The appropriate management of acute gout begins with confirming the diagnosis. When the diagnosis is uncertain consider other possible causes of joint inflammation, particularly sepsis. Anti-inflammatory therapy promptly relieves the pain of acute gout. The rapidity with which anti-inflammatory medication is commenced following the start of an attack is of greater importance than the specific drug chosen or the route of administration. Changes to therapy that aggravate the acute attack, such as altering hypouricaemic medication, should be avoided. Other conditions have the same presentation so confirming the diagnosis is a sound platform for immediate management and good long-term advice. The diagnosis must be certain if there is a decision to use life-long hypouricaemic therapy. Aspirating the joint is ideal management, but is not always possible. Gout is a common inflammatory arthritis that is increasing in prevalence. Non-steroidal anti-inflammatory drugs, colchicine and corticosteroids are options for the management of acute gout. They are equally efficacious and comorbidities guide the best choice. Allopurinol is an effective treatment for reducing concentrations of uric acid. Uricosuric drugs, such as probenecid, increase uric acid excretion. Renal function guides the starting dose of allopurinol and the baseline serum uric acid concentration guides the maintenance dose. New drugs in this class will soon become available and are likely to have a role in the treatment of patients who do not respond to other drugs. Hyperuricaemia is defined as a serum uric acid more than 0.36 mmol/L in women and more than 0.42 mmol/L in men. About 10% of people with hyperuricaemia develop gout, but 80–90% of patients with gout are hyperuricaemic. Gout results from a raised total body uric acid concentration with consequent deposition of crystals in joints and occasionally elsewhere.
Gout is a treatable form of arthritis that is associated with poor health and reduced life expectancy. Too often, gout management is focused on controlling the patient’s symptoms while their risk of irreversible joint damage and negative health outcomes continues to grow. Māori and Pacific peoples are disproportionately affected by gout and often receive sub-optimal care; it is time for a re-think to address this disparity. When urate levels in the blood reach saturation point, monosodium urate crystals can form. The inflammatory response to these crystals results in gout flares which are characterised by painful, red, hot, swollen joints. Over time, the duration and frequency of these flares may increase, resulting in chronic gouty arthritis and subcutaneous deposits of crystals referred to as tophi, both of which can lead to the destruction of joints. Detecting chronic kidney disease (CKD) early and preserving renal function is therefore an important gout-prevention strategy. Arthritis caused by gout (i.e., gouty arthritis) accounts for millions of outpatient visits annually, and the prevalence is increasing. Gout is caused by monosodium urate crystal deposition in tissues leading to arthritis, soft tissue masses (i.e., tophi), nephrolithiasis, and urate nephropathy. The biologic precursor to gout is elevated serum uric acid levels (i.e., hyperuricemia). Asymptomatic hyperuricemia is common and usually does not progress to clinical gout. Acute gout most often presents as attacks of pain, erythema, and swelling of one or a few joints in the lower extremities. The diagnosis is confirmed if monosodium urate crystals are present in synovial fluid. First-line therapy for acute gout is nonsteroidal anti-inflammatory drugs or corticosteroids, depending on comorbidities; colchicine is second-line therapy.
Prednisone lowers serum uric acid levels in patients with decompensated heart failure by increasing renal uric acid clearance. Chao Liu,ab. The appropriate management of acute gout begins with confirming the. Prednisone 10 mg twice daily for three to five days depending on the.