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A Case of Cerebral Venous Sinus Thrombosis (CVST)

A Case of Cerebral Venous Sinus Thrombosis (CVST). McGill Stroke Rounds Chenjie Xia (R2) Wednesday, April 28 th , 2010. Outline. Case introduction Overview of CVST Anticoagulation in CVST Role of steroids in CVST Management of seizures in CVST. Outline. Case introduction

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A Case of Cerebral Venous Sinus Thrombosis (CVST)

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  1. A Case of Cerebral Venous Sinus Thrombosis (CVST) McGill Stroke Rounds Chenjie Xia (R2) Wednesday, April 28th, 2010

  2. Outline • Case introduction • Overview of CVST • Anticoagulation in CVST • Role of steroids in CVST • Management of seizures in CVST

  3. Outline • Case introduction • Overview of CVST • Anticoagulation in CVST • Role of steroids in CVST • Management of seizures in CVST

  4. Mr. GC • ID: • 38M, right handed • originally from Australia, now works as oceanography researcher in Honolulu • PMHx: • Nil • no known previous clotting d/o • FMHx: • DVT in maternal grand-mother • Meds: • Nil at home • Habits: • non-smoker, occasional EtOH

  5. Mr. GC • HPI: • July 19th2009: flight of 10hrs on from Honolulu to Montreal for oceanography conference • Drank ½ litre of wine prior to flight (slightly unusual consumption) • Slight HA and nausea for 3 days PTA • PTA: no fever or other malaise, no focal neurological signs (aphasia, visual changes, motor or sensory changes), no recent infection/fever/weight loss or other constitutional symptoms

  6. Mr. GC • HPI (continued): • July 20th: brought to MGH by EMS with sudden onset GTC seizure lasting 1 minute at the conference • Repeated GTC seizure while in the MGH ER • Course at MGH: • O/E : expressive aphasia, Rt hemiplegia • CT head: left frontal 24 x 35mm ICH with edema, mild mass effect, no midline shift • Given Dilantin load and Ativan PRN for seizure control • Transferred to MNH NICU

  7. Mr. GC • O/E at MNH (July 21st): • Neck supple, afebrile, vitals normal • Mental status • Severe expressive aphasia (answers mostly limited to yes/no, < 4 words sentences, good repetition, able to read without difficulty) • Follows first-second order command • CNs: • pupils b/l reactive 4mm, fundi right normal, left not well seen, VFs normal • right facial droop (UMN distribution) • rest of the CNs unremarkable

  8. Mr. GC • O/E at MNH (July 21st): • Motor: •  toneRight UE and b/l LEs • Dense right hemiplegia, normal left side strength • reflexes (3+ at right arm and bilateral legs, right ankle 4-5 bts clonus, equivocal toes) • Sensory exam (normal to LT, T and vibration) • Cerebellar: normal left UE FTN and RAM

  9. Mr. GC CT head (July 20th) MRI T2 FLAIR (July 21st)

  10. Mr. GC MRV (July 20th)

  11. Mr. GC • Imaging: • CT head: • left frontal hematoma at high convexity with +++ edema • Thickening / hyperdensity of SSS, suspicion of venous thrombosis • MRI/MRV: • left frontal intraparenchymal bleed (with focal mass effect and effacement of subarachnoid spaces, minimal compression of the left lateral ventricle) • Signal void involving the anterior and middle portions of the SSS, highly compatible with sinus thrombosis • MRV reveals thrombosis of anterior and mid portion of the SSS

  12. Outline • Case introduction • Overview of CVST • Anticoagulation in CVST • Role of steroids in CVST • Management of seizures in CVST

  13. CVST - Epidemiology • 3-4 cases / million in adults; 7 cases / million in children; 5-8 cases / year in a tertiary care centre • 75% of adults are women, M:F = 1.5/5 • Peak incidence in third decade in adults • Highly variable symptoms and clinical course • > 80% have good neurologic outcome

  14. CVST - Pathogenesis • Mechanisms: 1) Thombosis of cerebral veins • localized edema and venous infarction • combination of cytotoxic and vasogenic edema 2) Thrombosis of major venous sinuses •  venous pressure and impaired CSF absorption intracranial hypertension • No pressure  between subarachnoid spaces at surface of the brain and ventricles no hydrocephalus

  15. CVST - Pathogenesis Jan Stam. Thrombosis of the cerebral veins and sinuses. The New England Journal of Medicine, April 28, 2005.

  16. CVST – Causes and Risk Factors • Prothrombotic risk factor (genetic or acquired) • Dehydration • Head trauma • Neurosurgical procedures • Obstetrical delivery (12 / 100 000 deliveries) • OCPs • LP • Infections (otitis, mastoiditis, paranasal sinusitis, orbit or facial infections) • 43% of patients will have > 1 RF

  17. CVST – Clinical Manifestations • Headache • most common, 90% of all cases • Focal neurological signs • motor, sensory deficits, aphasia, hemianopsia • Seizures • Behavioural problems • Amnesia, personality change • Thalamic lesions • Stupor or coma • from herniation, seizures, bilateral thalamic involvement • Isolated intracranial hypertension • 20-40% • Headache, n/v, papilledema, diplopia

  18. CVST - Diagnosis • Delay from onset of Sx to Dx: • Average = 7 days • Diagnostic modalities: • MRI, MRV • best tools for Dx and F/u • CT, CTV • Can be used for Dx • limited for F/u (radiation, contrast) • Conventional angio • Previous gold standard • May be useful in cases of isolated thrombosis of cortical veins without sinus thrombosis

  19. CVST - Treatment • Acute management of patients with impaired LOC • Role of anticoagulation (controversial…) • Role of thrombolysis • Control of seizures • Chronic intracranial hypertension management

  20. Back to our case…

  21. Mr. GC • Course of hospitalization: • Initial decision made not to A/C for now given hemorrhage • Plan repeat MRI/MRV in 1 week, then reconsider A/C • 1 week later…

  22. Mr. GC CT head (July 27th) MRI T2 FLAIR (July 27th)

  23. Mr. GC • Imaging: • CT head: • Evidence of edema causing significant mass effect with right midline deviation of 6 mm. • The left lateral ventricle is compressed • no interval change in the size of left frontal hemorrhage. • more conspicuously seen edema and mass effect • MRI/MRV: • increased surrounding edema, midline shift to the right • further compression of the lateral ventricle • no evidence of recent hemorrhage • Again demonstrated is hyperintensity in the two anterior thirds of the SSS in keeping with thrombosis • MRV does not demonstrate any significant change

  24. Mr. GC • July 27: • Clinical progress • Increasing ease in word-finding • Start to form short complete sentences • Increasing strength of right hemibody • Again, decision made not to A/C due to clinical stability / improvement. • Plan: repeat imaging in one week and then reevaluate need for A/C…

  25. What is the role of anticoagulation in CVST?

  26. Outline • Case introduction • Overview of CVST • Anticoagulation in CVST • Role of steroids in CVST • Management of seizures in CVST

  27. A/C in CVST – The Controversy • Not a new problem… • Hugo Krayenbuhl, Swiss neurosurgeon (1902-1985) said in his 1966 summary of 73 patients with CVST: “We have no proof that cerebral hemorrhages occur more often and are more severe in anticoagulated cases. The group without any treatment has the highest mortality.” http://www.societyns.org/society/bio.aspx?MemberID=14400

  28. A/C in CVST – The Controversy • Rationale FOR use of A/C in CVST • Avoid thrombus extension • Favour spontaneous thrombus resolution • Prevent pulmonary embolism • Rationale AGAINSTuse A/C in CVST • Promote or worsen ICH • Promote extracerebral bleeding complications

  29. A/C in CVST – The Evidence • Einhaupl et al. Lancet 1991  2 groups of 10 patients each  average delay to treatment 10 days

  30. A/C in CVST – The Evidence 2) De Bruijn et al. Stroke 1999  2 groups of 30 patients each  average delay to treatment 4 weeks

  31. A/C in CVST – The Evidence • Cochrane review: primary outcome (death) Stam et al. Anticoagulation for cerebral sinus thrombosis (Review). The Cochrane Collaboration, 2008

  32. A/C in CVST – The Evidence • Cochrane review: primary outcome (death or dependency) Stam et al. Anticoagulation for cerebral sinus thrombosis (Review). The Cochrane Collaboration, 2008

  33. A/C in CVST – The Evidence • Cochrane review: secondary outcome (new or recurrent intracerebral hemorrhage)  CI = 0-9% Stam et al. Anticoagulation for cerebral sinus thrombosis (Review). The Cochrane Collaboration, 2008

  34. A/C in CVST – The Evidence • Cochrane review: secondary outcome (extracerebral hemorrhage) Stam et al. Anticoagulation for cerebral sinus thrombosis (Review). The Cochrane Collaboration, 2008

  35. A/C in CVST – The Evidence • Is A/C safe in patients with CVST complicated by hemorrhage? • Fink et al. Neurology, 2001 • Starting points: • Increasing evidence heparin is safe for CVST with hemorrhage • Uncertainties about safety of heparin in presence of large hemorrhages

  36. A/C in CVST – The Evidence • Fink et al. Neurology, 2001 • Findings • 25 cases of CVT: 14 with ICH, 9 of which > 4cm3 • 7/9 ICH patients treated with heparin: • 0/7 had significant recurrent ICH or clinical deterioration • 3/9 patients were initially not treated with heparin: • 2/3 had recurrent ICH in different vascular territory (1 eventually died) • 1/3 was subsequently treated with heparin and clinical deficits resolved completed

  37. A/C in CVST – The Evidence • Fink et al. Neurology, 2001 • Conclusions • Heparin is safe in CVT with large hemorrhage • De novo recurrent ICH (i.e. in different vascular territory) occurred only in those not treated with heparin & subsequent improvement occurred only if heparin was instituted • Limitations of study: retrospective, non-randomized

  38. A/C in CVST – The Evidence • ISCVT (International Study on Cerebral Vein and Dural Sinus Thrombosis): • prospective multinational observational study involving 89 centres in 21 countries • 624 consecutive adult patients with symptomatic CVT (recruited from May 1998 to May 2001) • Dx confirmed by angio, CTV, MRV, surgery or autopsy • Choice of treatment left up to treating physician (i.e. no randomization)

  39. A/C in CVST – The Evidence • ISCVT (cont’d): • 83% of patients received UFH or LMWH in the acute phase  reflects general consensus among neurologists re: A/C in acute CVST? • Safety of heparin • ¾ with early ICH were treated with therapeutic heparin (rate similar to non-ICH patients) • Heparin associated with better outcome (all delayed ICH patients who had good outcome were treated with heparin) • Limitation: use of heparin was not randomized nor blinded

  40. A/C in CVST – The Evidence Girot et al. Predictors of outcome in patients with cerebral venous thrombosis and intracerebral hemorrhage. Stroke, 2007.

  41. A/C in CVST – The Conclusion • Cochrane review 2008: • “A/C treatment for CSVT appeared to be safe and was associated with potentially important reduction in risk of death or dependency which did not reach statistical significance” • Future RCTs with A/C vs placebo may be difficult to initiate due to lack of equipoise • May still be reasonable to collect more data from cohort series or case-control studies to estimate A/C-related risk

  42. A/C in CVST – The Conclusion • EFNS (European Federation of Neurological Societies) 2010 guidelines: • Level B recommendation for use of A/C • Concomitant ICH is not a contraindication • LMWH may be preferable • Studies with DVT shows  risk for extracerebral bleed with LMWH compared to UFH

  43. A/C in CVST – The Consensus? • Letters to the editor, Archives of Neurology 2008: • AGAINST (Walsay et al.) • Good natural history without treatment • No statistically significant  from RCTs • Physicians choose to A/C because “they find it extremely difficult to do nothing.” • AMBIVALENT (Roach) • Data favoring A/C is suggestive, but not compelling • More RCTs needed? • FOR (Stam) • A/C corrects underlying mechanism of hemorrhage: thrombosis  capillary pressure  local cerebral edema  petechial hemorrhage • Cannot ignore the ARR of 13% found in RCT (p = 0.08) from meta-analysis

  44. A/C in CVST – Long-term • Long-term oral anticoagulation • Recanalization • Occurs within first 4 months irrespective of further OAT • Even if incomplete or no recanalization, CVST recurrence rare • CVST Recurrence • Risk may be lower than in extracerebral VTE • ISCVT: during 16 months f/u 2.2% recurrence • Despite above… • Most still offer long-term OAT • ISCVT: at 6 months, 80% of patients were on OAT; median time on OAT = 7.7 months

  45. A/C in CVST – Long-term • EFNS guidelines • Optimal duration unclear, target INR 2-3

  46. A/C in CVST – Final Words • Still the same problem: • Hugo Krayenbuhl (1966): “We have no proof that cerebral hemorrhages occur more often and are more severe in anticoagulated cases. The group without any treatment has the highest mortality.”

  47. Again, back to our case…

  48. Mr. GC • July 27: • Clinical progress • Increasing ease in word-finding • Start to form short complete sentences • Increasing strength of right hemibody • Again, decision made not to A/C due to clinical stability / improvement… • Plan: repeat imaging in one week and then reevaluate need for A/C

  49. Mr. GC CT head (August 4th)

  50. Mr. GC • Imaging of August 4th: • size and density of the left frontal hematoma have diminished significantly • surrounding vasogenic edema has diminished slightly • left frontal horn is starting to reexpand • midline shift has improved

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