Laryngospasm refers to the phenomenon that involves the involuntary and forceful contraction of laryngeal muscles, which results from the depolarization of the superior laryngeal nerve. Contraction of the laryngeal muscles results in vocal cord adduction, complete airway obstruction, and impaired ventilation. Incidence of laryngospasm is higher in children and hypoxia develops more quickly compared to adults, requiring vigilance and prompt treatment.
Three structures are involved in the laryngospasm reflex: aryepiglottic folds, false vocal cords, and true vocal cords. The muscles most involved in the laryngospasm are the lateral cricoarytenoid and the thyroarytenoids (adductors of the glottis) and the cricothyroid (a tensor of the vocal cord). During laryngospasm, either the true vocal cords alone or the true and false vocal cords both become apposed in the midline and close the glottis. Folding in of the aryepiglottic folds results in a true ball-valve closure of the larynx and involves contraction of the infrahyoid (“strap”) muscles of the neck (sternohyoid, sternothyroid, thyrohyoid, and omohyoid muscles).
Stimuli that may trigger laryngospasm include “light” anesthesia, irritant volatile anesthetics or failure of the anesthesia delivery system, regurgitation of enteric contents into the oropharynx and oropharyngeal secretions or blood contacting adjacent laryngeal structures, the contact of the endotracheal tube with laryngeal structures during tracheal intubation/extubation causing airway irritation as well as the presence of nociceptive stimuli during surgical stimulation. Laryngospasm is more common after upper airway procedures, particularly ENT procedures in which blood, secretions, and surgical debris are present.
Laryngospasm may manifest with inspiratory stridor, increased inspiratory efforts (ie, tracheal tug), paradoxical chest and abdominal movements that can quickly progress to complete airway obstruction, desaturation, bradycardia, and central cyanosis.
Different approaches that may be used in preventing laryngospasm under anesthesia include intravenous lidocaine, topical lidocaine, intravenous magnesium, and “deep” extubation.
Early management of laryngospasm includes clearing blood and secretions from the airway and applying chin lift and jaw thrust, and insertion of an oral-pharyngeal airway followed by the application of end-expiratory pressure (PEEP) or continuous airway pressure (CPAP) via a tight-fitting mask and 100% oxygen to aid in splinting open the laryngeal musculature. The cricothyroid muscle is the only tensor of the vocal cords and a gentle stretching of this muscle may overcome moderate laryngospasm. Jaw thrust will aid in lifting up the tongue and unfurling of the aryepiglottic fold, and opening of the anterior commissure to allow passage of some flow with CPAP.
The laryngospasm notch, also called Larson point, is located behind the lobule of the pinna of each ear (Figure 106-1). Firm digital pressure is applied at the most superior portion of the laryngospasm notch inward, toward the base of the skull with both fingers and simultaneously the mandible is lifted at right ...