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Indian J. Anim. Hlth.

(2017), 56(1) : 111-112


Short Communication

ASCITES OF CARDIAC ORIGIN IN A DOG


- A CASE STUDY
P. MUKHERJEE, J. MUKHERJEE1*, S. S. KESH AND P. K. DAS1
Department of Teaching Veterinary Clinical Complex
Faculty of Veterinary and Animal Sciences, Mohanpur Campus
West Bengal University of Animal and Fishery Sciences
Mohanpur, Nadia, West Bengal, Pin- 741 246

A four years old male Labrabor Retriever dog was presented to the clinic with a history of anorexia
since last 45 days with dyspnoea and enlarged abdomen. Physical examination, ultrasonographic scan
and ECG study revealed ascites with myocardial ischemia. The present study describes different
diagnostic modalities along with treatment options for ascites in canine due to cardiac origin.

Key words: Ascites, ECG, Haematology, Ultrasonography, Ventricular enlargement

A four years old, male, Labrador Retriever dL, bilirubin (total) 1.23 mg/dL, bilirubin-
dog was presented to the clinic (TVCC, direct 0.50 mg/dL, bilirubin- indirect 0.73
WBUAFS, West Bengal, India) as outdoor mg/dL, SGPT 65.8 IU/L, SGOT 87.9 IU/
patient. The dog exhibited the symptoms
L, ALP 471.2 IU/L, BUN 23.6 mg/dL and
of anorexia since last 45 days, dyspnoea and
creatinine 1.89 mg/dL.
abdominal enlargement with pear shaped
appearance. The physical examinations Upon USG, the urinary bladder appeared
revealed normal body temperature (101° F) relatively normal in contour and thickness
and pale mucous membrane. On percussion, without any overt obstruction, uroliths or
fluid wave was evident in the abdomen. neoplasia. Both the kidneys appeared
Haematological examination reported normal in size and shape with clear cortico-
haemoglobin 10.2 gm %, TLC 12,000/cu medullary dimensions. The spleen appeared
mm and DLC with Neutrophils 86%, normal without any focal lesions. The liver
Lymphocyte 12%, Eosinophils 01% and lobes appeared normal floating in anechoic
Monocytes 01%. free fluid (Fig. 1) suggestive of ascites. The
Serum biochemistry revealed blood glucose gallbladder wall thickness was found to be
(Random) 65 mg/dL, total protein 5.9 gm/ 2.84 mm (Fig. 2). The ECG showed ST
dL, albumin 3.8 gm/dL, globulin 2.1 gm/ segment depression indicative of
*
Corresponding Author
1
Dept. of Veterinary Physiology, West Bengal University of Animal and Fishery Sciences
112 Indian Journal of Animal Health, June, 2017

myocardial ischemia (Fig 3). supply to the myocardium might lead to


cardiac systolic dysfunction resulting in
Ascites is referred to as accumulation of
increased end diastolic volume which
serous fluid in peritoneal cavity. The interns causes accumulation of free fluids
underlying cause of ascites may be in interstitial spaces due to increased
hypoproteinemia, neoplasia of an pressure in the blood vessels.
abdominal organ, ruptured urinary bladder
and haemorrhage from trauma as well as Treatment modalities of ascites depends
cardiac disturbances (Kumar and Srikala, upon the underlying causes. If cardiac origin
2014). Common cardiac complications is diagnosed the standard treatment protocol
responsible for manifestation of ascites are should start with diuretics (Furosemide @
congestive cardiomyopathy, right heart 2-4 mg/kg BID PO) and ACE inhibitors
(Benazepril/ Enalapril @ 0.5 mg/kg SID to
failure and congenital pulmonic stenosis
BID PO). In dogs with arrhythmias, beta
(Kumar and Srikala, 2014). In this present
adrenergic blockers or calcium channel
case the serum biochemistry revealed blockers are used to improve oxygenation
almost normal except for ALP. A rise in of the heart and to slow down the heart
the serum ALP may be due to thickening rate. In recent days, Pimobendan @ 0.25 mg/
of gall bladder (Kumar and Srikala, 2014). kg BID PO is also being used to improve
From the biochemical and USG reports, survival of the patients.
urinary functions appeared normal.
Therefore the renal involvement in this case Conflict of Interests
can be ruled out. Ascites due to myocardial The authors declare there is no conflict of
dysfunction (Tidholm et al., 2001 and interests amongst them.
Meurs, 2005) and ventricular enlargement
(Izabela et al., 2014) was well documented ACKNOWLEDGEMENT
in dogs. Here in the present case we found Authors are extremely grateful to the Vice-
severe myocardial ischemia. Poor blood Chancellor, WBUAFS for providing
financial support to complete the study.
REFERENCES
Izabela J, Agnieszka NN, Marcin N, Alicja C Meurs KM, 2005. Primary myocardial disease in
and Rafa C et al., 2014. Myocarditis in dogs: the dog. In: Ettinger SJ, Feldman EC, editors.
etiology, clinical and histopathological Textbook of Veterinary Internal Medicine:
features (11 cases: 2007–2013). Ir Vet J, Diseases of the Dog and Cat. 6th ed.
Philadelphia: WB Saunders, pp 1077–1082
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Tarducci A, 2001. Canine idiopathic dilated
Kumar KS and Srikala D, 2014. Diagnosis and cardiomyopathy. Part I: Aetiology, clinical
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Article received on 13.02.2017 and accepted for publication on 08.04.2017