Why does gout affect extremities

For men, gout usually attacks the large joints in their lower extremities, typically the big toes. Gout flare-ups often occur at night. There are several reasons why gout flares at night, including:. Inflammation and swelling in your affected joints is another sign that gout may be present. The final telltale signs of gouty arthritis include changes in your skin, such as redness and heat.

The system by Janssens and colleagues was based on a scale of For patients with a score of 8 or higher, the diagnosis of gout was confirmed in more than 80 percent of these patients.

It is well noted that the identification of monosodium urate crystals in joint fluid and tophi is considered a gold standard for the diagnosis of gout. Under polarized light, they exhibit strong negative birefringence. The crystals appear yellow with a line parallel to the slow vibration of the compensator and appear blue when the line is perpendicular to it.

If one suspects a sepsis process, the synovial fluid analysis is absolutely essential. Measuring the increased uric acid levels may be unreliable for diagnosis and can be misleading in either direction.

Serum urate levels may aid in supporting the diagnosis of gout. However, be aware that serum urate levels can be misleading in some cases and unreliable for the diagnosis of gout.

For example, a patient with joint pain with elevating serum urate may be inappropriately diagnosed with gout. Someone with a truly gouty attack who has normal serum urate levels may not actually have gout. Laboratory testing is only part of making a diagnosis. One may consider X-rays, ultrasound or magnetic resonance imaging MRI.

More recently, researchers noted that a new therapeutic imaging technique — dual-energy computed tomography CT — can identify four times as many areas of involvement than the standard clinical assessment. It may actually replace the gold standard of joint aspiration.

The clinical presentation of gout is typically acute monoarticular arthritis. It is usually located in a joint of the lower extremity but can occur in joints other than the feet including ankles, elbows, knees, wrists and fingers. With gout, one will typically note a warm, erythematous, swollen, tender joint with painful range of motion.

It is also important to note that acute inflammatory gout may occur in adjacent soft tissue or connective tissues, and is not limited to joint involvement itself. Typically, gout attacks last from six to 72 hours of onset, usually subsiding in three to 10 days.

Other clinical symptoms may involve the complaints of headache, fatigue and chills often with the onset of symptoms at night. The presentation may be symmetric or asymmetric, monoarticular or polyarticular. One should check the other body parts including the elbow olecranon bursa. Tophi may present with a chalky, usually painless irregular substance from the tips of fingers and toes as well as the joints themselves.

Also be aware of atypical gout presentations in patients taking cytotoxic drugs, immunocompromised patients with diabetes, those on dialysis, patients who have had an organ transplant and those who have high fructose ingestion. These all may influence the turnover of uric acid.

Hyperuricemia is defined as urate levels greater than 6. Levels of uric acid of greater than 6. The uric acid levels reflect a balance of dietary factor synthesis and excretion of uric acid. The uric acid concentration is caused either by decreased intravascular volume dehydration or truly increased total body uric acid levels. It is critical to remember that increased uric acid levels can result from increased uric acid production, decreased uric acid secretion or drugs that alter uric acid levels.

It is well known that the incidence of gout is higher in people with increased dietary intake of purines, particularly meat and seafood, as well as ingestion of beer and spirits, soft drinks and fructose. It must be clarified that coffee and tea can also increase uric acid levels and the presentation of gout.

Purine-rich fruits, vegetables and foods include oranges and citrus fruits, cranberries, tomatoes, pineapples, pomegranates, peanuts, beans, lentils, peas, spinach and asparagus. All of the aforementioned foods affect the balance between urate reabsorption and secretion, which is critically linked to the net uric acid elimination in the urine. One should diagnose patients on an acute presentation with aspiration and I strongly advise obtaining an analysis of the synovial fluid.

It is also important to use lab tests to assess the overall state of patient. This includes a complete metabolic panel, urinalysis, blood urea nitrogen, serum creatinine, C-reactive protein and erythrocyte sedimentation rate ESR.

With clinical judgment, additional tests may be advised, especially in light of other suspicions for metabolic involvement. Sometimes, even though there is an acute attack, the uric acid levels may not be above 6.

Consider obtaining repeat labs two to four weeks after the initial presentation. The treatment of gout is generally divided into two major phases of management: therapy for acute gouty attacks and chronic therapy for prophylaxis of these episodes. Treatment for an acute gout attack should begin as soon as possible. The choices of agent, appropriate dosage and duration of therapy are dependent on coexisting illnesses, clinical circumstances and the severity of the gout attack.

Therapeutic options for the management of acute gout include: nonsteroidal anti-inflammatory drugs NSAIDs ; low-dose colchicine; glucocorticoids; intraarticular or oral steroids; corticotropins; and interleukin-1 IL-1 inhibitors.

Rilonacept is a subcutaneous injection for the prevention of gout flares in patients during the initial months of therapy. The drug would be used in combination with the standard of care for uric acid lowering therapies. One may use a Medrol dose pak for six days or possibly prednisone 10 mg tapering of 10 mg BID for five days, 10 mg qd for five days and 5 mg for five days. It is generally recommended that NSAID dosages continue for five to seven days after an acute attack but gradually taper off.

Colchicine is highly effective when patients take it within the first 12 to 36 hours of the attack. It acts as an anti-inflammatory but not an analgesic. This drug has been utilized for decades in acute gout. The FDA removed intravenous colchicine for acute gout from the market in the U. High doses of colchicine may potentially lead to side effects, particularly troublesome diarrhea.

Colcrys is currently the only single-agent colchicine with FDA approval. Other FDA-approved colchicine formulations contain probenecid Benemid. Low doses of colchicine 0. This would be followed by a second dose of 0. The recommended prophylactic use for acute gout is 0. Colchicine is a tricyclic alkaloid. When the use of NSAIDs or colchicines is contraindicated, not properly tolerated or inappropriate for the patient, then one can give glucocorticoids or corticotropins orally or parenterally for acute gouty inflammation depending on the clinical presentation.

For single joint involvement, intraarticular aspiration followed by subsequent injection of a corticosteroid into the joint can be effective. This usually involves the use of a short tapering, oral, low-dose systemic corticosteroid such as prednisone or methylprednisolone, typically p. These include anakinra, canakinumab and rilonacept.

Therapy should begin immediately after the acute attack. Many suggest giving patients the option of initiating the next course of therapy because if they do not, they may risk another episode of an acute flare-up.

As mentioned previously, one should redo lab work two to four weeks after the acute episode. It is generally accepted that in patients with tophi or with two or more attacks in one year, one should initiate therapy for chronic gout.

The key in the urate lowering therapy is the reduction and maintenance of a serum uric acid level of less than 6. At this level, there is a decreased number of flares, less uric crystal accumulation in joints and dissolved tophi.

Allopurinol Zyloprim is a xanthine oxidase inhibitor and is most commonly used to reduce hyperuricemia regardless of its etiology. The dosing of allopurinol is individually based. Typically, the initial dose of allopurinol is mg but again, depending on the severity, mg 1 to 3 tabs p. Hypersensitivity syndrome and refractoriness to the drug 2 percent of patients on allopurinol have hypersensitivity syndrome or refractoriness could create an erythematous rash, hepatitis, eosinophilia, fever, declining renal function or even fatality.

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Copied to clipboard. Pertinent Pearls On Addressing Metabolic Issues Bear in mind that treating acute attacks does not treat the underlying disease. Emerging Modalities In Gout Treatment Recent research has produced two more drugs that will be helpful for managing chronic gout. The clinical examination was remarkable for marked swelling involving the left first MPJ.

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AMP Europe. Amputation Prevention Symposium. Cape Cod Symposium on Addictive Disorders. It most often affects the joint of the big toe. Gout attacks are caused by deposits of crystallized uric acid in the joint. Uric acid is present in the blood and eliminated in the urine, but in people who have gout, uric acid accumulates and crystallizes in the joints.

Uric acid is the result of the breakdown of purines, chemicals found naturally in our bodies and in food. Some people develop gout because their kidneys have difficulty eliminating normal amounts of uric acid, while others produce too much uric acid.

Gout occurs most commonly in the big toe because uric acid is sensitive to temperature changes. At cooler temperatures, uric acid turns into crystals. Since the toe is the part of the body that is farthest from the heart, it is also the coolest part of the body and, thus, the most likely target of gout.