Convulsions Induced by Ropivacaine During Interscalene Brachial Plexus Block

Ropivacaine is a new amide local anesthetic with a reportedly high threshold for systemic toxicity and high selectivity for sensory fibers ^[1]. We present a case of central nervous system (CNS) toxicity after ropivacaine during induction of a brachial plexus block.

Case Report

A 66-yr-old, 65-kg woman (ASA physical status I) was scheduled for right acromioplasty with general anesthesia. There was no medical history of epilepsy. Physical examination was unremarkable. An interscalene brachial plexus block was planned to provide intra- and postoperative analgesia. A venous catheter was inserted, and the patient was placed in the supine position with her head turned to the left. Arterial blood pressure was 140/90 mm Hg, and the heart rate was 68 bpm. With the use of a nerve stimulator and locator, an insulated 22-gauge short-beveled needle was inserted into the interscalene groove ^[2]. Bright red blood was obtained, and the needle was withdrawn slightly. No further blood could be aspirated, and paresthesia in the hand was elicited intentionally. A test dose of 2 mL 0.75% ropivacaine was injected. After approximately 2 min, the patient reported no unusual sensations. A further 18 mL of 0.75% ropivacaine was injected slowly.

Immediately after the injection, the patient convulsed. The seizure was characterized by clonic spasms of the facial muscles and was accompanied by loss of consciousness. A second seizure occurred soon afterward. No arrhythmias were seen on the electrocardiogram. Thiopental 100 mg was given intravenously (IV), and bag-mask ventilation was initiated. Succinylcholine 75 mg was given to facilitate tracheal intubation. During this time, the patient's systolic blood pressure was recorded to be 50 mm Hg. Epinephrine 1 mg was given, and blood pressure returned to preoperative levels. Nitrous oxide, isoflurane, and fentanyl were administered. When the effect of the succinylcholine began to wane, further relaxation was achieved with rocuronium. The decision was made to abandon surgery.

Approximately 20 min later, anesthetics were discontinued. While being transferred from the operating Table toher bed, the patient regained consciousness. There was no evidence of brachial plexus blockade. The incident was explained, and the patient was given the option of continuing with surgery. Despite the presence of a tracheal tube, the patient made it clear to all staff present with appropriate gestures that the surgery should continue.

General anesthesia was induced, and the operation proceeded. The following morning, the patient was given a full explanation of the incident. She had no memory of the episode, and her recovery was uneventful.

Discussion

Ropivacaine has been reported to be a suitable local anesthetic for brachial plexus block in a dose of 2.5-2.6 mg/kg without evidence of CNS or cardiovascular toxicity ^[3]. In our case, a total dose of 2.3 mg/kg ropivacaine was used. Despite the negative aspiration for blood before injection, it is probable that ropivacaine was injected directly into a vessel. Doses of bupivacaine as small as 2.5 mg have been reported to induce convulsions when injected into the vertebral artery ^[4]. The rapid onset of convulsions is more suggestive of intraarterial rather than IV injection ^[5], although a large volume of local anesthetic injected IV could also induce both CNS and cardiovascular toxicity. Both the total dose and time course of administration contributed to the local anesthetic systemic toxicity. Incremental administration of local anesthetic while simultaneously assessing the patient for evidence of toxicity might have alerted us to the inadvertent placement of the needle within a vessel ^[6].

There are no published cases of convulsions in humans with the use of ropivacaine. In a laboratory study in which beagles were given convulsant doses of IV ropivacaine (4.9 mg/kg), all animals made a complete recovery after thiamylal administration and controlled ventilation ^[7]. In a study of pregnant and nonpregnant ewes given IV local anesthetics, Santos et al. ^[8] found that ropivacaine 7.5 mg/kg produced more convulsions compared with bupivacaine 5.0 mg/kg and that ropivacaine 12.9 mg/kg produced more cardiovascular collapse compared with bupivacaine 8.5 mg/kg. In a study of human volunteers receiving infusions (10 mg/min) of either ropivacaine or bupivacaine, there were fewer CNS symptoms with ropivacaine, and the mean dose of ropivacaine tolerated was 124 mg, compared with bupivacaine 99 mg ^[9]. The onset of symptoms from the start of the infusion was, on average, 4 min with bupivacaine and 6 min with ropivacaine, but the duration of symptoms did not differ significantly.

New local anesthetics such as ropivacaine may have better safety profiles than bupivacaine, but toxicity can still occur. Recognition and prompt treatment of such incidents should result in a favorable outcome. This case serves as a reminder that CNS toxicity resulting from intravascular injection remains a potential problem even in the presence of negative aspiration or when test doses are used in the manner we have described. Therefore, when potentially toxic doses of local anesthetics are to be used, an incremental injection technique with an adequate delay between boluses is advisable to allow detection of adverse clinical effects.