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PubMed2006

[Effects of midazolam and estazolam as hypnotics in hypertensive patients with chronic insomnia: a multicentre, open labeled, randomized clinical trial].

OBJECTIVE: To compare the safety and efficacy of midazolam and estazolam in hypertensive patients with chronic insomnia. METHODS: In this multicentre, open labeled, randomized clinical trial, 217 adult (18 - 75 years) hypertensive patients (BP range 140 mm Hg or= 3 times/week for more than 1 month) were randomly divided into midazolam (7.5 - 15 mg before sleep, n = 113) or estazolam group (1 - 2 mg before sleep, n = 104). Patients took medication according to own need. Sleep diary should be completed within 15 minutes after getting up next morning. Follow-up analysis was performed in patients completed 8 sleep diaries or received midazolam or estazolam for 1 month. Patients' sleep diaries were evaluated, blood pressure and heart rate before and after therapy were measured and adverse events were recorded. RESULTS: (1) Blood pressure was equipotent reduced after both treatments (-11.8/7.3 mm Hg for midazolam group, and -9.1/5.6 mm Hg for estazolam group, all P < 0.05 vs. before treatment). (2) The total sleep score was also significantly decreased in both groups after medication (P < 0.01) and midazolam was significantly superior to estazolam in shortening sleep latency, reducing awakening frequency, improving objective sleep evaluation and decreasing daytime sleepiness, but there were no differences in dream frequency and total sleep time. (3) The adverse reactions such as dizziness, headache and nausea was similar in midazolam (3%) and estazolam group (7%, P > 0.05). CONCLUSIONS: It is safe to take midazolam or estazolam for hypertensive patients with chronic insomnia and both drugs reduced blood pressure. Midazolam is superior to estazolam in shortening sleep latency, reducing awakening frequency, improving objective sleep evaluation and decreasing daytime sleepiness.

Aged↗
PubMed1986

Influence of food on midazolam absorption.

The influence of food on the absorption of midazolam, a new benzodiazepine derivative, was investigated in 18 healthy volunteers in a four-way, randomized, crossover study with a one-week washout period between treatments. Single 15-mg oral doses of midazolam were administered one hour before, with, and one hour after a standard meal as well as under fasting conditions (control). Following serial blood sampling over the next 24-hour period, midazolam plasma concentrations were determined by gas chromatography and mass spectrometry for pharmacokinetic evaluation. The maximum plasma concentration (Cmax), time of maximum concentration (tmax), lag time prior to absorption (tlag), area under the plasma concentration-time curve (AUC), and elimination rate constant of midazolam and 1-hydroxymethylmidazolam were determined. Significant changes in these parameters were not found when midazolam was taken one hour before or with a meal as compared with the control condition. Significant changes in the Cmax, tmax, and AUC parameters for both midazolam and its metabolite were seen when midazolam was ingested one hour after a meal: There was a delayed and reduced rate of absorption as well as a small reduction in the extent of absorption. Thus, ingestion of midazolam within one hour after a meal may result in a delay in the onset of the pharmacologic effect. These changes may be of some clinical significance in that they may potentially delay the onset of sleep.

Adult↗
PubMed1989

Pharmacokinetics of midazolam following intravenous and oral administration in patients with chronic liver disease and in healthy subjects.

To study the effects of cirrhosis of the liver on the pharmacokinetics of midazolam single IV (7.5 mg as base) and p.o. (15.0 mg as base) doses of midazolam were administered to seven patients with cirrhosis of the liver and to seven healthy control subjects. One cirrhotic patient did not receive the oral dose. The distribution of midazolam in both study groups was alike as indicated by similar values of t1/2 alpha, V1 and Vss. Also the plasma protein binding of midazolam was unchanged in the patients with cirrhosis. The elimination of midazolam was significantly retarded in the patients as indicated by its lower total clearance (3.34 vs. 5.63 ml/min/kg), lower total elimination rate constant (0.400 vs. 0.721 h-1), and longer elimination half-life (7.36 vs. 3.80 h). The bioavailability of oral midazolam was significantly (P less than 0.05) higher in patients than controls (76% vs. 38%). The antipyrine-half-life was 32.4 h in the patients and 11.8 h in the controls. There were statistically significant (P less than 0.01) correlations between the clearances of the two drugs (r = 0.680) and between their half-lives (r = 0.755). The hypnotic effects of midazolam were similar in both groups. However, on a pharmacokinetic basis a reduced dosage of midazolam to patients with advanced cirrhosis of the liver is recommended.

Administration, Oral↗
PubMed1989

Discriminative stimulus properties of midazolam: comparison with other benzodiazepines.

Rats (N = 12) were trained to discriminate midazolam (1 mg/kg, IP) from vehicle in a food reinforced operant conditioning procedure. Midazolam, flunitrazepam, diazepam, chlordiazepoxide and pentobarbital showed dose-dependent substitution for midazolam. Buspirone and Ro 15-1788 did not substitute for midazolam. The midazolam cue was dose-dependently antagonized by Ro 15-1788. In rats (N = 12) trained to discriminate chlordiazepoxide (3 mg/kg, IP) from vehicle midazolam, flunitrazepam, diazepam and chlordiazepoxide substituted completely and dose dependently for chlordiazepoxide. The relative potency of chlordiazepoxide and diazepam was three times less in the midazolam-trained animals than in the chlordiazepoxide-trained animals. Response rate and latency data further support the main finding that the midazolam cue is similar, but not identical to the cue of classical benzodiazepines.

Animals↗
PubMed2005

Intramuscular midazolam vs intravenous diazepam for acute seizures.

OBJECTIVE: To determine effectiveness of intramuscular midazolam to control acute seizures in children as compared to intravenous diazepam. METHODS: 115 children in the age group of 1 month to 12 years who presented with acute convulsions were enrolled in the study. Patients who already had an intravenous access present were treated intravenous diazepam. Patients without an i.v. access at the time of convulsions were randomised into 2 groups and treated with either intramuscular midazolam or intravenous diazepam for control of seizures. Time interval from administration of drug to cessation of seizures was compared. Effectiveness of i.m. midazolam in various age groups, types of convulsions and etiology of convulsions was analyzed. Side effects of both drugs were evaluated. RESULTS: The mean interval to cessation of convulsions with i.m. midazolam was 97.22 seconds whereas in diazepam group without prior i.v. access it was 250.35 seconds and in diazepam group with prior i.v. access it was 119.4 seconds. i.m. midazolam acted faster in all age groups and in patients with febrile convulsions, which was statistically significant. i.m. midazolam was equally effective in various types of convulsions be it GTC or focal convulsions. 7 patients (10.8%) had thrombophlebitis associated with i.v. diazepam administration whereas none of the patients in the midazolam group had any side effects, which was statistically significant. CONCLUSION: i.m. midazolam is an effective agent for controlling acute convulsions in children especially in children with febrile convulsions. It has relatively no side effects as compared to Intravenous diazepam and can be used as a first line agent for treatment of acute convulsions in patients with difficult intravenous access.

Anticonvulsants↗
PubMed1995

Midazolam for caudal analgesia in children: comparison with caudal bupivacaine.

In a randomized, double-blind study we have examined the analgesic efficacy of caudal administration of midazolam, bupivacaine, or a mixture of both drugs in 45 children, undergoing inguinal herniotomy. They were allocated randomly into three groups (n = 15 in each) to receive a caudal injection of either 0.25% bupivacaine 1 ml.kg-1 with or without midazolam 50 micrograms.kg-1 or midazolam 50 micrograms.kg-1 with normal saline 1 ml.kg-1. There were no differences in quality of pain relief, postoperative behaviour or analgesic requirements between the midazolam group and the other two groups. Times to first analgesic administration (paracetamol suppositories) were longer (P < 0.001) in the bupivacaine-midazolam group than in the other two groups. Further, the bupivacaine-midazolam group received fewer (P < 0.05) doses of paracetamol than the bupivacaine group. Side effects such as motor weakness, respiratory depression or prolonged sedation were not observed in patients who received caudal epidural midazolam only. We conclude that caudal midazolam in a dose of 50 micrograms.kg-1 provides equivalent analgesia to bupivacaine 0.25%, when administered postoperatively in a volume of 1 ml.kg-1 for children following unilateral inguinal herniotomy.

Analgesia, Epidural↗
PubMed1997

Midazolam versus propofol for long-term sedation in the ICU: a randomized prospective comparison.

OBJECTIVE: To compare the efficacy, safety, and cost of midazolam and propofol in prolonged sedation of critically ill patients. DESIGN: Randomized, prospective study. SETTING: General intensive care unit (ICU) in a 1100-bed teaching hospital. PATIENTS: 67 critically ill, mechanically ventilated patients. INTERVENTIONS: Patients were invasively monitored and mechanically ventilated. A loading dose [midazolam 0.11 +/- 0.02 (SEM) mg.kg-1, propofol 1.3 +/- 0.2 mg.kg-1] was administered, followed by continuous infusion, titrated to achieve a predetermined sedation score. Sedation was continued as long as clinically indicated. MEASUREMENTS AND RESULTS: Mean duration of sedation was 141 and 99 h (NS) for midazolam and propofol, respectively, at mean hourly doses of 0.070 +/- 0.003 mg.kg-1 midazolam and 1.80 +/- 0.08 mg.kg-1 propofol. Overall, 68% of propofol patients versus 31% of midazolam (p < 0.001) patients had a > 20% decrease in systolic blood pressure after the loading dose, and 26 versus 45% (p < 0.01) showed a 25% decrease in spontaneous minute volume. Propofol required more daily dose adjustments (2.1 +/- 0.1 vs 1.4 +/- 0.1, p < 0.001). Nurse-rated quality of sedation with midazolam was higher (8.2 +/- 0.1 vs 7.3 +/- 0.1 on a 10-cm visual analog scale, p < 0.001). Resumption of spontaneous respiration was equally rapid. Recovery was faster after propofol (p < 0.02), albeit with a higher degree of agitation. Amnesia was evident in all midazolam patients but in only a third of propofol patients. The cost of propofol was 4-5 times higher. CONCLUSIONS: Both drugs afforded reliable, safe, and controllable long-term sedation in ICU patients and rapid weaning from mechanical ventilation. Midazolam depressed respiration, allowed better maintenance of sedation, and yielded complete amnesia at a lower cost, while propofol caused more cardiovascular depression during induction.

Adult↗
PubMed2006

Population pharmacodynamic modelling of lorazepam- and midazolam-induced sedation upon long-term continuous infusion in critically ill patients.

OBJECTIVE: The objective of the present investigation was to develop a population pharmacodynamic model for midazolam- and lorazepam-induced sedation upon long-term continuous infusion in critically ill patients. METHODS: The study was conducted in 59 patients receiving lorazepam and 54 patients receiving midazolam by continuous infusion for at least 24 h. Repeated blood samples were obtained for determination of the concentrations of lorazepam and midazolam. The level of sedation was assessed using a 5-point sedation scale. RESULTS: The pharmacokinetics of lorazepam and midazolam was described with previously proposed pharmacokinetic models. For the pharmacodynamics, the probability that the sedation was equal to or more than a specific score was described using a sigmoid E(max) model. The EC(50) values of lorazepam for the sedation scores equal or larger than 2-5 were 6.1, 57, 184 and 529 ng/ml, respectively. The corresponding values for midazolam were 216, 483, 1,100 and 2,200 ng/ml. Inter-individual variability in the EC(50) values was relatively high with a CV of 68% for lorazepam and 86% for midazolam (p=0.035). No covariates explaining part of the observed inter-individual variability were identified. CONCLUSION: The population pharmacodynamic model shows a similarly wide intra- and inter-individual variability in the pharmacodynamics of both lorazepam and midazolam. Thus, the previously observed differences in "ease of titration" between lorazepam and midazolam are unrelated to pharmacodynamic factors.

Adult↗
PubMed1988

Involvement of the macrolide antibiotic inducible cytochrome P-450 LM3c in the metabolism of midazolam by microsomal fractions prepared from rabbit liver.

This report characterizes the cytochrome P-450 isozyme involved in midazolam metabolism. This study was undertaken into liver microsomal fractions prepared from untreated rabbits or animals treated with drugs known to specifically induce various cytochrome P-450 isozymes such as form LM2 by phenobarbital, LM4 and LM6 by 3-methylcholanthrene and beta-naphthoflavone, LM3a by ethyl alcohol and acetone, and LM3c by macrolide antibiotics (rifampicin, erythromycin and triacetyloleandomycin). Among this library of characterized microsomal preparations, only those obtained from macrolide antibiotic-treated rabbits exhibited a Type I binding spectrum upon addition of midazolam (Ks = 3.2-5.3 micrograms/ml; 10.6-17.5 microM) and significantly metabolized midazolam to its various hydroxylated metabolites (Km = 2.52 +/- 0.22 micrograms/ml; 8.32 +/- 0.73 microM and Vmax = 20 micrograms metabolites formed/min/mg proteins; 66 nmoles metabolites formed/min/mg proteins). The following observations further confirmed the specific involvement of the cytochrome P-450 LM3c isozyme: (i) only anti-cytochrome P-450 LM3c isozyme antibodies intensively inhibited midazolam metabolism, (ii) incubation of microsomes, prepared from TAO-treated rabbits, with midazolam in the presence of potassium ferricyanide which restored the functional cytochrome P-450 LM3c isozyme, increased midazolam metabolism to a similar extent, and (iii) in the presence of Cyclosporin A, a specific substrate of the rabbit cytochrome P-450 LM3c isozyme, midazolam metabolism was inhibited in a concentration-dependent manner. These data demonstrated that the rabbit cytochrome P-450 LM3c isozyme was predominantly involved in midazolam metabolism.

Animals↗
PubMed1995

The erythromycin breath test predicts the clearance of midazolam.

Midazolam, a commonly used sedative and amnestic medication, has recently been shown to be largely metabolized in the liver by a cytochrome P450, termed CYP3A4. There is at least a tenfold intersubject variability in the liver content and catalytic activity of CYP3A4, which may in part account for the known interpatient differences in the kinetics of midazolam. To test this hypothesis, we determined the intravenous midazolam kinetics of 20 medically stable, hospitalized patients, whose hepatic CYP3A4 activities were determined with use of the [14C-N-methyl]erythromycin breath test. During the kinetic study, we also performed psychometric testing designed to quantitate the level of sedation and amnesia. We found a significant positive correlation between the erythromycin breath test results and weight adjusted clearance (in milliliters per minute per kilogram) of both total midazolam (r = 0.52; p = 0.03) and unbound midazolam (r = 0.61; p < 0.01). The relatively low dose of midazolam used (0.0145 mg/kg) produced significant but transient sedation and memory impairment in some of the patients. We conclude that interpatient differences in liver CYP3A4 activity in part account for the variations in midazolam kinetics. Our observations account for reported drug interactions involving midazolam and suggest that patients with low CYP3A4 activity may be most susceptible to prolonged amnestic effects occasionally produced by this short-acting benzodiazepine.

Adult↗
PubMed1995

The spinal potentiating effect and the supraspinal inhibitory effect of midazolam on opioid-induced analgesia in rats.

The authors investigated the effects of spinal and supraspinal administration of the benzodiazepine receptor agonist midazolam alone and with opioids on tests of nociception (tail-flick and hot-plate tests) and motor function (catalepsy) in rats. At the spinal level, the dose-response curves for peak effect and area under the curve for morphine were shifted to the left (indicating potentiation) by a submaximal dose of intrathecal (i.t.) midazolam (20 micrograms) in both nociceptive tests. Additionally, 2.5 micrograms of i.t. midazolam, a dose having no effect when given alone, increased antinociception in both tests when given with i.t. morphine. Isobolographic analysis confirmed that i.t. injection of midazolam potentiated antinociception induced by i.t. morphine. At the supraspinal level, intracerebroventricular (i.c.v.) injection of 4 micrograms of midazolam inhibited morphine antinociception, i.e., the dose-response curve for morphine in the hot-plate test shifted to the right. Midazolam did not affect morphine antinociception in the tail-flick test. Catalepsy occurred only when the highest doses of i.t. or i.c.v. morphine or midazolam were injected alone. The differing effect of midazolam on morphine-induced antinociception suggests that different mechanisms are involved in the spinal cord and brain.

Analgesia↗
PubMed1991

Comparison of the discriminative stimulus effects of midazolam after intracranial and peripheral administration in the rat.

Rats were trained in a two-lever drug discrimination paradigm to discriminate midazolam (0.32 mg/kg, i.p. or 1.0 mg/kg, i.p.) from the no-drug condition. After completion of i.p. and s.c. midazolam generalization gradients (0.032-1.0 mg/kg), rats were surgically implanted with unilateral cannulae into the lateral ventricles. Intracerebroventricular (i.c.v.) doses of 1.1-44.2 micrograms midazolam were delivered to unrestrained rats. Midazolam produced dose-dependent increases in drug-appropriate responding by all three routes of administration, but was 2.4- to 4.3-fold more potent when given i.c.v. than when given s.c. or i.p. Midazolam, over the dose range tested, did not produce substantial decreases in response rate by any route of administration. The discriminative-stimulus effect of i.c.v. midazolam was blocked by peripherally administered flumazenil, and such antagonism was surmounted by a 2- to 5-fold increase in the i.c.v. midazolam dose. Taken together, these data suggest that the discriminative-stimulus effects of midazolam are mediated via central benzodiazepine (BZ) receptors.

Animals↗
PubMed1991

Behavioral effects of chronic buspirone administration in the pigeon: comparison to midazolam.

The effects of acute and chronic administration of buspirone and midazolam were examined in White Carneau pigeons (N = 5) responding under a fixed-ratio 30 (FR 30) schedule of food presentation. Each drug was studied in all pigeons. For three pigeons, buspirone was studied before midazolam, while the order was reversed for the other two subjects. For each drug, a dose-response curve was determined before (prechronic) and two weeks after (postchronic) discontinuation of chronic administration. Prior to chronic drug administration, buspirone (0.3-5.6 mg/kg) and midazolam (0.1-3.0 mg/kg) decreased response rates in all subjects, in a dose-dependent manner. Midazolam was more potent than buspirone; midazolam's ED50 (95% C.I.) was 0.53 (0.41-0.69) mg/kg compared to 2.55 (1.48-4.41) mg/kg for buspirone. For each subject, the lowest dose that decreased responding by at least 50% was administered daily, immediately before the session, for up to 6 weeks. At the lowest daily dose of buspirone, complete recovery of baseline rates was observed in 3 pigeons. However, when the buspirone dose was increased, responding remained below control rates in all but one pigeon. During chronic midazolam administration, tolerance developed to the rate-decreasing effects of midazolam in 4 subjects. When saline was substituted for buspirone or midazolam, suppressed responding returned to predrug rates in all subjects. When the dose-response curves were redetermined, the postchronic ED50 for buspirone was 3.79 (2.10-6.82) mg/kg, which was not significantly different from the prechronic ED50, suggesting that tolerance did not develop to buspirone's rate-decreasing effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Midazolam withdrawal and discriminative motor control: effects of FG 7142 and Ro 15-1788.

Rats chronically drank either water or midazolam solution (0.1 mg/ml) in daily, 3-h schedule-induced polydipsia sessions and were evaluated in daily motor control sessions after polydipsia when midazolam metabolite levels had fallen to zero (withdrawal). Under midazolam polydipsia, animals orally self-administered between 21 and 38 mg/kg daily. The effect of acute drug administration [midazolam (0.75-3 mg/kg, SC), FG 7142 (1-8 mg/kg, IP), Ro 15-1788 (10-20 mg/kg, IP)] on motor control performance was similar after either chronic water or midazolam polydipsia. Thus chronic, oral midazolam self-administration did not lead to tolerance to the motor impairment produced by SC midazolam, nor did the daily discontinuation lead to impaired motor performance, nor had these performances, which occurred after daily elevated midazolam metabolite levels had reached zero (withdrawal), become sensitized to the effects of either the benzodiazepine inverse agonist FG 7142 or the agonist Ro 15-1788.

Animals↗
PubMed1994

Effect of morphine-induced catalepsy, lethality, and analgesia by a benzodiazepine receptor agonist midazolam in the rat.

Previously we have shown that intrathecal administration of midazolam can increase or decrease morphine-induced antinociception, depending upon relative concentration of these drugs by modulating spinal opioid receptors, and it also can inhibit morphine-induced tolerance and dependence in the rat. Now we report that midazolam also influences catalepsy, lethality, and analgesia induced by morphine in the rat. In the acute treatment, animals were first treated with saline or midazolam (0.03 to 30.0 mg/kg, b.wt., IP), and 30 min later with a second injection of saline or morphine (1.0 to 100.0 mg/kg, b.wt., SC). The catalepsy was measured 60 min after the second injection and lethality was checked after 24 h. Midazolam injection increased the morphine-induced catalepsy and lethality. In the chronic treatment, animals were injected with two injections daily for 11 days. The first injection consisted of saline or midazolam (0.03 to 3.0 mg/kg, b.wt., IP), and 30 min later with a second injection of saline or morphine (10.0 mg/kg, b.wt., IP) was given. Lethality, antinociception, and body weight were measured. Chronic morphine treatment also increased lethality in a dose-dependent manner. Chronic treatment with midazolam and morphine increased the antinociception on day 11, as measured in the tail-flick and hot-plate tests. Midazolam administration also prevented the morphine-induced weight loss. These results suggest a strong interaction between midazolam and morphine in altering catalepsy, lethality, and analgesia in rat.

Analgesics↗
PubMed1990

Midazolam use in the emergency department.

Midazolam is the first water-soluble benzodiazepine. As with other benzodiazepines it has amnestic, sedative, hypnotic, anxiolytic, and anticonvulsant properties. Midazolam is about two to four times more potent than diazepam. Midazolam has been extensively used for a variety of outpatient procedures, but there has been no documentation of its safety in emergency department patients. The authors retrospectively reviewed all patients receiving midazolam during a 2-year period at the University of Cincinnati Center for Emergency Care. The study population consisted of 389 patients (men 56%; women 44%) with an average age of 33.3 years. Midazolam was used intravenously for sedation before a wide variety of painful procedures and for agitation control. The average dose was 3.86 mg, with a range of 0.5 mg to 20.0 mg. The majority of patients (79.2%) received narcotics or sedative/hypnotic agents in addition to midazolam. There was an overall complication rate of 1.0%. Two patients (0.5%) developed clinically significant respiratory depression after midazolam use. Both patients had also received fentanyl citrate and the respiratory depression was reversed with naloxone. Two patients (0.5%) receiving several other drugs developed short periods of hypotension. There were no apparent long term sequelae. The authors conclude that midazolam can be safely used in the emergency department setting. Careful dosing and titration to the desired clinical effects is mandatory. Patients should be closely monitored to maximize safety.

Adolescent↗
PubMed1994

Midazolam's effects on myocardial load and coronary perfusion: reduced regional O2 consumption and lactate production during ischemia in dogs.

It is hypothesized that because of its potential to increase coronary flow and simultaneously decrease myocardial performance and O2 consumption, midazolam would minimize regional metabolic impairment during myocardial ischemia. Therefore, the hemodynamic and regional metabolic effects of systemic midazolam administration were compared during moderate and severe constrictions of the left anterior descending artery (LADa) to nontreated but ischemic animals in a canine model of acute coronary occlusion. In 16 anesthetized, ventilated, surgically prepared, and catheterized dogs, resting flow in the LADa was decreased by 50% and 75% for 15 minutes with 1 hour of normal flow in between. By arbitrary assignment, 7 dogs received midazolam (0.3 mg/kg and then 0.05 mg/kg/min) before thoracotomy. In all dogs, heart rate, electrocardiogram, LADa flow, left ventricular (LV) first time-derivative, and aortic, pulmonary artery, LADa, and LV pressures were measured continuously. Before and during constrictions, cardiac output by thermodilution and regional myocardial blood flow by microspheres were measured and blood was sampled for analysis. Data (mean +/- SEM) were compared within and between groups using ANOVA. Before placement of the LADa ligature, midazolam decreased heart rate and mean aortic pressure. Before ischemia, heart rate and LADa pressure were lower with midazolam than without it, but baseline metabolic variables were similar between the two groups (except for O2 consumption in the ischemic zone, which was lower with midazolam than without it). During 75% constriction with midazolam, LV end-diastolic pressure, coronary resistance, and ischemic zone O2 consumption were lower than without midazolam. Ischemic zone O2 delivery/consumption ratio was higher.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Etomidate versus midazolam for out-of-hospital intubation: a prospective, randomized trial.

STUDY OBJECTIVE: The primary objective of this study is to compare the intubation success rates of etomidate and midazolam when used for sedative-facilitated intubation, without paralytics, in out-of-hospital adult patients. METHODS: This prospective, double-blind, randomized trial was conducted with 2 ground out-of-hospital advanced life support systems (ALS); all patients aged 18 or older who required out-of-hospital sedative-facilitated intubation were eligible for participation. The ambulances were stocked with blinded numbered syringes containing either 7 mg of midazolam or 20 mg of etomidate. No paralytics were used. If sedation was not achieved with the study drug, medics could request additional sedation from a medical command physician; only midazolam or diazepam were available outside of the study. RESULTS: One hundred ten patients were enrolled in the study; 55 patients received midazolam and 55 patients received etomidate. The 2 groups were similar with regard to age, sex, initial vital signs, and reasons for intubation or sedation. The overall intubation success rate was 76% (95% confidence interval [CI] 68% to 84%); 75% (41/55) for midazolam (95% CI 64% to 86%) and 76% (42/55) for etomidate (95% CI 65% to 87%). There was also no difference in incidence of hypotension, number of intubation attempts, or perceived difficulty of intubation. Additional sedation was requested almost equally for the 2 groups: 14 patients in the midazolam group and 12 patients in the etomidate group. A benzodiazepine was successful for rescue of a failed etomidate intubation 10 of 12 times (83%; 95% CI 62% to 100%). When used for rescue of failed midazolam intubations, benzodiazepines were effective in only 5 of 14 (36%, 95% CI 11% to 61%) attempts. CONCLUSION: There were no observed differences between midazolam and etomidate in sedation-facilitated intubation success rates; we could not fully evaluate global outcomes of these agents or the sedative-facilitated intubation strategy itself.

Adolescent↗