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Once the offending allergens are identified, counsel patients on how to avoid them. Efforts should focus on the home, where specific triggers include dust mites, animals, cockroaches, mold, and pollen. See Treatment and Medication for more detail. Asthma is a common chronic disease worldwide and affects approximately 26 million persons in the United States.

It is the most common chronic disease in childhood, affecting an estimated 7 million children, and it is a common cause of hospitalization for children in the United States. The mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity.

Varying degrees of mononuclear cell and eosinophil infiltration, mucus hypersecretion, desquamation of the epithelium, smooth muscle hyperplasia, and airway remodeling are present.

The mechanisms involved include direct stimulation of airway smooth muscle and indirect stimulation by pharmacologically active substances from mediator-secreting cells such as mast cells or nonmyelinated sensory neurons.

The degree of airway hyperresponsiveness generally correlates with the clinical severity of asthma. Spirometry with postbronchodilator response should be obtained as the primary test to establish the asthma diagnosis. Exercise spirometry is the standard method for assessing patients with exercise-induced bronchospasm. Physical findings vary with the severity of the asthma and with the absence or presence of an acute episode and its severity. The severity of asthma is classified as intermittent, mild persistent, moderate persistent, or severe persistent.

Patients with asthma of any level of severity may have mild, moderate, or severe exacerbations. With severe exacerbations, indications for hospitalization are based on findings after the patient receives 3 doses of an inhaled bronchodilator. In general, patients should be assessed every 1-6 months for asthma control. The airways of the lungs consist of the cartilaginous bronchi, membranous bronchi, and gas-exchanging bronchi termed the respiratory bronchioles and alveolar ducts.

The smallest non-gas-exchanging airways, the terminal bronchioles, are approximately 0. Basophils, eosinophils, neutrophils, and macrophages also are responsible for extensive mediator release in the early and late stages of bronchial asthma.

Stretch and irritant receptors reside in the airways, as do cholinergic motor nerves, which innervate the smooth muscle and glandular units.

Evidence also suggests a key and expanding role for viral respiratory infections in these processesThe onset of asthma for most patients begins early in life, with the pattern of disease persistence determined by early, recognizable risk factors including atopic disease, recurrent wheezing, and a parental history of asthmaCurrent asthma treatment with anti-inflammatory therapy does not appear to prevent progression of the underlying disease severityThe mechanism of inflammation in asthma may be acute, subacute, or chronic, and the presence of airway edema and mucus secretion also contributes to airflow obstruction and bronchial reactivity.

Some of the principal cells identified in airway inflammation include mast cells, eosinophils, epithelial cells, macrophages, and activated T lymphocytes.

T lymphocytes play an important role in the regulation of airway inflammation through the release of numerous cytokines. Other constituent airway cells, such as fibroblasts, endothelial cells, and epithelial cells, contribute to the chronicity of the disease.

Other factors, such as adhesion molecules (eg, selectins, integrins), are critical in directing the inflammatory changes in the airway. Finally, cell-derived mediators influence smooth muscle tone and produce structural changes and remodeling of the airway. The presence of airway hyperresponsiveness or bronchial hyperreactivity in asthma is an exaggerated response to numerous exogenous and endogenous stimuli.

A study by Balzar et al reported changes in airway resident mast cell populations from a large group of subjects with asthma and normal control subjects. Chronic inflammation of the airways is associated with increased bronchial hyperresponsiveness, which leads to bronchospasm and typical symptoms of wheezing, shortness of breath, and coughing after exposure to allergens, environmental irritants, viruses, cold air, or exercise.

In some patients with chronic asthma, airflow limitation may be only partially reversible because of airway remodeling (hypertrophy and hyperplasia of smooth muscle, angiogenesis, and subepithelial fibrosis) that occurs with chronic untreated disease.

Airway inflammation in asthma may represent a loss of normal balance between two "opposing" populations of Th lymphocytes.

Two types of Th lymphocytes have been characterized: Th1 and Th2. Th2, in contrast, generates a family of cytokines (IL-4, IL-5, IL-6, IL-9, and IL-13) that can mediate allergic inflammation. A study by Gauvreau et al found that IL-13 has a role in allergen-induced airway responses. However, unequivocal support for the "hypgiene hypothesis" has not been demonstrated. Acute bronchoconstriction is the consequence of immunoglobulin E-dependent mediator release upon exposure to aeroallergens and is the primary component of the early asthmatic response.

Airway edema occurs 6-24 hours following an allergen challenge and is referred to as the late asthmatic response. Chronic mucous plug formation consists of an exudate of serum proteins and cell debris that may take weeks to resolve. Airway remodeling is associated with structural changes due to long-standing inflammation and may profoundly affect the extent of reversibility of airway obstruction.

These changes lead to a decreased ability to expel air and may result in hyperinflation. Uneven changes in airflow resistance, the resulting uneven distribution of air, and alterations in circulation from increased intra-alveolar pressure due to hyperinflation all lead to ventilation-perfusion mismatch.

Vasoconstriction due to alveolar hypoxia also contributes to this mismatch. In the early stages, when ventilation-perfusion mismatch results in hypoxia, hypercarbia is prevented by the ready diffusion of carbon dioxide across alveolar capillary membranes. Thus, patients with asthma who are in the early stages of an acute episode have hypoxemia in the absence of carbon dioxide retention.

Hyperventilation triggered by the hypoxic drive also causes a decrease in PaCO2. An increase in alveolar ventilation in the early stages of an acute exacerbation prevents hypercarbia.

With worsening obstruction and increasing ventilation-perfusion mismatch, carbon dioxide retention occurs. In the early stages of an acute episode, respiratory alkalosis results from hyperventilation. Later, the increased work of breathing, increased oxygen consumption, and increased cardiac output result in metabolic acidosis. Respiratory failure leads to respiratory acidosis due to retention of carbon dioxide as alveolar ventilation decreases.

Most patients experience symptoms during the third to fourth decade. A single dose can provoke an acute asthma exacerbation, accompanied by rhinorrhea, conjunctival irritation, and flushing of the head and neck.

It can also occur with other nonsteroidal anti-inflammatory drugs and is caused by an increase in eosinophils and cysteinyl leukotrienes after exposure. Primary treatment is avoidance of these medications, but leukotriene antagonists have shown promise in treatment, allowing these patients to take daily aspirin for cardiac or rheumatic disease. Aspirin desensitization has also been reported to decrease sinus symptoms, allowing daily dosing of aspirin.

Patients with asthma are 3 times more likely to also have GERD. More than 300 specific occupational agents have been associated with asthma. High-risk jobs include farming, painting, janitorial work, and plastics manufacturing.

Given the prevalence of work-related asthma, the American College of Chest Physicians (ACCP) supports consideration of work-related asthma in all patients presenting with new-onset or worsening asthma. An ACCP consensus statement defines work-related asthmas as including occupational asthma (ie, asthma induced by sensitizer or irritant work exposures) and work-exacerbated asthma (ie, preexisting or concurrent asthma worsened by work factors).

Immune-mediated asthma has a latency of months to years after exposure.