Clinical and ultrasonographic investigations of ascites in dogs

Abstract

Study entitled “Clinical and Ultrasonographic Investigation of Ascites in Dogs” was conducted in ten dogs. The study aimed at understanding the etiopathogenesis of ascites in dogs. The parameters observed were signalment, history and detailed clinical examination, electrocardiography, ultrasonography of liver, kidney and heart, course of illness, estimation of haemoglobin concentration packed cell volume(PCV), total plasma protein, albumin, A: G ratio, liver enzymes like alanine amino transferase (ALT) and alkaline phosphatase (ALP), protein content in ascitic fluid , ascitic fluid to plasma protein ratio, blood urea nitrogen (BUN), serum creatinine, sodium and potassium.

Inappetance and lethargy were observed in dogs with liver diseases. Cardiac palpitation, loud heart sounds and strong femoral pulse were noticed in dogs with CHF. Non- specific and vague signs were noticed in dogs with nephrotic syndrome. Deep ‘Q’ waves in leads I, II and aVF, prolonged ‘QRS’ duration, S-T slurring, tall ‘R’ waves, mild sinus arrhythmia and S1, S2 and S3 pattern were the abnormal ECG findings in dogs with CHF. No marked changes could be observed in the ECG of dogs with ascites of hepatic and renal origin.

Ultrasonography of liver revealed hyperechogenicity of parenchyma, specks of hyperechogenicity and mildly echogenic gall bladder contents in three out of five dogs with ascites of hepatic origin. Two dogs had uneven and eroded borders along with hyperechoic liver parenchyma in dogs with ascites of hepatic origin. Nephrosonogram was unremarkable in all the ten dogs. Ultrasonographic findings and serum biochemical findings were coinciding with each other. Ultrasonography was an efficient tool in studying the changes of liver parenchyma and portal vasculature. ECG in cardiac diseases was complementary to echocardiography. Echocardiography was efficient in diagnosing DCM (two dogs) and HCM (one dog).

All the dogs with liver diseases had mild to marked elevation in serum levels of ALT and/ or ALP. Hypoproteinemia and hypoalbuminemia were observed in dogs with liver and kidney diseases. Liver and kidney function tests were unremarkable in dogs with nephrotic syndrome and heart diseases. Treatment regimen involved administration of furosemide and/ or furosemide + spironolactone, silymarin, Liv- 52 Vet, enalapril, digoxin and prednisolone as the case may be. Six out of 10 dogs survived beyond 30 days following the therapy instituted. Nephrotic syndrome in dogs could be concluded by progressing hypoproteinemia especially hypoalbuminemia, low- protein ascites, negative ECG and echocardiographic findings and non- responsiveness to therapy. Nephrotic syndrome can be confirmed by biopsy and / or urine protein: creatinine ratio. Liver diseases can be confirmed and characterized only with biopsy.