Carotico cavernous fistula and its managment

ccf is an complex topic as one should know the anatomy to deal with it

1. Carotico cavernous fistula Nerella Sai Krishna, Resident Neuro Surgery

2. LOCATION OF CS Middle cranial fossa lateral to the body of the sphenoid bone

3. VENOUS SYTEM The two sinuses are connected by intercavernous sinuses which are anterior and posterior to the hypophysis

4. Numerous trabeculae cross the interior of the sinus

5. Content of CS Artery inside CS The internal carotid artery enters the sinus from its base, runs forward and superiorly and then exits at the superior wall of the sinus. Nerve related to CS CNs: III, IV, V1, V2, VI, Sympathetic

6. INTRODUCTION The caroticocavernous fistula is a specific type of dural arteriovenousfistula characterized by abnormal arteriovenous shunting within the cavernous sinus. A caroticocavernous fistula results in high-pressure arterial blood entering the low-pressure venous cavernous sinus. This interferes with normal venous drainage patterns and compromises blood flow within the cavernous sinus and the orbit.

7. Epidemiology Caroticocavernous fistulas represent approximately 12% of all dural arteriovenous fistulas. Direct CCFs are often secondary to trauma: head trauma: Youngs: Presentation: acute/rapid. indirect CCFs : Post menopause: insidious.

8. CLASSIFICATION Two main types: 1. Direct 2. Indirect

9. Barrow's Classification of CCFs. Type A: direct connection between the intracavernous ICA and CS Type B: dural shunt between intracavernous branches of the ICA and CS Type C: dural shunts between meningeal branches of the ECA and CS Type D: B + C

10. Pathophysiology Direct: typeA: ICACS Indirect: Br of ICA/ECSCS; types B , C, D The most frequent among indirect is type C , with meningeal branches of the ECAforming the fistula.

11. Clinical presentation Their symptoms range from benign to extremely severe ophthalmologic or neurologic complications. Clinical presentation is consequence of the elevated intracavernous pressure. In direct, high-flow CCFs, symptoms appear suddenly. Symptoms caused by CCFs are related to their size, duration, location, adequacy and route of venous drainage, and presence of arterial and venous collaterals

12. CLINICALPRESENTATION Pulsatile exophthalmos: ~75% Chemosis and subconjunctival haemorrhage Proptosis Progressive visual loss: 25-32% Pulsatile tinnitus (usually objective) Raised intracranial pressure Cranial nerve (III, IV, V c, VI) palsies The Dandy’s triad: pulsatile exophthalmos, bruit and chemosis

13. Moreover, other factors like dominant pattern of venous drainage the size and location of CCF and the presence of collateral vessels (arterial or venous) are important in this setting. Diplopia, pain, cephalic bruit, ophtalmoplegia, visual loss (Ophth. vein) Intracranial haemorrhage : (sphenoparietal sinus and deep middle cerebral vein) External haemorrhage: Otorrhagia, epistaxis (Pterygoid plexus)

14. Radiographic features CT • Proptosis Enlarged superior ophthalmic veins• Extraocular muscles may be enlarged• Orbital o edema• May show SAH/ICH from a ruptured cortical vein Angiography (DSA) • Rapid shunting from ICA to CS• Enlarged draining veins• Retrograde flow f rom CS, most commonly into the ophthalmic veins Ultrasound • Arterialised ophthalmic veins may be seen on Doppler study

15. MRI

16. DSA a. Digital angiogram of carotid circulation confirming carotid-cavernous fistula b. Digital angiogram of vertebral circulation showing right ophthalmic vein ingurgitated. c. Digital angiogram with final image after treatment of the traumatic CCF

17. Treatment and prognosis The natural history of CCF is highly varied, ranging from spontaneous closure to rapidly progressive symptoms. Poor treatment outcome indicators include feeding vessel aneurysms (indirect CCF) and retrograde filling of cortical veins (increased risk of haemorrhage). Direct fistulas have a relatively high spontaneous rate of haemorrhage (8.4%) subarachnoid, intracerebral or external haemorrhage (epistaxis, or otorrhagia). Subconjunctival hemorrhage is also common but does not carry the same poor prognosis

18. GOAL OF TREATMENT Direct CCF: Occlude the tear between ICAand CS, preserving the patency of ICA Indirect CCF : Interrupt fistulous communications/reduce CS pressure

19. Treatment options

20. Carotid compression therapy Contralateral hand: 10sec: 4-6/hr: Reduces AV shunting + Increase outlet venous pressures~ Thrombosis. Most useful in the treatment of indirect fistulas resulting in spontaneous closure in most of cases

21. Surgery Options Ligation of the CCF Surgical trapping of the fistula, and Surgical transvenous packing - Both direct and indirect CCFs Disadv: Cranial nerve deficits and residual fistulous communications. Indications for surgical repair include 1. Compromised proximal arterial access that prevents endovascular repair or causes it to fail 2 Salvage: failed endovascular treatments.

22. PARENT ARTERY OCCLUSION Arterial sacrifice may be required as a life-saving emergency treatment Indication: Difficult case Extensive traumatic vessel wall damage Active hemorrhage or A rapidly expanding hematoma of the soft tissues

23. Transarterial balloon embolisation TOC: Symptomatic direct CCF If not possible, detachable coils may be use Both arterial and venous access (including superior ophthalmic vein) Indirect fistulas typically require a combined transarterial (closure of feeders) and transvenous (closure of cavernous sinus) approach Indirect types are more difficult to treat and have a higher rate of spontaneous closure

24. Balloon Occlusion This procedure requires that the CS must be large enough to put the balloon for embolization and the size of fistula must be smaller than the inflated balloon, but large enough to allow a deflated balloon The balloon has the advantage of being able to be flow-directed through the fistula and CS, and must be inflated to a volume larger than the fistula orifice to prevent its retrograde migration into ICA Angiography is repeated to ensure closure of the fistula and patency of the ICA

25. Transarterial embolization Mainstay of treatment in high-flow direct CCEs It's an alternative when residual AV shunt remains in dural CCF Embolization can be made with detachable platinum coils and liquid èmbolic agents (n-butyl cyanoacrylate, ethylene-vinyl alcohol copolymer); Coils are preferred because of their reliable and controlled deployment into CS Complications of this procedure includes thromboembolus and ICA dissection

26. Covered stent graft placement Recent Advance: poly flurotetraethylene-covered stents Traumatic arterial damage immediate obliteration of a direct CCF, while preserving ICA patency Disadv Longitudinal flexibility: difficult navigation: tortuosity of the intracranial vasculature. Vasospasms: Intra-arterial nimodipine and papaverine infusion Endoleak, coverage of vital perforators, dissection and rupture

27. Transvenous embolization Is the current method of choice in treatment of indirect CCF's. The goal of this technique is to catheterize the abnormal CS superselectively and occlude the fistula without re-routing venous drainage to cortical structures. Several routes: Most: inferior petrosal sinus (IPS)

28. RADIOSURGERY Indirect CCFs Gamma knife radiosurgery can be used either alone or as an adjunct therapy before/after endovascular intervention Preliminary data : safe and effective alternative treatment

29. Fistulous point located at left CS, with ICA supply by meningo-hipofisary trunks (red arrow) and ECA supply by middle meningeal artery (blue arrow)and clivus branches from ascendent pharyngeal artery. Venous drainage to superior ophtalmic vein (yellow arrow) and to inferior petrous sinus.

30. Transarterial embolization Coil embolization of the fistula (red arrows) was performed via middle meningeal artery

31. Treatment Algorithm

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