Abstract

The incidence and mortality of sepsis in the intensive care unit (ICU) are extremely high. Thrombocytopenia, one of the most common laboratory abnormalities, is correlated with prognosis in sepsis. The pathophysiology of sepsis-associated thrombocytopenia (SAT) remains unclear and may be associated with several factors such as platelet activation due to vascular injury and pathogen, suppression of bone marrow, platelet-targeted antibodies and desialylation. This review summarized all these possible mechanisms in the 3 subtypes of SAT: increased platelet consumption, reduced platelet production and increased platelet destruction. Based on the clinically available platelet parameters, the evidence for identifying SAT subtypes and the recent progress in treatments according to these subtypes are proposed to provide new prospects for the management of SAT.

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