PAIN MANAGEMENT 1. PHARMACOTHERAPY

2. PAIN MANAGEMENT1. PHARMACOTHERAPY Salah N A El-Tallawy Prof. of Anesthesia and Pain Management, Faculty of Medicine, Minia University & NCI, Cairo University, Egypt Associate Prof. KSU, KSA

3. Objectives Introduction. Pain control strategies. Special painful conditions. Rules for pharmacotherapy. Algorithms for pain management.

21. Drug Strategies Non Opioid Analgesics: NSAA NSAIDs Non-selective COX inhibitors Selective COX-2 inhibitors Opioids Weak Opioids. Strong opioids. Mixed agonist � antagonists Adjuvants Antidepressants Anticonvulsants Substance P inhibitors NMDA inhibitors LA Drugs for Headache Drugs for Bone pain Others .

22. Alternative medicine: Acupuncture TENS Cupping Chiropractice Physical Therapy ice, heat, massage Exercise Psychological therapy Cognitive-behavioral therapy Relaxation techniques Biofeedback Hypnosis Non-Drug Strategies

23. WHO step Ladder

24. 1. Drug Therapy * All acidic analgesic / anti inflammatory Ds are highly bound to pp ? high conc in spleen, liver, bone marrow, GIT & especially in inflammed tissue ? almost complete local inhibition of cyclooxygenases. This explains that only acidic AA & NSAIDs are anitiinflammatory and cause acute side effects in the GIT, -- of platelets aggregation and kidney (fluid and K retention). Also, chronic inflammation of URT as in asthma, may lead to accummulation of NSAIDs in mucosa �Aspirine Asthma� in asthmatic pts. * In contrast, acetaminophen with neutral pka values and low pp are equally distributed uniformly throughout the body. * All acidic analgesic / anti inflammatory Ds are highly bound to pp ? high conc in spleen, liver, bone marrow, GIT & especially in inflammed tissue ? almost complete local inhibition of cyclooxygenases. This explains that only acidic AA & NSAIDs are anitiinflammatory and cause acute side effects in the GIT, -- of platelets aggregation and kidney (fluid and K retention). Also, chronic inflammation of URT as in asthma, may lead to accummulation of NSAIDs in mucosa �Aspirine Asthma� in asthmatic pts. * In contrast, acetaminophen with neutral pka values and low pp are equally distributed uniformly throughout the body.

26. 1.a.) NSAA - Acetaminophen Acetaminophen blocks prostaglandin synthesis centrally , this account for its antipyretic effect. However, it does not act on prostaglandins peripherally, so it cannot block local inflammation. Therefore, acetaminophen only lowers temperature and has analgesic properties because of its antiprostaglandin activity in the CNS. Long-term or large doses are both hepatotoxic and nephrotoxic. Toxic metabolite: benzoquinones Antidote: N-acetylcysteine or glutathioneAcetaminophen blocks prostaglandin synthesis centrally , this account for its antipyretic effect. However, it does not act on prostaglandins peripherally, so it cannot block local inflammation. Therefore, acetaminophen only lowers temperature and has analgesic properties because of its antiprostaglandin activity in the CNS. Long-term or large doses are both hepatotoxic and nephrotoxic. Toxic metabolite: benzoquinones Antidote: N-acetylcysteine or glutathione

27. NSAA � AcetaminophenCOX-3 inhibitor

28. Salicylates (e.g. aspirin) Aspirine has antipyretic and analgesic effects as well as anticoagulant and anti-inflammatory actions. Theoretically, these actions result from the antiprostaglandin activity, both centrally and peripherally. Unfortunately, these additional actions predispose this medication to produce GIT problems, including gastritis, bleeding ulcer, in susceptible individuals. Despite these problems, aspirin is still the cheapest and most readily available analgesic preparation.Aspirine has antipyretic and analgesic effects as well as anticoagulant and anti-inflammatory actions. Theoretically, these actions result from the antiprostaglandin activity, both centrally and peripherally. Unfortunately, these additional actions predispose this medication to produce GIT problems, including gastritis, bleeding ulcer, in susceptible individuals. Despite these problems, aspirin is still the cheapest and most readily available analgesic preparation.

29. 1.b.) NSAIDs

30. NSAIDs Blocks the production of Prostaglandin Very effective in mild � moderate pain Effective in other types of pain e.g. Musculoskeletal pain OR & RA Cancer Pain May be used alone or in combination with opioids

31. Practical guide for NSAID�s In Postoperative sitting: Pre-op administration ? ? post-op pain. e.g. Leroxicam 8-16 mg IV or Celebrex 400mg, P.O. pre-op Ketorolac & Leroxicam are effective in acute pain (IV) Precautions: Gastric effects: PPI are the drugs of choice to treat gastric complications. H2 blockers only mask the disease Check the renal function routinely prior to administration COX2 inhibitors doesn�t affect the platelet function

32. Practical guide for NSAID�s Usage (Contin) All specific or non-specific NSAID�s may cause: Water retention and edema Hypertension Renal dysfunction May delay bony fusion in chronic usage

33. Mechanism of Renal dysfunction: PGE2 and PGI2 are medullary VD. TXA2 is: cortical VC, regulate the renal vascular resistance and Renin secretion. Both can influence: The action of ADH. Loss of local renal Haemo-regulation (e.g. in hypotension) Reduction of GFR. Electrolyte and Na imbalance. PGDs depletion can result in: Acute tubular necrosis & papillary necrosis, Interstitial nephritis Local haemoregulation of the kidney is dependant on prostaglandins: PgE2 and PgI2 are medullary vasodilator. TxA2 is cortical vasoconstrictor and regulate the renal vascular resistance and Renin secretion. Accordingly, glumerular filtration rate is greatly dependant on this mechanism. Both can influence the action of ADH. Kidney affection by NSAIDs usually due to loss of local haemodynamic regulation.The early sign of affection is plasma sodium disturbance, this is followed by interstitial nephritis, then tubular and papillary necrosis. In early cases this process is recoverable. This mechanism is important in operative cases when hypotension is present, and NSAIDs are used as analgesic.Local haemoregulation of the kidney is dependant on prostaglandins: PgE2 and PgI2 are medullary vasodilator. TxA2 is cortical vasoconstrictor and regulate the renal vascular resistance and Renin secretion. Accordingly, glumerular filtration rate is greatly dependant on this mechanism. Both can influence the action of ADH. Kidney affection by NSAIDs usually due to loss of local haemodynamic regulation.The early sign of affection is plasma sodium disturbance, this is followed by interstitial nephritis, then tubular and papillary necrosis. In early cases this process is recoverable. This mechanism is important in operative cases when hypotension is present, and NSAIDs are used as analgesic.

34. Choice of NSAIDs 1. NSAIDs with Low Potency & Short t� e.g. Ibuprofen Acute pain: 200 � 800 mg Chronic pain: 2 � 3 gm/day

35. Choice of NSAIDs 2. NSAIDs with High Potency & Short t� e.g. Diclofenac Less against COX-1 compared to COX-2 Less GIT side effects. 1st pass metabolism ? oral bioavailability 50% ? Liver toxicity. Other drugs: Indomethacin Ketoprofen

36. Choice of NSAIDs 3. NSAIDs with Intermittent Potency & t� e.g. Naproxen Clinical use in: Migraine Musculoskeletal pain

37. Choice of NSAIDs 4. NSAIDs with High Potency & Long t� e.g. Oxicams (melo-, piro- & teno-xicam). They are not recommended in: Acute pain, Pain of short duration Recommended in: Inflammatory pain that persist for longer duration Arthritis & bone pain & cancer pain The High Potency & Long t� ? ?? of side effects GIT & renal.

38. Selective COX-2 Inhibitors

39. COX-2 inh. & GIT: COX-1 confer cytoprotection in the GIT COX-2 inhibitors improve risk/benefit regarding GIT safety COX-2 inh. & Kidney: they do not spare kidney ~ edema & HP COX-2 inh. & CVS: ? prostacyclin ++ Do not � platelet COX-1 ~ -- throm. /prost. balance ? thrombogenic risk Some studies reported IHD in some pts received celecoxib. Selective COX-2 Inhibitors

40. Drug Therapy2. Opioids- Weak Opioids.- Strong opioids. - Mixed agonist � antagonists

41. Weak Opioids e.g. Tramadol hydrochloride Potency: 100 mg equivalent to 100 mg pethidine. Dose 200 � 400 mg/d. Advantages: Less postoperative respiratory depression. Efficient in reduction of postoperative shivering. Acute & Chronic pain Cancer & non cancer pain Side effects: Nausea and vomiting.

42. Strong Opioids e.g. Morphine, Pethidine and Fentanyl. Duration of action is: Morphine: (10 mg) 3-4 hours. Pethidine: (100 mg) 3-4 hours. Fentanyl: (100 ?g) 45- 60 minutes. Main side effects: Nausea and vomiting. Respiratory depression. Extrapyramidal rigidity.

43. Agonist Antagonist Opioids Members are: Butorphanol �Stadol� (2 mg) Nalbuphine �Nubain� (10 mg) Duration of action is very short ( 2 hours). Suitable to be used in infusion pumps and PCA. Side effects: Hallucination is a famous one. Agonist antagonist opioids are group of drugs that specifically acting on one opioid receptor and antagonize the other opioid eceptor.They are introduced into clinical practice in a trial to get an opioid without famous opioid side effects mainly addiction, respiratory depression, constipation, and tolerance. Buprenorphine: known as tamgesic, not registered in the Egyptian market, is a parial agonit -antagonist on mu opioid receptor. In clinical concentrations it can produce analgesia,and if the dose increases I turns to be an antagonist. Butorphanol (Stadol), and Nalbuphine (Nubaine) are k-opioid agonists, mu-opioid antagonists. They can produce spinal analgesia, and sedation without respiratory depression. They are all having a very high lipid solubility and can pass easily through membranes, and can be used in transmucosal route. Buprenorphine, sublingual tablets are present, but not in the Egyptian market (Dose= 0.4 mg I.M.). Stadol 1-2 mg., and Nubaine 10 mg. Injectable forms are present in the Egyptian market. I.M 2 mg stadol, and 10 Nubaine are equipotent to 10 mg. Morphine. No oral forms are present for this group of drug. Main side effect is hallucination.Agonist antagonist opioids are group of drugs that specifically acting on one opioid receptor and antagonize the other opioid eceptor.They are introduced into clinical practice in a trial to get an opioid without famous opioid side effects mainly addiction, respiratory depression, constipation, and tolerance. Buprenorphine: known as tamgesic, not registered in the Egyptian market, is a parial agonit -antagonist on mu opioid receptor. In clinical concentrations it can produce analgesia,and if the dose increases I turns to be an antagonist. Butorphanol (Stadol), and Nalbuphine (Nubaine) are k-opioid agonists, mu-opioid antagonists. They can produce spinal analgesia, and sedation without respiratory depression. They are all having a very high lipid solubility and can pass easily through membranes, and can be used in transmucosal route. Buprenorphine, sublingual tablets are present, but not in the Egyptian market (Dose= 0.4 mg I.M.). Stadol 1-2 mg., and Nubaine 10 mg. Injectable forms are present in the Egyptian market. I.M 2 mg stadol, and 10 Nubaine are equipotent to 10 mg. Morphine. No oral forms are present for this group of drug. Main side effect is hallucination.

44. Opioid / Local Anesthetic Mixture Epidural Marcaine and fentanyl is a useful mixture: Used epidurally Can be used in pediatrics. High quality of pain relief. Potentiation for action and duration.

45. Positioning of Opioid Therapy Opioid therapy is the mainstay approach for Acute pain Cancer pain Pain in advanced illnesses Moderate - Severe non cancer pain AIDS pain The broad international consensus is that opioid therapy serves as the mainstay approach for treatment of pain associated with acute pain and pain due to serious illnesses, such as cancer. Notwithstanding, we have abundant evidence that undertreatment is common, even in these populations. The broad international consensus is that opioid therapy serves as the mainstay approach for treatment of pain associated with acute pain and pain due to serious illnesses, such as cancer. Notwithstanding, we have abundant evidence that undertreatment is common, even in these populations.

46. Opioid Therapy in Chronic Non-Cancer Pain Under-treatment is a major problem because: Published experience of multidisciplinary pain programs showed that opioids associated with: Poor function Psychiatric disorders Poor outcome Consider the following: Are opioids likely to work well? Are there reasonable alternatives? Are drug-related behaviors likely to be used? We have no consensus about the role of opioid therapy in nonmalignant pain�and, hence, no certain data about the degree of undertreatment that exists. However, the individual and systemic barriers to opioid use, as well as the bias against opioid therapy that developed from the experience of multidisciplinary pain management programs, make undertreatment likely. The data published from the aforementioned programs do reveal associations between opioid use and negative characteristics and outcomes, and they suggest the potential for adverse responses to this therapy. However, because of the selection biases inherent in these programs, which attracted the most difficult patients, this experience cannot be used to evaluate the larger role of opioid therapy. We have no consensus about the role of opioid therapy in nonmalignant pain�and, hence, no certain data about the degree of undertreatment that exists. However, the individual and systemic barriers to opioid use, as well as the bias against opioid therapy that developed from the experience of multidisciplinary pain management programs, make undertreatment likely. The data published from the aforementioned programs do reveal associations between opioid use and negative characteristics and outcomes, and they suggest the potential for adverse responses to this therapy. However, because of the selection biases inherent in these programs, which attracted the most difficult patients, this experience cannot be used to evaluate the larger role of opioid therapy.

47. Opioid Therapy: Prescribing Principles Prescribing principles Drug selection Dosing to optimize effects Route of administration Treating side effects Managing the poorly responsive patient Many published guidelines reflect consensus views about the best approaches for management of long-term opioid therapy. The principles in these guidelines must be understood to optimize the likelihood of successful outcomes.Many published guidelines reflect consensus views about the best approaches for management of long-term opioid therapy. The principles in these guidelines must be understood to optimize the likelihood of successful outcomes.

48. Opioid Therapy: 1. Drug Selection Immediate-release preparations Used mainly For acute pain For stabilization phase For �rescue� dosing Can be used for long-term management in select patients Immediate-release opioids are usually used for a limited period to treat acute pain or to help identify a useful starting dose for a long-acting drug. These drugs can be administered on a long-term basis as well, usually as supplemental doses given �as needed� to patients who are receiving a concomitant long-acting drug (an approach known as �rescue� dosing). Immediate-release opioids are usually used for a limited period to treat acute pain or to help identify a useful starting dose for a long-acting drug. These drugs can be administered on a long-term basis as well, usually as supplemental doses given �as needed� to patients who are receiving a concomitant long-acting drug (an approach known as �rescue� dosing).

49. Immediate-release preparations Single-entity drugs e.g. Tramadol Morphine Combination products Codeine + ASA Propoxene + Acetaminophen. Opioid Therapy: Drug Selection Short-acting opioids include the combination products, single-entity pure mu-agonists, and tramadol. Dose escalation of the combination products is subject to the limits of safe dosing with the nonopioid constituent. Acetaminophen-containing combinations, for example, generally should not be given at doses that deliver more than 4 grams of acetaminophen per day. Single-entity drugs, such as morphine, oxycodone, and hydromorphone, have no such top doses. Tramadol is a unique centrally-acting analgesic that acts via both an opioid mechanism and a nonopioid, monoaminergic mechanism. Short-acting opioids include the combination products, single-entity pure mu-agonists, and tramadol. Dose escalation of the combination products is subject to the limits of safe dosing with the nonopioid constituent. Acetaminophen-containing combinations, for example, generally should not be given at doses that deliver more than 4 grams of acetaminophen per day. Single-entity drugs, such as morphine, oxycodone, and hydromorphone, have no such top doses. Tramadol is a unique centrally-acting analgesic that acts via both an opioid mechanism and a nonopioid, monoaminergic mechanism.

50. Extended-release preparations Preferred because of improved pt�s compliance. Morphine, oxycodone, hydromorphone, codeine, tramadol, buprenorphine Fentanyl-TTS (72 hs). Opioid Therapy: Drug Selection Numerous extended-release formulations are available in different countries. The oral drugs allow dosing 1 to 3 times per day and the transdermal drugs allow dosing every 2 to 3 days. Usually, steady-state is approached with these formulations within a few days and dose adjustments are best made in this time frame. Numerous extended-release formulations are available in different countries. The oral drugs allow dosing 1 to 3 times per day and the transdermal drugs allow dosing every 2 to 3 days. Usually, steady-state is approached with these formulations within a few days and dose adjustments are best made in this time frame.

51. 2. Dose adjustments for opioids Increase the dose (not the number of opioids) until: pain relief is adequate or intolerable side effects occur Only one long acting opioid should be ordered at any given time. (e.g. Oramorph, Oxycontin, Duragesic) Only one opioid combination should be ordered at any given time. Opioid responsiveness can be defined as the likelihood that a favorable balance between analgesia and side effects will be attained as the opioid dose is slowly titrated. A patient cannot be said to be a �nonresponder� unless the dose has been increased to the point of treatment-limiting side effects. Responsiveness varies with characteristics of a particular patient and his or her particular pain. Studies have suggested that responsiveness is inversely related to neuropathic mechanism, breakthrough pain, previous opioid exposure, cognitive impairment, and psychologic distress. However, no evidence exists that any characteristic imparts opioid resistance. Opioid responsiveness can be defined as the likelihood that a favorable balance between analgesia and side effects will be attained as the opioid dose is slowly titrated. A patient cannot be said to be a �nonresponder� unless the dose has been increased to the point of treatment-limiting side effects. Responsiveness varies with characteristics of a particular patient and his or her particular pain. Studies have suggested that responsiveness is inversely related to neuropathic mechanism, breakthrough pain, previous opioid exposure, cognitive impairment, and psychologic distress. However, no evidence exists that any characteristic imparts opioid resistance.

52. 3. Poor Opioid Responsiveness If dose escalation ? adverse effects Strategy to lower opioid requirement + Add non-opioid analgesic + Adjuvant analgesic + Non-pharmacologic strategy. Changes of opioid therapy: Change the route: e.g. Spinal opioids �Opioid rotation� Surveys in the cancer population suggest that 10% to 30% of patients will experience a poor response to an optimally titrated opioid regimen. Poorly-responsive patients can be considered for a variety of alternative opioid strategies. These include: 1) more sophisticated management of opioid side effects (eg, a psychostimulant for opioid-induced sedation or mental clouding), 2) use of a pharmacologic approach to reduce the systemic opioid requirement (either a trial of intraspinal therapy or coadministration of a nonopioid or adjuvant analgesic), 3) opioid rotation, or 4) a trial of a nonpharmacologic approach to reduce the opioid requirement (eg, a stimulatory, rehabilitative, anesthesiologic, surgical, or complementary approach). Comparative studies of these strategies have been conducted, and selection of one over another involves a detailed assessment, careful judgments about risks and benefits, and discussion of patient preferences. Surveys in the cancer population suggest that 10% to 30% of patients will experience a poor response to an optimally titrated opioid regimen. Poorly-responsive patients can be considered for a variety of alternative opioid strategies. These include: 1) more sophisticated management of opioid side effects (eg, a psychostimulant for opioid-induced sedation or mental clouding), 2) use of a pharmacologic approach to reduce the systemic opioid requirement (either a trial of intraspinal therapy or coadministration of a nonopioid or adjuvant analgesic), 3) opioid rotation, or 4) a trial of a nonpharmacologic approach to reduce the opioid requirement (eg, a stimulatory, rehabilitative, anesthesiologic, surgical, or complementary approach). Comparative studies of these strategies have been conducted, and selection of one over another involves a detailed assessment, careful judgments about risks and benefits, and discussion of patient preferences.

53. 4. Opioid Rotation Based on inter individual variation in response to different opioids Reduce equianalgesic dose by 25%�50%: Reduce less ? if pain is severe Reduce less ? if same drug by different route Reduce less ? fentanyl Reduce more ? methadone (75%�90%) Opioid rotation is common practice and is based on the clinical observation of large individual variation in the response to different opioids. Guidelines for switching drugs assure safety and yield a reasonable starting dose of the new drug, which then must be titrated. Opioid rotation is common practice and is based on the clinical observation of large individual variation in the response to different opioids. Guidelines for switching drugs assure safety and yield a reasonable starting dose of the new drug, which then must be titrated.

54. 5. The Equianalgesia

56. 6. Opioid Therapy: Side Effects Common Constipation Somnolence, mental clouding Less common N / V � Sweating Myoclonus � Amenorrhea Itch � Sexual dysfunction Urinary retention � Headache For most patients, the goal during long-term therapy is to identify a favorable balance between analgesia and opioid side effects. The common side effects are constipation and mental clouding. Other side effects occur less often. For most patients, the goal during long-term therapy is to identify a favorable balance between analgesia and opioid side effects. The common side effects are constipation and mental clouding. Other side effects occur less often.

57. Prevention # management of constipation �The hand that writes the �opioid order� ? also writes the bowel regimen� In every patient receiving opioids Increase fluids and fibers Scheduled stool softeners/stimulant laxatives

63. Drug Therapy3. Adjuvant's Therapy

64. 3. Adjuvant Therapy Clonidine Anxiolytic drugs Anticonvulsants Antidepressants Ketamine LA Corticosteroids Others

65. Clonidine Alpha-2 agonist. Routes of adminstration: Oral, neuraxial & TTS Pain control properties by itself Excellent adjuvant for opioid dependent patients Decrease the requirement of opioids Decrease tolerance Effective control for neuropathic pain Caudal block for children 1?g/kg ? pain relief / 24h

66. Ketamine NMDA receptors antagonist ? Neuropathic pain Potent analgesic effect Small doses in combination of opioids ? ? pain control Post-op in chronic opioid users: Bolus dose of 100 ?g/kg followed by a continuous drip of 1-3 ?g/kg/min.

67. Anti-Convulsant Drugs in Pain Gabapentin Carbamazipine Phenytoin Depakine

68. Mechanisms of Anti-Convulsant Drugs in Pain

69. Usage of Anti-Convulsants Drugs in Acute Pain Gabapentin: Mainly for neuropathic pain Studies showed that: giving 600-1200 mg of Gabapentin 1 h pre-op.: decreases the opioids requirement post-op & better pain relief without increased sedation Combining Gabapentin + opioids is ideal for: re-do back surgery cases with chronic opioids usage These class of drugs are also mode stabilizers Every surgical incisional pain has Neuropathic component Studies showed giving 1200 mg of Gabapentin 1 h prior to surgery: decreases the opioids requirement post-op & better pain relieg without increased sedation Combining Gabapentin with opioids is ideal for re-do back surgery cases with chronic opioids usage These class of drugs are also mode stabilizersEvery surgical incisional pain has Neuropathic component Studies showed giving 1200 mg of Gabapentin 1 h prior to surgery: decreases the opioids requirement post-op & better pain relieg without increased sedation Combining Gabapentin with opioids is ideal for re-do back surgery cases with chronic opioids usage These class of drugs are also mode stabilizers

70. Antidepressant Drugs in Pain Managements This type of drug may be divided into 4 categories: Drugs that inhibit synaptic neurotransmitter reuptake.�� Drugs that have direct receptor stimulation. Drugs that produce receptor blockade. Drugs that inhibit the activity of enzymes such as monoamine oxidase.

71. Mechanism of Action of Antidepressants

73. Adjuvant Analgesics for Cancer Pain

74. Adjuvant Analgesics for Chronic Headache

75. Other Adjuvant Analgesics

79. Routes of Administrations Use the oral route whenever possible Except e.g. post op period, Try other routes e.g. buccal, sublingual, or rectal routes before initiating parenteral routes Parenteral: SQ and IV preferred & feasible for short-term therapy Always avoid IM. Oral and transdermal: preferred

80. I.M. not recommended but it is commonly used: Painful Serum levels are unpredictable. Rectal route: For pediatric patients. Simple procedures. Slow absorption: longer duration. Neuraxial: Intrathecal generally preferred for long-term use Epidural for a shorter periods. Routes of Administrations

81. Intravenous Route Desired. Easy titrated. Serum level is controllable. Can be used in: drip form , by pumps , best is by PCA.

82. Used for IV, SC & Epidural. Pre-set by the physician. Activated by the patient. Programming modalities include: Loading dose or infusion. Demand bolus dose. Constant background infusion rate. Lock-out interval. Maximum hourly dose.

83. Advantages: Patients can titrate their own analgesia Improved: Pain relief Pulmonary function. Decreased: Total daily dose. Over sedation. Postoperative complications.

88. Pain Management Algorithm

91. Trauma pain management Algorithm

92. Trauma pain management Algorithm

93. Trauma pain management Algorithm

94. Trauma pain management Algorithm

95. Trauma pain management Algorithm

96. Summary of Pain Management �the basics

97. Do Not Use Placebos! Unethical They don�t work Not helpful in diagnosis Effect is short lived Destroys trust

98. Match the therapy to the type of pain Intensity of pain Mild, moderate or severe. Type of pain e.g. Somatic & Visceral pain # Neuropathic pain Duration of pain Continuous # intermittent pain. Acute # chronic Drug combinations Never order more than one SR preparation at a time Only one combination analgesic should be ordered at a time

99. Basics of Pain Management 1st step: is the good pain assessment. Pain medications must be taken: ? when the pain is first perceived. Doses of opioids are increased: ? with the patient�s report of pain Adjuvant medications are used for: ? opioid non-responsive & neuropathic pain. Non-pharmacologic approaches are always a part of ? any pain management protocol. The pain assessment: so the pain syndrome can be identified and appropriately treated. The oral route is used whenever possible. If the patient is unable, buccal, sublingual, rectal, and TTS routes are considered before parenteral routes. IM route is avoided. The pain assessment: so the pain syndrome can be identified and appropriately treated. The oral route is used whenever possible. If the patient is unable, buccal, sublingual, rectal, and TTS routes are considered before parenteral routes. IM route is avoided.

101. �By any reasonable code, freedom from pain should be a basic human right, limited only by our knowledge to achieve it ...� Wall P & Melzack R 1987