Cardiotoxicidad Bupivacaina Reporte de Caso

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Case Report Recurrence of Cardiotoxicity After Lipid Rescue from Bupivacaine-Induced Cardiac Arrest Peter C. Marwick, MBChB, DA(SA) Andrew I. Levin, MBChB, DA(SA), MMed, PhD, FCA Andre R. Coetzee, MB, ChB, PhD, MMed, FFA(SA), FFARCS, MD, PhD Accidental intravascular administration of bupivacaine during performance of a brachial block precipitated convulsions followed by asystole. The patient was rapidly resuscitated using cardiopulmonary resuscitation, supplemented by 150 mL of 20% lipid emulsi
  Case Report Recurrence of Cardiotoxicity After Lipid Rescue fromBupivacaine-Induced Cardiac Arrest Peter C. Marwick, MBChB,DA(SA)Andrew I. Levin, MBChB,DA(SA), MMed, PhD, FCAAndre R. Coetzee, MB, ChB, PhD,MMed, FFA(SA), FFARCS, MD,PhD Accidental intravascular administration of bupivacaine during performance of a brachial block precipitated convulsions followed by asystole. The patient wasrapidly resuscitated using cardiopulmonary resuscitation, supplemented by 150mL of 20% lipid emulsion. Nonetheless, cardiac toxicity reappeared 40 min aftercompletion of the lipid emulsion. In the absence of further lipid emulsion,amiodarone and inotropic support were used to treat cardiotoxicity. This casesuggests that local anesthetic systemic toxicity may recur after initial lipid rescue.Since recurrence of toxicity may necessitate administration of additional doses oflipid emulsion, a sufficient quantity of lipid emulsion should be available whenregional anesthesia is performed. (Anesth Analg 2009;108:1344–6)  T  he use of lipid emulsions to treat systemic localanesthetic toxicity has recently been highlighted incase reports 1–9 and editorials. 10–16 We present a case oflipid rescue in which systemic toxicity recurred 40 minafter successful treatment with lipid emulsion. CASE REPORT  A 33-yr-old man (72 kg, 168 cm) presented for debridementof a compound fracture of his right humerus. The patient’svital signs, clinical examination, preoperative hemoglobin con-centration and urine analysis were unremarkable.A single injection infraclavicular paracoracoid block wasperformed after placement of an 18-gauge ported IV can-nula. No sedation was administered. The brachial plexuswas located using a 50 mm insulated needle (Stimuplex  , BBraun, Melsungen, Germany) attached to a nerve stimulator(Neuro-Trace III  , HDC  Corporation, Milpitas, CA).Evoked responses of finger and wrist flexion were firstelicited at 2 mA and disappeared at 0.4 mA. After injectionof 30 mL of 0.375% bupivacaine hydrochloride withoutepinephrine (Micro Healthcare, Bethlehem, South Africa)over 3 min, with aspiration at 5 mL intervals, the patientabruptly reported the new onset of a dry sensation in histhroat and eyes. These symptoms prompted immediatecessation of local anesthetic injection and removal of theinsulated needle. This was immediately followed by gener-alized convulsions and apnea. Facemask intermittent posi-tive pressure ventilation delivering 100% oxygen wasinitiated. Intralipid  (Fresenius Kabi  , South Africa) that washeld in the postanesthesia care unit was available within 30 sof the onset of convulsions. Convulsions were terminatedwithin 60 s by the administration of IV thiopental, 100 mgsucceeded by a further 150 mg.After termination of convulsions, the electrocardiogramtrace became visible and revealed a narrow complex tachy-cardia, which accelerated to a peak rate of 160 bpm. Over90 s, the tachycardia was succeeded by broadening of theQRS complexes, slowing of the heart rate and asystole.Intralipid 150 mL was administered over approximately90 s, the infusion commencing just prior to asystole. Externalcardiac compressions were begun, tracheal intubation was per-formed and epinephrine 1 mg was administered IV. Duringcardiopulmonary resuscitation, capnography (Dra¨ger  , Lu¨- beck, Germany) recorded an end-tidal carbon dioxide partialpressure (P etco 2 ) of 19 mm Hg.Within 3 min of completing the first 150 mL of lipidemulsion, the patient converted from asystole to a narrowcomplex rhythm at 130 bpm. This rhythm was associatedwith an arterial blood pressure of 160/120 mm Hg, P etco 2 of 61 mm Hg and an oxygen saturation (as measured bypulse oximetry) of 100%. Analysis of arterial blood samplesobtained from a radial arterial catheter 5 min after return ofspontaneous circulation revealed a pH  6.8, Pa co 2 113.3mm Hg, Pa o 2 180 mm Hg, lactate more than 15 mmol/L,potassium 3.2 mmol/L and glucose 10.9 mmol/L. Repeatanalysis 11 min after return of spontaneous circulationrevealed similar values, albeit Pa co 2 had decreased to 55mm Hg. The blood gas analyzer could not estimate bicar- bonate levels nor base deficit. These measurementsprompted an increase in minute ventilation and IV admin-istration of sodium bicarbonate, insulin, and potassium. Afurther blood gas analysis 110 min after return of spontane-ous circulation revealed pH 7.30, Pa co 2 53 mm Hg, Pa o 2 257mm Hg, bicarbonate 21.0 mmol/L, base deficit 5.2, lactate8.5 mmol/L, potassium 2.5 mmol/L, and glucose concentra-tions 7.9 mmol/L.Over the 30 min after return of spontaneous circulation,the remaining 350 mL contained in the Intralipid bag wereinfused. During this time, his heart rate and rhythm revertedto sinus tachycardia at 110 bpm. The circulation was sup-ported with an epinephrine infusion that was progressivelydecreased to 0.06  g  kg  1  min  1 at this time. From the Department of Anesthesiology and Critical Care,University of Stellenbosch and Tygerberg Academic Hospital, Ty-gerberg, South Africa.Accepted for publication November 24, 2008.Reprints will not be available from the author.Address correspondence to Andrew Levin, MBChB, DA(SA),MMed, PhD, FCA, Department of Anesthesiology and Critical Care,Stellenbosch University, Room 2044, Clinical Building, Francie vanZijl Avenue, Tygerberg 7505, South Africa. Address e-mail © 2009 International Anesthesia Research Society DOI: 10.1213/ane.0b013e3181979e17 Vol. 108, No. 4, April 2009 1344  The patient remained hemodynamically stable and, at theend of this 30 min period, it was decided by the anesthesi-ologist and surgeon to proceed with the planned debride-ment. This was facilitated by administering a 5 mg bolus ofmidazolam and isoflurane (end-tidal partial pressure 0.5kPa). The debridement was completed within 10 min.After surgery, the patient remained in the operatingroom until intensive care unit admission was possible.However, at the end of the next 30 min period, (approxi-mately 40 min after the conclusion of Intralipid infusion), aprogressively accelerating sinus tachycardia at a rate of 140 bpm, accompanied with frequent multifocal ventricular ex-trasystoles and short, self-terminating runs of ventriculartachycardia were observed. In view of what was presumedto be the recurrence of bupivacaine cardiotoxicity, addi-tional Intralipid was ordered. However, the recovery room’semergency stock was comprised of only one 500 mL bagwhich had now been used and no additional Intralipid could be obtained for several hours. Therefore, an amiodaroneinitial loading dose of 300 mg in 200 mL of 5% dextrose wasinfused over 30 min.Admission to the intensive care unit took place 1 h aftercompletion of the amiodarone loading dose by which timethe arrhythmias had terminated and inotropic support wasdiscontinued. The patient was tracheally extubated 5 h afterhis initial episode of systemic toxicity. Despite an initialserum amylase concentration of 608 IU/L, no clinical signsof pancreatitis were noted. On the first postarrest day, totalcreatine kinase of 2378 IU/L, MB fraction 26  g/L andTroponin I 1.255  g/L suggested that myocardial damagehad occurred. Four days later, cardiac enzyme levels de-creased to 765 IU/L, 1.1  g/L and 0.059  g/L, respectively.Hospital discharge occurred 4 days after the initial event. DISCUSSION The outstanding feature of this case was the recur-rence of cardiovascular instability 40 min aftercompletion of Intralipid administration for bupiva-caine cardiotoxicity. We attributed the cardiovascularinstability to recurrence of local anesthetic toxicityafter lipid rescue, a scenario not previously described.The cause of recurrence of toxicity was likely multi-factorial. The serum concentration of Intralipid wouldhave decreased due to redistribution and metabolism.The elimination half-life of IV bupivacaine is longerthan all other currently used local anesthetics, report-edly 3.5 h. 17 This may have been prolonged because ofpoor hepatic function and perfusion in the aftermathof the cardiac arrest. Bupivacaine may have redistrib-uted back into the central compartment. Initial tissueentry and subsequent acidosis-related ion trapping, 17 with later release into the plasma as the acidosisresolved, would have increased the plasma concentra-tions of bupivacaine. Furthermore, pulmonary uptakeof local anesthetics decreases arterial concentrations by 20%; subsequent release of local anesthetic occursover an unknown time, in an exponentially decreasingmanner. 18 For treatment of local anesthetic toxicity, both theAssociation of Anesthetists of Great Britain andIreland (AAGBI) 19 and Weinberg 20–22 currently rec-ommend an initial bolus of 1.5 mL/kg of 20% lipidemulsion administered over 1 min. This bolus may berepeated twice at 5 min intervals if an adequate circu-lation has not been restored. The bolus should befollowed by an infusion of 0.25 to 0.5 mL  kg  1  min  1 ,the AAGBI recommending administration over 20 min,whereas Weinberg recommends the infusion be contin-ued for 30 min. Weinberg suggests that a total doseexceeding8mL/kg20%lipidemulsionisnotlikelytobeneeded. 21,22 These recommendations imply that a single500 mL bag will suffice for most 60–70 kg patients.However, our case lends support to the AAGBI recom-mendation that at least 1000 mL 20% lipid emulsionshould be available. 23,24 The postoperative increase in serum amylase couldindicate pancreatic injury. While pancreatitis is aknown complication of chronic hyperlipidemia, 25 thesignificance of the hyperamylasemia seen in our pa-tient is currently unclear. Although we cannot findanother documented increase in amylase or pancreaticinjury after the use of lipid emulsion in resuscitation,this issue must be considered after lipid rescue.In summary, we report a case of recurrent systemiclocal anesthetic toxicity after successful treatment withlipid emulsion. Because no additional lipid emulsionwas available, the recurrent dysrhythmias were treatedwith amiodarone. This case documents the impor-tance of the availability of a sufficient quantity of lipidemulsion when regional anesthesia is performed. REFERENCES 1. Smith HM, Jacob AK, Segura LG, Dilger JA, Torsher LC.Simulation education in anesthesia training: a case report ofsuccessful resuscitation of bupivacaine-induced cardiac arrestlinked to recent simulation training. Anesth Analg 2008;106:1581–42. Ludot H, Tharin JY, Belouadah M, Mazoit JX, Malinovsky JM. Successful resuscitation after ropivacaine and lidocaine-induced ventricular arrhythmia following posterior lumbarplexus block in a child. Anesth Analg 2008;106:1572–43. Zimmer C, Piepenbrink K, Riest G, Peters J. [Cardiotoxic andneurotoxic effects after accidental intravascular bupivacaineadministration. Therapy with lidocaine propofol and lipidemulsion]. Anaesthesist 2007;56:449–534. Foxall G, McCahon R, Lamb J, Hardman JG, Bedforth NM.Levobupivacaine-induced seizures and cardiovascular collapsetreated with Intralipid. 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