John K. House, Consulting Editor Recent studies in Denmark, The Netherlands, North America, and Sweden indicate that the prevalence of bovine perinatal mortality is increasing, particularly in Holstein primiparae.1 The peripartum period is a high-risk period for the fetus and dam. Approximately 5% to 10% of the annual calf crop and 15% to 20% of the annual lamb crop in the United States dies prior to weaning.2–4 Between 50% and 70% of neonatal mortality occurs in the first 3 days of life with dystocia, starvation, and hypothermia responsible for 50% to 60% of these losses.3,5 The incidence of dystocia is particularly high in Holsteins with reports of 50% of heifers and 30% of cows requiring calving assistance.6 The risk of neonatal morbidity and mortality is largely influenced by sire selection (calving ease), maternal management, and subsequently maternal health during the peripartum period. Uterine torsion, vaginal prolapse, hydrops allantois, hydrops amnii, and metabolic disorders are disorders of pregnancy and the peripartum period that negatively impact on the health of the dam and the fetus during late gestation. Over the past 10 years, there has also been increasing application of advanced reproductive technologies with the production of in vitro and cloned embryos. The initial application of these methods has been associated with a higher incidence of complications during pregnancy and neonatal mortality. Uterine torsion is more common in cattle than other domestic species. The exact etiology is unclear, with most occurring during late first-stage or early second-stage labor.7 Proposed risk factors include poor maternal muscle tone, strong fetal movement, and reduced rumen fill. Retrospective studies have reported no significant seasonal affect but a higher incidence in Brown Swiss cows and a lower risk in Hereford, Angus, and Jersey cows compared with Holstein-Friesians.8 Calf birth weight is typically above average and a greater proportion of fetuses are male (63%).8 The incidence is also significantly higher in cows compared with heifers.7 Clinical signs associated with uterine torsions include fever, tachycardia, tachypnea, straining, anorexia, and vaginal discharge.8 The diagnosis of uterine torsion is based on a history of advanced pregnancy and the presenting clinical signs. On transrectal palpation, the orientation of the broad ligaments is distinctly altered; depending on whether the torsion is to the left or the right, the respective broad ligament is pulled tightly across the uterus.9 Approximately 60% of torsions involve the vagina, and spiral folds can be palpated per vagina.9 Most torsions are to the left (counterclockwise); in general the uterus rolls toward and over the nongravid horn (approximately 60% of all pregnancies in the cow are in the right horn).9 Torsions between 45 and 90 degrees are uncommon; 20% are 90 to 180 degrees, 57% are 180 to 270 degrees, and 22% are 270 to 360 degrees.8 With severe torsion, circulation is compromised. Treatment involves correction of the torsion and delivery of the calf. In a retrospective study of 164 cases, vaginal delivery was possible after manual correction (20%) or rolling of the cow (18%). Cesarean section was performed immediately in 35% of the cases, after failed detorsion attempts in 7% and because of failure of the cervix to dilate following successful correction of the torsion in 20%. When manually manipulating the fetus per vagina, it sometimes helps to have a person assist by pushing on the calf externally. Fetal survival rate is generally low, with fetal death often occurring prior to presentation if there has been delayed recognition of parturition. The primary predisposition to cervicovaginal prolapse in cattle is elevated plasma estrogen concentrations during late gestation.9 The higher prevalence in certain beef breeds implies a genetic predisposition, with Bos indicus, Herefords, Charolais, Limousin, and Shorthorns affected more frequently than other breeds.10–12 Other factors that contribute to the risk of vaginal prolapse include increased intraabdominal pressure in late pregnancy, obesity, and poor vaginal conformation. The pathogenesis and development of vaginal prolapses is progressive; it starts with the exposure of some of the vaginal mucous membrane. The prolapsed mass moves in and out as the cow gets up and lies down. Exposed mucosa dries out and becomes irritated, leading to straining and further prolapse. The prolapsed tissues become edematous, leading to circulatory impairment and swelling. Ultimately the cervix and occasionally the bladder may become involved.9 The objective of treatment in the case of pregnant animals is to replace and retain the vagina within the pelvic canal and to deliver a live calf. Numerous treatment options are described for vaginal and cervical eversions.12 These methods include suturing the vulva (caslick, Bruhners), vaginopexy (Minchef procedure), or cervicopexy (Winkler procedure). Close observation of the cow for signs of impending parturition is required following suture of the vulva. Failure to release the sutures prior to parturition can lead to severe laceration of the vulva and potentially the death of the calf. If the patient is close to parturition, induction is recommended to expedite the process and prevent recurrence prior to parturition. Since vaginal prolapse is likely to recur during the next pregnancy, it is recommended that the cow be culled when the calf is weaned. Ringwomb, or incomplete dilation of the cervix, causes sporadic dystocia, mainly in multiparous ewes bearing multiple fetuses. It is most commonly observed in sheep and may be heritable in some instances.13 Ringwomb has no predisposition associated with breed, age, or body condition score, but it is associated with a significantly higher lambing percentage.13 Correction with gentle manual stretching can be attempted; the use of PGE 2, administered as an intracervical gel in the treatment of ringwomb in ewes, is not effective at causing dilation of the cervix.14 Because of the significant risk of tearing, a cesarean delivery is often required.15 Ewes with diseases that cause abortion as a result of infectious agents may exhibit signs similar to ringwomb, as can pregnancy toxemia, consumption of poisonous plants, consumption of estrogenic plants, and lasalocid toxicity.15 Early dilation syndrome is a condition of sheep that is similar to but considered separate from ringwomb. In early dilation syndrome, incomplete dilation of the cervix occurs approximately 7 to 14 days before term. The ewe has little or no udder development or a sudden overnight blooming of the udder and placental membranes protruding when presented. The cervix usually can be dilated by hand, but the lambs, although born alive, are not viable. The syndrome occurs most frequently in ewe lambs and first-lambing 2-year-olds, but occasionally in older ewes. Affected flocks can have over 30% morbidity. The syndrome occurs in all breeds and in all flock management situations. No common link has been found from nutritional, physiologic, toxicologic, or infectious disease investigations.15 Fetal loss associated with abnormal placentation occurs sporadically and is reflected by alterations in volume and composition of allantoic and amniotic fluid. In a study of 60 cases of bovine hydrops, 88% were hydrallantois, 5% hydramnios, and 7% a combination of both.16 Hydrallantois is often associated with disease of the uterus and hydramnios with genetic or congenital defects of the fetus (e.g., Dexter cattle with bulldog calves, Angus calves with osteopetrosis, Guernsey calves with pituitary hypoplasia or pituitary aplasia).17 Hydrops allantois is a sporadic condition of cattle in which progressive excessive accumulation of allantoic fluid occurs. Accumulation of allantoic fluid from mid gestation is associated with placental dysfunction.9 Placental dysfunction is characterized by a reduced number of placentomes (normal 75 to 100) and the development of more primitive villous placentation.18 An increased incidence of hydrops allantois has been reported with pregnancies derived from in vitro fertilization (IVF)–produced embryos. In a comparative study of IVF and artificial insemination (AI)–derived pregnancies, the percentage of cows with hydroallantois was 1.8% and 0.07%, respectively.19 A herd outbreak of hydrops allantois has also been associated with severe nutritional deficiency.9 Allantoic fluid volume may exceed 100 L (normal 8 to 15 L near term), leading to rapid abdominal enlargement; rectal examination reveals tight distention of the uterus. The fetus and placentomes are not palpable due to the tightness of the uterine wall. Affected cows become anorectic, leading to dehydration, constipation, and eventually recumbency. The concentration of sodium and chloride in allantoic fluid of cattle during the last 12 weeks of gestation is normally low (Na = 52 ± 20 mEq/L and Cl = 17 ± 11 mEq/L) and the concentration of creatine high (1224 ± 458 µg/mL).20 With hydrallantois, allantoic fluid sodium and chloride concentrations rise toward extracellular fluid concentrations (Na = 116 ± 13 mEq/L and Cl = 81 ± 12 mEq/L) and allantoic creatine concentration decreases (193 ± 73 mEq/L).20 Normal amniotic fluid has electrolyte concentrations similar to those of plasma (Na = 132 ± 7 mEq/L and Cl = 115 ± 8 mEq/L) and a lower creatine concentration than allantoic fluid (70 ± 26 µg/mL).20 Cows with hydrallantois are also often hyponatremic and hyperglycemic.16,21 Because of the poor prognosis, salvage slaughter is generally recommended. Parturition can be induced if the cow is reasonably close to term and is recommended for the salvage of the calf. Attempts at medical management of affected cows include slow decompression and supportive fluid therapy. The grossly distended uterus is slow to involute and prone to severe metritis. The prognosis for future fertility is guarded. Hydramnios is rare, accounting for 5% to 10% of uterine dropsy cases.22 It has been associated with a genetic (autosomal recessive) or congenitally defective fetus in which swallowing is impaired, and the amount of amniotic fluid gradually increases over several months.22 It may affect only one of twin fetuses.9 Normal amniotic fluid volume at parturition is about 4 to 8 L; cattle with hydrops amnii may accumulate 20 to 100 L of amniotic fluid.23 The slowly progressive accumulation of fluid during the latter half of gestation means that the abdominal muscles become stretched and the cow develops the typical “pear-shaped” abdomen. In contrast to the situation with hydrallantois, placentomes and often the fetus are palpable per rectum. The prognosis for the life and future fertility of cattle that have hydramnios is good.23 The fetus itself is invariably defective and will not be viable. If the owner elects to keep the cow, the genetic implications should be considered. Clinical features that distinguish hydrops amnii and hydrops allantois are presented in Table 18-1. TABLE 18-1 Differential Diagnosis between Hydrallantois and Hydramnios in Cattle9 From Drost M. 2007. Complications during gestation in the cow. Theriogenology 68:487. The transfer of bovine embryos produced and manipulated in vitro results in abnormalities in some conceptuses, fetuses, placentas, and offspring.24,25 The term abnormal offspring syndrome is used to describe the range of abnormalities observed.26 The exact etiology of the syndrome is uncertain, although developmental abnormalities of the fetus, placenta, and offspring have been predominantly attributed to the presence of serum in the culture medium.27 In utero manifestations include prolonged gestation, abnormal placental development (placentomegaly, hydroallantois, and edematous placentomes in reduced numbers), and suboptimal embryonic and fetal survival.18,28 Increased birth weight and incidence of dystocia, congenital deformities, and perinatal mortality are neonatal manifestations of this syndrome. Respiratory disease is often a limiting factor in the survival of cloned calves during the neonatal period.29 Possible causes of compromised respiratory function include hypoventilation, ventilation perfusion mismatch, right-to-left shunt resulting from persistent fetal circulation, and respiratory distress syndrome resulting from inadequate surfactant production. Nasal insufflation at birth is recommended to support the respiratory function of cloned calves.29 Reduced fetal viability often reflects mismanagement of maternal nutrition during the last trimester of pregnancy and/or during the prepartum and peripartum period. Maintenance of adequate nutrition throughout pregnancy is essential to provide for the growing fetus and to maintain a healthy dam capable of delivering and nursing the fetus. Pregnancy toxemia, hypocalcaemia, protein energy malnutrition, micronutrient deficiencies, and obesity may all impair the health of the fetus directly, or else indirectly by affecting the health or capacity of the dam to deliver the fetus. Underfeeding of energy (40% to 70% of requirements)30 or protein (65% of requirements)31 during late gestation in beef cattle produces calves that are less able to generate heat to maintain body temperature after birth. This effect was observed despite no significant difference in birth weight.30,31 The fetal response to growth-restrictive environmental conditions is to partition nutrients toward the development of organs essential to life, such as the brain, at the expense of less vital organs and tissues.32,33 In humans, the repartitioning of nutrients to support fetal development has been demonstrated to have long-term effects on postnatal growth and metabolism, apparent as an increased propensity to develop insulin resistance, high blood pressure, more rapid weight gain, and increased adiposity.34 Similarly, nutrient restriction during gestation has been demonstrated to alter postnatal glucose metabolism in calves.35 The consequences of overnutrition during gestation on the developing fetus are less clear. A number of overfeeding trials have resulted in increased birth weight, whereas other studies have not.36,37 Maternal consequences include deposition of fat in the pelvis that increases the risk of dystocia and subsequently fetal compromise.38 For high-producing dairy cows, good nutritional and cow management during the transition period is pivotal for maintaining cow health. Hypocalcemia and negative energy balance contribute to the risk of dystocia and subsequently the risk of neonatal morbidity and mortality.39 Recently, there has been a paradigm shift in the thinking regarding the nutrition of nonlactating cows prior to calving. Previously, the focus had been on increasing the amount of energy in the ration fed to cows during the last 3 to 4 weeks prior to calving to meet the increasing energy needs associated with pregnancy in the face of the cows’ declining dry matter intake.40 Paradoxically, overfeeding energy during the dry period has been found to contribute to negative energy balance postpartum and an increased incidence of disease in the peripartum period.41 This phenomenon appears to be associated with increased insulin resistance, similar to type 2 diabetes. The current recommendation is to feed cows throughout the nonlactating period a ration that meets but does not exceed caloric needs. Straw is added to the ration to promote rumen health and to prevent overeating.39 In regard to trace minerals, selenium and copper deficiency may contribute to neonatal morbidity and mortality. Copper deficiency has been associated with impaired fertility, weak calves, and high calf mortality.42 In a larger Canadian study, myopathy and cardiomyopathy were common findings in stillborn and neonatal mortality, suggesting the possible contribution of nutritional myopathy.43 Investigation of perinatal morbidity and mortality should begin with assessment of maternal management. Some of the more common causes of stillbirth and perinatal mortality are listed in Box 18-1. Environmental stress prior to or around the time of parturition may also compromise the fetus or neonate. Heat stress affects fetal viability by impeding calf growth in the last trimester of pregnancy44 and by depressing colostral quality45 and immunoglobulin transfer.46 Uterine blood flow and placental mass are reduced and endocrine profiles altered when cattle are heat stressed during the last trimester of pregnancy. Heat stress during the last 3 weeks of pregnancy lowers dry matter intake, contributing to a negative energy balance at this time and promoting mobilization of body fat and ketogenesis. Transfer of immunoglobulins to colostrum is impaired and the concentration of protein, casein, lactalbumin, fat, and lactose in colostrum reduced.45 Cold, windy, and wet conditions also adversely affect calf survival. The magnitude of the effect of climate on neonatal survival depends on the age of the dam, the sex and size of the calf, and the incidence of dystocia in the herd.47 Cold stress sufficient to cause hypothermia in calves leads to subcutaneous hemorrhages and delayed absorption of colostral immunoglobulins.48 Fetal viability is rarely evaluated during the prepartum period in production animals but is a serious consideration when the prepartum dam is diseased or debilitated. Assessment of fetal viability is diagnostically challenging, but a number of methods are available to evaluate the fetus and fetal environment. During the physical examination of cattle, uterine blood flow, uterine tone, and presence of a vaginal discharge may be evaluated via rectal palpation and a vaginal speculum examination. Reduced fremitus in the uterine arteries and increased uterine tone may be appreciated by rectal palpation following fetal death. Abdominal ultrasound is useful for examining the uterus, placenta, and fetuses of small ruminants.49 When the gestational age of the fetus is known, fetal growth retardation can be detected by using ultrasound by measuring abdominal circumference as well as femur and tibial length.50 Examination of the fetus may detect gross congenital abnormalities, and ultrasound of the fetal chest allows visualization of a beating heart and determination of fetal heart rate. The normal heart rate of full-term lambs is 108 to 126 beats/min.51 After fetal death, the following may be observed: absence of fetal heartbeat, thickening of the uterine wall, increased echogenicity of chorioallantoic and amniotic fluid, altered fetal posture and definition, altered contour of the amnion, and reduced definition and ultimately reduced size of the caruncles. The uterus and placenta of cattle can be examined by transrectal ultrasound, but examination of the fetal calf via transrectal or transabdominal ultrasound is often compromised by limited access. Fortnightly ultrasound of the uterus and placenta of recipient cows carrying cloned calves is conducted to detect evidence of hydroallantois and placental edema in these high-risk pregnancies.52 The absence of fetal heartbeat is a specific sign of fetal death. The presence of large quantities of echoic particles in uterine fluids is also a sign of fetal distress or death. Fetal hyperactivity or inactivity over a 30-minute period of examination suggests fetal compromise.53 Repeated examinations are required since hyperactivity or sleeping periods have been infrequently observed in other species and the criteria for this classification are based on limited observations in cattle.54 Measuring the heart rate of fetal calves is more difficult than of small ruminants but can be achieved via transabdominal Doppler using a 1.5-MHz probe. The normal heart rate of full-term calves is 90 to 125 beats/min.55 In human medicine, fetal heart rate is used as a measure of fetal viability; fetal heart rate accelerations associated with fetal movement are considered a sign of fetal well-being, and persistent bradycardia or tachycardia are considered a sign of fetal stress.56 Normal fetal heart rate patterns of ruminants need to be characterized in more detail before fetal heart rate measurements are used for prenatal clinical assessment of ruminant fetal well-being.54,57 Estrone sulfate is a marker of a viable fetoplacental unit and has been used to assess fetal viability in cattle.58 Estrogen synthesized by embryonic tissue is converted to estrone sulfate by the endometrium, which contains the enzyme sulfotransferase. Estrone sulfate assays can be used to diagnose pregnancy in small ruminants after 50 days59 and in cattle after 100 days.60 Estrone sulfate may be measured in plasma or milk44,60; baseline values are low after fetal loss, regardless of the stage of pregnancy. Compromise of the fetoplacental unit reduces estrone sulfate production. In a study of the effects of heat stress on pregnant cattle, plasma estrone sulfate concentrations were significantly lower throughout pregnancy in cows that gave birth to low-birth-weight calves.44 Plasma concentrations of estrone sulfate rise slowly during the second trimester of pregnancy from 0.74 ng/mL to 3.66 ng/mL between day 90 and day 210 of pregnancy. The last trimester of pregnancy is associated with a rapid rise in the concentration of estrone sulfate to 13.36 ng/mL around 10 days prior to parturition.61 In human medicine, diagnosis of surfactant deficiency is based on the ratio of two phospholipids in amniotic fluid: lecithin (L) and sphingomyelin (S). If the L/S ratio is greater than 2.0, the surfactant system is mature and respiratory distress syndrome is rare.62 The L/S ratio in amniotic fluid collected from cattle may also be used to assess surfactant system maturity,63 thus providing a measure of readiness for birth, but is rarely used in clinical veterinary medicine. Crude surfactant harvested from bovine lungs at a slaughterhouse has been used intratracheally with calves that appeared to be in respiratory distress shortly after birth.64 Manipulation of parturition may be considered for maternal, fetal, or management reasons. Fetal viability following induced parturition is variable among species. The viability of calves induced within 14 days of anticipated calving date is good65; viability of lambs and kids induced greater than 5 days prior to anticipated parturition date is poor.17 Absorption of colostral immunoglobulins by premature calves is reduced, so colostral transfer should be monitored closely in induced neonates.66 Induction of parturition or cesarean section is often necessary to prevent mortality of small ruminants with pregnancy toxemia.67 Fetal viability is often improved by induction of parturition with dexamethasone; however, delivery of the fetuses via cesarean section is often necessary due to the debilitated state of the dam. Secretion of glucocorticoid hormones from the adrenal cortex increases markedly during the final days of gestation. The prenatal increase in fetal glucocorticoid secretion plays an important role in the cascade of endocrine events leading to parturition, and it stimulates maturational events in the lungs, liver, kidney, and gastrointestinal tract in preparation for postnatal life.68 Steroids stimulate production of surfactant phospholipids by alveolar type II cells, enhance the expression of surfactant-associated proteins, reduce microvascular permeability, and accelerate overall structural maturation of the lungs.69 Administration of flumethasone (10 mg) or dinoprost (25 mg) to pregnant cows 30 hours prior to elective cesarean section increases the lecithin-to-sphingomyelin ratio, thus improving lung function and reducing complications associated with respiratory acidosis in the calf.70 Induction of parturition has been used to reduce the incidence of dystocia in herds or breeds experiencing a high incidence of dystocia associated with fetomaternal disproportion.71 Large birth weights are strongly correlated with fetomaternal disproportion.72,73 Induction of parturition within 14 days of anticipated calving date is associated with good calf viability and a 3.2-kg reduction in birth weight of beef calves.65 Exogenous glucocorticoids, prostaglandin F2α (PGF2α), or a combination may be used to induce parturition in cattle (dexamethasone 20 to 30 mg alone or in combination with 25 mg of PGF2α) or in sheep and goats (10 to 20 mg dexamethasone and/or 15 mg PGF2α).17 Glucocorticoids are more effective than prostaglandin for inducing parturition in sheep.74 A lower incidence of dystocia and higher viability of calves has been reported in cattle induced with glucocorticoids compared with cows induced with prostaglandin.75 Cows treated with dexamethasone or prostaglandin within 14 days of the anticipated calving date usually calve within 72 hours of treatment.65 Combination of dexamethasone with prostaglandin increases the efficacy and reduces the interval to parturition (36 hours).76,77 Retention of fetal membranes is a common complication of induced parturition in cattle.78 Induction of parturition with dexamethasone causes a failure of immune-assisted detachment of the fetal membranes and the accompanying release of chemotactic factors.79 Retention of fetal membranes may be associated with reduced first-service conception and subsequent pregnancy rates.80 Treatment of cows with prostaglandin at calving was reported to reduce the incidence of retained fetal membranes,81 but subsequent studies failed to support this.76,82 Induction of cattle by administration of 25 mg of triamcinolone (Opticortinol) at day 270 followed by treatment with dexamethasone and prostaglandin 6 days later appears to reduce the incidence of retained fetal membranes associated with induction.78,83 Where calving induction is used to align calving patterns to pasture availability, cows are induced to calve at around 7 months’ gestation. Induced cows have increased rates of mastitis, metabolic disease, and retained placenta84,85 and have reduced milk production in the lactation of treatment.86,87 Calves born to cows induced at 7 months’ gestation are often stillborn, die, or are subject to euthanasia shortly after birth because they are too weak or suffer from other neonatal diseases.88,89
The Peripartum Ruminant
Late-Term Complications of Gestation
Uterine Torsion
Vaginal Prolapse
Ringwomb
Early Dilation Syndrome
Hydropic Conditions
Hydrops Allantois (Hydrallantois)
Hydrops Amnii (Hydramnios)
Characteristic
Hydrallantois
Hydramnios
Prevalence
85%-95%
5%-15%
Rate of development
Rapid (within 1 month)
Slow over several months
Shape of abdomen
Round and tense
Piriform, not tense
Transrectal detection of placentomes and fetus
Nonpalpable (tight uterus)
Palpable
Gross characteristics of fluid
Watery, clear, amber-colored transudate
Viscid, may contain meconium
Fetus
Small, normal
Malformed
Placenta
Adventitious
Normal
Refilling after trocarization
Rapid
Does not occur
Abnormal Offspring Syndrome
Maternal Nutrition
Environmental Management
Assessment of Fetal Viability.
Induction of Parturition
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
The Peripartum Ruminant
Chapter 18
