Lower extremity bursitis

Lower extremity bursitis

Janus D. Butcher

Bursitis is a common cause of lower extremity pain in people of all ages and activity levels. Typically, these patients have painful swelling, which is exacerbated by activity. The onset of symptoms may be insidious, resulting from chronic overuse, or acute, resulting from a single traumatic event. Because of the pr-oximity of bursae to other major structures, SYMPtoms may be vague and the diagnosis difficult to make. An understanding of the regional anatomy, typical clinical history and clinical manifestations is necessary to differentiate bursitis from the many other causes of lower extremity pain.

Bursitis has been reported to account for 0.4 percent of all visits to primary care clinics.[1] However, in runners the incidence may be as high as 10 per-cent.[2] Often the symptoms are mild enough that the patient may successfully “self-treat” through activity modification and other conservative measures. In more severe cases, the patient may be quite disabled, requiring a physician’s care. However, treatment is often frustrating for both patient and physician. A systematic approach to evaluation and treatment, with a well-structured rehabilitation program and a realistic recovery schedule, greatly facilitates the healing process and allows a fun return to activity.

Anatomy and Pathophysiology

Two types of bursae are described, constant and adventitial. While they are different in development and histology, both types can be involved in acute or chronic injuries. Constant bursae, which are formed during normal embryonic development, are sac-like structures lined with endothelial cells. They are generally present between tendon and bone or skin, and serve tb facilitate a gliding motion at points of high friction. The bursa may communicate with the adjacent joint (e.g., the supra-patellar or iliopsoas bursae) or may be understanding (e.g., the prepatellar bursa). The scant synovial cells secrete a fluid rich in collagen, proteoglycans and several enzymatic proteins, which act as a lubricant.

Adventitial bursae form later in life through a process of myxomatous degeneration of fibrous tissue in response to stress at the site of friction between adjacent structures (e.g., the bunion bursae).[3] These bursae lack an endothelial lining and do not contain synovial fluid. The location of adventitial bursae is quite variable, and many unique locations have been reported, including the mid-pretibial area, the area over the fifth metatarsal/ phalangeal bunion and the area over bony prominences in the kyphotic spine.

Many causes of bursitis have been described, the most common of which are trauma (inflammatory or hemorrhagic bursitis, crystal deposition and infection. Inflammatory bursitis often arises from repetitive subacute injury to the bursa. This repetitive injury results in local vasodilatation and increased vascular permeability, with the extravasation of serum proteins and extracellular fluid into the bursa.[4] This “foreign” material stimulates the inflammatory cascade and leukocyte reaction. Inflammatory bursitis also occurs in conjunction with systemic diseases such as rheumatoid arthritis, spondyloarthropathies, syphilis, hypothyroidism and systemic scleroderma.

Hemorrhagic bursitis is usually caused by a direct blow to the overlying tissues, resulting in hemorrhage into the bursa. The rapid collection of blood leads to pronounced swelling and pain, which may result in limited motion of the adjacent joint. This type of bursitis frequently occurs in the superficial bursae, such as the prepatellar bursa of the knee.

Crystal deposition, a less common cause of bursitis, is associated with rheumatoid arthritis, gout, pseudogout and the spondyloarthropathies. The types of crystals involved indude monosodium urate, calcium pyrophosphate, hydroxyapatite, cholesterol and calcium oxalate (Table 1). Calcific bursitis is the result of abnormal deposition of calcium, usually in the form of hydroxyapatite, into the collagenous matrix in response to chronic inflammation.

Infectious bursitis is most common in the superficial bursae. Approximately 90 percent of these infections are caused by Staphylococcus aureus or Staphylococcus epidermidis, and about 9 percent are caused by streptococcal species.[5] Mycobacterium tuberculosis, Mycobacterium marinum and Haemophilus influenzae have been isolated in rare cases. Physical examination reveals exquisite tenderness, erythema and significant warmth. Associated findings of lymphadenitis, cellulitis and fever further support the diagnosis. There is often evidence of damage to the overlying skin. It may be difficult to distinguish infectious bursitis from inflammatory bursitis, and bursal fluid analysis is frequently necessary.


A careful history, including discussion of inciting events or precipitating activities, symptom modifiers (medications, rest), past history of similar problems and past medical history will often suggest the diagnosis.

The physical examination reveals tenderness over the affected bursa, with swelling, erythema and warmth. Range of motion at the adjacent joint may be reduced because of pain. In chronic bursitis, the affected limb may show disuse atrophy and weakness. The adjacent tendons may also be involved, and examination may reveal tenderness along the tendon.

Aspiration should be performed in cases that suggest an infectious etiology. After sterile preparation of the area, the skin is anesthetized with 1 percent lidocaine. A 19- or 20-gauge needle is inserted into the bursa under sterile conditions, and the contents are aspirated into a 20- or 30-mL syringe. The aspirate should be sent for an analysis that includes these factors: appearance, ceu count, Gram stain, culture and microscopy (Table 2).

Radiographs may be helpful in identifying osteophytes or other underlying bony pathology that may contribute to the development of bursitis. A bone scan is not generally needed to make the diagnosis; however, a scan may help to rule out other causes of lower extremity pain (such as stress fractures) if the diagnosis is in doubt. Magnetic resonance imaging (MRI) and computed tomographic (CT) scanning have been used in the evaluation of bursitis[6]; however, their high cost and the commonly abundant clinical findings usually render them unnecessary.

If infectious bursitis is suspected, a laboratory evaluation that includes a complete blood cell count and an erythrocyte sedimentation rate should be performed. Tests for rheumatoid factor, antinuclear antibody, thyroid function or rapid plasma reagent may be indicated if an autoimmune disease or other systemic disease is suspected.


The treatment of bursitis has two parts: first, control of inflammation and pain, and, second,”rehabilitation and prevention of reinjury. The acronym “PRICEMM” (protection, relative rest, ice, compression, elevation, medication and modalities) is useful in designing an anti-inflammatory and analgesic treatment plan.[7] The following discussion outlines each component of PRICEMM.


Padding or bracing is particularly important for superficial bursae such as the retrocalcaneal or prepatellar bursa. Soft foam padding or orthopedic felt can be cut into pads to prevent continued friction injury. Commercially available athletic pads may also be useful.


Prescribed rest should be active rest. Encouraging alternative exercise activities that eliminate exacerbating motions allows patients to maintain their level of fitness and speeds their recovery. Examples of alternative exercises include swimming, pool running, cycling or ski machines. The physician should also offer strategies for altering vocational activities to decrease irritation to the bursa.


Ice is a very effective anti-inflammatory and analgesic agent. A convenient method is to use foam coffee cups, which are filled with water and frozen. The foam is then peeled back from the ice, and the* overlying skin is massaged in small circular motions with direct application of the ice. The patient should apply the ice for 10 minutes at a time, at least twice a day, until symptoms resolve.


When anatomically feasible, an elastic bandage can be applied and the affected extrimity elevated above the level of the heart to assist in reducing swelling.


Physical modalities such as ultrasound and high-voltage electrical stimulation may be useful in reducing the inflammation and pain associated with bursitis.[8]


Nonsteroidal anti-inflammatory drugs (NSAIDs) are the initial pharmacologic agents of choice. While they should never be used as the sole treatment for bursitis, they offer pain relief that allows the patient to resume activity and begin rehabilitation. It is important to give the patient a realistic expectation of the results of medication. NSAIDS do not cure the bursitis but, rather, attenuate the inflammatory process.

Injection of a corticosteroid such as betamethasone (Celestone) or triamcinolone (Aristocort) into the bursa provides excellent anti-inflammatory activity and pain relief. One method is to combine 20 to 40 mg of triamcinolone (or 6 mg of betamethasone) with 3 to 15 mL of lidocaine and inject the mixture into the bursa at the point of maximal tenderness.

Because of the potential complications of corticosteroid administration, including subcutaneous fat atrophy, skin depigmentation, infection, tendon rupture, hyperglycemia and steroid flare, it is important to carefully counsel the patient before the injections are begun. Injections are usually limited to three in a 12-month period, spaced at least 30 days apart to minimize the risk of complications. Corticosteroid injection should be reserved for patients who fail to respond to more conservative measures.

Rehabilitative exercise is the cornerstone of treatment, in most cases of bursitis. Friction over the affected bursa can be reduced by improving flexibility, and symmetrically strengthening the muscles involved in adjacent joint motion, to improve, joint mechanics.[7] Muscle atrophy is common in patients with chronic pain, and this problem should be addressed in the rehabilitation program.

On occasion, patients fail to improve with conservative therapy and require surgery to correct an underlying bony defect or exostosis. In some cases, excision of the bursa may be required.

Infectious bursitis requires drainage followed by antibiotic therapy. Pending culture results, the use of an antibiotic effective against staphylococcal species should be instituted. Good options include the penicillinase-resistant synthetic penicillins (e.g., dicloxacillin, given at a dosage of 500 mg four times per day), or a first-generation cephalosporin (e.g., cephalexin [Keflex], given in a dosage of 500 mg four times per day). The antibiotic choice should be adjusted according to culture and sensitivity results.

Specific Injury Sites

More than 150 bursae in the body have been described, all of which can become injured. Several sites in the lower extremity are frequently involved and are discussed below. Because of the relationship of bursae to nearby structures, it is often difficult to differentiate bursitis from other causes of lower extremity pain. A careful history and physical examination usually allow an accurate diagnosis to be made without expensive imaging studies.


Ischiogluteal Bursitis (Weaver’s Bottom). The ischiogluteal bursa lies deep to the gluteus maximus over the ischial tuberosity. Inflammation of this bursa is associated with the chronic and continuous direct stress that occurs in sedentary occupations.

Typically, patients have pain with sitting and walking. They have tenderness over the ischial tuberosity, which may be exacerbated by passive flexion and resisted extension of the hip. In patients with pain in the gluteal region, the possibility of sciatica, lumbar disc disease and piriformis syndrome should also be considered in the diagnosis.

Treatment includes employing the PRICEMM guidelines and instituting active rehabilitation by improving flexibility and strength. Lifestyle or occupational modifications to decrease direct pressure on this area should be prescribed. If vocational demands r-equire continued sitting, a foam pad or air-filled “doughnut” that decreases direct pressure over the affected ischial tuberosity should be used.

Greater Trochanter Bursitis. The greater trochanter has up to three bursae, which are associated with the gluteal muscle groups (Figure 1). Trochanteric bursitis occurs most frequently in overweight, middle-aged women. It results from acute trauma, overuse or mechanical factors, including shortened hip abductors or external rotators, and increased varus angulation of the hip due to leg-length discrepancy or a broad pelvic structure.[9] Calcific bursitis also occurs, but the incidence is relatively low.[10]

Clinically, these patients have deep, aching, lateral hip pain that may extend into the buttocks or the lateral knee. Pain is aggravated by activity, local pressure or stretching, and is often worse at night (which may interfere with sleep). Palpation over the bony prominence of the greater trochanter and slightly inferiorly or posteriorly elicits exquisite tenderness. Pain can also be elicited with resisted hip abduction and external rotation.

The differential diagnosis of lateral hip pain includes local soft tissue injury, neuropathies involving the lumbar nerve roots (L2 to L4) and branches of the iliohypogastric or subcostal nerves, and irritation of lumbar facet joints and paraspinous ligaments.[9] Other considerations include vertebral disc disease, femoral head and neck pathology such as avascular necrosis or stress fractures, and metastatic tumors.[10]

Conservative treatment includes the general PRICENM guidelines and rehabilitative exercises. Weight loss, conditioning and use of proper lifting techniques can aid in preventing recurrent or chronic injury.” The local injection of a corticosteroid is often very effective in relieving symptoms. Because of the relatively large volume of this bursa, up to 15 mL of lidocaine with 40 mg of triamcinolone can be injected at the point of maximal tenderness.


Eleven bursae are located around the knee. Five of these bursae are commonly involved in painful injuries: the pes anserine bursa, prepatehar bursa, medial collateral ligament bursa (Figure 2) and the bursae of the popliteal space (medial gastrocnemius bursa or semimembranosus bursa), commonly referred to as popliteal cysts.

Medial Collateral Ligament Bursa (No-Name, No-Fame Bursa of Stuttle). This bursa is usually located at the anterior border of the tibial segment of the medial collateral ligament. Injury to this bursa commonly follows a twisting injury with external tibial rotation. 12 The patient has medial knee pain below the joint line, which may prevent full extension of the knee. Palpating along the anteroinferior portion of the medial collateral ligament elicits tenderness, and a mass is often felt. Pain can be elicited by briskly extending the knee from a position of 90 degrees flexion.

On occasion, MRI may be required to differentiate this condition from a tear in the medial meniscus. Other causes of medial knee pain, such as medial collateral ligament injury or synovial plica, are usually excluded by the physical examination. This injury usually responds well to conservative measures and corticosteroid injection.

Pes Anserine Bursa. The pes anserine bursa lies behind the medial hamstring, which is composed of the tendons of the sartorius, gracilis and semitendinosus (SGT) muscles. Inflammation of the anserine bursa occurs commonly in overweight, middle-aged women, where it is associated with osteoarthritis of the knee. It also occurs in athletes, particularly those

engaged in activities such as running, basketball and racquet sports.

Typically, the patient has pain and tenderness over the anteromedial aspect of the knee, 4 to 5 cm below the joint line, which is exacerbated by active flexion of the knee. Examination reveals swelling over the anteromedial tibia just proximal to the insertion of the SGT tendons; the swelling can be mistaken for a cyst or a mass.[6] The tenderness may track along the SGT tendons, indicating an associated tendinitis. There is often evidence of patellar malalignment, as well as poor flexibility, particularly in the hamstrings and quadriceps tendons.

The differential diagnosis for this injury includes degenerative joint disease, meniscal injury and collateral ligament injury. These diagnoses are readily excluded by the location of the symptoms which, in patients with these disorders, will involve the joint line or the peripatellar soft tissues.

Treatment follows the general guidelines noted above. Often a diagnostic injection of 1 percent lidocaine into the bursa aids in making the diagnosis. Injected corticosteroids can be very useful; however, because of potential tendon rupture, care must. be taken not to inject directly into the SGT tendons. In addition, patients should be instructed to pay particular attention to stretching the hamstrings, quadriceps and Achilles tendons.

Prepatellar Bursa. Prepatellar bursitis (housemaid’s knee, or coal miner’s knee). presents as swelling anterior to the knee cap. It is usually associated with trauma, either chronic, as with repetitive kneeling (housemaid’s knee) or an acute injury, such as a blow to the knee.

The prepatellar bursa is one of the most common sites for septic bursitis. Infection should be considered if there is evidence of injury to the skin overlying the bursa. Other frequent findings in patients with infectious bursitis include increased warmth, redness and severe tenderness.

Aspiration should always be performed if infection is suspected. As previously mentioned, staphylococcal species are the most common infectious agents involved, and initial therapy should be directed against these organisms.

In noninfectious cases, treatment follows the general guidelines described previously. Wrapping the knee with an elastic bandage or padding for protection against further injury is helpful.

Popliteal Cysts. Popliteal (Baker’s) cysts usually arise from an intra-articular effusion that causes herniation of the articular synovial membrane through the posterior joint capsule into the popliteal space. Swelling of the medial gastrocnemius or semimembranosus bursae may also cause a painful popliteal cyst. These bursae can also become enlarged by an intra-articular effusion through the natural communication between these bursae and the knee joint. Popliteal cysts usually result from a significant intra-articular knee injury, osteoarthritis, rheumatoid arthritis and, less commonly, gouty arthritis.

Symptoms due to gastrocnemius or semimembranosus bursitis include painful local swelling or popliteal mass, which worsens with walking, jumping or squatting. Physical examination usually demonstrates a tender mass in the popliteal fossa. A careful examination of the knee must be done to rule out associated internal derangement. Ultrasound examination or MRI is useful to differentiate an isolated semimembranosus bursa that communicates with the joint from a synovial hernia related to intra-articular pathology.

In adults, treatment often requires surgery to correct intra-articular injury or to remove the cyst. These cysts are generally not injected with steroids because of the risk of neurovascular injury. In children, popliteal cysts are usually not associated with intra-articular pathology and may be treated by observation after the diagnosis is confirmed by imaging studies.


Retrocalcaneal Bursa. The retrocalcaneal bursa lies anterior to the Achilles tendon and posterior to the calcaneus (Figure 3). Bursitis is commonly caused by local trauma associated with a poorly designed shoe or worn heel counter on the shoe. Groups with the highest incidence of this condition include female adolescents transitioning to the use of high heels, ice skaters (with a female predominance) and distance runners.

Typically, the patient has posterolateral heel pain, particularly with passive dorsiflexion or resisted plantar flexion. A posterior heel prominence, local swelling and tenderness at the medial or lateral aspect of the Achilles tendon insertion is indicative of retrocalcaneal bursitis. Other causes of posterior heel pain should be differentiated, including gout, rheumatoid arthritis, Achilles tendinitis, osteomyelitis, Reiter’s syndrome and fracture of the os trigonum, or loose bodies in the posterior ankle.

In treating retrocalcaneal bursitis, the physician should identify offending footwear and have the patient modify or replace it as necessary to relieve the source of friction. Open heels (clogs), bare feet or a heel lift can be used to reduce the precipitating stress. PRICEMM guidelines and improved flexibility of the Achilles tendon are often effective. Surgical correction of an underlying bony abnormality (e.g., Haglund’s deformity) may be required if symptoms persist following conservative measures. Surgical correction should be a last resort, as the end result is not always satisfactory.[13] Corticosteroid injection should be done with extreme caution because of the proximity to the weight-bearing Achilles tendon.



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JANUS D. BUTCHER, MAJ, MC, USA is currently a faculty member in the Family Practice Department at Dwight David Eisenhower Army Medical Center, Fort Gordon, Ga. He received his medical degree from the University of Minnesota-Duluth School of Medicine, and completed a family practice residency at Madigan Army Medical Center, Tacoma, Wash. He also completed a primary care sports medicine fellowship at the Uniformed Services University of the Health Sciences, Bethesda, Md., and the Nirschl Orthopedic Clinic, Arlington, Va.

KEITH L. SALZMAN, MAJ, MC, USA is a faculty member in the Family Practice Residency at Tripler Army Medical Center, Honolulu. He received his medical degree from the Mayo Medical School, Rochester, Minn., and completed a famiiy practice residency at Dwight David Eisenhower Army Medical Center, Fort Gordon.

WADE A. LILLEGARD, M.D. is currently a faculty member of the Duluth (Minn.) Center for Sports Medicine. He graduated from the Uniformed Services University of the Health Sciences, Bethesda, Md., and completed a family practice residency at Martin Army Community Hospital, Fort Benning, Ga. He also completed a primary care sports medicine fellowship at Michigan State University College of Human Medicine, East Lansing.

Address correspondence to Janus Butcher, MAJ, MC, USA, Dept. of Family Medicine, Dwight David Eisenhower Army Medical Center, Fort Gordon, GA 30905.

COPYRIGHT 1996 American Academy of Family Physicians

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