Annals of African Medicine Annals of African Medicine Society ISSN: 1596-3519 Vol. 10, Num. 2, 2011, pp. 193-195

Annals of African Medicine, Vol. 10, No. 2, April-June, 2011, pp. 193-195

Letter to the Editor

Acute acalculous cholecystitis due to hepatitis A infection in a child: A rare cause of acute abdomen

Özkan Herek¹, Nergül Çördük¹, Duygu Herek², Senol Bagci¹

¹ Department of Pediatric Surgery, Pamukkale University, Denizli, Turkey
² Department of Radiology, Pamukkale University, Denizli, Turkey

Correspondence Address: Özkan Herek Department of Pediatric Surgery, Pamukkale University, Denizli Turkey oherek@pau.edu.tr

Code Number: am11040

PMID: 21691032

DOI: 10.4103/1596-3519.82059

Dear Sir,

Hepatitis A virus (HAV) infection is common in the developing countries. Although HAV infection usually has a benign clinical course, it may exceptionally cause the fulminan hepatitis, pleural effusion, ascites, acute cholecystitis. ^{[1],[2],[3],[4]} Acute acalculous cholecystitis due to HAV infection is very rarely reported in childhood. However, it may cause misdiagnosis and mistreatment when it occurs. For this reason, HAV infection should be kept in mind in differential diagnosis of acute acalculous cholecystitis. In this paper, we describe a case with acute cholecystitis due to HAV infection, and discuss the diagnostic challenge.

A 9-year-old boy presented with a five-day history of nausea, vomiting, fever, and a two-day history of abdominal pain. He was admitted to another hospital where an ultrasound (US) examination revealed a gallbladder wall thickening and pericholecystic free fluid. Then he was transferred to our department with a presumed diagnosis of gallbladder perforation. On admission to our department, his body temperature was 37.9 ⁰ C, heart rate was 84 beats/min, blood pressure was 100/55 mmHg, and mild jaundice of skin and sclera was present. At physical examination, we found tenderness and pain on the right upper quadrant. The liver was palpable, 4 cm below the costal margin. Laboratory findings were as follows: hemoglobin level, 15.1 g/dl; white blood cell count (WBC), 8100/mm ³ ; platelet count, 254 000/mm ³ ; C-reactive protein (CRP), 0.63 mg/dl; total bilirubin, 4.8 mg/dl; conjugated bilirubin, 3 mg/dl; albumin, 3.6 g/dl; aspartate aminotransferase, 2261 IU/L; alanine aminotransferase, 2586 IU/L; alkaline phosphatase, 276 IU/L; gamma glutamyl transferase, 192 IU/L; amylase, 34 IU/L. Serological screening test for hepatitis revealed positive anti-HAV IgM [38.89 (+)] and anti-HAV IgG [>76 (+)]. The surface antigen and antibodies to hepatitis B and C were negative. On the radiological examinations, plain abdominal radiography and chest X-ray were normal. US showed that the gallbladder was contracted with thick edematous wall [Figure - 1]. The thickness of gallbladder wall was measured as 9.8 mm. No gallstones were present. In addition to these findings, intra-abdominal free fluid was found mainly in pericholecystic area, Morrison pouch, and pelvic region [Figure - 2]. We decided to treat conservatively, because WBC count and CRP were normal and hepatitis A antibodies were positive. During the follow-up, he remained afebrile and clinically well. The pain and tenderness on the right upper quadrant of abdomen were regressed by the conservative treatment. On the fifth day, the thickness of the gallbladder wall was found to be 9.7 mm. Intra-abdominal fluid was seen only at pericholecystic area. On the same day, we started peroral feeding and he tolerated. On the seventh day, US showed that the thickness of the gallbladder wall was 8 mm. There was no abdominal fluid. In addition to these findings, an enlarged lymph node (11 x 15 mm in size) located in the hepatic hilum appeared on this US examination. On the 10 ^th day, the findings of abdominal examination were completely normal. The thickness of gallbladder wall was found to be 5.8 mm and the size of the lymph node was 16 x 10 mm as well. He was discharged on the 10 ^th day of his admission. On the 25 ^th day of the follow-up, the thickness of gallbladder wall was found to decrease nearly to normal values (2.7 mm), and the enlarged lymph node had disappeared. During the 6 months follow-up period, he was doing well.

Hepatitis A infection usually has a benign and self-limited clinical course. However in the literature, gangrenous cholecystitis, pleural effusions, and ascites due to HAV infection are rarely reported. ^{[1],[2],[3],[4]} Although these complications of HAV infection are very rare, gallbladder abnormalities commonly occur during acute viral hepatitis infections. ^[5],[6] These abnormalities include gallbladder wall thickening, gallbladder sludge, double-wall appearance. Maudgal et al.^[5] found a significant increase in the gallbladder wall thickness (5.16 ± 0.4 mm) in patients with viral hepatitis compared with the control group (2 ± 0.06 mm) in their study. In another study, Sharma and Dasarathy ^[6] prospectively evaluated gallbladder abnormalities in acute viral hepatitis. They reported that gallbladder wall thickness significantly increased (mean 6.1 ± 4.3 mm) in 98% of the patients with acute viral hepatitis and there was complete resolution in 96.4% of the cases within 12 weeks. ^[6] Recently, Toppet et al. ^[7] found a new sonographic feature in addition to gallbladder wall thickening. They reported that enlarged lymph node in the hilum of the liver were seen in all of the cases with acute viral hepatitis A at US examination. This finding was previously reported as an operator observation by Black and Mann. ^[1] This may be a more diagnostic finding for acute viral hepatitis than only gallbladder wall thickening which may occur in other clinical conditions such as cirrhosis, hypoalbuminemia, chronic renal failure, cardiac failure, or Kawasaki disease. ^[2],[3] In conclusion, although gangrenous cholecystitis and perforation due to HAV infection are previously reported in childhood, generally the gallbladder abnormalities seen in the disease have a benign course and are self-limited. Generally, when perforation or other causes are excluded, acute cholecystitis due to HAV infection is treated satisfactorily by conservative treatment. However, it can easily be misdiagnosed or mistreated when it is not kept in mind as differential diagnosis or when it is complicated with ascites or pleural effusions. In these situations, the detection of the gallbladder wall thickening/enlarged lymph nodes at the hilum by US or computerized tomography may be very useful in prompt diagnosis of complicated HAV infection.

References

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