e6 208 Nakagawa TA, Morris A, Gomez RJ, Johnston SJ, Sharkey PT, Zaritsky AL Dose response to inhaled nitric oxide in pediatric patients with pulmonary hypertension and acute respiratory dis tress syn[.]
e6 208 Nakagawa TA, Morris A, Gomez RJ, Johnston SJ, Sharkey PT, Zaritsky AL Dose response to inhaled nitric oxide in pediatric patients with pulmonary hypertension and acute respiratory distress syndrome J Pediatr 1997;131(1 Pt 1):63-69 209 Bloomfield GL, Holloway S, Ridings PC, et al Pretreatment with inhaled nitric oxide inhibits neutrophil migration and oxidative activity resulting in attenuated sepsis-induced acute lung injury Crit Care Med 1997;25(4):584-593 210 Fioretto JR, Campos FJ, Ronchi CF, et al Effects of inhaled nitric oxide on oxidative stress and histopathological and inflammatory lung injury in a saline-lavaged rabbit model of acute lung injury Respir Care 2012;57(2):273-281 211 Stubbe HD, Westphal M, Van Aken H, et al Inhaled nitric oxide reduces lung edema during fluid resuscitation in ovine acute lung injury Intensive Care Med 2003;29(10):1790-1797 212 Wu HS, Zhang L, Chen Y, et al Effect of nitric oxide on toll-like receptor and gene expression in rats with acute lung injury complicated by acute hemorrhage necrotizing pancreatitis Hepatobiliary Pancreat Dis Int 2005;4(4):609-613 213 Gries A, Bode C, Peter K, et al Inhaled nitric oxide inhibits human platelet aggregation, P-selectin expression, and fibrinogen binding in vitro and in vivo Circulation 1998;97(15):1481-1487 214 Gries A, Herr A, Kirsch S, et al Inhaled nitric oxide inhibits platelet-leukocyte interactions in patients with acute respiratory distress syndrome Crit Care Med 2003;31(6):1697-1704 215 Samama CM, Diaby M, Fellahi JL, et al Inhibition of platelet aggregation by inhaled nitric oxide in patients with acute respiratory distress syndrome Anesthesiology 1995;83(1):56-65 216 Qi Y, Qian L, Sun B, Liu L, Wu P, Sun L Inhaled NO contributes to lung repair in piglets with acute respiratory distress syndrome via increasing circulating endothelial progenitor cells PLoS ONE 2012;7(3):e33859 217 Jean D, Maitre B, Tankovic J, et al Beneficial effects of nitric oxide inhalation on pulmonary bacterial clearance Crit Care Med 2002;30(2):442-447 218 Ader F, Le Berre R, Lancel S, et al Inhaled nitric oxide increases endothelial permeability in Pseudomonas aeruginosa pneumonia Intensive Care Med 2007;33(3):503-510 219 Nishina K, Mikawa K, Takao Y, Obara H Inhaled nitric oxide does not prevent endotoxin-induced lung injury in rabbits Acta Anaesthesiol Scand 1997;41(3):399-407 220 Rayhrer CS, Edmisten TD, Cephas GA, Tribble CG, Kron IL, Young JS Nitric oxide potentiates acute lung injury in an isolated rabbit lung model Ann Thorac Surg 1998;65(4):935-938 221 Shanley TP, Zhao B, Macariola DR, Denenberg A, Salzman AL, Ward PA Role of nitric oxide in acute lung inflammation: lessons learned from the inducible nitric oxide synthase knockout mouse Crit Care Med 2002;30(9):1960-1968 222 Tsukahara Y, Horita Y, Anan K, Morisaki T, Tanaka M, Torisu M Role of nitric oxide derived from alveolar macrophages in the early phase of acute pancreatitis J Surg Res 1996;66(1):43-50 223 Afshari A, Brok J, Moller AM, Wetterslev J Inhaled nitric oxide for acute respiratory distress syndrome (ARDS) and acute lung injury in children and adults Cochrane Database Syst Rev 2010(7): CD002787 224 Afshari A, Brok J, Moller AM, Wetterslev J Inhaled nitric oxide for acute respiratory distress syndrome and acute lung injury in adults and children: a systematic review with meta-analysis and trial sequential analysis Anesth Analg 2011;112(6):1411-1421 225 Adhikari NK, Dellinger RP, Lundin S, et al Inhaled nitric oxide does not reduce mortality in patients with acute respiratory distress syndrome regardless of severity: systematic review and meta-analysis Crit Care Med 2014;42(2):404-412 226 Demirakca S, Dotsch J, Knothe C, et al Inhaled nitric oxide in neonatal and pediatric acute respiratory distress syndrome: dose response, prolonged inhalation, and weaning Crit Care Med 1996;24(11):1913-1919 227 Fioretto JR, de Moraes MA, Bonatto RC, Ricchetti SM, Carpi MF Acute and sustained effects of early administration of inhaled nitric oxide to children with acute respiratory distress syndrome Pediatr Crit Care Med 2004;5(5):469-474 228 Goldman AP, Tasker RC, Hosiasson S, Henrichsen T, Macrae DJ Early response to inhaled nitric oxide and its relationship to outcome in children with severe hypoxemic respiratory failure Chest 1997;112(3):752-758 229 Day RW, Allen EM, Witte MK A randomized, controlled study of the 1-hour and 24-hour effects of inhaled nitric oxide therapy in children with acute hypoxemic respiratory failure Chest.112(5):1324-1331 230 Dobyns EL, Cornfield DN, Anas NG, et al Multicenter randomized controlled trial of the effects of inhaled nitric oxide therapy on gas exchange in children with acute hypoxemic respiratory failure J Pediatr.134(4):406-412 231 Ibrahim T, El-Mohamady H Inhaled nitric oxide and prone position: how far they can improve oxygenation in pediatric patients with acute respiratory distress syndrome? J Med Sci 2007;7(3):390-395 232 Bronicki RA, Fortenberry J, Schreiber M, Checchia PA, Anas NG Multicenter randomized controlled trial of inhaled nitric oxide for pediatric acute respiratory distress syndrome J Pediatr 2015;166(2):365-369 e361 233 Tamburro RF, Kneyber MCJ Pulmonary specific ancillary treatment for pediatric acute respiratory distress syndrome Pediatr Crit Care Med 2015;16:S61-S72 234 Richter T, Bellani G, Scott Harris R, et al Effect of prone position on regional shunt, aeration, and perfusion in experimental acute lung injury Am J Respir Crit Care Med 2005;172(4):480-487 235 Tang R, Huang Y, Chen Q, et al Relationship between regional lung compliance and ventilation homogeneity in the supine and prone position Acta Anaesthesiol Scand 2012;56(9):1191-1199 236 Albert RK, Hubmayr RD The prone position eliminates compression of the lungs by the heart Am J Respir Crit Care Med 2000;161(5):1660-1665 237 Lee DL, Chiang HT, Lin SL, Ger LP, Kun MH, Huang YC Proneposition ventilation induces sustained improvement in oxygenation in patients with acute respiratory distress syndrome who have a large shunt Crit Care Med 2002;30(7):1446-1452 238 Hyatt RE, Bar-Yishay E, Abel MD Influence of the heart on the vertical gradient of transpulmonary pressure in dogs J Appl Physiol (1985) 1985;58(1):52-57 239 Bar-Yishay E, Hyatt RE, Rodarte JR Effect of heart weight on distribution of lung surface pressures in vertical dogs J Appl Physiol (1985) 1986;61(2):712-718 240 Lee HJ, Im JG, Goo JM, et al Acute lung injury: effects of prone positioning on cephalocaudal distribution of lung inflation—CT assessment in dogs Radiology 2005;234(1):151-161 241 Vieillard-Baron A, Rabiller A, Chergui K, et al Prone position improves mechanics and alveolar ventilation in acute respiratory distress syndrome Intensive Care Med 2005;31(2):220-226 242 Galiatsou E, Kostanti E, Svarna E, et al Prone position augments recruitment and prevents alveolar overinflation in acute lung injury Am J Respir Crit Care Med 2006;174(2):187-197 243 Valenza F, Guglielmi M, Maffioletti M, et al Prone position delays the progression of ventilator-induced lung injury in rats: does lung strain distribution play a role? Crit Care Med 2005;33(2):361-367 244 Broccard A, Shapiro RS, Schmitz LL, Adams AB, Nahum A, Marini JJ Prone positioning attenuates and redistributes ventilatorinduced lung injury in dogs Crit Care Med 2000;28(2): 295-303 245 Cornejo RA, Diaz JC, Tobar EA, et al Effects of prone positioning on lung protection in patients with acute respiratory distress syndrome Am J Respir Crit Care Med 2013;188(4):440-448 246 Demory D, Michelet P, Arnal JM, et al High-frequency oscillatory ventilation following prone positioning prevents a further impairment in oxygenation Crit Care Med 2007;35(1):106-111 e7 247 Guerin C, Badet M, Rosselli S, et al Effects of prone position on alveolar recruitment and oxygenation in acute lung injury Intensive Care Med 1999;25(11):1222-1230 248 Jozwiak M, Teboul JL, Anguel N, et al Beneficial hemodynamic effects of prone positioning in patients with acute respiratory distress syndrome Am J Respir Crit Care Med 2013;188(12):1428-1433 249 Vieillard-Baron A, Charron C, Caille V, Belliard G, Page B, Jardin F Prone positioning unloads the right ventricle in severe ARDS Chest 2007;132(5):1440-1446 250 Dupont H, Mentec H, Cheval C, Moine P, Fierobe L, Timsit JF Short-term effect of inhaled nitric oxide and prone positioning on gas exchange in patients with severe acute respiratory distress syndrome Crit Care Med 2000;28(2):304-308 251 Hale DF, Cannon JW, Batchinsky AI, et al Prone positioning improves oxygenation in adult burn patients with severe acute respiratory distress syndrome J Trauma Acute Care Surg 2012;72(6):1634-1639 252 Fernandez R, Trenchs X, Klamburg J, et al Prone positioning in acute respiratory distress syndrome: a multicenter randomized clinical trial Intensive Care Med 2008;34(8):1487-1491 253 Lemasson S, Ayzac L, Girard R, Gaillard S, Pavaday K, Guerin C Does gas exchange response to prone position predict mortality in hypoxemic acute respiratory failure? Intensive Care Med 2006;32(12):1987-1993 254 Taccone P, Pesenti A, Latini R, et al Prone positioning in patients with moderate and severe acute respiratory distress syndrome: a randomized controlled trial JAMA 2009;302(18):1977-1984 255 Gattinoni L, Vagginelli F, Carlesso E, et al Decrease in PaCO2 with prone position is predictive of improved outcome in acute respiratory distress syndrome Crit Care Med 2003;31(12): 2727-2733 256 Charron C, Repesse X, Bouferrache K, et al PaCO2 and alveolar dead space are more relevant than PaO2/FiO2 ratio in monitoring the respiratory response to prone position in ARDS patients: a physiological study Crit Care 2011;15(4):R175 257 Abroug F, Ouanes-Besbes L, Dachraoui F, Ouanes I, Brochard L An updated study-level meta-analysis of randomised controlled trials on proning in ARDS and acute lung injury Crit Care 2011;15(1):R6 258 Guérin C, Reignier J, Richard JC, et al Prone positioning in severe acute respiratory distress syndrome N Engl J Med 2013;368(23): 2159-2168 259 Mancebo J, Fernandez R, Blanch L, et al A multicenter trial of prolonged prone ventilation in severe acute respiratory distress syndrome Am J Respir Crit Care Med 2006;173(11):1233-1239 260 Papazian L, Gainnier M, Marin V, et al Comparison of prone positioning and high-frequency oscillatory ventilation in patients with acute respiratory distress syndrome Crit Care Med 2005;33(10):2162-2171 261 Lee JM, Bae W, Lee YJ, Cho YJ The efficacy and safety of prone positional ventilation in acute respiratory distress syndrome: updated study-level meta-analysis of 11 randomized controlled trials Crit Care Med 2014;42(5):1252-1262 262 Beitler JR, Shaefi S, Montesi SB, et al Prone positioning reduces mortality from acute respiratory distress syndrome in the low tidal volume era: a meta-analysis Intensive Care Med 2014;40(3):332-341 263 Curley MA Prone positioning of patients with acute respiratory distress syndrome: a systematic review Am J Crit Care 1999;8(6): 397-405 264 Curley MA, Thompson JE, Arnold JH The effects of early and repeated prone positioning in pediatric patients with acute lung injury Chest 2000;118(1):156-163 265 Kornecki A, Frndova H, Coates AL, Shemie SD A randomized trial of prolonged prone positioning in children with acute respiratory failure Chest 2001;119(1):211-218 266 Casado-Flores J, Martinez de Azagra A, Ruiz-Lopez MJ, Ruiz M, Serrano A Pediatric ARDS: effect of supine-prone postural changes on oxygenation Intensive Care Med 2002;28(12):1792-1796 267 Relvas MS, Silver PC, Sagy M Prone positioning of pediatric patients with ARDS results in improvement in oxygenation if maintained 12 h daily Chest 2003;124(1):269-274 268 Curley MAQ, Hibberd PL, Fineman LD, et al Effect of prone positioning on clinical outcomes in children with acute lung injury: a randomized controlled trial JAMA 2005;294(2):229-237 269 Curley MA, Arnold JH, Thompson JE, et al Clinical trial design— effect of prone positioning on clinical outcomes in infants and children with acute respiratory distress syndrome J Crit Care 2006;21(1):23-32; discussion 32-27 270 Emeriaud G, Newth CJL Monitoring of children with pediatric acute respiratory distress syndrome Pediatr Crit Care Med 2015;16:S86-S101 271 Essouri S, Carroll C Noninvasive support and ventilation for pediatric acute respiratory distress syndrome Pediatr Crit Care Med 2015;16:S102-S110 272 Mayordomo-Colunga J, Pons M, López Y, et al Predicting noninvasive ventilation failure in children from the SpO2/FiO2 (SF) ratio Intensive Care Med 2013;39(6):1095-1103 273 Essouri S, Chevret L, Durand P, Haas V, Fauroux B, Devictor D Noninvasive positive pressure ventilation: Five years of experience in a pediatric intensive care unit* Pediatr Crit Care Med 2006;7(4):329-334 274 Demaret P, Mulder A, Loeckx I, Trippaerts M, Lebrun F Noninvasive ventilation is useful in paediatric intensive care units if children are appropriately selected and carefully monitored Acta Paediatr (Oslo, Norway : 1992) 2015;104(9):861-871 275 Erickson, S Extra-corporeal membrane oxygenation in paediatric acute respiratory distress syndrome: overrated or underutilized? Annu Transl Med 2019;7(19):512-521 276 Dalton HJ, Macrae DJ Extracorporeal support in children with pediatric acute respiratory distress syndrome Pediatr Crit Care Med 2015;16:S111-S117 277 Zabrocki LA, Brogan TV, Statler KD, Poss WB, Rollins MD, Bratton SL Extracorporeal membrane oxygenation for pediatric respiratory failure: Survival and predictors of mortality Crit Care Med 2011;39(2):364-370 278 Barbaro RP, Xu Y, Borasino S, et al Does extracorporeal membrane oxygenation improve survival in pediatric acute respiratory failure? Am J Respir Crit Care Med 2018;197(9):1177-1186 279 Schmidt M, Pham T, Arcadipane A, et al Mechanical ventilation management during extracorporeal membrane oxygenation for acute respiratory distress syndrome An international multicenter prospective cohort Am J Respir Crit Care Med 2019;200(8):10021012 280 Rozencwajg S, Guihot A, Franchineau G, et al Ultra-protective ventilation reduces biotrauma in patients on venovenous extracorporeal membrane oxygenation for severe acute respiratory distress syndrome Crit Care Med 2019;47(11):1505-1512 281 Schmidt M, Pham T, Arcadipane A, et al Mechanical ventilation management during ECMO for ARDS: An international multicenter prospective cohort Am J Respir Crit Care Med 2019 e8 Abstract: Acute respiratory distress syndrome (ARDS) is a restrictive lung disease with severe hypoxemia and, often, hypercarbia Diffuse disruption of the alveolar epithelial-endothelial barrier resulting in noncardiogenic pulmonary edema is the main pathologic finding Lung protective ventilation strategies that use lower tidal volume, lower inspiratory driving pressure, and higher positive end-expiratory pressure have been supported in the adult literature Differences in practice patterns, comorbidities, and outcomes specific to pediatric patients led to a pediatric definition of ARDS in 2015 Key words: acute respiratory distress syndrome, hypoxemia, acute hypoxemic respiratory failure, restrictive lung disease, ventilatorinduced lung injury, ventilator-associated lung injury, lung-protective ventilation, ventilation-perfusion mismatch, shunt, dead space 49 Acute Viral Bronchiolitis KATHERINE N SLAIN AND STEVEN L SHEIN • Bronchiolitis accounts for 5% to 10% of total pediatric intensive care unit admissions in the United States Treatment for critical bronchiolitis is predominantly supportive, particularly for hypoxia, hypercarbia, dyspnea, and dehydration Lower respiratory tract infection is a leading cause of global morbidity and mortality in young children; viral bronchiolitis comprises approximately one-quarter of these infections.1,2 While overall mortality is low in high-resource areas, morbidity and associated healthcare costs are increasing In 2009, the hospital charges related to bronchiolitis were approximately $1.7 billion in the United States alone.3 In the United States, bronchiolitis is the most common cause of hospitalization among infants.3 It accounts for approximately 5% to 10% of total pediatric intensive care unit (PICU) admissions in the United States, 8% of PICU admissions among children younger than years in the United Kingdom, and 28% of nonelective PICU admissions in Australasia.4–7 As such, the pediatric intensivist should be familiar with the diagnosis and management of bronchiolitis, understand the high morbidity and cost associated with the disease, and appreciate the paucity of PICU-specific data and need for continued research This chapter will review the microbiology, epidemiology, pathophysiology, clinical presentation, current therapeutics, and common complications associated with severe bronchiolitis requiring PICU admission, termed critical bronchiolitis Microbiology The most common pathogen causing bronchiolitis is respiratory syncytial virus (RSV), accounting for approximately 50% to 80% of cases.8–10 The development of sensitive viral testing methods, including polymerase chain reaction, has increased the number of viruses implicated in lower respiratory tract infections.11,12 Rhinovirus; parainfluenza virus types 1, 2, and 3; influenza types A, B, and H1N1; human metapneumovirus; coronaviruses; enterovirus; and adenovirus are all associated with bronchiolitis.13–16 Up to one-third of children with RSV and nearly three-quarters of children with rhinovirus are coinfected.14 There is some evidence to suggest that RSV causes more severe disease than other viruses and that coinfections predispose children to more hypoxia and prolonged hospital length of stay (LOS).13,17 These findings are 546 • • PEARLS Use of medications and respiratory support modalities vary widely by region and between institutions without clear benefits on clinical outcomes not consistent across all studies; thus, there are currently no recommendations to change medical treatments based on viral etiology.18,19 Epidemiology and Risk Factors The timing and duration of the bronchiolitis “season” varies annually and geographically The Centers for Disease Control and Prevention monitor the temporal and circulation patterns of viruses, including RSV, through the National Respiratory and Enteric Virus Surveillance System From 2014 to 2017, the median duration of the RSV season in the United States was 31 weeks, from mid-October to early May, with a peak in early February.20 This pattern is not repeated internationally, however RSV global surveillance data from low- and middle-income countries show that onset, duration, and peak activity vary widely between countries and coincide with rainy seasons and low temperatures, suggesting that indoor crowding likely contributes to RSV transmission.21 Most children admitted to the PICU with bronchiolitis are otherwise generally healthy, but several comorbidities have been consistently identified as risk factors for severe illness and PICU admission.4,6,22,23 Prematurity is a well-established risk factor.24 In one single-center study, a history of preterm birth conferred an odds ratio of 24.5 (95% confidence interval, 3.2–186.9) for PICU admission.25 In addition to prematurity, hemodynamically significant congenital heart disease, chronic lung disease, neuromuscular disease, and being profoundly immunocompromised are well-known risk factors for severe disease Accordingly, these children are candidates for palivizumab prophylaxis.24 There is also evidence that some demographic and social factors may predispose children to more severe disease These include younger age, male gender, cigarette smoke exposure, and low socioeconomic status.23 Young infants are more likely to require hospitalization, PICU admission, mechanical ventilation, and have longer LOS.26–28 In a meta-analysis including 60 studies, CHAPTER 49 Acute Viral Bronchiolitis exposure to household smoking increased the risk of bronchiolitis by an odds ratio of 2.51 (95% CI, 1.96–3.21).29 A child’s socioeconomic status may have an impact on illness severity in bronchiolitis Children living in disadvantaged communities have been shown to have higher risk of hospital admission, higher risk of PICU admission, and longer hospital LOS.30–32 Pathophysiology The pathology of viral lower respiratory tract infection is best described in RSV infection Not all infected children will develop the clinical symptoms of lower respiratory tract illness, and host anatomic and immunologic properties likely play an important role in the severity of disease In acutely ill children, the innate immune system is activated as the infected airway cells secrete cytokine and chemokine inflammatory mediators Infectious bronchiolitis is characterized by intense neutrophilic and mononuclear peribronchial infiltration leading to tissue edema.33,34 In severe RSV infection, the peak viral load corresponds to peak disease severity As the viral load decreases, an influx of plasma neutrophil precursors occurs, followed by activation of CD81 T cells The neutrophil-mediated inflammation of the lower respiratory tract is an important mechanism of pathophysiology in a variety of viral lower respiratory tract illnesses, including RSV, influenza A, human metapneumovirus, adenovirus, rhinovirus, and coronavirus.35 In an autopsy study, children who died from RSV infection were found to have extensive RSV antigen in lung epithelium, sloughed epithelial cells blocking the small airways, significant apoptosis, low quantities of lymphocyte cytokines, and a near absence of CD81 lymphocytes and natural killer cells.36 These findings suggest that the pathogenesis of fatal RSV infection may be secondary to the failure of the child to develop an appropriate adaptive cytotoxic T cell response to infection.36 A larger autopsy study included 250 children who died from a variety of acute respiratory infections, including RSV, adenovirus, influenza, and parainfluenza.37 This study described RSV as causing the most profound damage and inflammation to the bronchiolar epithelial cells More recent studies have described a pattern of necrotic RSV-infected epithelial cells contributing to small airway inflammation.36,38,39 Furthermore, RSV likely destroys ciliated cells, contributing to impaired mechanical clearance of the distal airways.40 Young children and infants are disproportionately burdened by viral lower respiratory tract disease In addition to functionally immature immune systems, infant respiratory anatomy and mechanics predispose to severe disease The viral-induced inflammatory response occurring in proportionally smaller bronchioles leads to alveolar obstruction and collapse with edema, mucus, and cellular debris.33 The increased resistance affects both inspiration and expiration in the small airways, ultimately leading to a “ballvalve” mechanism of air-trapping, hyperinflation, and resorption atelectasis The subsequent pulmonary ventilation and perfusion mismatch may lead to hypoxemia Clinical Features and Diagnosis Bronchiolitis is a clinical diagnosis, often defined by an age of less than years with low-grade fever, tachypnea, dyspnea, upper respiratory tract symptoms (e.g., rhinorrhea), and lower respiratory tract symptoms (e.g., cough, wheezing, and rales).41 Tachypnea may progress to respiratory embarrassment manifested by 547 retractions, nasal flaring, head bobbing, and grunting, ultimately leading to respiratory failure necessitating ventilatory support Mechanical ventilation may also be needed to support infants with apnea Apnea occurs in approximately 5% of hospitalized children and is more likely in younger infants presenting with more severe respiratory distress.42 In one single-center study, the relative risk for mechanical ventilation was 6.5 (95% CI, 3.3–12.9) for infants with recurrent apnea.43 While only 2% to 3% of children with severe bronchiolitis require mechanical ventilation, this percentage may be as high as 35% in high-risk children with chronic comorbidities.3,27,44 Predicting the subset of children who will go on to require intensive care management is challenging for clinicians Clinical scoring systems may be helpful; however, none has been proved universally beneficial to date Originally developed for use in controlled trials of therapeutics, the respiratory distress assessment instrument (RDAI) and the respiratory assessment change score (RACS) may be predictive of illness severity.45–50 In a recent multicenter, international retrospective study, investigators developed a severity prediction score for children presenting to the emergency department Predictive variables included patient age, poor feeding, oxygen desaturation, apnea, flaring or grunting, retractions, and dehydration.51 In a large population, the score was able to quantify risk for escalated care— defined as PICU care, or need for noninvasive or invasive ventilatory support—with good discrimination and stability.51 Diagnostic testing is not recommended in current clinical practice guidelines for children with bronchiolitis in the non-ICU setting.41 In children with mild disease, multiple studies have suggested that chest radiographs are not needed and may lead to longer hospital LOS.52–54 Routine laboratory tests have not been shown to improve clinical outcomes of mild disease, including little utility of either abnormally low (,5000) or high (.15,000) white blood cell count in identifying children with a concurrent serious bacterial infection.55 However, the utility of radiographs and laboratory testing in children with critical bronchiolitis has been less studied; thus, fewer specific recommendations regarding diagnostic studies for children with critical bronchiolitis are available The American Academy of Pediatrics (AAP) suggests that radiography “should be reserved for cases in which respiratory effort is severe enough to warrant ICU admission” or when the diagnosis is unclear.41 The differential diagnosis of respiratory distress and wheeze in infants is broad and includes potentially life-threatening illness, such as congestive heart failure, anatomic abnormalities, mediastinal mass, foreign body, and bacterial pneumonia These alternate or coexisting diagnoses may be more likely in children presenting with an atypical course of bronchiolitis, including disease severe enough to warrant PICU admission.56–58 Additionally, clinicians should consider monitoring electrolytes, as children with severe bronchiolitis may be at risk for syndrome of inappropriate diuretic hormone release, and hyponatremia has been shown in multiple studies to be associated with greater illness severity.59–62 It is our practice to routinely obtain chest radiographs, complete blood cell count, and serum electrolytes in children with critical bronchiolitis Studies of the utility of these tests in the PICU setting are needed Prevention Viruses that cause bronchiolitis, such as RSV and rhinovirus, are spread via multiple mechanisms, including aerosols, direct contact with virus-containing secretions, and indirect contact (e.g., fomites).63,64 RSV can survive on surfaces for several hours Many ... with the disease, and appreciate the paucity of PICU-specific data and need for continued research This chapter will review the microbiology, epidemiology, pathophysiology, clinical presentation,... coronaviruses; enterovirus; and adenovirus are all associated with bronchiolitis.13–16 Up to one-third of children with RSV and nearly three-quarters of children with rhinovirus are coinfected.14... the United States was 31 weeks, from mid-October to early May, with a peak in early February.20 This pattern is not repeated internationally, however RSV global surveillance data from low- and