Product(s) used in this publication: Absolutely Quantified Peptides SpikeTides™ TQL
Plateletfunction during sepsis-related disseminated intravascular coagulation (DIC) is only sparsely investigated. We aimed to determine 1) platelet aggregation, independently of platelet count, and platelet activation among septic shockpatients and 2) whether platelet aggregation or platelet activation differed among patients with and without DIC.
MATERIALS AND METHODS:
We included 38 septic shockpatients at the Intensive Care Unit, Aarhus University Hospital, Denmark. Blood samples were obtained within 24 h of admission and the two consecutive days. Platelet aggregation was measured by impedance aggregometry including a model defining expected platelet aggregation relative to platelet count. Platelet activation was measured employing flow cytometry.
Platelet aggregation was significantly lower in septic shockpatients than in healthy controls (p < .0001) and was lower in patients with DIC than in patients without DIC (p < .05). However, patients with septic shock, regardless of DIC-status, had platelet aggregation as expected for their platelet counts and were within the 95% prediction interval calculated from healthy controls. Platelet activation was significantly higher in septic shockpatients than in healthy controls indicated by higher platelet surface-bound fibrinogen and CD63 (p < .05). Surface-bound P-selectin was significantly lower among septic shockpatients than in healthy controls (p < .001), but plasma soluble P-selectin was significantly higher among septic shockpatients than in healthy controls (p < .0001).
Patients with septic shock displayed no impairment of platelet aggregation when interpreted relative to platelet count. Platelet activation, measured with flow cytometry, was increased among septic shockpatients compared with healthy controls.