Local anesthetic system toxicity following brachial plexus anesthesia is severe complication of regional block. We reported a case of central nervous system toxicity following brachial plexus anesthesia, who was rescued successfully with intravenous lipid emulsion.
JOURNAL OF MILITARY PHARMACO-MEDICINE N07-2016 CASE REPORT: INTRAVENOUS LIPID EMULSION FOR TREATMENT OF LOCAL ANESTHETIC TOXICITY FOLLOWING BRACHIAL PLEXUS ANESTHESIA Vo Van Hien*; Nguyen Trung Kien* SUMMARY Local anesthetic system toxicity following brachial plexus anesthesia is severe complication of regional block We reported a case of central nervous system toxicity following brachial plexus anesthesia, who was rescued successfully with intravenous lipid emulsion * Key words: Local anesthetic system toxicity; Lipid emulsion INTRODUCTION Local anesthetic system toxicity (LAST) is a recognized complication of major conduction anesthesia The estimate of clinically important local anesthetic toxicity is from 7.5 to 20 occurrences per 10,000 peripheral nerve blocks [6] The incidence of toxicity is greater with brachial plexus techniques than most others, because larger than usual doses of local anesthetics are used and the injections are made in and around large vascular channels in the head, neck and axillary regions LAST includes two major types: central nervous system toxicity and cardiovascular system toxicity that can be treated with lipid emulsion [1] CASE REPORT A 73 years old man, 164 cm tall, 50 kg of weight, was admitted with right hand injury due to labour accident which required an emergency for wound resection and reformed index and middle finger amputation under supraclavicular approach anesthesia on Monday 27 of June, 2016 - Biochemical test: glucose 7.5 mmol/L, ure 7.1 mmol/L, creatinine 76 µmol/L, GOT 122 U/L, GPT 117 U/L, K+ 3.8 mmol/L, Na+ 136 mmol/L; ECG was normal at rate of 67/min, sinus rythm - Blood test: red blood cell 3.48 Tera/L, hemoglobin 101 g/L, hematocrit 0.32 l/L, platelet 100 G/L - Continuously monitored of ECG, heart rate, oxygen saturation (SpO2) Blood pressure was monitored in 2.5 mins interval; oxygen was given via facemask at a rate of L/min Blood pressure was 132/73 mmHg; respiratory rate 18 per minute - In the operating room: an IV 18G was placed After given IV 100 µg of fentanyl and 20 mg of propofol, ultrasound guided supraclavicular approach anesthetizes was done with 300 mg of lidocaine in 25 mL (6 mg/kg) and 50 mg of ropivacaine (1 mg/kg) The patient was awake during the block No blood or paresthesias was seen during procedure The patient felt numbness in his arm minutes after brachial block, motor block was assessed by Bromage score at level * 103 Hospital Corresponding author: Nguyen Trung Kien (drkien103@gmail.com) 77 JOURNAL OF MILITARY PHARMACO-MEDICINE N07-2016 - Approximately 10 minutes after the needle removement, patient became confused and unconscious, stopped breathing, SpO2 decreased from 100% to 50% - Supported ventilation through facemask with 100% oxygen for minutes and SpO2 recovered in normal range 98 - 100%, hemodynamic was stable pattern during that time Spontaneous respiratory rate recovered at rate of 18 per minute but consciousness was still not recovered and the patient did not response to verbal commands as well as deep pain stimulation any more Pupils were in normal size and responded well with light - Monitoring closely and surgeons started procedure - 20 minutes after becoming unconciousness, lipid emulsion (10%) therapy was started with bolus dose of mL/kg (150 mL) intravenously over minute - The patient opened his eyes and responded well to verbal commands and got full recovery immediately from finishing bolus dose - We did not use continuous infusion and operation finished at 64 minutes after brachial plexus anesthesia The patient was transfered to postoperative care unit with normal parameter of hemodynamic and respiratory He was discharged after days of treatments DISCUSSION Some reasons of unconsciousness and stopped breathing in this patient might be caused by injecting 100 µg of fentanyl and 20 mg of propofol before brachial plexus anesthesia However, stopped 78 breathing and unconsciousness due to fentanyl and propofol effects could be excluded because the patient was still awake during and after taking ultrasound guided supraclavicular approach block Small dose of propofol just brought a sedation meaning and could not bring general anesthesia effect in this situation He also felt numbness in his arm minutes and motor block at level according to Bromage score after brachial plexus block Thus, unconsciousness and stopped breathing could not have been blaimed for fentanyl or propofol effects Local anesthetic toxicity happened in this patient may be due to high dose of lidocaine (6 mg/kg) combined with ropivacaine (1 mg/kg) without combination with epinephrine Some authors indicated that toxicity occured most frequently following accidental intravascular injections and rarely following absorption of injected solutions from peripheral sites [2, 3] However, absorption was thought as a crucial reason in this patient because ultrasound guided for brachial block with inplane technique was performed Thus, doctor could see the needle as well as the tip of the needle clearly before injecting local anesthetics Further more, negative aspiration test was confirmed before injection local anesthetics Local anesthetics are widely and commonly used for regional anesthesia Although it is rare for patients to manifest serious adverse effects or experience complications secondary to local anesthetic administration, adverse events can occur, even it is taken under ultrasound guided, let alone take blind techniques These range from the mild symptoms that may JOURNAL OF MILITARY PHARMACO-MEDICINE N07-2016 follow systemic absorption of local anesthetics from a correctly sited and appropriately dosed regional anesthetic procedure to major central nervous system (CNS) and/or cardiac toxicity (most often from unintentional intravascular injection) that can result in disability or death [2] A variety of factors influence the likelihood and severity of local anesthetic systemic toxicity (LAST), including individual patient risk factors, concurrent medications, location and technique of block, specific local anesthetic compound, total local anesthetic dose (concentration, volume), timeliness of detection, and adequacy of treatment Although the patient had a higher GOT and GPT than normal level, that was not reason for this complication Slight anemia may have been a contributive factor for making higher free level concentration of local anesthetics in plasma That is the reason this patient was diagnosed central nervous system toxicity in a typical type and lipid emulsion was transfused after that Local anesthetic dose is very important factor to evoke the LAST According to Felice [5], maximal dose of lidocaine is - mg/kg But, in this patient, brachial plexus block was done with medium dose (6 mg/kg of lidocaine and mg/kg ropivacaine) without combination with epinephrine Moreover, elderly patient with low level of protein (55 g/L) could make a higher free concentration of local anesthetics (LA) in plasma In fact that one confounder in the interpretation of serum concentrations of LA is protein binding, which generally decreases with increasing drug concentrations In the clinical setting of probable LA toxicity, an elevated total drug concentration may be reflective of a high free drug concentration It is noted that, the serum concentration of LA may correlate with clinical signs and symptoms of toxicity Lidocaine administration in regional blocks usually results in a serum concentration of - µg/mL and therapeutic plasma concentrations of lidocaine are to µg/mL when used for ventricular arrhythmias Symptoms of toxicity may occur at concentrations µg/mL, convulsions may occur at concentrations 10 µg/mL, and cardiovascular collapse with levels 30 µg/mL [7] Our patient did not have symptoms of cardiac toxicity The commercial products of intravenous lipid emulsion (IVLE) are available in various concentrations The 20% formulation of IVLE contains 20% soybean oil, 1.2% egg yolk phospholipids, 2.25% glycerin, and the remainder is water The osmolality of IVLE is approximately 350 mOsm/kg water and 260 mOsm/kg lipid emulsion In this case, it was not available of IVLE 20% and IVLE 10% was injected with double volume in compare with guidline [7] There are multiple theories about the mechanism of action of IVLE in LA toxicity One theory is that IVLE serves as a “lipid sink,” providing a large lipid phase in the serum that is able to extract LAs from the plasma This may be true at the tissue level, as well Another theory is that IVLE has metabolic effects by inhibiting mitochondrial metabolism of lipids, reducing tissue acidosis and decreasing carbon dioxide production during times of myocardial 79 JOURNAL OF MILITARY PHARMACO-MEDICINE N07-2016 ischemia Also, as LAs may impair fatty acid delivery to the mitochondria, IVLE may work to saturate this impaired fatty acid delivery to enable further energy production Additionally, fatty acids, as found in IVLE, have been shown to activate calcium and potassium channels, which have been associated with LA-induced cardiotoxicity [4] Treatment of central nervous system (CNS) complications and toxicity remains controversial Seizures have been treated successfully with benzodiazepines or barbiturates (eg, phenobarbital) However, Weinberg [7] recommended that lipid infusion should be considered early, and the treating physician should be familiar with this method He also recommends avoiding vasopressin and using epinephrine only in small dose Obviously, vigilance, preparedness, and quick action will improve outcomes of this dreaded complication In this case, we used lipid emulsion (10%) therapy and the bolus dose was started with of mL/kg (150 mL) intravenously and obtained good outcomes According to Weinberg [7], if LAST happended, we should use intralipid emulsion and follow protocol for recovering includes: bolus 1.5 mL/kg (lean body mass) intravenously over minute (~100 mL) Then, continuous infusion 0.25 mL/kg/min (~18 mL/min; adjust by roller clamp); repeat bolus once or twice for persistent cardiovascular collapse Double the infusion rate to 0.5 mL/kg/min if blood pressure remains low; continue infusion for at least 10 minutes after attaining circulatory stability and recommended upper limit: 80 approximately 10 mL/kg lipid emulsion over the first 30 minutes Thus, plan for management of this complication should be established, and a Local Anesthetic Toxicity Kit and posting instructions should be ready to use CONCLUSIONS Intravenous lipid emulsion infusion provided a good effective treatment for central nervous system toxicity due to complication of regional anesthesia REFERENCES Aya AG, Ripart J, Sebbane MA, de La Coussaye JE Lipid emulsions for the treatment of systemic local anesthetic toxicity: Efficacy and limits Ann Fr Anesth Reanim 2010, 29 (6), pp.464-469 Di Gregorio G, Neal JM, Rosenquist RW, Weinberg GL Clinical presentation of local anesthetic systemic toxicity: a review of published cases, 1979 to 2009 Reg Anesth Pain Med 2010, 35 (2), pp.181-187 Dillane D, Finucane BT Local anesthetic systemic toxicity Can J Anaesth 2010, 57 (4), pp.368-380 Faccenda KA, Finucane BT Complications of regional anaesthesia Incidence and prevention Drug Saf 2002, 24 (6), pp.413-442 Felice K, Schumann H Intravenous lipid emulsion for local anesthetic toxicity: a review of the literature J Med Toxicol 2008, (3), pp.184-191 Finucane Brendan T Complications of brachial plexus anesthesia, complications of regional anesthesia Springer Science + Business Media, LLC: USA 2007, pp.121-144 Weinberg GL Treatment of local anesthetic systemic toxicity (LAST) Reg Anesth Pain Med 2010, 35 (2), pp.188-193 ... Complications of brachial plexus anesthesia, complications of regional anesthesia Springer Science + Business Media, LLC: USA 2007, pp.121-144 Weinberg GL Treatment of local anesthetic systemic toxicity. .. Complications of regional anaesthesia Incidence and prevention Drug Saf 2002, 24 (6), pp.413-442 Felice K, Schumann H Intravenous lipid emulsion for local anesthetic toxicity: a review of the literature... presentation of local anesthetic systemic toxicity: a review of published cases, 1979 to 2009 Reg Anesth Pain Med 2010, 35 (2), pp.181-187 Dillane D, Finucane BT Local anesthetic systemic toxicity