Acute Low Back Pain:

Acute Low Back Pain:

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 a previous article (CONSULTANT, September 1, 2002, page 1277), we reviewed the key aspects of the initial examination, with an emphasis on "red flags" that identify patients at risk for serious disease. Here we focus on the evaluation and treatment of back pain syndromes, including acute lumbosacral strain, low back pain with sciatica, and epidural compression syndromes (spinal cord compression, cauda equina syndrome, and conus medullaris syndrome). We also address the diagnostic dilemma of back pain in patients with a history of cancer. In an upcoming article, we will review the evaluation and treatment of low back pain in children and adolescents.


Most patients with acute low back pain have conditions that may be classified as acute lumbosacral strain. This symptom complex has different names, including back strain/sprain, 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. Perhaps a 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

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 90% of patients with acute nonspecific low back pain recover spontaneously during this period.2 "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

Relapses of nonspecific low back pain occur in approximately 40% of patients within the first 6 months.3 A recurrence unaccompanied by red flags may not require immediate referral or diagnostic evaluation.

Treatment. Management involves activity and analgesia. Manipulation and other physical modalities are sometimes used, although their value 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 7.4 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 for 2 days or who performed back mobilizing exercises.5,6

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.7 However, one meta-analysis showed that NSAIDs vary in their side-effect profiles and toxicity.8 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.8

Most clinicians consider NSAIDs first-line therapy for acute low back pain; no single drug has been shown to be most efficacious. However, there is no evidence that NSAIDs are more effective than acetaminophen for symptomatic relief of low back pain or other musculoskeletal syndromes.8 Thus, we 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, 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.7

Narcotic 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.7 Combinations containing acetaminophen and either codeine phosphate or oxycodone hydrochloride are listed in the Table. When prescribing narcotic 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.7 Muscle relaxants are most useful for treating back pain accompanied by muscular spasms.7 Corticosteroids injected locally or in the epidural space are occasionally used, although their benefit has not been demonstrated.7

Manipulation. Manipulative therapy is one of the more controversial treatments of low back pain. Numerous older trials of short-term manipulative therapy compared with other treatments, such as medication, indicate that manipulation may decrease pain and improve function but that it has little or no lasting benefit.2,4 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.9 A second study demonstrated that clinical outcomes with manipulation were no better than with standard medical therapy.10 Because the utility and cost-effectiveness of manipulation have not been adequately demonstrated, we do not routinely recommend it.

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


Sciatica affects only 2% to 3% of all patients with low back pain but is present in 95% of patients with a symptomatic herniated nucleus pulposus (disk).11 A herniated disk 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 we will discuss sciatica caused by disk herniation and then address sciatica attributable to epidural compression of the spinal cord and cauda equina.

Symptoms and diagnosis. Patients who present with sciatica more frequently have radicular symptoms than back pain. Because more than 95% of disk herniations occur at the L4-5 or L5-S1 level (Figure 1), the radicular pain typically extends below the knee.1,4 This radicular component is useful in differentiating true sciatica from nonsciatic conditions, such as trochanteric bursitis, hip osteoarthritis, and meralgia paresthetica.12

The approximately 5% of patients who have disk herniation above the L4-5 level are older persons. In this group, there is a relatively increased risk of disk 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.4

An additional distinguishing feature of sciatica caused by a herniated disk is that the pain is aggravated by sitting, coughing, or Valsalva maneuver and is relieved by lying supine.1,4,12,13 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 our previous article).

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.1,2,12-14 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 disk but to rule out other possible causes of the patient's symptoms, such as tumor, fracture, spondylolisthesis, and infection.13

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 disk, consider further evaluations, including plain radiography of the lumbar spine, complete blood cell count, erythrocyte sedimentation rate, urinalysis, and a chemistry profile.14

Medical treatment. The treatment of patients with sciatica is similar to that of patients with lumbosacral strain. 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.15 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.

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.7

Corticosteroids. One might suppose that these agents would relieve sciatic pain because of presumed nerve root inflammation by the herniated disk. 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.7 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.7 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 disk. However, this study did not show any significant functional benefit, nor did injection obviate the need for surgery.16

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.4

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 drawn up by the Agency for Health Care Policy and Research recommend manipulation for patients with sciatica only as an optional treatment that has limited effectiveness.2 Forceful manipulation may cause or aggravate neurologic deficits.4

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 disk may be treated and monitored without specialist referral. Approximately 80% of patients improve with nonsurgical therapy; more than 50% recover in 6 weeks.1,4,12

Most spine surgeons agree that surgery is appropriate only when the following criteria are met13:

Definitive evidence of herniation as demonstrated by 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 cure the sciatica and that only about 70% of patients who undergo surgery obtain relief of back pain.13 Emergency decompressive surgery is required only in patients with acute epidural compression syndromes.4

Conservative nonsurgical treatment has been compared with surgery for herniated disks in 2 studies.1,4 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.


This term encompasses spinal cord compression (Figure 2), 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 disk herniation. Transverse myelitis is a noncompressive condition that may present exactly like a compressive lesion of the spinal cord.17

History. The history of patients with epidural compression usually includes back pain with associated neurologic deficits, incontinence, and sciatica in 1 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 helpful.

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%.18 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%.18 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.18 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.18

Treatment. When you clinically suspect epidural compression, especially when it might be associated with a tumor, administer high-dose intravenous corticosteroids before ordering other tests or attempting to make a definitive diagnosis. Instituting such treatment immediately may help minimize progression of the compression and the resulting neurologic damage. Although there have been no controlled studies, one review of epidural compression resulting from neoplasm recommends dexamethasone, 100 mg IV.19 This recommendation is based on several studies that showed rapid relief of pain, as well as one animal study that demonstrated improved function. A dose of 10 mg of dexamethasone is reasonable for a patient whose symptoms are minimal or ambiguous. No studies have evaluated whether corticosteroids improve the outcome of epidural compression resulting from disk herniation, infection, or hemorrhage.

Imaging. After administering the corticosteroid, obtain plain radiographs of the suspected area of spine involvement. These may be omitted if you plan to order an emergent MRI. If you suspect epidural compression resulting from neoplasm, an MRI 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.19 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 disk herniation, it is reasonable to obtain a localized MRI.

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 disk. 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 a radiation therapist and an oncologist is recommended.

Outcome. For patients who have spinal cord 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.19 Of patients who require a catheter for urinary retention before treatment, 82% will continue to require the catheter afterwards.20 These poor outcomes are the reason we recommend immediate aggressive management with corticosteroids and MRI in patients with suspected epidural compression. n



1. Deyo R, Weinstein J. Low back pain. N Engl J Med. 2001;344:363-370.

2. Bigos S, Bowyer O, Braen G, et al. Acute Low Back Problems in Adults: Clinical Practice Guideline: Quick Reference Guide Number 14. Rockville, Md: Agency for Health Care Policy and Research, US Dept of Health and Human Services; 1994. AHCPR publication 95-0643.

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

4. Frymoyer J. Back pain and sciatica. N Engl J Med. 1988;318:291-300.

5. Malmivaara A, Hakkinen U, Aro T, et al. The treatment of acute low back pain: bed rest, exercise, or ordinary activity. N Engl J Med. 1995;332: 321-325.

6. Hagen KB, Jamtvedt G, Winnem MF. The Cochrane review of bed rest for acute low back pain and sciatica. Spine. 2000;25:2932-2939.

7. Deyo RA. Drug therapy for back pain. Which drugs help which patients. Spine. 1996;21:2840-2850.

8. Gotzsche PC. Non-steroidal anti-inflammatory drugs. BMJ. 2000;320:1058-1061.

9. Cherkin D, Deyo R, Battie M, et al. A compari-son of physical therapy, chiropractic manipulation, and provision of an educational booklet for the treatment of patients with low back pain. N Engl J Med. 1998;339:1021-1029.

10. 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;341:1426-1431.

11. Connelly C. Patients with low back pain. Postgrad Med. 1996;100:143-156.

12. Mazanec D. Back pain: medical evaluation and therapy. Cleve Clin J Med. 1995;62:163-168.

13. Deyo RA, Loeser JD, Bigos SJ. Herniated lumbar intervertebral disk. Ann Intern Med. 1990;112:598-603.

14. Deen G. Diagnosis and management of lumbar disk disease. Mayo Clin Proc. 1996;71:283-287.

15. Vroomen P, de Krom M, Wilmink J, et al. Lack of effectiveness of bed rest for sciatica. N Engl J Med. 1999;340:418-423.

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

17. Schmidt R, Markovchick V. Nontraumatic spinal cord compression. J Emerg Med. 1992;10:189-199.

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

19. Portenoy R, Lipton R, Foley K. Back pain in the cancer patient: an algorithm for evaluation and management. Neurology. 1987;37:134-138.

20. Helweg-Larsen S. Clinical outcome in metastatic spinal cord compression: a prospective study of 153 patients. Acta Neurol Scand. 1996;94:269-275.

21. Sasso R, Cotler HB, Guyer RD. Evaluating low back pain: the role of diagnostic imaging. J Musculoskel Med. 1991;8(5):21-37.

Loading comments...
Please Wait 20 seconds or click here to close