acute pain - dr. jongco

acute pain - dr. jongco

Transcript

1. Robert D. Jongco, MD Associate Professor of Anesthesiology Rutgers University – Robert Wood Johnson Medical School April 27, 2020
2. Learning Objectives • Define acute pain • Discuss the anatomy of acute pain • Define the elements involved in pain processing • Identify the chemical mediators of transduction and transmission of pain • Discuss Neural Plasticity as it relates to sensitization • Briefly identify various methods for assessing acute pain • Overview of treatment options for acute pain
3. Definition • Acute pain – normal, predicted, physiological response to an adverse chemical, thermal or mechanical stimulus o Typically resolves within 1 month o Poor management can result in increased morbidity and mortality, delayed recovery, patient dissatisfaction, adverse psychological effects and neuronal plasticity
4. Types of Acute Pain • Nociceptive – adaptive, transient pain in response to a noxious stimulus o Visceral – Sympathetic and parasympathetic o Somatic • Inflammatory – in response to tissue damage and inflammation o Burn, arthritis • Neuropathic – primary lesion or dysfunction of peripheral or central nervous system o Central post-stroke pain syndrome, Tumor, Trigeminal neuralgia, CRPS, diabetic neuropathy, Spinal stenosis • Non-inflammatory/Non-neuropathic – Abnormal central processing o Fibromyalgia, irritable bowel syndrome
5. Anatomy of Acute Pain • Ascending pathways with descending modulation o Spinothalamic tract  thalamus  somatosensory cortex o Spinoparabrachial tract  ventral medial nucleus of hippocampus and central nucleus of the amygdala (Limbic System)
6. Pain Pathways Central Projections of the Nociceptor Ascending Pathways and the Supraspinal Processing of Pain The Nociceptor: A Bidirectional Signaling Machine Limbic Sensory Descending Modulatory pathways DRG PAG RVM PB Amygdala Cingulate cortex Somatosensory cortex Insular cortex
7. Nociceptors • Free nerve endings in the periphery with cell body in DRG and central branches that synapse in the dorsal horn
8. Primary Afferent Nerves Fiber Type Diameter (micrometers) Myelinated Velocity (m/s) Stimulus ABeta 12-20 yes >40-50 touch ADelta 1-4 yes 10-40 Pain, temperature C 0.5-1.5 no <2 “second pain”
9. Rexed Laminae • Primary afferent neurons synapse in Rexed Laminae I, II, V o V – wide dynamic range neurons (WDR) involved in windup/sensitization • Response intensity increases as the frequency of the the stimulus increases
10. Pain Processing • Transduction – noxious stimuli converted to an action potential • Transmission – AP is conducted through the nervous system via 1st, 2nd and 3rd order neurons from the periphery through the dorsal horn to the thalamus and cortex • Modulation – altering of afferent transmission o Inhibition vs. augmentation • GABA/glycine release • Activation of descending inhibitory efferent pathways from motor cortex, hypothalamus, PAG  NE, 5-HT, endorphin release in dorsal horn • Central sensitization – windup occurs due to repetitive stimulation of WDR neurons by C fibers • Perception – integration of painful input into somatosensory or limbic cortex
11. Pain mediators Substance Source Effect Bradykinin Macrophages and plasma kinogen Activates nociceptors Serotonin platelets Activates nociceptors Histamine Platelets and mast cells Vasodilation, edema, pruritis; preteniates nociceptor response to bradykinin Prostaglandin Tissue injury and COX pathway Sensitizes nocicpetors Leukotriene Tissue injury and lipoxoxygenase pathway Sensitizes nociceptors Hydrogen ions Tissue injury and ischemia Increases pain and hyperalgesia associated with inflammation Cytokines (Ils, TNFs) macrophages Excites and sensitizes nociceptors Adenosine Tissue injury Pain and hyperalgesia Neurotransmitters/neuro peptides (glutamate, substance P) Antidromic release by peripheral nerve terminals follow tissue injury Glutamate activates nociceptors; substance P activates marophages and mast cells Nerve Growth Factor macrophages Stimulates mast cell release of histamine and 5-HT; induces heat hyperalgesia; sensitizes nociceptors
13. Pain Receptors • NMDA o Ca channel dependent o Activated following prolonged depolarization of cell membrane • Crucial role in sensitization o Substance P  removal of Mg blockade  glutamate activation of NMDA receptor • AMPA • Kainate o Na channel dependent  fast synaptic afferent input • Metabotropic
15. Neural Plasticity • Change in pathways, synapses and function as a result of various factors such as injury o Pain-induced changes in the CNS • Central sensitization – hyperexcitability of dorsal horn neurons due to NMDA receptor signaling, disinhibition, microglia activation o Wind-up • Peripheral Sensitization o Allodynia o Hyperalgesia • Primary and secondary
16. Persistent Pain: Central Sensitization • Glutamate/NMDA Receptor-Mediated Sensitization • Loss of GABAergic and Glycinergic Controls: Disinhibition • Glial-Neuronal Interactions HSP or mRNA KCC2 Basbaum AI, Bautista DM, Scherrer G, Julius D. Cellular and molecular mechanisms of pain. Cell. 2009;139:267-84.
17. Descending Pain Modulating System: Serotonin and Norepinephrine • Descending pathways modulate ascending signals (inhibitory) • NE and 5-HT are key neurotransmitters • Central sensitization decreases inhibition of ascending pain pathways
18. Acute Pain Assessment • Visual Analog Scale (VAS) • FACES • McGill Pain Questionnaire • Brief Pain inventory
19. Treatment • Poorly controlled acute pain can cause significant morbidity • Sensitization and windup chronic pain conditions
20. Treatment Strategies
21. Opioid Receptors
22. Opioids
23. Multimodal Analgesia Interventions • Patient Education • NSAIDS • Acetaminophen • Gabapentinoids • NMDA receptor antagonist • α2 agonists • Perioperative steroids • Regional Anesthesia (peripheral nerve blocks) • Local anesthetic infiltration • Magnesium • Intravenous lidocaine
24. Negative Expectations Shindo M, Lim J, Leon E, et al. Opioid prescribing and needs in thyroid and parathyroid surgery. JAMA. 2018;12:1098-1103.  Education can be used to discuss potential adverse effects of opioids  Also shown to reduce postop opioid consumption Expectations
25. NSAIDs • Tissue damage releases arachidonic acid • Arachidonic acid metabolized to prostaglandins which decreases threshold of peripheral nociceptors • Inhibition of COX-1 and COX-2 stops conversion of arachidonic acid to prostaglandins • PGs (PGE2) responsible for sensitization of nociceptors to other pain mediators
26. • Limit dose to < 3 gm/day • IV $33 a dose vs 5 cents oral • Are opioid requirements reduced? Acetaminophen
27. Gabapentinoids • Reduces acute postoperative pain and opioid consumption • Anticonvulsant, membrane stabilizing • Gabapentin dose is 300- 1200mg TID PO • Sedation is common side effect
28. Ketamine • Block NMDA glutamate receptors o Glutamate is the primary excitatory neurotransmitter in the CNS • Dose is sub-anesthetic (hallucinations uncommon) • Single doses 0.2-0.5 mg/kg IV given incrementally • Continuous IV infusions 0.1-0.2 mg/kg/hr.
29. Alpha 2 Agonists • Inhibit NE release in brain and spinal cord • Decreases transmission of painful signals • Commonly used agents: dexmedetomidine, tizanidine and clonidine. o Dex > Clonidine at alpha2 receptor •Both reduce pain, opioid consumption , postop N/V, postop shivering •Dexmedetomidine IV loading dose 0.5- 1mcg/kg; IV infusion 0.2-1.7 mcg/kg/hr
30. Corticosteroids • Effective in limiting postop pain and opioid consumption in ortho and abdominal procedures • IV dose 0.1mg/kg, given preoperatively or shortly after induction seems optimal • Even single dose 4mg can increase blood sugar • Delayed wound healing with chronic usage • Can increase serum glucose levels by 50g/dL
31. Regional Anesthesia • Important component of multimodal analgesia • Reduces opioid consumption and side effects in multiple surgical procedures • Multiple regional techniques available
32. Local Anesthetic Infiltration • Demonstrated benefits • Lack of motor impairment • Surgeon can administer • Depot forms may be beneficial? • IV Lidocaine – anti- inflammatory effects o Reduces pain scores and opioid usage, earlier return of bowel function o Mechanism of action is unclear
33. Magnesium • Mechanism unclear • Anti-inflammatory and NMDA receptor antagonist • Most common dose is 30-50 mg/kg and infusion • Optimal dosing unknown • Potentiates neuromuscular blockade
34. Intravenous Lidocaine o Most evidence for abdominal surgery o Decreased pain scores o Early return of bowel function o Shorter hospital LOS o 1 mg/kg bolus, 1-2 mg/kg/hr infusion