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Asthma is a chronic inflammatory disorder characterized by increased responsiveness of the airways to multiple stimuli. In susceptible individuals, the inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and coughing, particularly at night or in the early morning. These episodes—acute asthma—usually have widespread and varying airflow obstruction.

Although most acute asthma episodes improve spontaneously or within minutes to hours with treatment, with symptom-free intervals in between, many patients with asthma develop chronic airflow limitation. This impacts the diagnosis and management of episodes and the attempts to prevent recurrent acute asthma.

Asthma affects approximately 8% of the U.S. population, is the most common chronic disease of childhood (9% prevalence), and has a similar prevalence in developed nations around the world.1-3 Approximately one half of asthma cases develop before the age of 10 years, and another one third develop by the age of 40 years.


Asthma sufferers have an abnormal accumulation of eosinophils, lymphocytes, mast cells, macrophages, dendritic cells, and myofibroblasts in airways. The pathophysiologic hallmark of asthma is a reduction in airway diameter caused by smooth muscle contraction, vascular congestion, bronchial wall edema, and thick secretions. These changes create pulmonary function changes, increased work of breathing, and abnormal distribution of pulmonary blood flow (Table 69-1). Large and small airways contain plugs composed of mucus, serum proteins, inflammatory cells, and cellular debris. Inflammation affects all bronchial pulmonary structures.

TABLE 69-1Physiologic Consequences of Airflow Obstruction in Acute Asthma

Asthma is a continuum from acute bronchospasm through airway inflammation to permanent airway remodeling. Airway remodeling, with sub-basement membrane thickening, subepithelial fibrosis, airway smooth muscle hypertrophy and hyperplasia, angiogenesis, and mucous gland hyperplasia and hypersecretion, can become a trigger for nonreversible loss of lung function.4

Acute allergic bronchoconstriction results from immunoglobulin E–dependent release of mediators from mast cells. These mediators include histamine, leukotrienes, tryptase, and prostaglandins that directly contract airway smooth muscle.4 Bronchospasm induced by aspirin and other NSAIDs also involves mediator release from airway cells.4 Airway inflammation occurs as inhaled antigens activate immunoglobulin E, mast cells, dendritic cells, T helper cells, and epithelial cells in the airway and induce inflammatory mediators and cytokines. In turn, this initiates a cascade of inflammatory response, which is multicellular, redundant, and self-amplifying.

Acute asthma is an exaggerated airway response to a variety of external exposures. Viral acute respiratory infections are the most common acute asthma stimulus,5 accounting for 40% to 80% of episodes in adults and 80% in children....

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