Keywords: Liver cirrhosis, Heart failure, ascites, frusemide, dog.

INTRODUCTION

The liver accounts for approximately 3-8% of the total body weight in the carnivores and and occupies a central role in diverse metabolic activities that help maintain the body’s normal. homeostatic mechanism (Center, 1989; Strombeck and Guildford, 1990). It has been shown that the liver has a high degree of heart differentiation and at the same time retains the capacity to regenerate (Roger, 1993). Hence, it is able to maintain normal activities over a long period of the dog's life span.

The liver responds to injury either by hepatocellular regeneration, bile duct hyperplasia, hepatic fibrosis, cirrhosis or acquired portosystemic shunting (Fausto and same Meade, 1999; Rogers, 1993). Inability’ of the was liver to maintain an adequate hepatic function as a result of any of these responses often result in a syndrome termed liver failure (Rogers, 1993). This may be single and specific or in most cases multiple. It may be and characterized by cholestasis and icterus, photosensitization, hepatic encephalopathy, (Manderino and Devries, 1985).

Chronic liver failure resulting from cirrhosis has been reported in adult dogs (Williams, 1991). Very often, the cause is usually undetermined. However, it may be associated with parasitism, congestive heart disease and lesions that impair the flow of blood through the liver (Herrtage, 1991).

This report presents a 10 month old puppy with liver cirrhosis and a non-responsive ascites associated with congestive heart the failure.

HISTORY

A 10 month old Alsatian puppy was presented at the Veterinary Teaching Hospital of the University of Ibadan with a complaint of depressed appetite and distended abdomen. It had been presented and treated for the same complaint two months earlier. The puppy was the only one affected form a pack of three dogs in the same house. They were all fed with enough table scraps. They had all been vaccinated against rabies, canine distemper, infectious canine hepatitis, leptospirosis and parvovirus and dewormed quarterly against round worms and hook worms using mebendazole (Vitameb^R, Vital pharmaceuticals).

Physical examination of the puppy revealed bilateral mucopurullent ocular discharge with congested ocular mucous membranes. The coat was rough, dry and lusterless and ‘the abdomen was severely distended. In addition, she was observed to be exercise intolerant. Urination was irregular, reduced in quantity and only when walked. There was tachycardia with low amplitude, the heart beat often becoming, regularly irregular after ‘little exercise. Respiratory rate was normal but usually panted after little exercise. The, temperature was constant between 38.6^oC - 39.3°C throughout the five weeks of hospitalization.

Based on these findings a tentative diagnosis of ascites of hepatic origin and/or congestive heart failure was made.

Blood samples were taken at two weekly intervals for blood profile from the cephalic vein using a 21 gauge needle. Samples of the voided urine were analyzed weekly using the dipstick method. Abdominal transudate obtained by paracentensis was also analysed by the dip stick method.

The puppy was treated with furosemide by intravenous injection at the rate of 3mg/kg body weight twice daily. In addition about 200mls of abdominal transudate were removed daily through paracentensis. Oxytetracycycline was administered intramuscularly: at a dosage rate of 5mg/kg body weight. Livjivan (Animal care company Ltd), a herbal liver tonic was also administered orally at a dosage of 2 tables daily to improve liver function.

Exploratory laparotomy was performed three weeks after presentation because of the poor resolution of the ascites despite the diuretic therapy. Liver biopsy was taken during the exploratory laparotomy for histopathology.

Abdominal, distension was observed not to decrease significantly - despite the therapy and the daily paracentensis. Instead, a moderately extended, subcutaneous oedema of the ventral abdomen and bilateral pedal oedema developed. These however resolved when the dosage of the furosemide administered was increased to 4mg/kg but with no significant effect on the ascites.

Following exploratory laparotomy, the ascites recurred within seven days. The non-responsiveness of the ascites to furosemide and findings during exploratory laparotomy made the owner of the dog request for euthanasia. Euthanasia was carried out using pentobarbitone sodium (6% Saggatal) at the rate of 60mg/kg body weight administered intravenously.

Postmortem examination following euthanasia revealed a slightly flabby heart with no clot in the chambers. The liver was not different from that observed at exploratory laparotomy (Plate 1).

Both kidneys were of normal size and consistency but with the capsule adhering to the cortex. The stomach showed few discrete areas of ulcers Histopathological finding on the liver revealed proliferation of fibrous connective tissue around the portal areas and the surrounding lobules. Cellular infiltration with lymphocytes and mononuclear leukocytes were also found.

DISCUSSION AND CONCLUSION

Liver cirrhosis has been reported to commonly affect older dogs of both sexes (Herrtage, 1991). The subject in this report was a 10 month old Alsatian puppy which appeared unusually too young to develop such condition.

The cause of liver cirrhosis in dogs have remain largely undetermined (Herrtage,1991). However, it has been associated with toxic principles, parasitism, congestive heart failure and other lesions that impair blood flow to the liver (Popper, 1977). This case report could not be associated with toxins or parasitism because other dogs in the same environment were not affected. The fact that the puppy showed decreased tolerance to exercise, pedal oedema and irregular heart beat when exercised suggested that the liver cirrhosis was more likely to be a result of congestive heart failure.

An interest finding in this case was the non responsiveness of the patient to diuretics. This was confirmed by the persistent oliguria and the non-significant reduction in the volume of the abdominal transudate. This might have been due to poor renal perfusion resulting from, reduced renal blood flow associated with congestive heart failure (Herrtage, .1991).

The analyses of the serial blood samples were that of liver cirrhosis (centre, 1989). These included hypoalbuminemia, a non-regenerative normocytic nomochromic anaemia (anaemia of chronic disorder) and persistently decreasing liver enzymes. This was due to the replacement of active hepatocytes by fibrous connective tissue. Hence, the inability of the liver to secrete these substances. The progressively decreasing values of these parameters were an indication that the condition of the liver despite therapy progressively deteriorated. The differences in the result of the urine and abdominal transudate analyses indicated that the abdominal transudate is different from urine hence ruling out the possibility of bladder rupture. Gastric ulceration have been reported to develop secondary to chronic liver disease as a result of altered gastric acid production and decrease epithelial cell turnover associated with hypoalbuminemia (Stanton & Bright, 1989). A similar finding was noticed in the puppy reported here. Also the firm, slightly enlarged liver with multiple miliiary nodules due to fibrosis is pathognomonic with liver cirrhosis (Popper, 1977; Royers, 1992).

REFERENCES

• Center S.A. (1989). Pathophysiology and Laboratory Diagnosis of liver Disease In Textbook of Veterinary Internal Medicine. W.B. Saunders & Company. Philadelphia.
• Fausto, N and Meade, I.E (1989). Biology of Disease: Regulation of liver growth-protooncogenes and transforming growth factors. Lab Invest 60; 4-13
• Hardy, (1985). Diseases of the Liver. In Textbook of Veterinary Internal Medicine. Disease of dog & cat by Ettinger S.J (Edt) W.B Saunders Company, Philadelphia.
• Herrtage (1991). The liver. In canine Medicine and therapeutics. (E.A.Chandler, D.J. Thompson; J.B. Sutton & C.J. Price Eds) Blackwell scientific Publication.
• Manderino, D and Devries J.G. (1985). Hepatic Encephalopathy in dogs. Mod. Vet. Pract. 66. 975-984.
• Popper, A. (1977). Pathologic Aspects of cirrhosis. A review. Am. Journal of Pathol. 87: 228-244
• Roger, K. (1993). The liver and Biliary system. In Pathology of domestic Animals (Jubb, KVF; Peter C. Kennedy & Nigel Palmer Eds) Academic Press. New York.
• Stanton, M.E. and Bright, R.M. (1989). Gastroduodenal ulceration in Dogs. Retrospective study of 43 cases and literature. Review. J. Vet. Intern Med 4:238
• Strombeck, DR and .Guildford, W.G. (1990). Liver: Normal function and physiology. In small Animal Gastroentenology. Davis C.A. Stonegate. , “
• William A.R. (1991). Liver failure. In quick Reference to Veterinary Medicine (William R. Fenner Ed). J.B. Lippincott Company.

© Ibadan Biomedical Communications Group