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CEREBRAL VENOUS THROMBOSIS
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CEREBRAL VENOUS THROMBOSIS

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  • 1. Cerebral Venous Thrombosis
    DR.SRIRAMA ANJANEYULU
  • 2. Introduction
    Uncommon compared to arterial stroke
    Significant morbidity
    Recognised early and more commonly with newer imaging techniques
  • 3.
  • 4.
  • 5.
  • 6.
  • 7.
  • 8. Incidence
    0.5% of all strokes.
    In 1973, Towbin reported CVT in 9% of 182 autopsies.
    In 1995, Daif reported a frequency in Saudi Arabia of 7 cases per 100,000 hospital patients.
    Venous to arterial strokes-1:62.5.
    Towbin A.  Stroke. May-Jun 1973;4(3):419-30.
    Daif A, Awada A, al-Rajeh S, et al. Stroke. Jul 1995;26(7):1193-5. 
  • 9. Mortality &morbidity
    Mortality in untreated CVT- 13.8-48%.
    Analyzed 91 consecutively admitted patients from 1995 to 1998 over a mean 1-year follow-up interval.
    7% died in the acute phase
    1% died during the one year follow-up
    82% recovered completely
    1% were dependent
    59% developed thrombotic events during the follow-up
    10% had seizures
    11% complained of severe headaches
    1 patient experienced severe visual loss.
    Ferro JM, Lopes MG, Rosas MJ, et al. results of the venoport study. Cerebrovasc Dis. 2002;13(4):272
  • 10. series of 34 patients with confirmed cerebral venous thrombosis.
    10 patients (30%) -episodic headaches
    3 patients (8.8%) - seizures
    4 patients (11.7%) -pyramidal signs
    2 (5.9%) - visual deficits
    Mild nonfluent aphasia in 3 patients
    Working memory deficit and depression of mood in 6 patients (17.6%)
    Buccino G, Scoditti U, Patteri I, et al.  ActaNeurol Scand. May 2003;107(5):330-5. 
  • 11. SEX&AGE
    In a series of 110 cases, Ameri and Bousser found a female-to-male ratio of 1.29:1.
    61% of women with CVT were aged 20-35 years.
    Ameri A, Bousser MG.  NeurolClin. Feb 1992;10(1):87-111
  • 12. Mechanisms Leading to the Clinical Manifestations
    The occlusion of a cerebral vein -localized brain edema and venous infarction.
    HPE- swollen veins, edema, ischemic neuronal damage and petechialhges that can merge - large hg.
    Cytotoxic edema by local ischemia damages the energy-dependent cellular membrane pumps and induce intracellular swelling.
    Vasogenic edema by disruption in the BBB and leakage of plasma into the interstitial space is reversible .
    The occlusion of a major sinus - development of intracranial hypertension due to impaired absorption of CSF.
    Stam J. Adv Neurol 2003;92:233-40.  
  • 13. Headache
    MC symptom of CVT
    Stretching of nerve fibres in the walls of the occluded sinus and local inflammation .
    1.Headache of unusual type that started a few days or wks earlier with other CNS symptoms.
    2.In a context of isolated intracranial hypertension.
    3.Only symptom , in the absence of intracranial hypertension, SAH or meningitis.
    Isolated headache is sometimes of the thunderclap type, mimicking a subarachnoid hemorrhage
  • 14. Isolated focal neurological deficits
    long-lasting focal neurological deficits due to stroke (either venous ischemia or intra-cerebral hemorrhage) or edema.
    Transient focal neurological deficits mimicking transient ischemic attacks.
  • 15. Diffuse encephalopathies with seizures
    In patients with parenchymal lesions, the clinical picture is more severe and may include at various degrees:
    Coma
    motor deficits or aphasia
    seizures (focal or generalized seizures, including status epilepticus).
    Seizures - more common in sagittal sinus and cortical vein thrombosis.
  • 16. Other clinical presentations
    Attacks of migraine with aura
    Isolated psychiatric disturbances
    Pulsatile tinnitus
    Isolated or multiple cranial nerve involvement
  • 17. Clinical manifestations and the site of venous occlusion
    Cortical veins -motor or sensory deficits, seizures or both.
    Sagittal sinus- motor deficits that are alternating or bilateral,seizures and rarely isolated intracranial hypertension.
    Lateral sinus -isolated intracranial hypertension, associated with aphasia when the left transverse sinus is occluded.
    Deep cerebral veins -severe clinical presentation with coma, delirium and bilateral motor deficits, symptoms may be of milder if the thrombosis is limited.
    Cavernous sinus- orbital pain, chemosis, proptosis and oculomotor palsies.
    Leys D, Cordonnier C. Ann Indian AcadNeurol 2008 ;11:79-87.
  • 18. Specificities of clinical manifestations in the elderly
    In ISCVT, 8.2% of patients were aged 65 years or over.
    Isolated intracranial hypertension -less frequent
    Impaired consciousness and mental status impairment-more frequent .
    CVT-DD for impaired consciousness in elderly
    Cancers more frequently found as the cause than in younger CVT pts.
    Ferro JM, Canhao P, Bousser MG, Stam J, Barinagarrementeria F; ISCVT Investigators. Stroke 2005;36:1927-32.  
  • 19. I. Gosk-Bierskaetal,Neurology 2006;67;814-819
  • 20.
  • 21.
  • 22. Laboratory Studies
    Diagnosis made on cl. presentation and imaging studies.
    For determining the possible causes of CVT.
    CBC -polycythemia,PC decreased in TTP; leukocytosis in sepsis.
    Antiphospholipid and anticardiolipin antibodies .
    protein S, protein C, antithrombin III, lupus anticoagulant, and Leiden factor V mutation.
    Sickle cell preparation or hemoglobin electrophoresis .
    ESR,ANA-systemic lupus erythematosus, Wegener granulomatosis, and temporal arteritis.
    Urine protein –NS.
    LFT-cirrhosis.
  • 23. D-Dimers
    18 pts with CVT, Tardy et al reported that D-dimer levels < 500 ng/mL had a negative predictive value for ruling out the diagnosis in pts with acute headache.
    54 consecutive pts with headache suggestive of CVT, Lalive found that 12 had CVT and, of those, 10 had D-dimer levels >500 ng/mL.
    Kosinski et al (2004) -343 pts with symptoms s/o CVT.
    The diagnosis was confirmed in 35, with 34 of these pts showing elevated D-dimer levels > 500 mcg/L.
    Of the 308 pts not having CVT, 27 had positive values.
    Sensitivity was 97.1%, with a negative predictive value of 99.6%.
    Specificity was 91.2%, with a positive predictive value of 55.7%.
    Tardy B, Tardy-Poncet B, Viallon A, et al.  Am J Med. Aug 15 2002;113(3):238-41.
    Lalive PH, de Moerloose P, Lovblad K, et al. Neurology. Oct 28 2003;61(8):1057-60. 
    Kosinski CM, Mull M, Schwarz M, et al.  Stroke. Dec 2004;35(12):2820-5. 
  • 24. Imaging Studies MRI
    • Infarct that does not follow the distribution of an expected arterial occlusion.
    • 25. Show absence of flow void in the normal venous channels.
    • 26. MRV is an excellent method of visualizing the dural venous sinuses and larger cerebral veins.
    • 27. Single-slice phase-contrast angiography (SSPCA) takes less than 30 seconds and provides rapid and reliable information. Procedure of choice in diagnosing cerebral venous thrombosis.
    • 28. In a study of 21 patients, Adams demonstrated a specificity and sensitivity of 100% for SSPCA when compared to alternative imaging techniques.
    Adams WM, Laitt RD, Beards SC, et al. EurRadiol. 1999;9(8):1614-9. 
  • 29. MRI
    Very early stage of an acute thrombosis, MRI alone is limited by flow artefacts that can lead to false positives and the lack of hyperintense signal on T1- and T2-w images.
    During the first 3-5 days, the thrombosed sinus appears as an isointense signal on T1-w sequences and a hypointense signal on T2-w sequences: it can, therefore be very difficult to differentiate it from normal veins.
    The diagnostic yield of MRV alone is limited ,cannot differentiate between an occluded sinus and hypoplasia, particularly for lateral sinuses.
    Even with the combination of MRI and MRV, the diagnosis can still remain difficult, particularly for isolated cortical vein thrombosis: if the characteristic cord sign is not present on noncontrast-enhanced CT- or MRI-scan, a conventional angiography may sometimes still be required.
  • 30. Magnetic resonance venogram - axial view; A = transverse sinus; B = sigmoid sinus; C = confluence of sinuses; D = superior sagittal sinus.
  • 31. Magnetic resonance venogram - sagittal view; A = lateral (transverse) sinus; C = confluence of sinuses; D = superior sagittal sinus; and E = straight sinus.
  • 32. Contrast-enhanced MRI showing lack of filling of left transverse sinus.
  • 33. Axial view of MR venogram demonstrating lack of flow in transverse sinus.
  • 34. Coronal view of MR venogram demonstrating lack of flow in the left transverse and sigmoid sinuses.
  • 35.
  • 36.
  • 37. CT
    • CT - often the first imaging study obtained. infarction that does not correspond to an arterial distribution.
    • 38. In the absence of a hemorrhagic component, demonstration of the infarct may be delayed up to 48-72 hours.
    • 39. Useful in ruling out other conditions such as neoplasm and in evaluating coexistent lesions such as subdural empyema.
    • 40. CT of the sinuses is useful in evaluating sinusitis; CT of the mastoids may be helpful in lateral sinus thrombosis.
    • 41. Empty delta sign appears on contrast scans as enhancement of the collateral veins in the superior sagittal sinus (SSS) walls surrounding a nonenhanced thrombus in the sinus.
    • 42. Early division of the SSS can give a false delta sign.
    • 43. The dense triangle sign formed by fresh coagulated blood in the SSS and the cord sign representing thrombosed cortical vein are extremely rare.
  • Empty delta sign in a patient with superior sagittal sinus thrombosis. Transverse contrast-enhanced CT image reveals low-attenuating thrombus (arrow) within the superior sagittal sinus, surrounded by a triangular area of enhancement.
  • 44. DENSE TRIANGLE SIGN
  • 45. PROGNOSIS
    Predictors of 30-day case fatality
    Impaired consciousness
    Mental status disorder
    Thrombosis of the deep venous system
    Posterior fossa lesions
    The main cause of death is transtentorialherniation, secondary to a large hemorrhagic lesion, multiple lesions or diffuse brain edema.
    Other causes of acute death include status epilepticus, medical complications and pulmonary embolism.
    Deterioration after admission occurs in approximately 23% pts.
    Mortality after the acute phase is prominently associated with the underlying cause, especially cancer.
  • 46. Out come
    The predictors of poor long-term outcomes
    Infection of CNS
    Cancer
    Deep venous system thrombosis
    Intracranial hemorrhage
    GCS score at admission >9
    Mental status disorder
    Age >37 yrs
    Male gender
    The overall outcome is better than that of arterial stroke as 2/3 pts recover without sequelae.
    In elderly pts, most frequent cause is a carcinoma, the outcome is worse, 49% of patients being dead or dependent at the end of follow-up.
  • 47.
  • 48. GENERAL MANAGEMENT
    Pts with altered mental status or hemiplegia should be given NBM.
    IVF should not be hypotonic solutions.
    NS @ 1000 mL in 24 hrs.
    To decrease ICP the head elevated 30-40° at all times.
    Seizures –Fosphenytoin in those patients who require a parenteral formulation.
    Phenobarbital or sodium valproateinj , if the pt has allergy to phenytoin.
    Diazepam or lorazepam to treat SE, pt should be given an AED with a longer duration of action to prevent recurrent szs.
  • 49. Heparin & procedures of recanalization
    The aims of heparin therapy in CVT
    (i) to prevent the extension of the thrombus
    (ii) to treat the underlying prothrombotic state
    (iii) to prevent venous thrombosis in other parts of the body or PE
    (iv) to prevent the recurrence of CVT
  • 50. The German trial that compared iv unfractionated heparin with placebo was stopped after the recruitment of 10 pts in each arm because the interim analysis showed a significant benefit .
    Another analysis, based on more usual scales of stroke outcome, failed to show any statistically significant difference between the two groups but showed just a clear tendency.
    The Dutch trialcompared fixed high-dose of SC nadroparin with placebo in 60 pts.
    Failed to show any statistically significant difference between groups.
    Imbalance at baseline that favored the placebo group.
    The Indian trialcompared the effect of IV unfractionated heparin with placebo in 57 Indian women with puerperal sinus thrombosis in whom the diagnosis had not been confirmed by MRI or angiography.
    Showed an insignificant tendency for a benefit of anticoagulant treatment .
    A meta-analysis of these 3 trials showed a insignificant reduction in the relative risk of death or dependency of 0.46 (95% CI, 0.16-1.31).
    Based on these 3 trials and the meta-analysis, most neurologists now start treatment with heparin as soon as the diagnosis is confirmed, even in the presence of hemorrhagic infarcts.
    Einhaupl KM et al. Lancet 1991;338:597-600.  
    de Bruijn SF, Stam J. Stroke 1999;30:484-8.  
    Nagaraja D, Rao B, Taly A, NIMHANS J 1995;13:111-5.  
  • 51. HEPARIN
    Increases the action of antithrombin III, leading to inactivation of coagulation enzymes thrombin, factor Xa, and factor Ixa.
    Initial infusion: 18 U/kg/h IV
    aPTT checked in 6 h and q6h after any dosage change, as well as every am
    adjust dose according to aPTT
    aPTT ; <1.2 times : 80 U/kg bolus with increase of 4 U/kg/haPTT : 1.2-1.5 times : 40 U/kg bolus with increase of 2 U/kg/haPTT : 1.5-2.3 times : No change in infusion rate aPTT : 2.3-3 times : Decrease infusion rate by 2 U/kg/haPTT : > 3 times : Hold infusion for 1 h and decrease rate by 3 U/kg/h
  • 52. THROMBOLYTIC THERAPY
    Infusion of a thrombolytic agent into the dural venous sinus utilizing microcatheter technique.
    Limited to specialized centers ,should be considered for patients with significant deficit.
    Rheolytic catheter device in pts who fails to responded to microcatheter instillation of urokinase.
    The rheolytic catheter was designed for use in the coronary circulation and delivers 6 high-velocity saline jets through a halo device at the tip of the catheter.
    leads to breaks up the thrombus.
    Particulate debris is directed into an effluent lumen for collection into a disposable bag.
  • 53. Alteplase
    1 mg/cm infused via venous sinus catheter throughout clot, then 1-2 mg/h
    Urokinase
    250,000 U/h instilled directly or via venous sinus catheter; additional doses of 50,000 U; total dose 1,000,000 U over 2 h
    Streptokinase
    Loading dose: 1000-3000 IU/kg; followed by infusion of 1000-1500 IU/kg/h; in CVT, administered by direct infusion via catheter
  • 54. ORAL ANTICOAGULANTS
    After acute stage, heparin replaced by oral anticoagulation.
    To prevent any recurrence of CVT, any other venous thrombosis and pulmonary embolism.
    Following EBM data and recommendations in deep venous thrombosis oral anticoagulation is recommended for 6-12 months, aiming at INR 2-3.
    Prolonged oral anticoagulation necessary in pts with inherited or acquired prothrombotic disorders, including APLA.
  • 55. Warfarin
    Interferes with action of vitamin K, a cofactor essential for converting precursor proteins into factors II, VII, IX, and X.
    5 mg PO qd; adjust dose by monitoring INR (target, 2.5)
    0.2 mg/kg PO up to 10 mg,Maintenance: 0.1 mg/kg/d.(paed)
    ginger and Ginkgo biloba should be avoided.
    green leafy vegetables have high levels of vitamin K, which may decrease INR.
  • 56. Drugs that may decrease anticoagulant effects
    griseofulvin
    Carbamazepine
    Glutethimide
    Estrogens
    Nafcillin
    Phenytoin
    Rifampin
    Barbiturates
    Cholestyramine
    vitamin K
    Spironolactone
    oral contraceptives
    sucralfate
  • 57. Medications that may increase anticoagulant effects
    Phenylbutazone
    Salicylates
    Sulfonamides
    chloral hydrate
    Clofibrate
    Diazoxide
    anabolic steroids
    Ketoconazole
    ethacrynic acid
    Miconazole
    nalidixic acid
    Sulfonylureas
    Allopurinol
    Chloramphenicol
    Cimetidine
    Disulfiram
    Metronidazole
    phenylbutazone
    Phenytoin
    Sulfonamides
    acetaminophen
    sulindac
  • 58. HolgerAllroggen, Richard J Abbott,Postgrad Med J 2000;76:12–15
  • 59. Thank you