THE NERVOUS SYSTEM ANALGESIC REVIEW

1. THE NERVOUS SYSTEMANALGESIC REVIEW ANALGESIC REVIEW CSHALDERS/GOIT/2008

2. CSHALDERS/GOIT/2008

3. PAIN • Pain is a symptom of many conditions • It is what the client says it is • Pain can be medically induced • Pain triggers fear and anxiety and can hinder the healing process CSHALDERS/GOIT/2008

4. PAIN • Classification of pain • Productive pain- occurs immediately after tissue damage • This is a warning pain that one can react to therefore avoid deteriorating sequele • EG. Touching something hot CSHALDERS/GOIT/2008

5. PAIN • Non Productive Pain • Often caused by tissue injury one has minimal control over it • Eg. Occurs when stomach ulcer perforates CSHALDERS/GOIT/2008

6. PAIN • Visceral pain – emanates from the internal organs and involuntary tissues of the torso • Non narcotic drugs have little effect on visceral pain • Musculoskeletal pain – responds well to non narcotic analgesia • Pain that originates in the nervous system – called neuropathic pain requires treatment from non analgesics such as phenytoin or carbamazepine CSHALDERS/GOIT/2008

7. PAIN • Acute pain is characterised by sudden onset and transient in nature • Site of pain usually well identified • Chronic pain is prolonged lasting longer than 6 months • Treatment rarely offers complete relief • A sense of hopelessness and depression can accompany chronic pain CSHALDERS/GOIT/2008

8. PAIN • Pain Transmission • Starts in the periphery with the stimulation of pain receptors connected to the afferent nerve fibers • Large myelinated fibers (A fibers) conduct impulses very quickly • This usually transmits sharp localised pain to the CNS CSHALDERS/GOIT/2008

9. PAIN • Unmyelinated small fibers (C fibers) have slow transmission rates in chronic severe pain • Tend to transmit dull diffuse pain such as aching sensations • C fibers are usually activated by strong stimuli. • The cell bodies of the afferent fibers lie in the dorsal root ganglia just outside the spinal cord • These ganglia may be resented to produce nerve blocks CSHALDERS/GOIT/2008

10. PAIN • In pain transmission the spinothalmic tracts are the most important ascending pathways • Within the brain the information is sorted and sent to the cortex for final processing • The pain is perceived or felt at this level • Pain information is also processed in the brainstem , midbrain limbic areas. CSHALDERS/GOIT/2008

11. PAIN • These brain areas triggers the emotional and autonomic nervous system responses to pain • The experience of pain can be altered through the neuromodulation of these pathways from the periphery to the brain CSHALDERS/GOIT/2008

12. PAIN • Pain Assessment • Individual, subjective, and complex influenced by culture, prognosis, diagnosis, values, fears and anxiety • Different descriptors can be used to rate a persons pain • No pain, mild, moderate, severe • The verbal numerical scale 1-10 CSHALDERS/GOIT/2008

13. PAIN • Pain assessment • It is important to assess during movement, activity and rest • Document to ensue that the clients ongoing analgesic needs are effectively monitored and evaluated CSHALDERS/GOIT/2008

14. PAIN • Pain assessment • Establish the pathology of the pain • Identify the appropriate analgesics for this pain • How will patients co morbidities influence our management plan • Are symptoms of chronic pain developing CSHALDERS/GOIT/2008

15. Pain CSHALDERS/GOIT/2008

16. ANALGESICS • ANALGESICS • Pain “an unpleasant sensory and emotional experience associated with actual or potential tissue damage” CSHALDERS/GOIT/2008

17. Pain • Paracetamol • Analgesic and antipyretics • Hepatic Toxicity may increase in chronic alcoholism • Do not exceed 4 grams/day in adults • Routes oral IV PR • Remember to check other analgesics do not contain paracetamol eg. Mersyndol digesic CSHALDERS/GOIT/2008

18. Pain • NSAIDS • Analgesic and Anti inflammatory • Also antipyretic and anti-platelet actions • Precautions • Gastrointestinal irritation • Dehydrated/Shocked patient may cause acute renal failure • Route oral IV PR • Review after 2-3 days treatment CSHALDERS/GOIT/2008

19. Pain • Tramadol • Weak opiod effects • Precautions • Avoid in patients with seizures • Renal failure and elderly patients • Elderly patients reduced elimination(leading to accumulation or active opiod metabolites) • Routes Parental & PO CSHALDERS/GOIT/2008

20. Pain • Opiods • Drugs that have morphine like action • Calculated by age rather than weight in adults CSHALDERS/GOIT/2008

21. Pain • MORPHINE • Standard at which all opiods are compared • Naturally occurring opiod (papaver somniferum) • Routes IV SC PO PR • Fentanyl • Routes IV Lozenges Transdermal CSHALDERS/GOIT/2008

22. Pain • Pethidine • Useshould be discouraged in favour of other opiods • Oxycodone • Ususually well tolerated • Metabolised by liver • Codeiene • Regarded as a weak opiod • Not metabolised in some patients CSHALDERS/GOIT/2008

23. Pain • Local anesthetics • Act by binding to receptor sites in the sodium channel preventing the influx of sodium ions and therefore blocking conduction of the nerve impulse. The nerve size and degree of myelination will determine the speed of local anesthetic onset. ie the smaller the nerve the more rapid the onset CSHALDERS/GOIT/2008

24. Pain • IV SC SL Intrathecal Epidural • Short acting : lignocaine • Longer acting : ropivicaine bupivicaine • Be aware of local anesthetic toxicity CSHALDERS/GOIT/2008

25. Pain • Bupivicaine • More toxic but has widespread use • When injected caudally it becomes highly protein bound, which lessens its toxic effect • If giving during labour doesn’t cross the placental barrier hence little effect on foetus • Long duration of action 3-14 hours useful for spinal blocks • Onset of action 15-20 mins after injection CSHALDERS/GOIT/2008

26. Pain • Ropivicaine • Slightly more potent • More action on sensory nerve transmission • Less action on CNS and cardiovascular • Used regional blocks and epidural CSHALDERS/GOIT/2008

27. Pain • Lignocaine • Commonest local anaesthetic • Used spinal, injecatable, gels etc • Used intravenously as an antidysrythmic • Also added to some agents to prevent local irritation CSHALDERS/GOIT/2008

28. Pain • Vasoconstrictors such as adrenaline can be used to prolong the action of local anaesthetics and reduce the incidence of adverse effects CSHALDERS/GOIT/2008

29. Pain • Neuropathic agents • Tricyclic antidepressants eg. Amitriptyline in low doses • Anticonvulsants eg sodium valprate phenytion • Antiarrythmics eg IV lignocaine followed by oral mexilitene • Topical agents eg. Capsaicin, lignocaine CSHALDERS/GOIT/2008

30. Pain • Non Pharmacological Treatments • Heat/Cold packs • Massage • Exercise • Physiotherapy • Acupuncture • TENS • Reassurance, education relaxation hypnosis CSHALDERS/GOIT/2008

31. Physiology of pain • THE GATE CONTROL THEORY • The gate control theory proposes that a mechanism in the dorsal horn of the spinal cord the can modify the transmission of painful sensations from the peripheral nerve fibers to the thalamus and cortex of the brain. The gate is influenced by control systems with noradrenaline, serotonin, substance P and enkephalins in particular as neurotransmitters. CSHALDERS/GOIT/2008

32. Physiology of pain • Facilitation in the dorsal horn area results in increased insensitivity, which spreads beyond the injured area. Conversely techniques of afferent stimulation to relieve pain such as TENS, acupuncture, and rubbing the skin are thought to act through inhibitory circuits within the dorsal horn to diminish nociceptive transmission through the C fibers thus decreasing pain. (closing the gate) CSHALDERS/GOIT/2008

33. ENDOGENOUS OPIODS • ENDOGENOUS OPIODS • There are high concentrations of receptors for the body’s natural options, the endorphins and encephalin, in many areas of the CNS, particularly the grey matter of the mid brain, in the limbic system and at the interneurons in the dorsal horn areas. CSHALDERS/GOIT/2008

34. ENDOGENOUS OPIODS • The enkephalins, endorphins and dynorphin are thought to be the body’s natural pain relieving chemicals and to act by enhancing inhibitory effect at opiods receptors. • The analgesic drugs, opiods such as morphine and codeine, cause their effect by mimicking the actions of endorphins and enkephalins on opiod receptors. CSHALDERS/GOIT/2008

35. PROSTAGLANDINS • PROSTAGLANDINS • Damage to tissue may directly activate sensory nerves and sets in chain the processes of inflammation, in which are large number of inflammatory mediators are released. Prostaglandins lower the threshold of nocicetors to other mediators. CSHALDERS/GOIT/2008

36. TACHYKININS • TACHYKININS • Another group in the nociceptive pathway are the tachykinins. They are involved in the inflammatory and neurogenic pain. • Acute pain at state in which an individual experiences the sensation of nerve discomfort, has a sudden onset, and usually subsides with treatment. EG. Myocardial infarction, burn appendicitis and kidney stones. CSHALDERS/GOIT/2008

37. Chronic pain • Chronic pain is a persistent or recurring pain that continues for a long time and may be difficult to treat effectively. Regular medication with NSAID analgesics and in addition of an antidepressant is advised. CSHALDERS/GOIT/2008

38. NOCICEPTIVE PAIN • Arises from stimulation of superficial or deep nocieptors by noxious stimuli such as tissue injury or inflammation • Somatic nociceptive pain originates in the skin, mucosal surfaces, bones and joints, pleura and peritoneum. Described as throbbing, burning, stinging or a dull • ache. Responds best from treatment with NSAIDs CSHALDERS/GOIT/2008

39. Visceral nociceptive pain originates in organs and large muscle masses. Described as deep, diffuse and nagging and may be associated with nausea and vomiting or sweating. • Examples include pain from bowel obstruction, abdominal tumors, ischemic muscle or major surgery. Respond best with treatment from opiod analgesics CSHALDERS/GOIT/2008

40. NEUROGENIC PAIN • NEUROGENIC PAIN • Arises from a primary lesion, alteration or dysfunction in the peripheral or central nervous system. May be due to nerve compression. Neuropathic neurogenic pain is caused by peripheral nerve injury rather than stimulation It is often associated with parathesia. Eg Limb amputation, diabetic neuropathy or cancer tumor invasion may be accompanied by sympathetic nervous system dysfunction. Responds to adjunct medication (eg anticonvulsant, local anaesthetic or tricyclic antidepressants. CSHALDERS/GOIT/2008

41. PSYCHOGENIC PAIN • PSYCHOGENIC PAIN • Has psychological, psychiatric or psychosocial causes. It is a CNS syndrome and may have no obvious somatic cause. Responds with drug therapy and psychotherapy. CSHALDERS/GOIT/2008

42. PRINCIPLES OF PAIN MANAGEMENT • Treat the cause of pain where possible • Accurate diagnosis and assessment to select the right analgesic • Keep the patient pain free • Dose at regular specified intervals • Prevent adverse effects • Step up doses where required CSHALDERS/GOIT/2008

43. ROUTES OF ADMINISTRATION • Oral route, simplest and most acceptable • Continuous infusion used when there is severe pain over a period of days • The rectal route useful for patients who cannot swallow, or who are vomiting and for slower absorption • Transdermal administration effective for chronic administration. • Intravenous injection is the fastest route for rapid pain relief CSHALDERS/GOIT/2008

44. Narcotic Analgesics • They have an action only on the CNS. These drugs act to suppress pain. • Centrally acting narcotic analgesics stimul;ate opiod receptors within the CNS • Chemoreceptor trigger zone (CTZ) within the medulla is stimulated by many narcotics • This can lead to nausea and vomiting, this is worse in the ambulant patient CSHALDERS/GOIT/2008

45. Narcotic Analgesics • GIT tract has many opiod receptors which can cause decrease in peristaltic movements • This leads to an increase in water absorption and a consequent thickening of the bowel, resulting in constipation • Narcotics contract biliary smooth muscle which may result in spasm therefore contraindicated in bilary colic CSHALDERS/GOIT/2008

46. Narcotic Analgesics • Most cause depression of the cough and resp centre in the CNS • Chronic tolerance is another problem, and develops quite rapidly • Miosis (pupil restriction) occurs with narcotic drugs Profound constriction is indictive of an overdose CSHALDERS/GOIT/2008

47. Narcotic Analgesics • Clinical Considerations • Analgesic required varies between patients due to tolerance, previous experience with pain • Start with lower dose when changing narcotic • Narcotic analgesic combined with a non steroidal anti inflammatory drug, esp for bone pain or tumour metastasis CSHALDERS/GOIT/2008

48. OPIOD ANLGESICS • OPIOD ANLGESICS • The prototype opiod analgesic most commonly used is morphine • High affinity binding sites for enkephalines and endorphins are located in the membranes of the central neurons and are responsive to various opiods. • At the spinal level morphine stimulates opiod receptors and thus inhibits release of substance P from the dorsal horn neurons. • At the supraspinal level iods act to close the gate in the dorsal horn thus inhibiting afferent transmission. Opiods also alter perception and emotional responses to pain. Pain perception is inhibited which enhances analgesic effect of morphine. CSHALDERS/GOIT/2008

49. OPIOD ANLGESICS • Central effects • Effects of opiods in the CNS include • Analgesia • Suppression of the cough reflex • Suppression of the respiratory centre • Sedation and sleep • Euphoria • Dysphoria (hallucinations) • Miosis (pinpoint pupils) • Hypotension and bradycardia • Tolerance and dependence of addiction CSHALDERS/GOIT/2008

50. OPIOD ANLGESICS • Effects of opiods in the PNS include • Decreased motility of the gut • Spasms of sphincter muscles, delayed gastric emptying, urinary retention • Suppression of some spinal reflexes • Release of histamine causing bronchoconstriction and itching CSHALDERS/GOIT/2008