Tropical Medicine Central Resource

Imaging Diagnosis

The chronic granulomatous reaction which occurs in alveolar hydatid disease of the liver, with central necrosis and cavitation, may eventually result in characteristic calcifications. In 19 patients with alveolar hydatidosis from Alaska (Thompson et al), there was hepatomegaly in 42% and hepatic calcifications in 68%. Typically, the latter are small spheres with central radiolucencies and range from 2-4 mm in diameter (Fig. 3.159-3.163).

As with the more common unilocular cystic hydatid disease, there are many different ways to image alveolar cystic lesions in the liver. Ultrasound, CT, MRI and radionuclide scanning can be supplemented by selective hepatic or celiac arteriography, inferior vena cavography, and cholangiography. Each modality has a selected diagnostic role.

Scanning (US, CT or MRT) is the most effective way to identify the one or more masses which may develop within any part of the liver. As the lesions grow older, the wall thickens and a necrotic center develops, filled with debris. All methods of scanning may show displacement of the common bile duct and/or the right and left hepatic ducts and their branches within the liver caused by one or more alveolar hydatid masses (Figs. 3.162 & 3.163). Since these lesions are often of considerable size, the displacement of the biliary duct system may be pronounced. Contrast medium may leak during cholangiography from the bile ducts into a large necrotic lesion, partially outlining its ragged interior (Figs. 3.162 & 3.163).

Selective arteriography will likely show displacement of the hepatic artery branches around one or more avascular, often irregular filling defects in the liver; abrupt narrowing and cut-offs of arteries can be seen due to the diffuse infiltrating process. An inferior vena cavogram may reveal partial or complete obstruction of the IVC with collateral circulation via the azygos, hemiazygos, and lumbar venous plexus, if the liver mass has extended posteriorly or metastasized to regional lymph nodes, blocking the vena cava (Fig. 3.162D).

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Fig. 3.159 E. multilocularis calcifications in the liver of an asymptomatic 42-year-old Alaskan Eskimo woman who had skinned many foxes; there were also many dogs in her village. Except for occasional postprandial epigastric discomfort, she was otherwise asymptomatic. She had a diffusely nodular and slightly tender liver palpable 5 cm below the right costal margin. There was an 8% blood eosinophilia. Echinococcus hemagglutination and flocculation titers were strongly positive. (A) AP radiograph of the right upper quadrant shows the characteristic small radiolucencies surrounded by calcification, forming spheres measuring 2-4 mm in diameter (arrow). These calcifications were visible on a lumbosacral spine radiograph taken four years earlier and had increased in size in the interval. A radioisotope liver scan showed a large area of decreased uptake anteriorly in the region of the porta hepatis. Cholelithiasis was noted on oral choleccstogram and the calcified mass was anterior to the gallbladder. Hepatic arteriography showed an anterior avascular mass in the liver, possibly involving both lobes. At cholecystectomy, a pedunculated hydatid lesion was attached to the anterior inferior edge of the liver involving the right and left lobes without extensive parenchymal invasion in the bulk of the liver.
A radiograph of the surgically resected specimen (B) showed both scattered, amorphous, nondiagnostic calcium and the small radiolucencies surrounded by calcium thought to be diagnostic of alveolar hydatid disease (arrow). The resected hepatic tissue measured 10 x 8 x 8 cm and was virtually replaced by a large cyst with a thick irregular wall. At the periphery of this large cyst, there were multiple small cysts 5-6 mm in diameter, many of which budded from the wall of the large cyst while some were discrete within the adjacent liver parenchyma. The large cyst was filled with thick, white, pasty material and contained translucent membranes, forming small 2-4 mm translucent spheres. The small peripheral cysts were lined by such membranes and many contained clear fluid. (C) Section of the resected hydatid lesion showing necrotic, diffusely stippled (with finely divided calcium), amorphous material (center of lesion) containing pale eosinophilic, laminated membranes which were acellular, PAS positive, and diastase resistant. The small peripheral cysts ( bottom of lesion) were also lined by laminated membranes and surrounded by fibrous walls, which were separated from the liver parenchyma by a thin rim of granulation tissue and inflammatory cells. The calcification associated with these small cysts was primarily between the parasitic membranes and the adjacent fibrous wall, both as finely divided calcium and as somewhat larger granules. Focally, there were small calcific deposits between laminae of the parasitic membrane. There were also granulomas with necrotic centers surrounded by epithelioid cells, giant cells, and other inflammatory cells. No germinal epithelium or scolices were identified. (D) Enlargement of the cysts at the periphery of the multilocular lesion. (E) Photomicrograph showing a portion of one cyst with the cyst wall (right) and surrounding reactive tissue (center). Several liver cells are seen (lower left). (H & E, X 45) (A-E Courtesy of Dr. W. Thompson, et al, and AJR, 1972.) (F) Gross photograph of liver of another patient with alveolar hydatidosis, showing multiple cysts on the cut surface. (Courtesy of Drs. R.L. Rausch and D.H. Connor).

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Fig. 3.160 Typical E. multilocularis calcifications in the liver of a patient with surgically proven alveolar hydatid disease. (A) Oblique radiograph of the right upper quadrant. (B) The calcifications have shown some increase in extent six years later. (C) After another six years there is further increase in the amount of calcification. (D) Enlargement of an area in (C) shows numerous small radiolucencies surrounded by calcification, a finding felt to be diagnostic of alveolar hydatid disease. (Courtesy of Dr. W. Thompson, et al, and AJR, 1972).

		Imaging Diagnosis The chronic granulomatous reaction which occurs in alveolar hydatid disease of the liver, with central necrosis and cavitation, may eventually result in characteristic calcifications. In 19 patients with alveolar hydatidosis from Alaska (Thompson et al), there was hepatomegaly in 42% and hepatic calcifications in 68%. Typically, the latter are small spheres with central radiolucencies and range from 2-4 mm in diameter (Fig. 3.159-3.163). As with the more common unilocular cystic hydatid disease, there are many different ways to image alveolar cystic lesions in the liver. Ultrasound, CT, MRI and radionuclide scanning can be supplemented by selective hepatic or celiac arteriography, inferior vena cavography, and cholangiography. Each modality has a selected diagnostic role. Scanning (US, CT or MRT) is the most effective way to identify the one or more masses which may develop within any part of the liver. As the lesions grow older, the wall thickens and a necrotic center develops, filled with debris. All methods of scanning may show displacement of the common bile duct and/or the right and left hepatic ducts and their branches within the liver caused by one or more alveolar hydatid masses (Figs. 3.162 & 3.163). Since these lesions are often of considerable size, the displacement of the biliary duct system may be pronounced. Contrast medium may leak during cholangiography from the bile ducts into a large necrotic lesion, partially outlining its ragged interior (Figs. 3.162 & 3.163). Selective arteriography will likely show displacement of the hepatic artery branches around one or more avascular, often irregular filling defects in the liver; abrupt narrowing and cut-offs of arteries can be seen due to the diffuse infiltrating process. An inferior vena cavogram may reveal partial or complete obstruction of the IVC with collateral circulation via the azygos, hemiazygos, and lumbar venous plexus, if the liver mass has extended posteriorly or metastasized to regional lymph nodes, blocking the vena cava (Fig. 3.162D). .... ... ... Fig. 3.159 E. multilocularis calcifications in the liver of an asymptomatic 42-year-old Alaskan Eskimo woman who had skinned many foxes; there were also many dogs in her village. Except for occasional postprandial epigastric discomfort, she was otherwise asymptomatic. She had a diffusely nodular and slightly tender liver palpable 5 cm below the right costal margin. There was an 8% blood eosinophilia. Echinococcus hemagglutination and flocculation titers were strongly positive. (A) AP radiograph of the right upper quadrant shows the characteristic small radiolucencies surrounded by calcification, forming spheres measuring 2-4 mm in diameter (arrow). These calcifications were visible on a lumbosacral spine radiograph taken four years earlier and had increased in size in the interval. A radioisotope liver scan showed a large area of decreased uptake anteriorly in the region of the porta hepatis. Cholelithiasis was noted on oral choleccstogram and the calcified mass was anterior to the gallbladder. Hepatic arteriography showed an anterior avascular mass in the liver, possibly involving both lobes. At cholecystectomy, a pedunculated hydatid lesion was attached to the anterior inferior edge of the liver involving the right and left lobes without extensive parenchymal invasion in the bulk of the liver. A radiograph of the surgically resected specimen (B) showed both scattered, amorphous, nondiagnostic calcium and the small radiolucencies surrounded by calcium thought to be diagnostic of alveolar hydatid disease (arrow). The resected hepatic tissue measured 10 x 8 x 8 cm and was virtually replaced by a large cyst with a thick irregular wall. At the periphery of this large cyst, there were multiple small cysts 5-6 mm in diameter, many of which budded from the wall of the large cyst while some were discrete within the adjacent liver parenchyma. The large cyst was filled with thick, white, pasty material and contained translucent membranes, forming small 2-4 mm translucent spheres. The small peripheral cysts were lined by such membranes and many contained clear fluid. (C) Section of the resected hydatid lesion showing necrotic, diffusely stippled (with finely divided calcium), amorphous material (center of lesion) containing pale eosinophilic, laminated membranes which were acellular, PAS positive, and diastase resistant. The small peripheral cysts ( bottom of lesion) were also lined by laminated membranes and surrounded by fibrous walls, which were separated from the liver parenchyma by a thin rim of granulation tissue and inflammatory cells. The calcification associated with these small cysts was primarily between the parasitic membranes and the adjacent fibrous wall, both as finely divided calcium and as somewhat larger granules. Focally, there were small calcific deposits between laminae of the parasitic membrane. There were also granulomas with necrotic centers surrounded by epithelioid cells, giant cells, and other inflammatory cells. No germinal epithelium or scolices were identified. (D) Enlargement of the cysts at the periphery of the multilocular lesion. (E) Photomicrograph showing a portion of one cyst with the cyst wall (right) and surrounding reactive tissue (center). Several liver cells are seen (lower left). (H & E, X 45) (A-E Courtesy of Dr. W. Thompson, et al, and AJR, 1972.) (F) Gross photograph of liver of another patient with alveolar hydatidosis, showing multiple cysts on the cut surface. (Courtesy of Drs. R.L. Rausch and D.H. Connor). ... ... Fig. 3.160 Typical E. multilocularis calcifications in the liver of a patient with surgically proven alveolar hydatid disease. (A) Oblique radiograph of the right upper quadrant. (B) The calcifications have shown some increase in extent six years later. (C) After another six years there is further increase in the amount of calcification. (D) Enlargement of an area in (C) shows numerous small radiolucencies surrounded by calcification, a finding felt to be diagnostic of alveolar hydatid disease. (Courtesy of Dr. W. Thompson, et al, and AJR, 1972). Next Page Previous Page