Symptomatic Progression of Asymptomatic Rotator Cuff Tears

A recent study from the major orthopedic journal investigated the progression of painful rotator cuff tendon tears.  I have excerpted a portion of the article below.  This is a question that I am frequently asked by patients.  

The study demonstrates that a substantial proportion of subjects with asymptomatic rotator cuff tears become symptomatic after a short-term follow-up period. Pain development in asymptomatic rotator cuff tears is associated with tear size progression. Collectively, the subjects who developed new shoulder pain showed significant tear size increases compared with baseline measurements, whereas those who remained asymptomatic had no significant change in tear size. Likewise, the rate of tear progression, as defined in this study, for the symptomatic group (23%) was significantly greater than the rate for the asymptomatic group (4%). Tear progression manifested as both enlargement of full-thickness tears as well as conversion of partial-thickness to full-thickness tendon defects. The lack of tear progression seen in the majority of newly symptomatic tears, however, suggests that factors other than tear progression likely play a role in the evolution of symptoms for these patients. Given the high prevalence of asymptomatic rotator cuff disease, especially in individuals older than sixty years or in patients with a painful rotator cuff tear in the contralateral shoulder, these findings are clinically relevant. The onset of shoulder pain in a patient with a known preexisting asymptomatic tear may indicate an increase in tear size, which would potentially affect the clinical management of these patients.

Compared with the group of subjects who remained asymptomatic, the subjects who developed pain were found to have significantly larger tears at the time of enrollment. This suggests that the absolute size of an asymptomatic tear may be a predictor of future pain development. Previously, we reported the average size of symptomatic tears to be 30% larger than that of asymptomatic tears. There may be a cuff tear size threshold that predisposes a subject to future pain development, irrespective of tear progression. Future studies are necessary to define the relationship of absolute tear size and tear progression with pain development in the shoulders with an asymptomatic rotator cuff tear. In addition, a significant difference in predilection toward hand dominance was seen between the shoulders that developed pain (56% were on the dominant side) and those that remained asymptomatic (26% were on the dominant side). This may be explained by the finding that the dominant-side shoulders initially had larger tears than the nondominant shoulders. It is also possible that hand dominance, irrespective of tear size, predisposes a shoulder with an asymptomatic tear to develop symptoms.

This study demonstrates that shoulder function deteriorates as asymptomatic rotator cuff tears became painful.  All measures of active range of motion of the shoulder, with the exception of external rotation at 90° of abduction, decreased significantly after pain development. Interestingly, the subjects who remained asymptomatic also showed a decrease in forward elevation and internal rotation in extension. These findings suggest that progressive loss of range of motion of the shoulder may be a consequence of the presence of a rotator cuff tear, regardless of the presence of symptoms. The declines in active range of motion seen in this study were small at this short-term time point and would be difficult to appreciate clinically. Furthermore, the differences seen between symptomatic and asymptomatic shoulders were not clinically important. Further studies are needed to determine if this loss of shoulder motion progresses over time and if specific strategies can prevent or correct the functional changes in this patient cohort. 

External rotation strength of the shoulder was not significantly affected by new pain development. This can be explained by the fact that the tears included in this study were relatively small in size. These tears primarily involved the supraspinatus tendon, whereas the majority of the infraspinatus tendon was preserved, thus minimizing external rotation weakness. Furthermore, degenerative changes within the rotator cuff musculature were minimal, likely preserving cuff strength. It is possible that scapular plane abduction strength may have been a more sensitive test for the detection of disease progression in these subjects as this test is more sensitive to detect supraspinatus tears and has been previously correlated to the size of asymptomatic rotator cuff tears.

This study demonstrates that pain development in asymptomatic rotator cuff tears is not associated with progression of fatty degeneration of the rotator cuff muscles. This may be explained by the relatively short time period (one year) between the evaluation time points and the relatively small size of the tears included in this study. Nonetheless, it is notable that progressive fatty degeneration is not associated with pain development or tear enlargement in previously asymptomatic rotator cuff tears.

In summary, the risk of symptom progression for asymptomatic rotator cuff tears after a short-term follow-up interval is substantial. In this study, shoulders that developed pain had significantly larger tears at baseline and demonstrated a higher rate of tear progression than those that remained asymptomatic. Shoulder function and active range of motion deteriorated with symptom onset; however, no significant changes were found in external rotation strength or fatty degeneration of the rotator cuff muscles after pain development. There was an increase of compensatory scapulothoracic motion during early shoulder abduction after pain development; however, no increase in proximal humeral migration was seen.

The message here is that tears that are not treated and repaired will progress and get bigger over time.  Bigger tears get worse faster and are more likely to cause pain and impairment.  Patients with rotator cuff tears will often have to use their upper back muscles to fully lift the shoulder which is why we examine the neck and upper back (thoracic spine) for shoulder examinations.  Further study is needed to follow these tears over longer periods of time.

Reference:  The Journal of Bone and Joint Surgery (American). 2010;92:2623-2633.

Thanks,

JTM, MD

Lateral Epicondylitis Tennis Eblow

Lateral epicondylitis, or tennis elbow, is a commonly encountered problem in orthopedic practice. 

Problem 
Lateral epicondylitis (tennis elbow) is an overuse injury involving the extensor muscles that originate on the (outer elbow) lateral epicondylar region of the distal humerus. It is more properly termed a tendinosis that specifically involves the origin of the extensor carpi radialis brevis muscle (one of the tendons that extends the wrist.

Frequency
Lateral epicondylitis (tennis elbow) has been demonstrated to occur in up to 50% of tennis players. However, this condition is not limited to tennis players and has been reported to be the result of overuse from many activities. Lateral epicondylitis is extremely common in today's active society.

Causes
Any activity involving wrist extension and/or supination (turning the forearm in a clockwise direction as if turning a screwdriver) can be associated with overuse of the muscles originating at the lateral epicondyle (outer elbow). Tennis has been the activity most commonly associated with the disorder. The risk of overuse injury is increased 2-3 times in players with more than 2 hours of play per week and 2-4 times in players older than 40 years. Several risk factors have been identified, including improper technique, size of racquet handle, and racquet weight.

I see more work related elbow pain.  For work-related lateral epicondylitis, a systematic review identified 3 risk factors: handling tools heavier than 1 kg, handling loads heavier than 20 kg at least 10 times per day, and repetitive movements  for more than 2 hours per day.  The review also found that low job control and low social support were psychosocial factors associated with lateral epicondylitis. 

What happens to the tendon
The cause of tennis elbow is a microscopic tearing with formation of reparative tissue (ie, angiofibroblastic hyperplasia) in the origin of the extensor carpi radialis brevis (ECRB) muscle.  This is one of the wrist extensors.  This microtearing and repair response can lead to macroscopic tearing and structural failure of the origin of the ECRB muscle.
Concomitant intra-articular lesions (eg, loose bodies, synovitis, bone spurs, early arthritic lesions) have been visualized during elbow arthroscopy in patients with lateral epicondylitis. However, while concomitant intra-articular pathology has been noted, this process is currently considered an extra-articular process. 

Presentation
Patients present complaining of lateral elbow and forearm pain exacerbated by use. The typical patient is a man or woman aged 35-55 years who either is a recreational athlete or one who engages in rigorous daily activities.

Upon examination, the patient has a point of maximal tenderness just distal (5-10 mm) to the lateral epicondyle in the area of the extensor carpi radialis brevis (ECRB) muscle. Wrist extension or supination (but not flexion or pronation) against resistance with the elbow extended should provoke the patient's symptoms. Another helpful test is the chair raise test. The patient stands behind their chair and attempts to raise it by putting their hands on the top of the chair back and lifting. In patients with lateral epicondylitis, pain results over the lateral elbow. 

Indications
Approximately 90-95% of patients with lateral epicondylitis (tennis elbow) respond to conservative measures and do not require surgical intervention. Patients whose condition is unresponsive to 6 months of conservative therapy (including corticosteroid injections) are candidates for surgery. 

Relevant Anatomy
The extensor carpi radialis brevis (ECRB) muscle arises from the lateral epicondyle. The ECRB muscle lies deep to the extensor carpi radialis longus (ECRL) muscle and superficial to the joint capsule. The annular and collateral ligaments are located beneath and just distal to the origin of the ECRB muscle. 

Contraindications
No absolute contraindications to lateral epicondylitis (tennis elbow) surgery exist. It is advisable to offer surgery only after patients have failed 3-6 months of nonoperative modalities, such as steroid injections, splinting, and occupational therapy. Relative contraindications include any comorbidities that would place the patient at a more serious level of surgical risk. 

Workup 

Imaging Studies

• Radiographs (x-rays) can be helpful in ruling out other disorders or concomitant intra-articular pathology (eg, osteochondral loose body, posterior osteophytes, bone spurs). Calcification in the degenerative tissue of the extensor carpi radialis brevis (ECRB) muscle origin can be seen in chronic cases.
• Magnetic resonance imaging can help confirm the presence of degenerative tissue in the ECRB muscle origin and can help diagnose concomitant pathology. A guideline from the American College of Radiology (ACR) recommends MRI as the most appropriate imaging study for patients with suspected chronic epicondylitis when radiographs are nondiagnostic.
• I usually do not require an MRI to diagnose and treat tennis elbow. 

 Other Tests

• If the clinical examination indicates a possible neural etiology for the patient's symptoms, electromyography can be helpful in excluding posterior interosseous nerve compression syndrome as the diagnosis. 

Diagnostic Procedures

• Anesthetic injections into the origin of the extensor carpi radialis brevis (ECRB) muscle can help confirm the diagnosis, as the patient should experience relief from symptoms. 

Histologic Findings

  Despite the misnomer of lateral epicondylitis (tennis elbow), the histology of lesions shows neither acute nor chronic inflammatory cell infiltrate. Lesions are characterized by fibroblastic invasion with neovascularization. However, most other studies indicate degenerative changes. 

Staging
There are 4 progressive stages:

• Stage 1 - Inflammatory changes that are reversible
• Stage 2 - Nonreversible pathologic changes to origin of the extensor carpi radialis brevis (ECRB) muscle
• Stage 3 - Rupture of ECRB muscle origin
• Stage 4 - Secondary changes such as fibrosis or calcification 

Treatment 

Medical Therapy

  Nonsurgical treatment is the mainstay of care for patients with lateral epicondylitis (tennis elbow). The goal of initial treatment is cessation of the offending activity. Rest, use of a counterforce brace (a tennis elbow band), and nonsteroidal anti-inflammatory drugs (NSAIDs) often provide relief of symptoms. Often, wrist splinting is necessary.  

I find wrist immobilizers to be more effective than tennis elbow bands in the early phases of painful tennis elbow.  The wrist splint puts the injured tendon at rest allowing the inflammation to calm down thereby relieving pain.

Other researchers found the tennis elbow band to be more effective.  One study compared 3 common types of braces for their effect on grip strength in patients with lateral epicondylosis. In a randomized, controlled study of 52 patients, maximum and pain-free grip strength were assessed with the patient wearing an elbow strap orthosis, an elbow sleeve orthosis, a wrist splint, or a placebo orthosis. Use of the elbow strap and sleeve orthoses resulted in an immediate and equivalent increase in pain-free grip strength; consequently, the researchers suggest that either of these types of orthosis may be used. The wrist splint provided no immediate improvement in either pain-free or maximum grip strength.


Both corticosteroid and autologous blood injections have been shown to be effective. Corticosteroid injections at the lateral epicondyle have been shown to significantly decrease pain scores in the early post-injection period. 

 

When the patient is free of pain through a full range of motion, begin strengthening therapy in a very slow and progressive way. When the patient regains strength and nears resumption of activity, place the emphasis on preventing future irritation (eg, correct technique or address equipment concerns in athletes who participate in racquet sports, modify jobs or activities in patients who are not athletes).

Therapy in patients who are having considerable pain from inflammation seems to be counter productive as it often aggravates the pain.  Controlling inflammation and reducing pain enables patients to do more productive physical therapy.

The use of shockwave therapy raised initial excitement. However, 2 prospective, randomized, blinded trials showed no benefit of this intervention over placebo. 

Surgical Therapy
A myriad of surgical procedures has been described for the treatment of lateral epicondylitis (tennis elbow). However, most surgical procedures involve debridement of the diseased tissue of the extensor carpi radialis brevis (ECRB) muscle with decortication of the lateral epicondyle. This procedure has been performed through open, percutaneous, and arthroscopic approaches.  

Preoperative Details
Note the length of time of the patient's symptoms. Also note the conservative therapeutic course that has been implemented, including any corticosteroid injections. Consider the patient's workers' compensation status, as patients with workers' compensation claims may not respond as well to intervention.


A full evaluation should be performed on patients with lateral epicondylitis (tennis elbow) so that any other associated conditions can be detected. 

Intraoperative Details
In the classic open-release procedure for lateral epicondylitis (tennis elbow), the patient is positioned supine.  A 3-cm longitudinal incision is made over the lateral epicondyle. An incision is made through the extensor aponeurosis (outer elbow). The extensor carpi radialis brevis (ECRL) muscle is retracted medially, revealing the degenerative origin of the ECRB. All pathologic tissue is excised. The lateral epicondyle is decorticated with an osteotome, burr or by drill holes. The ECRL is sewn to the extensor aponeurosis in an attempt to repair the defect.

Lateral epicondylitis. Incision for open debridement of lateral epicondyle. Lateral epicondyle is circled.

Revision debridement for lateral epicondylitis. The fascia covering the origin of the extensor carpi radialis brevis muscle and the extensor carpi radialis longus muscle is fibrotic.

The extensor origin exposed

Lateral epicondylitis. Osteotome positioned over lateral epicondyle. 

Postoperative Details 

Surgical treatment of lateral epicondylitis (tennis elbow) is an outpatient surgical procedure. If the open approach is used, the elbow is usually protected initially with a splint or brace at 90°. 

Follow-up
Early motion in a brace may be initiated at 2-3 days after surgical treatment of lateral epicondylitis (tennis elbow), with strengthening exercises usually started by 3 weeks, depending on the patient's symptoms. Return to racquet sports can be expected by 4-6 months. Depending on the specific job requirements, patients can return to work in 6-12 weeks, although job modification or persistent use of a counterforce brace during work activities may be necessary.

I usually advise patients to wear the tennis elbow band for up to 6 months post op for heavy or demanding physical tasks to protect the healing tendon. 

Complications

One of the most concerning complications of aggressive surgical debridement for lateral epicondylitis (tennis elbow) is lateral elbow instability. The proximity of the lateral collateral ligaments and the annular ligament makes them susceptible to injury. Other complications include recurrence or incomplete relief of pain. 

Outcome and Prognosis
Surgical treatment of lateral epicondylitis (tennis elbow) has yielded predictably favorable results, with approximately 85% of patients reporting complete pain relief. Some patients may have persistent symptoms despite surgical treatment, and these patients may benefit from a more aggressive debridement.

Reference

Patients can link to my web site tennis elbow information here.  You can download a booklet on lateral epicondylitis here and a booklet on medial epicondylitis here.

Thanks,


JTM, MD

Tai Chi Exercise Reduces Knee Osteoarthritis Pain in the Elderly

Researchers from Tufts University School of Medicine have determined that patients over 65 years of age with knee osteoarthritis (OA) who engage in regular Tai Chi exercise improve physical function and experience less pain. Tai Chi (Chuan) is a traditional style of Chinese martial arts that features slow, rhythmic movements to induce mental relaxation and enhance balance, strength, flexibility, and self-efficacy.

The elderly population is at most risk for developing knee OA, which results in pain, functional limitations or disabilities and a reduced quality of life. According to the Centers for Disease Control and Prevention (CDC) there are 4.3 million U.S. adults over age 60 diagnosed with knee OA, a common form of arthritis that causes wearing of joint cartilage. A recent CDC report further explains that half of American adults may develop symptoms of OA in at least one knee by age 85.

For this study, 40 patients from the greater Boston area with confirmed knee OA who were in otherwise good health. The mean age of participants was 65 years with a mean body mass index of 30.0 kg/m². Patients were randomly selected and 20 were asked to participate in 60-minute Yang style Tai Chi sessions twice weekly for 12 weeks. Each session included: a 10-minute self-massage and a review of Tai Chi principles; 30 minutes of Tai Chi movement; 10 minutes of breathing technique; and 10 minutes of relaxation.

Tai Chi is a mind-body approach that appears to be an applicable treatment for older adults with knee OA. Physical components of Tai Chi are consistent with current exercise recommendations for OA, which include range of motion, flexibility, muscle conditioning, and aerobic work out. Researchers believe the mental feature of Tai Chi addresses negative effects of chronic pain by promoting psychological well being, life satisfaction, and perceptions of health.

The remaining 20 participants assigned to the control group attended two 60-minute class sessions per week for 12 weeks. Each control session included 40 minutes of instruction covering OA as a disease, diet and nutrition, therapies to treat OA, or physical and mental health education. The final 20 minutes consisted of stretching exercises involving the upper body, trunk, and lower body, with each stretch being held for 10–15 seconds.

At the end of the 12-week period, patients practicing Tai Chi exhibited a significant decrease in knee pain compared with those in the control group. Researchers noted a reduction in pain between the Tai Chi and control group. Researchers also observed improved physical function, self-efficacy, depression, and health status for knee OA in subjects in the Tai Chi group. 

Wow.  Exercise (including Tai Chi in this study and Yoga as well) is good for knee artrhritis.  Who knew?  Actually, my patients knew this since I have been an advocate of these kind of exercise programs for many years.

Of course,  all of my knee arthritis patients will be required to demonstrate the yoga pose below after completing their treatment for their knee arthritis.

References

• Article: "Tai Chi Is Effective in Treating Knee Osteoarthritis: A Randomized Controlled Trial." Chenchen Wang, Christopher H. Schmid, Patricia L. Hibberd, Robert Kalish, Ronenn Roubenoff, Ramel Rones, and Timothy McAlindon. Arthritis Care & Research; Published Online: October 29, 2009 (DOI:10.1002/art.24832); Print Issue Date: November 2009.

Thanks,

JTM, MD

SLAP Lesions

Reference, adapted, with permission, from one of the best shoulder sites on the web, www.shoulderdoc.co.uk.

What is a SLAP lesion?

The shoulder is a ball-and-socket type of joint and is anatomically referred to as the glenohumeral joint, describing the two bony structures involved. The socket is the glenoid cavity, a cup-shaped piece of bone that juts out from a corner of the shoulder blade (scapula). The rim of the glenoid is formed by cartilage called the labrum. The ball that fits into the socket is the head (upper part) of the humerus (arm bone). 

The upper (superior) part of the labrum anchors one of the two tendons of the biceps muscle. The feature that makes SLAP possible is the way the upper biceps tendon hooks over the head of the humerus. If the arm is forcefully bent inward and twists at the shoulder, the humeral head acts as a lever and tears the biceps tendon and labrum glenoid bone in a front-to-back (anterior-posterior) direction. And that is how the name SLAP is derived - Superior Labrum Anterior-Posterior or, in plain English, Upper Rim Front-Back.  cartilage from the

 

SLAP area and SLAP Lesion - pull-off of the Biceps origin (superior labrum) from the glenoid.

Causes and Risk Factors

Often an initial forceful movement of the labrum attached to the biceps tendon to be torn away from the bone (glenoid). This may be associated with a dislocation of the joint, but commonly occurs in athletes and workers with a pull on the arm, weightlifting, throwing injury or tackle. Laborers can tear the labrum with a slip and fall while holding on a railing with the injured arm.  If the initial condition does not heal properly, pain will result and worsen over time.

The typical symptoms are pain at the top of the shoulder, clicking and pain with overhead activities. These may be confused with AC Joint problems , but athletes with SLAP tears have pain with eccentric biceps loading (such as going down in a bench press). AC Joint pain is usually felt when pressing out at the end of a shoulder or bench press.

Risk Factors: Overhead and contact sports pose a greater risk of labral tears (SLAP lesions).  Workers performing heavy lifting or pulling tasks are also at risk.  Sudden traction injuries to the arm are common causes of SLAP lesions.

Types of SLAP Tears - Depending on the type and severity of injury, the labrum will tear in different ways and degrees. These are classified as a guide to treatment.

If you have been diagnosed with a SLAP tear, your surgeon may have called it a 'Type 1 or 2 or 3, etc'. SLAP tears have been classified according to their severity of tear. Please note that it does not mean that the outcome of surgery is worse, it just gives us surgeons a guide to management and a form of communication. The common types are types 1 to 4. There are other types, but these are rare. 

SLAP Type 1

This is a partial tear and degeneration to the superior labrum, where the edges are rough and fray along the free margin, but the labrum is not completely detached.

Treatment is usually to 'debride' (clean) the edges. 

 

SLAP Type 2

Type 2 is the commonest type of SLAP tear. The superior labrum is completely torn off the glenoid, due to an injury. This type leaves a gap between the articular cartilage and the labral attachment to the bone. Type 2 SLAP tears can be further subdivided into (a) anterior (b) posterior, and (c) combined anterior-posterior lesions.

Treatment is reattachment of the labrum (SLAP repair). This is done arthroscopically using suture anchors.  Recent data suggests that type 2 SLAP lesions do very well with a debridement and biceps tenodesis rather than repair of the labrum. Tenodesis seems to be associated with a lower rate of complications and a faster return to work.  Many shoulder surgeons limit SLAP repairs to overhead throwing athletes.  

 

SLAP Type 3

A Type 3 tear is a 'bucket-handle' tear of the labrum, where the torn labrum hangs into the joint and causes symptoms of 'locking' and 'popping' or 'clunking'.

Treatment usually involves removal of the 'bucket-handle' segment and then repair of any remaining detached, unstable labrum (SLAP repair). This is done arthroscopically using suture anchors.

Biceps tenodesis seems to be associated with a lower rate of complications and a faster return to work.  Many shoulder surgeons limit SLAP repairs to overhead throwing athletes.   

  

SLAP Type 4

The Type 4 SLAP tear is one where the tear of the labrum extends into the long head of biceps tendon.  Treatment is reattachment of the labrum (SLAP repair) and repair of the biceps tear, or a biceps tenodesis. This is done arthroscopically using suture anchors.

Prevention of SLAP lesions


Strong shoulder muscles remain the best defense against shoulder injuries. Exercises that build up these muscles around the shoulder should be done. Adequate warm-up before activity and avoidance of high-contact sports will help prevent of an instability-causing injury.

Treatment
 
Painkillers and anti-inflammatories - help control the pain.

Physical therapy can be helpful is some cases of SLAP lesions and should be considered if shoulder motion is limited or if there is weakness of the shoulder related to the initial injury.

Surgery may be recommended if an patient wants to continue their work, sports and training - SLAP lesions are sometimes repaired by arthroscopically through 2 or 3 small incisions. Some SLAP lesions can be simply debrided and cleaned, while most need repairing depending on the severity of the lesion. The associated lesions are also treated such as labrum and ligament lesions with instability.

You can see an animation of a SLAP repair on my website here.  Go to the shoulder section and select SLAP repair.


Try this link as well for a SLAP repair.

Recent data and reports suggests that the only patients who should have their SLAP lesion repaired should be overhead throwing athletes.  Other with SLAP lesions seem to have superior outcomes with an arthroscopic debridement and tenodesis of biceps tendon.

Biceps Tenodesis  

In this procedure the long head of the biceps tendon is detached from it's attachment in the shoulder and reattached to the humerus bone just below the shoulder. This procedure is more complex than a tenotomy, but avoids the risks of biceps discomfort (rare), and a 'popeye' appearance of the biceps muscle. Weakness is usually not a problem after biceps tenotomy.

Tenodesis, rather than tenotomy, may be preferable for more active, younger, thinner patients and those concerned about the appearance of the arm after surgery. Using modern fixation screws the repair is strong enough to move the arm early after surgery, without immobilization.

---

The Procedure:

1. The long head of the biceps tendon is released via the arthroscope:
 
arthroscopic scissors inserted via small puncture hole in skin and cutting the long head of biceps (arthroscopic view on the right).

2. A small incision (5cm) is made over the front of the shoulder and the tendon retrieved through this hole:

3. The tendon is fixed back into the bone of the humerus with a special interference screw:
 

Information before your surgery

You must not eat or drink anything after midnight the day before your surgery. When you wake up following the procedure you will be wearing a sling with a body belt. The sling should be worn for a few days to up to 6 weeks depending on the procedure performed and the time required for healing.

You will probably not be in hospital overnight after your operation, and should be able to go home about 4 hours after the surgery. Your may be given some exercises on your post operative discharge instructions and instructions on when to begin them.

At your first post operative visit in the office, I will review the procedure performed and your restrictions.  You should also prepare to see the physical therapist in the office who will teach you the appropriate exercises. You will need physiotherapy after the surgery and should return to your own therapist. 

Pain


A nerve block is usually used during the surgery. This means that immediately after the operation the shoulder and arm often feel completely numb. This may last for a few hours. After this the shoulder may well be sore and you will be given painkillers. These can be continued after you are discharged home. Ice packs or a cold compression wrap may also help reduce pain. Wrap crushed ice or frozen peas in a damp, cold cloth and place on the shoulder for up to 15 minutes. Ensuring you cover the wound site with a piece of gauze and tape to keep the area dry.

Wounds

This arthroscopic operation is usually done through two or three 5mm puncture wounds. There may be stitches under the skin and there may be paper strips over the wounds.  These can be kept dry until healed. In some cases, I will give you permission to shower and get the wounds wet after surgery.  It depends on the size of the incision.

Sleeping

For the first 3 - 6 weeks your sling must be worn in bed. Sleeping can be uncomfortable if you try and lie on the operated arm. We recommend that you lie on your back or on the opposite side, as you prefer.  

Sleeping in a reclined position in a reclining chair or on a couch surrounded by pillows is usually the most comfortable position.   

Ordinary pillows can be used to give you comfort and support. If you are lying on your side one pillow slightly folded under your neck gives enough support for most people. A pillow folded in half supports the arm in front and a pillow tucked along your back helps to prevent you rolling onto the operated shoulder during the night. If you are lying on your back, tie a pillow tightly in the middle (a "butterfly pillow") or use a folded pillow to support your neck. Place a folded pillow under the elbow of the operated arm to support that.

 

Follow up appointments

An appointment will be made for you to see the me in the office on the first office day after surgery. 

Daily activities

After a SLAP repair, for the first three weeks all activities of daily living for example feeding, dressing, cooking etc must be carried out using your un-operated arm. If appropriate an physical therapist will be available to give you advice on how to do this. Activities may also be limited for as long as 6 weeks after a repair.  My patients usually see the therapist at the first post op visit the day after surgery.

If you had a SLAP debridement and biceps tenodesis (reattachment of the biceps to the upper humerus), I usually allow patients to move the shoulder immediately after surgery.  You may not use the operative arm / hand to lift or pull anything since this may result in a rupture of the biceps tenodesis.  Moving the shoulder is permitted.  

If you had a SLAP debridement and biceps tenotomy (biceps cut and released and not repaired), you may use the arm as tolerated without restrictions immediately after surgery.  You activities are limited by you pain.

 

Your physical therapist and surgeon will advise you when it is safe to resume your leisure activities. This will vary according to your sport and level, as well as the period required to retrain your shoulder muscles with physical therapy.

  

Driving

You may not be able to drive for a minimum of 4 weeks. Your surgeon will confirm when you may begin. 

Return to work

This will depend upon whether the SLAP lesion was repaired, which requires additional healing time or whether a SLAP debridement and biceps tenodesis was performed. 

In my experience, patients may return to work sooner if they have had a debridement and tenodesis or tenotomy than those who have had a SLAP repair.  Patients having a SLAP repair seem to develop more stiffness and more post op discomfort than those having tenodesis of tenotomy.

You will need to discuss this with your surgeon.

Reference, adapted from one of the best shoulder sites on the web, www.shoulderdoc.co.uk.

Thanks for the reminder and permission, Prof. Funk.



Thanks,

JTM, MD

Nutrient-Dense Diet May Reduce Risk for Low-Trauma Fracture

Since the recent post have been about calcium and vitamin D as it relates to bone health, I thought one more related article could not hurt.

A nutrient-dense diet high in vegetables, fruit, and whole grains may reduce the risk for low-trauma fracture, particularly in older women, according to the results of a retrospective cohort study reported online November 10 in the American Journal of Clinical Nutrition.

 

In 2005, 2 million fractures occurred in the United States, which were associated with 17 billion in direct costs, and these figures are expected to increase by ≥50% over 20 years. Fractures also led to long-term disability, decreased health-related quality of life, and increased mortality. Identification and treatment of individuals with low bone mineral density (BMD) can reduce the burden of fracture, [but] alternative strategies for population health are necessary because many individuals who fracture do not have a low BMD.

Using a randomly selected, population-based cohort enrolled in the Canadian Multicentre Osteoporosis Study, the investigators aimed to determine the association between dietary patterns and incident fracture and to evaluate whether body mass index (BMI), BMD, or falls affected this relationship. In year 2 of the study (1997-1999), they used self-administered food frequency questionnaires to evaluate dietary patterns. The main study endpoint was low-trauma fracture occurring before the 10th annual follow-up in 2005 to 2007.

Factor analysis revealed 2 dietary patterns: nutrient dense, which emphasized intake of fruit, vegetables, and whole grains; and energy dense, which had higher intake of soft drinks, potato chips, French fries, meats, and desserts.

In association with the nutrient-dense factor, the risk for fracture was reduced in both men overall women overall.  No associations with fracture were identified for the energy-dense pattern.

Conclusion

 

A diet high in nutrient-dense foods (vegetables, fruits, whole grains) may reduce the risk of low-trauma fracture, especially among older women, the study authors conclude.  Because older women are also at the highest risk of fracture, population measures to encourage increased intake of fruit, vegetables, and whole grains have the potential to lower the population burden of fracture, including hip fracture. Few recent studies have assessed dietary patterns related to fracture outcomes. The results here are complementary to those of studies that assessed the relation of specific foods and nutrients, because synergistic effects of food combinations might exist.

Reference

 

Am J Clin Nutr. Published online November 10, 2010. Abstract

So, I guess the message here is to eat your fruits and vegetables.  I am off to search for more earth shattering information for the newsletter.

Thanks,

JTM, MD 

Calcium and Vitamin D

Previous postings have review the intake of calcium and vitamin D.  Here is a summary of some of the recommendations.

Calcium citrate (not calcium carbonate):  1000mg per day

Calcium carbonate will not be absorbed if you are taking medications to reduce stomach acid.  The carbonate needs stomach acid to be broken down and absorbed.

Current daily requirements of Calcium

Child:   700mg

Teen-Young adult:   1300mg

Adult:   800mg

Pregnancy:   1500mg

Lactation (breast feeding):   2000mg

Post menopausal:   1500mg

Major fracture:   1500mg

Vitamin D3:   2000 units per day.  

There seems to no disadvantage and there may even be a benefit to more Vitamin D.

Vitamin C:   500mg per day.

Thanks,

JTM, MD

The Evolving Role of Obesity in Knee Osteoarthritis

Here is an adapted review of a study on the effect of obesity on knee osteoarthritis.  I see a many patients in the office with knee arthritis.  Many are significantly obese.  Obese patients may not do as well with treatments provided for knee osteoarthritis.  Complications from total knee replacements are more common in obese patients as well. When counseling patients, part of the discussion about the treatments for their arthritis will include weight loss. 

The frequency of knee osteoarthritis continues to accelerate, likely because of the increasing proliferation of obesity, particularly in men and women 40–60 years of age at the leading edge of the 'baby boom' demographic expansion. The increasing pervasiveness of obesity and the growing appreciation of obesity's accompanying metabolic/inflammatory activities suggest rethinking the knee osteoarthritis paradigm.

Whereas once knee osteoarthritis was considered a 'wear-and-tear' condition, it is now recognized that knee osteoarthritis exists in the highly metabolic and inflammatory environments of body fat. 

Cytokines associated with adipose tissue, including leptin, adiponectin, and resistin, may influence osteoarthritis though direct joint degradation or control of local inflammatory processes. Further, pound-for-pound, not all obesity is equivalent for the development of knee osteoarthritis; development appears to be strongly related to the co-existence of disordered glucose and lipid metabolism. Additionally, obesity loads may be detected by mechanoreceptors on chondrocyte surfaces triggering intracellular signaling cascades of cytokines, growth factors, and metalloproteinases.

This review summarizes recent literature about obesity, knee osteoarthritis and joint pain. Consideration of adipocytokines, metabolic factors, and mechanical loading-metabolic factor interactions will help to broaden the thinking about targets for both prevention and intervention for knee osteoarthritis.

Before continuing with the posting, you can calculate you body mass index (BMI) here.

Introduction

Osteoarthritis is a highly prevalent joint disorder estimated to affect more than 37% of adults over the age of 60; it is a leading cause of pain and disability. Osteoarthritis is associated with considerable loss in productivity and health care expenditures, accounting for 97% of the total knee replacements and 83% of the total hip replacements in 2004. Using national data, the Healthcare Cost and Utilization Project showed that osteoarthritis accounted for US$ 10.5 billion in hospital charges in 2006, making it a more expensive condition than pneumonia, stroke, or complications from diabetes. Hospital admissions for arthritis more than doubled from 1993 to 2006.
 
The frequency of knee osteoarthritis continues to accelerate, likely because of the aging of the population and the increasing proliferation of the primary risk factor, obesity. There is an increasingly greater proportion of the total population, both in the United States and worldwide, over age 60, the age range typically associated with having osteoarthritis. Although the prevalence of obesity is rising in this elderly segment of the population, it is the escalating prevalence of obesity in those men and women aged 40–60 years, who are simultaneously at the leading edge of the baby boomer demographic expansion, that are the major contributors to the burgeoning osteoarthritis population.

Obesity has long been recognized as a risk factor for prevalent osteoarthritis, especially knee osteoarthritis although the obesity definition based on a BMI (body mass index) more than 30 kg/m² was not widely adopted until the 1990s. 

Data from a British study suggested that women with the highest BMI had six-fold increased odds of knee osteoarthritis (OAK) and nearly 18 times higher odds of bilateral OAK, compared with women with the lowest BMI. Similarly, a study of US African-American and Caucasian women identified higher risk of prevalent knee osteoarthritis with higher BMI levels. Researchers reported that for every standard deviation increase in BMI (3.8 kg/m²), there was a 40% increased risk for developing osteoarthritis of the knee. Studies show that increased weight precedes the presentation of osteoarthritis of the knee.

How does Obesity Increase the Likelihood of having Knee Osteoarthritis?

Because of the magnitude of obesity as a risk factor for osteoarthritis, especially knee osteoarthritis, as well as the growing prevalence of obesity, including morbid obesity, there is new effort being developed to understand how obesity increases the likelihood of having knee osteoarthritis. These efforts have as their long-term goal the development of focused prevention and intervention efforts. However, not all obese persons develop knee osteoarthritis, nor are all individuals with knee osteoarthritis obese. 

Osteoarthritis, Obesity, and Adipocytokines

Rheumatoid arthritis has long been recognized as having a vigorous inflammatory component, and as a result, some treatments were directed at modulating the deleterious elements of that inflammatory response. In contrast, osteoarthritis was considered a 'wear-and-tear' condition with a minimal inflammatory response. However, this framework for considering osteoarthritis, especially knee osteoarthritis, is now shifting with the increasing pervasiveness of obesity and the recognition of the inflammatory reaction associated with obesity. Fat tissue, once considered a passive storage portal of energy, is now recognized as a highly metabolic endocrine organ with the capacity to secrete active agents including adipocytokines, such as leptin, resistin, and adiponectin. Over the past decade, interest in these adipocytokines has quickly become an area of intense study with respect to osteoarthritis based on evidence that they may play an important role in cartilage metabolism.

Leptin, adiponectin and resistin levels have been detected in the joint fluid and plasma of patients with osteoarthritis.  Leptin, adiponectin, and resistin are thought to influence osteoarthritis through direct joint degradation or through control of local inflammatory processes.

Leptin is generally higher in obese individuals; the extremely high amounts of circulating leptin have led investigators to suggest a leptin resistance syndrome as a parallel concept to insulin resistance. BMI and body weight are consistently associated with leptin levels among those with osteoarthritis. Leptin and its receptor have been identified in human tissue that make both bone and cartilage.

Examination of cartilage, subchondral bone, and the bone spurs associated with arthritis show evidence of increased leptin levels.  Increased leptin levels have been directly associated with the degree of cartilage degeneration. 

Inflammation is an important hallmark of osteoarthritis, and the adipocytokines may be important in the creation of the inflammatory processes. Leptin and resistin levels may be associated with the promotion of inflammation but adiponectin appears to reduce production of pro-inflammatory cytokines.  

Osteoarthritis, Obesity, and Metabolic Factors

In addition to the adipocytokines, obesity may generate other systemic effects related to osteoarthritis, including abnormal glucose and fat metabolism. Metabolic changes resulting from insulin resistance and increased glucose load are closely related to proinflammatory cytokine production, characteristic of a chronic inflammatory state.

A recent report considered both obesity status and cardiac risk factors. Mid-aged women who were obese (defined as BMI ≥30 kg/m²) and had two or more cardiovascular risk factors had more than six times increased odds of having prevalent knee osteoarthritis as compared with nonobese women without cardiac risk factors.

Osteoarthritis, Obesity, and Mechanical Loading

Obesity has the potential for a major impact metabolically in the presentation of osteoarthritis while concurrently contributing to a major mechanical load on the joint. Studies of joint loading have provided evidence that abnormal loads can lead to changes in the composition, structure, and mechanical properties of joint cartilage. These abnormal loads have been attributed to obesity, joint instability, or trauma. 

Muscle forces are a major determinant of how loads are distributed across a joint surface. Decreasing the muscle forces (as a result of inactivity or age related weakness) acting about a joint or misaligned joints will ultimately change the mechanical forces on the knee. Failure by the quadriceps (the thigh muscle) to adequately absorb forces about the knee can cause greater dynamic loads being placed on the joint cartilage, resulting in progressive degeneration. As a result, quadriceps weakness has been shown to be an important risk factor for osteoarthritis in some studies.

^{This makes a case for physical therapy as a potential treatment for certain types of arthritis in certain patients.}
 
Loss of muscle strength may reduce the shock-absorbing potential of the joint, thereby causing cartilage breakdown.  Changes to the cartilage structure may initiate a local immune response, resulting in systemic inflammatory responses throughout the joint. Increased loading on the knee joint may be detected by mechanoreceptors on the surface of cartilage cells; this may trigger release of cytokines, growth factors, and other chemicals which break down cartilage.  
 
The role of body composition, however, is not unique to the compartment representing skeletal muscle mass. Some researchers have suggested that loss of muscle is the primary event for osteoarthritis onset, but this then contributes to fat gain, which then reinforces further muscle loss. The process of fat gain and muscle loss may act simultaneously within and around the joint to not only initiate joint damage, but also allow further progression through the effects of insulin and inflammation.

This is an abridged version of  an article modified for increased patient understanding from Current Opinion in Rheumatology.


In my experience, patients with arthritis have a hard time exercising in order to lose weight.  Studies have shown that even after a knee replacement, when their knee pain has been relieved, they remain unable to lose the weight.  This can lead to continued pain despite a technically well done knee replacement.


Thanks,


JTM, MD

Vitamin D and Bone Health

Vitamin D plays an important role in protecting your bones. It may also help prevent other conditions including certain cancers. Your body requires vitamin D to absorb calcium. Children need vitamin D to build strong bones, and adults need it to keep bones strong and healthy. When people do not get enough vitamin D, they can lose bone. Studies show that people with low levels of vitamin D have lower bone density or bone mass. They are also more likely to break bones when they are older. Vitamin D also appears to play a role in reducing the risk of certain cancers, autoimmune conditions, cardiovascular disease and other health problems.

Severe vitamin D deficiency is rare in the United States. It can cause a disease known as osteomalacia where the bones become soft. In children, this is known as rickets. These are both different conditions from osteoporosis.

National Osteoporosis Foundation Recommendations for Vitamin D

NOF recommends that adults under age 50 get 400-800 International Units (IU) of vitamin D every day, and that adults age 50 and older get 800-1,000 IU of vitamin D every day. Some people need more vitamin D.

There are two types of vitamin D supplements. They are vitamin D² and vitamin D³. Previous research suggested that vitamin D³ was a better choice than vitamin D². However, more recent studies show that vitamin D³ and vitamin D² are equally good for bone health. Vitamin D³ is also called cholecalciferol. Vitamin D² is also called ergocalciferol.

Experts disagree on the safe upper limit for vitamin D. In the past, experts said that people should not get more than 2,000 IU of vitamin D per day. Because of recent studies, some experts now say that a much higher amount is safe. It is difficult to get too much vitamin D unless a person is taking a prescription dose (usual dose 50,000 IUs once a week). In that case, healthcare providers can easily monitor a patient’s vitamin D level with a blood test to make sure they aren’t getting too much of the vitamin. Problems associated with getting too much vitamin D are very rare.

Sources of Vitamin D

There are three ways to get vitamin D:

• Sunlight
• Food
• Supplements and medications

Sunlight

Your skin makes vitamin D from the ultra-violet light (UVB rays) in sunlight. Your body is able to store the vitamin and use it later. The amount of vitamin D your skin makes depends on time of day, season, latitude, skin pigmentation and other factors. Depending on where you live, vitamin D production may decrease or be completely absent during the winter. It is difficult to measure the amount of vitamin D that your skin makes.
People with fair skin make more vitamin D than people with darker skin. People who live in higher latitudes such as New York, instead of lower latitudes such as Florida, may get less vitamin D from sunlight. Window glass and air pollution also decrease the amount of vitamin D that your skin can make.

 

 People who are housebound and do not get outside in the sun are unable to make vitamin D. As adults age, the ability to make vitamin D also decreases. Because of concerns about skin cancer, many people stay out of the sun, cover up with clothing and use either sunscreen or sunblock to protect their skin. Probably the most important factor which limits the ability of the skin to make vitamin D is the use of sunscreen and sunblock. Even an SPF (sun protection factor) of 8 reduces the production of vitamin D by 95 percent. These products help protect the skin from the harmful effects of the sun. Because of the cancer risk from staying in the sun, many people need to get vitamin D from other sources.

Food

Vitamin D is naturally available in only a few foods. It is very difficult to get all the vitamin D you need from food. Foods that have vitamin D include fatty fish (examples are mackerel, salmon and tuna). Vitamin D is also added to milk and to some brands of other dairy products, orange juice, soymilk and cereals.
Check the food label to see if vitamin D has been added to a particular product. One eight ounce serving of milk usually has 25% of the daily value (DV) of vitamin D. The DV is based on a total daily intake of 400 IUs of vitamin D. Therefore a serving of milk with 25% of the DV of vitamin D contains 100 IUs of the vitamin.

Supplements and Medications

Many people do not get enough vitamin D. These individuals should consider taking a supplement. Before adding a vitamin D supplement, check whether any supplements, multivitamins or medications you already take contain vitamin D. You can also estimate the amount of vitamin D that you get from foods.
Subtract the total amount of vitamin D you are already getting each day from the total amount you need to get each day. For example, a 55 year old woman who gets 400 IUs of vitamin D from her calcium supplement should take between 400 and 600 additional IUs of vitamin D to meet the 800-1,000 IUs of vitamin D that is recommended for her age.
Vitamin D supplements can be taken with or without food. While your body needs vitamin D to absorb calcium, you do not need to take vitamin D at the same time as a calcium supplement. If you need help choosing a vitamin D supplement, ask your healthcare provider or pharmacist to recommend one.

People Who May Not Get Enough Vitamin D

In the U.S. today, many people do not get enough vitamin D. People most likely at risk for not getting enough vitamin D include:

• older adults
• people who spend little time in the sun
• people living in nursing homes or other institutions
• people with certain medical conditions such as serious diseases of the nervous or digestive systems
• people with very dark skin
• obese or very overweight people

It’s important to be aware that many people can have low vitamin D levels regardless of their age, health status and some of the other factors listed above.

How to find out if you’re getting enough vitamin D

You can find out if you’re getting enough vitamin D for your body’s needs by having a simple blood test that checks your vitamin D level.
Discuss with your healthcare provider whether you should have this test done. It measures 25-hydroxyvitamin D, which is also written as 25(OH)D. This test should not be confused with a test for 1,25-dihydroxy-vitamin D.

To protect your bone health, most experts agree you need one of the following levels of 25(OH)D:

• 75 nmol/L or higher
• 30 ng/mL or higher

If you have osteoporosis and your blood test shows that you do not have enough vitamin D, your healthcare provider may prescribe a higher dose of vitamin D. In this case, most people take a weekly dose of 50,000 IUs of vitamin D2 until the blood level increases. Most healthcare providers do this for a short time to quickly boost the vitamin D level. After you get your vitamin D level up, you will still need to take a vitamin D supplement. The amount of vitamin D needed to maintain a normal vitamin D level can vary from person to person. Ask your healthcare provider how much vitamin D you should take.

In general, we can make the following recommendations, assuming you are in good health.


Calcium citrate (not calcium carbonate):  1000mg per day

Calcium carbonate will not be absorbed if you are taking medications to reduce stomach acid.  The carbonate needs stomach acid to be broken down and absorbed.

Vitamin D3: 2000 units per day.  There seems to no disadvantage and there may even be a benefit to more vitamin D.

Vitamin C: 500mg per day.   



From the National Osteoporosis Foundation.


Thanks,


JTM, MD