Lu v overview of pain


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  • Good day! For our first lecture, we will have an overview of pain.
  • At the end of this lecture, you will be able to define pain, discuss the differences between acute and chronic pain, and classify pain based on pathophysiologic mechanisms.
  • At the end of this lecture, you will be able to discuss the basic principles of pain management, identify pain measurement scales/tools, and
    discuss therapeutic options.
  • Pain can be defined in so many ways. Pain consists of a complex constellation of unpleasant sensory, perceptual and emotional experiences and certain associated autonomic, psychologic, emotional, and behavioral responses. In 1979, the International Association for the Study of Pain came up with this operational definition.
  • Acute pain is the normal, predicted physiological response to an adverse chemical, thermal or mechanical stimulus associated with surgery, trauma and acute illness. As our friendly surgeon cuts with his scalpel, pain is perceived by the body through its nociceptors. It’s good that we now have anesthesiologists to take care of us intraoperatively so we wont feel the pain. After the anesthesia has worn off, we expect to feel a bit of pain from the incision site because we deem it as normal.
  • Acute pain acts as a warning of potential damage. It tells us to stop working too hard beyond our limits. It tells us we need to rest. If not, further damage and more severe pain can ensue. It tells us to withdraw our finger from a hot object and not to play with fire later.
  • In acute pain, pain is usually well localized and transient. Pain is expected to be gone once the injury heals. It may be associated with increased autonomic response such as hypertension, tachycardia, and tachypnea. The nervous system remains intact. The stimulus-response is the same as with other sensory modalities, like touch which means that the greater the stimulus or the injury, the greater the pain response is.
  • Under “physiologic” conditions, low intensity, non-noxious stimuli activate low-threshold receptors to generate innocuous sensations. High intensity, noxious stimuli activate high threshold nociceptors which may lead to the sensation of pain. Pain (A delta and C fibers) can be differentiated from touch (A beta fibers).
  • Throughout the world, chronic pain is the most frequent cause of suffering and disability that seriously impair the quality of life. Chronic pain persists beyond expected healing periods. Although some clinician use the arbitrary figure of 6 months, this is not appropriate because many acute injuries or diseases heal in 2-3 weeks. A simple needle stick in the index finger is expected to heal in a few days. However, if pain persists, the patient might be developing reflex sympathetic dsytrophy that requires immediate effective therapy. If overlooked, the process may become irreversible. Chronic pain may be due to chronic pathologic processes in somatic structures or viscera or there may be frequently have no clearly identifiable cause.
  • As such, pain becomes the disease itself. The physiologic, affective, and behavioral responses to chronic pain are quite different from those to acute pain. It is a malefic force that often imposes severe physical, emotional, economic and social stresses on the patient and on the family. Anxiety, depression, and vegetative signs like anorexia, lassitude, and decreased libido often accompany chronic pain.
  • Central and peripheral changes lead to abnormal excitability in the nervous system. Hyperexcitable dorsal horn neurons interpret low intensity stimulus as pain thus producing allodynia (non-painful stimulus perceived as pain).
  • When does acute pain become chronic pain? There is no definite time because it’s a spectrum of events relating to neuroplasticity or changes in the nervous system. Morphological changes in cellular level
    Altered gene expression
    Functional changes – rewiring, sympathetic involvement
    Structural changes: “sprouting”
    A β fiber (allodynia)
    Altered modulation - ↓ inhibitory
    - ↑ excitatory
    Altered pain perception/interpretation in sensory cortex, limbic system
  • Somatic pain is pain from primary afferent nerves in somatic tissues (skin, muscle, bone, connective tissues). It involves A delta (fast pain) and C fibers (slow pain).It may be acute or chronic.
  • SOMATIC PAIN (CUTANEOUS) is pain derived from skin, subcutaneous tissue, and mucous membrane. It is localized, sharp, pricking, burning, throbbing, stabbing in character. It follows dermatomes of segmental nerves. There could be areas of primary and secondary hyperalgesia.
  • SOMATIC PAIN (DEEP) is pain derived from muscles, tendons, joints, and bones. It is less localized, sharp/dull, aching in character. It follows myotomes and sclerotomes. There could be areas of spread of pain depending on the degree and duration of stimulus. Not infrequently, a localized pain from a minor injury, but unrelieved, becomes diffuse, poorly localized, and referred to a site that is remote from the site of injury. Deeply situated muscles or bones refer pain not to dermatomes but segmental distributions. There may be associated hyperalgesia, tenderness, reflex muscle spasm, and sympathetic hyperactivity.
  • VISCERAL PAIN is pain from afferent nerves in thoracic, abdominal, and pelvic viscera. It involves sympathetic and parasympathetic afferent fibers. It may be acute, chronic, or recurrent.
  • VISCERAL PAIN (TRUE) occurs in the midline, early in the disease, vague, poorly localized, dull, aching and associated with marked autonomic phenomena such as nausea, vomiting, diaphoresis.
  • Viscerotomes. Appropriate superficial areas to which visceral pain is referred, with related dermatomes in brackets. The dark areas are those most commonly associated with pain in each viscus. The gray areas indicate approx. larger area that may be associated.
  • Viscero-somatic convergence. Visceral nociceptive afferents converge on the same dorsal horn neuron as do somatic nociceptive afferents. It is then conveyed thru the STT. Referred pain is felt in the cutaneous area corresponding to the dorsal horn neurons with hyperalgesia and allodynia. Reflex somatic motor activity results in muscle spasm w/c may stimulate the parietal peritoneum. Reflex sympathetic activity may result in spasms of sphincters of viscera over a wide area and ischemia. Only a small number of visceral afferent fibers converge compared with somatic thus dull, vague and poorly localized
  • VISCERAL PAIN (PARIETAL) Pleura or peritoneum ;Localized, sharp, stabbing, lancinating; Hyperalgesia,
    skeletal muscle spasm; sympathetic hyperactivity
  • NEUROPATHIC PAIN is pain from aberrant somatosensory processing in the peripheral or central nervous system. It is often related to nerve injury. Neuropathic pain is a pathological pain. Such syndromes comprise a complex combination of negative symptoms or sensory deficits, such as partial or complete loss of sensation, and positive symptoms that include dysesthesia, paresthesia, and pain.
  • Many patients with neuropathic pain exhibit persistent or paroxysmal pain that is independent of a stimulus. This stimulus-independent pain can be shooting, lancinating, or burning and may depend on activity in the sympathetic nervous system. Allodynia is the sensation of pain elicited by a non-noxious stimulus and can be produced in two ways: by the action of low threshold myelinated Aß fibres on an altered central nervous system; and by a reduction in the threshold of nociceptor terminals in the periphery. Stimulus-evoked hyperalgesias are commonly classified into subgroups on the basis of modality--ie, mechanical, thermal, or chemical. Mechanical hyperalgesias are further classified as brush-evoked (dynamic), pressure-evoked (static), and punctate hyperalgesias. The neuroma, a swelling at the proximal end of the injured nerve which contains regenerative axon sprouts, commonly exhibits exquisite mechanical sensitivity because of altered membrane properties of both C and A fibre axons.
  • Neuropathic pain is currently classified on the basis of the etiology of the insult to the nervous system or the anatomical distribution of the pain. No pain mechanism is an inevitable consequence of a particular disease process; only a few patients are affected and there are no predictors to indicate which patient will develop neuropathic pain.
  • A small but significant number of patients (up to 5%) who have undergone radical mastectomy develop pain in the posterior arm, axilla, and anterior chest wall because of damage to the intercostobrachial nerve, the lateral cutaneous branch of T2, and other upper thoracic nerves. The pain which usually develop 1-2 months after operation is tight, constricting, and burning in nature. It is often associated with hyperesthesia making wearing of bra uncomfortable. The pain is exacerbated by arm movement; pts often posture the arm in a flexed position close to the chest wall, and thus incur a high risk of developing a frozen shoulder.
  • ESCC develops from metastasis to one or more vertebral bodies, with spread into the spinal canal consequent encroachment on the spinal cord, or is a result of tumor extension thru the intervertebral foramina. ESCC is a common cause of dull, aching back pain and tenderness in the affected vertebra, and is often associated with radicular pain and later with neurologic signs. Compression fractures occur with weakened bones causing impingement of the spinal cord or nerve roots. This presents as acute severe pain with neurologic deficits.
  • Infiltration, compression or damage of brachial plexus by tumor presents with more severe, dull, aching pain which is first located in the shoulder and arm and vertebral border of scapula and later extends to medial part of arm, elbow forearm and hand. In direct tumor expansion, the C7-T1 distribution is affected first. There may be Horner’s syndrome. It could also occur as a result of radiation fibrosis post treatment. It occurs 6-12 months after. The roots C5-C6 are affected first presenting as numbness and paresthesia.
  • PSYCHOGENIC PAIN is pain in one or more sites that is the predominant focus of clinical attention, which is not fully accounted for by a nonpsychiatric medical or neurological condition. It is associated with emotional distress and functional impairment.
  • Untreated pain has several adverse effects. Illustrated in the following tables are the systems affected, the mechanisms of effect and clinical effects of pain. Respiratory effects include increased muscle tension and decreased lung compliance leading to hypoxemia, hypercapnia, perfusion problems, and atelectasis. Endocrine-wise, increased ACTH/epinephrine and decreased insulin concentrations result to protein catabolism, and hyperglycemia. Uncontrolled pain causes increased myocardial work which may lead to arrhythmias, angina, myocardial infarction ,or CHF.
  • Pain could lead to decreased immune cell production and function, urinary retention, and ileus. All of these could result to delayed recovery as well as increased morbidity and mortality.
  • Aside from physiological effects, pain has psychological effects. Uncontrolled pain causes anxiety, depression, anger, and sleeplessness, all perpetuating each other in a viscious cycle.
  • Effective pain management’s advantages include increased patient comfort and satisfaction, earlier mobilization, reduced number of hospital days and decreased costs.
  • The Joint Commission on Accreditation of Healthcare Organizations in 1999 advocated these rights of the patients: Patients have the right to appropriate assessment and management of pain, the patient’s right to pain management is respected and supported, and patients are involved in all aspects of their care, including pain management.
  • What are the keys to proper pain management? Assessment and education.
  • In 1998, the American Pain Society advocated pain assessment to be the 5th vital sign. Along with the other vital signs, pain should be assessed regularly and accurately.
  • Each of us has a different perception of pain. Pain is subjective and may be influenced by: age, gender, culture, communication/language skills, and previous experience.
  • Pain has several components that could be measured for us to have an objective way of assessing pain. Acute pain has been known to change physiologic parameters like blood pressure, heart rate, palmar sweating, and Spo2. Physiologic parameters however has been shown to have no discriminant power to detect analgesic demand during the postoperative period. Pain causes behavioral changes like crying, kicking and thrashing, or just being more still and quiet. As such behavioral scales have been developed.
  • Among the pain assessment tools developed, the self-report scales are still the gold standard.
  • The categorical scale probably is the simplest to use. It could be translated into the vernacular as
    No pain “walang kirot” Mild pain“konting kirot” Moderate pain“katamtamang kirot”
    Severe pain “malubhang kirot”
  • The visual analog scale or VAS makes use of a 10 cm line with one end denoting no pain and the other extreme as pain as bad as it could possibly be. Patients are asked to point where their pain level is, then the evaluator will measure using a ruler.
  • The Numeric Pain Intensity Scale makes use of a line numbered 0-10 with 5 being moderate pain.
  • The Wong-Baker FACES Scale uses a range of faces from smiling to crying to denote pain intensity.
  • Faces Pain Scale – Revised is another tool using cartoon images to denote pain.
  • OUCHER (African American version) scale makes use of real pictures.
  • The FLACC Behavioral Scale is one of the behavioral scales now being used around the world. This scale makes use of parameters that are found to consistently change with changing pain intensity. FLACC is an acronym for Face, Legs, Activity, Crying and Consolability for easy recall. The observer rates the child from 0 to 2 for each parameter for a lowest score of 0 and a highest score of 10. This scale is used for children less than 5 years or those who cant self-report their pain yet.
  • In taking the pain history, we could use the mnemonic: OLD CART :
    O – onset
    L – location
    D – description/duration
    C - contributing factors
    A – aggravating factors
    R – relieving factors
    T – therapies tried
  • The WHO advocated the use of a step-ladder approach to pain management. Step 1 for mild pain uses NSAIDs. Step 2 for moderate pain uses weak opioids in addition to NSAIDs. Step 3 fro severe pain makes use of strong opioids in adiotion to NSAIDs. All steps may employ the addition of adjuvant drugs. This treatment strategy should be the standard against which all other treatments for pain in patients with cancer are tested.
  • WHO recommends taking medications By the mouth By the clock By the ladder For the individual
    With attention to details
  • Multimodal analgesia combines two or more drugs to address the pain. In this way, there is reduced doses of each analgesic, improved antinociception due to synergistic/additive effects, and reduced severity of side effects of each drug.
  • NSAIDs decrease levels of inflammatory mediators generated at the site of tissue injury by inhibiting the enzyme cyclooxygenase, which catalyzes the conversion of arachidonic acid to prostaglandins and leukotrienes.
    NSAIDs have a ceiling effect on their analgesic potential
    Antipyretic and anti-inflammatory effect
  • The following are the common non- opioids in use with their dosages.
    Acetaminophen/Paracetamol 650 mg q4H or
    Aspirin 650 mg q4H or
    Ketorolac 30 mg PO/IV q6-8H or
    Ketoprofen 100 mg PO/IV q8-q12H or
    Ibuprofen 400-800 mg q6-q8H or
    Naproxen 250-500 mg q12H or
  • The newer COX-2 specific inhibitors include:
    Meloxicam* 7.5-15 mg OD or
    Nimesulide * 100-200 mg BID or
    Valdecoxib* 40 mg PO/IV OD-BID or
    Etoricoxib* 90 mg BID or 120 mg OD or
    Celecoxib* 200 mg BID
  • Opioids exert analgesia by binding to specific receptors both within and outside the CNS. Morphine is the most commonly used opioid for moderate to severe pain. Other opioids include tramadol, oxycodone and fentanyl in different preparations.
  • Weak opioids include tramadol and codeine. Tramadol comes in several preparations as below.
    Tramadol 50-100 mg immediate release tablet/capsules q4-6H
    Tramadol 100, 150, and 200 mg sustained release tablet form q8-12H
    Tramadol 50-100 mg IV q4-8H
    Note: Maximum daily dose: 600 mg
  • The table shows the strong opioids with their equi-analgesic doses. Pure agonists include morphine, pethidine, oxycodone
    and fentanyl. Mixed agonist antagonist include nalbuphine and butorphanol.
  • Adjuvant Drugs include Tricyclic antidepressants, Anticonvulsants, Corticosteroids, and Local anesthetics.
  • Interventional Techniques include Epidural and intrathecal drug delivery systems , Neural Blockade, and Cordotomy among others.
  • Radiotherapy is most effective for painful bone metastases. Radioactive strontium should be considered for the management of pain due to widespread bone metastases from prostatic carcinoma.
  • Aside from pharmacologic treatment, Nonpharmacologic Treatment are equally essential. These include Cognitive-Behavioral therpies like
    Preparatory information
  • Application of Physical Agents
    Application of superficial heat and cold
    Immobilization (eg, to provide rest and maintain alignment after musculoskeletal procedures)
  • Electroanalgesia (eg, TENS)
    Chiropractic techniques
  • Lu v overview of pain

    1. 1. OverviewOverview of Painof Pain
    2. 2. ObjectivesObjectives  Define pain.Define pain.  Discuss the differencesDiscuss the differences between acute and chronicbetween acute and chronic pain.pain.  Classify pain based onClassify pain based on pathophysiologicpathophysiologic mechanisms.mechanisms.
    3. 3. ObjectivesObjectives  Identify pain measurementIdentify pain measurement scales/tools.scales/tools.  Discuss therapeutic options.Discuss therapeutic options.
    4. 4. CASE 1. Patient is a 44yo/M, no comorbidities, coming with a chief complaint of right upper quadrant pain. Pt was diagnosed with calculous cholecystitis and underwent elective open cholecystectomy under general anesthesia. At the recovery room, patient complained of pain during inspiration. Pain was localized to the surgical site and described as sharp and tender on palpation.
    5. 5. ASSESSMENT: What is your assessment What are your differentials Is the pain acute or chronic?
    6. 6. What are your treatmentWhat are your treatment options?options?  Opioids?Opioids?  NSAIDs?NSAIDs?  Adjuvant analgesia?Adjuvant analgesia?  Regional Analgesia?Regional Analgesia?
    7. 7. CASE 2. Patient is a 50 yo/F, with a 10 yr history of mandibular pain described as burning, shooting and intermittent pain VAS of 9-10 seeks consult for this symptom. The patient was subjected to multiple dental extractions with no relief of symptoms. Patient was then referred to the pain service.
    8. 8. ASSESSMENT: What type of pain is the patient feeling? Differentiate the character of somatic, visceral and neuropathic pain? Is this acute or chronic in character?
    9. 9. Treatment Options?Treatment Options?  Opioids?Opioids?  NSAIDs?NSAIDs?  Adjuvants?Adjuvants?  What is the role of Gabapentinoids?What is the role of Gabapentinoids? Tricyclic antidepressants?Tricyclic antidepressants? Anticonvulsants?Anticonvulsants?
    10. 10. CASE 3. Patient is a 55 year old female diagnosed with stage 4 breast cancer, who came in for generalized weakness with low back pain radiating to the back of thigh. The pain was further characterized as lightning like with deep , gnawing pains on both upper flanks. Intake of around–the-clock tramadol with paracetamol afforded partial relief. Her pain score remains 5/10 with a feeling of doom.
    11. 11. ASSESSMENT: What type of pain is the patient experiencing ? Acute or chronic? Somatic, visceral or neuropathic? TREATMENT: Describe the WHO stepladder approach to pain control.
    12. 12. What is Pain?What is Pain?  EtymologicallyEtymologically – Greek –Greek – “poine”“poine” – LatinLatin – “poena”– “poena” ** Words suggesting punishment and theWords suggesting punishment and the consequent effect thereofconsequent effect thereof
    13. 13. What is Pain?What is Pain?  As used todayAs used today – Greek –Greek – “algos”“algos” – Latin –Latin – “dolor”“dolor” – Italia –Italia – “dolore”“dolore” – French –French – “douleur”“douleur”
    14. 14. What is Pain?What is Pain?  From the dictionaryFrom the dictionary – Suffering or loss inflicted for an offenseSuffering or loss inflicted for an offense – A primary condition of sensation orA primary condition of sensation or consciousness, the opposite of pleasureconsciousness, the opposite of pleasure – The sensation that one feels when hurtThe sensation that one feels when hurt (in body or mind)(in body or mind)
    15. 15. What is Pain?What is Pain?  From the dictionaryFrom the dictionary – The bodily suffering or distressing sensationThe bodily suffering or distressing sensation of soreness in a particular part of the bodyof soreness in a particular part of the body (physical)(physical) – Mental suffering, trouble, grief, or sorrowMental suffering, trouble, grief, or sorrow (psychological)(psychological)
    16. 16. What is Pain?What is Pain? ““Pain is an unpleasantPain is an unpleasant sensory andsensory and emotionalemotional experience associated withexperience associated with actual or potential tissue damage oractual or potential tissue damage or described in terms of such damage.”described in terms of such damage.” International Association for the Study of Pain, 1979
    17. 17. ACUTE PAINACUTE PAIN  the normal, predictedthe normal, predicted physiologicalphysiological response to anresponse to an adverse chemical, thermal oradverse chemical, thermal or mechanical stimulusmechanical stimulus associated with surgery,associated with surgery, trauma and acute illnesstrauma and acute illness
    18. 18. ACUTE PAINACUTE PAIN  Pain acts as a warningPain acts as a warning of potential damageof potential damage
    19. 19. ACUTE PAINACUTE PAIN  Pain is well localizedPain is well localized  Pain is transientPain is transient Features:Features: • intact nervous systemintact nervous system • increased autonomic responseincreased autonomic response
    20. 20. ACUTE PAINACUTE PAIN  PainPain (A delta and C fibers)(A delta and C fibers) can becan be differentiated from touchdifferentiated from touch (A beta fibers)(A beta fibers)
    21. 21. CHRONIC PAINCHRONIC PAIN  Pain that persistsPain that persists beyond expectedbeyond expected healing periodshealing periods  no clearly identifiableno clearly identifiable causecause
    22. 22. CHRONIC PAINCHRONIC PAIN  Clinical painClinical pain (pain is disease itself)(pain is disease itself)  Depression/anxiety  Vegetative signs
    23. 23. CHRONIC PAINCHRONIC PAIN • Pain can be elicited by A delta, C fibersPain can be elicited by A delta, C fibers andand A beta fibersA beta fibers
    24. 24.  No definite timeNo definite time  It’s aIt’s a spectrumspectrum of eventsof events When does acute painWhen does acute pain become chronic pain?become chronic pain?
    25. 25. NeuroplasticityNeuroplasticity  Morphological changes in cellular levelMorphological changes in cellular level  Altered gene expressionAltered gene expression  Functional changesFunctional changes –– rewiring, sympatheticrewiring, sympathetic involvementinvolvement  Structural changes:Structural changes: “sprouting”“sprouting”  AA ββ fiber (allodynia)fiber (allodynia)  Altered modulation -Altered modulation - ↓↓ inhibitoryinhibitory -- ↑↑ excitatoryexcitatory  Altered pain perception/interpretation inAltered pain perception/interpretation in sensory cortex, limbic systemsensory cortex, limbic system
    26. 26. SOMATIC PAINSOMATIC PAIN  Pain from primary afferentPain from primary afferent nerves in somatic tissuesnerves in somatic tissues (skin, muscle, bone,(skin, muscle, bone, connective tissues)connective tissues)  Involves A deltaInvolves A delta (fast pain)(fast pain) and C fibersand C fibers (slow pain)(slow pain)  May be acute or chronicMay be acute or chronic
    27. 27. SOMATIC PAIN (CUTANEOUS)SOMATIC PAIN (CUTANEOUS)  Pain derived from skin,Pain derived from skin, subcutaneous tissue, andsubcutaneous tissue, and mucous membranemucous membrane  Localized, sharp, pricking,Localized, sharp, pricking, burning, throbbing,burning, throbbing, stabbingstabbing  Follows dermatomesFollows dermatomes
    28. 28. SOMATIC PAIN (DEEP)SOMATIC PAIN (DEEP)  Pain derived fromPain derived from muscles, tendons, joints,muscles, tendons, joints, and bonesand bones  Less localized,Less localized, sharp/dull, achingsharp/dull, aching  Follows myotomes andFollows myotomes and sclerotomessclerotomes
    29. 29. VISCERAL PAINVISCERAL PAIN  Pain from afferent nerves inPain from afferent nerves in thoracic, abdominal, and pelvicthoracic, abdominal, and pelvic visceraviscera  Involves sympathetic andInvolves sympathetic and parasympathetic afferent fibersparasympathetic afferent fibers  May be acute, chronic, orMay be acute, chronic, or recurrentrecurrent
    30. 30. VISCERAL PAIN (TRUE)VISCERAL PAIN (TRUE)  MidlineMidline  Occurs early in the diseaseOccurs early in the disease  Vague, poorly localized,Vague, poorly localized, dull, achingdull, aching  Marked autonomicMarked autonomic phenomenaphenomena
    31. 31. VISCERAL PAINVISCERAL PAIN (REFERRED)(REFERRED) ViscerotomesViscerotomes
    32. 32. VISCERAL PAINVISCERAL PAIN (REFERRED)(REFERRED) Viscero-somatic convergenceViscero-somatic convergence
    33. 33. VISCERAL PAINVISCERAL PAIN (PARIETAL)(PARIETAL)  Pleura or peritoneumPleura or peritoneum  Localized, sharp,Localized, sharp, stabbing, lancinatingstabbing, lancinating  Hyperalgesia,Hyperalgesia,  skeletal muscle spasmskeletal muscle spasm  sympatheticsympathetic hyperactivityhyperactivity
    34. 34. NEUROPATHIC PAINNEUROPATHIC PAIN  Pain from aberrantPain from aberrant somatosensory processingsomatosensory processing in the peripheral or centralin the peripheral or central nervous systemnervous system  Related to nerve injuryRelated to nerve injury
    35. 35. NEUROPATHIC PAINNEUROPATHIC PAIN  Dysesthesia:Dysesthesia: abnormal pain complaintabnormal pain complaint – Burning, shooting, shock-like, lancinating,Burning, shooting, shock-like, lancinating, numbing, heavynumbing, heavy  Allodynia:Allodynia: pain from a stimulus that does notpain from a stimulus that does not normally evoke painnormally evoke pain  Hyperalgesia:Hyperalgesia: an increased response to aan increased response to a stimulus that is normally painfulstimulus that is normally painful
    36. 36. Neuropathic pain Predominantly “central” pain generator Predominantly “peripheral” pain generator Deafferentation pain Sympathetically- maintained pain Mononeuropathies Lancinating neuralgias Nerve compression or inflammation Nerve transection Polyneuropathies
    37. 37. NEUROPATHIC PAINNEUROPATHIC PAIN Post-mastectomy Pain SyndromePost-mastectomy Pain Syndrome
    38. 38. NEUROPATHIC PAINNEUROPATHIC PAIN Epidural Spinal Cord CompressionEpidural Spinal Cord Compression metastasis
    39. 39. NEUROPATHIC PAINNEUROPATHIC PAIN Brachial PlexopathyBrachial Plexopathy
    40. 40. PSYCHOGENIC PAINPSYCHOGENIC PAIN  Pain in one or more sites that is thePain in one or more sites that is the predominant focus of clinical attention,predominant focus of clinical attention, which is notwhich is not fullyfully accounted for by aaccounted for by a nonpsychiatric medical or neurologicalnonpsychiatric medical or neurological conditioncondition  Associated with emotional distress andAssociated with emotional distress and functional impairmentfunctional impairment
    41. 41. SystemSystem AffectedAffected Mechanism ofMechanism of EffectEffect Clinical EffectClinical Effect RespiratoryRespiratory Increased muscle tensionIncreased muscle tension Decreased lung complianceDecreased lung compliance Hypoxemia, hypercapnia,Hypoxemia, hypercapnia, perfusion problems,perfusion problems, atelectasisatelectasis EndocrineEndocrine Increased ACTH/epinephrineIncreased ACTH/epinephrine Decreased insulinDecreased insulin concentrationsconcentrations Protein catabolism,Protein catabolism, hyperglycemiahyperglycemia CardiovascularCardiovascular Increased myocardial workIncreased myocardial work Arrhythmias, angina,Arrhythmias, angina, myocardial infarction, CHFmyocardial infarction, CHF Physiologic Effects of PainPhysiologic Effects of Pain
    42. 42. SystemSystem AffectedAffected Mechanism ofMechanism of EffectEffect Clinical EffectClinical Effect ImmunologicalImmunological Depression of immune cellDepression of immune cell productionproduction Decreased immune functionDecreased immune function GenitourinaryGenitourinary Increased sphincterIncreased sphincter tone/decreased muscle tonetone/decreased muscle tone Urinary retentionUrinary retention GastrointestinalGastrointestinal Increased sphincterIncreased sphincter tone/decreased muscle tonetone/decreased muscle tone IleusIleus Physiologic Effects of PainPhysiologic Effects of Pain
    44. 44. Advantages of EffectiveAdvantages of Effective Pain ManagementPain Management  Patient comfort andPatient comfort and satisfactionsatisfaction1,2,31,2,3  Earlier mobilizationEarlier mobilization44  ↓↓ hospital stayhospital stay3,43,4  ↓↓ costscosts44 1. Eisenach JC, et al. Anesthesiology. 1988;68:444–448. 2. Harrison DM, et al. Anesthesiology. 1988;68:454–457. 3. Miaskowski C, et al. Pain. 1999;80:23–29. 4. Finley RJ, et al. Pain. 1984;2:S397.
    45. 45. JCAHO Revised Standards:JCAHO Revised Standards: The Patient’s RightsThe Patient’s Rights  Patients have the right to appropriatePatients have the right to appropriate assessment and management of pain.assessment and management of pain.  The patient’s right to pain management isThe patient’s right to pain management is respected and supported.respected and supported.  Patients are involved in all aspects of theirPatients are involved in all aspects of their care, including pain, including pain management. Joint Commission on Accreditation of Healthcare Organizations. 1999
    46. 46. Assessment andAssessment and EducationEducation Are the Keys to ProperAre the Keys to Proper Pain ManagementPain Management
    47. 47. Pain: ThePain: The 5th5th Vital SignVital Sign 1.1. TemperatureTemperature 2.2. Blood PressureBlood Pressure 3.3. PulsePulse 4.4. Respiratory RateRespiratory Rate American Pain Society. 1998 5. Pain Assessment5. Pain Assessment
    48. 48. Patient’s Perception of PainPatient’s Perception of Pain Pain is subjective and may bePain is subjective and may be influenced by:influenced by:  AgeAge  GenderGender  CultureCulture  Communication/languageCommunication/language skillsskills  Previous experiencePrevious experience
    49. 49.   ComponentsComponents MeasurementMeasurement 1. Physiologic Physiologic1. Physiologic Physiologic techniquestechniques 2. Behavioral2. Behavioral BehavioralBehavioral observationobservation 3. Cognitive3. Cognitive Self-reportSelf-report PAINPAIN
    50. 50. SELF-REPORT SCALESSELF-REPORT SCALES ““GOLD STANDARD”GOLD STANDARD” Manne et al Pain 1992Manne et al Pain 1992 McGrath et al Pain 1996McGrath et al Pain 1996 Chambers et al Pain 1999Chambers et al Pain 1999 Soetenga et al Pediatric Nursing 1999Soetenga et al Pediatric Nursing 1999 Voepel-Lewis et al Anesthesia and Analgesia 2002Voepel-Lewis et al Anesthesia and Analgesia 2002 Willis et al Pediatric Nursing 2003Willis et al Pediatric Nursing 2003
    51. 51. Categorical ScaleCategorical Scale  No painNo pain “walang kirot”“walang kirot”  Mild painMild pain “konting kirot”“konting kirot”  Moderate painModerate pain “katamtamang kirot”“katamtamang kirot”  Severe painSevere pain “malubhang kirot”“malubhang kirot”
    52. 52. Visual Analogue Scale (VAS)Visual Analogue Scale (VAS)
    53. 53. Numeric Pain Intensity ScaleNumeric Pain Intensity Scale
    54. 54. Wong-Baker FACES ScaleWong-Baker FACES Scale
    55. 55. Faces Pain Scale - RevisedFaces Pain Scale - Revised 0 2 4 6 8 10
    56. 56. OUCHER (African American version)OUCHER (African American version)
    57. 57. FLACC Behavioral ScaleFLACC Behavioral Scale PARAMETERPARAMETER 00 11 22 FACEFACE no particularno particular expression or smileexpression or smile occasional grimaceoccasional grimace or frown;or frown; disinteresteddisinterested frequent to constantfrequent to constant quivering chin;quivering chin; clenched jawclenched jaw LEGSLEGS normal position ornormal position or relaxedrelaxed uneasy; restless;uneasy; restless; tensetense kicking or legskicking or legs drawn updrawn up ACTIVITYACTIVITY lying quietly; normallying quietly; normal position; movesposition; moves easilyeasily squirming; shiftingsquirming; shifting back and forth;back and forth; tensetense arched; rigid orarched; rigid or jerkingjerking CRYCRY no cryno cry (awake or asleep)(awake or asleep) moans or whimpers;moans or whimpers; occasionaloccasional complaintscomplaints crying steadily;crying steadily; screams or sobs;screams or sobs; frequent complaintsfrequent complaints CONSOLABILITYCONSOLABILITY content, relaxedcontent, relaxed reassured byreassured by occasional touchingoccasional touching hugging or beinghugging or being talked to;talked to; distractabledistractable difficult to console ordifficult to console or comfortcomfort
    58. 58. Taking the Pain HistoryTaking the Pain History OLD CART :OLD CART : O – onsetO – onset L – locationL – location D – durationD – duration C - characteristicC - characteristic A – aggravating factorsA – aggravating factors R – relieving factorsR – relieving factors T – therapies triedT – therapies tried
    59. 59. WHO Analgesic LadderWHO Analgesic Ladder 1 2 3 Freedom from cancer pain Opioid for moderate to severe pain ± Non-opioid ± Adjuvant Opioid for mild to moderate pain ± Non-opioid ± Adjuvant Pain persisting or increasing Non-opioid ± Adjuvant Pain persisting or increasing
    60. 60. WHO RecommendationsWHO Recommendations  By the mouthBy the mouth  By the clockBy the clock  By the ladderBy the ladder  For the individualFor the individual  With attention to detailsWith attention to details
    61. 61. Multimodal AnalgesiaMultimodal Analgesia  Reduced doses of eachReduced doses of each analgesicanalgesic  ImprovedImproved antinociceptionantinociception due todue to synergistic/additivesynergistic/additive effectseffects  May reduce severity ofMay reduce severity of side effects of eachside effects of each drugdrug MorphineMorphine NSAIDs,NSAIDs, acetaminophen,acetaminophen, nerve blocksnerve blocks PotentiationPotentiation
    62. 62. Nonsteroidal Anti-Inflammatory DrugsNonsteroidal Anti-Inflammatory Drugs (NSAIDs)(NSAIDs)  Decrease levels of inflammatory mediators byDecrease levels of inflammatory mediators by inhibiting the enzymeinhibiting the enzyme cyclooxygenasecyclooxygenase, which, which catalyzes the conversion of arachidonic acid tocatalyzes the conversion of arachidonic acid to prostaglandins and leukotrienesprostaglandins and leukotrienes  NSAIDs have aNSAIDs have a ceiling effectceiling effect on their analgesicon their analgesic potentialpotential  Antipyretic and anti-inflammatory effectAntipyretic and anti-inflammatory effect
    63. 63. NSAIDsNSAIDs – Acetaminophen/Paracetamol 650 mgAcetaminophen/Paracetamol 650 mg q4H orq4H or – Aspirin 650 mg q4H orAspirin 650 mg q4H or – Ketorolac 30 mg PO/IV q6-8H orKetorolac 30 mg PO/IV q6-8H or – Ketoprofen 100 mg PO/IV q8-q12H orKetoprofen 100 mg PO/IV q8-q12H or – Ibuprofen 400-800 mg q6-q8H orIbuprofen 400-800 mg q6-q8H or – Naproxen 250-500 mg q12H orNaproxen 250-500 mg q12H or
    64. 64. NSAIDsNSAIDs – Meloxicam* 7.5-15 mg OD orMeloxicam* 7.5-15 mg OD or – Nimesulide * 100-200 mg BID orNimesulide * 100-200 mg BID or – Valdecoxib* 40 mg PO/IV OD-BID orValdecoxib* 40 mg PO/IV OD-BID or – Etoricoxib* 90 mg BID or 120 mg OD orEtoricoxib* 90 mg BID or 120 mg OD or – Celecoxib* 200 mg BIDCelecoxib* 200 mg BID *COX-2 specific*COX-2 specific
    65. 65. OpioidsOpioids  analgesia by binding to specific receptorsanalgesia by binding to specific receptors both within and outside the CNSboth within and outside the CNS  morphine, codeine, oxycodone, andmorphine, codeine, oxycodone, and fentanyl, tramadolfentanyl, tramadol  Morphine is the most commonly usedMorphine is the most commonly used opioid for moderate to severe painopioid for moderate to severe pain
    66. 66. Weak OpioidsWeak Opioids – Tramadol 50-100 mg immediate releaseTramadol 50-100 mg immediate release tablet/capsules q4-6Htablet/capsules q4-6H – Tramadol 100, 150, and 200 mgTramadol 100, 150, and 200 mg sustained release tablet form q8-12Hsustained release tablet form q8-12H – Tramadol 50-100 mg IV q4-8HTramadol 50-100 mg IV q4-8H  Note: Maximum daily dose: 600 mgNote: Maximum daily dose: 600 mg
    67. 67. Strong OpioidsStrong Opioids opioidopioid parenteraparentera ll oraloral agonistagonist morphinemorphine 10 mg10 mg 30 mg30 mg pethidinepethidine 100 mg100 mg 300 mg300 mg oxycodoneoxycodone 15 mg15 mg 20-30 mg20-30 mg fentanylfentanyl 100 ug100 ug NANA partialpartial agonistagonist nalbuphinenalbuphine 10 mg10 mg
    68. 68. Adjuvant DrugsAdjuvant Drugs  Tricyclic antidepressantTricyclic antidepressant – ImipramineImipramine 25-50 mg tab at bedtime25-50 mg tab at bedtime  AnticonvulsantsAnticonvulsants – CarbamazepineCarbamazepine 200 mg tab BID200 mg tab BID (max: 1,200 mg/day)(max: 1,200 mg/day) - GabapentinGabapentin 100 mg cap TID100 mg cap TID (max: 3,600 mg/day)(max: 3,600 mg/day)
    69. 69. Adjuvant DrugsAdjuvant Drugs  CorticosteroidsCorticosteroids – DexamethasoneDexamethasone  Local anestheticsLocal anesthetics – Lidocaine patchLidocaine patch  KetamineKetamine – Subanesthetic dosesSubanesthetic doses – N-methyl-d-aspartate (NMDA)N-methyl-d-aspartate (NMDA) receptor blocker in the dorsal hornreceptor blocker in the dorsal horn
    70. 70. Interventional TechniquesInterventional Techniques  Epidural and intrathecal drugEpidural and intrathecal drug delivery systemsdelivery systems  Neural BlockadeNeural Blockade  CordotomyCordotomy
    71. 71. RadiotherapyRadiotherapy  for painful bone metastasesfor painful bone metastases  Radioactive strontiumRadioactive strontium should beshould be considered for the management of painconsidered for the management of pain due to widespread bone metastases fromdue to widespread bone metastases from prostatic carcinoma.prostatic carcinoma.
    72. 72. Nonpharmacologic TreatmentNonpharmacologic Treatment Cognitive-BehavioralCognitive-Behavioral  RelaxationRelaxation  Preparatory informationPreparatory information  ImageryImagery  HypnosisHypnosis  BiofeedbackBiofeedback
    73. 73. Nonpharmacologic TreatmentNonpharmacologic Treatment Physical AgentsPhysical Agents  Application of superficial heat and coldApplication of superficial heat and cold  MassageMassage  ExerciseExercise  Immobilization (eg, to provide rest andImmobilization (eg, to provide rest and maintain alignment after musculoskeletalmaintain alignment after musculoskeletal procedures)procedures)
    74. 74. Nonpharmacologic TreatmentNonpharmacologic Treatment  Electroanalgesia (eg, TENS)Electroanalgesia (eg, TENS)  Chiropractic techniquesChiropractic techniques  AcupunctureAcupuncture
    75. 75. Thank YouThank You