Chief complaints in medical emergencies: do they relate to underlying disease and outcome? The Charité Emergency Medicine Study (CHARITEM)

Objectives: To evaluate the relationship between chief complaints and their underlying diseases and outcome in medical emergency departments (EDs).\ud \ud Methods: All 34 333 patients who attended two of the EDs of the Charite Berlin over a 1-year period were included in the analysis. Data were retrieved from the hospital information system. For study purposes, the chief complaint (chest pain, dyspnoea, abdominal pain, headache or 'none of these symptoms') was prospectively documented in an electronic file by the ED-physician. Documentation was mandatory.\ud \ud Results: The majority of patients (66%) presented with 'none of these symptoms', 11.5% with chest pain, 11.1% with abdominal pain and 7.4% with dyspnoea. In total, 39.4% of all patients were admitted to the hospital. The leading diagnosis was acute coronary syndrome (50.7%) for chest pain in-patients and chronic obstructive pulmonary disease (16.5%) and heart failure (16.1%) for in-patients with dyspnoea. The causes of abdominal pain in in-patients were of diverse gastrointestinal origin (47.2%). In-hospital mortality of in-patients was 4.7%. Patients with chest pain had significantly lower in-hospital mortality (0.9%) than patients with dyspnoea (9.4%) and abdominal pain (5.1%).\ud \ud Conclusion: The majority of emergency patients lack diagnosis-specific symptoms. Chief complaints help preselect patients but must not be mistaken as disease specific. Mortality largely differs depending on the chief complaint. In chest pain patients, standardized processes may be one factor that explains the low mortality in this group

Heparin strongly induces soluble fms-Like tyrosine kinase 1 release in vivo and in vitro: brief report

Objective: Soluble fms-like tyrosine kinase 1 (sFlt1) is involved in the pathophysiology of preeclampsia and coronary artery disease. Because sFlt1 has a heparin-binding site, we investigated whether or not heparin releases sFlt1 from the extracellular matrix.\ud \ud Methods and Results: We measured sFlt1 before and after heparin administration in 135 patients undergoing coronary angiography, percutanous coronary intervention, or both. sFlt1 was increased directly after heparin administration (from 254 to 13 440 pg/mL) and returned to baseline within 10 hours. Umbilical veins and endothelial cells treated with heparin released sFlt1. Heparinase I and III also increased sFlt1. Mice treated with heparin had elevated sFlt1 serum levels. Their serum inhibited endothelial tube formation.\ud \ud Conclusion: Heparin releases sFlt1 by displacing the sFlt1 heparin-binding site from heparan sulfate proteoglycans. Heparin could induce an antiangiogenic state