Hand, wrist, or elbow pain is a clinical presentation of discomfort in the upper extremity that may arise from musculoskeletal, neurological, or inflammatory conditions such as carpal tunnel syndrome, tendinopathy, arthritis, or epicondylitis.

Elbow Pain

2. Epidemiology and Risk Factors

Condition	Prevalence / Incidence	Key demographics
Carpal tunnel syndrome	Most common entrapment neuropathy; prevalence ~3–5% in general population	Aging, female predominance ^[1]^[2]
Lateral epicondylitis (tennis elbow)	Point prevalence 1–3%; more common than medial epicondylitis	Peak age 35–55 y; dominant arm ^[2]
Medial epicondylitis (golfer's elbow)	~0.4% general population	Similar age range; less common ^[2]
De Quervain's tenosynovitis	Incidence ~0.5/1000 person-years	Female 30–50 y, pregnancy ^[2]
Trigger finger	Lifetime prevalence 2–3%	Elderly female, occupation with prolonged gripping ^[2]
Osteoarthritis of hand	Radiographic OA in >50% over age 55	F > M; 1st CMC, DIP, PIP joints
Rheumatoid arthritis (hand)	0.3–0.4% in Chinese, 1–2% in Caucasians	F:M ≈ 3:1; peak onset 35–55 y ^[3]
Gout (wrist/hand/elbow)	~1–2% overall prevalence	M >> F; 4th–5th decade in men ^[4]
Cubital tunnel syndrome	2nd most common entrapment neuropathy	More in males, occupations with prolonged elbow flexion ^[2]

3. Relevant Anatomy and Function

Understanding the anatomy is the key to localising the pain. Let's build it from proximal to distal.

Six extensor compartments on the dorsal aspect of the wrist, separated by fibrous septa ^[2]:

Compartment	Tendons	Clinical relevance
1st	APL (abductor pollicis longus) & EPB (extensor pollicis brevis)	De Quervain's tenosynovitis
2nd	ECRL & ECRB	Intersection syndrome
3rd	EPL (extensor pollicis longus)	Rupture after Colles' fracture (Lister's tubercle)
4th	EDC & EIP	Extensor tenosynovitis (RA)
5th	EDM (extensor digiti minimi)
6th	ECU (extensor carpi ulnaris)	ECU tendinopathy

Nerve	Motor	Sensory	Clinical test
Median	Thenar muscles (LOAF = Lumbricals 1&2, Opponens pollicis, Abductor pollicis brevis, Flexor pollicis brevis superficial head)	Palmar: lateral 3.5 digits; Dorsal: tips of same	Abductor pollicis brevis strength; pen-touching test
Ulnar	Hypothenar muscles, interossei, medial 2 lumbricals, adductor pollicis	Medial 1.5 digits (palmar and dorsal)	Froment's sign (tests adductor pollicis)
Radial (superficial)	Nil intrinsic hand muscles	Dorsum of hand (1st web space) — "anatomical snuffbox" area	Sensory only in hand

Why does median nerve compression cause thenar wasting but not hypothenar?

Because the median nerve supplies LOAF muscles (all in the thenar eminence and radial lumbricals). The ulnar nerve supplies everything else intrinsic to the hand. In carpal tunnel syndrome, the median nerve is compressed under the flexor retinaculum, so only its territory is affected.

4. Etiology (Focused on Hong Kong Context) and Pathophysiology

Murtagh's diagnostic strategy for arm and hand pain organises causes by clinical likelihood ^[1]:

Diagnosis	Pathophysiology
Dysfunction of the cervical spine (lower)	C5–C8 radiculopathy → referred pain to arm/hand via dermatomal distribution. Disc herniation or spondylosis compresses nerve roots in the neural foramen.
Disorders of the shoulder	Rotator cuff pathology or adhesive capsulitis → pain radiates distally. The brain poorly localises deep somatic pain, so shoulder pathology is "felt" in the upper arm/elbow.
Medial or lateral epicondylitis	Repetitive overuse → micro-tears at tendon origin → chronic inflammation → angiofibroblastic degeneration (actually a tendinopathy more than a true "-itis") ^[2].
Overuse tendonopathy of the wrist	De Quervain's, intersection syndrome, ECU tendinopathy — repetitive motion causes frictional inflammation within tendon sheaths.
Carpal tunnel syndrome	Anything that ↑ pressure within the carpal tunnel (oedema, tenosynovitis, mass) → median nerve compression → ischaemia of nerve → paraesthesia, pain, then motor loss.
Osteoarthritis of the thumb (1st CMC) and DIP joints	Mechanical wear → cartilage loss → subchondral sclerosis → osteophyte formation. Heberden's (DIP) and Bouchard's (PIP) nodes are bony osteophytes ^[5].

Category	Diagnoses	Why it matters
Cardiovascular	Angina (referred), myocardial infarction, axillary vein thrombosis, arm claudication (left arm)	MI can present as isolated left arm pain. Visceral afferents from the heart enter the spinal cord at T1–T4, converging with somatic afferents from the left arm → referred pain.
Infection	Septic arthritis (shoulder/elbow), osteomyelitis, infections of tendon sheath and fascial spaces of hand, sporotrichosis ("gardener's arm")	Tendon sheath infections (esp. flexor tenosynovitis) can destroy the flexor tendon and spread along the Parona space. Kanavel's signs are cardinal: fusiform swelling, flexed posture, tenderness along sheath, pain on passive extension.
Neoplasia	Pancoast tumour, bone tumours (rare)	A Pancoast tumour (apical lung SCC) invades the brachial plexus (C8–T1) → shoulder/arm/hand pain with Horner's syndrome. Always do a CXR if pain is atypical.

Don't Miss This

Left arm pain + jaw pain + diaphoresis → think MI first, even in a young patient. In Hong Kong, where ischaemic heart disease is a leading cause of mortality, always rule out cardiac causes of arm pain before attributing it to MSK pathology.

Diagnosis	Why it's missed
Entrapment neuropathies (e.g. median nerve, ulnar nerve)	Symptoms mimic cervical radiculopathy. Always do Tinel's/Phalen's and nerve conduction studies to localise the lesion.
Pulled elbow (children)	"Nursemaid's elbow" — subluxation of the radial head from the annular ligament when a child is pulled by the forearm. The child holds the arm pronated and slightly flexed, refuses to use it. Easily reduced by supination-flexion manoeuvre.

5. Detailed Etiology and Pathophysiology by Condition

Etymology: "thoracic outlet" = the space between the clavicle and first rib through which the brachial plexus, subclavian artery, and subclavian vein pass.

Risk factors: cervical rib, fibrous bands, scalene muscle hypertrophy, repetitive microtrauma (athletes), poor posture ^[2].

Classification ^[2]:

Type	Structure compressed	Signs	Treatment
Neurological (nTOS)	Lower brachial plexus	Lower brachial plexus injury (paraesthesia/weakness along ulnar distribution)	Physiotherapy ± Botox injection to relax scalene muscles
Venous (vTOS)	Subclavian vein	Deep vein thrombosis (Paget-Schroetter syndrome)	Thrombolysis, anticoagulation, surgical decompression
Arterial (aTOS)	Subclavian artery	Claudication, acute limb ischaemia	Embolectomy, surgical decompression

Special tests: Adson's manoeuvre, Roos test, Elvey's test ^[2].

Investigations: CXR (cervical rib?), Doppler USG, nerve conduction studies, MRI, CT angiogram ^[2].

6. Classification

Process	Examples
Mechanical/Degenerative	OA, epicondylitis, De Quervain's, trigger finger
Inflammatory/Autoimmune	RA, gout, CPPD, psoriatic arthritis, SLE
Compressive/Entrapment	CTS, cubital tunnel, TOS, Guyon's canal
Infective	Septic arthritis, tendon sheath infection, osteomyelitis
Vascular	Buerger's disease, Raynaud's, DVT, arterial embolism
Neoplastic	Pancoast tumour, bone tumours, enchondroma
Referred	Cervical radiculopathy, cardiac

Green's Classification of Trigger Finger ^[2]:

Grade	Description
I	Palm pain and tenderness at A1 pulley
II	Catching of digit, can actively extend
III	Locking of digit, passively correctable
IV	Fixed flexion deformities

Frozen Shoulder Phases ^[2] (relevant because shoulder pathology can present as "arm pain"):

Phase	Duration	Features
Freezing (pain)	2–9 months	Progressive pain, especially at night
Frozen (pain + stiffness)	4–12 months	Marked loss of ROM, especially ER/IR
Thawing (stiffness)	5–24 months	Gradual improvement, may not fully resolve

7. Clinical Features — Symptoms and Signs (with Pathophysiological Basis)

7.2 Condition-Specific Symptoms

7.3 Key Clinical Signs (Examination Findings)

Finding	Condition	Mechanism
Heberden's nodes (DIP)	OA	Osteophyte formation at DIP margins
Bouchard's nodes (PIP)	OA	Osteophyte formation at PIP margins
Ulnar deviation at MCPs	RA	Synovitis → ligament/tendon laxity → ulnar drift
Swan-neck deformity	RA	PIP hyperextension + DIP flexion from extensor mechanism disruption
Boutonnière deformity	RA	Central slip rupture → PIP flexion + DIP hyperextension
Z-deformity of thumb	RA	MCP flexion + IP hyperextension
Gottron's papules	Dermatomyositis	Autoimmune → scaly papules over finger joints
Thenar wasting	CTS (advanced)	Chronic median nerve compression → denervation atrophy of APB
Hypothenar/intrinsic wasting	Ulnar neuropathy	Ulnar nerve compression → denervation of intrinsic muscles
Fusiform swelling of finger	Flexor tenosynovitis (Kanavel)	Pus distends the tendon sheath uniformly
Dupuytren's contracture	Fibromatosis	Palmar fascia thickening → progressive MCP/PIP flexion contracture

Test	Condition	Technique	Positive finding	Mechanism
Phalen's test	CTS	Wrist held in full flexion for 60 s	Paraesthesia in median nerve distribution	Flexion ↑ carpal tunnel pressure → reproduces nerve compression
Tinel's sign (wrist)	CTS	Tap over flexor retinaculum at wrist	Tingling in median nerve territory	Percussing a compressed nerve produces distal dysaesthesia
Finkelstein's test	De Quervain's	Thumb grasped in fist, sharply deviate wrist ulnarly	Acute pain at radial styloid and along EPB/APL tendons ^[2]	Ulnar deviation stretches the inflamed APL/EPB tendons over the narrowed first compartment
Cozen's test	Lateral epicondylitis	Pronate + radially deviate forearm → extend wrist against resistance ^[2]	Pain at lateral epicondyle	Resisted wrist extension loads the ECRB at its origin on the lateral epicondyle
Mill's test	Lateral epicondylitis	Pronate forearm, flex wrist, and extend elbow ^[2]	Pain at lateral epicondyle	Passively stretching the extensor origin by fully flexing the wrist with the elbow extended
Reverse Cozen's/Golfer's test	Medial epicondylitis	Resist wrist flexion with forearm supinated	Pain at medial epicondyle	Loads the common flexor origin
Tinel's sign (elbow)	Cubital tunnel	Tap over cubital tunnel (posterior to medial epicondyle)	Tingling in ulnar distribution	Percussion of compressed ulnar nerve
Elbow flexion test	Cubital tunnel	Hold elbow in full flexion for 60 s	Paraesthesia in ulnar distribution	Flexion narrows the cubital tunnel, compressing the nerve
Froment's sign	Ulnar neuropathy	Ask patient to hold paper between thumb and index finger; pull paper away	Thumb IP flexes (uses FPL — median nerve) instead of adducting	Adductor pollicis (ulnar nerve) is weak; patient compensates with FPL
Grind test	1st CMC OA	Forcefully push thumb against CMC joint with rotation ^[2]	Pain and crepitus	Axial loading of arthritic joint surfaces
Phalen-like for Guyon's	Guyon's canal	Sustained wrist extension	Ulnar paraesthesia	Extension compresses ulnar nerve/artery in the canal
Adson's manoeuvre	TOS	Extend neck, rotate head to affected side, deep breath; palpate radial pulse	Loss/diminution of radial pulse	Scalene muscle contraction compresses the subclavian artery

Finkelstein's vs. Eichhoff's Test

Strictly, Finkelstein's original test involves the examiner passively deviating the wrist ulnarly while the patient grips the thumb. The commonly performed version (patient makes a fist over the thumb, then actively deviates) is actually Eichhoff's test. Both are acceptable clinically, but Eichhoff's has a higher false-positive rate because it also stretches the 1st CMC joint. If Eichhoff's is positive, consider checking the grind test to exclude 1st CMC OA.

Finding	Nerve	Lesion site	Why?
Loss of sensation in palmar lateral 3.5 digits + thenar wasting	Median	Carpal tunnel	Median nerve compressed under flexor retinaculum
Loss of sensation in medial 1.5 digits (palmar AND dorsal) + intrinsic wasting + less claw	Ulnar	Cubital tunnel (elbow)	High lesion: dorsal branch affected (branches proximal to Guyon's canal); FDP 4/5 paralysed → less clawing
Loss of sensation in medial 1.5 digits (palmar only) + more prominent claw	Ulnar	Guyon's canal (wrist)	Low lesion: dorsal sensation spared; FDP 4/5 intact → IP flexion preserved → more clawing
Wrist drop + loss of sensation in 1st dorsal web space	Radial	Spiral groove (humerus)	Radial nerve compressed against humerus (Saturday night palsy)

A systematic approach for the clinical exam:

History:

Pain characteristics (SOCRATES).
Functional impact (grip strength, fine motor, ADLs).
Occupational history (repetitive tasks?).
Systemic review (constitutional symptoms → infection/malignancy; other joint involvement → RA/gout; cardiac symptoms → angina).
Past medical history (DM, thyroid, RA, pregnancy).
Drug history (diuretics → gout).

Examination — the "LOOK, FEEL, MOVE, SPECIAL TESTS" approach:

Look: Deformities, swelling, wasting, skin changes, nodules.
Feel: Tenderness (localise!), warmth, crepitus, pulses.
Move: Active and passive ROM of each joint; compare sides.
Special tests: As per table above, guided by clinical suspicion.
Neurovascular assessment: Sensory (light touch, pinprick), motor (intrinsic hand muscles), reflexes, pulses.

High Yield Summary

Top-line take-aways for exams:

Probability diagnoses for arm/hand pain (Murtagh): cervical spine dysfunction, shoulder disorders, epicondylitis, overuse tendinopathy of wrist, CTS, OA of thumb/DIP ^[1].
Serious conditions not to miss: MI/angina (referred left arm pain), septic arthritis, tendon sheath infection, Pancoast tumour ^[1].
CTS risk factors = aging, female, DM, hypothyroid, RA, obesity, pregnancy. Night pain + flick sign + Phalen's/Tinel's = classic presentation ^[2].
Lateral epicondylitis > medial epicondylitis. Tests: Cozen's and Mill's (lateral); reverse Cozen's (medial) ^[2].
De Quervain's = 1st extensor compartment (APL + EPB). Finkelstein's test. DDx: 1st CMC OA (grind test), Wartenberg's syndrome, intersection syndrome ^[2].
Trigger finger = A1 pulley stenosis. Green's grading (I–IV). Risk: DM, prolonged gripping, elderly female ^[2].
Cubital tunnel = ulnar nerve at elbow. High lesion → LESS claw (ulnar paradox). Distinguish from Guyon's canal by dorsal sensation ^[2].
RA hand = MCP ulnar deviation, swan-neck, boutonnière, Z-thumb. SPARES DIP. OA = Heberden's (DIP) + Bouchard's (PIP) ^[3]^[5].
Kanavel's signs (flexor tenosynovitis): fusiform swelling, flexed posture, sheath tenderness, pain on passive extension — a surgical emergency.
Always consider referred pain (cervical spine, cardiac) before attributing to local MSK pathology.

Active Recall - Hand/Wrist/Elbow Pain

Differential Diagnosis of Hand / Wrist / Elbow Pain

The differential diagnosis (DDx) for hand/wrist/elbow pain is broad because three anatomical segments, multiple tissue types (bone, joint, tendon, nerve, vessel), and several pathological processes (mechanical, inflammatory, compressive, infective, vascular, neoplastic, referred) all converge in one presenting complaint. The clinical task is to localise (where?) and characterise (what process?) — then the DDx narrows dramatically.

Murtagh's Diagnostic Strategies ^[1] provide the single best exam-oriented framework. Every cause of arm/hand pain slots into one of five tiers:

Tier	Meaning	Examples
Probability diagnosis	Common, high-prevalence conditions you'll see most days	Dysfunction of the cervical spine (lower); Disorders of the shoulder; Medial or lateral epicondylitis; Overuse tendonopathy of the wrist; Carpal tunnel syndrome; Osteoarthritis of the thumb and DIP joints
Serious disorders not to be missed	Low-prevalence but high-mortality/morbidity; must be actively excluded	Cardiovascular: angina (referred), myocardial infarction, axillary vein thrombosis, arm claudication (left arm); Infection: septic arthritis (shoulder/elbow), osteomyelitis, infections of tendon sheath and fascial spaces of hand, sporotrichosis ("gardener's arm"); Neoplasia: Pancoast tumour, bone tumours (rare)
Pitfalls (often missed)	Conditions commonly overlooked that cause diagnostic delay	Entrapment neuropathies (e.g. median nerve, ulnar nerve); Pulled elbow (children)
Seven masquerades	Common systemic diseases mimicking MSK pain	Depression, diabetes, drugs, anaemia, thyroid disease, spinal dysfunction, UTI
Is the patient trying to tell me something?	Psychogenic / functional overlay	Chronic pain syndrome, secondary gain

Exam Tip — Murtagh's Tiers

For any OSCE or written question that asks "Give the differential diagnosis of arm/hand pain", structuring your answer by Murtagh's five tiers (probability → serious → pitfalls → masquerades → psychogenic) demonstrates systematic thinking and scores well. Always mention the serious disorders explicitly — examiners want to hear that you won't miss an MI or septic arthritis.

3. Detailed Differential Diagnosis — Distinguishing Features

The real clinical question isn't just "what are the differentials?" but "how do I tell them apart?" Below is a condition-by-condition breakdown, grouped by region, with the key discriminating features.

Condition	Key discriminating features	Why this pattern? (Pathophysiological basis)
Lateral epicondylitis (tennis elbow)	Lateral elbow pain radiating down extensor forearm; worse with gripping/wrist extension; Cozen's test +, Mill's test + ^[2]	Micro-tears at ECRB origin on lateral epicondyle; resisted wrist extension reproduces the load on damaged tendon
Medial epicondylitis (golfer's elbow)	Medial elbow pain; worse with wrist flexion/pronation; may have associated ulnar paraesthesia ^[2]	Micro-tears at common flexor origin on medial epicondyle; proximity of ulnar nerve → concurrent neuropathy
Olecranon bursitis	Discrete, fluctuant swelling over olecranon; may be warm if infected or gouty	The olecranon bursa is superficial and prone to friction, trauma, or crystal/bacterial inflammation
OA elbow	Stiffness, loss of terminal extension, crepitus; XR: osteophytes, joint space narrowing	Cartilage wear → mechanical block from osteophytes → loss of ROM
Cubital tunnel syndrome	Medial 1.5-digit paraesthesia (palmar AND dorsal); less prominent claw hand; cubital valgus, Tinel sign at elbow, elbow flexion test + ^[2]	High ulnar nerve lesion → dorsal cutaneous branch affected (branches proximal to wrist); FDP 4/5 paralysed → less clawing (ulnar paradox)
PIN compression (radial tunnel syndrome)	Deep aching in proximal extensor forearm; weakness of finger/thumb extension WITHOUT wrist drop (ECRL spared — branches above arcade of Frohse); no sensory loss	PIN is purely motor after it dives through the supinator; compression at arcade of Frohse → motor deficit only
Pulled elbow (children) ^[1]	Toddler (1–4 y) refuses to use arm after being pulled; arm held pronated and slightly flexed; no swelling, no XR abnormality	Sudden longitudinal traction on extended elbow → radial head subluxes out of the annular ligament (which is relatively lax in toddlers)
Septic arthritis ^[1]^[3]	Hot, swollen, extremely painful elbow with restricted ROM in ALL directions; fever; ↑WBC/CRP; joint aspiration shows purulent fluid	Bacterial invasion → synovitis → purulent effusion → cartilage destruction in days if untreated
Gout/CPPD of elbow	Acute monoarthritis; olecranon bursitis common in gout (tophaceous deposits); gout: negatively birefringent needle crystals; CPPD: weakly positively birefringent rhomboid crystals ^[4]	Crystal deposition → NLRP3 inflammasome → IL-1β → neutrophilic inflammation

Lateral vs. Medial Epicondylitis — Quick Rule

Lateral = extensors = "tennis" = pain on resisted wrist extension (Cozen's)
Medial = flexors = "golfer's" = pain on resisted wrist flexion (reverse Cozen's) The side of the epicondyle tells you which muscle group is involved.

Condition	Key discriminating features	Pathophysiological basis
De Quervain's tenosynovitis	Radial wrist pain at 1st extensor compartment; swelling over radial styloid; Finkelstein's test + ^[2]	Stenosing tenosynovitis of APL/EPB → pain reproduced by stretching these tendons (ulnar deviation with thumb tucked)
1st CMC joint OA (DDx for De Quervain's)	Pain at base of thumb; Grind test + (axial load + rotation of thumb against trapezium) ^[2]; XR: joint space narrowing at CMC	Cartilage loss at trapeziometacarpal articulation; the grind test bypasses the tendons and directly loads the joint surfaces
Wartenberg's syndrome (DDx for De Quervain's)	Paraesthesia over radial dorsal hand; common in those wearing tight watch/jewellery ^[2]; no tendon tenderness	Neuritis of the superficial branch of the radial nerve — compressed by external pressure, NOT a tendon problem
Intersection syndrome (DDx for De Quervain's)	Pain/swelling ~4 cm proximal to Lister's tubercle on dorsal forearm; crepitus	APL & EPB cross over 2nd compartment (ECRL & ECRB) tendons ^[2] → frictional peritendinitis at the intersection point
Carpal tunnel syndrome	Nocturnal paraesthesia in lateral 3.5 digits; flick sign; thenar wasting (late); Phalen's +, Tinel's + ^[2]	Median nerve compression under flexor retinaculum → ischaemia → sensory then motor loss
Guyon's canal syndrome	Medial 1.5-digit paraesthesia (palmar only, dorsal spared); more prominent claw; hypothenar wasting; cyclist/handlebar use	Ulnar nerve compressed between pisiform and hook of hamate; dorsal branch already departed proximally → dorsal sensation intact
Scaphoid fracture/non-union	History of FOOSH; anatomical snuffbox tenderness; pain on axial loading of thumb ^[2]	Blood supply enters distally and runs retrograde → proximal pole fractures have highest AVN risk; non-union → SNAC wrist (progressive arthritis)
Kienbock's disease	Dorsal wrist pain over lunate; ↓grip strength; occurs in young adults with negative ulnar variance	AVN of the lunate → collapse → altered carpal mechanics → secondary OA
TFCC injury	Ulnar-sided wrist pain; ↑ with pronation/supination and ulnar deviation; "fovea sign" (tenderness in soft spot between FCU and ulnar styloid)	Triangular fibrocartilage complex acts as cushion/stabiliser between ulna and carpus; tear disrupts load transmission
RA wrist	Symmetrical synovitis of wrists; dorsal tenosynovitis; radial deviation of wrist (with ulnar deviation of fingers); morning stiffness > 30 min ^[3]^[5]	Pannus erodes cartilage and ligaments; the extensor tendons in compartments 4–6 are commonly involved
Ganglion cyst	Dorsal wrist (70%), painless, spherical, smooth, firm, transilluminable; no malignant potential ^[6]^[7]	Periarticular mucoid degeneration → herniation of connective tissue → cyst filled with synovial/mucinous fluid ^[6]
Gout / CPPD of wrist	Acute monoarthritis; wrist is the 2nd most common site for CPPD after knee ^[4]; chondrocalcinosis on XR in CPPD	Crystal deposition in wrist cartilage (especially TFCC for CPPD) → acute inflammatory flare

De Quervain's vs. 1st CMC OA vs. Intersection Syndrome vs. Wartenberg's

All four cause radial-sided wrist/thumb pain. The distinguishing tests are:

De Quervain's → Finkelstein's test (tendon stretch)
1st CMC OA → Grind test (joint compression)
Intersection syndrome → tenderness is more proximal (~4 cm above Lister's tubercle), with crepitus
Wartenberg's → sensory symptoms, no tendon findings; history of external compression

Condition	Key discriminating features	Pathophysiological basis
Trigger finger	Clicking/locking in flexion; tenderness at A1 pulley (MCP palm side); Green's grading I–IV ^[2]	Flexor tenosynovitis → nodule cannot pass through stenosed A1 pulley on extension
OA hand	Heberden's nodes (DIP), Bouchard's nodes (PIP); 1st CMC squaring; bony hard swelling; < 30 min morning stiffness ^[5]	Cartilage degeneration → osteophyte formation; mechanical process → symptoms improve with rest
RA hand	Symmetrical MCP/PIP swelling (spares DIP); ulnar deviation, swan-neck, boutonnière, Z-thumb; morning stiffness > 30 min; pannus on USG ^[3]^[5]	Autoimmune synovitis → pannus → cartilage/bone erosion → ligament laxity → deformities
Psoriatic arthritis (DIP pattern)	DIP arthritis with nail changes (pitting, onycholysis, oil-drop sign); dactylitis ("sausage digit"); may be asymmetric	Enthesitis-driven inflammation with predilection for DIP (close to nail matrix); distal periostitis
Gout of hand	Acute monoarthritis of small hand joints; tophi on fingers/olecranon; also affects small hand joints, wrist, elbow ^[4]	MSU crystal deposition → NLRP3 → IL-1β → acute neutrophilic inflammation
Dupuytren's contracture	Painless progressive flexion contracture of MCP/PIP (ring > little finger); palpable palmar cord/nodule; cannot lay hand flat	Fibroblastic proliferation in palmar fascia → contracture; associated with alcohol, DM, epilepsy, N. European ancestry
Flexor tendon sheath infection ^[1]	Kanavel's signs: fusiform swelling, flexed posture, tenderness along sheath, pain on passive extension	Bacteria within the closed tendon sheath → pus under pressure; distension causes the finger to rest in flexion
Herpetic whitlow	Painful vesicles on fingertip; healthcare workers; Tzanck smear shows multinucleated giant cells	HSV-1/2 direct inoculation → epidermal vesicle formation
Felon (pulp space infection)	Tense, throbbing fingertip; no fluctuation (septa prevent free drainage)	Infection in the closed pulp space compartment → ↑ pressure → ischaemia → can progress to osteomyelitis of distal phalanx
Paronychia	Red, swollen, tender nail fold; may have pus at nail margin	Disruption of the eponychium (cuticle) → bacterial/candidal entry into the periungual space
Dermatomyositis (Gottron's papules)	Red, sometimes scaly papules erupting on any of the finger joints ^[5]; proximal muscle weakness; heliotrope rash	Autoimmune vasculopathy affecting skin over joints (high-shear areas) + inflammatory myopathy
Systemic sclerosis (scleroderma)	Skin tightening, sclerodactyly, digital ulcers, Raynaud's, calcinosis	Fibrosis of skin and microvasculature → ischaemic ulcers at fingertips

Condition	Key discriminating features	Why the pain is "felt" in the hand/arm
Cervical radiculopathy (C5–T1)	Neck pain radiating in dermatomal distribution; ↑ with neck movement, Valsalva; Spurling's test +; ± segmental LMN weakness/reflex loss ^[1]^[8]	Disc herniation/osteophyte compresses nerve root → pain referred along the affected dermatome (C6 → thumb, C7 → middle finger, C8 → little finger)
Cervical myelopathy	Clumsy hands (myelopathic hand signs: 10-second test, finger escape sign, Hoffman's); UMN signs in legs; Lhermitte's ^[8]	Cord compression → disruption of corticospinal and dorsal column tracts → upper limb LMN at level + lower limb UMN below level
MI / Angina ^[1]	Constricting central chest pain radiating to left arm/jaw; diaphoresis; cardiac risk factors; ECG changes, ↑troponin	Cardiac visceral afferents converge with C8–T2 somatic afferents at the dorsal horn of the spinal cord → the brain misattributes the pain to the arm (viscero-somatic convergence)
Axillary vein thrombosis ^[1]	Acute UL swelling, pain, warmth; usually young athletic male with strenuous UL activity (effort thrombosis / Paget-Schroetter syndrome) ^[9]	Subclavian/axillary vein thrombosis → venous outflow obstruction → oedema + pain
Thoracic outlet syndrome	Variable: nTOS → lower brachial plexus (ulnar distribution paraesthesia/weakness); vTOS → arm DVT; aTOS → arm claudication ^[2]	Compression of neurovascular bundle at the thoracic outlet (between scalenes, clavicle, and first rib)
Pancoast tumour ^[1]	Shoulder/arm pain (C8–T1 distribution); Horner's syndrome (ptosis, miosis, anhidrosis); apical lung mass on CXR	Apical SCC invades the lower trunk of the brachial plexus and paravertebral sympathetic chain
Shoulder pathology ^[1]	Pain localised to shoulder/deltoid area; positive impingement/rotator cuff tests; full elbow/wrist/hand ROM preserved	Shoulder pain radiates to the upper arm because the deep somatic afferents from the glenohumeral capsule travel via the C5–C6 roots, which also supply the lateral arm
Acromegaly	Large hands with broad palms, spatulate fingers; CTS symptoms; sweaty palms; coarsened facial features ^[10]	GH/IGF-1 excess → soft tissue and periosteal overgrowth → carpal tunnel narrowing + joint hypertrophy

Don't Forget Referred Causes

A common exam pitfall is to focus entirely on local MSK causes and forget that arm/hand pain can be referred from the neck (cervical radiculopathy) or the heart (angina/MI). Murtagh specifically lists angina/MI and cervical spine dysfunction in the top-tier differentials ^[1]. Always screen for neck symptoms and cardiac risk factors.

Sometimes it helps to flip the approach and think by process rather than location, especially when the history is vague.

Process	Clues in History/Exam	DDx to consider
Degenerative / Mechanical	Insidious onset; worse with activity, better with rest; < 30 min morning stiffness; bony swelling	OA (hand, elbow), epicondylitis, De Quervain's, trigger finger, scaphoid non-union, Kienbock's
Inflammatory / Autoimmune	Morning stiffness > 30 min; symmetric joint swelling; extra-articular features; ↑ESR/CRP	RA, SLE, PsA, crystal arthritis (gout, CPPD), dermatomyositis, systemic sclerosis
Crystal	Acute onset, exquisitely painful, red-hot joint; history of hyperuricaemia/diuretics; joint aspiration diagnostic	Gout (MSU crystals — needle, negatively birefringent), CPPD (CPP crystals — rhomboid, weakly positively birefringent)
Infective	Fever (may be absent in elderly); monoarticular hot swollen joint; penetrating wound; immunosuppressed	Septic arthritis, osteomyelitis, flexor sheath infection, herpetic whitlow, sporotrichosis
Compressive / Entrapment	Paraesthesia/numbness in a specific nerve territory; worsened by sustained postures (flexion, extension); night symptoms; muscle wasting	CTS, cubital tunnel, Guyon's canal, PIN syndrome, Wartenberg's, pronator teres syndrome, TOS
Vascular	Colour changes (pallor → cyanosis → rubor); digital ulcers; rest pain; claudication; pulse changes	Raynaud's, Buerger's disease, arterial embolism, axillary vein thrombosis
Neoplastic	Insidious progressive pain; night pain/rest pain not relieved by position change; weight loss; bony swelling	Pancoast tumour, enchondroma, osteosarcoma (rare), metastasis
Referred	Pain distribution doesn't match a single nerve; neck pain; cardiac risk factors; Spurling's test +	Cervical radiculopathy, MI/angina, shoulder pathology

5. DDx Specific to Key Presentations — Pattern Recognition

For exams, you'll often be given a clinical vignette. Here are the most common patterns and what to think about:

RA	OA	PsA
MCP + PIP; spares DIP	DIP + PIP + 1st CMC; spares MCP	DIP (+ nail changes)
Symmetric	May be asymmetric	Asymmetric
Soft, boggy synovial swelling	Hard, bony nodes	Dactylitis ("sausage digit")
Morning stiffness > 30 min	< 30 min	Variable
Erosions on XR	Osteophytes on XR	Pencil-in-cup on XR

Population	Specific DDx to consider	Why?
Children	Pulled elbow ^[1]; osteomyelitis; juvenile idiopathic arthritis; fractures (supracondylar)	Immature annular ligament → subluxation; growing bone metaphysis is highly vascular → bacterial seeding
Pregnant women	CTS (physiological) ^[2]; De Quervain's (post-partum)	Fluid retention → carpal tunnel pressure ↑; repetitive lifting of newborn → 1st compartment tendinopathy
Diabetics	CTS, trigger finger, Dupuytren's, adhesive capsulitis ("diabetic hand syndrome")	Glycosylation of collagen → thickened tendon sheaths/joint capsules; diabetic neuropathy → entrapment susceptibility ^[2]
Young male smokers	Buerger's disease	Thromboangiitis obliterans → small/medium vessel thrombosis of hands/feet; virtually exclusive to smokers ^[9]
Elderly	OA, CPPD, CTS, cervical spondylosis, gout	Degenerative processes accumulate; CPPD prevalence ↑ with age (30–60% in > 85 y) ^[4]
Athletes / manual workers	Epicondylitis, De Quervain's, intersection syndrome, stress fractures, TOS	Repetitive loading → tendon overuse → degeneration

Category	Condition	Typical patient	Location	Character	Key discriminating test/feature
Probability	Cervical radiculopathy	Middle-aged, sedentary	Arm/hand (dermatomal)	Shooting/burning	Spurling's test; MRI cervical spine
Probability	Lateral epicondylitis	35–55 y, tennis/manual	Lateral elbow	Aching	Cozen's test, Mill's test ^[2]
Probability	Medial epicondylitis	Golfer, manual worker	Medial elbow	Aching	Reverse Cozen's; check ulnar nerve
Probability	De Quervain's	F 30–50, pregnancy	Radial wrist	Sharp with thumb use	Finkelstein's test ^[2]
Probability	CTS	Aging F; DM; pregnancy	Lateral 3.5 digits	Tingling/burning, nocturnal	Phalen's, Tinel's; NCS ^[2]
Probability	OA hand	Elderly F	DIP, PIP, 1st CMC	Aching, stiffness	Heberden's/Bouchard's nodes; grind test
Probability	Trigger finger	Elderly F; DM; gripping	MCP palm	Clicking/locking	Palpable nodule; Green's grading ^[2]
Serious	MI/Angina	Cardiac risk factors	Left arm (± chest)	Constricting	ECG, troponin; ↑ with exertion
Serious	Septic arthritis	Immunocompromised; RA	Any joint	Hot, constant	Joint aspiration: WBC > 50k, +ve culture
Serious	Flexor sheath infection	Penetrating wound	Finger	Throbbing	Kanavel's signs
Serious	Pancoast tumour	Smoker	Shoulder → C8/T1 arm	Constant, progressive	CXR: apical mass; Horner's syndrome
Serious	Osteomyelitis	Children; DM; IVDU	Near joint/bone	Deep, constant	MRI; blood cultures; ↑CRP
Pitfall	Cubital tunnel	Elbow flexion occupation	Medial 1.5 digits	Tingling	Tinel's at elbow; NCS ^[2]
Pitfall	Pulled elbow	Toddler 1–4 y	Whole arm (won't use)	Refusal to use arm	History of arm traction; reduces with supination-flexion
Other	RA hand	F 35–55; FHx	MCP, PIP, wrist	Stiffness, swelling	RF, anti-CCP; symmetrical; spares DIP ^[3]
Other	Gout	M; hyperuricaemia	1st MTP > wrist/hand	Excruciating, acute	Crystal analysis: MSU neg birefringent ^[4]
Other	CPPD	Elderly; OA	Knee > wrist	Acute or chronic	Chondrocalcinosis on XR; CPP weakly +ve birefringent ^[4]
Other	Ganglion cyst	F 20–40	Dorsal wrist 70%	Painless lump	Transillumination +; USG ^[6]^[7]
Other	Dupuytren's	Elderly M; alcohol; N. European	Palmar MCP/PIP	Contracture (not pain)	Palmar cord; inability to lay hand flat
Other	TOS	Young; cervical rib	C8/T1 + vascular	Variable	Adson's, Roos; CXR, Doppler USG ^[2]
Other	Buerger's disease	Young male smoker	Digital arteries	Rest pain, ulcers	Angiogram: corkscrew collaterals; no atherosclerosis ^[9]

High Yield Summary

Structure your DDx by Murtagh's tiers: probability → serious (don't miss) → pitfalls → masquerades → psychogenic ^[1].
Top probability diagnoses: cervical radiculopathy, shoulder disorders, epicondylitis, overuse tendinopathy (De Quervain's), CTS, OA of thumb/DIP ^[1].
Emergencies to exclude first: septic arthritis (hot joint = septic until proven otherwise), flexor sheath infection (Kanavel's signs), MI (left arm pain + cardiac risk factors), Pancoast tumour (smoker + Horner's) ^[1].
Key DDx for radial wrist pain: De Quervain's (Finkelstein's +) vs. 1st CMC OA (Grind test +) vs. Wartenberg's (sensory, external compression) vs. intersection syndrome (proximal, crepitus) ^[2].
Key DDx for finger joint deformity: RA = MCP/PIP, spares DIP, symmetric ^[3]; OA = DIP/PIP, Heberden's/Bouchard's nodes ^[5]; PsA = DIP + nail changes, dactylitis.
Nocturnal hand paraesthesia DDx: CTS (lateral 3.5, Phalen's +) vs. cubital tunnel (medial 1.5, dorsal affected) vs. C6/C7 radiculopathy (Spurling's +, NCS normal at wrist) vs. TOS (lower trunk symptoms) ^[2].
Ganglion cyst: most common soft tissue tumour of hand, dorsal wrist 70%, transilluminable, never malignant ^[6]^[7].
Crystal arthritis at wrist/hand: gout (MSU, neg birefringent) vs. CPPD (CPP, weakly pos birefringent); CPPD — wrist is 2nd most common site after knee ^[4].

Active Recall - DDx of Hand/Wrist/Elbow Pain

References

^[1] Lecture slides: murtagh merge.pdf (p19, Arm and hand pain) ^[2] Senior notes: maxim.md (Sections on epicondylitis, De Quervain's, trigger finger, carpal tunnel syndrome, cubital tunnel syndrome, thoracic outlet syndrome, hand anatomy, compression neuropathy) ^[3] Senior notes: Ryan Ho Rheumatology.pdf (Sections 2.6 RA, 2.8 Septic arthritis, 2.1 Approach to acute monoarthritis) ^[4] Senior notes: Ryan Ho Rheumatology.pdf (Sections 2.4.1 Gout, 2.4.2 CPPD) ^[5] Senior notes: Ryan Ho Fundamentals.pdf (p17 Hands and Upper Limbs; p130 Rheumatoid Hands; p406-408 Monoarthritis/Polyarthritis) ^[6] Senior notes: maxim.md (Ganglion cyst section) ^[7] Senior notes: felixlai.md (Ganglion cyst section) ^[8] Senior notes: Ryan Ho Neurology.pdf (p45 Where is the Lesion; p54 Roots/Plexuses/Peripheral Nerves; p173 Cervical myelopathy/spondylosis) ^[9] Senior notes: Ryan Ho Cardiology.pdf (p218 Buerger's Disease; Ryan Ho Haematology.pdf p131 VTE/Axillary vein thrombosis) ^[10] Senior notes: Ryan Ho Endocrine.pdf (p111 Acromegaly)

Diagnostic Criteria, Algorithm and Investigation Modalities

2. Diagnostic Criteria for Key Conditions

Most hand/wrist/elbow conditions lack formal "criteria" the way RA or gout do — they are diagnosed clinically. However, several important conditions do have established diagnostic or classification criteria. Here they are:

CTS is a clinical diagnosis ^[2], but nerve conduction studies provide objective confirmation.

Clinical diagnostic features (a combination of):

Pain and numbness in the distribution of the median nerve (first 3½ digits) ^[2]
Thenar area spared — because the palmar cutaneous branch of the median nerve branches proximal to the flexor retinaculum ^[2]
Worse at night, relieved by hanging over the side of bed or shaking ^[2]
Thenar muscle wasting and weakness of thumb abduction (late) ^[2]
Positive provocative tests: Phalen's test, Tinel's sign, Durkin's compression test

NCS criteria for CTS (electrophysiological confirmation):

Parameter	Finding in CTS	Why?
Distal motor latency (median nerve)	Prolonged ( > 4.2 ms)	Demyelination at the carpal tunnel slows conduction across the compressed segment
Sensory nerve conduction velocity	Slowed across the wrist	Same reason — focal demyelination at the tunnel
Compound muscle action potential (CMAP) amplitude	Reduced (late)	Axonal loss → fewer motor units firing
Comparison with ulnar nerve	Median delayed relative to ulnar	The ulnar nerve does NOT pass through the carpal tunnel, so serves as an internal control

NCS in CTS — The Nuance

Normal conduction does not rule out CTS ^[2]. Early or mild CTS may have normal NCS because demyelination hasn't progressed enough to affect conduction velocities measurably. Always treat the patient, not the NCS result. However, NCS demonstrating axonal loss is an indication for surgery ^[2].

Indications for surgery based on NCS/clinical findings ^[2]:

CTS unresponsive to conservative treatment for 6 weeks
Associated sensory/motor deficit
Axonal loss on NCS

RA commonly presents in the hands/wrists. The 2010 criteria are scored (≥ 6/10 = classified as RA):

Domain	Score
Joint involvement: 1 large joint (0); 2–10 large joints (1); 1–3 small joints (2); 4–10 small joints (3); > 10 joints incl ≥ 1 small (5)	0–5
Serology: RF and anti-CCP both negative (0); low-positive RF or anti-CCP (2); high-positive RF or anti-CCP (3)	0–3
Acute phase reactants: normal CRP and ESR (0); abnormal CRP or ESR (1)	0–1
Duration of symptoms: < 6 weeks (0); ≥ 6 weeks (1)	0–1

Requires ≥ 1 joint with definite clinical synovitis not better explained by another disease.

Key hand/wrist features ^[3]^[5]:

Classically starts in MCP, PIP, wrists and MTP joints and spares DIP ^[5]
Symmetrical involvement
Morning stiffness > 30 minutes

Applicable when septic arthritis has been excluded and MSU crystals have not been demonstrated (if crystals are found, the diagnosis is confirmed without needing the criteria).

Sufficient criterion: Detection of MSU crystals in a symptomatic joint/bursa → diagnostic, score not needed.

Classification criteria (≥ 8 points = classified as gout) ^[4]:

Domain	Finding	Score
Pattern of joint involvement	Ankle or midfoot (1); 1st MTP (2)	0–2
Characteristics of episode	Erythema, can't bear touch, great difficulty walking (each present = +1, max 3)	0–3
Time course	Max pain < 24h (0.5); resolution ≤ 14 days (0.5); complete resolution between episodes (1)	0–2
Clinical evidence of tophi	Present (4)	0–4
Serum urate	< 4 mg/dL (−4); 4– < 6 (0); 6– < 8 (2); 8– < 10 (3); ≥ 10 (4)	−4 to 4
Imaging: urate deposition	USG: double contour sign or DECT demonstrating urate deposition (4)	0–4
Imaging: gout-related damage	XR hands/feet showing ≥ 1 erosion (4)	0–4

Note: gout also affects small hand joints, wrist, elbow — not just the 1st MTP ^[4].

Joint fluid analysis — the gold standard:

MSU crystals: elongated needle-shaped, negative birefringent crystals ± engulfment by PMN ^[4]^[5]
CPPD crystals: pleomorphic or rhomboid shaped, weakly positive birefringence ^[5]

Clinical diagnosis graded by severity ^[2]:

Grade	Description	Implication
I	Palm pain and tenderness at A1 pulley	Conservative management
II	Catching of digit, can actively extend	Steroid injection
III	Locking of digit, passively correctable	Steroid injection; consider surgery
IV	Fixed flexion deformities	Surgical release required

No formal "scoring criteria" but the clinical rule is:

Hot, swollen, tender joint = septic arthritis until proven otherwise, even without fever, ↑WBC, ↑ESR/CRP ^[3]

Joint fluid analysis is mandatory if septic arthritis is suspected ^[5]:

Parameter	Non-inflammatory	Inflammatory	Septic
Appearance	Clear, yellow	Translucent, yellow-green	Opaque, purulent
Viscosity	High	Low	Very low
WBC count (/mL)	< 2,000	2,000–50,000	> 50,000 (often > 100,000)
Neutrophils	< 25%	> 50%	> 90%
Gram stain	Negative	Negative	Positive (60–80%)
Culture	Negative	Negative	Positive (if not pre-treated)

4. Investigation Modalities — Detailed Breakdown

Test	When to order	Key findings and interpretation
FBE (CBC) ^[1]	Any suspected inflammatory, infective, or systemic cause	↑WBC (neutrophilia) → infection/gout flare; ↓Hb → chronic disease (RA, malignancy); ↑platelets → reactive (inflammatory arthritis)
ESR/CRP ^[1]^[5]	Any inflammatory or infective condition	↑ESR/CRP → inflammatory (RA, crystal, septic) vs. normal → mechanical (OA, tendinopathy). CRP usually normal/mildly ↑ in SLE ^[5]. CRP is more specific for active inflammation; ESR is affected by age, anaemia, pregnancy
Serum urate	Suspected gout	Elevated in chronic gout BUT can be normal or low during an acute flare (12–43% normal/↓) → should be deferred to ≥ 2 weeks after resolution ^[4]
RF + anti-CCP	Suspected RA	RF: anti-IgG IgM antibody, positive in ~70% RA (not sensitive, not specific — also positive in infections, other autoimmune disease, elderly). Anti-CCP: more specific (~95%) for RA ^[5]
ANA, anti-ENA, C3/C4	Suspected SLE	ANA screening; anti-dsDNA, anti-Sm for SLE; complement consumption (↓C3/C4) in active disease
HbA1c	CTS, trigger finger, frozen shoulder, Dupuytren's	Screen for DM — a common underlying cause of soft-tissue entrapment syndromes ^[2]
TFTs	CTS	Screen for hypothyroidism → myxoedematous soft tissue swelling → carpal tunnel pressure ↑ ^[2]
Blood cultures	Suspected septic arthritis	Positive in ~50% of non-gonococcal septic arthritis; essential before starting antibiotics
Cardiac enzymes (Troponin)	Left arm pain + cardiac risk factors	Elevated troponin = myocardial injury. Rule out MI before attributing arm pain to MSK ^[1]

Plain X-ray: if in doubt, X-ray and compare both sides ^[1]

Why XR first? XR has the highest spatial resolution of all imaging modalities ^[11] — excellent for detecting bony pathology (fractures, erosions, osteophytes, calcifications). It is readily available, inexpensive, and usually the first-line imaging study.

Limitations: XR can only distinguish four densities — calcium, water (soft tissue), fat, and air ^[11]. Therefore it is poor for soft tissue lesions (tendons, ligaments, nerves, cartilage).

Condition	XR views	Key findings
OA hand	PA hand	Joint space narrowing (JSN), subchondral sclerosis, osteophytes (Heberden's/Bouchard's), subchondral cysts. 1st CMC: "squared" trapezium
RA hand/wrist	PA + lateral hand	Soft tissue swelling (early), periarticular osteopaenia (early), joint space narrowing, periarticular erosions (late), subluxations, ankylosis. Typically MCP/PIP/wrist; spares DIP
Gout	PA hand/foot	XR hands/feet showing ≥ 1 erosion ^[4]: "rat-bite" / punched-out erosions with overhanging edges and sclerotic borders; periarticular soft tissue tophi; joint space preserved until late. Typically normal in acute flare
CPPD	PA wrist/knee	Chondrocalcinosis: linear calcification in hyaline cartilage (parallel to bone) and fibrocartilage (e.g. TFCC at wrist, menisci at knee) ^[4]. May also see OA-like changes
Scaphoid fracture	AP, lateral, scaphoid view (30° wrist extension, 20° ulnar deviation) ^[2]	Fracture line across scaphoid waist (may be subtle initially). If high clinical suspicion but negative XR → thumb splint + repeat XR in 14 days or MRI wrist ^[2]
Epicondylitis	AP + lateral elbow	Usually normal. May show calcification at tendon insertion or loose bodies in chronic cases. Mainly used to rule out OA elbow, fracture
Pancoast tumour	CXR ^[1]	Apical lung mass ± rib erosion ± mediastinal widening
Cervical spondylosis	Lateral + AP C-spine	Disc space narrowing, osteophytes, neural foraminal narrowing. Not sensitive for disc herniation (need MRI)
Kienbock's disease	PA + lateral wrist	Sclerosis → fragmentation → collapse of the lunate (Lichtman staging)

Special XR Views You Must Know

Scaphoid view (30° extension, 20° ulnar deviation): elongates the scaphoid to reveal fracture lines hidden by foreshortening on standard views ^[2]^[11].
Ball-catcher's view (Nørgaard view, semi-supinated oblique): for early erosions in RA — shows the radial margins of the MCP joints which are the first sites of erosion.
Carpal tunnel view (tangential): shows the carpal tunnel contents projected en face — useful for hook of hamate fracture or calcification within the tunnel.

Ultrasound for soft tissue injuries (e.g. tendonopathy) ^[1]

Why USG? It is dynamic (can assess tendons during movement), radiation-free, inexpensive, and widely available. It is excellent for soft tissue — tendons, tendon sheaths, effusions, cysts, nerve thickening.

Condition	USG findings
Epicondylitis	Tendon thickening, hypoechoic areas (degeneration), increased Doppler signal (neovascularisation), calcification, partial/full-thickness tears
De Quervain's	Thickened 1st extensor compartment retinaculum, tendon sheath fluid, thickened APL/EPB tendons
Trigger finger	Thickened A1 pulley ( > 1 mm), tendon nodule, restricted tendon gliding on dynamic assessment
CTS	Swollen median nerve (cross-sectional area > 10 mm² at tunnel inlet), flattening at tunnel, flexor retinaculum bowing
RA	Synovial hypertrophy (pannus), joint effusion, power Doppler signal = active synovitis, erosions (more sensitive than XR for early erosions)
Gout	Double contour sign: hyperechoic irregular band overlying the surface of joint cartilage ^[4] — represents MSU crystal deposition on the articular cartilage surface
Ganglion cyst	Well-defined margins, thick wall with acoustic enhancement ^[2] — the cyst contents are fluid → posterior acoustic enhancement is expected
Tendon rupture	Discontinuity of tendon fibres, retracted tendon stump, haematoma
Septic arthritis	Joint effusion ± synovial thickening; can guide aspiration

Consider nerve conduction studies ^[1]

NCS/EMG are the key investigations for entrapment neuropathies — the "pitfalls often missed" in Murtagh's framework ^[1].

Principle ^[8]:

NCS: percutaneous electrical stimulation of a peripheral nerve → record the generated impulse distally. Measures conduction velocity, distal latency, and amplitude.
EMG: needle recording of bioelectric activity in muscles. Detects denervation (fibrillations, positive sharp waves) and reinnervation (polyphasic units).

NCS is useful for ^[8]:

Differentiation between focal and multifocal neuropathy
Differentiation between demyelinating and axonal neuropathy
Assessment of severity
Monitor progress and response to treatment
Prognostication after nerve trauma

NCS is NOT useful for ^[8]:

Exclude or confirm neuropathy/myopathy (clinical findings should suffice)
Cervical myelopathy (does NOT assess CNS function)
Define aetiology of peripheral neuropathy

Condition	NCS/EMG findings	Clinical significance
CTS	Prolonged distal motor latency; slowed sensory conduction across wrist; ↓CMAP amplitude if axonal loss	Severity grading: mild (sensory only) → moderate (motor + sensory) → severe (axonal loss). Axonal loss = surgical indication ^[2]
Cubital tunnel	Slowed motor conduction across the elbow segment; ↓CMAP amplitude of ADM/FDI; fibrillations in ulnar-innervated muscles on EMG	Localises the lesion to the elbow (vs. Guyon's canal, vs. C8/T1 root)
Cervical radiculopathy	NCS often normal (the lesion is proximal to the dorsal root ganglion, so sensory NCS is preserved); EMG shows denervation in a myotomal distribution	This is the key differentiator: in CTS, NCS is abnormal at the wrist; in radiculopathy, NCS is normal but EMG shows segmental denervation
TOS (nTOS)	May show ↓SNAP of medial antebrachial cutaneous nerve; ↓CMAP of ulnar nerve	Often normal or equivocal — nTOS remains a clinical diagnosis in many cases

CTS vs. Radiculopathy on NCS

The single most important NCS finding to differentiate CTS from C6/C7 radiculopathy:

CTS: median sensory NCS abnormal at the wrist (prolonged latency, reduced amplitude) — the lesion is at the wrist.
C6/C7 radiculopathy: sensory NCS normal at the wrist — the lesion is proximal to the dorsal root ganglion (DRG), so the peripheral sensory axon remains intact (Wallerian degeneration does not occur because the cell body in the DRG is still connected to the distal axon).

When to order: MRI is the investigation of choice for soft tissue detail (tendons, ligaments, cartilage, nerves, spinal cord) and when initial XR is non-diagnostic.

Condition	MRI indication	Key findings
Scaphoid fracture (occult)	High clinical suspicion but negative initial XR ^[2]	Bone marrow oedema (T1 low, T2/STIR high) at fracture site — MRI sensitivity ~100%
Cervical radiculopathy/myelopathy	Persistent radicular symptoms, myelopathic signs, pre-surgical planning	Disc herniation, foraminal stenosis, cord compression, cord signal change (T2 high = myelomalacia)
Kienbock's disease	Early detection before XR changes	AVN of lunate: T1 low signal (loss of marrow fat), T2 variable
TFCC injury	Ulnar wrist pain with equivocal clinical exam	Tear seen as high signal within the normally low-signal TFCC on T2/PD sequences
Epicondylitis (refractory)	Failure of conservative treatment > 6 months	Tendon thickening, intrasubstance signal change, partial/complete tear
Soft tissue mass	Atypical ganglion or suspected malignancy	Characterise mass: cystic (ganglion) vs. solid (tumour); gadolinium enhancement suggests malignancy
Frozen shoulder	Rule out other pathology (rotator cuff, SAIS)	Thickened joint capsule ^[2], particularly at the rotator interval; axillary pouch thickening

Modality	Indication	Key findings
CT (with 3D reconstruction)	Complex fractures (distal radius, carpal), pre-operative planning	Precise fracture geometry, fragment displacement, comminution
DECT	Demonstrating urate deposition in gout ^[4]	Colour-coded urate crystal deposits around joints/tendons — highly specific; used in 2015 ACR/EULAR gout criteria
CT angiogram	TOS (arterial/venous) ^[2]	Subclavian artery/vein compression during provocative positioning; thrombus visualisation

Joint fluid analysis: MOST IMPORTANT TEST when septic or crystal arthritis is suspected ^[5]

Indications ^[5]:

Suspicious of septic arthritis
Suspicious of crystal-induced arthritis
Suspicious of haemarthrosis
Differentiating inflammatory vs. non-inflammatory arthritis

What to send ^[5]:

Macroscopic: colour, viscosity, turbidity
Microscopy: wet films, WBC count/differential, crystal microscopy
Microbiology: Gram stain (urgent), bacterial culture, AFB smear/culture if indicated

Interpretation table ^[5]:

Parameter	Normal	Non-inflammatory (e.g. OA)	Inflammatory (e.g. RA, gout)	Septic
Colour	Clear, colourless	Clear, straw/yellow	Translucent, yellow-green	Opaque, yellow-green, purulent
Viscosity	High	High	Low (enzymes degrade hyaluronic acid)	Very low
WBC (/mL)	< 200	< 2,000	2,000–50,000	> 50,000 (often > 100k)
PMN %	< 25%	< 25%	> 50%	> 90%
Crystal microscopy	None	None	Gout: needle-shaped, strongly negative birefringent; CPPD: rhomboid, weakly positive birefringent ^[5]	Usually none (but crystals + infection can coexist)
Gram stain	Negative	Negative	Negative	Positive in 60–80%
Culture	Negative	Negative	Negative	Positive (diagnostic)

Crystals + Infection Can Coexist

Finding crystals in joint fluid does NOT exclude septic arthritis. Up to 1–2% of patients with gout have concurrent infection. Always send Gram stain and culture even if crystals are identified, especially if the clinical picture is atypical (e.g. prolonged fever, lack of improvement with anti-inflammatory treatment).

Investigation	When	Findings
ECG ^[1]	Left arm pain, cardiac risk factors	ST elevation/depression, T-wave inversion, new LBBB → ACS. Normal ECG does not exclude ACS — serial ECGs needed
CXR ^[1]^[2]	Suspected Pancoast tumour; TOS (cervical rib); shoulder pathology	Apical mass (Pancoast); cervical rib (TOS); calcific tendinopathy of shoulder
Doppler USG ^[2]	TOS (vascular); axillary vein thrombosis	Non-compressible vein (DVT); absent/reduced flow in subclavian artery (aTOS); vein distension (vTOS)
Bone scan (99mTc)	Occult fracture, osteomyelitis, metastasis, CRPS	Increased uptake at fracture/infection/tumour sites; three-phase positive in CRPS
Arthroscopy	Diagnostic when imaging equivocal; therapeutic	Direct vision: assess cartilage damage, synovial biopsy, debridement, removal of loose bodies ^[5]

Condition	First-line investigation	Confirmatory / Second-line
Lateral/medial epicondylitis	Clinical diagnosis ^[2]	USG or MRI if refractory
De Quervain's	Clinical diagnosis; plain XR to r/o DDx ^[2]	USG for tendon detail
Trigger finger	Clinical diagnosis ^[2]	USG (dynamic) if equivocal
CTS	Clinical diagnosis ^[2]; NCS	USG (nerve swelling); MRI (mass lesion)
Cubital tunnel	Clinical + NCS	MRI elbow if mass suspected
Scaphoid fracture	XR: AP, lateral, scaphoid view ^[2]	MRI if XR negative + high suspicion ^[2]
OA hand	XR hand (PA)	N/A — clinical + XR sufficient
RA	Bloods (RF, anti-CCP, ESR/CRP) + XR hands/feet	USG (early erosions, synovitis); MRI
Gout (acute)	Joint aspiration (crystal analysis)	Bloods (urate deferred 2 weeks); USG (double contour); DECT
CPPD	XR (chondrocalcinosis); joint aspiration	Bloods to screen for metabolic causes (Ca, PO4, Mg, Fe studies, PTH)
Septic arthritis	Urgent joint aspiration + Gram stain + culture	Blood cultures; bloods (WCC, CRP); XR to rule out osteomyelitis
TOS	CXR, Doppler USG ^[2], NCS	CT angiogram; MRI
Pancoast tumour	CXR ^[1]	CT thorax with contrast; biopsy
MI/Angina	ECG + Troponin ^[1]	Coronary angiography

High Yield Summary

Most hand/wrist/elbow conditions are clinical diagnoses. Investigations are to confirm, exclude serious mimics, or guide management.
Key investigations (Murtagh): FBE, ESR/CRP, ECG, NCS, plain XR ("if in doubt, X-ray and compare both sides"), USG for soft tissue ^[1].
CTS: clinical diagnosis + NCS for confirmation. Normal NCS does not rule it out. Axonal loss on NCS = surgical indication ^[2].
Joint aspiration = MOST IMPORTANT TEST for acute monoarthritis ^[5]. Must send crystal microscopy + Gram stain + culture. Gout: needle-shaped, negative birefringent. CPPD: rhomboid, weakly positive birefringent.
Scaphoid fracture: XR (incl. scaphoid view) first → if negative but clinically suspected → thumb splint + repeat XR 14 days OR MRI ^[2].
Gout imaging criteria: USG double contour sign or DECT urate deposition; XR erosion with overhanging edges ^[4].
Murtagh's nocturnal pain rule: TOS = can't fall asleep; CTS = wakes mid-night then settles; cervical spondylosis = wakes and persists ^[1].
RA: XR hands/feet (erosions, JSN, periarticular osteopaenia); bloods (RF, anti-CCP, ESR/CRP); USG (early erosions, active synovitis with power Doppler). 2010 ACR/EULAR criteria ≥ 6/10 ^[3]^[5].
NCS localises entrapment: CTS → prolonged distal latency at wrist; cubital tunnel → slowed across elbow; radiculopathy → NCS normal at wrist, EMG shows myotomal denervation ^[8].
Crystals + infection can coexist — always send culture even if crystals found.

Active Recall - Diagnosis and Investigations for Hand/Wrist/Elbow Pain

References

^[1] Lecture slides: murtagh merge.pdf (p19–20, Arm and hand pain) ^[2] Senior notes: maxim.md (Sections on epicondylitis, De Quervain's, trigger finger, CTS, cubital tunnel, scaphoid fracture, frozen shoulder, ganglion cyst) ^[3] Senior notes: Ryan Ho Rheumatology.pdf (Section 2.6 RA, Section 2.8 Septic arthritis) ^[4] Senior notes: Ryan Ho Rheumatology.pdf (Sections 2.4.1 Gout, 2.4.2 CPPD — including 2015 ACR/EULAR criteria) ^[5] Senior notes: Ryan Ho Fundamentals.pdf (p407–410, Approach to monoarthritis/polyarthritis — joint fluid analysis, physical examination, initial investigations) ^[8] Senior notes: Ryan Ho Neurology.pdf (p38, Electrodiagnostic Studies; p178, Approach to generalised weakness) ^[11] Senior notes: Ryan Ho Diagnostic Radiology.pdf (p13, Plain Film Radiography)

Management Algorithm and Treatment Modalities

3. Condition-Specific Management — Detailed

Management ^[2]:

Step 1 — Conservative (first-line):

Activity modification — identify and reduce the aggravating activity (e.g. adjust racket grip, ergonomic mouse, change technique). This is the single most important intervention because the pathology is driven by repetitive overloading of the ECRB tendon origin.
PT (physiotherapy): stretching, strengthening exercise ^[2] — eccentric loading exercises (slowly lowering a weight with the wrist extended) stimulate tendon remodelling by promoting aligned collagen synthesis. This is the most evidence-based conservative treatment.
Orthoses, e.g. elbow brace ^[2] — a counterforce brace applied ~2 cm distal to the lateral epicondyle reduces the load transmitted through the common extensor origin by redistributing force to the brace.

Step 2 — Pharmacological:

Analgesics — oral NSAIDs (short course, ≤ 2 weeks) for pain relief; topical NSAIDs are preferred for localised pain.
Local steroid injection ^[2] — corticosteroid (e.g. methylprednisolone 40 mg + lignocaine) injected at the point of maximal tenderness over the lateral epicondyle. Provides rapid short-term relief (weeks) but no long-term benefit and may actually weaken the tendon if repeated. Limit to ≤ 3 injections per site.
- Why does it work short-term? Steroids suppress local inflammation and oedema, reducing nociceptor stimulation.
- Why no long-term benefit? The pathology is primarily degenerative (angiofibroblastic), not inflammatory; steroids don't reverse tendinosis and may inhibit collagen synthesis.

Step 3 — Surgical (if refractory > 6–12 months):

Open/arthroscopic debridement of tendinosis, repair of damaged tendon insertions, tendon transfer if > 50% damage ^[2].
Surgery removes the degenerated tendon tissue and stimulates a healing response. Tendon transfer (e.g. using anconeus muscle) is reserved for massive defects.

Medial epicondylitis: Similar management as tennis elbow ^[2]. Additionally, always assess and address associated ulnar nerve neuropathy — may require concurrent ulnar nerve decompression if symptomatic ^[2].

Management ^[2]:

Step	Modality	Details and rationale
1. Conservative	Lifestyle (avoid repetitive actions)	Remove the mechanical trigger — the tendon sheath thickening is driven by friction
	Wrist splint (thumb spica)	Immobilises the 1st extensor compartment, preventing APL/EPB gliding and allowing inflammation to resolve
2. Pharmacological	Local steroid injection	Injected into the 1st extensor compartment sheath → reduces inflammation and sheath thickening. Cure rate ~60–80% with a single injection
3. Surgical	Surgical decompression: percutaneous/endoscopic release → widen the tunnel roof for tendons to move ^[2]	Division of the fibrous septum overlying the 1st compartment. Takes pressure off APL/EPB. Cure rate > 90%

Surgical complication to know: injury to the superficial branch of the radial nerve (Wartenberg's syndrome iatrogenically!) — it runs directly over the 1st compartment.

Management ^[2] — guided by Green's classification:

Green's Grade	Recommended treatment	Rationale
I (pain/tenderness only)	Splint that holds the finger in extension position at night ^[2]	Prevents the flexor tendon nodule from being pulled through the A1 pulley during nocturnal finger flexion; allows oedema to settle
II (catching, can actively extend)	Local steroid injection (into A1 pulley) ^[2]	Steroid reduces the tenosynovitis and nodule size, allowing freer tendon gliding. Success rate ~60–70% after 1 injection, up to 90% after 2
III (locking, passively correctable)	Steroid injection (1–2 attempts); if fails → surgical release of A1 pulley ^[2]	The nodule is now large enough to regularly catch; if steroids don't shrink it, mechanical release is needed
IV (fixed flexion deformity)	Surgical release of A1 pulley ^[2]	Fixed deformity means the tendon/nodule is physically trapped; no injection will resolve a structural problem

Steroid injection technique: Inject into the tendon sheath (NOT the tendon itself) at the level of the A1 pulley (MCP joint crease, palm side). Use a 25G needle; inject 0.5 mL triamcinolone + 0.5 mL lignocaine.

Surgical release: Can be done percutaneously (with a needle/blade) or open. Division of the A1 pulley allows the tendon to glide freely. Key risk is digital nerve injury (the digital nerves run immediately lateral to the sheath).

Why Not Just Operate on Everyone?

Steroid injections are tried first in Grades I–III because they are effective in most cases and avoid surgical risks (digital nerve injury, flexor tendon bowstringing if the wrong pulley is cut, wound infection). Surgery is reserved for failures and Grade IV because the structural problem is too severe for pharmacological resolution.

Management ^[2]:

Step 1 — Conservative:

Night-time wrist splint ^[2] — a rigid splint holds the wrist in neutral position (0–15° extension). Why night-time? During sleep, people tend to flex their wrists, which ↑ carpal tunnel pressure. Neutral positioning minimises pressure and allows the oedema to resolve overnight.
Physiotherapy — nerve gliding exercises, tendon gliding exercises, stretching. These mobilise the median nerve within the tunnel and prevent adhesion formation.
Lifestyle modification — ergonomic adjustments (e.g. keyboard height, mouse position); treat underlying cause (control DM, replace thyroxine in hypothyroidism, weight loss in obesity) ^[2].

Step 2 — Pharmacological:

Local steroid injection ^[2] — injected into the carpal tunnel (typically ulnar to palmaris longus tendon at the wrist crease). Reduces swelling within the tunnel → ↓ pressure on median nerve. Provides temporary relief; useful as a diagnostic/therapeutic test.
Pyridoxine (vitamin B6) ^[2] — mechanism unclear; may have a mild neuroprotective effect. Evidence is weak.
Diuretics ^[2] — may help in CTS related to fluid retention (e.g. pregnancy). Rarely used in practice.

Step 3 — Surgical:

Indications ^[2]:
- CTS unresponsive to conservative treatment for 6 weeks
- Associated sensory/motor deficit (thenar wasting, weakness of APB)
- Axonal loss on NCS
Procedure: Carpal tunnel release (division of flexor retinaculum): open vs endoscopic ^[2]
- Open release: 2–3 cm incision over the carpal tunnel; direct visualisation of the flexor retinaculum which is divided longitudinally. Gold standard.
- Endoscopic release: smaller incision, faster recovery, but slightly higher risk of incomplete release.
- Why does cutting the retinaculum work? The flexor retinaculum is the "roof" of the carpal tunnel. Dividing it decompresses the tunnel, immediately reducing pressure on the median nerve. The retinaculum eventually heals in a lengthened position.
Specific complications ^[2]:
- Persistent CTS symptoms (inadequate release) — incomplete division of the retinaculum
- Nerve injury: palmar cutaneous branch — sensory loss/painful neuroma over thenar eminence
- Vascular injury: superficial palmar arch — lies just deep to the retinaculum
- Wound infection, scar tenderness ("pillar pain")

Surgical Timing in CTS

Do NOT delay surgery in a patient with thenar wasting or axonal loss on NCS. Prolonged denervation leads to irreversible motor endplate degeneration — even if the nerve is later decompressed, the muscle may not recover. The window for reversible damage is approximately 6–12 months.

Management ^[2]:

Step	Modality	Details
1. Conservative	Soft elbow extension splint ^[2]	Worn at night. Prevents elbow flexion during sleep, which narrows the cubital tunnel and compresses the ulnar nerve. The splint keeps the elbow at ~30° flexion (not full extension, which can also stretch the nerve)
	Physiotherapy, lifestyle modification ^[2]	Avoid prolonged elbow flexion (e.g. holding phone), avoid leaning on elbow; nerve gliding exercises
2. Pharmacological	Local steroid injection, pyridoxine ^[2]	Less effective than in CTS because the cubital tunnel is not a "closed box" in the same way; steroid reduces local inflammation around the nerve
3. Surgical	Decompression in-situ, medial epicondylectomy, anterior transposition of ulnar nerve ^[2]	See below

Surgical options ^[2]:

Simple decompression in-situ: release of Osborne's ligament (roof of cubital tunnel) without moving the nerve. Simplest; suitable for mild-moderate cases without subluxation.
Medial epicondylectomy: remove a portion of the medial epicondyle to widen the tunnel. Less commonly performed.
Anterior transposition of ulnar nerve ^[2]: the nerve is moved from behind the medial epicondyle to a new position anterior to it (subcutaneous, intramuscular, or submuscular). This eliminates the stretch placed on the nerve during elbow flexion. Preferred when there is ulnar nerve subluxation or cubital valgus deformity.

Management varies by type ^[2]:

Type	Treatment	Rationale
Neurological (nTOS)	Physiotherapy ± Botox injection to relax scalene muscles ^[2]	Most cases are due to scalene muscle hypertrophy/spasm compressing the lower trunk. PT stretches the scalenes; Botox chemically denervates them → ↓ compression
Venous (vTOS)	Thrombolysis, anticoagulation; surgical decompression ^[2]	The subclavian vein is thrombosed → catheter-directed thrombolysis to restore flow; anticoagulation to prevent propagation; 1st rib resection removes the structural cause
Arterial (aTOS)	Embolectomy; surgical decompression ^[2]	The subclavian artery is compressed/thrombosed → embolectomy for acute ischaemia; 1st rib/cervical rib excision to decompress

Surgical procedures to decompress thoracic outlet ^[2]:

Supraclavicular/transaxillary excision of 1st rib/cervical rib
Scalenectomy

These are seldom required ^[2] — most nTOS cases respond to conservative management.

Treatment ^[6]^[13]:

Step	Modality	Details
1. Non-surgical (1st line)	Observation with brace → ~50% spontaneous resolution ^[6]^[13]	Many ganglions are asymptomatic and self-limiting
	Needle aspiration → up to 50% recurrence within a year ^[6]^[13]	Aspiration decompresses the cyst and provides immediate relief, but the stalk/connection to the joint capsule remains → recurrence
2. Surgical	Surgical excision of cyst and stalk if persistent or recurrent ^[6]^[13]	Complete excision of the cyst and its stalk/pedicle reduces recurrence (still up to 5–20% recurrence). Complications: wound complications, recurrence (up to 50% in some series), injury to neighbouring structures ^[13]

Important: The old practice of "Bible therapy" (smashing the cyst with a heavy book) is NOT recommended — it causes tissue damage, pain, and high recurrence.

Management ^[2]:

Scenario	Treatment
Undisplaced fracture	Non-operative: immobilisation in thumb spica cast ^[2] for 6–12 weeks (waist fractures ~8 weeks; proximal fractures ~12 weeks)
High clinical suspicion, normal XR	Thumb splint + repeat XR in 14 days or MRI wrist ^[2]
Displaced/proximal fracture	Operative: percutaneous screw fixation ^[2] (e.g. Herbert screw). Allows earlier mobilisation and reduces non-union/AVN risk

Why prolonged immobilisation? The scaphoid has a retrograde blood supply (enters distally, flows proximally) and is mainly surrounded by articular cartilage → limited periosteal blood supply → relies on primary bone healing without callus → requires absolute immobilisation for union ^[2].

Agent	Mechanism	Indication in hand/wrist/elbow pain	Key contraindications / side effects
Paracetamol	Central COX inhibition + serotonergic pathways	First-line analgesic for OA, mild MSK pain	Hepatotoxicity in overdose; avoid in liver disease
Oral NSAIDs (ibuprofen, naproxen, diclofenac)	COX-1/2 inhibition → ↓ prostaglandin → ↓ pain/inflammation	Epicondylitis, OA, acute gout, CPPD	GI ulceration, renal impairment, CVS risk (especially with prolonged use). Avoid in CKD, active PUD, heart failure
Topical NSAIDs (diclofenac gel)	Same but local delivery → lower systemic exposure	Epicondylitis, OA hand, De Quervain's	Skin irritation; preferred over oral for localised conditions to minimise systemic SE
COX-2 selective inhibitors (celecoxib, etoricoxib)	Selective COX-2 inhibition → less GI SE	Gout flare, inflammatory arthritis in patients with GI risk	↑ CVS risk; avoid post-CABG; still renal risks
Colchicine	Inhibits microtubule polymerisation → ↓ neutrophil migration/NLRP3 inflammasome	Acute gout, CPPD flare; gout prophylaxis during ULT initiation	Diarrhoea (most common), marrow suppression. C/I: severe renal/hepatic impairment. Drug interaction: clarithromycin, cyclosporin (↑ toxicity)
Corticosteroid (local injection)	Potent anti-inflammatory → ↓ oedema, ↓ cytokine release	CTS, epicondylitis, trigger finger, De Quervain's, OA (IA), acute gout (IA)	Tendon weakening/rupture if injected into tendon; skin depigmentation; infection risk; hyperglycaemia in DM patients. Limit to ~3 injections per site
Oral corticosteroid (prednisolone)	Systemic anti-inflammatory	Acute gout (when NSAIDs/colchicine C/I); RA flare; CPPD flare	DM control disruption, osteoporosis, immunosuppression, peptic ulcer. Short courses preferred
Allopurinol	Xanthine oxidase inhibitor → ↓ urate production	Chronic gout — ULT	Allopurinol hypersensitivity syndrome (HLA-B*5801 — screen in Chinese/Southeast Asian patients); start low, go slow
Febuxostat	Selective xanthine oxidase inhibitor	Gout — ULT in allopurinol intolerance/HLA-B*5801 +	↑ CVS mortality in CARES trial (controversial); avoid in severe CVD
Methotrexate	Folate antagonist → ↓ lymphocyte proliferation	RA — first-line DMARD	Hepatotoxicity, marrow suppression, pneumonitis. C/I: pregnancy, severe hepatic/renal disease. Supplement with folic acid 5 mg weekly
Pyridoxine (B6)	?Neuroprotective	Adjunct in CTS, cubital tunnel ^[2]	Generally safe; mega-doses can paradoxically cause neuropathy
Pregabalin / Gabapentin	α2δ Ca²⁺ channel ligand → ↓ excitatory neurotransmitter release	Neuropathic pain (cervical radiculopathy, post-surgical neuropathic pain)	Drowsiness, dizziness, weight gain, oedema

HLA-B*5801 Screening Before Allopurinol

In Hong Kong's Chinese population, the prevalence of HLA-B5801 is ~6–8%. This allele confers a high risk of allopurinol hypersensitivity syndrome (DRESS/SJS/TEN — mortality ~25%). Always screen for HLA-B5801 before starting allopurinol in Chinese patients. If positive, use febuxostat instead.

Splinting is the workhorse of conservative management for hand/wrist/elbow conditions. Different conditions require different splint types:

Condition	Splint type	Position	Rationale
CTS	Night-time wrist splint ^[2]	Wrist neutral (0–15° extension)	Minimises carpal tunnel pressure by avoiding flexion
Cubital tunnel	Soft elbow extension splint ^[2]	Elbow ~30° flexion	Prevents full elbow flexion which narrows the cubital tunnel
De Quervain's	Thumb spica splint	Wrist neutral, thumb immobilised	Prevents APL/EPB gliding through inflamed 1st compartment
Trigger finger	Extension splint at night ^[2]	MCP in extension (PIP/DIP free)	Prevents flexion → stops nodule from catching on A1 pulley
Scaphoid fracture	Thumb spica cast ^[2]	Wrist neutral, thumb immobilised	Absolute immobilisation for primary bone healing
Mallet finger	Stack splint	DIP in full extension	Allows extensor tendon healing at DIP

Steroid injection is used across multiple conditions. Here is a summary of injection sites and considerations:

Condition	Injection site	Agent	Notes
Lateral epicondylitis	Point of maximal tenderness at lateral epicondyle	Methylprednisolone 40 mg + lignocaine 1%	Do NOT inject into the tendon substance; peritendinous injection
De Quervain's	Into the 1st extensor compartment sheath	Triamcinolone 10 mg + lignocaine	Confirm placement: syringe should flow easily if within the sheath
Trigger finger	Into the flexor tendon sheath at A1 pulley	Triamcinolone 10–20 mg + lignocaine	Inject at MCP crease; resistance = tendon (withdraw slightly)
CTS	Into carpal tunnel, ulnar to palmaris longus	Methylprednisolone 40 mg + lignocaine	Avoid injecting directly into the median nerve (paraesthesia = stop)
OA 1st CMC	Into the 1st CMC joint under USG guidance	Triamcinolone 10 mg	Small joint → USG guidance improves accuracy

General contraindications to local steroid injection:

Septic arthritis or local skin infection (would worsen infection)
Overlying cellulitis or broken skin
Poorly controlled diabetes (steroid → hyperglycaemia for 1–2 weeks)
Coagulopathy (↑ bleeding risk)
Previous tendon rupture at the site
More than 3 injections in the same site within 12 months

A quick-reference for when conservative management should be abandoned and surgery considered:

Condition	Surgical indication
CTS	Unresponsive to conservative treatment for 6 weeks; sensory/motor deficit; axonal loss on NCS ^[2]
Cubital tunnel	Failure of splinting/PT for 3–6 months; progressive weakness/wasting; ulnar nerve subluxation
Lateral epicondylitis	Refractory symptoms > 6–12 months despite PT, bracing, injection
De Quervain's	Failure of splinting + ≥ 1 steroid injection
Trigger finger Grade IV	Fixed flexion deformity — surgery is first-line ^[2]
Septic arthritis	All cases — urgent aspiration/washout
Flexor sheath infection	All cases — urgent surgical drainage ^[1]
Scaphoid fracture (displaced/proximal)	Percutaneous screw fixation ^[2]
RA (emergency)	Septic arthritis, C1/2 instability, tendon rupture, CTS ^[3]
Ganglion cyst	Persistent/recurrent despite aspiration; symptomatic (nerve compression) ^[13]
OA hand	Severe ADL impairment; pain despite conservative Rx → trapeziectomy (1st CMC), arthrodesis (DIP) ^[12]

High Yield Summary

Universal ladder: conservative (activity modification, splinting, PT) → pharmacological (analgesics, steroid injection) → surgical.
CTS management: night-time wrist splint → steroid injection → carpal tunnel release (division of flexor retinaculum) if failure > 6 weeks, motor/sensory deficit, or axonal loss on NCS ^[2].
Lateral epicondylitis: activity modification + PT (stretching, strengthening, elbow brace) → analgesics/steroid injection → surgery (debridement, tendon repair/transfer if > 50% damage) ^[2].
De Quervain's: avoid repetitive actions + wrist splint → local steroid injection → surgical decompression (widen tunnel roof) ^[2].
Trigger finger: guided by Green's classification. Extension splint (I) → steroid injection (II–III) → surgical release of A1 pulley (III–IV) ^[2].
Cubital tunnel: soft elbow extension splint → steroid/pyridoxine → anterior transposition of ulnar nerve ^[2].
TOS: nTOS = PT ± Botox; vTOS = thrombolysis + anticoagulation + surgical decompression; aTOS = embolectomy + surgical decompression ^[2].
Septic arthritis: urgent aspiration + IV antibiotics + surgical washout — delay = permanent cartilage destruction.
Gout: acute flare (NSAIDs/colchicine/steroids) → chronic ULT (allopurinol first-line; screen HLA-B*5801 in Chinese patients). Never start/stop ULT during a flare.
RA surgical priority: LL before UL; proximal before distal; winner operation first (e.g. CTR, tenosynovectomy) ^[3].
Ganglion: observe/aspirate (1st line, ~50% spontaneous resolution) → excision if persistent ^[13].

Active Recall - Management of Hand/Wrist/Elbow Pain

References

^[1] Lecture slides: murtagh merge.pdf (p19–20, Arm and hand pain) ^[2] Senior notes: maxim.md (Sections on epicondylitis, De Quervain's, trigger finger, CTS, cubital tunnel syndrome, TOS, scaphoid fracture management) ^[3] Senior notes: Ryan Ho Rheumatology.pdf (p56, Role of surgery in RA; p62, SpA management — NSAIDs/biologics principles) ^[4] Senior notes: Ryan Ho Rheumatology.pdf (Sections 2.4.1 Gout — acute flare management, intercritical/tophaceous gout, ULT) ^[5] Senior notes: Ryan Ho Fundamentals.pdf (p407, Joint fluid analysis and initial investigations for monoarthritis) ^[6] Senior notes: maxim.md (Ganglion cyst management) ^[12] Senior notes: maxim.md (OA management — conservative and operative options) ^[13] Senior notes: Ryan Ho Rheumatology.pdf (p173, Ganglion — treatment)

Complications of Hand / Wrist / Elbow Conditions

Complications are the consequences of either the disease itself (if untreated or poorly controlled) or of the treatment (surgical or medical). Understanding complications from first principles means tracing them back to the underlying pathology — if you understand why cartilage is destroyed in septic arthritis, you understand why the complication is permanent joint stiffness. Below, we systematically cover complications condition by condition, then the cross-cutting complications that apply across multiple conditions (e.g. compartment syndrome, CRPS).

1. Disease Complications — By Condition

Complication	Mechanism	Clinical significance
Thenar muscle wasting ^[2]	Chronic compression → axonal loss of median nerve motor fibres → denervation atrophy of abductor pollicis brevis, opponens pollicis	Loss of thumb opposition and abduction → inability to grip, pinch, or oppose thumb. Irreversible if denervation exceeds ~6–12 months because motor endplates degenerate
Permanent sensory loss	Prolonged ischaemia → Wallerian degeneration of sensory axons	Numbness in lateral 3.5 digits → loss of fine touch discrimination; patients drop objects, burn fingers without noticing
"Ape hand" deformity	Loss of thenar opposition → thumb falls back into the plane of the palm	Thumb cannot oppose to other fingers → functional hand disability

Treatment complications of carpal tunnel release ^[2]:

Persistent CTS symptoms (inadequate release) — if the flexor retinaculum is not completely divided, residual compression persists; the most common cause of "failed" CTR.
Nerve injury: palmar cutaneous branch — this small branch of the median nerve crosses the operative field and can be transected during open CTR → painful neuroma or numbness over the thenar eminence.
Vascular injury: superficial palmar arch — the arch lies just deep to the retinaculum; overzealous deep dissection can lacerate it → haematoma and ischaemia to the digital arteries.
Pillar pain — post-operative pain at the thenar and hypothenar eminences (the "pillars") where the retinaculum was attached. Due to altered load transmission after the retinaculum is divided. Usually self-limiting over weeks.
Wound infection and scar tenderness — as with any surgical procedure.
Recurrence — rare ( < 5%) but may occur from scar tissue reformation or incomplete initial release.

Why Timing Matters in CTS

The key teaching point: irreversible thenar wasting is the most feared complication of CTS. Once axonal loss progresses beyond ~6–12 months, the motor endplates at the neuromuscular junction undergo fibrotic degeneration and cannot be reinnervated even if the nerve is subsequently decompressed. This is why sensory/motor deficit and axonal loss on NCS are urgent surgical indications ^[2].

Complication	Mechanism
Intrinsic hand muscle wasting	Ulnar nerve denervation → atrophy of interossei, hypothenar muscles, medial 2 lumbricals
Claw hand deformity	Loss of lumbrical/interosseous function (MCP flexion + IP extension) → unopposed MCP hyperextension + IP flexion by long flexors. Paradoxically less severe in cubital tunnel than in Guyon's canal (ulnar paradox — FDP 4/5 also denervated in high lesion)
Permanent sensory loss (medial 1.5 digits)	Axonal degeneration of ulnar sensory fibres
Grip and pinch weakness	Interossei (finger ab/adduction) and adductor pollicis (key pinch) denervated

Treatment complications:

Anterior transposition ^[2] — risk of devascularising the ulnar nerve during mobilisation; haematoma; medial antebrachial cutaneous nerve injury (numbness over medial forearm).
Medial epicondylectomy — instability of the elbow's medial column if too much bone is removed.

Complication	Mechanism
Chronic pain / treatment failure	The pathology is tendinosis (degenerative), not inflammatory → response to conservative treatment can be slow (6–12 months); ~10–20% become chronic despite treatment
Tendon rupture	Repeated steroid injections weaken the collagen matrix → ↑ risk of ECRB/common extensor tendon tear. This is why injections should be limited to ≤ 3 per site
Recurrence after surgery	Incomplete debridement or failure to address the underlying biomechanical cause (e.g. poor ergonomics)
Associated ulnar nerve neuropathy (medial) ^[2]	In medial epicondylitis, inflammation at the common flexor origin is in direct proximity to the ulnar nerve → concurrent ulnar neuritis

Complication	Mechanism
Chronic stenosing tenosynovitis	If the repetitive mechanical trigger is not eliminated, the 1st compartment sheath continues to thicken → persistent pain despite treatment
Post-injection skin depigmentation / fat atrophy	Steroid injection → local lipocyte atrophy + melanocyte suppression → visible skin dimple and whitening at injection site. More noticeable in darker skin tones
Superficial radial nerve injury (post-surgery)	The nerve passes directly over the 1st compartment. During surgical release, it can be transected → Wartenberg's syndrome (iatrogenic neuritis: numbness/dysaesthesia over dorsal thumb/1st web space)

Complication	Mechanism
Fixed flexion deformity (Green's Grade IV) ^[2]	Prolonged locking → secondary contracture of the PIP joint capsule and volar plate; even after A1 pulley release, the PIP may remain flexed
Tendon bowstringing (post-surgical)	If the A2 pulley is inadvertently released during A1 pulley surgery, the flexor tendon lifts away from the phalanx during flexion → reduced mechanical efficiency and visible bowstringing
Digital nerve injury (post-surgical)	The digital nerves lie immediately lateral to the flexor sheath at the A1 pulley level → risk during percutaneous or open release
Steroid-related tendon weakening	Repeated intrasheath steroid → collagen degradation → tendon rupture (rare but documented)

Complications ^[2]:

Complication	Mechanism	Clinical consequence
Avascular necrosis (AVN) (~30%)	The scaphoid's blood supply enters distally (dorsal branch of radial artery) and travels retrograde towards the proximal pole → higher risk if more proximal fracture ^[2] because the proximal fragment is cut off from its blood supply	Proximal pole becomes necrotic → sclerotic on XR → collapse → secondary OA
Scaphoid non-union advanced collapse (SNAC)	Progressive arthritis due to prolonged non-union ^[2]. The scaphoid is mainly surrounded by articular cartilage (no periosteal blood supply for callus formation) → relies on primary bone healing ^[2] → difficult to achieve union if not absolutely immobilised	Predictable pattern of wrist OA: radioscaphoid → capitolunate → pancarpal arthritis. End-stage → wrist fusion
Malunion	Fracture heals in an abnormal position (e.g. flexed "humpback" deformity) → altered carpal mechanics	Restricted wrist ROM, pain, secondary OA

RA is a systemic disease, but the hand/wrist bears the brunt of local joint destruction. Complications arise from pannus formation eroding cartilage, bone, and soft tissues ^[3]^[5]:

Complication	Mechanism
Joint deformities ^[5]: ulnar deviation, swan-neck, boutonnière, Z-thumb, volar subluxation	Pannus → ligament/capsule destruction → tendon imbalance → deformity. E.g. swan-neck: volar plate laxity at PIP → unopposed extensor pull → PIP hyperextension + compensatory DIP flexion
Tendon rupture ^[3]	Tenosynovitis weakens tendons from within; bony spicules at the DRUJ or Lister's tubercle can abrade tendons. The most common is extensor tendon rupture (EPL after Colles' fracture; EDC to ring/little finger from dorsal DRUJ osteophyte — the "Vaughan-Jackson" lesion)
Nerve palsy: CTS, PIN palsy ^[3]^[5]	Synovial proliferation within the carpal tunnel compresses the median nerve; synovitis around the elbow compresses the posterior interosseous nerve → finger drop
Trigger finger ^[5]	Flexor tenosynovitis → nodule formation → A1 pulley stenosis
Cervical myelopathy from C1/2 instability ^[3]	Pannus erodes the transverse ligament of C1 → atlantoaxial subluxation → spinal cord compression. A life-threatening complication — always check lateral C-spine in flexion before general anaesthesia in RA patients
Joint dislocation ^[5]	Ligament destruction at MCP/wrist → subluxation/dislocation
Secondary OA	End-stage RA → cartilage destruction → secondary degenerative changes on top of inflammatory disease

Complication	Mechanism
Chronic tophaceous gout ^[4]	Persistent hyperuricaemia → MSU crystal deposition in soft tissues → gouty tophi (extensor surface of fingers, hands, forearm, elbows, Achilles tendons, helix of ear) ^[4]. Tophi cause progressive joint destruction and functional impairment
Tophus complications ^[4]: ulceration, infection, inflammation mimicking dactylitis	Tophi thin the overlying skin → ulceration discharging whitish gritty material (crystalline urate). Ulcerated tophi are portals of entry for bacteria → secondary infection. Inflammation around a tophus can mimic dactylitis
Urate renal stones, uric acid nephropathy ^[4]	Hyperuricaemia → urate crystallisation in renal collecting system → stones; chronic urate deposition in renal interstitium → nephropathy
Progressive joint destruction ^[4]	Chronic crystal-induced inflammation → cartilage and bone erosion → deformity and disability
Recurrent flares with shortening intercritical periods ^[4]	Untreated: 2nd flare ≤ 1 year (62%), ≤ 2 years (78%), ≤ 10 years (93%) ^[4]. Flares become increasingly prolonged, disabling, polyarticular and may be associated with fever

Complication	Mechanism
Permanent cartilage destruction	Bacterial proteases + neutrophil-derived enzymes (collagenases, elastases) degrade the cartilage matrix within days. Cartilage is avascular and cannot regenerate → irreversible joint damage. This is why septic arthritis is a rheumatological emergency ^[3]
Secondary OA	Post-infective joint damage leads to early-onset degenerative changes
Joint ankylosis / stiffness	Inflammatory granulation tissue → fibrous adhesions → loss of ROM
Osteomyelitis	Infection extends from the joint into underlying bone, especially in children (where the metaphyseal blood supply communicates with the joint)
Tendon necrosis (flexor sheath infection)	Pus within the closed tendon sheath → ↑ pressure → ischaemic necrosis of the flexor tendons → loss of finger flexion
Spread to deep spaces — horseshoe abscess	The radial bursa (thumb FPL sheath) and ulnar bursa (little finger FDS/FDP sheath) communicate at the wrist in the Parona space → infection can spread between thumb and little finger
Amputation	End-stage: necrotic tendon, destroyed joint, uncontrolled infection → may require digital or ray amputation

2. Cross-Cutting Complications

These complications can occur across multiple conditions, especially trauma-related ones:

Always keep regional pain syndrome in mind for persistent burning pain in hand following injury, trivial or severe ^[1]

Etymology: "complex" = multifaceted; "regional" = localised to a body region; "pain syndrome" = chronic pain state.

Types:

CRPS Type I (reflex sympathetic dystrophy): no definable nerve lesion.
CRPS Type II (causalgia): follows a defined nerve injury.

Pathophysiology: Not fully understood. After injury (fracture, surgery, even minor trauma), an aberrant inflammatory and sympathetic nervous system response develops:

Initial injury → nociceptor sensitisation + neurogenic inflammation.
Peripheral sensitisation → central sensitisation (spinal cord wind-up).
Sympathetic-afferent coupling → sympathetic nervous system activity maintains pain.
Cortical reorganisation → chronic pain state with trophic changes.

Clinical features — three phases:

Phase	Features
Acute (0–3 months)	Burning pain disproportionate to injury; red, warm, oedematous hand; ↑ sweating; rapid nail/hair growth
Dystrophic (3–9 months)	Pain persists; cool, cyanotic skin; stiff joints; brawny oedema; osteoporosis on XR
Atrophic ( > 9 months)	Irreversible trophic changes: smooth shiny skin, fixed contractures, severe osteoporosis, muscle atrophy

When to suspect: persistent burning pain in hand following injury, trivial or severe ^[1] — the pain is out of proportion to the original insult.

Management: Early recognition is crucial. Multidisciplinary approach: physiotherapy (graded motor imagery, mirror therapy), analgesics (pregabalin/gabapentin for neuropathic component), vitamin C prophylaxis (500 mg daily after wrist fractures may reduce incidence), and psychological support.

CRPS After Wrist Fracture — Prevention

CRPS is listed as a rare but important complication under Murtagh's framework ^[1]. It occurs in ~5–25% of distal radius fractures. Evidence suggests that vitamin C 500 mg daily for 50 days starting from the day of fracture may reduce the risk. Tight casts should be avoided (↑ swelling → ↑ pain → ↑ CRPS risk).

Treatment modality	Complication	Mechanism
Steroid injection (any site)	Tendon rupture	Steroid inhibits collagen synthesis → tendon weakening (especially if injected directly into tendon substance rather than peritendinous)
	Skin depigmentation / fat atrophy	Local melanocyte and lipocyte suppression
	Hyperglycaemia	Systemic absorption of corticosteroid → hepatic gluconeogenesis ↑. Important to warn DM patients
	Infection (rare)	Introduction of bacteria through needle puncture; aseptic technique essential
Carpal tunnel release ^[2]	Persistent CTS, palmar cutaneous nerve injury, superficial palmal arch injury	See 1.1 above
Trigger finger release	Digital nerve injury, flexor tendon bowstringing	Digital nerves immediately lateral to A1 pulley; A2 pulley inadvertent release
De Quervain's release	Superficial radial nerve injury (Wartenberg's)	Nerve crosses the surgical field
Cubital tunnel surgery ^[2]	Ulnar nerve devascularisation, medial antebrachial cutaneous nerve injury	Nerve mobilisation disrupts vascular supply; MABC nerve runs in operative field
Prolonged casting	Joint stiffness/contracture, disuse muscle atrophy, pressure sores, CRPS	Immobility → capsular fibrosis; muscle disuse → atrophy; tight cast → ↑ pressure → CRPS
NSAIDs (chronic)	GI ulceration, renal impairment, CVS events	COX-1 inhibition → ↓ mucosal protection; renal prostaglandin inhibition → vasoconstriction; prothrombotic COX-2 relative excess
Allopurinol	Allopurinol hypersensitivity syndrome (DRESS/SJS/TEN)	HLA-B5801-mediated T-cell activation → severe cutaneous adverse reaction. Prevalence of HLA-B5801 ~6–8% in Chinese/Hong Kong population
DMARDs (methotrexate)	Marrow suppression, hepatotoxicity, pneumonitis	Folate antagonism → bone marrow toxicity; hepatocyte damage; immune-mediated pulmonary inflammation

The hand is the primary tool for interacting with the world. Any complication affecting the hand has outsized functional impact ^[2]:

Domain	Specific functional loss	Assessment
ADL — Upper limb ^[2]	Buttoning, combing, chopstick use	Ask the patient to perform these tasks
Grip and pinch	Inability to grip objects (jar, door handle) or perform key pinch (turning a key)	Dynamometer, key grip test
Fine motor	Dropping objects, difficulty writing, unable to pick up coins	Practical tests: writing, undo button
Occupational	Inability to perform work duties (manual workers, surgeons, musicians)	Occupational therapy assessment
Psychological	Frustration, depression, anxiety — especially if dominant hand affected	Screen for depression (Murtagh's masquerade: depression ^[1])
Social	Inability to shake hands, embarrassment from deformity, loss of independence	Social work referral if needed

Hand dominance is a critical part of the history ^[2] — complications affecting the dominant hand have far greater functional impact.

Condition	Disease complications	Treatment complications
CTS	Thenar wasting (irreversible), permanent sensory loss, ape hand	Persistent CTS, palmar cutaneous nerve injury, superficial palmar arch injury ^[2]
Cubital tunnel	Intrinsic hand wasting, claw hand, sensory loss	Nerve devascularisation, MABC nerve injury
Lateral epicondylitis	Chronic pain, tendon rupture (from repeated injections)	Recurrence post-surgery
De Quervain's	Chronic stenosing tenosynovitis	Superficial radial nerve injury (Wartenberg's)
Trigger finger	Fixed flexion deformity (Grade IV) ^[2]	Digital nerve injury, tendon bowstringing
Scaphoid fracture	AVN (~30%), SNAC wrist, malunion ^[2]	Screw migration, non-union despite fixation
RA hand	Deformities, tendon rupture, CTS, C1/2 instability ^[3]^[5]	DMARD toxicity (MTX), surgical complications
Gout	Tophi (ulceration, infection), renal stones, joint destruction ^[4]	Allopurinol hypersensitivity, colchicine toxicity
Septic arthritis	Cartilage destruction, secondary OA, osteomyelitis, ankylosis	Inadequate washout → persistent infection
Flexor sheath infection	Tendon necrosis, horseshoe abscess, amputation	Stiffness from adhesions
Ganglion	Nerve impingement ^[13]	Recurrence (up to 50%), wound Cx, injury to neighbours ^[13]
Any fracture/trauma	Compartment syndrome, Volkmann's contracture, CRPS ^[1]^[14]	Cast complications (stiffness, pressure sores)

High Yield Summary

CTS: most feared complication = irreversible thenar wasting from axonal loss. Surgical complications: persistent CTS (inadequate release), palmar cutaneous nerve injury, superficial palmar arch injury ^[2].
Scaphoid fracture: AVN (~30%, higher in proximal fractures) because blood supply is retrograde; SNAC wrist from non-union ^[2].
RA hand: progressive deformities (ulnar deviation, swan-neck, boutonnière), tendon rupture (Vaughan-Jackson lesion), CTS, and C1/2 instability (always check before GA) ^[3]^[5].
Gout: untreated → tophaceous gout with progressive joint destruction, tophi complications (ulceration, infection), and renal disease (urate stones, nephropathy) ^[4].
Septic arthritis: cartilage destruction within days — the defining reason it is a rheumatological emergency ^[3].
CRPS: always keep in mind for persistent burning pain in hand following injury, trivial or severe ^[1]. Disproportionate pain + trophic changes after injury. Prevention: vitamin C, avoid tight casts.
Volkmann's contracture: end-stage of missed compartment syndrome in the forearm. Classic scenario: supracondylar fracture → brachial artery injury → ischaemic necrosis of flexor compartment → claw deformity ^[2]^[14].
Steroid injection complications apply across all conditions: tendon weakening/rupture, skin depigmentation, hyperglycaemia in DM, infection. Limit to ≤ 3 per site.
Allopurinol hypersensitivity (DRESS/SJS/TEN): screen HLA-B*5801 in Chinese patients before starting. Mortality ~25%.
Functional impact: always assess ADL (buttoning, combing, chopstick use) and hand dominance ^[2] — hand complications disproportionately affect quality of life.

Active Recall - Complications of Hand/Wrist/Elbow Conditions

References

^[1] Lecture slides: murtagh merge.pdf (p19–21, Arm and hand pain — including CRPS mention) ^[2] Senior notes: maxim.md (Sections on CTS complications, scaphoid fracture complications, trigger finger, De Quervain's, supracondylar fracture/Volkmann's contracture, cubital tunnel, epicondylitis, forearm fractures, history taking — hand dominance/ADL) ^[3] Senior notes: Ryan Ho Rheumatology.pdf (p56, Role of surgery in RA — emergency indications, surgical options; p38, Tophaceous gout complications; p10, RA hand examination complications) ^[4] Senior notes: Ryan Ho Rheumatology.pdf (Section 2.4.1.2, Intercritical and chronic tophaceous gout — tophus complications, prognosis, renal manifestations; p40, Surgical treatment of gout complications) ^[5] Senior notes: Ryan Ho Fundamentals.pdf (p129–131, Rheumatoid hands examination — deformities and complications including joint dislocation, nerve palsy, trigger finger) ^[6] Senior notes: maxim.md (Ganglion cyst — complications: nerve impingement) ^[13] Senior notes: Ryan Ho Rheumatology.pdf (p173, Ganglion — treatment complications: recurrence, wound Cx, injury to structures) ^[14] Senior notes: maxim.md (Complications of trauma — compartment syndrome, Volkmann's contracture, CRPS; Ryan Ho Cardiology.pdf p212, compartment syndrome mechanism and management)

High Yield Summary

Top-line take-aways for exams:

Probability diagnoses for arm/hand pain (Murtagh): cervical spine dysfunction, shoulder disorders, epicondylitis, overuse tendinopathy of wrist, CTS, OA of thumb/DIP ^[1].
Serious conditions not to miss: MI/angina (referred left arm pain), septic arthritis, tendon sheath infection, Pancoast tumour ^[1].
CTS risk factors = aging, female, DM, hypothyroid, RA, obesity, pregnancy. Night pain + flick sign + Phalen's/Tinel's = classic presentation ^[2].
Lateral epicondylitis > medial epicondylitis. Tests: Cozen's and Mill's (lateral); reverse Cozen's (medial) ^[2].
De Quervain's = 1st extensor compartment (APL + EPB). Finkelstein's test. DDx: 1st CMC OA (grind test), Wartenberg's syndrome, intersection syndrome ^[2].
Trigger finger = A1 pulley stenosis. Green's grading (I–IV). Risk: DM, prolonged gripping, elderly female ^[2].
Cubital tunnel = ulnar nerve at elbow. High lesion → LESS claw (ulnar paradox). Distinguish from Guyon's canal by dorsal sensation ^[2].
RA hand = MCP ulnar deviation, swan-neck, boutonnière, Z-thumb. SPARES DIP. OA = Heberden's (DIP) + Bouchard's (PIP) ^[3]^[5].
Kanavel's signs (flexor tenosynovitis): fusiform swelling, flexed posture, sheath tenderness, pain on passive extension — a surgical emergency.
Always consider referred pain (cervical spine, cardiac) before attributing to local MSK pathology.

High Yield Summary

Structure your DDx by Murtagh's tiers: probability → serious (don't miss) → pitfalls → masquerades → psychogenic ^[1].
Top probability diagnoses: cervical radiculopathy, shoulder disorders, epicondylitis, overuse tendinopathy (De Quervain's), CTS, OA of thumb/DIP ^[1].
Emergencies to exclude first: septic arthritis (hot joint = septic until proven otherwise), flexor sheath infection (Kanavel's signs), MI (left arm pain + cardiac risk factors), Pancoast tumour (smoker + Horner's) ^[1].
Key DDx for radial wrist pain: De Quervain's (Finkelstein's +) vs. 1st CMC OA (Grind test +) vs. Wartenberg's (sensory, external compression) vs. intersection syndrome (proximal, crepitus) ^[2].
Key DDx for finger joint deformity: RA = MCP/PIP, spares DIP, symmetric ^[3]; OA = DIP/PIP, Heberden's/Bouchard's nodes ^[5]; PsA = DIP + nail changes, dactylitis.
Nocturnal hand paraesthesia DDx: CTS (lateral 3.5, Phalen's +) vs. cubital tunnel (medial 1.5, dorsal affected) vs. C6/C7 radiculopathy (Spurling's +, NCS normal at wrist) vs. TOS (lower trunk symptoms) ^[2].
Ganglion cyst: most common soft tissue tumour of hand, dorsal wrist 70%, transilluminable, never malignant ^[6]^[7].
Crystal arthritis at wrist/hand: gout (MSU, neg birefringent) vs. CPPD (CPP, weakly pos birefringent); CPPD — wrist is 2nd most common site after knee ^[4].

High Yield Summary

Most hand/wrist/elbow conditions are clinical diagnoses. Investigations are to confirm, exclude serious mimics, or guide management.
Key investigations (Murtagh): FBE, ESR/CRP, ECG, NCS, plain XR ("if in doubt, X-ray and compare both sides"), USG for soft tissue ^[1].
CTS: clinical diagnosis + NCS for confirmation. Normal NCS does not rule it out. Axonal loss on NCS = surgical indication ^[2].
Joint aspiration = MOST IMPORTANT TEST for acute monoarthritis ^[5]. Must send crystal microscopy + Gram stain + culture. Gout: needle-shaped, negative birefringent. CPPD: rhomboid, weakly positive birefringent.
Scaphoid fracture: XR (incl. scaphoid view) first → if negative but clinically suspected → thumb splint + repeat XR 14 days OR MRI ^[2].
Gout imaging criteria: USG double contour sign or DECT urate deposition; XR erosion with overhanging edges ^[4].
Murtagh's nocturnal pain rule: TOS = can't fall asleep; CTS = wakes mid-night then settles; cervical spondylosis = wakes and persists ^[1].
RA: XR hands/feet (erosions, JSN, periarticular osteopaenia); bloods (RF, anti-CCP, ESR/CRP); USG (early erosions, active synovitis with power Doppler). 2010 ACR/EULAR criteria ≥ 6/10 ^[3]^[5].
NCS localises entrapment: CTS → prolonged distal latency at wrist; cubital tunnel → slowed across elbow; radiculopathy → NCS normal at wrist, EMG shows myotomal denervation ^[8].
Crystals + infection can coexist — always send culture even if crystals found.

High Yield Summary

Universal ladder: conservative (activity modification, splinting, PT) → pharmacological (analgesics, steroid injection) → surgical.
CTS management: night-time wrist splint → steroid injection → carpal tunnel release (division of flexor retinaculum) if failure > 6 weeks, motor/sensory deficit, or axonal loss on NCS ^[2].
Lateral epicondylitis: activity modification + PT (stretching, strengthening, elbow brace) → analgesics/steroid injection → surgery (debridement, tendon repair/transfer if > 50% damage) ^[2].
De Quervain's: avoid repetitive actions + wrist splint → local steroid injection → surgical decompression (widen tunnel roof) ^[2].
Trigger finger: guided by Green's classification. Extension splint (I) → steroid injection (II–III) → surgical release of A1 pulley (III–IV) ^[2].
Cubital tunnel: soft elbow extension splint → steroid/pyridoxine → anterior transposition of ulnar nerve ^[2].
TOS: nTOS = PT ± Botox; vTOS = thrombolysis + anticoagulation + surgical decompression; aTOS = embolectomy + surgical decompression ^[2].
Septic arthritis: urgent aspiration + IV antibiotics + surgical washout — delay = permanent cartilage destruction.
Gout: acute flare (NSAIDs/colchicine/steroids) → chronic ULT (allopurinol first-line; screen HLA-B*5801 in Chinese patients). Never start/stop ULT during a flare.
RA surgical priority: LL before UL; proximal before distal; winner operation first (e.g. CTR, tenosynovectomy) ^[3].
Ganglion: observe/aspirate (1st line, ~50% spontaneous resolution) → excision if persistent ^[13].

High Yield Summary

CTS: most feared complication = irreversible thenar wasting from axonal loss. Surgical complications: persistent CTS (inadequate release), palmar cutaneous nerve injury, superficial palmar arch injury ^[2].
Scaphoid fracture: AVN (~30%, higher in proximal fractures) because blood supply is retrograde; SNAC wrist from non-union ^[2].
RA hand: progressive deformities (ulnar deviation, swan-neck, boutonnière), tendon rupture (Vaughan-Jackson lesion), CTS, and C1/2 instability (always check before GA) ^[3]^[5].
Gout: untreated → tophaceous gout with progressive joint destruction, tophi complications (ulceration, infection), and renal disease (urate stones, nephropathy) ^[4].
Septic arthritis: cartilage destruction within days — the defining reason it is a rheumatological emergency ^[3].
CRPS: always keep in mind for persistent burning pain in hand following injury, trivial or severe ^[1]. Disproportionate pain + trophic changes after injury. Prevention: vitamin C, avoid tight casts.
Volkmann's contracture: end-stage of missed compartment syndrome in the forearm. Classic scenario: supracondylar fracture → brachial artery injury → ischaemic necrosis of flexor compartment → claw deformity ^[2]^[14].
Steroid injection complications apply across all conditions: tendon weakening/rupture, skin depigmentation, hyperglycaemia in DM, infection. Limit to ≤ 3 per site.
Allopurinol hypersensitivity (DRESS/SJS/TEN): screen HLA-B*5801 in Chinese patients before starting. Mortality ~25%.
Functional impact: always assess ADL (buttoning, combing, chopstick use) and hand dominance ^[2] — hand complications disproportionately affect quality of life.

Hand/wrist/elbow Pain

Hand / Wrist / Elbow Pain

2. Epidemiology and Risk Factors

3. Relevant Anatomy and Function

4. Etiology (Focused on Hong Kong Context) and Pathophysiology

5. Detailed Etiology and Pathophysiology by Condition

6. Classification

7. Clinical Features — Symptoms and Signs (with Pathophysiological Basis)

7.2 Condition-Specific Symptoms

7.3 Key Clinical Signs (Examination Findings)

Active Recall - Hand/Wrist/Elbow Pain

Differential Diagnosis of Hand / Wrist / Elbow Pain

3. Detailed Differential Diagnosis — Distinguishing Features

5. DDx Specific to Key Presentations — Pattern Recognition

Active Recall - DDx of Hand/Wrist/Elbow Pain

References

Diagnostic Criteria, Algorithm and Investigation Modalities

2. Diagnostic Criteria for Key Conditions

4. Investigation Modalities — Detailed Breakdown

Active Recall - Diagnosis and Investigations for Hand/Wrist/Elbow Pain

References

Management Algorithm and Treatment Modalities

3. Condition-Specific Management — Detailed

Active Recall - Management of Hand/Wrist/Elbow Pain

References

Complications of Hand / Wrist / Elbow Conditions

1. Disease Complications — By Condition

2. Cross-Cutting Complications

Active Recall - Complications of Hand/Wrist/Elbow Conditions

References

On this page

Hand/wrist/elbow Pain

1. Definition and Scope

2. Epidemiology and Risk Factors

2.1 Epidemiology

2.2 Risk Factors — General Framework

3. Relevant Anatomy and Function

3.1 Elbow Joint

3.2 Forearm

3.3 Wrist Joint

3.4 Dorsal Extensor Compartments of the Wrist

3.5 Hand — The Flexor Pulley System

3.6 Nerve Supply of the Hand

4. Etiology (Focused on Hong Kong Context) and Pathophysiology

4.1 Probability Diagnoses (Common — the ones you'll see most in clinic)

4.2 Serious Disorders Not To Be Missed

4.3 Pitfalls (Often Missed)

5. Detailed Etiology and Pathophysiology by Condition

5.1 Lateral Epicondylitis ("Tennis Elbow")

5.2 Medial Epicondylitis ("Golfer's Elbow")

5.3 De Quervain's Tenosynovitis ("Gamer's Thumb")

5.4 Trigger Finger

5.5 Carpal Tunnel Syndrome (CTS)

5.6 Cubital Tunnel Syndrome

5.7 Thoracic Outlet Syndrome (TOS)

5.8 Osteoarthritis of the Hand

5.9 Rheumatoid Arthritis — Hand Involvement

5.10 Crystal Arthropathies Affecting the Hand/Wrist/Elbow

5.11 Septic Arthritis of Hand/Wrist/Elbow

5.12 Flexor Tendon Sheath Infections

5.13 Referred Pain

6. Classification

6.1 By Anatomical Location

6.2 By Pathological Process

6.3 Key Condition-Specific Classifications

7. Clinical Features — Symptoms and Signs (with Pathophysiological Basis)

7.1 Symptom Analysis Framework

7.2 Condition-Specific Symptoms

Carpal Tunnel Syndrome

Lateral Epicondylitis

Medial Epicondylitis

De Quervain's Tenosynovitis

Trigger Finger

Cubital Tunnel Syndrome

7.3 Key Clinical Signs (Examination Findings)

Inspection

Special Tests

7.4 Nerve Examination Pearls

8. Approach to the Patient — Putting It All Together

Active Recall - Hand/Wrist/Elbow Pain

References

1. Organising Framework — Murtagh's Diagnostic Strategy

2. DDx by Anatomical Region

3. Detailed Differential Diagnosis — Distinguishing Features

3.1 Elbow Region

3.2 Wrist Region

3.3 Hand / Finger Region

3.4 Referred / Systemic Causes

4. DDx by Pathological Process — A Complementary Lens

5. DDx Specific to Key Presentations — Pattern Recognition

Pattern A: Radial-sided wrist pain

Pattern B: Ulnar-sided wrist pain

Pattern C: Diffuse wrist swelling + pain

Pattern D: Finger locking/triggering

Pattern E: Finger joint pain + deformity

Pattern F: Nocturnal hand paraesthesia

6. DDx for Special Populations

7. Approach to Narrowing the DDx — Clinical Algorithm

8. Comprehensive DDx Summary Table

Active Recall - DDx of Hand/Wrist/Elbow Pain

1. General Principles — Why We Investigate

2. Diagnostic Criteria for Key Conditions

2.1 Carpal Tunnel Syndrome (CTS)

2.2 Rheumatoid Arthritis (2010 ACR/EULAR Classification Criteria)

2.3 Gout (2015 ACR/EULAR Classification Criteria)

2.4 Lateral and Medial Epicondylitis

2.5 De Quervain's Tenosynovitis

2.6 Trigger Finger — Green's Classification

2.7 Septic Arthritis

3. Diagnostic Algorithm

4. Investigation Modalities — Detailed Breakdown