Bronchiolitis

• Bronchiolitis is a viral infection of the very small airways of the lung in children under 2 years of age, most common between 3 and 6 months. ^[1]. ^[4]
• Respiratory syncytial virus (RSV) is the dominant cause, responsible for roughly two thirds of cases overall and for 50 to 80 percent of cases depending on the setting and season. ^{[2] [3]}.
• It starts like a cold with runny nose and cough; over one to three days it becomes tachypnoea, wheeze or crackles, and feeding difficulty. ^[1].
• No medication helps: bronchodilators, corticosteroids, antibiotics, hypertonic saline and chest physiotherapy do not improve outcomes and are not used. ^{[1] [4]}.
• Management is entirely supportive: give oxygen when saturation is persistently low, maintain hydration by mouth, tube or intravenous fluid, and use high-flow nasal oxygen only if standard oxygen fails; prevention is offered to selected infants with palivizumab or nirsevimab. ^{[1] [4] [3] [5]}.

By the end of this page you should be able to:

1. Explain why bronchiolitis happens mainly in young infants and why RSV is the principal cause.
2. Recognise the typical history and examination findings, including red flags and apnoea.
3. Assess severity using current threshold-based criteria and decide who needs referral, admission or discharge.
4. Manage bronchiolitis supportively: oxygen, high-flow nasal cannula, fluids, and what not to give.
5. Explain why bronchodilators, steroids and antibiotics do not help, and describe the mixed evidence for hypertonic saline.
6. Outline palivizumab and nirsevimab eligibility, dosing and how each is used.
7. Counsel families about expected course, complications and the link between early RSV infection and later wheeze.
8. Distinguish bronchiolitis from its main mimics, including viral wheeze, pneumonia and heart failure.

Bronchiolitis is an acute viral infection of the bronchioles, the smallest conducting airways, in children under 2 years of age. It is the most common acute viral lower respiratory illness of early childhood and remains a leading cause of hospitalisation in infants worldwide. ^{[1] [2]}.

A single virus, respiratory syncytial virus (RSV), produces the majority of cases, although several other viruses cause an identical or similar picture. Because the disease is driven by airway inflammation and mucus plugging rather than by smooth muscle spasm, treatment is supportive: oxygen, fluids and, when necessary, non-invasive respiratory support. Drugs that are useful in asthma are not useful here, and the temptation to try them is a common reason for over-treatment. ^{[1] [3] [4]}.

The illness is usually self-limiting and most children recover fully. Even so, it can be severe in the very young and in infants with chronic disease, and early infection leaves a real risk of recurrent wheezing in the first few years of life. ^{[2] [3]}.

There is no formal severity score in widespread use for bronchiolitis, so assessment rests on the history, examination and the objective thresholds below rather than on a number. ^[1]. Severe illness is a clinical judgement supported by oxygen saturation, work of breathing, feeding and risk factors.

Think of viral-induced wheeze or early asthma rather than bronchiolitis when an older infant or young child has persistent wheeze without crackles, recurrent episodic wheeze, or a personal or family history of atopy; these are unusual under 1 year of age. ^[1].

Bronchiolitis is a seasonal disease. In temperate climates cases peak in winter to early spring in line with RSV circulation; in warmer and tropical climates RSV may circulate for much of the year and outbreaks are less distinct. ^{[2] [5]}.

RSV itself is the commonest respiratory pathogen of infancy. Global estimates attribute to RSV more than 60 percent of acute respiratory infections in children and more than 80 percent of lower respiratory tract infections in infants under 1 year at the peak of the season. ^[3]. Older (2014) estimates attributed roughly 125,000 RSV hospitalisations and about 250 infant deaths per year in the United States to RSV ^[3]; more recent CDC estimates cite approximately 58,000 to 80,000 RSV-associated hospitalisations and 100 to 300 deaths annually among US children under 5 ^{[5] [7]}. RSV hospitalisation rates in US infants vary with study design: older series from 1997 to 2006 reported 26 per 1000 children under 1 year (48.9 per 1000 under 3 months) ^[2], while a systematic review of studies published through 2020 reported a pooled rate of 19.4 per 1000 infants under 1 year (range 8.4 to 40.8) ^[8], and CDC estimates that 2 to 3 percent of young infants are hospitalised for RSV ^[7]. Infection is acquired by almost all children by 2 years of age, though severity is greatest at 2 to 3 months, when maternal antibody is lowest. ^{[2] [3]}. ^[4]

About 1 to 3 percent of infants under 12 months are hospitalised with bronchiolitis each year, and 80 percent of those are under 6 months. ^[2]. Around 40 percent of under-1-year-olds who reach an emergency department with bronchiolitis are admitted, with an average stay of about 3.3 days. ^[2]. Mortality has fallen to fewer than 400 deaths per year in the United States; most deaths (79 percent) occur in infants under 1 year, mainly in the first few months of life. ^[2].

Risk factors for severe or hospitalised disease include young age (especially under 6 months), prematurity (especially under 32 weeks), chronic lung disease of prematurity, haemodynamically significant congenital heart disease, chronic neurological conditions, immunodeficiency, growth restriction, exposure to tobacco smoke, crowded living conditions, older siblings, lack of breastfeeding, low socioeconomic status and certain indigenous or ethnic groups with higher baseline rates. ^{[1] [2] [3]}. Boys are affected more often than girls by about 1.5 to 1. ^[2]. ^[6]

Bronchiolitis is a clinical syndrome produced by viruses. RSV is the principal agent in about two thirds of cases, and the proportion is higher in hospitalised patients. ^[2]. Other viruses commonly found singly or together in children with bronchiolitis are human metapneumovirus, parainfluenza viruses (types 1 and 3 especially), influenza A and B, rhinoviruses, human bocavirus and human coronaviruses. ^[2].

Infection is usually acquired from older children or adults with mild or subclinical illness; RSV survives on hard surfaces for up to 6 hours, on gloves for 90 minutes and on skin for 20 minutes. ^[3].

Whether dual infection makes illness worse is uncertain, but RSV plus human metapneumovirus co-infection has been linked to more severe disease in some studies. ^[2].

The clinical picture of bronchiolitis follows the anatomy of the problem. RSV begins replicating in the nasopharyngeal epithelium and spreads within days to the lower airways, especially the terminal bronchioles. Viral replication kills epithelial cells, which slough into the airway lumen; submucosal oedema, infiltration by inflammatory cells and thick, pooled mucus narrow and plug the small airways. Smooth muscle constriction is not a major contributor to the obstruction. ^{[2] [3]}.

Because an infant's airways are narrow and collateral ventilation is poorly developed, even modest oedema and mucus cause widespread partial obstruction. Air is trapped by a ball-valve mechanism (the airway narrows more on expiration than on inspiration) producing hyperinflation; when gas behind an obstruction is absorbed, patchy atelectasis results. Ventilation-perfusion mismatch produces hypoxaemia, and if the infant tires, hypercapnia and respiratory acidosis follow. ^{[2] [3]}.

Two features explain the timing and severity. First, maternal anti-RSV immunoglobulin reaches its lowest concentration at 2 to 3 months of age, exactly when infection incidence peaks. ^[3]. Second, preterm infants and those with chronic lung disease have smaller airway reserve and a pro-inflammatory milieu, and miss some of the third-trimester transfer of protective antibody and maturation of T-cell responses. ^{[2] [3]}.

This mechanism is the reason that asthma-type drugs do not work: the narrowing is fixed structural and mucous obstruction rather than reversible bronchospasm. ^{[3] [4]}.

The illness has a recognisable sequence. Parents usually describe one to three days of coryza (runny nose), sneezing and mild cough, then a prominent cough, tachypnoea, feeding difficulty and sometimes fever. According to NICE (Ref1), symptoms usually peak between 3 and 5 days; the Royal Children's Hospital Melbourne (Ref4) describes peak severity around day 2 to 3 from the onset of increased work of breathing. Most children improve over three to four days, with full recovery taking one to two weeks. Cough may persist for weeks (a median illness duration of about 12 days, with 18 percent still symptomatic at 3 weeks). ^{[1] [2]}. ^[4]

Symptoms that parents report include:

• a blocked or runny nose and sneezing. ^[3];
• cough, often harsh and persistent. ^{[1] [2]};
• fast breathing, sucking in at the ribs or grunting. ^[2];
• wheeze, sometimes heard without a stethoscope. ^[1];
• fever, present in about 30 percent of cases, usually below 39 °C. ^[1];
• poor feeding, typically after three to five days of illness. ^{[1] [2]};
• irritability or lethargy. ^[2];
• in young infants, episodes of stopped breathing (apnoea), sometimes the first or only sign. ^{[1] [3]}.

Feeding problems are common and prolonged: 82 percent of hospitalised children in one UK series had feeding difficulties lasting an average of 27 hours. ^[2]. Dehydration arises from cough-induced vomiting, poor intake and high insensible losses with tachypnoea. ^[2].

Red flags from the history include breathing that is worsening, fluid intake of only 50 to 75 percent of normal (or no wet nappy for 12 hours), any apnoea or cyanosis, and exhaustion such as not responding to social cues or waking only with prolonged stimulation. ^[1].

The child may look only mildly unwell or profoundly distressed. Inspection may show tachypnoea, nasal flaring, and intercostal, subcostal or supraclavicular recession, grunting, and in severe cases a silent chest with diminished air movement. Auscultation is variable and may be only wheeze, only crackles, both, or neither; diffuse polyphonic wheeze, prolonged expiration and coarse crackles are typical, and a falling breath-sound intensity with rising dyspnoea suggests progressive obstruction. ^{[2] [3]}.

Other examination findings:

• fever, usually mild; a high fever over 39 °C should raise suspicion of pneumonia. ^[1];
• tachycardia and prolonged capillary refill if dehydrated. ^[1];
• otitis media, which is the commonest bacterial coexisting infection. ^[3];
• soft tissue (chest wall) recession and, in small babies, periodic breathing or apnoea. ^[3].

Clinical findings also change minute by minute, so a single examination can mislead; re-examine after a period of settling. ^[2].

Examination of the nose matters: young infants are obligate nose breathers, so nasal saline drops and gentle superficial suction at feeds can reduce distress. ^[4].

No universal scoring system exists, so clinicians use the thresholds below plus judgement. ^[1].

Consider referral (or observe in hospital) if any of:

• Respiratory rate over 60 breaths per minute. ^[1];
• Inadequate oral intake of 50 to 75 percent of the usual volume, or clinical dehydration. ^[1];
• Persistent oxygen saturation under 92 percent in air. ^[1].

Risk factors that should lower the threshold for referral or admission include chronic lung disease, haemodynamically significant congenital heart disease, age under 3 months, prematurity under 32 weeks, neuromuscular disorders and immunodeficiency. ^[1]. Social factors (carer confidence, distance to care) also matter. ^[1].

Admit if any of:

• Apnoea (observed or reported). ^[1];
• Persistent oxygen saturation in air under 90 percent for children 6 weeks and over, or under 92 percent for babies under 6 weeks and for any child with an underlying condition. ^[1];
• inadequate oral intake of 50 to 75 percent of usual volume. ^[1];
• Persisting severe respiratory distress, for example respiratory rate over 70 per minute. ^[1].

High-flow nasal oxygen is not an admission criterion on its own; it is a treatment step for children already in hospital. ^[4].

Discharge when the child is clinically stable, taking adequate oral fluids, and has maintained oxygen saturation in air over 90 percent (over 92 percent if under 6 weeks or with underlying disease) for 4 hours including a period of sleep. ^[1]. Infants under 8 weeks carry higher risk of representation. ^[4]. Give written safety-net advice covering worsening work of breathing, fluid intake below 50 to 75 percent or no wet nappy for 12 hours, apnoea or cyanosis, and exhaustion. ^[1].

Bronchiolitis is a clinical diagnosis. Tests are neither required nor helpful for most children and should be reserved for deterioration or diagnostic uncertainty. ^{[1] [2] [4]}.

• Oxygen saturation (pulse oximetry): measure in every child presenting, including in primary care when available. ^[1].
• Chest radiograph: not routinely indicated; changes can mimic pneumonia and lead to unnecessary antibiotics. Consider it if intensive care is being considered, or if there is suspected cardiac disease (look for cardiomegaly). ^{[1] [2]}.
• Blood tests: not routinely indicated, including full blood count and blood cultures. ^[1].
• Blood gases: not routine; consider capillary sampling in severe worsening distress if supplemental oxygen exceeds 50 percent or if impending respiratory failure is suspected. ^[1].
• Virological testing: not indicated for individual management and should not guide treatment, though it may be useful for infection control or surveillance. ^[4].
• If imaging is done, expect bilateral hyperinflation, patchy atelectasis, peribronchial thickening or, with severe disease, parenchymal consolidation. ^[3].

The differential diagnosis of wheeze in an infant is broad and a careful history and examination are needed, especially because RSV occurs in epidemics that make other causes seem unlikely. ^[2].

Management is supportive from first presentation. ^{[2] [3] [4]}. The aim is to keep the child oxygenated, hydrated and comfortable while the airway inflammation resolves, avoiding unnecessary handling and interventions.

For previously healthy infants, give supplemental oxygen when saturation is persistently less than 90 percent (less than 92 percent for babies under 6 weeks or any child with an underlying condition). ^{[1] [2]}. Use warm humidified oxygen; brief dips below target are common and are not a reason to start oxygen. ^{[3] [4]}.

• Target 90 percent (92 percent in the groups above). Do not chase values in the mid to high 90s. ^[4].
• Wean to the minimum effective flow. ^[4].
• Trial off oxygen every 6 hours; reinstate if saturation stays low. ^[4].
• Once a child has been off oxygen for 2 hours, discontinue continuous monitoring and observe, rechecking if the child deteriorates. ^[4].
• Pulse oximetry used without signs of distress in an otherwise healthy child increases service use and cost and is not routinely recommended in some guidelines; always measure in a child with visible respiratory distress. ^[2].

High-flow nasal cannula (HFNC) should be reserved for children who have failed low-flow oxygen: persistently low saturation despite 2 hours of nasal prong oxygen with no improvement in respiratory state. ^[4]. It is not recommended when saturation is consistently 92 percent or more. ^[4].

Escalate or refer if an oxygen requirement on HFNC needs an inspired oxygen fraction above 50 percent, or if there is deterioration. ^[4]. Continuous positive airway pressure may be considered in children with impending respiratory failure, and in the few who progress, mechanical ventilation, high-frequency oscillation or extracorporeal membrane oxygenation may be needed. ^{[1] [3]}.

Continue comfort oral feeds if safe; young infants are obligate nose breathers and nasal toilet helps. ^[4]. If oral intake is inadequate, use a nasogastric or orogastric tube for fluids. ^{[1] [4]}.

• Nasogastric feeding is the preferred route when non-oral fluids are needed and is safe in children on respiratory support. ^{[1] [4]}.
• Start nasogastric bolus feeding at two-thirds maintenance, because of a risk of increased antidiuretic hormone secretion. ^[4].
• Give intravenous isotonic fluids with glucose when the child cannot tolerate tube feeds or has impending respiratory failure. ^{[1] [4]}.
• Avoid overfeeding: aspiration has been demonstrated in a significant proportion of hospitalised infants with bronchiolitis. ^[3].

• Deep nasal suction beyond the nasopharynx is not recommended; superficial suction may be used in moderate disease to help feeding. ^[4].
• Nasal saline drops may be used at feeds. ^[4].
• Chest physiotherapy is not indicated. ^{[1] [4]}.

Therapies that work in asthma or bacterial pneumonia do not work in bronchiolitis. Most hospitalised infants historically received at least one unnecessary drug. ^[2]. NICE lists specifically: do not use antibiotics, hypertonic saline, nebulised adrenaline, salbutamol, montelukast, ipratropium bromide, systemic or inhaled corticosteroids, or a combination of systemic corticosteroids and nebulised adrenaline. ^[1].

• Bronchodilators (salbutamol, ipratropium, adrenaline): there is no consistent benefit. Airway narrowing is due to mucous and oedema, not smooth muscle spasm, and wheeze may transiently improve without changing outcomes. The adverse effects (tachycardia, tremor, hypokalaemia, hyperglycaemia) can be serious in infants with lung or heart disease. ^{[1] [3] [4]}. One older North American review allowed a brief, objectively assessed trial of inhaled beta-agonist with discontinuation if no clear improvement, but this conflicts with the current advice of NICE and of the Royal Children's Hospital; it is no longer recommended. ^{[3] [1] [4]}.
• Corticosteroids: neither systemic nor inhaled steroids show consistent benefit, and viral bronchiolitis usually occurs in the first year, when lung growth is rapid and the safety of steroids is unknown and unapproved by regulators. ^{[1] [3]}. Post-bronchiolitis wheeze is usually a non-atopic phenotype and tends to respond poorly to steroids. ^[3].
• Antibiotics: use only when there is specific evidence of bacterial infection. Bacterial co-infection occurs in 0 to 7 percent of cases and is usually an unrelated urinary tract infection. ^{[1] [2]}.
• Hypertonic saline: evidence is conflicting. Older Cochrane data and some studies reported faster improvement and shorter stay with 3 percent saline; other studies show no benefit and there is a theoretical risk of bronchospasm. It is not recommended for emergency department use, and NICE and RCH advise against it. ^{[1] [2] [4]}.
• Chest physiotherapy: no evidence of benefit; avoid. ^{[1] [2] [4]}.
• Ribavirin: no longer recommended routinely, though it may be considered in selected immunocompromised children who continue to shed virus for months. ^{[2] [3]}.
• Montelukast: not effective and not recommended. ^{[1] [3]}.
• Caffeine: insufficient evidence for prevention of bronchiolitis-associated apnoea. ^[4].
• Sedation: chloral hydrate may reduce agitation in worsening distress (0 to 2 years: 10 mg per kg initial dose every 4 to 6 hours, rising to 15 then 20 mg per kg if needed, with increased monitoring), but it carries risks of excess sedation, respiratory depression, hypotension and paradoxical agitation. ^[4].

• CPAP or high-flow support should be in a monitored area with staff able to escalate. ^{[1] [4]}.
• Upper airway suctioning: do not perform routinely; do perform if the child presents with apnoea even without visible secretions, and consider it for respiratory distress or feeding difficulties caused by secretions. ^[1].
• Chloral hydrate note caveats above. ^[4].

RSV spreads by direct contact with infected secretions, survives on surfaces for hours, and incubation is 2 to 8 days (infectious shedding usually around 8 days, but up to 3 weeks, and months in immunocompromised children). ^[3]. The most effective measures remain hand hygiene (soap and water or alcohol rub), contact precautions, gloves, limiting crowding and visitor contact, eliminating tobacco smoke, promoting breastfeeding and limiting group daycare exposure. ^{[2] [3]}. Airborne masks are not routinely recommended because RSV is rarely airborne. ^[3].

Palivizumab is a humanised monoclonal antibody against the RSV F protein given as a 15 mg per kg intramuscular dose each month during the RSV season, for a maximum of five monthly doses. ^{[3] [6]}. It reduces hospitalisation in high-risk infants but does not treat infection and should not be used in hospital outbreaks or in established disease. ^{[3] [6]}.

Current AAP guidance restricts it to:

• Infants born before 29 weeks without chronic lung disease, under 12 months at season start. ^{[3] [6]};
• Infants with chronic lung disease of prematurity (oxygen for at least 28 days after birth), under 24 months, still needing medical therapy within 6 months of season start. ^[3];
• Infants under 12 months with haemodynamically significant congenital heart disease (especially acyanotic), children under 24 months after cardiac transplantation, infants under 12 months with airway abnormalities or neuromuscular disease impairing cough, and severely immunocompromised children under 24 months. ^[3];
• Special consideration in regions with high RSV burden (for example some indigenous populations). ^[6].

Palivizumab is not recommended for infants born at 29 weeks or later without lung disease, for lung disease infants 12 months or older who are off therapy, after a breakthrough RSV hospitalisation (the risk of a second in the same season is very low), or for Down syndrome or cystic fibrosis without specific indications. ^[3]. For infants born during the season, fewer than five doses are usually needed; the first dose may be given 48 to 72 hours before discharge or promptly after discharge. ^[6]. Monotherapy RSV passive antibody is expensive and benefits are limited, which is why guidelines reserve it for a small, high-risk group. ^[3].

Nirsevimab is a long-acting monoclonal antibody given as a single intramuscular dose; in 2023 the US Advisory Committee on Immunization Practices (ACIP) recommended:

• all infants under 8 months born during or entering their first RSV season, dosed 50 mg if under 5 kg and 100 mg if 5 kg or more. ^[5];
• infants and children 8 to 19 months at increased risk of severe RSV disease entering their second season, given 200 mg as two 100 mg injections at different sites. ^[5].

Infants born shortly before or during the season should receive nirsevimab within one week of birth, during the birth hospitalisation or in the outpatient setting. Based on pre-pandemic patterns, in most of the continental United States administration runs from October to the end of March; local epidemiology should guide timing in tropical or remote regions. ^[5]. Either maternal vaccination during pregnancy or infant immunisation is recommended to prevent RSV lower respiratory disease, but both are not usually needed for the same infant. ^{[5] [7]}.

Efficacy in pooled trials was about 79 percent against medically attended RSV lower respiratory infection, 81 percent against RSV hospitalisation and 90 percent against ICU admission through 150 days. ^[5]. Nirsevimab is contraindicated after a severe allergic reaction to a previous dose or component. ^[5].

Severe RSV bronchiolitis in infancy is followed by recurrent wheezing in about 20 to 40 percent (some series say 30 to 50 percent) of infants who are hospitalised. ^{[2] [3]}. A non-atopic wheezing phenotype is typical, tends to respond poorly to steroids, and usually resolves before adolescence. ^[3].

In otherwise healthy preterm infants (33 to 35 weeks), monthly palivizumab during the RSV season reduced wheezing days by 61 percent and recurrent wheeze from 21 percent to 11 percent in the first year. ^[3]. This is strong evidence that RSV contributes causally to early wheezing, but it comes from preterm infants and cannot yet be generalised to healthy term infants. ^[3]. RSV prevention is therefore encouraged on the basis of preventing severe acute disease, and any long-term wheeze benefit remains an additional, still-developing argument. ^[3].

• Premature infants and chronic lung disease: highest risk of severe disease, apnoea, hospitalisation and long-term wheeze; lower threshold for admission and for palivizumab. ^{[1] [3]}.
• Congenital heart disease (haemodynamically significant): worse course and hypoxaemia; consider palivizumab or nirsevimab eligibility. ^{[2] [3]}.
• Infants under 3, and especially under 1, months: peak severity and apnoea risk; keep admission threshold low. ^{[1] [3]}.
• Immunocompromised children: prolonged shedding, more severe and atypical disease; consider ribavirin in select cases and immunoprophylaxis. ^{[3] [2]}.
• Neuromuscular or airway abnormalities (and severe tracheomalacia): may need chest physiotherapy assessment for secretion clearance, a specific exception to the "no physio" rule. ^[1].
• Indigenous and high-prevalence communities: higher hospitalisation rates; local guidelines may extend eligibility. ^{[2] [5]}.

Where tests and drugs are scarce, bronchiolitis is diagnosed on clinical grounds and managed supportively:

• Use history and examination (prodrome, tachypnoea, wheeze or crackles) and pulse oximetry if available. ^{[1] [2]}.
• Keep affected infants separated from newborns; enforce hand washing and basic contact precautions among staff and families. ^{[2] [3]}.
• Give low-flow oxygen to keep saturation around target; do not waste oxygen chasing higher numbers. ^{[1] [4]}.
• Maintain feeds by mouth if safe; otherwise nasogastric fluids at two-thirds maintenance; use intravenous isotonic fluids only if tube feeding fails or respiratory failure is impending. ^{[1] [4]}.
• Avoid bronchodilators, steroids, routine antibiotics and chest physiotherapy; reserve antibiotics for clear bacterial infection such as otitis media. ^{[1] [4]}.
• Watch for apnoea in infants under 2 months: keep them observed in hospital even if they do not need fluids or oxygen. ^[4].
• Refer early when high-flow oxygen above 50 percent inspired fraction is needed, when risk factors exist, or when transport can be arranged; treatment of respiratory failure needs mechanical support available. ^[4].
• Palivizumab or nirsevimab is unavailable in many systems; prevention then relies on infection-control measures and delaying early infection where possible. ^[3].

• Bronchiolitis is a viral infection of small airways in children under 2 years; RSV is the cause in around two thirds to four fifths of cases depending on setting. ^{[1] [2]}.
• It is a clinical diagnosis: coryzal prodrome of one to three days followed by persistent cough plus tachypnoea or chest recession plus wheeze or crackles. ^[1].
• Fever is present in about 30 percent and is usually below 39 °C; a fever above 39 °C or persistently focal crackles should make you think of pneumonia. ^[1].
• Symptoms usually peak between 3 and 5 days by NICE (Ref1) or around day 2 to 3 from the onset of increased work of breathing by RCH Melbourne (Ref4); most children improve over three to four days, and cough can last weeks. ^{[1] [2] [4]}.
• Infants under 6 weeks may present with apnoea alone; apnoea occurs in up to 20 percent of hospitalised infants under 6 months. ^{[1] [3]}.
• No single severity score exists; use objective thresholds (respiratory rate, oxygen saturation, feeding, red flags) and risk factors. ^[1].
• Refer as an emergency for apnoea, a seriously unwell child, respiratory rate over 70, central cyanosis or exhaustion. ^[1].
• Admit if saturation is persistently under 90 percent (under 92 percent if under 6 weeks or with comorbidity), intake is 50 to 75 percent of normal, or severe distress persists. ^[1].
• Oxygen target is 90 percent (92 percent in the young or comorbid groups); do not chase higher. ^{[1] [4]}.
• High-flow nasal cannula is reserved for failure of low-flow oxygen; escalate if more than 50 percent inspired oxygen is needed. ^[4].
• Hydration is maintained by mouth, then nasogastric or orogastric tube, then intravenous isotonic fluids. ^{[1] [4]}.
• Chest physiotherapy, bronchodilators, steroids, antibiotics and routine hypertonic saline do not help and are avoided. ^{[1] [4]}.
• Ribavirin is not routine; reserve for selected immunocompromised children. ^{[2] [3]}.
• Palivizumab: 15 mg per kg intramuscularly each month, up to five doses, for selected high-risk infants. ^{[3] [6]}.
• Nirsevimab: single dose for infants under 8 months entering their first RSV season (50 mg if under 5 kg, 100 mg if 5 kg or more) and for at-risk children 8 to 19 months entering their second season (200 mg). ^[5].
• Recurrent wheezing follows severe RSV bronchiolitis in 20 to 50 percent of hospitalised infants but usually improves by adolescence. ^{[2] [3]}.

Viral-induced wheeze and early asthma in children; community-acquired pneumonia in children; respiratory syncytial virus and RSV infection; apnoea in infants; dehydration in children; cystic fibrosis; congenital heart disease; asthma; smoking cessation and infant health; immunisation and passive antibody prophylaxis.