目的：分析血清中Caspase酶切割细胞角蛋白18的裂解产物CCCK-18与单纯硬膜外血肿并脑疝患者 术后继发性脑梗死发生发展的关系，评价CCCK-18对继发性脑梗死的早期预测能力及临床决策价值。方 法：回顾性分析206例单纯硬膜外血肿并脑疝患者术前血清CCCK-18浓度与术后继发性脑梗死占位体积的 潜在关系。结果：术后继发脑梗死49例（23.78%），其中占位体积＞20 mL 32例（15.53%）纳入大面积脑梗死 组；占位体积＜20 mL 17例（8.25%）纳入小面积脑梗死组，无脑梗死157例（76.21%）纳入无脑梗死组。大面 积脑梗死组患者术前 CCCK-18 浓度显著高于小面积脑梗死组和无脑梗死组（均 P＜0.001）。术前血清 CCCK-18 水平与继发性脑梗死的占位体积呈线性相关（P＜0.001）。受试者工作曲线分析提示术前血清 CCCK-18水平对术后继发性大面积脑梗死的曲线下面积为0.814（P＜0.001），以241 U/L为预测界值的准确 度达到83.50%。多因素logistic回归分析表明，CCCK-18＞241 U/L是单纯硬膜外血肿并脑疝患者术后继发 大面积脑梗死的独立危险因素（P＜0.001）。术后随访6个月，术前血清CCCK-18＞241 U/L患者的格拉斯哥 预后量表（GOS）评分明显低于CCCK-18＜241 U/L的患者（P＜0.001）。结论：术前血清CCCK-18增高与单 纯硬膜外血肿致脑疝患者术后继发性大面积脑梗死密切相关，可作为辅助决策此类患者去骨瓣减压手术模 式并预估长期神经功能预后的生物标志物。

To analyze the correlation between serum caspase-cleaved cytokeratin 18 (CCCK-18) elevation and the occurrence and development of cerebral infarction secondary to traumatic epidural hematoma and concurrent cerebral herniation, and to clarify its early predictive ability and clinical decision-making value for secondary cerebral infarction. Methods: Preoperative serum CCCK-18 levels in 206 enrolled patients with cerebral herniation from isolated epidural hematoma were analyzed retrospectively for its potential correlation with the occupying volume of postoperative secondary cerebral infarction. Results: Post-operative secondary cerebral infarction was determined in 49 patients (23.78%). Among them, 32 cases (15.78%) had an occupying volume larger than 20 mL and were assigned to the massive cerebral infarction group; 17 cases (8.25%) had an occupying volume smaller than 20 mL and were assigned to the moderate cerebral infarction group, and the remaining 157 cases (76.21% ) were assigned to the non-cerebral infarction group. The concentration of CCCK-18 in the massive cerebral infarction group was significantly higher than that in the moderate cerebral infarction group and that in the non-cerebral infarction group (each P<0.001). The preoperative serum CCCK-18 level was linearly correlated with the occupying volume of secondary cerebral infarction (P<0.001). Receiver Operating Characteristic (ROC) showed that the area under the curve (AUC) of preoperative serum CCCK-18 was 0.814 (P<0.001), and the accuracy of assigning 241 U/L as the predictive threshold value was 83.50% . Multivariate logistic regression analysis showed that a >241 U/L preoperative serum CCCK-18 was an independent risk factor for postoperative massive cerebral infarction secondary to traumatic epidural hematoma and concurrent cerebral herniation. At the end of the 6-month follow-up, the GOS (Glasgow Outcome Scale) score of patients with serum CCCK-18 higher than 241 U/L was significantly lower than that of patients with levels lower than 241 U/L (P<0.001). Conclusion: Preoperative increased serum CCCK-18 is closely related to secondary massive cerebral infarction in patients with cerebral herniation from isolated epidural hematoma. It can serve as a useful biomarker for assisting decision-making of decompressive craniectomy surgery and predicting long-term neurological function.