---

Orthopaedic History Taking and Examination - Undergraduate Level

---

PART 1: HISTORY TAKING

General Approach

---

1. Presenting Complaint (PC)

• Pain
• Swelling
• Deformity
• Stiffness
• Weakness / loss of function
• Instability / giving way
• Locking / clicking
• Altered sensation / paraesthesia

---

2. History of Presenting Complaint (HPC)

• Mechanical vs. inflammatory pattern:
  • Mechanical: worse with activity, better with rest, no morning stiffness (or < 30 min)
  • Inflammatory: morning stiffness > 1 hour, worse at rest, improves with movement
• Night pain (suggests serious pathology: infection, tumour, inflammatory disease)
• Radicular pattern (dermatomal radiation suggests nerve root involvement)

---

• Onset (acute = haemarthrosis/fracture; chronic = effusion/synovitis)
• Fluctuant, hard, or soft?
• Warm or cold?

• Congenital vs. acquired
• Progressive or static?

• Direction (anterior, posterior, multidirectional)
• Triggering activity
• Frequency of episodes

• True locking (joint stuck in flexion, cannot fully extend) vs. pseudolocking (pain-inhibited)

---

3. Functional Enquiry

• Activities of daily living (ADLs): dressing, washing, cooking
• Mobility: walking distance, need for walking aids
• Work: occupation (manual vs. sedentary) and effect on ability to work
• Sport and recreation
• Sleep disturbance

---

4. Past Medical History (PMH)

• Previous musculoskeletal problems or surgery to the same or related region
• Previous trauma or fractures
• Relevant systemic diseases:
  • Rheumatoid arthritis, osteoarthritis, gout, pseudogout
  • Osteoporosis (fragility fractures)
  • Diabetes (peripheral neuropathy, poor wound healing)
  • Malignancy (metastatic bone disease)
  • Inflammatory bowel disease (associated arthropathy)
  • Psoriasis (psoriatic arthritis)
  • Neurological disease (e.g. cerebral palsy, spina bifida - affects joint biomechanics)

---

5. Drug History

• NSAIDs, analgesics (current pain management)
• Corticosteroids (long-term use - osteoporosis, avascular necrosis)
• Bisphosphonates, denosumab (bone health)
• DMARDs / biologics (rheumatological disease)
• Anticoagulants (relevant to surgery planning)
• Allergies (especially antibiotics relevant to surgery)

---

6. Family History

• Rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis
• Osteoporosis
• Bone tumours (familial predisposition)
• Congenital conditions (e.g. DDH - developmental dysplasia of hip)

---

7. Social History

• Occupation (type of work, manual labour, repetitive movements)
• Handedness (for upper limb problems)
• Smoking (impairs bone healing, increases surgical risk)
• Alcohol (falls risk, osteoporosis, avascular necrosis)
• Living situation: house/flat, stairs, support at home
• Mobility aids currently used

---

8. Systems Review

• Red flags in orthopaedics (require urgent investigation):
  • Unexplained weight loss
  • Night sweats / fever
  • Night pain not relieved by any position
  • History of malignancy
  • Age > 50 with new back pain
  • Bladder/bowel disturbance with back pain (cauda equina)
  • Saddle anaesthesia
  • Bilateral leg weakness

---

PART 2: PHYSICAL EXAMINATION

"Look, Feel, Move, then Special Tests"

---

General Inspection

• Gait (antalgic, Trendelenburg, steppage, spastic)
• Use of walking aids
• Body habitus, posture
• Obvious deformities
• Muscle wasting

---

The "LOOK, FEEL, MOVE" Framework

LOOK (Inspection)

• Skin: scars (previous surgery), sinuses (infection), erythema, bruising, skin changes (psoriasis)
• Shape: deformity (valgus/varus, flexion deformity), swelling (localised vs. diffuse), muscle wasting
• Position: resting posture of the limb, alignment

• Valgus - distal part deviated away from midline (e.g. hallux valgus, genu valgum)
• Varus - distal part deviated toward midline (e.g. genu varum)
• Flexion deformity - cannot achieve full extension
• Fixed deformity - cannot be corrected passively

---

FEEL (Palpation)

• Temperature: use dorsum of hand; warmth suggests inflammation or infection
• Tenderness: localise precisely (joint line, specific bony landmarks, soft tissues). Ask patient to indicate when it hurts. Map the tender area
• Swelling: differentiate:
  • Bony swelling - hard, non-fluctuant
  • Effusion - fluctuant, ballottement (knee), bulge sign (knee)
  • Soft tissue swelling - boggy (synovial thickening) vs. cystic
• Crepitus: felt during movement
• Neurovascular assessment: distal pulses, capillary refill, sensation

• Shoulder: acromion, AC joint, coracoid, bicipital groove, rotator cuff insertion
• Elbow: medial/lateral epicondyles, olecranon
• Wrist/hand: anatomical snuffbox (scaphoid), individual carpal bones, MCP/IP joints
• Hip: greater trochanter, ischial tuberosity, ASIS
• Knee: joint line (medial/lateral), tibial tuberosity, patella, collateral ligaments, popliteal fossa
• Ankle/foot: malleoli, Achilles tendon, calcaneum, base of 5th metatarsal

---

MOVE (Range of Motion)

1. Active movement first (patient moves themselves - tests neuromuscular function)
2. Passive movement (examiner moves the joint - tests joint integrity and end-feel)
3. Note: pain, limitation, and crepitus during movement

• Normal bony end-feel (elbow extension)
• Normal soft tissue end-feel (knee flexion)
• Abnormal: springy (meniscal block), empty (guarding due to pain)

---

Special Tests by Region

Shoulder

---

Elbow

---

Wrist and Hand

---

Spine

• Flexion, extension, lateral flexion, rotation
• Spurling's test (axial compression with rotation): radiculopathy
• Upper limb neurology: power (C5-T1), reflexes (biceps C5/6, brachioradialis C6, triceps C7), sensation

• Inspection: scoliosis, kyphosis, lordosis
• Schober's test: lumbar flexion (mark 10 cm above and 5 cm below lumbosacral junction; should increase by > 5 cm on full flexion in adults)
• Straight leg raise (SLR / Lasegue's): L4/L5/S1 nerve root irritation. Positive if pain radiates below knee at < 60°
• Crossed SLR: contralateral leg raise causes ipsilateral radicular pain - highly specific for disc prolapse
• Femoral nerve stretch test (prone knee bend): L2/3/4 root
• Lower limb neurology: power (L3-S2), reflexes (knee L3/4, ankle S1), sensation

---

Hip

• True leg length: ASIS to medial malleolus (structural shortening)
• Apparent leg length: umbilicus to medial malleolus (pelvic tilt contributing)

---

Knee

---

Ankle and Foot

---

Neurovascular Assessment

• Distal pulses (dorsalis pedis, posterior tibial in lower limb; radial, ulnar in upper limb)
• Capillary refill (< 2 seconds normal)
• Sensation in relevant dermatomes
• Motor power (MRC grading 0-5):

• Reflexes: graded 0 (absent), + (reduced), ++ (normal), +++ (brisk), ++++ (clonus)

---

PART 3: PRESENTING YOUR FINDINGS

"On inspection, there was [X]. On palpation, there was [Y] tenderness at [location] with [Z] swelling. Range of motion was limited to [X degrees] with [pain/crepitus]. Special tests showed [positive Lachman's], suggesting [ACL tear]. Neurovascular status was intact distally."

---

Summary: Key Mnemonics

---

---

Rheumatoid Arthritis - MBBS Level

---

1. Definition

• Robbins & Kumar Pathologic Basis of Disease

---

2. Epidemiology

• Harrison's Principles of Internal Medicine, 22nd Ed

---

3. Aetiology and Risk Factors

• HLA-DRB1 alleles carrying the "shared epitope" (SE) are the strongest genetic risk factor
  • *0401, *0404 alleles predominate in northern Europeans
  • *0405, *0901 in East Asians
• PTPN22 gene (encodes lymphoid tyrosine phosphatase) - regulates T and B cell activation; risk allele exclusive to ACPA-positive disease
• PADI4 gene - encodes enzyme converting arginine to citrulline; associated with anti-CCP antibody production, especially in East Asian populations

• Smoking - strongest environmental risk factor; promotes citrullination of proteins in the lung, triggering ACPA production
• Periodontal disease (Porphyromonas gingivalis produces citrullinating enzyme)
• Hormonal factors (female sex, postpartum period)
• Gut microbiome dysbiosis
• Harrison's 22nd Ed

---

4. Pathogenesis

Genetic susceptibility + Environmental trigger
        ↓
Abnormal citrullination of self-proteins (fibrinogen, collagen, vimentin, enolase)
        ↓
CD4+ T cells (Th1, Th17) react to citrullinated antigens presented by HLA-DR4
        ↓
Activation of B cells → Plasma cells → Rheumatoid factor + Anti-CCP antibodies
        ↓
Synovial inflammation → Pannus formation → Joint destruction

• Pannus = a thickened, vascular, fibroblast-rich membrane derived from hyperplastic synovium
• Invades and destroys underlying cartilage and bone at the pannus-bone interface
• Osteoclasts at this interface form resorption lacunae → marginal bone erosions (hallmark of RA on X-ray)
• Robbins & Kumar Pathologic Basis of Disease; Harrison's 22nd Ed

---

5. Morphology / Histopathology

• Synovial lining hyperplasia (normally 1-3 cells thick → becomes 8-10 cells thick)
• Dense infiltrate of CD4+ T cells, B cells, plasma cells, dendritic cells, mast cells
• Formation of lymphoid follicles and germinal center-like structures
• Neovascularisation (new blood vessels to supply the expanding tissue)

• Pannus covers articular cartilage and invades bone
• Generalised loss of proteoglycan from cartilage matrix
• Periarticular osteopenia (bone marrow inflammation)
• Progressive narrowing of joint space → eventual ankylosis

• Central zone of fibrinoid necrosis
• Surrounded by palisading macrophages/histiocytes
• Peripheral zone of granulation tissue and chronic inflammatory cells

• Robbins & Kumar Pathologic Basis of Disease

---

6. Clinical Features

Articular Features

• Symmetrical polyarthritis - hallmark feature
• Affects small joints first: MCP (metacarpophalangeal), PIP (proximal interphalangeal), wrists, MTP (metatarsophalangeal)
• Spares DIP (distal interphalangeal) joints - distinguishes from OA and psoriatic arthritis
• Later: larger joints (knees, shoulders, hips, elbows, ankles)
• Cervical spine (C1-C2 atlantoaxial) - can be involved; risk of atlanto-axial subluxation

• Morning stiffness > 1 hour (hallmark - inflammatory pattern)
• Pain and swelling of affected joints
• Joint warmth and tenderness
• Loss of grip strength

Classic Hand Deformities (late/chronic RA)

Extraarticular Features

• Rheumatoid nodules - subcutaneous, firm, non-tender; found over pressure points (olecranon, sacrum, occiput); pathognomonic when present
• Vasculitic skin lesions (nailfold infarcts, leg ulcers)
• Palmar erythema

• Pleuritis / pleural effusion (exudative; low glucose, low complement)
• Interstitial lung disease (ILD) - UIP or NSIP pattern on HRCT; more common in males and smokers
• Caplan syndrome: RA + pneumoconiosis → large pulmonary nodules
• Bronchiectasis, obliterative bronchiolitis

• Pericarditis / pericardial effusion
• Accelerated atherosclerosis → increased risk of MI and stroke (major cause of mortality)
• Myocarditis, cardiac nodules (rare)

• Keratoconjunctivitis sicca (secondary Sjögren syndrome) - most common
• Episcleritis (mild, self-limiting)
• Scleritis (severe, can be sight-threatening)
• Scleromalacia perforans (rare)

• Anaemia of chronic disease - most common haematological finding
• Felty syndrome: RA + splenomegaly + neutropaenia (recurrent infections)
• Thrombocytosis (reactive)

• Peripheral neuropathy (sensorimotor, mononeuritis multiplex)
• Carpal tunnel syndrome (median nerve compression)
• Atlanto-axial subluxation → cervical myelopathy

• Secondary amyloidosis (AA type) - uncommon; presents as proteinuria / nephrotic syndrome
• Drug-related nephrotoxicity (NSAIDs, gold, penicillamine)

• Fatigue, weight loss, low-grade fever, anorexia
• Lymphadenopathy
• Generalised osteoporosis (disease + corticosteroid use)

---

7. Laboratory Investigations

Immunological Tests

Seronegative RA = RF and ACPA both negative (~25% of patients). Still RA if clinical/radiological criteria met.

Acute Phase Reactants (markers of inflammation)

• ESR - elevated; correlates with disease activity
• CRP - elevated; more rapid response to inflammation
• Both are used in disease activity scores

Full Blood Count

• Normocytic normochromic anaemia (anaemia of chronic disease)
• Thrombocytosis (reactive to inflammation)
• Neutropaenia in Felty syndrome

Synovial Fluid Analysis

Imaging

X-ray changes are used for staging (Larsen score, Sharp score).

---

8. Diagnosis - ACR/EULAR 2010 Classification Criteria

• Harrison's Principles of Internal Medicine, 22nd Edition

---

9. Differential Diagnosis

---

10. Management

Treatment Goals ("Treat-to-Target" strategy)

• Achieve clinical remission (or low disease activity)
• Prevent joint damage and functional disability
• Minimise drug toxicity
• Improve quality of life

Drug Categories

A. NSAIDs

• Adjunctive role only (symptom relief)
• Inhibit COX-1 and COX-2 → reduce prostaglandin synthesis
• Examples: ibuprofen, naproxen, diclofenac
• Not disease-modifying - do not prevent erosions
• Side effects: GI ulceration, renal impairment, cardiovascular risk

B. Glucocorticoids

• Bridging therapy: rapid control while waiting for DMARDs to take effect (onset weeks-months)
• Short courses for disease flares
• Low-dose maintenance (prednisone 5-10 mg/day) in inadequate DMARD responders
• Side effects (long-term): osteoporosis, diabetes, hypertension, infections, adrenal suppression, cataracts, Cushingoid features
• Intra-articular injection for monoarticular flares

C. Conventional DMARDs (cDMARDs)

Methotrexate is the anchor DMARD. Combined DMARD regimens (e.g. MTX + HCQ + sulfasalazine = "triple therapy") are superior to monotherapy.

D. Biologic DMARDs (bDMARDs)

E. Targeted Synthetic DMARDs (tsDMARDs)

Management Algorithm (simplified)

Step 1: Start MTX (± short-term glucocorticoids as bridge)
        ↓ (if inadequate response at 3-6 months)
Step 2: Combination cDMARDs (MTX + HCQ + SSZ) OR MTX + biologic (anti-TNF)
        ↓ (if inadequate response)
Step 3: Switch biologic (different class) or JAK inhibitor
        ↓ (disease refractory)
Step 4: Rituximab / other biologics

Non-pharmacological Management

• Physiotherapy: joint protection, maintain ROM, muscle strengthening
• Occupational therapy: assistive devices, splinting, joint protection techniques
• Patient education: disease understanding, self-management
• Orthopaedic surgery: synovectomy, joint replacement (hip, knee), tendon repair, atlanto-axial fusion

---

11. Disease Activity Assessment

---

12. Prognosis and Complications

• High RF / high anti-CCP titres
• High baseline disease activity (DAS28)
• Early radiological erosions
• Extraarticular manifestations
• Functional disability at presentation
• Female sex
• Smoking

• Progressive joint destruction and disability
• Accelerated cardiovascular disease (leading cause of death in RA)
• Secondary amyloidosis (AA type)
• Osteoporosis and fragility fractures
• Drug-related toxicity
• Infections (especially with immunosuppressive therapy)
• Atlantoaxial subluxation → cord compression

---

13. Comparison: RA vs Osteoarthritis (OA)

• Robbins & Kumar Pathologic Basis of Disease

---

Key Examination Points for MBBS

1. RA is symmetrical small joint polyarthritis with morning stiffness > 1 hour
2. Spares DIP joints - key distinguishing feature
3. RF is sensitive but not specific; anti-CCP is more specific (~95%)
4. X-ray shows marginal erosions + periarticular osteopenia + uniform joint space loss
5. Methotrexate is the anchor/first-choice DMARD
6. Rheumatoid nodules = central fibrinoid necrosis + palisading macrophages
7. Pannus = key pathological structure that destroys cartilage and bone
8. ACR/EULAR 2010 criteria: score ≥ 6 = definite RA
9. Extraarticular complications: ILD (lung), pericarditis (heart), secondary Sjögren (eyes), anaemia of chronic disease, Felty syndrome
10. Treat-to-target strategy: aim for remission; step up therapy if target not met at 3-6 months

---