Addition of nebulised lidocaine to prevent refractory bronchospasms in a patient receiving serial bronchoscopies

Background

Perioperative bronchospasm is a common concern particularly in patients with reactive airway disease. Although there are numerous treatment options for bronchospasms, there are no current therapeutic guidelines or recommendations for the prevention of refractory perioperative bronchospasms. We present a case of a young patient with a history of granulomatosis with polyangiitis who underwent 15 bronchoscopies with balloon dilations over the course of 1 year. During these serial procedures, he developed increasingly severe and refractory bronchospasms which lead to multiple occurrences of prolonged hypoxaemia, reintubation and ICU admission. We present this case to highlight the paucity of guidelines regarding the prevention of refractory bronchospasm in susceptible patients and to encourage further research into the utility of nebulised lidocaine in their prevention.

Case presentation

A man in his 20s with a history of granulomatosis with polyangiitis presented to the preoperative area in preparation for his eighth bronchoscopy with bronchial dilations in the past 12 months due to recurrent bronchial stenosis and copious secretions causing severe shortness of breath (figures 1 and 2). At the time of presentation, the patient was medically managed on albuterol inhalers, albuterol/ipratropium and budesonide/formoterol nebulisers, 30 mg prednisone daily and avacopan. He had previously been treated with cyclophosphamide and rituximab. He had no other significant medical history. His surgical history was notable for a myringotomy with tympanostomy tubes as a child. As part of the preanesthetic evaluation, it was determined that during his most recent bronchoscopies, the patient experienced increasingly severe bronchospasms necessitating the usage of increasingly aggressive treatment strategies to facilitate their resolution.

His first four bronchoscopies and bronchial dilations were completed with preoperative stress dose of 100 mg intravenous hydrocortisone and 3 mL 0.083% nebulised albuterol prior to the induction of general anaesthesia with an endotracheal tube using sevoflurane vapour as the primary anaesthetic. At the completion of the procedure, the patient was extubated while breathing spontaneously with an end-tidal concentration ranging between 2.0% and 2.5% sevoflurane. No intraoperative or postoperative complications were noted.

During the fifth procedure following the same anaesthetic plan, mild bronchospasms were noted intraoperatively and were successfully treated with albuterol puffs delivered via the endotracheal tube. More severe bronchospasms were noted during the sixth procedure necessitating the intraoperative administration of albuterol puffs, 1 mg/kg propofol and 1 µg/kg epinephrine prior to their resolution.

During the seventh procedure, the patient was again pretreated with nebulised albuterol and hydrocortisone in the preoperative area. After the induction of general anaesthesia and endotracheal intubation, he was given 0.5 mg/kg ketamine and started on an infusion of 0.5 µg/min epinephrine in order to prevent bronchospasm. Intraoperatively, he experienced a severe bronchospasm necessitating the administration of two boluses of 1 µg/kg epinephrine. At the conclusion of the procedure, the patient was extubated while breathing spontaneously with an end-tidal concentration of 3% sevoflurane. Shortly after extubation, the patient’s tidal volumes decreased from around 500 mL to under 50 mL, his oxygen saturation fell from 100% to 85% and his lung sounds were very distant.

Two boluses of 1 mg/kg propofol and 1 µg/kg epinephrine were administered with poor effect. A decision was made to reintubate the patient to improve oxygenation and rule out any endotracheal or endobronchial mucus plugs. After successful endotracheal intubation, the patient’s oxygenation began to improve. Additional doses of 1 µg/kg epinephrine and five puffs of albuterol via the endotracheal tube were simultaneously administered, and the sevoflurane concentration was increased to 4%. With these changes, the tidal volumes normalised. The proceduralist completed a second bronchoscopy, a chest X-ray was taken and arterial blood gas was obtained. Bronchoscopy and chest X-ray were both unchanged from baseline, and arterial blood gas was notable only for mild hypercapnia (figure 3).

After extensive discussion with the proceduralist, a decision was made to extubate the patient while breathing spontaneously with an end-tidal concentration of 4% sevoflurane. The patient was uneventfully extubated and directly monitored by an anesthesiologist until he regained consciousness. He was then transferred to the post-anaesthesia care unit, where he was observed for an additional 90 min before being discharged home in stable condition.

The next morning the patient presented to the hospital with respiratory distress due to severe bronchospasm. He was intubated in the emergency department and transferred to the ICU where he was treated with albuterol, epinephrine and hydrocortisone. He responded well to the treatment regimen and was extubated the next morning. He was discharged home in stable condition 2 days later.

Approximately 2 months later, the patient reported with progressively worsening shortness of breath and was scheduled for his eighth bronchoscopy with endobronchial dilation. After extensively reviewing the literature for additional suggestions to prevent bronchospasm, we decided to administer 3 mL 0.083% nebulised albuterol followed by 5 mL nebulised 4% lidocaine and 100 mg hydrocortisone in the preoperative area. We intended to administer subcutaneous terbutaline and intravenous magnesium as well; however, both were on national backorder and tightly restricted by our pharmacy department. After the induction of general anaesthesia and endotracheal intubation, he was again given 0.5 mg/kg ketamine and started on an infusion of 0.5 µg/min epinephrine. There were no intraoperative bronchospasms. The patient was extubated breathing spontaneously with an end-tidal concentration of 4% sevoflurane. He was closely monitored by an anesthesiologist until he regained consciousness and was transferred to the post-anaesthesia care unit. After a brief observational period, he was discharged in stable condition.

Over the next 6 months, the patient underwent a total of seven additional bronchoscopies with endobronchial dilations. Due to the remarkable difference in clinical status with the addition of nebulised lidocaine, we elected to reduce preoperative and intraoperative bronchospasm prevention by one medication with each subsequent procedure (first we decreased sevoflurane concentration to 2% at extubation, then we eliminated ketamine and then we eliminated the epinephrine infusion) until we were only pretreating the patient with 100 mg of stress dose hydrocortisone, 3 mL 0.083% nebulised albuterol and 5 mL nebulised 4% lidocaine. There were zero incidents of intraoperative or postoperative bronchospasms or hospital admissions with the subsequent procedures in this strategy.

Outcome and follow-up

Since his last bronchoscopy, the patient completed an intravenous immunoglobulin and rituximab course, which had excellent results. It has now been 3 months since his last bronchoscopy. Prior to the intravenous immunoglobulin infusion, the longest duration since his initial diagnosis that he had without receiving a bronchial dilation was roughly 3 weeks. He made a full return to his office-based job and is fully independent. He has not experienced any further symptoms of shortness of breath at rest or with moderate activity, although he is still limited when he attempts to exercise. Given the risk-versus-benefit ratio of further bronchoscopies, the patient and the proceduralist have declined to pursue any additional intervention at this time.