Rotator Cuff Disease and Tears

• Spectrum: subacromial impingement and tendinopathy → partial-thickness tear → full-thickness tear, usually degenerative in older adults and traumatic in the young.
• Presentation: lateral shoulder pain worse with overhead activity, night pain when lying on the affected side, and weakness. Long-standing full-thickness tears produce visible atrophy of the supraspinatus and infraspinatus fossae.
• Examination:
• Empty can (Jobe) test — supraspinatus.
• External rotation against resistance — infraspinatus and teres minor.
• Lift-off and belly-press — subscapularis.
• Neer and Hawkins–Kennedy — impingement.
• Drop arm sign — a large full-thickness tear.
• Distinguish adhesive capsulitis, where passive as well as active range is lost, from cuff disease, where passive range is usually preserved.
• Imaging: radiographs to exclude arthritis and show a high-riding humeral head in chronic tears; MRI or ultrasound to characterise the cuff.
• Management: most tendinopathy and many degenerative tears respond to physiotherapy, NSAIDs and selective subacromial injection. Surgical repair is favoured for acute traumatic full-thickness tears in younger, active patients.

Extrinsic (mechanical) mechanisms

• Subacromial impingement: compression of the supraspinatus tendon and subacromial bursa between the greater tuberosity and the coracoacromial arch during elevation.
• Acromial morphology: a hooked (type III) acromion, subacromial or acromioclavicular osteophytes, and os acromiale narrow the outlet.
• Scapular dyskinesis and posterior capsular tightness: loss of scapular upward rotation and anterosuperior humeral translation functionally narrow the space in overhead athletes.

Intrinsic (degenerative) mechanisms

• Age-related tendinopathy: disorganised collagen, mucoid degeneration and calcium deposition within the tendon substance, worst in the relatively hypovascular critical zone near the greater tuberosity insertion.
• Attritional partial tearing: articular-sided fibres fail first (PASTA lesion) because they bear the greatest tensile load and are least vascular.

Traumatic mechanisms

• Fall on an outstretched hand or a sudden eccentric traction load (catching a heavy object, a violent throw) produces an acute full-thickness tear, typically in a younger patient.
• Anterior shoulder dislocation in a patient over roughly 40 years — the classic exam trap: the cuff tears rather than producing a Bankart lesion, so persistent weakness after reduction demands cuff imaging (and an axillary nerve check).

Non-modifiable risk factors

• Increasing age (prevalence of asymptomatic tears rises steeply after the sixth decade), male sex, acromial shape, family history, prior dislocation, and a known contralateral cuff tear.

Modifiable risk factors

• Smoking: impairs tendon microvascular perfusion and healing — the strongest modifiable predictor of tear progression and of failed repair.
• Diabetes mellitus, obesity and hyperlipidaemia: glycation and lipid deposition stiffen collagen and worsen tendon quality.
• Occupational and athletic overhead loading: painters, electricians, swimmers, throwers, and manual labourers.
• Repeated intratendinous corticosteroid injection and fluoroquinolone exposure, both of which weaken collagen.

• The outlet is the problem: the supraspinatus tendon runs through a fixed corridor bounded above by the acromion and coracoacromial ligament and below by the humeral head. Elevation between roughly 60° and 120° brings the tendon and bursa directly under the arch, which is why pain is arc-shaped rather than present throughout motion.
• Repetitive compression → bursitis and tendinopathy: mechanical irritation causes subacromial bursal thickening, neovascularisation and nociceptor ingrowth. Inflamed bursa, not the tendon itself, generates much of the early pain.
• The critical zone: the watershed segment of supraspinatus near its insertion is relatively hypovascular, so degenerated collagen is repaired poorly. Micro-tears accumulate faster than they heal.
• Partial → full-thickness progression: articular-sided fibres fail first; as the defect enlarges, load is transferred to the remaining intact fibres, which then fail in turn — a self-propagating cascade that explains why untreated degenerative tears enlarge over time.
• Loss of the force couple: the cuff's job is to compress and depress the humeral head so the deltoid can pull the arm up around a stable fulcrum. When supraspinatus and infraspinatus fail, unopposed deltoid pull translates the humeral head superiorly, narrowing the acromiohumeral interval. This produces the radiographic high-riding humeral head and, mechanically, worsens impingement — a vicious cycle.
• Weakness versus pain inhibition: early on, weakness is reflex inhibition from pain (abolished by subacromial lidocaine). With a true full-thickness tear, weakness persists after anaesthetic — the basis of the drop arm sign.
• Chronic changes: retraction, muscle atrophy and irreversible fatty infiltration (graded by the Goutallier classification) develop over months, which is why chronic massive tears become irreparable.
• Night pain: recumbency raises intrabursal pressure and causes venous congestion in the inflamed bursa; lying on the affected side also compresses the subacromial space directly.
• End stage: sustained superior migration erodes the glenoid and acromion, producing cuff tear arthropathy and pseudoparalysis.

Symptoms

• Anterolateral shoulder pain referred to the deltoid insertion: bursal and tendon nociceptors share C5 segmental innervation. Pain radiating below the elbow, with neck movement or paraesthesiae, points instead to cervical radiculopathy.
• Painful arc between roughly 60° and 120° of abduction: the tendon and bursa are squeezed under the arch through that range and clear it above.
• Night pain, worse lying on the affected side — often the symptom that finally brings the patient in.
• Weakness and difficulty with overhead tasks (reaching a shelf, combing hair); catching or crepitus with rotation.

Signs, each mapped to its structure

• Empty can (Jobe) — resisted elevation in the scapular plane with the thumb down isolates supraspinatus.
• Resisted external rotation with the elbow at the side — infraspinatus/teres minor; an external rotation lag sign or hornblower's sign indicates a large posterosuperior tear.
• Lift-off and belly-press — subscapularis; also look for increased passive external rotation.
• Neer and Hawkins–Kennedy — provoke impingement by driving the tuberosity under the arch; sensitive but not specific.
• Drop arm sign — inability to lower the arm smoothly from 90°, indicating a large full-thickness tear.
• Atrophy of the supraspinatus and infraspinatus fossae — chronic, denervation-independent disuse and fatty change.
• Subacromial lidocaine injection test: if strength normalises once pain is abolished, weakness was pain inhibition rather than a complete tear.

• Reduced acromiohumeral interval with a high-riding humeral head — indicates a chronic, often massive, full-thickness tear.
• Greater tuberosity sclerosis or cysts, subacromial spurs, hooked acromion.
• Calcific deposits (calcific tendinitis) and glenohumeral osteoarthritis, both important mimics.
• Radiographs cannot exclude a cuff tear — a normal film in a weak shoulder does not end the workup.

Step 3 — cuff-specific imaging.

• Ultrasound: operator-dependent but accurate for full-thickness tears, cheap, dynamic, and allows contralateral comparison. Reasonable first-line where expertise exists.
• MRI without contrast: the practical standard. A full-thickness tear shows a fluid-signal gap through the tendon on T2/fat-suppressed sequences with fluid in both the glenohumeral joint and subacromial bursa. MRI also grades retraction and fatty infiltration (Goutallier grading) — the two findings that determine reparability.
• MR arthrography: most sensitive for partial-thickness, articular-sided tears and for concurrent labral pathology; useful in young athletes and post-operative shoulders.

• Structured physical therapy: scapular stabiliser and cuff strengthening plus posterior capsular stretching, to restore the humeral head–depressing force couple. This, not medication, is the therapy that changes function.
• Activity modification: temporary avoidance of overhead loading; avoid prolonged sling immobilisation, which invites adhesive capsulitis.
• NSAIDs — a representative agent is naproxen or ibuprofen — for short-term analgesia; acetaminophen where NSAIDs are contraindicated (CKD, peptic ulcer disease, anticoagulation, heart failure).

Escalation

• Subacromial corticosteroid injection (a glucocorticoid such as triamcinolone with local anaesthetic) gives short-term pain relief and can unlock participation in therapy. AAOS notes the benefit is limited and time-bound; repeated or intratendinous injection is discouraged because steroid degrades tendon collagen and worsens repair outcomes.
• Reassess after an adequate therapy trial (on the order of 6–12 weeks); persistent pain or progressive weakness prompts advanced imaging and surgical consultation.

Definitive/surgical options

• Arthroscopic rotator cuff repair for acute traumatic tears, for symptomatic full-thickness tears failing non-operative care, and for young patients with high functional demand. Post-operative protocol: sling protection, then staged passive → active-assisted → resisted rehabilitation.
• Massive irreparable tears (Goutallier grade 3–4, marked retraction): debridement, superior capsular reconstruction, or tendon transfer.
• Cuff tear arthropathy with pseudoparalysis: reverse total shoulder arthroplasty, which medialises and lowers the centre of rotation so the deltoid can substitute for the absent cuff.

Of the disease

• Tear progression: untreated degenerative partial tears enlarge as load shifts to remaining fibres; signalled by new weakness rather than new pain.
• Fatty infiltration and retraction: irreversible muscle change after months of tendon discontinuity; on MRI (Goutallier grade 3–4) it predicts irreparability and repair failure.
• Cuff tear arthropathy: chronic superior humeral migration erodes the acromion and glenoid, producing arthritis and pseudoparalysis — the patient cannot actively elevate the arm despite full passive motion.
• Long head of biceps rupture: the degenerated tendon, destabilised by a subscapularis tear, ruptures and the muscle belly balls up distally (Popeye sign).
• Secondary adhesive capsulitis: pain-driven disuse causes capsular contracture; the signal is new loss of passive external rotation.
• Chronic pain and deconditioning, with sleep disruption from night pain.

Of treatment

• Corticosteroid injection: tendon weakening and rupture with repeated or intratendinous injection, skin/fat atrophy and depigmentation, transient hyperglycaemia in diabetics (warn every diabetic patient), and — rarely — septic arthritis, an emergency presenting with fever, a hot shoulder and severe pain on passive motion; treat with urgent aspiration, culture and drainage, not with more injections.
• NSAIDs: gastrointestinal bleeding, acute kidney injury, hypertension and fluid retention.
• Post-operative retear: the most common surgical complication; risk rises with tear size, older age, smoking and diabetes. Suspect it when early strength gains reverse.
• Post-operative stiffness from over-cautious rehabilitation.
• Nerve injury: axillary nerve with deltoid-splitting approaches, suprascapular nerve with mobilisation of a retracted cuff.
• Deep infection: shoulder surgery is characteristically complicated by Cutibacterium acnes, an indolent organism with normal-appearing wounds, minimal fever and slow-growing cultures — hold cultures for an extended period.
• Reverse arthroplasty: dislocation, scapular notching, acromial stress fracture and periprosthetic infection.

• Supraspinatus is the answer unless the stem says otherwise. It traverses the narrow subacromial outlet and has a hypovascular critical zone; empty can (Jobe) positivity localises it.
• Weakness that persists after subacromial lidocaine = structural tear; weakness that resolves = pain inhibition. This is the cleanest way a stem separates tendinopathy from a full-thickness tear, and the drop arm sign is its bedside equivalent.
• Passive range is the discriminator. Cuff disease loses active motion with preserved passive motion; adhesive capsulitis loses both, external rotation first, and clusters with diabetes and thyroid disease — the single association examiners test most often.
• Shoulder dislocation in a patient over 40: expect a rotator cuff tear, not a Bankart lesion. Persistent weakness after successful reduction means imaging the cuff — and always document axillary nerve function (deltoid contraction, lateral shoulder sensation).
• Best next step after a suggestive exam is plain radiographs, not MRI. Films exclude arthritis, calcific tendinitis and fracture and reveal the high-riding humeral head of a chronic massive tear; MRI or ultrasound follows to characterise the cuff.
• First-line management is physical therapy plus NSAIDs, per the AAOS rotator cuff guideline. Subacromial corticosteroid injection buys short-term relief only; repeated injections weaken tendon and are a wrong answer.
• Operate early on the acute traumatic full-thickness tear in a young, active patient — delay permits retraction and irreversible fatty infiltration. Conversely, an atraumatic degenerative tear in a low-demand older adult is managed non-operatively first.
• Common distractors: pain radiating below the elbow with paraesthesiae or reflex loss is cervical radiculopathy, not cuff disease; a hot, febrile shoulder with severe pain on passive motion is septic arthritis, needing aspiration, not MRI; and pseudoparalysis with an eroded, high-riding head is cuff tear arthropathy, treated with reverse — not anatomic — shoulder arthroplasty.