Fatty liver or fat cow syndrome (hepatic lipidosis, pregnancy toxaemia in cattle)

Fatty liver or hepatic lipidosis is a major metabolic disease of dairy cows. It is caused by decrease in energy intake and negative energy balance during parturition associated with excessive mobilization of body fat to liver.

Aetiology: A decrease in energy intake due to shortage of feed or inability of cows to consume adequate amount of feed during late pregnancy or lactation usually contribute to fatty liver disease. The condition develops prior to and during calving when the hepatic uptake of lipids exceeds the oxidation and secretion capacity of liver due to mobilization of excessive quantities of fat from body depots. Sudden demand of energy during immediate post-partum period in over-conditioned cows and deprivation of feed in high yielding pregnant cows precipitate fatty liver disease.

Generally, diary cows are in a state of negative energy balance in late pregnancy, which continues to early lactation due to drop in voluntary dry matter intake. Most cows adapt to the negative energy balance and the total amount of fat in liver that has elevated physiologically before calving declines slowly to the normal level within few weeks of calving. However, low hepatic glucogenesis capacity is associated with low blood glucose concentration, low insulin level and high rate of mobilization of fatty acid and elevated levels of non-esterified fatty acids (NEFA) in blood leading to severe lipidosis. Hepatic uptake of NEFA is proportional to NEFA concentration in blood. Liver processes NEFA either by oxidation or esterification. The triglyceride is the primary esterified product, which accumulates under elevated hepatic uptake of NEFA.

The disease conditions that predispose fatty liver include metritis, mastitis, ketosis,acidosis, retained placenta, milk-fever and left-side abomasal displacement.Overfeeding of cows during dry period predisposes fatty liver. Genetic factors are also proposed to influence mobilization of body lipid reserves.

Clinical findings: Fatty liver cows do not show any characteristic signs. Affected animals are generally obese and palpation over flank indicates excessive subcutaneous fat. There is drop in milk yield and reduced feed intake. The rumen movement may be absent in anorectic animals. The temperature, pulse and respiration rates are within normal range. ketonuria, hypoglycaemia, hyperammonaemia and endocrine changes may accompany fatty liver. The severely affected cows gradually become weak and recumbent, and die within 7-10 days. Most cases of fatty liver recover albeit in several days.

Diagnosis: Clinical diagnosis of fatty liver is difficult. The biopsy of liver is the reliable method to detect severity of the condition. Disease conditions associated with the clinical signs similar to fatty liver disease should be differentiated. Left side abomasal displacement is characterized by pings over the abdomen, ketosis and inappetance. Metritis and retained placenta may be accompanied by fever, inappetance, ruminal atony and foul smelling discharge from vagina. Changes in activities of liver specific enzymes, lipid profile, glucose and NEFA concentrations in blood are used as laboratory diagnostic tools.

Treatment and Prevention: Severe cases of fatty liver do not respond very well to the treatment and prognosis for  such cases,  particularly with nervous signs, is poor. Animals should be provided plenty of good quality feed and water. Intravenous administration of 5% glucose and balanced salt solution along with intraruminal administration of rumen fluid (5-10 litres) from normal cows are effective. Glucagons,10 mg/day intravenously or 15 mg/day subcutaneously for 14 days is effective in reducing liver triglyceride. Glucocorticoides, propylene glycol and insulin are also useful in treatment of fatty liver.Reducing severity and duration of negative energy balance is important to reduce occurrence of fatty liver. Propylene glycol can be given orally @ 500-1000 ml day during the last week of gestation.