POSTHEMORRHAGIC
ANEMIA
AND
SHOCK
IN THE
NEWBORN
DUE TO
HEMORRHAGE
DURING
DELIVERY
Report
of
8
Cases
By Henry N. Kirkman, M.D., and Harris D. Riley, Jr., M.D.
Department of Pediatrics, Vanderbilt University School of Medicine
(Accepted February 3, 1959; submitted November 28, 1958.)
l)r. Kirkman is now at the National Institutes of Health, Bethesda, Maryland.
PRESENT ADDRESS: (H.D.R.) Department of Pediatrics, University of Oklahoma Medical Center, 800
N.E. 13th Street, Oklahoma City 4, Oklahoma.
92
PEDIATRICS, July 1959
LTHOUCII the hazards of maternal
hem-orrhage during labor and delivery are
vell recognized, it is seldom realized that
the mother and fetus share the placenta as
a mutual appendage through which the
fetus, as well as the mother, might bleed.
In addition, certain conditions predispose
the umbilical vessels to tearing. The causes
of fetal hemorrhage are such that they
usu-ally give rise to bleeding during labor or
expimlsion. As a consequence, the infants
may be live-born and, if prompt measures
are taken against the shock resulting from
blood-loss, their lives can he saved. Seven
cases from this hospital, including two
ob-served by the authors, and one case from
the military experience of one of the
au-thors, are presented to illustrate the
mani-festations and diverse etiology of this
con-dition.
Case 1
CASE
REPORTS
A multiparous woman (VDRL-negative,
Rh-positive) was admitted in labor to an Air Force
hospital at an estimated 38 weeks of pregnancy.
A 1,928-gm, male imifant was delivered
pre-cipitously. Immediately after expulsion, the
in-famit was noted to be extremely pale and weak,
although it breathed and cried promptly. A
second male infant, of similar weight, was then
delivered spontaneously and appeared normal.
The contrast imi appearance between the two
imifants was striking. The first infant, receiving
oxygen by mask, had obvious pallor without
cyanosis or respiratory retractions. The
respira-tions were irregular and gasping, the cry feeble.
Neither peripheral nor precordial pulses of the
first baby were palpable, but a faint, rapid heart
beat was heard on auscultation.
The second infant was pink, active, and
cry-ing vigorously, even without the administration
of oxygen. Neither baby had edema, a palpable
spleen or liver.
A diagnosis of posthemorrhagic shock in the
first infant was made.
Soon thereafter, a single placenta with
vela-mentous insertions of the cords (Fig. 1) at each
side was delivered. The umbilical vessels of
one cord were totally avulsed at the
velamen-tous insertion, except for a thread-like strand
which later separated in handling.
Thirty milliliters of dextran were injected
im-mediately into a cutaneous vein of the first
infant, approximately 15 minutes after
de-livery. The baby immediately became much
more vigorous and developed a discernible
pulse. Further improvement occurred when 30
ml of Group-O, Rh-negative blood was
in-jected, approximately 30 minutes later.
The first hemoglobin determination, deferred
until 20 hours of age to avoid unnecessary
han-dhing, was 10.6 gm/100 ml in the first infant,
as compared to 16 gm/100 ml in the second.
Further replacement and comparative studies
are shown in Figure 2. Neither infant
devel-oped icterus during the stay in the nursery.
Both infants received a transfusion toward the
end of the hospitalization. Blood studies and
development of both imifants were normal at
2 and 5 months, respectively.
Case 2 (85440)
A 26-year-old primiparous woman
(Wasser-man-negative) was delivered of a set of
mono-chorionic twins at an estimated 38 weeks of
pregnancy.
The first infant, a 2,240-gm female, was
ARTICLES 93
Fic. 1. Case 1. The placenta of a set of nionochorionic twins. Velamientous insertiomis of
the cords at each side, one insertion being avulsed.
to breathe. A “more than usual” amount of
bleeding was stated to have occurred during
and after delivery of the first baby.
The second infant, a 2,126-gm girl, was
de-hivered by breech extraction. She cried
spon-taneously but appeared moderately pale and
weak.
Both umbilical cords were found to be
in-serted eccentrically into a single placenta, but
no other abnormality of the placenta or
yes-sels was recorded.
Thirty minutes after delivery, the capillary
hemoglobin of the second infant was found to
be 5.5 gm/100 ml. After a transfusion of 40 ml
of whole blood at 3 hours of age, the baby
ap-peared more vigorous and the color improved.
Another transfusion of 45 ml was given on the
second day.
The hemoglobin of the first infant was 16.5
gm/100 ml on the third day.
Although the first twin died of congenital
heart disease at 2 ‘ears of age, the second twin
appeared normal when last seen at 9 years of
age.
Case 3 (256921)
A 22-year-old womami (Rh-positive,
Kahn-miegative), who had experienced one previous,
uneventful pregnancy and delivery, delivered
spontamieously amid at term a 2,835-gm female.
Nlild vaginal bleeding occurred during the
second stage.
The infant, quite pale and weak, had a
de-layed cry.
Examination of the placenta revealed rupture
of a vessel which coursed between the main
lobe of the placenta and a succenturiate lobe
(Fig. 3).
The capillary hemoglobin was 13.5 gm/100
ml. The pulse exceeded 150/mm and was faint.
A polyethylene catheter was inserted into
the umbilical vein and the venous pressure
hastily measured as between 40 amid 60 mm of
blood. Forty milliliters of Group-O, Rh-negative
blood was then injected through the catheter,
resulting in immediate improvement as
mani-fested by increased vigor and a loud cry. A
second 40 ml was given at 43. hours, after
which the pallor was less.
The infant’s hemoglobin remained between
14.0 and 16.0 gm/100 ml during the remainder
of the 7-day nursery stay. No icterus was
noticed. She was given ferrous sulfate orally
before discharge and appeared miormal at 1
month of age.
Case 4 (235048)
A 26-year-old, white woman (Kahn-negative,
Group A, Rh-positive) was admitted in
approxi-mately the thirty-fourth week of her fourth
pregnancy. Vaginal bleeding, subsequently
found to be due to placenta previa, had begun
a few hours before admission. Shortly following
...
:
Erythrocytes 4.0
-(millions)
-3.0
-16
‘4
Hemoglobin I 2
(gm/IO0 ml) ,
8
50
-Hematocrit
(%)
)
0 2 3 4 5
DAYS AFTER BIRTH
6
94 ANEMIA AND SHOCK IN THE NEWBORN
FIG. 2. Case 1. Comparative hemimtologic values in a set of twins following hemorrhage at birth.
operating room, profuse l)leeding and mild
shock occurred. A CdSaiClI1 section ‘as
per-formiied imiimuediately.
The 1)htCeIlta \%LS overlvmg the cervix and
sittmated against the anterior wall of the uterus.
The infant, a 2,637-gm female, was pale and limp but SOOfl cried after aspiration of the
respiratory passages. The pallor persisted and
the respiratiomis became more irregular with
periods of apnea.
Several attempts failed to yield sufficient
blood for a ca)illary hemoglobin
determina-tiomi, ammd the infant’s con(litioml was coIlSi(lere(l
too precarious to attempt venil)nncture or
further laboratory examimiatiomis.
No jatmmidice developed. The baby died at
4
hours. The hemoglobin at the time of deathwas 11.1 gm/100 ml.
Case 5 (213-225)
A 25-year-old, white woman (Kahn-negative,
Group 0, Rh-positive) was admitted at term,
5.0
0 = First Twin
L Second Twin
. = Transfusion of 20-30 ml whole blood to first twin.
ARTICLES 95
Fsc. 3. Case 3. The placenta of an infant found to be anemic at birth. A vessel joining the main lobe of
the placenta to a succenti.mriate lobe has been rupttmred.
in her second pregnancy, with vaginal bleeding.
A diagnosis of marginal placenta previa was
made. After three days of intermittent bleeding
a cesarean section was performed through the
lower uterine segment. No mention was made
of the placenta havimig been incised.
The infant, a 4,763-gm female, breathed
im-mediately and spontaneously but was quite pale
and weak. There was no edema or
spleno-megalv.
The infamit’s blood was Group 0, Rh-positive,
with a negative slide-albumin test. The
capil-lary hemoglobin was 8.0 gm/100 ml.
At age 3 hours, she received 85 ml of whole
blood intravenously. Two other transfusions
were given until, at age 3 days, the hemoglobin
was 15 gm/100 ml. No icterus was noticed.
She was discharged home in apparently good
health. At age 4 years, 10 months she appeared
normal in every respect.
Case 6 (252-606)
A 16-year-old primiparous woman
(Kahn-negative) was delivered at an estimated 36
weeks of gestation by low-cervical cesarean
section because of a prolapsed cord. No
men-tion was made of the placenta having been
in-cised.
The baby, a 2,807-gm female, had depressed
activity at birth, a delayed cry and “peripheral
cyanosis of all extremities.” The spleen was not
palpable.
The capillary hemoglobin at that time was
11.0 gm/100 ml. The direct Coombs’ test was
negative.
She was immediately given a transfusion of
40 ml of whole blood with prompt
improve-ment. Another transfusion of 30 ml was given
the following day. Mild icterus was noticed on
the third day but cleared by the seventh day.
She appeared normal except for a mild
alveolar cleft at 1 year of age, when the
hemo-globin was 14 gm/100 ml.
Case 7 (238-639)
A 36-year-old, white woman (Kahn-negative,
Group B, Rh-positive) was admitted in the
96
ANEMIA AND SHOCK IN THE NEWBORNearly labor. A classic cesareami section was clone
because of a previous section. The placenta
was found to lie anteriorly and was separated
after “considerable bleeding.”
The baby, a 3,515-gm male, appeared pale
but otherwise normal. The spleen and liver
were not palpable.
On the second day, the capillary hemoglobin
was found to be 11.5 gm/mI; the blood, group
0, Rh-negative; the direct Coombs’ test,
nega-tive.
The baby remained pale but vigorous. At 3
weeks of age the hemoglobin was 9.4 gm/100
ml. After ferrous sulfate therapy, the
hemo-globin rose to 11.0 gm/100 ml at 3 months.
At 27 months of age he appeared normal.
Case 8 (213-063)
A 31-year-old, multiparous woman (Group 0,
Rh-positive, Kahn-negative), who had
experi-emiced two previous normal pregnancies, was
admitted in labor at term. A cesarean section
was performed because of a contracted pelvis
and previous sections. At operation the uterus
was found to have ruptured and the abdominal
cavity was partly filled with blood. The
pla-centa was seen partly protruding through the
dehiscence in the uterine wall.
The infant, a 3,317-gm male, had a slightly
delayed cry and mild pallor but otherwise
appeared in good condition.
At 6 hours of age the capillary hemoglobin
was 12 gm/100 ml; blood, Group 0,
Rh-negative. The liver and spleen were not
en-larged.
A diagnosis of anemia due to acute blood
loss was made and whole blood was made
available for transfusion. However, the
sub-sequent course was uneventful so transfusion
was withheld. Mild icterus appeared on the
third day. The hemoglobin remained between
12.0 and 13.0 gm/100 ml throughout the
nur-sery stay.
He was discharged in good condition on the
eleventh day. At 5 months of age the
hemo-globin was 9.0 gm/100 ml, but the diet was
somewhat inadequate according to his local
physician. He was started on iron therapy, and
6 weeks later the hemoglobin had risen to
12.5 gm/100 ml. He was followed until 5 years
of age, with no subsequent decrease in
hemo-globin, and was considered normal in every
respect.
COMMENT
A comprehensive review of all aspects of
posthemorrhagic anemia and shock in the
newborn, based on the experience in this
clinic and cases reported in the literature,
has been provided in another paper by the
authors.1
Cases 1 and 2 represent examples of
post-hemorrhagic shock resulting from tearing
of a velamentous insertion of the umbilical
vessels. Case 3 is an example of fetal blood
loss due to tearing of a vessel
communicat-ing between a succenturiate lobe and the
main body of the placenta. Cases 4-7 in all
probability
represent
examples
of
acute
fetal blood-loss due to incision or
disrup-tion
of
the
placenta.
Although
the
source
of bleeding was not recorded for Cases 2
or 4-7, a posthemorrhagic state could be
presumed by the condition of the infants
and the coexistence of obstetric conditions
with which fetal bleeding is commonly
as-sociated.25 Case 8 is an example of acute
fetal blood-loss due to disruption of the
placenta after uterine rupture.
REFERENCES
1. Kirkman, H. N., and Riley, H. D., Jr. :
Post-hemorrhagic anemia and shock in the
newborn; a review. PEDIATRICS, 24:97,
1959.
2. Novak, F. : Posthemorrhagic shock in
new-horns during labor and after delivery.
Acta. med. iugoslav., 7:280, 1953.
3. Torrey, W. E. : Vasa previa. Am.
J.
Obst.& Gynec., 63:146, 1952.
4.
Siddall, R. S., and West, R. H. : Incision ofplacenta at cesarean section; cause of
fetal anemia. Am.
J.
Obst. & Gynec., 63:425, 1952.
5. Wickster, G. A. : Post-hemorrhagic shock in
the newborn. Am.
