The feasibility of low dose barbiturate administration by intra-carotid infusion to achieve EEG burst suppression--a preliminary report.

More than 10 years have elapsed since the introduction of high dose barbiturate administration in the management of patients with severe head injuries. Barbiturate therapy became an accepted method of treatment for increased intracranial pressure when other measures fail. One of the major limiting factors in the use of high dose barbiturate therapy is its significant hypotensive effect on the systemic arterial blood pressure. In seeking ways and means of minimising this hypotensive effect, we designed a study in which the systemic administration of barbiturates is avoided and replaced by selective perfusion of the concerned hemisphere with the drug utilising the intra-carotid route. Twenty-two rats, divided into two groups, were used in the study. Since monitoring of electroencephalographic (EEG) burst suppression serves as a good indicator of the lowest level of cerebral metabolic activity, we used this as the method for determining the desired endpoint of sodium amytal administration in both groups of animals. Group I, the intravenous group, consisted of eleven animals who received sodium amytal intravenously until burst suppression on the EEG was documented. Group II, the intra-carotid group, comprised eleven animals who received intra-carotid sodium amytal until EEG burst suppression was induced. In the intravenous group, a mean dose of 35 mg/kg of sodium amytal was administered before EEG burst suppression was achieved. This dose, however, was accompanied by an almost 50% reduction in systemic blood pressure compared to the pretreatment level. The intra-carotid group required a mean dose of 3.8 mg/kg sodium amytal and this was accompanied by only minor changes in systemic arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)