Cerebral energy failure after subarachnoid hemorrhage: the role of relative hyperglycolysis.
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 energy supply. This phenomenon is known in head injury but has not as yet been shown after SAH. This study was conducted to test the hypothesis that hyperglycolysis is present in SAH patients and is associated with vasospasm. A total of 105 measurements were conducted on 21 SAH patients (age 49+/-15 years, median World Federation of Neurosurgical Societies Grade 4) over the first 5 days following admission. Arteriovenous differences were calculated for oxygen (avDO2) and glucose (avDGlc). Relative hyperglycolysis was defined as metabolic ratio (MR=avDO2[mmol/L]/avDGlc[mmol/L])<3.44. Jugular-venous saturation for oxygen (SjvO2), mean arterial blood pressure (MAP), intracranial pressure (ICP), cerebral perfusion pressure (CPP) were monitored. Relative hyperglycolyis was recorded in 34% of studies after SAH. In hyperglycolytic studies both jugular-venous lactate and SjvO2 were significantly elevated (jugular-venous lactate 14.9+/-9.9 vs. 11.8+/-5.5 mg/dL, p=0.04; SjvO2: 70.0+/-18% vs. 81.7+/-9%, p=0.002). Relative hyperglycolysis is associated with outcome after SAH. In patients who died after SAH almost 50% of studies showed hyperglycolysis, whereas patients who survived without neurological deficit had no hyperglycolytic events. Relative hyperglycolysis is a common event after SAH. It may be associated with relative hyperemia but most importantly with outcome.
Oertel
Matthias F
MF
Department of Neurosurgery, University Hospital Giessen-Marburg, Klinikstrasse 29, 35385 Giessen, Germany. matthias.oertel@neuro.med.uni-giessen.de
Schwedler
Madlen
M
Stein
Marco
M
Wachter
Dorothee
D
Scharbrodt
Wolfram
W
Schmidinger
Andrea
A
Böker
Dieter-Karsten
DK
D000328:Adult; D001794:Blood Pressure / Q000502:physiology; D001928:Brain Diseases, Metabolic / Q000209:etiology* / Q000378:metabolism* / Q000401:mortality; D002545:Brain Ischemia / Q000209:etiology* / Q000378:metabolism* / Q000401:mortality; D002536:Cerebral Arteries / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D054022:Cerebrum / Q000098:blood supply / Q000378:metabolism / Q000503:physiopathology; D004734:Energy Metabolism / Q000502:physiology; D005260:Female; D005947:Glucose / Q000378:metabolism; D006019:Glycolysis / Q000502:physiology*; D006801:Humans; D007427:Intracranial Pressure / Q000502:physiology; D019344:Lactic Acid / Q000097:blood; D008297:Male; D053858:Metabolic Networks and Pathways / Q000502:physiology; D008875:Middle Aged; D008991:Monitoring, Physiologic; D010101:Oxygen Consumption / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D015996:Survival Rate; D020301:Vasospasm, Intracranial / Q000150:complications / Q000503:physiopathology
D019344:Lactic Acid; D005947:Glucose