Uric Acid Crystals. (Photo contributor: Michael Bezzerides, MS4.)
Gout is the most common form of inflammatory arthritis in the United States. Its incidence has been rising significantly over recent years. This has been at least partially attributed to an increasing prevalence of obesity. The disease is caused by deposition of monosodium urate in joints and periarticular structures. This process is typically asymptomatic but does set the patient up for acute flares of inflammatory arthritis.
An acute gout flare is characterized by rapid-onset pain, redness, and swelling in the affected joint area. The acute attack often starts at night or during the early morning hours. The signs of inflammation can extend well beyond the primarily involved site. This “pseudo-cellulitis” can cause diagnostic confusion because it may be difficult to distinguish from a soft-tissue infection.
While the 1st metatarsophalangeal (MTP) joint is the 1st joint affected in most patients, gout can involve any joint or periarticular structure. This is particularly true for recurrent gout. Polyarticular gout flares are more frequently seen in patients with long-standing and poorly controlled disease.
When a patient with acute inflammatory arthritis presents to the emergency department (ED), several factors should raise suspicion that the patient may be affected by a gout attack. These include a history of prior gout flares, renal failure, use of medications that impair uric acid excretion such as thiazide diuretics, and location in the 1st MTP joint. Importantly, gout can coexist with other types of inflammatory joint diseases such as septic arthritis. Therefore, even in the patient with an established history of gout, the possibility of an alternative process needs to be assessed.
Gout—Acute Flare. Recurrent first metatarsophalangeal joint redness, swelling, pain, and tenderness consistent with an acute gout flare. (Photo contributor: Lawrence B. Stack, MD.)
Management and Disposition
The majority of patients with a suspected gout flare will require a joint aspiration. Testing of the synovial fluid should include a cell count with differential, Gram stain and culture, and crystal analysis (polarizing microscopy).
The synovial fluid or white blood cell count in patients with an acute gout flare is usually in the 10,000 to 100,000 cells/µL range. Importantly, this range overlaps with the cell counts typically seen in septic arthritis. Therefore, the white blood cell count in joint fluid does not allow separation of these two conditions.
The demonstration of intracellular urate crystals does confirm a diagnosis of gout. However, it does not exclude a 2nd overlapping process such as septic arthritis. Therefore, select patients who are at high risk for infection should be admitted and empirically treated for septic arthritis even if crystals are present.