Treatment of cerebral sinus/venous thrombosis.

Strokes in the young account for nearly 30% of all cases of stroke in India1 and cerebral venous thrombosis (CVT) accounts for 10-20% of these cases.2 Two-thirds of them develop the same in the post-partum period. In the recent years, a number of inherited and acquired pro-thrombotic states have been identified. However, the exact etiology of CVT remains unidentified in a significant proportion of cases. The treatment approach of CVT has undergone significant re-appraisal, especially in the last decade, with the advent of novel strategies like selective sinus catheterization and thrombolysis. Current therapeutic options for CVT treatment include anti-thrombotic therapy with un-fractionated heparin, low-molecularweight heparins (LMWH), oral anticoagulants, intravenous thrombolysis, local thrombolysis by selective sinus catheterization and a combination of thrombolysis and anticoagulation in addition to symptomatic therapy. Anticoagulation can prevent further thrombus formation and thereby prevent the progression of infarction and pulmonary embolism. However, in patients with hemorrhagic infarctions, worsening of bleeding was feared. Some authors recommended the use of anticoagulation only in patients with CVT without radiological evidence of hemorrhage, while most favor a more aggressive approach and recommend anticoagulation in all. The risk of hemorrhagic complications due to heparin has been over-estimated. A number of individual case reports, uncontrolled series,3,4 retrospective studies and randomized trials5 have demonstrated the efficacy and safety of heparin in CVT, even in the presence of hemorrhagic infarctions. A number of welldocumented case reports described worsening of the clinical condition when heparin was replaced by oral anticoagulants and rapid improvement after restarting heparin.6 Diaz et al7 reviewed 203 CVT cases between 1942 and 1990 and compared the outcome of patients treated with and without heparin. Ninety-one percent survived in the first group compared with 36% in the second. Randomized trials8,9 demonstrated the safety of intravenous/sub-cutaneous heparin in patients with non-hemorrhagic and hemorrhagic venous infarctions. The results of the two prospective controlled trials at National Institute of Mental Health and Neurosciences5,9 support the use of even lower doses (15,000 units per day in three divided doses) of heparin in puerperal CVT. A more recent multicentric, double blind placebo controlled trial of nadroparin, a low molecular weight heparin, by de Bruijn and Stam10 randomized 59 patients to receive nadroparin and placebo for 3 weeks, followed by oral anticoagulation for 3 months (nadroparin group only). After 3 weeks, there was no difference in the outcome measured by death or Barthel index score. After 12 weeks, 13% in the nadroparin group and 21% in the placebo group had poor outcome. However, this difference was not significant, probably because of the small number of patients. The bulk of evidence favors the use of heparin in CVT, but the best indications for its use are not universally agreed upon. All would agree that heparin is indicated in patients with coexistent pelvic or deep leg vein thrombosis and pulmonary embolism or in conditions associated with prothrombotic states. Neonatal CVT is the only situation in which heparin has not been shown to improve the outcome and most authors do not recommend its use in this situation. Most of the studies have used higher doses of heparin to maintain activated partial thromboplastin time (APTT) 2.5 times the control. But, in puerperal CVT smaller dose (5000 unit 8th hourlysubcutaneous) is safe and effective and obviates APTT monitoring which is not available at peripheral centers.