What is the management of CVT due to TBM in regions where it is a common cause?

Management of CVT Due to Tuberculous Meningitis

In regions where tuberculous meningitis (TBM) is a common cause of cerebral venous thrombosis (CVT), immediate anticoagulation with either intravenous unfractionated heparin or subcutaneous low-molecular-weight heparin must be initiated alongside standard antitubercular therapy, even in the presence of intracranial hemorrhage. 1, 2

Immediate Anticoagulation Protocol

Start anticoagulation immediately upon CVT diagnosis confirmation—this is non-negotiable even with hemorrhagic transformation. 1

• Intravenous unfractionated heparin: Dose-adjusted to aPTT 1.5-2.5× control 1
• Subcutaneous low-molecular-weight heparin: Body weight-adjusted dosing (typically enoxaparin 1 mg/kg twice daily) 1
• The presence of intracranial hemorrhage is explicitly NOT a contraindication to anticoagulation in CVT—this is a critical pitfall to avoid 1

Concurrent Antitubercular Therapy

• Initiate standard four-drug antitubercular therapy immediately (rifampicin, isoniazid, pyrazinamide, ethambutol) 2, 3
• Add adjunctive dexamethasone for TBM to reduce inflammation and vascular complications 2, 4
• The hypercoagulable state in TBM is driven by decreased protein S (anticoagulant) and increased factor VIII (procoagulant), along with deficient fibrinolysis from elevated PAI-1 5

Diagnostic Confirmation

• MRI with MR venography is the preferred diagnostic method for CVT 1
• CT venography if MRI is unavailable or contraindicated 1
• Confirm TBM diagnosis through CSF analysis showing lymphocytic pleocytosis, elevated protein, low glucose, and positive Mycobacterium tuberculosis testing 2
• Measure CSF opening pressure (typically >20 cmH2O in CVT) 1

Acute Care Setting and Monitoring

• Admit to stroke unit or neurocritical care setting for close neurological monitoring every 2-4 hours 1
• Monitor specifically for signs of neurological deterioration, worsening headache, decreased consciousness, or new focal deficits 1
• The vascular involvement in TBM is almost universal, with smaller arterial branches carrying the brunt of disease (94% MCA branches, 100% basilar artery branches affected), leading to widespread microscopic infarctions 4

Management of Increased Intracranial Pressure

• Consider acetazolamide or serial lumbar punctures if intracranial pressure remains severely elevated despite anticoagulation 1
• Treat seizures aggressively with antiepileptic medications if they occur (40% of CVT patients develop seizures) 1
• Monitor for papilledema and sixth nerve palsy (diplopia), which indicate elevated intracranial pressure present in >80% of CVT cases 6, 1

Transition to Long-Term Anticoagulation

• Transition to oral anticoagulation (warfarin with INR target 2-3 or direct oral anticoagulant) after initial heparin therapy, typically 5-10 days 1
• Duration of anticoagulation: 6-12 months for TBM-associated CVT, as the infectious/inflammatory etiology represents a transient but prolonged risk factor 1
• Continue until complete resolution of TBM and documented recanalization on imaging 1

Follow-Up Imaging

• Perform follow-up MR venography or CT venography at 3-6 months to assess recanalization 1
• Earlier imaging (1-3 months) is indicated if symptoms persist or evolve despite treatment 1

Regional Considerations for India and Endemic Areas

• TBM remains a significant public health concern in India, where it represents a common cause of CVT in younger patients 2, 7
• Over the last decade, a change in trends of causative factors for CVT has been noted from India, with infectious etiologies like TBM becoming more prominent 7
• Vascular complications occur in approximately 20% of TBM patients clinically, though autopsy studies show much more extensive vascular damage with widespread microscopic infarctions in brainstem and cerebellum 4, 3

Critical Pitfalls to Avoid

• Do not withhold anticoagulation due to fear of hemorrhagic complications—this is the most common error and worsens outcomes 1
• Do not delay anticoagulation while awaiting complete microbiological confirmation of TBM if clinical suspicion is high 2
• Do not underestimate the extent of vascular involvement—microscopic infarctions are far more common than visible on routine imaging 4
• The hypercoagulable state in TBM is more pronounced in advanced disease (stage 3 vs stage 2), requiring more aggressive management 5

Supportive Care

• Antiemetic drugs for symptom control 2
• Aggressive management of fever and metabolic derangements 3
• Consider aspirin or other antiplatelet agents as adjunctive therapy, though evidence is limited 3