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Clinical Presentation
Initial gout attacks are usually monoarthric. However, polyarthric attacks can also occur.
More than 75 percent of acute gout attacks affect a joint in the lower extremity, especially the first metatarsophalangeal joint.
Podagra, an acute attack of gout in
the great toe, accounts for over 50 percent of all acute attacks.
Approximately 85 to 90 percent of patients with gout experience podagra at some
point in the disease.
Patients with recurrent attacks of gout have a longer duration of illness and
are more likely to have polyarthric disease.
Joint involvement in polyarthric attacks appears to have an ascending, asymmetric pattern. In addition to the great toe, other areas affected include the insteps, heels, ankles, knees, fingers, wrists and elbows.
Recurrent attacks: poly-articular gout, usually more severe, more prolonged and associated with fever
May be difficult to differentiate from other inflammatory arthropathies or infection
Joint erosions: chronic pain, stiffness and deformity
Tophi may appear around joints, olecranon and pinna of the ear
May ulcerate through the skin: discharge chalky material
Only a minority of patients develop visible tophi, permanent joint changes or chronic symptoms
Renal calculi may form and parenchymal renal disease occur secondary to crystal deposition with some renal dysfunction occurring in 90% of patients with gouty arthritis
In 10% gout is preceded by nephrolithiasis
Typically the first attack occurs during the night and tends to subside after 3 - 10 days
Tophi generally noted an average of 10 years after the first attack
Acute Gouty Arthritis
Sudden attack of joint pain lasting several days
May follow trauma, surgery, drugs, exercise or alcohol
Commonly affects MTP joint of great toe (at least 50% of initial attack and 90% at some stage), also ankle and finger joints and the olecranon bursa
Joints feel hot and extremely tender
Hyperuricaemia is present at some stage
7% never have a second attack
60% recurrent attack within one year
Negative birefringent crystals are seen in synovial fluid
X-Rays: Soft tissue swelling
Acute gouty arthritis attacks may occur without provocation, or they may be precipitated by a number of conditions that raise uric acid levels.
Modifiable risk factors for gout attacks include alcohol consumption, obesity, hypertension and occupational and environmental exposure to lead.
Any abrupt change in the serum uric acid concentration may provoke an acute attack of gouty arthritis. Fluctuations in the serum acid concentration may occur in persons who are fasting, who consume binge amounts of alcohol or who ingest large amounts of protein and purine-rich foods (e.g., bacon, salmon, sweetbreads, scallops, turkey).
The chief complaint associated with an acute attack of gout is agonizing pain accompanied by signs of inflammation, including swelling, erythema, warmth and tenderness.
A low-grade fever may occur in conjunction with the inflammation. Acute attacks usually peak within one to two days of symptom onset. Untreated attacks may last seven to 10 days.
Most acute gout attacks occur in a lower extremity joint, often the first metatarsophalangeal joint.
Attacks usually start during the night, and moderate pain in a joint is first noticed. The pain becomes persistently worse and has a continuous, gnawing quality. The joints in the great toe and other parts of the lower extremity are generally the first articulations to be affected.
These joints are common sites of attack because of lower body temperature and decreased monosodium urate solubility. Lower extremity trauma can also lead to an attack.
Trauma induced in weight-bearing joints as a result of routine activities causes synovial effusions during daytime hours. At night, water is reabsorbed from the joint spaces, leaving a supersaturated concentration of monosodium urate.
Pain and inflammation are produced when uric acid crystals activate the humoral and cellular inflammatory processes. Because an acute attack begins suddenly, the swelling, erythema and tenderness in a joint may be misdiagnosed as septic arthritis or cellulitis.
Interval Gout
Interval or intercritical gout is the condition that occurs after the acute attack has resolved and the patient has become asymptomatic. At this point, the physician usually decides whether or not to initiate prophylactic hyperuricemic therapy.
Generally, patients with hyperuricemia and recurrent attacks, chronic gout, tophi, gouty arthritis or nephrolithiasis should be treated.
Some investigators argue that the first attack of acute gouty arthritis is grounds for the initiation of hyperuricemic treatment. Others contend that a first attack is easily treated and recommend withholding prophylactic therapy until additional attacks occur.
Tophaceous Gout
Tophi are nodular masses of monosodium urate crystals deposited in the soft tissues of the body. They are a late complication of hyperuricemia.
Rarely, tophi can develop without previous acute gouty arthritis. The most common sites of urate deposition are the base of the great toe, and the fingers, wrist, hand, olecranon bursae and Achilles tendon.
Tophi occur, on average, approximately 12 years after the initial attack (reported range: three to 42 years after initial symptoms).
Complications of tophi include pain, soft tissue damage and deformity, joint destruction and nerve compression syndromes such as carpal tunnel syndrome.
Renal Manifestations
The three renal complications of gout are nephrolithiasis and acute and chronic gouty nephropathy.
Nephrolithiasis occurs in approximately 10 to 25 percent of patients with primary gout. The solubility of uric acid crystals increases as the urine pH becomes more alkaline. Acidic urine saturated with uric acid crystals may result in spontaneous stone formation.
Other types of stones may also develop, because uric acid can act as a nidus for calcium oxalate or phosphate stones.
Acute gouty nephropathy usually results from the massive malignant cell turnover that occurs with the treatment of myeloproliferative or lymphoproliferative disorders.
The blockage of urine flow secondary to the precipitation of uric acid in the collecting ducts and ureters can lead to acute renal failure.
Long-term deposition of crystals in the renal parenchyma can cause chronic urate nephropathy. The formation of microtophi causes a giant cell inflammatory reaction. This results in proteinuria and inability of the kidney to concentrate urine.
Diagnostic Evaluation
The temptation to treat patients without a proven diagnosis must be resisted. Unrecognized septic arthritis can lead to loss of life or of limb. Distinguishing septic arthritis from crystal-induced arthritis is not possible without an examination of joint fluid.
Diagnostic arthrocentesis is indicated for every patient with new onset of acute monoarthritis or in whom a diagnosis has never been proven by joint aspiration and for those in whom a possibility of septic arthritis exists, it is strongly recommended for those with recurrent attacks whose diagnosis has never been proven by microscopic visualization of crystals
A prior history of gout or pseudo gout does not rule out the possibility of acute septic arthritis.
Septic arthritis must be diagnosed and treated promptly.
Irreversible damage can occur within 4-6 hours, and the joint can be completely destroyed within 24-48 hours.
Joint fluid analysis
Send joint fluid for fluid analysis, including cell count and differential, Gram stain, culture and sensitivity, and microscopic analysis for crystals. If crystals are seen, their shape and appearance under polarized light can aid in diagnosis.
In gout, crystals of MSU appear as needle-shaped intracellular and extracellular crystals. When examined with a polarizing filter, they are yellow when aligned parallel to the axis of the red compensator, but they turn blue when aligned across the direction of polarization (ie, they exhibit negative birefringence).
In pseudo gout, CPP crystals appear shorter and often rhomboidal. Under a polarizing filter, CPP crystals do not change color depending upon their alignment relative to the direction of the red compensator.
In crystal arthritis, the WBC count in the joint fluid is usually 50,000-100,000.
Even in the presence of crystals in the joint fluid, blood cultures are indicated if any sign of systemic toxicity is present. Septic arthritis can occur in patients with active crystalline arthropathy.
Pseudo gout attacks can be triggered by many metabolic abnormalities. Thus, patients who have an initial attack of arthritis with CPP crystals should have a workup including a chemistry screen; magnesium, calcium, and iron levels; and thyroid function tests.
White blood cell (WBC) count usually is elevated.
Erythrocyte sedimentation rate (ESR) usually is elevated during acute attacks.
Hyperuricemia may be present but is not diagnostic.
Because patients with gout typically have hypertension and impaired renal function, examination of the renal and cardiovascular systems is essential. Baseline laboratory tests should include a complete blood cell count, urinalysis, and serum creatinine, blood urea nitrogen and serum uric acid measurements.
Because an acute gout attack may be associated with edema, erythema, warmth and tenderness, the differential diagnosis includes septic arthritis and cellulitis.
The diagnosis of gout is confirmed by the presence of polymorphonuclear leukocytes and intracellular monosodium urate crystals in synovial fluid aspirated from an inflamed joint. Gouty attacks are triggered by crystal formation in synovial fluid. They are not related to serum levels of uric acid.
Examination of aspirated joint fluid can also rule out other disorders that mimic gout, such as septic arthritis and pseudo gout.
Occasionally, patients with gout may present without uric acid crystals in the synovial fluid aspirate. However, aspiration repeated five hours to one day later shows crystals in the synovial fluid of most of these patients
The goals of therapy are early resolution of inflammation, prevention of recurrent attacks, and reversal of complications arising from deposition of urate crystals in joints, kidneys, and tophi.
The treatment approach consists of medications to
treat the acute attack,
prevent future attacks, and
lower uric acid levels.
Acute attacks may be terminated with the use of nonsteroidal anti-inflammatory agents, colchicine or intra-articular injections of corticosteroids.
Probenecid, sulfinpyrazone and allopurinol can be used to prevent recurrent attacks.
In addition, attention should be given to controlling conditions commonly associated with gout (eg, Obesity, alcohol intake and certain foods and medications can contribute to hyperuricemia, hyperlipidemia) and modifying diet and other factors that contribute to the disease. These potentially exacerbating factors should be identified and modified.
Dosage adjustments may be needed in patients with renal insufficiency, liver disease, cardiac disease, peptic ulcer disease, allergies, bleeding diatheses, hypertension, or diminished oral intake.
Treatment of asymptomatic hyperuricemia usually is not necessary. However, prophylactic urate-lowering therapy is mandatory for clinical conditions that promote hyperuricemia (eg, lymphoproliferative diseases).
The above opinionated views and information serves to educated and informed consumer . The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition. .It should not replaced professional advise and consultation.A licensed physician should be consulted for diagnosis and treatment of any and all medical conditions
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