Sedation and analgesia for the brain-injured patient

• Published in: Annales françaises d'anesthésie et de réanimation 2008-07, Vol.27 (7-8), p.596
• Main Authors: Abdennour, L, Puybasset, L
• Format: Article
• Language: fre
• Subjects: Analgesia - methods; Analgesics - administration & dosage; Analgesics - adverse effects; Analgesics - therapeutic use; Antipsychotic Agents - therapeutic use; Brain Damage, Chronic - etiology; Brain Damage, Chronic - prevention & control; Brain Injuries - complications; Brain Injuries - metabolism; Brain Injuries - therapy; Critical Care - methods; Deep Sedation - methods; Drug Therapy, Combination; Epilepsy - etiology; Epilepsy - prevention & control; Humans; Hypnotics and Sedatives - administration & dosage; Hypnotics and Sedatives - adverse effects; Hypnotics and Sedatives - therapeutic use; Intracranial Hypertension - drug therapy; Intracranial Hypertension - etiology; Intracranial Hypertension - prevention & control; Ketamine - adverse effects; Ketamine - therapeutic use; Narcotics - administration & dosage; Narcotics - adverse effects; Narcotics - therapeutic use; Neuroprotective Agents - administration & dosage; Neuroprotective Agents - therapeutic use; Propofol - administration & dosage; Propofol - adverse effects; Propofol - therapeutic use; Psychomotor Agitation - drug therapy; Psychomotor Agitation - etiology; Psychomotor Agitation - prevention & control; Respiration, Artificial; Substance Withdrawal Syndrome - drug therapy; Substance Withdrawal Syndrome - etiology; Substance Withdrawal Syndrome - prevention & control; Syndrome
• ISSN: 1769-6623
• DOI: 10.1016/j.annfar.2008.04.012

Sedation-analgesia occupies an essential place in the specific therapeutic arsenal of the brain-injured patients. The maintenance of the perfusion of the brain, its relaxation and its protection are the fundamental objectives whose finality is to avoid the extension of the lesions and to preserve the neuronal capital. Sedation is instituted when patients are severely agitated or present a deterioration of their state of consciousness (GCS< or =8). Under cover of mechanical ventilation, sedation is the first line treatment of intracranial hypertension, a common pathway of various acute brain diseases of traumatic, vascular or other origin. The use of the combination of hypnotic and opioids is the rule. The combined action of these two classes reinforces and improves their sedative effects. Midazolam is the 2 benzodiazepine of reference. Propofol is more and more frequently added to the combination of hypnotic and opioids. The "propofol infusion syndrome" is a severe limitation to its long term administration in particular among patients presenting a severe septic or inflammatory state. Propofol will be imperatively stopped in the event of metabolic acidosis, rhabdomyolysis, acute renal insufficiency, hyperkaliemia or increase in the blood triglyceride levels. The use of thiopental is restricted to the most severe cases. Its use as a monotherapy at high doses is abandoned to the profit of a co-administration with midazolam or even with the combination of midazolam and propofol. Thiopental overdose is very frequent in the event of associated hypothermia. Etomidate does not have its place apart from induction in fast sequence. The neuro-protective effects of ketamine require to be demonstrated in man before being recommended routinely. Withdrawal of sedation can be responsible for a state of agitation which can be controlled by neuroleptics.