Viral croup and upper-airway obstruction

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

Parainfluenza viruses are typical causes, with RSV, influenza, adenovirus, coronavirus and metapneumovirus also implicated. Viral identification does not usually change acute treatment.

Inflammation and oedema narrow the cricoid-bounded subglottic airway. A small reduction in radius sharply increases resistance, especially in a young child.

Turbulent inspiratory flow through the narrowed extrathoracic airway produces stridor. Progression increases recession and respiratory effort until fatigue reduces flow and may make stridor deceptively quiet.

A calm hands-off view provides the safest severity assessment. Count respiration and observe chest and abdomen without forcing a mask, tongue depressor or supine examination.

Dexamethasone reduces mucosal oedema over several hours and lowers return visits and escalation. The 0.15 mg/kg oral dose is widely used for mild and moderate croup in current UK pathways.

Nebulised adrenaline vasoconstricts mucosal vessels within minutes, buying time for corticosteroid and airway planning. It is rescue therapy, not proof that discharge is safe.

Atypical features change the diagnosis. Drooling and refusal to swallow suggest supraglottic disease; toxic appearance with secretions suggests bacterial tracheitis; sudden onset suggests foreign body.

Spasmodic or recurrent croup may occur without fever, but frequent, prolonged, very young or poor-response episodes warrant ENT or respiratory assessment for subglottic stenosis, airway malacia or reflux-related and allergic mimics.

Croup usually resolves within 48 hours to several days. Caregivers need to know that night-time recurrence can occur even after a good daytime assessment.

Hydration is supportive, but never force a distressed child to drink. Small cool fluids can be offered once breathing allows safe swallowing.

Antibiotics do not treat viral croup. Bacterial tracheitis is a separate emergency requiring airway management and broad intravenous antibacterial treatment directed by microbiology and local policy.

Documentation should state stridor at rest, recession, mental state and response at defined times; labels such as mild or severe without these observations are unsafe.

Key points

Croup is viral subglottic inflammation, usually between 6 months and 6 years, causing a seal-like barking cough, hoarse voice and inspiratory stridor, often worse at night.
Assess before touching: position, mental state, stridor at rest, recession, air entry, colour and hydration. Agitation worsens dynamic obstruction, so keep the child on the caregiver's lap.
Mild croup has barking cough without stridor or recession at rest. Moderate disease has stridor and/or recession at rest without agitation or lethargy. Severe disease adds marked distress, agitation or lethargy.
First-line medicine for croup of any clinically significant severity is a single oral dose of dexamethasone 0.15 mg/kg. Follow the product and local maximum; avoid delaying treatment for unnecessary tests.
If oral medicine cannot be taken without dangerous distress or vomiting, nebulised budesonide 2 mg once is an accepted alternative in UK paediatric pathways.
For severe or worsening obstruction, give nebulised adrenaline 1 mg/mL at 400 micrograms/kg, equivalent to 0.4 mL/kg, maximum 5 mg or 5 mL. Improvement is rapid but temporary.
Observe after nebulised adrenaline under paediatric care because symptoms can recur as its effect wanes; repeat after senior review when severe obstruction persists and escalate the airway plan.
Oxygen treats hypoxaemia but does not relieve the narrowing. Hypoxaemia in croup is a late, dangerous sign; deliver oxygen in the least upsetting manner.
Do not routinely request radiographs, blood tests, swabs or arterial gases. Investigations can distress the child and are unnecessary in typical croup.
Do not use steam: it lacks evidence and causes scalds. Avoid cough suppressants, sedatives, forced examination and unnecessary venepuncture.
Do not inspect the pharynx when epiglottitis is possible. Maintain spontaneous breathing and involve anaesthesia and ENT for a controlled airway.
Discharge only when stridor at rest and significant recession have resolved, the child drinks safely and caregivers understand recurrence and emergency signs.

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

Parainfluenza infection

Parainfluenza viruses commonly infect laryngeal and tracheal mucosa, producing the characteristic seasonal barking-cough illness. within the child-specific clinical phenotype.

Other respiratory viruses

RSV, influenza, adenovirus, coronavirus and metapneumovirus can cause the same clinical subglottic syndrome. within the child-specific clinical phenotype.

Anatomical susceptibility

The narrow, non-expandable young child's subglottic airway develops major resistance from relatively little circumferential oedema. within the child-specific clinical phenotype.

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

1
Subglottic mucosal oedema
Viral inflammation narrows the airway below the vocal cords, where cricoid cartilage limits outward expansion. during progression of the respiratory disorder.
2
Turbulent inspiratory flow
Air accelerating through an extrathoracic narrowing creates audible stridor and negative-pressure chest-wall recession. during progression of the respiratory disorder.
3
Dynamic deterioration
Crying increases airflow demand and turbulence, while progressive fatigue reduces ventilation and may silence previously loud stridor.
4
Temporary vasoconstriction
Nebulised adrenaline rapidly shrinks mucosal vascular volume, but its short effect can wear off before corticosteroid benefit is established.

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

Typical sound and cough

Identify barking cough, hoarse voice and inspiratory stridor after a viral prodrome, often with nocturnal worsening.

Severity at rest

Observe stridor, sternal and intercostal recession, air entry, agitation, lethargy, colour and respiratory effort while calm.

Failure signs

Look for exhaustion, poor effort, reduced consciousness, cyanosis and diminishing air movement rather than relying on stridor volume.

Swallow and secretions

Drooling, dysphagia, muffled voice or copious secretions suggests a dangerous alternative and makes throat examination unsafe.

Onset and recurrence

Ask about viral prodrome, sudden choking, allergen exposure, previous intubation, recurrent episodes and persistent voice change.

Hydration and context

Assess drinking, urine, distance from care, night-time supervision and caregiver ability to recognise recurrent stridor.

Red flags requiring action

Cyanosis, reduced consciousness, exhaustion, poor effort or reduced air entry indicates impending respiratory arrest even if stridor becomes quieter.
Drooling, dysphagia, muffled voice, tripod posture, absent bark and a toxic child suggests epiglottitis; do not examine the throat or distress the child.
High fever, toxic appearance, rapidly progressive obstruction and copious secretions suggests bacterial tracheitis and often requires airway control and intravenous antibiotics.
Abrupt onset during eating or play, focal air-entry change or no viral prodrome suggests an airway foreign body.
Urticaria, facial or tongue swelling, wheeze, hypotension or gastrointestinal symptoms with stridor suggests anaphylaxis and requires intramuscular adrenaline.
Age under 6 months, recurrent atypical episodes, persistent hoarseness or poor response warrants assessment for structural airway disease.

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
First-line: calm clinical severity assessmentFirst stepFirst line
Why
Diagnose typical croup and detect impending failure without worsening obstruction.
Interpretation and limitations
Stridor and recession at rest indicate at least moderate disease; exhaustion, cyanosis or reduced consciousness indicates critical disease.
02
Pulse oximetry when tolerated
Why
Detect late hypoxaemia in moderate or severe obstruction.
Interpretation and limitations
A low saturation is dangerous; a normal value does not exclude severe upper-airway obstruction and must not delay treatment.
03
No routine imaging or blood tests
Why
Avoid distress and low-value testing in a classic presentation.
Interpretation and limitations
Investigation is reserved for an atypical or uncertain diagnosis after the airway is safe and senior expertise is present.
04
Controlled airway endoscopy
Why
Evaluate suspected epiglottitis, bacterial tracheitis or structural obstruction while enabling treatment.
Interpretation and limitations
This is performed in a prepared theatre or intensive-care environment by anaesthesia and ENT, not as bedside throat inspection.
05
Targeted microbiology
Why
Identify bacterial or specific viral disease when it changes infection control or antibacterial treatment.
Interpretation and limitations
Samples are obtained only when safe, often after airway control in bacterial tracheitis.

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

Epiglottitis

Drooling, dysphagia, muffled voice, tripod posture and toxicity without a typical bark requires a controlled airway pathway.

Bacterial tracheitis

High fever, toxicity, copious secretions and poor response to adrenaline or corticosteroid suggests bacterial airway infection.

Foreign-body aspiration

Sudden choking without prodromal coryza and focal or variable airway findings favours an inhaled object. when timing, examination and trajectory are integrated.

Anaphylaxis

Rapid stridor with swelling, urticaria, wheeze, vomiting or cardiovascular compromise requires intramuscular adrenaline. when timing, examination and trajectory are integrated.

Structural upper-airway disease

Recurrent atypical stridor, weak cry or symptoms outside the usual age range suggests stenosis, malacia, haemangioma or vocal-cord dysfunction.

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

01MildGive corticosteroid and adviceFirst stepBarking cough is present without stridor or recession at rest.

1Give oral dexamethasone 0.15 mg/kg once using the local product maximum.
2AlternativeConfirm safe drinking and no feature of a dangerous alternative.
3Discharge with night-time recurrence, hydration and emergency breathing advice when context is safe.

02ModerateTreat and observe responseStridor or recession persists at rest without lethargy or critical signs.

1Keep the child calm and give oral dexamethasone 0.15 mg/kg, or nebulised budesonide 2 mg if oral treatment is unsafe.
2Observe until stridor at rest and significant recession resolve and drinking is safe.
3EscalationGive nebulised adrenaline and escalate paediatric review if obstruction worsens or fails to improve.

03SevereBuy time and secure helpMarked distress, agitation, lethargy or worsening obstruction is present.

1Call senior paediatric and anaesthetic help, minimise handling and give oxygen if hypoxaemic.
2Give nebulised adrenaline 1 mg/mL at 0.4 mL/kg, maximum 5 mL, plus corticosteroid.
3Monitor continuously, repeat adrenaline after senior review if needed and prepare controlled airway support.

04AlternativeProtect the uncertain airwayAlternativeDrooling, toxicity, sudden onset, allergy features or poor treatment response is present.

1Do not inspect the throat, force the child supine or separate them from the caregiver.
2Summon anaesthesia, ENT and paediatrics and maintain spontaneous breathing during controlled assessment.
3Treat anaphylaxis, foreign body or bacterial infection according to the specific emergency pathway.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

First-line corticosteroid that reduces subglottic inflammation and subsequent escalation.

Dexamethasone

Child with croup: 0.15 mg/kg orally as a single dose; use the age-appropriate preparation and local product maximum. If oral treatment is not feasible, follow the local parenteral or nebulised-budesonide pathway.

Do not delay airway management in critical obstruction. Verify formulation concentration and weight, and avoid repeated courses for recurrent atypical stridor without specialist assessment.

Rapid temporary relief of severe subglottic mucosal oedema while definitive support is organised.

Adrenaline 1 mg/mL nebulised

Severe or worsening croup: 400 micrograms/kg, equivalent to 0.4 mL/kg of 1 mg/mL solution, maximum 5 mg or 5 mL, by nebuliser; repeat only with senior review and continuous monitoring.

Hospital resuscitation treatment only. Monitor heart rate and recurrence, involve paediatrics and anaesthesia, and never use improvement as justification for immediate discharge.

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

Acute respiratory failure

Progressive obstruction causes hypoxaemia, exhaustion, carbon-dioxide retention and ultimately cardiorespiratory arrest. when recognition or effective treatment is delayed.

Dehydration

Tachypnoea, fever and fear of swallowing can markedly reduce fluid intake during repeated night-time episodes. when recognition or effective treatment is delayed.

Airway intervention

A small proportion of severe cases require controlled intubation and paediatric intensive-care support. when recognition or effective treatment is delayed.

Treatment-related harm

Forced examination, sedation, steam burns or premature discharge after adrenaline can convert manageable obstruction into crisis.

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

Repeat mental state, stridor at rest, recession, air entry, colour and respiratory rate using the same calm approach.
After nebulised adrenaline, observe in hospital under paediatric care for recurrence as the effect wanes.
Monitor drinking and urine only once breathing is sufficiently settled for safe swallowing.
Document time, dose and response to corticosteroid and every adrenaline nebulisation.
Escalate when stridor becomes quieter alongside worsening effort or consciousness.
Reassess the diagnosis if response is poor, fever is high or secretions become copious.
Refer recurrent atypical disease for airway evaluation rather than issuing repeated unsupervised steroid courses.

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

Quiet is not always better

Stridor may fade when airflow fails; reduced sound with exhaustion or cyanosis is a pre-arrest sign.

Calm is an airway intervention

Keeping a child upright with a caregiver reduces crying, turbulent flow and avoidable worsening before medicines work.

Adrenaline buys time

Rapid improvement does not remove the underlying inflammation, so observation and corticosteroid remain essential.

Drooling changes the examination

Possible epiglottitis requires a controlled airway environment; a tongue depressor in an unprepared room is hazardous.

Steam adds harm

Humidified steam has no established clinical benefit and causes preventable scald injury.

11Common pitfallsFrequent interpretation and management errors.

01
Do not force an upset child to lie flat for examination.
02
Do not judge severity by loudness of stridor alone.
03
Do not inspect the throat when epiglottitis is possible.
04
Do not delay corticosteroid for a radiograph or viral test.
05
Do not use steam, cough suppressants or sedatives.
06
Do not regard oxygen as treatment of the obstruction itself.
07
Do not discharge immediately after nebulised adrenaline.
08
Do not repeatedly label atypical or recurrent stridor as viral croup without airway review.