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
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 status. Persistent or acute allergen or irritant exposure promotes inflammation, bronchoconstriction, and airway hyperresponsiveness on an ongoing basis. Allergen exposure triggers a biphasic response. The “early response” occurs within minutes of allergen exposure resulting in rhinorrhea, sneezing, itching of the eyes and nose, and bronchospasm due to the release of histamine and other preformed mediators of inflammation. The “late-phase response” peaks 6 to 8 hours after allergen exposure with the development of eosinophilic inflammation and T-cell infiltration of the airway. During an asthma exacerbation due to allergen exposure, both phases must be treated with medications to treat the symptoms of the early phase as well as the resultant inflammation of the late phase.9
Viral infections cause asthma symptoms by promoting eosinophilic or neutrophilic airway inflammation.4 Viral-induced asthma exacerbations are common in children, and in fact, a majority of acute asthma admissions are associated with viral infections in children and adults, especially rhinovirus.10,11 The risk of an asthma exacerbation can be modified by a patient’s underlying inflammatory state and level of airway hyperreactivity. A patient with reduced airway inflammation due to adequate controller therapy is less likely to have a severe asthma flare when exposed to offending agents.
The presentation of acute asthma may vary, but all patients experience worsening airflow obstruction associated with respiratory distress. Patients often complain of shortness of breath, chest tightness, and wheezing. Some patients describe chest pain, cough, or fatigue. Caregivers may report observations of breathlessness, trouble speaking, decreased activity, retractions, rapid breathing, wheezing noises, or relentless cough.12
On physical examination, tachypnea is present, often accompanied by tachycardia. Pulse oximetry may reveal decreased oxygen saturation. There is evidence of increased respiratory effort, such as intercostal, supraclavicular, or subcostal retractions. Infants and young children may demonstrate nasal flaring or head bobbing. Paradoxical motion of the thoracoabdominal wall (i.e. expansion of the abdominal girth with inspiration) is another useful sign of increased work of breathing. Auscultation of the chest often reveals wheezing and a prolonged expiratory phase. Rales or crackles are often heard, and may shift in location over minutes to hours (“migratory atelectasis”). An assessment of air movement is determined by the loudness of breath sounds in various areas of the chest and may also vary over time. Patients with poor air movement may have minimal wheezing since the passage of air through the airway is what generates wheezing sounds. As air exchange improves, wheezing may become more pronounced. Conversely, patients with a deteriorating clinical course may have diminishing wheezing indicative of worsening air movement and perhaps respiratory insufficiency. Agitation or somnolence are worrisome signs and may indicate hypoxemia or hypercarbia with impending respiratory failure.
Some patients present without significant wheezing but with prominent cough as their manifestation of asthma, often referred to as “cough-variant” asthma. It is believed that the pathophysiology and response to treatment are similar to classic asthma.
Many conditions result in acute or chronic respiratory symptoms that mimic an asthma syndrome. Some of these conditions are discussed below.
Anatomical abnormalities should be considered in young children with frequent episodes of cough or wheeze. Inhaled foreign bodies are most common in toddler-aged children (see Chapter 145). These problems may present with cough, stridor, or wheeze. In all age groups, gastroesophageal reflux can mimic or contribute to underlying asthma13,14 (see Chapter 82). Cystic fibrosis is a genetic disorder that can also present with chronic cough or recurrent episodes of wheezing (see Chapter 144).
Viral infections often cause wheezing in childhood as well. Respiratory syncytial virus (RSV) is the most common cause of infantile bronchiolitis, but other respiratory viruses such as rhinovirus, parainfluenza virus, coronavirus, adenovirus, and influenza viruses are other common infectious agents.15 Viral bronchiolitis is associated with edema, bronchospasm, and increased mucus production of the smaller airway, features which overlap with asthma (see Chapter 100). As these respiratory viral infections are known to precipitate asthma exacerbations, it may be difficult to determine if the wheezing represents and isolated episode of bronchiolitis or an asthma exacerbation triggered by the respiratory illness.
Atypical respiratory infections with agents such as Mycoplasma, Chlamydia pneumoniae, Bordetella pertussis, or parapertussis can present with chronic cough. Coughing associated with these infections can persist for several months.
Functional disorders can coexist with or mimic asthma and include vocal cord dysfunction (VCD) and psychogenic cough. VCD usually presents in adolescence, with upper airway (laryngeal) inspiratory and/or expiratory stridor, which may be difficult to distinguish from lower airway wheezing. The diagnosis of VCD is confirmed by laryngoscopy demonstrating paradoxical adduction of the vocal cords seen during inspiration.16-19 Psychogenic cough is a habitual cough that can also persist for months, often occurring after an acute respiratory illness.20 Habitual cough has a characteristic sound described as barky or honking. The cough is exaggerated by stress or attention to the cough and will disappear with sleep.20 These features help distinguish this entity from cough-variant asthma. A key feature of VCD and psychogenic cough is the lack of response to asthma therapy.16-20 In addition, they are not associated with hypoxia.
In the United States, the NHLBI Guidelines for the Diagnosis and Management of Asthma (EPR-3) are available to guide clinicians through the diagnosis and management of chronic asthma. These guidelines are complementary to the material presented in this chapter (http://www.nhlbi.nih.gov.easyaccess2.lib.cuhk.edu.hk/guidelines/asthma/).
The initial evaluation of a patient presenting with an asthma exacerbation should include the assessment of the acute respiratory symptoms, signs or symptoms of coexisting or precipitating conditions, and treatments initiated prior to presentation. History should be obtained regarding the characteristics of the patient’s asthma symptoms, the pattern and frequency of the symptoms, any precipitating or aggravating factors as well as features indicative of the severity and level of control of their asthma (Tables 141-1 and 141-2).4
| Types of Symptoms (Impairment) | Cough |
| Wheeze | |
| Shortness of breath | |
| Chest tightness | |
| Sputum production | |
| Frequency of Symptoms (Impairment) | Daily, weekly, none |
| Perennial, seasonally | |
| Do they have a night cough? | |
| Do they cough with activity? | |
| How often do they use their albuterol? | |
| Severity of Symptoms (Risk) | How often do they have flares of their asthma? How many times in the last year? |
| How many times have they used oral steroids? How many times in the last year? | |
| How many emergency room visits? | |
| How many visits to the hospital? | |
| Have they ever been in the ICU? |
Asthma history Previous severe exacerbation (e.g. intubation or ICU admission for asthma) Two or more hospitalizations for asthma in the past year Three or more ED visits for asthma in the past year Hospitalization of ED visit for asthma in the past month Using >2 canisters of SABA per month Difficulty perceiving asthma symptoms or severity of exacerbations Social history Low socioeconomic status or inner-city residence Major psychosocial problems Comorbidities Cardiovascular, other chronic lung, or chronic psychiatric disease |
The physical examination provides clues to the severity of the current illness as well as the presence of comorbidities. Important physical parameters include respiratory rate, work of breathing, air entry, wheezing, and oxygen saturation. Work of breathing refers to the use of accessory muscles of respiration and also includes parameters such as nasal flaring, abdominal retractions, and depth of respiration.
During an asthma exacerbation, physical findings may vary and evolve with treatment or progression of the acute condition. A quiet or silent chest is a worrisome sign as poor movement of air can be associated with respiratory insufficiency or failure. Asymmetry of auscultatory findings may indicate other conditions. Unequal breath sounds can be found with pneumonia, effusion (especially in dependent regions of the lung), or atelectasis. Unilateral breath sounds may indicate an aspirated foreign body or a pneumothorax on the side with diminished breath sounds,4 and may be accompanied by hyperresonance on that side, especially if there is significant air trapping. Chest radiographs are typically not needed for patients with known asthma and a straightforward asthma exacerbation.21 Typical radiographic findings include hyperinflation, peribronchial thickening, and atelectasis (Figure 141-1). Chest radiographs may be helpful when there is concern for pneumonia, effusion, pneumothorax, pneumomediastinum, or foreign body aspiration.
A classification system for the severity of an asthma exacerbation is provided in Table 141-3. Patients in mild distress typically have slightly increased respiratory rates, may not use accessory muscles of respiration, and have end-expiratory wheezes with good air entry. Patients in severe distress are working hard to breathe, with inspiratory and expiratory wheezes, and are often hypoxic. Signs of impending respiratory failure are provided in (Table 141-4). For infants and children under 5 years of age, clues to breathlessness include difficulty or reluctance to feed and changes in crying pattern (e.g. softer or shorter). Changes in vital signs in these younger patients must be interpreted in the context of normal values for the age of the patient. Interestingly, paradoxical thoracoabdominal movement, a sign associated with severe respiratory distress in older children, may be seen in young children and infants even in states of mild or moderate respiratory distress.
| Exacerbation Severity | Mild | Moderate | Severe | Subset: Respiratory Arrest Imminent |
|---|---|---|---|---|
| Symptoms | ||||
| Breathlessness | While walking | While talking (infants: softer, shorter cry; difficulty feeding) | While at rest (infants: stop feeding) | |
| Positioning | Can lie down | Prefers sitting | Sits upright | |
| Speaks in | Sentences | Phrases | Words | |
| Alertness | May be agitated | Usually agitated | Usually agitated | Drowsy or confused |
| Signs | ||||
| Respiratory rate | Increased | Increased | Often >30/min | |
| Use of accessory muscles, suprasternal retractions | Usually not | Commonly | Usually | Paradoxical thoracoabdominal movement |
| Wheeze | Moderate, often only end expiratory | Loud; throughout exhalation | Usually loud, throughout inhalation and exhalation | Absence of wheeze |
| Pulse/min | <100 | 100-120 | >120 | Tachycardia or bradycardia |
| Pulsus paradoxus | Absent (<10 mm Hg) | May be present (10-25 mm Hg) | Often present (>25 mm Hg for an adult, 20-40 mm Hg for a child) | Absence suggests respiratory muscle fatigue |
| Functional Assessment | ||||
| PEF % predicted or % personal best | >70% | 40% to 69% or response lasts <2 hours | <40% predicted or personal best | <25% Note: PEF test may not be needed for severe attacks |
| PaO2 (on room air) | Normal (test not usually necessary) | >60 mm Hg (test not usually necessary) | <60 mm Hg, possible cyanosis | |
| And/or PaCO2 | <42 mm Hg | <42 mm Hg | >42 mm Hg, possible respiratory failure | |
| SaO2 % (on room air) at sea level | >95% | 90% to 95% | <90% | |
| Poor air movement or silent chest in combination with increased respiratory effort, bradypnea, or disorganized breathing pattern |
| Inability to speak |
| Increasing pulsus paradoxus or decreasing pulsus paradoxus in an exhausted patient |
| PCO2 > 42 mm Hg |
| Inability to lie supine |
| Deteriorating mental status, lethargy, or agitation |
| Diaphoresis |
| Respiratory or cardiac arrest |
Objective measures of acute asthma include pulmonary function testing, pulse oximetry, and arterial blood gases. Patients with asthma exacerbations are at risk for hypoxemia. As a result, patients require frequent monitoring to ensure adequate oxygenation. During a severe exacerbation, continuous pulse oximetry is recommended whereas intermittent oximetry may be acceptable as the clinical course improves.
Arterial blood gases are typically performed in critically ill patients and those with clinical deterioration or signs of respiratory insufficiency or failure. Arterial blood gases may reveal hypoxemia due to ventilation-perfusion mismatch and respiratory alkalosis with hypocapnia due to hyperventilation. A normal or elevated partial pressure of carbon dioxide (PaCO2) may be the harbinger of respiratory failure22 and may be associated with a decreased blood pH due to respiratory acidosis. In addition, lactic acidosis is a particularly concerning finding in status asthmaticus and patients with lactic acidosis are also at high risk of respiratory failure.
Pulmonary function tests can be used to assess lung function even during an asthma exacerbation. Spirometric indices such as the measurement of the forced expiratory volume at 1 second (FEV1), or peak expiratory flow rate (PEFR) are most useful to assess the severity of asthma. However, since spirometry is often not readily available in the emergency setting, PEFR can be used instead. The hand-held peak flow meter measures PEFR, and normal values have been established according to age, gender, and height23 (Table 141-5). PEFR provides a measure of large airway flow by measuring the rate of airflow in liters per minute. As a flare or asthma exacerbation worsens, PEFR typically becomes lower than baseline and may reflect the severity of the exacerbation. In patients presenting to an emergency room with an asthma exacerbation, the FEV1 is typically 30% to 35% of normal,24 and the PEFR is less than 50% of normal.
| Height | Males & Females | Height | Males & Females | Height | Males & Females | |||
|---|---|---|---|---|---|---|---|---|
| (in) | (cm) | (in) | (cm) | (in) | (cm) | |||
| 43 | 109 | 147 | 51 | 130 | 254 | 59 | 150 | 360 |
| 44 | 112 | 160 | 52 | 132 | 267 | 60 | 152 | 373 |
| 45 | 114 | 173 | 53 | 135 | 280 | 61 | 155 | 387 |
| 46 | 117 | 187 | 54 | 137 | 293 | 62 | 157 | 400 |
| 47 | 119 | 200 | 55 | 140 | 307 | 63 | 160 | 413 |
| 48 | 122 | 214 | 56 | 142 | 320 | 64 | 162 | 427 |
| 49 | 124 | 227 | 57 | 145 | 334 | 65 | 165 | 440 |
| 50 | 127 | 240 | 58 | 147 | 347 | 66 | 168 | 454 |
Monitoring PEFR can also assist in tapering medication during the recovery phase of an acute hospitalization. The PEFR is effort- and technique-dependent and therefore, reliability remains a concern. It should be used in conjunction the other parameters of severity for assessments.
Asthma exacerbations are treated with a combination of supportive therapy and pharmacological interventions. Treatment is tailored to the severity of the symptoms and adjusted based on response to therapy. Adequate hydration should be established and maintained either orally or with intravenous fluids. Physiologic monitoring should include vital signs and pulse oximetry. Oxygen supplementation is provided to maintain oxygen saturations in a safe range. This range is widely debated, but most agree that levels >90% are needed, and many target levels >93% to 95%.
This class of medications works by stimulating the β2-adrenergic receptor causing activation of adenylate cyclase, which increases the production of cyclic 3’5-adenosine monophosphate (cAMP). This increase in cAMP depending on the site of stimulation results in bronchial smooth relaxation, skeletal muscle and cardiac muscle stimulation, and inhibition of the release of inflammatory mediators via stabilization of the mast cell membrane. Albuterol is one of the short-acting β2-adrenergic agents used as first-line therapy for an acute asthma exacerbation, and this class of agents is used first line due to their ability to rapidly and reliably open the airways. Albuterol can be administered by nebulizer, either continuously or intermittently, or by metered-dose inhaler (MDI) with a spacer device. Studies have compared the amount of medication delivered to the lungs when given by MDI with spacer versus nebulizer.25-27 The two modes are considered equivalent if the patient can use proper technique with the MDI-spacer method of delivery. Dosing information is provided in Table 141-6.
| Medications | Adult Dose | Child Dose (<12 yrs of age) | Onset of Action | Duration | Comments |
|---|---|---|---|---|---|
Inhaled Short-Acting β-2 Agonists | |||||
Albuterol nebulizer 5.0 mg/ml 2.5 mg/3 ml 1.25 mg/3 ml 0.63 mg/3 ml |
2.5-5.0 mg every 20 minutes for 3 doses then 2.5-10 mg every 1-4 hours as needed or 10-15 mg/hour continuously |
0.15 mg/kg (minimum dose 2.5 mg) every 20 minutes for 3 doses then 0.1-5 to 0.3 mg/kg up to 10 mg every 1-4 hours as needed, or 0. mg/kg/hour by continuous nebulization | 15 minutes | 3-4 hours | Only selective β-2 agonists are recommended. For optimal delivery, dilute aerosols to minimum of 4 mL at gas flow of 6-8 L/min. As effective as nebulized therapy if patient is able to coordinate. |
Albuterol MDI (90 mcg/puff) | 4-8 puffs every 20 minutes up to 4 hours, then every 1-4 hours as needed | 4-8 puffs every 20 minutes for 3 doses, then every 1-4 hours inhalation maneuver Use VHC; add mask in children <4 years | |||
Levalbuterol via nebulizer (0.63 mg/3 ml, 1.25 mg/0.5 ml 1.25 mg/3 ml) | 1.25-2.5 mg every 20 minutes for 3 doses, then 1.25-5 mg every 1-4 hours as needed | 0.075 mg/kg (minimum dose 1.25 mg) every 20 minutes for 3 doses, then 0.075-0.15 mg/kg up to 5 mg every 1-4 hours as needed | Levalbuterol administered in one-half the mg dose of albuterol provides comparable efficacy and safety. Has not been evaluated by continuous nebulization.
MDI has not been studied in severe asthma exacerbations. | ||
Levalbuterol metered- dose inhaler | See albuterol MDI dose | See albuterol MDI dose | |||
| Anticholinergics | |||||
Ipratropium bromide nebulizer solution (0.25 mg/ml) |
0.5 mg every 20 minutes for 3 doses then as needed |
0.25-0.5 mg every 20 minutes for 3 doses, then as needed |
20-30 minutes
Peak 60-90 minutes |
Duration 3-6 hours |
May mix in same nebulizer with albuterol. Should not be used as first-line therapy, should be added to SABA therapy for severe exacerbations. The addition of ipratropium has not been shown to provide further benefit once the patient is hospitalized. Should use with VHC and face mask for children <4 years. Studies have examined ipratropium bromide MDI for up to 3 hours. |
| MDI (18 mcg/puff) | 8 puffs as needed up to 3 hours | 4-8 puffs as needed up to 3 hours | |||
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