Sepsis is the most common cause of thrombocytopenia in intensive care unit (ICU)
patients, with an incidence rate as high as 35%-59%. Severe thrombocytopenia (≤50×10⁹/L)
accounts for 30% of cases, and the degree of thrombocytopenia is positively correlated
with mortality risk [1-3]. Studies have shown that patients with sepsis-associated
thrombocytopenia (SAT) not only experience prolonged ICU stays and mechanical ventilation
duration but also have significantly increased rates of major bleeding events and renal
replacement therapy. Meanwhile, the 28-day mortality rate rises with the severity of
thrombocytopenia [4, 5]. Platelets play a dual role in sepsis: on one hand, they act as
"innocent bystanders" reflecting disease severity; on the other hand, they participate in
the pathological process through immune regulation and microvascular protection. For
example, platelets contribute to host defense by facilitating neutrophil extracellular
traps (NETs) formation mediated by Toll-like receptor 4 (TLR4), but a reduction in
platelet count can lead to impaired endothelial barrier function, exacerbating organ
edema and bleeding risk [6, 7]. Furthermore, dynamic changes in platelet morphological
parameters, such as mean platelet volume (MPV) and platelet distribution width (PDW), are
independently associated with inflammatory response and mortality, highlighting the
importance of platelet function monitoring [8].
In clinical practice, the primary goal of exogenous platelet transfusion in SAT patients
is to rapidly increase circulating platelet counts in cases of inadequate platelet
production or excessive consumption, thereby reducing bleeding risk. Due to the complex
mechanisms of thrombocytopenia in sepsis-including bone marrow suppression, peripheral
consumption (e.g., disseminated intravascular coagulation (DIC), immune-mediated
destruction), and splenic sequestration-endogenous platelet recovery is often delayed.
Exogenous transfusion provides immediate platelet supplementation, particularly for
patients with severe thrombocytopenia (≤50×10⁹/L) accompanied by bleeding tendencies or
those requiring invasive procedures (e.g., surgery, central venous catheterization) [9].
Compared to endogenous platelet production (which typically takes 5-7 days), exogenous
transfusion helps to rapidly correct hemostatic function, reduce the risk of spontaneous
bleeding (such as gastrointestinal or intracranial bleeding); improve endothelial barrier
function, decrease microvascular leakage, thereby alleviating organ edema and hypoxic
injury; and provide platelets with immunomodulatory activity, potentially regulating
excessive inflammatory responses through the release of anti-inflammatory factors (e.g.,
TGF-β, IL-10) [10, 11].
However, current treatment strategies for SAT remain controversial. Some studies indicate
that platelet transfusion may increase in-hospital mortality, particularly in patients
with severe thrombocytopenia (≤50×10⁹/L), where transfusion is associated with higher
28-day and 90-day mortality rates, along with risks such as transfusion reactions and
alloimmunization [12, 13]. Potential mechanisms include: the inflammatory
microenvironment in septic patients may cause rapid activation or destruction of
transfused platelets, reducing transfusion efficacy; allogeneic platelets may carry
pro-inflammatory mediators (e.g., mitochondrial DNA, high mobility group box 1 (HMGB1)),
further exacerbating systemic inflammatory response; and transfusion-related
complications, such as transfusion-related acute lung injury (TRALI),
transfusion-associated circulatory overload (TACO), and alloimmune reactions, may
contribute to adverse clinical outcomes [14, 15]. Additionally, recent studies have found
that platelet function may be impaired in septic patients (e.g., increased glycoprotein
Ibα (GPIbα) shedding), leading to reduced adhesion and aggregation capacity of transfused
platelets and potentially worsening endothelial dysfunction [16].
Previous studies on platelet transfusion and outcomes in SAT patients were all based on
database analyses. The results showed that platelet transfusion in septic patients with
thrombocytopenia was associated with increased mortality [17, 18]. Currently, there are
no multicenter studies on platelet transfusion specifically for SAT patients, and the
benefits and risks of platelet transfusion still require further validation based on
large-sample data.
In summary, investigating the correlation between platelet transfusion during ICU stay
and 28-day mortality in SAT patients, as well as evaluating the impact of platelet
transfusion on bleeding and thrombotic events and inflammation control, is of great
significance for optimizing SAT management strategies. This study aims to analyze the
effect of platelet transfusion on the prognosis of SAT patients, thereby providing an
evidence-based foundation for clinical decision-making.
