Gout - Clinical Presentation and Diagnosis
Most patients will have elevated levels of uric acid in the blood for many years before having their first gout attack and do not need to be treated during this period. The solubility of uric acid in the serum is about 7 mg/dl. The risk of a gout attack increases with increasing uric acid levels but many patients will have attacks with "normal" levels of uric acid and some will never have an attack despite very high levels of uric acid.(ref 1)
| Serum uric acid level (mg/dl) | Incidence of gout |
| >9.0 | 7.0-8.9 |
| 7.0-8.9 | 0.5-0.37 |
| <7.0 | 0.1% |
An acute attack of gout is a highly inflammatory arthritis often with intense swelling, redness and warmth surrounding the joint. The inflammatory component is so intense, an acute attack of gout is often mistaken for a bacterial cellulitis. Even among other types of inflammatory arthritis, gout is considered the most painful with the patient unable to bear weight or put on a shoe over the affected joint and often prompting an off hour trip to the emergency room. Chills, a low grade fever and an elevated white blood cell count can occur, mimicking an infection. Characteristically, early gout attacks resolve spontaneously after 3 to 4 days. The first MTP joint (podagra) is the first joint affected in 50% of cases followed other lower extremity joints. Over 90% of patients who present with acute polyarticular gout have a history of podagra.
No presentation of gout would be complete without Thomas Sydenham's 1683 description of an acute gout attack. Dr. Sydenham was himself a sufferer of gout:
The victim goes to bed and sleeps in good health. About 2 o'clock in the morning, he is awakened by a severe pain in the great toe; more rarely in the heel, ankle or instep. This pain is like that of a dislocation, and yet the parts feel as if cold water were poured over them. Then follows chills and shiver and a little fever. The pain which at first moderate becomes more intense. With its intensity the chills and shivers increase. After a time this comes to a full height, accommodating itself to the bones and ligaments of the tarsus and metatarsus. Now it is a violent stretching and tearing of the ligaments-- now it is a gnawing pain and now a pressure and tightening. So exquisite and lively meanwhile is the feeling of the part affected, that it cannot bear the weight of bedclothes nor the jar of a person walking in the room.
Acute attack of gout at the ankle and 1st MTP joints.
An attempt should be made to document gout in the affected joint by aspiration and examination for crystals, particularly in a large joint that is easily accessible. Infection needs to be ruled out in an acute monoarthritis. Joint fluid from gouty joints are highly inflammatory and can often have >50,000 WBC/cu mm, predominantly polys. The definitive finding is a needle shaped negatively birefringent crystal (yellow when parallel to the axis of polarization). Intracellular crystals within a neutrophil are characteristic during the acute attack. Fluid should be sent to the lab in a green top and purple top tubes to facilitate the joint count and crystal exam. Crystals may be present in the joint several days after the acute attack of gout resolves.
Intracellular uric acid crystal under polarized light (top), non-polarized light (bottom).
After years of gouty attacks, patients will develop a chronic arthritis resulting in bone and cartilage destruction and deformity. Uric acid crystals deposit within and surrounding the joint causing a chronic destructive inflammatory process. X-rays characteristically show well demarcated "punched out" erosions.
X-ray showing soft tissue swelling and erosion of 2nd PIP.
Tophi or deposits of uric acid crystals are often found around joints, in the olecranon bursa or at the pinna of the ear.
Tophi at helix of ear.
Large tophaceous deposits surrounding joints.
This phase of gout is different than the highly inflammatory, self-limited presentation of the acute gouty flare. Chronic gout is often confused with other forms of chronic inflammatory arthritis such as rheumatoid arthritis and is associated with chronic pain and joint swelling resulting in bone and cartilage destruction. Evidence of tophi or a chronic arthritis is a clear indication for the initiation of uric acid lowering therapy.
1. Campion EW, Glynn RJ, deLabry LO. Asymptomatic Hyperuricemia Risks and Consequences. Am J Med 82:421, 1987.
2. Groft GD, Franck WA, Raddarz DA. Systemic Steroid Therapy for Acute Gout: A clinical trial and review of the literature. Semin Arthritis Rheum 19:329, 1990.
3. Roberts WN, Liang MH, Stein SH. Colchicine in Acute Gout Reassessment of Risks and Benefits. JAMA 257:1920, 1987.
4. Wallace SL, Singer JZ. Review: Systemic Toxicity Associated with Intravenous Administration of Colchicine--Guidelines for Use. J Rheumatol 15:495, 1988.
5. Gutman AB. Gout. Textbook of Medicine. 12th ed., Beeson PB and McDermott W (eds), Philadelphia: W. B. Saunders, 1958, p 595.
6. Paulus HE, Schlosstein LH, godfrey RL, et al. Prophylactic Colchicine Therapy of Intercritical Gout. A placebo-controlled study of probenecid-treated patients. Arthritis Rheum 17:609, 1987.
7. Kelly WN, Wortmann RL. Gout and Hyperuricemia. Textbook of Rheumatology. 5th ed., Kelly WN, Harris ED Jr., Ruddy S, Sledge CB (eds), Philadelphia: W. B. Saunders, 1997, p 1313-1347.
8. Emmerson BT. The Management of Gout. N Engl J Med 344:445, 1996.
9. Halz-LeBlanc BAE, Reynolds WJ, MacFadden DK. Allopurinol Hypersensitivity in a Patient with Chronic Tophaceous Gout: Success of intravenous desensitization after failure of oral desensitization. Arthritis Rheum 34:1329, 1991.