Induced coma
Template:Short description Template:Infobox medical intervention
An induced comaTemplate:Spaced en dashalso known as a medically induced coma (MIC), barbiturate-induced coma, or drug-induced comaTemplate:Spaced en dashis 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.<ref name=Mariano2014/><ref name =An2018>Template:Cite journal</ref>
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,<ref name =An2018/> and in refractory intracranial hypertension following 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 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.Template: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.<ref>Template:Cite journal</ref>
Brain disruption from sedation can lead to an eight times<ref>Template:Cite journal</ref> increased risk of the development of ICU delirium. This is associated with a doubled risk of mortality<ref>Template:Cite journal</ref> during hospital admission. For every one day of delirium, there is a 10% increased risk of death.<ref>Template:Cite journal</ref> Medically induced comas that achieve a RASS level of −4 or −5 are an independent predictor of death.<ref>Template:Cite journal</ref>
Although patients are not sleeping while sedated, they can experience hallucinations and delusions<ref>Template:Cite journal</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>Template:Cite journal</ref>
Considering the high risks of medically induced comas, protocols such as the ABCDEF Bundle<ref>Template:Cite journal</ref> and PADIS guidelines<ref>{{#invoke:citation/CS1|citation |CitationClass=web }}</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.
Survivors of prolonged medically induced comas are at high risk of suffering from post-ICU syndrome<ref>Template:Citation</ref> and may require extended physical, cognitive, and psychological rehabilitation.
TheoryEdit
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.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</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>{{#invoke:citation/CS1|citation |CitationClass=web }}</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>{{#invoke:citation/CS1|citation |CitationClass=web }}</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>{{#invoke:citation/CS1|citation |CitationClass=web }}</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 trials have failed to demonstrate any survival or morbidity benefit of induced coma in diverse conditions such as neurosurgical operations, head trauma,<ref>Template:Cite journal</ref> intracranial aneurysm rupture, intracranial hemorrhage, ischemic stroke, and status epilepticus. If the patient survives, cognitive impairment may also follow recovery from the coma.<ref>Template:Cite journal</ref> Due to these risks, barbiturate-induced coma should be reserved for cases of refractory intracranial pressure elevation.<ref name=Mariano2014>Template:Cite book</ref>
See alsoEdit
ReferencesEdit
External linksEdit
- Medically induced Coma – LiveScience