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In this VetGirl blog, we interview Dr. Søren R. Boysen, DACVECC, Associate Professor at University of Calgary on his recent study on “Effects of rapid intravenous 100% L-isomer Lactated Ringer’s administration of plasma lactate concentrations in healthy dogs” published in JVECC (2014). In this blog, we find out the whether or not the “L” in LRS is potentially detrimental when used to fluid resuscitate veterinary patients in the emergency room who may have a lactic acidosis. More importantly, we review the differences between d- and l-lactate, and whether or not LRS should still be one of the favorite fluids of emergency clinicians and criticalists (Yes, VetGirl likes it). We also briefly review the use of the handheld Accutrend lactate devices, and what we’re measuring with these devices. Finally, we review the importance of lactate when evaluating patients with gastric-dilatation voluvulus (GDV) and whether or not LRS can be used in these situations!

References:
1. Boysen SR, Dorval P. Effects of rapid intravenous 100% L-isomer Lactated Ringer’s administration on plasma lactate concentrations in healthy dogs. J Vet Emerg Crit Care 2014;24(5):571-577.

2. dePapp E, Drobatz KJ, Hughes D. Plasma lactate concentration as a predictor of gastric necrosis and survival among dogs with gastric dilatation-volvulus: 102 cases (1995-1998). J Am Vet Med Assoc 1999;215(1):49-52.

Boysen et al. ABSTACT:
Objective: To determine if rapid intravenous administration of lactated Ringer’s solution containing 28 mmol/L of l-lactate (L-LRS) can result in an increase in plasma lactate concentration in healthy dogs.

Design: Prospective cross over study with a 4-week washout period.

Setting: Veterinary teaching hospital.

Animals: Six healthy adult Beagles.

Interventions: Dogs received 180 mL/kg/h of L-LRS over 60 minutes, followed by a 4-week washout period, then 180 mL/kg/h of 0.9% sodium chloride (NaCl) over 60 minutes.

Measurements and Main Results:  Blood samples were drawn at baseline (T0), every 10 minutes during fluid administration (T10 to T60), and 60 minutes after fluid administration (T120). Samples were measured in duplicate at all time points with a handheld meter and at T0, T60, and T120 with a blood gas analyzer. Data were analyzed with 1-way or 2-way ANOVA for repeated measures and post hoc tests with Dunnett’s or Bonferroni’s correction for within-group and between group analyses, respectively. P values < 0.05 were considered significant. Results are mean ± SD. There was no difference between groups at T0 (L-LRS = 1.1 ± 0.6 mmol/L, NaCl = 1.2 ± 0.9 mmol/L). Within the L-LRS group, T0 was significantly lower than all other time points except T120. At T50 and T60, the L-LRS group was higher than the NaCl group. There was a statistical significance between the 2 groups over time.

Conclusions: The rapid administration of intravenous L-LRS to healthy dogs significantly increases plasma lactate concentration within 10 minutes and returns to baseline values within 60 minutes after cessation of administration. This could have implications in how plasma lactate concentration is interpreted with respect to prognosis, particularly in patients receiving resuscitative rates of L-LRS. Interpretation of plasma lactate concentrations should be considered in light of the rate, quantity and type of fluid administered, and timing of blood samples.

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