Bronchiolitis

1. Overview and Epidemiology
2. Pathophysiology
3. Risk Factors for Severe Disease
4. Clinical Presentation
5. Severity Assessment
6. Diagnosis
7. Treatment — Supportive Care
8. Treatment — High-Flow Nasal Cannula
9. What Does NOT Work
10. Indications for Hospitalization
11. Prevention
12. Key Research Papers
13. Connections

Overview and Epidemiology

Bronchiolitis is an acute viral lower respiratory tract infection causing inflammation and obstruction of the small airways (bronchioles). It is the single leading cause of infant hospitalization in the United States, accounting for approximately 50,000–80,000 hospitalizations per year in children under two years of age and generating roughly 2.1 million outpatient and emergency department visits annually.

The condition is caused by a range of respiratory viruses, not a single pathogen:

• Respiratory syncytial virus (RSV): The dominant cause, responsible for 50–75% of bronchiolitis cases. RSV has two circulating antigenic subtypes (A and B) and follows a predictable winter epidemic pattern in temperate climates.
• Rhinovirus: The second most common cause, accounting for 20–30% of cases. Rhinovirus-associated bronchiolitis tends to be less severe overall but peaks in autumn and spring, extending the season beyond RSV's winter dominance.
• Human metapneumovirus (hMPV): Responsible for approximately 5–10% of cases; clinically similar to RSV bronchiolitis and peaks in late winter and early spring.
• Parainfluenza viruses (types 1–3): Contribute a smaller but notable proportion; type 3 in particular can cause bronchiolitis in very young infants.
• Adenovirus, bocavirus, coronavirus, influenza: Less frequent but recognized causes, especially in immunocompromised or hospitalized children.

Peak vulnerability occurs between 2 and 6 months of age, when maternally derived antibody wanes and the infant's own immune system remains immature. The disease is uncommon after 24 months of age because larger airway caliber blunts the obstructive impact of mucosal edema. Seasonality in the Northern Hemisphere runs from November through March, with RSV epidemics peaking in December–January.

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Pathophysiology

Bronchiolitis results from a cascade of viral-driven injury to the small conducting airways rather than from true bronchospasm, a distinction that directly explains why bronchodilators fail.

The sequence of events:

1. Viral inoculation and replication: Inhaled virus attaches to apical ciliated columnar epithelial cells of the bronchioles. RSV uses the G protein to bind ICAM-1 and other surface receptors; rhinovirus uses ICAM-1 on lower airway epithelium. Replication occurs rapidly within 1–2 days of exposure.
2. Epithelial necrosis and sloughing: Infected cells undergo necrosis and apoptosis. Ciliated epithelium is destroyed, impairing mucociliary clearance and depositing cellular debris into the bronchiolar lumen.
3. Peribronchiolar inflammation: Innate immune activation triggers mast cell degranulation and recruitment of neutrophils and lymphocytes into the airway wall and submucosa, causing pronounced mucosal edema.
4. Luminal obstruction: The combination of sloughed epithelium, inflammatory exudate, excess mucus production, and edematous walls dramatically narrows the lumen of airways that are already only 1–2 mm in diameter. Small absolute reductions in radius cause disproportionately large increases in resistance (Poiseuille's law: resistance ∝ 1/r⁴).
5. Air trapping and atelectasis: Partial obstruction acts as a check-valve, allowing air in on inhalation (when airways dilate) but preventing it from exiting on exhalation (when airways narrow). This creates distal air trapping and hyperinflation. Complete obstruction leads to resorption atelectasis of distal alveoli. Both processes coexist in the same lung, often in adjacent segments.
6. Ventilation-perfusion (V/Q) mismatch: Atelectatic segments receive perfusion but no ventilation (shunt), while hyperinflated regions are ventilated but overstretched and poorly perfused (dead space). The resulting V/Q mismatch drives hypoxemia and, in severe cases, hypercapnia as the infant's respiratory muscles fatigue.

Because the obstruction is mechanical — not smooth-muscle mediated — inhaled beta-2 agonists (albuterol) cannot reverse it. This distinguishes bronchiolitis from asthma, where smooth-muscle bronchospasm is the primary mechanism.

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Risk Factors for Severe Disease

Most infants with bronchiolitis experience a self-limiting illness managed at home. The following factors predict a higher risk of severe disease, hospitalization, and need for intensive respiratory support:

• Prematurity (<35 weeks gestational age): Underdeveloped airways, surfactant deficiency, and blunted immune responses make premature infants significantly more vulnerable. Risk is highest in the first two RSV seasons.
• Age <3 months: Narrow airway caliber and obligate nasal breathing make even mild mucosal edema clinically significant. Apnea — sometimes the presenting symptom — is far more common in this age group.
• Congenital heart disease (CHD): Particularly lesions with increased pulmonary blood flow (VSD, AV canal) or those relying on pulmonary vascular resistance balance. Hypoxemia from bronchiolitis is poorly tolerated.
• Chronic lung disease (CLD) / bronchopulmonary dysplasia (BPD): Already-compromised gas exchange reserves leave little margin for additional V/Q mismatch.
• Immunodeficiency: T-cell deficiencies, severe combined immunodeficiency (SCID), DiGeorge syndrome, and transplant immunosuppression allow prolonged viral replication and atypical severe presentations.
• Tobacco smoke exposure: Prenatal and postnatal exposure impairs mucociliary clearance, increases airway inflammation, and roughly doubles the risk of severe RSV disease.
• Absence of breastfeeding: Breast milk provides secretory IgA, lactoferrin, and anti-inflammatory cytokines that reduce RSV severity; formula-fed infants have measurably higher hospitalization rates.
• Household crowding and daycare attendance: Increases viral exposure density, particularly for RSV and rhinovirus.

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Clinical Presentation

Bronchiolitis evolves in a predictable biphasic pattern over 7–14 days:

Upper respiratory prodrome (days 1–3): The illness begins with symptoms indistinguishable from a common cold — rhinorrhea (often copious and clear), mild cough, and low-grade fever (38–38.5°C). Parents frequently report that a sibling or caregiver had a "cold" the week before. Feeding remains mostly normal in this phase.

Lower respiratory phase (days 3–7): Virus descends to the bronchioles and the picture changes rapidly. The cardinal signs are:

• Tachypnea: Respiratory rate above 60 breaths/min in young infants is common and is the most sensitive early sign of lower tract involvement.
• Wheezing: Polyphonic expiratory wheeze from multiple narrowed airways; may be audible without a stethoscope. Crackles (rales) on auscultation reflect airway secretions and atelectasis.
• Retractions: Subcostal and intercostal retractions signal increased work of breathing. Suprasternal and sternal retractions indicate more severe obstruction.
• Nasal flaring: An accessory respiratory muscle sign, particularly prominent in young infants.
• Poor feeding: Increased work of breathing, nasal congestion, and tachypnea disrupt the suck-breathe-swallow sequence, reducing oral intake significantly.

Apnea: In infants under 2 months (especially former premature infants), apnea may be the presenting or predominant sign, occurring before or in the absence of obvious respiratory distress. Central apnea from RSV has distinct pathophysiology involving brainstem effects of viral neuroinvasion or hypoxia-triggered respiratory inhibition.

Peak and resolution: Symptoms peak on days 3–5. SpO2 naturally nadirs during this period. Feeding difficulty often persists beyond resolution of wheezing. Cough may linger for 2–3 weeks. Most previously healthy infants recover fully within 14 days.

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Severity Assessment

The American Academy of Pediatrics (AAP) and most clinical protocols stratify bronchiolitis severity to guide disposition decisions. Pulse oximetry is the cornerstone of objective assessment.

Mild bronchiolitis:

• SpO2 ≥95% on room air
• Respiratory rate <60 breaths/min
• Mild retractions or none
• Alert and interactive; adequate feeding (≥50% of normal intake)
• No apnea

Moderate bronchiolitis:

• SpO2 90–94% on room air
• Respiratory rate 60–70 breaths/min
• Moderate intercostal or subcostal retractions
• Irritable but consolable; reduced but present oral intake
• No apnea

Severe bronchiolitis:

• SpO2 <90% on room air
• Respiratory rate >70 breaths/min
• Severe retractions; suprasternal or sternal involvement; head bobbing
• Markedly decreased or absent feeding; lethargy or poor responsiveness
• Apnea (any episode)
• Cyanosis

Respiratory distress scoring systems such as the Respiratory Distress Assessment Instrument (RDAI) or the Bronchiolitis Severity Score (BSS) combine auscultatory findings, retractions, and respiratory rate into a composite score. These are research tools more than bedside mandates, but they improve inter-rater reliability and are commonly used in clinical trials.

Apnea as a danger sign: Any documented or witnessed apnea in an infant with bronchiolitis — regardless of current oxygen saturation — warrants hospital admission and cardiorespiratory monitoring. Apnea can be abrupt and silent; it remains one of the leading causes of bronchiolitis-related death.

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Diagnosis

The AAP 2014 Clinical Practice Guideline (updated 2021) is explicit: bronchiolitis is a clinical diagnosis. The history and physical examination are sufficient in the vast majority of cases, and the guideline actively discourages reflex testing that does not change management.

What clinicians should do:

• Pulse oximetry: Essential for all infants with suspected bronchiolitis. SpO2 is the primary objective parameter guiding oxygen therapy, admission, and discharge decisions.
• History and examination: Age, gestational age, risk factors, feeding intake, apnea episodes, and careful auscultation (wheeze, crackles, air entry) drive management decisions more reliably than any test.

What clinicians should NOT routinely do:

• Viral testing (RSV, influenza, respiratory panel): The AAP guideline recommends against routine viral testing because it rarely changes management. A positive RSV test does not alter treatment; a negative result does not exclude bronchiolitis from another virus. Exception: cohorting of hospitalized patients to reduce nosocomial spread may justify RSV rapid testing in an inpatient setting.
• Chest radiography (CXR): Routine CXR is not recommended. Radiographic findings in bronchiolitis (peribronchial thickening, hyperinflation, patchy infiltrates from atelectasis) are nonspecific and frequently misinterpreted as pneumonia, leading to unnecessary antibiotic prescriptions. CXR is indicated when the diagnosis is uncertain (e.g., unilateral findings, suspected foreign body, clinical deterioration), in severe disease requiring intensive care, or when a complication such as pneumothorax is suspected.
• Complete blood count (CBC): A normal or mildly elevated white cell count does not exclude secondary bacterial infection, and an elevated count does not confirm it. CBC is not part of routine bronchiolitis evaluation.
• Blood cultures and lumbar puncture: Reserved for infants who appear septic, are under 1 month of age, or have an unusually toxic presentation suggesting bacterial co-infection.

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Treatment — Supportive Care

Supportive care is the cornerstone and only evidence-based treatment for bronchiolitis. No pharmacologic intervention has demonstrated consistent benefit in unselected infants with bronchiolitis. The goals are to maintain oxygenation, preserve hydration, reduce work of breathing, and allow the natural viral illness to resolve.

Supplemental oxygen:

• Indicated when SpO2 falls below 90–92% on room air. The AAP 2014 guideline uses a threshold of 90%; many centers use 92% to allow a safety margin and reduce the frequency of desaturations triggering nursing interventions.
• Delivery method escalates from nasal cannula (low-flow) → high-flow nasal cannula → CPAP → mechanical ventilation depending on severity.
• Continuous SpO2 monitoring is appropriate in admitted infants; intermittent monitoring is sufficient once the infant is clinically stable and feeding well.

Nasal suctioning:

• Bulb syringe or wall-suction nasal suctioning to clear secretions before feeding and as needed for comfort.
• Nasopharyngeal (deep) suctioning temporarily relieves obstruction in mechanically ventilated or HFNC patients but causes transient desaturation; reserve for clinical need rather than routine schedule.
• Saline drops before suctioning loosen thick secretions and may improve feeding tolerance.

Hydration:

• Adequate hydration maintains mucociliary function and prevents dehydration from reduced oral intake and increased insensible losses from tachypnea.
• Oral or nasogastric (NG) feeding is preferred over IV fluids when safely tolerated, as it avoids the risks of peripheral IV insertion and hyponatremia from excessive hypotonic IV fluids.
• IV fluids (isotonic saline-based solutions) are indicated when respiratory rate exceeds 60–70 breaths/min (making safe swallowing impossible) or when the infant is significantly dehydrated.

Positioning and environment:

• Head-of-bed elevation at 30° reduces aspiration risk and may slightly reduce work of breathing, though evidence is limited.
• A calm, low-stimulation environment reduces crying — which dramatically worsens V/Q mismatch — and lowers oxygen demand.
• Clustering of nursing care (vital signs, assessments, suctioning) minimizes disturbance intervals.

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Treatment — High-Flow Nasal Cannula

High-flow nasal cannula (HFNC) therapy has become the standard of care for moderate-to-severe bronchiolitis that fails conventional low-flow oxygen. It represents the most significant advance in bronchiolitis management of the past two decades.

How HFNC works:

• Flushing nasopharyngeal dead space: High gas flows wash out CO2 that accumulates in the nasopharynx, reducing rebreathing and improving effective alveolar ventilation.
• Positive distending pressure: Flows exceeding the infant's peak inspiratory flow generate a small but consistent positive end-expiratory pressure (PEEP, typically 2–5 cmH2O), stenting open edematous bronchioles and recruiting atelectatic alveoli.
• Heated humidification: Gas is warmed to 37°C and humidified to 100% relative humidity, preventing cold-dry gas-induced mucosal injury and reducing metabolic cost of airway humidification.
• Reduction in work of breathing: By reducing resistive and elastic work, HFNC decreases respiratory rate, retractions, and accessory muscle use within 1–4 hours of initiation in most responders.

Dosing and initiation:

• Standard starting flow: 2 L/kg/min (commonly capped at 20–25 L/min in larger infants).
• FiO2 is titrated to maintain SpO2 ≥92–95%.
• An appropriately sized cannula should occlude no more than 50% of the naris to allow pressure equilibration and prevent inadvertent excessive PEEP.

Evidence base:

• Multiple randomized controlled trials and large observational cohort studies demonstrate that HFNC reduces escalation to intensive care, decreases intubation rates, and improves physiologic parameters more rapidly than standard low-flow oxygen.
• The PARIS trial (Franklin et al., NEJM 2018, PMID 29561606) — the largest bronchiolitis HFNC RCT — found that early HFNC in the emergency department reduced treatment failure by 50% compared with standard low-flow oxygen (12% vs. 23%).
• HFNC is now widely considered standard of care for moderate-to-severe bronchiolitis at centers with PICU backup. It is initiated in the emergency department or general pediatric ward and allows many infants to avoid PICU transfer.

Failure criteria and escalation:

• Failure to improve within 1–2 hours of HFNC at adequate flow and FiO2 should prompt consideration of CPAP, non-invasive positive pressure ventilation (NIPPV), or intubation.
• HFNC does not negate the need for close monitoring; deterioration can be sudden, particularly with apnea.

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What Does NOT Work

Evidence-based medicine in bronchiolitis is largely a story of negative trials. Decades of rigorously conducted RCTs have failed to demonstrate benefit from interventions that remain intuitively attractive or are widely requested by parents. The AAP guideline reflects this evidence by issuing strong recommendations against several common treatments.

Albuterol (and other beta-2 agonists):

• The AAP recommends clinicians should not administer albuterol (salbutamol) or other beta-2 agonists to infants with bronchiolitis (strong recommendation, Grade A evidence).
• Rationale: Airway obstruction in bronchiolitis is mechanical (debris, edema, cellular necrosis), not bronchospasm. There is no smooth-muscle component to relax.
• Multiple placebo-controlled trials — including a large JAMA 2020 RCT (Schuh et al., PMID 32155268) — show no reduction in hospitalization rate, length of stay, or symptom duration. Transient perceived improvements on clinical scoring may represent arousal effects of aerosol administration.

Racemic epinephrine:

• While nebulized epinephrine produces short-term (30–60 min) improvements in clinical scores through vasoconstriction and brief bronchodilation, multiple trials demonstrate no benefit on hospitalization rate or length of stay when given in the outpatient or emergency department setting.
• A landmark NEJM 2009 RCT (Plint et al., PMID 19494219) and Cochrane meta-analysis (Hartling et al., 2011, PMID 21328266) confirm no sustained benefit.
• The rebound effect after epinephrine wears off means infants who appear improved at 2 hours may deteriorate upon return home — a safety concern that makes outpatient epinephrine use problematic.

Systemic corticosteroids (dexamethasone, prednisolone):

• Multiple large RCTs, including the Plint et al. epinephrine-plus-dexamethasone trial and subsequent Cochrane reviews (Fernandes et al., 2013, PMID 22696338), show no benefit of systemic steroids for bronchiolitis hospitalization rate, length of stay, or symptom duration.
• The AAP recommends clinicians should not administer systemic corticosteroids to infants with bronchiolitis in any setting (strong recommendation, Grade A evidence).
• This differs from croup and from true asthma exacerbations, where steroids are first-line. Bronchiolitis is not asthma — the two conditions are mechanistically distinct.

Inhaled hypertonic saline:

• Initial trials suggested benefit in hospitalized infants; however, a 2015 NEJM RCT (Florin et al., and the SABRE trial) showed no reduction in hospitalization rate when administered in the emergency department. The AAP guideline (updated 2021) does not recommend hypertonic saline for the ED setting but allows for its use in hospitalized patients, where the evidence is mixed.

Ribavirin:

• The antiviral ribavirin has theoretical activity against RSV but is not recommended for routine bronchiolitis given poor clinical efficacy, high cost, significant toxicity, and difficult administration (inhaled). Its use is limited to severely immunocompromised patients in consultation with specialists.

Antibiotics:

• Bronchiolitis is a viral disease. Antibiotics have no role unless a secondary bacterial infection (pneumonia, otitis media, urinary tract infection) is specifically identified. Secondary bacterial pneumonia complicating bronchiolitis is uncommon. Reflexive antibiotic prescribing contributes to antimicrobial resistance without clinical benefit.

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Indications for Hospitalization

The decision to admit reflects a gestalt of oxygen saturation, work of breathing, hydration status, age, risk factors, and parental ability to monitor and return quickly. The following are evidence-based criteria:

Definitive indications:

• SpO2 <90–92% on room air that requires supplemental oxygen to maintain; the infant cannot be safely weaned to room air in the emergency department.
• Apnea — any witnessed or documented apneic episode, regardless of current SpO2.
• Severe respiratory distress — respiratory rate >70/min, significant retractions, head bobbing, grunting, inability to maintain oxygenation despite supplemental oxygen.
• Dehydration — inability to tolerate sufficient oral intake (typically defined as <50% of usual intake), signs of dehydration, or need for IV or nasogastric hydration.

High-risk patient characteristics that lower the threshold:

• Age <2 months (corrected gestational age preferred for premature infants)
• Gestational age <35 weeks at birth in first 2 RSV seasons
• Congenital heart disease (especially hemodynamically significant)
• Chronic lung disease / BPD
• Immunodeficiency or active immunosuppression
• Neuromuscular disease impairing respiratory reserve
• Social factors: distant home, limited transport, parental inability to recognize deterioration or return promptly

Discharge criteria:

• SpO2 ≥90–92% on room air consistently for 4–6 hours (not just transiently between feeds)
• Adequate oral hydration maintained without assistance
• Respiratory distress resolved or mild and stable
• No apnea in preceding observation period
• Parents/caregivers comfortable with monitoring and have explicit return precautions

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Prevention

RSV-specific prevention has been transformed since 2023 by the FDA approval of nirsevimab (brand name Beyfortus), a long-acting monoclonal antibody that provides passive immunity through an entire RSV season from a single intramuscular injection.

Nirsevimab (Beyfortus):

• Mechanism: A recombinant IgG1 monoclonal antibody with half-life-extended Fc modifications (YTE mutations), targeting the RSV prefusion F protein. Unlike older antibodies, its engineered half-life (~70 days) enables a single-dose seasonal strategy.
• Efficacy: The MELODY trial (FDA pivotal trial) demonstrated 74.5% reduction in medically attended RSV lower respiratory tract disease and 77.3% reduction in RSV-associated hospitalization versus placebo. The HARMONIE open-label trial (Griffin et al., NEJM 2023, PMID 37615996) showed 83.2% reduction in RSV-associated hospitalization.
• Dosing: Single IM injection: 50 mg for infants <5 kg; 100 mg for infants ≥5 kg.
• Recommendation: The CDC Advisory Committee on Immunization Practices (ACIP) recommends nirsevimab for all infants born within or entering their first RSV season (October–March), and for high-risk children up to 24 months entering their second RSV season.
• Safety: Comparable safety profile to placebo in trials; most common adverse events were injection-site reactions. No significant safety signals in post-market surveillance through 2024.

Maternal RSV vaccine (Abrysvo):

• FDA approved in 2023 for pregnant individuals at 32–36 weeks gestation. The bivalent prefusion F protein subunit vaccine achieves 82% efficacy against severe RSV lower respiratory illness in infants through the first 90 days of life via transplacental antibody transfer. It provides an alternative or complementary strategy to nirsevimab.

Palivizumab (Synagis) — for high-risk infants in second season:

• Palivizumab remains indicated for high-risk infants (premature <29 weeks, hemodynamically significant CHD, CLD) who are entering their second RSV season. It requires monthly IM injections (15 mg/kg) for up to 5 doses per season. The AAP Committee on Infectious Diseases updates eligibility criteria annually; eligibility narrowed in 2014 but expanded slightly for certain populations.

Non-pharmacologic prevention:

• Hand hygiene: The most effective intervention for interrupting viral transmission in household and healthcare settings.
• Breastfeeding: Associated with 36–56% reduction in RSV hospitalization risk; secretory IgA and other immune mediators in breast milk provide local mucosal protection.
• Tobacco smoke avoidance: Eliminates a major modifiable risk factor for severity.
• Cohort isolation: RSV-positive hospitalized infants should be cohorted or placed in contact precautions to prevent nosocomial spread.

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Key Research Papers

The following citations represent landmark studies and current guidelines informing bronchiolitis management:

1. Ralston SL, Lieberthal AS, Meissner HC, et al. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics. 2014;134(5):e1474–e1502. PMID: 25349312
2. Franklin D, Babl FE, Schlapbach LJ, et al. A randomized trial of high-flow oxygen therapy in infants with bronchiolitis (PARIS trial). N Engl J Med. 2018;378(12):1121–1131. PMID: 29561606
3. Schuh S, Freedman SB, Coates AL, et al. Effect of oximetry on hospitalization in bronchiolitis: a randomized clinical trial. JAMA. 2014;312(7):712–718. PMID: 25138332
4. Plint AC, Johnson DW, Patel H, et al. Epinephrine and dexamethasone in children with bronchiolitis. N Engl J Med. 2009;360(20):2079–2089. PMID: 19494219
5. Hartling L, Bialy LM, Vandermeer B, et al. Epinephrine for bronchiolitis. Cochrane Database Syst Rev. 2011;(6):CD003123. PMID: 21678340
6. Fernandes RM, Bialy LM, Vandermeer B, et al. Glucocorticoids for acute viral bronchiolitis in infants and young children. Cochrane Database Syst Rev. 2013;(6):CD004878. PMID: 23794256
7. 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. PMID: 32726528
8. Hammitt LL, Dagan R, Yuan Y, et al. Nirsevimab for prevention of RSV in healthy late-preterm and term infants (MELODY trial). N Engl J Med. 2022;386(9):837–846. PMID: 35196372
9. Piedimonte G, Perez MK. Respiratory syncytial virus infection and bronchiolitis. Pediatr Rev. 2014;35(12):519–530. PMID: 25452661
10. Zorc JJ, Hall CB. Bronchiolitis: recent evidence on diagnosis and management. Pediatrics. 2010;125(2):342–349. PMID: 20100768
11. Milési C, Matecki S, Jaber S, et al. 6 cmH2O continuous positive airway pressure versus conventional oxygen therapy in severe viral bronchiolitis. Pediatr Pulmonol. 2013;48(1):45–51. PMID: 22573568
12. Hall CB. Respiratory syncytial virus and parainfluenza virus. N Engl J Med. 2001;344(25):1917–1928. PMID: 11419430

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Connections

• RSV Bronchiolitis
• Croup
• Febrile Seizures
• Neonatal Jaundice
• RSV (Respiratory Syncytial Virus)
• Asthma
• Pneumonia