Bursae Injections

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11 Bursae Injections

Bursitis is commonly diagnosed and treated in clinical practices that focus on musculoskeletal medicine. Inflamed bursae often respond to conservative treatments including rest, cryotherapy, compression, physical/occupational therapy and nonsteroidal antiinflammatory drugs (NSAIDs).1a In patients who fail to respond to conservative rehabilitation, a corticosteroid injection into the bursa can serve as a useful diagnostic and therapeutic adjunct to a comprehensive course of rehabilitation.

Bursae are purse-like sacs containing fluid and function to reduce friction at a joint. They are positioned between two muscles or between a muscle and its tendon or bone. Inflammation may occur during repetitive activities involving poor body mechanics or following direct trauma. An accurate diagnosis includes a thorough history, and an investigation of the occupational and recreational factors predisposing a patient to repetitive overload or joint stress. Correction of improper biomechanics is essential to reduce joint tension early in the course of treatment to avoid chronic bursitis.

Physical examination will reveal focal tenderness, swelling, and pain during direct palpation. If the injury is due to acute trauma, a fracture or ligamentous instability of the joint should be considered. In cases of chronic bursitis, calcifications may be identified on plain radiographs. However, the most common etiology combines repetitive motion with improper biomechanics. The physical examination should include a survey of peripheral joints to rule out a systemic process such as an underlying rheumatic disease. Skin overlying the area of tenderness should be examined for evidence of warmth, redness, swelling, or penetrating trauma. Rarely an infected bursa is diagnosed, and skin warmth appreciated on palpation may be the most sensitive physical indicator.1 The treatment of bursitis requires that an infection be considered prior to initiating treatment protocols. Aspiration of a septic bursa and identification of a bacterial pathogen are necessary to initiate appropriate antibiotic treatment. Laboratory studies of the serum should include an erythrocyte sedimentation rate, complete blood cell count, and microscopic examination to screen for leukocytosis, bacteria on Gram stain, or crystals. Operative incision and drainage of a septic bursa may be required for effective treatment.2,3 Contraindications to bursal injection with corticosteroids include cellulitis, generalized infection, and coagulation disorders.

Bursal injections serve a diagnostic and a therapeutic role. An initial bursal injection with local anesthetic alone can provide important information that will confirm the diagnosis. Bursitis from a noninfectious etiology may be considered for an injection of corticosteroid and anesthetic reducing bursal pain and inflammation, thereby allowing the patient to engage in a comprehensive rehabilitation program. Following the injection, the patient should be given instructions to ice and observe relative rest prior to resumption of a therapeutic exercise program. The clinician should direct the patient in a home exercise program and a physical therapist may be consulted for soft tissue mobilization and instruction in a stretching and strengthening program. Ice may be a useful adjunct during the initial phases of treatment, and NSAIDs may provide additional relief. Each of these options should be individualized for the clinical situation, and none of these, especially bursal injections, is to be used as the primary form of therapy. Re-examination should be scheduled within the first few weeks, and the rehabilitative program should be tailored to the patient as symptoms subside.

This chapter describes the basic approach to injection of many of the bursae encountered in clinical practice. Although the rehabilitation program for each bursa has not been detailed to allow for closer attention to procedural techniques, it is essential to employ a comprehensive rehabilitation to maximize the success of injections.

Subacromial (Subdeltoid) Bursitis

The subacromial bursa rests on the supraspinatus and is covered by the acromion, the coracoacromial ligament, and the deltoid. This is the most common site of bursitis of the shoulder, with inflammation usually occurring secondary to rotator cuff tendinitis or shoulder impingement syndrome. In a pure subacromial bursitis, the impingement signs may be absent, and the inflamed bursa may limit full passive abduction due to compression at the near end range of shoulder motion.4 More commonly, subacromial bursitis coexists with impingement syndrome or rotator cuff syndrome. Determining the etiology of shoulder pain may be difficult, and a diagnostic injection into the bursa can narrow the field of possibilities. A diagnostic injection may help distinguish weakness and loss of range of motion secondary to a painful bursitis from a full-thickness rotator cuff tear. The patient should be thoroughly examined prior to the administration of local anesthetic and then reexamined 5 to 10 minutes after injection. Postinjection, the patient may be less guarded and more cooperative during the physical examination, yielding further diagnostic information.

Although an anterior, posterior, or lateral approach may be used, the posterolateral approach is preferred. Following sterile technique, the skin is cleansed with povidone-iodine, and the patient is directed to retract the shoulder to a neutral posture. The posterolateral angle of the acromion is identified by palpation, and the needle is advanced in an anteromedial and slightly inferior direction (Figs. 11-1 and 11-2).5 If the soft tissues resist needle insertion, a small volume can be injected to expand the bursa so that the needle can be advanced further, resulting in optimal needle position. A mixture of 2 to 4 mL of 1% or 2% lidocaine hydrochloride and 2 to 4 mL of 0.5% bupivacaine hydrochloride is injected into the bursa after a 25-gauge, 1.5-inch needle is introduced approximately 1 inch.6 In the authors’ experience, an inflamed subacromial bursa accepts 4 to 6 mL of total volume. Following the injection, a reduction of pain with improved strength supports the diagnoses of shoulder impingement, supraspinatus tendinitis, and subdeltoid bursitis. Patients who respond with greater than 50% relief are good candidates for an immediate follow-up injection with 1 mL of betamethasone sodium phosphate.6 Alternatively, the anesthetics can be mixed with the corticosteroids and administered in a single injection when the clinical examination is clear. Subacromial bursography is helpful when the initial blind anesthetic injection is unsuccessful or in a patient whose diagnosis is unclear. A normal bursogram casts doubt on a diagnosis of subacromial impingement.7

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Figure 11-2 Schematic of subacromial bursa injection.

(Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

The strengthening component of a rehabilitative program should not progress too rapidly after corticosteroid injection, to avoid aggravation of inflammation and to avoid the rare risk for tendon rupture.

Trochanteric Bursitis

Several bursae may be implicated in trochanteric bursitis. The subgluteus maximus bursa lies lateral to the greater trochanter and the insertion of the gluteus medius and minimus. The subgluteus medius bursa is situated superior and posterior to the trochanter. The gluteus minimus bursa lies anterior to the trochanter. All three bursae may be part of a greater trochanteric pain syndrome.

Trochanteric bursitis is commonly seen in an elderly population and manifests as pain in the lateral thigh during ambulation.5a Patients may describe a pseudoradicular pattern with the pain extending down the lateral aspect of the lower extremity and into the buttock. The symptoms can be elicited by placing the lower extremity in external rotation and abduction. Direct palpation or deep pressure applied posterior and superior to the trochanter will reproduce the pain.8 The patient should be examined for limitations in flexibility involving the gluteus maximus, medius, and minimus and the tensor fasciae latae. Trendelenburg gait as a result of hip abduction weakness may contribute to increased friction and irritation of the bursa. If the history and physical examination are consistent with bursitis, a corticosteroid combined with anesthetic agent is delivered via a 3.5-inch, 22-gauge needle directed at the point of maximal tenderness overlying the greater trochanter (Fig. 11-4).5,9 Persistent hip pain despite injection therapy and comprehensive rehabilitation should alert the physician to alternate sources of pain including the lumbar spine, hip joint, and distal lower extremity joints.10,11

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Figure 11-4 Greater trochanteric bursal injection.

(Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

Ischial Bursitis

The ischial bursa lies between the ischial tuberosity and the gluteus maximus. The examiner’s index of suspicion must be high because ischial bursitis—so-called “tailor’s or weaver’s bottom”—is not common. Classically, ischial bursitis occurs from friction and the trauma of prolonged sitting on a hard surface. It may occur in adolescent runners, often in conjunction with ischial apophysitis. Pain is most commonly aggravated during uphill running.13 The pain is distributed down the posterior aspect of the thigh and occurs with activation of the hamstring muscles. Initial treatment approaches should address modification of the patient’s activity, including a decrease in the duration and frequency of running. If an alternative to running includes cycling, the patient should be advised to avoid the use of toe clips, which increase activation of the hamstrings. When the etiology is due to prolonged sitting, the patient’s work station should be modified to allow activities to be conducted in a standing position, and a cushion should be used during sitting. Ice and NSAIDs are helpful in controlling symptoms. Adolescent athletes may require a radiologic series to screen for callus formation secondary to ischial apophysitis if the pain does not resolve with conservative measures. Persistent pain may benefit from injection as an adjunct to rest, ice, and NSAIDs. To perform this, the patient lies on his or her side with the knees fully flexed to relax the hamstrings. A 3-inch, 22-gauge needle is held in a horizontal position and directed toward the point of maximal tenderness overlying the ischial tuberosity. The injection of contrast dye into the bursa under fluoroscopy may be necessary to verify needle placement.

Anserine Bursitis

The anserine bursa separates the three conjoined tendons of the pes anserinus, or goose’s foot (semitendinosus, sartorius, and gracilis muscles), from the medial collateral ligament and the tibia. It is one of the most commonly inflamed bursae in the lower extremity. Anserine bursitis is commonly seen in women with heavy thighs and osteoarthritis of the knees. The bursa may also become inflamed as the result of direct trauma in athletes, especially soccer players.4,13 Patients report pain inferior to the anteromedial surface of the knee with ascension of stairs. Moving the patient’s knee in flexion and extension while internally rotating the leg will reproduce the symptoms. The palpatory examination will localize the pain to the anserine bursa. The injection is straightforward and effective in reducing inflammatory symptoms. After sterile preparation, the knee is fully extended and a 1.0- to 1.5-inch, 22-gauge needle is directed at the point of maximal tenderness (Fig. 11-5)5 to deliver a 1- to 3-mL combination of anesthetic and corticosteroid. The patient should enter a rehabilitation program emphasizing flexibility, and the athlete at risk for repetitive trauma may benefit from padded knee protection.

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Figure 11-5 Anserine bursal injection.

(Modified from Vander Slam TJ: Atlas of Bedside Procedures. Boston, Little, Brown, 1988.)

Tibial Collateral Ligament Bursitis

The tibial collateral ligament (TCL) bursa, referred to as the “no name, no fame” bursa,14 is located between the deep and superficial aspects of the tibial collateral ligament.14a The bursa does not adhere to the medial meniscus, and it appears to reduce friction between the superficial layer of the TCL and the medial meniscus. TCL bursitis should be considered in any patient with medial joint line tenderness. During a 3-year study, Kerlan found that 5% of orthopedic patients presenting with medial knee pain suffered from TCL bursitis.15 Physical examination will not show evidence of new ligamentous or capsular instability. Treatment consists of a local injection of lidocaine (2 to 4 mL) and 1 mL of triamcinolone (40 mg/mL)15 directed perpendicular to the medial joint line at the point of maximal tenderness (Fig. 11-6).

Pharmacologic Agents for Bursal Injection

A number of local anesthetics are available for bursal injections, and clinicians should be familiar with their pharmacologic properties. Concentrations of 0.5% to 1.0% lidocaine or 0.25% to 0.5% bupivacaine are appropriate for bursal injection. The onset and duration of the anesthetic effect is related to the volume and concentration injected. Lidocaine has an onset of action within 5 to 15 minutes and may last 3 to 4 hours, whereas bupivacaine begins to work in 10 to 20 minutes, but the anesthetic effect can last 4 to 6 hours.17 Bach describes the benefits of using a combination of lidocaine hydrochloride and bupivacaine hydrochloride in subacromial space injections to obtain an early onset of action with prolonged anesthesia.6

Corticosteroids are widely available and very effective in alleviating bursal inflammation. Corticosteroids of intermediate or long duration are suitable for treatment of bursitis. Triamcinolone acetonide (10 mg/mL and 40 mg/mL) is a commonly used intermediate-acting agent with a half-life of 24 to 36 hours. Betamethasone is a longer acting corticosteroid with a half-life of 36 to 72 hours and a relative antiinflammatory potency five times greater than triamcinolone.17 The dosage is adjusted to the size of the bursa, and the lowest effective dose should be delivered to the bursa. Clinicians may want to avoid corticosteroid injection acutely (the first 7 days after an initial injury) because corticosteroids theoretically inhibit the healing process.18 About 14 to 21 days after injury, glucocorticoids can control the inflammation and edema of the proliferative phase. The Achilles, patellar, and rotator cuff tendons should be avoided because direct injection into the tendon can place the patient at risk for rupture.18

The clinician must be careful to select a combination of medications within the recommended volumes to avoid further injury to the bursae. Table 11-1 may be used as a guideline for selecting the type and volume of corticosteroid and anesthetic to be administered.

References

1. Smith D.L., McAfee J.H., Lucas L.M., et al. Septic and non-septic olecranon bursitis: Utility of the surface temperature probe in the early differentiation of septic and nonseptic cases. Arch Intern Med. 1989;149:1581-1585.

1a. Kelley W.N., Harris E.D., Ruddy S., Sledge C.B. Textbook of Rheumatology. Philadelphia: WB Saunders; 1993. 545-560

2. Kerr D.R. Prepatellar and olecranon arthroscopic bursectomy. Clin Sports Med. 1993;12:137-142.

3. Waters P., Kasser J. Infection of the infrapatellar bursa. A report of two cases. J Bone Joint Surg Am. 1990;72A:1095-1096.

4. Magee D.J. Orthopedic Physical Assessment. Philadelphia: WB Saunders; 2008. p 706

5. Vander Slam T.J. Atlas of Bedside Procedures. Boston: Little Brown; 1988. 455, 459, 461

5a. Swezey R.L. Pseudo-radiculopathy in subacute trochanteric bursitis of the subgluteus maximus bursa. Arch Phys Med Rehabil. 1976;57:387-390.

6. Bach B.R., Bush-Joseph C. Subacromial space injections: A tool for evaluating shoulder pain. Physician Sportsmed. 1992;2:93-98.

7. Nicholas J.A., Hershman E.B. The Upper Extremity in Sports Medicine. St. Louis: Mosby; 1995. 124-125

8. Klippel J.H., editor. Primer on the Rheumatic Diseases. Atlanta: Arthritis Foundation. 2008:143-146.

9. Ege Rasmussen K.J., Fanø N. Trochanteric bursitis: Treatment by corticosteroid injection. Scand J Rheumatol. 1985;14:417-420.

10. Collée G., Dijkmans B.A., Vandenbroucke J.P., Cats A. Greater trochanteric pain syndrome (trochanteric bursitis) in low back pain. Scand J Rheumatol. 1991;20:262-266.

11. Traycoff R.B. “Pseudotrochanteric Bursitis”: The differential diagnosis of lateral hip pain. J Rheumatol. 1991;18:1810-1812.

12. Shbeeb M.I., Matteson E.L. Trochanteric bursitis (greater trochanter pain syndrome). Mayo Clin Proc. 1996;71:565-569.

13. Reid D.C. Sports Injury Assessment and Rehabilitation. New York: Churchill Livingstone; 1992. 631, 1564, 1625–1626, 1636

13a. Hemler D.E., Ward W.K., Karstetter K.W., Bryant P.M. Saphenous nerve entrapment caused by pes anserine bursitis mimicking stress fracture of the tibia. Arch Phys Med Rehabil. 1991;72:336-337.

14. Stuttle F.L. The no-name, no-fame bursa. Clin Orthop. 1959;15:197-199.

14a. Lee J.K., Yao L. Tibial collateral ligament bursa: MR imaging. Radiology. 1991;178:855-857.

15. Kerlan R.K., Glousman R.E. Tibial collateral ligament bursitis. Am J Sports Med. 1988;16:344-346.

16. Young J.L., Press J.M. Rehabilitation of running injuries. In: Buschbacher R.H., Braddom R.L., editors. Sports Medicine and Rehabilitation: A Sport-Specific Approach. Philadelphia: Hanley & Belfus; 1994:123-134.

17. Covino B.G., Scott D.B. Handbook of Epidural Anesthesia and Analgesia. Orlando: Grune & Stratton; 1985. 58-74

18. Saal J.A. General principles and guidelines for rehabilitation of the injured athlete. Phys Med Rehabil State Art Rev. 1987;1:523-536.