Perinatology

Chapter 14


Perinatology





Chapter contents



INTRODUCTION


ENDOCRINOLOGY OF THE PERIPARTURIENT PERIOD



PERIPARTURIENT COMPLICATIONS



MANAGEMENT OF THE HIGH-RISK PREGNANCY



PHYSICAL EXAMINATION OF THE NEONATAL FOAL



COMMON FOAL DISORDERS



NUTRITIONAL AND RESPIRATORY SUPPORT FOR THE NEONATAL FOAL



NEONATAL RESUSCITATION



DEVELOPMENT OF A NEONATAL INTENSIVE CARE SERVICE




INTRODUCTION


This chapter highlights the contributions of theriogenology, intensive care medicine and neonatology to the emerging clinical specialty of perinatology. Historically, research focused on infertility and early pregnancy loss in mares. The endocrinology of estrus and early pregnancy was investigated and strategies developed to manipulate estrus and ovulation. The introduction of transrectal ultrasonography allowed pregnancy detection as early as 15 days post ovulation with positive pregnancy diagnosis awaiting sonographic detection of a fetal heartbeat by Day 23. Ultrasonography improved the ability to detect twin conceptions early enough to allow crushing of one embryo as a means of ensuring a viable pregnancy with the remaining conceptus.


Endocrinologic confirmation of pregnancy has also been explored using maternal serum (and occasionally urine) concentrations of various hormones including pregnant mare serum gonadotropin, estrone sulfate, relaxin and progesterone. Unfortunately, most of these hormones are not sensitive enough markers of pregnancy loss, since elevated hormone concentrations frequently persist for variable intervals following embryonic or fetal death.


Impending embryonic/fetal demise is difficult to predict. Careful sonographic examination of the “embryo at risk” may reveal a small-for-date conceptus. An abnormally slow fetal heart rate during the first trimester suggests an unhealthy outcome. The value of attempts to intervene and maintain such pregnancies is controversial. If an abnormal uterine environment or fetal chromosomal anomaly is responsible for early fetal wastage, then intervention to try and maintain the pregnancy is probably unwise. An unhealthy in utero environment so early in gestation is likely to predispose to abnormal fetal growth and development. Conversely, intervention can be justified in pregnancies at risk due to extrauterine stresses such as endotoxemia. Progesterone supplementation and flunixin meglumine administration have been shown to exert a protective effect when given to mares before or soon after the onset of endotoxemia during early gestation (<90–120 days).


Mid-gestation appears to be the safest period for fetal development. The same maternal illnesses that may have terminated the pregnancy in early gestation as a result of luteolysis and progesterone deficiency are unlikely to have the same deleterious effect during the second trimester when the primary source of progestogens has become the fetoplacental unit. Drugs administered to the mare are more likely to have a teratogenic effect on the fetus during early pregnancy than during the second trimester when organogenesis has already been completed. Causes of fetal death during mid-gestation are still poorly understood. Often pregnancy loss is not detected until weeks after it has occurred.


Late pregnancy remains the focus of most fetal monitoring techniques, with the goal being to recognize fetal compromise early enough to prevent irreversible damage. In women, the two most popular tests of fetal well-being during the third trimester are the non-stress test (NST) and biophysical profile (BPP). The NST requires simultaneous, continuous monitoring of fetal heart rate and movement, and is based on the premise that fetal heart rate should accelerate in response to fetal movement. During a 20 min observation window, the healthy human fetus should experience two heart rate accelerations exceeding 15bpm in amplitude above the baseline heart rate and lasting for at least 15s. An NST meeting these criteria is termed reactive and is a reassuring sign of fetal well-being. The BPP involves a 30 min sonographic survey of fetal heart reactivity, muscle tone, body movements and breathing movements and an evaluation of amniotic fluid volume (AFV).


Developmentally, fetal muscle tone is the first of these parameters to emerge. Fetal movement can be characterized by flexion and extension of the extremities and rolling movements of the torso. Three episodes of fetal activity during a 30 min period are considered normal. If fetal movement is observed, then muscle tone is considered to be present. Breathing movements in the human fetus develop during the end of the first trimester. At least 30s of fetal breathing should be observed during the diagnostic window in late gestation. AFV is a measure of fetal renal function and general placental nutritive function. Amniotic fluid in women corresponds to allantoic fluid in mares, in that both contain fetal urine. Oligohydramnios (decreased AFV) in women has been associated with premature membrane rupture and hypoxia.


Each of the parameters is assigned a score of 2 (present) or 0 (absent). A significant decrease in AFV is considered an ominous sign even if the other parameters are still normal. As the BPP score decreases to <6/10 the incidence of perinatal complications and uteroplacental insufficiency increases.


During a transabdominal sonogram, the placenta is also evaluated for thickness, textural changes and premature separation. Fetal presentation and size are determined. Normal indices for the BPP in the equine fetus are being established.


While transabdominal ultrasonography may not become a routine screen for all pregnant mares, its use should be considered for those individuals with a history of previous perinatal loss, premature placental detachment, twinning or premature delivery (q.v.). Sonographic evaluation of fetal well-being can also be justified in those mares with unexplained or excessive abdominal enlargement, vaginal discharge, premature udder development or other severe systemic illness. If sonographic evaluation suggests fetal well-being, then therapy can be directed at maintaining pregnancy as long as possible to permit continued fetal maturation. If fetal distress is detected, then timely termination of the pregnancy can be coordinated with preparations to stabilize and treat a compromised neonate.


Management strategies for the abnormal pregnancy vary with the problem. A purulent vaginal discharge (q.v.) in a late pregnant mare may or may not result in placental insufficiency and the birth of a compromised and possibly infected foal. Observation of a generalized increase in placental thickness and fetal fluid echogenicity raises the index of suspicion that fetoplacental function has been affected. Marked elevations in maternal concentrations of equine fetal protein provide biochemical confirmation of this condition. Such pregnancies need not be lost. Affected mares may be treated with antibiotics, and low (anti-endotoxic) doses of flunixin meglumine, progesterone and β-sympathomimetic drugs such as isoxsuprine hydrochloride to help maintain pregnancy. If signs of fetal compromise develop, induction is performed in a suitable intensive care environment (q.v.).


Sonographic determination of anterior fetal presentation (q.v.) in late pregnant mares provides reassurance that dystocia will not be a problem due to posterior presentation. Several studies have shown that after the ninth month it is extremely unlikely that the equine fetus will change its presentation between anterior and posterior.


Transabdominal ultrasonography may also provide insight into another common periparturient problem, premature placental separation. In most cases, it is unknown when the placenta begins to detach. Foals that are the product of premature placental separation are at increased risk for hypoxic organ damage. Although neonatal intensive care units have become quite adept at saving such foals, preventing or limiting fetal exposure to hypoxia is preferred. If significant areas of premature placental detachment are detected in a late pregnant mare, induction of parturition should be considered, rather than waiting for increasing hypoxia and fetal compromise to occur.


In utero determinants of fetal size are still being evaluated. If intrauterine growth retardation could be identified early in gestation, perhaps therapy could be directed at trying to improve uteroplacental blood flow. Intrauterine growth retardation is still being investigated in human medicine and perhaps the equine fetus might serve as a model for future research.


A successful perinatal program requires the collaborative efforts of those trained in reproduction and neonatology. A working knowledge of equine obstetric procedures and therapies for the more common periparturient emergencies is essential. Enhanced neonatal survival depends on a thorough understanding of foal physiology, an ability to recognize early signs of neonatal compromise, and the expertise, facility and equipment required to provide neonatal resuscitation and intensive nursing care. Successful management of the critically ill neonate requires rapid diagnosis and treatment of specific disease processes while addressing the unique metabolic demands and physiologic instability of the newborn.


The most serious threats to perinatal survival include septicemia, hypoxia and dysmaturity (q.v.). Treatment of these conditions post partum has become increasingly successful, but is still limited by how quickly the problem is recognized, how rapidly patient stabilization can begin, the economic restraints of the owner, and the limitations of the veterinary facility. Farm managers and foal owners must be fully informed of a sick foal’s condition, the intensity of treatment required, and the possible sequelae. The decision to treat requires the complete commitment of both owner and veterinarian; otherwise, foal mortality will remain disappointingly high and many of the survivors will have their future performance limited by lingering disabilities associated with neonatal disease.


Frequently, disruptions in fetal maturation/adaptation begin prior to or during parturition. Recognition of the perinatal risk factors associated with disturbed fetal development allows the most important management change to occur: increased surveillance of a mare with a potentially abnormal pregnancy. Once the mare is identified as a high-risk candidate, more sophisticated periparturient monitoring techniques can be employed. Arrangements can be made to allow her to foal in a facility equipped to provide emergency care ranging from controlled parturition or Cesarean section (q.v.) to neonatal resuscitation and intensive care. Learning more about the perinatal events of an abnormal pregnancy will in turn improve reproductive management of the mare and care of the newborn foal. Successful integration of prenatal and neonatal care should reduce periparturient foal mortality in an economically sound manner.



ENDOCRINOLOGY OF THE PERIPARTURIENT PERIOD



GESTATION


To understand the endocrinology of the periparturient period, it is necessary to review the endocrinologic events of gestation (q.v.).



Progestogens


Progesterone (q.v.) plays a role in maintaining cervical and uterine tone, embryo motility, fixation and orientation, and uterine secretion of nutrients to the embryo. It is the only ovarian hormone necessary to maintain the first 70 days of pregnancy.


The primary corpus luteum starts to produce progesterone at ovulation and plasma concentrations rise >4ng/mL within 6–8 days. The presence of the mobile embryo prevents the release of endometrial prostaglandin F (PGF) into the maternal circulation, thus preventing luteolysis. Progesterone concentrations decrease between Days 14 and 30. A second increase in plasma progesterone concentrations occurs again between Days 35 and 40 due to the resurgence of the primary corpus luteum (due to stimulation by equine chorionic gonadotropin). Additional follicles develop and ovulate between Days 40 and 70. The luteinization of these secondary follicles between Days 40 and 150 forms the secondary corpora lutea. Progesterone concentrations plateau near Day 60 of gestation at approximately 15ng/mL.


There is great variation in plasma progesterone concentrations among normal mares during early gestation. Pregnancy should be maintained as long as plasma concentrations of progesterone are >4ng/mL prior to 120 days of gestation. The luteal structures function until Day 150 and then progesterone gradually decreases to low plasma concentrations (1–2ng/mL) at approximately 180 days. The ovaries have little activity throughout the remainder of gestation.


Between Days 30 and 60 of gestation, the conceptus begins to secrete progestogens, primarily pregnanes and 20-α-dihydroprogesterone. Concentrations gradually increase until Day 300 and then rise more sharply during the last month before parturition. The 5-α-pregnanes reach high concentrations (some up to 2000ng/mL) during late gestation. Progestogens decrease from as early as 2–3 days to as late as 4–12 h before parturition.


Both the stage of gestation and the assay specificity must be known to interpret progesterone assay results correctly for pregnant mares. Assays that have cross-reactivity between pregnanes and progesterones will have progestogen concentrations normally high in late gestation. Assays specific for progesterone will indicate low progesterone concentrations for normal mares in late gestation.



Equine chorionic gonadotropin


Trophoblastic cells from the chorionic girdle invade the endometrium to form endometrial cups. Endometrial cups secrete a glycoprotein called equine chorionic gonadotropin (eCG) (q.v.), formerly known as pregnant mare serum gonadotropin (PMSG).


Equine chorionic gonadotropin is present in the mare’s blood between Days 35 and 120, with peak concentrations around Day 60. There is great variation among mares in the amounts of eCG produced and the timing of its production. Relatively small amounts of eCG are present in the urine and milk of pregnant mares. Demise of the endometrial cups is due to a lymphocytic immune reaction by the mare that destroys the endometrial cups.


Because use of exogenous eCG in cattle and sheep has both follicle- stimulating hormone (FSH) and luteinizing hormone (LH) activity that stimulates superovulation and ovulation, it was previously thought that eCG caused the development and ovulation of additional follicles in the mare to form secondary corpora lutea. However, many follicles are present on mare ovaries prior to the appearance of eCG and, therefore, it is not thought to have FSH-like activity in mares. Also, exogenous eCG does not increase follicular activity in mares. Equine chorionic gonadotropin does, however, have LH-like activity in mares and is luteotropic to the primary corpus luteum on Day 35, causing a resurgence of progesterone secretion prior to causing ovulation and/or luteinization of the secondary follicles of pregnancy. The primary and secondary corpora lutea also produce estrogens and, possibly, androgens.


Bioassays based on ovarian and uterine weight changes in immature rats were the first quantitative measurements of eCG. An LH radioimmunoassay can be used to estimate eCG because there is high cross-reactivity with LH. Immunoassays using anti-eCG serum-absorbed inhibition assay and hemagglutination inhibition assays are also available. Enzyme-linked immunosorbent assays (ELISA) are once again commercially available as a pregnancy test (q.v.) in the mare, although false positive results may occur because the endometrial cups are maintained until 120 days even if the fetus has died. False negative results may occur if the mare is tested before Day 35 or after Day 120 of gestation.



Estrogens


The equine conceptus is capable of estrogen production as early as Day 14 but increases in maternal circulation of estrogen (q.v.) are not seen until after Day 35. At 35–40 days, total plasma estrogens increase and a plateau of 3ng/mL is reached on Days 40–60. Estrone sulfate is secreted by the fetoplacental unit after Day 80 and steadily increases during the fourth month. High concentrations are maintained until the eighth or ninth month.


Conjugated equilin also increases during the fourth month and does not decrease until the last month of gestation. It is thought that the fetal gonads contain large amounts of estrogen precursors that the placenta subsequently converts to estrogens. Interestingly, estrogen concentrations decrease during the last month of gestation.


Interpretation of estrogen assays must be made carefully because estrogens of pregnancy exist in many forms and may be conjugated (bound to sulfates) or unconjugated (free in blood). The pregnant mare excretes huge amounts of estrogen in urine, principally estrone and equilin, which are used to produce commercial preparations of estrogen.


Assay of estrone sulfate can be used as a pregnancy test (q.v.) after the third month of gestation. Estrone sulfate assays can also be used to indicate fetal well-being because the fetus must be alive for concentrations to be elevated.


Estrogens are believed to have a positive effect on uterine, placental and fetal growth, perhaps through regulation of blood flow through the uterine and placental blood vessels and in the synthesis and storage of prostaglandin precursors in the endometrium and myometrium. During late gestation estrogens stimulate prostaglandin production, gap junction formation and oxytocin receptor synthesis. Gonadectomizing horse fetuses in mid to late gestation results in decreased maternal estrogen levels, weak ineffective labor associated with low prostaglandin levels, and the birth of dysmature foals.



Relaxin


The placenta is thought to be the sole source of relaxin in the mare. Placental secretion of relaxin (q.v.) begins on about Day 80 of pregnancy and peaks initially at approximately Day 175. A 50% decline occurs by Day 225, but concentrations then increase again gradually until parturition. Relaxin decreases the collagen content in the extracellular matrices of the pubic symphysis and uterine cervix, inhibits uterine contractility, and may play a role in mammary gland development.


Relaxin has been demonstrated to be an indicator of fetoplacental health in the late gestational mare. Low relaxin concentrations have been associated with varying types of placentitis and placental insufficiency.


Mares exposed to endophyte-infected tall fescue (q.v.) experience a decrease in circulating relaxin levels that coincides with placental dysfunction and fetal distress. When affected mares are treated successfully with domperidone, a D2 dopamine agonist capable of reversing the signs of fescue toxicosis, the mares’ clinical signs resolve and relaxin levels return to normal. This hormone represents a promising marker of fetoplacental function. No commercial assay for relaxin is currently available.




PARTURITION


The hormonal events controlling parturition (q.v.) affect maturation of the fetus and cause physical changes in the dam necessary to allow delivery, including relaxation of the pelvic ligaments and cervix, and uterine contractions. Lactation and maternal behavior are also influenced by hormones. In domestic farm animals, parturition is initiated by the fetus, but the mare can delay delivery temporarily if she is disturbed. Progestogen concentrations appear to decrease from 2–3 days before foaling.


Mare plasma PGF2α concentrations are higher in late gestation (≥270 days) than in early gestation. PGF2α and 13,14-dihydro-15-keto-prostaglandin-F2α (PGFM) dramatically increase during parturition, but concentrations are minimal within 1–2 days after parturition. Prostaglandin E2 (PGE2) concentrations gradually increase near term and are thought to play a role in cervical softening.


In sheep, the hypothalamus stimulates the anterior pituitary to produce ACTH that causes the fetal adrenal to increase secretion of cortisol during the last 48–72 h of gestation. Cortisol is thought to activate placental enzyme systems that convert progesterone to estrogen, which is needed for PGF2α production and increase of oxytocin receptors. PGF2α causes release of oxytocin from the posterior pituitary and softens the cervix. The oxytocin in turn stimulates myometrium contraction that results in delivery of the fetus.


The exact mechanism regulating parturition in the mare is not known, but it is thought to be similar to that in sheep. There is evidence that the fetus plays an important role. Equine fetal adrenals undergo rapid hypertrophy immediately before parturition and fetal plasma cortisol increases slightly near term. Concentrations of cortisol in the amniotic fluid also increase near term. In the mare, there is no change in plasma concentrations of glucocorticoids before parturition. Ovarian hormones are not necessary for parturition and pregnant, ovariectomized mares have normal parturitions. Exogenous progesterone will not prolong gestation.


In the mare, PGF and oxytocin are involved with parturition but are not necessary for luteolysis. Oxytocin receptor formation seems to be controlled by estrogen–progesterone ratios and increased PGF2α production. Oxytocin (q.v.) is only increased during second stage labor and until the placenta is passed. As oxytocin is a neurohormone under the control of the mare’s central nervous system, this may be the mechanism by which she can “select” timing of delivery.


As the fetus and placenta are passed, steroid production by the conceptus is lost. Within 30 min of parturition, progestogen and estrogen concentrations in the mare decline precipitously. A surge of FSH occurs at the time of parturition, beginning a few days before and reaching a peak on or just before the day of parturition. Follicular development, therefore, soon resumes and estrogen concentrations increase during the first estrus (foal heat), which occurs approximately 7–11 days after foaling.


FSH (q.v.) concentrations then gradually decrease due to the inhibitory effect of the developing follicles associated with foal heat. However, LH (q.v.) concentrations are low prior to parturition due to the suppressing effect of progestogens. LH increases after the progestogens decrease following parturition. Further increases in LH concentrations occur due to estrogens produced by follicles during foal heat. After foal heat ovulation, progesterone increases due to its production by the corpus luteum, and a normal estrous cycle ensues.



HORMONE ASSAYS


Before the 1960s, investigations on hormone regulations were performed with bioassays that measured changes in organ size or weights due to stimulation by a particular substance. In the late 1960s, competitive protein binding assays and later radioimmunoassays confirmed information learned from the bioassays. Very sensitive radioimmunoassays allowed for much more accurate determination of hormone concentrations.


Much work has been done to develop assays that do not require long, tedious laboratory techniques and radioactive isotopes. ELISA tests use highly specific monoclonal antibodies and involve enzyme-induced color changes that do not require radioactive agents. Assays can be performed quickly and outside laboratories that have to meet the regulated requirements for handling and disposing of radioactive materials. Some assays are in a simple dipstick form and give qualitative results indicating the presence or absence of the hormone. Quantitative results can be obtained using plate readers that give an accurate determination of hormone concentrations. ELISA tests are available for progesterone, equine LH and eCG. Interpretation of results must be made carefully, after following assay directions, using appropriate control standards, and with comparison to concentration ranges in normal mares for the particular reproductive stage.



PERIPARTURIENT COMPLICATIONS



VARICOSE VESSELS IN THE VAGINA


A distended blood vessel with possible hemorrhage may be seen in the vulva/vagina of the pregnant mare near term. Varicose veins are more common in older mares.







UTERINE TORSION


Torsion of the uterus (q.v.) occurs during late gestation but is not usually associated with parturition as in the cow. The uterus rotates about its long axis and typically does not directly involve the cervix. The degree of rotation is quite variable and can range from 90 to >360°. The severity of clinical signs is related to the degree of torsion, and any gastrointestinal organ involvement or vascular compromise.







Treatment

Uterine torsion can be corrected surgically, manually or by rolling. Surgical correction by rotation of the uterus can be made through a flank incision in a standing, sedated mare. If there is a suspicion that the uterus has been severely compromised and/or rupture has occurred, a ventral midline incision with the mare under general anesthesia (q.v.) is recommended.


If the mare is near term and the torsion not severe, manual correction per vaginam is possible provided the torsion is <270°. The mare should be prepared as for dystocia evaluation. The cervix must be adequately dilated and a portion of the fetus palpable. If the fetal membranes are intact they should be ruptured to release fluids and reduce the size and weight of the uterus. The fetus may be rocked to flip the uterus into normal position. The foal may then be delivered immediately. Parturition may be hastened by induction with oxytocin after the torsion has been corrected.


The mare can be rolled to correct uterine torsion. This procedure should not be used near term because of the increased risk of uterine rupture (q.v.). Anesthesia is induced using a short-acting injectable anesthetic and maintained with inhalation anesthesia (q.v.). The mare is placed in lateral recumbency with the side in the direction of the torsion down. The legs should be hobbled and ropes applied to the limbs. Place a plank (3.5 m long ×0.3 m wide ×5 cm thick) perpendicularly against the mare’s back and flank. While one person kneels on the plank to hold the uterus in place, roll the mare such that her legs swing over her back in the direction of the torsion. Care should be taken to protect the mare’s head from injury. Success of correction can be evaluated by palpation per rectum for the proper positioning of the broad ligament. If the torsion has not been corrected, the procedure can be repeated. Pregnancy should be monitored closely for several days.


Complications associated with correction of uterine torsion include premature placental separation with fetal compromise and/or death and abortion, uterine wall necrosis and rupture, peritonitis and recurrence of the torsion during the same pregnancy.



HYDROPS AMNII AND HYDROPS ALLANTOIS


Hydrops amnii (excessive accumulation of amniotic fluid) in the mare has been associated with foals with hydrocephalus (q.v.) and with umbilical cord anomalies. Hydrops allantois is an excessive accumulation of allantoic fluid that occurs during the last trimester of gestation. Although both conditions are rare in the mare, hydrops allantois is the more common of the two.





Clinical signs

Hydrops allantois is associated with dramatic and rapid enlargement of the abdomen over several weeks. Mares with hydrops amnii develop mild abdominal distension over a more prolonged time period of weeks to months. The increased volume of fetal fluids exerts pressure on the gastrointestinal tract and thoracic cavity and results in maternal anorexia, tachycardia, tachypnea, dyspnea, depression, colic, decreased manure production, difficulty walking and marked ventral edema (q.v.).


Advanced cases may develop ventral abdominal hernia or prepubic tendon rupture (q.v.). Other complications include uterine rupture and uterine inertia (q.v.). Palpation per rectum reveals a large, fluid-distended uterus. It is often difficult or impossible to feel the fetus. In the early stages of hydrops, an absolute diagnosis may be difficult to make. The condition is confirmed via transabdominal ultrasonography. Large volumes of clear fetal fluids are observed.



Treatment

Hydrops allantois tends to be more life threatening for the mare due to its rapid onset and the excessive volume of fluids that accumulate. Prognosis for both mare and fetus is grave unless the mare is at term. The fetus may be normal in these pregnancies, but survival depends on how late in the pregnancy the condition develops and how successfully the mare is supported during labor. Often the best chance for saving the mare is by termination of the pregnancy.


Hydrops amnii is often associated with fetal birth defects and/or umbilical cord anomalies. In cases of hydrops amnii the prognosis for the pregnancy is poor because abortion and premature delivery are common. Future fertility is often not impaired if there is no accompanying prepubic tendon rupture or ventral abdominal herniation.


If the mare is comfortable and close to term, fluid accumulation is mild to moderate and fetal viability is reasonable, then the mare can be supported with IV fluids supplemented with B vitamins and dextrose, a laxative diet, oral vitamin E and altrenogest (0.044–0.088 mg/kg PO q 24 h).


In advanced cases of hydrops, parturition should be induced to relieve pressure on the mare’s internal organs and avoid prepubic tendon rupture, abdominal hernia formation or uterine rupture which can end a mare’s reproductive career and increase the risk of colic post foaling. The mare’s muscle enzymes should be monitored. Sudden increases in maternal serum creatine phosphokinase (CPK) concentrations herald increasing muscle damage and impending prepubic tendon rupture or hernia formation.


During delivery the sudden expulsion of large volumes of fetal fluids results in hypotensive shock (q.v.) in the mare. Manual rupture of the chorioallantois is often too blunt and results in rapid fluid expulsion. A sharp 20 to 32 French trocar catheter can be used to make a puncture through the chorioallantois to drain off allantoic fluid as slowly as possible. To prevent maternal shock, the mare should be pre-treated with at least 20L of IV fluids. One to two liters of hypertonic saline or hetastarch (10 mL/kg) can be administered to improve oncotic pressure and combat hypotension.


Corticosteroids can also be given to treat shock (q.v.). Oxytocin is administered to stimulate uterine contractions, but uterine inertia should be anticipated and chains should be available to help extract the fetus as rapidly as possible to minimize peri partum asphyxia. Post partum, flunixin administration can improve maternal comfort.


Retained fetal membranes (q.v.) are common and are treated with repeated doses of oxytocin (10–20IU IV/IM) q 3–4 h. The mare should be started on antibiotics and NSAIDs to reduce the risk of metritis, endotoxemia and laminitis (q.v.). Uterine involution may be delayed and additional oxytocin, IV calcium supplementation and uterine lavages may be indicated.



RUPTURED PREPUBIC TENDON AND VENTRAL ABDOMINAL HERNIA


Prepubic desmorrhexis (ligament rupture) and abdominal hernia formation are more common in older draft mares and other heavier breeds, but have been reported in other breeds including Arabs and ponies. Conditions that cause severe distension of the body wall such as hydrops, twins, severe ventral edema, or trauma may result in rupture of the prepubic tendon or abdominal hernia. It may be difficult to distinguish between prepubic desmorrhexis and abdominal hernia (q.v.), and clinical progression of the two conditions is similar.






Management

Repair of the acute condition is not possible. Confine the mare to a stall, limit exercise, and avoid giving bulky feeds. The mare should be fitted with a wide abdominal support heavily padded over the back. Because abdominal contractions during parturition will not be effective, parturition should be induced when the mare is near term so that delivery can be assisted. Affected mares should not be expected to carry a pregnancy again.


Complications include death of the mare due to internal hemorrhage and/or bowel damage, ventral evisceration following rupture of the body wall, and colic after delivery associated with bowel trauma and intra-abdominal adhesions.


Minor rents in the body wall can be surgically repaired. Larger tears are not amenable to successful repair. Foals delivered from mares with hydrops or prepubic tendon rupture are at increased risk for problems associated with chronic placental insufficiency such as compromised growth and development and hypoxic ischemic encephalopathy.


Deliveries associated with these conditions are often difficult and protracted, thereby adding the additional insult of acute hypoxia to already stressed neonates. Many of these foals are weak, slow to stand and nurse, and unable to absorb adequate amounts of colostral antibodies, thereby rendering them more susceptible to early sepsis.





Indications




1. Mares that have previously produced dead or severely hypoxic foals due to premature placental separation associated with delayed parturition.


2. Mares that have suffered problems during a previous foaling(s) such as dystocia, lacerations or other injuries, and that require professional assistance with delivery and immediate foal care.


3. Mares in which gestation is greatly prolonged beyond 12 mo and is associated with a very large fetus. NB Usually, mares with a prolonged gestation (>365 days) have small or normal size foals.


4. Mares in which there is the presence or possibility of rupture of the prepubic tendon.


5. Mares with hydrops.


6. Mares that have produced foals affected by neonatal isoerythrolysis, so the newborn foal may be prevented from ingesting colostrum before its red blood cells can be checked against the mare’s serum.


7. Mares that have sustained pelvic fractures or other injury to the birth canal such that the canal is reduced and manual assistance during delivery is anticipated.


8. Preparation of nurse mares.



Criteria for induction




1. Length of gestation. Induction should only be performed when the fetus is mature enough to adapt to the environment outside the uterus. A minimum of 330 days usually ensures adequate fetal maturity at the time of induction if all other criteria are fulfilled.


2. Adequate mammary development. The udder should be enlarged and the teats distended with colostrum. In uncomplicated pregnancies, concentrations of calcium, sodium and potassium undergo distinct changes in pre partum mammary secretions associated with fetal maturity and readiness for birth. Calcium concentrations >40 mg/dL are associated with a mature fetus and values <12 mg/dL are associated with reduced fetal viability. As delivery approaches, sodium concentrations decrease to <30 mg/dL and potassium levels increase >35 mg/dL. Water hardness test strips can be used to monitor calcium concentration.


3. Relaxation of the vulva and sacrosciatic ligaments. Maximum relaxation occurs very close to foaling and can dramatically increase during the first stage of labor. The degree of these changes is quite variable among mares.


4. Relaxation of the cervix. The cervix should be soft and easily compressed, with some degree of dilatation. Cervical relaxation may normally occur as early as 1 mo before term or as late as first stage labor.



Methods of induction


Oxytocin (q.v.) is the most commonly used agent for inducing parturition. Parturition will occur rapidly and safely with small doses of oxytocin. Oxytocin, 20IU administered IM, will cause a slow, quiet foaling. An IV bolus of 5–10IU is also effective. Smaller IV doses such as 2.5–5IU given every 20–40 min produce a more gradual onset of labor in late term mares and may reduce the risk of dystocia and premature placental separation that is observed with the use of larger doses of oxytocin.


Infusion of 60IU oxytocin in 1L of physiologic saline IV at a rate of 0.5–1IU oxytocin/min produces parturition that appears physiologically normal. Second stage labor usually occurs 20–35 min after the start of infusion. Often, the mare will deliver while standing, which may be an advantage if one suspects that manual intervention will be necessary. Oxytocin may be continued until the placenta is passed.


Natural PGF2α is not recommended for induction of parturition in the mare. Because of the strong uterine contractions it induces there is a high incidence of premature placental separation and fetal morbidity and mortality associated with its use. Some synthetic prostaglandins have however been used on a limited basis in mares. One synthetic PGF2α that can be used is fluprostenol sodium (2.2μg/kg). Doses of 1000μg for mares and 250μg for ponies administered IM are effective and signs of first stage labor will commence within 30 min of injection. Birth usually occurs within 2 h. There is some controversy over the safety and efficacy of fluprostenol for induction. Other synthetic prostaglandins that have been used in the mare are prostalene and fenprostalene. These drugs are dosed at 4 mg SC and 0.5 mg SC respectively. Studies using these drugs indicate that a viable fetus can be obtained approximately 4 h after administration.


Large doses of corticoids are necessary to induce parturition in the mare. Daily administration of 100 mg of dexamethasone for 4 days starting after Day 321 will induce parturition between 6.5 and 7 days after initiation of treatment. This delay between administration and delivery of the foal decreases the usefulness of this drug for induction. There is some thought that it may be beneficial to a potentially dysmature foal to administer corticosteroids for 2–3 days pre partum and then induce parturition with oxytocin.



PLACENTITIS


Placentitis (q.v.) describes inflammation of the fetal membranes and is a common cause of reproductive losses in mares. Most cases of placentitis are infectious in origin; the infection ascends by direct extension from the mare’s lower reproductive tract or spreads hematogenously from the mare’s systemic circulation. Acute placentitis may cause abortion or premature birth with or without infection of the newborn. Chronic placentitis can result in growth retardation of the newborn or death of the fetus.




Etiology

The most common cause of placentitis is bacterial infection that ascends from the dam’s urogenital tract through a relaxing cervix. Early placental lesions are first detected around the cervical pole of the fetal membranes.


The bacteria most commonly isolated include Streptococcus equi var. zooepidemicus, Escherichia coli, Enterobacter agglomerans, Klebsiella pneumoniae and Pseudomonas aeruginosa (q.v.).


In Kentucky, a slightly different form of placentitis has been recognized. It is characterized by focally extensive inflammation located predominantly at the junction of the uterine horns and the body of the placenta. The affected area is covered with thick, tenacious brown mucoid exudate and the underlying chorionic villi are necrotic, absent or reduced in size. This form is associated with infection by a group of Gram-positive, branching, filamentous nocardioform-like organisms.


A far less common route of infection is hematogenous as part of systemic disease in the dam. This form of placentitis is often diffuse in nature as seen with leptospirosis and Corynebacterium pseudotuberculosis (q.v.).

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Jul 8, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Perinatology
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