Gout is considered a form of crystal deposition arthritis, hence the name, gouty arthritis. Uric acid, a chemical that is found in the serum component of our blood, is the key to understanding gout. Excessively high levels of uric acid lead to the deposition of monosodium urate crystals into joints and certain subcutaneous spaces in the body. To understand the way that acute gouty attacks occur, let's use a simple example;

Example - As children, we would make our own rock candy. We'd get a pot of water and begin to heat it on the stove. As the water warmed, we'd add sugar. The hotter the water became, the more sugar we could dissolve. When the water was close to a boil and saturated with sugar, we would remove it from the heat and allow the sugar to crystallize on a string as the water cooled.

Acute gouty attacks occur in much the same manner. Most acute gouty attacks occur in the late hours of the night. As we sleep, our bodies tend to focus on the primary metabolic functions such as digestion, breathing, etc. The extremities, such as the feet tend to cool as a result of this 'lack of attention'. As they cool, and if the dissolved amount of uric acid is high enough, the result is the change of uric acid from a liquid to a crystal. The hallmark symptoms of gout are a) an acute onset of pain and b) an onset that occurs while you're sleeping in the early hours of the night.

Uric acid is measured in the serum (liquid) component of our blood. Normal levels for men are less that 7mg/dl of serum and slightly less for most women. This level tends to rise in women following menopause. The vast majority of gout patients are men with an onset during the 4th to 5th decade of life. If serum uric acid levels surpass 10mg/dl, the likelihood of a gout attack is very probable.

High levels of uric acid result from high levels of intake or low levels of excretion of purines. The inability to metabolize purines may be inherited or acquired. Purines are protein components in foods that are found commonly in the following foods;

Heavy red meats and organ parts (sausage, liver, kidney, tongue, heart)
Dark fillet fish (mackerel, anchovies, sardines, herring and fish roe)
Peanuts
Alcohol
Dairy products (milk, ice cream, cottage cheese)

Individuals who have had acute gouty attacks should limit their intake of these foods. This does not mean that they need to completely eliminate them from their diets, but rather they should consume these foods with moderation. Serum uric acid is also significantly influenced by the ability of the kidney to excrete uric acid. Factors that may change normal renal function may result in limited excretion of uric acid. These factors include the use of thiazide (HCTZ -hydrochlorthizide) diuretic therapy, dehydration and renal failure. Many antihypertensive (blood pressure lowering) medications include HCTZ and include Dyazide, Maxide, Moduretic, indapamide, Microzideand Zaroxolyn. Other factors that may contribute to the onset of gout include trauma, the stress of surgery, emotional stress, fatigue, infection or the use of penicillin.

Treatment of gout and gouty arthritis

The most significant consideration in the treatment of gout is the frequency of attacks. Frequent attacks (more than one a year) will result in progressive erosion of the joint, leading to painful chronic arthritis. Isolated attacks (less that one a year) lead to minimal destruction of the joint. The frequency of gouty attacks determines whether treatment is merely for each attack, or whether daily medication should be taken to lower levels of serum uric acid.

Treatment of acute attacks includes the use of prednisone or non-steroidal anti-inflammatory medications such as Indocin or Clinoril. Control of pain may require a mild narcotic such as codeine. Other treatment may include Colchicine which yields dramatic results but carries severe side effects which include nausea and severe diarrhea. Colchicine is dosed once every two hours until the desired (or undesired) effects are achieved.

Treatment of recurrent attacks includes the modifications in diet as previously discussed and the use of Allopurinal, an inhibitor of uric acid synthesis. Probenecid and sulfinpyrazone are also used to increase the output of uric acid by the kidney. Dosing and combination therapy depends upon the level of serum uric acid which is measured periodically during therapy. Individuals prone to gouty attacks should also maintain a high fluid intake to promote the excretion of uric acid and decrease the tendency to form uric acid stones in the kidney and bladder.

Gouty arthritis is the sequela of multiple untreated attacks that progressively destroy the cartilage of the joint. Surgical debridement of a joint with chronic damaged by chronic gout shows depositions of a material called gouty tophi that resemble cottage cheese. These gout crystals erode the surface cartilage resulting in premature destruction of the joint. Debridement of the joint, fusion or joint replacement is often indicated.

Abarticular - referring to gout that occurs in structures other than joints.
Gout - derived from the Latin term gutta meaning to drop.
Gouty - relating to gout.
Podagra - gout of the great toe joint.
Purine - a purine is an organic compound consisting of a pyrimidine ring fused to an imidazole ring. 
Saturnine - gout that occurs related to lead poisoning.
Secondary gout - gout that occurs as a secondary problem due to other illness such as diseases of he bone marrow or lead poisoning.
Uric acid - the chemical metabolite of purines.

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The symptoms of gout usually appear at night with an abrupt onset. The weight of the bed sheets is often intolerable. One joint or several may be involved. The most common site is the first metatarsal phalangeal joint (big toe joint). The pain is described as crushing and excruciating. Attacks tend to last several days.

Gouty arthritis can be visualize on X-rays after several attacks. The bone adjacent to the joint becomes eroded with a characteristic punched out lesion referred to as a Martel's Sign or 'rat bite sign'. The erosion is very distinctive and represents a pocket of gouty tophi. Tophi are the accumulation of monosodium uric acid crystals. Tophi are often found in joints but may also be found at extensor surface (back) of the elbow, the rim of the ear and at the back of the heel. When viewed surgically, tophi appear to have the same consistency of cottage cheese.

The differential diagnosis for this condition should include:

Chondrocalcinosis

Fracture

Infection of the joint (septic joint)

Osteoarthritis

Pseudogout

Rheumatoid arthritis

Rheumatic fever

• Pseudogout

• Turf Toe

• Hallux Limitus

• Bursitis

• Forefoot Pain

This article was written by Jeffrey A. Oster, DPM and last updated 1-28-10.

No additional information is available for this condition.