Lauren M. Smith
Asthma is characterized by increased airway responsiveness to various stimuli. Asthma is caused by a variety of processes including bronchoconstriction, widespread bronchial wall edema, and increased mucous secretions. However, airway inflammation is the primary pathophysiologic mechanism. Although the reversibility of airflow obstruction was once considered a cornerstone of the diagnosis, it is now recognized that reversibility may be incomplete in some patients because of airway remodeling (1).
Asthma affects between 5% and 10% of adults in the United States and the prevalence of asthma has been on the rise for the last three decades. However, mortality has declined. Asthma accounts for just over 2 million emergency department (ED) visits per year, adult and pediatric. Most deaths occur prior to hospital arrival and the highest rates of death occur in those older than 65. About half of all cases are diagnosed before the patient reaches age 10, and another one-third are detected before age 40. The male-to-female ratio of this disease is higher during childhood but reverses in adulthood. Higher asthma prevalence is seen in lower socioeconomic households and in the Afro-American population (2).
The natural course of asthma has not been investigated thoroughly, but studies suggest that 50% to 80% of patients have a good prognosis, especially those with mild disease or disease that develops in childhood. Chronic asthma is categorized by severity, ranging from intermittent to mild, moderate, or severe persistent. Treatment is focused on reduction of impairment and reduction of risk. Periods of symptom-free intervals are interspersed with exacerbations, which trigger visits to the ED. Only about l0% or less of asthmatics are considered to have severe or refractory asthma, and it is these patients that are difficult to control and are prone to exacerbations.
Asthma is a heterogeneous disease. Clinically, it can be separated into two groups: allergic or extrinsic asthma, and nonallergic or intrinsic asthma. Many patients have components of both types. Extrinsic asthma accounts for <10% of patients with asthma and tends to develop early in life. It is associated with a well-defined sensitivity to inhaled allergens, a family history of allergic diseases, increased serum levels of immunoglobulin (Ig) E, positive immediate skin tests, and blood eosinophilia. It may be seasonal (trees, grasses, and spores) or perennial (animals, gardens, and house dust). A good response to bronchodilator therapy is usually observed.
Intrinsic asthma is the more common type of the disease. An inciting allergen cannot be identified, a family history of allergies is less common, IgE levels may be normal or low, and skin tests are negative. Intrinsic asthma is perennial, tends to be more severe than extrinsic asthma, and has a limited response to bronchodilator therapy.
All individuals with asthma have hyperresponsive airways that narrow when exposed to various stimuli: allergic, infectious, pharmacologic, environmental, occupational, exercise-related, or emotional stimuli.
Allergic asthma occurs when inhaled allergens bind to IgE molecules that are bound to mast cells in the lining of the tracheobronchial tree. During the early response, various mediators are released, causing increased vascular permeability, mucosal edema, and bronchial smooth-muscle contraction. A second wave of reaction, the late response, is seen hours to days later and involves the accumulation of inflammatory cells in the bronchial mucosa, thereby perpetuating the reaction.
Although several theories attempt to explain the pathophysiologic changes that occur in nonallergic asthma, none adequately explains all clinically observed phenomena. Research suggests that even patients without atopy have the same pathophysiologic basis for the disease as atopic patients.
Respiratory infections, particularly viral infections, commonly precipitate bronchospasm. Viruses cause mucosal inflammation and lower the firing threshold of the subendothelial vagal receptors, resulting in enhanced airway reactivity. This hyperactivity may last up to 8 weeks, even in nonasthmatic persons.
Pharmacologic agents also may induce acute asthma. The agents most frequently implicated are aspirin and nonsteroidal anti-inflammatory compounds, coloring agents, and β-adrenergic antagonists.
Up to 10% of adults with asthma experience the triad of aspirin-induced bronchospasm, nasal polyps, and eosinophilia. Ingestion of aspirin, nonsteroidal anti-inflammatory compounds, and tartrazine (FDC yellow dye no. 5) and other dyes may induce severe asthma in these patients, possibly by diverting arachidonic acid metabolism toward the lipoxygenase pathway and causing the production of leukotrienes, which are potent bronchoconstrictors.
Sulfating agents are used widely as food preservatives and antioxidants in pharmaceutical products. Exacerbation of asthma has been reported after food ingestion and after the use of sulfite-containing drugs, including some inhalation bronchodilators.
A large variety of occupational dusts and fumes may provoke acute airway obstruction. Patients with occupational asthma typically give a cyclic history. They are symptom-free during weekends, vacations, and on arrival at work. As the workday progresses, wheezing develops. A history of similar symptoms in fellow employees may be noted. Three mechanisms are involved in occupational asthma: immunologic reactions (e.g., animal handlers), direct liberation of bronchoconstrictors (e.g., cotton workers), and direct irritant effects (e.g., meat wrappers).
Exercise also may stimulate an asthma attack. Exercise-induced bronchospasm is usually noted within 5 to 20 minutes after the completion of exercise and is related to thermal changes in the respiratory tree. Exercising in a cold, dry environment causes a more marked response than exercising in a warm, humid environment.
Endocrine factors have been recognized as yet another cause of airway hyperresponsiveness. Normal variations in progesterone and estradiol levels are believed to modulate airway reactivity.
Psychological factors also influence asthma exacerbations, probably through modification of vagal efferent activity. The extent to which psychological factors participate in the induction and continuation of an asthma attack is unknown but probably varies from patient to patient and from episode to episode.
Regardless of the underlying precipitant, airway narrowing, bronchial wall edema, bronchial smooth muscle contraction, and mucosal plugging ensue. These changes result in increased airway resistance, decreased forced expiratory volumes and flow rates, lung hyperinflation, increased work of breathing, and ventilation–perfusion mismatch.
CLINICAL PRESENTATION
The classic triad of symptoms during an asthma attack is cough, dyspnea, and wheezing, but chest tightness and nonproductive cough may precede dyspnea and wheezing. Asthmatic patients coming to the ED are frequently anxious, tachypneic, tachycardic, and mildly hypertensive. As airway obstruction worsens, the expiratory phase becomes prolonged and lung hyperinflation, accessory respiratory muscle use, muscle retraction, and pulsus paradoxus may be noted. Patients may attempt to sit upright or lean forward (tripod position) in an effort to ease the work of breathing. However, these signs may be absent despite severe airway obstruction. A silent chest indicates insufficient air movement or extensive mucous plugging and is an ominous sign. Cyanosis may appear only immediately before respiratory arrest and should not be relied on as an indication of the severity of the attack. The termination of an exacerbation is often marked by a cough productive of thick mucous plugs and bronchial casts (Curschmann spirals).
A subset of asthmatic patients experiences the sudden onset of severe symptoms. These individuals tend to respond rapidly to treatment but appear to be at significant risk for a fatal outcome.
Occasionally, an asthmatic patient may complain of intermittent dyspnea or cough on exertion. Patients with cough-equivalent asthma tend to have normal breath sounds on examination, even during an exacerbation, but reversible bronchospasm may be demonstrated on pulmonary function testing.
Complications of asthma include pneumothorax, pneumomediastinum, and subcutaneous emphysema. Pneumothoraces may require insertion of a chest tube for evacuation. Mild atelectasis may occur as a result of bronchial mucous plugging but rarely requires intervention other than conventional bronchodilator therapy. In addition, rib fractures and costochondral strain may occur as a result of excessive coughing. Cough syncope, a rare complication of asthma, is noted most frequently in moderately obese, middle-aged asthmatic men. Finally, dysrhythmias may occur as a result of hypoxia, especially in patients who have received oral adrenergic agents.
DIFFERENTIAL DIAGNOSIS
Wheezing, coughing, and dyspnea are present in many conditions. Common problems include pneumonia, bronchitis, croup, bronchiolitis, chronic obstructive lung disease, congestive heart failure, pulmonary embolism, allergic reactions, and upper airway obstruction from edema or a foreign body. Less common problems include cystic fibrosis, hypersensitivity pneumonitis, carcinoid syndrome, and exposure to odors, dust, and gas. A careful history and physical examination should help differentiate asthma from these conditions.
ED EVALUATION
The ability to perform a thorough history and physical examination before initiating treatment is often limited by the patient’s dyspnea. Aggressive therapy directed at relieving airway obstruction begins as soon as a diagnosis of asthma is established. Meanwhile, an attempt is made to obtain a history from family members or the patient. Important points to establish include the following (3,4).
• Duration and onset of the current attack
• Identification of precipitating causes
• Type and amount of medications (inhaler/nebulizer) used before arrival in the ED
• Response to prior therapy, including current or previous use of steroids
• Frequency of ED visits and hospitalizations
• Previous need for intubation or ventilation
• History of concurrent medications and allergies
• History of concurrent medical problems
• History of illicit drug use
Patients at high risk of asthma-related death include those with previous intubations; more than two hospitalizations or more than three ED visits in the past year; use of more than two canisters of short-acting β2-agonist (SABA) per month; difficulty perceiving airway obstruction or worsening asthma; low socioeconomic status or inner-city residence; illicit drug use; major psychosocial or psychiatric disease; age; and comorbidities such as cardiovascular or other chronic lung diseases.
Immediate attention is also directed to the patient’s appearance and work of breathing (i.e., use of accessory muscles), vital signs, chest, heart, mental status, and skin examination. The presence of a pulsus paradoxus (a drop of SBP of more than 12 mm Hg during inspiration) may be noted. However, judging the state of a patient’s ventilatory status and pulmonary function on clinical grounds alone can be misleading. The failure to recognize impending respiratory failure is a key contributor to patient death. The degree of tachycardia and tachypnea often do not correlate well with the degree of airway obstruction. Pulsus paradoxus may be absent in up to one-third of severe asthmatics (5). Furthermore, wheezing is absent if airflow is minimal. To complicate matters, all of the aforementioned clinical parameters can normalize with even minimal improvement in pulmonary function (6). Therefore, quantification of airway changes must be assessed by using either the forced expiratory volume in 1 second (FEV1) or the peak expiratory flow rate (PEFR). An initial FEV1 of <1 L (<30% predicted) or a PEFR of <100 L/min (<20% predicted) indicates very severe obstruction (3,4).
Hypoxemia is not common during most acute exacerbations. Pulse oximetry may be useful in assessing and following oxygenation. A saturation of <91% generally correlates with severe hypoxemia. Arterial blood gas (ABG) measurements are rarely needed in the management of acute asthma, unless the practitioner desires to know the pCO2 or pH. In general, hypercapnia, severe hypoxemia, or metabolic acidosis does not occur until the PEFR or FEV1 is <25% of predicted values (7), but young children and elderly patients commonly present exceptions to this rule. The degree of hypoxemia determined by ABG generally reflects the extent of ventilation–perfusion mismatch. A normal or increased PaCO2 indicates severe airway obstruction and impending ventilatory failure (7).
Expectorated sputum may appear purulent because of the presence of eosinophils, but this finding may not reflect infection. A wet preparation of sputum may contain Charcot-Leyden crystals (eosinophilic granules), Curschmann spirals (mucous casts), and bacteria.
Chest radiographs may demonstrate hyperinflation and atelectasis but are usually nondiagnostic. A chest radiograph is necessary only if pneumonia, pneumothorax, or pneumomediastinum is suspected or if the patient fails to respond to aggressive bronchodilator therapy.
Although electrocardiography occasionally reveals evidence of right ventricular strain, it is generally not helpful except to rule out concurrent cardiac problems. However, all older patients, especially those with cardiac disease, should be monitored during therapy.
Blood tests, including a complete blood count, are unlikely to help guide the acute management of an asthma attack. Asthma scores that incorporate subjective and objective criteria (pulse, respiratory rate, pulsus paradoxus, subjective dyspnea, accessory muscle use, wheezing, and PEFR) should not be relied on for predicting emergency treatment or determining disposition.
ED MANAGEMENT
ED interventions are guided by pulmonary function tests (FEV1, PEFR), vital signs, chest, heart and mental status examinations, and the patient’s subjective assessment of dyspnea. The goal of emergency treatment is to ensure adequate oxygenation and to relieve airflow obstruction.
Supplemental oxygen, inhaled β-adrenergic agonists, oral or intravenous corticosteroids, and, to a lesser extent, inhaled anticholinergic agents are the mainstays of asthma treatment in the ED. It is now thought that timely administration of glucocorticoids for serious exacerbations is the single most effective strategy for reducing ED visits and hospitalizations (8,9). The methylxanthines (e.g., theophylline) are not a component of emergency care (10). The benefits of ketamine remain largely anecdotal and have not been substantiated in controlled trials (11). The National Asthma Education and Prevention Program (NAEPP) Expert Panel (Fig. 76.1) (3,4) has established guidelines for the diagnosis and management of acute exacerbations of asthma. Acute pharmacologic therapy can be divided into three categories: β-adrenergic agonists, glucocorticoids, and anticholinergics. Chronic management is primarily composed of treatment with inhaled corticosteroids and long-acting inhaled β-agonists; however, these have no role in the acute setting. Despite effective therapies for chronic management, there is still frequently poor compliance, leading to poor control (1). Much work is being done to develop medications that further address the inflammatory component of asthma. This includes anti-IgE therapy and blockers of specific mediators (e.g., IL-5, 9, and 13) or receptors. These remain under investigation and their potential utility in the acute setting remains unclear (1).
FIGURE 76.1 Management of asthma exacerbations: Emergency department and hospital-based care. Key: FEV1, forced expiratory volume in 1 second; ICS, inhaled corticosteroid; MDI, metered-dose inhaler; PCO2, partial pressure carbon dioxide; PEF, peak expiratory flow; SABA, short-acting β2-agonist; SaO2, oxygen saturation. (Adapted from National Asthma Education and Prevention Program, Expert Panel Report 3: Guidelines of the Diagnosis and Management of Asthma (NIH Publication Number 08–5846). Baltimore, MD: Department of Health and Human Services, National Institutes of Health, 2007.)
Table 76.1 outlines the preferred treatments recommended by the NAEPP Expert Panel (3,4).
TABLE 76.1
Dosages of Drugs for Asthma Exacerbations in Emergency Medical Care or Hospital
β-Adrenergic Agonists
SABAs are the drugs of choice for the management of acute bronchospasm. They produce bronchodilation by stimulating β-receptors, resulting in the formation of cyclic adenosine monophosphate (cAMP), which results in relaxation of bronchial smooth muscle, inhibition of mediator release, and increase in mucociliary clearance. Drugs in this category include resorcinols, saligenins, and catecholamines (Table 76.1).
Resorcinols and saligenins available in the United States include albuterol (salbutamol), levalbuterol, pirbuterol, formoterol, metaproterenol, and terbutaline. Aerosol forms are available for albuterol, levalbuterol, and metaproterenol. All are available in metered-dose inhalers (MDIs). Aerosol agents and MDIs are rapid-acting, are theoretically long-lasting, and may be repeated every 20 to 30 minutes in an acute situation. Levalbuterol, the R-isomer of albuterol, offers little advantage over albuterol and is more expensive. Salmeterol is a chemical derivative of albuterol with an extended duration of action and a bronchodilator effect 10 times that of albuterol. Formoterol is similar but is even longer acting than salmeterol. Neither is appropriate for use in acute exacerbations of asthma. Albuterol, metaproterenol, and terbutaline are also available in oral form. Terbutaline and epinephrine are available for subcutaneous injection.
The resorcinols and saligenins are highly β2-selective and are virtually devoid of cardiac side effects when given in inhaled or aerosol form. A frequent noncardiac side effect is tremor. Inhaled or aerosolized β-agonists rapidly promote bronchodilation comparable with that produced by parenteral agents, appear to be longer lasting, and cause fewer side effects. Treatments given every 20 to 30 minutes or in a continuous fashion result in more effective and sustained improvement of pulmonary function than treatments given less frequently (12). The use of spacer devices enhances drug delivery and reduces oral deposition of the medication. Recent studies suggest that albuterol by MDI/spacer is as efficacious as higher doses of albuterol delivered by nebulizer (13).
Subcutaneous administration of β-agonists (epinephrine or terbutaline) may be of use in the treatment of asthmatics who cannot use inhalation devices effectively, in patients in extremis, in patients for whom initial treatment with aerosol β-adrenergic agents fails, or when preparation of aerosol or metered-dose agents for acute use risks delaying the initiation of therapy.
The catecholamines (epinephrine, isoproterenol, and isoetharine) have largely been supplanted by their more selective and longer-acting derivatives. Epinephrine, a nonselective α- and β-adrenergic agonist, may be given by oral inhalation (in a nonprescription preparation) or subcutaneously. The usual subcutaneous dose in adults is 0.3 to 0.5 mL of a 1:1,000 solution, which may be repeated every 20 minutes to a total of three doses. Epinephrine reaches peak blood levels 20 to 40 minutes after injection, and its bronchodilating effects last up to 4 hours. Side effects include increased myocardial irritability, dysrhythmias, and nervousness. Although some studies suggest that epinephrine may be safely used in asthmatics older than 40 years of age, extreme caution should be used in patients with coronary artery disease (14).
Isoetharine is more β2-selective than epinephrine and is an effective a bronchodilator. It is supplied as a 1% aerosol solution or in an MDI preparation. Its duration of action is 30 to 90 minutes. Doses may be repeated every 20 to 30 minutes during an acute attack.
Isoproterenol is a potent selective β-adrenergic agent. It is available in aerosol form, in a new MDI, and as an intravenous solution. The duration of action of the inhaled form is 3 hours, and inhalations may be repeated every 3 hours. Use of isoproterenol inhalants was associated with a number of asthmatic deaths in England and Wales in the 1960s, suggesting that the agent should be used cautiously, although a cause-and-effect relationship was not demonstrated. In addition, inhaled isoproterenol may cause paradoxical bronchospasm. Intravenous isoproterenol should be reserved for dire emergencies, and strict monitoring of heart rate, rhythm, and blood pressure is required.
Glucocorticoids
Glucocorticoids should be administered to any patient whose acute airway obstruction is not promptly relieved by an inhaled β-adrenergic agent. Patients who receive glucocorticoids early require fewer hospital admissions and sustain fewer relapses after discharge from the ED (8). Corticosteroids are thought to exert their effect on acute asthma by reducing airway inflammation. The initial dose is 60 to 125 mg of intravenous methylprednisolone or 40 to 80 mg of oral prednisone (3). Additional doses of methylprednisolone (60 to 80 mg intravenous) or prednisone (40 to 80 mg PO) with a frequency range of daily to every 6 to 8 hours should follow the initial dose. Oral administration of corticosteroids is equivalent to intravenous administration. Inhaled corticosteroid use has led to improved asthma control; however, data on the use of inhaled corticosteroids during the acute ED treatment of asthma has yet to be clearly defined (15,16). Because the effects of steroids are not noted for 4 or more hours, vigorous concomitant bronchodilator therapy must be continued.
Anticholinergic Agents
There has been a resurgence of enthusiasm for the use of anticholinergic agents to treat acute bronchoconstriction. These medications, including ipratropium bromide and glycopyrrolate, antagonize the neuromuscular transmitter acetylcholine at the postganglionic parasympathetic receptor, reducing vagally mediated bronchoconstriction in the larger central airways. There appears to be an additive effect when β-adrenergic agents and anticholinergic agents are used together, although this effect is not dramatic (17). Nebulized ipratropium (see Table 76.1) mixed with albuterol should be used in severe asthmatics. Peak anticholinergic bronchodilation is achieved within 1 to 2 hours. Aerosolized atropine sulfate and glycopyrrolate, although effective, have fallen out of favor because of the high incidence of anticholinergic side effects (tachycardia, restlessness, irritability, dry mouth, thirst, and difficulty swallowing).
Other Agents
Magnesium sulfate, a physiologic regulator of intracellular calcium flux, is an effective bronchodilator. In addition to preventing histamine release from mast cells and opposing the action of acetylcholine, magnesium directly inhibits bronchial smooth-muscle contraction. Both aerosolized magnesium (0.66 g in 10 mL of saline) and intravenous magnesium solutions (2 g over 20 minutes) have been used investigationally to treat patients with asthma for whom maximal standard therapy has failed, although neither form is currently approved for this indication in the United States. Bronchodilation is observed within 2 to 5 minutes after administration, but it disappears rapidly after treatment is discontinued; therefore, additional bronchodilator therapy must accompany the use of magnesium. Side effects include hypotension, malaise, and a warm sensation. Cardiac rhythm, blood pressure, pulse, neurologic status, and renal function must be monitored closely. Magnesium appears to be safe and may be helpful in some patients with severe asthma exacerbations (18).
Nedocromil and cromolyn inhibit the release of inflammatory cytokines from mast cells, but they have no role in acute management. Likewise, leukotriene inhibitors, although useful in long-term management, are not indicated for ED treatment.
Heliox, an 80:20 mixture of helium and oxygen, is sometimes considered for treatment in patients with respiratory acidosis who fail conventional therapy. Helium is a low-density, biologically inert gas that lowers airway resistance and decreases respiratory work. Significant improvement may be noted within 10 to 20 minutes of initiating therapy but there are currently insufficient data on whether heliox can avert tracheal intubation or change intensive care and hospital admission rates and duration or mortality; so while safe and well tolerated, no evidence exists that supports its use in the emergency setting (19,20).
Theophylline and its salts have been used to treat acute bronchospasm for more than 50 years. Studies suggest that the methylxanthines, when used alone or in combination with β-agonists during an acute episode, are associated with an increased incidence of side effects but do little to relieve bronchospasm. Methylxanthines have a narrow therapeutic-toxic window, are subject to many interactions with other drugs, and should not be used in the treatment of acute asthma exacerbations. Toxicity may result in life-threatening cardiac dysrhythmias or seizures.
Noninvasive Assisted Ventilation
Noninvasive assisted ventilation can be in the form of continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP). Noninvasive ventilation decreases the load on the respiratory muscles, improves oxygenation, and can prevent the need for intubation and invasive ventilation (21). Noninvasive ventilation does have some advantages over intubation, including the avoidance of sedation and ventilator-associated complications. Although this intervention is widely used and is reported anecdotally to be successful, literature is lacking to support its use and no guidelines currently exist. Patients most likely to benefit from noninvasive ventilation are those with a high work of breathing a pCO2 <45, and who are alert cooperative, and hemodynamically stable, with minimal coughing or vomiting (7). Bronchodilator treatments may still be administered via the ventilation circuit. Frequent monitoring must be maintained, as some patients do not improve with this internvention and may become hypercapneic and require intubation and invasive ventilation.
Invasive Assisted Ventilation
If the patient’s condition deteriorates or fails to improve despite intensive therapy, use of intubation and mechanical ventilation must be considered. Although there are no absolute criteria other than respiratory arrest and coma, the following patients should be considered for intubation and mechanical ventilation, via RSI (rapid sequence intubation).
• Those with worsening pulmonary function tests despite vigorous bronchodilator therapy
• Those with decreasing PaO2, increasing PaCO2, or progressive respiratory acidosis
• Those exhibiting respiratory muscle fatigue or exhaustion
• Those with declining mental status
Ventilatory strategies yielding low tidal and low respiratory rates are recommended to minimize the risk of producing or exacerbating dynamic lung hyperinflation (11). Expiratory airflow obstruction can result in air-trapping and higher lung volumes in mechanically ventilated asthmatics. This condition may result in “auto-PEEP,” a continuously increased intrathoracic pressure that may decrease venous return and cause hypotension. Auto-PEEP may be avoided in mechanically vented patients by using a rapid inspiratory flow rate, a reduced respiratory frequency, and a prolonged expiratory phase. This type of mechanical ventilation is commonly referred to as “permissive hypercapnea.” Hemodynamic instability or hypoxemia may occur after intubation; possible causes to consider besides “auto-PEEP” include displaced endotracheal tube, pneumothorax, over-sedation, and equipment failure.
Opioids, sedatives, and tranquilizers should be avoided in acute asthma, because respiratory arrest may occur after their use. Mucolytics, expectorants, and hydration do not aid in the treatment of asthma. Antibiotics are advisable only for those patients with fever and purulent sputum, evidence of pneumonia, or suspected bacterial sinusitis (3).
Asthma in Pregnancy
Asthma is the most common chronic medical condition that complicates pregnancy, and affects an estimated 4% to 8% of pregnancies. One-third of pregnant patients with asthma improve during pregnancy, one-third of patients remain unchanged, and one-third become worse. Asthma therapy during pregnancy is directed at providing adequate oxygenation for both mother and fetus. The management of pregnant asthmatics is essentially the same as that for nonasthmatics. The use of subcutaneous or inhaled β-adrenergic agents and corticosteroids appears to be safe during pregnancy (22).
CRITICAL INTERVENTIONS
• Measure either the FEV1 or the PEFR to quantify the degree of airway obstruction.
• Administer IV or oral glucocorticoids early to patients whose acute airway obstruction is not promptly relieved by an inhaled β-adrenergic agent.
• Prescribe oral corticosteroids on discharge to patients who have received glucocorticoids in the ED.
• In intubated patients, avoid auto-PEEP by using a rapid inspiratory flow rate, a reduced respiratory frequency, and a prolonged expiratory phase.
DISPOSITION
Several asthma-scoring indices have been proposed to predict the need for hospitalization, but all have proven disappointing. The following patients should be admitted to the hospital or observation unit.
• Those whose condition deteriorates in the ED
• Those with repeat exacerbations after previous recent ED visits
• Those who have dyspneic and significant hypoxemia (PaO2 <60), hypercapnea, or acidosis
• Patients with a pretreatment FEV1 of <10 L (<30% predicted) or a PEFR of <100 L/min (<20% predicted), and a post treatment FEV1 <2.1 L (<60% predicted) or a PEFR <300 L/min (<60% predicted)
• Patients who remain subjectively dyspneic after aggressive therapy
• Patients with continued abnormal vital signs after therapy
• Unreliable patients
Even patients who improve enough to be discharged from the ED have residual airway obstruction for up to several weeks after the acute episode subsides. Therefore, arrangements must be made for ongoing treatment and early follow-up. A nontapering 3- to 10-day course of oral corticosteroids (40 to 60 mg/d of prednisone) and a 5- to 10-day treatment regimen of a β2-adrenergic MDI with spacer (two puffs as needed, up to every 4 to 6 hours) should be prescribed. In addition, a chronic regimen of inhaled corticosteroids (preferred) or leukotriene modifier-inhibitor should be prescribed for all patients who have persistent asthma in accordance with NAEPP guidelines (3,4). Instruction in the proper use of the inhaler is essential, as is a brief educational intervention, as well as cessation of smoking and illicit drug use. Patients receiving chronic theophylline therapy should be continued on a long-acting preparation pending follow-up with their physician.
Common Pitfalls
• Failure to recognize that a silent chest or a normal PaCO2 is a sign of severe obstructive disease that may result in respiratory arrest.
• Withholding β-agonist therapy in the ED because of β-agonist use at home.
• Failure to use objective measurements of pulmonary function, in addition to clinical and subjective parameters of dyspnea, when judging the adequacy of bronchodilator therapy.
• Failure to give glucocorticoids to all but the mildest asthmatics, especially those who fail to respond to one or two doses of β-agonists.
• Failure to consider chronic asthma management in discharge planning.
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