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Hans-Peter Haring, MD; Klaus Berek, MD; Andreas Kampfl, MD; Bettina Pfausler, MD; Erich Schmutzhard, MD
Department of Neurology Neuro Intensive Care Unit University Hospital Anichstrasse 35 A-6020 Innsbruck Austria

Arch Neurol. 1994;51(1):13.

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Responding to Goldman's comment, we, indeed, assume that heparinization was one strategy for favorable outcome in our patients.¹ Both bacterial and venous cerebrovascular complications account for still high mortality rates and long-term sequelae in bacterial meningitis, in particular in pneumococcal meningitis.^2,3 Our data point to an obstructive process of the basal cerebral blood vessels with highest risk of developing brain ischemia throughout the first 5 days. There is strong evidence that these hemodynamic changes reflect secondary vasculitis⁴; additionally, following initial inflammatory damage of endothelium, the endogenous coagulation cascade might be activated, converting prothrombin into thrombin. Heparin as a thrombin antagonist should, thus, counteract possible development of local thrombosis, which—in addition to narrowing of the blood vessel—could lead to cerebral ischemia or even infarction.

However, anticoagulant therapy is associated with some risk due to well-known side effects. Heparin causes transient mild thrombocytopenia in up to 25% . . . [Full Text PDF of this Article]

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