Bronchospasm is one of the most feared complications occurring in anesthesia. 7% of all anesthesia-related deaths in France are attributed to bronchospasm [1]. 9% of asthmatic patients will experience intraoperative bronchospasm during general anesthesia. Additionally, adverse respiratory events, including bronchospasm, accounted for 28% of claims regarding anesthesia-related brain damage or death, and resulted in the highest mean cost per closed claim in anesthesia [2].

Bronchospasm is a sudden constriction of bronchial smooth muscle resulting in narrowing of the small airways, which causes increased work of breathing, decreased airflow, air trapping, dynamic hyperinflation, and VQ mismatch. Additionally, it can increase pulmonary vascular resistance resulting in right ventricular overload [3]. Bronchospasm can be separated into two categories based on its precipitating factors: allergic and non-allergic. Allergic bronchospasm is IgE-mediated and typically presents with cutaneous symptoms, prolonged episodes of desaturation, and shock. Non-allergic bronchospasm, most commonly, occurs following intubation or instrumentation of the airway. Non-allergic bronchospasm typically lacks cutaneous manifestations and cardiovascular shock seen in allergic bronchospasm [4]. 

In patients with known or suspected asthma, elective surgery should be delayed in the event of wheezing, cough, or dyspnea [4]. Patients with suspected asthma should be evaluated in concert with a pulmonologist prior to elective surgery. Patients with peak flow or FEV1 less than 80% of their normal may benefit from a short course of oral steroids prior to surgery. Asthmatic patients may dramatically reduce their risk of intraoperative bronchospasm if they stop smoking 2 months prior to their operation. Frequent asthma exacerbations, hospitalizations, and previous intubation for asthma exacerbation are risk factors for intraoperative bronchospasm. Recent respiratory infections are a trigger for asthma exacerbation, so it may be valuable to screen for recent fever, cough, or changes in sputum. Interestingly, a frequently-cited retrospective study found no increase in perioperative bronchospasm in asthmatic patients with recent upper respiratory tract infections, so the value of such screening is still debated [5].

When considering the intraoperative treatment of bronchospasm, the first and most important step is recognition. It typically presents with wheezing, high peak pressures on the ventilator, and prolonged expiratory times. The waveform on capnography is classically described as either a saw tooth or a shark fin with a gradual slope in the transitional phase. Visible slowing or complete cessation of chest rise is also a common finding in severe bronchospasm, but visualization of chest rise does not rule out bronchospasm. The differential diagnosis for bronchospasm is broad and includes a kinked endotracheal tube, mucus plugging, pulmonary embolism, pulmonary edema, or a bronchial intubation [6].

Once bronchospasm has been recognized, it is imperative to act quickly. The first steps are to increase the oxygen level to 100% FiO2 and to stop any surgical stimulation. Regardless of experience, it is also imperative to call for assistance. Switching to bag-mask ventilation is helpful because it allows one to directly assess pulmonary compliance and to increase the inspiratory rate to achieve an adequate I:E ratio. Ventilators may not be capable of delivering a rapid enough inspiration to compensate for the long expiratory times required in bronchospasm. As volatile anesthetics cause relaxation of bronchial smooth muscle, this should be one of the first steps in treatment. Isoflurane and sevoflurane are particularly useful, but desflurane should be avoided as it has notable airway irritant effects [4]. Propofol has direct bronchodilatory effects, so it may also be prudent to increase propofol sedation in patients receiving total intravenous anesthesia with propofol.

If bag-mask ventilation and deepening of anesthesia are not effective, the use of a rapid-acting beta-2-selective agonist should be utilized via nebulizer or metered-dose inhaler with an airway adapter if available. Because of a tendency for metered-dose inhalers to deposit medication on the endotracheal tube, a larger than normal dose is required to achieve the desired effect (8-10 puffs). While their onset of action is 4-6 hours, high-dose corticosteroids may be useful in the setting of refractory bronchospasm [3]. With severe, unresponsive bronchospasm, consider intravenous pushes or a continuous infusion of epinephrine.  Magnesium sulfate given intravenously can be helpful in difficult cases but may result in muscle weakness and CNS depression in high doses [7]. Finally, nitroglycerine has been reported anecdotally to reverse acute bronchospasm through direct smooth muscle relaxation [8].

If acute bronchospasm persists at the end of the case, a postoperative course of mechanical ventilation may be needed to allow time for airway recovery. Additionally, repeat administration of a short-acting beta-2 agonist is warranted prior to emergence. Neostigmine used for reversal of neuromuscular blockade increases the risk of bronchospasm because of its muscarinic and pro-secretory effects, but these can be counteracted with co-administration of glycopyrrolate [3]. 

In conclusion, bronchospasm is a serious complication of everyday anesthetic practice and can result in significant morbidity and mortality. It often presents in the operating room with rising peak pulmonary pressures, desaturation, and a saw-tooth-shaped end-tidal CO2 tracing. Once bronchospasm occurs, take rapid action by increasing FiO2, increasing sedation, and rapid-acting beta-2-selective agonists. Finally, after an episode of bronchospasm, a patient is more likely to have subsequent episodes of bronchospasm, so it is important to inform patients of the episode; therefore, incidents should be properly documented in the chart, allowing future providers to adequately prepare [9]. 

References

Auroy, Y., et al., Mortality related to anaesthesia in France: analysis of deaths related to airway complications. Anaesthesia, 2009. 64(4): p. 366-70.

Kumeta, Y., et al., [A survey of perioperative bronchospasm in 105 patients with reactive airway disease]. Masui, 1995. 44(3): p. 396-401.

Woods, B.D. and R.N. Sladen, Perioperative considerations for the patient with asthma and bronchospasm. Br J Anaesth, 2009. 103 Suppl 1: p. i57-65.

Dewachter, P., et al., Case scenario: bronchospasm during anesthetic induction. Anesthesiology, 2011. 114(5): p. 1200-10.

Warner, D.O., et al., Perioperative respiratory complications in patients with asthma. Anesthesiology, 1996. 85(3): p. 460-7.

Butterworth, J.F., et al., Morgan & Mikhail’s clinical anesthesiology. 2018, McGraw-Hill Education,: New York. p. 1 online resource.

Alter, H.J., T.D. Koepsell, and W.M. Hilty, Intravenous magnesium as an adjuvant in acute bronchospasm: a meta-analysis. Ann Emerg Med, 2000. 36(3): p. 191-7.

Baraka, A., et al., Nitroglycerin for intra-operative bronchospasm. Anaesthesia, 1999. 54(4): p. 395-6.

Westhorpe, R.N., G.L. Ludbrook, and S.C. Helps, Crisis management during anaesthesia: bronchospasm. Qual Saf Health Care, 2005. 14(3): p. e7.

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