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798 SECTION 12: Pediatrics FIGURE 126-11. CT showing soft tissue stranding and inflammation representing infection in the submandibular space ( arrow) in a patient with Ludwig’s angina. secretions or skin lesions. In cases of pharyngeal diphtheria, symptoms include sore throat, malaise, dysphagia, and low-grade fever. Charac teristic thick gray membranes (pseudomembranes) can develop over the tonsils and soft palate and potentially cause respiratory obstruction and death. Laryngeal diphtheria is characterized by a classic “barking” cough, stridor, hoarseness, and difficulty breathing, accompanied by marked edema of the neck referred to as “bull neck. ” Complications include myocarditis and neuritis potentially leading to diaphragmatic paralysis and death from respiratory failure. Diagnosis is confirmed by isolation of bacteria by culture of a nasopharyngeal swab. Treatment includes antitoxin, antibiotics, and respiratory support as needed.  OROPHARYNGEAL TRAUMA Traumatic oropharyngeal injuries in children typically occur during a fall with an object within the mouth. Such injuries are often referred to as “pencil injuries” and most commonly occur in patients between 2 and 4 years of age. When evaluating these injuries, ask if the entire foreign body was removed intact or if part of the object may have broken off into the soft tissue. Pencils, straws, toothbrushes, and toothpicks are the most common culprits. 53-55 There are rare, but well-known complications of penetrating pharyngeal injury. Entrance of free air into the neck or chest can result in stri dor and acute airway obstruction. Subsequent retropharyngeal infection from introduction of oral flora/bacteria into the penetrating wound can occur. A more severe complication of oropharyngeal trauma is carotid artery injury, as the carotid artery courses along the lateral aspect of the oropharynx and is therefore at risk of injury from both blunt and pen etrating impact forces. Penetrating injury can result in anything from hematoma formation to massive hemorrhage. Blunt injuries can cause compression of the carotid artery between the object and upper cervical vertebrae. The resultant shearing effect can cause an intimal tear in the vessel with subsequent thrombosis formation. Problems such as neck/ mediastinal emphysema, retained foreign bodies, abscess formation, thrombosis, and arterial dissection should be considered, as these find ings may be delayed after time of presentation. Symptoms may evolve over hours to days and can result in significant neurologic sequelae (stroke in the distribution of the common carotid territory).  CLINICAL FEATURES Children with acute oropharyngeal trauma may present with bleeding, drooling, or dysphagia. Children may also present in a delayed fashion with complications of oropharyngeal trauma such as retropharyngeal abscess (discussed separately earlier), or even neurologic symptoms of stroke in cases of carotid artery injury or thrombosis from prior trauma.  DIAGNOSIS Neither mechanism nor degree of injury is helpful in determining the possibility of neurovascular compromise. Soft tissue lateral neck films can assist in the evaluation of air in soft tissues, radiopaque foreign bodies, and evaluating for abscess. CT is superior to plain radiographs for the detection of free air, inflammation, or abscess. No consensus or specific clinical criteria exist with regard to advanced imaging for vascular injury.

ateral neck films can assist in the evaluation of air in soft tissues, radiopaque foreign bodies, and evaluating for abscess. CT is superior to plain radiographs for the detection of free air, inflammation, or abscess. No consensus or specific clinical criteria exist with regard to advanced imaging for vascular injury. CT angiography is necessary if carotid injury is suspected and should be considered for patients who are unstable or have neurologic sequelae, who cannot be adequately assessed, and for whom lateral pharyngeal trauma raises concern for vascular injury. 55,56 The risks of radiation from CT may outweigh the potential benefits in well-appearing children, however.57  TREATMENT Most wounds do not require surgical intervention and closure, but large gaping wounds and those with persistent bleeding may require closure under sedation or anesthesia. Lateral wounds adjacent to the path of the carotid artery have a greater risk of arterial injury than more mid line injuries, and those involving the soft palate have higher infectious complication rates than those limited to the hard palate. Oral wounds are tetanus prone, and prophylaxis should be given to unimmunized children. The incidence of infectious complications following penetrating palate trauma is approximately 1%, and thus the role of prophylactic antibiotics is unclear. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Wheezing in Infants and Children Gabrielle Freire Allan Evan Shefrin Roger Zemek INTRODUCTION Wheezing is a high-pitched sound that occurs when there is an eleva tion of airway resistance due to an obstructive process. The clinician must differentiate between stridor and wheeze because this determines location of the airway obstruction. Stridor is a sign of upper airway obstruction (above the thoracic inlet) that is more marked during CHAPTER Tintinalli_Sec12_p0669-0996.indd 798 8/2/19 7:52 PM

esistance due to an obstructive process. The clinician must differentiate between stridor and wheeze because this determines location of the airway obstruction. Stridor is a sign of upper airway obstruction (above the thoracic inlet) that is more marked during CHAPTER Tintinalli_Sec12_p0669-0996.indd 798 8/2/19 7:52 PM CHAPTER 127: Wheezing in Infants and Children 799 FIGURE 127-1. Normal inspiration and expiration (A, B) and dynamic airway compression (C) with development of auto–positive end-expiratory pressure (Auto-PEEP). TABLE 127-1 Important Historical Features and Their Significance in Infants and Children With Wheezing Feature Significance Age <1 y: bronchiolitis more common 1–2 y: mixed >2 y: asthma more common Family history Positive family history of wheeze suggests atopy, making asthma more likely Pattern Single episode: any etiology possible Recurrent: asthma Chronic illness: asthma, cystic fibrosis, congestive heart failure, anatomic abnormality Onset Sudden onset: foreign body aspiration, allergic reaction, asthma Identifiable trigger Concurrent viral illness: bronchiolitis, asthma Pollens, pets, dust, smoke and other irritants: asthma Choking episode: foreign body aspiration Response to bronchodilators Improvement with β2-agonist treatment is diagnostic for asthma Bronchiolitis may improve with inhaled epinephrine Previous hospitalization More severe disease, inability to care for child at home Previous critical care unit admission ± intubation More severe or life-threatening disease inspiration, whereas wheeze signifies lower airway obstruction dis tal to the thoracic inlet that is more marked during expiration (see Chapter 126, “Stridor and Drooling in Infants and Children”). 1-4 Wheezing implies a generalized obstructive airway disease when diffuse and focal obstruction when localized. However, severe flow limitation may exist without wheezing, for example, the silent chest in a severe asthma exacerbation. Bronchiolitis is the most frequent cause of wheezing in infants, and asthma is the most frequent cause in children and adolescents. RESPIRATORY PHYSIOLOGY The conducting airways extend from the trachea to the terminal bron chioles and do not participate in gas exchange. The distal transitional and respiratory zones are the gas-exchanging units. Lung tissue has elastic properties; functional residual capacity is the resting balance of stretch and recoil forces. Normally, at functional residual capacity, the tissue is relaxed at end expiration, and inspiration begins with minimal effort at the onset of inspiratory muscle contraction. Inspiration is an active process generated by the diaphragm and external intercostal muscles. During exertion, inspiration is aided by the use of accessory muscles including scalene and sternocleidomastoid muscles. 5 Expiration is normally a passive process, facilitated by elastic recoil of the stretched lung. In the presence of diffuse (e.g., asthma, bronchiolitis) or focal (e.g., foreign body) intrathoracic airway obstruction, the normally passive process of expiration becomes active in an attempt to overcome airway resistance. Abdominal and internal intercostal muscles are recruited. Positive intrapleural pressure is generated, and increasing external pressure is applied to the airways. This leads to progressively increasing airway obstruction as expiration proceeds, a phenomenon referred to as dynamic airway compression (Figure 127-1). Dynamic airway compression results in prolonged expiratory time. The net result is failure of alveoli and distal airways to fully empty at end expiration, resulting in air trapping and increased functional residual capacity.

as expiration proceeds, a phenomenon referred to as dynamic airway compression (Figure 127-1). Dynamic airway compression results in prolonged expiratory time. The net result is failure of alveoli and distal airways to fully empty at end expiration, resulting in air trapping and increased functional residual capacity. Before subsequent inspiratory flow can begin, inspiratory muscles must overcome this increased elastic recoil, which substantially increases the work of breathing, a phenomenon referred to as auto– positive end-expiratory pressure. Finally, air trapping and subsequent atelectasis result in areas with ventilation–perfusion mismatch and hypoxemia. Infants have smaller airways, highly compliant bronchial and bronchiolar cartilage, and more peripheral airway smooth muscle than older children and adults. These factors result in an even greater tendency toward airway collapse during expiration, air trapping, and auto–positive endexpiratory pressure. Thus, infants not only are more likely to experience wheezing illnesses but are also more likely to suffer the physiologic consequences of airway obstruction.  WHEEZING Approximately 25% to 30% of infants will have one episode of wheez ing, and nearly 50% of children will have a history of wheezing by 6 years of age. 2,7,8 Obtain a thorough history for any child with wheezing (Table 127-1), and consider age, family history, onset, pattern, season ality, positional changes, and associated symptoms. 2 A recurrent and episodic pattern, history of cough, association with identifiable triggers, and documented response to bronchodilators are highly suggestive of asthma in a child >2 years old. 9-11 A prior history of hospitalization, particularly to a critical care unit, and prior endotracheal intubation are important risk factors for severe disease. An exposure to sick contacts during a viral season, nasal congestion, poor feeding, and age <1 year Tintinalli_Sec12_p0669-0996.indd 799 8/2/19 7:52 PM

ars old. 9-11 A prior history of hospitalization, particularly to a critical care unit, and prior endotracheal intubation are important risk factors for severe disease. An exposure to sick contacts during a viral season, nasal congestion, poor feeding, and age <1 year Tintinalli_Sec12_p0669-0996.indd 799 8/2/19 7:52 PM 800 SECTION 12: Pediatrics TABLE 127-2 Age-Specific Respiratory Rate Ranges Age Respiratory Rate (breaths/min) <1 y 30–60 1–2 y 24–40 2–5 y 22–34 6–12 y 18–30 >12 y 12–16 TABLE 127-3 Differential Diagnosis for Wheezing in Infants and Children Potential Diagnosis Typical Age of Onset Cardinal Symptoms and Signs Confirmatory Tests Asthma >1–2 y Recurrent episodes of wheeze and/or nighttime cough, identifiable triggers such as seasonality, allergens, exercise Responsive to bronchodilators Trial of β-agonist Pulmonary function tests Allergy testing Bronchiolitis <1–2 y URI symptoms, seasonal (winter months), nasal flaring and congestion, wheezes, rales, rhonchi Consider viral antigen testing Gastroesophageal reflux Tracheoesophageal fistula Present from birth Cough, gagging, emesis related to feeding Esophageal pH probe Barium swallow Vascular ring, sling, malformation, or airway hemangioma or polyp Laryngomalacia Tracheomalacia Early infancy Present from birth, improves during first year of life Stridor that changes with position of the neck, exacerbations with URI CXR, CT angiography, bronchoscopy, barium swallow Laryngoscopy Congenital heart disease with left-to-right shunting and congestive failure Myocarditis 2–6 mo Any age Diffuse or basilar rales, tachycardia, hepatomegaly, cardiac murmur/gallop CXR, ECG, echocardiography ECG, CXR, troponin, echocardiography Foreign body aspiration Vocal cord dysfunction (paradoxical vocal cord motion) Usually >6 mo From birth (paralysis) Late school age/adolescents History of choking episode with subsequent acute onset of stridor and/or wheezing Stridor and/or wheezing, poor response to β-agonists Inspiratory and expiratory CXRs *

ECG, CXR, troponin, echocardiography Foreign body aspiration Vocal cord dysfunction (paradoxical vocal cord motion) Usually >6 mo From birth (paralysis) Late school age/adolescents History of choking episode with subsequent acute onset of stridor and/or wheezing Stridor and/or wheezing, poor response to β-agonists Inspiratory and expiratory CXRs * Flexible fiberoptic laryngoscopy Epiglottitis School age or adolescent Stridor and high fever, toxic appearance, drooling and tripod positioning Soft tissue radiographs of the neck* Pneumonia Any age Fever, cough, tachypnea, rales, grunting CXR Cystic fibrosis Ciliary dyskinesia Immunodeficiency Present from birth Recurrent lower respiratory tract infections, failure to thrive Sweat chloride concentration Ciliary biopsy Immunoglobulin assays *Consider portable radiographs because patients with possible foreign body aspiration or epiglottitis outside of the ED may experience sudden and complete airway obstruction. Abbreviations: CXR = chest x-ray; URI = upper respiratory infection. suggest bronchiolitis. 2 Choking or gagging indicates possible foreign body aspiration. CLINICAL FEATURES On physical examination, use the pediatric assessment triangle to assess appearance, work of breathing, and circulation .12 Assess the general appearance of the child using the TICLS mnemonic (tone, interactivity, consolability, look, and speech). Assess work of breathing by observ ing the child’s position (e.g., sniffing, tripod), accessory muscle use (nasal flaring, tracheal tug, scalene retraction, intercostal muscle use, abdominal breathing), and presence of stridor or wheeze. Assess circulation rapidly by observing the patient’s color, especially noting cyanosis. Determine respiratory rate (Table 127-2 shows age-related ranges). Monitor oxygen saturation by either intermittent or continuous pulse oximetry. It is common for some infants and children with asthma or bronchiolitis to develop ventilation–perfusion mismatch, which may result in mild hypoxemia (92% to 94%) that is correctable with minimum supplemental oxygen (1 to 2 L/min). More severe hypoxemia (≤92%) suggests moderate to severe disease. Hypoxemia refractory to bronchodilators and supplemental oxygen may suggest alternative diagnoses such as pneumonia, pneumothorax, pulmonary shunt, or congenital cardiac lesion (especially in the hypoxemic neonate). Diaphoresis, confusion, and drowsiness are ominous signs indicating imminent respiratory failure. Check for audibility and symmetry of breath sounds to assess adequacy of ventilation. Inspiratory-to-expiratory ratios of less than the normal 2:1 (e.g., 1:2 or 1:3) reflect the prolonged expiratory times seen with obstructive airway disease. Perhaps more important than the initial physical examination findings are the changes in these findings in response to bronchodilators and other treatments. DIAGNOSIS Table 127-3 lists the differential diagnosis of wheezing. Asthma and bronchiolitis account for the majority of wheezing episodes in children, although a broader differential diagnosis must always be considered and ruled out on history, on physical exam, or with ancillary investigations. This is particularly important when the patient’s history or physical findings are not consistent with a diagnosis of asthma or bronchiolitis or when the illness does not respond to interventions appropriate to these disease processes. Table 127-3 outlines the signs, symptoms, context, and ancillary testing for the different causes of wheezing. The association of wheezing with feedings suggests gastroesophageal reflux or tracheoesophageal fistula with aspiration.

en the illness does not respond to interventions appropriate to these disease processes. Table 127-3 outlines the signs, symptoms, context, and ancillary testing for the different causes of wheezing. The association of wheezing with feedings suggests gastroesophageal reflux or tracheoesophageal fistula with aspiration. Grunting, a physiologic response to generate positive end-expiratory pressure in an attempt to maintain alveolar inflation, suggests alveolar disease, although it may also result from severe abdominal distention. Inspiratory crackles or rales may be present in bronchiolitis as a result of atelectasis, although pneumonia is also a consideration. Consider the possibility of foreign body aspiration and congestive heart failure because these disorders may also cause wheezing. Tintinalli_Sec12_p0669-0996.indd 800 8/2/19 7:52 PM

ion. Inspiratory crackles or rales may be present in bronchiolitis as a result of atelectasis, although pneumonia is also a consideration. Consider the possibility of foreign body aspiration and congestive heart failure because these disorders may also cause wheezing. Tintinalli_Sec12_p0669-0996.indd 800 8/2/19 7:52 PM CHAPTER 127: Wheezing in Infants and Children 801 TABLE 127-4 Risk Factors for Severe Disease in Infants With Bronchiolitis Preexisting risk factors •   Prematurity (<37 wk gestational age, especially if <32 wk gestational age) •   Age <2 mo •   Underlying cardiac or pulmonary disease •   Immunodeficiency Acute risk factors •   Oxygen saturation ≤91% on room air at triage •   Increased work of breathing (retractions, nasal flaring, grunting) •   Dehydration (observed or reported poor feeding) •   Apnea  BRONCHIOLITIS Bronchiolitis is the most common lower respiratory tract infection in infants and children ≤2 years of age and is the leading cause for hos pitalization in children <1 year of age. 13 The most common cause is respiratory syncytial virus, although bronchiolitis may be caused by other viruses including, but not limited to, human metapneumovirus, adenovirus, influenza, rhinovirus, and parainfluenza viruses. PATHOPHYSIOLOGY The viral infection in bronchiolitis causes inflammation of the lower respiratory tract, with resultant edema, epithelial cell necrosis, bronchospasm, and increased mucus production within the bronchioles. 15 This results in variable degrees of air trapping, atelectasis, and hyperinflation of the lower airways. The increase in airway resistance and develop ment of lower airway obstruction result in increased work of breathing. Because the nasal passages account for 50% of total airway resistance, increased nasal mucus production may cause upper airway obstruction due to the small nasal passages of infants. This in itself can cause modest respiratory distress, particularly in young infants, who are obligate nasal breathers. Respiratory syncytial virus is transmitted by direct contact with contaminated secretions. Because respiratory syncytial virus is highly infectious, self-contamination and nosocomial spread are common. Hand washing and contact precautions are important to limit the spread of disease. CLINICAL FEATURES Although bronchiolitis can be seen throughout the year, its peak occurrence in North America is from November to March. Typical symptoms are rhinorrhea, tachypnea, wheezing, and coughing. Use of accessory muscles, nasal flaring, and fever may also occur. These symptoms last on average 7 to 21 days and are often the worst in the first week of the illness. 16 The peak of symptoms is often between the third and fifth day after onset. Associated symptoms include irritability, cyanosis, and poor feeding. A subset of infants with bronchiolitis will develop severe disease and apnea. Apneic episodes may be brief and self-limited or progress to more frequent and prolonged episodes that lead to hypoxia and the need for endotracheal intubation. Some infants presenting with apnea have minimal other symptoms. Several factors associated with a greater risk of severe disease and apnea are listed in Table 127-4. 15,17 Infants with bronchiolitis and these risk factors may have prolonged hospital stays, greater need for mechanical ventilation, and higher mortality rates. Consider bronchiolitis in infants with apparent life-threatening events and monitor such infants closely (see Chapters 117 and 118, “Brief Resolved Unexplained Events and Apparent Life-Threatening Events” and “Sudden Infant Death Syndrome”). On chest examination, wheezing and crackles are heard diffusely throughout both lung fields.

hiolitis in infants with apparent life-threatening events and monitor such infants closely (see Chapters 117 and 118, “Brief Resolved Unexplained Events and Apparent Life-Threatening Events” and “Sudden Infant Death Syndrome”). On chest examination, wheezing and crackles are heard diffusely throughout both lung fields. Respiratory rates should be measured for 1 full minute and may vary from normal to profound tachypnea (Table 127-1). Accessory muscle use and intercostal or subcostal retractions develop as respiratory distress worsens. Patients with bron chiolitis are at risk for dehydration as blocked nasal passages inhibit feeding while increased work of breathing and a higher metabolic rate contribute to increased insensible losses. Assess for signs of dehydra tion including dry mucous membranes, tachycardia, lethargy, delayed capillary refill, inadequate urine output, and a sunken fontanelle. DIAGNOSIS Bronchiolitis is a clinical diagnosis based on the findings of the history and physical examination, which include typical symptoms of rhinorrhea, tachypnea, crackles, and/or wheezing in a child <2 years of age. There are several published scoring systems for assessing the severity of illness and change over time used for research purposes, although none has been validated or gained wide acceptance in clinical application. Obtain pulse oximetry readings at presentation to detect hypoxemia that may not be readily suspected on physical examination and repeat readings during the course of the ED visit. Obtain intermit tent oxygen saturation monitoring for children with mild disease and continuous monitoring for those with moderate or severe disease. Rapid viral antigen detection tests are not helpful in the diagnosis of bronchiolitis but should be considered in certain clinical situations. Viral testing should be performed for patients on respiratory syncytial virus prophylaxis presenting with bronchiolitis. In this situation, the presence of respiratory syncytial virus infection may warrant discontinuation of the prophylaxis for the rest of that bronchiolitis season. Viral testing should also be considered in the context of planned admission for the purpose of patient cohorting and infection control. Ancillary tests, such as blood work and radiographs, are not routinely needed unless other diagnoses need to be excluded .15 The incidence of serious bacterial infections in infants <28 days of age with bronchiolitis and fever is 3% to 10%, similar to that in other neonates with fever, so the standard testing of blood, urine, and cerebrospinal fluid is indicated. In infants >30 days of age, the incidence of seri ous bacterial infection in association with bronchiolitis remains 3% to 5%, with the most common infection being a urinary tract infection. 18 Chest radiographs are not routinely indicated but may be considered when the illness is severe or associated with hypoxia or when pneumothorax is suspected. 19 Although the chest radiograph in bronchiolitis may demonstrate atelectasis, bacterial pneumonia is unusual. Point-of-care US can be a useful adjunct for the assessment in patients with bronchiolitis. Point-of-care US can be used by the clinician to identify diagnoses such as pneumonia, asthma, and pneu mothorax and may also be helpful in identifying patients with more severe bronchiolitis. 20-22 TREATMENT Figure 127-2 outlines an ED algorithm for bronchiolitis treatment based on severity of illness. In 2014, the American Academy of Pedi atrics published an updated clinical practice guideline for the treat ment of bronchiolitis in children age 1 to 23 months that highlights some of the challenges clinicians encounter in the inpatient and ED settings.

gorithm for bronchiolitis treatment based on severity of illness. In 2014, the American Academy of Pedi atrics published an updated clinical practice guideline for the treat ment of bronchiolitis in children age 1 to 23 months that highlights some of the challenges clinicians encounter in the inpatient and ED settings. The main interventions recommended for treatment of children with bronchiolitis are symptomatic supportive measures. As upper airway obstruction is often the main issue for children with bronchiolitis, the most important treatment is frequent instillation of saline into the nares followed by suctioning. Mild dehydration should be managed with more frequent and smaller feeds and the use of prefeed suctioning. If there is concern for more significant dehydration, options include temporary support with nasogastric feeds or IV hydration. In children with respiratory distress requiring respiratory support, the IV route is favored to reduce the risk of aspiration. The evidence behind the most common interventions to reduce respiratory distress is summarized below.  OXYGEN The American Academy of Pediatrics recommends maintaining an oxygen saturation of >90%. Tintinalli_Sec12_p0669-0996.indd 801 8/2/19 7:52 PM

ry support, the IV route is favored to reduce the risk of aspiration. The evidence behind the most common interventions to reduce respiratory distress is summarized below.  OXYGEN The American Academy of Pediatrics recommends maintaining an oxygen saturation of >90%. Tintinalli_Sec12_p0669-0996.indd 801 8/2/19 7:52 PM 802 SECTION 12: Pediatrics  BRONCHODILATORS No benefits have been shown on oxygen saturation, hospitalization rates, or duration of hospitalization by using β 2-agonists (including salbutamol/albuterol, ipratropium bromide, and terbutaline),23,24 and they should not be given routinely. Inhaled epinephrine does not reduce rates of admission, although some studies suggest that it may provide temporary clinical improve ment when used in the ED. This therapy should not be used routinely but may have a role to play in the management of children with severe or acutely deteriorating bronchiolitis. 15,24,25  CORTICOSTEROIDS The combined use of dexamethasone and epinephrine decreased admission rates in a large, multicenter, Canadian study. However, a recent meta-analysis incorporating these data with other studies on the topic did not confirm this association. Therefore, combination therapy should not be used routinely for the treatment of children with bronchiolitis. 24,26,27 There is no literature to support the use of systemic or inhaled corti costeroids alone in the treatment of bronchiolitis, and most guidelines advise against it.  NEBULIZED HYPERTONIC SALINE The data on the effect of hypertonic saline in bronchiolitis are mixed. Hypertonic saline may improve mucociliary clearance by loosening mucus plugs through osmotic draw of fluid from submucosal and adventitial spaces. The preponderance of evidence suggests no mean ingful clinical benefit from nebulized hypertonic saline (3% or 7%) in the ED, and the 2014 American Academy of Pediatrics clinical practice guidelines recommend against its routine use. FIGURE 127-2. ED algorithm for the treatment and disposition of a patient with bronchiolitis. ICU = intensive care unit; MD = physician; NG = nasogastric. MD Assessment (Respiratory assessment, history, physical exam) Presentation to ED Mild-Moderate BronchiolitisWell Severe, Life-Threatening Apnea • Aggressive nasal suctioning • Intermittent/continuous pulse oximetry • Supplemental oxygen maintaining SaO2 ≥90% • Assess hydration (Supplement with IV or NG as necessary) • Consider epinephrine nebulization (0.1% solution–0.5 mL in 3.5 mL NaCI) every 1–2 h • Consider dexamethasone (1 milligram/kg) combined with epinephrine • Nasal suction with normal saline • Assess hydration (Supplement with IV or NG as necessary) • Intermittent pulse oximetry • ICU consultation or transfer to tertiary pediatric hospital • Consider noninvasive ventilatory support • Consider intubation Assess Response (Observe for 2–4 h, assess feeding) Deterioration Improvement • Persistent O 2 requirement Assess Admission Criteria: • Apnea monitoring • Fluid/nutritional support needed • Inability to care for patient at home One or more criteria met No criteria met Consider admission to inpatient unitNasal suction as needed Caregiver education (signs, symptoms, natural history) Arrange for early follow-up with primary care physician Discharge home Tintinalli_Sec12_p0669-0996.indd 802 8/2/19 7:52 PM

d • Inability to care for patient at home One or more criteria met No criteria met Consider admission to inpatient unitNasal suction as needed Caregiver education (signs, symptoms, natural history) Arrange for early follow-up with primary care physician Discharge home Tintinalli_Sec12_p0669-0996.indd 802 8/2/19 7:52 PM CHAPTER 127: Wheezing in Infants and Children 803  VENTILATORY SUPPORT Noninvasive ventilation measures, such as high-flow nasal cannula oxygenation, nasal continuous positive airway pressure, and bilevel positive airway pressure, may help avoid or delay the need for endotracheal intubation and mechanical ventilation.29-31 While continuous positive airway pressure is a more effective respiratory support tool, high-flow nasal cannula is better tolerated by children and may be sufficient for patients who require support but do not have evidence of impending respiratory failure. When other measures do not work, endotracheal intubation with mechanical ventilation may be necessary. DISPOSITION AND FOLLOW-UP The majority of children with bronchiolitis can be discharged from the ED. Educate caregivers regarding the signs and symptoms of increasing respiratory distress and dehydration and tell them to bring the child for immediate reevaluation if they develop respiratory distress or dehydra tion. Demonstrate proper nasal suctioning techniques to caregivers. Counsel parents that symptoms may persist for up to 3 weeks to help avoid unnecessary ED returns for persistent mild symptoms. Factors that should prompt consideration for admission are listed in Table 127-4. Infants with 1 or more of these risk factors are at risk of requiring more significant interventions and should at least be observed for a period of time in the ED. Alternatively, infants without any risk factors can be safely discharged home, assuming that there are no social concerns and that adequate follow-up can be arranged. Factors such as sex, race, duration of symptoms, parental history of asthma, and prior ED visits are not related to safety for discharge.  ASTHMA Asthma is a chronic disease characterized by episodic and reversible airflow obstruction due to bronchial smooth muscle hyperreactivity and inflammation that is responsive to bronchodilator and corticosteroid treatments. 9,10,33 More than 95% of children age 2 to 18 years presenting to the ED with asthma exacerbations exhibit wheezing, shortness of breath, cough, and/ or dyspnea secondary to decreased expiratory airflow. 34 Milder cases of acute asthma exacerbations may present with only wheezing or mild dyspnea, whereas severe exacerbations present with dyspnea at rest, inability to speak, and marked increased work of breathing. 10 Severe exacerbations may progress to status asthmaticus and respiratory failure, which may be lifethreatening. 35,36 PATHOPHYSIOLOGY The three pathophysiologic processes of asthma are inflammation, bronchospasm, and airway obstruction. The inflammatory cascade either directly leads to or contributes to the severity of bronchospasm and airway obstruction. Multiple inflammatory pathways are activated in asthma and involve a complex interplay of cytokines, chemokines, immunoglobulin E, lymphocytes, mast cells, and eosinophils. Bronchospasm results in decreased airflow during exacerbations and may be precipitated by triggers such as infection, irritants, or allergens. Irritant-induced bronchospasm may involve non–immuno globulin E–dependent pathways (e.g., aspirin, NSAIDs), and may also involve as yet undefined mechanisms (e.g., exercise, emotional stress). Allergens precipitate bronchospasm as a result of immunoglobulin E–dependent release of histamine, leukotrienes, and other mediators from mast cells. The third primary pathophysiologic process in acute asthma is airway obstruction.

s), and may also involve as yet undefined mechanisms (e.g., exercise, emotional stress). Allergens precipitate bronchospasm as a result of immunoglobulin E–dependent release of histamine, leukotrienes, and other mediators from mast cells. The third primary pathophysiologic process in acute asthma is airway obstruction. Inflammation causes airway mucosal edema and contrib utes to airway obstruction indirectly as a result of mucus hypersecre tion, formation of mucus plugs, and structural airway changes. These changes, in a process termed airway remodeling, include hyperplasia and hypertrophy of airway smooth muscle, subepithelial fibrosis, and thickening of the sub-basement membrane. As a result of airway remodeling, some asthmatic patients may experience progressive loss of lung function that may not be reversible. CLINICAL FEATURES AND INITIAL ASSESSMENT Obtain a thorough, detailed history to determine the progression of illness and ability for ongoing care at home and for disposition planning. Identify possible triggers, such as viral illnesses, pneumonia, or allergens 37; progression of symptoms at home; and home treatments. Ask about past ED visits, hospitalizations, prior intensive care admission, and any invasive and noninvasive airway support. Obtain any family history of asthma or eczema. Assess airway and breathing immediately; the degree of respiratory distress and impaired ventilation dictate the tempo of the evaluation and intensity of interventions. Serial assessments are key to ED management because changes in clinical status and response to treatment are usu ally more relevant to outcome and need for admission than the level of severity at presentation. Physical signs are useful in determining the severity of airway obstruction. Mental status changes such as agitation may indicate hypoxemia, whereas somnolence may indicate hypercarbia. Respiratory rate (Table 127-2) and air entry indicate the adequacy of gas exchange and ventilation. Determine oxygen saturation at presentation. Perform continuous pulse oximetry for patients who are hypoxemic or severely ill. Intermittent oximetry should be done in mild to moderate exacerbations or once the patient has improved and does not require bronchodilators more frequently than hourly. Provide supplemental oxygen for oxygen saturation <92%, and maintain at 93% to 98%, because very high saturations of oxygen may decrease minute ventilation and result in elevations of pulmonary end tidal carbon dioxide (ETCO 2).38,39 Oxygen and β 2-agonists are pulmonary vasodilators and may con tribute to ventilation–perfusion mismatch by augmenting perfusion of underventilated lung units. This phenomenon may worsen hypoxemia, but generally resolves by 1 to 2 hours as pulmonary autoregulation cor rects mismatch. If oxygen saturation remains <92% after initial treat ment, consider worsening asthma, pneumothorax, or pneumonia. 40-42 Consider ETCO 2 monitoring in all children with severe or lifethreatening asthma exacerbations, because a rising ETCO 2 is a marker of fatigue or worsening of the disease. 43,44 Paco 2 should be lower than normal in children with asthma exacerbations due to increased minute ventilation (normal range, 35 to 40 mm Hg). 45,46 Accessory muscle use reflects the work of breathing necessary to overcome auto–positive end-expiratory pressure and airway resistance. 47,48 Subcostal and intercostal muscle use occurs with mild to moderate obstruction, whereas neck muscle use suggests severe obstruction. Wheezing is pathognomonic for airway obstruction and typically occurs more during expiration than during inspiration; however, the quiet chest is an ominous sign of severely compromised ventilation and indicates insufficient airflow to generate wheezing.

obstruction, whereas neck muscle use suggests severe obstruction. Wheezing is pathognomonic for airway obstruction and typically occurs more during expiration than during inspiration; however, the quiet chest is an ominous sign of severely compromised ventilation and indicates insufficient airflow to generate wheezing. The severity of an acute asthma exacerbation may be assessed based on signs and symptoms, and classified as mild, moderate, severe, or imminent respiratory failure. Asthma scoring systems are a means to assess severity and response to treatment and to communicate among providers. The Pediatric Respiratory Assessment Measure ( Figure 127-3) has been validated in patients 2 to 17 years old with asthma and is responsive to changes in a patient’s respiratory status. 49-51 DIAGNOSIS There are three essential diagnostic questions for the child with signs and symptoms suggestive of an acute asthma exacerbation: (1) Does this patient have asthma? (2) What is the severity of airway exacerbation? (3) Is there a treatable trigger for this exacerbation? For children >2 years old who do not have a history of health profes sional–diagnosed asthma, a provisional diagnosis of asthma is made when there are signs and symptoms of wheezing, shortness of breath, Tintinalli_Sec12_p0669-0996.indd 803 8/2/19 7:52 PM

rbation? (3) Is there a treatable trigger for this exacerbation? For children >2 years old who do not have a history of health profes sional–diagnosed asthma, a provisional diagnosis of asthma is made when there are signs and symptoms of wheezing, shortness of breath, Tintinalli_Sec12_p0669-0996.indd 803 8/2/19 7:52 PM 804 SECTION 12: Pediatrics FIGURE 127-3. The Pediatric Respiratory Assessment Measure (PRAM). Pediatric Respiratory Assessment Measure (PRAM) SIGNS/SCORING PATIENT’S SCORE (MAX 12) (max 2) (max 2) (max 3) (max 3) (max 2) 01 23 Suprasternal retractions Absent Absent Absent Normal Decreased at bases Present Present Widespread decrease Absent/minimal Audible without stethoscope/silent chest with minimal air entry Inspiratory and expiratory Expiratory only ≥95% *If asymmetric findings between the right and left lungs, the most severe is rated. PRAM Score 0–3 MILD Asthma PRAM Score 4–7 MODER ATE Asthma PRAM Score 8–12 SEVERE Asthma IMPENDING RESPIRATORY FAILURE is based on clinical presentation 1Chalut DS, Ducharme FM, Davis GM: The Preschool Respiratory Assessment Measure (PRAM): A responsive index of acute asthma severity. J Pediatr 137: 762, 2000. 2Ducharme F, Chalut D, Plotnick L, et al: The Pediatric Respiratory Assessment Measure: A valid clinical score for assessing acute asthma severity from toddlers to teenagers. J Pediatr 152: 467 , 2008. PRAM SCORE TOTAL 92%–94% <92% Scalene muscle contraction Air entry* Wheezing* O2 saturation in room air cough, dyspnea, diminished air entry, or retractions and demonstration of reversibility with β 2-agonist bronchodilators (e.g., salbutamol/ albuterol).33 Children 1 to 2 years old with viral-induced wheeze may be treated as having either asthma or bronchiolitis. 51 Children <1 year old with first episode of wheeze should be treated as having bronchiolitis. Although spirometry may be a useful adjunct to clinical assessment, spirometry cannot be performed in children <6 years old and is chal lenging to perform in severe respiratory distress. Atelectasis is common in children with acute asthma exacerbations, whereas bacterial pneumonia is much less common. A chest radiograph for a child with acute asthma and fever is likely to demonstrate atelectasis and is therefore not recommended unless additional features are pres ent, as presented in Table 127-5. 52,53 Point-of-care US is an alternative to chest radiographs in the management of children with respiratory illnesses. Point-of-care US is more sensitive than chest radiographs in distinguishing a viral illness from bacterial pneumonia and for detect ing pneumothorax, with the added benefits of bedside availability and easy repeatability without any radiation exposure. 54-57 As in bronchiolitis, point-of-care US findings in children with asthma may indicate more serious disease. TREATMENT Acute asthma exacerbations often require multiple medications (Table 127-6), review of current medication use, and an individual ized discharge plan. The Pediatric Respiratory Assessment Measure helps identify the severity of exacerbations and may be incorporated into treatment algorithms such as the Ontario Lung Association Pediatric Asthma Care Pathway ( Figure 127-4). Dosages of drugs for acute exacerbations are listed in Table 127-7, and treatment recommendations for acute exacerbations by severity are provided in Table 127-8.  SHORT-ACTING β2-RECEPTOR AGONISTS β2-Agonists are the mainstay of acute asthma therapy. They act specifi cally on β2-receptors to relax bronchial wall smooth muscles and are the most effective agents for relieving acute bronchospasm. Salbutamol/ albuterol is the most widely available and used β 2-agonist.

able 127-8.  SHORT-ACTING β2-RECEPTOR AGONISTS β2-Agonists are the mainstay of acute asthma therapy. They act specifi cally on β2-receptors to relax bronchial wall smooth muscles and are the most effective agents for relieving acute bronchospasm. Salbutamol/ albuterol is the most widely available and used β 2-agonist. After inhalation, the onset of action is within 3 to 5 minutes, the peak effect is seen within 30 to 120 minutes, and the duration of action is 2 to 5 hours. Levosalbutamol (levalbuterol), the R-enantiomer of salbutamol, is not any more effective or safer than salbutamol and is much more expensive. β2-Agonists are frequently delivered by metered-dose inhalers with an age-appropriate valved holding chamber or via wet nebulization . TABLE 127-6 Treatment for Acute Asthma Exacerbations Treatment Comments Short-acting β2-agonist bronchodilators For all patients with acute asthma exacerbations in the ED. Add ipratropium bromide for severe or life-threatening exacerbations. Systemic steroids For all patients with moderate or worse exacerbations as early as possible in course. May be given orally or parenterally. Oxygen In patients with arterial oxygen saturation ≤92%. Magnesium sulfate IV or nebulized smooth muscle–relaxing bronchodilator for severe exacerbations not responding to initial therapy. Inhaled corticosteroids No role in acute ED management, but prescribe inhaled corticosteroids for home use. TABLE 127-5 Indications for Imaging in Acute Asthma •   Fever not explained by apparent viral illness (rule out pneumonia) •   Chest pain, cardiovascular instability, or absent breath sounds (rule out pneumothorax) •   Poor response to treatment (consider congestive heart failure or foreign body aspiration) •   Life-threatening exacerbation (consider alternate diagnoses, comorbidities) Tintinalli_Sec12_p0669-0996.indd 804 8/2/19 7:52 PM

a) •   Chest pain, cardiovascular instability, or absent breath sounds (rule out pneumothorax) •   Poor response to treatment (consider congestive heart failure or foreign body aspiration) •   Life-threatening exacerbation (consider alternate diagnoses, comorbidities) Tintinalli_Sec12_p0669-0996.indd 804 8/2/19 7:52 PM CHAPTER 127: Wheezing in Infants and Children 805 FIGURE 127-4. The Ontario Lung Association Pediatric Asthma Care Pathway. CXR = chest x-ray; FEV1 = forced expiratory volume in 1 second; ICU = intensive care unit; MD = physician; MDI = metered-dose inhaler; PEF = peak expiratory flow; PRAM = Pediatric Respiratory Assessment Measure; q = every. [Reproduced with permission from The Ontario Lung Association. In: Paediatric Emergency Department Asthma Care Pathway: Information Package March 2014 . The Lung Association Ontario; 2014:4. Available at: http://machealth.ca/programs/paediatricemergency-department-asthma-care-pathway/m/mediagallery/1921/download.aspx.] Tintinalli_Sec12_p0669-0996.indd 805 8/2/19 7:52 PM

sociation. In: Paediatric Emergency Department Asthma Care Pathway: Information Package March 2014 . The Lung Association Ontario; 2014:4. Available at: http://machealth.ca/programs/paediatricemergency-department-asthma-care-pathway/m/mediagallery/1921/download.aspx.] Tintinalli_Sec12_p0669-0996.indd 805 8/2/19 7:52 PM 806 SECTION 12: Pediatrics TABLE 127-8 Summary of Treatment Recommendations by Severity for Acute Asthma Exacerbations β 2-Agonist Systemic Corticosteroid Anticholinergic Mild + − − Moderate ++ + − Severe* +++ + + *Severe patients not responding to full therapy should be considered for IV magnesium and/or other adjuvant therapies. TABLE 127-7 Dosages of Medications for Asthma Exacerbations Medication American Pediatric Dosages59 Alternative Pediatric Dosages Bronchodilators Salbutamol/albuterol (aerosol or nebulized) MDI (90 micrograms/puff); delivered via valved holding chamber: ≤1 y: 2 puffs/dose 1–3 y: 4 puffs/dose ≥4 y: 8 puffs/dose Nebulization (unit dose nebule or 5 milligrams/mL solution): 0.15–0.3 milligram/kg/dose (minimum 2.5 milligrams) IV: Not available PO: Not recommended MDI (100 micrograms/puff); delivered via valved holding chamber: ≤1 y: 2 puffs/dose 1–3 y: 4 puffs/dose 4–6 y: 6 puffs/dose ≥7 y: 8 puffs/dose Nebulization (unit dose nebule or 5 milligrams/mL solution): <10 kg: 1.25-milligram nebule or 0.25 mL of 5-milligram/mL solution * 10–20 kg: 2.5-milligram nebule or 0.5 mL of 5-milligram/mL solution * >20 kg: 5-milligram nebule or 1 mL of 5-milligram/mL solution * IV: 0.5–3 milligrams/kg/h continuous infusion (maximum 15 milligrams/h) PO: Not recommended Ipratropium bromide (aerosol or nebulized) MDI (20 micrograms/puff); delivered via valved holding chamber: 4–8 puffs/dose PRN, alternated with salbutamol Nebulization: 250–500 micrograms for all patients, mixed with salbutamol MDI (20 micrograms/puff); delivered via valved holding chamber: 3 puffs/dose for all patients, alternated with salbutamol Nebulization: 250 micrograms for all patients, mixed with salbutamol Systemic corticosteroids Prednisone (PO) 1–2 milligrams/kg/dose (maximum 60 milligrams) for 3–10 d 2 milligrams/kg (maximum 50 milligrams) in ED, then 1 milligram/kg/d for 4 d Methylprednisolone (IV, IM) 2 milligrams/kg/dose load, then 0.5–1 milligram/kg/dose every 6 h 1 milligram/kg/dose (maximum 125 milligrams/dose), repeated every 6 h or change to oral regimen Dexamethasone (PO, IV, IM) 0.6 milligram/kg/dose (maximum 16 milligrams) for 1–2 d Multiple dosing regimens: 0.6 milligram/kg/d for 1–2 d 0.3 milligram/kg/d for 3–5 d Other medications Magnesium sulfate (IV) 25–75 milligrams/kg/dose (maximum 2 grams) × 1 50 milligrams/kg/dose × 1 (monitor blood pressure) Ketamine (IV) † 1–2 milligrams/kg/dose × 1 2 milligrams/kg/dose × 1 (may alleviate need for intubation, given as induction agent for intubation) *Mixed in 3 mL of normal saline solution. †Consider only if standard therapies have failed in order to prevent intubation. Abbreviations: MDI = metered-dose inhaler; PRN = as needed. Metered-dose inhalers are as effective as nebulizers for mild to moder ate exacerbations and decrease length of ED stay while causing fewer side effects such as nausea, tachycardia, and tremor. 61 A primarily metered-dose inhaler–based algorithm may also confer benefits for infection control and may be more cost effective than a nebulizer-based algorithm. There is no therapeutic advantage of β 2-agonist administration by the IV route versus the inhaled route in the child who is ventilating reasonably well. However, for the patient with significantly dimin ished air entry, the IV route may allow for critical initial broncho dilation that permits subsequent inhaled medications to reach distal airways.

age of β 2-agonist administration by the IV route versus the inhaled route in the child who is ventilating reasonably well. However, for the patient with significantly dimin ished air entry, the IV route may allow for critical initial broncho dilation that permits subsequent inhaled medications to reach distal airways. 63,64 Oral albuterol is not recommended due to the delayed onset and prominent tachycardia, tremulousness, and behavioral changes accom panying this form. Epinephrine has α- and β-agonist properties that facilitate vasocon striction and rapid resolution of mucosal edema and can be an effec tive emergency treatment for asthma. An Epi-Pen may be used if more readily available than β-selective medication. However, because it is not as selective for lower airways as β 2-agonists, epinephrine causes more short-term side effects.  CORTICOSTEROIDS Systemic corticosteroids inhibit the inflammatory cascade and enhance β-receptor expression, sensitivity, and function. They provide rapid beneficial physiologic effects, usually within 4 hours, which reduces both the need for hospitalization and the likelihood of relapse. All patients presenting with a moderate or severe exacerbation should be treated immediately with systemic corticosteroids. Early administration of corticosteroids by a triage nurse can decrease ED length of stay and admission rates. 65-67 Oral corticosteroids should be given within the first hour of ED presentation and are usually followed by a short regimen upon discharge. Different regimens have been described in the literature and seem to be equivalent in efficacy and rates of adverse events (Table 127-7). 68,69 Tintinalli_Sec12_p0669-0996.indd 806 8/2/19 7:52 PM CHAPTER 127: Wheezing in Infants and Children 807 TABLE 127-9 Drugs for Rapid-Sequence Intubation of a Child With Near-Fatal Asthma Drug Dose Intubation Induction Ketamine* Short-term paralysis during intubation (Use caution with paralysis) Succinylcholine Rocuronium 2 milligrams/kg <10 kg: 2 milligrams/kg; >10 kg: 1 milligram/kg 1 milligram/kg Postintubation paralysis † Vecuronium 0.1 milligram/kg/h Postintubation sedation Ketamine† Fentanyl and Midazolam 2–3 milligrams/kg/h

CHAPTER 127: Wheezing in Infants and Children 807 TABLE 127-9 Drugs for Rapid-Sequence Intubation of a Child With Near-Fatal Asthma Drug Dose Intubation Induction Ketamine* Short-term paralysis during intubation (Use caution with paralysis) Succinylcholine Rocuronium 2 milligrams/kg <10 kg: 2 milligrams/kg; >10 kg: 1 milligram/kg 1 milligram/kg Postintubation paralysis † Vecuronium 0.1 milligram/kg/h Postintubation sedation Ketamine† Fentanyl and Midazolam 2–3 milligrams/kg/h 1–2 micrograms/kg bolus then 1 microgram/kg/h 0.1 milligram/kg/h *The use of ketamine for sedation may also obviate the need for paralysis. †Patient–ventilator dyssynchrony may necessitate postintubation paralysis. Historically, prednisone was the popular agent, with a total treatment course of 5 days. However, prednisolone suspension is more palatable and therefore has better compliance. 70 Dexamethasone is a less expen sive oral corticosteroid that has gained popularity following a series of clinical trials showing that a single dose or a 2-day course is therapeuti cally equivalent to a 5-day course of prednisolone. 71-73 When the patient is severely ill or not responding to therapy, IV methylprednisolone may be given every 6 hours. Inhaled corticosteroids have no role in the acute ED management, but are an essential part of maintenance therapy and should be prescribed to all patients with persistent asthma at discharge (see “Disposition and Follow-Up” section for further discussion).  ANTICHOLINERGIC AGENTS Anticholinergic agents such as ipratropium bromide relieve bronchiole obstruction by blocking muscarinic receptors in the bronchiole wall, leading to bronchodilation and decreased mucus secretion. However, they are not as potent or rapid as β 2-agonists. When used in combination with short-acting β 2-agonists, anticholinergics decrease hospitalization rates versus using short-acting β 2-agonists alone.75,76 Addition of mul tiple high doses of ipratropium (0.5 milligram) to nebulized albuterol treatments has additive benefit and results in reduced hospitalization in children with severe exacerbations.  MAGNESIUM IV magnesium sulfate acts as a bronchodilator by inhibiting smooth muscle contraction 77,78 and may reduce the need for hospitaliza tion or intensive care admission. 78-80 Nebulized magnesium is not effective. 81-86  KETAMINE Ketamine is a dissociative sedative agent that is commonly used for both procedural sedation and as an induction agent for endotracheal intubation. The sympathomimetic properties of ketamine and its bronchodilation effect make it the ideal induction agent for the patient with respiratory failure due to asthma. While case reports describe that ketamine alleviated the need to intubate when given as part of induction in children, 87 several randomized controlled trials demonstrated a lack of benefit.88-91  HELIOX Heliox, a mixture of helium and oxygen, is less dense than air, leading to laminar instead of turbulent airflow in obstructed airways. 92,93 It may be a better vehicle for medication delivery and improves gas exchange. It has no direct pharmacologic or biologic effect and has an extremely low risk profile. The evidence for routine heliox use is conflicted, and the equipment required to use it makes this treatment difficult in the ED setting.  METHYLXANTHINES Methylxanthines (theophylline and aminophylline) have been replaced by safer and more effective short-acting β 2-agonists. Adverse effects include tachycardia, vomiting, and CNS excitation, including seizures.94,95 Current treatment guidelines recommend against its use primarily due to its side effect profile and narrow therapeutic window. 96,97 TREATMENT OF NEAR-FATAL ASTHMA Patients with acute severe asthma who do not respond adequately to maximal medical therapy and who continue to manifest severe airway obstruction and hyperinflation are at risk for fatal asthma.

against its use primarily due to its side effect profile and narrow therapeutic window. 96,97 TREATMENT OF NEAR-FATAL ASTHMA Patients with acute severe asthma who do not respond adequately to maximal medical therapy and who continue to manifest severe airway obstruction and hyperinflation are at risk for fatal asthma. One third of pediatric deaths from asthma are in children who previously had only mild asthma. Clinical signs of this progression include worsening hypoxemia, increasing respiratory rate, diaphoresis, inability to speak, somnolence, and fatigue. The decision to undertake advanced airway management for near-fatal asthma is based on clinical judgment. One must weigh the need for intubation against the potential adverse outcomes, including worsening bronchospasm, laryngospasm, pneumothorax, ventilator-associated pneumonia, and hemodynamic instability. 98,99  NONINVASIVE POSITIVE-PRESSURE VENTILATION Bilevel positive airway pressure is the preferred noninvasive modal ity in the care of the patient with severe, nonresponsive asthma. It delivers different pressures during inspiration and expiration to decrease the work of breathing, stent the airways open, and improve gas exchange. It also appears to have a bronchodilator effect. 100 The largest study of bilevel positive airway pressure use in children found that 88% tolerated the intervention and demonstrated clinically sig nificant improvements in respiratory rate and oxygenation without adverse effects. 101 Bilevel positive airway pressure may be effective in preventing the need for endotracheal intubation even if applied for only several hours. Use of a well-fitting facemask and close attention to patient comfort are essential. Most patients tolerate bilevel positive airway pressure well, but sedation is frequently required with low doses of benzodiazepines (0.05 to 0.1 milligram/kg of midazolam or lorazepam) or ketamine (0.5 to 1 milligram/kg followed by 0.25 milligram/kg/h). Reasonable initial applied bilevel positive airway pressures for severe asthma are an inspi ratory positive airway pressure of 12 cm H 2O and expiratory positive airway pressure of 6 cm H 2O, with ranges of 12 to 18 cm H 2O and 6 to 12 cm H2O, respectively.100-102 Aerosolized medications can be adminis tered through the bilevel positive airway pressure airway circuit.  ENDOTRACHEAL INTUBATION AND ASSISTED VENTILATION An extremely small number of children will require intubation despite aggressive management. It is best to try to avoid the need to intubate due to challenges in ventilatory management and potential for adverse effects due to air trapping, and noninvasive ventilation strategies such as bilevel positive airway pressure may prevent the need for intubation. Select the largest appropriate cuffed endotracheal tube. Preoxygenate with 100% oxygen. If reasonable, give a normal saline fluid bolus (20 mL/kg) prior to intubation to minimize hypotension. Drugs for rapid-sequence intubation in severe asthma are listed in Table 127-9 and should be administered with the patient sitting up or Tintinalli_Sec12_p0669-0996.indd 807 8/2/19 7:52 PM

oxygenate with 100% oxygen. If reasonable, give a normal saline fluid bolus (20 mL/kg) prior to intubation to minimize hypotension. Drugs for rapid-sequence intubation in severe asthma are listed in Table 127-9 and should be administered with the patient sitting up or Tintinalli_Sec12_p0669-0996.indd 807 8/2/19 7:52 PM 808 SECTION 12: Pediatrics TABLE 127-10 Initial Ventilator Settings for the Intubated Pediatric Patient With Asthma Ventilator Parameter Setting Mode Synchronized intermittent mandatory ventilation/ pressure-regulated volume control Tidal volume 6–10 mL/kg Peak pressure 45 cm H2O Respiratory rate 8–15/min Inspiratory time 0.5–1.0 s Expiratory time 4–8 s TABLE 127-11 Recommended Dose Ranges for Inhaled Corticosteroids* Drug Dosage Alternate Formulations Budesonide (Pulmicort® ) dry powder inhaler (90 or 180 micrograms/spray) 180–360 micrograms twice daily Budesonide nebulizer suspension (Pulmicort Respules® ) (0.25, 0.5, 1 milligram/2 mL units) 0.5–1 milligram divided once or twice daily Fluticasone MDI (Flovent® ) (44, 120, or 220 micrograms/spray) 88–440 micrograms twice daily For children <5 y: 1 puff of 120 micrograms twice daily 50, 125, or 250 micrograms/spray MDI: 50–250 micrograms twice daily Beclomethasone (QVAR ® ) MDI (40, 80 micrograms/spray) 40–80 micrograms twice daily 50, 100 micrograms/spray MDI: 50–100 micrograms twice daily Ciclesonide MDI (Alvesco ® ) (80, 160 micrograms/spray) 80–320 micrograms twice daily 100, 200 micrograms/spray MDI: 100 micrograms once daily to 200 micrograms twice daily *Prescribers should use the lowest effective doses to prevent side effects including adrenal suppression. Abbreviation: MDI = metered-dose inhaler. in another comfortable position to maximize preoxygenation. Ketamine is the preferred induction agent because it provides bronchodilation and does not directly cause hypotension . Give it immediately before the paralytic agent. Atropine is only indicated to treat symptomatic bradycardia. For full discussion of pediatric intubation, refer to Chapter 113, “Intubation and Ventilation in Infants and Children. ” Once the endotracheal tube is in place, an appropriate tidal volume and a sufficiently low respiratory rate to allow for expiratory emptying and avoid hyperinflation should be provided manually. Management of ventilation must consider key pulmonary mechanics of the disease process including hyperinflation, auto–positive endexpiratory pressure, and markedly prolonged expiratory time constants that result in failure of the airways to empty. Therefore, use low respiratory rates and tidal volumes, long expiratory times, and high flow rates (Table 127-10). 103,104 The practice of controlled hypercapnic hypoventilation is a recommended ventilator strategy .10 The aim is to minimize hyperinflation and airway pressures while providing adequate oxygenation. 105 This mode of ventilation may be key to allowing for the prolonged expira tory times necessary to minimize auto–positive end-expiratory pressure and hyperinflation. Provide adequate sedation to avoid ventilator dys synchrony, tachypnea, and breath stacking. Ketamine, benzodiazepines, and opiates, or a combination of these, are appropriate, and paralysis is usually necessary. DISPOSITION AND FOLLOW-UP The decision regarding hospital admission or discharge of the child with asthma must consider both the adequacy of response to treatment and the ability of the patient and caretaker to provide necessary ongoing care. The ED relapse rate of 7% to 15% reflects the potential uncer tainty of disposition decisions . 40,106,107 Clinical improvement so that only minimal symptoms remain is a useful guide for discharge. Most patients should be observed for at least 60 minutes after the most recent bronchodilator dose.

ecessary ongoing care. The ED relapse rate of 7% to 15% reflects the potential uncer tainty of disposition decisions . 40,106,107 Clinical improvement so that only minimal symptoms remain is a useful guide for discharge. Most patients should be observed for at least 60 minutes after the most recent bronchodilator dose. A PRAM score of 8 or higher at 3 hours after ED presentation strongly predicts the need for admission. 108 If more aggressive therapies have failed, consider early admission. Dischargeable patients should be prescribed an inhaled short-acting β2-agonist on discharge from the ED. An age-appropriate valved holding chamber (e.g., AeroChamber ® ) must be prescribed with the metereddose inhaler and proper instructions for inhaler technique reviewed. Patients treated with systemic corticosteroids should be prescribed an oral corticosteroid course upon discharge, unless a single-dose dexa methasone regimen (0.6 milligram/kg) was used in the ED. Inhaled corticosteroids should be prescribed at discharge for all classes of asthma severity except mild intermittent asthma. 109 (See Table 127-11 for dosing guidelines.) In 2015, the Canadian Thoracic Society and Canadian Pediatric Society published a joint position statement recommending the use of inhaled corticosteroids for all preschool children 1 to 5 years of age with asthma who require systemic steroids in the ED for a moderate or severe asthma exacerbation or who have persistent symptoms . The statement recommends a 3-month trial of daily inhaled corticoste roids. The guidelines from the United Kingdom and United States also recommend consideration for initiation of inhaled corticosteroids when good reversibility is demonstrated after β 2-agonist treatment in children <5 years old with wheezing.9,33,110,111 Partner with the primary care physician to ensure appropriate followup, symptom and trigger management, monitoring of anti-inflamma tory therapy, and implementation of other elements of the National Asthma Education and Prevention Program guidelines. National and international guidelines recommend treatment with long-term controller medications in all children with persistent asthma.10 However, primary care physician adherence to these guidelines has been suboptimal. Despite published guidelines stating that inhaled steroids should be prescribed at discharge, fewer than 50% of children with persistent asthma treated by pediatric emergency physicians receive them. A visit to the ED is an indication of inadequate long-term asthma management and insufficient understanding of how to manage an exacerbation. The goal upon discharge should be to prevent future exacerbations requiring ED visits. A written asthma action plan focused on patient symptoms is superior to action plans based on peak flows. 113,114 The provision of a combined asthma action plan plus prescription increases patient adherence to medications and improves asthma control. 115 One of the proposed benefits of a combined plan with prescription may be the reinforcement of the medical recommen dations by the family physician as well as by the pharmacists filling the prescription. 115 At the time of discharge, the physician, nurse, and/or respiratory therapist should review the appropriate use, technique, and timing of all prescribed medications and review early symptom iden tification and management. Provide clear plans for follow-up appoint ments and instructions for managing relapse or future exacerbations (Figure 127-5). Tintinalli_Sec12_p0669-0996.indd 808 8/2/19 7:52 PM

hould review the appropriate use, technique, and timing of all prescribed medications and review early symptom iden tification and management. Provide clear plans for follow-up appoint ments and instructions for managing relapse or future exacerbations (Figure 127-5). Tintinalli_Sec12_p0669-0996.indd 808 8/2/19 7:52 PM CHAPTER 127: Wheezing in Infants and Children 809 FIGURE 127-5. The Ontario Lung Association Pediatric Asthma Action Plan Pathway. [Reproduced with permission from The Ontario Lung Association. In: Paediatric Emergency Department Asthma Care Pathway: Information Package March 2014 . The Lung Association Ontario; 2014:4. Available at: http://machealth.ca/programs/paediatric-emergency-departmentasthma-care-pathway/m/mediagallery/1921/download.aspx.] Tintinalli_Sec12_p0669-0996.indd 809 8/2/19 7:52 PM 810 SECTION 12: Pediatrics REFERENCES The complete reference list is available online at www.TintinalliEM.com. FIGURE 127-5. (Continued) Tintinalli_Sec12_p0669-0996.indd 810 8/2/19 7:52 PM