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“Pain is a more terrible
lord of mankind than
death itself.”
Albert
Schweitzer
NEMESIS (REVENGE) AND TYKHE ( FORTUNE)
HISTORY OF PAIN
GREEK GODDESS OF REVENGE AND
VENGENCE “ NEMESIS” HAD AN
ATTENDANT NAMED “POINE” WHO
WAS RESPONSIBLE FOR THE
PUNISHMENTS

PAIN, PENALTY, PENAL, PENAL CODE
Pain…

Definition:
An unpleasant sensory and emotional experience
associated with actual or potential tissue damage.
May not be directly proportional to amount of tissue
injury. Highly subjective, leading to under treatment
Major Categories of Pain
Classified by inferred pathophysiology:
1.
2.

Nociceptive pain (stimuli from somatic
and visceral structures)
Neuropathic pain (stimuli abnormally
processed by the nervous system)
Why Don’t We Do a Better Job
of Treating Pain?
Introduction
Many, if not most,
medical conditions
cause pain.
Introduction
Pain is a protective
mechanism and
occurs whenever
any tissues of the
body are being
damaged.
Introduction
Pain occurs
whenever the cells
or tissues are being
damaged—
whatever the
underlying cause.
Introduction
The reaction to
pain may be rapid,
as seen when one
touches a hot pan.
Introduction
Or slow, as when
one has been
seated in the
same position for
an extended
period of time.
Introduction
One of the oldest
roles of medical
practitioners is to
help alleviate pain.
Introduction
Analgesia
• The relief of pain without a loss of
consciousness.
Introduction
Analgesia can be provided by:
•
•
•
•

Drugs
Surgical Procedures
Physical Modalities
Other
Introduction
Analgesia:
• Eliminate the source of the pain.
• Block or attenuate the pathways that
transmit pain impulses to the brain.
• Combination of the two.
Introduction
Pain elicits a strong
emotional response
that is often
recorded in our
memory.
Problems in Pain Management
Problems
Pain appears to be under treated:
•
•
•
•

Failure to assess pain.
Failure to quantify pain.
Fear of addiction.
Legal constraints of utilizing controlled
substances.
• Ignorance
Problems
Grady Memorial Hospital:
• Black patients with isolated long-bone
fractures were less likely to receive
adequate analgesia when compared to
their white counterparts.
– Todd KH, Deaton C, D’Adamo AP, Goe L.
Ethnicity and analgesic practice. Ann Emerg
Med. 2000;35(1):11-16
Prehospital Pain
Management is even worse!
Prehospital Pain Management
Pain in the prehospital setting is
often:
• Not identified,
• Under treated,
• Both.
– Ricard-Hibon A, Leroy N, Magne M, et al.
Evaluation of acute pain in prehospital
medicine. Ann Fr Anesth Reanim.
1997;16(8):945-9
Prehospital Pain Management
Patients with extremity fractures
receive inadequate analgesia.
• Study of 1,073 patients found only 1.5%
received analgesia in the prehospital
setting.
– White LJ, Cooper LJ, Chambers RM,
Gradisek RE. Prehospital use of analgesia
for suspected extremity fractures. Prehosp
Emerg Care. 2000;4(3):205-8
Prehospital Pain Management
Prehospital patients with lowerextremity fractures (including hip
fractures):
• Only 18.3% of eligible patients received
analgesia.
– McEachin CC, McDermott JT, Swor R. Few
emergency medical services patients with
lower extremity fractures receive prehospital
analgesia. Prehosp Emerg Care.
2002;6(4):406-410
Prehospital Pain Management
Femoral neck
fractures are among
the most common
orthopedic injuries
encountered in
prehospital care.
Prehospital Pain Management
Hip fractures:
• Only a modest proportion of these
patients receive prehospital analgesia for
this painful and debilitating injury.
– Vassiliadis J, Hitos K, Hill CT. Factors
influencing prehospital and emergency
department analgesia administration to
patients with femoral neck fractures. Emerg
Med (Fremantle). 2002:14(3):261-6
Types of Pain
Acute pain:
• Pain associate with an acute event

Chronic pain:
• Pain that persists after an acute event is
over
• Pain that last 6 months or more
Pathophysiology
The generation of
pain involves
interaction
between all parts
of the nervous
system.
Pathophysiology
Perceiving pain:
• Algogenic substances—chemicals
released at the site of injury.
• Nociceptors—Afferent neurons that carry
pain messages.
• Referred pain—pain that is perceived as
if it were coming from somewhere else in
the body.
Pathophysiology
Nociception
• Derived from the word noxious meaning
harmful or damaging to the tissues.
• Mechanical event that occurs in tissues
undergoing cellular injury.
Pathophysiology
Nociceptive stimulus is detected by
free nerve endings in the tissues.
Three type of stimuli excite pain
receptors:
• Mechanical
• Thermal
• Chemical
Pathophysiology
Pain fibers are free
fibers.
Pathophysiology
Pain fibers principally located in the
superficial layers of the skin.
Pain fibers also located in:
•
•
•
•

Periosteum
Arterial walls
Joint surfaces
Falx and tentorium of the cranial vault.
Pathophysiology
Deep structures:
• Sparsely supplied with pain fibers
• Widespread tissue damage still causes
the slow, chronic, aching-type pain.
Pathophysiology
Visceral Pain:
• Ischemia
• Chemical stimuli
• Spasm of hollow
viscus
• Over distension of a
hollow viscous
Pathophysiology
Chemicals that excite pain receptors:
•
•
•
•
•
•
•

Bradykinin
Serotonin
Histamine
Potassium ions
Acids
Acetylcholine
Proteolytic enzymes
Pathophysiology
Chemicals that enhance the sensitivity
of pain endings, but do not
necessarily excite them:
• Prostaglandins
• Substance P
Pathophysiology
Types of pain:
• Fast Pain:
– Felt within 0.1 second after painful stimulus
– Also called: sharp pain, pricking pain, electric
pain and acute pain.
– Felt with needle stick, laceration, burn
Pathophysiology
Types of pain:
• Slow Pain:
– Felt within 1.0 second or more after painful
stimulus
– Also called: dull pain, aching pain, throbbing
pain and chronic pain.
– Usually associated with tissue destruction
Pathophysiology
Pain fibers transmit impulse to spinal
cord through fast or slow fibers:
• A-δ (delta) fibers—small myelinated
fibers that transmit sharp pain.
• C fibers—small unmyelinated fibers that
transmit dull pain or aching pain.
Pathophysiology
Pain is often a “double” sensation as
fast pain is transmitted by the Aδ
fibers while a second or so later it is
transmitted by the C fiber pathway.
Pathophysiology
Pain impulses enter the spinal cord
from the dorsal spinal nerve roots.
Fibers terminate on neurons in the
dorsal horns.
Pathophysiolgy
Pain ultimately transmitted to:
• Thalamus
• Medulla oblongata
• Somatosensory areas of the cerebral
cortex.
Analgesia
The brain’s opiate
system:
• Endorphins
• Enkephalins
Assessment of Pain
Pain, in most instances, is selfreported.
This should be considered along with
physical signs and symptoms when
assessing pain.
Assessment of Pain
Self-Report of pain:
• Have patient describe how they feel.
• For infants and children, rely on care
givers.
• Obtain important historical information
OPQRST-ASPN System
Onset of Problem
Provocative / Palliative factors
Quality
Region / Radiation
Severity
Time
Associated Symptoms
Pertinent Negatives
Assessment of Pain
Behavioral Observations:
•
•
•
•

Vocalizations (cry, scream, moan)
Facial expressions (frown, grimace)
Body posture (fetal position)
Motor responses (decreased movement,
restlessness)
Assessment of Pain
Physiological measurements:
•
•
•
•
•
•

Skin flushing
Diaphoresis
Restlessness
Tachycardia
Tachypnea
Elevated BP
Assessment of Pain
Physical
examination will
often give a clear
indication of the
source of the
patient’s pain.
Adult Pain
Visual “Ten Scale”:
Pain Management
Pain Management
Priorities are priorities!
•
•
•
•

Scene safety
BSI
Treat any life-threatening illness of injury
Treat pain
Pain Management
Strategies:
• Removing or
correcting the source
of the pain
Pain Management
Strategies:
• Blocking or
attenuating the
transmission of pain
impulses to the brain
Pain Management
Strategies:
• Or, a combination of
both
Pain Management
Non-medication therapies:
•
•
•
•
•
•
•

Recognition and empathy
Distraction
Muscle relaxation
Position of comfort
Temperature regulation
Physical therapies
Treat underlying cause
Pain Management
RICE:
•
•
•
•

Rest
Ice
Compression
Elevation
Pain Management
Medications that relieve pain are
called analgesics
Medication therapies:
• Peripherally-acting agents
• Centrally-acting agents
Pain Management
Peripherally-acting agents
• Considerable reaction locally to cellular
and tissue damage:
– Pain
– Swelling
– Inflammation
Pain Management
Peripherally-acting agents:
• Corticosteroids
• Non-steroidal anti-inflammatory agents
(NSAIDs)
• Local Anesthesia
Pain Management
Peripherally-acting agents:
•
•
•
•

Methylprednisolone
Acetaminophen
Ibuprofen
Aspirin
Pain Management
NSAIDs
• Effective for pain and inflammation
• Good side-effect profile
• Second generation NSAIDs have better
side-effect profiles
• Inhibit prostaglandins and other
mediators of pain and inflammation
Pain Management
Centrally-acting agents:
• Opiates
• Anesthetic gasses used in analgesic
quantities
• Atypical agents (ketamine)
Opiates
Mainstay of
analgesic practice
Originally derived
from the opium
poppy plant
Many now
synthetically
manufactured
Opiate Receptors
Μu (μ ) receptors
Kappa (κ) receptors
Delta (δ) receptors
Actions:
•
•
•
•

Inhibit pain
Cause sedation
Respiratory depression
Cardiovascular depression
Opiates
Actions:
• Act on CNS and organs containing
smooth muscle
• Analgesia without loss of consciousness
Opiates
Effects:
•
•
•
•
•
•
•
•

Analgesia
Suppresses cough reflex
Respiratory depression
Mental clouding
Mood changes
Euphoria
Dysphoria
Nausea and vomiting
Opiates
Effects:
• Meiosis
• Decreased gastric, biliary and pancreatic
secretions
• Reduce gastric motility
• Delay digestion of food in the small
bowel
• Decreases peristalsis in the colon
(constipation)
Opiates
Effects:
• Certain opiates (morphine) cause an
increase in biliary tract pressure
• Certain opiates (morphine) cause
peripheral vasodiation
• Histamine release (red eyes, pruritis,
flushing)
Opiates
Morphine
Morphine
Named after Greek
god Morpheus—god
of sleep and dreams
Morphine
Onset of action: < 5 minutes IV
Peak effects: 20 minutes
Duration: 7 hours
Typical IV dose: 2.5-10.0 mg
Opiates
Synthetic opiate agonists /
antagonists
• Nalbuphine
• Butorphanol
Synthetic Mixed Opiates
Sub-class of opiates with both
agonistic and antagonistic property
Activate some opiate receptors while
blocking others
Reportedly decreases the likelihood of
abuse and respiratory depression
Not controlled in many states
Synthetic Mixed Opiates
Nalbuphine
Nalbuphine
Most common mixed agent used in
prehospital care
Antagonistic properties decrease the
potential for abuse.
Nalbuphine
Initial studies indicated it was an
effective alternative to morphine.
– Chambers JA, Guly HR. Prehospital
intravenous nalbuphine administered by
paramedics. Resuscitation. 1994;27-153-8.
– Stene JK, Stofberg L, MacDonald G, et al.
Nalbuphine analgesia in the prehospital
setting. Am J Emerg Med. 1988;6(6):634-9.
Nalbuphine
Subsequent studies seem to suggest
not as effective as once thought.
English study found it offered poor
pain control to a high proportion of
patients in the prehospital setting.
– Wollard M, Jones T, Vetter N. Hitting them
where it hurts? Low dose nalbuphine
therapy. Emerg Med J 2002;19:565-570.
Nalbuphine
Because of antagonistic properties,
prehospital nalbuphine usage
appears to be responsible for
increased opiate requirements once
patients arrive in the ED.
– Houlihan KPG, Mitchell RG, Flapan AD, et al.
Excessive morphine requirements after
prehospital nalbuphine analgesia. J Accid
Emerg Med 1999;16:29-31
Nalbuphine
Also appears to interfere with general
anesthesia and maintenance.
– Robinson N, Burrow N. Excessive morphine
requirements after pre-hospital nalbuphine
analgesia. J Accid Emerg Med. 1999;16:1237.
Nalbuphine
Probably should have a limited role in
emergency medicine and EMS.
Nalbuphine
Onset of action: 2-3 minutes IV
Peak effects: < 30 minutes
Duration of effect: 3-6 hours
Typical IV dose: 5-20 mg
Gasses
Nitrous Oxide (N2O):
•
•
•
•
•

Anesthetic at high concentrations
Analgesic at low concentrations
Initially used in dentistry and obstetrics
Introduced into EMS in the 1970s.
Effective in treating virtually all types of
pain.
Acetaminophen
–
–
–
–

Mechanism – unknown
Route - PO, PR
Onset - variable, half life = 2-3 h
Side effects - hepatotoxicity, AIN/tubular
necrosis
– Contraindications
• Relative—, liver disease (max daily dose
reduction), renal disease (prolonged use)
– History – 1894, 35% current pain med
market, more ER visits for OD than all other
pain meds.
NSAIDS
–

Mechanism - COX inhibitors, lipoxygenase
inhibitors
– Route - PO, PR, IV, IM
– Side effects- platelet inhibition, PUD, dyspepsia,
CNS dysfunction, headache, renal dysfunction
– Contraindications
• Relative - ASA/NSAID induced asthma, periop CABG, GI bleed, Renal dysfunction, liver
disease.
NSAIDS
Mefenamic acid Global Standard of
Pain Relief

Mefenamic
acid

Inhibits prostaglandin
(PG)synthetase
Blocks prostaglandin
action at receptor sites

(Budoff P.W.JAMA. June 23,1979.volume 241.)
Anti Prostaglandin's
MEFENAMIC ACID which blocks the action
of cyclo-oxygenase are effective in checking
MENORRHAGIA.

(Menstrual disorders Pg 174 ,GYNAECOLOGY By ten Teachers ,Edited by
GEOFFREY V P CHAMBERLAIN MD FRCS FRCOG , 16TH Edition , ELBS .)
Fenamates .
Fenamates potentially inhibit cyclooxygenase and also block
responses to certain PGs .The
effect varies in different tissues but
can be very potent. (Collier & Sweatman.)
Mefenamic acid a Global
Standard of Pain Relief

“Mefenamic acid produces highly significant
reduction in menstrual blood loss in most women
with Menorrhagia”.
(Fraser etal Am.J.Obestet Gynecol 58-5-5543.Nov.1981.)

Upto 45% reduction in median blood loss in
Menorrhagia- The evidence
• In a trial involving 22 patients, there was a significant
reduction in blood loss from 137ml/cycle at present to
76ml/cycle on treatment.
(Haynes,P.J. etal Update . Bri. J. Obstet Gyne 1979.)
Adjuvants/Other classes
–
–
–
–

Gabapentin/Pregabalin, anticonvulsants neuropathic pain
Tricyclics - neuropathic and chronic pain
Caffeine - useful as an adjuvant with NSAIDS
Things we shouldn’t use acutely
•
•

Benzodiazepines: no role for acute pain relief
unless due to muscle spasm
Antihistamines, dextroamphetamine, steroids,
intrathecal clonidine
Some analgesics relieve pain primarily
by decreasing the sodium and
potassium transfers at the neuron level,
thereby slowing or stopping pain
transmission. Examples—local
anesthetics, anticonvulsants used for
neuropathic pain, migraines.
Future Trends
Methoxyflurane Inhalers
Intranasal fentanyl
Alfentanil (Alfenta)
Tramadol (Ultram)
Entonox
Non-Pharmacological interventions
Tramadol
Synthetic
analogue of
codeine.
Has weak opioid
agonistic
properties.
Slight abuse
potential
Non-controlled
Tramadol
1/10 as potent as morphine
Onset of action: 1-5 minutes IV
Peak effects: 15-45 minutes
Duration:
4.5 hours
Typical IV dose: 100 mg
Tramadol
Analgesia and side-effects similar to
morphine.
Concluded tramadol is an effective
alternative to morphine in the
prehospital setting.
– Vergnion M, Desgesves S, Garcey L,
Magotteaux V. Tramadol, an Alternative to
Morphine for Treating Posttraumatic Pain in
the Prehospital Situation. Anest Analg.
2001;92:1543-6.
Topicals/Local
–
–
–

–

Mechanism—local receptor effect
Route—topical
Side effects—local reaction, accidental IV
injection, burning, erythema, hives, seizures,
respiratory arrest, asthma
Contraindications
•

Relative—liver dysfxn, renal dysfxn, heart block
Non-Pharmacological
Interesting Austrian study for victims
of minor trauma using acupressure.
Patients randomly assigned to receive
acupressure at “true points,” at “sham
points” or “no acupressure.”
Different values measured before and
after treatment.
Acupressure
At the end of transport, patients who
received acupressure at “true points” had
less pain, less anxiety, a slower heart rate,
and greater satisfaction with the care
provided.
They concluded that acupressure is an
effective and easy-to-learn treatment of
pain in prehospital care.
– Kober A, ScheckT, Greher M et al. Prehospital
analgesia with acupressure in victims of minor
trauma: a prospective, randomized, doubleblinded trial. Anest Analg. 2002;95(3):723-7.

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