Diagnosis and therapeutic management of ascites of hepatic origin in a Labrador dog: A case report

Introduction

Ascites is a serious, possibly life-threatening medical condition and a frequently encountered entity in dogs. It is a common clinical manifestation in dog as a result of fluid accumulation in the peritoneal cavity due to escape of fluid between the parietal and visceral peritoneum from blood vessels, lymphatics, internal organs or abdominal masses. It is also one of the sequelae of various primary diseases (Ettinger et al., 2005) [3] . Which include chronic hepatic failure, congestive heart failure, nephritic syndrome, malnutrition, ancylostomiasis and protein losing enteropathy in canine (Randhawa et al., 1980) [9] . It has become necessary to rule out organ involvement in development of clinical ascites by use of biochemical tests as well as imaging studies. Ascites can be treated after diagnosis of underlying cause (Turkar et al., 2009) [9] .

Case history and clinical observations

A one and half year old female Labrador was presented to Veterinary Clinical Complex, College of Veterinary Science, Rajendranagar, Hyderabad with a major complaint of abdominal distension, inappetance, lethargy and weakness. Vaccination and deworming were upto date. Physical examination revealed fluid thrill upon tactile percussion and pear shaped abdomen (Fig. 2), heart rate was 120 BPM, respiratory rate was 24 BPM and temperature was 102⁰ F. Clinical examination revealed pale mucous membrane, dyspnea, dehydration and rough body coat. A series of investigations were ZAadvised to rule out the etiology of ascites. Hematological examination (table 1) revealed normal parameters except for hemoglobin (9.03 g/dl) which is less than normal suggesting anemia. Serum biochemistry (table 2) revealed elevated levels of ALT (566.1 U/L) and AST (120 U/L) and decreased total proteins, Serum albumin and glucose levels suggesting hepatic damage. Creatinine and BUN levels were normal suggestive of no renal involvement. Fecal sample examination revealed no parasitic ova's. Skiagram of abdomen revealed ground glass appearance (Fig. 3) suggestive of grade 2 ascites with gas filled intestines floating in ascitic fluid. Sonogram revealed hyperechoic liver parenchyma with rounded borders floating in anechoic fluid (Fig. 4) with no change in echogenicity in other organs. Abdominocentesis (Fig. 5) was done to relieve stress on diaphragm and ascetic fluid was subjected to various physical, biochemical and microscopic examination to determine the etiology of ascites. Physical examination of ascitic fluid reveled yellow colour (Fig. 6) Biochemical constituents of ascitic fluid, which include Total Protein 2.65 grams/dl, Albumin 1.20g/dl, Specific gravity 1.015 and pH 7.6 was estimated. Cytology of the ascitic fluid revealed few mesothelial cells and neutrophils indicating moderately transudate fluid. SAAG was estimated which is a marker of portal hypertension. SAAG was calculated which is less than 1.1 g/dl suggesting low gradient ascites and suggesting inflammation and vascular leakage. Based on the above physical, clinical, biochemical, radiographic and sonographic examination the above case was diagnosed as ascites due to hepatic origin.

Treatment and Discussion

The animal was treated with Inj. DNS 10ml/kg bwt IV for 3 days, Amoxicillin @ 12.5 mg/kg bwt IV for 5 days, inj. Chlorophenaramine maleate @ 1ml IM 3 days, inj. Furesamide @ 2 mg/kg bwt for 7 days, inj. Pantoprazole @ 0.4 mg/kg IV for 3 days, inj. Astymin 1ml/kg bwt IV for 7 days, and Inj. Toxol 1ml/kg bwt IM for 3 days, with an additional liver supportive therapeutic regimens include Susp. SAMe pet @ 20 mg/kg bwt PO, Milk thistle @ 6 mg/kg bwt PO for 30 days. The owner was advised to give the animal egg white and chicken soup for 1 month along with salt restricted diet. Reduction in abdominal distension was seen from day 3 (Fig. 7,8) of treatment and the animal became apparently healthy by day 10. The hemato biochemical parameters were back to normal. The owner was advised to continue egg protein and chicken soup. Low levels of Hb correlation with findings of (Bhatt et al., 2011) [1] (Ihedioha et al. 2013) [4] and Saravanan et al. 2014) [8] . Increased ALT and AST indicates hepatic insufficiency with extensive damage resulting into the leakage of enzymes from hepatic cell into blood stream was in correlation with findings of (Vijayakumar, 2002, Bhatt et al. 2011, and Jain et al. 2013) [10,1,5] . BUN and creatinine were normal indicate normal function of kidney. Hypoglycemia and hypoproteinaemia was indicative of inappetance/anorexia complemented by malabsorbtion from the intestines, decreased gluconeogenesis and glucogenolysis. Microscopic examination of ascitic fluid did not reveal presence of epithelial cells or pus cells. Similar findings were reported by (Ihedioha et al. 2013 and Jain et al. 2013) [4,5] . Direct examination of faecal sample revealed no parasitic eggs which were in correlation with findings of (Chakrabarti et al. 1994) [2] . Skiagram of lateral abdomen revealed characteristic 'Ground glass' appearance due to presence of ascitic fluid. Abdominal ultrasonography revealed presence of free floating anechoic abdominal fluid which was in correlation with findings of (Saravanan et al. 2014) [8] . Hepatic sonogram revealed hyperechoic liver suggestive of hepatic involvement in development of clinical ascites. Kidneys did not show any ultra-sonographic changes. Dextrose 10% has been well established in checking dehydration, depleting liver glycogen and preventing tissue catabolism, and antibiotics were given to prevent any secondary bacterial infection. Egg albumin was given as protein supplements that have high biological value (Mosier JE, et al., 1979) [7] . The animal was given sodium free diet to check sodium retention or secondary hyperaldosteronism (Wyllie R et al., 1980) [11] . Ascites is a clinical sign, not a disease, and it can occur due to multiple non-infectious as well as infectious causes. Finding the etiology is important in treating ascites. Delay in treatment may leads some other complication and may even lead to death some times.

Conclusion

In ascites effected dog, invesitigations like Physical, clinical, hematological, serobiochemical, radiography, ultrasonographic examination paves way for the diagnosing the origin of ascites as hepatic and was treated accordingly.

References

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