ABSTRACT
After subarachnoid hemorrhage (SAH) the detection of hemodynamically significant vasospasm is frequently difficult, especially in comatose patients. Most clinicians use transcranial Doppler sonography (TCD) to detect increasing mean blood flow velocities in the basal arteries as markers of cerebral vasospasm, without accounting for the effects of sedation and variations in blood pressure or pCO(2). This study was conducted to test the hypothesis that the arteriovenous difference of oxygen (avDO(2); in terms of % volume) could also be useful for the evaluation of vasospasm. A total of 22 SAH patients (M : F = 1 : 1.75, age 58+/-10 years, median Hunt and Hess grade 4) were prospectively enrolled. All patients were sedated with continuous doses of midazolam/fentanyl and/or propofol. TCD studies and avDO(2) measurements were conducted at the same time or in close succession. The blood flow velocity of the middle cerebral artery was recorded. A cranial CT scan was conducted if the avDO(2) increased by at least 0.8%. Overall, 82 measurements were recorded in 22 patients between days 1 and 13 after SAH. TCD mean flow velocities increased as expected. In contrast, avDO(2) decreased until post-hemorrhage day 4 before it increased again. Overall, after SAH, avDO(2) was significantly lower than in normal individuals. Cerebral infarction occurred primarily in patients with a maximal change of avDO(2) of more than 1%. TCD velocities alone are poor indicators of the severity of vasospasm. In contrast, daily avDO(2) seems to be a more robust parameter. However, collection of additional metabolic information is warranted.
Subject(s)
Cerebrovascular Circulation/physiology , Oxygen/metabolism , Subarachnoid Hemorrhage/diagnostic imaging , Subarachnoid Hemorrhage/metabolism , Vasospasm, Intracranial/diagnosis , Aged , Blood Flow Velocity/physiology , Female , Humans , Male , Middle Aged , Prospective Studies , Time Factors , Tomography, X-Ray Computed , Ultrasonography, Doppler, Transcranial , Vasospasm, Intracranial/etiologyABSTRACT
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.
