PAIN

MANAGEMENT

Dr. Prabowo Wicaksono SpAn

BAGIAN/SMF ANESTESI FK UNISSULA/RSISA
2007

DEFINITION
(IASP:
The
International
Association for the Study of Pain):
An unpleasant sensory and/emotional experience associated
with actual or potential tissue damage.
This definition recognizes the interplay of both physical and
psychological factors of pain and suggest that combined modality
therapy may often be required to treat pain syndromes.

TYPES OF PAIN
There are two qualitatively different types of pain: fast pain and slow
pain.
Fast pain: short, well-localized, stabbing sensation that is
matched the stimulus, such as pinprick or surgical stimulus. This
pain starts abruptly when the stimulus is applied and ends
promptly when stimulus is remove. Resulted from stimulation of
small, myelinated type A-delta nerve fibers with conduction
velocities of 12-30 m/s.
Slow pain: is characterized as a throbbing, burning, or aching
sensation that is poorly localized and less specifically related to
the stimulus. Resulted from stimulaton of more primitive,
unmyelinated type C nerve fibers with conduction velocities of
0.5-2m/s.

PAIN MECHANISM
TRANSDUCTION

TRANSMISSION

MODULATON

PERCEPTION
4

TRANSDUKSI
Multiple stimuli are perceived from skin,somatic structures, joints ,and
viscera.
Nociceptors (pain receptors) convert the physical attributes of
chemical, thermal, and mechanical stimuli into action potentials
that are transmitted along their axons to the spinal cord.
Pain receptors are naked, afferent nerve endings of myelinated A-delta
and unmyelinated C fibers that encode the occurance, intensity, duration,
and location noxious stimuli and signals pain sensation.
Three catagories of pain receptors are described in skin.
Mechanosensitive pain receptors: activated by mechanical
stimulation
A-delta fibes
Mechanothermal receptors: activated by mechanical and thermal
(>43C)
Polynodal pain receptor: responds to mechanical, chemical and
thermal injury , conduct impuls by unmyelinated C fibers.
Chemicals capable of activating these receptors include bradykinin,
histamin, prostaglandins.

TRANSDUKSI

TRANSMISSION OF PAIN SIGNALS

Pain signals are transmitted from pain receptors along myelinated Adelta fibers (rapid conduction) and unmyelinated C fibers (slow
conduction). These afferent fibers enter the spinal cord through the
dorsal nerve roots and terminate on cells in the dorsal horn of spinal
cord. At this site, release of excitatory neurotransmitters, such as
glutamate or substance P, are necessary for further cephalad
transmission of pain.
The spinothalamic tracts as well as other ascending pathways are
responsible for cephalad transmission of pain impulses after they have
been processed in the dorsal horn of spinal cord.
Pain impulses travel from the thalamus to the somatosensory
areas of the cerebral cortex, where it is ultimately perceive as pain.

MODULATION PERCEPTION
Considerable modulation of pain sensation, both facilitatory and
inhibitory, occurs within the CNS and the peripheral afferent nerve
endings. Endogenous opioids peptides are found in high density in
area of the CNS involved in nociception. Three groups of endogenous
opioids (enkephalins, endorphins an dynorphins) modulate
nociception by binding to specific receptors, mediating a
pharmacological effects, including spinal analgesia ( and receptor)
and supraspinal analgesia ( receptor).
Transmission of pain impulses may be modulated by activation of
descending inhibitory pain pathways that pass from brain to the
spinal cord. Activation of these inhibitatory pathways blocks the
release of substance P or other excitatory NT and thus prevents
the cephalad transmission of pain impulses. A central nervous systems
substance, possibly endorphins, is responsible for activating these
descending inhibitatory pain pathways.

HYPERALGESIA
Tissue damage induces a state of hyperalgesia (increased response to a
given stimulus intensity).
Primary hyperalgesia occurs within the area of injury and is due to
sensitization of primary afferent neurones by inflammatory mediators
Secondary hyperalgesia develops in the surroundings uninjured tissue and is
thought to be due to activation of the N-methyl-D-aspartate (NMDA) receptors
(a subtype of glutamate receptor) in the dorsal horn of the spinal cord.

REACTION TO PAIN
Although pain treshold are similar in individuals, their reaction
to pain vary greatly.
Pain causes both reflex motor and psychic reactions.
Involuntary reflex withdrawal reactions occur in spinal cord even before
pain signals reach the brain.
Psychic reactions to pain include anxiety, depressions, anger, and
skeletal muscle excitability.
Pain and anxiety are interrelated such that anxiety makes pain
less tolerable, whereas increases in pain enhance anxiety.
Indeed, the preoeprative level of anxiety is a useful predictor of the
likely intensity of postoperative pain.

DESCRIPTION OF PAIN
Organic pain may be subdivided into nociceptive or neuropathic pain.
Nociceptive pain includes visceral and somatic pain and refers to pain due to
peripheral stimulation of nociceptors in visceral or somatic structures.
Nociceptive pain is usually responsive to opioid or nonopioid analgesics.
Neurophatic pain involves peripheral or central afferent neural pathways and
commonly is described as burning pain respond poorly to opioids analgesics.

The relief of pain is purchased

always at a price
(Ralph Waters)

ACUTE POST OPERATIVE PAIN

PAIN SCORING
Knowledge of the incidence and severity of postoperative pain is essential for
the establishment of effective pain treatment programmes.
The simplest subjective measures of pain is to ask the patient whether or not he or
she feels any pain. A simple VRS (Verbal Rating Scale) with which a patient is
asked to describe the amount of pain that he or she feels according to an arbitrary
scale is:
None
Mild/ slight pain
Moderate pain
Severe pain
Very severe/ intolerable

INCIDENCE OF POSTOPERATIVE PAIN

Between one-third and a half of all surgical patients experience significant
postoperative pain. The incidence and severiy of acute surgical pain depend on:
1.The site of operation: 74% of thoracic cases; 63% of upper abdominal cases;
51% of lower abdominal cases and 23% of body-wall operation.
2. Age
3. Sex
4. Premedications
5. Anaesthetic agents
6. Psychological factors
7. Diurnal factors.

THE PROBLEM OF POSTOPERATIVE PAIN

Opioids analgesics are the mainstay for relief of postoperative pain but have
tended to be underused because of excessive concern about creating drug
dependency and fear of inducing respirtory depression. These risk are
overstated; the incidence of addiction among patients who receive opioids for
pain relief is less than 0.1% and the incidence of respiratory depression is no
more than 1%.
Several approaches has been made to solve this problem:
1.Use of non-opioids analgesics on their own or in combination with
opioid analgesics.
2.Use of regular injection of opioids rather than injections at the discretion of
the nurse
3.Use of continuous infusion of opioids
4.Use of patient Controlled Analgesia (PCA)
5.Use of extradural route of opioids administrations.
6.Use of very long acting oral opioids
7.Use of long acting regional blocks.

DRUGS USED IN ACUTE POSTOPERATIVE PAIN

MANAGEMENT
NON STEROIDAL ANTI-INFLAMMATORY DRUGS (NSAIDs)
NSAID drugs may be sufficiently effective as sole analgesics after minor to
intermediate surgery. They are also useful after major surgery when their
opioid sparring effect (up to 30%) will help contribute towards a reduction in
overall side effects.

SUMMARY OF ACTION
Inhibitions of prostaglandin biosynthesis is considered to be the main
mechanism of analgesics actions of NSAIDs. However, there is evidence that
some NSAIDs also exhibit significant prostaglandin-independent mechanism of
action, which augment the analgesia.

COX2-SELECTIVE NSAIDs
Theoritically the ideal NSAIDs would inhibit COX-2 without influencing COX-1.
It is possible that COX-2 selective inhibitors might produce analgesia with fewer
adverse effects.

NSAIDs ACTION

NormalTissue

ArachidonicAcid

COX1
Constitutive

InflammationSite
+

Cytokines
Growthfactors

COX2
Inducible
COX2
Inhibitors

NSAIDs
Physiolgical
Prostaglandin
Production

NormalFunctions

Pathological
Prostaglandin
Production

Inflammation,pain,fever
19

14

ADVERSE EFFECTS
NSAIDs can damage gastrointestinal mucosa, impair renal fuction and may be
associated with an increase risk of postoperative haemorrhage. They can also
provoke asthma in susceptible patients.
They should be avoided in patiens with a history of GI ulceration or bleeding, when
there is evidence of fluid retention or renal impairment , in patients with hepatic
impairment or who are in hypovolaemic or in circulatory arrest. Used with caution in
the elderly.
NSAIDs :

KETOROLAC (unselective cox inhibitor)

Provide analgesia equivalent to opioids. May adversely affect renal function. Peak
plasma concentration achieved within 30-60 minutes after oral and parenteral
administrations. It is metabolized in the liver, conjugated and excreted by the
kidneys. Dose and duration should be reduce in the elderly. Dose: 10-30 mg i.m or
i.v.

OPIOIDS ANALGESICS DRUGS

Opiates are very effective as postoperative analgesics. Opiates influences the
emotional aspects of pain, such as anxiety and fear. They act on specific opioids
receptors in the brain and spinal cord.
SUMMARY OF ACTION OF OPIOIDS
CENTRAL NERVOUS SYSTEM
Depress: awareness, anxiety, pain sensation and respiration.
Stimulate: vomiting centre, secretion of ADH, Edinger-Westphal nucleus (causing
small pupils), hallucination (rarely)
SMOOTH MUCLE
Depress: vascular tone and peristalsis
Stimulate : bronchoconstriction, bowel sphincters, billiary sphincters
OTHER
Stimulate: secretion of catecolamine
Depress: metabolism
Release: histamine
Induce: vagally mediated bradycardia (especially short-acting opioids)

ADVERSE EFFECTS
1.Nausea and vomiting up to 50% of cases
2.Respiratory depression
3.Considerable variation of individual response (up to 10 fold), making it dificult to
predict the correct dose
4.Bradycardia
5.Relatively slow onset of analgesia. Intravenous alfentanil and pethidine are
fastest (1-2 min), fentanyl may take 15-20 min to produce analgesia, but
respiratory depression has a faster onset.
6.Addiction in susceptible individuals

OPIOIDS
1.MORPHINE (naturally occuring alkaloids of opium)
(Morpheus, Greek: good of dreams)
Has been is use for over 2000 years and is still the best available analgesic.
Opium comes from the dried latex of unripe capsules of the poppy head (Papaver
somniferum). Morphine is one of 25 alkaloids contained in opium; the
concentration of morphine in opium is 9-17%.
Pharmacodynamics:
CNS: analgesic, sedatives, anxiolytic, euphoric, addictive, a respiratory
depressant, and cause nausea and vomiting. More effective against dull,
continuous visceral, than against sharp, intermitten pain. The intracranial
pressure is increased because of PaCO2
Eye: miosis by central action, via the oculomotor nerve, stimulating the Edinger
Westpal nucleus.
CVS: mild vasodilatation in clinical doses, sometimes bradycardia
Respiratory system: the response of the respiratory centre for PaCO2 is
diminished. Respiratory rate, rather than tidal volume is decresed. Breathing
may become irregular. Bronchoconstriction occurs, worse in asthmatic
patients. Depressed the cough reflex.
GI Tract: Constricts the sphincter of the gut and reduce peristalsis. Nausea and
vomiting due to central stimulation.

Morphine contracts the sphincters of Oddi, rarely cause severe pain.

Genitourinary Tract: The tone of vesical sphincter is increased and may
hinder micturition. Diuresis decreases due to secretion of ADH.
Other: crosses placental barrier, depresses fetal respiration. Causes itching,
especially o the nose. Occasionally cause anaphylactoid and allergic reaction,
due to hisamine release.
Dose: 0.15 mg/kg I.M, 0.03mg/kg iv. Infusion rate 0.03 mg/kg/h.
Onset of analgesia: 3-10 min (I.V) and 10-20 min (I.M)

2. CODEINE PHOSPHATE
A superb cough supressant, useful in opthalmic and neuroanaesthesia. It
depresses respiration less, causes less constipation and vomiting than
morphine. Analgesic effect is one-tenth of morphine. Non sedating, non
addictive. Widely used as a pediatric analgesic (1 mg/kg oral/IM), but may
release histamine. Should not be given IV as by this route it depressed cardiac
output. Adult dose: 15-50 mg IM, oral as analgesic, antitussive and
antidiarrhoeal agent. Duration 4-12 h.

3. PETHIDINE/MEPERIDINE
opium)

(Synthetic

alkaloid

of

Pharmacodynamics
1.Analgesic: relieve most types of pain, especially those associated with plain
muscle spasm. Depresses respiration centre and cough reflex. No effect on
iris. Can cause addiction.
2.Has an atropine like effect on cholinergic nerve endings
3.May release histamine from tissue
4.Side effects include sweating, hypotension, vertigo and limb tingling. Post
operative nausea is similar to that following morphine, but comes on earlier.
Like morphine, may cause hypotension, if the head of the patient is raised, or
with sudden movement. Circulatoy depressant.
5.Precautions: the administration of pethidine to patient receiving monoamine
oxidase inhibitors may cause severe reactions and even death. There is
restlessness, hypertension, convulsions and coma. The reaction is said to be
due to interference with microsomes in liver cells which detoxicate pethidine.
Treatment is supportive, and wit 25 mg prednisolone or CPZ.
Pharmacokinetics:
Dose: 0.5 mg.kg IV, 1.5 mg/kg IM. Onset: 2-5 min. Duration: 2-4 h

4. TRAMADOL
A synthetic analogue of codeine. Potency comparable to pethidine. Less likely
to depress respiration than morphine. Dose: 100 mg PO, IV to maximum 250
mg. Duration 3-6 h.

5. FENTANYL CITRATE
Effects: intense analgesia, respiratory depression which precedes the
analgesia, miosis, nausea and vomiting, which outlast the analgesia,
bradycardia, and addiction.
Adult dose: 0.025-0.1 mg. Respiratory depression is managed by IPPV or
antagonized by naloxone. Onset: respiratory depression in 30-60 s, analgesia in
5-7 min (dose related). Duration: 30-60 min. Fentanyl is mostly destroyed in the
liver.
Interaction: with diazepam it causes serious hypotension. With midazolam
it causes serious respiratory depression and hypoxia. It attenuates the
hypertension resulting from ketamine. Intravenous boluses of fentanyl can
cause a cough. Large doses of fentanyl may result in muscular rigidity, making
IPPV difficult, but a relaxant will overcome this effect.

Thank you..............