What is Gout? Sign, Diagnosis & Treatment

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Historically, gout was thought to be a condition of royalty and the very rich, with which the disease attributed to “high living”. This has not been shown tone entirely true. Gout is a common inflammatory condition related to a genetic defect of purine metabolism that results in hyperuricemia. Oversecretion of uric acid or a renal defect resulting in decreased excretion of uric acid or a combination of both occurs. The Prevalence rate is reported to be about 2% and appears to be on the rise. The incidence of gout increases with age and body mass index, and the disorder occurs more commonly in women than in man.

Primary hyperuricemia, in this condition the elevated serum urate levels or manifestations of urate deposition appear to be consequences of faulty uric acid metabolism. It may be caused by severe dieting or starvation, excessive intake of foods that are high in purines (shellfish, organ meats, beans) or heredity.

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Secondary hyperuricemia, gout is a clinically manifested secondary to any of a number of hereditary or acquired processes, including conditions in which there is an increase in cell turnover (leukemia, multiple myeloma, type of anaemia or psoriasis) and an increase in cell breakdown. Altered renal tubular function, either as a major action or as an unintended side effect of certain medications (e.g. diuretics such as thiazides and furosemide), low-dose salicylates or ethanol, can contribute to uric acid underexcretion.

Pathophysiology of Gout

Hyperuricemia (serum concentration greater than 7mg/dl) can but does not always cause urate crystal deposition. However, as uric acid levels increase, the risk becomes greater. Attacks of gout seem to be related to sudden increase or decrease of serum uric acid levels. When the urate crystals deposits within a joint, an inflammatory process occurs, and an attack of gout begins. With recurrent attacks, accumulation of sodium urate crystals, called Tophi, are deposited in peripheral areas of the body, such as great toe, the hands, and the finger joints. Renal urate kidney stones with chronic renal disease secondary to urate deposition may develop. The finding of urate crystals in the synovial fluid of asymptomatic joints suggests that factors other than crystals may be related to the inflammatory reaction.

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Signs and symptoms of Gout

The clinical features of the gout syndrome include acute gouty arthritis  (recurrent attacks of severe articular and periarticular inflammation), tophi (crystalline deposits accumulating in articular tissue, osseous tissue, soft tissue, and cartilage), gouty renal impairment and uric acid urinary calculi. The four stages of gout can be identified:

  1. Asymptomatic Hyperuricemia
  2. Acute gouty arthritis
  3. Intercritical Gout
  4. Chronic tophaceous gout

The subsequent development of gout is directly related to the duration and magnitude of the hyperuricemia. Therefore, the commitment to the Lifelong pharmacologic treatment of hyperuricemia is deferred until there is an initial attack of gout.

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  • Acute arthritis of gout is the most common early sign.
  • The metatarsophalangeal (MTP) joint of the big toe is the most commonly affected; the tarsal area, ankle or knee may also be affected in 90% of patients.
  • The acute attack may be triggered by trauma, alcohol consumption, dieting, medication, surgical stress or illness.
  • Abrupt onset occurs at night, causing severe pain, redness, swelling and warmth over the affected joint.
  • Early attacks tend to subside spontaneously over 3 to 10 days without treatment.
  • The next attack may not come for months or years; in time, attacks tend to occur more frequently, involving more joints and lasting for a longer period.
  • Higher serum concentration of uric acid is associated with tophus formation.
  • Tophi occur in the synovium, olecranon bursa, subchondral bone, infrapatellar and Achilles’ tendons, subcutaneous tissue and overlying joints.
  • Tophi have also have been found in aortic walls, heart valves, nasal and ear cartilage, eyelids, cornea, and sclera.
  • Enlargement of joint may cause a loss of joint motion.
  • Uric acid deposits may cause renal stones and kidney damage.

Diagnostic assessment

  • A definitive diagnosis of gouty arthritis is established by polarised light microscopy of the synovial fluid of the involved joint. Uric acid crystals are seen within the polymorphonuclear leukocytes in the fluid.  
  • Specific treatment is based on the examination of serum uric acid level, 24-hour urinary uric acid excretion, and renal function test.

Medical management

  • The medications used for treating gout include colchicine, an NSAIDs such as indomethacin, or a corticosteroid which is prescribed to relieve an acute attack of gout.
  • Management of hyperuricemia, tophi, joint destruction and renal disorders is usually initiated after the acute inflammatory process has subsided.
  • Uricosuric agents such as probenecid (Benemid), correct hyperuricemia and dissolve deposited urate. When reduction of the serum urate level is indicated, Uricosuric agents are the medications of choice.
  • If the patient has or is at risk for renal insufficiency or renal kidney stones, allopurinol, a xanthine oxidase inhibitor is recommended.
  • Corticosteroids may also be used in patients who have no response to other therapy.
  • If the patient experiences several acute episodes or there is evidence of tophi formation, prophylactic treatment is considered.
  • A new medication, febuxostat (uloric), was approved by FDA in 2009 for the treatment of gout that does not respond to usual treatment.

Nursing care

  • Although severe dietary restriction is not that necessary, the nurse should encourage the patient to restrict consumption of foods containing high purines, especially organ meats (liver, red meat), beans and to limit alcohol intake or if the possible complete cessation of alcohol.
  • Maintenance of normal body weight should be encouraged.
  • In an acute episode of gouty arthritis, pain management with prescribed medications is essential.
  • Avoidance of factors that increases pain and inflammation such as trauma, stress, and alcohol.
  • Acute attacks are most effectively treated if therapy is begun early in the course.
  • Encourage to drink plenty of water for the stability of uric acid levels which tends to increase if the water is less in the body.
  • Rest of the joints is suggested.
  • Use of cold compression on the joints for 20 to 30 minutes for few days, if the pain is not that bad.
  • Refer to the home remedies if you are not satisfied with the medical management which includes dietary Intake and different types of work out to relieve the pain in joints.

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