Rotator Cuff Tendinopathy

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Rotator cuff disease (RCD) describes a wide range of shoulder issues, from simple tendon inflammation to complete tears. The condition is understood to have multifactorial causes, stemming from both extrinsic factors like mechanical impingement and intrinsic factors such as age-related degeneration within the tendon itself. This article explores the causes, natural progression, diagnosis, and management of this common source of shoulder pain and dysfunction.

Anatomy and Biomechanics

Main article: Shoulder Biomechanics

The rotator cuff is a functional unit composed of four muscles - the supraspinatus, infraspinatus, teres minor, and subscapularis - and their tendons, which envelop the humeral head. Its primary biomechanical function is to stabilize and depress the humeral head within the glenoid fossa, providing a stable center of rotation for arm movements.

This stability is maintained by two critical force couples: the coronal couple, which balances the upward pull of the deltoid muscle against the inferior cuff muscles, and the transverse couple, which balances the forces of the anterior subscapularis and posterior infraspinatus/teres minor muscles to prevent abnormal migration of the humeral head.

Key anatomical structures contributing to stability include the rotator interval, a complex region containing the coracohumeral and superior glenohumeral ligaments which support the long head of the biceps tendon, and the rotator cable, a thick fibrous band acting as a "suspension bridge" to disperse stress away from the vulnerable rotator crescent. The integrity of these muscular and ligamentous structures, along with the balance of the force couples, is essential for normal shoulder function.

Etiopathogenesis

Rotator cuff disease (RCD) is a spectrum of conditions ranging from tendinopathy to full-thickness tears. The pathogenesis is multifactorial, involving both extrinsic compression and intrinsic degeneration of the tendon.

Extrinsic Factors

The extrinsic theory, famously proposed by Neer, suggests that impingement of the rotator cuff against the coracoacromial arch during forward elevation of the arm leads to tendinitis and subsequent tearing. Factors contributing to extrinsic compression include:

Acromial Morphology: A hooked (Type III) acromion is strongly associated with rotator cuff tears].

Other Anatomical Variants: Acromial spurs, os acromiale, and acromioclavicular joint spurs can also contribute to impingement. The lateral extension of the acromion, measured by the acromion index, is also linked to a higher incidence of cuff disease.

Intrinsic Factors

The intrinsic theory posits that degenerative changes within the tendon itself are the primary cause of rotator cuff tears. Key intrinsic factors include:

Age-Related Degeneration: The prevalence of rotator cuff tears increases with age, suggesting a normal attritional process. Histological changes such as collagen disorganization, fatty infiltration, and vascular proliferation weaken the tendon over time.

Vascularity: A "critical zone" of hypovascularity exists on the articular side of the rotator cuff, which may predispose this area to degeneration and tearing. However, some studies have questioned the significance of this hypovascular zone.

Genetic Predisposition: Evidence suggests an inherited predisposition to rotator cuff disease.

Other Risk Factors: Smoking, hypercholesterolemia, and poor posture have also been identified as contributing factors.

Natural History

Rotator cuff tears are common, with an age-dependent increase in prevalence. Many tears are asymptomatic, especially in older individuals.

Progression of Tears

Asymptomatic tears can become symptomatic over time, and this progression is often associated with an increase in tear size. Full-thickness tears are more likely to increase in size compared to partial-thickness tears. This progression is thought to be driven by increased strain on the remaining intact tendon fibers.

Chronic Pathological Changes

Chronic rotator cuff tears can lead to several irreversible changes:

Tendon Retraction and Adhesions: The torn tendon can retract and form adhesions, making surgical repair more challenging.

Fatty Infiltration and Muscle Atrophy: Disuse of the torn muscle leads to fatty infiltration and atrophy, which are associated with higher rates of repair failure and are generally not reversible, even after successful surgery. Tear size is a significant determinant of fatty degeneration.

Glenohumeral Joint Degeneration: Chronic, large tears can lead to rotator cuff tear arthropathy, a condition characterized by degenerative changes in the glenohumeral joint and superior migration of the humeral head.

Clinical Presentation

The most common symptom of RCD is pain, typically in the anterolateral shoulder and arm, especially with overhead activities. Night pain is also a frequent complaint. Weakness and loss of motion may be due to pain or true muscle dysfunction.

Inspection may reveal atrophy of the supraspinatus and infraspinatus muscles. Comparing active and passive range of motion can help differentiate RCD from conditions like adhesive capsulitis.

Several clinical tests can aid in diagnosis:

Pain Provocation Tests:

Painful Arc Test: Pain between 60° and 120° of abduction is suggestive of subacromial impingement or a rotator cuff disorder. It is a valuable test for detecting RCD, with a positive likelihood ratio of 3.7.
Hawkins and Neer Tests: These tests are commonly used but have limited diagnostic value on their own.

Strength Tests:

External and Internal Rotation Lag Tests: A positive result on these tests is highly indicative of a full-thickness tear. The internal rotation lag test, when normal, is particularly useful for ruling out a full-thickness tear.
Drop Arm Test: A positive result increases the likelihood of RCD.

Composite Tests:

External Rotation Resistance Test: This test, which is positive if it elicits either pain or weakness, is accurate for detecting RCD.

No single test is definitive, and a combination of findings improves diagnostic accuracy.

Investigations

Ultrasonography: US is a valuable, non-invasive tool for visualizing rotator cuff tendons. It has good sensitivity and specificity for both partial and full-thickness tears and can also detect fatty infiltration. However, its accuracy is operator-dependent.

Magnetic Resonance Imaging: MRI is considered the gold standard for diagnosing rotator cuff tears, providing excellent detail on tear size, location, retraction, and associated pathologies like fatty infiltration and muscle atrophy. MR arthrography, involving the injection of contrast material into the joint, can enhance the visualization of rotator interval structures

Management

Treatment for RCD ranges from non-operative management to various surgical interventions. The choice of treatment depends on factors such as tear type, patient age, activity level, and symptom severity.

Non-Operative Management

Non-operative treatment is the initial recommendation for most patients with RCD and includes:

Physical Therapy: A structured rehabilitation program focusing on pain control, range of motion, and strengthening of the rotator cuff and scapular muscles is a cornerstone of conservative management.
Medications: Analgesics and NSAIDs can help manage pain and inflammation.
Injections: Subacromial corticosteroid injections can provide short-term pain relief.

Many patients with RCD, including those with full-thickness tears, can achieve satisfactory function with non-operative treatment. However, there is a risk of tear progression and the development of chronic changes, particularly in younger, more active individuals with larger tears.

See physiotherapy protocol by Roberta Ainsworth for massive rotator cuff tears.^[1]

Surgical Management

Surgical intervention is considered for patients who fail to improve with non-operative treatment, or for those with acute traumatic tears. Surgical techniques have evolved from open procedures to minimally invasive arthroscopic repairs. A recent pragmatic randomized trial found that for RCD overall, non-surgical and surgical treatments provided equivalent improvements in pain and function at a two-year follow-up. However, for patients with full-thickness tears who did not improve with initial rehabilitation, surgery yielded superior outcomes in terms of pain relief and functional improvement.^[2]

Partial-Thickness Tears (PTT):

Debridement: For low-grade PTTs (less than 50% thickness), arthroscopic debridement can yield good results.
Repair: For higher-grade PTTs, repair is often recommended. This can be done via a trans-tendon technique or by converting the PTT to a full-thickness tear and then repairing it. Both methods have shown comparable and effective outcomes.

Full-Thickness Tears (FTT):

The goal of FTT repair is to anatomically reattach the torn tendon to its footprint on the greater tuberosity.

Repair Techniques:

Single-Row (SR) Repair: This involves placing a single row of suture anchors at the footprint. It is a simpler, quicker, and less expensive technique.
Double-Row (DR) Repair: This technique uses two rows of anchors to create a larger, more anatomical footprint restoration. DR repair is biomechanically stronger and has shown lower re-tear rates, especially for larger tears.
Transosseous-Equivalent (TOE) Repair: This is a suture-bridge technique that compresses the cuff over the footprint, potentially preserving tendon vascularity. TOE repairs have shown excellent biomechanical properties and low re-tear rates.

Tear Pattern and Repair Strategy: The geometric shape of the tear influences the repair strategy:

Crescent-Shaped Tears (Type 1): These short, wide tears are typically repaired directly to the bone with good to excellent prognosis.
Longitudinal (L- or U-shaped) Tears (Type 2): These long, narrow tears are best managed with side-to-side margin convergence to reduce strain before fixing the converged margin to the bone.
Massive Contracted Tears (Type 3): For these large, immobile tears, techniques like interval slides or partial repair may be necessary.
Rotator Cuff Arthropathy (Type 4): These are irreparable tears associated with significant glenohumeral arthritis, often requiring arthroplasty.

Subacromial Decompression (Acromioplasty): The routine performance of acromioplasty during cuff repair remains controversia. While it can improve visualization and may be beneficial for hooked acromions, its routine use is not supported by strong evidence, as studies have shown similar outcomes with and without the procedure.

Post-Operative Rehabilitation and Healing

Rehabilitation after rotator cuff repair is critical for a successful outcome. The process typically involves a period of immobilization followed by a gradual progression of passive and active range of motion, and finally, strengthening exercises.

The timing of mobilization is a subject of debate. While early mobilization may prevent stiffness, it also carries a risk of re-tear, especially for larger repairs. Several studies have shown that both early and delayed rehabilitation protocols can lead to comparable long-term outcomes, though some evidence suggests that a more cautious, delayed approach may lead to better structural healing.

Healing of the repaired tendon to the bone is a slow biological process, and the repaired tissue does not fully replicate the native tendon-to-bone insertion. Several factors can negatively affect healing, including:

Patient Factors: Advanced age, smoking, diabetes, and osteoporosis are associated with poorer healing.
Tear-Related Factors: Larger tear size, multiple tendon involvement, significant retraction, and advanced fatty infiltration and muscle atrophy are all predictors of poorer healing outcomes.