Perinatology

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

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.

Etiology

During late gestation, the blood vessels supplying the genital tract enlarge; blood flow to the genitalia increases under the influence of estrogens, and retrograde pressure exerted by the weight of the fetus and uterus may compromise venous return in some areas, resulting in a varicose vein. Common sites for such varicosities are the hymen (transverse fold) and floor of the vagina. Occasionally, a varicose vein may rupture and cause frank bleeding that appears as a bloody vulval discharge. This clinical sign may cause great alarm to the novice mare breeder.

Clinical signs

A frank bloody vulval discharge may be present. The source of the bleeding is determined by vaginal speculum examination. If rupture of the vessel has not occurred, there may be no obvious clinical signs.

Treatment

Usually, no treatment is indicated. If severe hemorrhage occurs, the vessel may be ligated or cauterized. Light exercise may help improve circulation and lessen the occurrence of this problem. The condition will resolve after parturition.

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.

Etiology

Uterine torsion may be caused by the mare falling down or rolling or by increased activity of the fetus, but often there may not be any history of these events.

Clinical signs

The mare may appear as if she is in first stage labor. There may be restlessness, sweating, anorexia, frequent attempts to urinate, and signs of intermittent colic that is unresponsive to treatment. Severity of pain is related to degree of torsion and/or concurrent involvement of gastrointestinal viscera. Dystocia (q.v.) may be the presenting sign if uterine torsion occurs near term.

Diagnosis

On palpation per rectum, the broad ligament will feel very tense on one side as it is pulled under the pregnant uterus and the opposite side will seem to bulge up over the uterus. The uterine wall should be palpated carefully to assess the degree of congestion, necrosis or possible rupture.

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.

Etiology

Amniotic fluid is comprised of saliva and upper respiratory tract secretions and is cleared in part by fetal swallowing. Therefore any condition that impedes or results in impaired fetal swallowing may contribute to development of hydrops amnii. The exact cause of hydrops allantois is unknown but it is thought to be related to a dysfunction of the chorioallantois resulting in abnormal allantoic fluid maintenance. Some cases have been associated with fetal anomalies, heavy edematous placentas and umbilical cord disorders.

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.

Etiology

The rupture tends to occur during the last 2 mo of gestation due to the excessive weight of the gravid uterus.

Clinical signs

Prior to rupture, the mare may be noted to be lying down frequently. A marked, thick, painful edema extending from the udder to the xiphoid region often precedes rupture of the prepubic tendon. Serum concentrations of CPK are usually elevated. After rupture has occurred, the mare will have a stiff, cautious gait and refuse to lie down. The mare will often assume a “sawhorse” stance with an elevation of the tail head and the ischial tuberosities. The udder and teats will be flattened and stretched cranially.

If rupture occurs suddenly, intense pain and colic may be accompanied by sweating, increased respiration, rapid weak pulse, internal hemorrhage and shock (q.v.) that often progress to death of the mare and fetus.

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.

INDUCTION OF PARTURITION

The main advantage of induction is that it ensures the presence of assistance for mares that have a history of complications or that have experienced problems during gestation. It is very important to evaluate carefully the mare and her reproductive status and to be sure that several criteria are met before making a decision to induce parturition. Poor timing of and preparation for induction of parturition can result in a premature foal and/or dystocia. Once owners have become accustomed to inducing parturitions, it may become difficult to convince them to wait when a mare is not yet ready.

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 PGF₂_α 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 PGF₂_α 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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Tags: The Equine Manual

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

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Perinatology

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