Asthma is characterized by reversible hyperresponsiveness, obstruction, and inflammation of the lower airways. About 13% of children are affected and, despite recent therapeutic advances, morbidity continues to be substantial, especially among inner-city residents.
Common triggers include irritants (cigarette smoke), viral infections, weather changes, allergens (dust, animals), exercise, cold air, and emotional stress. Children with a history of bronchopulmonary dysplasia (BPD) or other acute lung injury (smoke inhalation, hydrocarbon ingestion, near-drowning) are at increased risk for hyperactive airways or asthma. The greatest risk of mortality is in children who have a history of respiratory failure or hypoxic seizures, are under-treated (at home or after a medical visit), or delay seeking medical attention.
Acute asthma presents with dyspnea, cough, and expiratory and, to a lesser extent, inspiratory, wheezing. Cough-variant asthma presents with episodes of dry or productive cough and little or no wheezing. Airway obstruction can lead to retractions and decreased air entry, with little or no audible wheezing. Tachycardia, tachypnea, and, in severe attacks, cyanosis may be present; altered mental status (agitation, lethargy) occurs with impending ventilatory failure. URI is also often present.
Immediately evaluate a patient with a reported asthma exacerbation or wheezing. After the initial brief assessment, institute treatment promptly. While the first bronchodilator treatment is given, perform a focused history and physical examination related to the acute exacerbation. A more detailed history and physical examination can be delayed until after the initial therapy is given.
A trial of an inhaled β2 agonist (albuterol) may simultaneously confirm the diagnosis and provide clinical improvement. Relief of airway obstruction occurs in <15 minutes (often <5 minutes), and peak flow (PEFR) typically improves by >20% from baseline. Less improvement may occur with severe or prolonged episodes associated with more inflammation, leaving the diagnosis uncertain unless the patient has a history of previous wheezing episodes. Laboratory studies do not help in establishing the diagnosis of asthma, and chest x-rays are not necessary for most first episodes of wheezing. A chest x-ray may be indicated in the setting of localized posttreatment findings in association with significant tachypnea (rate >60/min in infants, >40/min in older children) or persistent tachycardia (rate >160/min) 20–30 minutes after the completion of a β2 agonist treatment in an afebrile child.
Inquire about a history of prematurity, mechanical ventilation, BPD, previous wheezing episodes, or heart disease. Check for a family history of asthma, recurrent bronchitis, eczema, allergic rhinitis, or other allergies.
Consider the possibility of complicating factors or a diagnosis other than asthma if a child or infant has protracted (more than three days), recurrent, or persistent localized wheezing in the face of adequate therapy for asthma. See Table 20.1 for the differential diagnosis and Table 20.2 for selected risk factors for death in asthma.
|≥2 hospitalization in the past year|
|Difficulty in perceiving asthma symptoms|
|Hospitalization or ED visit for asthma during past month|
|Low socioeconomic status or inner-city residence|
|Previous severe asthma exacerbation necessitating ICU care or intubation|
Rapidly assess the airway and breathing, measure the peak flow in all children older than 5–6 years of age, and determine whether the patient has a mild, moderate, or severe asthma exacerbation (Table 20.3). To facilitate evaluation of the PEFR and changes following therapy, always record the PEFR as a percentage of the child’s predicted normal PEFR from a table of standards by height or best value (if known), rather than an absolute number. Provide supplemental oxygen (40% by mask) to a patient with mild or moderate wheezing; use 100% oxygen if the attack is severe. In addition, some patients may have an initial drop in pO2 during β2 agonist therapy due to ventilation–perfusion (V/Q) mismatch, particularly if the aerosol is administered with room air rather than oxygen. Monitor a severely ill patient with pulse oximetry, and consider obtaining an ABG if the breath sounds are barely audible and do not improve within 5–10 minutes following the initial therapy.
|Symptoms||Peak expiratory flow rate|
|Mild||Dyspnea only during activity||≥70% predicted or personal best|
|Moderate||Dyspnea interferes with usual activity||40–69% predicted or personal best|
|Severe||Dyspnea at rest||<40% predicted or personal best|
|Interferes with speech|
|Life-threatening||Too dyspneic to speak||<25% predicted or personal best|
Inhaled β2 Agonists
Give 0.15 mg/kg (2.5 mg minimum; 10 mg maximum) of albuterol every 20 minutes for three doses, then 0.15–0.3 mg/kg every 1–4 hours as needed for mild to moderate exacerbations. As an alternative, give 0.25 mg for a patient weighing <20 kg and 5 mg if ≥20 kg. Substitute 4–8 puffs of an albuterol MDI (90 mcg/puff) with a spacer every 20 minutes for nebulized albuterol if the patient is cooperative. The onset of action is within five minutes and the duration is 4–6 hours. Give repeat doses every 20–30 minutes until no further improvement is noted in peak flow, oxygen saturation, or respiratory rate. For severe exacerbations, give 0.5 mg/kg/hour by continuous administration. Levalbuterol does not appear to provide superior therapeutic effect or diminish adverse effects. Reserve it for patients with a history of extreme tachycardia following albuterol administration.
Subcutaneous Epinephrine and Terbutaline
A dose of subcutaneous epinephrine or terbutaline may be given for severe attacks (peak flow <15% predicted or nearly absent breath sounds) when aerosolized medication may not reach the target small airways. The epinephrine dose is 0.01 mL/kg to 0.3 mL maximum of the 1:1000 preparation. For terbutaline, use 0.01 mL/kg up to 0.25 mL maximum. Common epinephrine side effects include nausea, palpitations, tachycardia, agitation, tremor, and, less frequently, hypertension and ventricular dysrhythmias. Terbutaline may cause less nausea and vomiting. Simultaneously begin nebulized β2 agonist treatments.
requires ≥2 β2 agonist aerosol treatments;
oxygen saturation is <93% on any assessment;
>2 days of coughing or awakening from sleep due to asthma in the past week;
chronically uses (every day or every other day) oral corticosteroids;
ED visit within the past two weeks, has had a past ICU admission;
hospitalized (for asthma) within the past two weeks;
≥3 hospitalizations during the past year;
has maximized β2 agonist treatment at home.
Use prednisone or prednisolone, 1 mg/kg (40 mg maximum) or dexamethasone 0.6 mg/kg (10 mg maximum). If the patient cannot tolerate oral medication, give IM dexamethasone (same dose as above). For a patient with impending respiratory failure, give a bolus of IV methylprednisolone (2 mg/kg, 125 mg maximum, followed by 1 mg/kg q 6h).
Ipratropium bromide is an anticholinergic that produces bronchodilation by antagonizing the activity of acetylcholine at the level of airway smooth muscle. Compared to inhaled β-agonists, the effect on airway obstruction is modest and generally results in approximately a 10% improvement in FEV1. Dilute albuterol (<20 kg: 0.25 mg; ≥20 kg: 5 mg) in a vial of ipratropium (250 mcg <12 years of age or 500 mcg ≥12 years of age). Give three consecutive ipratropium–albuterol inhalations to a patient with a severe exacerbation. The onset of action of ipratropium is relatively slow (20 minutes), and the peak effect occurs in about 60 minutes.
Ipratropium, unlike atropine, is poorly absorbed across mucous membranes, has little toxicity at the stated dose, and does not inhibit mucociliary clearance. There are, however, infrequent reports of paradoxical bronchoconstriction with the administration of anticholinergic agents. Monitor the patient carefully, and stop the nebulization if there are any signs or symptoms of worsening asthma.
The IV administration of magnesium sulfate may be useful for a patient whose condition worsens or fails to improve significantly (peak flow increases <50% from presentation and is <60% of predicted; intercostal retractions persist; or oxygen saturation <93%) after administration of β-agonists and systemic corticosteroids. The dose is 50–75 mg/kg (2 g maximum) in 50 mL of normal saline administered IV over 30 minutes. Side effects include hypotension, mild sedation, and cutaneous flushing; do not use the drug in patients with significant hypotension or renal failure. Monitor the blood pressure every ten minutes during the infusion and every 30 minutes thereafter for four hours, but do not stop the infusion for mild reductions in blood pressure in the absence of hypotensive symptoms.
Encourage oral fluids and provide IV hydration if the patient is seriously ill, but limit IV hydration to maintenance plus replacement of ongoing losses. If a patient with absent or minimal breath sounds or a PEFR <15% of expected has been vomiting or drinking poorly, assess the hydration status and obtain blood for electrolytes when placing the IV line. In general, most hospitalized asthma patients do not need an IV placed.
Heliox (a mixture of helium and oxygen) can be used as a nebulizing agent for albuterol when there has been a poor response to conventional therapy. Heliox provides a low-density gas mixture which can decrease turbulence in air flow though constricted airways and improve gas exchange and albuterol delivery. Request Heliox (70% helium/30% oxygen) in a premixed tank from the respiratory therapy department, then administer a continuous nebulization of albuterol via a nonrebreathing mask at 10 L/min. Discontinue Heliox if the oxygen saturation is <93% and initiate treatment with 100% oxygen via a nonrebreather mask.
If the above-described therapy fails to achieve adequate oxygenation, attempt a trial of BPAP (bilevel positive airway pressure), if available, with an initial expiratory positive airway pressure (EPAP) of 4–5 cmH2O and inspiratory positive airway pressure (IPAP) of 8–10 cmH2O.
If the patient’s respiratory mechanics fail to improve, endotracheal intubation and mechanical ventilation are necessary. Use ketamine (1–2 mg/kg) to provide sedation and bronchodilation. Use smaller tidal volumes than average (6–8 mL/kg) on a volume-preset ventilator, with normal-to-somewhat-lower respiratory rates for age, and long expiratory times. The required inspiratory pressures can exceed 50–60 cm H2O. Assess breath sounds and obtain an ABG. Permissive hypercapnia may lessen the risk of barotrauma, so the goal is incomplete correction of the respiratory acidosis (permit a pCO2 up to 50–60 mg Hg). An intubated patient will usually require a sedative (midazolam 0.1–0.3 mg/kg IV q 1–2h, 5 mg maximum) and a neuromuscular relaxant (vecuronium 0.05–0.1 mg/kg IV q 1–2h, 10 mg maximum) to minimize barotrauma.
A patient with acute asthma can be discharged home when the peak flow is >60–70% predicted for height, the oxygen saturation is >92% in room air, wheezing is minimal, there are no signs of significant obstruction (retractions, tachypnea, decreased air entry), and the patient denies having trouble breathing. Ensure that the parent can give the medications confidently, knows how to use a spacer device with an MDI, can monitor the child frequently, and is able to return to the ED if necessary. Ongoing bronchodilator therapy is usually necessary for two weeks. Prepare a written asthma action plan for worsening symptoms and a follow-up appointment within a week or two of the ED visit.
Inhaled β2 agonists are preferred for all patients with documented asthma and are first-line therapy, sometimes as single-drug therapy, but more commonly in combination with steroids. Infants and young children can use an MDI attached to a spacer with the proper-sized facemask, while older children do not need a face mask. The albuterol MDI dose is two puffs every 4–6 hours. For a nebulizer, use albuterol 0.5% (<20 kg: 0.5 mL; ≥20 kg: 1.0 mL) or levalbuterol (<10 kg: 0.63 mg; ≥10 kg: 1.25 mg) in 3 mL of normal saline given over 5–10 minutes.
Give an outpatient course of oral steroids if the patient required two or more acute albuterol treatments or has required acute therapy twice (or more) within 24 hours or three times in the past week. Avoid steroids in a child who has been exposed to viruses in the herpes family (especially varicella). Give oral prednisone or prednisolone (1 mg/kg/day q day or div bid, 40 mg/day maximum) for 3–4 more days. A single dose of oral dexamethasone (0.6 mg/kg q day, 10 mg maximum) is an alternative.
Prescribe inhaled steroids to patients whose risk (likelihood of exacerbations) and impairment (frequency and intensity of symptoms and functional limitations) characteristics classify them as having persistent asthma (see Table 20.4). Use fluticasone (44 mcg/puff 4–11 years; 110 mcg/puff ≥12 years) one puff bid. Prescribe budesonide inhalation suspension for nebulization (0.25–0.5 mg) for children 0–4 years of age whose other asthma medications are given via nebulizer.
|Exacerbations requiring oral steroids||Symptoms||Nighttime awakenings|
|≥2 in six months||>2 days/week||1–2/month||Mild persistent|
|≥2/year||>2 days/week||3–4/month||Moderate persistent|
|≥2/year||Throughout day||Often 7/week||Severe persistent|
Indications for Admission
Status asthmaticus: continued moderate or severe wheezing or other evidence of significant airway obstruction after therapy with nebulized β2 agonists, ipratropium, corticosteroids, or subcutaneous epinephrine, or any wheezing after IV magnesium sulfate
Repeated emergency visits over several days when therapy is maximal or compliance uncertain
Persistent tachypnea, inability to tolerate fluids or medications, altered mental status
Hypercapnia: pCO2 >40 mg Hg
Hypoxemia: pO2 <60 mg Hg or oxygen saturation < 93% in room air despite aggressive therapy
Pneumothorax, pneumomediastinum, or significant atelectasis
Bacterial tracheitis (BT) is the most common life-threatening bacterial infection of the airway, including the larynx, trachea, and bronchi. The pathology involves copious purulent secretions and pseudomembranes within the trachea. Staphylococcus aureus is most frequently implicated, followed by Streptococcus pyogenes, Moraxella catarrhalis, and Streptococcus pneumoniae. Influenza type A is often detected as well, suggesting a primary viral process followed by bacterial superinfection.
Any age patient can be affected, although the mean is about four years of age. Following a brief prodrome of cough, rhinorrhea, and low-grade fever, the initial presentation resembles moderate to severe viral croup, with hoarseness, sore throat, barking cough, and stridor. Then, instead of the expected improvement after several days, the patient develops high fever with significant respiratory distress. Drooling is uncommon.
Suspect BT in a febrile child with stridor that does not respond to racemic epinephrine administration or that gets worse after a number of days (when croup is usually resolving), particularly if the cough seems productive. In a stable patient, a portable lateral neck radiograph obtained in the ED may reveal an irregular tracheal margin characteristic of BT. Viral croup (pp. 638–641), epiglottitis (pp. 641–643), retropharyngeal abscess (pp. 166–167) and foreign body aspiration (pp. 643–645) are major differential diagnostic considerations.
If BT is suspected, allow the patient to assume a position of comfort on the parent’s lap. Provide supplemental oxygen in an unobtrusive manner, but defer completing a physical examination or inserting an IV. Immediately notify an anesthesiologist and otolaryngologist to prepare for laryngoscopy and possible orotracheal intubation in the operating suite. If the patient’s respiratory status suddenly deteriorates (usually due to movement of a pseudomembrane within the airway) perform bag-mask ventilation.
Definitive treatment includes airway stabilization, most frequently with tracheal intubation in the operating suite and meticulous pulmonary toilet and suctioning of secretions. Treat with broad-spectrum antibiotics, cefotaxime (150 mg/kg/d IV divided q 6h, 8 g/day maximum) plus MRSA coverage with vancomycin (40 mg/kg/day div q 6h, 4 g/day maximum) or clindamycin 40 mg/kg/day IV div q 8h, 4.8 g/day maximum).
Indications for Admission
Suspected bacterial tracheitis
Bronchiolitis is the most common wheezing-associated respiratory illness in children under two years of age. Epidemics in the winter (December through early February) are most frequently caused by respiratory syncitial virus (RSV). Human metapneumovirus (hMPV) causes bronchiolitis in somewhat older children (median age 11 months), typically in the spring (March through April). Less common causes of bronchiolitis include parainfluenza, influenza, and adenovirus, Mycoplasma, pertussis, Chlamydia, and Ureaplasma.
A prodrome of URI with rhinorrhea and coryza is followed by cough, audible wheezing, and varying degrees of respiratory distress. An infant with severe disease has tachypnea (>50/min), subcostal and intercostal retractions, poor feeding, nasal flaring, and grunting. In all cases, symptoms are likely to be most prominent at night. Fever is variable and usually low-grade. Although wheezing is the typical auscultatory finding, rhonchi and coarse rales may also be heard. In most patients, the condition worsens for 3–4 days and then rapidly resolves, although some patients may have a persistent cough for weeks afterward. Neonates and young infants may present with apnea and a sepsis-like picture.
Acute wheezing, cough, and respiratory distress in a young infant are most often secondary to bronchiolitis. Other diagnoses include the following.
Asthma (reactive airway disease) can cause a clinical picture with wheezing that is indistinguishable from bronchiolitis. Some infants with a first RSV exposure may already manifest hyperreactive airways. Consider asthma if the patient has had previous episodes of wheezing that were responsive to bronchodilators, a history of bronchopulmonary dysplasia, eczema, or a family history of asthma or atopic disease.
Foreign Body Aspiration
An aspirated foreign body may present with wheezing after a coughing or choking episode in an infant typically more than six months of age. There is no URI prodrome. Unless there is acute infection distal to the foreign body, there is usually no fever. Auscultatory findings are often localized. An esophageal foreign body can impinge on the trachea and also cause respiratory distress.
These conditions can cause airway obstruction and wheezing, which are exacerbated by a URI. Consider congenital lobar emphysema and intrapulmonary cysts (bronchogenic or cystadenomatoid malformation) when the wheezing is unilateral or localized. The chest x-ray is often diagnostic. With tracheomalacia, stridor from inspiratory collapse of a floppy trachea predominates over expiratory wheezing. Wheezing from a vascular ring is typically loudest over the trachea and midlung fields.
Inquire about a history of apnea, wheezing, prematurity, or mechanical ventilation (BPD), and check for a family history of asthma or allergies. Perform the examination with the infant undressed from the waist up and sitting on the parent’s lap. Obtain an accurate respiratory rate, note any signs of respiratory distress (flaring, grunting, retractions, cyanosis) or heart disease (murmur, hepatosplenomegaly), and assess the activity level and ability to drink.
Respiratory Rate >60/min or Signs of Respiratory Distress
Check the oxygen saturation in room air by pulse oximetry and suction the nares, if necessary. Provide supplemental oxygen (usually 30–40% by oxyhood or nasal prongs) to hypoxic patients to maintain an oxygen saturation >90% or a pO2 >65 mm Hg. Do not use albuterol, racemic epinephrine, hypertonic saline, or oral steroids. Start an IV and give maintenance fluids with D5 ½ NS unless the patient is dehydrated (see pp. 245–249). If there is no substantial improvement, admit the patient as clinical deterioration, with persistent hypoxemia, elevation of pCO2, or the development of acidosis may portend exhaustion and respiratory failure requiring mechanical ventilation.
Respiratory Rate 40–60/min
Supportive therapy (fluids, acetaminophen as necessary) is all that is needed if the infant is alert, tolerating fluids well, and has no signs of distress. Close follow-up is warranted.
Chest radiographs are not routinely indicated in patients with bronchiolitis. Obtain a chest x-ray if the infant has known underlying pulmonary or heart disease or does not respond to aggressive inpatient management.
Indications for Admission
Respiratory rate 60–70/min with lethargy or poor oral intake
Infant <3 months of age with a respiratory rate 60–70/min after maximal ED therapy
Respiratory distress, oxygen saturation <90% or pO2 <65 mm Hg in room air, or normal-to-elevated pCO2 (>40 mm Hg)
Infants with congenital heart disease, chronic lung disease, or immunodeficiency (at risk for complications of RSV infection) in the progressive stage (first day or two) of the illness
Cough is a very common symptom that is most often caused by a minor URI. However, a cough may also signal a more serious problem, such as pneumonia, asthma, or congestive heart failure. A thorough clinical evaluation is necessary before assuming that the patient just has a “cold.”
Clinical Presentation and Diagnosis
The clinical presentation varies, depending on the etiology (Table 20.5). Usually these can be differentiated with a careful history and physical exam, with only the occasional need for laboratory tests. Three features of a cough that help determine the cause are its quality, timing, and whether it is productive of sputum.