ABSTRACT
BACKGROUND: Acute chest pain of non-traumatic origin is a common reason for presentation to physician's offices and emergency rooms. Coronary heart disease is the cause in up to 25% of cases. Because acute chest pain, depending on its etiology, may be associated with a high risk of death, rapid, goal-oriented management is mandatory. METHODS: This review is based on pertinent articles and guidelines retrieved by a selective search in PubMed. RESULTS: History-taking, physical examination, and a 12-lead electrocardiogram (ECG) are the first steps in the differential diagnostic process and generally allow the identification of features signifying a high risk of lifethreatening illness. If the ECG reveals ST-segment elevation, cardiac catheterization is indicated. The timedependent measurement of highly sensitive troponin values is a reliable test for the diagnosis or exclusion of acute myocardial infarction. A wide variety of other potential causes (e.g., vascular, musculoskeletal, gastroenterologic, or psychosomatic) must be identified from the history if they are to be treated appropriately. Elderly patients need special attention. CONCLUSION: Acute chest pain is a major diagnostic challenge for the physician. Common errors are traceable to non-recognition of important causes and to an inadequate diagnostic work-up. Future studies should be designed to help optimize the interdisciplinary management of patients with chest pain.
Subject(s)
Chest Pain/diagnosis , Coronary Artery Disease/diagnosis , Critical Care/methods , Medical History Taking/methods , Thoracic Diseases/diagnosis , Troponin I/blood , Acute Disease , Biomarkers/blood , Chest Pain/blood , Chest Pain/etiology , Coronary Artery Disease/blood , Coronary Artery Disease/complications , Delivery of Health Care, Integrated , Electrocardiography/methods , Evidence-Based Medicine , Humans , Patient Care Team/organization & administration , Thoracic Diseases/blood , Thoracic Diseases/complicationsABSTRACT
BACKGROUND: Recently, clinical trials revealed renal impairment induced by hydroxyethyl starch (HES) in septic patients. In prior studies, we managed to demonstrate that HES accumulated in renal proximal tubule cells (PTCs). The related pathomechanism has not yet been discovered. To validate our hypothesis that the HES molecule itself is harmful, regardless of its molecule size or origin, we conducted a comprehensive study to elucidate the influences of different HES preparations on PTC viability in vitro. METHODS: Cell viability of human PTC was measured with a cytotoxicity assay, quantifying the reduction of tetrazolium salt to colored formazan. Experiments were performed by assessing the influence of different carrier solutions of HES (balanced, nonbalanced, culture medium), different average molecular weights (70, 130, 200 kDa), different origins (potato or corn derived), and various durations of incubation (2-21 hours). Furthermore, HES 130/0.4 was fractionated by ultrafiltration, and the impact on cell viability of average single-size fractions with <3, 3 to 10, 10 to 30, 30 to 50, 50 to 100, and >100 kDa was investigated. We also tested the possible synergistic effects of inflammation induced by tumor necrosis factor-α. RESULTS: All tested HES solutions, regardless of origin or carrier matrix, decreased cell viability in an equivalent, dose-dependent manner. Coincubation with tumor necrosis factor-α did not reduce HES-induced reduction of cell viability. Minor differences were detected comparing 70, 130, and 200 kDa preparations. Analysis of fractionated HES revealed that each fraction decreased cell viability. Even small HES molecules (10-30 kDa) were significantly deleterious. CONCLUSIONS: For the first time, we were able to show that only the total mass of HES molecules applied is responsible for the harmful impact on renal PTC in vitro. Neither molecular size nor their origin showed any relevance.