357 cerebral venous and sinus thrombosis

Cerebral venous and sinus thrombosis

Youmans Chapter 357Kenneth C. Liu

Bronwyn E. HamiltonStanley L. Barnwell

Outline• Pathogenesis• Incidence• Clinical findings• Diagnostic evaluation• Treatment

Pathogenesis• Thrombosis in cerebral vein venous hypertension

hypoxia of the brain neurolonal ischemia• Cerebral edema, massive hemorrhage, bilateral cerebral

infarction• Mechanism

– alteration in the physical activity of dural sinuses and vein

– chemical properties of blood– hemodynamic properties of blood flow

Pathogenesis• Vascular injury from trauma local endothelial damage

and altered hemodynamic• Abnormality of blood coagulation factor : dysfunction of

protein C,protein S, antithrombin III, plasminogen hypercoagulable states

• Risk factor :Factor V, prothrombin gene mutation, lupus anticoagulant, anti-phospholipid,anticardiolipin antibodies

Pathogenesis• Infection : alter coagulation cascade and inducible

hypercoagulable state– Cavernous sinus thrombosis, transverse sinus

thrombosis : sinusitis, otitis, mastoiditis– Staphylococcus aureus,gram negative rod,

Aspergillus• More common in young women, puerperium, oral

contraceptive• Idiopathic

Incidence• Rare disease• All age group• Both sex, women 20-40 years old

Clinical finding• Most common : headache(earliest symptoms) and

Seizure• Nausea, vomiting, visual change, Papilledema from

increase intracranial pressure• Confusion, agitation, mental status change• Focal neurological deficit from venous hypertension and

cerebral infarction• Aphasia, hemianopia, hemisensory• Acute mimic acute ischemic stroke, subacute are more

common• Fluctuating or progressive

Clinical finding• Clinical feature to the site

– Superior saggital sinus or transverse sinus : isolated intracranial hypertension

– Extend to cortical vein : focal deficit, seizure– Bilateral deficit : late sign of superior saggital sinus– Transverse sinus CVT may associated with otalgia,

otorrhea, cervical tenderness and lymphadenopathy

Clinical finding• Clinical feature to site

– Cavernous sinus CVT : eyelid edema, chemosis, retroorbital pain and exophthalmos, paralysis of CN III,IV, V1,V2,VI

– Involve deep venous system : akinetic mutism, coma, decerebration

– Memory disturnance, minor confusion– Cerebellar vein thrombosis : extremely rare and often

lethal

Diagnostic evaluation• Key diagnostic because clinical highly variables• CT

– Dense vein– Cord sign : hyperdense on NC CT– Dense triangle sign(delta sign) : specific to SSS on Contrast CT– First 1-2 wk after thrombosis– False positive : neonate, dehydrate, elevated hemoglobin– False negative is high

Diagnostic evaluation• MRI

– MRA, MRV : best method– Thrombus, edema, hemorrhagic infaction– False positive : sinus congenital absent or hypoplastic– False negative : methemoglobin mimic flowing blood, pt not

cooperate, poor technic

• Peripheral dural leaf enhancement along with nonopacified thrombus

A : axial,NC : 59 yrs old woman c headache, wedge-shaped, Hemorrhagic mass-like at lt.fronto-parietal areaDdx : hemorrhagic stroke, vascular malformation, tumour, cortical vein thrombosisB : angiogram : filling defect in superior saggital sinus but no dominant superior cortical vein of Trolard identified hemorrhagic stroke

• A : Man 41 Yrs old : new-onset headache and seizure, Lt frontal mass c internal hemorrhagic, surgical explore was performed for suspected cavernous malformation, Finding : anterior third of SSS and the associated cortical vein was thrombosed

• B : CTA in same PT : delta sign• C : lateral venous-phase angiography : lack of contrast enhancement in SSS• D : lateral venous-phase angiography : venous collateral

• A : vasogenic edema, superimposed hemorrhage, R/O vein of Labbe occlusion

• B : MRV transverse sinus thrombosis• C : source image

Treatement• Cause• Symptoms from increase ICP• Seizure or focal deficit

Antithrombotics• Heparin

– Early stage(< 7 days)– PTT 2-2.5 upper normal limit– Condition stabilize, add warfarin– Keep INR 2-3 – No underlying cause : 6 Mo– Hypercoaguable state : lifelong

• Complication : intracerebral hemorrhage

Systemic thrombolytics• Streptokinase, urokinase, tissue plasminogen activator (t-PA)• Complication

• GI bleeding• ICH

• Contraindication• Recent child birth• History of a bleeding diathesis• Recent major surgery• Recent major trauma• Active GI bleeding• Inflammatory bowel disease

• No strong data support

Interventional Neuroradiology• Direct mechanical manipulation and remove clot• Local infusion of thrombolytics • Route : transfemoral, transjugular• Endovascular local thrombolysis and mechanical

thrombectomy are generally safe and effective in opening venous occlusion

• Pt had better outcome

Urokinase

Urokinase

rt-PA• Urokinase not available in USA• Advantage

– Shorter half-life (5 vs 15 min)– Better clot lysis

Surgery• Indicaiton

– Malignant intracranial hypertension– Acute visual loss– Intracranial hemorrhage

• Ventriculostomy– Diversion of CSF– Monitoring of intracranial pressure

• Craniotomy with direct puncture of the dural sinuses and thrombectomy

Outcome• Mortality rate 30-80 %• Prognosis

– Coma– Extreme age : infant, elderly– Site of thrombosis : deep venous system,cerebellar system– Severe intracranial pressure– Underlysis : sepsis, malignancy

Thank you