Hydatid cysts in the pulmonary artery: A rare cause of pulmonary embolism

A 38-year-old man presented with complaints of haemoptysis and dyspnoea. His physical examination revealed an increased respiratory rate of 26 cycles/minutes. The ECG was normal. The patient had increased D-dimer levels.

Computed tomography angiography (CTA) revealed a large, well-defined cystic lesion in the right ventricular apex (Fig. 1, white arrow), attached to the right ventricular apical wall. There was no internal enhancement or calcification within the cyst. The pulmonary arteries were dilated with cystic attenuation filling defects in bilateral descending pulmonary arteries, causing their complete occlusion (Fig. 1, yellow arrow). These features were suggestive of pulmonary arterial dissemination of the hydatid cysts. A triangular-shaped peripheral opacity was noted in the lung parenchyma in the right middle lobe as a result of lung infarction secondary to pulmonary embolism (Fig. 1, red arrow).

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FIG 1.

(a) Axial contrast-enhanced computed tomography (CECT) of the thorax showing the large hydatid cyst in the right ventricular apex (white arrow). (b) Axial CECT of the thorax showing a cystic lesion in the left descending pulmonary artery (yellow arrow). (c) Sagittal CECT of the thorax showing the hydatid cyst in the right ventricle (white arrow) and cystic lesion in the pulmonary artery (yellow arrow). (d) Axial CT of the thorax, lung window showing a lung infarct in the right middle lobe (red arrow). RV right ventricle LV left ventricle

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The patient subsequently underwent surgical management. Cystotomy and capitonnage of the right ventricular hydatid cyst were done under cardiopulmonary bypass, and partial pulmonary endarterectomy was done for the pulmonary daughter cysts. Subsequently, medical therapy with anti-helminthics was started, and the patient was given oral Albendazole 400 mg once a day to prevent recurrence.

The patient had an uneventful post-operative period for 3 years, following which he developed dyspnoea. High-resolution computed tomography (HRCT) of the thorax was done, which showed the residual calcified membrane of the right ventricular hydatid cyst (Fig. 2, white dashed circle). New onset development of multiple cystic structures of different sizes was noted scattered in both lung fields (Fig. 2, red dashed arrow), which suggested a possibility of disseminated hydatidosis.

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FIG 2.

(a) Axial computed tomography (CT) of the thorax mediastinal window showing the residual calcific hydatid cyst (dashed circle). Also note the cystic lesions in the bilateral lung fields (red dashed arrows). (b) Axial CT of the thorax mediastinal window showing the cystic lesions in bilateral lung fields (red dashed arrows). (c) Sagittal CT of the thorax mediastinal window showing the residual calcific hydatid cyat (dashed circle) and cystic lesion in the pulmonary arteries (red dashed arrow). (d) Axial CT of the thorax, lung window, showing lesions in bilateral lung fields.

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Hydatidosis or cystic echinococcosis is a zoonotic parasitic infection caused by the larval stage of cystode tapeworms belonging to the genus Echinococcus. Its most common location is the liver (70–80%), followed by the lungs (18%– 35%), together accounting for at least 90% of cases.^1,2 Cardiac involvement is rare, yet potentially life-threatening, with frequency ranging from 0.5 to 2% of all cases of hydatid disease.³ The left ventricle is the most commonly affected chamber (55–60%), probably because of its large myocardial mass and blood supply. Right ventricular involvement is rare, accounting for 10–15% of all intracardiac cases.⁴ Right ventricular cysts have the propensity to grow within the lumen of the ventricle, thus having a high risk of intracavitary rupture. Pulmonary arterial extension of the hydatid cysts is extremely rare, but it is a life-threatening complication requiring prompt diagnosis and early surgical treatment to avoid potentially fatal complications.⁵