Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 1998
Comparative StudyCerebral oxygenation in contusioned vs. nonlesioned brain tissue: monitoring of PtiO2 with Licox and Paratrend.
Brain tissue PO2 in severely head injured patients was monitored in parallel with two different PO2-microsensors (Licox and Paratrend). Three different locations of sensor placement were chosen: (1) both catheters into non lesioned tissue (n = 3), (2) both catheters into contusioned tissue (n = 2), and (3) one catheter (Licox) into pericontusional versus one catheter (Paratrend) into non lesioned brain tissue (n = 2). Mean duration of PtiO2-monitoring with both microsensors in parallel was 68.1 hours. ⋯ During a critical reduction in cerebral perfusion pressure (< 60 mm Hg), PtiO2 decreased measured with both microsensors. Elevation of inspired oxygen fraction, normally followed by a rapid increase in tissue PO2, only increased PtiO2 when measured in pericontusional and nonlesioned brain. To recognize critical episodes of hypoxia or ischemia, PtiO2-monitoring of cerebral oxygenation is recommended in nonlesioned brain tissue.
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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
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
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.
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Acta Neurochir. Suppl. · Jan 1998
Continuous intracranial multimodality monitoring comparing local cerebral blood flow, cerebral perfusion pressure, and microvascular resistance.
Maintaining cerebral perfusion pressure (CPP) above 70 mmHg is currently a mainstay of neurosurgical critical care. Shalmon, et al. recently showed poor correlation between CPP and regional cerebral blood flow (CBF) [1]. To study the relationship between CPP and CBF, at a microvascular level, we retrospectively analyzed multimodality digital data from 12 neurosurgical critical care patients in whom a combined intracranial pressure (ICP)--laser Doppler flowmetry (LDF) probe (Camino, San Diego) had been placed. ⋯ Autoregulation was impaired or absent in all monitored patients. We conclude that with disrupted autoregulation, CPP above 70 mmHg does not necessarily insure adequate levels of cerebral perfusion. Restoration and maintenance of adequate cerebral perfusion should be performed under the guidance of direct CBF monitoring.