Chapter 34: Asthma

• Asthma is the most common chronic disease of childhood and is associated with significant morbidity and mortality.

• It is now defined as ‘a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation'

• There is emerging evidence that pre-school wheezers should be treated differently to classic atopic wheezing in older children.

• Inhaled albuterol remains the first line therapy for acute asthmatic exacerbations. Delivery of albuterol by metered dose inhaler and spacer device has been shown to be superior to delivery by nebulization.

• The addition of ipratroprium to the first two to three albuterol doses has been associated with a decreased need for hospitalization in pediatric patients with moderate-to-severe asthma exacerbations.

• Early administration of oral corticosteroids in the emergency department has been shown to enhance recovery from an acute asthma exacerbation and decrease rates of hospitalization.

• Oral dexamethasone (one–two doses) has been shown to be as efficacious as a 5-day course of oral prednisone.

• Magnesium sulfate is of benefit in patients with moderate-to-severe exacerbations who do not respond to initial bronchodilator therapy, and should be the first-line parenteral bronchodilator in severe/critical asthma.

• Asthma education, including asthma action plans on ED discharge, provided to children and their parents while in the ED results in fewer future ED visits and hospital admissions.

Asthma is the most common chronic disease of childhood.¹ The International Study of Asthma and Allergies in Childhood (ISAAC) has identified differences in the prevalence of asthma internationally, ranging from 1.6% in Indonesia to 36.7% in the United Kingdom.² Prevalence of asthma in the United States is estimated at 8.9%, affecting an estimated 7.1 million children under 18 years of age.³ The overall prevalence is highest in developed countries and is highest in urban versus rural areas. Most children develop asthma under 5 years of age.

Acute exacerbations of asthma are often managed in emergency departments (EDs). The CDC reported that in 2008 approximately 775,000 US children were treated for an acute exacerbation of asthma in the ED⁴ and accounted for approximately 14.4 million lost school days.

Asthma has been defined as intermittent, reversible obstructive airway disease and is a chronic inflammatory disorder of the airways with acute exacerbations. The most recent National Heart Lung and Blood Institute (NHLBI) expert panel guidelines (2007) define asthma as “a common chronic disorder of the airways that is complex and characterized by variable and recurring symptoms, airflow obstruction, bronchial hyperresponsiveness, and an underlying inflammation.” The interaction of these features determines the clinical manifestations, severity of asthma, and response to treatment.⁵

The major pathophysiology of asthma includes increased airway responsiveness, inflammation, mucous production, and submucosal edema. Airway responsiveness is defined as the ease with which airways narrow in response to various non-allergic stimuli. The level of airway responsiveness correlates with the severity of symptoms and medication requirements. Airway inflammation plays a critical role in the development of obstruction and the degree of hyperresponsiveness. Increased mucous production and submucosal edema add to the obstruction. There are anatomic and physiologic differences in a child compared with an adult which make them more prone to obstruction and more vulnerable to respiratory failure. The peripheral airways are smaller and thus offer greater resistance to airflow. Infants do not possess collateral channels for ventilation that are present in older children and adults. In infancy, the diaphragm is the primary muscle of respiration and possesses muscle fibers that are more prone to fatigue. Any degree of abdominal distention will interfere with diaphragmatic function and lead to secondary ventilatory insufficiency.

Children with acute exacerbations of asthma often seek care in an ED (Fig. 34-1). Exacerbations are characterized by decreases in expiratory airflow that can be documented and quantified by simple measurement of lung function (spirometry). These objective measures more reliably indicate the severity of an exacerbation than does the severity of symptoms.⁵ Unfortunately, spirometry is difficult to obtain in young children.⁶ Obtain an initial focused history and physical examination to guide treatment and then obtain a detailed history during treatment. Classification of the severity of the exacerbation is important in selecting therapy. Tables 34-1 and 34-2 illustrate the classification of asthma severity recommended by the NHLBI expert panel report.⁵ Numeric asthma scores can classify severity and measure effectiveness of treatment.^7–9 Scores which have been developed and validated include the pediatric asthma severity score (PASS) and the pediatric respiratory assessment measure (PRAM).¹⁰

The brief history should assess⁵:

• Time of onset and any potential causes or triggers of the current exacerbation;

• Severity of symptoms, especially compared with previous exacerbations;

• Treatment given before arrival to the ED and response to this treatment;

• All current medications and time of last dose, especially of asthma medications;

• Estimate of number of previous unscheduled office visits, ED visits, and hospitalizations for asthma, particularly within the past year;

• Any prior episodes of respiratory insufficiency or intensive care unit admissions due to asthma; and

• Other potentially complicating illness.

Complete a rapid physical examination and start treatment. Focus on the severity of the exacerbation (see Table 34-2). Obtain a general assessment of distress. Important clues include alertness, anxiety, general health, positioning, ability to speak, fluid status, and presence of cyanosis. Vital signs may have some prognostic value. Fever, unusual in asthma, may point to a more complicated course and significant underlying disease. Increased pulse rate may be a sign of hypoxia. Pulsus paradoxus (a drop in systolic blood pressure of 10 mm Hg or more with inspiration) was believed to correlate with a worsening status but its usefulness has been questioned. Increased respiratory rates are usually seen in asthmatic exacerbations, but respiratory rate may decrease with fatigue in severe asthma. The lung examination may reveal a number of findings including diffuse wheezing. Wheezing results from turbulent airflow and occurs first on expiration alone, progressing to both inspiration and expiration. The wheezing may be localized and may shift in location with time as the relative degree of obstruction may vary. If airway obstruction is severe, there will be little airflow and the chest may be quiet. Thus, wheezing is not a reliable indicator of the degree of obstruction. Lung examination may also reveal diffuse or localized rales or as a persistent cough with a clear lung examination. The presence of rales in asthma may be misinterpreted as indicative of concomitant pneumonia. Accessory muscle use is a more reliable indicator of degree of obstruction. The presence of air leak is suggested by asymmetric breath sounds, tracheal deviation, or subcutaneous edema.

A chest radiograph is rarely indicated in acute asthma exacerbations and rarely provides additional useful information.¹¹ Obtaining a chest x-ray may be important for the child with first-time wheezing, as there are many illnesses that can present with wheezing (see Differential Diagnosis below). Thereafter, specific indications for a chest radiograph include clinical suspicion of consolidation, effusion, pneumothorax, or impending respiratory failure. Typical chest radiograph findings are hyperinflation, peribronchial cuffing, and areas of subsegmental atelectasis (Fig. 34-2). These findings are nonspecific.

Spirometry can assess a patient's degree of respiratory compromise. However, many children are unable to cooperate. The simplest spirometry test, peak expiratory flow rate (PEFR), is reliable in children older than 5 years,⁶ but is probably not practical to assess severity in children younger than 8 years. A PEFR of less than 30% to 50% of predicted or of the patient's personal best indicates severe airway obstruction.

Oximetry is another tool that may help assess severity. It correlates with ventilation perfusion mismatching and thus degree of obstruction. An initial pulse oximetry may assess severity but not predict the need for hospital admission.¹²

Blood gases may be useful in severe exacerbations but are not necessary for management. Hypoxia will be present early due to ventilation perfusion mismatch. PCO₂ will be decreased early in the disease secondary to compensatory hyperventilation. As the obstruction progresses, the number of alveoli being adequately ventilated and perfused decreases and CO₂ retention occurs. Thus, a “normal” or slightly elevated PCO₂ in a patient with an asthma exacerbation may be a sign of muscle fatigue and impending respiratory failure. Eventually, the hypoxia and hypercapnia lead to acidosis. If a blood gas is warranted, a venous sample is usually acceptable.

Demonstrating episodic and reversible airway disease allows one to make a definitive diagnosis of asthma. This is most reliably accomplished by performing pulmonary function tests (PFTs). As outlined, children younger than 8 years are generally unable to perform the tasks needed to get accurate PFTs in the ED. The diagnosis in young children is usually made on a clinical basis. Consider the diagnosis of asthma in children with recurrent wheezing and symptom-free intervals, especially if there is a family history of asthma, atopy, or allergies. A personal history of atopy or allergies is also suggestive of the diagnosis of asthma. Some children with asthma have their first episode prior to 6 months of age. In infants, as in older children, viral infections are the most common trigger for asthma. Both infants who have asthma and those who do not may become infected with respiratory syncytial virus (RSV) or other viruses, and develop bronchiolitis as their first episode of wheezing. Therefore, in an infant with wheezing, it is impossible to clinically differentiate between bronchiolitic wheezing and asthma. The most important clue to infantile asthma is a history of recurrent episodes of wheezing or persistent cough, especially a nocturnal cough.

Other possible etiologies for wheezing in an infant or child are provided in Table 34-3. A history of prematurity or ventilatory support will help in identifying the infant with bronchopulmonary dysplasia (BPD). Clinical signs, which favor a congenital heart or cardiac cause for wheezing, include digital clubbing, cyanosis, organomegaly, an audible murmur, and an active precordium. An association of signs and symptoms with feeding may suggest a tracheoesophageal fistula, gastroesophageal reflux, or recurrent aspiration. Clues to identifying the presence of a lower airway foreign body may come from the history (sudden onset and observed aspiration), chest examination (asymmetry), or radiographic studies (localized air trapping). A patient with cystic fibrosis may have clubbing of the digits, poor weight gain, symptoms of malabsorption or a family history of cystic fibrosis. It is often quoted that all that wheezes is not asthma. This is especially true in children, and remember that even patients with a previous diagnosis of asthma may have another etiology for wheezing.

Obtain a cardiopulmonary assessment on every patient with an acute asthma exacerbation on arrival to the ED. The choice and intensity of therapy depends on the severity of the exacerbation and the patient's response to initial treatment. Recommended doses for asthma therapies are summarized in Table 34-4. Consider applying oxygen in all ED patients with an acute exacerbation of their asthma. Hypoxia can lead to hypoventilation and acidosis, which can cause pulmonary vasoconstriction, pulmonary hypertension, and right heart failure. Check for signs of dehydration due to decreased intake or vomiting and provide intravenous (IV) fluids if needed. However, in acute asthma exacerbation, there may be increased secretion of antidiuretic hormone and increased capillary permeability, thus IV fluids should be used in moderation to avoid overhydration resulting in pulmonary edema. Antibiotics should be used only if evidence of concurrent infection exists. However, most exacerbations are secondary to viral upper respiratory infections (URIs) and hence antibiotics are rarely indicated.

The aims of pediatric asthma treatment should be effective acute phase treatment, prevention of recurrent exacerbations, minimization of medication side effects, prevention of recurrent visits to the ED or hospitalizations, and optimization of long-term management. The use of a severity assessment clinical algorithm with an asthma care pathway can reduce hospital length of stay, reduce physician prescribing errors, and improve patient education, without a corresponding increase in treatment costs.¹³ Figure 34-1 provides an example of a treatment algorithm which can be used in an ED.

β-Adrenergic Agonists

Short-acting adrenergic bronchodilators are the first line of emergency treatment of asthma. Bronchodilation is produced by stimulation of β₂-adrenoreceptors, which mediate an increase in cyclic AMP via the enzyme adenyl cyclase. Cyclic AMP stimulates binding of calcium ions to the cell membrane, reducing the mycoplasmal calcium concentration with resultant bronchodilation (smooth muscle relaxation), and stabilization of mast cells (Fig. 34-3). Stabilization of mast cells retards the release of histamine and other inflammatory products. β-adrenergic agonist, when given efficiently and in high doses, will quickly relieve acute bronchospasm without many side effects.¹⁴

Albuterol (also known as salbutamol) is most commonly used in the United States. It is a short-acting β₂-agonist (SABA). Aerosol therapy is most commonly used. It is as effective as IV or SC therapy and more effective than oral therapy.¹⁵ There are two main methods of delivering aerosolized medications. Numerous studies suggest comparable efficacy of metered dose inhalers (MDIs) and nebulization.^16,17 MDIs are less expensive and more convenient, but require a cooperative child who understands the technique of administration. The concurrent use of an aero chamber or spacer will allow the younger children to use an MDI more effectively. For a child under 3 years of age, apply a mask to the mouthpiece of the spacer device to help administer the medications. The inhaler is actuated into the spacer device and the child inhales the medication immediately using five tidal breaths. Doses of 0.5 puffs/kg with a maximum of 10 to 12 puffs per dose are recommended for treatment of an acute exacerbation. The transition from general clinical use of jet nebulization to spacer/MDI in pediatric asthma has been categorized as slow but consistent, with concerns (unfounded) raised around cost, efficacy, and safety of spacer/MDI.^18,19

Particles generated by aerosolization vary in size. Only those in the 1 to 5 μm range are useful drug vehicles and are deposited in the lower airways. These represent only 10% of the output from an MDI, and 1% to 5% from jet nebulizer. The rest escape into the room, or are dissolved in mucous membranes and swallowed. Low flow rates and greater breath-holding periods optimize drug deposition in the lower airways. Oxygen flow rates of 6 to 7 L/min are recommended. Since so much of the drug escapes into the atmosphere, especially when being delivered to very young children, many physicians will administer “unit doses” (usually, 2.5 or 5 mg albuterol/3 mL NS) to all patients regardless of size. Larger nebulizer chambers allow for multiple drug unit doses (such as albuterol and ipratropium bromide) to be placed in the chamber and run over a period of time. This is less time-consuming for ED staff and avoids breaks in therapy in patients with moderate or severe exacerbations. Doses of 7.5 mg of albuterol mixed with 500 μg ipratropium for patients weighing less than 35 kg, and 15 mg albuterol with 1000 μg ipratropium in children weighing more than 35 kg can be mixed in the holding chamber and run over 1 hour. Continuous nebulization of albuterol, typically reserved for severe/critical asthma, at initial rates of greater than 3 mg/kg/h appears to be safe and effective.²⁰ Continuous nebulization is usually started at approximately 0.5 mg/kg/h and titrated up or down as needed. The repeat assessments of the patient's clinical status and response should guide the frequency of aerosols and the rate of continuous nebulization.

Other Adrenergic Agonists

It has been hypothesized that IV bronchodilators may result in a more rapid clinical response due to the potentially higher systemic distribution of the medication.²¹ The role of IV adrenergic agonists, such as IV salbutamol, in addition to nebulized solutions remains unclear. They are currently recommended in international asthma treatment guidelines as second-line treatment in children who do not respond to regular inhaled β-agonist and corticosteroid therapy. A Cochrane review in 2001 concluded that there was little evidence to support IV use over any other regimens in the management of acute severe asthma.¹⁵ It further reported no significant clinical improvements whether given by continuous infusion or by bolus and also resulted in more clinical side effects. IV terbutaline (also a β₂-selective agent) is safe and effective in both adult and pediatric patients with severe asthma exacerbations.^22,23 However, more recently, a randomized double-blind placebo controlled trial recommended the physician exercise caution in its use and advised further trials to investigate its efficacy and safety.²⁴

Salmeterol is a long-acting β₂-agonist (LABA) that has a longer duration of action but slower onset than albuterol. It is used primarily in the management of chronic moderately severe asthma to reduce the need for SABA. It is not intended for frequent repetitive administration or use in acute asthmatic exacerbation.

Levalbuterol (Levosalbutamol or Xopenex) is the R-enantiomer of the SABA albuterol. It is promoted as an alternative to racemic albuterol to decrease the incidence of side effects. However, no studies have demonstrated such a benefit from this medication.^25–27

Inhaled epinephrine does not have any advantages over inhaled albuterol in acute asthma exacerbations.²⁸ Epinephrine is also available as a SC injection. It is more toxic and no more effective than inhalation of a β₂-selective drug. Parenteral administration (0.01 mL/kg up to 0.3 mL of the 1:1000 solution SC) should be reserved for those patients who are unable to generate adequate tidal volume to deliver aerosolized drug to the bronchial tree such as in severe asthma exacerbations. SC terbutaline (0.01 mg/kg up to 0.25 mg), which is more β₂-specific, may be used as an alternative to SC epinephrine.

Side effects associated with all β-adrenergic agonists are largely due to sympathomimetic effects and include tremors, anxiety, nausea, headache, vomiting, tachycardia, arrhythmia, hypertension, and hypotension. Non-sympathomimetic side effects include decreased oxygen saturation (secondary to altered V/Q matching), which is common, and paradoxical bronchospasm, which is rare. Metabolic side effects include hypokalemia, hypophosphatemia, hyperglycemia, and lactic acidosis. These side effects are often related to dose and route of administration and rarely require cessation of therapy. However, all patients receiving prolonged high-dose β-adrenergic therapy or IV adrenergic therapy should have their oxygen saturation, heart rate, blood pressure, and serum electrolytes monitored closely.

Anticholinergics

Asthmatics have profound bronchoconstriction in response to cholinergic agonists; thus, anticholinergic agents play an important role in the treatment of asthma (Fig. 34-4). There has been a resurgence of interest in the use of anticholinergic agents due to better understanding of the cholinergic mechanisms that control airway caliber, and the development of synthetic analogs that are not appreciably absorbed across mucous membranes, minimizing side effects. Ipratropium bromide is a quaternary amine that fits into this category. It is a less potent bronchodilator, has a slower onset of action than the more commonly used β-adrenergic agonists, and is not recommended as first-line treatment in an acute exacerbation of asthma.²⁹ Its use in combination with multiple dosing of β-agonists in pediatric patients is helpful in reducing rates of hospitalization.³⁰ It is most efficacious when given as two to three doses in combination with the initial two to three albuterol treatments. This study included school-age children with asthma only. A 2005 review concluded that the indiscriminate use of anticholinergic agents was not advantageous in the treatment of wheezing children under the age of 2 years.³¹ Reported side effects of anticholinergic agents include dry mouth and a metallic taste.

Corticosteroids

Multiple studies have demonstrated the effectiveness of corticosteroids in the treatment of asthma. Benefits include rate of improvement measured by clinical scores and pulmonary function studies, decreased duration of symptoms, decreased hospitalization rates, decreased relapse rates, and decreased need for β-agonists.^32,33 A clearer understanding of the inflammatory mechanisms involved in the pathogenesis of even mild asthma has led to a greater emphasis on the use of steroids. Corticosteroids have multiple mechanisms of action in improving asthmatic patients. They restore responsiveness to β-adrenergics by increasing receptor numbers and lowering their threshold. Two mechanisms by which they reverse inflammation are inhibition of arachidonic acid metabolites via phospholipase and suppression of the polymorphonuclear response to chemotactic stimuli. Oral corticosteroids are preferred over parenteral corticosteroids in children as they are less invasive and equally efficacious.³⁴ IV dosing is reserved for those patients who cannot tolerate oral medications, require continuous β-agonist therapy, or have impending respiratory failure. Following a short course of corticosteroid therapy, adrenal suppression is minimal and clinically insignificant. Toxicity is chiefly related to duration of use and not to dose. Therefore, doses at the top of the dose–response curve should be used and they should be stopped as soon as clinically allowable.

Early administration of corticosteroids improves outcomes for asthma patients.^35,36 A recent study showed that administration of systemic corticosteroids within 75 minutes of triage reduced admission rates and length of active treatment.³⁷ Prednisone is the most commonly used corticosteroid; doses vary from 1 to 2 mg/kg/day for a duration of 3 to 5 days. Prednisone has a bitter taste and one of its most common side effects, whether taken in tablet or liquid form, is vomiting. There is some concern regarding the compliance of children and their caregivers in completing the 5-day course of prednisone. One study found that at least 7% of children seen in a pediatric ED never have their prescriptions filled.³⁸ In another study, caregivers reported adherence to the prescribed length of oral corticosteroid therapy only 64% of the time.³⁹ Investigators and clinicians have sought alternatives to this traditional therapy. Several clinical trials have examined the use of dexamethasone as an alternative.^40–46 A dosage of 0.6 mg/kg of dexamethasone was used in two of these studies, giving a second dose on the following day.^43,46 Three studies chose the intramuscular route for the administration of dexamethasone.^42,44,45 Each of these seven studies found dexamethasone to be equally effective as a course of prednisone. One study further examined the cost-effectiveness of a dexamethasone versus prednisone regimen on relapse rates, representations, and hospital admissions and found a decreased rate of return visits to the ED, a reduction in subsequent hospitalizations, and significant cost savings in the dexamethasone group.⁴⁷ The use of inhaled corticosteroids in the acutely ill asthmatic patient has been investigated but no significant benefit has been reported.⁴⁸

Magnesium

In patients who have not responded to the above therapy, one should consider administering magnesium sulfate. Magnesium produces bronchodilation via counteraction of calcium-mediated smooth muscle constriction. There is conflicting literature on its benefits for pediatric patients with an acute asthma exacerbation.^49,50 A systematic review of the literature on IV magnesium for asthmatics of all ages did demonstrate a decrease in admission rate for those with severe acute asthma exacerbations.⁵¹ Doses of 25 to 75 mg/kg IV over 20 minutes are recommended for patients with a moderate or severe asthma exacerbation who do not respond to initial therapy with albuterol and ipratropium. More recently the MAGNETIC study, a double-blind randomized placebo controlled trial comparing the use of nebulized magnesium to nebulized placebo following standard acute asthma management, has shown a reduction in asthma severity scores in children. The greatest difference in scores was seen in children who had the shortest duration of exacerbation at time of presentation.⁵² A recent well-designed clinical Argentinian study examined the use of intravenous magnesium within the first hour of initiation of standard treatment in acute severe asthma.⁵³ They found a significant reduction in the number of patients requiring ventilation compared with those managed with standard treatment and no IV magnesium. A further magnesium study in adults, the 3MG trial, a double-blind randomized controlled trial comparing nebulized and IV magnesium in acute severe asthma, showed no benefit from magnesium.⁵⁴

Other Agents

Methylxanthines

IV methylxanthines, for example, aminophylline, historically played an important role in the management of acute severe asthma. However, there is little consensus on their current use in the management of acute severe asthma.⁵⁵ One randomized trial found aminophylline use to be of equivocal benefit when compared with IV β-adrenergic use.⁵⁶ A Cochrane review in 2005 concluded that the addition of IV aminophylline to the routine treatment plan of β₂-agonists and corticosteroids showed an improvement in lung function within 6 hours, but did not show a reduction in symptoms, in hospital length of stay, or nebulized treatments required.⁵⁷ The review also concluded no role for methylxanthines in the management of mild-to-moderate asthma.

Leukotriene Antagonists

There is, as yet, no basis to recommend routine use of leukotriene antagonists in the ED management of asthma exacerbations. Early treatment with oral montelukast in the management of a mild asthma exacerbation, after ED care in a multi-center, randomized, placebo controlled study resulted in a reduction in asthma signs and symptoms and also a reduction in the need for further health care visits and in school absenteeism.⁵⁸ Its utility has not yet been proven for moderate-to-severe acute asthma.^59,60 Doses of 5 to 10 mg have been recommended depending on age of the child.

Heliox

Inhalation of a blend of helium and oxygen may be helpful for severe asthmatic patients unresponsive to other therapies. Current published literature is inconclusive as to its benefit and has not shown any significant complications with its use.^61,62 New evidence suggests certain beneficial effects in patients with more severe obstruction. Since these conclusions are based upon between-group comparisons and small studies, they should be interpreted with caution.⁶³

Hypertonic Saline

Hypertonic saline nebulization use and its benefits are well described for the treatment of bronchiolitis and cystic fibrosis. Its use in the treatment of acute asthma is much newer. A recent randomized controlled double-blind study compared albuterol nebulization mixed with hypertonic saline (5%) with albuterol mixed with normal saline.⁶⁴ It found that regular albuterol with hypertonic saline nebulization resulted in a shorter length of stay and a lower admission rate in preschool children.

Intubation/Mechanical Ventilation

Indications for intubation of an asthmatic patient include decreased level of consciousness, apnea, exhaustion, rising PaCO₂ after treatment, PaO₂ <60 mm Hg, and pH <7.2. An asthmatic may not immediately improve with intubation, since intubation does nothing to change lower airway obstruction. Intubation and mechanical ventilation may also put the patient at risk for serious complications. When intubating an asthmatic patient, the largest-diameter tube appropriate for the patient's size is used to avoid further increasing resistance. Although sedation is normally contraindicated in patients with asthma,⁵ sedation and paralysis may be indicated to avoid barotrauma secondary to the child struggling during passage of the endotracheal (ET) tube. A modified rapid sequence induction should be used. The dissociative anesthetic ketamine is known to have bronchodilatory properties and therefore is a good choice for a sedative. Paralysis with succinylcholine may increase secretions but is not contraindicated. Vecuronium or rocuronium are recommended by most authors, when muscle paralysis is indicated in a pediatric patient with a severe asthmatic exacerbation. Once intubated, patients will require sedation and paralysis to maintain effective ventilation. They also require a long expiratory time to avoid air trapping due to airway obstruction. Otherwise, the ventilator may be providing a second inspired breath before the first breath has been fully expired (stacking breaths). Intrinsic PEEP may cause an increase in intrathoracic pressure that leads to decreased venous return to the heart and can cause hypotension. Intubated asthmatic patients need to be watched carefully for the development of pneumothorax, or pneumomediastinum. Sudden changes in their respiratory or hemodynamic status may be due to a tension pneumothorax until proven otherwise. Ventilator settings should be adjusted to provide for adequate oxygenation with as low a peak pressure and PEEP as possible. The use of permissive hypercapnea (PCO₂) levels (as high as 70–90 mm Hg) has been associated with decreased morbidity and mortality rates in intubated asthmatic patients.

Challenges in Preschool Wheezers

One area that continues to challenge emergency physicians is the treatment of preschool wheezers due to a number of factors including difficult clinical assessment, their inconsistent response to the usual asthma medications, and frequent intermittent wheeze secondary to a primary viral infection such as RSV or adenovirus. This leads to episodic wheezing with no inter-illness symptoms or signs. Bronchiolitis is the main diagnostic consideration for such presentations in this age group. There is now a body of evidence which supports the hypothesis that the pathophysiology underlying wheezing in the preschool population is different to that in atopic asthma in the school-age population.^65,66

The treating physician can give a trial of a bronchodilator in an infant under 2 years presenting with recurrent symptoms. If there is no response to the inhaled β-agonist treatment, then the differential diagnosis should be reviewed and other treatment measures considered. In infants, in whom a diagnosis of mild-to-moderate asthma is suspected, the use of inhaled β-agonist MDI medication with a spacer device is equally as effective, if not better, than nebulized formulations.^67,68 Oral β-agonist treatment is not recommended in this age group as it does not affect symptom scores or length of stay when compared with placebo.⁶⁹ No clinical benefit has been found for oral corticosteroids for episodic wheezing in preschool children,^70,71 and oral corticosteroids should only be prescribed for critically ill preschoolers with wheezing.⁷²

Despite appropriate therapy, approximately 10% to 25% of ED patients with acute asthma will require hospitalization.⁷³ The decision to admit or discharge a patient from the ED can be difficult. Risk factors associated with admission to hospital for children with asthma include prior asthma hospitalization, environmental tobacco smoke exposure, family history of maternal asthma, allergen sensitization, and onset of asthma-like symptoms before 1 year of age.⁷⁴ In allergic asthmatic children, the combination of high-allergen sensitization and exposure and virus detection significantly increases the risk for hospital admission.⁷⁵

Numerous published studies have tried to establish objective criteria for admission. Clinical examination and scoring systems perform poorly in identifying who requires hospital admission.^9,76–79 These assessments may help to determine which patients should be admitted after an initial 1- to 2-hour period of treatment.⁵ An initial pulse oximetry in infants and young children might be useful for assessing exacerbation severity but not for predicting the need for hospital admission.⁸⁰ However, a repeat pulse oximetry of <92% to 94% at 1 hour was a better predictor of need for hospitalization.⁷⁹ Another predictor of early relapse is desaturation with ambulation. The child can be monitored by pulse oximetry and walk around the room. Various spirometric parameters have also been proposed but have not proved to have adequate sensitivity and are often difficult to obtain in children.⁶ To date, no objective criteria are uniformly helpful in making this decision.

A further knowledge gap exists in the area of “step down” therapy, in particular use of β-agonists. Most centers will have protocolized approaches to initial therapy in the ED, but transitional therapy from the ED to the inpatient setting, and indeed to the community setting, lacks evidence and appears opinion-based or experiential only.

The following risk factors have been identified as being associated with mortality: previous intubation (greatest predictor of subsequent death), two or more hospitalizations in the last year, three or more ED visits in the last year, use of systemic steroids, rapid progression of attacks, hypoxic seizures, severe nighttime wheezing, barotraumas, self-weaning from medications, lack of perception of the severity of the disease, poor medical management, poor access to medical care, and smoke exposure.

Patients discharged from the ED after an acute asthma exacerbation should be instructed to continue β-agonist use and take a short course of corticosteroids. Steroid bursts for 5 days or less, if done no more than four times per year, do not require tapering. Immune suppression is clinically insignificant in patients with normal baseline immune function. Growth suppression does not occur, and the incidence of adverse psychiatric effects is low. One or two doses of dexamethasone phosphate have equivalent efficacy. The use of inhaled steroids is encouraged for chronic treatment at home in patients with moderately severe asthma. The addition of inhaled steroids to oral steroids in patients discharged from the ED can decrease the rate of relapse. The most recent NHLBI 2007 guidelines urge that those treating acute exacerbations of asthma should work to prevent relapse of the exacerbation or recurrence of another exacerbation by providing:

• Referral for follow-up asthma care within 1 to 4 weeks;

• An ED asthma discharge plan with instructions for medications prescribed at discharge and for seeking further medical care if asthma symptoms worsen or for increasing medication use;

• Review of inhaler technique whenever possible; and

• Consideration of initiating inhaled corticosteroids.⁵

A recently updated Cochrane systematic review found that asthma education provided to children and their parents while in the ED resulted in fewer future ED visits and hospital admissions. However, the long-term benefit of such interventions remains unclear.⁸¹

Despite the mortality and morbidity associated with this disease, the prognosis for most children with asthma is good. At least half of all children with asthma will be symptom-free by adulthood.