Teaching Case

A 6-year-old male patient presented with vomiting and 37,8°C temperature. He had returned from a holiday in Central Africa 3 weeks prior to the onset of symptoms. The clinical examination revealed localised pain in the right-upper quadrant and positive Murphy's sign. Laboratory test showed an important increased level of ALT, AST, LDH, total and conjugated bilirubin, CRP and serology positive for hepatitis A infection (HAV).

Abdominal ultrasound (US) showed: - A distended gallbladder with thickening and striated walls (alternating echogenic and hypoechoic layers); a little fluid collection and positive Murphy’s sign were seen; no visible calculi inside; - Enlarged liver with homogenous echotexture, without solid or cystic focal lesions; - Multiple small porta hepatise lymphnodes; - No splenomegaly; - No ascites.

Acute cholecystitis is an inflammation of the gallbladder that can be divided into two different forms: calculous cholecystitis, generally caused by the presence of gallstones (90%), and acalculous cholecystitis (AAC), related to bile stasis in gallbladder due to the hypomobility of the wall, which leads to an increased pressure within the organ [1]. AAC is more frequent among chronic, especially those who are under parenteral nutrition, traumatised or burned patients. Other less frequent risk factors are uncontrolled diabetes, vascular or infectious diseases [2]. HAV is a single-stranded RNA virus from the Picornaviridae family, and in humans the transmission is through the fecal-oral route of transmission. After ingestion, the virus reaches the portal system through the gastrointestinal tract, followed by a self-limiting infection of the liver. The incubation period is between 2 and 6 weeks [3]. The infection usually occurs with symptoms in adult patients, while it's more frequently asymptomatic in childhood. The most common symptoms include acute pain in the right-upper quadrant associated with nausea, fever, vomiting and a positive Murphy's sign. Less common symptoms are represented by acute liver failure, ascites, haematologic alterations, pericardial effusion, pleural effusion, nephrotic syndrome, pancreatitis, AAC, vasculitis, reactive arthritis [3-5]. US is the first tool readily available to evaluate AAC. Thanks to the B-mode technique is possible to evaluate wall thickening (>3 mm), wall striation, pericholecystic and perihepatic fluid, gallbladder distention, intramural gas, and echogenic bile or sludge in the lumen; positive sonographic Murphy sign may be present. Computed tomography (CT) is not performed for the preliminary study, but it can provide detailed information about possible complications such as ischaemia, infection, gangrene, and perforation that occurs in about 10% of cases. Magnetic resonance imaging (MRI) may be useful in AAC complicated but is not routinely used [6]. In childhood, AAC is a rare complication and imaging findings resolve when viremia levels go back to normal [7]. Generally, symptoms resolve completely and do not cause chronic disease. AAC by HAV is treated conservatively and surgical intervention is not indicated [8]. Although AAC is less common than acute lithiasic cholecystitis, it has higher morbidity and mortality because of patient’s chronic diseases or conditions are usually sicker at baseline [8]. Take home message: AAC is an unusual complication of HAV. US is the preferred initial imaging test and imaging findings must be correlated with the clinical and laboratory test of the patient. CT or MRI may be helpful in equivocal cases or to identify complications. Written informed patient consent for publication has been obtained.