Uterine Torsion

By | 2012-10-25

The causes of uterine torsion in the mare are not well-defined. The condition is much more common in cattle; in that species a large, term fetus has been implicated as a major risk factor. The majority of uterine torsions in cows occur at term and most are thought to be a direct result of fetal positional changes during late first-stage and early second-stage labor. A striking difference between the mare and the cow is that more than 50% of uterine torsions in mares occur before the end of gestation. In this author’s clinical experience the vast majority occur before term, and other authors have reported on cases from as early as 8 months of gestation. Owners who work closely with their mares may mention that they have observed excessive fetal movements in the flank area. In a recent equine obstetrical study, 80% of term fetuses were found to be in dorsosacral position when the uterine torsion was corrected. This finding suggests that fetal righting reflexes may have played a role in creating the torsion. This author believes that vigorous fetal movements during the latter stages of gestation are likely to be a significant factor in the etiology of this condition in the mare ().

Diagnosis of Uterine Torsion

Correction of Uterine Torsion

Prognosis For The Fetus

The prognosis for cases of equine uterine torsion depends on the degree of vascular compromise. Severity and duration of the condition will affect placental circulation and subsequent fetal viability. In this author’s experience, if the fetus is alive and the uterine wall is not severely congested and edematous, then the prognosis for both the mare’s survival and for the birth of a live foal at term is good. The concept of progestin supplementation after the first 100 days of gestation remains controversial. Luteolysis can occur during early pregnancy as a result of endotoxin-mediated prostaglandin F2a release, and progestin supplementation has been shown to be effective in maintaining pregnancies. In late gestation a viable placenta should produce adequate amounts of progestins. If the fetoplacental unit is compromised to the extent that it is incapable of producing sufficient progestins to maintain pregnancy then it is probable that insufficient oxygen and nutrients will be available to support the rapidly growing late gestation fetus anyway. However, progestin supplementation during late gestation may still be indicated to ensure myometrial quiescence, and thus maintenance of the placental attachment. Recent studies support the premise that progestins may suppress myometrial activity by inhibition of endogenous prostaglandin F2a production. Although supplementation after a uterine torsion would be in the last 2 to 3 months of gestation, reports exist of mares retaining a nonviable (died at 3 to 5 months gestation) fetus while being administered progestins. Thus if progestin supplementation is administered to a mare after correction of a uterine torsion, fetal viability should be monitored at regular intervals.