Acute viral hepatitis: don't miss subtle and potentially misleading MRI signs

Clinical History

A 39-year-old overweight woman with a history of appendectomy and cholelithiasis presented to the emergency department suffering from nausea, epigastric pain, jaundice and dark urine.
Laboratory tests confirmed elevated serum bilirubin (total 10 mg/dL, direct 6 mg/dL) and prothrombin time, markedly increased liver enzymes (2700 U/L aspartate-, 3700 U/L alanine-aminotransferase).

Imaging Findings

Emergency ultrasound (Fig.1) showed homogeneous liver echotexture, cholelithiasis and a markedly thickened (1cm) stratified gallbladder wall: considering the local tenderness at physical examination, the attending surgeon suggested the possibility of acute cholecystitis.
However, the gallbladder was not overdistended and the leukocyte count was normal: therefore, radiologists opted for an early MR-cholangiopancreatography (Fig.2), which showed perihepatic and right parietocolic peritoneal effusion, non-dilated intrahepatic and common bile ducts, normal signal features of liver parenchyma on all sequences, including diffusion-weighted imaging (DWI), and "tram-track" hyperintensities consistent with periportal oedema. The thickened gallbladder wall showed fluid-like signal features and a visually low DWI signal indicating unrestricted diffusion, consistent with non-suppurative mural oedema from liver dysfunction.
Findings were interpreted as consistent with a serologic diagnosis of acute hepatitis with high viral load (3.000.000 UI/ml HBV DNA), which was treated with the antiviral drug tenofovir, lactulose, vitamin K supplementation, but without antibiotics.
A repeated ultrasound (Fig.3) at discharge showed regression of mural oedema.

Discussion

Acute viral hepatitis (AVH) is generally caused by hepatitis A, B (HBV), C, or E viruses, rarely by other agents such as herpes and Coxsackie viruses. Following the introduction of vaccines, the prevalence of HBV progressively decreased in industrialised countries. However, a HBV infection is still encountered in immigrants, in elderly and adult people without immunisation. Risk factors include cohabitation with HBV carriers, unsafe sexual activity, intravenous drug use and iatrogenic exposure. Regardless of the causative agent, AVH may range from a subclinical infection to fulminant liver failure. Characteristic manifestations include fever, jaundice, upper abdominal discomfort plus laboratory signs of hepatocyte necrosis, decreased liver function and hyperbilirubinemia. Most patients (95%) ultimately do not develop chronic hepatitis [1, 2].
Traditionally, the diagnosis of AVH relied on clinical features, consistent biochemistry and positive serologic tests, and the role of imaging was limited to a differential diagnosis from other disorders. Sonographically, the affected liver may appear enlarged with diffusely decreased echogenicity. On dynamic cross-sectional imaging, the most consistent feature of AVH is heterogeneous liver perfusion in the arterial phase, which reflects severity and is reversible as inflammation subsides. However, unremarkable ultrasound and CT appearances do not rule out AVH [3-5].
Nowadays, MRI is increasingly used even in emergency conditions to investigate acute hepatobiliary disorders, particularly in young patients or with equivocal clinical, laboratory and ultrasound findings. Its advantages include biological non-invasiveness, excellent tissue contrast and sensitivity for inflammation, visualisation of biliopancreatic ducts using MR-cholangiopancreatography [6, 7].
As in this case, radiologists shouldn’t miss subtle unenhanced MRI features of mild AVH, particularly the T2-weighted high signal “tracking” reflecting periportal oedema. Similar appearances, associated with biliary ductal abnormalities, are observed in bacterial cholangitis. In AVH, the liver parenchyma may appear normal on all sequences including diffusion-weighted imaging (DWI), or may show geographical oedematous changes [3-5].
Furthermore, AVH is generally (70% of cases) associated with ascites and oedematous gallbladder wall thickening reflecting transient liver dysfunction. Gallbladder thickening is often marked and should not be misinterpreted as cholecystitis, thus leading to inappropriate treatment including surgery. As in this patient, the routine use of DWI may be useful to rule out acute cholecystitis, in which the inflamed gallbladder is overdistended with mural hyperintensity on high b-value DWI images, visually low signal on apparent diffusion coefficient (ADC) maps, and pericholecystic fluid. Conversely, in liver failure and hypoproteinaemic states ascites is generally diffuse, and the non-suppurative mural oedema does not show restricted diffusion [5-9].

Differential Diagnosis List

Final Diagnosis

Cholestatic-type acute viral hepatitis B

URL:	https://www.eurorad.org/case/15035
DOI:	10.1594/EURORAD/CASE.15035
ISSN:	1563-4086