Table of Contents
Primary Category
Neurocritical Care
P-Category
Secondary Category
S-Category
Authors:
Introduction
- Thrombosis of cerebral veins and sinuses
- Relatively rare and frequently unrecognized condition
- Potentially severe and fatal condition
Epidemiology
- 0.5% of all strokes
- Prevalence: 5/1,000,000 people
- Common in Asia and the Middle East due to increased rates of pregnancy and infection in these nations
- Important cause of stroke in young people
- Common in 20-50 years age group, less common after age 65
- More common in females (2.9:1) due to estrogen changes, hormone replacement therapy, and pregnancy
- Superior sagittal sinus thrombosis
- most common type
- Frequently presents with bilateral deficits
Etiology
- Risk Factors: related to factors affecting Virchow’s triad (hypercoagulability, endothelial injury and venous stasis)
- Both hereditary and acquired prothrombotic conditions predispose to CVT
- Causes and risk factors
- Hereditary coagulopathies
- Antithrombin III deficiency
- Protein C and S deficiency
- Factor V leiden
- Factor II gene mutations
- Methylenetetrahydrofolate reductase gene mutation
- Von willebrand disease.
- Acquired coagulopathies
- Nephrotic syndrome
- Antiphospholipid antibody syndrome
- Hyperhomocysteinemia
- Prothrombotic condition
- Pregnancy
- Puerperium
- Infectious causes
- Otitis media
- Sinusitis
- Meningitis
- Mastoiditis
- Drugs
- Oral contraceptive pills
- L-asparaginase
- Corticosteroids
- Androgens
- Inflammatory conditions
- Systemic Lupus erythematosus
- Sarcoidosis
- Granulomatosis with polyangiitis
- Inflammatory bowel disease
- Hematological disorders
- Paroxysmal nocturnal hemoglobinuria
- Primary polycythemia
- Sickle cell disease
- Disseminated intravascular coagulation
- Thrombocythemia
- Leukemia
- Trauma
- Neoplasms
- Idiopathic
Pathophysiology
- Cortical vein thrombosis
- Raised venous and capillary pressure
- Disruption of blood brain barrier
- Formation of cerebral edema that develops into hemorrhagic venous infarction
- Venous infarction causes focal neurological deficits and seizures
- Cerebral sinus thrombosis
- CSF outflow obstruction
- Development of intracranial hypertension
- Headache and vision problems
Clinical Features
- 4 prominent clinical syndromes present
- Isolated intracranial hypertension
- Focal syndrome
- Diffuse encephalopathy
- Cavernous sinus syndrome
- Headache: Most common
- Seizures
- Focal neurological deficit
- Aphasia
- Hemiparesis
- Altered consciousness
- Loss of vision
Differential Diagnosis
- Idiopathic intracranial hypertension (pseudotumor cerebri)
- Arterial ischemic stroke
- Primary intracerebral hemorrhage
- Hemorrhagic stroke due to a vascular malformation
- Meningitis/encephalitis
- Brain abscess
- Systemic lupus erythematosus
- Sarcoidosis
- Antiphospholipid syndrome
Figure 1: Cerebral Sinus Thrombosis on CT Brain
Case courtesy of Dr Bruno Di Muzio, Radiopaedia.org, rID: 41031
Diagnosis
- Combined MRI of brain and Magnetic resonance venography: Gold standard for diagnosis
- MRI of brain
- Identifies thrombosed blood vessels
- Early thrombus formation: Hypodense from deoxyhemoglobin
- Late thrombus formation: Hyperdense from methemoglobin
- MR venography
- empty delta sign (triangular filling defect due to thrombus in sagittal sinus)
- CT scan of Head and CT venography
- Inferior to MRI due to bone infarct and radiation exposure
- Non-contrast CT head: hyperdense cortical veins or dural sinus
- CT venography: Ideal for subacute or chronic thrombosis due to difference in density of thrombosed sinus
- Catheter angiography
- Associated with complications
- Used only
- When MRI and CT are inconclusive
- Endovascular procedure is required
- D-dimer Test: Increased in current patients with cerebral venous thrombosis. Hence, negative d-dimer in such patients rules out CVT. This does not apply in case of a patient with CVT with a current isolated headache where d-dimer can be normal
Treatment
- Admit patients to the stroke unit
- Correct underlying causes like infection and dehydration
- Antithrombotic treatment
- Subcutaneous Low molecular weight heparin or
- IV heparin
- Worsening of medical condition despite adequate anticoagulation and ruling out other causes of worsening of condition
- Local IV thrombolysis or
- Mechanical thrombectomy
- Prevention of recurrent/future thrombotic events
- Oral anticoagulation
- 3-6months: for brief risk factors
- 6-12 months: idiopathic CVT/mild hereditary thrombophilia
- Indefinite: recurrent CVT/ severe hereditary thrombophilia
- Symptomatic treatment
- Treatment of raised ICP
- Monitor ICP
- Elevate head of bed
- Hyperventilation
- Sedation
- Treat with glycerol and mannitol
- Lumbar puncture in presence of vision threatening papilloedema, drain CSF before initiating heparin
- Surgery: VP shunt, Lumboperitoneal shunt, optic nerve fenestration surgery
- Impending herniation: Decompressive hemicraniectomy
- Antiepileptics in patients with seizures
Complications
- Hydrocephalus
- 15% of patients
- Obstructive type due to basal ganglia and thalamus edema
- Associated with worse prognosis
- Intracranial hypertension
- Headache with or without papilloedema
- Vision threatening: treat with immediate lumbar puncture, Shunt surgery
- Transtentorial herniation
- Major cause of immediate mortality
- Treatment: Decompressive hemicraniectomy
Prognosis
- Death rate: 8-10%
- 80% recover without any sequelae
- Overall good clinical outcome when compared to arterial stroke
- Poor prognostic factors
- Brain infection
- Presence of any neoplasms
- Deep vein thrombosis
- Intracerebral hemorrhage
- GCS>9 at the time of admission
- Male gender
- Age>37 years
- Altered mental status
- Death prognostic factors at 30 days
- Decreased consciousness
- Deep venous thrombosis
- Right sided intracranial bleeding
- Injury at the posterior fossa
- Major cause of acute mortality
- Herniation of the brain (transtentorial)
- Increase in size of hematoma
- Widespread cerebral edema
- Pulmonary embolism
- Status epilepticus
Bibliography
- Ribes MF. Des recherches faites sur la phlébite. Revue Médicale Française et Etrangère et Journal de Clinique de l’Hôtel-Dieu et de la Charité de Paris 1825; 3: 5–41.
- Bousser MG, Ferro JM. Cerebral venous thrombosis: an update. Lancet Neurol 2007;6(2):162Y170.
- Khealani, B. A. et al. Cerebral venous thrombosis: a descriptive multicenter study of patients in Pakistan and Middle East. Stroke 39, 2707–2711 (2008).
- Stam J (2005) Thrombosis of the cerebral veins and sinuses. N Engl J Med 352:1791–1798.
- Janghorbani, M. et al. Cerebral vein and dural sinus thrombosis in adults in Isfahan, Iran: frequency and seasonal variation. Acta Neurol. Scand. 117, 117–121(2008).
- Coutinho JM (2015) Cerebral venous thrombosis. J Thromb Haemost 13:S238–S244. https://doi.org/10.1111/jth.12945
- Coutinho JM, Zuurbier SM, Aramideh M, Stam J (2012) The incidence of cerebral venous thrombosis: a cross-sectional study. Stroke 43:3375–3377. https://doi.org/10.1161/STROKEAHA.112.671453
- Crassard I, Soria C, Tzourio Ch, et al. A negative D-dimer assay does not rule out cerebral venous thrombosis: a series of 73 patients. Stroke 2005; 36: 1716–19.
- Ferro JM, Canhao P, Stam J, Bousser MG, Barinagarrementeria F. Prognosis of cerebral vein and dural sinus thrombosis: results of the International Study on Cerebral Vein and Dural Sinus Thrombosis (ISCVT). Stroke 2004; 35: 664–70.
- Canhão P, Ferro JM, Lindgren AG, Bousser MG, Stam J, Barinagarrementeria F. Causes and predictors of death in cerebral venous thrombosis. Stroke 2005; 36: 1720–25.
- Piotr R and Barbara K. Cerebral venous and sinus thrombosis. Udar Mo´zgu 2010; 12: 47–50.
- Wasay, M. et al. Cerebral venous thrombosis: analysis of a multicenter cohort from the United States. J. Stroke Cerebrovasc. Dis. 17, 49–54 (2008).
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