To investigate the safety and feasibility of midazolam for conscious sedation in transcatheter device closure of atrial septal defects guided solely by transthoracic echocardiography.

A retrospective analysis was performed on 55 patients who underwent transcatheter device closure of atrial septal defects from October, 2019 to May, 2020. All patients received intravenous midazolam and local anesthesia with lidocaine to maintain sedation. A group of previous patients with unpublished data who underwent the same procedure with general anesthesia was set as the control group. The relevant clinical parameters, the Ramsay sedation scores, the numerical rating scale, and the post-operative satisfaction questionnaire were recorded and analyzed.

In the midazolam group, the success rate of atrial septal defect closure was 98.2%. Hemodynamic stability was observed during the procedure. None of the patients needed additional endotracheal intubation for general anesthesia. Compared with the control group, the midazolam group had no statistically significant differences in the Ramsay sedation score and numerical rating scale scores. Patients in the midazolam group experienced more post-operative satisfaction than those in the control group.

Conscious sedation using midazolam is a safe and effective anesthetic technique for transcatheter device closure of atrial septal defects guided solely by transthoracic echocardiography.

There are several agents used for conscious sedation by various routes in children. The aim of this prospective randomised study is to compare the effectiveness of three commonly used sedatives: intranasal ketamine, intranasal midazolam, and oral chloral hydrate for children undergoing transthoracic echocardiography.

Children who were referred to paediatric cardiology due to a heart murmur for transthoracic echocardiography were prospectively randomised into three groups. Seventy-three children received intranasal midazolam (0.2 mg/kg), 72 children received intranasal ketamine (4 mg/kg), and 72 children received oral chloral hydrate (50 mg/kg) for conscious sedation. The effects of three agents were evaluated in terms of intensity, onset, and duration of sedation. Obtaining high-quality transthoracic echocardiography images (i.e. absence of artefacts) were regarded as successful sedation. Side effects due to medications were also noted.

There was no statistical difference in terms of sedation success rates between three groups (95.9, 95.9, and 94.5%, respectively). The median onset of sedation in the midazolam, ketamine, and chloral hydrate was 14 minutes (range 7–65), 34 minutes (range 12–56), and 40 minutes (range 25–57), respectively (p < 0.001 for all). However, the median duration of sedation in study groups was 68 minutes (range 20–75), 55 minutes (range 25–75), and 61 minutes (range 34–78), respectively (p = 0.023, 0.712, and 0.045). Gastrointestinal side effects such as nausea and vomiting were significantly higher in the chloral hydrate group (11.7 versus 0% for midazolam and 2.8% for ketamine, respectively, p = 0.002).

Results of our prospectively randomised study indicate that all three agents provide adequate sedation for successful transthoracic echocardiography. When compared the three sedatives, intranasal midazolam has a more rapid onset of sedation while intranasal ketamine has a shorter duration of sedation. Intranasal ketamine can be used safely with fewer side effects in children undergoing transthoracic echocardiography.

To evaluate the efficacy and safety of a simple linear midazolam-based protocol for the management of impending status epilepticus in children up to 18 years of age.

This is a descriptive, quality assessment, retrospective chart review of children presenting with the chief complaint of seizure disorder in the emergency department (ED) of a tertiary care pediatric hospital and a triage category of resuscitation or urgent from April 1, 2009, to August 31, 2011. In children with at least one seizure episode in the ED treated according to the linear protocol, three main outcomes were assessed: compliance, effectiveness, and complications.

Of the 128 children meeting the above study criteria, 68 had at least one seizure episode in the ED, and treatment was required to terminate at least one seizure episode in 46 of 68 patients (67.6%). Fifty-five seizure episodes were treated in the 46 patients: 51 of 55 seizure episodes were treated with midazolam (92.7%) and 4 of 55 with lorazepam or diazepam (7.3%). Of those treated with midazolam, 86.3% (44 of 51) were successfully treated with one or two doses of midazolam. The median seizure duration for all treated patients was 6 minutes. Of the 42 patients treated with midazolam, 7 required either continuous positive airway pressure or intubation, and two patients were treated for hypotension. One patient died of pneumococcal meningitis.

This simple linear protocol is an effective and safe regimen for the treatment of impending status epilepticus in children.

Palliative sedation is a common treatment in palliative care. The home is a difficult environment for research, and there are few studies about sedation at home. Our aim was to analyze this practice in a home setting.

We conducted a retrospective cross-sectional descriptive study in a home cohort during 2011. The inclusion criteria were as follows: 18 years or older and enrolled in the Palliative Home Care Program (PHCP) with advanced cancer. The variables employed were: sex, age, primary tumor location, and place of death. We also registered indication, type, drug and dose, awareness of diagnosis and prognosis, consent, survival, presence or absence of rales, painful mouth, and ulcers in patients sedated at home. We also collected the opinions of family members and professionals about the suffering of sedated patients.

A total of 446 patients (56% at home) of the 617 admitted to the PHCP between January and December of 2011 passed away. The typical patient in our population was a 70-year-old man with a lung tumor. Some 35 (14%) home patients required sedation, compared to 93 (49%) at the hospital. The most frequent indication was delirium (70%), with midazolam the most common drug (mean dose, 40 mg). Survival was around three days. Rales were frequent (57%) as well as awareness of diagnosis and prognosis (77 and 71%, respectively). Perception of suffering after sedation was rare among relatives (17%) and professionals (8%). In most cases, the decision was made jointly by professionals and family members.

Our study confirmed the role of palliative sedation as an appropriate therapeutic tool in the home environment.

This study was designed to investigate the potential existence of the response of neurons in the parafascicular nucleus of the thalamus to acute myocardial ischaemia induced by selective coronary artery occlusion and the effects of midazolam on the response in rats.

The left anterior descending branch of the coronary artery was instrumented with a snare occluder in anaesthetized Sprague-Dawley rats. A single-barrel glass microelectrode was used for recording the unit discharges of the neuron in the parafascicular nucleus. The neuron responding only to noxious somatic stimulation was further examined for the response to coronary artery occlusion. Once the effect of coronary artery occlusion on the discharges was detected, the pharmacological effects of midazolam and flumazenil were examined.

It was observed that the discharge rate of the neuron was markedly increased following coronary artery occlusion. Midazolam attenuated the increase in the discharges of the neuron induced by coronary artery occlusion (P < 0.05). The effect of midazolam was reversed by flumazenil.

The parafascicular nucleus is involved in the modulation of cardiac nociception and midazolam possesses antinociceptive property in modulating cardiac pain.

Intrathecal ketamine produces a short period of analgesia with stable haemodynamics. Midazolam with bupivacaine prolongs the duration of analgesia when administered intrathecally but does not prevent hypotension. The objective of this study was to assess the effect of a combination of intrathecal bupivacaine, ketamine and midazolam on the duration of analgesia and haemodynamic parameters.

A prospective, randomized, double-blind study was carried out in 60 ASA I and II patients undergoing lower limb surgery under spinal anaesthesia. Patients were divided into three groups of 20 each. Patients in all the three groups received 3 mL of hyperbaric bupivacaine (0.5%) intrathecally. In addition, patients in Groups II and III received intrathecal ketamine (0.1 mg kg−1) and the same dose of ketamine along with midazolam (0.02 mg kg−1), respectively. All patients were evaluated for block characteristics, duration of pain-free period, total rescue analgesic requirement in the 24-h postoperative period, total dose of mephenteramine to treat hypotension and any central or neurological complication.

No patients in Group II required mephenteramine while 40% of patients in Group I and 10% in Group III required mephenteramine to maintain blood pressure after spinal anaesthesia. The mean ± standard deviation duration of pain-free period was 331.5 ± 89.9, 369.7 ± 124.2 and 730.5 ± 81.5 min in Group I, II and III, respectively. The pain-free interval was significantly greater in Group III compared to Groups I and II (P < 0.001). No patient had any complications.

A low dose of midazolam and ketamine with bupivacaine intrathecally results in prolonged analgesia and less haemodynamic fluctuations. However, the safety of this combination needs to be proved before its use in clinical practice.

Hypoxia-reperfusion injury is an important determinant of secondary brain injury. In the acute phase of cerebral reperfusion, pro-inflammatory events enhance expression of cerebral endothelial (intercellular adhesion molecule-1 and P-selectin) adhesion molecules, which play an important role in brain hypoxia-reperfusion injury. Midazolam is the most commonly used sedative in patients with brain injury. The objective of this investigation was to examine the effect of midazolam on the expression of cerebral endothelial intercellular adhesion molecule-1 and P-selectin during hypoxia-reperfusion injury invitro.

The up-regulation of mouse cerebral endothelial cells intercellular adhesion molecule-1 and P-selectin was assessed following hypoxia-reoxygenation (hypoxia-reperfusion). Cells were pre-treated with three different concentrations of midazolam (0, 5 and 50 μg mL−1) prior to hypoxia. Flow cytometry was used to estimate adhesion molecule expression mean channel fluorescence. Data are presented as mean ± SD.

Mouse cerebral endothelial cell intercellular adhesion molecule-1 and P-selectin expression was greater after exposure to hypoxia-reoxygenation compared to normoxia (mean channel fluorescence) 241 ± 12 vs. 140 ± 7 and 120 ± 14 vs. 46 ± 7, respectively, P < 0.05. Intercellular adhesion molecule-1 and P-selectin expression was decreased by midazolam (5 μg mL−1) pre-incubation compared to control, mean channel fluorescence 184 ± 10 vs. 241 ± 12 and 51 ± 7 vs. 120 ± 14, respectively, P < 0.05. Midazolam at 50 μg mL−1 had the same effect as 5 μg mL−1.

Pre-treatment with midazolam diminishes increased expression of cerebral endothelial intercellular adhesion molecule-1 and P-selectin expression following hypoxia-reoxygenation.

Postoperative nausea and vomiting is a common complication following strabismus surgery. This randomized and double-blind study was designed to evaluate the efficacy of midazolam alone or in combination with dexamethasone in reducing the incidence of postoperative nausea and vomiting in children undergoing strabismus repair.

One hundred ASA I children, aged 4–12 yr, scheduled to undergo elective strabismus surgery, were enrolled. No premedication was given. Anaesthesia was induced with sevoflurane, nitrous oxide and oxygen. After induction, fentanyl 2 μg kg−1 and cisatracurium 0.1 mg kg−1 were administered and an endotracheal tube was inserted. After induction of anaesthesia and before start of surgery, patients were randomly allocated into one of four groups of 25 children each to receive placebo, midazolam 50 μg kg−1, dexamethasone 0.5 mg kg−1 or a combination of midazolam 50 μg kg−1 and dexamethasone 0.5 mg kg−1. Episodes of nausea, and retching and vomiting were recorded during the first 24 h after surgery.

The incidence of postoperative nausea was 48%, 32%, 12% and 0% with placebo, dexamethasone, midazolam and the midazolam–dexamethasone combination, respectively. The incidence of vomiting was 52% and 32% with placebo and dexamethasone, respectively; no child vomited with midazolam alone, or with the midazolam–dexamethasone combination.

Prophylactic midazolam with or without dexamethasone reduces the incidence of PONV in children undergoing strabismus repair.

Dynamic balance involving movement of the centre of gravity is important for the evaluation of street fitness after sedation. The purpose of this study was to compare the recovery of dynamic balance after intravenous sedation with propofol or midazolam, and to investigate the usefulness of simple dynamic balance tests in evaluating the recovery.

Fourteen young male volunteers underwent intravenous sedation with propofol and midazolam for 1 h each at an interval of more than 1 week. Computerized dynamic posturography using a multi-axial tilting platform, the 10-m maximum-speed walking test and the timed ‘up & go’ test (subjects stand up from a chair, walk 5 m and back with maximum speed and sit down again) were performed before and after sedation. The increase in each variable of the tests described above represents a reduction of function.

The score of the computerized dynamic posturography was significantly lower in propofol sedation than that in midazolam sedation until 40 min after the end of sedation (P = 0.006). The scores of maximum-speed walking test and timed ‘up & go’ test were significantly lower in propofol sedation than those in midazolam sedation till 60 min after the end of sedation, respectively (P = 0.035 and 0.042). The timed ‘up & go’ and maximum-speed walking tests were well and significantly correlated with computerized dynamic posturography in midazolam sedation (timed ‘up & go’ test vs. computerized dynamic posturography: r = 0.66, P < 0.01; and maximum-speed walking test vs. computerized dynamic posturography: r = 0.53, P < 0.01).

The timed ‘up & go’ and maximum-speed walking tests are useful simple dynamic balance tests well correlated with precise computerized dynamic posturography for the evaluation of the recovery of dynamic balance from midazolam sedation in younger adults.

The A-Line® auditory evoked potential index (AAI) (AEP Monitor/2, Danmeter A/S, Odense, Denmark) is a newly developed composite parameter representing the degree of hypnosis. We conducted a prospective, observational study to explore the performance and validity of the AAI during conventional sedation for gastrointestinal (GI) endoscopy.

Thirty adults of either sex, age <65, scheduled for combined oesophagogastroduodenoscopy (OGD) and colonoscopy under sedation with intravenous (i.v.) midazolam and alfentanil were enrolled. The sedative end-point was set at the Observer’s Assessment of Alertness/Sedation (OAA/S) score less than 4. An AEP Monitor/2 was used in all patients. AAI, sedation scores, heart rate (HR), blood pressure (BP) and SPO2 were recorded every 2 min up to the end of the procedure. Receiver operator characteristic analysis was used to test validity and to select optimal sedation.

There was a significantly positive correlation between AAI and OAA/S scores (ρ = 0.886; P < 0.001). The AAI also showed significant differences between subsequent levels of sedation scores (P < 0.001). AAI greater than 54 indicated fully awake or minimal sedation and values between 54 and 42 were suggestive of moderate sedation. Values between 42 and 34 were associated with moderate to deep sedation and readings below 34 were associated with deep sedation. The relative risk of SPO2 < 95% for OAA/S = 2 compared with 3 was 15.98 (95% confidence interval (CI): 3.94–64.81).

AAI is an effective tool for monitoring sedation during GI endoscopy induced by i.v. midazolam and alfentanil.