A 70-year-old man was referred to the Respiratory Service at Christchurch Hospital for investigation of haemoptysis by bronchoscopy. The patient had ischaemic heart disease and atrial fibrillation. His medications included atenolol, frusemide, allopurinol, captopril, Mylanta and warfarin (INR 3). He had history of neither seizure activity nor other diseases of the central nervous system. Morphine 10 mg IM and atropine 0.6 mg IM were given 60 minutes prior to the procedure. No short-acting benzodiazepine was used.

The following regimen for local anaesthesia of the airway was used. Fifteen minutes prior to the procedure the patient received lignocaine 5 ml 4% (200 mg) via a nebulizer. Thereafter, 10 ml 4% lignocaine gel (400 mg) was applied within the nasal passage. At the beginning of the bronchoscopy, 10 ml of 4% lignocaine (400 mg) was applied to the vocal cords. Two applications of 10 ml of 1% lignocaine (200 mg) were then made to the right and left upper lobes. In total, the patient received 1200 mg of lignocaine.

The procedure was uncomplicated. Oxygen saturations were maintained above 95% using 2 l/min of oxygen via nasal prongs. Bronchial washings were taken; no cause for the haemoptysis was identified. The total time taken to complete the bronchoscopy following intubation was 10 minutes.

About five minutes following the procedure, the patient became drowsy and experienced a generalized tonic-clonic seizure. The seizure lasted about two minutes and was self-limiting. Thirty minutes after this event, the patient’s prolactin level was 823 mIU/L (normal range 80 to 350 mIU/L). The patient was observed for 24 hours and discharged without any further treatment. He remained well six weeks following this episode.

His lignocaine level was 32.7 μmol/l 30 minutes following the procedure. Lignocaine is potentially toxic at levels greater than 30 μmol/l. The lignocaine level may have been as high as 40 μmol/l at the time of the seizure. According to the ‘Adverse Drug Reaction Probability Scale’,1 this patient probably had a seizure secondary to lignocaine toxicity through mucosal absorption. Nebulization and absorption through the mucosa is a potent form of drug delivery used in therapeutic settings.

Morphine is a useful drug to minimize the cough reflex and sedate the patient, but it also lowers the seizure threshold.2 Seizures have also been particularly noted on the withdrawal of narcotic drugs.3

The 1200 mg of lignocaine used equates to 16 mg/kg although some would be suctioned out or swallowed. Little of the swallowed lignocaine would be absorbed. There is also no correlation between doses of lignocaine and peak concentrations.4,5 Neurotoxicity may begin with plasma concentrations of 5–6 g/l.6 However, in a series of 12 patients receiving on average 622 mg lignocaine, no patients exceeded the toxic concentration.4 In a position paper on fibre-optic bronchoscopy in adults published by the Thoracic Society of Australia and New Zealand,7 the maximal dose of lignocaine suggested was 512 mg.5 This is far less than the doses of lignocaine used in our institution.

Although neurotoxicity through mucosal absorption is a rare complication following a bronchoscopy, this case highlights that topical lignocaine should be used sparingly.

Author information: Karl Rodins, House Officer; Michael Hlavac, Advanced Trainee; Lutz Beckert, Respiratory Physician, Department of Respiratory Medicine, Christchurch Hospital, Christchurch

Correspondence: Dr Lutz Beckert, Respiratory Physician, Department of Respiratory Medicine, Christchurch Hospital, Christchurch. Fax: (03) 364 0914; email: Lutz.Beckert@cdhb.govt.nz