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Bursae are subcutaneous spaces lined with synovial membranes that secrete fluid to allow smooth and nearly frictionless motion among muscles, ligaments, tendons, bones, and skin. Some bursae are present at birth and are constant throughout life, whereas others are ""formed"" in response to repetitive physical pressure (e.g., bursae under metatarsal heads that may occur in rheumatoid arthritis). Although there are approximately 150 bursae in the body, most are not likely to be of pathologic significance. Bursal inflammation may be a clinical problem, however, in a few predictable anatomic sites: the subacromial bursa of the shoulder, olecranon bursa at the elbow, iliopsoas bursa near the hip, trochanteric-subtrochanteric bursae below the hip, gastrocnemiosemimembranous bursa of the knee, and retrocalcaneal bursa of the heel.
Subacromial bursitis is usually secondary to inflammatory lesions of the rotator cuff or bicipital tendon, both of which are anatomically contiguous to the bursal floor. Subacromial bursitis causes severe pain in all planes of movement but usually is worse with abduction and internal-external rotation movements. Subacromial bursitis should be distinguished from the more frequently encountered tendinitis problems of the shoulder, as the latter are more indolent and longer tolerated by patients. Subacromial bursitis causes prompt and severe pain and is distinguished on physical examination from the tendinitis overuse syndromes.
The olecranon bursa overlies the distal portion of the triceps tendon and the olecranon of the ulna. With inflammation, swelling is seen at the point of the elbow and pain may be present. If so, it occurs most typically with resisted extension of the arm (i.e., with increased tension in the adjacent triceps tendon). If pain is present, particularly with accompanying skin erythema, suspicion of an infection or a crystal-induced process is heightened and a bursal aspiration is indicated. Presumably, bacteria can access the olecranon bursa through the skin even without a visible skin wound. Typically, septic olecranon bursitis is seen in manual laborers and in alcohol abusers; chronic obstructive pulmonary disease patients may also be disproportionately affected. Hemorrhagic olecranon bursitis may be seen in uremic patients undergoing dialysis.
The iliopsoas bursa overlies the hip capsule (lateral to the femoral blood vessels, between the iliopsoas muscle and the anterior surface of the hip joint). The iliopsoas bursa is large (about 6 x 3 cm) and may communicate with the hip joint in select patients. Most often the iliopsoas bursa becomes symptomatic in a patient with predicate hip pathology (often osteoarthritis) and may manifest as an enlarging inguinal mass with pressure on adjacent tissues. These protruding bursae may be confused with a hernia, hydrocele, adenopathy, or psoas abscess. Computed tomography or magnetic resonance imaging scan is diagnostically useful and will demonstrate a well-defined water density mass in the appropriate anatomic site, often with a concurrent hip joint effusion.
The trochanteric bursae, several in number, overlie the lateral hip region. The largest and most important structure lies between the gluteus maximus and the tendon of the gluteus medius muscles. Patients usually complain of a deep, dull, aching pain in the lateral hip area, but half also describe anterolateral proximal lower extremity pain radiating to the knee, often worsening with activity and sometimes disturbing sleep. Differential diagnostic considerations here may include herniated nucleus pulposus of L3-4 (i.e., with symptoms in the L-4 nerve root distribution), spinal stenosis, or an entrapment neuropathy (namely, meralgia paresthetica).
Distention of the gastrocnemiosemimembranous bursa (Baker s cyst) often is a subclinical finding. Baker s cysts may be present and not palpable and may be palpable but not of clinical significance. In inflammatory knee conditions there is usually communication with the knee joint and a one-way synovial fluid flow into the bursa. If dissection or rupture of a Baker s cyst occurs, differentiation from deep vein thrombophlebitis can be difficult (""pseudothrombophlebitis""). Diagnostic ultrasonography is sensitive in detecting the presence of an intact Baker s cyst, but it becomes less reliable when bursal dissection or rupture into the calf occurs. Associated thrombophlebitis must be definitively excluded by venography or reliable, noninvasive means before accepting knee cyst-related phenomena as the sole cause of calf-foot pain and swelling.
Between the calcaneus bone and the Achilles tendon lies the retrocalcaneal bursa. Symptoms in the area of this bursa may be mistaken for Achilles tendinitis, and care should be taken to differentiate these conditions. A swollen retrocalcaneal bursa commonly will show bulging on the medial and lateral sides of the Achilles tendon. The swollen bursa may be extremely sensitive to pressure on direct palpation and with dorsiflexion of the foot. (Caution regarding the introduction of corticosteroid agents in the vicinity of the Achilles tendon is discussed in the treatment section later.)
Common sites of tendon inflammation are the frequently used tendons of the upper extremities where they pass over bony prominences. Although the rotator cuff refers generically to a collection of four muscles about the shoulder, it is specifically the supraspinous muscle that is most commonly involved in tendinitis, perhaps owing to the stress resulting from humeral impingement against the coracoacromial arch. Patients note pain subacromially and laterally over the shoulder with abduction of the arm. Bicipital tendinitis affects the long head of the biceps muscle and characteristically causes shoulder pain anteriorly and over the bicipital groove (particularly with flexion of the shoulder against resistance, elbow extended, and forearm supinated).
Lateral epicondylitis at the elbow (""tennis elbow"") results from inflammation and degeneration of extensor tendons of the forearm, particularly the extensor carpi radialis brevis, with eventual fibrous adherence to the capsule of the lateral elbow. Contracture of the wrist extensor muscles then chronically pulls on the capsule, producing pain about 2 cm distal to the lateral epicondyle. Medial epicondylitis
The dorsum of the wrist contains six compartments through which numerous tendons glide. Although an inflammatory process may affect any of these, inflammation of the abductor pollicis longus and extensor pollicis brevis tendons in the first compartment (i.e., most radial) may result in a lack of smooth excursion of the enclosed tendons, a condition known as de Quervain s disease (stenosing tenosynovitis). Patients describe pain at the radial aspect of the wrist, especially with pinch gripping. Palpation of the tendons in the anatomic ""snuff box"" area may reveal swelling compared with the uninvolved side.
Immobilization of an inflamed musculoskeletal part, whether partial or complete, is an important adjunct in management and helps to expedite and optimize chances for recovery. The exception to this general rule is with tendinitis or bursitis of the shoulder, where immobilization may foster development of a ""frozen"" shoulder and, except for brief periods (e.g., 24 to 48 hours), should be avoided. Splints are especially useful in epicondylitis of the elbow (""elbow band"") and in de Quervain s disease of the thumb. Ice during the acute phase and moist heat during the chronic phase are useful, and nonsteroidal anti-inflammatory drugs (NSAIDs) are helpful in many cases. The choice of a specific NSAID is not critical, but all such agents should be given in ample doses and with food (ideally in the middle of a meal) to lessen the risk of gastropathy. An enteric-coated aspirin preparation, 975 mg every 6 to 8 hours; naproxen (Naprosyn), 250 to 500 mg twice daily; and oxaprozin (Daypro), 1200 mg once a day, are representative examples. For patients with a bleeding diathesis, persons on warfarin (Coumadin) therapy, or those otherwise unable to tolerate the standard NSAIDs, possible treatment options include a nonacetylated salicylate (e.g., Trilisate or Disalcid) or a course of a centrally acting synthetic analgesic such as tramadol (Ultram), 50 to 100 mg every 6 hours as needed.
Physical therapy, ultrasound, or hydrotherapy has application in many cases but is most important in shoulder tendinitis or bursitis, in which there is greater risk of permanent compromise in range of motion. Acute tendinitis or bursitis may render such severe pain, however, that physical therapy intended to augment range-of-motion function becomes impractical or ignored. In such a clinical setting selective local anesthetic-corticosteroid injections are often valuable. The anatomic area is cleaned with povidone-iodine (Betadine) and alcohol, and an ethyl chloride spray may be applied as a topical anesthetic. Selection of corticosteroid is based on the extent of symptoms and, for practical reasons, the relative depth of involved tissue pathology owing to the potential for soft tissue atrophy (especially likely with synthetic fluorinated preparations such as triamcinolone). Consideration should be given to the relative solubility and potency when selecting a corticosteroid preparation (or combination) for soft tissue injection. Medium-potency agents include prednisolone sodium phosphate and prednisolone tebutate; these agents are useful at superficial injection sites. A high-potency fluorinated corticosteroid, such as triamcinolone hexacetonide (Aristospan Intra-articular, slow onset but prolonged duration of action) should be used only for injection of deep structures or for intra-articular injections, to minimize the danger of leakage to the skin with resultant atrophy and/or depigmentation of skin. Ideal technique favors injection near the affected tendon but not directly into the structure itself. A frequently used narrow tendon, such as the bicipital tendon, may be prone to rupture with direct injection; the Achilles tendon and surrounding areas should not be directly exposed to corticosteroid agents because this structure is inherently weak and prone to tear. Although more than a single corticosteroid injection may not be necessary to modify a soft tissue pain syndrome, caution should be taken not to exceed three injections in the same anatomic site over a 12-month period. Under sterile conditions, the incidence of iatrogenic infection with soft tissue injection is extremely low. A patient with glucose intolerance may have a transient effect from local corticosteroid injection. A period of reduced activity of 24 to 48 hours is best to optimize therapeutic results.
Surgical attention is seldom necessary in tendinitis or bursitis, but with structural rupture or recalcitrance to full conservative measures, surgical excision or repair may become a consideration.
Patients with recurrent symptoms must be instructed to avoid provocative or aggravating activities that strain susceptible anatomic structures by overuse. Warm-up and stretching exercises should always precede aerobic conditioning activities.
In the nomenclature of soft tissue pain syndromes, ""myofascial pain"" infers regional discomfort, often with a discernible soft tissue focus palpable on physical examination and radiating pain with modest pressure (4 kg) (""trigger zone""). The development of an anatomic trigger zone may result from trauma (of even minimal severity) or from overuse. Although often post-traumatic, or ostensibly autonomous, myofascial pain may also occur in systemic illnesses. The lack of gross ""swelling"" should not mislead the physician to conclude that the patient has no ""sensation of swelling."" The importance of a careful and ""hands-on"" physical examination cannot be overstated in this setting. Documentation of palpable soft tissue abnormalities is obviously important, but assessment of joint range of motion (passive and active), possible joint hypermobility, and subtle synovial warmth and/or thickening is useful whether any abnormalities are, in fact, present.
Myofascial pain appears to be distinct from the condition of fibromyalgia. Unlike the generalized
Fibromyalgia is a common pain amplification syndrome characterized by generalized chronic pain (longer than 3 months in duration), stiffness, gelling, and fatigue. Typically, patients are women of middle age with predictable tender points on physical examination and a disturbed sleep pattern such that they awaken nonrefreshed from sleep (a nonrestorative sleep pattern). The most frequently affected anatomic sites in fibromyalgia include (bilaterally) at the occiput, low cervical region, midpoint of the trapezius, supraspinatus at the medial border of the scapula, second ribs at costochondral junctions, 2 cm distal to the lateral epicondyles of the elbow, gluteal area in the upper-outer quadrants of the buttocks, 2 cm posterior to the greater trochanter, and at the medial fat pads of the knees proximal to the joint line. Predictable features of fibromyalgia (100% incidence) include generalized pain for at least 3 months and widespread local tenderness at 11 or more of the aforementioned 18 anatomic sites; characteristic features (greater than 75% incidence) are fatigue, sleep disturbance, and morning stiffness; common features (greater than 25% incidence) may be headache, paresthesias, psychologic abnormality, subjective swelling, and functional disability.
The diagnosis of fibromyalgia is based on a characteristic history, the exclusion of systemic diseases that may cause musculoskeletal pain (e.g., rheumatoid arthritis, systemic lupus erythematosus, inflammatory muscle disease, polymyalgia rheumatica, and hypothyroidism), the finding of nonarticular tender points with an essentially normal joint examination, and a normal laboratory profile (i.e., complete blood count, acute phase response, and thyroid functions). Occasionally, a low titer of antinuclear antibody is found but in the absence of an obvious cause such as connective tissue disease or a drug-induced effect.
The pathophysiology of fibromyalgia is not well understood, although an association with psychologic abnormalities has been suggested. There may be a subgroup of fibromyalgia patients with significant coexisting psychologic problems, especially depression, and there appears to be an increased incidence of depression in first-degree relatives of fibromyalgia patients. Most patients with fibromyalgia, however, are not depressed.
The most characteristic sleep abnormality in fibromyalgia is the loss of ""slow-wave"" deep sleep with a relative loss of the restorative phase of sleep. Sleep apnea may be seen disproportionately in male patients with fibromyalgia, and polysomnography is a reasonable consideration in selected patients. The natural history of fibromyalgia is not established definitively. Although symptoms may be chronic, perhaps lasting 10 to 15 years or longer, a majority of patients show symptomatic improvement when fully informed and optimally managed.
Fibromyalgia may occur following motor vehicle accidents or other trauma. Although some have suggested that no scientific data support a causality link between soft tissue trauma and the development of fibromyalgia, it seems presumptuous to rule out completely any possible linkage between trauma and fibromyalgia when so little is definitively understood about the latter condition itself. Patients who develop neck, upper back, or upper extremity pain after automobile trauma may have experienced sudden extreme movements of the cervical spine (""whiplash"") and may stretch an individual nerve root with impingement or a herniated disk. Some patients may continue to complain of soft tissue pain a year or more after traumatic injury yet have no objective evidence of neurologic pathology or radiographic abnormalities. A diagnostic-prognostic paradigm is not easily applied to the work-up, disposition, or compensatory claims of post-traumatic nonarticular pain patients. Although doubtlessly there are self-serving motives in some cases, it would seem reckless to categorically discount or dismiss the potential problems patients may encounter in the post-traumatic setting.
Proper management of fibromyalgia must begin with a definite diagnosis and assurance regarding the noncrippling nature of the process. Physician-patient dialogue is essential for the initiation of an effective treatment program, and printed educational material, including that from the Arthritis Foundation, often is also useful. Pharmacologic intervention is used most effectively in attempting to rectify the underlying sleep abnormality. Favorable results often are seen by instituting amitriptyline * (Elavil), 10 mg 2 hours before bedtime with increments of 10 mg every 2 weeks if necessary, not to exceed 50 mg total dose. These are not, of course, antidepressant dosages of amitriptyline, and depression is usually not the pathologic focus of managing fibromyalgia. A concurrent morning dose of a selective serotonin reuptake inhibitor such as paroxetine (Paxil), 20 mg, may be useful in depressed patients. The improvement of sleep pattern with the resulting attenuation or amelioration of pain symptoms is the single most important application of pharmacology in fibromyalgia. Cyclobenzaprine * (Flexeril), 10 mg at bedtime, may also be useful in improving sleep patterns. Owing to their similar side effects, though, antidepressants and muscle relaxants should not be prescribed concurrently. NSAIDs sometimes are helpful as analgesics but not as the sole drug used to alleviate the symptoms of fibromyalgia. Generally, NSAIDs should
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