Hazem Sharaf Pain Pathophysiology

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Dr. Hazem Sharaf Dr. Hazem Sharaf Anesthesia Consultant Anesthesia Consultant KFH Al-Baha KFH Al-Baha [email protected] [email protected] Pain Mechanisms & Pathophysiology

Transcript of Hazem Sharaf Pain Pathophysiology

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Dr. Hazem SharafDr. Hazem SharafAnesthesia ConsultantAnesthesia Consultant

KFH Al-BahaKFH [email protected]@yahoo.com

Pain Mechanisms & Pathophysiology

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ObjectivesUnderstand acute pain mechanisms

Phases of painModes of analgesiaTypes of painCan pain kills!!Can pain kills!!Myths of pain

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Understanding Acute Pain

Mechanisms

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Many, if not most, medical conditions cause pain.

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Pain is a protective mechanism and occurs whenever any tissues of the body are being damaged.

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One of the oldest roles of medical practitioners is to help alleviate pain.

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Pain elicits a strong emotional response that is often recorded in our memory.

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What is Pain!Pain!““An unpleasant sensory An unpleasant sensory andand emotional experience emotional experience associated with actual associated with actual oror potential tissue damage.”potential tissue damage.”

Pain is uniquely experienced by Pain is uniquely experienced by each individual; each individual; it cannot be it cannot be adequately defined, adequately defined, identified, identified, or measured by an observeror measured by an observer

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“the inability to communicate verbally does not negate that the individual is in pain and needs treatment”- unconscious.

-pre-verbal.-intellectually

disabled.-impaired communication

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Problems in Problems in PainPain Management Management

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Pain appears to be under-treated due to:Failure to assess or quantify pain.Fear of addiction & Legal restrictions of utilizing controlled drugs.

Ignorance.

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Terminology

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Noxious – harmful, injuriousNoxious stimuli – stimuli that activate nociceptors (pressure, cold/heat extremes, chemicals)

Nociceptor – nerve receptors that nerve receptors that transmits pain impulsestransmits pain impulses

Pain Threshold – level of noxious stimulus required to alert an individual of a potential threat to tissue

Pain Tolerance – – amount of pain a amount of pain a person is willing or able to tolerateperson is willing or able to tolerate

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Hyperesthesia – abnormal acuteness of sensitivity to touch, pain, or other sensory stimuli

Paresthesia – abnormal abnormal sensation, such as burning, sensation, such as burning, pricking, tinglingpricking, tingling

Analgesia – a neurologic or pharmacologic state in which painful stimuli are no longer painful

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AnalgesiaRelief of pain without loss of consciousness.Analgesia by:

DrugsSurgical ProceduresPhysical ModalitiesOther

Analgesics:Eliminate the source of the pain.Block or attenuate the pathways that

transmit pain impulses to the brain.Combination of the two.May 2, 2023

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Prehospital Pain ManagementIs usually Without adequate analgesia!

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Qualities of Pain:Organic Vs. Psychogenic

Acute Vs. ChronicMalignant Vs. BenignContinuous Vs. Episodic

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Acute pain:Pain associated with an acute event

Chronic painChronic pain:Pain that persists after an acute event & lasts 6 months or more

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Major Categories of Pain

Classified by pathophysiology:1. Nociceptive pain (stimuli

from somatic and visceral structures)

2. Neuropathic pain (stimuli abnormally processed by the nervous system)May 2, 2023

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The generation of pain involves interaction between all parts of the nervous system.

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Perceiving pain:Allogeneic 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.

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Nociceptive stimulus Nociceptive stimulus is detected by free nerve endings in the tissues.

Three types of stimuli excite pain receptors:MechanicalThermalChemical

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Pain fibers principally located in the skin superficial layers.

Pain fibers also located in:PeriosteumArterial wallsJoint surfacesFalx and tentorium of the cranial vault.

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Substances released…Released from the traumatized

tissue that excite pain receptors:BradykininSerotoninHistaminePotassium ionsAcidsAcetylcholineProteolytic enzymes

Chemicals that enhance the sensitivity of pain endings, but do not necessarily excite them:ProstaglandinsSubstance P

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So, for example:Non-steroidal anti-inflammatories, such as ibuprofen, are effective in minimizing pain because they minimize the effects of these substances released, especially prostaglandins.

Corticosteroids, such as dexamethasone used for cancer pain, also interferes with the production of prostaglandins.

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Deep structures:Lightly supplied with

pain fibersWidespread tissue

damage still causes the slow, chronic, dull-aching pain.

Visceral Pain:IschemiaChemical stimuliSpasm of hollow

viscousOver distension of a

hollow viscousMay 2, 2023

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Phases of Nociceptive PainNociceptive

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Modulation

Pain stimulus

Dorsal horn

Sensorycortex

Dorsal rootganglia

Perception

Transduction

Transmission

Peripheral nociceptors

Adapted with permission from Nicholson BD. J Am Acad Nurse Pract. 2003;15(12 suppl):3-9.May 2, 2023

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Process #1—TransductionNoxious stimuli cell membrane of the

neuron (nervous system cell) to become permeable to sodium ionssodium ions, allowing the ions to rush into the cell and creating a temporary positive charge.

Then potassium transfers back into the cell, thus charge back to a negative one. With this depolariztion and repolarization, the noxious stimuli is converted to an impulseimpulse. This impulse takes just milliseconds to occur.

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Some analgesics relieve pain primarily by decreasing the sodium & potassium transfers at the neuron level, thereby slowing or stopping pain transmission.

Examples—local anesthetics & anticonvulsants used for neuropathic pain & migraines.

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Process #2—TransmissionNeurotransmitters are needed to conduct the pain impulse from the spinal cord to the brain—opioids (narcoticsnarcotics) are effective analgesics because they block the release of neurotransmitters

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Process #3—Perception of PainOccurs in the cortical structures, so, behavioral strategies and therapy can reduce pain

(Non-pharmacological Pain relief)(Non-pharmacological Pain relief). Brain can accommodate a limited number of signals, So, distraction, imagery, relaxation signals may get through the same gategate, leaving limited signals (such as pain) to be transmitted to the higher structures.May 2, 2023

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Gate Control Theory

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Gate Control TheoryGate - located in the dorsal horn of the spinal

cordSmaller, slower (A-beta fibers) carry pain

impulseLarger, faster C fibers carry other

sensationsImpulses from faster fibers arriving @

gate 1st inhibit pain impulses (e.g. acupuncture/pressure, cold, heat, chem. skin irritation).

Brain

Pain

Heat, Cold, Mechanical

Gate (T cells/ SG)

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Process #4—Modulation of Pain►Descending fibers also release

substances such as norepinephrine and serotonin (referred to as endogenous endogenous opioids /endorphinsopioids /endorphins) which have the capability of inhibiting the transmission of noxious stimuli. Helps explain wide variations of pain threshold among people.

►Cancer pain responds to antidepressants which interfere with the reuptake of serotonin and norepinephrine which increases their availability to inhibit noxious stimuli.

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Modulation animationModulation

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Other types of painFast Fast Pain Pain (with rapid reaction):(with rapid reaction):

Felt within 0.1 second after painful stimulusAlso called: sharp pain, pricking pain, electric

pain and acute pain.Felt with needle stick, laceration, burn

Slow Slow Pain Pain (with slow reaction):(with slow reaction):Felt within 1.0 second or more after painful

stimulusAlso called: dull pain, aching pain, throbbing

pain and chronic pain.Usually associated with tissue destruction

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Pain FibersPain 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.

Pain is often a “double” sensation as fast pain is transmitted by the Aδ fibers while a second or later it is transmitted by the C fiber pathway.

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Pain Fibers

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Centrally acting agentsCentrally acting agentsOpiates: Natural or SyntheticOpiates act on mu, kappa, and deltamu, kappa, and delta receptors.Inhibiting pain; and may cause sedation, and respiratory and cardiovascular depression.

Acting on the CNS and smooth muscles.

Principal actions are analgesia and sedation without loss of consciousness.

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Opiate receptorsOpiate receptorsmumu**: euphoria, analgesia, respiratory

depression.mu1: analgesia.mu2: constipation, euphoria, physical

dependence, and respiratory depression.delta: analgesia.sigma: respiratory system, vasomotor activity,

hallucinations, and dysphoria.kappakappa**: spinal analgesia, sedation, and

pupillary constriction.epsilon: analgesia*Opiates have an affinity for mu and kappa

receptorsMay 2, 2023

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mu receptors

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Harmful Effects of PAINCardiovascular and respiratory systems are significantly affected by the pathophysiology of pain:

adrenergic stimulationhypercoagulation, leading to DIC heart rate & cardiac output myocardial oxygen consumption

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pulmonary vital capacity & alveolar ventilation

functional residual capacityarterial hypoxemiasuppression of immune functions, predisposing trauma patients to wound infections and sepsis

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The Stage of Alarm

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The Stage of ResistanceThe Stage of Resistance(everything is being used up)

Energy

Nutrients

Oxygen

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Exhaustion Stage (homeostasis Exhaustion Stage (homeostasis vsvs. death). death)

The body can no longer sustain its adaptive responses

Devastating sequelae

Irreversible organ damage and death of the patient

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Pain can kill

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What influences pt. resistance?Past and present condition of the patient

Available energy resources (pain consumes energy)

Amount of energy required for adaptation

Patient’s perception of the stressMay 2, 2023

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Providing timely and effective pain management Providing timely and effective pain management to the injured patient can help strengthen the to the injured patient can help strengthen the patient’s lines of resistancepatient’s lines of resistance

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Myths of Pain Management

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MYTH #1: If I give my patient a narcotic, he will not be competent enough to consentconsent for surgery later.

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Myth # 1: FALSEConcern about rendering patient incompetent is unfounded.

Withholding analgesia can be looked upon as a form of “compulsion” to sign consent for surgery.

Gabbay DS, Dickenson ET. Refusal of base station physicians to authorize narcotic analgesia. Prehosp Emerg Care. 2001;3(5):293-5.

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MYTH #2: If I give my patient a narcotic for abdominal pain, it will change the physical examination findings, making diagnosis difficult.

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Myth # 2: FalseSeveral researchers have examined this question:208 patients presented with abdominal pain.

152 morphine & 156 placebo The presence of peritoneal signs did not change in patients that received morphine and the accuracy of diagnosis did not differ between the two groups of patients as well as between the emergency physicians and the surgeons.

In fact, there was also a trend that the examination may be more reliable after treatment with morphine.

Pace S, Burke TF. Intravenous morphine for early pain relief in patients with acute abdominal pain. Acad. Emerg. Med. 1996;3:1086–1092

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Myth # 2: False108 children with abdominal pain.

52 morphine56 placebo (saline)

Morphine effectively reduces the intensity of pain and does not impede the diagnosis of appendicitis.

Green R. et al. Early analgesia for children with acute abdominal pain. Pediatrics. 2005;116:978-983.

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MYTH #3: If I give my patient narcotic, he will develop respiratory arrest.

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Myth # 3: FalseRespiratory depressant effects often offset by sympathetic stimulation in the pain patient. Different than from respiratory depression in pain-free opiate addicts.

Key is to use correct analgesic dose

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MYTH #4: If I give my patient narcotic, he will abuse narcotics

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Myth # 4: FalseBecause of a few patients malinger and drug-seek is no reason to withhold from reasonable pain patients.

Most people who become addicted to pain killers have underlying addictive tendencies.

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Myth # 4: FalseIn a 5-year review, the medical use of opiates increased while the incidence of opiate abuse actually decreased.

Joranson DE, Ryan KM, Gilson AM, Dahl JL. Trends in medical use and abuse of opioid analgesics. JAMA. 2000;283(13):1710-4.

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So, I hope we got:Acute pain mechanismsPhases of painModes of analgesiaTypes of painTheories of painYes, Pain can kill.Yes, Pain can kill.STOP STOP Myths of pain.

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ThankThank You & You & Have A Have A

Painless DayPainless DayMay 2, 2023