Abstract
Subcapsular hepatic haematoma is a rare, potentially life-threatening complication of laparoscopic cholecystectomy. A previously well woman in her 30s developed severe right upper quadrant pain and vomiting immediately after an apparently uncomplicated laparoscopic cholecystectomy. Multiphase computed tomography the next day showed a haematoma exceeding 19 cm with active bleeding from segments IVb and V. Angiography identified multifocal bleeding from hepatic arterial branches, including an accessory branch from the gastroduodenal artery. Selective gelatin-sponge embolization achieved angiographic haemostasis. Despite the haematoma subsequently rupturing into the peritoneal cavity and haemoglobin falling to 58 g/L, the patient remained haemodynamically stable and was managed with blood transfusion and surveillance without reoperation or drainage. This case supports early vascular imaging for disproportionate postoperative pain and physiology-guided management after embolization.
Introduction
Laparoscopic cholecystectomy is the standard treatment for symptomatic gallstone disease. Postoperative haemorrhage occurs in fewer than 1% of procedures and usually arises from the cystic artery, gallbladder bed, abdominal wall or liver capsule [1]. Subcapsular hepatic haematoma is substantially rarer; a 2019 review identified only 16 cases across 13 publications, predominantly managed by laparotomy or percutaneous drainage with only one case of management with embolization [2]. We describe a massive, actively bleeding subcapsular hepatic haematoma caused by multifocal hepatic arterial bleeding after an apparently uncomplicated laparoscopic cholecystectomy. Selective transarterial embolization achieved haemostasis, and subsequent rupture of the haematoma was managed without reoperation or percutaneous drainage.
Case report
A female Caucasian patient in her 30s presented with 6 months of intermittent biliary colic and recurrent transient choledocholithiasis. Other than an elevated BMI of 36.6, she had no significant medical history or regular medications; her only previous operation was tubal ligation. She was a non-smoker, consumed one to two alcoholic drinks most evenings, and denied recreational drug use. Pre-operative bilirubin was 73 μmol/L, alanine aminotransferase 669 U/L, aspartate aminotransferase 667 U/L, and haemoglobin 129 g/L. Ultrasonography demonstrated numerous small gallstones, mild intrahepatic duct prominence and no common bile duct dilatation.
Laparoscopic cholecystectomy with intraoperative cholangiography demonstrated mild acute cholecystitis, multiple gallstones and the liver was noted to be large. The critical view of safety was obtained, cholangiography showed normal biliary duct anatomy, and no choledocholithiasis. Haemostasis appeared satisfactory with no hepatic capsular injury. Immediately postoperatively, the patient developed severe right upper quadrant and epigastric pain with persistent vomiting requiring escalating analgesia. On postoperative Day 1, haemoglobin had fallen to 104 g/L. Missed choledocholithiasis was suspected, but magnetic resonance cholangiopancreatography demonstrated an 18-cm right subcapsular hepatic collection. Urgent multiphase computed tomography (CT) confirmed a haematoma exceeding 19 cm, marked hepatic mass effect and active intra-parenchymal bleeding from segments IVb/V, without bleeding from the gallbladder fossa, pseudoaneurysm or arteriovenous fistula (Fig. 1).
Coronal maximum intensity projection (MIP) CT in the arterial phase, post-operative Day 1, demonstrating the large subcapsular haematoma and multiple sites of active bleeding (arrows) arising from segment IVb.
The patient maintained normal blood pressure and heart rate without haemodynamic compromise. Following open disclosure and multidisciplinary review, emergency angiography was performed by interventional radiology, demonstrating multifocal bleeding from branches supplying segments IVb and V. An accessory branch arising from the gastroduodenal artery was also seen to supply these segments (Fig. 2). Selective gelatin-sponge embolization was performed until completion angiography showed no further extravasation (Fig. 3A and B).
Selective angiography from the common hepatic artery revealing variant arterial anatomy with accessory hepatic arterial branch (arrow) originating from the gastroduodenal artery (GDA).
(A) Super-selective angiography from the hepatic arterial branch arising from the GDA demonstrating multiple sites of active arterial bleeding (white arrows) into the subcapsular haematoma. (B) Fluoroscopy image after gelatin sponge embolization demonstrating stasis of flow in the accessory branch supplying the bleeding site.
Despite angiographic haemostasis, haemoglobin fell to 61 g/L on postoperative Day 2. Two units of packed red cells increased it to 84 g/L, but it decreased to 58 g/L within 24 hours. Repeat CT showed new moderate-volume haemoperitoneum, consistent with interval rupture of the subcapsular haematoma. A tiny possible focus of active bleeding adjacent to segment VII was not confirmed on later phases (Fig. 4).
Repeat multiphase CT Day 2 after embolization showing new moderate-volume haemoperitoneum consistent with interval rupture of the subcapsular haematoma.
The patient developed extensive right flank ecchymosis and transient hyperbilirubinaemia to 121 μmol/L but remained haemodynamically stable. After multidisciplinary review, repeat embolization and surgery were deferred because there was no physiological deterioration. She was managed with serial examinations, haemoglobin monitoring, analgesia and transfusion support. She was discharged 7 days after embolization. At 2-week review, haemoglobin was 104 g/L and imaging showed an organizing haematoma. At ~6 weeks, haemoglobin was 138 g/L, liver biochemistry had normalized and imaging demonstrated continued reduction of the haematoma to ~4.6 cm in maximal depth (Fig. 5).
Follow-up CT at ~6 weeks, (A) showing interval reduction of the right subcapsular hepatic haematoma, (B) to ~4.6 cm in maximal depth.
Discussion
Earlier reports have attributed subcapsular hepatic haematoma to excessive gallbladder traction, capsular injury, trocar or thermal trauma, non-steroidal anti-inflammatory drugs and anticoagulation [2, 3]. This patient had no coagulopathy or recognizable intraoperative injury, and CT showed no gallbladder-fossa bleeding. We postulate that excessive cranial traction on the gallbladder resulted in disruption of intraparenchymal hepatic vessels while the liver capsule remained intact, allowing substantial internal bleeding without externally visible capsular injury at time of operation. The subsequent demonstration of multifocal bleeding from segment IVb/V arterial branches, including variant supply from the gastroduodenal artery, supports an occult intra-parenchymal arterial injury. Variant peripheral arterial anatomy may make the bleeding source difficult to recognize laparoscopically and particularly amenable to endovascular treatment.
In this patient, early, severe pain was coupled with new onset anaemia despite the absence of haemodynamic compromise. A contained subcapsular space can accommodate substantial blood volume and may initially mask conventional signs of haemorrhage. Disproportionate pain, persistent vomiting and an unexplained haemoglobin fall should prompt early contrast-enhanced vascular imaging rather than attribution to expected postoperative pain or retained stones.
Although most cases of subcapsular haematoma have been described to have been managed by laparotomy and haematoma evacuation, or percutaneous drainage, De Castro et al. described delayed active bleeding from a segmental right hepatic branch treated by coil embolization, though the haematoma later became infected and required percutaneous drainage [3]. By comparison, the haematoma in this case was acute, exceeded 19 cm and arose from multiple arterial branches, yet gelatin-sponge embolization achieved durable haemostasis without infection or need for drainage. Importantly, subsequent rupture with haemoperitoneum did not represent clear embolization failure. In a stable patient without progressive extravasation, rupture may reflect decompression of an established haematoma rather than recurrent uncontrolled arterial bleeding. Decisions regarding repeat embolization or surgery should be driven by physiology and repeat vascular imaging, not haematoma size or haemoperitoneum alone. This case supports transarterial embolization for stable patients with active arterial bleeding, observation after haemostasis, drainage for infection and surgery for persistent bleeding or instability.
Acknowledgements
The authors would like to thank the surgical, interventional radiology, anaesthetic, nursing and allied health teams involved in the patient’s care for their contributions to her multidisciplinary management and recovery.
Conflicts of interest
None declared.
Funding
None declared.
Patient consent
Written informed consent was obtained from the patient for publication of this de-identified case and associated clinical details using the Oxford University Press Patient Consent Form.
