GOUT

•      A metabolic disease marked by red, swollen, and acutely painful joints

 

 

 

–  Gout affects any joint but is found mostly in the of the feet

•   Great toe

•   Ankle

•   Midfoot

 

 

Pathophysiology

(Note: Click here for supplemental pathogenesis information on gout.)

•      Men over 30 and postmenopausal women who take diuretics.

•      Follows an intermittent course

–   Pt can be symptom free for years between attacks

•      Underlying cause of primary gout is unknown

–   In many patients it results from κ excretion of uric acid by the kidneys.

–   Can be a genetic defect called hyper-uricemia that causes an overproduction of uric acid

•      Secondary gout may develop from another disease such as:

–   Obesity

–   Diabetes

–   High blood pressure

–   Leukemia

–   Bone cancer

–   Kidney disease

 

 

•      Secondary gout can also follow treatment with certain drugs such as hydrochlorothiazid  or pyrazinamide

A Painful Progression

•      Four Stages of Progression (if untreated):

•      1.  Pt develops asymptomatic hyperuricemia

–   Urate levels rise but don’t produce symptoms

•      2.  Acute gouty arthritis

–   Painful swelling and tenderness

–   When pt seeks medical attention

 

 

•      3.  The interictal stage

–   May last for months to years

–   Pt may be asymptomatic or may experience exacerbations

•      4.  Chronic stage

–   urate pools in the joints

–   tophi (clusters of urate crystals) develop in cartilage, synovial membranes, tendons, and soft tissues.

•      Final unremitting stage called tophaceous gout

 

 

Tale of the Tophi

•      Tophi - clusters of urate crystals surrounded by inflamed tissue

–   Can cause deformity and destruction of hard and soft tissues

–   In joints tophi lead to destruction of cartilage and bone

•      Tophi form in diverse areas:

–   hands

–   knees

–   feet

–   outer sides of the forearms

–   pinna of the ear

–   Achilles tendon

•      Rarely, internal organs such as the kidneys and heart may be affected and cause dysfunction

Hyperuricemia

•      Urates are uric acid salts

•      hyperuricemia is a plasma urate level Ψ 7 mg/dl

•      Hyperuricemia results from

–   ι urate production

–   κ excretion of uric acid

–   a combination of the above

•      With hyperuricemia, plasma and extracellular fluids are supersaturated with urate

•      This leads to urate crystal formation

•      When crystals are deposited in other tissues, a gout attack strikes

Provoking Factors

•      Stress

•      Trauma

•      Infection

•      Hospitalization

•      Use of some medications

•      Surgery

•      Starvation

•      Weight reduction

•      Excessive food intake

•      Use of alcohol

Relief in Sight

•      A sudden increase in serum urate may cause new crystals to form.

•      A drop in serum and extracellular urate may cause previously formed crystals to partially dissolve and be excreted

What to Look for

•      First attack strikes suddenly and peaks quickly

•      First attack is extremely painful

•      Attacks resolve in 10-14 days

•      Second attacks are usually 6 months to 2 years later

Tophi are

–    hard

–    irregular

–    • yellow-white nodules

•      Found especially on

–    ears

–    hands

–    feet

•      In late chronic stage gout the skin over the tophi may ulcerate and release a chalky white exudate or pus results in joint degeneration, deformity and disability

–   joints may be warm and tender

–   pts may have a hx of HTN and kidney stones

•      Pain often wakes the pt in the night with pain in the great toe or other part of the foot

•      Pain may become so severe that pt can’t bear weight of bed linens or even vibrations

•      May report chills and fever

Complications

•      Renal calculi

•      Infections

•      Nerve damage

•      Circulatory problems

•      CVA

•      Coronary thrombosis

•      HTN

•      Cardiovascular lesions

Tests

•      Needle aspiration of synovial fluid or tophi reveals sodium crystals (mono-sodium urate) in the cells

•      Blood and urine tests to determine serum and urine uric acid levels

•      X-rays initially produce normal results.

•      Chronic gout shows damage to cartilage and bone

Treatment

•      Three goals:

–   1.  Terminate the acute attack

–   2.  Reduce uric acid levels

–   3.  Prevent recurrent gout and renal calculi

Treatment of Acute Attacks

•      Bed rest and elevation of the extremity

•      Immobilization and protection of the inflamed, painful joins

•      Local application of cold

•      Bed Cradle

•      Tylenol for relief of mild pain

•      NSAIDs or cortisone for acute inflammation

•      Cholchicine or corticosteroids are occasionally used to treat acute attacks

•      Drink 2 L fluids per day to help prevent renal calculi

•      Acute attacks can occur 24-96 hours after any kind of surgery

–   Cholchicine  may be administered before and after to help attacks

Treatment of Chronic Gout

•      Serum uric acid levels are reduced to less than 6.5 mg/dl

•      Overproduction of uric acid θ allopurinol

•      Underproduction of uric acid θ probenecid or sulfinpyrazone

•      Serum uric acid levels monitored

•      NaH2CO3 given to make urine alkaline

Adjunctive Therapy

•      Avoiding alcohol especially beer and wine

•      Avoiding purine rich foods such as anchovies, liver, sardines, kidneys, sweetbreads, and lentils

Weight  Loss

•      Obese pts. should begin a weight-loss program because weight reduction decreases uric acid levels and stress on painful joints