Page 443 - WSAVA2018
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L. Smart1
1Murdoch University, College of Veterinary Medicine, Murdoch, Australia
In the setting of shock, rapid fluid administration is often life-saving. Isotonic crystalloids remain the first choice
in the majority of patients, with the least amount of evidence for causing harm. However, there is growing discussion that the administration of large volumes of crystalloid fluid may cause harm, especially for patients with systemic inflammation and increased vascular permeability. This talk will outline the potential adverse effects of large volumes of crystalloid, including those related to the constituents of the fluid (chloride, acetate), wash-out of the endothelial glycocalyx, and pro- inflammatory responses.
Constituents of isotonic crystalloids
The adverse effects of using 0.9% saline are probably the most well-recognised detriment of using high volumes of crystalloid fluid. The two main concerns
with using 0.9% saline for blood volume expansion are dilutional acidosis and acute kidney injury. Dilutional acidosis is created by delivery of excessive chloride
and subsequent dilution of bicarbonate, an effect that has been documented in dogs with haemorrhagic shock.(1) However, in this study, the change in blood pH was small and self-limiting. Still, if a patient is already severely acidaemic, reducing the blood pH further may have adverse consequences. The second concern is increasing the risk of acute kidney injury; which has been raised as a potential in human medicine.(2) The theory is that delivery of large amounts of chloride to the macula densa may reduce much-needed renin-angiotensin- aldosterone system activation in times of need (i.e. reduced renal perfusion). It is unknown if this effect is clinically relevant for veterinary medicine but suffice to say, 0.9% saline can be easily avoided and should only be used in alkalaemic patients.
The remaining choices for isotonic crystalloid administration belong in the group of ‘balanced’ fluids, which avoid excessive chloride by providing other anions such as lactate, gluconate and acetate. The most commonly used fluid is lactated Ringer’s solution or compound sodium lactate. The provision of lactate does not contribute to lactic acidosis but provides a substrate for bicarbonate production. However, in a patient that can’t metabolise lactate due to liver dysfunction, this fluid may cause mild hyperlactataemia. This is only inconvenient in the sense that it is difficult to then
use lactate as a marker of perfusion. The remaining
choices are fluids containing combinations of acetate and gluconate, such as Plasmalyte-148. These anions
are metabolised by the kidneys and skeletal muscle, providing a source of buffer. One possible adverse effect of injecting acetate rapidly is vasodilation,(3) which may momentarily worsen perfusion. Also, acetate has been shown in rats to be somewhat pro-inflammatory when used for fluid resuscitation.(4, 5) Therefore, if a choice can be made between a balanced crystalloid with either lactate or acetate, then the fluid with lactate is probably the better choice.
Shedding of the endothelial glycocalyx
The endothelial glycocalyx (EG) is a carbohydrate-rich scaffold of proteoglycans and glycosaminoglycans on the luminal surface of endothelial cells (Figure 1). The meshwork of carbohydrates and proteins creates an immobile plasma layer and barrier, preventing interaction between cells in circulation and endothelial cells. This prevents adhesion of platelets and white blood cells, and discourages thrombosis.
Figure 1 – The main components of the endothelial glycocalyx
The EG also plays an important role in fluid flux across the endothelium, which has led to a revision of the traditional Starling’s forces.(6) Albumin molecules within the EG layer provides some oncotic pressure, and it is the oncotic balance between the intravascular (flowing) compartment and the EG compartment that affects fluid flux according to protein levels. This explains why raising oncotic pressure in the intravascular compartment does not actually draw fluid from the interstitial space, much
to the disappointment of clinicians attempting to reduce peripheral oedema.
It is likely that shedding of the EG is one of the first steps in inflammation and coagulation, which then allows interactions between endothelial cells and circulating leucocytes and platelets.(7-11) There is some evidence that rapid intravenous crystalloid fluid therapy, without coinciding injury or inflammation, can increase EG shedding.(12) It is unknown if this response to blood volume expansion is related shear stress, release of atrial natriuretic peptide, dilution of EG constituents,
or a combination of these factors. In studies using euvolaemic models, it is difficult to separate the effects
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