pain

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  1. what is nociception?
    -Nocioception is the process of transduction ,transmission, perception and modulation of pain-Nocioception is similar for individuals,however the circle surrounding which is pain experience, pain behavior &system response are highly variable-Differentpeople react differently to the same intensity of painful stimuli. Personality& ethnic origin are thought to affect the perception of pain and theresulting pain behavior
  2. pain threshold
    pain threshold: the point where a stimulus is perceived as painful.  Painthreshold is fairly uniform from one person to another
  3. pain tolerance
    pain tolerance: maximum intensity or duration of pain that a person is willing toendure before a person wants some action taken on that. This is extremelyvariable from one person to another
  4. classifications of pain
    two main classification of pain:1.Nocioceptive:whichcan either somatic or visceral. Nocioceptive pain,  is pain resulting fromongoing stimulation of nerve by noxious stimuli.  Somatic has identifiable focal point and follows distribution ofnerve.  it is well localized, sharp, and pain at point of stimulusvisceral:diffuse, can be referred to another area, often described as dull andvague.   Ex . occurs when organ capsule is distended or when there is obstructionof hollow viscosnociocpetive pain whether somatic of visceralresponds well to nsaids and opiodanalgesics2. Neuropathicpain:caused by abnormal processing of painful stimuli.  Dysfunction of CNS thatallows for spontaneous excitation leading to severe pain. can be generatedperipherally or centrally. Difficult to treat.  Pain described as burning,tingling, or shock like.canbe associated w/ subjective numbness, loss of sensation , and weakness.•doesnot respond well to NSAIDS or opiods analgesic alone,  adjunctiveanalgesic may be efficacious in treating neuropathic pain.•adjunctiveanalgesic : med that is approved and used for other reasons than analgesicsproperties:  ex) tricyclic antidepressant & anticonvulsantdrugs. Acutepain-ismostly nocioceptive- itis caused by noxious stimuli which activate peripheral nocioceptive response-itassociated w/ neuro-endocrine stress response that isproportional to intensity of stimulus.-mostforms of acute pain are self limited or resolves w/ tx resolve txsuch as w/ opioids or stimulus with in a few days or weeks.   If paindoes not resolve it can become chronic.Chronicpain: painthat lasts longer than course of disease or injury -may be nociocpetive or neuropathicin this type of pain, psychological mechanisms or environmental factors play amajor role.next we will discuss nerve classification as it results in noxious stimulitransmission
  5. Nocioceptive pain
    Nocioceptive: which can either somatic or visceral. Nocioceptive pain,  is pain resulting fromongoing stimulation of nerve by noxious stimuli.  Somatic has identifiable focal point and follows distribution of nerve.  it is well localized, sharp, and pain at point of stimulusvisceral: diffuse, can be referred to another area, often described as dull and vague.   Ex . occurs when organ capsule is distended or when there is obstructionof hollow viscosnociocpetive pain whether somatic of visceralresponds well to nsaids and opiodanalgesics
  6. Neuropathic pain
    Neuropathic pain: caused by abnormal processing of painful stimuli.  Dysfunction of CNS that allows for spontaneous excitation leading to severe pain. can be generated peripherally or centrally. Difficult to treat.  Pain described as burning, tingling, or shock like.can be associated w/ subjective numbness, loss of sensation , and weakness.•does not respond well to NSAIDS or opiods analgesic alone,  adjunctive analgesic may be efficacious in treating neuropathic pain.•adjunctive analgesic : med that isapproved and used for other reasons than analgesics properties:  ex) tricyclic antidepressant & anticonvulsant drugs.
  7. acute vs chronic pain
    Acute pain-is mostly nocioceptive- it is caused by noxious stimuli which activate peripheral nocioceptive response-it associated w/ neuro-endocrine stress response that is proportional to intensity of stimulus.-most forms of acute pain are self limited or resolves w/ tx resolve tx such as w/ opioids or stimulus with in a few days or weeks.   If pain does not resolve it can become chronic.Chronic pain: pain that lasts longer than course of disease or injury - may be nociocpetive or neuropathicin this type of pain, psychological mechanisms or environmental factors play a major role.next we will discuss nerve classification as it results in noxious stimuli transmission
  8. specific nerves that carry pain
    specific nerves that carry pain = A delta (carry fast pain, sometimes referred to asfirst pain) & C fibers (carry slow pain sensation aka second pain)
  9. fast pain
    So fast pain results from activation of A-delta fibers and as you can see these fibers are myelinated. Pain transmitted along these fibers consists of a sharp, prickling sensation which is accurately localized and the duration of pain carried by the A-delta fibers coincides with the duration of the painful stimulus.
  10. slow pain
    Slow pain carried by C-fibers is burning or diffuse pain which has slower onset and greater persistence and less clear location. Slow pain results from the activation of C-fibers which unmyelinated and often the duration of pain carried by these C-fibers exceeds the duration of the stimulus.
  11. is acute pain fast or slow pain
    So acute pain is fast pain and is due to nocioception. It’s a physiologic pain, it’stransient, usually of brief duration, and easily treated with NSAIDS or opioids
  12. what are the neuronal changes seen in chronic pain?
    Chronic pain is different, it’s a pathologic problem with the sensations carried byC-fibers. It persists beyond the usual course of acute disease or injury, generally persists 1-6 months post healing. When chronic is associated with aloss of sensory input such as an amputation it is called deafferentation pain. Chronic pain is complex andinvolves changes within the nervous system both centrally and peripherally.There are changes in synaptic efficiency, nerve sprouting, and formation of newsynapses. There are different types of chronic pain. There can be sympatheticmediated pain which involves changes in adrenal receptor function and there canbe chronic pain which is sympathetically independent.
  13. A delta fibers & C fibers
    specific nerves that carry pain = A delta (carry fast pain, sometimes referred to asfirst pain)• & C fibers (carry slow pain sensation aka second pain)fast pain results as activation of a delta fibers, these fibers are myelinated
  14. A delta fibers & C fibers
    specific nerves that carry pain = A delta (carry fast pain, sometimes referred to asfirst pain)• & C fibers (carry slow pain sensation aka second pain)fast pain results as activation of a delta fibers, these fibers are myelinated
  15. C-fibers carry which type of pain?
    Slow pain carried by C-fibers is burning or diffuse pain which has slower onset and greater persistence and less clear location. Slow pain results from the activation of C-fibers which unmyelinated and often the duration of pain carried by these C-fibers exceeds the duration of the stimulus.
  16. chronic vs acute pain
    So acute pain is fast pain and is due to nocioception. It’s a physiologic pain, it’stransient, usually of brief duration, and easily treated with NSAIDS or opioids. Chronic pain is different, it’s a pathologic problem with thesensations carried by C-fibers. It persists beyond the usual course of acute diseaseor injury, generally persists 1-6 months post healing. When chronic is associated with a loss of sensory input such as an amputation it is called deafferentation pain. Chronic pain is complex and involves changes within the nervous system both centrally and peripherally.There are changes in synaptic efficiency, nerve sprouting, and formation of newsynapses. There are different types of chronic pain. There can be sympatheticmediated pain which involves changes in adrenal receptor function and there canbe chronic pain which is sympathetically independent.
  17. periaqueductal gray
    Some of this afferent input goes to an area of the brain called the periaqueductalgray, which is gray matter in the mid brainWhen there is is afferent stimulation of the periaqueductal gray, the efferent ordownward neural pathway is activatedEfferent neurons located in the periaqueductal gray form synapses w/ structures in themedulla that inhibit painThis efferent pathway is responsible for the modulation or inhibition of painsignals
  18. look this up
    Transmissionthrough C-fibers is relatively slow, and this may be due to the lack of themyelin sheath. Also, the the A-delta fibers and the C-fibers synapse atslightly different places in the spinal cord. The A-delta fibers that carryfast pain synapse at lamina 1 and 5. They then cross the spinal cord and travelto the mid-brain specifically the thalmus via the neospinothalamictract. Asyou may recall there are the main afferent or sensory pathways is the spinothalamic tract. There are 2 divisions of spinothalamic tract, the neospinothalamic tract carroes fast pain to the mid-brain. The paleospinothalamic tract carries slow pain fromC-fibers to the reticular formation of the brain stem. So we talked aboutA-delta fibers synapsing at lamina 1 and 5. C-fibers synapse at a differentplace, in lamina 2 which is also called the substantia gelatinosa. and also in lamina 3. Lamina 2,the substantia gelatinosa, contains many intra-neurons and plays amajor role in processing and modulating nocioceptive input. It is also a major site ofthe action of opioids. So as far as the anatomy you can see in this slide thesynapse of A-delta fibers and C-fibers is at slightly different places in thedorsal horn. Spinal cord gray matter is divided into 10 lamina, the first 6 ofthese lamina make up the dorsal horn. So the dorsal horn receives all afferentneuron activity and is the principal site for the modulation of pain by bothascending and descending neuro pathways. So once the A-delta andC-fibers, carrying the pain sensations, synapse in the dorsal horn, they ascendor descend 1 to 3 segments in the Tract of Lissauer. Then there is a synapse with a 2nd order neuron, which crosses themidline and ascends via the contralateral spinothalamic tract to the brain. So the painpathway is the spinothalamic tract. In the dorsal there are 2nd order neurons and these 2nd order neurons can either be nocioceptive, which means they only servenoxious stimuli, or they can be wide dynamic range neurons, which can carryboth noxious and non-noxious stimuli. The wide dynamic range neurons arecapable of windup.This means that during repeated stimulation, wide dynamic range neurons canincrease their firing rate in a graded fashion called wind up, even with thesame stimulus intensity. This does have implications in our practice. Forexample, preemptive analgesia is thought to be effective by preventing the windup of wide dynamic range neurons. In the thalmus, the 2nd order neurons synapse with 3rd order neurons which transmitsignals upward towards the cerebral cortex. Some of this afferent input goes toan area of the brain called the periaqueductal gray, which is gray matter in themid-brain.
  19. what is the most well known NT in pain transmission?
    substance P
  20. what is the major neurotransmitter released from C fibers?
    In the dorsal horn of the spinal cord, there are receptor systems that function to modulate the transmission of painSpeaking specifically about the chronic pain pathway, the C fibers synapse with interneurons in the substantia gelatinosa of the spinal cord and release the excitatory transmitter substance P to these interneuronsThe major NT released from C fibers is substance P
  21. what happens when enkephalin is released?
    he C fibers synapse with interneurons When enkephalin is released into the nerveterminal the release of substance P is decreasedYou can see in the inner block diagram, the release of substance P and you can alsosee the inhibitory release of enkephalin on second order neurons When the release of substance P is decreased via enkephalin release, the number of actionpotentials initiated in the interneuron of the pain pathway is reduced and theperception of pain is decreased
  22. what is enkephalin's effect on pain transmission?
    The effect of enkephalin on the pain transmission is inhibitory similar to that of the endorphins and serotoninThis has implications for pain managementThis explains the benefits of lose dose serotonin reuptake inhibitors in chronicpain ptsThe acute pain pathway is differentThe major NT released from the A delta fibers is glutamate à excitatory NTThe glutamate binds to AMPA and NMDA receptors on the post synaptic membrane
  23. What is the major NT released from the A delta fibers?
    The major NT released from the A delta fibers is glutamate à excitatory NTThe glutamate binds to AMPA and NMDA receptors on the post synaptic membrane
  24. Substance P, a major NT of pain, facilitates transmission of pain via________ receptor activation
    Substance P, a major NT of pain, facilitates transmission of pain via NK-1 receptoractivation
  25. NMDA receptors and AMPA receptors are________  receptors located ________  on the __________
    • glutamate
    • post synaptically
    • 2nd order neuron
  26. describe how  NMDA antagonists, such as ketamine work?
    Substance P, a major NT of pain, facilitates transmission of pain via NK-1 receptoractivationNMDA receptors and AMPA receptors are glutamate receptors located post synaptically on the 2nd order neuronWhen glutamate, an excitatory NT, is released from the primary nerve terminal it binds to these post synaptic receptors, and then the 2nd order neuron depolarizes and the pain impulse continues its transmission to the brainPain management strategies include NMDA antagonists, such as ketamineKetamine an be used in chronic pain syndromes such as neuropathic pain and diabetic neuralgia
  27. tell me about alpha 2 receptors
    there is an alpha 2 receptor, there are certain drugs such as clonidine and dexmedetomidine (precedex) that are alpha 2 adrenoceptor agonists The activation of alpha 2 leads to inhibitionAn alpha 2 agonist such as precedex causes an inhibitory affect on pain transmissionAlpha 2 receptors are located in the dorsal horn
  28. tell me about GABA
    GABA is a NT affecting receptors A and B and inhibiting the transmission of painBaclofen is a GABA agonist that acts on the spinal cord to inhibit painIt has proven quite useful in the tx of trigeminal neuralgia
  29. how does nitrous oxide affect pain?
    Nitrous oxide produces analgesia via complex mechanisms including activation of thedescending inhibitory pathway, activation of alpha 2 spinal adrenoreceptors, and possibly by inhibiting an NMDA receptor function
  30. Mu, delta, and kappa
    Mu, delta, and kappa, now called opioid 1, 2, and 3, are opioid receptors that haveinhibitory effects on nociception
  31. describe what happens When there is an intense or prolonged noxious stimuli?
    When there is an intense or prolonged noxious stimuli, there’s a sustaineddepolarization of the dorsal horn neurons which leads to series of intracellular eventsThe membrane depolarizes and NMDA receptors (excitatory receptors) are activatedand there’s a calcium influx into the neuronThe calcium influx causes phospholipase a2 to be activated, this is not shown in this illustration, but once phospholipase a2 is activated, there’s an increased production of intracellular arachadonic acid and the products of the prostaglandin cascade
  32. Opioid agonists have a high affinity for___ receptors
    mu
  33. Spinal analgesia is mediated by all opioid receptors, but it’s primarily mediated by the ____
    mu 2 receptors
  34. Supra spinal analgesia, likewise, ismediated by all opioid receptors, but it’s primarily mediated by the ______
    mu 1 receptors
  35. Most opioids will affect all of the opioid receptors, except __________?
    Most opioids will affect all of the opioid receptors, except remifentanil, an ultra short acting opioid, which is metabolized by non-specific plasma esterases, and unlike the other opioids, remi is a potent mu receptor agonist that appears to lack delta and kappa agonist activity
  36. where do IV opioids work?
    IV opioids, work directly in the region of the brain referred to as the peri aqueductal grey, so IV / IM opioids result in both supra spinal and spinal analgesia, however after epidural or spinal administration of the opioid, spinal analgesia results from the action of theopioids in the substantia gellatinosa, remember, the dominant receptor mediating supra spinal analgesia is the mu 1 receptorWhen the peri aqueductal grey area is affected, for example, with IV opioids, the pt’s response to pain is altered, so pts may feel the pain, but don’t care as much about it, it alters their tolerance to the pain
  37. where does modulation of pain occur?
    So modulation of pain can occur peripherally at the site of the nocioceptor, in the SC, or in the brainAnd modulation can be either facilitation or inhibition of the pain impulses, so there can be peripheral or central modulation of painIn peripheral modulation nocioceptor neurons displace sensitization following repeated stimulation
  38. peripheral modulation of pain
    Can have enhanced response to noxious stimuli or increased responsiveness to wider range of stimuli even no noxious stimuli•Can be primary hyperalgesia or secondary hyperalgesia•Primary•Mediated by the release of substances from damaged tissues•Commonly results after tissue injury•Prostaglandin produced after tissue damage, because phospholipids are leased from the tissue, phospholipids through the action of phospholipase a2 form arachodinic acidand set of the arachodonic cascade•Secondary•Neurogenic inflammation•Red flush around the site of infury,local tissue edema, sensitization to noxious stimuli resulting from release ofsubstance P•Substance P•Degranulates mast cells which causes the release of many substances•Histamine-dilation of vessels and tissue edema•When ever tissue is damaged there is allergens which are substance that cause painreleased from damage tissue•Examples•Bradykinin, Vasophils, 5HT•May activate nerve endings causing pain•Reaction is decreased by the injection of a local anesthetic such as lidocaineThis is an example of peripheral modulation
  39. central modulation
    •Central Modulation•Can facilitate or inhibit pain•Three major mechanisms for central sensitization in spinal cord•Wind up and sensitization of second order neurons-wide dynamic range  increase their frequency of discharge with the same repetitive stimuli and continue to discharge after the noxious stimuli has stopped•Receptor field expansion-dorsal horn neurons increase their receptor fields such that adjacent neurons become active to stimuli to which they were previously unresponsive•Hyperexcitablity of flexion reflexes•Caused by excitatory neurotransmitters•Glutamate and esbartate-activate mda receptors and increase intracellular calcium which activates phospholipase a2 and sets off arachodonic cascade
  40. tell me about the arachodonic cascade
    • Arachodoniccascade•
    • Twopathways•
    • Lipoxygenasepathway which leads to leukotrienes•
    • Cyclooxygenasepathway which leads to prostaglandins•
    • Wouldbe advantageous to interrupt cascade

    • •Releaseof substances leads to pain and inflammation
    • •Allogen-painproducing substance
    • •All end products of arachodoniccascade are allogens
  41. How do corticosteroids, aspirin and tylenol cause analgesia?
    •Corticosteroidsand nsaids interrupt the cascade

    •Aspirin and acetaminophen interrupt the cyclooxygenase pathway(same as NSAIDS)

    •Analgesic effect of corticosteroids is likely the result of inhibition of prostaglandinproduction through blockade of phospholipase A2 activation
  42. Ascending sensory spinal cord tract, what is it?  what does  it transmit?  what is it a component of?
    •Ascending sensory spinal cord tract-pain and temperature

    •Lateral spinothalamic tract which is a component of the anterolateral system
  43. Dorsallateral fasciculus-descending tract.  what does it do?  what is it's site of origin?
    •Dorsallateral fasciculus-descending tract

    •Modulates pain

    •Site of origin

    •Periaqueductal gray area along with reticular formation and nucleus raphe magnus

    • From there fibers relay inhibition to the dorsal horn neurons via the dorsolateral fasciculus, so for example, TENS (transcutaneous electrical nerve stimulation) is thought to produce analgesia by stimulating large afferent fibers, this involves the gate control theory of pain that activation of large afferent
    • fibers inhibit wide dynamic range second order neurons thereby inhibiting pain.
    • This plays a role with patients with mild to moderate acute pain and those with
    • chronic Low Back Pain, arthritis, and neuropathic pain. So the blocking of
    • large afferent pain fibers is thought to block conduction in the small afferent
    • pain fibers. Another method that uses the same logic is spinal cord stimulators
    • which also modulate pain by the gate control theory this involves stimulation
    • of the dorsal column which produces analgesia by stimulating the large alpha
    • fibers in the dorsal column of the spinal cord.
  44. how does TENS produce analgesia?
    •by stimulating large afferent fibers 







    • this
    • involves the gate control theory of pain that activation of large afferent
    • fibers inhibit wide dynamic range second order neurons thereby inhibiting pain.
    • This plays a role with patients with mild to moderate acute pain and those with
    • chronic Low Back Pain, arthritis, and neuropathic pain. So the blocking of
    • large afferent pain fibers is thought to block conduction in the small afferent
    • pain fibers. Another method that uses the same logic is spinal cord stimulators
    • which also modulate pain by the gate control theory this involves stimulation
    • of the dorsal column which produces analgesia by stimulating the large alpha
    • fibers in the dorsal column of the spinal cord.
  45. the endocrine response to pain
    • So the endocrine response to pain is complex, there’s an increase in the secretion
    • of hormones such as adrencorticotropin hormone, cortisol, glucagon and so
    • forth. Insulin secretion is decreased. There are also neuro and hormonal changes in the dorsal horn neurons themselves which lead to increased wound sensitivity.  Sensitivity this can involve hyperalgesia which is sensitization of nociceptors and a decreased pain threshold.
  46. Neuroplasticity
    • refers
    • to change in the dorsal horn such as windup of second order neurons and
    • sensitization of second order neurons and receptor field expansion these changes facilitate nociceptor transmission of pain.
  47. how can pain affect multiple body systems?
    • There is also as you know sympatho-adrenal activation leading to release of renin and angiotensin resulting in tachycardia and hypertension.
    • There can be decreased pulmonary function associated with splinting and immobility. Pain and trauma upsets the competence of the immune system through neuro-endocrine pathways the degree of immunosuppression is closely linked to the magnitude of tissue damage and pain. So patients who are at higher risk of immune system dysfunction are benefitted by a higher level of pain control, as are all patients.
  48. How do NSAIDS work?
    • NSAIDS are often used in the management of mild to moderation postoperative pain and
    • pain related to inflammation. NSAIDs, ASA, and Tylenol inhibit the action of
    • cyclooxygenase thereby preventing conversion of arachidonic acid to prostaglandins. Prostaglandins sensitize and amplify peripheral nociceptor response to substance P.  We’ve talked about the cyclooxygenase pathway. Cyclooxygenase exists in 2 forms: cox 1 widespread in body;  cox2 is present in very small amounts and synthesized only in the presence of inflammation so our more recent generation of cox 2 inhibitors are much less likely to produce side effects like gastric irritation and leukotriene production, that the older COX inhibitors caused. Evidence suggests that gibing NSAID’s before inflammation begins as part of a preemptive analgesia is very effective.
  49. Sympathetic blocking drugs
    • Sympathetic
    • blocking drugs given orally can be effective in managing chronic pain, but in
    • acute pain they’re mainly given to treat tachycardia and HTN which accompany
    • the sympathetic response t conduction blockade of the nerves would be effective. It also shows the interruption of the pathway through alpha 2 agonist activity at the level of spinal cord, this is how Clonidine or Dexmedetomidine act.
  50. where do systemic opioids work?
    • Systemic opioids are effective at
    • BOTH the dorsal horn and the supra-spinal level. As far as parenteral opioids,
    • we know that SubQ and IM routes are less reliable for pain control. There is more patient dissatisfaction, the blood levels are
    • less consistent, there are delays of drug administration, and injections are
    • painful. Drug levels are better maintained by continuous infusion and PCAs is often used.
  51. opioid dosing for pca
  52. Risk factors for respiratory depression with a PCA
    include basal infusion, advanced age, hypovolemia, and OSA
  53. what are the most common side effects of opioids?
    The most common side effects of opioids as you know are vomiting itching and ileus.
  54. what is a consideration when giving opioid agonist/antagonists?
    • Care should be Taken not to give a drug with mixed opioids receptor actions to a patient taking pure agonist drugs because of the
    • unpredictable effects of this combination
  55. opioid anatagonists, what do they do?
    • Opioids antagonist Naltrexone similar to
    • naloxone is sometimes given as a maintenance drug for addicts and treatment
    • programs it is a pure antagonist like

    • naloxone but with a longer half life, it
    • completely blocks the effects of heroin, which is why it’s given to this population. Side effects of Naloxone can be serious such as tachycardia, cardiac dysfunction, HTN, pulmonary edema. These SE of is reflection of sudden increase in SNS activity when analgesia is suddenly reversed.
  56. in cardiac cases and adult non cardiac surgery which pain control mechanism shows lower mortality?
    • Cardiac and non-cardiac surgeries- both
    • adult and pediatric

    • •Reduced mortality with continuous IV
    • narcotic vs PRN IV narcotic

    • •Better analgesia is correlated with
    • decrease incidence of ST depression

    Suppression of pain can improve intermediate ST depression and  clinical cardiac outcomes
  57. what is the benefit of thoracic epidurals?
    • •Thoracic epidural analgesia can improve
    • myocardial oxygen supply

    •75% of atherosclerotic coronary artery stenosis – constrict in response to SNS stim

    •Dilates stenotic arteries

    •Lumbar epidural would not have this effect in fact it may lower the perfusion pressure

    •Epidurals only work where they are

    •Must be thoracic for segmental blockade to be beneficial

    •Effective for its who have thoracic or upper and surgery

    •Decreased postop diaphragmatic dysfunction

    Blocking the afferent limb of the inhibitory reflex arch
  58. how does an epidural improve outcomes in a GI case or vascular case?
    Lumbar epidural

    • •May result in decreased perfusion
    • pressure

    Effective pain management

    •Reduces the stress response

    •Reduced Activation of the SNS

    •May decrease thromboembolic morbidity

    • Epidural anesthesia followed by epidural
    • analgesia

    • •Improves survival of lower extremity
    • vascular grafts

    • •Been shown to decrease risk of DVT
    • following orthopedic and urologic surgery

    GI surgery

    • •Both epidural and systemic opioids
    • inhibit GI motility

    • •Faster recovery of GI function from
    • epidural vs systemic
  59. Does routine administration of opioids and NSAID attenuate the stress response?
    routine administration of opioids and NSAIDS does not attenuate the stress response
  60. what are some potential complications of opioids and how should meperidine be used?
    Incidences of respiratory depression after opioid administration approx: 0.9% PRN  0.8% PCA admin

    Use of mepereidine is discouraged for acute pain management and routine use

    In elderly and impaired renal function: accumulation of normeperidine can lead to anxiety, tremors, myoclonis and seizures

    American pain society: meperedine Not used for chronic pain management, if used for acute, not used for more then 48 hours and dosage should not exceed 600mg in a 24 hr period
  61. complications from epidurals?
    Epidural: common complications from LA: motor block, hypotension, urinary retention

    Larger doses increase risk of motor block and hypotension

    Placement of catheter in thoracic area decreases risk of motor block, complications may be minimized by smaller doses
  62. complications of epidural clonidine
    • Clonidide is the most commonly used alpha2
    • adrenergic agonist for epidural analgesia, common complications include:
    • hypotension and bradycardia and sedation due to systemic absorption from the epidural space, clonidine causes a reduction of sympathetic outflow from the brain stem, in contrast there is direct peripheral
    • vasoconstriction from increased systemic levels of clonidine

    • Main affects have to do with sympathetic outflow from the brain stem, sedation which
    • is dose related, no risk of resp depression, clonidine doesn’t potentiate resp depression from opioids, alpha adrenergic agonist such as clonidine, precedex, dexmetatomidine: provide analgesia via inhibition of second order neurons in the dorsal horn of the spinal cord
  63. complications of neuraxial opioids: reported incidence
  64. Effects of spinal and epidural fentanyl
    • Onset time is DIRECTLY proportional to lipid solubility; fentanyl is highly lipid
    • soluble therefore it has rapid onset

    • Lipophillic opioids such as fentanyl readily
    • diffuse into lipid membrane such a neural tissue, when it is placed in the subarachnoid space it rapidly diffuses out of the CSF, lipophillic and hydrophobic, subarachnoid fentanyl rapid onset short duration, early respiratory depression can occur with either subarachnoid or epidural injection because there is systemic uptake. rostral spread, toward the brain, is minimal because the fentanyl doesn’t stay in CSF is fixed to neural tissue easily because it is lipophillic so late depression of respiration is minimal
  65. Morphine: neuraxial placement
    • Onset is slow duration is longer, when placed
    • in subarachnoid space is diffuses out of csf slowly because hydrophillic, increased rostral spread

    Systemic absorption is minimal, can be late depression of ventilation, 6-12 hrs after injections

    • Most serious side effects of epidural hydrophillic opioids, is late respiratory depression  which is dose dependent, most reported cases involve systemic opioids for
    • sedatives risk is higher in elderly and sleep apnea

    • Small doses of naloxone 0.04mg reverse side effects of respiratory depression,
    • without necessary reverses analgesia

    IMPORTANT: nursing staff needs to be aware of late resp depression with neuraxial administration of morphine with appropriate monitoring

    Side effects: pruritus, nausea, urinary retention, resp depression, CNS depression, sedation
  66. Chronic Pain: Divided into complex regional pain syndromes 1 and 2 
    what are they?
    CRPS1 – formally known as reflex sympathetic dystrophy

    CRPS2 - causalgia
  67. How is pain sympathetically maintained in complex regional pain syndrome?
    Sympathetic nervous system dysfunction is involve in the generation of diffuse burden pain.

    The peripheral nociceptor fibers become very sensitive to norepinephrine, and so pain is sympathetically maintained.
  68. What are the Clinical features of CRPS?
    • reflex autonomic dysfunction. There are vasomotor abnormalities, abnormalities of hair and nail growth, and osteoporosis, accompanied by sensory symptoms of burning
    • pain, hyperalgesia, and allodynia (state of altered perception such that normally innocuous stimuli cause pain) There may be disturbance of motor function.
  69. How does one develop CRPS?
    • CRPS
    • 1 - effects the extremities, most commonly, and often follows relatively minor
    • trauma (sprained ankle). Hand and Foot are the most common sites

    • CRPS
    • 2 – typically follows high velocity injury, such as gun shot wounds, to large
    • nerves. Most cases involve brachial plexus or sciatic nerve.



    • There are very complex and incompletely understood changes involving the sympathetic
    • nervous system that are responsible for the development of CRPS.
  70. what are the changes in the sympathetic nervous system in CRPS?
    that injury results in sympathetic activation, at multiple sites.

    increased alpha adrenal receptors which are activated by locally released catecholamine's

    •  
    • with the nerve injury, and there are increased adrenal receptors

    • outgrowths of alpha adrenal receptors which drive ganglionic activity at the dorsal root ganglia. This is what is meant by nerve sprouting. There is sprouting of sympathetic nerves into the dorsal root ganglion following injury.
    • Peripheral inflammation results in release of prostaglandins and norepinephrine
    • and resulting sensitization.

    So pain in this case is sympathetically driven.
  71. treatment for CRPS
    Pain problems that are sympathetically maintained may respond to sympatheticblockade by agents administered systemically, regionally, or around the sympathetic ganglion. There is some dispute about the long term efficacy of repeated sympathetic blocks. Most patients require 3-7 sympathetic blocks along with physical therapy.  Sympatheticallydriven pain can be helped by low dose antidepressants, which inhibit the uptakeof norepinephrine and serotonin.
  72. chronic pain management strategies in CRPS?
    • Chronic
    • pain management strategies:

    • Local
    • anesthetic blockade – can be useful diagnostically as well as therapeutically.
    • Often as little as 1 ml of LA is injected and if pain relief occurs, then the
    • pain is said to be sympathetically driven. Once it has been established that
    • there is a sympathetic component treatment may consists of a series of LA
    • sympathetic blocks.
  73. cervicothoracic sympathetic block
    A LA is injected into the anterior tubercle of C6, hoping that the LA will spread to the Stellate ganglion (the ganglion formed by the fusion of the inferior cervical and first thoracic ganglions, sympathetic innervation to the face and upper extremities passes through the stellate ganglion) To determine if it spread, you are looking to see if there is sympathetic denervation of the upper extremity.
  74. useful drugs in CRPS
    Clonidine - Systemic sympathetic blocking drug

    Steroids –reduce inflammation

    In addition

    Therapy for chronic pain is directed towards stopping pain behavior, increasing strength and mobility and developing coping strategies
  75. Other procedural intervention for chronic pain syndromes:
    Epidural injection of corticosteroids for chronic back pain.

    •   -Low back pain is a common chronic pain
    • condition, and lumbosacral radiculopathy involves mechanical nerve root
    • compression which   often causes
    • inflammation and intra neural accumulation of protein and fluid

      -Epidural injection of corticosteroids reduce the inflammation at the nerve root. This tends to benefit patients with sciatica symptoms, and there is little risk of serious complications

    •   -Steroids are never injected in the sub
    • arachnoid space because of the possibility of archanoiditis.
  76. facet joint syndrome
    • Facet joints may also become inflamed and pathology in this aprt of the vertebra may be demonstrated by CT scans. The diagnosiscan be confirmed by injection of LA into the facet joint under fluoroscopy, which is what this slide shows. The patient is prone with the effected side tilted upward, proper needle placement is confirmed with contrast dye, them 1 ml of LA is injected. This produces analgesia lasting 6 months or longer in
    • about 1/3 of patients. NASIDs may also benefit pt’s with facet joint pathology.
  77. Entrapment syndromes
    Entrapment syndromes occur when nerves are compressed at the nerve passage through ananatomically narrow passage- ulnar nerve is common
  78. Myofacial pain
    patients have distinct areas (trigger points) of marked tenderness in one or more muscles. Palpation of the muscle reveals tight ropy bands over trigger points

    • pain radiates in a fixed pattern that does not follow a dermatome, it often occurs
    • after trauma

    Trigger point injection with 1-2 ml of local anesthetic have been helpful
  79. Low back pain
    arthritis, muscle sprain, herniated disk

    >3 months is considered chronic and requires a mulidisciplinary approach
  80. what is the most effective for sympromatic
    relief of pain associated with nerve root compression (radiculopathy
    epidural steroids

    Steroids are superior to local anesthetics alone- long term studies have been equivocal
  81. Spinal Stenosis
    progressive narrowing of the intervertebral foramina by osteophyte

    Spinal stenosis- (reads slide)  problem of advanced age, also called apondolosis, epidural steroids are helpful
  82. opioids and adjuvants for chronic pain
    Opioids can be used for chronic pain but neuropathic pain is less likely to respond

    Substance abuse correlates with a high risk of treatment failure

    Opioids are usually given in extended release forms such as a fentanyl patch

    •  Need to individuallize treatment with opioids.  If one has side effects or isn’t working
    • well, need to try another

    Patients on long term therapy may have incomplete cross tolerance between opioids

    Adjuvant drugs are often needed such as antidepressants

    Antidepressants- Tricyclic antidepressants have analgesic effects in neuropathic pain they block NMDA mediated activity

    SSRIs are also used, they block the reuptake of serotonin and norepi

    Serotonin is an important inhibitory neurotransmitter in the pain pathway

    Sympatholytics- clonidine

    •  prazosin     
    • propranolol have been helpful with neuropathic pain

    Anticonvulsants-phenytoin and clonazepam  effective by altering ion channels along nerve fiber and blocking the action potential

    • Na channel blockers inhits gluconate? 
    • Release

    Oral Mexilitine?

    Psychologic counseling is important too
  83. Mexilitine and anticonvulsants in chronic pain
    • In chronic pain management there are many PHARMACOLOGIC INTERVENTIONS.Drugs like Mexilitine and anticonvulsants stabilize the
    • neural membrane and suppress firing of traumatized neurons

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