View source for Medicine:Induced coma

{{Short description|Medical procedure}}
{{Infobox medical intervention
| name         = Induced coma
| synonym      = Medically induced coma
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| specialty    = [[Biology:Neurology|Neurology]]
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An '''induced coma'''{{spaced en dash}}also known as a '''medically induced coma''' ('''MIC'''), '''barbiturate-induced coma''', or '''drug-induced coma'''{{spaced en dash}}is a temporary [[Medicine:Coma|coma]] (a deep state of [[Medicine:Unconsciousness|unconsciousness]]) brought on by a controlled dose of an anesthetic drug, often a [[Chemistry:Barbiturate|barbiturate]] such as [[Chemistry:Pentobarbital|pentobarbital]] or thiopental. Other intravenous anesthetic drugs such as [[Chemistry:Midazolam|midazolam]] or [[Chemistry:Propofol|propofol]] may be used.<ref name=Mariano2014/><ref name =An2018>{{cite journal | vauthors = An J, Jonnalagadda D, Moura V, Purdon PL, Brown EN, Westover MB | title = Variability in pharmacologically-induced coma for treatment of refractory status epilepticus | journal = PLOS ONE | volume = 13 | issue = 10 | pages = e0205789 | date = 2018 | pmid = 30379935 | pmc = 6209214 | doi = 10.1371/journal.pone.0205789 | bibcode = 2018PLoSO..1305789A | doi-access = free }}</ref>

Drug-induced comas are used to protect the [[Biology:Brain|brain]] during major [[Medicine:Neurosurgery|neurosurgery]], as a last line of treatment in certain cases of [[Medicine:Status epilepticus|status epilepticus]] that have not responded to other treatments,<ref name =An2018/> and in [[Disease#Refractory disease|refractory]] intracranial hypertension following [[Medicine:Traumatic brain injury|traumatic brain injury]].<ref name=Mariano2014/>

Induced coma usually results in significant systemic adverse effects. The patient is likely to completely lose respiratory drive and require [[Medicine:Mechanical ventilation|mechanical ventilation]]; gut motility is reduced; [[Medicine:Hypotension|hypotension]] can complicate efforts to maintain [[Biology:Cerebral perfusion pressure|cerebral perfusion pressure]] and often requires the use of vasopressor drugs. [[Medicine:Hypokalemia|Hypokalemia]] often results. The completely immobile patient is at increased risk of bed sores as well as infection from [[Medicine:Catheter|catheter]]s.{{citation needed|date=December 2022}}

The presence of an endotracheal tube and mechanical ventilation alone are not indications of continuous sedation and coma. Only certain conditions such as intracranial hypertension, refractory status epileptics, the inability to oxygenate with movement, et cetera justify the high risks of medically induced comas.<ref>{{Cite journal |last=Eikermann |first=Matthias |last2=Needham |first2=Dale M |last3=Devlin |first3=John W |date=May 12, 2023 |title='Multimodal, patient-centred symptom control': a strategy to replace sedation in the ICU |url=https://www.thelancet.com/pdfs/journals/lanres/PIIS2213-2600(23)00141-8.pdf |journal=The Lancet}}</ref>

Brain disruption from sedation can lead to an eight times<ref>{{Cite journal |last=Pan |first=Yanbin |last2=Yan |first2=Jianlong |last3=Jiang |first3=Zhixia |last4=Luo |first4=Jianying |last5=Zhang |first5=Jingjing |last6=Yang |first6=Kaihan |date=2019-07-10 |title=Incidence, risk factors, and cumulative risk of delirium among ICU patients: A case-control study |url=https://pubmed.ncbi.nlm.nih.gov/31508442/ |journal=International Journal of Nursing Sciences |volume=6 |issue=3 |pages=247–251 |doi=10.1016/j.ijnss.2019.05.008 |issn=2352-0132 |pmc=6722464 |pmid=31508442}}</ref> increased risk of the development of ICU delirium. This is associated with a doubled risk of mortality<ref>{{Cite journal |last=Salluh |first=Jorge I. F. |last2=Wang |first2=Han |last3=Schneider |first3=Eric B. |last4=Nagaraja |first4=Neeraja |last5=Yenokyan |first5=Gayane |last6=Damluji |first6=Abdulla |last7=Serafim |first7=Rodrigo B. |last8=Stevens |first8=Robert D. |date=2015-06-03 |title=Outcome of delirium in critically ill patients: systematic review and meta-analysis |url=https://www.bmj.com/content/350/bmj.h2538 |journal=BMJ |language=en |volume=350 |pages=h2538 |doi=10.1136/bmj.h2538 |issn=1756-1833 |pmid=26041151|pmc=4454920 }}</ref> during hospital admission. For every one day of delirium, there is a 10% increased risk of death.<ref>{{Cite journal |last=Ely |first=E. Wesley |last2=Shintani |first2=Ayumi |last3=Truman |first3=Brenda |last4=Speroff |first4=Theodore |last5=Gordon |first5=Sharon M. |last6=Harrell |first6=Frank E. |last7=Inouye |first7=Sharon K. |last8=Bernard |first8=Gordon R. |last9=Dittus |first9=Robert S. |date=2004-04-14 |title=Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit |url=https://pubmed.ncbi.nlm.nih.gov/15082703/ |journal=JAMA |volume=291 |issue=14 |pages=1753–1762 |doi=10.1001/jama.291.14.1753 |issn=1538-3598 |pmid=15082703}}</ref> Medically induced comas that achieve a [[Medicine:Richmond Agitation-Sedation Scale|RASS]] level of −4 or −5 are an independent predictor of death.<ref>{{Cite journal |last=Shehabi |first=Yahya |last2=Bellomo |first2=Rinaldo |last3=Reade |first3=Michael C. |last4=Bailey |first4=Michael |last5=Bass |first5=Frances |last6=Howe |first6=Belinda |last7=McArthur |first7=Colin |last8=Seppelt |first8=Ian M. |last9=Webb |first9=Steve |last10=Weisbrodt |first10=Leonie |last11=Sedation Practice in Intensive Care Evaluation (SPICE) Study Investigators |last12=ANZICS Clinical Trials Group |date=2012-10-15 |title=Early intensive care sedation predicts long-term mortality in ventilated critically ill patients |url=https://pubmed.ncbi.nlm.nih.gov/22859526/ |journal=American Journal of Respiratory and Critical Care Medicine |volume=186 |issue=8 |pages=724–731 |doi=10.1164/rccm.201203-0522OC |issn=1535-4970 |pmid=22859526}}</ref> &nbsp;

Although patients are not sleeping while sedated, they can experience hallucinations and delusions<ref>{{Cite web |last=Ali |first=Mohammed |title=ICU Delirium |date=2023 |url=http://www.ncbi.nlm.nih.gov/books/NBK559280/ |work=StatPearls |access-date=2023-08-15 |place=Treasure Island, FL |publisher=StatPearls Publishing |pmid=32644706 |last2=Cascella |first2=Marco}}</ref> that are often graphic and traumatizing in nature. This can lead to post-ICU PTSD after hospital discharge. Patients that develop ICU delirium are at 120 times greater risk of long-term cognitive impairments.<ref>{{Cite journal |last=Girard |first=Timothy D. |last2=Jackson |first2=James C. |last3=Pandharipande |first3=Pratik P. |last4=Pun |first4=Brenda T. |last5=Thompson |first5=Jennifer L. |last6=Shintani |first6=Ayumi K. |last7=Gordon |first7=Sharon M. |last8=Canonico |first8=Angelo E. |last9=Dittus |first9=Robert S. |last10=Bernard |first10=Gordon R. |last11=Ely |first11=E. Wesley |date=July 2010 |title=Delirium as a predictor of long-term cognitive impairment in survivors of critical illness |url=https://pubmed.ncbi.nlm.nih.gov/20473145/ |journal=Critical Care Medicine |volume=38 |issue=7 |pages=1513–1520 |doi=10.1097/CCM.0b013e3181e47be1 |issn=1530-0293 |pmc=3638813 |pmid=20473145}}</ref>

Considering the high risks of medically induced comas, protocols such as the ABCDEF Bundle<ref>{{Cite journal |last=Pun |first=Brenda T. |last2=Balas |first2=Michele C. |last3=Barnes-Daly |first3=Mary Ann |last4=Thompson |first4=Jennifer L. |last5=Aldrich |first5=J. Matthew |last6=Barr |first6=Juliana |last7=Byrum |first7=Diane |last8=Carson |first8=Shannon S. |last9=Devlin |first9=John W. |last10=Engel |first10=Heidi J. |last11=Esbrook |first11=Cheryl L. |last12=Hargett |first12=Ken D. |last13=Harmon |first13=Lori |last14=Hielsberg |first14=Christina |last15=Jackson |first15=James C. |date=January 2019 |title=Caring for Critically Ill Patients with the ABCDEF Bundle: Results of the ICU Liberation Collaborative in Over 15,000 Adults |url=https://pubmed.ncbi.nlm.nih.gov/30339549/ |journal=Critical Care Medicine |volume=47 |issue=1 |pages=3–14 |doi=10.1097/CCM.0000000000003482 |issn=1530-0293 |pmc=6298815 |pmid=30339549}}</ref> and PADIS guidelines<ref>{{Cite web |title=SCCM {{!}} PADIS Guidelines |url=https://sccm.org/Clinical-Resources/ICULiberation-Home/Guidelines |access-date=2023-08-15 |website=Society of Critical Care Medicine (SCCM)}}</ref> have been developed to guide ICU teams to avoid unnecessary sedation and comas. ICU teams that master these protocols to keep patients as awake and mobile as possible are called "Awake and Walking ICUs". These are teams that only implement medically induced comas when the possible benefits of sedation outweigh the high risks during specific cases.&nbsp;

Survivors of prolonged medically induced comas are at high risk of suffering from post-ICU syndrome<ref>{{Citation |last=Smith |first=Sarah |title=Post-Intensive Care Syndrome |date=2023 |url=http://www.ncbi.nlm.nih.gov/books/NBK558964/ |work=StatPearls |access-date=2023-08-15 |place=Treasure Island, FL |publisher=StatPearls Publishing |pmid=32644390 |last2=Rahman |first2=Omar}}</ref> and may require extended physical, cognitive, and psychological rehabilitation.

== Theory ==
Barbiturates reduce the metabolic rate of brain tissue, as well as the cerebral blood flow. With these reductions, the [[Biology:Blood vessel|blood vessel]]s in the brain narrow, resulting in a shrunken brain, and hence lower [[Medicine:Intracranial pressure|intracranial pressure]]. The hope is that, with the swelling relieved, the pressure decreases and some or all [[Medicine:Brain damage|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 [[Biology:Electroencephalography|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> intracranial aneurysm rupture, [[Medicine:Intracranial hemorrhage|intracranial hemorrhage]], ischemic [[Medicine:Stroke|stroke]], and [[Medicine:Status epilepticus|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>

== See also ==
* [[Medicine:Insulin shock therapy|Insulin shock therapy]]
* [[Medicine:Traumatic brain injury|Traumatic brain injury]]

== References ==
{{Reflist|30em}}

== External links ==
*[https://www.livescience.com/39483-what-is-a-medically-induced-coma.html Medically induced Coma] – LiveScience

{{Intensive care medicine}}

[[Category:Intensive care medicine]]
[[Category:Coma]]

{{Sourceattribution|Induced coma}}