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The Perfect Storm approaches

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1 The Perfect Storm approaches
Post-Op Pain management in Specific Patient Populations by Dr. William Crowley, SAMC Anesthesiologist The Perfect Storm approaches

2 2001 JCAHO pain standards The new standards require all institutions to: Recognize the right of patients to appropriate assessment and management of their pain. Identify patients with pain in an initial screening assessment. Record the results of the assessment. Educate relevant providers in pain management. Assure staff competency in pain management. Ensure that pain does not interfere with rehabilitation. Monitor and record the effectiveness of pain management. Establish accountability for quality pain management.

3 Accountability In 1999, the Oregon Board of Medical Examiners sanctioned a board certified pulmonologists’ medical license for one year for failing to adequately assess and manage his patients’ pain In July of 2001, a jury awarded the family of a man who died of metastatic lung cancer in California $1.5 million in a verdict against a physician for inadequate pain assessment and management. (The doctor was sued for “elder abuse/civil negligence” in civil court, as “pain and suffering” losses due to malpractice can’t be awarded in civil court in California after the patient dies. Malpractice insurance doesn’t cover civil negligence.

4 Accountability (continued)
In 2003, a physician, a hospital and a nursing home were sued (all three settled out of court) for improper pain assessment and management. *The physician was also disciplined by the state medical board, and ordered to take a 2 day comprehensive assessment program followed by a minimum of 40 hours of clinical education directed by the findings of the assessment. The federal government has arrested over 450 pain doctors since 1994, and there are now less that 5000 doctors in the US that are willing to prescribe high volume opioid drugs. ROCK----you----HARD PLACE

5 What is Pain? (IASP) The International Association for the Study of Pain (IASP) defines pain as, “An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.”

6 What is Pain? (Margo McCaffrey)
Margo McCaffery is a registered nurse and pioneer in the field of pain management. McCaffery suggested as early as 1968 the widely accepted definition, "Pain is whatever the experiencing person says it is, existing whenever the experiencing person say it does." (McCaffery and Beebe 1989, p. 7)

7 Pain comes in two physiologic forms:
Nociceptive pain Neuropathic pain Somatic pain results from injury to parts of the body that are NOT nerves or internal organs. It is usually well localized, and described with words such as: aching throbbing sharp dull Visceral pain results from inflammation, ischemia, or deformation of an internal organ. It is usually NOT well localized, and can even be “referred” to another part of the body, such as left arm or jaw pain in cardiac ischemia. It is often described with words like: deep pain pressure cramping The result of injury to nerves in either the central or the peripheral nervous system, and usually described with words like: burning tingling stabbing shocking lancinating *These descriptors are very important, and should be recorded in detail along with the patients’ pain rating!

8 The Nociceptive Pain Mechanism
The Nociceptive pain pathway consists of four processes: 1.) Transduction: The conversion of noxious stimuli into electrical current that depolarizes the cell membrane and creates an action potential. (Tissue injury triggers the release of prostaglandins which drastically increase the algesic effect of bradykinin and serotonin, exciting nociceptors. Cyclooxygenase converts arachidonic acid to prostaglandin, a conversion that gets blocked by NSAIDS) 2.) Conduction: The movement of the action potential from the periphery to the dorsal horn of the spinal cord. (Local anesthetics can stop an action potential in its tracks)

9 The Nociceptive Pain Mechanism (continued)
3.) Transmission: Neurotransmitters(substance P, glutamate, aspartate) are released from the nociceptor central terminus into the synapse between the nociceptor and the Dorsal Horn neurons, activating them. Some researchers refer to this step as “modulation” as this is where the impulses can be inhibited or facilitated by your own body) 4.) Perception: These signals are sent up the spinal cord to the brain where they are perceived as pain. These received signals themselves stimulate the brain to send signals back down the spinal cord that either inhibit or facilitate pain signals. These four processes are very important, as they each represent a step in the pathway that can be modulated (inhibited or facilitated) or even blocked entirely (in some cases). Local anesthetics are the ONLY way to completely block pain.

10 The normal pain response to injury
Pain intensity The normal pain response to injury Injured tissue releases “algesic” substances (leukotrienes, protons, bradykinin, histamine, serotonin) resetting the pain response curve to the left.

11 Pain pathways

12 A basic Pharmacologic guide to multimodal pain therapy

13 Multimodal Pain Therapy
Multimodal pain therapy is simply using two or more mechanisms to reduce pain at two or more sites, maximizing analgesia and minimizing side effects (mostly opioid related side effects). Multimodal pain therapy is often referred to as “opioid sparing”. It is “multidisciplinary”, involving Doctors, pharmacists, nurses (both med/surg and APN’s) Preemptive analgesics (Cox-2 inhibitors, pre-incision wound infiltration) NSAIDS and acetaminophen Local anesthetics (epidural, nerve blocks, infiltration of incision site) Alpha-2 agonists (clonidine) NMDA antagonists (ketamine) Opiates

14 The Neuropathic pain mechanism
An injured nerve is a dangerous nerve. When a nerve axon is damaged, it can degenerate. Degenerating nerves want to re-grow and release Nerve Growth Factor (NGF) to facilitate this. However NGF doesn’t just help a damaged nerve to repair itself. It also causes sodium channel and adreno-receptor proliferation on what’s left of the damaged nerve, and (importantly) channel and receptor proliferation on near-by, uninjured nerve fibers (both nociceptor and non-nociceptive mechano-receptor nerves.) All these extra channels and receptors lead to spontaneous nociceptor activity (in the absence of noxious stimuli) and the virtual bombardment of the dorsal horn of the spinal cord. This constant input leads to hyper-excitability of the dorsal horn neurons, sometimes to the extent that non-nociceptive neural input can be misinterpreted by the spinal cord as painful stimuli(Central Sensitization). A patient with diabetic neuropathy may complain that something as slight as a cool breeze can be excruciating on their feet (allodynia). Neuropathic pain has long been considered to be very difficult to treat. However, new research has brought a possible understanding of neuropathic pain.

15 Recent developments in neuropathic pain.
Nociceptors release glutamate, aspartate, and substance P as neurotransmitters. The dorsal horn cells of the spinal cord express both NMDA(N-methyl-D-aspartate) and AMPA receptors. When both are stimulated, “Long Term Potentiation” (pain memory) can occur. When glutamate binds to an AMPA receptor (at least 2 of the four subunits) Na+ ions pour into the cell and it depolarizes. Once depolarized via an AMPA receptor, glutamate can further depolarize the cell by binding to an NMDA receptor (which opens when the cell is depolarized). AMPA receptors are sodium channels only, whereas NMDA receptors are sodium and calcium channels. The influx of calcium into the cell causes an upregulation of AMPA receptors on the cell surface, leading to an increase in amplitude of the Excitatory Post-Synaptic Potential (EPSP). The cell now responds more strongly to ALL incoming signals. These mechanisms are self propagating, and may lead to a change in genetic expression, an example of “neuroplasticity” that can lead to pain in the absence of stimulus (phantom limb pain) Thus, you might guess that an NMDA receptor antagonist could alleviate neuropathic pain. And you’d be right.

16 Recent developments in neuropathic pain. (continued)
Ketamine is a potent NMDA antagonist, and as a low dose constant infusion has been shown to reduce the intensity of neuropathic pain. You’ll be seeing it on the floors in some patients in the near future. One study even showed that epidural verapamil (calcium channel blocker) was effective. Epidural analgesia works in neuropathic pain, often when everything else has failed. *{There will have to be a change in the current “universal” use of antithrombolytics (Lovenox), which preclude the use of epidurals in just about every patient who walks in the door, if pain relief is to be a reality for some patients.}

17 Pain physiology in specific populations
The Elderly: (the fastest growing segment of our population, with 1 in 5 expected to be older than 65 by 2050, according to the census bureau.) Chronic pain is the single most common complaint in the elderly, and has the greatest impact on quality of life. And treating pain in the elderly just got a lot more complicated…. High Grade Opioid Tolerance: (HGOT) In the last year federal statistics are available(2006) 180 million prescriptions for narcotic pain medicines were written. Researchers at the American Association of Pain Management estimate that nearly 3 million* Americans could be regarded as opioid tolerant, and that number is growing rapidly. *Does not include illicit drug users. This number could be as high as 15 million!

18 NSAIDs and the Elderly NSAIDS are not harmless!
18% of the elderly use NSAIDS everyday 60 million prescriptions annually and 63% take a prescription analgesic for > 6mo 72% take O.T.C. analgesics, for a median of > 5yr G-I adverse events: 20% 107,000 hospitalizations per year 16,500 DIE from ulcer complications *80% of patients with severe G-I complications have no prior G-I symptoms.

19 NSAIDS and the Elderly In light of all the negative press concerning NSAID use, The American Geriatric Society recently reversed its position and stated in its guidelines for treating persistent pain in the elderly (somewhere between 35-80% of elderly patients have persistent pain), that NSAIDS should be considered rarely, and with extreme caution, in highly select individuals. The new guidelines recommend that all patients with moderate to severe pain or diminished quality of life due to pain should be considered for opioid therapy. NSAIDS are STILL a valuable part of multi-modal post-operative pain management.

20 Elderly Patients with Chronic Pain who had seen a Doctor in the Last Year
Saw a pain specialist? 5% Had seen more than 5 doctors? % Saw primary care physicians? % The vast majority of chronic pain in this country is handled by primary care physicians.

21 Age related changes: JCAHO doesn’t just want pain managed, they want it assessed and recorded in a methodical, reproducible fashion. Challenges of pain assessment in older patients: 1.) Under-reporting: The elderly patient is much more likely than younger patients to remember later being in much more pain than was reported at the time. 2.) Lack of congruence between the patients’ and the caregivers’ perceptions of pain. 3.) Co-morbidities complicating the clinical picture. 4.) Sensory and cognitive impairments. Presentation: The elderly are more likely to present with lethargy, restlessness, confusion, or anorexia when in pain than other populations.

22 Age related changes: Pain assessment in Dementia:
Patient self reports are still reliable, as are caregiver/family member reports if they are familiar with the patient. Pain Assessment in Advanced Dementia (PAINAD): Assess breathing independent of vocalization Negative vocalization Facial expression Body language Consolability Each behavior scored 0-2, the higher the score, the more severe the pain.

23 Opiates and the elderly
Opiate dosing in the elderly is a “start low and go slow” process. Opiates should never be used as a monomodal therapy, and Demerol use is strongly discouraged. “Sustained release” oral opioids (OxyContin) are NOT for PRN dosing! Older patients experience side effects of opioids more frequently than younger adults. Sedation precedes respiratory depression. Decreased respiratory rate is a late sign of respiratory depression. Most people who suffered an opioid related In-Hospital Cardiopulmonary Arrest (IHCA) last year had a “normal” respiratory rate at the last vitals check before they were found. *There are between 370,000 and 750,000 IHCA’s every year, 50% are opioid related! Supplemental oxygen decreases the effectiveness of Oximetry in detecting hypoventilation. Does everybody over 30 need supplemental Oxygen?

24 High Grade Opioid Tolerance (HGOT)
Individuals requiring the equivalent of 1 mg or more intravenous or 3 mg or more oral morphine per hour for a period greater than one month may be considered to have High Grade Opioid Tolerance. (Sinatra, MD, PhD, Yale University)----It can happen a lot faster than that, and at much smaller doses. Tolerance: A state in which an increased dosage of a psychoactive substance is needed to produce a desired effect, a predictable and probably unavoidable result of chronic opiate use, even if taken exactly as prescribed by a physician. Tolerance develops to the opioid effects of analgesia, euphoria, sedation, respiratory depression and nausea, but not to miosis or constipation. Pharmacokinetic Tolerance: Opioids are biotransformed in the liver in reactions catalyzed by enzymes of the cytochrome P-450 system. The P-450 system can be induced by a host of unrelated compounds, and once induced can metabolize opioids much faster, leading to tolerance.

25 HGOT: Pharmacodynamic Tolerance: Neuroadaptive changes that take place after long-term exposure to the drug. 1.) Opioid receptor desensitization and down-regulation (not proven) 2.) Up-regulation of the cAMP pathway. Acutely, opiates inhibit the functional activity of the cAMP pathway, leading to hyperpolarization and inhibition of pro-nociceptor neurotransmitters like glutamate and substance P, but after long-term exposure the cAMP pathway recovers, and tolerance develops. Once recovery occurs, the cAMP pathway increases far above baseline levels after abrupt discontinuation of opioid binding, possibly responsible for the physiologic changes associated with withdrawal, dependence, and Opioid Induced Hyperalgesia. “Cross tolerance” is not 100% with opioids. Being tolerant to one opioid does not mean you’re tolerant to another opioid. If your HGOT patient isn’t getting relief despite high doses of one opioid, try another one.

26 Opioid Induced Hyperalgesia (OIH)
Central sensitization: Only recently has OIH been accepted as a “real” phenomenon worthy of research. Since that time, it has been recognized as a predictable and reproducible condition when patients treated with opioids long term had their dosages acutely reduced. This has particular relevance to the perioperative HGOT patient because more often than not, HGOT patients do not have their preoperative opioid drugs continued once admitted to the hospital, especially those patients who use illicit opioids. OIH and tolerance are two distinct entities.

27 How to Avoid OIH South Austin Hospital is not a detox center.
Recent reports have documented the occurrence of hyperalgesia when administration of opioids is abruptly tapered or discontinued, and that the hyperalgesia and allodynia that normally occurs after an injury is additive to that which is now known to occur when opioids are abruptly tapered. Find out the daily pre-surgical opioid dosage, and keep it going in the perioperative period.

28 Opioid conversion table There are even web sites that will calculate the conversion for you. Conversion tables rely on changing patient opioid dosage to “equianalgesic doses of Morphine.

29 How to use an opioid conversion table
Step 1: Set up the equation Values from the table Patient opioid values Value of opioid 1 = hour dose of current opioid(1) = Solve for X Value of opioid X amt. of new opioid (2) hour dose for opioid 2 Example: Mr. J takes 100 mg MSContin q8 hr, but is now NPO, and needs a new drug and a new route. Values from the table Patient opioid value Solve for X Morphine 30 mg PO = Morphine 300 mg PO = 15 mg Dilaudid Dilaudid 1.5 mg IV Dilaudid X mg IV IV/24 hrs *Reduce that dose by 25%(cross tolerance is NOT complete) 15 x .75= mg IV over 24 hours (0.5 mg/hour) by continuous infusion, with rescue dose of 10-20% Of the 24 hour dose(in this case 1-2 mg q 1 hour as needed for breakthrough pain.

30 Physiologic effects of pain *From the Journal of Perioperative Practice
Cardiovascular effects: Increased heart rate Increased blood pressure Increased stroke volume Increased myocardial oxygen demand Reduced myocardial oxygen supply Reduced blood flow to viscera and skin (delayed wound healing) Respiratory effects: Increased respiratory rate (respiratory alkalosis) for peripheral surgery Diaphragmatic splinting, hypoxia, atelectasis, pneumonia, for abdominal, thoracic surgery.

31 Pain effects: Endocrine effects: Increased Catabolism
Decreased insulin production (increased blood sugar levels) Decreased testosterone production Fluid retention Immune suppression Gastro-intestinal effects: Delayed gastric emptying Nausea Reduced G-I motility-Ileus Hemostatic effects: Hypercoagulability-> DVT

32 Pain effects: Psychological effects: Fear and avoidance behavior
Hyper-vigilance, insomnia Anxiety Anger Depression Catastophising

33 Pain effects: Chronic pain:
Incidence of post-operative chronic pain by procedure type: Thoracotomy: >50% Predictors of chronic pain included extent of acute post-operative pain and intercostal nerve dysfunction. Breast Surgery: Ranged from 11-57% Predictors of chronic pain included extent of acute post-operative pain presence of pre-operative pain, adjuvant radiation therapy, and intercostal nerve damage. Cholecystectomy: Ranges from 3-56% Predictors are numerous and varied, but it is suspected that post operative somatic incisional pain plays a significant role. *Perkins, FM, Kehlet, H Anesthesiology 2000

34 Summary Assess your patients’ pain, and record it!
Treat your patients’ pain, and then reassess and record it! Extended release opiates are NOT for break-through pain. Demerol is not recommended for anybody. Use opioid conversion tables to keep your HGOT patients on their normal preoperative opioid dosages, and then expect to add more for postoperative pain control. Any orders, written or verbal, stating or even implying that the attending physician is not to be notified of pain issues, is grounds for referral to peer-review.

35 Questions

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