Osteoarthritis is usually evidenced by joint space narrowing on x-ray.42
Bacterial cellulitis will present similarly to gout, but the erythema of bacterial cellulitis will more likely extend beyond the involved joint.16
Sarcoid arthropathy often presents as a polyarthritis, as in advanced gouty arthritis. However, in sarcoid arthropathy, serum calcium and angiotensin-converting enzyme will likely be elevated.43 Synovial or tendon sheath biopsy will show non-caseating granulomas, which are the hallmark for sarcoid disease. Additionally, joint fluid analysis will demonstrate a predominance of mononuclear or polymorphonuclear cells.43
Diagnostic Tests
Diagnostic tests to consider are analysis and culture of the synovial fluid, complete blood count (CBC), blood urea nitrogen (BUN), creatinine, radiography, ultrasonography, serum uric acid, and blood culture if septic arthritis is suspected.28 While serum urate levels may be normal during an acute gout attack, measurement may still be helpful for comparison, since elevation is a likely finding two weeks after an attack—if the patient was, in fact, experiencing an acute gout attack.42
Since renal dialysis increases the risk for gout, pseudogout, and septic arthritis, synovial fluid analysis is essential in patients undergoing renal dialysis.42
Various imaging techniques may aid in confirming a diagnosis of gout and monitoring its progression, but further studies are needed to more clearly define the role of these techniques in management of gout.45 Plain radiographic evidence of asymmetric swelling in a joint (one of the ACR/ARA preliminary criteria34) was shown to have a 60% positive predictive value for a diagnosis of gout.39 Late in the disease process, an affected joint may be affected by characteristic “punched out” intra-articular lesions, with a normal amount of joint space.45
Ultrasound is a safe and inexpensive test that can reveal soft tissue edema and increased vascularity during an acute gout attack. Chronic changes include the double contour sign and tophus-like lesions surrounded by a thin, anechoic rim.45
CT will also show tophi and bony erosion. While CT is more specific than other techniques, it is also more expensive and exposes the patient to increased radiation. MRI can help monitor the complications of gout, especially entrapment neuropathies.45
TREATMENT/MANAGEMENT
According to current evidence, treatment is not indicated for asymptomatic hyperuricemia.16
Acute Gout Management
Pharmacologic treatments available for an acute gout attack include NSAIDs, colchicine, and local or systemic corticosteroids.24,46 At the onset of an attack, patients should start high-dose NSAID therapy, and continue for two to three days after symptoms are resolved.6 Oral indomethacin (50 mg tid) or oral ibuprofen (800 mg tid) are both reasonable options.6 It may be prudent to consider a proton pump inhibitor (eg, omeprazole) to protect the gastric mucosa in patients who are susceptible to gastrointestinal problems.27
In addition to high-dose NSAID therapy, adding colchicine (1.2 mg by mouth at onset of symptoms, followed by 0.6 mg one hour later) has proven to be effective in relieving the symptoms of gout, but its serious gastrointestinal adverse effects, particularly diarrhea, must be considered.6,47
In patients with monoarticular gout who cannot tolerate NSAIDs, intra-articular aspiration and corticosteroid injections may provide relief.
Long-acting triamcinolone, administered by intra-articular injection, has been found to relieve pain and inflammation in patients with gout. Septic arthritis must be ruled out by way of joint aspiration and culture before injection of corticosteroids.47
Oral or IM-administered corticosteroids may be considered for patients with polyarticular involvement. Prednisone (60 mg/d, tapered over 10 days) is an appropriate option for outpatients or inpatients; methylprednisone (80 to 120 mg IM) may be suitable for inpatients.6 Again, septic arthritis must be ruled out before corticosteroids are administered.47
For the patient who is currently taking a thiazide diuretic for hypertension, substituting a different medication may be warranted; the angiotensin receptor blocker losartan, for example, has uricosuric action.27,29,47 Nonpharmacologic strategies, such as rest, ice, elevation, and avoiding trauma to the affected joint, are also recommended.27
Of note, allopurinol therapy should be neither initiated nor discontinued during an acute gout attack.27
Management of Chronic and Intercritical Gout
Urate-lowering therapy, such as allopurinol (50 to 300 mg/d29), should be considered for patients who experience frequent attacks (ie, three or more per year), patients with chronic tophi, patients with radiographically demonstrated joint damage,47 or patients with a documented state of uric acid overproduction.29
Allopurinol dosage should be adjusted based on creatinine clearance; dosing as high as 800 mg/d has been recommended in patients with normal renal function.2 Again, allopurinol should never be started or discontinued during an acute attack,27 because abrupt fluctuations in uric acid levels may heighten the inflammation. The target serum urate level is 6.0 mg/dL.29