Advances in Pharmacology
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1 Advances in Pharmacology Antidotes in anaesthesia Meyer-Overton revisited Hugh C. Hemmings Jr, MD, PhD, FRCA Joseph F Artusio Jr Chair and Professor of Anesthesiology Senior Associate Dean for Research Professor of Pharmacology Weill Cornell Medicine Anesthesiologist-in-Chief NewYork Presbyterian-Weill Cornell Medical Center 17 May 2018 hchemmi@med.cornell.edu
2 Declaration of interests Research funding from the National Institutes of Health Editor-in-Chief of the British Journal of Anaesthesia
3 Definition antidote: an agent that counteracts a poison Are anaesthetics poisons? Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition by Saunders, an imprint of Elsevier, Inc. All rights reserved.
4 The father of toxiciology Paracelsus (born Phillippus Aureolus Theophrastus Bombastus von Hohenheim, 11 November or 17 December 1493 in Einsiedeln, Switzerland 24 September 1541 in Salzburg, Austria) Renaissance physician, botanist, alchemist, astrologer, and occultist All things are poison and nothing is without poison, only the dose permits something not to be poisonous First to recognize the analgesic effect of ether and advocate the use of chemicals in medicine Never went anywhere without his sword, prodigious drinker, died in a tavern brawl in Salzburg at age 48
5 Types of antidotes chemical antidote interacts with a poison and changes its chemical nature to form a harmless substance (pralidoxime-organophosphate) physiological antidote counteracts the effects of the poison by producing opposing effects (neostigmineglycopyrrolate) complex formation leading to sequestration (NMBsugammadex) mechanical antidote prevents absorption of the poison (activated charcoal, ipecac)
6 Classical anaesthesia antidotes Drug/poison Acetaminophen/paracetamol Anticholinergic Anticholinesterase Benzodiazepine Ca 2+ channel blocker Digoxin Heparin Malignant hyperthermia Neuromuscular blocker Opioids Warfarin Antidote Acetylcysteine Physostigmine Atropine/Pralidoxime Flumazenil Calcium chloride Anti-digoxin Fab Protamine sulfate Dantrolene Anticholinesterase Naloxone Vitamin K
7 Novel anaesthesia antidotes Drug/poison Local anaesthetics Neuromuscular blockers Neuromuscular blockers DOAC (dabigatran; DTI) DOACs (FXa inhibitors) General anaesthesia Antidote Lipid emulsion Encapsulation: sugammadex, calabadion Degradation: cysteine Idarucizumab Adexanet alpha Methylphenidate/ketamine
8 Local anaesthetic toxicity Local anaesthetics act by blocking voltage-gated Na + channels essential for neuronal function Multiple off-target effects as well Selectivity based on precise delivery Relatively common spectrum of dose-related side effects due to systemic absorption
9 Diagnosis of local anaesthetic toxicity Central nervous system signs (~50%; may be subtle or absent) Excitation (agitation, confusion, muscle twitching, seizure) Depression (drowsiness, obtundation, coma or apnea) Sensory (metallic taste, circumoral numbness, diplopia, tinnitus, dizziness, hallucination) Cardiovascular signs (often the only manifestation of severe toxicity) Can appear late (>15 min after injection) Initially may be hyperdynamic (hypertension, tachycardia, ventricular arrhythmias), then Progressive hypotension Conduction block, bradycardia or asystole Ventricular arrhythmia (ventricular tachycardia, Torsades de Pointes, ventricular fibrillation)
10 Immediate treatment Stop injecting/call for help ABC: intubate, 100% O 2, IV access Control seizures: benzodiazepines, not propofol CPR/alert cardiopulmonary bypass team Avoid vasopressin, calcium channel blockers, beta blockers, lidocaine Epinephrine <1 mcg/kg doses Consider lipid emulsion rescue therapy 1.5 ml/kg bolus of 20% Intralipid over 1 min with infusion of ml/kg/min
11 Evidence to support intravenous lipid rescue therapy Low quality evidence: anecdotal case reports and laboratory studies only Side effects: rarely pancreatitis, ARDS, fat complex overload syndrome Unclear mechanism of action Sequestration of hydrophobic lipophilic local anaesthetic molecules questionable pharmacokinetic effect to accelerate redistribution from brain and heart Other mechanisms: inotropic effect by activation of VGCC relief of fatty acid inhibition of VGSC adrenergic receptor activation activation of fatty acid receptor GPCR40
12 Evidence for intravenous lipid rescue therapy Published on-line this month in Anesthesiology
13 New approaches to reversing neuromuscular blockade: encapsulation Acetylcholinesterase inhibitors reverse only shallow levels of block (To4R>0.4) Nonselective: indirectly increases ACh at all cholinergic synapses Requires a third drug to prevent undesired antimuscarinic effects Ceiling effect, slow (at least 10 min) Encapsulating agent sugammadex reverses even deep levels of block Bind free extracellular drug to reduce effect-site concentration (NMJ) Side effects due to nonspecific binding of other molecules or anaphylaxis Sugammadex: steroidal hormone (oral contraceptives)
14 Sugammadex A gamma-cyclodextrin that binds and sequesters steroidal NMBs Cyclic oligosaccharide with hydrophobic interior Unique mechanism that does not involve cholinergic system; but profound bradycardia can still occur Reduced residual muscular weakness compared to neostigmine Availability and cost are still concerns Pinterest.com
15 Sugammadex More rapid and effective in deep block with fewer side effects Jones et al., Anesthesiology 2008;109:
16 Calabadion Acyclic flexible oligomer that can accommodate larger molecules Reverses both steroidal and benzylisoquinolinium NMBs In preclinical development Grosse-Sundrup et al., 2012
17 New approaches to reversing neuromuscular blockade: cysteine Benzylisoquinolinums react with thiols and are reversible by cysteine through an intermolecular reaction React with endogenous Cys Accelerated by exogenous Cys N-acetylcysteine is FDA approved In preclinical development Heerdt et al., 2015
18 Specific antidotes against direct oral anticoagulants Direct oral anticoagulants: small molecule inhibitors of thrombin (DTI) or FXa Tummala et al., 2016 Nonspecific agents include activated charcoal, haemodialysis, prothrombin complex concentrate (PCC) Approved without an antidote
19 Idarucizumab Humanized monoclonal antibody Fab domain Specific high affinity for the DTI dabigatran Renal excretion; short half life, given by infusion Immediate, complete sustained reversal of dabigatran
20 Andexanet alpha Mutated FXa fragment lacking protease (procoagulant) activity Reverses rivaroxaban, apixaban, edoxaban, fondaparinux Binds FXa inhibitors with higher affinity acting as a decoy protein and drug sink Short half life; requires infusion Positive interim results In clinical development; not yet approved
21 In the pipeline Aripazine: synthetic small molecule that reverses FXa inhibitors Anivamersen/ pegnivacogin: an RNA aptamer pair (known as REG-1) including (anivamersen) developed to reverse the FIXa inhibitor pegnivacogin an alternative to heparin:protamine
22 Active emergence from general anaesthesia Pharmacological approaches reverse/accelerate emergence from general anaesthesia Methylphenidate accelerates emergence from isoflurane anaesthesia and induces return of righting reflex (Solt et al., 2011) Reduced time to emergence by 68% Mediated by D1 receptor activation (Taylor et al., 2013) Also effective for propofol and sevoflurane anaesthesia Subanaesthetic dose of ketamine accelerates emergence from isoflurane anaesthesia in rats (Hambrecht-Wiedbusch et al., 2017 Increased burst suppression ratio by 125% Reduced emergence time by 44% Paradoxical emergence
23 Thank you! Questions?
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