Strictly Clinical
  • Repeated Postanesthetic Laryngospasm in a Male Adult

    Laryngospasm is a potential complication after general anesthesia that is universally dreaded because the failure to act swiftly and effectively could be fatal for the patient. This case report involves a morbidly obese male patient who received his first general anesthetic and experienced 4 episodes of laryngospasm within an hour after emergence. Laryngospasm occurs when the vocal cords adduct, closing the glottis, thereby preventing gas exchange in a spontaneously ventilating individual. This patient was able to physically indicate his impending glottic closure, thus warning his caregivers of the imminent airway emergency. He was safely intubated during the fourth episode and admitted to the intensive care unit for monitoring. After 2 days, the patient was extubated and recovered otherwise uneventfully. This case demonstrates the high level of vigilance required during all phases of anesthesia care.

    Keywords: General anesthesia, laryngospasm, recurrent laryngospasm.

    Laryngospasm is a complication of anesthesia caused by reflexive adduction of the laryngeal musculature in the setting of an unsecured airway. In a spontaneously ventilating patient, this closure of the glottis can rapidly cause hypoxemia, pulmonary edema, or even death.1 Certain situations are considered hallmarks for association with laryngospasm events, such as pediatric cases, pungent volatile anesthetic gases, direct airway irritants, environmental events, or unknown etiology.2 In such cases, laryngospasm may be associated with irritation of the pharyngeal mucosa by the chemical irritants of the volatile agent, the physical irritant of airway secretions or other liquid, or other mechanical action to cause reflex of the vocal cords and surrounding tissues. Removal of the causative agent and swift action to reopen the glottic airway are required to prevent potentially catastrophic outcomes. This case involves an obese, Hispanic man receiving his first general anesthetic.

    Case Summary

    A 47-year-old Hispanic male patient presented to the day surgery outpatient unit for cystoscopy and transurethral resection of the prostate. His medical history was remarkable for morbid obesity, with a weight of 134.1 kg (298 lb), height of 172.7 cm (68 in), and body mass index of 48 kg/m2. (A BMI over 30 kg/m2 represents obesity and a BMI greater than 40 kg/m2 signifies morbid obesity.) No other comorbidities were reported by the patient or listed in the surgeon’s history and physical examination findings. The patient had no known food or drug allergies. The preoperative vital signs were within normal limits, and the patient was not nervous. He was easily conversant with staff and had a pleasant affect.

    Airway assessment revealed a modified Mallampati class 2 airway (soft palate, fauces, and uvula visible), with full cervical extension and a thyromental distance of 4 fingerbreadths. Although the Mallampati airway assessment may be performed to gather information regarding potential difficulty with laryngoscopy, the assessment is not always the best indicator of problems with pharyngeal visualization3 and thus should not be the sole determinant of a potentially difficult intubation. This man had never undergone general anesthesia and thus reported no prior problems with anesthesia. He also denied having any family history of problems with or complications from anesthesia.

    A general endotracheal anesthetic was planned and performed for this patient. Because the patient demonstrated full cervical extension, with a thyromental distance of 4 fingerbreadths, and clear pharyngeal structures were visible on physical examination, no special equipment such as an intubating ramp (to facilitate proper alignment of airway axis) or video laryngoscope (to facilitate visualization of the vocal cords) was used during induction or intubation. Laryngeal mask airways and a flexible endotracheal introducer were, however, present in the operating room (OR). Before induction, the patient was asked to lift his chin into a sniffing position, which was easily accomplished. Preoxygenation was accomplished with an adult size 5 circuit face mask for 5 minutes with 100% oxygen fresh gas flow.

    Induction was performed with the following intravenous (IV) medications: 50 mg of lidocaine, 300 mg of propofol, and 160 mg of succinylcholine. Direct laryngoscopy revealed a grade 1 view of the vocal cords and tracheal rings. A 7.0-mm oral endotracheal (ET) tube with a stylet was placed easily and atraumatically using a Macintosh 4 laryngoscope blade. Lidocaine jelly was applied around the oral ET tube, above the cuff, before placement to decrease pharyngeal irritation from the tube. Intraoperative anesthesia was maintained with 1.2 minimum alveolar concentration of sevoflurane, 50% oxygen and air fresh gas flow, and 20 mg of IV rocuronium. No IV opioids were administered. Postoperative nausea and vomiting prophylaxis was administered intravenously and consisted of 20 mg of famotidine, 10 mg of metoclopramide, 10 mg of dexamethasone, and 4 mg of ondansetron. The intraoperative course was uneventful and lasted approximately 75 minutes. Before extubation, 30 mg of ketorolac, 5 mg of neostigmine, and 1 mg of glycopyrrolate were administered intravenously. Train-of-four demonstrated 4 of 4 twitches with sustained tetany. Spontaneous ventilations resumed approximately 10 minutes before extubation. Tidal volumes inspired before extubation were consistently greater than 400 mL. The oropharynx was suctioned of secretions, and the patient responded to his name, opened his eyes on command, and lifted his head without prompting before extubation. Extubation was accomplished, and the patient continued to respond appropriately to questions as he continued to maintain arterial oxygen saturation (Sao2) greater than 93% with spontaneous ventilations (no supplemental oxygen required).

    Immediately before transfer of the patient from the OR table to the transport gurney, the patient stopped conversing with staff and was no longer effectively ventilating on his own. Positive pressure oxygen was applied, with no exchange of carbon dioxide possible. Positive pressure ventilation was again attempted after placement of a 100-mm oral airway with a simultaneous jaw thrust. The Sao2 concentration quickly decreased into the 80% range while 100% oxygen was applied. The inability to ventilate the patient led to the rapid assessment of a laryngospasm. Additional help was summoned as 40 mg of the IV muscle relaxant succinylcholine was administered. Another staff member provided positive pressure ventilations, and jaw thrusts and 2-handed mask seal were accomplished while awaiting the effects of the succinylcholine. The patient was quickly reintubated with a Macintosh 4 laryngoscope blade and a 6.5-mm oral endotracheal tube. Oxygen saturations immediately rose to 94%. After 2 minutes, the patient was again awake.

    The situation of laryngospasm was explained to the patient in lay terms, and he nodded his head in confirmation of understanding what was being said to him. After another 10 minutes had passed, the patient demonstrated return of muscle strength by demonstrating strong bilateral hand grips on request, and the ability to again raise his head with and without prompting. The oropharynx was suctioned of secretions, and again extubation was accomplished.

    Before leaving the OR suite, the patient was fully awake, conversant, and oriented. A simple face mask was placed for transport to the postanesthesia care unit (PACU). On arrival at the PACU, the Sao2 concentration was 98% with 6 L/min of oxygen and was maintained when the oxygen mask was removed. As the transfer of care report was completed, the patient was monitored for airway obstruction. Approximately 3 minutes after arriving in the PACU, as he was being assessed for comfort, the patient again experienced laryngospasm. This time, he was able to clearly look at staff as he “froze in place.” A jaw thrust was performed while a bag-valve-mask (Ambu bag, Ambu) was obtained and connected to oxygen. Positive pressure was applied. The second laryngospasm was broken approximately 90 seconds after it was first noted. Again, the patient was conversant. The simple face mask was again placed with oxygen at 10 L/min.

    At this point, the anesthesia provider remained at the head of the gurney even though the patient was apparently stable and awake. Eight minutes later, while the patient was speaking with his bedside PACU nurse, again the patient “froze in place” and ceased exhalations. No decrease in Sao2 concentration occurred because a jaw thrust and positive pressure were applied immediately as the third laryngospasm was identified. The third laryngospasm was broken approximately 60 seconds after it was first noted.

    Arrangements were made to admit the patient to the intensive care unit (ICU) for overnight observation. Also, additional staff brought the emergency airway cart along with succinylcholine to the bedside to use if needed. More questions were posed to the patient about his prior health, and additional staff completed a full physical examination to determine if the patient was experiencing an allergic reaction. Physical examination findings indicated his lungs were clear, and there was no change from prior examinations during the day. Oxygen via simple face mask was again applied at 10 L/min.

    After questions were completed and no signs or symptoms of allergic reaction were identified, the patient again experienced laryngospasm, approximately 7 minutes after the third laryngospasm was broken. For this fourth episode, 100 mg of succinylcholine was administered intravenously, and the patient was intubated with a 7.0-mm oral ET tube with a stylet and a Macintosh 4 blade. This intubation also yielded a full view of the vocal cords and was accomplished without trauma. Once the effects of the muscle relaxant had abated, the situation was again explained to the patient. However, this time we explained to him that we planned to keep him intubated overnight with sedation so that he could tolerate the oral endotracheal tube and rest overnight. He was transported to the ICU 30 minutes later in stable condition.

    This patient was extubated 2 days later with no apparent sequela. His affect remained as it had been before surgery: cheerful and personable. Results of all diagnostic and laboratory tests performed while he was in the ICU were normal, showing no potential cause of the airway hyperreactivity or any possible sequela related to the repeated laryngospasms. He was discharged to home on postoperative day 2. Neither the patient nor his family could add any specific information to help determine why he might have had particularly reactive airways.


    The occurrence of laryngospasm is possible whenever general endotracheal anesthesia is performed. Occurrence rates vary from 0.75% to 5%.2,4 Typical causes of laryngospasm include a history of smoking; use of pungent volatile anesthetics that may irritate the airways; or possible fluid or secretions in the airway from saliva, gastric fluid, or possibly blood. The patient in this case said he had no history of smoking or tobacco use or of a reactive airway disease, and pungent volatile agents were not used. The patient did not have copious secretions during the anesthetic, and before extubation, scant secretions were noted during suctioning.

    A patient experiences laryngospasm when the glottis muscles adduct while the airway is not secured (ie, an ET tube is not in place) and the patient is spontaneously ventilating. For a patient who is awake and alert, this event can be terrifying because he or she is no longer able to ventilate effectively. Intervention must happen quickly to prevent sequelae such as hypoxia, negative pressure pulmonary edema, cardiovascular collapse, or death. Laryngospasm is also possible for the nonalert patient who is either awake or in a state of depressed consciousness. The commonality is that the airway is not secure when laryngospasm occurs. External stimulation (eg, movement of the patient or the bed that the patient is resting on) and sympathetic stimulation from surgical insults while the patient is in a light plane of general anesthesia are also recognized as precipitating factors for laryngospasm.5 No matter the cause, laryngospasm is always a clinical event that demands rapid assessment and management.

    Although the rate of laryngospasm is fairly low, the manifestation of repeated laryngospasm in the same awake and alert adult patient is not described in the recent literature. In this patient receiving his first general anesthetic, all the usual causes were quickly ruled out. The patient’s muscle relaxant was fully reversed, and both objective and subjective parameters were used to establish that adequate strength was present before extubation. Deep oral suctioning was performed before extubation. During the surgery, this patient received sevoflurane, the least pungent of all the volatile agents. The sevoflurane end-tidal concentration was 0 before extubation. Before the extubation in the OR suite, the only possible external stimulation was aligning the transport gurney to the OR table and preparing the patient to be transferred to the gurney. The patient was not being moved or jostled during extubation. He was, however, logrolled onto a transfer assist roller board before the first laryngospasm. With all other common precipitating factors being equal and noncontributory, it is possible that this degree of movement could have precipitated the first laryngospasm. However, this does not explain the second, third, or fourth laryngospasm. This patient reported no asthma, chronic obstructive pulmonary disease, recent upper respiratory tract infection, tobacco use, or obstructive sleep apnea, nor allergy to any drug classification that was used during, before, or after the anesthetic.

    This case demonstrates the high level of vigilance required during all phases of anesthesia care. Rapid teamwork contributed to this patient’s positive outcome despite the occurrence of a potentially life-threatening clinical event 4 times within an hour after an otherwise uneventful surgical procedure.


    1. Naqvi SE, Khan RA, Ahmed N, Malik UA, Rafiq MY. Frequency of laryngospasm in awake versus deep extubation after intranasal surgery. Pakistan Armed Forces Med J. 2018;68(5):1293-1299. Accessed January 15, 2019.

    2. Lee JH, Lee JH, Lee MH, Cho HO, Park SE. Postoperative negative pressure pulmonary edema following repetitive laryngospasm even after reversal of neuromuscular blockade by sugammadex: a case report. Korean J Anesthesiol. 2016;70(1):95-99. doi:10.4097/kjae.2017.70.1.95

    3. Lundstrøm LH, Vester-Andersen M, Møller, AM, Charuluxananan S, L’hermite J, Wetterslev J; Danish Anaesthesia Database. Poor prognostic value of the modified Mallampati score: a meta-analysis involving 177 088 patients. Br J Anaesth. 2011;107(5):659-667. doi:10.1093/bja/aer292

    4. Aljonaieh KI. Effect of intravenous lidocaine on the incidence of postextubation laryngospasm: a double-blind, placebo-controlled randomized trial. Saudi J Anaesth. 2018;12(1):3-9. doi:10.4103/sja.SJA_440_17

    5. Visvanathan T, Kluger MT, Webb RK, Westhorpe RN. Crisis management during anaesthesia: laryngospasm. Qual Saf Health Care. 2005;14(3):e3. doi:10.1136/qshc.2002.004275


    Pamela Chambers, DNP, EJD, MSN, CRNA, is an Army veteran and active consultant in healthcare law to Certified Registered Nurse Anesthetists, attorneys, administrators, and other healthcare providers. She is serving as a member of the National Board of Certification & Recertification for Nurse Anesthetists (NBCRNA) board of directors in her second term.


    The author has declared no financial relationships with any commercial entity related to the content of this article. The author did not discuss off-label use within the article. Disclosure statements are available for viewing upon request.


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