Pain

Dr Ruwan Kuruppu

Pain

an unpleasant sensory and

emotional experience associated
with actual or potential tissue
damage

Pain Process
The

neural mechanisms by which

pain is perceived involves a process
that has four major steps:
Transduction
Transmission
Modulation
Perception

Facilitating Transduction

Biochemical mediators: Chemical Soup

Prostaglandins
Bradykinins
Serotonin
Histamines
Cytokines
Leukotrienes
Substance P
Norepinephrine

Peripheral Excitatory
Mediators
(Pain)
Substanc
e
Substance P
(SP)

Receptor
NK1

Prostaglandin ?
(PG)
Bradykinin

B2

Mechanism
neuronal excitability,
edema
Sensitize nociceptors,
inflammation, edema

(normal)

B1

Sensitize nociceptors
PG production

(inflammation)

Histamine

H1

C-fiber activation, edema,

vasodilatation

Serotonin

5-HT3

C-fiber activation, release SP

Norepinephri
ne

Sensitize nociceptors
Activate nociceptors

Peripheral sensitization
Peripheral

opioid receptors
Management of histamine

Postoperative Pain Relief..

Why

is it important?

Ethical
Minimize the systetmic responses

to pain

What are the systemic

responses to pain?

CVS
Hypertension
Tachycardia
SVR increased
CO increased or decreased
Myocardial O2 demand increased

RS

Increased MV due to increase of total body O2

consumption and CO2 production
Increased work of breathing
Thoracic and abdominal incisions further compromise
pulmonary function due to splinting effect
Reduced movement of chest wall

low TV
reduced FRC
promote atelectasis
intrapulmonary shunting
Hypoxaemia
Reduced VC
impair coughing and clearing secretion
prolong bed rest or immobilization can produce similar
changes in pulmonary changes.
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GI and Urinary Effects

Increased sympathetic tone

sphincter tone increased and reduced intestinal

& urinary motility promoting ileus urinary

retention respectively

hypersecretion of gastric acid

promote stress ulceration.

gastric acid, ulceration, reduces motility

potentially predisposes sever aspiration
pneumonitis
nausea, vomiting and constipation are
common
Abdominal distention further aggravate loss
of lung volume and pulmonary dysfunction.

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Endocrine Effects

The hormonal response to stress catabolic

hormone (catecholamines, cortisol, glucagon) and
reduced anabolic hormone (insulin, testosterone)
Patient develop ve nitrogen balance, carbohydrate
intolerance and increased lypolysis
increased cortisol and renin, aldestorone,
angiotensin, ADH results in Na retention, H2O
retention, secondary expansion of the extracellular
space.

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Continue.
Haematologic effects
Stress mediated increased in platelet adhesiveness
reduced fibrinolysis and hypercoagulability
together with immobility lead to DVT
Immune effects
Stress response produces leukocytosis with
lymphopenia depress the reticuloendothelial system
The later predispose patients to infection

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Pain Assessment

P recipitating/Alleviating Factors:
What causes the pain? What aggravates it? Has

medication or treatment worked in the past?

Q uality of Pain:

Ask the patient to describe the pain using words like

sharp, dull, stabbing, burning

R adiation

Does pain exist in one location or radiate to other areas?

S everity

Have patient use a descriptive, numeric or visual scale to

rate the severity of pain.

T iming

Is the pain constant or intermittent, when did it begin,

and does it pulsate or have a rhythm

Pain Assessment Tools:

Wong-Baker

Pain Assessment Tools:

Non-Verbal Pain Scale (FLACC)

TYPES OF PAIN
SURGICAL PAIN
Sensitization of nerve
ends causes
spontaneous firing
driving the pain
system
in the spinal cord
Glutamate receptor
(NMDA subtype) not
essential
Cox 1 blocks

INFLAMMATORY
PAIN
No sensitization in
simple
inflammation
Glutamate
receptor
essential

ACUTE PAIN MANAGEMENT

Simple

analgesics
- Paracetamol
Stronger analgesics
- NSAID
Weak opiates
- codeine, tramadol
Strong opiates
- morphine
Local anaesthetics
- bupivacaine
General anaesthetics - ketamine

OTHER METHODS
Immobilization
Relaxation techniques
Heat & cold fomentation
Massage
Exercise
TENS, Acupuncture
Hypnosis

CHRONIC PAIN
Acute Pain: Mechanisms, Management, and Treatment Options

WHO Analgesic Ladder

1
World Health Organization, 1990. Used with permission.

CHRONIC PAIN
LA

io
Op

id

LA

LA

LA
LA

ol
ad
am
/ tr
AID
S
N

LA
m
eta
r ac
Pa

ol

Multimodal Anaelgesia
Acute Pain: Mechanisms, Management, and Treatment Options

Multimodal Analgesia
An Example
Morphine

Reduced doses of each

analgesic
Potentiation

NSAIDs,
NSAIDs,
acetaminophen,
acetaminophen,
nerve
nerve blocks
blocks

Kehlet H, Dahl JB. Anesth Analg. 1993;77:10481056.

Improved
antinociception due to
synergistic/additive
effects
May reduce severity of
side effects of each
drug

Non-opioid simple analgesic

paracetamol, asprin,NSAIDS
Mechanism of actions
Advantages:1.
2.
3.
4.
5.

Devoid major side effects

Cost effectiveness
Easy to use
Well absorb enterally
No CNS impairment

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Non-opioid analgesic paracetamol,

NSAIDS

Disadvantages:1. Effective only for mild to moderate

2. NSAIDS
Peptic ulceration
Platelet dysfunction
Acute renal insufficiency and renal
capillary necrosis
? Asthma

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Mild-opioid analgesic
Codeine, tramadole
Codeine
Effective for moderate pain
Commonly use in combination of nonopioid
simple analgesic
Well absorb but first- pass metabolism limits
systemic delivery
If prescribe on a fixed schedule, stools
softeners or laxatives may be indicate

25

Tramadol

Mode of action
Pharmacokinetics
Advantages
Contraindication
Adverse effects

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Major-opioid analgesic pethidine,

morphine

Effective for severe pain

Analgesia is achieved at a specific blood level
for each patient for a given pain intensity. That
point is referred to as the minimum effective
analgesic constrain (MEAC). Small increases
above this point produces a large increasing
analgesia

27

Major-opioid analgesic
Continues
Can be administered in various roots SC, IM,
IV, PCA, Intra spinal
What ever the mode of administration, one has
to aware of the side effects

28

SC & IM
Advantages:1. Very familiar technique
2. Not involve with sophisticated equipment
or special skills
Disadvantages:3. Pain on injection
4. Unpredictable blood level

29

IV
Solve the problem with unpredictable absorption
but not necessary those of correct dosing. An
optimal balance between adequate analgesia,
sedation and respiratory depression can be
achieved by frequent intermittent small doses of
opioid.
Therefore, this technique is very labour intensive
and require close monitoring of reparative
depression.
Useful in:
1. Recovery area
2. Before physiotherapy
30

PCA
Advantages:1. Cost effective
2. Very high patient satisfaction
3. Minimal fluctuation in blood level
4. Very flexible
5. Patients has the control of his/her pain

31

PCA

continued.

Disadvantages:1. Possibility in over dosing

2. Respiratory depression is still possible
3. Not suitable for all patients
4. Need patients education
5. Patient may not press the button due to
sedative effect of anaesthetic
6. Mechanical error
. Malfunction of the PCA
. Siphoning backing of IV line
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Safety precautions
1.
2.
3.
4.
5.
6.

Lockout period and set up maximum amount

that can be given over a period
Syringe is kept at below the patients level to
avoid siphoning
Incorporate anti-siphoning value and
unidirectional value to the tubing
Patients monitors hourly
Instruction to the nursing staff in how to deal
the over dose and under dose
Naloxone and equipment to give oxygen and
facilities to ventilate should be available at
hand
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Intrathecal or epidural Opioid

Excellent

analgesia 4 24 hrs
Significant synergism with diluted LA

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Contradiction - Side Effects

Serious side effects are dose dependent
1. Delayed respiratory depression
2. Itching-response small doses of
naloxone 0.04mg
3. Nausea and vomitingmetoclopramide 5-10 mg,
ondansetron 4 6mg, droperidol
0.625mg
4. Urinery retention
5. Ileus
6. Sedation
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Local Anaesthetic
1.
2.
3.

Local infiltration
Peripheral nerve blocks
Central neural block

Disadvantage sympathetic and

motor block

36

Contradiction
Same as intrathecal opioid
Preemptive Analgesia
Multi Model drug therapy
Simple analgesic + opioid + LA

37

TREATMENT OF CHRONIC
PAIN
Na

channel block
Anti-depressants : phenytoin, Na valproate,
clonazepam
Anti-convulsants : carbamazepine
Ca channel block
: Gabapentin, Mg,
NMDA block
: ketamine, canabinoids
Sympathetic block
: guanethidine
GABA enhanced
: midazolam, baclofen
Inhibitory receptor stim. : opiate, cannabinoid
Release & deplete transmitter : capsacin
Prevent re-uptake of transmitter adr,nor : TCA,
tramadol

Thank you

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