Although it is commonly not palpable clinically, in the event of inflammation, the examiner may be able to detect effusion and thickening due to synovial irritation. The bursal synovium is subject to pathological change due to trauma, infection, metabolic disease, occupational strains, and neoplasms. Of course, this writing is dedicated to those aspects of treatment which relate to physiatry.
Acute direct trauma typically results in distention of the bursal sac with synovial effusion and may appear as a local swelling. Although this swelling may resolve spontaneously, from a therapeutic perspective, resolution may be enhanced by a compression wrap and rest. Initially, cryotherapy may reduce the intensity of the swelling and, after 3-4 days, heat packs may enhance the absorption of localized edema. One percent hydrocortisone pulsed phonophoresis @ 0.5 W/cm2 X 5 minutes, t.i.d., p.r.n. for pain and/or swelling may be administered.
In chronic traumatic bursitis, where the bursal wall becomes thickened and fibrotic with small accumulations of fibrin within the synovial cavity, synovectomy is commonly required, after which a compress is applied and a new bursa then forms.
Acute and chronic infectious bursitis is treated with appropriate antibiotic therapy. The area of the genicular region overlying this bursa may appear reddened, be markedly warm to palpation, with muscle spasm limiting local joint ROM. There may be fever, neutrophilia, and an elevated ESR. These clinical features usually resolve with continued use of the appropriate antibiotics.
Gouty bursitis involves urate deposits in the bursal wall with symptoms comparable to the infectious signs/symptoms. Biopsy, microscopy, and sometimes radiographic imaging reveal the effects of urate crystals interstitially. Although contrast therapy may provide for some initial relief, any treatment must be accompanied by antigout therapy in the form of purine restriction, increase in dietary vegetables, and possibly colchicine derivatives per oral.
There is no specific, effective, physiatric treatment for malignant lesions of the bursae. These lesions would be referred to other specialties for appropriate care.
Although seldom observed at this site, calcific bursitis may be considered a by-product of recurrent lesions of a sprain/strain/trauma character. Since this process favors the Glimcher hypothesis, it is capable of shifting from a soluble to an insoluble state and back again based on the chemical modification of the interstitial fluids. It is therefore possible to modify this calcific lesion to a noncalcific state with appropriate treatment. Acetic acid phonophoresis (three percent) may be effective, but care must be exercised in its application to avoid tissue irritation due to the effects of hydrogen ion concentration. Ultrasonic energy is applied with the lesion submerged in a one percent or two percent acetic acid solution (vinegar is three percent to four percent) @ 0.5 to 0.75 W/cm2 X 7 minutes. Any complaint of discomfort by the patient, for any reason, should result in immediate discontinuation of treatment and rinsing of the submerged tissue. There is some question as to the efficacy of this treatment.
Although the foregoing therapeutic regimen is commonly effective, in the event of continued complaints and/or objective findings, referral for orthopedic consultation is recommended.
Davis RV. Therapeutic Modalities for the Clinical Health Sciences, 2nd ed., 1989, Library of Congress Card TXU 389-661.
Griffin and Karselis. Physical Agents for Physical Therapists, 2nd ed., Thomas Publishers, 1982.
Krupp and Chatton. Current Medical Diagnosis and Treatment, Lange Publications, 1980.
Turek. Orthopedics -- Principles and Their Application, 3rd ed, Lippincott.
R. Vincent Davis, DC, PT, DNBPM