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A postal survey was conducted to determine how thiopental is used in UK neurosurgery critical care units. Thirty units were contacted and 26 replied. Thiopental is used in 23 units. The majority (60%) of these units govern the use of thiopental with protocols or guidelines and 74% use cerebral monitoring to guide dosage. When patients have had thiopental, 20 units delay brain stem testing, two will not perform tests and one unit incorporates cerebral angiography into their protocol. Twelve units use serum thiopental assays in their brain stem testing procedures, but there is wide variation in the interpretation of the results. We found inconsistency and confusion surrounding brain stem testing in this patient group, raising the possibility of misdiagnosis of brain stem death.

Two patients who underwent surgery for cerebral aneurysms are presented. In the first case 31 g thiopentone were given postoperatively over 20 h after the patient had already been comatose for many hours. Such high doses raise considerable problems in patient management. In the second case a loading dose of 50 mg/kg thiopentone was given prophylactically to a patient undergoing cerebral aneurysm surgery beginning at the induction of anaesthesia and before surface cooling was begun. Cerebral activity was monitored continuously with a cerebral function monitor (CFM). There was no significant cardiovascular depression, little delay in postoperative recovery and no permanent neurological sequelae. In cerebral aneurysm surgery, cerebral oedema following cerebral ischaemia, either associated with vasospasm or resulting from surgical occlusion of vessels, remains a major problem postoperatively and may be an indication for preventive treatment with barbiturates. The author contend that this technique merits further evaluation in cerebro-vascular surgery, especially in high risk cases.

The induction doses of thiopentone in eight elderly male patients (60--80 years) were significantly lower (p less than 0.01) than in eight young male patients (ranges 3.09--5.06 mg/kg body weight in the elderly and 4.88--8.11 mg/kg in the young). The sleep concentrations in venous as well as in arterial blood did not differ between the two groups. In the elderly the arterial concentrations were significantly higher than the venous (p less than 0.05). A three compartment open model was used to describe the disappearance of the drug from the venous blood. Significant increases were found in V3 (means 145.9 and 51.2 litres) and in T 1/2 beta (means 781 and 427 minutes) in the elderly. The redistribution rate constant, k1.2, was decreased in the elderly (p less than 0.05). By impedance cardiography 5 minutes after sleep mean percentages of the pre-induction value of cardiac output were 94.6% in the young and 87.0% in the elderly (p less than 0.05). In the young a correlation was found between cardiac output and induction dose (4 = 0.85, p less than 0.01).

Plasma total and unbound concentrations of thiopentone were investigated during exponentially decreasing infusions in seven patients undergoing cardiopulmonary bypass. Total plasma thiopentone concentrations reached a plateau (10.2, SD 2.1 micrograms/ml) soon after the initial bolus dose and commencement of the infusion. Concentrations were maintained until the onset of cardiopulmonary bypass, whereupon total plasma thiopentone concentration fell abruptly to 50.0 (SD 5.8) percent of the prebypass level. The unbound fraction of thiopentone increased from 16.6 (SD 1.9) percent before bypass to a maximum of 29.3 (SD 5.6) percent during bypass (p less than 0.01), decreased to 22.9 (SD 3.3) percent at the end of bypass (p less than 0.01), but was still elevated 5-7 hours later (20.5, SD 2.5 percent). The result of the changes in binding was a smaller decline in unbound thiopentone concentration at the onset of bypass to 76.4 (SD 15.7) percent of the prebypass level. Also, unbound levels returned to the prebypass level by the end of bypass, whereas total levels remained low.

During an infusion of thiopentone to control status epilepticus secondary to hypoxic brain damage, thiopentone and pentobarbitone levels were measured in the serum and cerebrospinal fluid (CSF). Pentobarbitone was found to be present in the serum between 7.8 and 11.1% of the thiopentone levels. There was a prompt response in serum levels of thiopentone to changes in the infusion rate. The CSF thiopentone varied between 15 and 40% of the serum levels. The CSF anticonvulsant threshold for thiopentone for this patient was between 5 and 15 mg/litre.