Acute Joint Pain (Case 44)
Case: A 45-year-old man presents to the emergency department complaining of pain, swelling, and redness in his right knee and inability to walk for 1 day. The symptoms appeared acutely yesterday without any history of trauma. No other joints were painful. He also felt feverish but did not take his temperature; he had no relief with acetaminophen. Past medical history is significant for hypertension controlled with hydrochlorothiazide and a kidney stone 5 years ago. He was recently divorced but has been sexually active, and he has had no recent travel or insect bites. He drinks two to three glasses of wine nightly. There is no family history of arthritis or gout. The review of systems is negative for rash, sore throat, history of heart murmur, recent dental work, inflammatory bowel disease, urethral discharge, or any recent infection. Physical examination shows a temperature of 101°F and a tender, warm, erythematous, swollen right knee.
Nongonococcal septic arthritis
Pseudogout/calcium pyrophosphate dihydrate (CPPD) deposition
When seeing a patient with acute arthritis, it is necessary to think first of the potential emergencies: undiagnosed trauma and septic joint. The former diagnosis, which is handled by orthopedic surgeons, is usually easily eliminated by the physical exam, negative radiographs, and non-bloody joint fluid. Septic joints, which require laboratory confirmation, are an emergency because antibiotics must be initiated quickly and the fluid drained from the joint to reduce the risk of damage from inflammatory mediators and collagenases. Untreated septic joints can show radiographic changes in as little as a week, and there may be irreversible joint damage if drainage is inadequate; the general approach is to treat presumptively while awaiting confirmation by Gram stain and culture.
• In cases in which aspiration of the affected joint is not possible (perhaps because of available resources or experience), treating for the possibility of septic arthritis until a definitive diagnosis can be made is extremely important.
• A prior history of an acute episode of arthritis suggests a crystal-induced process. Fifty percent of gout patients have a first episode in the first metatarsophalangeal (large toe) joint; historically, that classic presentation is called podagra. Middle age (older for women), obesity, alcoholism, thiazide or cyclosporine use, and a family history of gout are all risk factors.
• Fifty percent of first attacks of gout occur in a first metatarsophalangeal joint, the classic presentation called podagra. The knee and ankle are the next most common; upper extremity involvement is rarely seen unless the disease is long-standing.
• Tophi, deposits of uric acid seen in some patients with long-standing untreated gout, are palpable subcutaneous deposits of uric acid usually felt in the olecranon bursa or along the proximal ulnar surface.
• Clinical findings in gonococcal arthritis depend on the stage of the disease. Classically the earlier infection is characterized by a migratory joint pattern where one joint is inflamed but resolves before another is involved. Extensor tenosynovitis of the wrist or ankle is common. There is often a rash in this phase with a very small number of individual pustules, each on an erythematous base. A monoarticular septic joint is considered a later manifestation but often is present at the time of diagnosis.
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Nongonococcal Septic Arthritis
The overwhelming majority of these cases are caused by staphylococci and streptococci as a result of hematogenous dissemination. Acute joint infection can also be the result of trauma to the joint or may have spread from other localized areas where there may be an infection, such as bursitis, overlying cellulitis, or a nearby abscess or osteomyelitis. Rarely, a patient can develop a septic joint as a complication of a diagnostic or therapeutic arthrocentesis via direct inoculation or following use of contaminated tissue allografts. Risk factors for the development of a nongonococcal septic arthritis include rheumatoid arthritis (RA), immunodeficient states, immunosuppressive therapy, diabetes, preexisting joint damage, age, injection drug use, prosthetic joints, indwelling catheters, tissue allograft surgery, and malignancy.
Patients present with pain and limited movement in one joint. The joint is usually red, warm, and swollen, and most patients have accompanying constitutional symptoms such as fever and malaise. The knee is the most commonly affected joint, followed by the hip and ankle.
The gold standard for diagnosis is the isolation of the causative organism in a synovial fluid culture. Arthrocentesis fluid is sent for cell count and differential, Gram stain, and culture. The white blood cell (WBC) count in the fluid is usually >50,000 cells/μL and is mostly made up of neutrophils. A Gram stain is positive in half of the patients at presentation but results depend on the causative organism. Cultures will grow in 80% to 90% of patients and blood cultures are positive in 50% to 70% of patients. Peripheral blood may show an elevated WBC count, erythrocyte sedimentation rate (ESR), or C-reactive protein (CRP). Radiographs are not generally helpful but may show soft-tissue swelling.
Immediately treating the patient with drainage of the affected joint and appropriate IV antibiotics is imperative. A septic arthritis can destroy a joint within the first 24 hours, so many patients with suspected joint infection are treated before the culture results are available to help prevent long-standing joint damage. Initial antibiotic choice is based on the Gram stain and the patient’s underlying disease. Normal individuals are treated with antibiotics to cover gram-positive bacteria; this is usually vancomycin pending in vitro susceptibility testing. Broader spectrum antibiotics (vancomycin plus an agent with coverage against gram-negative bacilli, including Pseudomonas aeruginosa) are reserved for patients with more debilitating illness or immunocompromised states. Daily joint aspirations or definitive surgical drainage is also often necessary in the early stages of the illness. See Cecil Essentials 68.
Neisseria gonorrhoeae is the most common cause of septic arthritis in the United States, especially in young, sexually active people. Joint infection occurs in half of patients with disseminated gonococcal infection (DGI), and it always follows a mucosal infection by the organism. An important host factor that may increase risk of DGI is the presence of terminal complement component deficiency (C5–C8).
This form of septic arthritis is more common in women and in younger patients. The disease has two distinct clinical presentations. The first is a dermatitis–arthritis syndrome that includes rash, fever, bacteremia, and polyarthralgias that are usually asymmetric. There is often a tenosynovitis, usually of the hands and fingers. The rash can be maculopapular, vesicular, pustular, or necrotic on an erythematous base, and it can occur anywhere on the body. The second presentation is that of a frank purulent arthritis usually in a single joint (or less often in a few joints) in the absence of any skin manifestations.
Arthrocentesis with synovial culture is positive in only 50% of monoarticular cases and in <30% of disseminated cases. Polymerase chain reaction is somewhat helpful to distinguish the causative agent (sensitivity of 80% in patients with DGI). Rectal, pharyngeal, and genitourinary tract cultures can also be helpful in identifying the organism.
IV ceftriaxone is the initial treatment of choice for the first 2–4 days, followed by oral therapy with a cephalosporin or a fluoroquinolone (if the organism is sensitive) for 7–10 days. Gonorrhea is highly associated with concomitant chlamydial infection, so oral doxycycline is also given throughout the course of treatment. Patients should be screened and treated for other common STDs. See Cecil Essentials 104.
In patients with a uric acid level > 6.7 mg/dL, monosodium urate supersaturates in the serum and deposits in tissues. Over years this may lead to the development of arthropathy and tophi.
Gout presents as intermittent attacks of joint pain. There is usually redness, swelling, warmth, and significant pain in the joint, sometimes accompanied by fever and chills. Gout commonly presents as a monoarthropathy in the lower extremities. Half of all first episodes of gout occur in the first metatarsophalangeal joint. This presentation is also referred to as podagra.
Definitive diagnosis of gout requires the identification of monosodium urate crystals from a joint or tophus aspirate. The crystals are needle-shaped and can be seen as negatively birefringent with polarized light microscopy. The serum uric acid level often does not correlate with disease and is not useful in diagnosis.
Gout attacks usually last about a week and are often self-limited. Treatments for an acute exacerbation include nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and colchicine. It becomes important to treat underlying hyperuricemia in patients who have had multiple attacks of gout, kidney stones, or the development of tophi. The goal is to lower the uric acid level below 6.0 mg/dL. Allopurinol or febuxostat are the agents of choice to lower uric acid levels in most patients. It is also important to modify risk factors for the disease. This includes limiting alcohol use, restricting dietary purine intake, losing weight, and occasionally discontinuing certain prescription medications (e.g., thiazide diuretics or salicylates). See Cecil Essentials 87.
CPPD crystals form in patients with alterations of inorganic pyrophosphate metabolism and abnormalities in calcium metabolism. CPPD crystals precipitate in cartilage and provoke an inflammatory response. Other conditions commonly associated with CPPD arthritis include hypophosphatemia, hypomagnesemia, hypothyroidism, hemochromatosis, and hyperparathyroidism.
Many patients are asymptomatic, but when the disease presents as an inflammatory arthropathy it mimics the presentation of gout—thus the nickname pseudogout. These attacks are often seen in postsurgical patients or following an illness. Knees and wrists are the most common joints involved.
Diagnosis depends on the presence of weakly positive birefringent CPPD crystals in a joint aspirate. Inflammatory synovial fluid is characteristic of pseudogout. Patients may also have chondrocalcinosis on radiography.
The treatment for CPPD deposition disease is essentially the same as the treatment for acute gout, with NSAIDs as the mainstay of treatment and maintenance therapy with colchicine for some patients. Evaluation for possible associated conditions will be appropriate in some cases. See Cecil Essentials 73.
The most common viral joint pathogens are parvovirus B19, rubella, and hepatitis B and C viruses.
Viral arthritis typically presents as a mild to moderate polyarthritis. Parvovirus B19 usually involves the small joints of the hands and feet and the knees, and may mimic the pattern of RA. It is usually self-limited and sometimes associated with a rash. Acute rubella has a concomitant rash, fever, and lymphadenopathy. Patients can develop a polyarthritis after a rubella vaccination, usually about 2 weeks after immunization.
Parvovirus B19 is diagnosed by the presence of specific serum IgM antibodies. These patients may also develop autoantibodies such as rheumatoid factor and antinuclear antibodies that can persist for years.
Viral arthritis is self-limited and care is supportive, although symptoms can persist for some time. The arthritis is nonerosive in nature. See Cecil Essentials 79, 104.
a. Rarer forms of septic arthritis from tuberculosis and fungi can be seen in immunocompromised patients. These entities, though sometimes accompanied by fever, develop more gradually and inflammation is less intense than with the usual bacterial organisms or crystal-induced arthritides.
b. Patients with chronic renal failure may develop symptoms of acute arthritis from oxalate crystal deposition. Knees or hands are the most characteristic sites for inflammation. In contrast to gout and pseudogout, synovial fluid WBC counts are generally <2000 cells/mm3.