Epiglottitis is an acute, potentially life-threatening infection causing inflammation and swelling of the epiglottis and surrounding supraglottic structures, leading to rapid airway obstruction.

Exam domain	One-glance essentials
Definition / diagnosis	Epiglottitis = supraglottic cellulitis — acute inflammation of the epiglottis and aryepiglottic folds due to loose areolar tissue that swells rapidly, causing life-threatening airway obstruction ^[1]^[2] *Medical emergency* — can progress from sore throat to complete airway obstruction within hours; primarily affects children but increasing adult cases in post-vaccine era ^[3]^[4] Swelling limited to supraglottis — tightly bound epithelium at the vocal cords prevents spread to subglottis, distinguishing it from croup ^[5]^[2]
Epidemiology / risks	*Hib was the most common cause in children pre-vaccination; incidence dropped dramatically with Hib vaccination — pre-vaccine peak age 2–4 yr; post-vaccine, epiglottitis in children is now rare and organisms include Strep, Staph, and non-typeable H. influenzae ^[6]^[2] Adults: other organisms (Strep, Staph, non-typeable H. influenzae); risk factors include immunodeficiency, incomplete vaccination, diabetes ^[3]^[7] Poiseuille's law* (resistance ∝ 1/r⁴) explains why children deteriorate faster than adults with equivalent mucosal oedema ^[5]^[1] Recurrent or unusual epiglottitis should prompt investigation for underlying immunodeficiency (check IgG, IgA, IgM) ^[7]
Core mechanism	Bacteraemia (commonly Hib) seeds the epiglottic mucosa → inflammatory oedema of loose supraglottic areolar tissue → rapid narrowing of the supraglottic inlet ^[2]^[1] Progressive oedema → ball-valve obstruction at laryngeal inlet; upright/tripod posture maximises airway diameter; lying flat or agitation precipitates complete obstruction ^[5]^[8] *Blood cultures positive in ~75% of Hib epiglottitis* — confirms bacteraemic spread and risk of metastatic infection (meningitis, septic arthritis, pneumonia) ^[2]^[9]
Clinical picture	*4 D's: Drooling, Dysphagia, Dysphonia (muffled "hot potato" voice), Distress* — all absent in croup, serving as key discriminators ^[10]^[3] Rapid onset high fever, toxic appearance, tripod position, inspiratory stridor, NO barking cough (vs croup's barking cough + hoarse voice) ^[2]^[5] *Do NOT examine the throat with a tongue depressor* in suspected paediatric epiglottitis — risk of precipitating complete airway obstruction ^[4]^[8] Quiet stridor in a worsening child = near-complete obstruction = pre-arrest sign; adults present more indolently with severe sore throat and odynophagia ^[1]^[2]
Investigations	Clinical diagnosis based on the 4 D's in a toxic febrile child; *never delay airway management for investigations* — bloods and cultures taken AFTER airway is secured ^[8]^[2] Gold standard: *direct visualisation of cherry-red swollen epiglottis* — via controlled intubation (children) or flexible nasopharyngoscopy (cooperative adults) ^[1]^[2] Lateral neck X-ray may show the *thumbprint sign, but accuracy is imperfect — a normal film does not* exclude epiglottitis and imaging must not delay airway control ^[11]^[12] AP neck X-ray "steeple sign" = croup (subglottic narrowing), NOT epiglottitis; CT neck reserved for adults with uncertain diagnosis or suspected abscess ^[10]^[2]
Management	*Airway first, everything else second; do NOT agitate the child* — avoid throat exam, lying flat, IV access, or separating from parents until airway is secured in OT ^[8]^[4] *Controlled intubation under inhalational GA (sevoflurane)* maintaining spontaneous ventilation; use ETT 0.5–1 size smaller; *do NOT use LMA* (sits in inflamed supraglottic space) ^[8]^[1] *After the airway is secured: IV third-generation cephalosporin; add anti-MRSA cover only when indicated, then tailor to cultures and local microbiology guidance ^[12] Failed intubation → needle cricothyroidotomy (children) or surgical cricothyroidotomy/tracheostomy; aim extubation at 48–72 hours* after air-leak test confirms oedema resolution ^[8]^[1]
Complications	*Airway obstruction and death* — can occur within hours; the defining must-not-miss complication prevented by early controlled airway management ^[8]^[1] *Epiglottic abscess* — more common in adults; suspect if no improvement after 48–72 h IV antibiotics → CT neck with contrast → surgical drainage ^[2]^[13] *Secondary bacteraemic infections — pneumonia, meningitis, septic arthritis; 3rd-gen cephalosporins provide dual cover including CSF penetration ^[2]^[9] Iatrogenic intubation complications*: accidental extubation (extremely dangerous), post-extubation stridor, subglottic stenosis — minimise intubation duration ^[8]^[1]
Prevention / follow-up	*Hib vaccination* is the most effective preventive strategy; check vaccination status of index patient and all contacts ^[6]^[2] *Rifampicin prophylaxis: 20 mg/kg/day PO × 4 days* for household contacts where there is a child < 4 years who is incompletely immunised against Hib ^[2]^[6] Post-episode: ensure completion of Hib vaccination series; investigate immunodeficiency if recurrent episodes ^[7]^[6]
Exam traps	*A normal lateral neck X-ray does NOT exclude epiglottitis* — diagnosis is clinical; never let imaging delay controlled airway management ^[12]^[11] Confusing epiglottitis with croup: croup has barking cough, hoarse voice, gradual onset, younger age (6 mo–3 yr), steeple sign; epiglottitis has 4 D's, NO cough, toxic child ^[10]^[5] *Examining the throat with a tongue depressor or agitating the child* can convert partial to complete obstruction — the single most dangerous exam mistake ^[4]^[8] Bacterial tracheitis mimics "croup that worsens" — toxic child with purulent tracheal secretions after viral prodrome; requires different management from epiglottitis ^[10]^[2]

References

^[1] Lecture slides: GC 220. Upper airway obstruction and tracheostomy.pdf ^[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.137, 140, 143–144 ^[3] Lecture slides: GC 021. Upper respiratory tract infections.pdf, p.25, 28 ^[4] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.143 ^[5] Lecture slides: Assessment of stridor in children - UpToDate.pdf, p.3, 7 ^[6] Lecture slides: CFB (PAE03) Immunization.pdf ^[7] Lecture slides: Investigations of Imm Disorders 2025.pdf, p.13 ^[8] Senior notes: Ryan Ho Critical Care.pdf, p.10, 12 ^[9] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.147 ^[10] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.144 (DDx table) ^[11] Systematic review: Fujiwara et al. Diagnostic accuracy of radiographs for detecting supraglottitis (2017) ^[12] Guideline: Royal Children's Hospital Melbourne. Sore throat clinical practice guideline (epiglottitis and acute upper-airway obstruction) ^[13] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf, p.259

Epiglottitis

Epiglottitis (also termed supraglottitis) is an acute inflammation of the epiglottis and adjacent supraglottic structures — including the aryepiglottic folds, arytenoids, and valleculae — that can lead to life-threatening airway obstruction ^[1]^[2]. The name breaks down as: "epi-" (upon/above) + "glottis" (the opening between the vocal cords) + "-itis" (inflammation) — literally, inflammation of the structure that sits above the glottis.

Airway obstruction can be rapidly progressive resulting in cardiopulmonary arrest. Prompt recognition and treatment is critical to minimize morbidity and mortality. ^[2]

Why is epiglottitis so dangerous?

The epiglottis and supraglottic tissues are composed of loose areolar connective tissue that swells dramatically when inflamed. Because they sit directly above the narrowest part of the paediatric airway (the subglottis), even modest swelling can reduce the airway calibre to a critical degree within hours. In adults, the airway is slightly larger, but the same principle applies — rapid oedema → obstruction → asphyxia → cardiac arrest.

Epidemiology

Children previously 2–4 years old are most commonly affected but this has changed to 6–12 years old after development of Hib vaccination ^[2].
Occasionally occurs in adults ^[2]. In fact, in the post-vaccine era, the adult-to-child ratio has increased significantly — adults now account for a large proportion of epiglottitis cases in developed countries.
In the pre-vaccine era, incidence was approximately 5 per 100,000 children per year (peak 2–4 years). Post-Hib vaccine, paediatric incidence has dropped by > 90%.

Slight male predominance (M:F ≈ 1.5–2.5:1) in both children and adults.

Hib vaccination was introduced into the Hong Kong Childhood Immunisation Programme in 2007 (as part of the DTaP-IPV/Hib pentavalent vaccine given at 2, 4, 6 months and 18 months). Since then, Hib-related epiglottitis has become rare in Hong Kong children ^[3].
Non-Hib cases still occur — increasingly in adults and immunocompromised patients.
With rising Hib vaccine coverage, the incidence of epiglottitis has shifted from a predominantly paediatric disease to an increasingly adult disease worldwide.

No strong seasonal pattern (unlike croup, which peaks in autumn/winter). This is because the predominant pathogen (Hib) is bacterial, not a seasonal respiratory virus.

Anatomy and Function

Understanding the anatomy is crucial for understanding why epiglottitis is so dangerous and how it presents.

A leaf-shaped elastic cartilage covered by mucous membrane, attached inferiorly to the thyroid cartilage (via the thyroepiglottic ligament) and anteriorly to the hyoid bone (via the hyoepiglottic ligament).
Function: During swallowing, the epiglottis folds posteriorly and inferiorly to cover the laryngeal inlet, diverting food and liquid into the piriform fossae and oesophagus — it is the "trapdoor" that protects the airway during deglutition.
The lingual (anterior) surface of the epiglottis is covered by stratified squamous epithelium (which is tightly bound to cartilage), while the laryngeal (posterior) surface is covered by respiratory (pseudostratified ciliated columnar) epithelium overlying loose areolar submucosa.

Aryepiglottic folds: Mucosal folds running from the lateral edges of the epiglottis to the arytenoid cartilages. They form the boundaries of the laryngeal inlet.
Arytenoid cartilages: Paired cartilages that attach to the vocal cords; involvement causes pain on phonation.
Valleculae: Two pockets between the base of the tongue and the anterior surface of the epiglottis (the "vallecula epiglottica"). This is the space where the tip of a Macintosh (curved) laryngoscope blade sits during intubation.
False vocal cords (vestibular folds): May also become oedematous in supraglottitis.

The supraglottic submucosa on the laryngeal surface of the epiglottis and aryepiglottic folds is composed of loose areolar connective tissue — unlike the tightly bound tissue on the lingual surface. This loose tissue:

Has high capacity for fluid accumulation (oedema)
Swells rapidly and dramatically during inflammation
Can double or triple the thickness of the epiglottis within hours

This is the pathophysiological basis for the rapidity of airway obstruction in epiglottitis.

Feature	Paediatric Airway	Adult Airway
Shape	Funnel-shaped (narrowest at subglottis — cricoid ring)	Cylindrical (narrowest at glottis)
Epiglottis	Omega (Ω)-shaped, floppier, angled more posteriorly	Flatter, more rigid
Submucosal tissue	Looser, more vascular → swells more readily	Less loose
Airway diameter	Smaller absolute diameter → small amount of oedema causes proportionally greater obstruction (Poiseuille's law: resistance ∝ 1/r⁴)	Larger diameter, more reserve

Poiseuille's Law and Airway Obstruction

According to Poiseuille's law, airway resistance is inversely proportional to the fourth power of the radius. So if 1 mm of circumferential oedema reduces a 4 mm paediatric airway to 2 mm, resistance increases by 16-fold (2⁴/1⁴ → (4/2)⁴ = 16). The same 1 mm of swelling in a 10 mm adult airway (reducing it to 8 mm) increases resistance by only ~2.4-fold. This is why children deteriorate faster.

Aetiology

Organism	Details
Haemophilus influenzae type b (Hib)	MOST common infectious cause of epiglottitis in children ^[2]. Gram-negative coccobacillus; polysaccharide capsule type b is the virulent serotype. Decreased incidence of Hib epiglottitis after introduction of Hib vaccination ^[2].
Staphylococcus aureus	Gram-positive coccus; increasingly important in the post-vaccine era; can cause severe, necrotising supraglottitis ^[2].
Streptococcus pneumoniae	Gram-positive diplococcus; also causes pneumonia, meningitis, otitis media ^[2].
Streptococcus pyogenes (GAS)	Group A Streptococcus; important cause in both children and adults ^[2].
Other bacteria	Non-typeable H. influenzae, Moraxella catarrhalis, Klebsiella, anaerobes (in adults with comorbidities)
Viruses	Parainfluenza, influenza, HSV, EBV, VZV — more commonly associated with croup but can occasionally cause supraglottitis
Fungi	Candida spp. — in immunocompromised patients (HIV, post-transplant, haematological malignancies)

Cause	Mechanism
Thermal injury	Inhalation of hot gases/steam → direct thermal damage to supraglottic mucosa
Chemical/caustic injury	Ingestion or inhalation of caustic substances
Foreign body	Lodged in vallecula or supraglottic region → mechanical irritation + secondary infection
Crack cocaine / illicit drug inhalation	Direct thermal and chemical irritation
Post-radiation	Mucositis and oedema in patients receiving radiotherapy for head and neck cancers
Angioedema	Hereditary or ACE-inhibitor–induced angioedema can mimic or cause supraglottic swelling

Risk Factor Category	Examples
Age	Children 2–12 years (varies with vaccination status); adults with comorbidities
Vaccination status	Unvaccinated or incompletely vaccinated against Hib — single most important risk factor in children
Immunocompromised	HIV/AIDS, haematological malignancies, post-transplant immunosuppression, asplenia, complement deficiencies
Concurrent infections	Recent URTI may predispose to secondary bacterial supraglottitis
SLE/immunodeficiency	Functional asplenia in SLE; primary immunodeficiency states

Hong Kong Immunisation Context

Hib vaccination is part of the Hong Kong Childhood Immunisation Programme (given as DTaP-IPV/Hib at 2, 4, 6, and 18 months) ^[3]. Since its introduction, Hib epiglottitis has become exceedingly rare in vaccinated Hong Kong children. However, cases still occur in unvaccinated children (e.g., new immigrants, vaccine refusal) and adults.

Pathophysiology

Understanding the pathophysiology explains every clinical feature.

Bacteraemia: Hib epiglottitis is typically a bacteraemic illness — blood cultures are positive in ~75% of Hib cases in children. This explains the high fever and toxic appearance, and the risk of seeding other sites (meningitis, septic arthritis, pneumonia).
Cellulitis of the supraglottic structures: Unlike croup (which is a subglottic mucosal oedema), epiglottitis is a supraglottic cellulitis. The inflammation involves the epiglottis, aryepiglottic folds, arytenoids, and sometimes the uvula and base of tongue.
Airway obstruction mechanism: The swollen epiglottis prolapses posteriorly over the laryngeal inlet during inspiration (because negative intrathoracic pressure during inspiration sucks the floppy, oedematous epiglottis downward like a ball-valve). This is why obstruction is primarily inspiratory → producing inspiratory stridor.
Rapid progression: Because of the loose areolar tissue and rich blood supply in the supraglottic region, oedema can progress from mild sore throat to complete obstruction in 6–12 hours (sometimes faster in children).
Position of comfort: Patients adopt the "tripod" or "sniffing" position (sitting upright, leaning forward, with neck extended and chin protruded) to maximise the anteroposterior diameter of the supraglottic airway and prevent the swollen epiglottis from completely obstructing the laryngeal inlet. Forcing a child to lie supine can precipitate complete obstruction.

Classification

Infectious epiglottitis (most common): bacterial, viral, fungal
Non-infectious epiglottitis: thermal, chemical, traumatic, angioedema

Stage	Description
Stage 1 — Mild	Sore throat, muffled voice, low-grade fever; no respiratory distress; able to swallow (but painful)
Stage 2 — Moderate	High fever, toxic appearance, drooling, sitting upright; stridor at rest; tachycardia
Stage 3 — Severe	Severe respiratory distress, tripod positioning, cyanosis, altered consciousness, impending arrest

Paediatric epiglottitis: Typically more acute and fulminant; higher risk of rapid complete obstruction
Adult epiglottitis: Often more indolent; sore throat may be predominant for 1–2 days before progression; airway obstruction less common but still possible; higher rate of epiglottic abscess

Clinical Features

The Classic Epiglottitis Presentation

Think of the "3 D's": Dysphagia, Drooling, Distress — in a toxic-looking, febrile child who is sitting upright and leaning forward with a muffled ("hot potato") voice, refusing to lie down. Onset is typically rapid (hours, not days).

Symptom	Pathophysiological Basis
Rapid onset fever (high-grade, > 39°C)	Systemic bacteraemia and release of pyrogenic cytokines (IL-1, IL-6, TNF-α) → hypothalamic set-point elevation. Hib epiglottitis is characteristically a septic, toxic illness.
Severe sore throat / odynophagia	Inflammation and oedema of the epiglottis and surrounding structures → irritation of sensory nerve endings (internal branch of the superior laryngeal nerve, CN X) → pain on swallowing. The pain is often out of proportion to pharyngeal findings on inspection ("sore throat with a normal-looking throat" is a red flag).
Dysphagia	Swollen epiglottis and aryepiglottic folds cannot fold properly during swallowing → pooling of secretions in the hypopharynx → inability to swallow effectively → drooling ^[2]^[4].
Drooling (sialorrhoea)	Consequence of dysphagia — the child cannot swallow their own saliva because: (a) swallowing is extremely painful, and (b) the swollen supraglottic structures physically impede swallowing. Drooling is a hallmark sign and differentiates epiglottitis from croup (where drooling is absent).
Muffled / "hot potato" voice	Oedema of the supraglottic structures (especially aryepiglottic folds) changes the resonance of the pharynx without directly involving the vocal cords → produces a thick, muffled quality (like speaking with a hot potato in the mouth). Note: this is NOT hoarseness (hoarseness = glottic involvement, as in croup) ^[4].
Inspiratory stridor	Swollen supraglottic tissues narrow the laryngeal inlet → turbulent airflow during inspiration → audible stridor. This is an extrathoracic obstruction → dynamic collapse during inspiration (negative intrathoracic pressure sucks floppy, oedematous supraglottic tissue inward). Stridor indicates significant airway narrowing (>50% obstruction).
Respiratory distress / dyspnoea	Progressive narrowing of the airway → increased work of breathing → use of accessory muscles → respiratory distress ^[2]^[4].
Preference for sitting upright / refusal to lie down	Upright posture allows gravity to pull the swollen epiglottis anteriorly, away from the posterior pharyngeal wall, maintaining airway patency. Lying supine allows the oedematous epiglottis to fall posteriorly and obstruct. Children instinctively find this position and become extremely agitated if forced supine.
Anxiety / agitation	Hypoxia and air hunger → sympathetic activation → agitation. This may progress to lethargy (a late and ominous sign indicating hypercarbic respiratory failure).
Absence of spontaneous cough	Unlike croup (where barking cough is prominent), epiglottitis typically presents without significant cough because the inflammation is supraglottic (above the cough reflex trigger zone at the subglottis/trachea). Any cough that occurs is muffled ^[4].

Sign	Pathophysiological Basis
Toxic appearance	Systemic bacteraemia → sepsis physiology → high fever, tachycardia, flushed, ill-looking. Hib epiglottitis produces a more "toxic" child compared to viral croup.
Tripod / "sniffing" position	The child sits upright, leans forward with hands on knees, neck extended, chin protruded, and mouth open — this maximises the anteroposterior diameter of the supraglottic airway. This is a classic posture that should trigger immediate concern for epiglottitis.
Tachycardia	Fever, pain, anxiety, hypoxia → sympathetic drive → increased heart rate.
Tachypnoea	Compensatory mechanism for hypoxia and hypercarbia due to obstructed airflow.
Inspiratory stridor	Turbulent flow through narrowed supraglottic airway during inspiration. A quiet stridor or sudden cessation of stridor in a worsening child is an ominous sign → indicates near-complete obstruction (no airflow = no stridor).
Drooling	Inability to swallow secretions → saliva pools in the mouth and drips from the lips.
Suprasternal and intercostal recession (retractions)	Increased negative intrathoracic pressure generated to overcome the obstruction → visible indrawing of the suprasternal notch, intercostal spaces, and subcostal areas.
Cyanosis	Late sign → severe hypoxaemia → desaturation of haemoglobin → bluish discolouration of lips, tongue, peripheral extremities.
"Cherry-red" swollen epiglottis	If visualised (by experienced clinician during controlled intubation, or on lateral neck X-ray), the epiglottis appears swollen, erythematous, and oedematous — classically described as "cherry-red." Do NOT attempt to visualise the throat with a tongue depressor in a child with suspected epiglottitis — this may precipitate laryngospasm and complete airway obstruction.
Anterior neck tenderness	Palpation over the hyoid/thyroid cartilage region → tenderness due to underlying supraglottic inflammation.
Cervical lymphadenopathy	Reactive lymphadenopathy draining the infected supraglottic region → jugulodigastric and anterior cervical nodes.

CRITICAL: Do NOT Examine the Throat

In a child with suspected epiglottitis, do NOT use a tongue depressor to examine the oropharynx, do NOT attempt direct laryngoscopy at the bedside, and do NOT force the child to lie flat. Any of these manoeuvres may trigger complete airway obstruction via laryngospasm or posterior displacement of the swollen epiglottis. Keep the child calm, in their position of comfort (usually sitting on parent's lap), and arrange for controlled airway management in the operating theatre by an experienced anaesthetist/ENT surgeon.

This is a very high-yield comparison for exams ^[1]^[2]^[4]^[5].

Feature	Epiglottitis	Croup
Age	2–6 years (pre-vaccine); 6–12 years (post-vaccine)	6 months – 3 years (peak 1–2 years)
Aetiology	Hib (most common); other bacteria	Parainfluenza virus (most common); other viruses
Onset	Rapid (hours) — fulminant	Gradual (days) — prodrome of coryza
Fever	High (>39°C), toxic	Low-grade to moderate
Cough	Absent or muffled	Barking cough (seal-like) ^[4]
Voice	Muffled / "hot potato"	Hoarse (due to subglottic oedema involving vocal cords) ^[4]
Stridor	Inspiratory	Inspiratory (may be biphasic)
Drooling	Present	Absent
Dysphagia	Present	Absent
Position	Sitting, leaning forward (tripod)	May prefer to be held upright, but less specific
Appearance	Toxic, anxious, still	Miserable but not toxic
Preceding URTI	Absent or minimal	Present (1–3 days of coryza)
Site of obstruction	Supraglottic	Subglottic
Lateral neck X-ray	"Thumbprint sign" (swollen epiglottis)	"Steeple sign" (subglottic narrowing) on AP view
Response to nebulised adrenaline	Poor / not indicated as primary treatment	Good (first-line for moderate-severe croup)
Airway management	Intubation often required	Rarely requires intubation

Acute epiglottitis: H. influenzae type b infection of epiglottis esp affecting children resulting in rapid onset fever, dysphonia, dysphagia and respiratory distress (medical emergency) ^[4]

Tracheolaryngobronchitis (croup): viral subglottic infection leading to fever, hoarseness and stridor ^[4]

Epiglottitis sits within the broader differential of upper airway obstruction and stridor ^[5]^[6].

Causes of upper airway obstruction include: ^[5]

Depressed consciousness (tongue falls back)
Intraluminal: secretions, blood, vomitus, foreign body aspiration
Mural: infections (tonsillitis, peritonsillar/retropharyngeal abscess, epiglottitis, croup), trauma, tumour, oedema (anaphylaxis, angioedema, post-op), laryngospasm
Extramural: penetrating neck injury, tumour, oesophageal foreign body

Assessment of stridor should be systematic, evaluating for the above causes. Key features that distinguish epiglottitis from other causes of stridor include: the toxic appearance, rapid onset, drooling, dysphagia, muffled voice, and absence of barking cough ^[1]^[6].

Inability to speak = life-threatening (airway, breathing or neurologically compromised) ^[5]

For completeness and to contextualise epiglottitis within ENT, the larynx is divided into three regions ^[7]:

Division	Boundaries	Relevance to Epiglottitis
Supraglottic	Epiglottis → false vocal cords	This is where epiglottitis occurs
Glottic	True vocal cords (± 1 cm above and below)	Involved in croup (subglottic component)
Subglottic	Below vocal cords → inferior border of cricoid	Croup primarily affects this region

The larynx extends from the epiglottis superiorly to cricoid cartilage inferiorly and includes supraglottic larynx, glottic larynx and subglottic larynx ^[7].

Special Considerations

Increasingly common relative to children in the post-vaccine era.
Presentation may be more indolent: severe sore throat predominates for 1–2 days before respiratory symptoms develop.
Complete airway obstruction is less common but still occurs (adult airway is larger and less compliant).
Epiglottic abscess is more common in adults — may require surgical drainage.
Organisms: Streptococcus spp., Staphylococcus aureus, non-typeable H. influenzae, polymicrobial.
Flexible nasopharyngoscopy (fibreoptic laryngoscopy) can be performed in cooperative adults to confirm the diagnosis (unlike in children where this is contraindicated at the bedside).
All adults with epiglottitis still warrant close airway monitoring (ideally in an ICU or high-dependency setting).

Consider fungal epiglottitis (Candida, Aspergillus) in severely immunocompromised patients.
May have atypical organisms or polymicrobial infection.
May have blunted fever response.

High Yield Summary

Epiglottitis = supraglottic cellulitis — inflammation of the epiglottis and aryepiglottic folds due to loose areolar tissue that swells rapidly.
Hib is the most common cause in children; incidence has dropped dramatically with Hib vaccination.
Post-vaccine era: age shifted from 2–4 to 6–12 years in children; increasing proportion of adult cases.
Classic presentation: rapid onset, high fever, toxic, drooling, dysphagia, muffled voice, tripod position, inspiratory stridor, NO barking cough (vs croup).
Medical emergency — can progress from sore throat to complete airway obstruction in hours.
Do NOT examine the throat with a tongue depressor in suspected paediatric epiglottitis — risk of precipitating complete obstruction.
Lateral neck X-ray: "thumbprint sign" (swollen epiglottis); AP neck X-ray: "steeple sign" = croup, not epiglottitis.
Management priority: secure the airway first (controlled intubation in OT) → IV antibiotics (3rd-gen cephalosporin) → supportive care.
Poiseuille's law explains why children deteriorate faster (resistance ∝ 1/r⁴).
Adults: more indolent presentation, epiglottic abscess more common, flexible nasopharyngoscopy can be performed in cooperative adults.

Active Recall - Epiglottitis (Clinical Features & Pathophysiology)

^[1] Lecture slides: Assessment of stridor in children - UpToDate.pdf ^[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.143 ^[3] Lecture slides: CFB (PAE03) Immunization.pdf ^[4] Senior notes: Ryan Ho Respiratory.pdf, p.48 ^[5] Senior notes: Ryan Ho Critical Care.pdf, p.6 ^[6] Lecture slides: GC 220. Upper airway obstruction and tracheostomy.pdf ^[7] Senior notes: MBBS Final MB (Surgery) (Felix PY Lai).pdf, p.259

Differential Diagnosis of Epiglottitis

The clinical challenge with epiglottitis is that it presents as acute upper airway obstruction with stridor, fever, and respiratory distress — a constellation shared by several other conditions. The differential diagnosis is therefore best framed around the question: "What else could cause acute stridor and/or severe sore throat with airway compromise in a child (or adult)?"

The key to differentiating these conditions lies in understanding where in the airway the pathology sits (supraglottic vs glottic vs subglottic vs extrathoracic), how fast it progresses, and which clinical features are present or absent.

The differential of epiglottitis falls into two overlapping clinical presentations:

Acute stridor / upper airway obstruction (the airway emergency DDx)
Severe acute sore throat with systemic toxicity (the ENT/infectious DDx)

Differential diagnosis of acute upper airway obstruction ^[2]^[8]:

Croup
Diphtheria
Bacterial tracheitis
Peritonsillar or retropharyngeal abscess
Foreign body aspiration
Tonsillar and adenoid hypertrophy
Laryngomalacia (floppy larynx)
Angioedema (anaphylaxis or hereditary)

Sore throat — Emergency: acute epiglottitis (drooling of saliva). Serious causes: bacterial tonsillitis, abscess (quinsy), TB, lymphoma. Pitfalls: postnasal drip, irritation, foreign body, infectious mononucleosis. ^[9]

Hoarseness — Serious causes: acute epiglottitis, croup, carcinoma of the larynx. ^[9]

Detailed Differential Diagnoses

This is the single most important differential because it is far more common than epiglottitis and the two conditions present with stridor in young children, yet they require completely different management ^[2]^[4]^[8].

Feature	Why it differs from Epiglottitis
Site	Subglottic (below the vocal cords at the cricoid ring) — vs supraglottic in epiglottitis ^[2]. The cricoid is a complete cartilaginous ring that cannot expand, so subglottic mucosal oedema causes significant narrowing.
Aetiology	Parainfluenza virus (types 1 and 3 most common); also RSV, influenza, adenovirus — viral, NOT bacterial ^[4]
Age	6 months – 3 years (peak 1–2 years) — younger than epiglottitis ^[2]
Onset	Gradual over days with preceding coryzal prodrome (runny nose, mild cough for 1–3 days) ^[2]
Fever	Low-grade (< 38.5°C) ^[2]
Cough	Seal-barking cough — characteristic loud, brassy cough due to subglottic oedema vibrating the vocal cords ^[2]^[4]
Voice	Hoarse — because the subglottic inflammation extends to involve the vocal cords directly ^[2]^[4]
Drooling	Absent — the child can swallow because the supraglottic structures are normal ^[2]
Dysphagia	Absent ^[2]
Appearance	Relatively well-looking — miserable but not toxic ^[2]
Stridor	Loud, harsh, and rasping — vs soft and whispering in epiglottitis ^[2]
X-ray	AP neck: "Steeple sign" (inverted V of subglottic narrowing) ^[1]^[8]. Lateral: normal epiglottis, distended hypopharynx, subglottic haziness.
Treatment	Nebulised adrenaline + oral/IM dexamethasone (responds well)

The 4 D's of Epiglottitis vs Croup

Epiglottitis (4D's): Drooling, Dysphagia, Dysphonia (muffled "hot potato" voice), Distress — these are all absent in croup ^[2]. This mnemonic is the fastest way to differentiate the two at the bedside. Add a 5th D: Death (rapid progression to arrest if not managed).

Why is the cough different?

In croup, the subglottic oedema directly involves the vocal cords → the cords vibrate abnormally during coughing → producing the characteristic seal-barking cough and hoarse voice. In epiglottitis, the vocal cords are spared (inflammation stops at the tightly bound epithelium at the vocal cord level) ^[2] → no barking cough, no hoarseness. Instead, the swollen supraglottic structures change the resonance chamber above the cords → muffled, "hot potato" voice.

Feature	Explanation
Concept	Secondary bacterial infection of the trachea, often following viral croup. Think of it as "croup that doesn't get better or suddenly worsens".
Aetiology	Staphylococcus aureus (most common), Streptococcus pneumoniae, Moraxella catarrhalis, H. influenzae
Age	Similar to croup — typically < 6 years
Key differentiator from epiglottitis	Productive cough with purulent secretions (thick mucopurulent tracheal exudates/pseudomembranes); preceding croup-like illness that worsens despite treatment; high fever and toxic appearance (similar to epiglottitis); does NOT typically have drooling or dysphagia
Why it's dangerous	Thick tracheal secretions and pseudomembranes can cause sudden complete obstruction; one of the most frequent paediatric airway emergencies requiring ICU admission ^[1]
X-ray	Subglottic narrowing (like croup) + irregular tracheal soft tissue densities (pseudomembranes); epiglottis normal

Feature	Explanation
Concept	Suppurative infection of the retropharyngeal lymph nodes and space, located posterior to the pharynx and anterior to the prevertebral fascia
Age	Most common in children 2–4 years — because retropharyngeal lymph nodes involute by age 6 ^[1]
Key features	Fever, dysphagia, drooling, unwillingness to move neck (neck stiffness/torticollis — because neck extension stretches the inflamed retropharyngeal space), muffled "hot potato" voice, inspiratory stridor ^[1]
Why it mimics epiglottitis	Shares drooling, dysphagia, muffled voice, fever, and stridor. However, retropharyngeal abscess has neck stiffness/torticollis (child holds neck in extension or refuses to move it), and on physical examination, midline or unilateral swelling of the posterior pharyngeal wall may be seen ^[2]
Differentiator	Neck stiffness + posterior pharyngeal wall swelling; slower onset (days, not hours); X-ray: retropharyngeal space > 7 mm anterior to C2 or > 14 mm anterior to C6 ^[1]
Risk	Rupture → aspiration of pus → aspiration pneumonia; extension to mediastinum → mediastinitis

Feature	Explanation
Concept	Collection of pus between the tonsillar capsule and the pharyngeal constrictor muscle, typically a complication of tonsillitis/pharyngitis
Age	Peaks in children > 10 years and adolescents/young adults (when streptococcal pharyngitis is more common) ^[1]
Key features	Severe unilateral sore throat, fever, muffled "hot potato" voice, trismus (difficulty opening the mouth — because the pterygoid muscles adjacent to the abscess are in spasm), drooling, deviation of the uvula to the contralateral side, tonsillar asymmetry ^[2]
Why it mimics epiglottitis	Shares muffled voice, drooling, fever, and dysphagia. However, peritonsillar abscess has trismus (epiglottitis does NOT cause trismus), unilateral tonsillar swelling with uvula deviation (visible on oropharyngeal exam — which IS safe to perform in peritonsillar abscess, unlike epiglottitis), and onset is more gradual (preceded by tonsillitis).

Feature	Explanation
Concept	Toxin-mediated infection by Corynebacterium diphtheriae, a gram-positive rod. The exotoxin causes local tissue necrosis and systemic toxicity.
Key features	Airway pseudomembrane formation (tough, grey membrane over the pharynx/larynx that bleeds when removed), fever, sore throat, extensive cervical lymphadenopathy ("bull's neck appearance") ^[4], rarely peripheral neuritis and myocarditis
Why it mimics epiglottitis	Can cause upper airway obstruction via laryngeal pseudomembrane; presents with stridor, fever, and toxicity
Key differentiator	Grey pseudomembrane visible in oropharynx; "bull's neck" cervical lymphadenopathy; slower onset; travel history or unvaccinated (diphtheria vaccination is part of DTaP in HK); cardiac and neurological complications
Diagnosis	Throat swab and PCR for toxins ^[4]
Treatment	Antitoxin + macrolide/penicillins ^[4]

Diphtheria in Hong Kong Context

Diphtheria is extremely rare in Hong Kong due to universal DTaP vaccination. However, it should be considered in unvaccinated individuals (e.g., recent immigrants from endemic areas, vaccine refusers). Always ask about vaccination history.

Feature	Explanation
Concept	Aspiration of a foreign body (food, small toy) that lodges in the airway (supraglottic, glottic, subglottic, or bronchial)
Age	Typically 6 months – 3 years (oral exploratory phase)
Key features	Sudden onset choking episode while eating or playing; no fever (unless secondary infection develops); no prodrome; may have unilateral decreased breath sounds or wheeze (if bronchial); stridor if supraglottic/glottic
Why it mimics epiglottitis	Can cause acute stridor and respiratory distress. However, foreign body aspiration has a clear history of choking, no fever, no toxic appearance, and abrupt onset without preceding illness.
Key differentiator	History of witnessed choking event; absence of fever and toxicity; may have no systemic features at all initially; chest/neck X-ray may show radio-opaque FB or unilateral air trapping

Feature	Explanation
Concept	Angioedema = swelling of deep dermis, subcutaneous/submucosal tissue. Can be allergic (mast cell–mediated), hereditary (C1-esterase inhibitor deficiency), or drug-induced (ACE inhibitors). Anaphylaxis = severe systemic allergic reaction.
Key features	Rapid onset (minutes to hours); swelling of lips, tongue, uvula, larynx; stridor; urticaria (if allergic); hypotension (if anaphylaxis); no fever (unless infection coexists)
Why it mimics epiglottitis	Supraglottic oedema causing stridor and dysphagia. However, angioedema/anaphylaxis has no fever, no toxic appearance, and is associated with urticaria, allergen exposure, or ACE inhibitor use.
Key differentiator	Allergen exposure history; urticaria/angioedema of face/lips; hypotension; no fever; very rapid onset (minutes); responds to IM adrenaline

Feature	Explanation
Concept	"Floppy larynx" — congenital condition where supraglottic structures (especially the aryepiglottic folds and epiglottis) are abnormally soft and prolapse into the airway during inspiration ^[2]
Key features	Chronic inspiratory stridor since birth (or shortly after); worse with feeding, crying, and supine position; generally well-appearing; normal cry; no fever; usually self-limiting (resolves by 12–18 months)
Why it mimics epiglottitis	Supraglottic obstruction causing inspiratory stridor. However, laryngomalacia is chronic and present since birth, the child is well and afebrile, and there is no acute deterioration (unless there is a superimposed infection).

Feature	Explanation
Concept	Paradoxical adduction of the vocal cords during inspiration — a functional (non-organic) disorder. Also called vocal cord dysfunction (VCD).
Key features	Recurrent acute episodes of dyspnoea and stridor; may be misdiagnosed as asthma ^[1]; typically in adolescents/young adults; associated with anxiety; resolves spontaneously; no fever
Key differentiator	Recurrent episodes; no fever; no toxicity; normal between episodes; diagnosis by laryngoscopy showing paradoxical vocal cord movement

In adults presenting with severe sore throat and potential airway compromise, also consider:

Condition	Key Differentiating Features
Ludwig's angina	Submandibular space infection → floor of mouth elevation, "woody" induration of submandibular region, tongue protrusion; usually from dental infection
Parapharyngeal abscess	Lateral neck swelling, trismus, medial displacement of tonsil/lateral pharyngeal wall; high fever; may follow dental/tonsillar infection
Laryngeal carcinoma	Chronic progressive hoarseness in an older patient (typically male, smoker); no fever; weight loss; may present with stridor if advanced ^[9]
Infectious mononucleosis	EBV infection → severe pharyngitis with exudates; massive tonsillar hypertrophy can occasionally compromise airway; splenomegaly, atypical lymphocytes; rarely causes stridor ^[9]

Feature	Epiglottitis	Croup	Bacterial Tracheitis	Retropharyngeal Abscess	Peritonsillar Abscess	Foreign Body	Angioedema
Age	2–12 yr	6 mo–3 yr	< 6 yr	2–4 yr	> 10 yr	6 mo–3 yr	Any
Onset	Hours	Days	Days then sudden ↑	Days	Days	Seconds–minutes	Minutes
Fever	High	Low	High	High	High	None	None
Cough	Absent	Barking	Productive	Variable	Absent	Variable	Absent
Voice	Muffled	Hoarse	Hoarse	Muffled	Muffled	Normal	Normal/muffled
Drooling	Yes	No	No	Yes	Yes	No	Variable
Trismus	No	No	No	No	Yes	No	No
Neck stiffness	No	No	No	Yes	No	No	No
Position	Tripod	Any	Any	Neck extension	Any	Any	Any
X-ray sign	Thumbprint	Steeple	Irregular tracheal densities	Wide retropharyngeal space	N/A	FB visible/air trapping	N/A

High Yield Exam Points — Differential Diagnosis

The 4 D's of epiglottitis (Drooling, Dysphagia, Dysphonia, Distress) differentiate it from croup — all are absent in croup ^[2].
Croup: barking cough, hoarse voice, gradual onset, viral prodrome, younger age (6 mo–3 yr), subglottic → "steeple sign" ^[2].
Bacterial tracheitis: "croup that worsens" — toxic child with productive cough + purulent tracheal secretions after initial viral illness ^[1].
Retropharyngeal abscess: drooling + neck stiffness/torticollis + posterior pharyngeal wall swelling; age 2–4 years ^[1]^[2].
Peritonsillar abscess (quinsy): trismus + unilateral tonsillar swelling + uvula deviation; older child/adolescent ^[1]^[2].
Diphtheria: grey pseudomembrane + "bull's neck" + unvaccinated; ask about DTaP vaccination history ^[4].
Foreign body aspiration: witnessed choking, no fever, no prodrome, sudden onset ^[2].
Angioedema/anaphylaxis: urticaria, allergen exposure, no fever, minutes onset ^[2].
Sore throat — > 90% viral URIs. Emergency = epiglottitis (drooling). Serious = tonsillitis, quinsy, TB, lymphoma. ^[9]
The "thumbprint sign" on lateral neck X-ray = epiglottitis; "steeple sign" on AP neck X-ray = croup ^[1]^[8].

Active Recall - Differential Diagnosis of Epiglottitis

References

^[1] Lecture slides: Assessment of stridor in children - UpToDate.pdf ^[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.137, 140, 143–144 ^[4] Senior notes: Ryan Ho Respiratory.pdf, p.48 ^[8] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.144 (DDx table) ^[9] Lecture slides: GC 021. Upper respiratory tract infections.pdf, p.25, 28

Diagnostic Criteria, Algorithm & Investigations for Epiglottitis

Epiglottitis does not have a formal set of "diagnostic criteria" in the way that rheumatic fever (Jones criteria) or SLE (ACR/EULAR criteria) does. Instead, the diagnosis is made on a clinical basis — pattern recognition of the classical constellation of features — confirmed by direct visualisation of the swollen epiglottis and/or lateral neck radiography.

The practical diagnostic framework can be summarised as:

Clinical Diagnosis = High Clinical Suspicion + Supportive Findings

Component	Details
1. Clinical Presentation	Rapid onset (hours) of high fever, toxic appearance, sore throat, drooling, dysphagia, muffled voice, inspiratory stridor, tripod posture — the 4 D's: Drooling, Dysphagia, Dysphonia, Distress ^[2]
2. Direct Visualisation	Cherry-red, swollen epiglottis seen at controlled intubation in the operating theatre (children) or via flexible nasopharyngoscopy (cooperative adults). This is the gold standard for confirmation.
3. Lateral Neck Radiograph	"Thumbprint sign" — a swollen, rounded epiglottis replacing the normal thin, leaf-shaped shadow; enlarged aryepiglottic folds and ballooned hypopharyngeal airway ^[1]
4. Supporting Investigations	Leukocytosis, positive blood cultures (especially in Hib epiglottitis), elevated inflammatory markers

Clinical Diagnosis First, Investigations Second

In a child with suspected epiglottitis, the priority is AIRWAY MANAGEMENT, not investigations. Do NOT delay securing the airway to obtain blood tests or X-rays. If the clinical picture is classical and the child is in distress, proceed directly to the operating theatre for controlled intubation. Investigations are obtained after the airway is secured. A lateral neck X-ray is only appropriate if the diagnosis is uncertain and the child is stable enough to be accompanied by an airway-competent clinician to radiology.

The algorithm below reflects the real-world decision pathway: clinical assessment first → secure the airway → then investigate.

Key Principle: The diagnostic algorithm is fundamentally an airway management algorithm. The diagnosis is confirmed at the time of securing the airway (direct visualisation during intubation), not before. Investigations serve to identify the causative organism and guide antibiotic therapy, not to make the initial diagnosis.

Investigation Modalities

Investigations in epiglottitis serve three purposes:

Confirm the diagnosis (when uncertain)
Identify the causative organism (to guide targeted antibiotic therapy)
Assess for complications (bacteraemia, concurrent infections)

The investigations are presented in the order of clinical priority.

Why this investigation? — A non-invasive way to visualise the epiglottis without examining the throat directly. Only appropriate when the diagnosis is uncertain and the child is stable.

Feature	Details
Indication	Uncertain diagnosis; child stable enough for imaging; MUST be accompanied by clinician capable of emergency intubation
Technique	True lateral projection; patient upright (NEVER supine); neck in slight extension; during inspiration (to maximally silhouette the epiglottis against the air column)
Normal appearance	Epiglottis appears as a thin, finger-like projection — the "little finger" sign

Key findings in epiglottitis:

Finding	Description & Pathophysiological Basis
"Thumbprint sign" (thumb sign)	The normal thin, leaf-shaped epiglottis is replaced by a thickened, rounded, club-shaped shadow resembling a thumbprint. This occurs because the epiglottis is massively oedematous due to the inflammatory cellulitis in the loose areolar submucosa. ^[1]^[2]
Enlarged aryepiglottic folds	The aryepiglottic folds, normally thin mucosal folds, become thickened and prominent due to oedema — further narrowing the supraglottic airway. ^[1]
Ballooned hypopharyngeal airway	The hypopharynx (piriform fossae area) becomes distended with trapped air because the swollen supraglottic structures act as a partial obstruction, causing air to pool above the level of obstruction. ^[1]
Loss of the vallecula air space	Normally, the vallecular space (between the base of the tongue and epiglottis) is aerated. In epiglottitis, the swollen epiglottis obliterates this space.
Normal subglottic region	Unlike croup, the subglottis appears normal — swelling is stopped by the tightly bound epithelium at the level of the vocal cords ^[2]

Sensitivity of Lateral Neck X-ray

As many as 70% of patients with epiglottitis may have radiographic findings interpreted as normal ^[1]. Therefore, a normal lateral neck X-ray does NOT exclude epiglottitis. If clinical suspicion is high, proceed with direct visualisation regardless of X-ray findings. The X-ray is a supportive investigation, not a definitive one.

Comparison — Croup X-ray findings (for contrast):

AP neck X-ray: "Steeple sign" — inverted V-shaped narrowing of the subglottic airway (because the subglottic mucosa is oedematous within the rigid cricoid ring)
Lateral neck X-ray: normal epiglottis, distended hypopharynx, subglottic haziness ^[1]

This is the gold standard for confirming the diagnosis.

Method	Context	Details
Direct laryngoscopy during intubation	Children	Performed in the OT under inhalational general anaesthesia (typically sevoflurane). The swollen, cherry-red epiglottis is directly visualised as the laryngoscope blade is inserted. The senior anaesthetist proceeds to intubate (usually with a tube 0.5–1 size smaller than age-predicted due to supraglottic narrowing).
Flexible nasopharyngoscopy (fibreoptic laryngoscopy)	Cooperative adults	A thin flexible fibreoptic scope is passed through the nose to the nasopharynx, allowing visualisation of the supraglottic structures. Can be performed at the bedside in adults but intubation equipment must be immediately available in case of airway deterioration. Shows erythematous, oedematous epiglottis and aryepiglottic folds.

NEVER Do This in Children

Do NOT attempt to visualise the epiglottis in a child with a tongue depressor or direct laryngoscopy at the bedside ^[2]. This may trigger laryngospasm or complete airway obstruction. Direct visualisation should ONLY occur in the controlled setting of an operating theatre with full anaesthetic and surgical airway capability.

Why? — Hib epiglottitis is characteristically a bacteraemic illness. Blood cultures are positive in approximately 75% of children with Hib epiglottitis and help identify the causative organism for targeted antibiotic therapy.

Feature	Details
Timing	Obtained after the airway is secured (during or after intubation). Do NOT delay airway management to draw blood cultures.
Expected findings	Growth of H. influenzae type b (most common in unvaccinated children), S. aureus, Streptococcus spp.
Clinical significance	Positive blood cultures confirm bacteraemic epiglottitis; guide de-escalation of antibiotics from empiric to targeted therapy. Also raise concern for metastatic seeding — if blood cultures are positive, consider concurrent meningitis, septic arthritis, or pneumonia.

Feature	Details
Why?	Assess for leukocytosis (indicating bacterial infection) and evaluate for anaemia or thrombocytopenia (suggesting sepsis)
Expected findings	Leukocytosis is common — typically elevated WBC with neutrophil predominance (left shift), consistent with acute bacterial infection ^[2]. However, the WBC count can be low, normal, or high ^[2] — a normal WBC does not exclude the diagnosis.
Interpretation nuance	A low WBC in a toxic child is actually a more ominous finding — may indicate overwhelming sepsis with bone marrow exhaustion.

CBC with differentials: Leukocytosis is common but the WBC count can be low, normal or high. Neutrophil or lymphocyte predominance may be present. ^[2]

Marker	Expected Finding	Clinical Utility
CRP	Elevated (often markedly, > 100 mg/L in severe bacterial infection)	Non-specific marker of inflammation; helps distinguish bacterial (high CRP) from viral (low CRP) aetiology; useful for monitoring treatment response
ESR	Elevated	Less useful acutely (rises and falls slowly); generally not ordered in the acute setting
Procalcitonin	Elevated in bacterial infection	More specific for bacterial infection than CRP; can help distinguish bacterial epiglottitis from viral croup if diagnosis is uncertain

Feature	Details
When?	Obtained at the time of intubation — the anaesthetist or ENT surgeon swabs the surface of the epiglottis before or during intubation
Why?	Directly identifies the causative organism from the site of infection; may be positive even when blood cultures are negative
Findings	Culture and sensitivity of the pathogenic organism (Hib, S. aureus, Streptococcus spp., etc.)

Feature	Details
Pulse oximetry	Continuous monitoring; desaturation (SpO₂ < 92%) indicates significant hypoxaemia and critical airway compromise — a late finding. Avoid agitating the child by applying the probe; if possible, apply while the child is on the parent's lap.
ABG	Generally obtained after the airway is secured. May show: respiratory acidosis (↑PaCO₂ — from hypoventilation due to obstruction), hypoxaemia (↓PaO₂), and metabolic acidosis (lactic acid from tissue hypoperfusion in severe cases).
Interpretation	Type II respiratory failure (hypoxaemic + hypercarbic) is expected in severe obstruction — the patient cannot ventilate adequately due to the physical obstruction.

Feature	Details
Indication	NOT first-line for epiglottitis — reserved for adults with uncertain diagnosis or when abscess formation is suspected (epiglottic abscess, retropharyngeal abscess). Also useful when the differential includes retropharyngeal or parapharyngeal abscess.
Findings in epiglottitis	Diffuse soft tissue swelling of the epiglottis and aryepiglottic folds; thickened epiglottis ("thumbprint" on sagittal reformats); narrowed airway lumen; may show rim-enhancing abscess if epiglottic abscess has formed.
Findings in retropharyngeal abscess	Widened retropharyngeal space (> 7 mm anterior to inferior border of C2, or > 14 mm anterior to inferior border of C6 ^[1]); ring-enhancing fluid collection; cervical retroflexion.
Safety	Only if patient is stable with a secure airway (or in mild cases in adults). A child with severe respiratory distress should NEVER be sent to CT.

Investigation	Rationale
Throat swab / nasopharyngeal aspirate	May help identify viral pathogens if a viral aetiology is suspected (atypical presentation); also to identify concurrent viral–bacterial co-infection
Lumbar puncture	Consider in young children with Hib bacteraemia — Hib can also cause meningitis. If there are features of meningitis (altered consciousness, neck stiffness, bulging fontanelle), LP should be performed after the airway is secured and the child is stabilised.
Chest X-ray	To exclude concurrent pneumonia (especially in Hib bacteraemia with respiratory signs beyond the upper airway)
Hib antigen detection	Can be performed on blood or urine; rapid diagnostic test but less commonly used now

Investigation	Timing	Key Finding	Sensitivity/Limitation
Lateral neck X-ray	Pre-intubation (if stable + uncertain Dx)	Thumbprint sign, enlarged aryepiglottic folds, ballooned hypopharynx	Up to 70% may be normal ^[1]; supportive, not definitive
Direct visualisation	During intubation (OT) or fibreoptic scope (adults)	Cherry-red swollen epiglottis	Gold standard; diagnostic
Blood cultures	Post-airway securing	Positive in ~75% of Hib cases	Identifies organism; guides antibiotic de-escalation
CBC with differential	Post-airway securing	Leukocytosis with neutrophilia (variable)	WBC can be low, normal, or high ^[2]
CRP / Procalcitonin	Post-airway securing	Elevated	Non-specific; useful for monitoring
Epiglottic swab	During intubation	Pathogen identification	High yield from site of infection
ABG	Post-airway securing	Respiratory acidosis, hypoxaemia	Indicates severity of ventilatory failure
CT neck with contrast	If abscess suspected or uncertain Dx in adults	Soft tissue swelling; abscess formation	NOT first-line; only in stable patients

Feature	Epiglottitis	Croup
Best X-ray view	Lateral neck	AP neck
Pathognomonic sign	"Thumbprint sign" (swollen epiglottis)	"Steeple sign" (subglottic narrowing)
Epiglottis	Thickened, rounded	Normal
Subglottis	Normal	Narrowed (oedematous subglottic mucosa within rigid cricoid ring)
Hypopharynx	Ballooned (air trapping above obstruction)	Distended
Limitation	70% may appear normal ^[1]	Signs not consistently present ^[1]

High Yield Summary — Diagnosis & Investigations

Epiglottitis is a CLINICAL diagnosis — pattern recognition of the 4 D's in a toxic, febrile child. Formal diagnostic criteria do not exist.
Gold standard confirmation: Direct visualisation of a cherry-red swollen epiglottis — during controlled intubation (children) or flexible nasopharyngoscopy (adults).
Lateral neck X-ray: "Thumbprint sign" = swollen epiglottis; enlarged aryepiglottic folds; ballooned hypopharynx. BUT up to 70% may be interpreted as normal — a normal X-ray does NOT exclude epiglottitis.
Never delay airway management for investigations. Blood cultures, CBC, CRP, and epiglottic swab are obtained AFTER the airway is secured.
Blood cultures positive in ~75% of Hib epiglottitis — confirms bacteraemia and guides targeted antibiotics. Also prompts screening for metastatic infection (meningitis, septic arthritis).
CBC: leukocytosis common but WBC can be low, normal, or high.
CT neck: reserved for uncertain diagnosis in adults or if abscess is suspected — NOT first-line.
AP neck X-ray "steeple sign" = croup (subglottic), NOT epiglottitis.
Swelling is stopped by the tightly bound epithelium at the level of the vocal cords ^[2] — explains why the subglottis is normal on X-ray in epiglottitis.

Active Recall - Diagnosis & Investigations of Epiglottitis

References

^[1] Lecture slides: Assessment of stridor in children - UpToDate.pdf, p.3, 7 ^[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.137, 140, 143–144 ^[4] Senior notes: Ryan Ho Respiratory.pdf, p.48 ^[9] Lecture slides: GC 021. Upper respiratory tract infections.pdf, p.25, 28

Management of Epiglottitis

The management of epiglottitis is governed by one absolute priority:

Maintaining airway patency is of utmost importance and should be the initial action preceding diagnostic tests when epiglottitis is suspected. ^[2]

Everything else — antibiotics, blood cultures, IV access — comes after the airway is secured. Think of it as a two-phase approach:

Phase 1 (Emergency): Secure the airway
Phase 2 (Definitive): Treat the infection + supportive care + prevent spread

Phase 1: Emergency Airway Management

This is the most critical phase. Deterioration can occur rapidly regardless of the apparent severity of disease at the time of diagnosis. ^[2]

Action	Rationale
Keep the child calm	Agitation increases oxygen demand and can worsen dynamic airway obstruction (increased negative intrathoracic pressure during forceful inspiration sucks the oedematous epiglottis further into the airway).
Allow position of comfort (usually sitting upright on parent's lap)	The upright/tripod position uses gravity to keep the swollen epiglottis anterior, away from the posterior pharyngeal wall, maintaining airway patency.
Do NOT examine the oral cavity	Risk of triggering laryngospasm and precipitating complete airway obstruction ^[2].
Do NOT lie the child supine	Supine position allows the oedematous epiglottis to prolapse posteriorly → complete obstruction.
Do NOT place IV lines or perform anxiety-provoking interventions	Anxiety-provoking interventions such as IV line placement, placing child supine, direct inspection of oral cavity should be avoided until airway is secured. ^[2]
Administer supplemental oxygen	Only if it can be given without agitating the child — e.g., "blow-by" oxygen held near the face by the parent. Do NOT strap a mask tightly on a distressed child.
Continuous pulse oximetry	Apply gently, ideally to the toe while the child sits on the parent's lap — minimises disturbance.

Epiglottitis requires a multidisciplinary emergency response:

Team Member	Role
Senior/consultant anaesthetist	Leads airway management; performs inhalational induction and intubation
ENT surgeon	Stands by for surgical airway (tracheostomy) if intubation fails
Paediatric intensivist / PICU team	Post-intubation care, ventilator management, sedation
Paediatrician	Coordinates investigation and antibiotic therapy

The Most Junior Person Should NOT Attempt Intubation

Intubation in epiglottitis is technically extremely difficult — the landmarks are distorted by oedema, the airway is critically narrow, and there is ZERO margin for error. This must be performed by the most senior available anaesthetist. Failed intubation in this context can be rapidly fatal.

This is the preferred approach for all children with suspected epiglottitis and for adults with significant airway compromise.

Step	Details
Setting	Operating theatre — full anaesthetic equipment, surgical airway tray ready
Induction	Inhalational induction with sevoflurane in 100% oxygen. The child breathes spontaneously throughout — NO paralytic agents are given initially because if you paralyse a child with epiglottitis and then fail to intubate, you cannot ventilate them (the floppy, oedematous epiglottis collapses completely when muscle tone is lost). Maintaining spontaneous ventilation is the safety net.
Positioning	Supine only once deeply anaesthetised; slight head-up tilt; "sniffing position" to align oral-pharyngeal-laryngeal axes ^[5]
Direct laryngoscopy	The anaesthetist carefully visualises the supraglottic structures → cherry-red, swollen epiglottis is seen. The epiglottic opening (laryngeal inlet) may appear as a tiny slit or bubble of air emerging from the oedematous tissue.
Intubation	An ETT 0.5–1 size smaller than age-predicted is used (because the supraglottic narrowing will not accommodate a standard-sized tube). Paediatric ETT size = (age/4) + 4 ^[5]. For epiglottitis, use one size smaller.
Epiglottic swab	Swab the surface of the epiglottis for culture and sensitivity at the time of intubation.
Secure the ETT	Tie securely — accidental extubation in a child with epiglottitis can be catastrophic.

Do NOT attempt placement of a supraglottic airway device such as a laryngeal mask airway (LMA) ^[2]. Why? Because the LMA sits in the supraglottic space — the very area that is swollen and inflamed. It will not seal properly, may worsen oedema, and cannot reliably maintain the airway.

Scenario	Action
Cannot intubate, CAN ventilate with BVM	Continue BVM ventilation while preparing for surgical airway. Bag-mask ventilation → Endotracheal tube intubation ^[2] is the sequence. BVM may work temporarily because positive pressure can push the oedematous epiglottis anteriorly.
Cannot intubate, CANNOT ventilate	Surgical airway is indicated — this is a "can't intubate, can't oxygenate" (CICO) emergency ^[2]^[5]

Surgical Airway Option	Details
Needle cricothyroidotomy	Emergency temporising measure — a large-bore cannula (14G) is inserted through the cricothyroid membrane. Provides oxygenation but NOT adequate ventilation. Used as a bridge to definitive surgical airway. Preferred in children < 12 years because formal surgical cricothyroidotomy risks damaging the cricoid (the only complete cartilaginous ring and the narrowest point of the paediatric airway). ^[5]
Surgical cricothyroidotomy	Incision through the cricothyroid membrane; insertion of a small tracheostomy or ETT. More appropriate in adolescents and adults.
Emergency tracheostomy	Definitive surgical airway. The ENT surgeon performs a tracheostomy (incision through the 2nd–4th tracheal rings) if other methods fail. More time-consuming than cricothyroidotomy but provides a more stable and long-term airway. ^[6]

Surgical airway such as cricothyroidotomy is indicated in case endotracheal intubation fails or cannot be accomplished in a timely manner. ^[2]

Phase 2: Definitive Medical Treatment

Once the airway is secured, the focus shifts to treating the underlying infection and preventing complications.

This is the cornerstone of definitive treatment. The choice of antibiotic must cover the likely causative organisms, especially Hib and other common pathogens.

Augmentin + 3rd generation cephalosporin for at least 10 days ^[2]

Antibiotic	Rationale	Dose (Paediatric)
3rd generation cephalosporin (ceftriaxone or cefotaxime)	Excellent activity against Hib (including β-lactamase–producing strains), S. pneumoniae, and Streptococcus pyogenes. Penetrates well into inflamed tissues. "Cef-" = cephalosporin; "tri-" = third; "-axone" = long half-life (once daily dosing). ^[2]	Ceftriaxone 50–100 mg/kg/day IV (max 4g), once or twice daily; or Cefotaxime 150–200 mg/kg/day IV in 3–4 divided doses
Amoxicillin-clavulanate (Augmentin)	Amoxicillin provides broad Gram-positive and some Gram-negative coverage; clavulanate ("clav" = clavulanic acid) is a β-lactamase inhibitor that protects amoxicillin from enzymatic degradation by β-lactamase–producing organisms (e.g., Hib, some S. aureus). ^[2]	90 mg/kg/day IV (of amoxicillin component) in 3 divided doses initially; switch to oral when improving
Vancomycin	Should be used when MRSA is suspected ^[2]. Glycopeptide antibiotic that inhibits cell wall synthesis by binding D-Ala-D-Ala. Indicated when: (a) high local prevalence of MRSA, (b) patient not responding to initial therapy, (c) culture grows MRSA.	15 mg/kg/dose IV every 6 hours; monitor trough levels (target 15–20 µg/mL for serious infections)

Why a 3rd-generation cephalosporin specifically?

Many strains of H. influenzae produce β-lactamase, making ampicillin alone unreliable. 3rd-generation cephalosporins are β-lactamase stable — their molecular structure resists hydrolysis by β-lactamase enzymes. They also achieve excellent CSF penetration, which is important because Hib bacteraemia can seed the meninges (concurrent meningitis must be covered empirically until excluded).

Duration: At least 10 days ^[2]. Typically 7–10 days IV initially, then step down to oral antibiotics (e.g., oral amoxicillin-clavulanate) to complete the course if the child is improving clinically.

De-escalation: Once culture and sensitivity results return (blood cultures, epiglottic swab), narrow the antibiotic spectrum accordingly.

Antibiotic Choice — Exam Summary

Scenario	Antibiotic
Standard empiric	3rd-gen cephalosporin (ceftriaxone/cefotaxime) ± Augmentin
MRSA suspected	Add vancomycin
Culture-directed	Narrow based on sensitivities
Duration	≥ 10 days
Route	IV initially → step down to PO when improving

Feature	Details
Agent	IV dexamethasone (0.5–0.6 mg/kg, max 10 mg)
Rationale	Reduces supraglottic oedema by suppressing the inflammatory cascade (inhibits phospholipase A₂ → decreases prostaglandin and leukotriene synthesis → reduces vascular permeability and oedema). May shorten the duration of intubation and hasten resolution.
Evidence	Evidence is largely extrapolated from croup (where corticosteroids are strongly evidence-based) and from adult supraglottitis studies. Not universally recommended for epiglottitis (unlike in croup), but commonly used in practice.
Timing	Given after the airway is secured; not a substitute for airway management.

Steroids in Epiglottitis vs Croup

In croup, steroids are first-line and dramatically effective (NNT ~5 to prevent return to care). In epiglottitis, the evidence is weaker because epiglottitis is a bacterial cellulitis (not just mucosal oedema) and the primary treatment is antibiotics + airway management. However, many centres use adjunctive dexamethasone to reduce oedema and potentially shorten the intubation period.

Aspect	Details
Sedation	The intubated child requires sedation to tolerate the ETT — typically IV midazolam infusion ± morphine/fentanyl. Inadequate sedation → agitation → risk of accidental self-extubation (which can be fatal in the still-oedematous airway).
Humidified oxygen	Delivered via the ventilator circuit; humidification prevents drying and crusting of airway secretions around the ETT.
Fluid resuscitation	IV maintenance fluids; the child is likely dehydrated from poor oral intake (dysphagia) and increased insensible losses (fever, tachypnoea).
Monitoring	Continuous SpO₂, ECG, BP, temperature. Serial ABGs as needed.
Hand restraints	May be needed (with parental consent) to prevent the child from pulling out the ETT.
Fever management	Paracetamol (antipyretic); avoid NSAIDs in young children (Reye syndrome risk with aspirin; GI/renal concerns with others in dehydrated children).

Feature	Details
Timing	Typically 48–72 hours after intubation — by this time, antibiotics have begun to take effect and supraglottic oedema has usually subsided substantially.
Air leak test	With the ETT cuff deflated (or in uncuffed tubes, simply by listening), positive-pressure ventilation is applied. If air is heard leaking around the ETT, it means the supraglottic swelling has reduced enough to create a gap between the ETT and the airway wall → safe to consider extubation.
Direct visualisation before extubation	Some centres perform flexible laryngoscopy through the nose to directly assess the degree of residual supraglottic swelling before extubation.
Setting	Extubation should occur in a controlled setting (ICU or OT) with re-intubation equipment immediately available.

Phase 3: Prevention & Prophylaxis

Feature	Details
Primary prevention	Hib vaccination is the single most effective preventive measure. In Hong Kong, Hib vaccine is given as part of the DTaP-IPV/Hib pentavalent vaccine at 2, 4, 6, and 18 months ^[3].
Catch-up vaccination	Any unvaccinated or incompletely vaccinated child diagnosed with Hib epiglottitis should receive Hib vaccination before discharge (after recovery from the acute illness).
Effectiveness	Hib conjugate vaccines have reduced the incidence of invasive Hib disease (including epiglottitis) by > 99% in populations with high vaccine coverage.

Rifampin prophylaxis: Haemophilus influenzae type b (Hib) prophylaxis. Dosage = PO 20 mg/kg once a day for 4 days (Max = 600 mg). Indicated for all household members that has a child within the home who is younger than 4 years of age and incompletely immunized (unvaccinated). ^[2]

Feature	Details
Why rifampicin?	Rifampicin ("rif-" = rifamycin derivative; "-ampicin" = broad-spectrum) eradicates nasopharyngeal carriage of Hib. Household contacts of a patient with invasive Hib disease are at increased risk of secondary infection, especially young children who are not fully vaccinated.
Indication	All household contacts where there is a child < 4 years old who is incompletely immunised ^[2]. The index patient should also receive rifampicin before discharge to eradicate their own nasopharyngeal carriage (since 3rd-gen cephalosporins treat the systemic infection but may not reliably eradicate nasopharyngeal carriage).
Dose	Adults: 600 mg PO once daily × 4 days. Children: 20 mg/kg PO once daily × 4 days (max 600 mg). Neonates < 1 month: 10 mg/kg PO once daily × 4 days.
Side effects	Orange-red discolouration of urine, tears, sweat (warn the family); hepatotoxicity (rare); potent CYP450 inducer → multiple drug interactions (e.g., reduces efficacy of oral contraceptives, warfarin).
Contraindications	Severe hepatic impairment; concurrent use of protease inhibitors (HIV treatment).

Rifampicin Prophylaxis — When is it NOT Needed?

If ALL household contacts and children in the household are fully vaccinated against Hib AND are ≥ 4 years old, rifampicin prophylaxis is not required. The risk of secondary disease in fully vaccinated individuals is negligible.

Adult epiglottitis management shares the same principles but differs in some practical aspects:

Aspect	Adult-Specific Considerations
Airway assessment	Flexible nasopharyngoscopy can be performed in cooperative adults to confirm the diagnosis and assess severity — unlike in children.
Intubation	Not always required. Many adults with epiglottitis can be managed with close observation in ICU/HDU + IV antibiotics without intubation, provided there is no severe airway compromise. The adult airway is larger and less prone to complete obstruction.
Indications for intubation in adults	Stridor at rest, severe respiratory distress, inability to manage secretions, rapid progression, epiglottic abscess with impending rupture.
Antibiotics	Same principles: 3rd-gen cephalosporin ± Augmentin; vancomycin if MRSA suspected. In adults, polymicrobial and non-Hib infections are more common.
Steroids	IV dexamethasone is more commonly used in adults (some evidence for reducing oedema and avoiding need for intubation).
Epiglottic abscess	More common in adults. May require CT neck with contrast to confirm, and surgical drainage (needle aspiration or incision & drainage under GA) in addition to antibiotics.
Hib prophylaxis	Generally not needed for adult contacts as adults are not at significant risk of secondary invasive Hib disease.

Treatment	Indication	Contraindication / Caution
Controlled intubation under inhalational GA	All children with epiglottitis; adults with severe airway compromise	Do NOT use IV induction agents with paralysis initially (risk of total airway loss if unable to intubate); do NOT use LMA ^[2]
Needle cricothyroidotomy	CICO emergency; bridge to surgical airway; preferred in children < 12	Not a definitive airway; provides oxygenation only
Surgical cricothyroidotomy / tracheostomy	Failed intubation; cannot intubate cannot oxygenate ^[2]^[5]	Only by experienced surgeon; tracheostomy preferred if ENT surgeon available
IV 3rd-gen cephalosporin (ceftriaxone/cefotaxime)	All confirmed/suspected epiglottitis ^[2]	Cephalosporin allergy (use meropenem or chloramphenicol as alternative)
IV Augmentin (amoxicillin-clavulanate)	Empiric, to broaden Gram-positive coverage ^[2]	Penicillin allergy (true anaphylaxis)
IV Vancomycin	MRSA suspected ^[2]	Monitor for nephrotoxicity and ototoxicity; requires trough level monitoring
IV Dexamethasone	Adjunctive, to reduce supraglottic oedema	Not a substitute for airway management; evidence weaker than in croup
Rifampicin prophylaxis	Household contacts with children < 4 years who are incompletely immunised ^[2]	Severe liver disease; potent CYP inducer (drug interactions); orange discolouration of body fluids
Hib vaccination	All incompletely vaccinated children; catch-up for index patient ^[3]	Severe allergic reaction to previous Hib vaccine dose

High Yield Summary — Management of Epiglottitis

Airway first, everything else second. Do NOT delay airway management for investigations or IV access.
Do NOT agitate the child: avoid examining the throat, lying the child flat, placing IV lines, or separating from parents until airway is secured ^[2].
Do NOT use LMA — it sits in the supraglottic space (the inflamed area) and will not work ^[2].
Controlled intubation under inhalational GA (sevoflurane) in the OT, maintaining spontaneous ventilation until the ETT is placed. Use an ETT 0.5–1 size smaller than predicted.
Failed intubation → needle cricothyroidotomy (children) or surgical cricothyroidotomy/tracheostomy (adolescents/adults) ^[2].
Antibiotics: 3rd-gen cephalosporin (ceftriaxone/cefotaxime) ± Augmentin, for ≥ 10 days. Add vancomycin if MRSA suspected. ^[2]
Adjunctive dexamethasone — commonly used to reduce oedema, but evidence weaker than in croup.
Extubation typically at 48–72 hours — air leak test to confirm resolution of oedema.
Rifampicin prophylaxis: 20 mg/kg/day PO × 4 days for household contacts where there is a child < 4 years who is incompletely immunised ^[2].
Hib vaccination is the most effective preventive strategy; check vaccination status of index patient and contacts ^[3].

Active Recall - Management of Epiglottitis

References

^[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.147 ^[3] Lecture slides: CFB (PAE03) Immunization.pdf ^[5] Senior notes: Ryan Ho Critical Care.pdf, p.7, 9 ^[6] Lecture slides: GC 220. Upper airway obstruction and tracheostomy.pdf

Complications of Epiglottitis

Epiglottitis is a medical emergency not only because of the immediate airway threat, but also because of a cascade of complications that can arise from the disease itself, from the bacteraemia that often accompanies it, and from the interventions used to manage it. Understanding each complication from first principles — why it happens — allows you to anticipate, recognise, and prevent them.

Complications of acute epiglottitis: ^[2]

Airway obstruction and death
Epiglottic abscess
Necrotizing epiglottitis
Secondary infection
- Pneumonia
- Meningitis
- Septic arthritis

These can be organised into three categories:

Local complications (arising from the supraglottic inflammation itself)
Systemic / metastatic complications (arising from bacteraemia)
Iatrogenic complications (arising from intubation and management)

1. Local Complications

Airway obstruction and death ^[2]

This is the most feared and the defining complication of epiglottitis. It is the reason the condition is classified as an ENT emergency ^[10].

Aspect	Explanation
Mechanism	Progressive oedema of the epiglottis and aryepiglottic folds → progressive narrowing of the laryngeal inlet → eventually complete obstruction of the supraglottic airway. During inspiration, negative intrathoracic pressure sucks the floppy, oedematous epiglottis posteroinferiorly like a ball-valve, occluding the laryngeal inlet. Complete obstruction → no airflow → asphyxia → hypoxic cardiac arrest within minutes.
Time course	Deterioration can occur rapidly regardless of the apparent severity of disease at the time of diagnosis ^[2]. A child who appears only mildly distressed can progress to complete obstruction in as little as 30 minutes to several hours.
Risk factors for fatal outcome	Delayed presentation, delayed airway management, agitation of the child (throat examination, forced supine positioning, IV cannulation before airway is secured), very young age (smaller absolute airway diameter → Poiseuille's law), unvaccinated children with Hib (more virulent, more oedema).
Pre-vaccine era mortality	Approximately 6–7% in children, often from sudden complete obstruction before reaching hospital.
Post-vaccine era mortality	< 1% in settings with early recognition and controlled airway management. The dramatic reduction is due to both decreased incidence (vaccination) and improved awareness/airway protocols.
Prevention	Maintaining airway patency is of utmost importance and should be the initial action preceding diagnostic tests ^[2]. Early recognition + controlled intubation in the OT by senior anaesthetist + ENT standby for surgical airway.

Why 'Quiet Stridor' Is Ominous

Stridor is caused by turbulent airflow through a narrowed airway. If a child with epiglottitis who previously had audible stridor becomes quiet — and this is NOT accompanied by clinical improvement — it means the airway has become so narrow that there is almost no airflow at all. No flow = no turbulence = no stridor. This is a pre-arrest sign. Immediate intervention is required.

Epiglottic abscess ^[2]

Aspect	Explanation
Definition	A localised collection of pus within or adjacent to the epiglottis, formed when the supraglottic cellulitis progresses to suppuration and walling-off.
Mechanism	The initial cellulitis (diffuse infection of the loose areolar submucosa) may progress to frank abscess formation, especially if antibiotic therapy is delayed or inadequate, or if the causative organism is particularly virulent (e.g., S. aureus). The loose areolar tissue provides a favourable environment for pus accumulation.
Epidemiology	More common in adults than in children. In the post-vaccine era, as adult epiglottitis has become proportionally more common, epiglottic abscess has become a more recognised complication.
Clinical features	Persistent or worsening symptoms despite appropriate antibiotic therapy; persistent fever; failure to improve after 48–72 hours of IV antibiotics; worsening airway compromise; fluctuant swelling visible on flexible laryngoscopy (adults).
Diagnosis	CT neck with IV contrast — shows a ring-enhancing fluid collection within or adjacent to the epiglottis, with surrounding oedema. Flexible nasopharyngoscopy may show a bulging, fluctuant epiglottis.
Management	Surgical drainage (needle aspiration or incision and drainage under GA with secured airway) + continued IV antibiotics. Drainage is essential because antibiotics alone cannot adequately penetrate an abscess cavity (the abscess wall creates a barrier, and the acidic, hypoxic environment within the abscess impairs antibiotic efficacy).
Risk if untreated	Rupture of the abscess → aspiration of pus into the trachea and lower airways → aspiration pneumonia or acute airway obstruction. Extension to adjacent deep neck spaces (parapharyngeal, retropharyngeal) → deep neck space infection → mediastinitis.

Necrotizing epiglottitis ^[2]

Aspect	Explanation
Definition	Tissue necrosis (death) of the epiglottic cartilage and surrounding soft tissues due to overwhelming infection.
Mechanism	Severe infection → thrombosis of the small vessels supplying the epiglottis → ischaemic necrosis of the epiglottic cartilage. This is analogous to necrotising fasciitis in soft tissues elsewhere. Organisms that produce toxins and tissue-destructive enzymes (e.g., S. aureus producing coagulase and haemolysins; Group A Streptococcus producing streptokinase and hyaluronidase) are most likely to cause this.
Risk factors	Immunocompromised patients (diabetes, HIV, haematological malignancies), infection with virulent organisms (S. aureus, GAS), delayed treatment.
Clinical features	Failure to respond to antibiotics; persistent toxicity; airway compromise; on direct visualisation, the epiglottis appears necrotic (grey-black, sloughing tissue rather than the "cherry-red" of simple cellulitis).
Consequences	Loss of structural integrity of the epiglottis → permanent damage to the epiglottis → chronic aspiration risk (because the epiglottis can no longer fold to protect the airway during swallowing). May require long-term tracheostomy or reconstructive surgery.
Management	Aggressive IV antibiotics (broad-spectrum, including anti-staphylococcal and anti-streptococcal coverage); surgical debridement of necrotic tissue; prolonged airway support (tracheostomy).

2. Systemic / Metastatic Complications

These arise because Hib epiglottitis is characteristically a bacteraemic illness — blood cultures are positive in ~75% of paediatric Hib cases. Bacteria circulating in the bloodstream can seed other organs, causing secondary infections at distant sites.

Pneumonia ^[2]

Aspect	Explanation
Mechanism	Two pathways: (1) Haematogenous seeding — bacteraemia seeds the lungs directly, causing secondary bacterial pneumonia. (2) Aspiration — the child with severe dysphagia may aspirate oral secretions (which are now colonised with the pathogenic organism) into the lower airways, causing aspiration pneumonia. Additionally, rupture of an epiglottic abscess can cause direct aspiration of purulent material.
Organisms	Same as the causative organism of the epiglottitis — Hib, S. aureus, Streptococcus spp.
Clinical features	Persistent or recurrent fever after intubation; new cough or increased sputum production; new crackles/crepitations on auscultation; new infiltrates on CXR.
Diagnosis	CXR (new consolidation or infiltrates); tracheal aspirate for culture (obtained via the ETT); blood cultures if not already positive.
Management	The empiric antibiotic regimen for epiglottitis (3rd-gen cephalosporin ± Augmentin) already covers the likely pulmonary pathogens. Adjust based on culture results.

Meningitis ^[2]

Aspect	Explanation
Mechanism	Haematogenous seeding of the meninges. Hib has a particular tropism for the meninges — the polysaccharide capsule (polyribosylribitol phosphate, PRP) helps the organism evade complement-mediated killing in the bloodstream and cross the blood-brain barrier. Hib meningitis was one of the most common causes of bacterial meningitis in children in the pre-vaccine era.
Why it matters in epiglottitis	A child with Hib epiglottitis and positive blood cultures is at risk of concurrent meningitis. The early signs of meningitis (irritability, lethargy, poor feeding) may be masked by the sedation and intubation required for airway management.
Clinical features to watch for	Altered level of consciousness disproportionate to sedation; persistent high fever despite adequate antibiotics; seizures; bulging fontanelle (in infants); neck stiffness (difficult to assess in an intubated, sedated child).
Diagnosis	Lumbar puncture (LP) — should be performed if there is clinical suspicion of meningitis, but only after the airway is secured and the child is haemodynamically stable. CSF analysis: elevated WBC (neutrophilic pleocytosis), elevated protein, decreased glucose, positive Gram stain/culture.
Management	The 3rd-gen cephalosporins used for epiglottitis (ceftriaxone, cefotaxime) have excellent CSF penetration and are also the first-line treatment for Hib meningitis — so the standard epiglottitis antibiotic regimen already covers this complication. Consider adding dexamethasone before or with the first dose of antibiotics to reduce the inflammatory response in the meninges and decrease the risk of hearing loss (a well-established adjunctive therapy for bacterial meningitis in children).

Why 3rd-Gen Cephalosporins Are Ideal

The choice of ceftriaxone/cefotaxime for epiglottitis is partly because these antibiotics treat not only the epiglottitis itself but also its most dangerous metastatic complication — meningitis. They are β-lactamase stable (covering Hib), achieve high CSF concentrations (crossing the blood-brain barrier), and have a broad spectrum against the common causative organisms. This is a "one drug covers multiple bases" scenario.

Septic arthritis ^[2]

Aspect	Explanation
Mechanism	Haematogenous seeding of a joint space. Bacteria in the bloodstream lodge in the highly vascular synovial membrane, triggering an acute inflammatory response within the joint. The synovial membrane has no basement membrane, making it susceptible to bacterial invasion from the bloodstream.
Joints affected	Large joints — hip, knee, shoulder — are most commonly affected in haematogenous septic arthritis. In children, the hip is a particular concern because the femoral head blood supply courses through the joint capsule, making it vulnerable to damage from intra-articular inflammation.
Clinical features	Acutely swollen, warm, erythematous, exquisitely painful joint; refusal to weight-bear or move the affected limb; fever (which may be attributed to the epiglottitis itself and thus missed).
Diagnosis	Joint aspiration (arthrocentesis) — turbid synovial fluid with elevated WBC ( > 50,000/μL, predominantly neutrophils), positive Gram stain/culture.
Management	IV antibiotics (already being administered for epiglottitis) + orthopaedic referral for joint washout (especially the hip, where delayed treatment can cause avascular necrosis of the femoral head).

Although not listed explicitly in the lecture notes, the following can also occur via haematogenous spread in the context of Hib bacteraemia:

Complication	Mechanism
Pericarditis	Bacteraemic seeding of the pericardium → purulent pericarditis → risk of cardiac tamponade
Cellulitis	Hib bacteraemia can seed the skin/subcutaneous tissue, especially in young children — classically causing a buccal cellulitis (violaceous swelling of the cheek)
Osteomyelitis	Seeding of bone — particularly in growing bones with rich metaphyseal blood supply
Septicaemia / septic shock	Overwhelming bacteraemia → systemic inflammatory response → multi-organ dysfunction → shock

Because virtually all children with epiglottitis require endotracheal intubation, the complications of intubation itself are clinically relevant.

Complication	Mechanism & Explanation
Accidental extubation	The child may self-extubate if inadequately sedated or if the ETT is not properly secured. In epiglottitis, accidental extubation is extremely dangerous because the supraglottic structures are still oedematous → re-intubation may be very difficult or impossible → may require emergency surgical airway. Prevention: adequate sedation, secure ETT fixation, hand restraints with parental consent.
Post-extubation stridor	After removal of the ETT, residual oedema (now both from the original disease AND from the mechanical irritation of the ETT itself) may cause transient stridor. Usually self-limiting; may respond to nebulised adrenaline.
Subglottic stenosis	Prolonged intubation (especially > 7–10 days) or use of an oversized ETT can cause pressure necrosis of the subglottic mucosa → granulation tissue → cicatricial (scar) stenosis. This is why (a) the ETT should be 0.5–1 size smaller than predicted, (b) intubation should be kept as short as possible (aim for extubation at 48–72 hours), and (c) cuffed tubes should have the cuff pressure monitored.
Laryngeal trauma / vocal cord injury	Difficult intubation in a swollen, distorted airway increases the risk of traumatic injury to the vocal cords, arytenoids, or subglottic region. May cause temporary hoarseness or, rarely, permanent voice changes. ^[5]
Endobronchial intubation	If the ETT is advanced too far, it enters the right main bronchus (because it is straighter and more vertical than the left) → left lung atelectasis ± right tension pneumothorax. Prevented by confirming ETT position with capnography and CXR. ^[5]
Oesophageal intubation	Unrecognised oesophageal intubation → no ventilation → progressive hypoxia → death. Confirmed by capnography (absent or very low end-tidal CO₂), absent chest wall movement, gurgling sounds over epigastrium. Capnography (etCO₂) is the MOST RELIABLE method of confirming tracheal tube placement ^[5].
Aspiration	Regurgitation during intubation attempts (especially if RSI technique is used without cricoid pressure) → aspiration of gastric contents → chemical pneumonitis ± aspiration pneumonia.
Ventilator-associated pneumonia	Intubated patients on mechanical ventilation for > 48 hours are at risk of developing pneumonia caused by nosocomial organisms (Gram-negative bacilli, MRSA). Prevention: elevation of head of bed, oral hygiene, subglottic secretion drainage.

Complications of intubation: dental damage, lacerations of lips/gums/tongue/pharynx/oesophagus, laryngeal trauma, oesophageal or endobronchial intubation, accidental extubation, insufficient cuff inflation, laryngospasm or bronchospasm. ^[5]

One important consideration is that epiglottitis — particularly recurrent epiglottitis or epiglottitis caused by unusual organisms — may be the presenting manifestation of an underlying immunodeficiency.

Patient Mr. M: M/46, Caucasian. Referred for low IgG, IgA in 2016. 2011 — epiglottitis. Followed by recurrent neck abscess × 4. ^[11]

This case from the immunology lecture illustrates that a patient presenting with epiglottitis followed by recurrent deep neck infections should raise suspicion for primary immunodeficiency, particularly:

Common Variable Immunodeficiency (CVID) — low IgG and IgA → inability to mount effective antibody responses against encapsulated organisms (including Hib)
IgA deficiency — the most common primary immunodeficiency; IgA is the predominant immunoglobulin in mucosal secretions, so its deficiency predisposes to recurrent upper and lower respiratory tract infections
Complement deficiencies — particularly deficiency of C3 or terminal complement components, which impair opsonisation and killing of encapsulated bacteria

Clinical Pearl — Think About Immunodeficiency

If a patient has epiglottitis + recurrent deep neck infections + low immunoglobulins, think of CVID or other primary antibody deficiencies. This is a high-yield connection between ENT emergencies and immunology. Always check immunoglobulin levels (IgG, IgA, IgM) in patients with recurrent or unusual infections ^[11].

Phase	Complications
Acute (hours)	Airway obstruction and death — can occur at any point before the airway is secured
Early (24–72 hours)	Epiglottic abscess; secondary infections (pneumonia, meningitis, septic arthritis) from ongoing bacteraemia; iatrogenic complications of intubation
Subacute (days to weeks)	Necrotising epiglottitis (if severe or delayed treatment); post-extubation stridor; subglottic stenosis (if prolonged intubation)
Long-term	Permanent epiglottic damage → chronic aspiration risk; subglottic stenosis; vocal cord dysfunction; recurrent infections if underlying immunodeficiency undiagnosed

High Yield Summary — Complications of Epiglottitis

Airway obstruction and death — the defining complication; can occur within hours; prevented by early recognition and controlled airway management ^[2].
Epiglottic abscess — more common in adults; suspect when not improving after 48–72 hours of IV antibiotics; diagnose with CT neck with contrast; requires surgical drainage ^[2].
Necrotising epiglottitis — tissue necrosis from vascular thrombosis in overwhelming infection; risk of permanent epiglottic damage ^[2].
Secondary infections from bacteraemia — pneumonia, meningitis, septic arthritis ^[2]. The 3rd-gen cephalosporins used for epiglottitis also cover meningitis (excellent CSF penetration).
Iatrogenic complications of intubation — accidental extubation (extremely dangerous in epiglottitis), post-extubation stridor, subglottic stenosis, oesophageal/endobronchial intubation ^[5].
Recurrent epiglottitis or unusual infections should prompt investigation for underlying immunodeficiency (check IgG, IgA, IgM) ^[11].
Quiet stridor in a worsening child = near-complete obstruction = pre-arrest sign.
Prevention of complications: early controlled intubation, appropriate antibiotics (≥ 10 days), shortest intubation duration possible (aim extubation at 48–72 hours), Hib vaccination, rifampicin prophylaxis for contacts.

Active Recall - Complications of Epiglottitis

References

^[2] Senior notes: MBBS Final MB (Pediatrics) (Felix PY Lai).pdf, p.147 ^[5] Senior notes: Ryan Ho Critical Care.pdf, p.10, 12 ^[10] Lecture slides: CFB WCS29_Common ENT conditions 2023.pdf, p.45 ^[11] Lecture slides: Investigations of Imm Disorders 2025.pdf, p.13

High Yield Summary

Epiglottitis = supraglottic cellulitis — inflammation of the epiglottis and aryepiglottic folds due to loose areolar tissue that swells rapidly.
Hib is the most common cause in children; incidence has dropped dramatically with Hib vaccination.
Post-vaccine era: age shifted from 2–4 to 6–12 years in children; increasing proportion of adult cases.
Classic presentation: rapid onset, high fever, toxic, drooling, dysphagia, muffled voice, tripod position, inspiratory stridor, NO barking cough (vs croup).
Medical emergency — can progress from sore throat to complete airway obstruction in hours.
Do NOT examine the throat with a tongue depressor in suspected paediatric epiglottitis — risk of precipitating complete obstruction.
Lateral neck X-ray: "thumbprint sign" (swollen epiglottis); AP neck X-ray: "steeple sign" = croup, not epiglottitis.
Management priority: secure the airway first (controlled intubation in OT) → IV antibiotics (3rd-gen cephalosporin) → supportive care.
Poiseuille's law explains why children deteriorate faster (resistance ∝ 1/r⁴).
Adults: more indolent presentation, epiglottic abscess more common, flexible nasopharyngoscopy can be performed in cooperative adults.

High Yield Summary — Diagnosis & Investigations

Epiglottitis is a CLINICAL diagnosis — pattern recognition of the 4 D's in a toxic, febrile child. Formal diagnostic criteria do not exist.
Gold standard confirmation: Direct visualisation of a cherry-red swollen epiglottis — during controlled intubation (children) or flexible nasopharyngoscopy (adults).
Lateral neck X-ray: "Thumbprint sign" = swollen epiglottis; enlarged aryepiglottic folds; ballooned hypopharynx. BUT up to 70% may be interpreted as normal — a normal X-ray does NOT exclude epiglottitis.
Never delay airway management for investigations. Blood cultures, CBC, CRP, and epiglottic swab are obtained AFTER the airway is secured.
Blood cultures positive in ~75% of Hib epiglottitis — confirms bacteraemia and guides targeted antibiotics. Also prompts screening for metastatic infection (meningitis, septic arthritis).
CBC: leukocytosis common but WBC can be low, normal, or high.
CT neck: reserved for uncertain diagnosis in adults or if abscess is suspected — NOT first-line.
AP neck X-ray "steeple sign" = croup (subglottic), NOT epiglottitis.
Swelling is stopped by the tightly bound epithelium at the level of the vocal cords ^[2] — explains why the subglottis is normal on X-ray in epiglottitis.

High Yield Summary — Management of Epiglottitis

Airway first, everything else second. Do NOT delay airway management for investigations or IV access.
Do NOT agitate the child: avoid examining the throat, lying the child flat, placing IV lines, or separating from parents until airway is secured ^[2].
Do NOT use LMA — it sits in the supraglottic space (the inflamed area) and will not work ^[2].
Controlled intubation under inhalational GA (sevoflurane) in the OT, maintaining spontaneous ventilation until the ETT is placed. Use an ETT 0.5–1 size smaller than predicted.
Failed intubation → needle cricothyroidotomy (children) or surgical cricothyroidotomy/tracheostomy (adolescents/adults) ^[2].
Antibiotics: 3rd-gen cephalosporin (ceftriaxone/cefotaxime) ± Augmentin, for ≥ 10 days. Add vancomycin if MRSA suspected. ^[2]
Adjunctive dexamethasone — commonly used to reduce oedema, but evidence weaker than in croup.
Extubation typically at 48–72 hours — air leak test to confirm resolution of oedema.
Rifampicin prophylaxis: 20 mg/kg/day PO × 4 days for household contacts where there is a child < 4 years who is incompletely immunised ^[2].
Hib vaccination is the most effective preventive strategy; check vaccination status of index patient and contacts ^[3].

High Yield Summary — Complications of Epiglottitis

Airway obstruction and death — the defining complication; can occur within hours; prevented by early recognition and controlled airway management ^[2].
Epiglottic abscess — more common in adults; suspect when not improving after 48–72 hours of IV antibiotics; diagnose with CT neck with contrast; requires surgical drainage ^[2].
Necrotising epiglottitis — tissue necrosis from vascular thrombosis in overwhelming infection; risk of permanent epiglottic damage ^[2].
Secondary infections from bacteraemia — pneumonia, meningitis, septic arthritis ^[2]. The 3rd-gen cephalosporins used for epiglottitis also cover meningitis (excellent CSF penetration).
Iatrogenic complications of intubation — accidental extubation (extremely dangerous in epiglottitis), post-extubation stridor, subglottic stenosis, oesophageal/endobronchial intubation ^[5].
Recurrent epiglottitis or unusual infections should prompt investigation for underlying immunodeficiency (check IgG, IgA, IgM) ^[11].
Quiet stridor in a worsening child = near-complete obstruction = pre-arrest sign.
Prevention of complications: early controlled intubation, appropriate antibiotics (≥ 10 days), shortest intubation duration possible (aim extubation at 48–72 hours), Hib vaccination, rifampicin prophylaxis for contacts.

Epiglottitis

Definition

Epidemiology

Age Distribution

Sex Distribution

Geographic / Hong Kong Context

Seasonality

Anatomy and Function

The Epiglottis

Supraglottic Structures

Why the Loose Areolar Tissue Matters

Paediatric vs Adult Airway

Aetiology

Infectious Causes

Non-Infectious Causes

Risk Factors

Pathophysiology

Step-by-Step Pathogenesis

Key Pathophysiological Concepts

Classification

By Aetiology

By Severity (Clinical Staging)

By Age Group

Clinical Features

Symptoms (with Pathophysiological Basis)

Signs (with Pathophysiological Basis)

Comparison: Epiglottitis vs Croup (Viral Laryngotracheobronchitis)

Upper Airway Obstruction Context

Relevant ENT Anatomy: Laryngeal Divisions

Special Considerations

Epiglottitis in Adults

Epiglottitis in the Immunocompromised

Active Recall - Epiglottitis (Clinical Features & Pathophysiology)

References

Systematic Framework for the Differential

Differential Diagnosis Decision Algorithm

Detailed Differential Diagnoses

1. Croup (Viral Laryngotracheobronchitis)

2. Bacterial Tracheitis (Pseudomembranous Croup)

3. Retropharyngeal Abscess

4. Peritonsillar Abscess (Quinsy)

5. Diphtheria

6. Foreign Body Aspiration

7. Angioedema / Anaphylaxis

8. Laryngomalacia

9. Inducible Laryngeal Obstruction (Vocal Cord Dysfunction)

Additional Differential Considerations in Adults

Summary: Key Differentiating Features at a Glance

Active Recall - Differential Diagnosis of Epiglottitis

Diagnostic Criteria

Diagnostic Algorithm

Investigation Modalities

1. Lateral Neck Radiograph (Soft Tissue Lateral Neck X-ray)

2. Direct Visualisation of the Epiglottis

3. Blood Cultures

4. Complete Blood Count (CBC) with Differential

5. Inflammatory Markers (CRP, ESR, Procalcitonin)

6. Epiglottic Surface Swab / Culture

7. Arterial Blood Gas (ABG) / Pulse Oximetry

8. CT Neck with Contrast

9. Additional Investigations (Post-Airway Securing)

Summary Table: Investigations and Their Timing

Radiological Comparison: Epiglottitis vs Croup

Active Recall - Diagnosis & Investigations of Epiglottitis

Overarching Principles

Management Algorithm

Phase 1: Emergency Airway Management

A. Immediate Actions at Presentation

B. Mobilise the Team

C. Controlled Intubation in the Operating Theatre

D. Failed Intubation — Surgical Airway

Phase 2: Definitive Medical Treatment

A. Intravenous Antibiotics

B. Adjunctive Corticosteroids

C. ICU/PICU Management Post-Intubation

D. Assessment for Extubation

Phase 3: Prevention & Prophylaxis

A. Hib Vaccination

B. Rifampicin Chemoprophylaxis for Household Contacts

Management in Adults