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Carotid surgery is often performed under regional or local anesthesia because of improved cerebral perfusion monitoring, shorter hospital stay, and, perhaps, a lower incidence of associated complications, such as cerebrovascular accident or myocardial ischemia. We describe a patient undergoing elective carotid endarterectomy under cervical plexus block who had an epileptic seizure intraoperatively after infiltration of local anesthetic into the region of the internal carotid artery. The mechanism, treatment, and implications are discussed.
A 76-yr-old man, with a history of a left sided cerebrovascular accident three months before, presented for carotid endarterectomy (CEA). Carotid duplex ultrasound revealed a left internal carotid artery (ICA) stenosis of 6080% and a right ICA stenosis of 42%. Preexisting medical conditions included hypertension, controlled with furosemide 20 mg once daily and ticlopidine 250 mg twice daily. The patient had undergone an uneventful right CEA under regional anesthesia 18 mo previously. There was no history of epilepsy or ischemic heart disease. A 12-lead electrocardiograph revealed sinus rhythm, rate 80 bpm, with incomplete right bundle branch block. On the morning of the surgery, the patient (weight, 91 kg) was admitted to the holding room for cardiovascular monitoring, vascular access, and placement of the regional block. Oxygen 4 L/min via a face mask and sedation with diazepam emulsion 7.5 mg IV in divided doses were administered. Hemodynamic monitoring, consisting of invasive arterial blood pressure from the contralateral radial artery, noninvasive blood pressure, 5-lead electrocardiography, and pulse oximetry were started. We positioned a single-injection deep cervical plexus block at C4 using bupivacaine 0.375% 25 mL (1). This involved the injection of local anesthetic onto the cervical transverse process of C4, which lies 12 cm deep on the skin, 1 cm posterior to the posterior border of sternocleidomastoid. Within 10 min, the patient reported numbness of the left side of his neck. Sensory testing of analgesia to pinprick over the C2, C3, and C4 dermatomes confirmed that the regional block was adequate. A superficial cervical plexus block with bupivacaine 0.375% 15 mL was also successfully placed. This involved injection of local anesthetic solution subcutaneously up and down the posterior border of sternomastoid, starting from the midpoint between the mastoid process and the clavicular head of sternomastoid. No supplemental local anesthetic was required during the incision or the dissection phase of the operation. A trial period of cross-clamping of the ICA 35 min after the start of surgery was uneventful in terms of neurological dysfunction, but the patient reported mild discomfort during manipulation of the carotid artery. To treat this, the surgeon injected lidocaine 0.5% 1 mL into the region of the ICA. Within 5 s, the patient became unresponsive, showing generalized tonic-clonic seizure activity of the face and upper limbs, particularly the right side. Surgery was discontinued while the patients condition was assessed. A close-fitting anesthetic face mask was applied, and intermittent positive pressure ventilation with 100% oxygen commenced. Within 30 s of the start of the seizure, and before the administration of benzodiazepines, the seizure activity stopped, and spontaneous ventilation returned. Shortly after this, the patients consciousness level started to improve until verbal contact was resumed after 2 min. There was no loss of continence. Neurological testing revealed a slight weakness of the right arm that resolved fully within 10 min. The patient was orientated as to person, space, and time, with no residual global or focal deficits. Heparin 5000 international units, IV was therefore administered. Cross-clamp time was 27 min, and the rest of the operation proceeded uneventfully. Labetalol 5 mg incrementally (total 30 mg) was administered to control intraoperative hypertension (highest blood pressure recorded 202/100 mm Hg). Postoperatively, the patient remained in the postanesthesia care unit for 4 h before transfer back to the ward area. Full neurological testing was unremarkable. He was discharged from hospital the following day and was well at follow-up 1 mo later.
The temporal relationship between the lidocaine injection and onset of seizure activity was highly suggestive of direct injection of lidocaine into the internal carotid artery. This has been described previously during CEA under general anesthesia, when changes in the electroencephalogram were noted after injection of 40 mg lidocaine in two patients undergoing CEA (2). However, in our case, not only was the patient awake and therefore additionally had potential airway compromise, but the lidocaine dose involved was considerably smaller (5 mg). The fact that the patient had received diazepam 7.5 mg IV may have conferred some cerebral protection on this patient, because diazepam itself may be used to terminate seizures. A seizure occurring during CEA is a potential disaster, because it may compromise the airway, raise cerebral oxygen consumption, and exacerbate cerebral ischemia. The differential diagnosis of seizures occurring during CEA is multifactorial. Seizures may occur as a result of an overdose of local anesthetics, described after interscalene brachial plexus block (3), but not specifically after cervical plexus block. Interscalene and supraclavicular regional blocks have a higher incidence of seizure than other regional techniques (3), and high local anesthetic plasma concentrations have been described after cervical block (4). Cerebral seizure activity may occur as a manifestation of cerebral ischemia (5), but the carotid artery was not clamped at the time of the seizure. Seizures may also occur postoperatively (6), usually caused by a hyperperfusion syndrome (7). The fact that this seizure occurred 61 minutes after placement of the regional block and only lasted a few seconds suggests that it was not a result of a local anesthetic overdose. Bupivacaine blood levels may be very high initially after deep and superficial cervical plexus blocks, but very large doses of local anesthetic were used in the case described by Tissot et al. (8). Indeed, the bupivacaine dose used in this case was well under the recommended maximum dose (total 40 mL 0.375% bupivacaine = 150 mg, which is approximately 1.6 mg/kg). In animal models, lidocaine and bupivacaine are additive with respect to central nervous system toxicity (9), in contrast to cardiorespiratory toxicity, in which lidocaine potentiates bupivacaines toxicity (10) Active airway management was started after seizure activity commenced but was not required because of the very brief duration of the seizure. This was presumably a result of the small amount of lidocaine involvedonly 5 mgwhich would be "washed out" rapidly by the blood passing through the carotid artery. Supplementation of local anesthetic by the surgeon is commonly required during CEA under regional anesthesia, because the carotid artery may have additional afferent autonomic innervation, and a cervical plexus block will not necessarily prevent this (11,12). However, patients under general anesthesia may also have a local anesthetic injected into the vicinity of the ICA to block the carotid sinu, which may affect hemodynamic stability postoperatively (13). There are no data on the incidence of accidental intraarterial injection of local anesthetic under these circumstances or on the potential deleterious effects of this approach. Performing this operation using regional or local anesthesia thus enables immediate detection and treatment of such a complication, which might be missed with a patient receiving general anesthesia. In summary, a seizure occurring in a patient undergoing CEA under regional anesthesia was managed conservatively, but draws attention to the serious complications which may occur during this procedure and the requirement for constant vigilance by the anesthesiologist.
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