Pregnancy Toxemia in Goats
- Kendra R. Shatswell
- Jul 24
- 9 min read
Updated: Sep 8
Pregnancy toxemia, often called ketosis, is a metabolic disorder. Very simply, it occurs when the energy demands of the kid(s) are higher than the doe is able to meet.
When a doe experiences a negative energy balance, her body tries to compensate by mobilizing fat for energy, which requires the liver to metabolize these lipids into energy. But the production of ketones is secondary to this process and too many ketones will be released into the blood and urine. For an incredibly detailed article on the actual mechanisms behind the disease, please refer to this open access article - Pregnancy Toxemia in Ewes: A Review of Molecular Metabolic Mechanisms and Management Strategies
RISK FACTORS
Many factors contribute to the risk of pregnancy toxemia, but body condition and diet are arguably the most important. Does on either end of the body condition score are most likely to be affected.
In order to meet both her own energy demands and those of her fetus/fetuses, the doe needs to be in good body condition - most sources point at BCS 3-4 being ideal - and ingesting nutritious roughage. (For more information on body condition scoring, click here.) It is important that roughage is high-quality and easily digestible because the doe’s rumen capacity is decreased when the uterus is full of growing kids. The doe that has limited body capacity has little room for food so it must be excellent food. Note that pasture might be high protein but it is also less dry matter than hay and so the doe would have to eat significantly more pasture to achieve the same dry matter intake. Concentrates like grain are good sources of energy and protein but it is helpful to divide grain into more than one meal a day, to avoid ruminal acidosis. Interestingly, feral goats are more likely to abort kids if they are too undernourished during pregnancy but this is seen far less frequently in domestic goats (6).
If the doe is over-conditioned, she can experience pregnancy toxemia just as her under-conditioned herdmate might. Why? An over-conditioned goat stores fat around the organs and abdomen. This significantly decreases rumen capacity. As stated earlier, decreased rumen capacity means the doe can’t physically ingest enough to meet energy demands. Additionally, “Leptin, a hormone produced by adipose [fat] cells, may also contribute to a reduction in feed intake by decreasing the obese animals’ appetite” (Smith and Sherman 759). Do not diet an overweight doe late in gestation or you’ll likely cause the problem you’re trying to prevent. Exercise helps reduce the chances of pregnancy toxemia especially in over-conditioned does; some research in sheep indicates it will trigger the ewe’s body to use the fat for energy (1). In this interesting opinion piece, one producer noticed a serious difference between pregnant does kept in confinement versus those with more freedom for exercise.
It is important to make sure that all does have adequate access to food, so keep an eye out for any timid animals getting bullied away from the feeders to avoid fat bullies and skinny timid does.
Because of the increased energy demand with multiples, pregnancy toxemia is more likely to occur in litters but it is possible with a single kid. The kids will grow most towards the end of gestation: “Seventy percent of the weight of the kid is acquired between the one hundredth day of gestation and parturition.’’ (Smith and Sherman 757). Other sources claim 80% of kid growth might occur during this time. Multiples in utero take up a lot of body capacity and demand a lot of energy, making it more likely the doe will suffer a negative energy balance. In this article there is a chart from the textbook Nutrient Requirements of Small Ruminants that illustrates how requirements for crude protein, total digestible nutrients, and dry matter all increase during pregnancy and lactation. According to Penn State: “Generally, energy requirements for a doe carrying a single kid increase approximately 50% over her maintenance requirements, while energy requirements for a doe carrying twins increase 75%.” For additional charts: https://extadmin.ifas.ufl.edu/media/extadminifasufledu/nflag/pdfs/Nutrient-Requirements-of-Sheep-and-Goat.pdf
Older advice was to decrease feed during late gestation to avoid “large kids” but this is poor advice; a multitude of factors determine birthweight including genetics, litter size, season, dam age and/or freshening, and other factors like sex of the kids. Kids might be slightly smaller born to feed restricted does but as this article illustrates several times over, it is vital to meet the doe’s energy demands. Suddenly decreasing her intake when she needs it most will do more harm than good and can likely cause a myriad of issues, including pregnancy toxemia (6,9,10). In this interesting study, the progesterone of female offspring of the late gestation does who were feed restricted was negatively affected: “The main finding of the present paper is that after mating, plasma progesterone concentrations rose more slowly to reach a maximum in females born to late gestation feed-restricted goats compared to controls” (8)
Pregnancy toxemia cannot be ruled out entirely before the last couple months of pregnancy - one study indicated a very small number of does experienced pregnancy toxemia as early as three months into pregnancy (Smith and Sherman 758).
Do not underestimate the negative effect of stress on a pregnant doe. Bad weather, transportation, changing routine or changing the herd dynamics, or any other stressful event might trigger an acute onset of pregnancy toxemia. Pregnancy toxemia might piggy-back off of other issues such as a severe parasite infection or any other issue that would cause a doe to be losing energy, or occur concurrently with hypocalcemia. Ruminal acidosis can occur from both pregnancy toxemia and aggressive treatment of it with oral sugars. Besides the already mentioned disruptions in the rumen and liver, pregnancy toxemia can negatively affect the brain and kidneys, especially in the late stages (2,3,4,6)
After kidding a doe might experience lactational ketosis. It is essentially the same problem as gestational ketosis - too much energy demand as the doe feeds herself and produces milk for her kids. High production does are especially susceptible. “Glucose is required by the mammary gland for synthesis of lactose. After parturition, the quantity of milk produced and thus nutrient requirements of the goat increase more rapidly than the level of intake” (Goat Medicine 763).
SYMPTOMS
Symptoms of pregnancy toxemia can be quite subtle initially; the doe might just be “off” and show no other symptoms, a little slower and dull in general and eat with less gusto. She might isolate herself from the herd a bit. More noticeable symptoms might include going off feed entirely, swelling in the lower limbs, and teeth grinding. As mentioned earlier, her breath may smell like acetone. If left untreated or if it is sudden and severe, affected does will likely experience neurological symptoms due to the lack of glucose in the brain - eye twitching or even blindness, head-pressing or star-gazing, and incoordination - followed by recumbency or sometimes a coma in the terminal stage (2, 6).
DIAGNOSING
Producers can test urine using ketone strips or blood by using a livestock blood meter. The urine stripes are semi-quantitative, meaning the color change will give you a range from trace to high while the blood meters are quantitative and will give an amount in mmol/l or mg/dl. Acetone is one of the three major ketones that might be present in a toxemic doe - some producers are able to smell a sweet fruity scent or a nail-polish remover scent on the doe’s breath. The strips are more sensitive to the ketone acetoacetate while the blood meters are beta-hydroxybutyrate, aka BHB (Goat Medicine 760). No matter urine strips or blood strips, make sure they’re not expired and have been stored according to the manufacturer’s instructions.
Below is a blood ketone and glucose testing kit from PBS Animal Health. It is recommended to use a ruminant specific meter, not a human one.
There isn’t a lot of goat-specific research out there and there will be some variation depending on the source, but these are some suggested thresholds for BHB ketones via the blood meter :
≤ 0.8mmol/l normal
0.8-2mmol/l ketosis
≥2mmol/l severe ketosis
TREATMENT
Treatment means addressing the negative energy balance and the severity of the condition dictates the treatment course. In very mild cases, simply identifying and correcting the deficit might do the trick i.e. improving diet by safely increasing quality and/or quantity. Keep a drench gun handy because clinical cases will require treating with large volumes of energy supplements, usually propylene glycol or dextrose. Fortified vitamin b injections and/or electrolytes are helpful supportive care as is offering the doe a wide variety of safe forages and hays to eat. As far as dosages, the exact amount will vary with meter or strip reading and the size of the doe - a common recommendation is 30-60cc of propylene glycol two or three times a day. Note that exceedingly high dosages (one reference states 350cc - 500cc) might do more harm than good as the excess is “likely to overwhelm the ability of the rumen flora of an already sick goat to digest it” (Goat Medicine 760) and a toxicity can cause neurological issues - check out the term “plasma hyperosmolality” for more details.
A dextrose solution, such as the 50% injectable version labeled for cattle, can be given orally in similar dosages as the aforementioned propylene glycol - 30-60cc a few times a day - or with an IV - note that it is necrotic to tissue and so subcutaneous is not recommended (12,14).
In a pinch, other oral sugars such as corn syrup or molasses can be used but these are not going to supply sugar as quickly as dextrose (2, 14).
In the case of severely ketotic doe, time is of the essence. An intravenous solution is strongly suggested, either done by an experienced breeder or a veterinarian, as this will be the fastest way to correct the issue. If this is not an option, some breeders give the recommended 30-60cc of dextrose or propylene glycol as often as every 2 or 3 hours (2,12,14). Calcium borogluconate or calcium carbonate might also be necessary if toxemia has caused hypocalcemia, though this will most likely occur in lactational ketosis (2, 13). A further complication worth considering is the possibility of abomasal ulcers. There is little literature about ulcers in goats, and thus nothing on label for treatment. Long time breeder Kelley Hines had a fantastic write up about her experience with it (as well as her experience and protocol with pregnancy toxemia - here is a great podcast where she speaks about it and here is the Facebook link to the post - she did offer a pdf for fellow breeders) - if you are not on Facebook, I found a copy of her write up on ulcers here. Symptoms of ulcers might be very vague, just going off feed or general gut discomfort. Off-label treatments include ulcer paste marketed for horses or prescription pantoprazole under the guidance of a veterinarian (11,12).
Unfortunately, the reality of pregnancy toxemia is sometimes the best course of action is ending the pregnancy. Depending on the severity of the disease and the due date, the producer may have to decide between saving the kids or saving the doe. A rule of thumb is kids are likely viable at 135 days gestation in miniature breeds and 142 in standard breeds. This is NOT set in stone, especially in the case of multiples. (A good friend had 2 out of triplet Nubians survive at 133 days gestation!) Early kids will likely need some assistance, perhaps requiring to be warmed, tube fed, and/or given oxygen, or even enemas; truly premature kids are quite labor intensive. Induction is usually achieved through dexamethasone and a prostaglandin like Lutalyse® . An emergency cesarean might also be necessary as ketotic does are more likely to experience dystocia. (6,13,14)
Conclusion
Sometimes, as with many goat illnesses, pregnancy toxemia is just rotten luck. But it is one disease that’s frequency can be limited by proper management. Learn the symptoms and have some medications on hand as well as either a blood meter or urine strips - being prepared gives you the best chance for a successful outcome for both the doe and her kids. P.S. Keep an eye out for an upcoming post about my experience with pregnancy toxemia in the herd in Spring 2025.
Sources
Marteniuk, J.V. & Herdt, T. H. (1988). Pregnancy toxemia and ketosis of ewes and does. The Veterinary Clinics of North America: Food Animal Practice, 4(2), 307-315.
Smith, M.C. & Sherman, D.M. (2009). Goat Medicine. (2nd ed.). Ames, Iowa, The United States of America: Wiley-Blackwell.
Rowe, J.D. (2014). Teaching goat clients to prevent pregnancy toxemia. The AABP Proceedings, 47, 99-103.
Ji, X., Liu, N., Wang, Y., Ding, K., Huang, S., & Zhang, C. (2023). Pregnancy Toxemia in Ewes: A Review of Molecular Metabolic Mechanisms and Management Strategies. Metabolites, 13(2), 149. https://doi.org/10.3390/metabo13020149
VFF Stock Sense. (2025, February 6). Goat Webinar Series Part Two: Pregnancy toxemia in goats, kidding, and care of newborns. [Video]. YouTube. https://youtu.be/fPuKIhnYOM4?si=SQ3wCfiJU7m_gwDU
Bérengère Laporte-Broux, Christine Duvaux-Ponter, Sabine Roussel, Julie Promp, Pascale Chavatte-Palmer, Andrew A. Ponter, Restricted feeding of goats during the last third of gestation modifies both metabolic parameters and behaviour, Livestock Science, Volume 138, Issues 1–3, 2011, Pages 74-88, ISSN 1871-1413, https://doi.org/10.1016/j.livsci.2010.12.008.
Bérengère Laporte Laporte-Broux, Sabine Roussel, Andrew A. A. Ponter, Julien J. Perault, Pascale Chavatte-Palmer, et al.. Short-term effects of maternal feed restriction during pregnancy on goat kid morphology, metabolism, and behavior. Journal of Animal Science, 2011, 89, pp.2154-2163. ff10.2527/jas.2010-3374ff. Ffhal-00999873f