Artikel
In vitro analysis of platelet function in subarachnoid hemorrhage – an analysis of the clinical course in patients with subarachnoid hemorrhage
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Autoren
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Christian von der Brelie
- Klinik für Neurochirurgie, Universitätsklinikum Schleswig Holstein, Campus Kiel, Germany; Klinik für Neurochirurgie, Universitätsklinikum Bonn, Germany
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Alexander Subai
- Klinik für Neurochirurgie, Universitätsklinikum Bonn, Germany
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Verena Limperger
- Institut für Klinische Chemie, Universitätsklinikum Schleswig Holstein, Campus Kiel, Germany
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Astrid Dempfle
- Institut für Medizinische Informatik und Statistik, Universitätsklinikum Schleswig Holstein, Campus Kiel, Germany
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Azize Boström
- Klinik für Neurochirurgie, Universitätsklinikum Bonn, Germany
| Veröffentlicht: | 8. Juni 2016 |
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Gliederung
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Objective: Platelet function might play an essential role in the pathogenesis of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (SAH). The aim of this study is to evaluate the rate of DCI, the clinical course with respect to bleeding complications and the neurological outcome in patients with impaired platelet function proven with in-vitro diagnosis.
Method: This is a retrospective observational study. Patients in whom in vitro platelet function was tested have been extracted from an initial cohort of 787 patients with SAH being treated from 2005 to 2010. Only patients with aneurysmal SAH and PFA testing within the first 24 hours after aneurysm rupture have been included. Seventy nine patients were included in the study.
Results: The overall rate of DCI in the present study was 41.7%. In vitro platelet function showed pathological platelet function in 69%. DCI was detected significantly more often in patients with regular platelet function. (p = 0.01). This became also true in multivariate testing adjusted for age, gender, initial Hunt & Hess Grade and Fisher score. Patients with impaired platelet function did not display a higher rate of recurrent hemorrhage or hemorrhage complications during the initial treatment course. The patients in whom pathological platelet function was corrected with the patients who were managed without correction statistical analysis revealed no difference regarding development of DCI.
Conclusions: Pre-existing impairment of platelet function might lead to a lower rate of DCI after aneurysmal SAH. Thus, in vitro testing of platelet function might be useful to predict the occurrence of DCI in the course. The results imply that pathological platelet function is influencing the pathogenesis of DCI at a very early stage after onset.
