Orthopaedics

Definition

Osteoarthritis (OA) is the commonest joint disease — a degenerative disorder of synovial joints characterised by progressive loss of articular cartilage with accompanying subchondral bone changes, osteophyte formation and secondary synovitis. It is best regarded as a whole-joint failure rather than simple ‘wear and tear’. It may be primary (idiopathic) or secondary to a pre-existing abnormality (trauma, dysplasia, avascular necrosis, previous infection or inflammatory arthritis).

Pathology

The initiating event is cartilage damage: fibrillation and softening progress to fissuring and full-thickness loss, exposing bone. The subchondral bone responds with sclerosis (eburnation) and cyst formation, while at the joint margins new bone and cartilage form osteophytes. A secondary low-grade synovitis and capsular fibrosis contribute to pain and stiffness.

Clinical Features

Typically an older patient with activity-related joint pain that is relieved by rest, short-lived (<30 min) morning stiffness or ‘gelling’ after inactivity, and progressive loss of function. Examination shows crepitus, bony enlargement, restricted movement and, later, deformity (e.g. varus knee) and instability. The commonly affected joints are the knee, hip, first CMC joint of the thumb, and the DIP joints (Heberden’s nodes) and PIP joints (Bouchard’s nodes) of the hand.

Investigations

The diagnosis is largely clinical and radiographic. Plain radiographs show the ‘LOSS’ features: Loss of joint space (usually asymmetrical), Osteophytes, Subchondral sclerosis and Subchondral cysts. Blood tests are normal (helping to exclude inflammatory arthritis); joint aspiration is done only to exclude infection or crystals.

Management

Treatment is a stepwise, largely conservative programme. Non-pharmacological: patient education, weight loss, exercise and physiotherapy (quadriceps strengthening for the knee), activity modification, walking aids and footwear/orthoses. Pharmacological: topical NSAIDs and paracetamol, oral NSAIDs (with gastric caution), and intra-articular corticosteroid injections for flares. Surgical options for advanced disease refractory to conservative care include osteotomy (to realign and offload a compartment in the younger patient), arthroplasty (joint replacement — the definitive treatment for end-stage hip and knee OA) and arthrodesis (for selected small joints).

Complications

Progressive pain, deformity (varus knee, fixed flexion), instability, muscle wasting and loss of function and independence. Complications of treatment include the risks of NSAIDs and of joint-replacement surgery.

• Degenerative whole-joint disease: cartilage loss + subchondral changes + osteophytes.
• Mechanical pain (worse with use), brief (<30 min) morning stiffness, bony swelling, crepitus.
• Hands: Heberden’s (DIP) & Bouchard’s (PIP) nodes; also knee, hip, thumb base.
• X-ray ‘LOSS’: Loss of space, Osteophytes, Sclerosis, Subchondral cysts.
• Conservative first (weight loss, exercise, analgesia); arthroplasty for end-stage disease.

Definition

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune inflammatory disease characterised by a symmetrical, deforming polyarthritis that primarily attacks the synovium of small and large joints, together with extra-articular manifestations. It affects women more than men and typically begins in the third to fifth decades.

Pathology

The hallmark is synovitis: the inflamed, proliferating synovium forms a pannus — a mass of vascular granulation tissue that spreads over and erodes articular cartilage and subchondral bone from the joint margins, and stretches or destroys the capsule, ligaments and tendons. This leads progressively to joint destruction, instability and the characteristic deformities.

Clinical Features

Insidious onset of symmetrical pain, swelling and stiffness of the small joints of the hands and feet — typically the MCP, PIP and wrist joints (sparing the DIP joints) — with prolonged early-morning stiffness (> 1 hour) and systemic features (fatigue, malaise, low-grade fever). Established disease produces characteristic hand deformities: ulnar deviation of the fingers, swan-neck and boutonnière deformities, Z-thumb, and volar subluxation at the wrist.

Extra-articular Features

RA is a systemic disease: rheumatoid nodules (over pressure points), anaemia, vasculitis, lung involvement (nodules, fibrosis, effusions), eye disease (episcleritis, scleritis, dry eyes in secondary Sjögren’s), pericarditis, and, importantly for orthopaedics, cervical spine (atlanto-axial) instability.

Investigations

Serology: rheumatoid factor and anti-CCP antibodies (more specific), raised ESR/CRP, and a normochromic normocytic anaemia. Radiographs show peri-articular osteoporosis, soft-tissue swelling, marginal erosions, joint-space narrowing and, later, deformity and subluxation. The diagnosis uses the ACR/EULAR classification criteria.

Management

Management is by a rheumatology-led multidisciplinary team aiming for early control (‘treat to target’). The mainstay is disease-modifying anti-rheumatic drugs (DMARDs) — methotrexate first-line — started early, with biologic agents (anti-TNF and others) for resistant disease. NSAIDs and short courses of corticosteroids control symptoms and flares. Physiotherapy, occupational therapy and orthoses preserve function. Surgery (synovectomy, tendon repair, joint replacement or arthrodesis) is reserved for pain, deformity or loss of function despite medical treatment.

Complications

Beyond joint destruction and deformity, patients face the complications of chronic inflammation and its treatment: accelerated cardiovascular disease (the leading cause of excess mortality), osteoporosis (disease- and steroid-related), secondary amyloidosis, increased infection risk from immunosuppression, and cervical (atlanto-axial) instability. Regular monitoring of disease activity, drug toxicity and cardiovascular risk is an integral part of care.

• Chronic systemic autoimmune synovitis; symmetrical small-joint polyarthritis; F>M.
• Pannus erodes cartilage/bone; MCP/PIP/wrist affected, DIP spared; >1 h morning stiffness.
• Deformities: ulnar deviation, swan-neck, boutonnière, Z-thumb; extra-articular disease common.
• RF/anti-CCP positive, ↑ESR/CRP; marginal erosions & peri-articular osteoporosis on X-ray.
• Early DMARDs (methotrexate) ± biologics; beware atlanto-axial instability before anaesthesia.

Definition

Avascular necrosis (AVN, osteonecrosis) of the femoral head is death of bone and marrow due to interruption of its blood supply, leading progressively to structural failure, collapse of the articular surface and secondary osteoarthritis of the hip. The femoral head is especially vulnerable because of its precarious, largely intracapsular blood supply.

Causes

Traumatic: displaced femoral neck fracture and hip dislocation (which tear the retinacular vessels). Non-traumatic: corticosteroids and alcohol (the two commonest), sickle-cell disease, caisson (decompression) disease, Gaucher’s disease, SLE, radiation, and idiopathic. In children the equivalent idiopathic condition is Perthes disease.

Clinical Features

Insidious groin pain (sometimes referred to the thigh/knee) worse on weight-bearing, with an antalgic limp and progressive restriction of hip movement (early loss of internal rotation and abduction). Early disease may have few signs, so a high index of suspicion in at-risk patients is needed.

Investigations & Staging

Radiographs may be normal early; the first specific sign is the subchondral ‘crescent sign’ (a lucent line beneath the necrotic segment), progressing to flattening and collapse of the head and then joint-space loss. MRI is the most sensitive early investigation, detecting marrow changes before radiographic signs. The Ficat and Arlet classification stages the disease (I normal X-ray/abnormal MRI → II sclerosis/cysts → III crescent sign/subchondral collapse → IV secondary OA).

Management

Treatment depends on the stage. Pre-collapse (early) disease may be treated with protected weight-bearing and joint-preserving surgery such as core decompression (± bone grafting or vascularised graft) to relieve intraosseous pressure and encourage revascularisation; osteotomy can move the necrotic segment out of the load-bearing zone. Post-collapse (advanced) disease with a damaged joint is treated by total hip replacement. Underlying risk factors (steroids, alcohol) should be addressed.

Complications

The natural history is progressive: an untreated or late-presenting necrotic segment collapses, the femoral head flattens and becomes incongruent, and secondary osteoarthritis supervenes with pain, stiffness and shortening. Bilateral disease is common in the systemic (steroid/alcohol/sickle-cell) causes, so the opposite hip should always be imaged and monitored.

• Death of femoral-head bone from interrupted (precarious intracapsular) blood supply.
• Causes: femoral neck fracture/dislocation; steroids & alcohol commonest non-traumatic.
• Groin pain, limp, early loss of internal rotation/abduction.
• MRI most sensitive; crescent sign then collapse; Ficat staging.
• Pre-collapse → core decompression/joint preservation; post-collapse → total hip replacement.

Definition & Aims

Arthroplasty is the surgical reconstruction or replacement of a joint to relieve pain and restore movement and function. Total joint replacement (arthroplasty) replaces both articulating surfaces with prosthetic components; the hip and knee are the commonest and most successful. The principal aim is relief of pain, with improvement of function and correction of deformity.

Indications

The main indication is severe joint pain and disability from end-stage arthritis (osteoarthritis, rheumatoid arthritis, post-traumatic arthritis, AVN) that has failed adequate conservative treatment. Other indications include certain fractures (e.g. displaced femoral neck fracture in the elderly) and tumours requiring joint resection.

Types & Fixation

Components may be fixed to bone with cement (PMMA) or by cementless (press-fit, bone-ingrowth) fixation; hybrid constructs combine both. Bearing surfaces pair a metal or ceramic head with a polyethylene, ceramic or metal counterface. Replacement may be total (both surfaces) or partial (e.g. hemiarthroplasty of the hip, unicompartmental knee replacement).

Complications

Early: infection, venous thromboembolism (DVT/PE), dislocation (especially the hip), neurovascular injury, and peri-prosthetic fracture. Late: aseptic loosening (the commonest cause of long-term failure, driven by wear-particle osteolysis), polyethylene wear, late infection, peri-prosthetic fracture and implant failure. Revision surgery is more complex and less durable than primary replacement.

Post-operative Care

Multimodal analgesia, thromboprophylaxis, early mobilisation and physiotherapy, and measures to prevent dislocation (hip precautions) optimise outcome. Patients are counselled that a modern hip or knee replacement typically lasts many years but is not permanent and may eventually need revision.

Pre-operative Assessment

Careful patient selection and preparation underpin success. This includes optimising medical comorbidities (anaemia, diabetes, cardiac and respiratory disease), assessing and eradicating sources of sepsis (dental, urinary, skin), templating the radiographs to plan implant size and restore limb length and offset, and counselling the patient on the risks, the rehabilitation required and the finite lifespan of the implant. Body weight, activity level and bone quality all influence the choice of implant and fixation.

Revision Arthroplasty

When a replacement fails — through infection, aseptic loosening, wear, instability or peri-prosthetic fracture — revision surgery is required. Revision is technically more demanding than the primary operation: bone stock is often deficient, exposure is harder, and specialised implants (augments, longer stems, constrained bearings) may be needed. Outcomes are generally less good and complication rates higher than primary replacement, which is why preserving bone and avoiding infection at the first operation matters so much.

• Arthroplasty replaces joint surfaces; hip/knee commonest; main aim is pain relief.
• Indication: end-stage arthritis failing conservative care (also some fractures/tumours).
• Fixation cemented (elderly/soft bone) vs cementless (younger/good bone) vs hybrid.
• Feared complication: deep prosthetic infection; also VTE and dislocation early.
• Aseptic loosening (wear-particle osteolysis) is the main long-term cause of failure.

Definition

Ankylosing spondylitis (AS) is a chronic seronegative inflammatory arthropathy that principally affects the axial skeleton — the sacroiliac joints and spine — leading to inflammation, ossification and progressive bony ankylosis. It is the prototype of the seronegative spondyloarthropathies and is strongly associated with HLA-B27. It typically affects young men in the second and third decades.

Clinical Features

The hallmark is inflammatory back pain: insidious onset in a young adult, worse in the morning and with rest, improved by exercise, with prolonged morning stiffness and buttock pain (sacroiliitis). As the disease progresses the spine stiffens, with loss of lumbar lordosis, a fixed thoracic kyphosis and reduced chest expansion; advanced disease produces the rigid ‘bamboo spine’ and the stooped ‘question-mark’ posture. A reduced Schober’s test quantifies loss of lumbar flexion.

Extra-articular Features (the ‘A’s)

AS has systemic associations conveniently remembered as Anterior uveitis (the commonest extra-articular feature), Aortic regurgitation and conduction defects, Apical pulmonary fibrosis, Achilles tendinitis/enthesitis, Amyloidosis, and Atlanto-axial subluxation. Peripheral arthritis and enthesitis (plantar fasciitis) also occur.

Investigations

Radiographs of the sacroiliac joints show sacroiliitis (erosions, sclerosis, later fusion) — the earliest and most important sign; the spine shows syndesmophytes bridging vertebrae (the ‘bamboo spine’), squaring of vertebral bodies and ligamentous ossification. MRI detects early sacroiliitis before radiographic change. HLA-B27 is usually positive; rheumatoid factor is negative (seronegative); ESR/CRP may be raised.

Management

There is no cure; management aims to control pain and inflammation and preserve posture and mobility. The cornerstone is regular exercise and physiotherapy (to maintain spinal extension and chest expansion) together with NSAIDs for symptom control. Biologic agents (anti-TNF, IL-17 inhibitors) are highly effective for active disease not controlled by NSAIDs. Conventional DMARDs help peripheral (not axial) disease. Surgery (corrective osteotomy for severe kyphosis, hip replacement for hip involvement) is reserved for advanced deformity or joint destruction.

Diagnostic Criteria & Course

AS is one of the seronegative spondyloarthropathies, a family that also includes psoriatic arthritis, reactive arthritis and enteropathic (IBD-associated) arthritis, sharing features such as HLA-B27 association, enthesitis, dactylitis and sacroiliitis. The diagnosis rests on inflammatory back pain, restricted spinal movement and reduced chest expansion supported by imaging evidence of sacroiliitis. The course is one of intermittent flares over decades; early diagnosis and sustained exercise are the best predictors of preserved function.

Complications

Advanced disease leads to a rigid, kyphotic spine with impaired posture, forward gaze and respiratory reserve; the fused spine is brittle and prone to unstable fracture after minor trauma. Systemic complications include anterior uveitis, aortic regurgitation, apical pulmonary fibrosis and, rarely, amyloidosis and cauda equina syndrome. Osteoporosis of the ankylosed spine compounds the fracture risk.

• Seronegative axial spondyloarthropathy; HLA-B27; young men; sacroiliitis is the key lesion.
• Inflammatory back pain: worse with rest, better with exercise; ‘bamboo spine’, reduced Schober’s.
• Extra-articular ‘A’s: Anterior uveitis, Aortic regurgitation, Apical fibrosis, etc.
• SI-joint X-ray/MRI; syndesmophytes; HLA-B27+, RF negative.
• Exercise + NSAIDs ± biologics; ankylosed spine fractures easily and unstably.