Back pain for all medical students need.pptx

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1. Back pain III 28.2.2017

2. FACET SYNDROME General • Facet joints are true synovial joints containing a capsule, meniscus, and a synovial membrane. • These joints also sustain progressively increasing compressive loads down the spine, reaching approximately 12–25% in the lumbar region. • As the disc decreases in height, greater loads are imparted on the joints and influence the degenerative cascade.

3. Etiology • Somatic dysfunction/facilitated segment • Positional overload • Capsular tears/injury • Meniscoidal /synovial impingement • Spondylosis

4. Clinical Features • Back pain exacerbated with rotation and extension. • Referred pain pattern can be seen in a nondermatomal presentation. • No neurologic abnormalities.

5. Imaging • Imaging: x-ray, CT, MRI. – Degenerative changes may be noted but are not diagnostic. – MRI may show hypertrophy of the capsule and facets. – Fluoroscopic Z-joint injections or medial branch blocks may have a higher diagnostic value.

6. Treatment Conservative care – Relative rest. Medications for pain control. – Rehabilitation program: focus on lumbar spine stabilization in flexion-biased or neutral postures, proper body mechanics. – Interventional procedures may include facet joint injections or dorsal rami medial branch radiofrequency ablation.

7. SPRAIN/STRAIN General • This may be an overutilized term pertaining to muscular or ligamentous disruption due to overload injuries. Etiology • Overuse syndromes • Excessive eccentric contraction • Acceleration-deceleration injuries • Acute trauma

8. Clinical Features • Muscle aches with associated spasm and guarding in the region of injury. • Delayed onset muscle soreness can occur within 24–48 hours after an eccentric overload injury. • Facilitated segmental or somatic dysfunction may be more commonly involved than actual tissue disruption. • Normal neurologic exam.

9. Imaging • Increased lordotic curvature may be seen on lateral x-rays due to muscle spasm Treatment Conservative care Relative rest Medication. Rehabilitation program: focus on flexibility, range of motion, strengthening, and spinal stabilization exercises.

10. VERTEBRAL BODY COMPRESSION FRACTURE General Typically associated with osteoporosis, these fractures are more commonly seen in the thoracolumbar junction This is due to the transition between the fixed rigid thoracic and the highly mobile lumbar vertebra. Denis described a 3-column model for evaluating thoracolumbar fractures and determining their stability

11. Etiology Trauma Osteoporosis Osteomalacia Medication related (corticosteroids) Neoplasm

12. Clinical Features Sudden onset of constant thoracolumbar pain. Exacerbated with Valsalva maneuvers, turning in bed, coughing, or incidental trauma such as stepping off a curb.

13. Imaging Imaging: x-rays, bone scan, SPECT, CT, MRI. Anterior vertebral body wedging typically seen on imaging studies Bone scan with SPECT may have increased sensitivity

14. Treatment Conservative care Indicated for fractures causing < 25% decrease of vertebral height Short-term bedrest followed by activity restriction. Medications for pain control Rehabilitation program: focus on hyperextension exercises Bracing

15. • Surgical care – Spinal procedures are indicated for fracture causing > 50% decrease of vertebral height, instability, and late kyphotic deformity leading to neurologic compromise

16. SACROILIAC JOINT DYSFUNCTION/SACROILIITIS General • L-shaped articulation between the sacrum and the ilium that has a synovial joint anteriorly and syndesmosis posteriorly . • It is innervated by the L5 dorsal ramus and lateral S1 to S3 (S4) dorsal rami .

17. Etiology • Hyper/ hypomobile joint patterns • Repetitive overloads • Trauma • Capsular tears/injury

18. Clinical Features Acute or gradual back, buttock, leg, or groin pain with tenderness over the joint. Abnormal sacroiliac joint motion patterns, increased discomfort with positional changes. Discomfort within associated muscles, which may include the quadratus lumborum , erector spinae , and piriformis muscles. No neurologic abnormalities.

19. Imaging • X-ray, bone scan, CT, MRI • These studies can be considered to rule out alternative pathologies in resistant cases. • Fluoroscopic sacroiliac joint injections can have higher diagnostic value. • Serology workup can be indicated for underlying arthropathies .

20. Treatment • Conservative care – Relative rest. Medications. Rehabilitation program: manual medicine, SI joint injections, SI joint belt.

21. MYOFASCIAL PAIN SYNDROMES General • Denotes a regional pain disorder, characterized by hypersensitive areas called myofascial trigger points. • A myofascial trigger point is distinguished from a tender point by a circumscribed area of tenderness with a palpable tense band of muscle fibers that causes concordant pain in a referred pain pattern with an associated local twitch response upon palpation • It may also cause decreased range of motion and weakness.

22. Etiology • Postural mechanics • Overuse injuries • Trauma • Stress

23. Clinical Features • Muscle tenderness. Spasm, decreased range of motion, weakness, trigger points. • Nonmuscular symptoms including; paresthesias , poor sleep patterns, and fatigue. • Normal neurologic exam.

24. Imaging • None available. Consider further work-up to rule out other potential pathologies. Treatment • Conservative care – Correct underlying causes. Medications (analgesics, tricyclics ) for discomfort or sleep. – Rehabilitation program: focus on flexibility, strengthening, and aerobic exercises. – Spray and stretch or trigger point injections or botulitum toxin injections may be beneficial. – Psychologic counseling.

25. FIBROMYALGIA CLINICAL FEATURES • Diffuse aching stiffness and fatigue with multiple tender points in specific areas – Headaches – Neck and upper trapezius discomfort – Upper extremity paraesthesias – Fatigue—lack of sleep

26. • Females—20–60 years old • May experience morning stiffness but it varies throughout the day • Triggers may exacerbate symptoms: 1. Physical activity 2. Inactivity 3. Sleep disturbance 4. Emotional stress • May be associated with Irritable bowel syndrome, RA, Lyme, hyperthyroidism

27. ACR CLASSIFICATION OF FMS: • Widespread pain: pain found in all 4 quadrants of the body: the left and right side of the body as well as above and below the waist. – Axial involvement—cervical, anterior chest, thoracic, and low back • Pain in 11–18 tender points (Figure 3–5) – Bilateral involvement. –Occipital, lower cervical, trapezius, supraspinatus, second rib, lateral epicondyle, gluteal, greater trochanter, knee

28. Diagnosis of FMS • Needs to fulfill both criteria. • Symptoms present for at least 3 months

29. TREATMENT OF FMS • Patient education and reassurance • Medications – Tricyclic antidepressants (amitriptyline, nortryptyline ) – Pregabalin ( Lyrica ) and duloxetine (Cymbalta): only medications currently FDA-approved to treat fibromyalgia. – Muscle relaxants: cyclobenzaprine , tizanidine – Tramadol • Combination therapy is effective. • Biofeedback, tender point injections • Acupuncture • Low-impact, graded aerobic exercise

30. Infectious disorders of the spine Vertebral body osteomyelitis and discitis General • An embolic infection of the vertebral body metaphysis causing ischemia, infarct, and bony destruction with disc involvement Risk factors include advanced age, diabetes, immunodeficiency, penetrating trauma, GU procedures, and invasive spinal procedures.

31. It is most commonly seen in the lumbar spine, but increases in the cervical region with intravenous drug abuse and in the thoracolumbar junction with tuberculosis

32. Etiology • Staphylococcus aureus (most common) • Pseudomonas (intravenous drug abuse) • Mycobacterium tuberculi ( Pott’s disease) Clinical Features • Fever and back pain exacerbated with extension. • Spinal deformity evolves with collapse of vertebral body. • Neurologic involvement including radicular pain, myelopathy, or paralysis can occur due to direct dural invasion with compression from an epidural abscess.

33. Diagnostic Studies • X-rays – By 2 weeks, radiographs demonstrate disc space narrowing and blurred endplates. • Bone scan and SPECT • CT shows hypodensity with trabecular, cortical, and endplate destruction.

34. • MRI – Most sensitive and specific – T1 imaging: hypointense focus – T2: hyperintense focus and gadolinium enhancement • Labwork – Leukocytosis, increased ESR and C-reactive protein – Positive Gram stain and cultures • Positive bone biopsy

35. Treatment • Conservative care – Spinal immobilization with casting or bracing. Early ambulation. – Intravenous and oral antibiotics: Staphylococcus aureus : penicillin; first- or second-generation cephalosporins Pseudomonas: extended spectrum penicillins Tuberculosis: 12 months mycobacterial agents (rifampin, INH, ethambutol , pyrazinamide) • Surgical care – Spinal procedure including decompression and / or fusion

36. Nonorganic sources of back pain General • Patients may exhibit exaggerated complaints with a nonanatomical basis and without an organic pathology. Multiple screening tests exist. In particular for patients with low back pain are the Waddell’s signs. • Waddell’s signs are designed to delineate a nonorganic component for the patient’s low back pain. – Demonstration of more than 3 out of 5 signs may be cause for suspicion. – These signs can be remembered with the acronym DO ReST . – Be aware that an organic component is not excluded with positive Waddell’s signs. – It also does not diagnose any specific disorders.

37. Malingering General • Patients may misrepresent their condition due to secondary gain issues. More than pure symptom magnification or a deceptive distortion of events, malingering is a DSM-IV disorder. • Malingering is defined as an intentional production of falsely or grossly exaggerated physical and psychological symptoms for primary or secondary gain. • Criteria for diagnosing malingering are defined by DSM-IV.

38. Etiology • Motivated by external incentives • Avoiding work • Avoiding military duty • Obtaining financial compensation • Obtaining drugs • Evading criminal prosecution

39. Imaging • There are no specific studies to determine if a patient is malingering or demonstrating associated disorders. Certain psychological tests may offer insight on a patient’s condition but diagnosis rests mainly on clinical suspicion. Treatment • This rests on addressing the underlying issues involved with each patient’s individual situation. It may require a multidisciplined approach incorporating diverse aspects of the medical field, as well as confronting certain social matters.

40. MEDICAL SOURCES OF BACK PAIN General Factors causing spinal pain can be associated with nonmechanical conditions. These disorders must be considered with any pain presentation as they can be the primary dysfunction, though the predominating symptom appears spinal.

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42. Causes of Low Back Pain Congenital Dysplastic spondyloleisthesis Scoliosis Degenerative Degenerative joint disease, osteoarthritis, lumbar spondylolysis Facet joint disease, facet DJD Degenerative spondylolisthesis Degenerative disc disease Diffuse idiopathic skeletal hyperostosis Musculoskeletal Acute or chronic lumbar strain Mechanical low back pain Myofascial pain syndromes Fibromyalgia Postural abnormalities, pregnancy Traumatic Fracture or dislocations Sprain (lumbar, lumbosacral , sacroiliac)

43. Causes of Low Back Pain Inflammatory Spondyloarthropathies Rheumatoid arthritis Infectious Pyogenic vertebral spondylitis Intervertebral disc infection Epidual abscess Metabolic Osteoporosis or osteopenia Paget’s disease of bone Neoplastic Benign Spinal (benign bony tumours of spine) Intraspinal ( meningiomas , neurofibromas , neurilemmomas , low grade ependymomas ) Malignant Spinal (malignant bony or soft tissue tumours , metastasis) Intraspinal (metastasis, high grade ependymomas , astrocy tomas , meningeal carcinomatosis )

44. Causes of Low Back Pain Viserogenic Upper genitourinary disorders Retroperitoneal disorders (often neoplastic) Vascular Abdominal aortic aneurysm or dissection Renal artery thrombosis or dissection Stagnation of venous blood (nocturnal back pain of pregnancy) Psychogenic Compensation neurosis Conversion disorder Post operative and multiply operated–on back

45. Vertebral Deformities in Adults Clinical Presentation Varies from asymptomatic to severely disabled The most frequent clinical problem of AS is LBP LBP at the site of the curve can be localized either at the apex, on the prominence/hump, or in its concavity. It can be combined with radicular leg pain .

46. It can be the expression of a muscular fatigue or of a genuine mechanical instability. When the lumbar curve is accompanied by the loss of lumbar lordosis , the overloaded and stressed paravertebral back muscles may become a source of diffuse, permanent muscular pain.

47. The pain is axial LBP, and patients can control their pain well when lying down flat or on their side, and when the spine is relieved of its axial load. The second important symptom of AS is radicular pain and claudication symptoms when standing or walking

48. The radicular pain may be due to a localized compression or root traction whereas claudication may be due to single- or multiple-level LSS. The third important clinical presentation is a real neurologic deficit, including individual roots, several roots, or the whole cauda equina with apparent bladder and rectal sphincter problems.

49. Diagnosis, Classification, and Prognosis The diagnosis of AS is made on conventional x-rays Type 1 : Primary degenerative scoliosis , mostly on the basis of a disc and/or facet joint arthritis, affecting those structures asymmetrically with predominantly LBP symptoms, often accompanied with signs of LSS or without such signs .(These curvatures are often classified as de novo scoliosis) Type 2 : Idiopathic adolescent scoliosis of the thoracic and/or lumbar spine, which progresses in adult life and is usually combined with secondary degeneration and/or imbalance. Such patients may develop secondary degeneration and progression of the adjacent curve .

50. Type 3a : Secondary adult curvature in the context of an oblique pelvis, for example, due to a leg length discrepancy or hip pathology , or as a secondary curve in idiopathic; as neuromuscular and congenital scoliosis or as asymmetrical anomalies at the lumbosacral junction. Type 3b : Secondary adult curvature due to metabolic bone disease (mostly OP) combined with asymmetric arthritic disease and/or vertebral fractures.

51. Imaging • X-rays help establish diagnosis and prognosis. – Follow-up x-rays will depend on skeletal maturity, patient age, and degree of curvature . – Younger patients with rapidly progressing curves warrant earlier x-ray follow-up.

52. Rotation– Pedicle portion estimates the amount of vertebral rotation on the PA view. – Grading: 0 (no rotation) to 4 (complete pedicle rotation out of view). Curve: Cobb angle – An angle formed by the perpendicular lines drawn from the endplates of the most tilted proximal and distal vertebrae to measure the scoliotic curve .

53. Treatment Treatment Degree of angulation Observation < 20° Bracing 20–40° Surgery > 40° (< 35° for neuromuscular diseases) • Conservative care – Rehabilitation program – Bracing Worn 23 hours a day until spinal growth is completed. Weaning off can begin when radiographs display signs of maturity and curves are stable .

54. Patients should be evaluated at 2–3 year intervals for life after the brace is discontinued. Types Milwaukee brace High thoracic curves (apex at T8) Low profile TLSO Lower thoracic, thoracolumbar, and lumbar curves (apex below T8)

55. • Surgical care – Spinal procedures are indicated for scoliosis with: Relentless progression > 40° curvature in the skeletally immature, > 50° in the skeletally mature, < 35° in neuromuscular diseases, or progressive loss of pulmonary function