Induced coma

An induced coma, also known as a medically induced coma, a barbiturate-induced coma, or a 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, 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.

Induced coma
Specialtyneurology

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 indwelling lines.

Induced coma was a feature of the Milwaukee protocol, a now-discredited method that was promoted as a means of treating rabies infection in people.[1][2]

Theory

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.[3][4][5]

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.[6] 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.[7] The infusion dose rate of barbiturates is increased under monitoring by electroencephalography until burst suppression or cortical electrical silence (isoelectric "flatline") is attained.[8] Once there is improvement in the patient's general condition, the barbiturates are withdrawn gradually and the patient regains consciousness.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 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,[9] intracranial aneurysm rupture, intracranial hemorrhage, ischemic stroke, and status epilepticus. If the patient survives, cognitive impairment may also follow recovery from the coma.[10]

See also

References
  1. Jackson AC (2016). "Human Rabies: a 2016 Update". Curr Infect Dis Rep (Review). 18 (11): 38. doi:10.1007/s11908-016-0540-y. PMID 27730539.
  2. Zeiler FA, Jackson AC (2016). "Critical Appraisal of the Milwaukee Protocol for Rabies: This Failed Approach Should Be Abandoned". Can J Neurol Sci (Review). 43 (1): 44–51. doi:10.1017/cjn.2015.331. PMID 26639059.
  3. "Use of barbiturates in the control of intracranial hypertension". Journal of Neurotrauma. Mary Ann Liebert, Inc. 17 (6–7): 527–30. 2000. doi:10.1089/neu.2000.17.527. PMID 10937896.
  4. Lee MW, Deppe SA, Sipperly ME, Barrette RR, Thompson DR (1994). "The efficacy of barbiturate coma in the management of uncontrolled intracranial hypertension following neurosurgical trauma". J. Neurotrauma. 11 (3): 325–31. doi:10.1089/neu.1994.11.325. PMID 7996586.
  5. Nordby HK, Nesbakken R (1984). "The effect of high dose barbiturate decompression after severe head injury. A controlled clinical trial". Acta Neurochir (Wien). 72 (3–4): 157–66. doi:10.1007/BF01406868. PMID 6382945.
  6. Grocott HP. "Update on Techniques for Neuroprotection during Hypothermic Arrest" (PDF). Society of Cardiovascular Anesthesiologists. Archived from the original (PDF) on 23 April 2016. Retrieved 14 April 2016. approximately 60% of CMRO2 is utilized for neuronal function (with the remainder being required for cellular integrity)
  7. "Cerebral protection and resuscitation". CNS Clinic – Jordan – Amman. Retrieved 16 April 2016. The primary mechanism of protection involves a reduction in CMRo2 of up to 55% to 60% at which point the EEG becomes isoelectric.
  8. "Barbiturate Coma". Trauma.org. Archived from the original on 19 August 2016. Retrieved 16 April 2016. Therapeutic EEG response: burst suppression or cortical electrical silence (with preservation of SSEP and BAEF).
  9. Schwartz ML, Tator CH, Rowed DW, Reid SR, Meguro K, Andrews DF (1984). "The University of Toronto head injury treatment study: a prospective, randomized comparison of pentobarbital and mannitol". Can J Neurol Sci. 11 (4): 434–40. doi:10.1017/s0317167100045960. PMID 6440704.
  10. Schalén W, Sonesson B, Messeter K, Nordström G, Nordström CH (1992). "Clinical outcome and cognitive impairment in patients with severe head injuries treated with barbiturate coma". Acta Neurochir (Wien). 117 (3–4): 153–9. doi:10.1007/BF01400613. PMID 1414516.
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