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Get full access to all EB Medicine articles published 3 years (or more) ago, including evidence-based, peer-reviewed diagnosis and treatment recommendations.
You must have JavaScript enabled in your browser to utilize the functionality of this website. In strength testing for low back pain, thepatient is asked to walk a few steps on his or her toesand then on the heels.
Nonphysiological physical responses should alert the clinician to potential problems with symptom magnification or even frank malingering. Patients who experience acute LBP often fear serious, progressive, or debilitating consequences.
Sleeping flat on the back with a pillow beneath the knees or sleeping on the side with the top leg flexed on a pillow or with a pillow between the legs may enhance comfort for some patients. Both NSAIDs and skeletal muscle relaxants have been shown to reduce the duration of symptoms.
NSAIDs and, more recently, the cyclooxygenase-2 (COX-2) inhibitors often mainly are used to manage both pain and inflammation. Celecoxib appears to improve pain and decrease inflammation to the same degree as traditional NSAIDs. Topical medications, such as lidocaine patches and topical diclofenac, also may provide adequate analgesia.
There is a conspicuous lack of evidence to indicate that chronic opioid therapy improves functional outcome for patients with LBP. Some clinical scenarios (eg, trauma) invite capitalizing on the sedative impact seen with methocarbamol, carisoprodol, cyclobenzaprine, and other agents. All patients should be counseled to call you if the problem worsens or does not improve within 48 to 72 hours after following your advice.
Slideshare uses cookies to improve functionality and performance, and to provide you with relevant advertising. Inability to toe walk indicatesS1 root nerve damage; inability to heel walk may indicateL4 or L5 involvement. These responses may include exaggerated pain response to light palpation, lack of pain when distracted, nonreproducibility of pain (eg, negative straight-leg raising test result when patient is seated but positive result with lying down), and pain produced by stress on noninvolved tissues (eg, pressure on the top of the head or rotation of the torso producing increased LBP).
Warn patients that applying ice directly to skin can cause burns; it should be wrapped in a towel or some barrier between the ice and the skin should be in place.
Direct patients to avoid activities that clearly worsen pain but to continue to be as active as possible. Analgesics (usually traditional NSAIDs) and skeletal muscle relaxants can enhance mobilization and comfortable return to activity during the natural recuperative period. Either acetaminophen or any of the NSAIDs usually offer adequate short-term relief.5-7 If pain is more intense than would be anticipated to respond adequately to these measures, more potent analgesics may be used as "rescue medication" for short periods (less than 3 weeks). It also has been determined that the mechanism of action of muscle relaxants is independent of sedation. Both classes of agents appear to provide analgesia principally through inhibition of peripheral inflammation, although central mechanisms may play an important role. Selective COX-2 inhibitors cause fewer GI problems (dyspepsia, abdominal pain, and nausea) than the older nonselective NSAIDs. Most patients prefer not to be sedated, but newer skeletal muscle relaxant formulations (lower doses and extended-release products) provide for a reduced incidence of and less intense sedation. Although few patients with acute LBP require any bed rest, if it is used, 2 days has been shown to be as efficacious as 7 days; protracted leave from work should be the exception rather than the rule.
Patients with more persistent symptoms may be offered physical therapy, chiropractic or osteopathic manual medicine techniques, or a combination. Persons who demonstrate persistent or progressive symptoms merit further investigation or intervention. Scientific approach to the assessment and management of activity-related spinal disorders: a monograph for clinicians. Pharmacologic pain treatment of musculoskeletal disorders: current perspectives and future prospects.

Clinical course and prognostic factors in acute low back pain: an inception cohort study in primary care practice. Training in back care to improve outcome and patient satisfaction: teaching old docs new tricks. Acute back pain and spasm: a controlled multicenter trial of combined analgesic and antispasm agents.
Tizanidine and ibuprofen in acute low-back pain: results of a double-blind multicentre study in general practice. Cyclobenzaprine and naproxen versus naproxenalone in the treatment of acute low back pain and muscle spasm. Low back pain in the elderly has a much wider range of possible causes than in younger patients. Inability to toe walk indicates S1 root nerve damage; inability to heel walk may indicate L4 or L5 involvement.
Consider mentioning that, in most cases, acute LBP resolves within days to weeks without long-term sequelae.
After 24 hours, ice and heat can be alternated for 20 minutes every 3 to 4 hours (warn against excessive application of heat, which can result in burns). Progressive exercise generally is fully acceptable within the first 72 to 96 hours after the onset of acute LBP. However, the use of opioid analgesics in chronic noncancer pain continues to be controversial. However, for hyperacute LBP—the phase of marked intensity where a patient may be immobilized by pain, unable to move or straighten up, or even unable to get up on the examining table—it is reasonable to use short-term opioid analgesia (48 to 72 hours). Diazepam is the only benzodiazepine approved by the FDA for the treatment of patients with LBP resulting from muscle spasm. Avoidance of sedation with skeletal muscle relaxants increases the likelihood of rapid, unimpaired return to full, normal activity. Do not put the appointment too far in the future; doing so may lead to the perception that you are not concerned. Serious “geriatric” conditions include certain malignancies, polymyalgia rheumatica, and aortic aneurysm. Localized LBP pain, in the absence of bladder or bowel changes or other indicators of secondary disease, should be reassuring to both the clinician and the patient.
Good counsel might be to avoid driving; advise patients that driving risk is increased before awareness of impairment is present.
Many other pathologies, such as Paget’s disease, Parkinson disease, and osteoporosis with compression fracture, occur almost exclusively in older adults.29While malignancy is rarely an acute emergency, with the exception of epidural compression syndromes, it is an important diagnosable cause of back pain. It may take more than one message about the likely favorable outcome of acute LBP to convince the reluctant or apprehensive patient.
It is the first diagnosis to rule out by history, physical, or imaging studies in the older patient with back pain. While a complete epidural compression syndrome with paraplegia is obvious, mild or early compression can be difficult to discern. However, the consequences of  misdiagnosis can be catastrophic, as most cases are progressive and often irreversible.
Diagnosing the early or subtle cases is made more difficult because MRI, the gold standard test in making the diagnosis, can be difficult, if not impossible, to obtain emergently.Epidural compression syndrome is a collective term encompassing spinal cord compression, cauda equina syndrome, and conus medullaris syndrome. Cauda equina syndrome differs from spinal cord compression in that it occurs below the level of the cord and involves the spinal nerve roots of the cauda equina. Typically, patients present with a classic syndrome of urinary retention with resultant incontinence, saddle anesthesia, anal sphincter laxity, and associated bilateral weakness and sensory deficits in the lower extremities. In the early stages, conus medullaris syndrome commonly presents with bladder dysfunction and possibly fecal incontinence, with later development of lower lumbar and sacral motor, sensory, and reflex impairment.There are two reasons why these syndromes are grouped together. First, individual syndromes are frequently indistinguishable based on the presenting history and physical examination. For example, an incomplete spinal cord compressive lesion at T10 may initially present like a cauda equina syndrome.

Secondly, the initial ED evaluation and management for these syndromes is similar.EtiologiesIn the younger adult population, epidural compression usually results from a cauda equina syndrome due to a large central disc herniation. However, other etiologies to consider in all age groups include primary or metastatic umors, epidural abscess, and trauma. While back pain is frequent, it may not predominate.The most important factors to consider are the bilaterality of the symptoms and the involvement of more than one spinal level. Lower extremity symptoms and signs may be associated with bowel or bladder incontinence and saddle anesthesia. Physical examination usually reveals bilateral lower extremity weakness, hyporeflexia, and abnormal sensation.
Often, there is no specific nerve root distribution as multiple spinal levels are involved, although one should attempt to determine a spinal level. Urinary incontinence results from bladder spasms secondary to associated urinary retention. Urinary retention is approximately 90% sensitive for cauda equina syndrome, while decreased anal sphincter tone occurs in 60-80% of cases.21 Urinary retention or a complaint of urinary incontinence is easily evaluated by obtaining a post-void residual through catheterization. Alternatively, ED ultrasonography may determine post-void residual in a non-invasive manner.ManagementWhen an emergency physician suspects an epidural compression syndrome, he or she must take quick action. Begin steroids immediately, and call a neurosurgeon—the deficit is often progressive and potentially irreversible.
Epidural compression syndrome is one of the few occasions when an emergency physician should obtain a stat MRI.
If MRI is not available, then CT with myelography is the next best study.PrognosisThe prognosis of epidural compression syndrome depends upon the patient’s neurological status at the time of intervention. Specifically, for those patients with epidural compression due to malignancy, those who are ambulatory generally remain so. These patients typically have prolonged symptoms, and in more than half of those with osteomyelitis, the pain has been present for three or more months.16,17,22,32Pain is nearly a universal complaint in spinal infections. Plain films may be useful, but a spinal MRI (the gold standard) or CT is more sensitive and specific than radiographs. Piriformis syndrome is a lesser-known cause of sciatica whereby trauma or injury to the piriformis muscle results in spasm and inflammation that may produce concomitant sciatic nerve impingement. 2,35 In one study, it accounted for 6% of patients with chronic back pain.36Ninety-five percent of herniated discs occur at the L4-L5 or L5-S1 levels, which results in compression of the L5 or S1 nerve roots, respectively.
This compression produces a radiculopathy along the dermatomes of the involved nerve root, as well as sensory, muscular, and reflex changes for the involved nerve root.2 Patients with L5 compression may have difficulty with heel walking (and may demonstrate a foot drop), while those with an S1 problem may not be able to walk on their toes. Older patients have a higher incidence of more proximal disc herniation, such as L2-L3 and L3- L4.2 These patients may complain of pain in the anterior thigh, and demonstrate sensory deficits in the L3 or L4 dermatomes as well as quadriceps weakness with an associated diminished patellar reflex.
The history may reveal some recent trauma; however, more often the patient complains of mild to moderate back pain that preceded the sciatica for a period of days to weeks. Namely, the straight leg raise test and the lower extremity neurologic exam may be abnormal in patients with nerve root compression. Radiographic imaging for sciatica is generally not necessary in the ED because plain films will not demonstrate disc  herniation. However, plain radiographs may be indicated if there are red flags for malignancy, epidural compression, infection or fracture.2,9,11,24,37,38 If the physician is concerned about a more serious etiology for the sciatica, he or she may consider ordering an MRI or CT scan rather than plain radiography. However, this approach has not been evaluated for cost-effectiveness and utility.Acute Lumbosacral StrainThe majority of patients presenting with low back pain suffer from a benign condition commonly called lumbosacral strain (LSS).
This is an injury, possibly with subsequent inflammation, of the lumbosacral ligaments and musculature.
The pain of LSS is well localized to the lower back and upper buttocks, and typically worsens with activity and improves with rest. Often, tenderness over the paravertebral musculature is present, although exact reproduction of the pain is atypical.

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