Clinical Terms - Bone & Joint

Complications of gout include the following:

Complications of ______ include: • Severe degenerative arthritis • Secondary infections • Urate or uric acid nephropathy • Increased susceptibility to infection • Urate nephropathy • Renal stones • Nerve or spinal cord impingement • Fractures in joints with tophaceous gout

Tophi

A deposit of monosodium urate crystals in the body, caused by high levels of uric acid in the blood. As a general rule, asymptomatic hyperuricemia should not be treated. Patients with levels higher than 11 mg/dL who overexcrete uric acid are at risk for renal stones and renal impairment; therefore, renal function should be monitored in these individuals. Tophi should not be surgically removed unless they are in a critical location or drain chronically. Although colchicine was once the treatment of choice for acute gout, it is now less commonly used than nonsteroidal anti-inflammatory drugs because of its narrow therapeutic window and risk for toxicity. To be effective, colchicine therapy is ideally initiated within 36 hours of onset of the acute attack.

Gout Management - Acute

Acute treatment of proven crystal-induced arthritis is directed at relief of the pain and inflammation. Agents used in this setting include the following: • Nonsteroidal anti-inflammatory drugs (NSAIDs), such as indomethacin • Corticosteroids • Colchicine (now less commonly used for acute gout than it once was) • Adrenocorticotropic hormone (ACTH) • Combinations of drugs (colchicine plus NSAIDs, oral corticosteroids plus colchicine, intra-articular steroids plus colchicine or NSAIDs)

Gout

An extremely painful inflammation of joints, especially of the big toe, caused by a metabolic defect resulting in the accumulation of uric acid in the blood and the deposition of urates around the joints. It is caused by monosodium urate monohydrate crystals; pseudogout is caused by calcium pyrophosphate crystals and is more accurately termed "calcium pyrophosphate disease". Crystal deposition can be asymptomatic, but gout and calcium pyrophosphate disease can develop into debilitating illnesses marked by recurrent episodes of pain and joint inflammation that result from the formation of crystals within the joint space and deposition of crystals in soft tissue. If untreated, these disorders can lead to joint destruction and, in the case of uric acid crystals, renal damage. Comorbidity: Hypertriglyceridemia

polyarthritis

Arthritis involving five or more joints. Often autoimmune.

Gout Management - treatment alternative due to underside effects of normal treatments:

Because these agents change serum and tissue uric acid levels, they may precipitate acute attacks of gout. This undesired effect may be reduced by prophylaxis with the following: • Colchicine or low-dose NSAIDs • Low-dose prednisone (if patients cannot take colchicine or NSAIDs) Other therapeutic agents that may be considered include the following: • Uricase and pegloticase • Vitamin C • Anakinra • Fenofibrate

Gout Diagnostic Studies

Diagnostic studies for _______ • Joint aspiration and synovial fluid analysis • Serum uric acid measurement (though hyperuricemia is not diagnostic of gout) • 24-hour urinary uric acid evaluation • Blood studies (including white blood cells [WBCs, triglyceride, high-density lipoprotein, glucose, and renal and liver function tests)

arthropathies

Diseases of the Joint

Podagra

Gout (also known as _________ when it involves the big toe) is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint.

Gout Comorbidities

Hypertriglyceridemia Certain comorbid conditions are associated with a higher incidence of gout, including the following: Hypertension Diabetes mellitus Renal insufficiency Hypertriglyceridemia Hypercholesterolemia Obesity Anemia

Monoarticular

Involving a single joint

Gout Management - Nonpharmacologic

Nonpharmacologic measures that may be warranted are as follows: • Avoidance or restricted consumption of high-purine foods • Avoidance of excess ingestion of alcoholic drinks, particularly beer • Avoidance of sodas and other beverages or foods sweetened with high-fructose corn syrup • Limited use of naturally sweet fruit juices, table sugar, and sweetened beverages and desserts, as well as table salt • Maintenance of a high level of hydration with water (≥8 glasses of liquids daily) • A low-cholesterol, low-fat diet, if such a diet is otherwise appropriate for the patient • Weight reduction in patients who are obese

Gout radiographic studies

Plain radiographs may show findings consistent with ______. Erosions with overhanging edges are generally considered pathognomonic for ______ (though also found in other diseases). Characteristics of erosions typical of ____ include the following: • Maintenance of the joint space • Absence of periarticular osteopenia • Location outside the joint capsule • Sclerotic (cookie-cutter, punched-out) borders • Asymmetric distribution among the joints, with a strong predilection for distal joints, especially in the lower extremities

Gout (also known as _________ when it involves the big toe) is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis—a red, tender, hot, swollen joint.

Podagra

What is the treatment for gout?

Renal function should be monitored in patients with uric acid levels > 11 mg/dL

Which of the following tests is commonly misused in the diagnosis of gout?

Serum uric acid test Measurement of serum uric acid is the most misused test in the diagnosis. The presence of hyperuricemia in the absence of symptoms is not diagnostic. In addition, as many as 15% of patients with symptoms may have normal serum uric acid levels at the time of their attack. Thus, the diagnosis can be missed if the joint is not aspirated. Remember that situations that decrease uric acid levels can trigger attacks. In such cases, the patient's medical records may reveal prior elevations of uric acid.

Gout Symptoms

Symptoms include the following: • Podagra (initial joint manifestation in 50% of gout cases and eventually involved in 90%; also observed in patients with pseudogout and other conditions) • Arthritis in other sites - In gout, the instep, ankle, wrist, finger joints, and knee; in pseudogout, large joints (eg, the knee, wrist, elbow, or ankle) • Monoarticular involvement most commonly, though polyarticular acute flares are not rare, and many different joints may be involved simultaneously or in rapid succession • In gout, attacks that begin abruptly and typically reach maximum intensity within 8-12 hours; in pseudogout, attacks resembling those of acute gout or a more insidious onset that occurs over several days • Without treatment, symptom patterns that change over time; attacks can become more polyarticular, involve more proximal and upper-extremity joints, occur more often, and last longer • In some cases, eventual development of chronic polyarticular arthritis that can resemble rheumatoid arthritis

Gout Management - Long Term

Therapy to control the underlying hyperuricemia generally is contraindicated until the acute attack is controlled (unless kidneys are at risk because of an unusually heavy uric acid load). Long-term management of gout is focused on lowering uric acid levels. Agents used include the following: • Allopurinol • Febuxostat • Probenecid

Gout ultrasonic, CT and MRI Studies

Ultrasonographic findings in established gout include the following: • A "double-contour" sign, consisting of a hyperechoic, irregular line of MSU crystals on the surface of articular cartilage overlying an adjacent hyperechoic bony contour • "Wet clumps of sugar," representing tophaceous material, described as hyperechoic and hypoechoic heterogeneous material with an anechoic rim • Bony erosions adjacent to tophaceous deposits Other imaging modalities that may be considered include the following: • Computed tomography (CT) - Complementary to plain radiography for recognizing erosions in gout Magnetic resonance imaging (MRI) - MRI with gadolinium is recommended when tendon sheath involvement must be evaluated and when osteomyelitis is in the differential diagnosis

When is MRI useful in diagnosing Gout?

When tendon sheath involvement must be evaluated MRI is not part of any routine evaluation for acute arthritis. MRI evidence of edema is minimal in gout, unless concomitant osteomyelitis is present. However, MRI with gadolinium is recommended when tendon sheath involvement must be evaluated and when osteomyelitis is in the differential diagnosis. Large deposits of crystals may be seen in bursae or ligaments. MRI examination of erosions reveals tophi but no bone edema or synovitis.

How long do gout attacks initially take to reach maximum intensity?

attacks initially take 8-12 hours to reach maximum intensity. attacks begin abruptly and typically reach maximum intensity within 8-12 hours. Affected joints are red, hot, and exquisitely tender; even a bedsheet on the swollen joint is uncomfortable. The onset of symptoms in pseudogout can resemble acute gout or be more insidious and may occur over several days. Untreated, the first attacks resolve spontaneously in less than 2 weeks. A history of intermittent inflammatory arthritis, in which the joints return to normal between attacks, is typical of crystalline disorders and is characteristic of gouty arthritis early in its course.

Osteomalacia

softening of the bones, typically through a deficiency of vitamin D or calcium.

Gout - Physical Findings

• Involvement of a single (most common) or multiple joints • Signs of inflammation - Swelling, warmth, erythema (sometimes resembling cellulitis), and tenderness Fever (also consider infectious arthritis) Migratory polyarthritis (rare) • Posterior interosseous nerve syndrome (rare) Tophi in soft tissues (helix of the ear, fingers, toes, prepatellar bursa, olecranon) • Eye involvement - Tophi, crystal-containing conjunctival nodules, band keratopathy, blurred vision, anterior uveitis (rare), scleritis

Gout Management

• Treating the acute attack • Providing prophylaxis to prevent acute flares • Lowering excess stores of urate to prevent flares of gouty arthritis and to prevent tissue deposition of urate crystals