Neurological research
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Neurological research · Jun 1997
Multiparametric continuous monitoring of brain metabolism and substrate delivery in neurosurgical patients.
Brain function and tissue integrity are highly dependent on continuous oxygen supply and clearance of CO2. Aerobic metabolism is the major energy source to normal brain, however, during hypoxia and ischemia, lactate accumulation may sometimes be seen, indicating anaerobic glycolysis after severe head injury. Current monitoring techniques often fail to detect such events which can affect substrate delivery to the injured brain. ⋯ Brain pH was inversely related to brain CO2 for all patients. Brain glucose and lactate in patients with poor outcome were 639 microM l-1 +/- 330, and 1642 microM l-1 +/- 788, whereas patients with good outcome had brain glucose levels of 808 microM l-1 +/- 321 and lactate levels of 1001 microM l-1 +/- 417. Extended neuromonitoring using a combined sensor for brain oxygen, CO2, pH and temperature measurements, as well as a microdialysis probe for glucose and lactate analysis may optimize the management of comatose neurosurgical patients in the future, by allowing a fuller understanding of dynamic factors affecting brain metabolism.
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Neurological research · Jun 1997
Brain tissue pO2-monitoring in comatose patients: implications for therapy.
Monitoring of brain tissue partial pressure of O2 (ti-pO2) is a promising new technique that allows early detection of impending cerebral ischemia in brain-injured patients. The purpose of this study was to investigate the effects of standard therapeutic interventions used in the treatment of intracranial hypertension in comatose patients on cerebral oxygenation. In the neurosurgical intensive care unit ti-pO2, arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and jugular bulb oxygen saturation (SjvO2) were prospectively studied (0.1 Hz acquisition rate) in 23 comatose patients (21 with severe traumatic brain injury, 2 with intracerebral hematoma) during various treatment modalities: elevation of CPP with dopamine (n = 35), lowering of the head (n = 22), induced arterial hypocapnia (n = 13), mannitol infusion (n = 16), and decompressive craniotomy (n = 1). ⋯ Based on the present data, our understanding of many interventions previously believed to improve brain oxygenation might have to be re-evaluated. A CPP > 60 mmHg emerges as the most important factor determining sufficient brain tissue pO2. Any intervention used to further elevate CPP does not improve ti-pO2, to the contrary, hyperventilation even bears the risk of inducing brain ischemia.
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Neurological research · Jun 1997
Influence of body position on tissue-pO2, cerebral perfusion pressure and intracranial pressure in patients with acute brain injury.
It is a common practice to position head-injured patients in bed with the head elevated above the level of the heart in order to reduce intracranial pressure (ICP). This practice has been in vivid discussion since some authors argue a horizontal body position will increase the cerebral perfusion pressure (CPP) and therefore improve cerebral blood flow (CBF). However, ICP is generally significantly higher in the horizontal position. ⋯ However, regional ti-pO2 was unaffected by body position (30 degrees vs. 0 degree: 24.9 + 13.1 vs. 24.7 + 12.9 mmHg). In addition, there was no change in the time course after trauma concerning these findings in the individual patients. The data indicate that a moderate head elevation of 30 degrees reduces ICP without jeopardizing regional cerebral microcirculation as monitored using a polarographic ti-pO2 microcatheter.
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Neurological research · Jun 1997
Dynamic changes of cerebral oxygenation measured by brain tissue oxygen pressure and near infrared spectroscopy.
The aim of this study was to find out whether a correlation exists between changes in brain tissue oxygen pressure (ti-pO2) and hemoglobin oxygenation (HbO2) measured by near-infrared spectroscopy. We studied 10 patients with severe head injury. A ti-pO2 monitoring device was introduced in the frontal white matter as soon as possible after administration. ⋯ In 3 patients the correlation was poor. The reason for poor correlation might be poor signal quality of the NIRS sensor or inhomogenous distribution of ischemic areas in the whole brain. We conclude that under the condition of a stable NIRS signal and a diffuse brain lesion, changes of ti-pO2 are well reflected by NIRS.