Persistent Pyrexia after Portal Vein Embolisation: Diagnostic Contribution of ¹⁸F FDG PET/CT

INTRODUCTION

Radical surgeries of the malignant neoplasm limited to the biliary tract and liver parenchyma require major liver resections. Portal vein embolisation (PVE) is an image-guided technique that induces hypertrophy of the future liver remnant (FLR) by diverting portal venous flow toward the nontumorous liver parenchyma. The production of intrahepatic growth factors and cytokines, such as transforming growth factor-α, tumour necrosis factor-α, and hepatocyte growth factor, and the release of nitric oxide from altered portal pressure, induce hepatic hypertrophy. PVE is typically performed under ultrasound guidance via a percutaneous transhepatic approach. Alternative access routes include transileocolic and trans-splenic approaches.^[1] Embolic agents used include absolute ethanol, polyvinyl alcohol, gelatin sponge, fibrin glue, NBCA–lipiodol mixtures, and polidocanol foam, often used alone or in combination with coils or vascular plugs.^[2,3]

PVE is generally well tolerated, with patients rarely experiencing nausea, fever, or pain,^[4] Complications of PVE include subscapular hematoma, hemobilia, hemoperitoneum, vascular injuries, pneumothorax, and cholangitis. In experienced hands, the incidence of minor and major complications is up to 25% and 5%, respectively.^[5] In rare cases, PVE may be complicated by infection, presenting as cholangitis, liver abscess, or systemic sepsis. These infections adversely affect liver regeneration and are associated with poor outcomes following major hepatectomy. These patients have higher postoperative serum bilirubin levels, increased morbidity, and longer hospital stays compared to those without.^[6] Here, we report a case of PVE-induced hepatic infection in a suspected case of gall bladder carcinoma who initially underwent percutaneous transhepatic biliary drainage (PTBD) followed by PVE, subsequently developing infection in the embolized hepatic segments. However, imaging features of post-PVE hepatic infections, particularly on ¹⁸F FDG PET/CT, remain poorly described. We report a case highlighting the diagnostic utility of ¹⁸F FDG PET/CT in persistent pyrexia following PVE.

CASE REPORT

A 27-year-old male presented with a two-month history of progressive, painless jaundice, characterised by yellowish discolouration of the sclera, dark-coloured urine, and pruritus. There was no history of fever or abdominal pain. Baseline laboratory evaluation revealed cholestasis with markedly elevated serum alkaline phosphatase (ALP: 347 U/L, normal range 35-150) and total bilirubin (34.9 mg/dL, normal range 0.1-1.3), including a conjugated fraction of 13.16 mg/dL (0-0.4). Serum carbohydrate antigen (CA 19-9) was elevated at 299 U/mL (<37).

Ultrasonography demonstrated gallbladder wall thickening with distal common bile duct obstruction. Contrast-enhanced computed tomography revealed significant bi-lobar intrahepatic biliary radicle dilatation with irregular gallbladder wall thickening. Magnetic resonance cholangiopancreatography (MRCP) revealed wall thickening involving the body and neck of the gallbladder, with contiguous extension into the cystic duct, common hepatic duct, and reaching up to the primary biliary confluence. Both secondary confluences were patent. The patient underwent bi-lobar PTBD of liver segments III and VI. Following PTBD, serum bilirubin levels declined to 8.9 mg/ dL. [¹⁸F]FDG PET/CT was performed for metastatic workup, which revealed tracer-avid, irregular, asymmetrical gallbladder wall thickening involving the body and neck [Fig 1 A-E].

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Fig 1: (A-E): Before embolization - (A) Maximum intensity projection (MIP) image of baseline ¹⁸F FDG PET/CT done before PVE with abnormal increased tracer uptake in Gall bladder (green arrow). (B and C) Irregular asymmetrical GB wall thickening ~ 1.0 cm (green arrow in B), with SUVmax 5.0 (green arrow in C). (D) - Normal hepatic parenchyma with (E) CBD stent in-situ (yellow arrow in E); (F-J): 4 weeks after embolization – (F) Maximum intensity projection (MIP) image of ¹⁸F FDG PET/CT done 4 weeks after embolization showing increased FDG uptake of liver in branching pattern (yellow arrow) & diffuse bone marrow hypermetabolism (SUVmax- 4.1) reflecting sepsis induced bone marrow activation (blue arrows). (G) GB wall thickening with increased tracer uptake, SUVmax 10.4 (green arrow). (H) Corresponding axial, (I) Coronal and (J) Sagittal plane views of liver showing increased FDG uptake (SUVmax 7.2) in branching pattern along the embolization territory (yellow arrows in H-J).

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In view of planned major hepatic resection, the patient underwent right portal vein and hepatic vein embolisation to induce hypertrophy of the future liver remnant (FLR). The immediate post-procedural period was uneventful, and the patient was discharged after two days in stable condition, being afebrile, pain-free, and hemodynamically stable. One week later, the patient developed high-grade fever and abdominal pain. He was admitted, and laboratory investigations showed raised ALP (356 U/L), total bilirubin (2.47 mg/dL), conjugated bilirubin (1.22 mg/dL), with transaminases (AST: 46 U/L, ALT: 28 U/L). He had anaemia (Hb 7.9 g/dL), leucocytosis (TLC 23.28 × 10³/µL) with absolute neutrophilia (84%). Initial blood and bile cultures were negative. The patient remained persistently febrile despite empirical antibiotic therapy.

The patient was again referred for ¹⁸F FDG PET/CT four weeks following Portal vein embolisation (PVE) to evaluate pyrexia of unknown origin. The study revealed a metabolically active gallbladder mass, linear hyperdensities along embolized vascular branches with corresponding linear FDG uptake, and the uptake was extending in a branching pattern along respective vascular territories. No discrete abscess was noted. Mild diffuse bone marrow uptake was noted [Fig 1 F-J]. Microscopy and bile cultures were performed from both PTBD drainage tubes. Bile culture from the segment VI drain grew Pseudomonas aeruginosa, confirming a localised post-interventional infective complication. The patient started on treatment with ceftazidime and sulbactam, following which clinical and laboratory improvement was observed, including a decline in serum bilirubin levels. After remaining afebrile for 3 consecutive days and achieving clinical stabilisation, the patient was taken up for surgery in the following week. A staging laparoscopy was performed, followed by right modified hepatectomy with caudate lobectomy and left duct hepaticojejunostomy.

DISCUSSION

Portal vein embolisation (PVE) is considered a safe, preoperative intervention to induce hypertrophy of the future liver remnant (FLR) before major hepatectomy. Post-embolisation fever or post-embolisation syndrome is a common complication. It classically presents with low- to moderate-grade fever (often >38°C), pain, nausea, and occasionally leucocytosis within 1–3 days of the procedure. The fever is usually self-limited, related to the tumour site, hepatic ischemia–necrosis, and cytokine release, and not due to infection in the vast majority of cases.^[7] True infectious complications (bacteremia, liver abscess) are very rare (<0.2–0.5% of procedures), clinically important, and may adversely impact outcomes. have a high in-hospital mortality of 9.6%.^[8] They present with prolonged high-grade fever, hemodynamic instability, focal signs on imaging, and leucocytosis and liver dysfunction. In the present case, the patient developed persistent fever and deranged biochemical parameters, along with marked leucocytosis and absolute neutrophilia. These findings occurred one week after the procedure, beyond the expected time window (1-3 days) of post-embolisation syndrome (PES), and are therefore more suggestive of a true infective complication.

Pre-existing biliary-enteric anastomosis, external drainage, malfunctioning , diabetes mellitus, and residual iodised oil from TACE procedures predispose to hepatic abscesses. The inadequate function of the duodenal predisposes the to bacterial influx from the bowel.^[9] Patients with PTBD are at risk due to biliary contamination and bacterial translocation into the embolized liver segments.^[10,11] The combination of ischemic hepatic parenchyma and colonised bile creates a favourable milieu for infection, leading to cholangitis, infected necrosis, or hepatic abscess. ¹⁸F FDG PET/CT may play a valuable adjunctive role in the early detection of post-procedural hepatic infection before the dissemination to systemic sepsis manifestations. It may allow the timely initiation of antibiotic therapy, preventing clinical deterioration.^[12] On ¹⁸F FDG PET/CT, the differential diagnosis in this setting includes post-embolisation syndrome (PES), infection (hepatic abscess), cholangitis, and tumour progression. Post-embolisation syndrome (PES) typically demonstrates mild, diffuse homogeneous uptake, whereas hepatic abscess shows intense rim uptake with central photopenia, cholangitis presents with linear uptake along the biliary tree, and tumour progression manifests as focal nodular uptake with a corresponding CT lesion.^[13] In the present case, the delayed timing, persistent clinical symptoms, and FDG uptake along the PVE territory in a branching pattern favoured an infective aetiology over PES. The existing literature provides limited data on the imaging characteristics of hepatic infections after PV.^{[5, 14-16]} This knowledge gap is pronounced for ¹⁸F FDG PET/ CT, where systematic descriptions of imaging patterns, diagnostic pitfalls, and differentiation from post-procedural inflammatory changes or tumours remain scarce. Existing evidence suggests that ¹⁸F FDG PET/CT demonstrates increased uptake in infectious and inflammatory processes, facilitating early detection of infection. However, its role in accurately identifying and characterising post-PVE hepatic infections in this specific clinical setting remains inadequately defined, highlighting the need for further studies. This case highlights a distinctive ¹⁸F FDG PET/CT pattern and differs from focal abscess patterns described in previous studies.

CONCLUSION

Post-portal vein embolisation hepatic infection is a rare but clinically significant condition. ¹⁸F FDG PET/CT demonstrates characteristic segmental, linear branching uptake. It suggests potential utility in early diagnosis, the initiation of appropriate culture-guided antimicrobial therapy, and aids in early detection of systemic sepsis.