Gout

Populations and Risk Factors

Men aged 40-50 most commonly affected. Postmenopausal women (estrogen normally aids uric acid excretion)
Males of African American descent have higher prevalence
Premenopausal women rarely affected (estrogen is uricosuric)
Comorbidities: hypertension, obesity, metabolic syndrome, renal insufficiency, type 2 diabetes
Dietary contributors: high-purine foods (organ meats, red meat, shellfish), alcohol (especially beer), high-fructose beverages
Medications that reduce uric acid excretion: thiazide diuretics, low-dose aspirin, cyclosporine

Hyperuricemia: Uric acid is the end product of purine metabolism. Levels rise from either overproduction (10%) or underexcretion (90%) by the kidneys
Crystal deposition: When serum uric acid exceeds the saturation threshold (~6.8 mg/dL), MSU crystals precipitate in peripheral joints, tendons, and soft tissues — peripheral joints are cooler, which promotes crystallization
Acute attack mechanism: Crystals in the joint space trigger an intense neutrophilic inflammatory response with massive cytokine release. This produces the cardinal signs of acute gouty arthritis: exquisite pain, redness, heat, and swelling
Chronic tophaceous gout: After 10-20 years of inadequately treated hyperuricemia, large deposits of urate crystals (tophi) form visible hard nodules around joints, ears, tendons, and bursae. These can erode bone, producing a "punched-out" erosion pattern on X-ray
Renal involvement: Uric acid crystals can deposit in the kidneys, causing uric acid nephropathy and kidney stones

Acute attack: Joints red, hot, swollen, shiny, and exquisitely painful — even the weight of a bedsheet is intolerable. Sudden onset, often at night with throbbing pain
Moderate fever and chills may accompany acute episodes
Skin over gouty joint feels dry and tight (vs. moist in septic joints — a key differential finding)
"Punched-out" bony erosion pattern on X-ray in chronic cases
Tophi: large, hard, chalky nodules around joints, ears, and tendons (chronic disease)
Waddling gait if the great toe or foot joints are involved
Red flags: Acute gouty joint with fever requires medical referral to rule out septic arthritis; do not apply ice (cold promotes crystallization)

CMTO Appendix category A1 (MSK conditions) / A3 (systemic conditions)
Key differential: gout (dry, tight skin over joint) vs. septic arthritis (moist skin; fever higher; emergent condition)
Key differential: gout (elevated uric acid) vs. pseudogout (calcium pyrophosphate crystals; different joint distribution)
Acute gouty joint with systemic fever requires urgent medical referral — do not treat
Never apply ice to a suspected gouty joint (cold promotes MSU crystallization)
Aspirin inhibits uric acid excretion — should be avoided in gout patients

Acute gouty joints strictly contraindicate local massage — the inflammation is crystal-mediated and cannot be resolved by manual therapy. Even light touch is intolerable
Systemic massage contraindicated if fever or malaise is present (indicates systemic inflammatory response)
During remission: Massage is safe and helps manage stress, provide relaxation, and address secondary musculoskeletal tension
Never attempt to "grind out" crystals — this is clinically inappropriate and damages tissue
No ice: Do not apply ice to suspected gouty joints. Cold promotes uric acid crystallization and may worsen the attack
Aspirin note: Aspirin inhibits uric acid excretion and should be avoided. If a client is taking aspirin for cardiovascular reasons, this may complicate gout management

Acute gouty joints strictly contraindicate local massage. Systemic massage contraindicated if fever or malaise is present
Never apply ice to a suspected gouty joint — cold promotes uric acid crystallization
Do not attempt to "grind out" crystals. This is inappropriate and damages tissue
Distinguish from septic arthritis: gouty skin feels dry and tight (vs. moist in septic joints)
During remission, massage is safe and helps manage stress. During acute attacks, joints are exquisitely painful to even light touch
Gout is caused by hyperuricemia from either overproduction (10%) or underexcretion (90%) of uric acid