• Etiologic agents include: Haemophilus influenzae type B (accounted for >90% of cases in pre-vaccine era), Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes (group A b-hemolytic streptococcus), and group C b-hemolytic streptococcus (rare). Candida albicans may be an etiologic agent in immunocompromised patients. Pasteurella multocida has been implicated in a handful of cases after exposure to nasopharyngeal secretions from a cat.
• The inhaled anesthetic, sevoflurane, has been implicated in a few cases of epiglottitis.
• Erythema and edema of the uvula, aryepiglottic folds, arytenoids, epiglottis, and vocal cords include an exudate rich in neutrophils and fibrin, which usually proceed to organization and fibrous scarring.

• Disease due to H. influenzae type B occurs most often between the ages of 2 and 7 years (overall range: infancy to adulthood).
• Epiglottis and other invasive disease (including epiglottitis) secondary to H. influenzae have been reduced by 98% since the introduction of the conjugate vaccines in 1989 (approved at 15 months) and 1990 (approved at 2, 4, and 6 months)
• Year-round occurrence
• Affects boys and girls equally
• All geographic areas
• Rare in populations in which the peak incidence of meningitis is shifted towards infancy (i.e., Alaskan Eskimos, Native Americans)
• Occasional secondary cases in households or daycare centers
• May be more frequent in children with sickle cell anemia, asplenia, immunoglobulin defects, or leukemia
• Disease due to S. pyogenes occurs most often in early school-age children during the winter and early spring.

• Without prompt medical intervention, complete airway obstruction leading to respiratory arrest, hypoxia, and death
• Necrotizing cervical fasciitis (rarely)
• Therapeutic complications include: aspiration, endotracheal tube dislodgment and extubation, tracheal erosion or irritation, pneumomediastinum, pneumothorax, and pulmonary edema.
• Complications of H. influenzae type B bacteremia include: septic shock, pneumonia, cervical lymphadenopathy, and, rarely, arthritis and pericarditis.

• Mortality is estimated at 8% in hospital series.
• Virtually all cases in which arrest occurred prior to transfer to tertiary center resulted in fatality.
• Mortality should approach zero with appropriate airway management.

• Viral laryngotracheobronchitis (croup) with secondary bacterial tracheitis
• Severe parainfluenza or influenza infection
• Peritonsillar or retropharyngeal abscess
• Uvulitis
• Retropharyngeal abscess
• Peritonsillar abscess
• Foreign-body aspiration in a child with an upper respiratory infection
• Upper respiratory infection, including croup, in a child with a congenital or acquired airway problem (e.g., premature infant with subglottic stenosis, laryngeal web, vascular ring, tracheal stenosis)
• Diphtheria: rare in United States
• Laryngeal infections, including laryngeal tuberculosis

• Abrupt onset of high fever (39°C–40°C), sore throat, and dysphagia
• Very limited or no prodrome of mild upper respiratory illness
• Rapid onset of toxicity and respiratory distress
• Cough and hoarseness are late symptoms, if they occur at all.
• Time from onset of symptoms to presentation with progressive respiratory distress is generally less than 12 hours.
• Has the child been immunized against H. influenzae type B?
• How does the child prefer to hold itself? (i.e., sitting upright, leaning forward with chin hyperextended)

• Extremely anxious appearance
• Child prefers to remain sitting up.
• Child often leaning forward with chin hyperextended to maintain airway
• Slow and labored respiratory effort
• Drooling is seen as a manifestation of dysphagia.
• Inspiratory stridor, retractions, and late cyanosis
• Diagnosis can be suspected on history and observation of child’s appearance alone.
• Do not attempt to examine the throat if epiglottitis is a serious consideration.

• CBC: increased white blood cell count with left shift
• Cultures of blood (positive in up to 90%) and epiglottis (only performed in the operating room): may be positive for the causative organism.

• Lateral neck radiograph: showing characteristic “thumb sign” of edematous epiglottis, with narrowing of the posterior airway and ballooning of the hypopharynx

• Airway management: maintain child upright, never supine. Personnel experienced in airway management should accompany the child at all times, including during transport and in radiology.
• Rapid assembly of a team, which should include an anesthesiologist, an otolaryngologist, and a pediatrician, if possible.
• Allow the child to assume his or her most comfortable position (usually in the mother’s arms).
• Oxygen by mask or blown by face
• Transport to operating room as soon as possible for anesthesia and intubation, followed by positive pressure ventilation as necessary.
• Institute intravenous catheterization and blood collection and culturing of epiglottis only after the airway is secured.
• Perform emergent cricothyrotomy if obstruction occurs prior to controlled airway management.
• Use fluid resuscitation in cases of septic shock.

• Empiric antibiotic coverage to include gram-positive cocci and b-lactamase-producing H. influenzae type B. Duration of therapy: 7 to 10 days for all but staphylococcal disease (14–21 days). Switch may be made to oral medication after extubation and resumption of feeding.
• Cefuroxime: 150 mg/kg/d divided every 8 hours
• Ampicillin/sulbactam: 200 mg/kg/d divided every 6 hours
• Chloramphenicol: 75 to 100 mg/kg/d divided every 6 hours
• Ampicillin: 100 to 200 mg/kg/d divided every 6 hours for non-b-lactamase-producing H. influenzae type B (approximately 80% of isolates)
• Penicillin: 100,000 to 200,000 U/kg/d divided every 4 to 6 hours for streptococcal disease
• Oxacillin: 100 to 200 mg/kg/d for staphylococcal disease

• Extubation is usually possible within 24 to 48 hours. Criteria include: decreased epiglottis erythema and edema upon direct inspection, and development of an air leak around the endotracheal tube.
• Defervescence is usually prompt after initiation of appropriate antimicrobial therapy.

• Rifampin: 20 mg/kg/d in single dose for 4 days to eradicate colonization
• Universal immunization with H. influenzae type B capsular polysaccharide conjugate vaccines at 2, 4, and 6 months, with booster at 12 to 18 months

• Prophylaxis for index case and susceptible children in household, child care setting, and intimate contacts

• A radiograph is indicated only when the diagnosis is in doubt, and should not delay airway management.
• Blood collection should be avoided until the airway has been secured, so as not to upset the child unnecessarily.
• Failure to ensure appropriate airway management prior to any other interventions, including laryngeal examination, radiographs, and laboratory studies

Q: What is the incidence of epiglottitis since the introduction of conjugate vaccines against H. influenzae type B?
A: Because H. influenzae type B caused 90% of epiglottitis, and the incidence of all invasive disease due to H. influenzae type B has decreased by 98% in children under 5 years of age, one can estimate that the incidence of epiglottitis has been reduced by almost 90%.

Q: Have there been reports of epiglottitis caused by H. influenzae type B after complete vaccination?
A: Yes, eight cases due to H. influenzae type B were reported in the United States during the 2-year period of 1994 to 1995.

Q: How many of the cases of invasive disease due to H. influenzae type B occur in children with inadequate vaccination?
A: During 1994 and 1995, 47% of children under 4 years of age were too young (aged 5 months or younger) to have completed a primary series with an Hib-containing vaccine. Among children old enough to be fully vaccinated, 63% of those developing disease were undervaccinated, and the remainder (37%) had completed a primary series in which vaccine failed.

Q: Should a fully vaccinated child who develops invasive disease due to H. influenzae type B be tested for an underlying immunodeficiency?
A: Probably. In one study, about one-third of children diagnosed with invasive disease due to H. influenzae type B were found to have a previously undiagnosed immunoglobulin deficiency.

Q: Can epiglottitis recur?
A: Yes, but rarely.

Q: Are corticosteroids of any value in the management of epiglottitis?
A: There appears to be no benefit.

American Academy of Pediatrics. Haemophilus influenzae infections. In: Peter G, ed. 1997 red book: report of the Committee on Infectious Diseases, 24th ed. Elk Grove, IL: American Academy of Pediatrics, 1997:220–230.

Blackstock D, Adderly RJ, Steward DJ. Epiglottitis in young infants. Anesthesiology 1987;67:97–100.

Gonzalez-Valdepena H, Wald ER, Rose E, et al. Epiglottitis and Haemophilus influenzae immunization: the Pittsburgh experience—a 5-year review. Pediatrics 1995;96:424–427.

Grodin M. Epiglottitis. J Emerg Med 1983;1:13–19.

Hickerson SL, Kirby RS, Wheeler JG, Schutze GE. Epiglottitis: a 9-year case review. South Med J 1996;89:487–490.

Wenger JK. Supraglottitis and group A streptococcus. Pediatr Infect Dis J 1997;16:1005–1007.