Cerebral venous
and sinus thrombosis
Youmans Chapter 357
Kenneth C. Liu
Bronwyn E. Hamilton
Stanley 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 area
Ddx : hemorrhagic stroke, vascular malformation, tumour, cortical vein
thrombosis
B : 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

357 Cerebral venous and sinus thrombosis

  • 1.
    Cerebral venous and sinusthrombosis Youmans Chapter 357 Kenneth C. Liu Bronwyn E. Hamilton Stanley L. Barnwell
  • 2.
    Outline • Pathogenesis • Incidence •Clinical findings • Diagnostic evaluation • Treatment
  • 3.
    Pathogenesis • Thrombosis incerebral 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
  • 4.
    Pathogenesis • Vascular injuryfrom 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
  • 5.
    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
  • 6.
    Incidence • Rare disease •All age group • Both sex, women 20-40 years old
  • 7.
    Clinical finding • Mostcommon : 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
  • 8.
    Clinical finding • Clinicalfeature 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
  • 9.
    Clinical finding • Clinicalfeature 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
  • 10.
    Diagnostic evaluation • Keydiagnostic 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
  • 11.
    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
  • 13.
    • Peripheral duralleaf enhancement along with nonopacified thrombus
  • 14.
    A : axial,NC: 59 yrs old woman c headache, wedge-shaped, Hemorrhagic mass-like at lt.fronto-parietal area Ddx : hemorrhagic stroke, vascular malformation, tumour, cortical vein thrombosis B : angiogram : filling defect in superior saggital sinus but no dominant superior cortical vein of Trolard identified  hemorrhagic stroke
  • 15.
    • 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
  • 16.
    • A :vasogenic edema, superimposed hemorrhage, R/O vein of Labbe occlusion • B : MRV transverse sinus thrombosis • C : source image
  • 17.
    Treatement • Cause • Symptomsfrom increase ICP • Seizure or focal deficit
  • 18.
    Antithrombotics • Heparin – Earlystage(< 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
  • 19.
    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
  • 20.
    Interventional Neuroradiology • Directmechanical 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
  • 21.
  • 22.
  • 23.
    rt-PA • Urokinase notavailable in USA • Advantage – Shorter half-life (5 vs 15 min) – Better clot lysis
  • 25.
    Surgery • Indicaiton – Malignantintracranial hypertension – Acute visual loss – Intracranial hemorrhage • Ventriculostomy – Diversion of CSF – Monitoring of intracranial pressure • Craniotomy with direct puncture of the dural sinuses and thrombectomy
  • 26.
    Outcome • Mortality rate30-80 % • Prognosis – Coma – Extreme age : infant, elderly – Site of thrombosis : deep venous system,cerebellar system – Severe intracranial pressure – Underlysis : sepsis, malignancy
  • 27.

Editor's Notes

  • #22 1.Midline craniotomy c direct catheterization to SSS 2.Direct puncture to SSS , without craniotomy 3.Direct transjugular thrombolytic 4.Direct transfemoral thrombolytic 5.Direct infusion of Urokinase