All About Gout for Primary Care: The Diagnosis

The diagnosis of gout is based on clinical data, laboratory evaluation, and imaging. Crystal examination is the “gold standard.” Recent clinical classification criteria for gout in the absence of crystal visualization have a sensitivity of 0.92 and specificity of 0.89.¹

[[{"type":"media","view_mode":"media_crop","fid":"57821","attributes":{"alt":"","class":"media-image media-image-right","id":"media_crop_8049292642329","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"7295","media_crop_rotate":"0","media_crop_scale_h":"0","media_crop_scale_w":"0","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"height: 162px; width: 220px; float: right;","title":"","typeof":"foaf:Image"}}]]The elements of crystal examination

The gold standard in gouty arthropathy diagnosis is microscopic visualization of negatively birefringent, needle-shaped monosodium urate (MSU) crystals, usually engulfed by neutrophils and macrophages, from an aspirated joint or tophus.^2,3 MSU crystals may be identified in synovial fluid obtained from asymptomatic joints.^3,4 Acute gouty arthritis may occasionally coexist with another joint disease, such as septic arthritis or pseudogout. Therefore, in most circumstances, arthrocentesis should be performed and the sample should be sent for crystals, cell count, and culture.

High and low uric acid levels

High serum urate levels obtained during an acute attack support a diagnosis of gout. However, serum urate levels may be paradoxically low during an acute attack and typically are highest about 2 weeks after the attack.⁵

Chronic hyperuricemia is the most important risk factor for gout.² Uric acid values > 6.8 mg/dL can promote attacks because this is the limit of solubility of uric acid in the serum.⁶ However, there are patients with asymptomatic hyperuricemia in whom gout never develops.

Next: Hallmarks of an acute gout attack

Distinguishing acute gouty arthritis

A thorough history may help distinguish an acute gout attack from other causes of acute arthritis. Hallmarks of an acute gout attack include the following³:

• Episodes of monoarticular arthritis followed by intercritical periods completely free of symptoms

• Maximum inflammation within 12 to 24 hours after the onset of the attack

• Rapid resolution of synovitis after anti-inflammatory therapy

• A unilateral first metatarsophalangeal (MTP) joint attack (first presentation in about 50% of patients with gout and eventually 90% will have first MTP involvement)

• Erythema, warmth, and swelling

• Pain in the affected region with even light touch.

Nighttime or early morning episodes

Episodes of acute gouty arthritis often begin at night or in the early morning with rapidly escalating pain and swelling. The joint quickly becomes warm, red, and tender, potentially mimicking cellulitis or a septic joint.

The first acute attack affects the first MTP joint (known as podagra) about 50% of the time, but tarsal joints, ankles, knees, elbows, and interphalangeal joints are all frequently affected. Although it is not common, gout can affect the shoulders, hips, and spine.⁷

Untreated acute gout usually resolves in 7 to 10 days.⁸ Most patients have a second attack 6 months to 2 years later. Subsequent attacks frequently last longer than the initial attack and are more likely to affect proximal joints or be polyarticular.⁹

Chronic gouty arthritis may follow

When left untreated, acute attacks of gout can lead to chronic gout, which is characterized by chronic destructive polyarticular involvement with low-grade joint inflammation and joint deformity. Tophaceous gout (tophi are uric acid deposits frequently seen in bursa or joints) develops within 5 years of onset of gout in 30% of untreated patients.¹⁰

Next: Imaging options

Imaging options for acute gout

The following are imaging options for the diagnosis of acute gout:[[{"type":"media","view_mode":"media_crop","fid":"57757","attributes":{"alt":"","class":"media-image media-image-right","id":"media_crop_2346225760023","media_crop_h":"0","media_crop_image_style":"-1","media_crop_instance":"7283","media_crop_rotate":"0","media_crop_scale_h":"0","media_crop_scale_w":"0","media_crop_w":"0","media_crop_x":"0","media_crop_y":"0","style":"float: right; border-width: 0px; border-style: solid; margin: 5px; height: 440px; width: 240px;","title":" ","typeof":"foaf:Image"}}]]

• Radiographs are generally not useful for diagnosis of acute gout, but they may show evidence of chronic disease, classically described as “rat bite” or “punched out” erosions.

In the accompanying figure, note the periarticular rat bite erosions (arrows) of the 1st and 5th MTP joints and the radiopaque tophus (arrowhead) over and adjacent to the 5th MTP joint. The periarticular punched out erosions occur along the long axis of the bone with overhanging edges and sclerotic rims. The joint space is very well preserved until late in the course of disease.

• Musculoskeletal ultrasonography has the capacity to visualize intra-articular crystal deposits with a characteristic “double contour sign,” hyperechoic enhancement of the outer surface of the hyaline cartilage.

• Computed tomography (CT), particularly dual energy CT, and MRI also may be useful in confirming erosions and tophi.¹¹

Next in this Special Report: Management of an acute gout attack and pharmacological interventions for acute gout.

References:

1. Neogi T, Jansen TL, Dalbeth N, et al. 2015 Gout classification criteria: an American College of Rheumatology/European League Against Rheumatism collaborative initiative. Ann Rheum Dis. 2015;74:1789-1798.

2. Zhang W, Doherty M, Pascual E, et al. EULAR evidence based recommendations for gout, part I: Diagnosis. Report of a task force of the Standing Committee for International Clinical Studies Including Therapeutics (ESCISIT). Ann Rheum Dis. 2006;65:1301-1311.

3. Pascual E, Doherty M. Aspiration of normal or asymptomatic pathological joints for diagnosis and research: indications, technique and success rate. Ann Rheum Dis. 2009;68:3-7.

4. Pascual E. Persistence of monosodium urate crystals and low-grade inflammation in the synovial fluid of patients with untreated gout. Arthritis Rheum. 1991;34:141-145.

5. Singh G, Triadafilopoulos G. Appropriate choice of proton pump inhibitor therapy in the prevention and management of NSAID-related gastrointestinal damage. Int J Clin Pract. 2005;59:1210-1217.

6. Perez-Ruiz F, Liote F. Lowering serum uric acid levels: what is the optimal target for improving clinical outcomes in gout? Arthritis Rheum. 2007;57:1324-1328.

7. Choi H. Epidemiology of crystal arthropathy. Rheum Dis Clin North Am. 2006;32:255-273, v.

8. Fisher MC, Pillinger MH, Keenan RT. Inpatient gout: a review. Curr Rheumatol Rep. 2014;16:458.

9. Liebman SE, Taylor JG, Bushinsky DA. Uric acid nephrolithiasis. Curr Rheumatol Rep. 2007;9:251-257.

10. Schumacher HR Jr, Becker MA, Palo WA, et al. Tophaceous gout: quantitative evaluation by direct physical measurement. J Rheumatol. 2005;32:2368-2372.

11. Dalbeth N, Clark B, Gregory K, et al. Computed tomography measurement of tophus volume: comparison with physical measurement. Arthritis Rheum. 2007;57:461-465.