Low Back Pain

From WiserWiki

Jump to: navigation, search

Contents

[edit] Low Back Pain

James J. Heffernan


Low back pain is the most common musculoskeletal complaint among adult patients seen in primary care practice and second only to limb pain (generally related to injury) among patients seen in urgent care settings.Potential causes of low back pain are legion, but a specific pathoanatomic diagnosis is established in fewer than 20% of patients.

The back is a complex mechanical structure, a composite of vertebrae, intervertebral disks, and apophyseal joints stabilized by ligaments and the paraspinal and abdominal musculature.It supports the trunk and transmits, through the sacroiliac joints, upper body loads to the pelvis and lower extremities.The posterior vertebral elements encase and protect the spinal cord and cauda equina.Connections to thebulk of the body's peripheral nervous system run through the vertebral neural foramina.The spine and its supporting structures have extensive innervation.The posterior rami of the lumbosacral spinal nerves supply the apophyseal joints, the interspinous ligament, the paravertebral muscles, and associated cutaneous areas; at each vertebral level, the sinuvertebral nerve, joined by a sympathetic branch, innervates the anterior dura mater and dural sleeve, the posterior vertebral periosteum, the posterior longitudinal ligament, epidural blood vessels, and the anulus fibrosus.

Most episodes of low back pain arise from regional (i.e., nonsystemic) processes, a result of mechanical derangements to the complex anatomic relationships within and around the spine.Approximately 1% of patients with acute low back pain have sciatica, defined as pain in the distribution of a lumbar or sacral nerve root, with or without associated neurosensory and motor deficits.The presence of sciatica increases the likelihood that a herniated intervertebral disk is the cause of back pain.Systemic causes and the more serious local pathologic processes generally present with specific clinical features.


[edit] EPIDEMIOLOGY

Low back pain is extremely common, producing at least short-term impairment in 70% to 80% of a general population.The point prevalence of low back pain is 5% to 7% among adults.Nearly 2% of adults lose time from work annually as a result of low back pain, and 2% to 5% consult a physician for treatment.This ailment takes its toll in the productive years, with most patients between ages 30 and 60.Although most cases resolve in a relatively short period, 14% of adults report at least one episode lasting longer than 2 weeks, and 1.6% have features of sciatica.

Among chronic conditions, back and spine impairment is the leading cause of disability in persons under age 45 and ranks third behind heart disease and arthritis in the 45 to 64 age range.[1] It is the second most common complaint of pain for which treatment by a physician is sought.The annual cost of direct medical care for low back pain has been estimated at $13 to $16 billion, and the total annual societal costs in the United States are estimated at $20 to $50 billion.[2]

Men and women are comparably affected, but the incidence is somewhat higher for women in occupations requiring heavy exertion.Women also report low back symptoms more often after age 60, whereas men more frequently present with low back pain in their younger adult years.Most studies have demonstrated a precipitating event in a minority of cases (6% to 28%).The natural history of low back problems is one of recurrence, reported variably in 33% to 60% of patients with occupational low back pain during the ensuing 1 to 3 years.Symptoms tend to be mild and transient in young workers but more persistent and severe with increased age.Incidence rates are similar among heavy, light, and sedentary workers, although a higher proportion of heavy workers are incapacitated with low back pain.Those bored or dissatisfied with their occupations are more likely to report low back problems.In a given work setting, low back pain appears more frequently in those who consider their work to be physically demanding.Specific risk factors include occupations that require repetitive lifting in a forward bent-and-twisted position, exposure to vibrations caused by vehicles or heavy machinery, and cigarette smoking.Low back pain is common in persons who either sit or stand for prolonged periods; however, jobs requiring sudden maximal efforts are also associated with higher incidence rates.

No convincing evidence shows that patients with moderate kyphosis, scoliosis, or lordosis are more at risk for low back pain than those with normal spine curvature.Likewise, moderate differences in body habitus do not predict differences in incidence rates, although massive obesity and major skeletal abnormalities are associated with increased rates of low back pain.Isthmic spondylolisthesis, spinal osteochondrosis, and the spinal stenosis associated with achondroplasia appear to predispose affected patients to low back problems.Recreational activities have not been associated convincingly with low back pain syndromes, although isthmic spondylolisthesis is reportedly increased fourfold among gymnasts and interior linemen on football teams.

Attempts to characterize the low back pain patient psychologically have produced a variety of profiles.Although most studies have been performed retrospectively on patients in treatment programs, patients with low back pain have demonstrated greater levels of psychopathology than extremity-injured peers or noninjured industrial workers.A tendency toward neurotic depression rather than hysteria has been described, although other data support increased rates of hysteria and hypochondriasis along with anxiety and depression.Increased rates of alcoholism and divorce have also been noted among individuals disabled by low back pain.


[edit] PATHOPHYSIOLOGY

The potential causes of low back pain are myriad (Box 127-1).Systemic illness, regional cancer, and local infection account for only a trivial percentage of total cases.Most low back pain arises from uncharacterized regional processes.Although many putative causes have been identified by invasive studies and postmortem examinations, the specific anatomic cause of backache in a given patient most often goes unidentified (Figs.127-1 and 127-2).

Figure 127-1 Anatomy of the lumbosacral spine, lateral view. n., Nerve.  (From Cramer GD, Darby SA, editors:Basic and clinical anatomy of the spine, spinal cord, and ANS, St Louis, 1995, Mosby.)
Figure 127-1 Anatomy of the lumbosacral spine, lateral view. n., Nerve. (From Cramer GD, Darby SA, editors:Basic and clinical anatomy of the spine, spinal cord, and ANS, St Louis, 1995, Mosby.)
Figure 127-2 Relationships of lumbar nerve roots to vertebrae and disk.
Figure 127-2 Relationships of lumbar nerve roots to vertebrae and disk.


Box 127-1 - Causes of Low Back Pain
Primary Mechanical Derangements (Generally Putative)
  • Ligamentous strain
  • Muscle strain/spasm
  • Facet joint disruption/degeneration
  • Intervertebral disk degeneration/herniation
  • Vertebral compression fracture
  • Vertebral end plate microfractures
  • Spondylolisthesis
  • Spinal stenosis
  • Diffuse idiopathic skeletal hyperostosis
  • Severe scoliosis or kyphoscoliosis
  • Scheuermann's disease (vertebral epiphyseal aseptic necrosis)
    Infection
  • Epidural abscess
  • Vertebral osteomyelitis
  • Septic diskitis
  • Pott's disease (tuberculosis)
  • Nonspecific manifestation of systemic illness
    • Bacterial endocarditis
    • Influenza

      Neoplasia
  • Epidural/vertebral carcinomatous metastases
  • Multiple myeloma, lymphoma
  • Primary epidural or intradural tumors
    Metabolic Disease
  • Osteoporosis
  • Osteomalacia
  • Hemochromatosis
  • Ochronosis
    Inflammatory Rheumatologic Disorders
  • Ankylosing spondylitis
  • Reactive spondyloarthropathies (including Reiter's syndrome)
  • Psoriatic arthropathy
  • Polymyalgia rheumatica
    Referred Pain
  • Abdominal or retroperitoneal visceral process
  • Retroperitoneal vascular process
  • Retroperitoneal malignancy
  • Herpes zoster
    Other Causes
  • Paget's disease of bone
  • Primary fibromyalgia
  • Psychogenic pain
  • Malingering

The herniated vertebral disk is probably the best known cause of low back pain (Fig.127-3).Disk herniations tend to occur in a lateral or central posterior direction.Posterior prolapse of a herniated vertebral disk accounts for only a small subset of cases, however, and generally manifests through the classic neural impingement syndrome of sciatica.Herniation of the nucleus pulposus occurs in 95% to 98% of cases at the disk between the fourth and fifth lumbar vertebrae (L4-5) or between the fifth lumbar vertebra and sacrum (L5-S1), with herniation at two levels in 10% of cases.Older individuals have an increased risk of disk herniation at higher lumbar disk levels.Other causes of sciatica include spinal stenosis, synovial cysts, congenital anomalies of lumbar nerve roots, primary neural and osseous tumors, metastatic cancer, and epidural abscesses.Retroperitoneal neoplastic processes and endometriosis may cause sciatica by involvement of the lumbosacral plexus.Sciatica from local pressure to the sciatic nerve may result from toilet seats, especially in thin individuals, or from habitual placement of a wallet in a back pocket.

Figure 127-3 Magnetic resonance images demonstrating right posterior herniated L4-5 disk.
Figure 127-3 Magnetic resonance images demonstrating right posterior herniated L4-5 disk.


With aging the intervertebral disk degenerates, and much low back pain is probably related to small tears in the anulus fibrosus, compression of end plate cartilage, and microfractures of subchondral bone in the end plates; these processes cannot be demonstrated acutely.As these processes continueover time, however, subtle anatomic derangements are integrated, and spondylosis develops, manifested radiographically in thinning of the intervertebral disk with narrowing of neural foramina and bony spurring and lipping, especially at the disk margins. Spondylolisthesis refers to slippage of one vertebra over another, usually at the L5-S1 level.Studies using fluoroscopically directed injections of hypertonic saline and anesthetic agents with or without corticosteroids have reproduced and relieved low back pain, respectively, in a variety of patients.Injection sites have included the facet joints, ligamentum flavum, interspinous and supraspinous ligaments, intradiskal space, and epidural space.Derangement of posterior structures may therefore cause or contribute to low back pain in a given patient.

Spinal stenosis resulting from bony encroachment by osteoarthritis, generally superimposed on congenital narrowing of the lumbar spinal canal, can result in lumbosacral radiculopathy and neural claudication (or pseudoclaudication) with pain on ambulation or standing, relieved by sitting.The pain of spinal stenosis probably represents reversible cord or root ischemia.

Muscle pain and spasm are common features in low back pain, but a primary role for muscle strain remains uncertain.Axial myalgias associated with polymyalgia rheumatica and the low back pain and tender points associated with idiopathic fibromyalgia (fibrositis) are relatively common syndromes that cause low back pain nonskeletally.An inflammatory spondyloarthropathy may affect up to 2% of the population and most often presents as low back pain and stiffness, especially in the morning after sleep.Diffuse idiopathic skeletal hyperostosis, noted predominantly in middle-aged and elderly men, may be dominated by complaints of low back pain and stiffness.

The systemic process of osteoporosis is a major public health problem (see Chapter 45 ).This condition can produce back pain by the mechanism of vertebral collapse, though more often in the thoracic spine.Chronic, poorly localized back pain associated with osteoporosis in the absence of overt vertebral collapse probably results from multiple microfractures near vertebral end plates and can be a debilitating condition among the elderly population.

The spectrum of causes of back pain differs above and below the lumbosacral area.The thoracic spine is the region most often affected by vertebral compression fractures resulting from osteoporosis; the lower thoracic and upper lumbar vertebrae are the most common sites of bony metastatic disease.Middle and upper back pain may result from axial loading of the spine, as in football or jumping injuries, or after strenuous upper extremity trauma, as in the vertebral spinous process avulsion fractures or “clay shoveler's back,” a condition noted among manual laborers in whom shear forces are transmitted to the spine from abrupt unloading of upper extremity loads.Sacral fractures, a form of traumatic spondylolisthesis, may result from direct trauma to a flexed hip and extended leg.Coccygeal fracture may likewise result from direct trauma, usually a fall, and rarely from difficult childbirth.Pelvic malignancies may involve coccyx or sacrum by direct extension and lymphatic or hematogenous spread.

The clinical course of low back pain associated with systemic illness is that of the underlying disease.Excluding such patients from consideration, as well as those few with local infections and neoplastic processes whose prognosis depends on the specific cause and available treatment, the physician is left with the core of typical patients with low back pain.Among this group the natural course is remission and recurrence.Acute low back pain is generally a self-limited disease, with remission rates of 40% after 1 week, 50% to 85% in 3 weeks, and 90% in 2 months.Evenwhen low back pain is considered a work-related compensable injury, 85% to 90% of patients return to work within 12 weeks.Among patients who have sought medical attention for low back pain, recurrences are noted in 90% and are generally longer lasting than the initial attack.


[edit] PATIENT EVALUATION

Although a firm anatomic diagnosis is seldom made, the history and physical examination are generally discriminating enough to focus attention on the more serious causes of low back pain.


[edit] History

Severe backache after serious trauma suggests a fracture or acute disk herniation.Pain after a pure flexion injury suggests a pathologic condition of the disk or end plate, whereas pain after a torsional injury is more often associated with disruption of posterior structures (e.g., facet joint) and ligamentous injury.With either injury, pain may radiate to the buttocks or upper thigh.The pain associated with an acutely herniated intervertebral disk is often sharp or lancinating with radiation down the back of a leg, often to the ankle or foot.The patient resists movement and generally finds relief in a fixed, somewhat awkward supine posture or in the lateral decubitus position with the leg of the affected side in partial flexion.Bilateral sciatica associated with bowel or bladder dysfunction (incontinence or retention) and weakness suggests a massive central disk herniation or another epidural (and rarely intradural) mass lesion, especially hemorrhage, abscess, or metastasis.A patient writhing in pain suggests a visceral or vascular source (e.g., rupturing abdominal aortic aneurysm, ureteral colic).Backache, associated with fever, especially when unremitting or progressive, may represent vertebral osteomyelitis, septic diskitis, epidural abscess, or Pott's disease.Other febrile processes associated with back pain include early herpes zoster, influenza, or the nonseptic musculoskeletal manifestations of bacterial endocarditis.

Morning back pain and stiffness persisting several months after an insidious onset in a younger man who derives relief from exercise indicate ankylosing spondylitis.Similar symptoms coupled with conjunctivitis, urethritis, skin rash, balanitis, and diarrheal illness suggest a reactive inflammatory arthropathy (e.g., Reiter's syndrome; see Chapter 137 ).Most patients with typical mechanical low back pain present with pain, often severe, and muscle stiffness involving the back, buttocks, and often the thigh.Pain typically arises hours or days after a new or unusual exertion and is generally relieved by assumption of the supine position.In the patient with chronic sciatica, pain is often confined to the buttocks and leg and is usually described as dull or aching and exacerbated by sitting.Low or middle back pain in an elderly patient may result from osteoporosis with or without overt compression fractures, from polymyalgia rheumatica, or from neoplasia.Dull, progressively worsening bone pain in an elderly patient, especially pain that worsens with recumbency, suggests metastatic carcinoma or multiple myeloma.Spinal stenosis may also present as pain in a recumbent or standing position, relieved by sitting.Diffuse, poorlylocalized back pain may be a manifestation of Paget's or Cushing's disease.Associated pelvic or abdominal disease may refer pain to the low or middle back.


[edit] Physical Examination

A systematic approach to examination of the back complements the history in focusing attention on the identifiable causes of low back pain.Inspection and palpation yield important initial clues.Severe idiopathic kyphoscoliosis is associated with degenerative arthritis; mild scoliosis or loss of lumbar lordosis is a common finding in the acute setting, the result of paravertebral spasm.Prominent dorsal kyphosis in an elderly patient suggests vertebral collapse as a result of osteoporosis or malignancy.Most patients with acute low back pain have restricted vertebral mobility.However, diminished chest expansion (less than 3 cm) in association with decreased mobility of the spine, especially when sacroiliac joint tenderness coexists, strongly suggests ankylosing spondylitis (see Chapter 137 ).Tenderness of the sciatic nerve in the sciatic notch suggests a component of radiculopathy or neuropathy.

A tender spinous process in the setting of fever and backache suggests vertebral osteomyelitis, septic diskitis, or an epidural abscess; a tender spinous process in the setting ofmalignancy and backache suggests vertebral or epidural metastatic disease.In both cases, aggressive emergency evaluation is indicated, especially if neurologic deficits are noted.

Simple maneuvers can provide further diagnostic clues.Induction of pain on torsion or hyperextension of the spine suggests ligamentous or facet joint injury, most often at the L4-5 level.Increased discomfort with spinal extension also suggests spinal stenosis.Reduction of lateral flexion is more suggestive of spondyloarthropathy than a herniated disk or other cause of mechanical low back pain.

The most useful simple maneuver in assessing nerve root impingement is the straight leg raising (SLR) test, which places the lower lumbosacral nerve roots under tension.With the patient supine the examiner slowly raises the straightened leg of the affected side through the arc of hip flexion.If pain occurs in a radicular distribution with straight leg elevation through an arc of 60 degrees or less, the test is positive.The probability that herniation is the cause of back pain increases as the angle necessary to produce radicular pain decreases, although there is little or no traction on nerve roots with arcs of less than 20 to 30 degrees.This test is moderately sensitive (80%) for herniated lumbosacral disks, but not specific (40%).[3] To exclude false-positive results, the examiner should attempt repeated trials, some conducted while distracting the patient.The angle associated with pain should be reproducible when the examiner passively flexes the patient's hip with the knee in flexion, then slowly extends the foreleg.An important supplement to the direct SLR is the crossed SLR, which entails elevation of the unaffected leg in the patient with sciatica.A positive test results when radicular pain is produced in the unraised leg.The crossed SLR is substantially less sensitive (25%) but strikingly more specific (90%) than the direct SLR.[3] A similar but less well-quantified provocative test for eliciting pain in the setting of L3-4 disk herniation involves forcing full or exaggerated extension of the hip of the affected side while the knee is flexed and the patient is prone or in the lateral decubitus position.

In most patients, deep tendon reflexes are not affected by mechanical low back pain.The ankle jerk (Achilles tendon reflex), however, is subserved by the S1 root and is often diminished or absent in the compression radiculopathy produced by L5-S1 disk herniation.The Achilles tendon reflex is frequently absent in normal, elderly individuals.No reflex deficits occur with L4-5 disk herniations.The infrequent occurrence of L3-4 disk herniation with L4 root compression is manifested as a diminished knee jerk (patella tendon reflex).

Motor deficits are often subtle but can usually be demonstrated in the setting of true sciatica.Compression radiculopathy of the S1 root by L5-S1 disk herniation is associated with weakness of plantar flexion, best demonstrated by having the patient walk on the toes.Dorsiflexion weakness is associated with L5 radiculopathy from L4-5 disk herniation, as demonstrated by the patient walking on the heels or dorsiflexing the great toe against resistance.Quadriceps weakness results from L4 radiculopathy associated with L3-4 disk herniation.

Sensory deficits with sciatica are also often subtle but demonstrable.Compression of the S1 root by L5-S1 disk herniation may result in sensory deficits of the posterior calf and lateral aspect of the foot.Compression of the L5 root by disk herniation at L4-5 manifests as hypesthesia on the dorsum of the foot and great toe, especially in the first web space.Hypesthesia over the lateral aspect of the thigh is consistent with L4 root compression from L4-5 disk herniation.Saddle anesthesia in the patient with bilateral sciatica and loss of anal sphincter tone suggests the cauda equina syndrome from massive central disk herniation or another space-occupying lesion and warrants further emergency evaluation.

Hallmarks of malingering or of a psychiatric origin for low back pain include overreaction; reproduction of back pain by “tests” that should not elicit such pain on physiologic grounds (e.g., axial loading by the application of downward pressure on the head of the standing patient); variable results of true provocative tests (e.g., SLR) when the patient is distracted; superficial, nonanatomic tenderness; and motor or sensory disturbances with nonphysiologic components.


[edit] DIAGNOSIS

[edit] Diagnostic Procedures

Blood tests are of little diagnostic use in most patients with low back pain.Leukocytosis, an elevated erythrocyte sedimentation rate, and anemia are nonspecific markers of possible infection, neoplastic disease, or inflammatory spondyloarthropathy.Serum or urine immunoelectrophoresis may corroborate the suspicion of multiple myeloma.Abnormalities of serum calcium, phosphate, and alkaline phosphatase are crude indices of metabolic bone disease.The diagnosis of spondyloarthropathy usually rests firmly on the history, physical examination, and radiographs of the spine and sacroiliac joints; HLA-B27 determination is corroborative.

Lumbosacral spine radiographs are abnormal in most persons over age 50 and often in younger persons.Radiographs are neither sufficiently sensitive nor sufficiently specific to justify routine use in evaluating backache, especially in the acute setting.Findings of degenerative disk disease, osteoarthritis, spina bifida occulta, and transitional or asymmetric vertebrae are common in individuals with and without back pain.Spondylolisthesis has been noted in 5% to 20% of spinal radiographs (Fig.127-4).

Figure 127-4 Spondylolisthesis.
Figure 127-4 Spondylolisthesis.


Radiographs may be extremely helpful, however, if an inflammatory spondyloarthropathy or a destructive lesion associated with either malignancy or an infectious process is suspected.Anteroposterior and lateral views may also provide an overall view of the degree of osteoporosis and associated vertebral collapse.In major trauma, radiographic studies may demonstrate fractures and dislocations.Oblique views may better visualize the facet joint but rarely add to the evaluation process.Selective use of spinal radiographs based on specific criteria may increase the diagnostic yield threefold.Indications for spinal radiography in the patient with acute low back pain may include (1) age over 50, (2) history of serious trauma, (3) known cancer, (4) pain at rest, (5) unexplained weight loss, (6) drug or alcohol abuse, (7) treatment with corticosteroids, (8) temperature above 38° C, (9) suspicion of ankylosing spondylitis, and (10) demonstrable neuromotor deficit.[4] Spinal radiographs may also be appropriate for a patient with pain that persists beyond 3 to 4 weeks, even without neurologic findings.

Until the 1980s, contrast myelography was the procedure of choice when epidural compression by a tumor or infectious process was suspected or when neurologic deficits suggested intervertebral disk herniation, especially when a surgicalprocedure was contemplated.The sensitivity of contrast myelography for herniated lumbar disk is 90% and the specificity 70% to 90%.Diskography demonstrates disk herniation reliably at a given level only, is somewhat less sensitive and specific than myelography, and is seldom necessary.

Computed tomography (CT) scans of the lumbosacral spine have better sensitivity and specificity than myelography for herniated intervertebral disks and may also reveal bony abnormalities, tumors, and vascular lesions.Unfortunately, CT scans of the lumbosacral spine demonstrate significant abnormalities in more than one quarter of asymptomatic persons.CT has often been employed in place of or in addition to myelography when evaluating patients with low back pain.

In studies comparing different diagnostic modalities, CT, magnetic resonance imaging (MRI), and CT with myelography have demonstrated comparable true-positive and true-negative rates for diagnosing lumbar disk herniation, and all are more accurate than traditional myelography.[5] MRI best differentiates between recurrent disk herniation and scar tissue and is recommended when imaging is indicated in the patient who has undergone previous surgery.As with CT, MRI identifies substantial abnormalities (e.g., disk herniation, spinal stenosis) in up to one third of patients with no prior low back pain[6]; disk bulging or degeneration at least one lumbar level is found in nearly all individuals over age 60 (see Fig.127-3).Where available, MRI has generally become a standard in evaluating patients with suspected epidural abscess or malignancy.

Radionuclide bone scans are more sensitive than standard radiographs in identifying metastatic lesions (other than the plasmacytomas of multiple myeloma) and are also useful in characterizing the spondylolysis associated with isthmic spondylolisthesis.Nuclear medicine studies are sometimes helpful in identifying abscesses and osteomyelitis.When nerve root compression is suspected, electromyography may be confirmatory.“Therapeutic” facet joint injections are not beneficial, and injection studies to localize the source of low back pain are generally not indicated.


[edit] Differential Diagnosis

See Tables 127-1 and 127-2.


Table 127-1 Differential Diagnosis of Common Low Back Pain Syndromes

Clinical entityHistoryPhysical examinationSupporting studies
Mechanical low back painPain in back, buttocks, possibly thigh; may be severeParavertebral tenderness/spasmNone necessary
 Onset after new or unusual exertionScoliosis or loss of lumbar lordosis common 
 No history of major trauma, systemic infection, or malignancyNo neurologic signs (see Table 127-2) 
 Relief of pain in supine position  
Herniated intervertebral diskAcutely, pain in back severe and lancinatingStriking paravertebral tenderness/spasm with splinting in awkward posturesMRI, CT, or myelogram
 Antecedent flexion strain injury or traumaSigns of radicular irritation/injury usually present in acute settingElectromyography may provide supporting documentation of level of denervation
 Sciatica  
 Relief of pain supine with hip flexed  
 Bilateral weakness, possible bowel/bladder dysfunction with massive central disk prolapse  
 With chronic disk herniation, pain usually dull and possibly confined to leg  
Referred visceral or vascular painPatient writhes in discomfort, with no relief in any positionAbdominal findings usually predominateImaging studies directed at abdomen and retroperitoneum may visualize aortic aneurysm or abnormality of viscera (e.g., ureteral calculus, pancreatitis)
 Pain may occur in wavesFever or incipient shock often present 
Metastatic malignancy (or multiple myeloma)Unremitting or progressive pain at restTender spinous process at level of involvementStandard radiographs may reveal destructive bony lesions
 Known or suspected malignancyVariable neurologic findings, up to full paraplegiaRadionuclide bone scan sensitive for metastatic carcinoma but not for myeloma
 Weight loss, fever, other systemic symptoms Epidural impingement of spinal cord or roots best delineated by MRI, myelography, or CT
 History of weakness, possible bowel/bladder dysfunction ESR elevated
Epidural abscess, vertebral osteomyelitis, or septic diskitisUnremitting or progressive pain at restTender spinous process at level of involvementStandard radiographs may reveal destructive bony lesions
 FeverVariable neurologic findings, up to full paraplegiaRadionuclide scans may suggest abscess
 Drug abuse, diabetes mellitus, immunosuppressionStigmata of systemic infectionBlood cultures often positive
 Suspected or known systemic infection MRI probably best imaging modality to delineate extent of lesion and neural impingement
 Previous spinal or genitourinary surgery ESR elevated
 History of weakness, possible bowel/bladder dysfunction  
Ankylosing spondylitisInsidious onsetPainful or ankylosed sacroiliac jointsSacroiliac joints and lumbosacral spine ankylosed on standard radiographs
 Progressive morning back pain and stiffness over several monthsReduced mobility of spineESR elevated
 Relief with exerciseReduced chest wall expansionHLA-B27 confirmatory
 Age at onset: 40 years or youngerPossible associated uveitisUveitis may be confirmed on ophthalmologic examination
Reactive spondyloarthropathiesAs with ankylosing spondylitisAs with ankylosing spondylitisAs with ankylosing spondylitis
 Antecedent urethritis, rash, or colitisConjunctivitis, balanitis, urethritis, keratoderma blennorrhagicumBowel studies may reveal infectious or idiopathic inflammatory bowel disease
  PsoriasisInfectious urethritis may be confirmed
Spinal stenosisBack pain may vary from severe to absentNeurologic findings vary: often evidence of impairment at multiple spinal levelsStandard radiographs generally show extensive vertebral osteophytes and degenerative disk disease
 Pseudoclaudication often prominent, often involving L4 root (anterior thigh)Findings of osteoarthritis may be prominentImaging with MRI or CT/myelography supports diagnosis if neurologic and imaging findings are concordant
 Pain worsens during the day, aggravated by standing and relieved by rest  
 Weakness, possible bladder/bowel dysfunction  
CT, Computed tomography;MRI, magnetic resonance imaging;ESR, erythrocyte sedimentation rate.



Table 127-2 Radiculopathies Associated With Intervertebral Disk Herniations

Disk syndromeRootRate (%)Pain radiationSensory deficitMotor deficitReflex deficit
L5-S1S145-55Posterior thighPosterior calfPlantar flexorsAnkle
   Posterior and lateral calfLateral foot  
   Heel   
L4-5L530-40Lateral thighAnterior calfDorsiflexorsNone
   Anterior calf and dorsum of footMedial foot  
   ± Great toeFirst web space  
    ± Great toe  
L3-4L42-12Lateral and anterior thighMedial calf and footQuadricepsKnee
   Medial calf and foot± Great toe  
   ± Great toe   
Cauda equina (massive central anterior prolapse)Multiple<1Bilateral, including any or all of the aboveSaddle anesthesiaMultiple, including any or all of the aboveAny or all of the above
    Any or all of the above, usually bilaterallyBladder/bowel dysfunctionAnal wink
      Cremasteric

✢More than one level of involvement in up to 10% of cases. L, Lumbar;S, sacral.



[edit] MANAGEMENT

An exhaustive evidence-based review of the management of acute low back pain culminating in a detailed clinical practice guideline was published by the Agency for Health Care Policy and Research (AHCPR) of the U.S.Public Health Service in December 1994.[5] Algorithms incorporating elements of assessment and treatment were promulgated, keying on the presence or absence of clinical “red flags” (Figs.127-5,127-6,127-7,127-8 to 127-9 and Table 127-3).

Figure 127-5 Initial assessment of acute symptoms of low back pain. CBC, Complete blood count;ESR, erythrocyte sedimentation rate;U/A, urinalysis;CT, computed tomography;MRI, magnetic resonance imaging.  (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642, Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)
Figure 127-5 Initial assessment of acute symptoms of low back pain. CBC, Complete blood count;ESR, erythrocyte sedimentation rate;U/A, urinalysis;CT, computed tomography;MRI, magnetic resonance imaging. (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642, Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)
Figure 127-6 Treatment of acute low back problems on initial and follow-up visits.  (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642.Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)
Figure 127-6 Treatment of acute low back problems on initial and follow-up visits. (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642.Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)
Figure 127-7 Evaluation of low back symptoms in patient with slow recovery and limitations beyond 4 weeks. AP, Anteroposterior;EMG, electromyography;SEP, serum electrophoresis.  (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642, Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)
Figure 127-7 Evaluation of low back symptoms in patient with slow recovery and limitations beyond 4 weeks. AP, Anteroposterior;EMG, electromyography;SEP, serum electrophoresis. (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642, Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)
Figure 127-8 Surgical considerations for patients with persistent sciatica.  (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642, Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)
Figure 127-8 Surgical considerations for patients with persistent sciatica. (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642, Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)
Figure 127-9 Further care of acute low back problems.  (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642, Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)
Figure 127-9 Further care of acute low back problems. (From Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642, Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.)


Table 127-3 Clinical “Red Flags” for Use With Management Algorithms

Modified from Bigos S, Bowyer O, Braen G, et al:Acute low back problems in adults, Clinical practice guideline no 14, AHCPR pub no 95-0642, Rockville, Md, 1994, Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services.
Suspected clinical conditionRed flag
Cancer or infectionHistory of cancer
 Unexplained weight loss
 Duration of pain longer than 1 month
 Immunosuppression (e.g., corticosteroids, transplant, HIV infection)
 Fever
 Urinary infection
 Intravenous drug use
 Back pain not improved with rest, or worse supine
 Age >50
Spinal fractureHistory of “significant” trauma
  Major trauma at any age
  Minor trauma if potentially osteoporotic
 Prolonged use of corticosteroids
 Age >70
Cauda equina syndrome (severe compromise)Acute onset urinary retention/overflow incontinence
 Loss of anal sphincter tone or fecal incontinence
 Saddle anesthesia
 Global or progressive lower extremity weakness
 



[edit] Nonpharmacologic Therapy

The favorable short-term prognosis of most variants of low back pain supports a standard approach of conservative management for 4 weeks, even with suspected intervertebral disk herniation.The generally self-limited course of low back pain has made it difficult to interpret the success of interventions other than in prospective clinical trials.Invasive studies have shown reductions of intradiskal pressure with subjects in the supine position.Previous management recommendations, based to some extent on a study of military recruits, included substantial periods of bed rest.Subsequent data demonstrated that 2 days of bed rest is as effective as 7 days and results in 45% less time lost from work.[7] In ambulatory patients with acute low back pain, continuation of ordinary activities, as permitted by the pain, may lead to more rapid recovery than either bed rest or back-mobilizing exercises.[8] While on bed rest, partial flexion of the hips and knees while in the supine or lateral decubitus position further reduces symptoms.Sitting in bed to read or watch television should be prohibited when disk herniation is suspected, because sitting increases intradiskal pressure.Intradiskal pressures are only minimally higher in the standing position than they are lying on the side, and it is reasonable to allow ambulation to the bathroom and brief periods of walking to prevent deconditioning.

In the experimental setting, traction has been shown to reduce intradiskal pressure; however, the weight required to overcome lower segment resistance and produce dimensional changes in the intervertebral disk space approximates 60% of total body weight.Clinical trials of “therapeutic” vs.“sham” traction have demonstrated no convincing benefit from the former.[9] No trials have studied inversion devices or other gravity traction methods.

No well-designed studies have demonstrated benefit from physical measures.[5] Ice massage or local heat, however, may reduce pain from muscle spasm in select patients; heat may be more effective when muscle stiffness is prominent.No data support the use of transcutaneous electrical nerve stimulation (TENS) in acute back pain, with only weak support in chronic back pain.Studies of acupuncture in the treatment of low back pain are generally of poor quality and do not support a recommendation.[5] Spinal manipulation has some benefit, particularly among patients with uncomplicatedacute low back pain,[10] whose probability of recovery at 3 to 4 weeks is slightly increased.Manipulation is not recommended for patients with radiculopathy.[5]

In experimental situations, corsets and braces can reduce intradiskal pressure, the load on the lumbar spine, and the arc of motion in flexion; however, no convincing clinical data from controlled trials demonstrate their effectiveness for acute low back pain.Their use in the chronic setting also carries the risk of muscular disuse atrophy.Nonetheless, patients sometimes derive relief from low back pain with binders or braces.Lumbar corsets, used preventively, may reduce time lost from work due to low back problems in workers who do frequent lifting.[5] Flexion braces are generally most effective for patients with lumbar spinal stenosis or when examination suggests predominantly facet joint injury (with pain on spine extension and torsion).Other patients with less well-defined sources of low back pain may obtain relief with the hydraulic splinting of abdominalbinders.The choice of device and restriction of a specific range of motion are best established after assessment by a physical therapist.Serious injury from use of back braces has been associated primarily with rigid devices in patients with scoliosis.

Low-stress aerobic exercise can prevent debilitation caused by inactivity during the first month of acute low back pain.[5] In general, patients can safely begin a slowly graduated endurance training program when they can sit comfortably.Advocated back exercise regimens include (1) spinal mobilization exercises emphasizing flexion, (2) paravertebral strengthening exercises stressing extension, and (3) modified isometric exercises directed at strengthening abdominal muscles and hip extensors.The few randomized controlled trials evaluating specific exercises for acute low back pain are limited in scope and size.The general consensus is that aprogram of gradually increased aerobic activity and back-strengthening exercises is superior to no exercise.

In occupational settings an effective low-technology intervention for backache is low back school, a multifaceted educational course on body mechanics and back care.Although results have been variable, low back schools appear to help injured workers return to their jobs more quickly than manipulation or detuned diathermy and may reduce the incidence of injuries.


[edit] Pharmacologic Therapy

Analgesics and muscle relaxants are often prescribed to treat low back pain.Several randomized, double-blind studies demonstrated that nonsteroidal antiinflammatory drugs (NSAIDs) are superior to placebo for short-term relief from low back pain.[5] A recent meta-analysis reported a pooled odds ratio for pain relief after 1 week of 0.53 (95% confidence interval, 0.32 to 0.89) in four evaluable trials comparing NSAIDs with placebo in low back pain.[11] Anumber of NSAIDs have demonstrated efficacy.Some patients with mild low back pain respond adequately to therapeutic doses of acetaminophen, 1 gm every 4 to 6 hours, although no placebo-controlled studies have been reported.Since no data support one NSAID over any other in treating low back pain, choice of therapy may be based on cost and side effects.Patients with moderate or severe low back pain who are either intolerant of or allergic to NSAIDs may take a narcotic such as codeine or oxycodone with acetaminophen, but for no more than 7 days, given the natural history of most low back pain and the potential for abuse of these agents.No clinical trials have studied the cyclooxygenase-2 inhibitors in the management of low back pain, but in prerelease studies they were no more effective than NSAIDs in treating osteoarthritis and rheumatoid arthritis.

The putative muscle relaxants carisoprodol, diazepam, and cyclobenzaprine have also proved beneficial in controlled studies of patients with low back pain, although their efficacy is partly related to central nervous system effects.No data support improved efficacy over NSAIDs, although use of one of these agents in conjunction with an NSAID may have additive benefit.Cyclobenzaprine, carisoprodol, and diazepam are all sedating.Carisoprodol and diazepam possess significant addiction potential; cyclobenzaprine, which is similar in structure to the tricyclic antidepressants, has a striking atropine-like effect.As with narcotics, these agents generally should be taken by patients with acute low back pain for no more than 7 days.

More limited clinical data exist for orphenadrine and chlorzoxazone.These agents demonstrate muscle relaxant capabilities in animals and have reduced discomfort in humans, but the mechanism is more likely related to central analgesia and mild sedation than to muscle relaxation.

In patients with chronic low back pain, tricyclic antidepressant agents have demonstrated efficacy.[12] Response to a tricyclic antidepressant may reflect a combination of mood elevation with improvement in pain threshold, improved sleep pattern with reduction in symptoms of associated fibromyalgia, and a direct effect on neuropathic pain pathways by norepinephrine reuptake blockade.Painreduction may be noted at doses less than those effective in treating depression.%No data support the use of oral corticosteroids in the management of either acute or chronic low back pain.

Injection of long-acting anesthetic agents and corticosteroids into facet joints, ligamentous structures, or the epidural space has often been used to treat low back pain.Because corticosteroid injection into facet joints is no better than saline injection, however, and because 80% of low back pain patients have no definitive anatomic diagnosis and thus no specific target for injection, this therapy should not be considered part of the standard of care for low back pain.

Chemonucleolysis involves the injection of a chymopapain to dissolve herniated disk material.It was developed as a less invasive and potentially safer intervention than disk surgery in the treatment of sciatica.Although chemonucleolysis proved effective in relieving sciatica in a prospective clinical trial—77% of those treated with chymopapain responded 6 weeks after injection, compared with 47% of controls—both anaphylaxis and severe neurologic complications (e.g., transverse myelitis) have been reported.Morbidity is comparable to or worse than that associated with disk surgery, and surgery yields more predictable early relief from sciatica.


[edit] Emotional and Behavioral Therapy

Because conservative therapy is usually effective, the initial management of most patients with acute or recurrent low back pain should be at home; this avoids reinforcing illness behavior through hospitalization and reduces health care costs and inconvenience.A major source of patient dissatisfaction is the failure of health care providers to adequately describe the problem.Because the natural history of low back pain and sciatica is generally favorable, reassurance and education are important.Prescriptions for bed rest and graded activity should be explicit, with the anticipated course of improvement.Medications should be presented as temporary adjuncts to rest and graded exercise.The physician should also discuss recurrence and encourage lifestyle changes, including weight reduction, cessation of tobacco use, and regular exercise, to minimize long-term risk.Ergonomic changes at work (e.g., work position, lifting posture) and at home (e.g., firm mattress, chairs with firm lumbar support, elevated toilet seat) reduce ongoing discomfort and lower the risk of recurrence.

The patient impaired by chronic low back pain poses a special challenge.Attention must be directed at disruptions in family dynamics caused by this chronic condition, which may have no physical findings.Substance abuse is common among patients with chronic pain and includes alcohol, prescription medications, and illegal substances.Headache, fibromyalgia, and other somatic complaints may be a proxy for depression; the patient may benefit from counseling and pharmacologic intervention.Exercise and retraining programs with psychologic support may result in a return to work.


[edit] Surgery

Emergency surgical referral is clearly indicated when epidural abscess, malignancy, or hematoma is suspected; when neurologic deficits are severe or progressive (e.g., cauda equina syndrome); or when the pattern suggests referred pain from an impending intraabdominal or retroperitoneal catastrophe (e.g., leaking abdominal aortic aneurysm).Elective surgical referral is also appropriate when severe pain and neuromotor deficits from sciatica persist despite 4 to 8 weeks of appropriate conservative therapy and are associated with clinical evidence of root compression.Surgery is also considered for persistent pain or neurologic deficits from spondylolisthesis or spinal stenosis, but generally not until at least 3 months of conservative management have been completed.

During the past decade, nearly 200,000 diskectomies were performed annually in the United States, most electively to relieve sciatica.An estimated 5% to 15% of these procedures resulted in poor outcomes and reoperation, largely because of inappropriate patient selection.[13] Serious complications occur in less than 1% of patients.The results of standard diskectomy are excellent for short-term relief from sciatica in appropriate patients.Three quarters of such patients are sciatica-free 1 year after surgery, compared with one third of patients treated conservatively.Approximately one half of patients are completely pain-free (i.e., without sciatica or back pain) 1 year after surgery.However, long-term outcomes of diskectomy and conservative care are comparable after 4 to 10 years.[5] Standard diskectomy entails a posterior longitudinal incision, removal of laminar bone, incision of the ligamentum flavum, exploration for other abnormalities, and removal of herniated disk material.Complications include dural tears, diskitis, nerve root damage, and spinal instability.Recuperation is often lengthy.

Microdiskectomy employs a magnifying scope, allowing smaller incisions with fewer anatomic disruptions.Disk fragments are more likely to be missed than with standard diskectomy, and occasionally the wrong level is entered.However, microdiskectomy and standard diskectomy have similar efficacy.

Percutaneous diskectomy uses an automated percutaneous cutting and suction probe to aspirate the nucleus pulposus of the herniated disk, with minimal risk to the spinal cord or posterior elements.Few patients are candidates for this procedure, and recurrent herniation from the same disk is common.Percutaneous diskectomy is less efficacious than chymopapain injection therapy, and neither is as effective as standard diskectomy or microdiskectomy.

Overall, only a small percentage of patients with back pain and sciatica should require surgery.Those who meet criteria for surgery generally do well, with 90% achieving at least partial relief from sciatica and back pain.Preoperative markers of a poor outcome include physical findings suggesting a behavioral disturbance; distribution and quality of pain that deviate from expected anatomic pain radiation; pending workers' compensation claims; and psychologic tests showing hysteria, hypochondriasis, and somatization.A delay in surgery beyond 12 weeks may compromise the ultimate result, especially in patients with demonstrable weakness.


[edit] Image:B0323008283501321_g000001.jpg EVIDENCE-BASED MEDICINE

Primary sources for this chapter include MEDLINE, searched through PUBMED, and the clinical practice guideline Acute Low Back Problems in Adults of the Agency for Health Care Policy and Research of the U.S.Public Health Service, published in December 1994.Electronic searches dating back to 1994 were conducted through May 1999, with a focus on systematic reviews, meta-analyses, and large randomized clinical trials.


[edit] REFERENCES

  1. LS Cunningham, JL Kelsey: Epidemiology of musculoskeletal impairments and associated disability. Am J Public Health 1984; 74:574.
  2. AL Nachemson: Newest knowledge of low back pain: a critical look. Clin Orthop 1992; 279:8.
  3. 3.0 3.1 RA Deyo, J Rainville, DL Kent: What can the history and physical examination tell us about low back pain?. JAMA 1992; 268:760.
  4. RA Deyo, AK Diehl: Lumbar spine films in primary care: current use and effects of selective ordering criteria. J Gen Intern Med 1986; 1:20.
  5. 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 S Bigos, O Bowyer, G Braen,et al.: Acute low back problems in adults, Clinical practice guideline no 14. Rockville, Md: Agency for Health Care Policy and Research, Public Health Service, US Department of Health and Human Services; 1994:AHCPR pub no 95-0642
  6. SD Boden, DO Davis, TS Dina,et al.: Abnormal magnetic-resonance scans of the lumbar spine in asymptomatic subjects. J Bone Joint Surg 1990; 72A:403.
  7. RA Deyo, AK Diehl, M Rosenthal: How many days of bed rest for acute low back pain? A randomized clinical trial. N Engl J Med 1986; 315:1064.
  8. A Malmivaara, U Hakkinen, T Aro,et al.: The treatment of acute low back pain: bed rest, exercises, or ordinary activity?. N Engl J Med 1995; 332:351.
  9. AJ Beurskens, HC de Vet, AJ Koke,et al.: Efficacy of traction for nonspecific low back pain: 12-week and 6-month results of a randomized clinical trial. Spine 1997; 22:2756.
  10. PG Shekelle, AH Adams, MR Chassin,et al.: Spinal manipulation for low-back pain. Ann Intern Med 1992; 117:590.
  11. BW Koes, RJ Scholten, JM Mens, LM Bouter: Efficacy of non-steroidal anti-inflammatory drugs for low back pain: a systematic review of randomised clinical trials. Ann Rheum Dis 1997; 56:214.
  12. JH Atkinson, MA Slater, RA Williams,et al.: A placebo-controlled randomized clinical trial of nortriptyline for chronic low back pain. Pain 1998; 76:287.
  13. RM Hoffman, KJ Wheeler, RA Deyo: Surgery for herniated lumbar discs: a literature synthesis. J Gen Intern Med 1993; 8:487.
Personal tools
related