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http://www.rheumatology.org/publications/primarycare/number5/hrh0026598.html Regional Pain Syndromes: Diagnosis and Management JUAN J. CANOSO Regional pain syndromes (1,2), which occur one time or another in most people past the age of 40 years, are central to primary care medicine. They are also fairly frequent in younger people; however, their true frequency and characteristics in the pediatric group have yet to be defined. Because regional pain syndromes are so diverse and ubiquitous, simplistic attempts at classification are not applicable. It is more effective to pose the clinical problem according to region and syndrome, discuss differential diagnosis, review the need for imaging or other diagnostic documentation, and tailor a treatment program on the basis of what is known about the natural course of the syndrome. For most regional pain syndromes, treatment is empirical and extrapolated from pathophysiology rather than based on hard science; nevertheless, there is a growing mass of reliable data that will be commented on where applicable in this review. This article reviews common regional pain syndromes affecting the upper and lower extremities, emphasizing diagnosis, treatment, and circumstances in which referral is advisable. A few less common, but more serious, conditions are also described. A GROSSLY SWOLLEN TENDON SHEATH Clinical appearance In subacute or chronic tenosynovitis, one or a few contiguous tendon sheaths swell strikingly over the course of weeks or months (3,4). Pain and tenderness are minimal, and motion is at first preserved. As an example, a tendon sheath may be grossly enlarged at the dorsal wrist, but flexion and extension of the joint may be relatively unimpaired. The same is found in flexor digital tenosynovitis, or in enlargement of a dorsal tendon sheath of the ankle. Differential diagnosis Conditions that cause subacute or chronic tenosynovial enlargement may be generalized or local (Table 1). Rheumatoid arthritis and psoriatic arthritis may have predominant involvement of one or more tendon sheaths. However, in both conditions, findings elsewhere (articular, cutaneous, etc.) provide the clue toward the correct diagnosis. Similarly, sarcoidosis usually has characteristic chest x-ray findings. In other conditions, however, a swollen tendon sheath is the one and only finding. In such a patient, chronic infection and foreign body reaction are the most common conditions to be considered. Mycobacterial tenosynovitis must be suspected in individuals who are immunosuppressed, or have immigrated from a country where tuberculosis is highly endemic. When confronted with a patient with overt proliferative tenosynovitis, appropriate actions include looking for evidence of systemic disease by careful history and examination, and a chest radiograph. If such evidence is not forthcoming, the patient should be referred for tendon sheath biopsy. Treatment Treatment in proliferative tenosynovitis depends on the etiology: systemic rheumatic disease, microbial, or other. Role of the primary care physician Appropriate actions include early referral to an orthopedic surgeon, consultation with an infectious disease specialist if infection is shown or suspected, and provision of appropriate treatment and followup. Key issues Isolated bulky tenosynovitis requires biopsy with special stains and culture for chronic infection. The most common cause is mycobacterial infection. In an immunosuppressed person or an immigrant from highly endemic areas, Mycobacterium tuberculosis infection is a strong possibility. AN ACUTELY INFLAMED DIGITAL FLEXOR TENDON SHEATH Clinical appearance The affected finger is held in semiflexion. It is swollen, red, and tender on the palmar side. Digital creases are erased (the presence of digital creases suggests cellulitis rather than acute tenosynovitis). Differential diagnosis There are two main clinical settings in which the condition appears: 1) a patient who has sustained an abrasion, cut, or puncture wound in the palmar side of a finger, and 2) a patient with severe Raynaud's phenomenon (e.g., scleroderma and other connective tissue diseases) with or without fingertip ulcers. Tendon sheath calcifications are common in this second group and may tempt the clinician to attribute the findings to microcrystalline inflammation; however, pyogenic infection with Staphylococcus aureus or Streptococcus pyogenes must be strongly suspected in both settings. Treatment Acute digital tenosynovitis is a true emergency. If the condition is not treated quickly, tendon necrosis is inevitable. The patient should be immediately referred for hand surgery. The tendon sheath must be drained and irrigated, usually through proximal and distal incisions. Role of the primary care physician Primary care physicians must be aware of the signs and symptoms of acute flexor digital tenosynovitis and the need for immediate tendon surgery. Key issues Acute pyogenic tenosynovitis leads to tendon necrosis unless effective drainage is implemented. Antibiotic choice is based on findings from Gram stain. TRIGGER FINGER Clinical appearance A trigger finger is the locking of one or several fingers in flexion so that the patient may have to pull the finger to straighten it (5-7). Any digit may be affected, however the thumb and the middle finger are most commonly involved. The cause is cartilaginous metaplasia at the first retaining pulley (at the palmar aspect of the metacarpophalangeal joint) which normally becomes taut during finger flexion. When 3 or more digits are affected, the conditions shown in Table 2 should be considered, especially diabetes and hypothyroidism. Differential diagnosis Trigger finger should be distinguished from systemic inflammatory conditions such as rheumatoid arthritis and psoriatic arthritis in which the sheath is diffusely thickened and the trigger phenomenon is unusual. In Dupuytren's contracture, the finger contracture is caused by palmar fascia fibrosis and cannot be reduced. Treatment Spontaneous improvement occurs in only 20% of cases. If untreated, the process can lead to an inability to straighten the finger and a permanent contracture. Trigger finger is treated with corticosteroid infiltrations, as described in the next article. With appropriate treatment, including up to 3 infiltrations, the success rate is over 95%. Complications, including iatrogenic infection or tendon rupture, are rare. Patients should be informed that asymptomatic fat atrophy may occur at the injection site. Rarely, surgery may be required for patients who refuse infiltrations or in whom infiltrations fail. Role of the primary physician Primary care physicians should be familiar with the diagnosis of trigger finger and, with appropriate training, may feel comfortable performing corticosteroid infiltrations of the second, third, or fourth digits. Infiltrations of the thumb and fifth digits are technically difficult and should be performed by those with special expertise (e.g., rheumatologists, hand surgeons, or orthopedic surgeons). Key issues A trigger finger rarely improves without corticosteroid infiltration(s). Involvement of multiple digits may signify a metabolic or infiltrative disorder. De QUERVAIN`S TENOSYNOVITIS Clinical appearance This condition is characterized by disabling pain in the radial aspect of the wrist at the base of the thumb. Its pathogenesis is similar to the trigger finger. There is swelling and tenderness of the common sheath of the abductor pollicis longus and extensor pollicis brevis, both tendons outlining the anterior edge of the anatomic snuffbox. Women are more frequently affected than men. De Quervain's tenosynovitis is particularly common in two settings: in mothers who repeatedly lift infants and young children and in people who use their hands in repetitive activities, such as knitting, sewing, and gardening. A positive Finkelstein's test is characteristic of the condition; in the painful hand, (a) the fully flexed thumb rests on the palm; (b) the fingers are curled over the thumb; and (c) the wrist is very gently deviated to the ulnar side. Acute pain along the tendon is diagnostic of de Quervain's tenosynovitis. Additional findings can include a diffusely swollen and tender sheath or loculated tenosynovial effusions near the radial styloid. Differential diagnosis Conditions that cause radial wrist pain could be confused with de Quervain's tenosynovitis. These conditions are listed in Table 3. Treatment Corticosteroid infiltrations (1 to 3) are very effective in de Quervain's tenosynovitis, although the success rate is slightly less than in trigger finger (8). Surgery is indicated in the event of treatment failures. Role of the primary care physician The primary care physician should be able to diagnose de Quervain's tenosynovitis and distinguish it from other causes of wrist pain. Infiltrations for this condition are technically demanding and may be best approached by a specialist. Key issues De Quervain's tenosynovitis causes severe pain and disables the hand. Diagnosis is confirmed by Finkelstein's maneuver. Treatment promptly eliminates pain and leads to a rapid restoration of hand function. GANGLIA Clinical appearance Ganglia are ubiquitous uni- or multilocular cystic lesions that arise in paratendinous, pararticular, or intraosseous locations (9). Pararticular lesions communicate with the joint unidirectionally via a narrow and tortuous stalk, resulting in enlargement following excessive joint use. Nerve compression may result (Table 4). Common locations of ganglia include the vicinity of the A1 pulley in the digital flexor sheath, the dorsum of the wrist, the carpal tunnel region causing the carpal tunnel syndrome (Figure 1), and the dorsum of the foot. Unusual locations include the scapula at the suprascapular or the spinoglenoid notch, the vicinity of the proximal fibular head, the popliteal fossa, and intraosseous sites. Scapular and fibular lesions may cause suprascapular and common peroneal nerve compression neuropathy, respectively. Ganglia can be confidently diagnosed in most cases on the basis of location, typical increase in size and symptoms caused by joint use, and palpatory findings (cystic). Aspiration, which must be made with a large-bore needle, yields a thick jelly-like material. Echography, computed tomography (CT), and magnetic resonance imaging (MRI) facilitate the diagnosis of ganglia that occur in deep and atypical locations. Differential diagnosis It is essential to rule out a malignant tumor. An imaging procedure should be performed whenever there is doubt about the diagnosis. Because of its low cost and excellent resolution, echography is a useful imaging procedure to investigate soft tissue lesions. Treatment Surprisingly, little research has been done on ganglia. There are no published controlled trials comparing different forms of treatment. Aspiration followed by injection of a long-acting corticosteroid is an appropriate treatment. Technical details can be found in the accompanying article. Surgery is generally required for lesions greater than 3 cm in diameter, for anterior wrist ganglia, and for intraosseous ganglia, as well as in cases where there is nerve compression. Role of the primary care physician Most ganglia can be treated by primary care physicians. Lesions that are not amenable to infiltration should be appropriately referred for surgical resection. Key issues Ganglia are common and can cause compression neuropathies that necessitate surgical resection. However, the majority of ganglia can be treated by aspiration and corticosteroid infiltration. TENNIS ELBOW Clinical appearance Tennis elbow, or lateral epicondylitis (this is also a misnomer, as no inflammation is present at the site), is common in middle-aged people, most of whom are not tennis players (10,11). Tennis elbow results from overuse of the extensor carpi radialis brevis, a muscle that spans the lateral epicondyle, and the base of the third metacarpal, a wrist dorsiflexor. Undue tension and shock are placed on the enthesis (the tendon-bone attachment site), resulting in vascular hyperplasia, increased proteoglycans, bony metaplasia, and tissue distortion, causing pain. The diagnosis is suggested by the lateral location of the pain, which characteristically affects the soft tissues just distal to the epicondyle, plus pain reproduction by resisted dorsiflexion of the wrist. Passive elbow flexion and extension are normal. Swelling (a synovial bulge) and lack of extension are not characteristic of tennis elbow and may indicate synovitis or local growths. Medial epicondylitis (golfer's elbow) will not be addressed specifically in this review but represents the mirror image of lateral epicondylitis (12). Differential diagnosis Conditions to be considered in the diagnosis of pain in the radial elbow are shown in Table 5. Lack of evidence of synovitis (no synovial swelling, full flexion and extension) and reproduction of the pain on resisted dorsiflexion of the wrist are important clinical signs. An important cause of chronic elbow region pain is the radial tunnel syndrome (compression neuropathy of the posterior branch of the radial nerve at the supinator muscle) (13). The site of tenderness is anterior, 3 cm distal to the flexor elbow crease and just medial to the outer third of the forearm. Radial tunnel syndrome is distinct from compression neuropathy of the posterior interosseous nerve, which is caused by an impinging mass lesion, including a synovial cyst, and results in weakness and changes in nerve conduction velocity as well as pain. Treatment Tennis elbow resolves spontaneously with time and rest of the affected arm. The Froimson band, a forearm compression band, can provide symptomatic relief. It should be snugly wrapped at the proximal forearm (not at the painful site itself) and, by reducing tendon pull, it assists in resting the enthesis. Patients should be given isometric and range of motion exercises for the entire upper extremity, including the shoulder, elbow, wrist, and fingers. Exercises should not create prolonged (more than two hours) post-exercise pain. In tennis players, alteration of technique and revision of equipment may be essential for good long-term results. Medical therapy includes local and systemic analgesics (capsaicin 0.025% 3-4 times a day plus acetaminophen 1g 3 times a day) and nonsteroidal anti-inflammatory drugs (NSAIDs) (often just prior to the offending exercise). Corticosteroid infiltrations are frequently used in tennis elbow, and at least 50% of patients find immediate relief. However, recurrence is seen in 30% of these patients. About 10% of patients have chronic symptoms despite medical treatment, and repeated corticosteroid injections have been implicated in chronicity. Therefore, more than one injection is ill advised. What should be done in chronic or recurrent cases? First, other causes of elbow pain must be excluded. For true chronic tennis elbow, surgery has a success rate of over 90%. Detachment of the extensor carpi radialis brevis from the lateral epicondyle eliminates the offending pull. For chronic tennis elbow a trial is being conducted of Clostridium botulinum toxin injection, which results in prolonged muscle paralysis and entheseal rest. Role of the primary care physician The majority of patients with tennis elbow cases can be treated by primary care physicians. An understanding of the pathophysiology is key to success. Primary care physicians should institute a program of rest and progressive exercises, including isometric strengthening. Corticosteroid infiltrations should be used only sparingly. Cases that persist for more than 3 months should be referred to a specialist for diagnostic confirmation and further treatment. Key issues Tennis elbow, as with other overuse-related syndromes, continues to be a problem because long-term modification of activity is so difficult to achieve. After the pain subsides, sudden increases in muscle pull often produce a flare. This underscores the importance of a strict adherence to prophylactic measures, including isometric strengthening of wrist extensors and a very gradual resumption of activities. Surgery may be required for recalcitrant cases. OLECRANON AND PREPATELLAR BURSITIS Clinical appearance Olecranon bursitis causes an easily detectable saccular swelling at the tip of the elbow. The sac may or may not be tender, warm, or red. Surrounding edema may be present, and pitting edema may extend down the back of the forearm distally to the dorsum of the hand. In acute cases elbow flexion is limited by pain over the bursa. Passive extension, however, is always full and pain free. This differentiates acute olecranon bursitis from acute elbow synovitis which results in semiflexion of the elbow. Olecranon bursitis may be caused by trauma, bacterial infection, gout, rheumatoid arthritis, and many other conditions. Traumatic bursitis usually results from recurrent microtrauma, such as undue leaning on the elbow, but rarely by a memorable trauma. Septic bursitis is caused by direct penetration of skin bacteria, with only the occasional case resulting from hematogenous spread. Hence, the etiology is predominantly staphylococcal (80%) or streptococcal (17%). In the United States, the staphylococci grown from bursal fluid are almost always resistant to penicillin. Bursal gout occasionally occurs before articular gout, and some gout patients have recurrent gouty bursitis rather than arthritis. Rheumatoid involvement of the olecranon bursa usually occurs because of intrabursal discharge of necrotic nodules from the bursal wall, a common site for rheumatoid nodules. Differential diagnosis It is usually not difficult to distinguish olecranon bursitis from other processes that affect the posterior elbow. Occasionally, surrounding cellulitis from bursal rupture or infection may be so intense that confusion with septic arthritis is possible. The physical finding of an unrestricted passive joint extension strongly supports a diagnosis of bursitis. Although these cases are almost always septic, similar findings may occur with gouty or traumatic bursitis. Superficial bursae have only a limited capability to respond to inflammatory stimuli, and it is not unusual for the leukocyte count in cases of septic bursitis to be in the range of 5-10,000/mm3, especially in early cases. Thus, a relatively clear fluid in no way rules out bacterial infection or gout. Samples should be routinely sent for leukocyte count and differential, polarizing microscopy, Gram stain, and aerobic culture. Additional studies such as anaerobic, fungal, and mycobacterial cultures should be obtained in immunosuppressed patients. Septic bursitis can be tentatively diagnosed and empirically treated pending culture results (Table 6). Rapid improvement with antibiotics, even with negative cultures, points to a bacterial etiology. A bacterial etiology can be proven only by culture; however, Gram stains are negative in over 50% of cases, and bacterial growth is often sparse and may be delayed several days because of low bacterial counts. Treatment Traumatic olecranon bursitis is unsightly but harmless. Protecting the bursa from further pressure results in spontaneous recovery within 3 months. Once infection has been excluded by a negative bursal fluid culture, the bursa may be injected with 20 mg of methylprednisolone acetate (14). Methylprednisolone acetate is preferable to triamcinolone hexacetonide, as skin atrophy and secondary infection have been described with the use of the latter (15). The bursal fluid is usually resorbed within a week. Septic bursitis in the olecranon bursa in a nonimmunocompromised patient may be treated with daily aspiration and 500 mg of oral dicloxacillin every 6 hours or 500 mg of cephalexin every 6 hours until the fluid culture reverts to negative, usually within 7-10 days. In patients with penicillin or cephalosporin allergy, vancomycin or another antibiotic that is bactericidal to staphylococcal and streptococcal species may be used. Older and immunocompromised patients as well as patients with prepatellar septic bursitis are best treated with parenteral antibiotics initially, and duration of treatment should be at least 2 weeks. Sterile bursal effusions occur in approximately 30% of patients who have completed antibiotic therapy. They do not signify recurrence of infection and are best left untreated. Gouty bursitis is treated in the same manner as acute gouty arthritis. Role of the primary care physician The key steps to diagnosis are aspiration and submission of the bursal fluid for cell count, differential, polarizing microscopy, and culture. Primary care physicians can treat traumatic and gouty bursitis. Septic bursitis, especially of the prepatellar bursa, is more complicated, and patients should be referred for specialist care. Key issues It is important to watch for infection. Intrabursal corticosteroids should not be administered unless the bursal fluid culture report is negative. Corticosteroid infiltration will expedite recovery in traumatic bursitis, a self-resolving condition. SHOULDER PAIN Clinical appearance The prevalence of shoulder ailments is extremely high (16). Patients report pain, limited motion, or both. The onset of symptoms may be abrupt or gradual. The process may be acute, subacute, or chronic. The pain may originate not only in the shoulder complex proper (sternoclavicular joint, acromioclavicular [AC] joint, glenohumeral joint, scapulothoracic mechanism), but also in neural and other structures. A history of trauma, limb overuse, upper extremity or neck pain, or arthritis may be present. Particular emphasis should be placed on determining whether paresthesias are present and, if so, their location. The common shoulder pain syndromes include rotator cuff tendinitis, subacromial impingement, frozen shoulder, and AC disease. Rotator cuff tendinitis. Inflammation of the common tendon of the subscapularis, supraspinatus, infraspinatus, and teres minor may result from microcrystalline deposits (apatites), overuse, impingement on the tendon from above or below, or degenerative changes that occur with aging (2,17,18). Specific shoulder motions are painful, particularly abduction when combined with rotations. As is characteristic of tendinitis, stretching of the involved tendon, or muscle contraction acting on the involved tendon, causes pain. Range of passive motion is typically normal. Calcific rotator cuff tendinitis (Figure 2) occurs when a pre-existing calcium deposit undergoes resorption, resulting in acute inflammation, extreme pain, and loss of shoulder motion (18). The stages of calcific tendinitis are listed in Table 7. Subacromial impingement. The rotator cuff tendon, which courses through a narrow space between the acromion and the proximal humerus, may be impinged from above or below, or because increased tendon bulk acts as a tight-fitting wedge between the two bony boundaries. Impingement from above may be caused by osseous or soft tissue structures such as an abnormally shaped acromion (J-shaped, for example), a prominent coracoacromial ligament, osteophytes protruding inferiorly from the AC joint, or a swollen AC joint. Impingement from below can occur when muscle fatigue or joint hyperlaxity allow excessive upward motion of the humerus during abduction. Intrinsic impingement results when the tendon itself is thickened. A large, inactive calcium deposit may be the cause. Impingement symptoms are largely those of tendinitis. In some cases, there are also symptoms related to the condition that causes the impingement, such as tenderness at an osteoarthritic AC joint. Frozen shoulder. The pathogenesis of this syndrome is only partially understood (19). Inflammatory infiltrates with local cytokine production (including growth factors that promote collagen synthesis) lead to capsular fibrosis (20). Frozen shoulder may occur in diabetic fibrosis, Medsger's syndrome (a paraneoplastic syndrome) (21), and occasionally in scleroderma. Many other conditions exist that underscore the pathogenetic heterogeneity of the syndrome (Table 8)<>. Frozen shoulder should be distinguished from synovitis such as that seen in rheumatoid arthritis and ankylosing spondylitis, reduced motion caused by inactivity, rotator cuff tendinitis, and posttraumatic and postsurgical capsular retraction with limited joint motion. Because the joint capsule encircles the joint, passive and active shoulder motions are equally lost in all directions. Three partially overlapping stages may be distinguished during the clinical course of frozen shoulder. In stage I, due to active inflammation, nocturnal boring pain is prominent, and mild limitation of motion is found. This stage lasts weeks. In stage II night pain is less pronounced, and pain occurs with movements that stretch the capsule, resulting in painful restricted motion. This stage lasts months. Stage III features little or no night pain, and movement is painless but markedly restricted. During this stage, which lasts from months to years, fibrosis slowly resolves, although not completely, since only 70-80% of the initial motion is ultimately restored. AC joint disease. The AC joint is a tightly packed, meniscus-partitioned joint with little motion except during elevation of the arm, when the anterior surface of the bone is increasingly directed upward, which explains the terminal pain experienced during the arc of elevation maneuver. Conditions affecting the AC joint include osteoarthritis, which is particularly prevalent beyond the age of 60 years, synovitis secondary to rheumatoid arthritis, and osteolysis of the distal end of the clavicle, which is seen in weight lifters, unusual cases of bacterial infection, and hyperparathyroidism (22). Differential diagnosis The single feature that best assists in the diagnosis of shoulder pain is its location. The pain may be located at the top, side, front, back, or axillary sides of the joint. Differential diagnoses by pain location are listed in Table 9<>. Lateral pain is characteristic of rotator cuff or glenohumeral disease, superior pain of AC or sternoclavicular conditions, anterior pain of bicipital tendinitis and early frozen shoulder, posterior pain of tears in labrum glenoidale and suprascapular neuropathy, and axillary pain of various neural causes. Pain location results from the segmental innervation of shoulder structures: AC and sternoclavicular joints, C4 (top); joint capsule and rotator cuff, C5 (side). Other causes of shoulder region pain include radiculopathy, carpal tunnel syndrome with retrograde radiation of pain, cervical spine pathology, myofascial pain and local pathology, including infections, and intraosseus conditions. Partial or complete rupture of the supra- or infraspinatus (other components of the cuff rupture infrequently) may be marked by a sudden increase in symptoms or the appearance of nocturnal pain; however, rupture may also be asymptomatic. An important maneuver in establishing the presence of rotator cuff tendinitis and AC joint arthropathy is the arc of elevation test (Table 10, Figure 3). Several maneuvers have been proposed to establish the presence of impingement (17), but in reality they demonstrate tendinitis rather than impingement. Impingement merely designates a causal mechanism of tendinitis. To diagnose impingement, an impinging mechanism, whether bone pathology at the acromion, inferior spurs at the AC joint, a big calcific lump, joint hyperlaxity, or muscle fatigue, must be demonstrated. Structural subacromial impingement is usually visible in shoulder x-rays (inferior AC osteophytes). In chronic shoulder pain due to rotator cuff tendinitis, x-rays provide direct evidence of rotator cuff attrition if the space between acromion and proximal humerus is narrowed. Finally, x-rays can identify bone lesions (neoplastic and others) that may be the cause of shoulder pain. Ultrasound is an excellent imaging method for the diagnosis of tendinitis, calcific deposits, partial or complete tears, and some bone pathology. Finally, MRI shows the soft tissues in exquisite detail, but its high cost restricts its use to patients in whom surgery is being considered, e.g., complete rotator cuff tears (Figure 4). Treatment Physical therapy. Broad physical therapy principles apply to shoulder pain treatment (Table 11) (23). Periodic supervision by a physiotherapist is important to supervise a program of daily exercises that are done predominately at home. Shoulder physical therapy should begin with pendular exercises during the acute and subacute phases, followed by stretching and strengthening exercises later in the course of the disease. Heating the area with warm packs (or ultrasound) is particularly helpful prior to exercising because it facilitates stretching and provides analgesia. Although widely used, there are no proven benefits of laser therapy or electrical muscle stimulation. Medications. Nonsteroidal anti-inflammatory drugs are helpful in rotator cuff tendinitis, including cases of impingement and calcific tendinitis. They should be used in full anti-inflammatory doses with due attention to gastric protection, particularly in older individuals, and are generally used for short courses of treatment (two weeks or less). Persisting pain suggests a structural condition not always amenable to medical treatment, such as a complete rotator cuff tear, an impingement syndrome, or a diagnostic error. Corticosteroid infiltrations are a very useful treatment in rotator cuff tendinitis, the initial phases of frozen shoulder, and AC osteoarthritis (24). Surgery. Surgery can relieve structural subacromial impingement, which is generally resistant to physical and anti-inflammatory therapy. Arthroscopic surgery has two advantages: it allows a more complete exploration of the joint and subacromial bursa, and it has a lower morbidity. Prior to surgery, an MRI should be obtained to fully reveal the anatomy, including the integrity of the rotator cuff tendon. Tears should be repaired whenever strength restoration is required. In older and sedentary people for whom the primary goal is pain relief, decompressive surgery may suffice. Role of the primary care physician Primary care physicians see the majority of patients with shoulder pain. Good diagnostic skills will result in improved patient management. Diagnosis is based on the history, an assessment of passive and resisted motion, the results of the arc of elevation maneuver, and plain x-rays obtained in external and internal rotation. Treatment should be based on the results of this analysis. The physical therapy components of treatment should be emphasized. Corticosteroid infiltrations of the shoulder are not difficult, although injecting the frozen shoulder may be technically demanding. Patients who fail to respond to two or more treatment courses should be referred to a rheumatologist or orthopedic surgeon. Key issues The sources of shoulder pain are: musculotendinous, articular, soft tissue, osseus, or referred. Rotator cuff tendinitis is the most frequent cause of shoulder pain and should be distinguished from a frozen shoulder. A pathophysiologic-based treatment can be implemented that includes local and systemic medications and physical therapy. HIP PAIN Clinical appearance Pain in the hip region may originate in tendinous, bursal, articular, or osseus structures or other soft tissues. It may also be due to radiculopathy or peripheral nerve injury, or be referred from elsewhere. The initial assessment should be based on the actual location of pain. Never take for granted that "hip pain" actually originates in the hip joint! To the presenting report "my hip hurts," ask "where in the hip?" The patient may point to the anterior, the lateral, or the posterior aspect of the joint (Table 12). Differential diagnosis Anterior pain. Pain originating in the hip joint is experienced anteriorly, mainly in the groin and anteromedial thigh. Other possible projection areas, concurrent with the former, include the trochanteric region and sometimes the gluteal region. Hip joint disease is usually associated with limitation of motion and endpoint pain. Additional causes of anterior hip pain include iliopsoas tendinitis, capsular stretching, and iliopsoas bursitis (25). Both tendinitis and capsular stretching feature pain on traction, whereas tendinitis also causes pain on resisted motion. Pain on direct compression is a feature of iliopsoas bursitis. Lumbar radiculopathy, plexopathy, and femoral nerve neuropathy are identified by patellar tendon hyporeflexia, a positive inverted Lasθgue's sign (pain reproduction on hyperextension of the thigh), and anteromedial thigh and/or medial leg hypoesthesia. Iliohypogastric, ilioinguinal, and genitoinguinal neuropathies may occur as a complication of a McBurney muscle splitting incision, after a herniorrhaphy, or by muscle entrapment neuropathy. A band of hypoesthesia over the lower abdominal wall, the inguinal ligament, and the base of the scrotum (or labia) is highly suggestive of the diagnosis. Lateral pain. Diagnosis of lateral hip pain may be difficult. Hip arthritis in general does not solely cause lateral pain. Trochanteric bursitis affects the bursa between the fascia lata and the greater trochanter. Bursal inflammation of the bursae underlying the gluteus medius or minimus has also been described. Trochanteric bursitis is usually idiopathic, but other causes include leg length discrepancy (pain develops in the long leg side), painful processes of the lower extremity at any level, and scoliosis. Iliotibial band shortening may be a contributing factor. Clinical features that suggest iliotibial tightness include lateral thigh pain while sitting with the legs crossed (in the adducted thigh), lateral knee pain, and a positive Ober or Gautam test (26). Septic or tuberculous trochanteric bursitis is extremely rare. Radiating pain from the lumbar spine is dull and is associated with lumbar/gluteal pain. Neuropathies affecting the subcostal, iliohypogastric, and lateral cutaneous nerve of the thigh (meralgia paresthetica) cause lateral pain, paresthesias, and hypoesthesia in the corresponding territories near the iliac crest, the area just below it, and the lateral thigh, respectively. Bone pathology in the femoral neck, such as a bone insufficiency fracture, and occasionally aseptic necrosis of the femoral head may cause predominantly trochanteric pain. Also, soft tissue or bone malignancy may affect the trochanteric region, and their presence should be suspected whenever a bulge is felt. Radiographic studies are negative in routine cases of trochanteric bursitis but are very helpful in defining bone lesions. Echography and MRI effectively detect soft tissue tumors and trochanteric bursitis. Bone scans detect intraosseus or intraarticular processes. Posterior pain. Posterior hip pain is less common than anterior and lateral pain. Pain may originate in the lumbar spine, occasionally in the sacroiliac joint, and in some cases in the hip joint, although hip joint disease almost always has coexistent anterior pain. Pain that originates in the ischial tuberosity (ischial bursitis) is aggravated by sitting. Calcific tendinitis of the posterior thigh is a self-limited condition in which calcification, sometimes with lysis of the underlying cortical bone, develops at the femoral insertion of the gluteus maximus and/or vastus lateralis tendons. The lesion may be visible on plain x-rays or may require CT for diagnosis. Treatment The treatment of trochanteric pain caused by trochanteric bursitis involves identification of underlying factors, such as a 2.5-cm leg length discrepancy in favor of the affected side plus ipsilateral iliotibial band contracture, and is key to a successful long-term treatment. In such a patient, a 1.25-cm heel lift should be provided for the short limb, and the patient should be referred to physical therapy for instruction on iliotibial band stretching exercises. Corticosteroid infiltration is an effective mode of therapy (27). Patients refractory to medical therapy should be evaluated by an orthopedist. A longitudinal split of the iliotibial band, which relieves pressure on the underlying trochanteric bursae, often alleviates the pain (28). Role of the primary care physician The primary care physician should determine whether the pain has an articular or extra-articular origin. Articular hip pain most often arises in the groin or anterior thigh and may be due to osteoarthritis, avascular necrosis, or systemic rheumatic disease. Occasionally, hip articular disease causes referred pain at the knee. If articular disease is found, the patient should be referred to a rheumatologist for further evaluation and treatment recommendations. Trochanteric bursitis and fibromyalgia can be treated by primary care physicians. Ultrasound or MRI are needed to diagnose a soft tissue lesion that will ultimately require a tissue diagnosis. Key issues In hip region pain, the main issue is to distinguish hip joint disease from soft tissue problems or radiating pain. Early identification of hip joint disease is important. Trochanteric bursitis, the most common cause of pain in the hip region, responds well to corticosteroid infiltrations and has an excellent prognosis if causative factors are corrected. Because sarcomas have a predilection for the root of the limbs, particularly in the lower limb, any soft tissue bulge must be viewed with great suspicion. KNEE PAIN Clinical appearance Knee pain may be intrinsic or it may radiate from a proximal structure such as the hip or the lumbar plexus. If knee motion is free and painless while the patient is lying on the contralateral side, knee disease can be safely ruled out. While in the same position, if hip hyperextension, but not rotation or flexion, reproduces the pain, the source of the pain may be in the lumbar plexus or the femoral nerve. However, if all 4 motions reproduce the "knee pain," the source of pain is the hip. Intrinsic knee pain may affect the front, the medial side, the lateral side, or the posterior aspect of the joint (Table 13). Knee examination should include inspection, range of passive motion, patellofemoral function, stressing of the medial and lateral compartments, and an assessment of joint stability. Inspection may reveal swelling at the suprapatellar pouch and parapatellar gutters indicative of a synovial effusion, prepatellar swelling from prepatellar bursitis, and patellar tendon region swelling caused by pretendinous bursitis, tendon inflammation, fat pad hyperplasia/inflammation (Hoffa's disease), or infrapatellar bursitis. Swelling at the medial or lateral articular lines usually represents a meniscal cyst. A bulge in the popliteal fossa may be caused by a Baker's cyst (Figure 5), but other soft tissue lesions should be excluded. Palpation is used to confirm or refute the above findings, because fat and synovial proliferation can cause bulges around the knee joint. Identification of focal tenderness may be critical for diagnosis. Classic findings include tenderness at the medial or lateral articular lines in meniscal disease; patellar or tibial insertion of the patellar tendon in calcific enthesopathy and patellar tendon enthesitis, respectively; tibial insertion of the pes anserinus in the anserine bursitis syndrome; and lateral femoral condyle in patients with the iliotibial band syndrome. Valgus and varus stress while flexing and extending the joint will identify unicompartmental abnormalities, such as lateral and medial meniscal lesions. The Lachman test, which can be described as a drawer sign elicited by pulling forward the upper tibia with the knee flexed 20 degrees, is positive in anterior cruciate ligament tears. Differential diagnosis Anterior pain. Pain in the anterior knee (29) may be caused by one or more of the lesions listed in Table 13. The "shrug sign" is particularly useful in the diagnosis of patellofemoral syndrome (chondromalacia patella). To perform this test the supine patient is asked to relax the quadriceps. The patella, firmly held between the observer's index and thumb, is displaced distally and kept in a firm posterior contact. The patient is then asked to contract the quadriceps, and a positive test result is the occurrence of pain, often excruciating, as the roughened patella slides proximally against the roughened femoral condyle. A tender, inflamed medial plica (a vestigial synovial fold that has become swollen by inflammation and fibrosis) will jump under the examining finger in a medial parapatellar location during flexion and extension movements of the joint. Prepatellar bursitis is evident as a tender, soft tissue lump in front of the patella. Conditions affecting the quadriceps-tendon-patella-patellar ligament-tibia unit result in pain on resisted extension and display tenderness over the patella or at the tibial insertion of the patellar ligament. By actively elevating the straight leg, one can distinguish pretendinous bursitis, which still bulges, from deep infrapatellar bursitis, which tends to get buried under the taut ligament. Osgood-Schlatter's disease in pediatric cases results in a tender, hard lump at the tibial tuberosity. Successful treatment of anterior knee pain requires consideration of these potential causes. Medial pain. Pain over the medial aspect of the knee is usually caused by a meniscal tear in a younger patient and medial compartment osteoarthritis in patients past the age of 50 years. However, there are other considerations. Anserine bursitis (not truly a bursitis in most instances) hurts on pressure 3-5 cm distal to the medial articular line (30). Medial collateral ligament bursitis, which overlaps the articular line, hurts more on pressure in flexion when the bursa is exposed than in extension when the sac gets covered by the medial collateral ligament. Meniscal cysts characteristically soften and may become undetectable in full flexion and full extension, while they are hard and prominent when the knee is flexed 30-40 degrees. Lateral pain. Pain in the lateral knee is seen in the iliotibial band syndrome (31), a condition that results from the excessive friction of a tight iliotibial band on the lateral femoral condyle. Patients with this syndrome report lateral knee pain while running, going up or downstairs, and bicycling. On examination with the knee in semiflexion, a tender spot is found on the lateral femoral condyle anterior to the band. Tenderness decreases or disappears when the knee is fully extended. Other conditions affecting the lateral knee include meniscal tears and cysts, as well as the biceps femoris tenosynovitis in which there is tenderness in the posterolateral corner of the joint. Posterior pain. Pain in the posterior knee may be caused by popliteal (Baker's) cysts, various lesions affecting the popliteal artery, venous thrombosis, hematomas, ganglia, and soft tissue tumors including sarcomas (32). Foucher's maneuver is very useful in distinguishing popliteal cysts from other mass lesions. When the knee is flexed 30-40 degrees, Baker's cysts become soft or undetectable (a positive Foucher's sign) while other popliteal masses remain unchanged (33). Echography, with Doppler, is particularly helpful in the analysis of posterior knee pain. Venous disease, popliteal artery aneurysms, solid tumors, and ganglia can be reliably identified by this method. Treatment Painful knee conditions lead to quadriceps weakness, and quadriceps weakness alters patellar biomechanics and results in further pain. Thus, in addition to specific measures for the diagnosed condition, all patients with a painful knee should be instructed on isometric quadriceps exercises. The use of a cane on the opposite side helps relieve pain and provides stability and safety while the condition improves. Depending on the cause of the pain, local or systemic analgesics or NSAIDs may be used. Both warm packs and cold compresses are analgesic, the effect varying with the individual patient. Prepatellar bursitis is treated in a similar fashion as olecranon bursitis, although it is generally more problematic. Septic cases often require hospitalization, catheter or surgical drainage, and parenteral antibiotics for a few days until the process is controlled. At this point, oral antibiotics may be started and continued to complete 2-3 weeks of therapy. In some of the regional syndromes, one or more corticosteroid infiltrations will eventually be required. Anserine bursitis, medial collateral ligament bursitis, and the iliotibial band syndrome respond particularly well to corticosteroid infiltrations. Technical aspects of this procedure are discussed in the accompanying article. On the other hand, the medial plica syndrome, tight lateral retinaculum, and meniscal pathology including ruptured menisci and meniscal cysts are amenable to arthroscopic surgery. Baker's cysts almost always reflect intraarticular pathology that results in excess synovial fluid production and distention of a pre-existent communicating gastrocnemius-semimembranous bursa. They are best treated by addressing the knee problem that causes the bursal distention. Provided that infection has been ruled out, knee drainage followed by intraarticular corticosteroids is an effective method to reduce a symptomatic Baker's cyst and avert the risk of rupture. Long-term treatment is aimed at the underlying knee process. Role of the primary care physician Primary care physicians should be able to diagnose and treat anserine bursitis, patellofemoral syndrome, and prepatellar bursitis. Other causes of knee pain may require referral to a rheumatologist or orthopedist. Primary care providers should educate patients about the importance of the correct technique of quadriceps strengthening exercises. A well-integrated program of analgesics, anti-inflammatory drugs (including corticosteroid infiltrations), and physical therapy, including a cane when needed, provides interim comfort to patients with knee pain. Key issues Many of the knee conditions are within the field of primary care medicine, including anserine bursitis, prepatellar bursitis, patellofemoral syndrome, and early tibiofemoral osteoarthritis. Primary care physicians should learn to identify and treat patients with these conditions and refer others to the appropriate specialists. POSTERIOR HEEL PAIN Clinical appearance Several structures in the posterior heel may cause distressing pain (Table 14) (34,35). One is a subcutaneous bursa between the skin and deep fascia. This adventitious bursa develops under a hard heel counter particularly in women who wear high heels. The Achilles tendon lacks a defined synovial sheath. Stresses on the Achilles tendon are enormous and often result in fatigue damage. Overuse and fluoroquinolone toxicity cause noninsertional tendinosis (tender swelling) 2-6 cm proximal to the calcaneal insertion. Interstitial rupture, which is clinically characterized by nodular thickening at this site, often portends a complete rupture. In contrast, Achilles enthesitis in the spondylarthropathies occurs at the calcaneal insertion, hence the designation insertional tendinitis. Wedged in the angle between the Achilles tendon and calcaneus is the retrocalcaneal or Achilles bursa. This heterogeneous structure (fibrocartilage front and back, synovium at the top) is an almost constant association of insertional tendinitis in the spondylarthropathies and is frequently involved by itself in rheumatoid arthritis. A frequent calcaneal deformity, Haglund's deformity, is a cause of posterior heel pain and is recognizable as a tender, hard lump high in the posterolateral calcaneus. Differential diagnosis The clinician's first task is to determine the anatomic location of the heel pain. More than one structure may be affected. An enlarged superficial bursa can be readily identified superficial to the Achilles tendon, which is best determined while the tendon is tense. Thickening and tenderness may be felt at the insertional or noninsertional Achilles tendon. The presence of nodules at the noninsertional area (in the absence of nodular rheumatoid arthritis and tophaceous gout) suggests partial rupture and is therefore a warning sign for a complete rupture. The extent and severity of the lesion can be fully disclosed by echography or MRI. Insertional tendinitis can be diagnosed clinically. A lateral x-ray of the heel may show an intrabursal effusion characteristic of retrocalcaneal bursitis. Treatment Superficial bursitis requires better shoes in the long run, but NSAIDs may be used temporarily. Noninsertional tendinitis patients should be referred to an orthopedist with broad experience in foot pathology, as tendon debridement or repair may be indicated. In fluoroquinolone-related cases, re-exposure to these agents should be avoided. Insertional tendinitis in the spondylarthropathies usually responds to systemic treatment. Refractory cases may be treated with a walking cast. Corticosteroid infiltrations in the retrocalcaneal bursa are very effective treatment but care must be taken not to infiltrate the tendon, which could lead to tendon rupture. Posterior heel pain from Haglund's disease may be improved with modified shoes and anti-inflammatory drugs. A wedge osteotomy that removes the posterior/superior corner of the calcaneus is curative and should be considered in chronically symptomatic cases. Ancillary measures for all types of posterior heel pain include the use of heel lifts to decrease traction on the Achilles tendon and gently performed tendon stretching exercises. Also, the use of a night splint that holds the foot at 90 degrees has been recommended for pain relief. Role of the primary care physician Posterior heel pain, with the exception of cases obviously caused by inappropriate footwear, should be best evaluated by specialists. Insertional Achilles tendinitis and retrocalcaneal bursitis are commonly seen in rheumatic disorders. On the other hand, noninsertional tendinitis could lead to complete tendon rupture. These patients, as well as patients with Haglund's disease, should be referred for orthopedic evaluation. Key issues Noninsertional Achilles tendonopathy should be considered as potentially leading to Achilles tendon rupture, even if induced by fluoroquinolones. Swelling at the distal portion of the tendon and the retrocalcaneal bursa is a sign of spondylarthropathy. In contrast, isolated bursal swelling is characteristic of rheumatoid arthritis. PLANTAR HEEL PAIN Clinical appearance Plantar heel pain is frequently encountered in general medical practice (36,37). The pain is maximal when the patient first stands in the morning and tends to decrease with walking. There are 4 clinical contexts in which the symptom develops (Table 15). Fat pad failure is seen in obese patients with attrition of the plantar fat pad, in patients with a thin and flabby plantar pad, and as an iatrogenic condition in patients who sustained multiple plantar corticosteroid infiltrations for heel spurs. "Plantar fasciitis" is seen in runners with interstitial fascial rupture, in patients with flat, pronated feet in whom a collapsed longitudinal arch stretches the fascia, and in patients with spondylarthropathy and enthesitis at the calcaneal insertion. The tarsal tunnel syndrome results in plantar pain and paresthesias. It is due to a pressure neuropathy of the calcaneal branches of the posterior tibial nerve or the first branch of the lateral plantar nerve. Both are more likely to occur in patients with flat, pronated feet from excessive pressure on the medial edge of the heel. Stress fractures of the calcaneus and calcaneal cysts can also cause plantar heel pain. Differential diagnosis Fat pad failure pain is associated with central tenderness in the heel pad. Interstitial rupture hurts diffusely in the proximal plantar fascia. Traction enthesopathy and spondylarthropathy-related enthesitis cause tenderness at the medial calcaneal tubercle, which is the main insertion site of the plantar fascia. Entrapment neuropathy is characterized by a positive Tinel sign when the medial edge of the heel is percussed. Bone-type calcaneal pain can be readily detected by firmly squeezing the heel from the sides. An MRI or a bone scan will reveal the osseus lesion. It should be noted that a well-developed heel spur is frequently present in painful heels. However, similar spurs are often present in the asymptomatic contralateral heel. Furthermore, heel spurs are equally frequent in patients with and without heel pain, which further detracts from their clinical significance. On the other hand, ragged, poorly developed (inflammatory) spurs are often present in patients with spondylarthropathy (Figure 6). These spurs are not seen in normal individuals. Treatment Plantar heel pain should be treated with nonspecific measures, along with treatment aimed at the underlying condition (38). A heel cup, a firm plastic device that squeezes the plantar fat pad at its edges and increases its thickness, helps most patients. Anti-inflammatory drugs help, particularly in patients with spondylarthropathy. Achilles tendon and plantar fascia stretching exercises are useful once the condition becomes inactive and may help prevent recurrences. Corticosteroid infiltrations can be quite helpful in patients with an inflammatory cause. Because the procedure is technically difficult and very painful, it is generally reserved for those patients who have not benefited from a more conservative program including NSAIDs in full doses for 6 weeks. Additional measures that have been reported to be useful include a night splint that holds the ankle at 90 degrees and dexamethasone iontophoresis. Laser therapy was found ineffective in a well-designed controlled trial. Because spurs do not cause the pain in noninflammatory cases, they should not be surgically removed. Plantar fasciotomy is a salvage procedure for severe, long-standing cases (39). There is a partial collapse of the longitudinal arch following this procedure. Role of the primary care physician Primary care physicians should be aware of the major types of plantar heel pain (mechanical and inflammatory) and be able to implement basic treatment. Patients with inflammation may require referral to a rheumatologist, whereas patients with traction enthesopathy and tarsal tunnel syndrome should be referred for orthopedic evaluation. The suspicion of a bone origin of pain should lead to investigation by bone scan or MRI. Key issues Plantar calcaneal pain is caused by fat pad failure; plantar fascial pain by interstitial rupture, traction enthesopathy, or enthesitis; bone pain from fatigue fracture and bone cysts; and pain and paresthesias by pressure neuropathy. Each has different treatment implications. FOREFOOT PAIN Clinical appearance Anterior foot pain may have articular, neural, and bone causes (Table 16) (40,41). In hallux valgus, fibular deviation of the big toe often results in overlapping toes and severe metatarsalgia. Because it is caused by pointy-toed shoes and elevated heels, hallux valgus is almost entirely confined to women. Hallux rigidus is a degenerative condition in which a cartilaginous/bony ridge prevents dorsiflexion of the big toe. Ligamentous failure of the second metatarsophalangeal (MTP) joint is an obscure condition, albeit well-recognized by foot surgeons, in which instability results in premature osteoarthritis of the joint. A collapsed transverse metatarsal arch causes inordinate metatarsal head stress and pain. Morton's neuroma, a poorly understood tender thickening of the digital nerve between the third and fourth toes or the second and third toes, causes forefoot pain. Tarsal tunnel syndrome, the result of entrapment of the posterior tibial nerve by tenosynovitis, exostosis, aberrant muscle bellies, or other causes, leads to diffuse plantar forefoot pain and paresthesias (42). An important predisposing factor is a valgus deviation of the heel. Sympathetic dystrophy occasionally complicates this syndrome. Sensory neuropathies, such as diabetic neuropathy, may also cause distressing plantar pain. Finally, bone insufficiency metatarsal fractures are a prominent cause of forefoot pain in older individuals with osteoporosis as well as in runners. Differential diagnosis A careful physical examination usually yields the cause of forefoot pain. In articular disease, tenderness is sharply localized to the MTP joint(s). Morton's neuroma is best identified by 2-finger compression, one dorsal and one plantar at the symptomatic intermetatarsal space. The neuroma may be felt as a tender fusiform swelling under the plantar skin. In the tarsal tunnel syndrome, percussion in back of the medial malleolus causes showers of plantar paresthesias. Metatarsal fractures are best detected by 2-finger palpation. These are characteristically placed near the metatarsal heads. Treatment Forefoot pain is usually the result of faulty footwear. An extra wide, extra deep shoe may be all that is required in hallux valgus; however, patients often refuse to wear such unsightly shoes. If symptoms are severe, orthopedic referral for surgical correction of the deformity is warranted. Surgical consultation should also be requested in patients with an unstable second MTP joint, stress fractures, and tarsal tunnel syndrome. The best form of treatment of Morton's neuroma has not been established. Some authorities favor its surgical removal, and there are technical considerations that may decrease the rate of recurrence. Others believe that initial treatment with 1-3 corticosteroid infiltrations results in a cure in 50% of cases. A controlled trial comparing the two procedures is needed. Role of the primary care physician Primary care physicians should be able to prevent many instances of forefoot pain simply by explaining the characteristics of sound footwear. A patient with Morton's neuroma should be referred to a specialist for corticosteroid injections. Systemic inflammatory conditions such as rheumatoid arthritis can begin with MTP joint arthritis and could mimic Morton's neuroma. Key issues Forefoot pain may have an articular, osseous, or neurogenic basis. The two most common painful conditions are hallux valgus, caused by faulty footwear, and metatarsalgia from flat feet. Juan J. Canoso, MD: The American British Cowdray Hospital, Mexico City, Mexico, and Adjunct Professor of Medicine, Tufts University School of Medicine, Boston, Massachusetts. REFERENCES 1. Canoso JJ. Rheumatology in primary care. Philadelphia: WB Saunders; 1997. 2. Teitz CC, Garrett WE Jr, Miniaci A, Lee MH, Mann RA. Tendon problems in athletic individuals. J Bone Joint Surg Am 1997;79A:138-52. 3. Canoso JJ, Barza M. Soft tissue infections. Clin Rheum Dis 1993;19:293-309. 4. Regnard P-J, Barry P, Isselin J. 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Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone Joint Surg Am 1996;78:1685-9. 25. Johnston CA, Wiley JP, Lindsay DM, Wiseman DA. Iliopsoas bursitis and tendinitis: a review. Sports Med 1998;25:271-83. 26. Gautam VK, Anand S. A new test for estimating iliotibial band contracture. J Bone Joint Surg Br 1998;80B:474-5. 27. Schbeeb MI, O'Duffy JD, Michet CJ Jr, O'Fallon WM, Matteson EL. Evaluation of glucocorticosteroid injection for the treatment of trochanteric bursitis. J Rheumatol 1996;23:2104-6. 28. Slawski DP, Howard RF. Surgical management of refractory trochanteric bursitis. Am J Sports Med 1997;25:86-9. 29. Arroll B, Ellis-Pegler E, Edwards A, Sutcliffe G. Patellofemoral pain syndrome: a critical review of the clinical trials on nonoperative therapy. Am J Sports Med 1997;25:207-12. 30. Cohen SE, Mahul O, Meir R, Rubinow A. Anserine bursitis and non-insulin dependent diabetes. J Rheumatol 1997;24:2162-5. 31. Orchard JW, Fricker PA, Abud AT, Mason BR. Biomechanics of iliotibial band friction syndrome in runners. Am J Sports Med 1996;24:375-9. 32. Damron TA, Sim FH. Soft-tissue tumors about the knee. J Am Acad Orthop Surg 1997;5:141-52. 33. Canoso JJ, Goldsmith M, Gerzof SG, Wohlgethon JR. Foucher's sign of the Baker's cyst. Ann Rheum Dis 1987;46:228-32. 34. Canoso JJ. The premiere enthesis. J Rheumatol 1998;25:1254-6. 35. Myerson MS, McGarvey W. Disorders of the Achilles tendon insertion in Achilles tendinitis. Instr Course Lect Am Acad Orthop Surg 1999;48:211-8. 36. Myerson MS. Achilles tendon ruptures. Instr Course Lect Am Acad Orthop Surg 1999;48:219-30. 37. Olivieri I, Barozzi L, Padula A, De Matteis M, Pierro A, Cantini F, et al. Retrocalcaneal bursitis in spondyloarthropathy: assessment by ultrasonography and magnetic resonance imaging. J Rheumatol 1998;25:1352-7. 38. Schepsis AA, Leach RE, Gorzyca J. Plantar fasciitis: etiology, treatment, surgical results, and review of the literature. Clin Orthop 1991;266:185-96. 39. Daly PJ, Kitaola HB, Chao EYS. Plantar fasciotomy for intractable plantar fasciitis: clinical results and biomechanical evaluation. Foot Ankle 1992;13:188-95. 40. Mann RA. Disorders of the first metatarsophalangeal joint. J Am Acad Orthop Surg 1995;3:34-43. 41. Weinfeld SB, Myerson MS. Interdigital neuritis: diagnosis and treatment. J Am Acad Orthop Surg 1996;4:328-35. 42. Bailie DS, Kelikian AS. Tarsal tunnel syndrome: diagnosis, surgical technique, and functional outcome. Foot Ankle Int 1998;19:65-72. Figure 1. Ganglion cyst: wrist (magnetic resonance imaging). In this T2-weighted axial image, a lobulated mass, representing a benign ganglion cyst, has a homogenous signal of high intensity (white). The flexor tendons, which have a signal of low intensity (black), are also visible. (Reprinted from the American College of Rheumatology Clinical Slide Collection on the Rheumatic Diseases.) Figure 2. Shoulder, calcific tendinitis (roentgenogram). This anteroposterior projection of the shoulder was taken with the tube angled 10 degrees cephalocaudad, which allows better visualization of the subacromial bursal region. A large amorphous calcific deposit is present in the region of the supraspinatus tendon near its insertion. The shoulder joint is normal. (Reprinted from the American College of Rheumatology Clinical Slide Collection on the Rheumatic Diseases). Figure 3. The arc of elevation maneuver. Because the greater tuberosity of the humerus has to clear under the acromion/coracoacromial ligament during abduction, patients with subacromial impingement hurt during arc A. Once the greater tuberosity has cleared, pain ceases in arc B. A similar phenomenon occurs as the arm is brought down: no pain in arc B, pain in arc A, then no pain in full dependency. Because the acromioclavicular (AC) joint has its greatest motion in terminal elevation, patients with AC arthritis hurt in arc B. Finally, when the AC joint causes impingement, e.g., in osteoarthritis, there will be pain in arc A from impingement, plus pain in arc B from stress on the diseased joint. (Reproduced, with permission, from ref. 1.) Figure 4. Rotator cuff tear: shoulder (magnetic resonance imaging). In this T2-weighted coronal image, a high-intensity signal (white) in the supraspinatus tendon indicates that the patient has a tear in the rotator cuff. There is synovial fluid, which also has a high-intensity signal (white), medially in the glenohumeral joint and laterally in the subdeltoid bursa, indicating a communication through the torn rotator cuff. (Reprinted from the American College of Rheumatology Clinical Slide Collection on the Rheumatic Diseases). Figure 5. Popliteal cyst: knee (magnetic resonance imaging). In this T2-weighted image, the oval smooth mass behind the knee is a popliteal cyst with a homogenous signal (white) of high intensity. There are degenerative changes of the knee with joint space narrowing seen best posteriorly. A knee effusion extends into the suprapatellar bursa and has a high-intensity signal (white). (Reprinted from the American College of Rheumatology Clinical Slide Collection on the Rheumatic Diseases.) Figure 6. Ankylosing spondylitis: calcaneal erosion and spur (roentgenograms). Top, This lateral view of the os calcis shows a small spicule of new bone formation at the site of insertion of the plantar aponeurosis. There is also a small erosion of the posterior aspect of the os calcis just anterior to the Achilles tendon. Bottom, The calcaneal spur is represented as a loosely woven bony projection in the region of the plantar aponeurosis. This may progress to form a hard or dense spur. However, the inferior surface will be flat and the anterior aspect will not curve anteriorly and superiorly, as does the usual degenerative spur. Changes in the os calcis similar to those of ankylosing spondylitis also occur in Reiter's syndrome and rheumatoid arthritis. A large erosion is present near the attachment of the Achilles tendon. (Reprinted from the American College of Rheumatology Clinical Slide Collection on the Rheumatic Diseases.) Table 1. Conditions that cause subacute or chronic proliferative tenosynovitis -------------------------------------------------------------------------------- Generalized Rheumatoid arthritis Psoriatic arthritis Sarcoidosis Localized Chronic infection--tuberculosis, fungal, algae (Prototheca) Foreign bodies (plant thorn tenosynovitis) Tenosynovial chondromatosis Pigmented villonodular synovitis Soft tissue sarcoma -------------------------------------------------------------------------------- Table 2. Causes of multiple trigger fingers -------------------------------------------------------------------------------- Idiopathic Diabetes Hypothyroidism Mucopolysaccharidoses Amyloidosis (L type) Ochronosis -------------------------------------------------------------------------------- Table 3. Differential diagnosis of de Quervain's tenosynovitis -------------------------------------------------------------------------------- Proliferative tenosynovitis Osteoarthritis of the trapeziometacarpal joint Osteoarthritis of the radiocarpal joint Pressure neuropathy of the superficial branch of the radial nerve (Wartenberg's syndrome) Carpal tunnel syndrome -------------------------------------------------------------------------------- Table 4. Sites of nerve compression by ganglia -------------------------------------------------------------------------------- Superficial branches of radial nerve Median nerve within carpal tunnel Suprascapular nerve at suprascapular notch or spinoglenoid notch Tibial nerve at popliteal fossa Common peroneal nerve at proximal fibula -------------------------------------------------------------------------------- Table 5. Differential diagnosis of tennis elbow -------------------------------------------------------------------------------- Elbow synovitis Other enthesopathies (fluoroquinolones) Radial tunnel syndrome Pressure neuropathy of the posterior interosseous nerve Shoulder pain radiation Radiculopathy Fibromyalgia Myofascial pain Soft tissue lesions including sarcoma Panner's disease (osteonecrosis of the capitulum) -------------------------------------------------------------------------------- Table 6. Empirical criteria for the initiation of antibiotic treatment in olecranon and prepatellar bursitis pending culture results* -------------------------------------------------------------------------------- (a) Erosion, fissure, puncture, or other violation to the elbow or knee skin (b) Local inflammatory changes (may vary in intensity) (c) Leukocyte count in bursal fluid greater than 2,000/mm3 (d) A bursal fluid differential count of greater than 60% polymorphonuclear leukocytes (e) Intracellular bacteria on Gram stain -------------------------------------------------------------------------------- *Patients meeting clinical criteria (a) through (d) with crystals in the fluid, or (b) through (d) in the absence of crystals, or (e) justify initiation of antibiotic therapy. Table 7. Stages of calcific tendinitis* -------------------------------------------------------------------------------- 1. Precalcified (cartilaginous metaplasia) 2. Calcified (a) Formation (calcium in fibrocartilage) (b) Quiescence (calcium in fibrous tissue) (c) Resorption (inflammation) 3. Resolution (tendon once again normal) -------------------------------------------------------------------------------- *Pain in all stages except 2(c) is due to a predisposing cause or impingement due to a large calcified mass. Pain in 2(c) is inflammatory. Radiographically, calcified deposits in (c) appear ragged and are of lower density. Table 8. Diseases associated with frozen shoulder -------------------------------------------------------------------------------- None (idiopathic frozen shoulder) Cervical radiculopathy Contralateral stroke Intrathoracic pathology (lung cancer, thoracotomy, myocardial infarction) Brachial artery cardiac catheterization Endocrine disease (hypo- and hyperthyroidism, diabetes) Medsger's syndrome Polymyalgia rheumatica Prolonged immobilization Rotator cuff tendinitis Posttraumatic and postsurgical (asymmetric) -------------------------------------------------------------------------------- Table 9. Differential diagnosis of shoulder pain based on location -------------------------------------------------------------------------------- Lateral Rotator cuff tendinitis (senile, impingement, calcific, fluoroquinolones) Frozen shoulder Glenohumeral arthropathy Radiculopathy including herpes zoster Suprascapular nerve entrapment at suprascapular notch Axillary neuropathy Anterior Frozen shoulder, early Bicipital tendinitis Carpal tunnel syndrome Posterior Early cervical disc/facet joint pathology Labral tear Myofascial pain Scapulothoracic pathology Suprascapular nerve entrapment at spinoglenoid notch Superior Acromioclavicular arthropathy Sternoclavicular arthropathy Neck pathology Supraclavicular fossa pathology Phrenic nerve irritation Fibromyalgia Axillary Radiculopathy (including herpes zoster) Thoracic outlet syndrome Sulcus cancer, post-cancer treatment -------------------------------------------------------------------------------- Table 10. The arc of elevation maneuver -------------------------------------------------------------------------------- "Raise the extended arms fully along the scapular plane, and then bring them down, and while you are doing it tell me how you feel." No pain No diagnostic help Pain in middle third Rotator cuff tendinitis Pain in terminal third Acromioclavicular (AC) joint Pain in middle and terminal third Impingement due to AC pathology (usually osteoarthritis spurs) -------------------------------------------------------------------------------- Table 11. Principles of physical therapy for the shoulder (rotator cuff tendinitis, frozen shoulder, impingement syndromes) -------------------------------------------------------------------------------- Complete rest of the joint complex is ill advised. Pendular exercises, in which the weight of the arm distracts the subacromial space, are basic to maintain motion and provide analgesia. Stretching exercises help regain motion. Strengthening of rotator cuff muscles helps prevent relapses. Table 12. Differential diagnosis of hip pain based on location -------------------------------------------------------------------------------- Anterior Hip disease Hernia Disk pathology (L2 innervation of lower discs) Iliohypogastric (L1) neuropathy Ilioinguinal (L1) neuropathy Genitofemoral (L1-2) neuropathy Femoral nerve (L2-4) neuropathy Lumbar plexopathy (L1-4) Iliopsoas bursitis Calcific tendinitis of the iliopsoas tendon Capsular/ligamentous distention in hypermobility syndromes Bone insufficiency fractures of pubic rami Lateral Trochanteric bursitis Iliotibial band tightness (Ober) Lumbar spine pain radiation Subcostal nerve syndrome (T12) Iliohypogastric (L1) neuropathy Lateral cutaneous nerve of the thigh (L2-3) neuropathy ("meralgia paresthetica") Tendinitis Leg length discrepancy Dercum's disease Sarcoma, soft tissues and bone Metastatic cancer Incomplete fracture of femoral neck Osteomyelitis Aseptic necrosis Fibromyalgia Posterior Lumbar spine and sacroiliac joint pain radiation Hip disease Ischial bursitis Ischial bone lesions Calcific tendinitis in the posterior proximal thigh Sarcoma -------------------------------------------------------------------------------- Table 13. Etiology of knee pain according to location -------------------------------------------------------------------------------- Anterior Patellofemoral syndrome (chondromalacia patella) Prepatellar bursitis Recurrent patellar dislocation Tight lateral retinacular ligament Medial plica syndrome Quadriceps tendon calcific enthesopathy Patellar ligament calcific enthesopathy Patellar ligament enthesitis Pretendinous bursitis Deep infrapatellar bursitis Osgood-Schlatter's disease Medial Anserine bursitis Medial compartment arthropathy Hip pain radiation Meniscal tears Meniscal cysts Collateral ligament bursitis Semitendinous bursitis Medial plica syndrome Fibromyalgia Lateral Lateral compartment arthropathy Meniscal tears Iliotibial band syndrome Biceps femoris tendinitis Meniscal cysts Posterior Baker's cyst Thrombophlebitis Tight hamstring muscles Popliteal artery aneurysms Mucinous degeneration of the popliteal artery Popliteal fossa tumors, particularly sarcomas Genu recurvatum Popliteus bursitis -------------------------------------------------------------------------------- Table 14. Posterior heel pain -------------------------------------------------------------------------------- Subcutaneous bursitis Insertional Achilles tendinitis Noninsertional Achilles tendonopathy Stress interstitial and complete rupture Fluoroquinolone toxicity Nodular (sarcoma, tophi, rheumatoid arthritis nodules, leukemia) Retrocalcaneal bursitis Haglund's disease -------------------------------------------------------------------------------- Table 15. Plantar heel pain -------------------------------------------------------------------------------- Fat pad failure Obesity Constitutional Iatrogenic (corticosteroid infiltrations) Plantar "fasciitis" Interstitial fatigue rupture Traction enthesopathy (congenital flat foot, posterior tibial tendon failure) Enthesitis (spondylarthropathies) Entrapment neuropathy (tarsal tunnel syndrome) Calcaneal branches of the posterior tibial nerve First branch of the lateral plantar nerve Calcaneus lesions Fatigue fractures Calcaneal cysts -------------------------------------------------------------------------------- Table 16. Forefoot pain* -------------------------------------------------------------------------------- Faulty footware Flat foot with metatarsal arch failure MTP arthritis Hallux valgus Ligamentous failure of the second MTP joint Morton's neuroma Tarsal tunnel syndrome Neuropathy Metatarsal fracture -------------------------------------------------------------------------------- *MTP = metatarsophalangeal. |
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