Olof Brattström
Karolinska Institutet
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Featured researches published by Olof Brattström.
Acta Anaesthesiologica Scandinavica | 2010
Olof Brattström; Fredrik Granath; Patrik Rossi; Anders Oldner
Background: We investigated the incidence and severity of post‐injury morbidity and mortality in intensive care unit (ICU)‐treated trauma patients. We also identified risk factors in the early phase after injury that predicted the later development of complications.
Intensive and Critical Care Nursing | 2011
Anna Schandl; Olof Brattström; Anna Svensson-Raskh; Elisabeth Hellgren; Magnus D. Falkenhav; Peter V. Sackey
OBJECTIVES To describe a multidisciplinary intensive care follow-up and the methods used for identifying and managing physical and psychological problems in ICU survivors. METHODS Patients treated>four days in an intensive care unit (ICU) were invited three, six and 12 months after intensive care for screening of physical problems with function tests and psychological problems with the Impact of Event Scale (IES) and the Hospital Anxiety and Depression Scale (HADS). RESULTS 40 of 61 patients had clinically impaired physical function, with no ongoing physical rehabilitation at three months. Twenty-two patients received specific training instructions and 18 patients were referred for physiotherapy. 34 of 61 patients had symptoms of moderate to severe posttraumatic stress and/or symptoms of clinically significant anxiety or depression. Twelve patients accepted referral for psychiatric evaluation and treatment. CONCLUSION Multidisciplinary follow-up after intensive care can be of value in identifying untreated physical and psychological problems in ICU survivors. Liaison with specialists enables referral for identified problems. Patients screened and treated in the first six months appear to have little need for further follow-up after intensive care.
BJA: British Journal of Anaesthesia | 2012
Andreas Andersson; M. Rundgren; S. Kalman; O. Rooyackers; Olof Brattström; Anders Oldner; Stefan Eriksson; Robert Frithiof
BACKGROUND Microcirculatory and mitochondrial dysfunction are important factors in the development of septic shock. In this study, we investigated the effects of fluid resuscitated endotoxaemic shock and norepinephrine treatment on intestinal microcirculation and mitochondrial function in sheep. METHODS Eight anaesthetized sheep received an i.v. infusion of endotoxin. After 24 h, mean arterial pressure (MAP) was restored to baseline levels with a norepinephrine infusion. Five sheep served as sham experiments. Central and regional haemodynamics were monitored, and ileal microcirculation was evaluated with laser Doppler and sidestream dark-field videomicroscopy techniques. Gut mucosal acidosis was assessed by air tonometry, and ileal wall biopsies were analysed for mitochondrial activity. RESULTS After 24 h of endotoxaemia, the animals had developed hyperdynamic shock with systemic and mucosal acidosis. Although superior mesenteric artery (SMA) flow was higher than the baseline values, ileal microcirculatory perfusion and mitochondrial complex I activity decreased. After norepinephrine was started, SMA flow, ileal microcirculation, and mucosal acidosis remained unchanged. Although no statistically significant difference could be demonstrated, norepinephrine increased mitochondrial complex I activity in five of the six animals from which ileal biopsies were taken. CONCLUSIONS Although fluid resuscitated endotoxaemic shock increased regional blood flow, microcirculatory and mitochondrial alterations were still present. Restoring MAP with norepinephrine did not affect ileal microcirculation or mucosal acidosis, indicating that perfusion pressure manipulation is of limited importance to the intestinal microcirculation in established endotoxaemic shock.
Journal of Trauma-injury Infection and Critical Care | 2015
Mikael Eriksson; Olof Brattström; Johan Mårtensson; Emma Larsson; Anders Oldner
BACKGROUND The trauma patient sustains numerous potentially harmful insults that may contribute to a notable risk of acute kidney injury (AKI). The aim of this study was to investigate the incidence of and to identify risk factors for AKI in severely injured trauma patients admitted to the intensive care unit (ICU). The patients were followed up for 1 year with respect to survival and end-stage renal disease. METHODS Trauma patients admitted to the ICU for more than 24 hours at a Level I trauma center were included. The outcome measure was AKI diagnosed Days 2 to 7 of ICU treatment. Regression analysis was performed to identify factors associated with AKI development. RESULTS A quarter of the patients (103 of 413) developed AKI within the first week of ICU admission. AKI was associated with increased 30-day (17.5% vs. 5.8%) and 1-year (26.2% vs. 7.1%) mortality. Risk factors for AKI were male sex, age, nondiabetic comorbidity, diabetes mellitus, Injury Severity Score (ISS) greater than 40, massive transfusion, and volume loading with hydroxyethyl starch (HES) within the first 24 hours. Unexpectedly, sepsis before AKI onset, admission hypotension, and extensive contrast loading (>150 mL) were not associated with AKI development. None of the surviving AKI patients had developed end-stage renal disease 1 year after injury. CONCLUSION AKI in ICU-admitted trauma patients is a common complication with substantial mortality. Diabetes, male sex, and severe injury were strong risk factors, but age, nondiabetic comorbidity, massive transfusion, and resuscitation with HES were also associated with postinjury AKI. Based on the results of the current study, volume resuscitation with HES cannot be recommended in trauma patients. LEVEL OF EVIDENCE Prognostic study, level III; therapeutic study, level IV.
Acta Anaesthesiologica Scandinavica | 2013
P. Hyllienmark; Olof Brattström; E. Larsson; Claes-Roland Martling; J. Petersson; Anders Oldner
Trauma patients are susceptible to post‐injury infections. We investigated the incidence, as well as risk factors for development of pneumonia in intensive care unit (ICU)‐treated trauma patients. In addition, we report pathogens identified in patients that developed pneumonia.
Acta Anaesthesiologica Scandinavica | 2013
Joakim Johansson; Olof Brattström; Folke Sjöberg; Lennart Lindbom; Heiko Herwald; Eddie Weitzberg; Anders Oldner
Trauma and its complications contribute to morbidity and mortality in the general population. Trauma victims are susceptible to acute respiratory distress syndrome (ARDS) and sepsis. Polymorphonuclear leucocytes (PMNs) are activated after trauma and there is substantial evidence of their involvement in the development of ARDS. Activated PMNs release heparin‐binding protein (HBP), a granule protein previously shown to be involved in acute inflammatory reactions. We hypothesised that there is an increase in plasma HBP content after trauma and that the increased levels are related to the severity of the trauma or later development of severe sepsis and organ failure (ARDS).
British Journal of Surgery | 2016
Mikael Eriksson; Olof Brattström; Emma Larsson; Anders Oldner
Studies on mortality following trauma have been restricted mainly to in‐hospital or 30‐day death. Mortality risk may be sustained several years after trauma, but the causes of late death have not been elucidated. The aim was to investigate mortality and analyse causes of late death after trauma.
Free Radical Biology and Medicine | 2017
Jesper Eriksson; Andreas C. Gidlöf; Mikael Eriksson; Emma Larsson; Olof Brattström; Anders Oldner
Background: Thioredoxin (TRX), an endogenous anti‐oxidant protein induced in inflammatory conditions, has been shown to increase in plasma and to be associated with outcome in septic patients. This biomarker has never been studied in a trauma setting. We hypothesized that TRX would be increased after trauma and associated with post‐injury sepsis. Methods: Single‐centre prospective observational study conducted at the intensive care unit (ICU) at the Karolinska University Hospital, Stockholm, Sweden, a level‐1 trauma centre. Eighty‐three severely injured trauma patients, 18 years or older, with an ICU stay of three days or more were included. Plasma samples were obtained on day 1 and 3 after informed consent. Clinical, physiological and outcome data were retrieved from the trauma and ICU research registries. Plasma samples were also obtained from 15 healthy subjects. In addition, a standardized porcine trauma model was conducted where a femur fracture followed by a controlled hemorrhage period were inflicted in four pigs. Results: In pigs, however not significant, there was a continuing increase in plasma‐TRX after femur fracture and sequential hemorrhage despite near normalisation of cardiac index and lactate levels. In patients, median injury severity score was 29 and 48 patients developed sepsis during their ICU stay. A three‐fold increase in initial TRX was seen in trauma patients when compared to healthy volunteers. Thioredoxin was significantly higher in patients in shock on admission, those subject to massive transfusion and in the most severely injured patients. No difference was seen between survivors and non‐survivors. Plasma‐TRX on day 1 was significantly increased in patients who later developed post‐injury sepsis. In a logistic regression analysis including TRX, C‐reactive protein, injury severity, massive transfusion, and admission blood pressure, TRX was the only variable independently associated with post‐injury sepsis. Conclusions: This study demonstrates that TRX is released into plasma in response to severe trauma and independently associated with post‐injury sepsis. The use of TRX as a biomarker in trauma patients needs further evaluation in larger studies. Level of evidence: Retrospective cohort study, level III. HIGHLIGHTSThioredoxin (TRX) in plasma is shown to be increased after traumatic injury.TRX levels correspond to injury severity, shock on arrival and massive transfusion.TRX is independently associated with later sepsis development.TRX shows promise as an early future biomarker for post‐injury sepsis.
BJS Open | 2018
Mikael Eriksson; E. von Oelreich; Olof Brattström; J. Eriksson; Emma Larsson; Anders Oldner
High levels of circulating catecholamines after multiple trauma have been associated with increased morbidity and mortality. Beta‐adrenergic receptor antagonist (beta‐blocker) therapy has emerged as a potential treatment option, but the effect of preinjury beta‐blockade on trauma‐induced mortality is unclear. The aim of this study was to assess whether preinjury beta‐blocker therapy is associated with reduced mortality after multiple trauma.
Acta Anaesthesiologica Scandinavica | 2017
Erzsebet Bartha; Mathias Bertilsson; Rebecca Ahlstrand; Max Bell; Håkan Björne; Olof Brattström; Lena Nilsson; Egidijus Semenas; Andreas Wiklund; Sigridur Kalman
Background: Postoperative complications increase the risk of death 2–3 years postoperatively. Prediction of complications can support clinical decisions. Before clinical use of any prediction model, validation is reasonable. We aimed to validatethree models: Revised Cardiac Risk Index (RCRI), ARISCAT and POSSUM.Methods: The PROF S-study was performed in four Swedish university hospitals. Patients werere cruited between 2015-11-01 and 2016-02-15. Inclusion criteria were adults, ASA classification ≥3, major/complex upper and lower gastrointestinal, urogenital or orthopedic surgery. Complications were screened on days 3, 7 and 10 by the postoperative morbidity survey (POMS). Only patients with grade≥2 (Clavien-Dindo classification) were accounted for. Study outcomes were cardiovascular (RCRI model) and pulmonary (ARISCAT model) complications, and a composite of the POMS domains (POSSUM model). Discrimination was evaluated by C-statistics (area under receiver operator characteristic curve; AUC ROC).Results: The number of patients included was 1089. Thirteen patients were excluded due to wrong inclusion, and another three were lost to follow-up. Presen ce of malignancy was 41%. Patient characteristics and outcomes are displayed in Table 1. The RCRI underestimated the risk for cardiovascular complications, and discrimination was low (AUC ROC 0.64; 95% CI 0.59–0.68). The prediction by the ARISCAT model was fair (AUC 0.72; CI 0.69–0.76). The POSSUM model had poor /fair discrimination (AUC 0.70; CI 0.67–0.73).Conclusions: The ARISCAT model predicted pulmonary complications with fair discrimina-tion and so could be used as decision support. Parameters with significant odds ratios of the RCRI and POSSU M models might be used as complements of clinical judgement.Background: In elderly reclassification of ASA3 class by functional dependency improved prediction of postoperative mortality. We hypothesized that such a reclassification could improve the risk pred ...