The effect of midazolam premedication on discharge time in pediatric patients undergoing general anesthesia for dental restorations.

PURPOSE: The purpose of this study was to evaluate the effect of oral premedication with midazolam on recovery times of children undergoing dental restorations under general anesthesia. METHODS: The records of 106 children (1.2-11.3 years, ASA I or II) undergoing ambulatory dental restorations were randomly selected and retrospectively reviewed: 50 subjects received midazolam (M) 0.5 mg/kg orally approximately 30 minutes prior to their procedure and 56 control subjects received no premedication (C). General anesthesia consisted primarily of inhalational anesthesia. Time in the operating room (OR), post-anesthesia care unit (PACU) and same day surgery (SDS) were determined and compared between groups. RESULTS: Both groups were similar with respect to age and weight. There were no significant differences between groups in time spent in the OR, PACU or SDS (p>0.05). In a subset of children having shorter dental procedures (OR time < or =75 minutes, n=29), there remained no significant difference in discharge times between groups. CONCLUSIONS: Preoperative administration of oral midazolam does not delay discharge of children undergoing general anesthesia for dental rehabilitation.

Enteral methadone to expedite fentanyl discontinuation and prevent opioid abstinence syndrome in the PICU.

STUDY OBJECTIVE: To determine if enterally administered methadone can facilitate fentanyl discontinuation and prevent withdrawal in children at high risk for opioid abstinence syndrome. DESIGN: Retrospective analysis. SETTING: Pediatric intensive care unit (PICU) in a tertiary care children's hospital. PATIENTS: Twenty-two children (aged 6.1 +/- 5.4 yrs) who received continuous fentanyl infusion for 9 days or longer. INTERVENTION: Guidelines for initiating enteral methadone, rapidly tapering and discontinuing fentanyl infusions, and tapering methadone were implemented in the PICU. Development of opioid abstinence syndrome was evaluated during fentanyl and methadone dosage reductions and for 72 hours thereafter. MEASUREMENTS AND MAIN RESULTS: Children received fentanyl by continuous infusion for 17.8 +/- 8.4 days. Peak fentanyl infusion rate was 5.9 +/- 3.8 microg/kg/hour, and the median cumulative dose was 1302 microg/kg (range 354-7535 microg/kg). Methadone 0.50 +/- 0.22 mg/kg/day was begun 1.6 +/- 1.9 days before tapering fentanyl. The fentanyl infusion rate on starting the taper was 5.0 +/- 3.6 microg/kg/hour. Fentanyl was tapered and discontinued in a median of 2.6 days (range 0-11.9 days). Twenty-one patients had no opioid abstinence syndrome during or after fentanyl taper. One patient experienced significant opioid withdrawal after fentanyl discontinuation, which resolved after reinstitution of fentanyl and increasing the dosage of methadone to 0.3 mg/kg every 6 hours. Overall, methadone was tapered and discontinued in 18.2 +/- 11.9 days without precipitating opioid abstinence syndrome. CONCLUSION: Enteral administration of methadone may expedite fentanyl discontinuation and reduce the risk of withdrawal in critically ill children at high risk for opioid abstinence syndrome.

Use of propofol sedation in a pediatric emergency department: a prospective study.

The purpose of this study was to determine the efficacy and safety of propofol sedation for pediatric procedures in the emergency department. For patients needing painful procedures, propofol was administered intravenously. Vital signs, complications, and time to recovery were recorded. Patient amnesia and parent, patient, and operator satisfaction with sedation were assessed. The mean age was 7.4 years; 65% were male. Most underwent fracture reduction. Mean total dose was 3.3 mg/kg. Thirty percent experienced desaturation. One required assisted ventilation. Most had decreases in blood pressure. Mean recovery time was 18 minutes. Satisfaction with sedation was rated "excellent." Propofol was an effective sedation with minimal complications in the emergency department setting.

Invasive group A streptococcus infection of the scrotum and streptococcal toxic shock syndrome.

We report a case of invasive group A streptococcus infection of the scrotum that presented as epididymoorchitis and rapidly progressed to streptococcal toxic shock syndrome. The presentation, pathophysiology, and management of invasive group A streptococcus and streptococcal toxic shock syndrome are reviewed. Rapid recognition is necessary to avoid the significant morbidity and mortality associated with these invasive infections.

Ultrasound guidance for placement of central venous catheters: a meta-analysis of the literature.

OBJECTIVE: To evaluate the effect of real-time ultrasound guidance using a regular or Doppler ultrasound technique for placement of central venous catheters. DATA SOURCES: We searched for published and unpublished research using MEDLINE, citation review of relevant primary and review articles, conference abstracts, personal files, and contact with expert informants. STUDY SELECTION: From a pool of 208 randomized, controlled trials of venous and arterial catheter management, eight published randomized, controlled trials were identified. DATA EXTRACTION: In duplicate, independently, we abstracted data on the population, intervention, outcome, and methodologic quality. DATA SYNTHESIS: Ultrasound guidance significantly decreases internal jugular and subclavian catheter placement failure (relative risk 0.32; 95% confidence interval 0.18 to 0.55), decreases complications during catheter placement (relative risk 0.22; 95% confidence interval 0.10 to 0.45), and decreases the need for multiple catheter placement attempts (relative risk 0.60; 95% confidence interval 0.45 to 0.79) when compared with the standard landmark placement technique. CONCLUSIONS: When used for vessel location and catheter placement real-time, ultrasound guidance or Doppler ultrasound guidance improves success rates and decreases the complications associated with internal jugular and subclavian venous catheter placement.

An unusual cause of intraoperative hypoxemia.

Congenital anomalies of the tracheobronchial tree are rare occurrences; however, they can lead to pulmonary complications. A tracheal bronchus is an anatomic variant in which an ectopic bronchus originates directly from the tracheal wall above the carina. Presented is a case of intraoperative hypoxemia due to right upper lobe collapse. Despite what appeared to be proper endotracheal tube positioning, this clinical scenario was found to be the result of endotracheal tube obstruction of a tracheal bronchus supplying the right upper lobe. Fiberoptic bronchoscopy proved to be a rapid diagnostic and therapeutic tool, as the endotracheal tube was able to be visually positioned above this aberrantly located bronchus.

Amrinone and the pulmonary vascular pressure-flow relationship in conscious control dogs and following left lung autotransplantation.

BACKGROUND: Amrinone, a bipyridine compound, is known to improve left ventricular function via its positive inotropic and afterload-reducing effects. The goal of this study was to assess the efficacy of amrinone as a pulmonary vasodilator, an effect that could be beneficial in the setting of right heart failure associated with pulmonary hypertension. METHODS: Investigated were the effects of intravenous amrinone (750 micrograms/kg loading dose plus 1-20 micrograms.kg-1.min-1 maintenance dose) on the left pulmonary vascular pressure-flow (LPQ) relationship in chronically instrumented, conscious dogs. The effects of amrinone on the LPQ relationship were assessed in a series of conscious control dogs with (n = 10) and without (n = 9) acute preconstriction with the thromboxane analog U46619 and in a series of conscious dogs 2-4 weeks after left lung autotransplantation (LLA) with (n = 8) and without (n = 8) acute U46619 preconstriction. Left pulmonary vascular pressure-flow plots were generated by continuously measuring the pulmonary vascular pressure gradient (pulmonary arterial pressure/left atrial pressure [PAP/LAP]) and left pulmonary blood flow during gradual (approximately 1 min) inflation of a hydraulic occluder implanted around the right pulmonary artery. RESULTS: Amrinone had no effect on the baseline LPQ relationship in control dogs. U46619 caused acute pulmonary vasoconstriction. For example, PAP/LAP at left pulmonary blood flow of 70 ml.min-1.kg-1 was increased (P < 0.01) from 16 +/- 2 to 37 +/- 2 mmHg during U46619 administration. In this setting of acute preconstriction, amrinone caused pulmonary vasodilation, i.e., PAP/LAP was decreased (P < 0.05) from 37 +/- 2 to 32 +/- 2 mmHg. Left lung autotransplantation was associated with a marked shift in the LPQ relationship, indicating a chronic increase in pulmonary vascular resistance, i.e., PAP/LAP was increased (P < 0.01) from 15 +/- 2 to 32 +/- 3 mmHg. Despite the chronic increase in pulmonary vascular resistance after LLA, amrinone had no effect on the baseline LPQ relationship. However, after acute preconstriction with U46619 after LLA, amrinone caused pulmonary vasodilation, i.e., PAP/LAP was decreased (P < 0.05) from 45 +/- 4 to 39 +/- 4 mmHg. CONCLUSIONS: These results indicate that amrinone exerts a significant, although relatively modest pulmonary vasodilator influence in the setting of acute pulmonary vasoconstriction in conscious control dogs and in conscious dogs after LLA. However, amrinone did not reverse the chronic increase in pulmonary vascular resistance associated with LLA.

Pulmonary vascular alpha 1-adrenoreceptor activity in conscious dogs after left lung autotransplantation.

We investigated the extent to which sympathetic alpha 1-adrenoreceptor activation is involved in chronic pulmonary vascular regulation in conscious dogs after left lung autotransplantation (LLA). Continuous left pulmonary vascular pressure-flow plots were generated in conscious dogs 3-4 wk post-LLA and in identically instrumented conscious dogs not subjected to LLA (sham-operated controls). LLA resulted in a marked upward shift in the baseline left pulmonary vascular pressure-flow relationship compared with the control group (P < 0.01), i.e., LLA caused a chronic increase in pulmonary vascular resistance. The sympathetic alpha 1-adrenoreceptor antagonist prazosin partially reversed (P < 0.01) the LLA-induced increase in pulmonary vascular resistance. Circulating concentrations of norepinephrine and epinephrine at 2 and 4 wk post-LLA were not significantly different from values measured in control dogs. However, the dose-response relationship to the exogenous administration of the sympathetic alpha 1-adrenoreceptor agonist phenylephrine was shifted (P < 0.05) to the left post-LLA compared with control, which indicates an increase in pulmonary vascular reactivity to alpha 1-adrenoreceptor activation. This effect was not due to a generalized increase in pulmonary vascular reactivity to vasoconstrictor stimuli because the dose-response relationship to the thromboxane analogue U-46619 was not significantly altered post-LLA compared with control. Thus LLA results in a chronic increase in pulmonary vascular resistance in conscious dogs. A component of the increase in pulmonary vascular resistance resulting from LLA is mediated by an enhanced reactivity to sympathetic alpha 1-adrenoreceptor activation.

N omega-nitro-L-arginine and pulmonary vascular pressure-flow relationship in conscious dogs.

We investigated the effects of an inhibitor of nitric oxide (NO) synthesis, N omega-nitro-L-arginine (L-NNA), on the pulmonary vascular pressure-flow relationship in chronically instrumented conscious dogs. The L-arginine analogue L-NNA (20 mg/min for 60 min iv) had no effect on the baseline pressure-flow relationship. This result indicates that tonic release of endothelium-derived relaxing factor (EDRF), which is thought to be NO or a labile NO-generating molecule, is not responsible for low resting pulmonary vasomotor tone in conscious dogs. In contrast, L-NNA caused a leftward shift in the dose-response relationship to the thromboxane mimetic U-46619, indicating that the endogenous release of EDRF modulates the pulmonary vascular response to this vasoconstrictor. Finally, after preconstriction with U-46619, L-NNA abolished the pulmonary vasodilator response to bradykinin (1-10 micrograms.kg-1.min-1) but had no effect on the pulmonary vasodilator response to sodium nitroprusside (1-10 micrograms.kg-1.min-1). Thus EDRF does not appear to tonically regulate the baseline pulmonary vascular pressure-flow relationship in conscious dogs. However, EDRF does act to attenuate the magnitude of U-46619-induced pulmonary vasoconstriction. Moreover, the pulmonary vasodilator response to bradykinin is entirely mediated by EDRF in conscious dogs.

Intra-aortic balloon counterpulsation in newborn lambs infected with group B streptococcus.

To determine the efficacy of intra-aortic balloon counterpulsation (IABC) in neonatal group B Streptococcal (GBS) infection, we studied five lambs, 10-14 days old, weighing from 4.7 to 6.7 kg. The lambs were instrumented with arterial and venous catheters, and a 5 French intra-aortic balloon catheter with balloon volumes of 3-5 ml was inserted into the femoral artery. A continuous infusion of heat-killed GBS organisms was infused at a rate of 1.7 to 6.2 x 10(8) org/kg/min, until a 30-50% decrease in cardiac output was attained. IABC was then instituted for 30 minutes, hemodynamic measurements repeated, and IABC was stopped. GBS infusion caused significant decreases in cardiac output (282 +/- 62 vs. 165 +/- 38 ml/min/kg) and pH (7.39 +/- 0.02 vs. 7.33 +/- 0.06), and significant increases in mean pulmonary artery pressure (14.4 +/- 2.1 vs. 36.2 +/- 12.1 mm Hg) and pulmonary vascular resistance (1.20 +/- 0.38 vs. 5.08 +/- 1.49 mm Hg/L/min/kg). Institution of IABC during continuous GBS infusion significantly increased cardiac output (225 +/- 1.27 ml/min/kg). The institution of the IABC also resulted in a significant decrease in pulmonary vascular resistance (2.6 +/- 1.3 mm Hg/L/min/kg). The authors conclude that IABC improves cardiac output and decreases pulmonary vascular resistance in newborn lambs with GBS infection.

Clinical manifestations of exacerbations of cystic fibrosis associated with nonbacterial infections.

The purpose of this study was to determine whether acute pulmonary exacerbations of cystic fibrosis associated with nonbacterial infections are clinically distinguishable from other exacerbations. Eighty exacerbations in 54 patients were studied. Exacerbations associated with influenza (n = 8) were compared with those associated with other nonbacterial infections (n = 15) and those in which no nonbacterial infection was detected (n = 57). Patients with influenza had lower Shwachman scores and were more likely to be seropositive for C-reactive protein than patients in the other two groups. Patients with influenza had a mean decrease in forced expiratory volume per second of 26%, compared with test results obtained before the exacerbation. In contrast, the mean decrease in forced expiratory volume per second was 6% for other nonbacterial infections and 12% for the group without nonbacterial infection (p less than 0.05 for both comparisons). The forced expiratory flow in first 25% of vital capacity decreased 44% in the influenza group compared with 13% and 17% in the other two groups, respectively (p less than 0.01 for both comparisons). The influenza group also had a higher proportion of patients with at least a 20% decrease in forced expiratory volume per second and forced expiratory flow in first 25% of vital capacity than the other two groups had (p less than 0.05 for all comparisons). These data suggest that influenza is associated with severe exacerbations in patients with cystic fibrosis and support recommendations for efforts to prevent influenza in this population.