Emergency Department and Hospital Management of Asthma Exacerbations (Excerpt)
March 1, 1999 5 minutes read
Emergency Department and Hospital Management of Asthma Exacerbations (Excerpt)
Severe exacerbations of asthma are potentially life-threatening. Care must be prompt. Effective initial therapies (i.e., a short-acting ß2 agonist and the means of giving it by aerosol and a source of supplemental oxygen) should be available in a physician’s office. However, severe exacerbations require close observation for deterioration, frequent treatment, and repetitive measurement of lung function. Therefore, most severe exacerbations of asthma require prompt transfer to an emergency department for a complete course of therapy. An overview of the treatment strategies in emergency departments and hospitals is detailed below.
Assessment
An expert panel of the National Institutes of Health, National Heart, Lung, and Blood Institute in Bethesda, MD, recommends all clinicians treating asthma exacerbations be familiar with the characteristics of patients at risk for life-threatening deterioration. In the emergency department, treatment should be started as soon as an asthma exacerbation is recognized and assessment of lung function is made.
While treatment is given, obtain a brief, focused history and physical examination pertinent to the exacerbation. Take a more detailed history and complete physical examination and perform laboratory studies only after initial therapy has been completed.
Objectives of functional assessment are to:
• Obtain objective information on the severity of airflow obstruction and the patient’s response to treatment.
• In the emergency department, obtain forced expiratory volume in one second (FEV1) or peak expiratory flow (PEF) on presentation, after initial treatment, and at frequent intervals thereafter, depending on the patient’s response to therapy. Rarely, a patient’s airflow obstruction may be so severe as to prevent performance of a maximal expiratory maneuver.
• In the hospital, measure FEV1 or PEF before and 15-20 minutes after bronchodilator therapy during the acute phase of the exacerbation. Thereafter, measure FEV1 or PEF at least daily after discharge. Values <30% of predicted that improve by <10% after bronchodilator therapy or that fluctuate widely over 24 hours indicate a heightened risk of life-threatening deterioration.
In patients with severe distress or with FEV1 or PEF <50% of predicted, assess the adequacy of arterial oxygen saturation by pulse oximetry.
Objectives of the brief history are to determine:
• time of onset and cause of current exacerbation;
• severity of symptoms, especially compared with previous exacerbations;
• all current medications and time of last dose;
• prior hospitalizations and emergency department visits for asthma, particularly within the last year;
• prior episodes of respiratory insufficiency due to asthma (loss of consciousness or intubation and mechanical ventilation);
• other potentially complicating illness, especially other pulmonary or cardiac disease or diseases that may be aggravated by systemic corticosteroid therapy such as diabetes, peptic ulcer, hypertension, and psychosis.
Objectives of the physical examination are to:
• assess the severity of the exacerbation as indicated by the findings;
• assess overall patient status, including level of alertness, fluid status, and presence of cyanosis, respiratory distress, and wheezing. Wheezing can be an unreliable indicator of obstruction; in rare cases, extremely severe obstruction may be accompanied by a "silent chest"
• identify complications (e.g., pneumonia, pneumothorax, or pneumomediastinum);
• identify other diseases that may affect asthma (e.g., allergic rhinitis or sinusitis);
• rule out upper-airway obstruction. Both intrathoracic and extrathoracic central airway obstruction can cause severe dyspnea and may be diagnosed as asthma. Causes include epiglottis, organic diseases of the larynx, vocal cord dysfunction, and extrinsic and intrinsic tracheal narrowing. Clues as to their presence include dysphonia, inspiratory stridor, monophonic wheezing loudest over the central airway, normal values for PO2, and unexpectedly complete resolution of airway obstruction with intubation. When upper airway obstruction is suspected, obtain further evaluation by flow-volume curves and referral for laryngoscopy.
The most important objective of laboratory studies is detection of actual or impending respiratory failure; other objectives include detection of theophylline toxicity and conditions that complicate the treatment of asthma exacerbations. Do not permit these studies to delay initiation of treatment. For example:
Consider arterial blood gas (ABG) measurement for evaluating arterial carbon dioxide tension (PCO2) in patients with suspected hypoventilation, with severe distress, or with FEV1 or PEF 30% of predicted after initial treatment. (Note: Respiratory drive is typically increased in asthma exacerbations, so a "normal" PCO2 of 40 mm indicates severe airflow obstruction and a heightened risk of respiratory failure.)
Complete blood count (CBC) may be appropriate in patients with fever or purulent sputum; keep in mind modest leukocytosis is common in asthma exacerbations and corticosteroid treatment causes a further outpouring of polymophonuclear leukocytes within one to two hours of administration.
Measure serum theophylline concentration in patients taking theophylline prior to presentation.
It may be prudent to measure serum electrolytes in patients who have been taking diuretics regularly and patients with coexistent cardiovascular disease, because frequent ß2 agonist administration can cause transient diseases in serum potassium, magnesium, and phosphate.
Chest radiography is not recommended for routine assessment but should be obtained in patients suspected of a complicating cardiopulmonary process, such as pneumothorax, pneumomediastinum, pneumonia, lobar atelectasis, or congestive heart failure.
Electrocardiograms need not be routinely obtained, but a baseline electrocardiogram and continual monitoring of cardiac rhythm are appropriate in patients older than 50 years of age and those with coexistent heart disease or chronic obstructive pulmonary disease. The electrocardiogram may show a pattern of right ventricular strain that reverses promptly with treatment of airflow obstruction.
Assessment considerations unique to children and infants are as follows:
It is often difficult for physicians and parents to determine the severity of the airway obstruction in infants and small children with asthma. However, using a combination of the subjective and objective parameters permits a fairly accurate assessment to guide initial therapy. Many of these parameters have not been systemically studies, so they serve only as general guides.
The differences in the anatomy and physiology of the lungs of infants place them at greater risk for respiratory failure. These differences include greater peripheral airway resistance, fewer collateral channels of ventilation, further extension of airway smooth muscle into the peripheral airways, less elastic recoil, and mechanical disadvantage of the diaphragm. Viral infections, particularly respiratory syncytial virus, are the most common cause of acute wheezing illness in infants. The edematous inflammatory response in the airways leads to air trapping and hyperinflation, atelectasis, increased respiratory rate, and wheezing. This sequence of changes can rapidly progress to respiratory failure. Close monitoring is crucial.
It is particularly important to monitor O2 saturation by pulse oximetry in infants because their ventilation/perfusion characteristics lead them to become hypoxemic more readily than adults. SaO2 should be normal for altitude (>95% at sea level). Decreased oxygen saturation is often an early sign of severe airway obstruction, and an SaO2 <91% on room air is a good predictor of the need for hospitalization in small infants.
Capillary or ABG measurements should be performed in infants suspected of respiratory failure. PCO2 is the best measurement of ventilation in infants, as it is in adults. Children with a normal PCO2, but in obvious respiratory distress are at high risk for respiratory failure.
Source: Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma, National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, MD.
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