Department of Anaesthesiology and Intensive Care Medicine, Carl Gustav Carus University Hospital, Dresden, Germany*Corresponding author: Department of Anaesthesiology and Intensive Care Medicine, Carl Gustav Carus University Hospital, Fetscherstrasse 74, D-01307 Dresden, Germany
Accepted for publication: May 18, 2001
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Abstract |
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Br J Anaesth 2001; 87: 7847
Keywords: complications, convulsions; anaesthetics local, ropivacaine
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Introduction |
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Case report |
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The patient did not receive any sedation before surgery. In the induction room, monitoring was placed (ECG, pulse oximetry and non-invasive arterial blood pressure) and peripheral venous access was established. The left arm was abducted at a right-angle with the forearm flexed towards the head. The skin was infiltrated with 2% lidocaine 20 mg after sterile preparation, and a 23 gauge short bevel needle with an injection line was inserted parallel and close to the artery and directed towards the apex of the axilla. The perivascular sheath was identified with the loss of resistance technique. No spontaneous blood flow was observed in the connected injection line. After careful negative aspiration, 20 ml of ropivacaine 0.5% was injected over 1 min in 5 ml increments, with intermittent negative aspiration. Verbal contact was made during the injection and no early signs of systemic toxicity occurred. The brachial artery was then palpated again in order to insert the needle for a second injection. Suddenly, the patient lost consciousness without any prodromal signs, such as perioral numbness or dizziness, and a grand mal seizure started. During the convulsion, heart rate increased from 70 to 80 beats min1 and arterial blood pressure increased from 130/80 to 145/85 mmHg. The lungs were ventilated immediately with 100% oxygen using a mask. General anaesthesia was induced with thiopentone 400 mg, fentanyl 0.2 mg and succinylcholine 60 mg and the trachea was intubated. The convulsions stopped immediately after induction of general anaesthesia. For the following 30 min, anaesthesia was maintained with desflurane 2% in oxygen/nitrous oxide (30%/68%). ECG showed no signs of arrhythmia or changes in PQ or QT interval or QRS width. After this observation period, the scheduled surgery was performed under general anaesthesia. Three hours after the inadvertent intravascular injection of the local anaesthetic, the tracheal tube was removed. The patient had an incomplete sensory block of the ulnar nerve, evaluated by pinprick test, which lasted 4 h. The remaining brachial plexus showed no impairment of sensory function. The patient did not recall the seizure episode.
Venous blood samples were taken 15, 45, 75 and 155 min after the injection of ropivacaine. After immediate centrifugation, plasma samples were stored at 20°C. Total plasma concentrations of ropivacaine were determined using high-performance liquid chromatography (Institute of Clinical Pharmacology, Technical University, Dresden). The linear calibration curve was validated using four samples with known ropivacaine concentrations (0.5, 1.0, 2.0 and 4.5 mg litre1). The detection limit of the method was below 0.5 mg litre1 and the relative standard deviation of the method was 4.2%. The measured plasma concentrations of ropivacaine at 15, 45, 75 and 155 min were 3.3, 1.6, 1.2 and 1.0 mg litre1 respectively (Fig. 1).
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Discussion |
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Cardiac or central neurological complications after the administration of ropivacaine have been described after brachial plexus46 and sciatic blockade7 and after epidural anaesthesia.8 9 The wide range of administered doses of ropivacaine causing the symptoms confirms the inter-individual variation in threshold obtained in healthy volunteers (Table 1). Plowman and co-workers reported the onset of a grand mal seizure in a 13-yr-old boy after injecting ropivacaine 0.5 mg kg1 into the epidural space.9 The total plasma concentration of ropivacaine 30 min later was 1.4 mg litre1, suggesting a much larger value at the time of the incident. In our patient, we measured a total plasma concentration of ropivacaine of 3.3 mg litre1 15 min after inadvertent intravascular injection, and extrapolated to a concentration of 5.75 mg litre1 immediately after the end of the injection period. This value is well above the venous plasma concentration of ropivacaine found to produce neurological symptoms in humans.1 Unfortunately, we did not measure the concentrations of -1 glycoprotein, which are known to affect the unbound concentration of local anaesthetic. Knudsen and co-workers demonstrated that the total and the unbound concentrations of ropivacaine in arterial plasma are consistently higher than the corresponding venous concentrations during and up to 20 min after an i.v. infusion.1 After i.v. administration, the arterial circulation carries the local anaesthetic to various parts of the body, while the peripheral venous flow also returns from poorly perfused tissues. Therefore, during rapid i.v. injection the peak venous concentration probably does not represent the concentration at the site of action until equilibrium is reached.10 In our patient, the first sample was taken 15 min after the injection and the difference, if any, between the arterial and the venous concentrations was probably minor.
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Our patient showed no signs of cardiac toxicity and the changes in heart rate and arterial pressure were probably a consequence of the seizure, although a small increase in heart rate and arterial pressure has been described at similar plasma concentrations of ropivacaine.1 In one published case, severe cardiac arrhythmias were reported in addition to convulsions. The venous plasma concentrations 7 min after the inadvertent i.v. injection of ropivacaine were similar (3.6 mg litre1).7 The authors extrapolated to a peak plasma concentration at the time when the arrhythmia occurred of 78 mg litre1. This confirms that the cardiovascular system is more resistant to the effects of local anaesthetics than the central nervous system.13
Although brachial plexus blockade with 40 ml of ropivacaine 5 or 7.5 mg ml1 has been shown to be safe,5 administering the smallest clinically reasonable dose reduces the risk of severe toxic side-effects. Coventry and colleagues showed recently that brachial plexus blockade could be achieved with 30 ml of local anaesthetic using a nerve stimulator technique.14 The choice of local anaesthetic is also an important issue. The short-acting local anaesthetics prilocaine and lidocaine have been shown to be safer regarding systemic toxicity. We chose ropivacaine in the present case because of its long-lasting beneficial effects on arterial and venous blood flow after brachial plexus blockade15 and its better safety profile when compared with bupivacaine.1 2
In summary, we report a case of inadvertent intravascular injection of 1.1 mg kg1 of ropivacaine leading to a total venous plasma concentration of 3.3 mg litre1. Its initial plasma concentration after the end of the injection period was estimated at 5.75 mg litre1 using a two-compartment model. A grand mal seizure but no symptoms of cardiovascular toxicity occurred and the patient recovered without sequelae. This case emphasizes that regional anaesthetic techniques have to be applied very carefully and that appropriate monitoring of the patient is necessary. In the absence of contraindications, the addition of epinephrine to the local anaesthetic solution should be considered in order to detect inadvertent intravascular injection.
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Acknowledgements |
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References |
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