Acute epiglottitis (supraglottitis) is an acute, rapidly progressive cellulitis of the
epiglottis and adjacent structures that can result in complete—and potentially
fatal—airway obstruction in both children and adults. Before the widespread use
of H.
influenzae type b (Hib) vaccine, this
entity was much more common among children, with a peak incidence at ±3.5years of age. In some countries, mass vaccination
against Hib has reduced the annual incidence of acute epiglottitis in children
by >90%; over the same period, the annual incidence in
adults has changed little. Because of the danger of airway obstruction, acute
epiglottitis constitutes a medical emergency, particularly in children, and
prompt diagnosis and airway protection are of utmost
importance.
Etiology After the introduction of the Hib vaccine, disease
incidence among children in the United States declined dramatically.
Nevertheless, lack of vaccination or vaccine failure have meant that many
pediatric cases seen today are still due to Hib. In adults and (more recently)
in children, a variety of other bacterial pathogens have been associated with
epiglottitis, the most common being group A Streptococcus. Other pathogens seen less frequently include S. pneumoniae, Haemophilus parainfluenzae,
and S.
aureus. Viruses have not yet been established
as a cause of acute epiglottitis.
Manifestations and
Diagnosis Epiglottitis typically
presents more acutely in young children than in adolescents or adults. On
presentation, most children have had symptoms for <24 h, including high fever, severe sore throat,
tachycardia, systemic toxicity, and (in many cases) drooling while sitting
forward. Symptoms and signs of respiratory obstruction may also be present and
may progress rapidly. The somewhat milder illness in adolescents and adults
often follows 1 or 2 days of severe sore throat and is commonly accompanied by
dyspnea, drooling, and stridor. Physical examination of patients with acute epiglottitis
may reveal moderate or severe respiratory distress, with inspiratory stridor
and retractions of the chest wall. These findings diminish as the disease progresses and the patient tires.
Conversely, oropharyngeal examination reveals injection that is much less
severe than would be predicted from the symptoms—a finding that should
alert
the clinician to a cause of symptoms and obstruction that lies beyond the
tonsils. The diagnosis is often made on clinical grounds, although direct
fiberoptic laryngoscopy is frequently performed in a controlled environment
(e.g., an operating room) in order to visualize and culture the typical
edematous “cherry-red” epiglottis and to facilitate placement of an
endotracheal tube. Direct visualization in an examination room (e.g., with a
tongue blade and indirect laryngoscopy) is not recommended because of the risk
of immediate laryngospasm and complete airway obstruction. Lateral neck
radiographs and laboratory tests can assist in the diagnosis but may delay the
critical securing of the airway and cause the patient to be excessively moved
or repositioned, risking further airway compromise. Neck radiographs typically
show an enlarged edematous epiglottis (the “thumbprint sign”), usually with a
dilated hypopharynx and normal subglottic structures. Laboratory tests
typically show mild to moderate leukocytosis with a predominance of
neutrophils. Blood cultures are positive in a significant proportion of cases.
Treatment Security of the airway is always of primary concern in
acute epiglottitis, even if the diagnosis is only suspected. Mere observation
for signs of impending airway obstruction is not routinely recommended,
particularly in children. Many adults have been managed in this way since the
illness is perceived to be milder in this age group, but some data suggest that
this approach may be risky and probably should be reserved only for adult
patients who have yet to develop dyspnea or stridor. Once the airway has been
secured and blood and epiglottis specimens have been obtained for culture,
treatment with intravenous antibiotics
should be given to cover the most likely organisms, particularly H. influenzae. Because rates of ampicillin resistance in this
organism have risen significantly in recent years, therapy with a ß-lactam/ ß
-lactamase inhibitor combination or a second- or third-generation cephalosporin
is recommended. Typically, ampicillin/sulbactam, cefuroxime, cefotaxime, or
ceftriaxone is given, with clindamycin and TMP-SMX reserved for patients
allergic to _-lactams. Antibiotic therapy should be continued for 7
to 10 days and should be tailored, if necessary, to the organism recovered in
culture. If the household contacts of a patient with H. influenzae epiglottitis include an unvaccinated child under the
age of 4, all members of the household (including the patient) should receive
prophylactic rifampin for 4 days to eradicate H. influenzae carriage.
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