This article was originally printed in the Mar/Apr 2026 issue of the California Veterinarian magazine.

Two things are inevitable in the springtime: tax season and kidding season. Veterinarians will be pulling kids and lambs, cutting c-sections, treating the onslaught of neonatal diarrhea, and mainlining caffeine. Although we all know the adage “an ounce of prevention is worth a pound of cure,” occasionally we treat cases of pregnancy toxemia, also known as ketosis. Ketosis is a metabolic condition that occurs because of negative energy balance—feed intake cannot keep up with the energy demands of gestation and lactation.

Cases of pregnancy toxemia can be fatal for the dam and fetuses or result in the birth of weak lambs or kids, or prolonged recovery for the dam that may impair their ability to feed offspring. While ketosis is more common immediately post-partum/during early lactation in cattle, ketosis generally occurs in the last 2-4 weeks of pregnancy in small ruminants. Pregnancy toxemia can be primary or present secondarily with other comorbidities like pneumonia, lameness, or gastrointestinal parasites. Early recognition of clinical signs, use of stall-side tests, and careful treatment and monitoring for comorbidities are critical for the management of this condition.
The metabolic events of late pregnancy are a formidable task for small ruminants—exponentially increasing fetal size, fetal bone development, and colostrogenesis will increase energy demands on the dam several-fold. In addition, the expanding uterus will decrease the abdominal space available for the dam to eat enough feed to keep up with these demands, and ewes or does carrying >2 fetuses face even more challenges. For these reasons, late gestation ewes and does may decrease their dry matter intake by up to 30% at a critical timepoint.

When small ruminants enter a state of negative energy balance, they will mobilize fat, which is transported to the liver and used to create ketone bodies, or ketones. Ketones are weakly acidic and can be used as an energy source by tissues but are much less efficient. When production of ketones outpaces their use by tissues, animals may experience ketoacidosis. Pregnancy toxemia is the clinical syndrome for systemic illness due to ketoacidosis.

In high concentrations, ketones are pro-inflammatory, immunosuppressive, and appetite-suppressing, creating a vicious cycle of poor appetite and negative energy balance, as well as predisposition to periparturient comorbidities like mastitis, metritis, pneumonia, and GI parasitism. Ewes or does that are thin will face challenges related to fat stores available for mobilization, and overweight ewes or does may struggle with poor insulin sensitivity or fatty liver syndrome, further complicating late gestation and predisposing to pregnancy toxemia.

Small ruminants with pregnancy toxemia will run the spectrum of mild, subclinical cases barely noticeable to the owner all the way to severe clinical cases with high risk of mortality for both the dam and kids without immediate intervention. Often, the clinical signs are vague and may encompass several different body systems.

In the early stages, owners may notice a slightly decreased appetite, decreased activity levels or more time spent lying down, separating from herdmates, or decreased fecal output. In severe cases, owners may find animals down, completely anorexic, groaning with respiration, star-gazing, or abnormal licking/chewing (a condition called nervous ketosis). Since animals can present with such a constellation of vague clinical signs, it is important to educate owners on carefully watching high-risk animals and during high-risk times (in the last 2-4 weeks of pregnancy or after severe weather events).

Ewes or does with >2 fetuses, a history of pregnancy toxemia in previous pregnancies, thin or obese ewes/does, animals with a history of heavy lactation, and animals with signs of other primary diseases like pneumonia, GI parasites, lameness, mastitis should be considered high risk. The sooner animals with pregnancy toxemia can be identified, the greater the chance of successful intervention.

Several diagnostic tests can be run on-farm or in-clinic to support a diagnosis and estimate the severity of pregnancy toxemia. Using a thorough physical exam, diagnostics (including severity), and estimated due date of the dam can help veterinarians make decisions regarding treatment and recommendations about decision-making related to the pregnancy. The two main goals of treatment for pregnancy toxemia are increasing energy intake and utilization and decreasing energy losses.

Although a majority of subclinical and early clinical cases can be managed on farm with oral medications and feed supplementation, more severe cases may require escalation of care, including IV fluids with dextrose supplementation and insulin, among other treatments. In some cases, veterinarians may need to recommend termination of the pregnancy to increase the chances of dam survival, either through induction of parturition, cesarean section, or abortion, depending on the condition of the dam and gestation age of the offspring.

Although treatment decision-making can seem complex for cases of pregnancy toxemia in small ruminants, frameworks can be used by veterinarians to inform our recommendations to owners or producers and high-quality client education surrounding avoidable or manageable causes of pregnancy toxemia can be strong prevention measures.

So, for those of us gearing up for lambing and kidding season—may your coffee mugs be ever-filled and your patients’ pregnancies remain non-toxic!