Bronkiolitis

01Pathophysiology

Bronchiolitis is an acute inflammatory disease of the small airways (bronchioles) caused by viral infection, most commonly RSV. Understanding the pathophysiology is essential because every symptom the patient develops can be traced directly back to what happens at the level of the bronchiole.

The virus is transmitted via respiratory droplets or fomite contact and initially infects the nasopharyngeal epithelium, which explains the 2-3 day prodrome of rhinorrhea, sneezing, and low-grade fever. The virus then spreads distally to the bronchiolar epithelium. Once in the small airways, the virus causes direct necrosis of the ciliated epithelial cells lining the bronchioles. This triggers an inflammatory cascade with edema of the submucosa, increased mucus secretion, and accumulation of cellular debris within the airway lumen.

Because infant airways are already anatomically narrow (airway resistance is inversely proportional to the fourth power of the radius, per Poiseuille's law: $R\propto \frac{1}{r^4}R\; \backslash propto\; \backslash frac\{1\}\{r^4\}$), even a small amount of mucosal swelling dramatically increases resistance. This is why bronchiolitis disproportionately affects infants and is rarely clinically relevant in older children whose airways are larger.

The combination of edema, mucus plugging, and cellular debris leads to partial or complete obstruction of the bronchioles. Partial obstruction creates a ball-valve mechanism: air enters during inspiration (when airways dilate) but cannot escape during expiration (when airways narrow further). This produces air trapping and hyperinflation, which is the hallmark finding on chest radiography. Complete obstruction of some bronchioles leads to absorption atelectasis in the distal lung segments.

The clinical consequences follow logically. Wheezing is caused by turbulent airflow through narrowed, partially obstructed bronchioles. Crackles result from the reopening of collapsed small airways and fluid in the distal air spaces. Tachypnea and retractions reflect the increased work of breathing needed to overcome high airway resistance. Hypoxemia results from ventilation-perfusion mismatch due to atelectasis and mucus plugging. Feeding difficulty occurs because a tachypneic infant cannot coordinate suck-swallow-breathe cycles, which is a key trigger for hospitalization.

A critical pearl: apnea may be the presenting sign in very young infants (< 2 months) or those born prematurely, even before classic wheezing develops. This occurs because of immature central respiratory drive and is an important reason for admission and monitoring.

02Classification and Clinical Manifestation

Bronchiolitis does not have a formal staging system like some other diseases, but severity assessment is the primary clinical framework used to guide disposition (outpatient vs. inpatient vs. ICU).

Severity Classification

Clinical Course by Phase

High-Risk Features Warranting Hospitalization

03Diagnostic Workup

Bronchiolitis is a clinical diagnosis. This is one of the most tested concepts. The diagnosis is made based on the history and physical examination in an infant presenting with a viral upper respiratory prodrome that has progressed to lower respiratory tract signs (wheezing, crackles, respiratory distress). No laboratory test or imaging study is required to confirm the diagnosis in a typical presentation.

Pulse oximetry is the single most important objective measurement. The AAP guideline (2014, reaffirmed 2022) uses an $Sp{O}_{2}SpO\_2$ threshold of < 90% as the trigger for supplemental oxygen. Some institutions use 92%, but for exam purposes the key principle is that mild, transient desaturations in a well-appearing child do not mandate oxygen therapy or hospitalization.

RSV testing (rapid antigen detection or RT-PCR nasal swab) identifies the causative virus but does not change management in the outpatient setting. In the hospital, a positive RSV test is useful for infection control and cohorting (isolating RSV-positive patients together to prevent nosocomial spread). It may also reduce unnecessary antibiotic use by confirming a viral etiology. However, testing is not required for diagnosis.

Chest X-ray is not routinely recommended. This is a high-yield testing point. Studies have shown that obtaining CXRs in straightforward bronchiolitis leads to increased unnecessary antibiotic prescriptions because nonspecific findings (e.g., atelectasis, peribronchial thickening) are often misinterpreted as pneumonia. A CXR should only be obtained when the diagnosis is uncertain, when the clinical course is atypical (e.g., high fever, toxic appearance, lack of improvement), or when the severity warrants ICU-level evaluation. When obtained, findings include bilateral hyperinflation (flattened diaphragms, increased AP diameter), peribronchial thickening ("dirty" or prominent perihilar markings), and scattered areas of subsegmental atelectasis.

Laboratory studies (CBC, CMP, blood cultures) are similarly not indicated in uncomplicated cases. They should be reserved for infants who appear septic, febrile neonates in whom bacterial infection must be excluded, or cases with clinical deterioration suggesting secondary bacterial superinfection.

04Management and Treatment

Outpatient (Mild Cases)

The foundation of management is supportive care. Parents should be instructed on frequent nasal suctioning with a bulb syringe before feeds and sleep to maintain airway patency. Small, frequent feeds help maintain hydration. Antipyretics (acetaminophen 10-15 mg/kg/dose every 4-6 hours, or ibuprofen 10 mg/kg/dose every 6-8 hours if > 6 months) may be given for fever and discomfort. Parents must be counseled on return precautions: worsening respiratory distress, refusal to feed, signs of dehydration, or cyanosis.

Inpatient (Moderate Cases)

Hospitalization is indicated for infants with persistently, inability to maintain oral hydration, signs of moderate-to-severe respiratory distress, apneic episodes, or high-risk comorbidities. The management approach includes:

Supplemental oxygen is delivered via nasal cannula, titrated to maintain $Sp{O}_2\ge 90\mathrm{\%}SpO\_2\; \backslash geq\; 90\backslash \%$. The goal is to avoid over-oxygenation and the resulting prolonged hospitalization from waiting for weaning.

IV fluids (typically D5-normal saline or D5-half-normal saline at maintenance rates) are used when oral intake drops below 50% of normal or when tachypnea is severe enough to increase aspiration risk during feeding. Alternatively, nasogastric tube feeds can maintain enteral nutrition.

Nasal suctioning remains the single most impactful bedside intervention and should be performed regularly.

Inpatient (Severe Cases / ICU)

If the infant fails to improve on low-flow nasal cannula, high-flow nasal cannula (HFNC) at rates of 1-2 L/kg/min provides heated, humidified oxygen with a degree of positive airway pressure that helps recruit collapsed alveoli and reduce work of breathing. If HFNC is insufficient, CPAP or intubation with mechanical ventilation is the next escalation for true respiratory failure marked by recurrent apnea, rising $PaC{O}_{2}PaCO\_2$, or clinical exhaustion.

Therapies That Do NOT Work (Heavily Tested)

This is where exam questions are built. The following interventions have been studied and are not recommended by the AAP for routine use:

• Bronchodilators (albuterol): Bronchiolitis involves inflammation and mucus plugging, not bronchospasm. Smooth muscle constriction is not the primary mechanism, so beta-agonists do not provide meaningful benefit. A single trial of albuterol may occasionally be attempted in older infants with a family history of atopy, but if there is no objective improvement, it should be discontinued.

• Systemic corticosteroids (dexamethasone, prednisolone): Multiple large trials have shown no benefit in bronchiolitis. Steroids reduce inflammation in asthma (eosinophilic, Th2-driven), but the inflammation in bronchiolitis is neutrophilic and driven by direct viral cytotoxicity. Different pathophysiology, different response.

• Antibiotics: Bronchiolitis is viral. Antibiotics should only be given if there is documented secondary bacterial infection (e.g., acute otitis media, urinary tract infection, or pneumonia confirmed on culture).

• Chest physiotherapy: No evidence of benefit; may increase distress.

• Nebulized hypertonic saline (3%): May have a small benefit in hospitalized patients by drawing fluid osmotically into the airway lumen and improving mucociliary clearance, but it is not recommended in the emergency department or outpatient setting.

Prophylaxis: Palivizumab

Palivizumab is a monoclonal antibody against the RSV F protein, given as an IM injection (15 mg/kg/dose) monthly during RSV season (typically November through March, up to 5 doses). It is approved for prophylaxis, not treatment, and is indicated for:

• Infants born at < 29 weeks gestational age and < 12 months old at the start of RSV season

• Infants with hemodynamically relevant congenital heart disease

• Infants with chronic lung disease of prematurity requiring medical therapy within the preceding 6 months

Additionally, nirsevimab (a long-acting monoclonal antibody) has been approved as a single-dose alternative for RSV prophylaxis in all infants < 8 months entering their first RSV season, as well as high-risk children aged 8-19 months entering their second season.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most common way students lose points on bronchiolitis questions is by selecting an active pharmacologic intervention when the correct answer is supportive care. Exam vignettes are designed to present a sick-looking infant with respiratory distress, priming you to "do something" such as ordering albuterol, prescribing steroids, or starting antibiotics. The correct answer in a straightforward bronchiolitis presentation is almost always nasal suctioning, oxygen if hypoxemic, and IV fluids if dehydrated. Resist the urge to treat; this diagnosis tests your ability to recognize when doing less is doing right.

A second common trap involves chest X-ray interpretation. When a vignette describes a CXR with "patchy infiltrates" or "atelectasis" in the setting of classic bronchiolitis, students often pivot to pneumonia and select antibiotics. Remember that atelectasis from mucus plugging is an expected finding in bronchiolitis and does not indicate bacterial superinfection by itself. Antibiotics require additional clinical evidence: persistent high fever beyond what is expected (> 5 days), clinical toxicity, or a confirmed bacterial source.

Third, watch for the apnea presentation. A premature or very young infant (< 6-8 weeks) who presents with apneic episodes without prominent wheezing is still bronchiolitis until proven otherwise. The vignette may try to lead you toward central apnea workup or sepsis, but if there is a clear viral prodrome and RSV risk factors, bronchiolitis with apnea is the best answer, and the infant needs admission for cardiorespiratory monitoring.

Fourth, know the distinction between first-episode wheezing (bronchiolitis) and recurrent wheezing (reactive airway disease). If the vignette says "third episode of wheezing triggered by viral illness in a 14-month-old with eczema," that is no longer bronchiolitis. That child has reactive airway disease and may benefit from bronchodilators and possibly inhaled corticosteroids. The response to albuterol is a key differentiator.

Finally, remember that palivizumab is prophylaxis, not treatment. If a vignette asks about managing an infant who already has bronchiolitis, palivizumab is never the answer. It is only correct as a preventive measure in high-risk infants before RSV season.

The core competency being tested in bronchiolitis questions is clinical reasoning under pressure: recognizing a viral, self-limited disease in a distressed infant and resisting the impulse to overtreat. The exam rewards restraint, evidence-based practice, and understanding the natural history of the illness.