久坐会导致臀部皮下组织缺血,从而导致压力性溃疡的发生。

Johan Thorfinn, Folke Sjoberg, Disa Lidman
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引用次数: 10

摘要

更好地了解臀部压疮是如何形成的,将改善预防措施。我们的目的是研究坐着时臀部皮下脂肪灌注减少和缺血的迹象。用微电极定量氧(pO(2))。指示有氧或无氧代谢的代谢物(葡萄糖、乳酸、丙酮酸和甘油)通过微透析进行量化。研究人员对16名健康人进行了研究,他们分别坐在轮椅坐垫和坚硬的表面上。绘制坐姿压力图,测量皮下脂肪层厚度。结果表明,坐下时,pO(2)和葡萄糖显著减少,而坐在坚硬表面上对pO(2)的影响更为深远。加载后葡萄糖和pO(2)均显著升高。我们得出结论,坐骨结节的皮下脂肪组织在坐着时发生缺血。这一发现支持了一种理论,即不仅皮肤参与了压疮的早期发展,深层组织也参与了压疮的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sitting can cause ischaemia in the subcutaneous tissue of the buttocks, which implicates multilayer tissue damage in the development of pressure ulcers.

A better understanding of how pressure ulcers develop in the buttocks will improve prophylactic measures. Our aim was to investigate signs of reduced perfusion and ischaemia in the subcutaneous fat in the buttocks during sitting. A microelectrode was used to quantify oxygen (pO(2)). Metabolites that indicate aerobic or anaerobic metabolism (glucose, lactate, pyruvate, and glycerol) were quantified using microdialysis. Sixteen healthy people were studied while they sat on a wheel chair cushion, and a hard surface. Sitting pressures were mapped, and the thickness of the subcutaneous fatty layer was measured. The results showed that pO(2) and glucose were significantly reduced during sitting, and for pO(2) the effect is significantly more profound during sitting on a hard surface. After loading, both glucose and pO(2) increased significantly. We conclude that the subcutaneous adipose tissue covering the ischial tuberosities becomes ischaemic during sitting. This finding supports the theory that not only is the skin involved in early development of pressure ulcers, but also the deeper tissues.

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