The Case

A 48-year-old woman with a history of obesity (body mass index [BMI] of 32), but without any history of smoking, gastroesophageal reflux disease, or current or recent upper respiratory tract infection, was admitted for elective removal of metal hardware from her foot.  After induction of general anesthesia, a laryngeal mask was inserted easily and general anesthesia was maintained with sevoflurane in 35% oxygen. The patient was breathing spontaneously. The anesthesiologist was distracted briefly by the anesthesia technologist to sign for opioid drugs in a register, but during this time, the end-tidal carbon dioxide alarm sounded. The anesthesiologist immediately increased the oxygen to 100% and attempted to manually ventilate the patient, but this proved impossible. He called for help from the technologist, who was outside the operating room (OR), and asked for urgent delivery of suxamethonium (succinylcholine). However, the drug refrigerator was broken and contained no drugs. Suxamethonium had to be retrieved from another room, resulting in marked arterial hemoglobin desaturation without bradycardia or cardiac arrest. After suxamethonium was administered, the patient’s trachea was intubated and she was manually ventilated with a rapid increase in her arterial oxygen saturation to 98%. Her postoperative course was uneventful without any clinical sequelae.

The Commentary

By Christian Bohringer MBBS

Background

Laryngospasm is a narrowing or complete closure of the glottis due to reflex constriction of the laryngeal muscles. This phenomenon represents an exaggerated response to protect the lungs from inhaling irritant gases or from aspirating oropharyngeal contents. Laryngospasm can occur at any stage of anesthesia, including the postoperative period.¹ It is a potentially life-threatening complication that occurs more frequently in smokers, children, and during procedures that irritate the larynx or the vocal cords.^2,3,4 The classic presentation of laryngospasm is with high-pitched inspiratory stridor, which indicates that airway obstruction is incomplete. When laryngospasm is severe, complete airway obstruction may result in the loss of stridor as there is no longer any gas flowing across the vocal cords, despite continued respiratory effort. The movement of the chest and abdomen becomes non-synchronous, a pattern often described as paradoxical breathing. During normal breathing, the chest and the abdominal walls move outwards together during inspiration. During airway obstruction, the abdomen moves out while the chest moves in because of the negative pressure created within the thorax.⁵ This type of complete airway obstruction needs to be corrected emergently to prevent negative pressure pulmonary edema and/or hypoxic cardiac arrest.⁶

Laryngospasm usually occurs in a light plane of anesthesia when the patient is not sedated deeply enough to tolerate noxious chemical or physical stimuli.⁷ The depth of anesthesia therefore needs to be adjusted continuously by assessing the clinical signs of depth of anesthesia or by monitoring the processed electroencephalogram (EEG).⁸ The incidence of laryngospasm appears to be similar irrespective of whether the patient is intubated or not.⁹

Some medications are more likely to trigger laryngospasm, although this reaction is not predictable. Inhalational agents with irritant physicochemical characteristics like desflurane and high concentrations of isoflurane are more likely to cause laryngospasm than non-irritant agents like sevoflurane and halothane.¹⁰ Intravenous ketamine is associated with laryngospasm, perhaps because it induces salivation and saliva flowing over the vocal cords may trigger coughing and laryngospasm to prevent aspiration.¹¹ For this reason, all intubated patients should have their oropharynx suctioned properly prior to extubation to prevent the saliva that accumulates during the operation from flowing over the vocal cords. Appropriate oropharyngeal suctioning can reduce the incidence of laryngospasm after extubation.

Potential adverse effects of laryngospasm

Hypoxemia with hypoxic cardiac arrest, hypoxic ischemic encephalopathy and death may occur if airway obstruction is complete and not treated in a timely manner. A sedated patient must therefore be carefully monitored at all times for signs of impending airway obstruction. The team administering the sedation and anesthesia must be vigilant and competent to rapidly diagnose and treat laryngospasm, if it occurs.¹²

Laryngospasm may also precipitate post-obstructive pulmonary edema,¹³ which is diagnosed when the patient coughs up pink fluid and has a low oxygen saturation on pulse oximetry and arterial blood gas analysis. Positive pressure applied to the lung via either high flow nasal oxygen or continuous positive airway pressure is an essential component of treatment for post-obstructive pulmonary edema.¹⁴ The pulmonary edema is produced by the excessive negative pressure applied to the lung tissues, which pulls fluid into the pulmonary interstitial space.¹⁵ The expectorated pulmonary edema fluid is often pink because it is stained by red blood cells from ruptured pulmonary capillaries. Capillary rupture occurs because of excessive negative pressure created in the lung when the patient tries to inhale against the closed glottis. Negative pressure pulmonary edema is seen more frequently in fit young patients because their strong chest wall muscles can create much higher negative intrathoracic pressures than those of elderly patients.

Treatment of laryngospasm

To treat laryngospasm, continuous positive airway pressure should be applied to the airway, if circumstances permit. This intervention may terminate laryngospasm by pushing saliva off the vocal cords, as saliva on the larynx is a common precipitating factor. However, positive pressure should not be relied upon as the main modality to break laryngospasm because it can make the problem worse.¹⁶

Deepening the level of anesthesia with intravenous anesthetic agents may be sufficient if laryngospasm is mild. Intravenous propofol and lidocaine have been used successfully to treat laryngospasm.^17,18 When laryngospasm is severe, however, a small dose of muscle relaxant should be administered to reverse the laryngospasm without paralyzing the laryngeal muscles completely. This low dose treatment is usually effective because the larynx is more sensitive to neuromuscular blockers than the diaphragm and other respiratory muscles. Low dose succinylcholine has in fact also been used to reduce the incidence of laryngospasm during LMA insertion, which is why the anesthesiologist appropriately called for it in this case.^19,20 Succinylcholine has historically been the most commonly used drug for breaking laryngospasm because of its rapid onset and relatively short duration of action.²¹ A dose of 10 mg administered intravenously is usually sufficient to abolish the laryngospasm in an adult without requiring the patient to be ventilated. In children the recommended dose is 0.1mg/kg. When higher doses are necessary in children atropine is often administered before succinylcholine to prevent bradycardia. Succinylcholine is contraindicated in patients with stroke, spinal cord injury, burns, or myotonic dystrophy.

If succinylcholine is not immediately available or it is contraindicated in the patient with laryngospasm, a small dose of rocuronium can be used instead. If the dose of rocuronium is too large and the patient becomes too weak to breathe spontaneously, the effects of rocuronium can be rapidly reversed with sugammadex. The effects of rocuronium can be adequately reversed even from a profound level of paralysis.²² Sugammadex is an antagonist drug that has been specifically developed to reverse the paralysis caused by rocuronium.

During severe laryngospasm with extreme hypoxia and bradycardia, it may be necessary to administer a larger dose of muscle relaxant to speed up the onset of paralysis to prevent a hypoxic cardiac arrest. Following this larger dose, the patient will need to be mechanically ventilated. Bag valve resuscitators, laryngoscopy blades and endotracheal tubes therefore must be readily available in areas where patients are sedated or anesthetized.

Physical maneuvers may help reverse laryngospasm. Pressure applied bilaterally between the mastoid process and the ear lobule may abolish laryngospasm.^23,24 Another physical maneuver that has been recommended is pulling the mandible forward. These maneuvers are not as reliable as the administration of neuromuscular blocking drugs, however, and they should not be relied upon exclusively when treating severe life-threatening laryngospasm.

With adequate preparation, hypoxic cardiac arrest due to laryngospasm is preventable and it should occur only very rarely in patients who are being cared for in the hospital setting.

Approach to Improving Patient Safety

Avoid noxious stimulation of the patient before the depth of anesthesia is adequate

This patient manifested laryngospasm following insertion of the laryngeal mask airway (LMA) because she was not sufficiently anesthetized for either the LMA insertion or the intensity of the surgical stimulation. Assessing the position of the eyes, the pupil diameter, the frontalis muscle and the heart rate and blood pressure can help the anesthesiologist assess the depth of anesthesia.²⁵ Processed electro-encephalography (EEG) is now frequently used as an addition to these clinical signs to confirm that the depth of anesthesia is adequate.

Require ready availability of neuromuscular blocking drugs and airway equipment

Succinylcholine and rocuronium need to be readily available in the operating room to be able to treat severe laryngospasm. Availability is also necessary in other places like interventional radiology or endoscopy suites, post anesthesia care units, or any location where major nerve blocks are performed. The availability of these drugs should be assured by the scrub or circulating nurse using a standardized checklist. A capnograph should be available in any location where patients receive sedation because it is an excellent monitor for apnea. With upper airway obstruction the chest and abdomen still move but no CO2 will be measured by the capnograph. The absence of CO2 will precede hypoxemia and a capnograph therefore allows for early intervention to correct the airway obstruction. It can also be used to confirm the position of the ETT tube if intubation should become necessary like in this case. A cardiac defibrillator also should be readily available in all anesthetizing locations; the operational function of this equipment should be checked daily. If the drug refrigerator becomes inoperative, it should be replaced immediately or operations requiring general anesthesia should be reassigned to other rooms.

Ensure that staff administering sedation are able to recognize and treat laryngospasm

Vigilant monitoring by anesthesia staff can identify laryngospasm early and prevent complete airway obstruction by either increasing the depth of anesthesia or employing other treatment modalities. Vigilant monitoring of the capnograph was of great help in this case because the low expired carbon dioxide level triggered an alarm and alerted the anesthesiologist to the complete airway obstruction at a time when he was distracted by administrative paperwork.

Laryngospasm may occur during monitored anesthesia care (MAC) and all staff administering sedation, irrespective of their designation, should therefore be trained to recognize and treat it. Drugs used to treat laryngospasm and airway equipment must be readily available whether the anesthesia plan is for MAC, laryngeal mask airway, or endotracheal intubation. A high level of preparation and flexibility is indispensable for providing safe anesthesia care.

Use drugs that are associated with lower risk of laryngospasm

Dexmedetomidine and propofol ablate airway reflexes well and are associated with a lower incidence of laryngospasm than other drugs like thiopental and ketamine.^26,27 Atropine and other anticholinergic medications reduce the salivation seen with ketamine and may thereby reduce the risk of laryngospasm. Sevoflurane and halothane are non-pungent volatile anesthetic agents and are therefore less likely to precipitate laryngospasm than desflurane, isoflurane and diethyl ether.

Avoid distractions for the anesthesiologist

The anesthesiologist in this case was distracted by having to sign for opioid drugs in a controlled medication register. This distraction could have led to a delay in diagnosing laryngospasm. Distractions in the operating room are increasingly common and the ever-increasing requirements for data entry and paperwork can impair the vigilance needed for monitoring the patient’s vital signs.²⁸ All preparations for anesthetic administration should be completed whenever possible before the induction of anesthesia to reduce distractions for the anesthesia care provider while the patient is under anesthesia.

Optimize availability of anesthesia technologists

Anesthesia technologists are very familiar with anesthesia equipment and anesthesia crisis scenarios. Their assistance is invaluable for providing safe patient care when an unanticipated emergency arises in the operating room. Anesthesia care providers should cultivate a good relationship with their technologists, and hospitals need to ensure adequate staffing ratios to ensure that experienced assistance is rapidly available in a crisis.

Conclusion

This patient became hypoxic during an episode of laryngospasm but fortunately did not suffer a hypoxic cardiac arrest or hypoxic brain damage. The rapid assistance of the anesthesia technologist saved the day, as inadequate resources such as the broken drug refrigerator otherwise could have led to irreversible injury to the patient. This case resulted in unnecessary hypoxemia but a cardiac arrest could be averted because the neuromuscular blocking drug was brought to the operating room just in time.  

Safe anesthesia requires a very high level of preparation and teamwork. Anesthetic emergencies are not always predictable and anesthesia care providers must be prepared for all potential problems in order to be able to correct them rapidly. The assistance of an anesthesia technologist is a very important component of providing safe anesthesia care.

Take Home Points

• Patients need to be adequately anesthetized for the intensity of the planned surgical and airway stimulation.
• Anesthesia care providers should be vigilant at all times when monitoring their patients, and distractions in the operating room should be minimized.
• A capnograph (end tidal carbon dioxide monitor) is very useful for monitoring the patient’s ventilation.
• Neuromuscular blocking drugs and airway resuscitation equipment must be present in the operating room and readily available in any patient care area where patients are likely to develop laryngospasm.
• An adequate number of well-trained anesthesia technologists is necessary to support the care team in responding promptly and effectively to emergencies.

Christian Bohringer, MBBS
Professor of Clinical Anesthesiology
Department of Anesthesiology and Pain Medicine
UC Davis Health
chbohringer@ucdavis.edu

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