Almost 5 million children in the United States have asthma1 and it is the most common reason for admission to pediatric hospitals.2 Each year, asthma results in 10 million school absences,2 5500 deaths,3 and 500,000 hospitalizations.4,5 Appropriate asthma treatment prevents hospital admissions and emergency room visits, reduces the risk of death, and improves the quality of life for children with asthma.4,6,7 The hospitalist is ideally situated to have a major impact on asthma by treating its acute manifestations, by implementing effective long-term therapy where indicated, and by diagnosing and managing any comorbidity that accompanies and/or exacerbates asthma.
Asthma results from airway inflammation and smooth muscle dysfunction. It is defined by the National Heart Lung and Blood Institute (NHLBI) and World Health Organization (WHO) as:
A chronic inflammatory disorder of the airways in which many cells and cellular elements play a role, in particular, mast cells, eosinophils, T lymphocytes, macrophages, neutrophils, and epithelial cells. In susceptible individuals, this inflammation causes recurrent episodes of wheezing, breathlessness, chest tightness, and cough, particularly at night and in the early morning. These symptoms are usually associated with widespread but variable airway obstruction that is often reversible either spontaneously or with treatment. The inflammation also causes an associated increase in the existing bronchial hyperresponsiveness to a variety of stimuli. Reversibility of airflow limitation may be incomplete in some patients with asthma.4
PATHOPHYSIOLOGY OF ASTHMA
The underlying cause of asthma is unknown and the course of pediatric asthma is dynamic. Early in the course of the disease, airway inflammation, bronchial hyperreactivity and loss of lung function are evident. Atopy and a family history of asthma are strongly correlated with asthma in childhood. Exposure to allergens activates mast cells and promotes inflammation and airway infiltration with neutrophils, eosinophils, and lymphocytes.8 Whatever the cause, the inflammation results in airway hyperresponsiveness, which causes bronchoconstriction, edema and mucus plugging, all of which contribute to bronchial obstruction. Chronically, collagen deposition below the epithelial basement membrane results in narrowing of the airway due to remodeling.
Asthma exacerbations are acute or subacute episodes of progressively worsening shortness of breath, cough, wheezing, and chest tightness, or some combination of these symptoms. Exacerbations are characterized by decreases in expiratory airflow that can be documented and quantified by measurement of lung function (spirometry or PEF). These objective measures more reliably indicate the severity of an exacerbation than does the severity of the symptoms. Status asthmaticus is continued or progressive airway obstruction despite bronchodilator therapy resulting in sustained or worsening respiratory distress.4
Acute asthma exacerbations can be triggered by infectious respiratory illness, environmental allergen or irritant exposure, exercise, cold air, or a combination of these. An asthma exacerbation involves either a slow onset of symptoms or a rapid decline in respiratory ...