Ankle Pain Intra-articular: Situated within.

Occurring within Extra-articular: Situated outside of a joint Intra-articular Pain Often felt anteriorly Or dull achey pain (difficult to localize) Pain with dorsiflexion and plantarflexion Ankle effusion

Signs and Symptoms Ankle effusion Ankle Equinus

Differential Diagnosis Acute onset Leading causes infection and crystal induced arthritis Spondytoarthropathies (reactive arthritis)

Chronic pain Rheumatoid arthritis Spondylo arthropathies

Persistent Ankle Pain (post injury) Talar Dome injury (osteoarthritis dessicans. Transchondral fractures)

OA of ankle joint (rare) May be secondary to trauma

Neuropatiiic arthriropathy Severe degenerative disease, pt usually diabetic Hallux Valgus Lateral deviation of the great toe

Osteoarthritis A degenerative Form of Arthritis in which cartilage within joints gradually break down Non-inflammatory arthritide Degenerative Joint Disease Characterized by progressive loss of articular cartilage and remodeling and change the structure of subchondral bone Most common form of arthritis

The Pathogenisis of Osteoarthritis 1) 2) 3) 4) 5) 6) 7) Damage to the hyaline Cartilage (acute: Arthrocentisis) (chronic: Repetitive trauma) Impact of injury (avascular tissue worn away) Bone Sclerosis Growth of osteophytes at joint margins Weakness/muscle atrophy Ligamentous laxity Synovitis may result Joint Misalignment increased load (uneven distribution)

Primary Versus Secondary OA Osteoarthritis can be categorized as: 1) Primary OA occurring spontaneously (Avascular necrosis) 2) Secondary OA as a result of trauma or other insult to the joint Diagnosis of Osteoarthritis 1) Joint pain brought on and exacerbated by activity and relieved by rest 2) Stiffness that is self- limited on walking in the morning or after a period of extended activity 3) Absence of systemic symptoms 4) Increased bony prominence at joint margins (1st MPJ), crepitus, tenderness over joint line 5) Radiographic changes may be evident (Growth of osteophytes at joint magins) Clinical Findings Primary Lesions located in the metacarpels Heberdens Nodes (distal interphalangeal joints) Bouchards Nodes (Proximal Interphalangeal joints

Laboratory findings Synovial Fluid: not blood, Greater than 3000 WBC o Negative for Bifringent Crystals, bacterial

Blood Tests: o Erythrosedimentation Rate (ESR) normal in OA (Non rheumathological) o CRP Normal C-reactive Protein o Negative for Rheumathoid Factor

**Chronic cases of OA may present with increases of ESR and CRP** Radiographic Hallmarks of Osteoarthritis Sclerosing and Eburnation (hardening o subdural bone) Osteophyte development SPURRING (Osteophytic Lipping) Non uniform joint space narrowing Subchondral cysts

Differential Diagnosis Gout Definition: - Disease caused by deposition of monosodium urate monohvdrate crystals in joints and/or surrounding soft tissues Usually associated with hyperuricemia Extremely painful condition with warmth, erythema and swelling Usually begins as monoarthritis Affinity for 1st MPJ Other forms of arthritis (RA, Gout, CPPD) Occult Malignancy (Cancer) Meniscal or ligamentous tear

Definitive Diagnosis involves joint aspiration demonstrating strongly negative birefringent crystals from aspirated synovial fluid ** Under Polarized light microscope crystal are bright, and needle shaped Hyperuricemia is defined as serum (blood) urate concentrations greater >7.0 mg/dL Hyperuricemia alone is not sufficient to diagnose gout o Hyperuricemia may result from increased urate production (<5% of cases) or decreased exreation of Uric acid ( 90% of cases) by the kidneys Or a combination of both

Four phases of Gout 1) 2) 3) 4) Asymptomatic hyperuricemia Acute gouty arthritis Intercritical gout (asymptomatic) Chronic Tophaceous Gout presents with Tophi

1) Asymptomatic Hyperuricemia (no symptoms present)

Abnormally high serum urate levels without gouty arthritis or renal stones present Risk factors include: poor renal function, use of diuretics (treatment of hypertension) Treatment at this stage none required, modification and correction of underlying causes 2) Acute Gouty arthritis Symptoms include a sudden onset of pain, swelling of local synovial joint Diagnosis Joint aspiration Differential diagnosis include conditions affecting the 1st MPJ (Osteoarthritis), CPPD, Treatment includes NSAIDs, Corticosteriods

3) Intercritical Gout Asymptomatic phase Complte resolution of symptoms (pain, swelling) Uric acid levels still high (above 7.0 mg/dL)

4) Chronic Tophaceous Gouty Arthritis Signs Development of tophi chalky deposits of sodium urate present along the affected synovial joint

Pseudogout: Calcium Pyrophosphate Dihydrate (CPPD) Crystal Deposition disease Etiology is unknown idiopathic Crystal Deposition disease can mimic gout, rheumatoid arthritis or osteoarthritis Pseudogout causes an intermittent monoarthritis, often of knee or wrist For the diaganosis of CPPD (Calcium Pyrophosphate Dihydrate) CPPD crystals need to be present within the joint fluid for firm diagnosis

Clinical Findings of CPPD Lab Findings Demonstration of CPPD crystals Increased White Blood cell counts Inflammatory presentation

Specific Tests include: 1. serum calcium

2. phosphorus 3. magnesium 4. alkaline phosphate 5. Thyroid Stimulating Hormone 6. Ceruloplasim Image Studies Radiographic findings Screenlngfor CPPD crystal deposition disease involves 4 radiographs 1) Anteriorposterior view of the knee 2) Anterioposterior view of the pelvis 3) Posteroanterior view of both hands 4) Posteroanterior view of both wrists

Diagnostic Criteria 1 Demonstration of CPPD crystals In tissue or synovial fluid 2) Identification of monoclinic or triclinic crystals Showing no or weakly positive birefringence by compensated polarized light microscopy 3) Presence of typical radiographic calcifications 4) Acute arthritis, especially of knees or other large joints 5) Chronic arthritis, especially of the knee, hip, wrist, carpus, elbow, shoulder or Metacarpal Phalangeal Joint especially if accompanied by acute exacerbations Complicatoins May lead to progressive degenerative joint damage If disease is severe 1) Joint collapse may occur 2) Charcot like degenerations

Treatment NSAIDs Oral or I.V. Colchicine IV or IA glucocorticoids

Birefrigence (radiographs) Bone Degeneration Uric acid is the end product of purine metabolism (catabolism) position of urate crustals in the joints and Kidneys cuases gout (sympotomatic)

Blood Concentrations of Uric Acid: 1) Male 4.0 8.5 mg/dL 2) Female 2.7 7.3 mg/dL 3) Elderly slightly elevated levels

** Critical Values of blood concentrations of Uric Acid: Greater >12mg/dL Four Treatment options for Acute Gouty Arthritis 1) NSAIDs most important factor how quickly it is administered Indomethacine

Colchincine 0.5 0.6 mg hourly until a) Significant clinical improvements seen with early administration b) may cause severe G.I. upset if this occurs omit the use of Colchincine c) 10 doses no relief (check differential diagnosis) 2) Corticosteriods - glucocorticoids may be used if the medication above do not work - I.M. or I.A. 10 40 mg of prednisone can be used **Analgesics and narcotics may also be administered in severe cases Intercritical Period of Gout Low does of colchicines Prophylactic Therapy NSAIDS

** Ultimate goal is to decrease Blood urate levels to 5mg or less Chronic Gout 1) Allopurinal Blocks the production of Uric Acid by inhibiting purine synthesis - prevents reabsorption of Uric acid in the blood) - Probenicid is used in patients who do not tolerate Allopurinol NSAIDS Maximum safe dosage (MSD)

a) continous in the first few minutes of critical attack

b) 4 hours of symptoms use atleast 2 days for attack until symptoms subside - continue dose once symptoms subside for 48 hours

Summary Characteristics of NSAIDS Traditional NSAIDs 1) indomethacin -