Prevention and Treatment Patrick Levelle, MD
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1 Prevention and Treatment Patrick Levelle, MD
2 LOCAL ANESTHETIC TOXICITY 1. PERIPHERAL NERVE BLOCKS 2. ROLE OF THE PERIANESTHESIA RN 3. LOCAL ANESTHETIC TOXICITY Use of Lipid Emulsion
3 Regional and Peripheral Nerve Blocks: For surgical anesthesia and post-operative analgesia Better post-operative pain relief Faster emergence from GA Decreased use of narcotics Less risk of respiratory depression and PONV Can reduce length of stay, faster OP discharge Can decrease the cost of health care Improved patient satisfaction
4 For post-operative analgesia Injection of long acting local anesthetics or placement of indwelling catheter Common Sites: Brachial Plexus Femoral Nerve Sciatic Nerve
5 Primary risks include: Pain and discomfort at the site of injection Nerve injury Needle/Catheter Medications injected Vascular injury Local Anesthetic Systemic Toxicity-LAST
6 Pre-operative blocks: Created necessity for block nursing to ensure patient safety and comfort during and after placement of peripheral nerve blocks Some institutions have developed perioperative block nursing teams ARMC: Developed definition, policy and educational module for RN Assistant in peripheral nerve blocks
7 Post injection monitoring-treatment Peri-Anesthesia RN assists with: Patient positioning Patient monitoring Patient sedation and comfort Nerve identification Safe local anesthetic injection
8 Local Anesthetics Reversibly block conduction in nerve tissue Toxicity results from high (toxic) blood levels of local anesthetics
9 Toxicity from local anesthetic administration may occur with any: High volume block High concentration block Major nerve or plexus block Epidural block
10 LAST may occur from: Rapid intravascular absorption of LA Direct intravascular injection of LA Absorption of LA from depot site over time
11 Anytime high volume-high concentration local anesthetic administration occurs, THERE MUST BE A PLAN TO TREAT LAST!
12 POLICY
13 CME
14 ADEQUATE MONITORS
15 PLAN OF ACTION
16 RESUSCITATION EQUIPMENT & MEDS ON HAND
17 Use the least amount of LA required to achieve the desired block All patients should be monitored: EKG PULSE OXIMETRY NIBP VERBAL COMMUNICATION
18 Patients should be monitored after the block Onset usually occurs within first minute of injection Several cases reported a delay of onset of 5 minutes May be delayed as much as 30 minutes in high risk patients
19 LOW PLASMA PROTEINS Factors that increase risk of LAST ADVANCED AGE CHF ISCHEMIC HEART DISEASE CARDIAC CONDUCTION DISEASE LIVER/RENAL DISEASE
20 Risks-continued: METABOLIC/RESPIRATORY ACIDOSIS USE OF SODIUM CHANNEL BLOCKERS: CLASS I ANTIARRHYTHMICS: Procainamide Quinidine Disopyramide Mexiletine Flecainide PHENYTOIN CALCIUM
21 Aspirate before every injection, inject divided doses slowly Query the patient for symptoms of LAST Stop the injection if: Blood is present in the line Altered mental status Changes in neurological status CV instability develops Consider epinephrine marker in LA (5mcg/ml) with large volume injections or use as a test dose
22 Neurological symptoms may precede C/V symptoms CV symptoms may be the only manifestation of severe LAST studies indicate up to 40%
23 EXCITATORY Agitation Confusion Muscle Twitching Seizure DEPRESSIVE Drowsiness Obtundation Coma Apnea NON-SPECIFIC Metallic taste Circumoral numbness Diplopia Tinnitus Dizziness
24 CV symptoms can be HYPERDYNAMIC initially: Hypertension Tachycardia, ventricular arrhythmias V-tach / V-fib / Torsades If initially hyperdynamic, may progress to: Hypotension Conduction Block Bradycardia Asystole
25 Prompt recognition of LAST is key SEVERE TOXICITY SYMPTOMS: Sudden Mental Changes LOC Seizure Arrhythmias CV Instability
26 FOR SYMPTOMS OF SEVERE LAST: STOP the injection immediately CALL for help (CODE) MANAGE the airway-100% oxygen TREAT seizures promptly Benzodiazepines preferred Avoid Propofol with C/V instability
27 If no circulatory arrest: Use conventional resuscitation to treat hypotension, bradycardia & tachyarrhythmia's Manage arrhythmias with ACLS protocols, If circulatory arrest occurs: Start CPR ACLS Consider the use of cardiopulmonary bypass Arrhythmias may be refractory to treatment
28 LIPID EMULSION
29 20% LIPID EMULSION In use since 1962 for Parenteral Nutrition Weinberg-1998-Unexpected finding in study of Carnitine deficiency
30 Carnitine Required for fatty acid transport during metabolic energy production Deficiency produces inability to utilize certain fats for energy production Case Report Carnitine Deficiency-increased susceptibility to bupivacaine cardiotoxicity Hypothesis-Impaired FA oxidation led to increased LA cardiotoxicity Gave rats Lipid Emulsion prior to bupivacaine, expecting to see accelerated cardiotoxicity
31 Weinberg found the opposite: Lipid increased the lethal dose of bupivacaine by 50% Weinberg then demonstrated efficacy of lipids by rescuing dogs from bupivacaine cardiac arrest First successful use in clinical practice peer reviewed case reports by 2012 Guidelines for use in LAST ASRA-2010 Practice Advisory
32 METHOD OF ACTION NOT WELL DEFINED Studies support the formation of intravascular lipid sink Acts to absorb the circulating lipophilic local anesthetics reducing the amount of free toxin to bind to myocardial cells Bupivacaine concentration reduction 3X greater with lipids versus hemodilution alone
33 Initial IV bolus: 1.5ml/kg (lean body weight) Infusion: 0.25ml/kg/hour Continue infusion at least 10 minutes after achieving C/V stability May repeat bolus twice at 5 minute intervals May increase infusion to 0.5ml/kg/hour for refractory cases Maximum dose: 10ml/kg in first 10 minutes
34 Resuscitation may be prolonged-be prepared Consider CPB Avoid: Vasopressin Calcium channel blockers / Lidocaine for arrhythmia treatment Decrease doses of epinephrine to 0.5 mcg/kg. Evidence that higher doses of epinephrine may impede lipid resuscitation
35 If resuscitation is successful Monitor patient for at least 12 hours C/V depression can recur or persist Post LAST events at
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