Zed 451 logo11/20/2023 In a follow-up study, the dose was increased to 0.3-0.4 mg/kg. Induction was graded as good in only 59% of patients with 19% experiencing inadequate hypnosis. In the first clinical trial using etomidate in the pediatric population, etomidate (0.2 mg/kg) was used for the induction of anesthesia in a cohort of 198 children, ranging in age from 1-day to 15 years. The following manuscript reviews clinical reports regarding etomidate use in the pediatric population, outlines its physiologic effects and discusses recent concerns regarding its effects on corticosteroid metabolism and the implications for clinical use.Īnesthetic induction and endotracheal intubation In contrary to the large amount of clinical experience with its use in the adult population, the clinical experience in the pediatric-aged patient is somewhat limited. These properties have led to its use as an anesthetic induction in both adult and pediatric patients with altered myocardial performance, congenial heart disease, or hypovolemia. A similar lack of hemodynamic changes with no change in shunting were noted in 30 children with congenital heart disease, 15 with right-to-left shunts and 15 with left-to-right shunts. Using a balloon-tipped pulmonary artery catheter to evaluate hemodynamic changes following a bolus dose of 0.3 mg/kg in a cohort of 12 children, there were no significant changes in right atrial, aortic, or pulmonary artery pressure oxygen saturation, calculated shunt (Qp:Qs) ratio or systemic/pulmonary vascular resistance. When compared to other commonly used anesthetic induction agents such as propofol or the barbiturates, etomidate is generally devoid of adverse effects on cardiovascular function and hemodynamic performance. The average mean arterial pressure for all patients increased after etomidate resulting in an increase in the cerebral perfusion pressure (CPP) from 49.1 ± 5.3 mmHg at baseline to 65.3 ± 13.1 mmHg. The average ICP for the 5 min before etomidate administration was 32.8 ± 6.6 mmHg, decreasing to 21.2 ± 5.2 mmHg with the greatest difference being noted at 5-10 min after etomidate administration. In a prospective study of 8 children with traumatic brain injury, etomidate (0.3 mg/kg) was administered when there was a sustained ICP elevation ≥20 mmHg for >5 min. These physiologic effects result in a decrease of cerebral blood volume and intracranial pressure (ICP) especially in the setting of intracerebral hypertension. As with the barbiturates and propofol, etomidate decreases the cerebral metabolic rate for oxygen thereby leading to cerebral vasoconstriction with a reduction of cerebral blood flow (CBF) and volume. Following the intravenous administration of a single bolus dose, loss of consciousness occurs in 15-20 s with the rapid recovery of 5-10 min related to rapid drug redistribution and not primary metabolism. Unlike other sedative and hypnotic agents, only the R(+) enantiomer has clinical effects. It was released for clinical use in the United States in 1972. Etomidate is an intravenous anesthetic agent whose clinical effects are the result of potentiation of the gamma-amino butyric acid inhibitory neurotransmitter system with the alteration of transmembrane chloride conductance.
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