back pain

Acute Low Back Pain: Guidelines for Treating Common—and Uncommon—Syndromes

DAVID DELLA-GIUSTINA, MD
Yale University

Dr Della-Giustina is the chief of education and the director of the emergency medicine residency program at the Yale University School of Medicine in New Haven, Connecticut.

 

 

ABSTRACT: Most patients with nonspecific low back pain recover spontaneously within 4 to 6 weeks. Patients who resume their normal activities as soon as possible generally recover faster than those who stay in bed; analgesics speed recovery. Sciatica is usually caused by a herniated disc. Administer high-dose intravenous corticosteroids immediately to patients with suspected epidural compression syndrome. Back pain in a patient with a history of cancer may indicate metastasis to the spine. If a cancer patient has new or aggravated symptoms, consider corticosteroid therapy and order an MRI scan.

Key words: back pain, herniated disc, epidural compression syndrome


Although acute low back pain usually resolves within 6 weeks—with or without treatment—the pain may signal a significant neurologic or life-threatening disease that warrants immediate intervention.

In my article on page 436 of this issue, I reviewed the key aspects of the initial examination, with an emphasis on “red flags” that identify patients at risk for serious disease. Here I focus on the evaluation and treatment of back pain syndromes, including nonspecific back pain, low back pain with sciatica, and epidural compression syndromes (spinal cord compression, cauda equina syndrome, and conus medullaris syndrome). I also address the diagnostic dilemma of back pain in patients with a history of cancer. In an upcoming article, I will review the evaluation and treatment of low back pain in children and adolescents.

NONSPECIFIC BACK PAIN

Most patients with acute low back pain have conditions that may be generally classified as nonspecific back pain. This symptom complex has different names, including back strain/sprain, acute lumbosacral strain, mechanical back pain, and lumbago (acute low back pain without sciatica or neurologic deficit). Strain and sprain have never been histopathologically documented in these patients, however. The more accurate term would be “idiopathic” or “nonspecific” low back pain, since a more precise diagnosis will never be made in up to 85% of these patients.1,2

Symptoms and diagnosis. The patient typically complains of mild to moderate low back pain that is aggravated with movement and relieved with rest. There is usually no significant identifiable cause of the pain, nor are there noteworthy findings on the physical examination. The evaluation of any red flags noted in the history or on physical examination typically reveals no significant underlying condition.

Monitor such patients for 4 to 6 weeks to see if symptoms improve. Some studies suggest that 85% to 90% of patients with acute nonspecific low back pain recover spontaneously during this period.1,3 “Watchful waiting” thus ensures that the patient will not lose time and money by undergoing unnecessary procedures. If any red flags appear or if the patient fails to improve, further evaluation using plain radiography, MRI, or laboratory testing is indicated.1,3

Relapses of nonspecific low back pain occur in approximately 40% of patients within the first 6 months.4 A recurrence unaccompanied by red flags may not require immediate referral or further diagnostic evaluation.

Treatment. Management involves activity and analgesia. Manipulation and other physical modalities are sometimes used, although the value of these treatments is questionable.

Activity. In recent years, the therapeutic benefit of activity in treating nonspecific low back pain has gained increasing recognition. Until the mid 1980s, 7 days of strict bed rest was commonly prescribed. In 1986, a study showed that 2 days of bed rest was as effective as 7 days.5 More recently, it has been demonstrated that patients who resumed their normal activities to the extent tolerable recovered faster than those who stayed in bed or who performed back mobilizing exercises.1,6,7

Counsel patients with acute nonspecific low back pain to continue their routine activities insofar as possible, using their pain as the limiting factor. Discourage exercise until the acute pain has resolved or improved significantly.

Analgesia. The mainstays of pharmacologic therapy are NSAIDs and acetaminophen. Although not all NSAIDs have been evaluated for the treatment of low back pain, it seems likely that they are about equally effective.1,8-10 However, one meta-analysis showed that NSAIDs vary in their side-effect profiles and toxicity.11 Ibuprofen was the least toxic of the 12 agents studied, particularly with regard to upper GI tract bleeding complications. Furthermore, there appears to be a linear relationship between dose and toxicity, so the lowest dose possible should be used in patients at risk. The concomitant use of misoprostol or omeprazole reduces the risk of clinically important GI tract bleeding during NSAID therapy.11

Most clinicians consider NSAIDs first-line therapy for acute low back pain. However, there is no evidence that NSAIDs are more effective than acetaminophen for symptomatic relief of low back pain or other musculoskeletal syndromes.1,11 Thus, I recommend using acetaminophen in combination with NSAIDs or as the sole initial agent when treating patients at risk for adverse effects of NSAIDs, such as the elderly and patients with renal disease or peptic ulcers. One regimen is acetaminophen, 650 to 975 mg q4 to 6h, either alone or in conjunction with either ibuprofen, 600 to 800 mg tid, or naproxen, 250 to 500 mg bid (Table). A parenteral NSAID, such as ketorolac, is no more effective than oral ibuprofen in patients with musculoskeletal pain.8

table back pain

 

(Click to enlarge)

Opiate analgesics may be prescribed for patients with moderate to severe pain. It is best not to prescribe more than 1 to 2 weeks’ worth of medication. Combinations containing acetaminophen and either codeine phosphate or oxycodone hydrochloride are listed in the Table. When prescribing opiate analgesics that include acetaminophen, warn patients not to combine them with other acetaminophen products.

Other medications used to treat acute low back pain include muscle relaxants and corticosteroids. Muscle relaxants, such as diazepam, 5 to 10 mg q6 to 8h, and methocarbamol, 1000 to 1500 mg qid, are as effective as NSAIDs; however, there does not seem to be any synergistic benefit when these agents are used in combination.1,8 Muscle relaxants are most useful for treating back pain accompanied by muscular spasms.1,8 Systemic corticosteroids are not recommended because their benefit has not been demonstrated.1,8,12

Manipulation. Manipulative therapy is one of the more controversial treatments of acute low back pain. Numerous older trials of short-term manipulative therapy compared with other treatments, such as medication, indicated that manipulation may decrease pain and improve function but that it has little or no lasting benefit.3,5 However, more recent research has shown that manipulation administered acutely was no better than physical therapy and only slightly better, in terms of patient satisfaction with care at 1 and 4 weeks, than an inexpensive educational booklet.13 A second study demonstrated that clinical outcomes with manipulation were no better than those with standard medical therapy.14 Finally, a recent Cochrane Review concluded that spinal manipulative therapy was no better than standard interventions for acute low back pain.15

Other physical modalities. These include traction, diathermy, cutaneous laser treatment, exercise, ultrasound treatment, and transcutaneous electrical nerve stimulation. None of these modalities has been proved effective for acute low back symptoms. Heat or ice may provide temporary symptomatic relief in some patients. Massage has not been adequately studied, but initial evidence is promising.1,2

SCIATICA AND DISC HERNIATION

Sciatica is a broad term that is defined as a radicular pain into the leg in the distribution of a lumbosacral nerve root, which is often accompanied by a sensory or motor deficit.1,5 Sciatica affects only 2% to 3% of all patients with low back pain but is present in 95% of patients with a symptomatic herniated disc.1,2,5,16 A herniated disc is the most common cause of sciatica; others include foraminal stenosis, intraspinal tumor or infection, extraspinal plexus compression, piriformis syndrome, and lumbar canal stenosis (spinal stenosis). Here I will discuss sciatica caused by disc herniation and then address sciatica attributable to epidural compression of the spinal cord and cauda equina.

Symptoms and diagnosis. Patients who present with low back pain with sciatica more frequently complain of the radicular symptoms than the back pain. Because more than 95% of disc herniations occur at the L4-5 or L5-S1 level, the radicular pain typically extends below the knee in the dermatomal distribution of that specific nerve root.1,2,5,16 This radicular component is useful in differentiating true sciatica from nonsciatic conditions, such as trochanteric bursitis, hip osteoarthritis, and meralgia paresthetica.17

The approximately 5% of patients who have disc herniation above the L4-5 level are older persons. In this group, there is a relatively increased risk of disc herniation at the L2-3 and L3-4 levels. These herniations cause pain in the anterior thigh, weakness of the quadriceps, and a diminished patellar reflex on the affected side.5,16

An additional distinguishing feature of sciatica caused by a herniated disc is that the pain is aggravated by sitting, coughing, or Valsalva maneuver and is relieved by lying supine.2,5,16,17 The physical examination generally demonstrates localization of pain, a neurologic deficit in a unilateral single nerve root distribution, and usually a positive result on a straight leg raise test (as discussed in my article on page 436).

If the patient has no other red flags, treat him or her conservatively and do not perform any diagnostic tests for the first 4 to 6 weeks of treatment.1,2,5,16,17 If the patient has a demonstrable neurologic deficit, consider obtaining plain radiographs at the initial evaluation. These films are not used to diagnose the herniated disc but to rule out other possible causes of the patient’s symptoms, such as tumor, fracture, spondylolisthesis, and infection.

If the patient’s condition worsens or the sciatica fails to improve, order an imaging study, preferably MRI. If you suspect any condition other than a herniated disc, consider further evaluations including a complete blood cell count, erythrocyte sedimentation rate, urinalysis, and a chemistry profile.18

Medical treatment. The treatment of patients with sciatica is similar to that of patients with nonspecific back pain. In one study of patients with sciatica, 2 weeks of bed rest was no more effective than watchful waiting when such factors as intensity of pain, bothersomeness of symptoms, and functional status were assessed. If your patient’s symptoms are severe enough to warrant bed rest, recommend the shortest possible period—in most instances, no longer than 2 to 3 days.1,6,19

The use of analgesics and muscle relaxants is the same as that described for nonspecific back pain. NSAIDs are not as effective for sciatica as they are for nonspecific back pain.1,8,10,16

Corticosteroids. One might suppose that these agents would relieve sciatic pain because of presumed nerve root inflammation by the herniated disc. In fact, the usefulness of corticosteroid treatment has long been debated. Clinical tests of epidural injection have yielded conflicting results. A meta-analysis demonstrated a measurable, if slight, 10% to 15% reduction of pain following epidural corticosteroid injection compared with placebo.8 Proponents of corticosteroid administration may interpret such a reduction as a useful temporary measure that allows the patient to get through the acute pain episode without surgery. However, avoidance of surgery was not evaluated as an end point in most of the studies in this meta-analysis, so such a benefit would be speculative.8

A more recent study of epidural corticosteroid injection demonstrated short-term improvement in leg pain and sensory deficits in patients with sciatica attributable to a herniated disc. However, this study did not show any significant functional benefit, nor did injection obviate the need for surgery.20

Systemic administration of corticosteroids has not been studied as extensively as epidural injections. The results of most studies have been inconclusive, and none have compared the effectiveness of systemic corticosteroid administration with that of epidural corticosteroid injection.5

Manipulation and other physical modalities.The use of manipulation as treatment for sciatica is more controversial than its use in nonspecific back pain. Proponents of this technique do not view sciatica as a contraindication to manipulation. Guidelines developed by the Agency for Health Care Policy and Research recommend manipulation for patients with sciatica only as an optional treatment that has limited effectiveness.3 Forceful manipulation may cause or aggravate neurologic deficits.5

Other physical modalities have not been shown to be useful in managing sciatica, although, as in the case of nonspecific back pain, heat or ice may provide temporary relief.

Surgery. Most patients with a herniated disc may be treated and monitored without specialist referral. Approximately 80% of patients improve with nonsurgical therapy; more than 50% recover in 6 weeks.1,2,5,16,21

Most spine surgeons agree that surgery is appropriate only when the following criteria are met16,21:

•Definitive evidence of herniation on an imaging study.

•A corresponding clinical picture and neurologic deficit.

•Failure of conservative treatment to produce improvement in 4 to 6 weeks.

Remember that the major benefit of surgery is to relieve the radicular symptoms and neurologic deficit and that only about 70% of patients who undergo surgery obtain relief of back pain.16 Emergency decompressive surgery is required only in patients with acute epidural compression syndromes.5,21

Conservative nonsurgical treatment has been compared with surgery for herniated discs in several studies. The results showed that patients who underwent surgery had improved function and fewer symptoms at 1 and 2 years postoperatively, compared with those treated conservatively; however, by 4 and 10 years postoperatively, the results in both groups were comparable.2,5,21,22

EPIDURAL COMPRESSION SYNDROME

This term encompasses spinal cord compression, cauda equina syndrome, and conus medullaris syndrome. The conditions are grouped together because their presentations are similar (except for the level of neurologic deficit) and because the evaluation and management are similar until the diagnosis is known.

Symptoms and diagnosis. The most serious diagnosis in a patient who presents with back pain is epidural compression syndrome. Although the diagnosis of complete epidural compression is obvious, evaluating patients with early signs and symptoms is more difficult; the initial differential diagnosis is broad and includes most conditions that cause weakness, sensory changes, or autonomic dysfunction. The history and physical examination will enable you to narrow the differential to a compressive lesion of the spinal cord or cauda equina. Confirm your evaluation by diagnostic testing.

Possible causes of epidural compression include spinal canal hemorrhage, tumors of the spine or epidural space, spinal canal infections, and massive midline disc herniation. Transverse myelitis is a noncompressive condition that may present exactly like a compressive lesion of the spinal cord.

History. The history of patients with epidural compression usually includes back pain with associated neurologic deficits, incontinence, and sciatica in one or both legs. The duration of symptoms does not help differentiate these syndromes from benign causes of back pain. Important features are a history of malignancy (Box) and rapid progression of neurologic symptoms, especially bilateral symptoms. With these exceptions, the history is not generally helpful.

highlights back pain nsaids

Physical examination. The physical examination findings depend on the level of compression and the extent to which the spinal cord or cauda equina is compressed. The most common finding in cauda equina syndrome is urinary retention with overflow incontinence; it has a sensitivity of 90% and a specificity of about 95%.1,23 This proves useful in patients who present with back pain and an ambiguous history of urinary incontinence. Evaluate these patients by checking urinary postvoid residual volume. The absence of postvoid residual volume has a negative predictive value for cauda equina syndrome that approaches 99.9%.23 However, we do not recommend relying on this test alone to evaluate a patient who presents with other major neurologic deficits.

Other common findings in patients with epidural compression include weakness or stiffness in the lower extremities, paresthesias or sensory deficits, gait difficulty, and abnormal results on straight leg raising.23 The most common sensory deficit—usually called “saddle anesthesia”—occurs over the buttocks, posterosuperior thighs, and perineal regions. Anal sphincter tone is decreased in 60% to 80% of patients.23

Treatment. When you clinically suspect epidural compression, especially when it may be associated with a tumor, administer corticosteroids before ordering tests or attempting to make a definitive diagnosis. The acute use of corticosteroids in the patient with epidural compression from disc herniation, epidural abscess, or hematoma is controversial, and there is no definitive answer. For the patient with potentially metastatic disease, a wide range of dosing for dexamethasone (10 to 100 mg IV) has been suggested.24-26 The current recommended approach is to administer 10 to 16 mg of dexamethasone IV to the patient with known cancer and signs of epidural compression.24,27

Imaging. After administering the dexamethasone, the patient requires emergent imaging with MRI. In the past, it was recommended that one obtain plain radiographs initially and then use them to help determine whether further imaging was necessary. This is no longer recommended because plain films add time and expense but not much clinically important information to the initial evaluation.25,27 Plain films will completely miss epidural metastases. For example, more than 60% of patients with lymphoma and epidural metastases have normal plain radiographs.26

If you suspect epidural compression resulting from neoplasm, an MRI scan of the entire spine is recommended, because 10% of patients with vertebral metastases have additional silent epidural metastases that would be missed by a localized imaging study.25-27 The presence of these tumors remote from the symptomatic site may change the management strategy. If you suspect cauda equina syndrome resulting from a massive central disc herniation, it is reasonable to obtain a localized MRI scan.

back pain cancer

Specialist referral. Which specialist you consult for further management depends on your initial diagnostic suspicion and the MRI results. Generally, if the patient is younger than 50 years and has no history of cancer, his condition is more likely to be caused by a dysfunction that requires surgery, such as a midline herniated disc. Consultation with a spine surgeon would thus be appropriate. If the patient has a history of cancer or is older than 50 years, metastatic disease is more likely; consultation with both a radiation oncologist and an oncologist is recommended.

Outcome. For patients who have epidural compression attributable to tumors, the outcome depends on presenting symptoms. Patients who cannot walk before treatment, rarely walk again. Those who are too weak to walk without assistance but who are not paraplegic have a 50% chance of walking again. Those who are able to walk when treatment begins are likely to remain ambulatory.25-28 Of patients who require a catheter for urinary retention before treatment, most will continue to require the catheter afterwards.25,27,28 

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4.Carey TS, Garrett JM, Jackman A, et al. Recurrence and care seeking after acute back pain: results of a long-term follow-up study. North Carolina Back Pain Project. Med Care. 1999;37(2):157-164.

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7.Malmivaara A, Hakkinen U, Aro T, et al. The treatment of acute low back pain—bed rest, exercises, or ordinary activity? N Engl J Med. 1995;332(6):351-355.

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14.Andersson GB, Lucente T, Davis AM, et al. A comparison of osteopathic spinal manipulation with standard care for patients with low back pain. N Engl J Med. 1999;341(19):1426-1431.

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19.Vroomen PC, de Krom MC, Wilmink JT, et al. Lack of effectiveness of bed rest for sciatica. N Engl J Med. 1999;340(6):418-423.

20.Carette S, Leclaire R, Marcoux S, et al. Epidural corticosteroid injections for sciatica due to herniated nucleus pulposus. N Engl J Med. 1997;336(23):1634-1640.

21.Awad JN, Moskovich R. Lumbar disc herniations: surgical versus nonsurgical treatment. Clin Orthop Relat Res. 2006;443:183-197.

22.Hahne AJ, Ford JJ, McMeeken JM. Conservative management of lumbar disc herniation with associated radiculopathy: a systematic review. Spine (Phila Pa 1976). 2010;35(11):E488-E504.

23. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA. 1992;268(6):760-765.

24. Chamberlain MC. Neoplastic meningitis and metastatic epidural spinal cord compression. Hematol Oncol Clin North Am. 2012;26(4):917-931.

25. Penas-Prado M, Loghin ME. Spinal cord compression in cancer patients: review of diagnosis and treatment. Curr Oncol Rep. 2008;10(1):78-85.

26. Portenoy RK, Lipton RB, Foley KM. Back pain in the cancer patient: an algorithm for evaluation and management. Neurology. 1987;37(1):134-138.

27. Cole JS, Patchell RA. Metastatic epidural spinal cord compression. Lancet Neurol. 2008;7(5):459-466.

28. Helweg-Larsen S. Clinical outcome in metastatic spinal cord compression. A prospective study of 153 patients. Acta Neurol Scand. 1996;94(4):269-275.