Search PubMed⌕ Search
Home/Archive/PubMed

PubMed · 9142575

Platelet function in septic multiple organ dysfunction syndrome.

M Gawaz·T Dickfeld·C Bogner·S Fateh-Moghadam·F J Neumann
View original source ↗Export metadata ↓

Abstract

OBJECTIVE: Altered platelet function plays a role in the pathophysiology of multiple organ failure in sepsis. The purpose of the present study was to evaluate various aspects of platelet adhesive function in septic patients and its putative relevance for prognosis. DESIGN: Prospective clinical study. SETTING: Intensive Care Unit of the University Hospital. PATIENTS AND METHODS: A total of 41 patients admitted to the medical Intensive Care Unit were studied. On the day of admission, patients were evaluated by intensive care scoring systems (Elebute, APACHE II) to assess the severity of sepsis and multiple organ dysfunction syndrome (MODS), and platelet function tests were performed. All patients were observed for 28 days to assess their clinical outcomes. Eleven patients revealed septicemia without MODS (Elebute > or = 12, APACHE II < 20) and 20 septic patients suffered from MODS (Elebute > or = 12, APACHE II > or = 20). Ten non-septic patients without MODS served as a control group (Elebute < 12, APACHE II < 20). Flow cytometric determination of the activated fibrinogen (fg) receptor GPIIb-IIIa and as well as thrombospondin (TSP) on platelets and platelet-neutrophil adhesion (CD 41 immunofluorescence) ex vivo was performed using monoclonal antibodies. The effect of plasma obtained from patients on normal platelet aggregation in vitro, and adhesion to cultured endothelial cells was evaluated. RESULTS: The surface expression of TSP on platelets was increased in septic patients with MODS compared to controls (p < 0.03). Platelet-neutrophil adhesion was not significantly altered in septicemia (p < 0.09) but decreased significantly in the presence of MODS (p < 0.05) when compared to controls. Logistic regression analysis showed that platelet-neutrophil adhesion was an independent predictor for poor clinical outcome (p < 0.01). Plasma from septic patients sensitized normal platelets to hyperaggregate and to adhere to cultured endothelium (p < 0.01). CONCLUSION: In septic patients platelets become activated and are hyperadhesive to other vascular cells including neutrophils and endothelium. This may induce sequestration of platelets and microcirculatory arrest, thus the development of MODS.

Explore related subjects

APACHEAdultAgedBiomarkersCase-Control StudiesCell Adhesion MoleculesCross-Sectional StudiesEndothelium, VascularFemaleHumansIntensive Care UnitsLogistic ModelsMaleMembrane GlycoproteinsMiddle AgedMultiple Organ FailureNeutrophilsPlatelet ActivationPlatelet Glycoprotein GPIIb-IIIa ComplexProspective StudiesSurvivorsSystemic Inflammatory Response SyndromeThrombospondinsJournal ArticleResearch Support, Non-U.S. Gov't

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

M Gawaz, T Dickfeld, C Bogner, S Fateh-Moghadam, F J Neumann. 1997. Platelet function in septic multiple organ dysfunction syndrome.. https://doi.org/10.1007/s001340050344

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2001

[Hospital infections and risk factors in the intensive care units of 16 Dutch hospitals, results of surveillance of quality assurance indicators].

OBJECTIVE: To gain insight into the incidence of nosocomial infections and associated risk factors in Intensive Care Units (ICUs). DESIGN: Prospective. METHOD: From July 1997 to December 1999, standardised surveillance of nosocomial infections was implemented in ICUs in 16 hospitals in the Netherlands. Surveillance was performed in patients with an ICU stay of > or = 48 hrs; data were collected from admission until discharge from ICU. Data-collection included demographic data and patient- and treatment-related risk factors. The data were aggregated in a national database. RESULTS: In the research period, hospitals sent good quality data for aggregation in the national database on 2795 patients (61% male) and 27,922 ICU patient days. The median length of stay was six days, the median 'Acute physiology and chronic health evaluation' (APACHE) II score was 17 and the median age was 67 years. A total number of 749 infected patients were found with 1,177 nosocomial infections (27% of patients, 42 infections/1000 patient days), consisting of 43% pneumonia, 20% sepsis, 21% urinary tract infections, 16% other types of infections. Out of all the patients, 62% was on mechanical ventilation, 64% had a central venous line and 89% had a urinary catheter in situ. Selective decontamination of the gastrointestinal tract was used for 12% of the patients, and systemic antibiotics for 68%. Micro-organisms most frequently isolated were Pseudomonas aeruginosa in patients with pneumonia, Staphylococcus epidermidis in catheter-related bloodstream infections and Escherichia coli in patients with urinary tract infections. Large differences in device use and incidence of infections were observed between the ICUs. CONCLUSION: The aggregated data gave insight into the incidence of nosocomial infections and associated risk factors in ICUs. The data are meant as references to support decision- and policy-making in local infection control programs.

APACHE↗
PubMed2001

Reduction in mortality after inappropriate early discharge from intensive care unit: logistic regression triage model.

OBJECTIVE: To develop a predictive model to triage patients for discharge from intensive care units to reduce mortality after discharge. DESIGN: Logistic regression analyses and modelling of data from patients who were discharged from intensive care units. SETTING: Guy's hospital intensive care unit and 19 other UK intensive care units from 1989 to 1998. PARTICIPANTS: 5475 patients for the development of the model and 8449 for validation. MAIN OUTCOME MEASURES: Mortality after discharge and power of triage model. RESULTS: Mortality after discharge from intensive care was up to 12.4%. The triage model identified patients at risk from death on the ward with a sensitivity of 65.5% and specificity of 87.6%, and an area under the receiver operating curve of 0.86. Variables in the model were age, end stage disease, length of stay in unit, cardiothoracic surgery, and physiology. In the validation dataset the 34% of the patients identified as at risk had a discharge mortality of 25% compared with a 4% mortality among those not at risk. CONCLUSIONS: The discharge mortality of at risk patients may be reduced by 39% if they remain in intensive care units for another 48 hours. The discharge triage model to identify patients at risk from too early and inappropriate discharge from intensive care may help doctors to make the difficult clinical decision of whom to discharge to make room for a patient requiring urgent admission to the unit. If confirmed, this study has implications on the provision of resources.

APACHE↗