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Emergency And Acute Medicine - Gout/Pseudogout
Basics Description
Gout is a crystalline arthropathy caused by deposition of monosodium urate in tissues, most commonly affecting middle-aged men and postmenopausal women. It is the most common crystal-induced arthritis and classically progresses through four phases: asymptomatic hyperuricemia (serum urate >7 mg/dL), acute gout, intercritical gout with symptom-free intervals, and chronic tophaceous gout, which occurs in up to 45% of cases.
Risk factors include age >40 years, male sex (male-to-female ratio 2:1–6:1 before age 65, approaching 1:1 thereafter), hypertension, use of loop or thiazide diuretics, high intake of alcohol, meat, seafood, and fructose-sweetened beverages, and obesity. Uric acid nephrolithiasis may lead to renal dysfunction. Chronic disease can result in avascular necrosis and deforming arthritis.
Gout preferentially involves previously damaged tissues such as synovium, subchondral bone, bursae (olecranon, infrapatellar, prepatellar), Achilles tendon, and extensor surfaces of the forearms, toes, fingers, and ear. Rare involvement of the CNS or cardiac valves has been described.
Pseudogout is caused by calcium pyrophosphate crystal deposition and is the most common cause of acute monoarthritis in patients older than 60 years. Risk factors include hypercalcemia, hemochromatosis, hypothyroidism or hyperthyroidism, hypophosphatemia, hypomagnesemia, amyloidosis, and underlying gout.
Etiology
Gout results from deposition of monosodium urate crystals due to underexcretion (most common) or overproduction of uric acid. Acute attacks are often triggered by rapid changes in uric acid levels such as initiation or withdrawal of diuretics, alcohol intake, salicylates, niacin, cyclosporine, lead exposure, or starting uricosurics or allopurinol.
Pseudogout occurs due to excess accumulation of calcium pyrophosphate crystals within the synovium. Minor trauma and acute systemic illness, including surgery or ischemic heart disease, may precipitate attacks of either condition.
Diagnosis Signs And Symptoms
Both gout and pseudogout typically present as acute monoarticular or polyarticular arthritis with warmth, erythema, swelling, and pain. Early attacks often resolve spontaneously within 3–21 days, while later attacks may be longer, more severe, clustered, and polyarticular.
Gout symptoms usually peak within 12–24 hours. Tophi and skin desquamation may be present in advanced disease. Women often present after menopause and more commonly have polyarticular involvement. Presentations may be less dramatic in elderly or immunosuppressed patients. The first metatarsophalangeal joint is most commonly affected, followed by the ankle, knee, hand, and wrist.
Pseudogout more often involves large joints, particularly the knee, followed by the wrist, metacarpals, shoulder, elbow, ankle, hip, and tarsal joints. It may be monoarticular, asymptomatic, mimic osteoarthritis with symmetric degeneration, or present as a pseudorheumatoid arthritis variant with fever and confusion in elderly patients.
Essential Workup
Arthrocentesis with synovial fluid analysis is essential to confirm diagnosis and exclude infection. Aspirate should be examined for crystals, Gram stain, culture, leukocyte count, and differential. Gout fluid typically contains 20,000–100,000 WBC/mm³ without bacteria. Pseudogout fluid usually has fewer than 50,000 WBC/mm³.
Polarized light microscopy shows needle-shaped, strongly negatively birefringent crystals in gout and rhomboid-shaped, weakly positively birefringent crystals in pseudogout.
Diagnosis Tests And Interpretation
CBC often reveals leukocytosis. Chemistry panels assess renal function. Magnesium, calcium, TSH, and iron studies may identify associated conditions. Serum uric acid has limited diagnostic value during acute attacks. Blood and urine cultures are indicated if infection is suspected.
Plain radiographs may show soft tissue swelling in acute gout, while chronic gout demonstrates calcified tophi and characteristic erosions. Pseudogout may show chondrocalcinosis and calcification of cartilage or ligaments. Dual-energy CT can identify urate deposits or nephrolithiasis.
Differential Diagnosis
Septic arthritis, trauma, osteoarthritis, reactive arthritis, rheumatoid arthritis, systemic lupus erythematosus, avascular necrosis, osteomyelitis, sickle cell disease, and other crystal arthropathies.
Treatment Initial Stabilization Therapy
Primary goals are pain control and exclusion of infectious arthritis.
Ed Treatment Procedures
NSAIDs are first-line therapy if tolerated. If contraindicated or ineffective, corticosteroids (oral, IM, IV, or intra-articular) or colchicine may be used. Joint aspiration can provide symptomatic relief. Aspirin should be avoided.
Long-term urate-lowering therapy and prevention strategies are generally not initiated in the ED and include withdrawal of precipitating agents, uricosurics, allopurinol, hydration, urine alkalinization, and prophylactic colchicine or NSAIDs.
Medication
Therapeutic options include NSAIDs, colchicine, corticosteroids, allopurinol, febuxostat, probenecid, and biologic agents for refractory disease. Dosing should be adjusted for renal or hepatic impairment and patient age.
Follow-Up Disposition
Admission is indicated for suspected septic arthritis, acute renal failure, or intractable pain.
Patients without evidence of infection and with adequate pain control may be discharged.
Issues For Referral
Referral is indicated for septic arthritis, renal failure, or refractory disease.
Follow-Up Recommendations
Rheumatology follow-up is recommended for severe or difficult-to-control cases. Nephrology or urology referral is indicated for renal insufficiency or uric acid nephrolithiasis. Orthopedic follow-up is required for septic arthritis or significant joint damage. Patients should be counseled on a low-purine diet.
Key Clinical Insights And Frequent Errors
Septic arthritis may coexist with acute gout and must always be excluded. NSAIDs remain first-line therapy when tolerated. Acute attacks are often self-limited, but recurrent gout and pseudogout can result in progressive bony and cartilaginous damage if not appropriately managed.
Basics Description
Gout is a crystalline arthropathy caused by deposition of monosodium urate in tissues, most commonly affecting middle-aged men and postmenopausal women. It is the most common crystal-induced arthritis and classically progresses through four phases: asymptomatic hyperuricemia (serum urate >7 mg/dL), acute gout, intercritical gout with symptom-free intervals, and chronic tophaceous gout, which occurs in up to 45% of cases.
Risk factors include age >40 years, male sex (male-to-female ratio 2:1–6:1 before age 65, approaching 1:1 thereafter), hypertension, use of loop or thiazide diuretics, high intake of alcohol, meat, seafood, and fructose-sweetened beverages, and obesity. Uric acid nephrolithiasis may lead to renal dysfunction. Chronic disease can result in avascular necrosis and deforming arthritis.
Gout preferentially involves previously damaged tissues such as synovium, subchondral bone, bursae (olecranon, infrapatellar, prepatellar), Achilles tendon, and extensor surfaces of the forearms, toes, fingers, and ear. Rare involvement of the CNS or cardiac valves has been described.
Pseudogout is caused by calcium pyrophosphate crystal deposition and is the most common cause of acute monoarthritis in patients older than 60 years. Risk factors include hypercalcemia, hemochromatosis, hypothyroidism or hyperthyroidism, hypophosphatemia, hypomagnesemia, amyloidosis, and underlying gout.
Etiology
Gout results from deposition of monosodium urate crystals due to underexcretion (most common) or overproduction of uric acid. Acute attacks are often triggered by rapid changes in uric acid levels such as initiation or withdrawal of diuretics, alcohol intake, salicylates, niacin, cyclosporine, lead exposure, or starting uricosurics or allopurinol.
Pseudogout occurs due to excess accumulation of calcium pyrophosphate crystals within the synovium. Minor trauma and acute systemic illness, including surgery or ischemic heart disease, may precipitate attacks of either condition.
Diagnosis Signs And Symptoms
Both gout and pseudogout typically present as acute monoarticular or polyarticular arthritis with warmth, erythema, swelling, and pain. Early attacks often resolve spontaneously within 3–21 days, while later attacks may be longer, more severe, clustered, and polyarticular.
Gout symptoms usually peak within 12–24 hours. Tophi and skin desquamation may be present in advanced disease. Women often present after menopause and more commonly have polyarticular involvement. Presentations may be less dramatic in elderly or immunosuppressed patients. The first metatarsophalangeal joint is most commonly affected, followed by the ankle, knee, hand, and wrist.
Pseudogout more often involves large joints, particularly the knee, followed by the wrist, metacarpals, shoulder, elbow, ankle, hip, and tarsal joints. It may be monoarticular, asymptomatic, mimic osteoarthritis with symmetric degeneration, or present as a pseudorheumatoid arthritis variant with fever and confusion in elderly patients.
Essential Workup
Arthrocentesis with synovial fluid analysis is essential to confirm diagnosis and exclude infection. Aspirate should be examined for crystals, Gram stain, culture, leukocyte count, and differential. Gout fluid typically contains 20,000–100,000 WBC/mm³ without bacteria. Pseudogout fluid usually has fewer than 50,000 WBC/mm³.
Polarized light microscopy shows needle-shaped, strongly negatively birefringent crystals in gout and rhomboid-shaped, weakly positively birefringent crystals in pseudogout.
Diagnosis Tests And Interpretation
CBC often reveals leukocytosis. Chemistry panels assess renal function. Magnesium, calcium, TSH, and iron studies may identify associated conditions. Serum uric acid has limited diagnostic value during acute attacks. Blood and urine cultures are indicated if infection is suspected.
Plain radiographs may show soft tissue swelling in acute gout, while chronic gout demonstrates calcified tophi and characteristic erosions. Pseudogout may show chondrocalcinosis and calcification of cartilage or ligaments. Dual-energy CT can identify urate deposits or nephrolithiasis.
Differential Diagnosis
Septic arthritis, trauma, osteoarthritis, reactive arthritis, rheumatoid arthritis, systemic lupus erythematosus, avascular necrosis, osteomyelitis, sickle cell disease, and other crystal arthropathies.
Treatment Initial Stabilization Therapy
Primary goals are pain control and exclusion of infectious arthritis.
Ed Treatment Procedures
NSAIDs are first-line therapy if tolerated. If contraindicated or ineffective, corticosteroids (oral, IM, IV, or intra-articular) or colchicine may be used. Joint aspiration can provide symptomatic relief. Aspirin should be avoided.
Long-term urate-lowering therapy and prevention strategies are generally not initiated in the ED and include withdrawal of precipitating agents, uricosurics, allopurinol, hydration, urine alkalinization, and prophylactic colchicine or NSAIDs.
Medication
Therapeutic options include NSAIDs, colchicine, corticosteroids, allopurinol, febuxostat, probenecid, and biologic agents for refractory disease. Dosing should be adjusted for renal or hepatic impairment and patient age.
Follow-Up Disposition
Admission is indicated for suspected septic arthritis, acute renal failure, or intractable pain.
Patients without evidence of infection and with adequate pain control may be discharged.
Issues For Referral
Referral is indicated for septic arthritis, renal failure, or refractory disease.
Follow-Up Recommendations
Rheumatology follow-up is recommended for severe or difficult-to-control cases. Nephrology or urology referral is indicated for renal insufficiency or uric acid nephrolithiasis. Orthopedic follow-up is required for septic arthritis or significant joint damage. Patients should be counseled on a low-purine diet.
Key Clinical Insights And Frequent Errors
Septic arthritis may coexist with acute gout and must always be excluded. NSAIDs remain first-line therapy when tolerated. Acute attacks are often self-limited, but recurrent gout and pseudogout can result in progressive bony and cartilaginous damage if not appropriately managed.
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