Strange and Schafermeyer's Pediatric Emergency Medicine, Fourth Edition (Strange, Pediatric Emergency Medicine), 4th Ed.

CHAPTER 33. Upper Airway Emergencies

Richard Cantor

Linnea Wittick Roy

HIGH-YIELD FACTS

• Acute respiratory emergencies in the pediatric patient are common and may, if improperly treated, result in significant morbidity and mortality.

• The clinician must maintain an awareness of the unique anatomic and physiologic characteristics of the respiratory tract in the growing infant and child.

• Stridor may originate anywhere in the upper airway from anterior nares to subglottic region.

• The most common causes of acute upper airway obstruction are croup, epiglottitis, and foreign-body obstruction. Additional processes include peritonsillar abscess, bacterial tracheitis, and retropharyngeal abscess.

Acute upper airway emergencies are common in the pediatric patient and can result in significant morbidity and mortality. Calm, decisive, and deliberate intervention ensures the most effective outcome. Accurate assessment of the child in respiratory distress remains the most critical step in patient care and an expanded knowledge of the most frequent airway problems encountered will assist in the proper evaluation, treatment, and disposition of these patients.

PATHOPHYSIOLOGY

The small caliber of the upper airway in children results in greater baseline airway resistance and makes it vulnerable to occlusion. Any process that further narrows the airway will cause an exponential rise in airway resistance and, as a result, will increase in the work of breathing. As the child perceives distress, an increase in respiratory effort augments turbulence and increases resistance to an even greater degree.

Since the young infant is primarily a nasal breather, any degree of nasopharyngeal obstruction may result in significant increase in work of breathing. The large tongue of infants and small children can occlude the oropharynx, especially with altered mental status and decreased muscle tone. Interventions such as tilting the head or lifting the chin may correct this effect. Insertion of an orotracheal or a nasotracheal airway may assist in alleviating respiratory distress. Older children will frequently present with enlarged tonsillar and adenoidal tissues. The pediatric trachea is easily compressible because of incomplete closure of the cartilaginous rings. Any maneuver that overextends the neck contributes to compression of this structure and secondary upper airway obstruction.

SIGNS OF DISTRESS

Abnormalities in respiratory function are eventually reflected in physical symptoms and signs ranging from subtle changes to obvious distress. Respiratory failure ensues when respiratory efforts cannot maintain adequate respiratory function, either oxygenation or ventilation.

Tachypnea represents the most common response of the child to increased respiratory needs. Although most commonly caused by hypoxia and hypercarbia, tachypnea may also be a secondary response to metabolic acidosis, pain, or central nervous system insult. Tachycardia represents a sign of distress of any etiology in the pediatric patient. This would include the patient with respiratory compromise.

Infants and children use accessory muscles as a compensatory mechanism to support the increased work of breathing. Intercostal, subcostal, sub- and supersternal, and supraclavicular retractions as well as nasal flaring are commonly seen.

Many infants and children with upper airway compromise will assume a “position of comfort,” which represents the most adequate anatomic compensation they can generate relative to their disease state. Children with stridor will often assume an upright position, lean forward, and generate their own jaw thrust maneuver to facilitate opening of the upper airway. Patients with upper airway compromise may also prefer to breathe through an open mouth, which suggests dysphagia with inability to swallow secretions, or the general presence of air hunger. This is in contrast with patients with lower airway disease, specifically those with reactive airway components, who assume a “tripod position” consisting of upright posture, leaning forward, and support of the upper thorax by the use of extended arms.

The presence of cyanosis is an ominous sign in the pediatric patient. It represents inadequate oxygenation within the pulmonary bed or inadequate oxygen delivery by the cardiovascular system. Cyanosis of respiratory origin tends to be central rather than peripheral. A secondary effect of cyanosis may be the development of somnolence. The most common symptoms and signs of hypoxemia include agitation, irritability, and failure to maintain feeding efforts in the young infant.

By far, the most reliable sign of respiratory failure in the infant or child is an ineffective respiratory effort and an altered level of consciousness. Auscultation of the chest may reveal decreased air entry, poor breath sounds, and bradypnea as the child progresses toward respiratory failure. Concomitant with hypoxemia in infants is the development of bradycardia. Although bradycardia may also be due to excessive vagal stimulation, hypoxemia should be ruled out in all such cases of respiratory distress.

GENERAL MANAGEMENT PRINCIPLES

Give any child with respiratory distress supplemental oxygen. Oxygen may be delivered in a variety of ways, including mask with or without rebreather apparatus, nasal prongs, face tent, or via an oxygen hood. Infants and children who feel threatened by the use of frightening equipment may be placed in the mother’s arms and receive oxygen by tubing alone (at maximal flow) or by inserting the end of the tubing in a cup.

Specific diagnostic categories of respiratory distress offer the clinician various therapeutic modalities that will improve the patient’s status. Use a standardized approach to the patient in mild-to-moderate distress. Provide supplemental oxygen; allow the child to assume a position of comfort, and create a comfortable, nonthreatening environment for both parent and child. Avoid any noxious stimuli in the form of unnecessary procedures. Also maintain normothermia and hydration. Assess the degree of respiratory distress, at presentation and at appropriate intervals.

ASSESSMENT AND MANAGEMENT OF SPECIFIC CLINICAL SCENARIOS

Stridor, the hallmark of upper airway compromise, results from the generation of inspiratory turbulence transmitted against a narrowed lumen (see Fig. 33-1). Stridor may originate anywhere in the upper airway from the anterior nares to the subglottic region. In the young infant, stridor is most often the result of a congenital anomaly involving the tongue (macroglossia), larynx (laryngomalacia), and trachea (tracheomalacia). Congenital forms of stridor are often chronic in their presentation.

image

FIGURE 33-1. Algorithm for stridor.

In the emergency department (ED), the most common causes of acute upper airway obstruction are croup and foreign-body obstruction. Additional processes include bacterial tracheitis, epiglottitis, peritonsillar abscess, and retropharyngeal abscess (Tables 33-1 and 33-2).

TABLE 33-1

Features of Upper Airway Disorders

image

TABLE 33-2

Clinical Features of Acute Upper Airway Disorders

image

image CROUP (VIRAL LARYNGOTRACHEOBRONCHITIS)

Laryngotracheobronchitis (croup) accounts for 90% of stridor with fever affecting children most commonly from 6 months to 3 years of age.13 The subglottic region becomes edematous and inflamed with a fibrinous exudate. Agents responsible for croup include parainfluenza types 1, 2, and 3 (most common); adenovirus; respiratory syncytial virus (RSV); and influenza. The seasonal predominance (fall and winter) is related to the epidemiology of the most common causative agents.

Children usually present after several days of nonspecific upper respiratory infection (URI) symptoms with a characteristic brassy or barking cough that is almost unique to croup. Inspiratory stridor eventually develops, ranging in severity from mild (only when crying or agitated) to severe (present at rest). Temperatures to 102°F are common. Higher temperatures or the presence of a toxic appearance should alert the clinician to consider other diagnoses. Physical examination reveals a child with hoarse voice, coryza, and a slightly increased respiratory rate. The usual evolution of the disease is worsening of symptoms for 3 to 5 days followed by resolution over a period of days. The vast majority of children tolerate this common disease without significant morbidity; however, a small percentage may develop complete upper airway obstruction.

A variety of croup scores have been developed that quantify and qualify a constellation of physical findings. Most of these are more beneficial for research purposes, but some have been developed to assist the clinician in estimating the severity of subglottic obstruction as mild, moderate, or severe (Table 33-3).1,2,4

TABLE 33-3

Clinical Croup Score

Image

Most commonly, children present with mild croup and may be treated as an outpatient as long as the physician is comfortable with parental reliability. These patients present with a history of a barky cough, mild respiratory distress, and stridor only with activity or agitation. As croup is a self-limited disease with treatment aimed solely at relieving symptoms, discharge patients with mild croup if the parents are reliable, the child is well hydrated and taking adequate fluids and the child is older than 6 months. Give most of these patients a dose of oral decadron before they return home. Cool mist therapy may be suggested,5 although the effectiveness of mist treatment has been called into question.6,7 The classic technique is to fill the bathroom with steam by running a hot shower. The parents can then sit with the child in this home version of a Turkish bath, for no more than 30 minutes at a time. A car ride in the cool night air with the windows slightly open may also diminish the child’s symptoms. Arrange follow-up within 24 hours if the patient is discharged with instructions to return if symptoms worsen.

Patients with a moderate croup score require more aggressive treatment and a longer period of observation. The use of oxygen and racemic epinephrine delivered by nebulizer will usually result in symptomatic improvement of the patient for up to 2 hours. The recommended dose for racemic epinephrine is 0.5 mL of a 0.25% solution dissolved in 2.5 mL of normal saline.811 Effects peak at 10 to 30 minutes, with duration of action lasting up to 2 hours. Racemic epinephrine does not shorten the duration of illness. The child may experience a return to a pretreatment level of obstruction 1 to 2 hours after therapy as the effects of the medication wear off. Repeat the dose of racemic epinephrine as needed until stridor at rest resolves.

Corticosteroids may prevent the progression of croup to complete obstruction by decreasing the amount of swelling of the laryngeal mucosa. Steroids lessen the duration of illness, amount of time in the hospital, and the number of racemic epinephrine nebulizer treatments given.4,1114 Administer steroids as early in the course of disease as possible. Dexamethasone 0.15 to 0.6 mg/kg given one time orally or intramuscularly causes significant improvement in symptoms within 6 hours.15,16

A child may be safely discharged to home after receiving both corticosteroids and racemic epinephrine treatments if, after 2 hours of ED observation, they demonstrate a normal respiratory effort, a normal level of consciousness, and no stridor at rest. Prompt follow-up should be arranged.

If a child has severe croup or a decrease in oxygen saturations, admit that child to an intensive care setting. Allow them to remain in a position of comfort, usually in a parent’s arms or lap. Initiate treatment with oxygen, racemic epinephrine, and corticosteroids as soon as possible. Antibiotics may be needed if a bacterial etiology is suspected. Children should be electively intubated for respiratory failure (lethargy, inability to maintain respiratory efforts, Pao2<70 on 100% oxygen, or Paco2 >60), but this decision is best made in the intensive care setting. Children who develop severe upper airway obstruction from this disease do not do so suddenly but progress gradually over time. If intubation must be performed in the ED, use an endotracheal (ET) tube 1 mm smaller than that calculated for age to accommodate the subglottic edema and airway narrowing. Some studies have also suggested using heliox in treatment of severe coup, but no definitive benefit has been demonstrated yet.17,18

As the diagnosis of croup is usually made on clinical grounds alone, further workup is not usually necessary. Upright lateral neck radiographs may be obtained for patients with suspicion of epiglottitis. Maintain close supervision of the patient while the films are obtained. The characteristic “steeple sign” with narrowing of the subglottic area may be noted but does not make the diagnosis of croup.

image EPIGLOTTITIS (SUPRAGLOTTITIS)

Epiglottitis represents a true upper airway emergency with life-threatening complications if handled improperly. It may occur at any time of the year and in any age group. Traditionally, it most commonly involved children from 2 to 5 years of age. Since the advent of the Haemophilus influenzae type B vaccine, the age range has shifted to affect older children and adults.1923

Epiglottitis presents with acute onset of fever, sore throat, and dysphagia with progression to signs of respiratory distress. The child will often assume a position of comfort by sitting upright, mouth open, with head, neck, and jaw in extension. The voice will be muffled, and stridor, if present, will be quite minimal in intensity. These children often appear “toxic.” In severe cases, airway and swallowing mechanisms may be compromised to such a degree that profound drooling ensues. Some children will be devoid of any respiratory symptoms. They will, however, complain of a severe sore throat and dysphagia with an absence of signs of pharyngeal or tonsillar pathology. The presence of pharyngitis or uvulitis in no way excludes the possibility of epiglottic involvement. Croup-like presentations in patients who fail to respond to traditional therapies should also alert the clinician to the possibility of epiglottitis.

Since the widespread use of the Hib vaccine, H. influenzae type b with accompanying bacteremia is a less frequent cause of epiglottitis with Streptococcus pneumoniaeStaphylococcus aureus, and group A-hemolytic streptococci becoming more common.1921,24 However, H. influenzae type B should not be discounted as it still causes disease in both unimmunized and immunized patients. Blood cultures are positive in 80% to 90% of affected individuals. Other noninfectious etiologies of epiglottitis such as trauma, burns, leukemia, and angioneurotic edema have been reported as well.

For patients with unrecognized epiglottitis, the most important clinical consideration remains that airway obstruction and respiratory arrest will most certainly occur. Factors contributing to airway and ventilatory deterioration include patient fatigue, aspiration of secretions, and sudden laryngospasm. Avoid all maneuvers that agitate the child, including separation from parents, alteration of optimal airway posture (avoid lying down), fearful events (rectal temperatures, blood work, and radiographs), and gagging (forcible tongue blade examination of the oral cavity, suctioning).25

Be prepared to emergently intubate and ventilate these patients at all times and in all places within the ED. Radiographs, when obtained, should include anteroposterior and -lateral views of the soft tissues of the neck. Obtain a chest x-ray in patients with suspected pneumonia. Do not perform these evaluations if they promote agitation and subsequent worsening of airway compromise. In most cases, direct visualization and culture of the epiglottis itself will be performed in the operating suite prior to intubation (Fig. 33-2). Antibiotics can be started once airway is secured.

image

FIGURE 33-2. Epiglottitis. A. Lateral neck x-ray of a child with epiglottitis. B. Endoscopic view of almost complete airway obstruction secondary to epiglottitis. Note the slit-like opening of the airway.

While the patient is in the ED, avoid agitating the child in any way. Provide supplemental oxygen in a nonthreatening manner and allow the patient to assume a position of comfort. Prepare equipment for bag-valve-mask (BVM) ventilation, ET intubation, needle cricothyrotomy, cricothyrotomy, and tracheostomy. Consult an expert in intubation and provision of a surgical airway and alert the operating room. Take the child to the operating room for direct visualization of the epiglottis and intubation. If the child suffers a respiratory arrest, open the airway. Attempt BVM ventilation (usually effective). If unable to ventilate, intubate. If unable to intubate, perform needle or surgical cricothyroidotomy, depending on the age of the patient. Provide adequate sedation and restraint postintubation and transfer the patient to an intensive care unit for further treatment and monitoring. Treat with ceftriaxone IV.

image BACTERIAL TRACHEITIS

Bacterial tracheitis, also referred to as membranous tracheitis, represents a true upper airway emergency since, like epiglottitis it may progress to full airway obstruction. Bacterial tracheitis is an infection of the subglottic region causing subglottic edema and pseudomembrane formation in the trachea and bronchi. With the decreasing incidence of H. influenzae, this uncommon upper airway infection has surpassed the incidence of epiglottitis, making it an important etiology of upper airway obstruction for the emergency physician to consider. It is more likely to cause respiratory failure than croup and epiglottitis combined.26,27 Bacterial tracheitis is polymicrobial, most commonly involving S. aureusS. pneumoniiH. influenzaePseudomonas, and Moraxella. This entity occurs in the same age group as croup, with the average age at presentation being 3 years and occurs primarily during the fall and winter. Mortality lies between 18% and 40%, so prompt recognition and treatment is warranted. Significant morbidity such as ARDS, respiratory failure, shock, and multiorgan failure and cardiopulmonary arrest may occur.

Symptoms begin with a prodrome of a mild upper respiratory tract infection lasting for 1 to 2 weeks. The patient then experiences a rapid deterioration with respiratory distress, increased work of breathing, high fevers, and a toxic appearance. These patients often appear anxious and lethargic. On physical examination, typical signs of upper airway obstruction such as stridor, tachypnea, retractions, and a barky cough are present. Occasionally, the infection extends into the lower airways, and wheezing may be present as well. If lateral neck radiographs are performed, subglottic and tracheal narrowing may be seen along with a ragged tracheal border secondary to the pseudomembrane. A chest radiograph may demonstrate a concomitant pneumonia in many children. Laboratory evaluation may demonstrate a leukocytosis with a left shift. Blood cultures are rarely useful. Obtain tracheal cultures by bronchoscopy if the patient is intubated to guide therapy.

Usually, patients with bacterial tracheitis experience a rapid deterioration of their respiratory status which requires mechanical ventilation. Definitive diagnosis occurs with visualization of a normal epiglottis and the presence of pus, inflammation, and in some cases a pseudomembrane in the subglottic region upon intubation. Intubate with an ET tube 1 mm smaller than usual to accommodate tracheal wall edema. Meticulous ET tube suctioning in a pediatric intensive care unit (PICU) setting will usually maintain airway patency. Bronchoscopy may be necessary if suctioning is ineffective. Begin broad-spectrum antibiotics that include coverage for S. aureus with a third-generation cephalosporin, such as ceftriaxone along with vancomycin until culture results are known. Toxic shock syndrome can occur with staphylococcal tracheitis.

image RETROPHARYNGEAL ABSCESS

Retropharyngeal abscesses are seen predominantly in children younger than 3 years secondary to suppurative cervical lymphadenopathy.28 Older children may present with this entity, in many instances following penetrating trauma to the posterior oropharynx. Common organisms include group A-hemolytic Streptococcus and S. aureus, including, more frequently, methicillin-resistant S. aureus (MRSA).29Symptoms include high fever, muffled voice, difficulty swallowing, drooling, and, occasionally, inspiratory stridor. Dysphagia and drooling are more frequent findings than upper airway compromise. Cervical lymphadenitis and trismus also commonly present with retropharyngeal abscesses. Children frequently present with a stiff neck or torticollis and often are initially thought to have meningitis.

A high index of suspicion must be maintained to accurately identify the child with a retropharyngeal abscess. Clinically noting a swelling of the wall of the posterior pharynx may make the diagnosis. Laboratory findings often show a leukocytosis with elevated acute phase reactants. Lateral neck radiographs may demonstrate prevertebral soft-tissue swelling greater than 7 mm at the level of the second cervical vertebrae or greater than 14 mm at the level of the sixth cervical vertebrae and a normal epiglottis and aryepiglottic folds (Fig. 33-3). In most suspected cases, a computed tomography (CT) scan of the neck will identify any soft-tissue infection and abscess formation. An experienced radiologist may be able to visualize an abscess by ultrasound.

image

FIGURE 33-3. Retropharyngeal abscess lateral soft-tissue neck x-ray demonstrating prevertebral soft-tissue density consistent with retropharyngeal abscess.

All patients with a suspected retropharyngeal abscess should have an ENT consult. Children with cellulitis, without a collection of pus, are often treated with IV antibiotics. Children with partial airway obstruction, who do not demonstrate signs of respiratory failure, must have meticulous observation with all equipment and personnel on hand to intervene (a PICU setting is acceptable). Antibiotics must cover the common organisms. Start the patient on clindamycin plus a third-generation cephalosporin as empiric treatment. Definitive therapy involves intraoperative drainage of the abscess in the OR.

image PERITONSILLAR ABSCESS

Peritonsillar abscesses usually affect children older than 8 years. They are the most common deep infections of the head and neck, usually representing complications of recurrent bacterial tonsillitis, or in some cases, a superinfection of an existent Epstein–Barr infection.30 Most are polymicrobial in origin, including group A Streptococcus (predominant), PeptostreptococcusFusobacterium, and other mouth flora, including anaerobes.

These patients present with increasing dysphagia and ipsilateral ear pain, with progression to trismus, dysarthria, and toxicity. Drooling is common. Patients will often have a “hot potato” phonation, representing splinting of the palatine muscles during normal speech.

The pharynx will be erythematous, with unilateral tonsillar swelling, which, in some cases, may displace the uvula toward the unaffected side. The soft palate may be displaced medially. Fluctuance may confirm the presence of underlying purulent fluid. Reactive cervical adenopathy is common. Severe, although uncommon, complications have been reported, including sternocleidomastoid muscle spasm and torticollis, fasciitis, mediastinitis, thrombophlebitis of the internal jugular vein (Lemierre’s syndrome) and airway obstruction.

Often, the diagnosis is made on examination alone.31 If obtained, the complete blood count will demonstrate an elevated white blood count. Obtain throat cultures in all cases, and consider serologic testing for Epstein–Barr virus infection. Perform a CT scan of the neck with contrast if any doubt exists as to the existence of a peritonsillar abscess after the examination. A clinician experienced with the procedure should perform direct tonsillar needle aspiration after adequate sedation/analgesia has been administered.32 Selected individuals, after adequate drainage, may be considered for discharge from the ED after careful follow-up is arranged. Continue these patients on appropriate antibiotics and analgesics. Some patients require admission for drainage, intravenous hydration, and antibiotics.

image FOREIGN-BODY OBSTRUCTION

Most foreign-body aspirations occur in children younger than 5 years, with 65% of deaths affecting infants younger than 1 year.3335 Common offending agents are foods (e.g., peanuts, hard candies, frankfurters) and items commonly found in the home (e.g., disc batteries, coins, and marbles).36 Symptoms range from mild (cough only) to full-blown upper airway obstruction. It is imperative that the clinicians maintain a high index of suspicion relative to the possibility of foreign-body aspiration, especially in the afebrile child with sudden onset of symptoms. In >50% of cases, there is no history of foreign-body ingestion or a choking spell. Often, patients present multiple times for a respiratory illness that does not improve before the correct diagnosis is made. Some children with chronic foreign-body aspiration may present with a recurring pneumonia or lung abscess.

Most patients will present with symptoms of partial obstruction. Obtain radiographs including anteroposterior and lateral views of the upper airway extending from the nasopharynx to the abdomen so it includes the diaphragm in the evaluation for foreign body. More extensive radiographic investigations include inspiratory and expiratory chest radiographs, or, in younger, uncooperative patients, bilateral decubitus views. These examinations may help in diagnosing foreign bodies that are radiolucent. Although the utility of these views is debated, the foreign body may act as a ball valve causing the affected lung to appear more inflated than usual.37 Atelectasis may also be seen in the affected lung. Maintain a high index of suspicion in all suspected cases as the radiographs can appear normal. Esophageal foreign bodies, if positioned at the thoracic inlet or carina, can compress the upper airway and cause symptoms and signs of airway obstruction.

Foreign-body obstruction can cause complete or incomplete obstruction. In children younger than 1 year with complete obstruction, first, give four back blows followed by chest thrusts. In children older than 1 year, employ repetitive abdominal thrusts. If unsuccessful, use Magill forceps under direct laryngoscopy to attempt removal of the foreign body. If still unsuccessful, attempt vigorous BVM ventilation in preparation for bronchoscopy. Consider attempting to intubate the R mainstem bronchus around the foreign body to maintain an airway until the foreign body can be removed in the OR.

For incomplete obstruction (phonation, coughing present) in children of all ages, provide supplemental oxygen. Allow a position of comfort and avoid noxious stimuli. Arrange for controlled airway evaluation in the operating room. Aspirated foreign bodies must be removed by rigid bronchoscopy.

SUMMARY

Competency in the management of the pediatric patient with respiratory distress is a necessary skill for the emergency physician. This chapter has provided an outlined overview of the most common upper airway disorders that one will encounter in general practice. Standardized therapeutic interventions will maximize overall clinical outcomes.

REFERENCES

1. Bjornson CL, Johnson DW. Croup-treatment update. Pediatr Emerg Care. 2005;21:863.

2. Malhotra A, Krilov LR. Viral croup. Pediatr Rev. 2001;22:5–12.

3. Rosekrans JA. Viral croup: current diagnosis and treatment. Mayo Clin Proc. 1998;73:1102–1106.

4. Guideline for the diagnosis and management of croup. www.topalbertadoctors.org, 2007. Accessed April 30, 2014.

5. Neto G, Kentab B, Klassen T, et al. A randomized controlled trial of mist in the acute treatment of moderate croup. Acad Emerg Med. 2002;9:873–879.

6. Moore M, Little P. Humidified air inhalation for treating croup. Cochrane Database Syst Rev. 2006, (6):CD002820.

7. Scolnik D, Coates AL, Stephens D, et al: Controlled delivery of high vs. low humidity vs. mist therapy for croup in emergency departments: a randomized controlled trial. JAMA. 2006;295(11):1274–1280.

8. Kelly PB, Simon JE. Racemic epinephrine use in croup and disposition. Am J Emerg Med. 1992;10:181.

9. Ledwith CA, Shea LM, Mauro RD. Safety and efficacy of nebulized racemic epinephrine in conjunction with oral dexamethasone and mist in the outpatient treatment of croup. Ann Emerg Med. 1995;25:331.

10. Prendergast M, Jones JS, Hartman D. Racemic epinephrine in the treatment of laryngotracheitis: can we identify children for outpatient therapy? Am J Emerg Med. 1994;12:613.

11. Rizos JD, DiGravio BE, Sehl MJ, et al. The disposition of children with croup treated with racemic epinephrine and dexamethasone in the emergency department. J Emerg Med. 1998;16:535.

12. Donaldson D, Poleski D, Knipple E, et al. Intramuscular versus oral dexamethasone for the treatment of moderate-to-severe croup: a randomized, double-blind trial. Acad Emerg Med. 2003;10:16–21.

13. Jonson DW, Jacobson S, Edney PC, et al. A comparison of nebulized budesonide, intramuscular dexamethasone, and placebo for moderately severe croup. N Engl J Med. 1998;339:498.

14. Rittichier KK, Ledwith CA. Outpatient treatment of moderate croup with dexamethasone: intravenous versus oral dosing. Pediatrics. 2000;106:1344–1348.

15. Dobrovoljac M, Geelhoed GC. 27 Years of croup: an update highlighting the effectiveness of 0.15 mg/kg of dexamethasone. Emerg Med Australas. 2009;21(4):309–314.

16. Chub-Uppakarn S, Sangsupawanich P. A randomized comparison of dexamethasone 0.15 mg/kg vs..6 mg/kg for the treatment of moderate to severe croup. Int J Pediatr Otorhinolorygol. 2007;71(3):474–477.

17. Wright RB, Rowe BH, Arent RJ, et al. Current pharmacological options in the treatment of croup. Expert Opin Pharmacother. 2005;6(2):255–261.

18. Vorwerk C, Coats TJ: Use of heliox-oxygen mixtures in t treatment of croup: a systematic review. Emerg Med J. 2008;25(9):547–550.

19. Hickerson SL, Kirby RS, Wheeler JG, et al. Epiglottis: a 9-year case review. South Med J. 1996;89:487.

20. Losek JD, Dewitz-Zink BA, Melzer-Lange M, et al. Epiglottitis: comparison of signs and symptoms in children less than 2 years old and older. Ann Emerg Med. 1990;19:55–58.

21. Mauro RD, Poole SR, Lockhart CH. Differentiation of epiglottitis from laryngotracheitis in the child with stridor. Am J Dis Child. 1988;142:679.

22. Shah RK, Roberson DW, Jones DT. Epiglottitis in the Hemophilus influenzae type B vaccine era; changing trends. Laryngoscope. 2004;114:557.

23. Kumar RK, Mashell K. Acute epiglottitis. J Pediatr Child Health. 1998;34:594.

24. Guardian E, Blis M, Harley E, et al. Supraglottitis in the Era following widespread immunization against Haemophilus influenzae type B: evolving principles in diagnosis and management. The Laryngoscope. 2010;120(11):2183–2188.

25. Fulginiti VA. Acute supraglottitis (epiglottitis): to look or not? Am J Dis Child. 1988;142:597.

26. Hopkins A, Lahiri T, Salerno R, Heath B. Changing epidemiology of life-threatening upper airway infections: the reemergence of bacterial tracheitis. Pediatrics. 2006;188:1418–1421.

27. Bernstein T. Is bacterial tracheitis changing? A 14-month experience in a pediatric intensive care unit. Clin Infect Dis. 1998;27:458–462.

28. Craig FW, Schunk JE. Retropharyngeal abscess in children: clinical presentation, utility of imaging, and current management. Pediatrics. 2003;111:1394.

29. Abdel-Hag N, Quezada M, Asmar BI. Retropharyngeal abscess in children: the rising incidence to methicillin resistant Staphylococcus aureusPediatr Infect Dis. 2012;31(7):696–699.

30. Hammerschlag PE, Hammerschlag MR. Peritonsillar, retropharyngeal, and parapharyngeal abscesses. In: Feigin RD, Cherry JD, eds. Textbook of Pediatric Infectious Diseases. Vol. 1. 5th ed. Philadelphia, PA: WB Saunders; 2004:172.

31. Herzon FS. Pediatric peritonsillar abscess: management guidelines. Curr Probl Pediatr. 1996;26:270–278.

32. Blotter JW. Otolaryngology consultation for peritonsillar abscess in the pediatric population. Laryngoscope. 2000;110:1698–1701.

33. Brownstein DR. Foreign bodies of the gastrointestinal tract and airway. In: Barkin RM, ed. Pediatric Emergency Medicine Concepts and Clinical Practice. 2nd ed. St. Louis, MO: Mosby-Year Book; 1997:371.

34. Chiu CY, Wong, KS, Lai SH. Factors predicting early diagnosis of foreign body aspiration in children. Pediatr Emerg Care. 2005;21:161.

35. Rovin J, Rodgers BM. Pediatric foreign body aspiration. Pediatr Rev. 2000;21:86–89.

36. Shah RK, Patel A, Laner L, et al. Management of foreign bodies obstructing the airway in children. Arch Otolarygology Head Neck Surg. 2010;136(4):373–379.

37. Brown JC, Chapman T, Klein EJ, et al. The utility of adding expiratory or decubitus chest radiographs to the radiographic evaluation of suspected pediatric air way foreign bodies. Ann Emerg Med. 2013;61(1):19–26.