Annals of Long Term Care

INTRODUCTION
Gout is a clinical syndrome caused by tissue (synovial, bursa, cartilage) deposition of monosodium urate (MSU) crystals in a patient with an elevated body pool of uric acid.1 New-onset gouty arthritis is common in the elderly population, and prevalence of gout is on the rise. In a study using a managed care population database, the prevalence of gout and/or hyperuricemia (defined as serum uric acid level > 6.8 mg/dL) in persons over age 75 years increased from 20.55 to 41.28 cases per 1000 enrollees over a 10-year period.2

This seems to be related to increasing lifespan, and thus the age-related diseases such as hypertension and effects of associated treatment as with diuretics (see Tables I and II). Under age 65 years, men are affected four times the number of women.2 Due to loss of the uricosuric effect of estrogen with increasing age, this ratio is reduced to 3:1 after age 65 years. The majority of patients who develop gout have been hyperuricemic for about two decades. However, the majority of individuals with hyperuricemia never develop gout. Most patients with idiopathic gout have a defect (possibly inherited) leading to underexcretion of uric acid, even when the renal function is otherwise normal.1 Diuretic therapy, renal insufficiency, hypertension, and hypertriglyceridemia can be other contributing factors. It has been estimated that at least half of patients who present with an initial attack of gout are taking a diuretic. Approximately 10% of patients with gout have increased uric acid production, resulting from excessive purine ingestion, alcohol abuse, genetic defect of purine synthesis, or increased nucleic acid turnover as in myeloproliferative and lymphoproliferative disorders. Gout in the elderly differs from classical gout found in middle-aged men and middle-aged women in several respects: it has a more equal gender distribution, frequent polyarticular presentation with involvement of the joints of the upper extremities, fewer acute gouty episodes, a more indolent chronic clinical course, and an increased incidence of tophi.4

Gout has four distinct stages:

1. Asymptomatic hyperuricemia
2. Acute gouty arthritis
3. Intercritical gout
4. Chronic tophaceous gout

CLINICAL FEATURES
Acute Gouty Arthritis

In an acute presentation, patients will notice severe pain, redness, swelling, and warmth in one or more joints. Severe tenderness will be noted in involved joints. Symptoms worsen within first 24 hours. Joint involvement (in order of decreasing frequency) includes the metatarsophalangeal joint (podagra), the instep/forefoot, the ankle, the knee, the wrist, and the fingers.5 In elderly women, an initial presentation may be acute arthritis of fingers, having inflamed Heberden’s and Bouchard’s nodes.3 Untreated acute gout usually resolves within 1-3 weeks.

Intercritical Gout
This is the period between two attacks of gout. Approximately 60% of patients have a second attack within the first year, and 78% have a second attack within 2 years. Only 7% of patients do not have a recurrence within a 10-year period.6

Chronic Tophaceous Gout
Tophaceous disease is more likely to occur in patients with the following: a polyarticular presentation, a serum urate level higher than 9.0 mg per dL, and a younger age at disease onset (ie, 40.5 years or younger).7 The rate of urate deposition and, consequently, the rate of tophi formation, correlate with the duration and severity of hyperuricemia.6 The most common sites include the joints of the hands and feet. The helix of the ear, the olecranon bursa, and the Achilles tendon are classic, though less common, locations for tophi. Additionally, urate deposition in kidneys could lead to nephrolithiasis.

DIAGNOSIS
Routine Laboratory Data

Consider obtaining complete blood count, basic metabolic panel, erythrocyte sedimentation rate, and serum uric acid level routinely in patients with acute gouty arthritis.