Pregnancy toxemia in cows is similar to the condition in small ruminants and is the result of fetal carbohydrate or energy demand exceeding maternal supply during the last trimester of pregnancy. It is precipitated by large or multiple fetuses, feed low in energy or protein, and health conditions that increase energy demand or decrease ability to take in nourishment (eg, lameness and oral diseases). The fetoplacental unit uses carbohydrate for energy and removes these compounds from the blood in an insulin-independent fashion. When this demand exceeds maternal supply, adipose tissue is mobilized to supply energy as acetate or ketone bodies, sparing carbohydrate consumption by other maternal tissues. However, only a small amount of new carbohydrate is generated from fat metabolism (from glycerol). This condition is more severe than ketosis (see Ketosis in Cattle) because fetal demand increases during pregnancy, while milk demand can decline in response to negative energy balance.
Although the mechanism is unknown, clinical disease develops in some cows with negative energy or carbohydrate balance. Proposed mediators of clinical disease include glucose deficiency with intermittent hypoglycemia, ketone body accumulation with metabolic acidosis or appetite suppression, and death of the fetus with secondary infection and toxemia. Individual cows of any breed can be affected, but herd problems are most common in beef cattle, which frequently are managed so that late pregnancy coincides with the poorest availability of feed. Both thin and fat cows can be affected, but the first noted abnormality often is loss of body condition over 1–2 wk. Decreased appetite, rumination, fecal production, and nose-licking are general signs of illness. With time, affected cows become markedly depressed, weak, ataxic, and recumbent. Opisthotonos, seizures, or coma may be seen terminally. Ketonuria is present from the early stage of disease and is the most specific finding; even mild ketonuria should not be found in normal pregnant cows until a few days before calving. Hypoglycemia is also common, but excited or seizuring cows may have hyperglycemia. With more advanced disease, there may be variable increases in serum activities of muscle or liver enzymes, as well as clinicopathologic evidence of infection, metabolic acidosis, internal organ dysfunction or failure, and circulatory collapse. Hepatic lipidosis in conjunction with large or multiple fetuses is a common necropsy finding; evidence of muscle pressure necrosis and toxemia may also be found.
Successful treatment requires early identification of the disease. There are few differential diagnoses, and pregnancy toxemia must be considered a factor in any disease that affects cattle in late gestation. Cattle that have lost weight but are still eating may be managed by feeding concentrate or propylene glycol (0.5–1 g/kg/day). Anorectic cattle must be treated aggressively, because the decrease in energy intake causes the disease to progress rapidly. Propylene glycol can be force-fed, or dextrose given IV (0.5 g/kg). Cattle with dehydration, organ dysfunction, or metabolic acidosis should be treated with large volumes (20–60 L/day, PO or IV) of electrolyte fluids; if IV fluid administration is practical, continuous dextrose infusion (5%) is recommended. Protamine zinc insulin (200 U, SC, every 48 hr) may be given after dextrose administration to suppress ketogenesis. Insulin is not approved for use in cattle in the USA, however. Recumbent cattle may benefit from good nursing care (see Bovine Secondary Recumbency) but rarely respond to treatment. To decrease the energy drain of any cow with pregnancy toxemia, induction of parturition or removal of the fetus by cesarean section should be considered.
On the herd level, the disease can be prevented by adequate attention to nutrition and health care of cattle in late gestation. For the individual cow, recognition of the precarious state of energy and carbohydrate balance during late gestation dictates careful monitoring of energy intake, attitude, and fat mobilization, especially during times of illness or other stress.
Last full review/revision July 2011 by Christopher K. Cebra