Patients with severe asthma exacerbations may have such severe restriction of airflow that they do not exhibit wheezing on examination.
Beta-2 agonists are the mainstay of treatment for acute asthma exacerbations.
Corticosteroids should be given to patients who do not respond initially to beta-2 agonists and in those with moderate to severe exacerbations.
Peak expiratory flow rate and forced expiratory volume in 1 second are objective measures of the severity of a patient’s asthma exacerbation and should be followed serially to measure improvement.
Asthma is a chronic disorder of the airways that is associated with inflammation, bronchial hyperreactivity, and intermittent airflow obstruction. The most common chronic disease in childhood, it is also common in the adult population. Presentations of acute asthma account for more than 2 million emergency department (ED) visits annually. The causes are multifactorial, but the pathophysiology is characterized by the release of inflammatory cell mediators that lead to airway smooth muscle constriction, pulmonary vasculature leakage, and mucous gland secretion.
Asthma is characterized by progressive shortness of breath, variable airflow obstruction, and wheezing. Symp-toms fluctuate over time, and patients with worsening symptoms due to a trigger are considered to have an “exacerbation” and require prompt treatment to reverse the airflow obstruction.
An acute asthma presentation is due to a decrease in expiratory airflow and is characterized by progressive symptoms of shortness of breath, a nonproductive cough, and wheezing in all lung fields. Symptoms may develop over a period of hours, days, or weeks, but often there is an acute worsening that prompts the patient to seek medical care. The most common trigger of acute asthma is an upper respiratory tract infection, but other factors may lead to sudden worsening of symptoms (Table 21-1).
Obtaining a thorough history may not be possible in an acute asthma exacerbation. A focused history should be obtained in parallel with initiation of therapy to reverse airflow obstruction, regardless of the trigger. Once the patient has improved and is able to provide more history, an attempt should be made to characterize the triggering event, rapidity of symptom onset, and the severity of the exacerbation, which will help guide further treatment and disposition. Characterization of the severity of the patient’s underlying asthma may help predict mortality (Table 21-2).
Risk factors for mortality in asthma.
Chronic steroid usage |
>2 canisters of short acting beta-2 agonists per month |
≥2 hospitalizations in the past year |
≥3 emergency department visits in the past year |
History of intensive care unit admissions |
Previous intubations for asthma |
Cardiopulmonary comorbidities |
Illicit drug use |
Low socioeconomic status or inner-city residence |
Attempting to define the patient’s underlying long-term asthma control does not aid in the management of an acute exacerbation, but will be important to understand when prescribing outpatient therapeutic regimen and follow-up. Patients should be asked about the frequency and duration of their current asthma symptoms and recent beta-agonist usage.
Numerous medical conditions can present in a similar fashion to asthma, including pulmonary embolism (PE), pneumonia, congestive heart failure (CHF), acute myocardial infarction (AMI), or chronic obstructive pulmonary disease (COPD). The initial history should focus on differentiating asthma from other life-threatening causes of shortness of breath and wheezing.
Patients may present with a wide spectrum of severity, from an increase in coughing to obvious respiratory distress with tachypnea and accessory muscle use. Mental status should be assessed initially because alterations in consciousness may affect the patient’s ability to protect their airway. A diminished level of consciousness is an indicator of impending respiratory arrest. The neck should be palpated for tracheal deviation and crepitus, as might occur with spontaneous pneumothorax. The lung exam is variable and demonstrates prolonged expiration with wheezing. However, the severity of the airflow obstruction cannot be gauged by the loudness of the wheezing. The patient who is audibly wheezing may still have good air movement on auscultation, whereas the quiet sounding chest with little air movement is a sign of severe disease because there is not enough airflow to produce a wheeze. Percussion of the thorax reveals hyper-resonance due to air trapping. Evaluation of extremity edema will help differentiate asthma from other causes of difficulty breathing.
The use of diagnostic studies is limited in the evaluation of a patient with an asthma exacerbation. However, certain diagnostic modalities may be indicated, depending on the clinical situation.