Intraoperative Bronchospasm Management
Immediately deepen anesthesia with 100% oxygen and increase volatile anesthetic concentration (if using inhalational agents), then administer inhaled albuterol (2.5-5 mg via nebulizer or 4-8 puffs via MDI with spacer) as first-line bronchodilator therapy. 1
Immediate Initial Steps
- Increase FiO2 to 100% and manually ventilate with smaller tidal volumes and slower respiratory rates to reduce airway pressures and allow adequate expiratory time 1
- Deepen anesthesia using volatile anesthetics (sevoflurane or isoflurane at 2-3 MAC) which provide direct bronchodilation through smooth muscle relaxation 2
- Remove any potential triggers (endotracheal tube malposition, surgical stimulation, aspiration) 1
First-Line Pharmacologic Treatment
Inhaled short-acting beta-2 agonists (SABAs) are the definitive first-line treatment:
- Albuterol 2.5-5 mg via nebulizer in 3 cc saline, or 4-8 puffs (400-800 mcg) via MDI with spacer adapter on the breathing circuit 1
- May double the dose for severe bronchospasm 1
- Onset of action within 5-15 minutes with peak effect at 30-60 minutes 3
- Levalbuterol 0.63-1.25 mg is an alternative with potentially fewer cardiac side effects 1
Second-Line Adjunctive Therapy
If bronchospasm persists despite adequate SABA administration, add:
- Ipratropium bromide 0.5 mg (500 mcg) via nebulizer mixed with albuterol 1, 4
- Provides additive benefit to SABA therapy by blocking cholinergic-mediated bronchospasm 1, 5
- Particularly effective when bronchospasm may be triggered by vagal stimulation from airway manipulation 4, 5
- Note: Ipratropium has slower onset (15-30 minutes) compared to albuterol, so should not be used as monotherapy in acute situations 4
Systemic Corticosteroids
- Methylprednisolone 40-60 mg IV or equivalent dose of alternative corticosteroid 1
- Prevents late-phase inflammatory response and reduces risk of recurrent bronchospasm 1
- Effects take 4-6 hours to manifest, so this is prophylactic rather than immediate treatment 1
Critical Pitfalls to Avoid
Regarding the neostigmine/atropine context:
- The bronchospasm is NOT caused by neostigmine or atropine - these agents were given for neuromuscular blockade reversal, which is appropriate and necessary 1
- Neostigmine increases acetylcholine at the neuromuscular junction (nicotinic receptors), not at bronchial smooth muscle (muscarinic receptors) 6, 7
- The co-administered atropine blocks muscarinic side effects of neostigmine, including any potential bronchospasm from muscarinic stimulation 2
- Do not withhold or delay appropriate neuromuscular blockade reversal in patients with reactive airway disease 1, 6
Other critical considerations:
- Paradoxical bronchospasm from albuterol itself is extremely rare but documented - if bronchospasm worsens after albuterol, immediately discontinue and switch to alternative bronchodilators 8
- Avoid excessive positive pressure ventilation which can worsen air trapping and cause barotrauma 1
- In patients with known severe asthma or COPD, consider prophylactic bronchodilator administration before extubation 1
Monitoring and Escalation
- Continuously monitor peak inspiratory pressures, end-tidal CO2 waveform (prolonged expiratory phase), oxygen saturation, and auscultation 1
- If bronchospasm remains refractory after the above measures, consider: