caa a22 4500 477107923 CHVBK 20180405111600.0 cr unu---uuuuu 170330e19960401xx s 000 0 eng 10.1007/BF01420305 doi (NATIONALLICENCE)springer-10.1007/BF01420305 Brain tissue pO2 in relation to cerebral perfusion pressure, TCD findings and TCD-CO2-reactivity after severe head injury [Elektronische Daten] [J. Dings, J. Meixensberger, J. Amschler, B. Hamelbeck, K. Roosen] Summary: As a reliable continuous monitoring of cerebral blood flow and/or cerebral oxygen metabolism is necessary to prevent secondary ischaemic events after severe head injury (SHI) the authors introduced brain tissue pO2 (ptiO2) monitoring and compared this new parameter with TCD-findings, cerebral perfusion pressure (CPP) and CO2-reactivity over time on 17 patients with a SHI. PtiO2 reflects the balance between the oxygen offered by the cerebral blood flow and the oxygen consumption by the brain tissue. According to TCD-CO2reactivity PtiO2-CO2-reactivity was introduced. After initally (day 0) low mean values (ptiO2 7.7 +/−2.6 mmHg, TCD 60.5 +/−32.0 cm/sec and CPP 64.5 +/−16.0 mmHg/, ptiO2 increased together with an increase in blood flow velocity of the middle cerebral artery and CPP. The relative hyperaemic phase on days 3 and 4 was followed by a decrease of all three parameters. Although TCD-CO2-reactivity was except for day 0 (1.4+/−1.5%), sufficient. ptiO2-CO2-reactivity sometimes showed so-called paradox reactions from day 0 till day 3, meaning an increase of ptiO2 on hyperventilation. Thereafter ptiO2-CO2-reactivity increased, increasing the risk of inducing ischaemia by hyperventilation. The authors concluded that ptiO2-monitoring might become an important tool in our treatment regime for patients requiring haemodynamic monitoring. Springer-Verlag, 1996 Severe head injury nationallicence cerebral perfusion pressure nationallicence brain tissue oxygen pressure nationallicence continuous monitoring nationallicence Dings J. Department of Neurosurgery, University of Wuerzburg, Germany aut Meixensberger J. Department of Neurosurgery, University of Wuerzburg, Germany aut Amschler J. Department of Neurosurgery, University of Wuerzburg, Germany aut Hamelbeck B. Department of Neurosurgery, University of Wuerzburg, Germany aut Roosen K. Department of Neurosurgery, University of Wuerzburg, Germany aut Acta Neurochirurgica Springer-Verlag 138/4(1996-04-01), 425-434 0001-6268 138:4<425 1996 138 701 https://doi.org/10.1007/BF01420305 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01420305 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Dings J. Department of Neurosurgery, University of Wuerzburg, Germany aut NATIONALLICENCE 700 1- Meixensberger J. Department of Neurosurgery, University of Wuerzburg, Germany aut NATIONALLICENCE 700 1- Amschler J. Department of Neurosurgery, University of Wuerzburg, Germany aut NATIONALLICENCE 700 1- Hamelbeck B. Department of Neurosurgery, University of Wuerzburg, Germany aut NATIONALLICENCE 700 1- Roosen K. Department of Neurosurgery, University of Wuerzburg, Germany aut NATIONALLICENCE 773 0- Acta Neurochirurgica Springer-Verlag 138/4(1996-04-01), 425-434 0001-6268 138:4<425 1996 138 701 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer