Shoulder Impingement Syndrome Medication

During the acute and subacute phases of shoulder impingement syndrome, it is appropriate to use a short course of nonsteroidal anti-inflammatory drugs (NSAIDs) for analgesic and anti-inflammatory effects as an adjunct to the therapy program and other treatment modalities. Choices in this drug classification are extensive, so only selected examples are discussed. Patient response to differing NSAIDs may vary. For information on the full array of NSAIDs available, dosing, and schedule, please refer to the latest edition of the Physician's Desk Reference.

The major mechanism of action of NSAIDs is inhibition of the synthesis of prostaglandin (PG), specifically PGE2 via blocking of cyclo-oxygenase (COX), which is the enzyme that converts arachidonic acid into PG. PGs lower the threshold to noxious stimuli by sensitizing the nociceptors to the actions of other noxious endogenous substances (eg, bradykinin, histamine, substance P, serotonin). PGE2 causes pain and inflammation in soft tissues, is cytoprotective in the GI tract by increasing secretion of mucus and bicarbonates and decreasing secretion of gastric acids and digestive enzymes, and enhances renal salt and water excretion in the renal system by acting as a vasodilator of small arterial blood vessels.

The COX pathway is subdivided into COX1, which is responsible for PGE2 production in the GI tract and kidneys, and, COX2, which is responsible for inflammatory PG synthesis during soft tissue injury. NSAIDs serve as competitive inhibitors of COX activity, and either selectively inhibit the COX2 enzymes or nonselectively inhibit both COX1 and COX2 enzymes, making the nonselective NSAIDs potentially ulcerogenic and renal toxic.

All NSAIDs have similar adverse drug reactions, as follows:

• Hepatotoxicity: Liver function profile must be monitored in patients taking NSAIDs, periodically every 1-2 months, especially in high-risk individuals.
• Renal toxicity: Renal function profile must be monitored periodically every 1-2 months, especially in high-risk individuals.
• GI toxicity: Symptoms may include nausea, diarrhea, acid reflux, and periumbilical cramping. The physician may consider administering NSAIDs in conjunction with GI protective medications (eg, misoprostol, omeprazole, H2-blockers) and instruct patients to take NSAIDs with food. If GI symptoms persist for more than 2 weeks or if the patient has evidence of complication (eg, iron deficiency anemia, GI bleeding, unexplained weight loss, dysphagia), endoscopic evaluation is indicated
• Aplastic anemia: Monitor CBC, especially platelets, periodically for 1-2 months.
• Anaphylaxis: Inquire about and check medical records for history of allergic reactions.

Class Summary

NSAIDs are the most widely used drugs in the world, exhibiting anti-inflammatory, antipyretic, and analgesic activities. They primarily are used for treating inflammatory conditions that are musculoskeletal in origin. Numerous drugs are available in this category and all have similar drug profiles.

Ibuprofen (Ibuprin, Advil, Motrin)

An arylpropionic acid, it is the prototypical NSAID and causes less epigastric pain, GI occult blood loss, and less hepatotoxicity. Mostly indicated for rheumatoid arthritis and osteoarthritis for mild to moderate pain. Compared to other available NSAIDs, it has a short half-life.

Diclofenac sodium/potassium (Voltarem, Cataflam)

Chemical composition is heteroaryl acetic acid with a short half-life. The delayed-release enteric-coated form is diclofenac sodium and the immediate release form is diclofenac potassium. Both primarily are indicated for rheumatoid arthritis, osteoarthritis, and ankylosing spondylitis. Can cause hepatotoxicity; hence liver enzymes should be monitored in the first 8 weeks of treatment. Has a relatively low risk for bleeding GI ulcers.

Etodolac (Lodine, Lodine XL)

Indole NSAID with intermediate half-life indicated for rheumatoid arthritis and osteoarthritis. The short-acting form is approved for analgesic use comparable to aspirin/Tylenol (with codeine). Lower risk of GI complications and is especially well tolerated by elderly patients.

Naproxen (Aleve, Anaprox, Naprelan, Naprosyn)

Probably most potent arylpropionic acid with a long half-life. Indicated for rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, juvenile arthritis, acute gout, and mild to moderate pain. Comes in a controlled release form (also used for acute pain) and an enteric-coated form (not used for acute pain).

Oxaprozin (Daypro)

Arylpropionic acid with 40-50 h half-life. Can be administered qd.

Nabumetone (Relafen)

An alkanone NSAID with long half-life (24 h) that can be administered qd. Lower risk of GI complications and is indicated for rheumatoid arthritis and osteoarthritis.

Piroxicam (Feldene)

Enolic acid with a long half-life (50 h) that can be administered qd. Indicated for rheumatoid arthritis and osteoarthritis. Has high GI toxicity, greater than ASA.

Class Summary

Although increased cost can be a negative factor, the incidence of costly and potentially fatal 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)

Selective COX-2 inhibitor, NSAID approved by the FDA on 12/31/98. Indicated for osteoarthritis and rheumatoid arthritis and moderate to severe pain. Potentially presents less GI complications and platelet aggregation problems than nonselective COX-inhibitor NSAIDs. Renal complications are comparable. Celecoxib has a sulfonamide chain and is primarily dependent upon cytochrome P450 enzymes (a hepatic enzyme) for metabolism.

Class Summary

May offer improved relieve over either agent alone.

Tramadol 37.5 mg and acetaminophen 325 mg (Ultracet)

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 d or less) management of acute pain.