Acute severe and life-threatening asthma

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

Acute airway smooth-muscle constriction, mucosal oedema and mucus plugging increase expiratory resistance and cause dynamic hyperinflation. Work and gas trapping can culminate in fatigue and arrest.

Children often compensate with tachypnoea and low carbon dioxide. A normalising or rising carbon dioxide in a child who remains distressed reflects failing ventilation, not recovery.

Initial assessment and treatment occur simultaneously. Observe speech, feeding and mental state, listen for air movement and measure saturation; peak flow is useful only when it does not delay therapy.

Metered-dose inhaler with spacer deposits bronchodilator effectively in many attacks and avoids nebuliser-generated aerosol. Oxygen-driven nebulisation is used when severe effort or hypoxaemia prevents reliable spacer delivery.

Beta2 agonist causes tremor, tachycardia, hypokalaemia and lactate elevation. Persistent tachypnoea after high doses can reflect lactic acidosis, but bronchospasm must be reassessed before reducing treatment.

Ipratropium adds bronchodilation in severe disease but is not continued indefinitely once the acute intensive sequence is complete.

Systemic steroid benefit takes hours, so give it early. Vomiting shortly after a dose may require replacement according to the product and local policy.

Intubation is hazardous because severe airflow obstruction causes gas trapping and hypotension. It is performed by an experienced team using a strategy that allows long expiration and accepts permissive hypercapnia where appropriate.

Sedation outside a controlled airway removes respiratory drive. Anxiety is managed through calm caregivers and efficient treatment, never respiratory-depressant medicine.

An attack signals long-term treatment failure or overwhelming trigger. Before discharge, establish diagnosis, ICS access, spacer skill, smoke exposure and the reason treatment did not prevent escalation.

Adolescents need confidential assessment of vaping, adherence, mental health and intentional over- or under-use. Include them directly in action-plan decisions.

A post-attack review prevents recurrence by adjusting maintenance, identifying risk, replacing used relievers and ensuring school and home plans align.

Key points

Grade severity from the most dangerous feature. A child does not need every criterion, and falling tachycardia or respiratory rate with exhaustion is deterioration.
First line: give oxygen to target 94–98% and salbutamol immediately. Mild-to-moderate attacks can use a pressurised metered-dose inhaler and spacer; severe or hypoxaemic attacks use an oxygen-driven nebuliser.
Spacer regimen: give one salbutamol 100-microgram puff at a time with tidal breaths, repeating up to 10 puffs and reassessing; use a mask when a mouthpiece seal is unreliable.
Severe nebuliser dose: salbutamol 2.5 mg under 5 years or 5 mg age 5 and over, repeated or continuously under senior monitoring according to response.
Add nebulised ipratropium 250 micrograms to each of the first three salbutamol nebulisers in acute severe or life-threatening asthma.
Give oral prednisolone early: commonly 20 mg age 2–5 and 30–40 mg age over 5 for at least 3 days, or follow BNF-C weight-based/local dosing. Use intravenous hydrocortisone if oral treatment cannot be taken.
Reassess after every bronchodilator: mental state, speech or feeding, effort, air entry, saturation, heart and respiratory rates and peak flow if age and effort allow.
Do not request chest radiography routinely. Image for suspected pneumothorax, focal collapse, foreign body or failure suggesting another diagnosis.
Obtain blood gas in life-threatening or nonresponding disease. Do not stop bronchodilator to obtain it, and avoid arterial puncture if a venous or capillary sample answers the question.
For poor response, senior-led intravenous magnesium sulfate 40 mg/kg, maximum 2 g, over 20 minutes is a common first intravenous bronchodilator option; monitor blood pressure.
Intravenous salbutamol or aminophylline requires paediatric intensive-care-level expertise, dose verification and cardiac, potassium, lactate and glucose monitoring.
Discharge requires sustained improvement on spaced inhaled treatment, normal activity and oxygenation, an ICS-containing preventer plan, observed technique, written action plan and review within 2 working days.

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

Viral or allergen trigger

Respiratory viruses, seasonal allergen exposure, exercise, pollution and smoke commonly trigger sudden inflammation and bronchoconstriction. within the child-specific clinical phenotype.

Inadequate anti-inflammatory treatment

Absent, interrupted or poorly delivered ICS leaves airway inflammation vulnerable to a modest trigger. within the child-specific clinical phenotype.

High-risk asthma phenotype

Previous intensive care, severe attacks, low lung function and psychosocial barriers increase rapid deterioration risk. within the child-specific clinical phenotype.

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

1
Acute bronchoconstriction
Airway smooth muscle contracts rapidly, narrowing expiratory flow and creating wheeze and prolonged expiration. during progression of the respiratory disorder.
2
Oedema and mucus
Inflamed mucosa and plugs further obstruct small airways and can create a silent poorly ventilated region.
3
Dynamic hyperinflation
Incomplete expiration traps gas, flattens the diaphragm, increases work and reduces venous return during severe attacks.
4
Ventilatory failure
Muscle fatigue eventually lowers minute ventilation, raising carbon dioxide and causing acidosis, hypoxaemia and reduced consciousness.

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

Function

Assess speech, feeding, walking, posture and alertness; inability to speak or feed indicates severe limitation.

Breathing

Record rate, recession, accessory use, wheeze, air entry, symmetry, exhaustion and paradoxical movement.

Objective severity

Measure saturation, heart rate and peak flow when feasible, using age-specific thresholds and the worst feature.

Failure

Recognise silent chest, cyanosis, poor effort, hypotension, arrhythmia and altered consciousness as life-threatening signs.

Risk history

Ask previous ventilation or admission, recent attacks and steroid, reliever use, ICS adherence and safeguarding or psychosocial barriers.

Red flags requiring action

Silent chest, cyanosis, poor effort, exhaustion, confusion, drowsiness, hypotension or arrhythmia is life-threatening irrespective of respiratory rate.
Age over 5: saturation below 92%, peak flow 33–50%, respiratory rate above 30, heart rate above 125 or inability to complete sentences indicates acute severe asthma.
Age 2–5: saturation below 92%, inability to talk or feed, heart rate above 140, respiratory rate above 40 or marked accessory-muscle use indicates severe disease.
Normal carbon dioxide during a severe attack may be ominous; a raised PaCO2 indicates fatigue and respiratory failure.
Previous ventilation, intensive-care admission, recent oral steroid, high SABA use or absent ICS increases near-fatal risk and lowers escalation thresholds.
Asymmetry, sudden choking, stridor, urticaria, fever with focal signs or no bronchodilator response suggests foreign body, anaphylaxis, pneumonia or another diagnosis.

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: continuous clinical reassessment and oximetryFirst stepFirst line
Why
Grade response and identify hypoxaemia or fatigue while treatment proceeds.
Interpretation and limitations
Use the worst feature; saturation below 92% places the child in at least acute severe disease.
02
Peak expiratory flow age over 5
Why
Quantify airflow relative to the child's best or predicted value when performance is safe.
Interpretation and limitations
33–50% indicates acute severe and below 33% life-threatening asthma; inability to perform can itself reflect severity.
03
Blood gas
Why
Detect ventilatory failure in life-threatening or nonresponding asthma.
Interpretation and limitations
Normal or raised carbon dioxide with ongoing distress is concerning; acidosis and rising PaCO2 accelerate intensive-care support.
04
Electrolytes, glucose and lactate
Why
Monitor severe disease and toxicity during repeated or intravenous beta2 agonist.
Interpretation and limitations
Hypokalaemia and lactate elevation require contextual management without mistaking metabolic tachypnoea for persistent bronchospasm.
05
Targeted chest radiograph
Why
Assess pneumothorax, focal collapse, foreign body or unexpected nonresponse.
Interpretation and limitations
Routine imaging is unnecessary and hyperinflation alone does not change standard asthma treatment.

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

Foreign-body aspiration

Sudden choking, unilateral findings and poor bronchodilator response requires urgent bronchoscopy assessment. when timing, examination and trajectory are integrated.

Anaphylaxis

Acute wheeze with urticaria, swelling, gastrointestinal or circulatory features requires intramuscular adrenaline. when timing, examination and trajectory are integrated.

Pneumonia or pneumothorax

Fever, focal crackles, pleuritic pain or unilateral absent air entry warrants targeted imaging and treatment. when timing, examination and trajectory are integrated.

Upper-airway or dysfunctional breathing

Inspiratory stridor, throat tightness or tingling with normal oxygenation can mimic asthma but may coexist. when timing, examination and trajectory are integrated.

Additional chapter-specific clues

Alternative emergency

Look for stridor, allergy, focal infection, unilateral findings, choking and cardiac signs before assuming every wheeze is asthma.

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

01ImmediateTreat while assessingFirst stepA child presents with a current asthma attack.

1Give oxygen for hypoxaemia and salbutamol by spacer or oxygen-driven nebuliser according to severity.
2Give systemic corticosteroid early and add ipratropium for severe or life-threatening disease.
3Reassess after every cycle and summon senior help at the first life-threatening feature.

02SevereEscalate inhaled treatmentEscalationSevere criteria persist after initial salbutamol.

1Use repeated or continuous oxygen-driven salbutamol with the first three ipratropium doses.
2Monitor saturation, ECG, potassium, glucose and clinical air movement.
3Discuss intravenous magnesium and intensive-care transfer before fatigue develops.

03FailurePrepare controlled ventilationSilent chest, exhaustion, altered consciousness or rising carbon dioxide develops.

1Call PICU and the most experienced airway clinician immediately and continue bronchodilator and oxygen.
2Avoid sedation outside airway control and correct shock or pneumothorax.
3Use a controlled ventilation strategy with long expiratory time and specialist intravenous bronchodilator decisions.

04DischargePrevent the next attackImprovement is sustained on safely spaced inhaled therapy.

1Confirm oxygenation, activity, drinking and inhaler technique and provide an ICS-containing regimen.
2Give written action and emergency plans, spacer and adequate medicines.
3Arrange GP or asthma-team review within 2 working days and specialist follow-up after severe or life-threatening disease.

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

First-line rapid bronchodilator for every acute asthma attack.

Salbutamol

Spacer: 100 micrograms per puff, one puff at a time up to 10 puffs with reassessment. Severe attack by oxygen-driven nebuliser: 2.5 mg under 5 years or 5 mg age 5 and over, repeated according to response and protocol.

Monitor heart rate, potassium, glucose and lactate when doses are repeated or continuous. Use a spacer where effective and oxygen-drive the nebuliser in hypoxaemia.

Early systemic anti-inflammatory treatment for moderate, severe or poorly responsive attacks.

Prednisolone

Common UK acute regimen: age 2–5 years 20 mg orally once daily; age over 5 years 30–40 mg once daily, usually for at least 3 days. Verify current BNF-C, weight and local protocol.

Give promptly and do not taper a short course routinely. Use intravenous hydrocortisone if oral medicine cannot be retained; account for recent steroid exposure and adrenal risk.

Senior-led intravenous bronchodilator option before or alongside intensive-care escalation.

Magnesium sulfate intravenous

Severe nonresponse under senior care: 40 mg/kg, maximum 2 g, intravenously over 20 minutes using the local paediatric acute-asthma protocol.

Monitor blood pressure and cardiorespiratory state; verify concentration and infusion rate. It never replaces repeated inhaled bronchodilator, steroid or airway planning.

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

Respiratory arrest

Progressive obstruction and fatigue can produce hypoxic cardiac arrest unless ventilation is supported. when recognition or effective treatment is delayed.

Air leak

Severe gas trapping can cause pneumothorax or pneumomediastinum and sudden asymmetric deterioration. when recognition or effective treatment is delayed.

Medicine toxicity

Repeated beta2 agonist can cause hypokalaemia, tachyarrhythmia, hyperglycaemia and lactic acidosis. when recognition or effective treatment is delayed.

Early recurrent attack

Discharge without ICS access, technique correction or action planning creates preventable rapid reattendance. when recognition or effective treatment is delayed.

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

Record response after each bronchodilator cycle, including air entry and function rather than wheeze alone.
Use continuous oximetry and cardiac monitoring in life-threatening disease or intravenous treatment.
Monitor potassium, glucose and lactate with high-dose or intravenous beta2 agonist.
Repeat blood gas when clinical ventilation worsens, not on a fixed schedule in a recovering child.
Watch for sudden unilateral deterioration from pneumothorax.
Before discharge, observe technique with the actual inhaler and spacer supplied.
Review maintenance and risk within 2 working days and update school and family action plans.

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

The worst sign defines severity

A child with a modest respiratory rate but a silent chest remains life-threatening and must not be averaged into a lower category.

Normal carbon dioxide is abnormal

A distressed child should hyperventilate; a normalising PaCO2 can mark loss of ventilatory reserve.

Wheeze needs airflow

Less wheeze can mean improvement or critically reduced air movement, so function and auscultated entry determine meaning.

Lactate can imitate failure

Beta2-agonist-associated lactic acidosis may sustain tachypnoea after bronchospasm improves; reassess the whole child before endless escalation.

Discharge is active prevention

An attack is incomplete care until anti-inflammatory treatment, technique, access and early review are secured.

11Common pitfallsFrequent interpretation and management errors.

01
Do not require every severe criterion before escalating.
02
Do not interpret a quiet chest as improvement without checking air entry.
03
Do not delay salbutamol and oxygen for imaging or venepuncture.
04
Do not use sedation for agitation in an acute attack.
05
Do not routinely prescribe antibiotics or request radiography.
06
Do not give intravenous bronchodilator without senior dose verification and monitoring.
07
Do not discharge on SABA alone.
08
Do not omit a 2-working-day review and written action plan.