Therapeutic management of ascites in Rottweiler

Introduction

True ascites is defined as collection of serous or serosanguinous fluids in the peritoneal cavity (Ettinger and Feldman, 2005) [1] . The development of ascites is associated with changes in Starling's forces which involve an increase in hydrostatic pressure within the venous or lymphatic systems and a reduction in oncotic pressure of capillaries (Richter, 2003 [2] ; Singh et al., 2019b) [3] . Ascites is a manifestation rather than a disease. It can be a secondary symptom of cardiac, hepatic, renal and various systemic diseases in dogs (Ihedioha et al., 2013) [4] and also secondary to hypoalbuminemia and portal hypertension (Center, 2015) [5] . It occurred more frequently with hepatic origin compared to instances involving a single affected organ or a combination of the two or more organs (Kumar et al., 2003 [6] ; Dixit et al., 2018) [7] . In this report diagnosis and therapeutic management of ascites has been discussed. Case history and observations A three year old Rottweiler bitch was presented to Veterinary Clinical Complex, Tirupati with the history of abdominal distension since one week (Fig 1). Respiratory distress, anorexia and vomiting has been observed for three days. Water intake and urination were normal. Deworming was done eight months ago. Regular vaccination of the animal. The dog whelped two months ago. On Physical examination temperature, heart rate and respiratory rate were 102.8ºF, 120 beats/min and 40/min respectively. Conjunctival mucus membrane was pale pink and popliteal lymph node was slightly enlarged. Fluid thrill was observed up on abdominal palpation. No parasitic ova were identified on faecal examination. The dog was negative for leptospirosis by Microscopic Agglutination Test (MAT) and negative for Babesia canis, Babesia gibsoni and Ehrlichia canis on PCR.

Treatment and Discussion

Abdominocentesis was performed in order to relieve the animal from respiratory distress. About 1 litre of ascitic fluid was drained out by abdominocentesis. Administered Inj. Amoxirum forte @ 12.5 mg/kg body weight IM twice daily for a period of 5-7days. Inj. Vomikind @ 0.2 mg/kg body weight IV twice daily was given as per the requirement for 3 days. Advised the owner to use Tab. Lasilactone 50mg @ 2 mg/kg body weight PO twice daily until the regression of ascites. Tab. Lisybin large PO once daily for a period of one month. Syrup. Fe-folate @ 8 ml PO twice daily for one month. Threptin biscuits @ 2 biscuits PO once in a day for one month. Advised the owner to offer salt free and protein rich diet including egg white, chicken and cheese etc. Abdominal distension was reduced with in 10 days and animal resumed to normal appetite within 10 days.

Ascites is characterized by the abnormal accumulation of fluid in the peritoneal cavity resulting from the leakage of fluid between parietal and visceral peritoneum. This leakage may originate from blood vessels, lymphatic system, internal organs or abdominal masses as explained by Vijayakumar (2002) [8] . Anorexia in ascitic dogs may result from the buildup of harmful metabolic waste products or from a reduced elimination of specific hormones such as leptin and ghrelin, which are responsible for regulating the hunger centre in the brain (Kumar et al., 2020) [9] . Vomiting may be attributed to the direct stimulation of the chemotactic trigger zone resulting from the inability of the liver and kidneys to effectively clear endotoxins. (Wills and Simpson, 1994) [10] . The respiratory distress may be attributed to significant fluid accumulation within the peritoneal cavity (Peden and Zenoble, 1982 [11] and Singh et al., 2019a) [12] . Bhadesiya et al. (2015) [13] stated that the presence of abdominal effusion in dogs with ascites hinders the radiographic assessment of the liver and other abdominal organs which typically exhibit a characteristic "ground glass" appearance. The hyperechoic liver parenchyma accompanied by anechoic free fluid in the abdomen that separated the intra-abdominal organs creating the appearance of floating intestines was indicative of ascites resulting from hepatic involvement (Jana et al., 2019) [14] . Anaemia and neutrophilic leukocytosis was observed and anaemia occurs due to chronic inflammatory disease or various factors which impair the DNA synthesis leading to maturation arrest of pro-rubicyte to rubicyte stage (Willard and Tvedten 1999 [15] and Singh et al., 2019b) [3] and neutrophilic leukocytosis occur as result of the inflammatory response associated with chronic hepatitis which subsequently progress to cirrhosis (Elhiblu et al., 2015) [16] , in pathological conditions like infection, acute haemolysis (Singh et al., 2019b) [3] . Hypoproteinaemia and hypoalbuminemia in the present study might be due to reduced capacity of the liver to synthesize proteins in hepatic diseases (Webster, 2005) [17] and hepatic fibrosis (Ihedioha et al., 2013) [4] . Elevated ALT has been reported earlier in hepatic anoxia, hepatic perfusion, chronic hepatitis, liver cirrhosis, cholangitis and cholangiohepatitis (Willard and Tvedten, 1999 [15] and Singh et al. 2019b) [3] . Hepato cellular damage results in elevated serum ALT, ALP activity and the magnitude of the increase in enzyme levels is proportionate to the liver damage (Singh et al., 2019b) [3] . The findings of ascitic fluid was in concurrence with findings of Mondal et al., 2012 [18] . Amoxicillin and sulbactam was used along with diuretics and supportive medication for successful treatment of ascites as reported by Regmi and Shah, 2017 [19] , Neelam et al., 2019 [20] and Samad 2019 [21] . Amoxicillin and sulbactam proved to minimize bacterial infection in ascites cases (Neelam et al., 2019 [20] and Sundararajan et al., 2022) [22] . Furosemide and Spironolactone which effectively drained out excess ascitic fluid Kumar et al. (2016) [23] , Singh et al. (2019b) [3] and Dhillon et al. (2020) [24] . The hepatoprotective activity of silybin can be attributed to its antioxidant, antifibrotic, antiinflammatory and cellular signalling properties (Loguercio and Festi, 2011) [25] . Threptin biscuits were useful in relieving ascites and improving health as they contains essential amino acids, minerals and vitamins.

Conclusion

Ascites is a sign rather than a disease. It occurs mainly due to hepatic abnormalities. Ascites can be diagnosed by radiography, ultrasonography, haemato-biochemical and ascitic fluid analysis. Earlier diagnosis and prompt treatment will give good prognosis in ascitic cases.

Acknowledgement

AcknowledgementThe authors thank Sri Venkateswara Veterinary University, Tirupati, Andhra Pradesh for providing facilities and funds to carryout research.

References

1. Ettinger SJ, Feldman EC. Disease of dog and cat. In: Textbook of veterinary internal medicine. 6th ed. Philadelphia: WB Saunders; 2005. p. 137-145.
2. Richter KP. Diseases of the liver and hepatobiliary system. In: Handbook of small animal gastroenterology. 2003. p. 286-352.
3. Singh SK, Shukla SK, Bhatt P, Singh AK. Clinico therapeutic studies on ascites in canines. Int J Curr Microbiol Appl Sci. 2019;8(9):1120-1137.
4. Ihedioha JI, Anosa VO, Esievo KA. Prevalence of and clinicopathologic findings associated with ascites in dogs in Enugu State, Nigeria. Comp Clin Pathol. 2013;22:185-193.
5. Center SA. Portal hypertension and ascites in small animals. Merck Vet Man. 2015.
6. Kumar S, Ahuja A, Bihani DK, Gahlot AK. Studies on canine ascites. J Canine Dev Res. 2003;3(2):9-17.
7. Dixit AA, Roy K, Shukla PC, Swamy M. Epidemiological studies in canine ascites. Indian J Vet Med. 2018;38(1-2):85-87.
8. Vijayakumar G. Therapeutic management of ascites in dogs. Intas Polivet. 2002;3(2):179-184.
9. Kumar GKC, Kamran CA, Shrikrishna I. Clinical signs observed in different stages of chronic kidney disease in dogs. Int J Livest Res. 2020;10(10):249-252.
10. Wills JM, Simpson KW. The Waltham book of clinical nutrition of the dog and cat. 1994.
11. Peden WM, Zenoble RD. Canine ascites. Am Vet Med Assoc. Iowa State Univ Vet. 1982;44(1):12-16.
12. Singh S, Shukla SK, Bhatt P, Singh AK. Prevalence of ascites in canines in and around Tarai region of Uttarakhand. J Entomol Zool Stud. 2019;7(2):11941197.
13. Bhadesiya CM, Jani RG, Parikh PV, Pandey AM, Rao N, Shai A. Haemato-biochemistry and imaging study on ascites with hepatic and cardiac involvement in a German shepherd pup. Int Res J Chem. 2015;11:23212845.
14. Jana S, Das PK, Banerjee D, Ghosh D, Mukherjee P, Mukherjee J. A case study on ascites of hepatic origin in a dog. Indian J Anim Health. 2019;58(1):135-138.
15. Willard MD, Tvedten H. Small animal clinical diagnosis by laboratory methods. Saunders Publication; 1999. p. 38-61, 208-246.
16. Elhiblu MA, Dua K, Mohindroo J, Mahajan SK, Sood NK, Dhaliwal PS. Clinico-hemato-biochemical profile of dogs with liver cirrhosis. Vet World. 2015;8(4):487491.
17. Webster CRL. History, clinical signs and physical findings in hepatobiliary disease. In: Textbook of veterinary internal medicine. 2005;2:1422-1434.
18. Mondal DB, Kumar M, Saravanan M, Sharma K. Peritoneal fluid analysis in canine disease diagnosis. J Adv Vet Res. 2012;2(4):307-313.
19. Regmi B, Shah MK. A case study on ascites of hepatic origin and their proper management in a male German Shepherd dog. Int J Appl Sci Biotechnol. 2017;5(4):555-558.
20. Neelam N, Bhagwan J, Jain V. Ascites in a bully female pup-a case report. Int J Curr Microbiol Appl Sci. 2019;8(2):2949-2951.
21. Samad MA. Therapeutic management of ascites in an Indian breed of Spitz dog in Bangladesh with a brief review on canine ascites. J Vet Med Res. 2019;1(1):4962.
22. Sundararajan RC, Pavithra P, Vijayanand V, Balagangatharathilagar M, Gopal K, Kokila S, et al. Ascites due to hepatic origin in two dogs. Pharma Innov J. 2022;SP-11(10):297-299.
23. Kumar A, Das S, Mohanty DN. Therapeutic management of ascites in GSD female dog. Int J Sci Environ Technol. 2016;5(2):654-657.
24. Dhillon KS, Kaur SJ, Singh A. Ascites of hepatic origin in a female beagle pup: Diagnosis, treatment and management. J Entomol Zool Stud. 2020;8(2):19421944.
25. Loguercio C, Festi D. Silybin and the liver: from basic research to clinical practice. World J Gastroenterol. 2011;17(18):2288-2301.