Chapter 123: Stridor and Drooling in Infants and Children

Stridor is a high-pitched, harsh sound produced by turbulent airflow through a partially obstructed airway. Both inspiratory and expiratory stridor are associated with airway obstruction. As air is forced through a narrow tube, it undergoes a decrease in pressure (the Venturi effect). The decrease in lateral pressure causes the airway walls to collapse and vibrate, generating stridor. Airway resistance is inversely proportional to the fourth power of the airway radius. This translates into a 16-fold increase in resistance when the radius is reduced by half. Even 1 mm of edema in the normal pediatric subglottis reduces its cross-sectional area by >50%. A small amount of inflammation can result in significant airway obstruction in children.

Immediately assess the child with stridor, because stridor indicates a difficult airway, and advanced airway management may be necessary (see chapter 111, "Intubation and Ventilation in Infants and Children"). A thorough history and examination will often lead to a "working diagnosis." If time permits, ask about the time and events surrounding the onset of stridor, the presence of fever, known congenital anomalies, perinatal problems, prematurity, and previous endotracheal intubation.

The level of obstruction can often be identified on examination. Partial obstruction of the upper airway at the nasopharynx and oropharyngeal levels produces sonorous snoring sounds, called stertor. Obstruction of the supraglottic region may cause inspiratory stridor or stertor. Obstruction of the glottis and subglottic and tracheal areas often cause both inspiratory and expiratory stridor. Consider airway foreign body until proven otherwise if there is marked variation in the pattern of stridor. The noise made by a child with stridor is often interpreted as wheezing by parents unfamiliar with stridor. Clarify what the parent means when the word "wheezing" is used—whether the sound occurs when the child breathes in or breathes out. The provider can imitate a stridor sound to help ED diagnosis. The differential diagnosis of stridor depends on the child's age (Table 123-1).

An infant <6 months old with a long duration of symptoms typically has a congenital cause of stridor. The major causes are laryngomalacia, tracheomalacia, vocal cord paralysis, and subglottic stenosis. Less common but important considerations include airway hemangiomas and vascular rings and slings. Stridor presenting in the first 6 months of life will often require direct visualization of the airway through endoscopy or advanced imaging. The timing of this evaluation (emergent or outpatient) is dictated by the severity of symptoms and clinical suspicion.

Laryngomalacia accounts for 60% of all neonatal laryngeal problems and results from a developmentally weak larynx. Collapse occurs with each inspiration at the epiglottis, aryepiglottic folds, and arytenoids. Generally, stridor worsens with crying and agitation but often improves with neck extension and when the child is prone. Laryngomalacia usually manifests shortly after birth, which is a key diagnostic feature, and generally resolves by age 18 months old. In many cases, the tracheal support structures are similarly affected, resulting in laryngotracheomalacia. Symptom exacerbations may occur with upper respiratory infections or increased work of breathing from any cause. Definitive diagnosis can often be made with flexible fiberoptic laryngoscopy. Surgery may be required if a child suffers from failure to thrive, apnea, or pulmonary hypertension.

Vocal cord paralysis can be congenital or acquired. Unilateral vocal cord paralysis is more common than bilateral cord paralysis and presents with feeding problems, stridor, hoarse voice, and cry changes. Children with bilateral cord paralysis often have a normal voice associated with stridor and dyspnea, and symptoms include cyanosis and apneic episodes. Diagnosis is by flexible nasolaryngoscopy. Endotracheal intubation can be difficult with bilateral cord paralysis, and needle cricothyroidotomy and subsequent tracheotomy may be required to secure the airway.

Subglottic stenosis may be acquired or congenital and is diagnosed when there is a narrowing of the laryngeal lumen. Congenital stenosis is usually diagnosed in the first few months of life when the child is noted to have persistent inspiratory stridor. Mild cases may present later in childhood as recurrent or persistent croup. Prolonged endotracheal intubation in premature babies is the most common cause of acquired subglottic stenosis. Treatment is based on the severity of the stenosis, but symptoms typically resolve by a few years of age.

Hemangiomas are benign congenital tumors of endothelial cells or vascular malformations that can occur anywhere on the body (80% are located above the clavicles), including the airway where they can cause obstruction and stridor. Hemangiomas typically enlarge throughout the first year of life, may not be noticed at birth, and tend to spontaneously regress by age 5 years old. For infants <6 months old, thoroughly examine the skin, because cutaneous hemangiomas, especially in a beard distribution, may be a clue to the presence of an airway hemangioma. Consider airway hemangioma in new-onset stridor beginning after the first month of life without another explanation; definitive diagnosis requires airway visualization through endoscopy. Although most hemangiomas spontaneously regress, large malformations and those causing significant respiratory symptoms may require treatment with β-blockers, steroids, laser, or surgery.^1,2,3

Vascular rings and slings are rare congenital anomalies of the aortic arch and pulmonary artery in which anomalous vessels can compress the trachea or esophagus. Examples include a double- or right-sided aortic arch. Symptoms are often present from birth or early in the first month of life, and may be progressive and exaggerated during intercurrent upper respiratory infections; difficulty with feeding may also occur if the esophagus is compressed. Because these anomalies are rare, a high index of suspicion is required for diagnosis. Chest x-ray may reveal subtle narrowing or anterior compression of the trachea on the lateral view or an abnormal (e.g., right-sided) aortic arch. Further evaluation includes bronchoscopy, CT angiography, and echocardiography to evaluate for associated congenital heart anomalies. Definitive treatment is surgical.

The child >6 months old with a relatively short duration of symptoms (hours to days) characteristically has an acquired cause of stridor. Causes are either inflammatory/infectious, such as croup or epiglottitis, or noninflammatory, such as a foreign body aspiration (Table 123-2).

CROUP

Croup (viral laryngotracheobronchitis) is the most common cause of stridor outside the neonatal period, commonly affecting children 6 months to 3 years old, with a peak in the second year of life. The incidence is highest in the fall and the early winter months, and more cases occur during odd-numbered years.⁴ Croup is acquired through inhalation of the virus. The most common viruses are parainfluenza virus and rhinovirus, followed by enterovirus and respiratory syncytial virus, influenza virus, human metapneumovirus, and human bocavirus. Co-infection by more than one virus is common.^5,6,7

CLINICAL FEATURES

The clinical course of croup varies, but symptoms typically begin after 1 to 3 days of nasal congestion, rhinorrhea, cough, and low-grade fever. Classic symptoms are a harsh barking cough, hoarse voice, and stridor. Symptoms may be worse at night. The severity of symptoms is related to the amount of edema and inflammation of the airway. Assess for tachypnea, stridor at rest, nasal flaring, retractions, lethargy or agitation, and oxygen desaturation. The "typical" duration of symptoms ranges from 3 to 7 days. Symptoms are most severe on the third and fourth days of illness and then improve.

DIAGNOSIS

Diagnosis is clinical. Laboratory studies, viral tests, or radiographs are needed only in children who fail to respond to conventional therapy or if considering another diagnosis such as epiglottitis, retropharyngeal abscess, or aspirated foreign body.⁸ If radiographs are ordered, provide physician monitoring during the procedure, because agitation may worsen existing airway obstruction.⁵ Radiographs may demonstrate subglottic narrowing ("steeple sign") (Figure 123-1). However, the steeple sign may be present in normal children and can be absent in up to 50% of those with croup.

TREATMENT

Croup is often classified as mild, moderate, or severe (Table 123-3), and treatment is directed primarily at decreasing airway obstruction. Croup scoring systems are more useful as research tools than for clinical practice. The score, if calculated, should only be used as one piece of data in the decision-making process.

Place children in a position of comfort, often in the lap of the caretaker. Assess respiratory distress through observation, without disturbing the child. Agitation and crying increase oxygen demand and may worsen airway compromise. Humidified air or cool mist do not appear to improve clinical symptoms.^9,10 However, anecdotally, exposing children with croup to cold air at home reduces the intensity of symptoms.⁵

Current standard treatment is nebulized epinephrine for moderate to severe croup and corticosteroids for all (Table 123-4).

Epinephrine Mild croup generally does not require epinephrine. Give nebulized epinephrine for moderate to severe croup. For those with moderate or severe croup who receive nebulized epinephrine, observe in the ED for 3 hours before considering discharge.¹¹

Epinephrine decreases airway edema through vasoconstrictive alpha effects. Clinical effects of epinephrine are seen in as few as 10 minutes and last for more than 1 hour.^12,13 Use of epinephrine decreases the number of children with croup requiring intubation, intensive care unit admission, and admission to the hospital in general. Studies comparing l-epinephrine with racemic epinephrine show no significant difference in response initially; however, at 2 hours after administration, patients receiving l-epinephrine have lower croup scores.^14,15 Administration of nebulized intermittent positive-pressure breathing has no benefit over simple nebulization.¹⁶

ED observation for about 3 hours is recommended because an increase in croup scores can occur between the second and third hours after epinephrine nebulization in those patients ultimately requiring admission.^17,18

Corticosteroids All patients with croup, whether mild, moderate, or severe, benefit from the administration of oral steroids as a one-time dose. Steroids reduce the severity and duration of symptoms^19,20 and result in a decrease in return visits and ED or hospital length of stay. Dexamethasone is equally effective if given parenterally or orally. Currently, a single dose of 0.6 milligram/kg PO of the oral dexamethasone preparation is recommended, but doses as low as 0.15 milligram/kg of dexamethasone may be considered.^{19,20,21,22,23} Traditionally, onset of action for oral dexamethasone is considered to be 4 to 6 hours after oral administration, but effects can be seen within 1 hour of oral administration.²¹ Most clinicians initially prescribe oral corticosteroids because of ease of administration. The volume of a PO dose of IV dexamethasone is smaller than the volume of the PO dexamethasone preparation and may be associated with less vomiting. Nebulized budesonide and IM dexamethasone are alternatives to PO dexamethasone in children who are vomiting.

Agents with No Benefit in Croup Heliox, in a 70% helium/30% oxygen ratio, has theoretical treatment benefits for severe, refractory croup. Replacing nitrogen with the less dense helium decreases airway resistance and improves gas flow through a compromised airway. An important limitation is the low fractional concentration of inspired oxygen in the gas mixture. Despite its theoretical benefits, studies show no definitive advantage of heliox over conventional treatment.^{24,25,26,27,28}

Although historically used in children with mild to moderate croup, the use of humidified air is likely ineffective.²⁹

There are insufficient data to determine whether nebulized β₂-agonists are beneficial in children with croup.²⁷ In addition, there is theoretical risk of worsening upper airway obstruction with β-agonists in croup: β-receptors on the vasculature cause vasodilation (as compared to the vasoconstrictive α effects of epinephrine), which might worsen upper airway edema in croup, and there is no smooth muscle in the upper airway. Therefore, β-agonists are not recommended for treatment of croup.

DISPOSITION AND FOLLOW-UP

Most children with croup can be safely discharged to home (Table 123-5). Children who have received nebulized epinephrine should be observed in the ED for 3 hours after administration. Children with persistent stridor at rest, tachypnea, retractions, and hypoxia or those who require more than two treatments of epinephrine should be admitted to the hospital.^5,17,18 Intubation is reserved for cases of severe croup not responding to medical treatment. When intubation is necessary, use endotracheal tubes smaller than recommended for patient size and age to avoid traumatizing the inflamed mucosa.

EPIGLOTTITIS

Epiglottitis, or supraglottitis, is an acute inflammatory condition of the epiglottis that may progress rapidly to life-threatening airway obstruction. Widespread administration of Haemophilus influenzae type B vaccine has significantly reduced the number of cases of childhood epiglottitis. In the postvaccine era, most cases of infectious epiglottitis are caused by streptococcal and staphylococcal species. Candida species can cause epiglottitis in the immunocompromised patient. Noninfectious causes, such as thermal injury, caustic burns, and direct trauma, may cause swelling and inflammation of the epiglottis with a clinical picture identical to that of infectious epiglottitis in the absence of fever.

CLINICAL FEATURES

Infection typically presents with the abrupt onset of fever, drooling, and sore throat. Symptoms may progress rapidly, with inability to handle oral secretions followed by stridor and respiratory distress. Cough is often absent, but the voice may be muffled. Most children appear toxic and anxious and may assume a tripod or sniffing position with the neck hyperextended and the chin forward to maintain the airway.³⁰

DIAGNOSIS

The ideal approach to the diagnosis of epiglottitis varies, depending on the practice and the environment. Each institution should have a written "suspected epiglottitis management protocol." Important components of all protocols are listed in Table 123-6.

In older children and those with mild respiratory distress, gentle direct visualization of the epiglottis may be attempted. Despite concerns that such maneuvers could trigger worsening distress, no documented reports show this to be unsafe. Patients with suspected epiglottitis who are initially seen in an office or clinic without pediatric or otolaryngologic subspecialty support should be transported to a referral center accompanied by personnel who can manage the airway.

Lateral neck radiographs are usually unnecessary in patients with the classic presentation of epiglottitis. When the diagnosis is uncertain, obtain soft tissue neck radiographs with the neck extended during inspiration. Affected children typically hold their heads in a sniffing position and have prolonged inspiration already, making it quite simple to obtain radiographs. Lateral neck radiographs may show an enlarged epiglottis protruding from the anterior wall of the hypopharynx (often called the "thumb sign") and thickened aryepiglottic folds (Figure 123-2). If suspicion for the diagnosis still exists despite normal-appearing radiographs, direct visualization of the epiglottis is necessary to exclude the diagnosis (Figure 123-3).

TREATMENT

Keep the child seated and upright in a position of comfort. Provide oxygen. Administer nebulized racemic or l-epinephrine to decrease airway edema. Alert the referral center or pediatric otolaryngologist as soon as possible so decisions concerning intubation or tracheotomy can be made in concert with consultants and support personnel can be mobilized. The most skilled individual available should perform intubation as soon as the diagnosis is made. Use sedation, paralytics, and vagolytics as needed. For a child who is able to maintain an airway, the decision to administer paralytics must be accompanied by absolute certainty that intubation will be successful. Have multiple endotracheal tube sizes immediately available. If endotracheal intubation is unsuccessful, an emergent surgical airway is required. Administer a second- or third-generation cephalosporin, such as cefuroxime (50 milligrams/kg IV) or ceftriaxone (50 milligrams/kg IV), to ensure adequate coverage of the most common infectious pathogens. With the increasing incidence of Staphylococcus aureus and highly resistant Streptococcus pneumoniae as a cause of epiglottitis, one may also empirically add vancomycin (10 milligrams/kg IV) to the antibiotic regimen. Antibiotics are typically continued for 7 to 10 days. Steroids are often employed to decrease mucosal edema of the epiglottis.

BACTERIAL TRACHEITIS

Bacterial tracheitis, also known as membranous laryngotracheobronchitis or bacterial croup, is an uncommon infection that can cause life-threatening upper airway obstruction. It can be a primary or secondary infection. The mean age of presentation is now 5 to 8 years of age compared with the 4 years of age that has been classically described.^31,32

Bacterial tracheitis often develops secondarily after a viral upper respiratory tract infection. A history of upper respiratory infection symptoms followed by sudden worsening with high fever, stridor, and cough (which may be productive of thick sputum) and a toxic appearance suggest the diagnosis. Thick mucopurulent secretions of the trachea result in upper airway obstruction. Children with tracheitis often complain of sore throat and will point to their trachea when asked where it hurts; there is often tenderness with palpation of the trachea. Management is similar to that of epiglottitis, with patients ideally going to the operating room for sedation, intubation, and bronchoscopy. Cultures and Gram stain of the mucopurulent secretions should be obtained at this time, because Gram stain findings may help guide the antibiotic therapy. Bronchoscopy may be therapeutic, because the removal of purulent pseudomembranes improves tracheal toilet and may lessen upper airway obstruction. For continued management, most patients with bacterial tracheitis require intubation and ventilatory support.

The most commonly isolated pathogen obtained from culture at bronchoscopy is S. aureus. Other organisms implicated in bacterial tracheitis include S. pneumoniae, Streptococcus pyogenes, Moraxella catarrhalis, H. influenzae, and anaerobes.^33,34,35,36 Initial antibiotic choices include ampicillin/sulbactam or the combination of a third-generation cephalosporin and clindamycin. Add vancomycin for methicillin-resistant S. aureus. Laboratory studies other than tracheal cultures are of limited use in the diagnosis. Neck radiographs are not needed to make the diagnosis. When obtained to evaluate for other potential diagnostic entities, neck films may show subglottic narrowing of the trachea and irregular tracheal margins in patients with tracheitis (Figure 123-4). Because no single clinical or radiographic feature can definitively make a diagnosis, bronchoscopy is the diagnostic method of choice in bacterial tracheitis.

AIRWAY FOREIGN BODY

Airway foreign body aspiration occurs most commonly in children between 1 and 3 years old as a result of increasing mobility and oral exploration. Foreign body aspiration in children <6 months old often involves a well-meaning sibling who places an object in the infant's mouth. The most common objects aspirated fall into two groups: food and toys. Commonly aspirated foods include peanuts, sunflower seeds, carrots, raisins, grapes, and hot dogs.

A high index of suspicion is needed for diagnosis. Consider foreign body aspiration in a young child with respiratory symptoms, regardless of the duration of symptoms, because many children may present >24 hours after foreign body aspiration. If the clinical scenario clearly indicates the presence of a foreign body or airway obstruction, immediately implement a protocol for obstructed airway management. Suspect foreign body aspiration with a history of sudden coughing and choking in the child; this is the most predictive of all signs and symptoms in foreign body aspiration.^37,38 In many cases, the choking episode is not witnessed by a caregiver.

CLINICAL FEATURES

Although the location of the aspirated foreign body plays a role in determining the symptoms and signs on presentation, there is great overlap between groups, and some children may be asymptomatic on presentation. "Classic dogma" is that laryngotracheal foreign bodies cause stridor and hoarseness, whereas bronchial foreign bodies cause unilateral wheezing and decreased breath sounds. Eighty percent to 90% of airway foreign bodies are found in the bronchi. Children may develop severe immediate-onset stridor or even cardiopulmonary arrest, but a significant proportion will have no cough, wheeze, or stridor. The most important factor in reducing mortality from an airway foreign body is the recognition of the child in acute airway distress.

DIAGNOSIS

Radiographs are helpful to confirm the diagnosis of airway foreign body but should not be used to exclude the diagnosis, because plain chest radiographs are normal in >50% of tracheal foreign bodies and one fourth of bronchial foreign bodies.³⁹ Laryngeal and tracheal foreign bodies often constitute an acute emergency, and radiography is omitted. If performed, posteroanterior and lateral neck radiographs are the radiographic examinations of choice. Foreign bodies lodged in the proximal esophagus may also present with airway compression. Tracheal and esophageal foreign bodies can be differentiated on neck radiographs: foreign bodies typically lodge in the trachea in profile and in the esophagus en face (see Figure 77-2). Suspected bronchial foreign bodies can be evaluated with the use of posteroanterior and lateral chest films (Figure 123-5). More than 75% of airway foreign bodies in children <3 years of age are radiolucent.^37,40,41,42 Indirect radiologic signs of a radiolucent airway foreign body include unilateral obstructive emphysema, atelectasis, and consolidation. Unilateral obstructive emphysema is seen when a foreign body obstructs airflow, mainly on expiration. This generates a check-valve obstruction that results in hyperinflation of the affected side and mediastinal shift to the opposite side (Figure 123-6). A foreign body that obstructs a bronchus may produce focal atelectasis and consolidation visible on chest films. Inspiratory and expiratory chest radiographs can aid in the diagnosis by showing hyperinflation (air trapping) on expiratory films. Bilateral decubitus chest films have been used to demonstrate air trapping; however, they increase false positives without increasing true positives, suggesting a lack of clinical benefit.⁴³ A clinically suspected foreign body aspiration should ultimately be ruled out by bronchoscopy, regardless of the chest radiograph findings.^44,45,46,47

TREATMENT

Children with complete airway obstruction are typically unable to breathe or speak and require emergency basic life support measures to relieve airway obstruction. For detailed discussion, see chapters 108, "Resuscitation of Neonates" and 109, "Resuscitation of Children." If basic life support maneuvers fail, direct laryngoscopy and foreign body extraction with Magill forceps should be attempted. When the foreign body is not visible or able to be removed, orotracheal intubation with dislodgment of the foreign body more distally (often into the right mainstem bronchus) can relieve the complete obstruction and may be life-saving. If the foreign body cannot be removed and ventilation cannot be provided through an endotracheal tube, needle cricothyroidotomy or emergency tracheostomy should be performed. Those patients who do not have complete airway obstruction should have their respiratory status closely monitored while preparations are made for bronchoscopic removal under general anesthesia.

RETROPHARYNGEAL ABSCESS

The retropharyngeal space occupies the space between the posterior pharyngeal wall and the prevertebral fascia and extends from the base of the skull to approximately the level of the second thoracic vertebrae. This space is fused down the midline and contains two chains of lymph nodes extending down each side. These lymph nodes tend to regress by age 4 years old, obliterating this potential space, which explains the decreasing frequency of retropharyngeal abscess in older children. The formation of a retropharyngeal abscess is believed to be secondary to suppuration of these lymph nodes that have been seeded from a distant infection. Localized penetrating trauma with subsequent invasion of this space by bacteria is another cause of retropharyngeal infection. This most commonly occurs in children who fall with a stick or other similar object in their mouth. Infection can also occur from traumatic esophageal instrumentation or ventral extension of vertebral osteomyelitis. Retropharyngeal infection typically progresses from an organized phlegmon to a mature abscess.

CLINICAL FEATURES

Most cases of retropharyngeal abscess evolve insidiously over a few days after a relatively minor upper respiratory infection. Fever is typically present but may be absent in >10% of patients.^48,49,50,51 Signs and symptoms include neck pain, fever, dysphagia, excessive drooling, and neck swelling. The child may maintain the neck in an unusual position, with stiffness, torticollis, and hyperextension. A unique finding is bulging of the posterior oropharynx. Abscess progression can lead to stridor and respiratory distress. Pleuritic chest pain is an ominous sign, indicating extension of the infection into the mediastinum.

DIAGNOSIS

Initial imaging includes a soft tissue lateral neck radiograph. The radiograph should be taken during inspiration with the neck extended to limit false-positive results. The diagnosis of retropharyngeal abscess/cellulitis is suggested when the retropharyngeal space at C2 is twice the diameter of the vertebral body or greater than one half the width of the C4 vertebral body (Figure 123-7). Rarely, gas may be seen within the mass. Contrast-enhanced CT scan may demonstrate necrotic nodes, inflammatory phlegmon, or fluid collection within a ring-enhancing abscess (Figure 123-8). CT is helpful for diagnosing and defining the extent of the infection and planning a surgical procedure. However, CT scans are limited in their ability to differentiate between abscess and cellulitis/phlegmon. Therefore, imaging results should be correlated to clinical findings when guiding the decision of conservative versus surgical treatment.^{52,53,54,55,56,57} Unstable patients should be intubated before going to the radiology suite for CT scan. Patients requiring sedation to obtain a scan may require presedation intubation if airway obstruction is present. A physician accustomed to managing the difficult pediatric airway should escort patients without airway compromise to radiology, and appropriate equipment should accompany the patient.

TREATMENT

Carefully monitor and stabilize the airway. Obtain IV or IO access to administer fluids, antibiotics, and CT contrast. Retropharyngeal cellulitis and small, localized abscesses may be treated successfully with antibiotic therapy alone. All other cases should undergo operative incision and drainage, usually by an otolaryngologist. Steroids can reduce airway edema, inflammation, and the progression of cellulitis into an abscess. Most retropharyngeal abscesses are found to contain mixed flora when cultured.³¹ Common organisms include S. aureus, S. pyogenes, Streptococcus viridans, and β-lactamase–producing gram-negative rods. Oral anaerobes are also frequently seen. Single-agent antimicrobial therapy includes ampicillin/sulbactam or clindamycin. Unusual complications of retropharyngeal abscess include airway obstruction, spontaneous abscess perforation, mediastinitis, sepsis, aspiration, and jugular venous thrombosis.

PERITONSILLAR ABSCESS

Peritonsillar abscess is a deep oropharyngeal infection. It can occur in patients of any age, but most commonly occurs in adolescents and young adults. The disease typically begins as a superficial infection that progresses to an accumulation of pus in a space between the tonsillar capsule and the superior constrictor muscle. Most are unilateral, and <10% are bilateral at the time of diagnosis.

CLINICAL FEATURES AND DIAGNOSIS

Patients with peritonsillar abscess typically present with sore throat, fever, chills, trismus, and voice change ("hot potato voice"). Patients will often complain of "the worst sore throat" of their life and may drool due to difficulty swallowing their saliva. Ipsilateral ear pain and torticollis may be present. On examination, bulging of the affected tonsil and deviation of the uvula away from the involved tonsil are evident (Figure 123-9).

Differentiating peritonsillar cellulitis from peritonsillar abscess can be difficult. If the child is toxic, consider a peritonsillar abscess until proven otherwise. Imaging with CT scan or US can differentiate between the two.

TREATMENT

In nontoxic-appearing adolescents with good follow-up and with findings most consistent with peritonsillar cellulitis, a trial of oral antibiotics (e.g., penicillin) may be the best choice for treatment. Most cases of peritonsillar abscess are managed as outpatients with prompt aspiration or incision and drainage using local anesthetics in the ED. Young and uncooperative children may require procedural sedation to facilitate adequate evaluation and drainage. Complications of needle aspiration and incision and drainage include hemorrhage, puncture of the carotid artery, and airway aspiration of purulent material. CT with IV contrast is the imaging modality of choice for assessment of suspected infection in patients who have failed incision and drainage and in whom trismus or lack of cooperation prevents a thorough intraoral examination.

Most peritonsillar abscesses are polymicrobial infections. Predominant organisms include anaerobes, group A β-hemolytic streptococci, S. aureus, and H. influenzae.⁵⁸ The fluid obtained from needle aspiration should be sent for Gram stain and culture. IV antimicrobial therapy may include ampicillin/sulbactam or clindamycin. Outpatient management antibiotic choices include penicillin, clindamycin, and amoxicillin/clavulanate. Single high-dose steroid administration may improve symptoms in patients with peritonsillar abscess.⁵⁹

LUDWIG'S ANGINA

Ludwig's angina is a potentially life-threatening, rapidly expanding infection of the submandibular space. The submandibular space is composed of two spaces subdivided by the mylohyoid muscle into the sublingual and submylohyoid space (submaxillary space) and extends from the floor of the mouth to muscular attachments at the hyoid bone. Infectious expansion into this space spreads superiorly and posteriorly and often involves the entire submandibular space (Figure 123-10). Most cases arise from an odontogenic source, often from the spread of periapical abscesses of mandibular molars.

CLINICAL FEATURES

Ludwig's angina usually begins with a mild infection that progresses rapidly to severe mouth pain, drooling, trismus, tongue protrusion, and brawny neck swelling. The child may lean forward to maximize airway diameter. Stridor may develop with subsequent progressive airway obstruction. Control the airway early, because intubation can be extremely difficult late in the clinical course of the disease. One case series reports that 11 of 20 patients had an unsuccessful attempt at intubation resulting in emergent tracheotomy.⁶⁰ Treatment is antibiotics and oral surgery to remove the dental abscess that is the source of the infection. IV antibiotics should cover β-lactamase–producing aerobic or anaerobic gram-positive cocci and gram-negative bacilli. Consideration must be given to including coverage of community-acquired methicillin-resistant S. aureus as well.

DIPHTHERIA

Diphtheria is an acute toxin-mediated disease caused by Corynebacterium diphtheria and has largely been eradicated in developed nations through widespread vaccination. It is transmitted from person to person through respiratory secretions or skin lesions. In cases of pharyngeal diphtheria, symptoms include sore throat, malaise, dysphagia, and low-grade fever. Characteristic 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 C. diphtheria by cultures of a nasopharyngeal swab. Treatment includes antitoxin and antibiotics (erythromycin or penicillin G) and respiratory support as needed.

OROPHARYNGEAL TRAUMA

Traumatic oropharyngeal injuries in children typically occur during a fall with an object in 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 a foreign body was removed intact or if part of the object may have broken off into the soft tissue. If there is suspicion of retained foreign body, imaging is required.

CLINICAL FEATURES

Children with oropharyngeal trauma may present with bleeding, drooling, or dysphagia. 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. Prophylactic antibiotics play an inconclusive role in the treatment of intraoral wounds.⁶¹ There are rare but well-known complications of penetrating pharyngeal injury. Entrance of free air into the neck or chest can result in stridor and acute airway obstruction. Subsequent retropharyngeal infection from introduction of bacteria into the penetrating wound can occur. A more severe complication of oropharyngeal trauma is carotid artery injury. The carotid artery is closely associated with the lateral oropharynx and is at risk of injury from penetrating and blunt impact forces. Penetrating injury results in massive hemorrhage, whereas 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. Symptoms may evolve over hours to days and can result in significant neurologic sequelae (stroke in the distribution of the common carotid territory).

DIAGNOSIS AND TREATMENT

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. Normal retropharyngeal soft tissue in airway films is no more than one half of the width of the adjacent vertebral body. An increase in the width and the presence of air in the retropharyngeal space indicate pharyngeal injury and may warrant further investigation. CT is superior to plain radiographs for the detection of free air, inflammation, or abscess. CT angiography is needed if carotid injury is suspected and should be considered for patients who are unstable, who cannot be adequately assessed, and for whom lateral pharyngeal trauma raises concern for vascular injury.⁶² Treatment is specific for the complication and involves consultation with surgery or otolaryngology.