The most common form of inflammatory arthritis, reported to be 3.9% of the population. Men are three to four times more likely to be diagnosed with gout. Incidence increases with age, BMI, alcohol consumption, hypertension, and diuretic use. Another risk factor is the consumption of fructose-rich beverages. Gout increases the risk for cardiovascular disease.
Pathophysiology
Gout is caused by hyperuricemia. Uric acid is a by-product of purine metabolism. Purines are basic chemical compounds found in high concentrations in meat products. Urate levels are affected by diet, medications, overproduction in the body, and inadequate excretion by the kidneys.
- Hyperuricemia (greater than 6.8 mg/dL) may lead to urate crystal deposition.
- The initial cause for the gout attack occurs when macrophages in the joint space phagocytize urate crystals. After various immunologic steps, inflammation occurs. This process is increased with free fatty acid concentrations, which by themselves can trigger gout attacks.
- With repeated attacks, accumulations of sodium urate crystals (tophi) are deposited in peripheral areas of the body such as the great toe, hands, and the ear. Renal uratelithiasis, a type of kidney stone, with chronic kidney disease secondary to urate deposition, may develop.
Primary hyperuricemia may be caused by severe dieting or starvation, excessive intake of foods that are high in purines (shellfish, organ meats), or heredity. In secondary hyperuricemia, gout is a clinical feature secondary to any number of genetic or acquired processes, including conditions in which there is an increase in cell turnover and an increase in cell breakdown. Altered renal tubular function can also contribute to underexcretion of uric acid.
Clinical Manifestations
Acute gouty arthritis (recurrent attacks of severe articular and periarticular inflammation), tophi (crystalline deposition in periarticular tissues), gouty nephropathy (renal impairment), and uric acid renal calciuli. There are four stages of gout:
- Asymptomatic hyperuricemia
- Acute gouty arthritis: most common early clinical manifestation. The metatarsophalangeal joint of the big toe is a commonly affected joint. The tarsal area, ankle, or knee may also be affected. The same structures for the upper extremities may also be affected, but it less common. This attack may be triggered by trauma, alcohol ingestion, dieting, medications, surgical stress, or illness. Abrupt onset often occurs at night, awakening the patient with severe pain, redness, swelling, and warmth of the affected joint. Early attacks spontaneously subside over 3 to 10 days without treatment.
- Intercritical gout: a symptom-free symptom until the next attack, which may not occur for months to years. Over time, attacks become more frequent, involves more joints, and lasts longer.
- Chronic tophaceous gout: tophi are associated with more frequent and severe inflammatory episodes. Worse hyperuricemia produce more extensive tophus formation. They most commonly form in the synovium, aolecranon bursa, subchondral bone, infrapatellar and Achilles tendons, and subcutaneous tissue on the extensor surface of the forearms and overlying joints. They have also been found in the aortic walls, heart vales, nasal and ear cartilage, eyelids, cornea, and sclera. Joint enlargement may cause a loss of joint motion. uric acid deposits may cause renal and kidney damage.
Medical Management
A definitive diagnosis of gouty arthritis is established by polarized light microscopy of the synovial fluid of the involved joint. Uric acid crystals are seen within the polymorphonuclear leukocytes in the fluid during a disease flare up.
- Acute attacks are managed with Colchicine (oral or parenteral), an NSAID (Indomethacin), or a corticosteroid.
- Administered as soon as an attack begins. Dosage is increased until pain is relieved or diarrhea develops, then medication is stopped. When used chronically, GI upset occurs in most patients.
- Hyperuricemia, tophi, joint destruction, and renal disorders are managed after the acute inflammatory process has subsided. Uric acid lowering therapies should be considered. Xanthine oxidase inhibitors such as allopurinol and febuxostat are agents of choice.
- Management during intracritical gout (stage 3) includes lifestyle changes such as avoiding purine-rich foods, weight loss, decreasing alcohol consumption, and avoiding certain medications. Uricosuric agents (probenecid) may be indicated in patients with frequent acute attacks, as they decrease uric acid levels and dissolve deposited urate.
- Corticosteroids may be used for patients who do not respond to other therapies.
- Pegloticase has been shown to be effective in patients whose refractory chronic gout are not controlled with previous therapies.
Nursing Management
Ensure adequate patient knowledge. Use written and verbal materials for education. Severe dietary restriction is not necessary, but the nurse should restrict consumption of foods high in purines, especially organ meats, and to limit alcohol intake. Maintenance of normal body weight should be encouraged.
- In an acute episode of gouty arthritis (stage 2), pain management with prescribed medications is essential, along with avoidance of factors that increase pain and inflammation (trauma, stress, alcohol). Medication adherence is critical, but remains poor among patients prescribed urate lowering therapies. Reinforce the importance of taking prescribed medications. Between acute episodes, medications and preventive behaviors may be abandoned.