pain management

“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


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 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


Femoral neck fractures are among the most common orthopedic injuries encountered in prehospital care.


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.

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