pain management
Post on 07-May-2015
338 Views
Preview:
TRANSCRIPT
“Pain is a more terrible lord of mankind than death
itself.”
Albert Schweitzer
NEMESIS (REVENGE) AND TYKHE ( FORTUNE)
HISTORY OF PAINGREEK 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. Nociceptive pain (stimuli from somatic and visceral structures)
2. 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 lower-extremity 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 self-reported.
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;16:123-7.
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, peri-op CABG, GI bleed, Renal dysfunction, liver disease.
NSAIDS
Mefenamic acid Global Standard of Pain Relief
Mefenamic Mefenamic acidacid
Blocks prostaglandinaction at receptor sites
Inhibits prostaglandin(PG)synthetase
(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 cyclo-oxygenase 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 58-5-5-543.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, double-blinded trial. Anest Analg. 2002;95(3):723-7.
top related