Pediatric Reactive Airway Disease 

  • Author: Eric S Chin, MD; Chief Editor: Richard G Bachur, MD   more...
 
Updated: Dec 1, 2011
 

Background

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]

  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 short-acting beta2-agonist
  4. Alternative diagnoses have been excluded

On June 25, 2009, The American Thoracic Society and the European Respiratory Society jointly released new official standards on asthma evaluation for clinical trials and practice.[2] The Medscape Medical News article, New Guidelines Issued for Asthma Assessment, has a more detailed discussion.

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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, resulting in increased work of breathing. A complex interaction occurs between inflammatory cells and airway epithelium. Mediators released from mast cells induce edema, mucous secretion, and bronchospasm. These mediators include histamine, tryptase, heparin, leukotrienes, platelet-activating factor, cytokines, interleukins, and tumor necrosis factor. The other inflammatory cells (ie, eosinophils, lymphocytes) also release mediators and create a toxic environment to respiratory epithelial cells.

In infants and 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.

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.

Rhinovirus infections are an important contributor to asthma exacerbations in children. Hence, therapies against rhinovirus might reduce the risk of severe exacerbations.[3]

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.[4]

Hygiene hypothesis suggests that early exposure to infections and allergens might protect children from developing asthma later in life because of improved immune system.[4]

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.

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Epidemiology

Frequency

United States

Risk of developing asthma is 7% if neither parent has asthma, 20% if one parent has asthma, and 64% if both parents have asthma. In the United States, approximately one half of all ED and clinic visits for asthma are children younger than 18 years. Pediatric asthma is a chronic, multifactorial, lower airway disease that affects 5-15% of children (2.7 million children in the United States alone). ED visits peak in the fall. School holidays disrupt the spread of infections with a subsequent decrease in hospitalization. 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.[5] Homes in poverty areas were more likely to have high cockroach allergen levels. Asthma may develop in children from early exposure to cockroach allergen.[6]

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.

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.[7] 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.

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.[8]

International

Worldwide, the prevalence of asthma is increasing. Asthma is found to be 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.

Mortality/Morbidity

  • 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.

Race

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.

No correlation exists with income or education level from a retrospective review.

Sex

The male-to-female ratio is 1.5:1.

Age

The peak prevalence of asthma is in those aged 6-11 years.

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Contributor Information and Disclosures
Author

Eric S Chin, MD  Consulting Staff, Department of Emergency Medicine, Kaiser Permanente Hospital, South San Francisco

Disclosure: Nothing to disclose.

Specialty Editor Board

Debra Slapper, MD  Consulting Staff, Department of Emergency Medicine, St Anthony's Hospital

Debra Slapper, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Grace M Young, MD  Associate Professor, Department of Pediatrics, University of Maryland Medical Center

Grace M Young, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Emergency Physicians

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Richard G Bachur, MD  Associate Professor of Pediatrics, Harvard Medical School; Associate Chief and Fellowship Director, Attending Physician, Division of Emergency Medicine, Children's Hospital of Boston

Richard G Bachur, MD is a member of the following medical societies: American Academy of Pediatrics, Society for Academic Emergency Medicine, and Society for Pediatric Research

Disclosure: Nothing to disclose.

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Patient peak flow record.
This nomogram results from tests carried out by S. Godfrey, MD, and his colleagues on a sample of 382 healthy boys and girls aged 5-18 years. Each child blew 5 times into a standard Wright Peak Flow Meter, and the highest reading was accepted in each case. All measurements were completed within a 6-week period. The outer lines of the graph indicated that the results of 95% of the children fell within these boundaries.
Stepwise approach for managing asthma in children 0 to 4 years of age. National Institutes of Health. National Heart, Lung, and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the diagnosis and management of asthma. August 2007. NIH publication no. 07-4051. Available at: http://www.nhlbi.nih.gov/guidelines/asthma/index.htm. 3 Accessed December 30, 2007. PRN, As necessary.
Table 1. Peak Flow Rates in Liters per Minute[12]
Height in



Inches



Average



Rate



Range*Height in



Inches



Average



Rate



Range*
40150110-19056330240-420
41160115-20557340240-420
42170120-22058360260-460
43180130-22059375270-480
44190135-24560390280-500
45200145-25561400290-510
46210150-27062415300-530
47220160-28063430310-550
48230165-29564445320-570
49240175-30565460330-590
50250180-32066480345-615
51260190-33067500360-640
52270195-34568515370-660
53280200-36069530380-680
54300215-38570550395-705
55315225-40571570410-730
*Includes 95% of white males aged 7-20 years.



Derived and adapted from J Pediatr 1979;95:192-6.



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