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      Drugs & Diseases > Rheumatology

      Gout and Pseudogout Clinical Presentation

      Updated: Aug 29, 2023
      • Author: Bruce M Rothschild, MD; Chief Editor: Herbert S Diamond, MD  more...
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      Presentation

      History

      The spontaneous onset of excruciating pain, edema, and inflammation in the metatarsal-phalangeal joint of the great toe (podagra; see the image below) is highly suggestive of acute crystal-induced arthritis. Podagra is the initial joint manifestation in 50% of gout cases; eventually, it is involved in 90% of cases. Podagra is not synonymous with gout, however: it may also be observed in patients with pseudogout, sarcoidosis, gonococcal arthritis, psoriatic arthritis, and reactive arthritis.

      Gout. Acute podagra due to gout in elderly man. Gout. Acute podagra due to gout in elderly man.
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      Other than the great toe, the most common sites of gouty arthritis are the instep, ankle, wrist, finger joints, and knee. In early gout, only 1 or 2 joints are usually involved. Consider the diagnosis in any patient with acute monoarticular arthritis of any peripheral joint except the glenohumeral joint of the shoulder.

      The most common sites of pseudogout arthritis are large joints, such as the knee, wrist, elbow, or ankle. Case reports have documented carpal tunnel syndrome as an initial presentation of pseudogout. Case reports of calcium pyrophosphate (CPP) crystals forming masses in the spinal ligamentum flavum have been documented. [87] These have led to both single-level and multilevel myelopathy.

      Although crystal-induced arthritis is most commonly monoarticular, polyarticular acute flares are not rare, and many different joints may be involved simultaneously or in rapid succession. Multiple joints in the same limb often are involved, as when inflammation begins in the great toe and then progresses to involve the midfoot and ankle.

      Gout attacks begin abruptly and typically reach maximum intensity within 8-12 hours. Affected joints are red, hot, and exquisitely tender; even a bed sheet on the swollen joint is uncomfortable. The onset of symptoms in pseudogout can resemble acute gout or be more insidious and may occur over several days.

      Untreated, the first attacks resolve spontaneously in less than 2 weeks. A history of intermittent inflammatory arthritis, in which the joints return to normal between attacks, is typical of crystalline disorders and is characteristic of gouty arthritis early in its course.

      Gout initially presents as polyarticular arthritis in 10% of patients. Elderly women, particularly women with kidney insufficiency who are taking a thiazide diuretic, can develop polyarticular arthritis as the first manifestation of gout. These attacks may occur in coexisting Heberden and Bouchard nodes. Such patients may also develop tophi more quickly, occasionally without prior episodes of acute gouty arthritis. [88, 89, 90]

      The pattern of symptoms in untreated gout changes over time. The attacks can become more polyarticular. More proximal and upper-extremity joints become involved. Attacks tend to occur more frequently and last longer.

      Eventually, patients may develop chronic polyarticular arthritis, sometimes nearly symmetrical, that can resemble rheumatoid arthritis. Indeed, chronic polyarticular arthritis that began as an intermittent arthritis should prompt consideration of a crystalline disorder in the differential diagnosis.

      Acute flares of gout can result from situations that lead to increased levels of serum uric acid, such as the consumption of beer or liquor, overconsumption of foods with high purine content, trauma, dehydration, or the use of medications that elevate levels of uric acid. Acute flares of gout also can result from situations that lead to decreased levels of serum uric acid, such as the use of radiocontrast dye or medications that lower the levels of uric acid, including allopurinol and uricosurics. (See Overview/Etiology.)

      Patients with gout have as much as 1000 times more uric acid in the body as unaffected individuals do and are almost twice (1.97 times) as likely to develop renal stones as healthy individuals are [91] ; therefore, they may have a history of renal colic and hematuria. Indeed, renal stones may precede the onset of gout in 14% of affected patients. Whereas 52% of these patients may have stones composed entirely of uric acid, 20% may develop calcium oxalate or sometimes calcium phosphate stones. [92]

      Because gout is frequently present in patients with the metabolic syndrome (eg, insulin resistance or diabetes, hypertension, hypertriglyceridemia, and low levels of high-density lipoproteins) and because the presence of these associated disorders can lead to coronary artery disease, these problems should be sought and treated in patients diagnosed with gout.

      It is important to ask about a history of peptic ulcer disease, kidney disease, or other conditions that may complicate the use of the medications used to treat gout.

      Fever, chills, and malaise do not distinguish cellulitis or septic arthritis from crystal-induced arthritis, because all 3 illnesses can produce these signs and symptoms. A careful history may uncover risk factors for cellulitis or septic arthritis, such as possible exposure to gonorrhea, a recent puncture wound over the joint, or systemic signs of disseminated infection.

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      Physical Examination

      Patients experiencing an acute attack of gout or pseudogout most often present with involvement of a single joint. However, all joints must be examined to determine whether the patient’s arthritis is monoarticular or polyarticular. Involved joints have all the signs of inflammation: swelling, warmth, erythema, and tenderness.

      The erythema over the joint may resemble cellulitis; the skin may desquamate as the attack subsides. The joint capsule becomes quickly swollen, resulting in a loss of range of motion of the involved joint.

      Patients may be febrile during an acute gout attack, particularly if it is polyarticular. However, it is important to look for sites of infection that may have seeded the joint and caused an infectious arthritis resembling or coexisting with acute gouty arthritis.

      Migratory polyarthritis is a rare presentation. Polyarticular gout commonly involves the small joints of the fingers and toes, as well as the knees. An inflammatory synovial effusion may be present. Uncommonly, acute gout may present as carpal tunnel syndrome.

      Posterior interosseous nerve syndrome is a rare compression neuropathy that manifests as inability to extend the fingers actively. The syndrome has been reported in a patient with elbow swelling from an attack of pseudogout; in this case, treatment with intra-articular steroids led to resolution of the nerve palsy. [93]

      Patients with established gout may have chronic arthritis. Affected joints evidence tenderness and swelling, with or without redness, warmth, or joint damage.

      Tophi

      Although gout typically causes joint inflammation, it can also cause inflammation in other synovial-based structures, such as bursae and tendons. Tophi are collections of urate crystals in the soft tissues. They tend to develop after about a decade in untreated patients who develop chronic gouty arthritis. Tophi may develop earlier in older women, particularly those receiving diuretics. [88, 89, 90]

      Tophi are classically located along the helix of the ear, but they can be found in multiple locations, including the fingers, the toes, the prepatellar bursa, and along the olecranon, where they can resemble rheumatoid nodules (see the images below). Rarely, a creamy discharge may be present. [94, 95] The finding of an apparent rheumatoid nodule in a patient with a negative rheumatoid factor assay or a history of drainage from a nodule should prompt consideration of gout in the differential diagnosis. [96]

      Gout. Tophaceous deposits in ear. Gout. Tophaceous deposits in ear.
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      Gout. Tophaceous deposits on elbow. Gout. Tophaceous deposits on elbow.
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      Gout. Chronic tophaceous gout in untreated patient Gout. Chronic tophaceous gout in untreated patient with end-stage renal disease.
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      Eye involvement

      The folklore surrounding gout has also involved the eye, and before the 20th century, a myriad of common and unusual ocular symptoms were falsely ascribed to gout. Medical science has since documented eye involvement as a rare but definite aspect of gout. All manifestations of gout in the eye are secondary to deposition of urate crystals within the ocular tissue. [97, 98]

      Tophi have been described in the eyelids. [99, 100, 101] Conjunctival nodules containing needlelike crystals have been described within the interpalpebral areas, sometimes associated with a mild marginal keratitis. Band keratopathy with refractile, yellow crystals in the deep corneal epithelial cells and at the level of the Bowman membrane are not uncommon. [102]

      Blurring of vision from the corneal haze or a foreign body sensation due to epithelial breakdown may occur. Gout rarely can be associated with anterior uveitis; Duke-Elder mentions this as a cause of hemorrhagic iritis in his classic Text Book of Ophthalmology. Scleritis and tendinitis have also been described. Besides the cornea, the iris, anterior chamber, lens, and sclera have been found to harbor urate crystals; on postmortem examination, urate crystals have also been found in tarsal cartilage and in the tendons of extraocular muscles. [97, 98]

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      Complications

      Complications of gout include the following:

      • Severe degenerative arthritis
      • Secondary infections
      • Urate or uric acid nephropathy
      • Increased susceptibility to infection
      • Urate nephropathy
      • Renal stones
      • Nerve or spinal cord impingement [103, 104]
      • Fractures in joints with tophaceous gout [105]

       Calcification of the atlas transverse ligament has been reported in 44-70% of individuals with calcium pyrophosphate disease (CPPD), with frequency increasing with age. [106]  A significantly elevated rate of non-union of type II and III odontoid fractures has been reported in patients with CPPD (90.3%, versus 32% in controls). [107]

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