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