Post Your Cases > Supraventricular tachycardia after an intercostal nerve block with bupivacaine treated with 10% intralipid’
The use of 20% intralipid as a rescue drug for bupivacaine cardiotoxicity has been reported. There are laid down guidelines to treat severe toxicity but there are conflicting reports on the success of 10% intralipid to treat it.1 We report a case of severe cardiotoxicity by racemic bupivacaine treated successfully by 10% intralipid. A 26-year-old, 75 kg, male with fracture 9th thoracic vertebra and fractures 8, 9, 10, 11 right-sided ribs, with paraparesis, underwent transthoracic fixation of affected dorsal vertebra under general anesthesia with one lung ventilation. Towards the end of surgery, intercostal nerve block at three levels was planned for post-operative analgesia and to facilitate early tracheal extubation. The patient developed supraventricular tachycardia soon after the administration of the first injection of 5ml of 0.5% racemic bupivacaine. The heart rate peaked to 244-250/minute and invasive arterial pressures came down to 50-56/30-36mm Hg. Further injection of local anesthetic was stopped and 10% intralipid, which was available at that time, was started through the right internal jugular vein (canulated at the beginning of the surgery). Figure 1 shows the photograph of the monitor taken five minutes after starting treatment. Sinus rhythm returned after 150 ml of intralipid was injected over 15 mins. The hemodynamics returned to normal and the patient remained stable in post-operative period and did not need vasopressors or anti-arrhythmics. The patient was electively ventilated and weaned off successfully the next day. There was no evidence of any cardiac or neurological sequelae in the follow up period. The blood levels of bupivacaine could not be measured due to non-availability of the required facility, though clinically it is beyond doubt that bupivacaine was the cause of tachyarrhythmia. Intercostal nerve blocks are associated with a higher incidence of local anesthetic toxicity because of increased vascularity. Injection of a small amount of drug can cause toxic symptoms if injected rapidly. Bupivacaine usually slows down ventricular conduction because of its effect on sodium channels. At higher plasma drug concentration, bupivacaine acts on calcium and potassium channels and causes slowing of conduction with decreased contractility and certain metabolic changes. Supra-ventricular arrhythmias are sometimes due to re-entry of an impulse around an arc of functional conduction block. 2 The lipid sink theory 3 describes how intralipid forms a lipid phase inside plasma into which bupivacaine is extracted from the cardiac tissues and thus reduces the amount of free bupivacaine in the aqueous phase of plasma. Cardiotoxicity with bupivacaine is known but what was remarkable in this case is that it occurred almost immediately with a small volume of injected drug and presented as supraventricular tachycardia with severe hypotension. The electrocardiographic changes reverted completely with 2ml/kg of 10% intralipid within 15 mins. We were successful using 10% intralipid in the same volume and in a short time possibly because we had the central venous catheter in place or 10% intralipid was effective. Adult cardiac life support guidelines should be followed simultaneously in all cases where required. Weinberg et al 4 have suggested that propofol should not be used for treating cardiotoxicity though it contains 10% intralipid because propofol itself may be detrimental in such situation. The authors suggest that if 20% intralipid is unavailable, 10% intralipid may be used. It is strongly recommended that intralipid be kept available in the theatres where nerve blocks are practised routinely so that immediate action may be taken in case of local anesthetic toxicity.
References 1. The Association of Anaesthetists of Great Britain & Ireland. Guidelines for the management of Severe Local Anaesthetic Toxicity. London, UK: AAGBI; 2007 2. De La Coussaye JE, Brugada J, Allessie MA. Electrophysiologic and arrthymogenic effects of bupivacaine: a study with high resolution ventricular epicardial mapping in rabbit hearts. Anesthesiology 1992; 77: 132-141 3. Weinberg GL. Lipid infusion therapy: translation to clinical practice. Anesth Analg 2008; 106:1340–1342 4. G Weinberg, P Hertz, J Newman. Lipid, Not Propofol, Treats Bupivacaine Overdose. Anesth Analg 2004; 99: 1875-1876
Nice save, Dr. Goyal!! Good to know that 10% might help if it's the only lipid emulsion available. Obviously, the preferred choice is 20% formulation. However, if that is not available, it makes sense as you did, to use 10%. I'm glad the patient responded so well. Thanks for the very nice discussion. Guy
A 26-year-old, 75 kg, male with fracture 9th thoracic vertebra and fractures 8, 9, 10, 11 right-sided ribs, with paraparesis, underwent transthoracic fixation of affected dorsal vertebra under general anesthesia with one lung ventilation. Towards the end of surgery, intercostal nerve block at three levels was planned for post-operative analgesia and to facilitate early tracheal extubation. The patient developed supraventricular tachycardia soon after the administration of the first injection of 5ml of 0.5% racemic bupivacaine. The heart rate peaked to 244-250/minute and invasive arterial pressures came down to 50-56/30-36mm Hg. Further injection of local anesthetic was stopped and 10% intralipid, which was available at that time, was started through the right internal jugular vein (canulated at the beginning of the surgery). Figure 1 shows the photograph of the monitor taken five minutes after starting treatment. Sinus rhythm returned after 150 ml of intralipid was injected over 15 mins. The hemodynamics returned to normal and the patient remained stable in post-operative period and did not need vasopressors or anti-arrhythmics. The patient was electively ventilated and weaned off successfully the next day. There was no evidence of any cardiac or neurological sequelae in the follow up period. The blood levels of bupivacaine could not be measured due to non-availability of the required facility, though clinically it is beyond doubt that bupivacaine was the cause of tachyarrhythmia.
Intercostal nerve blocks are associated with a higher incidence of local anesthetic toxicity because of increased vascularity. Injection of a small amount of drug can cause toxic symptoms if injected rapidly. Bupivacaine usually slows down ventricular conduction because of its effect on sodium channels. At higher plasma drug concentration, bupivacaine acts on calcium and potassium channels and causes slowing of conduction with decreased contractility and certain metabolic changes. Supra-ventricular arrhythmias are sometimes due to re-entry of an impulse around an arc of functional conduction block. 2
The lipid sink theory 3 describes how intralipid forms a lipid phase inside plasma into which bupivacaine is extracted from the cardiac tissues and thus reduces the amount of free bupivacaine in the aqueous phase of plasma. Cardiotoxicity with bupivacaine is known but what was remarkable in this case is that it occurred almost immediately with a small volume of injected drug and presented as supraventricular tachycardia with severe hypotension. The electrocardiographic changes reverted completely with 2ml/kg of 10% intralipid within 15 mins. We were successful using 10% intralipid in the same volume and in a short time possibly because we had the central venous catheter in place or 10% intralipid was effective. Adult cardiac life support guidelines should be followed simultaneously in all cases where required.
Weinberg et al 4 have suggested that propofol should not be used for treating cardiotoxicity though it contains 10% intralipid because propofol itself may be detrimental in such situation. The authors suggest that if 20% intralipid is unavailable, 10% intralipid may be used. It is strongly recommended that intralipid be kept available in the theatres where nerve blocks are practised routinely so that immediate action may be taken in case of local anesthetic toxicity.
References
1. The Association of Anaesthetists of Great Britain & Ireland. Guidelines for the
management of Severe Local Anaesthetic Toxicity. London, UK: AAGBI; 2007
2. De La Coussaye JE, Brugada J, Allessie MA. Electrophysiologic and arrthymogenic effects of bupivacaine: a study with high resolution ventricular epicardial mapping in rabbit hearts. Anesthesiology 1992; 77: 132-141
3. Weinberg GL. Lipid infusion therapy: translation to clinical practice. Anesth Analg 2008; 106:1340–1342
4. G Weinberg, P Hertz, J Newman. Lipid, Not Propofol, Treats Bupivacaine Overdose. Anesth Analg 2004; 99: 1875-1876