Supraspinatus Tendonitis

Etiology

The supraspinatus tendon muscle unit sees its greatest stress forces during shoulder abduction. It acts to depress the humeral head during abduction and forward flexion positions. This depression keeps the humeral head centered on the glenoid and functions to allow for the deltoid to maintain its mechanical advantage, and thereby its power.[8] The tendon itself inserts into the most superior and anterior portions of the greater tuberosity. The insertion footprint is triangular and has a maximum footprint of 6.9 mm medial to lateral and 12.6 mm anterior to posterior.[9] The point of susceptibility is along this short tendonous insertion nearest the tuberosity underneath the acromion.[6]

Sources of rotator cuff dysfunction can include traumatic events as well as degenerative tears. As discussed above, supraspinatus tendonitis is on the spectrum of rotator cuff syndrome/dysfunction.[4] Neer's original landmark description of shoulder impingement described at-risk patients as heavy laborers, overhead laborers, or those who are anatomically predisposed.[6] Some early Finnish population data suggests about half of rotator cuffs repairs were from traumatic mechanisms, with the other half coming after tendon degeneration (the classic "wear and tear" patterns).[10] These can occur after specific injuries, including lifting events, shoulder subluxation/dislocation events, falls, or other unexpected arm loading events.  

While traumatic tears can be from a single event, Neer estimated that 95% of rotator cuff tears might find their origin in supraspinatus tendonitis associated with anatomic impingement predisposition environments. The impingement pathway supposes a slower erosive degeneration of the tendon during arm abduction and overhead lifting events. The latter describes the classic scenario now more accurately referred to as "external impingement" of the shoulder.

Indeed, several studies have challenged the previously proposed 95% external impingement pathway.  Moreover, there is some data to suggest there is a significant genetic predisposition to rotator cuff pathologies, which may predispose to rotator cuff tendonitis or tearing from either etiology.[11] With those factors in mind, it is difficult to assign exact values in a heterogeneous population, but it is reasonable to say that either pathway may contribute to the supraspinatus tendonitis continuum.

Epidemiology

The prevalence of rotator cuff breakdown is so common that the reported incidence in octogenarians is at least 50%.[12] Multiple studies detail the prevalence of rotator cuff pathology by age group.  One landmark magnetic resonance imaging (MRI) study of asymptomatic shoulders detailed that partial rotator cuff tears were present in 20% of the population, and 15% had full-thickness tearing.[13] Sher et al. reported pathology was found significantly more often in shoulders over the age of 60 years compared to younger patients.  

Owens et al. reported on the epidemiology in the military, showing subacromial impingement occurred at roughly 7.77 per 1000 person-years amongst military personnel.[14] The authors subsequently reported an age over 40 increased the risk of subacromial impingement and, therefore, may increase the risk of supraspinatus tendonitis. While it remains difficult to know the true epidemiology of supraspinatus tendonitis, we can use these data points as surrogates to potentially extrapolate and demonstrate the commonality of the rotator cuff, and therefore supraspinatus, tendonitis.  Also, it is worth noting the differentiating element of internal impingement, which classically involves the articular (as opposed to bursal) side of the posterior rotator cuff, which often presents in throwers and overhead athletes.[15][16][17]

Pathophysiology

There are multiple proposed etiologies for rotator cuff tendonitis. It is important to appreciate the difference between external and impingement mechanisms as these result in differing clinical presentations and underlying rotator cuff pathologies. 

Traditionally, Neer's hypothesis of a predictable breakdown in three stages is still commonly used.[6] He proposed a predictable breakdown in three stages: edema and hemorrhage, fibrosis and tendonitis, and eventual tendon rupture.[6] He reported that overhead activities and heavy labor might predispose a patient to this pathway. Smith et al. showed lower blood supply in pathologic supraspinatus tendons when compared to their healthy counterparts, suggesting that there may be a significant vascular component to tendon breakdown as well.[18] Some constellation of genetic predisposition, activity, and possible threshold event can lead to supraspinatus tendonitis.

History and Physical

Rotator cuff dysfunction does not always isolate the most superior aspect of the shoulder. Pain is the most common reason for presentation in rotator cuff injury, and pain lateral or anterior are the most common sites of pain in all comers.[19] The astute clinician should recognize the different potential sources of pain generators in the shoulder. For example, anterior pain may be indicative of proximal biceps tendon pathologies,[20][21][22] while anterolateral or straight lateral pain may be indicative of subacromial impingement or rotator cuff dysfunction,[5][3] and posterior shoulder pain may include, but not be limited to, degenerative conditions of the shoulder and/or referred pain from the neck.[7][20]

Patients with subacromial impingement will often complain of pain with overhead activities and may also endorse weakness. In one study, >98% of presenting patients had pain as an element of their presentation.[23] Patients may describe pain with overhead activities, feelings of weakness, sleep disturbances, and deep aching of the shoulder.

To examine the shoulder, first inspect the shoulder, as well as the scapula, for any obvious asymmetry. Evaluate for scapular winging or dyskinesia.  There may or may not be wasting about the scapula if rotator cuff pathology is present. To perform a focused examination of the supraspinatus, ask the patient to forward flex the arm. Pain at liftoff or pain at 90 to 120 degrees of active elevation may indicate rotator cuff pathology.

Furthermore, pain during active slow de-elevation of the arm may indicate cuff pathology.[23] Care is necessary to rule out adhesive capsulitis as out as a diagnosis. In this scenario, the clinician should evaluate both active and passive (supine) range of motion. In isolated supraspinatus tendinitis (or rotator cuff syndrome/dysfunction), passive ROM should be full in all planes.[7] 

The neurovascular exam should be normal in patients with isolated rotator cuff dysfunction or tendonitis. Decreased pulsed with overhead arm positioning, radicular or dermatomal sensory abnormalities, or focal weakness outside of the shoulder should raise the evaluator to look for alternate or concomitant diagnoses including cervical radiculopathy, thoracic outlet syndrome, brachial plexopathy, or peripheral nerve compression.

The Hawkins test (90 degrees forward flexion and passive significant internal rotation of the arm) may also recreate acromial contact with the inflamed bursa/tendon creating pain. Furthermore, the Jobe (or empty can) test has the patient hold their arm in 90 degrees of abduction, 30 degrees of forward flexion, and resist a downward force while in the thumbs down position.[24] Pain and/or weakness in this position may indicate supraspinatus pathology.  One can also evaluate the patient is the same manner with a thumbs up (or full can) test to further interrogate the cuff.

Some constellation of positive findings may lead to the diagnosis of subacromial bursitis, external shoulder impingement, or supraspinatus tendonitis. Weakness that is frank or painless may be more indicative of a complete supraspinatus tear, but a lack of this finding does not rule out the diagnosis. 

Evaluation

The initial evaluation of the patient complaining of shoulder pain is variable. Many patients can be diagnosed based on exam and do not require additional workup at the initial presentation. The presence of profound weakness marked swelling, erythema, or deformity should prompt a more aggressive workup. Initial imaging of the shoulder with routine radiographs including an AP, axillary lateral, true AP, and scapular-Y view may help visualize pathology about the shoulder. Furthermore, using a true supraspinatus outlet view instead of a regular scapular-Y view may improve acromial characterization.[25]

The Dutch Orthopedic Association published guidelines for treating what they refer to as subacromial pain syndrome. Their recommendations include early anti-inflammatories, injections for persistent cases, and advanced imaging (MRI) for cases lasting longer than six weeks.[26] MRI will help to quantify any partial or full-thickness tearing, as well as help characterize tendon inflammation. These recommendations may be useful in guiding an algorithmic approach to care.

In cases when the evaluator may be less certain regarding the diagnosis, an MRI of the shoulder without contrast is the best study to characterize the soft tissues. Usually, this is indicated in patients who fail a conservative treatment effort of more than six weeks, who have profound symptoms, or who have an unclear diagnosis.

Secondary impingement, which is usually associated with swimmers or overhead athletes, is a part of the constellation of symptoms of overuse and instability. There are reports regarding athletic patients who have lax shoulders, scapular dyskinesia, and train often. The mainstay of treatment in that population involves rest, physical therapy, and a gradual return to activities. It is a separate entity from degenerative shoulder pathologies and may be on the differential in a younger or more athletic population.[27]

Treatment / Management

Less than one in every four patients will require surgery even if the condition progresses to a symptomatic full-thickness tear.[28] The vast majority of patients will improve with comprehensive non-operative care, including anti-inflammatories and physical therapy. In a 2017 meta-analysis, physical therapy proved effective, as were NSAIDS (when compared to placebo), for the treatment of subacromial impingement, although the evidence was of low quality.[29] Subacromial injections with a combination of corticosteroids and a local anesthetic may provide some diagnostic and therapeutic benefit for the patient as well.[30]  (A1)

Multiple authors have debated the importance of corticosteroids beyond eight weeks.[30] If the patient does go on to need rotator cuff repair, there has been some debate about the effect of corticosteroids pre-operatively effecting the healing potential post-operatively.[31] Baverel et all suggest in their data evaluation that injections with corticosteroids may only cause increased re-rupture rates if injected after surgical repair. With that in mind, a single subacromial injection for patients who do not improve with initial NSAIDs and exercises may provide benefits. Multiple injections without advanced imaging and a discussion of the risks (tendon atrophy) are not a recommendation.(A1)

At this time, there is much debate about the surgical treatment of the supraspinatus tendonitis and its associated pathology. Some studies show good improvement with isolated subacromial decompression with or without acromioplasty.[32] Other studies state they see no role for the use of surgical intervention without the presence of a symptomatic rotator cuff tear.[26] At this point, current knowledge discourages the routine use of subacromial decompression and acromioplasty for the treatment of supraspinatus tendonitis without MRI evidence of a tear. However, surgical intervention remains a reasonable consideration and alternative once the patient has exhausted all attempts at non-operative management, and when anatomic risk factors may exist in the presence or absence of significant levels of subacromial/subdeltoid bursitis, in addition to possible partial tears in the rotator cuff tendon(s).

With regards to prognosis, a significant portion of untreated supraspinatus tendonitis may go on to rotator cuff tears. In some patients, these early changes may be subclinical and may not present until the tear has been present for some time. Keener et al. described asymptomatic shoulders with rotator cuff changes visible on ultrasound. He found that a significant portion of these patients had a rotator cuff defect that enlarged and became symptomatic over time.[33] This information about the natural history of tears leads us to believe that patients presenting with rotator cuff tendonitis may benefit from early non-surgical interventions, as mentioned above, to improve their prognosis.  

Differential Diagnosis

The differential diagnosis should include subacromial impingement, rotator cuff tear (partial versus full-thickness), bicipital tendonitis, glenohumeral arthritis, acromioclavicular arthritis, adhesive capsulitis, and calcific tendonitis.  Note that many of these occur as a continuum of supraspinatus tendonitis and can occur concomitantly. 

Complications

Complications of supraspinatus tendonitis include progression to a rotator cuff tear. Rotator cuff tears were initially described by near to be the produce of untreated impingement secondary to tendon hemorrhage and tendonitis.[6] The literature on tendonitis may also indicate that patients with multiple episodes may progress to surgery and that those patients may have some attrition of the rotator cuff noted at the time of surgery.[34] Keener et al. have discussed this at length in multiple ultrasound-based papers in asymptomatic shoulders.  When subclinical rotator cuff tendinopathy was present in these shoulders, they had a greater than 50% chance of progressing to becoming clinically symptomatic.[33]