PAIN MANAGEMENT

Dr. Prabowo Wicaksono SpAn

BAGIAN/SMF ANESTESI FK UNISSULA/RSISA
2007
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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.

It is the immediate, stabbing pain that instanly tells the person that tissue damage is
occuring, whereas burning pain become the source of sustained discomfort.
PAIN MECHANISM
TRANSDUCTION

TRANSMISSION

MODULATON

PERCEPTION
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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 fiber
Mechanothermal receptors: activated by mechanical and thermal (>43°C)

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

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TRANSMISSION OF PAIN SIGNALS
Pain signals are transmitted from pain receptors along myelinated A-delta 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, ß endorphins an dynorphins) modulate nociception by
binding to specific receptors, mediating a pharmacological effects, including spinal
analgesia (κ and δ receptor) and supraspinal analgesia (μ 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
Normal Tissue Inflammation Site
Arachidonic Acid
Cytokines
+ Growth factors

COX-1 COX-2
Constitutive Inducible

COX-2
NSAIDs
Inhibitors
Physiolgical Pathological
Prostaglandin Prostaglandin
Production Production

Normal Functions Inflammation, pain, fever

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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 (Synthetic alkaloid of
opium)
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..............