Background Delirium is acute brain dysfunction associated with serious illness. Emerging data indicate that delirium occurs in greater than 20% of children in pediatric intensive care units. Cardiac bypass surgery is a known risk factor for delirium in adults, but has never been systematically studied in pediatrics. Objectives To describe the incidence of delirium in pediatric patients after cardiac bypass surgery, and explore associated risk factors and effect of delirium on in-hospital outcomes. Design Prospective observational single-center study. Setting Fourteen-bed pediatric cardiothoracic intensive care unit (PCICU). Patients One hundred and ninety four consecutive admissions following cardiac bypass surgery, age one day to 21 years. Interventions Subjects were screened for delirium daily using the Cornell Assessment of Pediatric Delirium. Measurements and Main Results Incidence of delirium in this sample was 49%. Delirium most often lasted 1–2 days, and developed within the first 1–3 days after surgery. Age less than two years, developmental delay, higher RACHS-1 score, cyanotic disease, and albumin less than three were all independently associated with development of delirium in a multivariable model (all p values <0.03). Delirium was an independent predictor of prolonged ICU LOS, with patients who were ever delirious having a 60% increase in ICU days compared to patients who were never delirious (p<0.01). Conclusions In our institution, delirium is a frequent problem in children after cardiac bypass surgery, with identifiable risk factors. Our study suggests that cardiac bypass surgery significantly increases children’s susceptibility to delirium. This highlights the need for heightened, targeted delirium screening in all PCICUs to potentially improve outcomes in this vulnerable patient population.

Objectives: Assessing outcomes after pediatric critical illness is imperative to evaluate practice and improve recovery of patients and their families. We conducted a scoping review of the literature to identify domains and instruments previously used to evaluate these outcomes. Design: Scoping review. Setting: We queried PubMed, EMBASE, PsycINFO, Cumulative Index of Nursing and Allied Health Literature, and the Cochrane Central Register of Controlled Trials Registry for studies evaluating pediatric critical care survivors or their families published between 1970 and 2017. We identified articles using key words related to pediatric critical illness and outcome domains. We excluded articles if the majority of patients were greater than 18 years old or less than 1 month old, mortality was the sole outcome, or only instrument psychometrics or procedural outcomes were reported. We used dual review for article selection and data extraction and categorized outcomes by domain (overall health, emotional, physical, cognitive, health-related quality of life, social, family). Subjects: Manuscripts evaluating outcomes after pediatric critical illness. Interventions: None. Measurements and Main Results: Of 60,349 citations, 407 articles met inclusion criteria; 87% were published after 2000. Study designs included observational (85%), interventional (7%), qualitative (5%), and mixed methods (3%). Populations most frequently evaluated were traumatic brain injury (n = 96), general pediatric critical illness (n = 87), and congenital heart disease (n = 72). Family members were evaluated in 74 studies (18%). Studies used a median of 2 instruments (interquartile range 1–4 instruments) and evaluated a median of 2 domains (interquartile range 2–3 domains). Social (n = 223), cognitive (n = 183), and overall health (n = 161) domains were most frequently studied. Across studies, 366 unique instruments were used, most frequently the Wechsler and Glasgow Outcome Scales. Individual domains were evaluated using a median of 77 instruments (interquartile range 39–87 instruments). Conclusions: A comprehensive, generalizable understanding of outcomes after pediatric critical illness is limited by heterogeneity in methodology, populations, domains, and instruments. Developing assessment standards may improve understanding of postdischarge outcomes and support development of interventions after pediatric critical illness.

The first PCC orientation training integrated with simulation was effective and logistically feasible. The train to success concept with repetitive practice was highly valued by participants. Continuation and expansion of this novel multi-institutional training is planned.

Adverse tracheal intubation associated events and desaturations are common and associated with longer mechanical ventilation in critically ill children. Severe tracheal intubation associated events are associated with higher ICU mortality. Potential interventions to decrease tracheal intubation associated events and oxygen desaturation, such as tracheal intubation checklist, use of apneic oxygenation, and video laryngoscopy, may need to be considered to improve ICU outcomes.

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Neutrophils accumulate during the acute inflammatory response to brain injury, but their role in the injury process remains controversial. We tested the hypothesis that neutrophils contribute to cerebral edema, tissue injury, and disturbed cerebral blood flow (CBF) (hyperemia or ischemia) during the first 24 h after traumatic brain injury. Wistar rats (n = 51) were injected with either vinblastine sulfate to induce neutropenia or the saline vehicle. Five days later, under halothane anesthesia, right hemispheric trauma was produced by weight drop (10 g x 5 cm) onto exposed dura. At 24 h after trauma, brain water (wet-dry weight), traumatic infarct size (percent of hemispheric section infarcted), or local CBF (lCBF, 14C-iodoantipyrine autoradiography) was assessed. Vinblastine treatment produced profound neutropenia on the day of trauma (absolute neutrophil count 0.024 +/- 0.008 x 10(9)/L vs 1.471 +/- 0.322 x 10(9)/L, p < 0.05 in neutropenic vs saline, respectively, mean +/- SEM). Neutropenia did not reduce the development of brain edema in the injured hemisphere (brain water 82.38 +/- 0.29% vs 82.73 +/- 0.37% in neutropenic and saline, respectively, mean +/- SEM) or traumatic infarct size (34.5 +/- 3.3% vs 33.2 +/- 2.1% in neutropenic vs saline respectively). In contrast, neutropenic rats exhibited 52%, 41%, and 57% reductions in lCBF in the frontal cortex, parietal cortex, and amygdala, respectively, of the injured hemisphere 24 h after trauma (all p < 0.05 vs nonneutropenic controls). These data suggest that neutrophils and the acute inflammatory process contribute to the level of CBF observed 24 h after trauma, but effects on edema or early posttraumatic infarct size could not be demonstrated.

Polymorphonuclear leukocytes (PMN) are implicated in the pathogenesis of traumatic brain injury. We tested the following hypotheses: (1) leukocyte accumulation is present in brain tissue 24 h posttrauma, (2) leukocyte accumulation represents PMN, and (3) prior systemic PMN depletion attenuates brain tissue PMN accumulation. Trauma was induced in exposed right parietal cortex by weightdrop in anesthetized Wistar rats (n = 24). Of the traumatized rats, 12 were PMN-depleted with vinblastine sulfate i.v. Controls were 12 normal rats and 5 sham-operated rats (craniotomy). Sections of traumatized and contralateral hemispheres were analyzed for myeloperoxidase (MPO) activity. Brain MPO activity was increased fivefold at 24 h posttrauma, but only in the traumatized hemisphere (0.448 +/- 0.133 U/g vs 0.090 +/- 0.022 U/g in trauma vs normal, respectively, p < 0.05, mean +/- SEM). PMN depletion attenuated this increase in MPO activity and decreased circulating PMN counts (0.07 +/- 0.032 x 10(9)/L vs 0.894 +/- 0.294 x 10(9)/L PMN-depleted-trauma vs trauma rats, respectively, p < 0.05). Leukocyte accumulation in the brain posttrauma was confirmed by MPO assay. Inhibition of MPO activity in the PMN-depleted group and the specificity of vinblastine treatment for depletion of circulating PMN suggest that leukocyte accumulation in the brain at 24 h posttrauma is largely due to PMN.

Few recent studies have assessed the epidemiology of health care-associated infections (HAIs) in the pediatric population after cardiac surgery. A retrospective cohort study was performed to assess the epidemiology of several types of HAIs in children 18 years of age or younger undergoing cardiac surgery from July 2010 to June 2012. Potential pre-, intra-, and postoperative risk factors, including adherence to the perioperative antibiotic prophylaxis regimen at the authors' hospital, were assessed by multivariable analysis using Poisson regression models. Microorganisms associated with HAIs and their susceptibility patterns were described. Overall, 634 surgeries were performed, 38 (6 %) of which were complicated by an HAI occurring within 90 days after surgery. The HAIs included 7 central line-associated bloodstream infections (CLABSIs), 12 non-CLABSI bacteremias, 6 episodes of early postoperative infective endocarditis (IE), 9 surgical-site infections (SSIs), and 4 ventilator-associated pneumonias (VAPs). Mechanical ventilation (rate ratio [RR] 1.07 per day; 95 % confidence interval [CI] 1.03-1.11; p = 0.0002), postoperative transfusion of blood products (RR 3.12; 95 %, CI 1.38-7.06; p = 0.0062), postoperative steroid use (RR 3.32; 95 % CI 1.56-7.02; p = 0.0018), and continuation of antibiotic prophylaxis longer than 48 h after surgery (RR 2.56; 95 % CI 1.31-5.03; p = 0.0062) were associated with HAIs. Overall, 66.7 % of the pathogens associated with SSIs were susceptible to cefazolin, the perioperative antibiotic prophylaxis used by the authors' hospital. In conclusion, HAIs occurred after 6 % of cardiac surgeries. Bacteremia and CLABSI were the most common. This study identified several potentially modifiable risk factors that suggest interventions. Further studies should assess the role of improving adherence to perioperative antibiotic prophylaxis, the age of transfused red blood cells, and evidence-based guidelines for postoperative steroids.