Copyright 2019 Jason McLott All Rights Reserved Disclosure Statement I have no financial relationships with any commercial interest related to the content of this activity I will discuss the off label use of many medications ID: 908804
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Slide1
Opioid Free Anesthesia Techniques
Copyright 2019. Jason McLott. All Rights Reserved.
Slide2Disclosure StatementI have no financial relationships with any commercial interest related to the content of this activity
I will discuss the off label use of many medications
Slide3Learner OutcomesReview pain physiology.Review fundamentals of opioid free anesthesia.Understand how and when to use interfascial plane blocks.
Understand how to select the correct medications for an opioid free anesthetic.
Identify and formulate an opioid free anesthesia cocktail for infusion from multiple classes of medications.
Slide4Anatomy of Pain
Slide5What Is Pain?A stimulus that causes protective behaviors that promote healingAn alarm to signal the body of actual or potential tissue damageWell defined onset associated with tissue injury from surgery, trauma, or disease related injury from inflammation
Slide6Types of PainSomatic painWell-localized painDescribed as sharp, crushing, tearing painFollows a dermatomal patternVisceral painPoorly localizedDescribed as dull, cramping, or colicky painAssociated with peritoneal irritation, dilation of smooth muscle or a tubular passage
Slide7Anatomy Of Pain Afferent nociceptive fibersAδ fibersC fibers
Slide8Aδ FibersLightly myelinated and small diameter (2-5 μm)
Respond to mechanical and thermal stimuli
Transmit rapid, sharp pain
Allow localization of pain
Responsible for initial response to acute pain
Slide9C FibersUnmyelinated and smallest fiber (<2μm) Respond to chemical, mechanical, and thermal stimuli
Transmit slow, diffuse, dull pain
Slide10Substances Released By Nociceptive FibersAδ fibers release glutamate C fibers release both Substance P and glutamate
Slide11Substance P Key excitatory neuropeptide in the somatosensory systemReleased by C fibers primarilyActivate NK1 receptors in Lamina I and II
Slide12Glutamate Key excitatory neurotransmitter in the somatosensory systemActivates postsynaptic AMPA and NMDA receptors
Slide13NMDA And Mg2+NMDA receptors are inactive due to Mg2+ ion plugConstant depolarization and activation of NMDA receptor causes Mg2+ ion to releaseRelease of Mg2+ ion allows influx of Ca
2+
Ca
2+
increases NO production causing increased release of glutamate
Slide14Phases of Pain
Slide15TransductionNociceptorsFree nerve endings of Aδ and C fibersLocated in the skin, viscera, muscles, joints, and meninges.Stimulated by mechanical, thermal, or chemical stimuli.Transform stimuli to electrical signals that are sent to the central nervous system (CNS).
Slide16Peripheral SensitizationTissue injury causes release of numerous chemicals (i.e. bradykinin, prostaglandins, serotonin, cytokines, and hydrogen ions)These chemicals may:Directly induce pain transmissionIncrease excitability of nociceptors and decrease pain threshold
Slide17TransmissionImpulse previously translated into electrical signal is sent through afferent nerve fibers to the dorsal horn of the spinal cord, and then along the sensory tracts to the brain through 2nd and 3rd order neurons
Slide18ModulationDampening or amplifying of pain signalDampening of pain signal by descending inhibitory pathwayPeriaqueductal Gray (PAG)Rostral Ventromedial MedullaOpioid receptors on presynaptic afferent nerve and postsynaptic 2nd order interneurons are responsible for dampening effect
Slide19Descending Inhibitory PathwayMidbrain periaqueductal gray (PAG)primary control center for descending inhibitory pathwayStimulated by ascending pathway or endorphins (endogenous and exogenous)PAG stimulation activates neurons in the rostral ventromedial medulla, causing release of serotonin in dorsal hornSerotonin released in dorsal horn activates interneurons in Lamina II (aka substantia gelatinosa)
These interneurons release endogenous opioid neurotransmitters
Slide20Endogenous Opioid NeurotransmittersEndorphins activate mu opioid receptorsDynorphins activate kappa opioid receptors Enkephalins activate mu and delta opioid receptors Activation of opioid receptor inhibits the release of substance P and glutamate from afferent fibers, decreasing transmission of pain to brain for perception
Slide21PerceptionConscious awareness of painEnd result of transduction, transmission, modulation, and psychological aspects
Slide22Opioid Induced Hyperalgesia
Slide23MOA Of OpioidsActivate intracellular G-proteinsHyperpolarization of afferent neuronInhibition of excitatory neurotransmitter release (Glutamate and Substance P)Stimulate postsynaptic opioid receptorsAntagonize the depolarizing effects of Substance P and glutamate
Slide24Opioid Induced Hyperalgesia (OIH)State of nociceptive sensitization caused by exposure to opioidsPatient becomes more sensitive to certain painful stimuliPatients have a prolonged period of hypersensitivity to painMay occur after single dose of an opioidRemifentanil>Fentanyl>Morphine
Slide25Causes Of OIHAlteration of glutamate activitySpinal dynorphinsDescending inhibitory pathwaysGenetic influences
Slide26Glutamate Role In OIHGlutamate plays a central role in development of OIHOpioids activate Gs protein which increases the amount of glutamate released Activation of NMDA receptors increases NO production and decreases postsynaptic μ-opioid receptors’ functionInhibition of NMDA receptor prevents tolerance and OIH
Slide27Spinal DynorphinsDynorphin levels increase with prolonged mu-receptor agonist administrationIncreased dynorphin levels cause release of excitatory neuropeptides such as calcitonin gene related peptide, which increases pain transmissionStudies show that reversal of dynorphin can restore analgesic effects of morphine
Slide28Descending Inhibitory Pathway OIHOpioid modulation of pain at the supraspinal level has a unique action on a subset of neurons in the RVMThere is an actual increase in spinal nociceptive processing when they are activated by opioidsLesioning of the dorsolateral funiculus prevents the release of excitatory neuropeptidesInjection of local anesthetics into the RVM prevented or reversed OIH and tolerance to opioids
Slide29Genetic Influences On OIHThe primary genetic influence is the activity of Catechol-O-methyltransferase (COMT)The substitution of the amino acid valine for methionine decreases the breakdown of dopamine and noradrenaline by up to 400%Increased dopamine/noradrenaline levels increase pain sensitivity
Slide30Opioid Free Anesthesia
Slide31What Is Opioid Free Anesthesia (OFA)The absence of using mu-receptor agonist opioids intraoperativelyIt is not the total absence of opioids in the entire perioperative period, but use of opioids as the last line of treatment instead of the first in the postoperative periodIt is a scientifically-based, systematic treatment of the surgical patient
Slide32Why Use Opioids?Opioids were primarily used initially because of their safe intraoperative profileMinimal cardiac depressionBlunting of pain transmissionProvide the basis of postoperative pain control
Slide33Why To Avoid OpioidsNegative side effect profileRespiratory depression, N/V, pruritus, urinary retentionOpioids suppress the immune responseSuppression of Natural Killer cellsCause cognitive/sleep dysfunctionIncreased risk for addiction postoperativelyIncreased risk of chronic pain with opioid administration
Slide34Benefits Of OFAStable hemodynamics intraoperativelyDecreased risk of respiratory depressionPrevention of chronic painIncreased effectiveness of opioids administered postoperativelyDecreased incidence of N/V, pruritus, constipation, urinary retention, immune suppression, and cognitive/sleep dysfunction
Slide35Methods Of OFAManagement of peripheral sensitizationManagement of central sensitizationPrevention of OIHWeight based dosing on drugsIBW Adjusted body weight for patients whose actual body weight is 30% greater than IBW
Slide36Management Of Peripheral SensitizationLocal AnestheticsPeripheral nerve blocksLidocaine infusionSteroidsDecadronNSAIDSToradolCelebrexCannabinoids
Slide37Regional AnesthesiaIf It Can Be Blocked, Block It!Upper extremity surgeriesBrachial plexus blocksAxillary blockTerminal nerve blocksLower extremity surgeriesFascia
iliaca
block, PENG
FNB or ACB
Popliteal Sciatic Block
Genicular
nerve block
IPACK block (posterior)
Lateral
Anterior
Interfascial
Plane BlocksTAP blockMidaxillary vs SubcostalIL/IH blockRectus sheath blocksQuadratus Lumborum blockErector Spinae blockPECS 1& 2 Blocks
Slide38Interfascial Plane Blocks
Slide39Midaxillary TAP Blocks
Somatic analgesia for dermatomes T10-L1
Adequate postop analgesia for
surgeries
with incision at or below umbilicus
Appendectomy
Umbilical hernia repair
Inguinal hernia repair
Colectomy
C-section
Slide40Midaxillary TAP Block
Slide41Subcostal TAP Block
Somatic pain coverage of T7 to T10 dermatomes
Adequate post op analgesia for surgeries with incision above the umbilicus
Cholecystectomy
Colectomy
Upper ventral hernia repair
Slide42Subcostal TAP Block
Slide43Quadratus Lumborum Block
Provides somatic and visceral coverage of T7 to L3 dermatomes
Provides analgesia for abdominal surgeries, hip surgeries, and lumbar back surgeries
Typical duration up to 48 hours
Slide44Quadratus Lumborum Block Type 2
Slide45Quadratus Lumborum Block Type 3
Slide46Erector Spinae Plane Block
Provides somatic and visceral coverage
Erector Spinae block is done at either T5 or T8 transverse process
T5 adequate for thoracic surgeries/rib fractures, thoracic spine surgery
T8 adequate for abdominal surgeries
Can be done on an anticoagulated patient
Slide47Erector Spinae at T5
Slide48PECS 1 Block
Injection of local anesthetic between pectoralis major and pectoralis minor at level of 3
rd
rib
Blocks the lateral and medial pectoral nerves
Provides pec major muscle relaxation, appropriate for
portacath
insertion, pacemaker insertion, and breast expanders
Slide49PECS 2 Block
Injection of local anesthetic between pectoralis minor and serratus anterior muscles at level of 4
th
rib
Adequate for tumor resections, mastectomies, sentinel node biopsies, and axillary incisions
Slide50PECS Blocks
Slide51Lidocaine InfusionAnti-inflammatory effect by prostaglandin inhibitionUseful in abdominal and urological proceduresDosage Initial bolus: 1.5mg/kgMaintenance: 2mg/kg/hrPostoperative: 1.33mg/kg/hr
Slide52DecadronGlucocorticoid steroidInhibits the production of prostaglandins, bradykinin, histamine and leukotrienesCaution in diabetic patientsAdvise that insulin requirement may be increased for next 24 hoursLiterature disputes any wound healing effectsDosage
0.2mg/kg
(10-20mg on average)
Slide53ToradolInhibits production of prostaglandins, bradykinin, and histamineStrong analgesic effectEquipotent to morpine 10mg Caution in elderly, renal failure, or platelet dysfunctionDosage15mg at induction, 15mg at endHalf dosages for elderly
Some studies say 15mg is as effective as 30mg dose
Slide54CelebrexCOX-2 inhibitorInhibits prostaglandin synthesisDecreased risk of bleeding, GI side effects, and AKIUsage postoperatively decreases narcotic use and durationDosage:Preoperatively 400mg POPostoperativeley 200mg PO BID for 7 days
Slide55CannabinoidsEndocannabinoid system is a major endogenous pain control systemAnti-inflammatory and analgesic propertiesPromising studies involve inhibiting the enzymes that are released during stress that inhibit the endocannabinoid system from functioningLigands that activate CB1 receptors are promising for nociceptive alterationLigands that activate CB2 receptors are promising for anti-inflammatory properties
Slide56Management Of Central SensitizationSubstance P inhibitionClonidineDexmedetomidineGlutamate antagonistKetamineN2OMagnesiumGabapentinoids
Slide57Substance P Inhibitors
Slide58Clonidinea2-adrenoreceptor agonistDecreases sympathetic outflow from lower brainstem regionDecreases release of NE at both peripheral and central terminalsAnalgesic properties are due to both peripheral and central a2-adrenoreceptor agonism
Slide59ClonidinePeripheral analgesiaBlocking of pain transmission conducted through C fibersResult of interaction with inhibitory G coupled proteinsCNS analgesiaActivation of a2-adrenoreceptors in the dorsal hornDecreased release of Substance P and NEActivation of a2-adrenoreceptors in locus coeruleus responsible for supraspinal analgesia and sedation
Slide60ClonidineAvoid in patients with:BradyarrthymiasPatients who are afterload dependentIe severe ASCoronary artery disease due to possible HOTNStrong considerationsRenal patients require less doseLow starting BP
Slide61ClonidinePO dose: 3-5mcg/kg (IBW) given 1-2 hours preopBioavailbility is 75-95%IV dose: Give 1.5mcg/kg (IBW) on induction, following incision if a sympathetic response is detected give additional 1.5mcg/kgTotal dose 3mcg/kg, may give up to 5mcg/kg (increased SE and sedation)Dose may be given over 30 minutes in
preop
Long half life up to 18 hours with both PO and IV dose
Slide62DexmedetomidineStrong a2-adrenoreceptor agonist (1600:1)Same MOA as clonidineLess SE profile than clonidineStronger analgesic effect than clonidine
Slide63DexmedetomidineUse with caution in patients with:Heart blockSevere ventricular dysfunctionHypovolemic patientsUncontrolled hypertension
Slide64DexmedetomidineDosage:Initial bolus: 0.3-1mcg/kg over 10 minutes in preopMaintenance: 0.3-0.5mcg/kg/hrPostoperative infusion: 0.2-0.5mcg/kg/hrIntrathecal 5-10mcgEpidural 0.5mcg/mLShort half-life of 2-2.6
hrs
Slide65Glutamate Antagonists
Slide66KetamineNMDA antagonistPrevents glutamate from activating NMDA receptorReverse opioid tolerance and opioid induced hyperalgesiaRecent research shows efficacy in treating CPRS, PTSD, anxiety, and depressionLow dose over long infusion times for repeated exposures
Slide67KetamineDosage:Initial bolus: 0.5mg/kgASRA guidelines advocate for 0.35mg/kg bolusMaintenance: 5-10mcg/kg/minASRA guidelines state up to 1mg/kg/hrAlternative use is to administer 10-20mg prior to administration of opioidSubanesthetic dose decreases risks of postoperative hallucinations
Slide68N2ONMDA antagonistMinimal acute pain analgesiaShort duration of action may be reason whyStrong evidence may prevent development of chronic pain in at risk patientsENIGMA trial
Slide69MagnesiumSupplementation with exogenous magnesium changes concentration gradient and prevents disassociation of Mg2+ ion from NMDA receptor channel, preventing depolarization of postsynaptic neuronDosageInitial bolus 20-50mg/kg over 10-15 minutesMaintenance 10-25 mg/kg/hr
Slide70GabapentinoidsPresynaptic binding to the α-2-δ subunit of voltage-gated Ca+2 channels inhibiting Ca+2 influx Prevents release of glutamate, norepinephrine, substance P, and calcitonin gene-related peptide
Gabapentin and Pregabalin
Slide71GabapentinOriginally used as an anticonvulsant medication to treat epilepsyDecreases opioid use and PONVDosageInitial: 300mg-1200mg PO At least 1 hour prior to surgeryMaintenance: 300mg-600mg PO BID
Slide72PregabalinFaster absorption and onset than gabapentinAnalgesia effects similar to gabapentinDosageInitial: 150-300mg POAt least 1 hour prior to surgeryMaintenance: 75-150mg PO BID
Slide73Analgesics
Slide74AnalgesicsAcetaminophenEsmololNubain
Slide75AcetaminophenMetabolite AM 404 Activates CB1 receptor in rostral ventromedial medullaPO vs IVBest to give either prior to incisionDosageInitial: 1gm PO or IVMaintenance 1gm PO or IV q 6-8 hours
Slide76EsmololSelective β1-adrenoreceptor antagonistMetabolized by RBC esteraseAnalgesic MOA theories Central analgesia by inhibition of β-adrenoreceptors altering G protein activation
Inhibition of neurotransmitter release in substantia gelatinosa neurons
Slide77EsmololDosageInitial: 0.5-1mg/kg bolusMaintenance: 5-15 mcg/kg/min
Slide78NubainMechanism of actionFull kappa agonist and partial mu antagonistPotencyEquipotent to morphine¼ potency of NarcanDosage
Induction: 0.1-0.2mg/kg
PACU: 5-10mg up to total dose of 20mg
Side effects
Sedation, HOTN, bradycardia
Slide79Typical GA inductionKetamine 10mg/Precedex 10mcg/mL 0.25-0.5mL/10kg, divided into several small dosages from preop to OR
Toradol
15mg
Nubain
5-10mg
Magnesium 0.5-1gm bolus
Lidocaine
2mg/kg
Propofol
1mg/kg
*based on IBW or AdjBW
Slide80Cocktail Maintenance InfusionLidocaine 2mg/kg/hr, Ketamine 5mcg/kg/min, Magnesium 10mg/kg/hr, Dexmedetomidine 0.4mcg/kg/hrSyringe (50mL)Lidocaine 2% 10mL, Ketamine 30mg, Dexmedetomidine
40mcg, Magnesium 1gm, fill rest of syringe with IV fluid
NS 100mL bag remove 20mL
Inject
Lido 2% 20mL, Ketamine 60mg, Magnesium 2gm, and Dexmedetomidine 80mcg into bag
Infuse at 0.5mL/kg/hr
Run infusion up until starting incision closure
Slide81Emergent Ectopic Rupture
Ectopic pregnancy rupture
Hgb 7,
tranfused
2 units of PRBC
OFA technique
Slide82Transverse Colectomy
Bilateral QL3 block
OFA technique
Required Morphine 4mg night of surgery
Bowel function returned next morning
Discharged POD2
Slide83Laparoscopic Appendectomy
16yo WPW
Prior surgery opioid based anesthetic
Avoided any sympathomimetic medications
Stable VS perioperatively
High risk cardiac patient, no opioids!!
Slide84Tips To Starting OFADo not administer opioidsCommunicateEducateNetwork
Slide85Contactjmclott@gmail.com