The mechanisms of TP in the ICU are numerous, and multifactorial mechanisms often act simultaneously, mainly because of a lack of production and excessive consumption, including abnormal megakaryocyte counts caused by bone marrow suppression, disseminated intravascular coagulation, immune-mediated destruction of platelets, and direct and indirect platelet activation during sepsis.[17,19,20] However, the presence of an increase in thrombopoietin (TPO) levels in septic patients with low platelet counts[21] suggests that the rate of platelet consumption is faster than that of sepsis. Here, THPO is linked to Sepsis.