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Case Report: Case Report

Intravenous Lipid Infusion in the Successful Resuscitation of Local Anesthetic-Induced Cardiovascular Collapse After Supraclavicular Brachial Plexus Block

Warren, Julio A. MD; Thoma, R Brian MD; Georgescu, Alexandru MD; Shah, Saurin J. MD

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doi: 10.1213/01.ane.0000281434.80883.88
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Rescue from bupivacaine-induced cardiovascular collapse with IV lipid therapy has been investigated in animal models.1–3 As a result, lipid therapy was proposed for treatment of such local anesthetic toxicity4–6 and was described in resuscitations of patients with bupivacaine and ropivacaine-induced asystole.7,8 We report the successful resuscitation of a patient with IV lipid infusion following cardiovascular collapse after supraclavicular brachial plexus block with mepivacaine and bupivacaine.


A 60-yr-old man, weighing 83 kg, presented for revision of left upper extremity basilic vein fistula. Pertinent history and physical examination were performed, and preoperative evaluations were reviewed (Fig. 1). Routine monitors (pulse oximetry, plethysmography, and noninvasive arterial blood pressure) were placed. His arterial blood pressure was 147/73 and heart rate was 63 bpm. He received 3 L/min of nasal cannula oxygen, and IV midazolam 6 mg was titrated to an appropriate level of anxiolysis. A single-injection supraclavicular brachial plexus block was performed in the preoperative holding area using a Braun Stimuplex® 2-inch, 22-gauge needle. Local anesthetic with 1:200,000 epinephrine (30 mL 1.5% mepivacaine with 3 mL 8.4% sodium bicarbonate, followed by 10 mL 0.5% bupivacaine, in separate 10-mL syringes) was administered over several minutes after frequent negative aspirations of blood (Fig. 2). Rather than making multiple needle passes to elicit nerve stimulation, the entire drug volume was deposited after contacting the first rib. Neither pain nor paresthesia was reported by the spontaneously breathing and easily arousable patient. Immediately postprocedure, the patient was continually monitored in the preoperative holding area; he followed commands appropriately, and his vital signs were stable.

Figure 1.
Figure 1.:
Pertinent medical history and preoperative evaluation. NSR = normal sinus rhythm; RBBB = right bundle branch block; LAD = left axis deviation; LVEF = left ventricular ejection fraction; MR = mitral regurgitation.
Figure 2.
Figure 2.:
Timeline of critical events with cardiac rhythm strips. BP = arterial blood pressure; V-fib = ventricular fibrillation.

Five minutes later, he began to exhibit labored respirations with bilateral breath sounds, followed by apnea and unresponsiveness. Pulselessness developed, and cardiopulmonary resuscitation (CPR) was initiated. His cardiac rhythm degenerated. He was given atropine 1 mg IV, epinephrine 1 mg IV increments (total 3 mg), vasopressin 40 U, 100 mL 8.4% sodium bicarbonate, and magnesium sulfate 6 g over 10 min, including 11 successive defibrillations (up to 360 J) with minimal brief periods of perfusing heart rhythms but no restoration of sustained cardiovascular activity. Liposyn III 20% IV fat emulsion (Hospira, Inc., Lake Forest, IL) was administered centrally via infusion without bolus (250 mL over 30 min) beginning 10 min after CPR was initiated. Repeated defibrillations during lipid infusion produced successively longer intervals of sustained cardiac rhythm until wide complex tachyarrhythmia developed. Arterial blood samples were drawn. The unbound bupivacaine level (NMS Labs, Willow Grove, PA) drawn 2 min after lipid infusion had begun was 0.49 μg/mL. IV lipid infusion and CPR (including 15 additional defibrillations) were continued. Hemodynamic stability was achieved, chest compressions were suspended, and spontaneous respiratory efforts were noted. He was transferred to the surgical intensive care unit where examination 2 h later revealed the desired peripheral nerve blockade in the left upper extremity as evidenced by sensory and motor deficits. Twelve-lead electrocardiography and serial cardiac enzymes did not suggest pulmonary embolism or myocardial infarction. He was discharged 3 days later.


Bupivacaine exhibits narrower safety margins than other local anesthetics at similar concentrations.9,10 Cardiac toxicity of bupivacaine has long been documented.11 Weinberg et al. demonstrated that IV lipids confer resistance to and enhance resuscitation of animals exposed to toxic bupivacaine doses.1–3 Various mechanisms of lipid rescue of bupivacaine-induced cardiac arrest have been proposed, including “lipid sink” and metabolic theories.1,2,12

Our delayed recovery, in contrast to a similar case report of lipid rescue,7 may be attributed to infusion (rather than bolus) delivery of lipids. Early symptoms of bupivacaine central nervous system toxicity are associated with unbound concentrations of 0.11 μg/mL.13 Although the bupivacaine level was markedly lower than established cardiotoxic bupivacaine concentrations, collection of peripheral arterial blood with poor circulation (rather than central) or timing of collection (after lipids had begun infusing) could explain this difference. No mepivacaine level was drawn during the resuscitation. Thus, we cannot exclude the possible synergistic contribution of mepivacaine to this cardiac event. In summary, we report the first use of Liposyn III 20% IV fat emulsion in successful human resuscitation of local anesthetic-induced cardiovascular collapse. The use of 20% Intralipid (Baxter Pharmaceuticals) has been described.7,8 Regardless of branded preparation, we agree with Weinberg14 that 20% lipid emulsion should be available in perioperative areas, obstetric units, and any sites where local anesthetics are administered. Lipid rescue for presumed local anesthetic toxicity should be considered during resuscitative efforts in prolonged CPR refractory to standard Advanced Cardiac Life Support protocols.


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