Pes Anserine Bursitis Medication
- Author: P Mark Glencross, MD, MPH, FACOEM, FAAPMR; Chief Editor: Consuelo T Lorenzo, MD more...
In general, medications are not frequently used to treat pes anserine bursitis. In cases where pharmacologic therapy may be warranted to help alleviate symptoms, the addition of an over-the-counter or prescribed anti-inflammatory medication, such as a nonsteroidal anti-inflammatory drug (NSAID), may be indicated. In addition, injection of a local anesthetic, with or without a corticosteroid, may be helpful.
Nonsteroidal Anti-inflammatory Drugs
NSAIDs have analgesic, anti-inflammatory, and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase (COX) activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions.
Although increased cost can be a negative factor, the incidence of costly and potentially fatal gastrointestinal (GI) bleeding is clearly lower with COX-2 inhibitors than with traditional NSAIDs. Ongoing analysis of the cost of preventing GI bleeding will further define the populations that will find COX-2 inhibitors the most beneficial.
Anesthetic (local) and corticosteroid combinations may be used. Local anesthetics stabilize neuronal membranes and prevent the initiation and transmission of nerve impulses, thereby producing local anesthesia. Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects; in addition, they modify the body’s immune response to diverse stimuli. This compounded medication consists of 0.5 mL of betamethasone and 2.0 mL of 1% lidocaine without epinephrine.
Ibuprofen is the drug of choice for patients with mild to moderate pain. It inhibits inflammatory reactions and pain by decreasing prostaglandin synthesis.
Naproxen is used for relief of mild to moderate pain; inhibits inflammatory reactions and pain by decreasing the activity of cyclooxygenase, thereby decreasing prostaglandin synthesis.
Indomethacin is rapidly absorbed; metabolism occurs in the liver by demethylation, deacetylation, and glucuronide conjugation. It inhibits prostaglandin synthesis.
Ketoprofen is used 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 greater than 75 mg do not yield increased therapeutic effects. Administer high doses with caution, and closely observe the patient for response.
Celecoxib primarily inhibits COX-2. COX-2 is considered an inducible isoenzyme, 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 effective dose of celecoxib for each patient.
Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. They modify the body’s immune response to diverse stimuli.
Triamcinolone decreases inflammation by suppressing migration of polymorphonuclear leukocytes (PMNs) and reversing capillary permeability.
Methylprednisolone decreases inflammation by suppressing migration of PMNs and reversing increased capillary permeability.
Betamethasone decreases inflammation by suppressing migration of PMNs and reversing increased capillary permeability.
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