Bronchiolitis is an acute inflammatory disease of the lower respiratory tract that is characterized by acute inflammation, edema, and necrosis of epithelial cells lining small airways, increased mucous production, and bronchospasm.¹ The term describes a clinical syndrome that occurs in infancy and is characterized by a prodromal upper respiratory tract infection, rapid respiration, chest retractions, wheezing, and frequently, hypoxia. It is a disease that occurs almost exclusively in children younger than 2 years. It is the leading cause of hospitalization in infancy in the United States, accounting for 3% of all admissions. This results in nearly 100,000 hospitalizations per year, with an associated annual cost over $1.73 billion.² It is the cause of death for less than 100 children annually in the United States³; however, it causes nearly 200,000 deaths internationally annually, especially in resource-poor settings.⁴ There is evidence that hospitalization rates are increasing as well. It has a seasonal pattern, being most common in the winter and spring.⁵

The most common etiologic agent is the respiratory syncytial virus (RSV), which is responsible for 70% of all bronchiolitis cases, and even higher in winter months.⁶ Nearly all children are RSV seropositive by the age of 2. Infection with RSV does not grant permanent or long-term immunity; reinfections are common throughout life.⁷ Many other viruses have been implicated in bronchiolitis including rhinovirus, human bocavirus, metapneumovirus, enterovirus, coronavirus, parainfluenza, adenovirus, influenza, mumps, picornavirus, and echovirus. These viruses are associated with varying severity of disease and seasonality from the more typical RSV bronchiolitis, and coinfection with multiple viruses is common.^8–13 Mycoplasma pneumoniae and Chlamydia trachomatis also have been associated with bronchiolitis. The principal agent in school-aged children with bronchiolitis is Mycoplasma.

Infection produces inflammation of the bronchiolar epithelium, causing necrosis, sloughing, and luminal obstruction. Ciliated epithelium that has sloughed is replaced by cuboidal cells without cilia. The absence of ciliated epithelium prevents adequate mobilization of secretions and debris. The bronchioles and small bronchi are obstructed by submucosal edema, peribronchiolar cellular infiltrate, mucous plugging, and intraluminal debris. The obstruction is not uniform throughout the lungs, leading to ventilation/perfusion mismatching, resultant hypoxia, and compensatory hyperventilation. If the obstruction is severe, hypercapnia may occur. Distal to the obstructed bronchiole, air trapping or atelectasis may occur. The epithelium usually regenerates from the basal layer within 3 to 4 days. However, functional regeneration of the ciliated epithelium usually requires approximately 2 weeks.

Adenovirus is associated with a particularly severe reaction termed bronchiolitis obliterans. In this disease, the destruction of the normal ciliated epithelium is extensive. The normal cells are replaced by stratified undifferentiated epithelium with an intense inflammatory response extending to the alveoli. During the reparative phase, extensive fibrosis and scarring lead to obliteration of the small airways.

Typically, a child with bronchiolitis will have a prodrome of an upper respiratory tract infection. Parents describe runny nose, low-grade fever, and decreased appetite for 1 to 2 days prior to the development of tachypnea and evidence of increased work of breathing. However, in some children lower-tract symptoms may develop over hours. Often, there will be a family or contact history of upper respiratory tract infection. Increased work of breathing may compromise patients’ abilities to tolerate oral intake; this, combined with increased insensible losses from tachypnea and fever, may result in dehydration (Fig. 36-1).

Hyperventilation occurs as a compensatory response for hypoxia secondary to ventilation–perfusion mismatch. Respiratory rates of 70 to 90 per minute or more are common. Flaring of the nasal alae and use of intercostal muscles may also be present. Respirations are shallow because of persistent distention of the lungs by the trapped air. Wheezing, prolonged expiration, and musical rales are common. The chest is often hyperexpanded and hyper resonant due to the air trapping. The liver and spleen may be displaced downward because of the hyperinflation and flattening of the diaphragm. Thoracoabdominal asynchrony may be present with breathing. Fever is present in two-thirds of children with bronchiolitis. Despite these findings, the patient often has a nontoxic appearance.

Respiratory fatigue may occur due to the increased work of breathing. Apnea may occur, chiefly in infants less than 2 months of age and typically prior to the onset of other respiratory symptoms. Rates of apnea range from 1% in healthy, term infants to as high as 24% in very young and premature infants or those with comorbidities.¹⁴

Hypoxia is common, and the patient should have oxygen saturations assessed with a pulse oximeter. Hypercarbia will be present in those with more severe obstruction. Respiratory rates greater than 60 breaths/min correlate well with carbon dioxide retention noted on blood gas analysis.

In many patients, a chest radiograph will reveal hyperinflation, peribronchial cuffing (thickening of the bronchiole walls), and areas of subsegmental atelectasis that can be difficult to differentiate from pneumonia. Although no study has convincingly demonstrated an association between radiographic findings and severity of disease,¹⁵ chest radiography may help rule out other disease processes in the differential diagnosis of bronchiolitis. The American Academy of Pediatrics (AAP) practice guideline for bronchiolitis states that the current evidence does not support routine radiography in children with bronchiolitis.¹ The use of bedside ultrasound to evaluate bronchiolitis is an area of ongoing research.^16,17

Laboratory studies are generally not helpful and are not indicated in the acute management of bronchiolitis.¹⁸ Virologic tests for RSV, if obtained during peak RSV season, have a high predictive value. These tests are helpful in hospital cohorting to minimize nosocomial transmission; however, such testing rarely alters management decisions or outcomes for the majority of children with clinically diagnosed bronchiolitis.^19,20 The use of complete blood counts is not useful in diagnosing bronchiolitis or guiding its therapy. Research has demonstrated that young febrile infants with clinical bronchiolitis are less likely to have a serious bacterial illness than febrile infants without bronchiolitis.²¹ One systematic review estimated the rate of urinary tract infection in patients younger than 90 days to be 3.3%; there were no cases of meningitis identified and few cases of bacteremia.²² Another study found positive urine cultures in 6.7% of febrile bronchiolitis patients between 2 and 12 months.²³ Acute otitis media may occur concomitantly with bronchiolitis and warrants standard therapy.