Hepatitis A Virus Induced Acute Acalculous Cholecystitis Diagnosed Postoperatively: Case Report
Hepatitis A Virus Induced Acute Acalculous Cholecystitis Diagnosed Postoperatively: Case Report
41-year-old previously healthy patient presented with right upper quadrant abdominal pain. Pain started two days prior to presentation when an abdominal ultrasound in a peripheral hospital showed a 10 mm gallbladder stone with normal laboratory tests; however, her pain was resolved on analgesics. Now the pain was persistent and associated with vomiting and laboratory tests showed elevated bilirubin. Laparoscopic cholecystectomy with intraoperative cholangiography was done that showed inflamed gallbladder but with no stones and normal cholangiography. Day one post-operation, while the pain resolved, labs showed elevated liver function tests and hepatitis workup showed acute HAV infection attributing her presentation to HAV induced AAC.
Introduction: acute acalculous cholecystitis (AAC) is defined as gallbladder inflammation without the presence of stones. Contrary, hepatitis A virus (HAV) causes acute hepatitis A and can present with different symptoms; however, HAV causing and presenting as AAC is rare.
Case presentation: 41-year-old previously healthy patient presented with right upper quadrant abdominal pain. Pain started two days prior to presentation when an abdominal ultrasound in a peripheral hospital showed a 10 mm gallbladder stone with normal laboratory tests; however, her pain was resolved on analgesics. Now the pain was persistent and associated with vomiting and laboratory tests showed elevated bilirubin. Laparoscopic cholecystectomy with intraoperative cholangiography was done that showed inflamed gallbladder but with no stones and normal cholangiography. Day one post-operation, while the pain resolved, labs showed elevated liver function tests and hepatitis workup showed acute HAV infection attributing her presentation to HAV induced AAC.
Discussion: AAC is usually caused by stasis of the gallbladder due to different causes; however, HAV as the cause of AAC has been reported. While cholecystectomy is the mainstay treatment for AAC, this might not be the case for HAV induced AAC. For instance, unless there is necrotic gallbladder or persistence of symptoms, the AAC can be managed conservatively in this case. Even though our diagnosis was cleared post-operatively, had we know the diagnosis of HAV induced AAC before, we would still opt for surgery due to the severity and persistence of pain.
Conclusion: More cases should be reported and more studies should be done to further define the presentation and management of HAV induced AAC.
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