Gallbladder perforation complicated by intrahepatic abscess: multimodal imaging diagnosis

Clinical History

Elderly woman with longstanding cholelithiasis, complaining of persistent fever, right hypocondrium pain, malaise and progressive weight loss for 3 months. Moderate pain evoked during liver palpation without frank Murphy’s sign.
Mild anaemia (12.1 g/dL), raised inflammatory markers (8800/mmc neutrophils, C-reactive protein 138 mg/L), ALP, GGT and LDH enzymes.

Imaging Findings

Ultrasound performed at another institution (not shown) detected cholelithiasis, gallbladder mural thickening and a vast hypoanechoic inhomogeneous pericholecystic lesion, initially interpreted as gallbladder cancer with parenchymal invasion.
Transferred to our hospital, the patient underwent contrast-enhanced MDCT with multiplanar reformations: a large multilobular, centrally hypodense lesion with peripheral enhancement occupied most of 4th and 5th liver segments, abutting the thickened enhancing gallbladder fundus.
Further investigation with contrast-enhanced MRI confirmed internally fluid-like liver abscess surrounded by oedematous parenchyma and allowed identification of fistulisation to the discontinuous gallbladder fundus. MRCP excluded abnormalities of both intrahepatic and common bile ducts.
Following MRI, focused ultrasonographic re-evaluation confirmed gallbladder with sludge content and dominant obstructing infundibular stone, plus fistulous communication identifiable between its fundus and adjacent hypoanechoic liver lesion.
Laparotomic surgery (including cholecystectomy with liver abscess drainage) and pathologic findings confirmed acute and chronic cholecystitis complicated by fistulous communication with intrahepatic abscess.

Discussion

Gallbladder perforation (GBP) is a rare but life-threatening complication of cholecystitis. Risk factors include advanced age, arteriosclerosis, diabetes, immunosuppression and steroidal treatment. GBP may occur acutely during cholecystitis or weeks after onset. Pathogenesis involves overdistension and increased intraluminal pressure from neck cystic duct obstruction causing mural oedema, ischemia and gangrene [1, 2].
Often GBP manifests acutely with right upper or diffuse abdominal pain, fever and vomiting along with variable peritoneal irritation, local tenderness or positive Murphy’s sign. Conversely, some patients present insidiously with malaise, weight loss and a palpable mass, mimicking a malignant process [1-4].
According to the 1934 Niemeier classification, spontaneous GBP is classically categorised as acute (type 1) with biliary peritonitis, subacute (type 2) with pericholecystic abscess and chronic (type 3) forms with fistulisation between the gallbladder and adjacent organs. Intrahepatic perforation with cholecystohepatic communication and liver abscess formation is even rarer, with less than 15 cases reported in literature, mostly diagnosed weeks to months after onset of acute cholecystitis symptoms [1, 5, 6].
Ultrasound may detect signs of cholecystitis along with most hepatic abscesses with varying degrees of internal echoes, but the gallbladder wall defect is rarely identified and misinterpretation as malignancy is not uncommon [3, 5, 6].
Currently, cross-sectional imaging allows correct diagnosis of complicated cholecystitis, differentiation from malignancy, planning and timing of laparoscopic or laparotomic surgery. Most usually, GBP is preoperatively diagnosed with CT, through identification of mural discontinuity, intramural/intraluminal gas or membranes, intraperitoneal air o ascites. Close inspection of the gallbladder wall may allow (in 70% of cases) identification of defects indicating perforation, most usually at the fundus [3, 7]. As with this case, pericholecystic or hepatic abscesses appear as unilocular hypoattenuating or otherwise complex, septated cystic lesions, usually well-demarcated with rim enhancement, whereas intralesional gas is uncommon [3, 4, 8].
MRI diagnoses acute cholecystitis and complications, proving useful with equivocal sonographic findings: abscesses appear as solitary or multilocular fluidlike lesion, usually with low T1 and high T2 signal intensities depending on their protein content, enhancing walls and identifiable perilesional oedema [4, 9]. In this patient, MRI allowed precise identification of gallbladder fundus perforation with cholecystohepatic fistulisation causing liver abscess formation.

Differential Diagnosis List

Final Diagnosis

Intrahepatic abscess due to perforated cholecystitis with cholecystohepatic communication

URL:	https://www.eurorad.org/case/9573
DOI:	10.1594/EURORAD/CASE.9573
ISSN:	1563-4086