Nature of Disease: A metabolic disease or ketosis occurring in late gestation when maternal glucose homeostasis is disrupted.
Primary Cause: Nutrition is inadequate to meet the high energy demands of the developing fetus and gravid uterus.
Primary Targets: Predominantly occurs in beef cows because their last trimester often coincides with seasonal poor feed availability.
Etiology & Risk Factors:
Dietary Factors: Poor-quality diets low in energy or protein, or high in poorly digestible fiber.
Fetal Demands: Large or multiple fetuses significantly increase energy requirements.
Environmental Stress: Cold, snowy weather which increases energy needs and covers available forage.
Concurrent Health Issues: Conditions that decrease the ability to eat, such as lameness or oral diseases.
Pathophysiology:
Substrate Consumption: The gravid uterus consumes 50%–60% of maternal glucose and 30%–40% of amino acids.
Maternal Adaptation Failure: Reduced insulin secretion and sensitivity are meant to direct glucose to the fetus; however, when severe, this leads to excessive adipose tissue mobilization.
Metabolic Consequences:
Increased nonesterified fatty acids (NEFA) for maternal energy.
Excessive ketone body production leading to metabolic acidosis.
Hepatic Lipidosis: Fatty infiltration of the liver due to massive fat mobilization.
Clinical Findings:
Early Signs: Rapid loss of body condition over 1–2 weeks and decreased appetite.
General Signs: Depression, decreased rumination, reduced fecal production, and nose-licking.
Advanced/Terminal Signs: Weakness, ataxia, recumbency, seizures, and coma.
Postmortem Lesions: Lack of subcutaneous fat, serous atrophy of internal fat depots (omental, perirenal, pericardial), and liver damage (hepatic lipidosis).
Diagnosis:
Clinical Indicators: History of late gestation and marginal feed quality.
Ketonuria: The earliest and most specific finding; even mild ketonuria is abnormal in healthy pregnant cows.
Blood Chemistry:
Hypoglycemia: Low blood glucose (though hyperglycemia may occur with seizures).
Energy Markers: Increased beta-hydroxybutyrate (BHB >1.5 mmol/L) and NEFA (>0.6 mmol/L).
Nutritional Markers: Low BUN, hypoproteinemia, hypoalbuminemia, and hypokalemia.
Treatment Protocols:
Early Intervention (Still Eating): High-quality forage/concentrate and oral propylene glycol (0.5–1 g/kg/day).
Aggressive Therapy (Anorectic):
Transfaunation: Rumen fluid from a healthy animal to restore microbial populations.
Nutritional Slurry: Force-feeding a mix of alfalfa pellets, beet pulp, and soybean meal.
IV Dextrose: Bolus (0.5 g/kg) or continuous 5% infusion for hospitalized cases.
Insulin: Protamine zinc insulin may be used to suppress ketogenesis.
Termination of Pregnancy: Induction of parturition or C-section to remove the metabolic drain of the fetus.
Prevention Strategies:
Body Condition Management: Target a BCS of >5 (1–9 scale) for beef cattle as they enter the final trimester.
Nutritional Analysis: Feed analysis to ensure adequate protein (9%–10% of dry matter) and fiber digestibility.
Ionophores: Daily administration of monensin to facilitate ruminal propionate generation and increase glucose availability.
Stress Monitoring: Careful observation during weather events or periods of illness.