Article
Elevated blood glucose level early after aneurysmal subarachnoid hemorrhage – Caused by early brain injury or due to pre-existing hyperglycemic metabolism?
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Authors
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Kerim Beseoglu
- Klinik für Neurochirurgie, Heinrich-Heine-Universität Düsseldorf, Medizinische Fakultät, Düsseldorf, Deutschland
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Nima Etminan
- Klinik für Neurochirurgie, Heinrich-Heine-Universität Düsseldorf, Medizinische Fakultät, Düsseldorf, Deutschland
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Daniel Hänggi
- Klinik für Neurochirurgie, Heinrich-Heine-Universität Düsseldorf, Medizinische Fakultät, Düsseldorf, Deutschland
| Published: | June 2, 2015 |
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Outline
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Objective: Elevated blood glucose levels are frequently detected early after aneurysmal subarachnoid hemorrhage (aSAH) and are considered a risk factor for poor neurological outcome. However it remains unclear whether hyperglycemia is caused by the SAH ictus or reflects a pre-existing hyperglycemic metabolism. To further elucidate this, we prospectively analysed glycated haemoglobin levels (HbA1c) in patients with aSAH and its influence on outcome.
Method: Prospectively, 90 patients with confirmed aSAH were included between July 2012 and July 2014 (NCT02081820). Within the first 72 hours HbA1c was assessed as a measure for elevated blood glucose levels in the weeks preceding aSAH. Blood glucose levels along with epidemiological data were recorded upon admission. Patient outcome was recorded after 6 months using modified Rankin scale (mRS). Statistical analysis included correlation analysis of HbA1c with initial neurological status and blood glucose level as well as uni- and multivariate analysis of ist impact on outcome.
Results: HbA1c level did not correlate with initial neurological status (p=0.984, r=-0.004) or the amount of subarachnoid blood (Fisher grade, p=0.322, r=0.187). On the contrary, initial blood glucose level correlated significantly with neurological status at admission (p=0.030, r=0.396) independent of HbA1c level (p=0.114). Additionally, HbA1c failed to show a significant influence on the occurrence of delayed cerebral ischemia (DCI) (p=0.791) or outcome after 6 month (p=0.374).
Conclusions: A pre-existing hyperglycaemic metabolism, as reflected by elevated HbA1c levels, is not a relevant contributor to the impact of SAH nor does it influence the quality of neurological recovery. Initially elevated blood glucose levels are independent of HbA1c and are more likely caused by early brain injury.
