Journal of Postgraduate Medicine Medknow Publications and Staff Society of Seth GS Medical College and KEM Hospital, Mumbai, India ISSN: 0022-3859 EISSN: 0972-2823 Vol. 47, Num. 1, 2001, pp. 37-39

Journal of Postgraduate Medicine, Vol. 47, Issue 1, 2001 pp. 37-39

Hepatic Hydatid Cyst Rupturing Into Sub-diaphragmatic Space And Pericardial Cavity

Ahuja SR, Karande S, Koteyar SR*, Kulkarni MV

Departments of Pediatrics and Radiology*, LTM Medical College and LTMG Hospital, Sion, Mumbai - 400 022, India.

Code Number: jp01010

Abstract

A ten-year-old male child presented with a large hepatic hydatid cyst which ruptured into the sub-diaphragmatic space and pericardial cavity, giving rise to a pericardial effusion. This communication between the hydatid cyst and the pericardium was documented on computerised tomographic scan of the chest and abdomen. The cyst was aspirated carefully and then enucleated. There was an associated right sided reactionary pleural effusion. The pericardial effusion and pleural effusion resolved on albendazole therapy and did not require surgical intervention.

Hydatid disease or echinococcosis is a systemic zoonosis. The word ‘hydatid’ is of Greek origin and literally means a ‘watery vesicle’. (1) The commonest sites affected in children are the lungs and the liver. (2) Cysts have also been reported in the pain, eye, spleen, bones, genitourinary tract, heart, endocrine glands and subcutaneous tissues. We report a rare presentation of echinococcosis in a child wherein a hydatid cyst in liver ruptured into the sub-diaphragmatic space as well as the pericardial cavity. The child also had an associated reactionary right-sided pleural effusion.

Case History

A ten-year-old male child residing at Satara, Maharashtra, presented with high grade fever, abdominal pain, vomiting and abdominal distention since 15 days. The abdominal pain was continuous, dull-aching and localized to the epigastrium and right hypochondrium. He also complained of chest pain and difficulty in peathing, two days prior to admission. There was no history suggestive of congestive cardiac failure. There was no history of contact with tuberculosis. The child had a history of prolonged close proximity to dogs.

On examination, the child was afepile with a heart rate of 96/min, respiratory rate of 36/min with mild subcostal and intercostal retractions. His blood pressure was normal. There was no pallor, icterus and evidence of cardiac tamponade. The abdomen was distended; liver was palpable 7 cm below costal margin in the midclavicular line. Spleen was not palpable. Heart sounds were muffled but there was no murmur. peath sounds were diminished in the right inframammary and infrascapular regions with fine crepitations. Investigations revealed a haemoglobin of 10 gm/dl, total white cell count of 11200/mm3, serum albumin was 3.2 gm/dl and serum globulin 3.7 gm/dl. X-ray chest showed a cardiothoracic ratio of 0.65, elevation of the right dome of diaphragm and a right-sided pleural effusion (Figure 1). Ultrasound (USG) scan of abdomen showed hepatomegaly with a 6.5 x 4.5cm anechoic lesion in the posterosuperior quadrant of the right lobe of liver. The lesion was cystic, well defined with multiple echogenic septae within its cavity suggestive of a hydatid cyst. The surrounding liver parenchyma appeared normal. Echocard-iography showed a moderate pericardial effusion with fipin strands in the pericardial cavity. There was no evidence of tamponade. Heart valves were normal. Computerised tomographic (CT) scan of abdomen showed a large hydatid cyst in the liver communicating with the pericardial cavity (Figure 2) and the right sub-diaphragmatic space. Twelve days later an exploratory laparotomy was done which revealed a large hepatic hydatid cyst rupturing into the sub-diaphragmatic space. The cyst was carefully aspirated after injecting 0.5% cetrimide, a scolicidal solution and then enucleated. Oral albendazole in a dose of 15 mg/kg/day was given two days preoperatively and continued for four weeks postoperatively. On follow up after a month, x-ray chest and echocardiography showed complete resolution of the pericardial and right pleural effusions.

Discussion

Hydatid disease remains endemic in various parts of the world due to the close association that exists between sheep, dogs and humans. (2) Most persons are infected as children but often do not present with symptoms until adulthood. (3) The clinical manifestations of hepatic hydatid disease depend upon the site, size and stage of development of the cyst; on whether the cyst is dead or alive and whether it is secondarily infected or not. (1) As hydatid cysts grow, they can rupture into the surrounding tissues. Unusual complications of a hepatic hydatid cyst include rupture into the stomach, duodenum or small intestine. Rupture into the biliary tree can cause cholangitis, biliary colic and jaundice with excretion of germinative mempanes in the stools. (1)

Literature search did not reveal any report of a hepatic hydatid cyst simultaneously rupturing into sub-diaphragmatic space and pericardial cavity associated with pleural effusion in a child. In our case, this was documented on CT scan. Whenever there is rupture or leakage of a cyst, an allergic response is evoked due to spillage of antigenic cyst contents in the surrounding tissues.1 Since the first case of cardiac involvement was reported in 1901, less than 100 cases have been reported worldwide. (4) Rupture of a hydatid cyst into the pericardial cavity can give rise to a pericardial effusion, which is an allergic inflammatory process. (5) The effusion can be massive and cause cardiac tamponade. In our case since there was no evidence of tamponade, it was not tapped. Also, tapping of a pericardial effusion due to hydatid disease can further aggravate the effusion since tapping is known to reactivate the pericardial inflammation. (5)

USG is the primary diagnostic modality for hepatic hydatid disease and is often all that is required when the appearance is classical. (3) Hydatid cysts are seen as well defined, circumscribed, anechoic lesions with no infiltration of surrounding liver tissue. USG shows the morphological characteristics of the cyst, its wall thickness and the extent to which the biliary tree is affected. (6) Gharbi et al (7) have described five types of echinococcal cysts on USG: purely cystic except for hydatid sand; detached mempane; multiseptated; peripheral or diffuse distribution of coarse echoes in a complex heterogenous mass; and calcified wall. These five types are believed to correspond to evolutionary stages of the hydatid cyst. USG by its universal availability is not only very useful for initial diagnosis, but is also an ideal modality for follow up of patients with hydatid disease. With successful treatment, cysts appear hyper-echogenic on USG. (8) CT scan can be used alternately or in addition to USG. Hydatid cyst of liver is seen as a peripherally enhancing hypodense mass lesion. (3) Daughter cysts, hydatid sand and calcification of the cyst wall are well seen on CT scan. Fluid-fluid or air-fluid levels can be seen when the cyst ruptures. (3) Magnetic resonance imaging (MRI) is useful only when the diagnosis of hydatid disease is questionable. Cysts are typically of low intensity on T1-weighted scans and of high intensity on T2-weighted scans. MRI is very sensitive in detecting cyst wall irregularity which is a sign of reduced parasite viability. (3)

The treatment of hydatid cyst involves surgical enucleation of the cyst and peri-operative medical treatment with albendazole. Total cystopericystectomy is the procedure of choice; however operative strategy is best individualised. (9) A newer modality of diagnosis and treatment is percutaneous drainage of the hepatic hydatid cyst under CT/USG guidance. However this method has a high risk of spillage of cyst contents and is hence not recommended for routine use. (10) The use of albendazole before and after surgery is known to reduce the risk of intraoperative dissemination and recurrence. (2) Drug therapy is essential to eliminate the disease, otherwise the disease may progress due to continued growth of daughter cysts. In case the initial four-week therapy with albendazole is not fully successful, a second course for another four weeks is indicated after a gap of 14 days. The efficacy of albendazole is better when used for three months against when used for a month. (11) Our patient received albendazole for 28 days. Long-term follow up is required in our case to watch for the later development of constrictive pericarditis.

References

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