Special Feature

Nontraumatic Monoarticular Arthritis-Evaluation and Management

By Frederic Kauffman, MD, FACEP

Case: a 50 year-old male with a history of alcohol abuse presents to the ED at 3:00 a.m. with a 12-hour history of severe pain and swelling in his right knee. The pain is excruciating, and even the weight of his bed sheet worsens the pain. He denies a history of trauma, fevers, chills, other joint involvement, or rash. He does recall that, one year prior to admission, he developed severe pain in his right great toe that prevented him from walking but not drinking; the "attack" lasted seven-to-10 days and resolved without therapy. The patient takes no medications.

Physical examination reveals normal vital signs and temperature. All joints are normal except for the right knee, which is warm and erythematous; a large joint effusion is present, and range of motion is severely limited by pain. Skin examination reveals no rash or evidence of trauma, and genital examination reveals no penile discharge.

What is the differential diagnosis for nontraumatic monoarticular arthritis?

Monoarticular arthritis must be evaluated on an urgent basis since septic arthritis is listed first on the "worst is first" differential diagnosis. Other entities that commonly involve only a single joint include gout, pseudogout, and osteoarthritis.1

Why is a septic joint a medical emergency?

Nongonococcal bacterial arthritis may lead to joint destruction within 48 hours of onset if not properly diagnosed and treated.2 Gonococcal arthritis, which classically presents in a migratory fashion rather than a true monoarticular fashion, is less destructive and amenable to more conservative management.

How are bacteria introduced into a joint?

A septic joint may develop due to hematogenous spread of bacteria from other sources such as, introduction of bacteria from local sources such as skin or bone (osteomyelitis); direct open trauma; or from surgery/arthrocentesis.3

Who tends to get septic arthritis?

Immunocompromised patients are classically at risk, and include the aged, the very young, diabetics, alcoholics, patients with chronic renal failure, patients on immunosuppressive drugs, IV drug users, and patients with chronic and severe debilitating illnesses. In addition, patients with prosthetic joints are also at risk.3

What organisms tend to cause septic arthritis?

Staphylococcus aureus is the most common cause of septic arthritis overall. Infants may become infected with Gram-negative organisms, particularly Escherichia coli. Young children are predisposed to Haemophilus influenza infection, although routine Hib vaccination has made this etiology much less common. Sickle cell patients are at risk for septic arthritis caused by Salmonella. Patients with prosthetic joints may become seeded by Staphylococcus epidermidis, and intravenous drug users may develop septic arthritis from a multitude of organisms, including methicillin-resistant Staphylococcus and Gram-negatives such as Pseudomonas, Klebsiella, and Serratia.1

In addition to antibiotics, what other measures are crucial to the management of septic arthritis?

Antibiotics, based upon likely causative organisms and information obtained from Gram's stain of joint fluid, should be started urgently. In addition, proper joint drainage, not only at the time of presentation, but also on a daily basis, is imperative if joint destruction and long-term complications are to be avoided. Initial drainage often includes incision and drainage, with subsequent daily aspiration by large-bore needle or via arthroscopy with a drain.4

By history, what is the most likely diagnosis in the case presented?

Patients with gouty arthritis often have a history of alcohol consumption and a complaint of severe monoarticular joint pain and swelling that is so severe that minimal weight or touch produce excruciating pain. Although fever may be present, thereby mimicking septic arthritis, it often is not. As many as 75% of patients develop acute arthritis in the great toe metatarsal-phalangeal (MTP) joint.5 Typical joint involvement includes the great toe MTP joint, tarsal joints, ankle, and knee. Most patients with gout have monoarticular involvement. For all of these reasons, the most likely diagnosis in this case is acute gouty arthritis.

How is the diagnosis of gout made?

A compatible history, along with a physical exam revealing a monarticular arthritis, suggests the possibility of gout. Definitive diagnosis is made by demonstrating negatively birefringent crystals in the joint fluid, with an absence of bacteria by Gram's stain. If concerns still exist for septic arthritis, joint fluid culture must also be negative.

What is pseudogout?

Pseudogout may present in monoarticular or polyarticular symmetric fashion. The entity is caused by deposition of calcium pyrophosphate dihydrate crystals in articular hyaline or fibrocartilaginous tissue. Crystal shedding into the joint space results in acute inflammation, producing a clinical attack. Radiographic joint evaluation may reveal calcification in the joint, along with tendon insertions, ligaments, and bursae. Pseudogout usually has no underlying cause but may be seen in patients with hyperparathyroidism, hemochromatosis, hypothyroidism, hypomagnesemia, hypophosphatemia, and Wilson's Disease.6 Joint fluid analysis reveals positively birefringent crystals, which are blunted at the ends and less needle-like in appearance than gout crystals.

Can gout present in a polyarticular fashion?

Although classically a monoarticular arthritis, gout may present in a polyarticular fashion in up to 40% of cases.7 Over time, acute gouty attacks may become more frequent and are more likely to be polyarticular in presentation, especially in the elderly. Females are more likely than males to have polyarticular involvement at the time of initial presentation.8

Can gout and septic arthritis be present in the same joint?

Many of the clinical features of gout and septic arthritis overlap. Both are typically monoarticular, and involved joints are warm, erythematous, swollen, and tender. Range of motion is limited. Fever and elevated WBC counts may be present in both disorders. In such cases, joint fluid analysis is crucial to making the correct diagnosis. To rule-in gout, negatively birefringent crystals must be seen in the joint fluid. To rule-out septic arthritis, bacteria must be absent in joint fluid Gram's stain. In equivocal cases, joint fluid cultures should be sent and empiric treatment for septic arthritis instituted pending final culture results. Although uncommon in case-report literature, crystal-induced arthritis (gout and pseudogout) has been reported to coexist with septic arthritis.9 As such, the diagnosis of either entity should not preclude an adequate search for the other.

What is the treatment of an acute gout attack?

Several medical options are available to treat acute gout: colchicine, nonsteroidal antiinflammatory drugs (NSAIDs), and corticosteroids.

Colchicine has the longest history in the management of gout. It is most effective when used within the first 24-48 hours of an acute flare, and it has up to a 90% response rate when used in the first several hours of an attack. Colchicine may be given either orally or via the intravenous route. Gastrointestinal side effects may limit oral use. Colchicine-induced life-threatening granulocytopenia has been seen in the elderly, in patients with renal insufficiency, and after large drug doses administered both orally and intravenously.10

The most commonly used class of drugs for the management of an acute gouty attack is the NSAIDs. Maximum doses are administered at the beginning of an attack, and lowered within 1-2 days until symptomatic resolution. Caution or avoidance in the use of NSAIDs should be used in patients with peptic ulcer diseare, renal insufficiency, or anticoagulation.10

Corticosteroids generally are reserved for patients in whom colchicine and NSAIDs are ineffective or contraindicated. Oral doses equivalent to 20-40 mg prednisone may be given for several days, and then tapered over 1-2 weeks. Intraarticular steroids may also be used with involvement of large joints, as long as septic arthritis has been ruled out.10

The treatment of pseudogout is analogous to that of gout. However, treatment of associated diseases (such as hypothyroidism) will not result in crystal deposit resorption and may precipitate an acute arthritic flare.6

Summary

Nontraumatic monoarticular arthritis is a common entity to be evaluated by emergency physicians. Septic arthritis, if misdiagnosed or not treated promptly, may result in permanent joint destruction. Crystalline-induced acute arthropathy is self-limited, but pain relief can be achieved readily and safely with a thorough knowledge of treatment options.

References

    1. Talbot-Stern JK. Arthritis, tendinitis, and bursitis. In: Rosen P, et al (eds). Emergency Medicine Concepts and Clinical Practice. St. Louis, MO: Mosby-Year Book, Inc. 1998.

    2. Freed HA, et al (eds). Case Studies in Emergency Medicine. Boston, MA: Little Brown and Company 1997.

    3. Mahowald M. Infectious arthritis: Bacterial agents. In: Schumacher HR (ed). Primer on Rheumatic Diseases. Atlanta, GA: Arthritis Foundation 1993.

    4. Mikhail IS, Alarcón GS. Nongonococcal bacterial arthritis. Rheum Dis Clin North Am 1993;19:311.

    5. Tate GA, Schumacher HR. Gout: Clinical and laboratory features. In: Schumacher HR (ed). Primer on Rheumatic Diseases. Atlanta, GA: Arthritis Foundation 1993.

    6. McCarty DJ. Calcium pyrophasphate dihydrate crystal deposition disease. In: Schumacher HR (ed). Primer on Rheumatic Diseases. Atlanta, GA: Arthritis Foundation 1993.

    7. German DC, Holmes EW. Hyperuricemia and gout. Med Clin North Am 1986;70:419.

    8. Agarwal AK. Gout and pseudogout. Primary Care. 1993;20(4):839.

    9. Baer PA, Coexistent septic and crystal arthritis. Report of four cases and literature review. J Rheumatol 1986;13:604.

    10. Terkeltaub RA. Pathogenesis and treatment of crystal-induced inflammation. In: Koopman WJ (ed). Arthritis and Allied Conditions: A Textbook of Rheumatology. Baltimore: Williams and Wilkins 1997.