Pregnancy Toxemia in Ewes and Does: Signs and Care

By Dr. Zubair Khalid, DVM, MS, PhD · 2026-09-20

Pregnancy toxemia is a metabolic emergency that develops in the last weeks of pregnancy when a ewe or doe cannot eat enough energy to meet the demands of her growing fetuses. The result is a negative energy balance. Her blood glucose falls, her body mobilizes fat and protein for fuel, and ketone bodies such as beta-hydroxybutyrate (BHBA) build up in the blood. Without prompt treatment, pregnancy toxemia can progress from a picky eater to a down, unresponsive animal and can kill both the dam and her unborn young [1][2].

This article is educational and is not a substitute for veterinary diagnosis or treatment.

Owner Triage: What to Do Right Now

If you own a late-pregnant ewe or doe and she has gone off feed, separated from the flock or herd, or seems dull or unsteady, treat it as urgent.

1. Move her to a quiet, sheltered pen close to the barn so you can watch her.
2. Offer fresh, highly palatable feed and clean water. Do not force feed a down animal by mouth.
3. Take her rectal temperature and note her breathing and gum color.
4. Call your veterinarian and report how far along she is, how many fetuses she is likely carrying, her body condition, and whether she has been eating.
5. Ask your veterinarian whether a hand-held ketone meter or a blood glucose reading would help guide the decision to come out to the farm.
6. If she is down, do not leave her flat on her side. Roll her onto her sternum (chest) if she can tolerate it, and keep her off cold, wet ground.

The single most useful thing an owner can do is recognize the problem early. Early recognition combined with appropriate intervention is the best approach to limiting the impact of this disease in a flock or herd [1].

At a Glance: Pregnancy Toxemia Decision Table

What Is Pregnancy Toxemia?

Pregnancy toxemia, sometimes called ketosis or twin lamb disease, is a nutritional metabolic disease of late pregnancy in small ruminants. It is not simply a disease of overconditioned animals. It is more typically associated with inadequate energy intake relative to pregnancy requirements, which drives the mobilization of body protein and fat [1]. Older names such as twin lamb disease reflect the strong link to multiple fetuses, and pregnancy toxemia remains one of the most common metabolic diseases of late-pregnant ewes and does, with potentially devastating effects on health and performance [1].

The condition is characterized by disorders in carbohydrate and fat metabolism [2]. Obese and multiparous ewes are particularly susceptible, and the disease may lead to maternal death, abortion, or premature birth [2]. The same disease process occurs in goats, where pregnancy toxemia causes substantial economic losses through reduced productivity, reproductive failure, and high mortality [3].

There are two practical levels of the disease. Subclinical pregnancy toxemia describes animals with abnormal ketone levels but few or no obvious outward signs. Clinical pregnancy toxemia describes animals that are visibly sick. Subclinical disease matters because it silently reduces performance and can tip into the clinical form under stress such as cold weather, transport, or a feed change.

The Physiology Behind the Crisis

To understand why late pregnancy is the vulnerable window, it helps to follow the energy.

A pregnant ewe or doe must supply glucose to her own brain and tissues and to her fetuses. In late gestation, fetal demand for glucose climbs sharply. Under normal conditions the dam maintains blood glucose through gluconeogenesis, the process of making new glucose, largely in the liver from precursors such as propionate from rumen fermentation and amino acids.

When feed intake falls short, several things happen at once:

• Rumen propionate supply drops, so the liver has less raw material for glucose.
• Blood glucose falls, which is measurable as hypoglycemia.
• The body mobilizes stored fat, releasing non-esterified fatty acids (NEFAs) into the blood.
• The liver takes up these fatty acids and converts some to ketone bodies, including BHBA.
• Fat that the liver cannot fully oxidize or export accumulates, producing hepatic fatty infiltration and lipidosis.

This cascade has been reproduced experimentally. When pregnant ewes were subjected to a 70 percent feed restriction for 15 days to model pregnancy toxemia, blood BHBA, NEFAs, and cholesterol rose while blood glucose fell. Liver tissue from the affected ewes contained more NEFAs, BHBA, cholesterol, and triglyceride, and microscopic examination showed excessive fat vacuoles plus damage to hepatocyte nuclei, mitochondria, and endoplasmic reticulum [4]. Gene expression studies show that fatty acid oxidation and triglyceride synthesis pathways are enhanced in the toxemic liver while acetyl-CoA metabolism is repressed [4].

The liver is not the only casualty. In goats with pregnancy toxemia, serum cardiac troponin I was significantly higher than in healthy goats (0.43 ng/mL versus 0.06 ng/mL), and CK-MB was roughly three times higher, suggesting clinically significant myocardial damage can occur. Insulin was lower and cortisol was markedly higher in the affected goats [5]. This is why advanced pregnancy toxemia is a whole-body disease and not merely a feeding problem.

Metabolic profiling in does confirms the pattern. In a study of 153 clinically healthy late-pregnant does, 53 had subclinical pregnancy toxemia based on 3-hydroxybutyrate above 0.86 mmol/L. Those does had significantly lower glucose concentrations and significantly higher urea and total protein concentrations than pregnant controls [6]. In another study of goats with pregnancy toxemia, glucose was significantly lower and gluconeogenic amino acids such as valine were significantly higher than in controls, while histidine was lower, reflecting the body pulling amino acids into glucose production [7].

Oxidative stress and inflammation accompany the metabolic collapse. Does with pregnancy toxemia show elevated markers of oxidative stress such as MDA and reduced antioxidants including GSH, GPx, SOD, and CAT, plus increased pro-inflammatory cytokines including IL1 alpha, IL1 beta, IL6, and TNF alpha, with reduced IL10 [3]. Earlier work showed that does with pregnancy toxemia had significantly lower insulin and significantly higher cortisol than control goats [5].

Who Is at Risk

Risk is not random. Several factors cluster together.

Multiple fetuses

Pregnancy toxemia is strongly tied to twins, triplets, and quadruplets. In a hospital case series of 56 does with pregnancy toxemia, all pregnancies involved twins (11), triplets (37), or quadruplets (7). No singleton pregnancies appeared in that series [8]. In ewes, the last three weeks of gestation are the danger window. In a three-flock study, more than 20 percent of ewes were identified with moderate risk of developing ketosis during the last three weeks of gestation, and ewes carrying triplets had reduced body condition score and increased BHBA concentrations [9].

Body condition extremes

Both overconditioned and underconditioned animals are at risk. Fat ewes and does have less appetite capacity to take in the extra energy they need, and their livers are already loaded with fat. Thin animals have no reserves to mobilize. Interestingly, most does in one hospital series (15 of 36 with recorded scores) had appropriate body condition scores, which reinforces that pregnancy toxemia is not only a disease of fat animals [8]. A genetic component may also exist: Boer goats were overrepresented relative to the general hospital population in the last year of one study [8].

Late-gestation undernutrition

Simply not eating enough is the core driver. Any condition that reduces intake, such as a ration change, poor-quality forage, competition at the feeder, dental problems, lameness, or severe weather, can tip an animal over the edge [1].

Rumen health

The rumen microbiome differs between healthy and affected ewes. In one study, pregnancy toxemia ewes had lower serum glucose, cholesterol, LDL-C, uric acid, creatinine, acetate, propionate, butyrate, and microbial crude protein, and higher BHBA, AST, and ammonia nitrogen than healthy ewes. Differences in bacterial diversity were also observed at the phylum level [10]. This suggests poor rumen fermentation and reduced propionate production are part of the disease picture.

Age and parity

The disease is seen in adult pregnant females rather than the very young. In one clinical series of Iraqi Awassi ewes with pregnancy toxemia, affected animals ranged from 2 to 8 years old [11]. Multiparous animals are more often affected because they more often carry multiples [2].

Genetic and individual variation

Genomic work in Shami goats identified multiple single-nucleotide variants significantly associated with pregnancy toxemia susceptibility, and discriminant analysis using these variants achieved high classification accuracy [3]. Serum proteomics also separates healthy goats from those with subclinical and clinical pregnancy toxemia, with 25 proteins significantly differentially expressed [12]. This tells us some animals are inherently more vulnerable, but it does not give owners a practical genetic test today.

Early Signs Versus Advanced Signs

The disease has a predictable arc, and the earlier you catch it the better the outcome.

Early signs

• Anorexia, or going off feed, especially refusing grain
• Lethargy and dullness, separating from the group
• Ataxia, or unsteady, wobbly walking
• Weight loss
• Grinding of the teeth (a sign of abdominal discomfort in small ruminants)
• Dropping behind the flock or herd on pasture

In the Iraqi ewe series, recognized clinical signs included depression, loss of appetite, weight loss, lying down, a ketogenic odor on the breath, inability to walk, neurological signs, teeth grinding, jaundice, blindness, bloat, dystocia, and death, including fetal death [11]. Those descriptors span the full spectrum from early to advanced.

Advanced signs

• Recumbency, or being unable to rise
• Neurological signs such as head pressing, tremors, or unusual behavior
• Blindness
• A sweet or acetone-like odor to the breath (a ketogenic odor)
• Jaundice
• Bloat
• Coma and death

Temperature, respiration, and pulse may not differ significantly from healthy animals in early or moderate disease, which is a trap for owners who rely on a thermometer alone [11]. A normal temperature does not rule out pregnancy toxemia.

Progression can be fast. In an experimental model, induced ketosis shortened gestation to about 143 days compared with 150 days in normal twin-pregnant ewes. Clinical recovery and normal feed intake took about 3.4 days, and 3 of the ewes required treatment [13]. This tells us the disease both makes animals sick and pushes them toward premature delivery.

How Pregnancy Toxemia Is Diagnosed

Diagnosis rests on history, physical examination, and blood chemistry. Blood chemistries provide insight into diagnosis and may help predict responsiveness to treatment and outcome [1].

Glucose and ketones are the core tests

Hypoglycemia (low blood glucose) and elevated BHBA (beta-hydroxybutyrate) confirm the picture. In a clinical and biochemical study of affected ewes, BHBA and NEFAs were significantly elevated compared with healthy controls [11]. In does with clinical pregnancy toxemia, glucose was significantly lower than in controls [7].

Practical ketone monitoring

Hand-held meters make on-farm monitoring realistic. The Nova Vet Meter was evaluated for sheep-side BHBA monitoring. Against gold-standard laboratory analysis, accuracy and sensitivity for detecting BHBA in the 0.8 to 1.5 mmol/L range were 94.2 percent and 97.3 percent, and for detecting BHBA at or above 1.6 mmol/L were 98.0 percent and 50.0 percent [9].

Practical BHBA thresholds used in the literature:

• 0.8 mmol/L is a critical cut-off. Ewes with BHBA between 0.8 and 1.6 mmol/L are typically classified as having subclinical pregnancy toxemia [14].
• 0.8 to 1.5 mmol/L represents moderate risk to develop ketosis [9].
• At or above 1.6 mmol/L represents the greatest risk [9].
• Does with 3-HB above 0.86 mmol/L were classified with subclinical pregnancy toxemia in one herd study [6].
• A BHBA above 1.2 mmol/L was the threshold used to define pregnancy toxemia in does in a hospital cohort of newborn kids [15].

In a Romanov sheep study, no ewes in the group had BHBA above 1.6 mmol/L, and there was no significant difference in BHBA, NEFAs, or cholesterol based on birth type, though triglyceride was higher in ewes giving birth to triplets [14]. This shows the risk picture is not identical in every flock, and herd-specific monitoring matters.

Other laboratory findings

A veterinarian may also look at:

• NEFAs, which rise with fat mobilization [11][16]
• Liver enzymes such as AST, which may be elevated [10]
• Urea, creatinine, and total protein [6]
• Serum bicarbonate and BUN in goats, which carry prognostic weight (see Prognosis below) [8]
• Cholesterol and triglycerides [14][11]
• Cardiac biomarkers such as troponin I and CK-MB, which may indicate myocardial involvement [5][17]
• Inflammatory and oxidative stress markers, which research studies use but which are not routine farm tests [3]

Imaging can support the diagnosis. Hepatic ultrasonography in does with pregnancy toxemia indicated hepatic fatty infiltration [3].

A Step-by-Step Diagnostic and Treatment Path

The following flow shows the main decision points from recognizing a problem to monitoring recovery.

flowchart TD
    A[Late pregnant ewe or doe off feed] --> B[Check body condition and gestation stage]
    B --> C[Measure glucose and BHBA]
    C --> D{Glucose low and BHBA high}
    D -->|No| E[Look for other causes]
    D -->|Yes| F[Pregnancy toxemia suspected]
    F --> G[Contact veterinarian]
    G --> H[Start energy support and supportive care]
    H --> I[Monitor glucose ketones and appetite]
    I --> J{Improving}
    J -->|Yes| K[Continue care and plan delivery]
    J -->|No| L[Reassess for induction or cesarean section]

Treatment Principles

Pregnancy toxemia treatment rests on three pillars: restore energy, treat the individual animal, and resolve the pregnancy. This is a disease where a veterinarian should direct care, because the choice of when to intervene with the pregnancy can be as important as the glucose support itself.

Energy support

The foundation is supplying glucose and glucose precursors so the dam stops mobilizing fat. In practice this means veterinary-guided intravenous glucose therapy, oral energy drenches or gels designed for ruminants, and getting the animal eating again as soon as she safely can. The goal is to break the ketosis cycle and restore normal appetite and rumen function. Treatment also requires careful handling of the pregnancy, and this is a decision only a veterinarian should make.

Some cases are complicated by concurrent hepatic lipidosis, which is why blood chemistry results can predict how well an animal will respond to treatment and what the likely outcome is [1]. Animals with severe liver involvement may not recover with energy support alone.

Resolving the pregnancy

When the dam does not respond to energy support, the pregnancy itself must be addressed. Options include inducing parturition, delivering the fetuses, or performing a cesarean section. Research on induced parturition in ewes with pregnancy toxemia has examined protocols using agents such as aglepristone and dexamethasone. In one study, all ewes in the treated and untreated pregnancy toxemia groups developed clinical pregnancy toxemia, and parturition timing, placental measures, and most blood results did not differ significantly among groups [18]. This is technical territory in which the choice of agent, timing, and delivery method must be decided by the attending veterinarian based on the individual animal and her fetuses.

A key consideration is fetal readiness. Inducing parturition too early can produce premature newborns that cannot survive. Newborns from dams with pregnancy toxemia are already more fragile. Kids born to does with pregnancy toxemia were more acidemic and hyperlactatemic at birth than control kids, were more likely to require tube feeding at 0 and 12 hours of life, and control kids were slightly heavier [15]. Twins from dams that survived to delivery had a higher survival rate than quadruplets. Death was also more likely for offspring delivered by cesarean section than for those delivered vaginally in one hospital series, though this may reflect the severity of cases needing surgery [8].

Supportive care

Supportive care for a down or weak animal typically includes:

• Shelter, warmth, and soft, dry bedding
• Positioning changes to prevent muscle and nerve damage in a down animal
• Fluids and electrolyte balance as directed by the veterinarian
• Treating concurrent problems such as lameness, mastitis, or gastrointestinal disease
• Careful monitoring for the need to intervene in the pregnancy

Monitoring During Treatment

Monitoring is where owners and veterinarians work together. Two measurements drive most decisions.

Glucose

Blood glucose tells you whether energy support is working. A rising, stable glucose alongside returning appetite is a good sign. Persistent hypoglycemia despite treatment suggests the animal needs more aggressive intervention.

BHBA and ketones

BHBA tells you whether the ketotic state is resolving. Trending BHBA downward is the goal. A hand-held meter validated for sheep-side monitoring makes serial measurements practical [9]. In does, the same principles apply, with slightly different thresholds used in different studies [6][15].

A reasonable monitoring schedule for a treated animal includes glucose and ketone checks at least daily, plus appetite, attitude, and gait assessments several times a day. Down animals need more frequent checks. Return to normal feed intake took roughly 3.4 days in the experimental induced-ketosis model, which gives a sense of the typical recovery timeline when treatment works [13].

Prevention: Late-Gestation Nutrition and Body Condition

Prevention is far more effective than treatment. The entire strategy is to match energy intake to pregnancy demand and to enter late gestation with the right body condition.

Manage body condition before breeding

Do not try to fix body condition during late pregnancy. The time to do it is before breeding and in mid gestation. Both very thin and very fat animals are at higher risk, so aim for the middle [1][8]. Use body condition scoring at regular intervals to track your flock or herd.

Feed a proper late-gestation ration

Energy density matters. In a study comparing ewes fed a low-energy roughage-only diet versus a high-energy roughage and concentrate diet, significant differences appeared in glucose, folic acid, cobalamin, fructosamine, NEFAs, and BHBA, confirming that diet energy density directly shifts these metabolic markers [16]. Animals carrying multiples need more energy than those carrying singles. Work with your veterinarian or nutritionist to build a late-gestation ration for the animals that actually need it, and separate multiple-bearing animals so they get their share.

Provide enough feeder space

Competition is a hidden cause of underfeeding. Shy animals lose weight while the ration looks adequate on paper. Group animals by size and appetite, and provide generous feed space.

Monitor BHBA in the last weeks

In a three-flock study, more than 20 percent of ewes were identified with moderate risk of developing ketosis during the last three weeks of gestation [9]. Regular BHBA monitoring in the last 4 to 6 weeks lets you catch subclinical disease before it becomes clinical. A hand-held meter validated for ovine use makes this feasible on farm [9].

Reduce stress and manage weather

Cold, wet, and stormy weather raise energy needs. Provide shelter and consider extra feed during severe weather. Avoid unnecessary transport, handling, or ration changes close to lambing or kidding.

Treat other problems promptly

Lameness, dental disease, and any painful condition that reduces eating will raise pregnancy toxemia risk. Address them early.

Consider the genetic angle for the future

Genomic variants associated with pregnancy toxemia susceptibility have been identified in goats [3], and proteomic profiles differentiate affected from healthy animals [12]. These are research tools rather than on-farm tests, but they point toward future breeding strategies that could reduce susceptibility over time.

Unsafe Home Remedies and Common Mistakes

Some well-intentioned actions can make things worse.

• Do not pour large volumes of any liquid into the mouth of a down animal. A down ewe or doe can aspirate fluid into her lungs. Ask a veterinarian how much to give and by what route.
• Do not rely on "just give her more grain" once a true ketosis is established. Advanced cases often cannot eat enough to reverse the process, and a sudden grain load can cause rumen acidosis.
• Do not wait for a fever. Temperature can be normal in pregnancy toxemia, so a normal reading does not mean the animal is fine [11].
• Do not delay because the animal is only "a little off." The gap between mild anorexia and recumbency can be short.
• Do not induce parturition on your own. Timing affects whether the newborns survive, and the clinical consequence can be premature, nonviable young [8][15].
• Do not skip veterinary care for the newborns. Kids from dams with pregnancy toxemia have documented metabolic problems at birth and often need early feeding support [15].

Prognosis

Outcome depends on how early treatment starts, how much liver and organ damage has occurred, and whether the pregnancy can be resolved safely.

In a hospital cohort of 56 does with pregnancy toxemia, most (39) survived to hospital discharge. Does with high BUN concentration and those with serum bicarbonate concentration below 15 mEq/L were more likely to die than does without those findings [8]. Among 49 does that survived to delivery of their offspring, survival to discharge was positively associated with the survival of their offspring, meaning dam and newborn outcomes track together [8].

For ewes, the experimental induced-ketosis model showed that animals can recover with treatment, with a return to normal feed intake around 3.4 days, but three of the study animals still required treatment [13]. This reinforces that early intervention matters and that recovery is not guaranteed even with care.

Blood chemistry values can predict responsiveness to treatment and outcome, which is one reason veterinarians run laboratory tests rather than treating blind [1]. Cardiac involvement, reflected in elevated troponin I and CK-MB, may also influence how a goat tolerates the metabolic insult [5][17]. In ewes, shortened gestation is a common consequence, so be prepared for earlier-than-expected lambing [13].

Limitations and When to Contact a Veterinarian

This article covers general principles. Individual animals need individual veterinary assessment, because the right monitoring plan, treatment intensity, and timing of intervention in the pregnancy vary with the animal, her fetuses, her liver status, and your farm setup.

Call a veterinarian immediately if a late-pregnant ewe or doe:

• Refuses feed for more than a few hours, especially grain
• Is dull, wobbly, or unable to keep up with the group
• Cannot rise or shows neurological signs such as head pressing or blindness
• Has breath that smells sweet or acetone-like
• Has a known BHBA at or above 1.6 mmol/L, or a BHBA that continues to rise on monitoring
• Has a low blood glucose reading on a meter
• Is within 4 to 6 weeks of lambing or kidding and has stopped eating
• Has gone down and cannot be kept comfortable or clean
• Has a past history of pregnancy toxemia, twins, triplets, or quadruplets

Also contact a veterinarian if a newborn from an affected dam is weak, slow to suckle, or not thriving in the first hours of life. Kids born after maternal pregnancy toxemia are more likely to need tube feeding early and may have metabolic acid-base problems at birth [15].

Frequently Asked Questions

What causes pregnancy toxemia in ewes and does?

It is caused by a negative energy balance in late pregnancy. The animal cannot eat enough energy to meet the demands of her fetuses, so blood glucose falls and her body mobilizes fat and protein, producing ketones [1][2].

What are the earliest signs I should watch for?

Anorexia, lethargy, and unsteady walking are the earliest signs. An animal that is picking at feed and lagging behind the group is showing the start of the problem, before she goes down.

How is pregnancy toxemia confirmed?

Hypoglycemia plus elevated beta-hydroxybutyrate (BHBA) confirms it. A hand-held meter validated for sheep-side use can measure BHBA accurately in the moderate range [9].

What BHBA level is dangerous?

A BHBA at or above 1.6 mmol/L represents the greatest risk in ewes, and 0.8 to 1.5 mmol/L represents moderate risk [9]. Subclinical pregnancy toxemia in ewes is often defined as BHBA between 0.8 and 1.6 mmol/L [14].

Can a ewe or doe survive pregnancy toxemia?

Yes, many do, especially with early treatment. In one hospital series, most does with pregnancy toxemia survived to discharge [8]. Recovery depends on how early treatment begins and how much organ damage has occurred.

Is pregnancy toxemia only a problem in fat animals?

No. It is more typically linked to inadequate energy intake, and most does in one hospital series had appropriate body condition scores [1][8].

What should I feed a late-pregnant ewe or doe?

Feed a ration with adequate energy density for her stage and number of fetuses, and make sure she can actually eat it without competition. Diet energy density directly affects glucose, NEFAs, and BHBA levels [16].

Why do the newborns sometimes do poorly too?

Newborns from affected dams are more likely to be acidemic and hyperlactatemic at birth and more often need early tube feeding [15]. Have them examined and monitor their first feeds closely.

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Sources

1. Pregnancy Toxemia in Sheep and Goats.
2. Pregnancy Toxemia in Ewes: A Review of Molecular Metabolic Mechanisms and Management Strategies.
3. Genomic Variants, Transcriptomic Profile, Ultrasonographic Findings, and Antioxidant and Immunological Biomarkers Linked to Pregnancy Toxemia Susceptibility in Goats.
4. Molecular mechanisms of lipid metabolism disorder in livers of ewes with pregnancy toxemia.
5. Changes in cardiac biomarkers in goats naturally affected by pregnancy toxemia.
6. Metabolic profiles in goat does in late pregnancy with and without subclinical pregnancy toxemia.
7. Changes in free amino acid profile in goats with pregnancy toxemia.
8. Evaluation of prognostic indicators for goats with pregnancy toxemia.
9. Evaluation of the Nova Vet Meter for sheep-side monitoring of β-hydroxybutyric acid (BHBA) and description of ewe BHBA during late gestation in three flocks from the Northeastern U.S.
10. Relationship between rumen microbiota and pregnancy toxemia in ewes.
11. Clinical and Biochemical Study of Pregnancy Toxemia in Iraqi Ewes.
12. Changes in Serum Proteomic Profiles at Different Stages of Pregnancy Toxemia in Goats.
13. Maternal undernutrition during late pregnancy in sheep. Its relationship to maternal condition, gestation length, hepatic physiology and glucose metabolism.
14. Subclinical Pregnancy Toxemia Affects Blood Parameters of Ewes and Impairs Postnatal Growth and Development of Lambs.
15. Characterization of short- and long-term morbidity and mortality of goat kids born to does with pregnancy toxemia.
16. Serum concentrations of folic acid and cobalamin and energy metabolism of ewes as a function of the energy density of the diet, peripartum period, and pregnancy toxemia.
17. The cardiac biomarkers troponin I and CK-MB in nonpregnant and pregnant goats, goats with normal birth, goats with prolonged birth, and goats with pregnancy toxemia.
18. Evaluation of an alternative treatment protocol by aglepristone to induce parturition in ewes with an experimental model of early pregnancy toxemia.