HSS Manual Ch. 20 - Low Back Pain

From the HSS Manual of Rheumatology and Outpatient Orthopedic Disorders


H. Hallett Whitman, III
Assistant Professor of Clinical Medicine
Clinical and Research Associate
Cardiovascular Hypertension Center
Weill Medical College of Cornell University
Chief of Rheumatology
Summit Medical Group
Summit, New Jersey

Daniel J. Clauw
Professor of Medicine and Chief
Division of Rheumatology
Department of Medicine
Assistant Dean of Clinical and Transitional Research
University of Michigan Medical School
Ann Arbor, Michigan

John F. Beary, III
Clinical Professor of Medicine
University of Cincinnati
Attending Physician
Division of Rheumatology and Immunology
Veterans Administration Medical Center
Cincinnati, Ohio

KEY POINTS

  • Low back pain (LBP) is the second most common condition seen in primary care practice, and the most common problem seen by musculoskeletal specialists. It is essential that physicians be comfortable with the nuances of diagnosis and treatment of LBP.
  • Less common causes of low back pain such as infection (fever and focal pain) and cancer (weight loss, unexplained pain, and oncologic risk factors) must not be overlooked. If the pain persists and is unexplained, then it must be worked up further.
  • MRI images have a 30% false positive rate, and therefore must be used in a discriminating fashion. Remember that most patients with acute LBP and without neurological signs and symptoms will respond to conservative therapy, and need no diagnostic tests.
  • Prolonged bed rest is harmful. An extended period of inactivity is a risk factor for converting acute LBP into chronic LBP. Start an appropriate regimen of exercise as soon as possible to preserve strength and flexibility in the muscles that support the lumbar spine.
  • Sensitization of peripheral or central pain processing systems will explain some cases of chronic low back pain that persist despite the correction of anatomical factors. Thus the first 3-6 months of assessment and treatment of LBP patients are critical in regard to preserving and optimizing function of the lumbar spine.

INTRODUCTION

  1. Low back pain (LBP) can affect up to eighty percent of the population at some point in their life, making it second only to the common cold as an illness affecting mankind, and the fourth or fifth most common reason for a physician office visit in the United States.
  2. Acute LBP usually resolves spontaneously, but up to ten percent progress to chronic LBP resulting in temporary or permanent disability that results in loss of over 1000 work days per 1000 workers each year, costs over $20 billion annually, and disables several millions persons in the United States alone at any one time.
  3. Risk factors for the development of LBP include heavy manual work, poor job satisfaction, exposure to vibration, cigarette smoking, and probably sedentary life style and pregnancy.
  4. Most patients with acute and chronic LBP have “idiopathic” low back pain, meaning that despite testing no clear cause can be found for their pain.
  5. Most patients who present with acute LBP in the absence of significant neurologic physical findings need no diagnostic tests and will respond to conservative management.
  6. Patients who do not respond to a conservative regimen may need imaging studies and, rarely surgery.

ETIOPATHOGENESIS

Any of the components of the lumbosacral spine when combined with related conditions seen below may be responsible for LBP.

  1. Vertebral body (fracture, osteoporosis, metastatic disease, sickle cell disease, infection)
  2. Intervertebral disk (herniation, infection)
  3. Joints (osteoarthritis, ankylosing spondylitis)
    1. Apophyseal joints
    2. Sacroiliac joints
  4. Ligaments (strain, rupture)
    1. Anterior and posterior longitudinal ligaments
    2. Interspinous and supraspinous ligaments
    3. Iliolumbar ligaments
    4. Apophyseal ligaments
  5. Nerve roots (herniated nucleus pulposus, spinal stenosis)
  6. Paraspinal musculature (strain, spasms)
  7. Pain from adjacent structures (referred pain)
      1. Kidney (Pyelonephritis, perinephric abscess)
      2. Pelvic structures (pelvic inflammatory disease, ectopic pregnancy, endometriosis, prostate disease)
      3. Vascular (aortic aneurysm, mesenteric thrombosis)
      4. Intestinal (diverticulitis)
  8. Pain amplification syndromes where there is no identifiable abnormality of the peripheral tissue, but there is localized or widespread hyperalgesia (e.g., myofascial pain, regional forms of fibromyalgia)

PREVALENCE

Prevalence of LBP ranges from 38- 93 per 1000 population with female sex, Caucasian ancestry, and increasing age all being independent risk factors for increased incidence.

CLINICAL MANIFESTATIONS

  1. History is of great importance in obtaining associated symptoms and establishing a pattern of pain. A thorough review of symptoms is required to that would suggest a nonmechanical cause for low back pain, including:
    1. Fever or chills would raise the possibility of an infectious process.
    2. Weight loss, chronic cough, change in bowel habits, or night pain may suggest malignancy.
    3. Similar pain or morning stiffness in other areas of the body would increase the suspicion of a more generalized rheumatic condition such as ankylosing spondylitis, psoriatic arthritis or reactive arthritis.
    4. If fatigue or sleep disturbance is present, in the setting of a diffuse pain syndrome, the diagnosis of fibromyalgia should be considered.
    5. Morning stiffness or back pain that improves with exercise should promptconsideration of a spondyloarthropathy such as anklyosing spondylitis.
  2. Pain: The quality of pain, its distribution, and modulating factors are helpful in determining etiology
    1. Onset of pain:
      1. Sudden onset especially following trauma suggests injury.
      2. Indolent onset suggests a nonmechanical cause.
      3. Episodic or colicky pain suggests an intraabdominal or pelvic source.
    2. Localization of pain:
      1. Localized pain provides a focus for the diagnostic workup.
      2. Radicular, suggesting nerve root impingement.
      3. Pain that is not easily localized, migratory, or multifocal suggests fibromyalgia
    3. Modulating factors
      1. Exercise- induced pain especially walking, suggests osteoarthritis or spinal stenosis whereas pain that improves with exercise especially following morning stiffness suggests an inflammatory process, e.g. a spondyloarthopathy.
      2. Valsalva maneuvers such a coughing, sneezing, or bowel movements that worsen pain suggest nerve root impingement.
  3. Neurologic symptoms: The presence of neurologic symptoms should be specifically sought in patients with LBP. Their presence not only can help delineate the site of the abnormality but may also prompt more rapid intervention.
    1. Weakness, numbness, or paresthesias in a dermatomal distribution suggest nerve root impingement (Table 20-1). See also the dermatome figure in the Appendix
      1. The most common cause of nerve root impingement in persons between the ages of 20 and 50 is a herniated nucleus pulposus.
      2. Radicular symptoms in persons over the age of 60 are more likely to be secondary to spinal stenosis resulting from osteoarthritis.
    2. Bowel or bladder dysfunction suggest the presence of cauda equina syndrome and should prompt emergent investigation
    3. Low back pain in the presence of fever and neurologic symptoms should trigger the possibility if an epidural abscess.

PHYSICAL EXAMINATION

Specific abnormalities and provocative maneuvers designed to elicit pain in certain syndromes should be tested for in patients with low back pain.

  1. Patient standing:
    1. Note alignment of the spine looking for a pelvic tilt that may indicate paravertebral spasm, for loss of normal lumbar lordosis that could indicate either spasm or ankylosis, and for evidence of structural scoliosis.
    2. Evaluate gait, station, posture.
    3. Evaluate the patient’s ability to flex, hyperextend, rotate, and tilt the spine.
  2. Patient supine:
    1. Straight leg raising (SLR). Flex each leg at the hip with the knee extended and record the angle at which pain occurs and whether it radiates below the knee. A true positive SLR test is defined as radicular pain radiating below the knee, is a sensitive indicator of nerve root impingement, and should be confirmed by extending the knee while the patient is sitting to eliminate malingering.
    2. A crossed SLR test (radicular pain contralateral to the leg being raised) is highly predictive of nerve root compromise.
    3. Evaluate hip and knee range of motion to eliminate these areas as a source of pain.
    4. Carry out thorough neurologic (Table 20-1) and vascular examinations. The combination of the neurologic examination and symptoms define a “root signature”, allowing the physician to localize the source of the problem and potentially correlate it with the results of the imaging test.

 Site Pain Sensory Findings Motor Weakness Reflexes
 L3-4 Anterolateral thigh, medial knee Anterolateral thigh Knee extensors Patellar decreased
 L4-5 Posterior thigh, lateral calf, dorsum of foot, great toe Posterolateral calf, dorsum of foot, web of great toe Ankle dorsiflexors, extensor of great toe No specific reflex change
 L5-S1 Buttock, posterior thigh, calf, heel, ball of foot, lateral toes Buttock, posterior thigh, calf, lateral foot or lateral two toes Normal or weak plantar reflexes of ankle Achilles decreased

L3-4 disk affects the L4 nerve root.
L4-5 disk affects the L5 nerve root.
L5-S1 disk affects the S-1 nerve root.

  1. Patient prone
    1. Look for evidence of sciatic notch tenderness sometimes seen in sciatica.
    2. Results of the femoral stretch test (extending the hip) may be positive in L4 radiculopathy.
    3. Palpate bony structures, especially the vertebral structures, for localizedtenderness, and exam for the presence of trigger points, not only in the low back but also in other areas of the body.

DIAGNOSTIC INVESTIGATIONS

  1. LABORATORY TESTS should be performed as indicated by the history and physical examination, age of the patient, and duration of symptoms.
    1. The erythrocyte sedimentation rate and C-reactive protein reflect acute phase reactants and will usually be elevated in infection, inflammatory joint disease, and metastatic malignancies.
    2. Determinations of calcium, phosphorus, and alkaline phosphatase levels screen for metabolic bone disease.
    3. Serum and urine protein immunoelectrophoresis should be performed if multiplemyeloma is suspected because of the coexistence of back pain, elevated ESR and anemia.
  2. IMAGING STUDIES
    1. Imaging Studies are not performed until the patient fails a trial of conservative therapy or unless neurologic or constitutional symptoms are present
      1. Plain films should be taken as an initial study in the evaluation of low back pain.
        1. Anteroposterior, lateral, and cone down views of the lower two interspaces are standard.
        2. Oblique views will identify subtle spondylosis and help to visualize the neural foramina but are not routinely necessary
        3. Flexion extension views may be obtained to document instability and range of motion
      2. Bone scintigraphy is a useful as a screening study when malignancy (other thanMultiple myeloma), infection, or occult fracture not seen on plain films are suspected
      3. MRI has revolutionized the imaging of the lumbosacral spine and can visualize both bony and soft tissue structures well. MRI is now the study of choice for imaging intraspinal pathology. The prinicipal problem with MRI is the high rate of false-positive examinations. Up to 30% of asymptomatic persons will have significant abnormalities on MRI. Thus, MRI-defined abnormalities need to be placed into the context of the findings on history and physical examination.
      4. Computed tomography (CT). When used without intradural contrast, CT is the study of choice for delineating the bony structures of the spine (spinal stenosis). With the addition of intrathecal metrizamide, the sensitivity for detecting neural involvement is enhanced. CT does not detect intraspinal pathology as well as MRI and false positives exams may also be present as in MRI
      5. Myelography outlines the dural theca and its contents after injection of a contrast media into the dural sac. This is a good study to delineate neural compression. It remains the study of choice when metal hardware is present or when arachnoiditis may be present. Myelography is slowly falling from favor because of its invasiveness, side effects, and improvement in imaging with MRI and CT.
      6. Diskography is performed by injecting dye into the disk space. If symptoms are reproduced during the procedure, it may be particularly helpful, especially if other imaging studies have been nondiagnostic.
    2. Radiologic signs:
      1. Degenerative Disk Disease. Radiographic abnormalities correlate poorly withsymptoms and must be correlated with the results of the history and physical examinations.
        1. Narrowing of the intervertebral disc
        2. Vacuum phenomenon defined as radioluceny in the disk space
        3. Traction osteophytes defined as anterior osteophytes on the lumbosacral spine indicative of spinal instability
      2. Osteoarthritis
        1. Osteophyte formation
        2. Facet joint arthritis
        3. Spinal Stenosis
        4. Acquired spondylolisthesis
      3. Congenital and developmental defects
        1. Spondylolysis refers to the dissolution or failure of the neural arch, typically noted as a lucency in the “neck” of the “Scotty dog” noted on oblique spine radiographs (the “eye” of the Scotty Dog is the pedicle, the “ear” is the superior articulation of that vertebral body, and the “neck” is the par interarticularis). Failure of the pars can lead to slippage (usually anteriorly) of one vertebral body over the other.
        2. Spondylolisthesis is slippage of one vertebral body on another. It can be a consequence of spondylolysis or acquired conditions.
        3. Transitional vertebrae, with lumbarization of S-1 or sacralization of L-5.
        4. Schmorl’s nodes are defects in the vertebral end plates that allow vertical disc herniation
        5. Scoliosis or kyphosis
      4. Spondyloarthopathies (ankylosing spondyltiis, reactive arthritis, psoriatic arthritis, arthritis associated with inflammatory bowel disease)
        1. Erosions or sclerosis of the sacroiliac joints are best seen in a Ferguson (sacroiliac) view of the pelvis, a special view that allows better visualization of the joint
        2. Syndesmophytes. Calcification of the ligamentous structures leads to a bridging of the adjacent vertebral bodies
      5. Neoplasm
        1. Typically leads to destruction of the vertebral body
        2. Loss of the outline of the pedicle on the anteroposterior films
        3. Pathologic Fracture
      6. Infection should be suspected when destruction of adjacent vertebral end plates is present or bony destruction is accompanied by constitutional symptoms.
      7. Miscellaneous
        1. Osteoporosis. Loss in mineralization, compression fractures with characteristic anterior wedging, “fish mouth” appearance to the intervertebral spaces.
        2. Metabolic bone disease (i..e osteomalacia, Paget Disease, or hyperparathyroidism)
        3. Sickle cell disease

DIFFERENTIAL DIAGNOSIS

  1. Vertebral body diseases
    1. Fracture
    2. Metabolic bone disease
    3. Multiple myeloma
    4. Metastatic cancer
    5. Infection
  2. Intervertebral disc diseases
    1. Herniation
    2. Infection
  3. Joint Disease
    1. Apophyseal joint disease due to osteoarthritis
    2. Sacroiliac joints
  4. Ligamentous Disease
    1. Anterior and posterior long ligaments
    2. Interspinous and supraspinous ligaments
    3. Iliolumbar ligaments
    4. Apophyseal ligaments
  5. Nerve Root Impingement
    1. Herniated Nucleus Pulposus
    2. Spinal Stenosis
    3. Neoplasm
  6. Paraspinal Musculature
    1. Fibromyalgia
    2. Myofascial (localized pain)
  7. Referred Pain
    1. Renal
    2. Pelvic
    3. Vascular
    4. Gastrointestinal

TREATMENT

  1. Because more than 90% of cases of low back pain are self limited and resolve spontaneously, any treatment algorithm must account for this and should avoid immediate laboratory or imaging studies unless constitutional symptoms, weakness, or neurologic dysfunction suggests that there is an urgent problem.
  2. Acute Treatment:
    1. Rest vs. activity. Many longitudinal studies suggest that prolonged rest, and/or “fear” on the part of the patient that activity will worsen their pain, and are associated with a higher likelihood of the acute low back pain becoming chronic. Patients should avoid extended periods of inactivity.
    2. Spinal Traction has no direct benefit, but may help enforce bed rest if this is desirable for a very short period of time
    3. Pharmacologic treatment
      1. Pain control. This is often brought about with the use of single or combination drug therapy with NSAIDs, other classes of analgesics, and topical pain patches (i.e. Lidoderm 5%)
      2. Muscle relaxants. The mechanism of action of these drugs is not entirely clear, but they are helpful in some patients with acute low back pain. Examples include cyclobenzaprine (Flexeril) 5-10 mg either as a single nighttime dose or up to every six hours, methocarbamol (Robaxin) 750-1500 mg up to every six hours, and chlorzoxazone (Parafon Forte) 500-750 mg up to every six hours). Benzodiazepines such as diazepam (Valium) may also be used for a limited period of time.
    4. Physical measures
      1. Moist heat: heating pads, hot tubs, steam and sauna baths
      2. Massage, ultrasound
      3. Bracing for any extended period of time may lead to muscle weakness
  3. Failure of conservative treatment as outlined after 4 - 6 weeks is considered an indication to initiate a diagnostic workup and consider surgical intervention. Theworkup should include plain radiographs of the lumbosacral spine, and usually aMRI of the lumbosacral spine, as well as any other laboratory studies deemed necessary based on the history and physical exam
  4. Other Treatment Modalities:
    1. Injection of myofascial trigger points with lidocaine alone or combined with corticosteroids if the patient exhibits only a few specific areas of tenderness
    2. Facet or nerve block procedures can be both diagnostic and therapeutic but requires specific skills and experience.
    3. Trancutaneous electrical nerve stimulator (TENS).
    4. Physical therapy. See below.
  5. Invasive intervention should be considered if there is a failure of conservative therapy and when there is a radiographically demonstrable anatomic lesion that could explain the pain, or when malignancy or infection cannot be excluded with noninvasive techniques.
    1. Surgery should rarely be performed before 2 months of conservative therapy except in circumstances that require urgent intervention such as worsening neurologic deficit. However, a delay of more than six months may also be unwise because of a higher risk of the development of chronic pain.
    2. Types of surgical intervention. These operations usually are performed after conservative therapy has failed and intractable pain, other sensory findings, or motor weakness are present. Depending on the skill and experience of the surgeon usually the least invasive operation has the best chance of success. For pure disk disease artificial disk replacements are being developed and hold promise for less invasive surgery that does not disrupt the normal bony structures.
      1. Laminectomy or hemilaminectomy. Removal of all or part of the lamina while preserving the apophyseal joints or in the case of spinal stenosis trimming the joints to decompress the neural tissues
      2. Laminotomy or hemilaminotomy. An opening is created in the lamina without it being totally removed.
      3. Diskectomy. Removal of the nucleus pulposus by standard surgical approach or fiberoptic approach
      4. Microdiskectomy. Removal of a portion of the herniated nucleus pulposus under microscopic guidance with a fiberoptic scope
      5. Spinal fusion. The precise indications for this surgery are controversial; this is usually performed in combination with one of the above operations.
  6. Chronic Pain may arise from a failure of conservative or more aggressive therapies, and these patients remain difficulty to treat even in specialized settings. A subset of this group has fibromyalgia.
  7. Rehabilitation and exercise. Flexibility and strengthening exercise is frequently recommended for patients with low back pain. Basic principles regarding rehabilitation in these patients should be followed and physical therapists are very helpful in instructing patients in these programs.
    1. Postsurgical patients
      1. Ambulation is encouraged early and prolonged sitting is avoided
      2. Lifting should be avoided
    2. Non-surgical patients: “Exercises” for low back pain probably should not be initiated until the acute phase of recovery has been completed and the patient can move freely without pain, whereas resumption of normal “activities” should be encouraged as early as possible. In beginning an exercise program, patients should be instructed to begin with only three to five repetitions of each exercise and proceed slowly.
      1. Pelvic tilt. Buttocks are tightened, and the lumbar spine is flattened isometrically
      2. Modified sit ups. With the patient supine, knees bent and arms at the side, the head and shoulders are lifted off the ground for five seconds.
      3. Knee-chest stretch. With the patient supine, knees bent and arms at the side, each knee is brought to the chest one at a time and held with the arms for five seconds. Then the knee is extended and that leg is lowered to the ground slowly
      4. Wall exercise. Patient leans against the wall with their feet about one foot from the wall depending on their height. Knees are then bent to about 45 degrees or until the lumbar spine feels flat against the wall for a few seconds. Patient then returns the upright position
    3. Other suggestions
      1. Weight reduction
      2. Increase aerobic fitness with walking, swimming, or other low impact activities. Do stretching activities as a workup before aerobics.
      3. Life-style modifications: proper lifting techniques (while lifting, the knees should be flexed and the back straight. Twisting while lifting should be avoided); a firm mattress should be used; and vocational training may be helpful

PROGNOSIS

  1. In long-term follow-up the vast majority of LBP patients without a serious underlying disorder such as malignancy, herniated nucleous pulposus with spinal cord ornerve root compression, or significant spinal stenosis will do well with a short period of rest, a conservative exercise program (in some cases supervised by a physical therapist) that emphasizes flexion and extension exercises, stretching regimens, and gradual aerobic conditioning and weight loss.
  2. Factors associated with a worse prognosis include malignancy, fracture, multiple level spinal stenosis, or a herniated nucleus pulposis or other condition with spinal cord or nerve root impingement that it not corrected surgically in a timely manner.
  3. Patient characteristics that usually indicate the need for surgery are sphincter and sexual dysfunction due to the compression of the conus medullaris or cauda equina, persistent radicular symptoms especially if associated with neurologic motor deficits that progress. The surgical procedure chosen is determined by the anatomical lesion that needs correction, and the training and skill of the surgeon called upon to do the surgery. Picking a surgeon with extensive experience and good outcomes is a particular Role that medical consultants can play on behalf of their low back pain patients.
  4. Serious intraoperative or perioperative complications can occur during low back surgery if important neurologic structures are compromised due to surgical error, infection, or bleeding that causes pressure and subsequent damage to the spinal cord or nerve roots.
  5. Low back pain patients that have uncorrected pain for more than 3 – 6 months may have difficulty being totally free of pain even after the anatomic cause of their originalpain is corrected. This may occur because of behavioral (e.g. fear of movement leading to inactivity and isolation) or neurobiological (e.g. “sensitization”of peripheral or central pain processing systems) reasons, or misdiagnosis (e.g. pain coming from a different cause than that originally treated), or be due to multiple causes).

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