In a thorough discussion of ultrasonographically detectable signs of impending embryonic loss, Newcombe (2000) suggests the following criteria for predicting its occurrence:

On occasion, a mare in early pregnancy (14 to 17 days after ovulation) has development of pronounced uterine edema, sometimes associated with behavioral estrus. Assay of progesterone concentration sometimes reveals a low concentration consistent with estrus. Some such pregnancies can be salvaged with immediate administration of progesterone or progestogen, which should be continued until either another ovulation occurs and forms a functional corpus luteum or progesterone supplementation is no longer deemed necessary to support the pregnancy (usually by 100 to 150 days of gestation). Newcombe (2000) suggests that conceptuses in such mares are more likely to be abnormal, particularly when embryonic vesicles are smaller than expected at 12 to 14 days after ovulation; thus, they are more likely to fail even though progesterone supplementation is implemented. An additional cause to be considered is developing endometritis (Figure 8-7), which can precipitate endometrial prostaglandin-F ₂α (PGF ₂α) release. Close monitoring of embryonic development is warranted in such progesterone-supplemented mares.

With the exception of progesterone and progestogen supplementation of mares developing uterine edema during early pregnancy, the most prudent management of mares with signs of abnormal embryonic development is serial reexaminations at intervals of 1 to 3 days. Colorado workers suggest that if an embryo and heartbeat cannot be identified with ultrasound by day 25 (Figure 8-8), monitoring through day 30 is indicated. If a viable embryo with an evident heartbeat does not become apparent by this time, PGF ₂α should be administered to induce luteal regression and return to estrus for rebreeding. Newcombe (2000) also suggests that manual crushing of the conceptus at the time of induced luteolysis, immediately followed by uterine lavage to remove any remaining embryonic debris, might improve chances of conception when such mares are immediately rebred. We have noted that cloudy fluid accumulates in the uterus of some mares after the conceptus is manually crushed, so performing uterine lavage after the crush procedure is recommended. Treatment for more than 1 day may be necessary.

Early fetal death (i.e., abortion early in gestation), or pregnancy loss beyond 40 days gestation, usually occurs with no premonitory signs. The expelled fetus and membranes may be found in stall bedding or on pasture but frequently go unnoticed. Ultrasound examination during the period of early fetal death (before expulsion) may reveal intact membranes and fetal fluids of normal echogenicity but a dead fetus (no heartbeat, inactive) (Figure 8-9). In other cases, fetal fluids become more hyperechoic (flocculent or “fuzzy”) in appearance, suggesting the presence of debris or purulent material (Figure 8-10).

Most commonly, early fetal death is idiopathic and of sporadic incidence. Although no specific pathogens that restrict their attack to the early fetus have been identified, the agents involved in mare reproductive loss syndrome (MRLS) were first thought to have a predilection for pregnancy during the early fetal period. Texas and Kentucky workers showed that the increased fetal losses occurred without a concurrent increase in embryonic losses, despite that many mares carrying embryos (<40 days of gestation) were exposed on the same farms during the outbreak. University of Kentucky workers identified Eastern tent caterpillar involvement in MRLS, which presented as a multifaceted clinical syndrome with pericarditis and unilateral uveitis in adult horses, birth of weak foals, and early (40 to 150 days gestation) fetal loss. However, most susceptible pregnancies were in this early stage of gestation when the outbreak occurred. Later, less severe outbreaks with signs consistent with MRLS (abortion with amnionitis or funiculitis) involved fetuses of later gestational age. Outbreaks of abortion (early or late fetal loss) of similar presentation have been described elsewhere in the United States and in other countries.

When embryonic death (<35 to 40 days) occurs during the breeding season, there is a good chance the affected mare will return to a fertile estrus and thus become pregnant again before the breeding season ends. Regardless of the cause of early fetal death, if endometrial cups are present, the affected mare can rarely be successfully rebred with establishment of another pregnancy during the same breeding season (Figure 8-11). For this reason, early fetal death usually results in failure to produce a foal for another year.

Fetal susceptibility to teratogens decreases with increasing age, except for those structures that differentiate later (e.g., cerebellum, palate, and urogenital system). Regarding infection, the extent of fetal damage that occurs likewise depends on fetal age at the time of infection and degree of fetal immunocompetence, virulence of the infectious agent, and extent of placental lesions and degree of placental dysfunction.

Although the exact level of function necessary to support fetal life and development is difficult to define, a critical level of placental function is deemed necessary to support the developing embryo and fetus to term. Therefore, placental dysfunction is a common cause of pregnancy loss. Possible causes of placental dysfunction include acute or chronic placentitis, hypoxia resulting from alterations in perfusion ratios between uterine and placental blood flow (as occurs with uterine torsion), a defective placenta (e.g., as occurs in hydrallantois), inadequate placental attachment, edema of the placenta, local immunologic reactions in the placenta, and maternal disease or malnutrition. Placental dysfunction may result in a malformed fetus, fetal death, mummification, abortion, fetal growth retardation (Figure 8-12), prematurity, full-term stillbirth, and neonatal weakness and death.

Low birth weights in neonates are often attributed to placental dysfunction caused by infection with microorganisms. Signs in the neonate (such as neonatal weakness and septicemia) that may occur as a result of fetal infection in utero are usually encountered in the first week of life, particularly within the first 24 hours.

Abortion is the termination of pregnancy before the conceptus is capable of extrauterine life. Causes of abortion can be infectious or noninfectious. The overall rate of abortion reported in the horse population varies from 5% to 15%, but “abortion storms” (outbreaks) have been reported in populations of susceptible pregnant broodmares exposed to reproductive pathogens (e.g., Equine herpesvirus [EHV-1], Equine viral arteritis [EVA], MRLS) (Figure 8-13). Observed abortions after 4 months of gestation usually account for a small fraction of equine pregnancy wastage; however, abortions before 4 months of gestation are rarely observed because fetal and placental tissues are relatively small and often overlooked in bedding or on pasture and genital discharges are usually scant after abortion at this early stage. Therefore, most aborted fetuses examined are 6 to 11 months of gestational age. Most equine abortions are the result of placental dysfunction.