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