Lundsgaard-Hansen P, Pappova E
Ann Clin Res. 1981;13 Suppl 33:5-17.
With some amplifications, Starling's concept of the serum colloid osmotic or oncotic pressure as the determinant of fluid partition between the intravascular and the interstitial compartment has been confirmed by modern physiological research. The relationship between serum oncotic pressure and interstitial edema is non-linear, i.e. edema becomes progressively greater per mm decrease of the oncotic pressure. The intravascular volume effect of crystalloids is inseparable from interstitial edema, because it depends on an expansion of the interstitium which increases the hydrostatic pressure in that compartment sufficiently to compensate for a lowered capillary oncotic pressure. With large crystalloid fluid loads, about 90% of the total edema accumulates in skeletal muscle, subcutaneous fat, and the skin. The skin is particularly susceptible to the development of edema associated with a hypoproteinemic fluid overload, presumably because its extracellular space is three times larger than the average whole-body value. The intestine also shows a marked reaction to a hypoproteinemic fluid overload. There is evidence for a pathogenetic significance of hypoproteinemic edema in the myocardium, the intestine, and the skin. To rid a patient of this type of edema, concentrated albumin is indispensable, and its effects are demonstrable in the above-mentioned tissues, whereas a diuretic alone is ineffective. The therapeutic implications of these mechanisms and findings are discussed. In the lung, fluid exchange and distribution between the intravascular and the interstitial compartment is influenced by additional factors, and opinions on the use of colloids versus crystalloids continue to differ, particularly with respect to those circumstances where capillary permeability is presumably or demonstrably abnormal. However, the weight of the evidence still favours the concept that in patients with a much greater than respiratory distress syndromes much greater than, the serum oncotic pressure should at any rate not be permitted to drop below a certain critical level. A condensed review of these complex and as yet incompletely clarified problems is presented.
经过一些扩充后,现代生理学研究证实了斯塔林关于血清胶体渗透压或血浆渗透压是决定血管内和组织间隙间液体分配的概念。血清渗透压与组织间隙水肿之间的关系是非线性的,即渗透压每降低1毫米汞柱,水肿会逐渐加重。晶体液的血管内容积效应与组织间隙水肿密不可分,因为它依赖于组织间隙的扩张,这种扩张会使该间隙内的静水压充分升高,以补偿毛细血管渗透压的降低。大量输注晶体液时,约90%的总水肿积聚在骨骼肌、皮下脂肪和皮肤中。皮肤特别容易发生与低蛋白血症性液体超负荷相关的水肿,可能是因为其细胞外间隙比全身平均水平大三倍。肠道对低蛋白血症性液体超负荷也有明显反应。有证据表明低蛋白血症性水肿在心肌、肠道和皮肤中具有发病学意义。为了消除患者的这种类型水肿,浓缩白蛋白是必不可少的,其效果在上述组织中是可证实的,而单独使用利尿剂则无效。讨论了这些机制和发现的治疗意义。在肺中,血管内和组织间隙间的液体交换和分布受其他因素影响,关于胶体液与晶体液使用的观点仍然存在分歧,特别是在毛细血管通透性可能或明显异常的情况下。然而,现有证据仍支持这样的观点,即在患有远超过呼吸窘迫综合征的患者中,无论如何都不应使血清渗透压降至某个临界水平以下。本文对这些复杂且尚未完全阐明的问题进行了简要综述。