2. Development Committee
Mario H. Cardiel, MD, MSc
Rheumatologist
Morelia, Mexico
Andrei Danilov, MD, DSc
Neurologist
Moscow, Russia
Smail Daoudi, MD
Tizi Ouzou, Algeria
João Batista S. Garcia, MD, PhD
Anesthesiologist
São Luis, Brazil
Yuzhou Guan, MD
Beijing, China
Jianhao Lin, MD
Orthopedist
Beijing, China
Supranee Niruthisard, MD
Anesthesiologist, Pain Specialist
Bangkok, Thailand
Germán Ochoa, MD
Orthopedist, Spine Surgeon and Pain Specialist
Bogotá, Colombia
Milton Raff, MD, BSc
Consultant Anesthetist
Cape Town, South Africa
Raymond L. Rosales, MD, PhD
Neurologist
Manila, Philippines
Ammar Salti, MD
Consultant Anesthetist
Abu Dhabi, United Arab Emirates
Jose Antonio San Juan, MD
Orthopedic Surgeon
Cebu City, Philippines
Xinping Tian, MD
Rheumatologist
Beijing, China
Işin Ünal-Çevik, MD, PhD
Neurologist, Neuroscientist and Pain Specialist
Ankara, Turkey
Speaker’s Notes
Please acknowledge the members of the development committee.
This program was sponsored by Pfizer Inc.

3. Learning Objectives
After completing this module, participants will be able to:
Discuss the prevalence of acute pain
Understand the impact of acute pain on patient functioning and quality of life
Explain the pathophysiology of acute pain
Apply a simple diagnostic technique for the differential diagnosis of acute pain
Select appropriate pharmacological and non-pharmacological strategies for the management of acute pain
Speaker’s Notes
Review the learning objectives for this session. Ask the participants if they have any additional goals.

4. Table of Contents What is acute pain? How common is acute pain?
What is the impact of acute pain on patient functioning and quality of life?
How should acute pain be assessed in clinical practice?
How should acute pain be treated based on its pathophysiology?
Speaker’s Notes
This slide outlines the overall flow of the presentation.

5. Pain Is the 5th Vital Sign
Temperature
Respiration
Pulse
Blood pressure
Pain
Speaker’s Notes
In 2000, the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) unveiled new pain management standards. Central to these new standards was the concept of pain as the fifth vital sign – something that should be regularly monitored in all patients. While there is some controversy regarding whether pain should in fact be monitored at every visit, like blood pressure, this concept highlights the fundamental importance of pain in patient care.
Reference
Phillips DM. JCAHO pain management standards are unveiled. Joint Commission on Accreditation of Healthcare Organizations. JAMA 2000; 284(4):428-9.
Phillips DM. JAMA 2000; 284(4):428-9.

6. Overview of Pain Protective role: vital early warning system
Senses noxious stimuli
Triggers withdrawal reflex and heightens sensitivity after tissue damage to reduce risk of further damage
Unpleasant experience:
Suffering – physical, emotional and cognitive dimensions
Continuous unrelieved pain can affect physical (e.g., cardiovascular, renal, gastrointestinal systems, etc.) and psychological states
Maladaptive response:
Neuropathic and central sensitization/dysfunctional pain
Not protective
Lessens quality of life
Speaker’s Notes
The physiologic function of pain is to serve as an early warning system that senses noxious stimuli to provoke a reflexive withdrawal (nociception) and to heighten sensitivity after tissue damage to reduce risk of further damage through movement (inflammation).
However, continuous unrelieved pain can have a detrimental impact on both physical and psychological well-being. Unrelieved pain can lead to sympathetic activation of the pituitary-adrenal, affecting the cardiovascular , renal and gastrointestinal systems, increasing the risk of cardiac ischemia and ileus. Unrelieved pain is also frequently associated with anxiety and depression.
Thus, chronic pain states, often involving neuropathic and/or central sensitization/dysfunctional pathophysiologies are considered to be maladaptive rather than protective and lessen quality of life.
References
Costigan M et al. Neuropathic pain: a maladaptive response of the nervous system to damage. Annu Rev Neurosci 2009; 32:1-32.
Wells N et al. In: Hughes RG (ed). Patient Safety and Quality: An Evidence-Based Handbook for Nurses. Agency for Healthcare Research and Quality; Rockville, MD: 2008.
Woolf CJ et al. Pain: moving from symptom control toward mechanism-specific pharmacologic management. Ann Intern Med 2004; 140(6):
Costigan M et al. Annu Rev Neurosci 2009; 32:1-32; Wells N et al. In: Hughes RG (ed). Patient Safety and Quality: An Evidence-Based Handbook for Nurses. Agency for Healthcare Research and Quality; Rockville, MD: 2008; Woolf CJ et al. Ann Intern Med 2004; 140(6):

7. Acute pain may become chronic
The Pain Continuum
Insult
Time to resolution
Acute pain
Chronic pain
Normal, time-limited response to ‘noxious’ experience (less than 3 months)
Pain that has persisted beyond normal tissue healing time (usually more than 3 months)
Usually obvious tissue damage
Serves a protective function
Pain resolves upon healing
Usually has no protective function
Degrades health and function
Speaker’s Notes
This slide illustrates how acute and chronic pain are often classified along a pain continuum.
Acute pain may be seen as a message that follows an insult to tissue, signaling the presence of a pathologic condition, thus alerting the patient to the need to either seek treatment or protect the involved area from further injury. Most episodes of acute pain are self-limiting. Acute pain becomes chronic when it persists beyond the expected period of healing, usually considered to be three months. Recurrent acute pain is not chronic pain.
Chronic pain has also been defined as pain that ceases to serve a protective function, and instead degrades health and functional capability. Chronic pain conditions may be due to a single pathophysiology, that is nociceptive, neuropathic or central sensitization/dysfunctional pain only, or a may be due to a combination of more than one pathophysiological mechanisms.
It is important to differentiate chronic pain from a condition with recurrent episodes of acute pain because the treatment strategies are very different for these two situations.
References
Chapman CR, Stillman M. In: Kruger L (ed). Pain and Touch. Academic Press; New York, NY: 1996.
Cole BE. Pain Management: classifying, understanding, and treating pain. Hosp Physician 2002; 38(6):23-30.
International Association for the Study of Pain. Unrelieved Pain Is a Major Global Healthcare Problem. Available at: CM/ContentDisplay.cfm&ContentID=2908. Accessed: July 24: 2013.
National Pain Summit Initiative. National Pain Strategy: Pain Management for All Australians. Available at: Accessed: July 24, 2013.
Turk DC, Okifuji A. In: Loeser D et al (eds). Bonica’s Management of Pain. 3rd ed. Lippincott Williams & Wilkins; Hagerstown, MD: 2001.
Acute pain may become chronic
Chapman CR, Stillman M. In: Kruger L (ed). Pain and Touch. Academic Press; New York, NY: 1996; Cole BE. Hosp Physician 2002; 38(6):23-30; International Association for the Study of Pain. Unrelieved Pain Is a Major Global Healthcare Problem. Available at: Accessed: July 24: 2013; National Pain Summit Initiative. National Pain Strategy: Pain Management for All Australians. Available at: Accessed: July 24, 2013; Turk DC, Okifuji A. In: Loeser D et al (eds.). Bonica’s Management of Pain. 3rd ed. Lippincott Williams & Wilkins; Hagerstown, MD: 2001.

8. Somatic vs. Visceral Pain
Nociceptors are involved
Often well localized
Usually described as throbbing or aching
Can be superficial (skin, muscle) or deep (joints, tendons, bones)
Involves hollow organ and smooth muscle nociceptors that are sensitive to stretching, hypoxia and inflammation
Pain is usually referred, poorly localized, vague and diffuse
May be associated with autonomic symptoms (e.g., pallor, sweating, nausea, blood pressure and heart rate changes)
Speaker’s Notes
Nociceptive pain can have either a somatic or a visceral origin. Somatic pain, originating in the skin, muscles, joints, tendons or bones, is the better known of the two types and is what is often meant when people refer to nociceptive pain. However, visceral pain originating in the hollow organs and/or smooth muscles is also quite common, as exemplified by dysmenorrhea, infective cystitis and functional gastrointestinal disorders. Unlike somatic pain, visceral pain is usually diffuse rather than well localized. It may also be referred (i.e., experienced in a part of the body not associated with the initial injury or dysfunction).
References
McMahon SB, Koltzenburg M (eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006.
Sikandar S, Dickenson AH. Visceral pain: the ins and outs, the ups and downs. Curr Opin Support Palliat Care 2012; 6(1):17-26.
McMahon SB, Koltzenburg M (eds). Wall and Melzack’s Textbook of Pain. 5th ed. Elsevier; London, UK: 2006; Sikandar S, Dickenson AH. Curr Opin Support Palliat Care 2012; 6(1):17-26.

9. Referred Pain Speaker’s Notes
In the spinal cord, there is a convergence of visceral and somatic cutaneous afferent fibers. The ascending axons transmit the message to the brain. Thus, visceral nociceptor stimulation misinterprets the location of the pain as being in the skin.
The image shown on this slide depicts the regions of referred visceral pain.
References
Hudspith MJ et al. In: Hemmings HC, Hopkins PM (eds). Foundations of Anesthesia. 2nd ed. Elsevier; Philadelphia, PA: 2006.
Schmitt WH Jr. Visceral referred pain areas. Uplink 1998; 10:1-3.
Hudspith MJ et al. In: Hemmings HC, Hopkins PM (eds). Foundations of Anesthesia. 2nd ed. Elsevier; Philadelphia, PA: 2006; Schmitt WH Jr. Uplink 1998; 10:1-3.

10. Prevalence of Acute Pain
Lifetime prevalence in general population:
Approaches 100% for acute pain leading to use of analgesics1
Emergency room patients:
Pain accounts for >2/3 of emergency room visits2
Hospitalized patients:
>50% report pain3
Speaker’s Notes
Acute pain is an extremely common condition, with one international study suggesting the lifetime prevalence of acute pain leading to the use of analgesics approaches 100%.1
The proportion of patients in clinical settings who report pain reflects this high prevalence, with pain accounting for more than two-thirds of emergency room visits, and more than half of hospitalized patients reporting pain.2,3
References
Diener HC et al. Per-capita consumption of analgesics: a nine-country survey over 20 years. J Headache Pain 2008; 9(4):
Todd KH, Miner JR. In: Fishman SM et al (eds). Bonica’s Management of Pain. 4th ed. Lippincott, Williams and Wilkins; Philadelphia, PA: 2010.
Dix P et al. Pain on medical wards in a district general hospital. Br J Anaesth 2004; 92(2):235-7.
1. Diener HC et al. J Headache Pain 2008; 9(4):225-31; 2. Todd KH, Miner JR. In: Fishman SM et al (eds). Bonica’s Management of Pain. 4th ed. Lippincott, Williams and Wilkins; Philadelphia, PA: 2010; 3. Dix P et al. Br J Anaesth 2004; 92(2):235-7.

11. what are the most common types of acute pain you see in your practice?
Discussion Question
what are the most common types of acute pain you see in your practice?
Speaker’s Notes
Ask the question shown on the slide to participants to stimulate discussion. Suggest doing a poll.

12. Nociceptive Pain Visceral Somatic Visceral Trauma
Musculoskeletal injury
Ischemic, e.g., myocardial infarction
Abdominal colic
Speaker’s Note:
In our daily life there are many forms of acute pain, such as “somatic pain” of musculoskeletal origin due to sports injury /trauma, burn, incision (such as in post-operative pain) or infectious diseases (such as in pharingitis, otitis, etc.).
It may also be a “visceral pain” due to vascular occlusion such as in myocardial ischemia, visceral nociceptive/inflammatory pain due to stretching, hypoxia or inflammation of the hollow organs such as in abdominal colic, dysmenorrhea, etc. Trigeminal or C2-C3 nerve root irritation may lead to neurovascular inflammation in acute episodic headaches such as migraine.
Reference
Fishman SM et al (eds). Bonica’s Management of Pain. 4th ed. Lippincott, Williams and Wilkins; Philadelphia, PA: 2010.
Post-operative pain
Burn pain
Infection, e.g., pharyngitis
Dysmenorrhea
Fishman SM et al (eds). Bonica’s Management of Pain. 4th ed. Lippincott, Williams and Wilkins; Philadelphia, PA: 2010.

13. Epidemiology of Pain in General Practice
1 in 3 patients reported pain
Of patients in pain:
47.2% had acute pain
Location of pain was mainly in musculoskeletal areas and the limbs
2 in 3 pain patients had a drug prescription
Pain was more frequent in women
Speaker’s Notes
The data shown on this slide are drawn from a survey of 89 Italian general practitioners who reported that one in three of 1432 patients reported pain. Nearly half of these cases were diagnosed as acute pain. The main complaints were of musculoskeletal and abdominal origin, with the most frequent site of pain being the limbs.
Pain was 1.5 times more frequent in women than men and the female to male ratios for acute and chronic pain were 1.2:1 and 1.8:1 respectively. Approximately two thirds of contacts with pain led to a drug prescription.
Reference
Koleva D et al. Pain in primary care: an Italian survey. Eur J Public Health 2005; 15(5):475-9.
Koleva D et al. Eur J Public Health 2005; 15(5):475-9.

14. Most Common Types of Pain in General Practice
Speaker’s Notes
This slide shows the prevalence of pain at the primary care level during one year in a group practice serving an area in Stockholm, Sweden with approximately 14,000 inhabitants. Mean age of the population was 37 years with a mean income just below the Swedish average at the time.
Overall, 28% of the 6890 individuals who consulted a general practitioner had at least one pain-related problem – 37% of these patients had pain duration of less than 1 month, 13% duration of 1–3 months and 37% of more than 3 months. A total of 11% suffered from a chronic intermittent state of pain.
In terms of pathophysiology, 94% of cases were classified as nociceptive, 2% as neuropathic, 2% as psychogenic, <1% as idiopathic and 2% could not be classified.
Reference
Hasselström J et al. Prevalence of pain in general practice. Eur J Pain 2002; 6(5):
Note: types of pain are based on ICD-9 codes *The use of the symptom code suggests clinician could not identify the underlying cause of the pain
**MSK – other refers to musculoskeletal pain at sites other than the neck, back or soft tissue
ICD = International Classification of Disease; MSK = musculoskeletal
Hasselström J et al. Eur J Pain 2002; 6(5):

15. Impact of Acute Pain on Daily Activities
Speaker’s Notes
The data in this slide suggest that acute pain negatively impacts on daily activities and under treatment/insufficient relief of acute pain decreases the patient’s quality of life at both the physical and emotional levels.
Survey participants in this study were aged 18 years or older, experienced moderate to moderately severe pain at least 2–3 times per month, and had taken combination opioid products for any reason within the previous 6 months. A total of participants were classified as acute pain sufferers whose pain was managed through limiting strenuous activities, undergoing physical therapy and pharmacotherapy. Inadequate pain control was a major concern of these participants.
It should be noted that the chart shown on this slide is based on self-reported data gathered through an internet survey, rather than a true quality of life study.
Reference
McCarberg BH et al. The impact of pain on quality of life and the unmet needs of pain management: results from pain sufferers and physicians participating in an Internet survey. Am J Ther 2008; 15(4):
*Patients who responded “Sometimes”, “Often” or “Always”
Adapted from: McCarberg BH et al. Am J Ther. 2008; 15(4):

16. Consequences of Unrelieved Pain
Acute pain
Impaired physical function
Dependence
Extended recovery time
Increased risk of developing chronic pain
Reduced mobility
On medication
Hospital readmissions
Speaker’s Notes
Unrelieved acute pain can result in a number of physical, psychological, emotional and social issues that negatively influence a patient’s life. It can also result in progression to chronic pain.
Reference
Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. The National Academies Press; Washington, DC: 2011.
Disturbed sleep
On family members/other caregivers
Economic costs
Immune impairment
Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. The National Academies Press; Washington, DC: 2011.

17. Post-operative Pain
80% of patients undergoing surgery experience post-operative pain
<50% report adequate pain relief
10–50% develop chronic pain*
88% of these report the pain is moderate, severe or extreme
Speaker’s Notes
As indicated on this slide, post-operative pain is both pervasive and costly.
The trend towards outpatient surgery may compromise opportunities to appropriately assess post-operative pain and establish appropriate and necessary post-operative analgesia management. High unanticipated admissions and readmissions tax the already challenged hospital system. Accordingly, a vicious cycle is established.
References
Coley KC et al. Retrospective evaluation of unanticipated admissions and readmissions after same day surgery and associated costs. J Clin Anesth 2002; 14(5):
Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. The National Academies Press; Washington, DC: 2011.
For 2–10% of these,
pain is severe
Pain accounts for 38% of unanticipated admissions and readmissions following ambulatory surgery
*Depending on type of surgery
Coley KC et al. J Clin Anesth 2002; 14(5):349-53; Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. The National Academies Press; Washington, DC: 2011.

18. Importance of Pain Assessment
Pain is a significant predictor of morbidity and mortality.
Screen for red flags requiring immediate investigation and/or referral
Identify underlying cause
Pain is better managed if the underlying causes are determined and addressed
Recognize type of pain to help guide selection of appropriate therapies for treatment of pain
Determine baseline pain intensity to future enable assessment of efficacy of treatment
Speaker’s Notes
Appropriate assessment of patients presenting with pain is crucial in order to determine whether they are suffering from a condition that requires immediate management or referral. It can also help ensure optimal treatment of pain through identification of the underlying cause of the pain and recognition of the pathophysiologic mechanism behind the pain, which can help guide treatment selection. Finally, determining baseline pain intensity enables future assessment of treatment efficacy in order to guide titration and modification of the analgesic regimen.
References
Forde G, Stanos S. Practical management strategies for the chronic pain patient. J Fam Pract 2007; 56(8 Suppl Hot Topics):S21-30.
Sokka T, Pincus T. Pain as a Significant Predictor of Premature Mortality Over 5 Years in the General Population, Independent of Age, Sex and Acutely Life-threatening Diseases. Poster presentation at ACR 2005.
Forde G, Stanos S. J Fam Pract 2007; 56(8 Suppl Hot Topics):S21-30; Sokka T, Pincus T. Poster presentation at ACR 2005.

19. how do you assess acute pain in your practice?
Discussion Question
how do you assess acute pain in your practice?
Speaker’s Notes
Ask the question shown on the slide to participants to stimulate discussion.

20. Assessment of Acute Pain
Site of pain
Circumstances associated with pain onset
Character of pain
Intensity of pain
Associated symptoms (e.g., nausea)
Comorbidities
Treatment
Current and previous medications, including dose, frequency of use, efficacy and side effects
Relevant medical history
Prior or coexisting pain conditions and treatment outcomes
Prior or coexisting medical conditions
Factors influencing symptomatic treatment
Speaker’s Notes
This slide lists information that should be gathered in the course of taking a pain history.
Reference
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.

21. Locate the Pain
Speaker’s Notes
Body maps can help locate the pain.
In cases of nociceptive pain of somatic origin, the pain is generally well localized to the injured area. However, in cases of neuropathic pain, body maps may be useful for the precise systematization of pain according to individual dermatomes.
It should be noted that in cases of referred pain, the location of the pain and of the injury or nerve lesion/dysfunction may not be correlated.
References
Gilron I et al. Neuropathic pain: a practical guide for the clinician. CMAJ 2006; 175(3):
Walk D et al. Quantitative sensory testing and mapping: a review of nonautomated quantitative methods for examination of the patient with neuropathic pain. Clin J Pain 2009; 25(7):
Body maps are useful for the precise location of pain symptoms and sensory signs.*
*In cases of referred pain, the location of the pain and of the injury or nerve lesion/dysfunction may not be correlated
Gilron I et al. CMAJ 2006; 175(3):265-75; Walk D et al. Clin J Pain 2009; 25(7):

22. Determine Pain Intensity
Simple Descriptive Pain Intensity Scale
Mild pain
Moderate pain
Severe pain
Very severe pain
No pain
Worst pain
0–10 Numeric Pain Intensity Scale
No pain 1 2 3 4 5 6 7 8 9 10
Moderate pain
Worst possible pain
Speaker’s Notes
Various pain scales have been developed to help assess pain intensity, which can help guide treatment selection and adjustment.
This slide displays three of the most common pain intensity scales. The selection of which scale to use may depend on the literacy, numeracy and cognitive abilities of the patient. For instance, the more visual Faces Pain Scale may be the most useful in young children, especially those under three years of age, or in elderly patients suffering from cognitive decline.
References
International Association for the Study of Pain. Faces Pain Scale – Revised. Available at: GeneralResourceLinks/FacesPainScaleRevised/default.htm. Accessed: July 15, 2013.
Iverson RE et al. Practice advisory on pain management and prevention of postoperative nausea and vomiting. Plast Reconstr Surg 2006; 118(4):
Faces Pain Scale – Revised
International Association for the Study of Pain. Faces Pain Scale – Revised. Available at: Accessed: July 15, 2013; Iverson RE et al. Plast Reconstr Surg 2006; 118(4):

23. Look for Red Flags for Musculoskeletal Pain
Older age with new symptom onset
Night pain
Fever
Sweating
Neurological features
Previous history of malignancy
Speaker’s Notes
It is also important to screen patients presenting with pain for red flags indicative of a serious underlying condition. Depending on the condition suspected, clinicians should then initiate appropriate investigations or refer the patient to a specialist.
Reference
Littlejohn GO. Musculoskeletal pain. J R Coll Physicians Edinb 2005; 35(4):340-4.
Littlejohn GO. R Coll Physicians Edinb 2005; 35(4):340-4.

24. Acute Pain Evaluation and Treatment
Re-evaluate and adjust treatment if indicated
Treat appropriately
Pain is severe/disabling: requires opioids
Perform assessments
Perform diagnostic evaluation
Patient presenting with acute pain
Yes
Refer to specialist
Speaker’s Notes
This slide presents a simple flowchart for the management of acute pain.
Patients presenting with acute pain should be evaluated by obtaining a medical history and performing a physical examination. Factors that may influence choice and dose of analgesic should be evaluated, including comorbid medical conditions or laboratory anomalies and current medications with potential for drug interactions.
Next, pain severity should be quantified using a rating scale. Pain-related disability and functional impairment should likewise be quantified.
Patients with severe or disabling pain requiring opioids may required referral to a specialist for treatment. Other patients should be treated with appropriate analgesics and educated about doses, expected time to response, possible side effects, etc. Clinicians should also stress the benefits of behavioral interventions such as exercise and relaxation. The presence of anxiety and/or depression should be evaluated and these conditions should be treated as necessary. Finally, pain severity and functional impairment should be re-assessed at regular intervals and the treatment adjusted based on assessment of response.
Reference
Ayad AE et al. Expert panel consensus recommendations for the pharmacological treatment of acute pain in the Middle East region. J Int Med Res 2011; 39(4): No
Ayad AE et al. J Int Med Res 2011; 39(4):

25. Goals in Pain Management
Involve the patient in the decision-making process
Agree on realistic treatment goals before starting a treatment plan
Speaker’s Notes
It is important to discuss and agree on realistic treatment goals before starting a treatment plan. In cases of neuropathic pain, for example, total pain relief is usually an unrealistic goal and will result in frustration for both patient and doctor. A reduction in pain of about 30–50% is more realistic, and is clinically important to patients. With this in mind, patients need to accept reduced pain and improved function with minimum acceptable side effects as a goal of pain management.
References
Farrar JT et al. Clinical importance of changes in chronic pain intensity measured on an 11-point numerical pain rating scale. Pain 2001; 94(2):
Gilron I et al. Neuropathic pain: a practical guide for the clinician. CMAJ 2006; 175(3):
Optimized pain relief
Improved function
Minimized adverse effects
Farrar JT et al. Pain 2001; 94(2):149-58; Gilron I et al. CMAJ 2006; 175(3):

26. Multimodal Treatment of Pain Based on Biopsychosocial Approach
Lifestyle management
Sleep hygiene
Stress management
Interventional pain
management
Physical therapy
Pharmacotherapy
Speaker’s Notes
The 2011 Institute of Medicine (IOM) pain report suggested that a mind-body approach should be used when caring for patients with pain.
The biopsychosocial approach, combining physical and emotional factors in assessing and treating chronic pain, offers a uniquely valuable clinical perspective. This mind-body perspective is now generally accepted by pain researchers and has been found useful by clinicians in various disciplines.
This animated slide lists components that might be included in such a multimodal approach to pain therapy.
References
Gatchel RJ et al. The biopsychosocial approach to chronic pain: scientific advances and future directions. Psychol Bull 2007; 133(4):
Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research.; National Academies Press; Washington, DC: 2011.
Mayo Foundation for Medical Education and Research. Comprehensive Pain Rehabilitation Center Program Guide. Mayo Clinic; Rochester, MN: 2006.
Occupational therapy
Education
Complementary therapies
Biofeedback
Gatchel RJ et al. Psychol Bull 2007; 133(4): ; Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research.; National Academies Press; Washington, DC: 2011; Mayo Foundation for Medical Education and Research. Comprehensive Pain Rehabilitation Center Program Guide. Mayo Clinic; Rochester, MN: 2006.

27. Discussion Question
what non-pharmacological approaches to managing acute pain do you incorporate into your practice? are there non-pharmacological modalities your patients regularly ask about?
Speaker’s Notes
Ask the question shown on the slide to participants to stimulate discussion.

28. Physical Interventions for Acute Pain
Potential utility
Transcutaneous electrical nerve stimulation
Certain stimulation patterns effective in some acute pain settings (e.g., post-operative pain)
Acupuncture
Reduces post-operative pain as well as opioid-related adverse effects
May be effective in some other acute pain settings
Massage and manual therapy
Little consistent evidence for use in post-operative pain
Heat and cold therapy
Evidence for benefits from post-operative local cooling is mixed
Speaker’s Notes
According to the guidelines developed by the Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine, transcutaneous electrical nerve stimulation and acupuncture may be of benefit in some acute pain settings. Evidence regarding the benefits of massage, manual therapy and heat and cold therapy is mixed.
Reference
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.

29. Cognitive Behavioral Interventions for Acute Pain
Potential utility
Reassurance and provision of information
Evidence that information is effective in reducing procedure-related pain is tentatively supportive and not sufficient to make recommendations
Relaxation training
Evidence is weak and inconsistent
Attentional techniques (e.g., imagery, distraction, music therapy)
Listening to music produces a small reduction in post-operative pain and opioid requirement
Immersive virtual reality distraction is effective in reducing pain in some clinical situations
Hypnosis
Evidence of benefit is inconsistent
Coping methods/ behavioral instruction
Training prior to surgery reduces pain, negative affect and analgesic use
Speaker’s Notes
According to the guidelines developed by the Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine, patient education prior to surgery can be of benefit in reducing pain and use of analgesics. Attentional techniques such as music therapy and distraction may also be of benefit in some situations.
Evidence regarding the benefits of relaxation training and hypnosis is mixed.
Reference
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.

30. Ideal Characteristics for Acute Analgesic Therapy
Ideal drug characteristics for acute pain therapy:
Speaker’s Notes
Pharmacotherapy for acute pain needs to strike a balance between effective analgesia and limited adverse effects. Ideally, it combines these characteristics with rapid onset and long duration of analgesia.
Reference
Baumann TJ. In: DiPiro JT et al (eds). Pharmacotherapy: A Pathophysiologic Approach. 5th ed. McGraw-Hill; New York, NY: 2002.
Rapid onset
Long duration
Effective analgesia
Limited adverse effects
Baumann TJ. In: DiPiro JT et al (eds). Pharmacotherapy: A Pathophysiologic Approach. 5th ed. McGraw-Hill; New York, NY: 2002.

31. Patients Prefer Avoiding Side Effects to Complete Pain Control
Relative Importance Placed by Patients on Different Attributes of Acute Pain Therapy
47%
Speaker’s Notes
This slide shows the importance weights for setting/route, side effect type and severity, and pain control.
Fifty patients undergoing major abdominal surgery were enrolled and completed interviews prior to and 4 weeks after surgery.
Patients reported an average of 75% pain relief within 12 hours of transitioning from patient-controlled analgesia to oral analgesia. In all, 96% reported at least one side effect from pain medication of any level of severity, 82% reported at least one side effect that was moderate or severe, and 40% reported at least one side effect that was severe.
Effective pain control and side effect type/severity ranked about equally in importance, with the combined side effect percentage slightly higher (47%) than that for effective pain control (41%). Setting (e.g., at home or in hospital) and route (i.e., oral or intravenous) of administration of pain medications were ranked a distant third at 12%.
Reference
Gan TJ et al. Patient preferences for acute pain treatment. Br J Anaesth 2004; 92(5):681-8.
Gan TJ et al. Br J Anaesth 2004; 92(5):681-8.

32. Proportion of Patients Experiencing Adverse Events
Total n (%)
Constipation
25 (50%)
Mental cloudiness/dizziness
41 (82%)
Itching
27 (54%)
Nightmares/hallucinations
16 (32%)
Mood changes/alterations
17 (34%)
Nausea
35 (70%)
Sleep disorders
24 (48%)
Vomiting
Speaker’s Notes
This slide shows the proportion of patients experiencing side effect at any time during the study by maximum severity.
Fifty patients undergoing major abdominal surgery were enrolled and completed interviews prior to and 4 weeks after surgery.
Reference
Gan TJ et al. Patient preferences for acute pain treatment. Br J Anaesth 2004; 92(5):681-8.
Gan TJ et al. Br J Anaesth 2004; 92(5):681-8.

33. Why should we treat acute pain?
If acute pain IS NOT treated effectively:
It may cause severe suffering, loss of quality of life, loss of productivity, have economic considerations
Is associated with morbidity and even mortality
May develop into chronic pain
Speaker’s Notes
This slide highlights the importance of treating acute pain.
Reference
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.

34. So how do we treat acute pain?
Treat according to pain mechanisms involved
Speaker’s Notes
Treatment of pain is based on treating the underlying cause and treating according to pain mechanisms involved.
Since the transition from acute to chronic pain involves a complex web of noxious signal pathways, a multimodal management plan is most optimal to inhibit the progression of pain from acute to chronic.
Under normal conditions, noxious stimuli diminish as healing progresses and pain sensation lessens until minimal or no pain is detected. Persistent, intense pain, however, activates secondary mechanisms both at the periphery and within the central nervous system that cause allodynia, hyperalgesia, and hyperpathia that can diminish normal functioning. These changes begin in the periphery with upregulation of cyclo-oxygenase-2 (COX-2) and interleukin (IL)-1β-sensitizing first-order neurons, which eventually sensitize second-order spinal neurones by activating N-methyl-d- aspartic acid (NMDA) channels and signaling microglia to alter neuronal cytoarchitecture. Throughout these processes, prostaglandins, endocannabinoids, ion-specific channels, and scavenger cells all play a key role in the transformation of acute to chronic pain. A better understanding of the interplay among these substances will assist in the development of agents designed to ameliorate or reverse chronic pain.
Reference
VoscopoulosC et al. When does acute pain become chronic? Br J Anaesth 2010; 105(Suppl 1):i69-85.
Multimodal analgesia
Voscopoulos C, Lema M. Br J Anaesth 2010; 105(Suppl 1):i69-85.

35. Multimodal or Balanced Analgesia
Improved analgesia
 doses of each analgesic
 severity of side effects of each drug
Opioid
Potentiation
Acetaminophen
nsNSAIDs/coxibs
α2δ ligands
Ketamine
Clonidine
Nerve blocks
Speaker’s Notes
Optimal pain management that allows a patient to lead a normal life is unlikely to be achieved with a single analgesic.
The concept of multimodal or balanced management pivots around the notion that by combining analgesics that work on distinct parts of the pain transmission circuit, pain management can be improved with lower doses of the individual analgesic and accordingly yield less side effects.
Reference
Kehlet H, Dahl JB. The value of "multimodal" or "balanced analgesia" in postoperative pain treatment. Anesth Analg 1993; 77(5):
Coxib = COX-2 inhibitor; nsNSAID = non-specific non-steroidal anti-inflammatory drug
Kehlet H, Dahl JB. Anesth Analg 1993; 77(5):

36. Analgesics Should Be Given at Regular Intervals During Acute Pain Episodes
Speaker’s Notes
In this randomized controlled trial , the effectiveness of around-the-clock dosing of acetaminophen with hydrocodone was compared against PRN dosing with the same drugs in children (6–15 years) who had undergone tonsillectomy.
Over the 3 post-operative days, children in the PRN group had significantly higher mean pain intensity scores .
The results of this study support the use of around-the-clock dosing of acetaminophen with hydrocodone during the early postoperative recovery at home in an outpatient pediatric population undergoing tonsillectomy, particularly for the first 48 hours.
Reference
Sutters KA et al. A randomized clinical trial of the efficacy of scheduled dosing of acetaminophen and hydrocodone for the management of postoperative pain in children after tonsillectomy. Clin J Pain 2010; 26(2):
Sutters KA et al. Clin J Pain 2010; 26(2):

37. Nociception: Neural Process of Encoding Noxious Stimuli
Somatosensory
cortex
Thalamus
Perception
Noxious stimuli
Descending modulation
Ascending input
Speaker’s Notes
This slide illustrates some central and peripheral pathways by which painful stimuli are normally processed (nociceptive pain).
Transduction is the conversion of a noxious thermal, mechanical or chemical stimulus into electrical activity in the peripheral terminals of nociceptor sensory fibers. This process is mediated by specific receptor ion channels expressed only by nociceptors.
Conduction is the passage of action potentials from the peripheral terminal along axons to the central terminal of nociceptors in the central nervous system.
Transmission is the synaptic transfer and modulation of input from one neuron to another. Peripheral nerve fibers involved in pain include unmyelinated slowly conducting C fibers and thinly myelinated A fibers.
In the superficial layers of the dorsal horn, these fibers make synaptic connection with second-order neurons that transmit the impulses through the spinal cord to the brain (ascending transmission pathway). In the brain, the thalamus and certain specific cortical areas are critical for the sensory experience of pain. Transmission and processing of pain impulses is also modulated by descending pathways.
Reference
Scholz J, Woolf CJ. Can we conquer pain? Nat Neurosci 2002; 5(Suppl):
Conduction
Transmission
Transduction
Nociceptive afferent fiber
Spinal cord
Consequences of encoding may be autonomic (e.g., elevated blood pressure) or behavioral (motor withdrawal reflex or more complex nocifensive behavior). Pain perception is not necessarily implied.
Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):

38. Inflammation Changed responsiveness of neurons in CNS
Brain
Damaged tissue
Inflammatory cells
Tumor cells
Prostanoids
Cytokines
Growth factors
Kinins
Purines
Amines
Ions
Inflammatory chemical mediators
Changed responsiveness of neurons in CNS
(central sensitization)
Speaker’s Notes
Inflammation occurs when damaged tissue, inflammatory cells and/or tumor cells release inflammatory chemical mediators, such as cytokines, growth factors, kinins, purines, amines, prostanoids and ions. Some of these mediators directly activate nociceptors, provoking pain. Others heighten the responsiveness of the nociceptors, lowering the pain threshold while the damaged tissue heals – a process known as peripheral sensitization. This in turn changes the responsiveness of neurons in the CNS, which is called central sensitization.
Reference
Scholz J, Woolf CJ. Can we conquer pain? Nat Neurosci 2002; 5(Suppl):
Changed responsiveness of nociceptors
(peripheral sensitization)
Nociceptive afferent fiber
Spinal cord
CNS = central nervous system
Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):

39. nsNSAIDs/coxibs, opioids
Mechanism-Based Pharmacological Treatment of Nociceptive/Inflammatory Pain
Brain
α2δ ligands
Acetaminophen
Antidepressants
nsNSAIDs/coxibs
Opioids
Perception
Opioids
Noxious stimuli
nsNSAIDs/coxibs
Local anesthetics
Local anesthetics
Descending modulation
Ascending input
Transmission
Transduction
Speaker’s Notes
This slide outlines some treatment options for nociceptive and inflammatory pain, indicating where in the pain pathway these agents take effect.
Reference
Scholz J, Woolf CJ. Can we conquer pain? Nat Neurosci 2002; 5(Suppl):
Nociceptive afferent fiber
Inflammation
Spinal cord
Peripheral sensitization
Central sensitization
nsNSAIDs/coxibs, opioids
Coxib = COX-2 inhibitor; nsNSAID = non-specific non-steroidal anti-inflammatory drug
Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):

40. how do these medications work to reduce acute pain?
Discussion Question
how do these medications work to reduce acute pain?
Speaker’s Notes
Ask the question shown on the slide to participants to stimulate discussion.

41. What are NSAIDs (nsNSAIDs/coxibs)?
Analgesic effect via inhibition of prostaglandin production
Broad class incorporating many different medications:
NSAID = Non-Steroidal Anti-Inflammatory Drug
Examples of nsNSAIDs:
Diclofenac
Ibuprofen
Naproxen
Examples of Coxibs:
Celecoxib
Etoricoxib
Parecoxib
Speaker’s Notes
NSAIDs make up a broad class of medications that includes both nsNSAIDs and coxibs. Both nsNSAIDs and coxibs have an analgesic effect by inhibiting prostaglandin production through inhibition of the COX-2 enzyme. However, while coxibs selectively inhibit COX-2, nsNSAIDs also inhibit the constitutively expressed COX-1 enzyme.
Commonly used nsNSAIDs include diclofenac, ibuprofen and naproxen, while celecoxib, etoricoxib and parecoxib are coxibs.
Reference
Brune K. In: Kopf A et al (eds). Guide to Pain Management in Low-Resource Settings. International Association for the Study of Pain; Seattle, WA: 2010.
Coxib = COX-2-specific inhibitor; nsNSAID = non-specific non-steroidal anti-inflammatory drug
Brune K. In: Kopf A et al (eds). Guide to Pain Management in Low-Resource Settings. International Association for the Study of Pain; Seattle, WA: 2010.

42. How do nsNSAIDs/coxibs work?
Arachidonic acid
COX-1 (constitutive)
COX-2 (induced by inflammatory stimuli)
Coxibs
BLOCK
BLOCK
nsNSAIDs
BLOCK
Prostaglandins
Prostaglandins
Speaker’s Notes
nsNSAIDs and coxibs have both peripheral and central analgesic effects.
Peripheral trauma triggers the production of COX-2 both at the periphery and in the dorsal horn, which in turn stimulates the production of prostaglandins. Prostaglandins in the periphery increase sensitivity to noxious stimuli by affecting the transient receptor potential cation channel subfamily V member 1 (TRPV1) on nociceptors. In the dorsal horn, prostaglandins activate protein kinase A (PKA), which in turn phosphorylates glycine-receptor-associated chloride channels, reducing the probability of their opening and rendering the neuron more excitable to glutamate-transmitted stimuli.
Both nsNSAIDs and coxibs inhibit prostaglandin production by blocking the action of the COX-2 enzyme. However, while coxibs selectively inhibit COX-2, nsNSAIDs also inhibit the constitutively expressed COX-1 enzyme.
References
Gastrosource. Non-steroidal Anti-inflammatory Drug (NSAID)-Associated Upper Gastrointestinal Side-Effects. Available at: Accessed: December 4, 2010.
Vane JR, Botting RM. New insights into the mode of action of anti-inflammatory drugs. Inflamm Res 1995; 44(1):1-10.
Gastrointestinal cytoprotection, platelet activity
Inflammation, pain, fever
Pain relief
Coxib = COX-2-specific inhibitor; NSAID = non-steroidal anti-inflammatory drug
nsNSAID = non-specific non-steroidal anti-inflammatory drug
Gastrosource. Non-steroidal Anti-inflammatory Drug (NSAID)-Associated Upper Gastrointestinal Side-Effects. Available at: Accessed: December 4, 2010; Vane JR, Botting RM. Inflamm Res 1995;44(1):1-10.

43. Adverse Effects of nsNSAIDs/Coxibs
All NSAIDs:
Gastroenteropathy
Gastritis, bleeding, ulceration, perforation
Cardiovascular thrombotic events
Renovascular effects
Decreased renal blood flow
Fluid retention/edema
Hypertension
Hypersensitivity
Cox-1-mediated NSAIDs (nsNSAIDs):
Decreased platelet aggregation
Speaker’s Notes
This slide outlines some adverse effects associated with nsNSAIDs and coxibs.
References
Clemett D, Goa KL. Celecoxib: a review of its use in osteoarthritis, rheumatoid arthritis and acute pain. Drugs 2000; 59(4):
Grosser T et al. In: Brunton L et al (eds). Goodman and Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. (online version). McGraw-Hill; New York, NY: 2010.
Coxib = COX-2-specific inhibitor; NSAID = non-steroidal anti-inflammatory drug; nsNSAID = non-specific non-steroidal anti-inflammatory drug
Clemett D, Goa KL. Drugs 2000; 59(4):957-80; Grosser T et al. In: Brunton L et al (eds.). Goodman and Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. (online version). McGraw-Hill; New York, NY: 2010.

44. Discussion Question
how do you evaluate gastrointestinal risk in patients you are considering prescribing a nsNSAID or a coxib?
Speaker’s Notes
Ask the question shown on the slide to participants to stimulate discussion.

45. Odds ratio/relative risk for ulcer complications
Risk Factors for Gastrointestinal Complications Associated with nsNSAIDs/Coxibs 1 1 1 2 1 3 4 3
Speaker’s Notes
Most anti-inflammatory drugs have been associated with gastrointestinal side effects. Gastrointestinal mucosa damage can range from endoscopic lesions with no clinical manifestations to serious upper gastrointestinal complications that, in some instances, may be fatal. This graph provides the relative risk of a variety of factors for gastrointestinal complications associated with nsNSAIDs/coxibs. Previous upper gastrointestinal bleeding s the single most important predictor of future upper gastrointestinal bleeding.
References
Bardou M, Barkun AN. Preventing the gastrointestinal adverse effects of nonsteroidal anti-inflammatory drugs: from risk factor identification to risk factor intervention. Joint Bone Spine 2010; 77(1):6-12.
Gabriel SE et al. Risk for serious gastrointestinal complications related to use of nonsteroidal anti-inflammatory drugs. A meta-analysis. Ann Intern Med 1991; 115(10):
García Rodríguez LA, Hernández-Díaz S. The risk of upper gastrointestinal complications associated with nonsteroidal anti-inflammatory drugs, glucocorticoids, acetaminophen, and combinations of these agents. Arthritis Res 2001; 3(2):
García Rodríguez LA, Jick H. Risk of upper gastrointestinal bleeding and perforation associated with individual non-steroidal anti-inflammatory drugs. Lancet 1994; 343(8900): 1 3
Odds ratio/relative risk for ulcer complications
ASA = acetylsalicylic acid; coxib = COX-2-specific inhibitor; GI = gastrointestinal; NSAID = non-steroidal anti-inflammatory drug; nsNSAID = non-specific non-steroidal anti-inflammatory drug; SSRI = selective serotonin reuptake inhibitor
1. Garcia Rodriguez LA, Jick H. Lancet 1994; 343(8900):769-72; 2. Gabriel SE et al. Ann Intern Med 1991; 115(10):787-96; 3. Bardou M. Barkun AN. Joint Bone Spine 2010; 77(1):6-12; 4. Garcia Rodríguez LA, Hernández-Díaz S. Arthritis Res 2001; 3(2):

46. Gastrointestinal risk
Guidelines for nsNSAIDs/Coxibs Use Based on Gastrointestinal Risk and ASA Use
Gastrointestinal risk
Not elevated
Elevated
Not on ASA
nsNSAID alone
Coxib
nsNSAID + PPI
On ASA
Coxib + PPI
Speaker’s Notes
In 2006, the Third Canadian Consensus Conference recommended that all patients on ASA who are prescribed either a coxib or a nsNSAID should also receive a PPI, regardless of their level of gastrointestinal risk.
While this recommendation proved to be controversial, the rationale was that ASA is prescribed to patients with comorbidities that are themselves gastrointestinal risk factors. Of note, some patients may take ASA because they believe it to be beneficial without necessarily having any comorbidities.
Reference
Tannenbaum H et al. An evidence-based approach to prescribing nonsteroidal antiinflammatory drugs. Third Canadian Consensus Conference. J Rheumatol 2006; 33(1):
ASA = acetylsalicylic acid; coxib = COX-2-specific inhibitor; nsNSAID = non-selective non-steroidal anti-inflammatory drug; PPI = proton pump inhibitor
Tannenbaum H et al. J Rheumatol 2006; 33(1):

47. How Opioids Affect Pain
Modify perception, modulate transmission
and affect transduction by:
Altering limbic system activity; modify sensory and affective pain aspects
Activating descending pathways that modulate transmission in spinal cord
Affecting transduction of pain stimuli to nerve impulses
Brain
Perception
Descending modulation
Ascending input
Speaker’s Notes
Opioid analgesics produce their analgesic effect by mimicking the actions of endogenous peptides produced in response to noxious stimuli, such as endorphins, enkephalins and dynorphins, and binding to endogenous opioid receptors (known as mu, kappa and delta receptors) that are present both centrally and peripherally.
There are four major classes of opioid analgesics:
Opioid agonists, the most common class, bind to and stimulate opioid receptors.
Partial agonists, such as buprenorphine, have a high affinity but low agonist effect on the mu receptor, and a greater antagonist effect at the kappa receptor. Therefore, such agents have a ceiling to their analgesic effect, but the antagonist action enables their use in opioid abuse detoxification, deterrence and maintenance.
In contrast, opioid agonist-antagonists are functional mu receptor antagonists and kappa receptor agonists. Like partial agonists, these have a ceiling to their analgesic effect, beyond which increasing the dosage only increases opioid side effects.
Opioid antagonists have a high affinity for the mu receptors, but lack any activating activity.
Finally, tramadol is considered an atypical opioid as it has with central gamma-aminobutyric acid (GABA), catecholamine and serotonergic activities in addition to being a partial mu agonist.
References
Reisine T, Pasternak G. In: Hardman JG et al (eds). Goodman and Gilman’s: The Pharmacological Basics of Therapeutics. 9th ed. McGraw-Hill; New York, NY: 1996.
Scholz J, Woolf CJ. Can we conquer pain? Nat Neurosci 2002; 5(Suppl):
Trescot AM et al. Opioid pharmacology. Pain Physician 2008; 11(2 Suppl):S
Transmission
Transduction
Nociceptive afferent fiber
Spinal cord
Reisine T, Pasternak G. In: Hardman JG et al (eds). Goodman and Gilman’s: The Pharmacological Basics of Therapeutics. 9th ed. McGraw-Hill; New York, NY: 1996; Scholz J, Woolf CJ. Nat Neurosci 2002; 5(Suppl):1062-7; Trescot AM et al. Pain Physician 2008; 11(2 Suppl):S

48. Discussion Question
what potential side effects do you discuss with patients for whom you are considering prescribing an opioid?
Speaker’s Notes
Ask the question shown on the slide to participants to stimulate discussion.

49. Adverse Effects of Opioids
System
Adverse effects
Gastrointestinal
Nausea, vomiting, constipation
CNS
Cognitive impairment, sedation, lightheadedness, dizziness
Respiratory
Respiratory depression
Cardiovascular
Orthostatic hypotension, fainting
Other
Urticaria, miosis, sweating, urinary retention
Speaker’s Notes
The use of opioids in pain management can be associated with a variety of adverse effects, as shown on this slide. Gastrointestinal side effects can include nausea, vomiting and constipation, while central nervous system effects may include cognitive impairment, sedation, lightheadedness, and dizziness. Respiratory depression, orthostatic hypotension, fainting, urticaria, miosis, sweating and urinary retention are among the other potential adverse effects of opioids.
References
Moreland LW, St Clair EW. The use of analgesics in the management of pain in rheumatic diseases. Rheum Dis Clin North Am 1999; 25(1):
Yaksh TL, Wallace MS. In: Brunton L et al (eds). Goodman and Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. (online version). McGraw-Hill; New York, NY: 2010.
CNS = central nervous system
Moreland LW, St Clair EW. Rheum Dis Clin North Am 1999; 25(1):153-91; Yaksh TL, Wallace MS. In: Brunton L et al (eds). Goodman and Gilman’s The Pharmacological Basis of Therapeutics. 12th ed. (online version). McGraw-Hill; New York, NY: 2010.

50. Acetaminophen Action at molecular level is unclear
Potential mechanisms include:
Inhibition of COX enzymes (COX-2 and/or COX-3)
Interaction with opioid pathway
Activation of serotoninergic bulbospinal pathway
Involvement of nitric oxide pathway
Increase in cannabinoid-vanilloid tone
Speaker’s Notes
Acetaminophen is a common analgesic that was first synthesized more than a century ago. However, despite its long history of use, its action at the molecular level remains unclear. It appears to act centrally through interactions with the cyclooxygenase system, the endogenous opioid pathway, the serotoninergic inhibitory descending system, the nitric oxide pathway, and the endocannabinoid system.
It is generally safe, with rare hepatotoxicity events being mostly associated with overdose, either intentional or accidental. However, caution should be used in patients on anticoagulants as acetaminophen has an anti-aggregatory effect.
Reference
Mattia A, Coluzzi F. What anesthesiologists should know about paracetamol (acetaminophen). Minerva Anestesiol 2009; 75(11):
Mattia A, Coluzzi F. Minerva Anestesiol 2009; 75(11):

51. Use of pharmacological agents before, during and after surgery may:
Peri-operative Pain Management Aims to Control Pain and Decrease Likelihood of Developing Chronic Pain
Persistent post-operative pain
Acute post-operative pain
May lead to development of
Use of pharmacological agents before, during and after surgery may:
 acute pain
 subsequent development of chronic pain
 morbidity, costs and other consequences of chronic pain
Speaker’s Notes
This slide provides an overview of the role of pharmacological agents in preventing or reducing acute and/or chronic post-operative pain.
Acute post-operative pain is common and characterized by spontaneous resting and breakthrough pain referred to the site of surgery and surrounding tissues. Acute post-operative pain is followed by persistent or chronic post-operative pain (which usually lasts for 3–6 months or more after surgery) in 10–50% of individuals after common operations such as groin hernia repair, breast and thoracic surgery, leg amputation, and coronary artery bypass surgery.
Pain in the immediate post-operative period generally responds well to opiates and COX inhibitors, however, these agents are unlikely to prevent the development of chronic post-operative pain. Multimodal approaches to pain management in the peri-operative period have the potential to reduce or prevent both acute and chronic pain after surgery. Combination strategies directed at both the injured nerve and the neuroplastic changes subsequently produced are likely to produce the best results.
Effective peri-operative analgesia is essential for reducing post-operative morbidity, improving quality of life, and reducing healthcare costs.
References
Joshi GP et al. Consequences of inadequate postoperative pain relief and chronic persistent postoperative pain. Anesthesiol Clin N Am 2005; 23(1):21-36.
Kehlet H et al. Persistent postsurgical pain: risk factors and prevention. Lancet 2006; 367(9522):
Joshi GP et al. Anesthesiol Clin N Am 2005; 23(1):21-36; Kehlet H et al. Lancet 2006; 367(9522):

52. Controlling Post-operative Physiology
Supportive agents/therapy in high-risk patients
Pre-operative
information + teaching
Enteral nutrition
Attenuation of intra-operative stress
Pain
relief
Exercise
Speaker’s Notes:
No single technique or drug regimen has been shown to eliminate postoperative morbidity and mortality. Multimodal interventions may lead to a major reduction in surgical injury with improved recovery and reduction in postoperative morbidity and overall costs.
Reference
Kehlet H. Multimodal approach to control postoperative pathophysiology and rehabilitation. Br J Anaesth 1997; 78(5):
Reduced morbidity and accelerated convalescence
Kehlet H. Br J Anaesth 1997; 78(5):

53. Recommendations for Management of Acute Pain
Acetaminophen
If ineffective
Add nsNSAIDs/coxibs
Speaker’s Notes:
This slide shows the recommended algorithm for applying pharmacotherapy to manage acute pain. The algorithm was developed by the Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine.
Reference
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.
If ineffective
Add opioids (preferably short-acting agents at regular intervals; ongoing need for such treatment requires reassessment)
Coxib = COX-2-specific inhibitor; nsNSAID = non-selective non-steroidal anti-inflammatory drug
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine.
Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.

54. Algorithm for Treatment of Acute Pain Based on Severity
Acute pain due to:
Sport injury
Traumatic or inflammatory condition
Musculoskeletal injury
Mild or moderate acute pain
Severe acute pain
Inadequate analgesia
Step 1: acetaminophen
(4 g/day maximum dose; 4 h minimum interval between each 1 g dose)
Inadequate analgesia
Speaker’s Notes
This slide presents an alternative algorithm for the treatment of acute pain, based on severity. This algorithm is based on the expert panel consensus recommendations for the pharmacological treatment of acute pain in the Middle East region.
Reference
Ayad AE et al. Expert panel consensus recommendations for the pharmacological treatment of acute pain in the Middle East region. J Int Med Res 2011; 39(4):
Step 2: coxib or nsNSAID
(make choice based on patient risk profile)
Inadequate analgesia
Topical nsNSAID (with or without combined oral acetaminophen, coxib or nsNSAID)
Step 3: add 1 of following:
Acetaminophen/codeine
Acetaminophen/tramadol
Tramadol
Opioids
(refer patient to pain clinic or specialist)
Coxib = COX-2 inhibitor; nsNSAID = non-specific non-steroidal anti-inflammatory drug
Ayad AE et al. J Int Med Red 2011; 39(4):

55. Analgesia for Post-operative Pain Based on Type of Surgery
Surgical procedures
- Acetaminophen
- nsNSAIDs/coxibs*
- Wound infiltration
- Regional block analgesia
- Weak opioid or rescue analgesic, if necessary
- Peripheral nerve block or IV opioid
- Epidural or major peripheral nerve or plexus block or IV opioid
Major surgery
Moderate surgery
Minor surgery
Speaker’s Notes:
This slide provides an overview of the various types of multimodal approaches that can be applied depending on the surgical procedure performed.
Examples of minor surgery would include surgery to correct an inguinal hernia or varicose veins and laparoscopy, while moderate surgery might include hip replacement, hysterectomy and jaw surgery. Thoracotomy, aortic surgery and knee replacement would be examples of major surgery.
The PROSPECT group of surgeons and anesthesiologists have developed evidence- based, procedure-specific recommendations for post-operative pain management. Recommendations for post-operative pain management following abdominal hysterectomy, colonic resection, hemorrhoid surgery, herniorraphy, laparoscopic cholecystectomy, non-cosmetic breast surgery, radical prostatectomy, thoracotomy, total hip arthroplasty and total knee arthroplasty can be found on the PROSPECT website.
Reference
Sivrikaya GU. In: Racz G (ed). Pain Management – Current Issues and Opinions. InTech; Rijeka, Croatia: 2012.
PROSPECT Working Group. Procedure Specific Postoperative Pain Management. Available at: Accessed: July 24, 2013.
Treatment modalities
*Unless contraindicated
Coxib = COX-2-specific inhibitor; IV = intravenous; nsNSAID = non-selective non-steroidal anti-inflammatory drug
Sivrikaya GU. In: Racz G (ed). Pain Management – Current Issues and Opinions. InTech; Rijeka, Croatia: 2012.
PROSPECT Working Group. Procedure Specific Postoperative Pain Management. Available at: Accessed: July 24, 2013.

56. Discussion Question
in your practice, do you regularly assess risk for developing chronic pain? if so, how?
Speaker’s Notes
Ask the question shown on the slide to participants to stimulate discussion.

57. Risk Factors for Chronic Post-operative Pain
Pre-operative factors
Moderate to severe pain, lasting >1 month
Repeat surgery
Psychologic vulnerability (e.g., catastrophizing)
Pre-operative anxiety
Female gender
Younger age (adults)
Workers’ compensation
Genetic predisposition
Inefficient diffuse noxious inhibitory control
Intra-operative factors
Surgical approach with risk of nerve damage
Post-operative factors
Moderate to severe acute pain
Radiation therapy to area
Neurotoxic chemotherapy
Depression
Psychological vulnerability
Neuroticism
Anxiety
Speaker’s Notes:
This slide lists peri-operative risk factors for the development of chronic post-operative pain.
Reference
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.
Australian and New Zealand College of Anaesthetists and Faculty of Pain Medicine. Acute Pain Management: Scientific Evidence. 3rd ed. ANZCA & FPM; Melbourne, VIC: 2010.

58. Acute Pain Can Become Chronic
Life Cycle Factors Associated with Development of Chronic Pain
From birth
Genetics Female sex
Minority race/ethnicity Congenital disorders Prematurity
Parental anxiety
Irregular feeding/sleeping
Parents’ pain exposure and reactions
Personality
Childhood
Physical/sexual abuse and other traumatic events
Low socioeconomic status
Emotional, conduct and peer problems
Hyperactivity
Serious illness or injury
Separation from mother
Acute or recurrent pain experience
Adolescence
Changes of puberty Gender roles
Education level
Injuries
Obesity
Low levels of fitness
Adulthood
Vivid recall of childhood trauma
Lack of social support
Accumulated stress
Surgery
Overuse of joints and muscles
Occupation
Chronic disease
Aging
Speaker’s Notes:
This slide shows the individual factors throughout a person’s lifespan that could contribute to the eventual development of chronic pain.
Reference
Institute of Medicine of the National Academies. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. The National Academies Press; Washington, DC: 2011.
Institute of Medicine. Relieving Pain in America: A Blueprint for Transforming Prevention, Care, Education, and Research. The National Academies Press; Washington, DC: 2011.

59. Key Messages
Acute pain is extremely common, with musculoskeletal pain being the most common presentation in primary care
Clinicians should maintain high degree of awareness for “red flags” indicating potential serious disorders and should, when possible, treat the underlying cause of pain
In acute pain, normal nociception is modified by inflammation
Acetaminophen, nsNSAIDs/coxibs and opioids target common mechanisms of acute pain
Pain severity and individual patient risk profile should be considered when selecting pain management therapies
Timely and appropriate treatment may help prevent acute pain from becoming chronic pain
Speaker’s Notes
This slide can be used to summarize the main points of this presentation.
Coxib = COX-2-specific inhibitor; nsNSAID = non-selective non-steroidal anti-inflammatory drug;