Barbiturate coma therapy has been used in head injured patients to lower ICP when other therapies such as mannitol and hyperventilation have failed. Barbiturates may also be protective during periods of cerebral hypoxia. The mechanism of action of barbiturates is by inhibiting the synaptic transmission thereby decreasing the cerebral metabolic rate of oxygen consumption, reducing blood volume and ICP. In addition to lowering ICP, extracellular concentration of lactate and excitatory amino acids are reduced after barbiturate therapy.
Intensive monitoring including EEG, arterial blood pressure monitoring, PA catheter monitoring and frequent blood chemistries is required for barbiturate coma therapy. Treatment is started with a loading dose and maintained with an infusion. EEG monitoring is helpful in defining the limits of therapy by the occurrence of burst suppression. Once burst suppression is achieved then a constant infusion may be maintained. Controlled burst suppression should be present on EEG. Studies have indicated that plasma and CSF levels of pentobarbital do not accurately reflect the physiologic effects of pentobarbital and recommend monitoring the EEG instead of the pentobarbital levels.