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Print version ISSN 1413-8670
Braz J Infect Dis vol.13 no.1 Salvador Feb. 2009
Luiz José de SouzaI,II; Lílian Costa BragaII; Natally de Souza Maciel RochaII; Rachel Ribeiro TavaresII
IThe Brazilian Society of Internal Medicine
IIDengue Reference Center; Campos dos Goytacazes, RJ, Brazil
Acute viral hepatitis A is a common systemic infection in children, especially in developing countries. Acute acalculous cholecystitis in the course of this infection is a rare and poorly reported event that needs to be diagnosed because of the possibility of complications, such as gangrene and perforation of the gallbladder wall. We present the case of a 16-year-old teenager with clinical and ultrasonographic findings of acalculous cholecystitis during an episode of hepatitis A virus infection, which took place December 2007 in Plantadores de Cana Hospital.
Key-Words: Acute viral hepatitis A, acute acalculous cholecystitis.
Hepatitis A is a benign viral infection (HAV), self-limiting, common in childhood [1-5] and frequent in developing countries . Even though the majority of cases are asymptomatic, clinical presentation can begin with nausea, vomiting, diarrhea, fever and jaundice. Usually the recovery period ranges from two to three weeks. The main laboratorial alterations are: leukopenia, lymphocytosis, signs of altered hepatic functions and hepatitis IgM serology. Thrombocytopenia alone is a marker of severity . The main complications of HAV are acalculous cholecystites [1,2,4,7-12], ascites, pleural effusion [1,5,9] and acute renal failure [13-15].
Acute acalculous cholecystitis (AAC) is inflammation of the gallbladder free from calculi, clinically characterized by a state of typical biliary pain, jaundice, and mass in the right hypochondrium, which often is perceived as acute abdominal pain. The diagnosis is suspected clinically and then confirmed through ultrasound. When there is a delay in diagnosis, gangrene or perforation of the gallbladder wall can occur.
We report a case of acute acalculous cholecystitis as a complication of acute viral hepatitis A in a male teenager.
The patient, F.J.S.R.J., a 16-year-old male, born and raised in Campos dos Goytacazes, had complaints of abdominal pain, fever, nausea, vomiting and cephalalgia; he was admitted during the sixth day of evolution to the Plantadores de Cana Hospital. His medical history was unremarkable; there was no history of drug hypersensitivity or drug abuse. On physical examination, he presented fatigue, diffuse abdominal pain to superficial and deep palpation, and no abdominal masses or signs of peritoneal irritation. On the following day, laboratory studies revealed leukopenia with lymphocytosis and absence of band neutrophils, thrombocytopenia, decreased erythrocyte sedimentation rates (ESR), hyperbilirubinemia, mostly due to an increase in direct bilirubin, a large increase in liver enzymes levels, and anti-HIV serology and dengue fever antigen both negative. Only symptomatic medication was administered to the patient and he maintained similar clinical and laboratory findings during five days.
On the 11th day of illness, the patient's general state worsened. His abdominal pain and vomiting frequency increased, and he developed choluria and mild jaundice. Physical examination revealed a distended abdomen, with pain in the right upper quadrant, positive Murphy and Blumberg signs and reduced peristaltic sounds. Laboratory studies found leukopenia, increased total bilirubinemia liver enzymes, prolonged prothrombin time (PT), serum amylase and lipase within normal limits, negative anti-dengue fever IgM serology and positive hepatitis A IgM serology (using The Abbott Axsym microparticle enzyme immunoassay method). Abdominal ultrasound did not show dilation and tortuosity of the intra and extra hepatic bile ducts; his gallbladder wall was thickened (7.0 mm) and surrounded by echogenic content; there was no lithiasis inside the gallbladder (Figure 1). When the surgeon was contacted, he decided to follow a conservative treatment.
On the 16th day of illness, the patient had an improvement in his general state. Complementary exams showed a marked decrease in liver enzymes, normalization of the PT and persistence of hyperbilirubinemia due to direct and indirect bilirubin levels. On ultrasound scan, the liver appeared with enlarged dimensions, a smooth surface and homogeneous echogenicity (Figure 2); the gallbladder presented with the same aspect as previously (Figure 3) and a small quantity of fluid was visible at the anterior wall of the liver (Figure 4). The results of laboratory tests are shown in Table 1.
Fourteen days after admission, symptoms and signs gradually regressed. The patient was dismissed from the hospital and was referred to outpatient monitoring.
The case report here describes a hepatitis A virus infection that developed into severe acalculous cholecystitis. This complication is rare and poorly reported in the international literature [1-5]; this is the first Brazilian report of this type of event.
Even though the majority of cases are asymptomatic, the clinical presentation can begin abruptly with nausea, vomiting, diarrhea, fever, jaundice, asthenia, reduced appetite and abdominal distention. Usually the recovery period ranges from two to three weeks, with no development of a chronic infection or a carrier state. The main laboratorial alterations are: leukopenia, lymphocytosis, signs of altered hepatic functions and hepatitis A IgM serology. Specific laboratorial findings indicate a greater possibility of complications, such as thrombocytopenia, which alone is a marker of severity . Kim et al.  found that a group of patients with hepatitis A that presented thrombocytopenia not only had delayed recovery, but also had more frequent complications.
The possible complications of HAV are acalculous cholecystites [1,2,4,7-12], ascites, pleural effusion [1,5,9], transitory sinus bradycardia , acute renal failure [14,15], massive hepatic necrosis and fulminating hepatitis, the latter two complications being more common in the elderly. Acute acalculous cholecystitis (AAC) is the inflammation of the gallbladder free from calculi, clinically characterized by a state of typical biliary pain, jaundice, and a mass in the right hypochondrium, which many times simulates acute abdominal pain. The diagnosis is suspected clinically and then confirmed through ultrasound. The ultrasonographic criteria for diagnosing AAC include: (1) gallbladder distention; (2) thickening of the gallbladder wall (>3.5mm); (3) no acoustic shadow or biliary sludge; (4) perivesical liquid accumulation , and (5) no dilation of the intra- and extra hepatic bile ducts . The sensitivity of ultrasound for detection of AAC is 88.9%, the specificity and accuracy are 97.8 and 96.1%, respectively . Treatment is initially conservative [10,16], with indications for urgent cholecystectomy in cases of gangrene or perforation of the gallbladder wall.
Mourani el al.  reported a case of AAC caused by HAV in which a cholecystectomy was performed, followed by a biopsy with pathological and immunohistochemical analysis. Microscopic examination revealed severe portal inflammation, pericholangitis, hepatic cholestasis and lymphocytes in the gallbladder. The immunohistochemical analysis revealed the viral antigen in the gallbladder epithelium and in the intra- and extrahepatic bile ducts. These findings suggest three possible physiopathological mechanisms of AAC associated with hepatitis A. The presence of lymphocytes in the gallbladder inflammatory process suggests that the lesion is mediated by immunological mechanisms. The presence of the viral antigen in the biliary epithelium is consonant with direct viral invasion coming from the liver, while the presence of the antigen in the bile ducts suggests ascendant infection.
The case reported here referred to an adolescent who presented HAV, confirmed sorologically, with thrombocytopenia at the beginning of the disease, developing by the 11th day of disease, with symptoms suggestive of acute cholescystitis. On ultrasound examination, the vesicular inflammatory process was confirmed; however, no calculi or indirect signs of lithiasis were found. Thus, AAC was confirmed, based on the ultrasonographic criteria mentioned above.
Despite the severity of the patient's clinical manifestations, the patient received a conservative treatment under assisted monitoring. Clinical evolution was favorable, thus, surgical intervention was not necessary.
Acute acalculous cholecystitis is a rare complication of hepatitis A. Although there are only a few cases in the literature in which the clinical state is suggestive of cholecystitis during HAV, especially in the presence of thrombocytopenia, it is important to take into account the possibility of acute acalculous cholecystitis due to the complications it may cause, such as gangrene and perforation of the gallbladder wall.
1. Mourani S., Dobbs S.M., Genta R.M., et al. Hepatitis A virus - associated cholecystitis. Ann Intern Med 1994;120(5):398-400. [ Links ]
2. Ozaras Resat, Mert Ali, Yilmaz Mehmet Halit, et al. Acute viral cholecystitis due to hepatitis A virus infection. J Clin Gastroenterol 2003;37(1):79-81. [ Links ]
3. Saxena S.K. Acute viral cholecystitis in viral hepatitis. J Assoc Physicians India 1994;42(5):428. [ Links ]
4. Basar O., Kisacik B., Bozdogan E., et al. An unusual cause of acalculous cholecystitis during pregnancy: hepatitis A virus. Dig Dis Sci 2005;50(5):1532. [ Links ]
5. Black M.M., Mann N.P. Gangrenous cholecystitis due to hepatitis A infection. J Trop Med Hyg 1992;95(1):73-4. [ Links ]
6. Kim H.S., Kim H.S., Lee J.Y., et al. Initial thrombocytopenia as a simple, valuable predictor for clinical manifestation in acute hepatitis A. Scand J Gastroenterol 2008;43(7)81-8. [ Links ]
7. Casha P., Rifflet H., Renou C., et al. Acalculous acute cholecystitis and viral hepatitis A. Gastroenterol Clin Biol 2000;24(5):591-2. [ Links ]
8. Andrea Venuta, Paolo Bertolani. Acute Cholecystitis in a child with HAV infecção. The internet Journal of Pediatrics and Neonatology 2007;6(2). [ Links ]
9. Ciftci A.O., Karnak I., Tanyel F.C. The association of hepatitis A virus infection, acalculous cholecystitis and blunt abdominal trauma: a diagnostic challenge. Journal of Pediatric Gastroenterology and Nutrition 2001;32:92-4. [ Links ]
10. Hermier M., Descos B., Collet J.P., et al. Acute cholecystitis disclosing A virus hepatitis. Arch Fr Pediatr 1985;42(7):525-9. [ Links ]
11. Friberg J., Sönstabö R., Tjick J.G., et al. Eur J Radiol 1987; 7(2):153. [ Links ]
12. Dalgiç N., Ince E., Öncel S., Günes M. Acute viral acalculous cholecystitis due to viral hepatitis A. Dahili Bilimler Medical Sciences 2005;58:78-80. [ Links ]
13. Tanir G., et al. Transient sinus bradycardia in a child during the course of acute hepatitis A. Turk J Gastroenterol 2007;18(3):195-7. [ Links ]
14. Parakkadavathu R.T., Pisharath S.V., Chekkura A.P., et al. Acute renal failure in a patient with non-fulminant hepatitis A infection. Saudi J Kidney Dis Transpl 2007;(3):422-5. [ Links ]
15. Song K.S., Kim M.J., Jang C.S., et al. Clinical features of acute viral hepatitis A complicated with acute renal failure. Korean J Hepato 2007;13(2):166-7. [ Links ]
16. Imamoglu M., Haluk S., Sari A., Ahmetoglu Ali. Acute acalculous cholecystitis in children: diagnosis and treatment. Journal of Pediatric Surgery 2002;37(4)36-9. [ Links ]
17. Wu G.M., Laing F.C. Acute acalculous cholecystitis. BrighamRAD. 1994. [ Links ]
18. Weelde B.J., Oudkerk M., Koch C.W. Ultrasonography of acute cholecystitis: clinical and histological correlation. Diagn Imaging Clin Med 1986;55(5)190-5. [ Links ]
Address for correspondence:
Dr. Luiz José de Souza
Sociedade Brasileira de Clínica Médica/RJ
Avenida Alberto Torres, 217 - Centro
Zip code: 28035-580
Campos dos Goytacazes - Rio de Janeiro - Brazil
Telephone/Fax number: (22) 2723-9243
Received on 10 July 2008; revised 18 January 2009.