败血症患者血小板轨迹变化的预后意义:利用重症监护医学信息中心-IV 数据库进行的回顾性分析。

IF 2.7 3区 医学 Q2 CRITICAL CARE MEDICINE SHOCK Pub Date : 2024-10-10 DOI:10.1097/SHK.0000000000002493
Yingxin Wang, Jiaqian Wu, Tenghao Shao, Dan Su, Xin Ma, Zhanbiao Yu, Ning Li
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引用次数: 0

摘要

目的:脓毒症患者的血小板数量经常会减少或增加,但这些时间模式对预后的影响仍不清楚。本研究旨在探讨血小板轨迹的变化对脓毒症临床预后的影响:本研究是一项回顾性分析,使用的数据来自重症监护医学信息市场(MIMIC)-IV 数据库。根据脓毒症确诊后 14 天内血小板计数的变化,将脓毒症患者的血小板轨迹分为四种不同的模型。随后评估了这些轨迹对患者预后的影响:共纳入了 15,250 名脓毒症患者来构建模型,并确定了以下四种不同的血小板计数轨迹:血小板水平正常(表型 1);血小板水平持续偏低(表型 2);血小板水平逐渐升高,超出正常范围(表型 3);血小板水平持续显著升高(表型 4)。四种表型的 28 天死亡率、院内死亡率和 90 天死亡率在统计学上存在明显差异。多变量回归分析显示,与血小板水平正常组(表型 1)相比,血小板水平持续偏低组(表型 2)的院内死亡率(比值比 [OR] = 1.34,95% 置信区间 [CI]:1.16-1.54)、28 天死亡率(比值比 [OR] = 1.69,95% 置信区间 [CI]:1.47-1.94)和 90 天死亡率(比值比 [OR] = 1.50,95% 置信区间 [CI]:1.32-1.69)更高。与表型 1 相比,表型 3 和表型 4 的院内死亡率没有差异,但表型 4 的 28 天死亡率有所上升(P < 0.05),表型 3 的 90 天死亡率呈下降趋势(P < 0.05)。经回归调整的反概率加权结果与上述发现基本一致,只是表型 4 和表型 1 的 28 天死亡率没有统计学差异。在基于年龄、体重、抗血小板药物或疗法的亚组中,血小板水平与这些因素之间存在交互作用:结论:在败血症患者中,血小板计数减少与死亡率增加有关,而血小板计数适度增加可降低 90 天死亡率。然而,对于血小板计数持续升高的患者,在使用抗血小板药物或疗法时应谨慎,因为这可能会增加死亡率。
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Prognostic Implications of Changes in Platelet Trajectories in Patients With Sepsis: A Retrospective Analysis Using the Medical Information Mart for Intensive Care-IV Database.

Objective: Patients with sepsis often experience reductions or increases in platelet counts, but the implications of these temporal patterns on prognosis remain unclear. The aim of this study was to investigate the impact of changes in platelet trajectories on the clinical prognosis of sepsis.

Methods: This study was a retrospective analysis using data from the Medical Information Mart for Intensive Care (MIMIC)-IV database. Patients with sepsis were identified from the database, and their platelet trajectories were categorized into four distinct models based on the changes in platelet counts over a period of 14 days post-diagnosis of sepsis. The effect of these trajectories on patient prognosis was subsequently evaluated.

Results: A total of 15,250 patients with sepsis were included to construct a model, and the following four distinct platelet count trajectories were identified: normal platelet levels (phenotype 1); persistently low platelet levels (phenotype 2); gradually increasing platelet levels exceeding the normal range (phenotype 3); and consistently significantly elevated platelet levels (phenotype 4). Statistically significant differences were found in the 28-day mortality, in-hospital mortality, and 90-day mortality among the four phenotypes. Multivariate regression analysis showed that compared to the group with normal platelet levels (phenotype 1), the group with persistently low platelet levels (phenotype 2) had higher in-hospital mortality (odds ratio [OR] = 1.34, 95% confidence interval [CI]: 1.16-1.54), 28-day mortality (OR = 1.69, 95% CI: 1.47-1.94), and 90-day mortality (OR = 1.50, 95% CI: 1.32-1.69). There was no difference in in-hospital mortality between phenotypes 3 and 4 compared to phenotype 1, although phenotype 4 showed an increase in 28-day mortality (p < 0.05), and phenotype 3 showed a decreasing trend in 90-day mortality (p < 0.05). The results of inverse probability weighting adjusted by regression were basically consistent with the above findings, except that there was no statistical difference in 28-day mortality between phenotype 4 and phenotype 1. In the subgroups based on age, weight, and antiplatelet drugs or therapies, there was an interaction between platelet levels and these factors.

Conclusion: In patients with sepsis, a decrease in platelet count is associated with increased mortality, while a moderate increase in platelet count can reduce 90-day mortality. However, for patients with persistently elevated platelet counts, caution is advised when using antiplatelet drugs or therapies, as it may increase mortality.

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来源期刊
SHOCK
SHOCK 医学-外科
CiteScore
6.20
自引率
3.20%
发文量
199
审稿时长
1 months
期刊介绍: SHOCK®: Injury, Inflammation, and Sepsis: Laboratory and Clinical Approaches includes studies of novel therapeutic approaches, such as immunomodulation, gene therapy, nutrition, and others. The mission of the Journal is to foster and promote multidisciplinary studies, both experimental and clinical in nature, that critically examine the etiology, mechanisms and novel therapeutics of shock-related pathophysiological conditions. Its purpose is to excel as a vehicle for timely publication in the areas of basic and clinical studies of shock, trauma, sepsis, inflammation, ischemia, and related pathobiological states, with particular emphasis on the biologic mechanisms that determine the response to such injury. Making such information available will ultimately facilitate improved care of the traumatized or septic individual.
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