Diagnostic Radiology/Musculoskeletal Imaging/Joint Disorders/Gout

Gout is a form of peripheral arthritis resulting from the deposition of monosodium urate crystals secondary to hyperuricemia.

Prevalence in the United States: 1.6 to 13.6 per 1000. Typically occurs in middle aged or elderly males (90% of cases are in males). It is particularly rare in premonpausal women. Caucasians populations are more affected than those of African heritage. Interestingly, gout is relatively frequent in young male Polynesians.

Hyperuricemia and gout are often associated with hypertension, obesity, hyperlipidemia, atherosclerosis, and ethanol abuse.

While all gout patients have a high serum uric acid concentration at some point in their disease progression, most hyperuricemic individuals never show clinical signs of urate crystal deposition.

Pathophysiology

 * Uric acid under excretion (90% of cases)
 * Primary: Idiopathic reduced renal excretion
 * Secondary:
 * Chronic renal failure
 * Thiazide use
 * Alcohol
 * Hyper or hypoparathyroidism
 * Uric acid overproduction (10% of cases)
 * Primary: Enzyme defect in purine synthesis
 * Secondary:
 * Increased turnover of nucleic acids
 * Myeloproliferative and lymphoproliferative disorders
 * Hemolytic anemia
 * Chemotherapy
 * Alcohol

Clinical Presentation
The natural history of progressive urate crystal deposition manifests as three classic stages.
 * 1) Acute gouty arthritis: 80% of attacks involve and single joint with severe pain, redness, and swelling.
 * 2) Intercritical gout: These are asymptomatic intervals between acute attacks most common early in disease progression. This pattern is quite uncommon in other arthritic disorders and alone is very suggestive of gout.
 * 3) Chronic tophaceous gout: Collections of solid urate in connective tissues, which may be calcified.

Attacks may occur for 4–6 years before radiographic evidence.

Location

 * Lower extremity > upper extremity
 * Small joints > large joints
 * Random distribution in hands (helpful diagnostic distinction)
 * First MTP most common (podagra)

Characteristics

 * Marginal, pararticular or intra-articular erosions which may have overhanging edges
 * Well-defined erosions that may have a sclerotic border
 * Joint space preserved (unless very advanced)
 * Not usually associated with osteoporosis
 * Soft tissue and bursa deposition - tophi
 * MRI - Tophus has low intensity on T1 and variable low to high intensity on T2 depending on the amount of amorphous calcification.
 * CT - Tophi have density similar to soft tissue.

Misc. Points

 * Erosions and tophi usually only with longstanding disease
 * 40% of patients have concomitant CPPD
 * Can have many different appearances, but is quite common so always keep in mind.

Images


Fig. 1 Shows classic location at first MTP and small erosion with "overhanging" edge. Notice that the joint space and bone density are preserved.

Fig. 2 Another appearance showing multiple erosion locations including first MTP, base of third and fourth metacarpals, and possibly the head of the fifth metacarpal and second proximal phalanx.



Fig. 3 Advanced gout resulting in joint destruction from large erosions in first, fourth and fifth rays. Notice the large "overhanging" edges.



Fig. 4 Example showing tophaceous gout of fifth MTP joint.



Fig. 5 If you didn't appreciate the tophi on the last example, certainly you will here. Notice calcification of the tophus on the ulnar side of fifth MCP joint.



Fig. 6 Patient with known gout. This example shows chondrocalcinosis of the triangular fibrocartilage. 40% of gout patients have concomitant CPPD. Also notice erosion of the head of the 5th proximal phalanx.



Fig. 7 Tophaceous gout of the 1st MTP. Notice the tophi have a density similar to soft tissue and are both inside and surrounding the bone. Also note the cortical destruction of the proximal phalanx and the head of the metacarpal.

Treatment
First line is to control associated disorders such as hypertension, obesity, hyperlipidemia, atherosclerosis, and ethanol abuse.

Acute Attack

 * Goal is to quickly alleviate pain.
 * Anti-inflammatory therapy with NSAIDs, colchicine, or Cox-2 inhibitors.
 * Should resolve symptoms in hours to days.

Prophylactic

 * Goal is to prevent acute attacks.
 * Indomethacin or colchicine.
 * In patients without evident tophi, prophylaxis can be safely discontinued 6 to 12 months after serum urate levels have normalized.

Antihyperuricemic therapy

 * Goal is a serum urate concentration of 5 to 6 mg/dL which is below that at which monosodium urate is saturating in extracellular fluids.
 * Uricosuric drugs and allopurinol can be used to lower the serum urate concentration.

Surgery
Surgery is typically only indicated to treat the complications of tophaceous disease, which include infection, compression due to the mass effect of a tophus, joint deformity, and intractable pain. Tophaceous deposits may compress nerves or erode through the skin resulting in chronic ulcers which often lead to infection.