Epidemiology

Bronchiolitis is a common presentation to emergency departments, with a seasonal pattern. It typically affects children under the age of 12 months, but may occur in children up to 2 years of age. The peak age is between 2 and 8 months of age, with males more commonly affected. Approximately 1% of children will require admission for bronchiolitis, which is the leading cause of admission for children with lower respiratory tract disease in the Western world.¹ Epidemics of bronchiolitis occur during each winter, with the peaking of respiratory viruses. While respiratory syncytial virus (RSV) is the commonest organism responsible for bronchiolitis, others include parainfluenza virus, adenovirus, rhinovirus and influenza. Bronchiolitis may also complicate exanthems such as measles and varicella in young children. It is estimated that by the age of 2, 70% of children have been exposed to RSV. Despite the frequency, mortality is low at less than 1% of hospitalised babies. High-risk patients include those with underlying chronic lung disease, congenital heart disease, neuromuscular disorders or corrected age less than 2 months of age.¹

Pathophysiology

Infection with RSV is associated with direct invasion of epithelial cells in the respiratory tract. Primary infection in young children and infants involves the lower respiratory tract. The bronchiolar epithelium is predominantly affected and an inflammatory response follows. Lymphocytes infiltrate the affected areas and oedema develops in the submucosa. Smooth muscle spasm ensues. The net result is that small airways become narrowed by the combination of oedema and muscle spasm, giving the typical clinical picture of bronchiolitis.

How this clinical picture emerges is still unclear. The role of pro-inflammatory regulators interleukin (IL)-6, IL-8, interferon-γ, and macrophage inflammatory protein-1β, as well as of the regulatory cytokine IL-10 in causing the disease as we know it, as opposed to facilitating healing and repair still remains to be elucidated.^2–4

The incidence of concomitant or secondary bacterial infection is low, although otitis media may occur. In the very young infant, apnoea may be the predominant symptom, with few other respiratory signs. Likewise, in neonates a non-specific sepsis-like picture with collapse may occur. In reinfection with RSV or primary infection in older children, the symptoms are more limited to the upper respiratory tract, causing signs consistent with a severe common cold.

History

Bronchiolitis typically presents with a prodrome of upper respiratory tract infection over 1–2 days.

When the lower respiratory tract becomes involved, the hypersecretion of mucus causes the moist cough, onset of respiratory distress and resultant feeding difficulties. As ability to feed in an infant is an important index of bronchiolitis severity, a careful history of a change in feeds is paramount.

Examination

Examination of the child will reveal a combination of signs of upper respiratory tract infection (URTI), along with signs indicative of lower respiratory tract infection (LRTI), which may fluctuate between examinations. The fever is usually low grade. A moist cough is common and wheeze may be audible at the bedside.

Tachypnoea and tachycardia are usually in proportion to the illness severity. Infants who are estimated to be feeding less than 50% of normal feeds usually have oxygen saturations less than 94%. Cyanosis is seen in children with severe disease.

Chest examination may reveal hyperinflation and recessions of the chest wall due to increased work of breathing. Paradoxically, as an infant fatigues, the recessions will decrease. In this situation the diminishing air entry signifies progressive disease. Auscultation reveals wheezes that are generally symmetrical. There may be inspiratory crepitations. The auscultation findings are dynamic as coughing will move secretions to more proximal airways, with resultant temporary clearing of the wheeze. A short time later, as the fluid returns to the more peripheral airways, the wheeze returns. Hence, babies referred by a local doctor with ‘marked wheeze’ may initially appear to be wheeze free when seen in the emergency department (ED) a short time later. Re-examination later will confirm the presence of wheeze.⁵

Oxygen saturations fall with disease severity and SaO₂ levels below 94% indicate a need for admission.⁴ McIntosh graded severity of bronchiolitis by simply documenting children as needing no oxygen, requiring oxygen and needing ventilation.⁶ Certainly, increasing oxygen requirements will be associated with increasing severity of disease.

Assessment

In helping to assess an infant with bronchiolitis and the likely subsequent course, one needs to determine the onset of the respiratory distress or poor feeding phase of the illness. Most children have increasing work of breathing for 48–72 hours due to increasing secretions, before a plateau phase followed by resolution over 3–7 days.

The cough may persist for a further 7–10 days after resolution of the respiratory distress. In this way one can determine if a child is likely to deteriorate further, is probably stable at the peak of severity or improving at the time of the ED visit. It is the tiring consequence of the tachypnoea of bronchiolitis that impairs feeding ability, which is the important determinant of whether a child warrants interventions such as oxygen or intravenous fluids.

Assessment of the child with bronchiolitis requires several components to be considered. Several scoring systems for bronchiolitis have been developed to determine the severity of the disease. Table 6.6.1 shows the criteria used to help determine severity and management issues.

Table 6.6.1 Bronchiolitis severity and management

Severity Signs Management Mild Alert Discharge home   Feeding >50% normal     Mild respiratory distress Smaller/frequent feeds   SaO₂ ≥94% Review in primary care   NOT high-risk patient     Age >6 weeks   Moderate Lethargic, tired Admit   Feeding <50% normal O₂ to SaO₂ >94%   Marked respiratory distress Minimise handling   Dehydrated Consider NG or IV fluids   SaO₂ <94% Close observation   High-risk patient   Severe As above but with: Cardiorespiratory monitor   Increasing O₂ requirement Consider ABG   Fatigue Liaise with PICU   Signs of CO₂ retention     Apnoeic episode  

ABG, arterial blood gas; NG, nasogastric; PICU, paediatric intensive care unit.

Differential diagnosis

The differential diagnosis of bronchiolitis includes cardiac failure, asthma and pneumonia (Table 6.6.2). Cardiac failure can present with many of the features of bronchiolitis – dyspnoea, tachypnoea, tachycardia, crepitations and palpable liver. Feeding may also be poor. However, infants with bronchiolitis will usually have the URTI prodrome and the onset of poor feeding is acute. The feeding difficulty in children with cardiac failure is less acute, leading to poor weight gains. Additional signs, such as a gallop rhythm or murmur, suggest an underlying cardiac abnormality. Recurrent episodes of wheeze associated with URTIs, particularly in older infants, can be difficult to differentiate from asthma. Pneumonia in infants can mimic bronchiolitis and the differentiation can be difficult. Some infants have persistent wheezing, which does not compromise activity or feeds and is unresponsive to inhaled bronchodilators (‘fat happy wheezer’).

Table 6.6.2 Differential diagnosis of bronchiolitis

Asthma Cardiac failure Pneumonia Neonatal sepsis – presenting as collapse Happy wheezer – persistent wheezing in undistressed baby

Investigations

The diagnosis of bronchiolitis is clinical, based on history and examination. The role of chest radiography is limited and only indicated if the diagnosis is unclear or in severe cases. The typical radiological findings are hyperinflation of the lung fields, with bilateral increase in interstitial markings (particularly perihilar regions). There may be patchy atelectasis secondary to plugging or, in severe cases, collapse. Children with high fever, or a clinical impression of sepsis, may have superimposed bacterial infection, and a chest X-ray will aid exclusion of this diagnosis.⁷

Nosocomial infection and cross-infection can occur during bronchiolitis outbreaks. In patients being admitted to hospital, a nasopharyngeal aspirate (NPA) or posterior nasal aspirate (PNA) can be done to analyse for RSV or other respiratory viruses for isolation control. The development of near patient testing (NPT) kits for rapid diagnosis of RSV infection has aided infection control in some areas.⁸ The rapid testing for RSV may be useful in cases of neonates to help with decision making where a child presents with fever, collapse or apnoea.

Other tests such as full blood examination are generally not useful in diagnosis. Severe cases may demonstrate CO₂ retention on arterial blood gases or electrolyte disturbance.

Drug therapy

The role of various drug therapies in bronchiolitis is controversial and still undergoing research.

Two meta-analyses of the benefits of inhaled β agonists in bronchiolitis have proved inconclusive. A more recent Cochrane Review suggests some minimal benefit, while Patel has recently shown no benefit with albuterol (salbutamol).^9–12 Nebulised adrenaline (epinephrine) has similarly not been shown to provide benefit over a sustained timeframe. Isaacs suggested that if wheeze is the predominant sign then a trial of selective β agonist may help.¹

Systemic or inhaled glucocorticoids are widely used in some parts of the world, but the evidence for their use is variable. A recent meta-analysis has shown some marginal benefit with systemic glucocorticoid use.¹³ The role of ipratropium bromide is equally unclear and there is no clear-cut benefit to use.¹⁴

Nebulised adrenaline (epinephrine) and dexamethasone in combination have been shown in a multicentre trial in Canada to have some potential beneficial effect on the severity of the illness as determined by hospital admission.¹⁵

Ribavarin and antiviral immunoglobulins are not used in the ED setting, but may have a role in high-risk groups in intensive care. Ribavirin is expensive and has only marginal benefit when given aerolysed to high-risk patients with severe disease.¹⁶ The role of immunisation against RSV is still under investigation.