Dynamic changes of platelets and white blood cells in patients with traumatic brain injury and its clinical sigulficance
10.3760/cma.j.issn.1001-8050.2009.08.232
- VernacularTitle:创伤性脑损伤患者血小板、白细胞的动态变化及临床意义
- Author:
Yehua JIA
;
Xin CHEN
;
Jianhua XIONG
;
Jianning ZHANG
- Publication Type:Journal Article
- Keywords:
Brain injuries;
Thrombosis;
Inflammation;
Blood platelets;
Leukocytes
- From:
Chinese Journal of Trauma
2009;25(8):725-728
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the dynamic changes of platelets (PLT) and white blood cells (WBC) after traumatic brain injury (TBI) and discuss its clinical significance. Methods The number of PLT and WBC were examined in 63 patients with TBI by using cytoanalyze and also analyzed together with Glasgow Outcome Scale and concurrent infection, in the meantime, enzyme-linked immu-nosorbent was used to investigate concentration changes of C reactive protein (CRP) and thrombospondin 1 (TSPI) and analyze the correlation between CRP and TSP1. Results The number of WBC in all pa-tients, whether concurred with infection or not, was significantly increased within 24 hours after TBI (P < 0.01), with no statistical difference between patients without infection at day 4 and normal patients (P >0.05). However, the number of WBC was decreased to below 10 × 109/L in patients without infec-tion, which was significantly higher than that in normal patients (P < 0.05). In patients with infection and unfavorable prognosis, the number of WBC was increased again ay days 7-14, whereas that of PLT rose significantly at days 14-21 (P <0. 01). The concentration of TSPI was positively correlated with that of CRP (r = 0.720, P < 0.01). Conclusions Monitoring the dynamic changes of PLT and WBC is promising. The change of WBC at day 4 post injury is a key indicator to provide evidences of prophylactic antibiotic usage. Much attention should be paid to the dynamic change of PLT at days 14-21 post injury so as to evaluate the condition of hypercoagulability that can be potentially caused by inflammation response. Secondary increase of WBC and later increase, of PLT may affect prognosis of the patients. TSP1 and CRP may participate in thrombosis formation induced by inflammation.
