Jens Astrup

Rebleeding after aneurysmal subarachnoid hemorrhage: a literature review.

OBJECTIVE To summarize the current knowledge of the mechanisms leading to rebleeding and the prevention of rebleeding after subarachnoid hemorrhage (SAH). METHODS A literature search was performed to investigate factors associated with rebleeding after SAH. RESULTS The review of the literature revealed that rebleeding is a complex and multifactorial event involving hemostasis, pathophysiologic, and anatomic factors. Administration of antifibrinolytics has been shown to have a dramatic effect on the rebleeding rate, so changes in coagulation and fibrinolysis must be involved in rebleeding. CONCLUSIONS Further studies are warranted before the exact mechanisms leading to rebleeding are established and the optimal preventive measures are made available. At the present time, antifibrinolytic therapy remains the only realistic protective measure during the initial 6 hours after SAH during which the rebleeding rate is highest.

Reduced clot-stability during the first 6 hours after aneurysmal subarachnoid haemorrhage - a prospective case-control study

INTRODUCTION Early rebleeding is an important cause of death and disability following aneurysmal subarachnoid haemorrhage (SAH). Recent studies have shown that 50-90% of the rebleedings occurred within the first 6 hours after the primary bleeding. The mechanism leading to rebleeding remains to be established. In the present prospective case-control study we hypothesize that patients with SAH develop a coagulopathy characterized by reduced clot stability during the early period after the initial bleeding. METHODS Patients with aneurysmal SAH was studied with a dynamic clot lysis assay and markers of fibrinolysis and clot stabilizers in blood samples taken within and after 6 hours after onset of bleeding. Results were compared with blood samples from age and gender matched healthy controls. RESULTS 36 patients were enrolled, 26 patients had blood samples collected within 6 hours after the initial bleeding whereas 10 patients had blood samples taken later than 6 hours after the initial bleeding. Patients demonstrated significantly reduced clot stability during the first 6 hours after initial bleeding. Fibrinolytic activity was increased during the first 6 hours along with the inhibitors of fibrinolysis whereas the modulators of fibrinolysis were reduced or inactivated. CONCLUSION During the first 6 hours after SAH patients exhibit reduced clot-stability. Probably a consequence of activated fibrinolysis in combination with reduced or inactivated factor XIII and thrombin-activable fibrinolysis inhibitor.

The CT Normal But Low Flow Infarct Periphery: Selective Neuronal Necrosis?

Large infarcts in the MCA territory usually appear sharply demarcated from tissue of normal attenuation on CT. On 133-Xenon inhalation blood flow tomography, on the other hand, infarcts appear surrounded by a wide borderzone of low blood flow (1). Such low flow in the CT normal infarct periphery can be explained as low function and metabolism either due to deafferentiation and disconnection of neurons in the infarct surroundings, or as so-called incomplete infarction with CT invisible microfoci of infarction and wider zones of selective loss of neurons (2,3,4). This study explores the latter possibility.