Rotator Cuff Injuries

Populations and Risk Factors

• Prevalence increases with age: approximately 25% of adults over 60 and up to 50% of those over 80 have partial or full-thickness tears — many are asymptomatic (Magee & Manske, 2021)
• Overhead athletes: swimmers (shoulder of the swimmer), baseball pitchers, tennis players, volleyball players — repetitive overhead motion compresses the supraspinatus in the subacromial space during the late cocking and deceleration phases
• Occupational risk: painters, carpenters, electricians, and others performing repetitive overhead work — cumulative microtrauma exceeds tendon repair capacity
• More common in the dominant arm (increased cumulative loading)
• Age-related tendon degeneration is the strongest intrinsic risk factor — tendons lose cellularity, vascularity, and collagen organization progressively after age 40
• Acromial morphology: Type III hooked acromion has the highest association with impingement and RC tears (compared to Type I flat or Type II curved)
• Smoking: reduces tendon vascularity and impairs healing capacity
• Hypercholesterolemia and diabetes: associated with increased tendon degeneration through microvascular changes
• Acute tears may result from falls on an outstretched hand (FOOSH), forceful lifting, or sudden deceleration (e.g., grabbing a railing during a fall)

Causes and Pathophysiology

Subacromial Space Anatomy

• The subacromial space (normally 7–14 mm) lies between the acromion and coracoacromial ligament superiorly and the humeral head inferiorly. The supraspinatus tendon, subacromial bursa, and long head of biceps tendon occupy this space.
• The subacromial bursa provides frictionless gliding between the supraspinatus tendon and the acromion. Compression of the bursa during overhead activities produces bursitis, which further reduces the available space — creating a self-reinforcing impingement cycle.
• Acromial morphology (Type I flat, Type II curved, Type III hooked) directly influences the space available. A Type III hooked acromion narrows the outlet, increasing mechanical compression on the supraspinatus tendon with every overhead movement.

The Impingement Continuum

• Stage I — Edema and hemorrhage (age < 25): Repetitive overhead activity produces mechanical compression of the supraspinatus tendon in the subacromial space. The tendon responds with edema and microhemorrhage. This stage is reversible with activity modification and conservative treatment. Clinically: positive impingement signs (Neer's, Hawkins-Kennedy), painful arc, but no weakness on resisted testing and no structural tear.
• Stage II — Fibrosis and tendinopathy (age 25–40): Repeated episodes of compression cause cumulative tendon damage. The tendon develops fibrotic changes, thickening, and partial tearing. The subacromial bursa thickens (fibrotic bursitis), further narrowing the space. Clinically: persistent pain, positive impingement signs, pain and possibly mild weakness on resisted testing (Empty Can), but still no full-thickness disruption.
• Stage III — Tendon tear (age > 40): Continued mechanical compression combined with intrinsic tendon degeneration leads to partial-thickness and eventually full-thickness tears. The critical zone of hypovascularity makes the supraspinatus tendon particularly vulnerable because the watershed area cannot mount an adequate healing response. Clinically: significant AROM loss, weakness on resisted testing, positive Drop Arm test in full-thickness tears.

Critical Zone of Hypovascularity

• The critical zone lies approximately 1 cm proximal to the supraspinatus insertion on the greater tuberosity. Blood supply from two sources (osseous vessels from the tuberosity and muscular vessels from the muscle belly) creates a "watershed" area where both supplies are relatively diminished.
• This hypovascularity means the critical zone has a reduced capacity for repair — microdamage accumulates faster than the tendon can heal, making this the site where most tears initiate and propagate.
• The clinical significance is direct: the critical zone explains why supraspinatus tears are far more common than tears of the other three RC muscles, why healing is slow, and why full-thickness tears often require surgical intervention because the tissue cannot bridge the gap on its own.

Partial vs. Full-Thickness Tears

• Partial-thickness tears involve incomplete disruption of tendon fibers. They may be bursal-side (compressed against the acromion), articular-side (more common — exposed to tensile stress from the joint side), or intratendinous. AROM is reduced and painful, but PROM is preserved near-normal. Resisted testing shows pain with or without mild weakness.
• Full-thickness tears involve complete disruption of the tendon from the bursal to the articular surface. The key finding is a significant discrepancy between AROM (markedly reduced) and PROM (relatively preserved) — the passive structures (capsule, ligaments) are intact, but the contractile unit (tendon-muscle) cannot generate force to move the joint. Drop Arm test is positive. Marked weakness on specific resisted testing (Empty Can for supraspinatus, ER for infraspinatus).
• Massive tears involve two or more tendons or > 5 cm retraction. Pseudoparalysis (inability to actively elevate the arm despite full passive range) may be present. Marked atrophy is visible in the supraspinatus and infraspinatus fossae. Surgical referral is typically indicated.

Compensatory Patterns

• When the supraspinatus fails, the deltoid and remaining RC muscles attempt to compensate. The upper trapezius and levator scapulae become hypertonic to elevate and stabilize the scapula during arm elevation (shoulder hiking). The pectoralis minor shortens as the scapula protracts and anteriorly tilts — this further narrows the subacromial space, perpetuating impingement.
• Scapular dyskinesis (abnormal scapular movement) is both a cause and consequence of RC pathology. Insufficient scapular upward rotation during arm elevation forces the humeral head closer to the acromion, increasing impingement. This is why periscapular muscle balance is essential to RC treatment — the scapula must move correctly for the RC to function.

Signs and Symptoms

By Pathology Stage

General Presentation

• Pain location: Anterolateral shoulder, often radiating to the lateral deltoid insertion (C5 referral zone); patients frequently cannot localize the pain precisely, pointing to the general deltoid area
• Night pain: A characteristic finding across the spectrum — lying on the affected side compresses the subacromial space; arm position during sleep can maintain impingement
• Weakness: Specific to the affected muscle — difficulty reaching overhead (supraspinatus), external rotation (infraspinatus/teres minor), reaching behind the back (subscapularis)
• Crepitus: Grinding or clicking with shoulder movement from inflamed bursa or irregular tendon surface
• Functional complaints: Cannot reach overhead shelves, difficulty with hair washing/dressing, cannot throw

Assessment Profile

Subjective Presentation

• Chief complaint: "My shoulder hurts when I reach overhead"; "I can't sleep on that side"; "my arm feels weak when I lift things above my head"; pain described in the general deltoid area
• Pain quality: Deep, aching pain in the anterolateral shoulder; sharp with overhead movement (impingement provocation); dull ache at rest; night pain is characteristic, especially lying on the affected side
• Onset: Gradual in tendinopathy and degenerative tears (weeks to months of increasing shoulder pain with overhead activity); acute in traumatic tears (sudden onset after a fall, forceful lift, or deceleration event — "I felt a pop and couldn't lift my arm")
• Aggravating factors: Overhead activities (reaching, lifting above shoulder height), lying on the affected side, reaching behind the back (bra strap, back pocket), repetitive arm elevation, carrying heavy objects with the arm at the side
• Easing factors: Rest, arm supported at the side (reduces subacromial compression), NSAIDs (temporary), avoiding overhead positions, ice after activity
• Red flags: Acute traumatic onset with immediate inability to raise the arm and significant weakness → suspect full-thickness or massive tear; refer for imaging and orthopedic evaluation

Observation

• Local inspection: Atrophy in the supraspinatus fossa (above the scapular spine) and/or infraspinatus fossa (below the scapular spine) in chronic tears — compare bilateral; muscle bulk asymmetry is an important finding; mild swelling is uncommon (deep pathology)
• Posture: Forward head posture with protracted scapulae and increased thoracic kyphosis (upper crossed syndrome posture) — this narrows the subacromial space and perpetuates impingement; the affected shoulder may be held in slight internal rotation and adduction (guarding); shoulder height asymmetry from upper trapezius hypertonicity
• Gait: Not directly affected; however, arm swing may be reduced on the affected side due to pain avoidance

Palpation

• Tone: Upper trapezius and levator scapulae hypertonicity from the compensatory shoulder hiking pattern described in Pathophysiology. Pectoralis minor shortened from scapular protraction/anterior tilt. Infraspinatus and teres minor guarding. Deltoid may be hypertonic from compensatory use. The RC muscles themselves (supraspinatus belly, infraspinatus, subscapularis via the axillary fold) may show focal tenderness or atrophic, boggy quality in chronic tears rather than active guarding.
• Tenderness: Greater tuberosity (supraspinatus insertion) — the primary landmark; subacromial space tenderness (bursal involvement); bicipital groove (long head of biceps, often co-involved); acromioclavicular joint (rule out AC pathology); trigger points in upper trapezius, infraspinatus, and subscapularis (via axillary fold access); posterior glenohumeral joint line for posterior capsular tightness
• Temperature: Usually normal; mild warmth over the subacromial space suggests active bursitis or acute tendon inflammation
• Tissue quality: Supraspinatus and infraspinatus fossae may feel hollow or wasted in chronic tears. The RC muscles themselves may have fibrotic, ropy texture with trigger points — infraspinatus TrPs are particularly common and refer into the anterior/lateral shoulder. Posterior capsule may feel thickened and inelastic. Pectoralis minor feels shortened and taut.

Motion Assessment

• AROM: Painful arc between 60–120 degrees of active abduction (the subacromial compression zone) — pain diminishes above 120 degrees as the greater tuberosity clears the acromion. Active elevation may show shoulder hiking (upper trapezius substitution). Active ER and IR should be tested separately to identify which RC muscle is affected. Compare bilateral.
• PROM / end-feel: PROM exceeds AROM — this is the critical finding that distinguishes RC pathology (contractile tissue lesion) from adhesive capsulitis (capsular restriction where PROM = AROM in a capsular pattern ER > ABD > IR). End-feel for passive elevation and rotation is normal (tissue stretch or capsular) unless posterior capsular tightness is present (firm end-feel in horizontal adduction and IR). Pain at end-range of passive elevation indicates subacromial compression.
• Resisted testing: Isometric testing isolates individual RC muscles. Supraspinatus: resisted abduction or Empty Can position — pain indicates tendinopathy, weakness indicates tear. Infraspinatus/teres minor: resisted ER at 0 degrees abduction — pain and/or weakness. Subscapularis: resisted IR, Lift-Off test, Bear Hug test. The pattern of pain versus weakness distinguishes tendinopathy (strong and painful) from tear (weak and painful or weak and painless).

Special Test Cluster

Clinical test clustering improves accuracy: Impingement cluster (Neer's + Hawkins-Kennedy + painful arc) — if all 3 positive, high probability of subacromial pathology. Tear cluster (positive Drop Arm + weakness on Empty Can + ER weakness) — high probability of full-thickness tear requiring imaging referral.

Differential Diagnoses