Recognizing And Treating Lower Extremity Gout

Author(s): 
Nicholas Romansky, DPM, FACFAS

Given the increased prevalence of gout and how gout affects the lower extremity, the author discusses current concepts in diagnosis and treatment, and provides an
illuminating case study.

Gout is an inflammatory arthritis that results from hyperuricemia, from either the body’s overproduction or underexcretion of uric acid. It typically presents with acute onset, can be recurrent and the vast majority is monoarticular in presentation. The first metatarsophalangeal joint (MPJ) is involved in 90 percent of individuals with gout. Gout can result in joint deterioration and destruction.

   For the last two years, gout has been much more recognizable to the public in print, TV and other forms of media. The painful condition of gout is now more appreciated as the number of gout medications, formulations and reformulations has changed the landscape for the public and patient base, and thus changed the management by physicians.

   The formation of crystals that accumulate within a joint triggers gout. It is well known that just because patients have hyperuricemia, it does not mean they have gout. The actual number of true gout cases is likely underestimated. Many times, patients and physicians treat this with OTC analgesics or anti-inflammatories without the proper diagnosis and workup for gout.Hyperuricemia is the cause of gout. According to Chen and Schumacher, there is an increasing prevalence with significant comorbidities including cardiovascular disease, hypertension, renal insufficiency and metabolic syndrome.1

   At a recent Podiatry Institute meeting in August of 2011, researchers stated that gout affects approximately 5 to 6 million people in the United States with prevalence on the rise.2 Gout reportedly occurs more in men than women, affecting 2 percent of men older than 30 years of age. Risk factors for gout have been well documented in the medical literature. Risk factors include being male, postmenopausal, a strong family history, kidney disease, organ transplants, excessive alcohol use, a diet high in purines (red meat and seafood), metabolic syndrome, obesity, dehydration and exercise.

   Studies have shown that heavy alcohol use in general, particularly beer, increased the incidence of gout whereas moderate use of red wine did not.3 The growing public awareness and public presentation of gout in the last 10 years — with a two- to threefold increase in the incidence of gout — parallels the increases in obesity and metabolic syndrome.4

A Guide To The Stages Of Gout

Gout can be divided into three stages: acute gout, intercritical gout and chronic gout.
Acute gout can occur as a primary non-systemic episode or can be secondary to other systemic issues including kidney failure, myocardial infarction or cerebrovascular accident.

   Intercritical gout is typically the asymptomatic period between acute attacks of gouty inflammation. The disease may progress even though it is clinically silent. During this period, tophi may develop as the body stores of uric acid accumulate. Generally, acute gout attacks are infrequent and intercritical periods are long in duration. However, when the disease progresses, acute flare-ups may increase in frequency and intercritical periods may actually shorten.

   Chronic gout is characterized by the chronic deterioration and destruction of joints, which include bony erosions and the development of tophi. It is at this stage that acute gout may become polyarticular, occur more proximal than the foot and ankle, and are significantly more painful. These attacks usually last longer and are more severe in nature. They include the carpal tunnel and tarsal tunnel regions, spine, eye involvement, pancreatic involvement, solitary breast nodules or may be cardiac in nature with endocarditis.

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