Epiglottitis (Supraglottitis)

Epiglottitis — also called supraglottitis — is an acute, potentially life-threatening inflammation of the epiglottis and surrounding supraglottic structures. Once considered a disease almost exclusively of young children caused by Haemophilus influenzae type b (Hib), universal Hib vaccination has transformed the epidemiology: today adults account for the majority of cases, and the causative organisms are more varied. Regardless of age, the hallmark danger is rapidly progressive airway obstruction, making immediate recognition and airway management the cornerstones of care.

Table of Contents

  1. What Is Epiglottitis?
  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. References & Research
  13. Featured Videos

What Is Epiglottitis?

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:

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 — incidence in vaccinated populations fell by more than 90%. 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 has remained relatively stable 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, HIV infection, solid organ transplant recipients, and patients on corticosteroids — carry elevated risk and a more severe clinical course.

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:

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

Non-Infectious Causes

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, TNF-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:

Critical clinical rule in children: do NOT disturb the child's position, do NOT attempt to visualize the pharynx at the bedside, and do NOT attempt venipuncture or any painful procedure 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 must be 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:

Danger Signs and the Rule of No Examination

The following clinical findings predict imminent airway loss and require immediate escalation to a setting capable of surgical airway management:

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, flexible nasopharyngoscopy by an experienced otolaryngologist in a controlled setting with immediate airway backup is the appropriate diagnostic maneuver — but 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 but should never delay airway management in a deteriorating patient. Sensitivity is approximately 80–90% for significant epiglottitis.

CT Neck with Contrast

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. CT does not replace clinical assessment and should only be performed 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:

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 should not delay therapy.

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

Any child with suspected epiglottitis should be taken to the operating room for examination under anesthesia and intubation. The sequence:

  1. Maintain child in position of comfort, allow parent to accompany
  2. Provide supplemental oxygen by face mask if tolerated — do not force
  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:

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

Medical Treatment

Intravenous Antibiotics

Empirical broad-spectrum IV antibiotics should be started as soon as cultures are obtained (or immediately in children before cultures if airway is unstable). Recommended regimens:

De-escalation to organism-directed therapy should follow 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 universally administered to reduce supraglottic edema. 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.

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 must be monitored for rebound worsening ("rebound phenomenon") and should not be discharged 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:

Overall mortality in modern series from high-income countries is less than 1% in adult cases managed in centers with immediate airway expertise. 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

PCV13 and PPSV23 vaccines reduce the burden of pneumococcal upper respiratory tract disease, including pneumococcal epiglottitis, particularly in older adults and immunocompromised patients.

Prompt Treatment of Upper Respiratory Infections

In immunocompromised or diabetic individuals, pharyngitis or tonsillitis not responding to initial therapy warrants early reassessment for supraglottic spread. Early identification prevents progression to epiglottitis.

Awareness in Healthcare Settings

Emergency physicians, pediatricians, and otolaryngologists should maintain a high index of suspicion in any patient with severe sore throat disproportionate to pharyngeal findings, especially with drooling or muffled voice. The differential diagnosis of "sore throat" in an adult that mandates imaging includes epiglottitis, peritonsillar abscess, retropharyngeal abscess, and Ludwig's angina — all require rapid airway assessment.

References & Research

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  2. Carey MJ. Epiglottitis in adults. Am J Emerg Med. 1996;14(4):421–424. PMID: 8768161
  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. PMID: 8989757
  4. Britto J, Habibi P, Walters S, Levin M, Nadel S. Systemic complications associated with bacterial tracheitis. Arch Dis Child. 1996;74(3):249–250. PMID: 8787432
  5. 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. PMID: 14608570
  6. Guldfred LA, Lyhne D, Becker BC. Acute epiglottitis: epidemiology, clinical presentation, management and outcome. J Laryngol Otol. 2008;122(8):818–823. PMID: 18047756
  7. Hammoud K, Iram S, Zafar A, Khan MA. Adult acute epiglottitis from Group A streptococcus. Clin Pract. 2012;2(2):e43. PMID: 24765408
  8. Andreassen UK, Baer S, Nielsen TG, Srensen H, Thomsen J. Acute epiglottitis — 25 years experience with nasotracheal intubation, current management policy and future trends. J Laryngol Otol. 1992;106(12):1072–1075. PMID: 1479245
  9. Lassen HC. A preliminary report on the 1952 epidemic of poliomyelitis in Copenhagen with special reference to the treatment of acute respiratory insufficiency. Lancet. 1953;1(6749):37–41. PMID: 13008383
  10. Hebert PC, Ducic Y, Boisvert D, Lamothe A. Adult epiglottitis in a Canadian setting. Laryngoscope. 1998;108(1 Pt 1):64–69. PMID: 9432068
  11. Isakson M, Hugosson S. Acute epiglottitis: epidemiology and Streptococcus pyogenes serotype distribution in adults. J Laryngol Otol. 2011;125(4):390–393. PMID: 21176253
  12. Ward MA. Emergency department management of acute respiratory infections. Semin Respir Infect. 2002;17(1):65–71. PMID: 11891518

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