Abstract
Fascioliasis is caused by Fasciola
hepatica or Fasciola gigantica which are transmitted by ingesting raw
contaminated freshwater plants. Sheep and cattle are definite hosts with snails
being intermediate and humans are incidental hosts1.
The clinical manifestations are divided into two phases. Acute hepatic phase
occurring 6 to 12 weeks of ingestion with abdominal pain, fever, anorexia, loss
of appetite and weight, myalgia and marked eosinophilia. Chronic hepatic phase
starts from about 6 months to up to 10 years or more. Most are asymptomatic but
can develop common bile duct obstruction, gall bladder stones, cholangitis,
biliary cirrhosis and sclerosing cholangitis.
Keywords: Gall stone, Cholecystitis,
Adolescent, Abdominal pain
1. Case Study
A 13-year-old boy presented with abdominal pain, low grade fever
and non- bilious vomiting. Examination showed right upper quadrant tenderness,
hemodynamic stability with other systemic examinations being normal.
Investigations: WBC 19,000 cells/cu mm (polymorphs 74%, eosinophils 8%); CRP
100mg/dl; normal liver function test (LFT) and negative hepatitis serology (A,
B and E). Ultrasound abdomen showed partially distended gall bladder with
diffuse thickening of the wall, calculus of 1.5 cm and significant peri portal
lymphadenopathy. Clinical features were fitting with diagnosis of
cholecystitis, hence underwent laparoscopic cholecystectomy. Nodules over the
right lobe of liver were noted.
Histopathology of the nodules
showed features of Fascioliasis. Stool complete analysis showed eggs of both
Fasciola hepatica and Ascaris lumbricoides. He was commenced on Nitazoxanide
and Albendazole. After 2 days of treatment, developed jaundice, upper abdominal
pain, recurrent non-bilious vomiting and tender hepatomegaly was present.
Investigations showed increased inflammatory markers (WBC counts 34000 cells/cu
mm, CRP 89 mg/dl, increased total bilirubin 5.73mg/dl with predominant
conjugated hyperbilirubinemia (5.35mg/dl) and elevated liver enzymes (AST
91U/L, ALT 219U/L). In view of history fitting with cholangitis, was started on
broad spectrum antibiotics. MRI with MRCP showed abrupt narrowing at proximal
common hepatic duct and features of cholangitis. ERCP showed biliary stricture
and common bile duct stenting was done. Gradually improved clinically and
biochemically with hyperbilirubinemia/transaminases resolving. On follow up, he
gained weight with normalizing LFT.
Fascioliasis is caused by Fasciola
hepatica or Fasciola gigantica which are transmitted by ingesting raw
contaminated freshwater plants. Sheep and cattle are definite hosts with snails
being intermediate and humans are incidental hosts1.
The clinical manifestations are divided into two phases. Acute hepatic phase
occurring 6 to 12 weeks of ingestion with abdominal pain, fever, anorexia, loss
of appetite and weight, myalgia and marked eosinophilia. Chronic hepatic phase
starts from about 6 months to up to 10 years or more. Most are asymptomatic but
can develop common bile duct obstruction, gall bladder stones, cholangitis,
biliary cirrhosis and sclerosing cholangitis2.
Diagnosis is based on the clinical
picture, detection of eosinophilia, abnormal LFT, elevated ESR, typical
findings on ultrasound or computed tomography scans and identification of
Fasciola eggs in stool and duodenal or biliary aspirates3. It is treated with Triclabendazole or
Nitazoxanide. Our patient presentation fits with chronic hepatic phase and
symptoms due to cholecystitis followed by cholangitis improving with treatment.
2. Conclusion
Fascioliasis is treated with
Triclabendazole or Nitazoxanide. Our patient presentation fits with chronic
hepatic phase and symptoms due to cholecystitis followed by cholangitis
improving with treatment.
3. References