Daniel O Thomas-Rueddel1, Bernhard Poidinger2, Manfred Weiss3, Friedhelm Bach4, Karin Dey5, Helene Häberle6, Udo Kaisers7, Hendrik Rüddel8, Dirk Schädler9, Christian Scheer10, Torsten Schreiber11, Tobias Schürholz12, Philipp Simon7, Armin Sommerer5, Daniel Schwarzkopf13, Andreas Weyland14, Gabriele Wöbker15, Konrad Reinhart8, Frank Bloos8. 1. Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany; The Integrated Research and Treatment Center for Sepsis Control and Care, Jena University Hospital, Jena, Germany. Electronic address: daniel.thomas@med.uni-jena.de. 2. Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany. 3. Department of Anesthesiology, University Hospital Ulm, Ulm, Germany. 4. Department of Anesthesiology, Intensive Care Medicine, Emergency Medicine and Pain Therapy, Ev. Krankenhaus Bielefeld, Bielefeld, Germany. 5. Department of Anesthesiology and Intensive Care Medicine, Bundeswehrkrankenhaus Berlin, Berlin, Germany. 6. Department of Anesthesiology and Intensive Care Medicine, University Hospital Tübingen, Tübingen, Germany. 7. Department of Anesthesiology and Intensive Care Medicine, University Hospital Leipzig, Leipzig, Germany. 8. Department of Anesthesiology and Intensive Care Medicine, Jena University Hospital, Jena, Germany; The Integrated Research and Treatment Center for Sepsis Control and Care, Jena University Hospital, Jena, Germany. 9. Department of Anesthesiology and Intensive Care Medicine, University Medical Center Schleswig-Holstein, Campus Kiel, Germany. 10. Department of Anesthesiology and Intensive Care Medicine, Ernst-Moritz-Arndt-University Greifswald, Greifswald, Germany. 11. Department of Anesthesiology and Intensive Care Medicine, Zentralklinik Bad Berka GmbH, Bad Berka, Germany. 12. Department of Intensive Care Medicine, University Hospital Aachen, Aachen, Germany. 13. The Integrated Research and Treatment Center for Sepsis Control and Care, Jena University Hospital, Jena, Germany. 14. Department of Anesthesiology, Intensive Care Medicine, Emergency Medicine, and Pain Therapy, Hospital Oldenburg, Oldenburg, Germany. 15. Department of Intensive Care Medicine, HELIOS Klinikum Wuppertal, Wuppertal, Germany.
Abstract
PURPOSE: Current guidelines and most trials do not consider elevated lactate (Lac) serum concentrations when grading sepsis severity. We therefore assessed the association of different types of circulatory dysfunction regarding presence of hyperlactatemia and need for vasopressor support with clinical presentation and outcome of sepsis. METHODS: In a secondary analysis of a prospective observational multicenter cohort study, 988 patients with severe sepsis were investigated regarding vasopressor support, Lac levels, and outcome. RESULTS: Twenty-eight-day mortality regarding shock or hyperlactatemia was as follows: hyperlactatemia more than 2.5 mmol/L and septic shock (tissue dysoxic shock): 451 patients with a mortality of 44.8%; hyperlactatemia without vasopressor need (cryptic shock): 72 patients, mortality 35.3%; no hyperlactatemia with vasopressor need (vasoplegic shock): 331 patients, mortality 27.7%; and absence of hyperlactemia or overt shock (severe sepsis): 134 patients, mortality 14.2% (P < .001). These groups showed differences in source and origin of infection. The influence of hyperlactatemia on 28-day mortality (P < .001) (odds ratio 3.0, 95% confidence interval 2.1-4.1 for Lac >4 mmol/L) was independent of vasopressor support (P < .001) (odds ratio 2.0, 95% confidence interval 1.3-3.0 for norepinephrine >0.1 μg/kg per minute) in logistic regression. CONCLUSIONS: Hyperlactatemia increases risk of death independent of vasopressor need resulting in different phenotypes within the classic categories of severe sepsis and septic shock.
PURPOSE: Current guidelines and most trials do not consider elevated lactate (Lac) serum concentrations when grading sepsis severity. We therefore assessed the association of different types of circulatory dysfunction regarding presence of hyperlactatemia and need for vasopressor support with clinical presentation and outcome of sepsis. METHODS: In a secondary analysis of a prospective observational multicenter cohort study, 988 patients with severe sepsis were investigated regarding vasopressor support, Lac levels, and outcome. RESULTS: Twenty-eight-day mortality regarding shock or hyperlactatemia was as follows: hyperlactatemia more than 2.5 mmol/L and septic shock (tissue dysoxic shock): 451 patients with a mortality of 44.8%; hyperlactatemia without vasopressor need (cryptic shock): 72 patients, mortality 35.3%; no hyperlactatemia with vasopressor need (vasoplegic shock): 331 patients, mortality 27.7%; and absence of hyperlactemia or overt shock (severe sepsis): 134 patients, mortality 14.2% (P < .001). These groups showed differences in source and origin of infection. The influence of hyperlactatemia on 28-day mortality (P < .001) (odds ratio 3.0, 95% confidence interval 2.1-4.1 for Lac >4 mmol/L) was independent of vasopressor support (P < .001) (odds ratio 2.0, 95% confidence interval 1.3-3.0 for norepinephrine >0.1 μg/kg per minute) in logistic regression. CONCLUSIONS:Hyperlactatemia increases risk of death independent of vasopressor need resulting in different phenotypes within the classic categories of severe sepsis and septic shock.
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