Pain

1
Pain
An unpleasant sensory and emotional
experience associated with actual or
potential tissue damage, or described in
terms of such damage.
International Association for the Study of Pain
MYTHS
Anesthetics mask symptoms
Patient will harm itself if
theres no pain
Pain is difficult to assess
The Truth!
Pain is BAD:
Decreased cardiovascular function
Decresed appetite
Slows wound healing
Decreased immune function
Greater chance of infection
Increased fear and anxiety

STIMULATION ( )
TRANSMISSION ( )
PERCEPTION ( )
MODULATION ( )
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Mechanism
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Process #2Transmission
Impulsespinal cordbrain stem
thalamuscentral structures of brainpain
is processed.
Neurotransmitters are needed to continue the
pain impulse from the spinal cord to the
brainopioids (narcotics) are effective
analgesics because they block the release of
neurotransmitters
Process #4Modulation of Pain
Changing or inhibiting pain impulses in the
descending tract (brainspinal cord)
Descending fibers also release substances such as
norepinephrine and serotonin (referred to as
endogenous opioids or endorphins) which have the
capability of inhibiting the transmission of noxious
stimuli. Helps explain wide variations of pain among
people.
Cancer pain responds to antidepressants which
interfere with the reuptake of serotonin and
norepinephrine which increases their availability to
inhibit noxious stimuli.
Process #3Perception of Pain
The end result of the neural activity of pain
transmission
It is believed pain perception occurs in the cortical
structuresbehavioral strategies and therapy can be
applied to reduce pain. Brain can accommodate a
limited number of signalsdistraction, imagery,
relaxation signals may get through the gate, leaving
limited signals (such as pain) to be transmitted to the
higher structures.
Nociceptive
Neuropathic
-soft tissue
-bone
-skeletal muscle
-smooth muscle
Nerve
Compression
Nerve
Injury
Classification of Chronic Pain

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Nociceptive
(

)

( )

NSAID

Classification of Pain
Acute Chronic
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Postoperative pain can be divided into:
Acute pain is experienced immediately after
surgery (up to 7 days)
Pain which lasts more than 3 months after the
injury is considered to be chronic pain

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Describing pain only in terms of its
intensity is like describing music only
in terms of its loudness
von Baeyer CL; Pain Research and Management 11(3) 2006; p.157-162
PAIN HISTORY
Description: severity, quality, location,frequency,
aggravating & alleviating factors
Previous history
Context: social, cultural, emotional, spiritual
factors
Patient
Assessment
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Treatment
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Treatment
Non-pharmacologic
Pharmacologic
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Non-Pharmacologic
Stimulation Therapy:
electrical nerve stimulation
Psychological Intervention
relaxation training, and hypnosis, have proven
effective in the management of postprocedure pain
and in cancer-related pain
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Pharmacologic Therapy
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General Treatment Principles
In general, common causes of treatment failure
is Under-dosing
When treating chronic pain, elimination and
prevention of pain is best accomplished by
using analgesics at fixed time intervals rather
than on an as-needed basis
Effective analgesic therapy begins with an
accurate assessment of the patient
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+/- adjuvant
Non-opioid
Weak opioid
Strong opioid
By the
Clock
W.H.O. ANALGESIC LADDER
+/- adjuvant
+/- adjuvant
1
2
3
Guidelines for Cancer pain
The WHO 3-step Analgesic Ladder
Strong opioid
+non opioids
+
adjuvants
Weak opioid
+non opioid
+
adjuvants
Non opioid
(antipyretic)
+
adjuvants
Pain
Pain persisting or
increasing
Pain persisting or
increasing
Step 1.
Step 2.
Step 3.
90% respond well to oral medicines
Adjuvant Analgesics
first developed for non-analgesic indications
subsequently found to have analgesic activity in specific
pain scenarios
Common uses:
pain poorly-responsive to opioids (eg. neuropathic
pain), or
with intentions of lowering the total opioid dose and
thereby mitigate opioid side effects.
Adjuvants Used In Palliative Care
General / Non-specific
corticosteroids
cannabinoids (not yet commonly used for pain)
Neuropathic Pain
gabapentin
antidepressants
ketamine
topiramate
Clonidine
Pregabaline
Bone Pain
bisphosphonates
(calcitonin)
inflammation
edema
spontaneous nerve depolarization
tumor mass
effects
CORTICOSTEROIDS AS ADJUVANTS
}
Steroids: MOA
inhibit phospholipase A2>>>
inhibits prostoglandin/leukotrienes
Membrane Phospholipid
Arachidonic Acid
Bad Prostaglandins
Pain/Inflammation
Good Prostaglandins
GI Protection
Renal Blood Flow
Thromboxane
Platelets
COX-2
COX-1
Phospholipase A2
Steroids
inhibit here
NSAIDS inhibit here
Pain Level
Description
Numerical
Rating (0 to
10 Scale)
WHO Therapeutic
Recommendations
Example Medicines for
Initial Therapy
Mild pain 13
Nonopioid analgesic: taken
on a regular schedule, not as
needed (prn)
Acetaminophen 650 mg
every 4 hr
Acetaminophen 1,000 mg
every 6 hr
Ibuprofen 600 mg every 6
hr
Moderate pain 46
Add opioid for moderate pain
(e.g., moderate potency
analgesic). Use on a
schedule, not prn
Acetaminophen 325
mg/codeine 60 mg every 4 hr
Acetaminophen 325
mg/Oxycodone 5 mg every 4
hr
Tramadol 50 mg every 6 hr
Severe pain 710
Switch to a high potency
(strong) opioid; administer
on a regular schedule
Morphine 15 mg every 4 hr
Hydromorphone 4 mg every
4 hr
Morphine controlled release
60 mg every 8 hr
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36
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Dosing
The management of chronic pain is also best
accomplished by around-the-clock
administration
As-needed schedules are to be used in
conjunction with around-the-clock regimens
and are used when patients experience
breakthrough pain
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TOLERANCE
physiological phenomenon normal A
in which increasing doses are required
to produce the same effect
3 . 2 . 4 : Chapter 1993 Oxford Textbook of Palliative Medicine Inturrisi C, Hanks G.
PHYSICAL DEPENDENCE
physiological phenomenon in normal A
which a withdrawal syndrome occurs
when an opioid is abruptly discontinued
or an opioid antagonist is administered
3 . 2 . 4 : Chapter 1993 Oxford Textbook of Palliative Medicine Inturrisi C, Hanks G.
PSYCHOLOGICAL DEPENDENCE
and ADDICTION
A pattern of drug use characterized by a
continued craving for an opioid which is
manifest as compulsive drug-seeking
behaviour leading to an overwhelming
involvement in the use and procurement
of the drug
3 . 2 . 4 : Chapter 1993 Oxford Textbook of Palliative Medicine Inturrisi C, Hanks G.
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7 - 8

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Type of Pain Nonopioids Opioids
Other
Medications
Comments
Chronic low
back pain
Acetaminophen,
NSAIDs
Short-term use for
mild-to-moderate
flare-ups
TCAs, AEDs
Acetaminophen and
NSAIDS first; opioids in
selected patients; AEDs or
TCAs if neuropathic
symptoms
Fibromyalgia
Acetaminophen,
NSAIDs
Long-term use not
recommended
Tramadol,
TCAs; AEDs
Acetaminophen and
NSAIDs considered first;
tramadol may be better
alternative than opioids
Neuropathic
pain
Acetaminophen
or NSAIDs are
rarely effective
Considered first-
line therapy but
usually are tried
after AEDs and/ or
TCAs, tramadol,
lidocaine 5% patch
TCAs, AEDs,
SNRIs, trama
dol, topical
(e.g., 5% lido
caine patch,
capsaicin)
Gabapentin, 5% lidocaine
patch, tramadol, nortrip
tyline, desipramine, all
considered first-line agents;
opioids considered first-line
agents but usually are tried
after above
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Acetaminophen
Tynelol
Panadol
325 650 4 500 1000
6
4000


Mefenamic acid
Ponstan
500 250 6
1000

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Naproxen
Aleve
500 500 12 250 6
8
1000
Ibuprofen
Advil
200 400 6 8
OTC 400 8
5 10
6 8
3200
1200


OTC

NSAID
6

Celecoxib
Celebrex
Cobix
100 200 200

200

Diclofenac
Voltaren
25 50 6 8
100

200

Indomethacin
Indocin
25 2 3 150

2
25 6
150

NSAID

Tolmetin
200 400 8 1800
Meloxicam
Mobic
7.5 15 15

COX2
Piroxicam
feldene
10 2 20

Patient Control Analgesia (PCA)
Treatment of Neuropathic Pain
Pharmacologic treatment
Opioids
Steroids
Anticonvulsants gabapentin, topiramate
TCAs (for dysesthetic pain, esp. if depression)
NMDA receptor antagonists: ketamine, methadone
Anesthetics
Radiation therapy
I nterventional treatment
Spinal analgesia
Nerve blocks