eMedicine Specialties > Sports Medicine > Spine

Lumbosacral Disc Injuries: Treatment & Medication

Author: Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM, President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine
Coauthor(s): Kevin P Sullivan, MD, Consulting Staff, The Boston Spine Group; Erik D Hiester, DO, Fellow in Interventional Pain Management, Emory Medical School/Georgia Pain Physicians
Contributor Information and Disclosures

Updated: Jun 23, 2008

Treatment

Acute Phase

Rehabilitation Program

Physical Therapy

Physical therapy for acute radiculopathy should emphasize analgesia through passive modalities, stretching activities, and soft-tissue mobilization initially, and then the therapy should advance to McKenzie-type activities to regain segmental motion. Once segmental activity has been normalized or improved and the patient's pain has been reduced, then the patient may begin a walking program and a progressive lumbar stabilization program. The stabilization program should be steadily advanced, and the patient should have a generalized conditioning program initiated as well.

Surgical Intervention

The treatment of radiculopathy depends upon the pain severity, degree of functional limitation, and neurologic status. Surgical emergencies include cauda equina syndrome and a rapidly progressive neurologic deficit. Relative surgical emergencies include painless weakness with or without numbness, less than antigravity strength, or extreme leg pain that is unresponsive to a selective nerve root block (SNRB). The above clinical scenarios are thought to be biomechanical rather than biochemical in origin; thus, they are amenable to immediate surgical intervention. All other conditions require a minimum of 6-12 weeks of adequate nonsurgical care before the consideration of surgery. Treatment is directed toward alleviating pain.

For those patients with chronic LBP that is unresponsive to nonsurgical management, lumbar fusion remains the surgical procedure of choice. Unfortunately, suboptimal clinical results are obtained by a significant proportion of patients. Lumbar disc arthroplasty has been developed as a potential means to improve the long-term outcome of these patients.39,40  Although these devices have had relatively good early clinical results, questions still remain about their long-term efficacy in the maintenance of motion and relief of pain, the life span of the devices, and the results of randomized comparative trials with fusion.

Related Medscape topics:
Resource Center Pain Management: Advanced Approaches to Chronic Pain Management
Resource Center Pain Management: Pharmacologic Approaches
Resource Center Spinal Disorders
Specialty Site Neurology & Neurosurgery
Specialty Site Orthopaedics
Specialty Site Surgery

Other Treatment

Early in the care of radiculopathy, interventional procedures may be employed in cases of severe pain, lack of progress, or significant functional impairment. In a position statement, the NASS recommended the use of epidural steroid injections in lumbar radicular pain caused by structural abnormalities such as disc herniation and spinal stenosis.32 If no improvement occurs, confirmation of the diagnosis is required. MRI is the study of choice, but it is important for the lesion, as seen on MRI, to corroborate with the location of symptoms. In borderline or ambiguous cases, electrodiagnostic testing can be helpful. If the diagnosis remains uncertain, a fluoroscopically guided SNRB may be employed as a diagnostic aid.

Appropriate nonsurgical rehabilitative interventions include oral nonsteroidal anti-inflammatory drugs (NSAIDs), spine-specific physical therapy, avoidance of provocative influences, and a fluoroscopically guided steroid injection. If a comprehensive conservative program fails, an open surgical or other less invasive procedure (chemonucleolysis or percutaneous discectomy) is offered. Long-term analyses have not shown surgical intervention to be superior to a more conservative approach.41 Less invasive treatments may be successful in up to 80% of persons thought to be appropriate surgical candidates.

Intradiscal electrothermy (IDET) is perhaps one of the newest and most innovative treatments aimed at chronic LBP resulting from IDD. Targeted thermal therapy with the IDET procedure is designed to modify annular collagen, thermocoagulate annular nociceptive nerve fibers, and cauterize ingrowth granulation tissue. These effects promote collagen remodeling and changes in the annular integrity (causes contraction and thickening of the annulus collagen, thereby stabilizing annulus fissures). A study evaluating the outcome after IDET has shown success rates of 70-80% based upon an improvement of 2 points on a 10-point visual analog score (VAS) and sitting tolerance.42 This procedure has provided an alternative to major spinal surgery in the treatment of chronic LBP related to IDD.

Medication

Oral NSAIDs can help decrease pain and inflammation. Various oral NSAIDs can be used, but none of these agents holds a clear distinction as the drug of choice. The selection of an NSAID is largely a matter of convenience (eg, how frequently the doses must be taken to achieve adequate analgesic and anti-inflammatory effects) and cost.

Opioid analgesics may also be used to help control pain for short durations during treatment. These drugs should not be used long term, and there is not a clear drug of choice. Treatment should be individualized.

Related eMedicine topics:
 Cyclooxygenase Deficiency
Opioid Abuse
Toxicity, Narcotics
Toxicity, Nonsteroidal Anti-inflammatory Agents

Related Medscape topics:
Resource Center Adverse Drug Events Reporting
Resource Center Pain Management: Advanced Approaches to Chronic Pain Management
Resource Center Pain Management: Pharmacologic Approaches

Nonsteroidal Anti-inflammatory Drugs

NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. The mechanism of action of these agents is not known, but they may inhibit cyclooxygenase (COX) activity and prostaglandin synthesis. Other mechanisms may exist as well; these may include inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.

COX-2 inhibitors are equally effective. Although increased cost can be a negative factor, the incidence of costly and potentially fatal gastrointestinal (GI) bleeds is clearly less with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of cost avoidance of GI bleeds will further define the populations that will find COX-2 inhibitors the most beneficial.


Celecoxib (Celebrex)

For arthritis. Inhibits primarily COX-2, which is considered an inducible isoenzyme and is induced during pain and inflammatory stimuli. Inhibition of COX-1 may contribute to NSAID GI toxicity. At therapeutic concentrations, COX-1 isoenzyme is not inhibited, thus, GI toxicity may be decreased. Seek the lowest dose of celecoxib for each patient.

Adult

200 mg/d PO qd; alternatively, 100 mg PO bid

Pediatric

Not established

Coadministration with fluconazole may cause an increase in celecoxib plasma concentrations because of inhibition of the celecoxib metabolism; coadministration of celecoxib with rifampin may decrease celecoxib plasma concentrations.

Pregnancy

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

Precautions

May cause fluid retention and peripheral edema; caution in patients with compromised cardiac function, hypertension, conditions predisposing to fluid retention; caution in the presence of severe heart failure and hyponatremia because circulatory hemodynamics may deteriorate; NSAIDs may mask the usual signs of infection; caution in the presence of existing, controlled infections; evaluate symptoms and signs that suggest liver dysfunction, or in abnormal liver laboratory results


Ibuprofen (Motrin, Ibuprin)

DOC for patients with mild to moderate pain. Inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.

Adult

200-400 mg PO q4-6h while symptoms persist; not to exceed 3.2 g/d

Pediatric

<6 months: Not established

6 months to 12 years: 4-10 mg/kg/dose PO tid/qid

>12 years: Administer as in adults

Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; monitor PT duration closely (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease, recent GI bleeding or perforation, renal insufficiency, or high risk of bleeding

Pregnancy

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

Precautions

Caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of anticoagulation abnormalities or during anticoagulant therapy


Ketoprofen (Oruvail, Orudis, Actron)

For relief of mild to moderate pain and inflammation.
Small dosages are initially indicated in small and elderly patients and in those with renal or liver disease.

Doses over 75 mg do not increase the therapeutic effects. Administer high doses with caution and closely observe patient for response.

Adult

25-50 mg PO q6-8h prn; not to exceed 300 mg/d

Pediatric

<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 the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Pregnancy

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

Precautions

Caution in patients with congestive heart failure, hypertension, and decreased renal and hepatic function; caution in the presence of anticoagulation abnormalities or during anticoagulant therapy


Naproxen (Naprosyn, Naprelan, Anaprox)

For relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, which results in a decrease of prostaglandin synthesis.

Adult

500 mg PO followed by 250 mg q6-8h; not to exceed 1.25 g/d

Pediatric

<2 years: Not established

>2 years: 2.5 mg/kg/dose PO; not to exceed 10 mg/kg/d

Coadministration with aspirin increases the risk of inducing serious NSAID-related adverse effects; probenecid may increase the concentrations and, possibly, the toxicity of NSAIDs; may decrease the effect of hydralazine, captopril, and beta-blockers; may decrease the diuretic effects of furosemide and thiazides; may increase PT duration when taking anticoagulants (instruct patients to watch for signs of bleeding); may increase the risk of methotrexate toxicity; phenytoin levels may be increased when administered concurrently

Documented hypersensitivity; peptic ulcer disease; recent GI bleeding or perforation; renal insufficiency

Pregnancy

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

Precautions

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 the drug.

More on Lumbosacral Disc Injuries

Overview: Lumbosacral Disc Injuries
Differential Diagnoses & Workup: Lumbosacral Disc Injuries
Treatment & Medication: Lumbosacral Disc Injuries
Follow-up: Lumbosacral Disc Injuries
References
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Further Reading

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Contributor Information and Disclosures

Author

Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM, President and Director, Georgia Pain Physicians, PC; Clinical Associate Professor, Department of Physical Medicine and Rehabilitation, Emory University School of Medicine
Robert E Windsor, MD, FAAPMR, FAAEM, FAAPM is a member of the following medical societies: American Academy of Pain Medicine, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, American Medical Association, International Association for the Study of Pain, Physiatric Association of Spine, Sports and Occupational Rehabilitation, and Texas Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Kevin P Sullivan, MD, Consulting Staff, The Boston Spine Group
Kevin P Sullivan, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine, Association of Academic Physiatrists, and Physiatric Association of Spine, Sports and Occupational Rehabilitation
Disclosure: Nothing to disclose.

Erik D Hiester, DO, Fellow in Interventional Pain Management, Emory Medical School/Georgia Pain Physicians
Erik D Hiester, DO is a member of the following medical societies: American Academy of Family Physicians, American Medical Association, American Osteopathic Association, and American Pain Society
Disclosure: Nothing to disclose.

Medical Editor

Andrew D Perron, MD, Residency Director, Department of Emergency Medicine, Maine Medical Center
Andrew D Perron, MD is a member of the following medical societies: American College of Emergency Physicians, American College of Sports Medicine, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Henry T Goitz, MD, Chief, Sports Medicine, Associate Professor, Department of Orthopaedic Surgery, Medical College of Ohio
Henry T Goitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons and American Orthopaedic Society for Sports Medicine
Disclosure: Nothing to disclose.

CME Editor

Jon B Whitehurst, MD, Clinical Instructor of Surgery, University of Illinois College of Medicine; Partner and Executive Board Member, Rockford Orthopedic Associates; Orthopedic Chairman, Rockford Memorial Hospital
Jon B Whitehurst, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine, and Arthroscopy Association of North America
Disclosure: Nothing to disclose.

Chief Editor

Craig C Young, MD, Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Sports Medicine Fellowship Director, Medical College of Wisconsin
Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa, and Wilderness Medical Society
Disclosure: Nothing to disclose.

 
 
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