ANALGESIA and LOCAL ANAESTHESIA. Professor Donald G. MacLellan Executive Director Health Education & Management Innovations

Transcription

1 ANALGESIA and LOCAL ANAESTHESIA Professor Donald G. MacLellan Executive Director Health Education & Management Innovations

2 Definition of Pain Pain is an unpleasant sensory and emotional experience with actual or potential tissue damage or described in terms of such damage. Simpler Definition : International Association for the Study of Pain Pain is what the patient says is hurting. We have to BELIEVE what the patient says!

3 Peripheral nervous system Processing by brain (perception) PAIN Pain gate open Central Nervous System Central Nervous System Transmission by neurons Detection by nociceptors (sensory receptor cells) White & Harding, 2006

4 Nociception (the encoding and processing in the nervous system of noxious stimuli) Four Processses: Transduction Transmission Perception Modulation

5 Nociception - Transduction Nociceptors exposed to noxious stimuli Noxious stimuli mechanical (pressure, swelling, incision..) thermal (burn, scald) chemical (toxic substance, ischaemia, infection..) Release of chemical mediators from damaged cells (Pg, bradykinin, 5-HT, Sub P, K+, histamine) Free nerve endings of C fibres & A-delta fibres of primary afferent neurones respond

6 Nociception - Transmission C Fibres: Small unmyelinated Slow conducting Pain: Diffuse Dull, acing,burninng Slow or second pain A-Delta Fibres: Large myelinated Fast conducting Pain: Well localised Sharp, pricking Fast or first pain

7 Nociception - Transmission Three Stage Transmission: Damage site Fibres Dorsal Horn Sp Cord Brain Stem Spinal Cord Connections between thalamus, cortex & high levels of the brain

8 Nociception - Perception Responses from Multiple Cortical Areas: Reticular System - autonomic & motor response Somatosensory Cortex intensity, type, location of pain & relates to previous experiences Limbic System emotional & behavioural responses

9 Nociception - Modulation Changing or Inhibiting Transmission of pain Impulses: Multiple complex pathways Descending Modulatory Pain Pathways (DMPP) Inhibitory Neurotransmitters (endo opioids, 5- HT,Nor Adr, GABA, Neurotensin, Ach, Oxytocin)

10 Neuropathic Pain PNS damaged Neuroplasticity neuronal sprouting in Dorsal Horn Pain burning, tingling, shooting, like electric shocks, radiating Can be severe and unrelenting

11 ANALGESICS

12

13 WHO LADDER 1. Mild pain - NSAID + adjuvant 2. Moderate pain - weak narcotic + NSAID + adjuvant 3. Severe pain - strong narcotic + NSAID + adjuvant 4. Regional analgesia

14 ANALGESICS

15

16 NSAIDS Inhibit synthesis of cyclooxygenase (COX) Enzyme responsible for synthesis of: Prostaglandins Pain response Suppression of gastric acid secretion Promote secretion of gastric mucus and bicarbonate Mediation of inflammatory response Production of fever Promote renal vasodilation ( blood flow) Promote uterine contraction Thromboxane A 2 Involved in platelet aggregation

17 Aspirin (Acetylsalicylic Acid) Good Pain relief Fever Inflammation Bad GI ulceration: Gastric acidity GI protection Bleeding Renal elimination Uterine contractions during labor

18 Acetaminophen (Paracetamol) NSAID similar to aspirin Only inhibits synthesis of CNS prostaglandins Does not have peripheral side effects of ASA

19

20

21

22 Peripheral Effects Reduced motility of the gastrointestinal tract causing constipation (a major problem with chronic use) Contraction of the biliary tract which may be harmful in patients with biliary colic Histamine release causing itching, bronchoconstriction and hypotension

23 Opioid Medications Morphine: The prototype opioid to which all other are compared Administered orally or by injection, continuous infusion, patient controlled analgesia, spinally Slow release oral forms are available Short half-life (3-4 hours)

24 Opioid Medications Methadone: (long half-life >24 hours, slow onset) is used for chronic pain and for maintenance of addicts. Pethidine: has similar uses to morphine. Known in US as meperidine. Severe interaction with monoamine oxidase inhibitors. Buprenorphine: (long half-life - 12 hours, slow onset) is used in chronic pain. Partial agonist so is not as effective as morphine. Pentazocine: used to treat acute pain. p- receptor action produces dysphoria.

25 Opioid Medications Fentanyl: used for acute pain and anaesthesia. Short half-life of 1-2 hours. High potency allows transdermal patch administration. Codeine: used to treat mild pain and also cough. Little dependence liability. Dextropropoxyphene: similar to codeine but may cause respiratory depression and convulsions. Tramadol: is similar to codeine but also acts by a non-opioid mechanism to inhibit amine uptake.

26 SEDATIVES

27 Diazepam Benzodiazepine with sedative and amnesic properties Depresses the CNS at the limbic and subcortical levels of the brain Depresses the ventilatory response to PaCO 2

28 Diazepam Mild muscle relaxation mediated at the spinal cord level; not at the neuromuscular junction Highly alkaline ph No analgesic properties Drug of choice for seizures

29 ADVERSE REACTIONS & PRECAUTIONS-Diazepam apnoea, respiratory depression, post-op respiratory depression contraindicated narrow angle glaucoma or patients < 6 mths age (in oral form) incompatible with many drugs; when given IV with other medications, the IV line should be adequately flushed should be injected < 5 mg/min to avoid respiratory arrest

30 Midazolam benzodiazepine that has a rapid onset with sedative and amnesic properties depresses the CNS at the limbic and subcortical levels of the brain depresses the ventilatory response to PaCO 2

31 Midazolam no analgesic properties mild muscle relaxation mediated at the spinal cord; not at the neuromuscular junction water soluble - which allows for better absorption following IM injection

32 LOCAL ANAESTHESIA

33 ADVANTAGES patient remains conscious maintain their own airway aspiration of gastric contents unlikely smooth recovery requiring less skilled nursing care as compared to general anaesthesia

34 ADVANTAGES postoperative analgesia reduction in surgical stress earlier discharge for outpatients less expense

35 DISADVANTAGES patient may prefer to be asleep practice and skill is required for the best results some blocks require up to 30 minutes or more to be fully effective

36 DISADVANTAGES analgesia may not always be totally effective - patient may require additional analgesics, IV sedation or a light general anaesthetic toxicity may occur if the local anaesthetic is given intravenously or if an overdose is injected

37 Mechanism of Action - Local Anaesthetics produce a blockade of nerve impulse by preventing increases in permeability of nerve membranes to Na+ ions, slowing the rate of depolarization interact directly with specific receptors on the sodium channel, inhibiting sodium influx

38 Systemic Toxicity of Local Anaesthetics Addition of Epinephrine causes local vasoconstriction and slows absorption Follow recommended dose

39 CNS Toxicity Unconsciousness Generalized convulsions Coma Apnoea Numbness of the mouth and tongue, metal taste in the mouth

40 CNS Toxicity Light-headedness Tinnitus Visual disturbance Muscle twitching Irrational behaviour and speech

41 Cardiovascular Toxicity slowing of the conduction in the myocardium myocardial depression peripheral vasodilatation usually seen after 2 to 4 times the convulsant dose has been injected

42 Prevention of Toxicity Always use the recommended dose Aspirate through the needle or catheter before injecting the local anaesthetic. Intravascular injection can have catastrophic results. If a large quantity of a drug is required, use a drug of low toxicity and divide the dose into small increments, increasing the total injection time. always inject slowly (<10 ml/min) and communicate with the pt.

43 Treatment of Toxicity All necessary equipment to perform resuscitation, induction, and intubation should be on hand before injection of local anaesthetics Manage airway and give oxygen Stop convulsions if they continue for more than 15 to 20 seconds - Diazepam 5 mg to 20 mg IV

44 Avoid Bupivacaine CVS adv events

45

46

47 Application for Intact Skin

48

49 Lidocaine (Lignocaine) amide type anaesthetic the most commonly used local anesthetic rapid onset and a duration of minutes extended when solutions with epinephrine are used for up to 2 hours metabolized in the liver and excreted by the kidneys.

50 DOSE AND ROUTES- Lidocaine Percutaneous infiltration: 0.5%, 1.0% Max dose 4 mg/kg or 7 mg/kg with epinephrine Toxic IV dose: 250 mg Regional infiltration: 0.5% Peripheral nerve: 1.0%, 1.5%, 2.0%

51 ADVERSE REACTIONS & PRECAUTIONS-Lidocaine Contraindicated in patients with a known sensitivity to amide type anaesthetics All local anaesthetics can produce CNS stimulation, depression or both

52

53 Reversal Agent For Narcotics

54 Naloxone narcotic antagonist use in the management and reversal of overdoses caused by narcotics or synthetic narcotics

55 INDICATIONS - Naloxone For the complete and partial reversal of depression caused by the following drugs: Narcotics: Morphine, Heroin, Dilaudid, Percodan, Methadone, Demerol, Paregoric, Codeine, and Fentanyl Synthetic Narcotics: Nubain, Stadol, Talwin, Darvon

56 DOSE AND ROUTES Naloxone 1-2 MG IV q5min up to 3 times Continuos infusion may be started at 400 mcg/hr.

57 Bibliography Principles and Practice of Regional Anaesthesia Wildsmith & Armitage Illustrated Handbook in Local Anaesthesia Ejnar Erikson Tetzlaff JE. The pharmacology of local anesthetics. Anesthesiol Clin North Am 2000;18: Achar S, Kundu S. Principles of office anesthesia: part I. Infiltrative anesthesia. Am Fam Physician. 2002;66(1):91-4.