Platelet aggregation in severe sepsis.

Severe sepsis and multiple organ distress syndrome remain a diagnostic and therapeutic challenge for intensive therapy. Platelet activating factor forms a bridge between inflammation and clot formation. Our study surveys the effect of severe sepsis on platelet function and focuses on spontaneous aggregation in severely ill patients. Daily arterial blood samples were collected from 45 patients (average age of 60.7 ± 13) for five consecutive days following admission and 30 healthy controls. Platelet aggregation was measured using adrenaline (ADR), adenosine diphosphate (ADP), collagen (COL) and normal saline (SAL). Clinical status was observed using Multiple Organ Dysfunction Score (MODS) and Sequential Organ Failure Assessment (SOFA) score systems. Inducible aggregation deteriorated in septic patients in all 5 days with ADR, ADP and COL (P < 0.05) while SAL aggregation was increased during intensive care. Low platelet patients showed weak inducible aggregation with ADP throughout, with ADR on the 2nd, 3rd, 4th and 5th days and with COL on the 1st, 2nd and 3rd days. SAL aggregation showed no significance. No significant difference was seen between platelet functions comparing survivors and non-survivors. In the spontaneous aggregative group, platelet count was insignificantly higher, while procalcitonin levels were lower in 1st, 3rd and 4th days and no significant difference was observed in lactate levels. We demonstrated the presence of spontaneous platelet activity while overall inducible platelet aggregation is significantly deteriorated in septic patients. There were significant differences in inducible aggregation between normal and low platelet count groups. Inducible platelet function had no predictive value in the outcome.