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Induced coma

From Wikipedia, the free encyclopedia
Induced coma
Other namesMedically induced coma
SpecialtyNeurology

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. Other intravenous anesthetic drugs such as midazolam or propofol may be used.[1][2]

Drug-induced 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,[2] and in refractory intracranial hypertension following traumatic brain injury.[1]

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.[citation needed]

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 epilepticus, the inability to oxygenate with movement, et cetera justify the high risks of medically induced comas.[3]

Brain disruption from sedation can lead to an eight times[4] increased risk of the development of ICU delirium. This is associated with a doubled risk of mortality[5] during hospital admission. For every one day of delirium, there is a 10% increased risk of death.[6] Medically induced comas that achieve a RASS level of −4 or −5 are an independent predictor of death.[7]  

Although patients are not sleeping while sedated, they can experience hallucinations and delusions[8] 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.[9]

Considering the high risks of medically induced comas, protocols such as the ABCDEF Bundle[10] and PADIS guidelines[11] 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. 

Survivors of prolonged medically induced comas are at high risk of suffering from post-ICU syndrome[12] and may require extended physical, cognitive, and psychological rehabilitation.

Theory

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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.[13][14][15]

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.[16] 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.[17] 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.[1]

The infusion dose rate of barbiturates is increased under monitoring by electroencephalography until burst suppression or cortical electrical silence (isoelectric "flatline") is attained.[18] 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.[1] 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,[19] intracranial aneurysm rupture, intracranial hemorrhage, ischemic stroke, and status epilepticus. If the patient survives, cognitive impairment may also follow recovery from the coma.[20] Due to these risks, barbiturate-induced coma should be reserved for cases of refractory intracranial pressure elevation.[1]

See also

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References

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  1. ^ a b c d e Mariano GL, Fink ME, Hoffman C, Rosengart A (2014). "Intracranial pressure: monitoring and management.". In Hall JB, Schmidt GA, Kress JP (eds.). Principles of Critical Care (4th ed.). McGraw Hill. ISBN 978-0-07-173881-1.
  2. ^ a b An J, Jonnalagadda D, Moura V, Purdon PL, Brown EN, Westover MB (2018). "Variability in pharmacologically-induced coma for treatment of refractory status epilepticus". PLOS ONE. 13 (10): e0205789. Bibcode:2018PLoSO..1305789A. doi:10.1371/journal.pone.0205789. PMC 6209214. PMID 30379935.
  3. ^ Eikermann, Matthias; Needham, Dale M; Devlin, John W (May 12, 2023). "'Multimodal, patient-centred symptom control': a strategy to replace sedation in the ICU" (PDF). The Lancet. 11 (6): 506–509. doi:10.1016/S2213-2600(23)00141-8. PMID 37187192.
  4. ^ Pan, Yanbin; Yan, Jianlong; Jiang, Zhixia; Luo, Jianying; Zhang, Jingjing; Yang, Kaihan (2019-07-10). "Incidence, risk factors, and cumulative risk of delirium among ICU patients: A case-control study". International Journal of Nursing Sciences. 6 (3): 247–251. doi:10.1016/j.ijnss.2019.05.008. ISSN 2352-0132. PMC 6722464. PMID 31508442.
  5. ^ Salluh, Jorge I. F.; Wang, Han; Schneider, Eric B.; Nagaraja, Neeraja; Yenokyan, Gayane; Damluji, Abdulla; Serafim, Rodrigo B.; Stevens, Robert D. (2015-06-03). "Outcome of delirium in critically ill patients: systematic review and meta-analysis". BMJ. 350: h2538. doi:10.1136/bmj.h2538. ISSN 1756-1833. PMC 4454920. PMID 26041151.
  6. ^ Ely, E. Wesley; Shintani, Ayumi; Truman, Brenda; Speroff, Theodore; Gordon, Sharon M.; Harrell, Frank E.; Inouye, Sharon K.; Bernard, Gordon R.; Dittus, Robert S. (2004-04-14). "Delirium as a predictor of mortality in mechanically ventilated patients in the intensive care unit". JAMA. 291 (14): 1753–1762. doi:10.1001/jama.291.14.1753. ISSN 1538-3598. PMID 15082703.
  7. ^ Shehabi, Yahya; Bellomo, Rinaldo; Reade, Michael C.; Bailey, Michael; Bass, Frances; Howe, Belinda; McArthur, Colin; Seppelt, Ian M.; Webb, Steve; Weisbrodt, Leonie; Sedation Practice in Intensive Care Evaluation (SPICE) Study Investigators; ANZICS Clinical Trials Group (2012-10-15). "Early intensive care sedation predicts long-term mortality in ventilated critically ill patients". American Journal of Respiratory and Critical Care Medicine. 186 (8): 724–731. doi:10.1164/rccm.201203-0522OC. ISSN 1535-4970. PMID 22859526.
  8. ^ Ali, Mohammed; Cascella, Marco (2023). "ICU Delirium". StatPearls. Treasure Island, FL: StatPearls Publishing. PMID 32644706. Retrieved 2023-08-15.
  9. ^ Girard, Timothy D.; Jackson, James C.; Pandharipande, Pratik P.; Pun, Brenda T.; Thompson, Jennifer L.; Shintani, Ayumi K.; Gordon, Sharon M.; Canonico, Angelo E.; Dittus, Robert S.; Bernard, Gordon R.; Ely, E. Wesley (July 2010). "Delirium as a predictor of long-term cognitive impairment in survivors of critical illness". Critical Care Medicine. 38 (7): 1513–1520. doi:10.1097/CCM.0b013e3181e47be1. ISSN 1530-0293. PMC 3638813. PMID 20473145.
  10. ^ Pun, Brenda T.; Balas, Michele C.; Barnes-Daly, Mary Ann; Thompson, Jennifer L.; Aldrich, J. Matthew; Barr, Juliana; Byrum, Diane; Carson, Shannon S.; Devlin, John W.; Engel, Heidi J.; Esbrook, Cheryl L.; Hargett, Ken D.; Harmon, Lori; Hielsberg, Christina; Jackson, James C. (January 2019). "Caring for Critically Ill Patients with the ABCDEF Bundle: Results of the ICU Liberation Collaborative in Over 15,000 Adults". Critical Care Medicine. 47 (1): 3–14. doi:10.1097/CCM.0000000000003482. ISSN 1530-0293. PMC 6298815. PMID 30339549.
  11. ^ "SCCM | PADIS Guidelines". Society of Critical Care Medicine (SCCM). Retrieved 2023-08-15.
  12. ^ Smith, Sarah; Rahman, Omar (2023), "Post-Intensive Care Syndrome", StatPearls, Treasure Island, FL: StatPearls Publishing, PMID 32644390, retrieved 2023-08-15
  13. ^ "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 of Neurotrauma. 17 (6–7). Mary Ann Liebert, Inc.: 527–530 2000. doi:10.1089/neu.2000.17.527. PMID 10937896.
  14. ^ Lee MW, Deppe SA, Sipperly ME, Barrette RR, Thompson DR (June 1994). "The efficacy of barbiturate coma in the management of uncontrolled intracranial hypertension following neurosurgical trauma". Journal of Neurotrauma. 11 (3): 325–331. doi:10.1089/neu.1994.11.325. PMID 7996586.
  15. ^ Nordby HK, Nesbakken R (1984). "The effect of high dose barbiturate decompression after severe head injury. A controlled clinical trial". Acta Neurochirurgica. 72 (3–4): 157–166. doi:10.1007/BF01406868. PMID 6382945. S2CID 12215655.
  16. ^ 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)
  17. ^ "Cerebral protection and resuscitation". CNS Clinic – Jordan – Amman. Archived from the original on 4 November 2020. 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.
  18. ^ "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).
  19. ^ Schwartz ML, Tator CH, Rowed DW, Reid SR, Meguro K, Andrews DF (November 1984). "The University of Toronto head injury treatment study: a prospective, randomized comparison of pentobarbital and mannitol". The Canadian Journal of Neurological Sciences. Le Journal Canadien des Sciences Neurologiques. 11 (4): 434–440. doi:10.1017/s0317167100045960. PMID 6440704.
  20. ^ 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 Neurochirurgica. 117 (3–4): 153–159. doi:10.1007/BF01400613. PMID 1414516. S2CID 23032307.
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