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Management of Acute Pain Shada Y. Elhayek M.Sc. Clinical Pharmacy Content • • • • • Introduction Types of pain Management of pain Patient evaluation Monitoring What is Pain? • pain: an unpleasant sensory & emotional experience associated with actual or potential tissue damage or described in terms of such damage Pathophysiology Pain Nociceptive Neuropathic Neuropathic Functional Somatic Visceral Types of Pain • Acute pain: • Acute pain usually is nociceptive, but it can be neuropathic in nature • Common causes of acute pain: surgery, acute illness, trauma, labor, & medical procedures When should acute pain not be treated? • Traumatic head injury because medications can interfere with cognitive function • Acute abdominal pain until diagnosis is made. Although several studies support early pain management • Chronic Pain: • Pain persisting for > 6 months to years • Persistent (chronic) pain serves no biologic protective purpose & can cause undue stress & suffering • Can be nociceptive, neuropathic/ functional, or both Clinical Presentation of Acute Pain • Pain attributes: Clinical Presentation- Acute Pain • General • Obvious distress (e.g., trauma), infants may present with changes in feeding habits, increased fussiness. Those with dementia may exhibit changes in eating habits, increased agitation, calling out. Attention also must be given to mental/emotional factors that alter the pain threshold. Anxiety, depression, fatigue, anger, and fear in particular, are noted to lower this threshold, whereas rest, mood elevation, sympathy, diversion, and understanding raise the pain threshold. • Symptoms • • Can be described as sharp, dull, shock like, tingling, shooting, radiating, fluctuating in intensity, and varying in location (these occur in a timely relationship with an obvious noxious stimuli) • Signs • Hypertension, tachycardia, diaphoresis, mydriasis, and pallor, but these signs are not diagnostic • In some cases there are no obvious physical signs • Comorbid conditions usually not present • Outcome of treatment generally predictable • Laboratory Tests • • Pain is always subjective • • There are no specific laboratory tests for pain • • Pain is best diagnosed based on patient description and history Pharmacological management • Non opioid analgesics: 1. Paracetamol 2. Aspirin 3. NSAIDS Paracetamol • Has analgesic and antipyretic properties, and it is recommended for use in minor pain. • It has comparable effectiveness to aspirin, but it does not have peripheral anti-inflammatory activity or effects on platelet function. • Acetaminophen has fewer GI and renal adverse effects than NSAIDs. • Hepatic toxicity has been associated with acute acetaminophen overdose as well as with usual doses in certain high-risk conditions or situations (e.g., alcohol ingestion, cachexia or malnutrition, and concomitant drugs that induce hepatic enzymes). NSAIDS • Drugs: aspirin, choline salicylate, diflunisal, meclofenamate, mefenamic acid, etodolac, diclofenac, ibuprofen, fenoprofen, ketoprofen, magnesium salicylate, naproxen, ketorolac) and cyclooxygenase-II enzyme selective inhibitors (celecoxib) • Recommended for mild to moderate acute pain. MOA: NSAIDs relieve pain by inhibiting prostaglandin synthesis. • They must be used with caution: 1. in patients who are at risk for GI bleeding (>60 years old, history of a GI event, or taking medications, such as corticosteroids, that may cause bleeding). 2. There is the possibility of increased cardiovascular events in patients taking NSAIDs, and it has been recommended that cyclooxygenase-II enzyme inhibitors only be used when there are no other therapeutic options available, and that their dose and duration of therapy should be limited. Major concerns • • • • • Sodium retention GI ADR CV risk Bronchospasm and allergy Nephrotoxicity Opioids • Morphine is 1st line for moderate to severe pain • Administered oral, parenteral and rectal • Pentazocin and butophanol are mixed agonistantagonists MOA: • Analgesia via inhibiting µ, ĸ, ɛ and δ opioid receptors located in the central transmission and peripheral nervous systems and block the of pain and release of neurotransmitters that may be responsible for transmitting pain • Analgesia results because the perception of pain within the CNS as well as the patient’s emotional response to pain is altered, therefore modifying the sensory and affective response. • Opioid classes include the phenanthrenes (morphinelike), phenylpiperidine (meperidinelike), and diphenylheptane • (methadonelike). ADRs • • • • • Nausea, vomiting & constipation: Urinary retention, sedation, altered mental status Respiratory depression Hypotension. Tolerance to opioid induced side effects can be seen after a few days of administration. If the side effects do not lessen over time, adjunctive drug therapy, such as an antiemetic or stimulant, may need to be initiated. Importantly, tolerance to constipation does not occur and requires the use of routine stimulant laxatives for persons requiring chronic opioid therapy. • True type 1 hypersensitivity (anaphylactic) reactions uncommon after administration of opioid agonists. If this does occur, an opioid from a different chemical class may be prescribed under close medical supervision • The release of histamine resulting in itching (local or diffuse), flushing, or urticaria. If appropriate, a trial of oxymorphone or fentanyl may be an option because they have been associated with less histamine release and therefore less itching and urticaria. Premedication with antihistamines may also be helpful. • Tolerance to the analgesic effects of opioids is a common phenomenon, and its causes are complex and multifactorial. Tolerance is suspected when larger doses of an opioid are required to achieve the same level of analgesia once seen with lower doses. • Physical dependence is commonly observed in patients requiring chronic opioid analgesics and is manifested by signs and symptoms of withdrawal after abrupt discontinuation or rapid dose reduction of the medication.