Dr Hector Thomson
Peer review: Dr David McCreary
What is laryngospasm?
Laryngospasm is potentially life-threatening closure of the true vocal cords resulting in partial or complete airway obstruction. This is a primitive protective airway reflux that aims to protect against aspiration but can cause life threatening hypoxia.
In laryngospasm either the true cords alone or the false cords slam shut and close the glottis. Most laryngeal reflexes are produced by stimulation of the superior laryngeal nerve which provides sensory innervation to the supraglottic region. This is a branch of the vagus nerve. The muscles involved are the lateral cricoarytenoid and the thyroarytenoids (adductors) and the cricothyroid (vocal cord tensors). The cricothyroid muscle is the only tensor of the vocal cords. Gentle pressure from a jaw thrust may overcome moderate laryngospasm.
What causes it?
- Extubation: children with URTI symptoms (beware the snotty child)
- Airway manipulation (especially when under light anaesthesia)
- ENT procedures (usually involves lots of suctioning and prodding around the airway!)
- Secretions/blood/vomit in airway
- Foreign body
- Near drowning
- Drugs (rarely associated with ketamine sedation)
- Vocal cord dysfunction
- Past history
- Recent URTI
In the ED we will encounter this while performing procedural sedation. The feared situation being IM ketamine sedation then laryngospasm that doesn’t settle with first line measuring. Leading to a scramble to gain IV access. There is also a case report from RCH of a case during nitrous oxide sedation.
🤓 TOP TIP: Give your ketamine slowly to reduce complications (Credit: Dr Shaun Baxter) Ed: In particular this avoids the ‘stunned apnoea’ that a fast push can cause – which can cause some 🤨 in the room.
How do we recognise it?
Laryngospasm exists on a spectrum from partial to complete obstruction and occasionally presents atypically and without warning signs
🚨 Early warning = Loss of end-tidal CO2 🚨
- Inspiratory stridor/airway obstruction
- Increased inspiratory efforts/tracheal tug
- Paradoxical chest/abdominal movements
- No chest wall movements
- No airway sounds
- Inability fo ventilate
- Central cyanosis
In 189 cases reported to the Australian Incident Monitoring Study:
- 77% were clinically obvious
- 14% presented as airway obstruction
- 5% as regurgitation
- 4% as desaturation
PAUSE: Proceduralist stop the procedure
PERSONEL: Call for help – the situation can rapidly deteriorate An airway crisis needs a team and you will need but a team leader and an expert to manage the airway + drugs drawn up and equipment prepared
POSITION: Jaw thrust/Chin lift + Suction blood and secretions
PEEP:100% O2 via mask with PEEP valve Consider a guedel airway
PRESSURE POINT: Larson’s point bilaterally while forming jaw thrust
PROPOFOL: 0.5mg/kg IV to deepen sedation/anaesthesia If rapidly developing hypoxia proceed to next step
PARALYSE:1.5mg/kg IV and intubate -> 3-4mg/kg IM has been suggested but remember you can put an IO in quickly Give atropine 20mcg/kg as bradycardia can develop with hypoxia. The anaesthetic approach has been suggested to get a low dose suxamethonium to break the spasm. My thought is if I am giving a paralytic for laryngospasm it is an airway emergency requiring intubation.
What complications can arise?
- Desaturation (60%)
- Bradycardia (6%)
- Negative pressure pulmonary oedema (4%)
- Aspiration (3%)
- Cardiac arrest (0.5%)
- Ischaemic brain injury
Side Note - Where is Larson's Point?
Image: from Larson’s original paper
Don’t Forget the Bubbles have a fantastic section on procedural sedation. In it, they include a flowchart to be filled out for every patient prior to sedation. All the paediatric anaesthetists I worked with would check they had sux and atropine to hand and some would draw up emergency drugs to ward off the evil laryngospasm spirits. In ED I think this is a bit of a waste of medications but for every procedural sedation, I ensure I have sux, atropine and adrenaline to hand along with needles to draw them up.
🤓 Ed: I don’t have the drugs drawn up (massive waste given the frequency of the event), and I don’t have them on the side either. I do, however, specifically run through the steps we’d take for a laryngospasm event with the nursing staff as part of the pre-procedure timeout and in that I include that I could ask for sux and they should have eyeballed it and know where to get it immediately if needed.
Source: Don’t Forget The Bubbles
So remember – just stay calm and don’t fear the squeak!
- First10 EM
- Don’t Forget The Bubbles
- Life in the Fast Lane
- McCreary D, Neill A. NewinEM – Risk Factors for Adverse Events in Emergency Department Procedural Sedation for Children.
RCEMLearning Podcast February 2018.
- Hernández-Cortez E. Update on the management of laryngospasm. J Anesth Crit Care Open Access. 2018;8(2):1–6. DOI: 10.15406/jaccoa.2018.08.00327
- N D’souza, R Garg. Perioperative Laryngospasm – Review of literature. The Internet Journal of Anesthesiology. 2008 Volume 20 Number 1. Laryngospasm With Apparent Aspiration During Sedation With Nitrous Oxide Babl, Franz E. et al. Annals of Emergency Medicine , Volume 66 , Issue 5 , 475 – 478. doi: 10.1016/j.annemergmed.2015.04.029
- Bellolio MF, Gilani WI, Barrionuevo P. Incidence of Adverse Events in Adults Undergoing Procedural Sedation in the Emergency Department: A Systematic Review and Meta-analysis. Academic emergency medicine : official journal of the Society for Academic Emergency Medicine. 23(2):119-34. 2016. doi: 10.1111/acem.12875
- Visvanathan T, Kluger MT, Webb RK, Westhorpe RN. Crisis management during anaesthesia: laryngospasm. Qual Saf Health Care. 2005 Jun;14(3):e3. doi: 10.1136/qshc.2002.004275. PMID: 15933300; PMCID: PMC1744026.
- Al-Metwalli RR, Mowafi HA, Ismail SA. Gentle chest compression relieves extubation laryngospasm in children. J Anesth. 2010;24(6):854-857. doi: 10.1007/s00540-010-1036-9
- Philip C. Larson; Laryngospasm-The Best Treatment . Anesthesiology 1998; 89:1293–1294 doi: 10.1097/00000542-199811000-00056