Bronchiolitis

Bronchiolitis is an acute viral infection of the lower respiratory tract that primarily affects infants and young children under the age of two, characterized by inflammation, edema, and mucus accumulation in the bronchioles—the smallest airways in the lungs ^[1]. The condition is most commonly caused by respiratory syncytial virus (RSV), although other pathogens such as rhinovirus, parainfluenza virus, and adenovirus can also be responsible ^[2]. Bronchiolitis typically begins with upper respiratory symptoms like rhinorrhea and cough before progressing to lower respiratory signs including tachypnea, wheezing, and increased work of breathing due to airway obstruction ^[3]. The disease is self-limiting in most cases, with symptoms resolving within one to three weeks, but can lead to respiratory failure in severe instances, particularly in high-risk infants such as those born prematurely or with underlying cardiopulmonary conditions ^[4]. Diagnosis is primarily clinical, based on history and physical examination, with pulse oximetry used to assess hypoxia; routine imaging and laboratory testing are discouraged in uncomplicated cases per guidelines from the American Academy of Pediatrics ^[5]. Management centers on supportive care, including hydration, nasal suctioning, and supplemental oxygen when indicated, while therapies such as bronchodilators, corticosteroids, and antibiotics are not routinely recommended due to lack of proven benefit ^[6]. Hospitalization may be necessary for infants with severe respiratory distress, apnea, or inability to maintain oral intake ^[7]. Public health interventions such as palivizumab prophylaxis for high-risk infants and emerging preventive strategies like maternal RSV vaccines and long-acting monoclonal antibodies (e.g., nirsevimab) have shown promise in reducing hospitalization rates and the global burden of disease ^[8]. Ongoing surveillance through systems like the Respiratory Virus Hospitalization Surveillance Network helps monitor seasonal trends and guide preventive timing ^[9].

Pathophysiology and Etiology

Bronchiolitis is an acute viral infection of the lower respiratory tract that primarily affects infants and young children under two years of age, with peak incidence between 2 and 6 months ^[2]. The condition is characterized by inflammation, edema, and mucus accumulation in the bronchioles—the smallest airways in the lungs—leading to airway obstruction and impaired gas exchange ^[1]. The pathophysiological mechanisms and etiological agents of bronchiolitis are closely interwoven, with viral infection triggering a cascade of inflammatory and structural changes that disproportionately affect the immature respiratory systems of infants.

Etiological Agents and Viral Pathogenesis

The most common cause of bronchiolitis is respiratory syncytial virus (RSV), which accounts for approximately 50–80% of cases, particularly during seasonal epidemics in temperate regions ^[12]. RSV infects ciliated epithelial cells lining the bronchioles via fusion (F) and attachment (G) glycoproteins, leading to direct cytotoxic damage, cell lysis, and sloughing of cellular debris into the airway lumen ^[13]. This disruption of the epithelial barrier impairs mucociliary clearance and promotes mucus hypersecretion, contributing to luminal obstruction.

Other significant viral pathogens include rhinovirus (RV), human metapneumovirus (HMPV), and human parainfluenza viruses (HPIVs), particularly HPIV-3 ^[14]. Rhinovirus, traditionally associated with the common cold, is increasingly recognized as a major cause of bronchiolitis, especially in older infants and those with atopic predisposition ^[15]. HMPV, a member of the Pneumoviridae family closely related to RSV, induces similar clinical manifestations through epithelial necrosis and mucus accumulation ^[16]. HPIVs cause infection via hemagglutinin-neuraminidase (HN) and fusion (F) proteins, leading to syncytia formation, inflammation, and airway obstruction ^[17].

Each of these viruses elicits distinct immune responses that influence disease severity. RSV and HMPV are associated with a T-helper 2 (Th2)-skewed and Th17-polarized immune profile, characterized by elevated levels of IL-4, IL-13, and IL-17, which promote eosinophil recruitment, mucus overproduction, and airway hyperreactivity ^[18]. In contrast, rhinovirus induces a robust innate antiviral response via RIG-I and MDA5 sensors, leading to strong production of type I and III interferons (IFN-α/β and IFN-λ), although it may evade immunity through immunosuppressive mechanisms like upregulation of TGF-β and PD-L1 ^[19]. HPIVs trigger a strong Th1 response with IFN-γ and chemokine production, facilitating viral clearance but potentially contributing to tissue damage ^[20].

Pathophysiological Mechanisms of Airway Obstruction

The hallmark of bronchiolitis is obstructive breathing due to inflammation and luminal narrowing of the bronchioles. Viral replication in epithelial cells triggers a robust local immune response, with infiltration of inflammatory cells and release of pro-inflammatory cytokines such as interleukin-6 (IL-6), IL-8, and tumor necrosis factor-alpha (TNF-α), which exacerbate airway wall edema and mucosal swelling ^[21]. The combination of epithelial damage, inflammatory edema, and excessive mucus secretion narrows the bronchiolar lumen, which is particularly consequential in infants due to their inherently narrow airways and reduced respiratory reserve ^[22].

This obstruction leads to several physiological consequences:

Air trapping and hyperinflation: Difficulty expelling air through narrowed airways results in air being trapped distal to the obstruction, leading to lung hyperinflation ^[23].
Ventilation-perfusion (V/Q) mismatch: Obstructed airways reduce alveolar ventilation while perfusion remains intact, resulting in hypoxemia ^[23].
Increased work of breathing: Infants compensate by increasing respiratory rate and using accessory muscles, manifesting as tachypnea, nasal flaring, and subcostal retractions ^[25].
Wheezing and crackles: Turbulent airflow through narrowed bronchioles produces wheezing, while mucus plugging and atelectasis may lead to crackles on auscultation ^[23].

Role of Viral Load, Age, and Host Immunity

Disease severity in bronchiolitis is influenced by a triad of factors: viral load, infant age, and host immune response. Higher RSV viral loads, measured via quantitative real-time PCR, are consistently associated with more severe clinical outcomes, including prolonged oxygen requirement, longer hospitalization, and increased need for mechanical ventilation ^[27]. However, paradoxically, some infants with severe respiratory failure exhibit lower nasal viral loads and reduced interferon responses, suggesting that immunopathology—rather than viral burden alone—plays a critical role in disease progression ^[28].

Infant age is a major determinant of severity, with those under 12 weeks at highest risk for apnea, respiratory failure, and intensive care unit (ICU) admission ^[29]. This vulnerability stems from anatomical factors such as smaller airways, weaker respiratory muscles, and immature immune responses, including impaired regulatory T cell (Treg) function and blunted interferon signaling ^[30]. The interplay between viral load and age modifies clinical outcomes, with younger infants experiencing worse prognosis even at similar viral loads.

Seasonal and Transmission Dynamics

The epidemiology of bronchiolitis is shaped by the seasonal and transmission patterns of its causative viruses. In temperate regions, RSV follows a predictable annual cycle, with increased transmission from October to April, peaking in winter months ^[31]. This seasonality is influenced by climatic factors such as lower temperature and humidity, which enhance viral stability and reduce mucociliary clearance ^[32]. In tropical regions, RSV transmission is often associated with the rainy season and higher humidity ^[33].

RSV spreads primarily through respiratory droplets and contact with contaminated surfaces (fomites), with household transmission playing a significant role ^[34]. Infants and young children are key drivers of community transmission, with daycare settings facilitating rapid spread ^[35]. Rhinoviruses circulate year-round with peaks in fall and spring, contributing to bronchiolitis cases outside the typical RSV season ^[36]. These overlapping seasonal patterns result in a prolonged burden of viral bronchiolitis, with RSV responsible for the majority of severe cases.

Diagnostic Implications and Pathogen Detection

Accurate identification of the causative pathogen is critical for infection control and public health surveillance, though not routinely required for clinical management. Reverse transcription PCR (RT-PCR) is the gold standard for viral detection due to its high sensitivity and specificity, capable of identifying RSV, rhinovirus, HMPV, and HPIVs from nasopharyngeal specimens ^[37]. Multiplex PCR panels allow simultaneous testing for multiple pathogens and detection of coinfections, which may influence disease severity ^[38].

In contrast, rapid antigen tests offer faster results at the point of care but have lower sensitivity (~68% for RSV), increasing the risk of false negatives, especially in infants with low viral loads ^[39]. Therefore, negative antigen results in high clinical suspicion should be confirmed with PCR ^[40]. The integration of both methods—antigen testing for triage and PCR for confirmation—optimizes clinical decision-making and strengthens infection control through early cohorting and isolation ^[41].

Clinical Presentation and Disease Progression

Bronchiolitis typically follows a predictable clinical course, beginning with mild upper respiratory symptoms and progressing to lower respiratory tract involvement characterized by increased work of breathing, wheezing, and potential respiratory compromise. The disease progression is generally self-limiting in most infants, though severity and duration can vary significantly based on age, viral pathogen, and underlying health conditions. Clinical presentation evolves over several days, with symptoms peaking before gradually resolving.

Initial Symptoms and Early Phase

The onset of bronchiolitis usually occurs 4 to 6 days after exposure to the causative virus, most commonly respiratory syncytial virus (RSV) ^[42]. The initial phase mimics a common cold and includes non-specific upper respiratory symptoms such as rhinorrhea, nasal congestion, mild cough, sneezing, and low-grade fever ^[43]. Infants may also exhibit decreased appetite and irritability. These early signs are often subtle and can be mistaken for a simple viral upper respiratory infection, particularly in older infants or children with prior exposure to respiratory viruses.

During this stage, physical examination typically reveals only mild tachypnea and nasal flaring. The absence of significant respiratory distress at this point often allows for outpatient management, especially in otherwise healthy infants over 12 weeks of age. However, caregivers should be counseled on warning signs of progression, including worsening breathing effort and feeding difficulties.

Progression to Lower Respiratory Tract Involvement

As the infection spreads from the upper to the lower respiratory tract, the bronchioles—small airways leading to the alveoli—become inflamed and obstructed. This phase usually begins within 2 to 3 days of symptom onset and marks the transition to clinically apparent bronchiolitis ^[25]. The hallmark of this progression is the development of lower respiratory tract signs due to airway narrowing and mucus plugging.

Key progressive symptoms include:

Wheezing, a high-pitched whistling sound heard during expiration, resulting from turbulent airflow through narrowed bronchioles ^[3]
Tachypnea, with respiratory rates often exceeding 60 breaths per minute in infants
Increased work of breathing, manifested as nasal flaring, grunting, and use of accessory muscles such as the sternocleidomastoid and intercostal muscles
Chest retractions, visible as inward pulling of the skin between the ribs (subcostal) or above the clavicles (supraclavicular)
Difficulty feeding, due to the increased effort required for breathing, which can lead to poor oral intake and dehydration
Irritability or lethargy, particularly in more severely affected infants

The pathophysiology underlying this obstructive breathing pattern involves viral-induced damage to ciliated epithelial cells, immune-mediated inflammation, airway edema, and mucus hypersecretion ^[25]. These changes lead to air trapping, hyperinflation, and ventilation-perfusion mismatch, contributing to hypoxemia. The small caliber of infant airways amplifies the impact of even minor obstruction, making young infants particularly vulnerable to respiratory compromise.

Peak Disease Severity and High-Risk Indicators

Symptoms of bronchiolitis typically peak between days 3 and 5 of illness ^[25]. During this period, infants may exhibit the most pronounced signs of respiratory distress. In some cases, especially among very young or premature infants, apnea—defined as pauses in breathing lasting ≥20 seconds or shorter episodes associated with bradycardia or cyanosis—may occur and represents a medical emergency ^[23].

Infants under 12 weeks of age, particularly those born prematurely or with underlying conditions such as congenital heart disease or chronic lung disease, are at highest risk for severe disease and respiratory failure ^[29]. These high-risk subgroups often require lower thresholds for hospitalization and closer monitoring due to their limited respiratory reserve and immature immune responses.

Recovery Phase and Long-Term Symptoms

After the peak, most infants begin to show gradual improvement. The recovery phase typically starts around day 6 to 7, with a slow resolution of respiratory symptoms. However, cough and wheezing may persist for 1 to 3 weeks, and in some cases, up to 6 weeks, particularly in infants with a history of atopy or recurrent wheezing ^[6]. Full recovery is expected in the majority of cases with appropriate supportive care.

Despite clinical recovery, some infants who experience severe RSV bronchiolitis may be at increased risk for long-term respiratory sequelae, including recurrent wheezing and asthma-like symptoms. The exact mechanisms linking severe bronchiolitis to later respiratory morbidity are not fully understood but may involve persistent airway inflammation or epithelial damage. However, most children outgrow these symptoms without long-term pulmonary impairment.

Disease Course Summary

The typical clinical timeline of bronchiolitis can be summarized as follows:

Days 1–3: Upper respiratory symptoms dominate, including rhinorrhea, cough, and mild fever
Days 3–5: Progression to lower respiratory tract involvement with wheezing, tachypnea, and increased work of breathing; symptoms peak
Days 6–14: Gradual improvement in respiratory status; cough may linger
Beyond 2 weeks: Most children fully recover, though prolonged coughing may persist

This predictable pattern underscores the importance of anticipatory guidance for caregivers and careful monitoring for signs of deterioration, particularly in high-risk infants. Supportive care remains the cornerstone of management throughout the disease course, with interventions focused on maintaining hydration, oxygenation, and airway clearance ^[51]. Early recognition of severe disease indicators allows for timely escalation of care, including hospitalization or intensive respiratory support when necessary ^[52].

Diagnosis and Clinical Guidelines

The diagnosis of bronchiolitis is primarily clinical, relying on a thorough history and physical examination rather than routine laboratory or imaging studies. According to guidelines from the American Academy of Pediatrics (AAP), bronchiolitis should be diagnosed in infants and young children under two years of age who present with a viral upper respiratory prodrome—such as rhinorrhea and cough—followed by lower respiratory tract signs including tachypnea, wheezing, and increased work of breathing ^[5]. The diagnosis is supported by physical findings such as diffuse wheezing, crackles (rales), nasal flaring, chest retractions, and grunting, all indicative of respiratory distress ^[54].

Clinical Criteria for Diagnosis

The AAP emphasizes that bronchiolitis is a clinical diagnosis and does not require confirmatory testing in typical cases. Key diagnostic features include a history of recent upper respiratory symptoms progressing to lower respiratory signs, with peak severity typically occurring between days 3 and 5 of illness ^[25]. Infants often exhibit tachypnea (respiratory rate >60 breaths per minute), use of accessory muscles, and feeding difficulties due to labored breathing. Apnea, particularly in infants under two months of age or those born prematurely, may be a presenting feature and warrants close monitoring ^[56]. The clinical judgment of the provider, rather than isolated metrics, should guide diagnostic and management decisions.

Indications for Diagnostic Testing

Despite the clinical nature of the diagnosis, certain diagnostic tests may be used in specific circumstances. Routine chest imaging is not recommended for uncomplicated bronchiolitis, as findings such as hyperinflation and peribronchial thickening are non-specific and may lead to misdiagnosis (e.g., bacterial pneumonia) and unnecessary antibiotic use ^[57]. However, chest X-rays may be warranted in cases of severe respiratory distress, clinical deterioration, suspicion of complications (e.g., pneumothorax), or atypical presentation suggesting an alternative diagnosis such as foreign body aspiration or heart failure ^[58].

Viral testing, such as rapid antigen detection or reverse transcription-polymerase chain reaction (RT-PCR), is not routinely recommended but may be considered in high-risk infants (e.g., those with prematurity, chronic lung disease, or congenital heart disease), hospitalized patients for cohorting purposes, or when public health surveillance is a priority ^[59]. RT-PCR is the most sensitive method for detecting respiratory syncytial virus (RSV) and other pathogens like rhinovirus, parainfluenza, and human metapneumovirus, offering higher accuracy than rapid antigen tests ^[60]. However, antigen tests have lower sensitivity (~68%) and may yield false-negative results, particularly in later stages of illness or in children with low viral loads ^[39].

Pulse oximetry is commonly used to assess hypoxia and guide decisions about hospitalization or supplemental oxygen. An oxygen saturation below 90–92% on room air is often used as a threshold for admission, though clinical context should always inform interpretation ^[62]. Overreliance on oximetry can lead to overdiagnosis and overtreatment, so it should be used judiciously and not as a standalone criterion ^[63].

Risk Stratification and Severity Assessment

Clinical guidelines recommend a risk-stratified approach to management, with severity assessed based on respiratory effort, oxygenation, hydration status, and presence of apnea. Mild cases are characterized by minimal respiratory distress, oxygen saturation ≥95%, and preserved feeding ability, and can typically be managed at home with supportive care. In contrast, severe disease is marked by persistent hypoxemia (SpO₂ <90%), significant work of breathing, apnea, lethargy, or inability to maintain oral intake, all of which may necessitate hospitalization ^[52].

High-risk infants—including those born prematurely, with chronic lung disease of prematurity (bronchopulmonary dysplasia), or with hemodynamically significant congenital heart disease—are more likely to experience severe disease and require intensive care ^[65]. These populations often have lower thresholds for admission and closer monitoring, even with seemingly moderate symptoms.

Monitoring and Escalation of Care

For hospitalized infants, continuous cardiorespiratory monitoring is recommended for those at high risk of apnea, including preterm infants and those under 12 weeks of age ^[66]. However, recent evidence supports transitioning to intermittent pulse oximetry in stabilized patients to reduce alarm fatigue and unnecessary interventions ^[67]. Clinical assessment should remain central, with frequent evaluations of respiratory rate, work of breathing, hydration, and mental status.

Indications for escalation to high-flow nasal cannula (HFNC) include persistent hypoxemia despite low-flow oxygen, marked respiratory distress, or signs of fatigue. Mechanical ventilation is reserved for infants with respiratory failure, characterized by apnea, hypercapnia with acidosis, or hemodynamic instability ^[68]. Predictors of HFNC failure include younger age (<3 months), lower body weight (≤5 kg), higher Wood-Downes scores (≥9), and underlying comorbidities ^[69].

Summary of Guideline Recommendations

Current evidence-based guidelines strongly discourage routine use of chest X-rays, blood tests, viral panels, bronchodilators, corticosteroids, and antibiotics in uncomplicated bronchiolitis ^[70]. These interventions lack proven benefit, increase healthcare costs, and may lead to harm. Instead, management should focus on supportive care—nasal suctioning, hydration, and oxygen therapy when indicated—while reserving diagnostic testing and advanced respiratory support for specific clinical scenarios where results will directly impact patient management ^[5]. This approach aligns with principles of antimicrobial stewardship and promotes high-value, patient-centered care.

Risk Factors and High-Risk Populations

Bronchiolitis, while common in infants and young children, can manifest with varying degrees of severity. Certain factors significantly increase the likelihood of severe disease, hospitalization, or complications, particularly in vulnerable populations. These risk factors are rooted in host susceptibility, underlying medical conditions, environmental exposures, and viral characteristics. Identifying high-risk individuals is critical for clinical decision-making, preventive interventions, and resource allocation.

Age and Developmental Vulnerability

Infant age is one of the most significant determinants of bronchiolitis severity. The highest incidence and greatest risk of severe disease occur in infants under 12 months of age, with the peak vulnerability between 2 and 6 months ^[2]. Infants younger than 12 weeks are at particularly high risk for respiratory decompensation, intensive care unit (ICU) admission, and apnea ^[29]. This heightened susceptibility is due to anatomical factors such as narrow airways, which are more easily obstructed by inflammation and mucus, as well as immature immune responses that impair viral clearance and increase the risk of immunopathology ^[25]. The combination of small airway diameter and high metabolic demand amplifies the work of breathing during respiratory infections, making infants uniquely prone to respiratory failure.

Prematurity

Prematurity is a major risk factor for severe bronchiolitis and hospitalization. Infants born before 34 weeks' gestation have underdeveloped lungs, weaker respiratory muscles, and compromised immune function, all of which increase their vulnerability to respiratory syncytial virus (RSV) and other pathogens ^[65]. Studies show that preterm infants have nearly double the relative risk (RR = 1.9) of bronchiolitis hospitalization compared to term infants ^[76]. They are also more likely to require supplemental oxygen, high-flow nasal cannula (HFNC), and mechanical ventilation ^[65]. Due to their increased risk, preventive strategies such as palivizumab prophylaxis are recommended for select preterm infants during RSV season according to American Academy of Pediatrics guidelines ^[54]. The presence of prematurity lowers the threshold for hospital admission and necessitates closer monitoring for signs of deterioration.

Chronic Lung Disease of Prematurity

Infants with chronic lung disease of prematurity (CLD), also known as bronchopulmonary dysplasia, are at exceptionally high risk for severe bronchiolitis and prolonged hospitalization ^[79]. These children often have baseline respiratory compromise, including reduced lung compliance and impaired gas exchange, which diminishes their ability to compensate during an acute viral infection. Bronchiolitis in this population can lead to rapid clinical deterioration, requiring extended respiratory support and higher oxygen targets. Management focuses on minimizing additional lung injury while providing adequate support, with careful attention to hydration and nutrition ^[80]. The use of non-recommended therapies such as bronchodilators and corticosteroids is discouraged unless there is clear evidence of benefit, to avoid potential adverse effects.

Congenital Heart Disease

Children with congenital heart disease (CHD), particularly those with hemodynamically significant defects or cyanotic lesions, are at increased risk for severe bronchiolitis and adverse outcomes ^[81]. The mortality rate for bronchiolitis in children with CHD is approximately 3.5%, significantly higher than the general pediatric population (<1%) ^[81]. Viral lower respiratory tract infections can exacerbate baseline cyanosis through ventilation-perfusion mismatch and hypoxemia ^[83]. These infants often require longer durations of oxygen therapy (averaging about 7.5 days) and are more likely to need intensive care support ^[84]. Management requires careful oxygen administration to avoid both hypoxia and hyperoxia, which can affect pulmonary vascular resistance and cardiac function ^[79]. Antibiotics are frequently used in this population despite the viral etiology, reflecting concerns about bacterial superinfection and clinical instability ^[84].

Environmental exposures and socioeconomic conditions play a significant role in bronchiolitis risk. Maternal smoking during pregnancy and exposure to secondhand smoke are associated with increased disease severity and hospitalization rates ^[29]. Other environmental factors include lack of breastfeeding, which deprives infants of protective maternal antibodies, and crowded living conditions that facilitate viral transmission ^[88]. Attendance at group childcare settings increases the risk of viral exposure and subsequent infection ^[89]. Socioeconomic deprivation is strongly linked to higher bronchiolitis hospitalization rates, reflecting disparities in housing quality, access to healthcare, and environmental exposures such as indoor air pollution ^[90]. Racial and ethnic disparities also exist, with higher rates of severe disease observed among Black, Hispanic, and American Indian/Alaska Native populations in the United States ^[91].

Viral and Immunological Factors

The specific viral pathogen and host immune response also influence disease severity. Respiratory syncytial virus (RSV) is the most common cause of bronchiolitis and is associated with a higher risk of severe disease compared to other viruses ^[12]. Higher RSV viral loads correlate with increased disease severity, including prolonged oxygen requirement, longer hospital stays, and need for ventilatory support ^[27]. The host immune response, particularly a dysregulated or Th2-skewed profile, can exacerbate immunopathology and airway obstruction ^[18]. Co-infection with multiple respiratory viruses and secondary bacterial infections are also associated with increased disease severity and need for mechanical ventilation ^[95]. Immunodeficiency, whether primary or secondary, further increases susceptibility to severe viral infections and complications ^[96].

Summary of High-Risk Indicators

The presence of any of the following factors should prompt heightened clinical vigilance and lower thresholds for hospitalization and intensive monitoring:

Age ≤3 months, especially ≤12 weeks
Prematurity (gestational age <34 weeks)
Chronic lung disease of prematurity
Hemodynamically significant congenital heart disease
Neuromuscular disorders or central nervous system abnormalities
Immunodeficiency
Exposure to tobacco smoke
Socioeconomic deprivation and crowded living conditions

Early recognition of these high-risk factors allows for timely escalation of care, appropriate use of preventive measures like nirsevimab or maternal RSV vaccines, and implementation of infection control practices to reduce nosocomial transmission ^[97]. A comprehensive approach that integrates clinical, environmental, and social risk assessment is essential for optimizing outcomes in infants with bronchiolitis.

Management and Supportive Care

The management of bronchiolitis is primarily centered on supportive care, as the condition is typically self-limiting and driven by viral-induced inflammation and airway obstruction rather than bronchospasm. There are no routinely recommended antiviral therapies for respiratory syncytial virus (RSV), the most common cause of bronchiolitis ^[23]. Clinical guidelines from the American Academy of Pediatrics emphasize that treatment should focus on maintaining hydration, oxygenation, and airway clearance, while avoiding ineffective or potentially harmful interventions ^[5]. Most infants with mild bronchiolitis can be safely managed at home, while hospitalization is reserved for those with moderate to severe disease or high-risk conditions.

Mainstays of Supportive Care

Supportive care is the cornerstone of bronchiolitis management and includes several key components:

Hydration: Ensuring adequate fluid intake is essential to prevent dehydration, which can result from tachypnea, increased work of breathing, and difficulty feeding. Infants should continue breastfeeding or formula feeding, with smaller, more frequent feeds recommended if respiratory effort interferes with feeding ^[7]. For hospitalized infants unable to maintain oral intake, alternative routes such as nasogastric tube feeding or intravenous therapy may be necessary ^[6]. Special attention should be paid to fluid composition; isotonic solutions (e.g., 0.9% NaCl with potassium) are preferred over hypotonic fluids to reduce the risk of hospital-acquired hyponatremia, which is associated with worse outcomes ^[102].

Nasal Suctioning: Regular nasal suctioning using a bulb syringe or mechanical device helps relieve upper airway obstruction caused by mucus accumulation. This intervention is particularly beneficial before feeding and sleep, as it improves feeding tolerance and reduces respiratory effort ^[103]. Gentle suctioning is recommended to avoid mucosal trauma.

Fever and Symptom Management: Fever and discomfort can be managed with acetaminophen (paracetamol) or ibuprofen when indicated, although these do not alter the course of the illness ^[42]. The use of cool-mist humidifiers is common among caregivers, though evidence supporting their benefit is limited ^[105].

Monitoring: Close clinical monitoring is essential, especially in high-risk infants. Parameters include respiratory rate, work of breathing (e.g., nasal flaring, retractions), oxygen saturation, hydration status, and level of alertness ^[80]. In hospitalized infants, continuous pulse oximetry is recommended when supplemental oxygen is administered, although routine continuous monitoring in stable patients is discouraged to prevent alarm fatigue ^[67].

Avoidance of Ineffective Therapies

Numerous therapies are not recommended for routine use in bronchiolitis due to lack of proven benefit and potential for harm. The American Academy of Pediatrics and other major guidelines strongly advise against the use of:

bronchodilators (e.g., albuterol, salbutamol): Multiple randomized trials and meta-analyses have shown no significant improvement in oxygen saturation, hospitalization rates, or symptom duration. Transient improvement may occur in some infants, but routine use is discouraged due to side effects such as tachycardia and oxygen desaturation ^[108].
corticosteroids: Neither systemic nor inhaled corticosteroids have demonstrated benefit in typical cases of bronchiolitis. A 2011 meta-analysis found no reduction in hospital admissions or length of stay, and their use is associated with potential adverse effects, including immunosuppression ^[109].
antibiotics: These are not indicated unless there is strong evidence of a bacterial co-infection, which is uncommon. Overuse contributes to antimicrobial resistance and unnecessary costs ^[110].
hypertonic saline: While some studies suggest a modest reduction in hospital length of stay, the overall evidence is of low quality, and routine use in outpatient or emergency settings is not recommended ^[5].
chest physiotherapy: This is not recommended due to lack of benefit and potential discomfort.

Indications for Hospitalization

Hospitalization is necessary for infants who exhibit signs of moderate to severe illness or have underlying risk factors that increase the likelihood of complications. Key indications include:

Hypoxia, defined as oxygen saturation <90% on room air, which may require supplemental oxygen ^[54].
Inability to maintain adequate oral hydration due to respiratory distress or fatigue ^[7].
Severe respiratory distress, characterized by tachypnea (>60 breaths per minute), nasal flaring, grunting, chest retractions, or cyanosis ^[42].
Apnea, especially in infants under 6 months or those born prematurely ^[115].
Underlying medical conditions such as prematurity, chronic lung disease, congenital heart disease, or immunodeficiency ^[7].

In the hospital setting, care remains primarily supportive, with close monitoring, oxygen therapy, and fluid management as needed. Mechanical ventilation is reserved for cases of respiratory failure ^[79].

Fluid and Electrolyte Management

Optimal fluid management is critical to prevent complications such as hyponatremia and fluid overload. Infants with bronchiolitis are at risk for both dehydration and overhydration, particularly in the ICU. Fluid overload, defined as a positive fluid balance exceeding 10% of body weight, is associated with prolonged mechanical ventilation and increased need for intubation ^[118]. To mitigate this risk, fluid administration should be carefully titrated, and daily weights, strict intake and output monitoring, and regular assessment of serum sodium levels are recommended ^[119]. In select cases, fluid restriction at 50–75% of maintenance may be considered, particularly when there is concern for the syndrome of inappropriate antidiuretic hormone secretion (SIADH) ^[119].

Monitoring for Apnea

Apnea is a life-threatening complication, particularly in high-risk infants such as those born prematurely or younger than 3 months ^[52]. Continuous cardiorespiratory monitoring, including pulse oximetry and respiratory rate tracking, is recommended for these infants ^[66]. However, for stabilized patients, intermittent monitoring may be sufficient and is associated with fewer alarms and interventions ^[67]. Clinical assessment remains paramount, and monitoring should be combined with frequent physical evaluations.

In summary, the management of bronchiolitis emphasizes supportive care tailored to the severity of illness and individual risk factors. Avoiding unnecessary interventions, ensuring adequate hydration, and providing oxygen when indicated are the pillars of effective treatment. Adherence to evidence-based guidelines helps optimize outcomes and reduce the economic and clinical burden of this common pediatric illness ^[6].

Respiratory Support and ICU Interventions

Infants with bronchiolitis may require escalating levels of respiratory support depending on the severity of respiratory distress, hypoxemia, and risk of respiratory failure. The approach to respiratory support follows a stepwise progression, beginning with low-flow oxygen and advancing to high-flow nasal cannula (HFNC) or mechanical ventilation in severe cases. Clinical guidelines emphasize individualized assessment and timely escalation of care to prevent complications while avoiding unnecessary interventions ^[125].

Indications for Supplemental Oxygen and High-Flow Nasal Cannula

Supplemental oxygen is a cornerstone of respiratory support in bronchiolitis and is indicated when hypoxia is present. The threshold for initiating oxygen therapy is well established: oxygen should be administered if oxyhemoglobin saturation (SpO₂) falls below 90% on room air, as this level of hypoxemia increases the risk of complications such as apnea and respiratory failure ^[54]. Some recent evidence suggests that a target saturation of 90–94% is sufficient, and maintaining higher saturations (e.g., >94%) may not confer additional benefit and could lead to unnecessary oxygen use ^[127].

High-flow nasal cannula (HFNC) therapy has emerged as a key intervention for infants with moderate to severe bronchiolitis who fail to respond to conventional low-flow oxygen. HFNC delivers heated and humidified gas at flow rates that can exceed the infant’s inspiratory demand, reducing the work of breathing, improving secretion clearance, and providing mild positive airway pressure effects ^[128]. It is considered a safe and effective bridge to avoid intubation in many cases.

Indications for HFNC include:

Persistent hypoxemia (SpO₂ < 90%) despite low-flow oxygen therapy
Increased work of breathing (e.g., marked retractions, grunting, tachypnea)
Signs of respiratory fatigue or impending respiratory failure (e.g., lethargy, poor perfusion, apnea)
Age typically under 2 years, with some protocols specifying infants ≥44 weeks postmenstrual age ^[129]

Mechanical Ventilation and ICU Admission Criteria

Mechanical ventilation is reserved for infants with severe respiratory failure who do not respond to non-invasive support. Indications include:

Severe hypoxemia (e.g., SpO₂ < 90%) refractory to HFNC or non-rebreather masks
Hypercapnia with respiratory acidosis (pH < 7.25)
Apnea or central respiratory depression
Lethargy, decreased level of consciousness, or clinical signs of fatigue
Hemodynamic instability due to respiratory compromise ^[68]

Infants requiring mechanical ventilation are typically managed in a pediatric intensive care unit (PICU), where continuous monitoring and multidisciplinary care are available. Risk factors for intubation include young age (<3 months), prematurity, and underlying comorbidities such as chronic lung disease of prematurity (bronchopulmonary dysplasia) or congenital heart disease ^[68].

The decision to intubate is based on clinical assessment, blood gas analysis, and overall stability rather than isolated parameters ^[132]. According to the American Academy of Pediatrics and other consensus guidelines, mechanical ventilation should be reserved for critical cases where oxygenation and ventilation cannot be maintained with less invasive measures ^[132]. Bag-mask ventilation remains the first-line intervention during acute respiratory failure, with timely transition to invasive mechanical ventilation if needed ^[134].

Predictors of Respiratory Support Success and Failure

Success rates for HFNC in infants with bronchiolitis range from 70% to over 80%, with success defined as avoidance of mechanical ventilation ^[135]. Predictors of successful HFNC use include older age (>3 months), higher admission weight (>5 kg), and absence of significant comorbidities such as prematurity or chronic lung disease ^[69]. Infants who respond within the first hour—demonstrating reduced respiratory rate, improved work of breathing, and stable oxygenation—are more likely to succeed on HFNC ^[125].

Conversely, predictors of HFNC failure and subsequent need for mechanical ventilation include:

Younger age (<3 months)
Lower body weight (≤5 kg)
Higher disease severity, as indicated by Wood-Downes scores ≥9
Radiographic findings such as complete lobar consolidation
Presence of a nasogastric tube at initiation, possibly reflecting poor feeding or fatigue ^[138]

Prematurity, congenital heart disease, and chronic lung disease are well-established risk factors for progression to respiratory failure and mechanical ventilation ^[68]. Infants with these comorbidities require closer monitoring and lower thresholds for escalation of care ^[140].

Monitoring for Apnea and Neurological Deterioration

Apnea is a life-threatening complication of bronchiolitis, particularly in high-risk infants, and requires vigilant monitoring. Apnea, defined as a pause in breathing lasting ≥20 seconds or a shorter pause accompanied by bradycardia, cyanosis, or oxygen desaturation, may be the first sign of clinical deterioration ^[141]. Continuous cardiorespiratory monitoring, including pulse oximetry and respiratory rate tracking, is standard in intensive care settings for infants at risk of apnea ^[142].

High-risk subgroups for apnea include:

Premature infants, especially those born before 32 weeks' gestation, due to immature respiratory control centers ^[65]
Young infants under 12 weeks, particularly those ≤3 months ^[144]
Infants with chronic lung disease, congenital heart disease, neuromuscular disorders, or immunodeficiency ^[29]

Clinical assessment remains paramount, and monitoring should be combined with frequent physical evaluations, including assessment of work of breathing, level of consciousness, and feeding tolerance. The decision to escalate or de-escalate monitoring should be guided by institutional protocols and clinical judgment, with emphasis on avoiding alarm fatigue while ensuring patient safety ^[80].

Fluid and Electrolyte Management in the ICU

Optimizing fluid and electrolyte management is critical in hospitalized infants with bronchiolitis to prevent complications such as hyponatremia and fluid overload. Hypotonic intravenous (IV) fluids are associated with a significantly increased risk of hospital-acquired hyponatremia (serum sodium <135 mmol/L), particularly in critically ill infants who may have non-osmotic stimulation of antidiuretic hormone (ADH) due to hypoxia, hyperinflation, or stress ^[147].

Guidelines from the American Academy of Pediatrics recommend the use of isotonic maintenance fluids (e.g., 0.9% NaCl with added potassium) to mitigate this risk ^[102]. The use of isotonic fluids has been shown to reduce the incidence of hyponatremia and is now considered standard of care in hospitalized children ^[147].

Fluid overload, defined as a positive fluid balance exceeding 10% of body weight, is associated with adverse respiratory outcomes, including increased work of breathing and need for intubation ^[150]. To prevent fluid overload, fluid administration should be carefully titrated to maintenance needs, with consideration of fluid restriction at 50–75% of usual maintenance in selected cases, particularly when there is concern for syndrome of inappropriate antidiuretic hormone secretion (SIADH) ^[119]. Daily weights, strict intake and output monitoring, and clinical assessment for signs of fluid overload (e.g., weight gain, edema, hepatomegaly) are essential components of management ^[152].

Prevention Strategies and Immunoprophylaxis

Prevention of bronchiolitis, particularly that caused by respiratory syncytial virus (RSV), focuses on reducing viral transmission and providing passive immunity to infants during their most vulnerable period. Strategies include non-pharmaceutical interventions, targeted immunoprophylaxis for high-risk infants, and emerging population-level approaches such as maternal vaccination and long-acting monoclonal antibodies. These measures aim to reduce hospitalization rates, lower healthcare utilization, and mitigate the global burden of disease, especially in infants under one year of age who are at highest risk for severe outcomes.

Non-Pharmaceutical Interventions and Infection Control

Non-pharmaceutical interventions (NPIs) play a critical role in limiting the spread of RSV and other bronchiolitis-associated viruses. These include hand hygiene, respiratory etiquette, and environmental cleaning, particularly in high-transmission settings such as childcare centers and households. Regular handwashing with soap and water or use of alcohol-based sanitizers significantly reduces viral transmission ^[153]. In daycare environments, structured infection control protocols—such as exclusion of symptomatic children, surface disinfection, and cohorting—have been shown to reduce acute respiratory infections ^[154]. During the COVID-19 pandemic, widespread implementation of NPIs such as mask-wearing and social distancing led to an 80–94% reduction in bronchiolitis cases across multiple countries, demonstrating their effectiveness ^[155]^[156]. Public health messaging emphasizing staying home when ill and using well-fitting masks in crowded settings further supports community-level prevention ^[157].

Palivizumab Prophylaxis for High-Risk Infants

Palivizumab, a monoclonal antibody targeting the RSV fusion (F) protein, has been used for decades to prevent severe RSV disease in high-risk infants. It is administered as monthly intramuscular injections during the RSV season and is recommended for infants with specific risk factors, including prematurity (especially those born before 34 weeks' gestation), chronic lung disease of prematurity (bronchopulmonary dysplasia), and hemodynamically significant congenital heart disease ^[54]. Clinical trials and real-world data demonstrate that palivizumab reduces RSV-associated hospitalizations by approximately 55% in these populations ^[159]. Population-based studies in Canada and the United States report hospitalization rates of 4.8% to 6.6% among high-risk infants receiving prophylaxis, compared to significantly higher rates in unvaccinated cohorts ^[160]^[161]. However, partial or incomplete dosing—often due to logistical or financial barriers—is associated with increased hospitalization risk, particularly among Medicaid-insured populations ^[162]. Despite its clinical efficacy, palivizumab's high cost and logistical demands have led to ongoing debates about cost-effectiveness, especially for broader infant populations ^[163].

Maternal RSV Vaccination

Maternal immunization represents a major advancement in RSV prevention. Vaccines such as Pfizer’s RSVpreF, administered during the third trimester of pregnancy (32–36 weeks), induce high levels of neutralizing antibodies that are transferred transplacentally to the fetus. A large Phase 3 trial showed that maternal vaccination reduced the risk of medically attended RSV-associated lower respiratory tract infection (LRTI) by 68% in infants during their first six months of life ^[164]. Real-world data from the 2024–2025 RSV season confirm its effectiveness, with significant reductions in infant hospitalization rates where uptake is high ^[165]. In May 2025, the World Health Organization (WHO) issued a formal position paper recommending maternal RSV vaccination as a key strategy for infant protection ^[166]. The prequalification of Pfizer’s maternal RSV vaccine by WHO in March 2025 was a critical step toward global access, enabling procurement through UNICEF and Gavi, the Vaccine Alliance ^[167]. Integration of maternal vaccination into existing antenatal care programs offers a scalable approach to achieving high coverage.

Long-Acting Monoclonal Antibodies: Nirsevimab

Nirsevimab (Beyfortus) is a long-acting monoclonal antibody that provides passive immunity with a single intramuscular dose, offering protection for the entire RSV season. It targets the RSV F protein with high affinity and extended half-life, making it suitable for broad infant immunization. Clinical trials and post-implementation surveillance show approximately 74.5% efficacy against RSV-associated LRTI and about 80% effectiveness in preventing ICU admissions ^[8]^[169]. The HARMONIE phase 3b trial confirmed 180-day protection against RSV hospitalization in healthy term and preterm infants across Europe ^[170]. Real-world data from the 2024–2025 season indicate that the combined availability of maternal vaccines and nirsevimab contributed to a 28% to 43% reduction in infant RSV hospitalization rates compared to previous seasons ^[171]. The WHO recommends nirsevimab for all infants under 8 months entering their first RSV season, as well as for high-risk children up to 24 months ^[166]. Its single-dose regimen simplifies delivery compared to palivizumab and supports equitable access, particularly in resource-limited settings.

Challenges in Global Implementation and Equity

Despite the promise of these interventions, significant challenges remain in extending protection to high-risk infant populations, especially in low- and middle-income countries (LMICs) where the burden of RSV is greatest. The high cost of monoclonal antibodies and maternal vaccines limits availability, with nirsevimab and maternal RSV vaccines primarily accessible in high-income countries as of early 2026 ^[173]. Gavi has initiated a program to support LMICs in introducing maternal RSV vaccines, but pricing, supply constraints, and health system capacity remain barriers ^[174]. Programmatic hurdles include integrating maternal vaccination into antenatal care, ensuring timely administration of nirsevimab to newborns, and maintaining cold chain requirements. Additionally, disparities in access persist even within countries due to socioeconomic factors, rural-urban divides, and fragmented healthcare systems, necessitating targeted policies to ensure that preterm infants and those with chronic conditions receive priority protection ^[175].

Emerging Antiviral Therapies and Future Directions

While prevention remains the cornerstone of RSV control, emerging antiviral therapies may complement immunization by reducing disease severity in breakthrough infections. Candidates in clinical development include zelicapavir, an RSV nucleoprotein inhibitor with antiviral activity in pediatric trials ^[176], and obeldesivir, an oral nucleoside analog being evaluated for prophylactic and therapeutic use ^[177]. Lonafarnib, repurposed as an RSV fusion inhibitor, represents a novel mechanism in preclinical development ^[178]. These agents, if proven safe and effective in infants, could provide critical tools for treating high-risk or immunocompromised children. A comprehensive approach combining prevention, early diagnosis, and targeted treatment will be essential to ultimately reduce the global burden of RSV bronchiolitis.

Complications and Long-Term Outcomes

Bronchiolitis, while typically a self-limiting illness in most infants, can lead to a range of complications, particularly in those with underlying health conditions or in severe cases requiring intensive care. The acute phase of the disease may be complicated by respiratory failure, apnea, and secondary infections, while emerging evidence suggests potential long-term respiratory sequelae, including recurrent wheezing and an increased risk of asthma development. Understanding these complications and outcomes is critical for risk stratification, clinical management, and long-term follow-up.

Acute Complications in the ICU Setting

Infants with severe bronchiolitis admitted to the pediatric intensive care unit (PICU) are at risk for several life-threatening complications. The most common and critical is respiratory failure, which arises from progressive airway obstruction, increased work of breathing, and ventilation-perfusion mismatch. This often necessitates advanced respiratory support, including high-flow nasal cannula (HFNC), continuous positive airway pressure (CPAP), or invasive mechanical ventilation ^[68]. The need for mechanical ventilation is particularly elevated in infants under three months of age, those born prematurely, or those with underlying cardiopulmonary conditions such as congenital heart disease (CHD) or chronic lung disease of prematurity (CLD) ^[180].

Apnea is another significant acute complication, especially in very young infants and those born preterm. The immature respiratory control system in these infants is highly susceptible to disruption during viral illness. Apnea, defined as a pause in breathing lasting ≥20 seconds or a shorter pause with bradycardia or cyanosis, may be the first sign of clinical deterioration and often mandates ICU admission for continuous cardiorespiratory monitoring ^[181]. Studies indicate that apnea occurs in up to 20% of hospitalized infants with bronchiolitis, with higher rates in those with a history of prematurity or low birth weight ^[182].

Fluid overload and electrolyte imbalances are additional complications that can exacerbate respiratory status. Overzealous administration of intravenous (IV) fluids, particularly hypotonic solutions, can lead to hyponatremia and pulmonary edema. Fluid overload, defined as a positive fluid balance exceeding 10% of body weight, is associated with increased risk of intubation and prolonged mechanical ventilation ^[150]. The use of isotonic maintenance fluids is now standard to prevent hospital-acquired hyponatremia, which is also a marker of disease severity and is linked to longer ICU stays and higher intubation rates ^[147].

Secondary bacterial infections can occur, especially in mechanically ventilated infants, leading to ventilator-associated pneumonia, bacteremia, or urinary tract infections. The incidence of invasive bacterial co-infection in otherwise healthy infants with bronchiolitis is low, but it increases significantly in critically ill or ventilated patients ^[185]. Clinical indicators of bacterial co-infection include persistent high fever, marked leukocytosis, significantly elevated C-reactive protein (CRP) or procalcitonin, and radiographic findings such as lobar consolidation or pleural effusion ^[186]. Antibiotics should be reserved for confirmed or strongly suspected cases to avoid unnecessary antimicrobial exposure and support antimicrobial stewardship antibiotic resistance.

Distinguishing Viral Progression from Bacterial Co-Infection

A critical challenge in the ICU is differentiating between worsening viral bronchiolitis and a secondary bacterial infection. Viral progression typically follows a course of gradual improvement after a peak in symptoms, whereas bacterial co-infection often presents with clinical deterioration after initial stabilization. Key laboratory and radiographic findings aid in this distinction. Low procalcitonin levels are more indicative of a viral etiology, while elevated levels suggest bacterial infection ^[187]. Chest imaging, such as X-ray or ultrasound, may reveal focal consolidation or pleural effusion, which are more suggestive of bacterial pneumonia. In ventilated infants, endotracheal aspirate or bronchoalveolar lavage (BAL) may be necessary for microbiological diagnosis ^[186].

Long-Term Respiratory Sequelae

Emerging evidence indicates that severe bronchiolitis, particularly that caused by respiratory syncytial virus (RSV), may have long-term implications for respiratory health. A significant body of research links severe RSV bronchiolitis in infancy with an increased risk of recurrent wheezing and the subsequent development of asthma. The underlying mechanisms are complex and likely involve a combination of viral-induced airway damage, immune system modulation, and genetic predisposition. RSV infection can cause epithelial cell necrosis and disrupt the airway epithelial barrier, potentially leading to chronic airway hyperreactivity ^[25].

Furthermore, the host's immune response to RSV, which is often skewed toward a T-helper 2 (Th2) phenotype with elevated levels of IL-4, IL-5, and IL-13, may promote eosinophilic inflammation and mucus overproduction, contributing to a persistent wheezing phenotype ^[18]. This immunopathology is similar to that seen in asthma, suggesting a shared pathophysiological pathway. Rhinovirus, another common cause of bronchiolitis, is also strongly associated with recurrent wheezing and asthma development, possibly due to pre-existing airway hyperresponsiveness and epithelial barrier dysfunction ^[191].

In rare cases, severe bronchiolitis can lead to post-infectious bronchiolitis obliterans, a chronic obstructive lung disease characterized by fibrotic occlusion of the small airways. This condition is more commonly associated with adenovirus infection but can occur after other severe viral pneumonias ^[192]. It presents with persistent cough, wheezing, and exercise intolerance, and requires long-term pulmonary management.

Prognostic Factors and Risk Stratification

The prognosis of bronchiolitis is generally favorable, with most children making a full recovery within one to three weeks. However, several factors influence the risk of complications and long-term outcomes. Young age, particularly under 12 weeks, is a major predictor of severe disease and ICU admission ^[25]. Prematurity and underlying conditions such as CHD or CLD significantly increase the risk of respiratory failure, apnea, and prolonged hospitalization ^[65]. Higher viral load, especially of RSV, has been correlated with increased disease severity, longer hospital stays, and a greater need for ventilatory support ^[27]. However, the host immune response plays a critical modifying role, and paradoxically, some infants with severe disease may exhibit lower viral loads but a dysregulated immune response, leading to significant immunopathology ^[28].

Monitoring and Management of High-Risk Infants

For high-risk infants, including those with a history of apnea or severe respiratory distress, monitoring may extend beyond the acute phase. In some cases, home apnea monitoring may be considered after discharge, although this practice is increasingly reserved for specific, high-risk scenarios based on individual assessment ^[197]. In the ICU, readiness for non-invasive or mechanical ventilation should be anticipated in infants with recurrent apnea or progressive respiratory failure. Predictors of high-flow nasal cannula (HFNC) failure, such as younger age (<3 months), lower body weight (≤5 kg), and higher disease severity scores, help guide timely escalation of care ^[69].

In conclusion, while most cases of bronchiolitis resolve without long-term consequences, severe disease can lead to significant acute complications and potential chronic respiratory issues. Vigilant monitoring, careful fluid management, and the ability to distinguish viral progression from bacterial co-infection are paramount in the ICU. The long-term association with recurrent wheezing and asthma underscores the importance of ongoing follow-up and research into preventive strategies, such as RSV vaccines and monoclonal antibodies, to mitigate both the immediate and enduring burden of this common childhood illness ^[8].

Epidemiology and Surveillance

Bronchiolitis is a leading cause of acute respiratory illness in infants and young children globally, with a significant impact on pediatric healthcare systems. The condition primarily affects children under two years of age, with the highest incidence occurring between 3 and 6 months of life ^[200]. Approximately 1 in 3 infants under one year develops bronchiolitis, particularly during peak respiratory virus seasons ^[201]. The disease is most commonly caused by respiratory syncytial virus (RSV), which accounts for 50–80% of cases, though other pathogens such as rhinovirus, human metapneumovirus (HMPV), and parainfluenza virus also contribute ^[12]. Globally, RSV is responsible for an estimated 33 million lower respiratory tract infections annually in children under five, resulting in 3.6 million hospitalizations and over 100,000 deaths, with the majority occurring in low- and middle-income countries (LMICs) ^[203].

Seasonal and Geographic Patterns

The epidemiology of bronchiolitis is strongly influenced by the seasonal transmission dynamics of its causative viruses. In temperate regions such as the United States and Western Europe, RSV follows a predictable winter seasonal pattern, with activity typically beginning in October, peaking between December and February, and subsiding by spring ^[31]. However, recent years have seen disruptions to this pattern, particularly following the suppression of viral circulation during the COVID-19 pandemic. In 2020–2021, non-pharmaceutical interventions (NPIs) such as mask-wearing, social distancing, and enhanced hygiene led to dramatic reductions—up to 94% in some areas—of bronchiolitis and RSV cases ^[156]. As these measures were relaxed, a rebound effect occurred, with earlier and sometimes more intense outbreaks, attributed to a larger pool of immunologically naïve infants ^[206].

In tropical and subtropical regions, bronchiolitis seasonality is less predictable and often correlates with rainy seasons or periods of high humidity. For example, surveillance in Singapore and parts of Southeast Asia shows year-round transmission with peaks during wet seasons, when indoor crowding and reduced ventilation increase transmission risk ^[33]. Australia exhibits a mixed pattern, with temperate southern zones experiencing winter epidemics and tropical northern areas showing less defined, continuous transmission ^[208]. These geographic variations are influenced by climate variables such as temperature, humidity, and precipitation, which affect viral stability and human behavior ^[32].

Surveillance Systems and Data Collection

Bronchiolitis is not a nationally notifiable disease in many countries, including the United States, and is therefore monitored indirectly through surveillance of respiratory viruses, particularly RSV. The U.S. Centers for Disease Control and Prevention (CDC) utilizes several integrated systems to track disease activity:

Respiratory Virus Hospitalization Surveillance Network (RESP-NET): This system combines data from the Emerging Infections Program (EIP) and FluSurv-NET to monitor laboratory-confirmed RSV, influenza, and HMPV hospitalizations across multiple states, providing age-stratified rates ^[9].
National Respiratory and Enteric Virus Surveillance System (NREVSS): A voluntary, laboratory-based network that collects weekly data on RSV detections from clinical and public health labs nationwide ^[211].
Pediatric Acute Respiratory Illness (ARI) Interactive Dashboard: Offers real-time data on bronchiolitis-related hospitalizations and emergency department visits, integrating clinical and demographic information ^[212].

Internationally, surveillance varies. The UK Health Security Agency (UKHSA) monitors daily emergency department attendances for acute bronchiolitis, using statistical models to establish seasonal baselines and detect outbreaks ^[213]. Similarly, Public Health Scotland has implemented a national respiratory surveillance plan integrating data from primary care, hospitals, and laboratories ^[214]. The World Health Organization (WHO) supports global RSV surveillance through its Global Influenza Programme, leveraging existing influenza networks to expand monitoring in LMICs ^[215].

Limitations and Needed Improvements

Despite these systems, bronchiolitis surveillance faces critical limitations. The lack of standardized case definitions and reliance on indirect proxies like RSV testing result in underreporting and misclassification. Coding variability using ICD-10 codes across institutions further hampers data accuracy ^[216]. Reporting delays—often weeks between case occurrence and data availability—impede timely public health responses. Additionally, most systems focus on hospitalizations, missing milder cases managed in outpatient or urgent care settings, which are essential for understanding transmission dynamics.

Improvements are needed to enhance early detection and outbreak response. Integration of real-time digital surveillance using electronic health records, telehealth visits, and internet search trends could provide earlier warnings ^[217]. Standardizing clinical severity scores and coding practices would improve data comparability. Expanding syndromic surveillance in ambulatory care settings and applying statistical methods like the Moving Epidemic Method (MEM) to define outbreak thresholds could enable more proactive interventions ^[218]. Global harmonization of surveillance protocols, supported by WHO, is essential for equitable monitoring and response, particularly in LMICs where the burden is greatest.

Impact of Preventive Interventions on Epidemiology

Recent advances in prevention have begun to reshape the epidemiology of bronchiolitis. Nirsevimab, a long-acting monoclonal antibody, and maternal RSV vaccination have demonstrated high efficacy in reducing severe RSV disease. Real-world data from the 2024–2025 season show a 28% to 43% reduction in infant RSV hospitalization rates in areas with high uptake of these interventions ^[171]. The WHO has recommended both strategies for global implementation, with prequalification of Pfizer’s maternal RSV vaccine enabling procurement through UNICEF and Gavi, the Vaccine Alliance ^[166]. However, challenges remain in extending access to LMICs due to cost, supply constraints, and health system limitations ^[167].

Infection control measures in high-transmission settings, such as childcare centers, also play a critical role. Interventions including hand hygiene, environmental cleaning, and exclusion of symptomatic children have been shown to reduce acute respiratory infections ^[154]. During the pandemic, widespread NPIs led to near-elimination of bronchiolitis cases, underscoring their effectiveness ^[155].

In conclusion, the epidemiology of bronchiolitis is shaped by viral seasonality, geographic variation, and population immunity. While surveillance systems provide valuable insights, improvements in data integration, standardization, and real-time monitoring are needed. Emerging preventive strategies offer transformative potential to reduce disease burden, but equitable global access remains a critical challenge.

Health Disparities and Economic Burden

Bronchiolitis imposes a substantial economic burden on healthcare systems globally, while significant health disparities persist across socioeconomic, racial, and geographic lines. These inequities are driven by complex interactions between social determinants of health, access to preventive care, and structural barriers in healthcare delivery. Addressing both the financial costs and unequal outcomes associated with bronchiolitis requires coordinated public health strategies that prioritize equity and early intervention.

Socioeconomic and Racial Disparities in Bronchiolitis Outcomes

Socioeconomic deprivation is strongly linked to increased risk of bronchiolitis hospitalization and severe disease. Children from low-income households face higher rates of admission due to factors such as overcrowded housing, exposure to indoor air pollutants, and secondhand smoke—all of which exacerbate respiratory vulnerability ^[224]. In England, regional variations in bronchiolitis admission rates are stark, with up to a 15-fold difference across local authority areas, often aligning with levels of socioeconomic disadvantage ^[225]. Similarly, in the United States, Black, Hispanic, and American Indian/Alaska Native (AIAN) populations experience disproportionately higher hospitalization rates and worse clinical outcomes ^[91]. These disparities are compounded by unequal access to timely care, with Hispanic children, for example, less likely to receive diagnostic testing despite similar symptom severity ^[227]. Rural populations also face increased risks due to limited healthcare access and delayed care-seeking, particularly in low- and middle-income countries where acute respiratory infections remain a leading cause of childhood morbidity ^[228].

Economic Costs of Bronchiolitis

The economic burden of bronchiolitis is considerable, with average one-year healthcare costs estimated at $4,313 per patient, of which hospitalizations account for $2,847 ^[229]. Costs escalate dramatically in severe cases; hospitalization requiring intensive care can be up to 20 times more expensive than standard care ^[230]. In the U.S., trends from 2000 to 2016 show sustained high hospitalization rates, particularly among infants, placing growing pressure on pediatric healthcare infrastructure ^[231]. Similar patterns are observed in Canada and France, where seasonal outbreaks contribute to recurring financial strain on health systems ^[232], ^[233]. Beyond direct medical costs, families bear substantial indirect burdens, including lost wages, transportation expenses, and caregiving time, which further amplify the overall economic impact ^[234].

Impact of Preventive Interventions on Cost-Effectiveness

Emerging preventive strategies offer promising avenues for reducing both the clinical and economic burden of bronchiolitis. palivizumab, a monoclonal antibody used for RSV prophylaxis in high-risk infants such as those born prematurely or with chronic lung disease, has been shown to reduce RSV-associated hospitalizations by up to 55% ^[159]. However, its high cost limits broad population-level use, though it may be cost-effective in targeted high-risk groups ^[236]. The newer long-acting monoclonal antibody nirsevimab offers single-dose protection for an entire RSV season and has demonstrated approximately 80% efficacy in preventing hospitalizations ^[237]. Economic models suggest nirsevimab could be cost-saving in some settings by preventing ICU admissions and reducing overall healthcare utilization ^[238]. Similarly, maternal RSV vaccines such as Abrysvo (RSVpreF) confer passive immunity to newborns and show strong potential for cost-effectiveness when vaccine coverage and efficacy are high ^[239]. These interventions, when implemented equitably, could significantly reduce seasonal healthcare surges and flatten hospitalization peaks.

Public Health Strategies to Address Disparities and Reduce Costs

Effective public health policy must integrate clinical, structural, and community-based approaches to mitigate disparities and optimize cost-effectiveness. Standardized clinical pathways and quality improvement initiatives have been shown to reduce unnecessary treatments—such as bronchodilators, corticosteroids, and antibiotics—aligning care with American Academy of Pediatrics guidelines and improving resource use ^[240]. Community-led programs, such as the Respiratory Parent Champions model in Liverpool, UK, train caregivers in high-deprivation areas to manage respiratory illnesses, resulting in reduced hospitalization rates ^[241]. Expanding access to preventive therapies through public programs like the U.S. Vaccines for Children (VFC) initiative is critical for reaching underserved populations ^[242]. Additionally, enforcing infection control standards in childcare settings—including hand hygiene, surface disinfection, and exclusion of ill children—can reduce transmission, particularly in disadvantaged communities ^[154].

Surveillance and Data Equity

Current surveillance systems, such as the U.S. Respiratory Virus Hospitalization Surveillance Network (RESP-NET) and the UK Health Security Agency (UKHSA) dashboard, provide valuable insights into bronchiolitis trends but suffer from delays, fragmented data, and inconsistent coding practices ^[9], ^[213]. These limitations hinder timely public health responses and mask disparities. Improvements are needed in real-time digital surveillance, including the use of machine learning models to analyze electronic health records and telehealth visits for early outbreak detection ^[217]. Standardizing clinical severity scores and ICD coding would enhance data comparability, while probabilistic data linkage could integrate disparate datasets to create more accurate patient trajectories ^[247]. Globally, harmonizing surveillance protocols through initiatives like the World Health Organization (WHO) RSV surveillance strategy can support equitable monitoring and response ^[248].

In conclusion, bronchiolitis presents a dual challenge of high economic cost and persistent health inequities. Addressing these issues requires a multifaceted approach that combines targeted prevention, equitable access to care, standardized clinical practices, and enhanced surveillance. By integrating social, clinical, and policy interventions, public health systems can reduce the burden of bronchiolitis and ensure better outcomes for all children, regardless of background.