Bursae are fluid-filled sacs located at points of contact between bony landmarks and overriding tendons. There are at least 150 bursae symmetrically distributed throughout the human body. Additional bursae can develop in areas of increased friction. Each bursa acts as a cushion that minimizes friction and allows smooth gliding interactions between bones and tendons. The bursa is lined by a membrane that secretes synovial fluid. Synovial fluid serves to lubricate the area and facilitate motion in confined joint spaces. Without bursae, limb movement would be painful.
Bursitis is inflammation of the bursa. The most frequent sites of bursitis are the shoulder, elbow, hip, and knee—specifically the subdeltoid, olecranon, ischial, trochanteric, semimembranous-gastrocnemius, and prepatellar bursae. Irritation of the bursa can be acute or chronic. Various etiologies underlying bursitis include trauma (inflammatory or hemorrhagic bursitis), infection, and arthritic conditions such as osteoarthritis, rheumatoid arthritis, systemic lupus erythematosus, gout, and pseudogout. Overuse or repetitive microtrauma is the most common cause of bursitis. Bursitis is diagnosed in patients of all ages and levels of activity. The risk of bursitis increases with age; however, traumatic bursitis is more likely in patients under 35 years of age. Bursitis is predominantly diagnosed in males. Individuals who participate in repetitive or vigorous activity or who suddenly increase the intensity of activity are at increased risk for bursitis.
Patients with bursitis typically present with point tenderness directly over the bursa, dull ache or stiffness at the affected joint, increased pain with range of motion of overlying muscles and tendons, warmth, erythema, and swelling at the bursal site. Inflammation of the calcaneal bursa can cause swelling extending proximally to the knee.
Inflammatory bursitis is often due to repetitive microtrauma. Recurring injury to the bursa triggers local vasodilatation and increased vascular permeability, ultimately causing the infiltration of extracellular fluid and proteins into the bursa. Inflammation causes synovial cells to multiply and thereby increases fluid production. In the acute setting, early inflammation causes the bursa to become distended. The additional bulk is perceived as foreign by the immune system, and this stimulates further inflammation. In the cases of chronic microtrauma, the bursal wall becomes thickened and the contents of the bursal sac are altered. Rather than synovial fluid, the bursa is filled with granular, brown, inspissated blood and calcifications. Its gritty contents create more friction when bone and tendon move against the bursa.
Hemorrhagic bursitis is characterized by bleeding directly into the bursa. It is typically due to violent trauma inflicted on the overlying tissues, and most commonly occurs at the prepatellar bursa of the knee. Rapid accumulation of blood causes an acute enlargement of the bursa and accompanying pain. The increased bursal mass hinders mobility of the nearby joint.
Infectious bursitis most commonly affects the olecranon and prepatellar bursae. Predisposing factors include diabetes, alcoholism, steroid therapy, uremia, trauma, skin disease, and a history of noninfectious bursitis. Patients will present with extreme tenderness, warmth, and erythema at the site, and there is often evidence of injury to the overlying skin. Infection often occurs from direct introduction of bacteria through traumatic injury or by contiguous spread of cellulitis. Bacterial infection is most commonly due to Staphylococcus aureus and Staphylococcus epidermidis. Roughly 10 percent of cases have been linked to species of Streptococcus. Further support for infectious bursitis includes the presence of lymphadenitis, cellulitis, and fever. The absence of these findings, however, does not rule out infection. Acute swelling and erythema warrant aspiration of the bursa and analysis of the fluid—including cell count, Gram stain, culture, and microscopic evaluation. A bursal fluid white cell count greater than 1,000/mcL is consistent with infection. A measurement greater than 50,000/mcL suggests septic bursitis. Complete laboratory evaluation should also include a complete blood count and erythrocyte sedimentation rate.
Bursitis due to crystal deposition is associated with various arthritic conditions, including rheumatoid arthritis, gout, and pseudogout. On aspiration, various types of crystals may be seen based on the underlying illness: monosodium urate (gout), calcium pyrophosphate (pseudogout), cholesterol (rheumatoid chylous bursitis), and hydroxyapatite (hydroxyapatite crystal disease). Crystal deposition and the arthritides are less common causes of bursitis.
The differential diagnosis for upper extremity pain includes rotator cuff tear, adhesive capsulitis, tendonitis, shoulder dislocation, fracture, and referred pain from a neck injury. Other possible diagnoses for lower extremity pain include sciatica, lumbar disc disease, pelvic stress fracture, pelvic tumor, avascular necrosis of the femoral head, meniscal tear, thrombophlebitis, ligamentous injury or tear, Osgood-Schlatter disease, Achilles tendonitis, and Reiter syndrome.
Bursitis is typically diagnosed based on physical examination. Patients often present with abrupt onset of swelling and localized tenderness over the bursa, pain with range of motion of adjacent muscles and tendons, and erythema. One exception to note is olecranon bursitis—this condition may not be painful at presentation. Chronic bursitis may also present with disuse atrophy and weakness.
When considering bursitis, it is important to obtain a thorough medical history, including duration of symptoms, recent fever, history of repetitive movement (i.e., kneeling while cleaning floors or resting elbows on a computer desk), history of rheumatic conditions (i.e., RA, SLE, or gout), surgical history, and recreational activities.
Diagnostic testing may include aspiration of the bursa with fluid analysis, radiological studies (X-ray, magnetic resonance imaging, computerized tomography, bone scan), complete blood cell count, erythrocyte sedimentation rate, rheumatoid factor, rapid plasma reagent, antinuclear antibody, and uric acid. As stated previously, aspiration of the bursa should be done when an infectious etiology is under consideration. The bursal fluid may be tested for cell count with differential, appearance, culture, Gram stain, and presence of crystals. Fibrocartilaginous bodies (also known as “rice bodies”) in the bursa are associated with autoimmune disorders such as rheumatoid arthritis. Radiographs are not usually necessary, but they may be done in cases of acute trauma, joint instability, or significant deformity. Trauma cases may reveal a hooked acromion process, tendon calcification, or decreased acromiohumeral distance. MRI is usually reserved for cases requiring surgery. Bone scans assist clinicians in ruling out stress fracture, avascular necrosis, and osteomyelitis.
Treatment of bursitis should include pain control as well as rehabilitation and prevention of future potential injury. A seven-step plan, represented by the acronym PRICEMM, has gained wide acceptance among healthcare providers. PRICEMM has been used as a framework for tailoring a patient’s rehabilitation plan. The acronym stands for protection, relative rest, ice, compression, elevation, medication, and modalities.
The first step of treatment is to eliminate pressure from the affected area and to protect the joint. Movement and pressure of the inflamed area can exacerbate symptoms and impede healing. Soft foam padding, orthopedic felt, and braces can be used to protect the affected area from increased friction or pressure. A sling can be used to protect the arm and support the shoulder in some cases of upper extremity bursitis. Heel pads can be inserted into shoes to decrease friction at the calcaneal bursae. Sitting on a foam pad (referred to as a “doughnut” cushion) has also provided relief to patients with bursitis of the hip, particularly ischiogluteal bursitis.
Relative rest should be prescribed to encourage patients to continue participation in exercise, but to choose activities that will not further irritate the bursa. Initially, activity should be modified to avoid things that exacerbate the pain. The overall goal should be for the patient to refrain from the triggering activity, but to maintain their fitness level by participating in alternative activities such as swimming or cycling. Continued physical activity accelerates the rehabilitative process. Bed rest or immobilization of the associated joint after the inflammation subsides is not appropriate and should be discouraged in cases of bursitis.
Application of an ice pack will help to decrease inflammation and swelling, allowing the bursa to return to its normal shape and consistency. Ice is also an effective analgesic. Direct application of ice to the skin should be done at least twice a day for 10 minutes at a time. Compression of the affected bursa can be accomplished with an elastic bandage. While the bursa is wrapped, the extremity should be elevated above the level of the heart to decrease the amount of swelling. Elevation of the extremity for 20–30 minutes several times daily will facilitate removal of fluid from the affected area.
Various modalities have aided the healing of irritated and inflamed bursae. Electrical stimulation, ultrasound, and phonophoresis have been used to decrease inflammation and reduce pain. These practices are typically done by a physical therapist. Physical therapy is often prescribed for patients experiencing weakness in an extremity or a decline in range of motion.
Medications of choice for bursitis are nonsteroidal antiinflammatories (NSAIDs) or aspirin. The goal of using these medications is to alleviate pain and allow the patient to resume activity and participate in a rehabilitation program. NSAIDs are typically used for four to six weeks if symptoms have been present for fewer than three weeks at the time of diagnosis. While NSAIDs and aspirin are the preferred initial treatment, some patients will require additional medication if conservative management is not effective. Corticosteroid injections (betamethasone, triamcinolone) are the next step in treatment. Corticosteroids are powerful anti-inflammatory medications that provide rapid relief when injected into the bursa at the point of maximal tenderness. Patient education regarding the potential side effects of corticosteroid use should always be done. All patients should be informed of the possibility for subcutaneous fat atrophy, skin depigmentation, hyperglycemia, tendon rupture, and infection. Risk for these complications is decreased when the injections are spaced at least one month apart.
As discussed earlier, some cases of bursitis are due to a bacterial infection of the bursal fluid. If this is the case, the swollen bursa needs to be drained in order to evacuate the infected fluid. Antibiotics should be prescribed to cover potential infectious agents, typically Staphylococcus species; penicillinase-resistant penicillins (i.e., dicloxicillin, nafcillin, oxacillin) or first-generation cephalosporins (i.e., cephalexin) are frequently used for treatment. The chosen medication may need to be adjusted after culture and analysis of the fluid.
Surgery is another option for treatment of bursitis, but it is rarely done. The main surgical candidates are patients with chronic bursitis or infectious bursitis. In chronic cases that have not improved with traditional therapy, surgery may be done to correct an anatomical abnormality, such as a bone spur. In cases of infection, the bursa may be opened and drained (“incision and drainage” procedure) or removed entirely.
Elbow Injuries and Disorders; Knee Injuries and Disorders.
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