An assessment of the systematic effects and the intracranial effects of intensive care manoeuvres following traumatic brain injury
Introduction. During the intensive care of patients with traumatic brain injury, intracranial pressure and arterial pressure are commonly measured to derive cerebral perfusion pressure. The assumption is that provided cerebral perfusion pressure is maintained within normal limits cerebral blood flow will autoregulate and therefore meet cerebral metabolic demand. In this thesis cerebral perfusion pressure and cerebral venous oxyhaemoglobin saturation (SjO2) data are presented. The latter indicates the balance between cerebral blood flow and metabolism and therefore adequacy of cerebral oxygen delivery. Methods. Fibre optic technology makes continuous measurement of oxyhaemoglobin saturation possible, however the equipmenthad not been assessed in the jugular bulb. After assessment of the device, a cohort of brain injured patients with a Glasgow Coma Score (GCS) of less than 13 and/or an Injury Severity Score (ISS) of greater than 16 were studied before, during and after intrahospital transport. 10 patients with a GCS of 8 or less, without eye opening, were studied after the administration of the intravenous anaesthetics, Thiopentone and Propofol. Physiological variables were recorded every minute by a personal computer and abnormal values (insults) graded on an increasing three point scale. Results. After in vivo calibration the Oximetrix 3 and Opticath 40cm catheter demonstrated clinically satisfactory agreement when compared with in vitro reflection oximetry, mean difference 0.85% (95% confidence interval -4.5% to 5.2%). Abnormal physiology before intrahospital transport was predictive of further insults during and after transport. An increase in the frequency of insults was seen, that was associated with an increasing ISS (P< 0.01). Slow infusion of intravenous anaesthetic agent was superior to rapid infusion. Propofol, by slow infusion, produced a more sustained reduction of intracranial pressure and a higher cerebral venous oxyhaemoglobin saturation. However Thiopentone produced a higher cerebral perfusion pressure.