Perinatal Adaptation
At birth the fetus must successfully make a series of structural and physiologic changes to survive. Perinatal mortality is often attributable to cardiovascular, pulmonary, thermoregulatory, or metabolic physiologic abnormalities.
Dystocia and severe birth asphyxia compromises physiologic transitions, increasing the risk of neonatal mortality. Compromised neonates that survive the birth process are less likely to consume adequate colostrum and are subsequently more likely to die of hypothermia and infectious diseases.The placenta functions as the respiratory organ of the developing fetus, and efficiency of oxygen transfer to the fetus is increased by the high oxygen affinity of fetal versus adult hemoglobin.96 In utero the potential spaces of alveoli and the tracheobronchial tree are distended with fluid secreted by pulmonary tissue.97 Oxygenated blood is delivered to the fetus via the umbilical vein, which anastomoses with the portal vein near the liver, and approximately two thirds of the blood flow is shunted via the ductus venosus directly into the caudal vena cava.98 The caudal vena cava drains into the right atrium, where over 50% of the volume shunts directly into the left atrium via the foramen ovale.98 The relatively hypoxic in utero environment causes constriction of pulmonary vessels and dilation of the ductus arteriosus.98 Because pulmonary arterial resistance is higher than systemic arterial resistance, nearly 70% of pulmonary artery flow is shunted via the ductus arteriosus into the aorta, with the remainder perfusing the lung.99 Left ventricular output is distributed to the systemic circulation via the aorta. Two umbilical arteries arise from the aorta in the region of the last lumbar vertebra to carry predominantly venous blood back to the placenta via the umbilicus.
At birth some of the lung fluid is evacuated through the trachea during spontaneous delivery.100 When the umbilicus ruptures, asphyxia triggers reflex gasping, respiratory movements, and increased peripheral vascular resistance.99 The majority of lung fluid is absorbed through alveolar walls in the initial stages of ventilation.100 This mechanism is prompted by activation of adrenaline-mediated α-adrenergic receptors in the pulmonary epithelium.101 The rapidity of lung fluid absorption by the body is optimized at thoracic pressures between 35 and 40 cm H2O.100 Pulmonary ventilation reduces pulmonary vascular resistance, promoting perfusion of the ventilated alveolar tissue.98 The increased O2 saturation of blood stimulates closure of the ductus arteriosus within 4 to 5 minutes of birth.99 The foramen ovale functionally closes within 5 to 20 minutes of birth when increased pulmonary venous return raises blood pressure in the left atrium, reversing the right to left shunt.99 The septum secundum, a thin fold of tissue that lies in close apposition to the foramen, acts as a valve closing the opening. Healthy calves have mean pulmonary arterial pressures ranging from 40 to 82 mm Hg immediately after birth, declining to 22 to 25 mm Hg by 2 weeks of age.102 Systemic arterial pressure is approximately 100 mm Hg, and arterial saturation is greater than 90%.98 Transient mild metabolic and respiratory acidosis are observed following rupture of the umbilical cord due to anaerobic glycolysis in poorly perfused tissues during the transition between placental oxygen delivery
■ TABLE 18.2
Arterial and Venous Blood Gas Values for Newborn Calves
| Parameters | ||||||
| Calf Age | pH | pO2 | pCO2 | HCO3 | Base Excess | |
| Venousa | 1 hour | 7.219 (0.05) | N/A | 41.0 (5.9) | 24.2 (2.7) | -2.9 (3.2) |
| Arterialb | 1 hour | 7.3 (0.05) | 58.43 (11.61) | 50.40 (5.27) | 23.52 (2.78) | N/A |
aBlood was taken from the brachial artery while the calf was in lateral recumbency (N = 30).164
bBlood taken from the jugular vein immediately postpartum.103 Values represent mean with standard deviation parenthesis.
N/A, Not available.and establishment of respiratory function. The mild acidosis is normally corrected within 1 to 4 hours of birth.103 Anatomic closure of the foramen ovale and ductus arteriosus may take several weeks.99 Normal blood gas values for the calf during the immediate postpartum period are presented in Table 18.2.
Dystocia is commonly associated with prolonged hypoxia and acidosis. Hypoxia and acidosis maintains constriction of pulmonary arterioles, and the subsequent maintenance of high pulmonary vascular resistance favors continuation of in utero right to left vascular shunts, which contributes to systemic hypoxia. Following dystocia, neonates are less active, slow to stand, slow to nurse, and prone to hypothermia and hypogammaglobulinemia. The normal duration of stage 2 labor (from appearance of fetal membranes at the vulva to delivery of the fetus) in ruminants is generally shorter in multiparous animals (≈30 minutes) than primiparous animals (≈60 minutes).104 Fetal viability is improved with early intervention; multiparous animals should be assisted after 30 to 60 minutes of stage 2 labor and primiparous animals after 60 to 90 minutes.79
The range in ambient temperatures over which newborn animals are able to maintain homeothermy is much narrower than growing or adult animals. Neonates are more susceptible to fluctuations in environmental temperature due to their large surface area to mass, evaporation of amniotic fluid, and limited caloric reserves. Starvation and hypothermia is the second leading cause of death of neonatal lambs.3 Neonatal mortality increases with decreasing ambient temperature and with increasing precipitation on the day of birth.53 Thermoneutrality is maintained by shivering and metabolism of brown adipose tissue. Normally at birth, blood glucose concentration in calves ranges between 50 and 60 g/dL, rising to 100 mg/dL within the first 24 hours of life.98 Lambs born in warm weather can survive for up to 4 days without supplemental nutrition.
Severe weather stress may increase energy requirements by 500% and deplete the energy reserves of newborn lambs in 6 to 16 hours.105 Starvation exacerbates the effects of environmental stress by reducing the available substrates for heat production, and energy depletion leads to hypoglycemia. Administration of glucose to hypothermic neonates before and during warming is important to avoid deaths from cerebral hypoglycemia induced by increased utilization of glucose by peripheral tissues.106 Warming hypothermic lambs by immersion in 38° C water is more efficient than infrared lamps or wrapping the lamb in a cotton cloth.107No intrauterine transfer of immunoglobulin occurs in ruminants; hence, at birth, neonatal ruminants are agammaglobulinemic and immunologically naive. Infectious disease is the leading cause of morbidity and mortality in calves greater than 3 days of age.108 Failure of passive transfer increases the risk of neonatal mortality.109 Colostrum provides a concentrate source of energy and immunoglobulins. Immunoglobulins are concentrated in colostrum by an active, receptor-mediated transfer of IgG1 from the blood of the dam across the mammary gland secretory epithelium beginning several weeks before parturition.110 Colostral IgG1 concentrations may be 5 to 10 times the maternal serum concentrations. IgM, IgA, and IgG2 concentrations in colostrum are much lower.111 The large numbers of leukocytes also contribute to providing passive immunity to the newborn.112 Methods of assessing passive transfer and management of failure of passive transfer are discussed in detail in Chapter 19.
Dystocia
Forty to sixty percent of stillbirths are associated with dystocia. Calves that survive dystocia are more likely to have edema of the head and tongue, making suckling difficult. They are also weak and exhausted and likely to be recumbent for a longer period of time and expose themselves to more fecal pathogens.113 Dystocia affects the uptake of immunoglobulins by the calf, and calves that survive dystocia are more likely to become sick in the first 45 days of life.114 Maternal variables correlated with dystocia and consequently calf mortality at birth include parity and conformation.
Dystocia and stillbirths in heifers is most commonly secondary to fetopelvic incompatibility. Fetopelvic incompatibility accounts for a lower proportion of dystocias in multiparous cows, but weak labor secondary to hypocalcemia, uterine torsion, and incomplete cervical dilation are more common in older cows.44 The prevalence of stillbirths in dairy herds globally is reported to be increasing.1 In the U.S. dairy industry the incidence is currently 8% (11.3% in primiparae and 5.3% in pluriparae).115 Dam pelvic diameter is an important determinant of dystocia for heifers.116 Pelvic measurements can be used to identify abnormally small or abnormally shaped pelvises. Large frame size of the dam correlates with a reduced risk of dystocia; however, continued selection for large frame size tends to select for larger birth weight and dimensions of calves.117 Age at first calving for heifers is not correlated with risk of dystocia as long as heifers are fed and managed to achieve appropriate growth and stature before calving.118-120 The risk of dystocia in heifers is increased by poor nutrition in the last trimester.121 Appropriate nutrition and management of replacement heifers to achieve appropriate size and stature at parturition reduce maternal and neonatal losses by reducing the incidence of dystocias. Maternal consequences associated with calving difficulty and delivery of a stillborn calf include decreased milk production and reduced reproductive efficiency. Reductions in milk production ranging from 100 to 400 kg have been reported to be associated with the birth of a stillborn calf. If the stillborn calf is delivered by cesarean section, the reduction in milk yield is on the order of 300 to 500 kg.122 Delivery of a stillborn calf is also associated with depressed conception rates, increased services per conception, and delayed conception.Use of calving ease bulls over primiparous cows helps to reduce the incidence of dystocia and subsequently mortality during parturition.
The heritability of calving ease is relatively low; estimates of maternal calving ease range from 0.03 to 0.24,44,123,124 and paternal heritability is around 0.147. Despite the relatively low heritability of calving ease, selection for calving ease should not adversely affect other production parameters in dairy cattle as the genetic correlation between calving ease and other dairy production traits is generally close to 0.44 Calving ease evaluations are intended to increase the use of AI for heifers. To facilitate sire selection, most breed associations provide guidelines regarding calving ease or expected progeny difference for calf birth weights. An example of such a scheme is the calving ease and reliability values assigned to AI Holstein bulls. In this system the calving ease score is the expected percentage of difficult births predicted for calves delivered by primiparous cows.125 The reliability score provides an indication as to the number of births that were considered in deriving the calving ease score. The higher the reliability score, the larger the number of observations the calving ease score is based on and the more likely it is that the calving ease prediction will accurately reflect the outcome.Management variables that influence the risk of dystocia and perinatal mortality include stocking density of preparturient cows, timing of calving, and cow grouping. In a study of 123 beef herds, the dystocia rate was highest for cows housed in a barn and decreased progressively through barn/yard, barn/ pasture, and pasture-only calving location categories.126 The most common cause of dystocia in penned heifers was vulvar constriction, while dystocias in paddocked heifers were most commonly associated with malpresentations.127 Calving beef heifers 6 weeks before cows has been recommended to allow the heifers longer to recover and conceive after calving than cows.128 In a herd-level comparative study, this practice was associated with a higher incidence of dystocia and stillborn calves.126 Heifer dystocia rate is reduced the longer heifers are maintained as a separate group from cows before calving.126
Fetal variables that influence the risk of mortality include sex, size, and number. Calves born to primiparous cows, twins, and bull calves are more likely to die at birth than calves born r I* "i i ιι*r i 53129
from multiparous cows, single calves, and heifer calves. , Low- and high-birth-weight calves are at greater risk of mortality than average-birth-weight calves.53 Small calves experience greatest mortality at parities greater than one.118 Large-birthweight calves have greatest risk of mortality when delivered by heifers. Statistical modeling suggests that for every 1 kg increase in body weight, there is a 13% increased probability of dystocia.130 Compared with other dairy breeds, Holsteins have the highest ratio of calf birth weight to dam body weight, averaging 7.1%.131 Holstein cows subsequently have the highest incidence of dystocia.130,131 Fetal viability may be compromised in utero by a number of infectious agents. Common infectious agents associated with abortion and or birth of weak calves are listed in Box 18.1. Manifestations of disease in the newborn are dependent on the time of exposure to the infectious agent.
Peripartum Assessment of Fetal Vitality
During parturition fetal reflexes can be assessed to ascertain appreciable signs of life. The interdigital, bulbar, and swallowing reflexes can be assessed in calves presenting in an anterior presentation. The interdigital and anal reflex and pulse in the umbilical cord can be evaluated in calves presenting in a 132
posterior presentation.132 Depressed responsiveness is a feature of impaired acid-base status. An increasing proportion of calves fail to respond as the severity of the acidosis increases. Failure to elicit reflexes is not confirmatory of fetal death as an absence of reflexes has been observed in severely acidotic live calves.133 Six percent of fetuses with no reflexes intrapartum are normal at the time of delivery.134
Criteria commonly used to assess the vitality of the newborn calf are presented in Table 18.3. Timely assessment of the newborn calf is indicated as two thirds of perinatal mortality occur within an hour of birth and 95% of this loss occurs within 5 minutes of birth.135 Abnormal neonatal behavior in the immediate postnatal period is commonly secondary to perinatal hypoxia and a combination of metabolic and respiratory acidosis. Traditional Apgar parameters, heart rate, respiratory rate, and mucous membrane color, are not predictive of acidemia in newborn calves.136 Depressed tongue withdrawal and weak suck reflex are correlated with perinatal acidemia in calves.136
Calves and lambs normally have a head righting reflex almost immediately after birth. Sternal recumbency is usually attained within 2 to 4 minutes followed rapidly by attempts to stand, at 10 to 20 minutes for lambs and 15 to 30 minutes for calves.137-139 Failure for calves to achieve sternal recumbency within 15 minutes of birth is highly predictive (84%) of compromised vitality and risk of mortality.139 Hypoxic neonates may struggle and appear bright initially but have difficulty maintaining sternal recumbency, have depressed or absent suck reflex, are slow to stand or remain recumbent, and develop a depressed mentation within hours. Hypoxic calves can also have an impaired 140 response to environmental stressors such as cold temperature.140 Reduced muscle tonicity prevents shivering,141 and the metabolic activity of brown adipose tissue may be reduced, compromising nonshivering thermogenesis.142 Furthermore, calves with low vitality have a limited ability to generate heat through natural physical behavior, and delayed colostrum ingestion may limit the energy available to generate heat.131
■ TABLE 18.3
Assessing the Newborn Calf
| Criterion | Good Vitality | Poor Vitality |
| Respiration | 50-75 bpm and thoracic breathing | Gasping; primary apnea; irregular, abdominal breathing; bellowing and secondary apnea |
| Hair coat appearance | Placental fluid covered | Meconium stained |
| Peripheral edema | None | Capital, lingual, or limb edema |
| Mucous membranes | Pink and normal capillary refill time | Cyanotic, pale, and slow capillary refill time |
| Response to reflex stimulation | Vigorous head shake; strong corneal, suck, or pedal reflex | Weak or no response |
| Muscle tone | Active with head-righting within minutes | Inactivity and flaccid musculature |
| Heart rate | 100-150 bpm and regular | >150 bpm followed by bradycardia (or no attempts to suckle |
From Mee JF: Managing the calf at calving time. In Proceedings of the 41st Annual Conference American Association of Bovine Practitioners, Charlotte, NC, 2008, p 46.
The normal heart rate of calves is between 100 and 150 bpm immediately after birth. Heart rate normally stabilizes within minutes of calving, but in at-risk calves peripartal tachycardia (>150 bpm) is followed by a declining bradycardia.132 Following experimentally induced hypoxia, nonviable hypoxic calves had similar heart rates (118 ± 36 bpm) and body temperatures (39.6 ± 0.2° C) as viable calves but lower respiratory rates (14 and 18 vs. normal 49 ± 12).137 The rectal temperature of a normal newborn calf is higher than normal at calving 102° F to 104° F (39° C to 40° C) and gradually drops to normal within 3 to 5 hours. Calves that experience a protracted, difficult calving may experience hyperthermia (>103° F, >39.5° C) at birth, which drops in the hours following birth and is slow to return to normal.132
The normal time taken to stand and nurse varies between species and breeds. The average time from birth to standing and nursing for beef calves is 35 and 81 minutes, respectively. Dairy calves are more variable and take approximately twice as long.143 A high prevalence of delayed first sucklings has been reported among dairy calves. Failure of the newborn to nurse may result from reduced neonatal vigor, poor mothering, poor maternal conformation, or adverse conditions such as slippery flooring.144 Calves have difficulty locating teats on low slung udders (Meyer CL, Berger PJ, Koehler KJ: Interactions among factors affecting stillbirths in Holstein cattle in the United States, J Dairy Sci 83:2657, 2000.
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