ICU · Respiratory / ventilation
Severe & Near-Fatal Asthma in the ICU
Also known as Severe asthma · Near-fatal asthma · Status asthmaticus · Acute severe asthma · Life-threatening asthma · Critical asthma syndrome · Magnesium sulphate in asthma · Ketamine for asthma · Permissive hypercapnia in asthma · Volatile anaesthetics in asthma · Heliox · VV-ECMO for asthma
Severe or near-fatal asthma (status asthmaticus) is graded by the British Thoracic Society as acute severe, life-threatening, or near-fatal. The escalation ladder is oxygen (SpO2 94-98 per cent), repeated or continuous nebulised salbutamol with ipratropium 0.5 mg, an early systemic corticosteroid (oral prednisolone, or intravenous hydrocortisone when the oral route is unsuitable), intravenous magnesium sulphate 2 g over 20 minutes for severe disease not responding to initial treatment, and second-line aminophylline or IV salbutamol. If the patient tires or the PaCO2 rises, intubate with a bronchodilating induction agent such as ketamine and ventilate for permissive hypercapnia (low tidal volume, low rate, long expiration, plateau pressure kept below about 30 cmH2O). Refractory bronchospasm is treated with inhalational volatile anaesthetics (sevoflurane), Heliox, or VV-ECMO. Watch for the auto-PEEP arrest, tension pneumothorax, lactic acidosis, and hypokalaemia.
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Target exams
Red flags
- A normal or rising PaCO2 in acute asthma is pre-arrest — the patient is tiring, prepare for intubation
- A silent chest, cyanosis, exhaustion, or altered consciousness = life-threatening, escalate now
- Hypotension or PEA minutes after intubation = auto-PEEP arrest — disconnect the circuit, let the lung deflate
- Intubate with ketamine (a bronchodilator); propofol and thiopentone can worsen bronchospasm and cause hypotension
- High-dose salbutamol causes lactic acidosis (beta-2 effect) and hypokalaemia — monitor and replace potassium
- Avoid combining neuromuscular blockade with corticosteroids — high risk of critical-illness myopathy
- Barotrauma — pneumomediastinum, subcutaneous emphysema, tension pneumothorax — from hyperinflation and high airway pressures
Meet the patient
A 26-year-old who has been wheezing for hours becomes quiet in resus. She can no longer speak, her chest is almost silent, and PaCO2 has risen from 30 to 42 mmHg. The inexperienced response is relief that the gas is normal; the correct response is to prepare the airway.[5][7]
Three findings tell you she is near arrest: less sound, less speech, and more carbon dioxide. Asthma should produce vigorous hypocapnic ventilation. When that compensation disappears, the respiratory muscles are losing.[5][7]
References23ShowHide
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