Laryngospasm

T1Airway·950 words · ~5 min read·v0.1✓ Sourced · 4DRAFT

Why examiners ask this

Laryngospasm is the commonest airway emergency at emergence, and the examiner wants a stepwise escalation delivered in seconds, not a list. It tests organization (what first, what next), judgment about when to stop waiting and give succinylcholine, and adaptability when there is no IV in a child. It also leads naturally into negative-pressure pulmonary edema and the decision to extubate deep or awake.

The 60-second answer

A patient who was breathing and now has a silent chest, a flat or absent capnograph, paradoxical chest and abdominal movement, or inspiratory stridor after extubation has laryngospasm until I prove otherwise. I call for help, remove the stimulus, suction the pharynx, and apply a tight-fitting mask with 100% oxygen and continuous positive pressure while I perform a jaw thrust and press firmly in the laryngospasm notch behind the ramus of the mandible.¹ If that does not break it within about 30 seconds, or the saturation is falling, I deepen with propofol 0.5–1 mg/kg IV. If the spasm persists while the saturation keeps falling or the heart rate drops, I give succinylcholine 0.1–0.5 mg/kg IV, or a full 1–2 mg/kg and intubate if the spasm is severe, with atropine in a child.² Without an IV, I give succinylcholine 3–4 mg/kg IM, no more than 150 mg.³ Afterward I watch for pulmonary edema and aspiration.

Decision points and the "why"

CPAP before drugs — partial spasm often yields to positive pressure because it stents the false cords apart; forcing pressure against complete closure only insufflates the stomach, so I watch whether gas moves before I keep squeezing the bag.
Larson's maneuver — firm pressure in the notch between the condyle and the mastoid is painful enough to reflexly relax the cords; it is free and fast, so I do it with the jaw thrust, not after.²
Propofol as the second step — it deepens anesthesia and blunts the reflex within one circulation time; I choose it over more volatile because inhaled agent cannot reach the alveoli through a closed glottis.
Small-dose succinylcholine — 0.1–0.5 mg/kg relaxes the cords and often avoids reintubation; I move to a full intubating dose if the patient is desaturating or bradycardic, because I then need a secure airway rather than a trial.
Atropine in children — hypoxia plus succinylcholine is a vagal setup; I give atropine 0.02 mg/kg with or before the succinylcholine in any infant or small child, and immediately if the heart rate is falling.²
No IV — intramuscular succinylcholine 3–4 mg/kg (maximum 150 mg) into the deltoid or the tongue base usually takes 2–3 minutes;³ intraosseous access is faster for drugs if I already need resuscitation.
Deep or awake extubation — I extubate in a clearly deep plane or fully awake, never in between, because stage 2 is when the reflex is most active; a recent URI, secretions, blood in the airway, and passive smoke exposure push me toward awake; a URI within 6 weeks or second-hand smoke each raise the risk up to 10-fold.¹

The complication they will inject

The spasm breaks after succinylcholine, the child is reintubated, and pink frothy fluid appears in the tube with an SpO2 of 88% on 100% oxygen. This is negative-pressure pulmonary edema from vigorous inspiration against a closed glottis; laryngospasm is its commonest cause.⁴ I tell the surgeon and the team, keep the tube in, apply PEEP of 5–10 cmH2O, suction, and support oxygenation. I send the child to a monitored bed or PICU, get a chest radiograph to separate this from aspiration, and give furosemide only if there is volume overload, because the edema is driven by transmural pressure and usually resolves in 12–24 hours with PEEP alone.⁴ I reassess before any attempt at extubation.

Pitfalls that cost points

Reciting the treatments without a time trigger for moving from CPAP to drugs.
Giving succinylcholine to a bradycardic child without atropine.
Treating stridor as laryngospasm when the cause is a retained throat pack, blood clot or edema; I look and suction.
Forgetting post-event monitoring for pulmonary edema and aspiration in an ambulatory patient.
Extubating in a light plane "to be safe" after a tonsillectomy.

Rapid-why

Q: Why does the capnograph go flat but the chest still move? A: The patient is making inspiratory efforts against a closed glottis; no gas moves, so there is no CO2 waveform and the chest and abdomen move paradoxically.

Q: Why does IV lidocaine help? A: Lidocaine 1–1.5 mg/kg given about 2 minutes before extubation suppresses airway reflexes; I use it as prevention, not rescue.

Q: What makes children higher risk? A: A smaller functional residual capacity and higher oxygen consumption shorten the time to desaturation, and URIs, airway surgery and inhalational induction all raise reflex sensitivity.

Q: How do you tell laryngospasm from bronchospasm? A: Laryngospasm gives stridor or silence with no gas exchange; bronchospasm gives wheeze, a prolonged expiratory upslope on the capnograph and high airway pressures with some ventilation possible.

Numbers to know

Item	Value
Propofol to deepen	0.5–1 mg/kg IV
Succinylcholine, relaxing dose	0.1–0.5 mg/kg IV
Succinylcholine, intubating	1–2 mg/kg IV; 3–4 mg/kg IM, max 150 mg³
Atropine, child	0.02 mg/kg IV/IM²
Lidocaine for prevention	1–1.5 mg/kg IV before extubation
PEEP for negative-pressure edema	5–10 cmH2O

Sources

1.Laryngospasm · OpenAnesthesia (IARS), 2023 · openanesthesia.org
2.Laryngospasm · Life in the Fast Lane · litfl.com
3.QUELICIN (succinylcholine chloride) injection prescribing information · FDA / DailyMed · dailymed.nlm.nih.govSection 2.4: IM up to 3-4 mg/kg, total IM dose not to exceed 150 mg, onset about 2-3 min.
4.Negative pressure pulmonary edema (Review) · Experimental and Therapeutic Medicine, 2023 · ebi.ac.ukFull text via Europe PMC (PMC10443067).

Facts on this page were checked against these sources on Oct 14, 2026. Guidelines change; confirm doses against current institutional protocols.