Editing Induced coma (section)

== Theory ==
Barbiturates reduce the metabolic rate of brain tissue, as well as the [[cerebral blood flow]]. With these reductions, the [[blood vessel]]s 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.<ref>{{cite journal | vauthors =  | title = The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Use of barbiturates in the control of intracranial hypertension | journal = Journal of Neurotrauma | volume = 17 | issue = 6–7 | pages = 527–530 | year = 2000 | pmid = 10937896 | doi = 10.1089/neu.2000.17.527 | publisher = Mary Ann Liebert, Inc. }}</ref><ref>{{cite journal | vauthors = Lee MW, Deppe SA, Sipperly ME, Barrette RR, Thompson DR | title = The efficacy of barbiturate coma in the management of uncontrolled intracranial hypertension following neurosurgical trauma | journal = Journal of Neurotrauma | volume = 11 | issue = 3 | pages = 325–331 | date = June 1994 | pmid = 7996586 | doi = 10.1089/neu.1994.11.325 }}</ref><ref>{{cite journal | vauthors = Nordby HK, Nesbakken R | title = The effect of high dose barbiturate decompression after severe head injury. A controlled clinical trial | journal = Acta Neurochirurgica | volume = 72 | issue = 3–4 | pages = 157–166 | year = 1984 | pmid = 6382945 | doi = 10.1007/BF01406868 | s2cid = 12215655 }}</ref>

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.<ref>{{cite web | title= Update on Techniques for Neuroprotection during Hypothermic Arrest | publisher= Society of Cardiovascular Anesthesiologists | author= Grocott HP | url= http://www.scahq.org/files/Conference_2014_Annual_Syllabi_Sessions/SCA_2014_syllabus_Grocott_Update_on_techniques_for_neuroprotection_during_hypothermic_arrest.pdf | access-date= 14 April 2016 | quote= approximately 60% of CMRO2 is utilized for neuronal function (with the remainder being required for cellular integrity) | archive-url= https://web.archive.org/web/20160423192027/http://www.scahq.org/files/Conference_2014_Annual_Syllabi_Sessions/SCA_2014_syllabus_Grocott_Update_on_techniques_for_neuroprotection_during_hypothermic_arrest.pdf | archive-date= 23 April 2016 | url-status= dead }}</ref> 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.<ref>{{cite web| title =Cerebral protection and resuscitation| publisher =CNS Clinic – Jordan – Amman| url =http://www.neuroanesthesia.info/cerebralprotection.htm| access-date =16 April 2016| quote =The primary mechanism of protection involves a reduction in CMRo2 of up to 55% to 60% at which point the EEG becomes isoelectric.| archive-date =4 November 2020| archive-url =https://web.archive.org/web/20201104172132/http://www.neuroanesthesia.info/cerebralprotection.htm| url-status =dead}}</ref> Their action limits oxidative damage to lipid membranes and may scavenge free radicals. They also lead to reduced vasogenic edema, fatty acid release and intracellular calcium release.<ref name=Mariano2014/>

The infusion dose rate of barbiturates is increased under monitoring by [[electroencephalography]] until burst suppression or cortical electrical silence (isoelectric "flatline") is attained.<ref>{{cite web| title =Barbiturate Coma| publisher =Trauma.org| url =http://www.trauma.org/archive/anaesthesia/barbcoma.html| access-date =16 April 2016| quote =Therapeutic EEG response: burst suppression or cortical electrical silence (with preservation of SSEP and BAEF).| archive-url =https://web.archive.org/web/20160819000601/http://www.trauma.org/archive/anaesthesia/barbcoma.html| archive-date =19 August 2016| url-status =dead}}</ref> 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.<ref name=Mariano2014/> Furthermore, the reduction in intracranial hypertension may not be sustained. Some [[Randomized controlled trial|randomized trial]]s have failed to demonstrate any survival or morbidity benefit of induced coma in diverse conditions such as neurosurgical operations, [[head trauma]],<ref>{{cite journal | vauthors = Schwartz ML, Tator CH, Rowed DW, Reid SR, Meguro K, Andrews DF | title = The University of Toronto head injury treatment study: a prospective, randomized comparison of pentobarbital and mannitol | journal = The Canadian Journal of Neurological Sciences. Le Journal Canadien des Sciences Neurologiques | volume = 11 | issue = 4 | pages = 434–440 | date = November 1984 | pmid = 6440704 | doi = 10.1017/s0317167100045960 | doi-access = free }}</ref> [[cerebral aneurysm|intracranial aneurysm]] rupture, [[intracranial hemorrhage]], ischemic [[stroke]], and [[status epilepticus]]. If the patient survives, cognitive impairment may also follow recovery from the coma.<ref>{{cite journal | vauthors = Schalén W, Sonesson B, Messeter K, Nordström G, Nordström CH | title = Clinical outcome and cognitive impairment in patients with severe head injuries treated with barbiturate coma | journal = Acta Neurochirurgica | volume = 117 | issue = 3–4 | pages = 153–159 | year = 1992 | pmid = 1414516 | doi = 10.1007/BF01400613 | s2cid = 23032307 }}</ref> Due to these risks, barbiturate-induced coma should be reserved for cases of refractory intracranial pressure elevation.<ref name=Mariano2014>{{cite book | vauthors = Mariano GL, Fink ME, Hoffman C, Rosengart A | date = 2014 | chapter = Intracranial pressure: monitoring and management. | veditors = Hall JB, Schmidt GA, Kress JP | title = Principles of Critical Care | edition = 4th | publisher = McGraw Hill | chapter-url = https://accessmedicine.mhmedical.com/content.aspx?bookid=1340&sectionid=80036194 | isbn = 978-0-07-173881-1 }}</ref>