BACKGROUND: Postinjury multiple organ failure (MOF) remains the leading cause of morbidity and late mortality after severe trauma. Our previous work consistently identified an association between thrombocytopenia and progression to MOF. In addition, recent studies suggest that platelets play a critical role in postinjury hyperinflammation. Therefore, we hypothesized that postinjury thrombocytopenia is a marker for progression to MOF. METHODS: One thousand four hundred fifteen critically injured surgical intensive care unit patients surviving>48 hours were prospectively collected over 12 years. Variables studied included age, Injury Severity Score (ISS), red blood cell (RBC)/12 h, MOF (Denver MOF score), death, infectious complications, and noninfectious complications. Thrombocytopenia was defined as platelets<80k. Logistic regression was applied to identify independent predictors of MOF and death. RESULTS: Mean±standard error of the mean ISS, age, and RBC were 29.3±11.3; 37.4 years±16.6 years; and 4.4 units±5 units. MOF developed in 346 patients (24%) and 118 patients (8%) died. Thrombocytopenia occurred in 35% of patients within 48-hour postinjury and was associated with a significant increase in ISS, RBC transfused, and age. Logistic regression confirmed that thrombocytopenia was a major independent risk factor for all adverse outcomes with an odds ratio of 2.4 for developing MOF and 3.4 for death. After adjustment for these factors, a relative increase in platelet count from day 3 to day 10 was associated with a significantly lower likelihood of MOF and death. CONCLUSION: Early postinjury thrombocytopenia is an independent risk factor for MOF, death, and other complications. Following platelet count dynamics over the first several days postinjury can help predict which high-risk patient will develop these adverse outcomes.
BACKGROUND:Postinjury multiple organ failure (MOF) remains the leading cause of morbidity and late mortality after severe trauma. Our previous work consistently identified an association between thrombocytopenia and progression to MOF. In addition, recent studies suggest that platelets play a critical role in postinjury hyperinflammation. Therefore, we hypothesized that postinjury thrombocytopenia is a marker for progression to MOF. METHODS: One thousand four hundred fifteen critically injured surgical intensive care unit patients surviving>48 hours were prospectively collected over 12 years. Variables studied included age, Injury Severity Score (ISS), red blood cell (RBC)/12 h, MOF (Denver MOF score), death, infectious complications, and noninfectious complications. Thrombocytopenia was defined as platelets<80k. Logistic regression was applied to identify independent predictors of MOF and death. RESULTS: Mean±standard error of the mean ISS, age, and RBC were 29.3±11.3; 37.4 years±16.6 years; and 4.4 units±5 units. MOF developed in 346 patients (24%) and 118 patients (8%) died. Thrombocytopenia occurred in 35% of patients within 48-hour postinjury and was associated with a significant increase in ISS, RBC transfused, and age. Logistic regression confirmed that thrombocytopenia was a major independent risk factor for all adverse outcomes with an odds ratio of 2.4 for developing MOF and 3.4 for death. After adjustment for these factors, a relative increase in platelet count from day 3 to day 10 was associated with a significantly lower likelihood of MOF and death. CONCLUSION: Early postinjury thrombocytopenia is an independent risk factor for MOF, death, and other complications. Following platelet count dynamics over the first several days postinjury can help predict which high-risk patient will develop these adverse outcomes.
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