GOUT Katie Margelot NURS 870

Definition Gout is an acute, sudden inflammatory disease of the joint, caused by high concentrations of uric acid in the joints

Epidemiology One of most common causes of monoarticular arthritis Estimated US prevalence is 4% Effects males much more often… 9:1 ratio First attack usually after age 50 in men, age 60 in women

Pathogenesis Either body isn’t getting rid of uric acid or is producing too much of it For majority, gout is caused by genetic defect in renal excretion of uric acid, causing chronic hyperuricemia Decrease in renal excretion also caused by hyperinsulinism, renal failure, thiazide diuretics, and aspirin Excess uric acid can be caused by myeloproliferative disease, lymphoproliferative malignancies, consumption of high fructose corn syrup or alcohol, cyclosporine, thiazide and loop diuretics, obesity and HTN Usually presents after many years (mean ~30 yrs) of asymptomatic hyperuricemia

Pathogenesis Acute gout occurs when serum becomes supersaturated with uric acid, causing it to precipitate and collect in synovial fluid, causing an inflammatory response Attack may be precipitated by trauma, fall in temperature or pH, dehydration, starvation, high alcohol intake, new use of thiazide diuretics, emotional or physical stress, or rapid changes in serum uric acid concentration

Clinical Manifestations First attack usually is abrupt in onset and affects a joint in the lower extremity Usually one joint affected at a time Most common joint for initial presentation (50%): first metatarsophalangeal joint (big toe joint- “Podagra”) Other common sites are the midfoot, ankle, and knee Later episodes can involve upper extremity joints, but 80% occur in the lower extremities Hip or shoulder involvement is rare Polyarticular involvement occurs in only 5% of attacks, and usually limited to upper extremity joints Finger joint involvement more common in women

Clinical Manifestations Joint is swollen and erythematous Periarticular involvement common Low-grade fever Leukocytosis Serum uric acid level is often NORMAL at time of attack As attack resolves, skin over involved joint may peel

Differential Diagnosis Infection of joint (RED FLAG) Septic arthritis, osteomyelitis, prosthetic joint infection, disseminated gonorrhea Cellulitis Rheumatoid arthritis Psoriatic arthritis Lyme disease HIV Bursitis Trauma: Fracture, meniscus injury, hemarthrosis Pseudogout

History & Physical Exam Physical Exam Vitals May have low grade fever Inspection and palpation of joint Surrounding tissue may be inflamed Tophi? History Sudden onset, often occurs at night Painful, swollen, red joint 95% of time, only ONE joint is affected >80% of the time, it is a lower extremity joint Inflammatory s/s reach peak in hours, can last for days to weeks

Diagnostic Tests Definitive diagnosis: Aspiration and examination of synovial fluid for urate crystals Usually not needed, dx based on clinical findings CBC: May have leukocytosis ESR, CRP: May be elevated Serum uric acid: Can be WNL during attack…check 2 weeks after 24 hour urine uric acid excretion >900 mg Rheumatoid factor titer

Treatment PCP should be able to diagnose, treat, prevent recurrences, and reduce risk of developing chronic gouty arthritis Acute attacks are usually self-limited and resolve on their own in 7-10 days Severe attacks can last weeks Untreated gout can lead to chronic gout Initiating treatment at first sign of acute attack has excellent therapeutic outcome

Treatment DOC: NSAIDS (indomethacin, ibuprofen, naproxen) Colchicine If cannot take NSAIDs N/V/D Corticosteroids Refractory cases, or if cannot tolerate NSAIDs or colchicine Single IV dose equally effective as short course of high-potency oral prednisone or methylprednisolone Can give a single intra-articular injection if a large, weight-bearing joint is severely affected Associated with rebound attacks—may need to give concurrent low dose of colchicine Oxypurinol, febuxostat, uricase….Refer to rheumatology specialist

Treatment Reduction of uric acid level key to decreasing recurrence of attacks First line agents: Allopurinol and febuxostat Continue for 3 months after uric acid levels normalize, 6 months for patients with tophi Also can use probenecid, colchicine, pegloticase Recomment for patients who have >2 acute attacks in a year, tophi, or nephrolithiasis Goal range for serum uric acid is 5-6 mg/dL

Treatment YES: Joint rest—no heavy lifting or weight bearing activity Increase fluid intake Vegetables, low-fat dairy Lose weight if obese Losartan, calcium channel blockers Cherries?? NO: Aspirin Alcohol (esp. beer) High fructose corn syrup Purine-rich foods: organ meats, shellfish, oatmeal, asparagus, cauliflower, yeast, spinach, mushrooms, legumes Thiazide & loop diuretics

Chronic Gout Takes average of 10 years to develop Incidence greatly declined with introduction of anti hyperuricemic agents 15% will be affected Longstanding hyperuricemia causes deposits of uric acid crystals (tophi) Eventually results in chronic arthritis with cartilage erosion, joint deformity, and chronic swelling

Outcomes Cardiovascular event risk??? Concerns about correlation with renal failure have been disproved Nephrolithiasis…risk is less than 1% per year

References Adkins, J., & Cash, J. (2014). Gout. In J. Cash & C. Glass (Eds.). Family Practice Guidelines (3 rd ed.). ( ). New York: Springer Publishing Company. Becker, M.A. (2015). Clinical manifestations and diagnosis of gout. In P.L. Romain (Ed.), UpToDate. Retrieved from gout?source=search_result&search=gout&selectedTitle=2%7E150 Becker, M.A. (2015). Treatment of acute gout. In P.L. Romain (Ed.), UpToDate. Retrieved from gout?source=search_result&search=gout&selectedTitle=1%7E150 Goroll, A. (2014). Evaluation of acute monoarticular arthritis. In A. Goroll & A. Mulley (Eds.). Primary Care Medicine: Office Evaluation and Management of the Adult Patient (7 th ed.). ( ). Philadelphia, PA: Wolters Kluwer Goroll, A. (2014). Management of gout. In A. Goroll & A. Mulley (Eds.). Primary Care Medicine: Office Evaluation and Management of the Adult Patient (7 th ed.). ( ). Philadelphia, PA: Wolters Kluwer Hainer, B., Matheson, E., & Wilkes, R. (2014). Diagnosis, treatment, and prevention of gout. American Family Physician, 90(12), Retrieved from Zhang, Y., Neogi, T., Chaisson, C., Hunter, D., & Choi, H. (2012). Cherry consumption and decreased risk of recurrent gout attacks. Arthritis and Rheumatism 64(12), Retrieved from