pain management

• Based on Duration

  •Acute

  •Chronic

  •Acute on Chronic

  Based on nature of pain

  •Nociceptive

  •Neuropathic

  •Mixed

  •Visceral

  •Malignant / Cancer pain
• challenges in acute pain management

  • Variable response to analgesics

  •Older age = more sensitivity to opioids

  •Ethnicity – genetic factors can affect how drugs are metabolized, decreased effectiveness? Or is it a bias? 

  •Psychological issues

  •Type of surgical procedure

  •The use of pre-emptive analgesic techniques

  •Intraoperative anaesthetic techniques:

  •Regional anesthetic procedures vs GA

  •Use of Adjuncts : Ketamine etc..

  •Genetics: gene polymorphism
• Negative effects of inadequate acute pain management include:

  •Increased hospital stay, more frequent readmissions

  •Reduced quality of life (QOL)

  •Impaired physical function

  •Decreased functional recovery

  •Increased complications

  •Impaired sleep
• poorly managed acute pain is a risk factor for chronic pain postoperatively, effectively managing acute pain can reduce the risk of pain progression
• •Chronic pain is persistent or recurrent pain, lasting beyond the usual course of acute illness or injury, or more than 3 - 6 months, and adversely affecting the patient’s well-being
• chronic pain:

  •Difficult to diagnose & treat

  •Subjective personal experience

  •Cannot be measured except by behavior

  •May originate from a physical source but slowly it “out-shouts” and becomes the disease

  •It has no biologic value as a symptom

  •Life permanently disrupted (relentless)
• Acute pain

  •Physiologic response to tissue damage

  •Warning - signals damage/danger

  •Helps locate problem source

  •Has biologic value as a symptom

  •Responds to traditional medical model

  •Life temporarily disrupted (self limiting)
• Quality of Life

  •Physical functioning

  •Ability to perform activities of daily living

  •Work

  •Recreation
• Psychological Morbidity

  •Depression

  •Anxiety, anger

  •Sleep disturbances

  •Loss of self-esteem
• Socioeconomic Consequences

  •Healthcare costs

  •Disability

  •Lost workdays
• Social Consequences

  •Marital/family relations

  •Intimacy/sexual activity

  •Social isolation
• Nociceptive, or inflammatory, pain is pain resulting from activity in neural pathways caused by potentially tissue-damaging stimuli. Examples include postoperative pain, arthritis, mechanical low back pain, sickle cell crisis, and sports or exercise injuries.
• Neuropathic pain is pain caused by a primary lesion or dysfunction in the peripheral and/or central nervous systems.2 Examples of peripheral neuropathic pain syndromes include HIV sensory neuropathy, postherpetic neuralgia (PHN), and diabetic neuropathy. Examples of central neuropathic pain include central poststroke pain, spinal cord injury pain, trigeminal neuralgia, and multiple sclerosis pain.
• mixed type pain - chronic pain can be of mixed etiology with both nociceptive and neuropathic characteristics.
• Two types of neuropathic pain—PHN and diabetic neuropathy—will be emphasized within this module. These types of pain are being stressed because the great majority of randomized controlled trials of treatments for neuropathic pain have examined these two disorders, and because our understanding of the mechanisms of neuropathic pain is largely derived from those studies.
• pathophysiology of neuropathic pain:

  Excitotoxicity - nerve damage, nociceptive input to spinal cord, damage inhibitory cells, disinhibited pain system.

  Sodium channels: damaged nerves, abnormal sodium channels produced result in hyperexcitable nerve.

  Ectopic discharge: damaged nerves produce ectopic / abnormal, nerve impulses that may promote pain perceptions.

  Deafferentation: CNS deprived of normal nerve input (amputation or plexus avulsion) pain may result. (Classically severe pain in an insensate or absent limb)
• pathophysiology of neuropathic pain (2)

  • Central sensitization: repeated sensory input, CNS becomes hyperresponsive to peripheral input 'facilitated state' due to long-term changes in anatomy or physiology of the CNS by pain.
• peripheral nerve injury causes:

  1. Sensitization by spontaneous activity by neurons, lowered threshold for activation, increased response to given stimulus
  2. Formation of ectopic neuronal pacemakers along nerve and increased expression of sodium channels and voltage gated calcium channels.

  3. Adjacent demyelinated axons can have abnormal electrical connections channels and increased neuronal excitability.
• CENTRAL MECHANISMS: Sustained painful stimuli results in spinal sensitization (neurons within dorsal horn)

  1. Increased spontaneous activity of dorsal horn neurons, reduced activation thresholds, enhanced responsiveness to synaptic inputs.
  2. Expansion of receptive fields, death of inhibitory interneurons (intrinsic modulatory systems).
  3. Central sensitization mediated by NMDA receptors that further release excitatory amino acids and neuropeptides.
  4. Sprouting of sympathetic efferents into neuromas and dorsal root and ganglion cells.
• multimodal therapy

  •Synchronous administration of ≥ 2 pharmacological agents or approaches, each with a distinct mechanism of action

  Key Recommendation:

     Whenever possible, clinicians should use multimodal pain management therapy.
• MULTIMODAL THERAPY:

  Rationale:

  •Targeting of different pathways

  •Synergism of multiple agents

  •Allows dose reduction of individual agents, reducing the risk for adverse effects
• KETAMINE

  •Action: NMDA receptor antagonist

  •‘anti-hyperalgesic', 'anti-allodynic' and 'tolerance-protective' agent

  •Indication: Protective analgesia, NP treatment, opioid-tolerant patients

  •SE: Dysphoria, nightmares, “psychedelic” effects
• intervention of pain management:

  • Epidural or Perineural injections of local anesthetics/steroids – Precision (USG)

  • Sympathetic nerve blocks

  • Neural ablative procedures (RF/Rhizotomy)

  • Peripheral Neural Stimulation - PENS

  • Spinal cord stimulation (PNFS/DRG)

  • Implantation of intrathecal drug delivery systems.
• NONPHARMACOLOGICAL OPTIONS:

  • Biofeedback

  • Relaxation therapy

  • Physical and occupational therapy

  • Cognitive/behavioral strategies

  • meditation; guided imagery

  • Acupuncture

  • Transcutaneous electrical nerve stimulation
• nonopioid systemic analgesics include:

  paracetamol (few AEs), NSAIDs (improve pain score but have associated risks), gabapentioids (gabapentin and pregabalin).
• systemic opioids: provide pain relief, pain and tissue damage if injected, may have adverse reactions
• Central Regional Analgesia includes opioids intrathecally or epidurally

  Peripheral Regional Analgesia includes peripheral nerve blocks, intra-articular blocks and the infiltration of incisions