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


Although acute low back pain usuallyresolves within 6 weeks-with or withouttreatment-the pain may signal asignificant neurologic or life-threateningdisease that warrants immediateintervention.

ABSTRACT: Most patients with nonspecificlow back pain recover spontaneously within4 to 6 weeks. Patients who resume theirnormal activities as soon as possible generallyrecover faster than those who stay inbed; analgesics speed recovery. Sciatica isusually caused by a herniated disk. However,if the patient has a demonstrable neurologicdeficit, obtain plain radiographs to ruleout tumor, spondylolisthesis, fracture, andinfection. Administer high-dose intravenouscorticosteroids immediately to patients withsuspected epidural compression syndrome.Back pain in a patient with a history of cancermay indicate metastasis to the spine. Ifa cancer patient has new or aggravatedsymptoms, start corticosteroid therapy andorder plain radiographs and MRI scans.

Although acute low back pain usuallyresolves within 6 weeks-with or withouttreatment-the pain may signal asignificant neurologic or life-threateningdisease that warrants immediateintervention.

In a previous article (CONSULTANT,September 1, 2002),we reviewed the key aspects of the initialexamination, with an emphasis on"red flags" that identify patients at riskfor serious disease. Here we focus onthe evaluation and treatment of backpain syndromes, including acute lumbosacralstrain, low back pain withsciatica, and epidural compressionsyndromes (spinal cord compression,cauda equina syndrome, and conusmedullaris syndrome). We also addressthe diagnostic dilemma of backpain in patients with a history of cancer.In an upcoming article, we will reviewthe evaluation and treatment of lowback pain in children and adolescents.

Most patients with acute low backpain have conditions that may be classifiedas acute lumbosacral strain. Thissymptom complex has differentnames, including back strain/sprain,mechanical back pain, and lumbago(acute low back pain without sciaticaor neurologic deficit). Strain and sprainhave never been histopathologicallydocumented in these patients, however.Perhaps a more accurate termwould be "idiopathic" or "nonspecific"low back pain, since a more precise diagnosiswill never be made in up to85% of these patients.1

Symptoms and diagnosis. Thepatient typically complains of mild tomoderate low back pain that is aggravatedwith movement and relieved withrest. There is usually no significantidentifiable cause of the pain, nor arethere noteworthy findings on the physicalexamination. The evaluation of anyred flags noted in the history or onphysical examination typically revealsno significant underlying condition.

Monitor such patients for 4 to 6weeks to see if symptoms improve.Some studies suggest that 90% of patientswith acute nonspecific low backpain recover spontaneously duringthis period.2 "Watchful waiting" thusensures that the patient will not losetime and money by undergoing unnecessaryprocedures. If any red flagsappear or if the patient fails to improve, further evaluation using plainradiography, MRI, or laboratory testingis indicated.1

Relapses of nonspecific low backpain occur in approximately 40% of patientswithin the first 6 months.3 A recurrenceunaccompanied by red flagsmay not require immediate referral ordiagnostic evaluation.

Treatment. Management involvesactivity and analgesia. Manipulationand other physical modalities aresometimes used, although their valueis questionable.

Activity. In recent years, the therapeuticbenefit of activity in treatingnonspecific low back pain has gainedincreasing recognition. Until the mid1980s, 7 days of strict bed rest wascommonly prescribed. In 1986, astudy showed that 2 days of bed restwas as effective as 7.4 More recently,it has been demonstrated that patientswho resumed their normal activitiesto the extent tolerable recoveredfaster than those who stayed inbed for 2 days or who performedback mobilizing exercises.5,6

Counsel patients with acute nonspecificlow back pain to continue theirroutine activities insofar as possible,using their pain as the limiting factor.Discourage exercise until the acute painhas resolved or improved significantly.

Analgesia. The mainstays of pharmacologictherapy are NSAIDs andacetaminophen. Although not allNSAIDs have been evaluated for thetreatment of low back pain, it seemslikely that they are about equally effective.7 However, one meta-analysisshowed that NSAIDs vary in theirside-effect profiles and toxicity.8Ibuprofen was the least toxic of the 12agents studied, particularly with regardto upper GI tract bleeding complications.Furthermore, there appearsto be a linear relationship betweendose and toxicity, so the lowest dosepossible should be used in patients atrisk. The concomitant use of misoprostolor omeprazole reduces the riskof clinically important GI tract bleedingduring NSAID therapy.8

Most clinicians considerNSAIDs first-line therapy for acutelow back pain; no single drug hasbeen shown to be most efficacious.However, there is no evidence thatNSAIDs are more effective thanacetaminophen for symptomatic reliefof low back pain or other musculoskeletalsyndromes.8 Thus, we recommendusing acetaminophen incombination with NSAIDs or as thesole initial agent when treating patientsat risk for adverse effects ofNSAIDs, such as the elderly and patientswith renal disease or peptic ulcers.One regimen is acetaminophen,650 to 975 mg q4 to 6h, either aloneor in conjunction with either ibuprofen,800 mg tid, or naproxen, 250 to500 mg bid (Table). A parenteralNSAID, such as ketorolac, is no moreeffective than oral ibuprofen in patientswith musculoskeletal pain.7

Table - Drug therapy for acute lumbosacral strain: sample regimen

Acetaminophen + NSAIDs
Narcotic-analgesic combinations*
Muscle relaxants

650 - 975 mg q4 - 6h
Acetaminophen, 650 - 975 mg q4 - 6h, + either ibuprofen, 800 mg tid, or naproxen, 250 - 500 mg bid
Acetaminophen, Codeine phosphate, 30 mg, + acetaminophen, 300 mg, 1 or 2 tablets q4 - 6h; or oxycodone hydrochloride, 5 mg, + acetaminophen, 325 mg, 1 or 2 tablets q4 - 6h
Diazepam, 5 - 10 mg q6 - 8h, or methocarbamol, 1000 - 1500 mg qid

*When prescribing narcotic-analgesic combinations that contain acetaminophen, warn the patient not to take another form of acetaminophen.

Narcotic analgesics may be prescribedfor patients with moderate tosevere pain. It is best not to prescribemore than 1 to 2 weeks' worth of medication.7 Combinations containing acetaminophenand either codeine phosphateor oxycodone hydrochloride arelisted in the Table. When prescribingnarcotic analgesics that include acetaminophen,warn patients not to combinethem with other acetaminophenproducts.

Other medications used to treatacute low back pain include musclerelaxants and corticosteroids. Musclerelaxants, such as diazepam, 5 to 10mg q6 to 8h, and methocarbamol, 1000to 1500 mg qid, are as effective asNSAIDs; however, there does notseem to be any synergistic benefitwhen these agents are used in combination.7 Muscle relaxants are mostuseful for treating back pain accompaniedby muscular spasms.7 Corticosteroidsinjected locally or in the epiduralspace are occasionally used, althoughtheir benefit has not beendemonstrated.7

Manipulation. Manipulative therapyis one of the more controversialtreatments of low back pain. Numerous older trials of short-term manipulativetherapy compared with othertreatments, such as medication, indicatethat manipulation may decreasepain and improve function but thatit has little or no lasting benefit.2,4However, more recent research hasshown that manipulation administeredacutely was no better thanphysical therapy and only slightly better,in terms of patient satisfactionwith care at 1 and 4 weeks, than aninexpensive educational booklet.9 Asecond study demonstrated that clinicaloutcomes with manipulationwere no better than with standardmedical therapy.10 Because the utilityand cost-effectiveness of manipulationhave not been adequately demonstrated,we do not routinely recommendit.

Other physical modalities

. Theseinclude traction, diathermy, cutaneouslaser treatment, exercise, ultrasoundtreatment, and transcutaneous electricalnerve stimulation. None of thesemodalities has been proved effectivefor acute low back symptoms. Heat orice may provide temporary symptomaticrelief in some patients. Massagehas not been adequately studied, butinitial evidence is promising.


Sciatica affects only 2% to 3% of allpatients with low back pain but is presentin 95% of patients with a symptomaticherniated nucleus pulposus(disk).11 A herniated disk is the mostcommon cause of sciatica; others includeforaminal stenosis, intraspinaltumor or infection, extraspinal plexuscompression, piriformis syndrome,and lumbar canal stenosis (spinalstenosis). Here we will discuss sciaticacaused by disk herniation and then addresssciatica attributable to epiduralcompression of the spinal cord andcauda equina.

Figure 1

Symptoms and diagnosis. Patientswho present with sciatica more frequentlyhave radicular symptoms thanback pain. Because more than 95% ofdisk herniations occur at the L4-5 orL5-S1 level (Figure 1), the radicularpain typically extends below theknee.1,4 This radicular component isuseful in differentiating true sciaticafrom nonsciatic conditions, such astrochanteric bursitis, hip osteoarthritis,and meralgia paresthetica.12

The approximately 5% of patientswho have disk herniation above theL4-5 level are older persons. In thisgroup, there is a relatively increasedrisk of disk herniation at the L2-3 andL3-4 levels. These herniations causepain in the anterior thigh, weakness ofthe quadriceps, and a diminishedpatellar reflex on the affected side.4

An additional distinguishing featureof sciatica caused by a herniateddisk is that the pain is aggravatedby sitting, coughing, or Valsalva maneuverand is relieved by lyingsupine.1,4,12,13 The physical examinationgenerally demonstrates localization ofpain, a neurologic deficit in a unilateralsingle nerve root distribution, and usuallya positive result on a straight legraise test (as discussed in our previousarticle).

If the patient has no other redflags, treat him or her conservativelyand do not perform any diagnostictests for the first 4 to 6 weeks of treatment.1,2,12-14 If the patient has a demonstrableneurologic deficit, considerobtaining plain radiographs atthe initial evaluation. These films arenot used to diagnose the herniateddisk but to rule out other possiblecauses of the patient's symptoms,such as tumor, fracture, spondylolisthesis,and infection.13

If the patient's condition worsensor the sciatica fails to improve,order an imaging study, preferablyMRI. If you suspect any conditionother than a herniated disk, considerfurther evaluations, including plainradiography of the lumbar spine,complete blood cell count, erythrocytesedimentation rate, urinalysis,and a chemistry profile.14

Medical treatment. The treatmentof patients with sciatica is similarto that of patients with lumbosacralstrain. In one study of patients with sciatica,2 weeks of bed rest was no moreeffective than watchful waiting whensuch factors as intensity of pain, bothersomenessof symptoms, and functionalstatus were assessed.15 If yourpatient's symptoms are severe enoughto warrant bed rest, recommend theshortest possible period-in most instances,no longer than 2 to 3 days.

The use of analgesics and musclerelaxants is the same as that describedfor nonspecific back pain. NSAIDs arenot as effective for sciatica as they arefor nonspecific back pain.7

Corticosteroids. One might supposethat these agents would relieve sciaticpain because of presumed nerveroot inflammation by the herniateddisk. In fact, the usefulness of corticosteroidtreatment has long been debated.Clinical tests of epidural injection haveyielded conflicting results. A meta-analysisdemonstrated a measurable, ifslight, 10% to 15% reduction of pain followingepidural corticosteroid injectioncompared with placebo.7 Proponents ofcorticosteroid administration may interpretsuch a reduction as a useful temporarymeasure that allows the patientto get through the acute pain episodewithout surgery. However, avoidance ofsurgery was not evaluated as an endpoint in most of the studies in this metaanalysis,so such a benefit would bespeculative.7 A more recent study ofepidural corticosteroid injection demonstratedshort-term improvement in legpain and sensory deficits in patientswith sciatica attributable to a herniateddisk. However, this study did not showany significant functional benefit, nordid injection obviate the need forsurgery.16

Systemic administration of corticosteroidshas not been studied as extensivelyas epidural injections. The resultsof most studies have been inconclusive,and none have compared theeffectiveness of systemic corticosteroidadministration with that of epiduralcorticosteroid injection.4

Manipulation and other physicalmodalities. The use of manipulation astreatment for sciatica is more controversialthan its use in nonspecific backpain. Proponents of this technique donot view sciatica as a contraindicationto manipulation. Guidelines drawn upby the Agency for Health Care Policyand Research recommend manipulationfor patients with sciatica only asan optional treatment that has limitedeffectiveness.2 Forceful manipulationmay cause or aggravate neurologicdeficits.4

Other physical modalities havenot been shown to be useful in managingsciatica, although, as in the caseof nonspecific back pain, heat or icemay provide temporary relief.

Surgery. Most patients with aherniated disk may be treated andmonitored without specialist referral.

Approximately 80% of patients improvewith nonsurgical therapy; more than50% recover in 6 weeks.1,4,12

Most spine surgeons agree thatsurgery is appropriate only when thefollowing criteria are met13:

  • Definitive evidence of herniation asdemonstrated by an imaging study.
  • A corresponding clinical picture andneurologic deficit.
  • Failure of conservative treatment toproduce improvement in 4 to 6 weeks.

Remember that the major benefitof surgery is to cure the sciaticaand that only about 70% of patientswho undergo surgery obtain relief ofback pain.13 Emergency decompressivesurgery is required only in patientswith acute epidural compressionsyndromes.4

Conservative nonsurgical treatmenthas been compared withsurgery for herniated disks in 2 studies.1,4 The results showed that patientswho underwent surgery hadimproved function and fewer symptomsat 1 and 2 years postoperatively,compared with those treated conservatively;however, by 4 and 10 yearspostoperatively, the results in bothgroups were comparable.

Figure 2

This term encompasses spinalcord compression (Figure 2), caudaequina syndrome, and conus medullarissyndrome. The conditions aregrouped together because their presentationsare similar (except for thelevel of neurologic deficit) and becausethe evaluation and managementare similar until the diagnosisis 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 compressivelesion of the spinal cord orcauda equina. Confirm your evaluationby diagnostic testing.

Possible causes of epidural compressioninclude spinal canal hemorrhage,tumors of the spine or epiduralspace, spinal canal infections, andmassive midline disk herniation.Transverse myelitis is a noncompressivecondition that may present exactlylike a compressive lesion of thespinal cord.17

History. The history of patientswith epidural compression usually includesback pain with associated neurologicdeficits, incontinence, and sciaticain 1 or both legs. The duration ofsymptoms does not help differentiatethese syndromes from benign causesof back pain. Important features are ahistory of malignancy (Box) and rapidprogression of neurologic symptoms,especially bilateral symptoms. Withthese exceptions, the history is nothelpful.

Physical examination. The physicalexamination findings depend onthe level of compression and the extentto which the spinal cord or caudaequina is compressed. The most commonfinding in cauda equina syndromeis urinary retention with overflowincontinence; it has a sensitivity of90% and a specificity of about 95%.18This proves useful in patients who presentwith back pain and an ambiguoushistory of urinary incontinence. Evaluatethese patients by checking urinarypostvoid residual volume. The absenceof postvoid residual volume has a negativepredictive value for cauda equinasyndrome that approaches 99.9%.18However, we do not recommend relyingon this test alone to evaluate a patientwho presents with other majorneurologic deficits.

Other common findings in patientswith epidural compression includeweakness or stiffness in thelower extremities, paresthesias or sensorydeficits, gait difficulty, and abnormalresults on straight leg raising.18The most common sensory deficit--usually called "saddle anesthesia"--occursover the buttocks, posterosuperiorthighs, and perineal regions. Analsphincter tone is decreased in 60% to80% of patients.18

Treatment. When you clinicallysuspect epidural compression, especiallywhen it might be associated witha tumor, administer high-dose intravenouscorticosteroids before orderingother tests or attempting to make a definitivediagnosis. Instituting such treatmentimmediately may help minimizeprogression of the compression andthe resulting neurologic damage. Althoughthere have been no controlledstudies, one review of epidural compressionresulting from neoplasm recommendsdexamethasone, 100 mgIV.19 This recommendation is based onseveral studies that showed rapid reliefof pain, as well as one animal study thatdemonstrated improved function. Adose of 10 mg of dexamethasone is reasonablefor a patient whose symptomsare minimal or ambiguous. No studieshave evaluated whether corticosteroidsimprove the outcome of epidural compressionresulting from disk herniation,infection, or hemorrhage.

Imaging. After administering thecorticosteroid, 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 specialistyou consult for further managementdepends on your initial diagnosticsuspicion and the MRI results.Generally, if the patient is youngerthan 50 years and has no history ofcancer, his condition is more likely tobe caused by a dysfunction that requiressurgery, such as a midline herniateddisk. Consultation with a spinesurgeon would thus be appropriate. Ifthe patient has a history of cancer oris older than 50 years, metastatic diseaseis more likely; consultation witha radiation therapist and an oncologistis recommended.

Outcome. For patients who havespinal cord compression attributable totumors, the outcome depends on presentingsymptoms. Patients who cannotwalk before treatment rarely walkagain. Those who are too weak to walkwithout assistance but who are notparaplegic have a 50% chance of walkingagain. Those who are able to walkwhen treatment begins are likely to remainambulatory.19 Of patients who requirea catheter for urinary retentionbefore treatment, 82% will continueto require the catheter afterwards.20These poor outcomes are the reasonwe recommend immediate aggressivemanagement with corticosteroids andMRI in patients with suspected epiduralcompression.


REFERENCES: 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 BackProblems in Adults: Clinical Practice Guideline: QuickReference Guide Number 14. Rockville, Md: Agencyfor Health Care Policy and Research, US Dept ofHealth and Human Services; 1994. AHCPR publication95-0643.
3. Carey TS, Garrett JM, Jackman A, et al, for theNorth Carolina Back Pain Project. Recurrence andcare seeking after acute back pain: results of a longtermfollow-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. Thetreatment 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 Cochranereview of bed rest for acute low back pain and sciatica.Spine. 2000;25:2932-2939.
7. Deyo RA. Drug therapy for back pain. Whichdrugs help which patients. Spine. 1996;21:2840-2850.
8. Gotzsche PC. Non-steroidal anti-inflammatorydrugs. BMJ. 2000;320:1058-1061.
9. Cherkin D, Deyo R, Battie M, et al. A comparisonof physical therapy, chiropractic manipulation,and provision of an educational booklet for the treatmentof patients with low back pain. N Engl J Med.1998;339:1021-1029.
10. Andersson GB, Lucente T, Davis AM, et al. Acomparison of osteopathic spinal manipulation withstandard care for patients with low back pain. N EnglJ Med. 1999;341:1426-1431.
11. Connelly C. Patients with low back pain. PostgradMed. 1996;100:143-156.
12. Mazanec D. Back pain: medical evaluation andtherapy. Cleve Clin J Med. 1995;62:163-168.
13. Deyo RA, Loeser JD, Bigos SJ. Herniated lumbarintervertebral disk. Ann Intern Med. 1990;112:598-603.
14. Deen G. Diagnosis and management of lumbardisk disease. Mayo Clin Proc. 1996;71:283-287.
15. Vroomen P, de Krom M, Wilmink J, et al. Lackof effectiveness of bed rest for sciatica. N Engl J Med.1999;340:418-423.
16. Carette S, Leclaire R, Marcoux S, et al. Epiduralcorticosteroid injections for sciatica due to herniatednucleus pulposus. N Engl J Med. 1997;336:1634-1640.
17. Schmidt R, Markovchick V. Nontraumatic spinalcord compression. J Emerg Med. 1992;10:189-199.
18. Deyo RA, Rainville J, Kent DL. What can thehistory and physical examination tell us about lowback pain? JAMA. 1992;268:760-765.
19. Portenoy R, Lipton R, Foley K. Back pain in thecancer patient: an algorithm for evaluation and management.Neurology. 1987;37:134-138.
20. Helweg-Larsen S. Clinical outcome in metastaticspinal cord compression: a prospective study of153 patients. Acta Neurol Scand. 1996;94:269-275.
21. Sasso R, Cotler HB, Guyer RD. Evaluating lowback pain: the role of diagnostic imaging. J MusculoskelMed. 1991;8(5):21-37.

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