Gout and Pseudogout Clinical Presentation

Author: Bruce M Rothschild, MD; Chief Editor: Herbert S Diamond, MD more...

Updated: Mar 26, 2012

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History
Physical Examination
Complications
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History

The spontaneous onset of pain, edema, and inflammation in the metatarsal-phalangeal joint of the great toe (podagra) 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.

See the image of acute podagra below.

Gout. Acute podagra due to gout in an elderly man.

Podagra is not synonymous with gout, however. Podagra may be observed in patients with pseudogout, sarcoidosis, gonococcal arthritis, psoriatic arthritis, and reactive arthritis.

Other than the great toe, the most common sites of gouty arthritis are the ankle, wrist, and knee. In early gout, only 1 or 2 joints are usually involved. Consider the diagnosis in any patient with acute monarticular arthritis of any peripheral joint except the glenohumeral joint of the shoulder, in which a crystal-induced arthritis is more likely to be due to pseudogout.

In addition to the shoulder, the most common sites of pseudogout arthritis are the knee and wrist. Case reports have documented carpal tunnel syndrome as an initial presentation of pseudogout. Case reports of pseudogout forming masses in the spinal ligamentum flavum have been documented.^[49]These have led to both single and multi-level myelopathy.

Although crystal-induced arthritis is most commonly monarticular, 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 reach maximum intensity within 8-12 hours. The joints are red, hot, and exquisitely tender; even a bed sheet on the swollen joint is uncomfortable. The onset of symptoms in pseudogout is usually 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 typically caused by 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 renal 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.^{[50, 51, 52]}

The pattern of symptoms in untreated gout changes over time. The attacks become more polyarticular. Although more joints may become involved, inflammation in a given joint may become less intense. More proximal and upper-extremity joints become involved. Attacks 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 diagnoses.

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, hemorrhage, 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.

Patients with gout are profoundly more likely to develop renal stones than are healthy individuals (by a factor of 1000); therefore, they may have a history of renal colic and of hematuria. Indeed, renal stones may precede the onset of gout in 40% of affected patients. While 80% of these patients may have stones composed entirely of uric acid, 20% may develop calcium oxalate or calcium phosphate stones with a uric acid core.

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.

Importantly, ask about a history of peptic ulcer disease, renal 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.

Physical Examination

Patients with an acute attack of gout or pseudogout most often present with involvement of a single joint. However, examine all joints to determine if 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.

During an acute gout attack, patients may be febrile, particularly if it is an attack of polyarticular gout. However, look for sites of infection that may have seeded the joint and caused an infectious arthritis that can resemble or coexist 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.

Chronic arthritis with tenderness and swelling, with or without redness, warmth, or joint damage, may be present.

Posterior interosseous nerve syndrome has been reported because of elbow inflammation causing compression of the nerve. In patients presenting with a swollen elbow and inability to extend the fingers actively, this should be considered. Treatment with intra-articular steroids has led to resolution of the nerve palsy in a case report.^[53]

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 tend to develop earlier in women, particularly those receiving diuretics.^{[50, 51, 52]}

The classic location of tophi is along the helix of the ear but they can be found in multiple locations, including the fingers, toes, prepatellar bursa, and along the olecranon, where they can resemble rheumatoid nodules. Rarely, a creamy discharge may be present.^{[54, 55]}The finding of a rheumatoid nodule in a patient with a negative rheumatoid factor result or a history of drainage from a nodule should prompt consideration of gout in the differential diagnoses.^[56]

See the images of tophaceous gout below.

Gout. Tophaceous deposits in ear.

Gout. Tophaceous deposits on elbow.

Gout. Chronic tophaceous gout in an untreated patient with end-stage renal disease.

Eye involvement

The folklore surrounding gout has also involved the eye, and, prior to the 20th century, a myriad of common and unusual ocular symptoms were falsely ascribed to gout. All manifestations of gout in the eye are secondary to deposition of urate crystals within the ocular tissue.^{[57, 58]}

Tophi have been described in the eyelids.^{[59, 60, 61]}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.^[62]

Symptoms of visual blurring from the corneal haze or foreign body sensation due to epithelial breakdown may occur. Gout rarely can be associated with anterior uveitis and has been mentioned by Duke-Elder in his textbook as a cause of hemorrhagic iritis. Scleritis and tenonitis also have been described. In addition to the cornea, urate crystals have been described clinically in the iris, anterior chamber, lens, and sclera, and, on postmortem examination, in the tarsal cartilage and in the tendons of extraocular muscles.^{[57, 58]}

Complications

Complications of gout include the following:

Severe degenerative arthritis
Secondary infections
Urate or uric acid nephropathy
Nerve or spinal cord impingement
Increased susceptibility to infection
Urate or uric acid nephropathy
Renal stones
Nerve or spinal cord impingement^{[63, 64]}
Fractures^[65]

Proceed to Differential Diagnoses

Contributor Information and Disclosures

Author

Bruce M Rothschild, MD Professor of Medicine, Northeastern Ohio Universities Colleges of Medicine and Pharmacy; Adjunct Professor, Department of Biomedical Engineering, University of Akron; Research Associate, University of Kansas Museum of Natural History; Research Associate, Carnegie Museum

Bruce M Rothschild, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Rheumatology, International Skeletal Society, New York Academy of Sciences, Sigma Xi, and Society of Skeletal Radiology

Disclosure: Nothing to disclose.

Coauthor(s)

Anne V Miller, MD Assistant Professor of Medicine, Division of Rheumatology, Southern Illinois University School of Medicine

Anne V Miller, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Sriya K M Ranatunga, MD, MPH Associate Professor, Department of Clinical Medicine, Southern Illinois University School of Medicine

Disclosure: Nothing to disclose.

Mark L Francis, MD Consulting Staff, Arthritis and Osteoporosis Associates of New Mexico

Mark L Francis, MD is a member of the following medical societies: American College of Rheumatology, Illinois State Medical Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Chief Editor

Herbert S Diamond, MD Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Additional Contributors

Richard W Allinson, MD Associate Professor, Department of Ophthalmology, Texas A&M University Health Science Center; Senior Staff Ophthalmologist, Scott and White Clinic

Richard W Allinson, MD, is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Texas Medical Association