Management of Ketamine‑Induced Laryngospasm

Recognition and Immediate Airway Support

Recognize laryngospasm by an inspiratory “crowing” sound, suprasternal recession, use of accessory muscles, and paradoxical thoraco‑abdominal movements; complete obstruction presents as silent inspiration, requiring immediate action without waiting for spontaneous vocal‑cord opening. 1
Apply continuous positive airway pressure (CPAP) with 100 % oxygen using a reservoir bag and facemask while keeping the upper airway patent. 1
Avoid unnecessary upper‑airway stimulation during treatment, as it can worsen or prolong the spasm. 1
Perform Larson’s manoeuvre (jaw thrust with deep pressure applied at the “laryngospasm notch” between the posterior mandible and mastoid process) to help break the spasm. 1

Give propofol 1–2 mg kg⁻¹ intravenously if the spasm persists or oxygen saturation is falling; larger doses may be required for severe or total cord closure unresponsive to initial propofol. 1
Administer succinylcholine 1 mg kg⁻¹ intravenously when hypoxia worsens despite propofol, providing complete vocal‑cord relaxation for ventilation and possible intubation. 1
If intravenous access is unavailable, succinylcholine can be delivered intramuscularly (2–4 mg kg⁻¹), intralingually (2–4 mg kg⁻¹), or intraosseously (1 mg kg⁻¹). 1
Atropine may be required to treat bradycardia that follows succinylcholine administration. 1

Consider a surgical airway (e.g., cricothyrotomy) in extremis when all non‑invasive measures fail. 1

Ketamine exhibits a paradox: it can both precipitate and alleviate laryngospasm, so management should follow the standard algorithm regardless of ketamine use. 1
Do not delay escalation of treatment; laryngospasm can rapidly progress to complete airway obstruction and hypoxic cardiac arrest. 1
The belief that “hypoxia will break the laryngospasm” is dangerous—vocal cords will not reopen before fatal hypoxia occurs. 1

Monitor for post‑obstructive pulmonary edema, which occurs in approximately 4 % of laryngospasm cases; typical signs include dyspnea, agitation, cough, pink frothy sputum, and low oxygen saturation, resulting from negative intrathoracic pressure generated by forceful inspiratory attempts against a closed airway. 1

Laryngospasm risk is highest during lighter planes of anesthesia, but ketamine‑induced episodes can also happen under deep anesthesia. 1
Children, smokers, patients with pre‑existing airway infections, and procedures involving airway manipulation with increased secretions carry a higher risk of laryngospasm. 1

The American Society of Anesthesiologists recommends immediate treatment of laryngospasm with continuous positive airway pressure (CPAP) and 100% oxygen, as this condition can progress to hypoxic cardiac arrest and death if not promptly managed 2, 3, 4
Call for help immediately upon recognizing laryngospasm, as this is a potentially life-threatening emergency that requires prompt intervention 2, 3, 4

The Difficult Airway Society guidelines suggest administering propofol 1-2 mg/kg intravenously if laryngospasm persists and/or oxygen saturation is falling, with the strength of evidence being high for this recommendation 2, 3, 4
Administer intravenous succinylcholine 1 mg/kg if hypoxia worsens, as this provides complete vocal cord relaxation, permitting ventilation, re-oxygenation, and intubation if necessary, with a moderate level of evidence supporting this intervention 2, 3, 4
Succinylcholine can be administered via alternative routes, including intramuscular (2-4 mg/kg), intralingual (2-4 mg/kg), and intraosseous (1 mg/kg), in the absence of intravenous access, based on expert opinion 2, 3, 4

Laryngospasm presents with characteristic inspiratory 'crowing' sound, marked suprasternal recession, use of accessory respiratory muscles, and paradoxical thoracoabdominal movements, according to the American Academy of Pediatrics, with a high level of evidence for these clinical findings 3, 5

Post-obstructive pulmonary oedema develops in approximately 4% of laryngospasm cases, presenting with dyspnoea, agitation, cough, pink frothy sputum, and low oxygen saturations, as reported by the American Thoracic Society, with a moderate level of evidence for this complication 2

Do not delay escalation of treatment if initial measures fail, as laryngospasm can progress rapidly to complete airway obstruction and hypoxic cardiac arrest, according to the Difficult Airway Society guidelines, with a high level of evidence supporting prompt intervention 2, 3
Avoid unnecessary airway stimulation during treatment, as this can worsen or prolong the laryngospasm, with a moderate level of evidence supporting this recommendation 2, 3