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Chapter 15 PAIN MANAGEMENT Eileen Mann

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1 Chapter 15 PAIN MANAGEMENT Eileen Mann

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

3 PART 1: Epidural Analgesia

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.

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

6 Locating the Epidural Space
Spinal cord Spinal column

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

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

9 Epidural is performed with the patient sitting or lying down with their back curved outwards

10 Contraindications Patient refusal Coagulopathy Local infection
Inadequate facilities, equipment, training, staffing levels Anatomical abnormality Hypovolaemia Sepsis/fever Back problems Neurological condition Allergy

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.

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.)

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 mcg will last around hours Diamorphine mg will last hours

14 Opioid Side Effects Effects receptors in the medullary respiratory centre leading to potential respiratory depression Sedation Itching Nausea

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.

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

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.

18 Monitoring Consciousness level Colour Heart rate Blood Pressure
Respirations Oxygen saturation Temperature Wound Urine output Motor/sensory levels PAIN

19 PART 2: Postoperative Nausea and Vomiting (PONV)

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

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.

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

23 Chemical Receptors in the Vomiting Centre in the Brain
Acetylcholine: cyclizine, hyoscine Dopamine antagonist: droperidol, metoclopramide, phenothiazines 5 Hydroxytryptamine (serotonin): ondansetron Histamine

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?

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 : Ondansetron 8mg i.v. PLUS Dexamethasone 8mg i.v.

26 Summary Carry out a risk assessment Prophylaxis
Avoid emetogenic drugs if possible Combination therapies Complementary therapies Educate patients and staff

27 PART 3: The Multidimensional Nature of Pain

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

29 Acute pain will always respond to analgesia
Definition of Acute Pain ‘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

30 Definition of Chronic Pain
‘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

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?

32 Acute AND Chronic Pain Acute – nociceptive (biologically active)
Chronic – nociceptive/neuropathic, mixed Acute on Chronic episodic/background Visceral Idiopathic

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.

34 Types of Pain Syndromes (IASP 1986)
Chronic pain Cancer related pain Somatic pain (superficial & deep) Visceral pain Neuropathic pain Chronic pain Usually depression and anxiety Poor sleep, appetite Reduced social activity Work affected Not obvious they have pain Somatic pain 1) Superficial – cutaneous 2) Deep - connective tissue, muscle, bone, joints Visceral pain Affects visceral tissues – intestine Hollow viscus organs - stomach

35 Theories of Pain Specificity theory Pattern theory Neuromatrix
Gate Control Theory Specificity (Von Frey 1845) Rather like the other senses – touch, pressure. Direct link from receptor to the brain where it arrived at a specific pain centre. Pattern Specific receptors did not exist but instead free nerve endings responded to multiple stimuli. There is some support for this theory as afferent impulses are critical to the perception of pain. Gate control theory This still stands from it’s inception in The most highly thought of as it brought clinical observation and research together to explain the conundrums of pain. Neuromatrix Since the 1990’s a growing understanding of the dynamic nature of nervous system. Leaving an imprint…more later on this!

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 Sensory information from the nociceptors is carried to the brain through the spinal cord. The nerve fibres responsible for carrying this type of information from the nociceptors to the spinal cord are called A delta and C fibres. A delta fibres are fast conducting, large diameter ( 206 um ). Pain signals carried by these fibres appear as sharp, that is well localised. C fibres are slow conducting, smaller diameter ( um ) fibres that are unmyelated. The pain signals carried by these fibres are perceived as slow, burning, aching pain that is diffused. Beecher story 1946 – psychological aspects, the meaning of the pain. Major impact as it explained the pain as a research level and clinical level for the first time. Melzack and Casey went on to explain it in terms of sensory, affective and cognitive. Think back to your descriptions of pain

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 A beta fibres are responsible for the sensation of light touch. Interestingly they over ride the noicipceptors and can be stimulated using cutaneous stimulation such as TENS and massage,

38 Cross Section of the Spinal Cord
A Beta A Delta A- beta Large unmyelinated A-delta C fibres C Fibres Substantia Gelatinosa

39 Limbic system Autonomic response
“GATING” MECHANISMS Located within the dorsal horn of the spinal cord, but also found within the brain stem, hypothalamus and thalamus Somatosensory cortex 4 Limbic system Autonomic response Thalamus Hypothalamus 5 Brainstem Descending mechanism Ascending mechanism Use stimulation at the periphery – local anaesthetic injections and creams, but also massage, warmth, cool, this is how TENS is thought to work and aromatherapy and reflexology alter pain perception at a cutaneous level Some systemic drugs help to reduce the influence of the chemical soup such as the NSAIDs which block the synthesis of prostaglandin e. Opioids are powerful in blocking the transmission of pain at CNS level Other drugs can work at CNS level to influence pain perception on the seratonin/nor adrenalin pathways but also the influence of boredom, anxiety, fear and anger will alter pain perception. The modulating pathway that helps to close the Gate may be boosted by a perception of locus of control, attention/distraction techniques, endogenous opioids, laughter etc. 1 Sensory input from the periphery 3 2 Substantia gelatinosa

40 Physiology (Sensory) Nociceptors A-delta, B-delta, C fibres
Chemicals – histamine, bradykinin Neurochemical mediators Ascending transmission Descending transmission Pain systems dynamic and “plastic” Pain perception can be modulated by both pharmacological and non pharmacological strategies at all levels of the nervous system. Changes may become fixed - remapping C fibres Activity of the C fibres may be up-regulated peripherally by serotonin (i.e., 5-hydroxy tryptamine), prostaglandins, thromboxane, and leucotrienes in the damaged tissues. This is referred to as peripheral sensitization in contrast to central sensitization which occurs at the dorsal horn. Chronic pain. At the dorsal horn, in addition to releasing substance P, C fibres release other excitatory neurotransmitters: glutamate, aspartate, calcitonin gene related peptide (CGRP), and a gas, nitric oxide (see Jensen, 1996, fig.1, p.82).

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)

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.

43 Pain continuing or worsening when the cause is stable or improving.
“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.

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 that it impaired their work or leisure activity but only 4.5% had sought medical advice (Bay Nielsen et al 2001)

45 CHRONIC PAIN Once established often relatively difficult to treat. Can be resistant to ordinary analgesia. Psychosocial interventions needed, central changes, autoimmune components.

46 Recent Developments Better understanding of the mechanisms
Improved use of assessment tools Advances in imaging – CAT, PET and fMRI Evidence based health care – improved guidelines and algorithms New drugs for pain management New modes of delivery & more appropriate use The role of non pharmacological therapy - cognitive and behavioural strategies

47 Summary Pain is multidimensional
The assessment and management of pain should reflect the sensory, affective and cognitive components Sociocultural components are important Future developments are likely to focus on genetic variability

48 PART 4: Entonox

49 Identification Presented in cylinders that are painted blue with a white and blue shoulder. The gas is pressurised and is self administered by the patient via a pressure regulator and demand valve.

50 Mechanism of Action True mechanism of analgesia is not known.
The effects of Entonox take place within the pain centres of the brain and spinal cord. The gas forms an essential ingredient in general anaesthesia.

51 Pharmacokinetics Entonox is an analgesic agent that is composed of 50% nitrous oxide and 50% oxygen. It offers rapid onset of potent analgesia with speedy reversal of effects. It is inhaled, absorbed through the lungs into the blood within which it is carried to the brain where analgesia occurs.

52 Pharmacodynamics The effects of Entonox are felt within three to four breaths and maximised after 2 minutes. The effects rapidly disappear once Entonox inhalation is discontinued. Residual effects are hard to display after minutes. Despite this patients are usually advised not to drive for 12 hours.

53 Metabolism and Excretion
Entonox is rapidly excreted from the body. It is excreted, largely unchanged, by the lungs into the surrounding air.

54 Toxicity Prolonged use of Entonox in an enclosed space may subject staff to undue exposure. Prolonged use (exceeding 6-8 hours) may have an adverse effect on vitamin synthesis. Use over 6 hours may also interfere with folate metabolism and DNA synthesis which can impair bone marrow function.

55 Use of Entonox Ideal for situations where pain is of short duration.
Can be used in combination with other analgesics such as paracetamol, NSAIDs and opioids. A mouthpiece/face-mask and bacterial filter is required for individual patient use. The gas is safe for any age group as long as they are able to comprehend and physically operate the system.

56 Clinical Uses of Entonox
Changing dressings, packs and removing drains Suturing and removing sutures Redressing burns Invasive procedures : catheterisation, cannulation, sigmoidoscopy Changing and removing clothing Applying traction; removing skeletal pins Physiotherapy Renal colic; constipation Lifting and moving patient

57 Precautions Patient refusal or known allergy
Entonox will cause an enclosed air pocket in the body to expand rapidly in volume as the gas mixture is absorbed from the blood into the space. Therefore Entonox is contra-indicated in all cases where there is air trapped within a body space.

58 Contraindications Artificial, spontaneous or traumatic pneumothorax
Intestinal obstruction Air embolism, following a recent underwater dive/ decompression sickness Myringoplasty Intoxication Severe bullous emphysema Head injuries with impaired consciousness. Maxillofacial injuries with a risk of inhaling blood Patient non-compliance

59 Drug Interactions There are no major incompatibilities with other drugs and Entonox, when used with other analgesics, can form part of an effective multimodal approach to pain control.

60 Side Effects May cause drowsiness
Allergic and sensitivity reactions are rare Minor effects on the heart and cardiovascular system Minimal effects on respiration Can cause nausea


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