A Pain in the Back
On the next chart you pick up, the triage nurse has written, "Back pain, needs med refill." What is your honest reaction? Mine, too. But after evaluating the patient, sometimes I am embarrassed that my initial reaction was negative. Nationally, about 4% of emergency department visits are for back and spine pain, and most of these are for benign and self-limited conditions. However, in this diverse group are potentially serious and progressive conditions that can lead to bad outcomes. It's our job to detect these patients. This manuscript presents an organized approach to evaluate and classify patients with back pain. After reading this, I was able to approach the next "back pain, med refill" patient with a better attitude. Maybe you will, too.
J. Stephan Stapczynski, MD, FACEP, Editor
This article originally appeared in the October 2008 issue of Primary Care Reports.
Disclaimer: The opinions and assertions contained herein are the private views of the author and should not be construed as official or as reflecting the views of the Department of Army or the Department of Defense.
Introduction
Back pain is a ubiquitous complaint in medicine. The evaluation and management of these patients varies based on several risk factors for serious disease called the red flags of back pain. Consider the management of the following patient: A 44-year-old healthy female presents with back pain for 3 days. If she has a normal physical examination and no neurological complaints, then her management and disposition would be quick and without any major concerns. However, if she has a history of breast cancer, then the evaluation would be more thorough with the disposition requiring close follow-up. On the other hand, the evaluation and disposition would differ if she had no cancer history but had a history of injection drug use. These scenarios are just a few of several that physicians may face on a daily basis when caring for patients with back pain.
Epidemiology
Back pain is a common problem that accounts for approximately 4% of emergency department (ED) visits.1 Back pain affects up to 90% of the population at some point in their lives, with up to 85% of these patients having no definite etiology determined for their symptoms.2 In 2002, the three-month prevalence of low back pain in adults in the United States was 34 million.3 It is estimated that the economic burden for spine problems in 2005 was more than $85 billion, with only expenditures for heart disease and stroke being substantially higher.4 Fortunately, for almost 90% of patients with nonspecific back pain, their symptoms will resolve within 1 month.2
Clinical Presentation
The clinical presentation of the patient with back pain ranges from the patient with mild pain due to muscle spasm to the patient with the severe and unrelenting pain of an epidural abscess. It is more important to evaluate for the red flags in the history and physical examination (see Table 1) than to recognize a particular classic presentation for the various diseases. Identification of the red flags will direct whether further evaluation is required. One may classify patients with back pain into three broad categories: nonspecific back pain, back pain associated with radiculopathy or sciatica, and back pain associated with another specific cause.
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History
The red flags in the history are those historical factors that raise the clinician's suspicion for a serious etiology. The presence or absence of the red flags will guide the clinician to a cost-effective evaluation. The following are the historical red flags.
Duration of the Symptoms. Low back pain is divided into three groups based on the duration of the symptoms. Those with pain lasting 6 weeks or less are categorized as having acute pain. Those with symptoms lasting between six and 12 weeks are defined as having subacute pain. Those with pain lasting longer than 12 weeks are defined as having chronic back pain.5 This differentiation is important because in approximately 80-90% of patients with acute nonspecific low back pain, symptoms will resolve within 6 weeks. Thus, waiting this time period before undertaking diagnostic testing will significantly decrease the number of unnecessary tests. Pain lasting greater than six weeks suggests there is a higher likelihood that the patient may have cancer, infection, or a rheumatologic etiology.
One difficulty in applying this rule is how best to approach the patient who presents for the first time with pain that has been ongoing for six weeks or greater but has an otherwise normal evaluation. In these cases, it is reasonable to ensure that the patient has an appropriate treatment regimen and can follow up in approximately two to three weeks to ensure that symptoms are improving or resolved.
Age of the Patient. Patient age greater than 50 or less than 18 is a red flag because these age groups are more likely to have a serious etiology for their symptoms. Specifically, those younger than age 18 are at increased risk for congenital defect, tumor, infection, spondylolysis, and spondylolisthesis. Patients older than 50 are at increased risk for tumor, abdominal aortic aneurysm, and infection. Those older than 65 years have an increased probability of spinal stenosis.6,7
Location and Radiation of the Pain. Pain that is caused by muscular, ligamentous strain, or disk disease without nerve involvement is located primarily in the back, often with radiation into the buttocks or thighs. Sciatica is defined as a radicular pain into the leg past the knee and in the distribution of a lumbosacral nerve root, which is often accompanied by a neurosensory or motor deficit.8 Back pain with sciatica is a red flag as it affects only 1% of all patients with low back pain. Sciatica is concerning for nerve root inflammation or compression below the L3 nerve root based on the dermatomal distribution of the lumbosacral nerves.8 This radiculopathy is important to identify because approximately 95% of all herniated disks occur at the level of the L4-L5 or L5-S1 spaces.8,9 This corresponds to compression of the L5 or S1 nerve root and produces complaints corresponding to the pathways of these nerve roots.
History of Trauma. Major trauma is an obvious red flag for fracture. However, minor trauma in the elderly, those with known osteoporosis, or in the chronic steroid user is also a red flag for the possibility of vertebral fracture. Even injuries such as a fall from standing or a seated position may produce enough force to result in a fracture in some osteoporotic individuals.
Systemic Complaints. Constitutional symptoms such as fever, chills, night sweats, malaise, and an undesired weight loss are red flags suggestive of infection or malignancy. This is one of the areas that the provider is less likely to inquire about when evaluating patients with back pain. These complaints are more worrisome for infection if the patient has additional risk factors such as recent bacterial infection (pneumonia or urinary tract infection), immunocompromised status including diabetes, or if the patient has a history of injection drug use. One maxim regarding back pain in the patient with a history of injection drug use is that the patient should be assumed to have a spinal infection until ruled out by diagnostic studies. Additionally, recent invasive procedures such as colonoscopy may predispose the patient to infection secondary to transient bacteremia.
Atypical Pain Features. Similar to systemic complaints, this is an area that many providers overlook. In general, benign low back pain is usually described as a dull, achy pain that is worsened with movement and improved with rest. Atypical pain features raise red flags for infection and tumor. Atypical features of concern include the following: pain that is worse at night and often awakens the patient from sleep, pain that is not relieved with rest, and pain that is unrelenting despite proper analgesic use. A large number of patients complain of being uncomfortable and having difficulty getting to sleep at night due to their symptoms. While this is bothersome, it is not the symptom that raises a red flag. Rather, the severe pain that awakens the patient from sleep and is often worse than the daytime symptoms is concerning.
Other atypical pain features include pain that is worsened with prolonged sitting, coughing, and Valsalva. These symptoms are consistent with disk herniation. Symptoms due to spinal stenosis are worsened with activities such as walking, prolonged standing, and back extension and are relieved with rest and forward flexion.
Associated Neurological Deficits. Patients with benign back pain have no associated neurological deficits or complaints. In addition to asking about weakness, paresthesias, and sensory deficits, one must inquire about bowel and bladder incontinence. Any neurological complaint is a red flag for a pathologic process that is causing impingement on the spinal cord, cauda equina, or spinal nerve roots. If the patient has neurological complaints, focus further on the time course, whether that issue is stable, improving, or worsening, and whether the symptoms are unilateral or bilateral.
In regard to urinary incontinence, one issue that occasionally causes difficulty for the provider is how best to evaluate the patient who reports urinary incontinence but has an otherwise completely normal history and physical examination or has a known history of urinary incontinence. In these cases, residual bladder volumes can be measured. A large post-void residual volume in conjunction with low back pain suggests significant neurological compromise and warrants immediate evaluation for an epidural compression syndrome. A negative post-void residual volume (less than 100 mL) is reassuring and essentially excludes significant neurologic compromise as the etiology for the incontinence.10,11 Complaints of worsening or progressing paresthesias, weakness, and gait disturbances need to be evaluated to determine if the complaints can be explained by a single nerve root, likely from compression by a herniated disk, or multiple or bilateral nerve root complaints, which is concerning for epidural compression. These symptoms should be correlated with the physical examination findings.
History of Cancer. A history of cancer is a red flag due to the risk of metastatic spread to the vertebral bodies, spinal canal, or even the spinal cord. The most common cancers to metastasize are breast, lung, thyroid, kidney, or prostate. The probability of the back pain being due to cancer rises from 0.7% in those patients with no history of cancer to 9% in those patients with a history of cancer excluding nonmelanoma skin cancer.12,13 Primary tumors arising in the spine include osteosarcoma, lymphoma, multiple myeloma, and neurofibromas.
Urinary, Abdominal, or Chest Complaints. The provider should inquire about symptoms involving the pulmonary, gastrointestinal, and urinary systems. A failure to inquire into these areas could cause one to miss renal colic, urinary tract infection, pneumonia, abdominal aortic aneurysm, pancreatitis, or some other retroperitoneal process as the source for the patient's symptoms.
Physical Examination
The physical examination of the patient with low back pain does not need to be long or complex. The examination should be focused on evaluating red flags uncovered in the history and on localizing specific neurological complaints.
Vital Signs. Obvious derangements in the vital signs are of concern. The presence of fever is a red flag for infection. Fever is present in 27% of patients with tuberculosis osteomyelitis, 50% with pyogenic osteomyelitis, and up to 87% in spinal epidural abscess.10 However, in one review, approximately 2% of patients with idiopathic low back pain who presented in the primary care setting had a fever that was not due to a spinal infection but rather attributed to a coexistent viral syndrome.10 Therefore, the presence of a fever is concerning but not pathognomonic of a spinal infection. Conversely, the absence of fever does not exclude spinal infection.
General Appearance. Most patients with a benign etiology for their low back pain prefer to remain still. Those patients who are writhing in pain should raise the provider's suspicion for spinal infection, abdominal aortic aneurysm, or nephrolithiasis.
Back. The back should be exposed and palpated. Initially inspect the back for signs of trauma and other underlying disease. Erythema, warmth, swelling, and drainage suggest infection. When possible, the patient should be examined lying and standing, or at least palpate and percuss the vertebral bodies looking for point tenderness.
The final portion of the back examination is the straight leg raise test. This is a test that is used specifically to evaluate the patient for evidence of an intervertebral disc herniation. To perform this test, the patient is placed in the supine position and the leg is passively elevated by the examiner up to 70 degrees. A positive test produces a new or worsening radicular pain below the knee along the path of a nerve root somewhere between 30-70 degrees of elevation. A positive test result can be further verified by lowering the leg 10 degrees from the point of radicular pain and dorsiflexing the foot. This should reproduce the radicular pain that was felt at the higher degree of elevation. Reproduction of the patient's back pain or pain in the hamstring is not a positive test. It is important to clearly understand the results of the test, as a positive straight leg raise test is approximately 80% sensitive for a herniated disk at either the L4-L5 or L5-S1 levels, where 95% of herniated disks occur.8,9 Radicular pain in the affected leg when lifting the asymptomatic leg (positive crossed straight leg raise) is highly specific yet insensitive for nerve root compression by a herniated disk.2,8,9
Neurologic. The neurologic examination is the most important part of the physical examination to both exclude an impending neurosurgical emergency and localize neurologic deficits. The physical examination is best focused on evaluating specific nerve roots by evaluating strength, sensation, and reflexes. Sensation can be tested initially by using light touch over the dermatomes innervated by specific spinal nerve roots. If abnormalities are uncovered with light touch, then the examination can be further delineated by evaluating sharp/dull, temperature, proprioception, and vibration. The motor examination is focused on the muscles innervated by the specific spinal nerve roots as well as determining distal versus proximal weakness if there are any abnormalities. The Patellar and Achilles reflexes should be compared for symmetry. Finally, Babinski's test is performed to evaluate for an upper motor nerve syndrome. All deficits or abnormalities should be compared with the nerve root involved. For example, weak plantar flexion of the left foot in addition to a hyporeflexive Achilles reflex and diminished sensation on the lateral foot corresponds well with S1 nerve root compression. (See Table 2.)
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Rectal Examination. A digital rectal examination does not need to be performed on all patients suffering from low back pain. It is indicated, however, in those patients with red flags, especially those with neurological complaints or severe pain. On examination, evaluate for perianal sensation, rectal tone, and rectal and prostatic masses. Poor rectal tone in association with back pain and saddle anesthesia indicates an epidural compression syndrome.10
Tests for Non-Organic Pain. In 1980, Waddell described five physical signs that were associated with non-organic back pain. Waddell found that those patients who had three or more of the five signs (see Table 3) were more likely to have non-organic disease.14 These signs, which may be useful in identifying patients with non-organic back pain, should be used in conjunction with the entire presentation and not as the sole basis of discounting a patient's symptoms.
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Diagnostic Studies. The vast majority of patients suffering from acute low back pain are self-resolving in four to six weeks. Beyond the history and physical, a question always arises as to which ancillary studies need to be included in the work up of acute low back pain. When there are no red flags, a good history and physical examination should suffice. When red flags are elucidated, then further evaluation is warranted with diagnostic testing.
Laboratory Tests. The typical laboratory tests to consider for patients with low back pain are the complete blood count (CBC), erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), and urinalysis (UA). In patients with red flags for infection, physicians should order the CBC, ESR or CRP, and a UA. In infection, the white blood cell (WBC) count may be normal or elevated, although the ESR is almost universally elevated.15-21 The CRP is commonly substituted for or added to the ESR in screening for spinal infection. While it should have a similar result, its use as a screening test for spinal infection has not been studied. A UA should be obtained in those under consideration for spinal infection as a potential primary source of the infection.
In cases of cancer as the potential etiology for the back pain, the ESR is generally elevated but the other laboratory tests are usually normal.13
Plain Radiography. There is a sense among many patients that they should receive plain radiographs of the low back as part of their evaluation. However, plain radiographs rarely add helpful information in establishing the diagnosis. What they do add is cost, time, and unnecessary radiation. In the absence of red flags, plain radiographs are not necessary. If there is concern for fracture or perhaps rheumatologic disease, then AP and lateral views of the spine should be obtained. Oblique views are generally excluded in adults as they add little information and again increase cost and radiation exposure. In most settings when there is concern about infection, nervous system impingement, or metastatic disease, it is more cost effective to move directly to MRI, since this will be obtained if the studies are positive or if the studies are negative and the patient has persistent symptoms.
Magnetic Resonance Imaging (MRI). MRI is the gold standard imaging technique for evaluation for epidural compression syndromes, spinal infection including vertebral osteomyelitis and epidural abscess, and intervertebral disk herniation. MRI is also commonly used in evaluating spinal trauma whenever there is concern for spinal cord injury or potential spinal cord injury because MRI gives better visualization of the spinal canal and the spinal cord than CT. Unless there is concern for a compressive lesion of the spine, spinal infection, or spinal metastases, MRI may be delayed for 4-6 weeks, especially if the examiner is only concerned that the patient has a herniated disk.
Computed Tomography (CT). CT is the study of choice to evaluate the bony structure. This is most important in the setting of spinal trauma and determining the stability of the spinal column and integrity of the spinal canal. In the absence of MRI or in those cases where MRI is contraindicated for the patient, a CT-myelogram may be used to evaluate for epidural compressive lesions. CT is also a good imaging modality to determine the presence of vertebral osteomyelitis. However, due to poor resolution of the spinal canal, it can miss epidural abscess unless myelography contrast is used.
Radionuclide Imaging. Radionuclide imaging is much less commonly used today. Its primary use is for those patients in whom metastatic spread of cancer is a concern, but there are no neurologic symptoms. While inferior to MRI, radionuclide imaging allows a more global evaluation for metastases. It is also used to help identify infectious processes as well as vertebral stress fractures, especially in adolescents with low back pain. In general, most positive findings with radionuclide imaging are confirmed with MRI.
Back Pain Management
After the initial evaluation, the physician should be able to categorize the patient into three broad categories: nonspecific back pain, back pain associated with radiculopathy (sciatica) or spinal stenosis, and back pain associated with another specific cause.
The majority of patients with low back pain fall into the category of nonspecific back pain. This is the group of patients who have back pain without radiculopathy and no red flags or a negative evaluation of the red flags. Despite the term nonspecific, the connotation is not one to discount the patient's symptoms, but rather to note that there is no specific etiology that has been found that can account for the symptoms. These patients with nonspecific back pain can have significant pain and disability that may adversely affect them for a period of time. Despite the degree of pain and disability, it is important to educate these patients that they will most likely respond very favorably to conservative management over a 4-6 week period, with many responding well after only several days.2,22 In treating these and all patients with back pain, there are many treatment options that are helpful and are commonly used in combination. An important point is that no one treatment has been demonstrated to be clearly superior, so there is much confusion and debate both within the medical community and the lay population on what is the best treatment. The approach to the treatment of the patient with back pain is focused on the following areas: analgesic medications, activity modification, spinal manipulative therapy, and other physical modalities.
Analgesic Medications. Ample use of analgesic agents is paramount in treating back pain symptoms and allowing patients to increase their activity level, which is also important in the healing process. The primary medications are acetaminophen, non-steroidal anti-inflammatory medications (NSAIDs), and opiate analgesics. Acetaminophen (Tylenol) is medication that is commonly overlooked as it is readily available over the counter. However, patients commonly confuse acetaminophen with aspirin and are unwilling to combine it with an NSAID due to fear of toxicity. In reality, acetaminophen is an excellent analgesic that has proven efficacy comparable to NSAIDs in the treatment of pain due to musculoskeletal conditions.23 Furthermore, it is inexpensive and has a small side-effect profile in comparison to the NSAIDs. Acetaminophen is recommended in the treatment for all patients with back pain unless there is a specific contraindication such as liver disease or allergy.
Most NSAIDs are essentially equally efficacious in the management of acute pain.23-26 Choose a particular NSAID based on its side-effect profile and cost. The lowest dose of medication needed to reach the therapeutic effect of pain reduction should be attempted. In the past, COX-2 inhibitors were suggested as an alternative to NSAIDs in patients with concerns for gastrointestinal or renal toxicity. In light of recent literature regarding the COX-2 safety profile, however, these drugs should be used sparingly and only after discussion with the patient about the risks.25 The concomitant use of misoprostol (Cytotec) or omeprazole (Prilosec) has been shown to reduce the risk of clinically important gastrointestinal bleeding during NSAID therapy.24,27
The most common recommended approach is to use a combination of both acetaminophen and NSAIDs. A popular dosing regimen is acetaminophen 500-1000 mg orally every 4 to 6 hours either alone or in combination with either ibuprofen (Advil, Motrin) 400 to 800 mg three times daily or naproxen (Aleve) 250 to 500 mg twice daily.
The liberal use of opiate analgesics is recommended for those patients with moderate to severe pain. Prescribing opiate analgesia allows patients to break the pain cycle and gives them a stronger option when exacerbations of pain occur during the healing process. There are several precautions on the use of opiates. First, if prescribing an opiate-acetaminophen (Percocet or Vicodin) or opiate-NSAID combination, ensure that you warn the patient not to combine it with regular acetaminophen or NSAID depending on the combination used. Failure to warn patients may lead to accidental acetaminophen toxicity or increased side-effects from the NSAIDs. Second, prescribe the opiates for only a short period of time, generally no longer than seven to 10 days. This allows adequate use while limiting excessive use or the development of dependence. Finally, patients should be warned of the potential problems of driving motor vehicles while taking opiates.
Muscle relaxants, such as diazepam (Valium), methocarbamol (Robaxin), metaxalone (Skelaxin), or cyclobenzaprine (Flexeril), are effective in treating low back pain; however, they are no better than NSAIDs.28-31 Muscle relaxants commonly cause sedation and can become addictive with chronic use. The addition of cyclobenzaprine to high-dose ibuprofen (800 mg) in the first 48 hours of acute low back pain has no benefit over ibuprofen alone.30 However, if the patient demonstrates significant muscle spasm of the paraspinal musculature, then muscle relaxants may be useful.28,32 In spite of this, it is important to understand that most muscle relaxants exert benefit only in the first four days of an attack when spinal muscular spasm is at its peak. Spasm is rarely a significant component of the symptoms after the first week of the injury. Unless there are unusual circumstances, muscle relaxants should be avoided after the first week of treatment.
Some advocate the use of corticosteroids systemically or by local injection; however, this treatment has never been shown to be beneficial and should be avoided.5,23,24
Activity Modification. Patients with nonspecific back pain should continue their routine activities to the extent tolerable and use pain as their guide for activity modification. Bed rest has no benefit and may ultimately be harmful in the recovery of the patient.33 Even two days of bed rest are not beneficial in comparison to early mobilization and activity.33,34 Additionally, in patients with sciatica, bed rest is not beneficial in comparison to early mobilization.33,35 The issue of how long patients should stay home from work or how long they should modify work activities is difficult to define. Each case is individual, but the best method is to counsel patients to use the pain as the guide and to educate them that the symptoms will improve with time. Active exercise and back strengthening exercise are not beneficial during the acute crisis of back pain, although it may be important once the patient recovers to prevent future episodes.36,37 Patients should be advised to resume normal daily activities and to curtail activities that exacerbate the pain.
Manipulation. One of the most controversial treatments of acute low back pain is spinal manipulation. Numerous studies have evaluated the efficacy of spinal manipulation in patients with uncomplicated low back pain. For example, acute manipulation was shown to be no better than physical therapy and only slightly better, in terms of patient satisfaction with care at one and four weeks, than giving the patient a $1 educational booklet.38 And manipulation was no better than standard medical therapy in terms of clinical outcome.39 Finally, in those patients with uncomplicated low back pain, spinal manipulative therapy was superior only to sham therapy or other therapies previously judged to be ineffective or harmful.40 There is no statistically or clinically significant advantage of spinal manipulation over general care, analgesics, physical therapy, or back school.40 Similar results were obtained for those patients with chronic back pain.40 Manipulative therapy is not routinely recommended in most patients with acute nonspecific low back pain.
Other Physical Modalities. Other treatments common for low back pain include the following: traction, diathermy, cutaneous laser therapy, exercise, ultrasound, homeopathy, acupuncture, massage, and transcutaneous electrical nerve stimulation. None of these treatments has shown significant improvement in the recovery rate from acute low back pain.5 Thermal and ice therapy have the benefit of being very inexpensive and may be marginally effective in reducing the subjective complaints of acute low back pain. Corsets and lumbar braces have shown no benefit in the treatment of low back pain and only add to the cost of treatment.41 Physical exercise and strengthening in the acute phase of low back pain should be avoided. Early mobilization is beneficial, but strenuous rehabilitation in the acute phase may be harmful. As the acute pain subsides, moderate stretching and strengthening of both abdominal muscles and back muscles are beneficial.
Subacute and Chronic Low Back Pain
As previously mentioned, approximately 90% of patients suffering from low back pain will recover in 4-6 weeks. Those who do not improve in this time period are considered to have subacute or chronic low back pain. The initial management of these patients should be to evaluate them with laboratory and radiologic imaging to ensure that there is not a diagnosable etiology for their back pain such as tumor or infection. Plain radiographs may show spondylolysis with or without spondylithesis (see Figures 1A and 1B) or compression fractures (see Figure 2) as an explanation for the persistent pain. If the evaluation is negative, there are numerous steps that one may take to try to improve the patient's symptoms. Activity modification is important, so the patient should undergo instruction on proper lifting, carrying, and bending. Exercise is beneficial in the management of chronic low back pain.36,42 A common place to refer these patients for more formal instruction is to a "back school." These programs have proven efficacy in improving the outcomes of these patients and ensure a formal education is given to the patient.43 Smoking is correlated with chronic back pain, and cessation should be strongly encouraged. Reduction in body weight and improved cardiovascular fitness are also beneficial.
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Steroid Injection. There remains significant controversy as to the benefits, if any, of glucocorticoid injection into the lumbar disks, facet joints, or local tissues of the back.24,42,44 In general, patients with chronic nonspecific back pain without radiculopathy have no improvement with these injections.42,44 Epidural steroid injection, which is generally performed by an anesthesiologist, may be beneficial to those patients with post-surgical scarring or with severe impairment from spinal stenosis. The success of such treatment is debatable and inconclusive. If patients do improve, it is usually short term, with a return of symptoms in four to 10 months.24,45
Behavioral Therapy. Behavioral therapy, including biofeedback, has been shown to be beneficial when used in conjunction with a comprehensive rehabilitation approach including physical, mental, and behavioral approaches.46
Medications. Analgesics such as acetaminophen and NSAIDs remain the cornerstone analgesics. Opiates and muscle relaxants should be avoided in chronic pain as addiction becomes likely. Antidepressants, especially tricyclic and tetracyclic medications, have been shown to be beneficial in the treatment of chronic low back pain.42,47
Spinal Manipulative Therapy. Spinal manipulation is not superior to standard treatments for the management of chronic low back pain.40,42
Transcutaneous Electrical Nerve Stimulation. Transcutaneous electrical nerve stimulation (TENS) units have been shown to be no more effective than placebo in treatment of chronic low back pain.12,48
Acupuncture. Acupuncture may be beneficial in the treatment of chronic back pain. One study showed some improvement at 10 weeks but no difference at 1 year to standard therapy.12,49,50
Massage. Massage has some benefit for patients with chronic low back pain when combined with exercise.12,51
Low Back Pain with Radiculopathy or Sciatica
Back pain with associated sciatica is only a symptom in 1% to 4% of individuals with low back pain, whereas it is found in 95% of those with disk herniation.8,12 The more common diagnoses for this complaint are herniated disk in the younger population and spinal stenosis in the older population.
Herniated Disk. The outcome for patients with a herniated disk is generally positive, with 50% recovering in 6 weeks, and only 5-10% ultimately requiring surgery.2,8,9 Interestingly, two separate studies demonstrated that the beneficial results of surgery appear only in the first two years after the procedure with there being no difference in the patients' symptoms at four and 10 years post operatively.2,8
The management of patients with back pain with sciatica is similar to the management of the patient with uncomplicated low back pain. Analgesic use should include acetaminophen, NSAIDs, and short-term opiates when the pain necessitates it. Activity should be routine, using pain as the limiting factor. Manipulation should be avoided due to the risk of worsening the neurological deficit or symptoms. One difference is in the use of steroids. While there is no role for systemic steroids, epidural steroid injection has been shown to have a mild to moderate reduction in pain relief but with no proven reduction in need for operative management.24,52 The combination of analgesic pain control and early mobilization is the mainstay of treatment. The clinician should be diligent to detect progressive neurological function, and the patient should be educated to return earlier if the symptoms are worsening. MRI is rarely warranted in the first 4-6 weeks unless signs or symptoms of epidural compression or progressive nerve entrapment symptoms are seen. However, if the patient continues to have symptoms past six weeks then imaging with MRI is warranted to better define the etiology of the symptoms.
Spinal Stenosis. Spinal stenosis is a chronic cause of back pain that is very common in the elderly. In fact, it is the leading indication for lumbar spinal surgery in patients older than age 65.7 Spinal stenosis is defined as a narrowing of the spinal canal caused by degeneration of the bony and intraspinal soft tissues.7 This narrowing may involve the central canal, lateral recess, or intervertebral foramen at a single spinal level or multiple levels. The narrowing that results from the degenerative disease affects the spine by causing compression of vascular and neural structures. The symptoms include a central low back pain that is chronic and progressive. Later in the disease process the patient classically develops sciatica that is more commonly bilateral, although it may be unilateral.53 Commonly, patients develop neurogenic claudication, which is the hallmark for spinal stenosis. This is a bilateral thigh and leg pain followed by numbness and weakness that is brought about by walking, prolonged standing, and back extension. These symptoms are relieved with rest and forward flexion of the spine.6,7,53 Neurogenic claudication, which is also called pseudoclaudication, occurs in approximately 60% of patients with spinal stenosis. It is called pseudoclaudication because it is caused by neurologic compression, not arterial or vascular obstruction.6,7,53 One way to help differentiate it clinically from vascular claudication is that when ascending stairs, a patient is unlikely to develop neurogenic claudication due to the flexing of the trunk to go up the stairs, whereas ascending stairs should worsen vascular claudication.6 The diagnosis of spinal stenosis is elusive and based more on the patient's age and history because physical examination findings often are absent. The diagnosis is usually confirmed by CT scan or MRI. As in most cases of lumbar pain syndromes, surgery is rarely indicated. Over-the-counter analgesics provide adequate relief. Opioids may be needed and should be prescribed for short periods of time.
Epidural Compression Syndrome. Epidural compression syndrome is a collective term encompassing spinal cord compression, cauda equina syndrome, and conus medullaris syndrome. This is the current term of choice for these individual entities because the presentation for these syndromes is similar except for the level of the neurologic deficit. Furthermore, the initial evaluation and management for these syndromes is similar, until the actual diagnosis is known. Back pain is the earliest and most common symptom in metastatic epidural spinal cord compression.54-56 Epidural compression arises from pressure being placed on the central cord or cauda equina from some space-occupying lesion. Possible etiologies include a large central disk herniation, spinal canal hematoma, spinal canal abscess, primary or metastatic tumor, or traumatic compression.
An understanding of epidural compression syndrome is paramount, as a catastrophic neurological loss can develop if it is not recognized and treated promptly. Complete epidural compression syndrome is obvious to all practitioners; the ability to discern those patients who are presenting 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. One of the keys to discerning an epidural compression syndrome is that the symptoms are usually bilateral. Furthermore, there is a combination of motor, sensory, and autonomic nervous system deficits found on physical examination. Interestingly, these patients usually have only minor low back complaints or improvement in their back pain as their neurologic deficit progresses. In addition to the bilateral leg complaints, these individuals may experience constipation or incontinence of the bladder and bowel. A large post-void residual (greater than 100 mL or more than 20% of the voided sample) or urinary retention with overflow incontinence is indicative of a denervated bladder and commonly is seen in this condition.10,11,54,55,57 Patients often complain of saddle anesthesia and have a decrease in rectal tone.10 Major motor and sensory loss is also frequently noted.
It is advised to immediately treat these patients with steroids as soon as the condition is suspected; do not wait for the results of diagnostic tests as it may take several hours. Treatment consists of dexamethasone 10 mg to 100 mg IV at onset of evaluation.54-56 It is essential to understand that this dosing recommendation is based on studies with metastatic epidural compression that showed improved function and decreased pain, but were too small to make a definitive answer for the optimal dose. An intravenous dose of 10 mg of dexamethasone is a very reasonable approach when considering the benefits and the side-effects of the higher doses.54-56 There are no studies evaluating the utility of steroids in improving the outcome of epidural compression due to disk herniation, infection, or hemorrhage.
When epidural compression is considered, radiographic imaging should go directly to emergent MRI of the cervical, thoracic, and lumbosacral spine if there is concern for metastatic compression or infection. Otherwise, a regional MRI of the spinal area affected will suffice. In these cases, plain spinal radiographs typically will add little information to the case, yet they will delay the time that it takes to get a definitive diagnosis. Immediate consultation with the appropriate specialist (spine surgeon, radiation oncologist, oncologist) is required once the diagnosis is more clearly delineated.
Spinal Infection. Spinal infections, most commonly vertebral osteomyelitis and spinal epidural abscess, are uncommon yet very serious causes of back pain that providers can initially miss. Vertebral osteomyelitis is frequently unrecognized initially, with up to half of patients having symptoms for more than 3 months prior to their diagnosis. The history is very useful in considering the diagnosis of spinal infection. These infections occur more commonly in diabetics, other immunocompromised patients, injection drug users, and the elderly.58-61 More than 90% of patients with vertebral osteomyelitis or epidural abscess had back pain as a primary complaint.58-61 In those cases where no back pain was reported, patients either had altered mental status due to sepsis or had diminished sensation due to a preexisting spinal cord lesion.59,61 The back pain is often nocturnal, severe in nature, and unremitting despite appropriate rest and analgesics. Those with epidural abscess may have concomitant sciatica and neurologic symptoms. Fever is documented in only 50-70% of patients with either vertebral osteomyelitis or epidural abscess.58,59,61 Consequently, one cannot rely on the absence of fever to exclude this diagnosis. On examination the majority of patients will have localized spinal tenderness to palpation or percussion. On laboratory examination the WBC count is elevated in approximately 30-70% of patients, whereas the ESR is elevated in more than 90% of patients.58,59,61,62
Staphylococcus aureus is the most common microbe causing infection, but E. coli, Proteus and Pseudomonas are also known pathogens. Most of these infections are hematogenously spread. The treatment for epidural abscess is generally surgery, although there are some patients who will not be operated on at the discretion of the spine surgeon. The treatment for osteomyelitis usually requires six to eight weeks of IV. It is most beneficial if blood cultures with susceptibilities are known, but for empiric treatment assume Staphylococcal involvement and use nafcillin or cefazolin. If methicillin-resistant Staphylococcus aureus (MRSA) is suspected as a causative agent, vancomycin plus rifampin or linezolid is a treatment option. The antibiotic regimen may be tailored depending on the results of the blood cultures as well as the clinical response. It is important to identify the infecting organism so that proper antibiotics are utilized. The remainder of treatment is supportive and includes analgesics, bed rest until the symptoms improve, and immobilization with an orthosis. Surgery is reserved for those patients who have significant abscesses, spinal cord compression, significant bony destruction, or are refractory to typical medical treatment.
Back Pain in the Cancer Patient
Evaluating the cancer patient with back pain is more difficult because of the risk of spinal metastases and the potential devastating consequences if a significant lesion is missed. Roughly 5% of cancer patients will develop spinal metastases and epidural compression. The best way to approach this subset of patients with back pain is to separate them into three groups based on their symptoms.
Group 1. This group includes all patients with signs and symptoms of progressive epidural compression. This includes new or progressing bilateral or unilateral symptoms that involve more than one spinal nerve root. These patients represent a true emergency and should be treated with IV dexamethasone 10 mg and evaluated with an emergent MRI.
Group 2. These patients have stable and mild symptoms that have been present for several days to weeks. In addition to the back pain, patients in this group have isolated involvement of a single nerve root. These patients do not require high-dose steroids or emergent MRI. However, an evaluation with MRI is recommended in 24 to 48 hours as well as initiation of dexamethasone at a dose of 4 mg to 10 mg IV or orally while awaiting the MRI. Plain radiographs may assist in the diagnosis of metastases, but normal films do not rule out early metastases or tumors not involving the bone.
Group 3. The majority of cancer patients suffering from back pain fall into this category. These individuals have isolated back pain with no neurological deficits or complaints. There are two ways to approach these patients. The first method is to obtain plain radiographs of the area involved. If metastases are seen on the plain radiographs, these patients should undergo urgent imaging with MRI to better define the degree of involvement. If no bony pathology is noted, the patients should be followed closely for improvement over the next two to three weeks. At that point, if they continue to have symptoms, they should be imaged further with an MRI. It must be remembered that 50% bony destruction is needed before radiographs can detect a lytic lesion and 60% of patients with metastatic disease to the bone will have normal initial radiographs. This is why it is important to follow these patients closely.
The second approach is to go directly to MRI within the next week and to omit the plain radiographs. These patients do not require emergent MRI, but they are at much higher risk of metastases than the average patient with back pain and require a more diligent evaluation. The author generally follows this second course of action.
Back Pain in Children and Adolescents
Children and adolescents are much less likely to visit a physician for back pain. When they present with back pain, however, one must perform a more thorough diagnostic evaluation at the initial presentation, as there is a much higher probability of diagnosing a treatable etiology for the symptoms. The history should be the same as for the adult with the addition of asking about any recent increase in physical activity or involvement in sports such as football, dance, and gymnastics. These activities are associated with an increased likelihood of spondylolysis or spondylolisthesis, which is considered a stress fracture of the spine in children and adolescents. On the physical examination look for birthmarks such as café au lait spots that are indicative of neurofibromatosis, as well as midline skin abnormalities of the back that may indicate underlying developmental spinal abnormalities. Etiologies to consider in the child younger than age 10 are discitis, tumor, and osteomyelitis. Etiologies for those 10 and older include spondylolysis, spondylolisthesis, Scheuermann's disease, tumor, vertebral osteomyelitis, herniated disk, and ankylosing spondylitis. All children without an obvious etiology for their back pain should be evaluated with a CBC, ESR, UA, and plain spinal radiography to include oblique views if the initial AP and lateral views are normal.
Conclusion
Back pain is a very common complaint in the adult population. With a focused approach, the provider will be able to discern those cases that require further evaluation with diagnostic studies. In most patients, nonspecific back pain symptoms will resolve within four to six weeks with conservative treatment including analgesia and activity modification. However, in those patients who have concerning signs or symptoms in the history and examination, one needs to be aggressive in trying to determine the source of the patient's symptoms.
References
1. Deyo RA, Mirza SK, Martin BI. Back pain prevalence and visit rates: Estimates from U.S. national surveys, 2002. Spine 2006;31:2724-2727.
2. Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001;344:363-370.
3. Strine TW, Hootman JM. US national prevalence and correlates of low back and neck pain among adults. Arthritis Rheum 2007;57:656-665.
4. Martin BI, Deyo RA, Mirza SK, et al. Expenditures and health status among adults with back and neck problems. JAMA 2008;299:656-664.
5. Bigos SJ. Acute Low Back Problems in Adults Clinical Practice Guideline. Quick Reference Guide. In: Services, UDoHaH, ed. Vol 95-0643: Agency for Health Care Policy and Research; 1994.
6. Chad DA. Lumbar spinal stenosis. Neurol Clin 2007;25:407-418.
7. Markman JD, Gaud KG. Lumbar spinal stenosis in older adults: Current understanding and future directions. Clin Geriatr Med 2008;24:369-388, viii.
8. Frymoyer JW. Back pain and sciatica. N Engl J Med 1988;318:291-300.
9. Deyo RA, Loeser JD, Bigos SJ. Herniated lumbar intervertebral disk. Ann Intern Med 1990;112:598-603.
10. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992;268: 760-765.
11. Schmidt RD, Markovchick V. Nontraumatic spinal cord compression. J Emerg Med 1992;10:189-199.
12. Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med 2007;147:478-491.
13. Deyo RA, Diehl AK. Cancer as a cause of back pain: Frequency, clinical presentation, and diagnostic strategies. J Gen Intern Med 1988;3:230-238.
14. Waddell G, McCulloch JA, Kummel E, et al. Nonorganic physical signs in low-back pain. Spine 1980;5:117-125.
15. Auletta JJ, John CC. Spinal epidural abscesses in children: A 15-year experience and review of the literature. Clin Infect Dis 2001;32:9-16.
16. Baker AS, Ojemann RG, Swartz MN, et al. Spinal epidural abscess. N Engl J Med 1975;293:463-468.
17. Curry WT, Jr., Hoh BL, Amin-Hanjani S, et al. Spinal epidural abscess: Clinical presentation, management, and outcome. Surg Neurol 2005;63:364-371; discussion 371.
18. Pereira CE, Lynch JC. Spinal epidural abscess: An analysis of 24 cases. Surg Neurol 2005;63 Suppl 1:S26-29.
19. Wisneski RJ. Infectious disease of the spine. Diagnostic and treatment considerations. Orthop Clin North Am 1991;22:491-501.
20. Sapico FL, Montgomerie JZ. Pyogenic vertebral osteomyelitis: Report of nine cases and review of the literature. Rev Infect Dis 1979;1:754-776.
21. Darouiche RO. Spinal epidural abscess. N Engl J Med 2006;355:2012-2020.
22. Yelin EH, Henke CJ, Epstein WV. Work disability among persons with musculoskeletal conditions. Arthritis Rheum 1986;29:1322-1333.
23. Malanga GA, Dennis RL. Use of medications in the treatment of acute low back pain. Clin Occup Environ Med 2006;5:643-653, vii.
24. Deyo RA. Drug therapy for back pain. Which drugs help which patients? Spine 1996;21:2840-2849; discussion 2849-2850.
25. Roelofs PD, Deyo RA, Koes BW, et al. Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database Syst Rev 2008(1):CD000396.
26. van Tulder MW, Scholten RJ, Koes BW, et al. Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database Syst Rev 2000(2):CD000396.
27. Gotzsche PC. Non-steroidal anti-inflammatory drugs. BMJ 2000;320:1058-1061.
28. Borenstein DG. Epidemiology, etiology, diagnostic evaluation, and treatment of low back pain. Curr Opin Rheumatol 1999;11:151-157.
29. Browning R, Jackson JL, O'Malley PG. Cyclobenzaprine and back pain: A meta-analysis. Arch Intern Med 2001;161:1613-1620.
30. Turturro MA, Frater CR, D'Amico FJ. Cyclobenzaprine with ibuprofen versus ibuprofen alone in acute myofascial strain: a randomized, double-blind clinical trial. Ann Emerg Med 2003;41:818-826.
31. van Tulder MW, Touray T, Furlan AD, et al. Muscle relaxants for non-specific low back pain. Cochrane Database Syst Rev 2003(2):CD004252.
32. Cherkin DC, Wheeler KJ, Barlow W, et al. Medication use for low back pain in primary care. Spine 1998;23:607-614.
33. Hagen KB, Jamtvedt G, Hilde G, et al. The updated cochrane review of bed rest for low back pain and sciatica. Spine 2005;30:542-546.
34. Malmivaara A, Hakkinen U, Aro T, et al. The treatment of acute low back painbed rest, exercises, or ordinary activity? N Engl J Med 1995;332:351-355.
35. Vroomen PC, de Krom MC, Wilmink JT, et al. Lack of effectiveness of bed rest for sciatica. N Engl J Med 1999;340:418-423.
36. Hayden JA, van Tulder MW, Malmivaara AV, et al. Meta-analysis: Exercise therapy for nonspecific low back pain. Ann Intern Med 2005;142:765-775.
37. van Tulder MW, Malmivaara A, Esmail R, et al. Exercise therapy for low back pain. Cochrane Database Syst Rev 2000(2):CD000335.
38. Cherkin DC, Deyo RA, Battie M, et al. A comparison 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.
39. 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.
40. Assendelft WJ, Morton SC, Yu EI, et al. Spinal manipulative therapy for low back pain. Cochrane Database Syst Rev 2004(1):CD000447.
41. Van Tulder MW, Jellema P, van Poppel MN, et al. Lumbar supports for prevention and treatment of low back pain. Cochrane Database Syst Rev 2000(3):CD001823.
42. Carragee EJ. Clinical practice. Persistent low back pain. N Engl J Med 2005;352:1891-1898.
43. Heymans MW, van Tulder MW, Esmail R, et al. Back schools for nonspecific low back pain: A systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2005;30:2153-2163.
44. Khot A, Bowditch M, Powell J, et al. The use of intradiscal steroid therapy for lumbar spinal discogenic pain: A randomized controlled trial. Spine 2004;29:833-836; discussion 837.
45. Cuckler JM, Bernini PA, Wiesel SW, et al. The use of epidural steroids in the treatment of lumbar radicular pain. A prospective, randomized, double-blind study. J Bone Joint Surg Am 1985;67:63-66.
46. van Tulder MW, Ostelo R, Vlaeyen JW, et al. Behavioral treatment for chronic low back pain: A systematic review within the framework of the Cochrane Back Review Group. Spine 2000;25:2688-2699.
47. Salerno SM, Browning R, Jackson JL. The effect of antidepressant treatment on chronic back pain: A meta-analysis. Arch Intern Med 2002;162:19-24.
48. Weiner DK, Rudy TE, Glick RM, et al. Efficacy of percutaneous electrical nerve stimulation for the treatment of chronic low back pain in older adults. J Am Geriatr Soc 2003;51:599-608.
49. Cherkin DC, Eisenberg D, Sherman KJ, et al. Randomized trial comparing traditional Chinese medical acupuncture, therapeutic massage, and self-care education for chronic low back pain. Arch Intern Med 2001;161:1081-1088.
50. Furlan AD, van Tulder M, Cherkin D, et al. Acupuncture and dry-needling for low back pain: An updated systematic review within the framework of the Cochrane collaboration. Spine 2005;30:944-963.
52. Armon C, Argoff CE, Samuels J, et al. Assessment: Use of epidural steroid injections to treat radicular lumbosacral pain: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2007;68:723-729.
53. Amundsen T, Weber H, Lilleas F, et al. Lumbar spinal stenosis. Clinical and radiologic features. Spine 1995;20:1178-1186.
54. Byrne TN. Spinal cord compression from epidural metastases. N Engl J Med 1992;327:614-619.
55. Cole JS, Patchell RA. Metastatic epidural spinal cord compression. Lancet Neurol 2008;7:459-466.
56. Kwok Y, Tibbs PA, Patchell RA. Clinical approach to metastatic epidural spinal cord compression. Hematol Oncol Clin North Am 2006;20:1297-1305.
57. Curtis LA, Dolan TS, Cespedes RD. Acute urinary retention and urinary incontinence. Emerg Med Clin North Am 2001;19:591-619.
58. Bluman EM, Palumbo MA, Lucas PR. Spinal epidural abscess in adults. J Am Acad Orthop Surg 2004;12:155-163.
59. Carragee EJ. Pyogenic vertebral osteomyelitis. J Bone Joint Surg Am 1997;79:874-880.
60. Sapico FL, Montgomerie JZ. Vertebral osteomyelitis. Infect Dis Clin North Am 1990;4:539-550.
61. Schwartz ST SM, Ho G. Bacterial vertebral osteomyelitis and epidural abscess. Semin Spine Surg 1990;2:95-105.
62. Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: A meta-analysis of 915 patients. Neurosurg Rev 2000;23:175-204; discussion 205.-370.
3. Strine TW, Hootman JM. US national prevalence and correlates of low back and neck pain among adults. Arthritis Rheum 2007;57:656-665.
4. Martin BI, Deyo RA, Mirza SK, et al. Expenditures and health status among adults with back and neck problems. JAMA 2008;299:656-664.
5. Bigos SJ. Acute Low Back Problems in Adults Clinical Practice Guideline. Quick Reference Guide. In: Services, UDoHaH, ed. Vol 95-0643: Agency for Health Care Policy and Research; 1994.
6. Chad DA. Lumbar spinal stenosis. Neurol Clin 2007;25:407-418.
7. Markman JD, Gaud KG. Lumbar spinal stenosis in older adults: Current understanding and future directions. Clin Geriatr Med 2008;24:369-388, viii.
8. Frymoyer JW. Back pain and sciatica. N Engl J Med 1988;318:291-300.
9. Deyo RA, Loeser JD, Bigos SJ. Herniated lumbar intervertebral disk. Ann Intern Med 1990;112:598-603.
10. Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992;268: 760-765.
11. Schmidt RD, Markovchick V. Nontraumatic spinal cord compression. J Emerg Med 1992;10:189-199.
12. Chou R, Qaseem A, Snow V, et al. Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Ann Intern Med 2007;147:478-491.
13. Deyo RA, Diehl AK. Cancer as a cause of back pain: Frequency, clinical presentation, and diagnostic strategies. J Gen Intern Med 1988;3:230-238.
14. Waddell G, McCulloch JA, Kummel E, et al. Nonorganic physical signs in low-back pain. Spine 1980;5:117-125.
15. Auletta JJ, John CC. Spinal epidural abscesses in children: A 15-year experience and review of the literature. Clin Infect Dis 2001;32:9-16.
16. Baker AS, Ojemann RG, Swartz MN, et al. Spinal epidural abscess. N Engl J Med 1975;293:463-468.
17. Curry WT, Jr., Hoh BL, Amin-Hanjani S, et al. Spinal epidural abscess: Clinical presentation, management, and outcome. Surg Neurol 2005;63:364-371; discussion 371.
18. Pereira CE, Lynch JC. Spinal epidural abscess: An analysis of 24 cases. Surg Neurol 2005;63 Suppl 1:S26-29.
19. Wisneski RJ. Infectious disease of the spine. Diagnostic and treatment considerations. Orthop Clin North Am 1991;22:491-501.
20. Sapico FL, Montgomerie JZ. Pyogenic vertebral osteomyelitis: Report of nine cases and review of the literature. Rev Infect Dis 1979;1:754-776.
21. Darouiche RO. Spinal epidural abscess. N Engl J Med 2006;355:2012-2020.
22. Yelin EH, Henke CJ, Epstein WV. Work disability among persons with musculoskeletal conditions. Arthritis Rheum 1986;29:1322-1333.
23. Malanga GA, Dennis RL. Use of medications in the treatment of acute low back pain. Clin Occup Environ Med 2006;5:643-653, vii.
24. Deyo RA. Drug therapy for back pain. Which drugs help which patients? Spine 1996;21:2840-2849; discussion 2849-2850.
25. Roelofs PD, Deyo RA, Koes BW, et al. Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database Syst Rev 2008(1):CD000396.
26. van Tulder MW, Scholten RJ, Koes BW, et al. Non-steroidal anti-inflammatory drugs for low back pain. Cochrane Database Syst Rev 2000(2):CD000396.
27. Gotzsche PC. Non-steroidal anti-inflammatory drugs. BMJ 2000;320:1058-1061.
28. Borenstein DG. Epidemiology, etiology, diagnostic evaluation, and treatment of low back pain. Curr Opin Rheumatol 1999;11:151-157.
29. Browning R, Jackson JL, O'Malley PG. Cyclobenzaprine and back pain: A meta-analysis. Arch Intern Med 2001;161:1613-1620.
30. Turturro MA, Frater CR, D'Amico FJ. Cyclobenzaprine with ibuprofen versus ibuprofen alone in acute myofascial strain: a randomized, double-blind clinical trial. Ann Emerg Med 2003;41:818-826.
31. van Tulder MW, Touray T, Furlan AD, et al. Muscle relaxants for non-specific low back pain. Cochrane Database Syst Rev 2003(2):CD004252.
32. Cherkin DC, Wheeler KJ, Barlow W, et al. Medication use for low back pain in primary care. Spine 1998;23:607-614.
33. Hagen KB, Jamtvedt G, Hilde G, et al. The updated cochrane review of bed rest for low back pain and sciatica. Spine 2005;30:542-546.
34. Malmivaara A, Hakkinen U, Aro T, et al. The treatment of acute low back painbed rest, exercises, or ordinary activity? N Engl J Med 1995;332:351-355.
35. Vroomen PC, de Krom MC, Wilmink JT, et al. Lack of effectiveness of bed rest for sciatica. N Engl J Med 1999;340:418-423.
36. Hayden JA, van Tulder MW, Malmivaara AV, et al. Meta-analysis: Exercise therapy for nonspecific low back pain. Ann Intern Med 2005;142:765-775.
37. van Tulder MW, Malmivaara A, Esmail R, et al. Exercise therapy for low back pain. Cochrane Database Syst Rev 2000(2):CD000335.
38. Cherkin DC, Deyo RA, Battie M, et al. A comparison 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.
39. 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.
40. Assendelft WJ, Morton SC, Yu EI, et al. Spinal manipulative therapy for low back pain. Cochrane Database Syst Rev 2004(1):CD000447.
41. Van Tulder MW, Jellema P, van Poppel MN, et al. Lumbar supports for prevention and treatment of low back pain. Cochrane Database Syst Rev 2000(3):CD001823.
42. Carragee EJ. Clinical practice. Persistent low back pain. N Engl J Med 2005;352: 1891-1898.
43. Heymans MW, van Tulder MW, Esmail R, et al. Back schools for nonspecific low back pain: A systematic review within the framework of the Cochrane Collaboration Back Review Group. Spine 2005;30:2153-2163.
44. Khot A, Bowditch M, Powell J, et al. The use of intradiscal steroid therapy for lumbar spinal discogenic pain: A randomized controlled trial. Spine 2004;29:833-836; discussion 837.
45. Cuckler JM, Bernini PA, Wiesel SW, et al. The use of epidural steroids in the treatment of lumbar radicular pain. A prospective, randomized, double-blind study. J Bone Joint Surg Am 1985;67:63-66.
46. van Tulder MW, Ostelo R, Vlaeyen JW, et al. Behavioral treatment for chronic low back pain: A systematic review within the framework of the Cochrane Back Review Group. Spine 2000;25:2688-2699.
47. Salerno SM, Browning R, Jackson JL. The effect of antidepressant treatment on chronic back pain: A meta-analysis. Arch Intern Med 2002;162:19-24.
48. Weiner DK, Rudy TE, Glick RM, et al. Efficacy of percutaneous electrical nerve stimulation for the treatment of chronic low back pain in older adults. J Am Geriatr Soc 2003;51:599-608.
49. Cherkin DC, Eisenberg D, Sherman KJ, et al. Randomized trial comparing traditional Chinese medical acupuncture, therapeutic massage, and self-care education for chronic low back pain. Arch Intern Med 2001;161: 1081-1088.
50. Furlan AD, van Tulder M, Cherkin D, et al. Acupuncture and dry-needling for low back pain: An updated systematic review within the framework of the Cochrane collaboration. Spine 2005;30:944-963.
51. Furlan AD, Brosseau L, Welch V, et al. Massage for low back pain. Cochrane Database Syst Rev 2000(4):CD001929.
52. Armon C, Argoff CE, Samuels J, et al. Assessment: Use of epidural steroid injections to treat radicular lumbosacral pain: Report of the Therapeutics and Technology Assessment Subcommittee of the American Academy of Neurology. Neurology 2007;68:723-729.
53. Amundsen T, Weber H, Lilleas F, et al. Lumbar spinal stenosis. Clinical and radiologic features. Spine 1995;20:1178-1186.
54. Byrne TN. Spinal cord compression from epidural metastases. N Engl J Med 1992; 327:614-619.
55. Cole JS, Patchell RA. Metastatic epidural spinal cord compression. Lancet Neurol 2008;7:459-466.
56. Kwok Y, Tibbs PA, Patchell RA. Clinical approach to metastatic epidural spinal cord compression. Hematol Oncol Clin North Am 2006;20:1297-1305.
57. Curtis LA, Dolan TS, Cespedes RD. Acute urinary retention and urinary incontinence. Emerg Med Clin North Am 2001;19: 591-619.
58. Bluman EM, Palumbo MA, Lucas PR. Spinal epidural abscess in adults. J Am Acad Orthop Surg 2004;12:155-163.
59. Carragee EJ. Pyogenic vertebral osteomyelitis. J Bone Joint Surg Am 1997;79:874-880.
60. Sapico FL, Montgomerie JZ. Vertebral osteomyelitis. Infect Dis Clin North Am 1990;4:539-550.
61. Schwartz ST SM, Ho G. Bacterial vertebral osteomyelitis and epidural abscess. Semin Spine Surg 1990;2:95-105.
62. Reihsaus E, Waldbaur H, Seeling W. Spinal epidural abscess: A meta-analysis of 915 patients. Neurosurg Rev 2000;23:175-204; discussion 205.
On the next chart you pick up, the triage nurse has written, "Back pain, needs med refill." What is your honest reaction? Mine, too. But after evaluating the patient, sometimes I am embarrassed that my initial reaction was negative.You have reached your article limit for the month. Subscribe now to access this article plus other member-only content.
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