PERINATAL MORTALITY IN BEEF HERDS 0749-0720/94 $0.00 + .

20

DYSTOCIA-RELATED
RISK FACTORS
Lawrence E. Rice, DVM, MS

An extensive study of perinatal and neonatal losses in beef cattle

identified that 69% of all calf deaths between birth and weaning occurred
within the first 96 hours after birth.53 Based upon gross necropsy lesions,
64% of these losses were attributed to dystocia. The impact of dystocia on
overall calf mortality is even more dramatic if figures include the number of
stillborn calves that have no significant gross lesions but probably die of
acidosis and anoxia during or immediately after birth.58, 74, 75, 77 Other
reports indicate a similar importance of dystocia in calf death loss in beef
37
herds. , 41, 81
European Economic Community figures indicate that annual calf
mortality due to problem births in beef breeds varies between 1.8% and
43
9.4%. Furthermore, selection of cattle for increased muscularity has caused a
steady rise in the frequency of dystocia. Direct economic losses can be
estimated from such figures but indirect monetary losses are more difficult to
assess with respect to dam infertility, decreased dam and calf performance,
increased calf morbidity and mortality from subsequent disease that would be
observed in surviving but injured calves, and depressed calves that become
hypogammaglobulinemic because of inad-equate or delayed colostrum
absorption. This article reviews parturition, the causes and effects of dystocia,
and the management procedures sug-gested to reduce the incidence of dystocia
and the losses it causes.

CAUSES OF DYSTOCIA
Direct Factors
Incompatibility in the sizes of the fetus and dam's pelvis is the single
42
most important cause of dystocia in beef cattle. , 55, 81 The second most
From the Boren Veterinary Medical Teaching Hospital, Department of Medicine and Sur-
gery, Oklahoma State University, College of Veterinary Medicine, Stillwater, Okla-homa

VETERINARY CLINICS OF NORTH AMERICA: FOOD ANIMAL PRACTICE

VOLUME 10 • NUMBER 1 • MARCH 1994 53

54 RICE

commonly reported cause is abnormal presentation, position, or posture of the

fetus in utero. In some instances, this category was responsible for the greatest
41
number of dystocias. , 62 In first-calf heifers, vulvar constric-tion can be
another important cause of dystocia. In these cases, birth weight of the fetus was
not considered excessive and, characteristically, the fetal head and feet were
21
presented at the lips of the vulva. , 62 Consequently, delivery was not difficult
when forced extraction was performed with simultaneous stretching of the vulva
or aided by an episiotomy. If left unattended, this undoubtedly can be an
important factor associated with stillborn or weak calves. Other minor reported
causes of dystocia are uterine inertia, failure of cervix to dilate, and uterine
4
torsion. 1, 54,70
Certain hormonal imbalances have been linked to dystocia. Estrogen levels
in dams experiencing dystocia were found to be significantly be-low those of
24
normal calving COWS. , 50, 52 The relationship between the low estrogen
levels and dystocia is unknown and it can only be specu-lated that the normal
mechanism of parturition is altered when maternal estrogens are decreased at
parturition. In addition, a sire can confer to fetal genotype a depressing effect on
52
maternal estrogen levels and in-creased rates of dystocia. The placenta is the
source of elevated estro-gens at parturition, and other data show fetal genotype
can alter dam performance through differences in fetal hormone production?O

Contributing Factors

Birth weight consistently has been determined to be the most impor-

6

tant contributing factor associated with dystocia. , 36, 37, 54, 55, 62 The
relation-ship between increasing birth weight and frequency of dystocia may not
be linear, however, because it appears that dystocia increases markedly after
41
birth weight reaches a certain threshold. , 43 This would be espe-cially
important for calf viability with very large calves experiencing higher perinatal
mortality. Unfortunately, a specific threshold dependent on breed, parity, and
management cannot be set. The effects of birth weight on frequency of dystocia
in the aforementioned reports were analyzed by regression and correlation. In
these studies, birth weight accounted for 17% to 29% of the variability in
dystocia. Meijering41 re-ported that such analysis may underestimate
associative traits when categorical dependent variables (dystocia score) and
continuous indepen-dent variables (pelvic area, weight) are utilized. By
correcting for this discontinuity in the analysis, birth weight is found to account
for 30% to 50% of the variability in dystocia.
A popular concept held by producers is that calf shape is also very
important-i.e., "bulky" calves are most responsible for dystocia. With the
exception of the extreme bulk seen with double-muscled breeds/' 43 however,
other fetal measurements are not significant contributing fac-tors if birth weight
37
is considered first. , 48, 55
Birth weight is a function of genetic and environmental factors. Each
 DYSTOCIA-RELATED RISK FACTORS 55

parent supplies 50% of the genetic input to the fetus, but fetal environ-ment is
provided entirely by the dam. This means that each dam has the most influence
on birth weight. On a herd basis, however, the sire has a dramatic effect on birth
weight through the great number of
offspring that he sires. Birth weight is a moderately heritable trait (h 2 =
0.3_0.4).16,33,34
European and Israeli dairy breeders extensively studied genetic con-trol of
dystocia due to feto-pelvic incompatibility.4,38 They have reported large
differences in number of dystocias and stillbirths between progeny groups of
bulls, both as sires and as maternal grandsires. When this information was used
to select sires for mating to heifers, a reduction of approximately 60% in
dystocia rate and 40% in stillbirth rate was ob-served. Using a sire's own birth
weight as the only guide for selection of calving ease is fraught with error,
however, because of the fetal environ-ment's inherently large effect on birth
weight and genetics' only moder-ate (yet dominant) effect on the variation in
dystocia. Expected Progeny Difference (EPD) estimates for birth weight are
better predictors of po-tential calving ease because the complicated statistical
equation that com-putes EPD takes into consideration many genetic and
environmental variables. Scores of sires that are used widely for artificial
insemination soon develop high accuracies for birth weight EPDs, which can be
more useful in selecting for calving ease. Many North American breed associ-
ations now publish Sire Summaries containing estimates for birth weight that
may be used as a guide in selecting sires to breed to heifers. Some also include
maternal calving ease scores that reflect the influence of maternal grandsires.
Heritability estimates for direct calving ease and maternal calving ease are
reported in one Sire Summary to be 18% and 19%, respectively.68

The Sire Summary of some breeds lists a calving ease category in addition
to birth weight EPD to help breeders identify appropriate sires. Because each
breed association has a different summary, the definitions must be read
carefully before scores are put to use. In some summaries, for example, a high
numerical score means easier calving, whereas in others a lower score denotes
the same. At least one producer known to the author has increased dystocia by
improper interpretation of the calv-ing ease score.
Selection of a bull for his own calving ease may spell trouble in later
generations. This is best illustrated in the Simmental Sire Summary.68 One bull
remained a trait leader in calving ease for nearly 20 years. Progeny were small
at birth and remained small at weaning, as yearlings, and as adults. This sire's
daughters had increased dystocia rates, proba-bly because of their small stature,
which was reflected in the maternal calving ease category. When selecting a
sire, therefore, one should con-sider important maternal traits as well as the
sire's own calving ease.
Although calf genotype has the greatest effect on birth weight, the
maternal influence on birth weight must be reviewed. As previously stated, the
dam supplies half the genotype and all of the environment. This environment
includes factors such as age of dam, breed, size, pelvic dimensions, and
nutrition. The classical study of Joubert and Hammond
56 RICE

in 195831 illustrates best the effect that the combination of fetal genotype and
maternal environment can have on birth weight. They compared birth weights
of reciprocal crossbred calves from large South Devon cattle (average dam
weight, 1203 Ib) and small Dexter cattle (average dam weight, 614 lb).
Purebred South Devon calves weighed 97 lb and purebred Dexter calves
weighed 53 lb at birth. The 73-lb birth weight of crossbred calves from South
Devon dams was not different from the mid-parent average of 75 pounds,
whereas the crossbred calves from the Dexter dams were 15.5 lb lighter than the
mid-parent average and only 6.5 lb heavier than the average purebred Dexter
birth weight. The aver-age gestation was 287 days for both breeds yet the
Dexter dams bred to a South Devon sire gave birth on the 278th day (9 days
shorter) to calves averaging 6.5 lb heavier than the Dexter average. The
placental weight of Dexter dams was 3.3 lb compared with 11 lb for South
Devon dams. The authors concluded that the difference in gestation duration
and birth weight of the reciprocal crossbred calves was due to lack of uterine
space and reduced placental size in the Dexter dams. Similar differences have
been reported in Shetland pony-Shire reciprocal crossbred foals and in
Holstein-Jersey reciprocal crosses.19,76
A more recent study27 adds information regarding the maternal ef-fect on
birth weight. Reciprocal embryo transfers were done with Char-olais and
Brahman embryos in Charolais and Brahman cows. Cows were slaughtered at
232 days and 271 days of gestation. Uterine and fetal parameters were
evaluated. At 232 days, the Charolais calves were nearly twice as big as the
Brahman calves (50.5 versus 28.6 lb), but the breed of dam had no effect on
fetal weight. Between days 232 and 271, average daily growth of Charolais
fetuses in Charolais cows was 1.4 lb / day, compared with 0.57 lb / day for
Charolais fetuses in Brahman dams. At 271 days, Charolais fetuses in Charolais
cows weighed 28.5 Ib more than those in Brahman cows. Brahman fetuses in
Charolais cows were 10.8 lb heavier than Brahman fetuses in Brahman cows.
This study con-cluded that fetal genotype was the primary factor controlling
birth weight, but maternal factors could either allow full expression of fetal
genetic potential or markedly limit intrauterine growth. The primary maternal
factors in Brahman dams moderating birth weight appear to be reduced
placentome weight and reduced uterine perfusion.26
Crossbreeding studies also have shown that Brahman dams sup-press birth
weight through placentome size and function whereas dams of other breeds
complimented fetal growth.18 One study indicated a fetal genotype/ maternal
environment interaction on testosterone produc-tion? Dams carrying male
fetuses or fetuses sired by high-growth-rate bulls had higher testosterone levels
which were significantly and posi-tively correlated to placentome weight with
the exception of Brahman F1 dams that had the highest serum testosterone
levels but had the lowest placentome weight. The authors speculated that these
interactions con-tribute to wide ranges observed in birth weights of calves
produced by a single sire within and between breeds.
Depressed birth weights also may result from elevated environmen-tal
temperature. This is noticeable in the higher birth weight of calves
 DYSTOCIA-RELATED RISK FACTORS 57

born in the northern region of the United States versus lower birth weights in the
14
southern region. ,49 The cause, again, appears to result from altered uterine blood
flow and reduced placental mass.13 Blood volume of the dam is diverted away from
6o
viscera and toward skin, lungs, and other organs involved in thermal regulation.
The conclusion to be drawn from such studies is that if the maternal
environment is optimal, fetal birth weight will be expressed at its genetic
potential. If the maternal environment is restricted, however, fetal birth weight
will be restricted accordingly. Because we now know that the fetus initiates
parturition, we might conclude from the aforementioned Dexter-South Devon
crossbred study that a shorter gestation period of crossbred calves out of Dexter
dams was a fetal response to an unfavor-able environment. In this case, fetal
growth rate was increased but its genetic potential could not be realized because
of uterine space restric-tions and reduced availability of nutrients from a smaller
placenta. The interaction between fetal maturity and environmental stress set in
motion induction of parturition by the fetus.
An analogy to placental function can be drawn from the surviving
premature/dysmature calf born to a cow with chronic mycotic placenti-tis. Most
of these fetuses are aborted, but those that survive often are born premature,
with a low birth weight and poor body condition. These fetuses try to enhance
63
their nutritional supply by developing adventi-tious placentation. When they
reach a stage of maturity that permits them to respond to the stress of the
environment, parturition occurs.
This brings our discussion to the effect of nutrition on birth weight and
dystocia. By studying the effects of the genetic-environmental inter-action on
birth weight it becomes obvious that prepartum nutrition is an environmental
factor. The dam is very protective and sacrifices body condition, when
necessary, for the development and survival of the fetus. The fetus also appears
to possess self-preservation methods via increas-ing development of placental
tissue when subjected to nutritional stress. In a study at Oklahoma State
University,59 cows fed deficient diets pre-partum exhibited a thin body
condition (average score of 3.7) near calv-ing time. They were slaughtered at
260 days of gestation and found to have placentas significantly heavier than
cows in optimum body condi-tion (average score of 5.7). There were no
differences in fetal weights.
Prepartum energy intake levels have little effect on birth weight until
deficient diets reduce dam body condition to less than Body Con-dition Score
6
(BCS) 4, at which the nutritional environment limits birth weight. , 15, 23
Conversely, cows with BCS 4 or greater provide adequate nutrition and the
genetic potential for birth weight is not limited. Fat dams (BCS 7-9) do not have
heavier calves than dams in desired BCS of 5 or 6?9 In addition, when low
prepartum nutrition reduces birth rates, dystocia rates are not reduced but sometimes
are increased. Malnour-ished first-calf heifers are underdeveloped and weaker at
calving.
The effect of prepartum energy intake levels on reproductive per-formance
in first-calf heifers has been studied repeatedly.2, 6,15,23,35,36,78 In
these studies, prepartum protein levels were maintained at National
58 RICE

Research Council (NRC) requirements, whereas energy levels ranged from 25%
or 50% deficiency to adequate or excessive by 10% to 25%.
Inadequate prepartum energy levels resulted in reduced dam weights at
calving, reduced calf birth weights, and reduced pregnancy rates in the next
breeding season, but no difference in dystocia rates. Adequate or excessive
prepartum energy intake levels resulted in no difference in birth weights. Heifers
allowed to become extremely fat appear to suffer increased dystocia rates due to
pelvic fat, but calf birth weights are not increased. Three groups of heifers were
fed low, me-dium, or high levels of energy from weaning until calving at 2 years
of age?9 At calving, heifers in the low, medium, and high level groups weighed
609 lb, 862 lb, and 1085 lb, respectively. Calf birth weights were not different in
the medium and high level groups (61 lb) but were significantly higher than
those of the low level group (46 lb). Calf losses up to 24 hours postpartum were
45% in the high level group compared with 5% in the medium level group and
6% in the low level group. The extremely fat heifers had a high percentage of
stillbirths because of slow delivery or posterior presentation.
The effects of prepartum protein levels on birth weights and dysto-cia are
not as clear. Cowboy legend and veterinary folklore claim that high protein
levels increase birth weights and dystocia; most data do not support that belief,
however. A 2-year study at Oklahoma State Univer-sity compared calving
performance of heifers on wheat pasture (high energy, high protein), grain and
hay (high energy, adequate protein), or pasture and cottonseed protein
supplement (adequate energy, adequate protein) for the last 60 days of
gestation.67 Average body condition score at calving for the three groups were
6.1, 6.5, and 5.6, respectively. There were no differences in birth weights or
rates of dystocia. A similar study in Kansas comparing high protein (150% NRC
requirements) to adequate protein (100% NRC requirements) or deficient
9
protein (75% NRC require-ment) produced similar results. Another 2-year
study produced mixed results when comparing excess protein to adequate
protein with both protein rations being isocaloric. There was a significant
increase in birth weights and dystocia in the first year, but there were no
differences in the second year. 1
In summary, inadequate nutrition can lower birth weights but dys-tocia
rates are not altered unless heifers are small and weak or exces-sively fat. In
both cases, dystocia rates likely increase.

Pelvic Area

Pelvic area has been the maternal trait most frequently associated with
dystocia in first-calf heifers.6 , 17, 30, 43, 55, 62 In these studies, however,
calf birth weight accounted for more than twice as much of the variabil-ity in
dystocia rate as did dam pelvic area. A few studies showed no relationship
between pelvic area and dystocia or reported other body measurements such
as dam body weight at calving or external pelvic
 DYSTOCIA-RELATED RISK FACTORS 59

measurements as being more highly correlated to dystocia than internal pelvic

area.36, 42, 47
Efforts to use pelvic area and expected birth weights to select breed-ing
stock against dystocia have produced inconsistent results. 8o One method
involves establishing a pelvic area-to-calf birth weight ratio by dividing the
pelvic area by the expected calf birth weight.17 The guideline requires the
prebreeding pelvic area-to-birth weight ratio to be not less than 2.1:1 or 2.2:1
for average 600-to-700-lb heifers at 13 to 14 months of age. If a producer
expects heifers to deliver 75-lb calves unassisted (or with relative ease), for
2
example, prebreeding pelvic area should not be less than 165 cm . This figure
would be used as the minimum pelvic area for selecting replacement heifers.
Another procedure is to cull heifers with a selected bottom percent-age of
pelvic areas prior to breeding or at pregnancy testing time. 73 The owner and
veterinarian determine the percentage to cull based on num-ber available, their
size, number of replacements needed, postcalving history, and perhaps other
factors.
Several statistical and epidemiologic analyses have been performed to
predict dystocia or calving ease from prebreeding or precalving ani-mal values
such as dam pelvic area and estimated calf birth weights. The scientific data
raise questions concerning the accuracy and cost-effective-ness of using dam
pelvic area as a culling tool to prevent dystocia.8o
Regression analysis has shown that pelvic area is significantly re-lated to
dystocia,45, 55, 62 but this statistical method has not been successful in
predicting dystocia because the association between pelvic area and dystocia
has been too low to develop an accurate equation. Only 30% to 40% of the
variation in dystocia can be accounted for when an estimated or actual birth
weight plus dam pelvic area are used in the analysis. Regression analysis also is
reported to be inappropriate for this purpose because the dependent variable
(dystocia) has been reported as categori-cal data and the independent variable
(pelvic area) is continuous data. Regression analysis should be used only when
both variables are contin-uous data.
Discriminant analysis is the preferred statistical method to employ when
the dependent variable is categorical data and the independent variables are
45
continuous data. Using precalving pelvic area and cow age as independent
variables and assisted or unassisted birth as depen-dent variables, Morrison
reported discriminant analysis correctly classi-fied the dystocia rate in 85% of
45
134 cows and heifers. No estimated calf birth weights were used. The
analysis showed that if all dams would have been classified as unassisted, the
proportional chance of being cor-rect was 71.6%. Discriminant analysis
therefore correctly classified 13.4% more animals than would be expected by
chance alone.
An epidemiologic study of four Canadian herds was conducted to evaluate
the usefulness of pelvic area measurements taken prior to the breeding season or
at the time of pregnancy examination in identifying heifers that should be culled
because of higher risk of dystocia. 73 The conclusion was that neither
measurement was sufficiently accurate to predict the prevalence of dystocia
when culling based on either pelvic
60 RICE

area-to-birth weight ratio or heifers with pelvic areas in the bottom 25th
percentile. The sensitivity of the predictions was low, ranging from 19% to 44%,
indicating the majority of heifers that actually developed dysto-cia would not
have been identified. The positive predictive value (PPV) represents the
proportion of heifers with pelvic areas below the cut-off point that actually had
dystocia. In these herds, the PPV ranged from 23% to 50%, similar to the
average prevalence of dystocia and, therefore, no better than selecting against
dystocia by chance alone. The negative predictive value (NPV) represents the
proportion of heifers with pelvic area greater than the cut-off point that did not
suffer dystocia. The NPV was higher (72%-87%), but not different from
selecting for calving ease by chance alone.
When epidemiologic procedures are applied to the Morrison data (Table 1),
the sensitivity (78%) of discriminant analysis is much higher than reported in
the Canadian study. Specificity (86%) also was slightly improved. The high
number of false-positive predictions resulted in a PPV of only 55%. The NPV of
95% was quite high and, had the heifers with predicted dystocia been culled,
dystocia prevalence would have dropped from 17% to a very low 4.7%.
Achievement of this low preva-lence would be costly because the high number
of false-positives that did not suffer dystocia would have been culled. The
resulting cull rate (25%), however, would be the same as that of the Canadian
study.
Obviously, definite conclusions cannot be reached from anyone study.
Discriminant analysis cannot be done in most on-farm situations. Furthermore,
in the Morrison study, one dependent variable was dam age because both cows
and heifers were included in the study. A similar analysis with heifers only may
not produce similar results. The authors of this study, however, were
encouraged when the data revealed that all misclassified dams experiencing
dystocia were 3 years of age or older,

Table 1. AGREEMENT BETWEEN ACTUAL AND PREDICTED DYSTOCIA

PREVALENCE BY DISCRIMINANT ANALYSIS

Predicted - - ----------- - - Actual Dystocia ---------------

Dystocia Yes No Total
a b
Yes 18 15 33
c d
No 5 96 101
Total 23 111 134
Prevalence = 23/134 = 17%
Sensitivity = a/ (a+c) = 78%
Specificity = d/ (b + d) = 86%
PPV = a/ (a+b) = 55%
NPV = d/ (c+d) = 95%
% false + = b/ (a+b) = 45%
% false - = c/ (c+d) = 5%
Adapted from Morrison D, Humes P, Keith N, et al: Discriminant analysis for predicting dystocia in
beef cattle, II: Derivation and validation of a prebreeding prediction model. J
Anim Sci 60:617-621.
 DYSTOCIA-RELATED RISK FACTORS 61

whereas all2-year-olds with dystocia were correctly predicted. Although its

predictive value may be questionable, replacement heifers' pelvic area
remains a relatively important factor in dystocia rates.
Some producers who have used pelvic area measurements in heifer
selection regularly claim that the prevalence of dystocia decreased for the
first few years after implementing the practice. Even though pelvic area is
highly heritable14 (50%-60%), it is doubtful that females selected for large
pelvic areas would have a significant impact on frequency of dystocia for
several generations. Improvement in calving ease therefore likely is due to
improved management (nutrition, shorter calving season, and so on), which
often accompanies new procedures. In the author's experience, progressive
producers who have used pelvic area as a selec-tion tool often discontinue
its use after a few years because of a very low culling rate based on pelvic
area.
Because of the high heritability of pelvic area, perhaps measuring
yearling bulls, establishing EPDs for pelvic area, and selecting maternal
lines for calving ease may be additional steps toward reducing dystocia. 12, 67
The heritability of pelvic area is higher than that of birth weight. Over
several generations, the pelvic area-to-birth weight ratio would increase and,
theoretically, reduce dystocia. Confirmation of this theory is not yet
available but some breed associations are evaluating bull pelvic area data
for possible future use.
The best means of controlling the prevalence of dystocia is through
proper replacement heifer development and judicious sire selection. Heifers
should weigh 65% of their mature weight at breeding and 85% of their
mature weight at calving. If this type of heifer is bred to known calving ease
bulls, dystocia rates will be maintained at tolerable levels. 61

MANAGEMENT OF DYSTOCIA

Normal Parturition

Parturition in cattle is initiated by endocrinal events originating from

s
the fetus when it reaches a critical size and stage of maturation. The fetal
hypothalamo-pituitary-adrenal cortex axis coordinates release of
adrenocorticotrophic hormone and cortisol production approximately 2
weeks before parturition. A marked increase in these hormones occurs 2 to
3 days before delivery. The placenta is the target organ of fetal cortisol,
where increased placental estrogen production occurs. The rise in placental
estrogen causes production of prostaglandin F2 from the endometrium,
which subsequently results in lysis of the corpus luteum and removal of the
progesterone block that maintains pregnancy. Pros-taglandins also enhance
uterine contractions that previously have been inhibited by high
progesterone levels.
In swine, relaxin seems to be the principal hormone creating cervical
s
dilation. The role of relaxin in cattle is not clear. It has been isolated from
the bovine corpus luteum and from the bovine placenta, but its
62 RICE

activity is much lower than in swine. The administration of porcine relaxin

along with a short-acting corticosteroid to primiparous beef heif-ers enhanced
46
cervical dilation and increased pelvic size, resulting in easier deliveries.
Although this is interesting from the academic view-point (and may be of
therapeutic value in the future), the role of bovine relaxin in parturition remains
unclear, and availability of porcine relaxin has been limited to research.
The aforementioned endocrinal events set the stage for changes in uterine
activity that occur during the three stages of labor. During this time, the most
5
important hormones are estrogen, prostaglandins, and oxytocin. Oxytocin is
not effective until uterine receptors for oxytocin are developed and unless
calcium ions are available. Oxytocin receptors are developed in response to the
marked increase in the estrogen-to-progesterone ratio. Prostaglandins act by
liberating calcium ions from intracellular binding sites in the uterus, whereas
oxytocin apparently causes an influx of these calcium ions into myometrial
83
cells.
The smooth muscle of the uterus contains two types of receptors-ex and
~.64, 83 ex Receptors have a specific affinity for norepinephrine and are
primarily excitatory. ~ Receptors have a specific affinity for epineph-rine and
are primarily inhibitory. ~ Receptors are further divided into ~1 and ~2 receptors.
Stimulation of the ~l receptors results in cardiac stim-ulation and relaxation of
intestinal smooth muscle. Stimulation of ~2 receptors results in bronchodilation
and relaxation of uterus muscula-ture. Epinephrine release may stimulate the ~2
receptors and inhibit myometrial contractions during parturition. In one clinical
study, it was observed that closely confined first-calf heifers had delayed
parturition and increased dystocia compared with pastured heifers. The
supposition was that disturbances associated with close confinement increased
epi-nephrine release. Clenbuteral, a long-acting ~2 mimetic, has been shown to
delay parturition when administered early in stage 1 of parturition.57,82 It has
little or no effect if administered late in stage 1 or in stage 2 of parturition.
Clenbuteral is not available in the United States and its use in food animals is
illegal.

Obstetric Assistance

Despite the application of the best and/or most cost-effective man-agement

procedures meant to reduce the prevalence of dystocia, dystocia cases always
will confront producers and veterinarians. Nearly all unfor-tunate sequelae can
be avoided through proper and timely obstetric assistance.
Older veterinary textbooks and Extension fact sheets reported stage 2 of
63
parturition to last up to 4 hours for normal parturition in the bovine. It was
recommended to delay intervention for at least 2 hours after the appearance of
fetal membranes unless there was an obvious problem requiring assistance. It
also was recommended that first-calf heifers should be given more time to
allow expansion of soft tissue.
 DYSTOCIA-RELATED RISK FACTORS 63

Research at the United States Department of Agriculture Research Station

in Miles City, Montana, and at Oklahoma State University indi-cates normal
stage 2 of parturition is much briefer in cows and heifers than previously
thought. In both studies, dams were examined if they did not calve unassisted
within 2 hours after the appearance of mem-branes at the vulva. In Montana,
cows that calved unassisted did so in 34 minutes, and heifers in 58 minutes?O
In an Oklahoma State University study, unassisted heifers calved in 55 minutes
compared with 162 min-utes that passed before assisted calves were
56
delivered. Because the protocols at both locations called for assistance at 2
hours, it is not known how many animals might eventually have calved
unassisted, but at Okla-homa State University there was no indication that
parturition would have progressed satisfactorily. One study56 reported no
difference in dystocia rates in heifers related to pelvic area, but unassisted
heifers with below-average pelvic areas took nearly twice as long (112 minutes)
to calve than unassisted heifers with above-average pelvic areas (68 min-utes).
Neonates from slow calving heifers with below-average pelvic area required
more assistance in nursing.56 The protocol called for feeding colostrum to
calves that did not nurse within 2 hours of birth; the ques-tion therefore is
"When would these calves have nursed if they had not been hand fed?"

Effects of Dystocia

Dystocia presents the possibility of severe acid-base imbalances, resulting

from intense and prolonged labor contractions, inability to breathe, and trauma
during forced extraction. Prolonged hypoxia is an important cause of fetal death
during dystocia and, if not fatal, can be a serious factor determining
survivability.8, 10, 11, 27, 51, 77 Normal newborns suffer slight acidosis but
dystocial calves consistently have significantly reduced blood pH. Immediately
after birth, venous blood pH from eu-tocial calves has been reported to range
from 7.18 to 7.26, whereas dys-tocial calves had venous blood pH values
ranging from 6.84 to 7.11.22,27, 40,44, 76, 77 Physical activity is reduced and
51
dystocial calves are slow or unable to stand and suckle. , 58,74,75 All these
factors contribute to a high perinatal mortality rate and so-called "weak calf
syndrome" calves. In one study, the rectal temperature of dystocial calves
decreased 2.9°C shortly after birth and was slow to increase. The calves were
lethargic, anorexic, and later found to be hypogammaglobulinemic?5
The most commonly reported necropsy findings of dystocial calves are
localized edema of the head and cervical region, and atelectatic or hemorrhagic
63
lungs. Partially inflated yet atelectatic lungs are seen com-monly and some
39
show evidence of in utero aspiration of fluid containing meconium. ,58 Other
63
common traumatic lesions ,65 are ruptured dia-phragm, and fractures of the
vertebrae, ribs, or sternum. A consistent finding in hypoxia is meningeal
hemorrhage and congestion?2, 29 Meco-nium staining of hair coat is seen
39
commonly on dead or hypoxic calves. ,58
64 RICE

Some calves survive the trauma of forced extraction only to suffer

debilitating injuries. Commonly seen injuries are leg fractures and luxa-tions,
28
mandibular fractures, brachial nerve paralysis, and femoral nerve paralysis. ,
32, 63,71 Collapsed tracheal rings often are associated with ster-nal and rib
fractures near the thoracic inlet. 65
The adverse effect that dystocia can have on respiratory function, acid-base
balance, viability, and passive transfer of immunoglobulins in the newborn calf
(see articles by Perino and Rupp, Toombs et aI, and Wikse et al for discussion
of these problems) necessitates a review of our thinking on eutocia, dystocia,
and obstetric assistance?2, 33, 40, 51, 75, 77 Live-stock producers and some
veterinarians would define eutocia as a birth that occurred without assistance
regardless of calf viability, and dystocia as a birth that required assistance. A
more accurate definition of dystocia would be any birth that reduces calf
viability, causes maternal injury, or requires assistance.
Veterinarians also must inform livestock producers that normal stage 2 of
parturition is completed rather quickly and earlier intervention increases calf
viability. This author's recommendation is to assist cows in 30 to 60 minutes
after the appearance of membranes. Cows have large pelvic areas and expanded
soft tissues that allow parturition to progress rapidly. Slow parturition and
dystocia in these animals usually are the result of mechanical obstruction,
uterine torsion, uterine inertia, or other causes that must be corrected. Heifers
should be assisted within 60 to 90 minutes after the appearance of membranes.
They normally take longer to calve because of a smaller birth canal and the
necessity to expand the soft tissue, especially the vulva. Permitting too much
time to elapse for the expansion of soft tissue, however, often results in
unnecessary im-pacting of the fetal head in the pelvis. The force of contractions
and pelvic pressure creates fetal hypoxia and acidosis that can be avoided or
minimized with earlier intervention. Most of these calves are easily deliv-ered
with traction and manual stretching of the vulva or by performing an
episiotomy. All vital functions (respiratory, cardiovascular, thermo-regulation,
and acid-base balance) will be improved and passive transfer enhanced.

One must remember there is a cost associated with earlier interven-tion,

however. First, more labor is required. Second, more confinement is required,
especially for primiparous dams, which may expose the neo-nate to more
contamination and enteric pathogens.
Having made the proper recommendations to prevent dystocia and
minimize the unfortunate sequelae of dystocia does not mean the practi-tioner
will not be faced with the compromised neonate following dysto-cia or an
unassisted birth. Treatment of the hypoxic acidotic calf imme-diately
postpartum can be successful and includes correcting ventilation and acid -base
balance, and maintaining body temperatureY' 32, 58, 75, 77 The most rewarding
cases likely will be those delivered by the veterinarian and treated immediately.
In this author's experience, hypoxic weak calves presented more than 6 hours
postpartum have an unfavorable prognosis (Rice L, unpublished data, 1993).
Details of proper treatment are spelled out in the article by Dr. Kasari.
 DYSTOCIA-RELATED RISK FACTORS 65

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to
Lawrence E. Rice, DVM, MS
Boren Veterinary Teaching Hospital
Oklahoma State University
College of Veterinary Medicine
Stillwater, OK 74078