A lesson from Intraoperative Challenges: Fires, Laryngospasm, Bronchospasm, Aspiration, and POVL

Laryngospasm: Mechanism, Risk Factors, and Why Extubation Timing Matters

Apprehensions about triggering laryngospasm have made some practitioners hesitant to employ deep or sedated extubation methods that could mitigate these risks. It’s vital to understand the complex dynamics of laryngeal function to effectively manage post-extubation airway obstructions, including laryngospasm.

Put simply, laryngospasm is a condition characterized by the contraction of the glottis adductor muscles, which include the lateral cricoarytenoid and interarytenoid muscles, as well as the vocal cord tensor, the cricothyroid. This can lead to either a partial or complete spasm. In a partial spasm, there is still some air movement, which may be accompanied by crowing sounds or phonation and paradoxical chest movements. A complete spasm, however, results in no air movement at all, necessitating immediate identification due to the risks of hypoxia and negative-pressure pulmonary edema (NPPE).

However, the larynx can occlude reflexively at various levels, not just at the true vocal cords. This understanding challenges the notion that positive-pressure ventilation via mask can resolve laryngospasm, an assertion not backed by extensive literature. Moreover, diagnosing and treating laryngospasm or any form of airway obstruction promptly is crucial to prevent severe consequences like hypoxemia and cardiac arrest, which are particularly significant concerns in pediatric cases.

Addressing these airway challenges necessitates a comprehensive approach, including recognizing the multifaceted nature of the larynx, the factors contributing to laryngospasm, and the limitations of positive-pressure ventilation in these scenarios. Effective management strategies emphasize the importance of smooth extubation techniques that avoid triggering reflexive airway obstructions and leveraging a variety of medications and interventions tailored to the patient's needs.

Initial management is stepwise: deliver 100% oxygen, stop the triggering stimulus, and apply a firm jaw thrust with continuous positive airway pressure, pressing at the laryngospasm notch (Larson's point) behind each earlobe. If the spasm does not break, deepen the anesthetic, typically with a small bolus of propofol. Succinylcholine is reserved for spasm that persists despite these measures.

Stepwise management of laryngospasm from oxygen and CPAP to succinylcholine

For managing laryngospasm, particularly in situations where rapid intervention is required and intravenous access is already established or quickly achievable, the recommended intravenous (IV) dose of succinylcholine is:

0.1 to 0.2 mg/kg body weight for IV administration.

This lower dose, compared to the full dose used for tracheal intubation, is often sufficient to relieve laryngospasm. It acts quickly, usually within 30 to 60 seconds, and the effects typically last a few minutes, allowing for brief but effective intervention to alleviate the spasm and secure the airway.

For cases where IV access is not immediately available, especially in emergency situations or with pediatric patients, succinylcholine can be administered intramuscularly (IM). The recommended dose for IM administration is higher due to slower absorption:

4 to 5 mg/kg body weight for IM administration.

This IM dose can provide a rapid onset of action, though not as quick as IV administration, and can be a critical intervention in severe cases of laryngospasm where securing the airway is immediately necessary.

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