What is REACTIVE AIRWAY DISEASE (RAD)?
Reactive airway disease is another name for wheezing and coughing that happens when the airways in the lungs “react” to something, such as a respiratory infection. The small breathing tubes in the lungs react by getting narrow and becoming clogged with mucus. When air passes through a narrowed airway, it makes a high pitched whistling noise called wheezing. Some children with reactive airway disease may develop asthma later. While there is no way to predict exactly which children may have asthma, children with a family history of asthma are at a higher risk.
What are the symptoms of reactive airway disease?
Your child may have one or more of the following:
• Fast, shallow breathing
• Dry cough
• Chest retractions (skin pulls in between ribs with each breath)
• Nostrils flaring with each breath
What is the treatment?
Your child’s doctor will talk with you about specific care for your child. Some general
guidelines to follow are listed below:
• Your child’s doctor may prescribe aerosol treatments (breathing treatments) with
medicine that works to relax the airways that are reacting. Some children may use an
inhaler (puffer), also called a metered dose inhaler or MDI.
• Your child’s doctor may also prescribe steroids (for example, Prelone or Orapred) to be
taken for several days. The steroids help reduce inflammation and irritation in the airways.
• Keep your child away from cigarette smoke, perfumes and other strong fumes that may make the
• Do not use over-the-counter medicines, such as cough syrup, unless your child’s doctor tells you to.
When should I call the doctor?
Call 911 or your local ambulance service right away if your child:
• Is so lethargic that he hardly responds to you.
• Is working very hard to breathe or finds it hard to take a breath.
• Has chest retractions (skin pulling in around the ribs and chest when breathing).
• Grunts when he breathes.
• Has a blue or dark purple color to the nail beds, lips or gums.
• Stops breathing for more than 5 seconds.
• Cannot speak while trying to breathe.
• Has any breathing problem that needs care right away.
• Your child has persistent lethargy or irritability ( does not smile or show interest in play for at least a few
minutes during a four-hour period).
• Your child wheezes or breathes harder than he did when he was seen by the doctor
• Your baby is unable to breathe and suck at the same time or chokes when he sucks.
• Your child has fast, shallow breathing.
• Your child has a tight feeling in the chest.
• You child is inconsolable (cannot be calmed for at least a few minutes each hour using methods that
usually work for your child, such as holding, rocking, pacifiers or soothing talk.
• Continues to cough a lot even after taking medicine.
• You have any questions or concerns about how your child looks or feels.
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.
Clinical factors suggestive of childhood asthma include recurrent wheezing, symptomatic improvement with a bronchodilator, recurrent cough, exclusion of alternative diagnoses, and suggestive peak flow findings.
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.
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.
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. Homes in poverty areas were more likely to have high cockroach allergen levels. Asthma may develop in children from early exposure to cockroach allergen.
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 are needed in children using inhaled corticosteroid therapy.
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.
• One third of all children younger than 18 years are significantly affected.
• Reactive airway disease accounts for 13 million physician 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.
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.
Provide oxygen during transport, cardiorespiratory monitoring and pulse oximetry, beta-agonist nebulization, and intravenous access if the patient is in moderate-to-severe respiratory distress. Subcutaneous terbutaline or epinephrine may be considered if severe distress and very poor air movement are present.
Emergency Department Care
The initial components for ED management of reactive airway disease are oxygen, FEV1 or PEF by spirometry, and hydration with isotonic fluids.
Optimal management of status asthmaticus includes continuous inhaled beta-agonist of 0.5 mg/kg/h, inhaled ipratropium, intravenous corticosteroid (2 mg/kg/dose), and intravenous magnesium of 40 mg/kg given concurrently for the child in moderate-to-severe respiratory distress.
Frequent evaluation of the patient's cardiorespiratory status is imperative. If a child fails to improve with these interventions, admission to an ED observation area, inpatient unit, or pediatric critical care unit should be initiated. Continued failure to respond with mental status changes is an ominous finding and suggests rising pCO2. Consider noninvasive positive pressure ventilation (PPV) (eg, continuous positive airway pressure [CPAP] 3-5 cm H2O, intermittent positive airway pressure [IPAP] 10-18 cm H2O) prior to rapid sequence intubation. Consider the increased risk of pneumothorax if intubated. Optimize ventilator settings.
• Avoid intubation if possible.
• Consider all other measures first (eg, bilevel positive airway pressure, continuous beta-agonist, helium-oxygen mixture [heliox]).
• Consider ketamine for sedation/dissociative state, 1 mg/kg IV (provides 15 min anesthesia and may provide further bronchodilation for up to 30 min).
• For rapid sequence intubation, succinylcholine, 2 mg/kg IV preceded by atropine 0.02 mg/kg in the pediatric patient (older adolescent: 1-1.5 mg/kg IV without atropine) may be used.
• Tube size = (age/4) + 4
• Avoid nasal intubation. Oral intubation allows for a larger tube size and easier access for suctioning and bronchoscopy.
• Aerosolized albuterol, a beta2-agonist, relieves bronchospasm.
• Although studies suggest that delivery of albuterol by metered dose inhaler (MDI) with spacer is equally as effective as nebulization in children as young as 2 years, nebulization is recommended for those younger than 6 years or those with severe asthma or poor air movement. Infants and small children need doses of MDI equivalent to those used by adults because of decreased retention time of the drug in the lung, because of their inability to hold their breath, and because the size of the airway limits delivery of medication.
• The use of chlorofluorocarbon (CFC) inhalers is being phased out to protect the ozone layer. A decreased ozone layer may lead to health and environmental problems. No difference exists in efficacy between CFC and non-CFC inhalers.
• Continuous albuterol nebulization may reduce the need for endotracheal intubation in status asthmaticus.
• Levalbuterol, the single isomer, may result in higher patient discharge rates from the ED or hospital and hence may be more cost-effective than the traditional, racemic albuterol given.
• Ipratropium: The combination of a beta-adrenergic agonist and ipratropium improves FEV1 more effectively than either agent used alone. Other anticholinergics, such as glycopyrrolate, also may be nebulized.
• Prednisone or prednisolone given early during ED treatment reduces hospital admission rates. The dosages for both are 2 mg/kg/dose. Prednisone, in tablet form, is given to older children or adolescents. Prednisolone can be given orally (Prelone), or parenterally (Solu-Medrol). Prednisolone is preferred for the younger child or for those who cannot tolerate oral administration (eg, vomiting, severe respiratory distress, altered mental status).
• Nebulized corticosteroids could prove useful in the ED setting. Further studies are pending.
• Oral beta2-agonists have no role in the acute setting. Oral beta-agonists may be beneficial in preschool children for outpatient therapy.
• Theophylline has no role in the acute setting. It may be considered for outpatient treatment in patients with poor compliance with inhaled beta-agonist and for patients with nocturnal asthma exacerbation.
• Magnesium at 40 mg/kg IV may provide a "therapeutic bridge." Studies remain in conflict regarding magnesium's effectiveness.
Pediatric emergency medicine specialist
Pediatric critical care specialist
Pediatric pulmonary specialist