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Obstructive airway disease is the most common chronic pulmonary pathology encountered in emergency medicine. Its most common etiology, asthma, is characterized by bronchoconstriction and airway hyperresponsiveness to certain stimuli. These stimuli trigger inflammatory mediators that lead to airway inflammation, mucosal edema, and, ultimately, reversible bronchospasm.1
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Conversely, chronic obstructive pulmonary disease (COPD) is a disorder characterized by abnormal tests of expiratory flow demonstrating air flow obstruction that becomes fixed and does not change markedly over a period of months. It is a multifocal pathology encompassing the triad of emphysema, chronic bronchitis, and asthma.2 The increasing prevalence and the large burden these disease entities impose on emergency medical care make the diagnosis and management of acute exacerbations vital to any health care provider.
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Approximately 22.5 million Americans had asthma in 2005, conferring an estimated financial burden of $19.7 billion in annual health care costs.3 In the United States, there are approximately 2 million emergency department visits per year for acute asthma, with 12 million people reporting having had asthma “attacks” in the past year.4 Approximately 2–20% of all ICU admissions are attributed to severe asthma, with intubation and mechanical ventilation necessary in up to one third of ICU admissions5 and mortality rates in patients receiving intubation ranging from 10% to 20%.6
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COPD is the fourth most common cause of death in the United States, the third most common cause of hospitalization, and the only cause of death that is increasing in prevalence. The mortality of all patients while hospitalized for a COPD exacerbation is approximately 5–14%,7 while mortality of COPD patients admitted to an ICU for an exacerbation is 24%. For patients 65 years or older and discharged from the ICU after treatment of a COPD exacerbation, the 1-year mortality is 59%.7
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Asthma is characterized by airway inflammation with an abnormal accumulation of inflammatory mediators in response to various stimuli. Acutely this accumulation leads to a reversible reduction of airway diameter caused by smooth muscle contraction, vascular congestion, bronchial wall edema, and thickened secretions.
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Chronic asthma can lead to airway remodeling, with subepithelial collagen deposition and increased airway resistance that manifests as a progressive decline in forced expiratory volume in 1 second (FEV1) measurements. Once airway remodeling has occurred, the pathologic changes may become irreversible.
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Pathologic findings in patients with chronic asthma include bronchial wall thickening due to inflammation and edema, bronchial narrowing or obstruction, and the presence of mucus plugs that at times may be large and thick. This airway narrowing leads to alveolar hyperinflation and, in a subset of patients, may lead to the formation of bullae, the potential for bullae rupture, and the development of pneumothoraces (Figures 10-1 and 10-2).
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