1 / 96

KEY CONCEPTS IN ACUTE PAIN MANAGEMENT PGY-1 Faculty of Medicine University of Ottawa Feb.18, 2009

KEY CONCEPTS IN ACUTE PAIN MANAGEMENT PGY-1 Faculty of Medicine University of Ottawa Feb.18, 2009. John Penning MD FRCPC Director Acute Pain Service The Ottawa Hospital. Objectives. General Key Concepts The “real cost” of acute pain Multi-modal analgesia

guillermo
Download Presentation

KEY CONCEPTS IN ACUTE PAIN MANAGEMENT PGY-1 Faculty of Medicine University of Ottawa Feb.18, 2009

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. KEY CONCEPTS IN ACUTE PAIN MANAGEMENTPGY-1 Faculty of MedicineUniversity of Ottawa Feb.18, 2009 John Penning MD FRCPC Director Acute Pain Service The Ottawa Hospital

  2. Objectives • General Key Concepts • The “real cost” of acute pain • Multi-modal analgesia • New Dimensions in pain management • How and when to use naloxone

  3. Objectives • Discuss key concepts of each modality • COX-inhibitor as Foundational analgesic • Tylenol # 3 has it’s limitations • Opioids? – think outside the “box” • Tramacet – a “me too” drug? Or something new to add? • Anti-pronociceptive agents for difficult acute pain

  4. Consequences of poorly managed acute post-operative pain • The Patient suffers • CVS: MI, dysrhythmias • Resp: atelectasis, pneumonia • GI: ileus, anastamosis failure • Endocrine: “stress hormones” • Hypercoagulable state: DVT, PE • Impaired immunological state • Infection, cancer, wound healing • Psychological: • Anxiety, Depression, Fatigue, Sleep Deprivation • Chronic Post-surgery/trauma Pain

  5. Consequences of poorly managed acute post-operative pain • The Hospital • Increased costs $$$ • Poor staff morale • Reputation/Standing in the Community, Nationally • Accreditation • Canadian Council on Health Services Accreditation; Acute Care Standard 7.4 2005. • TOH Pain Management Council 2006 • TOH Pain Assessment and Management Policy ADM 8 • Litigation

  6. Consequences of poorly managed acute post-operative pain • The Healthcare professional • Morale • Complaints to College • Litigation

  7. Risk Factors for severe post-op pain • While incision size and type of surgery are predictors of post-op pain, the greatest source of variability is the PATIENT. • Younger age • Female • Pre-operative pain issues • Anxiety, depression, catastrophizing

  8. Chronic Post-Surgical PainRisk Factors • Brandsborg B. et al. Risk factors for chronic pain after hysterectomy. Anesthesiology 2007; 106: 1003 – 12. • Pre-operative pelvic pain as the main indication for surgery • Pain problems elsewhere • Previous C/S • Procedure done with spinal anesthesia shown to decrease incidence of CPSP.

  9. The New Challenges in Managing Acute Pain after Surgery and Trauma • Patients/Society more “aware” of their rights to have good pain control • We are being held accountable • Pressure from hospital to minimize length of stay • Control pain, yet limit the side-effect burden and complications secondary to opioids

  10. The New Challenges in Managing Acute Pain after Surgery and Trauma • The Opioid Tolerant Patient • The greatest change in practice/attitudes in the last 10 years is the now wide spread acceptance of the use of opioids for CHRONIC NON-MALIGNANT PAIN • Renders the “usual” standard “box” orders totally inadequate in these patients • Get an accurate Pain/Analgesic History • The Brief Pain Inventory – “BPI”

  11. Brief Pain Inventory: Charles Cleeland

  12. What is the “Best Way” to manage Acute Pain? • FIRST, DO NO HARM Therefore, the “best way” is a BALANCE Effective Analgesic Modalities Patient Safety

  13. Analgesia with Opioids alone • The harder we “push” with single mode analgesia, the greater the degree of side-effects Side-effects Analgesia

  14. Case Problem: Severe Respiratory Depression after Ketorolac? • Healthy 34 yr. patient c/o severe incisional pain in PACU after ovarian cystecomy • Received 200 g fentanyl with induction and 10 mg morphine during case, no foundational analgesic given • PCA morphine started in PACU, plus nurse supplements totaled 26 mg in 90 minutes • Still c/o pain, 30 mg ketorolac IV, given with some relief after 15 minutes, so patient sent to ward • 60 minutes later found unresponsive, cyanotic, RR 4/min.

  15. Case Problem: Severe Respiratory Depression after Ketorolac? • Pharmacodynamic drug interaction between morphine and NSAID • morphine’s respiratory depressant effect opposed by the stimulatory effects of pain, busy PACU environment • NSAID decreases pain, morphine’s effect unappossed

  16. Case Problem: Severe Respiratory Depression after Ketorolac? • Safer approach? • Add NSAID foundational analgesic ASAP • Gain control of acute pain with fast onset, short acting opioid(fentanyl) • In a patient previously “loaded” with opioids and c/o pain despite some sedation, Monitor closely for over-sedation and respiratory depression after pain isalleviated by any means!

  17. The problem with the “Little Pain – LittleGun”, “Big Pain – Big Gun” Approach • With opioids analgesic efficacy is limited by side-effects • “Optimal” analgesia is often difficult to titrate • 10 – fold variability in opioid dose : response for analgesia • A dose of opioid that is inadequate for patient A can lead to significant S/E or even death in patient B. • Many patient factors add to the difficulty • Opioid tolerance, anxiety, obstructive sleep apnea, sleep deprivation, concomitantly administered sedative drugs

  18. Multi-modal Analgesia • “With the multimodal analgesic approach there is additive or even synergistic analgesia, while the side-effects profiles are different and of small degree.” Side-effects Analgesia

  19. Pain Pathways There is as of yet no single silver bullet!!

  20. Acute Pain Management Modalities • Cyclo-oxygenase inhibitors • Non-specific COX inhibitors(classical NSAIDs) • Selective COX-2 inhibitors, the “coxibs” • Acetaminophen is probably COX-3 • Local anesthetics • Opioids • NMDA antagonists • Ketamine, dextromethorphan • Anti-convulsants • Gabapentin, Pregabalin

  21. NSAID, Coxibs and Acetaminophen CONCEPT # 1 The foundation of all acute pain Rx protocols. ”First on last off” • sole agent in mild /moderate pain • Analgesic efficacy is limited inherently • In contrast, with opioids efficacy is limited by S/E • Opioids added as required • opioid sparing effect 30-60 %

  22. COX-INHIBITORS vs. OPIOIDS • Efficacy Limited InherentlyLimited by S/E • Inter-patient dose variability SmallLarge, making dose titration difficult • Life threatening complications Upper GI bleedingResp. depression With chronic useRisk is early

  23. COX-INHIBITORS vs. OPIOIDS • Toxicity, S/E Tissue/organ toxicneurologic dysfunc • Drug tolerance Not evidenttolerance is part of normal response • Abuse potential Nil Yes

  24. Cyclo-oxygenase inhibitors Acetaminophen Naproxen Celecoxib Ketorolac Numerous others

  25. Cell Membrane Phospholipids Phospholipase Arachidonic Acid COX-2 COX-1 Prostaglandins Prostaglandins Acute Pain Gastric Protection Inflammation Platelet Hemostasis Fever

  26. Why a COX-2 inhibitor? • No effects on platelets! • Better GI tolerability • Less dyspepsia, less N/V • Equivalent analgesic efficacy with non-selective COX-inhibitors

  27. Celecoxib and “sulfa allergy” • Allergy to sulfa?? History, Please! • Most reported allergies are bogus: N/V, diarrhea • A rash with sulfonamide anti-biotics? Celecoxib belongs to the “other” class of sulfonamides: furosemide, glyberide, etc. • Do not use celecoxib is history of anaphylaxis or severe cutaneous reaction (Steven-Johnson sydrome. etc.) with a sulfonamide

  28. Two hours before surgery associated with post-op pain • Celecoxib 400 mg PO If severe allergy to sulfa? OR • Naproxen 500 mg PO Contra-indications to NSAID? Plus Acetaminophen 1000 mg PO

  29. Contra-indications to Celecoxib/NSAIDs • Patients with the “ASA triad” • Risk of severe asthma, angioedema precipitated with COX-inhibitor • Renal insufficiency or risk there of • especially if risk of hypovolemia periop • Patient on ACE inhibitors or ARBs • Vascular patients having aortic cross-clamp and/or probable angiogram peri-operatively • Poorly controlled hypertension • Especially if pt. is on ACE inhibitor, potent loop diuretics

  30. Contra-indications to Celecoxib/NSAIDs • Congestive heart failure • Fluid/sodium retention • Active peptic ulcer disease

  31. The Opioids • We have to stop trying to put every patient in the “analgesic dose box” Meperidine 75 mg IM Q4H prn Tylenol #3 1 – 2 PO Q4H prn

  32. Opioids CONCEPT # 2 Pharmacokinetic + Pharmacodynamic patient to patient variability results in 1000% variability in opioid dose requirements (standardized procedure, opioid naïve patient) • opioid dosage must be individualized • therefore, if parenteral therapy indicated, IV PCA much better suited to individual patient needs than IM/SC

  33. True or False? • One opioid is just like any other, in terms of analgesic efficacy and side-effects.

  34. Opioids – Are they all the same? • Morphine • Hydromorphone (dilaudid) • Fentanyl • Oxycodone (parenteral n/a) • Meperidine (demerol)

  35. Opioids – Do they all act the same? • Opioids work as analgesics by activating endogenous inhibitory pain modulating systems • Opioid receptors • Mu, Delta and Kappa • Large genetic variability in expression • Good choice in one patient may be poor choice in another • Analgesic efficacy • Side-effect profile

  36. Meperidine Morphine Atropine Fentanyl Bupivacaine

  37. Meperidine’s major problem • Normeperidine • The “ugly” metabolite • Neuroexcitatory: twitches, dilated pupils, hallucinations, hyperactive DTR, seizures • Non-opioid receptor mediated, no tolerance • Half-life is 15 – 20 hours N-demethylation

  38. True or False? • One opioid is just like any other, in terms of analgesic efficacy and side-effects. • Answer. There is considerable variability between patients in response to different opioids.

  39. Opioid Myths that still prevail! • Codeine is a “weak” opioid? • Codeine is inherently safer than the more potent opioids?

  40. CODEINE – A drug whose time has come and gone? N Engl J Med 351; 27 Dec. 30, 2004

  41. Problems with Codeine • 62 yr. male with CLL, presents with bilateral pneumonia. • Broncho-lavage revealed yeast • Anti-biotics: Ceftriaxone, clarithromycin, voriconazole • Codeine 25 mg PO TID for cough

  42. Problems with Codeine • Day 4 became markedly sedated, pin-point pupils and ABG reveals PaCO2 of 80 mmHg. Marked improvement with Naloxone. • What’s the expected morphine blood level? • Answer: 1 to 4 mcg/L • This patient’s morphine blood level? • 80 mcg/L

  43. Codeine Metabolism in Normal Circumstances • The major pathways convert codeine to inactive metabolites • CYP3A4 pathway yields norcodeine • Glucuronidation • The minor pathway, about 10%, yields morphine • CYP2D6, essential for analgesic effect 60 mg Codeine PO – approx. 4 mg morphine SC • Variability! 60 mg PO Codeine yields potentially 0 to 60 mg parenteral morphine

  44. Genetic Variability And drug interactions 1% Finland 10% Greek 30% East Africa

More Related