This study reports all complications and side effects occurring in 38 patients with severe traumatic brain lesions treated with barbiturate coma because of a dangerous increase in intracranial pressure. The treatment was induced by intravenous infusion of thiopentone (5-11 mg.kg-1) followed by a continuous infusion of 4-8 mg.kg-1.h-1. The subsequent rate of thiopentone infusion was governed by the level of the intracranial pressure with the intention of keeping ICP below 20 mmHg (2.7 kPa). The duration of treatment was 1-15 days. Arterial hypotension occurred in 58%, hypokalemia in 82%, respiratory complications in 76%, infections in 55%, hepatic dysfunction in 87% and renal dysfunction in 47% of the patients. Twenty patients survived. Mortality in 17 patients was caused by an untreatable increase in intracranial pressure. In one patient complications due to barbiturate treatment may have contributed to the fatal outcome. In none of the other cases were the noted complications and side effects associated with any permanent symptoms or dysfunctions.

SummaryThe cardiovascular response to laryngoscopy and intubation was investigated in lightly anaesthetised patients admitted to hospital for elective intracranial surgery. One group of patients was given fentanyl5 pglkg body weight before induction with thiopentone and suxamethonium. The other group served as controls. Fentanyl treatment caused a signijicant attenuation of the blood pressure and pulse response to laryngoscopy and intubation.DEfSerent techniques for induction of anaesthesia are discussed in relation to the demands ofneuroanaesthesia.

Mean hemispheric cerebral blood flow (CBF) and intracranial pressure (ICP) were measured in 19 severely head-injured patients treated with barbiturate coma. The CBF was calculated from the clearance of tracer substance monitored by extracranial scintillation detectors after intravenous administration of xenon-133. In 11 of the patients cerebral arteriovenous oxygen differences were measured simultaneously. In all patients the effects of pronounced hyperventilation were recorded prior to initiation of barbiturate treatment. A normal CBF response to hyperventilation (delta CBF/delta PaCO2 greater than or equal to 1) was obtained in eight patients. In these patients induction of barbiturate coma was accompanied by physiological decreases in CBF and in the calculated cerebral metabolic rate of oxygen (CMRO2); they also exhibited a rapid and lasting decrease in ICP. A decreased or an abolished CO2 reactivity was recorded (delta CBF/delta PaCO2 less than 1) in 11 patients. In 10 of these 11 patients the physiological decreases in CBF and CMRO2 were not obtained during barbiturate treatment and the decrease in ICP was transitory. This study demonstrates a correlation between cerebral vasoreactivity, physiological effects of barbiturate therapy, and clinical outcome.

Mean hemispheric cerebral blood flow (CBF) was studied in 11 comatose brain-injured patients following intravenous administration of xenon-133. Repeated measurements were performed in order to evaluate cerebral vasoreactivity following a decrease in PaCO2. In addition, the effect of induced barbiturate coma was evaluated in patients with intracranial hypertension. The cerebral vasoreactivity and the CBF response following induction of barbiturate coma varied. In patients with normal CO2 reactivity, barbiturate treatment was accompanied by a considerable decrease in CBF as compared to patients with decreased or abolished CO2 response. During barbiturate treatment the intracranial pressure (ICP) became normal in three of four patients with preserved CO2 response, but reached normal levels in only one of five patients with impaired CO2 reactivity. Patients whose ICP became normal recovered. The data suggest a positive correlation between CO2 reactivity and the effect of barbiturate treatment. Furthermore, preserved cerebral vasoreactivity after severe head injury may be of prognostic value.

There is a difference in the human rCBF distribution between halothane and isoflurane with higher relative flows in subcortical regions during isoflurane anesthesia. However, despite this redistribution, isoflurane anesthesia resulted in a lower mean CBFxenon than did anesthesia with halothane.