CASE REPORT / CAS CLINIQUE
CEREBRAL HYDATIDOSIS. CASE PRESENTATION AND LITERATURE REVIEW
Cerebral hydatidosis is a rare form of hydatid disease of the Central Nervous System accounting for 2 to 3 percent of all cases of hydatid disease. Hydatid disease is a major health problem in certain nomadic communities in Kenya. Treatment is surgical excision of the cyst. A four year old African boy presented with fits, progressive enlargement of the head and right hemiparesis at the Kenyatta National Hospital, Nairobi, Kenya. A computerised tomography (CT) scan of the head showed a large cystic mass in the left parietal area with no associated brain oedema or contrast enhancement. A left parietal craniotomy and total excision of the cystic mass was done. Histology showed laminated wall of cyst of echinococcus granulosus with numerous scolices. Post-operative recovery was good and follow-up has not revealed any evidence of recurrence.
Keywords : Cerebral Hydatidosis, Kenya
L’hydatidose cerebrale est observee chez environ 2 a 3% des patients qui presentent une hydatidose. L’hydatidose est un des problemes de sante publique majeur observe au sein de communautes nomades vivant au Kenya. Le traitement est 1’ablation chirurgicale du kyste. Un cas survenu chez un garcon agé de 4 ans ayant des crises d’epilepsies, une macrocephalie et une hemiparesie droile a ete observe a l’Hopital National de Kenyatta a Nairobi. L’examen tomodensitometrique cranien a montre I’existence d’un grand kyste situe dans la region parielale gauche sans oedeme cerebral et sans rehaussement apres injection de produil contraste. Une craniotomie parie’tale gauche a permis 1’excision totale du kyste, avec a l’examen histologique une confirmation de la nature du kyste qui contenait de nombreux scolex. Une regression des signes cliniques est apparue apres 1’intervention sans recidive de l’affection.
Cerebral hydatidosis is caused by the larval stage of hydatid of the dog tapeworm taenia echinococcus. Hepatic and pulmonary forms of the disease are the most common and account for almost 85% of the cases.
A four year old African male was admitted to the Neurosurgical Unit at Kenyatta National Hospital, Nairobi, Kenya, with a one year history of persistent headache and grandmal seizures. He had previously been admitted and treated in various hospitals elsewhere on several occassions for what was then thought to be attacks of malaria. He was referred to Kenyatta National Hospital from the Kakuma refugee camp where he was
On examination, he was found to be sick looking although fully conscious and co-operative. He had marked right side wcakeness with power in the upper and lower limbs reduced to grade 3/5. The deep tendon reflexes were brisk. His head circumference was 56cm. A computerised tomography (CT) scan of the head showed a large cystic mass in the left parietal area, with mass effect. There was no rim enhancement on injection of contrast materia (Fig 1)
Blood results were as follows:
Liver function tests were as follows:
Abdominal ultrasound showed features suggestive of hepatic hydatidosis. Patient was pre-operatively put on albendazole, prepared for surgery and underwent craniotomy under a general anaesthetic. The mass was excised in toto. Histology showed laminated wall of cyst, typical of echinoccocus granulosus with numerous scolices. His post operative recovery was uneventful with good recovery of power on the right side and improvement of his symptoms.
The existence of the hepatic form of hydatid disease was recognised by Hippocrates and Galen in their early writing (2). The first reports of cerebral hydatid disease and vertebral echinococcosis were by Guesnard and Chaussier respectively in 1807 (3). Hepatic and pulmonary forms of the disease arc the most common and account for almost 85 per cent of the cases (4). Cerebral hydatidosis accounts for 2 to 3 per cent of patients. Central nervous system forms of the disease may be cerebral (80 %), cranial (5%) and vertebral (15 %).
The ‘usual hostsfor the adult worms are dogs, wolves and foxes. Cattle, sheep and dogs serve as intermediate hosts. In the definite hosts, the scolex attaches to the intestinal mucosa. becomes the adult worm and releases eggs into the faeces of canines. After ingestion of the egg by man, the capsule is digested and hexacanth oncospherc is released in the jejunum where it penetrates the intestinal mucosa and passes into the portal circulation. Most become entrapped in the small intrahepatic venules while others pass to the lungs, central nervous system, bone and other site (1). The embryo, oncospheres, may be destroyed by normal hosts defense mechanisms or may increase rapidly in size and form unilocular cysts. The cyst wall differentiates into an internal granular layer (endocyst) and an outer cuticular laminated layer surrounded by an outer host adventitial fibrous capsule. The cavity of the cyst contains hydatid fluid, daughter cysts, brood capsules and scolices. Brood capsules arise from the germinal layer of the endocyst. Brood capsules and scolices within the hydatid cyst fluid form the hydatid sand (5).
Papilloedema is usually present. Seizures are also common.
Definitive diagnosis is dependent upon indentification of the parasite or its body parts in the lesion.
Successful operative treatment depends upon complete removal of the unruptured cyst. Attempts should therefore be made to remove the cyst in loto. If rupture of the cyst occurs, irrigation with hypertonic salin should be done (7) to destroy the organisms by osmotic dessication. Prognosis usually depends on location and size of the lesion, presence of single or multiple lesions and the presence of contamination. Fortunately cerebral lesion are usually single and accessible.