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General Clinical Characteristics of Cystic Hydatid Disease

It is surprising how many cysts there may be in small children (and also in adults) or how large a single cyst can grow without any clinical complaints from the patient. The location of the cyst is clinically the important factor: in the chest or abdomen, cysts may remain silent for many years. In the brain, orbit, or spine they become clinically apparent much sooner. As a general rule, significant symptoms and physical evidence of the mass are unusual before the cyst has reached at least 10 cm in diameter: many deep cysts are not easily palpable until they are almost 20 cm in diameter. Hydatid cysts are long-lived and, in some human hosts, may remain viable for up to 53 years.

As already noted, the severity of the infection depends on the species, but clinically it is also the other two factors of location and spread, which strongly influence the way hydatidosis will develop in any patient: clinical symptoms result from increasing pressure from the cyst(s) or from the sequelae of cyst rupture. In some patients, trauma will rupture a cyst and the symptoms then depend on the position of the cyst and which way it leaks. Thus, there may be acute abdominal pain if rupture occurs within the abdomen. Fever and an acute hypersensitivity reaction, including urticaria and, rarely, anaphylactic shock or death, may occur after cyst rupture at any site. Numerous scolices are discharged from the ruptured cyst to give rise to new daughter cysts (secondary hydatidosis) (Figs. 3.30 & 3.31). If the primary cyst erodes into a vein, metastatic hydatidosis may develop in the lungs and other organs.

When a cyst ruptures in the lungs, there may be abrupt onset of coughing and expectoration. Cardiac hydatids may give rise to metastatic hydatids or cardiac tamponade; there may be dyspnea from mediastinal cysts compressing the trachea or a tension pneumothorax if rupture occurs into the pleura. Pressure symptoms such as bone pain, spontaneous fracture and deformity, hemorrhage due to erosion of a major vessel, and cerebral symptoms of epilepsy and blindness may all occur.

Many hydatids in the liver will remain clinically silent for a long time, but with gradual enlargement most patients will eventually have symptoms, which may vary from slight pain in the upper quadrant to severe biliary colic and jaundice following communicating rupture of the cyst and discharge of its contents into a major bile duct. Embolic obstruction of the biliary tract by daughters or fragments of the endocyst may result. Ruptured cysts may undergo suppuration and clinically mimic a hepatic abscess.

The clinical spectrum is wide and satisfactory imaging is only possible if the radiologist has a clear perception of the natural history of hydatid disease and what happens during treatment. It is equally important to know the capabilities of the different methods that are available to image hydatid disease, so that the best choice for the patient can be made.

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Copyright: Palmer and Reeder