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The term reactive airway disease (RAD) is used to describe a family of diseases that share the common characteristic of airway sensitivity to physical, chemical, or pharmacological stimuli. This sensitivity results in a bronchoconstrictor response throughout the tracheobronchial tree and is seen in patients with asthma, chronic obstructive pulmonary disease (COPD), emphysema, viral upper respiratory illness, and some other respiratory disorders.
Asthma is airway hyperactivity and inflammation. There are two subgroups that respond well to bronchodilator treatment, allergic and idiosyncratic. Allergic asthma is thought to result from an immunoglobulin E–mediated response to antigens, such as dust and pollen. Among the mediators released are histamine, leukotrienes, prostaglandins, bradykinin, thromboxane, and eosinophilic chemotactic factor. Their release leads to inflammation, airway capillary leakage, increased mucus secretion, and bronchial smooth muscle contraction. Idiosyncratic asthma is mediated by nonantigenic stimuli, including exercise, cold, pollution, and infection. Bronchospasm results from increased parasympathetic (vagal) tone. Although the primary stimulus differs, the same mediators as those in allergic asthma are released (also note: some patients with allergic asthma have enhanced vagal tone).
Asthmatic bronchitis can develop from the progression of asthma or chronic bronchitis, where the patient always has some degree of airway obstruction and is less responsive to bronchodilator treatment.
Duration of disease
Frequency, initiating factors, and duration of attacks
Does the patient cough at night?
Has the patient ever required inpatient therapy? Did the patient ever require intensive care unit admission or intubation?
What are the patient’s medications, including daily and as-needed usage, over-the-counter medications, and steroids?
Common symptoms include coughing, shortness of breath, and tightness in the chest. The most common physical finding is expiratory wheezing. Wheezing is a sign of obstructed airflow and is often associated with a prolonged expiratory phase. As asthma progressively worsens, patients use accessory respiratory muscles. A significantly symptomatic patient, with quiet auscultatory findings, may signal impending respiratory failure because not enough air is moving to elicit a wheeze. Patients may also be tachypneic and probably are dehydrated; they prefer an upright posture and demonstrate pursed-lip breathing. Cyanosis is a late and ominous sign.
The mainstay of therapy remains inhaled β-adrenergic agonists. Selective short-acting β2 agonists, such as albuterol and terbutaline, offer greater β2-mediated bronchodilation and fewer side effects (e.g., β1-associated tachydysrhythmias and tremors). Albuterol can be nebulized, administered orally or by metered-dose inhaler (MDI). Terbutaline is effective via nebulizer, subcutaneously, or as a continuous intravenous (IV) infusion. Note that β2 agonists may result in hypokalemia, lactic acidosis, and cardiac tachydysrhythmias, particularly with IV use. Patients with coronary artery disease may have particular difficulty with tachycardia and need β2- specific agents given via the inhaled route. Long-acting β2 agonists, such as salmeterol and formoterol, are used for chronic dosing and are sometimes paired with a steroid. Lastly, epinephrine is available for subcutaneous use in severely asthmatic patients.
Class and Examples | Dose | Actions |
---|---|---|
β-Adrenergic agonists: albuterol, metaproterenol, fenoterol, terbutaline, epinephrine | 2.5 mg in 3 mL of normal saline for nebulization, or 2 puffs by MDI Terbutiline dose is 0.3–0.4 mg subcutaneously Epinephrine dose is 0.3 mg subcutaneously, 5–10 mcg IV |
Increases adenylate cyclase, increasing cAMP and decreasing smooth muscle tone (bronchodilation); short-acting β-adrenergic agonists (e.g., albuterol, terbutaline, and epinephrine) are the agents of choice for acute exacerbations |
Methylxanthines: aminophylline, theophylline | 5 mg/kg IV over 30 minutes as a loading dose | Phosphodiesterase inhibition increases cAMP; potentiates endogenous catecholamines; improves diaphragmatic contractility; central respiratory stimulant |
Corticosteroids: methylprednisolone, dexamethasone, prednisone, cortisol | Methylprednisolone, 60–125 IV every 6 hours; or prednisone 30–50 mg orally daily | Antiinflammatory and membrane stabilizing; inhibits histamine release; potentiates β agonists |
Anticholinergics: atropine, glycopyrrolate, ipratropium | Ipratropium, 0.5 mg by nebulization or 4–6 puffs by MDI; Atropine, 1–2 mg per nebulization | Blocks acetylcholine at postganglionic receptors, decreasing cGMP, relaxing airway smooth muscle |
Cromolyn sodium | Also a membrane stabilizer, preventing mast cell degranulation, but must be given prophylactically | |
Antileukotrienes: zileuton, montelukast | Inhibition of leukotriene production and/or zafirlukast, leukotriene antagonism; antiinflammatory; used in addition to corticosteroids; however, may be considered first-line antiinflammatory therapy for patients who cannot or will not use corticosteroids |
Corticosteroids: reverse airway inflammation, decrease mucus production, and potentiate β-agonist–induced smooth muscle relaxation. Steroids are strongly recommended in patients with moderate to severe asthma or in patients who have required steroids in the past 6 months. Onset of action is 1 to 2 hours after administration. Methylprednisolone is popular because of its strong antiinflammatory but weak mineralocorticoid effects. Side effects include hyperglycemia, hypertension, hypokalemia, and mood alterations, including psychosis. Long-term steroid use is associated with myopathy. Steroids may be given orally, via MDI, or intravenously.
Anticholinergic agents: produce bronchodilation by blocking muscarinic cholinergic receptors in the airway, therefore attenuating bronchoconstriction resulting from inhaled irritants (and, occasionally, β-blocker therapy). They are commonly prescribed to patients with severe airway obstruction (predicted forced expiratory volume in 1 second [FEV 1 ] < 25%) and in COPD. Ipratropium, glycopyrrolate, and atropine may be given via nebulizer, and ipratropium is available in an MDI.
Leukotriene receptor antagonists: act by inhibition of the 5-lipoxygenase pathway or antagonism of the cysteinyl-leukotriene type 1 receptors. They are commonly prescribed and may be used in conjunction with inhaled steroids.
Cromolyn sodium: a mast cell stabilizer useful for long-term maintenance therapy. Patients younger than 17 years of age and with moderate to severe exercise-induced asthma appear to benefit the most. Administered via MDI, side effects include some minimal local irritation on delivery. Cromolyn sodium is not indicated for acute asthmatic attacks.
The patient’s history guides the judicious ordering of preoperative tests. A mild asthmatic patient maintained on as-needed medication and currently healthy will not benefit from preoperative testing. Symptomatic patients with no recent evaluation may merit closer attention.
The most common test is a pulmonary function test (PFT), which allows simple and quick evaluation of the degree of obstruction and its reversibility. A comparison of values obtained from the patient with predicted values aids assessment of degree of obstruction. Severe exacerbation correlates with a peak expiratory flow rate (PEFR) or FEV 1 of less than 30% to 50% of predicted. In most adults, this is a PEFR of less than 120 L/min and an FEV 1 of less than 1 L. Tests should be repeated after a trial of bronchodilator therapy to assess reversibility and response to treatment.
Arterial blood gases are usually not helpful. Electrocardiograms, chest radiographs, and blood counts are rarely indicated for evaluation of asthma, unless particular features of the patient’s presentation suggest alternative diagnoses (e.g., fever and rales, suggesting pneumonia).
IV induction agents used in asthmatic patients include propofol and ketamine. Ketamine has well-known bronchodilatory effects secondary to release of endogenous catecholamines, with β2-agonist effects. Ketamine also has a small, direct relaxant effect on smooth muscle. Propofol decreases both airway resistance and airway reflexes after administration. IV lidocaine is a useful adjunct for blunting the response to laryngoscopy and intubation.
Mask induction with sevoflurane is an excellent method to block airway reflexes and to relax airway smooth muscles directly. This agent is much more palatable to the airway than isoflurane or desflurane.
The stimulus of intubation (and the presence of the endotracheal tube) causes significant increases in airway resistance and, in severely asthmatic patients, may precipitate a bronchospastic crisis. As a result, deep extubation (removal of the endotracheal tube, while the patient is breathing spontaneously, but still under general anesthesia) is a commonly used strategy to facilitate a smooth emergence. Deep extubations should be avoided in patients with difficult airways, who are morbidly obese, or who may be at risk for aspiration.
COPD encompasses a spectrum of diseases that includes emphysema, chronic bronchitis, and asthmatic bronchitis. It is characterized by progressively increased resistance to breathing. Airflow limitation may result from loss of elastic recoil or obstruction of small or large (or both) conducting airways. This increased resistance may have some degree of reversibility. Cardinal symptoms are cough, dyspnea, and wheezing.
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