Define pain. Difference between preventive and preemptive analgesia

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Here is a comprehensive summary drawn from the textbooks.

Definition of Pain

The International Association for the Study of Pain (IASP) defines pain as:
"An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage."
This updated definition (revised 2020) highlights several key points:
  • Pain is both a sensory and an emotional experience — it is not purely a physical signal.
  • It can occur with actual tissue damage (e.g., a cut), potential damage (e.g., a threat), or even in the absence of demonstrable tissue damage (e.g., neuropathic or psychogenic pain).
  • It is distinct from nociception, which is the unconscious neural activity induced by a harmful stimulus applied to sensory receptors — pain requires conscious awareness.

Classification of Pain

TypeCharacteristics
Acute (physiologic)Sudden onset; resolves with healing; serves a protective function (e.g., withdrawal reflex)
Chronic (pathologic)Persists beyond recovery; often refractory to NSAIDs and opioids
InflammatoryDue to tissue inflammation (peripheral sensitization)
NeuropathicDue to nerve injury; features burning, shooting, allodynia, hyperalgesia
Ganong's Review of Medical Physiology, 26e; Miller's Anesthesia, 10e; Barash's Clinical Anesthesia, 9e

Preemptive vs. Preventive Analgesia

These two terms are related but conceptually distinct:

Preemptive Analgesia

  • Defined as an analgesic intervention administered before surgical incision that is more effective than the same intervention given after surgery.
  • The rationale was to prevent the establishment of central sensitization caused by the incisional injury, thereby reducing postoperative pain hypersensitivity.
  • Mechanism: Block nociceptive afferent input before it reaches the CNS and triggers wind-up, facilitation, and long-term potentiation in dorsal horn neurons.
  • Clinical reality: Randomized controlled trials have had mixed (largely negative) results. A single pre-incision analgesic block cannot prevent central sensitization because once the block wears off, the ongoing surgical/inflammatory injury re-initiates central sensitization. The term is now considered obsolete.

Preventive Analgesia

  • A broader, more modern concept: includes any antinociceptive regimen delivered at any time during the perioperative period (before, during, or after surgery) that attenuates pain-induced sensitization.
  • Timing is less critical than the intensity and duration of the intervention.
  • The goal is to block NMDA receptor activation in the dorsal horn, preventing:
    • Wind-up
    • Central sensitization
    • Expansion of receptive fields
    • Long-term potentiation → chronic pain

Three Critical Principles for Preventive Analgesia to Succeed

  1. Depth: Analgesia must be adequate to block all nociceptive input during surgery.
  2. Extent: The analgesic technique must cover the entire surgical field.
  3. Duration: Analgesia must span both the surgical and postsurgical (inflammatory) periods — because inflammatory injury continues well into the postoperative period and perpetuates central sensitization.

Key Comparison Table

FeaturePreemptive AnalgesiaPreventive Analgesia
TimingStrictly before incisionAny time in the perioperative period
FocusTiming of interventionIntensity + duration of intervention
Mechanism targetIncisional-phase central sensitizationAll phases of sensitization (incisional + inflammatory)
Clinical evidenceMixed/negative; largely obsoleteSupported; replaces preemptive concept
GoalPrevent initial central sensitizationPrevent sustained/chronic pain development
Miller's Anesthesia, 10e; Barash's Clinical Anesthesia, 9e; Cummings Otolaryngology, 7e

Clinical implication: Because a single pre-incision block is insufficient to prevent postoperative sensitization, multimodal preventive analgesia (combining NSAIDs, opioids, NMDA antagonists such as ketamine, gabapentinoids, and regional/neuraxial techniques) extending into the postoperative inflammatory period is the recommended approach for reducing chronic post-surgical pain.

Causes of low back pain. Management of patient with prolapsed intervertebral disc

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Causes of Low Back Pain

Low back pain (LBP) is one of the most common conditions in clinical practice, affecting 60–80% of the population at some point in their lives. Causes can be classified as follows:

1. Musculoskeletal / Mechanical (Most Common)

CauseFeatures
Muscle/ligament strainAcute onset after injury; paraspinal tenderness, muscle spasm; no neurological signs
Lumbar disc herniation (PIVD)Shooting/stabbing LBP with radiation in dermatomal distribution; positive straight leg raise
Lumbar facet joint syndromeUp to 35% of LBP; pain aggravated by extension and lateral rotation; negative SLR
Sacroiliac (SI) joint syndromeUnilateral LBP radiating to hip/thigh; positive Patrick test; pain with stair climbing
Lumbar spinal stenosisUsually in older adults (>60 years); neurogenic claudication; bilateral leg pain with walking, relieved by flexion
SpondylolisthesisAnterior vertebral displacement; "step-off" on palpation; due to degenerative arthritis or spondylolysis
SpondylolysisBony defect in pars interarticularis; common in young athletes; pain with hyperextension

2. Disc-Related

  • Lumbar disc degeneration (discogenic LBP): degenerative disc disease without frank herniation; axial LBP
  • Prolapsed/herniated disc: nuclear material herniates through annulus fibrosus, compressing nerve roots (most commonly L4–L5 or L5–S1)

3. Degenerative / Arthritis

  • Lumbar spondylosis (osteophyte formation)
  • Facet joint arthropathy
  • Degenerative endplate changes (Modic changes on MRI)

4. Inflammatory

  • Ankylosing spondylitis: morning stiffness, sacroiliac tenderness, young males; HLA-B27 positive
  • Other seronegative spondyloarthropathies

5. Infective

  • Vertebral osteomyelitis / discitis: fever, local tenderness, elevated ESR/CRP; MRI confirms
  • Epidural abscess: pain + fever + neurological signs → surgical emergency

6. Neoplastic

  • Primary vertebral tumors (e.g., myeloma)
  • Metastases (breast, prostate, lung, renal, thyroid): worsening pain in recumbent position, night pain, systemic symptoms
  • Intradural/extramedullary tumors

7. Congenital / Developmental

  • Spina bifida occulta
  • Sacralization / lumbarization of vertebrae
  • Congenital scoliosis
  • Transitional vertebrae / asymmetric facet joints

8. Referred / Visceral Pain

  • Renal stones, pyelonephritis, renal cysts → costovertebral angle tenderness
  • Aortic aneurysm → pulsatile abdominal mass + back pain
  • Retroperitoneal pathology (lymphoma, pancreatic Ca)
  • Pelvic disease in women (endometriosis, PID)
  • Prostate disease in men

9. Vascular

  • Ischemia of lumbar spinal cord
  • Aortic aneurysm (see above)

10. Osteoporotic / Traumatic

  • Vertebral compression fractures (osteoporosis, trauma, malignancy)
  • Transverse process fractures

11. Psychogenic / Functional

  • Chronic LBP without structural pathology
  • Associated with somatization, depression, compensation claims

Red Flags Requiring Urgent Imaging (MRI)

  • Objective neurological deficits (radiculopathy, conus signs, sphincter dysfunction)
  • Pain worsening in recumbent position / at night
  • Pain aggravated by Valsalva maneuver
  • History of cancer
  • Fever + spinal tenderness
  • Post-trauma
  • Progressive pain
Adams & Victor's Principles of Neurology, 12e; Bradley & Daroff's Neurology in Clinical Practice

Management of Prolapsed Intervertebral Disc (PIVD)

Pathophysiology

The nucleus pulposus herniates through a defect in the annulus fibrosus, compressing adjacent nerve roots (most commonly L4–L5 → L5 root, or L5–S1 → S1 root). This produces:
  • L5 root: pain/numbness down dorsomedial foot; weakness of tibialis anterior (foot drop)
  • S1 root: pain/numbness to lateral foot/small toe; weakness of peroneus longus and brevis; absent ankle jerk

Investigations

  • MRI lumbosacral spine: investigation of choice — confirms level, degree of herniation, nerve root compression
  • CT spine: if MRI contraindicated
  • EMG/NCV: may not detect early radiculopathy; useful for chronic or atypical cases
  • X-ray: limited value; screens for structural anomalies, fractures

Conservative Management (First-Line, 6–12 Weeks)

Most patients improve with conservative treatment.
ModalityDetails
RestShort-term relative rest; prolonged bed rest not recommended
NSAIDsFirst-line; reduce disc-related inflammation and pain
Muscle relaxantsFor associated muscle spasm
Physical therapyCore strengthening, postural correction, McKenzie exercises
Massage therapyAdjunct for muscle pain
AcupunctureShown to be effective in some patients
AnalgesicsParacetamol ± weak opioids for breakthrough pain

Interventional / Minimally Invasive

  • Lumbar epidural steroid injections (LESIs): provide fast and effective pain relief when nerve root is not severely mechanically compressed; useful if conservative treatment fails within 6–8 weeks
  • Transforaminal / caudal epidural blocks: targeted root injection at the affected level
  • Medial branch blocks / facet injections: if facet joint involvement coexists

Surgical Management

Indications for surgery:
  1. Absolute (emergency):
    • Cauda equina syndrome: bilateral leg weakness, saddle anaesthesia, bowel/bladder dysfunction → emergency microdiscectomy
  2. Relative (elective):
    • Moderate-to-severe focal neurological deficit (weakness, significant numbness)
    • Severe disabling pain for >3 months not responding to aggressive pain management, with disc herniation confirmed on MRI/CT
Surgical options:
ProcedureDescription
MicrodiscectomyGold standard; minimally invasive removal of herniated nucleus material
Open discectomy (laminectomy/laminotomy)Wider exposure when needed
Endoscopic discectomyMinimally invasive; faster recovery
Spinal fusionFor instability, recurrent disc herniation, or associated spondylolisthesis
Postoperative care: Early mobilisation, physiotherapy, core rehabilitation.

Summary Algorithm

PIVD diagnosed (clinical + MRI)
        |
        ├── Cauda equina syndrome? → EMERGENCY SURGERY
        |
        ├── Severe/progressive neurological deficit? → Early surgery
        |
        └── Otherwise → Conservative (NSAIDs, PT, muscle relaxants) × 6–12 weeks
                            |
                    No improvement?
                            |
                    Epidural steroid injection
                            |
                    Still no improvement + confirmed herniation?
                            |
                    Elective microdiscectomy
Bradley & Daroff's Neurology in Clinical Practice; Adams & Victor's Principles of Neurology, 12e; Barash's Clinical Anesthesia, 9e; Cummings Otolaryngology, 7e
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