Page 444 - WSAVA2018
P. 444

 25-28 September, 2018 | Singapore
of hypervolaemia from the effects of the fluid infusion itself and the scenario is less applicable to emergency medicine. Several rodent haemorrhagic shock models comparing large volumes of isotonic crystalloids to plasma or albumin infusions have demonstrated that large-volume crystalloids are associated with greater glycocalyx shedding, vascular permeability and reduced glycocalyx thickness. Preliminary work conducted
by our group found that dogs given Plasmalyte-148
for haemorrhagic shock showed evidence for more glycocalyx shedding and inflammation, compared to those given synthetic colloid fluids or whole blood.
(13) These types of studies raise cause for concern
that large volumes of crystalloid, rapidly administered, may not be innocuous as previously thought, and may be contributing to a pro-inflammatory states that our patients may already be experiencing. Ongoing work is being conducted in this area, especially in the area of sepsis,(14) where systemic inflammation and vascular dysfunction may make patients particularly sensitive to further EG shedding.
Are synthetic colloid fluids safer?
Some may be tempted to use synthetic colloid fluid to avoid the administration of large volumes, which may reduce degree of shear stress and atrial distension (therefore avoiding release of natriuretic peptides). However, in order to achieve the same degree of
blood volume expansion, the blood will still be diluted. Therefore, there may still be some adverse effect on the endothelial glycocalyx. Also the choice of diluent for synthetic colloids may be limited; it is most commonly suspended in 0.9% NaCl, which is not ideal for the reasons discussed above.
Additional adverse effects of synthetic colloids include interference with haemostasis, either due to platelet dysfunction or interference with secondary coagulation. Therefore, in a patient with active bleeding, this may
not be the best choice. Also, an association between synthetic colloid fluids and acute kidney injury is currently being investigated.
1. McBride D, Raisis AL, Hosgood G, Smart L. Hydroxyethyl starch 130/0.4 compared with 0.9% NaCl administered to greyhounds with haemorrhagic shock. Veterinary Anaesthesia and Analgesia. 2017;44(3):444-451.
2. Yunos NM, Bellomo R, Hegarty C, Story D, Ho L, Bailey M. Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA 2012;308(15):1566-72.
3. Saragoca MA, Mulinari RA, Bessa AM, Draibe SA, Ferreira Filho SR, Ribeiro AB, Ramos OL. Comparison of the hemodynamic effects of sodium acetate in euvolemic dogs and in dogs submitted to hemorrhagic shock. Brazilian Journal of Medical and Biological Research 1986;19(3):455-8.
4. Schimmer RC, Urner M, Voigtsberger S, Booy C, Roth Z’Graggen B, Beck- Schimmer B, Schlapfer M. Inflammatory kidney and liver tissue response to different hydroxyethylstarch (HES) preparations in a rat model of early sepsis. PLoS One 2016;11(3):e0151903.
5. Voigtsberger S, Urner M, Hasler M, Roth Z’Graggen B, Booy C, Spahn DR, Beck-Schimmer B. Modulation of early inflammatory response by different balanced and non-balanced colloids and crystalloids in a rodent model of endotoxemia. PLoS One 2014;9(4):e93863.
6. Woodcock TE, Woodcock TM. Revised Starling equation and the glycocalyx model of transvascular fluid exchange: an improved paradigm for prescribing intravenous fluid therapy. British Journal of Anaesthesia 2012;108(3):384-94.
7. Mulivor AW, Lipowsky HH. Role of glycocalyx in leukocyte-endothelial cell adhesion. American Journal of Physiology Heart and Circulatory Physiology 2002;283(4):H1282-H91.
8. Chappell D, Dorfler N, Jacob M, Rehm M, Welsch U, Conzen P, Becker BF. Glycocalyx protection reduces leukocyte adhesion after ischemia/reperfusion. Shock. 2010;34(2):133-9.
9. Constantinescu AA, Vink H, Spaan JA. Endothelial cell glycocalyx modulates immobilization of leukocytes at the endothelial surface. Arteriosclerosis, Thrombosis, and Vascular Biology 2003;23(9):1541-7.
10. Pries AR, Secomb TW, Jacobs H, Sperandio M, Osterloh K, Gaehtgens P. Microvascular blood flow resistance: role of endothelial surface layer. American Journal of Physiology 1997;273(42):H2272-H9.
11. Gotte M, Bernfield M, Joussen AM. Increased leukocyte-endothelial interactions in syndecan-1-deficient mice involve heparan sulfate-dependent and -independent steps. Current Eye Research 2005;30:417-22.
12. Powell M, Mathru M, Brandon A, Patel R, Frolich M. Assessment of the endothelial glycocalyx disruption in term parturients receiving a fluid bolus before spinal anesthesia: a prospective observational study. International Journal of Obstetric Anesthesia. 2014;23(4):330-334.
13. Smart L, Boyd CJ, Claus MA, Bosio E, Hosgood G, Raisis A. Large-volume crystalloid fluid is associated with increased hyaluronan shedding and inflammation in a hemorrhagic shock model. Critical Care 2018;22(Suppl. 1):P293.
14. Macdonald SPJ, Taylor DM, Keijzers G, Arendts G, Fatovich DM, Kinnear
FB, Brown SGA, Bellomo R, Burrows S, Fraser JF, Litton E, Ascencio-Lane JC, Anstey M, McCutcheon D, Smart L, Vlad I, Winearls J, Wibrow B. REstricted Fluid REsuscitation in Sepsis-associated Hypotension (REFRESH): study protocol for a pilot randomised controlled trial. Trials. 2017;18(1):399.

   442   443   444   445   446