Radiology

A 28 year old lady presented with complaints of headache, vomiting and one episode of generalized tonic, clonic convulsions in the post partum period about two years ago. Contrast enhanced CT scan (Fig1 and 2) of the brain performed at that time had revealed venous sinus thrombosis, which was treated conservatively by anticoagulation.

Fig 1

Fig 2

The patient's symptoms subsided only to recur a year later. An MRI of the brain was performed then, which was thought to suggest chronic venous thrombosis. This was again treated conservatively. The patient's symptoms subsided after sometime. About 10 months later, the patient developed tinnitus and headaches. The MRI of the brain performed at this time revealed a few dilated veins in the posterior fossa along with a dilated right transverse sinus, suggestive of a dural fistula. The patient was referred for a four vessel cerebral angiogram. This revealed a dural arteriovenous fistula (AVF) of the right transverse sinus, which had multiple feeder arteries (Fig 3,4,5).

Fig 3	Fig 4

Fig 5

 

MANAGEMENT

Endovascular obliteration of this fistula was planned. Right femoral arterial and bilateral femoral venous accesses were secured. 6F guiding catheter were placed in the right internal jugular vein. Two microcatheters were positioned in the right transverse sinus, near the torcula at the site of fistula. (Jetstream II MIS and Tracker 18 Target therapeutics Fremont CA). The second microcatheter was placed as a safety measure to fill in the small remnants of the fistula, which may be residual after deployment of the coils. The right transverse sinus was then progressively packed with more than 30 coils. 15 GDC coils were used; additional free platinum coils and tungsten spirale wires were deployed (Fig 6). 33 % glue was then injected in the right transverse sinus, through the second microcatheter sealing off most of the residual fistula. .

 

Fig 6

 

A right common carotid angiogram performed immediately after the embolisation showed markedly reduced flow in the feeder vessels, late and slow opacification of the superior sagittal sinus and the straight sinus through the residual fistula which had significantly reduced in size. There was remarkable improvement in the brain circulation with antegrade flow in the sinuses (Fig 7,8,9) .

Fig 7	Fig 8

Fig 9

A check angiogram performed two days later revealed complete obliteration of the dural fistula. Patient was having mild headaches, which improved over a period of time. When seen 3 months after the procedure, the patient continues to be asymptomatic and a check angiogram revealed complete obliteration of the fistula. However she continued to have diminished vision in the left eye which was due to optic atrophy.

DISCUSSION

Dural AVFs represent abnormal shunts within the dura. Theoretically, they can occur at any site within the dura, but most frequently they develop near the venous sinuses. Arterial supply is usually through the branches of the neuromeningeal arteries. Although there is a lot of controversy regarding its etiology, it is probably secondary to venous obstruction, which may be secondary to congenital anomalies (hypoplasia, aplasia), trauma, infection and cerebral or craniofacial AVMs. Dural AVFs are believed to develop in the presence of a structural weakness in the dura, which is controlled by a trigger factor. The symptomatology of dural AVFs is highly variable and includes bruits, cranial nerve deficits, opthalmological complications, focal neurological deficits, intracranial hypertension, haemorrhage, hydrocephalus and congestive cardiac failure (especially in children). Dural AVFs are not static lesions. They may regress either spontaneously or following haemorrhage or angiography or manual compression of the cranial vessels. Spontaneous progression may also occur. The severity of symptoms depends on the topography and the type of initial venous drainage. This progression is due to venous rupture with haemorrhage and venous thrombosis. Active treatment for dural AVFs is considered only when the clinical symptoms and potential complications of the lesion affect the patient's life. Endovascular treatment is the treatment of choice as other form of treatment such as irradiation; electrothrombosis, estrogens and surgery are seldom successful in curing these lesions. The morphological goal is the permanent occlusion of the shunt at the site of abnormal Communication, with preservation of the venous outlet. This can be done successfully by navigating a microcatheter to the site of fistula from the venous route with coils or glue. If the fistula is not accessible, the flow in the fistula may be reduced via the arterial route (Using particles like PVA ), which may at times result in obliteration of the fistula.

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