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Department of Anesthesiology, Duke University Medical Center, Durham, North Carolina
Address correspondence and reprint requests to Stephen M. Klein, MD, Department of Anesthesiology, Box 3094, Duke University Medical Center, Durham, NC 27710. Address e-mail to klein006{at}mc.duke.edu
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Abstract |
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IMPLICATIONS: This case documents the successful cardiopulmonary resuscitation of a patient after accidental ropivacaine-induced ventricular fibrillation. Despite techniques used to detect intravascular injection, toxicity may still occur; early intervention is essential for an optimal outcome.
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Introduction |
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Case Report |
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Routine ASA monitors and supplemental oxygen were applied. Midazolam 3 mg and fentanyl 100 µg IV were titrated for sedation. Using an insulated needle and a nerve stimulator (Braun Medical, Bethlehem, PA), a femoral nerve block was performed using 20 mL of 1.5% mepivacaine with 1:400,000 epinephrine to provide anesthesia in the area of the tourniquet. The patient remained relaxed and conversant.
Five minutes later, using the same technique, an anterior sciatic block was done with 0.5% ropivacaine with 1:400,000 epinephrine for prolonged analgesia. Plantar flexion of the toes was obtained (at 0.4 mA) and stopped after injecting 1 mL. The remainder of the solution was injected over 120–180 s. A negative aspiration occurred between each 3- to 5-mL dose. No changes in heart rate or blood pressure (cycled every 3 min) were noted. After injecting 32 mL (160 mg), the patient became less responsive. The injection was aborted and 5–10 s later twitching of the hand and face as well as tachycardia developed. Midazolam 2 mg IV was administered; however, the twitching rapidly progressed to a tonic-clonic seizure.
Mask ventilation with 100% oxygen was initiated and additional assistance summoned. The convulsions were halted with propofol 20 mg IV. The patient remained unresponsive and the trachea was intubated. During this time, the pulse rate slowed. There was gradual widening of the QRS complex on the ECG. Three minutes after the injection, the ECG showed ventricular fibrillation and no pulse or blood pressure could be obtained. Chest compressions were initiated and the defibrillator was requested. After 60 s of compressions and just before direct current defibrillation and IV epinephrine, the patient converted to sinus bradycardia 50 bpm. Blood pressure was 90/40 and O2 saturation was 98%. Heart rate increased to 120 bpm, blood pressure returned to baseline, and the patient began to make respiratory efforts within 60 s of return of circulation.
Ten minutes after the injection, the patient was breathing regularly, opening her eyes, and following commands appropriately. The trachea was extubated and the patient was transferred to the emergency department. Thirty minutes later, she was alert and had a complete sensory and motor block of her femoral and sciatic nerve. The patient was admitted to the hospital and discharged the next morning without complications. The sciatic nerve block lasted 12 h.
A venous blood sample was collected 5 min after the ropivacaine injection to assess local anesthetic concentrations. Ropivacaine and mepivacaine plasma concentrations were measured using a gas chromatograph (3). Total ropivacaine was 3.2 mg/L, free ropivacaine was 0.5 mg/L, and total mepivacaine was 0.22 mg/L.
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Discussion |
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The sudden symptoms associated with injection and the serum ropivacaine concentrations suggest that a portion of the 160-mg dose entered the circulation contributing to the cardiac arrest. Some was correctly deposited providing a sciatic block. These bolus concentrations (3.2 and 0.5 mg/L) 5 minutes after injection are substantially larger than the mean maximally tolerated concentrations documented by Knudsen et al. (4) (2.2 and 0.15 mg/L) to produce central nervous system (CNS) toxicity when infused in volunteers, further supporting this etiology.
Several reports have documented ropivacaine CNS toxicity (5) and only two (6,7) have reported cardiovascular toxicity, both of which also involved a sciatic nerve block. Ruetsch et al. (6) described a block with ropivacaine 225 mg, CNS toxicity, and a severe dysrhythmia. That patient maintained spontaneous circulation and required only brief inotropic interventions to maintain perfusion. The (total and free) serum ropivacaine concentrations were 3.6 and 0.69 mg/L at 7 minutes and 1.6 and 0.3 mg/L at 12 minutes demonstrating a rapid decrease in a short time. Mullanu et al. (7) likewise reported CNS toxicity and junctional bradycardia with combined lower extremity blocks using ropivacaine 187.5 mg and mepivacaine 300 mg and obtained ropivacaine levels of 3.2 and 0.5 mg/L at 10 minutes.
Local anesthetic toxicity is an uncommon but well documented complication of regional anesthesia. To reduce its occurrence, frequent aspiration and slow fractionated injection are recommended. Despite following these recommendations, we were unable to avoid cardiovascular toxicity. Failure to aspirate blood or perceive an increase in heart rate from epinephrine is common in case reports of local anesthetic toxicity (5,8). An increase in blood pressure is considered a more reliable marker of epinephrine injection (9) but in our case it may have been missed, given the rate of injection and the three-minute interval between blood pressure cuff cycling. Rapid intervention with airway and circulatory support, however, is considered essential when toxicity occurs (10). We attribute much of our successful outcome to avoiding hypercarbia, hypoxemia, and maintaining circulatory perfusion to allow redistribution of local anesthetic. In addition, the relative safety profile of ropivacaine was likely helpful (2,4,11). Animal data also suggest that IV propofol may have protective effects against local anesthetic cardiotoxicity which may have been beneficial in this case (12,13).
The prior block with mepivacaine could have potentiated or added to the cardiotoxicity, although the toxic mechanisms of combined local anesthetics are controversial (14). When performing combined lower extremity blocks, it is common to administer large-milligram doses, and hence increase the possibility of toxicity from the total dose via intravascular or systemic reuptake. Nevertheless, we estimate this had little effect in our case because the total serum mepivacaine level was only 0.22 mg/L. Also, the patient was taking olanzapine and citalopram. Olanzapine is an atypical antipsychotic drug that binds to 
1, dopamine, histamine1, muscarinic, and serotonin type 2 receptors. Citalopram is a selective serotonin receptor inhibitor. These medications are reported to interrupt myocardial muscle repolarization early in phase 3 of the action potential by early after-depolarization (15). This causes QT interval prolongation and may have increased the sensitivity to the arrhythmogenic effects of ropivacaine. Additionally, the peripheral blockade of olanzapine may have further exacerbated hypotension caused by ropivacaine or masked the hypertensive response from the epinephrine marker. Furthermore, sedation with midazolam and fentanyl (16) as well as advanced age (17) or underlying disease may have also masked tachycardia from the epinephrine marker.
In summary, techniques used to detect intravascular injection may reduce but not eliminate catastrophic events. Consequently, regional anesthesia using large amounts of local anesthetic should be done in locations with resuscitation equipment and by individuals trained to recognize these complications and begin early treatment.
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S. L. Orebaugh The femoral nerve and its relationship to the lateral circumflex femoral artery. Anesth. Analg., June 1, 2006; 102(6): 1859 - 1862. [Abstract] [Full Text] [PDF]
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