Summary
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 ≤ 8). Age was 33.2 (±11.3) years. Total time of monitoring of PtiO2, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and endtidal PCO2 (ETCO2) was 119.3 (±65.7) hours. Data were continuously recorded by a computer system. Outcome was assessed at discharge and after 6 months post injury. 56% of the patients with more than 300 minutes of PtiO2 < 10 mm Hg died, 22% had an unfavourable outcome, 22% had a favourable outcome. Cerebral hypoxia was associated with intracranial hypertension (ICP > 20mmHg) in 11.5 (±15.1)%. CPP was compromised below 60mm Hg in 16.8 (±23.4)%. Hypocarbia (ETCO2 < 28mm Hg) was present in 48.0% of the time of PtiO2 < 10mmHg. 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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© 1998 Springer-Verlag Wien
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Bardt, T.F., Unterberg, A.W., Härtl, R., Kiening, K.L., Schneider, G.H., Lanksch, W.R. (1998). Monitoring of Brain Tissue PO2 in Traumatic Brain Injury: Effect of Cerebral Hypoxia on Outcome. In: Marmarou, A., et al. Intracranial Pressure and Neuromonitoring in Brain Injury. Acta Neurochirurgica Supplements, vol 71. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6475-4_45
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DOI: https://doi.org/10.1007/978-3-7091-6475-4_45
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