Artikel
Fatal subarachnoid hemorrhage from ruptured cerebral aneurysm – causes of in-hospital mortality in a large single centre patient series
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Autoren
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Kerim Beseoglu
- Neurochirurgische Klinik, Heinrich-Heine-Universität Düsseldorf, Deutschland
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Sven Eicker
- Neurochirurgische Klinik, Heinrich-Heine-Universität Düsseldorf, Deutschland
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Hans-Jakob Steiger
- Neurochirurgische Klinik, Heinrich-Heine-Universität Düsseldorf, Deutschland
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Daniel Hänggi
- Neurochirurgische Klinik, Heinrich-Heine-Universität Düsseldorf, Deutschland
| Veröffentlicht: | 16. September 2010 |
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Gliederung
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Objective: Subarachnoid hemorrhage (SAH) from ruptured intracranial aneurysms is a life-threatening incident requiring immediate medical care. Despite all treatment efforts mortality after SAH is still high. The goal of the present study was to identify causes of in-hospital mortality after SAH in patients treated surgically or endovascularly.
Methods: Of 591 patients with SAH from ruptured cerebral aneurysms from the years 2003 to 2009 102 patients died after admission to our department. We evaluated the medical course of each patient for the first 30 days after admission with regard to pre-existing medical conditions and other risk factors such as cardiac and pulmonary diseases. We complemented our data with a detailed analysis of treatment and complications after admission.
Results: The overall in-hospital fatality after SAH was 17.25% (n=102, mean age 59.4 yrs, 38 m:64 f) of which 38.8% (40 patients) died within 48 hours after initial hemorrhage. This was caused by massive cerebral edema (46.4%), mass shift due to intracerebral hematoma (25.0%) or early rebleeding from untreated aneurysm (21.4%).
53 (51.9%) patients were treated, 20 (19.6%) by surgical procedure, 33 (32.3%) by endovascular procedure. Major cause of death in treated patients was cerebral infarction (20 patients, 37.7%) followed by rebleeding from treated aneurysm (10 patients, 18.9%). Cerebral infarction was significantly higher in endovascular than in surgically treated patients (43.5% vs. 28.6%, p=0.039, χ2-test). Rebleeding after treatment was not significantly different in both groups (5 patients vs. 5 patients).
Conclusions: The present study demonstrated that early general cerebral edema caused by initial damage and cerebral infarction are the major reasons for in-hospital mortality. However, to further determine the association of cerebral infarction and endovascular procedure as well as the impact of vasospasm larger patient cohorts are required. As a consequence there should be a focus on the treatment of both etiologies.
