Perspective

Low back pain (LBP) is associated with large economic costs, both direct and indirect. Estimates vary depending on the types of care included (i.e., allopathic medicine versus chiropractic or complementary-alternative medicine), with direct costs being estimated at anywhere from $12 to $91 billion per year in the United States. Lost productivity is thought to be the major indirect costs of LBP; one study puts this annual U.S. cost at $24 billion for workers with LBP versus $7 billion for those without LBP.

Epidemiology

Most adults will experience LBP at some point in their lifetime, and about one in five adults experience LBP within a single year. LBP costs billions of dollars per year. About 85% to 90% of patients with LBP in a variety of outpatient settings are considered to have nonspecific LBP.¹ This may lead to physician complacence in the evaluation of a presumably benign disorder.

Conversely, LBP can be incapacitating, and the patient may perceive the problem as a harbinger of death or disability, regardless of the cause. Patient expectations of a specific diagnosis of the pain source and a complete cure are rarely met and are probably unrealistic. Psychologic, social, and economic factors play a role in the natural history of many pain-related conditions, including progression of LBP from an acute to a chronic condition. LBP often becomes a chronic condition subject to exacerbations, akin to asthma and diabetes mellitus.² These issues combine to make LBP a source of frustration for patients and physicians alike.

Pathophysiology

LBP is a symptom complex caused by a variety of diseases and anatomic abnormalities. Multiple potential sources of pain intrinsic to the spinal column (joints between vertebrae, sacroiliac joint, intervertebral disks, vertebral bones, periosteum, ligaments, meninges, paraspinous muscles, fascia, blood vessels, and nerves) have been implicated. Additionally, a number of visceral structures may be a source of pain referred to the low back region.

LBP is often classified as specific or nonspecific, mechanical or nonmechanical, or primary or secondary or is classified on the basis of presumed etiology (structural, neoplastic, referred pain or visceral, infectious, inflammatory, or metabolic). All these classification systems recognize that in the majority of cases a specific pathoanatomic diagnosis cannot be assigned. Indeed, clear correlation between a specific anatomic abnormality and pain is rarely established in patients, and proposed mechanisms of pain in the medical literature have been fraught with controversy. For example, many asymptomatic subjects have evidence of bulging, prolapsed, or herniated intervertebral disks.³

Presenting Signs and Symptoms

Differential Diagnosis and Medical Decision Making

Nonmechanical causes must be distinguished from mechanical causes of LBP. The key to such distinction rests on eliminating systemic (infectious, neoplastic, metabolic, or inflammatory) and visceral causes. Figure 92.1 shows one diagnostic approach, and Box 92.1 lists the differential diagnosis for LBP.

Fig. 92.1 Diagnostic approach to low back pain.

Specific causes of LBP are shown in Table 92.1, together with red flag signs or symptoms suggesting these diagnoses. When the history and physical examination suggest a nonmechanical cause of LBP, appropriate diagnostic testing or specialty consultation (or both) is necessary to confirm or rule out the suspected specific cause or causes.

Table 92.1 “Red Flags” in the History and Physical Examination of Patients with Low Back Pain

^* Age younger than 20 years is associated with increased risk for spondylolysis, spondylolisthesis, and stress fractures; age older than 50 years suggests increased risk for cancer and compression fractures.

^† Unexplained weight loss is defined as more than 10 lb over the preceding 6 months.

^‡ Most commonly caused by a herniated lumbar disk or lumbar spinal stenosis rather than malignancy.

^§ Significant trauma is a fall from a height or external trauma such as a motor vehicle accident.

^‖ Substance abuse can increase the risk for fracture through higher rates of trauma. Alcohol abuse can also increase the risk for fracture as a result of decreasing bone density.

Adapted from Atlas SJ, Deyo RA. Evaluating and managing acute low back pain in the primary care setting. J Gen Intern Med 2001;16:120–31.

Visceral and systemic causes of LBP, though rarely found in most ambulatory care settings, must be addressed. Visceral sources of referred pain that cause LBP can result from a variety of vascular, pelvic, renal, and gastrointestinal pathology. Pain from aortic dissection, for example, can be referred to the back. Similarly, retroperitoneal pathology of any source, including hematomas and metastatic disease, can cause LBP. Patients with pain from these sources may or may not have other clues to the source of their pain. Clues to the diagnosis of aortic dissection may include a diminished femoral pulse or mottling of a leg. Because testicular cancer metastasizes to the retroperitoneum, genitourinary examination might identify the pathology.

A retroperitoneal hematoma may be heralded only by tachycardia or, rarely, by hypotension from blood loss. More commonly, warfarin or an antiplatelet agent may be a contributing factor. Any of these clues may be subtle but may also be the only evidence of an important diagnosis.

Systemic causes of LBP are disease processes that involve the structures of the spinal column, including cancer, infection, inflammation, and degenerative processes. Cancer (with metastatic or primary tumor invasion of the spinal column) typically occurs in those older than 50 years. Weight loss, pain with bed rest, and failure of therapy (with pain lasting a month or longer) are frequent symptoms. Back pain in any patient with a history of cancer should be considered to be due to a cancerous lesion of the spine until ruled out.⁴

Infections involving the spine (spinal epidural abscess [SEA], osteomyelitis, and diskitis) are rare. Prudent suspicion, deliberate consideration, and attention to patient risks are the most important ways to facilitate successful diagnosis. Patients with sickle cell disease are predisposed to Salmonella osteomyelitis. Patients with immunosuppression, chronic corticosteroid therapy, injection drug use, and recent bacterial infections (cellulitis, pneumonia, urinary tract infection) are at increased risk for SEA, osteomyelitis, and diskitis. Patients with SEA may have isolated back pain, spotty neurologic changes that do not fit a discrete distribution, or pain that mimics sciatica.

Inflammatory arthritides such as ankylosing spondylitis can cause LBP but are frequently associated with other arthritic and systemic symptoms. Patients with these diseases usually report pain that worsens with lying down, as well as morning stiffness that gradually improves with activity. The pain is usually chronic, with a duration of 3 or more months, and is of gradual onset. Ankylosing spondylitis is most common in young men, with symptoms usually appearing before the age of 40.

Once possible visceral and systemic causes of the patient’s symptoms have been excluded, the focus should be shifted to determine whether neurologic compromise has occurred. Additionally, diagnoses that may lead to spinal instability (fracture and spondylolisthesis) should be considered.

LBP can be associated with leg pain secondary to radiating pain, but other causes include sciatica (or lumbosacral radiculopathy) with pain radiating from the back to the buttock and posterior or lateral aspect of the leg. Sciatica is frequently caused by lumbar degenerative disk disease. True sciatica usually causes pain below the knee; at least 95% of degenerative disks in the lumbar spine occur at the L4-L5 and L5-S1 vertebral levels. For this reason, the neurologic examination should be focused on both sensory and motor testing of the lumbosacral nerve roots. Table 92.2 details the motor, sensory, and reflex test components of the neurologic examination of patients with LBP. Note that functional strength testing is more likely than simple motor testing to detect subtle muscle weakness.

Passive straight leg raise (SLR) testing appears to help in the diagnosis of sciatica by stretching the sciatic nerve. A positive ipsilateral SLR test (which results in pain below the knee when the leg to which LBP radiates is raised higher than 30 to 60 degrees with the patient supine) is sensitive but not specific for sciatica, whereas a positive crossed SLR test (in which pain in the affected leg is provoked or worsened when the contralateral leg is raised) is specific but insensitive.⁵ A negative SLR test may be of greater value because patients with this finding generally have good long-term outcomes.

Spinal stenosis can result from a variety of processes that impinge on the spinal cord (usually hypertrophy of the ligamentum flavum) and cause pseudoclaudication—back and leg pain with walking and extension of the spine that improves with sitting and lumbar flexion. Most cases occur in patients 55 years or older; they usually report an insidious onset of symptoms.

Cauda equina syndrome (CES) results from compression of the conus medullaris of the spinal cord or the nerve roots that make up the cauda equina. It is typically caused by a large central disk herniation but can also be due to other space-occupying lesions such as spinal stenosis, tumor, SEA, and hematoma.² The most consistent findings in patients with CES are LBP, urinary symptoms, and sacral and perineal (“saddle”) paresthesias.⁶ Bilateral sciatica is also a concerning symptom. Central disk herniations may not cause sciatica, and back pain may be a minor component of the patient’s symptoms. The presence of urinary retention has good sensitivity and specificity for CES.⁷ Magnetic resonance imaging (MRI) is diagnostic and usually shows severe spinal canal impingement by a disk.

Expeditious diagnosis and therapy may help maximize the long-term outcome (in terms of pain and disordered bladder, bowel, and sexual function) in these patients. Despite some controversy regarding the role of impairments already present at diagnosis, there appears to be some improvement in the outcome of CES if decompression is performed within 48 hours of arrival in the emergency department (ED).⁸

LBP without a systemic or visceral cause and without neurologic compromise may nevertheless occur as a result of a specific mechanical cause, usually involving the spinal column itself. Lumbar fractures generally result from significant trauma (e.g., falls from heights, external trauma) but can be caused by minor trauma in older patients, in patients receiving chronic corticosteroid therapy, and in persons at risk for pathologic fractures (e.g., because of bony metastases or osteoporosis of the spine).

A history of trauma and bone tenderness (to palpation or percussion) suggests fracture as a possible cause of LBP. Stress fractures of the sacrum and lumbar spine and insufficiency fractures of the sacrum are other causes of LBP to which athletes (especially young athletes) and older patients (especially women), respectively, are predisposed.

Spondylolisthesis, or slippage of one vertebral body relative to an adjacent vertebral body, is a specific mechanical cause of LBP that can lead to progressive instability. It occurs as a result of a defect in the pars interarticularis from either a fracture or spondylolysis, which can be congenital or degenerative in etiology. Spondylolisthesis can also lead to degenerative disk disease and osteophyte development. Instability causes symptoms similar to those of spinal stenosis.

Children have back pain at higher rates than previously appreciated and are at higher risk for spondylolysis and spondylolisthesis, especially adolescent and teenage athletes. A one-legged hyperextension test may help diagnose these conditions. Bone scans using single-photon emission computed tomography may be the most appropriate initial test, assuming that the findings on plain radiography are normal.⁹

Finally, nonspecific mechanical causes of LBP may be the root of patients’ symptoms when possible systemic and visceral sources have been ruled out and no signs of instability or neurologic compromise are present. Nonspecific LBP syndromes have been called lumbago, lumbar sprain or strain, idiopathic LBP, myofascial strain, and a variety of other names. These patients tend to be most comfortable at rest, and their symptoms worsen with activity and movement. They do not have red flags (that suggest specific musculoskeletal, systemic, or visceral sources of their pain) in their history and physical examination, nor do they have signs or symptoms of neurologic compromise.

The Waddell signs have been promoted as tools to help demonstrate a “nonorganic” cause of patients’ symptoms, but they are mainly useful for predicting patients at risk for prolonged recovery from LBP.¹⁰ Waddell signs may also point to a diagnosis of depression or another psychoneurosis.

Diagnostic Testing

Plain films of the lumbosacral spine, rectal examination, postvoid residual bladder volume, the erythrocyte sedimentation rate, and MRI are useful diagnostic adjuncts in the ED (Table 92.3). Other studies such as myelography (plain or computed tomographic [CT]), electromyography, and diskography should be obtained at the discretion of consultants.

Table 92.3 Diagnostic Adjuncts for Low Back Pain

CES, Cauda equina syndrome; SEA, spinal epidural abscess.

^* Deyo RA, Weinstein JN. Low back pain. N Engl J Med 2001;344:363–70.

^† Henschke N, Maher CG, Refshauge KM. Screening for malignancy in low back pain patients: a systematic review. Eur Spine J 2007;16:1673–9.

^‡ Small SA, Perron AD, Brady WJ. Orthopedic pitfalls: cauda equina syndrome. Am J Emerg Med 2005;23:159–63.

^§ Gilbert FJ, Grant AM, Gillan MG, et al. Low back pain: influence of early MR imaging or CT on treatment and outcome—multicenter randomized trial. Radiology 2004;231:343–51.

If an abdominal aortic aneurysm or dissection is a consideration in the diagnosis, it must be ruled out by an appropriate imaging study, either ultrasound or CT scanning. Urinalysis (and culture as indicated) is recommended for patients in whom urinary tract infection or renal disease is likely. Other specific conditions causing LBP may be diagnosed with appropriate tests as indicated by their differential diagnosis.

Treatment

Admission and Discharge

Admission to the hospital may be required for further evaluation, testing, and treatment, including further diagnostic testing and consultation, as well as relief of symptoms.

Patients with nonspecific LBP can be discharged home in almost all circumstances; there appears to be limited need or utility in admitting patients for pain control. All patients with LBP who are discharged from the ED should be warned about the risk for CES and be told to return if they experience neurologic or bowel or bladder symptoms.¹⁴

Counseling patients with nonspecific LBP that the ED work-up has not found any concerning pathology, that they can expect their pain to get better, and that pain does not necessarily mean danger will help manage their expectations. They should be told to continue their normal activities of daily living as limited by their symptoms. Finally, they should be advised to arrange follow-up with a primary care provider because LBP can recur frequently and may better be managed with continuity of care.

Patients with specific systemic or visceral sources of their LBP require specialist consultation.