Epiglottitis (Supraglottitis)

Table of Contents

1. What Epiglottitis Is
2. Epidemiology: Before and After Hib Vaccine
3. Causes and Pathogens
4. Pathogenesis and Anatomy
5. Symptoms and Clinical Presentation
6. Danger Signs and the Rule of No Examination
7. Diagnosis
8. Airway Management
9. Medical Treatment
10. Complications
11. Prevention
12. Key Research Papers
13. Featured Videos

What Epiglottitis Is

The epiglottis is a leaf-shaped flap of fibroelastic cartilage that sits at the base of the tongue, directly above the laryngeal inlet. During swallowing it folds downward to prevent food and liquid from entering the trachea. When the epiglottis becomes acutely inflamed — along with the aryepiglottic folds and arytenoid cartilages that frame the glottic opening — the resulting edema can narrow or completely obstruct the airway within hours.

The term supraglottitis is more anatomically precise because the inflammation frequently extends beyond the epiglottis to involve the entire supraglottic larynx. However, epiglottitis remains the term most widely used in clinical practice and patient communication.

Key anatomical facts that explain epiglottitis risk:

• The epiglottis occupies the narrowest and most collapsible part of the upper airway
• In infants and toddlers the epiglottis is proportionally larger and the airway lumen smaller, so a small amount of edema produces a disproportionately large reduction in airflow
• The supraglottic mucosa is loosely attached to the underlying cartilage, allowing fluid to accumulate rapidly
• Edema stiffens the epiglottis, impairing its mobility and worsening both airway obstruction and swallowing dysfunction simultaneously

Epidemiology: Before and After Hib Vaccine

Before the conjugate Hib vaccine entered routine pediatric schedules in the late 1980s and early 1990s, epiglottitis was primarily a disease of children aged 2–6 years, with an incidence of approximately 3.5–10 per 100,000 children per year. H. influenzae type b was identified in the majority of cases, and the condition carried significant mortality from sudden, complete airway obstruction.

Following near-universal Hib vaccination, pediatric epiglottitis has become rare in high-income countries. In Sweden the overall rate fell from 4.5 to 0.98 cases per 100,000 people a year in the 16 years after childhood Hib vaccination began (Isakson 2011). In Denmark the rate in children fell to 0.02 cases per 100,000 a year, while the rate in adults stayed steady at about 1.9 per 100,000 a year (Guldfred 2008). The epidemiological center of gravity shifted decisively toward adults, who now constitute 60–80% of cases in most North American and European series. Adult incidence did not fall the same way because the Hib vaccine was introduced for children, not adults, and because adults acquire epiglottitis from a wider range of organisms than Hib alone.

The current adult peak is in the fourth and fifth decades, with men somewhat more frequently affected than women. Immunocompromised individuals — including those with diabetes mellitus, human immunodeficiency virus (HIV) infection, solid organ transplant recipients, and patients on corticosteroids — carry elevated risk and a more severe clinical course.

Several studies find adult epiglottitis becoming more common. In Israel, the yearly rate in adults rose from 0.88 per 100,000 (1986–1990) to 2.1 (1991–1995) and 3.1 (1996–2000), linked to a mix of bacteria rather than Hib (Berger 2003). Among adults seen in US emergency departments, the share with epiglottitis rose from 0.002% in 2014 to 0.005% in 2024, with the steepest rise in people aged 60–74 (O'Brien 2026).

Causes and Pathogens

The etiology of epiglottitis is heterogeneous and has evolved substantially since the Hib vaccine era.

Bacterial Causes (Most Common)

In the post-vaccine era, the bacterial landscape in adults is dominated by:

• Streptococcus pyogenes (Group A Streptococcus): One of the bacteria found in adult epiglottitis. Produces rapid, severe inflammation via superantigens and M protein-mediated host injury.
• Streptococcus pneumoniae: Common cause of respiratory tract infections. A Swedish study (Isakson 2011) concluded that it is the most important bacterial cause of epiglottitis in adults: the rate of pneumococcal epiglottitis in adults rose from 0.1 to 0.28 cases per 100,000 a year, and it was the cause in 10 adults. An Israeli series (Berger 2003) linked the rise in adult cases to a mix of bacteria.
• Staphylococcus aureus: Including methicillin-resistant S. aureus (methicillin-resistant Staphylococcus aureus, MRSA); associated with more severe disease and abscess formation.
• Haemophilus influenzae (non-typeable or type b): Persists as a cause in unvaccinated individuals and immunocompromised adults.
• Klebsiella pneumoniae: More frequent in diabetic and immunocompromised hosts; carries higher complication and mortality rates.
• Pseudomonas aeruginosa: Seen in neutropenic and severely immunocompromised patients.

In pediatric epiglottitis, blood cultures are positive in 60–80% of cases; positive culture rates are lower in adults (20–40%), reflecting more variable pathogen spectrum and possible prior antibiotic use.

Viral Causes

• Herpes simplex virus (HSV-1 and HSV-2): Causes ulcerative supraglottitis, particularly in immunocompromised hosts; responds to acyclovir.
• SARS-CoV-2: Case reports of acute epiglottitis as a presenting manifestation of COVID-19 infection have been documented.
• Other respiratory viruses (parainfluenza, influenza) may trigger or co-infect.

Non-Infectious Causes

• Thermal injury: Steam inhalation, hot liquid ingestion, or smoke inhalation can produce supraglottic edema indistinguishable from infectious epiglottitis.
• Caustic ingestion: Acid or alkali ingestion injures the supraglottic mucosa, producing edema and risk of airway loss.
• Foreign body: Impacted fishbone or other foreign body above the glottis can produce localized edema mimicking epiglottitis.
• Angioedema: Hereditary or drug-induced (particularly ACE-inhibitor-associated) angioedema can cause isolated supraglottic swelling without infection.

In up to one-third of adult cases, no specific pathogen is identified despite thorough microbiological workup.

Pathogenesis and Anatomy

Bacterial epiglottitis follows a rapid sequence from mucosal invasion to life-threatening airway compromise:

1. Mucosal colonization and invasion: Bacteria access the supraglottic mucosa via the respiratory or oropharyngeal route. The epiglottis and aryepiglottic folds — which are normally colonized by upper respiratory commensal flora — become infected with a virulent organism.
2. Acute inflammatory response: The host mounts an intense neutrophilic inflammatory response. Cytokines (interleukin-1, interleukin-6, tumor necrosis factor-alpha) drive rapid vascular permeability, and the loosely adherent supraglottic submucosa fills with inflammatory edema fluid.
3. Mechanical airway obstruction: The swollen epiglottis folds posteriorly (toward the posterior pharyngeal wall) rather than correctly closing over the laryngeal inlet during swallowing. In severe cases, the edematous epiglottis completely occludes the glottic opening during inspiration when negative intraluminal pressure draws the pliable structure downward.
4. Bacteremia and systemic spread: The highly vascular epiglottis provides an entry point for bacteremia, which occurs in a significant minority and can produce septic complications including meningitis and epiglottic abscess.

The "cherry-red epiglottis" seen on direct laryngoscopy reflects the intense hyperemia and edema of the epiglottic mucosa. This finding, once seen, is both diagnostic and an indicator of the degree of vascular engorgement — and the degree of obstruction risk.

Symptoms and Clinical Presentation

The clinical picture differs substantially between children and adults, making awareness of both presentations essential.

Classic Pediatric Presentation (now rare in vaccinated populations)

Children with Hib epiglottitis classically present with a sudden onset over 6–24 hours of:

• High fever (39–40°C), toxic appearance, severe distress
• Drooling — inability to swallow secretions; a key diagnostic sign
• Dysphagia and odynophagia — severe throat pain on swallowing
• Dysphonia ("hot potato voice"): muffled, thick-sounding voice from supraglottic obstruction; distinct from the hoarse or barking voice of croup (subglottic)
• Tripod position: the child sits bolt upright, leaning forward with arms extended behind, chin jutted forward and neck hyperextended — maximizing the effective airway diameter through positioning
• Inspiratory stridor — a late and ominous sign indicating severe airway compromise; hospitals treat its appearance as a signal for immediate airway control

Standard hospital practice in children: the child's position is not disturbed, no one tries to look at the throat at the bedside, and no blood draw or other painful procedure is done before a controlled airway is secured. These maneuvers cause agitation and crying, which dramatically increase airway demand and can precipitate complete laryngospasm with total airway occlusion. The child is taken to the operating room with a parent present and an anesthesiologist and otolaryngologist at the bedside before any examination is performed.

Adult Presentation

Adult epiglottitis typically evolves over 1–2 days and is less acutely dramatic, though the potential for airway loss remains:

• Severe sore throat — disproportionate to pharyngeal exam findings; the classic distinguishing feature in adults is that the pharynx looks relatively normal while the patient has extreme odynophagia
• Odynophagia — pain on swallowing; may be severe enough to prevent oral intake
• Muffled or "hot potato" voice
• Drooling — a sinister sign in adults as in children, indicating inability to handle secretions
• Fever — present in most but not all; absence does not exclude the diagnosis
• Neck tenderness — particularly over the hyoid bone and suprahyoid structures
• Stridor is a late and alarming sign; absence of stridor does not mean the airway is safe

Danger Signs and the Rule of No Examination

The following clinical findings predict imminent airway loss; hospitals treat them as an emergency calling for a setting capable of surgical airway management:

• Inspiratory stridor at rest
• Tripod positioning or refusal to lie flat
• Drooling (inability to manage secretions)
• Rapid progression of symptoms over hours
• Oxygen saturation falling despite supplemental oxygen
• Retractions (intercostal, suprasternal, or supraclavicular)
• Restlessness, agitation, or altered mental status from hypoxia

The rule of no examination applies to any child with suspected epiglottitis: no tongue depressor examination, no attempt to visualize the throat, no venipuncture, no nasopharyngeal swab. In adults, the standard diagnostic step is flexible nasopharyngoscopy by an experienced otolaryngologist in a controlled setting with immediate airway backup — used only in patients not showing signs of imminent obstruction.

Diagnosis

Epiglottitis is primarily a clinical diagnosis confirmed by imaging or direct visualization. The priority sequence is: stabilize the airway first, establish diagnosis second.

Lateral Neck Radiograph

The "thumbprint sign" is the classic radiographic finding: a markedly enlarged, rounded epiglottis on a lateral soft tissue neck film, resembling a thumbprint pressed against the hypopharynx. A normal epiglottis appears thin ("little finger sign") in the same view. Lateral neck films are useful in stable adults; in a deteriorating patient, airway management comes first. Sensitivity is approximately 80–90% for significant epiglottitis.

Computed Tomography Neck with Contrast

Computed tomography (CT) is the most informative imaging study in stable adult patients. It confirms epiglottic thickening (>8 mm is abnormal; normal <5 mm), defines extension to adjacent structures, identifies abscess formation (epiglottic or paraglottic), and evaluates for alternative diagnoses such as peritonsillar or retropharyngeal abscess, Ludwig's angina, or malignancy. Computed tomography does not replace clinical assessment and is done only in stable patients who can be closely monitored.

Flexible Nasopharyngoscopy

In adults without signs of impending obstruction, flexible laryngoscopy performed by an otolaryngologist (with the patient upright, with anesthesia and surgical airway equipment immediately available) directly visualizes the cherry-red swollen epiglottis and assesses the degree of glottic patency. It is both diagnostic and guides the urgency of airway intervention.

Microbiological Studies

Once the airway is secured or in a stable adult, the following cultures are obtained:

• Blood cultures (two sets, before antibiotics if possible) — positive in 20–40% of adults, 60–80% of children
• Throat swab culture — may identify organism if epiglottis is swabbed directly during laryngoscopy, though surface swabs do not reliably reflect the causative pathogen
• Epiglottic culture — obtained if abscess is drained at surgery

Laboratory Studies

Complete blood count typically shows leukocytosis with left shift. C-reactive protein and procalcitonin are elevated and help track treatment response. These tests do not diagnose epiglottitis, and treatment is not held back while waiting for them.

Airway Management

Airway management is the most critical determinant of outcome. The approach depends on the age of the patient and the severity of obstruction at presentation.

Children

Standard practice is to take any child with suspected epiglottitis to the operating room for examination under anesthesia and intubation. The usual sequence:

1. Maintain child in position of comfort, allow parent to accompany
2. Supplemental oxygen by face mask if tolerated — not forced
3. Alert otolaryngology and anesthesia immediately; have tracheotomy equipment at bedside
4. Inhalational anesthesia induction (sevoflurane) with child in sitting position — avoids needle fear response; allows maintenance of spontaneous ventilation
5. Direct laryngoscopy after induction — visualize cherry-red epiglottis, attempt nasotracheal intubation (preferred over orotracheal — more stable and better tolerated in the awake-to-sedated transition)
6. Tracheotomy immediately if intubation fails (rare, <2% of cases in experienced centers)
7. Obtain cultures (blood, epiglottis) after airway secured

Adults

Adults are stratified by clinical severity:

• Mild (no stridor, managing secretions, no retractions): Admission to intensive care unit for continuous monitoring, intravenous (IV) antibiotics, corticosteroids, humidified oxygen. Otolaryngology present with equipment for emergency intubation. Anesthesia on standby. Serial assessments every 30–60 minutes.
• Moderate (stridor at rest, drooling, retractions, rising work of breathing): Immediate preparation for intubation. Awake flexible nasolaryngoscopy to assess glottic patency. Nasotracheal or orotracheal intubation, preferably by experienced otolaryngologist or anesthesiologist with surgical airway backup.
• Severe (cyanosis, impending arrest, cannot maintain position): Emergency surgical airway (cricothyrotomy or tracheotomy), without prolonged intubation attempts.

Extubation is planned after 24–48 hours of intravenous antibiotics when direct inspection confirms edema resolution and there is an audible air leak around the endotracheal tube (indicating airway swelling has subsided).

How Many Adults Need a Breathing Tube

Not every adult with epiglottitis needs a breathing tube. In a Canadian study, a detailed review of 51 adult cases found that 18% were intubated straight away; patients who did not need intubation at first did not later need emergency airway procedures, and breathlessness on arrival (seen in 29%) was the only sign that predicted intubation (Hébert 1998). In a Danish series of 34 adults, 29% needed an artificial airway, breathing distress was linked to needing one, and all patients recovered completely (Guldfred 2008). In a Chinese series of 570 adults, high blood pressure, diabetes, heavy drinking and high inflammation markers in the blood were linked to needing an airway procedure (Shen 2026). The warning signs above — stridor, drooling, tripod posture, breathing distress — remain signs that hospitals treat as an emergency.

Medical Treatment

Intravenous Antibiotics

Hospitals start empirical broad-spectrum intravenous antibiotics as soon as cultures are obtained (or immediately in children before cultures if the airway is unstable). Regimens commonly used:

• Ampicillin-sulbactam (3 g intravenous every 6 hours) — provides coverage for H. influenzae, streptococci, and anaerobes; first-line choice for most adult cases
• Ceftriaxone (2 g intravenous every 24 hours) — appropriate for penicillin-allergic patients (non-anaphylactic allergy)
• Vancomycin (15–20 mg/kg intravenous every 8–12 hours) — added when methicillin-resistant Staphylococcus aureus is suspected (healthcare-associated, prior methicillin-resistant Staphylococcus aureus colonization, no improvement on beta-lactams)
• Clindamycin (900 mg intravenous every 8 hours) — alternative for anaerobic and streptococcal coverage in penicillin-anaphylaxis-allergic patients

Treatment is then narrowed to the organism found once culture and sensitivity results are available. Total antibiotic duration is typically 7–10 days, with transition to oral agents once the patient tolerates oral intake.

Corticosteroids

Intravenous dexamethasone (0.15 mg/kg per dose in children; 10 mg per dose in adults, every 6–8 hours) is widely given to reduce supraglottic edema, though not to everyone: in a 10-year series at a US children's hospital, steroids were given to 63% of patients (Shah 2004). High-quality randomized controlled trial evidence is limited because of the rarity and severity of the condition — most evidence is from observational series and expert consensus. Corticosteroids are generally continued for 24–48 hours or until edema resolves.

A 2026 US study looked back at the records of adults with epiglottitis seen in emergency departments from 2014 to 2024. Those given steroids within 24 hours were about half as likely to need a breathing tube (risk ratio 0.48) and less likely to go to intensive care (risk ratio 0.71); early antibiotics showed a similar link (risk ratio 0.54 for a breathing tube, 0.72 for intensive care). Older age, other illnesses and low oxygen were strong predictors of airway trouble. Because the study compared records rather than randomly assigning treatment, it shows a link, not proof of cause (O'Brien 2026).

Nebulized Racemic Epinephrine

Racemic epinephrine (2.25% solution, 0.5 mL in 2.5 mL normal saline by nebulizer) produces transient alpha-adrenergic vasoconstriction of the supraglottic mucosa, temporarily reducing edema and buying time. Its effect is short-lived (30–90 minutes) — patients are monitored for rebound worsening ("rebound phenomenon") and are not sent home after a single dose in the emergency department. It is a temporizing measure only, not a substitute for definitive airway management.

Supplemental Oxygen and Humidification

Humidified oxygen is delivered by face mask, high-flow nasal cannula, or heliox (70:30 helium-oxygen mixture). Heliox reduces the density of the inspired gas and decreases the work of breathing through a narrowed airway — it may provide several hours of additional stability while definitive treatment is arranged. It does not treat the underlying inflammation.

Complications

Even with appropriate treatment, epiglottitis can produce serious complications:

• Complete airway obstruction and respiratory arrest: The most feared complication; accounts for almost all mortality. Can occur suddenly and without warning, even in patients who appeared stable. Delayed airway obstruction can develop from a few hours to days after admission (Berger 2003). In a Canadian study of 813 adult cases, none of the eight fully documented deaths was a sudden obstruction without earlier breathlessness (Hébert 1998).
• Epiglottic abscess: Suppuration within the epiglottic tissue; may require surgical drainage; typically visible on computed tomography. In an Israeli series of 116 adults, an abscess was found in 29%, 21% and 24% of episodes across three five-year periods (Berger 2003).
• Bacteremia and septic complications: Hematogenous spread can produce meningitis, septic arthritis, pneumonia, and — rarely — pericarditis.
• Pulmonary edema (negative pressure/post-obstructive): Sudden relief of an obstructed airway can be followed by acute pulmonary edema from sudden change in intrathoracic pressure dynamics; requires diuresis and supportive ventilation.
• Tracheotomy scar and subglottic stenosis: Complications of emergency surgical airway; rare in elective tracheotomy but more common in emergency settings.
• Prolonged intensive care unit (ICU) stay and ventilator-associated pneumonia in patients requiring prolonged intubation.

In a Canadian study of 813 adult cases, 1.2% died (Hébert 1998); in a Danish series of 34 adults, all recovered (Guldfred 2008). Mortality in children has fallen from approximately 5–10% in the pre-vaccine era to near-zero in vaccinated populations managed at pediatric centers.

Prevention

Hib Vaccination

The Hib conjugate vaccine (administered as a 3- or 4-dose series in infancy, with a booster at 12–15 months) has been the single most effective intervention in the history of epiglottitis. In countries with high vaccination coverage it has essentially eliminated pediatric Hib epiglottitis. Adults who were not vaccinated in childhood and are at increased risk (asplenia, immunodeficiency) may benefit from Hib vaccination.

Pneumococcal Vaccination

In a Swedish study of adult pneumococcal epiglottitis, 9 of 10 bacterial strains could be typed, and all but one were types covered by the 23-valent pneumococcal polysaccharide vaccine (PPSV23); the authors concluded the infection is preventable by that vaccine (Isakson 2011). The US Centers for Disease Control and Prevention (CDC) schedule (updated February 2026) lists a 4-dose series of the 15- or 20-valent conjugate vaccine (PCV15 or PCV20) for children, and PCV15, PCV20 or PCV21 for all adults 50 and older who have not had a conjugate vaccine; PCV15 is followed by a PPSV23 dose one year later.

Prompt Treatment of Upper Respiratory Infections

In immunocompromised or diabetic individuals, pharyngitis or tonsillitis not responding to initial therapy can be an early sign of supraglottic spread, and early identification can catch it before it progresses to epiglottitis.

Awareness in Healthcare Settings

A severe sore throat out of proportion to what the throat looks like, especially with drooling or a muffled voice, is the classic warning pattern that emergency physicians, pediatricians and otolaryngologists are trained to recognise. The causes of this kind of adult "sore throat" that are checked with imaging include epiglottitis, peritonsillar abscess, retropharyngeal abscess, and Ludwig's angina — all handled with rapid airway assessment.

Key Research Papers

1. Shah RK, Roberson DW, Jones DT. Epiglottitis in the Haemophilus influenzae type b vaccine era: changing trends. Laryngoscope. 2004;114(3):557–560. — PubMed PMID: 15091234
2. Carey MJ. Epiglottitis in adults. Am J Emerg Med. 1996;14(4):421–424. — PubMed PMID: 8768171
3. Damm M, Eckel HE, Jungehulsing M, Roth B. Airway endoscopy in the interdisciplinary management of acute epiglottitis. Int J Pediatr Otorhinolaryngol. 1996;38(1):41–51. — PubMed PMID: 9119592
4. Berger G, Landau T, Berger S, Finkelstein Y, Bernheim J, Ophir D. The rising incidence of adult acute epiglottitis and epiglottic abscess. Am J Otolaryngol. 2003;24(6):374–383. — PubMed PMID: 14608569
5. Guldfred LA, Lyhne D, Becker BC. Acute epiglottitis: epidemiology, clinical presentation, management and outcome. J Laryngol Otol. 2008;122(8):818–823. — PubMed PMID: 17892608
6. Andreassen UK, Baer S, Nielsen TG, Dahm SL, Arndal H. Acute epiglottitis — 25 years experience with nasotracheal intubation, current management policy and future trends. J Laryngol Otol. 1992;106(12):1072–1075. — PubMed PMID: 1487663
7. Hébert PC, Ducic Y, Boisvert D, Lamothe A. Adult epiglottitis in a Canadian setting. Laryngoscope. 1998;108(1 Pt 1):64–69. — PubMed PMID: 9432069
8. Isakson M, Hugosson S. Acute epiglottitis: epidemiology and Streptococcus pneumoniae serotype distribution in adults. J Laryngol Otol. 2011;125(4):390–393. — PubMed PMID: 21106138
9. Ward MA. Emergency department management of acute respiratory infections. Semin Respir Infect. 2002;17(1):65–71. — PubMed PMID: 11891520
10. O'Brien J, Muccio DR, Schrock JW. Association of early steroid and antibiotic therapy with airway outcomes in adult epiglottitis: a 10-year multicenter retrospective cohort study. Acad Emerg Med. 2026;33(4):e70285. — PubMed PMID: 42023439
11. Shen BJ, Tang XL, Li CY, Liu YJ, Yi HL, Yin SK, Su KM, Liu SR. Active emergency management of adult acute epiglottitis: an analysis of 570 cases. World J Otorhinolaryngol Head Neck Surg. 2026 (online ahead of print). — PubMed PMID: 42500078

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Connections

• ENT
• Laryngitis
• Tonsillitis
• Dysphagia
• Laryngeal Cancer
• Vocal Cord Dysfunction
• Sleep Apnea
• Ear Infections
• Sepsis

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