IMPORTANCE Guidelines for declaration of brain death in children were revised in 2011 by the Society of Critical Care Medicine, American Academy of Pediatrics, and Child Neurology Society. Despite widespread medical, legal, and ethical acceptance, ongoing controversies exist with regard to the concept of brain death and the procedures for its determination. OBJECTIVES To determine the epidemiology and clinical characteristics of pediatric patients declared brain dead in the United States. DESIGN, SETTING, AND PARTICIPANTS This study involved the abstraction of all patient deaths from the Virtual Pediatric Systems national multicenter database between January 1, 2012, and June 30, 2017. All patients who died in pediatric intensive care units (PICUs) were included. MAIN OUTCOMES AND MEASURES Patient demographics, preillness developmental status, severity of illness, cause of death, PICU medical and physical length of stay, and organ donation status, as well as comparison between patients who were declared brain dead vs those who sustained cardiovascular or cardiopulmonary death. RESULTS Of the 15 344 patients who died, 3170 (20.7%) were declared brain dead; 1861 of these patients (58.7%) were male, and 1401 (44.2%) were between 2 and 12 years of age. There was a linear association between PICU size and number of patients declared brain dead per year, with an increase of 4.27 patients (95% CI, 3.46-5.08) per 1000-patient increase in discharges (P < .001). The median (interquartile range) of patients declared brain dead per year ranged from 1 (0-3) in smaller PICUs (defined as those with <500 discharges per year) to 10 (7-15) for larger PICUs (those with 2000-4000 discharges per year). The most common causative mechanisms of brain death were hypoxic-ischemic injury owing to cardiac arrest (1672 of 3170 [52.7%]), shock and/or respiratory arrest without cardiac arrest (399 of 3170 [12.6%]), and traumatic brain injury (634 of 3170 [20.0%]). Most patients declared brain dead (681 of 807 [84.4%]) did not have preexisting neurological dysfunction. Patients who were organ donors (1568 of 3144 [49.9%]) remained in the PICU longer after declaration of brain death compared with those who were not donors (median [interquartile range], 29 [6-41] hours vs 4 [1-8] hours; P < .001). CONCLUSIONS AND RELEVANCE Brain death occurred in one-fifth of PICU deaths. Most children declared brain dead had no preexisting neurological dysfunction and had an acute hypoxic-ischemic or traumatic brain injury. Brain death determinations are infrequent, even in large PICUs, emphasizing the importance of ongoing education for medical professionals and standardization of protocols to ensure diagnostic accuracy and consistency.

Background Mechanical power is a composite variable for energy transmitted to the respiratory system over time that may better capture risk for ventilator-induced lung injury than individual ventilator management components. We sought to evaluate if mechanical ventilation management with a high mechanical power is associated with fewer ventilator-free days (VFD) in children with pediatric acute respiratory distress syndrome (PARDS). Methods Retrospective analysis of a prospective observational international cohort study. Results There were 306 children from 55 pediatric intensive care units included. High mechanical power was associated with younger age, higher oxygenation index, a comorbid condition of bronchopulmonary dysplasia, higher tidal volume, higher delta pressure (peak inspiratory pressure—positive end-expiratory pressure), and higher respiratory rate. Higher mechanical power was associated with fewer 28-day VFD after controlling for confounding variables (per 0.1 J·min−1·Kg−1 Subdistribution Hazard Ratio (SHR) 0.93 (0.87, 0.98), p = 0.013). Higher mechanical power was not associated with higher intensive care unit mortality in multivariable analysis in the entire cohort (per 0.1 J·min−1·Kg−1 OR 1.12 [0.94, 1.32], p = 0.20). But was associated with higher mortality when excluding children who died due to neurologic reasons (per 0.1 J·min−1·Kg−1 OR 1.22 [1.01, 1.46], p = 0.036). In subgroup analyses by age, the association between higher mechanical power and fewer 28-day VFD remained only in children < 2-years-old (per 0.1 J·min−1·Kg−1 SHR 0.89 (0.82, 0.96), p = 0.005). Younger children were managed with lower tidal volume, higher delta pressure, higher respiratory rate, lower positive end-expiratory pressure, and higher PCO2 than older children. No individual ventilator management component mediated the effect of mechanical power on 28-day VFD. Conclusions Higher mechanical power is associated with fewer 28-day VFDs in children with PARDS. This association is strongest in children < 2-years-old in whom there are notable differences in mechanical ventilation management. While further validation is needed, these data highlight that ventilator management is associated with outcome in children with PARDS, and there may be subgroups of children with higher potential benefit from strategies to improve lung-protective ventilation. Take Home Message: Higher mechanical power is associated with fewer 28-day ventilator-free days in children with pediatric acute respiratory distress syndrome. This association is strongest in children <2-years-old in whom there are notable differences in mechanical ventilation management.

A sixth dose of tetanus, diphtheria, acellular pertussis (Tdap) vaccine in adolescents might produce a differing reactogenicity and/or immunogenicity response depending on the composition of the 5 prior doses of DTaP or DT-whole cell pertussis (DTwP) vaccine. Reactions and immune responses following receipt of the Sanofi Pasteur (Adacel) and GlaxoSmithKline (Boostrix) Tdap vaccines were assessed in 229 adolescents. No differences were observed for reactions to either Tdap vaccine regardless of the prior DTaP/DTwP vaccination history. Seroprotective levels and antibody concentrations were comparable regardless of prior DTaP/DTwP vaccine history. A sixth sequential dose of Tdap after 5 doses of DTaP appears safe and immunogenic.

The absorption of terramycin from the gastrointestinal tract is rather similar to that of aureomycin. Peak levels are low, tend to be achieved in 2 to 6 hours after ingestion, and are prolonged for several hours. Single oral doses of 11 mg/kg. body weight give peak serum levels ranging from 0.20 to 1.95 µg./cc., with a mean of 1.0 µg./cc. Doubling or tripling this single dose did not produce marked increases in serum levels. Dosage of 11 mg./kg. orally every six hours (44 mg./kg./24 hours) resulted in peak serum levels on the third day which were essentially identical with those after the initial dose. However, when a dosage of 33 mg./kg. was given orally every six hours (132 mg./kg./24 hours), marked cumulation in the serum was noted. The mean serum level on the first day on this schedule was 2.7 µg./cc., and on the third day, 8.0 µg./cc. Diffusion into the cerebrospinal fluid in three cases was poor. With spinal fluid and serum levels simultaneously obtained, the spinal fluid levels were ¼, ⅙ and ⅛, respectively of the serum levels. Intravenously administered terramycin in dosage of 6.6 mg./kg. gave peak serum levels at one-half hour, ranging from 10.0 to 12.8 µg./cc. Six hours after injection, serum levels ranged from 1.8 to 4.4 µg./cc., and at 12 hours, from 0.78 to 2.6 µg./cc. Terramycin given rectally in perforated capsules was well tolerated. However, in four patients given 66 mg./kg. by this route, peak serum levels ranged from 0 to 1.0 µg./cc. Recommended terramycin dosage: (a) Oral: 11 mg./kg./dose every six hours (44 mg./kg./24 hours). Adequate antibacterial serum levels for most susceptible organisms are produced with this dosage. Increasing the dosage to 33 mg./kg./dose every six hours (132 mg./kg./24 hours) may be done in cases when high serum levels seem indicated. (b) Intravenous: 6.6 to 11 mg./kg./dose every 6 to 8 hours.

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