CCF

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Classification
  • Barrow classification 1985
Direct
Type A
Direct high flow shunts between InternalCA → cavernous sinus
~Traumatic
~Iatrogenic: trigeminal rhizotomy, Endovascular procedure
~Spontaneous: rupture of ICA aneurysm
Indirect
Type B
Low flow shunts from meningeal branches (a dural artery branch of InternalCA) → cavernous sinus
Indirect
Type C
Low flow shunts from meningeal branches (a dural artery branch of ExternalCA) → cavernous sinus
Indirect
Type D
Low flow shunts from meningeal branches (a dural artery branch of both InternalCA and ExternalCA) → cavernous sinus
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Presentation (indirect have more gradual onset than direct): TRIAD for DIRECT: exophthalmos + chemosis + visual loss
  • Increased intracavernous pressure
    • Orbital and retro orbital pain
    • Chemosis: arterialisation of conjunctiva
    • Dec. Visual acuity/neovascularization of iris or retina: venous ischaemia —> hypoxia retinopathy—> neovascularization
    • Diplopia/pupillary dilation/Opthalmoplegia: venous engorgement of the orbital contents —> ischaemic compression of CN
    • Inc. intraocular pressure: increased back pressure as venous drainage is affected. Initially unilateral but can progress to bilateral
  • Transmitted arterial pulse to eye
    • pulsatile proptosis
  • Ocular/cranial bruit: High flow (type A) —> turbulent
  • Rare SAH 5%
Clinical features
Fq
Bruits
80%
Proptosis
72%
Chemosis
55%
CN4 palsy
49%
Complete ophthalmoplegia
24%
Visual lost
18%
Radiology
  • CT/MRI demonstrates
    • proptosis,
    • serpiginous and engorged intraocular vessels including superior ophthalmic vein (seen on T2 to diff from rectus muscles)
    • Convexity of lateral wall of cavernous sinus.
  • Angiography:
    • Shunt of blood from ICA into cavernous sinus —> rapid pacification of petrosal sinus/ ophthalmic veins
    • Manoeuvres to slow blood flow and slow down filling the shunting arteries
      • Huber: inject contrast up VA and press on affected carotid
      • Mehringer-hieshima: inject contrast up ICA and press ICA below catheter
Treatment
  • Low flow (indirect) CCF 20-50% spontaneously thrombose
    • Observe --> As long as vision is stable and intraocular pressure is not raised
    • 10 sec for every hour ICA compression
  • Symptomatic high flow CCF don’t resolve spontaneously and best to tx ASAP
    • Indications
      • Elevated intraocular pressure >20mmHg
      • Inc. filling of cortical veins on angiography —> can cause neurology due to back pressure like cognard type 2b to 5
      • Proptosis
      • Visual loss
      • CN4 palsy
      • Intractable bruits
  • Endovascular tx
    • Options
      • Electrolytically detachable coils
      • Amplatzer vascular plug
    • Route
      • Transarterial
        • Always to go transarterial if the vessel is large enough.
        • If it is Type B you can embolize the feeder artery with coils
        • Otherwise you have to embolize the whole cavernous sinus
        • Destructive option (Last option)
          • carotid artery occlusion on either side of fistula provided that the patient can tolerate this after occlusion test.
            • Distal occlusion must be done proximal to ophthalmic artery
            • Occlusion test can be false positive where after occlusion, while the fistula is still open, blood can be stolen by fistula —> reduce cerebral blood flow —> neurological symptoms
      • Transvenous:
        • better for indirect CCF because
          • small arterial feeders of indirect are small and hard to get to
          • if you just embolize the arterial feeders and you can't ensure that the small feeders have collaterals.
        • heart —> jugular —> petrosal sinus —> cavernous sinus
          • Lower success than transarterial route
        • Heart —> jugular —> supra-optic vein —> superior ophthalmic vein —> cavernous sinus
          • Best to wait for a while to allow for arterialisation of veins so that they have thicker wall and wont be so fragile —> can rupture
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