Gout

Gout is the oldest recognized arthropathy. It was originally called podagra, from the Greek pous , meaning foot, and agra , meaning attack. In ancient history all arthritis was called gout. Today we know it to be a specific arthropathy secondary to deposition of monosodium urate crystals. It occurs in 0.3 percent of the population, and it accounts for 5 percent of all patients with arthritis. It is predominantly a disorder of males, occurring 20 times more frequently in males than in females. When it occurs in females, it is in the postmenopausal female.

There are two types of gout: (1) primary idiopathic gout due to an inborn error of metabolism, leading to the increase in uric acid in the blood; and (2) secondary gout associated with various diseases that cause increased production or decreased excretion of uric acid. Secondary gout does not usually produce radiographic changes.

Only 45 percent of patients with gout manifest radiographic bone changes, and then only 6 to 8 years after the initial attack. The radiographic changes indicate the chronicity of the disease process. Urate crystals deposit in tissues with poor blood supply, including cartilage, tendon sheaths, bursa, and so on. The radiographic presentation is dependent upon where the urate crystals are deposited. If they are deposited in cartilage, then the radiographic picture will be that of osteoarthritis; if they are deposited in soft tissue, then it will be that of chronic tophaceous gout. The hallmarks of osteoarthritis are discussed elsewhere. The radiographic features of chronic tophaceous gout are as follows:

1.

Tophi
2.

Normal mineralization
3.

Joint space preservation
4.

Punched-out erosions with sclerotic borders
5.

Overhanging edge of cortex
6.

Asymmetrical polyarticular distribution
7.

Distribution in feet, ankles, knees, hands, and elbows, in decreasing order of frequency

Because the radiographic features of chronic tophaceous gout are pathognomonic of the disease no matter what joint is involved, the features are discussed in greater detail before describing the distribution. It must be remembered that osteoarthritis developing secondary to urate crystal deposition in cartilage cannot be distinguished from osteoarthritis secondary to any other etiology. One must rely on the radiographic findings of tophaceous deposit.

Tophi are soft tissue masses created by the deposition of urate crystals ( Fig. 16-1 ). Urate crystals are not radiographically opaque. However, calcium may precipitate with the urate crystals to varying degrees, creating variation in the density of tophi ( Fig. 16-2 ). Tophi are usually found in the periarticular area along the extensor surface of bone; however, they may be intraarticular or not associated with the joint at all.

Tophi over an extended period of time erode the underlying bone. Because of the indolence of the process, the erosion produced usually has a sclerotic border. The erosion looks “punched out” and has frequently been described as a “mouse bite” ( Fig. 16-3 ). Often as the erosion is developing, the proximal edge of cortex is remodeled in an outward direction, creating an overhanging edge ( Fig. 16-4 ). This is seen in connection with 40 percent of the erosions identified. If the tophus is intraarticular and involves adjacent bones, then its extensor location and the indolence of the erosion allow preservation of the flexor portion of the joint space. Therefore on a radiograph, even when part of the joint is involved, the joint space appears to be preserved ( Fig. 16-5 ).

Urate crystals may deposit within the bone, producing an intraosseous tophus; the bone involved shows a lytic lesion, which may be expansile, with or without calcification ( Fig. 16-6 ). The calcified tophus within the bone should not be mistaken for an infarct or enchondroma. Gout does not cause infarction; it replaces marrow.

Intraosseous deposit may also cause such destruction as to be misdiagnosed as infection. Usually preservation of the white cortical line of the involved joint surface will distinguish gout from infection ( Fig. 16-7 ). Once the bone changes have occurred, they cannot be reversed; however, the urate crystals can disappear with treatment. Therefore, it is possible to see the bone changes of chronic tophaceous gout without the presence of the actual tophi ( Fig. 16-8 ).