The low mortality compared with previous outcome studies strongly indicates that this therapy improves outcome for severe head injuries. However, a randomized, controlled study is needed to reach general acceptance of this new therapy.

The study documents that mitochondrial dysfunction is a common cause of disturbed cerebral energy metabolism in patients with SAH. Mitochondrial dysfunction may increase tissue sensitivity to secondary adverse events such as vasospasm and decreased cerebral blood flow. The separation of ischemia and mitochondrial dysfunction bedside by utilizing microdialysis offers a possibility to evaluate new therapies.

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.