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Caroticocavernous fistula


These are spontaneous or acquired connections between the carotid artery and the cavernous sinus and can be classified as direct or indirect.

Direct CCF represents direct connection between the ICA and cavernous sinus.  They occur as a result of a trauma causing rupture of ICA into cavernous sinus.  The shearing forces of severe head trauma, often accompanied by penetrating injury from bony spicules, can cause the ICA to be torn between its points of dural attachment. The other causes include rupture of intracavernous ICA aneurysm into cavernous sinus, collagen deficiency syndromes, fibromuscular dysplasia, arterial dissection or direct surgical trauma.

 Indirect CCF are actually dural arteriovenous malformations which are supplied either by dural branches of external carotid artery (ECA) or dural branches of ICA or both. They are not fistula per say. Most of the times they occur spontaneously.  However, factors associated with their development include pregnancy, sinusitis, trauma, surgical procedures and cavernous sinus thrombosis.


Type A: Direct rupture of intracavernous ICA into cavernous sinus.

Type B: Dural arteriovenous malformation between dural branches of ICA draining

into cavernous sinus.(Figure 1)

Type C: Dural arteriovenous malformation between dural branches of ECA draining

into cavernous sinus.(Figure 2)

Type D: Dural arteriovenous malformation between dural branches of ICA and ECA draining into cavernous sinus.

Another classification depending on therapeutic strategies is as follows:

Type 1: Post traumatic direct CCF.

Type 2: CCF caused by rupture of pre existing intracavernous  ICA aneurysm into the cavernous sinus resulting in two separate holes : one from ICA into the aneurysm and other from the aneurysm into the cavernous sinus.

Type 3: Dural type of CCF.

Type 4: Combination of Type 3 with either Type 1 or Type 2.


Clinical features are proptosis, chemosis, venous retinopathy, secondary glaucoma, decline in vision and increased intra ocular pressure, pulsatile tinnitus, dysfunction of cranial nerves III, IV, V1, VI. Diplopia and complete opthalmoplegia can occur due to cavernous sinus syndrome.

The clinical features are  related to the size, duration, location of fistula , adequacy and  routes of venous drainage and to the presence of arterial and venous collateral vessels.

Elevated venous pressure in veins draining the orbit may produce orbital venous congestion, transudation of interstitial fluid into the orbit with resultant proptosis, increased intraocular pressure due to impaired drainage of aqueous humour and secondary glaucoma.  These may compromise retinal perfusion and result in severely diminished visual acuity which may or may not be reversible.  Orbital symptoms are frequently related not only to the degree of shunt but also to the adequacy of external drainage of the superior ophthalmic vein.

The clinical presentation may not accurately reflect the pathology.

Emergency treatment is indicated if the intra ocular pressure rises above 40mm of Hg to prevent permanent loss of vision and when there is reversal of venous drainage into the spheno parietal sinus / cortical veins for the fear of intra cerebral haemorrhage.

Rarely, a unilateral CCF may present with bilateral orbital symptoms, by supplying the contralateral cavernous sinus with arterialized blood via the circular sinus creating free intercavernous communication.


Diagnosis is essentially clinical.  Gold standard imaging study  is Digital  Subtraction Angiography (DSA).

Role of CT & MRI is only in establishing the degree of associated brain injury and skull fractures.

Evaluation of CCF by DSA:

1)  Identifying the type of CCF.

2)  Size and location of fistula.

3)  Identification of and confirmation of patency of outflow pathways of cavernous sinus.

4)  Identification of high risk features like cortical venous drainage, pseudoaneurysm, cavernous sinus varix.

5)  Identification of associated vascular injuries in traumatic CCF or of ruptured aneurysm.

6)  To study cross circulation through circle of willis.



i)   Spontaneous closure  of  type B ,C ,D can  occur .

ii)  Intermittent manual carotid compression maneuver  for dural type of low flow fistulae

iii)  Transarterial balloon occlusion of Type A  fistulae using flow directed detachable latex / silicon balloons.( Figure 3)

iv)  Rarely occlusion of ICA for Type A CCF.

v)   Transcatheter coil embolization via an arterial or venous route using platinum microcoils.(Figure 4) (Figure 5)

vi)  Transarterial embolization of dural CCF using polyvinyl alcohol sponge particles for ECA branches.(Figure 6)


1)    Thromboembolic or ischemic events due to microcatheter and balloon manipulation injury to the parent vessel or inadvertent balloon detachment.

2)    Pseudoaneurysm formation due to balloon deflation or migration.

3)  Alteration of arterial flow resulting in haemorrhage, edema or worsening of ocular symptoms.

4)    Geopardizing supply to cranial nerves during embolization of dural CCF

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