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作 者:张海鹏[1] 张力[2] 苏峰[3] 李玉清[4] 朱颖波[1] 刘建平 赵宝山[1] 朱永[1]
机构地区:[1]河北省涿鹿县医院创伤外科,张家口075600 [2]河北北方大学药理生化研究所,张家口075000 [3]河北北方大学附属第一医院骨科,张家口075000 [4]河北省涿鹿县医院检验科,张家口075600 [5]河北省涿鹿县卫生防疫站检验科,张家口075600
出 处:《复旦学报(医学版)》2004年第4期425-428,共4页Fudan University Journal of Medical Sciences
摘 要:目的 探索长骨及骨盆骨折后脂肪栓子的干预时机和脂栓形成的因素。方法 分析了 172例长骨及骨盆骨折 ,包括其中临床和亚临床脂肪栓塞 [(sub - )CFE]的病例资料 ;比较长骨及骨盆骨折中尿酮体阳性 (PK)和阴性 (NK)者的发病情况 ;比较长骨及骨盆骨折 (LP组 )与创伤严重程度 (ISS)相当的颅面骨骨折 (CF组 )的血TG。结果 PK组 (sub - )CFE发生率高于NK组 ,差异有非常显著意义 (P <0 .0 1) ,其中 4例有进行性的血沉或血小板异常。LP组中的PK组TG水平高于NK组 ,差异有显著意义 (P <0 .0 5 ) ;LP组的TG及其阳性率高于同等ISS的CF组 ,差异分别有非常显著和极显著意义 (P <0 .0 1和P <0 .0 0 1)。结论 长骨及骨盆骨折后TG高至并发酮尿时 ,脂肪栓塞综合征的发病风险显著增高 ,可作干预TG增高和预防FES的临床时机。ISS不是脂栓形成中的主要因素 。Purpose: To probe a parameter of the hypertriglyceridemia due to fat emboli after fracture of long bone or pelvis(FLBP), and to analyze the generation of post-FLBP fat emboli. Methods: The clinical data of the cases with FLBP (LP group), including ones with clinical or sub-clinical fat embolism[(sub-) CFE], were analyzed. The prevalence rate of the (sub-)CFE in the group with ketonugia(PK group) was compared with that in the group without ketonugia(NK group). Serum triglyceride (TG) level of LP group was compared with that of the group with fracture of craniofacil bone (CF group), which was neither of long bone nor of pelvis. Results: A proved (sub-) CFE occurred in 9 cases with post-FLBP hypertrialuceridemia in association with ketonuria, merely of PK group, and prevalence rate of(sub-)CFE in PK group was significantly higher than that in the NK one(P < 0.01). Of the 9 cases, only 5 ones had ever been accompanied by the progressive fast blood sedimentation or by the progressive thrombocytopenia. TG of PK group was significantly higher than that of the NK one(P < 0.05) and the hypertriglyceridemia positive rate of LP group was far higher than that of the CF group (P < 0.001), nevertheless there was hardly different injury severity scores between LP and CF group. Conclusions: The results suggested that ketonuria concurrent with post-FLBP hypertriglyceridemia could basically enhance the risk of (sub-)CFE, which could be regarded as the time parameter for requiring medical interference to lower TG and for preventing from FES. Post-FLBP fat emboli showed its prime origin from intramedullary myelotriglyceride of the long bone or pevil. However, only for a few of post-trauma patients, might endovascular reaction be an important causal factor of fat emboli.
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