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Re: Convulsions associated with low plasma level of local anaesthesics
- Pierre Pasquier, [S. Ausset], [G. Pelee De Saint Maurice], [P Vest], [J.X Mazoit], and [Y. Auroy] (18 August 2009)
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Central nervous system toxicity after two-stage brachial plexus block with 300 mg of ropivacaine
- Simon J Parrington, Ricky Brull (25 February 2009)
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Local Anesthetic Dosing Ranges May Be Misleading
- James W. Heitz (10 January 2009)
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Re: Intralipid
- Tsuyoshi Satsumae, Makoto Tanaka (29 December 2008)
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Reply to Dr Marri
- Tsuyoshi Satsumae, Makoto Tanaka (29 December 2008)
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Convulsions associated with ropivacaine 300mg for brachial plexus block
- Sudhakar Marri, David Coventry (11 December 2008)
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Intralipid
- Muhammad Rahim Mansha Kayani (2 December 2008)
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Convulsion afte a toxic dose of ropivacaine
- Yasir Al-Tamimi (2 December 2008)
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Pierre Pasquier department of Anesthesiology and Intensive Care, Percy Military Hospital, Paris, France, [S. Ausset], [G. Pelee De Saint Maurice], [P Vest], [J.X Mazoit], and [Y. Auroy]
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We read with interest the case report by Satsumae and colleagues,¹ adressing the question of sensitivity to local anaesthesics (LA) -toxicity occuring at lower than expected dose. We met a quite similar case of a 51-yr-old women who presented myoclonic movements of the whole body after popliteal sciatic blockade through a non stimulating catheter, inserted with a peripheral nerve stimulator, using 24 mg ropivacaine administered 60 minutes after the injection of 300 mg of lidocaine. Dosages and time intervals between injections complied with guidelines of the French Society of Anesthesiology ². A venous blood sample drawn during myoclonic movements showed non toxic levels of local anaesthetics (0.12 and 0.1 mg.L–1 for ropivacaine and lidocaine respectively). The blood glucose level was normal and she had no medical history, neurological disease, or alcoholism and took no medication. The postoperative course was uneventful and an electroencephalogram performed 30 days later showed no abnormality. This case suggests that toxic complications may occur after administration of low dosages of local anaesthetics in the absence of intravascular injection. In healthy volunteers, Knudsen et al retrieved a mean plasma level of ropivacaine of 2.2 mg.mL-1 ± 0.8 for the first occurrence of signs of neurological toxicity. In this study myoclonic movements were considered as signs of systemic toxicity, as we did for our patient, and the lowest plasma level associated with this kind of symptoms was 0.5 mg.mL-1 ³. Two case reports have previously reported toxic symptoms of local anaesthetics associated with the administration of a small amount of local anesthesic ⁴, ⁵. In one case, symptoms occurred with low plasma levels of ropivacaine ⁴ suggesting that patients with a low tolerance to local anaesthetics may exist or that toxicity threshold varies according to factors such as: medications, hypercarbia, electrolytic abnormalities, carnitin deficiency. In addition, general anesthesia might have influenced the toxicity of ropivacaine by their central nervous system effects and changed the pharmacokinetics of local anaesthetics . The responsibility of LA toxicity can be discussed since the placement of the nerve catheter had not been radiologically assessed even if neither the timing of symptoms nor the normal blood level of local anaesthetics suggests an inadvertent intravascular injection. Furthermore, many drugs were used perioperatively and could have been implied in the symptomatology: hydroxyzine and alprazolam for preoperative medications; propofol at target-control infusion and alfentanyl for general anaesthesia; dexamethazone and droperidol in prevention of post operative nausea and vomiting. This case suggests that these complications may occur with low dosages despite careful attention to needle and catheter placement ⁶, fractionated dosing and frequent aspirations, in the absence of intravascular injection. It must also be pointed out that a 1 mg L-1 plasma level of lidocaine and 0.12 mg L-1 of ropivacaine seem to be very low, especially when it was measured during the myoclonia suggesting that patients with a low tolerance to local anaesthetics may exist. Therefore, safety in regional anaesthesia cannot rely only on the use of “safe” dose limits. Careful monitoring and preparedness for managing complications throughout the whole course of regional anaesthesia is of paramount interest. 1 Satsumae T, Tanaka M, Saito S, Inomata S. Convulsions after ropivacaine 300 mg for brachial plexus block. Br J Anaesth 2008; 101: 860-2 2 [Peripheral nerve block of limbs in the adult]. Ann Fr Anesth Reanim 2003; 22: 567-81 3 Knudsen K, Beckman Suurkula M, Blomberg S, Sjovall J, Edvardsson N. Central nervous and cardiovascular effects of i.v. infusions of ropivacaine, bupivacaine and placebo in volunteers. Br J Anaesth 1997; 78: 507-14 4 Dhir S, Ganapathy S, Lindsay P, Athwal GS. Case report: Ropivacaine neurotoxicity at clinical doses in interscalene brachial plexus block. Can J Anesth 2007; 54: 912-6 5 Iwama H. A case of normal ropivacaine concentration causing grand mal seizure after epidural injection. Eur J Anaesthesiol 2005; 22: 322-3 6 Marri S, Coventry D. Convulsions associated with ropivacaine 300 mg for brachial plexus block. Br J Anaesth 2009; 102: 562-3; author reply 3 Conflict of Interest:None declared |
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Simon J Parrington, Clinical fellow in Regional Anaesthesia Toronto Western Hospital Canada, Ricky Brull
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Editor -We read with interest the case report by Satsumae and colleagues[1] in which they describe convulsions in a young adult male following combined axillary and interscalene block with 300 mg of ropivacaine for open reduction and internal fixation of the right navicular (scaphoid) bone. Central nervous system (CNS) toxicity is a well-recognized phenomenon following sub toxic dose of local anaesthetic agents, the authors correctly point out that the symptoms of toxicity correlate poorly with plasma concentration. However we suspect that there are differences from standard North American practice in this case report which warrant further discussion. Sedation for regional anaesthesia remains a topic of controversy in our subspecialty.[2,3] Use of agents in combination such as hydroxyzine and atropine and the intramuscular route of administration can lead to variable absorption and unpredictable effects that may mask the signs of early CNS toxicity.[4] Intravenous midazolam at a dose used in clinical practice of 0.03 mg/kg did not mask the early symptoms of CNS toxicity in healthy volunteers who underwent intravascular injection of up to 60 mg of ropivacaine in divided doses[5] and has the advantage of being anticonvulsant. Inappropriate sedation may also prevent the detection of intraneural injection of local anaesthetic with the consequentrisk of temporary or permanent nerve damage. When performing a parasthesia guided interscalene block, the endpoint relies on constant verbal patient-to-clinician feedback to distinguish distal parasthesia from painful dysasthesiae which may herald nerve injury. Standard practice in our institution is the use of a single short acting sedative agent titrated to effect in order to reduce the likelihood of masking the early signs of Central nervous system (CNS) toxicity and potential nerve injury. Finally the use of a two stage-brachial plexus block in this case is also curious in that surgical anaesthesia for open reduction and internal fixation of the right navicular bone could be obtained by axillary block alone rather than adding a second approach to the brachial plexus such as an interscalene block which may further increase the risk of systemic toxicity and nerve injury. References 1 Satsumae T, Tanaka M, Saito S, Inomata S. Convulsions after ropivacaine 300 mg for brachial plexus block. Br J Anaesth 2008; 101: 860- 862. 2 Bernards CM, Hadzic A, Suresh S, Neal JM. ASRA. Practice Advisory on Neurologic Complications in Regional Anesthesia and Pain Medicine. Reg Anesth Pain Med 2008; 33: 449-460. 3 Regional Anaesthesia for limb surgery a review of anaesthetists beliefs and practice. Feely NM, Popat MT, Rutter SV. Anaesthesia 2008; 63: 621-625. 4 Mulroy MF, Neal JM, Mackey DC, Harrington BE. 2-Chloroprocaine and bupivacaine are unreliable markers of intravascular injection in the pre- medicated patient. Reg Anesth Pain Med 1998; 23: 9-13. 5 McCartney CJ, Murphy DB, Chan VW. Intravenous ropivacaine bolus is a reliable marker of intravascular injection in premedicated healthy volunteers. Can J Anesth 2003; 50: 795-800. Conflict of Interest:None declared |
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James W. Heitz
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To the Editors: I read with keen interest the case report of Satsumae, et. al., of grand mal seizure occurring after combined brachial plexus and interscalene blocks with 300 mg of ropivacaine.(1) While I agree with their conclusion that a generous dose of local anesthetic in combination with the patient’s subclinical epilepsy may have both been contributory to the adverse outcome, I think this case report raises several issues worthy of clarification and expansion. Local anesthetic dosing ranges assume a standard 70 kg patient. Adherence to these ranges has contributed to the inadvertent overdosing of pediatric and petite adult patients. Dosing based upon patient weight is safer and therefore preferable. While the authors cite a study comparing brachial plexus blocks with ropivacaine 7.5 mg ml-1 300mg with bupivacaine 5 mg ml-1 200 mg as proof of safety for their dose of ropivacaine, this analysis misses several crucial details.(2) First, all the patients in the cited study had premedication with either diazepam 10 mg orally or midazolam 2 mg intravenously and the antiepileptic properties of these drugs are well- known. However, the patient in this case report was premedicated with hydroxyzine and atropine which would not have been protective against seizure. The case report patient may not have tolerated the same dose of local anesthetic as the study patients due to the difference in premedication. Secondly, there was a higher incidence of dizziness in the ropivacaine group of the cited study. Although the study authors did not believe this was attributable to local anesthetic effect, they could not disprove it. There was one seizure in the ropivacaine group, but none in the bupivacaine group. The study did not detect a difference in local anesthetic toxicity between the bupivacaine and ropivacaine groups, but was not sufficiently powered to detect it. Third, careful reading of this study reveals an average weight of 77 +/- 12 kg in the ropivacaine group, so these patients were substantially heavier than the 60 kg patient in the case report. Finally, it may not appropriate to extrapolate that a certain local anesthetic dose which is safe for brachial plexus blockade is also safe when a portion is used in an interscalene block, as seizure may be more likely with an interscalene block.(3) Besides the sources quoted in case report, there is also the manufacturer’s recommendation that a dose range of 75 to 300 mg of ropivacaine 7.5 mg ml-1 is appropriate for brachial plexus blockade.(4) There is no dispute as to whether ropivacaine 7.5 mg ml-1 in the dose of 300 mg is recommended for upper extremity blockade. However, for the 60 kg patient in this case report, this dose was 5 mg kg-1. While the total dose of local anesthetic may be within the range of published recommendations, it was apparently excessive on a weight basis for this smaller than average man. As the authors’ literature search revealed, seizure from peripheral nerve block with ropivacaine has been reported in doses of 5 – 8 mg kg-1. The website AnaesthesiaUK operated by the Royal College of Anaesthetists recommends no more than 4 mg/kg of ropivacaine.(5) It may be true that a lower seizure threshold reduces tolerance to local anesthetics. but a predisposition to seizures would not be necessary to explain this adverse event since a supratherapeutic of local anesthetic was administered. This case report serves as powerful reminder to always consider patient weight when determining an appropriate local anesthetic dose. Yours truly, James W. Heitz, MD Assistant Professor of Anesthesiology and Medicine, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania USA, james.heitz@jefferson.edu 1. Satsumae T, Tanaka M, Saito S, et al., Convulsions after ropivacaine 300 mg for brachial plexus block. Brit J Anaesth 2008;101(6):860-2. 2. Raeder JC, Drosdahl S, Klasstad O, et. al., Axillary brachial plexus block with ropivacaine 7.5 mg/ml. A comparative study with bupivacaine 5 mg/ml. Acta Anesthesiol Scand 19999;43:794-8. 3. Brown DL, Ransom DM, Hall JA, Leicht CH, Schroeder DR and Offord KP. Regional anesthesia and local anesthetic-induced systemic toxicity: seizure frequency and accompanying cardiovascular changes. Anesth. Analg. 1995 81: 321-8. 4. http://www.naropin-us.com/pdf/NaropinPI.PDF Accessed December 31, 2008. 5. http://www.frca.co.uk/article.aspx?articleid=100816 Accessed December 31, 2008 Conflict of Interest:None declared |
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Tsuyoshi Satsumae, Assistant Professor University of Tsukuba, Tsukuba City, Japan, Makoto Tanaka
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We thank Drs Rahim and Kayani for their correspondence, and strongly agree with the opinion that IntralipidR 20% should be reserved in case of local anaesthetic toxicities, in any location where local anaesthetics are administered. Although the exact mechanism of reversal of local anaesthetic toxicity is unclear, more than ten published case reports described successful resuscitation in patients suffered from local anaesthetics-related cardiac (1-3) and central nervous system (2) toxicity. Additionally, no complication due to intralipid was observed after acute, short-term administration in these reports. Thus, we agree with Dr Brull stating that it would seem imprudent to withhold administration of the intralipid in local anaesthetic toxicity while awaiting scientific proof.(4) MedialipidR 20%, which is different from IntralipidR in structure, was also useful; suggesting that the formulation of the intralipid may not matter.(3) Intralipid is appreciably safe, cheap and has long shelf life. We have already prepared “lipid rescue kits” (http://lipidrescue.org/) in our operating theatres in order to improve patients’ safety. Finally, intravascular injection is unlikely to have been a cause in our case because seizure occurred 10 min after the second ropivacaine injection and total ropivacaine concentration 2 min after the seizure onset was only 2.13 mg liter-1. If intravascular injection concerned, seizure might have occurred earlier and the serum ropivacaine concentration would have been higher immediately after injection. T.Satsumae M.Tanaka Tsukuba, Japan References: 1. Rosenblatt MA, Abel M, Fischer GW, Itzkovich CJ, Eisenkraft JB. Successful use of a 20% lipid emulsion to resuscitate a patient after a presumed bupivacaine-related cardiac arrest. Anesthesiology 2006; 105: 217 -8. 2. Litz RJ, Roessel T, Heller AR, Stehr SN. Reversal of central nervous system and cardiac toxicity after local anesthetic intoxication by lipid emulsion injection. Anesth Analg 2008; 106: 1575-7. 3. Ludot H, Tharin JY, Belouadah M, Mazoit JX, Malinovsky JM. Successful resuscitation after ropivacaine and lidocaine-induced ventricular arrhythmia following posterior lumbar plexus block in a child. Anesth Analg 2008; 106: 1572-4. 4. Brull SJ. Lipid emulsion for the treatment of local anesthetic toxicity: patient safety implications. Anesth Analg 2008; 106: 1337-9. Conflict of Interest:None declared |
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Tsuyoshi Satsumae, Assistant Professor University of Tsukuba, Tsukuba City, Japan, Makoto Tanaka
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We would like to thank Dr Marri for his interest and thoughtful comments on our case report.(1) He pointed out mainly two problems associated with our selection of regional anaesthetic technique and the dose of ropivacaine used. First, we performed combined axillary /interscalene brachial plexus block. We added interscalene brachial plexus block to completely anaesthetize the upper extremity, as axillary brachial plexus block alone might result in sparing of the radial region of the forearm. As a result, performing two regional blocks facilitated central nervous system toxicity related to ropivacaine overdose. Secondly, minimum effective dose of a local anaesthetic should be used in small increments with a heightened vigilance when performing regional blocks. Although a definite criterion does not exist, we agree with Chazalon and colleagues stating that it is reasonable to accept a maximum ropivacaine dose of 3 mg kg-1 for an upper limb block.(2) Although the dose of ropivacaine used in our case was within the manufacture’s recommended dose for brachial plexus block in the UK, US, Japan, and many other countries, the fact that our case resulted in an overdose indicates that the recommended dose should be reconsidered. Intravascular injection is unlikely to have been an etiology in our case because the seizure occurred 10 min after the second ropivacaine injection and total ropivacaine concentration 2 min after the seizure onset was only 2.13 mg liter-1. If intravascular injection concerned, seizure might have occurred earlier and the serum ropivacaine concentration would have been higher. As Dr Marri also correctly states, only axillary brachial plexus block using peripheral nerve stimulator and/or ultrasound guidance would have been appropriate for the choice of regional anaesthesia in our case, which would facilitate reduction in the local anaesthetic requirement. Alternatively, we should have switched to general anaesthesia if axillary brachial plexus block didn’t achieve satisfactory analgesia. T. Satsumae M. Tanaka Tsukuba, Japan References: 1. Satsumae T, Tanaka M, Saito S, Inomata S. Convulsions after ropivacaine 300 mg for brachial plexus block. Br J Anaesth 2008; 101: 860- 2. 2. Chazalon P, Tourtier JP, Villevielle T, et al. Ropivacaine-induced cardiac arrest after peripheral nerve block: successful resuscitation. Anesthesiology 2003; 99: 1449-51. Conflict of Interest:None declared |
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Sudhakar Marri Ninewells Hospital & Medical school, Dundee, David Coventry
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Sir, We read with interest the case report by Satsumae and colleagues, describing convulsions associated with ropivacaine 300 mg for brachial plexus block. The article raises several questions about the authors’ selection of regional anaesthetic technique and the dose of local anaesthetic used. First, regarding the choice of regional anaesthetic technique for navicular (scaphoid) surgery; adequate intraoperative anaesthesia should be provided by axillary brachial plexus block alone. A blind technique without a peripheral nerve stimulator or ultrasound will inevitably result in a higher incidence of musculocutaneous and radial nerve failure but this is hardly an indication for additional interscalene blockade. Occasionally, additional interscalaene brachial plexus block or a specific low-volume block of C5/6 with ultrasound or peripheral nerve stimulator can be useful to provide analgesia of the shoulder when arm positioning is problematic, but this approach seems excessive if used for supplementation or tourniquet analgesia alone. Using a peripheral nerve stimulator or ultrasound will improve the success rate(1) and safety profile of the axillary technique by allowing accurate injection of local anaesthetic and more importantly facilitate reduction in the dose of local anaesthetic administered. Second, regarding the dose of local anaesthetic used, although the authors acknowledge that the dose of local anaesthetic used was excessive, we wish to highlight that the use of a “safer agent” should not be an excuse to use larger doses of local anaesthetic but to improve the margin of safety for a ‘conventional’ dose. In our practice, the majority of brachial plexus blocks can be performed with less than 170 mg of ropivacaine, despite the maximum dose limit of 250-300mg recommended by the manufacturer and the BNF. This should however take into account patient weight, co- morbidity and site of injection. For a single-shot brachial plexus block, ropivacaine has been shown to be equipotent to bupivacaine and has a similar pharmacokinetic profile. It is effective at a concentration of 5mg/ml, and there seems little benefit in increasing its concentration to 7.5 or 10mg/ml (2,3), although lack of a 5mg/ml ampoule is unhelpful in achieving this. In our practice we use a 30 ml mixture of 7.5 mg/ml and 2 mg/ml at 2:1 or 1:1 ratio to achieve concentrations of 5.6 mg/ml or 4.7mg/ml respectively. Finally, partial intravenous injection can acutely increase plasma concentration of local anaesthetic and therefore decrease the overall toxic dose necessary to provoke significant side effects following further systemic absorption. This may have been a contributing cause in this case. In conclusion, we wish to highlight the importance of choosing the most appropriate regional anaesthetic approach for a given procedure and use of the ultrasound guided techniques to minimise complications and reduce the total dose of local anaesthetic administered. References 1.Ultrasound guidance improves success rate of axillary brachial plexus block. Chan VW, Perlas A, McCartney CJ, Brull R, Xu D, Abbas S. Can J Anaesth. 2007 Mar;54(3):176-82. Erratum in: Can J Anaesth. 2007 Jul;54(7):594 2.Clinical application of ropivacaine for the upper extremity. Singelyn FJ. Curr Top Med Chem. 2001 Aug;1(3):219-25. Review. 3. Ropivacaine: an update of its use in regional anaesthesia. McClellan KJ, Faulds D. Drugs. 2000 Nov;60(5):1065-93. Review Conflict of Interest:None declared |
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Muhammad Rahim Mansha Kayani
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Editor- I have read with interest the case report on convulsions after ropivacane 300mg for brachial plexus block. In this case patient had both axillary and interscalene blocks.Though you have excluded the posibilty of intavascular injection. As axillary block has very high chances of intavascular injections it is very difficult to rule out just on the basis of time of onset of convulsions. Also I would like to know whether you have itralipid 20% in your theatres which is recommended by The Association of Anaesthetists of Great Britain & Ireland in the guidelines of severe Local Anaesthetic Toxicity. Conflict of Interest:None declared |
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Yasir Al-Tamimi, Consultant Anaesthetist Joondalup Hospital, Perth WA
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Dear sir I read with extreme interest the case report submitted by Satsumae et al. I would like to rasie the following issues: 1- The case highlights neurotoxicity caused by twice the normal dose of ropivacaine in a 60 kg, health young man. 2- I believe that the authors should have stated clearly the reason for putting another 150 mg of ropivacaine at the interscalene level of the brachial plexus. The second dose is an obvious overdose and I don't agree that it should've been given at all. I suggest that if the "axillary approach" didn't confer the right anaesthesia the authors should've moved to non-regional anaesthesia and save the patient a toxic dose. Although the blood levels done didn't reflect a significant toxic level of ropivacaine I would still call this an overdose of ropivacaine. 3- I am quiet puzzeled by the authors description in the last paragraph of their report that"No definite reason was identified...etc". I don't agree that this patient was oversensitive but he was rather fortunate that no cardivascular complications occurred and he survived an obvious overdose. 4- I believe the reader deserves an explanation for the 2nd dose of ropivacaine, was it a dose miscalculation or a normal practice ? . Many thanks, Yasir Al-Tamimi Joondalup Hospital Perth WA Australia altamimiy@ramsayhealth.com.au Conflict of Interest:None declared |
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