Department of Neurosurgery, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
Zhejiang Provincial Key Laboratory of Aging and Neurological Disorder Research, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China.
J Neurotrauma. 2022 Apr;39(7-8):508-519. doi: 10.1089/neu.2021.0388. Epub 2022 Mar 1.
In this study, we investigate the association of serum calcium with coagulopathy and hemorrhagic progression contusion (HPC) in patients with traumatic intraparenchymal hemorrhage (tIPH), and further explore the interaction and mediation effect between serum calcium and coagulopathy on HPC. We conducted retrospective analyses of patients with tIPH admitted to the First Affiliated Hospital of Wenzhou Medical University between January 2016 to December 2019. The clinical data, coagulation parameters, and serum calcium levels were collected for further analysis. Multi-variate logistic regression analysis was applied to identify the association of serum calcium level with coagulopathy and HPC. Causal mediation analysis (CMA) and additive interaction model were used to estimate the interaction and mediation effect between serum calcium as well as coagulopathy on HPC. Additionally, we repeated the analysis using corrected calcium. A total of 473 patients were included in this study. Of these, 54 (11.4%) patients had hypocalcemia at admission, 105 (22.2%) presented with coagulopathy, and 187 (39.5%) experienced HPC. Admission serum calcium level in patients presented with coagulopathy and HPC were 8.84 (interquartile range [IQR]: 8.44-9.40] and 8.92 (IQR: 8.48-9.40) mg/dL respectively, which were significantly lower than that of patients without coagulopathy (9.10 [IQR: 8.68-9.88] and 9.12 [IQR: 8.72-9.89] mg/dL; all < 0.001). Multi-variate logistic regression analysis identified that hypocalcemia emerged as an independent risk factor for coagulopathy and HPC. However, no significant interaction was detected between hypocalcemia and coagulopathy. CMA showed that the mediator coagulopathy explained 24.4% (95% confidence interval: 4.7-65.0%; = 0.006) of the association between hypocalcemia and HPC. Moreover, comparable results were held using corrected calcium, as well. Admission serum calcium level is associated with the HPC for patients with tIPH and this relationship is partially mediated by coagulopathy, but no significant interaction is detected. Further studies are needed to validate the findings and explore its mechanisms.
在这项研究中，我们探讨了血清钙与创伤性脑实质内出血（tIPH）患者凝血障碍和出血性进展性挫伤（HPC）的关系，并进一步探讨了血清钙与凝血障碍对 HPC 的相互作用和中介作用。我们对 2016 年 1 月至 2019 年 12 月期间温州医科大学附属第一医院收治的 tIPH 患者进行了回顾性分析。收集了临床资料、凝血参数和血清钙水平进行进一步分析。采用多变量逻辑回归分析来确定血清钙水平与凝血障碍和 HPC 的关系。采用因果中介分析（CMA）和加性交互模型来估计血清钙以及凝血障碍对 HPC 的交互和中介作用。此外，我们使用校正钙重复了分析。这项研究共纳入了 473 名患者。其中，54 名（11.4%）患者入院时血钙水平低，105 名（22.2%）患者出现凝血障碍，187 名（39.5%）患者发生 HPC。出现凝血障碍和 HPC 的患者入院时血清钙水平分别为 8.84（IQR：8.44-9.40）和 8.92（IQR：8.48-9.40）mg/dL，明显低于无凝血障碍患者的 9.10（IQR：8.68-9.88）和 9.12（IQR：8.72-9.89）mg/dL（均<0.001）。多变量逻辑回归分析确定低钙血症是凝血障碍和 HPC 的独立危险因素。然而，低钙血症和凝血障碍之间没有检测到显著的相互作用。CMA 显示凝血障碍作为低钙血症和 HPC 之间的中介物，解释了 24.4%（95%置信区间：4.7-65.0%； = 0.006）的关联。此外，使用校正钙也得到了类似的结果。入院时血清钙水平与 tIPH 患者的 HPC 相关，这种关系部分由凝血障碍介导，但未检测到显著的相互作用。需要进一步的研究来验证这些发现并探讨其机制。
