Summary
We report a case of local anaesthetic toxicity in an anaesthetic trainee participating as a subject for an awake tracheal intubation training course. The trainee experienced symptoms of toxicity despite the dose of lidocaine administered being less than the maximum safe dose recommended for airway topicalisation. We argue this highlights the variability in absorption of local anaesthetic and the importance of safety during awake tracheal intubation training courses. It is essential to use the minimum safe dose of local anaesthetic required during topicalisation for awake tracheal intubation. We have now made it our course policy that participants cannot undergo awake tracheal intubation less than 2 weeks following a period of coryzal illness. We recommend that operators remain vigilant for signs of local anaesthetic toxicity when undertaking this procedure and adhere to newly published Difficult Airway Society awake tracheal intubation guidelines.
Keywords: awake tracheal intubation, local anaesthetic: systemic toxicity, training
Introduction
The fourth National Audit Project recommends that all anaesthetic departments should have the skills and equipment readily available to perform awake tracheal intubation (ATI) 1. There are several courses that provide the opportunity to learn and practice this essential skill in a controlled environment. It is common for courses to rely on attendees participating as subjects so they can gain experience performing ATI on other participants.
Successful ATI depends to a large extent on adequate topicalisation of the airway. Lidocaine has several properties that makes it more favourable than other local anaesthetics for airway topicalisation. It has a moderate duration of action, lacks intrinsic vaso‐active effects and is less cardiotoxic than other local anaesthetics 2. The plasma concentration of lidocaine is affected by the dose and route of administration, in addition to its rate of metabolism and excretion. In an average healthy adult, signs and symptoms of toxicity can be seen at plasma levels above 4.5 μg.ml−1 3. Studies measuring the plasma concentration of lidocaine during flexible bronchoscopy and topicalisation have shown that peak plasma lidocaine concentration can vary between individuals and that the timing of the peak varies with the route of absorption. Inhalation absorption results in peak plasma levels at 20–30 min, whereas absorption through upper airway mucous membranes results in peak levels at 30–50 min 4.
Trials using total lidocaine doses of 8 mg.kg−1 and 9.3 mg.kg−1 have reported that no patients experienced symptoms of toxicity, however, some of their subjects had peak serum lidocaine concentrations above 4.5 μg.ml−1 4, 5. More recently, the Difficult Airway Society published guidelines for ATI recommending a maximum lidocaine dose of 9 mg.kg−1 based on lean body weight 6.
Report
A 35‐year‐old anaesthetic trainee (ASA I, 56 kg) volunteered as a participant on a training course for ATI. Prior to the course she received information regarding the procedure and the risks of ATI and signed a consent form to participate. The week before the course, the trainee contacted the course director to inform him that she had sinusitis following a coryzal illness. He advised that it would be best to avoid undergoing ATI on the course. However, following three days of nasal steroids, she was asymptomatic and it was agreed that she would participate on the second day of the course.
Before the procedure, written consent was obtained and the maximum dose of lidocaine was calculated independently by two consultant anaesthetists using her actual body weight of 56 kg. The participant was fasted for 6 h before the procedure. Standard monitoring was used throughout. After establishing intravenous (i.v.) access she was premedicated with 200 μg i.v. glycopyrrolate and two sprays of xylometazoline to each nostril. Her airway was nebulised with 5 ml lidocaine 4% for 10 min, 2.5 ml co‐phenylcaine nasal spray, and four sprays of lidocaine 10% to the oropharynx. Supplementary spray‐as‐you‐go lidocaine 4% (in 0.1 ml aliquots) was then applied to the airway by course delegates as they advanced the 4.2‐mm flexible bronchoscope (Karl Storz, Tuttlingen, Germany) (Fig. 1).
Figure 1.

The participant undergoing airway topicalisation for awake tracheal intubation with a flexible bronchoscope on a training course.
The operators had difficulty topicalising the airway and the vocal cords remained reactive with each spray of lidocaine resulting in coughing. Some trauma was caused to the oropharyngeal mucosa, and mucus was seen pooling in the oropharynx. The supervising consultants felt it was unsafe to proceed and the procedure was abandoned. A total of 5 ml lidocaine 4% was used for the spray‐as‐you‐go technique (Table 1).
Table 1.
Local anaesthetic used for awake tracheal intubation on the participant in this report
| Lidocaine concentration and route | Volume administered | Lidocaine dose |
|---|---|---|
| Lidocaine 4% nebulised | 5 ml | 200 mg (majority wasted as aerosol) |
| Co‐phenylcaine nose spray | 2.5 ml | 125 mg |
| Lidocaine 10% sprayed to the oropharynx | 4 × 0.1 ml | 40 mg |
| Lidocaine 4% spray as you go | 5 ml | 200 mg |
| Total lidocaine dose administered | 565 mg (10.1 mg.kg−1) | |
| Estimated dose available for absorption (only one‐third nebulised drug inhaled) | 431.6 mg (7.7 mg.kg−1) | |
| Maximum ‘safe dose’ for a 56‐kg adult | 504 mg (9 mg.kg−1) | |
Towards the end of the procedure, the participant began to feel dizzy. She was monitored for 20 min and then moved to a non‐clinical area for rest. However, the dizziness continued to worsen and was followed by nausea, vomiting and an unpleasant taste in her mouth. Approximately 30 min after the procedure she developed tinnitus and became agitated. She was transferred to the post‐anaesthetic care unit of the operating theatre complex and monitoring was recommenced. This revealed sinus bradycardia, which was present throughout, and a normal blood pressure. The participant was drowsy but no seizure activity was witnessed. She was given 4 mg i.v. ondansetron, 50 mg i.v. cyclizine and an infusion of 1000 ml Hartmann's solution was commenced. The vomiting and tinnitus continued for approximately 1 h and then subsided. Six hours following the procedure, the participant remained dizzy and could not mobilise safely. She was admitted to a medical ward for observation and discharged the following morning, and was asymptomatic. Plasma lidocaine levels were not measured at any time.
Discussion
Local anaesthetic systemic toxicity affects the central nervous and cardiovascular systems. Neurological features include an initial excitatory phase with features such as: tinnitus; circumoral tingling; a metallic taste in the mouth; light‐headedness; muscle twitching; agitation; and eventually seizures. Higher plasma lidocaine concentrations have a depressive effect on the central nervous system manifesting as respiratory depression and coma. Cardiovascular effects include: dysrhythmias; altered systemic vascular resistance; and cardiac arrest 2, 3. Our participant experienced: light‐headedness; tinnitus; an unpleasant taste in the mouth; agitation; and drowsiness.
Woodall et al. reported the experiences of 200 volunteers on an ATI training course where participants underwent a similar technique for airway topicalisation 7. As the majority of nebulised drug is lost as aerosol, and only a fraction is available for absorption, 25% of the nebulised lidocaine administered was included in their dosage calculation. They state that there were no overt signs of lidocaine toxicity when a maximal dose of 9 mg.kg−1 was used. That said, their subjects did report excitatory neurological symptoms, with 3% reporting circumoral tingling, 3% reporting paraesthesia and 14% reporting light‐headedness.
The total dose of lidocaine administered to our participant was 565 mg (10.1 mg.kg−1). Although it could be argued that this overdosed the participant, this includes the entire nebulised lidocaine dose. Aerosol released from nebulisers is only available for inhalation during inspiration, and the remainder is wasted during exhalation 8. In normal respiration, only one‐third of the respiratory cycle is inspiration. Therefore, the maximum amount of nebulised drug inhaled would have been estimated to be one‐third of the total dose (66 mg). Applying this dose reduction for the nebulised lidocaine lost as aerosol, the total dose of lidocaine administered was 431.6 mg (7.7 mg.kg−1). The dose calculation made before the procedure was on the assumption that only one‐third of the total nebulised dose was absorbed by the body. The onset of our participant's tinnitus (30 min after the procedure) is consistent with the timing of peak plasma lidocaine concentration demonstrated in other studies 4, 5, 7. The absence of seizures or cardiovascular effects in our participant would be consistent with a lower plasma concentration of lidocaine.
Plasma lidocaine levels were measured in 25 of Woodall et al.'s participants 7. None had a peak plasma concentration above the recognised level for toxicity. A study of 41 patients undergoing flexible bronchoscopy using an average lidocaine dose of 9.3 mg.kg−1 found that the mean peak plasma lidocaine concentration was 2.9 mg.l−1 5. Although no patients experienced signs of lidocaine toxicity, 15% did have a peak plasma concentration above 4.5 μg.ml−1. They also found that only 42% of the variation in peak plasma concentration was attributable to dose per unit body weight. In another study, two subjects that received total lidocaine doses of only 4.8 mg.kg−1 and 6.2 mg.kg−1 had peak serum lidocaine concentrations exceeding 4.5 μg.ml−1 4. These highlight the interindividual variability in serum lidocaine levels when calculating dose by body weight.
There have been reports of lidocaine toxicity when doses below 9 mg.kg−1 have been used 9. One case involved a patient with a base‐of‐tongue abscess who developed seizures and coma while undergoing ATI 10. The authors postulated that the patient's inflamed airway may have resulted in increased transmucosal absorption of local anaesthetic. Our participant was recovering from a sinus infection and her nasopharyngeal mucosa was noted to be hyperaemic. Increased absorption of lidocaine could explain why she experienced symptoms of lidocaine toxicity within the recommended dose. Due to the propensity for hyperaemic mucosae to result in higher plasma lidocaine levels, recently unwell volunteers should not receive ATI. However, this may be unavoidable in patients. Anaesthetists must be mindful of the potential for increased absorption of local anaesthetic in patients with infections, airway oedema and burns undergoing ATI.
The symptoms were apparent in our participant because she received no sedation or general anaesthesia. However, many patients undergoing ATI receive sedation and then have a general anaesthesia for surgery. Although cardiovascular features would still be apparent during general anaesthesia, neurological symptoms may be attributed to the effects of other drugs or may have subsided by the time patients are fully conscious. We recommend that operators use the minimal dose of lidocaine to safely anaesthetise the airway, and that they remain vigilant for signs of local anaesthetic toxicity.
This case highlights the importance of safety measures on ATI training courses. It is vital to ensure that the maximum recommended dose of lidocaine for lean body weight is not exceeded. Additional safety measures include the use of continuous monitoring, access to emergency drugs and airway equipment and the presence of an appropriate number of trained facilitators and dedicated recovery staff. Volunteers with recent respiratory tract symptoms should not have an ATI due to the potential for increased absorption of local anaesthetic and the increased likelihood of reactive airways. It is now the policy of this training course that recently unwell participants (within two weeks) are not permitted to undergo ATI. By maintaining vigilance and ensuring that these safety measures are adhered to, we hope that anaesthetists can continue to benefit from the invaluable learning experience that ATI courses provide.
Acknowledgements
We acknowledge and thank the entire faculty from the James Cook Airway Course and Dr A. Norrington, who treated the participant. The first author is the subject of this case report. The second author is the course director. No external funding or competing interests declared.
Presented in part at the Association of Anaesthetists Annual Congress, Glasgow, September 2019.
[Correction added on 19th March 2020, after first online publication: In the Summary, "2 weeks before" has been corrected to "2 weeks following" in this current version.]
Contributor Information
F. Pearson, Email: fiona.pearson7@nhs.net, @fi_pea.
P. Chiam, @Gasmanpat.
References
- 1. Cook TM, Woodall N, Harper N, Benger J. Major complications of airway management in the UK: results of the Fourth National Audit Project of the Royal College of Anaesthetists and the Difficult Airway Society. Part 2 Intensive Care and Emergency Department. British Journal of Anaesthesia 2011; 106: 632–42. [DOI] [PubMed] [Google Scholar]
- 2. El‐Boghdadly K, Pawa A, Chin KJ. Local anesthetic systemic toxicity: current perspectives. Local and Regional Anesthesia 2018; 11: 35–44. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3. Malamed S. Handbook of local anesthesia, 6th edn. Missouri: Mosby, 2013: 15–30. [Google Scholar]
- 4. Milman N, Laub M, Munch E, Angelo H. Serum concentrations of lignocaine and its metabolite monoethylglycinexylidide during fibre‐optic bronchoscopy in local anaesthesia. Respiratory Medicine 1998; 92: 40–3. [DOI] [PubMed] [Google Scholar]
- 5. Efthimiou J, Higenbottam T, Holt D, Cochrane G. Plasma concentrations of lignocaine during fibreoptic bronchoscopy. Thorax 1982; 37: 68–71. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6. Ahmad I, El‐Boghdadly K, Bhagrath R, et al. Difficult Airway Society guidelines for awake tracheal intubation (ATI) in adults. Anaesthesia 2019; 75: 6–8. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7. Woodall N, Harwood R, Barker G. Complications of awake fibreoptic intubation without sedation in 200 healthy anaesthetists attending a training course. British Journal of Anaesthesia 2008; 100: 850–5. [DOI] [PubMed] [Google Scholar]
- 8. Clay M, Clarke S. Wastage of drug from nebulisers: a review. Journal of the Royal Society of Medicine 1987; 80: 38–9. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 9. Haldar R, Samanta S, Gyanesh P. Lignocaine toxicity from topical anaesthesia of airway during awake fibreoptic intubation. Journal of Neuroanaesthesiology and Critical Care 2014; 1: 146–7. [Google Scholar]
- 10. Giordano D, Panini A, Pernice C, Raso M, Barbieri V. Neurologic toxicity of lidocaine during awake intubation in a patient with tongue base abscess. Case report. American Journal of Otolaryngology 2014; 35: 62–5. [DOI] [PubMed] [Google Scholar]
