Cerebral Venous Thrombosis

Reviewed and revised 15 August 2015


  • Cerebral venous thrombosis (CVT) refers to thrombus formation in either the deep or superficial venous drainage systems of the brain
  • The etiology is multifactorial and the presentation is variable, with diagnosis requiring a high index of suspicion
  • CVT is a rare condition (~1% of all strokes) that is more common in females (x3 risk) and younger adults (80% <50 years-old)
  • diagnosis is often delayed (median ~4 days), which leads to increased morbidity and mortality
  • the goals of therapy are to stabilse the patient, remove the occlusion in the vein, and stop clot propagation with anticoagulation


Venous drainage of the brain

  • Drained blood enters the major dural sinuses: Superior sagittal sinus (SSS), inferior sagittal sinus (ISS), lateral sinus (LS), cavernous sinus and straight sinus, and then to the internal jugular vein (IJV)
  • Superficial venous system has numerous anastomses and predominantly drain the SSS and the LS
  • Deep white matter and basal ganglia are drained by the deep venous system toward the vein of Galen

Pathophysiology of CVT

  • CVT causes increased venous pressure
    • decreases CSF drainage and increases intracranial pressure
    • increases venular and capillary pressure
      • decreases capillary perfusion and subsequently cerebral perfusion, causes ischemia, leads to cytotoxic edema
      • disrupts the blood-brain barrier causing vasogenic edema
      • causes venous and capillary rupture causing intrapaenchymal haemorrhage
  • Clinical presentation (e.g. headache +/- various neurological deficits) results from the above pathophysiology and depends on:
    • thrombosis location
    • time since onset
    • presence of parenchymal brain involvement (e.g. haemorrhage) or intracranial hypertension

Thrombus location is associated with certain signs and symptoms:

  • Cavernous sinus thrombosis: ocular signs (orbital pain, chemosis, proptosis, oculomotor palsy)
  • Cortical vein thrombosis: motor deficits, sensory deficits, seizures
  • Sagittal sinus thrombosis: motor deficits, bilateral deficits, seizures
  • Lateral sinus thrombosis: isolated intracranial hypertension
  • Left transverse sinus thrombosis: Aphasia
  • Deep venous sinus (straight) thrombosis: behavioural symptoms (thalamic lesions)

About 50% of CVT undergo haemorrhagic transformation prior to anticoagulation


CVT is often multi-factorial in aetiology

  • underlying thrombophilia (acquired or hereditary)
  • high estrogen exposure
    • estrogen-based oral contraceptives
    • pregnancy
    • in vitro fertilisation treatment
  • other pro-thrombotic states
    • neoplastic disorders (e.g. direct compression, invasion of cerebral sinuses, chemotherapy)
    • para-meningeal infections (e.g.sinusitis, otitis media, meningitis, head and neck infections)
    • mechanical injury to the sinuses or jugular veins (e.g. trauma, venous catheterisation, neurosurgical procedures)
    • drugs (e.g. androgens, IV immunoglobulin)
    • haematological disorders (e.g. paroxysmal nocturnal haemoglobinuria, myeloproliferative disorders)
    • systemic disorders (e.g. SLE, Behçet disease, Inflammatory bowel disease, Nephrotic syndrome)
  • low CSF volume (e.g. rare reports post-LP)


Suspect CVT if:

  • Headache (most common symptom, may be isolated; no specific pattern), especially if:
    • occurring in a pregnant female in the 3rd trimester
    • in a young female recently started on oral contraceptives
    • persistent and atypical in nature (can be gradual or sudden onset; can be localised or diffuse), especially in young adults
  • Stroke in the absence of typical cardiovascular risk factors (may have motor, visual or sensory deficits; seizures are common)
  • Haemorrhagic infarcts present on neuroradiological imaging that are:
    • multiple, and/or
    • do not conform to a particular arterial distribution
  • Intracranial hypertension that is otherwise unexplained (may be insidious in onset with papilloedema, or present as encephalopathy/ coma)
  • Altered vision in an individual with recent sinusitis
  • Neurological symptoms in patients with known risk factors for cerebral venous thrombosis (See above)



  • D-dimer (normal in 4% of cases and up to 40% of those presenting with isolated headache)
  • Lumbar puncture is not recommended unless needed to rule out meningitis or as therapy for raised ICP (CSF findings are non-specific in CVT: lymphocytic pleocytosis, elevated RBCs and protein)
  • Thrombophilia screen
    • generally indicated 2 to 4 weeks after completion of anticoagulation
    • limited value of testing in the acute setting or in patients taking warfarin


  • CTV (CT combined with venography)
    • 95% sensitive
    • more widely available
    • can diagnose associated conditions (e.g. sinusitis) or alternate differentials
    • findings on CTB include the “string sign”, the “dense triangle sign,” and the “empty delta sign”
  • MRI (gradient echo T2 susceptibility weighted sequence with MR venography)
    • avoids radiation exposure and problems with contrast allergy and nephropathy
  • Catheter cerebral angiography can be useful in patients with inconclusive CTV or MRV in whom a clinical suspicion for CVT remains high
    • a negative plain CT or MRI does not rule out CVT



  • attend to ABCs and address life-threats
    • coma
    • seizures
    • raised ICP

Specific therapy

  • anticoagulation (unless absolute contra-indication present)
    • therapeutic heparin or LMWH initially
      • presence of intracranial haemorrhage in conjunction with CVT is not be considered a contraindication for anticoagulation
      • can transition to warfarin once stable
    • duration
      • 3-6 months if provoked (modifiable risk factor)
      • 6-12 months if unprovoked
      • indefinite if recurrent CVT, a persistent highly pro-thrombotic state or occurrence of other thrombotic complications (e.g. PE)
  • thrombolysis (systemic or catheter-directed)
    • uncertain role use to risk of haemorrhage
    • can consider as last resort if anticoagulation fails (e.g. neurological deterioration despite therapeutic anticoagulation, in the absence of intracranial haemorrhage)
  • intravascular thrombolysis
    • emerging therapy with uncertain role
  • early follow-up CT or MR venogram in patients with persistent or evolving symptoms to rule out propagation of thrombus

Supportive care and monitoring

  • maintain adequate hydration
  • consider ICP monitoring if severe neurological deterioration (CSF drainage may be therapeutic)
  • periodic assessments of the visual fields and visual acuity

Seek and treat underlying cause and complications

  • address modifiable risk factors
    • e.g. avoid estrogen-based contraception (can use progestogen only pill or intra-uterine devices such as Mirena)
    • e.g. treat para-meningeal infection
  • treat complications
    • secondary seizure prophylaxis is indicated if a patient with CVT has a seizure
    • in patients with neurological deterioration due to severe mass effect or intracranial hemorrhage causing intractable intracranial hypertension, decompressive hemicraniectomy may be considered

Disposition, consults and follow up

  • early neurology and haematology consultation
  • admission to a stroke unit is preferable; may required management in an HDU/ ICU setting
  • follow-up CTV or MRV at 3 to 6 months after diagnosis is reasonable to assess for recanalization of the occluded cortical vein/sinuses in stable patients
  • “For women with a history of CVT, prophylaxis with LMWH during future pregnancies and the postpartum period is probably recommended” (Saposnik et al, 2011)


According to Thorell et al, 2015:

  • 4.3-5.6% mortality during acute hospitalization; ~8.3 at the end of follow up in one study (median 16 months)
  • good recovery in most, 88% survivors had complete recovery or only mild deficits
  • about half of survivors have ongoing headaches
  • 2/3 achieve recanalised cerebral veins in the first few months
  • recurrence is rare, ~3% (even in pregnancy-associated CVT)
  • other thrombotic complications may occur (~4%)

Worse long-term prognosis if:

  • Cause is:
    • malignancy
    • CNS infection
  • Associated intracranial haemorrhage
  • altered mental status or GCS <9 on admission
  • Male
  • Age >37 years
  • CVT affects the deep venous system

References and Links


Journal articles

  • Alvis-Miranda HR, Milena Castellar-Leones S, Alcala-Cerra G, Rafael Moscote-Salazar L. Cerebral sinus venous thrombosis. J Neurosci Rural Pract. 2013;4:(4)427-38. [pubmed] [free full text]
  • Coutinho JM, de Bruijn SF, deVeber G, Stam J. Anticoagulation for cerebral venous sinus thrombosis. Stroke. 2012;43:(4)e41-e42. [pubmed] [free full text]
  • Piazza G. Cerebral venous thrombosis. Circulation. 2012;125:(13)1704-9. [pubmed] [free full text]
  • Saposnik G, Barinagarrementeria F, Brown RD, et al. Diagnosis and management of cerebral venous thrombosis: a statement for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2011;42:(4)1158-92. [pubmed] [free full text]
  • Thorell SE, Parry-Jones AR, Punter M, Hurford R, Thachil J. Cerebral venous thrombosis-a primer for the haematologist. Blood Rev. 2015;29:(1)45-50. [pubmed] [free full text]

FOAM and web resources

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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