Induced coma

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.

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.[1][2][3]

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,[4] intracranial aneurysm rupture, intracranial hemorrhage, ischemic stroke, and status epilepticus. If the patient survives, cognitive impairment may also follow recovery from the coma.[5]

About 55% of the glucose and oxygen utilisation 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 in theory reduces the metabolic and oxygen demand. Once there is improvement in the patient's general condition, the barbiturates are withdrawn gradually and the patient regains consciousness.

Induced coma is used in the treatment of symptomatic rabies through the Milwaukee protocol, first attempted in 2004.[6]

See also

References

  1. ↑ "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.
  2. ↑ Lee M.W., Deppe S.A., Sipperly M.E., Barrette R.R., Thompson D.R. (1 June 1994). "The efficacy of barbiturate coma in the management of uncontrolled intracranial hypertension following neurosurgical trauma". Journal of Neurotrauma (Mary Ann Liebert, Inc.) 11 (3): 325–31. doi:10.1089/neu.1994.11.325. PMID 7996586.
  3. ↑ Nordby H. K., Nesbakken R. (1984). "The effect of high dose barbiturate decompression after severe head injury: A controlled clinical trial". Acta Neurochirurgica (Springer-Verlag) 72 (3–4): 157–66. doi:10.1007/BF01406868. PMID 6382945.
  4. ↑ Schwartz M.L., Tator C.H., Rowed D.W, Reid S.R, Meguro K., Andrews D.F. (1 November 1984). "The University of Toronto head injury treatment study: a prospective, randomized comparison of pentobarbital and mannitol". The Canadian Journal of Neurological Sciences 11 (4): 434–40. PMID 6440704.
  5. ↑ Schalén W., Sonesson B., Messeter K., Nordström G., Nordström C.H. (1992). "Clinical outcome and cognitive impairment in patients with severe head injuries treated with barbiturate coma". Acta Neurochirurgica (Springer-Verlag) 117 (3–4): 153–9. doi:10.1007/BF01400613. PMID 1414516.
  6. ↑ Rodney E. Willoughby, Jr., M.D.; Kelly S. Tieves, D.O., George M. Hoffman, M.D., Nancy S. Ghanayem, M.D., Catherine M. Amlie-Lefond, M.D., Michael J. Schwabe, M.D., Michael J. Chusid, M.D., and Charles E. Rupprecht, V.M.D., Ph.D. "Survival after Treatment of Rabies with Induction of Coma". New England Journal of Medicine. New England Journal of Medicine. Retrieved 16 June 2005.