ANALGESIA and LOCAL ANAESTHESIA - HEMI Australia · ANALGESICS . 1. Mild pain - NSAID + adjuvant 2. Moderate pain - weak narcotic + NSAID + adjuvant 3. Severe pain - strong narcotic

ANALGESIA and

LOCAL ANAESTHESIA

Professor Donald G. MacLellan

Executive Director

Health Education & Management Innovations

Definition of Pain

“ Pain is an unpleasant sensory and

emotional experience with actual or

potential tissue damage or described in

terms of such damage. ”

International Association for the Study of Pain

Simpler Definition :

“ Pain is what the patient says is hurting. ”

We have to BELIEVE what the patient says!

Pain gate open

Detection by

nociceptors (sensory receptor cells)

Transmission by

neurons

PAIN

Central

Nervous

System

Central

Nervous

System

White & Harding, 2006

Peripheral nervous system

Processing

by brain (perception)

Nociception (the encoding and processing

in the nervous system of noxious stimuli)

Four Processses:

Transduction

Transmission

Perception

Modulation

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

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

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

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

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)

Neuropathic Pain

• PNS damaged

• Neuroplasticity – neuronal sprouting in Dorsal

Horn

• Pain – burning, tingling, shooting, like electric

shocks, radiating

• Can be severe and unrelenting

ANALGESICS

1. Mild pain

- NSAID + adjuvant

2. Moderate pain

- weak narcotic + NSAID + adjuvant

3. Severe pain

- strong narcotic + NSAID + adjuvant

4. Regional analgesia

WHO LADDER

ANALGESICS

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 A2

–Involved in platelet

–aggregation

Aspirin

(Acetylsalicylic Acid)

Good

• Pain relief

• Fever

• Inflammation

Bad

• GI ulceration:

– Gastric acidity

– GI protection

• Bleeding

• Renal elimination

• Uterine

contractions during

labor

Acetaminophen

(Paracetamol)

• NSAID similar to aspirin

• Only inhibits synthesis of CNS

prostaglandins

• Does not have peripheral side effects

of ASA

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

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)

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.

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.

SEDATIVES

Diazepam

• Benzodiazepine with sedative and amnesic

properties

• Depresses the CNS at the limbic and

subcortical levels of the brain

• Depresses the ventilatory response to

PaCO2

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

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

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

PaCO2

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

LOCAL ANAESTHESIA

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

ADVANTAGES

• postoperative analgesia

• reduction in surgical stress

• earlier discharge for outpatients

• less expense

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

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

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

Systemic Toxicity of

Local Anaesthetics

• Addition of Epinephrine causes local

vasoconstriction and slows absorption

• Follow recommended dose

CNS Toxicity

• Unconsciousness

• Generalized convulsions

• Coma

• Apnoea

• Numbness of the mouth and tongue, metal

taste in the mouth

CNS Toxicity

• Light-headedness

• Tinnitus

• Visual disturbance

• Muscle twitching

• Irrational behaviour and speech

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

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.

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

Avoid Bupivacaine CVS

adv events

Application for

Intact Skin

Lidocaine

(Lignocaine)

• amide type anaesthetic

• the most commonly used local anesthetic

• rapid onset and a duration of 60-75 minutes

• extended when solutions with epinephrine

are used for up to 2 hours

• metabolized in the liver and excreted by the

kidneys.

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%

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

Reversal Agent

For Narcotics

Naloxone

• narcotic antagonist

• use in the management and reversal of

overdoses caused by narcotics or

synthetic narcotics

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

DOSE AND ROUTES

Naloxone

• 1-2 MG IV q5min up to 3 times

• Continuos infusion may be started at 400

mcg/hr.

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;18:217-33.

• Achar S, Kundu S. Principles of office anesthesia: part I. Infiltrative anesthesia. Am Fam Physician. 2002;66(1):91-4.