Rotator Cuff Tendonitis

Etiology

While subacromial impingement syndrome (SIS) is the most common cause of shoulder pain, rotator cuff (RC) tendonitis is often seen in association with shoulder impingement. Rotator cuff tendonitis can present in the acute setting following injury or, chronically, as a result of repetitive overuse activities or sport-related demands.[1][2][3] 

Acute Rotator Cuff Tendonitis

Acutely, rotator cuff tendonitis afflicts athletes at all levels of competition. Acute injuries often occur secondary to direct trauma to the shoulder in contact sports, poor throwing mechanics in overhead sports (i.e., baseball, javelin throwers), or from falls on an outstretched arm.[1]

Chronic Rotator Cuff Tendinopathy

Chronically, rotator cuff tendinopathy can occur secondary to a variety of proposed mechanisms:

Extrinsic compression

The extrinsic theory of mechanical impingement and pathologic contact between the undersurface of the acromion and the rotator cuff results in repetitive injury to the cuff. Rotator cuff tendinopathy results in weakened areas of the cuff, eventually resulting in PTTs and/or FTTs. The mechanical compression can occur secondary to a degenerative bursa, acromial spurring, and predisposing acromial morphologies (i.e., the hooked-type acromion). Theories were popularized and modified by Watson-Jones, Neer, and Bigliani.[2][4][5]

Intrinsic mechanisms

Several theories exist to support intrinsic degeneration of the cuff as the primary source of shoulder impingement. In general, the intrinsic degenerative theories cite that cuff degeneration eventually compromises the overall stability of the glenohumeral joint. Once compromised, the humeral head migrates superiorly, and the subacromial space decreases in size. Thus, the cuff becomes susceptible to secondary extrinsic compressive forces, ultimately leading to cuff degeneration, tendinopathy, and tearing.[2][6]

• Vascular changes - Advocates for intrinsic degenerative theories cite focal vascular adaptations that occur secondary to age-related changes and intrinsic cuff failure from repetitive eccentric forces directly experienced by the cuff itself. Lohr et al. initially demonstrated a distal area of the supraspinatous tendon on the articular side that lacks blood vessel supply 1 cm proximal to its insertional footprint.[7] Rudzki et al. demonstrated an age-dependent manner of increasing hypovascular regions in these distal cuff regions as well.[8] Controversy proposed by other studies, however, supports that the attritional areas develop secondary to the preceding impingement mechanisms. Subsequently, external impingement (EI) leads to blood vessel damage, ensuing ischemia, tenocyte apoptosis, gross tendinopathy, and attritional cuff damage.[2] Furthermore, many studies cite increased vascularity in focal areas of the cuff, and the hypervascularity has been associated with age-related changes, tendinopathy, and PTTs and/or FTTs.[9][10]
• Age, sex, and genetics - Histologically, age-related rotator cuff changes include collagen fiber disorientation and myxoid degeneration.[11] The literature favors increasing frequencies of rotator cuff abnormalities with increasing age. The frequency increases from 5% to 10% in patients younger than 20 years of age, to 30% to 35% in those in their sixth and seventh decades of life, topping out at 60% to 65% in patients over 80 years of age.[6][12][13]
• Tensile forces - A study by Budoff et al. proposed that the primary mode of failure of the cuff occurs intrinsically within the cuff itself as it repeatedly withstands significant eccentric tensile forces during physical activity.[14]

Epidemiology

Shoulder pain comprises the third-leading musculoskeletal complaint at physician office visits. Following spine and knee complaints, shoulder complaints account for 4.5 million visits and $3 billion in associated healthcare costs in the United States alone.[15] With a lifetime prevalence rate of 67%, shoulder pain is most commonly caused by subacromial impingement syndrome and/or rotator cuff pathologies.[2][6][12][13] Rotator cuff injuries afflict patient populations in an age-dependent fashion. Prevalence rates increase from 5% to 10% in patients younger than 20 years of age to over 60% in patients over age 80 years old.[6]

Pathophysiology

Acute rotator cuff tendonitis can occur secondary to direct blows to the shoulder, poor throwing mechanics in overhead sports, or from falls on an outstretched arm.[1]

Tendinopathy ensues after repetitive rotator cuff injury triggers a recurrent pathological cycle that results in acute on chronic tendonitis, increasing levels of tendinopathy and tendinosis, and ultimately, PTTs and/or FTTs to varying degrees of tear sizes and retraction. The exact pathogenesis of rotator cuff tears remains controversial, but most clinicians agree the underlying mechanism is comprised of a combination of extrinsic impingement from structures surrounding the cuff and intrinsic degeneration from changes within the tendon itself.[16]

Histopathology

Rotator cuff tendinopathic histologic changes include the following:[9][10][11][13][17]

• Rounded tenocytes (apoptosis)
• Extracellular matrix disorganization and myxoid degeneration
• Vascular changes (focal hypervascularity, focal hypovascular regions as well)
• Reduced total cellularity
• Calcified depositions
• Collagen fiber thinning
• Degenerative acromion, coracoacromial ligament (CAL)

History and Physical

A comprehensive history should be obtained by clinicians evaluating patients with acute or chronic shoulder pain. Characteristics of a history of potential rotator cuff injury include:

• Acute rotator cuff tendonitis: history of trauma and/or acute on chronic exacerbation
• Chronic rotator cuff tendinopathy: either acute on chronic history/mechanism or an atraumatic, insidious onset presentation
• Symptom exacerbation with overhead activity
• Pain at night

A thorough history includes current or history of sports participation (as well as specific positions played in each sport), occupational history and current status of employment, hand dominance, any history of injury/trauma to the shoulder(s) and/or neck, and any relevant surgical history.

Physical Examination Pearls

C-spine/neck exam:[18]

Coexisting cervical radiculopathy should be ruled out in any situation where neck and/or shoulder pathology is in consideration. Observation of neck posturing, muscular symmetry, palpable tenderness, and active/passive range of motion (ROM) should be evaluated. Special tests that are helpful in this regard include the Spurling maneuver, myelopathic testing, reflex testing, and a comprehensive neurovascular exam.

Shoulder exam:[2][6][19][20][21]

Clinicians must observe the overall shoulder girdle for assessment of symmetry, shoulder posturing, and overall muscle bulk and symmetry. Scapular winging should also be ruled out. The skin should be observed for the presence of any previous surgical incisions, lacerations, scars, erythema, or induration.

After the observational component of the physical examination, the shoulder should be palpated for any areas of tenderness. Classically, rotator cuff tendonitis correlates with anterolateral tenderness to palpation. Next, the active and passive ROM of both shoulders is documented. In cases of rotator cuff tendonitis, patients may demonstrate compromised active ROM but should exhibit full passive ROM. In the absence of advanced degenerative changes affecting the glenohumeral joint, limited passive ROM is considered diagnostic for adhesive capsulitis and involves a separate treatment algorithm from rotator cuff tendinopathy/impingement.

The clinician can assess motor strength grading for C5 to T1 nerve roots in addition to specific rotator cuff muscle strength testing. Specifically, rotator cuff strength and/or pathology can be determined via the following examinations:

1. Supraspinatus (SS)

• Jobe’s test: a positive test is pain/weakness with resisted downward pressure while the patient’s shoulder is at 90 degrees of forward flexion and abduction in the scapular plane with the thumb pointing toward the floor.
• Drop arm test: the patient’s shoulder is brought into a position of 90 degrees of shoulder abduction in the scapular plane. The examiner initially supports the limb and then instructs the patient to adduct the arm to the side of the body slowly. A positive test includes the patient’s inability to maintain the abducted position of the shoulder and/or an inability to adduct the arm to the side of the trunk in a controlled manner.

2. Infraspinatus (IS)

• Strength testing is performed while the shoulder is positioned against the side of the trunk, the elbow is flexed to 90 degrees, and the patient is asked to externally rotate (ER) the arm while the examiner resists this movement.
• External rotation lag sign: the examiner positions the patient’s shoulder in the same position, and while holding the wrist, the arm is brought into maximum ER. The test is positive if the patient’s shoulder drifts into internal rotation (IR) once the examiner removes the supportive ER force at the wrist.

3. Teres Minor (TM)

• Strength testing is performed while the shoulder positioned at 90 degrees of abduction, and the elbow is also flexed to 90 degrees. Teres minor (TM) is best isolated for strength testing in this position while ER is resisted by the examiner.
• Hornblower’s sign: the examiner positions the shoulder in the same position and maximally ERs the shoulder under support. A positive test occurs when the patient is unable to hold this position, and the arm drifts into IR once the examiner removes the supportive ER force.

4. Subscapularis (SubSc)

• IR lag sign: the examiner passively brings the patient’s shoulder behind the trunk (about 20 degrees of extension) with the elbow flexed to 90 degrees. The examiner passively internally rotates (IR) the shoulder by lifting the dorsum of the hand off of the patient’s back while supporting the elbow and wrist. A positive test occurs when the patient is unable to maintain this position once the examiner releases support at the wrist (i.e., the arm is not maintained in IR, and the dorsum of the hand drifts toward the back).
• Passive ER ROM: a partial or complete tear of the subscapularis can manifest as an increase in passive external rotation (ER) compared to the contralateral shoulder.
• Lift-off test: more sensitive/specific for lower subscapularis pathology. In the same position as the IR lag sign position, the examiner places the patient’s dorsum of the hand against the lower back and then resists the patient’s ability to lift the dorsum of the hand away from the lower back.
• Belly press: more sensitive/specific for upper subscapularis pathology. The examiner has the patient’s arm at 90 degrees of elbow flexion, and IR testing is performed by the patient pressing the palm of his/her hand against the belly, bringing the elbow in front of the plane of the trunk. The examiner initially supports the elbow, and a positive test occurs if the elbow is not maintained in this position upon the examiner removing the supportive force.

5. External impingement/Subacromial impingement

• Neer impingement sign: positive if the patient reports pain with passive shoulder forward flexion beyond 90 degrees.
• Neer impingement test: positive test occurs after the examiner gives a subacromial injection, and the patient reports improved symptoms upon repeating the forced passive forward flexion beyond 90 degrees.
• Hawkins test: positive test occurs with the examiner passively positioning the shoulder and elbow at 90 degrees of flexion in front of the body; the patient will report pain when the examiner passively IR’s the shoulder.

6. Internal impingement

•  Internal impingement test: the patient is placed in a supine position, and the shoulder is brought into terminal abduction and external rotation; a positive test consists of the reproduction of the patient’s pain.

Evaluation

Radiographic imaging should be obtained in all patients with acute or chronic shoulder pain.

Radiographs[2]

Recommended imaging includes a true anteroposterior (AP) image of the glenohumeral joint (i.e., the “Grashey” view). The true AP image is taken with the patient rotated between 30 and 45 degrees offset the cassette in the coronal plane. Alternatively, the beam can be rotated while the patient remains neutral in the coronal plane. The distance between the acromion and the humeral head (i.e., the acromiohumeral interval) can be calculated. A normal interval is between 7 and 14 mm, and this interval is decreased in cases of advanced degenerative arthritis and rotator cuff arthropathy (RCA).

Other radiographic imaging includes a 30-degree caudal tilt view that can be performed to visualize the presence of acromial spurring. In addition, the “scapular Y” or “supraspinatus outlet” view is used to determine acromial morphology.

Pertinent findings

The following are the most common radiographic changes associated with rotator cuff pathology:

• Rotator cuff arthropathy: Proximal humeral migration and decreases in the acromiohumeral interval to <7mm
• Degenerative findings:
• Osteophytes on the acromion, proximal humerus and/or glenoid are often seen in cases of advanced disease
• Calcification of the coracoacromial ligament (CAL) and/or coracohumeral ligament (CHL)
• Greater tuberosity cystic degeneration
• Acromioclavicular joint arthritis
• “Hooked” acromion: best appreciated on the supraspinatus outlet view
• Os acromiale: best seen on an axillary lateral radiograph

Ultrasound[6]

Ultrasound (US) is an often-underutilized imaging modality to detect rotator cuff  tendon and muscle belly integrity. In 2011, a meta-analysis of over 6,000 shoulders revealed a sensitivity of 0.96 and specificity of 0.93 in assessing shoulders for PTTs or FTTs.

Magnetic Resonance Imaging[2]

Magnetic resonance imaging (MRI) is useful in evaluating the overall degree of rotator cuff  pathology. MRI can be helpful in providing more accurate cuff tear details, including partial- versus full-thickness tears, the extent and size of the tear(s), location, and degree of retraction. In cases of chronic rotator cuff  pathology, the cuff can be assessed for fatty degenerative changes on the T1-weighted sagittal sequence series.

Subdeltoid and/or subacromial bursitis can also be evident and are important considerations as potential sources of pain. In addition, the acromioclavicular (AC) joint, acromial morphology, and long head of the biceps (LHB) tendon integrity are better appreciated. A systematic approach to reviewing shoulder MRIs is important, especially when correlating the MRI findings with the patient-reported symptoms and clinical examination.

Treatment / Management

Given the complex nature of rotator cuff tendonitis, we recommend the treatment and management be broken down into the following categories:

Group 1: Partial-Thickness (PTT) or Full-Thickness RC Tears (FTTs), Asymptomatic Patient[22](B3)

Patients presenting with MRI-evidence of PTTs or FTTs often present without any symptoms. The most recent American Academy of Orthopaedic Surgeons (AAOS) clinical practice guideline (CPG) summary reported the growing awareness of incidental rotator cuff  pathology revealed via shoulder MRIs in asymptomatic patient populations. Although there is evidence of increasing prevalence of rotator cuff  disease in the aging population, there is no reliable evidence that surgical intervention prevents tear propagation or the development of clinical symptoms. Thus, the committee recommended symptomatic management via nonoperative modalities alone.

Group 2: Partial-Thickness (PTT), Symptomatic Patients[22][23](B3)

Patients presenting with symptoms of external impingement/ subacromial impingement syndrome in the absence of FTTs are first managed with nonoperative treatment modalities. There is no agreed upon time interval when it is most appropriate to proceed with surgical intervention in this particular group of patients. The literature ranges from 3 months to 18 months. Surgical intervention should be individually tailored based on the patient’s symptoms, improvement with nonoperative modalities, and overall goals of the patient.

Group 3: Chronic RC Tears, Symptomatic Patients[22](B3)

The AAOS CPG reported a “weak” recommendation grade secondary to limited available evidence in the literature comparing rotator cuff repair (RCR) to continued nonoperative treatment modalities in this subset of patients. Certainly, the overall clinical picture must be considered, and the treatment tailored to the individual patient in each scenario.

Nonoperative Rotator Cuff Syndrome  Treatment Modalities[22][23](B3)

Physical therapy (PT)

• Physical therapy (PT) remains the mainstay of first-line treatment for RC tendonitis. Even in the setting of PTTs, patients can still be managed with PT alone.
• PT modalities include aggressive RC and periscapular stabilizer strengthening programs, as well as ROM exercises.

Anti-inflammatory medications

• First-line nonoperative management also includes the use of non-steroidal anti-inflammatory (NSAIDs) medications in conjunction with PT modalities.
• Although the AAOS CPG reported inconclusive evidence for the use of NSAIDs, iontophoresis, transcutaneous electrical nerve stimulations (TENS), and other similar therapy modalities in the presence of FTTs, the committee reported a “moderate” recommendation grade for exercises and/or NSAIDs in the presence of RCS symptoms in the absence of FTTs.

Cortisone injections

• For rotator cuff  tendonitis, the most utilized injection includes one into the subacromial space. Patients can experience symptomatic relief almost instantaneously after the injection is given, allowing them to participate in subsequent PT therapy sessions ideally.

 Rest/Activity modifications

• Patients benefit from an initial period of rest from the exacerbating activity (occupation or sport), especially repetitive overhead activity and heavy lifting.

Surgical Management

Rotator cuff syndrome surgical techniques range from debridement, subacromial decompression (SAD), and/or acromioplasty to rotator cuff  debridement and, when indicated, rotator cuff  bursal- or articular-sided tear completion with rotator cuff repair . The latter will not be discussed in this review. Assuming no rotator cuff full-thickness tears are present, the extent of surgical management for external impingement/subacromial impingement syndrome alone includes:[22][23][24](A1)

Subacromial decompression

• Extensive debridement of the subacromial space is beneficial in patients with persistent symptoms of external impingement/subacromial impingement syndrome after at least 4 to 6 months of failed nonoperative modalities.
• Comprehensive bursectomy allows for thorough and more accurate evaluation of the bursal side of the cuff itself.
• CAL debridement is recommended in the setting of substantial CAL fraying and/or calcification, as this is considered an additional source of impingement.
• A meta-analysis of 9 studies comparing open versus arthroscopic procedures yielded equivalent surgical times, outcomes, and complication rates at 1-year follow-up; the arthroscopic cohort returned to work quicker compared to the open cohort.

Acromioplasty

• Shaving the undersurface of the acromion, especially in the setting of significant spurring, improves the environment surrounding the cuff and allows additional clearance distance between the acromion and cuff itself throughout mid-arc and terminal range of motion and impingement positions.
• In the case of hooked acromion morphologies, care is taken to debride this area with a shaver, burr, or rasp to flatten the undersurface.
• The anterior extent of the acromioplasty is demarcated by the anterior deltoid origin. This area should be respected in the debridement process. The anteroinferior region of the acromion is a common site of spurring and causes impingement symptoms in these patients.

Os Acromiale

• In the case of persistent symptoms, a two-stage procedure is often utilized. First, the os acromiale is fused using bone grafting techniques, followed by a formal acromioplasty after healing is achieved.

Differential Diagnosis

The differential diagnosis for chronic shoulder pain includes several etiologies:

Impingement

• External/subacromial
• Subcoracoid
• Calcific tendonitis
• Internal (including SLAP lesions, glenohumeral internal rotation deficit (GIRD), little League shoulder, posterior labral tears)

Rotator Cuff (RC) Pathology

• Tendonitis (acute), tendinopathy (chronic or acute on chronic)
• Partial- versus full-thickness tears (PTTs versus FTTs)
• RC arthropathy

Degenerative

• Advanced degenerative joint disease, often associated with rotator cuff arthropathy
• Glenohumeral arthritis
• Adhesive capsulitis
• Avascular necrosis (AVN)
• Scapulothoracic crepitus

Proximal Biceps

• Subluxation – often seen in association with subscapularis injuries
• Tendonitis and tendinopathy

Acromioclavicular Joint Conditions

• AC joint separation
• Distal clavicle osteolysis
• AC joint arthritis

Instability

• Unidirectional instability – seen in association with an inciting event/dislocation (anterior, posterior, inferior)
• Multidirectional instability (MDI)
• Associated labral injuries/pathology

Neurovascular Conditions

• Suprascapular neuropathy – can be associated with paralabral cyst at the spinoglenoid notch
• Scapular winging – medial or lateral
• Brachial neuritis
• Thoracic outlet syndrome (TOS)
• Quadrilateral space syndrome

Other Conditions

• Scapulothoracic dyskinesia
• Os acromiale
• Muscle ruptures (pectoralis major, deltoid, latissimus dorsi)
• Fracture (acute injury or pain resulting from long-standing deformity, malunion, or nonunion)

Prognosis

The majority of patients with rotator cuff tendinopathy in the absence of FTTs improve with nonoperative management. The most recent AAOS CPGs touted a “moderate” recommendation grade for initial treatment of NSAIDs and/or exercises programs based on multiple level II studies in the literature.

Complications

Complications associated with rotator cuff syndrome are best broken down into nonoperative- versus operative-related complications:

Nonoperative Management

• Persistent pain/recurrent symptoms
• In the setting of PTTs, there is at least a theoretical risk of tear propagation, lack of healing, fatty infiltration, atrophy, and retraction
• Overall a controversial topic, a 2017 study analyzed independent risk factors for symptomatic rotator cuff tear progression over 19 months of nonoperatively managed shoulders; risk factors for tear progression included:
• The initial presence of an FTT
• Medium-sized cuff tears (1 to 3 cm)
• Smoking
• While PTTs were included in the study, the presence of a PTT was not a risk factor for cuff tear progression
• In the setting of chronic/atrophic tears, especially with rotator cuff tear propagation, degenerative joint disease and rotator cuff arthropathy  ensue

Surgical Management

• Surgical treatment tends to be most effective in patients that have failed or reported persistent or worsening symptoms despite at least 4-6 months of exhaustive nonoperative treatment modalities
• The standard risks of surgery, including recurrent pain/symptoms, infection, stiffness, neurovascular injury, and risks associated with anesthetic use
• Subacromial decompression/acromioplasty
• Deltoid dysfunction: can occur secondary to failed deltoid repair following an open acromioplasty or excessive debridement during arthroscopy
• Anterosuperior escape: occurs secondary to aggressive coracoacromial ligament  release–the coracoacromial arch and suspensory system becomes compromised, and with CAL release in the setting of massive, retracted, and irreparable RC tears, the humeral head migrates superiorly and anteriorly to compromise patient functional outcomes