What is Asthma?
Asthma is a common disease, affecting approximately 8–10% of the population. It is slightly more common in male children (younger than 14 years) and in female adults. There is a genetic predisposition to asthma. Prevalence, hospitalizations, and fatal asthma have all increased in the United States over the past 20 years. Each year, approximately 10 million office visits, 1.8 million emergency department visits, and more than 3500 deaths in the United States are attributed to asthma. Hospitalization rates have been highest among blacks and children, and death rates are consistently highest among blacks aged 15–24 years.
Causes of Asthma
Asthma is a chronic disorder of the airways characterized by variable airway
obstruction, airway hyperresponsiveness, and airway inflammation. No single
histopathologic feature is pathognomonic but common findings include
1.airway inflammatory cell infiltration with eosinophils, neutrophils, and lymphocytes (especially T cells); goblet cell hyperplasia, sometimes plugging of small airways with mucus.
2.collagen deposition beneath the basement membrane; hypertrophy of bronchial smooth muscle; airway edema; mast cell activation; and denudation of airway epithelium.
3.Interleukin-5 is important in promoting eosinophilic inflammation.
4.The strongest identifiable predisposing factor for the development of asthma is atopy, but obesity is increasingly recognized as a risk factor.
Pathogenesis
1.Nonspecific precipitants of asthma include exercise, upper respiratory tract
infections, rhinosinusitis, postnasal drip, aspiration, gastroesophageal reflux, changes in the weather, and stress. Exposure to products of combustion (eg, from tobacco, crack cocaine, methamphetamines, and other agents) increases asthma symptoms and the need for medications and reduces lung function.
2.Air pollution (increased air levels of respirable particles, ozone, SO2, and NO2) precipitate asthma symptoms and increase emergency department visits and hospitalizations.
3.Selected individuals may experience asthma symptoms after exposure to aspirin (aspirin-exacerbated respiratory disease), nonsteroidal anti-inflammatory drugs, or tartrazine dyes.
4.Occupational asthma is triggered by various agents in the workplace and may occur weeks to years after initial exposure and sensitization.
5.Women may experience catamenial asthma at predictable times during
the menstrual cycle.
6.Exercise-induced bronchoconstriction begins during exercise or
within 3 minutes after its end, peaks within 10–15 minutes, and then resolves by 60 minutes. This phenomenon is thought to be a consequence of the airways’ attempt to warm and humidify an increased volume of expired air during exercise.
7.“Cardiac asthma” is wheezing precipitated by decompensated heart failure. Cough-variant asthma has cough instead of wheezing as the predominant symptom of bronchial hyperreactivity.
Symptoms and Signs
Asthma is characterized by episodic wheezing, difficulty in breathing, chest tightness, and cough.
Excess sputum production is common.
The frequency of asthma symptoms is highly variable.
Some patients have infrequent, brief attacks of asthma while others may suffer nearly continuous symptoms.
Asthma symptoms may occur spontaneously or be precipitated or exacerbated by many different triggers as discussed above.
Asthma symptoms are frequently worse at night; circadian variations in bronchomotor tone and bronchial reactivity reach their nadir between 3 AM and 4 AM, increasing symptoms of bronchoconstriction.
Hunched shoulders and use of accessory muscles of respiration suggest an increased work of breathing.
Laboratory Findings (Diagnosis)
Arterial blood gas measurementsmay be normal during a mild asthma exacerbation, but respiratory alkalosis and an increase in the alveolar-arterial oxygen difference (A–a–DO2) are common. During severe exacerbations, hypoxemia develops and the PaCO2 returns to normal. The combination of an increased PaCO2 and respiratory acidosis may indicate impending respiratory failure and the need for mechanical ventilation.
Pulmonary Function Testing
The evaluation for asthma should therefore include spirometry (forced expiratory volume in 1 second [FEV1], forced vital capacity [FVC], FEV1/FVC) before and after the administration of a short-acting bronchodilator. These measurements help determine the presence and extent of airflow obstruction and whether it is immediately reversible. Airflow obstruction is indicated by a reduced FEV1/FVC ratio. Significant reversibility of airflow obstruction is defined by an increase of 12% or more and 200 mL in FEV1 or FVC after inhaling a short-acting bronchodilator. Exercise challenge testing may be useful in patients with symptoms of exercise induced bronchospasm.
Peak expiratory flow (PEF)
These meters are handheld devices designed as personal monitoring tools. PEF monitoring can establish peak flow variability, quantify asthma severity, and provide both patient and clinician with objective measurements on which to base treatment decisions. An absolute eosinophil count can identify patients eligible for anti–interleukin-5 therapy to manage eosinophilic airway disease.
Differential Diagnosis
Patients who have atypical symptoms or poor response to therapy may have a condition that mimics asthma. These disorders typically fall into one of five categories:
Systemic vasculitides
Cardiac disorders
Psychiatric disorders
Upper airway disordersthat mimic asthma include vocal fold paralysis, vocal fold dysfunction syndrome, foreign body aspiration, laryngotracheal masses, tracheal narrowing, tracheobronchomalacia, and airway edema (eg, angioedema or inhalation injury).
Lower airway disordersinclude nonasthmatic chronic obstructive pulmonary disease (COPD) (chronic bronchitis or emphysema), bronchiectasis, allergic bronchopulmonary mycosis, cystic fibrosis, eosinophilic pneumonia, hypersensitivity pneumonitis, sarcoidosis, and bronchiolitis obliterans.
Systemic vasculitideswith pulmonary involvement may have an asthmatic component, such as eosinophilic granulomatosis with polyangiitis.
Cardiac disordersinclude heart failure and pulmonary hypertension. Psychiatric causes include conversion disorders (“functional” asthma), emotional laryngeal wheezing, vocal fold dysfunction, or episodic laryngeal dyskinesis. Rarely, Münchausen syndrome or malingering may
explain a patient’s complaints.
Report of the National Asthma Education and Prevention
Program (NAEPP), in conjunction with the Global Initiative for Asthma, a collaboration between the National Institutes of Health/National Heart, Lung, and Blood Institute and the World Health Organization, provides guidelines for diagnosis and management of asthma. This report identifies four components of chronic asthma diagnosis and management:
(1) assessing and monitoring asthma severity and
asthma control
(2) patient education designed to foster a partnership for care
(3) control of environmental factors and comorbid conditions that affect asthma
(4) pharmacologic therapy for asthma.
Clinical Diagnosis
1.Episodic or chronic symptoms of wheezing, dyspnea, or cough.
2.Symptoms frequently worse at night or in the early morning.
3.Prolonged expiration and diffuse wheezes on physical examination.
4.Limitation of airflow on pulmonary function testing or positive bronchoprovocation challenge.
5.Reversibility of airflow obstruction, either spontaneously or following
bronchodilator therapy.
Pharmacologic Agents
Asthma medications can be divided into two categories:
(1) quick relief (reliever) medications that act principally by direct relaxation of bronchial smooth muscle, thereby promoting prompt reversal of acute airflow obstruction to relieve accompanying
symptom
(2) long-term control (controller) medications that act primarily to
attenuate airway inflammation and that are taken daily independent of symptoms to achieve and maintain control of persistent asthma. Anti-inflammatory agents, long-acting bronchodilators, and leukotriene modifiers comprise the important long-term control medications. Most asthma medications are administered by inhalation or orally. Inhalation of an appropriate agent results in a more rapid onset of pulmonary effects as well as fewer systemic effects compared with oral administration of the same dose. Proper inhaler technique and the use of an inhalation chamber (a “spacer”) with metered-dose inhalers
(MDIs) decrease oropharyngeal deposition and improve drug delivery to the lung. Nebulizertherapy is reserved for patients who are acutely ill and those who cannot use inhalers because of difficulties with coordination, understanding, or cooperation.
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