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Asthma is a chronic inflammatory disorder characterized by increased responsiveness of the airways to multiple stimuli. Many cells and cellular elements, such as mast cells, eosinophils, T-lymphocytes, macrophages, neutrophils, and epithelial cells, play a role in the development of the inflammatory response. 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 usually are associated with widespread, but variable, airflow obstruction that is often reversible spontaneously or with treatment.


Although most acute attacks are reversible and improve spontaneously or within minutes to hours with treatment and patients appear to recover completely clinically, many asthmatic patients develop chronic airflow limitation. The recognition that asthma is a chronic inflammatory disorder of the airways has significant implications for the diagnosis, management, and potential prevention of acute exacerbations.


Asthma affects approximately 4% to 5% of the population in the U.S.1 It is the most common chronic disease of childhood, with a prevalence of 5% to 10%. On the other end of the spectrum, asthma affects 7% to 10% of the elderly, accounting for 68,000 admissions to hospitals in 1991.2 Approximately one half of cases of asthma develop before the age of 10 years old and another one third before the age of 40 years old. The 2:1 male-to-female preponderance of asthma in childhood equalizes by age 30 years old. Self-reported prevalence rates for asthma in the U.S. increased by 74% from 1980 to 1996.1 Similar prevalence rates are reported in developed nations throughout the world. From 1980 to 1999, the estimated annual number of office visits for asthma in the U.S. increased by 83%, from 5.9 million to 10.4 million. Whereas the number of ED visits increased by 36% (from 1.5 million to 2 million) between 1992 and 1999, the number of hospitalizations and deaths seems to have declined since 1995.1 In the U.S. alone, the estimated direct and indirect costs of asthma in all age groups was $6.2 billion in 1990.3


Asthma is characterized by inflammation of the airways, with an abnormal accumulation of eosinophils, lymphocytes, mast cells, macrophages, dendritic cells, and myofibroblasts. 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 are reflected in pulmonary function changes, increased work of breathing, and abnormal distribution of pulmonary blood flow (Table 72-1). Large and small airways often contain plugs composed of mucus, serum proteins, inflammatory cells, and cellular debris. On a microscopic level, airways are infiltrated with eosinophils and mononuclear cells. Evidence of microvascular leakage, epithelial disruption, and vasodilation is frequently noted. The airway smooth muscle is hypertrophied and characterized by new vessel formation, an increased number of epithelial goblet cells, and deposition of interstitial collagen beneath the epithelium. Subepithelial fibrosis, an increase in the thickness of the reticular layer of the basement ...

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