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Update on management of cerebral venous sinus thrombosis and chronic venous outflow obstruction in the

endovascular era

Update on management of cerebral venous sinus thrombosis and chronic venous outflow obstruction in the

endovascular eraAdnan I. Qureshi MD

Professor of Neurology, Neurosurgery, and Radiology President, International Society of Interventional

Neurology

Shahram Majidi MD, Mikayel Grigoryan MD, Gustavo J. Rodriguez MD, M. Fareed K. Suri MD,

Zeenat Qureshi Stroke Research CenterUniversity of Minnesota, Minneapolis, MN

Adnan I. Qureshi MDProfessor of Neurology, Neurosurgery, and Radiology

President, International Society of Interventional Neurology

Shahram Majidi MD, Mikayel Grigoryan MD, Gustavo J. Rodriguez MD, M. Fareed K. Suri MD,

Zeenat Qureshi Stroke Research CenterUniversity of Minnesota, Minneapolis, MN

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Dural arteriovenous fistulas?

Anatomical considerations?

Endovascular treatment in acute CVST?

Venous insufficiency and multiple sclerosis?

Chronic intracranial hypertension?

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Dural arteriovenous fistulas?

Anatomical considerations?

Endovascular treatment in acute CVST?

Venous insufficiency and multiple sclerosis?

Chronic intracranial hypertension?

Cerebral venous systemCerebral venous system

Superficialvenous complex

Deepvenous complex

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Anatomical variantsAnatomical variants

Superficial venous complex

Deep venous complex

Paracavernous venous drainage

A (Complete)

Superior sagittal sinus and transverse sinus (es) connected directly +indirectly

Infratentorial drainage via basal vein (s) and vein of Galen

Supratentorial drainage via sylvian/middle cerebral vein (s)

B (Incomplete)

Above not present

Above not present

Above not present

Superficial venous complex-type ASuperficial venous complex-type A

Deep venous complex-type ADeep venous complex-type A Paracavernous venous complex-type AParacavernous venous complex-type A

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Intraluminal imaging using intravascular ultrasound

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Dural arteriovenous fistulas?

Anatomical considerations?

Endovascular treatment in acute CVST?

Venous insufficiency and multiple sclerosis?

Chronic intracranial hypertension?

Cerebral venous thrombosis-Pathophysiology

Cerebral venous thrombosis-Pathophysiology

Occlusion of dural sinus with thrombosis Impairment of cerebrospinal fluid resorbtion via

the arachnoid villi into the dural venous sinuses Increased intracranial pressure Venous engorgement, venous infarction with

hemorrhagic conversion

Occlusion of dural sinus with thrombosis Impairment of cerebrospinal fluid resorbtion via

the arachnoid villi into the dural venous sinuses Increased intracranial pressure Venous engorgement, venous infarction with

hemorrhagic conversion

Cerebral venous thrombosis-Pathophysiology

Cerebral venous thrombosis-Pathophysiology

Venousengorgement

CSFaccumulation

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Randomized Trials Evaluating Intravenous Heparin (Einhaupl et al. Lancet 1991;338:597-600)

Randomized Trials Evaluating Intravenous Heparin (Einhaupl et al. Lancet 1991;338:597-600)

20 patients with Sinus Venous Thrombosis (diagnosed by Angiography)

IV heparin (PTT 80-100s)

Continuous salineinfusion

10 patients 10 patients

lower higherClinical severity

3 MonthsComplete recovery

Slight neurological deficitsDeath

8/10 1/102/10 6/10

3/10none

Day 3 onwards

Randomized Trial Evaluating Subcutaneous Low Molecular Weight Heparin (de Bruijn SF et al. Stroke

1999:30;484-488)

Randomized Trial Evaluating Subcutaneous Low Molecular Weight Heparin (de Bruijn SF et al. Stroke

1999:30;484-488)

59 patients with Sinus Venous Thrombosis

Nadroparin(3 weeks) Placebo

30 patients 29 patients

6/30 7/29Barthel <15 or Death

3 MonthsDeath or Oxford Handicap 3

Other Complications

4/30 6/29

One major gastrointestinal bleed

One pulmonary embolism

3 Weeks

3 monthsOral anticoagulation Placebo

Meta-analysis of both trialsMeta-analysis of both trialsAnticoag-ulation

Placebo Relative risk reduction

Death or dependence

10% 23.1% 15.5% (95% CI, -37 to 6).

Trial Pre-existing ICHEinhaupl et al. Lancet 1991;338:597-600

3/10

de Bruijn SF et al. Stroke 1999:30;484-488

15/30

No new symptomatic ICH in either trial

Meta-analysis of both trialsMeta-analysis of both trialsAnticoag-ulation

Placebo Relative risk reduction

Death or dependence

10% 23.1% 15.5% (95% CI, -37 to 6).

Trial Mean time-symptom onset --initiation of treatment

Einhaupl et al. Lancet 1991;338:597-600

25-33 days

de Bruijn SF et al. Stroke 1999:30;484-488

10-11 days

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ASA/AHA guidelinesASA/AHA guidelines For patients with CVT, initial anticoagulation

with adjusted-dose UFH or weight-based LMWH in full anticoagulant doses is reasonable, followed by vitamin K antagonists, regardless of the presence of ICH

For patients with CVT, initial anticoagulation with adjusted-dose UFH or weight-based LMWH in full anticoagulant doses is reasonable, followed by vitamin K antagonists, regardless of the presence of ICH

Saposnik G; American Heart Association Stroke Council. Stroke. 2011;42(4):1158-92.

Mechanism of recoveryRecanalization versus collateral formation

Mechanism of recoveryRecanalization versus collateral formation

21 patients with documented cerebral venous thrombosis who had serial imaging using same modality (CTV→CTV or MRV→MRV)

Initial imaging →→Repeat imaging3 -12 m

21 patients with documented cerebral venous thrombosis who had serial imaging using same modality (CTV→CTV or MRV→MRV)

Initial imaging →→Repeat imaging3 -12 m

Farrag A, Irfan M, Guliani GK, Tariq N, Taylor RA, Suri MF, Qureshi AI. Neurocrit Care. 2010 Dec;13(3):373-9

Grade I Grade II Grade IIIPartial recanalization (antereograde flow through part of the sinus) of one or more occluded dural venous sinus with improved flow in branches

Completed recanalization (antereograde flow through all the sinus) of one dural venous sinus

Complete recanalization of all occluded venous sinuses

RECANALIZATION GRADES

Grade I Grade II Grade III

10 0 7

RECANALIZATION GRADES

Farrag A, Irfan M, Guliani GK, Tariq N, Taylor RA, Suri MF, Qureshi AI. Neurocrit Care. 2010 Dec;13(3):373-9

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Grade I Grade II Grade IIICollaterals bypass occluded segment of dural venous sinus but connect within the same sinus

Collaterals bypass occluded segment of dural venous sinus but connect with a different sinus

Collaterals bypass occluded segment of dural venous sinus but connect with a different circulation (through deep or cavernous venous sinus circulation)

COLLATERAL GRADES

Grade I Grade II Grade III3 1 4

COLLATERAL GRADES

Farrag A, Irfan M, Guliani GK, Tariq N, Taylor RA, Suri MF, Qureshi AI. Neurocrit Care. 2010 Dec;13(3):373-9

Figure demonstrates new grade 3 collaterals (see arrows) bypassing occluded segment of dural venous sinus and connect with a different circulation

Figure demonstrates new grade 3 collaterals (see arrows) bypassing occluded segment of dural venous sinus and connect with a different circulation

A B

Figure demonstrates complete recanalization (grade III, see arrows) and new grade 3

collaterals (see dashed arrows) bypassing occluded segment of dural venous sinus and connect with a

different circulation (Figure 3B)

Figure demonstrates complete recanalization (grade III, see arrows) and new grade 3

collaterals (see dashed arrows) bypassing occluded segment of dural venous sinus and connect with a

different circulation (Figure 3B)A B

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A B

Figure demonstrates complete recanalization (grade III, see arrows) of the transverse sinusFigure demonstrates complete recanalization

(grade III, see arrows) of the transverse sinus

A B

Figure demonstrates complete recanalization (grade III, see arrows) of the superior

sagittal sinus

Figure demonstrates complete recanalization (grade III, see arrows) of the superior

sagittal sinus

ASA/AHA guidelines:The role of endovascular treatment

ASA/AHA guidelines:The role of endovascular treatment Endovascular intervention may be considered if

deterioration occurs despite intensive anticoagulation treatment (Class IIb; Level of Evidence C).

Endovascular intervention may be considered if deterioration occurs despite intensive anticoagulation treatment (Class IIb; Level of Evidence C).

Saposnik G; American Heart Association Stroke Council. Stroke. 2011;42(4):1158-92.

Endovascular intervention may be considered if deterioration occurs despite intensive anticoagulation treatment (Class IIb; Level of Evidence C).

Endovascular intervention may be considered if deterioration occurs despite intensive anticoagulation treatment (Class IIb; Level of Evidence C).

23% of patients with cerebral venous thrombosisundergo neurological deterioration

1/3rd related to new parenchymal lesion----Increased likelihood of dying

Bousser MG, et al. Lancet Neurol 2007; 6: 162–70

ASA/AHA guidelines:The role of endovascular treatment

ASA/AHA guidelines:The role of endovascular treatment

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Can waiting for deterioration be avoided?Can waiting for deterioration be avoided?

Predictors of neurological deterioration/death

Coma (unrelated to mass lesion) Deep cerebral venous thrombosis Transverse sinus with posterior fossa

involvement

Predictors of neurological deterioration/death

Coma (unrelated to mass lesion) Deep cerebral venous thrombosis Transverse sinus with posterior fossa

involvement

Canhão P, et al. Stroke 2005; 36: 1720–25.

Endovascular modalities for treatment of cerebral venous thrombolysis

Endovascular modalities for treatment of cerebral venous thrombolysis

Prolonged infusion of

thrombolyticsAcute local

thrombolysis+thrombectomy

Acute local thrombolysis+thrombectomy

+ infusion

11 ptsCVST

4 pts completerecanalization

7 pts suboptimalrecanalization

No recanalization (n=3)

Partial recanalization (n=3)

Reocclusion (n=1)

3 pts completerecanalization

3 pts additionalrecanalization

Local rt-PA+thrombectomy

Local rt-PA infusion

(mean 19 h)

Grigoryan M, et al.AAN annual meeting2011-Honolulu, HI

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Dural arteriovenous fistulas?

Anatomical considerations?

Endovascular treatment in acute CVST?

Venous insufficiency and multiple sclerosis?

Chronic intracranial hypertension?

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Long-term sequelaeLong-term sequelaeThe incidence of dural arteriovenous fistula among CVST

survivors was:

1% to 3%The incidence of suspected idiopathic intracranial

hypertension was:

25%Underlying CVST in patients referred for idiopathic

intracranial hypertension was:

10%

The incidence of dural arteriovenous fistula among CVST survivors was:

1% to 3%The incidence of suspected idiopathic intracranial

hypertension was:

25%Underlying CVST in patients referred for idiopathic

intracranial hypertension was:

10%

Saposnik G; American Heart Association Stroke Council. Stroke. 2011;42(4):1158-92.

Long-term sequelaeLong-term sequelaeThe incidence of dural arteriovenous fistula among CVST

survivors was:

1% to 3%The incidence of suspected idiopathic intracranial

hypertension was:

25%Underlying CVST in patients referred for idiopathic

intracranial hypertension was:

10%

The incidence of dural arteriovenous fistula among CVST survivors was:

1% to 3%The incidence of suspected idiopathic intracranial

hypertension was:

25%Underlying CVST in patients referred for idiopathic

intracranial hypertension was:

10%

In patients with the clinical features of idiopathic intracranial hypertension,

imaging of the cerebral venous system is recommended to exclude CVST (Class I; Level of Evidence C).

Saposnik G; American Heart Association Stroke Council. Stroke. 2011;42(4):1158-92.

DAVF with right sigmoid sinus and internal jugular vein occlusion

DAVF with right sigmoid sinus and internal jugular vein occlusion

C

DAVF with right sigmoid sinus and internal jugular vein occlusion

DAVF with right sigmoid sinus and internal jugular vein occlusion

C

Activation of

existingchannels

ORNew vesselformation

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Peri-osteal arterial branchesfrom external carotid artery

Diploic veins from Transverse sinus

Arterial and venous channels within the occipital bone-magnified image of bone slices

Endovascular occlusion of segment proximal to occluded segement-

site of entry of fistulas

Endovascular occlusion of segment proximal to occluded segement-

site of entry of fistulasC

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Dural arteriovenous fistulas?

Anatomical considerations?

Endovascular treatment in acute CVST?

Venous insufficiency and multiple sclerosis?

Chronic intracranial hypertension?

Stent placement in transverse sinus-ΔP (mm Hg)

Re: Bussière M. AJNR Am J Neuroradiol. 2010;31(4):645-50.

Stent placement in transverse sinus-ΔP (mm Hg)

Re: Bussière M. AJNR Am J Neuroradiol. 2010;31(4):645-50.

Pre-stent

Post-stent

24

13

14

15

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Stent placement for cerebral venousstenosis

Stent placement for cerebral venousstenosis

52 pts with

intracranialhypertension

+Transverse

sinusstenosis

Symptomsimproved(100%)

Recurrenceof symptoms associated

with recurrentstenosis (n=6)

Ahmed RM, et al. AJNR Am J Neuroradiol. 2011;32(8):1408-14.

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Cerebral venous sinus thrombosis and chronic venous outflow obstruction

Dural arteriovenous fistulas?

Anatomical considerations?

Endovascular treatment in acute CVST?

Venous insufficiency and multiple sclerosis?

Chronic intracranial hypertension?

Chronic cerebrospinal venous insufficiency Chronic cerebrospinal venous insufficiency •Reflux in the internal jugular veins and/or vertebral veins in sitting and supine posture;

•Reflux in the deep cerebral veins;

•High-resolution B-mode evidence of internal jugular vein stenoses;

•Flow not Doppler-detectable in the internal jugular veins and/or vertebral veins;

•Reverted postural control of the main cerebral venous outflow pathways.

Re: J Neurol Neurosurg Psychiatry. 2009 Apr;80(4):392-9.

Chronic cerebrospinal venous insufficiencyand multiple sclerosis

Chronic cerebrospinal venous insufficiencyand multiple sclerosis

Re: Zamboni P. J R Soc Med. 2006 Nov;99(11):589-93.

Chronic cerebrospinal

venous insufficiency

Multiplesclerosis

Venous stasisFe deposit

Autoimmuneresponse

Venous changesrelated to MS duration

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Chronic cerebrospinal venous insufficiencyand multiple sclerosis

Chronic cerebrospinal venous insufficiencyand multiple sclerosis

Re: Zamboni P. J R Soc Med. 2006 Nov;99(11):589-93.

Chronic cerebrospinal

venous insufficiency

Multiplesclerosis

Venous stasisFe deposit

Autoimmuneresponse

Venous changesrelated to MS duration

Safety profile of endovascular treatment for chronic cerebrospinal venous insufficiency in

patients with multiple sclerosis

Safety profile of endovascular treatment for chronic cerebrospinal venous insufficiency in

patients with multiple sclerosis

Petrov I, et al. J Endovasc Ther. 2011 Jun;18(3):314-23.

495 pts with

multiple sclerosis

and venousinsufficiency

1012lesions were

treated

Vein rupture (0.4%), Vein dissection (3.0%),

Acute thrombosis (1.6%), Acute recoil (0.2%);

Cardiovascular and Interventional Radiological Society of Europe commentary on the treatment of chronic

cerebrospinal venous insufficiency

Cardiovascular and Interventional Radiological Society of Europe commentary on the treatment of chronic

cerebrospinal venous insufficiency

The basis for this new treatment rests on anecdotal evidence and successful testimonies by patients on the

Internet. CIRSE believes that this is not a sound basis on which to offer a new treatment, which

could have possible procedure-related complications, to an often desperate patient population

Re: Cardiovasc Intervent Radiol. 2011 Feb;34(1):1-2. Epub 2010 Dec 7.

ConclusionsConclusions With advancements in endovascular techniques, a

larger spectrum of acute and chronic cerebral venous diseases can be treated.

An evidence based approached is paramount to ensure that these new interventions are indeed beneficial to the patients.

With advancements in endovascular techniques, a larger spectrum of acute and chronic cerebral venous diseases can be treated.

An evidence based approached is paramount to ensure that these new interventions are indeed beneficial to the patients.

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ReferencesReferences Canhao P, Falcao F, Ferro JM. Thrombolytics for cerebral

sinus thrombosis: a systematic review. Cerebrovasc Dis 2003; 15: 159–66.

Canhao P, Falcao F, Ferro JM. Thrombolytics for cerebral sinus thrombosis: a systematic review. Cerebrovasc Dis 2003; 15: 159–66.