Laryngospasm: review of different prevention andTreatment

Marzieh Beigom Khezri

Department of Anesthesiology, Medical School, Qazvin University of Medical Science, Qazvin, Iran. E-mail:

Learning objective: Discusses laryngospasm with the emphasis on thedifferent prevention and treatment modalities,specially presentsgentle chest compression as an alternative to standardpractice for relief of laryngospasm.

Introduction:

Laryngospasm is areflex closure of the upper airway as a result ofthe glottic musculature spasm. It is essentially aprotective reflex that acts to prevent foreignmaterial entering the tracheobronchial tree. Theexaggeration of this reflex may result in completeglottic closure and consequently impeding respiration1. Morbidity and mortality may result from the immediate (hypoxemia and hypercapnia) and delayed (“negative-pressure pulmonary edema”) consequences of laryngospasm, and thus every effort should be made to rapidly relieve the airway obstruction caused by laryngospasm.2

Differential diagnosis:

  • Bronchospasm
  • Supraglottic obstruction
  • Vocal cord palsy(a bilateral complete recurrent laryngeal nerve palsy (affecting abduction and adduction) results in both vocal cords adopting a paramedian position. A partial bilateral recurrent laryngeal nerve palsy involving only the abductor fibers can result in bilateral adducted vocal cords, an inability to open the vocal cords on inspiration, serious compromise to airflow, and a critically obstructed airway, which may require immediate intervention. Bilateral incomplete palsy is more dangerous than complete palsy.3
  • Tracheomalacia
  • Psychogenic
  • Laryngomalacia
  • Airway edema
  • Hematoma, soft tissue obstruction,
  • The presence of foreign material such as throat packs.

Both supraglottic obstruction and partial laryngospasm are associatedwith inspiratorystridor and intercostal retractionswith rapidly deteriorating oxygenation. These twocomplications can be differentiated by directly visualizingthe vocal cords while the patient is makinginspiratory efforts .4

Risk factors

Risk factors can be classified into three categories:

  • Anesthesia-related factors
  • Patient-related factors
  • Surgery-related factors

Anesthesia-related factors:

  • Insufficient depth of anesthesia5,6,7
  • Airway irritation with volatile anesthetics,mucus or blood
  • Airway manipulation with suction catheter or laryngoscope blade 6,7
  • Among the intravenous (i.v.) induction agents, barbiturates such as thiopentone have been shown to increase the incidence of laryngospasm. 8-14 Ketamine is rarely associated with laryngospasm (0.4%) .15,16 However, ketamine may cause hyper-salivationwhich can precipitate laryngospasm by irritating the vocal cords.16 Also, anesthesia induction with propofol is less associated with laryngospasm than sevoflurane induction .17
  • Among all the volatile agents, the highest incidenceof laryngospasm is associated with desflurane(50%). Isoflurane is more associated with laryngospasmthan enflurane, halothane and sevoflurane.18-20 There is no difference in the incidence oflaryngospasm between sevoflurane and halothane.21
  • Age (The incidence of laryngospasm following generalanesthesia is inversely correlated with age.22
  • Upper respiratory tract infection
  • Active asthma(Children with upper respiratory tract infection or active asthma have irritable airway and are approximately 10-fold more prone to develop laryngospasm.Chronic smokers(There is a 10-fold increase in the incidence of laryngospasm in children who are exposed totobacco smoke.12
  • History of gastroesophageal reflux .23,24
  • Patients with elongated uvula and those with history of choking during sleep may also develop laryngospasm under general anesthesia .6,25,26

Surgery-related factors:

  • Tonsillectomy and adenoidectomy have the highest incidence of laryngospasm (21–26%) .1,11,27,28
  • Appendicectomy, cervical dilation, hypospadias surgery and skin transplant in children are highly associated with laryngospasm .8
  • Thyroid surgery29,30
  • Esophageal procedures8,31

Prevention

  • Identifying the patients at risk for laryngospasm.
  • Inhalational induction of anesthesia should be carried out by a nonirritant anesthetic such as sevoflurane.
  • Laryngoscopy and tracheal intubation should also be attempted after deepening the level of anesthesia.
  • Deep tracheal extubation.(The advantage of deep tracheal extubation over awake extubation in children undergoing tonsillectomy is that patients are less likely to cough and strain which can cause bleeding from the tonsilar bed and consequently increasing the risk of laryngospasm. On the other hand, awake tracheal extubation offers the advantage of protecting the airway against aspiration during this vulnerable period. Pounder et al.32 studied the incidence of respiratory complications in children undergoing minor surgery and found greater oxyhemoglobindesaturationin the awake extubation group than in the deep extubation group (P < 0.05). They also found 16% incidence of laryngospasm in the awake group versus 4% incidence in the anesthetized group (P > 0.05).
  • Positive pressure inflation of the lungs before tracheal extubation is followed by forcedexhalation ‘artificial cough’ after extubation which expels any secretions or blood and this in turn decreases vocal cord irritation and laryngospasm.
  • Premedication with anticholinergic agents(Premedication with anticholinergic agents to prevent larygospasm is controversial. However, anticholinergics decrease secretions which play a role in triggering laryngospasm and thus they play an indirect role in reducing the incidence of laryngospasm.9,22,27,33
  • Premedication with an oral benzodiazepine.34,33,35,36
  • Use of lidocaine (intravenous lidocaine37 or topical38
  • Use of magnesium(15 mg/kg) magnesium sulphate in 30 ml 0.9% NaCl over 20 min after trachea intubation.39
  • Use 5% carbon dioxide (CO2)( for 5 min prior to tracheal extubation).40
  • Acupuncture.11

Treatment

  • Identifying and removing the offending stimulus
  • Applying jaw thrust maneuver

  • LarsonManeur41(It involves placing the middle finger of each hand in what they term the ‘laryngospasmnotch’ (Figure 1). This technique consists of firmly pressing inward toward the base of the skull with both fingers, while at the same time applying jaw thrust maneuver .21On the otherhand LarsonManeur defined as a forcible jaw thrust with bilateral digital pressure on the body of the mandible just anterior to the mastoid process, known as Larson's point. This opens the airway and induces periosteal pain by pressing on the styloid process which helps relaxing the vocal cords by the autonomic nervous system .21,42

Figure 1Laryngospasm notch (located behind the lobule of the pinna of theear, bounded anteriorly by the ascending ramus of the mandibleadjacent to the condyle, posteriorly by the mastoid process of thetemporal bone and cephalad by the base of the skull). Larson's maneuver was described as a forcible jaw thrust with bilateral digital pressure on the body of the mandible just anterior to the mastoid process, known as Larson's point, may resolve laryngospasm by clearing the airway and stimulation.

  • Inserting an oral or nasal airway
  • Positive pressure ventilation with 100% oxygen.
  • Chest compression43-45(chest compressionwith 100% O2 via a tight-fitting face mask was effective in relieving extubation laryngospasm in most children(73.9%) after tonsillectomy or adenoidectomy surgery). Gentlechest compression should be performed by using the extended palm of the freehand placed on the middle of the chest, with the fingersdirected caudally and performing a compression force halfor less than half that used for cardiopulmonary resuscitation(CPR) at a rate of approximately 20–25 compressionsper min. Additionally, none of the patients managed by chest compression developed gastric distension compared to 86.5% of children in the Standard-Practice Group.45The mechanism of chest compression in the relief oflaryngospasm is unknown. However, some mechanismsmay be proposed. First, in laryngospasm, either the truevocal cords alone or the true and false vocal cords becomeopposed in the midline and close the glottis. When the truevocal cords are in opposition, they prevent the entrance ofair, but not its exit, whereas apposition of false vocal cords was capable of preventing both entrance and exit of air.46 Chest compression pushes air in the lung to act directly on the vocal cords to relieve the spasm. In cases oftrue vocal cord opposition; chest compression will force the air through a small lumen left open at the posteriorcommissure of the vocal cords. This will ensure ventilation and gas exchange between air trapped in the lung andoxygen in the pharynx, which will cause rapid relief of laryngeal spasm. In complete laryngeal spasm, in whichboth true and false vocal cords are opposed, This technique could help in converting complete to partial laryngealspasm as air force from below could push the area just above the false cords away from each other, opening theentrance of the larynx. Second, chest compression stimulates fast, shallow breathing with or without increases inminute ventilation .47-50This increased respiratory drive has been suggested as the mechanism of action .51Third, the Hering–Breuer deflation reflex, which is mediated via the vagus nerve, might be activated. It is initiatedeither by stimulation of stretch receptors or stimulation of proprioceptors activated by lung deflation. The impulsesthrough the vagus nerve, would favor relaxation of thevocal cords.52
  • Deepening the levelof anesthesia with i.v. or inhalational anesthetic. Propofol can be used at doses 0.25–0.8 mg/kg because of its rapid and predictable action, but if there is no i.v. line inhalational anesthesia can be used .22,53-56
  • Suxamethonium(0.1–3 mg/kg) : suxamethonium administration following hypoxia may be associated with severe bradycardia and even cardiac arrest. Thus, it is highly recommended to give atropine at 0.02 mg/kg) IV prior to administration of suxamethonium to treat laryngospasm.5,9,27 The two advantages of small dose (0.1—0.3 mg/kg)of suxamethonium arethe maintenance of spontaneous breathing thusavoiding further hypoxia and the avoidance ofbradycardia following repeated doses .57
  • Infusing doxapram at 1.5 mg/kg.58
  • I.v. nitroglycerin at 4 μg/kg7
  • Superior laryngeal nerve block6,59

Figure 2.Superior laryngeal nerve block .A 25 G needle is used to make contact with the hyoid bone, walking off the inferior marginof the bone and advancing 1–2 mm until it pierces the hyoid ligament..

When laryngospasm occurs during inhalational induction without previous i.v. access several

options can be used:

  • Suxamethonium can be administered at 4 mg/kg i.m.60
  • Establishing an i.v. access for the administration of drugs to treat laryngospasm.61
  • Using the intraosseous route62
  • Sublingual injection

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