Stridor in Children: A Review, Update, and Current Management Recommendations
Authors: Steven G. Rothrock, MD, FACEP, Research Director, Department of Emergency Medicine, Orlando Regional Medical Center and Arnold Palmer’s Hospital for Women and Children, Orlando, FL; Clinical Assistant Professor, Division of Emergency Medicine, University of Florida College of Medicine, Gainesville, FL.
The clinical presentation has life or death written all over it. And for good reason. An acutely ill child who presents to the ED with stridor invariably triggers consideration of an extensive differential diagnosis that includes both mild and life-threatening conditions. Because complete airway obstruction, respiratory collapse, and operative intervention are potential elements of the clinical scenario, swift action is mandatory. The best clinical outcome is achieved through implementation of a systematic, proven protocol for managing patients with stridor.
From a diagnostic perspective, several issues will challenge the emergency practitioner: First, what is the etiology of the stridor? Croup? Epiglottitis? Retropharyngeal abscess? Next, are diagnostic studies necessary to confirm the diagnosis? Or will they delay definitive intervention and precipitate clinical deterioration? Is immediate control of the airway required? If so, should a team experienced in pediatric airway control be assembled to provide support? Finally, what pharmacotherapeutic measures can provide rapid improvement without delaying targeted management of the airway?
Fortunately, the management of children with stridor has become increasingly focused and systematic. For one thing, the infectious agents producing clinical syndromes associated with stridor have changed dramatically since the introduction of vaccines directed against Haemophilus influenzae type b, which is fading from the scene as the principal offender in epiglottitis. More and more, the ED physician must have a high index of suspicion for atypical offenders, among them Candida species, herpes simplex, and Staphylococcal organisms.1
Changes in the causative organisms for stridor syndromes have been accompanied by significant departures from the accepted management catechism for diseases such as epiglottitis and croup. For example, whereas the use of racemic epinephrine once mandated admission to the hospital, recent studies have questioned this dogma.2 Moreover, the strict admonition against direct examination of the hypopharynx has also been questioned, with current recommendations permitting such evaluation providing specific clinical criteria are satisfied. Finally, newer treatment regimens, including nebulized epinephrine (L isomer) and intramuscular steroids, have proven effective in clinical management.3
With these evolving issues in clear focus, the purpose of this review is to provide a systematic, targeted approach that examines diagnostic options and management pathways that will improve outcomes for this commonyet anxiety-provokingclinical problem.
Stridor is a musical, high-pitched sound of respiration that is a sign of partial obstruction of the upper airway, which begins with the pharynx and includes the trachea and the main bronchi. The Venturi effect explains the sounds that are heard.6 The pressure exerted on a partially closed tube by a gas is equal in all directions except during linear movement. Linear flow creates additional pressure in a forward direction in the tube with a corresponding fall in lateral wall pressure. In other words, during inspiration, areas of the airway that are easily collapsible (e.g., posterior pharynx and above the glottis) are "suctioned" closed; during expiration, these areas are forced open. Thus, sounds are created due to the changing shape and size of the airway.
The fact that different parts of the airway are more collapsible than others accounts for differences in presentation of airway disease. For example, above the glottis (vocal cords), there is only soft tissue and no cartilage; therefore, this area collapses more easily during inspiration compared to airway at the vocal cords and the glottis. The trachea, on the other hand, is less collapsible. Therefore, obstructive lesions at this level lead to stridor that changes little during inspiration and expiration.
Anatomically, the upper airway can be divided into three main areas: 1) the supraglottic airway (above the vocal cords); 2) the glottic and subglottic airway; and 3) the intrathoracic airway. Depending on the location of obstruction, disorders that cause stridor have a variable propensity to develop complete obstruction, and they have different clinical features. (See Figure 1.)
Supraglottic Airway. The supraglottic airway comprises the section of the airway from the nose to just above the vocal cords. Importantly, this part of the airway is easily distensible and easily collapsible because there is no cartilaginous support. Due to the presence of multiple tissue planes, localized infections can spread easily and form abscesses. In young children (especially < 2 years old), the retropharyngeal space contains lymph nodes that may serve as a nidus for formation of abscesses. Eventually, these retropharyngeal lymph nodes atrophy, and the risk of abscess formation decreases as children age.
Classic important diseases that cause obstruction or stridor at this level include supraglottitis (epiglottitis), retropharyngeal abscess(es), and diphtheria, although many other supraglottic conditions also produce this finding. Stridor from supraglottic obstruction generally produces a sound that is heard primarily on inspiration, since the airway easily collapses from the negative pressure exerted with inspiration. With exhalation, the airway is reinflated and the obstruction improves. Drooling can be a prominent feature, since the obstruction is above the level of the esophagus and patients may be unable to swallow. A muffled or "hot-potato" voice may also be prominent. This is caused by an obstruction between the listener and the vocal cords, as the vocal cords are generally uninvolved. Therefore, the sound produced by the vocal cords is normal while the obstruction muffles what the examiner is hearing.
It should be stressed that disorders causing supraglottic obstruction have the potential to rapidly obstruct the airway. Obstruction may be swift and lethal since this part of the airway collapses the most easily.
Glottic and Subglottic Airway. The glottic and subglottic airway extends from the vocal cords to the trachea before entering the thoracic cavity. This part of the airway is not as collapsible as the supraglottic airway because cartilage (cricoid cartilage and incomplete tracheal cartilaginous rings) surrounds the majority of its length.
The most common disorder causing obstruction at this level is laryngotracheobronchitis (croup). Many congenital disorders can also cause stridor or partial obstruction at this level, including laryngomalacia, tracheomalacia, and vocal cord paralysis. The ED physician should appreciate that inflammation or obstruction at the glottis (vocal cords) leads to a hoarse-sounding voice and not muffling, as seen with supraglottic disease. Stridor may occur during inspiration (see Figure 1) or during inspiration and expiration since the shape and size of this part of the airway changes little during respiration. Although drooling implies obstruction above or at the esophagus and not at the level of the glottis or trachea, a large obstructing tracheal lesion or foreign body can compress the posterior wall of the trachea, leading to esophageal obstruction and drooling. Therefore, the presence of drooling should not be considered concrete evidence that a lesion is not at the level of the glottis or trachea.
Intrathoracic Airway. The intrathoracic airway is comprised of the trachea that lies within the thoracic cavity and the mainstem bronchi. Intrathoracic airway obstruction causes stridor that is loudest on expiration since intrathoracic pressure rises on expiration and tends to cause airway collapse. During inspiration, intrathoracic pressures fall, and the thoracic airway (and any existing obstruction) tends to expand, leading to a quieter sound. Congenital disorders are also a prominent cause of obstruction at this level (e.g., vascular slings and webs). Furthermore, although foreign bodies frequently lodge at this level, they can lodge at any site within the upper or lower airway.
Age is an important factor that can help identify the etiology of a child’s stridor. While generalizations can be made about the age at which certain disorders present, most non-congenital disorders can produce stridor at any age. Generally, congenital disorders (e.g., vocal cord paralysis, laryngomalacia, and tracheomalacia) present during the first few weeks of life. At about 6 months of age, infants begin to explore their environment and place objects in their mouth, which can lead to foreign body aspiration. Developmentally, the pediatric patient’s ability to grasp small, potentially aspirated objects progresses from a raking motion at 7 months to a distinct pincer grasp at 1 year of age. The incidence of foreign body aspiration peaks at around 2-3 years of age and tapers off by age 5. Croup also occurs primarily in infants under 3 years old. Importantly, retropharyngeal abscesses are most common in those under age 4, since retropharyngeal lymph nodes generally atrophy after this age.
In the past, epiglottitis was described as a disease that usually occurred in children 2-7 years of age. However, epiglottitis can occur at any age, from neonate to adult. In fact, since the introduction of the H. influenzae type b vaccine, the overall incidence of epiglottitis has dropped dramatically, and the peak age incidence for epiglottitis is now greater than 7 years.1 Peritonsillar abscesses are another important disorder causing stridor and upper airway obstruction in children. The incidence of this disorder peaks above age 10, when children are at highest risk for pharyngitis secondary to group A beta-hemolytic streptococci.7
Acuity of onset can also help identify the cause of a child’s stridor. An almost immediate onset of symptoms in the appropriately aged child should alert the physician to a foreign body as the cause of airway obstruction. Children with angioedema and allergic reactions generally have a very short (< 5 minutes) onset of stridor. Other features, such as rash, hypotension, and wheezing, should raise the suspicion of an allergic reaction. Epiglottitis can produce stridor within hours of onset of symptoms, although the prodrome may be protracted by one or two days.
Infants and children with airway disorders that are caused or preceded by viral infections often have a protracted prodromal phase lasting from several days to a week prior to seeking medical care. Acute laryngotracheobronchitis or viral croup typically has a prodrome of several days consisting of cough, rhinorrhea, and other upper respiratory symptoms before developing stridor. Bacterial tracheitis and retropharyngeal abscesses generally are preceded by viral upper respiratory infections that predispose to the development of these bacterial infections.
Appearance is another useful clue to the cause of a child’s stridor. Epiglottitis, upper airway abscesses, and bacterial infections (e.g., diphtheria) should be considered in children who are toxic-appearing, with obvious apprehension, air hunger, and tripoding (holding self up in sitting position with extended arms). Children with croup generally do not appear toxic, although airway edema may progress on occasion to cause a more toxic appearance. Depending on the location and severity of airway obstruction, children with congenital disorders and foreign body obstruction may either appear toxic or nontoxic.
Alterations in mental status (lethargy, anxiety) and evidence of increased respiratory effort (e.g., head bobbing, retractions, accessory muscle use) imply impending airway obstruction, although these signs do not point to a specific cause of stridor.
Associated Symptoms. Serious bacterial infections (e.g., epiglottitis, diphtheria, bacterial tracheitis) are associated with fever, while foreign bodies and congenital disorders as a rule do not cause temperature elevation. Temperature elevations in children with croup may be variable. However, reliance on temperature to diagnose or exclude serious bacterial infections is potentially hazardous. Up to 25% of cases with a serious bacterial cause (e.g., epiglottitis and abscesses) for airway stridor are not febrile on presentation to a physician, while a significant number of children with croup have an elevated temperature.8,9
Other symptoms may assist in localizing the site of airway obstruction. For example, drooling and muffled sounds imply that the obstruction is supraglottic (e.g., epiglottitis, diphtheria, or retropharyngeal abscess). Aspirated foreign bodies are an exception, as they can lodge in the trachea, compress the esophagus, and lead to drooling. Hoarseness (due to vocal cord inflammation) accompanied by cough is associated with glottic and subglottic disease (e.g., croup), neither of these features typically occur in epiglottitis.
Acoustics or the quality of stridor can be useful for identifying the site of airway obstruction. While inspiratory stridor implicates a supraglottic obstruction, biphasic stridor implicates glottic or subglottic obstruction, and expiratory stridor is indicative of intrathoracic obstruction, stridor that changes its timing and pattern implies an obstruction that is moving in location (e.g., an aspirated foreign body).
While texts state that the pitch and frequency (megahertz and decibel level) of a sound can aid in locating the source of obstruction, pitch has been found to be useless in differentiating among sources of stridor.10
Air-Shadow Interface (Radiographs). When indicated, radiographs are a useful tool for differentiating among disorders that cause stridor. Prior to obtaining radiographs, clinicians must realize that many children with stridor have the potential to completely obstruct their airway. Therefore, never send an unaccompanied child in whom a life-threatening disorder is suspected to a separate radiology suite. Obtain portable films or accompany the child to the radiology suite and bring appropriate equipment for airway intervention. Furthermore, an appropriate soft-tissue lateral film of the neck requires that the film be obtained with the child’s neck extended during the terminal phase of inspiration. It should be stressed that this position has the potential to obstruct an already compromised airway.
Indications for plain film radiography include upper airway abscesses and foreign bodies in children who are clinically stable. Generally, stable children suspected of having epiglottitis will have either a portable radiograph of the lateral neck or proceed directly to an emergency evaluation of their airway. Unstable children need immediate attention to their airway, either in the operating room or ED, by clinicians who are expert in pediatric airway management.
Classic findings of epiglottitis on plain radiography include an enlarged epiglottis with an appearance similar to a thumb, enlarged aryepiglottic folds, and a ballooned hypopharyngeal airway. However, these findings are subjective and are not obvious in all cases of pediatric epiglottitis. In fact, as many as 70% of all patients with epiglottitis have radiographs that are initially read as normal by radiologists.11,12 Objective findings that may be more accurate in detecting epiglottitis include an epiglottis width/the width of the third cervical vertebral body greater than 0.5, or an aryepiglottic width/width of the third cervical vertebral body greater than 0.35 on lateral radiography. A limited study found that these measurements were 100% sensitive in diagnosing epiglottitis.12
Findings that suggest retropharyngeal abscess include a retropharyngeal space greater than 7 mm anterior to the inferior border of the second cervical vertebral body, or a retrotracheal space greater than 14 mm in children (> 22 mm in adults) anterior to the inferior border of the sixth cervical vertebral body.13 Other suggestive findings include soft-tissue air-fluid levels and cervical retroflexion. Computed tomography is touted by some experts as being more accurate than plain films for detecting retropharyngeal abscesses.14
Soft-tissue radiographs of the neck are often used for evaluating children with croup. One series found that nearly 50% of pediatricians routinely obtained plain films in children with croup.15 Unfortunately, plain films are often misleading or non-diagnostic in this disorder. A prior study that evaluated radiologists’ interpretations of plain films in children with croup found that 24-28% of radiographs were diagnosed as possible epiglottitis, while only 33-38% of radiographs were called croup, proving the unreliability of plain films in diagnosing this disorder.16 When clinically indicated, it may be that plain films of the chest are probably more useful radiographs and can document the presence or absence of a concurrent pneumonia.
Airway foreign bodies are also a final important cause of stridor that can be detected with plain films. Unfortunately, less than 10% of aspirated foreign bodies are radio-opaque.17 Furthermore, even more sensitive radiographic indicators of a bronchial foreign body, such as mediastinal shift, unilateral atelectasis or hyperexpansion, and persistent expansion with expiration, may not completely rule out a foreign body. Therefore, never rely on plain films to exclude an airway foreign body when there is a strong clinical suspicion. In these cases, other airway visualization techniques (e.g., direct laryngoscopy or bronchoscopy) should be considered.
Airway Examination. Direct visualization is an important tool to consider for diagnosing the cause of a child’s stridor. In the past, it was commonly taught that direct visualization of the hypopharynx and use of a tongue blade or mirror (indirect laryngoscopy) was a hazardous technique that should be avoided at all costs in children with stridor and possible epiglottitis. However, several bodies of evidence suggest that this risk is overstated. A literature review dating back to 1964 reveals no recorded cases of tongue blade laryngospasm in children with epiglottitis.18 Furthermore, there has never been a case of laryngospasm in the more than 1000 adult cases of epiglottitis reported.19
Finally, several studies have evaluated the safety of direct visualization in children with suspected epiglottitis. At one pediatric ED, a policy of sequential visualization of the epiglottis in 155 consecutive stridorous children was safely performed by first having the child open his or her mouth.2 If the epiglottis was not visualized, a tongue blade was applied to the anterior tongue while the child was sitting up, then a laryngoscope was used while the child was sitting up; and, finally, direct laryngoscopy was performed while the child was lying down. Using these sequential techniques, the epiglottis was correctly identified in 148 of 149 children with croup and six of six children with epiglottitis. No complications occurred during direct visualization.
Two other series totaling 126 children with epiglottitis found that direct laryngoscopic visualization with care not to touch the epiglottitis and hypopharynx was uniformly safe.11,20 While these reviews suggest that stable children will usually tolerate careful laryngoscopy or application of a tongue blade to the mid or anterior tongue, only clinicians who are comfortable with all aspects of pediatric airway management should perform these techniques. Furthermore, equipment should be available to intervene if stridor worsens or laryngospasm occurs. In general, it is best to use these techniques only in children with a moderate or low suspicion of epiglottitis who are deemed clinically stable. Finally, each institution should develop protocols that outline clinical pathways for children who present with severe, acute, upper airway obstruction.
Specific Upper Airway Disorders. The list of disorders that can precipitate stridor is extensive. (See Table 1.) However, ED physicians must be aware of those disorders that are common (e.g., croup) and potentially life-threatening (e.g., bacterial infection, foreign bodies).
Prior to the late 1980s, Haemophilus influenzae type b (HIB) was the most common etiology of epiglottitis. With the introduction of an effective vaccine against this organism, the incidence of all diseases due to HIB dropped dramatically. In 1980, H. influenzae meningitis occurred in 19.3 of every 100,000 children under the age of 5.22 By 1991, only 3.7 of every 100,000 children at this age developed meningitisa greater than fivefold decrease.22 Furthermore, the average annual incidence of epiglottitis dropped from 11 cases per 10,000 hospital admissions prior to 1990 to fewer than two cases per 10,000 admissions.1
Finally, the changing pattern of epiglottitis is reflected by a newer age spectrum for this disease. Prior to 1990, the median age for children with epiglottitis was approximately 3 years, with a typical range of 2-5 years.1 Additionally, up to 24% of children with epiglottitis were less than 2 years of age.23 However, since 1990, the median age has risen to 7 years, with adolescents, teenagers, and even adults more frequently affected.1
Prior to 1990, HIB accounted for 85-90% of all childhood cases of epiglottitis.1 With the introduction of an effective HIB vaccine over the past decade, HIB currently accounts for only 25% of all cases.1 Due to a decrease in HIB cases and an increase in the number of immunocompromised patients (due to rising HIV rates, more children living with cancer, etc.), atypical organisms are more frequently recognized as a cause of epiglottitis, including Candida, herpes simplex, Staphylococcus aureus, and Streptococci.1,24 Acute supraglottitis secondary to varicella has also recently been reported.25
Presentation. Classically, children with epiglottitis present with high fever, toxicity, acute onset of stridor, drooling, the absence of a cough, and a preference for sitting up. Importantly, the triad of drooling, agitation, and the absence of a cough have been found to be useful in differentiating epiglottitis from croup.2 Although the median age for epiglottitis has risen from 3 years to 7 years, epiglottitis can occur at any age.
While early studies indicate that those under the age of 2 with epiglottitis generally present with subtle clinical features easily confused with croup,23 more recent comparisons indicate that features probably do not differ dramatically between those over and under the age of 2.8 However, adolescents, teenagers, and adults often present with atypical features.19 Older children may simply complain of a sore throat, without evidence of stridor or other features of airway obstruction and with few or no findings of inflammation on examination of the pharynx.19 Importantly, hyoid tenderness is present in almost all older patients.19 Furthermore, while initial clinical features may be subtle, the propensity to develop airway obstruction is still present.
If a child with severe stridor, toxicity, or other features strongly suggestive of epiglottitis presents to the ED, assessment and management must be swift and directed. Although a portable radiograph of the lateral neck soft tissues can be obtained, generally it is recommended to avoid radiography, as this wastes valuable time. If the child has an airway that is patent and maintained, do not disturb or manipulate the airway. A team consisting of an anesthesiologist and surgeon skilled in invasive airway surgical techniques should be assembled immediately in the operating room. Preferably, the composition of this team should be predetermined by protocol. If time allows, anesthetic induction with an inhalational agent should take place in the operating room under controlled circumstances by the physician most skilled in airway management. In children who are clinically stable, nasotracheal intubation is preferred, although oral endotracheal intubation is often necessary in unstable patients.
If airway compromise occurs prior to assembling an operating team, proceed with bag-mask ventilation. Mask ventilation can be easily accomplished in most patients with epiglottitis, since airway compromise is usually due to diaphragmatic fatigue rather than complete airway obstruction from a floppy, heavy epiglottis.11 Higher airway pressures than normal may be necessary to sufficiently balloon the hypopharynx and help mechanically lift the epiglottis to open the airway. If mask ventilation is unsuccessful, proceed with endotracheal intubation. It can generally be stated that with epiglottitis, unsuccessful mask ventilation means improper head position, and, consequently, a closed airway. Use a MacIntosh (curved) laryngoscope blade to avoid direct manipulation of the epiglottis. Prepare several endotracheal tubes that are 0.5 and 1.0 mm smaller than expected for that age with stylets. If vocal cords and the airway are not visualized, have an assistant apply gentle pressure to the sternum. Frequently, this maneuver will produce an air bubble between the vocal cords, allowing for airway visualization. Surgical airway techniques (cricothyrotomy vs tracheostomy), depending on the child’s age, are final options in children with complete airway obstruction. Finally, transtracheal jet ventilation is relatively contraindicated in children with complete airway obstruction due to the high risk from barotrauma in this group of patients.26
For patients who are stable, nontoxic, and have only minimal-to-moderate stridor, several evaluation and management options should be considered. First, assemble airway intervention equipment in case clinical deterioration occurs. Do not allow the patient to be unattended or to leave the department (e.g., to obtain radiographs). Plain film radiography may reveal an enlarged epiglottis, confirming the diagnosis of epiglottitis. However, false-negative (or falsely normal) radiographs have been reported in up to 70% of all cases.12 Alternately, clinicians who are comfortable with their airway skills may consider direct visualization of the epiglottis in children who are clinically stable and have a low-to-moderate suspicion of epiglottitis.
Management. To prevent sudden airway obstruction, all children with epiglottitis require intubation under controlled circumstances. In the past, children who were expectantly managed without intubation in intensive care units had a mortality rate greater than 5%.19 In contrast, mortality in intubated children is less than 1%.19 Consequently, all children with epiglottitis should be intubated until airway swelling resolves. Diligently search for concurrent infections (e.g., pneumonia, upper respiratory infections, meningitis, septic arthritis) in all children with epiglottitis, as 20-25% of children have a second infectious source.1,11 Administer antibiotics that are effective against HIB and other common organisms that cause epiglottitis (e.g., a third-generation cephalosporin). Steroids have not been proven effective in epiglottitis and are not recommended.27 No controlled studies have addressed the utility of racemic epinephrine; theoretically, use of this treatment modality might induce laryngospasm.
Retropharyngeal abscess is a rare but serious cause of supraglottic airway obstruction. This infection generally occurs in very young children prior to atrophy of retropharyngeal lymph nodes. The infection is often polymicrobial, and common oral pathogens are the most frequent causative organisms (e.g., Bacteroides, Peptostreptococci, Fusobacteria, Group A streptococci, Streptococcus viridans, and Staphylococcus aureus).13
Most children with retropharyngeal abscesses are younger than 4 years old.13 There is often a preceding viral upper respiratory infection with eventual seeding of the retropharyngeal lymph nodes by bacteria. With spread of the bacterial infection, an abscess forms, and children develop fever, drooling, stridor, and toxicity. Because of the abscess site adjacent to the cervical spine, the head is often hyperextended. Direct visualization carries the same theoretic risk of airway obstruction as epiglottitis. If the pharynx can be visualized without worsening the symptoms, unilateral or bilateral swelling of the posterior pharyngeal wall may be evident. However, this finding may not be obvious on clinical examination, especially if swelling is bilateral. In addition to airway obstruction, complications of mediastinitis, aspiration, and sudden death can occur with rupture of the abscess into adjacent tissue planes, airway, or vascular structures (e.g., jugular vein or carotid artery).13
Diagnosis. Rapid diagnosis and management are required to avoid complete airway obstruction. As in patients with suspected epiglottitis, children who are toxic with severe stridor, drooling, or other evidence of impending airway obstruction must be taken directly to the operating room. Gentle airway management and induction with a general anesthetic is necessary before the abscess ruptures, with leakage of contents into the lungs.
Although plain film radiography may reveal air-fluid levels or soft-tissue swelling anterior to the vertebral bodies (> 7 mm anterior to C2 or > 14 mm anterior to C6), computed tomography (CT) is more accurate at identifying retropharyngeal abscesses.14 Only children who are clinically stable should be allowed to proceed to CT. Furthermore, always ensure that airway equipment and personnel who are capable of managing airway compromise accompany the patient.
Management. If immediate airway intervention is required in a child with a retropharyngeal abscess, consider positioning the head in a downward and hyperextended position to avoid aspiration should the abscess rupture. Following airway management, surgical drainage of the abscess will be required. Antibiotics effective against oral pathogens including anaerobes should be administered. Penicillin is the recommended drug of choice. Clindamycin is an acceptable alternative. Additional coverage with a third-generation cephalosporin or an antistaphylococcal penicillin should be strongly considered.
Bacterial tracheitis is a rare disorder in children that causes features similar to those of epiglottitis and upper airway abscesses. Only 100 cases had been reported in the literature prior to 1989.28
Typically, patients with bacterial tracheitis develop a viral upper respiratory infection. Symptoms are initially mild and mimic those of croup. They consist of a cough, rhinorrhea, and low-grade fever. Over an ensuing three- to seven-day period, a bacterial superinfection of the trachea occurs with S. aureus. A purulent exudate of the trachea leads to severe stridor, and systemic toxicity occurs. Fifty percent of patients have an associated pneumonia.28 Intubation is generally required to secure the airway and prevent obstruction. Following intubation, frequent suctioning may be required in addition to bronchoscopy in order to unplug the airway and prevent total airway occlusion. Anti-staphylococcal antibiotics are also required.
Foreign body aspiration is an important and potentially fatal cause of acute stridor. Aspiration most commonly occurs in children under the age of 6, with 80% of cases occurring in those under 3 years old.29 This is the leading cause of home-related deaths in the United States for children under 6 years old, with 2000 deaths occurring each year.29 Fortunately, with the passage of the Consumer Products Safety Act of 1979, home safety has improved and the incidence is decreasing. Infants and children older than 6 months are particularly at risk because they lack dentition, are inherently curious, are still crawling, do not have a completely coordinated swallowing mechanism, and are increasingly adept at picking up small objects.29,30,31
Identifying children who have aspirated foreign bodies can be extremely difficult. Only 20-46% present within 24 hours of the initial aspiration while 17% wait more than 30 days from aspiration before seeking medical care.30 Generally, those with upper respiratory foreign bodies present more acutely than those with foreign bodies that have lodged in the lower respiratory tract. Furthermore, 24% of children with aspirated foreign bodies have previously been misdiagnosed, usually as having a respiratory illness such as pneumonia or bronchitis.30 In 25-50% of children, no history of foreign body ingestion can be elicited. Fewer than 10% of aspirated foreign bodies are radiolucent, which underscores the ease with which they can be missed on radiologic examination.32
Most foreign bodies (80-85%) lodge in the bronchial tree. Although the mainstem bronchi of a child branch at equal angles from the trachea, the right side is the most common position for a bronchial foreign body to lodge. Only 2-12% of foreign bodies lodge within or above the larynx, while 3% lodge within the trachea.30 Esophageal foreign bodies can also cause airway compromise through compression on the trachea.
Children with bronchial foreign bodies usually present subacutely, with recurrent cough, wheezing, or other respiratory symptoms. In contrast, children with laryngotracheal foreign bodies more frequently present with acute stridor or cardiopulmonary arrest. However, there is considerable overlap in the symptoms manifested by children with upper and lower airway foreign bodies. (See Figure 2.)
Diagnosis. The most difficult assignment in identifying a lodged foreign body is considering the diagnosis in a child with upper or lower respiratory symptoms. This diagnosis should be considered in any child with acute stridor or cardiopulmonary arrest. Never rely on plain films to exclude the diagnosis of an upper or lower respiratory foreign body. It should be stressed that most foreign bodies (> 90%) will not be visible on plain radiographs.32 Furthermore, inspiratory/expiratory films and decubitus films to detect air trapping have only a 67% sensitivity in detecting bronchial foreign bodies.32 Typical features of a lower respiratory foreign body include recurrent wheezing, pneumonia, or bronchitis, or a persistent cough. When the clinical suspicion is high for an airway foreign body, consider laryngoscopy or bronchoscopy regardless of radiographic findings.
Management. Immediate treatment of a child with an upper airway foreign body and respiratory failure consists of a series of five back blows and chest thrusts in those under 1 year of age. For children over 1 year, substernal abdominal thrusts are recommended with the child in the upright or supine position. Directly inspect the oropharynx between thrusts and do not perform blind finger sweeps. If these maneuvers are unsuccessful, directly inspect the hypopharynx, and inspect the larynx via laryngoscopy. Remove the foreign body with Magill forceps if it is accessible. If this procedure is unsuccessful, consider endotracheal intubation or needle cricothyrotomy.
Laryngotracheobronchitis or viral croup is the most common infectious cause of acute upper airway obstruction in children, accounting for greater than 90% of all cases of stridor and 20,000 hospital admissions per year.7 Most cases occur in the late fall and early spring. Viruses, including parainfluenza, respiratory syncytial virus (especially in patients < 12 months), rhinoviruses, and influenzae A and B, are responsible for croup.7
Stridor in children with croup occurs from mucosal and submucosal edema of the subglottic portion of the airway. The mucosa in this region is loosely adherent, permitting significant edema formation and potential airway compromise. In infants, 1 mm of subglottic edema will cause a 50% decrease in the cross-sectional area of the trachea.33 The subglottic portion of the airway is the narrowest portion of a child’s airway, which further increases the propensity for obstruction. In addition to the upper airway, inflammation often spreads to the trachea and bronchi, causing signs and symptoms of lower respiratory tract disease.
Clinical features include inspiratory and expiratory stridor, a cough (similar to the bark of a seal), hoarseness from vocal cord inflammation, fever, and, occasionally, lower tract symptoms such as wheezing. In contrast to viral croup, a non-seasonal allergic variant known as spasmodic croup may occur. This disorder typically has an abrupt onset, with no preceding upper respiratory infection and no fever.7
Diagnosis. Diagnosis of croup is primarily based on clinical features. The typical age is 2 years. Most children have a few days of prodromal upper respiratory tract symptoms, including nasal congestion, a mild cough, and fever, before stridor develops. Stridor is usually biphasic, although it is often louder on inspiration. Importantly, clinicians must rule out other more immediately life-threatening diseases, including epiglottitis, abscesses, and foreign bodies. Plain radiography has been promoted for the diagnosis of this disorder; however, the main use for this modality is to exclude other serious disorders.
Assessment of Severity. While most children with croup have mild symptoms that will not progress, a small subset of children may develop airway obstruction. Several clinical scoring systems have been proposed for assessing children with stridor. (See Table 2.) Features suggestive of impending airway obstruction have been identified, including age less than six months, rest stridor, cyanosis, decreased level of consciousness, hypoxia, and hypercarbia.7,33 Importantly, an experienced clinician’s evaluation may be more accurate than any scoring system for evaluating the degree of stridor.
Pulse oximetry and capnometry have been evaluated as tools for assessing the severity of a child’s stridor. Pulse oximetry should be routinely obtained on all children with stridor. One recent study found that clinicians were only 33% sensitive in identifying hypoxemia in children with acute respiratory disease.35 Importantly, a normal oxygen saturation may also serve to falsely reassure clinicians. Hypoxia generally indicates advanced disease and impending respiratory failure. While hypoxia signifies fatigue and impending airway obstruction, hypercarbia (detected by capnography or capnometry) has been found to be a much better (and earlier) predictor of clinical deterioration and the need for intubation in children admitted to an intensive care unit.36
Treatment. Humidified mist is usually recommended as first-line treatment for children with croup, although no controlled studies have proven its efficacy. The mist may directly decrease inflammation or reflexly slow respiration through an undefined mechanism.37 Oxygen administration may also benefit a subset of children.
Racemic epinephrine has been promoted as an effective treatment for croup. Racemic epinephrine is composed of 50% D and 50% L isomers of epinephrine. It was first used because the D isomer has 1/30 of the alpha effects of the pure L isomer (e.g., hypertension, tachycardia). However, racemic epinephrine is much more expensive than the L isomer (the form used for all other purposesasthma, allergy, anaphylaxis, and cardiac arrest). Moreover, direct comparisons of racemic epinephrine to an equal amount of the L isomer have shown no differences in outcome for the treatment of croup, including croup scores, side effects, heart rate, blood pressure and respiratory rate.3 Given the apparent rapid efficacy and significant cost differences, the L isomer is the recommended form of epinephrine for the treatment of acute laryngotracheobronchitis.3 The administered dose of the L isomer is 5 cc of the 1:1000 concentration.3
In the past, administration of epinephrine to children with croup mandated admission to observe for potential rebound or further closing of the airway after the medication wore off. This approach has been challenged for several reasons. First, the half-life of epinephrine is only 1-2 hours. Four studies of racemic epinephrine use in children with rest stridor have shown that the effects of epinephrine will wear off within two hours.38,39,40,41 Outpatient management was deemed safe in all children with mild symptoms who had been observed in the ED for two or three hours after epinephrine administration without a worsening of their stridor. In addition, a large number of children received intramuscular steroids in addition to epinephrine in these studies.38,39,40,41 Therefore, observe all children for at least 2-3 hours and administer steroids to all who receive epinephrine.
Steroids are an accepted adjunctive treatment for children with croup. Nebulized budesonide (2 mg) has been shown to decrease croup scores by 50% at two hours in admitted children with moderate-to-severe croup.4,42,43 A meta-analysis that included more than 1200 children with croup from 10 studies found that intramuscular dexamethasone (0.6 mg/kg) decreased croup scores at 12 and 24 hours and intubation rates in admitted children with croup.44 A single study also found that children treated as outpatients with moderately severe croup who received 0.6 mg/kg of dexamethasone IM were improved significantly at the 24-hour follow-up.5 Although clinical studies on outpatient experience with steroids in children with croup are limited, their use for this purpose is widespread in the pediatric community.45
Finally, the decision to admit or discharge a child with croup can be difficult. Generally, admit all children with: 1) a toxic appearance; 2) dehydration or inability to keep down fluids; 3) significant stridor or retractions at rest; 4) unreliable parents; or 5) no improvement with epinephrine administration or worsening at 2-3 hours following epinephrine administration.
Emergency physicians who care for children must be aware of both common and life-threatening causes of stridor. While most children with stridor do not have a serious illness, an important subset will harbor a serious illness that may progress to complete airway obstruction. Clues from the history and physical examination can be used to guide the assessment and management of most children with stridor. (See Table 3.) Importantly, clinicians must be aware of the limitations of plain film radiography in diagnosing the cause of a child’s stridor. In the past, direct visualization of the airway was felt to be uniformly contraindicated in children with stridor. However, this simple technique may provide useful information for clinicians who are trained and equipped to manage a child’s airway. Finally, clinicians must be aware of the different treatments available, as well as indications for emergent and urgent airway intervention in children with stridor.
[This article was originally published in Pediatric Emergency Medicine Reports, April, 1996.]
3. Waisman Y, Klein BL, Boenning DA, et al. Prospective randomized double-blind study comparing L-epinephrine and racemic epinephrine aerosols in the treatment of laryngotracheitis (croup). Pediatrics 1992;89:302-306.
35. Mancker AJ, Petrack EM, Krug SE. Contribution of routine pulse oximetry to evaluation and management of patients with respiratory illness in a pediatric emergency department. Ann Emerg Med 1995;25:36-40.
40. Ledwith C, Shea L, 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;25:331-337.
46. Handler SD. Stridor. In: Fleisher GR, Ludwig S, eds. Textbook of Pediatric Emergency Medicine. Baltimore: Williams & Wilkins; 1993:477.