Managing asthma in the pediatric ED
Managing asthma in the pediatric ED
By Blake Bulloch, MD; Richard M. Ruddy, MD
Peer Reviewer: Jeffrey Linzer, MD
Guest Editor: Larry B. Mellick, MD, MS, FAAP, FACEP
The American Thoracic Society defines asthma as "a disease characterized by an increased responsiveness of the trachea and bronchi to various stimuli and manifested by a widespread narrowing of the airways that changes in severity either spontaneously or as a result of treatment."1 While this definition was first used in 1962, it remains appropriate today.
To establish the diagnosis of asthma, clinicians should determine that 1) the patient has intermittent or recurring symptoms of airflow obstruction, 2) that the obstruction to airflow is reversible, and 3) that the airflow obstruction is not due to other diagnoses.2 Remember that "all that wheezes is not asthma" and that you must consider other disease entities in acutely wheezing children.3,4
To better guide the clinician's assessment of asthma severity and to optimize the management of patients with asthma, guidelines by an expert panel at the National Institute of Health and the National Heart, Lung, and Blood Institute were published initially in 1991 and updated in 1997.2 In the 1997 report, the classification of asthma severity was changed from mild, moderate, and severe to the new classification of mild intermittent, mild persistent, moderate persistent, and severe persistent.
This more accurately reflects the clinical and chronic manifestations of asthma. The panel does emphasize that no matter what classification of asthma a patient has, they can have mild, moderate, or severe exacerbations. (See chart, p. 20.) An asthma exacerbation is a worsening of symptoms that can be either abrupt in onset or gradual, but which is always associated with a decrease in expiratory airflow. This review will approach the diagnosis, clinical evaluation, and management of children presenting to the emergency department (ED) with an acute asthma exacerbation.
Etiology
Episodes of wheezing associated with respiratory infections are common in the first year of life. Many of these infants will have bronchiolitis, an infectious etiology of wheezing, but some have asthma. Martinez and colleagues prospectively studied factors affecting wheezing before the age of 3 years and their relation to wheezing at 6 years of age.8 Factors found to be independently associated with persistent wheezing were: maternal asthma, maternal smoking, rhinitis apart from colds, eczema during the first year of life, male sex, and Hispanic background. Among the children with non-recurrent (transient) wheezing, maternal smoking was the only independent factor.
Other studies have revealed that infants with documented viral infections of the lower respiratory tract are at greater risk for wheezing later in life.9 This includes not only those infants who had severe episodes of bronchiolitis but also those with mild forms of viral lower respiratory tract infections that were managed in the office setting. Also, patients born with impaired lung function at birth may be more susceptible to these infections, and therefore to wheezing. In contrast, lower respiratory tract infections from bacterial causes do not seem to predispose children to asthma.
Conditions that predispose or that may worsen lower airway disease include rhinitis and sinusitis. With this in mind, patients and parents should be questioned about nasal obstruction, nasal discharge, frequent colds, day and night coughing with post-nasal drip, and sore throat. Treatment of sinusitis will often result in improvement in airway obstruction. Management includes the use of antihistamines, decongestants, and antibiotics for common pathogens.10 Gastroesophageal reflux also may cause symptoms of dyspnea and wheezing often within a couple of hours of feeding and shortly after being laid supine. These infants often have histories of recurrent vomiting or regurgitation and gastroesophageal reflux must be considered as a cause of wheezing in infants.
Clinical Evaluation
The clinical evaluation of a patient who presents with an asthma exacerbation should begin with a rapid cardiopulmonary assessment and immediate institution of rescue therapy when required. Focus the assessment on the degree of respiratory distress, which determines the amount of airway obstruction and ventilatory compromise. Ventilation/perfusion changes, spirometry, and patient symptoms have been shown to poorly correlate with each other in a variety of situations. However, in each individual patient, assessing the degree of obstruction is best done by measuring the severity of symptoms and signs displayed on physical exam combined with an objective measure of airway obstruction such as peak expiratory flow rates.
History
The most common presenting symptoms in asthmatics include shortness of breath (SOB), wheezing, cough, and chest tightness. Patients frequently feel SOB although it is not entirely clear why. The chest is hyperinflated due to the air trapping. Because of increased elastic recoil at this distended lung volume, the work of exhalation is lessened but the work of inspiration is greatly increased.11 Tonic activity of the inspiratory muscles throughout inspiration and expiration has been shown in patients with asthma exacerbations, and this is a major contributor to the sensation of dyspnea. Dyspnea can be clinically assessed by determining the effect on the child's normal speech (i.e., the ability to speak in normal sentences without breaths).
Chest tightness is a manifestation of stimulation of vagal nerve irritant receptors. Subtle airway obstruction may have cough as the only clinical manifestation of an acute exacerbation. In mild cough-variant episodes as described, there may be no wheezing or prolonged expiration on clinical exam. Asthma with acute cough should be enough of a symptom complex to provide the patient with a trial of bronchodilators.
Other important historical data to obtain include the onset and duration of the current exacerbation and possible triggers of the epi sode. Triggers can be allergic, infectious, or irritant in nature. Viral URI is more common in infants and young children, while environmental allergens/irritants are more common in older children and adolescents. Duration of symptoms for greater than 24 hours is likely to suggest a greater component of inflammation. Obtain an inventory of current medications and the dose and frequency of each drug, including the use of systemic corticosteroids over the past several months. Identify patients who have had previous hospital admissions including the need for intensive care to identify the most high-risk patients.
Factors that have been identified that increase a patient's risk of a fatal asthma exacerbation include: previous life-threatening exacerbations, hospital admission for asthma in the last 12 months, suboptimal medical management, poor access to medical care, psychological or psychosocial problems, overuse of beta-agonists, black race, and age (with teenagers at increased risk).5-7 Finally, seek a history of allergies to help identify triggers. Some authors report that up to 90% of children may have allergy/atopy as part of their asthma.12
Physical exam
Initially, the physical exam should be brief and focused. Always begin by assessing the child's general appearance. Work of breathing as evidenced by the presence of chest wall retractions and abdominal excursion, skin color, and level of consciousness can be assessed within seconds and is a good indicator of the severity of respiratory compromise. Assess for an increase in the anterior-posterior diameter of the chest, the "barrel chest," to estimate the severity of air trapping. Observe the patient's respiratory rate and look for nasal flaring as a sign of distress. Occasionally, patients may grunt if there is significant pneumonia or atelectasis. Evaluate the use of accessory muscles by looking for intercostal, subcostal, and suprasternal retractions. The accessory muscles work to lift the entire rib cage cephalad. This generates high-negative intrapleural pressures in patients whose airways are partially obstructed to assist in ventilation. Use of the accessory muscles of respiration in this fashion places a larger metabolic demand on the child. This leads to more CO2 production and fatigue, which may contribute to respiratory acidosis.
Expiration is impaired in asthma due to intrathoracic small airway obstruction. Prolonged expiration is often subtle in mild asthma but can be pronounced in severe episodes. Most characteristic, but least prognostic, is the degree of wheezing on exam. Wheezing may be auscultated and is caused by rapid, turbulent airflow through the narrowed airways. Wheezing may be heard on both inspiration and expiration and tends to vary in intensity and pitch over time and often changes from place to place. After bronchodilator therapy, it may be louder due to improvement of the obstruction.
Be aware of the patient in whom no wheezing is auscultated, as wheezing is not heard when airflow has diminished over severely obstructed airways.
On physical exam, it is useful to calculate a standard score such as a clinical asthma score.13 (See table, p. 22.) Clinical asthma scores, such as the Wood-Downes' score shown in table 2, were designed to predict patients at high risk for respiratory failure. Obtain oxygen saturation by pulse oximetry to detect hypoxia and to assist in demonstrating the effect of small airways disease on oxygen shunting.
Measurement of pulsus paradoxus is useful in recognizing severe episodes, although it may be difficult to obtain in children. A paradoxical pulse is measured by inflating an appropriate-sized blood pressure cuff above the systolic blood pressure and slowly deflating it until you hear the first systolic sounds during expiration. Note this pressure and then continue to lower the pressure until you can hear the systolic sounds throughout the respiratory cycle. The difference is normally less than 4-5 mm Hg and is the change in systolic blood pressure between inspiration and expiration. A pulsus paradoxus is present when this value is 10 mm Hg or greater and is accurate in identifying patients with a greatly diminished FEV1.
Laboratory studies
Bedside pulmonary function tests provide a rapid, objective assessment of the patient and serve as a guide to the effectiveness of therapy. In moderate-to-severe obstruction, these tests may be delayed until after bronchodilators are administered and the patient shows some improvement. The forced expiratory volume in one second from maximal inspiration (FEV1) and the peak expiratory flow rate (PEFR) can be measured in the ED. These studies directly measure the degree of large airway obstruction. Patient cooperation is required for these tests to be reliable. Sequential measurements may be taken to monitor.
Peak expiratory flow (PEF) monitoring has been shown to play a useful role in the ED management of childhood asthma. It is effort-dependent and takes practice, so it is not always useful in children under 5 years of age. Appropriate normal values for age, corrected for height, are available. A decrease in PEFR to less than 50% of the patient's personal best indicates a severe exacerbation.2 Following improvement in PEFR by the titration of rescue medications to response can decrease ED admits when performed well.14
Pulse oximetry is a useful adjunct in the monitoring of patients with exacerbations, especially in those children younger than 5 years of age who are unable to perform PEFR. It is a noninvasive, painless method of assessing a patient's oxygenation and small airways disease. It is unreliable in cool, underperfused states, and it can be sensitive to movement and lighting. Some literature suggests that patients with initial oxygen saturation of less than 91% who respond to treatment well enough to be discharged home from the ED have a higher incidence of relapse, with return visits and often hospitalization. On the other hand, patients with an initial oxygen saturation of 95% or higher rarely relapse acutely.15 A disadvantage is that pulse oximetry does not reflect a decreased PaO2 until it has decreased to less than 80 mm Hg. It is not reliably consistent when the O2 saturation is less than 75% to 80%.
Arterial blood gas (ABG) analysis has not been a good predictor of clinical outcome in patients with acute asthma exacerbations.16 Hypoxia is a major concern in children with asthma. Pulse oximetry is useful and more convenient for assessing oxygenation, but an ABG is the only way to get an accurate measurement. It is the patient with an acute severe exacerbation in whom we are concerned about respiratory failure (increasing PCO2 and respiratory acidosis) and who has a significant O2 requirement in which the ABG may be useful. As such, the ABG can be reserved for those patients who may require intubation and mechanical ventilation or who are clinically difficult to assess. Keep in mind that obtaining an ABG may be difficult, especially in a child younger than 2 years of age, and may further aggravate the patient's respiratory distress.
The use of chest radiographs in patients with wheezing remains controversial. Radiographic findings of hyperinflation, peribronchial thickening, increased central lung markings, and subsegmental atelectasis are frequent findings in asthma exacerbations and usually do not change patient management.
Chest radiography has been previously recommended for patients presenting with their first episode of wheezing. However, Gershel and colleagues found 94.3% of radiographs in first-time "wheezers" to be normal.17 They found that patients with first-time wheezing and a respiratory rate above 60 or a pulse above 160, localized rales or localized decreased breath sounds before treatment, and localized rales and localized wheezing after bronchodilator treatment were more likely to have positive films.
Those in support of radiographs argue correctly that all that wheezes is not asthma. However, history and physical examination most often lead the clinician in the right diagnostic direction. It seems wise to follow the patient's response to medical management, and if the clinical picture seems discordant with the history, consider obtaining the radiographs. If a patient fails to respond to medical management or has fever, a radiograph is wise to help exclude pneumonia, pneumomediastinum, or the rare pneumothorax. Sinusitis may be an important comorbid factor for an asthma exacerbation, and it is occasionally beneficial to obtain a CT or radiograph of the sinuses.
The need for blood analysis is limited in patients with asthma exacerbations. While a CXR will detect cases of pneumonia, a white blood cell count is a nonspecific indicator of toxicity or of accompanying bacteremia in patients with pneumonia. Keep in mind that the use of corticosteroids or sympathomimetics will result in demargination of white blood cells and possibly cause leukocytosis. As such, the CBC is not a good indicator of infection in asthmatic patients. Beta-agonists have been shown to decrease serum levels of potassium, magnesium, and phosphate, although this is not usually of clinical significance in otherwise healthy children. Beta-agonists stimulate beta2-adrenergic receptors that are linked to membrane-bound sodium-potassium ATPase. In activating this enzyme, there is a direct influx of potassium into cells leading to a decreased serum potassium concentration. Catecholamines have also been shown to cause intracellular shifts of phosphate ions. If a patient is on theophylline at home, it is prudent to check a serum level.
Patients in status asthmaticus may have increased levels of plasma anti-diuretic hormone (ADH). This may occur secondary to hypovolemia, decreased left atrial pressures, or stimulation by adrenergic drugs. If given hypotonic fluids, patients have developed clinically significant hyponatremia. Therefore, hypotonic fluids should be avoided in patients with severe exacerbations, especially if they are not showing a significant response to therapy. ADH levels return to normal once there is relief of the airway obstruction.
On occasion, moderately severe asthma may affect serum electrolytes such as potassium, magnesium, or phosphate. Severe asthmatic patients are hypoxic and may have a respiratory alkalosis from hyperventilating. This, combined with low serum potassium and/or magnesium, may precipitate cardiac dysrhythmias. Hypo phos phate mia is reported to cause respiratory muscle fatigue and to cause a decrease in tissue oxygen extraction in patients with asthma exacerbations. Whether the decreases in serum concentrations of potassium, magnesium, or phosphate are clinically significant is unknown, and measurement of these electrolytes on a routine basis is not indicated.
References
1. American Thoracic Society. Chronic bronchitis, asthma, and pulmonary emphysema. Am Rev Respir Dis 1962; 85:762-768.
2. National Institutes of Health, National Heart, Lung and Blood Institute. Highlights of the expert panel report 2. Guidelines for the Diagnosis and Management of Asthma. May 1997. NIH Publication No. 97-4051A.
3. Kulick RM, Ruddy RM. "Allergic Emergencies." In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. 3rd ed. Baltimore: Williams and Wilkens; 1993, pp. 858-867.
4. Konig P. Asthma. A pediatric pulmonary disease and a changing concept. Pediatr Pulmonol 1987; 3:264-275.
5. Larsen GL. Asthma in children. N Engl J Med 1992; 326:1540-1545.
6. Call RS, Smith TF, Morris E, et al. Risk factors for asthma in inner city children. J Pediatr 1992; 121:862-866.
7. Newcomb RW, Akhtor J. Respiratory failure from asthma: A marker for children with high morbidity. AJDC 1988; 142:1,041-1,044.
8. Martinez FD, Wright AL, Taussig LM, et al. Asthma and wheezing in the first six years of life. N Engl J Med 1995; 332:133-138.
9. Hall WJ, Hall CB. "Bacteria and Viruses in Etiology and Treatment." In: Weiss EB, Stein M, eds. Bronchial Asthma, Mechanisms and Therapeutics. 3rd ed. Little, Brown and Company; 1993, pp. 564-576.
10. Senior BA, Kennedy DW. Management of sinusitis in the asthmatic patient. Ann Allergy Asthma Immunol 1996; 77:6-19.
11. Williams Jr. MH, Shim C. "Clinical Evaluation." In: Weiss EB, Stein M, eds. Bronchial Asthma, Mechanisms and Therapeutics. 3rd ed. Little, Brown and Company; 1993, pp. 447-454.
12. Kaliner M. Goals of asthma therapy. Ann Allerg Asthma Immunol 1995; 75:169-172.
13. Wood DW, Downes JJ, Lecks MS. A clinical scoring system for the diagnosis of respiratory failure. AM J Dis Child 1972; 123:227-279.
14. Taylor MRH. Asthma: Audit of peak flow rate guidelines for admission and discharge. Arch Dis Child 1994; 70:432-434.
15. Geelhoed GC, Landau LI, LeSouef PN. Evaluation of SaO2 as a predictor of outcome in 280 children presenting with acute asthma. Ann Emerg Med 1994; 23:1,236-1,241.
16. Nowak RM, Tomlanovich MC, Sarkar DD, et al. Arterial blood gases and pulmonary function testing in acute bronchial asthma. JAMA 1983; 249:2,043-2,046.
17. Gershel JC, Goldman HS, Stein RE. The usefulness of chest radiograph in first asthma attacks. N Engl J Med 1983; 309:336-339.
(Editor's note: Next month's column will cover the current standards in pharmacological treatment and disease management of asthma. The following month will cover care and treatment of asthmatic children in respiratory failure.
Richard M. Ruddy, MD, is the director of the Division of Emergency Medicine at the Children's Hospital Medical Center in Cincinnati. Blake Bulloch, MD, is a fellow with the Division.
Jeffrey Linzer, MD, is assistant professor of pediatrics at Emory University School of Medicine. Larry B. Mellick, MD, MS, FAAP, FACEP, is director of pediatric emergency medicine at the Medical College of Georgia in Augusta.)
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