Recipient(s) will receive an email with a link to 'Gout' and will have access to the topic for 7 days.
(Optional message may have a maximum of 1000 characters.)
Gout is an inflammatory arthritis related to a hyperuricemia (serum uric acid [SUA] level >6.8 mg/dL) 1.
Acute gouty arthritis can affect ≥1 joints; the first metatarsophalangeal joint is most commonly involved at presentation (podagra).
Although hyperuricemia is necessary for the development of gout, it is not the only determining factor.
Characterized by deposition of monosodium urate (MSU) crystals that accumulate in joints and soft tissues, resulting in acute and chronic arthritis, soft-tissue masses called tophi, urate nephropathy, and uric acid nephrolithiasis
After an initial flare, a second flare occurs in ∽60% of patients within 1 year and 78% within 2 years of the initial attack 2.
Management involves treating acute attacks and preventing recurrent disease by long-term reduction of SUA levels through pharmacology and lifestyle adjustments.
Uric acid 7 to 8.9 mg/dL is 0.5%.
Uric acid >9 mg/dL is 4.5%.
Increasing prevalence over the past decades 3
Overall prevalence of 3.9% (8.3 million) in the United States in 2008 3
2008 prevalence of hyperuricemia in the United States 3:
Hyperuricemia results from urate overproduction, underexcretion, or often a combination of the two.
Gout occurs when MSU, a product of purine metabolism, precipitates out of solution and accumulates in joints and soft tissues.
Transient changes in urate solubility caused by local temperature decrease, trauma, or acidosis may lead to an acute gouty attack.
Urate crystals that precipitate trigger an immune response.
Left untreated, this crystal deposition leads to permanent joint damage and tophus formation.
Phosphoribosyl pyrophosphate (PRPP) deficiency and hypoxanthine-guanine-phosphoribosyltransferase (HGPRT) deficiency (Lesch-Nyhan syndrome) are inherited enzyme defects associated with overproduction of uric acid.
Polymorphisms in the URAT1 and SLC 2A9 (GLUT9) renal transporters are hereditary enzyme defects resulting in primary underexcretion of uric acid.
Age >40 years
Increased purine uptake (meats and seafood)
Alcohol intake (especially beer)
High fructose intake
Congestive heart failure
Coronary artery disease
Maintain optimal weight.
Diet modification purine-rich foods)
Reduce alcohol consumption (beer and liquor).
Maintain fluid intake and avoid dehydration.
Nontraumatic joint disorders
Classic presentation of acute gouty arthritis:
Fever can be present.
Subcutaneous or intraosseous nodules, referred to as tophi, can be seen.
Pain with urination secondary to uric acid renal stones
Examine suspected joint(s) for tenderness, swelling, and range of motion (ROM).
Assess for presence of firm nodules known as tophi.
In patients with chronic gout, tophi can frequently be found in the helix of the ear, over the olecranon process, or on the Achilles tendon.
Patients with untreated chronic gout can have evidence of joint inflammation and deformity.
SUA (may be normal during an acute flare)
CBC (can see elevation of WBC during gout flare)
Synovial fluid analysis: urate crystals (negatively birefringent under polarizing microscopy), cell count (WBC usually 2,000 to 5,000 cells/mm3); culture to rule out infection.
Screen for uric acid overproduction using 24-hour urinary uric acid in those patients with gout onset before the age of 25 years or with a history of urolithiasis 1[C].
Radiograph's are normal early in disease but can reveal
Urate kidney stones are radiolucent and thus invisible on radiograph.
Ultrasound evidence of urate deposition—hyperechoic enhancement over surface of hyaline cartilage 4.
Dual-energy CT (DECT) imaging can show urate deposition at articular or periarticular sites 4.
ACR-EULAR Gout Classification calculator: (goutclassificationcalculator.aukland.ac.nz) validated classification criteria with sensitivity 92%, specificity 89% [with clinical criteria only sensitivity of 85% and specificity of 78%] 4.
SUA q2-5wk while titrating urate-lowering treatment to goal 1[C]
Regularly monitor CBC, renal function, liver function test, and urinalysis.
General lack of evidence regarding specific recommendations, although the American College of Rheumatology has outlined the following 1[C]:
Dietary and lifestyle modifications 1[B]
Instructions on initiating treatment on signs and symptoms of an acute gout attack without the need to consult health care provider for each attack 1[B]
Discussion that gout is caused by excess uric acid and that effective urate-lowering therapy is essential treatment 1[B]
Increased susceptibility to infection
M10.9 Gout, unspecified
M10.00 Idiopathic gout, unspecified site
M10.30 Gout due to renal impairment, unspecified site
M1A.30X0 Chronic gout due to renal impairment, unsp site, w/o tophus
M1A.9XX1 Chronic gout, unspecified, with tophus (tophi)
M10.09 Idiopathic gout, multiple sites
M10.39 Gout due to renal impairment, multiple sites
M10.079 Idiopathic gout, unspecified ankle and foot
M10.072 Idiopathic gout, left ankle and foot
M10.40 Other secondary gout, unspecified site
M10.49 Other secondary gout, multiple sites
M10.071 Idiopathic gout, right ankle and foot
M1A.9XX0 Chronic gout, unspecified, without tophus (tophi)
M10.379 Gout due to renal impairment, unspecified ankle and foot
M10.479 Other secondary gout, unspecified ankle and foot
M1A.30X1 Chronic gout due to renal impairment, unsp site, with tophus
274.9 Gout, unspecified
274.00 Gouty arthropathy, unspecified
274.10 Gouty nephropathy, unspecified
274.19 Other gouty nephropathy
274.89 Gout with other specified manifestations
274.11 Uric acid nephrolithiasis
274.03 Chronic gouty arthropathy with tophus (tophi)
274.02 Chronic gouty arthropathy without mention of tophus (tophi)
274.01 Acute gouty arthropathy
90560007 Gout (disorder)
190828008 gouty arthropathy (disorder)
239844009 Gout secondary to renal impairment (disorder)
190829000 chronic urate nephropathy (disorder)
24595009 Primary gout (disorder)
48440001 Articular gout (disorder)
402469004 Gouty tophus (disorder)
MSU crystals found in synovial fluid aspirate are pathognomonic for gout.
Pharmacologic treatment should begin within 24 hours of acute gout flare.
Asymptomatic hyperuricemia does not require treatment.