Periarticular Rheumatic Disorders

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[edit] Periarticular Rheumatic Disorders

Nancy Y.N. Liu

Juan J. Canoso

Periarticular rheumatic disorder, also referred to as soft tissue rheumatism, includes a wide range of musculoskeletal conditions often encountered by the primary care physician.In contrast to diseases that primarily affect the joint, these syndromes involve the periarticular region, which includes the tendons, bursae, fascia, nerves, and muscle (Fig.134-1).Because of the proximity of these structures to the joint, patients often complain of “arthritis.” Similarly, physicians unfamiliar with these conditions may diagnose articular rather than periarticular disease.This confusion may result in delayed or inappropriate therapy.Accurate diagnosis of periarticular rheumatic conditions requires knowledge about the various disorders, a thorough patient history to distinguish between these conditions, and musculoskeletal examination.Once a diagnosis is made, the physician can provide appropriate therapy and advice.Most of these conditions are localized to one region of the body, although some, particularly fibromyalgia, are diffuse (see Chapter 142 ).In addition, systemic diseases, such as rheumatoid arthritis (RA) or the spondyloarthropathies, may have associated periarticular involvement (see Chapters 133 and 137 ).

Figure 134-1 Common structures around the joint include muscle, tendon, enthesis, and bursa.

[edit] DEFINITIONS

[edit] Bursitis

Two forms of bursae exist in the body: the superficial bursae and the deep bursae.Superficial bursae (e.g., olecranon, prepatellar) enhance the gliding of skin over bone and are not filled with fluid unless trauma, infection, or an acute crystal event occurs.Superficial bursae do not communicate with the joint.In contrast, deep bursae (e.g., subacromial, iliopsoas, gastrocnemius-semimembranosus) often develop communication with joints as they age from constant friction and facilitate the gliding of one tendon over another tendon or bone.Pathologically, both bursae are composed of synovial lining cells and thus can become involved in systemic inflammatory disease.

[edit] Tendinitis

Tendons transmit the tension generated by muscle to move bone.The highly organized type I collagen in tendons provides tremendous tensile strength and elasticity.A sheath that is histologically identical to synovium lines some tendons.Tendinitis occurs with repetitive use, resulting in microscopic fraying of the collagen, fibrosis, and eventual limitation of tendon motion.Tendinitis may also develop secondary to systemic inflammatory disease (e.g., RA, spondyloarthropathies).Tendinopathy is associated with fluoroquinolone drugs in an estimated 15 to 20 per 100,000 patients.^[1]

[edit] Enthesopathy

Enthesis is defined as the point of attachment of tendon, fascia, or ligament to bone (see Fig.134-1).Typical areas include the Achilles tendon attachment to the calcaneus, the plantar fascia to the calcaneus, and the common origin of thewrist extensor muscles to the lateral epicondyle.These areas are susceptible to spur formation, calcification from hydroxyapatite deposition, and inflammatory changes from the spondyloarthropathies.Clinical findings include swelling or pain at or underneath the tendinous insertion.

[edit] Myofascial Pain

Regional myofascial syndromes are caused by localized areas of pain within muscle that often develop from overt or minor injury.Patients typically describe the pain as a vague, diffuse pain with burning.Clinically, a firm, discrete nodule or taut band, also known as a trigger point, can be palpated within the muscle.There is no visible swelling unless muscle spasm is present.When the trigger point is pressed, the pain radiates to a distant point in an atypical dermatomal distribution.A twitch response(a sudden contraction of the muscle area that has been palpated) may be pathognomonic for a trigger point.Trigger points and their zones of pain referral throughout the body most often involve the cervical, shoulder, and lower back regions^[2](Fig.134-2).The description of myofascial pain has been mostly anecdotal.Clinical attempts to separate regional myofascial pain from fibromyalgia based on physical findings of trigger points and tender points, respectively, have not shown definitive results, although many still believe the two entities are distinct.

Figure 134-2 Common myofascial trigger points.

[edit] Nerve Entrapment

Nerve entrapment and peripheral neuropathy are discussed in Chapter 167 .

[edit] REGIONAL PROCESSES

[edit] Cervical Area

Neck pain has many different etiologies, ranging from osteoarthritis to neoplastic disease (see Chapter 124 ).Neck pain and stiffness constitute a common complaint even in young adults.By age 45, more than 50% of the working population complains of neck stiffness and pain.History and physical examination are most helpful in differentiating the various diagnostic possibilities from myofascial neck pain.

Typically, myofascial neck pain starts after trauma, often delayed by days to weeks after the event.The patient may report no specific injury.The pain is localized to the posterior neck region and is sometimes associated with muscle contraction headaches.Patients may describe the pain be ginning after prolonged sitting or sleeping.Activity may improve the pain.No neurologic symptoms are present.

Physical examination reveals well-preserved passive range of motion in the neck, although patients may be unable to move the neck actively.Palpation of the posterior cervical region reveals trigger points within the trapezius and extensor neck muscles.The ligamentum nuchae may also be very tender (see Fig.134-2).If multiple trigger points exist, the referred area of pain can be extensive, although the neurologic examination is completely normal.

Laboratory tests may exclude other diseases but are not specific for myofascial neck pain.Radiographs may be normal or may reveal varying degrees of osteoarthritis.These latter findings, however, may not be responsible for the cervical pain.Further diagnostic tests, such as electromyography (EMG), nerve conduction studies (NCS), computed tomography (CT) scan of the neck, and magnetic resonance imaging (MRI), are not necessary at the initial stages unless the history or examination suggests other diagnoses.

The differential diagnosis of neck pain is broad and can be divided into inflammatory and noninflammatory processes (Box 134-1).Systemic inflammatory diseases include RA, spondyloarthropathies, and systemic juvenile RA.Osteoar-thritis, degenerative disk disease, diffuse idiopathic skeletal hyperostosis (DISH), and fibromyalgia are common noninflammatory diseases of the cervical region.Meningitis, osteomyelitis, and infectious diskitis are infectious etiologies.Neoplastic diseases include metastatic lesions, multiple myeloma, and primary spinal cord tumors.In addition, disorders of the temporomandibular joint, heart, and gastrointestinal (GI) tract may cause pain that is referred to the cervical area.

Treatment of myofascial neck pain is similar to that outlined at the end of this chapter.In cervical neck pain, proper working and sleeping positions are crucial to rehabilitation.Appropriate height of desks, computers, and workstations should be established.At night, patients should sleep in a neutral position (lying on back with legs raised) with only a flat or cervical pillow.Appropriate exercises to stretch and strengthen the neck muscles are helpful.

[edit] Shoulder Area

Shoulder pain may arise from pathology within the true glenohumeral joint, the periarticular structures, or the distant structures that refer pain to the shoulder region.Glenohumeral processes are discussed in Chapter 125 ; only adhesive capsulitis is discussed here.The periarticular structures surrounding the shoulder include the rotator cuff complex, subacromial/subdeltoid bursa, and long head of the biceps.Patients can misinterpret myofascial pain as shoulder pain.

The onset, quality, location, duration, and frequency of pain are important.In addition, factors that exacerbate or improve the pain may help in the diagnosis.Acute pain after trauma suggests a tear in the rotator cuff, joint capsule, or intraarticular structures; gradual pain is less specific.Burning or radicular pain may indicate neuropathy or reflex sympathetic dystrophy.Pain localized to the anterior aspect of the shoulder is common in bicipital tendinitis, whereas rotator cuff tendinitis is more subacromial in location.Glenohumeral processes typically have constant pain referred to the lateral aspect of the upper arm; however, constant pain that is not associated with shoulder movement is an ominous symptom for malignancy or referred pain.Systemic features of fever, chills, and weight loss, visible or progressive swelling in the shoulder area, and pain aggravated by deep inspiration may indicate nonmusculoskeletal etiologies of pain.Axillary pain is usually not from a shoulder source.

Examination of the shoulder includes inspection for asymmetry between the shoulders and palpation of various anatomic regions, including the common myofascial regions of the rhomboid, trapezius, serratus, and rotator cuff muscles.Joints participating in shoulder movement include the sternoclavicular, acromioclavicular, and glenohumeral joints.Scapulothoracic motion also contributes to shoulder movement.Passive range of motion (ROM) in abduction and internal and external rotation delineates the integrity of the glenohumeral joint.In contrast, active ROM provides information not only about the joint, but also about the function of the tendons and muscles surrounding the shoulder.Thus in acute rotator cuff tendinitis, passive ROM of the shoulder is normal (if the patient can relax and avoid guarding), whereas active ROM, particularly against resistance, is limited or painful.In adhesive capsulitis, however, both passive and active ROM are limited.

A general examination also provides clues, particularly if the shoulder examination is normal.Evidence for other joint involvement may suggest an inflammatory arthropathy.Neurologic deficits point to neuropathic processes.Pain referred to the shoulder may originate in the neck, lungs, heart, or abdomen.

[edit] Rotator Cuff Disorders.

The rotator cuff complex includes the supraspinatus, infraspinatus, and teres minor muscles, which attach to the greater tuberosity of the humerus, and the subscapularis, which attaches to the lesser tuberosity (Fig.134-3).The rotator cuff is the internal and external rotator of the shoulder and also depresses the humeral head during abduction.Most common shoulder problems are caused by rotator cuff pathology, categorized as impingement syndrome, acute tendinitis, and rotator cuff tears.

Figure 134-3 Shoulder with humeral head stabilized in shallow scapular glenoid by rotator cuff and capsule. A, Posterior view. B, Cross-sectional view.

[edit] Impingement Syndrome.

Impingement syndrome refers to compression of the rotator cuff (particularly supraspinatus and infraspinatus) and the long head of the biceps against the acromion, coracoacromial ligament, and sometimes the acromioclavicular joint.Impingement syndrome is divided into three different stages.^[3] Stage I usually occurs in patients 15 to 25 years old who perform repetitive overhead activities.Edema and hemorrhage are present in the rotator cuff.Stage II occurs in active individuals between ages 25 and 50 and is typically associated with pathologic changes of fibrosis.Stage III occurs in older individuals when the cuff progressively degenerates or tears, and secondary bony changes develop in the acromion and humerus.

The patient typically complains of pain that is often worse at night and is exacerbated by overhead activity.Pain may be localized to the area of the subacromial region or may diffusely radiate down toward the deltoid region.The pain can be intermittent or constant.In young patients, complete tear, usually resulting from trauma, is acutely painful, whereas in older patients the condition may be less symptomatic.

Examination reveals normal passive ROM of the glenohumeral joint, but active ROM may be limited by pain.Patients often use scapulothoracic movement to help in shoulder abduction.The arc of motion is a useful test (Fig.134-4).As the patient abducts, beginning at 45 degrees, the greater tuberosity impinges the supraspinatus tendon against the acromion or coracoacromial ligament.Once the arc is beyond 120 degrees, the greater tuberosity clears the acromion, and the impingement (or pain) ceases.^[4] In a rotator cuff tear, active abduction, internal rotation, and external rotation against resistance may be weak.The drop sign is positive if the patient's arm suddenly drops or gives way at 90 degrees when the arm is brought down from overhead (180 degrees) along the side.

Figure 134-4 Arc of motion test for impingement.As patient abducts, beginning at 70 degrees, greater tuberosity impinges supraspinatus tendon against acromion or coracoacromial ligament.Once arc is beyond 120 degrees, greater tuberosity clears acromion and impingement (or pain) ceases.

Radiographs in early impingement are usually normal, whereas advanced stages may reveal sclerosis and cystic changes of the distal acromion or greater tuberosity.If the rotator cuff is torn, the space between the acromion and humeral head (normally measuring greater than 5 mm) is lost, and proximal migration of the humerus occurs.Scalloping or erosions of the acromion are also present.MRI may be the most sensitive test to identify a tear, whether partial or complete.

Treatment of impingement syndrome depends on the stage.In early disease, conservative therapy with antiinflammatory medications, rest, and physical therapy to strengthen the rotator cuff muscles is usually adequate.In stages I and II,corticosteroid injections into the subacromial space may also be effective.Job and recreational modifications are necessary to prevent further injury.Patients unresponsive to conservative therapy that has included two or three corticosteroid injections or patients with functional impairment should be referred to an orthopedic surgeon for consultation.Arthroscopic decompression includes division of the coracoacromial ligament and acromioplasty; the latter is most successful in patients with an intact rotator cuff.The results of open and arthroscopic decompression are similar.

[edit] Acute Tendinitis.

Although supraspinatus and bicipital tendinitis typically result from impingement, they may occasionally occur as separate entities.Supraspinatus tendinitis is more common.This tendon helps abduct the shoulder and maintain the strength of the arm when carrying a heavy load with the shoulder abducted; thus it is susceptible to overuse and eventual degeneration.The biceps muscle functions as a flexor of the elbow, supinator of the forearm, and forward elevator of the upper arm.Again, tendinitis occurs as a result of overuse or repetitive motion.

In supraspinatus tendinitis, pain usually localizes in the region just above the scapular spine and lateral to the acromion, near the greater tuberosity of the humerus.Active abduction against resistance elicits severe pain, but passive motion is entirely normal.In bicipital tendinitis, pain is located anteriorly in the area of the biceps tendon, and discrete swelling is sometimes palpable in the tendon area.Supination of the hand against resistance (Yergason maneuver) is painful at the shoulder.Active and passive ROM of the shoulder are normal.

Acute calcific tendinitis occurs secondary to calcium hydroxyapatite deposition in a tendon that has developed degeneration from overuse or impingement.It can involve any tendinous location, but the supraspinatus and bicipital tendons are common areas.Symptoms are usually acute, mimicking gout or pseudogout, and may resolve spontaneously over several days.Calcium deposits within the supraspinatus tendon may eventually rupture into the subacromial bursa, and secondary bursitis develops.Radiographs may reveal amorphous or well-delineated calcific depositswithin the subacromial bursa, supraspinatus, or bicipital tendons.Treatment includes nonsteroidal antiinflammatory drugs (NSAIDs), local corticosteroid injection, or intramuscular adrenocorticotropic hormone (ACTH, 40 to 60 IU).Colchicine, 0.6 mg twice a day, may prevent recurrent postinjection flares.Multiple needlings, which manually disrupt the calcific deposits, and corticosteroid infiltration may help resolve resistant cases.If symptoms recur, surgical intervention may be necessary (see Chapter 125 ).

[edit] Bursitis.

The terms “subacromial” and “subdeltoid” bursitis have often been misused to describe pain in these regions.Acute bursitis is most likely caused by impingement syndrome or calcific tendinitis.Clinical symptoms, physical findings, and treatment are identical to those previously outlined.

[edit] Rotator Cuff or Biceps Tendon Tears.

See Chapters 125 and 143 .

[edit] Myofascial Shoulder Pain.

Myofascial pain around the shoulder region is often the result of overuse or poor positioning during work or play.The most common regions include the trapezius, the supraspinatus and infraspinatus, and the muscles along the medial border of the scapula (levator scapulae, serratus anterior, rhomboid) (see Fig.134-2).Pain may be diffuse and may include sites distant from the myofascial trigger point.On examination a taut band may be palpable in various regions.Treatment is primarily exercises that use these muscles.NSAIDs are given in a short course.Myofascial trigger point injections may be necessary.

[edit] Adhesive Capsulitis.

Adhesive capsulitis (frozen shoulder) is a slow, insidious loss of shoulder motion accompanied by varying intensities of pain.The condition is usually self-limited and resolves within 1 to 3 years unless there is an underlying disease.Often a patient is left with a 20% to 25% reduction in normal motion.Adhesive capsulitis typically develops following shoulder immobility after acute calcific tendinitis of the shoulder, acute stroke, or myocardial infarction.It is also associated with diabetes, hypothyroidism and hyperthyroidism, tuberculosis, apical lung tumors, and local primary neoplasms (Box 134-2).Women and middle-aged patients (40 to 60 years old) are at a slightly greater risk for developing adhesive capsulitis.Its pathology reveals capsular fibrosis and contracture, but it is not clear whether this is a result of inflammation or joint immobility.

Patients complain of slow, gradual onset of shoulder pain that can be severe, even at night.The pain is generalized and referred to the superolateral aspect of the shoulder and upper arm.Examination reveals no swelling at the glenohumeral joint.Passive and active ROM are greatly limited in all movements.

Diagnosis of adhesive capsulitis is based on the physical findings of limited shoulder motion.The physician should investigate associated diseases such as diabetes and thyroid disease.Laboratory studies and plain radiographs are not helpful except to exclude secondary etiologies.Shoulder arthrography can confirm the reduction of the joint cavity but is not necessary, since the diagnosis is established clinically.Routine arthroscopy is not indicated unless other processes (e.g., intraarticular pathology) are suspected or patients fail to improve from conservative therapy.

Numerous treatments for adhesive capsulitis have been described, but most studies are uncontrolled.Prevention is most important.ROM shoulder exercises are recommended for any painful shoulder.The Codman (pendulum) exercise is performed with the patient flexed forward at the waist with most of the body weight supported by the opposite arm on a table or chair back (Fig.134-5).The affected arm is dangled perpendicular to the ground.The patient then circles the arm clockwise for a set repetition and then counterclockwise.The circles should become bigger, and the patient can progress to holding weights with the affected arm while doing the pendulum exercises.NSAIDs have inconsistent effects on the pain.Intraarticular steroids or oral prednisone (20 mg daily, tapered by 2.5 mg per week until finished) appears to be effective in controlling the nocturnal pain in early disease.To regain motion, however, an intensive physical therapy program should be initiated by a physical therapist, followed by a home program.Patients must be informed that improvement is slow; symptoms may persist for 1 to 2 years.

Figure 134-5 Codman (pendulum) range of motion exercise for the shoulder.

Some patients have intractable pain unresponsive to conservative therapy, whereas others have severe shoulder limitation, impairing activities of daily living.Furtherevaluation with MRI scanning may be indicated to exclude intraarticular pathology.Distention arthrography with lidocaine and saline or manipulation under general anesthesia is often performed, but the true efficacy of these interventions has not been proved in well-designed trials.Arthroscopic examination with distention and debridement of capsular adhesions appears comparable to manipulation but offers the advantage of diagnosing and repairing unsuspected rotator cuff tears.

[edit] Reflex Sympathetic Dystrophy.

Reflex sympathetic dystrophy (RSD) (shoulder-hand syndrome) may present initially as shoulder pain or adhesive capsulitis.Risk factors are similar to those of adhesive capsulitis and range from traumatic soft tissue or bony injury to effects of myocardial or cerebrovascular injury.The etiology is unclear, but a disturbance of sympathetic outflow is assumed through the symptoms, physical findings, and response to treatment.RSD may also occur in the lower extremity.

In the earliest stage, patients complain of burning pain, swelling, temperature changes, and excessive perspiration in the extremity.About 3 to 6 months after the initial stage, the soft tissue swelling progresses to skin induration and muscle atrophy.Contractures of the digits, tight shiny skin, and limitation of motion characterize the late stage.Pain may extend proximally from the hand.

Radiographs in early to middle phases may be normal or may reveal patchy osteopenia, whereas late-stage findings show marked osteopenia.Triple-phase technetium bone scan classically demonstrates increased blood flow and pooling, as well as increased uptake in the periarticular structures of the affected extremity.Diagnostically, the improvement of pain and dysesthesia after regional sympathetic block is also characteristic.

The differential diagnosis of RSD includes cervical radiculopathy, carpal tunnel syndrome, the onset of systemic sclerosis, and RA.Treatment in the early phases includes high-dose systemic glucocorticoids (1 mg/kg/day) for 2 weeks.If the patient does not respond, the steroids are rapidly tapered; if improvement occurs, the steroids are tapered gradually over 4 to 6 weeks.Alternative treatments include interruption of sympathetic tone through regional ganglion block, sympathectomy, and medications.Rigorous physical therapy should follow all interventions to preserve motion.In later stages, physical therapy alone is indicated to help regain function and motion.Full recovery is limited if symptoms have been present for more than 6 months.

[edit] Differential Diagnosis.

The differential diagnosis of shoulder pain is broad and can be separated into four categories (Box 134-3).Intraarticular processes include internal derangement, synovitis, osteoarthritis, infection, osteonecrosis, adhesive capsulitis, and tumor.Periarticular processes primarily involve rotator cuff pathology, bicipital tendinitis, acromioclavicular arthritis, and localized or generalized myofascial disorders.Referred pain to the shoulder often is associated with cervical radiculopathy, Pancoast's tumor, subdiaphragmatic processes, gallbladder disease, and myocardial infarction.Other considerations include RSD, brachial neuritis, suprascapular nerve entrapment, and thoracic outlet syndrome.A differential diagnosis can also be generated by the location of shoulder pain (Box 134-4).

[edit] Elbow

True articular causes of elbow pain are extremely rare except for inflammatory processes of the elbow joint.Common soft tissue syndromes include olecranon bursitis, lateral and medial epicondylitis, and nerve entrapment syndromes.Pain often localizes over a particular region.Passive and active ROM of the elbow spans 0 degrees (full extension) to 135 degrees (full flexion).With joint inflammation the patient holds the elbow in semiflexion to accommodate inflammatory fluid or cellular infiltrate.Active and passive flexion and extension are limited.With periarticular disease, however, passive ROM is usually normal.

[edit] Olecranon Bursitis.

Systemic diseases such as gout, RA, and less often, pseudogout, oxalosis, and basic calcium phosphate deposition may all involve the olecranon bursa.Traumatic or infectious bursitis, however, is more common in primary care practice.Since the olecranon is a superficial bursa, it is susceptible to repetitive trauma and bacterial infection from direct skin penetration.Patients may not remember a particular event that precipitated the swelling but may have a longstanding habit of bearing pressure on the elbows.In acute crystal or infectious bursitis, pain tends to besevere, and systemic symptoms (e.g., fever, sweats, chills) may be present.

An important physical finding is swelling in a discrete sac at the tip of the olecranon.The region may be warm, erythematous, and painful to palpation.Soft tissue edema distal to the elbow may be present.Occasionally, if septic bursitis is advanced, the olecranon bursa ruptures, resulting in diffuse cellulitis of the elbow and forearm.Pain may be present (sometimes severe) in flexion, but full passive extension of the elbow is possible without pain, suggesting that true elbow joint involvement is unlikely.Rheumatoid nodules or tophaceous deposits may be palpable in the olecranon bursa.

Aspiration and analysis of the olecranon bursa fluid for total and differential white blood count, crystal search, Gram's stain, and culture are important in making the diagnosis.Unlike articular infections, the septic bursal fluid may have deceptively few leukocytes (less than 10,000/mm^[5]).Infection cannot be excluded until culture results are final.Radiographs typically reveal only soft tissue swelling.

The differential diagnosis for swelling in the olecranon region includes traumatic, septic, gouty, and rheumatoid bursitis.In addition, superficial bursitis sometimes occurs in systemic sclerosis, systemic lupus erythematosus (SLE), and hypertrophic pulmonary osteoarthropathy.

Therapy for traumatic bursitis includes protecting the olecranon region from further trauma by consciously avoiding pressure to the elbow.Corticosteroid injection into the bursa has been successful, but skin atrophy and secondary infections may occur.Surgical resection is rarely necessary.About 80% of all septic bursitis cases are caused by Staphylococcus aureus, followed by Streptococcus organisms in 14%.^[6] Rarely, gram-negative infection occurs, most often in debilitated or older patients.An oral antibiotic effective against Staphylococcus and Streptococcus organisms is the initial therapy for septic olecranon bursitis.When final cultures return, the antibiotic can be tailored.Along with antibiotic therapy, serial needle aspiration of the olecranon bursa fluid is necessary daily until culture results are negative.Antibiotics can be discontinued 5 days after the negative culture.If cultures reveal persistence of the organism despite antibiotic therapy and aspiration, surgical resection of the bursa is necessary.More aggressive initial therapy with intravenous antibiotics may be indicated for patients who are febrile, immunocompromised, or chronically debilitated.

[edit] Lateral and Medial Epicondylitis.

Lateral epicondylitis (tennis elbow) results from trauma to the insertion of the common extensor tendon onto the lateral epicondyle.The extensor carpi radialis brevis is most often involved, at its insertion on the lateral epicondyle.Patients typically describe an aching pain in the lateral aspect of the elbow that is aggravated by grasping or turning the wrist.Pain may be present at rest.Onset ranges from acute to subacute or chronic.Despite its name, tennis elbow develops with any occupation or activity that stresses the wrist extensors.

Medial epicondylitis is the counterpart to lateral epicondylitis but results from overuse of the flexor tendons of the wrist.The point of tenderness is located over the medial epicondyle.Although termed golfer's elbow, this condition may occur with other sports and occupational activities.

Physical examination reveals focal tenderness in the lateral or medial epicondyle region.In addition, extension of the finger or wrist against resistance produces pain in the lateral epicondyle region, whereas flexion of the wrist against resistance produces pain in the medial epicondyle region.

Bilateral lateral epicondylitis is rare.When present, the physician should consider fibromyalgia.Entrapment neuropathies, particularly the deep branch of the radial nerve, may be confused with lateral epicondylitis, whereas compressive neuropathy of the ulnar nerve may be mistaken for medial epicondylitis.In addition, cervical radiculopathy and carpal tunnel syndrome sometimes manifest as elbow pain.Entrapment neuropathy of the deep branch of the radial nerve should be suspected in chronic refractory tennis elbow.The tenderness is anterior, on the radius, approximately 2 cm distal to the elbow crease.

Treatment of lateral and medial epicondylitis begins with avoiding the aggravating condition and modifying it to prevent recurrent injury.This may require the assistance of a professional in sports medicine or an occupational therapist.Relative rest for 3 to 4 weeks, the use of a forearm compression band, and NSAIDs are initial measures.Gentle exercises to stretch the extensor or flexor muscles should progress to strengthening exercises.The success rate of these combined conservative modalities is nearly 75%.Local corticosteroid infiltration around the lateral and medial epicondyle has been a traditional alternative when conservative therapy fails.Although corticosteroid injection is more effective than lidocaine alone for acute pain management, the outcome at 6 months is the same.Thus conservative therapy is recommended for 6 months.If pain persists after that period, surgical consultation is recommended.

[edit] Wrist and Hand

The wrist and hand are prone to traumatic injuries as well as to systemic inflammatory disease.Periarticular processes of the wrist include tenosynovitis, median and ulnar nerve entrapment, and ganglions.In the hand, tenosynovitis and Dupuytren's contracture are common periarticular conditions.

Wrist flexion normally spans 80 degrees of flexion and extension, 40 degrees of ulnar deviation, and 20 degrees of radial deviation.Palpation of the ulnar styloid and radiocarpal joints provides clues for synovitis.Muscle atrophy on examination of the hand may suggest neuropathy.Skin changes (e.g., tightening, rashes) and nail changes are helpful in diagnosing systemic inflammatory diseases.ROM of the fingers can be grossly assessed by the patient's ability to make a complete fist.If the patient cannot, the examination must focus on passive and active ROM of the fingers to distinguish an articular process from a tendinous one.If the examiner can passively move the metacarpophalangeal (MCP), proximal interphalangeal (PIP), and distal interphalangeal (DIP) joints into full flexion, the pathology resides in the tendon mechanism.If passive motion of the joint is limited, however, articular pathology is present.

[edit] Tenosynovitis.

Although tenosynovitis is more common in the inflammatory arthritides (e.g., RA, psoriatic arthritis), stenosing tenosynovitis of the thumb and fingers results more often from overuse or repetitive motion.

[edit] De Quervain's Tenosynovitis.

Stenosing tenosynovitis of the abductor pollicis longus and extensor pollicis brevis tendons is also known as de Quervain's tenosynovitis.It is secondary to the thickening of the fibrous sheath over the radial styloid, which impinges on the two tendons.Patients have pain over the radial aspect of the wrist, which is often exacerbated by thumb or wrist motion.Physical findings may include focal soft tissue swelling over the radial styloid region, pain on palpation of the region, or severe pain when the wrist is deviated toward the ulna while the thumb is folded within the fingers (Finkelstein's test) (Fig.134-6).Differential diagnosis of pain in this region includes carpometacarpal disease from osteoarthritis, tendinitis of the extensors of the wrist, or tendinitis associated with systemic disease such as spondyloarthropathies or disseminated gonococcemia.Treatment includes NSAIDs, immobilization with a long thumb spica or opponens splint fashioned by an occupational therapist, and local corticosteroid injection into the tendon sheath.Activities that require repetitive motion of the thumb or wrist should be modified.

Figure 134-6 Finkelstein's test is positive in de Quervain's stenosing synovitis.Ulnar flexion of wrist produces pain over dorsal compartment containing extensor pollicis brevis and abductor pollicis longus tendons.

[edit] Stenosing Tenosynovitis.

Stenosing tenosynovitis of the finger, also known as trigger finger, develops secondary to excessive forces at the fibrous rings that affix the flexor tendon in place.As a result of these forces, fibrocartilaginous metaplasia develops and obstructs the normal gliding motion of the flexor tendon.Repetitive motion of the fingers and frequent clutching of the hand are associated with this entity.Patients classically complain of the inability to open a finger from flexion in the morning without active assistance from the other hand.Other patients describe a snapping of the finger from flexion to extension.Examination reveals swelling or nodularity, often tender to palpation, along the tendon sheath in the palmar surface of the hand.If the patient actively flexes and extends the finger, crepitation is palpable through the course of the tendon within the palm.Differential diagnosis includes suppurative tenosynovitis (an acute syndrome with redness and pronounced tenderness), mycobacterial infections, systemic inflammatory diseases, Dupuytren's contracture, and sarcoidosis.If multiple fingers are involved, diabetes mellitus, amyloidosis, and ochronosis should be excluded.Local corticosteroid injection of the tendon sheath is extremely effective.^[5] Modification of job or recreational activities is necessary.Referral to a hand surgeon is recommended if symptoms recur.

[edit] Median and Ulnar Nerve Entrapment.

Entrapment of the median and ulnar nerves at the wrist results in carpal tunnel syndromes (see Chapter 167 ).

[edit] Dupuytren's Contracture.

A progressive fibrotic condition involving the palmar fascia, Dupuytren's contracture leads to fixed flexion deformities at the MCP joint.This entity is painless and does not cause significant disability until the fingers develop contractures that limit function.Pathologically, fibroblasts proliferate in the palmar fascia without an inflammatory component.The flexor tendons, however, are not involved.Taut bands of fibrosis form, typically involving the fourth, fifth, and occasionally the third fingers, but rarely the thumb or index finger.Similar findings may occur in the plantar region.Men are affected more often than women.Previous reports associating Dupuytren's contracture with diabetes mellitus and alcoholism have not been consistently documented.Treatment consists of passive extension of the finger in early stages.Surgical intervention at later stages may be necessary, but recurrence is common.

[edit] Ganglions.

Ganglions are cystic outpouchings of the joint capsule or tendon sheath.They often occur asymptomatically on the dorsum of the wrist and resolve or recurspontaneously.The ganglion is filled with a gelatinous fluid and transilluminates, differentiating it from solid tumors.Lipoma, neuroma, synovial cyst of RA, calcific deposits, giant cell tumor, and sarcoma may have a similar appearance.Management includes observation only, aspiration and injection with corticosteroids, or surgical removal.

[edit] Anterior Chest Wall Pain

Costochondritis, or pain in the anterior chest wall along the costosternal junction, may mimic acute cardiac or pleuritic pain.Patients describe intermittent pain that lasts for several days, radiates to the chest wall, and is exacerbated by deep breath.The costosternal junctions are often tender to palpation at one or more locations and even along the intercostal muscles.If bilateral tenderness in the costochondral regions is elicited, spondyloarthropathies and fibromyalgia should be considered in the differential diagnosis.Referred pain from cardiac, pulmonary, esophageal, and vascular sources also must be excluded.

Tietze's syndrome is a possible diagnosis if swelling is associated with pain in the costochondral regions.The etiology of Tietze's syndrome is unknown, but pathology reveals proliferation of cartilage and increased vascularity in the costochondral region.This syndrome may be acute or chronic.Differential diagnosis includes spondyloarthropathy, infection, and tumor of the bone.

Treatment of both costochondritis and Tietze's syndrome includes eliminating the factors that may aggravate the pain, administering NSAIDs, instituting physical therapy with ultrasound, or administering local corticosteroid injections.Skin atrophy in the anterior chest wall region can occur secondary to local steroid injections.This complication may be particularly undesirable for some patients.

[edit] Low Back and Pelvis

Low back pain is one of the most common complaints in a primary care practice (see Chapter 127 ).Although the pain is usually self-limited, loss of productivity in the working population exacts an enormous financial cost to society.Soft tissue etiologies of low back pain include myofascial pain, bursitis, and localized muscle syndromes.

[edit] Myofascial Low Back Pain.

Myofascial low back pain can develop without associated conditions or can be secondary to mechanical back disease, nerve entrapment, and inflammatory diseases of the back.Patients complain of a dull, aching pain that is not well localized.Muscle spasm may be associated with the pain, and nondermatomal radicular symptoms may be present.Activity, prolonged sitting, and cool temperatures exacerbate the pain.More ominous symptoms that require further evaluation include fever, chills, weight loss, pain unrelated to position, urinary or fecal incontinence, and neurologic deficits.

Inspection of the lower back while the patient is standing may reveal asymmetry that suggests scoliosis or leg length discrepancy.Percussion of the vertebral bodies and palpation of the paravertebral musculature can localize the region of pain.Lower back ROM includes flexion, extension, lateral bending, and lateral rotation.Numerous myofascial trigger points may be palpable in the lower back (see Fig.134-2).^[2] When these points are pressed, the pain is reproduced and may radiate to distant regions.

The diagnosis of myofascial low back pain is based on the exclusion of other etiologies.The major categories include mechanical back pain secondary to degenerative disease, nerve entrapment syndromes, infection, inflammatory back disease, referred pain from abdominal or retroperitoneal sources, neoplasms, and psychogenic causes.

Treatment of myofascial low back pain includes recognition of aggravating factors at home, at work, or in recreational activities.Proper sitting, standing, and sleeping positions should be encouraged.Exercises to strengthen the abdominal musculature and back extensors, improvement of posture, and back protection are the foundation of lifelong back care.^[7] Referral to a formal back school or physical therapy program is recommended if patients have chronic pain.NSAIDs may be helpful to patients with myofascial pain secondary to degenerative diseases.Muscle relaxants such as cyclobenzaprine (10 to 20 mg at night and 5 to 10 mg in the morning) are helpful if muscle spasms are present.Alternatively, low-dose tricyclic antidepressants (e.g., amitriptyline) may help patients with chronic back pain.Myofascial trigger point injections with a long-acting anesthetic followed by muscle stretching provide relief of pain.Some believe this can provide lasting benefit without the need for chronic reinjections.^[7] Other modalities, including therapeutic massage and transcutaneous electric nerve stimulation (TENS), have variable results.

[edit] Piriformis Syndrome.

The piriformis muscle is an external rotator of the hip that occupies the area of the greater sciatic notch.Spasms of this muscle produce symptoms of buttock pain that are aggravated by sitting and improved with standing.Symptoms may mimic sciatica, but the neurologic examination is normal.Pain can be elicited in the sciatic notch and the lateral rectal wall.External rotation of the hip against resistance may produce pain.Treatment with local corticosteroid injections can provide relief.

[edit] Ischial Bursitis.

Tenderness at the ischial tuberosity results in difficulty sitting or lying down.Inflammation of the ischial bursa is assumed rather than proved. Tailor's bottom and weaver's bottom are common terms describing this condition.Although there is some association with prolonged sitting on hard surfaces, the exact etiology is unclear.Local fat atrophy is a common finding.Patients can localize the pain over the ischial prominence, which is exquisitely tender to palpation.Suppurative ischial bursitis may occur in paraplegic patients.Ischial tenderness has been associated with the spondyloarthropathies from enthesitis and can be mistaken for low back strain or even herniated nucleus pulposus.Treatment includes using foam cushions with holes cut for the two ischial tuberosities.Local corticosteroid injections should be avoided; they may result in further fat atrophy and pain.

[edit] Osteitis Pubis.

Inflammation of the symphysis pubis has multiple etiologies.Septic seeding of the symphysis occurs most often after genitourinary surgery or herniorrhaphy.Spondyloarthropathies, particularly in women, and calcium pyrophosphate dihydrate (CPPD) disease may also affect this region.Trauma from sports, stress fractures, or specific injury to the gracilis or adductor longus muscles may clinically resemble osteitis pubis.Patients complain of pain in the lower anterior pelvis that may radiate into the medial thighs.Walking may be painful, and palpation over the symphysispubis produces exquisite pain.Initial radiographs may be normal, but with advanced stages, erosions, widening of the joint space, and sclerosis are present.In CPPD disease, linear calcification in the symphysis is present.Treatment includes the use of NSAIDs during evaluation for other underlying diseases.The pain may resolve spontaneously.If infection is suspected, percutaneous aspiration must be performed.Local corticosteroid injection may be beneficial.Surgical intervention is reserved for intractable cases.

[edit] Hips

Periarticular structures and referred pain cause hip pain more often than true articular processes.In the latter, pathology in the joint results in pain localized to the groin or referred anatomically to the knee.Patients often use “hip pain” to refer to any area in the lower back, buttock, and lateral hip regions.

Inspection of the hips during weight bearing detects scoliosis or leg length discrepancy.The gait should be observed.An antalgic gait is characterized by the patient leaning over the painful hip during weight bearing to avoid contraction of the hip abductors.Alternatively, the pelvis may drop down on the opposite side when bearing weight on the affected hip (Trendelenburg's gait).

Measurement of leg lengths is performed in the supine position from the anterior superior iliac crest to the medial malleolus.Up to 1 cm of difference in length between the legs is considered normal.Passive ROM of the hip includes flexion (120 to 135 degrees), extension (20 degrees), internal rotation (35 to 45 degrees), and external rotation (45 degrees).The hips can also abduct to 60 to 70 degrees and adduct to 25 to 30 degrees.Patrick's (fabere) test involves placing the foot ipsilateral to the hip being examined onto the knee of the other leg; then the thigh is further abducted toward the table.If pain exists, intrinsic hip disease or sacroiliac disease is present.The Thomas test can detect hip contractures.With the patient supine, both hips are flexed initially, then the hip of concern is extended toward the table; the other hip remains flexed to fix the pelvis and flatten the lumbar lordosis.Limitation of full extension indicates a hip contracture on that side.Examination of the periarticular structures is detailed later.

[edit] Trochanteric Bursitis.

The trochanteric bursa is located between the tendon of the gluteus maximus muscle and the posterior aspect of the greater trochanter.Bursitis classically develops from overuse or stress of the hip abductors due to hip disease, degenerative disease of the lumbar spine, leg length discrepancy, and other lower extremity conditions.The trochanteric region is a common tender point for fibromyalgia.Thus any patient with bilateral trochanteric bursitis should be examined for other tender points associated with fibromyalgia (see Chapter 142 ).

Patients typically complain of localized lateral hip discomfort exacerbated by rising from a chair or car seat and walking and difficulty sleeping on the affected side.Sometimes the pain is diffuse, involving the lateral hip and thigh, buttock, and even the groin or knee.Localized point tenderness on or posterior to the greater trochanter is the classic finding.Occasionally the fascia lata is also tender.Active hip abduction against resistance and passive external rotation of the hip produce pain.Passive internal rotation is normal.

Differential diagnosis of lateral hip pain includes referred pain from the spine, particularly the upper lumbar region (L2 to L4), secondary to spinal stenosis, disk herniation, and facet syndromes.Entrapment of the cutaneous branches of the iliohypogastric or subcostal nerve can produce burning pain in the lateral hip.Occult stress fractures of the femoral neck in older patients may present as lateral hip pain.Fascia lata fasciitis may mimic trochanteric bursitis, but the pain usually extends below the trochanteric region along the tensor fascia lata.

Treatment of trochanteric bursitis includes moist heat and correction of associated pathology, such as leg length discrepancy or gait abnormalities.Physical therapy referral for ultrasound may be beneficial.Local corticosteroid injection mixed with lidocaine (Xylocaine) is most effective.Patients requiring frequent injections (more than three) warrant reevaluation and surgical consultation if no underlying cause is identified.

[edit] Iliopsoas Bursitis.

The iliopsoas bursa is a deep bursa located between the iliopsoas and the hip joint capsule.This bursa is in direct communication with the hip joint in approximately 15% of patients.It is not a common site for inflammation unless underlying hip pathology exists.Patients typically complain of groin or anterior hip pain.Examination may reveal a palpable mass in the middle third of the inguinal ligament.Extension of the hip produces pain.Occasionally a patient may have a pelvic mass, venous compression, secondary varices, or compression neuropathy of the femoral nerve resulting from the mass effect of the expanding bursa.^[8]

Differential diagnosis of inguinal pain with or without a mass includes intrinsic hip pathology, iliopsoas tendinitis, psoas abscess, hernias, adenopathy, femoral artery aneurysm, and tumor.Treatment is directed at the underlying hip pathology when inflammation is present.Local corticosteroid injections are effective but may require radiologic guidance.Surgical resection is sometimes necessary.

[edit] Meralgia Paresthetica.

See Chapter 167 .

[edit] Knee

Periarticular structures of the knee contribute substantially to knee complaints in the primary care setting.Intraarticular knee pathology can be divided into inflammatory processes, degenerative processes, and internal derangement. Chapter 143 discusses sports injuries that typically produce internal derangement; Chapters 132 and 133 cover osteoarthritis and RA.The periarticular structures of the knee include the prepatellar and infrapatellar bursae, the anserine bursa, the gastrocnemius and semimembranosus bursae (which may become a popliteal cyst), and the iliotibial band.

Examination of the knee begins with the patient standing while the physician looks for evidence of genu recurvatum (hyperextension of knee, suggestive of hyperlaxity), valgus or varus deformities, posterior or anterior knee swelling, and patellar malalignment.The knee joint is palpated medial and lateral to the patella for evidence of synovitis, anterior for prepatellar bursitis, and posterior for popliteal cysts.ROM includes flexion to 140 degrees and extension to 0 degrees.Instability of the knee can be detected by several maneuvers (see Chapter 129 ).

Pain in the knee may be diffuse or localized.Referred pain from the hip typically is perceived medially.The differential diagnosis of knee pain can be classified according to location (Box 134-5).

[edit] Prepatellar Bursitis.

The prepatellar is a superficial bursa that is easily infected from direct penetration of skin surface bacteria.It can be chronically thickened by constant trauma from occupations that require kneeling.Although gout or RA may occur in this bursa, inflammation in this region is usually infectious.Patients complain of sudden onset of redness, warmth, and swelling, accompanied by variable symptoms of fever or chills.Examination reveals erythema and swelling over the patella with surrounding soft tissue edema.Palpation of the knee joint reveals no synovitis or fluid.Passive extension of the knee is painless and full, which is in marked contrast to a septic knee joint.End flexion may produce discomfort resulting from tautness of the skin over the prepatellar bursa.

Diagnosis is based on bursal fluid aspiration, and analysis is similar to that for septic olecranon bursitis.Occasionally the prepatellar bursa ruptures before the patient visits the office.Aspiration of the cellulitic region near the prepatellar bursa is still indicated, since even a drop of fluid may provide the microbiologic diagnosis.

Septic prepatellar bursa is treated similar to olecranon bursitis and requires serial drainage and antibiotic therapy against S.aureus and Streptococcus until fluid cultures become sterile.The prepatellar area is more difficult to treat, however, and initial therapy with intravenous antibiotics, whether inpatient or outpatient, is more prudent.If patients do not improve within several days (less swelling and erythema, sterile cultures), intravenous antibiotics may be necessary.In addition, the knee must be immobilized to prevent constant irritation of the bursa, but the patient should be instructed on isometric exercises to maintain quadriceps muscle tone.Early orthopedic consultation is advised so that debridement or more extensive drainage can proceed if medical therapy fails.Pigtail catheter drainage of the bursa, inserted under ultrasound or CT guidance, is an effective alternative approach to surgery.Protection of the knee with pads and avoidance of kneeling should treat chronic prepatellar bursitis that is noninfectious.Most cases require surgical excision.

[edit] Infrapatellar Bursitis.

The infrapatellar bursa is located between the patellar tendon and the tibia.It is often associated with the spondyloarthropathies but can also be septic or associated with gout.Diagnosis and management are similar to those for prepatellar bursitis.

[edit] Anserine Bursitis.

The pes anserine bursa is located in the medial aspect of the knee, approximately 5 cm below the medial joint line and under the tendons of the sartorius, gracilis, and semitendinosus muscles as they attach to the tibia medially.Irritation of this region is often secondary to overexertion from running, valgus knee deformities, osteoarthritis, and fibromyalgia.Patients complain of medial knee pain with weight bearing and at night if the knees touch each other.Examination reveals exquisite tenderness over the anserine region.Obese patients may have overlying fat that is also painful.The knee joint is normal unless osteoarthritis is present.Differential diagnosis includes the various causes of medial knee pain (see Box 133-5 ).Treatment includes NSAIDs or local corticosteroid injections with an anesthetic.

[edit] Baker's Cyst (Popliteal Cyst).

Baker's cysts occur with any intrinsic pathology of the knee, including mechanical derangement, osteoarthritis, and all inflammatory arthritides, such as RA.Fluid from the knee enters the connecting gastrocnemius-semimembranous bursa but is unable to return easily to the joint space, thus mimicking a one-way valve mechanism.Patients complain of fullness or swelling in the posterior aspect of the knee with pain in the calf.The pain is aggravated by walking and relieved by rest.If the cyst has ruptured or blocks venous or lymphatic drainage through mass effect, peripheral edema of the lower extremity may be mistaken for deep venous thrombosis.

Swelling may be evident on inspection of the popliteal fossa.The Foucher sign (hardening of the mass in extension and softening of the mass in semiflexion of the knee) separates Baker's cyst from popliteal aneurysm or tumor, in which consistency is unchanged.Edema of the lower extremity with calf tenderness and a positive Homans' sign may be present if the cyst has leaked or ruptured (pseudothrombophlebitis).Other findings associated with a Baker's cyst may include secondary varices, ischemia, compressive neuropathies, and posterior compartment syndrome.

The differential diagnosis of a mass in the popliteal fossa includes popliteal artery aneurysm or cystic degeneration of the vessel wall, ganglion, lipoma, and sarcoma.Diagnosis is based on the physical examination.Ultrasonography visualizes the cyst, even if rupture has occurred, since residual fluid usually remains in the cyst.

A Baker's cyst is treated based on the underlying knee condition.Intraarticular steroids are effective if fluid is present in the knee and septic arthritis is excluded.Bed rest, heat, and elevation of the leg are necessary if the cyst has ruptured.True thrombophlebitis can develop from prolonged compression, preventing venous return, and patients then need anticoagulation.

[edit] Iliotibial Band Syndrome.

The iliotibial band is the extension of the fascia lata as it attaches to Gerdy's tubercle, located on the lateral aspect of the tibia.Runners often develop pain over the lateral aspect of the knee.Pain is caused by tightness of this band as it rubs against the lateral femoral condyle during knee flexion and extension.Pain is reproduced over the lateral femoral condyle.Treatment includes NSAIDs, ice, and ultrasound, as well as exercises to stretch the hip abductors and fascia lata and correction of any mechanical factors.

[edit] Ankle and Foot

Foot and ankle problems are common in the ambulatory population.The principal motions of the ankle and foot complex include dorsiflexion, plantar flexion, inversion, and eversion.The small bones of the foot also accommodate various terrains.The true ankle joint functions in dorsiflexion (10 degrees) and plantar flexion (30 degrees).The subtalar joint allows for inversion (30 degrees) and eversion (10 degrees).The metatarsophalangeal (MTP) joints provide the greatest motion in the foot, since their major role is in the push-off action.Thus dorsiflexion of the MTP joint is at least 70 degrees.In addition, the Achilles, posterior tibialis, and peroneal tendons function to plantar flex, invert, and evert, respectively, the ankle and foot.

Examination of the ankle and foot begins with inspection of the area anteriorly and posteriorly while the patient is standing.The loss of the medial longitudinal arch is a common problem for valgus deformities.If swelling or pain is present, isolation of specific joints of the ankle is important.In true ankle arthritis, the dorsum of the ankle along the joint line is diffusely swollen.In contrast, asymmetric swelling over the medial or lateral malleolus suggests tenosynovitis of the posterior tibialis or peroneal tendon, respectively.Limitation of passive motion suggests true joint involvement.Active motion, particularly against resistance, tests the function of the tendons.The insertion of the Achilles ten don and plantar fascia should be palpated.Vascular and neurologic status completes the examination.

[edit] Achilles Tendinitis.

The Achilles tendon is susceptible to acute injury, rupture, calcification, and inflammation associated with the spondyloarthropathies and RA.In addition, Achilles tendon inflammation and rupture have occurred with fluoroquinolone treatment.^[1] Common symptoms are pain localized to the posterior aspect of the heel and pain exacerbated by dorsiflexion of the ankle.Acute injury usually occurs in running sports, and tendon rupture is possible.When rupture occurs, the patient describes a snapping sensation followed by the inability to stand on the toes.Acute swelling and erythema may be present in calcific tendinitis.In systemic inflammatory processes the tendon may be diffusely tender and swollen, and the retrocalcaneal bursa may also be involved.Treatment consists of rest, NSAIDs, heel inserts, and an ankle splint used at night in neutral position to prevent tendon contractures.In acute ruptures, immobilization and surgical intervention are necessary.Corticosteroid injections into the Achilles tendon are not recommended because this predisposes the patient to subsequent tendon rupture.

[edit] Posterior Tibialis Tendinitis.

The posterior tibialis tendon inverts the foot and maintains the medial longitudinal arch.RA and the spondyloarthropathies often involve this tendon.Younger patients often injure the tendon while participating in high-stress activities, such as running and dancing.Older patients may note progressively flat arches and pain in the medial ankle secondary to gradual attrition of the tendon from microtrauma or degeneration.In patients with RA or other processes, acute rupture may suddenly result in a flat arch.Diagnosis is based on swelling and pain near the medial malleolus or pain and weakness with active inversion of the foot against resistance.In later stages after tendon rupture, flattening of the longitudinal arch on weight bearing is associated with hindfoot valgus deformity (Fig.134-7).^[9] MRI scans delineate the various stages of tendon degeneration.Treatment for initial stages includes rest, NSAIDs, and medial heel lift.If these approaches are ineffective, casting for a short time or local corticosteroid injection into the tendon sheath is necessary.Persistent inflammation, pain, and swelling may require surgical intervention.

Figure 134-7 Posterior view of normal foot (left) and hindfoot valgus (right). Right foot also has forefoot abduction, with “too many toes” seen lateral to ankle. (From Supple KM et al:Semin Arthritis Rheum 22:107, 1992.)

[edit] Peroneal Tendinitis.

The peroneal tendon everts the ankle and is susceptible to inflammatory conditions as well as mechanical injury.Examination reveals localized swelling and pain just posterior to the lateral malleolus.Active eversion against resistance is weak or painful.Therapy is similar to that for posterior tibialis tendinitis.

[edit] Retrocalcaneal Bursitis.

The retrocalcaneal bursa is located posterior to the calcaneus and anterior to the Achilles tendon at its insertion site onto the calcaneus.This bursa is usually associated with systemic inflammatory diseases such as the spondyloarthropathies, RA, and gout.Pain arises in the heel at the Achilles tendon's insertion.Focal swelling may be visible in this area.Therapy is similar to that for Achilles tendinitis.Intrabursal injection or surgery may be required if symptoms persist.

[edit] Plantar Fasciitis.

Inflammation of or strain on the plantar fascia is a common cause of foot pain.The plantar fascia is a thick, bandlike structure that attaches at the calcaneus and to each toe.Causes of plantar fasciitis include pes planus, prolonged standing, obesity, aerobic exercises that require jumping or bearing weight on the toes, fluoride or retinoid therapy, and the spondyloarthropathies.Patients complain of pain localized to the plantar surface of the foot that is exacerbated by pushing off with the toes.Examination with the dorsiflexed foot reveals tenderness along the plantar fascia or at the insertion of the fascia into the calcaneus.Heel spurs may be palpable or evident on radiographs.If fasciitis is associated with systemic inflammatory disease, plain films may demonstrate periostitis at the calcaneal insertion or even erosions.If clinically suspected, stress fractures of the metatarsals can be evaluated with serial radiographs or bone scan and Morton's neuroma by clinical examination.Treatment includes correction of underlying processes andthe use of a plastic heel cup that maintains the soft tissue of the heel pad under the weight-bearing portion of the heel.Longitudinal arch support may also help.Local corticosteroid injection of the plantar fascia is also effective but must be cautiously given to avoid extensive fat pad atrophy at the heel.

[edit] Nerve Entrapment or Compression.

Prominent nerve conditions include tarsal tunnel syndrome (see Chapter 167 ) and Morton's neuroma (see Chapter 130 ).

[edit] PRINCIPLES OF TREATMENT

[edit] Rehabilitation

Although treatment of the periarticular rheumatic disorders seems diverse, certain principles are applicable to tendinitis, bursitis, and myofascial pain.Overuse and injury predominate in the etiology of these processes.Thus a major focus of treatment is identifying the cause of overuse or injury and adjusting work or recreation to prevent further injury.

An occupational therapy consultation is often extremely helpful and cost-effective.An occupational therapist assesses a patient's needs and then establishes a program that maximizes joint protection, prevents disability, and optimizes joint function.Industrial rehabilitation may be required if a patient has significant limitations at work.Work hardening programs have been established to help employees with various regional soft tissue problems to return to work.

Physical therapy includes modalities that initially control pain, followed by passive and active exercises to stretch or move a joint or periarticular structure.The final step is muscle strengthening around the region to prevent reinjury or further damage.

Heat and cold are common modalities to treat various soft tissue pains.Heat from moist heating packs and ultrasound may provide relief, although usually short-lived.Since ROM improves after heat application, use of heat may be a useful adjunct and may allow patients to exercise.Cold, usually reserved for acute injuries, reduces swelling.

TENS has been used for chronic pain of the back, neck, and other regions.The mechanism of action is postulated to be interference of pain impulses to the brain by its own impulses (gate control theory of pain).The cost of a TENS unit may not be reimbursed by third-party insurance.

Exercises, both passive and active, are important to maintain ROM, strength, and function.In passive exercises the therapist or machine moves the muscle while the patient makes no muscle contraction.Active motion requires the patient to contract the muscle in an isometric (no joint motion) or isotonic (joint motion against resistance) manner.The optimal program for each patient's soft tissue problem is best gauged by a physical therapist.If the primary care physician wants to prescribe or supervise an exercise program, however, extensive exercises are available for each regional problem.^[7]

Splints or orthotic devices immobilize an affected area to reduce pain, hold a particular region in an optimal position for function, or redistribute stress from a painful region to surrounding structures.Examples of these functions include a neutral wrist splint for carpal tunnel syndrome, a hindfoot orthosis to reduce valgus deformities secondary to posterior tibialis tendon dysfunction, or a forearm band for lateral epicondylitis.Properly fitting shoes are crucial in many of the periarticular disorders, and consultation with an orthopedic surgeon or podiatrist may be necessary.

[edit] Medications

[edit] Nonsteroidal Antiinflammatory Drugs.

The use of NSAIDs in rheumatic diseases is discussed in Chapters 132 , 133 , and 137 .For the periarticular entities, NSAIDs provide analgesic and antiinflammatory effects.Numerous NSAIDs are available and differ in metabolism, dosing, and toxicity profile (see Table 137-2 ).A particular NSAID should beprescribed for at least 10 to 14 days before the medication is discontinued for lack of efficacy.Common toxicities include GI intolerance, gastritis, and superficial ulceration.Other toxicities include renal insufficiency, elevated liver enzyme levels, hyperkalemia, headaches, mood changes, and other central nervous system alterations.NSAIDs are not as effective for myofascial pain as for inflammatory musculoskeletal disorders.

[edit] Tricyclic Antidepressants.

Tricyclics are important in the treatment of chronic neck or low back pain.Possible mechanisms of action include their effect on brain neuropeptides, the direct role on stage IV sleep, endogenous opioids, and reduction of brainstem-mediated muscle spasm.In addition, these medications are helpful if there is component of depression.

[edit] Parenteral Corticosteroids.

Parenteral corticosteroids may be useful in the early stages of RSD or adhesive capsulitis.ACTH can be an alternative to NSAIDs in acute calcific tendinitis.The protocol is similar to the treatment of acute gouty arthritis.Patients receive 40 to 60 IU of ACTH intramuscularly; this is repeated up to 3 days if necessary.

[edit] Corticosteroid Injections.

Corticosteroid injections are a major form of treatment for the various soft tissue disorders (see Chapter 123 ).The primary care physician should be able to inject into common areas that include the subacromial, trochanteric, and anserine regions, along with the true knee joint.Utmost care is needed when injecting the tendon sheaths, carpal and tarsal tunnels, plantar fascia, and retro calcaneal bursa.Injection of these regions should be referred to a rheumatologist or orthopedist if the primary care physician is not experienced.The true glenohumeral or hip joint is difficult to enter, and a specialist, or a radiologist under fluoroscopic guidance, should perform these injections.

After an injection, the area is rested or splinted for 48 to 72 hours.Patients should be informed about possible postinjection flare and its treatment with ice and analgesics.If a tendon sheath is injected, strenuous activity of that tendon should be avoided for up to 2 weeks.

Injection of trigger points in myofascial pain is based on the theory of mechanical disruption of the trigger point by saline or an anesthetic, followed by passive muscle stretch.Some studies have reported a longer duration of improvement if corticosteroids are combined with the local anesthetic.Most studies have been uncontrolled; thus corticosteroids are not recommended for injection of trigger points.

[edit] Referral

Subspecialty referrals are indicated only if patients do not respond to initial management that includes avoidance of aggravating factors, pain control, and further strengthening exercises.

[edit] REFERENCES