Recognizing And Treating Lower Extremity Gout

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Author(s): 
Nicholas Romansky, DPM, FACFAS

   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.11 A podiatrist should be well aware of atypical presentations of gout that mimic other disorders such as rheumatoid arthritis, osteoarthritis, septic arthritis, myeloproliferative disorders, and lymphoproliferative disorders.

   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 6.8 mg/dL. Levels of uric acid of greater than 6.8 are considered to be above the saturated level, predisposing the patient to crystal formation/deposition. 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.12 It is lower in those with increased intake of coffee, dairy products and vitamin C (all lower uric levels). 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.13 The presence of yellow urate crystals, possible moderate amounts of white blood cells and negative cultures is truly the gold standard.

   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 6.8 mg/dL until two weeks after the attack has subsided. Consider obtaining repeat labs two to four weeks after the initial presentation.

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