Impaired platelet reactivity in patients with septic shock: a proof-of-concept study

Abstract

Coagulation disorders and thrombocytopenia are common in patients with septic shock, but only few studies have focused on platelet variables beyond platelet count. The aim of this study was to evaluate whether platelets reactivity predicts sepsis-induced thrombocytopenia in patients with septic shock.

We therefore enrolled consecutive patients with septic shock and platelets count >150*10³/μL on the day of the diagnosis. Platelets reactivity tests were performed daily from the diagnosis of septic shock until day five; platelet volume distribution and mean platelet volume were also recorded daily. Sepsis-induced thrombocytopenia was defined as a platelet count <150*10³/μL.

Thirty patients were included; sepsis-induced thrombocytopenia occurred in 11 (31%) patients. Platelets reactivity and platelet count at day of septic shock diagnosis were not correlated. Patients who experienced thrombocytopenia had lower maximal aggregation at diagnosis than others. Maximal aggregation tests were predictors of thrombocytopenia (AUROC from 0.756 to 0.797, depending on the agonist used). Both platelet volume distribution width and mean platelet volume were predictors of 90-day mortality (AUROC 0.866 and 0.735, respectively).

In this pilot study, impaired platelets reactivity was more common in patients who subsequently developed sepsis-induced thrombocytopenia; also, platelet volume distribution width and mean platelet volume were predictors of 90-day mortality.

Keywords:

• Critical care
• disseminated intravascular coagulation
• platelet reactivity
• sepsis
• Septic shock
• thrombocytopenia

Acknowledgements

The authors wish to acknowledge Veronica Lodolini (Cardiovascular Institute, Azienda Ospedaliera Universitaria di Ferrara, Cona (FE), Italy and Maria Cecilia Hospital, GVM Care & Research, Cotignola (RA)) and Elisa Mosele (Cardiovascular Institute, Azienda Ospedaliera Universitaria di Ferrara, Cona (FE), Italy and Maria Cecilia Hospital, GVM Care & Research, Cotignola (RA)) for their contribution.

Authors’ contributions

AF, SS, and GC designated the study protocol; AF had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. GM, BP, GF, RR, AE contributed to the acquisition, analysis, and interpretation of the data; FST and SS contributed to the drafting of the manuscript. JC and CAV contributed to the critical revision of the manuscript for important intellectual content. All authors read and approved the final manuscript and agree to be accountable for all aspects of the work.

Data availability statement

Dataset is available for researchers under reasonable requests.

Competing interests

The authors declare no competing interests.

List of abbreviations

SIT: sepsis-induced thrombocytopenia; PR: platelet reactivity; LTA: light transmission aggregometry; MPV: mean platelet volume; PDW: platelet size distribution width; HIT: heparin-induced thrombocytopenia; SAPS: Simplified Acute Physiology Score; SOFA: Sequential Organ Failure Assessment; INR: international normalized ratio; aPTT: activated partial thromboplastin time; ADP: Adenosine diphosphate; AA: Arachidonic acid; TRAP-6: Thrombin receptor-activating peptide-6; RBC: red blood cells; ICU: intensive care unit; LOS: length of stay; DIC: diffuse intravascular coagulation.

Supplementary material

Supplemental data for this article can be accessed here.

Additional information

Funding

This study was financially supported by the University of Ferrara, Ferrara, Italy.