Pain Control: Acute and Chronic Conditions

Pain Control: Acute and Chronic Conditions Frank C. Nacario MD DPBA Associate Professor Anesthesiology & Pain Medicine Palliative Care UERMMMCI Hippocratic precepts: “ the first duty of medicine is to heal- if it can to relieve often, to comfort always” 1. 2. 3. 4. 5. 6. 7. Definition of pain Acute vs Chronic pain Physiology of pain Effects of pain Pain scores in different surgical procedures Pain assessment Pain control in the postoperative period Pain “unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” International Association for the Study of Pain, 1979 “Pain is whatever the experiencing person says it is; existing whenever he or she says it does.” McCaffrey, 1980 “Pain is now recognized as a complex experience with at least four main components o o o o nociception sensation suffering or distress behaviour Champagne and Weisse,1994 Pain threshold refers to the point when stimulation is felt as painful. Pain tolerance refers to “how much” one can bear the pain experience; varies between individuals and cultures. i.e. females vs males pain as a form of punishment pain as a vital experience Two categories of pain Acute: primarily due to nociception  short-lived and reversible;less than six months  organic disease or injury is present Chronic: may be due to nociception but in which psychological and behavioral factors often play a major role  behavior state, initiated by a real injury  six months or longer; that it has itself become the disease Acute Pain ACUTE PAIN Chronic Pain Chronic Pain Two Types of Pain 1. Physiologic or nociceptive pain    Includes acute, subacute, chronic, and inflammatory pain Results from noxious stimuli and inflammation in an otherwise intact tissue Pain system is functioning as nature intends it to 1. Pathologic or neuropathic pain   Associated with frank injury to neural tissue Reflects abnormal functioning of the pain system Nociceptors: special sense receptors in the skin or internal organs ▫ receptors receive noxious (painful) stimuli produced by intense heat, extreme pressure, pricks and cuts, surgery or ischemia Noxious sensation: two components First pain Fast, sharp, well-localized Aδ fibers Second pain Slower onset, duller, poorly localized C fibers Peripheral Nociceptor System 1. Somatic structures  Cutaneous nociceptors: pain receptors at the termination of free-nerve endings in the skin (1) A-δ high- threshold mechanoreceptors (HTM) activated by mechanical noxious stimuli (2) A-δ myelinated mechanothermal nociceptors activated by noxious mechanical stimuli and noxious heat (3) C polymodal nociceptors activated by mechanical, thermal, and chemical noxious stimuli (4) miscellaneous C mechanical nociceptors and cold nociceptors ▫ Deep nociceptors: also supplied by A-δ and C fibers  Less sensitive to noxious stimuli than cutaneous nociceptors  Easily sensitized by inflammation; dull and poorly-localized  Muscle, fascia, tendons, and other deeper somatic structures 2. Visceral structures   Supplied by C afferents and some A-δ fibers Activated by disease, inflammation, contraction under isometric conditions, ischemia, rapid distention, and other adequate visceral nociceptive stimuli and endogenous algogenic substances Sensitization following Tissue Injury Peripheral Sensitization direct effect: injury > release of algogens (activate and sensitize nociceptors); indirect effect: (release of a complex soup of inflammatory substances further sensitizing injured tissue and surrounding tissues) make the nociceptors more sensitive to the painful stimulus, more prone to activation by: - weak touch - thermal stimuli - during movement lowered threshold to stimulation, and prolonged and enhanced response - ▫ Primary hyperalgesia  Sensitization at the site of injury  Characterized by lowered pain threshold, increased sensitivity to suprathreshold stimuli, and spontaneous pain – peripheral sensitization ▫ Secondary hyperalgesia  Refers to the pain and tenderness felt at the area adjacent to the site of the initial injury including the area without inflammation – central sensitization Central Sensitization - abnormal degree of amplification of the incoming sensory signal in the CNS - amplifies the signal of nociceptors, and amplifies the signal of low-threshold A-β sensory fibers (touch-sensitive & vibration) which previously are subliminal - A-β touch input is perceived as painful - key involvement of glutamate neurotransmitter and its NMDA receptor • Burn – produce tenderness in the burnt area (primary hyperalgesia); due to sensitized nociceptors (peripheral sensitization) also produce tenderness in a substantial zone of intact skin (secondary hyperalgesia) - due to spinal amplification of otherwise normal touch input (central sensitization) Lloyd/ Hunt Syste m Diamete r (m) Letter System Conduc tion Velocity (m/s) Myelin Receptor /Ending Types I-a 12-20 - 70-120 + Muscle spindle primary endings I-b 12-20 - 70-120 + Golgi tendon organs - 12-20 A-  70-120 + Muscle efferents (extrafusal) II 6-12+ A- 30-70 + Encapsulated endings - 2-10 A- 10-50 + Muscle efferents (intrafusal) III 1-6 A- 5-30 + A- specific nociceptors/ polymodal receptors, cold, most hair, some visceral receptor - <3 B 3-15 + Preganglionic autonomic <1.5 C 0.5-2.0 No C-nociceptors, C-polymodal receptor, warmth receptor, some mechanoreceptor, postganglionic autonomic, enteric nerve fibers IV Pain Pathways Synapse: release of neurotrans: Glutamate-aspartate, sP, FRAP, VIP CCK GRP, ENK,DYN = depolarization Release of neurotrans Lateral system:nSTT Medial system:pSTT, SMT,SRT A-δ fibers C fibers Endogenous Opiate System • Enkephalins ▫ Opiate-binding sites in the dorsal horn, periaqueductal gray (PAG), nucleus raphe magnus, globus pallidus and other areas involved with the pain pathway ▫ Neurons containing serotonin (5HT) also contain enkephalins • Dynorphins ▫ Hypothalamus, PAG, reticular formation, medulla, dorsal horn of the SC in laminae I, V • Β-endorphins ▫ Basal hypothalamus, limbic system, 3rd ventricle, midbrain, locus ceruleus Opioid Receptors & Ligands Receptor µ (mu) Natural Ligand Enkephalins Κ (kappa) Dynorphin δ (delta) Enkephalins Ε (epsilon) Β-endorphins Non-opiate Descending Inhibitory System • Serotonin ▫ The cell bodies of 5HT originate in the nucleus raphe, medulla and pons ▫ Their axons terminate in laminae I, IIo, IV and V of the spinal dorsal horn and near the central canal; others in the ventral horn ▫ the analgesic action of systemic opiates can be blocked by depletion of 5HT Non-opiate Descending Inhibitory System • NE (norepinephrine) descending system ▫ Axons descend in all of the laminae of the spinal cord ▫ Mediates analgesia and dorsal horn inhibition ▫ Appears to be critical for opiate-induced analgesia ▫ Hyperpolarizes 1st order neuron, internuncial neurons , and wide-dynamic range neurons in the STT Peripheral Nociceptor System 1. Somatic structures ▫ Cutaneous nociceptors: on free-nerve endings 1) A-δ high- threshold mechanoreceptors (HTM) activated by mechanical noxious stimuli (2) A-δ myelinated mechanothermal nociceptors activated by noxious mechanical stimuli and noxious heat (3) C polymodal nociceptors activated by mechanical, thermal, and chemical noxious stimuli (4) miscellaneous C mechanical nociceptors and cold nociceptors ▫ Deep nociceptors: supplied by A-δ and C fibers    Less sensitive to noxious stimuli than cutaneous nociceptors Easily sensitized by inflammation; dull and poorlylocalized Muscle, fascia, tendons, and other deeper somatic structures 2. Visceral structures ▫ ▫ Supplied by C afferents and some A-δ fibers Activated by disease, inflammation, contraction under isometric conditions, ischemia, rapid distention, and other adequate visceral nociceptive stimuli and endogenous algogenic substances Peripheral Nociceptor system Third Order neuron (thalamic) Second order neuron (dorsal horn) Primary afferent neuron (DRG) Peripheral tissues Gate Control Theory 2 competing pain mechanisms which influence gate control Aδ, (C) Aβ noxious stimuli Activation of large afferent epicritic fibers inhibits WDR neuron and inputSTT activity Painstimuli in one part of the body inhibits pain in other peripheral partschange (temperature or vibration) " Rubbing the injured area makes it better“ Transcutaneous electrical nerve stimulation, hot and cold therapies and stimulation therapies are thought to be effective other skin Effects of Pain Components of the Stress Response ACTH:protein catabolism a) Neuro-endocrine cortisol:lipolysis b) Cardiovascular glucagon: hyperglycemia c) Respiratory epinephrine ↓Insulin, ↓ protein anabolism d) Gastrointestinal Dec FRC ↑platelet adhesiveness ↓ testosterone myocardial work Impaired diaphragmatic e) Genitourinary ↓aldosterone: fibrinolysis ↑sphincteric toneand H2O retention Immobility - dysrhythmias salt ↑sphincteric tone Function(reflex inhibition Activation of coagulation f) Immunologic/ ↓ smooth muscle tone Insomnia ADH - anginatone ↓smooth muscle of phrenic nerve) cascade Anxiety congestive cortisol: - MI heart failure Coagulation = Atelectasis ═ urinary retention Helplessness -═CHF vasoconstriction, Ileus = Pneumonia g) General Well Being ═catecholamines: incidence of thromboembolic ═ Fear contractility myocardial phenomena heart rate angiotensin II Pain Scores: Common procedures • Appendectomy:5-7 • Cholecystectomy: 7 • Cesarian section: 4-7 • Thoracic surgery: 7-8 • Bowel surgery: 7-9 • Gynecologic surgery:7-8 • Hemorrhoidectomy: 9 • Opthalmologic procedures: 1-6 • Liposuction: 4-6 • Nephrectomy: 10 Pain Assessment Self-Report: Visual Analog Scale Numeric Rating Scale Visual Analogue Scale (VAS): 0 10 No pain Worst imaginable pain Numeric Rating Scale 0 1 2 3 8 9 10 No pain 4 5 6 7 The Whaley & Wong Faces Rating Scale Pain Faces Scale “Pain as the Fifth Vital Sign” “We need to train doctors and nurses to treat pain as a vital sign. Quality care means that pain is measured and treated” James Campbell, MD Presidential Address, American Pain Society November 11, 1996 Pain Interventions 1. Non-opioid and Opioid drug therapy via the Oral Transdermal Transmucosal Parenteral ▫ Intramuscular Intravenous intermittent Intravenous continuous Cyclooxygenase pathway Phospholipids Phospholipase A2 Arachidonic acid 5-lipoxygenase 5- HPETE COX Leukotrienes TXA2 PGI2 Vasodilator,hyperalgesic,inhib pl. aggr Pl. aggr, vasoconstric PGF2 PGE2 PGD2 Bronchoconstr, myomet contrac Vasodil,hyperalg Inh. Plt aggreg, vasodil Involvement of COX COX 1( constitutive) COX 2 (inducible) Inflammation Inflammation Nociception Nociception GI mucosal integrity GI mucosal integrity GI adaptive cytoprotection Renal sodium balance GF Kidney development Angiogenesis Angiogenesis Pl. TXA 2 synthesis Endothelial PGI2 synthesis Endothelial PGI2 synthesis Protection myocardial damage Non-opioid drugs Aspirin: non-selective COX inhibitor  COX 1 & 3 inhibitor Acetaminophen:  COX 3 inhibitor NSAIDs:  Non selective COX inhibitor      Ketorolac (Toradol): IV Ketoprofen (Orudis): IV, IM Mefenamic acid (Ponstan): oral Diclofenac (Voltaren, Diclowal): IM, oral, topical Ibuprofen (Alaxan, Advil): oral COX2 inhibitors  Etoricoxib, Celecoxib - oral  Parecoxib- IV  (Rofecoxib, Valdecoxib, Nimesulide) Non opioid drugs Mechanism of Action ▫ Inhibition of PG-mediated amplification of chemical and mechanical irritants on the sensory pathway. ▫ Inhibits COX (prostaglandin synthetase) ▫ Blocks response to inflammatory substances, bradykinins, acetylcholine, serotonin ═ mediation of peripheral inflammatory response Opioids Agonist on the opioid receptors ▫ Periaqueductal grey ▫ Periventricular gray ▫ Nucleus reticularis ▫ Gigantocellularis ▫ Medial thalamus ▫ Reticular formation ▫ Lateral hypothalamus ▫ Spinal cord Opioid Receptors Mu1 Supraspinal analg nv Mu2 Resp depression, dependence Spinal analgesia nv Delta Kappa Spinal analgesia, sedation Sigma Dysphoria Opioids Agonists: Mu receptor ▫ Morphine: oral, IV, IM, intrathecal, epidural ▫ Fentanyl: transdermal, transmucosal, IV ▫ Oxycodone: oral ▫ Hydromorphone: oral Weak Agonists :Mu  Tramadol: oral, IV, transmucosal  Meperidine: IV, IM, epidural Agonist-antagonists: kappa, sigma/ no activity on Mu; potential to reverse effect of agonist ▫ Nalbuphine: IM, IV ▫ Butorphanol: IM, IV 2. Central neuraxial analgesia ▫ Intrathecal: spinal opioid receptors (SG)  addresses the shortcomings of IV and IM  single dose 12 to 24hours pain relief  potential for both acute and delayed respiratory depression (rostral spread) ▫ Epidural  reduced incidence of side effects: pruritus, respiratory depression  catheter may be inserted for intermittent 12 to 24 hour interval doses or continuous infusion  PCA with background infusion achieves better analgesia Undesirable Effects of Opioids Sedation - k Nausea and Vomiting - m Suppression of cough reflex - m Psychological and Physical dependence Tolerance Constipation – most common - k Respiratory depression - m PCA – Patient-controlled Analgesia Background infusion with PCA boluses  IV or epidural  Better maintenance of therapeutic levels  Better patient satisfaction  Not dependent on care giver (no delay in meds)  Patient has control over own pain concerns  Usually, patients gives only to maintain tolerable pain level – less drug use Other interventions 3. Transcutaneous Electrical Nerve Stimulation 4. Psychological Intervention for Post op Analgesia Administration Round the clock vs prn RTC : maintain blood level decreases total opioid requirement prn: intermittent, peaks and troughs PCA – patient-controlled analgesia ▫ ▫ ▫ IV or epidural Better maintenance of therapeutic levels Better patient satisfaction  Not dependent on care giver (no delay in meds)  Patient has control over own pain control needs  Usually, patients demand only to maintain tolerable pain level – less drug use Ideal pain management RESCUE MEDICATIONS BREAKTHROUG H PAINS RTC MEDICATION PERSISTENT PAIN TIME Adjuvant drugs: Antidepressant Anxiolytic Steroids Antiemetic Management of drug related side effects Antacids Laxatives/stool softeners WHO Analgesic Ladder Three step sequence for pain control STEP - 3 If pain persist or increases If pain persist or increases STEP - 1 STEP - 2 Weak opioids Strong opioids Analgesics should be administered by the mouth, by the clock, by the ladder The three basic analgesics are: Aspirin, Codeine and Morphine PAI Non opioids N “Approaching this helps prevent the Doctor Kangarooing from Analgesics-analgesics in a desperate search for some drug that will suit the patient better”. Multimodal Pain Control • Inflammation & Analgesia ▫ NSAID • Analgesia ▫ Opioid • Adjuvants • Non-pharmacologic therapy ▫ Psychological support ▫ TENS Pharmacotherapy NMDA receptor inhibitors Counterirritation Triad of Pain Pain Depression Anxiety Impaired sleep Impaired ADL Control pain 24/7 Medicines for severe pain “Pain is perfect misery, the worst of evils, and excessive overturns all patience.” John Milton, Paradise Lost