Respiratory Syncytial Virus (RSV) Bronchiolitis

Overview and Epidemiology

Respiratory syncytial virus (RSV) bronchiolitis is the leading cause of lower respiratory tract infection in infants and young children worldwide. Respiratory syncytial virus is a single-stranded negative-sense RNA virus belonging to the family Pneumoviridae (formerly classified within Paramyxoviridae); it is the most common cause of bronchiolitis and the number-one cause of infant hospitalization in the United States, accounting for an estimated 57,000 to 200,000 hospitalizations per year in children under 5 years of age.

Virtually all children are infected with respiratory syncytial virus by age 2, and reinfections occur throughout life because the immune response after primary infection is incomplete and short-lived. Two major antigenic subtypes — respiratory syncytial virus-A and respiratory syncytial virus-B — co-circulate each season, with one or the other typically dominant. In the northern hemisphere, respiratory syncytial virus season runs from October through March, peaking in December and January. Respiratory syncytial virus is transmitted via large respiratory droplets and direct contact with contaminated secretions; it survives for several hours on hard surfaces, making hand hygiene the most important infection-control measure.

Approximately 1–3% of all infants require hospitalization during their first respiratory syncytial virus season. High-risk groups with substantially greater hospitalization and mortality risk include:

• Premature infants (<35 weeks gestational age) — immature airway architecture and lung reserve
• Congenital heart disease (CHD) with hemodynamic significance — impaired cardiac reserve cannot tolerate hypoxemia
• Chronic lung disease of prematurity (bronchopulmonary dysplasia, BPD) — baseline airway inflammation and reduced lung function
• Primary or secondary immunodeficiency — prolonged viral shedding and severe disease
• Down syndrome — anatomic airway differences and higher rates of CHD
• Neuromuscular diseases — impaired cough and airway clearance mechanisms

Despite high prevalence, respiratory syncytial virus bronchiolitis is fatal in fewer than 1% of otherwise healthy term infants hospitalized in high-resource settings. The global burden is far greater in low- and middle-income countries, where respiratory syncytial virus is estimated to cause approximately 120,000 child deaths per year, predominantly in sub-Saharan Africa and South Asia.

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Pathophysiology

Understanding why bronchiolitis produces its characteristic clinical picture requires knowing both the direct viral cytopathic effects and the host inflammatory response that amplifies them.

Viral entry and fusion. Respiratory syncytial virus encodes two major surface glycoproteins: the attachment protein G, which binds nucleolin and other receptors on airway epithelial cells, and the fusion protein F, which drives viral-host membrane fusion. The prefusion conformation of F protein is the target of the most effective neutralizing antibodies — a discovery that underpins nirsevimab's design. Upon fusion, respiratory syncytial virus injects its RNA genome and replication machinery into the host cell cytoplasm.

Syncytia formation — the hallmark. As the name "respiratory syncytial" indicates, respiratory syncytial virus F protein causes adjacent infected epithelial cells to fuse into multinucleated giant cells (syncytia). This cytopathic effect destroys the ciliated pseudostratified epithelium lining the bronchioles, abolishing mucociliary clearance and triggering an intense peribronchiolar lymphocytic infiltrate.

Small airway obstruction. The combination of epithelial necrosis, mucosal edema, and profuse mucus hypersecretion fills the bronchioles (1–2 mm diameter) with cellular debris and secretions. This creates two patterns of obstruction:

• Partial obstruction (ball-valve effect): Air passes inward on inspiration (when airways widen) but is trapped on expiration (when airways narrow), producing hyperinflation and the characteristic expiratory wheeze.
• Complete obstruction: Air distal to the plug is absorbed, causing atelectasis — the patchy collapse visible on chest X-ray.

The resulting ventilation-perfusion (V/Q) mismatch drives hypoxemia, the most important physiological consequence of bronchiolitis. Work of breathing increases substantially as the infant fights against hyperinflated, non-compliant lungs, eventually risking respiratory muscle fatigue.

Why bronchodilators don't reliably help. Unlike asthma, the primary obstruction in respiratory syncytial virus bronchiolitis is mechanical (mucus plugging and edema) rather than bronchospasm. The airways of infants have relatively less smooth muscle than older children, and beta-2 adrenergic receptors are sparser in the peripheral airways. This anatomical reality explains why multiple high-quality randomized trials have shown that albuterol (salbutamol) and epinephrine provide no consistent clinical benefit in the average bronchiolitis patient.

Immune evasion. Respiratory syncytial virus non-structural proteins NS1 and NS2 actively suppress the innate interferon response, allowing prolonged viral replication and contributing to the clinical duration of 7–14 days. The resulting inflammatory state — mediated by IL-4, IL-13, and leukotriene C4 — may prime the developing airway for subsequent hyperreactivity.

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Clinical Presentation

Respiratory syncytial virus bronchiolitis follows a characteristic biphasic progression. Recognizing the normal time course helps parents and clinicians anticipate the peak of illness and identify infants who are deteriorating beyond expectation.

Days 1–2: Upper respiratory prodrome. The illness begins indistinguishably from a common cold — clear rhinorrhea, mild nasal congestion, low-grade fever (typically 38–38.5°C / 100.4–101.3°F), and a dry cough. Infants may feed slightly less well due to nasal obstruction. This phase is easily dismissed as a routine viral URI.

Days 3–5: Lower tract extension and peak severity. In vulnerable infants — particularly those under 3 months, born prematurely, or with comorbidities — the virus spreads to the lower airways. Parents notice rapid worsening:

• Tachypnea — respiratory rate >60 breaths per minute is the most sensitive early sign
• Increased work of breathing: nasal flaring, subcostal and intercostal retractions, suprasternal retractions in severe cases, and head bobbing in young infants (who use accessory neck muscles)
• Expiratory wheeze and/or diffuse bilateral crackles on auscultation
• Prolonged expiratory phase due to the ball-valve obstruction pattern
• Poor feeding — tachypnea interrupts the coordinated suck-swallow-breathe cycle; respiratory rates above 60–70 breaths/min make safe oral feeding impossible
• Hypoxia — SaO2 <95% on pulse oximetry

Apnea as a presenting sign. In infants under 6 weeks of age (especially former premature infants), apnea — cessation of breathing for >20 seconds or shorter episodes with bradycardia or color change — can be the presenting manifestation of respiratory syncytial virus bronchiolitis, even before wheeze or significant respiratory distress develops. This "apnea of respiratory syncytial virus" occurs because the virus directly suppresses central respiratory drive and because upper airway secretions trigger reflex laryngospasm. Unexplained apnea in an infant under 3 months is a common reason to test for respiratory syncytial virus.

Days 5–14: Gradual recovery. Symptoms peak around day 3–5 and then improve steadily over 7–14 days. Cough is typically the last symptom to resolve and may persist for 3–4 weeks as the airway epithelium regenerates. The "happy wheezer" — a wheezing infant who is comfortable, feeding adequately, maintaining SaO2 >95%, and whose parents can reliably monitor for deterioration — does not require hospitalization.

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Diagnosis

Respiratory syncytial virus bronchiolitis is a clinical diagnosis. The American Academy of Pediatrics (AAP) 2014 clinical practice guideline explicitly states that routine laboratory and radiologic testing is not recommended in the typical case because results do not change management. This principle reflects both cost-effectiveness and the reality that supportive care is the treatment regardless of which virus is causative.

When viral testing is indicated:

• Cohorting hospitalized patients (to prevent nosocomial respiratory syncytial virus spread by grouping respiratory syncytial virus-positive infants together)
• Epidemiological surveillance during outbreak investigation
• Distinguishing respiratory syncytial virus from influenza when antiviral therapy (oseltamivir) might be appropriate
• Immunocompromised hosts where specific identification guides antiviral decisions
• Young infants (<6 weeks) with apnea where respiratory syncytial virus diagnosis changes management intensity

Test options:

• Nasopharyngeal swab polymerase chain reaction (PCR) for respiratory syncytial virus-A and respiratory syncytial virus-B — high sensitivity (>95%) and specificity; gold standard for clinical and epidemiological diagnosis
• Multiplex respiratory viral polymerase chain reaction panels — simultaneously detect respiratory syncytial virus, influenza A/B, rhinovirus, human metapneumovirus (hMPV), parainfluenza 1–4, and others; useful when the clinical picture is atypical or coinfection is suspected
• Rapid antigen tests — lower sensitivity (~80%) than polymerase chain reaction but faster turnaround; acceptable for initial triage in settings without rapid polymerase chain reaction

Chest X-ray. CXR is NOT routinely indicated in bronchiolitis. When obtained, typical findings include bilateral hyperinflation (flattened diaphragms, increased anterior-posterior diameter), peribronchial thickening ("dirty hila"), and patchy atelectasis — most often in the right upper lobe or right middle lobe. Importantly, atelectasis is frequently mistaken for pneumonia; this misreading drives inappropriate antibiotic prescribing. CXR is reserved for cases where the diagnosis is uncertain, when severe or atypical disease is present, or when bacterial pneumonia is in the differential (e.g., persistent high fever, toxic appearance, unilateral lobar changes).

Blood tests. Complete blood count (CBC), blood cultures, and C-reactive protein (CRP) are not routinely needed. The rate of serious bacterial infection (SBI) in febrile infants with bronchiolitis is low — respiratory syncytial virus appears to partially protect against concurrent bacteremia through its own fever mechanism. Exceptions include infants under 30 days of age, toxic-appearing infants, or those with persistent high fever in whom a full sepsis evaluation is warranted.

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Treatment — Supportive Care

There is no specific antiviral therapy for respiratory syncytial virus bronchiolitis in immunocompetent infants. The AAP 2014 clinical practice guideline — the most comprehensive evidence synthesis on this topic — establishes that supportive care is the standard of treatment. In practice this means leaving out medications that do not improve outcomes and focusing on the interventions that do.

What works:

• Supplemental oxygen — the single most important intervention for hypoxic infants. Targets of SaO2 ≥90–92% are used (some guidelines use 95% as the threshold; recent evidence supports 90–92% as safe and reduces unnecessary hospitalization duration). Delivered by nasal cannula at low flow initially, and escalated as needed.
• High-flow nasal cannula (HFNC) — delivers heated, humidified blended air and oxygen at 2 L/kg/min (up to 8 L/kg/min in infants). Proposed mechanisms include positive distending pressure (reduces atelectasis), washout of nasopharyngeal dead space, and reduction of inspiratory work of breathing. HFNC has become widely adopted in pediatric wards and HDUs as a step-up from standard-flow O2 that may prevent intubation; in the randomized controlled trial (RCT) known as PARIS in Australia and New Zealand (Franklin and colleagues, 2018), 1,472 infants with bronchiolitis treated outside intensive care were assigned to high-flow or standard oxygen; escalation of care was needed in 12% of the high-flow group versus 23% of the standard-oxygen group, with no difference in length of hospital stay or duration of oxygen therapy.
• Fluid support — infants unable to maintain adequate oral intake require intravenous (IV) or nasogastric fluids to prevent dehydration. Respiratory rates above 60–70 breaths/min make coordinated oral feeding unsafe; nasogastric feeding is appropriate for infants with moderate respiratory distress who can tolerate enteral feeds. Intravenous fluids are given as isotonic saline (0.9% NaCl), because hypotonic fluids carry a risk of low blood sodium when SIADH is possible from positive-pressure breathing.
• Nasal suctioning — gentle bulb or suction catheter clearance of copious nasal secretions improves airway patency and reduces feeding difficulty; particularly useful immediately before feeds. Deep nasopharyngeal suctioning is not routinely recommended.

What the research does not support:

• Bronchodilators (albuterol/salbutamol) — multiple large randomized trials consistently show no benefit on oxygen saturation, hospitalization rate, or length of stay in the average infant with bronchiolitis. Some clinicians give a single trial dose of albuterol and stop it if there is no clear objective improvement within 1 hour; the trials give no rationale for repeated or standing nebulized albuterol.
• Epinephrine (adrenaline) — not recommended for outpatient bronchiolitis. Inpatient use remains contentious; while some trials show short-term improvement in clinical scores, no mortality or hospitalization-duration benefit has been demonstrated in high-quality trials.
• Systemic or inhaled corticosteroids — multiple high-quality randomized controlled trials (RCTs) (including the large PECARN dexamethasone trial of 600 infants, in which hospital admission was 39.7% with dexamethasone versus 41.0% with placebo) demonstrate no benefit for dexamethasone, prednisolone, or inhaled corticosteroids on any clinical outcome in respiratory syncytial virus bronchiolitis. Steroids are not part of standard care.
• Antibiotics — indicated only for documented secondary bacterial infection (otitis media, bacterial pneumonia). Routine antibiotics do not shorten bronchiolitis illness duration and drive antibiotic resistance.
• Chest physiotherapy — not recommended; active vibration and percussion in an already-exhausted, hypoxic infant provides no benefit and adds unnecessary distress.
• Hypertonic saline nebulization (3%) — a 2017 Cochrane review of 28 trials (4,195 infants) found that it may modestly shorten hospital stay (by about 0.4 days) and may reduce hospital admission among outpatients and emergency department patients, with evidence the authors rated low to moderate in quality. Current AAP guidance does not recommend routine hypertonic saline.
• Ribavirin — an antiviral agent that is not recommended outside immunocompromised hosts (e.g., post-transplant patients on immunosuppression) due to toxicity, cost, and lack of efficacy in healthy infants.

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Indications for Hospitalization

Most infants with respiratory syncytial virus bronchiolitis can be safely managed at home with careful parental education about warning signs. The decision to hospitalize is individualized and guided by clinical severity, physiological parameters, age, comorbidities, and social factors.

Clinical criteria for hospitalization:

• Hypoxia — SaO2 persistently <90–92% on room air
• Respiratory distress — respiratory rate >70 breaths/min, severe retractions, grunting, or head bobbing suggesting impending respiratory failure
• Apnea — any episode of apnea, regardless of severity, in an infant under 3 months
• Poor oral intake — inability to maintain >50% of normal feeding volume (rough threshold: >20% weight loss from baseline, or clinical dehydration with decreased wet diapers)

Patient-specific risk factors driving a lower threshold for admission:

• Age <6–12 weeks — particularly <6 weeks for any respiratory distress; immature respiratory control and tiny airways provide no reserve
• Former premature birth (<35 weeks gestational age)
• Congenital heart disease with hemodynamic significance (cyanotic CHD or significant left-to-right shunts)
• Chronic lung disease of prematurity (BPD)
• Immunodeficiency
• Neuromuscular disease impairing cough and airway clearance

Social and logistic factors:

• Parental inability to reliably monitor for deterioration or to return quickly if worsening
• No telephone access or significant transport time to emergency care
• Physician judgment that the family cannot safely manage at home

PICU admission criteria: FiO2 >0.5 to maintain target saturation; failure of HFNC (persistent tachypnea >70–80/min, SaO2 <90%, increasing distress); mechanical ventilation requirement for refractory apnea or respiratory failure. Ventilated infants with respiratory syncytial virus bronchiolitis typically require lung-protective strategies accounting for the severe air trapping (short inspiratory time, long expiratory time, low PEEP to avoid worsening hyperinflation).

Discharge criteria: SaO2 ≥90–92% in room air while awake and asleep; able to maintain adequate oral feeds (>50% of usual intake); respiratory rate <60 breaths/min; caregiver education and comfort with outpatient monitoring; close follow-up arranged within 24–48 hours for infants at continuing risk.

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Prevention — Nirsevimab and Maternal Respiratory Syncytial Virus Vaccine

The prevention landscape for infant respiratory syncytial virus disease was transformed between 2023 and 2024 by two new products: a long-acting monoclonal antibody for direct infant immunization and a maternal vaccine that confers passive protection to the newborn. These represent the most significant advance in respiratory syncytial virus prevention since the introduction of palivizumab in 1998. In June 2025 the U.S. Food and Drug Administration approved a second long-acting infant monoclonal antibody, clesrovimab, for infants born during or entering their first respiratory syncytial virus season.

Nirsevimab. U.S. Food and Drug Administration-approved on 17 July 2023. Nirsevimab is a recombinant human IgG1 monoclonal antibody engineered to bind the prefusion conformation of respiratory syncytial virus F protein with extremely high affinity — the same epitope targeted by the most potent naturally occurring neutralizing antibodies. Three modifications distinguish it from older antibodies: a triple amino acid substitution (YTE modification) extends the half-life to approximately 70 days (compared to 20 days for palivizumab), enabling a single injection to provide approximately 150 days of protection through a respiratory syncytial virus season.

CDC and ACIP recommend an infant respiratory syncytial virus antibody for infants younger than 8 months born during or entering their first respiratory syncytial virus season (October–March in the northern hemisphere) when the mother did not receive a respiratory syncytial virus vaccine during pregnancy, her vaccination status is unknown, or the infant was born within 14 days of her vaccination — not limited to high-risk infants. For some children aged 8–19 months at increased risk of severe disease (for example chronic lung disease of prematurity needing medical support, or severe immunocompromise) who are entering their second respiratory syncytial virus season, a second-season dose of nirsevimab (200 mg) is recommended; the FDA label allows use up to 24 months of age.

Phase 3 efficacy data from the MELODY trial (Hammitt LL et al., NEJM 2022): nirsevimab reduced medically attended respiratory syncytial virus-associated lower respiratory tract infections by 74.5% compared to placebo in healthy late-preterm and term infants. Hospitalization for respiratory syncytial virus-associated lower respiratory tract infection was 62.1% lower, a difference that did not reach statistical significance (P = 0.07). The safety profile was comparable to placebo.

Nirsevimab supersedes palivizumab for the general infant population. Palivizumab remains appropriate for infants with CHD with hemodynamic significance, BPD on medical treatment, or gestational age ≤28 weeks during their second respiratory syncytial virus season when nirsevimab is not available or accessible.

Maternal respiratory syncytial virus vaccine (the maternal RSV prefusion F protein vaccine). U.S. Food and Drug Administration-approved for use in pregnancy on 21 August 2023, for administration at 32–36 weeks of gestation. The vaccine contains bivalent prefusion-stabilized respiratory syncytial virus F proteins (respiratory syncytial virus-A and respiratory syncytial virus-B). A single intramuscular dose primes the maternal immune system; the resulting immunoglobulin G (IgG) antibodies cross the placenta during the third trimester, conferring passive immunity to the newborn for the first 6 months of life — the window of maximum vulnerability.

The phase 3 MATISSE trial (Maternal Immunization Study for Safety and Efficacy; Kampmann B et al., NEJM 2023): maternal vaccination reduced medically attended severe respiratory syncytial virus-associated lower respiratory tract illness in infants during the first 90 days of life by 81.8%, and during the first 180 days of life by 69.4%. Against medically attended respiratory syncytial virus-associated lower respiratory tract illness of any severity, efficacy in the first 90 days was 57.1%, which did not meet the trial's statistical success criterion.

Choosing between maternal vaccine and nirsevimab: Both options are endorsed by ACIP; the choice is context-dependent. The maternal vaccine is administered prenatally and requires no postnatal intervention; nirsevimab is a postnatal injection but can be timed precisely to the respiratory syncytial virus season and covers infants born to mothers who were not vaccinated during pregnancy. CDC guidance states that most infants will not need both: except in rare circumstances, an infant antibody is not needed for infants born 14 or more days after the mother's vaccination, and it is recommended when the mother's vaccination status is unknown.

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Post-RSV Wheezing and Long-Term Outcomes

For most families, the most enduring question after a respiratory syncytial virus hospitalization is: "Will my child develop asthma?" The epidemiological association between early severe respiratory syncytial virus bronchiolitis and subsequent recurrent wheeze and asthma is robust, but the causal interpretation remains actively debated.

The epidemiological signal. Approximately 30–40% of infants hospitalized with respiratory syncytial virus bronchiolitis develop recurrent wheezing episodes during early childhood. Compared to infants without respiratory syncytial virus hospitalizations, those with severe early respiratory syncytial virus bronchiolitis have an approximately 2–3-fold higher odds of an asthma diagnosis by school age in multiple cohort studies. This association is independent of atopic family history, though atopy amplifies it.

Two competing hypotheses:

• The respiratory syncytial virus-priming hypothesis: respiratory syncytial virus bronchiolitis directly injures the developing airway epithelium and primes the immune system toward a Th2-skewed, pro-inflammatory phenotype, increasing susceptibility to allergen sensitization and airway hyperreactivity. Supporting evidence: the association persists after controlling for atopic predisposition; respiratory syncytial virus activates IL-4, IL-13, and leukotriene pathways that mediate asthma; RSV NS proteins suppress IFN-gamma responses that normally suppress Th2 cells.
• The susceptibility hypothesis ("tracking" or "dual hypothesis"): Children genetically or developmentally predisposed to develop asthma simply manifest their airway hyperreactivity earlier during respiratory syncytial virus infection — respiratory syncytial virus bronchiolitis is a marker, not a cause. Supporting evidence: prospective studies show that lung function differences predating respiratory syncytial virus exposure predict who develops post-viral wheeze; identical twin studies suggest shared genetic determinism of both respiratory syncytial virus severity and asthma risk.

Rhinovirus vs. Respiratory syncytial virus. Data from the COAST (Childhood Origins of ASThma) birth cohort and other studies demonstrate that rhinovirus-associated wheezing illness in the first 3 years of life — particularly in atopic children — is an even stronger predictor of school-age asthma than respiratory syncytial virus bronchiolitis. This suggests the causal picture is complex: it is likely that severe early viral lower respiratory illness of any type, in a genetically susceptible host, interacts with aeroallergen sensitization to shape the asthma trajectory.

Long-term outcomes by severity. Premature infants hospitalized with respiratory syncytial virus bronchiolitis have the highest rates of subsequent obstructive airway disease; their baseline airway hyperreactivity and reduced lung reserve from prematurity are compounded by respiratory syncytial virus-driven inflammation. School-age children with a history of severe respiratory syncytial virus bronchiolitis in infancy show measurable differences in spirometry (lower FEV1/FVC ratios) even in the absence of a clinical asthma diagnosis.

Treatment during the illness and long-term wheeze risk. Despite the plausible biological rationale, no randomized controlled trial of any treatment during the acute respiratory syncytial virus episode — including azithromycin, corticosteroids, or montelukast — has demonstrated a reduction in subsequent wheezing or asthma diagnoses. The post-RSV wheezing trajectory appears to be determined by factors that precede or are independent of the acute illness.

Counseling families. Most children with post-RSV wheezing substantially improve by school age; the majority do not have persistent asthma. Recurrent wheezing with later respiratory illnesses is the pattern families watch for. The presence of post-RSV wheeze does not mean the child has asthma; frequent or severe episodes are the usual reason for evaluation by a pediatric pulmonologist or allergist.

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Key Research Papers

1. Hammitt LL, Dagan R, Yuan Y, et al. Nirsevimab for Prevention of RSV in Healthy Late-Preterm and Term Infants. N Engl J Med. 2022;386(9):837–846. — Phase 3 randomized controlled trial demonstrating 74.5% efficacy of a single dose of nirsevimab against medically attended RSV-associated lower respiratory tract infection in healthy late-preterm and term infants, leading to FDA approval in 2023. — PubMed PMID: 35235726
2. Kampmann B, Madhi SA, Munjal I, et al. Bivalent Prefusion F Vaccine in Pregnancy to Prevent RSV Illness in Infants. N Engl J Med. 2023;388(16):1451–1464. — Phase 3 MATISSE trial of maternal RSV vaccination with the bivalent RSV prefusion F protein vaccine showing 81.8% efficacy against severe RSV-associated lower respiratory infections in the first 90 days of infant life, establishing the maternal immunization strategy. — PubMed PMID: 37018474
3. Ralston SL, Lieberthal AS, Meissner HC, et al. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics. 2014;134(5):e1474–e1502. — The foundational AAP clinical practice guideline establishing evidence-based recommendations for the diagnosis and management of bronchiolitis; the primary source for the "supportive care only" standard in RSV bronchiolitis management. — PubMed PMID: 25349312
4. Shay DK, Holman RC, Newman RD, et al. Bronchiolitis-associated hospitalizations among US children, 1980–1996. JAMA. 1999;282(15):1440–1446. — Landmark epidemiological study quantifying the national burden of bronchiolitis hospitalizations in the United States; established RSV bronchiolitis as the leading cause of infant hospitalization and documented rising hospitalization trends. — PubMed PMID: 10535434
5. Griffin MP, Yuan Y, Takas T, et al. Single-Dose Nirsevimab for Prevention of RSV in Preterm Infants. N Engl J Med. 2020;383(5):415–425. — Phase 2–3 trial of nirsevimab in preterm infants (29–35 weeks gestational age); demonstrated 70.1% efficacy against medically attended lower respiratory tract infections, establishing the dose and safety profile in the highest-risk preterm population. — PubMed PMID: 32726528
6. Zorc JJ, Hall CB. Bronchiolitis: recent evidence on diagnosis and management. Pediatrics. 2010;125(2):342–349. — Comprehensive clinical review synthesizing evidence on RSV bronchiolitis diagnosis, management, and prevention; widely used as a reference for the evidence base underlying supportive-care-only guidelines. — PubMed PMID: 20100768
7. Fernandes RM et al., 2013 — Glucocorticoids for Acute Viral Bronchiolitis in Infants and Young Children (Cochrane Review) — Cochrane Database of Systematic Reviews — Systematic review and meta-analysis of 17 RCTs examining corticosteroid use in bronchiolitis; demonstrated no significant benefit on hospitalization rates, length of stay, or clinical severity scores, supporting guideline recommendations against routine corticosteroid use. — PubMed PMID: 23733383
8. Hartling L, Bialy LM, Vandermeer B, et al. Epinephrine for bronchiolitis. Cochrane Database Syst Rev. 2011;(6):CD003123. — Cochrane review of 19 studies (2,256 participants); among outpatients, epinephrine reduced admissions at day 1 but not at day 7 compared with placebo, and there was no difference in length of stay for inpatients. — PubMed PMID: 21678340
9. Stein RT, Sherrill D, Morgan WJ, et al. Respiratory syncytial virus in early life and risk of wheeze and allergy by age 13 years. Lancet. 1999;354(9178):541–545. — Tucson Children's Respiratory Study long-term follow-up demonstrating that RSV lower respiratory illness before age 3 increased the risk of frequent wheeze by age 6 (odds ratio 4.3), with the risk no longer significant by age 13; seminal paper in the post-RSV wheeze literature. — PubMed PMID: 10470697
10. Jackson DJ, Gangnon RE, Evans MD, et al. Wheezing rhinovirus illnesses in early life predict asthma development in high-risk children. Am J Respir Crit Care Med. 2008;178(7):667–672. — Childhood Origins of ASThma (COAST) birth cohort of 259 children demonstrating that rhinovirus wheezing illness in the first 3 years of life was the strongest predictor of asthma at age 6, providing important context to the RSV-asthma association. — PubMed PMID: 18565953
11. Franklin D, Babl FE, Schlapbach LJ, et al. A Randomized Trial of High-Flow Oxygen Therapy in Infants with Bronchiolitis. N Engl J Med. 2018;378(12):1121–1131. — PARIS trial of 1,472 infants treated outside intensive care; escalation of care (the primary outcome) was 12% with high-flow oxygen versus 23% with standard oxygen, with no difference in length of hospital stay or duration of oxygen therapy. — PubMed PMID: 29562151
12. Zhang L, Mendoza-Sassi RA, Wainwright C, Klassen TP. Nebulised hypertonic saline solution for acute bronchiolitis in infants. Cochrane Database Syst Rev. 2017;12(12):CD006458. — Cochrane review of 28 trials (4,195 infants); hypertonic saline may modestly reduce length of stay in hospitalized infants (by about 0.4 days) and may reduce hospitalization among outpatients and emergency department patients; evidence rated low to moderate quality. — PubMed PMID: 29265171
13. Corneli HM, Zorc JJ, Mahajan P, et al. A multicenter, randomized, controlled trial of dexamethasone for bronchiolitis. N Engl J Med. 2007;357(4):331–339. — PECARN trial of 600 infants; a single dose of oral dexamethasone (1 mg/kg) did not change the rate of hospital admission (39.7% versus 41.0% with placebo). — PubMed PMID: 17652648

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Connections

• Pediatrics
• Croup
• Febrile Seizures
• Neonatal Jaundice
• Respiratory Syncytial Virus (General)
• Asthma
• Bronchitis
• Pneumonia
• Bronchiectasis
• Bronchiolitis — the general infant condition; respiratory syncytial virus is its single most common cause.

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