ANALGESIA and LOCAL ANAESTHESIA - HEMI Australia · ANALGESICS . 1. Mild pain - NSAID + adjuvant 2....
Transcript of ANALGESIA and LOCAL ANAESTHESIA - HEMI Australia · ANALGESICS . 1. Mild pain - NSAID + adjuvant 2....
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.