2 IntroductionThis 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 AnalgesiaPart 2 – Postoperative Nausea and VomitingPart 3 – The Multidimensional Nature of PainPart 4 - Entonox
4 Epidural AnalgesiaInvolves 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/bedstayNeeds much less opioid, resulting in reduced side effects such as PONV, delayed nutrition, sedationReduced respiratory infectionsIncreases mobility leading to less muscle wasting and deep vein thrombosis
6 Locating the Epidural Space Spinal cordSpinal column
7 Spinal NervesCervical - 8 pairs interconnect to form the cervical plexus and the brachial plexus. These innervate the back of the head, neck, shoulders, arms, hands and diaphragmThoracic - directly connected to the muscles between the ribs, deep back muscles, abdomen and thoraxLumbar - supplies the muscles of the lower limbs and trunk, external genitalia, groin and lower limbsSacral - forms the sacral and coccygeal plexus, innervating the thighs, buttocks, legs, feet and the anal/genital areaCoccyx - one pair of nerves supplies the skin in the region of the coccyx
8 Who may benefit from an epidural? Patients recently undergone abdominal incisionsSerious pelvic & leg fracturesMajor pelvic and leg surgeryParticularly useful following chest trauma
9 Epidural is performed with the patient sitting or lying down with their back curved outwards
11 Caudal AnalgesiaThis 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 AnaestheticsBlocks the initiation and spread of action potentials within the nervesBlocks 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 OpioidsThought to bind to opioid receptors in the substansia gelatinosa of the spinal cord interfering with the pain impulseProvides analgesia which lasts longer than systemic opioidsDoes not cause motor or sensory blockade, or hypotensionFentanyl mcg will last around hoursDiamorphine mg will last hours
14 Opioid Side EffectsEffects receptors in the medullary respiratory centre leading to potential respiratory depressionSedationItchingNausea
15 Local Anaesthetic Side Effects Local anaesthetics block conduction in all types of nerves:Sympathetic block - hypotension, urinary retentionSensory block - pressure soresMotor block - weakness, immobility, falls.
16 Complications of Combined Local Anaesthetic/Opioid Epidurals Early:HypotensionHigh sensory and motor blockRespiratory depressionSedationCardiovascular complicationsHead/neck/backacheAnaphylaxisLate:HaematomaEpidural abscessInfection and sepsisUnresolved motor and sensory lossItchingLeaking epidural
17 The Ideal Outcome A sensory pain block with no motor block and minimal side effects. An alertpatient capable of earlymobilisation and able to participate inactive physiotherapy.
19 PART 2: Postoperative Nausea and Vomiting (PONV)
20 Why Treat Nausea and Vomiting? Humanitarian reasonsIncrease in autonomic activityIncrease in closed compartment pressureDelayed hydration and nutritionDelayed discharge from hospitalDelayed 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 sicknessFemales > males (pre menopause)Young > oldType of procedure performedUse of opioids
23 Chemical Receptors in the Vomiting Centre in the Brain Acetylcholine:cyclizine, hyoscineDopamine antagonist:droperidol, metoclopramide, phenothiazines5 Hydroxytryptamine (serotonin):ondansetronHistamine
24 Antiemetics All give 30-45% reduction of symptoms at best May reduce vomiting more than nauseaPharmacodynamics/kinetics poorly understood for older drugsMultimodal 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. PLUSDexamethasone 8mg i.v.
26 Summary Carry out a risk assessment Prophylaxis Avoid emetogenic drugs if possibleCombination therapiesComplementary therapiesEducate patients and staff
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 1986Acute 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 1986Chronic 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, mixedAcute on Chronic episodic/backgroundVisceralIdiopathic
33 Acute TO Chronic PainPain 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 painCancer related painSomatic pain (superficial & deep)Visceral painNeuropathic painChronic painUsually depression and anxietyPoor sleep, appetiteReduced social activityWork affectedNot obvious they have painSomatic pain1) Superficial – cutaneous2) Deep - connective tissue, muscle, bone, jointsVisceral painAffects visceral tissues – intestineHollow viscus organs - stomach
35 Theories of Pain Specificity theory Pattern theory Neuromatrix Gate Control TheorySpecificity (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.PatternSpecific 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 theoryThis 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.NeuromatrixSince 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’ mechanismLarge diameter fibres (touch) ‘closed’ the gateSmall diameter fibres (nociceptors) ‘opened’ the gateAffective/cognitive descending ‘modulation’Pain is multidimensionalSensory 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” painBright, sharpSomaticC FIBRES:Unmyelenated, slow (.5-2 m/s) “slow” painDull diffuse, continuous, deepA 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 BetaA DeltaA- betaLarge unmyelinatedA-deltaC fibresC FibresSubstantia Gelatinosa
39 Limbic system Autonomic response “GATING” MECHANISMSLocated within the dorsal horn of the spinal cord, but also found within the brain stem, hypothalamus and thalamusSomatosensory cortex4Limbic systemAutonomic responseThalamusHypothalamus5BrainstemDescending mechanismAscending mechanismUse 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 levelSome 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 levelOther 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.1Sensory input from the periphery32Substantia gelatinosa
40 Physiology (Sensory) Nociceptors A-delta, B-delta, C fibres Chemicals – histamine, bradykininNeurochemical mediatorsAscending transmissionDescending transmissionPain 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 - remappingC fibresActivity 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 HyperalgesiaReduction in the pain threshold in the area of damage. e.g. skin burn, pharyngitis, sprained ankleLocally 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 painCentral 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 thresholdAugmented responseOngoing activityPain 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 PAINOnce 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 toolsAdvances in imaging – CAT, PET and fMRIEvidence based health care – improved guidelines and algorithmsNew drugs for pain managementNew modes of delivery & more appropriate useThe 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 componentsSociocultural components are importantFuture developments are likely to focus on genetic variability
49 IdentificationPresented 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 PharmacokineticsEntonox 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 PharmacodynamicsThe 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 ToxicityProlonged 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 drainsSuturing and removing suturesRedressing burnsInvasive procedures : catheterisation, cannulation, sigmoidoscopyChanging and removing clothingApplying traction; removing skeletal pinsPhysiotherapyRenal colic; constipationLifting 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 obstructionAir embolism, following a recent underwater dive/ decompression sicknessMyringoplastyIntoxicationSevere bullous emphysemaHead injuries with impaired consciousness.Maxillofacial injuries with a risk of inhaling bloodPatient non-compliance
59 Drug InteractionsThere 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 rareMinor effects on the heart and cardiovascular systemMinimal effects on respirationCan cause nausea