Changes in circulating inflammatory cells and the relationship to secondary brain injury in patients Changes in circulating inflammatory cells and the relationship to secondary brain injury in patients

Changes in circulating inflammatory cells and the relationship to secondary brain injury in patients

  • 期刊名字:中国神经再生研究(英文版)
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  • 论文作者:Xiaoping Tang,Tao Zhang,Yuanch
  • 作者单位:Department of Neurosurgery
  • 更新时间:2022-12-22
  • 下载次数:
论文简介

BACKGROUND: Recent studies have indicated that reactive encephalitis plays an important role in secondary tissue damage after craniocerebral injury.OBJECTIVE: To observe changes in white blood cells (WBC) and polymorphonuclear neutrophils (PMN)in peripheral blood, and to determine their role in secondary brain insult in patients with craniocerebral injury.DESIGN, TIME AND SETTING: A case-control study at the Department of Neurosurgery of the Affiliated Hospital North Sichuan University of Medical Sciences between August 2007 and May 2008.PARTICIPANTS: Sixty-three patients, admitted within 24 hours after craniocerebral injury and who received no surgery, were included in the study. The cohort consisted of 41 males and 22 females, aged 9-72years, with an average age of 42 years. Ten healthy volunteers, selected from the Department of Neurosurgery, were designated as the control group.METHODS: WBC and PMN from the peripheral blood were measured 0, 24, 48, 72, and 168 hours after admission to hospital. The Glasgow coma scale, area of cerebral hemorrhage, and degree of brain edema were simultaneously determined. The Glasgow outcome scale was evaluated six months after injury. The relationship between changes in WBC and PMN were analyzed. Sixty-three patients were divided into 0, 24,48, 72, and 168 hours groups, with admission time to hospital as the determining factor. As controls, WBC and PMN of peripheral blood were also detected in 10 healthy volunteers.MAIN OUTCOME MEASURES: The main outcome measures were WBC and PMN counts in the peripheral blood at 0, 24, 48, 72, and 168 hours after admission to hospital, the mutual relationship between GCS, WBC and PMN, and changes in brain hemorrhage volume and edema size.RESULTS: WBC peaked at 24 hours after injury, and PMN peaked at 48 hours after injury (P < 0.01).these="" measures="" negatively="" correlated="" to="" the="" glasgow="" coma="" scale="" (r="0.657," -0.541,="" respectively,="" p="">< 0.05).in="" patients="" with="" glasgow="" coma="" sale="">< 8,="" wbc="" and="" pmn="" were="" significantly="" higher="" than="" in="" the="" patients="" with="" gcs="" ≥="" 8="" (p="">< 0.05).="" cerebral="" hemorrhage="" reached="" a="" peak="" at="" 24="" hours="" after="" injury,="" and="" the="" degree="" of="" brain="" edema="" was="" maximal="" at="" 168="" hours="" after="" injury.="" wbc="" and="" pmn="" counts="" were="" positively="" correlated="" to="" cerebral="" hemorrhage="" volume="" and="" brain="" edema="" size="" (p="">< 0.05).conclusion:="" wbc="" and="" pmn="" counts="" significantly="" increased="" after="" craniocerebral="" injury="" and="" exhibited="" a="" correlation="" with="" the="" gcs="" score,="" volume="" of="" hemorrhage="" and="" edema,="" and="" glasgow="" outcome="" scale.="">

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