Induced coma

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Medically-induced coma
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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

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

Drug-induced comas are used to protect the

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

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 epileptics, 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

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

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 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

References

  1. ^
    ISBN 978-0-07-173881-1
    .
  2. ^
    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.
  4. PMID 31508442
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  5. PMID 26041151
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  6. PMID 15082703
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  7. PMID 22859526
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  8. PMID 32644706
    . Retrieved 2023-08-15.
  9. PMID 20473145
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  10. PMID 30339549
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  11. ^ "SCCM | PADIS Guidelines". Society of Critical Care Medicine (SCCM). Retrieved 2023-08-15.
  12. PMID 32644390
    , retrieved 2023-08-15
  13. PMID 10937896
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  14. PMID 7996586
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  15. S2CID 12215655
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  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. PMID 6440704
    .
  20. S2CID 23032307
    .

External links
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