Lactational Ketosis / Fatty Liver Disease

Lactational Ketosis / Fatty Liver Disease

by Robert Van Saun, DVM, MS, PhD Department of Veterinary Science Pennsylvania State University

Similar to the disease process described for pregnancy toxemia, dietary glucose deficiency occurring during peak milk production can result in a ketotic state in heavily lactating dairy goats.

This is generally not a disease problem in sheep or non-dairy breed goats.

Clinical Signs. Lactating does will initially reduce milk production. Refusal of grain and further reductions in milk production will ensue. Does will rapidly lose body condition during early lactation. Body temperature, pulse rate and respiratory pattern will be within normal limits. Rumen activity may diminish. In severe cases, neurologic signs (nervous ketosis) similar to those described for pregnancy toxemia will be observed.

Causes. Glucose demand to support lactose (milk sugar) production by the mammary gland tremendously increases the does requirement for dietary glucose precursors. Sugars and starches primarily in cereal grains are the predominate sources of glucose precursors. As lactation is initiated, dry matter intake starts at it’s lowest level on the day of kidding and then slowly increases. However, milk production by the mammary gland increases glucose demand more rapidly than accounted for by dietary intake. This results in a period of negative energy balance, resulting in body weight loss to support lactation. If grains are increased in the diet too rapidly, a condition of acidosis might result (see lactic acidosis). To compensate for the reduced glucose availability, the doe will mobilize body protein and reserve fat to meet increased energy and glucose needs. Excessive body fat mobilization results in large amounts of fatty acids being delivered to the liver for processing. The liver can only metabolize a fraction of the fat delivered and in the face of low blood glucose concentrations, will generate excessive amounts of ketone bodies. Fatty acids not metabolized to ketone bodies will be synthesized back into fat and stored in liver cells. Excessive liver fat storage will result in associated fatty liver disease.

Treatment. Similar to pregnancy toxemia, glucose supplementation in the form of intravenous dosing followed by 3 days of oral propylene glycol is needed. Repeat treatments may be necessary for full recovery. Corticosteroid therapy is also used to stimulate the doe’s ability to generate glucose from amino acids. In refractory cases, insulin therapy in conjunction with glucose infusions may be necessary. Supportive therapy to stimulate intake and dietary modification to increase glucose availability are also warranted. Prevention. Good supportive care following kidding and appropriate dietary management of the early lactation doe are important. Recently kidded does should be managed carefully to ensure adequate opportunity to eat a well-balanced diet without any obstacles. Recently kidded does may be more timid and reluctant to compete for food. Observe does carefully for any indications of other postparturient disease problems that may negatively impact appetite.

Ensure the early lactation diet has higher protein and energy content, but is not excessive in grain. Gradually increase grain over the first 2 weeks of lactation. Body condition score of the late pregnant doe is again critical. Does should enter lactation with some body reserve, but not excessive. Heavy body condition does will not only have more fat reserves to mobilize and be more susceptible to fatty liver disease, but their intake will be reduced. Excessively thin does will not have the nutrient reserves to support good lactational production.