Treating Low Back Pain

1. Treating Low Back Pain • Carmen P. Pichard-Encina, MD • Assistant Professor • Johns Hopkins Orthopaedic Surgery at • Good Samaritan Hospital • September 12, 2012

2. Disclosures • Nothing to disclose at this time.

3. Outline • Anatomy of the lumbar spine • Sources of low back pain • Evaluation of the lower back • Treatment Options

4. Anatomy • The lumbar region or lower back, consists of five vertebrae labeled L1 to L5. • This is the main weight-bearing section of the spinal column.

5. Anatomy • Vertebral bodies • Provide structural support. • Separated by intervertebral discs.

6. Anatomy • Pedicles • On either side of the vertebral canal, they connect the vertebral body to the lamina.

7. Anatomy • Lamina • The lamina creates an outer wall, which protects the spinal cord posteriorly. • The lamina ends at the transverse process. Transverse processes are the sites of attachment for ligaments and muscles.

8. Anatomy • Facet joints • The articular facets form the joints connecting each vertebrae with the vertebrae above and below (so that each vertebrae has four facets, two superior and two inferior). • The facet joints, like other mobile joints in the body, are covered with cartilage.

9. Anatomy • Spinal Cord • The spinal cord is the main bundle of nerve fibers connecting the brain to the rest of the body. • The spinal cord ends near the L1 and L2 vertebrae, where it divides into bundles of nerve roots called the cauda equina.

10. Anatomy • Nerve roots • Exiting from the spinal cord are nerve roots. • Nerve roots transmit signals between the spinal cord and the other parts of the body.

11. Anatomy • Each nerve root has a specific distribution • motor • sensory • reflex (patellar- L4, Achilles-S1)

12. Anatomy • Intervertebral disc • They provide a tough but flexible cushion for the vertebrae. • They allow movement. • They have a soft interior called the nucleus pulposus and an outer wall called the annulus fibrosus.

13. Sources of low back pain (LBP) • Degenerative Changes • Sprains and strain of muscles • Fractures • Infection • Tumor

14. Sources of LBP • Sprain or strain • Usually poor lifting technique, specific trigger event • Acute episode (less than 6 weeks) • 50% resolve by 2 weeks (NASS) • 80% resolve by 8 weeks.

15. Sources of LBP • Fractures • Osteoporosis • Chronic steroid use • Low energy trauma in elderly • Car accidents • Falls from heights

16. Compression fracture risk • 2 or more previous osteoporotic compression fractures (future fracture risk increased by 12 fold) • 2 SD decrease in BMD (4-6 fold) • Positive family history (2.7 fold) • Premature menopause (1.6 fold) • Smoking (1.2 fold)

17. Sources of LBP • Infection • Drug abuse • Diabetes • Recent spine surgery • Pain + constitutional symptoms. Bacteria has hyaluronase enzyme

18. Sources of LBP • Infection • Osteodiscitis (Usually nonop) • Only 50% have a fever. • ESR/CRP elevated in more than 90% but not specific • WBC only elevated in 42% • Blood cultures positive in 24% • XR lag behind up to 2-8 weeks. • MRI with gadolinium gold standard

19. Sources of LBP • Infection • Epidural abscess • Hematogenous or direct inoculation • Patients usually more systemically ill than osteodiscitis • Usually posterior • Surgical management usually necessary

20. Sources of LBP • Tumor • History of cancer • Weight loss • Night pain

21. Sources of LBP • Degenerative changes • 95% of the population will have degenerative changes of the spine by age 50.

22. By age 50ext

23. To image or not to image? • LBP does NOT correlate with radiographic evidence of low back DDD. • With no red flags can usually be deferred 6 weeks.

24. To image or not to image? • False positive rate of MRI is very high: • 35% of patients less than 40yo. • 93% of patients more than 60yo. MRI is effective when used as a confirmatory study only

25. Risk factors for LBP • 30-50 years old • Male • Job occupation • Lower income • Cigarette smoking (vasoconstriction, pain receptors) • Prolonged exposure to vibrations (truck drivers) • Weight

26. Natural history of LBP • 90% resolve spontaneously. • Lifetime incidence is 60-90%.

27. Degenerative changes in the lumbar spine • Glycosaminoglycan (GAG) levels in the nucleus gradually decline. • Water content decreases in the 6th decade and beyond. • Noncollagen glycoproteins replace GAG.

28. Degenerative changes of the lumbar spine • Phase 1: Dysfunctional phase (Kirkaldy-Willis) • Biochemical changes in aggregating proteoglycans. • Circumferential annular tears and fissures (scar weaker) Pain: Outer ring of annulus has pain sensors, and inflammation

29. Degenerative changes of the lumbar spine • Phase 2: Unstable phase • Loss of mechanical integrity (progressive) • Propagation of tears (herniations) Posterolateral herniated nucleus pulposus most common (weakest PLL site). Most common at L4-5.

30. Degenerative changes of the lumbar spine • Phase 2: Unstable phase • Loss of disc-space height • Facet joint/capsular laxity, subluxation

31. Degenerative changes of the lumbar spine • Phase 3: Final Stabilization Phase • Further disc degeneration • Endplate destruction. • Osteophyte formation • Less pain.

32. History • Timing of pain • Correlate with intradiscal pressure (highest sitting leaning forward with weight in hands)

33. History • Radicular pain • Usually radiates below the knee and has a dermatomal pattern. • Referred pain usually is deep and dull aching, usually to buttocks or hamstrings. Also rule out GT bursitis.

34. History • Cauda Equina Syndrome • Bowel and bladder difficulties • Perianal/saddle anesthesia • Diminished rectal tone • +/- motor deficits

35. History • Spinal stenosis (central) • More common in men because their spinal canal is smaller at the L3-5 level than women • Insidious pain • Few neurologic findings on exam. • Typically will have pain with extension. • 50% have neurogenic claudication

36. History • Spinal stenosis • Neurogenic claudication • Radiates from proximal to distal • Alleviated by flexing forward (sitting, grocery cart) • Heaviness and cramping of calves • Vascular claudication • Radiates retrograde • Alleviated by stopping/standing still.

37. Physical • Full neuro and motor exam • Tension signs for lumbar disc herniation • SLR (L4-5, L5-S1)- pain below the knee • Femoral nerve stretch (L2-3, L3-4) • Contralateral SLR (axillary HNP)

38. Physical • Waddell’s signs: • Tenderness to light touch. • Simulation (axial loading, pelvic rotation) • Distraction (SLR sitting versus supine) • Regional rather than anatomic distribution of pain. • Overreaction

39. Physical • Waddell’s Signs • Evaluates psychological component. • More than 2 suggest malingering, secondary gain or psych component.

40. Treatment of LBP • Initial treatment always conservative management: • Rest • 1-2 days • resume ADL • No lifting • Walking

41. Treatment of LBP • Initial treatment: • NSAIDs • Pain reliever initially • 5-10 days has antiinflammatory effect • Gastritis/stomach ulcers • +/- opioids and non-opioid pain medication.

42. Treatment of LBP • Initial treatment: • +/- opioids and non-opioid pain medication. • Muscle relaxers (CNS not skeletal muscle)

43. Treatment of LBP • Physical therapy • Core strenghtening • Hamstring stretching • Lifting techniques/back school. • Supervised

44. Treatment of LBP • Pain management for possible injections. • Epidural injections • Facet injections

45. Treatment of LBP • Epidural injections • Do not change underlying condition. • Anti-inflammatory action breaks the cycle of pain inflammation and pain. • Effects longer than the actual steroid.

46. Treatment of LBP • Epidural injections • Three different methods: • 1. Interlaminar • back of epidural space • wider space

47. Treatment of LBP • Epidural injections • 2. Caudal • Sacral hiatus • Several segments

48. Treatment of LBP • Epidural injections • 3. Transforaminal • “nerve block” • along side the nerve • One side/one segment

49. Treatment of LBP • Facet injections • Intraarticular or medial branch block

50. Treatment of LBP • Surgical • Usually after failed conservative management • Neurological deficits