• Clavicle ("little key" — Latin clavicula): S-shaped bone connecting sternum to acromion; fractures here are extremely common.
• Scapula ("shovel" — Latin): flat bone with the glenoid fossa (shallow socket), acromion (roof over the supraspinatus), coracoid process (attachment for short head of biceps, coracobrachialis, pectoralis minor).
• Humerus: The humeral head articulates with the glenoid (only ~25–30% of the head contacts the glenoid at any time → inherently unstable).

This is clinically the most important space for shoulder pain:

• Roof: Acromion + coracoacromial ligament + AC joint
• Floor: Humeral head (greater tuberosity)
• Contents: Supraspinatus tendon, long head of biceps tendon, subacromial bursa

When anything narrows this space (hooked acromion, AC joint osteophytes, humeral head migration superiorly due to weak rotator cuff) or enlarges the contents (bursitis, calcific tendinitis, swollen tendon), you get subacromial impingement ^[3].

The rotator cuff is a group of four muscles whose tendons form a confluent "cuff" that envelops the humeral head, providing dynamic stability and fine motor control.

• Glenoid labrum: Fibrocartilaginous ring deepening the glenoid by ~50%. The superior labrum is the attachment of the long head of biceps → SLAP (Superior Labrum Anterior to Posterior) lesions.
• Glenohumeral ligaments (superior, middle, inferior): Static stabilisers, especially the inferior glenohumeral ligament (most important for anterior stability in abduction).
• Coracoacromial ligament: Forms the "roof" of the subacromial space. Acts as a last restraint against superior humeral migration in massive cuff tears.
• Long head of biceps tendon: Runs through the bicipital groove and into the joint, attaching to the superior glenoid labrum. A common pain generator — it is intra-articular but extra-synovial.

Normal shoulder abduction involves a 2:1 ratio of glenohumeral to scapulothoracic motion. For every 3° of abduction, 2° occur at the GH joint and 1° at the scapulothoracic articulation. Disruption of this rhythm (scapular dyskinesis) is seen in rotator cuff disease and can perpetuate impingement.

• Axillary nerve (C5,6): wraps around the surgical neck of the humerus. At risk during shoulder dislocation and proximal humeral fractures. Supplies deltoid and teres minor. Regimental badge area sensory loss if damaged.
• Suprascapular nerve (C5,6): passes through suprascapular notch → infraspinous fossa via spinoglenoid notch. At risk of entrapment → supraspinatus/infraspinatus wasting.
• Long thoracic nerve (C5,6,7): supplies serratus anterior. Damage → winging of scapula ^[4].

• Labral tears (SLAP lesions, Bankart lesions)
• Septic arthritis of the shoulder ^[5] — hot, swollen tender joint = septic arthritis until proven otherwise ^[5]. Less common than knee but must not be missed. Most common organism: S. aureus.
• Crystal arthropathy: Gout (unusual site), pseudogout (calcium pyrophosphate deposition)

• Stage I: Oedema and haemorrhage of subacromial bursa/tendon (age < 25, reversible)
• Stage II: Fibrosis and tendinitis (age 25–40, recurrent pain)
• Stage III: Rotator cuff tear, bony changes (age > 40, progressive disability)

Rotator cuff syndrome (MC): pain during activity only, passive ROM > active ROM, external rotation spared (infraspinatus + teres minor) ^[2]

Why is this the most common? The supraspinatus tendon lives in a mechanically hostile environment — sandwiched between the acromion above and the humeral head below. Decades of overhead use lead to progressive tendon degeneration. By age 60, up to 30% of the population has an asymptomatic rotator cuff tear on MRI.

Distinguishing features within the rotator cuff continuum:

The key clinical discriminator: passive ROM > active ROM ^[2]. If the examiner moves the arm for the patient and it goes further than the patient can move it themselves, the joint is fine — the motor (rotator cuff) is the problem.

Frozen shoulder: DM as risk factor (check Hstix), symptoms change over time (pain → pain + stiffness → stiffness → resolution), night pain/rest pain (inflamed capsule); limited active + passive ROM ^[2]

Why does frozen shoulder look different from rotator cuff disease? Because the pathology is in the joint capsule, not the tendon. A contracted, fibrotic capsule physically prevents movement regardless of whether the patient or the examiner is trying to move the arm. Both active AND passive ROM are restricted — this is the capsular pattern.

Capsular pattern of the glenohumeral joint: ER > abduction > IR (external rotation is lost first and most). Why? The inferior glenohumeral ligament complex and axillary recess — the structures most affected by capsular fibrosis — are the primary check-reins to external rotation.

How to differentiate from GH OA and septic arthritis (which also restrict both active and passive ROM):

• Frozen shoulder: Insidious onset, no trauma, DM/thyroid association, three-phase disease course, no joint destruction on X-ray
• GH OA: Older patient, joint space narrowing and osteophytes on X-ray, crepitus, history of previous injury or cuff tear arthropathy
• Septic arthritis: Acutely unwell, fever, hot swollen joint, severely restricted in ALL directions, markedly elevated inflammatory markers

AC joint arthritis: more localised tenderness ^[2]

The AC joint sits superficially at the top of the shoulder. OA here produces pain that is precisely localised to the AC joint — you can point to it with one finger. This contrasts with the deeper, more diffuse pain of rotator cuff disease.

Why is it often missed? Because cross-body adduction (the scarf test) is not routinely performed, and clinicians may attribute the pain to the rotator cuff. The Paxinos sign (approach from behind, press up on posterolateral acromion while pressing clavicle down → pain) is specific for AC joint OA ^[4].

Biceps tendonitis: more localised tenderness ^[2]

The long head of biceps tendon runs through the bicipital groove on the anterior humerus. Pain is localised to this groove and is reproduced by resisted biceps contraction (Speed test, Yergason test). Why is it often associated with rotator cuff disease? Because the biceps tendon shares the same subacromial "neighbourhood" — it passes through the rotator interval, and inflammation from impingement often spills over to the biceps tendon.

Cervical radiculopathy: neck pain, radiating pain, weakness ^[2]

Dysfunction of the cervical spine (lower) is listed as the #1 probability diagnosis for arm and hand pain in Murtagh's framework ^[1]. This is critical — cervical spine pathology can perfectly mimic intrinsic shoulder disease.

Why does cervical radiculopathy cause shoulder pain? The shoulder is innervated by C5 (deltoid, supraspinatus via suprascapular nerve) and C6 (biceps, wrist extensors). A C5/6 disc herniation or osteophytic foraminal stenosis compresses the C5 or C6 root → pain perceived in the shoulder and radiating down the arm in a dermatomal distribution ^[8].

How to differentiate from intrinsic shoulder pathology:

There is no universally validated diagnostic criterion set, but the working clinical diagnosis rests on:

Investigations ^[3]: HbA1c (screen for DM); XR shoulder: rule out AC pathology; MRI shoulder: thickened joint capsule, rule out SAIS ^[3]

GCA should be screened for in every patient with PMR-type shoulder pain. The 1990 ACR Classification Criteria ^[9]:

≥ 3 of the following 5 criteria ^[9]:

1. Onset ≥ 50y
2. New headache
3. Abnormalities of temporal artery at clinical examination
4. ↑ ESR ( > 50 mm/h)
5. Abnormal findings on biopsy of temporal artery

Sensitivity ~93%, specificity ~91%. Note: temporal artery biopsy must be ordered urgently ( < 24–48h) because delay risks permanent visual loss from arteritic anterior ischaemic optic neuropathy ^[9].

Hot, swollen tender joint = septic arthritis until proven otherwise ^[5]. Diagnosis is confirmed by joint aspirate:

Joint fluid analysis is the MOST IMPORTANT TEST when septic arthritis is suspected ^[13].

No formal diagnostic criteria. Diagnosis is based on:

• Clinical: loss of active ROM (usually SIT) but intact passive ROM ^[3]; drop arm sign ^[3]; weakness on cuff-specific testing
• Imaging confirmation: USG shoulder (dynamic test for tear) ^[3] or MRI shoulder: gold standard, degree of tear (irreparable if fatty infiltration or muscle tendon atrophy) ^[3]

• Clinical: Painful arc + positive Neer/Hawkins
• Neer's test for impingement: if Neer's sign positive, repeat test after injecting 10mL 1% lignocaine into subacromial space → abolishment of pain helps confirm impingement ^[4][13]. This is both diagnostic and therapeutic — if the pain disappears with subacromial local anaesthetic, the pain generator is the subacromial space.

This is the first-line imaging for most shoulder conditions. It is cheap, fast, and widely available. The key is knowing exactly what to look for.

XR shoulder findings by condition ^[3]:

Views to request:

• Standard: AP (true AP in the plane of the scapula) + axillary lateral view
• Additional: Scapular Y-view (outlet view — shows acromion morphology); Zanca view (30° cephalad tilt — best for AC joint)
• Rule: Plain X-ray is not indicated in the absence of red flags and major trauma ^[1]. But in practice, XR is routinely done as baseline for chronic shoulder pain.

USG shoulder: dynamic test for tear ^[3]

Ultrasound is excellent for soft tissue evaluation around the shoulder and is increasingly the first-line imaging for suspected rotator cuff pathology in many centres, including Hong Kong.

Key USG findings:

MRI shoulder: gold standard for rotator cuff tear assessment ^[3]. MRI provides exquisite soft tissue contrast and is the investigation of choice when you need detailed information about:

Key MRI findings by condition:

When to order MRI:

• Suspected rotator cuff tear (especially if surgical candidate)
• Failed conservative management for 6 months (to assess for occult pathology)
• Suspected labral tear in young patient with instability
• Atypical frozen shoulder (to exclude intra-articular pathology)
• Cervical radiculopathy or myelopathy
• Suspected tumour or infection (with contrast)

Less commonly used for primary shoulder assessment but valuable in specific situations:

Consider nerve conduction studies ^[1] when:

Principle: NCS measures the speed and amplitude of electrical conduction along a nerve. A focal compression causes slowing (demyelination) or reduced amplitude (axonal loss) at the site. EMG detects denervation in muscle (fibrillations, positive sharp waves) — confirming active nerve injury.

Joint fluid analysis: MOST IMPORTANT TEST when septic arthritis, crystal arthropathy, or haemarthrosis is suspected ^[13].

Indications for shoulder joint aspiration:

• Acute hot swollen joint (septic arthritis until proven otherwise)
• Suspected crystal arthropathy
• Effusion of unclear aetiology
• Therapeutic drainage of large effusion

Synovial fluid interpretation ^[13]:

Why does inflammatory fluid have low viscosity? Inflammatory enzymes (proteases, hyaluronidases) released by activated neutrophils break down hyaluronic acid — the molecule responsible for the normal "stringy" viscosity of synovial fluid.

Neer's test for impingement ^[4][13]:

• Process: If Neer's sign positive, then repeat test after injecting 10mL 1% lignocaine into subacromial space ^[4][13]
• Interpretation: Abolishment of pain helps confirm impingement ^[4][13]
• Rationale: If the pain disappears when the subacromial space is anaesthetised, the pain generator must be within that space (supraspinatus tendon, subacromial bursa). If pain persists, consider an alternative source (AC joint, GH joint itself, referred).
• This is also therapeutic — if combined with corticosteroid, it treats the subacromial bursitis/tendinopathy.

Corticosteroids are potent anti-inflammatory agents that work by inhibiting phospholipase A2 → blocking the entire arachidonic acid cascade (both COX and lipoxygenase pathways) → profound ↓in prostaglandins, leukotrienes, and inflammatory cytokines. When injected locally, they deliver a high concentration directly to the site of inflammation with minimal systemic effects.

General contraindications to steroid injection: Active infection (local or systemic), overlying skin infection, uncontrolled DM (transient hyperglycaemia for 24–48h after injection), bleeding diathesis/anticoagulation (relative C/I).

Physiotherapy is the cornerstone of conservative management for virtually all shoulder conditions. The specific programme varies:

Conservative (first line): analgesia, steroid, physiotherapy (rotator cuff strengthening) ^[3]

Step-wise approach:

1. Activity modification — avoid overhead provocative activities
2. NSAIDs (oral) — 2–4 week course for acute flare
3. Subacromial corticosteroid injection — if oral analgesics inadequate. Provides a "window" of pain relief to allow effective physiotherapy
4. Physiotherapy (rotator cuff strengthening) ^[3] — this is the most important component. Evidence shows structured physiotherapy for 12 weeks is as effective as surgery in many patients
5. Reassess at 3–6 months

Operative ^[3]:

• Indications: failed conservative for 6 months ^[3]
• Approaches: usually arthroscopic ^[3]
• Procedures:
  • Surgical repair of supraspinatus / long head of biceps tendon → improve ROM ^[3]
  • Subacromial bursectomy: removes the inflamed bursa → increase subacromial space ^[3]
  • Acromioplasty (removal of a section of acromion — specifically the undersurface and any anterior hook) → increase subacromial space ^[3]
  • In practice, arthroscopic subacromial decompression (ASD) = bursectomy + acromioplasty + CA ligament release, performed as a single combined procedure

Why 6 months? The rotator cuff tendons have poor vascularity and slow healing biology. It takes at least 3–6 months of structured rehabilitation to see the maximum benefit from conservative treatment. Operating earlier may subject patients to unnecessary surgical risk.

Contraindications to surgery: Active infection, uncontrolled medical comorbidities, patient not motivated for post-operative rehabilitation (this is crucial — surgery without rehab often fails).

Management depends on a balance of factors:

Considerations ^[3]:

• Age & activity of patient — a 75-year-old sedentary patient with a small tear tolerates it well with conservative management; a 45-year-old labourer cannot
• Severity of tear (MRI) — size, retraction, irreparable if fatty infiltration or muscle tendon atrophy ^[3]
• Shoulder arthropathy status (shoulder not weightbearing thus primary OA uncommon) ^[3]

Conservative (Mainstay) ^[3]:

• Non-operative (mainstay): analgesics, steroid, PT ^[3]
• Appropriate for: partial tears, small full-thickness tears in older/low-demand patients, patients with significant comorbidities
• PT focuses on deltoid and periscapular muscle strengthening to compensate for the lost rotator cuff function

Operative ^[3]:

• Indications: failed conservative Tx / large and massive tears / > 2 weeks since injury ^[3]
  • The " > 2 weeks since injury" criterion applies to acute tears in young active patients — early repair (within 3 months) gives better outcomes because the tendon has not yet retracted and the muscle has not atrophied
• Procedures:
  • Surgical repair (arthroscopic / open) ^[3] — re-attach the torn tendon to its footprint on the greater tuberosity using suture anchors. Arthroscopic approach preferred for better cosmesis, less deltoid damage, and faster rehabilitation
  • Tendon transfer: if massive cuff tears ^[3] — when the cuff is irreparable. Common transfers:
    • Latissimus dorsi transfer → for irreparable posterosuperior cuff tears (replaces infraspinatus/teres minor function)
    • Pectoralis major transfer → for irreparable subscapularis tears
    • Lower trapezius transfer → emerging option for posterosuperior tears
  • Reverse total shoulder arthroplasty (fig.): if massive cuff tears + glenohumeral arthritis ^[3]
    • Why "reverse"? In a normal shoulder, the ball is on the humerus and the socket on the glenoid. In a reverse prosthesis, the ball (glenosphere) is placed on the glenoid and the socket on the humerus. This changes the biomechanics so that the deltoid (which is intact) can produce abduction without needing a functioning rotator cuff. The medialised centre of rotation increases the deltoid moment arm.
    • Indication: cuff tear arthropathy (massive irreparable tear + GH OA + pseudoparalysis)

Management is phase-dependent — this is the key concept:

Conservative (first line) ^[3]:

Additional conservative measures:

• Hydrodilatation (distension arthrography): Injection of saline + steroid + local anaesthetic into the GH joint under imaging guidance to physically distend and rupture the contracted capsule. Can provide rapid improvement in ROM. Growing evidence supports this in the frozen/early thawing phase.
• Oral corticosteroids: Short course (e.g., prednisolone 30mg tapering over 4–6 weeks) may provide rapid pain relief in the freezing phase, but effects may not be sustained.
• Optimise DM control: Check HbA1c — poor glycaemic control → more severe and prolonged disease due to ongoing collagen glycosylation ^[3].

Operative ^[3]:

• Indications: stiffness fails to improve after conservative management for 6 months ^[3]
• Modalities:
  • Manipulation under anaesthesia (MUA) ^[3]:
    • Technique: Patient under GA. Surgeon forcefully moves the shoulder through all planes of motion to mechanically rupture the contracted capsule.
    • Complications: fracture (esp. during ER) ^[3] — osteoporotic patients (e.g., elderly, prolonged steroid use) are at particular risk. The humeral shaft can fracture when the surgeon applies rotational force.
    • Must follow immediately with aggressive physiotherapy to prevent re-adhesion.
  • Arthroscopic capsular release ^[3]:
    • Technique: The contracted capsule (especially the rotator interval, anterior capsule, and inferior capsule/axillary recess) is directly divided under arthroscopic vision using electrocautery or a radiofrequency device.
    • Advantage: Controlled, precise release under direct vision — lower risk of fracture compared to MUA.
    • Complications: residual stiffness (early mobilisation) ^[3] — the most common complication. If the patient does not begin aggressive PT within 24–48h of surgery, the capsule may re-scar in the released position. Axillary nerve injury ^[3] — the axillary nerve runs very close to the inferior capsule (at the 6 o'clock position of the glenoid), which is the area that most needs release. Surgeons must stay above the 5:30 position to avoid it.

Management of tendinopathy ^[2]:

• Conservative (first line): analgesia, ice therapy, steroid, physiotherapy ^[2]
• Operative (rare): arthroscopic tenodesis (divide and reattach), tenotomy (divide the tendon) ^[2]
  • Tenodesis ("teno" = tendon, "desis" = binding): The long head of biceps is detached from the superior labrum and re-attached to the bicipital groove or proximal humerus using an interference screw. Preserves cosmesis and biceps function. Preferred in younger, active patients.
  • Tenotomy ("teno" = tendon, "tomy" = cutting): Simply cut the biceps tendon at its origin → the tendon retracts distally → Popeye deformity. Very simple procedure. Minimal rehab. Preferred in older, lower-demand patients who will tolerate the cosmetic deformity. Mild strength loss in supination (~15%) but usually not clinically significant.

Management of rupture ^[2]:

• Conservative: analgesia, physiotherapy — appropriate for proximal (long head) biceps rupture in older patients. The brachialis and supinator compensate for elbow flexion and forearm supination respectively. Elbow flexion and supination intact (due to brachialis & supinator) ^[2].
• Operative: form a bone tunnel in radius to re-insert tendon end (single-incision vs dual-incision technique) ^[2] — indicated for distal biceps rupture (complete avulsion from the radial tuberosity) in active patients, because distal rupture causes significant (30–40%) loss of supination strength and moderate loss of flexion strength.

Conservative:

• Activity modification (avoid cross-body movements, heavy pressing)
• Oral analgesia (paracetamol, NSAIDs)
• Intra-articular AC joint corticosteroid injection (diagnostic and therapeutic)

Operative:

• Indication: Failed conservative management
• Procedure: Arthroscopic distal clavicle excision (Mumford procedure) — remove 5–10mm of the distal clavicle → eliminates bone-on-bone contact while preserving the AC and CC ligaments for stability. Very reliable operation with good outcomes.

Conservative: analgesics, cervical collar, physiotherapy ^[8]

• First line: Most cervical radiculopathies (80–90%) resolve with conservative management over 6–12 weeks
• Analgesia: NSAIDs ± neuropathic agents (gabapentin/pregabalin if shooting/burning pain)
• Cervical collar: Short-term (max 2 weeks) — provides rest and reduces neck movement
• PT: Cervical traction, postural training, isometric strengthening of deep cervical flexors
• Epidural steroid injection: Considered for refractory radicular pain — delivers corticosteroid to the inflamed nerve root

Surgical: if intractable pain or progressive neurological deficits ^[8]

• Anterior decompression and fusion: removal of a core of bone and disc with its osteophytes ^[8] — the standard approach for single-level disc herniation. Removes the disc compressing the root and replaces it with a bone graft or cage → the two vertebrae fuse together.
• Posterior laminectomy: wide multilevel removal of spinal lamina for multilevel cord decompression ^[8] — used when there is multilevel stenosis causing myelopathy.
• Foraminotomy: drilling away overlying bone at IV foramina for decompression of radiculopathy ^[8] — preserves motion (no fusion required). Good for foraminal stenosis from osteophytes.

Urgent surgical indications:

• Progressive motor deficit (suggests ongoing nerve root destruction)
• Cervical myelopathy (cord compression → UMN signs) — this does NOT improve spontaneously and usually progresses
• Cauda equina equivalent features in the cervical cord (bilateral UMN signs, sphincter disturbance) → emergency

• Urgent prednisolone — the hallmark of PMR management is the dramatic response to low-dose prednisolone
• Starting dose: Prednisolone 15 mg/day (contrast with GCA which requires 40–60 mg/day)
• Response: > 70% improvement in symptoms within 1 week — if no response, reconsider the diagnosis
• Gradual ↓dosage to maintenance level according to ESR level ^[9] — taper very slowly (1–2 mg every 4–6 weeks). Most patients require 1–2 years of treatment. Relapses are common if tapered too fast.
• Steroid-sparing agent: Methotrexate (7.5–10 mg/week) considered if relapsing disease or unable to taper below 7.5 mg prednisolone
• Screen for GCA in all PMR patients — if headache, jaw claudication, visual symptoms, or temporal artery abnormalities develop → immediate high-dose prednisolone (60 mg) + urgent temporal artery biopsy ^[9]

This is a rheumatological emergency — joint cartilage can be destroyed within days:

Complications of SAIS ^[3]:

• Rotator cuff degeneration and tear
• Adhesive capsulitis (frozen shoulder)

Why does SAIS progress to rotator cuff tear? Chronic mechanical impingement of the supraspinatus tendon against the acromion causes repetitive microtrauma → collagen fibre disorganisation → tendinosis (failed healing response with mucoid degeneration and neovascularisation) → progressive weakening → partial tear → full-thickness tear. This is essentially Neer's Stage I → II → III progression. The tendon's poor vascularity at the watershed zone means it cannot repair itself adequately under ongoing mechanical stress.

Why does SAIS lead to frozen shoulder? Pain from impingement causes guarding and reduced shoulder use → disuse leads to capsular inflammation and fibrosis → secondary adhesive capsulitis. This is why early physiotherapy (within the pain-free range) is important even in SAIS — to prevent the secondary complication of capsular contracture.

Complication of rotator cuff tear ^[3]: adhesive capsulitis, recurrence

Cuff tear arthropathy: When a massive rotator cuff tear goes untreated, the humeral head is no longer held centred in the glenoid. The unopposed pull of the deltoid drives the humeral head superiorly → chronic articulation between the humeral head and the acromion (instead of the glenoid) → "acetabularisation" of the acromion and "femoralization" of the humeral head → secondary glenohumeral OA. This end-stage condition is called cuff tear arthropathy and is the primary indication for reverse total shoulder arthroplasty ^[3].

Why adhesive capsulitis? Same mechanism as with SAIS — pain leads to disuse, disuse leads to capsular fibrosis. Additionally, any shoulder surgery for rotator cuff repair inherently risks adhesive capsulitis from post-operative immobilisation (the very sling that protects the repair also immobilises the capsule).

Recurrence of tear after surgical repair: Re-tear rates after rotator cuff repair are significant — ranging from 20% for small tears to > 70% for massive tears. Why? The repaired tendon must heal back to bone (tendon-to-bone healing), which is biologically challenging because the normal enthesis (the gradual transition zone from tendon → fibrocartilage → mineralised cartilage → bone) is never fully regenerated. Instead, a weaker fibrovascular scar forms at the repair site.

Thawing phase: 5–24 months — may not completely resolve spontaneously ^[3]

While frozen shoulder is often described as "self-limiting," the reality is more nuanced:

• Up to 40% of patients have persistent restriction of motion (usually ER and IR) at long-term follow-up
• Diabetic patients have a worse prognosis — more severe stiffness, longer disease duration, and higher rates of residual restriction. This is because ongoing collagen glycosylation continues to drive capsular fibrosis even during the "thawing" phase.
• Muscle atrophy: Prolonged disuse leads to wasting of deltoid, supraspinatus, and infraspinatus. Even after ROM returns, the patient may have weakness from deconditioning that requires months of rehabilitation.

Complications of shoulder dislocation ^[15]:

• Recurrence — the Bankart lesion (avulsion of anterior-inferior labrum) creates a permanent defect in the static stabilising ring. Recurrence rate after first-time anterior dislocation: ~50–90% in patients < 20 years old, ~10–25% in patients > 40. Why such an age difference? Younger patients have more elastic capsules and ligaments, so the labral detachment does not scar down as firmly. They also tend to be more active and expose the shoulder to further risk.
• Chronic pain / stiffness — from capsulolabral scarring and inflammation
• Adhesive capsulitis — especially if prolonged immobilisation after reduction
• Rotator cuff injury — in patients > 40 with dislocation, the rotator cuff (especially supraspinatus) often tears at the time of dislocation because the ageing tendon is weaker than the capsulolabral complex ^[15]
• Nerve damage (especially axillary & suprascapular nerve) ^[15] — the axillary nerve wraps around the surgical neck of the humerus and is stretched during inferior displacement of the humeral head. Axillary nerve injury occurs in ~5–35% of anterior dislocations (higher in older patients). Results in: deltoid weakness + loss of sensation over the "regimental badge area" (lateral deltoid). Suprascapular nerve injury causes supraspinatus and infraspinatus weakness.
• Degenerative joint disease, e.g. secondary OA ^[15] — from damage to the articular cartilage at the time of dislocation (Hill-Sachs lesion = impression fracture of posterior humeral head; glenoid rim fractures) → altered joint mechanics → accelerated wear

If not treated urgently:

• Cartilage destruction: Bacterial proteases and inflammatory enzymes (matrix metalloproteinases, collagenases) released by activated neutrophils destroy the articular cartilage within 48–72 hours. Cartilage has no intrinsic blood supply and cannot regenerate — the destruction is irreversible.
• Osteomyelitis: Infection can spread from the joint into the adjacent bone
• Systemic sepsis: Bacteraemia from the infected joint → septic shock, multi-organ failure
• Secondary OA: Even after successful treatment, the damaged cartilage surface leads to premature OA
• Ankylosis: In severe cases, complete joint destruction leads to fibrous or bony fusion

If cervical spondylosis progresses from foraminal stenosis (radiculopathy) to central canal stenosis (myelopathy), the consequences are far more severe ^[8]:

• Arms: LMN signs at the level of compression + sensory loss
• Legs: UMN signs (spasticity, hyperreflexia, Babinski positive) + spastic scissoring gait
• Sphincter: Late feature — bladder dysfunction
• Key point: Unlike radiculopathy, which can often be managed conservatively, myelopathy usually does not improve spontaneously and typically progresses → earlier surgical decompression is warranted ^[8]

Shoulder pain from any cause that leads to prolonged immobilisation or disability can result in systemic complications. This is particularly relevant in the context of post-stroke shoulder ^[16]:

Prolonged immobilisation ^[16]: pressure sores, contractures, frozen shoulder, shoulder subluxation