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[脂肪栓塞与骨折,文献综述]

[Fat embolism and fracture, a review of the literature].

作者信息

Müller C, Rahn B A, Pfister U

机构信息

Labor für experimentelle Chirurgie, Städtisches Klinikum Karlsruhe.

出版信息

Aktuelle Traumatol. 1992 Jun;22(3):104-13.

PMID:1353289
Abstract

The reasons of fat embolism as well as the following fat embolism syndrome are most likely long bone fractures, especially if the femur is participated. On the other hand there are cases, where a severe concussion of the entire body caused fat embolism. But it is also supposed, that intramedullary reaming as well as the insertion of knee- and hip-prostheses could be a releasing factor, because the applicated pressure on the medullary canal can cause a fat release in the systemic blood system. The morbidity depends on age and fracture, which is on fractures between 0.9 and 2%. The most affected group are people between 18 and 28 years of age. The fat embolism is manifesting at 46-60% of the patients in the first 24 hours and over 90% of the patients are affected in the first three days. If you look at the metabolic changes, you will find shortly after the fracturing process a rapid increase of free fatty acids (FFA), as well as an increase of the plasmatic enzyme levels (lipase, GPT, GOT, GLDH, LDH, etc.), catecholamines and glucocorticoids. In order to discuss the pathogenesis in a fairly complete way, you have to take different theories into consideration, because several parallel running processes--which are influencing each other--are leading to the syndrome. Infloating theory: Proceeding on the assumption that contents of the bone marrow are floating out of the fracture gap into the venous system and are leading to fat embolism in the lungs. Lipase theory: You can diagnose in 50-70% of the fracture patients an increase of the lipase level, which is correlating with the manifestation of the fat embolism. The lipase releases fat from the body depositories in addition to the fat, who is coming out of the fracture gap. Shock and coagulation theory: During shock the microcirculation is decelerated, the blood viscosity is increased and the suspension stability of the cellular blood components is decreased, which is leading to the sludging phenomenon. So the capillaries of the lungs and the brain are a kind of sludge filter of the blood, that is changed in its suspensions stability. Free fatty acids theory: Primary existing capillary defects are reasonable caused by free fatty acids (FFA). They are hydrolyzed of the neutral fats and are histotoxic for the walls of the blood vessels.(ABSTRACT TRUNCATED AT 400 WORDS)

摘要

脂肪栓塞以及随后的脂肪栓塞综合征最常见的原因很可能是长骨骨折,尤其是涉及股骨的骨折。另一方面,也有因全身严重撞击导致脂肪栓塞的病例。但也有人认为,髓内扩髓以及膝关节和髋关节假体的植入可能是一个诱发因素,因为施加在髓腔内的压力会导致脂肪释放入全身血液系统。发病率取决于年龄和骨折情况,骨折患者的发病率在0.9%至2%之间。受影响最严重的群体是18至28岁的人群。46%至60%的患者在最初24小时内出现脂肪栓塞,超过90%的患者在头三天内受到影响。观察代谢变化时,会发现在骨折后不久游离脂肪酸(FFA)迅速增加,血浆酶水平(脂肪酶、谷丙转氨酶、谷草转氨酶、谷氨酸脱氢酶、乳酸脱氢酶等)、儿茶酚胺和糖皮质激素也会增加。为了较为全面地探讨发病机制,必须考虑不同的理论,因为几个相互影响的并行过程导致了该综合征。漂浮理论:基于骨髓内容物从骨折间隙漂浮到静脉系统并导致肺部脂肪栓塞的假设。脂肪酶理论:在50%至70%的骨折患者中可诊断出脂肪酶水平升高,这与脂肪栓塞的表现相关。脂肪酶除了使从骨折间隙出来的脂肪释放外,还能从身体储存部位释放脂肪。休克与凝血理论:休克期间微循环减慢,血液粘度增加,血细胞成分的悬浮稳定性降低,导致血液淤滞现象。因此,肺和脑的毛细血管是血液的一种淤滞过滤器,其悬浮稳定性发生了变化。游离脂肪酸理论:游离脂肪酸(FFA)合理地导致了原发性存在的毛细血管缺陷。它们由中性脂肪水解产生,对血管壁具有组织毒性。(摘要截选至第400个单词)

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