rs of age in humans (see precautions/pregnancy , pediatric use, animal pharmacology and/or toxicology ). some published studies in children suggest that similar deficits may occur after repeated or prolonged exposures to anesthetic agents early in life and may result in adverse cognitive or behavioral effects. these studies have substantial limitations, and it is not clear if the observed effects are due to the anesthetic/sedation drug administration or other factors such as the surgery or underlying illness. anesthetic and sedation drugs are a necessary part of the care of children needing surgery, other procedures, or tests that cannot be delayed, and no specific medications have been shown to be safer than any other. decisions regarding the timing of any elective procedures requiring anesthesia should take into consideration the benefits of the procedure weighed against the potential risks.

d under these circumstances, although usually smaller than the original induction dose, must be individualized. there are insufficient data to support this use of etomidate for longer adult procedures or for any procedures in pediatric patients; therefore, such use is not recommended. the use of intravenous fentanyl and other neuroactive drugs employed during the conduct of anesthesia may alter the etomidate dosage requirements. consult the prescribing information for all other such drugs before using. premedication: amidate is compatible with commonly administered pre-anesthetic medications, which may be employed as indicated. see also clinical pharmacology, adverse reactions , and dosage recommendations for maintenance of anesthesia. amidate anesthesia does not significantly alter the usual dosage requirements of neuromuscular blocking agents employed for endotracheal intubation or other purposes shortly after induction of anesthesia. parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. to prevent needle-stick injuries, needles should not be recapped, purposely bent, or broken by hand.

incidence (22.7% to 63%). most of these observations were judged mild to moderate in severity but some were judged disturbing. the incidence of disturbing movements was less when 0.1 mg of fentanyl was given immediately before induction. these movements have been classified as myoclonic in the majority of cases (74%), but averting movements (7%), tonic movements (10%), and eye movements (9%) have also been reported. no exact classification is available, but these movements may also be placed into three groups by location: a. most movements are bilateral. the arms, legs, shoulders, neck, chest wall, trunk and all four extremities have been described in some cases, with one or more of these muscle groups predominating in each individual case. results of electroencephalographic studies suggest that these muscle movements are a manifestation of disinhibition of cortical activity; cortical electroencephalograms, taken during periods when these muscle movements were observed, have failed to reveal seizure activity. b. other movements are described as either unilateral or having a predominance of activity of one side over the other. these movements sometimes resemble a localized response to some stimuli, such as venous pain on injection, in the lightly anesthetized patient (averting movements). any muscle group or groups may be involved, but a predominance of movement of the arm in which the intravenous infusion is started is frequently noted. c. still other movements probably represent a mixture of the first two types. skeletal muscle movements appear to be more frequent in patients who also manifest venous pain on injection. other adverse observations respiratory system: hyperventilation, hypoventilation, apnea of short duration (5 to 90 seconds with spontaneous recovery); laryngospasm, hiccup and snoring suggestive of partial upper airway obstruction have been observed in some patients. these conditions were managed by conventional countermeasures. circulatory system: hypertension, hypotension, tachycardia, bradycardia and other arrhythmias have occasionally been observed during induction and maintenance of anesthesia. one case of severe hypotension and tachycardia, judged to be anaphylactoid in character, has been reported. geriatric patients, particularly those with hypertension, may be at increased risk for the development of cardiac depression following etomidate administration (see clinical pharmacology ). gastrointestinal system: postoperative nausea and/or vomiting following induction of anesthesia with etomidate is probably no more frequent than the general incidence. when etomidate was used for both induction and maintenance of anesthesia in short procedures such as dilation and curettage, or when insufficient analgesia was provided, the incidence of postoperative nausea and/or vomiting was higher than that noted in control patients who received thiopental.

s before induction of anesthesia, probably because less etomidate is generally required under these circumstances (consult the package insert for fentanyl before using). the most characteristic effect of intravenous etomidate on the respiratory system is a slight elevation in arterial carbon dioxide tension (paco2) (see adverse reactions ). reduced cortisol plasma levels have been reported with induction doses of 0.3 mg/kg etomidate. these persist for approximately 6 to 8 hours and appear to be unresponsive to adrenocorticotropic hormone (acth) administration. the intravenous administration of up to 0.6 mg/kg of etomidate to patients with severe cardiovascular disease has little or no effect on myocardial metabolism, cardiac output, peripheral circulation or pulmonary circulation. the hemodynamic effects of etomidate have in most cases been qualitatively similar to those of thiopental sodium, except that the heart rate tended to increase by a moderate amount following administration of thiopental under conditions where there was little or no change in heart rate following administration of etomidate. however, clinical data indicates that etomidate administration in geriatric patients, particularly those with hypertension, may result in decreases in heart rate, cardiac index, and mean arterial blood pressure. there are insufficient data concerning use of etomidate in patients with recent severe trauma or hypovolemia to predict cardiovascular response under such circumstances. clinical experience and special studies to date suggest that standard doses of intravenous etomidate ordinarily neither elevate plasma histamine nor cause signs of histamine release. limited clinical experience, as well as animal studies, suggests that inadvertent intra-arterial injection of etomidate, unlike thiobarbiturates, will not usually be followed by necrosis of tissue distal to the injection site. intra-arterial injection of etomidate is, however, not recommended. etomidate induction is associated with a transient 20% to 30% decrease in cerebral blood flow. this reduction in blood flow appears to be uniform in the absence of intracranial space occupying lesions. as with other intravenous induction agents, reduction in cerebral oxygen utilization is roughly proportional to the reduction in cerebral blood flow. in patients with and without intracranial space occupying lesions, etomidate induction is usually followed by a moderate lowering of intracranial pressure, lasting several minutes. all of these studies provided for avoidance of hypercapnia. information concerning regional cerebral perfusion in patients with intracranial space occupying lesions is too limited to permit definitive conclusions. preliminary data suggests that etomidate will usually lower intraocular pressure moderately. etomidate is rapidly metabolized in the liver. minimal anesthetic plasma levels of unchanged drug are equal to or higher than 0.23 mcg/ml; they decrease rapidly up to 30 minutes following injection and thereafter more slowly with a half-life value of about 75 minutes. approximately 75% of the administered dose is excreted in the urine during the first day after injection. the chief metabolite is r-(+)-1-(1-phenylethyl)-1h-imidazole-5-carboxylic acid, resulting from hydrolysis of etomidate, and accounts for about 80% of the urinary excretion. limited pharmacokinetic data in patients with cirrhosis and esophageal varices suggest that the volume of distribution and elimination half-life of etomidate are approximately double that seen in healthy subjects. in clinical studies, elderly patients demonstrated decreased initial distribution volumes and total clearance of etomidate. protein binding of etomidate to serum albumin was also significantly decreased in these individuals. reduced plasma cortisol and aldosterone levels have been reported following induction doses of etomidate. these results persist for approximately 6 to 8 hours and appear to be unresponsive to acth stimulation. this probably represents blockage of 11 beta-hydroxylation within the adrenal cortex.