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Hydatid disease, caused by Echinococcus granulosus and multilocularis is seen commonly in the tropical countries and sheep rearing areas of New Zealand and Australia (Hadidi, 1979). The commonest organ affected is the liver but other organs that may be affected are spleen, kidneys, lungs, peritoneal cavity, and brain.
Ultrasonography not only determines the diagnosis of hepatic echinococcal cysts, but can also classify the cysts reflecting their pathology and natural history.
Echinococcal cysts are the larval stage of the Echinococcus tapeworm. The definitive host is a carnivore, usually a dog while man is the intermediate host. Hydatid disease of the liver may present as hepatomegaly, infection of cysts, rupture into the biliary tree with cholangitis and obstructive jaundice, or may remain asymptomatic (Lewall & Corkell, 1985).
Rarely, complications such as rupture into the peritoneal cavity, lung or colon, hydatid allergy, and membranous glomerulonephritis due to glomerular deposits of hydatid antigen may occur (Lewall & Corkell, 1985). Morphologically, these cysts are made up of an ectocyst composed of a multi layered acellular wall, and an endocyst, composed of a thin membrane. The pericyst is made up of compressed hepatic parenchyma, fibroblasts, and inflammatory cells arising in the surrounding hepatic parenchyma. These three layers and the free internal material (scoleces and brood capsule) account for the imaging features of echinococcal cysts.
A variety of ultrasonic appearances have been described with a natural maturational progression from single to multiple cysts, and then to a dead, calcified cyst (Beggs, 1983; Gharbi et al., 1981; Bezzi et al., 1987). When infected, hydatid cysts lose their characteristic sonographic appearances and appear diffusely hyperechoic. The various appearances include: type I, fluid filled cysts; type IR, lesions containing undulated membranes that represent detached endocyst secondary to rupture (sonographic water lily sign); type II, lesions that contain daughter cysts and/or formed echogenic material (matrix); and type III, dead, calcified lesions.
The gradual reduction in cyst size and the detachment is probably due to reduced ratio between fluid secretion and its resorption by the host parenchyma; a decreased production of cystic fluid with reduced pressure within the cyst may cause cyst regression and / or endocyst separation from pericyst (Bezzi et al., 1987). The changes in the echopattern and appearance of a pseudosolid or hyperechoic pattern are either following treatment or secondary infection (Bezzi et al., 1987; Lewall & Corkell, 1985). Given the risk of rupture with spill of cyst contents into the peritoneum, secondary infection, or rupture into the biliary tree, most lesions are resected. Well-calcified lesions are considered innocuous and if asymptomatic can be followed up without resection. In cases of inaccessible cysts, injection of sonographically guided scolicidal agents with drug therapy (albendazole) may be considered (Bret et al., 1988). spleen (4).
1. Beggs I. The radiological appearances of hydatid diseases of the liver. Clin Radiol 1983; 34: 555-63.
2. Bezzi M, Teggi A, Rosa FD, Capozzi A, Tucci G, Bonifacino A, Angelini L. Abdominal hydatid disease: US findings during medical treatment. Radiology 1987; 162: 91-5.
3. Bret PM, Fond A, Bretagnolle M, et al. Percutaneous aspiration and drainage of hydatid cysts in the liver. Radiology 1988; 168: 617-20.
4. Gharbi HA, Hassine W, Brauner MW, Dupuch K. Ultrasound examination of the hydatic liver. Radiology 1981; 139: 459-63.
5. Hadidi A. Ultrasound findings in liver hydatid cyst. J Clin Ultrasound 1979; 7: 365-8.
6. Lewall DB, Corkell SJ. Hepatic echinococcal cysts: sonographic appearances and classification. Radiology 1985; 155: 773-5.