Mrs. K, an 81-year-old golf-enthusiast admitted with congestive heart failure, now refuses to walk and complains of ankle pain. When you see her, she refuses to let even a bedsheet near her left ankle, and she claims that you did this to her.
Unfortunately, she’s probably right. Mrs. K also has a history of podagra, and she developed an acute gouty monoarthritis after receiving treatment with diuretics and aspirin. Gout—along with the other causes of inpatient acute monoarthritis (pseudogout, septic arthritis, and trauma)—are increasingly common diagnoses in the geriatric patient population. Because the elderly are uniquely predisposed to losing functional independence following an acute attack, making a timely diagnosis is particularly important in this age group. And though the patient’s clinical features may point toward an etiology, making the correct diagnosis ultimately depends on the results of the joint tap.
Gout occurs in patients with high serum levels of uric acid, though not all hyperuricemic patients develop gout. Among elderly hospitalized patients with hyperuricemia, approximately 65% have significant renal impairment, and others have advanced hypertension, coronary artery disease, and congestive heart failure. Over time, high serum uric acid levels may lead to the deposition of monosodium urate crystals in the joints; these lesions are the precursors of a gouty attack.
Gouty attacks occur when crystal deposits become inflamed. The inflammation may be triggered by a medication-induced change in uric acid concentration or by a medical condition, including acute illness, trauma, surgery, and dehydration. (See Table 1, p.18.) Though some elderly patients with acute gouty arthritis will manifest confusion or a sudden change in ambulatory status, most will present with a monoarthritis and a rise in temperature. Gout is suspected clinically when the first metatarsal phalangeal joint is involved (podagra), but other commonly involved joints include the ankle and the knee. Uric acid levels in the blood are usually elevated but can also temporarily normalize or even dip low during attacks. An X-ray of the involved joint may be normal or may already show the characteristic erosive lesion of gout, the “overhanging edge.”
Making the correct diagnosis is dependent upon visualizing intracellular, needle-shaped, negatively birefringent crystals in the synovial fluid. After the fluid is removed from the affected joint, it should be examined under polarized light within two hours; if more time is needed, the fluid can be refrigerated for up to 12 hours. Co-infection of a gouty joint has been described in the elderly population, and the synovial fluid should be sent to the laboratory for a cell count, Gram’s stain, and culture, as well as glucose and lactate levels. (See Table 2, below.)
Direct in-hospital treatment of gout toward alleviating the current attack, preventing future attacks, and providing appropriate antibiotic coverage in suspected co-infected cases until joint culture results are finalized. Treatment options for the acute attack include NSAIDs and corticosteroids—either oral or intra-articular. Hourly oral colchicine is not a good option for an elderly patient because the diarrhea that ensues is particularly disruptive. Nor is IV colchicine a good option thanks to its side-effect profile that renders it unusable in patients with reduced renal function. The treatment of hyperuricemia with allopurinol should not be undertaken during the acute attack because any change in the serum uric acid concentration will serve only to exacerbate the current inflammation.