Chapter 52 Bursae are potential spaces or sacs, subcutaneous and deep, that develop in relation to friction and facilitate the gliding motion of tendons and muscles. There are approximately 78 bursae on each side of the body as described by Monro and Spalteholz.1,2 Tendon sheaths are similar in composition to bursae but differ in overall shape. Tendon sheaths are long and tubular, whereas bursae are usually round and flat. Inflammation of bursae, as in bursitis, can be seen microscopically as a thickening of the normal thin surface of synovial cells lining the bursal wall.3 Tendinitis and tenosynovitis are used to describe similar inflammatory reactions in tendons and tendon sheaths, respectively. Because of the adjacent location of bursae and tendons, an inflammatory process in one may also involve the other.4 Common sites of tendinitis and bursitis in the body are depicted in Figure 52-1. Figure 52-1 Common sites of tendinitis and bursitis. Corticosteroid injection therapy for tendonitis and bursitis is universally accepted and practiced, and the initial relief may be dramatic. However, the actual long-term benefit over other modalities, such as physical therapy, nonsteroidal antiinflammatory drugs, time, and even oral corticosteroids, is somewhat debatable. If the practitioner is reluctant to inject steroids, a course of oral prednisone or methylprednisolone may give similar short-term benefit. In most cases it is prudent to limit the number of injections at a single site to two or three. See Table 52-1. Do not inject areas of Achilles tendinitis or patellar tendinitis since rupture of the weight-bearing tendons can occur. (Redrawn from Walker LG, Meals RM. Tendinitis: a practical approach to diagnosis and management. J Musculoskelet Med. 1989;6:24.) In addition, some forms of tendinitis may be caused by factors other than overuse, inflammation, trauma, and degenerative disease. Gonococcemia, for example, is one cause of tenosynovitis that should be considered in the appropriate setting.5 Another rare cause is hemodialysis.6 In 2008 the Food and Drug Administration added a black box warning to fluoroquinolone antibiotics highlighting the potential for tendinopathy and tendon rupture (Box 52-1). Clinicians should avoid tendon sheath injections in patients who are taking this class of drugs.7 Trigger points are hyperirritable areas, usually within a taut band of skeletal muscle or in the muscle fascia, that are painful on compression and associated with a characteristic pattern of referred pain, motor dysfunction, and autonomic phenomena (Box 52-2).8 Trigger points can also be identified by the local twitch response, a brisk contraction of muscle fibers elicited by snapping palpation or rapid insertion of a needle into the trigger point itself.9 Trigger points probably develop in response to muscle fiber injury. The injury may be an acute traumatic event or more subtle repetitive microtrauma. The underlying pathophysiology has not been fully elucidated but probably involves chronic muscle stress, excessive release of acetylcholine, and dysfunctional motor end plates.10 Trigger points can occur in any muscle or muscle group; they are generally unilateral, but bilateral trigger points have been reported. Since the stress associated with myofascial pain commonly affects both single muscles and whole muscle groups, trigger points tend to cluster. In the upper part of the trunk, a common trigger point cluster involves the muscles of the neck and shoulder area, including the trapezius, levator scapulae, and infraspinatus muscles (Fig. 52-2). In the lower part of the trunk, the quadratus lumborum, gluteus medius, and tensor fasciae latae are commonly affected. Trigger points often affect other muscles innervated by the same spinal segments, and subsequent treatment is usually directed at all muscles innervated by both the anterior and posterior branch of the same spinal nerve. Table 52-1 lists common trigger points and their associated myofascial pain syndromes. Management of the pain resulting from bursitis and tendinitis may be greatly enhanced by the proper selection and administration of local injections. Successful application of local injection and intrasynovial (bursa and tendon sheath) therapy requires an understanding of the diagnosis, accurate localization of the pathologic condition, and appropriate injection techniques. Lidocaine and corticosteroid preparations may be injected separately or together as adjuncts for pain control. The goal of corticosteroid injection therapy is relief of pain so that the patient is able to regain function and participate in a physical rehabilitation program.5 In many cases a single injection may be all that is required to ameliorate a painful condition. However, injection therapy is best viewed as an adjunct in the management of painful tendinitis and bursitis syndromes. It should not be viewed as a single quick fix, but a method to facilitate other modalities. The precise mechanisms for the lasting analgesia and beneficial therapeutic effects of local injection therapy have not been clarified. Few clinical trials have adequately measured the efficacy of corticosteroid therapy. Although steroids are known to reduce inflammation, it is unclear whether the antiinflammatory effect is responsible for the increased range of motion and relief of pain that the patient usually experiences. Histologic studies of chronic tenosynovitis lesions demonstrate degeneration, but not inflammation.5 It is therefore possible that the pain experienced with tendinitis and bursitis occurs as a result of mechanisms other than inflammation, such as mechanoreceptor stimulation by shearing, traction, or activation of nociceptive receptors by substance P and chondroitin sulfate.5 Though often performed in the emergency department (ED) and ubiquitous therapy by orthopedic surgeons, rheumatologists, and family practitioners, injection therapy may not be definitive care. Hence, follow-up and additional evaluations and interventions should be considered. In short, injection therapy should be considered an adjunct to a variety of treatment modalities, including pain control, physical therapy, occupational therapy, relative rest, immobilization, and exercise. Additional pain control can be achieved with such options as nonsteroidal antiinflammatory drugs (NSAIDs), acupuncture, ultrasound, ice, heat, and electrical nerve stimulation.5,11,12 Besides pain relief, early participation in rehabilitative activities and exercises can be an important aspect of patient recovery. Patients receiving only analgesics may have worse outcomes than those who also incorporate exercise as part of their treatment.4 Any factors that provoke the initial injury should also be identified because failure to eliminate these provoking factors can contribute to the injury developing into a chronic condition.5 Although opinions in the literature differ, we recommend that corticosteroid injections not be repeated in the same site unless at least a partial clinical response has occurred. In addition, an injection should not be repeated in the same site more than once every 3 months.5,11–14 Some limit corticosteroid injections at any given site to two or three injections before alternative therapy is pursued. Despite few data on the outcome of repeated injections, these recommendations are generally accepted and may limit the risk for adverse effects. Though universally practiced and generally considered safe and effective for short-term therapy, there are sparse scientific data defining a true benefit of corticosteroid injections for musculotendinous conditions. Inflammation is not always the cause of tendinopathy. Although true inflammatory tendonitis may respond quite well to corticosteroid injections, conditions such as posttraumatic shoulder impingement and rotator cuff tears may not be expected to benefit more from local injection than from treatment consisting of rest, time, physical therapy, and NSAIDs.13,14 Despite appearing to initially be effective for conditions such as olecranon bursitis, lateral epicondylitis, and de Quervain’s tenosynovitis, long-term relief of other conditions is often superior with other modalities. In addition, oral corticosteroids can be as effective as local injection and can be an alternative for emergency clinicians reluctant to perform an injection. Injection therapy is the most widely accepted and scientifically supported modality for treating trigger point pain.15 However, because it may place patients at risk for becoming dependent on injection for pain relief, some authors reserve injection therapy for patients who have failed other measures (Box 52-3).16 Various substances have been used for trigger point injections, including local anesthetics, botulinum toxin, sterile water, and sterile saline.16 Dry needling, a technique that involves multiple advances of a needle into the muscle at the region of the trigger point, provides as much pain relief as an injection of lidocaine.17 In fact, in a recent systematic review on needling therapies for trigger points, Cummings and White18 concluded that based on current medical evidence, “the nature of the injected substance makes no difference to the outcome and wet needling is not therapeutically superior to dry needling.” In support of these findings, it has been proposed that the needle (not the injected substance) reduces trigger point pain by mechanically disrupting dysfunctional activity at the motor end plate.16 Nevertheless, the addition of a local anesthetic is recommended to reduce the degree of postinjection soreness.17 The use of steroids for trigger point injection is controversial and without a clear rationale because there is little evidence to support an inflammatory pathophysiology for trigger point pain.16 Hence, the use of steroids for trigger point injection is not recommended. The indications for steroid injection are twofold: therapy and diagnosis. Injection therapy offers not only relief of pain, particularly when a local anesthetic is used concurrently, but also a medium to deliver therapeutic agents. In addition to relieving pain, injection therapy may aid in diagnosis. When injecting a bursa, for example, bursal fluid is sometimes collected for laboratory analysis. Finally, the relief of pain helps differentiate a localized site of injury from referred or visceral pain.12 Absolute contraindications to local injection therapy are limited and include specific infections such as bacteremia, infectious arthritis, periarticular cellulitis or ulceration, and adjacent osteomyelitis (Box 52-4). The procedure is also contraindicated in patients with bleeding disorders. A history of hypersensitivity, either to the corticosteroid or to the vehicle by which it is delivered, is an absolute contraindication. Finally, corticosteroid injections should not be performed in a patient who has a documented osteochondral fracture. Relative contraindications depend on both the clinician’s experience and the indication for the injection. Violation of the integrity of the skin or chronic foci of infection, either locally or in the vicinity of the site of involvement, is a relative contraindication. The procedure is also relatively contraindicated in patients taking anticoagulants, in patients with poorly controlled diabetes, and in those with internal joint derangements or hemarthroses. Patients with a preexisting tendon injury may be subject to tendon rupture if the corticosteroid injection relieves the pain and full activity is then resumed. Hence, partial tendon rupture is a relative contraindication. Consider trigger point injection once a myofascial pain syndrome has been identified (see Box 52-2 and Table 52-1). As mentioned previously, some authors reserve injection for patients who fail noninvasive modalities (Box 52-3). There are few contraindications to trigger point injection. Overlying infection is an absolute contraindication. Relative contraindications include proximity to sensitive structures, bleeding disorders, anticoagulation, an uncooperative patient, and lack of clinician experience. Dry needling is as effective as injection therapy, so in those with allergy to local anesthetics, the clinician may perform dry needling to avoid the problem. Local anesthetics should be mixed with a corticosteroid preparation to increase volume, decrease postinjection pain, and assess the accuracy of bursae and tendon sheath injections. Use of corticosteroids alone can be very painful. Local anesthetics may also be used alone, before injecting the corticosteroid. The major hazards with injection of local anesthetics are hypersensitivity and accidental intravenous or intraarterial injection (see Chapter 29). Serious or fatal hypersensitivity to procaine and other regional anesthetic compounds is encountered very rarely. This possibility is usually suggested by a previous history of reactions to these compounds. Ester solutions (e.g., procaine, tetracaine) that produce the metabolite paraaminobenzoic acid (PABA) account for the majority of these reactions. Amide solutions (e.g., lidocaine, bupivacaine) are rarely involved, and usually the preservative methylparaben, which is structurally similar to PABA, is responsible. When a definite history of sensitivity is present, use of any agent from that class of anesthetic agents is absolutely contraindicated. Although there is evidence of allergic reactions from corticosteroids given orally and parentally, the possibility of an allergic reaction caused by corticosteroid injection is highly unlikely, and such cases occur infrequently.19 Nevertheless, the clinician should be aware that anaphylaxis after injection of methylprednisolone acetate has been reported.20 In addition, an unusual rash after an intraarticular methylprednisolone injection, which appears to be consistent with a delayed type of hypersensitivity, has also been documented.21 Corticosteroid injections have been found to be safe procedures with few complications (Box 52-5).22 Although the possibility of introducing infection is one of the most serious potential complications, infections occurring as an aftermath of intrasynovial injections are extremely rare. In a study at the Mayo Clinic involving 3000 injections given in 1 year, no infections were reported.21 Others have found the risk for infection to be 4.6 per 100,000 intraarticular injections.23 Local undesirable reactions are usually minor and reversible. After steroid injection, about 2% of patients may experience an acute synovitis otherwise known as “postinjection” flare.10,16 This may be slightly more common with methylprednisolone acetate (Depo-Medrol) and less common with triamcinolone acetonide (Kenalog). Characterized by an increase in pain and joint swelling, symptoms usually begin a few hours after steroid injection and can last as long as 3 days. Histologically, steroid crystals have been seen within polymorphonuclear leukocytes, which makes it a true synovitis.13,19 This reaction may be difficult to differentiate from an infection, and infection must be ruled out if the symptoms last longer than 48 hours or are associated with fever, warmth, or other suspicious signs of infection. Postinjection flare appears to be more likely to develop with the more soluble (shorter-acting) steroid solutions and may be related to the carrier in which the steroid is manufactured.13,21 Limiting activity of the involved area for 2 days after the injection might help reduce the incidence.19 When it does occur, the reaction is usually mild and can be controlled adequately with the application of ice or cold compresses and analgesics as needed. Another relatively minor complication is localized subcutaneous or cutaneous atrophy at the site of the injection.13 This problem is chiefly of cosmetic concern and is recognized as a small depression in the skin frequently associated with depigmentation, transparency, and the occasional formation of telangiectases. These changes in the skin occur when injections are made near the surface and some of the injected steroid leaks back along the needle track. The skin depression usually recedes and the skin returns to normal when the crystals of the steroid have been completely absorbed. These changes are usually evident 6 weeks to 3 months after the initial injection and generally resolve within 6 months, although they can be permanent.11,13 In the two-syringe technique, the anesthetic is injected first, the needle is advanced into the bursa/peritendon area, and the syringe is then exchanged for another to inject steroid. This technique helps prevent injection site atrophy by avoiding any leakage of the steroid suspension to the skin’s surface.24 Use a small amount of lidocaine or normal saline to flush the suspension from the needle before removing it. The Z-tract technique is a method of creating an indirect route from the skin puncture to the ultimate site of the steroid injection.24 To perform this technique, insert the needle 0.5 to 1.0 cm from the actual target site. When the needle is halfway through the fat tissue, redirect it to the target site and inject both the anesthetic and the corticosteroid. Injection site atrophy is more likely to occur with preparations that are less soluble and thus longer acting.11 One of the most serious complications after local steroid injection is tendon rupture. In general, the risk is very low (<1%) and appears to be related to the dose used.11,13 Some believe that injecting steroids directly into the tendon leads to a decrease in the tendon’s tensile strength.13,19,25,26 Gray and Gottlieb,13 however, noted no cases of tendon rupture after more than 300 tendon sheath injections. We still advise that one be diligent and careful about injecting into the surrounding area of the tendon sheath and not into the tendon substance. Moreover, by using one size of needle and syringe, the operator is more likely to appreciate the increase in resistance when injecting directly into the tendon. We also suggest limiting the frequency of injections to no more than once every 3 months in the same site.5,11–13 Tendon rupture is more likely to occur in major stress-bearing tendons in athletes, such as the Achilles tendon and the patellar tendons. For this reason, injection of corticosteroids in these areas should be avoided in the ED.20 There have been reports of accidental nerve injury after corticosteroid injection, particularly of the ulnar nerve (for treating medial epicondylitis) and the median nerve (for treating carpal tunnel syndrome).27 In addition, pericapsular calcifications develop in up to 42% of patients undergoing local steroid therapy, although they are generally asymptomatic.13,24 Finally, within minutes to hours of injection, approximately 1% of patients may experience facial and neck flushing. This reaction may last a few days, but it is usually a benign and self-limited reaction. Facial flushing seems to be more common with triamcinolone preparations.11,13,19 Systemic absorption of local corticosteroid injections does occur, though at a slower rate than with oral steroids.12 As a result, patients are at low risk for systemic complications, but they do occur. Specifically, intrasynovial injections of steroids have been shown to suppress the hypothalamic-pituitary-adrenal axis for 2 to 7 days.11 This complication is more likely to occur in patients who receive repeated injections in a short period or multiple injections in different sites at one time.19 Corticosteroids can also exacerbate hyperglycemia in diabetics.12,24 Abnormal uterine bleeding has been reported as well.11,12,20 Other potential complications of corticosteroid and local anesthetic injections are outlined in Box 52-5. Commonly used corticosteroid repository preparations for the injection of bursae and tendon sheaths are described in Table 52-2. Local anesthetics such as lidocaine or bupivacaine can be mixed with the corticosteroid preparation in the same syringe. All corticosteroid suspensions, with the exception of cortisone and prednisone, can produce a significant and rapid antiinflammatory effect (in the synovial spaces). Corticosteroids should not be used for trigger point injections. Corticosteroid preparations are categorized by their solubility and relative potency. Solutions that are more soluble have a shorter duration of action, primarily because they are absorbed and dispersed more rapidly. The addition of tertiary butyl acetate to the solution causes decreased solubility and therefore a longer duration of action. For example, triamcinolone hexacetonide, the least soluble preparation, has the longest duration of action.13 Because the long duration of action increases its potential for subcutaneous atrophy, some authors use this preparation only for intraarticular injections.12,13 There is little consensus in the literature regarding which corticosteroid to use and what dosage is most appropriate for a given site.5,21,24 Centeno and Moore28 noted that the choice of injection agent is most dependent on the institution where the clinician trained. In 1995 a survey of 172 rheumatologists found that opinions differ regarding almost every facet of soft tissue and intraarticular injection, including patient preparation, choice of corticosteroid, and postinjection advice.29 Some clinicians advocate mixing both shorter- and longer-acting corticosteroids in the same syringe with little consideration for the location or type of condition.12,13 We do not recommend using longer-acting corticosteroids for soft tissue injections, particularly because of the increased risk for associated atrophy,5,12 including atrophy of surrounding structures such as ligaments and fascia.30 In general, use a short- or intermediate-acting agent for an acute or subacute condition such as bursitis or tendinitis; reserve longer-acting agents such as triamcinolone for chronic and prolonged conditions, including arthritis.11,13 Triamcinolone acetonide and methylprednisolone acetate are reasonable first choices for most ED procedures. The dose of any corticosteroid suspension used for intrasynovial injection may be selected arbitrarily. Factors that influence the dosage and expected response include the size of the affected area, the presence or absence of synovial fluid or edema, the severity and extent of any synovitis, and the steroid preparation selected (Table 52-3). Dosages may also need to be reduced in the elderly.31 Unlike intraarticular injections for synovitis in patients with chronic joint disease, repeated infiltration for soft tissue conditions such as bursitis and tendinitis is not generally recommended or required. However, if only a partial response occurs or if recurrence develops, a single injection can be repeated as long as one waits at least 12 weeks between injections.5,11–13,20 Preparation of the site before injection requires meticulous adherence to aseptic technique. Anatomic landmarks may be outlined with a skin pencil. It is important that the injection site and needle tip remain sterile with use of the “no-touch” technique, although sterile drapes are not generally considered necessary.5,22 For operator protection, universal precautions should be followed.12 The material required for local injection procedures includes antiseptic solution, needles, syringes, a hemostat, culture and laboratory tubes, bandages, and sterile gauze (Fig. 52-3). Special trays may be stocked for this purpose. The usual sizes of needles for injection sites and corticosteroid doses are listed in Table 52-3. Figure 52-3 Equipment required for injection therapy. Needle sizes and corticosteroid doses are listed in Table 52-3. For those reluctant to inject areas of tendonitis or bursitis, a short course of oral steroids, combined with rest, physical therapy, ice, and nonsteroidal antiinflammatory drugs, is appropriate. Local skin anesthesia is an option before injection but not universally practiced. For bursae and tendon sheaths, local anesthetics can be injected alone or with corticosteroids mixed together in the same syringe. Use the Z-tract technique to limit the risk for a fistulous tract in the soft tissue. Because the steroid may theoretically precipitate or layer in the barrel of the syringe during the injection, agitate the syringe immediately before using it to optimize its distribution. In addition to minimizing the pain associated with the injection, mixing an anesthetic with the corticosteroid also produces a larger volume for delivery.5 Successful treatment of a myofascial pain syndrome requires accurate diagnosis (see Box 52-2 and Table 52-1) and precise identification of the trigger point (a taut band of muscle fibers). There are three generally accepted methods for identification of trigger points: flat palpation, pincer palpation, and deep palpation.15 To perform flat palpation, slide a fingertip across the muscle fibers of the affected muscle group while using the opposite hand to retract the skin to either side until the taut band is identified (Fig. 52-4, left). Snap the band like a violin string to precisely identify the trigger point. Pincer palpation involves firmly grasping and rolling the muscle fibers between the thumb and forefinger until the taught band is found (Fig. 52-4, right). Use deep palpation when the taut band is obscured by superficial tissue. Place a fingertip over the muscle attachment of the area suspected of housing the trigger point and apply pressure in different directions. Reproduction of the patient’s symptoms identifies the trigger point. It may be helpful to mark the trigger point with a skin marker for easy identification before treatment. Once the trigger point has been found, therapy can be divided into invasive and noninvasive techniques (see Box 52-3). Noninvasive techniques used in the ED include spray and stretch, massage therapy, and ischemic compression therapy.15 Physical therapy, transcutaneous electrical stimulation, and ultrasound treatments are adjuncts that may be arranged by the patient’s primary care physician. Invasive techniques involve injecting the trigger point with local anesthetic or botulinum toxin or dry needling. Spray and Stretch: This technique of spray and stretch was once advocated by some as the single most effective treatment of trigger point pain.8 Place the patient in a comfortable position and ensure that the target muscle is well supported and under minimal tension and that one end of the trigger point is securely anchored. Anesthetize the skin overlying the trigger point with vapocoolant spray (ethyl chloride, dichlorodifluoromethane, or trichloromonofluoromethane) over the entire length of the muscle. Apply the spray at a 30-degree angle to the skin. After the first pass of spray, apply immediate pressure on the other end of the muscle to create a passive stretch. Perform multiple slow spray passes over the entire width of the muscle while maintaining passive stretch until the muscle achieves a full range of motion. Do not perform more than three repetitions before rewarming the area with moist warm heat, and do not allow each spray to last more than 6 seconds. Educate patients to not overstretch muscles after each therapy session. Massage Therapy: This technique, as described by Simons and colleagues, uses “deep stroking” or “stripping” massage to allow the affected muscle group to be lengthened and relaxed as much as possible.32 Ischemic Compression Therapy: The principle behind ischemic compression therapy is to use pressure to induce ischemia for ablation of the trigger point. To perform this technique, apply and maintain pressure on the trigger point with increasing resistance until tension in the muscle is relieved. The patient might perceive mild discomfort but not profound pain. Repeat the process for each trigger point encountered. Injection Therapy: Almost any trigger point is suitable for injection therapy. Those that fail to respond to noninvasive treatments should be strongly considered for injection. Historically, various substances have been used, including local anesthetics, botulinum toxin, sterile water, and sterile saline. Despite the different compositions, durations of action, and mechanisms of action of these substances, a common finding is that the duration of pain relief following the procedure outlasts the duration of action of the injected substance.15 As noted earlier, the authors of a recent systematic review concluded that based on current medical evidence, the nature of the injected substance makes no difference on the outcome and that wet needling is not therapeutically superior to dry needling.18 Nevertheless, the addition of a local anesthetic has been shown to reduce the degree of postinjection soreness and is recommended by most authors.17 The technique most often recommended for trigger point injection has been referred to as the universal technique. Position the patient in a recumbent position to assist in relaxation of the affected muscles, overall comfort, and prevention of syncope. Reidentify the previously marked trigger point of interest, and scrub the overlying skin with a topical antiseptic solution. For superficial trigger points, use a 22-gauge, 1.5-inch needle. Deeper muscles may require a 21-gauge, 2- or 2.5-inch needle (see Table 52-3). Grasp the skin overlying the trigger point between the thumb and index or middle finger of the nondominant hand. Insert the needle approximately 1 to 1.5 cm from the point and advance it into the trigger point at a 30-degree angle. Aspirate to confirm that a blood vessel has not been entered, and inject a small amount of the agent. Withdraw the needle to the skin, redirect it to another area of the trigger point, and inject again. Use a “fast-in, fast-out approach” to elicit a local twitch response, which has been shown to increase the effectiveness of the trigger point injection and allows the entire trigger point area to be treated.33,34 Severe cramping or paresthesias suggest inadvertent nerve entry and mandates withdrawal and redirection of the needle. For best results, it is critical to elicit a local twitch response with every injection. Following the procedure, the muscle group that was injected should undergo a full active stretch.15 Shoulder Region: Pain associated with disability may result from any of the intrinsic shoulder disorders, including bicipital tendinitis, calcareous tendinitis, and subacromial bursitis (Fig. 52-5). Because injection is easy and safe to perform, these areas are frequently injected, especially in patients who have failed more conservative therapy such as ice, rest, and oral antiinflammatory medications. Injections may also offer a diagnostic advantage when evaluating a patient with subacromial pain or a rotator cuff syndrome in differentiating shoulder weakness caused by impingement (shoulder strength improves after injection) and a true rotator cuff tear (no change in strength following injection). A potential long-term complication of untreated persistent inflammation is the development of a “frozen shoulder” (adhesive capsulitis).35 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. Approach.: Locate the point of maximal tenderness along the bicipital tendon. Make entry with a 22- or 25-gauge, 3.9- to 5.0-cm needle through an optional lidocaine skin wheal. Avoid an intratendinous injection, which may cause weakening of the tendon and predispose the patient to tendon rupture. Advance the needle along the side of the tendon at a 30-degree angle and aim at one border of the bicipital groove to perform a peritendinous infiltration. Administer one third of the injection at this point. Withdraw the needle slightly but keep it subcutaneous and redirect it upward approximately 2.5 cm for injection of another third of the drug. Withdraw it again and redirect it downward so that it touches the bicipital border gently. Deposit the remainder of the drug at this point. With any of these injections, resistance to injection suggests intratendinous needle placement, which should be avoided.37 If the two-syringe technique is used, instill 1 to 1.5 mL of an intermediate-acting corticosteroid suspension, such as prednisolone tebutate, at the point of maximum tenderness. Inject the anesthetic (2 to 4 mL of 1% lidocaine or 0.25% bupivacaine) along the upper and lower borders of the tendon. 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.
Treatment of Bursitis, Tendinitis, and Trigger Points
General Anatomic Considerations
Trigger Points
Rationale for Injection Therapy
Trigger Points
Indications and Contraindications
Trigger Points
Hazards and Complications
Corticosteroid Preparations
Dosage and Administration
Preparation of the Site
Techniques
Bursae and Tendon Sheaths
Trigger Points
Noninvasive Techniques
Invasive Techniques
Specific Regions and Clinical Entities
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