Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 1998
Cerebral hemodynamic changes during sustained hypocapnia in severe head injury: can hyperventilation cause cerebral ischemia?
Hyperventilation (HV) is routinely used in the management of increased intracranial pressure (ICP) in severe head injury. However, this treatment continues to be controversial because it has been reported that long-lasting reduced cerebral blood flow (CBF) due to profound sustained hypocapnia may contribute to the development or deterioration of ischemic lesions. Our goal in this study was to analyze the effects of sustained hyperventilation on cerebral hemodynamics (CBF, ICP) and metabolism (arterio jugular differences of lactates = AVDL). ⋯ According to AVDO2 and AVDL, no adverse effects were found during four hours of HV in hyperemic patients. Nevertheless, AVDO2 and AVDL are global measurements and might not detect regional ischemia surrounding focal lesions such as contusions and haematomas. We suggest that monitoring of AVDO2 or other haemometabolic variables should be mandatory when sustained HV is used in the management of head injury patients.
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Acta Neurochir. Suppl. · Jan 1998
Monitoring of brain tissue PO2 in traumatic brain injury: effect of cerebral hypoxia on outcome.
This study investigates the effect of hypoxic brain tissue PO2 on outcome, and examines the incidence of possible causes for cerebral hypoxia. We studied 35 patients with severe head injury (GCS < or = 8). Age was 33.2 (+/- 11.3) years. ⋯ Hypocarbia (ETCO2 < 28 mm Hg) was present in 48.0% of the time of PtiO2 < 10 mm Hg. No obvious cause for cerebral hypoxia was found in 45% of the data. These result underscore the association of cerebral hypoxia with poor neurological outcome and stress the meaning of monitoring of PtiO2 as an independent parameter in patients following TBI.
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Acta Neurochir. Suppl. · Jan 1998
Moderate hypothermia and brain temperature in patients with severe middle cerebral artery infarction.
Elevated temperature is known to facilitate neuronal injury after ischemia. After head injury a gradient between temperature and body temperature of up to 3 degrees C higher in the brain has been reported. Hypothermia may limit some of the deleterious metabolic consequences of such increased temperature. ⋯ After MCA stroke, human intracerebral temperature is higher than central body-core temperature. Mild hypothermia in the treatment of severe cerebral ischemia using cooling blankets is safe and does not lead to severe side effects. Mild hypothermia can help to control critically elevated ICP values in severe space-occupying stroke and may improve clinical outcome in these patients.
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Acta Neurochir. Suppl. · Jan 1998
Comparative StudySimultaneous continuous measurement of pO2, pCO2, pH and temperature in brain tissue and sagittal sinus in a porcine model.
The clinical use of brain tissue oxygen measurement in patients with severe head injury is increasing. It is important to compare the findings in brain tissue with cerebrovenous blood oximetry, to obtain normal values and to find out limitations of the method. We evaluated a newly available multisensor probe simultaneously in the brain tissue and in the sagittal sinus in a porcine animal model. ⋯ Measuring partial oxygen pressure in brain tissue is more responsive to physiological variations, and the absolute values are more sensitive than oxygen measurement in the cerebrovenous compartment. This is important for interpreting measured values and introducing new coefficients for patient monitoring.
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Acta Neurochir. Suppl. · Jan 1998
Effects of cerebral perfusion pressure on brain tissue PO2 in patients with severe head injury.
Ischemia causes secondary brain damage after severe head injury (SHI). Cerebral perfusion is commonly estimated by monitoring CPP, but the adequacy of cerebral oxygenation requires further measurements, such as jugular oxygen saturation or, more recently, PtiO2 monitoring. In 7 patients with severe head injury, ICP, MAP, CPP, SjO2 and PtiO2 were monitored for a mean time of 9.0 +/- 2.2 days. ⋯ Focusing on values under the thresholds of 60 mm Hg for CPP and 20 mm Hg for PtiO2, we found a relationship between CPP and PtiO2. Looking at the PtiO2 time-course, we observed a quite constant increasing trend during the first 48 hours of monitoring, then the values remained relatively constant within a normal range. Our data show that decreases of PtiO2 are not uncommon after severe head injury and therefore it seems that monitoring of PtiO2 in SHI may be useful in order to minimize secondary insults.