Reproductive disorders

1 The mare

Clinical examination of the mare (Figs. 12.1–12.2)

A thorough history of the mare’s breeding life should occur prior to any examination or evaluation. This will provide insight into the areas of concern and focus. Then a general physical examination should be conducted to include body condition score.

During examination of the reproductive tract adequate restraint, preferably the use of an examination stock or crush, is advisable so that undivided attention can be more safely given to the examination. It may be necessary to tranquillize some mares but a quiet, unhurried approach will often allow the initial examination to be made. The external genitalia should be assessed, recognizing length and position of the vulva relative to the rectum and the brim of the pelvis. Perineal body mass and angles should be noted. The perineum should be cleaned and the urogenital tract examined.

Manual palpation and ultrasonographic examination per rectum of the uterine body, horns, ovaries and cervix should follow. A speculum exam aids in identifying stage of the estrous cycle as well as the presence of hyperemia, exudate, urine, and traumatic injuries such as adhesions, scars and tears in the vaginal vault and cervix. Manual palpation provides further evaluation of the vaginal vault and during diestrus any cervical defects. Further evaluation of the reproductive tract can include endometrial culture and cytology, clitoral culture, endometrial biopsy, hysteroscopic evaluation and color Doppler studies.

The estrous cycle (Figs. 12.3–12.20)

The estrus cycle in the mare may be regarded as the period between the ovulation of a mature follicle through to the ovulation of the next mature follicle. This is usually a period of approximately 21 days in Thoroughbred mares and up to 25 days in pony mares. The period between ovulations may be conveniently divided into separate identifiable periods which reflect changes in behavior and in ovarian function. Estrus display and acceptance of the stallion begins before ovulation and normally lasts for 24–48 hours post ovulation. Thereafter the mare loses receptivity.

The luteal phase commences with the formation first of the corpus hemorrhagicum, which then matures into a corpus luteum. The corpus luteum is responsible for progesterone production, which peaks at approximately the sixth day after ovulation. If maternal recognition of pregnancy does not occur, prostaglandin (PGF2α) is released from the endometrium and luteal regression follows. Follicular waves continue through diestrus and the follicles that do not become atretic continue to enlarge from mid to late diestrus. With luteal regression and progesterone decreasing, these follicles (16–20 mm diameter) are stimulated by follicle-stimulating hormone (FSH). One or two dominant follicles will undergo final maturation with the remainder regressing. The growing follicles produce increasing amounts of estrogen bringing the mare into physiological and behavioral estrus. Luteinizing hormone from the anterior pituitary rises, inducing ovulation and the luteal phase commences.

The dimensions of mare ovaries, on average, are 50 mm × 28 m × 33 mm, and the average weight is 120 grams. Pony mares have smaller ovaries with an average weight of only 43 grams. Equine ovaries have distinctive differences from other species. There is a relatively small palpable ovulation fossa with the ovarian stroma having a very fibrous appearance. Large areas of the surface are usually devoid of follicles. Mature follicles may be as large as 70–80 mm and may be numerous. A palpably large follicle (>70 mm) should be carefully evaluated as this may, especially in Thoroughbreds, be due to the presence of more than one mature follicle, an anovulatory follicle or hematoma. Up to 40% of Thoroughbred mares may have a double ovulation. As ovulation approaches the dominant follicle with maximum mean size of 40–45 mm becomes softer and more tender on palpation. Ultrasonographic examination shows changes in shape going from spherical to non-spherical with thickening of the follicle wall (theca layer, basal lamina and granulose layer), and increased echogenicity of the granulosa layer with increased demarcation of an anechoic layer peripheral to the granulose layer. Color-flow Doppler ultrasonography can assess changing perfusion to the dominant follicle to predict if and when ovulation may occur. The presence of increased echogenicity within the follicular fluid can also indicate impending ovulation. Once collapse of the preovulatory follicle and release of the oocyte occurs, a large corpus hemorrhagicum, approximately 70% of the size of the preovulatory follicle, develops. This may often be difficult to differentiate manually (except for its meaty consistency) as it becomes smaller and is progressively luteinized. The primary corpus luteum, which on section has a yellowish hue, develops at the site.

Variations from this cycle of events include ovulation in the luteal phase in approximately 9% of mares, and this can be responsible for a prolonged luteal phase (diestrus). Estrus, service and pregnancy can, rarely, occur in this period, but more often, the mare remains unreceptive.

Small atretic follicles occur in the mare during a phase in the maturation process when the preovulatory follicle becomes dominant at 23–25 mm early in estrus; the preovulatory follicle’s growth rate increases relative to the subordinate follicles that will eventually regress and become atretic. Follicular cystic degeneration which occurs in other domestic species does not occur in mares. It is frequently diagnosed clinically but cannot be substantiated on gross or histological examination. Mares may exhibit a long transitional phase from winter anestrous to spring estrus, with estrus cycles up to 40 days being recorded. Typical ovaries show numerous slow-growing follicles to be present, leading to the erroneous belief that this represents a cystic condition. Other causes of multiple small follicles should additionally be ruled out such as granulosa cell tumor.

Prominent vessels are often present on the surface of the ovary and in some normal aged mares, may display even more marked varicosity.

Following conception, the developing embryo descends into the uterus 5–6 days post ovulation. At or around day 36, implantation of the girdle cells of the trophoblast occurs within the uterine mucosa, usually at the base of a uterine horn. These cells create the endometrial cups (see Fig. 12.21) which produce equine chorionic gonadotrophin (ECG). ECG has and ovulatory and luteinizing effect on the follicles present in the ovaries which form secondary and accesory corpora lutea. There is wide variation in their number between different mares. In the majority of mares regression of the endometrial cups occurs by day 150 of gestation, however cases of retained endometrial cups for up to 2 years post foaling have been documented. Both the primary and supplemental corpus luteum begin to regress and are usually completely atrophic by about 210–220 days. From this stage forward, the ovaries of pregnant mares show little follicular activity.

Figure 12.21 Normal uterus showing endometrial cups (50 days gestation).

The ovary

Non-infectious disorders

Anovulatory follicles (Fig. 12.25)

Ovulation failure occurs in approximately 8.2% of estrous cycles during the physiological breeding season. The follicles may be large (5–15 cm in diameter) and may persist for extended periods of time resulting in a prolonged interovulatory interval. Suggested causes include: insufficient estrogen production from the follicle; insufficient pituitary gonadotrophin stimulation to induce ovulation; decreased gonadotrophin receptors on the follicle; and hemorrhage into the lumen of the preovulatory follicle.

Diagnosis

• Ultrasonographic monitoring of the progression of the dominant follicle should be done during estrus.

• Initial indication of a problem may be the thickening of the follicle wall or the detection of echogenic particles within the follicular fluid, potentially progressing to fibrous strands traversing the lumen or the homogeneous appearance of hemorrhage.

• Some follicles may luteinize and produce low levels of progesterone while others do not and may persist for long periods of time. Uterine edema will usually subside and the mare behaviorally will be neither receptive nor unreceptive.

Treatment

• If the anovulatory follicle luteinizes then prostaglandin therapy will result in lysis and follicular regression. However, in the absence of progesterone and luteinization, initiating estrus will depend on when the regression of the anovulatory follicle occurs.

• A subsequent follicular wave may be initiated in the presence of a regressing anovulatory follicle with behavioral estrus, uterine edema and subsequent ovulation of the new dominant follicle.

• Human chorionic gonadotrophin (HCG) and deslorelin (a GnRH agonist) are generally not effective in inducing ovulation of the affected follicle.

Lack of follicular development (anestrus) (Figs. 12.26 & 12.27)

Seasonal anestrus occurs in most mares, however some mares may be placed under lights for 60 days and still have no follicular development. Mares may come off the race track to be bred and either seem to have a large follicle waiting to ovulate or have small inactive (anestrus) ovaries.

Clinical signs

• Small inactive ovaries may be present with 10–15 mm follicles to no follicular activity present.

• The uterus is flaccid and the cervix is wide open and pale due to lack of progesterone and estrogen.

Diagnosis and treatment

• Rectal palpation and ultrasound help to identify the size of the ovaries and the follicular activity.

• Presence or absence of uterine edema aids in determining if the mare is truly anestrus/transition or coming out of transition.

• There are many different drugs and protocols to help induce cyclicity (Table 12.1).

Table 12.1

Induction of cyclicity

Drug	Mechanism of action	Dose
Domperidone	DA₂ dopamine receptor antagonist	1.1 mg/kg PO sid–bid
Reserpine	Rauwolfian substance	0.01 mg/kg PO q 24 hour
Sulperide	Selective DA₂ dopamine receptor antagonist	3.3 mg/kg/day
Deslorelin	GnRH agonist	62.5 µg IM, q 12 h
Buserelin	GnRH agonist	12.5 µg IM, q 12h
eFSH	FSH	12.5 µg IM, q 12 h until a 35 mm follicle present; then coast for 24 hours, give hCG and breed in another 24 hours

Ovarian hematoma (Figs. 12.28 & 12.29)

Ovarian hematomas result from excessive hemorrhage into the follicular lumen following ovulation or may be the result of a hemorrhagic anovulatory follicle. As one of the common differentials for an enlarged unilateral ovary it is imperative to differentiate it from neoplastic disease (i.e. granulosa cell tumors).

Diagnosis and treatment

• Ultrasonographic evaluation of the enlarged ovary reveals hyperechogenic homogeneous blood within the lumen of an extremely large follicle, or a multicystic appearance due to fibrin strand formation spanning the diameter of the structure. The affected ovary has a clearly identifiable ovulation fossa on rectal palpation. The contralateral ovary on examination is of normal size and function and mares continue to cycle normally. Endocrine profiles and behavior are normal.

• Regression of the hematoma should occur over time, during which a normal interovulatory period will occur.

• If the hematoma becomes excessively large it can destroy the remaining normal parenchyma of the ovary and ovarian removal may be necessary because the ovary is left non-functional.

Ovarian tumors (Figs. 12.30 & 12.31)

Granulosa cell tumors (GCT) are the most common ovarian tumor in the mare. GCTs are usually extremely large or small and are usually steroid-producing, slow-growing, benign and unilateral. The opposite ovary is usually inactive probably due to the inhibin produced by the tumor’s granulosa cells suppressing the release of pituitary follicle-stimulating hormone. An elevated level of testosterone occurs in about 54% of mares due to the presence of a significant number of thecal cells within the tumor (granulosa thecal cell tumor). Behavioral changes can include aggressive or stallion-like behavior, nymphomania with persistent estrus or long periods of anestrous. Colic signs may occur if the ovary becomes so large that it pulls on the broad ligament lying ventrally in the abdominal cavity. Tumors vary in size from 6–40 cm diameter. Pregnancy may not be affected by the development of the tumors after conception and can be found post foaling on routine examination. Tumor-bearing ovaries are often grossly enlarged with a smooth thickened capsule but sometimes give an impression of follicular structures being present. On section, early tumors show multiple cysts with a thin stroma; older tumors show marked thickening of the stroma and may on occasion be filled with blood.

Germ cell tumors are very rare but dysgerminomas may be associated with hypertrophic osteopathy of the lower limb, loss of condition and stiffness when walking. They are reported to vary in size but appear to metastasize early to the regional lymph nodes.

Teratomas have also been reported in equine ovaries which are enlarged and the mass contains fluid and an amorphous material with hair-like structures.

Other mesenchymal tumors, such as hemangiomas, leiomyoma, fibroma and lymphoma, have been described but appear to be extremely uncommon.

Diagnosis and treatment

• Behavioral changes as described above in combination with lack of an ovulation fossa on rectal palpation, ultrasonographic imaging and serum hormone levels aid in diagnosis. Ultrasonographic appearance of GCTs can vary from enlarged multicystic, honeycomb appearing firm ovaries to a single large cyst or blood-filled structure.

• Differentiation between ‘autumn’ or anovulatory follicles and ovarian hematomas is imperative. The contralateral ovary is usually small with no to minimal follicular activity.

• Clinical diagnostic assays should include serum antimullerian hormone, inhibin, testosterone and progesterone. These, however, may be equivocal and ascertaining if continued growth with time or regression with hormone therapy (progesterone and estradiol) may be necessary.

• Removal of the affected ovary. This can be done via a flank laparotomy, midline or paramedian approach. Return to normal estrous cycles by the contralateral ovary may take 8–12 months.

Cyst adenoma (Fig. 12.31C)

Epithelial cell tumors are rare and reports are confined to cyst adenoma. These may be identifiable per rectum as large cystic masses; fertility of the other ovary appears to remain normal and pregnancy may be uninterrupted following the surgical removal of the tumor. Affected ovaries are large and enclose multiple, large cysts containing clear, yellow fluid; these masses probably originate from the epithelial cells of the ovulation fossa. Usually these tumors are not hormonally active.

Treatment

Surgically remove the ovary.

Pituitary Pars Intermedia dysfunction (PPID)

Reproductive abnormalities such as abnormal estrous activity, estrous suppression and reduced fertility have been described in mares with PPID. This may be due to the hypertrophy, hyperplasia or adenoma in the pars intermedia of the pituitary destroying or impinging on the gonadotrophic cells of the anterior pituitary or suppression of the gonadotrophin secretion due to elevated levels of androgens or glucocorticoids produced in response by the adrenal cortex. The mare’s ovaries are usually small to normal size, however they are firm on palpation with multiple small follicles that are observed on ultrasound deep within the ovarian parenchyma. The ovulation fossa is palpable.

Diagnosis and treatment

• Blood serum assays for glucose, insulin, adrenocorticotrophic hormone (ACTH), and cortisol levels can be indicative as well as abnormal responses to the dexamethasone suppression, ACTH stimulation and thyrotropin-releasing hormone (TrH) tests.

• See treatment for PPID.

Epithelial inclusion cysts

Epithelial inclusion cysts are multiple and occur in close proximity to the ovulation fossa increasing both in size and number with advancing age and these may interfere with ovulation. The other ovary usually continues to function normally and pregnancy may also occur.

Other structures occurring near the ovary include cysts of the mesonephric tubules; epoöphoron cysts and paroöphoron cysts. These slowly enlarge with time and consequently are more frequently found in aged mares. Epoöphoron cysts can reach up to 7 cm diameter and, on manual palpation, may be mistaken for part of the actual ovary. Paroöphoron cysts are smaller and less common.

The oviduct

Diagnosis and characterization of oviduct disease is difficult because the oviduct is not always palpable per rectum or visible on ultrasonographic examination. Therefore diagnosis often occurs after all other possible causes of infertility have been ruled out. Pathology within the oviduct would prevent the passage of the oocyte, spermatozoa or embryo into the uterus. Abnormalities affecting the oviduct can be categorized as inflammatory (salpingitis) or structural (blockage).

Salpingitis

Inflammatory disease of the oviduct or salpingitis is not common in the mare unlike other species due to the tight muscular sphincter around the uterine ostium (papillae). This tight utero-tubal junction appears to prevent the ascent of endometritis. The special anatomical position of the uterus of the mare in which the oviducts are in the dorsal part of the abdominal cavity above the uterus, rather than lying ventrally also aids in the prevention of inflammation. Salpingitis in the mare appears to be a widespread infiltrative, non-occlusive, and generally non-exudative process. Many cases however, have no identifiable pathogenic (or other) organism. Unilateral adhesions of the oviduct or fimbrae may also affect fertility by distorting the oviduct’s position relative to the ovary impairing passage of the oocyte. The cause of both the inflammatory changes and the adhesions is not clear.

Diagnosis and treatment

• This condition is difficult to diagnose unless visually evident on laparoscopic examination or laparotomy. Culture of the oviduct during the procedure.

• Treatment can be attempted based on antibiotic sensitivity testing.

Oviduct blockage (Fig. 12.32)

Blockage of the oviduct may occur due to malformation in younger mares or occlusions or plugs most commonly found in older mares. Abnormal development of the oviducts as with cystic oviducts or the absence of an oviduct lumen hinders movement of the oocyte, spermatozoa or embryo. It has not been clarified if oviduct plugs in the older mare form due to collagen-type masses or inspissations of degenerated oocytes and oviduct secretions, however infertility can be a consequence.

Diagnosis

• Cannulation of the oviductal fimbrae via flank laparoscopy in the standing mare, with infusion of fluorescent microsphere beads will allow for the direct visualization of oviduct anatomy and indirect assessment of oviduct patency by performing a uterine lavage at 24 and 48 hours post surgery to identify the microspheres. If the microspheres are not found in the lavage fluids it is assumed the oviduct is not patent.

• A ventral midline exploratory laparotomy will also allow for visualization of the ovaries and oviducts for anatomical defects. This may be difficult however in maiden mares whose mesovarians and broad ligaments have not been stretched. Infusion of a sterile 5% new methylene blue dye in normal saline through a catheter into the oviduct and detection of the dye within the uterus will determine patency.

Treatment

• Movement or passage of the blockage through the oviduct can be done using two different techniques, the first of which is flushing the oviducts either via ventral midline laparotomy or standing flank laparoscopy.

• The second and less invasive or detrimental to the oviduct is placement of prostaglandin E2 (PGE2) on the surface of the oviduct using a flank laparoscopic approach. The PGE2 potentiates muscular relaxation of the oviduct allowing movement of the oviductal plugs into the uterus.

The uterus

The uterus is comprised of two uterine horns and the uterine body.

Developmental disorders

Congenital abnormalities of the uterus are rare in the mare but the finding of a bifid placenta without avillous areas suggests that bifid uterus may occur, although this has not so far been described. Anatomical abnormalities can be related to chromosomal disorders (see section Ovarian developmental disorders).

Non-infectious disorders (barren mares)

Endometrial cysts (Figs. 12.33–12.37)

Endometrial cysts are not a cause of infertility, but a sign of lymphatic blockage and decreased uterine clearance, which have been shown to affect fertility. Uterine cysts are fluid-filled structures that can occur anywhere in the endometrium. They usually project outward or away from the surface of the endometrium. The incidence of endometrial cysts in the general mare population has been reported to be 1–22%, while in subfertile and older mares as high as 55%. It has been shown in some cases that the presence of numerous or large endometrial cysts (2.5 cm) can impede mobility of the embryonic vesicle and restrict the ability of the early conceptus to prevent luteolysis after day 10, thereby blocking maternal recognition of pregnancy. Additionally, by having the yolk sac or allantois in contact with a cyst versus the endometrium, absorption of nutrients may be prevented, resulting in early embryonic death.

Both lymphatic and glandular cysts occur in the endometrium of the mare. Lymphatic cysts are most common. They arise from collections of lymphatic fluid in the endometrium or myometrium, usually due to obstructed lymphatic channels or perhaps by gravitational effects of a pendulous uterus. Multiparous mares with uteri that have undergone fibotic changes are most prevalent, with size varying from a few millimeters up to 15 cm in diameter. Lymphatic cysts are cylindrical or spheroidal structures that can be pedunculated or sessile. They are usually thin-walled, round, elongated and may be individual or multilobular, divided by septa. Glandular cysts are a distension of uterine glands caused by periglandular fibrosis. They are usually microscopic to a few millimeters in diameter, are embedded in the endometrium and can be found in any area of the uterus.

Diagnosis

• Lymphatic cysts can be diagnosed through transrectal palpation, by direct intrauterine palpation via the cervix, through hysteroscopic examination, and endometrial biopsy, but most commonly by transrectal ultrasonography.

• The increased use of transrectal ultrasonography has enhanced the practitioner’s ability to differentiate early embryonic vesicles from endometrial cyst. In mares that have a few small cysts, ultrasounding the mare pre or post breeding or ovulation and mapping of endometrial cysts can aid in pregnancy diagnosis by comparing ultrasonographic images. Mares that have numerous clusters or multilobular cysts may need repeat examinations before determination of a pregnancy by increasing vesicular size or a visible heart beat can be established.

Treatment

• Most cysts do not cause a problem, but are usually a sign of an underlying one. These mares are usually older mares with poor uterine clearance and benefit tremendously by simply using uterine lavage and oxytocin in their breeding regimen. Where cysts create a problem is in the distinction or recognition from a pregnancy, however this is more of an inconvenience than a problem. Cyst removal therefore should be delegated to those mares with poor reproductive histories that have large cysts that may obstruct embryo movement or those mares with numerous small cysts that may prevent early embryonic growth or severely compromise the placenta.

• Various treatments have been proposed to include: endometrial curettage, puncture by uterine biopsy, aspiration, or lasering during hysteroscopic examination, snare electrocoagulation via hysteroscopy, repeated lavage with warm saline or ablate manually. Large pedunculated cysts are removed when the mare is in heat, by manually snaring the cyst with a gigli wire introduced through a steal double mare catheter. Once the snare is around the base a gradual sawing motion will cut the cyst from the endometrium. This can usually be accomplished without rupturing the cyst with minimal removal or damage to the underlying endometrium. Care must be taken not to remove more than the epithelial lining. A minimal amount of hemorrhage is associated with this procedure and it is recommended to lavage the mare’s uterus for the proceeding couple of days. Smaller more numerous cysts are usually removed via hysteroscopic laser. This technique has not been determined to be satisfactory for large cysts, since so much heat is generated in order to destroy the cyst that there is increased risk of damage to or tearing of the uterus. Smaller cysts, however, are easy to find and destroy. Lasering the cyst at the thinnest section until complete penetration through the wall has been made releases the fluid contents with immediate visible shrinkage. Care must be taken not to laser blood vessels on the cyst’s surface making visibility difficult.

Persistent endometrial cups (Figs. 12.38–12.40)

Around days 35–36 of gestation the chorionic girdle starts to invade the maternal endometrium and the endometrial cups are formed. These produce equine chorionic gonadotrophin (eCG). eCG has biological activities similar to FSH and LH. The LH component causes luteinization and/or ovulation of follicles, forming secondary and accessory CLs, and continues to produce progesterone until days 100–120 of pregnancy. eCG stimulates primary and secondary CLs to form and continue to produce progesterone until days 100–120 of pregnancy. Endometrial cups regress as the placenta forms and progestagens are produced. Most endometrial cups have regressed by 150 days of gestation, however there is increasing evidence that persistent endometrial cups in post foaling, post abortion or post embryonic loss after 45 days should be considered when mares fail to cycle properly within the expected time period.

Persistent endometrial cups should be considered when mares fail to show regular estrus activity. Mares will show behavioral estrus but instead of having a normal estrus period leading to ovulation, small multiple follicles will luteinize or hemorrhage forming the spider web appearance associated with secondary CLs (visible on ultrasound examination).

Diagnosis

• Positive blood serum eCG levels. Care must be taken with some commercial kits since they can cross react with LH.

• Transrectal ultrasonography can identify hyperechogenic spots in the base of a horn if the endometrial cups are large and able to be visualized.

• Hysteroscopic examination may reveal the circle of peanut-shaped cups in the base of a horn. These will vary in size and color depending on their activity and longevity.

Treatment

• Different treatments have been attempted to help regress existing endometrial cup tissue. These include laser, biopsy and kerosene endometrial curettage. Unfortunately, kerosene is the only treatment to be looked at critically in three mares and it is still questionable whether treatment is to no avail. Regression therefore finally occurs over time.

• The persistence of the endometrial cups has been evident in mares up to 2 years post foaling and post 45 day embryonic loss.

Non-infectious disorders (pregnant mares)

Uterine torsion (Figs. 12.41 & 12.42)

Uterine torsion is an infrequent complication of pregnancy, reported in 5–10% of all mares that have serious equine obstetric problems. Uterine torsion occurs in middle to late gestation and causes great risk to both mare and foal. The cause is unknown, although it has been postulated that uterine torsion may develop secondary to rolling as a result of gastrointestinal problems or trauma, or the righting reflexes and vigorous movements of the fetus, during the later stages of gestation.

Mares display signs of abdominal discomfort and colic, most commonly with mild intermittent episodes responsive to anti-inflammatories and analgesics. Eventually, inappetence and lethargy ensue. Severity of signs is dependent on degree of rotation, level of vascular or fetal compromise and intestinal involvement. Torsion of the uterus greater than 360° interferes with blood flow to and from the uterus and can result in local anoxia, congestion, fetal death and rupture of the uterus. Chronic oxygen deprivation to tissue and serosal injury further promote adhesion formation in the abdominal cavity.

Diagnosis

Physical examination can be within normal limits, with the problem evident only on rectal palpation of the broad ligaments. Torsion of the uterus can occur clockwise, to the right: the left broad ligament is stretched horizontally over the top of the uterus and the right broad ligament courses tightly ventrally or vertically under the uterus toward the opposite side. The uterus may also torse in a counter-clockwise direction, to the left: the right broad ligament is palpable as a dorsal sheet of tissue going to the left side and the left broad ligament is pulled ventrally, toward midline. Rotation can range from 180° to 360°. Unlike cattle, in the mare, the cervix and cranial vagina are usually not involved unless the degree of rotation is severe or fibrous tissue has formed.

Transrectal and transabdominal ultrasonography can aid in assessment of uterine compromise by enabling determination of uterine wall thickness, placental integrity, vascular distension, fetal viability and condition of the fetal fluid.

If there is concern about intestinal involvement, abdominocentesis may be performed to aid in determining the appropriate mode of replacement or prognosis.

Treatment

• Many methods have been used to correct uterine torsion in the mare. The most common are rolling the anesthetized mare and laparotomy via standing flank or ventral midline incision. Although non-surgical methods such as rolling are less expensive, this technique may predispose to separation of the placenta from the endometrium with subsequent abortion, premature birth or death of the fetus. Uterine rupture and tearing are severe complications associated with this procedure. Evaluation of uterine and intestinal compromise is not possible.

• Standing flank laparotomy has been more popular than the ventral midline approach and is especially easier earlier in gestation; in addition, general anesthesia is not necessary. The uterus should be palpated for signs of edema, congestion and hematomas. This method carries risks: the mesometrium is under considerable tension, and if the horse is standing during laparotomy, this can lead to perforation of the uterus and injuries to the mesometrium during manual retorsion.

• A ventral midline approach allows quick and clear access to the abdominal cavity, visual assessment of uterine wall viability, correction of concomitant gastrointestinal tract problems, and performance of hysterotomy if indicated. Continued monitoring is necessary for systemic compromise and laminitis. Prognosis for fetal survival is good with improvement as gestational age lessens.

Peripaturient hemorrhage (Figs. 12.43–12.46)

Hemorrhage from the middle uterine, external iliac, utero-ovarian and vaginal arteries has been described in late pregnancy and after parturition and accounts for 40% of peripaturient deaths in mares. Most cases occur in older, multiparous mares, but it is becoming an increasing problem in younger primiparous mares from 5–24 (median, 14) years of age. The etiology for rupture has not been definitively ascertained, although at least three hypotheses have been proposed:

1) Middle uterine a arterial rupture usually occurs on the right side of the mare’s uterus, possibly as a result of the cecum displacing the uterus and increasing tension on the right uterine artery in addition to additional direct pressure by the cecum on the artery

2) Normal age-related vascular degeneration

3) Copper deficiency interfering with elasticity of the vessels.

Mares with discomfort or colic in the middle or late stages of gestation or 24–72 hours after parturition should be considered to be potential hemorrhage candidates. In some instances, mares are simply found dead because of acute arterial hemorrhage. More often, however, mares develop signs within 24 hours of parturition, and most are associated with rupture of the right uterine artery.

Three clinical scenarios can occur. In the first, the hemorrhage is confined to the broad ligament. Although this type of hemorrhagic episode is usually self-limiting because containment within the ligament enhances hematoma formation, it can be incredibly painful, and most mares lie down and get up repeatedly, lie on their side or look frequently at their belly. Mucous membranes can be normal to pale, depending on the extent of hemorrhage. The second scenario occurs when the mare hemorrhages into the uterus. This is usually a post-partum event, unless there has been traumatic injury to the uterus. Finally, the most detrimental scenario is seen with rupture within the broad ligament and extension of hemorrhage into the abdomen. When this occurs, the only border for containment is the abdomen itself, which is not as conducive to clot formation. Mares may lie on their sides, adopt a sternal position, or circle and stagger; and will have pale mucous membranes, high heart rates, rapid breathing, cold sweat, low body temperature (96–98°F) and, possibly, acute death.