Epiglottitis
Mona Gangar
Emmagene Worley
THE CLINICAL CHALLENGE
Epiglottitis is an acute inflammatory condition of the epiglottis and supraglottic structures that can quickly progress to fatal airway obstruction. Although initially a pediatric condition, the advent and widespread use of the Haemophilus influenzae type B (Hib) vaccine in the 1990s has led to demographic shifts. By 1995, Hib disease levels had declined by more than 95%.1 Because this decrease was mostly caused by the significant decline in pediatric disease, adults now have the higher incidence and mortality. The most recent analysis found a mortality rate of 0.006 per 100 000 in adults and 0.001 per 100 000 in children, the majority in children ages 0 to 3 years. Of the 1187 US deaths from epiglottitis over 39 years, adults accounted for 63.5%.1 Hospital admissions show a similar pattern, with the mean admission age of a patient with epiglottitis of 45 years.2
Whereas children often have dramatic presentations with sudden onset sore throat, drooling, fever, respiratory distress, and tripoding, adults have a slightly more insidious onset, developing symptoms over the prior 24 hours. The most common presenting complaints are sore throat, dysphagia and odynophagia, along with muffled voice, hoarseness, and drooling. Because there is much overlap with common, unobstructive viral upper respiratory infections, the diagnosis of epiglottitis in adults remains challenging. In addition to timely diagnosis, airway management remains a central clinical challenge. Because of the infectious process and edema, the airway is tenuous and has distorted anatomy. This makes intervention more difficult, and even minor interventions can precipitate airway decompensation and laryngospasm.
PATHOPHYSIOLOGY
Acute inflammation and infection of the epiglottis and supraglottic structures lead to the clinical condition of epiglottitis. The microbiology of causative agents has shifted since the Hib vaccine, resulting in more similar adult and pediatric profiles. Streptococcus was the most common pathogen in a recent meta-analysis, found in 22.1% of swab cultures and 10.5% of blood cultures.3 Staphylococcus, other strains of Haemophilus, and Neisseria are also encountered. Most blood cultures do not grow a causative organism, and surface cultures from endoscopy are usually negative.
Of note, caustic or thermal injuries to the epiglottis present identically to infectious epiglottitis. Thermal injury can occur after ingestion of hot foods or beverages, and direct traumatic injury can occur after ingestion of a foreign body or retrieval of that foreign body with blind finger sweeps. Epiglottitis has even been reported owing to traumatic placement of a laryngeal mask airway.4
APPROACH/THE FOCUSED EXAM
When epiglottitis is suspected, great care should be taken with all physical exam maneuvers while maintaining a calm environment. Because the airway is precarious, patients should be evaluated in an environment suitable for managing a difficult airway, and ENT and anesthesia consults should be called immediately for airway support.
In adults, special attention should be paid to sore throat complaints that are disproportionate to physical exam findings. Stridor, voice change, and dyspnea are often later signs and are concerning for impending airway compromise. Tachycardia and tachypnea should be taken seriously as signs of respiratory distress and sepsis. Complications of epiglottitis include abscess formation, sepsis, and exacerbations of other underlying chronic diseases, such as asthma, chronic obstructive pulmonary disease (COPD), or diabetes.
The diagnosis of epiglottitis is clinical, and direct inspection on endoscopy is the gold standard for definitive diagnosis. Edema and erythema of the epiglottis, arytenoids, and aryepiglottic fold are the most common findings (Figure 16.1).
If flexible laryngoscopy is not readily available, imaging studies can aid in making the diagnosis and determining the need for airway intervention. Lateral neck films are low-cost and easily obtained. Radiographic features suggestive of epiglottitis include the thumb sign (Figure 16.2), vallecula sign, thickened aryepiglottic folds, and hypopharyngeal distention. According to two studies, an epiglottic width greater than 5 mm, especially when measured at the base of epiglottis, is the most accurate objective parameter.5,6 It is important to note that lateral neck films are dependent on positioning, and reporting of results is variable, leading to a false-negative rate of approximately 30%.5 Ultrasound has been investigated as a potential diagnostic modality for epiglottitis. In transverse views of the neck, an increase in the anterior-posterior width of the epiglottis and a “P-sign” in longitudinal view at the thyrohyoid membrane have been described.7 Ultrasound, however, suffers from being both operator-dependent for image acquisition and subjective in result interpretation. Computed tomography (CT) and magnetic resonance imaging (MRI) have also been used in this context and can be helpful for identifying associated deep neck space involvement or abscesses (Figure 16.3). However, these should be obtained judiciously—maintaining the airway is of utmost importance, and having the patient lie flat on an imaging table can precipitate further obstruction.
DIFFERENTIAL DIAGNOSIS
The differential diagnosis for epiglottitis includes other conditions affecting the upper airway structures. In adults, it is most often confused with either viral pharyngitis or strep throat. In comparison, epiglottitis is more abrupt in onset and the pain of the sore throat more severe. In children, the differential includes croup, bacterial tracheitis, and foreign body ingestion (Table 16.1).
Figure 16.2: Thumb sign as seen on lateral neck X-ray. Asterisk indicates thickened epiglottis or thumb sign and arrows indicate thickened aryepiglottic fold. (Courtesy of Stephen L. Done, MD, Seattle, Washington and from Iyer R. Upper airway obstruction. In: Iyer R, Chapman T, eds. Pediatric Imaging: The Essentials. 1st ed. Wolters Kluwer; 2016:1-8. Figure 1.5A.) |
TABLE 16.1 Differential Diagnosis Table | |||||||||||||||||||||||||||||||||||||||||||||
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