Serum Ascites Albumin Gradient (SAAG), Ascites Total Nucleated Cell Count (TNCCascites), Ascites Lactate Dehydrogenase (LDHascites), Ascites Total Protein (TPascites) and Their Serum Ratio (LDHratio and TPratio) in Canine Abdominal Effusion
G. Gianesini1; F. Busato1; M. Drigo2; A. Zoia3
Transudative ascites is caused from an elevation of the hydrostatic pressure (HP) gradient (transudates-HP) or from the decrease in colloid osmotic pressure (transudates-COP), while exudative ascites arises from an increase permeability of the peritoneal capillaries. SAAG (albuminserum–albuminascites), TNCCascites, LDHascites, LDHratio (LDHascites÷LDHserum), TPascites and TPratio (TPascites÷TPserum) have all been used to discriminate these 3 types of ascites, but evidences for their use in veterinary medicine are lacking. The aim of this study was to describe concentrations of these parameters in different type of canine ascites.
Cross-sectional study retrospectively evaluating client-owned dogs with ascites presented between 05-2015 and 12-2019. The disease causing the ascites was used as gold standard to establish the underlying pathophysiology. In accordance with human literature, ascites caused by protein losing enteropathy, nephrotic syndrome and severe hepatic insufficiency were classified as transudates-COP; ascites caused by portal hypertension were classified as transudates-HP and ascites caused by neoplasia, septic or non-septic peritonitis, and other miscellaneous inflammatory causes (including hemorrhage) were classified as exudates. Differences in SAAG, TNCCascites, LDHascites, LDHratio, TPascites and TPratio among transudate–COP, transudate–HP and exudates were analyzed using Kruskal-Wallis and post-hoc testing with Bonferroni correction for pairwise comparisons.
Two-hundreds and ninety-one ascitic dogs entered the study: 35 transudates-COP, 67 transudates-HP, and 189 exudates. Among groups results were as follow. SAAG concentrations: transudates-COP (0.90 g/dL; IQR=0.70–1.20), transudates-HP (0.80 g/dL; IQR=0.60–1.50), and exudates (0.50 g/dL; IQR=0.30–0.90); TNCCascites counts: transudates-COP (180 µL; IQR=90–270), transudates-HP (610 µL; IQR=260–920), and exudates (13490 µL; IQR=7470–29720); LDHascites concentrations: transudates-COP (17 IU/L; IQR=8–20), transudates-HP (31 IU/L; IQR=22–57), and exudates (615 IU/L; IQR=305–1183); LDHratio concentrations: transudates-COP (0.9 IU/L; IQR=0.04–0.15), transudates-HP (0.28 IU/L; IQR=0.11–0.45), and exudates (3.28 IU/L; IQR=1.14–7.46); TPascites concentrations: transudates-COP (0.2 g/dL; IQR=0.1–2.0), transudates-HP (3.4 g/dL; IQR=1.4–3.9), and exudates (4.3 g/dL; IQR=3.3–5.1); TPratio concentrations: transudates-COP (0.08 g/dL; IQR=0.03–0.61), transudates-HP (0.64 g/dL; IQR=0.29–0.77), and exudates (0.75 g/dL; IQR=0.62–0.88). Among transudates-COP, transudates-HP and exudates there was a significant difference for all the parameters analysed (p<0.001 for all comparisons). Pairwise comparisons showed that all the parameters analysed were significantly different between exudates and transudates-HP (p<0.001 for all comparisons) and between exudates and transudates-COP (p=0.001 for SAA and p<0.001 for all the other comparisons). Only TPascites and TPratio were significantly different between transudates-COP and transudates-HP (p<0.001 for both comparisons).
All parameters analysed have a diagnostic value in differentiating exudates from transudates, but only TPascites and TPratio show a diagnostic utility in discriminating transudates-COP from transudates-HP.
Disclosures
No disclosures to report.