Rotator Cuff Syndrome

Rotator cuff syndrome is a spectrum of shoulder pathology ranging from tendinitis and impingement to partial or complete tears of the rotator cuff tendons, resulting in pain, weakness, and limited shoulder movement.

2. Epidemiology

Risk Factor	Mechanism / Explanation
*Age*	Tendon degeneration accumulates over decades; collagen cross-linking ↓, vascularity ↓, repair capacity ↓
*Hand dominance*	The dominant shoulder undergoes more repetitive loading → more cumulative microtrauma
*Contralateral shoulder*	*Likelihood of bilateral tear after age 60 is as high as 50%* — this reflects systemic tendon biology rather than isolated trauma
*Smoking*	*Affects vascularity of tendon* — nicotine causes microvascular vasoconstriction, carbon monoxide ↓ oxygen delivery, directly impairs tenocyte metabolism
*Family history*	Genetic predisposition in collagen composition (e.g., COL5A1 polymorphisms), tendon ultrastructure
*Trauma*	Acute overload can cause macroscopic tear on a background of chronic degeneration
*Occupational demands of heavy labors*	Repetitive overhead lifting, vibration, sustained postures — painters, construction workers, warehouse workers

Additional risk factors to be aware of:

Metabolic disease: Diabetes mellitus (glycosylation of collagen → stiff, brittle tendons; microangiopathy), hypercholesterolaemia
Corticosteroid use: Both systemic and repeated local injections weaken tendon collagen
Anatomical variants: Hooked (Type III) acromion — discussed under aetiology

High Yield Exam Point

The bilateral nature of rotator cuff disease is important — if you find a tear in one shoulder of a 65-year-old, there is up to a 50% chance the other shoulder has one too. This supports the "intrinsic degeneration" theory: it's not just about one shoulder being overused, it's a systemic tendon ageing problem.

3. Anatomy and Function

The rotator cuff is a group of four muscles whose tendons coalesce to form a continuous cuff around the humeral head, blending with the glenohumeral joint capsule. Mnemonic: SITS (Supraspinatus, Infraspinatus, Teres minor, Subscapularis).

Muscle	Origin	Insertion	Nerve Supply	*Function* ^[1]
Supraspinatus	Supraspinous fossa of scapula	Superior facet of greater tuberosity	Suprascapular nerve (C5, C6)	*Abductor of the arm at shoulder* (initiates first 0–15° of abduction, then assists deltoid)
Infraspinatus	Infraspinous fossa of scapula	Middle facet of greater tuberosity	Suprascapular nerve (C5, C6)	*External rotation*
Teres minor	Lateral border of scapula	Inferior facet of greater tuberosity	Axillary nerve (C5, C6)	*External rotation*
Subscapularis	Subscapular fossa (anterior scapula)	Lesser tuberosity	Upper & lower subscapular nerves (C5, C6)	*Internal rotation*

The shape of the acromion affects the subacromial space:

Type	Shape	Clinical Significance
Type I	Flat	Lowest risk of impingement
Type II	Curved	Intermediate risk
Type III	Hooked	Highest risk — the anterior hook narrows the subacromial space and mechanically compresses the supraspinatus tendon

Type III acromion is strongly associated with rotator cuff tears. This is an important finding to look for on the supraspinatus outlet view (Y-view) X-ray.

4. Aetiology and Pathophysiology

The aetiology of rotator cuff syndrome is best understood as a combination of intrinsic (within the tendon) and extrinsic (outside the tendon) factors.

These relate to the tendon's own biology degenerating over time:

Factor	Pathophysiology
*Chronic microtrauma from repeated overhead activities*	*Swimming, lifting, painting* — cumulative micro-injury exceeds the tendon's repair capacity → tendinosis (degenerative, NOT inflammatory)
*Poor vascularity of tendons*	*Smoking* directly impairs tendon vascularity. The watershed zone (10–15 mm from insertion) has inherently poor perfusion → ↓ healing, ↓ collagen turnover
Degenerative tendinopathy	With age: ↓ cellularity, ↓ organised collagen, ↑ mucoid degeneration, ↑ calcification → weakened tendon prone to tearing
Rotator cuff muscle weakness	Disuse, neurological injury, or fatty infiltration → loss of dynamic stabilisation → humeral head migrates superiorly → mechanical impingement worsens → more damage (vicious cycle)

These relate to structures compressing the rotator cuff from above or around it:

Structure	Mechanism
Humeral head	Glenohumeral instability (e.g., in young overhead athletes) → superior subluxation of humeral head during abduction → narrows subacromial space from below
Acromion	Anatomical variation — curved or hooked (Bigliani Type II/III) acromion → narrows subacromial space from above
Coracoacromial ligament	Hypertrophy (thickening) of this ligament → reduces clearance in the coracoacromial arch
AC joint	Osteoarthritis of the AC joint → inferior osteophytes project downward into the subacromial space → mechanical compression of supraspinatus

5. Classification

5.2 Rotator Cuff Tear Classification [2]

Category	Description
Partial thickness	Incomplete tear — can be articular-side, bursal-side, or intratendinous
Full thickness	Complete tear through the entire tendon substance

Size	Dimension
Small	< 1 cm
Medium	1–3 cm
Large	3–5 cm
Massive	> 5 cm OR involving ≥ 2 tendons

This is assessed on MRI and is critical for surgical decision-making — it tells you whether the muscle is still viable and the tear is reparable:

Stage	Description
0	No fatty infiltration
1	Some fatty streaks
2	< 50% fatty infiltration
3	50% fatty infiltration
4	> 50% fatty infiltration

Goutallier ≥ 3 = generally considered irreparable because the muscle has been replaced by fat and cannot generate meaningful contraction even if re-attached.

Irreparable Tear Criteria

A rotator cuff tear is considered irreparable if there is significant fatty infiltration or muscle tendon atrophy on MRI ^[2]. Don't just focus on tear size — a "small" tear in a severely atrophied, fatty-infiltrated muscle may be functionally irreparable, while a "large" acute tear in healthy muscle may be readily repairable.

6. Clinical Features

6.1 Subacromial Impingement Syndrome

Symptom	Pathophysiological Basis
Progressive pain in anterosuperior aspect of shoulder ^[2]	The supraspinatus tendon and subacromial bursa are compressed beneath the anteroinferior acromion — the anterior and lateral deltoid region is where referred pain from C5 dermatome is perceived
*Pain exacerbated by abduction* ^[2]	Abduction (especially 60–120°) maximally narrows the subacromial space as the greater tuberosity approaches the acromion — this is the "impingement zone"
Pain relieved by rest ^[2]	Removing the mechanical compression allows the inflammatory response to settle
*Night pain, cannot sleep on affected side* ^[1]	Lying on the affected side directly compresses the inflamed subacromial space against the mattress; also, the recumbent position allows the humeral head to migrate superiorly slightly
*Pain sometimes radiates to the elbow* ^[1]	Referred pain along the C5 dermatome (the suprascapular nerve is C5,C6) — the brain poorly localises deep musculoskeletal pain

Sign	How to Elicit	Pathophysiological Basis
Limited ROM in forward flexion ^[2]	Ask patient to raise arm forward — compare active vs passive	Pain inhibits active elevation; the inflamed tendon/bursa is compressed during flexion
*Painful arc (60–120°)* ^[1]^[2]	Ask patient to actively abduct the arm slowly from 0° to 180°	Between 60–120°, the greater tuberosity passes directly beneath the acromion → maximal subacromial compression → pain. Below 60° and above 120°, the greater tuberosity rotates away from the acromion → less compression → no pain. *Positive test result: shoulder pain between 60° and 120° indicates subacromial or rotator cuff disorder* ^[1]
Neer's impingement sign ^[2]	Stabilise scapula with one hand; passively flex the shoulder to 180° with arm in internal rotation (thumb pointing down)	Forces the greater tuberosity against the anterior undersurface of acromion → reproduces impingement pain
Hawkins' sign ^[2]	Flex shoulder to 90°, flex elbow to 90°, then passively internally rotate the shoulder	Internally rotating the shoulder pushes the supraspinatus tendon against the coracoacromial ligament → reproduces impingement pain

6.2 Rotator Cuff Tear

Symptom	Pathophysiological Basis
Pain over lateral aspect of shoulder ^[2]	The deltoid insertion area/C5 dermatome receives referred pain from the supraspinatus and rotator cuff; the tear site itself may cause local nociception from the exposed subchondral bone and inflamed synovium
Inability to perform overhead activities ^[2]	Loss of the force couple — the torn supraspinatus can no longer initiate abduction or assist the deltoid in elevation; the patient cannot generate sufficient torque for overhead tasks
*Night pain, cannot sleep on affected side* ^[1]	Same mechanism as impingement — compression of inflamed structures + loss of muscle tone during sleep allows humeral head subluxation
*Weakness* ^[1]	Direct mechanical failure of the tendon–muscle unit; also pain-inhibited weakness (guarding)

Sign	How to Elicit	Pathophysiological Basis
Muscle atrophy: supraspinatus & infraspinatus ^[2]	Inspect the supraspinous and infraspinous fossae from behind — look for hollowing/wasting compared to contralateral side	Chronic disuse of the torn muscle → denervation-like atrophy; also fatty infiltration replaces muscle fibres over time
Loss of active ROM (usually SIT muscles) but *intact passive ROM* ^[2]	Test active vs passive abduction, external rotation, internal rotation	The joint surfaces and capsule are normal → passive movement is full. But the motor unit (tendon) is torn → active movement is weak/absent. This is the hallmark distinction from frozen shoulder (where BOTH active AND passive ROM are lost)
*Drop arm sign* ^[2]	Ask patient to actively abduct to 90° (or passively place arm at 90°), then ask to slowly lower the arm	The torn supraspinatus cannot eccentrically control the arm against gravity → the arm drops suddenly. This indicates a significant (usually full-thickness) rotator cuff tear
*Impingement syndrome* ^[1]	Painful arc, Neer's sign, Hawkins' sign (as above)	A tear often co-exists with impingement — the torn tendon edge catches on the acromion, and associated bursitis contributes to impingement signs
Lag signs	External rotation lag sign (infraspinatus), lift-off test (subscapularis), Hornblower's sign (teres minor)	When a specific tendon is torn, the patient cannot maintain the position the examiner places the limb in — the limb "lags" back due to loss of active motor control

Active vs Passive ROM — The Critical Distinction

Feature	Rotator Cuff Tear	Frozen Shoulder
Active ROM	↓	↓
Passive ROM	Normal/Near-normal	↓ (equally reduced)
Pattern	Depends on which tendon is torn	Global restriction, especially ER and IR
Mechanism	Motor unit failure (tendon torn)	Capsular contracture (joint stuck)

This is one of the most commonly tested exam points in shoulder pathology ^[2].

Test	What It Tests	Positive Finding
Painful arc	Subacromial impingement	Pain 60–120° abduction
Neer's sign	Subacromial impingement	Pain on forced passive flexion with IR
Hawkins' sign	Subacromial impingement	Pain on passive IR at 90° flexion
Drop arm test	Full-thickness supraspinatus tear	Cannot hold arm at 90° abduction
Empty can (Jobe's) test	Supraspinatus	Weakness/pain resisting downward force with arm at 90° abduction, 30° forward flexion, thumbs down
External rotation lag sign	Infraspinatus/teres minor	Arm falls into IR when released from ER position
Lift-off test (Gerber's)	Subscapularis	Cannot lift hand off back when placed behind back
Belly press test	Subscapularis (alternative)	Cannot press hand against belly without wrist flexion
Bear hug test	Upper subscapularis	Cannot maintain hand on opposite shoulder while examiner pulls
Speed's test	Biceps tendon/SLAP	Pain on resisted forward flexion with arm supinated
Yergason's test	Biceps tendon	Pain on resisted supination with elbow flexed 90°

7. Calcific Tendonitis — Special Subtype

Calcific tendonitis deserves mention as part of the rotator cuff syndrome continuum:

For completeness (this sets up the DDx section I'll cover in detail later):

Condition	Key Distinguishing Feature ^[2]
Rotator cuff syndrome (MC)	Pain during activity only, passive ROM > active ROM, external rotation spared
Frozen shoulder	DM risk factor, symptoms change over time (pain → stiffness → resolution), limited active + passive ROM
AC joint arthritis	More localised tenderness (over AC joint), cross-body adduction test positive
Biceps tendonitis	More localised tenderness (anterior shoulder, bicipital groove), Speed's/Yergason's positive
Cervical radiculopathy	Neck pain, radiating pain, weakness — Spurling's test positive

High Yield Summary

Definition: Rotator cuff syndrome = continuum of subacromial impingement → calcific tendonitis → partial tear → full-thickness tear

Epidemiology: Age-related disease; 20% at 60–69y, 40.7% at ≥70y; up to 50% bilateral after age 60

Risk Factors (ASHTON): Age, Smoking, Hand dominance, Trauma, Occupation (heavy labour), Nfamily history + contralateral shoulder

Anatomy: SITS muscles (Supraspinatus, Infraspinatus, Teres minor, Subscapularis); critical hypovascular zone 10–15 mm from insertion; force couple with deltoid

Aetiology: Intrinsic (microtrauma, hypovascularity, degeneration) + Extrinsic (acromion shape, AC joint OA, coracoacromial ligament hypertrophy, GH instability)

Classification: Partial vs full thickness; articular vs bursal side; tear size (small < 1 cm, medium 1–3 cm, large 3–5 cm, massive > 5 cm or ≥ 2 tendons); Goutallier fatty infiltration grading

Clinical Features:

Impingement: anterosuperior shoulder pain, painful arc (60–120°), Neer's sign, Hawkins' sign
Tear: lateral shoulder pain, weakness, night pain, muscle atrophy, ↓ active ROM but intact passive ROM, drop arm sign
Key distinction from frozen shoulder: passive ROM preserved in rotator cuff tear, lost in frozen shoulder

Active Recall - Rotator Cuff Syndrome

Differential Diagnosis of Shoulder Pain in the Context of Rotator Cuff Syndrome

When a patient walks into clinic complaining of shoulder pain, your job is not to jump straight to "rotator cuff tear" — it's to systematically work through a differential. The shoulder is a complex region where pathology from the joint itself, the periarticular soft tissues, and even distant structures (cervical spine, thorax) can all present as "shoulder pain." The key is pattern recognition based on first-principles understanding of anatomy and pathophysiology.

These are the conditions you must be able to distinguish from each other at the bedside. The senior notes lay them out clearly, and they are the most commonly tested:

Condition	Key Distinguishing Features ^[2]
Rotator cuff syndrome (MC)	Pain during activity only; passive ROM > active ROM; external rotation spared (infraspinatus + teres minor usually intact early)
Frozen shoulder	DM as risk factor (check HbA1c); symptoms change over time (pain → pain + stiffness → stiffness → resolution); night/rest pain; limited active + passive ROM
AC joint arthritis	More localised tenderness directly over the AC joint
Biceps tendonitis	More localised tenderness over the anterior shoulder (bicipital groove)
Cervical radiculopathy	Neck pain, radiating pain, weakness in dermatomal distribution

Let's unpack each one in detail, explaining why the clinical features differ based on pathophysiology.

"Frozen" = the capsule is literally stuck. "Adhesive capsulitis" → "adhesive" = sticking together, "capsul-" = joint capsule, "-itis" = inflammation.

Why does it present differently from rotator cuff syndrome?

The pathology is in the joint capsule, not the tendons. The glenohumeral capsule becomes inflamed, fibrosed, and contractured — it physically restricts joint motion in all directions. This is fundamentally different from a tendon problem:

Feature	Rotator Cuff Syndrome	Frozen Shoulder ^[2]
Active ROM	↓	↓
Passive ROM	Normal or near-normal	↓ (equally reduced)
Pattern of restriction	Depends on tendon involved; ER often spared	Global restriction, especially ER/IR and flexion ^[2]
Pain pattern	Activity-related	Changes over time: freezing → frozen → thawing
Risk factors	Age, occupation, smoking	DM (check HbA1c) ^[2], thyroid disease, post-trauma/surgery
Night pain	When lying on affected side	Prominent — inflamed capsule causes rest/night pain

Why is external rotation particularly affected in frozen shoulder? The anterior capsule and coracohumeral ligament (which tighten during ER) are the first to become fibrosed and contractured. Think of the capsule as a sleeve around the joint — when it shrinks, the movements that stretch the sleeve the most (ER, then IR, then flexion) are restricted first. This is the capsular pattern of the glenohumeral joint (ER > abduction > IR).

Temporal pattern of frozen shoulder ^[2]:

Freezing phase (2–9 months): Pain predominates — inflammatory capsulitis
Frozen phase (4–12 months): Pain + stiffness — fibrosis and contracture develop
Thawing phase (5–24 months): Stiffness gradually resolves — may not completely resolve spontaneously

Secondary frozen shoulder can occur as a complication of rotator cuff syndrome ^[2] — the patient guards against pain → disuse → capsular contracture. This is important clinically because what starts as a rotator cuff problem can evolve into a combined pathology.

This is the critical extrinsic/referred cause that must always be considered. The reason it's in the DDx is that cervical nerve root compression can present with shoulder pain that mimics intrinsic shoulder pathology.

Clinical features of cervical radiculopathy ^[3]:

Unilateral arm pain or sensory disturbance ^[3]
May have associated weakness ^[3]
Dermatomal distribution ^[3]
Neck pain ^[3]

Why does cervical radiculopathy cause shoulder pain? The C5 nerve root innervates the deltoid, supraspinatus, and infraspinatus. C5 radiculopathy causes pain radiating to the lateral arm and shoulder — the brain interprets this as "shoulder pain" because the afferent fibres from C5 dermatome converge at the same spinal cord level. The key giveaway is that the pain typically starts in the neck and radiates distally, follows a dermatomal distribution, and may be associated with neurological signs (weakness, numbness, reflex changes).

Dermatomal patterns ^[3]:

Level	Motor Weakness	Sensory Deficit / Pain Location	Reflex
C5	Deltoid	Lateral arm	Biceps
C6	Biceps, wrist extension	Radial forearm, radial two digits	Brachioradialis
C7	Triceps, wrist flexion	Middle finger	Triceps
C8	Finger flexors	Ulnar two digits	—
T1	Hand intrinsics	Ulnar forearm	—

Differential diagnosis of cervical radiculopathy itself includes ^[3]:

Cervical myelopathy (symptoms may overlap — patients can have myeloradiculopathy)
Peripheral nerve compression (e.g., carpal tunnel, cubital tunnel)
Shoulder pathology (i.e., the reverse — shoulder pathology can be mistaken for cervical radiculopathy)

Key distinguishing tests:

Spurling's test: Extend and laterally flex the neck toward the symptomatic side, then apply axial compression → narrows the neural foramen → reproduces radicular pain. If positive, strongly suggests cervical radiculopathy rather than primary shoulder pathology.
Shoulder examination is normal: Full passive and active ROM, no impingement signs, no tenderness over rotator cuff or AC joint
Neurological examination reveals dermatomal weakness and sensory changes that don't fit a peripheral nerve pattern

The Cervical Spine–Shoulder Trap

One of the most common clinical errors is attributing shoulder pain to rotator cuff syndrome when the actual culprit is cervical radiculopathy (or vice versa). Always examine the cervical spine in any patient with shoulder pain, and always examine the shoulder in any patient with neck pain. The two conditions can also coexist (especially in elderly patients with degenerative disease in both regions), making the clinical picture even more confusing.

6. Other Important Differentials to Consider

Feature	Rotator Cuff Syndrome	Frozen Shoulder	AC Joint Arthritis	Biceps Tendinopathy	Cervical Radiculopathy
Pain location	Anterolateral / lateral shoulder	Diffuse, deep shoulder	Superior shoulder, over AC joint	Anterior shoulder, bicipital groove	Neck → shoulder → arm (dermatomal)
Pain character	Activity-related, painful arc	Rest/night pain, changes over time	Localised, with overhead/cross-body	Localised, with biceps contraction	Radiating, shooting, ± paraesthesia
Active ROM	↓ (especially abduction)	↓↓	Mildly ↓ at extremes	Usually normal	Usually normal (unless motor deficit)
Passive ROM	Normal	↓↓ (equal to active)	Mildly ↓ at extremes	Normal	Normal
Key special test	Neer, Hawkins, drop arm	Capsular pattern (ER > Abd > IR)	Cross-body adduction	Speed's, Yergason's	Spurling's test
Key risk factor	Age, occupation, smoking	DM, post-surgery	Prior AC joint injury, manual labour	Overhead athletes, repetitive use	Cervical spondylosis, disc prolapse
Neurology	Normal	Normal	Normal	Normal	Dermatomal weakness/numbness/↓reflex

High Yield Summary

The Big Five DDx of shoulder pain: Rotator cuff syndrome (MC), Frozen shoulder, AC joint arthritis, Biceps tendonitis, Cervical radiculopathy

The single most important bedside distinction: Active vs passive ROM

Passive ROM preserved + active ROM reduced → Rotator cuff tear (motor unit failure)
Both active AND passive ROM reduced → Frozen shoulder (capsular contracture) or GH OA

Don't forget referred causes: Cervical radiculopathy (always examine the neck), Pancoast tumour (CXR), cardiac ischaemia, diaphragmatic irritation

Cervical radiculopathy mimics shoulder pain via C5 dermatome — key clue is neck pain, dermatomal distribution, positive Spurling's test, and normal shoulder examination

AC joint and biceps tendon pathology are distinguished by localised tenderness and specific provocation tests (cross-body adduction for AC joint; Speed's/Yergason's for biceps)

Active Recall - Differential Diagnosis of Shoulder Pain

References

^[1] Lecture slides: GC 236. Common Shoulder Problems [Updated in 2025].pdf (Module 2: Rotator cuff pathology, pages 77–105) ^[2] Senior notes: maxim.md (sections 3.3–3.6, pages 485–489) ^[3] Lecture slides: GC 227. Cervical Spine Pathology.pdf (pages 41–44)

Diagnosis of Rotator Cuff Syndrome

Systematic Clinical Assessment

Physical examination is the cornerstone and should follow the structured Look–Feel–Move approach ^[1]:

Jobe test (Empty Can Test) ^[1]:

Tests: Supraspinatus
Technique: Arm at 90° abduction, 30° forward flexion (in the scapular plane), fully internally rotated (thumb pointing down — like emptying a can). Resist downward force.
Positive: Pain and/or weakness → supraspinatus pathology
Why it works: This position isolates the supraspinatus by minimising the contribution of the deltoid, and the internal rotation places the supraspinatus insertion directly under the acromion

Lift-off test (Gerber's test) ^[1]:

Tests: Subscapularis
Technique: Place patient's hand behind their back (dorsum of hand resting on the lumbar spine). Ask patient to lift the hand away from the back.
Positive: Inability to lift the hand off the back → subscapularis tear
Why it works: Lifting the hand off the back requires active internal rotation against resistance — the subscapularis is the primary internal rotator, and if it's torn, the patient cannot generate force in this position

Other special tests (summary from the full examination framework ^[1]):

Test	Structure Tested	Technique	Positive Finding
Neer's impingement sign	Subacromial impingement	Passively flex shoulder to 180° with arm internally rotated	Anterior shoulder pain
Hawkins' sign	Subacromial impingement	Flex shoulder and elbow to 90°, passively IR	Anterior shoulder pain
Painful arc	Subacromial impingement	Active abduction 0–180°	Pain between 60° and 120° ^[1]
Drop arm test	Full-thickness supraspinatus tear	Hold arm at 90° abduction, slowly lower	Arm drops suddenly
External rotation lag	Infraspinatus	Passively place arm in maximal ER, release	Arm falls into IR
Hornblower's sign	Teres minor	Resist ER with arm at 90° abduction	Cannot hold position
Belly press test	Subscapularis (alternative to lift-off)	Press palm against abdomen; attempt to keep elbow forward	Elbow drifts posteriorly (compensating with wrist flexion)

The Impingement Test vs Impingement Sign

There is a subtle distinction:

Impingement sign = Neer's sign or Hawkins' sign is positive (pain reproduced)
Impingement test (Neer's injection test) = Inject local anaesthetic (e.g., 10 mL 1% lignocaine) into the subacromial space, then repeat the impingement signs. If pain is abolished, this confirms the pain originates from the subacromial space (rather than the AC joint, cervical spine, etc.). This is both diagnostic and therapeutic.

Investigation Modalities — Detailed Interpretation

Why do we get it? It's the first-line imaging for any shoulder complaint — cheap, fast, widely available. It does not directly visualise the soft tissue rotator cuff, but it provides critical indirect information and excludes other pathology.

Standard views:

AP view (true AP / Grashey view): Humeral head centred on glenoid
Axillary view: Visualises glenohumeral congruency, Hill-Sachs/Bankart lesions
Y-view (Supraspinatus outlet view): Assesses acromion morphology (Bigliani classification)

What to look for on X-ray ^[2]:

X-ray Finding	What It Tells You	Pathophysiological Basis
Acromiohumeral distance ^[2]	Normal: 7–14 mm. Decreased ( < 7 mm) = proximal migration of humeral head → suggests massive rotator cuff tear	Without the rotator cuff's depressor force couple, the deltoid's unopposed superior pull drags the humeral head upward against the acromion
Acromion morphology ^[2]	Bigliani Type I (flat), II (curved), III (hooked). Type III → ↑ risk of impingement	A hooked acromion physically narrows the subacromial space, directly compressing the supraspinatus
Bony spurs ^[2]	Subacromial spurs (inferior acromion), acromial enthesophytes	Traction spurs from chronic coracoacromial ligament stress; directly narrow the subacromial space
Calcification of supraspinatus tendon ^[2]	Radio-opaque deposits near the greater tuberosity → calcific tendonitis	Calcium hydroxyapatite deposition within the tendon substance in areas of hypoxia/degeneration
AC joint changes	Joint space narrowing, osteophytes, inferior osteophytes projecting into subacromial space	Osteoarthritis of AC joint; inferior osteophytes can contribute to extrinsic impingement
Fractures ^[2]	Exclude greater tuberosity fracture, proximal humerus fracture	Important in traumatic presentations — an acute fracture may mimic or co-exist with a rotator cuff tear
Glenohumeral OA	Joint space narrowing, subchondral sclerosis, osteophytes	Suggests primary GH OA or secondary cuff tear arthropathy
"Acetabularisation" of the acromion	The acromion becomes concave/cupped on the undersurface	In chronic massive cuff tears, the humeral head articulates with the acromion → the acromion remodels to accommodate the "new articulation" — a sign of cuff tear arthropathy

The Acromiohumeral Distance

This is one of the most important measurements on a shoulder X-ray. If the acromiohumeral distance is < 7 mm, it strongly suggests a massive, chronic rotator cuff tear with superior humeral migration. This finding has implications for surgical planning — a standard rotator cuff repair may not be feasible, and the patient may need a reverse total shoulder arthroplasty instead.

USG shoulder: dynamic test for tear ^[2]

Why USG? It's the first-line imaging for confirming a suspected rotator cuff tear ^[2]. It is:

Dynamic: You can examine the tendon while the patient actively moves the shoulder — this reveals tears, subluxation of the biceps tendon, and impingement in real-time
Operator-dependent: Accuracy is highly dependent on the skill of the sonographer — in experienced hands, sensitivity and specificity for full-thickness tears approach 90–95%
Cost-effective and non-invasive: No radiation, no contrast, performed in clinic
Bilateral comparison: Can easily scan the contralateral shoulder for comparison

Key USG Findings:

Finding	Interpretation
Hypoechoic / anechoic defect in tendon	Tendon tear (partial or full-thickness) — fluid or granulation tissue fills the gap
Non-visualisation of tendon	Complete retracted tear — the tendon has pulled away from the insertion
Tendon thickening / heterogeneity	Tendinopathy — disorganised collagen, mucoid degeneration
Subacromial bursal fluid / thickening	Subacromial bursitis — secondary to impingement
Cortical irregularity of greater tuberosity	Enthesopathy at the tendon insertion — chronic traction changes
Calcific deposit	Calcific tendonitis — hyperechoic focus with or without posterior acoustic shadowing
Dynamic impingement	Bunching of subacromial bursa/tendon during active abduction — confirms impingement
Biceps tendon subluxation/dislocation	May indicate subscapularis tear (the transverse humeral ligament and subscapularis hold the biceps in the groove)

Limitations of USG:

Cannot reliably assess fatty infiltration of the muscle (critical for assessing reparability)
Cannot assess intra-articular pathology (labral tears, SLAP lesions, glenohumeral cartilage)
Posterior structures (infraspinatus, teres minor) can be harder to visualise
Operator-dependent — results vary significantly with sonographer experience

MRI shoulder: gold standard, degree of tear ^[2] — irreparable if fatty infiltration or muscle tendon atrophy ^[2]

Why MRI? MRI provides the most comprehensive assessment of the rotator cuff and is the definitive pre-operative investigation. It answers the key surgical questions:

Which tendon(s) are torn? (Supraspinatus, infraspinatus, subscapularis, or multiple)
Is the tear partial or full-thickness? And if partial, is it articular-side, bursal-side, or intratendinous?
What is the tear size? (Small/medium/large/massive)
Is there tendon retraction? How far has the torn edge pulled back from the insertion?
Is there fatty infiltration of the muscle? (Goutallier classification — determines reparability)
Is there muscle atrophy? (Tangent sign — if the supraspinatus muscle belly sits below the tangent line drawn from the scapular spine to the coracoid, atrophy is present)
What is the condition of the remaining cuff? (Are other tendons degenerative?)
Are there associated pathologies? (Labral tears, biceps pathology, capsular thickening, GH OA)

Key MRI sequences and findings:

Sequence	What It Shows Best
T1-weighted	Anatomy, fatty infiltration (fat appears bright/hyperintense on T1)
T2-weighted / PD fat-sat	Fluid (bright on T2), tendon tears (fluid signal within tendon gap), oedema, bursitis
Oblique coronal	Best for supraspinatus and infraspinatus tears (perpendicular to the tendon)
Oblique sagittal	Best for assessing fatty infiltration, tear retraction, muscle bulk
Axial	Best for subscapularis, biceps tendon in the groove, labral pathology

MRI findings in specific conditions:

Condition	MRI Appearance
Tendinopathy	Thickened tendon with intermediate signal on T1/T2 (no discrete fluid-filled defect)
Partial-thickness tear	Focal area of increased T2 signal within the tendon substance that does not extend full-thickness
Full-thickness tear	Fluid signal (bright on T2) extending from bursal to articular surface; gap in the tendon
Massive retracted tear	Tendon stump retracted to or beyond the glenoid level; associated muscle atrophy and fatty infiltration
Fatty infiltration	Muscle replaced by fat (bright on T1 in the muscle belly) — Goutallier classification
Subacromial bursitis	Fluid in the subacromial-subdeltoid bursa (bright on T2)
Calcific tendonitis	Low signal focus on all sequences (calcium is dark on MRI — better seen on X-ray!)

Goutallier Classification on MRI — Reparability Assessment

The Goutallier classification was originally described on CT but is now routinely applied on MRI oblique sagittal images:

Stage	Fatty Infiltration	Reparability
0	None	Fully reparable
1	Fatty streaks	Reparable
2	< 50% fat	Reparable (borderline if Grade 2+)
3	50% fat	Generally irreparable
4	> 50% fat	Irreparable

Goutallier ≥ 3 means the muscle is too fatty/atrophied to function even if the tendon is re-attached surgically. These patients are candidates for tendon transfer or reverse total shoulder arthroplasty rather than primary repair.

MR Arthrogram (MRI with intra-articular gadolinium contrast):

When? When conventional MRI is equivocal, particularly for:
- Partial-thickness articular-side tears: Contrast leaking into a partial tear makes it more conspicuous
- Labral pathology / SLAP lesions: Contrast distends the joint and outlines labral tears
Not routinely needed for straightforward full-thickness tears (these are well-seen on standard MRI)

Investigation	When / Why
CT scan	Rarely needed for rotator cuff. Useful for assessing bony anatomy (acromion morphology, glenoid bone loss in instability, fractures). CT with 3D reconstruction helps pre-operative planning for arthroplasty.
CT arthrogram	Alternative to MR arthrogram if MRI is contraindicated (e.g., pacemaker). Contrast outlines intra-articular structures.
Blood tests	Not diagnostic for rotator cuff syndrome per se, but: HbA1c (if frozen shoulder suspected — screen for DM ^[2]); ESR/CRP (if infection or inflammatory arthritis suspected); FBC, CRP, blood cultures (if septic arthritis being considered)
Diagnostic subacromial injection (Neer's impingement test)	Inject 5–10 mL lignocaine into the subacromial space. If pain is abolished and strength improves → confirms subacromial impingement as the pain generator. If pain persists → pain source is elsewhere (AC joint, GH joint, cervical spine)
Nerve conduction studies / EMG	If cervical radiculopathy or peripheral nerve entrapment is suspected. Differentiates neurogenic weakness from tendon pathology.

The investigation strategy depends on where you are in the clinical pathway:

Clinical Scenario	Recommended Investigation
Acute traumatic shoulder pain in young patient	X-ray (exclude fracture/dislocation) → if weakness persists, USG → MRI
Chronic activity-related shoulder pain in middle-aged patient, responding to conservative Rx	X-ray (baseline) → clinical monitoring
Chronic shoulder pain, failed 6 weeks conservative Rx	X-ray + USG → if tear confirmed, MRI for pre-op planning
Suspected massive tear (drop arm+, severe weakness, wasting)	X-ray (acromiohumeral distance) → USG → MRI (assess reparability: fatty infiltration, retraction)
Suspected calcific tendonitis (acute severe pain, limited movement)	X-ray (calcification visible) → USG (guided barbotage if needed)
Diagnostic uncertainty: is this shoulder or cervical spine?	X-ray shoulder + C-spine → diagnostic subacromial injection → if negative, MRI C-spine / nerve conduction studies

Investigation including USG and MRI ^[1] — this is the lecture slide's explicit summary of the investigation modalities for rotator cuff pathology. In practice, X-ray is always the starting point, USG is the dynamic bedside/clinic assessment, and MRI is the gold standard for pre-operative planning.

High Yield Summary

Diagnosis is clinical, supported by imaging — no formal diagnostic criteria exist for rotator cuff syndrome.

Physical examination framework: Look, Feel, Move ^[1] → then Special tests: Jobe test (supraspinatus), Lift-off test (subscapularis) ^[1], Neer's sign, Hawkins' sign, painful arc, drop arm test.

Key clinical finding: Active ROM ↓ with passive ROM preserved → rotator cuff pathology. Both ↓ → frozen shoulder / GH OA.

X-ray ^[2]: First-line. Look for acromiohumeral distance ( < 7 mm = massive tear), acromion morphology, bony spurs, calcification, fractures.

USG ^[2]: Dynamic test for tear. First-line imaging to confirm tear. Operator-dependent. Cannot assess fatty infiltration.

MRI ^[2]: Gold standard for pre-operative planning. Grades tear size, fatty infiltration (Goutallier), muscle atrophy. Irreparable if fatty infiltration or muscle tendon atrophy ^[2].

Diagnostic subacromial injection: Confirms subacromial space as pain source when clinical picture is ambiguous.

Active Recall - Diagnosis and Investigations of Rotator Cuff Syndrome

References

^[1] Lecture slides: GC 236. Common Shoulder Problems [Updated in 2025].pdf (pages 23, 77, 80, 87–91, 105, 110, 115–116, 119) ^[2] Senior notes: maxim.md (sections 3.3–3.6, pages 485–489)

Management of Rotator Cuff Syndrome

A. Non-Operative (Conservative) Management

Conservative management is first-line for the majority of patients across the rotator cuff syndrome spectrum ^[2].

Components of Conservative Management

Agent	Mechanism	Role	Cautions
Paracetamol	Central COX inhibition, ↓ prostaglandin synthesis in CNS	First-line, safe for regular use	Hepatotoxicity at supratherapeutic doses
NSAIDs (e.g., ibuprofen, naproxen)	Peripheral COX-1/2 inhibition → ↓ prostaglandin synthesis → ↓ inflammation and pain	Short courses for acute flare-ups; effective for bursitis and tendinopathy	GI ulceration (COX-1), renal impairment, CV risk. Avoid long-term. Some concern about impaired tendon healing with chronic use
Topical NSAIDs (e.g., diclofenac gel)	Local COX inhibition with reduced systemic absorption	Alternative when oral NSAIDs are contraindicated	Less effective for deep structures like the subacromial space
Opioids	μ-opioid receptor agonism in CNS	Short-term for severe acute pain only (e.g., acute calcific tendonitis, post-op)	Dependence, constipation, sedation. NOT for chronic rotator cuff pain

B. Operative Management

Surgical Options

Operative treatment modalities ^[1]:

This is the primary surgical treatment for reparable rotator cuff tears:

Arthroscopic repair (most commonly used today):

Technique: Small portals (5 mm incisions), camera and instruments inserted into the subacromial space. The torn tendon edge is mobilised, the greater tuberosity footprint is prepared (to a bleeding bone bed that promotes healing), and the tendon is reattached using suture anchors drilled into the bone.
Advantages: Less soft tissue dissection → less post-operative pain, faster rehabilitation, better cosmesis, can address associated pathology simultaneously (bursectomy, acromioplasty, biceps tenotomy/tenodesis)
Single-row vs double-row fixation: Double-row fixation provides a larger footprint contact area and higher initial fixation strength, potentially improving healing rates for larger tears

Open repair:

When: Massive tears requiring extensive mobilisation, revision surgery, or when arthroscopic expertise is unavailable
Technique: Deltoid-splitting or deltoid-detaching approach to access the subacromial space and repair the tendon directly

Associated procedures commonly performed during rotator cuff repair:

Subacromial bursectomy ^[2]: Removal of the inflamed subacromial bursa → increases subacromial space, removes a pain generator, improves visualisation during arthroscopy
Acromioplasty ^[2]: Removal of a section of the undersurface of the acromion (usually the anteroinferior spur) → increases subacromial space, removes the source of extrinsic impingement. Also known as subacromial decompression.
Biceps tenotomy or tenodesis: If the long head of biceps is frayed/inflamed (common co-pathology). Tenotomy = simply cut the tendon (simpler, may cause cosmetic Popeye deformity). Tenodesis = cut and reattach the tendon to the humerus (preserves cosmesis and some supination strength).

When to Add Acromioplasty?

Acromioplasty is typically performed when there is radiographic evidence of a hooked (Type III) acromion, subacromial spurs, or clinical evidence of extrinsic impingement. It is NOT universally performed with every rotator cuff repair — recent evidence suggests that acromioplasty does not add significant benefit to arthroscopic rotator cuff repair in all patients. The decision is individualised based on the anatomy.

Condition	First-Line Management	Operative Indications	Operative Options
Subacromial impingement	Analgesia, steroid injection, PT (rotator cuff strengthening) ^[2]	Failed conservative for 6 months ^[2]	Arthroscopic subacromial decompression (bursectomy + acromioplasty)
Partial-thickness tear	Non-operative ^[1]: analgesics, steroid, PT	Failed conservative; tear progression; > 50% tendon depth	Debridement +/- repair; completion and repair
Small full-thickness tear ( < 1 cm)	Non-operative ^[1]: analgesics, steroid, PT	Failed conservative Tx ^[2]; functional impairment	Arthroscopic repair
Medium full-thickness tear (1–3 cm)	Trial of conservative Rx; consider early repair in young/active	Recurrent symptoms, weakness, tendon retraction ^[1]	Arthroscopic repair
Large full-thickness tear (3–5 cm)	Brief conservative trial; more likely to need surgery	Large tears, lack of healing, muscle atrophy ^[1]	Arthroscopic/open repair + bursectomy + acromioplasty
Massive tear ( > 5 cm / ≥ 2 tendons), reparable	Surgery usually indicated	Tear size > 1 cm, weakness, tendon retraction ^[1]	Repair +/- tendon transfer
Massive tear, irreparable (Goutallier ≥ 3), no arthritis	Conservative Rx or reconstruction	Failed conservative	Tendon transfer / SCR
Massive tear + GH arthritis (cuff tear arthropathy)	Limited conservative options	Pain and functional impairment	Reverse total shoulder arthroplasty ^[2]
Calcific tendonitis	NSAIDs, subacromial steroid injection	Failed conservative; refractory pain	USG-guided barbotage, ESWT, arthroscopic excision
Secondary frozen shoulder	Treat underlying cause + analgesics + PT ^[2]	Stiffness fails to improve after 6 months conservative ^[2]	MUA / Arthroscopic capsular release ^[2]

Post-operative rehabilitation is as important as the surgery itself. A perfectly repaired tendon will fail if not rehabilitated properly:

Typical post-rotator cuff repair protocol:

Phase	Timeframe	Goals	Activities
Phase 1: Protection	0–6 weeks	Protect the repair, control pain and swelling	Sling immobilisation, gentle pendulum exercises, passive ROM only
Phase 2: Early motion	6–12 weeks	Restore passive and active-assisted ROM	Remove sling, active-assisted exercises, gentle stretching
Phase 3: Strengthening	12–24 weeks	Restore active ROM, begin isometric then isotonic strengthening	Progressive resistance training, rotator cuff and scapular stabiliser exercises
Phase 4: Return to function	6–12 months	Full functional recovery, sport/occupation-specific	Full resistance training, overhead activities, sport-specific drills

Why Is Rehabilitation So Long?

Tendon-to-bone healing is inherently slow. The repaired tendon must integrate with the bone through a fibrocartilaginous transition zone — this biological process takes 12–16 weeks to achieve reasonable strength. Loading the repair too early (e.g., active overhead reaching at 4 weeks) can pull the suture anchors out of the bone and cause re-tear. Conversely, being too protective for too long causes stiffness. The rehabilitation protocol balances these competing risks.

As mentioned, adhesive capsulitis is a common complication of rotator cuff syndrome (both from the disease itself and post-operatively) ^[2]. The management approach for frozen shoulder in this context ^[1]^[2]:

Goals of treatment ^[1]: Pain relief and Restore ROM and function ^[1]

Management options ^[1]:

Continue physiotherapy? ^[1]
Steroid injection? ^[1]
MUA? ^[1]
Arthroscopic capsular release? ^[1]
Combined? ^[1]

The approach depends on the type and phase:

Frozen shoulder management algorithm ^[1]:

6- to 12-week trial of physiotherapy for all types
If clinical improvement → continued maintenance physiotherapy ^[1]
If no response:
- Diabetic frozen shoulder: Distension arthrography + intensive physiotherapy ^[1]
- Primary frozen shoulder: Progressive operative management
- Secondary frozen shoulder: Simultaneous treatment of underlying cause ^[1]
If still no response → Operative procedure: MUA or arthroscopic arthrolysis ^[1]
Surgical approach based on capsular tightness:
- Anterior capsule tight → Rotator interval/anterior capsular release only ^[1]
- A/P capsule tight → 360° release ^[1]
Intensive post-operative physiotherapy ^[1]

PREVENTION is the best treatment for post-traumatic shoulder stiffness ^[1]:

Early mobilisation ^[1]
Adequate pain relief ^[1]

Frozen Shoulder Management Key Points

No consensus exists in management of adhesive capsulitis ^[1]

Arthroscopic capsular release is one of the options ^[1]:

AVOID releasing too much ^[1] — excessive release can lead to instability
Consider when conservative treatments fail at 3 months ^[1]
Beware of surgical complications ^[1] — axillary nerve injury (runs 3–5 mm from the inferior capsule), residual stiffness

High Yield Summary

Non-operative is first-line for most patients — analgesics, subacromial steroid injection, physiotherapy (muscle strengthening, ROM exercise, pain relief) ^[1]

Non-operative candidates: Age of patient (elderly), demand of patients (low), partial tear, tear < 1 cm ^[1]

Operative indications: Tear > 1 cm, recurrent symptoms, weakness, lack of healing, tendon retraction, muscle atrophy ^[1]; failed conservative Tx, large and massive tears ^[2]

Operative options: Debridement → Repair (open vs arthroscopic) → Reconstruction if failed → Replacement if arthritis ^[1]

Key surgical adjuncts: Subacromial bursectomy and Acromioplasty to increase subacromial space ^[2]

Irreparable massive tears without arthritis: Tendon transfer (latissimus dorsi / pectoralis major)

Irreparable massive tears WITH arthritis: Reverse total shoulder arthroplasty ^[2]

Surgical repair usually achieves satisfactory results ^[1]

Bio-augmentation has no evidence to support routine use ^[1]

Post-op rehabilitation is critical: Phased protocol over 6–12 months; balance protection of repair vs prevention of stiffness

Active Recall - Management of Rotator Cuff Syndrome

References

^[1] Lecture slides: GC 236. Common Shoulder Problems [Updated in 2025].pdf (pages 82, 87–89, 93–96, 104–105, 117–119, 131) ^[2] Senior notes: maxim.md (sections 3.5–3.6, pages 486–489)

Complications of Rotator Cuff Syndrome

Complications of rotator cuff syndrome fall into two broad categories: (A) complications of the disease itself (natural history if untreated or progressive) and (B) complications of treatment (both conservative and operative). Understanding these from first principles is critical — every complication can be traced back to a specific anatomical or physiological mechanism.

A. Complications of the Disease (Natural History)

B. Complications of Treatment

Complication	Mechanism	Prevention / Management
Steroid-induced tendon weakening	Corticosteroids inhibit collagen synthesis by tenocytes, accelerate collagen degradation, and cause local fat necrosis → weakened tendon → increased risk of tear progression	Limit to 3 subacromial injections per year; never inject directly INTO the tendon substance; use USG guidance
Steroid-related skin/fat atrophy	Local corticosteroid causes adipocyte apoptosis and dermal thinning at the injection site → visible skin depression and depigmentation	Proper injection technique (ensure subacromial placement, not subcutaneous)
NSAID-related GI/renal/CV side effects	COX-1 inhibition → reduced gastric mucosal protection → ulceration; reduced renal prostaglandins → renal impairment; COX-2 inhibition → prothrombotic → CV risk	Short courses, gastroprotection (PPI) for high-risk patients, avoid in CKD/cardiac disease
Disease progression during conservative trial	While waiting, the tear may enlarge, retract, and develop fatty infiltration → may convert a reparable tear to an irreparable one	Close clinical monitoring; repeat imaging if symptoms worsen; don't blindly continue conservative Rx if there is progressive weakness
Secondary frozen shoulder	Immobility from pain → capsular contracture (as above)	Ensure PT includes ROM exercises alongside strengthening; adequate analgesia to enable participation

B2. Complications of Rotator Cuff Repair Surgery

Complication	Mechanism
Scapular notching	The humeral polyethylene component impinges on the inferior scapular neck during adduction → progressive bone erosion. Most common complication of RTSA. Usually asymptomatic but can cause loosening.
Instability / Dislocation	Altered biomechanics + loss of rotator cuff → reduced soft tissue tension → prosthesis can dislocate, especially in flexion-internal rotation
Infection	As with any arthroplasty; C. acnes is particularly common in shoulder arthroplasty (the shoulder has a high density of pilosebaceous glands)
Acromial / scapular spine fracture	RTSA increases the deltoid tension (to compensate for absent cuff). This increased tension can cause stress fractures of the acromion or scapular spine
Glenoid baseplate loosening	Mechanical failure of fixation → requires revision surgery
Periprosthetic fracture	Fracture of the humerus around the humeral stem

Prognosis / healing rate depends on comorbidities ^[1]:

DM ^[1] — glycosylation of collagen impairs tendon-to-bone healing; microangiopathy reduces blood supply to the repair site; delayed inflammatory resolution
Hypercholesterolaemia ^[1] — lipid deposition in tendons (xanthomatous tendinopathy); impaired tendon biology
Smoking status ^[1] — nicotine causes microvascular vasoconstriction → reduced oxygen delivery to healing tissue; carbon monoxide reduces oxygen-carrying capacity; directly toxic to tenocytes
All of the above may affect healing ^[1]

These are modifiable risk factors — optimising them pre-operatively improves surgical outcomes. This is why smoking cessation, HbA1c optimisation ( < 8%), and lipid management should be addressed before elective rotator cuff repair.

High Yield Summary

Disease complications:

Rotator cuff degeneration and tear ^[2] — impingement → tendinosis → partial tear → full-thickness tear (continuum)
Adhesive capsulitis (frozen shoulder) ^[2] — the most commonly cited complication of both impingement and rotator cuff tear; prevention via early mobilisation and adequate pain relief
Cuff tear arthropathy — end-stage massive tear with secondary GH OA; only treatable with reverse TSA
Muscle atrophy and fatty infiltration — irreversible beyond Goutallier 3; makes the tear irreparable even if tendon can be mobilised

Surgical complications:

Re-tear is the most common complication of rotator cuff repair (10–70% depending on tear size)
Healing rate depends on DM, hypercholesterolaemia, and smoking ^[1]
Post-operative stiffness, infection, nerve injury, anchor failure

Frozen shoulder procedure complications ^[1]: dislocation, axillary nerve injury (0.6%), superficial wound infection

Prevention of stiffness ^[1]: Early mobilisation + adequate pain relief

Active Recall - Complications of Rotator Cuff Syndrome

References

^[1] Lecture slides: GC 236. Common Shoulder Problems [Updated in 2025].pdf (pages 82, 88, 102, 105, 128, 130–131) ^[2] Senior notes: maxim.md (sections 3.5–3.6, pages 486–489)

High Yield Summary

Definition: Rotator cuff syndrome = continuum of subacromial impingement → calcific tendonitis → partial tear → full-thickness tear

Epidemiology: Age-related disease; 20% at 60–69y, 40.7% at ≥70y; up to 50% bilateral after age 60

Risk Factors (ASHTON): Age, Smoking, Hand dominance, Trauma, Occupation (heavy labour), Nfamily history + contralateral shoulder

Anatomy: SITS muscles (Supraspinatus, Infraspinatus, Teres minor, Subscapularis); critical hypovascular zone 10–15 mm from insertion; force couple with deltoid

Aetiology: Intrinsic (microtrauma, hypovascularity, degeneration) + Extrinsic (acromion shape, AC joint OA, coracoacromial ligament hypertrophy, GH instability)

Clinical Features:

Impingement: anterosuperior shoulder pain, painful arc (60–120°), Neer's sign, Hawkins' sign
Tear: lateral shoulder pain, weakness, night pain, muscle atrophy, ↓ active ROM but intact passive ROM, drop arm sign
Key distinction from frozen shoulder: passive ROM preserved in rotator cuff tear, lost in frozen shoulder

High Yield Summary

The Big Five DDx of shoulder pain: Rotator cuff syndrome (MC), Frozen shoulder, AC joint arthritis, Biceps tendonitis, Cervical radiculopathy

The single most important bedside distinction: Active vs passive ROM

Passive ROM preserved + active ROM reduced → Rotator cuff tear (motor unit failure)
Both active AND passive ROM reduced → Frozen shoulder (capsular contracture) or GH OA