An induced coma – also known as a medically induced coma (MIC), barbiturate-induced coma, or drug-induced coma – is a temporary coma (a deep state of unconsciousness) brought on by a controlled dose of an anesthetic drug, often a barbiturate such as pentobarbital or thiopental. Barbiturate comas are used to protect the brain during major neurosurgery, as a last line of treatment in certain cases of status epilepticus that have not responded to other treatments, and in refractory intracranial hypertension following traumatic brain injury.
|Other names||Medically induced coma|
Induced coma usually results in significant systemic adverse effects. The patient is likely to completely lose respiratory drive and require mechanical ventilation; gut motility is reduced; hypotension can complicate efforts to maintain cerebral perfusion pressure and often requires the use of vasopressor drugs. Hypokalemia often results. The completely immobile patient is at increased risk of bed sores as well as infection from catheters.
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, resulting in a shrunken brain, and hence lower 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.
About 60% of the glucose and oxygen used by the brain is meant for its electrical activity and the rest for all other activities such as metabolism. 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 under monitoring by electroencephalography until burst suppression or cortical electrical silence (isoelectric "flatline") is attained. Once there is improvement in the patient's general condition, the barbiturates are withdrawn gradually and the patient regains consciousness.
Controversy exists over the benefits of using barbiturates to control intracranial hypertension. Some studies have found 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.
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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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