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Lecture Title: Acute Pain Management. Lecturer name: Osama Ibraheim MD,SOB. Lecture date:. Lecture Objectives. Fundamental Considerations. Millions of patients worldwide undergo surgery.
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Lecture Title: Acute Pain Management Lecturer name:Osama Ibraheim MD,SOB. Lecture date:
Fundamental Considerations • Millions of patients worldwide undergo surgery. Although developing more effective techniques for postoperative analgesia, many patients experience pain.
PAIN An unpleasant sensory and emotional experience associated with actual or potential tissue damage. IASP, Subcommittee on Taxonomy, 1979
ETIOLGY OF PAIN • HEAT • COLD • CHEMICAL • MECHANICAL TORSION STRETCH CUT PINCH PRICK COMPRESS CRUSH
TYPOLOGY OF PAIN • Acute • Chronic benign • Chronic cancer
Chronic Pain vs Acute Pain Acute: A Symptom of Injury or Disease Chronic Benign: Pain itself is the disease Chronic Cancer: Actual Tissue destruction
Adverse Effects of Pain • Cardiovascular • Pulmonary • Gastrointestinal • Renal • Extremities • Endocrine • CNS • Immunologic
Adverse Effects of Pain Cardiovascular: Tachycardia, hypertension, increased SVR, increased cardiac work, increased myocardial O2 demand. Pulmonary: Hypoxia, hypercarbia, atelectasis, decreased cough, decreased vital capacity and function residual capacity, V/Q mismatch. Gastrointestinal: Nausea, vomiting, ileus, intolerance for oral intake. Renal: Oliguria, urinary retention.
Adverse Effects of Pain Extremities: Skeletal muscle spasm, limited mobility, thromboembolism. Endocrine: Excessive adrenergic activity, vagal inhibition, catabolic metabolism, increased O2 consumption. CNS: Sedation, fatigue, anxiety, and fear cause central sympathetic stimulation. Immunologic: Inhibited cellular immunity, increased risk of infection, ?? impaired wound healing ??
FREE NERVE ENDINGS ARE PRESENT IN ESSENTIALLY ALL BODY TISSUES IN VARYING AMOUNTS
ALGOGENIC(substances released by pain) SEROTONIN POTASSIUM HISTAMINE ACETLYCHOLINE BRADYKININS LEUKOTRIENES PROSTAGLANDINS SUBSTANCE P29 NOREPINEPHRINE
THE RECEPTORS IN THE FREE NERVE ENDINGS RESPOND TO THE SUBSTANCES BY BECOMING CHARGED ELECTROCHEMICALY
RECEPTORS THEN PROPAGATE AN ELECTROCHEMICAL STIMULUS TO DIFFERING NERVE FIBERS
NOCICEPTION This electrochemical event that occurs between the site of tissue damage or injury sets off a series of neural transmissions that eventually results in the perception of pain……Collectively this known as nociception
NERVE FIBERPAIN CLASSIFICATION A FIBER……..SHARP-STABBING-LOCAL “ FIRST PAIN” B FIBER....PHYSIOLOGIAL REACTION C FIBER....DULL-ACHE-BURN-THROB NONLOCALIZED-RADIATE “SECOND PAIN”
NERVE FIBER CLASSIFCATION TYPE FUNCTION A a myelinated motor A alpha myelinated touch-pressure A beta myelinated touch-pressure A delta myelinated pain-temperature A gamma myelinated proprioception
A Delta • 1 - 4 micrometers diameter • Myelinated, Rapid conduction • Sharp, localized • Heat, cold • “First pain”
B myelinated preganglionic autonomic C non-myelinated pain-temperature
C Fibers • Small • Slow Conduction • Unmyelinated • Postganglionic autonomic
C Fibers • Dull pain, burning, Aching throbbing • Nonlocalized - radiating - diffused • Temperature,Touch,Mechanical • “Second pain”
Gate Theory Balance between A delta and C fibers to dorsal horn determines the intensity of the stimulus that is passed to higher brain center
Area of High Nociceptor Concentration • Mucosal membranes • Periosteum • Deep fascia • Ligaments • Joint capsules • Cornea • Subcutaneous tissue
Areas of Moderate Nociceptor Concentration • Skeletal muscle • Cardiac muscle • Smooth muscle
Areas of Minimal Nociceptor Concentration • Bone • Cartilage • Marrow
Physiologic Processes of Nociception • Detection • Transduction • Transmission • Modulation • Perception
Detection • “First pain” • “Second pain”
TRANSDUCTION NOXIOUS STIMULI TRANSLATED INTO ELECTRICAL FIRING AT THE SENSORY NERVE ENDINGS
TRANSMISSION • PROPAGATION OF IMPULSE TRAVELS VIA NEURAL PATHWAYS. • SENSORY AFFERENT NEURONS PROJECT INTO THE SPINAL CORD • ASCENDING NEURONS RELAY TO BRAINSTEM AND THALAMUS • THALAMUS RELAYS TO CEREBRAL CORTEX
MODULATION INTRINIC PAIN MODIFICATION 1.DIFFERENT IN INDIVIDUALS 2.DEPENDS ON..... PAST EXPERIENCES CULTURE PSYCHIC
MODULATION-CONT • STIMULUS PRODUCED ANALGESIA • NEUROENDOCRINE ANALGESIA • CNS/PNS ANALGESIA • OPIOID ANALGESIA • SITUATION • PATHOLOGY • PHYSIOLOGY
Modulation – Excitatory Substances • Peripheral Prostaglandins, bradykinins, histamine, K, substance P, serotonin (5HT2) • Spinal Glutamate, aspartate, amino acids, substance P, norepinephrine (alpha 1)
Modulation - Inhibitory Supraspinal • Endorphins, enkephalins, dynorphins, norepinephrine (alpha 2), GABA, somatostatin (5HT1), neurotensin
First Neuron Pain Peripheral afferent fibers to dorsal horn Second Neuron Pain Dorsal horn to thalamic Third Neuron Pain Thalamus to cortex
Pain Pathways: • Tissue damage>>>Algesic substanses release>>>Noxious stimuli>>>A delta and C fibers>>>to the Neuraxis>>>Many to Ant. and Anterolat.Horns>>>Segmenal reflex responses , and others via the Spinothalamic and Spinoreticular tracts>>>Suprasegmental and cortical responses.
Classification & Function of Peripheral Nerve Fibers A. Myelinated A- Fibers: • a: Motor , Proprioception (afferent) • b: Motor, Touch (afferent) • g: Muscle spindles (efferent) • d: Pain, Temperature (afferent) B. Myelinated B-Fibers: • Pre-ganglionic Sympathetic Fibers C. Non-Myelinated C- Fibers: Pain, Temperature.
Spinothalamic tract Dorsal horn of spinal cord • Nociceptive sensory fibres are C-fibres and Ad fibres • C-fibres umyelinated • Ad myelinated • Slow conduction velocity • Signal variety of noxious stimuli - polymodal Dorsal Root Ganglion Peripheral nerve Sympathetic ganglion Viscera Blood vessels Skeletal muscle Tendon bundle C and Ad fibres Nociceptive terminals Muscle and skin receptors Nociceptive pathways: peripheral sensory nerves
Cortex Thalamus Mesencephalon Medulla oblongata Spinal cord Ascending Pain Pathways • Topographic representation maintained • Sites for pain modulation are spinal cord and thalamus Pons
Segmental reflex responses: Increased skeletal muscle tone , Increased oxygen consumption , Lactic acid production • Suprasegmental • reflex responses: Increased Sympathetic tone , Hypothalamic stimulation.
Chemical Mediators Membrane ion channels of Nociceptive neurons Directly coupling to membrane receptors Hydrogen ATP Serotonin 5HT3 Indirectly (more commonly) mediating intracellular secondary messages Bradykinins B1, B2 Cytokines Prostanoids Histamine H1 Serotonin 5HT1
Factors that modify perioperative pain : • 1- Site ,nature and duration of surgery. • 2- Type and extent of incision. • 3- Physiologic and psychologic makeup of the patient. • 4- Pre operative preparation of the patient. • 5- Presence of complications of surgery. • 6- Anesthetic management. • 7- Quality of perioperative care. • 8- Preoperative treatment of painful stimuli .
Preemptive Analgesia : • Antinociceptive treatment of that prevents the establishment of altered central prossesing, which amplifies postop. Pain. • Windup:functional changes in the dorsal horn because of pain . • This type of therapy ,in addition to reducing acute pain ,attenuates chronic postop. Pain.
Principles of Pain Management Anticipate pain Recognize patient: Ask the patient Look for signs (HR, BP, facial grimacing, tears, sweating, etc) Find the source Quantify pain (mild, moderate, severe) Treat: Quantify the patients perception of pain Correct the cause where possible Give appropriate analgesics regularly as required Remember most sedative agents do not provide analgesia Reassess
Modalities of Pain Relief Non-opioid analgesics+opioid analgesics Regular injections of opioids Continuous IV or SC infusion of opioids Patient controlled analgesia (PCA) Extradural opioids & or local anesthetics Combined exrtadural + spinal analgesia Long acting oral opioids Long acting regional blocks Ketamine (S+)
Modalities of Pain Relief Pharmacological Non-pharmacological
DRUGS NSAID’s COX-1 Minor – Moderate pain COX-2rofecoxib, parecoxib-inj Severe pain Actions: Inhibit synthesis of PG-E Direct analgesic effect on higher centers Modify nociceptive responses-bradykinins Antiplatelet Hypothrombinaemia Lowers body temp Hypoglycemia Metabolic acidosis Adverse gastrointestinal effects Lower doses only
Systemic Opioids : Analgesic effects of opioids : via receptors in the CNS. Roots of administeration :I.M. ,I.V. ,Transdermal ,Oral ,Topical ,I.V. regional ,Perineural ,etc. I.M. root is the most treatment choice after surgery. The” As Needed” part of the order is often interpreted to mean “As little as possible” . No relation exists between Gender and opioid requirement.
Analgesic Opiates • Morphine • Pethidine • Fentanyl • Sufentanil • Alfentanil • Remifentani • ANTIDOTE : Naloxone
Routes of administration of analgesics Oral Intravenous Sublingual/buccal Epidural (opioid) Oral transmucosal Intrathecal (opiod) Intranasal Intra articular (opioid) Transdermal Topical - EMLA cream Rectal Intradermal Inhalational Peripheral N block Subcutaneous Nerve plexus block Intramuscular Intravenous regional