Liver-gallbladder anatomical adjacency-related severe infection: a case report of liver abscess rupturing into the gallbladder inducing septic shock and literature review

Introduction

Hepatic abscess refers to a localized suppurative infection of the liver caused by pathogens such as bacteria, fungi, or parasites. It is characterized by necrosis and liquefaction of liver tissue, leading to the formation of a purulent cystic cavity (1,2). The complication rate of hepatic abscess ranges from approximately 10% to 30%, with common complications including abscess rupture (e.g., into the peritoneal cavity, inducing peritonitis) and biliary obstruction (3). In contrast, gallbladder perforation is primarily associated with intrinsic gallbladder diseases, such as cholecystitis or impacted gallstones. The incidence of gallbladder perforation secondary to hepatic abscess—due to anatomical proximity or inflammatory extension—is less than 3%.

The pathogenesis of liver abscess with secondary gallbladder perforation involves a cascade of direct infectious spread and tissue destruction (4). When an abscess abuts the gallbladder bed, pathogens can breach the hepatic capsule and invade the gallbladder wall, causing inflammation, ischemia, and necrosis. Progressive necrosis ultimately leads to perforation, creating a fistula between the abscess and gallbladder lumen. Pus, containing pathogens and toxins, may then enter the biliary tract or peritoneal cavity. Hematogenous dissemination of these pathogens can trigger systemic inflammatory response syndrome (SIRS), leading to bacteremia, sepsis, and potentially septic shock. This rare but severe complication arises from the specific anatomical and pathological confluence required for this cascade.

We describe a rare case of hepatic abscess leading to gallbladder perforation and subsequent sepsis. This report details the clinical course, diagnostic approach, and therapeutic interventions, aiming to provide clinical insights that may aid in the early recognition and management of similar complex cases. We present this article in accordance with the CARE reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0013/rc).

Case presentation

The patient was an 84-year-old male who presented to our hospital on July 24, 2025, with a chief complaint of right upper quadrant abdominal pain accompanied by high fever for 1 day. The pain was colicky in nature and progressively intensified, accompanied by nausea, vomiting, dizziness, hypotension (94/47 mmHg), and cold, clammy extremities. The patient had a history of chronic renal insufficiency. Admission labs showed serum creatinine 393 µmol/L and estimated glomerular filtration rate (eGFR) 11 mL/min/1.73 m², consistent with Chronic Kidney Disease (CKD) stage 5, with no recent significant change. The patient had been irregularly self-administering traditional Chinese medicines claimed to have renal protective effects, such as “Niaoduqing”. Upon admission, physical examination demonstrated peritoneal irritation signs, including abdominal muscle rigidity, and marked tenderness with rebound tenderness in the right upper quadrant. No abdominal mass was palpated, shifting dullness was negative, and bowel sounds were diminished. Initial laboratory tests indicated markedly elevated levels of C‑reactive protein (CRP) (221.8 mg/L), procalcitonin (PCT) (>100 ng/mL), white blood cell (WBC) (12.17×10⁹/L), neutrophil ratio (95.1%) and liver function tests [alanine aminotransferase (ALT; 63.3 U/L), aspartate aminotransferase (AST; 157.4 U/L), total bilirubin (25.1 µmol/L), direct bilirubin (19.7 µmol/L)]. The Sequential Organ Failure Assessment (SOFA) score was 11 on admission. Non‑contrast computed tomography (CT) examination revealed multiple patchy hypodense lesions in the liver, with the largest lesion measuring approximately 31 mm × 36 mm (segment V of the liver), accompanied by mild thickening of the gallbladder wall. No gallstones were observed within the gallbladder lumen or in the intrahepatic or extrahepatic bile ducts, and there were no signs of biliary duct dilatation. No acute abdominal signs such as perforation, obstruction, or stenosis were evident on imaging (Figure 1). The patient subsequently developed clinical deterioration, with worsening abdominal pain, persistent high-grade fever and hypotension. On the afternoon of hospital day 2, contrast-enhanced abdominal ultrasonography revealed a heterogeneous mixed-echo area in liver segment V, measuring approximately 49 mm × 36 mm, suggestive of a hepatic abscess with substantial liquefaction (Figure 2A). A communication was observed between the abscess area and the gallbladder lumen, indicating an abnormal connecting channel, consistent with fistula formation between the abscess and the gallbladder (Figure 2B). Blood culture identified Escherichia coli, indicating sepsis progression and diagnostic delay.

Figure 1 CT imaging demonstrates the evolutionary trends of the hepatic S5 abscess and gallbladder changes across different time periods. The left panel illustrates the hepatic S5 abscess, while the right panel depicts the gallbladder. (A) On admission, the boundary between hepatic S5 and the gallbladder was poorly defined, with significant surrounding exudation observed (red arrow). The gallbladder was enlarged. (B) Following drainage, the hepatic S5 abscess showed significant resolution, with a tubular hyperdense structure visualized (red arrow). The gallbladder volume returned to normal. (C) After catheter removal, the hepatic S5 abscess was nearly completely resolved (red arrow). The gallbladder volume remained within normal limits. CT, computed tomography.

Figure 2 Abdominal contrast-enhanced ultrasound demonstrating (A) the hepatic S5 abscess measuring approximately 49 mm × 36 mm, and (B) an abnormal communication pathway between the hepatic S5 abscess and the gallbladder, suggestive of perforation (red arrows).

Upon admission, the patient was initiated on a comprehensive protocol for septic shock management, which included empirical antibiotic therapy with meropenem (Mepem) administered at a dosage of 1 g every 6 hours, supplemented by nutritional support, fluid resuscitation and symptomatic treatment. On July 26, 2025, the patient underwent ultrasound-guided percutaneous catheter drainage (US-PCD) of the liver abscess. Grayish-red turbid purulent fluid was successfully drained from the puncture site. The procedure was completed successfully without any intraoperative complications. Additionally, the drained fluid was sent for pathogen culture. Blood cultures collected from both sides on July 27, 2025, and July 30, 2025, consistently identified Escherichia coli infection. After five days of culture, the drainage fluid also tested positive for Escherichia coli. In accordance with the antimicrobial susceptibility test results, the antibiotic regimen was adjusted on July 31, 2025, to cefoperazone-sulbactam administered at 3 g every 8 hours. The patient reported minimal postoperative pain, maintained patent drainage, and demonstrated favorable recovery with no observed postoperative complications. The patient was discharged on August 20, 2025. After discharge, the patient was treated with cefpodoxime proxetil dispersible tablets (0.1 g twice daily) for one week.

At the 1-month and 3-month post-discharge follow-up visits, the patient reported no recurrence of abdominal pain and displayed no signs of relapse. Follow-up imaging demonstrated a progressive reduction in the size of the hepatic abscess, with normalization of gallbladder wall thickness (Figure 1B,1C; Figure 3). Laboratory findings indicated a gradual decline in inflammatory markers, which ultimately returned to normal ranges. The drainage catheter was removed on September 11. One month after catheter removal, a repeat abdominal color Doppler ultrasound revealed that the abscess in liver segment 5 measured approximately 16 mm × 10 mm, with the gallbladder wall remaining intact. Both physical examination and ultrasonographic evaluation confirmed the absence of recurrence or complications, indicating that the patient had achieved a favorable recovery (Figure 4).

Figure 3 Ultrasound imaging demonstrates the evolution of the hepatic abscess across different time periods. (A) On admission, the hepatic S5 abscess measured approximately 49 mm × 36 mm. (B) In the early post-drainage phase, the hepatic S5 abscess measured approximately 48 mm × 33 mm. (C) During the later phase of drainage, the hepatic S5 abscess measured approximately 27 mm × 17 mm. (D) After removal of the drainage catheter, the hepatic S5 abscess measured approximately 16 mm × 10 mm.

Figure 4 Timeline of the clinical case. CEUS-Abd, abdominal contrast-enhanced ultrasound; CRP, C‑reactive protein; CT, computed tomography; PCT, procalcitonin; US-Abd, abdominal ultrasound; WBC, white blood cell count.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

This case report extends beyond a simple presentation of hepatic abscess; its pivotal contribution lies in elucidating the insidious nature of the rare complication wherein a hepatic abscess erodes into the gallbladder, and in demonstrating how insufficient awareness and consequent diagnostic delay can precipitate a septic crisis. It serves as an instructive clinical exemplar of the rapid systemic deterioration that can arise from a localized infectious focus.

The difficulty in diagnosis

Hepatic abscesses commonly rupture into the thoracic or abdominal cavity, yet the anatomically adjacent gallbladder is often overlooked as a potential “target organ”. Clinical assessment often focuses narrowly on the abscess itself, failing to actively consider direct erosion into neighboring hollow viscera. This condition has low incidence and an insidious onset, leading to frequent early misdiagnosis. Timely identification depends on clinical suspicion and precise imaging.

Anatomically, the inherent structure of the gallbladder wall, combined with the dense tissue barrier between the liver and gallbladder, restricts the local release of pus from the hepatic abscess. This not only delays the direct invasive progression of the abscess into the gallbladder wall but also further reduces the susceptibility to perforation (5). However, the medial segment of the left hepatic lobe (S4) lacks a sufficiently thick hepatic tissue barrier adjacent to the gallbladder bed. When an abscess occurs in this region, it is more prone to directly erode the adjacent gallbladder wall. In the present case, the abscess was located in segment V (S5). Although this differs from the medial segment of the left hepatic lobe, S5 is also anatomically adjacent to the gallbladder bed. Therefore, the high-risk anatomical feature of the abscess being immediately adjacent to the gallbladder bed remains valid. Early imaging signs are often subtle. In initial perforation stages, CT may show only close apposition of the abscess to the gallbladder wall, with direct fistulous tracts or subtle wall defects typically remaining undetectable.

Although rare, similar cases of liver abscess eroding into adjacent organs have been reported in the literature. Examples include a case of Klebsiella pneumoniae liver abscess penetrating the diaphragm to form a hepatopleural fistula, and a case of liver abscess eroding through the intestinal wall to form a hepatointestinal fistula. This mechanism is anatomically plausible: when a liver abscess is located adjacent to a hollow viscus (such as the gallbladder or diaphragm), the lack of a sufficiently thick tissue barrier may allow the abscess to directly erode into the neighboring organ. In the present case, the abscess was located in segment V of the liver (Figure 1A), immediately adjacent to the gallbladder bed, which corresponds to this high-risk anatomical feature, providing important corroborating evidence for the “abscess-first” mechanism proposed herein (6-8).

Discussion of the etiology of liver abscess

Liver abscesses typically arise from the following pathways: (I) biliary origin: caused by choledocholithiasis, cholangitis, etc., and represents the most common etiology, accounting for approximately 40–60% of cases; (II) portal venous origin: secondary to intra-abdominal infections (such as appendicitis, diverticulitis); (III) hematogenous spread: via bacteremia through the hepatic artery; (IV) direct extension: from contiguous infectious foci; (V) cryptogenic origin: no identifiable cause despite comprehensive investigation, accounting for approximately 15–20% of cases.

In the present case, the patient had no history of prior systemic disease evaluation. The initial admission CT scan revealed no evidence of cholelithiasis, biliary dilation, or cholangitis. The gallbladder wall demonstrated only mild edema, which was considered a reactive change secondary to the adjacent abscess rather than indicative of primary cholecystitis. These findings do not support biliary disease as the underlying etiology of the liver abscess. The patient had a past medical history of chronic kidney disease, representing a predisposing factor with impaired immune barrier function. Admission blood cultures grew “Escherichia coli”. After comprehensive investigation, no definite primary infectious focus was identified. Following exclusion of other sources of infection, this case exhibits features consistent with cryptogenic liver abscess. Literature reports indicate that approximately 15–20% of pyogenic liver abscesses have no identifiable etiology despite extensive workup. These cases are hypothesized to result from transient bacteremia: in immunocompromised hosts, transient bacteremia may lead to bacterial seeding within the liver, while the primary focus either resolves spontaneously or remains occult and undetectable.

Pathophysiological cascade

The patient presented with sepsis on admission, attributable to the liver abscess. Following the diagnosis of gallbladder perforation with communication between the abscess and the gallbladder lumen, the patient experienced clinical deterioration with worsening hemodynamic instability and altered mental status, suggesting that fistula formation contributed to further propagation of the septic process. This case comprehensively demonstrates the rapid deterioration cascade from a localized hepatic abscess to septic shock. The primary hepatic abscess, acting as the initial focus, eroded into the adjacent gallbladder, leading to perforation and establishing itself as a critical amplifier of infection (2). Following gallbladder perforation, a high load of pathogens and toxins spread via retrograde biliary flow and direct peritoneal diffusion. This transformed the infection from a relatively confined abscess to a widespread release within the extensive biliary-peritoneal system, resulting in massive and rapid systemic absorption of bacteria and toxins. This process triggered a dysregulated systemic inflammatory response, leading to endothelial damage, capillary leakage, and distributive shock, thereby completing the fatal transition from localized infection to a systemic life-threatening condition (9). The core mechanisms can be summarized as: trans-organ invasion by the localized infection, disruption of gallbladder wall integrity, and subsequent hematogenous systemic dissemination. This case serves as a critical reminder that, for hepatic abscesses adjacent to the gallbladder, the gallbladder must be regarded as a potential complication target. Once perforation occurs, the therapeutic window narrows dramatically, and any delay in diagnosis or intervention significantly heightens the risk of sepsis.

Therapeutic strategy evaluation and enhancement

We searched the PubMed database using the keywords “liver abscess” and “gallbladder perforation” to identify and compile case reports of gallbladder perforation secondary to liver abscess as well as organ perforation secondary to liver abscess. The results are summarized in Table 1 (6,7,10-26). In cases of liver abscess secondary to gallbladder perforation, the majority of patients had a history of cholelithiasis and were primarily managed with initial surgical intervention or drainage combined with surgery. Only a minority of cases achieved favorable clinical outcomes with percutaneous drainage alone. In contrast, in cases of organ perforation secondary to liver abscess, most patients achieved satisfactory outcomes with drainage therapy alone. This case report presents a special instance of liver abscess secondarily causing gallbladder perforation, in a patient with no prior history of cholecystitis or gallstones. This case fully demonstrates the importance of drainage in controlling the source of infection.

Percutaneous interventional drainage, characterized by minimal invasiveness, rapid execution, and low trauma, serves as the first-line treatment for well-liquefied hepatic abscesses complicated by localized gallbladder perforation and sepsis (27,28). Guided by imaging, it effectively drains pus and lowers pressure, controlling infection and inflammation with an 85–90% success rate in suitable liquefied cases (29). This approach is particularly beneficial for elderly patients, those with multiple comorbidities, or individuals at high surgical risk. Using local anesthesia reduces risks and aligns with the minimally invasive principle, enabling faster recovery, shorter stays, and lower mortality. However, its efficacy is limited in poorly liquefied or multifocal abscesses, and it cannot directly repair perforations or address persistent bile leaks. Post-procedure complications like catheter blockage or displacement require careful technique and monitoring (30).

However, surgical intervention enables definitive source control and comprehensive management of complications, serving as salvage therapy for percutaneous drainage failure or complex presentations (31,32). Surgical intervention, while definitive for infection control and complication management, is invasive. It entails higher complication rates, slower recovery, and added risks for critically ill or elderly patients.

Therefore, in clinical scenarios where a liver abscess-gallbladder fistula is confirmed or highly suspected, adopting a staged, damage-progression treatment strategy is crucial. The primary step involves performing ultrasound or CT-guided percutaneous drainage of the liver abscess, while concurrently assessing the need for combined percutaneous transhepatic gallbladder drainage (PTGBD) to achieve preliminary control of the infection source (33). This minimally invasive interventional approach aims to alleviate the septic state and stabilize the patient’s condition at the lowest physiological cost. If infection persists or clinical deterioration occurs despite adequate drainage, escalation to surgical intervention is warranted. The core advantage of this strategy lies in prioritizing minimally invasive measures to control the infection source, thereby creating safer physiological conditions for any subsequent definitive surgery, systematically reducing overall treatment risk and improving patient prognosis. Based on a systematic review and integrated analysis of multiple literature sources, this article comprehensively summarizes the standardized management strategies for liver abscess and its associated complications, as well as the optimal timing for interventional therapy and surgical intervention, aiming to provide reference for clinical practice (Table 2).

Diagnostic and interventional value of contrast-enhanced ultrasound (CEUS)

CEUS played a pivotal role in this case by confirming the communication between the liver abscess and the gallbladder—a finding not apparent on initial non-contrast CT due to timing (perforation occurred 24–48 hours after admission) and technical limitations (contrast avoided due to renal impairment). CEUS provided real-time dynamic assessment of contrast flow from the abscess cavity into the gallbladder lumen, definitively establishing the “abscess-first” mechanism. Most importantly, US-PCD, by accurately identifying the liquefied portions and communication tract, enabled effective source control while avoiding invasive surgery in a septic patient with renal impairment. In this case, the patient achieved clinical stabilization with drainage alone, without the need for further surgical resection. This process not only highlights the diagnostic value of CEUS but also underscores the critical role of timely, targeted drainage, fully demonstrating the importance of the drainage procedure itself.

Limitation

The main limitations of this study are as follows: first, a single case report cannot provide epidemiological data on the disease (such as incidence or prevalence rates), nor can a single observation establish causality or generalizability; thus, the findings may not be applicable to broader patient populations. Second, selection bias is difficult to exclude, as the decision to report this case was inherently influenced by its atypical presentation. Reporting bias is also inherent, as case reports tend to highlight rare manifestations or successful treatment outcomes. Third, the follow-up period was limited, which precludes a comprehensive assessment of long-term outcomes and potential complications. Last, incomplete documentation of procedural details may hinder the standardization of the treatment process.

Clinical significance and recommendations

Hepatic abscess-induced gallbladder perforation represents a critical condition requiring a high degree of clinical vigilance. This entity typically constitutes a “dual-focus high-pressure infectious complex”, often driving refractory sepsis. The key to successful management lies in establishing an early diagnosis through imaging and dynamically assessing the pressure dynamics within the infected system. Once confirmed, an aggressive drainage strategy should be implemented in conjunction with potent antimicrobial therapy and multidisciplinary supportive care. In the future, the development of standardized multidisciplinary management pathways and clinical early-warning scores for such complex intra-abdominal infections holds promise for further improving patient outcomes.

Conclusions

This case illustrates that in an elderly patient presenting with sepsis and organ dysfunction due to a liquefied hepatic abscess complicated by localized gallbladder perforation—and without diffuse peritonitis—percutaneous interventional drainage merits consideration as a first-line approach. The combination of imaging-guided drainage and targeted antibiotic therapy achieved prompt infection source control, promoted the healing process of the gallbladder wall, and resulted in a positive clinical course. It underscores the critical role of accurate clinical recognition and supports the preferential use of minimally invasive interventions in appropriately selected cases. Moving forward, refining individualized treatment strategies and accumulating further evidence will be essential to establish standardized, optimized management pathways for similar complex clinical scenarios.

Acknowledgments

We express our gratitude to the patient for consenting to the publication of anonymized clinical data. We also extend our sincere appreciation to the Department of Critical Care Medicine at the Affiliated Hospital of Guangdong Medical University (Zhanjiang, China), and to all healthcare professionals involved in the management of this case.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0013/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0013/prf

Funding: This study was supported by the Development Center for Medical Science & Technology National Health Commission of the People’s Republic of China (No. WKZX2024CX301205, to Y.Z.).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0013/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are 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 procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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