Bicipital Tendinitis (Tenosynovitis) (Fig. 52-6).: This is a nonspecific low-grade inflammation of the biceps tendon or its sheath (or both) that is more common in those who repeatedly flex the elbow against resistance, such as weight lifters and swimmers.4,36 The tendon courses through the joint and along the bicipital (intertubercular) groove, which can be appreciated when the elbow is held at 90 degrees of flexion and the arm is internally and externally rotated.³⁶ Patients may have restricted or normal range of motion and normal strength; however, they usually complain of tenderness on palpation over the bicipital groove.⁴ Efforts to elevate the shoulder, reach the hip pocket, or pull a back zipper all aggravate the symptoms. Tenderness over the bicipital groove does not confirm the diagnosis, however, because the supraspinatus tendon is in close proximity to the insertion of the bicipital tendon.³⁶ Other diagnostic clues include the Lipman test, in which “rolling” the bicipital tendon produces localized tenderness; the Yergason test, which elicits pain along the bicipital groove when the patient attempts supination of the forearm against resistance while holding the elbow flexed at a 90-degree angle against the side of the body; and the Speed test, in which pain is reproduced when the patient resists forward elevation of the humerus against an extended elbow. Radiographic findings are normal and they are not required if the clinical diagnosis is supported.

Calcareous Tendinitis, Supraspinatus Tendinitis, and Subacromial Bursitis.: These inflammations are so clinically similar that their symptoms and signs are difficult to differentiate. The musculotendinous rotator cuff is composed of the supraspinatus, infraspinatus, teres minor, and subscapularis muscles, which insert as the conjoined tendon into the greater tuberosity of the humerus. The subacromial bursa lies just superior and lateral to the supraspinatus tendon (Fig. 52-7). Both the tendon and the bursa are located in the space between the acromion process and the head of the humerus and are particularly prone to impingement in this “critical zone.” Impingement can occur when the shoulder moves forward and compresses the cuff and bursa under the anterior third of the coracoacromial arch. Injections into either the bursa or the tendon sheath area are commonly performed to relieve inflammation and overuse.

In calcareous (or calcific) tendinitis of the shoulder, a calcific deposit (hydroxyapatite) is located within the substance of one or more of the rotator cuff tendons (commonly the supraspinatus).³⁸ These calcium crystals can occasionally rupture into the adjacent subacromial bursa and cause acute pain and tenderness in the deltoid area (Fig. 52-8). The bursae in relation to the greater tuberosity and the subdeltoid (subacromial) bursa are the most common sites of calcific deposits.

During the acute or hyperacute stage, the patient holds the arm in a protective fashion against the chest wall. The pain may be incapacitating, and all ranges of motion are disturbed, with internal rotation being markedly limited. Tenderness is often diffuse over the perihumeral region. The patient may also complain of pain at night when lying on the affected side and with abduction of the arm. Supraspinatus tendon impingement is most apparent when the humerus is abducted and internally rotated. The Hawkins test elicits pain with forcible internal rotation while the patient’s arm is passively flexed forward at 90 degrees, and the Neer test elicits pain with full forward flexion between 70 and 120 degrees (Fig. 52-9). Both tests are fairly sensitive but not specific for supraspinatus tendon impingement.³⁹ Constitutional symptoms are rare, but swelling may sometimes be apparent with the hyperacute form, and a fever and accelerated sedimentation rate may even develop in some patients. When shoulder radiographs demonstrate a calcific deposit, the shadow appears “hazy” with lightening of the periphery caused by the pressure of inflammatory edema (see Fig 52-8B). Night pain may be intolerable and require opioids for control.

AC Joint Inflammation.: Pain arising in the acromioclavicular (AC) joint is frequently an aftermath of an acute injury, such as falling on an outstretched hand or the result of weight lifting. With this injury, all ranges of motion of the shoulder cause pain, and the joint is tender but rarely swollen. Be aware that an obvious deformity or mechanism of injury may suggest AC separation or dislocation. With AC joint inflammation, crepitus is not uncommon.³⁶ Adduction of the arm across the body with forward elevation to 90 degrees (the cross-arm test) may exacerbate the pain because the AC joint is compressed with this motion.³⁶ In a study by Jacob and Sallay,⁴² injection of corticosteroids provided short-term relief of symptoms but did not alter the long-term course of patients with AC joint arthropathy. Hence, some clinicians believe that AC joint injection should be performed only in patients with persistent pain despite a trial of rest, oral antiinflammatory medications, and modification of activity.³⁷

Radiohumeral Bursitis, Lateral Epicondylitis, and Medial Epicondylitis.: Radiohumeral bursitis occurs at the juncture of the radial head and the lateral epicondyle of the elbow. This condition is commonly found in combination with lateral epicondylitis, which is thought to result from repetitive microtrauma at the insertion of the extensor carpi radialis and extensor digitorum muscles. The symptoms of the two adjacent problems are indistinguishable, but tenderness overlies the radiohumeral groove with bursitis, whereas tenderness occurs chiefly at the lateral epicondyle with tennis elbow (Fig. 52-11). Although the term epicondylitis suggests an inflammatory cause of the pain, some evidence suggests that the injury in lateral epicondylitis results from a degenerative process causing a “tendinosis.”⁴³ Regardless of the exact pathophysiology, there is often a history of repetitive motion of the wrist (flexion, extension, supination, pronation, or any combination thereof), such as while golfing, gardening, or using tools.⁴ A clinical sign supporting the diagnosis of tennis elbow is provocation of pain when the patient attempts extension of the middle finger against resistance with the wrist and elbow held in extension. Alternatively, pain is reproduced at the elbow when the patient is asked to extend the wrist against resistance.

Medial epicondylitis (golfer’s elbow) is a similar condition, although it occurs on the side opposite that of lateral epicondylitis and is much less common (Fig. 52-12).⁴ This condition involves the origin of the pronator teres and flexor carpi radialis muscles. On physical examination the patient usually complains of pain when the wrist is flexed against resistance or when the forearm is pronated. Palpation of the medial epicondyle also elicits tenderness.

There is evidence supporting the short-term efficacy of corticosteroid injection for both lateral and medial epicondylitis.44–52 Successful injection of lateral epicondylitis produces a predictable short-term improvement (less than 6 weeks) in pain that is superior to that with nonsteroidal drug therapy and physical therapy.^45,49–52 However, after 6 weeks, physical therapy reduces symptoms more than corticosteroid injection does.⁵¹ A similar effect was noted with medial epicondylitis: at 6 weeks patients injected with corticosteroids also reported significantly less pain than did those receiving physical therapy, but at 3 months and 1 year there were no significant differences in pain between groups receiving corticosteroids and physical therapy and physical therapy alone.⁴⁷

Olecranon Bursitis (Aseptic).: Olecranon bursitis is an inflammation of the olecranon bursa of the elbow, located between the skin and the olecranon process (Fig. 52-15). The most common cause of olecranon bursitis is trauma,⁵⁴ which is usually minor, or activities that involve chronic leaning or repetitive elbow motion. Olecranon bursitis is also known as “barfly elbow” or “student’s elbow,” so named because prolonged leaning on the elbow can lead to bursitis. It may also be seen after an AstroTurf rug burn of the elbow during sporting activities. Other patients at risk for olecranon bursitis include gardeners, auto mechanics, carpet layers, gymnasts, and wrestlers.⁵⁵ More significant trauma, such as a direct blow to the elbow, can also cause olecranon bursitis. In this case, hemorrhage into the bursa results in acute hemorrhagic bursitis. Other causes of olecranon bursitis include hemodialysis⁵⁶ and systemic diseases such as rheumatoid arthritis, lupus, uremia, and gout.⁵⁷

The olecranon bursa is located superficially and is consequently susceptible to injury. Although most cases of olecranon bursitis are sterile, the olecranon bursa is the most frequent site of septic bursitis.⁵⁸ Therefore, it is important to accurately differentiate between the two entities. Steroid injections are absolutely contraindicated in cases of confirmed or suspected septic bursitis. Frequently, the diagnosis will be suggested by the history and physical examination, but it may be necessary to aspirate and analyze the fluid if septic bursitis is suspected.

In aseptic olecranon bursitis, findings on radiographs are usually normal, but soft tissue swelling may be evident. Bony spurs or amorphous calcific deposits may also be seen, especially in older patients.⁵⁴ Occasionally with rheumatoid arthritis and gout, nodules or tophi may be palpated within the bursal sac. The bursa and surrounding structures are not typically tender, and there is full and painless range of motion of the involved elbow. Signs of infection such as warmth and erythema of the overlying skin are also usually absent. It should be noted, however, that pain, warmth, tenderness, and erythema might be present in both septic and aseptic olecranon bursitis. If there is any suspicion of septic olecranon bursitis, aspiration should be performed and corticosteroid injection deferred until an infectious cause has been ruled out.⁵⁴

Aseptic olecranon bursitis may be cosmetically bothersome to the patient but does not usually cause discomfort and may resolve spontaneously. In cases of bursal swelling that are nontender and not tense, treatment is symptomatic and includes NSAIDs, compression, and avoidance of further injury.⁵⁴ In cases of acute hemorrhagic bursitis, aspiration of the bursa followed by a dressing and ice will decrease the incidence of chronic bursitis.⁵⁴ When the bursa is large, tense, and inflamed and infection has been excluded, aspiration with steroid injection has been shown to hasten the resolution of symptoms.⁵⁹ Smith and colleagues⁶⁰ demonstrated the superiority of intrabursal methylprednisolone acetate over oral naproxen or placebo at 6 months and noted faster resolution and less reaccumulation of fluid with the steroid injection. The addition of a course of an oral NSAID after steroid injection did not affect the outcome.⁶⁰ Following steroid injection, application of a compression dressing and a brief period of relative immobilization may be helpful.⁵⁴ Repetitive steroid injections for aseptic olecranon bursitis have been associated with triceps rupture and should be avoided.⁶¹

Septic Bursitis.: Septic bursitis is most common in the olecranon, prepatellar, and superficial infrapatellar bursae because of their superficial location and vulnerability to injury.⁶² Infection of the other bursae is much less common. The infection is most likely caused by direct percutaneous inoculation of common skin organisms into the bursae as a result of trauma or contiguous spread from an overlying cellulitis.^54,62,63 Septic bursitis secondary to hematogenous spread is rare.^54,62,63 Most cases of septic bursitis are caused by Staphylococcus aureus (80%), followed by streptococcal organisms.⁶⁴ Other less common organisms include coagulase-negative staphylococci, enterococci, and gram-negative organisms such as Escherichia coli and Pseudomonas aeruginosa.⁶² Isolated cases of bursitis caused by fungi (Aspergillus terreus, Candida lusitaniae), Brucella, and Mycobacterium tuberculosis have also been reported.⁵⁴ Such unusual organisms should be considered in cases of septic bursitis that are subacute or chronic and those discovered in an immunocompromised host.⁵⁴

The most common cause of olecranon septic bursitis is trauma. It has been estimated that as many as 70% of cases of septic bursitis are related to trauma, either chronic and caused by repetitive injury or acute and often associated with occupational or recreational activities.⁶² Other risk factors for the development of septic bursitis include chronic illnesses (e.g., diabetes mellitus, alcoholism) and previous inflammation of the bursa, as occurs with gout, rheumatoid arthritis, and uremia.⁶² Infection may follow an injection of corticosteroids into the bursae in up to 10% of cases.⁶⁵

At times the diagnosis of septic bursitis can be challenging. Acute gouty olecranon bursitis may have a very similar clinical picture and can often be accurately differentiated from septic arthritis only by fluid analysis (Fig. 52-16). Other conditions that may mimic bacterial septic olecranon bursitis include acute rheumatoid bursitis, aseptic bursitis secondary to oxalosis induced by dialysis, or infectious bursitis caused by unusual organisms such as Mycobacterium, Serratia marcescens, or fungi. About one third of all cases of olecranon bursitis are septic.⁵⁴

In some cases the diagnosis of septic bursitis is obvious (see Fig. 52-16A). The onset of pain and swelling may be quite rapid (over a period of 8 to 24 hours), as opposed to the more gradual onset of aseptic bursitis. The bursa is erythematous, tense, swollen, warm, and very painful. Flexion of the elbow is limited by pain; however, some joint mobility may be present because the bursa does not usually extend into the joint.⁶² The patient may report a history of trauma to the area, which may be evident on physical examination. Some patients will also have a fever. Smith and associates found that the infected bursa was generally 2.2°C or more warmer than the unaffected elbow.⁶⁶

Aspiration of infected bursal fluid with culture of bacteria from the aspirate confirms the diagnosis of septic bursitis. Fluid is usually easily obtained from the tense bursa and (in the case of established infection) may be cloudy or grossly purulent. The white blood cell count of the fluid in septic bursitis is usually 5000 to 100,000 cells/mm³ or greater, and the proportion of polymorphonuclear cells usually exceeds 90%. Neither fever nor systemic leukocytosis is considered sensitive or specific for the disease. However, in immunocompromised patients (e.g., those with diabetes mellitus, alcoholism), the white blood cell count in the bursal fluid tends to be higher.⁶⁷ Because of some overlap in the leukocyte count of bursal fluid in septic versus aseptic bursitis, it is important to remember that a low bursal white blood cell count does not exclude a septic cause. Moreover, the sensitivity of Gram stain may be 50% or less.⁶⁸ In a large study of 200 patients with olecranon bursitis, cell count and Gram stain were not always helpful in the acute evaluation and treatment of new cases of septic bursitis.⁶⁹ Therefore, if clinical suspicion for septic olecranon bursitis is high, even in the presence of a normal or equivocal fluid cell count or Gram stain, steroid injection should be delayed and empirical antibiotic therapy started until the results of culture are available.⁵⁴

Treatment of septic bursitis includes the use of antibiotics directed against penicillinase-producing Staphylococcus, splinting, warm soaks, and drainage of the bursa. Drainage may be performed by daily needle aspiration until the fluid is sterile.⁶³ However, open incision and drainage might be required, particularly if the infection is recurrent or refractory.⁷⁰ In addition to daily drainage of the bursa as necessary, administer antibiotics for at least 2 weeks.⁶³ Consider additional antibiotic coverage against methicillin-resistant S. aureus based on the patient’s risk factors and epidemiology.⁶² Outpatient therapy with oral antibiotics is generally acceptable, although this approach has been challenged for immunocompromised patients.⁶⁷ This decision is generally guided by the clinical appearance of the bursa, as well as associated comorbid conditions, compliance, and other factors regarding patient care. Response to antibiotic therapy might be slow. Thus, it is important to initiate antimicrobial treatment as soon as clinical suspicion of septic bursitis exists. Additional treatment with oral NSAIDs may help reduce the pain. Standard gout medications will generally resolve acute gouty bursitis.

Ganglion Cysts of the Wrist or Hand.: These cystic swellings occur frequently on the hands, especially on the dorsal aspect of the wrist (Fig. 52-17). Ganglion cysts are common and make up approximately 60% of all soft tissue tumors affecting the wrist and hand. They usually develop spontaneously in adults between 20 and 50 years of age, with a female-to-male ratio of 3 : 1. Ganglion cysts may also be seen on the foot and ankle, generally on the extensor surface.

The etiology of ganglia remains obscure; there is usually no history of trauma.⁷¹ The word ganglion is derived from the Greek word meaning “cystic tumor.” The mesothelium- or synovium-lined cystic structures are attached to or may arise from tendon sheaths or near the joint capsule and do not extend into the joint itself.⁷² Attachment is often by a pedicle. The wall of a ganglion is smooth, fibrous, and of variable thickness. The cyst is filled with a clear, gelatinous, sticky, or mucoid fluid of great density. The viscous fluid in the cyst may sometimes represent almost pure hyaluronic acid.

The types of ganglia vary with their location. The most common ganglia are located on the dorsal surface of the wrist and arise from the scapholunate joint. These constitute approximately 65% of ganglia. Volar wrist ganglia, which arise over the distal aspect of the radius, constitute another 20% to 25% of ganglia and are often adherent to the radial artery.⁷³ Flexor tendon sheath ganglia make up the remaining 10% to 15% and are found on the hand and wrist.

Most ganglia are of no great clinical significance and most do not require treatment. Spontaneous regression is common. However, if the appearance of the cyst is disturbing to the patient or if the ganglion is painful or tender (from soft tissue or nerve compression or bone erosion), simple aspiration with or without injection of a corticosteroid suspension is usually an effective approach. Up to three aspirations may be required before the technique is considered a failure. In one study, 69% of 116 patients required only a single aspiration for successful treatment.⁷⁴ Two or three aspirations were required in 19%, and only 12% of patients ultimately needed surgical excision.⁷⁴ It should be noted, however, that ganglia often recur after aspiration or surgery. In a study by Dias,⁷⁵ 42% of palmar wrist ganglia treated by surgical excision and 47% treated by aspiration recurred within 5 years. Because aspiration with or without steroid injection is associated with considerable cost savings and shorter recovery times than with surgery and because there is no difference in recurrence rates, aspiration appears to be the initial treatment of choice.⁷⁵ In the event that nonsurgical treatment fails, surgical excision may be indicated. The “old” treatment of attempting to rupture the ganglion with a heavy book is not advised because of the potential for local injury. Aspiration of volar wrist ganglia should also be undertaken with caution because the radial artery often adheres to the cyst and may be at risk for injury.⁷³

de Quervain’s Disease and Intersection Syndrome.: de Quervain’s disease, a relatively common disorder, is a stenosing tenovaginitis of the extensor pollicis brevis (EPB) tendon and the abductor pollicis longus (APL) tendon of the thumb (Fig. 52-18). Though commonly referred to as a tenosynovitis, which denotes inflammation of the synovial sheaths, this condition is more accurately described as a tenovaginitis.⁷⁸ Tenovaginitis refers to thickening of the fibrous sheath of the first extensor compartment. In 1912, de Quervain described “thickening of the dense fibrous connective tissues without any fresh sign of inflammation, neither round cell inflammation nor increase in numbers of cells.”⁷⁸ Histologically, the thickening is caused by the accumulation of mucopolysaccharide within the tendon sheath.^79,80

It is commonly thought that the disorder occurs more often after repetitive use of the wrists, especially with a wringing motion. The syndrome has been called “washerwoman’s sprain,” and often no specific cause is apparent. Women during pregnancy or within 12 months of childbirth are also frequently affected.⁵⁷ However, a study by Kay⁷⁸ challenged the association between repetitive motion and de Quervain’s disease. In a retrospective study of 100 cases, no strong correlation was found with occupation or history of repetitive activities in patients in whom de Quervain’s disease was diagnosed. Thus, it may be possible that repetitive activities exacerbate the pain associated with a condition for which the etiology is unclear.

Tenderness and occasionally palpable crepitation are elicited just distal to the radial styloid process, where both tendons come together in an osseofibrous tunnel. Patients usually have wrist pain and often mistakenly attribute the discomfort to some distant, albeit irrelevant trauma. The condition may be confused with first carpometacarpal arthrosis (osteoarthritis of the thumb) and intersection syndrome. Radiographs will have normal findings in de Quervain’s disease but might be appropriate to rule out other pathologic abnormalities. Ultrasound may demonstrate thickening and edema of the synovial sheath⁸¹ but has not yet been routinely used to make or confirm the diagnosis. Rarely, gonococcal tenosynovitis might simulate this inflammatory condition (Fig. 52-19).

A useful clinical maneuver that indicates de Quervain’s disease is the Finkelstein test (Fig. 52-20). Abduct the patient’s thumb into the palm of the hand, fold the fingers over the thumb, and then apply ulnar deviation at the wrist; severe pain at the site of the affected tendon sheaths indicates a positive test. When performing the Finkelstein test, also palpate the tender area for crepitus. If axial traction or compression (the carpometacarpal grind test) and rotation of the thumb produce pain, the condition is most likely due to degenerative changes in the carpometacarpal joint of the thumb rather than de Quervain’s disease. It should be noted that gonococcal tenosynovitis of the wrist may mimic de Quervain’s disease, and one should inquire about other symptoms (e.g., sore throat, penile or vaginal discharge, or fever) and carefully look for the characteristic rash of this sexually transmitted disease (see Fig. 52-19).

Local corticosteroid injection as the therapeutic preference for de Quervain’s tenovaginitis is well founded in the literature. In a study comparing steroid injection of de Quervain’s disease with immobilization and oral NSAID therapy alone, the latter was effective only in a small group of patients with minimal symptoms.⁸² In a retrospective study, 84% of 58 patients were effectively managed either with a single injection (60%) or with repeat injections (24%), with only 12% requiring surgical treatment.⁸³ These data support a metaanalysis of 495 subjects treated for de Quervain’s tenovaginitis in which an 83% cure rate was found with injection alone versus 61% for injection and splinting, 14% for splinting alone, and 0% for rest or NSAIDs.⁸⁴ The strikingly favorable response to local injection therapy suggests that surgery to release the tendon sheaths is seldom needed. Interestingly, some evidence suggests that failure of steroid injections may be due to an anatomic variant in which the EPB is located in a separate synovial compartment.^84,85 This is supported by a study in which steroids selectively injected into the EPB tenosynovium resulted in the resolution of symptoms in all 50 patients.⁸⁶ Clinical suspicion for this anatomic variant should be raised when previous steroid injections have failed and patients have pain with firm resistance to thumb metacarpophalangeal joint extension (the EPB entrapment test).⁸⁵ Consider selective injection into the EPB tenosynovium in these patients.

Accurate injection of the corticosteroid has been found to be an important aspect of the patient’s response to treatment.⁸⁷ Using radiographic dye to verify correct corticosteroid placement, researchers have found that when the corticosteroid and anesthetic injection did not successfully reach either the EPB or the APL compartment, the patient did not experience relief of pain. Conversely, when the medication was injected accurately, most patients reported an improvement in symptoms. If available, ultrasound may help guide the injection. In 2002, Kamel and coworkers⁸⁸ used ultrasound to guide steroid injection in 21 patients with the clinical diagnosis of de Quervain’s disease. No complications were reported, and all patients had decreased edema and thickening of the tendons at 6 and 12 weeks. A similar study by Jeyapalan and Choudhary used ultrasound as an adjunct for injection in 17 patients in whom de Quervain’s disease was diagnosed clinically. One patient was identified as having solitary EPB involvement and 15 of the remaining 16 patients (1 patient was lost to follow-up) had significant relief at a mean of 6.75 weeks with no immediate or delayed complications reported.⁸⁹ Larger studies are needed to confirm the benefits of ultrasound.

Intersection syndrome is a condition that may easily be confused with de Quervain’s disease. Because the treatment approach and the clinical course of intersection syndrome differ from that of de Quervain’s tenovaginitis, it is important that the clinician also be familiar with this entity. First described in 1841 by Velpea, intersection syndrome describes a clinical entity approximately 4 to 8 cm proximal to the location of de Quervain’s disease (see Fig. 52-18).⁹⁰ Although the cause is not yet clear, intersection syndrome is thought to result from inflammation of the second dorsal compartment of the wrist, which houses the extensor carpi radialis longus (ECRL) and extensor carpi radialis brevis (ECRB) tendons.⁹¹ Other possible causes include inflammation of a bursa that develops between the APL and the ECRB tendons⁷¹ and inflammation of the ECRL and ECRB tenosynovium where they cross the muscle bellies of the APL and EPB.⁹²

Intersection syndrome is characterized by pain, tenderness, edema, and occasional crepitus 4 to 8 cm proximal to the radial styloid and may be mistaken for de Quervain’s disease. This condition is seen in athletes who play sports that require forceful repetitive wrist flexion and extension, such as rowing, weight lifting, gymnastics, and tennis.⁷¹ Treatment includes rest, NSAIDs, and immobilization with a thumb spica splint in 15 degrees of wrist extension. After a 2- to 3-week trial of splinting, corticosteroid injection therapy is recommended. In contrast, steroid injection is recommended early in the course of de Quervain’s disease. Some authors, in fact, recommend corticosteroid injection therapy on initial diagnosis of de Quervain’s disease.⁹³ Most patients with intersection syndrome, on the other hand, respond well to nonoperative treatment, and surgery is generally reserved for refractory cases.⁹²

Carpal Tunnel Syndrome.: Carpal tunnel syndrome is the most common nerve entrapment neuropathy of the wrist.⁹⁴ Caused by median nerve compression in the fibroosseous tunnel of the wrist, carpal tunnel syndrome is characterized by pain at the wrist that sometimes radiates proximally into the forearm and is associated with tingling and paresthesias of the medial aspect of the thumb, palmar side of the index and middle fingers, and radial half of the ring finger. Typically, the patient wakes during the night with burning or aching pain, numbness, and tingling. Occasionally, the discomfort is extremely severe and causes the patient to seek emergency care. Clinical signs that support this diagnosis include a positive Tinel sign, which is elicited by reproducing the tingling and paresthesias by tapping (with a reflex hammer) over the median nerve at the volar crease of the wrist (Fig. 52-21).⁹⁵ In addition, one can perform the Phalen test, described as holding the dorsal sides of the flexed wrists at a 90-degree angle against each other for several minutes to provoke symptoms in the median nerve distribution.⁹⁵ Phalen’s test is more sensitive than Tinel’s sign and is more specific for carpal tunnel syndrome.⁹⁴ Severe muscle atrophy of the thenar eminence may develop in advanced or neglected cases. In many cases the disturbance is idiopathic, without a recognizable underlying cause. However, people who participate in repetitive activities of the wrist, such as typing, driving, assembly line work, and racquet sports, are at risk for the development of carpal tunnel syndrome.⁵⁷ Other conditions associated with carpal tunnel syndrome include rheumatoid arthritis (sometimes as the initial manifestation), pregnancy, hypothyroidism, diabetes, and acromegaly.

Initial therapy for carpal tunnel syndrome consists of modification of activity and splinting; the latter is particularly helpful at night.⁵⁷ Of the medications sometimes used to treat carpal tunnel syndrome, diuretics, NSAIDs, and pyridoxine have been shown to offer little to no relief.⁹⁶ In contrast, the benefits, at least in the short term (e.g., 4 to 6 weeks), of local steroid injections for carpal tunnel syndrome have been well proven.⁹⁷ In a Cochrane review of randomized trials by Marshall and colleagues,⁹⁸ local steroid injection provided greater clinical improvement 1 month after injection than did placebo and up to 3 months after injection than did oral steroid treatment. However, symptoms after local corticosteroid injection were no different from the symptoms after either NSAIDs or splinting at 8 weeks. The benefits of initial steroid injection versus surgical intervention for carpal tunnel syndrome are controversial because there is little scientifically valid information on which to draw any conclusions. In one small study, Hui and associates⁹⁹ found that surgery resulted in a better symptomatic outcome (but not grip strength) than did local steroid injection over a 20-week period. It appears that local steroid injection for carpal tunnel syndrome offers improvement in symptoms, but this improvement may not be permanent or long term. Current recommendations include a trial of conservative treatment (including possible steroid injection) for patients who have mild to moderate symptoms and lack thenar wasting.¹⁰⁰ Surgery is indicated for patients with persistent symptoms after conservative treatment and for those with severe weakness of the thumb abductors.⁹⁴ Nerve compression should be confirmed by nerve conduction studies before surgery.⁹⁷

Digital Flexor Tenosynovitis (“Trigger Finger”).: A “trigger” or “snapping” finger is one of the most common problems of the hand and is characterized by a stenosed tendon sheath at the level of the first annular pulley (A1), which is located on the palmar surface over the base of the metacarpal head (Fig. 52-22).¹⁰³ In this condition the A1 pulley becomes inflamed, and a nodule develops on the tendon as it gets “pinched” under the constricted sheath.¹⁰³ Locking occurs when the involved digit is in flexion and is especially troublesome when the patient awakens in the morning. This can occur in any finger but is seen most frequently in the ring and middle fingers.

Besides thickening and stenosing of the tendon sheath, a trigger finger may also be characterized by flexor tendon synovitis. The tendon sheaths are long and tubular, and the walls are lined with a thin layer of synovial cells. Symptoms develop when the tendon becomes trapped and is unable to glide within the tendon sheath. A nodule or fibrinous deposit may form at a site in the tendon sheath, usually over or just distal to the metacarpal head of the trigger finger. When the digit is flexed, the nodule moves with the tendon proximally, and on extension it gets “stuck” on the pulley, thereby leading to intermittent catching of the tendon.¹⁰³ The nodule may be palpable on physical examination, but this is not necessary for diagnosis.⁵⁷ Carpal tunnel syndrome commonly coexists with a trigger finger and may be caused by tenosynovitis. Common causes of tenosynovitis include trauma, diabetes mellitus, and rheumatoid arthritis, although it may also be a primary and idiopathic disorder.⁹¹

Conservative treatment, including local rest or splinting, application of moist heat, and NSAID therapy, is the usual initial approach for symptomatic tenosynovitis. If these simple measures fail to control the symptoms, corticosteroid injection is indicated. One double-blind, placebo-controlled, randomized study of trigger finger demonstrated that steroid injections were significantly more effective than placebo.¹⁰⁴ At follow-up 3 weeks after treatment, 9 of the 14 patients receiving a combination of lidocaine and steroid injections were asymptomatic versus 2 of the 10 patients receiving lidocaine injections alone. A similar study showed complete resolution of symptoms in 52% of patients who received corticosteroid injections and improvement of symptoms in 47%.¹⁰³ Steroid injections are more successful when performed in patients with a palpable nodule or symptoms for less than 6 months.¹⁰⁵ Alternatively, some evidence suggests that the efficacy of steroid injections for trigger fingers diminishes with each subsequent injection at the same site.¹⁰⁶ As a guideline, if treatment fails after three injections (separated by several weeks or months), consider surgery as treatment of the condition.⁵⁷ In addition, patients with diabetes mellitus more often require surgical release for trigger finger than do non–insulin-dependent diabetics.¹⁰³ Division of the first annular pulley, digital nerve injury, scarring, and recurrence are well-known complications of surgical release.¹⁰⁶

Carpal/Metacarpal Inflammation.: Overuse and aging can lead to pain at the base of the thumb and fingers. This is especially common in elderly women and can be quite painful. The first metacarpal articulates with the trapezium, a common site for this condition. Injection therapy is usually quite successful (Fig. 52-23).

Trochanteric Bursitis.: Trochanteric bursitis is the second leading cause of lateral hip pain after osteoarthritis.¹⁰⁸ However, trochanteric bursitis can be confused with other conditions at or near the hip, such as sacrolumbar disease, hip or femur pathology, and metastases.^109–111 Patients with trochanteric bursitis, though, usually demonstrate discrete tenderness on deep palpation at or adjacent to the greater trochanter; relief of symptoms with a proper corticosteroid injection can help confirm the diagnosis.¹⁰⁹

The principal bursae associated with this condition are the subgluteus maximus bursa, the subgluteus minimus bursa, and the gluteus minimus bursa, although other bursae of the hip may be affected (Fig. 52-24). The pain may be acute but is more often subacute or chronic; frequently, patients have already tried NSAIDs without success and have been assigned a number of incorrect diagnoses. The chief locus of the pathologic condition is in the abductor mechanism of the hip. Pain occurs near the greater trochanter and may radiate down the lateral or posterolateral aspect of the thigh and, rarely, into the knee.¹¹² The pain is described as “deep,” “dull,” and “aching,” and it often interferes with sleep.

Lying on the affected hip, stepping from curbs, and descending steps provoke pain. Tenderness may be elicited over and adjacent to the greater trochanter. In contrast to true hip joint involvement, the Patrick FABERE sign (flexion, abduction, external rotation, and extension) may be negative, and complete passive range of motion is relatively painless. Active abduction when the patient lies on the opposite side typically intensifies the discomfort, and sharp external rotation may accentuate the symptoms. Internal rotation does not usually affect the level of pain.¹⁰⁹ Hip radiographs may demonstrate a calcific deposit adjacent to the trochanter; however, the incidence of this finding is low.¹¹⁰

Corticosteroid injection for trochanteric bursitis is often an effective therapy.¹¹⁰ In one study, 77% of patients reported improvement of their pain after an injection of betamethasone mixed with lidocaine.¹¹³ In addition, 61% of the patients reported improvement in their pain 26 weeks after receiving the injection. Failure of corticosteroid therapy should prompt the clinician to seek alternative diagnoses, such as true hip joint disease, which can easily be confused with trochanteric bursitis.¹¹⁴ In addition, though rare, there have been case reports of septic trochanteric bursitis caused by tuberculosis.¹¹⁵

Ischiogluteal Bursitis.: “Weaver’s bottom” is a painful disorder characterized by pain over the center of the buttocks with radiation down the back of the leg.¹¹⁰ This condition is rarely diagnosed initially and is often mistaken for lumbosacral strain, a herniated disk, or a spinal cord tumor. When it is recognized, a skillful intrabursal injection, coupled with a few days’ rest, usually relieves the extreme pain. The ischial or ischiogluteal bursa is adjacent to the ischial tuberosity and overlies the sciatic and posterior femoral cutaneous nerves. Sitting on hard surfaces, bending forward, and standing on tiptoes may all provoke the pain. Tenderness is present over the ischial tuberosity. At times, a soft tissue mass may also be felt in this area.¹¹⁶

Prepatellar Bursitis.: “Housemaid’s knee” or “nun’s knee” is characterized by swelling with effusion of the superficial bursa overlying the lower pole of the patella (Fig. 52-26). In contrast to intraarticular pathology, passive motion of the knee is fully preserved and the pain is generally mild, except during extreme knee flexion or direct pressure. Although the disorder is usually caused by pressure from repetitive kneeling on a firm surface (“rug cutter’s knee”), it can also develop after direct trauma, and occasionally it is a manifestation of rheumatoid arthritis or gout.¹¹⁷ Though uncommon, the prepatellar bursa is one of the most frequent sites of septic bursitis.⁴ Moreover, patients with septic prepatellar bursitis may not have the classic signs of infection such as erythema, warmth, or fever, and this makes it difficult to differentiate from aseptic bursitis.¹¹⁸ The bursal aspirate should therefore always be sent for laboratory analysis.⁴

Suprapatellar Bursitis.: Suprapatellar bursitis is usually associated with synovitis of the knees. On occasion the bursa is largely separated from the synovial cavity with only a very minor communication, and the swelling and effusion are chiefly confined to the suprapatellar area. This may be traumatic in origin or a manifestation of an inflammatory arthropathy.

Anserine Bursitis.: “Cavalryman’s disease” now mainly occurs in heavy women with disproportionately large thighs in association with osteoarthritis of the knee, although this entity is also seen in athletes involved in running, baseball, and racquet sports.¹¹⁰ The bursa is on the anteromedial side of the knee, inferior to the joint line at the site of insertion of the conjoined tendons of the sartorius, semitendinous, and gracilis muscles and superficial to the medial collateral ligament. The entity is characterized by a relatively abrupt onset of knee pain along with localized tenderness and a sense of fullness in the vicinity of the anserine bursa about 4 to 5 cm below the anteromedial aspect of the tibial plateau. Pain is exacerbated by flexion of the knee. Corticosteroid injection for anserine bursitis has been shown in clinical trials to be an effective treatment.¹¹⁹

Medial Collateral Ligament Bursa.: This bursa is located anterior to the tibia and posterior to the medial collateral ligament. Injury to this bursa often occurs when the patient undergoes a twisting motion with concurrent external rotation of the tibia. Tenderness may be appreciated along the anteroinferior aspect of the medial collateral ligament, and the pain is exacerbated with extension of the knee. This condition may sometimes be confused with a medial meniscus tear, and magnetic resonance imaging might be necessary to differentiate the two conditions. Treatment is usually successful with conservative measures, including relative rest, compression, and NSAIDs.¹¹⁰

Popliteal Cyst.: “Baker’s cysts” are herniated fluid-filled sacs of the articular synovial membrane that extend into the popliteal fossa, sometimes through the natural communication between the bursa in the posterior of the knee and the joint itself. These cysts may also be due to swelling of the medial gastrocnemius or semimembranosus bursae alone. Baker’s cysts can occur secondary to trauma, although they are also seen in patients with rheumatoid arthritis, gout, and osteoarthritis.¹¹⁰ Patients will often complain of popliteal fossa tenderness and swelling that may extend into the calf. Activities that involve active flexion of the knee, such as walking or jumping, exacerbate the symptoms.

The clinical manifestation of Baker’s cysts can mimic that of deep venous thrombosis (DVT), and it is important to take great care in differentiating the two. For this reason, symptomatic Baker’s cysts are also known as pseudothrombophlebitis syndrome.¹²⁰ In most studies, 2% to 6% of patients suspected of having DVT actually have a popliteal cyst as the cause of their knee or calf pain. Ultrasound is an important tool in this diagnosis.

Many cases of Baker’s cyst resolve spontaneously over a few weeks. However, treatment of Baker’s cysts may require surgery to correct any articular injury or to remove the cyst. Steroid injections are not usually performed because of the risk for neurovascular injury.

Ankle Tendinitis.: This is a relatively uncommon condition that may result from unusual repetitive activity or, rarely, from acute trauma. The disorder is differentiated from ankle joint involvement by the lack of pain or restricted motion during passive flexion and extension of the ankle. Active flexion and extension of the toes produce pain. Local tenderness is elicited along the involved tendons. Initial treatment consists of rest, NSAIDs, and immobilization, sometimes for several weeks. Some patients may eventually need operative intervention for prolonged symptoms.¹²¹ Local steroid injections have been used successfully in patients who do not respond to conservative measures; however, the risk for tendon rupture is well documented. As a result, tendon sheath injections should be reserved for patients with persistent symptoms despite an adequate trial of conservative therapy and should be done in consultation with a foot and ankle specialist.

Bunion Bursitis.: It is common for bunion bursitis to overlie the first metatarsophalangeal joint at its medial surface on the great toe. On occasion, tense swelling occurs, and decompression is required. Aspiration with culture of the fluid should be performed.

Heel Pain.: Talalgia may be caused by many different conditions, including Achilles tendinitis, retrocalcaneal bursitis, and plantar fasciitis (Fig. 52-29). Additional discussion may be found in Chapter 51. The bursae of clinical significance around the heel include the retro-Achilles bursa (located in the space between the skin and the Achilles tendon), the retrocalcaneal bursa (located between the Achilles tendon and the calcaneus), and the subcalcaneal bursa. Achilles tendinitis or bursitis may be traumatic in origin but is more apt to be part of a systemic disease, such as rheumatoid or gouty arthritis. Although a normal Achilles tendon is thick and strong, when affected by an inflammatory arthropathy, it is predisposed to degeneration, and because the Achilles tendon is not invested by a full synovial sheath, it is more vulnerable to intratendon instillation. Because of the potential hazard of tendon rupture after local steroid injection, it is wise to avoid infiltration of steroids into this area. In a double-blind, randomized, controlled trial it was shown that injection of methylprednisolone and bupivacaine (Marcaine) had no benefit over injecting bupivacaine alone.⁵ It is preferable to treat Achilles tendinitis with rest, splinting, and oral NSAIDs and to avoid injection therapy.

Retrocalcaneal bursitis is often seen in association with Haglund’s deformity, a bony ridge on the posterosuperior aspect of the calcaneus. The bursa lies anterior to the Achilles tendon and posterior to the calcaneus. Local swelling and tenderness at the posterior aspect of the heel, proximal (and sometimes lateral) to the insertion of the Achilles tendon, characterize this bursitis. Treatment is focused on minimizing pressure on the bony ridge, which includes the use of open-heeled shoes (clogs), bare feet, sandals, or a heel lift. Conservative measures such as ice, oral NSAIDs, and rest are other common treatment modalities. Corticosteroid injections are not recommended because of the risk for Achilles tendon rupture.122,123

The condition in this region that is most amenable to injection therapy is plantar fasciitis, which is also the most common cause of heel pain in adults.¹²⁴ The plantar fascia is located deep to the fat layer of the foot and extends from the calcaneus to the base of the digits. It is responsible for support of the medial longitudinal arch of the foot.¹²⁵ Signs of this condition include pain on the plantar medial aspect of the heel, which is often worse in the morning, after long periods of rest, and with passive dorsiflexion of the toes.¹²⁴ The pain may be relieved with activity. Although patients may have a heel spur, many symptomatic patients do not, and the presence of a heel spur should not be considered pathognomonic for the condition. Though still debated, the pathology is generally thought to originate from microtears in the fascia, often as a result of overuse.^122,123 Obesity may also increase the risk for plantar fasciitis because of the excessive load on the fascia.¹²⁴

Most cases of plantar fasciitis eventually resolve with nonsurgical management.¹²⁶ Treatment begins with elimination of any precipitating activity, relative rest, strength and stretching exercises, arch supports, and night splints. If these conservative measures are not effective, injection of the painful heel will usually provide short-term improvement. In a recent Cochrane review, steroid injections for plantar fasciitis resulted in significant improvement at 1 month but not at 3 or 6 months when compared with control groups.¹²⁷ In addition, there is a risk for rupture of the plantar fascia and fat pad atrophy with corticosteroid injections.¹²² One study reported a rupture rate of close to 10%.¹²⁸ Therefore, caution should be exercised when injecting steroids into a painful heel. In addition, because this condition tends to be chronic or recurring, referral to an appropriate specialist is recommended.

Torticollis.: Myofascial causes of torticollis usually involve the trapezius, sternocleidomastoid, and levator scapulae muscles, either alone or in a synergistic manner. The splenius and semispinalis muscles may also be involved. As mentioned earlier, carefully inject trigger points in the trapezius muscle to avoid puncture of a high-rising apical pleura.

Levator Scapulae Muscle Syndrome.: Painful sensitive foci may occur at the origin of the levator scapulae muscle on the superior medial aspect of the scapula, along the flat muscle belly, or at the insertion on the transverse processes of the first four cervical vertebrae (Fig. 52-30A). Pain is usually referred to the posterior cervical region, the posterior aspect of the scalp, and the periauricular area.

Splenius Capitis and Semispinalis Capitis Muscle Syndrome.: Pain resulting from trigger points in the splenius capitis and semispinalis capitis muscles may be located over the muscles themselves or be perceived in the head and face and give rise to headache syndromes (see Fig. 52-30B). Some patients may also experience dizziness. Trigger points in the splenius capitis and semispinalis capitis muscles may be difficult to pinpoint, so having the patient point to the area of maximal tenderness is extremely helpful.

Trapezius Muscle Syndrome.: The trapezius muscle is a frequent source of muscle pain and headache, especially at the angle of the neck or at the occipital insertions, where trigger points are most commonly located (see Fig. 52-30C). When injecting trigger points at the angle of the neck be careful to not puncture the apical pleura.

Sternocleidomastoid Muscle Syndrome.: The sternocleidomastoid muscle is also a frequent source of neck pain and headache. Trigger points are most often found at its sternal and clavicular origins and occipital insertion, as well as in the upper two thirds of the muscle belly (see Fig. 52-30C). Dizziness, ipsilateral ptosis, lacrimation, and conjunctival injection may accompany trigger points located in the sternocleidomastoid muscle.¹²⁹ Pain may involve the muscle itself or be referred to the periauricular, facial, or frontal areas.

Scapula Muscles.: When injecting trigger points in the lateral scapular and periscapular muscles, place the patient prone with a pillow under the chest to round the shoulders and facilitate injection. Note the anatomy and boundaries of the shoulder before injection, and warn the patient to not move the shoulder. Stabilize the scapula with the nondominant thumb and fingers to prevent movement of the lower portion of the scapula, which could result in inadvertent puncture of the pleura.

Myofascial pain is also commonly associated with a number of muscle beds at the medial border of the scapula, including the rhomboids, the serratus anterior, the subscapular muscles, and the levator scapulae. To inject trigger points in these medially situated muscles, have the patient place the ipsilateral hand behind the back. This will cause “winging of the scapula” and a safer approach. Direct the needle tangentially for easy access to the serratus anterior and subscapularis muscles. As with the lower portion of the scapula, care should be taken to inject the levator scapulae at an oblique angle that is nearly parallel to the thorax to help reduce the chance of accidentally inducing pneumothorax.

Infraspinatus Muscle Syndrome.: Because of its multiple functions, this muscle is subject to earlier degeneration than other muscles of the rotator cuff and is more susceptible to trigger points (see Fig. 52-30D). Trigger points in the infraspinatus muscle invariably cause sympathetic hyperactivity and often contribute to dystrophy-like syndromes of the upper extremity. To identify trigger points in the infraspinatus muscle, it is important to palpate along the entire length of the muscle bundles, as well as across the “grain” of the muscle (see Fig. 52-4).

Rectus Abdominis Muscle Syndrome.: These muscles are frequent sites of anterior abdominal wall pain. They often flare up after abdominal surgery and may be a major cause of postoperative pain in some patients. Abdominal wall trigger points are most commonly found in the upper three segments of the rectus muscle and can more easily be located by placing the patient in a supine position with the head and neck flexed so that the rectus muscles are under tension (see Fig. 52-30E). Pain and tenderness are usually localized directly over the trigger point. Trigger points in the lower rectus segments may be a cause of low back pain. Lower segment trigger points may be associated with trigger points in the corresponding posterior lumbar spinal segments (i.e., L4, L5, S1).

Pectoralis Major/Pectoralis Minor Muscle Syndrome.: The pectoralis major muscle is a frequent site of myofascial pain, particularly at its insertion on the anterior medial portion of the shoulder (see Fig. 52-30E). The inferior belly of the muscle is also a common area for trigger points, so be sure to carefully search the entire muscle to avoid missing a treatable area. Pain is usually located at the trigger point, but patients with trigger points in the clavicular portion of the muscle may have referred pain in the uppermost part of the muscle, whereas others may experience referred pain in the arm.

Intercostal Muscle Syndrome.: In patients with musculoskeletal chest pain, palpate the intercostal muscles for areas of tenderness. Pain emanating from the exterior intercostal muscles is usually localized near the site of the trigger point and is emphasized during inspiration (see Fig. 52-30F). Intercostal muscle trigger points often flare after chest surgery or trauma. Exercise extreme care when injecting an intercostal muscle trigger point to avoid entry into the pleural space.

Tensor Fasciae Latae Muscle Syndrome.: Because the tensor fasciae latae muscle is easy to examine, trigger points located here are easy to identify (see Fig. 52-30G). Patients usually complain of pain along the lateral aspect of the thigh as far down as the knee.

Anterior Tibialis Muscle Syndrome.: Trigger points located in the anterior tibialis muscle usually cause pain along the anterior aspect of the ankle, but the entire ankle may be involved in severe cases. Trigger points are most commonly found in the upper third of the muscle and typically cause pain in the anterior portion of the leg and dorsal portion of the ankle (see Fig. 52-30H).

Gastrocnemius/Soleus Muscle Syndrome.: Myofascial pain related to trigger points in the gastrocnemius and soleus muscles is usually located behind the knee and along the Achilles tendon near the heel (see Fig. 52-30I). These trigger points are generally found along the lateral and medial margins of the muscle group or along the midline (or in both areas) and often flare in patients experiencing vascular insufficiency of the lower extremities. One author suggests locating and injecting these trigger points for relief of the pain associated with intermittent claudication.¹³⁵

Quadratus Lumborum Muscle Syndrome.: The quadratus lumborum is considered a hip hiker and lateral flexor of the spine. It also assists respiratory function by anchoring the 12th rib for the pull of the diaphragm. Trigger points may be found along the 12th rib, around the iliac crest, and along the lateral border of the muscle (see Fig. 52-30J) and are often associated with distress on deep inspiration and 12th rib pain. Pain can be local or referred to the anterior abdominal wall. In addition, these trigger points may accentuate postoperative pain or painful abdominal scars over the lower quadrant.

Gluteus Medius Muscle Syndrome.: Trigger points located in the gluteus medius may be the most critical trigger points in the lower extremities (see Fig. 52-30J). They are most commonly found along the iliac shelf and, with extensive involvement, along the entire gluteal ridge, including the gluteus minimus and the gluteus maximus muscles from the sacroiliac joint to the anterior superior iliac spine. It is estimated the 10% of people have legs that differ in length by at least 1 cm. This discrepancy in length may cause unilateral back pain and trigger points of the gluteus, erector spinae, and quadratus lumborum muscles.

Similar to the infraspinatus muscle syndrome, trigger points in the gluteus medius muscle are frequently associated with sympathetic hyperactivity. In addition, when these trigger points flare, they often recruit trigger points in the quadratus lumborum, tensor fasciae latae, and other gluteal muscles, where they induce diffuse lower back pain, or in the cervical muscles and cause neck pain and headaches. Though less common, isolated gluteus medius pain may also occur and usually projects along the iliac crest into the posterior of the hip, thigh, and calf.