DYSTOCIA
The carefully synchronized physiologic changes occurring in both the maternal and fetal systems
during the final weeks prepartum are critical to ensure that labor and delivery proceeds with
minimal stress for both the cow and her calf. Factors that disrupt either the fetal or maternal
system may result in dystocia. Current strategies for minimizing dystocia have emphasized the
use of calving ease sires for high-risk females, especially nulliparous heifers. Despite the
increased availability of calving ease data for sire selection, there has been a decrease in the
percentage of unassisted births and an increase in the percentage of births requiring considerable
force or extreme difficulty over the last 5 years. During the same period of time, the stillbirth
rate has increased 10%, and there has been a 37% increase in calf mortality from birth to weaning
over the last five years (excluding stillbirths). Calf mortality is now estimated at nearly 20% of
all calves born (compared to ~15% mortality rate 5 y ago). Similar mortality rates in beef herds
are estimated to reduce net profit by approximately 38% without including the impact of calf loss
on potential rate of genetic progress.
The impact of dystocia on cow performance has been well-documented. For the dam, increased
calving difficulty is associated with decreased lactational performance (decreased yields of milk,
fat, and protein), decreased reproductive performance (increased services per conception and
days open), increased numbers of cow deaths, and increased risk of other periparturient
metabolic disorders. Even slight assistance at calving results in significant effects on these
parameters, however, the economic losses are greatest with extremely difficult deliveries.
The economic costs associated with dystocic calves are not as clearly understood. Calf mortality
increases with increasing calving difficulty, and exceeds 50% in the most difficult deliveries.
The economic losses associated with high mortality rates vary with genetic merit of the herd;
estimates in 1981 exceeded 132 million dollars. The losses associated with decreased
performance of calves surviving dystocic births have not been well documented. Calves stressed
at birth are hypoxic and acidotic with reduced immune competence with high morbidity and
mortality rates as they develop.
Research on dystocia has primarily focused on the potential for reducing the incidence through
breeding programs. The physiological changes occurring in the dam and her calf during a normal
parturition are thoroughly documented, but the processes that differentiate a normal from a
difficult delivery are not as well documented. An objective definition of a difficult delivery has
never been developed and(or) accepted by researchers. A physiological approach to
understanding and defining dystocia with the goal of reducing losses to the dairy industry is
critical for several reasons. First, the potential for a significant reduction in the incidence of
dystocia is realistically achievable in a relatively short time frame and the economic rewards are
substantial. Secondly, the recent increases in both the incidence of dystocia and in calf mortality
rates suggest that the industry is not currently addressing the problem in an effective manner.
CONSEQUENCES OF DYSTOCIA
Dystocia is defined as any abnormal or difficult delivery process, encompassing
malpresentations, prolonged parturitions, and difficulties due to inappropriate assistance.
Currently, over 20% of all births receive some form of obstetrical assistance. The scoring system
for calving ease currently in use by the dairy industry is a 5-point system, with a calving ease of 1
indicating no assistance was provided and a score of 5 indicating that extreme difficulty was
encountered during delivery. The subjective nature of the system creates some difficulty in
interpreting the data acquired. A calving ease score of 1 indicates that no assistance was
provided, but provides no assurance that it was not needed. Unobserved calvings are scored 1 by
definition. Additionally, a calving scored as a 5 may be due to a prolonged and difficult delivery,
an uncorrected malpresentation of the fetus, or inappropriate timing of assistance. Although the
calving ease score is the same in all cases, the physiological basis for the dystocia is not. Despite
the inconsistencies and the subjective nature of the scoring system, the data collected clearly
show significant effects of dystocia on most parameters measured. Reducing the variability
inherent in the current system would only magnify the differences, suggesting that current
estimates of losses due to dystocia are underestimating true losses.
The most recently published data regarding effects of dystocia on the dam show that economic
losses are incurred from several sources. Milk production decreases as calving ease score
increases. Losses exceed 700 kg of milk per 305-day milk production with a calving ease score
of 5, although significant losses are apparent with even slight assistance (calving ease score of 2).
Changes in milk components are similar to those seen for milk volume. Milk fat losses exceed 24
kg and protein losses exceed 20 kg with a calving ease score of 5 when compared to component
production of cows following a calving ease score of 1.
Reproductive performance of the dam following a dystocic delivery is also impaired. Services
per conception increase with increasing calving ease score, exceeding 0.2 for cows following a
calving ease score of 5. Calving ease scores of 5 are associated with increases in days open of
over 30 days, although as with lactational performance, significant decreases in reproductive
performance (e.g., increases in days open of over 7 d) are observed even at calving ease scores of
2 (slight assistance). These estimates on cow performance may underestimate true losses,
because the effect of the increased culling rate of dystocic cows is not included. Culling rates for
dystocic cows of up to 30% have been reported. Increased cow deaths are also seen with
increasing calving ease scores, with over 4% more cows dying after a calving ease score of 5 than
after unassisted calvings. Field reports suggest the maternal death rate is highest when dystocia
is due to incomplete cervical dilation.
Increases in metabolic disorders and other periparturient disorders also occur at a much greater
frequency in dystocic cows. Dystocia is a significant risk factor for both mastitis and lameness
diagnosed before first service. Dystocia is associated with 2-fold increases in the risk of milk
fever, 3-fold increases in cystic ovaries, over 2-fold increases in the risk for left-displaced
abomasum, and 2- to 3-fold increases in retained placenta and metritis. The increase in several
of these metabolic disorders was present even following slight assistance. In most cases, the
difference between an unassisted calving and a calving where slight assistance is rendered has
more to do with the patience of the calving attendant than the needs of the cow. The impaired
performance and increased incidence in metabolic disorders of cows following only slight
assistance at calving may indicate that assistance itself is inducing the observed effects.
Losses associated with the calf are less well documented. Estimates of the percentage of calf
mortality attributable to stress at parturition range from 70% to 98%. Increases in calf mortality
occur with increasing calving ease scores. Nearly 50% of calves are stillborn following a birth
with a calving ease score of 5, with more of these calves dying by 48 h of age. It is important to
note that calf mortality is increased even with slight assistance at calving.
Most calf deaths are associated with perinatal asphyxia, although a surprisingly high number are
associated with trauma, suggesting that inappropriate timing of assistance or excessive force
during assistance also contributes to calf losses. A European study reported that 40% of stillborn
calves from veterinary-assisted deliveries had fractured ribs and 10% had fractured vertebra, with
heifers suffering more traumatic damage at the same force or calving difficulty than bulls. In
addition, there may be a genetic component influencing susceptibility to fractures during
parturition. As little as 275 kg of force will fracture long bones of neonatal calves, and this force
is exceeded easily by mechanical calf extractors or even by forceful manual extractions. The
amount of force required for extraction is dependent on many factors, including the size of the
calf, the size of the pelvis, dilation of the cervix, and relaxation of the musculature surrounding
the birth canal. In addition, less force is required for extraction if simultaneous traction is
applied to both forelimbs relative to that required for alternate traction of forelimbs. Fractures
due to forceful extraction have been reported by other investigators, and most traumatic injuries
are suspected to remain undiagnosed. Tracheal collapse typically occurs in calves older than one
week of age as a consequence of assisted delivery, and is easily misdiagnosed. Rupture of the
liver may occur as a direct result of compression during delivery, although death may not occur
for 12 to 24 h. Most investigators recommend extreme caution and restraint in providing
obstetrical assistance. By contrast, early obstetrical assistance in Hereford cows was reported to
improve subsequent reproductive performance in the cows and improve growth rates of assisted
calves.
Perinatal trauma and(or) asphyxia also have consequences for those calves surviving a dystocic
birth. Prolonged intermittent hypoxia, as would be expected to occur as a result of repeated
umbilical cord compressions during stage 2 labor, appears to be more damaging to the animal
than the same duration of continuous hypoxia, although most damage to the central nervous
system probably occurs as a result of oxygen free radical generation during the reventilation
period after birth. Delivery-associated bradycardia and subsequent decreases in umbilical oxygen
tension only occur with the onset of abdominal contractions during stage 2 labor. Heart rate
decelerations occur in conjunction with uterine contractions; decelerations in heart rate
continuing beyond the end of a contraction are indicative of fetal distress. The hypoxia
associated with dystocia also blunts the ventilatory response to hypercapnia after birth and may
inhibit initiation of spontaneous respiration. Calf survival and(or) severity of the hypoxic insult
to the calf at parturition is associated with the number, size, and weight of the cotyledons present
in the placenta. Severe hypoxia during delivery results in both discharge of meconium into
amniotic fluid and gasping movements by the fetus. Muscular contractions associated with
anoxia-induced gasping may be intense enough to fracture vertebrae. In addition, inspiration of
the meconium-contaminated amniotic fluid during gasping results in meconium aspiration
syndrome in calves postnatally. Meconium coats the alveoli, impairing gas exchange postnatally
and consequently increasing the duration and severity of acidosis in these calves. Hemorrhage
sites are apparent in many vital organs, including heart, thymus, spleen and the central nervous
system. More than 40% of asphyctic calves die by 3 wk of age, and morbidity rate is 2.4-fold
higher in dystocic calves during the first 45 days of life. In addition, calves requiring assistance
at birth are sick at a younger age than calves not requiring assistance at birth.
Factors that delay the development of homeostasis in neonatal calves often severely reduce their
chances for survival. Dystocia suppresses non-shivering thermogenesis, and decreased heat
production and increased heat loss occurs in dystocic calves through the first day of life. This is
due in part to decreased mobilization of lipid stores and decreased concentrations of plasma
thyroid hormone, and directly related to degree of acidosis present at birth. In addition, hypoxia
decreases both shivering and non-shivering thermogenesis in newborn. Inability to
thermoregulate severely compromises survivability of neonatal calves, especially during cold or
windy conditions. Dystocic calves quickly become hypoglycemic in response to cold stress,
while eutocic calves have increased concentrations of blood glucose under the same conditions.
Similar decreases in core body temperature are common in asphyxiated piglets and have been
associated with an increased incidence of necrotic bowel lesions.
Dystocic calves are acidotic, hypoxic, and clinically abnormal following birth. Numerous reports
have suggested that the normal newborn exhibits a mixed state of metabolic and respiratory
acidosis. Arterial blood [H+] in dystocic calves is 6.7 x 10-8 as compared to [H+] of 5.0 x 10-8 in
eutocic calves, although values for arterial Pco2 are not different between dystocic and eutocic
calves, possibly due to the subjectivity of the scoring system. Concentrations of hemoglobin are
decreased in dystocic calves; similarly, arterial oxygen tension is 32 mm Hg in dystocic calves at
birth and 41 mm Hg in their eutocic counterparts. Most abnormal physiological parameters in
dystocic calves reach normal values by 16 h of age, however, concentrations of hemoglobin and
oxygen tension remain low; as a result, total oxygen content is significantly decreased.
Interestingly, although 36-h means for heart rate, respiration rate, and rectal temperature were not
different, within-calf variability for these parameters were significantly different suggesting
possible defects in homeostatic regulation.
Stressed calves demonstrate delayed behavioral adaptations, irregular respiration rates, and
failure to thermoregulate; these same clinical problems were reported as responses to premature
rupture of the umbilical vessels in both foals and lambs. Premature rupture resulted in a loss of
~1500 ml of placental blood in foals, roughly 30% of the total blood volume at birth. The
decreased blood volume was theorized to result in decreased ability to perfuse vital organs,
especially the pulmonary system and the central nervous system, inducing many of the clinical
outcomes observed in these neonates. Blood flow continues through the placenta for
approximately 1.5 min after the first breath; constriction of umbilical vessels and stoppage of
placental flow (as well as initiation of placental separation) is initiated primarily by the change in
oxygen tension associated with the shift from placental to pulmonary respiration. Transfer of
placental blood into the fetal system is not complete until this umbilical constriction occurs.
Delayed umbilical cord clamping in premature infants results in increased packed cell volume
and arterial-alveolar oxygen tension differences and decreased reliance on supplemental oxygen.
In dairy cattle, the relatively short umbilical cord often ruptures as the hind legs are expelled
from the birth canal. Since all stressed calves in these experiments were assisted by definition,
and because the assistance process ruptures the umbilical cord prematurely, some of the problems
encountered by dystocic calves may be a result of improper assistance during delivery.
Dystocic calves often suffer from failure of passive transfer of immunity. Despite early
speculation to the contrary, this is not a consequence of altered glucocortioid concentration in
dystocic calves. Although severe, chronic hypoxia may alter rates of immunoglobulin
absorption, failure of passive transfer is primarily due to diminished maternal behavior by the
dam and delayed time to suckling in the calf rather than a diminished ability to absorb colostral
immunoglobulins. Voluntary consumption of colostrum is reduced by 74% during the first 12 h
following a dystocic delivery, however, dystocic calves that are force-fed equal quantities of
pooled colostrum have an equal absorptive capacity to eutocic calves. A study on management
factors contributing to calf mortality reported the highest mortality rates for dystocic calves that
were allowed to suckle their dams; mortality rates were reduced by practicing assisted suckling
or supplemental colostrum feeding.
Other components of the immune system and other consequences of dystocia may also contribute
to the increased susceptibility to disease. Glucocorticoids are potent suppressors of immune
function; some researchers have reported increased concentrations of glucocorticoids in dystocic
calves, although others have reported that glucocorticoids are decreased following a dystocic
delivery. Impaired neutrophil adherance, chemotaxis, and bactericidal activity have all been
demonstrated following a stressful birth in infants; these defects appear to be in part a
consequence of damage to cell membranes by oxygen free radicals. Neonatal hypoxia may also
impair respiratory burst directly; decreases in oxygen tension within physiological limits has been
shown to decrease the concentrations of oxygen free radicals produced by stimulated neutrophils.
In addition, neonatal hypoxia may have long-term effects on immune function. Neonatal rats
maintained in a hypoxic environment for the first week of life produced decreased amounts of
serum antibodies following sequential immunization at 9 wk postpartum; functional killing
ability of macrophages and neutrophils was also impaired.
FACTORS ASSOCIATED WITH DYSTOCIA
Many sources of variation in the incidence of dystocia have been identified; several have been
assumed to be causes of dystocia despite a lack of conclusive scientific evidence. Events
occurring as early as the first few days following conception may influence the parturition
process. Several assisted reproductive technologies, including in vitro fertilization and nuclear
transfer cloning, increase the incidence of dystocia and stillbirths in subsequent pregnancies. The
extent of this effect is dependent on the culture media used during embryo development and the
degree of manipulation of the embryo. In many cases, it appears that the increased incidence of
dystocia is associated with extended gestation lengths and abnormal fetoplacental development.
The number of placentomes is decreased, suggesting the potential for impaired blood supply to
the fetus. In addition, it has been suggested that IVF-derived calves also have an increased
susceptibility to infection postnatally leading to higher than normal postnatal mortality rates.
The sex of the fetus also affects the incidence of dystocia. Male calves have a higher incidence
of dystocia than female calves. This may be an effect of prolonged maternal exposure to fetal
testosterone production, although most researchers have assumed that male calves have more
difficulty simply because they are slightly larger at birth than their female counterparts.
Although many body dimensions are increased in male calves, none show a significant
relationship with dystocia when birthweight is included in the analysis as a covariable. The
incidence of dystocia increases 2.3% for every 1 kg increase in birth weight, however, the gender
effect is still apparent even when birth weights are equivalent. Interestingly, birth weights of
calves born from right horn pregnancies are significantly heavier than those born from left horn
pregnancies, although the effect of this difference on the incidence of dystocia has not been
examined. Excessive birth weight is often suggested to be the primary cause of dystocia,
although very small calves also have an increased incidence of dystocia relative to that seen in
more moderately sized calves. In addition, inbreeding decreases birth weight while increasing the
incidence of dystocia.
Many researchers have argued that dystocia is not simply a function of birth weight, but is a
function of the relationship between birth weight of the calf and pelvic size of the dam
(fetopelvic incompatibility). While the association between fetopelvic incompatibility and
dystocia is clear from many studies, the role of this incompatibility as a cause of dystocia has
never been established. In addition, fetopelvic incompatibility has not been associated with
dystocia in dairy animals in controlled studies, although it is often reported as a primary factor in
case studies. Accuracy of pelvic measurements is also questionable; measurements taken by
several technicians on the same animals in a controlled study were significantly different and the
predictive power of measurements taken at any time prior to calving for pelvic size at calving is
extremely poor. Fetopelvic incompatibility has shown very limited usefulness as a predictive tool
for managing dystocia; well over two-thirds of those heifers predicted to have difficult deliveries
actually require no assistance, and over 25% of dystocic deliveries are not detected.
Other factors associated with the dam include body weight, parity (first calf heifers have a much
greater chance of having a prolonged or difficult parturition while dystocia in multiparous cows
is more often associated with malpresentation of the fetus), and age at first calving (young heifers
have more difficulty). Although overfed, obese cattle have greater difficulty calving and a
greater incidence of fetal malpresentations at delivery, lead feeding in dairy cattle is associated
with a decreased incidence of dystocia. Obesity-induced dystocia is primarily associated with
excessive deposition of fat around the reproductive tract rather than fetal oversize. Severe energy
restriction of heifers decreases calf birth weight but increases the incidence of dystocia; by
contrast, less severe long-term energy restriction decreases calf birth weight but has no effect on
the rate of dystocia.
Several studies confirm that dystocic cows have altered concentrations of progesterone and
estrogen in the prepartum period compared to non-dystocic, and reduced estrone sulfate
concentrations during the final 10 days of gestation may be associated with reduced cotyledonary
surface area and decreased viability of the newborn calf. These should not be interpreted as true
dam effects, however, as the fetus influences the endocrine responses of the dam. Although
cortisol increases prior to and during parturition in all cows, and is highest following a dystocic
delivery, whether high cortisol is a factor in causing dystocia or only a response to the stress of a
difficult delivery has yet to be determined. Additionally, placental and cervical prostaglandin
synthesis may contribute to both the incidence of dystocia and the associated high incidence of
retained placentae. Prostaglandins are important in controlling cervical softening at parturition
and placental prostaglandin biosynthesis is decreased in cows experiencing retained placentae.
Calving ease scores of first and second parity cows are highly correlated with calving ease scores
of the same cows for their next calving, suggesting that maternal effects influence the process of
parturition independently of the sire effects. Similar repeatability estimates were reported in
Herefords. Although maternal effects are evident, breeding strategies for improving calving ease
have focused on sire selection. The primary focus of dairy herd breeding programs over the last
40 years has been milk production. Early studies demonstrated that although selection for high
milk production extends gestation length, it does not alter birthweight, suggesting that selection
strategies for increased milk production is not necessarily linked to dystocia. Sire selection for
calving ease tends to reduce birthweight of the resulting calves, and concerns have appeared in
the literature that these small calves will become small cows at increased risk for dystocia. These
concerns may have limited the use of calving ease sires in problem herds. However, studies
designed to test this hypothesis showed that while small calves become small cows and large
calves become large cows, calves born from difficult deliveries tended to have a higher incidence
of dystocia as cows than their unassisted counterparts. Daughter-dam heritability as a trait of the
dam was estimated at .24, suggesting that mature body size is less important than other maternal
traits. In addition, calves born from sires with low calving ease scores have less calving
difficulty as cows than those born from sires with high scores. Sire effects also are the most
important influence on the incidence of dystocia due to malpresentation, while calculated
heritabilities for malpresentations as traits of the dam and repeatabilities are low. Twice as many
bull calves present abnormally at delivery, and malpresentations are more commonly observed in
3 and 4 year old cows than in 2 year old cows. More than 2/3 of malpresentations in Angus and
Hereford cattle occur as posterior presentations, with true breech presentations comprising only
10% of total malpresentations.
Some of the factors that cause dystocia may be breed-specific. Holsteins have the highest
incidence of dystocia of any dairy breed; they also have the highest ratio of calf birth weight:dam
body weight (averaging 7.1% and often over 10%). By contrast, Jerseys rarely have prolonged or
difficult deliveries except in cases of malpresentation; their calf weight:dam weight ratio
averages 5.6 to 6.3% and rarely exceeds 8%. Breeding a Holstein sire to a Jersey dam results in
a lower incidence of dystocia relative to purebred Holsteins despite the smaller size of the dam
and increased calf birth weight:dam body weight. Maternal or (presumably uterine) constraints
on fetal growth are important, but can be at least partially overridden by sire effects.
Environmental effects provide an additional complication in interpreting the literature. Although
the incidence of dystocia is highly variable over time, the highest incidence rates occur in late fall
and winter periods. There are many potential explanations for this phenomenon, although one
intriguing possibility is an effect of heat stress on placental development. Exposure to high
environmental temperatures during mid-gestation or during the third trimester restricts placental
development and depresses fetal development to term. Likewise, higher stillbirth rates for
summer-born calves (during periods of lower rates of dystocia) may be heat stress related.
Adenosine stimulates respiration during periods of hypoxia, and has been suggested to be
important in initiation of respiration at birth, but adenosine suppresses respiratory efforts during
heat stress. Additionally, a 15-fold increase in sudden death syndrome is reported in infants
sleeping in overheated rooms compared to those sleeping in the same position in cooler rooms.
Many reports have also suggested that temperament of the cow may influence the process of
parturition, with veterinary practitioners reporting that stresses or inappropriate assistance during
calving causes spasm or constriction of the constrictor vestibuli muscle surrounding the vulva,
leading to vulvular stenosis. Vulvular stenosis has been reported to be a cause of severe dystocia.
Additionally, both stress and epinephrine decrease uterine motility around the time of parturition,
potentially prolonging the length of labor. Moving range cattle not accustomed to isolation into
restrictive maternity stalls prior to parturition increased the incidence of dystocia several-fold
compared to their pasture-calved herdmates; this increase was reported to be a consequence of
irregular labor and vulvular stenosis. A stress-free, familiar calving environment may be
important for the normal progress of parturition. Beef herds with higher frequency of
observation had an increased frequency of dystocia and higher rate of calf mortality, suggesting
that management errors and(or) inappropriate assistance was a major factor in determining the
incidence of dystocia.
CONCLUSION
Despite the increasing availability of sire evaluations for calving ease, trends for both the
incidence of dystocia and for stillbirth rates in calves suggest that losses to the industry are
increasing rather than decreasing. The percentage of unassisted births is approximately 6% lower
over the period from 1991-1996 than for the preceding 5-year period. This could be taken as an
indication of increased awareness by producers at parturition, however, during the last five years
there has been an increase of over 15% in the incidence of calvings requiring considerable force
or extreme difficulty as well as a 13.2% increase in stillbirth rate. Mortality rates from birth to
weaning, excluding stillbirths, have increased from 8% to over 11%. The average predicted
difficult first calvings for daughters of Holstein sires also increased during the same period.
Taken together, these data suggest a real trend for an increasing rate of dystocia and dystociarelated losses in the Holstein population. Research to determine the physiological basis of
dystocia is necessary to reverse these trends. An objective set of criteria for both the timing and
intensity of obstetrical assistance based on outcomes of both the dam and her calf are critical to
developing a scientifically valid and repeatable database.