Laryngospasm

• Laryngospasm


  A form of airway obstruction that is so common and different that most anesthesiologists consider it to be a separate entity
• Laryngospasm


  • The risk is greater in certain subgroups such as children with asthma or airway infections or those undergoing oesophagoscope or hypospadias repair, and adults undergoing anal surgery
  • It has the potential to cause morbidity and mortality, especially if managed poorly
  • It may present atypically and may be precipitated by factors which are not immediately recognized, increasing the potential for patient harm and further complications such as pulmonary aspiration and post obstructive pulmonary oedema
• Risk factors for laryngospasm

  • Difficult intubation
  • Nasal, oral or pharyngeal surgical site
  • Obesity with obstructive sleep apnea
• Signs of laryngospasm


  • Inspiratory stridor/airway obstruction
  • Increased inspiratory efforts/tracheal tug
  • Paradoxical chest/abdominal movements
  • Desaturation, bradycardia, central cyanosis
• Precipitating causes of laryngospasm

  • Airway manipulation
  • Blood/secretions in the pharynx
  • Regurgitation/vomiting
  • Surgical stimulus
  • Moving patient
  • Irritant volatile agent
  • Failure of anesthetic delivery system
  • Unable to determine
• Management of laryngospasm


  1. Cease stimulation/surgery

  2. 100% Oxygen

  3. Try gentle chin lift/jaw thrust

  4. Request immediate assistance

  5. Deepen anesthesia with an IV agent

  6. Visualize and clear the pharynx/airway

  7. Suspect aspiration

  8. Suspect airway obstruction

  9. Try mask CPAP/IPPV, if this is unsuccessful, give suxamethonium unless contraindicated, give atropine unless contraindicated. Again, try mask CPAP/IPPV

  10. Intubate and ventilate
• About 77% of laryngospasm cases were clinically obvious, 14% presented as airway obstruction, 5% as regurgitation, 4% as desaturation
• Cricothyroid muscle


  The only tensor of the vocal cords. Gentle stretching of this muscle may overcome moderate laryngospasm
• Jaw thrust


  Gentle pressure should be exerted on the angle of the mandible, and not on soft tissues
• Suxamethonium


  Delay in relieving severe laryngospasm was associated with post-obstructive pulmonary edema and were managed with suxamethonium without intubation. 0.5mg/kg IV to relieve laryngospasm, 1.0–1.5mg/kg IV for intubation, 4.0mg/kg IM for intubation (if no IV access)
• Atropine


  0.01mg/kg as bradycardia may occur
• Sequence for managing laryngospasm

  1. 100% Oxygen

  2. Cease all stimulation

  3. Remove airway devices and suction

  4. Apply gentle CPAP with thrust

  5. Call for help, the problem and delegate

  6. Deepen anesthesia

  7. Give Suxamethonium and continue CPAP

  8. Intubate if SpO2 does not improve

  9. Consider Atropine 10-20 mcg/kg for the treatment of associated bradycardia
• This is a sequence to be rehearsed. Time will not permit a checklist management approach
• Although stimulating airway devices contributing to spasm should be removed, the Guedel (oral) airway may be helpful in providing CPAP
• Call for assistance early. The situation deteriorates rapidly in children
• Delegate responsibilities clearly including ETT preparation and suxamethonium administration
• Some pediatric anesthetists will carry pre-drawn suxamethoniumin their pocket to reduce drug error and save time during desaturation
• Deepening anesthesia


  An option in adult anesthesia, but rapid development of hypoxia in children usually precludes this
• Spasm will 'break' with sufficient hypoxia and time, but predisposes to bradycardia, cardiac arrest, regurgitation and pulmonary edema. These can be prevented with early intervention
• Suxamethonium dosage


  0.1 to 1 mg/kg IV, 2 to 4 mg/kg IMI/IO/IL
• In complete obstruction, forced inflation attempts will add to obstruction (Fink ball/valve effect) and inflate the stomach
• Consider stomach deflation before emergence
• In a rapidly desaturating child, immediate intubation without relaxation may be the appropriate treatment
• Bronchospasm


  Usually manifests during anesthesia as an expiratory wheeze, prolonged expiration and/or increased inflation pressures during intermittent positive pressure ventilation (IPPV)
• Wheeze may be audible either with or without auscultation, but can only be present if there is gas flow in the patient's airways. Thus, in cases of severe bronchospasm, the chest may be silent on auscultation and the diagnosis may rest on correct assessment of increased inflation pressures
• Other signs of bronchospasm

  • Low oxygen saturation
  • Change in capnogram
  • Hypoventilation
  • Hypotension
• Causes of bronchospasm during induction of anesthesia

  • Bronchospasm due to airway irritation
  • Anaphylaxis
  • Misplacement of endotracheal tube
  • Aspiration of gastric contents
  • Pulmonary edema (following failed intubation)
  • Unknown, possibly allergy
• Causes of bronchospasm during maintenance of anesthesia

  • Anaphylaxis (or severe allergy)
  • Endotracheal tube or ventilator problem
  • Aspiration, laryngeal mask or mask anesthesia
• Causes of bronchospasm during emergence or recovery phase of anesthesia

  • Pulmonary edema
  • Anaphylaxis/ allergy
  • Accidental extubating
  • Extubation spasm
  • Aspiration
  • Unilateral bronchospasm and pulmonary edema (cause not determind)
  • No definded cause
• Management of bronchospasm


  1. Oxygen 100%

  2. Stop stimulation and surgery

  3. Deepen anesthesia

  4. If intubated, exclude esophageal or endobronchial intubation

  5. If mask or laryngeal mask, consider laryngospasm, regurgitation, vomitus and aspiration

  6. Give adrenaline or salbutamol
• Further management of severe bronchospasm

  1. Call for help, communicate the problem and delegate

  2. Hand ventilate and deepen anesthesia

  3. Check tube placement and switch to 100% O2

  4. Utilize in-circuit Salbutamol and Ipatropium Bromide

  5. Monitor EtCO2 waveform and airway pressures

  6. Consider IV fluids, arterial line and serial ABGs

  7. Commence Adrenaline or Salbutamol as an IV bolus and use infusions if indicated to maintain stability

  8. Use a long expiratory phase, intermittent disconnection and low pressure PEEP to reduce hyperinflation

  9. Consider hydrocortisone, aminophylline or magnesium as adjunctive or alternative treatment

  10. Prepare for ICU admission if required
• Adrenaline dosage


  Bolus: 0.1-1.0mcg/kg titrated to hemodynamics, Infusion: 0.1mcg/kg/min
• Salbutamol dosage


  Bolus: 5mcg/kg up to 2 years, 15mcg/kg up to 18 years (max 250mcg), Infusion: Start at 100mcg/kg/hr (up to 300mcg/kg/hr)
• Aminophylline dosage


  Loading dose of 5 to 7mg/kg over 15 minutes, Infusion of 0.5/kg/hr to follow
• Magnesium dosage


  50mg/kg over 20 minutes with a max dose of 2g
• Hydrocortisone dosage


  1. 2 mg/kg IV
• IV fluids


  Commence therapy with 10-20ml/kg of crystalloid
• Intermittent disconnection allows CO₂ escape and prevents hyperinflation. Hand ventilation with permissive hypercapnia may also be required to avoid the complications of high airway pressure ventilation
• Treatment can be assessed by hemodynamic parameters, airway pressure, ABGs and the CO₂ waveform. With resolution, the 'sloping' up ward trace of EtCO2 returns to normal with the more horizontal alveolar plateau