Medicine chapters
Asthma and acute severe asthma
Chronic asthma (diagnosis, triggers and stepwise inhaler treatment) and the recognition and emergency management of acute severe and life-threatening asthma.
- Asthma is variable, reversible airflow obstruction with airway hyper-responsiveness and eosinophilic inflammation; diagnose by variable peak flow, reversibility (FEV1 up >12–15%) or a positive methacholine challenge.
- Chronic control is stepwise: reliever, then inhaled corticosteroid, then LABA in the same inhaler, then LTRA/LAMA, then biologics; never use a LABA alone.
- Acute severe attack (PEF 33–50%, RR ≥25, HR ≥110, cannot finish sentences): oxygen to SpO2 94–98%, nebulised salbutamol + ipratropium, prednisolone or IV hydrocortisone, then IV magnesium; life-threatening signs need ICU review.
On this page
Overview
Asthma is a chronic inflammatory airway disease with three features:
- Variable airflow obstruction that improves on its own or after treatment.
- Airway hyper-responsiveness to many stimuli.
- Bronchial inflammation (eosinophils, mast cells, Th2 lymphocytes), mucus plugging and, over years, airway remodelling.
It usually starts in childhood, is commonly atopic, and kills mainly through under-treated acute attacks. The TOS stresses the treatment of acute severe asthma (status asthmaticus).
Causes and triggers
- Atopy: house-dust mite, pollens, animal dander, fungal spores; often with eczema and allergic rhinitis.
- Viral infections (the commonest trigger of attacks), cold air, exercise (wheeze usually comes after exercise), smoke and air pollution.
- Occupational agents: isocyanates (spray paint), flour, wood dust, latex, soldering fumes. Symptoms improve away from work.
- Drugs: aspirin and NSAIDs, beta-blockers (tablets and even timolol eye drops).
- Poor adherence to inhaled steroids.
Aspirin-sensitive asthma comes with nasal polyps and rhinitis. Blocking cyclo-oxygenase shunts arachidonic acid towards leukotrienes, so leukotriene receptor antagonists (montelukast) help.
Pathophysiology (exam points only)
- Early phase (minutes): mast cell IgE cross-linking releases histamine and leukotrienes → bronchospasm.
- Late phase (hours later): eosinophils and Th2 cells cause inflammation and persistent obstruction.
- Sputum may show Curschmann spirals and Charcot–Leyden crystals (from eosinophils).
Clinical features
- Episodic wheeze, breathlessness, chest tightness and cough, typically worse at night and early morning.
- Nocturnal cough may be the only symptom, especially in children.
- Between attacks the chest may be normal.
Investigations
| Test | Finding in asthma |
|---|---|
| Peak flow diary | Diurnal variation (morning dips) |
| Spirometry | Obstructive: FEV1/FVC reduced |
| Reversibility | FEV1 improves by more than 12–15% (and at least 200 mL) after a bronchodilator or a course of steroids |
| Bronchial provocation (methacholine or histamine) | A low dose causes a 20% fall in FEV1; useful when spirometry is normal |
| Fractional exhaled nitric oxide (FeNO) | Raised with eosinophilic inflammation; predicts steroid response |
| Blood and sputum eosinophils, total and specific IgE, skin-prick tests | Support atopic, eosinophilic asthma |
| Gas transfer (TLCO) | Normal (reduced in emphysema) |
| Chest X-ray | Usually normal; hyperinflation in attacks; excludes pneumothorax |
FEV1 before salbutamol: 2.0 L; 15 minutes after: 2.5 L
Change = (2.5 − 2.0) ÷ 2.0 × 100 = 25% (and 500 mL)
More than 12–15% → significant reversibility, consistent with asthma
A normal spirometry on the day does not exclude asthma, because obstruction is variable. Use a peak flow diary or a methacholine challenge.
Chronic asthma: stepwise treatment
Assess control, check inhaler technique and adherence, remove triggers, then move up or down the steps.
| Step | Treatment |
|---|---|
| Reliever for all | Short-acting β2 agonist (salbutamol) as needed, or as-needed low-dose ICS–formoterol (GINA preferred reliever) |
| 1–2 | Add regular low-dose inhaled corticosteroid (ICS) (beclometasone, budesonide, fluticasone) |
| 3 | Low-dose ICS plus a long-acting β2 agonist (LABA) in one inhaler; or maintenance and reliever therapy (MART) with budesonide–formoterol |
| 4 | Medium-dose ICS–LABA; add a leukotriene receptor antagonist (montelukast) or a long-acting antimuscarinic (tiotropium) |
| 5 | Specialist care: high-dose ICS, biologics (omalizumab anti-IgE; mepolizumab, benralizumab anti-IL-5 pathway), oral steroids as a last resort |
- Using a reliever three or more times a week means asthma is not controlled; step up.
- Step down slowly once controlled for about 3 months.
A LABA must never be used alone in asthma. Without an inhaled steroid it hides worsening inflammation and has been linked to more asthma deaths.
Drug points that are tested
| Drug | Mechanism | Key side effect or point |
|---|---|---|
| Salbutamol | β2 agonist → ↑cAMP → smooth muscle relaxation | Tremor, tachycardia, hypokalaemia, hyperglycaemia |
| Inhaled steroids | Switch off inflammatory genes | Oral thrush and hoarseness (rinse mouth, use a spacer) |
| Ipratropium, tiotropium | Muscarinic (M3) blockade | Dry mouth; ipratropium is quaternary so little systemic effect; can precipitate angle-closure glaucoma via a loose nebuliser mask |
| Montelukast | Blocks CysLT1 leukotriene receptor | Useful in aspirin-sensitive and exercise asthma |
| Theophylline / aminophylline | Phosphodiesterase inhibition, adenosine antagonism | Narrow therapeutic range; metabolised by CYP1A2: levels rise with ciprofloxacin, erythromycin and on stopping smoking; toxicity causes vomiting, arrhythmias, seizures |
| Sodium cromoglicate | Mast cell stabiliser | Prophylaxis only |
| Omalizumab | Binds circulating IgE | Severe allergic asthma |
Acute asthma: assessing severity
| Severity | Features (adults) |
|---|---|
| Moderate | PEF 50–75% of best or predicted, no severe features |
| Acute severe | Any one of: PEF 33–50%; RR ≥25/min; HR ≥110/min; cannot complete sentences in one breath |
| Life-threatening | Any one of: PEF <33%; SpO2 <92% or PaO2 <8 kPa; normal PaCO2 (4.6–6.0 kPa); silent chest; cyanosis; poor respiratory effort; exhaustion, confusion or drowsiness; arrhythmia, bradycardia or hypotension |
| Near-fatal | Raised PaCO2 and/or need for mechanical ventilation |
Best PEF 450 L/min; today 180 L/min; RR 28; HR 118; SpO2 94%
180 ÷ 450 × 100 = 40% → within 33–50%
With RR ≥25 and HR ≥110 → acute severe asthma (no life-threatening feature yet)
In an attack the patient should blow off CO2, so PaCO2 is usually low. A normal or rising PaCO2 means the patient is tiring and is a life-threatening sign.
Pulsus paradoxus reflects severe airway obstruction (large swings in intrathoracic pressure reduce left ventricular filling on inspiration), but it is present in only about half of severe attacks, so its absence does not mean the attack is mild.
Management of acute severe asthma (status asthmaticus)
Treat immediately; do not wait for blood gases.
- Sit up; oxygen by mask to keep SpO2 94–98%.
- Nebulised salbutamol 5 mg, driven by oxygen; repeat every 15–30 minutes, or give back-to-back (continuous) nebulisation if poor response.
- Nebulised ipratropium bromide 0.5 mg 4–6 hourly in acute severe or life-threatening attacks.
- Steroids: prednisolone 40–50 mg orally (continue for at least 5 days), or IV hydrocortisone 100–200 mg if the patient cannot swallow or is vomiting.
- IV magnesium sulphate 1.2–2 g over 20 minutes (single dose) if not responding or life-threatening, after senior review.
- Consider IV aminophylline (senior decision; check if already on theophylline) or IV salbutamol.
- Arterial blood gas if SpO2 <92% or life-threatening features; chest X-ray to exclude pneumothorax or consolidation (not routine otherwise).
- Do not give sedatives. Antibiotics only if there is evidence of bacterial infection.
- Check potassium (salbutamol and steroids lower it) and correct.
Refer to ICU (intubation may be needed)
- Deteriorating PEF despite treatment.
- Persisting or worsening hypoxia.
- Rising PaCO2 or falling pH.
- Exhaustion, drowsiness, confusion, feeble respiration.
- Respiratory arrest.
"Oh SHIM!" for acute asthma, in order: Oxygen, Salbutamol, Hydrocortisone or prednisolone, Ipratropium, Magnesium; then aminophylline and ICU.
Monitoring and discharge
- Repeat PEF 15–30 minutes after starting treatment, then regularly; keep SpO2 above 92%.
- Discharge when PEF is above 75% of best, symptoms are controlled on discharge medicines for 12–24 hours, and inhaler technique has been checked.
- Give oral prednisolone for at least 5 days (it can be stopped without tapering), start or step up inhaled steroid, and give a written action plan with follow-up.
Complications
- Pneumothorax, pneumomediastinum and surgical emphysema.
- Respiratory failure and death.
- Allergic bronchopulmonary aspergillosis (ABPA): poorly controlled asthma, eosinophilia, very high IgE, fleeting infiltrates and central bronchiectasis; treated with prednisolone with or without itraconazole.
- Eosinophilic granulomatosis with polyangiitis (late-onset asthma, eosinophilia, neuropathy, ANCA).
- Steroid side effects; growth delay in children on high doses.
Asthma in special situations
- Pregnancy: continue usual inhalers; treat attacks the same way. Prednisolone is preferred because the placenta inactivates most of it.
- Avoid beta-blockers (including eye drops) and NSAIDs in aspirin-sensitive asthma.
- Adenosine can trigger bronchospasm; in asthma, use verapamil for SVT instead.
- Carboprost (PGF2α) is avoided in asthmatic women with postpartum haemorrhage.
Expect: features of acute severe versus life-threatening asthma (PEF cut-offs, RR, HR, silent chest, normal PaCO2), the order of emergency treatment (oxygen, nebulised salbutamol, ipratropium, steroids, IV magnesium, aminophylline, ICU), salbutamol causing hypokalaemia and tremor, discharge criteria, the methacholine challenge when spirometry is normal, reversibility cut-offs, why a LABA is never given alone, leukotriene antagonists in aspirin-sensitive asthma with nasal polyps, beta-blocker and NSAID avoidance, and theophylline interactions.
Quick revision
- Asthma = variable, reversible obstruction + hyper-responsiveness; TLCO normal.
- Reversibility >12–15%; methacholine 20% FEV1 fall at low dose.
- Steps: reliever → ICS → ICS + LABA → add LTRA or LAMA → biologics.
- Acute severe: PEF 33–50%, RR ≥25, HR ≥110, broken sentences.
- Life-threatening: PEF <33%, SpO2 <92%, normal PaCO2, silent chest, exhaustion.
- Treat: O2 94–98%, salbutamol 5 mg neb, ipratropium 0.5 mg, prednisolone 40–50 mg or IV hydrocortisone, IV Mg 1.2–2 g.
- Rising CO2, drowsiness or exhaustion → ICU.
- Discharge when PEF >75%; prednisolone at least 5 days.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
What is status asthmaticus?
An older term for a severe asthma attack that does not respond to the usual bronchodilators; today it is graded as acute severe or life-threatening asthma and managed as an emergency.
Why is magnesium sulphate used in acute asthma?
It relaxes bronchial smooth muscle, and a single IV dose of 1.2–2 g over 20 minutes helps patients who have not responded to nebulised bronchodilators and steroids.
Why is a normal PaCO2 dangerous in an asthma attack?
A breathless asthmatic should be hyperventilating with a low PaCO2; a normal or high value means the patient is tiring and may soon stop breathing effectively.
Can the short prednisolone course be stopped suddenly?
Yes; a course of about 5 days (up to about 2 weeks) can usually be stopped without tapering, because adrenal suppression is unlikely in that time.