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Chapter 45. Pain Management

Bridget Fowler Scullion; Laurajo Ryan

  • Pain is a warning mechanism; tissue damage causes release of prostaglandins & other substances that send signals via peripheral nerves (nociceptors) to dorsal horn of spinal cord; from spinal cord, neurotransmitters transmit pain signals to spinothalamic tract & thalamus which process the pain signal in the brain; neurotransmitters (NE, 5HT) & endogenous opioids in brain & spinal cord modulate pain signal

  • Signs/symptoms → physical signs associated with acute pain (↑ HR, BP, diaphoresis) may be absent in those with chronic pain
    • Nociceptive pain: somatic pain & visceral pain
      • Somatic pain → injury to bones, joints, muscle, skin connective tissue; often described as dull, throbbing, aching; localized
      • Visceral pain → internal organs; GI tract, liver, stomach, pancreas; described as deep, cramping, sharp, stabbing; usually diffuse
    • Neuropathic pain: damage to peripheral or central nerves vs noxious stimuli; often described as burning, tingling
    • Pain Assessment
      • Effective pain relief requires a thorough pain assessment; a pain rating scale such as 0–10 describes intensity only—numerous acronyms available to identify elements of pain assessment

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Clinical Pearl 45-1

PAINED

  • Place: where is the pain?
  • Amount: present & past intensity of pain, worst? best? how often? constant? intermittent? when did it begin? (use numeric, verbal & visual analog scales depending on patient ability)
  • Intensifiers: what makes pain worse?
  • Nullifiers: what makes pain better? What pharmacological & non-pharmacological approaches (including complementary/alternative therapies) have been used? effective?
  • Effects: side effects from past/present therapies? quality of life: physical, psychological & social function?
  • Descriptors: what does it feel like? sharp, stabbing, burning, shooting, dull, aching, throbbing, crampy…?

  • Drug selection & dosing
    • Complete thorough pain assessment & determine etiology of pain → diagnosis should guide drug selection; World Health Organization (WHO) analgesic ladder helps determine approach
    • Individualize regimen → easier to prevent pain than relieve pain; keep dosing schedules simple & use least invasive therapy possible → PO preferred for convenience & cost-effectiveness; avoid IM administration → painful, erratic absorption; use scheduled doses vs PRN for persistent pain
    • Drug selection considerations → pain type & diagnosis, past medication use, age, organ function, & drug-specific factors (ex. PK, metabolism route, dose form)
    • Nonopioids indicated in mild-to-moderate somatic & visceral pain
      • APAP has ↓ AE, drug interactions & contraindications vs NSAIDs → considered 1st line; use may be limited by lack of anti-inflammatory effects
      • NSAIDs best for somatic or inflammatory pain; continue if/when opioids added → may be limited by hematologic, GI, CV, renal toxicity
    • Opioids indicated for moderate-to-severe acute & chronic pain → no max pharmacologic dose; dose often limited by side effects & individual patient response; combination opioids limited by max dose of nonopioid ingredient; may limit appropriate dose titration
      • Use round the clock long-acting or continuous infusion dosing for persistent pain; initiate 75% of prior 24h use & continue PRN dosing for breakthrough pain (BTP); adjust based on PRN use
        • BTP dose selection based on ...

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