Acute severe and life-threatening asthma

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

Death in acute asthma often follows under-recognition, delayed systemic corticosteroid or failure to escalate. Objective severity features are deliberately redundant because no single sign is sufficiently sensitive; a quiet, exhausted patient may be more dangerous than a loudly wheezing one.

The treatment hierarchy is oxygen to target, rapid inhaled beta2 agonist, antimuscarinic for severe disease, early systemic corticosteroid, then senior-led magnesium and ventilatory/critical-care decisions. Antibiotics, aminophylline and IV beta2 agonists are not routine first-line additions.

AIR/MART action plans may alter the patient's pre-arrival reliever steps, but once an adult has severe or life-threatening features the emergency pathway and full reassessment apply.

Key points

Treat first and assess in parallel: ABCDE, help, continuous monitoring, oxygen target 94-98%, bronchodilator and systemic corticosteroid.
Acute severe asthma is any of PEF 33-50%, respiratory rate at least 25/min, heart rate at least 110/min, or inability to complete sentences in one breath.
Life-threatening features include PEF below 33%, SpO2 below 92%, silent chest, cyanosis, poor effort, arrhythmia, hypotension, exhaustion or altered consciousness.
A normal PaCO2 is dangerous in a patient working hard to breathe; early attacks usually lower CO2, so normalisation can mean fatigue.
Initial nebulised salbutamol dose differs between current UK sources: the 2026 BTS/RCEM/SAM emergency pathway uses 2.5 mg, while the SIGN 158 acute algorithm uses 5 mg. Add ipratropium 500 micrograms in severe/life-threatening attacks and repeat or escalate according to response in a monitored emergency pathway.
Give prednisolone 40-50 mg orally promptly, or hydrocortisone 100 mg IV if oral treatment is not possible; oral is as effective when absorbed.
If inadequate response, use repeated or continuous salbutamol and consider IV magnesium sulfate 1.2-2 g over 20 minutes with senior oversight.
Do not sedate, do not rely on wheeze intensity, and do not delay ICU review for a chest radiograph.
Measure PEF before treatment if feasible without delay, then 15-30 minutes after and serially; record ability to speak, effort, SpO2, pulse and respiratory rate.
Discharge requires sustained clinical improvement, safe reliever spacing, ICS-containing maintenance, technique/action-plan review and prompt follow-up.

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

Poor baseline control

Inadequate anti-inflammatory treatment, poor adherence, incorrect inhaler technique or excessive reliever reliance leaves airway inflammation active and increases vulnerability to a severe attack.

Acute triggers

Viral respiratory infection, allergen exposure, smoke, pollution or workplace irritants can provoke rapid bronchoconstriction and inflammatory swelling in a susceptible airway.

Medicine-related risk

Non-selective beta-blockers, aspirin or other non-steroidal anti-inflammatory drugs in sensitive people, and abrupt corticosteroid withdrawal may precipitate dangerous deterioration.

High-risk history

Previous intensive-care admission, recent severe attacks, psychosocial difficulty or poor perception of airflow limitation identifies patients who may deteriorate before seeking help.

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

1
Acute airway narrowing
Smooth-muscle contraction combines with mucosal oedema and mucus plugging to sharply increase expiratory resistance throughout unevenly affected bronchi.
2
Dynamic hyperinflation
Incomplete expiration traps gas, raising end-expiratory lung volume and the work needed for each subsequent breath while reducing venous return when severe.
3
Gas-exchange failure
Patchy obstruction creates ventilation-perfusion mismatch and hypoxaemia; increasing carbon dioxide suggests fatigue or critically reduced ventilation rather than reassuring improvement.
4
Respiratory muscle exhaustion
Sustained high work of breathing eventually overwhelms respiratory muscles, causing reduced respiratory effort, altered consciousness and impending arrest.

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

Moderate attackRed flag

Increasing symptoms with PEF above 50-75% best/predicted and no acute severe features. Still assess risk and response; prior near-fatal asthma lowers the admission threshold.

Acute severe asthmaRed flag

Any one of PEF 33-50%, respiratory rate at least 25/min, pulse at least 110/min, or inability to complete sentences in one breath.

Life-threatening asthmaRed flag

Any one of PEF below 33%, SpO2 below 92%, PaO2 below 8 kPa, normal PaCO2 4.6-6.0 kPa, silent chest, cyanosis, poor effort, arrhythmia, hypotension, exhaustion or altered consciousness.

Near-fatal asthmaRed flag

Raised PaCO2 and/or need for mechanical ventilation. Involve critical care immediately; deterioration can be rapid and intubation is high risk.

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
PEF percentage best or predictedFirst step
Why
Objectively grade airflow and response.
Interpretation and limitations
Use personal best when reliable; below 50% is severe, below 33% life-threatening. Inability to perform due to distress is itself concerning and must not delay treatment.
02
Continuous SpO2 and vital signs
Why
Detect hypoxaemia, tachycardia, exhaustion and response.
Interpretation and limitations
Target 94-98%. SpO2 below 92% is life-threatening and an indication for ABG; absence of tachycardia does not reassure an exhausted patient.
03
ABG
Why
Assess life-threatening hypoxaemia, CO2 retention and acidosis.
Interpretation and limitations
Obtain when SpO2 below 92% or other life-threatening features. Normal or raised PaCO2 is ominous; repeat within about 1 hour if initial PaO2 below 8 kPa, PaCO2 normal/raised, or deterioration occurs.
04
Potassium, glucose and lactate
Why
Detect treatment-related and physiological metabolic disturbance.
Interpretation and limitations
Beta2 agonists can lower potassium and raise lactate/glucose. Persistent tachypnoea with improving airflow may reflect lactic acidosis; reassess rather than escalating blindly.
05
Chest radiograph
Why
Identify pneumothorax, consolidation or another complication.
Interpretation and limitations
Not routine in every attack. Obtain for suspected pneumothorax/consolidation, life-threatening disease, poor response or ventilation; never delay immediate treatment/escalation.
06
ECG and continuous rhythm monitoring
Why
Monitor severe hypoxaemia, tachyarrhythmia and high-dose beta2-agonist effects.
Interpretation and limitations
Look for arrhythmia/ischaemia and correlate with potassium; do not withhold essential bronchodilation solely for expected sinus tachycardia.

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

Anaphylaxis

Urticaria, angio-oedema, hypotension or gastrointestinal symptoms accompanying wheeze indicate a systemic allergic emergency rather than isolated asthma.

Pneumothorax

Sudden pleuritic pain, unilateral reduced breath sounds and rapid physiological decline suggest pleural air, particularly during severe asthma or positive-pressure support.

Pulmonary embolism

Pleuritic pain, haemoptysis, venous thromboembolism risk or unexplained hypoxaemia with limited objective bronchospasm should prompt probability-led PE assessment.

Upper-airway obstruction

Inspiratory stridor, voice change, throat symptoms or poor response to bronchodilation favours laryngeal or central-airway obstruction.

Cardiogenic pulmonary oedema

Crackles, orthopnoea, oedema and cardiac or radiographic evidence of congestion distinguish left-heart failure, although wheeze can occur in pulmonary oedema.

Additional chapter-specific clues

Complication or mimicRed flag

Sudden unilateral signs, pleuritic pain, subcutaneous emphysema, fever/focal crepitations, urticaria/airway swelling or inspiratory stridor suggests pneumothorax, pneumonia, anaphylaxis or upper-airway obstruction.

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

01First 10 minutesImmediate severe-attack bundleFirst stepAny acute severe or life-threatening feature.

1Call senior help; use ABCDE, continuous SpO2/ECG, IV access and document PEF if possible without delaying treatment.
2Give oxygen to SpO2 94-98%. For initial nebulised salbutamol, the 2026 BTS/RCEM/SAM pathway specifies 2.5 mg and SIGN 158 specifies 5 mg; use the current adopted emergency pathway and document the source. Add ipratropium 500 micrograms nebulised in severe/life-threatening disease.
3Give prednisolone 40-50 mg orally immediately or hydrocortisone 100 mg IV if oral absorption/route is unsuitable.
4If life-threatening features exist, obtain ABG and involve ICU/anaesthetics now; do not wait to see whether the first nebuliser works.

0215-30 minutesResponse-based escalationEscalationPersistent severe signs or inadequate improvement after initial treatment.

1Repeat salbutamol 5 mg every 15-30 minutes or use continuous nebulisation 5-10 mg/hour in a suitable monitored system; repeat ipratropium per acute protocol.
2Consider one IV magnesium sulfate dose 1.2-2 g over 20 minutes after senior review, particularly in life-threatening or poorly responding severe attack.
3Recheck PEF, speech, respiratory effort, SpO2, pulse, respiratory rate, potassium and blood gas when indicated; correct fluid/electrolyte problems.
4Discuss ventilation early. NIV is not routine acute-asthma treatment; impending arrest, worsening exhaustion/consciousness, refractory hypoxaemia or rising CO2 requires expert airway management.

03DischargeClose the post-attack risk loopSustained recovery without life-threatening features and a safe disposition.

1Confirm stable symptoms and observations, PEF preferably above 75% best/predicted, and bronchodilator need spaced to a safe interval; admit if severe features persist or social/risk factors make discharge unsafe.
2Complete prednisolone, restore or start an ICS-containing AIR/MART maintenance plan, demonstrate technique and supply a personalised action plan; do not discharge on SABA alone.
3Arrange follow-up with primary care within 2 working days and specialist respiratory review after admission, with explicit review of attack cause, adherence, SABA/steroid exposure and occupational/psychosocial risks.

04Peri-arrestCritical deteriorationSilent chest with poor effort, reduced consciousness, bradycardia/hypotension, severe acidosis or respiratory arrest.

1Activate the resuscitation/critical-care response, continue high-concentration oxygen and prepare controlled intubation by the most experienced available clinician.
2Treat tension pneumothorax immediately if clinically suspected; manage cardiac arrest with current RCUK ALS and consider dynamic hyperinflation/auto-PEEP during ventilation.
3Use low ventilatory rates and prolonged expiratory time under critical-care management; permissive hypercapnia may be necessary to limit barotrauma, guided by pH and haemodynamics.

Key medicines and prescribing safety5 treatments · regimens, roles and cautions

First-line rapid bronchodilation.

Salbutamol

Initial nebulised dose: 2.5 mg in the 2026 BTS/RCEM/SAM emergency pathway; 5 mg in the SIGN 158 acute algorithm. Repeat every 15-30 minutes if response is inadequate; monitored continuous nebulisation at 5-10 mg/hour may be used in refractory severe attacks. Spacer alternative: 4 puffs initially, then 2 puffs every 2 minutes up to 10 puffs.

Monitor pulse, rhythm, potassium, glucose and lactate with repeated/high doses. Use air-driven nebuliser plus supplemental oxygen in hypercapnic-risk contexts when applicable; do not let delivery logistics delay treatment.

Adds bronchodilation and reduces admission risk in severe attacks.

Ipratropium bromide

500 micrograms nebulised with the initial beta2 agonist in acute severe or life-threatening asthma; repeat according to the acute protocol, commonly every 4-6 hours once improving.

Avoid aerosol in the eyes, especially with glaucoma; not a substitute for beta2 agonist or steroid and not required indefinitely after recovery.

Treats airway inflammation and reduces relapse; give early.

Prednisolone or hydrocortisone

Prednisolone 40-50 mg orally once daily, usually for at least 5 days or until recovery; if oral route unsuitable, hydrocortisone 100 mg IV immediately then 100 mg every 6 hours while needed, switching to oral promptly.

Oral is preferred when absorbed. Monitor glucose, mood and infection risk; do not taper a short course solely because it lasted 5-7 days unless there is chronic steroid use/adrenal risk.

Second-line bronchodilator adjunct after initial inhaled therapy and steroid.

Magnesium sulfate

1.2-2 g IV infused over 20 minutes as a single dose after senior review for life-threatening or poorly responding acute severe asthma.

Monitor BP and renal function; flushing/hypotension can occur. Repeated dosing is not routine, and it must not delay critical-care escalation.

Rare third-line rescue when standard treatment has failed; evidence of added benefit is limited.

Aminophylline—specialist rescue only

If critical-care/respiratory specialists decide benefit outweighs harm: loading 5 mg/kg IV (maximum 500 mg) over at least 20 minutes, omitted if receiving theophylline, then infusion guided by age, comorbidity and levels.

Narrow therapeutic index, vomiting, arrhythmias and seizures; major interactions. Check theophylline exposure and levels and use continuous ECG—never routine first line.

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

Respiratory arrest

Progressive obstruction, hyperinflation and muscle fatigue can culminate in profound hypoventilation, loss of consciousness and cardiopulmonary arrest.

Air-leak syndromes

High intrathoracic pressures may rupture alveoli, producing pneumothorax or pneumomediastinum and abruptly worsening ventilation and haemodynamics.

Treatment-associated metabolic stress

Intensive beta-agonist exposure can contribute to tremor, tachycardia, hypokalaemia and raised lactate, potentially confusing reassessment of persistent tachypnoea.

Hypoxic injury

Prolonged severe hypoxaemia or arrest may injure the brain, heart and kidneys even after airflow obstruction is reversed.

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

Record PEF, speech, respiratory rate, pulse, SpO2, effort, auscultation and consciousness at baseline and 15-30 minutes after initial bronchodilator.
Use continuous SpO2 and ECG in severe/life-threatening attacks; monitor BP and fluid status without overhydration.
Repeat ABG within about 1 hour when initial PaO2 is below 8 kPa, PaCO2 is normal/raised, acidosis is present or the patient deteriorates.
Check potassium, glucose and lactate with repeated/high-dose beta2 agonist and interpret tachypnoea against improving or worsening airflow.
Before discharge document stability, bronchodilator spacing, ICS-containing regimen, technique, action plan, steroid course and follow-up.

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

Normal CO2 is abnormal here

A patient with a severe attack should usually hyperventilate and lower PaCO2. A normal value may indicate failing ventilation before it becomes frankly raised.

Wheeze can disappear for the wrong reason

A silent chest may mean minimal airflow, not resolution. Judge speech, effort, PEF, oxygenation and mental state.

Lactate can imitate treatment failure

High-dose beta2 agonist can cause lactic acidosis and tachypnoea while bronchospasm improves. Reassess PEF and chest movement before simply giving more salbutamol.

Intubation is not the moment to start planning

Dynamic hyperinflation and peri-intubation cardiovascular collapse make airway management hazardous. Early expert involvement is a treatment, not an administrative step.

Every attack is a prevention signal

Discharge without an ICS-containing plan, technique check and rapid follow-up leaves the mechanism of the next attack untouched.

11Common pitfallsFrequent interpretation and management errors.

01
Reassurance from a quiet chest or normal PaCO2.
02
Waiting for CXR or blood results before bronchodilator, steroid and escalation.
03
Giving sedatives to tolerate distress in an unventilated severe attack.
04
Using antibiotics routinely without evidence of bacterial infection.
05
Escalating beta2 agonist indefinitely without monitoring potassium/lactate or planning ventilation.
06
Discharging on SABA alone or without a written action plan and prompt review.