ASTHMA/ REACTIVE AIRWAY DISEASE

     Asthma is a chronic disorder of airway inflammation, edema, chronic mucus plug formation, and bronchoconstriction characterized clinically by recurrent episodes of wheezing, breathlessness, chest tightness, and coughing.  The inflammation, edema, and bronchoconstriction of asthma result in cross-sectional narrowing of the airways with resultant variable airflow obstruction that is generally reversible with appropriate medical therapy. The diagnosis is established by demonstrating reversibility on post bronchodilator PFT testing.

     Key indicators of asthma other than the above mentioned symptoms include nocturnal symptoms which interrupt sleep habits, plus worsening of symptoms in the presence of exercise, viral infections, animals with fur or feathers, house-dust mites, mold, smoke, pollens, changes in weather, laughing, crying, airborne chemicals or dusts, and menses.

     Conditions to consider in the differential diagnosis of asthma include COPD (chronic bronchitis and emphysema), cystic fibrosis, bronchiectasis, allergic bronchopulmonary aspergillosis, airway foreign bodies, laryngospasm, laryngeal edema, laryngotracheobronchomalacia, endobronchial tumors, pulmonary malignancies, congestive heart failure, pulmonary embolism, gastroesophageal reflux disease, carcinoid syndrome, allergic granulomatosis (Churg-Strauss syndrome), Loeffler’s syndrome, tracheal stenosis, and vocal cord dysfunction/paralysis.  Conditions which may cause exacerbation include sinusitis, allergic rhinitis, GERD, hyperthyroidism, pregnancy, and viral upper respiratory infections.  Often times, treatment of these conditions may improve the patient’s asthma symptoms.

     Spirometry measurements taken pre and post bronchodilator therapy should be used to establish the diagnosis in all patients suspected of having asthma.  Airflow obstruction will manifest as a reduced FEV1 and FEV1/FVC ratio on spirometry testing.  Reversibility will be present when the deficits in the above parameters improve by 12% or greater following inhalation of a short-acting bronchodilator.  Elderly patients may need oral steroid therapy for 2 to 3 weeks before demonstrating reversibility.  When the diagnosis is still in doubt, further testing with full pulmonary function tests (PFT) to include lung volumes, flow loops and diffusing capacity of carbon monoxide may be helpful.  Other studies to consider include chest radiography, arterial blood gas sampling, and bronchoprovocation testing with either methacholine, histamine, or an exercise challenge.  After establishing the diagnosis, spirometry should then be repeated once the patient’s symptoms and PEFR have stabilized, and then at 1 to 2 year intervals to monitor for evidence of remodeling which may lead to progressive irreversible damage (manifests as a decline in serial FEV1 measurements).

     Patients with asthma require therapy and follow up monitoring.  Patients should be taught to use a PEFR meter and to monitor this value frequently.  Patients should determine their own personal best value when they are asymptomatic and then use this value to gauge how their asthma is doing comparatively on any given day.  If the PEFR is low, patients should be instructed on how to adjust their therapy to abort a potential exacerbation.

     The first step in long-term asthma management is to identify and eliminate or reduce exposure to any stimuli which exacerbate the patient’s asthma.  There are many potential inducers of asthma to include inhalant allergens (animal allergens, house-dust mites, cockroach allergens, fungi/molds, and outdoor allergens), occupational exposures, irritants (tobacco smoke and pollution), allergic rhinitis, sinusitis, gastroesophageal reflux (GERD), NSAID sensitivity, sulfites (processed potatoes, shrimp, dried fruits, beer and wine), beta-blocker therapy, and viral respiratory infections.  The Asthma and Allergy Foundation of America (800-727-8462) has information on various companies which distribute products to aid in reducing allergen exposure.

     Emergency medical therapy for an asthma attack consists of inhaled beta-agonist therapy with or without ipratropium bromide therapy and if necessary, intravenous or oral corticosteroids.  Nebulized beta-agonist therapy equivalent to 2.5 mg of albuterol every 20-30 minutes for three consecutive doses or a single 7.5 mg dose is the recommended manner of administering treatment.  Beta-agonist therapy may be given with or without concomitant nebulized ipratropium bromide.  Delays in initiating therapy should be avoided.  Patients should also be administered supplemental oxygen.  Some physicians use heliox to administer aerosolized therapy to help abort acute attacks.  In emergent situations, subcutaneous epinephrine in a 1:1000 dilution should be administered in 0.3 mL doses.  Patients with an FEV1 less than 0.8 L or a PEFR less than 100 L/min after therapy should be hospitalized.  Once the FEV1 is greater than 1.6 L or the PEFR exceeds 300 L/min, the patient may be discharged home with outpatient therapy and close follow up.  Warning indicators of impending respiratory failure include mental impairment, fatigue, respiratory arrest, and a PCO2 greater than 42 mm Hg.  Intubation should be considered if the patient’s condition does not improve, and this procedure should be performed before the patient’s condition becomes severe.

     The complication of ventilator therapy in an asthmatic patient is that overly aggressive ventilation can result in poor exhalation which may result in hyperinflation, barotrauma, and potentially pneumothorax.  Therefore, it is important to maintain a normal respiratory rate (<15 breaths/min) and avoid greatly elevated tidal volumes.  Tidal volumes should be started at 6 to 7 mL/kg.  Plateau pressures should be monitored with a target below 35 cm H2O and an ideal level less than 30 cm H2O.  If sedatives are ineffective at maintaining a normal respiratory rate, muscle relaxants may prove effective.  Keep the duration of therapy brief when muscle relaxants are used in conjunction with steroids in order to avoid myopathy.

     Chronic therapy for asthma is directed against preventing attacks.  As needed beta-agonist therapy should be the sole form of therapy only for patients who suffer rare, infrequent attacks (mild, intermittent asthma).  In patients with recurrent regular attacks, sole therapy with beta-agonists alone is mismanagement.  Patients with more than mild, infrequent asthma should receive therapy with inhaled corticosteroids.  Therapy should initially be aggressive until symptoms are controlled and then the dosage of inhaled steroids should be reduced until the lowest effective dose is determined.  Long acting beta-agonist,tiotropium, or leukotriene inhibitor therapy may be added to inhaled steroids in order to reduce the daily dosage needed to prevent recurrance.  Patients should also be instructed on how to use beta-agonist metered dose inhalers in order to prevent exacerbations (indicated by worsening PEFR).  Other therapies for patients with moderate to severe asthma include leukotriene inhibitors and nedrocromil or cromolyn sodium.  Severe cases may require methylxanthines or chronic oral corticosteroids, but these cases should be referred to the care of a pulmonologist who specializes in asthma management.  Asthmatics should receive Tdap,  pneumoncoccal vaccine and annual influenza vaccinations. 

     Reasons for treatment failure include poor metered dose inhaler (MDI) technique, noncompliance with therapy, improper therapeutic regimen, or repeated exposure to inducers.  Patients should bring their MDIs with them to each visit and demonstrate their technique.  Patients should also demonstrate their technique for PEFRs.  Spacers are advisable to facilitate adequate medication delivery with MDIs.  Also, in patients with difficult to control asthma consider an alternative underlying etiology which may mimic asthma such as allergic bronchopulmonary aspergillosis, Churg-Strauss syndrome, bronchiectasis, or vocal cord dysfunction.

     Patients with exercise-induced asthma (EIA) should be instructed to prepare for exercise by warming up at a submaximal level for 10 minutes and if possible to avoid cold air exposure.  Following the warm up period, patients with EIA enter a refractory period for about 40 minutes, and it is during this period they may engage in exercise at any level.  If patients still suffer symptoms during exercise, a short-acting beta-agonist may be used prior to the exercise period.  Other therapies which may be offered to refractory cases include long-acting beta-agonists (salmeterol), leukotriene inhibitors, cromolyn or nedocromil sodium, and inhaled corticosteroids.

     Asthma may be secondary or exacerbated by GERD.  Since GERD is so common it is often difficult to determine the relationship of these two conditions in patients afflicted with both simultaneously.  For this reason it is best to initiate a trial of high dose proton pump inhibitor therapy in patients suspected of having GERD induced asthma.  If symptoms abate or decrease significantly, then continuation of therapy is probably advisable.