Epiglottitis and deep-neck-space infection

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Epiglottitis is supraglottic inflammation caused by bacteria, less often viral or non-infective injury. Vaccination has reduced Haemophilus influenzae type b disease, but streptococci, staphylococci and H influenzae still cause adult infection. Deep-neck-space infection develops when oral organisms cross tissue planes after tonsillar, dental, salivary or traumatic inoculation.

The shared danger is anatomy: small increases in oedema can narrow the supraglottic airway, while fascial spaces permit infection to track around carotid sheath, jugular vein and mediastinum. Treatment therefore pairs airway control with source control and tissue-active antimicrobials; antibiotics alone cannot drain a mature collection or reverse mechanical obstruction.

Key points

Airway safety comes before diagnostic certainty; keep a distressed patient upright and avoid procedures that may precipitate obstruction.
Adult epiglottitis often presents with severe throat pain, dysphagia, muffled voice and minimal oropharyngeal findings; stridor is a late warning.
Deep-neck infection follows tonsillar, dental, salivary, traumatic or instrument-related infection and may spread between fascial planes into the mediastinum.
Flexible nasendoscopy is performed only by an experienced team where immediate airway rescue is available; unstable patients proceed to controlled airway management.
Contrast CT neck and chest maps deep collections after the airway is secure; imaging must not delay intervention in a deteriorating patient.
Start intravenous ceftriaxone-based or local broad oral-flora treatment after blood cultures when safe, adding anaerobic and resistant-organism cover by source and exposure.
A mature parapharyngeal, retropharyngeal or odontogenic abscess usually requires drainage and removal of the dental or other source.
Review frequently for increasing oxygen need, secretion intolerance, swelling, cranial neuropathy, jugular thrombosis and mediastinal extension.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Respiratory bacterial infection

H influenzae, streptococci and staphylococci infect supraglottic tissue, with organism probability shaped by vaccination, age and immune status.

Dental and tonsillar spread

Odontogenic disease, tonsillitis, salivary infection, trauma and instrumentation seed polymicrobial oral flora into deep fascial spaces.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Supraglottic oedema
Inflammation expands the epiglottis and aryepiglottic tissues within a narrow airway, sharply increasing resistance and work of breathing.
2
Fascial-plane propagation
Loose connective planes allow pus and gas to track around pharynx, carotid sheath and mediastinum beyond visible surface disease.
3
Pressure and necrosis
A walled collection impairs perfusion and antibiotic delivery, while tissue pressure and toxins promote necrosis, thrombosis and sepsis.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Epiglottic phenotypeRed flag

Severe odynophagia, drooling, quiet muffled speech and preference to sit forward with little visible pharyngeal inflammation is a high-risk pattern.

Peritonsillar spreadRed flag

Unilateral throat pain, hot-potato voice, uvular deviation and trismus suggests a peritonsillar collection requiring ENT drainage assessment.

Ludwig anginaRed flag

Bilateral woody submandibular swelling, raised tongue and dental infection creates rapidly worsening airway difficulty.

Deep-space complicationRed flag

Neck stiffness, torticollis, cranial neuropathy, septic emboli or chest symptoms indicates extension beyond superficial pharyngitis.

Red flags requiring action

Stridor, drooling, inability to swallow secretions or exhaustion indicates critical airway narrowing requiring immediate expert control.
Trismus, floor-of-mouth elevation, tongue displacement or rapidly spreading submandibular swelling suggests Ludwig angina and difficult intubation.
Neck swelling with chest pain, crepitus or sepsis can indicate descending mediastinitis and needs urgent cross-sectional imaging after airway safety.
Severe pain with little visible tonsillar change can reflect epiglottitis or a deep parapharyngeal process rather than uncomplicated pharyngitis.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Continuous airway and physiological assessmentFirst step
Why
Detect deterioration before complete obstruction.
Interpretation and limitations
Increasing stridor, secretion intolerance, fatigue, hypoxia or hypercapnia mandates immediate airway intervention; normal saturation does not reassure early.
02
Senior flexible nasendoscopy
Why
Visualise supraglottic oedema in a controlled setting.
Interpretation and limitations
A swollen erythematous epiglottis supports diagnosis, but examination must stop if distress worsens and must have rescue capability.
03
Contrast CT neck and chest
Why
Map abscess, gas, vascular thrombosis and mediastinal spread.
Interpretation and limitations
Perform only after airway stability. A rim-enhancing collection or descending extension changes drainage and operative planning.
04
Blood and deep cultures
Why
Identify bacteraemia and guide narrowing from representative material.
Interpretation and limitations
Take blood cultures before antibiotics when safe and send aspirate or operative tissue; superficial throat swabs do not represent deep infection.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Anaphylaxis or angioedema

Rapid tongue or laryngeal swelling with urticaria, wheeze or exposure history requires immediate adrenaline rather than infection-only management.

Foreign body or tumour

Abrupt choking or progressive dysphagia, weight loss and unilateral findings can obstruct the airway without acute bacterial disease.

Severe tonsillitis or croup

Surface tonsillar inflammation and viral laryngotracheal illness can mimic voice change, but secretion intolerance and adult stridor demand broader airway assessment.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01ASSESSProtect the airwayFirst stepUpper-airway infection is suspected from pain, voice, swallowing or neck findings.

1Keep the patient upright, calm and nil by mouth while experienced anaesthesia and ENT attend with difficult-airway equipment.
2Avoid tongue depression, unnecessary cannulation attempts and unmonitored transfer when obstruction is plausible.
3Obtain rapid observations, glucose and cultures without postponing airway control; use controlled theatre intubation or surgical airway according to anatomy.
4After stabilisation, examine dental, tonsillar, salivary and traumatic sources and choose contrast imaging with the operating team.

02TREATTreat infection and drain the sourceThe airway is secure enough for antimicrobial and source-control treatment.

1Give intravenous ceftriaxone or a locally approved severe upper-airway regimen promptly, adding metronidazole for anaerobic deep-space infection when indicated.
2Drain accessible abscesses and remove the diseased tooth, device or necrotic focus through ENT, maxillofacial or thoracic teams.
3Use ICU observation after airway intervention and extubate only after oedema, leak and endoscopic assessment support safety.
4Narrow antimicrobial therapy to deep cultures and define duration from drainage adequacy, bacteraemia and mediastinal or bone involvement.

03REVIEWReassess anatomy and complicationsSymptoms or physiology fail to improve promptly or new regional signs appear.

1Repeat airway, neck, cranial-nerve, chest and sepsis assessment at short intervals rather than waiting for routine ward review.
2EscalationEscalate persistent fever or swelling to repeat CT and surgical review for an undrained pocket, thrombophlebitis or mediastinitis.
3Check renal, hepatic and concentration monitoring for chosen agents and transition to oral therapy only after swallowing and anatomy recover.
4Arrange dental or tonsillar source follow-up and vaccination or public-health action when the recovered organism makes it relevant.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Provides broad activity against H influenzae, streptococci and susceptible respiratory organisms.

Ceftriaxone for severe epiglottic infection

Give ceftriaxone 2 g intravenously once daily in adults, using meningitis dosing if central nervous system infection is suspected.

Check immediate beta-lactam allergy, biliary disease, renal and liver context and local resistance; airway control must never wait for antibiotic effect.

Covers oral streptococci, beta-lactamase producers and anaerobes while drainage is arranged.

Co-amoxiclav for polymicrobial deep-neck infection

Give co-amoxiclav 1.2 g intravenously every 8 hours for severe odontogenic or polymicrobial deep-neck infection when local guidance supports it.

Avoid in immediate penicillin allergy or previous co-amoxiclav liver injury, adjust for renal function and do not let treatment postpone drainage.

Adds activity against anaerobes in dental and deep fascial-space infection.

Metronidazole anaerobic component

Give metronidazole 500 mg intravenously every 8 hours when the selected beta-lactam does not provide adequate anaerobic cover.

Review liver disease, warfarin and neurological toxicity and avoid alcohol during treatment and for 48 hours afterwards.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Complete airway obstruction

Progressive oedema, fatigue and secretions can cause sudden hypoxic arrest, making controlled early airway management lifesaving.

Descending mediastinitis

Retropharyngeal infection can enter the chest, causing pleural, pericardial and mediastinal sepsis requiring urgent specialist thoracic drainage.

Septic thrombophlebitis

Internal jugular thrombosis can produce persistent bacteraemia, neck pain and pulmonary septic emboli after pharyngeal infection.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Observe airway work, voice, swallowing, secretions and oxygenation continuously until the risk of abrupt obstruction has resolved.
Trend fever, inflammatory markers, blood cultures and deep culture results while linking changes to drainage and imaging.
Inspect neck swelling, mouth opening, floor of mouth and cranial nerves and ask about chest pain suggesting descending infection.
Document airway grade, device plan, antimicrobial review, drain care and the clinician responsible for source eradication.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Pain can exceed the view

Minimal tonsillar inflammation does not exclude epiglottitis or a deep collection; severe disproportionate odynophagia is a useful warning.

CT follows airway safety

Cross-sectional anatomy is valuable only after the patient can tolerate lying flat and transfer without losing the airway.

Pus needs a route out

Clinical improvement may stall despite susceptible antibiotics when pressure and devitalised tissue remain behind fascial barriers.

Extubation is another airway decision

Removing a secured tube requires evidence that supraglottic swelling and secretions have improved, not merely a lower fever.

11Common pitfallsFrequent interpretation and management errors.

01
Forcing oral examination in a distressed stridulous patient and precipitating complete airway obstruction.
02
Sending an unstable patient supine to CT without senior airway escort and rescue equipment.
03
Treating a rim-enhancing deep collection with antibiotics alone despite persistent fever and mass effect.
04
Ignoring dental source, internal jugular thrombosis or mediastinal extension after initial throat symptoms improve.