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Level 2 of 6Must-remember

Acute severe asthma: grading and emergency treatment

Assess, manage and stay safe — enough on its own

The card — assess, manage, caution

Assessment— look, ask, measure

  • Assess from across the room before you touch the patient: speech (sentences, then phrases, then single words, then mute), posture (the patient unable to recline is severe — never nurse an asthmatic flat), work of breathing (accessory muscle use, suprasternal and intercostal retraction, and ominously paradoxical thoraco-abdominal movement), and mental state (agitation is usually hypoxaemia; drowsiness or confusion is pre-terminal).
  • History to ask for: the tempo of the attack (most build over hours to days, but brittle asthma strikes within minutes), how much reliever has already been used (a patient who has emptied a salbutamol canister before arrival is further into the attack than the first PEF suggests), and the previous worst attack — intensive care admission or intubation identifies a patient to be treated maximally from the outset.
  • Ask about drugs as a precipitant: aspirin and other NSAIDs (the classical patient is a woman presenting in middle age with asthma, rhinosinusitis and nasal polyps), beta-adrenoceptor antagonists even as ophthalmic drops, the oral contraceptive pill, cholinergic agents, prostaglandin F2α and arecoline in betel nut — and about viral upper respiratory infection, non-adherence to inhaled corticosteroid, allergen exposure and air pollution.
  • Risk factors for a fatal attack that must raise treatment intensity irrespective of how well the patient looks: a previous near-fatal attack requiring intubation or intensive care; any life-threatening exacerbation or hospital admission in the preceding 12 months; more than two courses of oral corticosteroid in the past 12 months; over-reliance on short-acting beta₂-agonists or long-acting beta₂-agonist monotherapy; brittle asthma; blunted perception of airflow limitation (a minority feel well at a PEF of 30% of best); psychiatric illness, social isolation, poor access to care, obesity, rhinosinusitis, reflux and continued smoking.
  • Measure a peak expiratory flow unless the patient is too ill to co-operate — inability to perform it is itself a life-threatening finding; upright, lips sealed tightly around a clean mouthpiece, a maximal short blast, best of three, interpreted as a percentage of the patient's own previous best on optimal treatment.
  • Apply the oximeter before anything else and obtain a room-air value if it can be done safely: SpO₂ below 92% is a life-threatening feature and the single strongest trigger for arterial blood gas analysis.
  • Acute severe asthma is defined by numbers, not impressions: PEF 33–50% of predicted or personal best (below 200 L/min), respiratory rate at least 25/min, heart rate at least 110/min, or inability to complete a sentence in one breath.
  • Life-threatening asthma is any one of: PEF below 33% (below 100–150 L/min) or unable to blow; SpO₂ below 92%; PaO₂ below 8 kPa (60 mmHg); a normal or raised PaCO₂; a silent chest; cyanosis; respiratory rate above 30/min or falling; pulse above 120/min or bradycardia; exhaustion, delirium or drowsiness; hypotension or arrhythmia.Not available at your setup — Arterial blood gas. Silent chest, cyanosis, feeble effort, bradycardia, drowsiness and inability to blow a PEF are clinical findings — grade the attack on them even without oximetry or gases.
  • Near-fatal asthma is a raised PaCO₂ and/or the need for mechanical ventilation with raised inflation pressures — the PEF is unrecordable, the patient mute, the effort feeble with paradoxical thoraco-abdominal movement.Not available at your setup — Arterial blood gas.
  • The single conceptual point: a patient in acute severe asthma is hyperventilating and should be blowing off carbon dioxide, so a normal PaCO₂ (4.6–6.0 kPa, 35–45 mmHg) in such a patient means the respiratory muscles are tiring, and a raised PaCO₂ above 6 kPa (45 mmHg) means they are failing.Not available at your setup — Arterial blood gas.
  • Auscultation: widespread polyphonic expiratory wheeze with a prolonged expiratory phase, but loudness reflects airflow, not severity — in a very severe exacerbation airflow may be too limited to generate a wheeze, leaving globally reduced breath sounds, the silent chest.
  • Paediatric thresholds are different: acute severe means SpO₂ below 92%, too breathless to talk or feed, heart rate above 140/min at 1–5 years or above 125/min over 5 years, respiratory rate above 40/min at 1–5 years or above 30/min over 5 years, and accessory muscle use; life-threatening adds SpO₂ below 92% despite oxygen, inability to vocalise, bradycardia, feeble or falling effort, silent chest, cyanosis, grunting, hypotension, exhaustion, agitation or reduced conscious level, and PEF below 33% in an older child.
  • In children, grunting, inability to feed, and a child who was working hard ten minutes ago and now appears calm are danger signs — the last is exhaustion, not improvement; PEF is unreliable below about 5–6 years and must never delay treatment.
  • The features that define exhaustion rather than recovery: a falling respiratory rate, a settled drowsy patient, bradycardia, hypotension or a new arrhythmia, and the disappearance of pulsus paradoxus in a previously paradoxical patient (pulsus paradoxus is present in only about 45% of cases, so its absence proves nothing).
  • Mimics to consider before committing to the diagnosis: anaphylaxis (seconds to minutes after a trigger, with urticaria, angio-oedema, hypotension, needing intramuscular adrenaline not a nebuliser), pneumothorax (sudden unilateral deterioration), pulmonary embolism, inhaled foreign body, inducible laryngeal obstruction (inspiratory stridor with normal SpO₂ and gases), cardiogenic pulmonary oedema, COPD exacerbation, bronchiolitis in the infant under 12 months, and croup at 6 months to 3 years.
  • Check the potassium and glucose: repeated beta₂-agonist doses drive potassium intracellularly and corticosteroids compound the effect, and hypokalaemia in a hypoxaemic patient is arrhythmogenic; both drug classes raise the glucose, and a raised lactate is common with repeated beta₂-agonist dosing.Not available at your setup — Serum electrolytes.

Management— do this, in order

  • Sit the patient upright and keep them upright — never nurse an asthmatic flat; after 20 weeks of pregnancy use left lateral tilt if she must be reclined.
  • Correct hypoxaemia immediately and completely: controlled supplemental oxygen to maintain SaO₂ 94–98%, starting in the sickest patients with a reservoir (non-rebreathing) mask at 15 L/min or 40–60% by face mask, then titrating down. Asphyxia is a common cause of asthma death.
  • Salbutamol 5 mg nebulised, driven by oxygen at 6–8 L/min, repeated every 15–20 minutes — at least three treatments in the first hour of a severe attack. Never drive the nebuliser with an air compressor in a hypoxaemic patient. Terbutaline is an acceptable alternative (published nebulised doses vary between 2.5 mg and 10 mg, so give a moderate dose and repeat rather than one large dose).
  • If no nebuliser is available: salbutamol 100 microgram metered-dose inhaler through a large-volume spacer, 4–10 puffs, one puff at a time with five tidal breaths each, repeated up to three times in the first hour (6–12 puffs every 30–60 minutes in severe exacerbations) — genuinely equivalent in a co-operative patient, because one 2.5 mg nebule delivers 25–30 times the dose of a single MDI actuation (0.09–0.1 mg), so two puffs is not treatment for an acute attack.
  • Add nebulised ipratropium bromide 500 microgram in the same chamber, repeated 4–6 hourly — give it routinely in life-threatening attacks and in any patient failing to respond to salbutamol, because adding it to a short-acting beta₂-agonist reduces hospital admission rates in moderate-to-severe exacerbations.
  • Give a systemic corticosteroid to every patient in the first minutes: prednisolone 40–50 mg orally once daily for at least 5 days (reported ranges 40 mg, 40–60 mg, or 0.5–1 mg/kg/day), with no taper needed for courses of three weeks or less. It takes 4–6 hours to act, which is precisely why it cannot wait for the response to the nebuliser.
  • If vomiting, unable to swallow or too breathless to take a tablet: hydrocortisone 200 mg intravenously, then 100 mg 6-hourly until oral therapy is possible — but there is no evidence the intravenous route is superior in a patient who can swallow, and the drug must never be delayed while access is obtained. A single intramuscular dose of methylprednisolone acetate 240 mg may substitute where vomiting or non-adherence is anticipated.Doctor / Nurse
  • For severe exacerbations requiring admission, an alternative steroid regimen is prednisolone or methylprednisolone 1 mg/kg every 6–12 hours for 48 hours, or until PEF reaches 50% of predicted or baseline, then 0.5 mg/kg/day until PEF reaches 70%.
  • Reassess formally after the first dose and again after three doses (60–90 minutes after starting) recording PEF, respiratory rate, SpO₂, pulse, speech and conscious level with a clock time; repeat the PEF 15–30 minutes after starting therapy and thereafter every 4–6 hours.
  • If the patient is not responding, escalate bronchodilator delivery: repeat salbutamol 5 mg with ipratropium 500 microgram, or move to continuous salbutamol nebulisation at 5–10 mg/hour, monitoring heart rate and potassium.
  • Intravenous magnesium sulphate 1.2–2 g over 20 minutes with cardiac monitoring, as a single dose, for the patient who has not responded to initial treatment — a 2 g infusion over 20 minutes reduces hospitalisation rates in acute severe asthma (FEV₁ below 25% of predicted on presentation, or failure to respond to initial therapy). Slow the infusion if blood pressure falls; repeat dosing is not established.Doctor / Nurse
  • Aminophylline only if used at all, and never without a pump and continuous cardiac monitoring: 5 mg/kg intravenously over 20 minutes, then 0.5–1 mg/kg/hour — and omit the loading dose entirely in a patient already taking oral theophylline.Doctor / NurseNot available at your setup — Infusion pump.
  • Fluids and potassium: 0.9% sodium chloride 500–1000 mL over the first one to two hours in an adult, titrated to pulse, blood pressure and urine output rather than given as a fixed prescription, and replace potassium once the level is known.Doctor / NurseNot available at your setup — Serum electrolytes.
  • Paediatric doses — estimate weight as (age in years + 4) × 2 kg for children aged 1–10 years, record it and calculate every dose from it: salbutamol nebulised 2.5 mg under 5 years and 5 mg from 5 years, oxygen-driven, every 20–30 minutes in the first hour; or MDI plus spacer (face mask under 3 years) 6 puffs under 6 years and 10–12 puffs from 6 years, one puff at a time with 5 tidal breaths each, up to 3 times in the first hour.
  • More paediatric doses: ipratropium nebulised 250 microgram under 12 years and 500 microgram from 12 years, every 20–30 minutes for the first 2 hours in a severe attack then 4–6 hourly; soluble prednisolone 1–2 mg/kg once daily to a maximum of 40 mg (in practice 20 mg at 2–5 years, 30–40 mg over 5 years) for 3–5 days; hydrocortisone 4 mg/kg intravenously (maximum 100 mg) 6-hourly if vomiting; magnesium sulphate 40 mg/kg intravenously over 20 minutes to a maximum of 2 g as a single dose with cardiac monitoring; aminophylline 5 mg/kg over 20 minutes then 1 mg/kg/hour; fluids 0.9% sodium chloride 10 mL/kg boluses reassessed after each.Doctor / Nurse
  • Pregnancy — treat exactly as in the non-pregnant adult, because foetal hypoxia is far more dangerous than any of the drugs used; a woman on maintenance prednisolone above 7.5 mg/day should receive hydrocortisone 100 mg three to four times daily during labour.
  • Assisted ventilation is indicated for coma, respiratory arrest, exhaustion, delirium or drowsiness, or deteriorating gases despite optimal therapy — PaO₂ below 8 kPa (60 mmHg) and falling, PaCO₂ above 6 kPa (45 mmHg) and rising, pH low and falling; intubation is technically difficult and is best performed semi-electively, before the crisis of respiratory arrest, after correcting volume status.DoctorNot available at your setup — Mechanical ventilator, Endotracheal intubation kit, Arterial blood gas.

Caution— what harms

  • Never grade severity by the loudness of the wheeze: a silent chest in a distressed patient means no air is moving, and is a life-threatening feature.
  • A normal PaCO₂ in a struggling, tachypnoeic asthmatic is abnormal — they should be hyperventilating. It means alveolar ventilation is falling and the patient is tiring; a rising PaCO₂ above 6 kPa (45 mmHg) is ventilatory failure, and above 8 kPa (60 mmHg) ventilation is very likely required.
  • Never reduce the oxygen because the carbon dioxide is high. Oxygen-induced hypoventilation is extremely rare in asthmatics; the 88–92% target belongs to chronic hypercapnic respiratory failure in COPD, not here. Failure to oxygenate despite high-concentration oxygen is itself an indication for assisted ventilation.
  • Do not read apparent calming as improvement: a falling respiratory rate and a settled, drowsy patient represent exhaustion; bradycardia, hypotension or a new arrhythmia in a struggling asthmatic are pre-terminal, not incidental, and cyanosis is late.
  • Sedatives, anxiolytics and hypnotics are contraindicated because of respiratory depression — agitation in an asthmatic is hypoxaemia, so treat the hypoxaemia.
  • Mucolytics (acetylcysteine, potassium iodide) may worsen cough and airflow obstruction, chest physiotherapy has no role in the acute bronchospastic phase, and doubling the inhaled corticosteroid dose does not prevent or abort an impending exacerbation.
  • Antibiotics are not indicated routinely — the yellow or green sputum of an exacerbation frequently contains eosinophils and shed epithelium rather than bacteria; reserve them for fever and purulent sputum with radiographic pneumonia or bacterial sinusitis.
  • Do not delay the corticosteroid while obtaining intravenous access, and do not make it conditional on the response to the nebuliser — it takes 4–6 hours to act because it works on transcription, not on smooth muscle.
  • Sudden unilateral deterioration is a pneumothorax until proven otherwise, and a tension pneumothorax is a clinical diagnosis requiring immediate needle decompression, not a radiological one.
  • Two MDI puffs is not treatment: one 2.5 mg nebule delivers 25–30 times the dose of a single actuation (0.09–0.1 mg), and a nebuliser remains preferable in the patient too breathless, too agitated or too young to co-ordinate an inhalation.
  • Never give aminophylline without omitting the load in a patient already on oral theophylline, and never without an infusion pump, continuous cardiac monitoring and drug level measurement.
  • Do not skip the monitoring: check and replace potassium (beta₂-agonists plus corticosteroids cause hypokalaemia and arrhythmia), check glucose, and repeat the blood gas if the initial PaCO₂ was normal or raised, if the PaO₂ was below 8 kPa, or if the patient deteriorates — always recording the oxygen device and flow rate alongside the result.Not available at your setup — Serum electrolytes, Arterial blood gas.
  • Do not use non-invasive ventilation to defer a decision about intubation: its evidence base in acute asthma is much weaker than in COPD, and if used at all it belongs in a critical care environment with intubation equipment immediately to hand. Heliox is a rescue measure only and limits the deliverable FiO₂.
  • Do not discharge on impression: the patient should be stable on discharge medication with nebulised therapy discontinued for at least 24 hours, with a PEF of 75% of predicted or personal best (some authorities accept 60–70% with minimal symptoms), and observed for at least 30 minutes after the last bronchodilator dose — "feeling much better" is not a criterion.

Refer / escalate

Call for critical care help immediately for any life-threatening or near-fatal feature — silent chest, SpO₂ below 92%, PEF below 33%, a normal or raised PaCO₂, cyanosis, feeble effort, bradycardia, hypotension, exhaustion, drowsiness or coma — or for failure to improve after three bronchodilator treatments in the first hour, and intubate semi-electively rather than waiting for respiratory arrest.

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