Gout is a crystal arthropathy due to deposition of monosodium urate crystals in and around the joints.
Typically occurs in those above 40 years. There is a strong male predilection of 20:1.
Acute gouty arthritis presents with a monoarticular red, inflamed, swollen joint, typically in the lower limb and classically affecting the first metatarsophalangeal joint ('podagra') 12. It often manifests during sleep, and can later involve more than one joint to become an oligoarthropathy or rarely, a polyarthropathy 12.
Once the acute phase is over, usually within 7-10 days, there is an intercritical asymptomatic period ('intercritical gout') between acute flares 12. This asymptomatic period is unique to crystal arthopathies and varies in length between patients, but often lasts months 12.
Patients with chronic uncontrolled hyperuricaemia, such as those with chronic kidney disease, may develop chronic tophaceous gout. In chronic tophaceous gout, there are solid urate crystal collections (‘tophi’) and chronic inflammatory and destructive changes in surrounding connective tissue 12. These tophi are typically yellow-white in colour, non-tender, and are typically located on the articular structures, bursae, or the ears 12.
Characterised by monosodium urate crystals deposition in periarticular soft tissues. The crystals are needle-shaped and are strongly birefringent in plane polarised light 10. The synovial fluid is generally a poor solvent for monosodium urate and therefore causes crystallisation at low temperatures. The crystals are chemotactic and activate complement.
There are five recognised stages of gout:
- asymptomatic hyperuricaemia
- acute gouty arthritis
- intercritical gout (between acute attacks)
- chronic tophaceous gout
- gouty nephropathy
The primary risk factor is hyperuricaemia, although only a small proportion of patients with hyperuricemia develop gout, often taking 20-30 years to develop. The two mechanisms by which hyperuricaemia can develop are either under-secretion of uric acid by the kidneys (most common) or overproduction of uric acid (only 10% of cases).
- under-secretion by kidneys:
Usually, has an asymmetrical polyarticular distribution:
- joints: 1st MTP joint most common (known as 'podagra' when it involves this joint); hands and feet are also common
- less common: bones, tendon, bursa
Most radiographic findings include the skeletal system.
Characteristic radiologic changes occur in the chronic stage, though not all patients progress to this. There is a predilection for the small joints of the hands and feet. Chondrocalcinosis is present in ~5%.
- joint effusion (earliest sign)
- preservation of joint space until late stages of the disease
- an absence of periarticular osteopenia
- eccentric erosions
- the typical appearance is the presence of well-defined “punched-out” erosions with sclerotic margins in a marginal and juxta-articular distribution, with overhanging edges (see case 12) also known as rat bite erosions
- punched-out lytic bone lesions
- overhanging sclerotic margins
- mineralisation is normal
Surrounding soft tissues
- tophi: pathognomonic
- olecranon and prepatellar bursitis
- periarticular soft tissue swelling due to crystal deposition in tophi around the joints is common
- the soft tissue swelling may be hyperdense due to the crystals, and the tophi can calcify (uncommon in the absence of renal disease)
While there can be variation in appearance, tophi tend to be hyperechoic, heterogeneous, have poorly defined contours. They can be multiple grouped and surrounded by anechoic halos 8.
Findings generally reflect those on the plain radiograph.
Dual-energy CT can distinguish between urate mineralisation and calcification, which may be useful for cases where the clinical and biochemical presentation is atypical 11.
Signal characteristics of gouty tophi are usually:
- T1: isointense
- variable 4
- the majority of lesions are characteristically heterogeneously hypointense
- T1 C+ (Gd): tophus often enhances
Treatment and prognosis
Acutely, gout can be managed with non-steroidal anti-inflammatory drugs (e.g. naproxen), colchcine, prednisolone, or newer cytokine blocking agents (e.g. IL-1 blockers such as anakinra or canakinumab) if refractory disease 12. In the long-term, xanthine oxidase inhibitors (e.g. allopurinol or feboxustat), uricosuric drugs (e.g. probenecid), or uricase agents (e.g. pegloticase) may be used to reduce urate levels and prevent further acute flares 12. Tophaceous gout can also be managed with surgical excision of symptomatic lesions 12.
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- 8. de Ávila Fernandes E, Kubota ES, Sandim GB et-al. Ultrasound features of tophi in chronic tophaceous gout. Skeletal Radiol. 2011;40 (3): 309-15. doi:10.1007/s00256-010-1008-z - Pubmed citation
- 9. Chowalloor PV, Siew TK, Keen HI. Imaging in gout: A review of the recent developments. Ther Adv Musculoskelet Dis. 2014;6 (4): 131-43. doi:10.1177/1759720X14542960 - Free text at pubmed - Pubmed citation
- 10. Ivorra J, Rosas J, Pascual E. Most calcium pyrophosphate crystals appear as non-birefringent. Ann. Rheum. Dis. 1999;58 (9): 582-4. doi:10.1136/ard.58.9.582 - Free text at pubmed - Pubmed citation
- 11. Desai MA, Peterson JJ, Garner HW, Kransdorf MJ. Clinical utility of dual-energy CT for evaluation of tophaceous gout. Radiographics : a review publication of the Radiological Society of North America, Inc. 31 (5): 1365-75; discussion 1376-7. doi:10.1148/rg.315115510 - Pubmed
- 12. Neogi T. Clinical practice. Gout. (2011) The New England journal of medicine. 364 (5): 443-52. doi:10.1056/NEJMcp1001124 - Pubmed
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