Bronchiolitis is a common lower respiratory tract infection in infants and young children, occurring most frequently in those under the age of two. The peak incidence is observed in children aged 2–6 months. Pure bronchiolitis affecting only the bronchioles, without involving alveoli and interalveolar walls, is rarely identified clinically. Therefore, it is considered a specific type of pneumonia referred to as asthmatic pneumonia.
Etiology
The condition is primarily caused by respiratory syncytial virus (RSV). Other causes include parainfluenza virus, adenovirus, rhinovirus, human metapneumovirus (hMPV), bocavirus, and Mycoplasma pneumoniae.
Pathology and Pathogenesis
The pathological changes mainly involve bronchioles with diameters of 75–300 μm. These changes include epithelial necrosis and lymphocytic infiltration in the surrounding tissue, along with submucosal congestion, edema, glandular hyperplasia, and increased mucus secretion. These changes result in narrowing or even obstruction of the bronchiolar lumen, leading to pulmonary emphysema and atelectasis. The inflammation may extend to the alveoli, alveolar walls, and pulmonary interstitium, resulting in ventilation and gas exchange disorders. These complications can further lead to hypoxemia, hypercapnia, respiratory acidosis or alkalosis, and metabolic acidosis.
Clinical Manifestations
The typical course of bronchiolitis begins with upper respiratory symptoms. Lower respiratory tract symptoms and signs usually appear 2–3 days later, peak at 3–5 days, and then gradually subside. A distinguishing feature of this condition is the simultaneous occurrence of cough and dyspnea. Wheezing and wheezing sounds upon auscultation of the lungs are prominent features. The condition primarily manifests as symptoms of lower airway obstruction, such as prolonged exhalation with wheezing. Severe cases may include expiratory respiratory distress. Respiratory distress may occur in episodes, with no wheezing observed during the intervals.
Severe cases may present with pale complexion, irritability, and perioral or lip cyanosis. Respiratory symptoms are often more pronounced than systemic symptoms at the onset, and body temperature may vary. Physical examination may reveal shallow and rapid breathing, with a rate of 60–80 breaths per minute or even over 100 breaths per minute, along with nasal flaring and inspiratory retraction. The heart rate may be accelerated to 150–200 beats per minute.
Lung auscultation often reveals expiratory wheezing; moist rales may be heard when dyspnea improves slightly. Percussion may reveal hyperresonant sounds. The liver and spleen may be palpable at the subcostal margin due to hyperinflation of the lungs pushing these organs downward. Increased insensible water loss due to excessive ventilation and inadequate fluid intake may lead to significant dehydration in some patients. Metabolic acidosis may occur in infants. Severe dyspnea may lead to carbon dioxide retention, resulting in respiratory acidosis, reduced arterial oxygen partial pressure, and respiratory failure.
The peak severity of this condition is often observed 48–72 hours after the onset of respiratory distress. The disease course typically lasts between 5 and 15 days, with an average duration of 10 days.
Auxiliary Examinations
The total white blood cell count and its differentiation in peripheral blood are often within normal ranges. Severe cases may show metabolic acidosis on blood gas analysis, and a small number of cases may demonstrate respiratory acidosis. Blood gas analysis is used to assess the degree of hypoxia and carbon dioxide retention. Monitoring of oxygen saturation is recommended in patients with risk factors for severe bronchiolitis, such as chronic lung disease or anatomical abnormalities of the airway.
Pathogen-based diagnosis includes testing for viral antigens and nucleic acids, as well as virus isolation. Chest X-rays may reveal varying degrees of pulmonary hyperinflation, patchy infiltration, localized atelectasis, peribronchial inflammation, and increased pulmonary markings.
Diagnosis and Differential Diagnosis
The diagnosis is generally straightforward in infants presenting with typical wheezing and wheezing sounds. However, differentiation from the following conditions is necessary:
Bronchial Asthma
The first episode of infectious wheezing in an infant is often bronchiolitis. However, recurrent wheezing episodes and a family history of asthma or other allergic conditions may indicate asthma.
Tuberculosis
Miliary tuberculosis may occasionally present with episodic wheezing, but rales are generally absent on auscultation. Wheezing may also occur in patients with bronchial lymph node tuberculosis due to lymph nodes compressing the airways. Differentiation is made based on a history of tuberculosis exposure, signs of tuberculosis intoxication, tuberculin skin tests, and chest X-ray findings.
Other Conditions
Conditions such as mediastinal masses, cardiogenic wheezing, foreign body aspiration, and congenital tracheobronchial abnormalities may also cause wheezing. A combination of medical history, clinical findings, and relevant diagnostic tests is used for differentiation.
Treatment
Currently, there is no specific or highly effective treatment available, so management primarily focuses on supportive and symptomatic care.
General Treatment
Frequent ventilation of the room is recommended to maintain adequate temperature and humidity levels. Nutritional intake should ensure sufficient caloric and hydration needs. Hospitalization is suggested for patients with moderate to severe respiratory distress, especially those in high-risk groups.
Symptomatic Treatment
Oxygen therapy is provided if blood oxygen saturation remains consistently below 90%–92%. High-flow nasal cannula oxygen therapy may be used if necessary. For patients with severe dyspnea, bronchodilators may be attempted; however, further use is discontinued if the initial treatment is ineffective. Routine use of systemic glucocorticoids is not recommended. For patients experiencing severe dyspnea, systemic glucocorticoids may be tried for 1–3 days, but the medication should be discontinued promptly if no improvement is observed.
Anti-Infective Treatment
Bronchiolitis is most commonly caused by RSV infection, for which there are currently no clearly effective antiviral drugs. Ribavirin, a broad-spectrum antiviral agent, has uncertain efficacy in treating RSV-induced bronchiolitis. For cases involving Mycoplasma pneumoniae infection, macrolide antibiotics may be used. Antibiotics may also be administered on a case-by-case basis for secondary bacterial infections.
Other Measures
Efforts should be made to maintain airway patency, ensure sufficient fluid intake, correct acidosis, and address respiratory failure or other critical conditions promptly if they arise.
Prevention
Education and Lifestyle Changes
Educational efforts to raise parental awareness of the disease are emphasized. Breastfeeding is promoted, passive smoking should be avoided, and measures to improve the physical health of infants and young children are encouraged.
Immunoprophylaxis
Vaccines targeting the most common pathogens of bronchiolitis (such as RSV, rhinovirus, human metapneumovirus, and parainfluenza virus) are currently unavailable. However, RSV monoclonal antibody (palivizumab) may be used for prevention in high-risk infants, including those born prematurely or those with bronchopulmonary dysplasia, congenital heart disease, or immunodeficiency disorders. Palivizumab has been shown to reduce the incidence and hospitalization rates related to RSV infections in these high-risk groups.