Pediatric Reactive Airway Disease

Updated: Jul 16, 2021
  • Author: Eric S Chin, MD; Chief Editor: Kirsten A Bechtel, MD  more...
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Overview

Practice Essentials

Not all children who wheeze have asthma. Most children younger than 3 years who wheeze are not predisposed to asthma. Only 30% of infants who wheeze go on to develop asthma. Reactive airway disease has a large differential diagnosis and must not be confused with asthma.

To establish the diagnosis of asthma, certain criteria should be met [1, 2] :

  1. At least 5 years of age

  2. Episodic symptoms of airflow obstruction or airway hyperresponsiveness

  3. Reversible airflow obstruction of at least 10% of predicted forced expiratory volume in one second (FEV1) after use of a short-acting beta2-agonist

  4. Alternative diagnoses have been excluded

The American Thoracic Society and the European Respiratory Society jointly released official standards on asthma evaluation for clinical trials and practice. [3]

Signs and symptoms of reactive airway disease

Clinical features that may be seen in patients with reactive airway disease include the following:

  • Fever
  • Tachycardia
  • Diaphoresis
  • Poor feeding
  • Flushing, cyanosis
  • Subcutaneous emphysema
  • Intercostal retractions
  • Increased anteroposterior diameter or pectus carinatum
  • Tachypnea, dyspnea
  • Wheezing
  • Coughing
  • Distant breath sounds, hyperresonance, poor air movement to result in wheezing ("silent chest")
  • Decreased peak expiratory flow rate
  • Inspiratory-to-expiratory ratio (normal ratios are 1:2 to 1:3)
  • Allergic shiner (dark semicircles of skin under the eyes)
  • Transverse nasal skin fold from repeatedly rubbing the nose
  • Flaring of nasal alae
  • Presence of nasal polyps and nasal secretions
  • Pulsus paradoxus (greater than a 10 mm Hg difference in systolic blood pressure during inspiration)
  • Murmur
  • Altered mental status
  • Clubbing

See Presentation for more detail.

Diagnosis of reactive airway disease

Laboratory studies

Laboratory studies that may be indicated for patients with reactive airway disease include the following:

  • Complete blood cell count
  • Arterial blood gas analysis or venous blood gas measurement
  • Assessment of electrolyte levels

Imaging studies

Radiography does not need to be routinely included in the evaluation of asthma. Consider chest radiography in the setting of increased temperature, absence of family history of asthma, or the presence of localized wheezes or rales.

Procedures

Procedures include the following:

  • Spirometry (FEV 1)
  • Peak expiratory flow (PEF) measurement
  • Barium swallow (may be indicated to determine any esophageal, pulmonary, or vascular pathology)

See Workup for more detail.

Management of reactive airway disease

Ultimately, the best treatment for reactive airway disease is to prevent an exacerbation from occurring. Knowing the provocative factors, such as infection, exercise, nonadherence to medication, weather, allergens, and irritants, can aid in early intervention.

See Treatment and Medication for more detail.

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Pathophysiology and Etiology

Pathophysiology

Numerous environmental stimuli induce an allergen-antibody interaction, causing a release of mediators that create airway inflammation. Airway inflammation is the primary factor responsible for smooth muscle hyperresponsiveness, edema, and increased mucous production. A complex interaction occurs between inflammatory cells and airway epithelium. Mast cells, eosinophils and lymphocytes secrete mediators include histamine, tryptase, heparin, leukotrienes, platelet-activating factor, cytokines, interleukins, and tumor necrosis factor and create an environment toxic to respiratory epithelial cells by causing edema, mucous secretion, bronchospasm and increased work of breathing.

Speculation exists that all infants are born with highly responsive airways. Increased immunoglobulin E (IgE) levels have been found in those younger than 2 years. A decrease in airway responsiveness may be associated with environmental allergens, viral respiratory diseases, and hereditary factors. In children younger than 3 years, the intrapulmonary airways are so small that any lower airway infection results in diminished airway function. Other anatomical factors, such as poor collateral ventilation, decreased elastic recoil pressure, and a partially developed diaphragm, may predispose the very young child to respiratory compromise.

Rhinovirus infections are an important contributor to asthma exacerbations in children. Hence, therapies against rhinovirus might reduce the risk of severe exacerbations. [4]  Fever and bronchospasm are not associated with a more severe clinical course. In fact, fever as a response to infection may have a beneficial effect and can be seen as a good prognostic indicator. [5]  Recently, it has been hypothesized that severe infection with Respiratory Syncytial Virus (RSV) may be a marker of a predisposing factor for asthma. [6]

There are several theories as to prevention of bronchospasm and asthma in children. The hygiene hypothesis suggests that early exposure to infections and allergens might protect children from developing asthma later in life because of improved immune system. [5]

Breastfeeding might protect children younger than 24 months of age against recurrent wheezing. The cytokine, TGF-B1, in human milk may have both suppression and enhancement functions in the immune reaction.

Exposure to maternal environmental tobacco smoke during pregnancy or the first year appears to predispose children to reactive airway disease.

Current research on the genetic basis for the pathogenesis of asthma may lead to new diagnostic and preventive treatments. The ADAM33 gene on the short arm of chromosome 20 is hypothesized as being important in the development and pathogenesis of asthma.

Etiology

The following are causes of pediatric reactive airway disease:

  • Precipitants of asthma exacerbation

    • Infection -Respiratory syncytial virus (RSV) most commonly isolated from infants and preschool-aged children; Mycoplasma pneumoniae most commonly isolated from school-aged children

    • Tobacco smoke

    • Pet dander, cockroach and dust mite allergen

    • Molds

    • Pollen

    • Exercise

    • Weather changes

    • Stress

    • Drugs

  • A precipitant of bronchiolitis is respiratory infection, usually due to RSV

  • Gastroesophageal fistula

  • Mediastinal mass (external compression of the airway)

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Epidemiology

United States statistics

Pediatric asthma is a chronic, multifactorial, lower airway disease that affects 5-15% of children (2.7 million children in the United States alone). In the United States, approximately one half of all ED and clinic visits for asthma are children younger than 18 years. ED visits peak in the fall, while school holidays disrupt the spread of infections, resulting in a subsequent decrease in ED visits and hospitalizations. Status asthmaticus appears to be on the rise; several retrospective studies reflect an increase in hospital admissions, particularly in those younger than 4 years. Fewer hospital and ED visits occur in children using inhaled corticosteroid therapy.

Asthma prevalence appears to be increasing worldwide. Air pollutants may play a role in the prevalence increase. Higher prevalence occurs in poverty stricken urban areas where children are less likely to have routine doctor visits and access to the availability of medications.

A correlation may exist between high levels of exposure to cockroach allergen and the frequency of asthma-related health problems in inner-city children. [7] Homes in poverty areas were more likely to have high cockroach allergen levels. Asthma may develop in children from early exposure to cockroach allergen. [8] An association may exist between obesity and childhood asthma. Increased resistin, an adipokine produced by adipose tissue, may play a negative predictive role in asthma. [9]

An algorithm has been developed to determine the risk factors for developing persistent asthma symptoms among children younger than 3 years of age who had 4 or more episodes of wheezing during the previous year. [10] The Asthma Predictive Index included either (1) one of the following: parental history of asthma, a physician diagnosis of atopic dermatitis, or evidence of sensitization to aeroallergens; or (2) two of the following: evidence of sensitization to foods, ≥4% peripheral blood eosinophilia, or wheezing apart from colds.

International statistics

Worldwide, the prevalence of asthma is increasing. Asthma is more common in Western countries than in developing countries. Asthma is more prevalent in English-speaking countries. Prevalence increases as a developing country becomes more Westernized and urbanized.

Race-, sex-, and age-related demographics

Reactive airway disease is more common in black and Hispanic children; hospitalization rates in African Americans are 4 times greater than in the white population. A correlation may exist between high levels of exposure to cockroach allergen and the frequency of asthma-related health problems in inner-city children. [7]  No correlation exists between education levels from a retrospective review.

The male-to-female ratio is 1.5:1. The peak prevalence of asthma is in those aged 6-11 years.

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Prognosis

The prognosis is excellent with attention to general health and appropriate use of medications. Fewer than 50% of patients "outgrow" asthma. Childhood asthma and wheezy bronchitis persisting into adulthood could lead to chronic obstructive lung disease (COPD) in later decades of life. [11]

Morbidity/mortality

One third of all children younger than 18 years are significantly affected. Reactive airway disease accounts for 13 million health care visits annually in the United States and 200,000 hospitalizations for which approximately $1.8 billion is spent annually. Mortality rates are increasing despite new pharmacologist advances.

Predictors of mortality risk include the following:

  • More than 3 ED visits per year

  • More than 2 hospitalizations per year

  • Hospitalization or ED visit in the last month

  • History of ICU admission

  • Mechanical ventilation

  • Use of 2 or more albuterol canisters in a month

  • Current use or recent discontinuation of systemic steroids

  • History of an acute onset of severe asthma exacerbation

  • Nocturnal symptoms

  • History of syncope

  • Comorbid cardiac disease

  • Illicit drug use

  • Serious psychosocial or psychiatric problems

  • Low socioeconomic situation

  • Limited access to health care

The European Respiratory Society (ERS) and American Thoracic Society (ATS) created a task force to evaluate and provide management recommendations for severe or therapy-resistant asthma, recognized as a major unmet need. Severe asthma is defined as requiring treatment with high-dose inhaler plus a second controller and-or systemic corticosteroids to prevent it from becoming "uncontrolled" or that remains "uncontrolled" despite this therapy. Current research based on phenotyping (epidemiology, pathogenesis, pathobiology, structure and physiology) to allow better diagnosis and targeted treatment. [12]

Complications

Complications of reactive airway disease include the following:

  • Respiratory failure/mechanical ventilation

  • Atelectasis

  • Flaccid paralysis (self-limited)

  • Death

  • Pneumothorax

  • Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

  • Altered theophylline metabolism

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Patient Education

Educate children and their families about asthma. Stress the following when you talk to them:

  • Avoidance of potential triggers

  • Emphasis on the use of anti-inflammatory inhalation

  • Instruct on peak expiratory flow and symptom monitoring

For excellent patient education resources, visit eMedicineHealth's Asthma Center. Also, see eMedicineHealth's patient education article Asthma.

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