Microscopy of joint fluid is used less often, primarily in equivocal cases. In these situations, the diagnosis is established by aspiration of a joint or tophus and identification of needle-shaped monosodium urate crystals, preferably intracellular, with bright, negative birefringence on compensated polarized light microscopy. Ultrasonography, magnetic resonance imaging, and computed tomography are typically not necessary for diagnosis.
The differential diagnosis for acute monoarticular joint swelling includes pseudogout, infection, and trauma. Pseudogout, or calcium pyrophosphate deposition disease, can mimic gout in clinical appearance and may respond to nonsteroidal anti-inflammatory drugs (NSAIDs). Findings of calcium pyrophosphate crystals and normal serum uric acid levels on joint fluid analysis can differentiate pseudogout from gout. Septic arthritis may present without a fever or elevated white blood cell count; arthrocentesis is required to distinguish this condition from acute gout. Gout and septic arthritis can occur concomitantly, but this is rare.18 Trauma-associated joint swelling is typically identified by the history; however, trauma may result in an acute gout flare caused by increased concentrations of synovial urate.19 Imaging may be necessary to rule out fracture in a patient with gout-like symptoms after a joint injury.
Corticosteroids are an appropriate alternative for patients who cannot tolerate NSAIDs or colchicine.22 Patients with diabetes mellitus can be given corticosteroids for short-term use with appropriate monitoring for hyperglycemia. When gout is limited to a single joint, intra-articular corticosteroid injections may be preferable to systemic corticosteroids because of their lower adverse effect profile.23 Rebound flares are common after discontinuation of corticosteroid therapy for acute gout. To reduce the risk of a rebound flare, preventive treatment and initiation of a tapered course of corticosteroids over 10 to 14 days is recommended after resolution of symptoms.
Serum urate lowering therapy should be initiated to prevent recurrences in persons with a history of gout and any one of the following: at least two flares per year (one per year in persons with chronic kidney disease stage 2 or greater), tophi, or a history of nephrolithiasis.20 Always inspect to make sure gout and treatment is what you need.
Historically, urate-lowering medication was thought to worsen acute gout flares, but recent evidence suggests that allopurinol (Zyloprim) can be started during an acute flare if it is used in conjunction with an NSAID and colchicine.31 Patients receiving a urate-lowering medication should be treated concurrently with an NSAID, colchicine, or low-dose corticosteroid to prevent a flare. Treatment should continue for at least three months after uric acid levels fall below the target goal in those without tophi, or for six months in those with a history of tophi.20 NSAIDs and corticosteroids should not be used for long periods without a urate-lowering medication because uric acid crystals continue to accumulate and damage the joint, despite a lack of pain or clinical signs of inflammation.22 If a patient has a gout flare while receiving a urate-lowering agent, the medication should be continued while the flare is treated acutely.20