OBJECTIVE: To investigate the relationships between slow vasogenic waves ('B waves') of intracranial pressure (ICP), pressure-reactivity and outcome after traumatic brain injury. MATERIAL AND METHOD: 193 head-injured patients (age 34 +/- 16.7 years; median GCS 6) were monitored from 1997 to 2002. ICP, arterial blood pressure (ABP) were continuously monitored. Pressure-reactivity index (PRx) and magnitude of ICP slow waves were evaluated using the bed-side computers. RESULTS: Distribution of PRx in different outcome groups indicated that pressure-reactivity was significantly worse in patients with fatal outcome. A magnitude of spontaneous slow waves of ICP was gradually decreasing in poorer outcome grades. Mortality indicated threshold rise from 20% to 70% when averaged PRx increased above 0.3 (p < 0.01). There was no threshold for mortality observed along distribution of magnitude of ICP slow waves. Mortality gradually increased when the magnitude of slow waves decreased (R = -0.26; p < 0.0001). CONCLUSION: Inadequate pressure-reactivity and low magnitude of slow vasogenic waves of ICP are associated with fatal outcome after head injury. Based on brain monitoring data, differentiation between favourable outcome and severe disability is more problematic than differentiation between survivors and non-survivors.
OBJECTIVE: To investigate the relationships between slow vasogenic waves ('B waves') of intracranial pressure (ICP), pressure-reactivity and outcome after traumatic brain injury. MATERIAL AND METHOD: 193 head-injured patients (age 34 +/- 16.7 years; median GCS 6) were monitored from 1997 to 2002. ICP, arterial blood pressure (ABP) were continuously monitored. Pressure-reactivity index (PRx) and magnitude of ICP slow waves were evaluated using the bed-side computers. RESULTS: Distribution of PRx in different outcome groups indicated that pressure-reactivity was significantly worse in patients with fatal outcome. A magnitude of spontaneous slow waves of ICP was gradually decreasing in poorer outcome grades. Mortality indicated threshold rise from 20% to 70% when averaged PRx increased above 0.3 (p < 0.01). There was no threshold for mortality observed along distribution of magnitude of ICP slow waves. Mortality gradually increased when the magnitude of slow waves decreased (R = -0.26; p < 0.0001). CONCLUSION: Inadequate pressure-reactivity and low magnitude of slow vasogenic waves of ICP are associated with fatal outcome after head injury. Based on brain monitoring data, differentiation between favourable outcome and severe disability is more problematic than differentiation between survivors and non-survivors.
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