基于决策树算法构建糖尿病酮症酸中毒患儿脑水肿风险预测模型

Predictive risk model of brain edema in children with diabetic ketoacidosis based on decision tree algorithm

  • 摘要:
    目的 探讨糖尿病酮症酸中毒(DKA)患儿并发脑水肿的影响因素,并构建决策树模型。
    方法 回顾性选取158例DKA患儿的病历资料,根据患儿是否并发脑水肿分为并发脑水肿组(n=36)和未并发脑水肿组(n=122)。收集分析所有患儿的一般临床资料,并比较相关指标之间的差异性。采用多因素Logistic回归分析筛选DKA患儿并发脑水肿的影响因素。采用SPSS Modeler软件构建DKA患儿并发脑水肿的决策树模型,并分析决策树模型的预测效能。
    结果 本研究共纳入158例DKA患儿,其中有36例患儿并发脑水肿,脑水肿的发生率为22.78%。并发脑水肿组在年龄≤6岁、血糖>20 mmol/L、pH值≤7.35、碳酸氢盐浓度>10 mmol/L、血钠上升缓慢、持续低钠血症、血尿素氮升高方面占比高于未并发脑水肿组,差异有统计学意义(P < 0.05)。年龄≤6岁、血糖水平>20 mmol/L、pH值≤7.35、碳酸氢盐浓度>10 mmol/L、血钠上升缓慢和血尿素氮水平升高是DKA患儿并发脑水肿的独立危险因素(P < 0.05)。将单因素分析中具有统计学差异的7个项目纳入决策树模型,共筛选出解释变量6个,分别为碳酸氢盐浓度>10 mmol/L、血糖水平>20 mmol/L、持续低钠血症、血钠上升缓慢、pH值≤7.35和血尿素氮水平升高。决策树模型共5层,13个节点,其中血钠上升缓慢是最重要的预测因子。DKA患儿并发脑水肿的决策树模型的曲线下面积(AUC)是0.880(95%CI: 0.819~0.927), Logistic回归模型的AUC是0.735(95%CI: 0.659~0.802), 2个模型的Delong检验结果为Z=2.790, P=0.005, 结果提示决策树模型的AUC更优(P < 0.05)。
    结论 本研究构建的DKA患儿脑水肿的决策树预测模型显著优于Logistic回归模型。本研究证实血钠上升缓慢是最强预测因子,并建立碳酸氢盐>10 mmol/L→血糖>20 mmol/L→血钠动力学的3步预警路径。模型具有直接临床指导价值,但需多中心验证。血钠动力学与脑水肿的机制关联有待进一步研究。

     

    Abstract:
    Objective To investigate the influencing factors of cerebral edema in children with diabetic ketoacidosis (DKA) and construct a decision tree model.
    Methods A retrospective selection of medical records from 158 children with DKA was conducted. The patients were divided into cerebral edema group (n=36) and non-cerebral edema group (n=122) based on the presence or absence of concurrent cerebral edema. General clinical data of all children were collected and analyzed, and differences in relevant indicators were compared between the two groups. Multivariate logistic regression analysis was employed toscreen for factors influencing the development of cerebral edema in children with DKA. The SPSS Modeler software was used to construct a decision tree model for predicting cerebral edema in children with DKA, and the predictive efficacy of the model was analyzed.
    Results A total of 158 children with DKA were included in this study, of whom 36 developed cerebral edema, resulting in an incidence rate of 22.78%. The cerebral edema group had significantly higher proportions of patients aged ≤6 years, with blood glucose levels >20 mmol/L, pH values≤7.35, bicarbonate concentrations >10 mmol/L, slow increases in serum sodium levels, persistent hyponatremia and elevated blood urea nitrogen levels compared to the non-cerebral edema group (P < 0.05). Age≤ 6 years, blood glucose levels >20 mmol/L, pH values ≤7.35, bicarbonate concentrations>10 mmol/L, slow increases in serum sodium levels and elevated blood urea nitrogen levels were identified as independent risk factors for cerebral edema in children with DKA (P < 0.05). Seven items showing statistical differences in univariate analysis were incorporated into the decision tree model, from which six explanatory variables were selected: bicarbonate concentration >10 mmol/L, blood glucose level >20 mmol/L, persistent hyponatremia, slow increase in serum sodium levels, pH value≤7.35 and elevated blood urea nitrogen level. The decision tree model consisted of 5 layers and 13 nodes, with a slow increase in serum sodium levels being the most important predictor. The area under the curve (AUC) of the decision tree model for predicting cerebral edema in children with DKA was 0.880 (95%CI, 0.819 to 0.927), while that of the logistic regression model was 0.735 (95%CI, 0.659 to 0.802). The Delong test results for the two models were Z=2.790, P=0.005, indicating that the decision tree model had a superior AUC (P < 0.05).
    Conclusion The decision tree prediction model for cerebral edema in children with DKA constructed in this study significantly outperforms the logistic regression model. This study confirms that a slow increase in serum sodium levels is the strongest predictor and establishes a three-step early warning pathway involving bicarbonate: >10 mmol/L, blood glucose >20 mmol/L and serum sodium dynamics. The model has direct clinical guiding value but requires multicenter validation. The mechanistic association between serum sodium dynamics and cerebral edema warrants further investigation.

     

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