The endothelial glycocalyx is a 1µm thick continuous network of proteoglycans and glycoproteins on the intravascular aspect of endothelial cells that covers fenestrations and intercellular clefts. It serves to prevent platelet and leukocyte adhesion in addition to its function as a semipermeable layer that allows water and electrolytes to move across while preventing the movement of proteins and other macromolecules. This leads to the creation of a subglycocalyceal layer of fluid between the glycocalyx and endothelium with a volume of 700-1000 mL that is low in protein but with electrolytes that are in equilibrium with the plasma. The traditional Starling equation should therefore be altered such that the plasma to subglycocalyceal layer protein gradient is part of the determination of transcapillary flow not the plasma to interstitial fluid protein gradient as was traditionally taught. In other words, the oncotic pressure in the intravascular space is dependent upon an intact glycocalyx.
Colloids are large enough that they remain in the intravascular space and increase the oncotic pressure when the glycocalyx is intact. However, the glycocalyx is degraded by natriuretic peptides (which can be present with acute excessive intravascular volume loads), hyperglycemia, and inflammatory mediators released during surgery, trauma, and sepsis (e.g. CRP, bradykinin, TNF). Impairment of the glycocalyx favors movement of fluid, crystalloid or colloid, into the interstitial space and edema formation if fluid accumulation exceeds lymphatic clearance. The clinical significance of this is that with the inflammation that accompanies surgical and critically ill patients as well as the administration of large amounts of intravascular fluid to those patients, the endothelial glycocalyx will become impaired leading to poor retention in the intravascular space no matter the choice of fluid, colloid or crystalloid.
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