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Trauma and sepsis, epidemiology and pathophysiology

Trauma and sepsis are common causes for intensive care admission. These conditions are closely linked and carry high mortality. We are conducting translational studies ranging from epidemiology to in vitro experiments in this field.

The epidemiological studies on traumatology utilise trauma registries from the Karolinska trauma centre, as well as local and national health registries. Our group is also studying the prevalence and dynamics of biomarkers induced by severe trauma and sepsis. Studies are based on our plasma biobank from ICU patients.

The endothelin system and its role in sepsis have been closely studied by our group for over a decade. The dominant peptide, endothelin-1 (ET-1), is largely released in sepsis and correlated to outcome. The group has shown that ET-1, a highly vasoconstrictive peptide, contribute to hypoperfusion, pulmonary hypertension, oedema formation and cardiac dysfunction in experimental sepsis. ET-1 has also been attributed to have pro-inflammatory effects, a field currently investigated by our group.

Financial support

  • LPS Medical Foundation
  • Magnus Bergvall Foundation
  • Swedish Society of Medicine
  • Swedish Cancer and Traffic Injury Society Fund
  • Laerdal Foundation
  • Carnegie Foundation
  • Swedish Research Council
  • Stockholm County Council

Publications

Heparin-binding protein (HBP): an early marker of respiratory failure after trauma?
Johansson J, Brattström O, Sjöberg F, Lindbom L, Herwald H, Weitzberg E, et al
Acta Anaesthesiol Scand 2013 May;57(5):580-6

Time dependent influence of host factors on outcome after trauma.
Brattström O, Larsson E, Granath F, Riddez L, Bell M, Oldner A
Eur. J. Epidemiol. 2012 Mar;27(3):233-41

Gut microcirculatory and mitochondrial effects of hyperdynamic endotoxaemic shock and norepinephrine treatment.
Andersson A, Rundgren M, Kalman S, Rooyackers O, Brattstrom O, Oldner A, et al
Br J Anaesth 2012 Feb;108(2):254-61

Impact of sepsis on levels of plasma cystatin C in AKI and non-AKI patients.
Mårtensson J, Martling CR, Oldner A, Bell M
Nephrol. Dial. Transplant. 2012 Feb;27(2):576-81

Endotoxin induces differentiated contractile responses in porcine pulmonary arteries and veins.
Persson BP, Boels PJ, Lövdahl C, Rossi P, Arner A, Oldner A
J. Vasc. Res. 2011 ;48(3):206-18

Neutrophil gelatinase-associated lipocalin in adult septic patients with and without acute kidney injury.
Mårtensson J, Bell M, Oldner A, Xu S, Venge P, Martling CR
Intensive Care Med 2010 Aug;36(8):1333-40

Early predictors of morbidity and mortality in trauma patients treated in the intensive care unit.
Brattström O, Granath F, Rossi P, Oldner A
Acta Anaesthesiol Scand 2010 Sep;54(8):1007-17

Inhaled tezosentan reduces pulmonary hypertension in endotoxin-induced lung injury.
Persson BP, Rossi P, Weitzberg E, Oldner A
Shock 2009 Oct;32(4):427-34

Left ventricular mechanical dyssynchrony is load independent at rest and during endotoxaemia in a porcine model.
A'roch R, Steendijk P, Oldner A, Weitzberg E, Konrad D, Johansson G, et al
Acta Physiol (Oxf) 2009 Aug;196(4):375-83

Endotoxemic pulmonary hypertension is largely mediated by endothelin-induced venous constriction.
Rossi P, Persson B, Boels PJ, Arner A, Weitzberg E, Oldner A
Intensive Care Med 2008 May;34(5):873-80

Cardiac effects of endothelin receptor antagonism in endotoxemic pigs.
Konrad D, Haney M, Johansson G, Wanecek M, Weitzberg E, Oldner A
Am. J. Physiol. Heart Circ. Physiol. 2007 Aug;293(2):H988-96

Group members

Anders Oldner – Adjunct Professor

Eddie Weitzberg – Professor, co-supervisor

Björn P. Persson – Associated

Emma Larsson – Associated

Olof Brattström – Associated

Halla Halldorsdottir – MD, Graduate student

Mikael Eriksson – Associated

Former group members:

Patrik Rossi, MD, PhD, former doctoral student

David Konrad, MD, PhD, former doctoral student

Michael Wanecek, MD, PhD, former doctoral student and co-supervisor

Contact us

Anders Oldner

Adjunct professor
Eriksson I Lars group - Section of Anesthesiology and Intensive Care
Department of Physiology and Pharmacology (FYFA), C3