Artikel
Delayed cerebral ischemia in patients with subarachnoid hemorrhage – The role of serum D-dimer and C-reachtive protein as early markers
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Autoren
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Helene Hurth
- Neurochirurgie
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Milan Stanojevic
- Neurochirurgie
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Marcos S. Tatagiba
- Neurochirurgie
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Jochen Steiner
- Neurochirurgie
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Ulrich Birkenhauer
- Neurochirurgie
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Ulrike Ernemann
- Neuroradiologie, Universitätsklinikum Tübingen
-
Florian H. Ebner
- Neurochirurgie
| Veröffentlicht: | 2. Juni 2015 |
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Gliederung
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Objective: To evaluate the role of the serum markers C-reactive protein (CRP) and D-dimer as prognostic factors regarding the occurrence of delayed cerebral ischemia (DCI) and outcome in patients with aneurysmatic subarachnoid hemorrhage (aSAH).
Method: From 2008 to 2014 all patients admitted to our Neurosurgical Intensive Care Unit (ICU) within one day after an aSAH were analyzed retrospectively. We documented the initial clinical condition by means of Hunt and Hess as well as WFNS SAH grading scales. The extent of bleeding in the initial CCT scan was determined by the Fisher Grade. CRP, D-Dimer, leukocyte count (LC) and procalcitonin were investigated on admission, one day after treatment, on day 4, on day 9, on day 14 after admission and on discharge from the ICU. CCT scans 24 hours after treatment and before discharge were compared for the occurrence of DCI. Occurrence and treatment of vasospasms were documented. Radiologic results were matched with clinical outcome on discharge and after a 3-15 month follow-up period determined by the extended Glasgow Outcome Scale (GOS-E). Treatment groups were divided into a surgical and an endovascular group.
Results: DCI occurred in 31% of patients. There was no difference in occurrence of DCI between the endovascular and the surgical treatment group. A significant correlation between radiologically confirmed vasospasms and DCI was observed. Patients suffering a DCI showed a significantly lower GOS-E on discharge. This difference declined in the follow-up. Serum CRP levels were highest on day 4 and decreased afterwards. Serum CRP levels differed in a significant manner on day 9 and 14 between patients with and without DCI. Serum D-Dimer reached the peak value on day 4 in patients without DCI but further increased on days 9 and 14 in those patients presenting with DCI on discharge. Significant alterations were observed on day 14. There was no correlation between the initial Hunt and Hess, WFNS SAH or Fisher score as well as leucocyte count and the occurrence of DCI.
Conclusions: Serum CRP and D-Dimer seem to be reliable laboratory markers for the occurrence of DCI and a consecutively worse outcome in patients with aSAH. This observation supports the hypothesis of both microthrombosis and inflammatory processes being part of the development of DCI. The value of D-Dimer and CRP monitoring for an early therapeutic intervention has to be evaluated in prospective studies.
