What are the symptoms of gout? is a big question to ask.
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Throughout its natural history, gout passes through three stages:
(1) asymptomatic hyperuricemia,
(2) episodes of acute gouty arthritis separated by asymptomatic intervals (termed intercritical or interval gout),
(3) chronic gouty arthritis, the period when tophi often become apparent.
The characteristics of gout pain includes
- rapid onset, reaching maximum severity in 2–6 hours, and often waking the patient in the early morning
- severe pain, often described as the ‘worst pain ever’
- extreme tenderness, such that the patient is unable to wear a sock or to let bedding rest on the joint
- marked swelling with overlying red, shiny skin
- self limiting over 5–14 days, with complete resolution.
Later, attacks may become polyarticular and are associated with fever. Attacks vary in duration but are time limited. Over time, attacks recur at shorter intervals, last longer, and eventually resolve incompletely. This leads to the development of chronic arthritis that slowly progresses to a crippling disease on which acute exacerbations are superimposed.
Asymptomatic hyperuricemia is a condition in which the serum urate level is high, but gout manifested by arthritis or uric acid nephrolithiasis has not yet occurred. Most people with hyperuricemia remain asymptomatic throughout their lifetimes. The tendency toward acute gout increases with the serum urate concentration. The risk of nephrolithiasis increases with the serum urate level and with the magnitude of urinary uric acid excretion. The phase of asymptomatic hyperuricemia ends with the first attack of gouty arthritis or urolithiasis. In most instances, this occurs after at least 20 years of sustained hyperuricemia. Between 10% and 40% of gouty subjects have one or more attacks of renal colic before the first articular event.
ACUTE GOUTY ARTHRITIS
The first attack of acute gouty arthritis usually occurs between age 40 and 60 years in men and after age 60 in women. Onset before age 25 should raise the possibility of an unusual form of gout, perhaps one related to a specific enzymatic defect that causes marked purine overproduction, an inherited renal disorder, or the use of cyclosporine.
A single joint is involved in about 85% to 90% of first attacks, with the first metatarsophalangeal joint being the most commonly affected site. The initial attack is polyarticular in 3% to 14%. Acute gout is predominantly a disease of the lower extremities, but eventually, any joint of any extremity may be involved. Ninety percent of patients experience acute attacks in the great toe at some time during the course of their disease. Next in order of frequency are the insteps, ankles, heels, knees, wrists, fingers, and elbows. Acute attacks rarely affect the shoulders, hips, spine, sacroiliac joints, sternoclavicular joints, acromioclavicular joints, or temporomandibular joints. Acute gouty bursitis, tendinitis, or tenosynovitis can also occur. Urate deposition and subsequent gout appear to have a predilection for previously damaged joints, such as in Heberden’s nodes of older women.
Some patients report a history of short, trivial episodes of “ankle sprains,” sore heels, or twinges of pain in the great toe before the first dramatic gouty attack. In most patients, however, the initial attack occurs with explosive suddenness and commonly begins at night after the individual has gone to sleep feeling well. Within a few hours of onset, the affected part becomes hot, dusky red, swollen, and extremely tender. Occasionally, lymphangitis may develop. Systemic signs of inflammation may include leukocytosis, fever, and elevation of the erythrocyte sedimentation rate. Radiographs usually show only soft tissue swelling during early episodes.
The course of untreated acute gout is highly variable. Mild attacks may subside in several hours or persist for only a day or two and never reach the intensity described for the classic attack. Severe attacks may last days to weeks. The skin over the joint often desquamates as the erythema subsides. With resolution, the patient becomes asymptomatic and enters the intercritical period.
Drugs may precipitate acute gout by either increasing or decreasing serum urate levels acutely. The occurrence of gout after the initiation of antihyperuricemic therapy is well established. In fact, the more potent the urate-lowering effect, the more likely there is to be an acute attack. Drug-induced gout secondary to increased serum urate levels occurs on occasion with diuretic therapy, intravenous heparin, and cyclosporine. Diuretic therapy in the elderly appears to be a particularly important precipitating factor for gouty arthritis. Other provocative factors include trauma, alcohol ingestion, surgery, dietary excess, hemorrhage, foreign protein therapy, infections, and radiographic contrast exposure. The risk of a patient with gout developing an attack during hospitalization is 20%.
The definitive diagnosis of gout is best established by aspiration of the joint and identification of intracellular needle-shaped crystals that have negative birefringence with compensated polarized light microscopy.
However, criteria have been proposed for a presumptive diagnosis. These include the triad of acute monarticular arthritis, hyperuricemia, and a dramatic response to colchicine therapy. There are limitations to using either of these schemes. First, although the diagnosis of acute gouty arthritis can be strongly suggested by the typical presentation, not all inflammation of the great toe (podagra) in hyperuricemic patients is caused by gout. Second, some patients with gout are normouricemic at the time of an acute attack, a phenomenon related to alcohol use or a consequence of interleukin (IL)-6 generation by the acute inflammatory process. Third, diseases other than gout can occasionally improve with colchicine therapy; these include pseudogout, hydroxyapatite calcific tendinitis, sarcoid arthritis, erythema nodosum, serum sickness, rheumatoid arthritis, and familial Mediterranean fever. Finally, the simultaneous presence of both gout and septic arthritis can be confusing clinically, with the former masking the latter.
Criteria for the Classification of Acute Gouty Arthritis
|The presence of characteristic urate crystals in the joint fluid, or a tophus proved to contain urate crystals by chemical means or polarized light microscopy, or the presence of 6 of the following 12 clinical, laboratory, and radiographic phenomena:|
|More than one attack of acute arthritis|
|Maximal inflammation developed within 1 day|
|Attack of monarticular arthritis|
|Joint redness observed|
|First metatarsophalangeal joint painful or swollen|
|Unilateral attack involving first metatarsophalangeal joint|
|Unilateral attack involving tarsal joint|
|Asymmetric swelling within a joint (radiograph)|
|Subcortical cysts without erosions (radiograph)|
|Negative culture of joint fluid for microorganisms during attack of joint inflammation|
The terms intercritical gout and interval gout have been applied to the periods between gouty attacks. Some patients never have a second attack. However, most patients suffer a second attack within 6 months to 2 years. The frequency of gout attacks usually increases over time in untreated patients. Later attacks have a less explosive onset, are polyarticular, become more severe, last longer, and abate more slowly. Nevertheless, recovery is complete. Radiographic changes may develop during the intercritical period despite no sign of tophi on physical examination. These changes are more likely in patients with more severe hyperuricemia and more frequent acute attacks.
The diagnosis of gout in a hyperuricemic patient with a history of acute attacks of monarthritis may be difficult or inconclusive during the intercritical phase. Aspiration of an asymptomatic joint, however, can be a useful adjunct in the diagnosis of gout if urate crystals are demonstrated. Joint fluids obtained from gouty patients during the intercritical phase revealed monosodium urate crystals in 12.5% to 90% of joints. Such crystals in asymptomatic joints are often associated with mild synovial fluid leukocytosis, which suggests the potential to contribute to joint damage even in the intervals between attacks.
CHRONIC GOUTY ARTHRITIS
Eventually, the patient may enter a phase of chronic polyarticular gout with no pain-free intercritical periods. At this stage, gout may be easily confused with other types of arthritis or other conditions. The time from the initial attack to the beginning of chronic symptoms or visible tophaceous involvement is highly variable in studies of untreated patients. Some reports say intervals are ranging from 3 to 42 years, with an average of 11.6 years between the first attack and the development of chronic arthritis. Ten years after the first attack, about half the individuals were still free of obvious tophi, and most of the remainder had only minimal deposits. Thereafter, the proportion of those with nontophaceous involvement slowly declined, to 28% after 20 years. Two percent of the patients had severe crippling disease some 20 years after the initial attack.
The rate of formation of tophaceous deposits correlates with both the degree and the duration of hyperuricemia. The principal determinant is the serum urate level. Some researchers found the mean serum urate concentration to be >9.1 mg/dL in many patients without tophi. The rate of tophus formation also increases with the severity of renal disease and the use of diuretics.
Tophaceous gout is the consequence of the chronic inability to eliminate urate as rapidly as it is produced. As the urate pool expands, deposits of urate crystals appear in cartilage, synovial membranes, tendons, soft tissues, and elsewhere. Tophi are rarely present at the time of an initial attack of primary gout; they are more likely to be present in gout secondary to myeloproliferative diseases, in juvenile gout-complicating glycogen storage diseases, in Lesch-Nyhan syndrome, or after allograft transplantation in patients treated with cyclosporine.
Tophi can occur in a variety of locations. Tophaceous deposits may produce irregular, asymmetric, moderately discrete tumescence of the fingers, hands, knees, or feet. Tophi also form along the ulnar surfaces of the forearm, as saccular distentions of the olecranon bursa, in the antihelix of the ear, or as fusiform enlargements of the Achilles tendon. The process of tophaceous deposition advances insidiously. Although the tophi themselves are relatively painless, acute inflammation can occur around them. Eventually, extensive destruction of the joints and large subcutaneous tophi may lead to grotesque deformities, particularly of the hands and feet, and to progressive crippling. The tense, shiny, thin skin overlying the tophus may ulcerate and extrude white, chalky, or pasty material composed of urate crystals. Secondary infection of tophi is rare. Tophi can produce a marked limitation of joint movement by involvement of the joint structure directly or of a tendon serving the joint. Any joint can be involved, although those of the lower extremity are affected primarily. Spinal joints do not escape urate deposition, but acute gouty spondylitis is unusual.
Musculoskeletal Manifestations of Crystal-Induced Arthritis:
Acute mono- or polyarthritis: -Destructive arthropathies
Bursitis: – Pseudo-rheumatoid arthritis
Tendinitis: – Pseudo-ankylosing spondylitis
Enthesitis: – Spinal stenosis
Tophaceous deposits:-Crowned dens syndrome
Peculiar type of osteoarthritis:-Carpal tunnel syndrome
Synovial osteochondromatosis:-Tendon rupture
Symptoms related to nerve or spinal cord compression by tophi have rarely been observed. Tophi rarely occur in myocardium, valves, cardiac conduction system, various parts of the eye, and larynx. Long standing hyperuricemia may cause renal stones and renal failure.
The serum uric acid is elevated (> 7.5 mg/dL) in 95% of patients who have serial measurements during the course of an attack. However, a single uric acid determination is normal in up to 25% of cases, so it does not exclude gout, especially in patients taking urate lowering drugs. Identification of sodium urate crystals in joint fluid or material aspirated from a tophus establishes the diagnosis. The crystals, which may be extracellular or found within neutrophils, are needle-like and negatively birefringent when examined by polarized light microscopy. A biochemical screen, including renal function, uric acid, glucose and lipid profile, should be performed because of the association with metabolic syndrome. Elevated ESR and CRP and a neutrophilia are typical of acute gout, and they return to normal as the attack subsides.
Early in the disease, radiographs show no changes. Later, punched-out erosions with an overhanging rim of cortical bone (“rat bite”) develop. When these are adjacent to a soft tissue tophus, they are diagnostic of gout.