The nurse is caring for a child with acute epiglottitis the child has a high-pitched

The Child With Stridor

A child with intrathoracic airway obstruction has expiratory stridor and prolonged expiration (e.g., bronchiolitis, asthma, intrathoracic foreign body).195 In contrast, a child with extrathoracic upper airway obstruction has inspiratory stridor (e.g., epiglottitis, laryngotracheobronchitis, laryngeal, subglottic foreign body). When agitated or crying, such children exhibit dynamic collapse of the airway (Fig. 77.12), which can significantly worsen airway obstruction and lead to respiratory failure and hypoxemia. Therefore events that can upset the child, such as drawing of blood for analysis of gases, venipuncture for blood tests, and separation from parents, must be minimized. The difficult-airway cart should also be present. The surgical team should be mobilized and prepared to perform an emergency tracheotomy should total airway obstruction occur and mask ventilation or tracheal intubation not be possible.

When inducing anesthesia in a child with stridor the following is suggested. To minimize upsetting the child, the child is brought to the operating room with the mother or father, who holds the child during induction (preferably lying down in a semi-upright position). Induction of anesthesia with sevoflurane in oxygen by mask is the preferred method because maintaining spontaneous respirations is critical. If the stridor worsens or mild laryngospasm occurs, then the pop-off valve is sufficiently closed to develop 10 to 15 cm H2O of positive end-expiratory pressure (PEEP). This procedure relieves most instances of airway obstruction caused by dynamic collapse of the airway and loss of pharyngeal muscle tone when the child attempts to inspire against an obstructed airway (Fig. 77.13). As the level of anesthesia deepens, gentle assistance with ventilation may be necessary; however, maintaining spontaneous respiratory effort is important if possible.

Any child with airway obstruction will have a long, slow induction of anesthesia before becoming sufficiently anesthetized to permit laryngoscopy and tracheal intubation. The issue of a full stomach is secondary to the airway problem. Rapid induction of anesthesia and paralysis is contraindicated in these children. A child with laryngotracheobronchitis or epiglottitis usually requires an uncuffed tracheal tube that is 0.5 to 1.0 mm internal diameter smaller than normal (Table 77.6); the use of a stylet facilitates its insertion.

Apnea and Stridor

These upper airway presentations have been linked with GERD in case reports and epidemiologic studies; temporal relationships between them and reflux episodes have been demonstrated in some patients by esophageal pH–multichannel intraluminal impedance studies, and a beneficial response to therapy for GERD provides further support in a number of case series. An evaluation of 1,400 infants with apnea attributed the apnea to GERD in 50%, but other studies have failed to find an association. Apnea and brief resolved unexplained event-like presentation (previously called an “apparent life-threatening event”) caused by reflux is generally obstructive, owing to laryngospasm that may be conceived of as an abnormally intense protective reflex. At the time of such apnea, infants have often been provocatively positioned (supine or flexed seated), have been recently fed, and have shown signs of obstructive apnea, with unproductive respiratory efforts.The evidence suggests that for the large majority of infants presenting with apnea and a brief resolved unexplained event, GERD is not causal. Stridor triggered by reflux generally occurs in infants anatomically predisposed toward stridor (laryngomalacia, micrognathia). Spasmodic croup, an episodic frightening upper airway obstruction, can be an analogous condition in older children. Esophageal pH probe studies might fail to demonstrate linkage of these manifestations with reflux owing to the buffering of gastric contents by infant formula and the episodic nature of the conditions. Pneumograms can fail to identify apnea if they are not designed to identify obstructive apnea by measuring nasal airflow.

Reflux laryngitis and other otolaryngologic manifestations (also known as laryngopharyngeal reflux) can be attributed to GERD.Hoarseness, voice fatigue, throat clearing, chronic cough, pharyngitis, sinusitis, otitis media, and a sensation of globus have been cited. Laryngopharyngeal signs of GERD include edema and hyperemia (of the posterior surface), contact ulcers, granulomas, polyps, subglottic stenosis, and interarytenoid edema. The paucity of well-controlled evaluations of the association contributes to the skepticism with which these associations may be considered. Other risk factors irritating the upper respiratory passages can predispose some patients with GERD to present predominantly with these complaints.

Many studies have reported a strong association between asthma and reflux as determined by history, pH–multichannel intraluminal impedance, endoscopy, and esophageal histology. GERD symptoms are present in an average of 23% (19–80%) of children with asthma as observed in a systematic review of 19 studies examining the prevalence of GERD in asthmatics. The review also reported abnormal pH results in 63%, and esophagitis in 35% of asthmatic children. However, this association does not clarify the direction of causality in individual cases and thus does not indicate which patients with asthma are likely to benefit from anti-GERD therapy. Children with asthma who are particularly likely to have GERD as a provocative factor are those with symptoms of reflux disease, those with refractory or steroid-dependent asthma, and those with nocturnal worsening of asthma. Endoscopic evaluation that discloses esophageal sequelae of GERD provides an impetus to embark on the aggressive (high dose and many months’ duration) therapy of GERD.

Medical management and approach

A.

In the patient’s history, ask the following questions: When did the stridor begin? Does the child have symptoms of an upper respiratory infection or cold, such as coughing or rhinitis? When did the cold symptoms begin? Is it difficult for the child to breathe? Is there fast breathing? Did the child recently choke on something and have difficulty breathing or turn blue? Does the child have a sore throat, hoarseness, or a change in voice? Can the child swallow? Is there drooling or fever?

In the physical examination, count the respiratory rate, note the heart rate, and assess the oxygen saturation for signs of impending respiratory failure. Listen for stridor at rest when the child is calm or an increase in stridor during crying or coughing. Note the phase of the breathing cycle that stridor is heard (during inspiration, expiration, or both). Most cases of acute stridor are inspiratory in nature. Listen for hoarseness, a barky cough, or a muffled voice. Look for retractions, cyanosis, extreme anxiety or confusion, restlessness, drooling, or a sniffing-type posture. With a stethoscope, note air exchange, wheezing, and rales. Determine whether the stridor is acute or chronic.

Angioedema usually presents with facial swelling, urticaria, and a history of similar allergic reactions. Foreign body aspiration can cause stridor, asymmetric breath sounds, or wheezing. The onset is sudden, and upper respiratory infection symptoms and fever are not usually present. An ingested foreign body can rarely lodge in the esophagus and cause upper airway obstruction. A forced expiratory chest film may demonstrate air trapping and possibly a shift of the mediastinum. Bronchoscopy is diagnostic and therapeutic, and should be performed if foreign body is suspected. Assess carefully for tonsillitis or peritonsillar abscess.

Assess the degree of respiratory distress and determine whether it is mild/moderate, severe, or very severe (Table 1). Antibiotics play no role in uncomplicated viral croup. Early corticosteroid treatment appears to modify the course of even mild/moderate viral croup and should be used to reduce the progression of the inflammation and to prevent return for care and/or hospitalization. Corticosteroids may be given orally, intramuscularly, or parenterally. Nebulized corticosteroids may be useful, although oral or intramuscular routes are preferred.

Encourage parents to give fluids to the child with uncomplicated, mild/severe viral croup. Instruct the parents to call or seek medical care if the child develops stridor at rest, has evidence of respiratory distress (retractions), or becomes too ill to drink. Children with croup whose stridor resolves after treatment with nebulized racemic epinephrine in an ambulatory setting should be observed for at least 3 hours before returning home because stridor and respiratory distress frequently recur.

When stridor is moderate to severe and does not respond to traditional therapy, hospitalization in a pediatric ward or pediatric intensive care unit (ICU) should be considered. If acute epiglottitis is suspected, it should be considered an airway emergency and airway visualization should be considered (Figure 1). It is important to assess the risk for acute airway obstruction before attempting to visualize the epiglottis in any patient suspected of having acute epiglottitis to allow for adequate preparation (Table 2). When there is severe distress, inspection of the epiglottis should be done in the operating room by an anesthesiologist whenever possible, with an otolaryngologist or pediatric surgeon available for emergency intubation and/or tracheostomy. In visualizing the epiglottis, it is important to have oxygen, a self-inflating Ambu bag, a laryngoscope, and an appropriately sized endotracheal tube (0.5–1 mm less than expected for the child’s age) available in case the examination precipitates acute upper airway obstruction. Never force a distressed sitting child to lie down. This may compromise the airway and cause immediate obstruction. Lateral neck radiographs should not be taken initially in patients at high risk for acute epiglottitis because of the danger of acute obstruction in the radiology department and the delay in diagnosis and treatment while waiting for the film. The value of lateral neck films as an alternative to direct visualization in cases with a moderate risk for epiglottitis is controversial.

Suspect bacterial tracheitis when croup is complicated by high fever, purulent tracheal secretions, and increasing respiratory distress. This may be the presenting pattern (resembling epiglottitis), or it may present after several days of stridor (secondary bacterial tracheitis). Endotracheal intubation is often necessary. Tracheal secretions should be cultured to allow for appropriate antibiotic therapy. Abundant purulent secretions and pseudomembrane formation require aggressive pulmonary toilet.

In hospitalized children, manage respiratory distress and stridor associated with viral croup with racemic epinephrine and corticosteroids. Corticosteroid treatment shortens the hospital stay. Although humidified mist therapy is used routinely in many centers, its efficacy has not been documented, and tents are a barrier to observation. Viral croup rarely requires endotracheal intubation, although extreme vigilance is required. Heliox (70% helium and 30% oxygen) may prevent intubation in severe cases, although there is not enough evidence to recommend its regular use. Ribavirin therapy is not indicated for viral croup. Always continue to reassess the patient if incomplete response to therapy for secondary infections such as bacterial tracheitis.

Manage acute epiglottitis with intubation in a controlled setting because of the high risk for acute airway obstruction. Initiate antibiotic therapy with an appropriate cephalosporin antibiotic (Table 3). Blood cultures will be positive in more than 50% of the cases caused by H. influenzae type b. Identify extraepiglottic foci of infections, such as pneumonia, septic arthritis, pericarditis, and meningitis. Consider bacterial pathogens other than H. influenzae in a child immunized against H. influenzae type b.

Causes of stridor identified by direct laryngoscopy or bronchoscopy include laryngomalacia, laryngeal web, laryngeal papilloma, redundant folds in the glottic area, and supraglottic masses. Diagnoses associated with pharyngeal or retropharyngeal masses include enlarged adenoids; abscess or cellulitis; benign neoplasms, such as cystic hygroma, hemangioma, goiter, and neurofibroma; and malignant neoplasms, such as neuroblastoma, lymphoma, and histiocytoma. Bronchoscopy can further identify tracheomalacia and/or tracheal compression from a variety of lesions including vascular malformations. Esophagram or barium swallow can also aid in the diagnosis of intrathoracic lesions, which often are characterized by expiratory or fixed stridor.

Discharge children from the hospital when stridor at rest and respiratory distress has resolved and they no longer need oxygen. They should be afebrile, eating well, and appropriately active. Schedule a follow-up visit 24 to 48 hours after discharge. Consider a visiting nurse referral. Instruct the parents to call the physician immediately if stridor or signs of respiratory distress (fast breathing or chest indrawing) return.

Frequently Recurring or Persistent Stridor

Stridor, a harsh, medium-pitched, inspiratory sound associated with obstruction of the laryngeal area or the extrathoracic trachea, is often accompanied by a croupy cough and hoarse voice. Stridor is most commonly observed in children with croup (seeChapter 412); foreign bodies and trauma can also cause acute stridor. A few children, however, acquire recurrent stridor or have persistent stridor from the 1st days or weeks of life (Table 401.5). Most congenital anomalies of large airways that produce stridor become symptomatic soon after birth. Increase of stridor when a child is supine suggestsairway malacia, such as laryngomalacia or tracheomalacia. It is important to note that when evaluating for a specific anatomic cause of abnormal breath sounds, it is not uncommon to identify additional congenital anomalies of the airway. An accompanying history of hoarseness or aphonia suggests involvement of the vocal cords. Associated dysphagia may also suggest a vascular ring. In a child with intermittent stridor (with wheezing) that accompanies physical activity and is not responsive to asthma therapies,paradoxical vocal cord dysfunction may be of consideration. Paradoxical vocal cord dysfunction may be highly supported by history and confirmed by laryngoscopy during an exercise challenge test if symptoms are successfully elicited. Speech therapy and behavior modification may be therapeutic.

Physical examination for recurrent or persistent stridor is usually unrewarding, although changes in its severity and intensity due to changes of body position should be assessed. Anteroposterior and lateral radiographs, contrast esophagography, fluoroscopy, computed tomography (CT), and magnetic resonance imaging (MRI) are potentially useful diagnostic tools. In most cases, direct observation by laryngoscopy is necessary for definitive diagnosis. Undistorted views of the larynx are best obtained with fiberoptic laryngoscopy.

Vocal Cord Palsy and Stridor in MSA

Stridor may occur in up to 30% of patients with MSA. It can be much worse during sleep. A normal laryngeal examination during wakefulness does not rule out the problem.36 The presence of stridor is associated with a poor prognosis (compared with MSA patients without stridor) and has traditionally been managed by tracheostomy. Recently, CPAP has been used to assist with stridor at night.36,37 Patients with MSA often have OSA as well as worsening stridor during sleep. The etiology of stridor is controversial but is likely due to overactivity of the vocal cord adductors (close vocal cords) and underactivity of vocal cord abductors (posterior cricoarytenoid muscles [PCAs]). A neuropathy of the recurrent laryngeal nerves that innervate the PCA muscles may be involved. The syndrome of stridor in many patients is a dystonia rather than vocal cord paralysis. In others, there is complete vocal cord immobility. Sudden death has been reported in MSA patients with stridor even though treated with tracheostomy or CPAP.37,38

Stridor

Stridor, a harsh medium-pitched sound typically heard on inspiration, is caused by turbulent airflow in the upper airway. The phase of respiration in which stridor occurs is helpful in identifying the site of the airway obstruction (see Fig. 3.1). The relative anatomy of the upper airway in an adult versus in an infant is shown in Fig. 3.6. The most common cause of stridor of infants and young children is laryngomalacia, Congenital anomalies should be suspected in children with recurrent or persistent stridor. Acute inspiratory stridor is most commonly caused by acute inflammation/infection, typically croup; however, an acute foreign body aspiration in the upper airway may also cause acute-onset stridor. Epiglottitis is the most serious life-threatening infection in this area and must be identified quickly. A history of prior intubation in a patient with stridor and respiratory distress should raise concern for vocal cord paralysis or subglottic stenosis. An age-related differential diagnosis is noted in Table 3.9. Differentiating features of common disorders are noted in Table 3.10.

3 Stridor

Stridor is a loud, musical sound of definite and constant pitch (usually about 400 Hz) that indicates upper airway obstruction.43,69 It is identical acoustically to wheezing in every way except for two characteristics: (1) stridor is confined to inspiration, whereas wheezing is either confined entirely to expiration (30% to 60% of patients) or occurs during both expiration and inspiration (40% to 70% of patients);73,74 and (2) stridor is always louder over the neck, whereas wheezing is always louder over the chest.74

In some patients with upper airway obstruction, stridor does not appear until the patient breathes rapidly through an open mouth.75

Stridor

Stridor, by definition, is a respiratory noise occurring predominantly in inspiration due to obstruction occurring primarily in the extrathoracic portion of the trachea or laryngeal structures (see SIGNS OF RESPIRATORY DISEASE | General Examination; SIGNS OF RESPIRATORY DISEASE | Lung Sounds). The two most common causes of stridor in children are acute laryngotracheobronchitis, (croup) (see CROUP) and laryngomalacia (see LARYNGITIS AND PHARYNGITIS). Stridor is more common in children due to the smaller size of the trachea where a relatively modest mucosal swelling can result in sufficient airway tracheal narrowing to limit flow during inspiration. Subglottic stenosis is a less common cause of stridor that may arise from congenital lesions; secondary to prolonged or difficult intubation, usually in infants born prematurely; or from subglottic cysts or hemangiomata (see LUNG DEVELOPMENT | Congenital Parenchymal Disorders; LARYNGITIS AND PHARYNGITIS). Stridor with an expiratory component implies more severe obstruction, such that flow limitation is also present in the extrathoracic trachea during expiration or an obstruction extending to the intrathoracic portion of the trachea.