Open repair results in less recurrent instability

For years I have selectively used arthroscopic techniques for stabilization of the shoulder for individuals who have had instability or recurrent dislocations.  I have, however, been skeptical of using arthroscopic surgery alone for all patients because I do not believe it yields satisfactory long term results and is associated with a higher rate of recurrence.  In other words, I believe that arthroscopic stabilization procedures have a higher rate of failure.  The review of the study below confirms this, as other studies have demonstrated in the past. 

I love studies that prove what I have believed for many years.

Study evaluates open, arthroscopic surgical techniques for shoulder repair

These results were presented during the American Orthopedic Society for Sports Medicine’s 2010 Specialty Day program.

Systematic reviews have evaluated whether an arthroscopic or open technique yields better results in patients with recurrent shoulder instability.  They have shown that an open procedure is less likely to result in recurrent instability; however, this remains a controversial topic.

Researchers performed the largest randomized trial to date on this subject and found more evidence in favor of the open technique.

They found no difference in disease-specific quality of life in patients who received open or arthroscopic repair for traumatic anterior shoulder dislocation, but patients who underwent open repair had a significantly lower risk of recurrent instability.

An expertise-based approach

In the randomized clinical trial, 196 patients with traumatic unidirectional anterior shoulder instability underwent open (Fig. 1) or arthroscopic (Fig. 2) repair (open, n = 98; arthroscopic, n = 98). Both groups consisted of 80 males and 18 females. The mean age in the open group was 27.8 years; in the arthroscopic group, it was 27.2 years. Expertise-based randomization allowed the participating surgeons to perform their preferred surgical technique for the repairs.

Fig. 1 A, Diagram of capsule during of open capsular repair for anterior instability.

Bankart lesions (tears of the stabilizing cartilage structures in the shoulder) were the primary pathology, and most of the open procedures were performed using the subscapular split approach.

The researchers measured disease-specific quality of life using the Western Ontario Shoulder Instability (WOSI) Index at baseline and at 3, 6, and 12 months postoperatively. They compared mean WOSI scores using an independent sample t-test.

Secondary outcome measures included range-of-motion, recurrent instability, surgical time, and scores from the American Shoulder and Elbow Surgeons (ASES) questionnaire. Patients were followed for a minimum of 1 year, and identical rehabilitation protocols were used.

Comparing outcomes

Investigators analyzed baseline characteristics and found no statistically significant differences regarding gender distribution, operative side, hand dominance, age, participation in sports, or WOSI scores between the two groups. On average, arthroscopic procedures were completed in 1 hour and 1 minute, while the open procedures took an average of 1 hour and 17 minutes.

At 12 months postoperatively, 175 patients (84 open, 91 arthroscopic) had completed follow-up. Researchers found no statistical difference in average WOSI scores, ASES scores, or range of motion between the two groups. 

A statistically significant difference was found in instability recurrence rates (open, 4 percent; arthroscopic, 12 percent; p = 0.042).

Younger age and the presence of a Hill Sachs lesion were two factors related to recurrence.

All patients with recurrent instability had a Hill Sachs lesion (this is a fracture of the humeral head from the dislocation).  The average age of patients with recurrence was 22 years, compared to 27 years in the total study population.

Overall, researchers concluded that there is no disease-specific quality of life difference between open and arthroscopic repairs, but that open surgical repair has a statistically lower chance of recurrent instability and a trend toward better disease-specific outcomes.

Bottom line

• Both open and arthroscopic approaches for treating traumatic anterior shoulder dislocation have similar functional and quality of life outcomes.
• Using an open, rather than arthroscopic, technique results in a lower rate of recurrence in patients with recurrent shoulder instability.
• The presence of a Hill Sachs lesion and younger age are likely associated with recurrent instability.

AAOS Now
May 2010 Issue
http://www.aaos.org/news/aaosnow/may10/clinical11.asp

  

Thanks,

JTM, MD 

 

An Common Cause of Anterior Knee Pain

A medial plica is a remnant of an embryonic partition in the knee, and runs along the inner aspect of the kneecap.

It may also be called a 'medial shelf' - more a vertical shelf than a horizontal one, mind - and runs down from above the patella to the fat pad below the patella.

---

As the knee bends the 'shelf' of tissue may also give a sudden snap over the rounded ends of the femur bone.

When a medial plica becomes abnormally thickened, it can be felt with the finger as a string-like object to the inner aspect of the kneecap.

Plica syndrome is often characterized by anterior knee pain, which is most commonly found along the superomedial aspect of the knee. The “plica” is due to remnant embryological tissue that compartmentalizes the knee during fetal development. The plica is considered a “vestigial” structure, which means that it has lost its ability to function over time and does not functionally affect an individual whether it is present or absent. It has been likened to the appendix, which can be a source of pain but lacks significant important function.


Symptoms

What are the symptoms of plica syndrome in athletes?

Usually plica syndrome is characterized by pain near the anteromedial (in front and toward the midline) side of patella (kneecap). Usually the pain is associated with bending of the knee and is irritated after and during exercise. Usually, no other symptoms other than pain is present, but it can occasionally be accompanied by swelling of the knee after prolonged physical activity.

How is plica syndrome diagnosed in athletes?

Plica syndrome is a difficult diagnosis in athletes, and is often made after “exclusion” of other common, structural causes of knee pain. Athletes will typically complain of discomfort along the front or inside of the knee. Usually there are no “mechanical symptoms” of locking or catching with a plica, but a sense of snapping or catching from a large plica can rarely occur. There may be tenderness in the region of the plica or medial femoral condyle where the plica is abrading the bone. Plain x-rays are usually normal. An MRI may show the plica on certain views, but is primarily useful to exclude bone bruises, meniscus tears, ligament injuries, and cartilage defects that can also cause similar pain and swelling of the knee joint. Routine labs are not beneficial to diagnose plica syndrome, but can help to identify other potential causes of knee pain.


Causes

What initially causes plica syndrome in athletes?

Most often plica syndrome is precipitated by a history of blunt trauma to the front of the knee or prolonged strenuous exercise. The plica is an embryologic remnant that is present throughout life, but is believed that a traumatic event or repetitive microtrauma is responsible for inciting inflammation and symptoms.

Treatment

What is the nonoperative treatment for plica syndrome in athletes?

Usually the first-line of treatment for plica syndrome in athletes includes rest from strenuous or precipitating activities. Physical therapy can be initiated to strengthen and stretch the muscles and soft tissues around the knee. In addition, oral non-steroidal anti-inflammatory medications and steroid injections can help alleviate the symptoms of plica syndrome by decreasing the inflammation and synovitis. If symptoms of pain and swelling completely resolve, a gradual rehabilitation program is started with a controlled return to competition. Steroid injections should be used judiciously, however. Occasionally, athletes may have a "flare" reaction after the injection with increased pain and swelling in the knee joint that resolves after 48 to 72 hours. Diabetics may have to monitor their blood sugar levels more closely due to a risk of hyperglycemia. In addition, there is a small risk of local “fat atrophy” and slight skin discoloration at the site of the injection.
What happens if conservative measures fail to help?

Failure to respond to months of nonoperative management may be an appropriate indication for surgical treatment in athletes. This procedure can be performed in a minimally invasive fashion (“arthroscopically”), using a camera and small instruments to excise the plica and associated inflammatory tissue around it that is causing the pain. The arthroscopic procedure also offers the benefit of allowing a thorough inspection of the knee for any other injuries or offending structures that may be a source of pain in athletes. The procedure has been reported with successful outcomes, allowing athletes to return to their previous level of competition without discomfort. However, the accurate diagnosis of a symptomatic plica remains the predominant challenge – not its surgical treatment. Many athletes will have asymptomatic plicas on imaging studies or arthroscopy that may not be the predominant cause of knee pain.
When can I return to play after surgery?

Arthroscopic surgery and plica excision is a relatively minor surgery. Unless associated procedures or repairs to knee ligaments or cartilage is required, a controlled rehabilitation program and quadriceps strengthening usually allows for an expeditious return to play 4 to 6 weeks after surgery.


Summary for the physician:

1. Definitions (based on arthroscopy) 
2. Pleats of synovial lining of the knee
3. Four Plicae
   1. Inferior plica (ligamentum mucosum)
      1. Intercondylar
      2. Anterior to anterior cruciate ligament
   2. Superior plica (plica synovialis suprapatellaris)
      1. Suprapatellar region (2 cm above patella)
   3. Medial plica (plica synovialis patellaris)
      1. Five anatomic subsets of the plica
      2. One finger breadth lateral to medial patella
   4. Lateral plica (rarely injured)
      1. Five anatomic subsets
5. Mechanism of Injury
   1. More common in teenage athletes
   2. Onset often after blunt or twisting knee injury
   3. Repetitive knee flexion-extension
      1. Rowing
      2. Swimming
      3. Cycling
6. Symptoms
   1. Medial patella pain
   2. Snapping sensation with knee flexion
   3. Provocative: Repeated flexion and extension motion
      1. Walking up and down stairs
      2. Squatting
7. Signs
   1. Painful arc at 30 to 60 degrees
   2. Medial to patella above joint line
   3. Painful cord palpable alongside medial edge of patella
   4. Palpation reproduces symptoms
8. Management
   1. Eliminate or reduce provocative activities
      1. Cycling
      2. Stair-step machine
   2. Local Cold Therapy
   3. Consider local Corticosteroid Injection
   4. Consider arthroscopic resection 
   
   
   Thanks.
   
   JTM, MD
   

Steroid Injections for Painful Shoulders

Here is a great review of steroid injections for the painful shoulder.   It is very technical and probably better for the medical professional rather than the average patient.

JTM, MD

From International Journal of Clinical Practice  by Allen D Bell, MD ; Doug Conaway, MD

Summary and Introduction

Summary

The painful shoulder is a common clinical entity with a broad array of possible causes. A caregiver for an affected patient needs to determine the etiology for the pain, often relying primarily on the history and physical examination and supplemented with laboratory testing and imaging when needed. However, initial treatment decisions are often made before ordering these tests in situations not involving trauma. Most conditions affecting the shoulder are treated with conservative measures such as rest, physical therapy and analgesics.
When such measures fail, local corticosteroid injections can be a valuable tool to help achieve symptom relief for a wide range of the most common conditions affecting the shoulder joint. This review aims to help the clinician distinguish among the commonly encountered causes of shoulder pain and guide therapy when the use of local corticosteroid injections is considered.

Introduction

Historically, injectable corticosteroids, often in combination with physical therapy, have been considered effective and valuable therapy for alleviating joint pain caused by inflammation.^[1-4] For over 50 years, clinicians have depended on such local corticosteroid treatment to provide safe, rapid, temporary relief of joint pain and suppression of inflammation.^[5-7] Despite this fact, there are few well-controlled studies demonstrating the benefits of injectable corticosteroids for shoulder pain, and hence debate continues regarding which types of shoulder pain are appropriate to treat by injection.^[8]
In current practice, corticosteroid injections are among the most accepted, successful and frequently administered treatments employed by rheumatologists, orthopaedic surgeons and primary care physicians.^[9] Roughly 90% of orthopedists and 95% of rheumatologists reported using corticosteroid injections for their patients in recent surveys.^[10-12] This is likely in part due to the paucity of practical alternatives to surgical intervention.^[13]
This review discusses and differentiates the conditions affecting the shoulder, which are candidates for injectable corticosteroid treatment. Corticosteroid injection indications, guidelines, techniques, efficacy and safety are also discussed.

Indications

Injections are appropriate when a symptomatic shoulder condition has a suspected underlying sterile inflammatory component that may respond to corticosteroids. Only commonly encountered conditions are discussed (Table 1). If the cause of an inflamed tendon, bursa or joint is unknown, infection should be excluded before considering the use of corticosteroids.

Table 1. Common Conditions Affecting the Shoulder for Which Corticosteroid Injections May Be of Benefit^[17,23,41]

Osteoarthritis (glenohumeral, acromioclavicular)

Rheumatoid arthritis

Adhesive capsulitis (frozen shoulder)

Rotator cuff impingement/tendinitis/tendinosis

Biceps tendinitis

Crystal deposition disorders (pseudogout, 'Milwaukee shoulder', calcium hydroxyapatite deposition)

Subacromial/subdeltoid bursitis

Rotator Cuff Impingement Syndromes

This broad entity refers to rotator cuff tendinitis/tendinosis and/or partial rotator cuff tendon tears due to impingement. It accounts for the majority of cases of clinically encountered shoulder pain.^[14] Such problems are typically encountered in older adults but can be seen in hard-driving young athletes as well. The underlying common pathophysiology is inflammation of the rotator cuff tendons, particularly the supraspinatus tendon, which is the most commonly affected.
Degeneration and/or inflammation of the common tendon of the subscapularis, supraspinatus, infraspinatus and teres minor (i.e. the rotator cuff muscles) most commonly results from overuse, impingement on the tendon from above or below, degenerative changes with aging or microcrystalline deposits.^[15]
Impingement of the rotator cuff is common because the tendons must course through a narrow space between the acromion above and the humeral head below (i.e. the impingement interval). This space becomes narrowest when the arm is abducted but is fairly narrow at rest as well; thus, any condition that further decreases this space or enlarges the tendon predisposes to impingement.^[15,16] Common possible etiologies include acromial-anatomic variants (e.g. downsloping or curved/hooked acromion, os acromiale), hypertrophic degenerative changes in the acromioclavicular (AC) joints, weight training and a thickened or calcified coracoacromial ligament.^[15-17]
Typical patient complaints include limited and/or painful range of motion and weakness, usually of abduction. Pain typically occurs with active range of motion and is worsened with overhead or above-the-shoulder activities, but night pain that disturbs sleep, particularly when the patient lies on the affected shoulder, is another fairly common symptom.^[16] Pain is typically located lateral to the glenohumeral joint and is generally less severe at rest.^[15] It often radiates laterally to the mid-upper arm.
Examination reveals no restriction of passive range of motion. However, active patient abduction of the affected arm is typically painful along the 'middle third' of a 180-degree arc (Figure 1).^[15] Decreased strength can also be elicited in this portion of the arc when the physician provides resistance to active motion and can be compared with the opposite side as a point of reference. Other commonly used physical examination maneuvers to demonstrate impingement and the associated rotator cuff tendon irritation include (i) flexing the arm to 90 degrees, then adducting it across the chest; the arm is then internally rotated with force by the examiner, who stabilizes the scapula with his other hand (Hawkins' test) (Figure 2); and (ii) passively flexing the internally rotated arm into full flexion with the scapula stabilized (Neer's test) (Figure 3).

Figure 1. (click image to zoom) The arc of elevation maneuver [adapted from (15)]. When a patient with shoulder pain elevates the extended arm from a relaxed, at-the-side position to completely overhead and parallel to the long axis of the trunk, a 180-degree arc is formed. Movement through the first 20-40 degrees (labeled part '1' of the arc) is generally not painful or only minimally symptomatic with rotator cuff tendinitis/tendinosis and impingement, but throughout the portion of the arc designated '2' in the diagram (i.e. the 'middle third', approximately 40-120 degrees), pain will occur with active motion. Movement through the terminal 30-60 degrees (labeled '3') of the arc is generally much less painful with rotator cuff pathology and typically affected by acromioclavicular arthritis/ pathology. The exception is when acromioclavicular arthritis and hypertrophic degenerative change are the cause of rotator cuff impingement, in which case both the second and the third labeled portions of the arc will be painful. Patients with glenohumeral arthritis, adhesive capsulitis, acute calcific tendinitis and subacromial bursitis often have pain throughout all the portions of the arc.

Figure 2. (click image to zoom) Hawkins' test for rotator cuff impingement. The arm is flexed to 90 degrees, adducted across the chest, then internally rotated forcefully by the examiner, who stabilizes the scapula with his other hand.

Figure 3. (click image to zoom) Neer's test for rotator cuff impingement. The arm is internally rotated, then passively lifted into full flexion with the scapula stabilized.

The 'drop arm' test will detect complete rotator cuff tears, the potential end result of continued impingement on degenerating and/or partially torn rotator cuff tendons: gentle downward pressure exerted by the physician on the forearm of an extended arm abducted to 90 degrees cannot be resisted and the arm drops or rapidly falls back to the patient's side.^[14] Another easy test is to simply ask the patient to actively abduct the arm from its resting position at the side - a patient with a full-thickness rotator cuff tear will be unable to do so. Magnetic resonance imaging (MRI), contrast arthrography or ultrasound is often used to confirm the diagnosis of a full-thickness tear if surgical intervention is being contemplated.^[18]

Subacromial/Subdeltoid Bursitis

The subdeltoid bursa lies in the subacromial space over the rotator cuff tendons, providing them with lubrication and protection against friction.^[16] This bursa does not normally communicate with the glenohumeral joint space, though it can do so in the presence of a full-thickness rotator cuff tear.^[13]
Subacromial/subdeltoid bursitis is usually secondary to surrounding irritation (e.g. partial rotator cuff tears, AC joint hypertrophy) or can be primary in rheumatoid or other inflammatory arthritides. A typical history is that of acute severe pain superimposed on a history of chronic milder pain. Tenderness may be elicited along the acromial border laterally, and there is often pain throughout the 180-degree arc of active motion (Figure 1).^[17,19]

Calcific Tendinitis

Calcific tendinitis is inflammation/irritation caused by calcium hydroxyapatite deposits around the shoulder, most commonly in the supraspinatus tendon. The exact aetiology is uncertain, but many believe initial tendon degeneration predisposes to dystrophic calcium deposition.^[15,18] Resorption of the crystals or rupture of the crystals into surrounding bursae can cause acute, severe pain symptoms thought to be related to a chemical irritation. The calcific deposits in the affected tendon(s) are usually visible on plain shoulder radiographs.^[18]
A combination of history, physical examination and radiographic findings is needed to make the diagnosis - as symptoms can mimic other causes of shoulder pain, tendon calcifications are often incidental/asymptomatic, and in some cases, radiographs may be negative due to the microscopic size of the calcifications. Most affected patients are middle-aged, and there is a slight female predominance.^[18]
Onset of pain is typically rapid. The pain is unrelated to shoulder position or activity and usually does not improve or change with rest, helping to distinguish this condition from impingement syndrome and glenohumeral arthritis. Patients may be unwilling to move the affected arm, and pain is typically out of proportion to objective physical examination findings. Because of the acute and severe nature of symptom onset, corticosteroid injection, non-steroidal anti-inflammatory drugs (NSAIDs) or both are often considered earlier in the treatment algorithm.^[17,18]

Glenohumeral Arthritis

The glenohumeral joint is less commonly affected by osteoarthritis than are the knees and hips because it is not a weight-bearing joint.^[18] Repetitive overhead lifters (e.g. occupational lifters, weight lifters and athletes) and those with prior trauma are more commonly affected. Chronic rotator cuff tears, neuropathy and other abnormalities affecting the shoulder can also lead to osteoarthritis and degenerative changes of the glenohumeral joint. Patients are typically aged over 50 years and complain of insidious onset of local pain, limitation of motion and/or weakness.^[20] The 'painful arc' with osteoarthritis is often the full 180 degrees, and crepitus may be present on examination (Figure 1).
In the absence of such risk factors, inflammatory conditions (e.g. rheumatoid arthritis, calcium pyrophosphate deposition disease, calcium hydroxyapatite deposition ['Milwaukee shoulder']) or other etiologies (e.g. prior avascular necrosis) should be considered. History, examination and laboratory and imaging tests help differentiate these causes. Osteoarthritis typically results in an insidious onset of chronic pain, and plain radiographs usually reveal joint space narrowing, osteophyte formation, sclerosis and/or subchondral cysts.^[4,17,18] Pain occurs with passive range of motion and at rest, helping to distinguish arthritis from rotator cuff impingement syndrome.

Adhesive Capsulitis

This condition describes a global and typically painful decrease in shoulder range of active and passive motion due to adherence of the shoulder capsule to the humeral head. This condition is sometimes referred to as 'frozen shoulder'.^{[20][14,15,17]} The cause is often long-standing pain that limits shoulder motion; trauma, rotator cuff tears, thyroid disorders and diabetes have been associated with this condition.

AC Joint Arthritis

Radiographic evidence of AC joint arthrosis and hypertrophic degeneration is common in people aged over 40 years but is often incidental and asymptomatic.^[18] AC joint disorders may also be traumatic, and hence radiographs may be warranted to exclude fracture or dislocation/separation.^[20] In the case of chronic idiopathic or post-traumatic degenerative changes of the AC joint, patients typically present with gradual and insidious onset of superior shoulder pain.
Classically, the pain is aggravated when the patient rolls onto the affected shoulder while sleeping or while the patient reaches across the chest with the affected arm towards the opposite axilla.^[20] On physical examination, the hallmarks of diagnosis are tenderness over the AC joint and AC joint pain with passive or active arm adduction across the body.^[17,18] Pain can be exacerbated when the examiner has the patient grab the opposite shoulder with the hand of the affected arm and pushes the patient's elbow towards the ceiling against resistance.^[17] Also, the arm can be extended to 90 degrees, then adducted across the chest to elicit AC joint pain (cross-arm test) (Figure 4).

Figure 4. (click image to zoom) Cross-arm test for acromioclavicular joint pain. The arm is extended to 90 degrees, then adducted across the chest.

Radiographs can help confirm degenerative changes in the AC joint and exclude the uncommon condition known as osteolysis of the distal clavicle, a similarly treated condition that results in resorption of the distal clavicle secondary to prior trauma or repetitive weight training.^[17,20] It is important to remember that hypertrophic osteoarthritis of the AC joint is one of the causes of rotator cuff impingement, and patients can therefore present with symptoms and signs of both conditions (Figure 1).

Biceps Tendinitis

The long head of the biceps tendon travels through the bicipital groove between the greater and lesser tuberosities of the humerus and inserts on the superior glenoid/glenolabral complex.^[18] Irritation of the long head of the biceps tendon is relatively common and typically occurs due to repetitive shoulder flexion, while the short head of the tendon is less commonly affected clinically.^[17] Patients typically complain of anterior shoulder pain and may relate a snapping or popping sensation or sound in the shoulder.
The diagnosis of biceps tendinitis (sometimes called bicipital tendinitis) is based on localising the patient's maximal site of tenderness to the bicipital groove, where the long head of the tendon lies.^[18] Yergason's supination sign refers to pain in the bicipital groove when patient-initiated forearm supination of a pronated forearm with the elbow at 90 degrees is resisted by the examiner (Yergason test) (Figure 5).^[18] A positive Speed's test refers to pain at the bicipital groove with resisted forward flexion of a supinated forearm while the shoulder is partially flexed.^[17]
 

Figure 5. (click image to zoom) Yergason test for biceps tendinitis. With the elbow flexed at 90 degrees, the patient's maximised site of tenderness is elicited as the examiner resists the patient's attempts to supinate his forearm.

Biceps tendon rupture results in objective weakness of biceps muscle function and often causes ecchymosis at the site of rupture. A bulge in the medial aspect of the distal upper arm ('Popeye' muscle) occurs as a result of unopposed contraction of the biceps muscle from the loss of tendon integrity.^[16] Most cases are in older patients and are managed conservatively, but the diagnosis can be confirmed with MRI if surgery is being considered.

Selecting Patients for Corticosteroid Injection Therapy

In general, all the above conditions should first be treated with conservative therapies, including rest, physical therapy and analgesics such as NSAIDs. In most cases, such therapy will suffice to alleviate symptoms. Corticosteroid injections are typically reserved for those who fail an adequate treatment regimen using one, or preferably a combination, of the above regimens.^[20] The severe and acute nature of symptoms of some of the above-mentioned conditions, such as subacromial bursitis, calcific tendinitis, rheumatoid arthritis, adhesive capsulitis and gout, may warrant earlier treatment with intrabursal or intra-articular corticosteroids to obtain satisfactory pain relief.^{[1,9,13,15,17,21,22]}
In special patient populations, such as those who are intolerant of or at high risk of complications from NSAIDs, corticosteroid injections may be a first-line therapy.^[22] Elderly patients and those with gastrointestinal upset or bleeding from NSAIDs, a history of peptic ulcer disease, and renal insufficiency are all at high risk from NSAID therapy. Joint-replacement candidates may also benefit from corticosteroid therapy prior to treatment, since the potential complications of repeated corticosteroid injections are less of a concern.

Injection Techniques

General Guidelines

Selection of Corticosteroid Agent and Dose. Relatively few studies have been published on the pharmacokinetics of intra-articular corticosteroids.^[23][24] Though difficult to predict in the individual patient, average duration of action is roughly 1-3 weeks and tends to be longer for the more non-soluble corticosteroid preparations.^{[21-23,25-27]} Less-soluble products may remain in the joint for 2-3 weeks; mean residence time in the joint is roughly 6 days. Selection of a particular injectable corticosteroid is often based on physician's comfort level and experience (Table 2).

Table 2. Commonly Used Injectable Corticosteroid Preparations [modified from (30)]

Solubility/generic (trade) name	Dose equivalent, mg*
Relatively insoluble
Dexamethasone acetate (Decadron-LA)	0.75
Hydrocortisone acetate (Hydrocortone)	20.0
Prednisolone acetate (Prednalone)	5.0
Triamcinolone acetonide (Kenalog)	4.0
Triamcinolone hexacetonide (Aristospan)	4.0
Slightly soluble
Methylprednisolone acetate (Depo-Medrol)	4.0
Prednisolone tebutate (Hydeltra-TBA)	5.0
Triamcinolone diacetate (Aristospan Forte)	4.0
Soluble
Dexamethasone sodium phosphate (Decadron)	0.75
Prednisolone sodium phosphate (Hydeltrasol)	5.0
Most soluble
Betamethasone sodium phosphate (Celestone)	0.6

*For example, 4 mg of methylprednisolone acetate is equivalent to 0.75 mg of dexamethasone sodium phosphate, which is equivalent to 5 mg of prednisolone acetate.

A suggested guideline is to use a more water-soluble preparation for acute inflammatory conditions such as tendinitis and a less water-insoluble preparation for chronic inflammatory conditions (e.g. impingement, bursitis and arthritis), recognizing that the trade-off is a shorter duration of action for the more soluble agents.^[10,26] Others believe that soluble formulations (e.g. hydrocortisone) have little role in infiltration therapy because they diffuse more readily from the injected region and can exert greater systemic effects.^[9] For chronic conditions, preparations of methylprednisolone and triamcinolone are often favored and appear to maximize the anti-inflammatory effects and duration of benefit relative to other currently available corticosteroid formulations.^[9,26][28] These were also the most widely used agents among members of the American College of Rheumatology in a previous survey.
The dose to be injected and needle size depend on the specific structure being injected, but are generally the same regardless of the underlying condition affecting each specific site. A proposed guideline for the various injections detailed in this review is provided (Table 3), but prescribing information should always be consulted.

Table 3. Needle Sizes and Doses for Injection of Various Shoulder Structures [modified from (19)]

Structure	Needle gauge size	Dose of methylprednisolone acetate, mg
Acromioclavicular joint	22-25	4-10
Biceps tendon (long head)	22	10-20
Glenohumeral joint	20	20-40
Subacromial bursa	20	20-40

The objective for any injection procedure is to insert the needle at the selected site in the shoulder with minimal pain and trauma and not introduce infection. For all injections, informed consent should be obtained and patients made as comfortable as possible. Sterile technique should be utilised and gloves worn. The desired entry site should be identified using standard anatomic landmarks and marked (e.g. thumbnail and retracted tip of a ballpoint pen or marker). The skin should be cleaned with betadine, alcohol swabs or chlorhexidine and allowed to dry completely. To minimise patient's discomfort from the procedure, an ethyl chloride spray may be applied for 5 s, after which a subcutaneous or topical anaesthesia such as lignocaine (lidocaine) can be applied to anaesthetise the shoulder. The operator should allow 3-5 min to ensure that the area is sufficiently anaesthetised before injecting the corticosteroid. The needle is then advanced to the desired point. Prior to injection, the plunger is withdrawn, which may return synovial fluid and confirm the correct location. This also ensures that a blood vessel has not been entered. When a bursa or joint space is injected, the solution should flow easily without significant resistance. An adhesive strip can be used to cover the injection site after the procedure.^[29-32]
Specific techniques for injection are somewhat varied but generally uncomplicated and are further delineated below.^[4,13] After the procedure, patients should be advised to limit activity for 48-72 h and counseled to use ice and analgesia for rare post-injection 'flares' related to chemical irritation from the corticosteroid preparation.^{[10,25,30,32,33]}

Techniques for Specific Sites

Subacromial Injection. Injection into the subacromial/subdeltoid bursal space can be utilized for rotator cuff impingement syndrome, calcific tendinitis, subacromial/subdeltoid bursitis and adhesive capsulitis.^[9,17,19] A lateral approach generally is used and is all that is discussed, though other approaches have been described.^{[13,14,17,19,34]}
The affected shoulder is palpated until the distal, lateral and posterior edges of the acromion are identified. The needle is inserted inferior to the posterolateral corner of the acromion, aiming the needle medially and slightly anteriorly under the acromion with the tip directed to the undersurface of the acromion (Figure 6).^[9,19] The practitioner may want to gently pull down on the upper arm at the elbow to open up the subacromial space.

Figure 6. (click image to zoom) Subacromial space injection technique to enter the subacromial/subdeltoid bursa [adapted from (9)]. The acromion is the palpable landmark, with the needle entry site and direction illustrated with an arrow in the figure and described in the text.

 
Glenohumeral Joint Injection. Injection directly into the glenohumeral joint space can be used for acute and chronic capsulitis (i.e. frozen shoulder), glenohumeral arthritis and synovitis (e.g. rheumatoid arthritis).^[9,14,17,19] The posterior entry is preferred by the author owing to the possibility of arterial or brachial plexus injury with an anterior approach, but both anterior and posterior approaches are commonly used.^[17,19]
For the posterior approach, the patient's arm can be internally rotated across the waist, and the needle inserted two fingerbreadths inferior and medial to the posterolateral corner of the acromion and directed antero-medially towards the coracoid process (Figure 7).^[9,14,17,19]
 

Figure 7. (click image to zoom) Posterior approach glenohumeral joint injection technique [adapted from (9)]. The goal of this injection is to enter the glenohumeral joint space. The skin entry site just below and medial to the posterolateral aspect of the labeled acromion is marked with an 'X', and from this posterior approach the needle tip is directed towards the labeled coracoid process.

The anterior approach involves inserting the needle tip a fingerbreadth lateral to and just below the coracoid process and directing the needle posteriorly and slightly laterally.^[19,35]
AC Joint. The AC joint space can be palpated about 1 cm medial to the top of the acromion and can be approached for injection from above and from a slight anterior position, though other techniques have been described.^[9,17,35] The patient should be seated with the arm hanging down to slightly open the AC joint.^[9,17] The needle tip can then be directed inferiorly into the joint (Figure 8).

Figure 8. (click image to zoom) Acromioclavicular joint injection technique to enter the acromioclavicular joint space [adapted from (9)]. The skin entry site is just above the acromioclavicular joint (which is labelled with an 'X') with the needle tip directed inferior as illustrated by the arrow in the figure.

 
 Biceps Tendon. The goal of this injection is to enter the tendon sheath of the biceps tendon and/or the bicipital groove around the tendon without injecting into the tendon itself.^[17,35] The tendon is identified in the bicipital groove of the humerus. A needle is inserted into the skin over the point of maximal tenderness and directed into the groove at an angle with the needle tip nearly parallel to the groove. Increased resistance to flow of the injection should suggest an intra-tendinous location and direct the caregiver to withdraw the needle tip slightly.^[17,35]

Efficacy Data

Though anecdotal data are strong, there are somewhat limited controlled trial data to support or refute corticosteroid injections for the painful shoulder.^[21,34] An extensive recent meta-analysis by Buchbinder et al.^[8] found a benefit of subacromial corticosteroid injection for rotator cuff disease and glenohumeral intra-articular corticosteroid injection for adhesive capsulitis compared with placebo. Short-term benefit has been demonstrated by others (not included in the meta-analysis of Buchbinder et al.) for AC joint pain, adhesive capsulitis and non-specific rest pain of the shoulder.^[1,21,36]
The American Academy of Orthopedic Surgeons includes corticosteroid injections as part of its recommended clinical guidelines for the treatment of rotator cuff disorders and AC joint pain, and the American College of Rheumatology has advocated corticosteroid injections to primary care providers for glenohumeral synovitis (e.g. rheumatoid arthritis), adhesive capsulitis (frozen shoulder), rotator cuff tendinitis, impingement syndrome, subacromial bursitis and AC joint arthritis.^[9,20]

Contraindications and Complications

Contraindications. Contraindications to intra-articular corticosteroid injection include infection in or around the joint (e.g. septic arthritis, periarticular cellulitis and osteomyelitis), bacteremia or sepsis, significant skin breakdown at the proposed injection site, known hypersensitivity to the proposed injection, the presence of a joint prosthesis, uncontrolled bleeding diathesis, osteochondral or other intra-articular fracture and severe joint destruction (e.g. Charcot's joint).^{[26,28,30,31]}
Relative contraindications include joint instability, adjacent superficial skin lesions or abrasions, hemarthrosis, severe osteoporosis of bones adjacent to the joint and an uncooperative patient.^{[26,28,30,31]} Diabetic patients should be warned that corticosteroid injections can cause elevation of their blood sugar for 2-3 days after the procedure. Caution should also be used in patients on anticoagulation therapy. Equally important is for the practitioner to make sure that one is not using injectable corticosteroids for a condition that would not be expected to be helped by the treatment (e.g. acute injury, pathology due to neurogenic disease, referred pain and neuropathic arthritis).
Complications. The administration of intra-articular corticosteroids is generally safe with minimal risk to the patient when used conservatively, appropriately, and with aseptic technique.^[37] As with any pharmacological agent, corticosteroids should not be administered indiscriminately, however, and no treatment is without risk.
Reported side effects of corticosteroid injection therapy include systemic effects, tendon weakening/rupture, fat atrophy, muscle wasting, skin pigment changes, septic arthritis, nerve and blood vessel damage, post-injection symptom flare/synovitis, facial flushing, anaphylaxis and steroid arthropathy.^{[10,22,30,32]} Almost all these complications can be minimized or prevented by taking a careful history, using an accurate and aseptic injection technique, and avoiding high doses and overly frequent injections.^{[10,22,30,32]} Most clinicians recommend at least a 3-month interval between corticosteroid injections to help prevent certain steroid-related complications, though little scientific data support this specific interval.^[26,28,30]
The most common significant clinically encountered side effect is likely the steroid flare reaction, which occurs in up to 5% of intra-articular injections. Flares probably are caused by inflammation related to phagocytosis of the corticosteroid crystals by leucocytes.^[9,32] The pain from this side effect typically starts a few hours after the injection and stops within 24-48 h as the anti-inflammatory effect of the glucocorticoid overrides the inflammatory effect of the corticosteroid crystals.^[9,32] Treatment includes rest, cold compresses and analgesics.^[9,32,33]
Injections directly into a tendon can cause rupture; this is particularly important to remember when performing subacromial and biceps tendinitis injections.^[4,38,39] Several case reports of avascular necrosis in months following corticosteroid injection have been published, but no causal evidence exists.^[23][4] The feared complication of introducing infection into a joint has an exceedingly low incidence if standard aseptic technique is used, and has been estimated in the range from 1 in 15,000 to 1 in 85,000 in larger series.^[30,40] There is a much stronger association for avascular necrosis with prolonged use of systemic corticosteroids, and the shoulder seems to be affected more than other upper limb joints.

Conclusion

Shoulder pain is a common clinical complaint, and a combination of history, physical examination, laboratory testing and imaging may be needed to determine the underlying cause of pain. Once the diagnosis is established, conservative measures are generally employed and give most patients symptomatic relief.
When initial conservative therapy fails, or for patients who have severe, acute symptoms, depot corticosteroid injections are a well-established therapy for painful shoulder joints and have a long track record of safety. Proper technique and accurate pre-procedural diagnosis help to assure the maximum benefit and safety of this treatment.

References

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2. Rasmussen S, Lorentzen JS, Larsen AS, Thomsen ST, Kehlet H. Combined intra-articular glucocorticoid, bupivacaine and morphine reduces pain and convalescence after diagnostic knee arthroscopy. Acta Orthop Scand 2002; 73: 175-8.
3. Jones A, Doherty M. Intra-articular corticosteroids are effective in osteoarthritis but there are no clinical predictors of response. Ann Rheum Dis 1996; 55: 829-32.
4. O'Driscoll SW. Surgery of the shoulder arthritis. In: Koopman WJ, ed. Arthritis and Allied Conditions: A Text of Rheumatology, 13th edn. Baltimore, MD: Williams & Wilkins, 1997: 899-911.
5. Lane NE, Thompson JM. Management of osteoarthritis in the primary-care setting: an evidence-based approach to treatment. Am J Med 1997; 103: S25-30.
6. Uthman I, Raynauld JP, Haraoui B. Intra-articular therapy in osteoarthritis. Postgrad Med J 2003; 79: 449-53.
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8. Buchbinder R, Green S, Youd JM. Corticosteroid injections for shoulder pain (Cochrane Review). In: Anonymous. The Cochrane Library, Issue 1, Chichester, UK: John Wiley & Sons Ltd, 2004.
9. Canoso JJ. Corticosteroid infiltrations (Available at http://www.rheumatology.org/publications/primarycare/number5/hrh0029598.asp, accessed June 9 2004).
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21. Roy S, Oldham R. Management of painful shoulder. Lancet 1976; 1: 1322-4.
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29. Schumacher HR Jr. Arthrocentesis of the knee. Hosp Med 1997: July: 60-64.
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31. Cellular Aspects of Rheumatoid Arthritis. Intrasynovial Injection Techniques Kalamazoo, MI: The Upjohn Company, 1982: 1-29[booklet].
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35. A How to Reference Guide. Periarticular and Intra-Articular Injections Kalamazoo, MI: Pharmacia, 2002.
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37. Hollander JL. Intrasynovial steroids for rheumatoid arthritis. Med Counterpoint 1974; 37-8.
38. Karpman RR, McComb JE, Volz RG. Tendon rupture following local steroid injection: report of four cases. Postgrad Med 1980; 68: 169-76.
39. Ford LT, DeBender J. Tendon rupture after local steroid injection. South Med J 1979; 72: 827-30.
40. Hollander JL. Intrasynovial corticosteroid therapy in arthritis. Md Med J 1970; 19: 62-6.
41. Salvarani C, Cantini F, Olivieri I et al. Corticosteroid injections in polymyalgia rheumatica: a double-blind, prospective, randomized, placebo controlled study. J Rheumatol 2000; 27: 1470-6.

 

This is a great review even if I did not write it.

Thanks

JTM, MD