Retained Fetal Membranes

CHAPTER 12 Retained Fetal Membranes

The functions of the fetal membranes, also referred to as the placenta, and fluids are to supply nutrition to the fetus, remove waste products from the fetus, exchange oxygen and carbon dioxide between the mare and the fetus, and serve as the major source of protection to the fetus.^1,² The amniotic fluid, which averages approximately 8 L at term, serves to protect the fetus from external mechanical injury and acts as a bactericidal medium in which the fetus can develop. It also serves as a slippery mucous fluid that prevents the fetus from becoming attached to the developing fetal membranes. The primary source of amniotic fluid is fetal nasopharyngeal secretions and saliva.¹ The allantoic cavity stores fetal urine until such time as it can be removed by the circulation to the mare. Urine enters the cavity through the urachus and reaches approximately 18 L by term. This fluid-filled cavity also acts to protect the fetus against external trauma. Hippomanes are generally located in the allantoic fluid and are formed from sediment and debris plus mucoproteins and calcium phosphate found in urine. Generally at least one hippomane is present but frequently two or three may be found. There is no clinical significance attached to their presence.^1,²

The fetal membranes must be examined following parturition to evaluate the attachment surfaces that existed during gestation and to determine the appearance of all other aspects, which may be normal or abnormal. The attachment surface of the chorioallantoic membrane is an excellent indicator of the endometrial surface during that gestation and possibly future pregnancies. Examination of the fetal membranes during gestation is also possible using ultrasonography and can be used to aid in the diagnosis of placentitis. Routine pregnancy examinations are performed by rectogenital examination at greater than 50 days of gestation unless there is reason to suspect a problem with the pregnancy. Indications of problems include vulvar discharges, premature udder development, edema of the ventral abdominal wall, illnesses or injuries of the mare that may affect the fetus and the pregnancy, extreme enlargement of the abdomen, and in some instances, prolonged gestation. In addition to evaluation of the fetal membranes during ultrasonographic examination, the fetus and fetal fluids should be examined. The thickness of the near-term amniotic membrane is approximately 2 mm.

Postpartum examination of the placenta is an excellent diagnostic aid, because the expense is minimal and the evaluation can be rapidly performed. The membranes can be inspected during the same visit in which the foal is examined. If the environmental temperature is high, the placenta should be refrigerated until it is examined to preserve many important characteristics. The first characteristic to observe is the location of the chorionic side of the membranes. This side should be inverted, with the allantoic side outermost, if the delivery was normal. The chorioallantoic membrane should be examined for thickness, absence of villi, and any area of abnormal color or appearance. The weight of the placenta, although previously stressed as being important, is probably the least significant placental characteristic and the author has chosen to eliminate this portion of the examination because of a lack of correlation of placental weight to any specific problem.

The next part of the examination is to carefully visualize the entire surface of the chorioallantoic membrane and place it in the T shape that normally exists; the gravid horn makes one side of the T much larger than the other. Several small sacculations may be present near the junction of the pregnant horn and body of the uterus on the allantoic surface. These areas contain sloughed endometrial cup material.^1,³ Another sacculation may be attached to the umbilical cord and can be fluid-filled and up to 20 cm in length.⁴ The umbilical cord is composed of two arteries, a vein, and the urachus, plus lymphatics. One artery originates from each of the two horns.² Twisting of the umbilical cord is normally very common and makes the diagnosis of umbilical torsion and occlusion somewhat more difficult than it is in other species. The normal approximate length of the twisted umbilical cord is 50 to 60 cm.^1,² It has been proposed that shorter-than-normal umbilical cords can result in umbilical herniation. It has been reported that umbilical cord torsion can result in vascular occlusion and urachal occlusion, which may result in death of the fetus and abortion or previous urachus and predisposition to rupture of the bladder.

The next portion of the examination is the amnion. This is examined to determine whether meconium is present. Meconium presence generally indicates a problem with fetal oxygenation resulting in fetal distress near term or partutrition.¹ The chorionic side of the allantochorionic membrane can be examined in detail following inversion so that the allantoic portion is once again internal to the chorionic surface. This examination provides an evaluation of the mirror image of the attachment surface that existed during gestation and cannot be replaced by any other diagnostic test. The surface should ideally be roughened with the presence of villi except where the papillae of the oviducts enter the uterus, where placental folds exist because of overlapping in the areas adjacent to the endometrial cups, where the yolk sac attachment existed, and where the internal os of the cervix was located.⁴ Any abnormal condition such as endometrial fibrosis, placentitis, or uterine cysts can reduce the attachment surface available and may be sufficient to result in fetal growth retardation or loss.⁵ The tips of the chorioallantoic membrane near the apical end of the uterine horns are frequently edematous, with the gravid horn more often affected than the nongravid one.^1,⁴

Placentitis caused by infectious organisms may account for up to approximately 16% of equine abortions. Streptococcal organisms were reported to be the most likely cause of placentitis, representing approximately 23% of those diagnosed. Escherichia coli, Pseudomonas spp., Klebsiella spp., and Staphylococcus spp. have also been reported as important causes of bacterial placentitis.⁶ Fungal infections of the fetal membranes account for approximately 41% of abortions reported by several investigators. Viruses account for the remainder of the infectious placentitis causes of abortion.^1,^2,⁶ Organisms enter the uterus through the cervix or by hematogenous spread. Organisms that enter by the cervical route include those that enter the uterus prior to or at the time of breeding and do not manifest themselves as a clinical problem until abortion. Ascending infections may result in lesions located near the internal cervical os.^1,⁶ Less than normal vulvar conformation can result in bacterial contamination of the vagina and cervical inflammation. This may cause the cervix to relax and bacteria or fungi to enter. It has also been suggested that cervical relaxation may also occur during transition of pastures from poor to lush vegetation. Bacterial infections that are acute in onset result in abortion, whereas chronic infectious often result in fetal growth retardation or emaciation.¹ Lesions associated with infections of the placenta include inflammation and thickening. The nature of the amniotic fluid may prevent spread of bacterial organisms directly to the fetus, but entry is possible by invasion through the umbilical vessels and cord.⁶

There was reportedly an increase in mycotic placentitis associated with the use of intrauterine antibiotics and with increased manipulations, which result in entry of these organisms into the reproductive tract. The chorioallantoic membrane may increase in thickness by five to ten times.⁶ The amnion is involved in fungal infections in only approximately 10% of cases, and the fetus may have the characteristic appearance of thickened and roughened skin. Severe placentitis accompanying fungal infections restricts nutrient supply to the fetus and reduces fetal size.

Retention of the fetal membranes is reported to be the most common problem in postpartum mares. Authors consider failure of passage of part or all of the allantochorionic membrane with or without the amniotic membrane within a predescribed period of time as retention of the fetal membranes. The length of time varies among authors from 30 minutes to 6 to 12 hours.² Retention of fetal membranes has also been described as retained placenta or retained afterbirth. This condition is reported to occur with a frequency of 2 to 10.5%. It is difficult to determine from the literature an exact incidence because variation exists in the point of time post partum at which a placenta is considered to be retained. Retained placenta is more common in draft breeds than in medium- or lightweight breeds. Following dystocia or prolonged gestation, there is also an increase in the incidence of retained fetal membranes. Dropsy of the fetal membranes and cesarean section have been related to an increased incidence of retained fetal membranes. There is disagreement between authors as to whether there is an increased incidence of retained fetal membranes following abortion, stillbirth, or twinning in lightweight horses. It appears that there may be no increase unless these conditions coexist with dystocia.

A more recent study found the following relationships to retained fetal membranes: mares that were bred naturally versus those that conceived by artificial insemination have an increased incidence of retained placentas when the breeding occurred at foal heat.⁷ There was no reported difference in placental passage in mares artificially inseminated at foal heat versus mares artificially inseminated at second, third, or later postpartum estrus. In mares that were barren or maiden or had foaled the previous year, there was no difference in the incidence of retained placenta following parturition. In mares older than 15 years of age there was a higher incidence of retained fetal membranes than there was in mares that were younger.

Time of year appeared to influence the incidence of retained fetal membranes only on certain farms, with a higher incidence after March 31. The sex of the foal did not influence the incidence of retained fetal membranes. There was no reported difference in the retention incidence between the birth of weak or diseased foals and that of healthy foals. During normal parturition, separation occurs between the allantochorionic membrane and the endometrium during stage III of labor. The mechanism responsible for separation is believed to involve cessation of blood flow through the umbilical cord and the corresponding collapse of fetal placental vessels and decrease in size of chorionic villi.² This is followed by uterine contractions, which enhance reduction of uterine size and separation of chorionic villi. Uterine horn contractions originating nearest the ovary and progressing toward the body of the uterus aid in separation and expulsion of fetal membranes from the uterine lumen. As the placenta enters the cervix, its presence enhances the release of oxytocin and results in increased uterine and abdominal contractions. Once the placenta passes between the vulvar lips, the weight of the placenta aids in expulsion by applying gentle pressure and stimulating separation.

Causes of retained fetal membranes are uncertain at the present time. A variety of situations or circumstances are related to retention of fetal membranes, but no specific single cause has been described. It is known that complete separation of the placenta cannot occur until the microvilli are released from the maternal crypts. These microcotyledons are firmly attached to the endometrium by the seventh month of gestation. It has been suggested that in mares with retained fetal membranes, retention is not necessarily caused by attachment of the fetal membranes in both uterine horns but rather in the previously gravid horn or the nongravid horn. An additional report suggests that attachment and failure to separate does not necessarily occur in either of the horns but actually occurs in the body of the uterus. It appears, however, that the majority opinion favors the failure of the previously nonpregnant horn to separate from the fetal membranes. Characteristics of the placenta that may account for the difference in horn separation include variations in allantochorion thickness, length of the villi, and the degree of attachment of the fetal membranes in the gravid horn or in the nongravid horn. Furthermore, because of the success of oxytocin therapy in mares with retained fetal membranes, it has been speculated that a hormonal imbalance accounts for membrane retention. It has been suggested that more microvilli are present in the uterine horns than in the body of the uterus and that these microvilli are much more branched and larger than in the nonpregnant horn. Reportedly, folding of the fetal membranes and the endometrium occurs more commonly in the nongravid horn than in the previously gravid horn or body of the uterus. Uterine involution may occur at a slower rate in the nongravid horn than in the previously gravid horn or in the uterine body. It is possibly one of these phenomena, a combination of two or more, or unknown events that are responsible for retention of fetal membranes in mares. Furthermore, the edema of the placenta may be partially responsible for retention. Edema apparently is more prevalent in the gravid horn than in the nongravid horn, which would add support to the hypothesis that the gravid horn is the primary site of fetal membrane retention.

Endometritis or inflammation of the uterine lumen during pregnancy has been suggested as a possible cause of fetal membrane retention. Inflammatory responses could create adhesions between the chorioallantoic membrane and the endometrium and delay separation of the fetal membranes. These infections could be introduced during breeding, could enter the uterus through the cervix during gestation, or could spread to the uterus via the blood. In addition, it has been postulated that air entering the uterus immediately following expulsion of the fetus could be a source of bacteria and other substances that could be responsible for a subsequent inflammatory response.² It is difficult to believe, however, that substances entering the uterus at the time of parturition could create circumstances that lead to endometrial inflammation, placental edema, decreased effectiveness of oxytocin, or any of the other possible causes of retained fetal membranes within a few minutes following parturition. The theory that bacteria enter the uterine lumen at breeding and remain dormant for a prolonged period of time appears to have more credibility than that of bacteria that enter at the time of parturition in regard to an effect on fetal membranes. It has been reported that infections occurring between the fetal membranes and the endometrium are much more prevalent near the external os of the cervix and the surrounding area of uterine body than at any other location within the uterine lumen. Because this area is rarely involved in fetal membrane retention, it appears that infection as a cause of fetal membrane retention is not a high probability.

Mares with retained fetal membranes reportedly do not exhibit the usual signs of colic and abdominal straining immediately post partum that occurs in mares that pass the placenta normally. If a hormonal imbalance were responsible for failure of myometrial contractions that normally occur after foaling, this would account for a decreased occurrence of straining and abdominal pain. Furthermore, excellent results have been reported with oxytocin in the treatment of retained fetal membranes.⁸ Oxytocin normally increases in the blood during the second and third stages of a normal parturition. Furthermore, oxytocin has been used to induce parturition, and increased doses reduce the time to the second and third stages of labor.

It has also been suggested that uterine inertia can be caused in mares by a decrease in the concentration of blood calcium; overstretching of the myometrium, which is seen in cases of hydrops allantois, twinning, or oversized fetuses; and in cases of myometrial degeneration resulting from bacterial infection. Uterine inertia has also been incriminated following premature deliveries when the proper sequence of hormonal interaction has not been established. In one mare with retained fetal membranes, high concentrations of progesterone persisted, in contrast to the decrease observed in unaffected mares. Relaxin concentration was reported to remain elevated in a mare with retained fetal membranes. It has been suggested that the presence of retained fetal membranes within the lumen of the uterus serves as a continued source of relaxin. The function of prostaglandin F_2αremains unknown in the normal physiologic passage of fetal membranes.

Clinical signs of retained fetal membranes primarily consist of a portion of the membrane protruding from the vulvar lips. The degree of membrane protrusion varies from a few centimeters to a situation in which the placenta protrudes from the vulva to the ground. Retained fetal membranes can be present without any visible signs. In affected mares, the entire fetal membrane or a portion thereof is retained within the uterine, cervical, or vaginal lumen. Diagnosis in these cases is more difficult than in those in which the fetal membranes are apparent. Retained fetal membranes that protrude from the vulva generally create no adverse side effects unless the placenta irritates the mare and causes her to kick at the placenta. Some mares unintentionally kick their foals while trying to get the placenta away from their hocks. For this reason it is suggested that the placenta be tied in a knot ventral to the vulvar lips. Another suggestion has been to place the placenta in a plastic sleeve and tie it so that the placenta is included inside the plastic sleeve. This can be done in such a way to keep the placenta from touching the hocks or distal extremities.

The complications most frequently reported following retained fetal membranes include metritis, laminitis, septicemia, and death of the mare.⁹ Acute metritis and laminitis appear to be more of a problem in the draft breeds than in the medium- to lightweight breeds. It has also been suggested that the risk of uterine infection and delay in uterine involution increase with the duration of placental retention. This observation resulted in veterinarians removing the retained fetal membranes manually from the mare’s uterus. This is no longer a recommended treatment. The relationship between laminitis and retention of the fetal membranes was thought to be the result of the delay in uterine involution because the environment is suitable for bacteria to multiply within the uterine lumen and result in absorption of bacteria and toxins.

Many types of gram-negative organisms capable of producing endotoxin and causing histamine release have been found in the uterus with retained fetal membranes.² In a report of 356 Standardbred mares with retained fetal membranes in which the fetal membranes were not manually removed, there were no reported cases of acute metritis, septicemia, toxemia, or laminitis during or following passage of the placenta.⁷ It should also be noted that postpartum laminitis can occur as a result of systemic acute metritis with or without a retained placenta.¹⁰ Septic or toxic metritis can result in systemic signs of elevated body temperature, changes in disposition, and changes in appetite. However, toxic or septicemic metritis can occur in the absence of obvious retained fetal membranes. There may be retention of many microvilli in large areas where they have broken free from their attachments and remained embedded in the maternal crypts of the endometrium. This is the primary reason that manual removal or attempts to separate retained fetal membranes from the endometrium should be avoided.² Although a major portion of a retained fetal membrane could be removed manually, the large number of remaining microvilli can serve as foci of infection and inflammation with fluid accumulation within the uterine lumen. It is imperative that following expulsion of fetal membranes the chorionic surface be examined carefully to determine its gross appearance.

Laminitis may occur when large numbers of microvilli remain attached to the endometrial surface, which is followed by systemic involvement from septic uterine contents or related to histamine release by the uterus. Laminitis has been attributed to degenerative changes that occur within the tissue between the third phalanx and the hoof wall. This is in contrast to the normal sequence of events, which include toxic capillary injury and edema. The substances produced within the uterus may also have a direct effect on the sensitive lamina of the hoof. The specific mechanism involved in the development of laminitis following septic metritis is not known. Two possibilities have been suggested that involve a vasoactive component and a coagulation component. The relationship of hormones or toxins acting on digital vessels and thus altering the circulation of blood to the feet has been included in what has been known as the vasoactive component. Furthermore, it has been suggested that peripheral blood circulation increases immediately postpartum because of a reduction in uterine size and increase in uterine tone, thus moving blood from the uterus to the peripheral circulation. It is suggested that this is the vasoactive component of laminitis. The coagulation component is thought to be related to intravascular coagulation and fibrogen degradation products; thus, treatment with heparin has been recommended to reduce the incidence of laminitis.

Laminitis associated with retention of fetal membranes or, more specifically, with toxic or septic metritis, is similar to that which occurs following gastrointestinal involvement. The initial signs of laminitis occur 2 to 4 days following the onset of septic or toxic metritis. At that time, the animal exhibits an unusual gait and unusual stance by attempting to bear more weight on the rear limbs than on the forelimbs; thus, the rear limbs are placed further forward under the animal than normal. In such a case, the hooves of the horse are warmer to the touch than normal and a characteristic pulse may be present in the digital artery. Many affected animals spend the majority of their time lying down or stationary in a standing position.

The literature suggests that any animal with retained fetal membranes be treated to prevent laminitis. This includes the use of ice or cold water foot baths, suitable footing, and intrauterine and systemic antibiotic therapy to prevent septic metritis. Substances such as antihistamines, phenylbutazone, nonsteroidal anti-inflammatory drugs, and tranquilizers have been included in recommended therapy for retained fetal membranes. Antihistamines apparently neither prevent nor cure laminitis following retained placenta and their use is not recommended. It has also been suggested that the quantity of roughage be reduced in animals demonstrating signs of laminitis and that grain be completely eliminated from the diet.² Some authors recommend flushing the uterus when septic or toxic metritis is present or manually removing the placenta immediately to reduce the possibility of laminitis.

It is this author’s opinion that neither flushing the uterus nor manual removal of the placenta is indicated in mares with uncomplicated retained fetal membranes or in mares affected by septic or toxic metritis. As stated previously, manual removal of the placenta may result in separation of microvilli from the larger portion of the fetal membranes. In such instances, the microvilli then have to liquefy from the maternal crypts and be expelled or be absorbed by the uterus. Whenever manipulation of the uterus is performed, either for the purpose of manual removal of retained fetal membranes or in uterine lavage, there is an increase in blood supply and potentially an increase the absorption of substances from the uterine lumen into the circulatory system. If these substances are of a septic or toxic nature, manipulation of the placenta or flushing of the uterus generally initiates a deterioration in the mare’s general clinical condition. Such treatment may be more detrimental than beneficial. Excellent results have been obtained with conservative therapy involving systemic medications, including antibiotics and supportive care when indicated during the first 2 days post partum. The conservative approach in treating retained fetal membranes permits the mare to establish the normal physiologic barrier that is responsible for prevention of septic or toxic signs following parturition in most mares. This supportive care may include systemic antibiotics, anti-inflammatory drugs such as phenylbutazone or flunixin meglumine, and systemic fluids if required. This approach to treatment of retained fetal membranes generally results in improvement in the mare’s condition within 24 to 48 hours. Once improvement has occurred, local treatment of the uterus may be initiated. Frequent measurement of body temperature and complete blood counts in systemically affected mares demonstrates subclinical relapses following manipulation of the uterus for examination, uterine infusion, or uterine lavage.

Treatment of retained fetal membranes varies widely and each has its advantages and disadvantages. The first reported treatment for retained fetal membranes was manual removal. A variety of methods are described in the literature for manual removal of fetal membranes from the uterus of a mare. These methods include grasping the free portion of the fetal membrane protruding from the vulvar lips and applying traction; inserting the hand between the chorion and the endometrium to force separation of the two; placing the hand between the chorion and the endometrium, applying massage rather than simply using the hand as a wedge to separate the two structures; grasping the chorioallantoic membrane and twisting it, thus forcing separation of the fetal membranes from the endometrium; and, possibly the most complex, placing a wooden ring over the fetal membranes and forcing it between the membranes and the endometrium.² It has been recommended that the time between parturition and manual removal be anywhere from immediate to 24 hours. The primary rationale for early removal is to avoid delay, thus reducing the time required for uterine involution and reducing the possibility of uterine infection. In the same report, however, the author states that manual removal of fetal membranes delays uterine involution. Several vaginal examinations at 4- to 12-hour intervals may be necessary to manually remove fetal membranes without causing injury to the mare. It was furthermore suggested that the membranes be manipulated no longer than 10 minutes at each visit.

Although manual removal has been reported to be the treatment of choice by many authors, it is accompanied by several undesirable complications, the first of which is severe hemorrhage. Mares can lose large quantities of blood into the lumen of the uterus following manual separation of the fetal membranes. Assuming that the mare survives, this blood serves as an excellent environment for bacterial growth. It has also been reported that pulmonary emboli follow manual removal of the placenta. Manual removal of fetal membranes has been accompanied by invagination or eversion of a uterine horn, as well as a delay in uterine involution. It has been reported that there is an increased amount of fluid accumulation in the uterine lumen following manual removal of fetal membranes. The primary reason for the increase in fluid is that during separation only the central branches of the chorionic villi within the maternal crypts are removed. The remainder of the microvilli are broken off and retained within the endometrium. Furthermore, rupture of the endometrial and subendometrial capillaries occurs adding fluid within the lumen of the uterus. The presence of microvilli remaining within the endometrial crypts has been related to an increased occurrence of endometritis, laminitis, uterine spasm, and delayed involution. One author acknowledged that manual removal should be discouraged because of the possibility of trauma, hemorrhage, and infection. Manual removal was then recommended after other methods failed. It has been postulated that manual removal of the fetal membranes can result in permanent endometrial damage. The author has observed an increase in endometrial fibrosis occurring in a number of mares from 3 to 14 years of age that had normal fertility until manual removal of the fetal membranes. Following manual removal, decreases in fertility and deterioration in endometrial biopsy classification due to an increase in endometrial fibrosis were observed. The cervices of mares in which the fetal membranes have been manually removed remain open longer than those of mares treated with more conservative approaches. It has been suggested that manual removal of the fetal membranes remains as a treatment from a time when draft horses predominated and retained fetal membranes were more of a problem. The use of antiseptics placed into the lumen of the uterus has been suggested as an alternative method of treatment. Povidone-iodine diluted in large volumes of warm water has been placed into the lumen of the uterus or inside the placenta. Another method describes the placement of 2 to 12 L of dilute povidone iodine solution into the allantochorionic space followed-by ligation of the cervical star. This procedure traps the fluid within the allantoic cavity ⁹ and stretches the uterus and dilates the cervix as the placenta is passed, thus initiating endogenous oxytocin release and separation of microvilli from their attachments. It is suggested that the placenta should be passed within 30 minutes following this procedure. A disadvantage of the use of antiseptics has been their possible depression of phagocytosis by uterine neutrophils. The clinical importance of this phenomenon is unknown. Flushing and siphoning of fluid from the uterus is reported by some authors to be successful in the management of retained fetal membranes but by others to be of questionable value.² Infusion of the uterus with warm water (42° C) has been used with beneficial results. Large volumes of intrauterine saline and uterine flushes containing antibiotics have reportedly prevented or cured laminitis. Much diversity with regard to uterine therapy obviously exists. The most conservative treatment for retained fetal membranes in the author’s opinion is the use of oxytocin. A variety of doses and routes of administration are described in the literature. The use of oxytocin in a slow intravenous drip with 30 to 60 units placed in 2 L of saline and administered over an hour or of 80 to 100 units added to 500 mL saline and administered over a 30 minutes were both successful. Oxytocin can be administered as a bolus intravenously or intramuscularly. Doses for bolus injection range from 20 to 120 units. The administration of oxytocin can be repeated at 1.5- to 2-hour intervals until the placenta is delivered. Owing to the extremely short half-life of oxytocin, there is no detrimental effect of repeated administration. The only disadvantages of administration of a bolus are the spasmodic myometrial contractions and abdominal straining that may follow. It has also been reported that signs of colic appear more frequently when oxytocin is administered as a bolus.⁸ The severe cramping and abdominal straining may be related to dose. This author has not observed colic requiring treatment following administration of 20 units of oxytocin intramuscularly at 1- to 2-hour intervals. Furthermore, if signs of colic do occur, they can be eliminated with sedatives or analgesics. As the interval between parturition and treatment increases, the dose of oxytocin may be slightly increased. Dosages administered shortly after parturition should not exceed 20 units. Oxytocin is effective up to at least 18 hours post partum. As the animal approaches 15 to 18 hours post partum, the dose of oxytocin may be increased to 40 units per injection. The route of administration does not appear to affect the clinical outcome.

Antibiotics have also been recommended in the treatment of retained fetal membranes. It is probable that antibiotic treatment does not result in a more rapid expulsion of retained fetal membranes but primarily aids in the prevention of metritis. One report indicated the successful use of oxytetracycline hydrochloride in capsule form. In this author’s experience, the use of powered antibiotics or antibiotics in capsule or tablet form is undesirable because these antibiotics must be dissolved before they can have contact with the endometrial surface. Liquid preparations are believed to be superior for intrauterine administration. Other antibiotics that have been used in treatment of retained fetal membranes include amikacin, polymyxin, ticarcillin, sulfanilamide, and penicillin. It has been recommended that intrauterine antibiotics be administered at approximately 8 hours post partum if fetal membranes are retained. The primary value of antibiotic treatment is reportedly to control the contaminating bacteria that enter the reproductive tract at the time of parturition. Furthermore, it has been suggested that the fetal membrane attachment to the endometrium be examined prior to each treatment. Mares treated with intrauterine antibacterial agents for placental retention have a significantly higher pregnancy rate at the end of the breeding season than do mares that have not been treated with intrauterine antibiotics.⁷ The incidence of abortion, however, is higher in this group than in mares that have not been treated with intrauterine antibiotics. There was no difference in the foaling percentage of mares treated or not treated with intrauterine antibiotics for retained fetal membranes. Another reason not to incorporate intrauterine antibiotic therapy as part of a “routine” treatment for retained fetal membranes is based upon a report indicating that by 5 hours following intrauterine administration of antibiotics, 45% of the mares expelled the fetal membranes, compared with 81% of mares treated with oxytocin alone.⁷

Protection against tetanus must always be a consideration following parturition but especially in cases of retained fetal membranes. The use of tetanus antitoxin or toxoid is recommended. The placement of sutures or metal clips in the dorsal vulva following parturition if indicated has been recommended to reduce uterine contamination.² The beneficial aspects of intrauterine therapy or the need to manually remove the placenta rapidly has not been established. It is established, however, that systemic oxytocin treatment for uncomplicated cases of retained fetal membranes is superior to all other forms of therapy. A heavy hunter mare that was treated only with systemic antibiotics following a cesarean section passed the placenta 5 days following delivery with no adverse side effects.¹¹ The animal was not given intrauterine medication because of her disposition. Another report involving a mare first examined 5 days following parturition indicated that she had passed the placenta on that day without signs of complications, having received no prior therapy. This author treated a mare following an abortion at 9 months of gestation with intrauterine oxytetracycline once daily for 3 days followed by intrauterine infusion of 2% Lugol’s solution every other day until passage of the fetal membranes. This mare received phenylbutazone for the first 4 days of treatment. The fetal membranes were passed 13 days following the abortion. The uterus was cultured 34 days following delivery and contained no bacteria. The mare was bred approximately 60 days following abortion and conceived, maintained the pregnancy, and delivered a healthy foal. A careful examination is indicated in all mares with retention of fetal membranes to determine that septic or toxic metritis is not present.

Follow-up examination of mares with retained fetal membranes is mandatory regardless of treatment. It is imperative to be certain that the uterus is involuting normally regardless of whether the mare is to be bred during that breeding season. Transrectal examination of the reproductive tract must be utilized to determine the degree of uterine involution. Additional diagnostic tests may be indicated, including uterine culture, endometrial biopsy, and ultrasonographic examination. Endoscopic examination and endometrial cytology may also be used. Waiting approximately 25 days following placental passage to breed the mare may be beneficial; however, late in the breeding season, mares have been bred at 10 to 20 days post partum following retention of fetal membranes with acceptable conception rates. Examination of the placenta should occur following passage; however, many times it is difficult to determine whether the placenta is complete because of the deterioration of the tissue during retention.

There appears to be no difference in conception rates following the first breeding or at the end of the breeding season. Pregnancy loss rates were similar in normal foaling mares and in mares with retained plactenta.⁷ This lack of a difference was obvious regardless of the duration of placental retention. Manual removal of the fetal membranes was not attempted. It has been suggested that fetal membranes that cannot be removed easily should not be removed and a more conservative approach should be taken.¹² This author suggests that if fetal membranes have not been expelled by 3 hours post partum, the mare should be treated. The author’s treatment of choice is the administration of 20 units of oxytocin intramuscularly every 1 to 2 hours until the mare passes the placenta or until 18 hours post partum. Oxytocin in syringes is dispensed to owners prior to parturition with specific instructions, including contacting the attending clinician at 3 hours post partum so that medication can begin immediately when it is obvious that the placenta is retained. This avoids the delay in the arrival of the veterinarian to the farm, which may not occur until later that day. Mares that foal in the middle of the night should be examined early the following morning to determine if any complications coexist with the retained fetal membranes or if passage of the membranes has been complete. This examination includes rectogenital palpation and examination of the placenta, if possible. Decrease in uterine tone has been an excellent indicator of potential complications following parturition. If the uterus has good to excellent tone at the time of the examination, no vaginal investigation is made of the vagina or uterus to locate a fetal membrane. If fetal membranes are present within the uterus but good to excellent tone is present, the uterus is infused with 5 to 8 g oxytetracycline in 500 mL of saline. The author is uncertain whether this treatment is necessary. If the uterine tone is diminished, the volume of uterine infusion fluid is increased. In lightweight breeds no other medication is given. In draft breeds or in any mare following correction of a dystocia, systemic penicillin with or without gentamicin and flunixin meglumine is administered. Because mares that have experienced severe dystocias appear to be at a higher risk for developing septic or toxic metritis in conjunction with retained fetal membranes or because of the dystocia itself, systemic medication is continued for 3 to 7 days, depending on the animal’s condition. Uterine infusions are changed from oxytetracycline to 2% Lugol’s solution on the second to fourth day unless a cesarean section was performed to enhance the contractility of the uterus, thereby increasing tone and decreasing uterine lumen size. The volume of dilute Lugol’s solution administered is determined by the size and tone of the uterus and may vary from 500 ml to 4 L. An important consideration regarding the administration of Lugol’s solution is to not overdistend the uterus.

References

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2 Roberts SJ. Veterinary obstetrics and genital diseases, 3rd ed., Woodstock, VT: Published by the author; 1986:26-28. 30, 41–49, 245–255, 298–352, 382.

3 Ginther OJ. Placentation and embryology. In: Reproductive biology of the mare. Ann Arbor: McNaughton and Gunn; 1979:225.

4 Whitwell KE, Jeffcott LB. Morphological studies on the fetal membranes of the normal singleton foal at birth. Res Vet Sci. 1975;19:44.

5 Steven DH, Jeffcott LB, Mallon KA. Ultrastructural studies of the equine uterus and placenta following parturition. J Reprod Fertil. 1979;Suppl 27:579.

6 Plat H. Infection of the horse fetus. J Reprod Fertil. 1975;Suppl 23:604.

7 Provencher R, Threlfall WR, Murdick PW, et al. Retained fetal membranes in the mare: a retrospective study. Can Vet J. 1988;29:903.

8 Cox JE. Excessive retainment of the placenta in a mare. Vet Rec. 1971;89:252.

9 Burns SJ, Judge NG, Martin JE, et al. Management of retained placenta in mares. Proc Am Assoc Equine Pract. 1977;23:381.