Chapter 15 PAIN MANAGEMENT Eileen Mann. Introduction This presentation focuses on the healthcare of...

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Transcript of Chapter 15 PAIN MANAGEMENT Eileen Mann. Introduction This presentation focuses on the healthcare of...

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Chapter 15 PAIN MANAGEMENT Eileen Mann Slide 2 Introduction This presentation focuses on the healthcare of patients experiencing pain. It adds to the knowledge you will already have gained by reading the book chapter. Part 1 Epidural Analgesia Part 2 Postoperative Nausea and Vomiting Part 3 The Multidimensional Nature of Pain Part 4 - Entonox Slide 3 PART 1: Epidural Analgesia Slide 4 Epidural Analgesia Involves the infusion of a local anaesthetic and commonly an opioid into the epidural space surrounding the spinal cord. The epidural space extends from the foramen magnum to the sacral canal. Slide 5 Why Use Epidurals? High quality analgesia Reduced complications/bedstay Needs much less opioid, resulting in reduced side effects such as PONV, delayed nutrition, sedation Reduced respiratory infections Increases mobility leading to less muscle wasting and deep vein thrombosis Slide 6 Locating the Epidural Space Spinal cord Spinal column Slide 7 Spinal Nerves Cervical - 8 pairs interconnect to form the cervical plexus and the brachial plexus. These innervate the back of the head, neck, shoulders, arms, hands and diaphragm Thoracic - directly connected to the muscles between the ribs, deep back muscles, abdomen and thorax Lumbar - supplies the muscles of the lower limbs and trunk, external genitalia, groin and lower limbs Sacral - forms the sacral and coccygeal plexus, innervating the thighs, buttocks, legs, feet and the anal/genital area Coccyx - one pair of nerves supplies the skin in the region of the coccyx Slide 8 Who may benefit from an epidural? Patients recently undergone abdominal incisions Serious pelvic & leg fractures Major pelvic and leg surgery Particularly useful following chest trauma Slide 9 Epidural is performed with the patient sitting or lying down with their back curved outwards Slide 10 Contraindications Patient refusal Coagulopathy Local infection Inadequate facilities, equipment, training, staffing levels Anatomical abnormality Hypovolaemia Sepsis/fever Back problems Neurological condition Allergy Slide 11 Caudal Analgesia This involves placing local anaesthetic into a continuation of the epidural space that is located at the lower end of the spine. It produces a block of the sacral and lumbar nerve roots which is ideal for perineal surgery. Slide 12 Local Anaesthetics Blocks the initiation and spread of action potentials within the nerves Blocks conduction in small diameter nerve fibres (A delta & C fibres) more readily than large fibres (A beta) Therefore pain sensation is blocked more easily than other sensory modalities (touch etc.) Slide 13 Opioids Thought to bind to opioid receptors in the substansia gelatinosa of the spinal cord interfering with the pain impulse Provides analgesia which lasts longer than systemic opioids Does not cause motor or sensory blockade, or hypotension Fentanyl 50 - 200 mcg will last around 3 - 6 hours Diamorphine 0.5 - 5 mg will last 6 - 12 hours Slide 14 Opioid Side Effects Effects receptors in the medullary respiratory centre leading to potential respiratory depression Sedation Itching Nausea Slide 15 Local Anaesthetic Side Effects Local anaesthetics block conduction in all types of nerves: Sympathetic block - hypotension, urinary retention Sensory block - pressure sores Motor block - weakness, immobility, falls. Slide 16 Complications of Combined Local Anaesthetic/Opioid Epidurals Early: Hypotension High sensory and motor block Respiratory depression Sedation Cardiovascular complications Head/neck/backache Anaphylaxis Late: Haematoma Epidural abscess Infection and sepsis Unresolved motor and sensory loss Itching Leaking epidural Slide 17 The Ideal Outcome A sensory pain block with no motor block and minimal side effects. An alert patient capable of early mobilisation and able to participate in active physiotherapy. Slide 18 Monitoring Consciousness level Colour Heart rate Blood Pressure Respirations Oxygen saturation Temperature Wound Urine output Motor/sensory levels PAIN Slide 19 PART 2: Postoperative Nausea and Vomiting (PONV) Slide 20 Why Treat Nausea and Vomiting? Humanitarian reasons Increase in autonomic activity Increase in closed compartment pressure Delayed hydration and nutrition Delayed discharge from hospital Delayed return to work and normal functioning Slide 21 P.O.N.V. A vastly underrated problem. Many patients fear nausea and vomiting more than postoperative pain. 30% elect to forgo opioids and tolerate pain if this stops the nausea. Slide 22 Patients at Risk from PONV History of PONV and/or motion sickness Females > males (pre menopause) Young > old Type of procedure performed Use of opioids Slide 23 Chemical Receptors in the Vomiting Centre in the Brain Acetylcholine: cyclizine, hyoscine Dopamine antagonist: droperidol, metoclopramide, phenothiazines 5 Hydroxytryptamine (serotonin): ondansetron Histamine Slide 24 Antiemetics All give 30-45% reduction of symptoms at best May reduce vomiting more than nausea Pharmacodynamics/kinetics poorly understood for older drugs Multimodal antiemetic therapy? Cyclizine, prochlorperazine and ondansetron all have more or less equal efficacy. Metoclopramide has no antiemetic action in the postoperative setting. The role of steroids? Slide 25 Antiemetics Ondansetron available as i.v.+ melts Cyclizine i.v.i ( side effect problems) Prochlorperazine P.O Buccastem (i.m., p.r.) Best evidence : PLUSOndansetron 8mg i.v. PLUS Dexamethasone 8mg i.v. Slide 26 Summary Carry out a risk assessment Prophylaxis Avoid emetogenic drugs if possible Combination therapies Complementary therapies Educate patients and staff Slide 27 PART 3: The Multidimensional Nature of Pain Slide 28 Definition of Pain An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage IASP 1986 Slide 29 Pain of recent onset and probably limited duration. It usually has an identifiable temporal and causal relationship to injury and disease. IASP 1986 Acute pain will always respond to analgesia Definition of Acute Pain Slide 30 Pain lasting for long periods of time. It usually persists beyond the time of healing of an injury and frequently there may not be any clearly identifiable cause. IASP 1986 Chronic pain may or may not be opioid responsive and other analgesic regimes may also be ineffective Definition of Chronic Pain Slide 31 The Acute/Chronic Debate Q. Where does acute pain end and chronic pain begin? Do changes happen much earlier than previously thought? Q. What is the biological mechanism that is driving pain? Q, What are the impact of psychosocial factors? Slide 32 Acute AND Chronic Pain Acute nociceptive (biologically active) Chronic nociceptive/neuropathic, mixed Acute on Chronic episodic/background Visceral Idiopathic Slide 33 Acute TO Chronic Pain Pain is usually event related and starts as an acute episode with a high level of biological activity. The pain is initially reversible. Changes tend to become fixed depending upon: the nature and duration of the original cause of pain, age of the patient, psychosocial influences such as pain memory, culture, pain affect and possibly genetic susceptibility. Slide 34 Types of Pain Syndromes (IASP 1986) Chronic pain Cancer related pain Somatic pain (superficial & deep) Visceral pain Neuropathic pain Slide 35 Theories of Pain Specificity theory Pattern theory Neuromatrix Gate Control Theory Slide 36 The Gate Control Theory Modulating gating mechanism Large diameter fibres (touch) closed the gate Small diameter fibres (nociceptors) opened the gate Affective/cognitive descending modulation Pain is multidimensional Slide 37 Nociceptors Two types of afferent fibres: A DELTA: Mylenated, fast (>30m/s) fast pain Bright, sharp Somatic C FIBRES: Unmyelenated, slow (.5-2 m/s) slow pain Dull diffuse, continuous, deep Slide 38 Cross Section of the Spinal Cord A Beta A Delta C Fibres Substantia Gelatinosa Slide 39 GATING MECHANISMS Located within the dorsal horn of the spinal cord, but also found within the brain stem, hypothalamus and thalamus Somatosensory cortex Thalamus Hypothalamus Brainste m Substantia gelatinosa Sensory input from the periphery Ascending mechanism Descending mechanism Autonomic response Limbic system 1 2 3 4 5 Slide 40 Physiology (Sensory) 1. Nociceptors A-delta, B-delta, C fibres 2. Chemicals histamine, bradykinin 3. Neurochemical mediators 4. Ascending transmission 5. Descending transmission 6. Pain systems dynamic and plastic 7. Pain perception can be modulated by both pharmacological and non pharmacological strategies at all levels of the nervous system. 8. Changes may become fixed - remapping Slide 41 Primary Hyperalgesia Reduction in the pain threshold in the area of damage. e.g. skin burn, pharyngitis, sprained ankle Locally released chemical inflammatory mediators: potassium, histamine, bradykinin, leukotrienes, serotonin, histamine, substance P, arachadonic acid metabolites (prostaglandins etc) Slide 42 Secondary Hyperalgesia Non-nociceptors acquire capacity to evoke pain Central pain pathways adjust and change pain memory? Brief stimulation of nociceptors can cause major changes in the receptive fields in the spinal cord. Repetitive peripheral stimulation causes response to progressively increase. Possibly due to loss of central inhibition. Acute gene expression altering receptors. Remapping at cord and brain level. Slide 43 Pain Windup Pain continuing or worsening when the cause is stable or improving. FEATURES: Reduced threshold Augmented response Ongoing activity Pain adjacent to but beyond the limits of tissue injury. Slide 44 Pain Management ACUTE PAIN Relatively easy to treat but needs effective early therapy to reduce the risk of wind up/cortical remapping. A narrow therapeutic window. ** **At one year following hernia surgery 29% of patients reported pain in the area of the hernia, 11% reported