Purpose <p>Contusion expansion is a key determinant of outcome after traumatic brain injury (TBI). Because many patients develop acute coagulopathy, it has been proposed that hemostatic changes may drive this expansion, but the link remains uncertain.</p> Methods <p>In this retrospective single-center cohort, we included adults with isolated moderate-to-severe TBI and no pre-injury antithrombotic therapy. The hemostatic markers activated partial thromboplastin time (APTT), prothrombin time (PT, reported as INR), platelet count (PLT), and fibrinogen were measured on admission and during the first 72&#xa0;h. Contusion volumes were derived from serial CT scans. Associations between hemostatic markers and contusion volumes over time were analyzed using generalized additive mixed models (GAMMs), adjusting for confounders.</p> Results <p>Among 109 patients, median admission values were fibrinogen 2.4&#xa0;g/L, PT-INR 1.0, APTT 29&#xa0;s, and PLT 233 × 10<sup>9</sup>/L. After admission, fibrinogen and PLT declined, whereas PT-INR and APTT increased modestly. Contusion volume increased from a median of 0.7&#xa0;ml at baseline to 4.6&#xa0;ml on the third CT. In univariable models, higher APTT and PT-INR values and lower platelet counts were associated with larger contusion volumes, but these associations lost significance after adjustment for age and time from injury.</p> Conclusion <p>Hemostatic disturbances, as measured by standard coagulation assays, were common after TBI but not independently associated with contusion volume over time.</p>

错误:搜索内容不能为空,请输入英文关键词
错误:关键词超出字数限制,请精简
高级检索

Association between hemostatic changes and contusion volume in traumatic brain injury: an observational cohort study

  • Alexander Fletcher-Sandersjöö,
  • Emma Hammarlund,
  • Caroline Lindblad,
  • Logan Froese,
  • Henrike Häbel,
  • Jennifer Sebghati,
  • Marc Maegele,
  • Mikael Svensson,
  • Bo-Michael Bellander,
  • David W. Nelson,
  • Eric Peter Thelin

摘要

Purpose

Contusion expansion is a key determinant of outcome after traumatic brain injury (TBI). Because many patients develop acute coagulopathy, it has been proposed that hemostatic changes may drive this expansion, but the link remains uncertain.

Methods

In this retrospective single-center cohort, we included adults with isolated moderate-to-severe TBI and no pre-injury antithrombotic therapy. The hemostatic markers activated partial thromboplastin time (APTT), prothrombin time (PT, reported as INR), platelet count (PLT), and fibrinogen were measured on admission and during the first 72 h. Contusion volumes were derived from serial CT scans. Associations between hemostatic markers and contusion volumes over time were analyzed using generalized additive mixed models (GAMMs), adjusting for confounders.

Results

Among 109 patients, median admission values were fibrinogen 2.4 g/L, PT-INR 1.0, APTT 29 s, and PLT 233 × 109/L. After admission, fibrinogen and PLT declined, whereas PT-INR and APTT increased modestly. Contusion volume increased from a median of 0.7 ml at baseline to 4.6 ml on the third CT. In univariable models, higher APTT and PT-INR values and lower platelet counts were associated with larger contusion volumes, but these associations lost significance after adjustment for age and time from injury.

Conclusion

Hemostatic disturbances, as measured by standard coagulation assays, were common after TBI but not independently associated with contusion volume over time.