Updated: Jul 16, 2009
Mechanical low back pain is one of the most common patient complaints expressed to emergency physicians in the United States accounting for more than 6 million cases annually. Approximately two thirds of adults are affected by mechanical low back pain at some point in their lives, making it the second most common complaint in ambulatory medicine and the third most expensive disorder in terms of health care dollars spent surpassed only by cancer and heart disease.1
Low back pain reportedly occurs at least once in 85% of adults younger than 50 years, and 15-20% of Americans have at least one episode of back pain per year. Of these patients, only 20% can be given a precise pathoanatomic diagnosis. Low back pain affects men and women equally. The onset most frequently occurs in people aged 30-50 years. Low back pain is the most common and most expensive cause of work-related disability in the United States.2 Low back pain is not a common complaint in children and, when present, is more likely to have a serious etiology, such as infection or malignancy.3
Many causes of mechanical low back pain exist. The most common causes are age-related degenerative disc and facet processes and muscle- or ligament-related injuries. Discussion in this article is limited to musculoskeletal causes. These can be divided into nerve root syndromes, musculoskeletal pain syndromes, and skeletal causes.
Nerve root syndromes
Classic nerve root syndrome is characterized by radicular pain arising from nerve root impingement due to herniated discs. A similar syndrome can also be produced by inflammation and irritation, which may explain why patients whose presentation is consistent with this diagnosis respond to conservative therapies.
Impingement pain tends to be sharp, well localized, and can be associated with paresthesia, whereas irritation pain tends to be dull, poorly localized, and without paresthesia. Impingement is associated with a positive straight leg raising sign (ie, shooting pain down contralateral leg with leg raising), while irritation is not. Neurologic deficits and pain radiation below the knee are rarely seen in irritation alone and are most commonly found with impingement.4
The cause of impingement syndrome is most commonly herniated discs, but it may also be caused by spinal stenosis, spinal degeneration, or cauda equina syndrome.
Herniated discs are produced as spinal discs degenerate. After growing thinner, the nucleus pulposus herniates out of the central cavity against a nerve root. Intervertebral discs begin to degenerate by the third decade of life, and herniated discs are found on autopsy in one third of adults older than 20 years. Only 3% of these, however, are symptomatic.5 The most common locations for herniation are L4, L5, and S1.6
Spinal stenosis occurs when disc spaces decrease as intervertebral discs lose moisture and volume with age. Even minor trauma under these circumstances can cause inflammation or nerve root impingement, which can produce classic sciatica pain without disc rupture. The pain can often be bilateral.7
Spinal degeneration is caused by alterations in the hygroscopic quality of the nucleus pulposus. This process progresses to annular degeneration. Coupled with progressive posterior facet disease, this process leads to spinal canal or foraminal encroachment. These retrogressive and proliferative changes in the disc anteriorly and the joints posteriorly produce clinical symptoms and radiographic findings termed 3-joint complex degeneration. Spinal degeneration has 3 distinct stages, as follows:
Cauda equina syndrome is produced by massive midline extrusion of nuclear material or tumor into the spinal canal, which compresses the caudal sac. The classic presentation is bilateral sciatica, with lower extremity bowel or bladder dysfunction present in 90% of patients. Urinary retention is initially observed and followed by overflow incontinence. Perineal or perianal anesthesia is present in 60-80% of patients.8
Musculoskeletal pain syndromes
Musculoskeletal pain syndromes that produce low back pain include myofascial pain syndromes and fibromyalgia.
Myofascial pain is characterized by pain and tenderness over localized areas (trigger points), loss of range of motion in the involved muscle groups, and pain radiating in a characteristic distribution but restricted to a peripheral nerve. Relief of pain is often reported when the involved muscle group is stretched.
Fibromyalgia results in pain and tenderness on palpation of 11 of 18 trigger points, one of which is the low back area, as classified by the American College of Rheumatology. Generalized stiffness, fatigue, and muscle ache are reported.
Other skeletal causes
Other skeletal causes of low back pain include osteomyelitis, sacroiliitis, and malignancy.
Osteomyelitis results from infectious processes involving the bones of the spine, while sacroiliitis results from inflammatory changes in the sacroiliac joints. This pain presents over the sacroiliac joints and radiates to the anterior and posterior thighs. This pain is usually worse at night and is exacerbated by prolonged sitting or standing.
Malignant tumors of the spine can be primary or metastatic. Most primary spinal tumors are found in patients younger than 30 years and usually involve the posterior vertebral elements. Metastatic tumors are found mostly in patients older than 50 years and tend to occur in the anterior aspects of the vertebral body.9
Mechanical low back pain is one of the most common patient complaints expressed to emergency physicians in the United States accounting for more than 6 million cases annually.
No differences exist in incidence of back pain between racial groups.
Both male and female populations are affected; however, there is a tendency towards a higher incidence in male patients.
Low back pain is a common complaint in adults of all ages.
Low back pain is not a common complaint in children and, when present, is more likely to have a serious etiology, such as infection or malignancy.
A thorough history and physical examination is paramount to arrive at a diagnosis, and initially imaging is often unnecessary.4
| Aneurysm, Abdominal | Pelvic Inflammatory Disease |
| Appendicitis, Acute | Perirectal Abscess |
| Ectopic Pregnancy | Prostatitis |
| Endometriosis | Renal Calculi |
| Neoplasms, Spinal Cord | Urinary Tract Infection, Female |
| Ovarian Cysts | Urinary Tract Infection, Male |
Perforated viscous
Pancreatitis
Large bowel obstruction
Improvement occurs in almost all patients within 4-6 weeks, except those with infection, occult malignancy, or systemic illness. If pain fails to significantly improve or resolve in this time frame, imaging is always indicated.13
If new neurologic deficits are noted accompanied by bowel or bladder dysfunction one should suspect cauda equina syndrome. This is a true emergency, and emergency imaging is mandated. MRI is the preferred imaging modality in this situation. If cauda equina syndrome is strongly suspected, the practitioner should consider giving dexamethasone without delay to prevent further loss of neurologic function while pursuing confirmatory testing.
Conservative therapy is the mainstay of treatment, as even those with true sciatica generally respond.14 Ultimately, only 2% of patients with sciatica and 4-6% of patients with true disc herniation require surgery. Conservative therapy traditionally includes the following:
Evidence-based clinical practice guidelines from the American Pain Society (APS) for patients with chronic low back pain describe the use of interventional diagnostic tests and therapies, surgeries, and interdisciplinary rehabilitation.19
The goal of pharmacotherapy is to reduce pain and inflammation.
NSAIDs are most commonly used to relieve mild to moderate pain. Although the effectiveness of NSAIDs tends to be patient specific, ibuprofen is usually the DOC for initial therapy. Other options include flurbiprofen, ketoprofen, and naproxen.
DOC to treat mild to moderate pain if no contraindications exist.
Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
600 mg PO tid
<6 months: Not established
6 months to 12 years: 20-40 mg/kg/d PO divided tid/qid
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain and inflammation.
Small dosages initially are indicated in patients who are small or elderly and in those with renal or liver disease. Doses over 75 mg do not increase therapeutic effects. Administer high doses with caution, and closely observe patient for response.
25-50 mg PO q6-8h prn; not to exceed 300 mg/d
<3 months: Not established
3 months to 12 years: 0.1–1 mg/kg PO q6-8h
>12 years: Administer as in adults
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Caution in congestive heart failure, hypertension, and decreased renal and hepatic function; caution in anticoagulation abnormalities or during anticoagulant therapy
For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.
500 mg PO initial, followed by 250 mg q6-8h; not to exceed 1.25 g/d
<2 years: Not established
>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d
Coadministration with aspirin increases risk of inducing serious NSAID-related adverse effects; probenecid may increase concentrations and, possibly, toxicity of NSAIDs; may decrease effect of hydralazine, captopril, and beta-blockers; may decrease diuretic effects of furosemide and thiazides; monitor PT closely (instruct patients to watch for signs of bleeding); may increase risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently
Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency; high risk of bleeding
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Acute renal insufficiency, interstitial nephritis, hyperkalemia, hyponatremia, and renal papillary necrosis may occur; patients with preexisting renal disease or compromised renal perfusion risk acute renal failure; leukopenia occurs rarely, is transient, and usually returns to normal during therapy; persistent leukopenia, granulocytopenia, or thrombocytopenia warrants further evaluation and may require discontinuation of drug
These agents reduce tonic somatic motor activity of the muscle.
Short-acting medication that may have depressant effects at spinal cord level.
Skeletal muscle relaxants have modest short-term benefit as adjunctive therapy for nociceptive pain associated with muscle strains and, used intermittently, for diffuse and certain regional chronic pain syndromes. Long-term improvement over placebo has not been established.
350 mg PO tid/qid
Not established
Increases toxicity of alcohol, CNS depressants, MAO inhibitors, clindamycin, phenothiazines
Documented hypersensitivity; acute intermittent porphyria
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in renal and hepatic impairment
Skeletal muscle relaxant that acts centrally and reduces motor activity of tonic somatic origins influencing both alpha and gamma motor neurons.
Structurally related to tricyclic antidepressants and thus carries some of the same liabilities.
10 mg PO tid with a range of 20-40 mg/d in divided doses; not to exceed 60 mg/d
Not established
Coadministration with MAOIs and tricyclic antidepressants may increase toxicity; cyclobenzaprine may have additive effect when used concurrently with anticholinergics; effects of alcohol, CNS depressants, and barbiturates may be enhanced with cyclobenzaprine
Documented hypersensitivity; patients who have taken MAOIs within the last 14 d
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in angle-closure glaucoma, urinary hesitance
Pain control is essential to ensure patient comfort, to promote pulmonary toilet, and to aid physical therapy regimens. Many analgesics have sedating properties that benefit patients who have sustained injuries.
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, in those with upper GI disease, or in those who are taking oral anticoagulants.
325-650 mg PO q4-6h or 1000 mg tid/qid; not to exceed 4 g/d
<12 years: 10-15 mg/kg/dose PO q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO q4h; not to exceed 5 doses/d
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; known G-6-PD deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; acetaminophen is contained in many OTC products, and combined use with these products may result in cumulative acetaminophen doses exceeding recommended maximum dose
A drug combination indicated for the treatment of mild to moderate pain.
30-60 mg/dose based on codeine content PO q4-6h or 1-2 tabs q4h; not to exceed 12 tabs/d
0.5-1 mg/kg/dose based on codeine content PO q4-6h; 10-15 mg/kg/dose based on acetaminophen content; not to exceed 2.6 g/d of acetaminophen
Toxicity increases with CNS depressants or tricyclic antidepressants
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients dependent on opiates because this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction
A drug combination indicated for the relief of moderate to severe pain.
1-2 tab or cap PO q4-6h prn
<12 years: 10-15 mg/kg/dose acetaminophen q4-6h PO prn; not to exceed 2.6 g/d acetaminophen
>12 years: 750 mg acetaminophen PO q4h; not to exceed 10 mg hydrocodone bitartrate in single dose; not to exceed 5 doses/d
Coadministration with phenothiazines may decrease analgesic effects; toxicity increases with CNS depressants or tricyclic antidepressants
Documented hypersensitivity; elevated intracranial pressure
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Tablets contain metabisulfite, which may cause hypersensitivity; caution in patients dependent on opiates because this substitution may result in acute opiate-withdrawal symptoms; caution in severe renal or hepatic dysfunction
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low back pain, mechanical low back pain, low back pain treatment, low back pain causes, musculoligamentous injury, classic nerve root syndrome, musculoskeletal pain syndrome, impingement syndrome, herniated disk, herniated disc, spinal degeneration, cauda equina syndrome, myofascial pain syndrome, fibromyalgia, osteomyelitis, sacroiliitis, spinal stenosis, degenerative joint disease, straight leg test
Debra G Perina, MD, Associate Professor, Director of Prehospital Care Division, Department of Emergency Medicine, University of Virginia Health Sciences Center
Debra G Perina, MD is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Edward Bessman, MD, Chairman, Department of Emergency Medicine, John Hopkins Bayview Medical Center; Assistant Professor, Department of Emergency Medicine, Johns Hopkins University
Edward Bessman, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine
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Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
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Eric L Legome, MD, Chair, Department of Emergency Medicine, St Vincent's Hospital Manhattan; Associate Professor, Department of Emergency Medicine, New York Medical College
Eric L Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
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John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
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