Laryngospasm
Formal Definition
Laryngospasm — an involuntary, sustained, reflex closure of the vocal cords and laryngeal muscles (primarily the adductor muscles, including the lateral cricoarytenoid, thyroarytenoid, and interarytenoid) in response to stimulation of the superior laryngeal nerve afferents from the glottic region (most often from secretions, blood, or stimulation during light anesthesia, or from intubation/extubation); remains open until the trigger is removed or the patient is fatigued enough to allow relaxation; can result in complete airway obstruction with inability to ventilate, severe hypoxia, and potentially negative pressure pulmonary edema if sustained; a classic intraoperative and post-extubation emergency.
How It's Used on the Ward
"Laryngospasm" on induction or emergence from anesthesia — when the patient's vocal cords slam shut and the anesthesiologist cannot ventilate them; recognized by the "can't ventilate, can't intubate" pattern with high inspiratory pressures and a characteristic stridor; treated with jaw thrust, positive pressure via mask, deepening of anesthesia, and ultimately small doses of muscle relaxant if needed.
Example
""35-year-old patient (Mallampati 2, normal airway exam) undergoing elective inguinal hernia repair under general anesthesia. After IV induction with propofol and successful LMA placement, surgery proceeds. On attempted LMA removal at end of case, patient coughs and light anesthesia is briefly inadequate; secretions above the LMA stimulate the larynx. Patient develops stridor and inability to ventilate. Anesthesiologist: 'Laryngospasm — jaw thrust, 100% O2, sustained positive pressure 25 cm H2O, prepare succinylcholine 20 mg IV if not resolved in 30 seconds.' Jaw thrust and sustained PPV break laryngospasm in 15 seconds; oxygen saturation rebounds from 89% to 99%; patient transferred to PACU stable.""
Clinical Context
Why it happens: larynx is highly reactive to stimulation (secretions, blood, instrumentation) under light anesthesia. Most common phases: (1) Induction, especially in semi-awake patient with stimulation. (2) Emergence from anesthesia, when the patient is light and being suctioned or extubated. Predisposing factors: recent URI (more reactive airway), GERD, asthma, smoking, tonsillar hypertrophy in pediatrics, young age (kids have more reactive airways). Recognition: absent or poor chest rise with positive pressure ventilation, characteristic inspiratory stridor, SpO2 dropping, no capnograph waveform (no gas exchange). Treatment ladder: (1) jaw thrust + chin lift + 100% O2. (2) Sustained positive pressure at 25–40 cm H2O via mask (overcomes laryngeal closure). (3) Larson maneuver (pressure on "notch" — pressure on the notch between the posterior border of the mandibular ramus and the mastoid process bilaterally). (4) IV propofol deepening. (5) IV succinylcholine (10–20 mg). (6) IM succinylcholine if no IV access. (7) Reintubate if unable to ventilate despite neuromuscular blockade. Complications: hypoxia, negative pressure pulmonary edema, dental trauma from forced ventilation, post-obstructive pulmonary edema. Pediatric laryngospasm is particularly common during emergence with sevoflurane; prevention includes gentle suction under deep anesthesia, IV lidocaine, extubation under deep anesthesia with help from airway exchange catheter.