{"id":5365,"date":"2011-07-14T20:25:51","date_gmt":"2011-07-14T20:25:51","guid":{"rendered":"http:\/\/crashtext.org\/misc\/5365.htm\/"},"modified":"2014-11-21T10:30:46","modified_gmt":"2014-11-21T15:30:46","slug":"pain-management","status":"publish","type":"post","link":"https:\/\/crashingpatient.com\/resuscitation\/pain-management.htm\/","title":{"rendered":"Pain Management"},"content":{"rendered":"

Is it the Pain or the Hurt that Matters<\/a> <\/p>\n

<\/span>Equivalency<\/span><\/h2>\n

Opioid Agonist<\/strong> IM\/IV\/SQ<\/strong> Oral<\/strong> Conversion Factor<\/strong> Half Life<\/strong> Starting Dose<\/strong>Morphine 10 30 3 2-3 hours 5 mg IV Q 4 Controlled Release Morphine (MS Contin) – 30 – 15 mg PO Q12 Codeine 130 200 NR 1.5 Hydromorphone (Dilaudid) 1.5 7.5 5 1 mg IV Q4 Levorphanol (Levo-Dromoran) 2 4 2 Methadone (Dolophine) 10 20 2 Meperidine (Demerol) 75 300 NR 4 Don’t Hydrocodone (Lorcet, Lortab,Vicodin, others) N\/A 30 N\/A 10 mg PO Q3-4 Oxymorphone (Numorphan) 1 (10 rectal) N\/A Fentanyl 100ug\/hr N\/A N\/A Fentanyl Patch 0.1 – 25 mcg\/hr=50 mg Morphine PO Q24hrs Controlled Release Oxycodone (Oxycontin) – 20 – 10 mg PO Q12 Oxycodone (Percocet, Tylox) N\/A 20 N\/A 5 mg PO Q4 Propoxyphene — ?NR N\/A Methadone 1-10 2-20   hydomorphone 1.5 mg = 10 mg morphine (10-20 minutes peak for hydro and morph) Br J Anesth 1984;56(8):813)   <\/p>\n

<\/span>Oxycodone and Hydrocodone<\/span><\/h2>\n

no difference in pain control between hydrocodone 5 mg and oxycodone 5 mg (Acad Emerg Med 2005;12(4):282)   <\/p>\n

<\/span>Hydromorphone<\/span><\/h2>\n

0.015 mg\/kg of dilaudad was equivalent to 0.1 mg\/kg   Rapid titration using 1+1 protocol. Use 1mg initially and an additional 1mg in 15 minutes (Ann Emerg Med 2009;54:221) and (54:561) <\/p>\n

<\/span>Morphine<\/span><\/h2>\n

  Oral Morphine per day\/2 = fentanyl patch per hour   Give 10% of 24 hour dose for breakthrough   Give everyone colace (softens), senna 2 tabs Qhs (stimulant), lactulose (large sugar)   IV opioids take 8 minutes, Oral 60-120 minutes, SC 20-30 minutes   Increasing dose, mild to moderate 25-50% Severe 50-100%   Rescue dose 20%   works at the \u03bc receptors 90% metab by liver conjugation contains Sodium Bisulfate which may cause allergic reactions histamine release may cause appearance of reactions     Dilaudad Toradol-no advantage over PO Fentanyl Nubain Ultram   Just b\/c one opioid doesn’t work does not mean another one in same class will not, start at 50% of prior dose with new med.   Life Sci. 2000;66(23):2221-31 > Lung opioid receptors: pharmacology and possible target for nebulized > morphine in dyspnea. > Zebraski SE, Kochenash SM, Raffa RB.   Chronic pain actually forms neuronal connections between somatic and pain sensory fibers causing pain with normal sensations= allodynia . Can also cause mood changes, depression, insomnia   12 hrs for fentanyl patch to work. warm temp allows more in, cold less.   Oxycontin gives a surge dose then the rest is time released.   Methadone’s analgesia lasts 6 hours.   Do not use NSAIDS unless no worry at all for GI Bleed   Instead use Bextra, as effective as Vioxx but without the side effects. Only worry in patients with renal failure (Audio Digest Chronic Pain) Can give 20 mg BID for 5 days and then 10 mg BID. <\/p>\n

<\/span>Codeine<\/span><\/h2>\n

The answer, it would seem, lies in the fact that there is highly variable expression in the brain of the gene to produce cytochrome P450 2D6 55. There appears to be moderate ethnic variability, with the most \u0091non-converters\u0092 being in whites. In this group, up to 10% are non-converters and up to another 10% are poor metabolizers 56. With Asians, only 1% are non-converters. This means to me that current studies suffer from the fact that there has not been an effort to look at how well this drug works in known converters. Taking the population as a whole, up to 20% can be expected to have diminished or no analgesic effects. Eliminating 1 in 5 people would significantly skew the results. I am still awaiting a study on codeine that takes this into account. I may still be convinced that it is a poor drug. Until then, I think it makes sense to NOT prescribe codeine as an unknown \u0096 i.e. for someone new to narcotic pain relief. This both because of the studies such as mentioned and because there is a finite chance (10-20%) the patient will be a non-converter. On the other hand, it is probably medical myth to assume it never works. With the occasional patient that requests it, and has felt it worked in the past, it is reasonable to use. (RaneyFacts) 5% expressed poorly 5% not expressed at all p450 enzyme needed to metab codeine to morphine   These studies also suggestthat the analgesic effect of codeine<\/strong> is either wholly or mostlydependent on its metabolism to morphine.6<\/a> 7<\/a> Metabolismof codeine<\/strong> to morphine is catalysed by the cytochrome P450 enzyme<\/strong> CYP2D6. Over 50 different genetic variants are known to existfor CYP2D6, which leads to a wide spectrum of metabolic capabilities within population<\/strong>s.8<\/a> 9<\/a> Individuals are normally classified as either poor metabolizers (PM) or extensive metabolizers (EM), depending on the activity of the enzyme<\/strong>, although this is knownto be an oversimplification. PMs will produce little or no morphinefrom codeine<\/strong> whereas EMs will produce morphine, although theactual amount may show wide variation.10<\/a>\u009612<\/a>   <\/p>\n

<\/span>Back Pain<\/span><\/h3>\n

Robaxin Take 1500 mg Q2hrs as long as no cognitive deficits as loading dose, then switch to the 1000 mg-1500mg QID. Do not use generic, it is not as good. If there is an inflammatory process, you need NSAIDs as well.   Use gabapentin for all of neuropathic pain. Worry about it only in renal patients. it does not affect drug levels.   Use Ultram instead of opioids for acute and chronic pain   Actin is the Fentanyl citrate lollipop Works very rapidly   Demerol’s metabolite normperidine causes seizures and highs.   Myofascial pain: true trigger points cause pain elsewhere when pressed. Travel lists the triggers. Reflex Sympathetic Dystrophy (RSD): calcitonin 200 IU IN OD, it takes a few days to work   Fentanyl Infusion at 2\/3 bolus dose\/hour     Analgesic adjuvants to opioids \u0095 Anesthesiology 1999: 0.5 mg\/kg ketamine PO q12h \u0096 Decreased need for breakthrough oral opioids, less somnolence \u0095 J Pain and Symptom Management 1999 \u0096 0.1 \u0096 0.2 mg\/kg\/hr infusion ketamine in terminal patients relieved pain morphine could not   Acute Pain Management in Trauma Give fentanyl bolus until relief then start drip at 2\/3 required dose per hour   Patient activated transdermal patches as good as IV PCA (JAMA 3\/16\/04)     <\/p>\n

Demorol<\/h4>\n

normeperedine can last up to 40 hrs in the elderly ——————————————————————————– Ketamine for Perioperative Pain Management (Anesthesiology Volume 102(1) January 2005 pp 211-220)   <\/p>\n

Opioid induced constipation<\/a><\/h4>\n

  Neuropathic Pain Use opioid and gabapentin in combination ( NEJM Volume 352:1324-1334 March 31, 2005 Number 13)     Use ketamine for the RSI and then keep it going for pain control 0.1 mg\/kg infusion   Topical anesthesia for all ng tubes 5 cc of lidocaine jelly 5 minutes before procedure   Intradermal lidocaine for IV starts   It is PROCEDURAL SEDATION, not conscious sedation Titrate analgesia and then sedation Even if you use incredibly potent sedative, patients still need pain control because pain is a spinal reflex and patients will have greater post-procedural pain. Pain is inducible   Best way to break spasm, like in lower back pain, is to stop the pain. Just keep titrating the opioids until pain is stopped. Then they must be treated with lower doses for 24-36 hours   NSAIDS require induction of Cox-2 receptors and give no relief in the first few hours   Canabinoid Canabinoid receptors receptors CB1 receptor stimulation produces receptor stimulation produces two effects: Analgesia Addictive behavior NOT endorphin sites that lead to addiction, only dependence   Methylnaltrexone Methylnaltrexone (MNTX) (MNTX) n No central antagonism No central antagonism \u0096 does not cross BBB does not cross BBB n Well absorbed PO Well absorbed PO n Alvimopan Alvimopan n Mu Mu selective antagonist selective antagonist n Minimal intestinal absorption Minimal intestinal absorption Bates 2004 Alvimopan Alvimopan 6 mg bid PO 6 mg bid PO n Shorter bowel recovery time, 1 day earlier discharge Alvimopan Alvimopan 6 mg pre 6 mg pre-op decreased post op decreased post-op op N&V from 23% to NONE N&V from 23% to NONE Taguchi 2001   NSAIDs NSAIDs n Can act as analgesic only if Can act as analgesic only if arachadonic arachadonic acid \/ acid \/ prostaglandin cascade activated prostaglandin cascade activated n Not effective in neuropathic pain Not effective in neuropathic pain \u0096 no tissue injury no tissue injury or inflammation or inflammation n Osteoarthritis good example of no inflammation, Osteoarthritis good example of no inflammation, little effect little effect n Requires 4 Requires 4-6 hours for blood 6 hours for blood-borne mediators to borne mediators to induce COX induce COX-2 receptors in dorsal horn 2 receptors in dorsal horn \u0096 cannot cannot obtain relief from obtain relief from NSAIDs NSAIDs in first few hours. Renal colic in majority of cases caused by raised intra intra-mural tension mural tension n NSAID will decrease that tension, requires 15 NSAID will decrease that tension, requires 15-20 20 minutes minutes n NOT effective in 15 NOT effective in 15-30% of patients as pain induced 30% of patients as pain induced by other mechanisms by other mechanisms n Note that pain control due to direct impact on mural Note that pain control due to direct impact on mural stretch receptors, so does not require COX stretch receptors, so does not require COX-2 induction induction   ACUTE PAIN MANAGEMENT IN THE EMERGENCY<\/strong> DEPARTMENT<\/strong> James Ducharme MD CM, FRCP Dalhousie University, Department of Emergency Medicine Saint John Regional Hospital Reference List \u00b7 Johnston CC, Gagnon AJ, Fullerton L, Common C, Ladores, Forlini S. One-week survey of pain intensity on admission to and discharge from the emergency department: a pilot study. Journal of Emergency Medicine 1998; 16(3):377-382. \u00b7 Unruh AM, Ritchie J, Merskey H. Does gender affect appraisal of pain and pain coping strategies? Clinical Journal of Pain 1999; 15(1):31-40. \u00b7 Raftery KA, Smith-Coggins R, Chen AHM. Gender-associated differences in Emergency Department pain management. Ann Emerg Med 1995; 26:414-421. \u00b7 Kelly AM. Does the clinically significant difference in visual analog scale pain scores vary with gender, age, or cause of pain? Academic Emergency Medicine 1998; 5(11):1086-1090. \u00b7 Horgas AL, Tsai PF. Analgesic drug prescription and use in cognitively impaired nursing home residents. Nursing Research 1998; 47(4):235-242. \u00b7 Acute pain management guideline panel. Acute pain management: Operative or medical procedures and trauma, Clinical Practice Guidleine No 1. Publication No. 920032. 1992. Rockville, Md, U.S. Department of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research. Ref Type: Report \u00b7 Singer AJ, Richman PB, Kowalska A, Thode HC, Jr. Comparison of patient and practitioner assessments of pain from commonly performed emergency department procedures. Annals of Emergency Medicine 1999; 33(6):652-658. \u00b7 Todd KH, Funk JP. The minimum clinically important difference in physicianassigned visual analog pain scores. Academic Emergency Medicine 1996; 3(2):142-146. \u00b7 Ducharme J, Beveridge RC, Lee JS, Beaulieu S. Emergency management of migraine: is the headache really over? Academic Emergency Medicine 1998; 5(9):899-905.     PAIN: OF COURSE IT\u0092S ALL IN YOUR HEAD NEUROBIOLOGY OF PAIN DEFINITION   IASP: “Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage”. Even the authors were aware of this definition\u0092s inadequacy, and hastened to add: “Pain is always subjective\u0085 This definition avoids tying pain to the stimulus”. Despite the disclaimer, this definition DOES tie the sensation to the stimulus, perpetuating the centuries old fallacy. It does not, and cannot, explain many of the perplexing aspects of pain experience, and it does not consider the crucial influence of the brain on the sensation and the perception of pain. <\/p>\n

    \n
  1. The brain can generate pain, create a perceptual experience, independent of the peripheral input, i.e., regardless of the presence or the extent of tissue damage or pathology.<\/li>\n
  2. The brain is continually modified by experience and sensory input.<\/li>\n<\/ol>\n

    THE PUZZLE OF PAIN   Without the contributions of modern neuroscience, it is impossible to unravel the multitude of the pain puzzles: <\/p>\n

      \n
    1. Well known instances of NO PAIN with major injuries<\/li>\n
    2. Excruciating PAIN in missing structures (phantom pains), or denervated structures (below spinal cord section in paraplegics)<\/li>\n
    3. PAIN persisting, after complete healing of injury<\/li>\n
    4. PAIN provoked by touch, or no stimulus at all<\/li>\n
    5. PAIN that is delayed, or non-anatomically spread<\/li>\n<\/ol>\n

      NOCICEPTION AND PAIN PATHWAYS   Stimuli from the periphery (mechanical, chemical, thermal) are transmitted to the spinal cord through the sensory afferent nerves. Damaged tissue is a source of many amines and peptides that stimulate sensory nerve endings: bradykinin, adrenaline, 5HT, PGE2, IL-1, IL-6, TNF-alpha, etc. These afferents synapse on the dorsal horn second order neurons in the spinal column (projection neurons), which form pathways extending to the brain \u0096 primarily thalamus and somato-sensory cortex. Acute, physiological pain is mediated in the spinal synapses mainly by the GLUTAMATE-activated AMPA type of glutamate receptors. In addition to glutamate, excitatory transmitters include AcCh, substance P, and CGRP, while GABA, enkephalin, 5HT and NA provide the inhibitory neurotransmission. NEUROBIOLOGY OF CHRONIC PAIN Chronic pain is not just a prolonged acute pain; it is a distinct entity, with many functional and structural alterations of the peripheral and central nervous system. ERIPHERAL SENSITIZATION \u0096 PRIMARY HYPERALGESIA Peripheral nociceptive hyperexcitability is induced through increased receptor (autosensitization) or cell membrane (heterosensitization) reactivity to stimuli, usually sustained presence of inflammatory factors. CENTRAL SENSITIZATION \u0096 SECONDARY HYPERALGESIA Central hyperexcitability is the key process in the generation of chronic pain. It is mediated by NMDA-type of post-synaptic glutamate receptors, and it results in transcriptional changes and manufacturing of the c-fos protein (the marker of central sensitization) in the second order dorsal horn projection neurons. Repetitious and intense activation of the high-threshold C-fibers and AMPA post-synaptic receptors results in activation of the NMDA post-synaptic receptors (through dislodging the Mg ions and opening the N and Ca channels to Ca influx) and the NMDA mediated WIND-UP phenomenon (augmented response of the dorsal horn neurons to the same intensity stimuli). Activation of the NMDA-receptors represents the first step in central sensitization, i.e., the transition from acute to chronic pain. Knowing this makes it easy to realize that adequate treatment of physiological, nociceptive pain is the most important goal of acute pain management \u0096 prevention of central sensitization! Other changes involved in central sensitization include substance P \u0096 NO (nitric oxide) cascade (with expansion of the receptive fields), increased release of NPY, VIP, galanin, and somatostatin from the pre-synaptic C-fiber terminals, hyper-sensitization of the WDR (wide dynamic range) neurons to non-nociceptive stimuli, expression of substance P by A-fiber pre-synaptic terminals, and sprouting of A-fiber terminals into the superficial layers of the dorsal horn (thus synapsing onto the nociceptive second order neurons). Reorganization or remodelling of the synapses at the dorsal horn level, as well as at the brainstem, thalamus, and somatosensory cortex levels, is a well-documented phenomenon, referred to as neuronal plasticity, responsible for a variety of chronic pain syndromes. Central sensitization and neuroplastic remodeling are responsible for all the main features of chronic pain: hypersensitivity to nociceptive stimuli (hyperalgesia), perception of pain upon non-nociceptive stimulation (NNP and allodynia), expansion of the pain-receptive fields and trigger-zones, and delayed pain. Changes in central sensitization can be viewed as: <\/p>\n

        \n
      1. FUNCTIONAL (NEUROCHEMICAL) HYPEREXCITABILITY:Activation of the NMDA- receptors, wind-up, sensitization of WDR neurons, expression of substance P by A-fibers<\/li>\n
      2. STRUCTURAL (NEUROANATOMICAL) HYPEREXCITABILITY:<\/li>\n<\/ol>\n

        Dying-off of C-fiber terminals, sprouting of A-fiber terminals, extensive reorganization of the somatosensory cortical maps, remodeling in the brainstem, cerebellum, basal ganglia, and motor cortical areas. DYSFUNCTIONAL DESCENDING INHIBITION \u0096 FAILURE OF INTERNAL ANTINOCICEPTION As illustrated in PAIN PATHWAYS, nociception activates not only the afferent pathways, but also a variety of segmental and descending, inhibitory or anti-nociceptive pathways (SLIDE 5). Increased brainstem CCK, and deficiencies in the descending enkephalin, 5HT, and NA pathways, can all contribute to dysfunctional anti-nociception. Processing of pain at the brain level has profound implications for both, the perception of pain, and for the management of pain. Ascending pain pathways are relayed through the thalamus to the somatosensory cortex, which is responsible for the initial localization and the intensity of the stimulus (SENSORY-DISCRIMINATIVE function), as well as to the limbic brain structures, esp. the anterior cingulated cortex, which is responsible for the unpleasant, aversive aspect of the experience (AFFECTIVE-MOTIVATIONAL function). Both of these areas communicate extensively and reciprocally with the prefrontal cortex, which brings the situational and memory context to the experience (COGNITIVE-EVALUATIVE function). These three aspects of pain experience (R. Melzack\u0092s gate and neuromatrix theory of pain) make a variety of pain treatment modalities potentially helpful, and at the same time provide the neurophysiological and neurostructural explanation of these modalities\u0092 efficacy (dismissing, in the process, all kinds of hogwash that has been written about “psychogenesis” of pain).   CHRONIC PAIN SYNDROMES Chronic pain is generally categorized, according to etiological factors, as stemming from tissue damage \u0096 inflammatory pain<\/strong>, or from nerve damage \u0096 neuropathic pain<\/strong>. The former is evident in various injuries (low back pain), infections, inflammatory diseases (RA, IBD, SLE) and immune\/neuroendocrine dysfunctions (possibly FM\/CFS, MPS). The latter is encountered in diabetes, certain infections (shingles), cancer, traumatic nerve injury, and following amputations (limb, breast). Opioids are exceedingly effective in managing inflammatory pain, whereas they are less effective in managing neuropathic pain, due to the loss of pre-synaptic opioid receptors, and the extensive re-wiring of the dorsal horn synaptic circuits. Low back pain In up to 85% of sufferers, there is no detectable damage (“no objectively demonstrable organic pathology”); in only about 15% can one of the five recognizable causes (herniated disc, arthritis, infection, tumor or fracture) be demonstrated. In addition, it is estimated that about 10% of low back pains develop a neuropathic dimension, making the picture even more puzzling. The vast majority of chronic low back pain sufferers continue to be under-treated or maltreated, labeled as “somatizers” or malingerers, despite ample evidence for central sensitization and somatosensory mapping reorganization in such patients. Fibromyalgia and Myofascial Pain Syndrome There is ample evidence in these disorders, as well, of altered central processing of the incoming nociceptive and non-nociceptive stimuli, at both the spinal and the brain level. Incoming stimuli from muscle C-fiber afferents are much more potent inducers of central sensitization than skin afferents, explaining lower pain threshold (hyperalgesia) and pain on movement (proprioceptive allodynia) in these patients. In addition, a dysregulated neuroendocrine stress response (decreased cortisol, growth hormone and IGF-1 secretion) may compound the picture in about a third of patients. Phantom limb pain Phantom pains affect over 70% of amputees, and persist for 2-7 years in about 60% of them; fewer than 15% obtain total pain relief. Extensive somatosensory cortex reorganization, with expansion of the trigger zones, has been demonstrated in numerous brain imaging studies. Peripheral ectopic discharges (from the stump neuroma), deafferentation hyperexcitability, and unmasking of the underlying silent connections, may all be contributory. In addition to phantom limb pain, phantom pains following mastectomy, and phantom body pains below the spinal cord section in paraplegics, are gaining increasing recognition. DIAGNOSIS OF CHRONIC PAIN: CARTESIAN DUALISM, PSYCHOBABBLE AND ARROGANT IGNORANCE Clinical features of chronic pain can be confusing and difficult to comprehend for the examining physician, leading to the characterization of the patient\u0092s complaints as “non-organic”, “psychogenic”, “hysterical”, “somatizing”, and “hypochondriacal”, or as evidence of “illness\/pain behavior”, “emotional overlay”, or even malingering. Especially puzzling is: <\/p>\n