embolism is an uncommon and mostly self-limiting complication after transarterial chemoembolization procedure for treatment of hepatocellular carcinoma. Usually, conservative management is sufficient for complete recovery of patients who develop this complication. If conservative treatment is ineffective, urgent surgical intervention may be required to prevent the progression of complications.

CASE SUMMARY

This article reports a rare and serious case of acute cholecystitis complicated by gallbladder necrosis and biliary peritonitis, which was initially treated conservatively but eventually necessitated emergency laparotomy. The patient initially presented with equivocal symptoms of fever and upper abdominal pain and distention, which worsened at the two weeks mark along with emergence of signs of peritonitis. This was managed by emergency laparotomy and cholecystostomy, allowing rapid symptom relief. The patient ultimately discharged and succumbed to advanced liver cancer 11 months after diagnosis.

CONCLUSION

After cholecystostomy, the patient showed symptom relief and was discharged, surviving 11 months post-stage IIIB liver cancer diagnosis.

Key Words: Cystic artery embolism; Transarterial chemoembolization; Hepatocellular carcinoma; Diagnosis; Symptoms; Case report

Core Tip: Acute cholecystitis due to cystic artery embolism after transarterial chemoembolization is an uncommon and mostly self-limiting complication. We present a rare case of acute cholecystitis complicated by gallbladder necrosis and biliary peritonitis, which required emergency laparotomy and cholecystostomy creation.

INTRODUCTION

Worldwide, hepatocellular carcinoma (HCC) ranks as the 6^th most common cancer as well as the 4^th leading cause of cancer-related mortality[1]. A range of treatment modalities, ranging from surgical resection to locoregional and systemic therapies, offer options for curative or palliative treatment across different stages of HCC[1]. In particular, the treatment modalities available for unresectable HCC include vascular interventions, local ablative techniques, radiotherapy, targeted therapies, immunotherapy, and chemotherapy[2]. The utilization of transarterial chemoembolization (TACE) has demonstrated enhanced survival rates in patients with unresectable liver cancer, establishing it as an efficacious therapeutic modality for the management of this malignancy[3]. The presence of various complications, however, may be a significant impediment to its extensive clinical utilization[4]. For example, unintended ischemic damage to hepatic and biliary structures may cause unwanted and potentially serious complications such as hepatic abscess, necrosis of the bile duct, and acute cholecystitis[4-8]. Acute cholecystitis is a rare, but well-established complication likely caused by reflux of embolic materials like gelatin sponge (GS) and lipiodol causing embolization of the cystic artery, which, unlike the dual blood supply of the liver, is the sole blood supply to the gallbladder[9]. Usually, serious complications arising from acute cholecystitis are uncommon and patients respond well to conservative treatment[10-12]. However, progression of cholecystitis to gallbladder necrosis combined with peritonitis can adversely affect the well-being of the patient and can even be life-threatening. Consequently, early recognition by symptoms, signs, and examinations and early treatment by medications, drainage, and surgeries play an important role in the patient’s prognosis.

CASE PRESENTATION

Chief complaints

Persistent left upper abdominal discomfort for 1 month, followed by fever and abdominal distension 2 weeks after TACE.

History of present illness

The patient, a 51-year-old woman, was admitted to Shaanxi Provincial People's Hospital due to recurrent left upper abdominal discomfort for a duration of 1 month. Computed tomography (CT) and magnetic resonance imaging (MRI) of the upper abdomen revealed a space-occupying lesion measuring 7.4 cm × 9.1 cm × 7.1 cm in the anterior right quadrant of the liver, with invasion of the middle hepatic vein (Figure 1A). The blood test results showed elevated levels of alanine aminotransferase (ALT) at 120 U/L, aspartate aminotransferase (AST) at 128 U/L, positive hepatitis B surface antigen, alpha fetoprotein (AFP) at 6.05 ng/mL, and CA19-9 at 201.23 U/mL. Puncture histopathology indicated necrotic tissue with a few degenerated hepatocytes present. No nodal involvement or distant metastasis was found. The initial diagnosis for the patient was HCC. TNM stage T4N0M0, which corresponds to AJCC stage IIIB. This was associated with hepatitis B virus-related cirrhosis.

Figure 1 Upper abdominal computed tomography images. A: A 7.4 cm × 9.1 cm × 7.1 cm space-occupying lesion in the anterior right liver; B: Manifestations of acute gallbladder inflammation induced by transarterial chemoembolization; C: Findings after gallbladder puncture and catheterization.

The treatment option consisted of sorafenib combined with TACE. Following the 3^rd TACE procedure, the patient presented with unexplained high fever, recurrent upper abdominal pain, and abdominal distention without nausea or vomiting. Laboratory results revealed a white blood cell count of 8.53 × 10⁹/L, neutrophil percentage of 80.9%, total bilirubin (TBiL) level of 11.29 μmol/L, and ALT level of 63 U/L (Table 1). Abdominal ultrasound examination did not reveal any obvious abnormalities. On the 10th day after the operation, an abdominal CT scan showed a round low-density shadow in the gallbladder fossa accompanied by gas accumulation and surrounding exudation (Figure 1B). Cystic artery embolism leading to acute cholecystitis was considered as a potential complication - a rare and serious occurrence following TACE procedures. Subsequently, percutaneous transhepatic gallbladder drainage (PTGD) was performed under local anesthesia to address this complication. During the procedure, no signs of perforation were observed and clear visibility of the gallbladder was maintained. After placement of a drainage tube, minimal bilious drainage contents were obtained, which did not significantly improve infection markers. Furthermore, bedside ultrasound indicated abnormal positioning of the puncture tube necessitating repeat PTGD alongside more aggressive treatment for resolution of the infection. Although there was improvement in abdominal symptoms post-treatment intervention, intermittent fever persisted.

Table 1 Alterations in full blood count and liver function tests in our patient following transarterial chemoembolization.

Blood test (reference value)	1 week after TACE	2 weeks after TACE	Before exploratory laparotomy	2 days after surgery	1 week after surgery
Hb (115-150 g/L)	111	115	86	73	112
PLT (125-350 × 109/L)	75	113	190	152	217
WBC (3.5-9.5 × 109/L)	8.53	13.12	15.34	15.11	10.69
N (0.4-0.75)	0.809	0.925	0.83	0.874	0.77
ALP (50-135 U/L)	122	160	157	117	443
TBil (0-23 umol/L)	11.29	19.93	31.17	16	35.9
ALB (40-55 g/L)	22.8	23.6	36.9	30.2	42.4
ALT (7-40 U/L)	63	118	37	30	19
AST (13-35 U/L)	44	77	29	30	27
GGT (7-45 U/L)	76	89	84	48	250

TBiL: Total bilirubin; TACE: Transarterial chemoembolization; Hb: Hemoglobin; PLT: Platelet; WBC: White blood cell; ALP: Alkaline phosphatase; ALB: Albumin; ALT: Alanine aminotransferase; AST: Aspartate aminotransferase; GGT: Gamma-glutamyl transferase.

Two weeks post-TACE, the patient presented with sudden abdominal distension, exacerbated abdominal pain, and evident signs of peritonitis. Blood analysis revealed a white blood cell count of 15.34 × 10⁹/L, with neutrophils accounting for 83% (Table 1). Urgent bedside ultrasound examination demonstrated multiple areas of peritoneal fluid accumulation that progressively increased in size, leading to a suspected diagnosis of biliary peritonitis.

History of past illness

The patient had no significant past medical history, with no history of liver disease, diabetes, hypertension, or other chronic conditions.

Personal and family history

The patient led a regular lifestyle with no harmful habits, and had no history of smoking or alcohol consumption. There was no history of long-term medication use. There was no family history of liver disease, malignancies, or hereditary diseases, and no history of hepatitis or liver cirrhosis in direct relatives.

Physical examination

The patient was conscious but in a poor mental state. There was no significant change in weight. The conjunctiva was not jaundiced, the oral cavity was clean, and the gingiva showed no signs of bleeding. There was no enlargement of bilateral cervical lymph nodes, the thyroid was not enlarged, and the trachea was in the midline. Breathing was stable, and bilateral lung sounds were clear, with no wheezing or crackles. The heart rate was regular, and no murmurs were heard on cardiac auscultation. The abdomen was distended, with tympanic percussion and tenderness on palpation mainly in the right upper quadrant, without rebound tenderness. The liver edge was palpable, firm in texture, and tender. No ascites was detected, and bowel sounds were normal. There was no obvious splenomegaly. There was no edema in the lower extremities, and the limbs were freely movable. No other abnormalities were noted on examination.

Laboratory examinations

At admission, the patient presented with elevated liver enzymes (ALT and AST), mild bilirubin elevation, and positive hepatitis B surface antigen, indicating liver damage and hepatitis B virus infection. The tumor markers AFP and CA19-9 were also elevated, suggesting the possibility of HCC.

After the third TACE treatment, the patient showed improvement in TBiL, with a reduction in ALT levels. However, blood tests still indicated mild infection, with white blood cell count and neutrophil percentage remaining elevated, suggesting an ongoing inflammatory response.

Ten days post-procedure, the patient's white blood cell count significantly increased, with a higher percentage of neutrophils, indicating acute infection. Although ALT levels remained stable, the patient continued to show signs of infection and inflammation, likely due to complications from the procedure.

Imaging examinations

Imaging at admission: A space-occupying lesion was identified in the anterior right quadrant of the liver, measuring 7.4 cm × 9.1 cm × 7.1 cm, with invasion of the middle hepatic vein (Figure 1A). This imaging finding suggests a possible HCC with vascular invasion.

Imaging after the 3^rd TACE treatment (10 days post-procedure): A round low-density shadow was observed in the gallbladder fossa, accompanied by gas accumulation and surrounding exudation (Figure 1B). This suggests acute cholecystitis with gas formation, possibly due to complications after TACE, such as gallbladder perforation or biliary infection.

Imaging after complications (2 weeks post-procedure): Multiple areas of peritoneal fluid accumulation were observed, progressively increasing in size, leading to a suspected diagnosis of biliary peritonitis. This imaging finding further supports the diagnosis of peritonitis, likely caused by biliary tract infection.

FINAL DIAGNOSIS

The patient is a middle-aged female with a confirmed diagnosis of HCC. Following the third session of TACE, she developed acute cholecystitis secondary to cystic artery embolization. Subsequent PTGD was performed, but her symptoms worsened, with laboratory findings indicating leukocytosis and ultrasound revealing signs of peritonitis. Biliary peritonitis was ultimately suspected.

TREATMENT

Consequently, an emergency laparotomy was performed, revealing severe local inflammation and necrosis of the gallbladder along with a distorted anatomy in the hepatic hilar region. Due to the distorted anatomy of the Calot’s triangle which increases risk of biliary tract damage if cholecystectomy was performed, the surgical intervention chosen involved irrigation and debridement as well as cholecystostomy (Figure 1C and Figure 2).

Figure 2 Surgical exploration and placement of a cholecystostomy tube. A: Ischemic necrotic gallbladder observed in the surgical exploration field; B: Cholecystostomy tube used during surgery; C: The gallbladder with the cholecystostomy tube in place.

OUTCOME AND FOLLOW-UP

Following surgery, the patient experienced symptom relief and was discharged two weeks later with a drainage tube. The patient received regular post-discharge follow-up and subsequently required repeated hospitalizations due to episodes of cholangitis and blockage of the drainage tube. Follow-up imaging revealed progressive tumor growth, accompanied by deterioration in liver function and overall condition. Ultimately, the patient succumbed to multiple organ failure resulting from advanced liver cancer 11 months after initial diagnosis.

DISCUSSION

Epidemiology

TACE is the recommended treatment modality for patients with inoperable HCC with preserved liver function[3,7,10,13,14]. It involves two main mechanisms to eliminate tumor cells: One the one hand, a chemotherapeutic agent, usually doxorubicin, exerts cytotoxic effects on tumor cells; on the other hand, embolization of the feeding artery of the tumor causes tumor cells to undergo ischemia and necrosis[8,13]. In terms of embolic agent selection, TACE with lipiodol mixed with anticancer drugs and GS particles, transarterial embolization with GS particles (GS-TAE), transarterial radioembolization with yttrium-90 microspheres (TARE), and TACE with drug-loaded microspheres (doxorubicin) have been reported to enhance tumor response and mitigate severe complications[13,15-20].

Complications from TACE are infrequent and predominantly benign[8]; studies have reported a range of such serious but rare complications including hepatic abscess leading to sepsis, bile duct necrosis, biloma formation, biliary stricture, intrahepatic bile duct dilation, hepatic infarction, tumor rupture, gastric mucosa injury and gastrointestinal bleeding, acute pancreatitis, liver rupture, pulmonary embolism, femoral artery pseudoaneurysm, acute tumor lysis syndrome, and acute cholecystitis[4,6,7,10,16,21-23]. Among these, acute cholecystitis is a relatively more common complication and its incidence ranges from 0.3% to 10%[6,10,12,13,20,23-26]. The majority of patients experiencing complications exhibited Child-Pugh Class B liver function and had a model for end-stage liver disease score of at least 9[27]. Multiple administrations can also increase the risk of acute cholecystitis[13]. Our patient underwent three TACE procedures that could have put her at higher risk of the complication. The risk of unintended embolization of the cystic artery can be reduced through techniques like highly selective microcatheter embolization[12].

In the case of radioembolization (TARE), a higher incidence of cholecystitis and other gallbladder related complications has been reported, at 2.4%-24%[12]. In TARE, cholecystitis is caused by radiation rather than ischemia[12].

Pathogenesis

The main cause of acute cholecystitis after TACE is likely from technical problems, reflux of embolized material, or embolization of the cystic artery leading to its occlusion[3,9]. Hence, it is crucial to tailor the choice of embolization and chemotherapy drugs to the patient and ensure precise placement of the catheter[7,27]. Despite that, the backflow of embolized material may occur even when a super-selective catheter is placed away from the origin of the cystic artery[4].

Because the cystic artery is the primary source of blood supply to the gallbladder, and, unlike the liver, the gallbladder does not have a dual blood supply[4], embolism of the cystic artery can result in gallbladder ischemia, leading to acute cholecystitis, which, if unresolved, can progress to gallbladder necrosis[4,9].

The cystic artery primarily originates from the right hepatic artery[28], thus when employing the proximal right hepatic artery (or proper hepatic artery) approach, there is a higher likelihood of cystic artery embolization[13,29]. Selective techniques comes with a lower risk of cholecystitis[13]; however, it has been reported that chemoembolization procedures in segments IV and V of the liver may also increase risk of cholecystitis and hence may require additional precaution[13]. At the same time, rare anatomical variations to the origin of the cystic artery also exist, such as that arising from the left hepatic artery, common hepatic artery, or the superior mesenteric artery[4,13]. In these cases, embolization of the left hepatic artery may have an increased risk of occluding the cystic artery.

Diagnoses and differentials

Patients who develop acute cholecystitis post-TACE may report symptoms of right upper abdominal pain (which can last from a few days to a month) and fever and show signs of guarding or tenderness[4,7,13]. Severe abdominal pain and/or persistent symptoms despite treatment may suggest more serious complications like gallbladder necrosis or perforation[4,22]. These non-specific symptoms make diagnosis difficult because most patients will often experience such nonspecific symptoms like fever, fatigue, abdominal pain (in the right upper quadrant), nausea, vomiting and ileus following TACE, and this has been has been extensively reported in the literature as the self-limiting “post-embolisation syndrome”[7,10,17,22], which can affect up to 20%-90% of patients[8]. Other complications such as hepatic abscess and hepatic infarction may also present similarly, with abdominal pain and fever as the main symptoms[9]. Yet, clinicians involved in the care of patients post-TACE should be more cautious of acute cholecystitis in particular in patients with right-sided HCC who report such symptoms post-TACE, especially if they persist.

It is important to note that most of the complications occur within a 2-week period following TACE[7]. Early recognition and prompt initiation of treatment are important because delayed recognition can carry the risk of progression to gangrenous cholecystitis and gallbladder necrosis[7,12,22]. Our patient presented initially with similar symptoms as those in the literature, with high fever, abdominal pain, and abdominal distention, which could have prompted a consideration of acute cholecystitis; however, there were insufficient clues, with laboratory indicators unspecific and imaging inconclusive. The development of more severe symptoms 2 weeks after the procedure, however, was suggestive of more serious complications, which was confirmed to be biliary peritonitis by bedside ultrasound.

Imaging and laboratory tests

Various imaging modalities may be necessary to aid the diagnosis of patients with acute cholecystitis (as well as other complications), including CT, MRI, digital subtraction angiography, and ultrasound[7,30]. CT and ultrasound findings of a dilated gallbladder with wall thickening may be suggestive of cholecystitis and are described in many reports[9,13,31]; other CT criteria for cholecystitis may include presence of “sandwich-like layering of the gallbladder wall” suggesting submucosal edema, “gas in the gallbladder”, “pericholecystic stranding” in fat surrounding gallbladder, “indistinct interface of gallbladder wall and adjacent liver”, and presence of “pericholecystic abscess”, as well as deposition of “lipiodol in the walls of the gallbladder”[31]. Discontinuous enhancement of the gallbladder wall seen on CT can suggest necrosis of the gallbladder[9], while interruption of the gallbladder wall together with fluid collection originating from the gallbladder (and sometimes gas) may suggest a perforated gallbladder[22]. In our case, initial ultrasound did not show any abnormalities; however, on the 10^th day after the procedure, abdominal CT showed a round low-density shadow in the gallbladder fossa accompanied by gas accumulation and surrounding exudation, which can suggest cholecystitis.

In terms of laboratory indicators, white blood cell count, neutrophil percentage, TBiL, alkaline phosphatase (ALP), procalcitonin, and other indicators can serve as markers for acute cholecystitis. Elevated white blood cell counts and an increase in neutrophil percentage can suggest the possibility of an infection[10]. However, leukocytosis and raised transaminases are also reported in post-embolisation syndrome[8,20,25,31]. These changes are probably due to necrosis of tumor cells and surrounding healthy hepatocytes, causing lysis and release of intracellular enzymes[4,31]. Thus, such indicators may not differentiate patients with acute cholecystitis from those without[31]. In our patient, initial laboratory values were inconclusive with leucocyte count (8.53 × 10⁹/L) and ALP (122 U/L) in the normal range and slight elevation of neutrophil ratio (80.9%); when her symptoms worsened two weeks after TACE, laboratory values also became more suggestive of a serious complication with a marked increase in leucocytes (13.12 × 10⁹/L), neutrophil percentage (92.5%), as well as ALP value (160 U/L).

Management/treatment and prognosis

HCC complicated with cholecystitis can impact the treatment and prognosis of patients[12]. However, as a complication of TACE, it is generally self-limiting for most patients[9,31], and most achieve complete recovery with conservative management[9,12,29,31]. Close observation, fasting, and intravenous administration of antibiotics such as piperacillin with tazobactam are usually sufficient[9,32].

However, a small subset may exhibit worsening local inflammation of the gallbladder leading to gallbladder necrosis and perforation accompanied by acute peritonitis[12,13,22]. Gangrenous cholecystitis, emphysematous cholecystitis, and lipoidal cholecystitis are other serious complications[13,31]. In such cases where conservative treatment proves ineffective, drainage or cholecystectomy may be considered[7,9,13,31]. For example, Karavias et al[11] reported a case involving gangrenous cholecystitis associated with TACE treatment for HCC and subsequently performed cholecystectomy on the patient. Some argue that prophylactic cholecystectomy could be beneficial for specific patient populations with malignancies[12]. Cholecystostomy can also be a viable alternative if there is already severe local necrosis of the gallbladder and performing a forced cholecystectomy may pose a risk of damaging the biliary tract. In our case, due to the presence of local necrosis in the gallbladder and difficulties in separating the Calot’s triangle, there was an increased risk of biliary injury. Therefore, we opted for cholecystostomy which effectively controlled inflammation and allowed for safe discharge. Additionally, the timing of the operation is crucial: In cases where local necrosis and gallbladder perforation are suspected, along with evident signs of peritonitis, immediate surgical intervention becomes necessary to achieve optimal prognosis, which was the case with our patient, where initial conservative treatment failed to resolve the patient’s condition. A review of relevant articles with acute ischemic cholecystitis following TACE is presented in Table 2.

Table 2 Summary of significant literature findings.

Ref.	Findings	Contributions
Marcacuzco Quinto et al[6]	Out of the 196 patients with liver tumors who had undergone 322 TACE procedures, 4 developed acute cholecystitis	To review the complications following TACE for liver tumors
Xue et al[10]	Severe complications were few (4.9%), acute cholecystitis (n = 4 in 511)	A large cohort study of TACE for huge HCC with a diameter over 10 cm
Cosgrove et al[14]	Severe procedure-related complications were seen in 3.2% (cholecystitis, n = 1 in 62 patients)	An open-label study of 62 patients with DEB-TACE for unresectable HCC
Dhamija et al[8]	Biliary complications of various severities developed in 6 (3.6%) patients, leading to an incidence of 1.9% (6/305)	The incidence and presentation of biliary complications following TACE in patients with HCC
Tu et al[7]	The incidence was 2.1% per patient and 0.84% per TAE/TACE procedure. The complications included cholecystitis (n = 2). Major complications are mostly benign, but some are lethal	The incidence and outcome of major complications following conventional TAE/TACE therapy for HCC
Tarazov et al[30]	Serious ischemic complications of TACE occur in about 5% of patients and can be successfully managed without open surgery	The frequency, character, methods of treatment, and outcome of ischemic complications after TACE
Jayakrishnan et al[12]	Hepatic artery-based therapies carry a risk of cholecystitis (0.02%-24%), although the risk is reduced with selective catheterization	Review of the impact of antineoplastic therapies on the risk for cholelithiasis and acute cholecystitis
Malagari et al[26]	Severe procedure-related complications were seen in 4.2% (cholecystitis: n = 1; liver abscess: n = 1; pleural effusion: n = 1)	The results of segmental transcatheter arterial chemoembolization with doxorubicin-loaded DC bead in the treatment of HCC in non-surgical candidates
Biselli et al[23]	A significantly more favorable survival was observed for TACE-treated patients compared with IAC-treated patients; the side effect after the intraarterial procedure was chemical cholecystitis (8%)	TACE and IAC have a primary role in treating patients with unresectable HCC larger than 5 cm
Chen et al[2]	Metaanalysis provides preliminary evidence for the comparative safety and efficacy of HAIC and TACE combined with sorafenib, and indicates the dominance of HAICoxaliplatin in HCC interventional therapy	A systematic review and network metaanalysis of comparative effectiveness of interventional therapeutic modalities for unresectable HCC
Hidaka et al[17]	Combined therapy involving bland GS-TAE followed by Lip-TACE can be performed safely and may improve survival in patients with huge HCCs. Severe adverse events were seen in two patients, acute cholecystitis and tumor rupture (n = 21)	To assess the efficacy of combined therapy involving bland TAE using gelatin sponge particles followed by TACE using lipiodol mixed with anticancer agents and GS particles
Llovet and Bruix[3]	Sensitivity analysis showed a significant benefit of chemoembolization with cisplatin or doxorubicin but none with embolization alone	Systematic review of randomized trials for unresectable HCC, and chemoembolization improves survival
Monier et al[29]	DEB-TACE was associated with increased hepatic toxicities compared to conventional TACE	Comparison between drug-eluting beads and lipiodol emulsion in liver and biliary damages following TACE of HCC
Wagnetz et al[31]	There was a 49% incidence of acute cholecystitis for TACE of HCC, and a lobar TACE of the right hepatic artery likely carries the highest risk of post-TACE cholecystitis	Acute ischemic cholecystitis is self-limiting and does not seem to require any intervention or surgery
Karaman et al[13]	The possibility of cholecystitis is always remembered during TACE-DEB for tumors in segments IV and/or V	A case of ischemic cholecystitis after DEB-TACE that required cholecystectomy
Karavias et al[11]	Super selective embolization significantly reduces the risk of cholecystitis. In most cases, management is conservative and only severe cases require further intervention	Gangrenous cholecystitis related to TACE treatment for HCC
Chung et al[20]	Important predisposing factors were major portal vein obstruction, compromised hepatic functional reserve, biliary obstruction, previous biliary surgery, excessive amount (> 20 mL) of iodized oil, hepatic arterial occlusion after repeated transcatheter oily chemoembolization (TOCE), and nonselective embolization	The major complications and their predisposing factors in TOCE for hepatic tumors
Kim et al[15]	Adjustments in the amounts of iodized oil or gelatin sponge particles and in the sites of embolization may reduce ischemic biliary injuries after TACE	The exact pathogenic mechanisms and clinical implications of the ischemic bile duct injury after TACE in patients with HCC
Song et al[21]	The biliary abnormality prone to ascending biliary infection was the most important predisposing factor to the development of liver abscess after TOCE	The incidence, predisposing factors for, and clinical outcome of liver abscess developing in patients with hepatic tumors after TOCE
Vasudevan et al[9]	The differential diagnosis in a patient with abdominal pain after TACE including post-embolization syndrome and, less commonly, hepatic abscess formation, one must consider cholecystitis especially for right-sided hepatic tumors	A case of acute ischemic cholecystitis following DEB-TACE
Lim et al[22]	The presence of gallbladder perforation must be recognized in patients with persisting symptoms and imaging evidence	A rare but serious complication: Gallbladder perforation following TACE
Kuroda et al[32]	Patients with post-TAE infarction of the gallbladder can be treated conservatively	Gallbladder infarction developing after TAE in patients with malignant hepatic tumors was studied
Sun et al[4]	If a hepatic resection is carried out after TACE, the gallbladder should be removed simultaneously. In addition, once a patient has developed an infarcted gallbladder, a cholecystectomy becomes necessary	The incidence, diagnosis, treatment, outcome, and mechanism of hepatic and biliary damage after TACE for malignant hepatic tumors

Lip-TACE: Lipiodol mixed with anticancer drugs and GS particles; TACE: Transarterial chemoembolization; HCC: Hepatocellular carcinoma; DEB-TACE: Drug-eluting bead transarterial chemoembolization; TAE: Transarterial embolization; IAC: Intraarterial chemotherapy; HAIC: Hepatic artery infusion chemotherapy.

CONCLUSION

In the case that we report, the patient presented with localized gallbladder necrosis accompanied by peritonitis following ectopic embolization of the cystic artery using lipiodol embolization. Following cholecystostomy treatment, the patient experienced symptom relief and was subsequently discharged. Ultimately, the patient achieved a survival of 11 months after being diagnosed with stage IIIB liver cancer.

ACKNOWLEDGEMENTS

We thank supports from the Department of Hepatobiliary Surgery of the Shaanxi Provincial People's Hospital and Professor Rong-Qian Wu for his contribution to the language aspect of the draft.