Treatment of Cerebral Venous Sinus Thrombosis
Immediate anticoagulation with either low-molecular-weight heparin (LMWH) or unfractionated heparin (UFH) should be initiated as first-line treatment for all patients with cerebral venous sinus thrombosis, even when intracerebral hemorrhage is present on imaging. 1, 2
Initial Anticoagulation Protocol
First-Line Treatment Options
LMWH is the preferred initial agent due to superior efficacy compared to UFH, with the following dosing regimens: 1
- Enoxaparin: 1.0 mg/kg subcutaneously twice daily OR 1.5 mg/kg once daily 1
- Dalteparin: 200 U/kg subcutaneously once daily 1
Intravenous UFH is the appropriate alternative when: 1
- LMWH is contraindicated or unavailable
- Severe renal failure is present (creatinine clearance <30 mL/min)
- Thrombolytic therapy may be needed
- Dosing: Initial bolus of 5000 IU, followed by continuous infusion of approximately 30,000 IU over 24 hours, adjusted to maintain aPTT at 1.5-2.5 times baseline 1
Critical Management Principle
The presence of intracerebral hemorrhage related to CVST is NOT a contraindication to anticoagulation. 1, 2 The risk of thrombus propagation outweighs bleeding concerns in this specific context, and anticoagulation should be started without delay regardless of hemorrhagic lesions present on imaging. 1
Transition to Oral Anticoagulation
Begin oral anticoagulants early while continuing parenteral anticoagulation for a minimum of 5 days and until INR is ≥2.0 for at least 24 hours. 1
For vitamin K antagonists (warfarin): Target INR range of 2.0-3.0 (target INR of 2.5). 1
Warfarin is preferred over direct oral anticoagulants (DOACs) in patients with: 1
- Mechanical heart valves
- Antiphospholipid syndrome
- Severe renal impairment
Duration of Anticoagulation
Minimum duration is 3 months for all patients. 1, 2 Beyond this, duration depends on underlying etiology:
- Provoked CVST (transient risk factors): 3-6 months 1, 3
- Unprovoked CVST or low-risk thrombophilia: 6-12 months 3
- Antiphospholipid syndrome: Consider indefinite anticoagulation 1
- Severe thrombophilia or recurrent thrombosis: Indefinite (lifelong) anticoagulation 2, 3
- Cancer-associated CVST: Continue anticoagulation as long as anti-cancer treatment is given 1
Special Populations
Severe renal failure (creatinine clearance <30 mL/min): Use UFH followed by early vitamin K antagonists OR LMWH adjusted to anti-Xa concentration. 1
Behçet's syndrome with CVST: High-dose glucocorticoids followed by tapering, with anticoagulants added for a short duration. 1
Monitoring and Follow-Up
Admit all patients to a stroke unit or neurocritical care setting for close monitoring and specialized care. 2, 3
Perform regular neurological assessments to detect clinical deterioration, including monitoring for: 1
- Worsening consciousness
- New focal deficits
- Seizures
- Signs of increased mass effect
Follow-up imaging at 3-6 months after diagnosis with CT venography or MR venography is reasonable to assess for recanalization of the occluded cortical vein/sinuses in stable patients. 1, 3
Investigate underlying prothrombotic conditions as this affects treatment duration. 2, 3
Escalation of Care
Consider mechanical thrombectomy in patients with: 1
- Absolute contraindications to anticoagulation
- Failure of initial therapeutic anticoagulation despite adequate dosing
Decompressive hemicraniectomy may be lifesaving in patients with severe mass effect or large intracerebral hemorrhage causing progressive neurological deterioration. 1
Common Pitfalls
Do not delay anticoagulation due to hemorrhagic transformation. The evidence from two randomized trials involving 79 patients showed that anticoagulant therapy was safe with no new symptomatic intracerebral hemorrhages observed, though one major gastrointestinal hemorrhage occurred. 4 While isolated case reports describe rebleeding with heparin 5, the consensus from major guidelines prioritizes immediate anticoagulation given the greater risk of thrombus propagation.
Do not use peripheral coagulation studies alone to guide therapy in refractory cases. Emerging evidence suggests potential differences between intracranial and peripheral anticoagulation levels, though this remains investigational. 6