Culture negative endocarditis (CNE) is a common concern in patients with fever, heart murmur, cardiac vegetation, and negative blood cultures. The diagnosis of CNE is not based only on negative blood cultures and a cardiac vegetation. The clinical definition of CNE is based on negative blood cultures plus the findings of culture positive infective endocarditis (IE), e.g., fever, cardiac vegetation, splenomegaly, peripheral manifestations. Because embolic splenic infarcts may occur with culture positive IE, some may assume that splenic infarcts are a sign of CNE. Previously, CNE was due to fastidious and non-culturable organisms. With current diagnostic methods, fastidious organisms grow in 2-3 days. Therefore, fastidious IE are a subset of culture positive IE, but do not represent true CNE. We describe a case of an elderly female who presented with a fever of unknown origin (FUO) and multiple splenic infarcts thought by some to represent CNE. An extensive workup for CNE pathogens was negative. The final cause of her splenic infarcts was a diffuse large B-cell lymphoma (DLBCL). Review of the literature, as well as this case, confirms that splenic infarcts are not a feature of CNE. In patients with fever, splenic infarcts, and negative blood cultures, physicians should search for an alternate explanation rather than CNE, e.g., malignancy and hypercoaguable state (lupus anticoagulant).
Introduction:Patients with Sickle Cell Disease (SCD) have numerous risk factors including but not limited to iron overload, avascular bone necrosis, infection especially acute chest syndrome and frequent pain crisis. Incidence of Clostridium Difficile infection (C. Diff) in sickle cell disease patients is lower than the general population but they are frequently hospitalized for vaso-occlusive crisis and are often given empirical antibiotic treatment which puts them at high risk for C. Diff (1). Here we are describing trends and predictors of C. Diff among SCD patients and how C.diff burgen has changed over the time in Sickle cell patients. Methods:We used National Inpatient Sample (NIS) for the years 2008-2017 by Healthcare Cost and Utilization Project. We extracted a study cohort of all-cause hospitalizations among SCD patients using International Classification of Diseases (9th/10th Editions) Clinical Modification diagnosis codes (ICD-9-CM/ICD-10-CM). Concurrent C. Diff and other comorbidities were identified by ICD-9/10-CM codes and Elixhauser comorbidity software. Our primary objective was to delineate temporal trends, and predictors of C. Diff infection in SCD patients. We utilized Cochran Armitage trend test and multivariable survey logistic regression models to analyze the trends, predictors and outcomes. Results:Out of a total 991,848 all-cause hospitalizations among SCD patients, 5,182 (1.81%) hospitalizations were complicated with C. Diff infection. Prevalence of C.Diff infection increased from 3/1000 hospitalizations in 2008 to 6/1000 hospitalizations in 2017 (pTrend<0.0001) with a 6% yearly increase (OR:1.06; 95%CI:1.04-1.09; p<0.001) (Figure.1). Patients who developed C.Diff infection had higher mean age (39 vs 33-years; p<0.001), and more likely to be females (62% vs 38%; p<0.001). Furthermore, in multivariable regression analysis, increasing age (OR:1.1; 95%CI:1.1-1.1; p<0.0001), females (OR:1.2; 95%CI:1.1-1.4; p<0.001), neurological disorders (OR:1.6; 95%CI:1.2-1.9; p<0.001), weight loss (OR:2.5; 95%CI:2.0-3.2; p<0.001), depression (OR:1.5; 95%CI:1.2-1.9; p<0.001), and renal failure (OR:1.3; 95%CI:1.2-1.6; p<0.001) were associated with higher odds of C. Diff infection. Also other concurrent conditions like liver disorders (OR:1.5; 95%CI:1.2-2.0; p<0.001), congestive heart failure (OR:1.3; 95%CI:1.1-1.6; p<0.001), and septicemia (OR:3.6; 95%CI:3.1-4.3; p<0.001) were also associated with increased odds of developing C.Diff infection. Among the patients who developed C.Diff infection, 15% were discharged to long term facilities and 4% died during the hospitalization. Moreover C.Diff infection was also associated with higher length of stay (11 vs 6-days; p<0.001). Discussion:In this nationally representative study, we observed that prevalence of C.Diff among SCD has been increasing over the last decade. We were also able to delineate several factors such as renal failure, liver disorder, CHF and septicemia which were significantly associated with development of C.Diff infection. Modifiable factors require better optimization which may eventually decrease the C.diff infection prevalence but this conclusion needs more in-depth studies to establish the causal relationship. References: (1) Ahmed J, Kumar A, Jafri F, Batool S, Knoll B, Lim SH. Low Incidence of Hospital-OnsetClostridium difficileInfection in Sickle Cell Disease.N Engl J Med. 2019;380(9):887-888. doi:10.1056/NEJMc1815711 Disclosures No relevant conflicts of interest to declare.
An index case of Legionnaires's disease with mediastinal adenopathy prompted us to review our recent experience with Legionnaires' disease to determine the incidence of mediastinal adenopathy of this finding in Legionnaires' disease. We reviewed the radiographic findings of 90 hospitalized adults with Legionnaires' disease from 2015 to 2017. Excluded were 11 patients with mediastinal adenopathy due to non-Legionnaires' disease causes, e.g., lymphoma. Thirty-seven of the remaining patients had both chest films and chest computed tomography (CT) scans. Of the 37 Legionnaires' disease cases, 13/37 (35%) had mediastinal adenopathy and 8/27 (24%) also had unilateral hilar adenopathy. These chest CT findings were not seen on chest films. Chest CT scans are needed to detect mediastinal adenopathy in Legionnaires' disease. Mediastinal adenopathy may be due to Legionnaires' disease or a malignancy. Some findings in Legionnaires' disease are also present in mediastinal adenopathy due to lymphomas, e.g., highly elevated erythrocyte sedimentation rate (ESR), lactate dehydrogenase (LDH), and ferritin. Hospitalized adults with Legionnaires' disease and mediastinal adenopathy should have serial chest CT scans to monitor resolution of the mediastinal adenopathy. In hospitalized adults with otherwise unexplained persistent mediastinal adenopathy, they should be considered as being due to another etiology, e.g., lymphoma, until proven otherwise.
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