Article
Cerebral energy failure after subarachnoid hemorrhage – the role of hyperglycolysis
Zerebrale Energiekrise nach Subarachnoidalblutung – die Rolle der Hyperglykolyse
Search Medline for
Authors
Published: | May 8, 2006 |
---|
Outline
Text
Objective: After subarachnoid hemorrhage (SAH) cerebral metabolism is significantly impaired. Hyperglycolysis describes the reduction of oxidative metabolism followed by a relative increase of anaerobic glycolysis to maintain the energy supply. This phenomenon is known in head injury but has not been shown after SAH, yet. This study was conducted to test the hypothesis that hyperglycolysis is present in patients with SAH and associated with vasospasm.
Methods: A total of 105 measurements were conducted on 21 SAH patients (age 49±15 years, median Hunt/Hess Grade 4) the first five days following admission. Arteriovenos differences were calculated for oxygen (avDO2) and glucose (avDGlc). Hyperglycolysis was defined as a Metabolic Ratio (MR=avDO2(Vol%)/avDGlc(mg/dl)) <0.58. Vasospasm was diagnosed by transcranial Doppler sonography (VMCA>120 cm/s and Lindegaard Ratio >3) in conjunction with neurological deterioration.
Results: All but one patient developed at least one episode of hyperglycolysis during the observation period. Those patients, who experienced hyperglycolysis in more than 50% (n=12) of the time were significantly older (45±13 vs. 52±16 years; p=0.004) with higher jugular-venous saturations (67.6±8.3 vs. 79.2±5.2%; p=0.002) All patients developed vasospasm after post-hemorrhage day 3. Before and after day 3 hyperglycolysis occurred in 45% and 55% of studies, respectively. (p=0.3)
Conclusions: Hyperglycolysis is a common event after SAH. It may be associated with relative hyperemia but is independent of the presence of vasospasm.