Hepatic lipidosis, commonly referred to as “fatty liver syndrome,” is a multifactorial syndrome of peri-parturient dairy cows.  It occurs most frequently in production situations that commingle dry cows and lactating cows in a single group.  These cattle are likely to become over-conditioned late in lactation or during their dry period.  Mortality can be as high as 25% without aggressive treatment and correction of  concurrent diseases.

  In over-conditioned cattle, fatty acids synthesized in the liver are stored as triglycerides in adipose tissue at extra-hepatic sites.  With an increased energy demand not met by a parallel increase in intake, triglycerides in adipose tissue are converted to glycerol and NEFAs (non-estrified fatty acids), which are bound to albumin in the blood.  The albumin bound NEFAs can be used as sources of energy by the mammary glands, liver, spleen, and muscle.  The liver receives much of the NEFAs due to its large blood supply and efficiency at extracting these substances.  In the liver, NEFAs are re-estrified back into triglycerides and remain in the liver until they can be oxidized or repackaged in an envelope of cholesterol, phospholipid, and protein.  Repackaging and export from the liver is a very slow process in cattle.  Cattle with hepatic lipidosis have smaller amounts of the packaging materials, further slowing hepatic output.  It is likely that glucose availability influences the course of the disease, with high glucose availability favoring fatty liver syndrome and the opposite favoring ketosis.

  Development of fatty liver syndrome can happen very quickly.  Triglycerides present can increase from 5% to more than 25% in 48 hours under extreme conditions of fat mobilization.  A prepartum decline in DMI (Dry Matter Intake) appears to increase the NEFAs in the serum at this time.  This is most severe in obese cows, those in stressful environments, or those under nutritional stress.  Endocrine changes that occur at parturition may contribute to the decrease in DMI.  It has been shown that force-feeding to prevent a DMI drop will reduce the amount of hepatic triglycerides accumulated at day 1 postpartum.

  Cows that develop fatty liver syndrome tend to be obese or well-conditioned with high amounts of omental and/or subcutaneous fat.  They show nonspecific signs of illness, including depression, anorexia, weight loss, and weakness that may lead to recumbency.  Decreased milk production and rumen motility are also evident.  Metritis, retained fetal membranes, mastitis, milk fever, and displaced abomasum are some concurrent diseases that can be present with fatty liver syndrome.  The number of days to first ovulation following calving has been shown to be increased with greater amounts of triglycerides within the liver.

  Most diagnostic tests are poor indicators of hepatic lipidosis.  The most common clinical pathological abnormalities are ketonuria, hypoglycemia, and increased serum free fatty acids.  Liver derived enzymes, such as GGT and AST, are usually higher than in a dry cow, but are still within normal limits.  Due to decreased functional liver mass, the triglycerides and cholesterol (mostly lipoproteins) may be decreased.  Serum bile acids, in one study, were found to be an unreliable indicator of hepatic fatty degeneration.

  A liver biopsy is the most accurate and reliable way to confirm and assess the degree of fatty degeneration of the liver antemortem.  A mild to moderate amount of fat can be present in the liver of most post-parturient high producing dairy cows without evidence of disease.  The amount of fatty degeneration can be quantitated via histopathology or flotation in copper sulfate solutions of varying specific gravities.  It has been shown that there is little correlation between the amount of fatty degeneration and clinical signs until it is marked and the liver will float in distilled water (SG=1).

  On necropsy, fatty livers are usually yellow or tan.  Fatty degeneration is especially prominent in the centrilobular and intermediate areas of hepatic lobules, and a pronounced reticular pattern, on both serosal and cut surfaces, can usually be observed.  A white discoloration may be evident in the abdominal fat due to accelerated lipolysis.

  The main goal in treatment of fatty liver syndrome is the elimination of the negative energy balance.  This includes administration of both glucose and insulin twice daily.  Corticosteroids can be used for treating the ketosis that may be present, but only for a short period of time.  Corticosteroids  will increase appetite, reduce milk production (to help alleviate the demand for energy), and stimulate synthesis of glucose from the stores present.    Vitamin E and selenium have been found to be low in cattle with fatty liver, and supplementation is recommended.  Transfaunation of rumen fluid from a normal cow may increase production of volatile fatty acids used for glucose precursors.

  The best policy regarding fatty liver syndrome is prevention.  Goals of a good prevention program include the prevention of obesity in cattle late in their lactation and during their dry period.  It is important to maintain a good breeding program so that there are appropriate dry period lengths (45-60 days).  The ration should be balanced according to maintenance and pregnancy requirements to maintain, not put on, condition.  At 2-4 weeks before calving, the grain content in the ration should be slowly increased to acclimate the rumen flora to the fresh cow ration.

  Fatty liver syndrome can be prevented with proper management.  In situations in which management is poor, fatty livers, in addition to the other problems mentioned, are likely to be much more prevalent.  With good management decisions, the owner will be much happier with the efficiency and productivity of the herd.

-by Lynne Catania, Class of 2002

-edited by Dr. Matt Renninger,  VPB Graduate Student

References:

Cebra DK, Garry GB, Getzy DM, Fettman MJ: 1994.  Hepatic lipidosis in anorectic, lactating Holstein cattle: a retrospective study of serum biochemical abnormalities. J Vet Int Med 11(4): 231-237.

Garry FB, Fettman MF, Curtis CR, Smith JA: 1994.  Serum Bile Acid Concentrations in Dairy Cattle with Hepatic Lipidosis.  J Vet Int Med  8(5): 432-438.

Howard JL and Smith RA, Ed.: 1999.  Current Veterinary Therapy 4 – Food Animal Practice.  SB Saunders Co, Philadelphia, PA.  pp 226-233.

Jones TC, Hunt RD, King NW: 1999. Veterinary Pathology 6^th ed.  WB Saunders Co., Philadelphia, PA.  pp 226-233

Jubb KVF, Kennedy PC and Palmer N: 1993.  Pathology of Domestic Animals, v.2.

Academic Press, San Diego, CA.  pp 331-350.

Rukkwamsuk T, Wensing T and Kruip TAM: 1999.  Relationship between triacylglycerol concentration in the liver and first ovulation in postpartum dairy cows.  Theriogenology.  51(6): 1133-1142.

Smith BP et al.: 2002.  Large Animal Internal Medicine 3^rd ed.  Mosby, Inc, St. Louis, MO.  Pp 810-817.