The effect of fluid bolus administration on cerebral tissue oxygenation in post-cardiac arrest patients.

PURPOSE: Fluid boluses (FB) are often used in post-cardiac arrest (CA) patients with haemodynamic instability. Although FB may improve cardiac output (CO) and mean arterial pressure (MAP), FB may also increase central venous pressure (CVP), reduce arterial PaO2, dilute haemoglobin and cause interstitial oedema. The aim of the present study was to investigate the net effect of FB administration on cerebral tissue oxygenation saturation (SctO2) in post-CA patients. METHODS: Pre-planned sub-study of the Neuroprotect post-CA trial (NCT02541591). Patients with anticipated fluid responsiveness based on stroke volume variation (SVV) or passive leg raising test were administered a FB of 500 ml plasma-lyte A (Baxter Healthcare) and underwent pre- and post-FB assessments of stroke volume, CO, MAP, CVP, haemoglobin, PaO2 and SctO2. RESULTS: 52 patients (mean age 64 ±â€¯12 years, 75% male) received a total of 115 FB. Although administration of a FB resulted in a significant increase of stroke volume (63 ±â€¯22 vs 67 ±â€¯23 mL, p = 0.001), CO (4,2 ±â€¯1,6 vs 4,4 ±â€¯1,7 L/min, p = 0.001) and MAP (74,8 ±â€¯13,2 vs 79,2 ±â€¯12,9 mmHg, p = 0.004), it did not improve SctO2 (68.54 ±â€¯6.99 vs 68.70 ±â€¯6.80%, p = 0.49). Fluid bolus administration also resulted in a significant increase of CVP (10,0 ±â€¯4,5 vs 10,7 ±â€¯4,9 mmHg, p = 0.02), but did not affect PaO2 (99 ±â€¯31 vs 94 ±â€¯31 mmHg, p = 0.15) or haemoglobin concentrations (12,9 ±â€¯2,1 vs 12,8 ±â€¯2,2 g/dL, p = 0.10). In a multivariate model, FB-induced changes in CO (beta 0,77; p = 0.004) and in CVP (beta -0,23; p = 0.02) but not in MAP (beta 0,02; p = 0.18) predicted post-FB ΔSctO2. CONCLUSIONS: Despite improvements in CO and MAP, FB administration did not improve SctO2 in post-cardiac arrest patients.

Variability of serum concentrations of cystatin C and urinary retinol-binding protein, neutrophil gelatinase-associated lipocalin, immunoglobulin G, and C-reactive protein in dogs.

BACKGROUND: Markers of kidney dysfunction and damage have potential to detect chronic kidney disease (CKD) in early stages. However, data on long-term variation of these markers in healthy dogs is lacking and is crucial for the interpretation of results. HYPOTHESIS/OBJECTIVES: To determine temporal variations of serum cystatin C (sCysC) and urinary retinol-binding protein (uRBP), neutrophil gelatinase-associated lipocalin (uNGAL), immunoglobulin G (uIgG), and C-reactive protein (uCRP) in healthy dogs. ANIMALS: Eight clinically healthy adult Beagles were evaluated. METHODS: Longitudinal observational study. Serum cystatin C was determined by particle-enhanced nephelometric immunoassay. Urinary retinol-binding protein, uNGAL, uIgG and uCRP were determined by ELISA and concentrations were indexed to urinary creatinine. Within- and between-dog variance components (VC) and within-dog coefficients of variation (CV) were determined from blood and urine collected at eight time points over 1.5 years. RESULTS: Urinary C-reactive protein (uCRP) concentrations were consistently below the detection limit (5.28 ng/mL). Mean ± within-dog standard deviation for sCysC, uRBP/c, uNGAL/c and uIgG/c was 0.15 ± 0.01 mg/L, 0.09 ± 0.03 mg/g, 2.32 ± 2.03 µg/g and 12.47 ± 10.98 mg/g, respectively. Within-dog CV for sCysC, uRBP/c, uNGAL/c and uIgG/c was 8.1%, 33.7%, 87.2% and 88.1%, respectively. CONCLUSIONS AND CLINICAL IMPORTANCE: Serum cystatin C, uRBP/c, uNGAL/c and uIgG/c exhibit a wide range of long-term within-dog variability. Researchers and veterinarians might need to take this into account when interpreting their results. To assess their diagnostic and predictive ability, future studies need to establish reference ranges for healthy dogs and dogs with CKD.