Date post: | 13-Apr-2017 |
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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