Updated: Oct 28, 2009
The lumbar vertebrae are the 5 largest and strongest of all vertebrae in the spine. These vertebrae comprise the lower back. They begin at the start of the lumbar curve (ie, the thoracolumbar junction) and extend to the sacrum. The strongest stabilizing muscles of the spine attach to the lumbar vertebrae. Fractures of lumbar vertebrae, therefore, occur in the setting of either severe trauma or pathologic weakening of the bone. Osteoporosis is the underlying cause of many lumbar fractures, especially in postmenopausal women. Osteoporotic spinal fractures are unique in that they may occur without apparent trauma. However, a thorough diagnostic workup is always required to rule out spinal malignancy. (See image below and Image 1.)
The lumbar spine provides both stability and support, allowing humans to walk upright. Proper function of the lumbar spine requires that it have a normal posture (ie, a normal lumbar curve). Any injury that changes the shape of a lumbar vertebra will alter the lumbar posture, increasing or decreasing the lumbar curve. As the body attempts to compensate for the alteration in the lumbar spine in order to maintain an upright posture, this will tend to distort the curves of the thoracic and cervical spine.
Lumbar compression fractures can be a devastating injury, therefore, for 2 reasons. First, the fracture itself can cause significant pain, and this pain sometimes does not resolve. Second, the fracture can alter the mechanics of the posture. Most often, the result is an increase in thoracic kyphosis, sometimes to the point that the patient cannot stand upright. In trying to maintain their ability to walk, patients with kyphosis report secondary pain in their hips, sacroiliac joints, and spinal joints. These patients are also at risk for falls and accidents, increasing the risk of secondary fractures in the spine and elsewhere.
Fractures in the lumbar spine occur for a number of reasons. In younger patients, fractures are usually due to violent trauma. Car accidents frequently cause flexion and flexion distraction injuries. Jumps or falls from heights cause burst fractures. These fractures can also result in serious neurological injury. In older patients, lumbar compression fractures usually occur in the absence of trauma, or in the context of minor trauma, such as a fall. The most common underlying reason for these fractures in geriatric patients, especially women, is osteoporosis. Other disorders that can contribute to the occurrence of compression fractures include malignancy, infections, and renal disease.
Traumatic fractures
Different types of fractures can occur in the lumbar (or thoracic) spine. Classification of these fractures is based on the 3-column anatomic theory of Denis, which describes anterior, middle, and posterior spinal columns consisting of aspects of the spine and their corresponding ligaments and other soft-tissue elements. The Denis system, however, was created to classify traumatic fractures. A similar classification system does not exist for compression fractures. The main reason to use such a classification is to help determine whether a fracture is stable. Instability in the Denis system implies that damage has occurred to at least 2 of the columns of the lumbar spine.
When any of the above injuries occurs with a severe rotational force, the degree of injury and of instability increases.
Nontraumatic fractures
In osteoporosis, osteoclastic activity exceeds osteoblastic activity, resulting in a generalized decrease in bone density. The osteoporosis weakens the bone to the point that even a minor fall on the tailbone, causing an axial load or flexion, results in one or more compression fractures (see Image 1). The fracture is usually wedge shaped. Without correction, a wedge fracture invariably increases the degree of kyphosis.
Malignancies that result in spinal fractures are most commonly metastases rather than primary bone cancers. Primary cancers that often spread to the spine via hematologic dissemination include cancers of the prostate, kidneys, breasts, and lungs. Melanoma is a less common but more aggressive cause of spinal metastasis. The most common primary cancer of the spine is multiple myeloma, but others, including a variety of sarcomas,2 can also manifest as a spinal fracture. Nonmalignant lesions that can cause fractures include aneurysmal bone cyst and hemangioma.
Spinal infections usually start in the lumbar intervertebral disk. From the disk, the infection spreads to bone, resulting in osteomyelitis. Severe pain is the hallmark symptom. The exception is spinal tuberculosis or Pott disease. In this case, the disk spaces are typically spared and a compression fracture may be the initial manifestation that leads to its discovery.
Most fractures of the lumbar spine that require operative treatment occur at the thoracolumbar junction. These injuries are primarily traumatic in origin. Most nontraumatic lumbar fractures are osteoporotic in origin. These are almost invariably wedge-type compression fractures. The National Osteoporosis Foundation (NOF) estimates that currently, 10 million individuals in the United States have osteoporosis, and 34 million more have low bone mass.3 In 2005, osteoporosis was responsible for more than 2 million fractures; approximately 547,000 of those were vertebral fractures. Approximately one third of osteoporotic vertebral injuries are lumbar, one third are thoracolumbar, and one third are thoracic in origin. Additionally, 75% of women older than 65 years who have scoliosis have at least 1 osteoporotic wedge fracture.
Osteoporosis occurs primarily in postmenopausal women. Type 1 osteoporosis occurs in women aged 51-65 years and is associated with wrist and vertebral fractures. Estrogen deficiency is the main etiologic factor. Type 2 osteoporosis (senile type) is observed in women and men older than 75 years, in a 2:1 ratio of women to men.
In young and middle-aged adults, most lumbar fractures are traumatic in origin. High-velocity falls can cause burst fractures, and seat-belt injuries can cause wedge fractures. As stated above, women 51-65 years old develop type 1 osteoporosis. After age 75 years, men also begin to develop type 2 osteoporosis.
Midline back pain is the hallmark symptom of lumbar compression fractures. The pain is axial, nonradiating, aching, or stabbing in quality and may be severe and disabling. The location of the pain corresponds to the fracture site, as seen on radiographs. In elderly patients with severe osteroporosis, however, there may be no pain at all as the fracture occurs spontaneously.
Young adults may present with severe back pain following an accident, such as a fall or a motor vehicle accident. Lower extremity weakness or numbness are important symptoms of neurologic injury from the fracture.
Vertebral fractures may also cause referred pain. Gibson et al presented a study of 350 patient encounters in 288 patients with 1 or more compression fracture without conus medullaris compromise or spinal nerve compression. They found that nonmidline pain was present in 240 of the 350 encounters. The pain was typically in the ribs, hip, groin, or buttocks. Treatment of the fracture with vertebroplasty (see Other Treatment) resulted in 83% of those patients gaining pain relief.4
Alternatively, many compression fractures are painless. Osteoporosis is a silently progressive disease. Osteoporotic compression fractures are often diagnosed when an elderly patient presents with symptoms such as progressive scoliosis or mechanical lower back pain and the physician obtains routine lumbar radiographs.
Finally, patients may present with a known (or unknown) malignancy. Routine spinal screening via magnetic resonance imaging (MRI; if focal or referred pain occurs), or via bone scan (as a survey if pain has not occurred) reveals the pathologic fracture. The most common malignancies leading to spinal involvement in the form of fractures are metastasis and multiple myeloma. Often, the compression fracture is the presenting manifestation that leads to the diagnosis of malignancy. However, patients may also have unexplained fevers, night sweats, past history of malignancy, or weight loss.
Finally, patients who have recently traveled outside of the United States, or who live in the inner city, may have symptoms of infection, such as general malaise, fever, or severely increasing pain. In these patients, osteomyelitis and Pott disease (tuberculosis spondylitis) must be ruled out.
A detailed neurologic examination is essential in all patients presenting with back pain, spine deformity, or traumatic spine injury. Most interventional procedures to alleviate pain in compression fractures are contraindicated in cases of neurologic compromise. Thus, a rectal examination is required to assess for rectal tone and sensation in trauma patients.
Upon inspection of the spine, the patient typically has a kyphotic posture that cannot be corrected. The kyphosis is caused by the wedge shape of the fractured vertebra; the fracture essentially turns the lateral conformation of the vertebra from a square to a triangle.
Hip flexor contractures due to iliopsoas shortening are typically present.
Palpation is important to correlate any reports of pain to the radiographic level of injury. Extreme pain elicited with superficial palpation is often observed in patients with spinal infections. Moderate pain is usually present at the level of the fracture.
The principal underlying cause of lumbar compression fractures is osteoporosis. In women, the leading risk factor for osteoporosis is menopause, or estrogen deficiency. Additional risk factors that may worsen the severity of osteoporosis include cigarette smoking, physical inactivity, use of prednisone and other medications, and poor nutrition. In males, all of the above nonhormonal risk factors apply; however, low testosterone levels also may be associated with compression fractures.
Renal failure and liver failure are both associated with osteopenia. Nutritional deficiencies can decrease bone remodeling and increase osteopenia. Finally, genetics also play a role in the development of compression fractures; osteoporosis can be observed in closely related family members.
Malignancy may manifest initially as a compression fracture. The most common malignancy in the spine is metastasis. Typical malignancies that metastasize to the spine are renal cell, prostate, breast, and lung, although other types can metastasize to the spine on rare occasions. The 2 most common primary spine malignancies are multiple myeloma and lymphoma.
Infection that results in osteomyelitis can also result in a compression fracture. Typically, the most common organisms in a chronic infection are staphylococci or streptococci. Tuberculosis can occur in the spine and is called Pott disease.
| Coccyx Pain | Osteoporosis (Primary) |
| Lumbar Degenerative Disk Disease | Osteoporosis (Secondary) |
| Lumbar Facet Arthropathy | |
| Lumbar Spondylolysis and
Spondylolisthesis | |
| Mechanical Low Back Pain |
Spinal malignancy resulting in fracture
Renal failure
Hemangioma of vertebral body
Osteomyelitis
Pott disease
PET scanning has been used to differentiate benign compression fractures from malignant ones. However, therapy with bone marrow–stimulating agents may result in false-positive scans for malignant fracture.6
The indications for surgical management of lumbar compression fractures are discussed in Surgical Intervention. Nonoperative treatment consists of pain relief, bracing, and rehabilitation.
Traumatic injuries with neurologic compromise usually require comprehensive inpatient rehabilitation. Mobility and strength rehabilitation programs are individualized to each patient's capabilities. All therapy disciplines comprising the multidisciplinary team participate in the comprehensive program. In most cases, rehabilitation begins with the patient in a thoracic-lumbar-sacral orthosis (TLSO). More information on comprehensive spinal cord rehabilitation is available in Spinal Cord Injury and Aging.
Elderly patients with osteoporotic compression fractures are often treated with TLSO bracing and rehabilitation. To facilitate progress in the rehabilitation program, some patients can be treated in a less restrictive corset or abdominal binder if their pain is well controlled. Early mobilization is important to prevent secondary complications of immobility. The therapy occasionally begins in an inpatient setting and then moves to an outpatient setting. Weight-bearing exercises are usually part of the program and are believed to be the main type of therapy required to prevent progression of the osteoporosis in the future. Extension exercises are also considered beneficial. Radiographic monitoring of the fracture over the ensuing months is important, because some fractures can worsen to the point at which they require surgical stabilization.
Used primarily when a patient requires inpatient rehabilitation, occupational therapy is essential to restore the patient's maximal level of function.
Recreational therapy is an essential component of the inpatient rehabilitation program. For many patients, recreational therapists bridge the gap between the hospital and the community.
Early mobilization is extremely important to decrease the frequency of secondary medical complications. Complications can occur in young adults and in elderly patients.
Surgical intervention is required when neurologic dysfunction and/or instability occurs as a result of the lumbar fracture.
In patients thought to have a pathologic cause for lumbar fractures, appropriate consultations with medical specialists are required to assist with either the diagnostic workup or medical management of these conditions.
Oral medications are useful in patients with lumbar fractures for many reasons. The initial goal for most patients is pain relief. In geriatric patients, the goal of pain relief must be balanced by the potential adverse effects of some of the stronger pain medications. Often, the strongest pain medications can cause severe disorientation, respiratory depression, and constipation.
The second goal is to prevent further osteoporosis in these patients. A variety of agents may be used for this purpose, including parathyroid hormone, antiosteoporotic agents, bisphosphonates, and selective estrogen modulators.
Patients with spinal cord injuries need many different medications to assist with their rehabilitation and daily function (eg, to treat spasticity or autonomic dysreflexia).
Ohtori et al found that an L2 spinal nerve block may provide temporary relief of low back pain from acute osteoporotic lumbar vertebral fractures.31 In a randomized, controlled study, 60 patients with acute L3 or L4 osteoporotic vertebral fractures received 1.5 mL of 1% lidocaine in a spinal nerve root block or a subcutaneous injection. Patients who received the L2 block showed greater improvement in pain relief, as measured by the visual analog scale score, at 1 hour, 1 week, and 2 weeks after treatment (P <.05). From 1 month to 4 months after treatment, however, significant pain-score differences between the groups no longer existed (P >.05). The authors concluded that, although L2 spinal nerve blocks had no long-term effects on pain and social function, they provided effective pain relief for 2 weeks.
Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained fractures or other trauma.
A centrally acting analgesic, often appropriate in elderly patients with moderate back pain.
1 tab PO q4-6h prn; often a tid/qid dosing schedule can prevent cycling of pain; not to exceed 4000 mg/d; codeine can then be given independent of acetaminophen
Administer weight-based dosing
Toxicity increases with CNS depressants or TCAs
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Caution in patients dependent on opiates because this substitution may result in acute opiate withdrawal symptoms; caution in severe renal or hepatic dysfunction
Reserved for patients with more severe back pain from their fracture; can be given in short- or long-acting form.
5-10 mg PO q4-6h prn; 10-20 mg of long-acting form can be given bid with fewer fluctuations in pain level
Not established
Phenothiazines may antagonize analgesic effects; MAOIs, general anesthesia, CNS depressants, and TCAs may increase toxicity
Documented history of dependence or abuse of these medications; need to operate heavy machinery or drive
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
Pregnancy category D if used for prolonged periods or in high doses at term; caution in COPD, emphysema, and renal insufficiency
DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.
375-650 mg PO q4-6h prn or 1000 mg PO q6-8h prn; 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 in 24 h
Rifampin can reduce analgesic effects; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; known G-6-P deficiency
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Hepatotoxicity possible in people with long-term alcoholism 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 doses exceeding recommended maximum dose
Centrally acting analgesics. Although mode of action is not completely understood, from animal tests, at least 2 complementary mechanisms appear applicable: binding of parent and M1 metabolite to micro-opioid receptors and weak inhibition of reuptake of norepinephrine and serotonin.
Ultram: 50-100 mg PO q6-8h
Ultram ER: 100-300 mg PO qd
Not established
Significantly decrease carbamazepine effects; cimetidine increases toxicity; risk of serotonin syndrome with coadministration of antidepressants
Documented hypersensitivity; opioid-dependent patients; concurrent use of MAOI or within 14 d; use of SSRIs, TCAs, or opioids; acute alcohol intoxication
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Seizures have been reported in patients receiving Ultram within the recommended dosage range; spontaneous postmarketing reports indicate that seizure risk is increased with doses of Ultram above the recommended dosing range; risk of convulsions may also increase in patients with epilepsy, history of seizures, or a recognized risk for seizure (eg, head trauma, metabolic disorders, alcohol and drug withdrawal, CNS infections); in Ultram overdose, naloxone administration may increase risk of seizure; administer Ultram cautiously in patients at risk for respiratory depression; may impair mental and or physical abilities required for performance of potentially hazardous tasks such as driving car or operating machinery
Drug combination indicated for relief of moderate to severe pain.
1-2 tab/cap PO q4-6h prn for pain
0.05-0.15 mg/kg/dose oxycodone PO; not to exceed 5 mg/dose of oxycodone PO q4-6h prn
Phenothiazines may decrease analgesic effects; toxicity increases with coadministration of either CNS depressants or TCAs
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
Duration of action may increase in elderly patients; be aware of total daily dose of acetaminophen patient is receiving; do not exceed 4000 mg acetaminophen in 24 h; higher doses may cause liver toxicity
Potent semisynthetic opiate agonist similar in structure to morphine. Approximately 7-8 times as potent as morphine on mg-to-mg basis with shorter or similar duration of action.
1-4 mg PO q4-6h prn; alternatively, 1-2 mg IV/IM/SC q4-6h prn; adjust dose according to pain scale assessment
Not established
Hydantoins may decrease effects; phenothiazines, CNS depressants, and TCAs may increase toxicity
Documented hypersensitivity; obstetrical analgesia, increased intracranial pressure, respiratory depression, ulcerative colitis, Crohn disease, abdominal cramping and distention
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
Pregnancy category D in prolonged use or high doses at term; caution in patients with head injuries because may increase respiratory depression and CSF pressure (use only if absolutely necessary); caution postoperatively and with history of pulmonary disease (suppresses cough reflex); increased dosing levels, due to tolerance, may aggravate or cause seizures (even without prior history); adjust dose in renal insufficiency (do not use in severe renal dysfunction); normeperidine metabolite accumulation may induce CNS toxicity; monitor closely for morphine-induced seizure activity if prior seizure history
A synthetic opioid that is 75-200 times more potent with much shorter half-life than morphine sulfate. Has less hypotensive effects and is safer in patients with hyperactive airway disease than morphine because of minimal-to-no associated histamine release. By itself, it causes little cardiovascular compromise, although addition of benzodiazepines or other sedatives may result in decreased cardiac output and blood pressure.
Highly lipophilic and protein-bound. Prolonged exposure leads to accumulation in fat and delays weaning process.
Consider continuous infusion because of short half-life.
Parenteral form is DOC for conscious sedation analgesia. Ideal for analgesic action of short duration during anesthesia and during immediate postoperative period.
Excellent choice for pain management and sedation of short duration (30-60 min) and easy to titrate. Easily and quickly reversed by naloxone.
After initial parenteral dose, subsequent parenteral doses should not be titrated more frequently than q3h or q6h thereafter.
Transdermal form is used only for chronic pain conditions in opioid-tolerant patients. When using transdermal dosage form, most patients are controlled with 72-h dosing intervals; however, some require dosing intervals of 48 h.
Emergency: 0.5-2 mcg/kg/dose IM/IV
Analgesia: 0.5-1 mcg/kg/dose IM/IV q30-60min
Transdermal: Apply a 25-mcg/h system q48-72h
<2 years: 2-3 mcg/kg/dose IM/IV q30-60min
2-12 years: 1-2 mcg/kg/dose IM/IV q60min
>12 years: Administer as in adults
Phenothiazines may antagonize analgesic effects of opiate agonists; TCAs may potentiate adverse effects when both drugs are used concurrently
Documented hypersensitivity; hypotension or potentially compromised airway in which establishing rapid airway control would be difficult
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 hypotension, respiratory depression, constipation, nausea, emesis, and urinary retention; idiosyncratic reaction known as chest wall rigidity syndrome may require neuromuscular blockade in order to increase ventilation
DOC for analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone.
Various IV doses are used; commonly titrated until desired effect obtained.
Starting dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h
Relatively hypovolemic patients: Start with 2 mg IV/IM/SC; reassess hemodynamic effects of dose
Infants and children: 0.1-0.2 mg/kg dose IV/IM/SC q2-4h prn; not to exceed 15 mg/dose; may initiate at 0.05 mg/kg/dose
Phenothiazines may antagonize analgesic effects of opiate agonists; TCAs, MAOIs, and other CNS depressants may potentiate adverse effects
Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult
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 hypotension, respiratory depression, nausea, emesis, constipation, urinary retention, atrial flutter, and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate
Centrally acting pain medication that combines tramadol hydrochloride with acetaminophen. Clinical trials demonstrated that the combination offers better pain relief over either medication alone. Indicated for the short-term (5 days or less) management of acute pain.
2 tab PO q4-6h prn pain for 8 d maximum
Not established
Tramadol decreases carbamazepine effects significantly; cimetidine increases toxicity; risk of serotonin syndrome increases with coadministration of antidepressants
Rifampin can reduce analgesic effects of acetaminophen; coadministration with barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity
Documented hypersensitivity; opioid-dependent patients; concurrent use of MAOI or within 14 days; use of SSRIs, TCAs, opioids; acute alcohol intoxication; known G-6-PD deficiency
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Tramadol can cause dizziness, nausea, constipation, sweating, pruritus; additive sedation with alcohol and TCAs; abrupt discontinuation can precipitate opioid withdrawal symptoms; adjust dose in liver disease, myxedema, hypothyroidism, hypoadrenalism; pregnancy, breast-feeding; seizure; development of tolerance or dependency with extended use
Hepatotoxicity possible with acetaminophen in chronic alcoholics following various dose levels; severe or recurrent pain or high or continued fever may indicate a serious illness; APAP is contained in many OTC products and combined use with these products may result in cumulative APAP doses exceeding recommended maximum dose
Promote new bone formation on trabecular and cortical (periosteal and/or endosteal) bone surfaces by preferential stimulation of osteoblastic activity over osteoclastic activity.
Recombinant human parathyroid hormone rhPTH(1-34), which has identical sequence to 34 N-terminal amino acids (biologically active region) of 84-amino acid human parathyroid hormone. Acts as endogenous parathyroid hormone, thus regulating calcium and phosphate metabolism in bone and kidney. Works primarily to stimulate new bone by increasing number and activity of osteoblasts (bone-forming cells). Additional physiological actions include regulation of bone metabolism, renal tubular reabsorption of calcium and phosphate, and intestinal calcium absorption. When administered with calcium and vitamin D, teriparatide increases bone mineral density and decreases risk of fractures in patients with osteoporosis.
20 mcg SC qd
Not established
None reported
Documented hypersensitivity; increased risk for osteosarcoma (including those with Paget disease of bone or unexplained elevations of alkaline phosphatase, open epiphyses, or prior radiation therapy involving the skeleton); children or growing adults; patients with bone metastases or history of skeletal malignancies and those with metabolic bone diseases other than osteoporosis
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Monitor for hypercalcemia; may cause orthostatic hypotension (particularly following first several doses), dizziness, or leg cramps
Used to prevent worsening of osteoporosis and occasionally can reverse the process.
Administered most often intranasally. Advantage is that it also can relieve some of the back pain associated with fracture.
1 puff 200 IU/d in alternating nostrils; 100 IU SC qd/qod
Not established
None reported
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
Hypocalcemia may occur; examine urine sediment during prolonged therapy
Analogs of pyrophosphate that act by binding to hydroxyapatite in bone matrix, thereby inhibiting dissolution of crystals. Prevent osteoclast attachment to bone matrix and osteoclast recruitment and viability.
A bisphosphonate that acts as a specific inhibitor of osteoclast-mediated bone resorption. Patients should be upright and not lie down for 30 min after taking medication.
10 mg PO qd; must take at least 30 min before first food intake of day
Not established
None reported
Documented hypersensitivity; abnormalities of the esophagus that delay esophageal emptying; inability to sit upright for at least 30 min; hypocalcemia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Hypocalcemia must be corrected before initiating treatment; not recommended for patients with renal insufficiency
May act like estrogen to prevent bone resorption.
Selective estrogen receptor modulator that decreases bone loss.
60 mg PO qd
Not established
Concomitant use with estrogen replacement medication not recommended; coadministration of cholestyramine not recommended
Documented hypersensitivity; breastfeeding; women who could become pregnant; history of thromboembolic events
D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus
Not associated with an increased risk of breast cancer; hot flashes and leg cramps are most common adverse effects
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[Best Evidence] Ohtori S, Yamashita M, Inoue G, et al. L2 spinal nerve-block effects on acute low back pain from osteoporotic vertebral fracture. J Pain. Aug 2009;10(8):870-5. [Medline].
lumbar compression fracture, compression fracture, kyphoplasty, vertebroplasty, burst fracture, wedge fracture, balloon kyphoplasty, percutaneous vertebroplasty, spine compression fracture, lumbar spine compression fracture, lumbar crush fracture, osteoporotic fracture, collapse fracture, osteoporosis, vertebra fracture, vertebral fracture, spinal wedge fracture
Andrew L Sherman, MD, MS, Associate Professor of Clinical Rehabilitation Medicine, Vice Chairman, Chief of Spine and Musculoskeletal Services, Program Director, SCI Fellowship and PMR Residency Programs, Department of Rehabilitation Medicine, Leonard A Miller School of Medicine, University of Miami
Andrew L Sherman, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Sports Medicine, American Medical Association, American Paraplegia Society, American Spinal Injury Association, and Association of Academic Physiatrists
Disclosure: pfizer Honoraria Speaking and teaching
Nizam Razack, MD, FACS, Assistant Professor of Neurological Surgery, Orthopedics, and Rehabilitation, University of Miami; Neurosurgeon, Spine and Brain Neurosurgery Center; Chairman, Department of Neurosurgery, Orlando Regional Medical Center
Nizam Razack, MD, FACS is a member of the following medical societies: American Association of Neurological Surgeons, American College of Surgeons, Congress of Neurological Surgeons, Florida Medical Association, and Society for Neuro-Oncology
Disclosure: Nothing to disclose.
Curtis W Slipman, MD, Director, University of Pennsylvania Spine Center; Associate Professor, Department of Physical Medicine and Rehabilitation, University of Pennsylvania Medical Center
Curtis W Slipman, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists, International Association for the Study of Pain, and North American Spine Society
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Patrick M Foye, MD, FAAPMR, FAAEM, Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School
Patrick M Foye, MD, FAAPMR, FAAEM is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society
Disclosure: Nothing to disclose.
Kelly L Allen, MD, Regional Medical Director, IMX-Medical Management Services
Disclosure: Nothing to disclose.
Rene Cailliet, MD, Professor-Chairman Emeritus, Department of Rehabilitation Medicine, University of Southern California School of Medicine; Former Director, Department of Rehabilitation Medicine, Santa Monica Hospital Medical Center
Rene Cailliet, MD is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American Pain Society, Association of American Medical Colleges, International Association for the Study of Pain, and Pan American Medical Association
Disclosure: Nothing to disclose.
Related eMedicine topics:
Lumbar Spine Fractures and Dislocations
Lumbar Spine, Trauma
Nonoperative Treatment of Osteoporotic Compression Fractures
Vertebral Fracture
Vertebroplasty and Kyphoplasty, Percutaneous
Clinical guidelines:
ACR Appropriateness Criteria® osteoporosis and bone mineral density. American College of Radiology - Medical Specialty Society. 1998 (revised 2007). 12 pages. NGC:005990
Clinical trials:
Comparison of Balloon Kyphoplasty, Vertebroplasty and Conservative Management in Acute Osteoporotic Vertebral Fractures (OSTEO-6)
Comparison of Balloon Kyphoplasty and Vertebroplasty in Subacute Osteoporotic Vertebral Fractures (OSTEO+6)
KAVIAR Study - Kyphoplasty And Vertebroplasty In the Augmentation and Restoration of Vertebral Body Compression Fractures
Tapentadol IR vs Oxycodone IR vs Placebo in Acute Pain From Vertebral Compression Fracture Associated With Osteoporosis
To Evaluate Success of Cement Treatment of Spinal Compression Fractures
Treatment of Malignant Vertebral Fractures With Percutaneous Balloon Kyphoplasty. (KYPHOK)
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