A barbiturate-induced coma, or barb coma, is a temporary coma (a deep state of unconsciousness) brought on by a controlled dose of a barbiturate drug, usually pentobarbital or thiopental. Barbiturate comas are used to protect the brain during major neurosurgery, and as a last line of treatment in certain cases of status epilepticus that have not responded to other treatments. Because patients are often seriously ill or injured, and are under general anesthesia and in a coma, careful airway management, which involves some form of mechanical ventilation, is needed.
Barbiturates reduce the metabolic rate of brain tissue, as well as the cerebral blood flow. With these reductions, the blood vessels in the brain narrow, decreasing the amount of space occupied by the brain, and hence the intracranial pressure. The hope is that, with the swelling relieved, the pressure decreases and some or all brain damage may be averted. Several studies have supported this theory by showing reduced mortality when treating refractory intracranial hypertension with a barbiturate coma.
Controversy exists, however, over the benefits of using barbiturates to control intracranial hypertension. Some studies have shown that barbiturate-induced coma can reduce intracranial hypertension but does not necessarily prevent brain damage. Furthermore, the reduction in intracranial hypertension may not be sustained. Some randomized trials have failed to demonstrate any survival or morbidity benefit of induced coma in diverse conditions such as neurosurgical operations, head trauma, intracranial aneurysm rupture, intracranial hemorrhage, ischemic stroke, and status epilepticus. If the patient survives, cognitive impairment may also follow recovery from the coma.
About 60% of the glucose and oxygen use by the brain is meant for its electrical activity and the rest for all other activities such as metabolism. This is recognized by a device such as an electroencephalogram (EEG), which measures electrical activity in the brain. When barbiturates are given to brain injured patients for induced coma, they act by reducing the electrical activity of the brain, which reduces the metabolic and oxygen demand. The infusion dose rate of barbiturates is increased until EEG burst suppression or cortical electrical silence (isoelectric "flatline" EEG) is attained. Once there is improvement in the patient's general condition, the barbiturates are withdrawn gradually and the patient regains consciousness.
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approximately 60% of CMRO2 is utilized for neuronal function (with the remainder being required for cellular integrity)
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The primary mechanism of protection involves a reduction in CMRo2 of up to 55% to 60% at which point the EEG becomes isoelectric.
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Therapeutic EEG response: burst suppression or cortical electrical silence (with preservation of SSEP and BAEF).
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