Monoarticular arthritis update: Current evidence for diagnosis and treatment in the emergency department
Department of Emergency Medicine, Mount Sinai School of Medicine, New York, NY, USA.Emergency medicine practice 05/2012; 14(5):1-19; quiz 19-20.
Monoarticular arthritis presentations in the emergency department are increasing as the population ages and gets heavier. Many etiologies--from trauma to infection to autoimmune-mediated inflammation--are associated with significant disability or early mortality, and their treatments are associated with adverse effects. A systematic approach to evaluating patients with monoarticular arthritic complaints is important for relieving pain, diagnosing systemic illness, and unmasking true arthritis emergencies. Septic arthritis is a rapidly destructive process that can cause significant disability in a matter of hours or days, with relatively high mortality. Other causes of monoarticular arthritis may cause disability in the long term. In all cases, accurate diagnosis and appropriate therapies are crucial for resuming activities and preventing long-term deficits. This review examines the diagnosis and treatment of monoarticular arthritis, with a focus on recent evidence in the diagnosis of septic arthritis and new research on gout therapies. Modalities for pain control and new techniques for imaging are discussed.
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ABSTRACT: Arthrocentesis is an essential emergency step in managing patients with acute arthritis. To identify a bacterial infection, Gram staining is performed promptly. However, crystal analysis may not be immediately performed in many facilities. Being considered not to be stable over time, synovial fluid (SF) is sometimes discarded instead of being stored for crystal identification. The aim of this study was to assess the detectability of monosodium urate (MSU) and calcium pyrophosphate (CPP) crystals in SF over a period of 3 days. Consecutive SF samples from 75 joints were analyzed for MSU, CPP crystals, and pH. Two independent observers evaluated the samples by regular light and polarization microscopy immediately after arthrocentesis and after 1, 2, and 3 days at room temperature or at 4°C. Of 75 samples, 27 contained crystals (16 MSU, 6 CPP, 5 both); semiquantitative counts of both MSU and CPP crystals did not change significantly after 3 days. There was no new formation of crystals in any of the crystal-negative samples, which was independent of the storage temperature. Synovial fluid pH was not predictive of crystals and did not change over time. Although immediate workup for microbiology, including Gram stain and culture, is indispensable and well established, crystal analysis may at times not be immediately performed. Our study suggests that when crystal identification cannot be done immediately, it can be safely performed up to 3 days after arthrocentesis when SF is stored at 4°C or even at stable room temperature (20°C).
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ABSTRACT: Acute angioedema represents a cause of admission to the emergency department requiring rapid diagnosis and appropriate management to prevent airway obstruction. Several drugs, including angiotensin-converting enzyme inhibitors (ACE-I), nonsteroidal anti-inflammatory drugs (NSAIDs) and oral antidiabetics, have been reported to induce angioedema. The aim of this prospective observational study conducted in a setting of routine emergency care was to evaluate the incidence and extent of drug-induced non-histaminergic angioedema in this specific clinical setting, and to identify the class of drugs possibly associated with angioedema. Patients admitted to seven different emergency departments (EDs) in Rome with the diagnosis of angioedema and urticaria were enrolled during a 6-month period. Of the 120,000 patients admitted at the EDs, 447 (0.37 %) were coded as having angioedema and 655 (0.5 %) as having urticaria. After accurate clinical review, 62 cases were defined as drug-induced, non-histaminergic angioedema. NSAIDs were the most frequent drugs (taken by 22 out of 62 patients) associated with the angioedema attack. Of the remaining patients, 15 received antibiotic treatment and 10 antihypertensive treatment. In addition, we observed in our series some cases of angioedema associated with drugs (such as antiasthmatics, antidiarrheal and antiepileptics) of which there are few descriptions in the literature. The present data, which add much needed information to the existing limited literature on drug-induced angioedema in the clinical emergency department setting, will provide more appropriate diagnosis and management of this potentially life-threatening adverse event.
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