434 Labor

11 percent at 32 weeks, and then decreases to approximately

TABLE 22-1. Fetal Presentation in 68,097 Singleton
3 percent at term. The high incidence of breech presentation in
Pregnancies at Parkland Hospital
hydrocephalic fetuses is in accord with this theory, as the larger
Presentation Percent Incidence fetal cephalic pole requires more room than its podalic pole.
SECTION 7

Cephalic 96.8 —
Breech 2.7 1:36 Breech Presentation
Transverse lie 0.3 1:335
Compound 0.1 1:1000 When the fetus presents as a breech, the three general con-
Face 0.05 1:2000 figurations are frank, complete, and footling presentationss and
Brow 0.01 1:10,000 are described in Chapter 28 (p. 559). Breech presentation
may result from circumstances that prevent normal version
from taking place. One example is a septum that protrudes
less commonly, the fetal neck may be sharply extended so that into the uterine cavity (Chap. 3, p. 42). A peculiarity of fetal
the occiput and back come in contact, and the face is fore- attitude, particularly extension of the vertebral column as seen
most in the birth canal—face
— presentation (Fig. 23-6, p. 466). in frank breeches, also may prevent the fetus from turning. If
The fetal head may assume a position between these extremes, the placenta is implanted in the lower uterine segment, it may
partially flexed in some cases, with the anterior (large) fonta- distort normal intrauterine anatomy and result in a breech
nel, or bregma, presenting—sinciput presentation—or partially presentation.
extended in other cases, to have a brow presentation (Fig. 23-8,
p. 468). These latter two presentations are usually transient.
■ Fetal Attitude or Posture
As labor progresses, sinciput and brow presentations almost
always convert into vertex or face presentations by neck flexion In the later months of pregnancy, the fetus assumes a char-
or extension, respectively. Failure to do so can lead to dystocia, acteristic posture described as attitude or habitus as shown in
as discussed in Chapter 23 (p. 455). Figure 22-1. As a rule, the fetus forms an ovoid mass that cor-
The term fetus usually presents with the vertex, most logi- responds roughly to the shape of the uterine cavity. The fetus
cally because the uterus is piriform or pear shaped. Although becomes folded or bent upon itself in such a manner that the
the fetal head at term is slightly larger than the breech, the back becomes markedly convex; the head is sharply flexed so
entire podalic polee of the fetus—that is, the breech and its flexed that the chin is almost in contact with the chest; the thighs are
extremities—is bulkier and more mobile than the cephalic flexed over the abdomen; and the legs are bent at the knees.
pole. The cephalic polee is composed of the fetal head only. Until In all cephalic presentations, the arms are usually crossed over
approximately 32 weeks, the amnionic cavity is large compared the thorax or become parallel to the sides. The umbilical cord
with the fetal mass, and the fetus is not crowded by the uterine lies in the space between them and the lower extremities. This
walls. Subsequently, however, the ratio of amnionic fluid vol- characteristic posture results from the mode of fetal growth and
ume decreases relative to the increasing fetal mass. As a result, its accommodation to the uterine cavity.
the uterine walls are apposed more closely to the fetal parts. Abnormal exceptions to this attitude occur as the fetal head
If presenting by the breech, the fetus often changes polarity becomes progressively more extended from the vertex to the
to make use of the roomier fundus for its bulkier and more face presentation (see Fig. 22-1). This results in a progressive
mobile podalic pole. As discussed in Chapter 28 (p. 559), the change in fetal attitude from a convex (flexed) to a concave
incidence of breech presentation decreases with gestational age. (extended) contour of the vertebral column.
It approximates 25 percent at 28 weeks, 17 percent at 30 weeks,
■ Fetal Position
Position refers to the relationship
of an arbitrarily chosen portion
of the fetal presenting part to the
right or left side of the birth canal.
Accordingly, with each presentation
there may be two positions—right
or left. The fetal occiput, chin (men-
tum), and sacrum are the determining
points in vertex, face, and breech pre-
sentations, respectively (Figs. 22-2 to
22-6). Because the presenting part
may be in either the left or right posi-
tion, there are left and right occipital,
A B C D left and right mental, and left and
FIGURE 22-1 Longitudinal lie. Cephalic presentation. Differences in attitude of the fetal body right sacral presentations. These are
in (A) vertex, (B) sinciput, (C) brow, and (D) face presentations. Note changes in fetal abbreviated as LO and RO, LM and
attitude in relation to fetal vertex as the fetal head becomes less flexed. RM, and LS and RS, respectively.
 435

CHAPTER 22
A B
FIGURE 22-2 Longitudinal lie. Vertex presentation. A. Left occiput anterior (LOA). B. Left occiput posterior (LOP).

A B
FIGURE 22-3 A. Right occiput posterior (ROP). B. Right occiput transverse (ROT).
 436 Labor
SECTION 7

FIGURE 22-6 Longitudinal lie. Breech presentation. Left sacrum

posterior (LSP).

FIGURE 22-4 Longitudinal lie. Vertex presentation. Right occiput

anterior (ROA).

Left mento-anterior Right mento-anterior Right mento-posterior

FIGURE 22-5 Longitudinal lie. Face presentation. Left and right mentum anterior and right mentum posterior positions.
 Normal Labor 437

■ Varieties of Presentations and Positions

For still more accurate orientation, the relationship of a given
portion of the presenting part to the anterior, transverse, or

CHAPTER 22
posterior portion of the maternal pelvis is considered. Because
the presenting part in right or left positions may be directed
anteriorly (A), transversely (T), or posteriorly (P), there are six
varieties of each of the three presentations as shown in Figures
22-2 to 22-6. Thus, in an occiput presentation, the presenta-
tion, position, and variety may be abbreviated in clockwise
fashion as:

OA

ROA LOA

ROT LOT

ROP LOP

OP

Approximately two thirds of all vertex presentations are in the

left occiput position, and one third in the right.
In shoulder presentations, the acromion (scapula) is the
portion of the fetus arbitrarily chosen for orientation with the
maternal pelvis. One example of the terminology sometimes FIGURE 22-7 Transverse lie. Right acromiodorsoposterior (RADP).
employed for this purpose is illustrated in Figure 22-7. The The shoulder of the fetus is to the mother’s right, and the back is
acromion or back of the fetus may be directed either poste- posterior.
riorly or anteriorly and superiorly or inferiorly. Because it is
impossible to differentiate exactly the several varieties of shoul-
dus. The breech gives the sensation of a large, nodular mass,
der presentation by clinical examination and because such spe-
whereas the head feels hard and round and is more mobile and
cific differentiation serves no practical purpose, it is customary
ballottable.
to refer to all transverse lies simply as shoulder presentations.
Performed after determination of fetal lie, the second
Another term used is transverse lie, with back up or back down,
maneuver is accomplished as the palms are placed on either
which is clinically important when deciding incision type for
side of the maternal abdomen, and gentle but deep pressure
cesarean delivery (Chap. 23, p. 468).
is exerted. On one side, a hard, resistant structure is felt—the
back. On the other, numerous small, irregular, mobile parts
■ Diagnosis of Fetal Presentation are felt—the fetal extremities. By noting whether the back is
and Position directed anteriorly, transversely, or posteriorly, fetal orientation
Several methods can be used to diagnose fetal presentation and can be determined.
position. These include abdominal palpation, vaginal examina- The third maneuver is performed by grasping with
tion, auscultation, and, in certain doubtful cases, sonography. the thumb and fingers of one hand the lower portion
Rarely, plain radiographs, computed tomography, or magnetic of the maternal abdomen just above the symphysis pubis.
resonance imaging may be used. If the presenting part is not engaged, a movable mass will be
felt, usually the head. The differentiation between head and
breech is made as in the first maneuver. If the presenting
Abdominal Palpation—Leopold Maneuvers part is deeply engaged, however, the findings from this
Abdominal examination can be conducted systematically maneuver are simply indicative that the lower fetal pole
employing the four maneuvers described by Leopold in 1894 is in the pelvis, and details are then defined by the fourth
and shown in Figure 22-8. The mother lies supine and com- maneuver.
fortably positioned with her abdomen bared. These maneuvers To perform the fourth maneuver, the examiner faces the
may be difficult if not impossible to perform and interpret if mother’s feet and, with the tips of the first three fingers of each
the patient is obese, if there is excessive amnionic fluid, or if the hand, exerts deep pressure in the direction of the axis of the pel-
placenta is anteriorly implanted. vic inlet. In many instances, when the head has descended into
The first maneuver permits identification of which fetal the pelvis, the anterior shoulder may be differentiated readily
pole—that is, cephalic or podalic—occupies the uterine fun- by the third maneuver.
 438 Labor

In attempting to determine
presentation and position by vagi-
nal examination, it is advisable to
pursue a definite routine, com-
SECTION 7

prising four movements. First, the

examiner inserts two fingers into
the vagina and the presenting part
is found. Differentiation of vertex,
face, and breech is then accom-
plished readily. Second, if the ver-
tex is presenting, the fingers are
directed posteriorly and then swept
forward over the fetal head toward
the maternal symphysis (Fig. 22-9).
During this movement, the fingers
necessarily cross the sagittal suture
A B and its linear course is delineated.
Next, the positions of the two
fontanels are ascertained. For this,
fingers are passed to the most ante-
rior extension of the sagittal suture,
and the fontanel encountered there
is examined and identified. Then,
with a sweeping motion, the fingers
pass along the suture to the other
end of the head until the other fon-
tanel is felt and differentiated (Fig.
22-10). Last, the station, or extent
to which the presenting part has
descended into the pelvis, can also
be established at this time (p. 449).
Using these maneuvers, the various
sutures and fontanels are located
readily (Fig. 7-11, p. 139).

C D
Sonography and
FIGURE 22-8 Leopold maneuvers (A–D) performed in a fetus with a longitudinal lie in the left Radiography
occiput anterior position (LOA).
Sonographic techniques can aid
fetal position identification, espe-
Abdominal palpation can be performed throughout the latter cially in obese women or in women with rigid abdominal
months of pregnancy and during and between the contractions walls. Zahalka and associates (2005) compared digital exami-
of labor. With experience, it is possible to estimate the size of nations with transvaginal and transabdominal sonography for
the fetus. According to Lydon-Rochelle and colleagues (1993), fetal head position determination during second-stage labor
experienced clinicians accurately identify fetal malpresentation and reported that transvaginal sonography was superior.
using Leopold maneuvers with a high sensitivity—88 percent,
specificity—94 percent, positive-predictive value—74 percent, ■ Occiput Anterior Presentation
and negative-predictive value—97 percent. In most cases, the vertex enters the pelvis with the sagittal suture
lying in the transverse pelvic diameter. The fetus enters the pel-
Vaginal Examination vis in the left occiput transverse (LOT) position in 40 percent
Before labor, the diagnosis of fetal presentation and position by of labors and in the right occiput transverse (ROT) position in
vaginal examination is often inconclusive because the present- 20 percent (Caldwell, 1934). In occiput anterior positions—LOA
ing part must be palpated through a closed cervix and lower or ROA—the head either enters the pelvis with the occiput
uterine segment. With the onset of labor and after cervical dila- rotated 45 degrees anteriorly from the transverse position, or
tation, vertex presentations and their positions are recognized this rotation occurs subsequently. The mechanism of labor in
by palpation of the various fetal sutures and fontanels. Face all these presentations is usually similar.
and breech presentations are identified by palpation of facial The positional changes of the presenting part required to
features and fetal sacrum, respectively. navigate the pelvic canal constitute the mechanisms of labor.
 Normal Labor 439

pelvic inlet at labor onset. In this circum-

stance, the head is sometimes referred to
as “floating.” A normal-sized head usually

CHAPTER 22
does not engage with its sagittal suture
directed anteroposteriorly. Instead, the
fetal head usually enters the pelvic inlet
either transversely or obliquely. Segel and
coworkers (2012) analyzed labor in 5341
nulliparous women and found that fetal
head engagement before labor onset did
not affect vaginal delivery rates in either
spontaneous or induced labor.

Asynclitism. The fetal head tends to

FIGURE 22-9 Locating the sagittal suture by vaginal examination. accommodate to the transverse axis of the
pelvic inlet, whereas the sagittal suture,
while remaining parallel to that axis, may not lie exactly mid-
The cardinal movements of laborr are engagement, descent, way between the symphysis and the sacral promontory. The
flexion, internal rotation, extension, external rotation, and sagittal suture frequently is deflected either posteriorly toward
expulsion (Fig. 22-11). During labor, these movements not the promontory or anteriorly toward the symphysis (Fig.
only are sequential but also show great temporal overlap. For 22-12). Such lateral deflection to a more anterior or posterior
example, as part of engagement, there is both flexion and position in the pelvis is called asynclitism. If the sagittal suture
descent of the head. It is impossible for the movements to approaches the sacral promontory, more of the anterior parietal
be completed unless the presenting part descends simultane- bone presents itself to the examining fingers, and the condition
ously. Concomitantly, uterine contractions effect important is called anterior asynclitism. If, however, the sagittal suture lies
modifications in fetal attitude, or habitus, especially after the close to the symphysis, more of the posterior parietal bone will
head has descended into the pelvis. These changes consist present, and the condition is called posterior asynclitism. With
principally of fetal straightening, with loss of dorsal convex- extreme posterior asynclitism, the posterior ear may be easily
ity and closer application of the extremities to the body. As palpated.
a result, the fetal ovoid is transformed into a cylinder, with Moderate degrees of asynclitism are the rule in normal
the smallest possible cross section typically passing through labor. However, if severe, the condition is a common reason
the birth canal. for cephalopelvic disproportion even with an otherwise normal-
sized pelvis. Successive shifting from posterior to anterior asyn-
Engagement clitism aids descent.
The mechanism by which the biparietal diameter—the greatest
Descent
transverse diameter in an occiput presentation—passes through
the pelvic inlet is designated engagement. The fetal head may This movement is the first requisite for birth of the newborn.
engage during the last few weeks of pregnancy or not until In nulliparas, engagement may take place before the onset
after labor commencement. In many multiparous and some of labor, and further descent may not follow until the onset
nulliparous women, the fetal head is freely movable above the of the second stage. In multiparas, descent usually begins
with engagement. Descent is brought about by one or more
of four forces: (1) pressure of the amni-
onic fluid, (2) direct pressure of the fun-
dus upon the breech with contractions,
(3) bearing-down efforts of maternal
abdominal muscles, and (4) extension
and straightening of the fetal body.

Flexion
As soon as the descending head meets
resistance, whether from the cervix, pelvic
walls, or pelvic floor, it normally flexes.
With this movement, the chin is brought
into more intimate contact with the fetal
thorax, and the appreciably shorter sub-
occipitobregmatic diameter is substituted
for the longer occipitofrontal diameter
FIGURE 22-10 Differentiating the fontanels by vaginal examination. (Figs. 22-13 and 22-14).
 440 Labor
SECTION 7

1. Head floating, before engagement 5. Complete extension

2. Engagement, descent, flexion 6. Restitution (external rotation)

3. Further descent, internal rotation 7. Delivery of anterior shoulder

7

4. Complete rotation, beginning extension 8. Delivery of posterior shoulder

FIGURE 22-11 Cardinal movements of labor and delivery from a left occiput anterior position.
 Normal Labor 441

Anterior asynclitism Normal synclitism Posterior asynclitism

CHAPTER 22
Occipitoo-
Sagittal frontal plane
p
Anterior Posterior
suture Pelvic inlett
parietal parietal
plane

FIGURE 22-12 Synclitism and asynclitism.

A B

C D
FIGURE 22-13 Lever action produces flexion of the head. FIGURE 22-14 Four degrees of head flexion. The solid line
Conversion from occipitofrontal to suboccipitobregmatic diameter represents the occipitomental diameter, whereas the broken
typically reduces the anteroposterior diameter from nearly 12 to line connects the center of the anterior fontanel with the pos-
9.5 cm. terior fontanel. A. Flexion poor. B. Flexion moderate. C. Flexion
advanced. D. Flexion complete. Note that with complete flexion,
the chin is on the chest. The suboccipitobregmatic diameter, the
shortest anteroposterior diameter of the fetal head, is passing
through the pelvic inlet.
 442 Labor
SECTION 7

A B

C D
FIGURE 22-15 Mechanism of labor for the left occiput transverse position, lateral view. A. Engagement. B. After engagement, further
descent. C. Descent and initial internal rotation. D. Rotation and extension.

Internal Rotation into play. The first force, exerted by the uterus, acts more poste-
This movement consists of a turning of the head in such a man- riorly, and the second, supplied by the resistant pelvic floor and
ner that the occiput gradually moves toward the symphysis the symphysis, acts more anteriorly. The resultant vector is in the
pubis anteriorly from its original position or, less commonly, direction of the vulvar opening, thereby causing head extension.
posteriorly toward the hollow of the sacrum (Figs. 22-15 to This brings the base of the occiput into direct contact with the
22-17). Internal rotation is essential for completion of labor, inferior margin of the symphysis pubis (see Fig. 22-16).
except when the fetus is unusually small.
Calkins (1939) studied more than 5000 women in labor to
ascertain the time of internal rotation. He concluded that in
approximately two thirds, internal rotation is completed by the
time the head reaches the pelvic floor; in about another fourth,
internal rotation is completed shortly after the head reaches the
pelvic floor; and in the remaining 5 percent, rotation does not
take place. When the head fails to turn until reaching the pelvic
floor, it typically rotates during the next one or two contractions
in multiparas. In nulliparas, rotation usually occurs during the
next three to five contractions.

Extension
After internal rotation, the sharply flexed head reaches the vulva
and undergoes extension. If the sharply flexed head, on reaching
the pelvic floor, did not extend but was driven farther downward,
it would impinge on the posterior portion of the perineum and
would eventually be forced through the perineal tissues. When
the head presses on the pelvic floor, however, two forces come FIGURE 22-16 Mechanism of labor for left occiput anterior position.
 Normal Labor 443

CHAPTER 22
1

45º
3
45º
2
1 45º

FIGURE 22-17 Mechanism of labor for right occiput posterior position showing anterior rotation.

With progressive distention of the perineum and vaginal perineum soon becomes distended by the posterior shoulder.
opening, an increasingly larger portion of the occiput gradually After delivery of the shoulders, the rest of the body quickly
appears. The head is born as the occiput, bregma, forehead, passes.
nose, mouth, and finally the chin pass successively over the
anterior margin of the perineum (see Fig. 22-17). Immediately
■ Occiput Posterior Presentation
after its delivery, the head drops downward so that the chin lies
over the maternal anus. In approximately 20 percent of labors, the fetus enters the pel-
vis in an occiput posterior (OP) position (Caldwell, 1934). The
External Rotation right occiput posterior (ROP) is slightly more common than
the left (LOP). It appears likely from radiographic evidence
The delivered head next undergoes restitution (see Fig. 22-11). If that posterior positions are more often associated with a narrow
the occiput was originally directed toward the left, it rotates toward forepelvis. They also are more commonly seen in association
the left ischial tuberosity. If it was originally directed toward the with anterior placentation (Gardberg, 1994a).
right, the occiput rotates to the right. Restitution of the head to In most occiput posterior presentations, the mechanism of
the oblique position is followed by external rotation completion labor is identical to that observed in the transverse and ante-
to the transverse position. This movement corresponds to rotation rior varieties, except that the occiput has to internally rotate
of the fetal body and serves to bring its bisacromial diameter into to the symphysis pubis through 135 degrees, instead of 90 and
relation with the anteroposterior diameter of the pelvic outlet. 45 degrees, respectively (see Fig. 22-17).
Thus, one shoulder is anterior behind the symphysis and the other Effective contractions, adequate head flexion, and average
is posterior. This movement apparently is brought about by the fetal size together permit most posteriorly positioned occiputs
same pelvic factors that produced internal rotation of the head. to rotate promptly as soon as they reach the pelvic floor, and
labor is not lengthened appreciably. In perhaps 5 to 10 per-
Expulsion cent of cases, however, rotation may be incomplete or may
Almost immediately after external rotation, the ante- not take place at all, especially if the fetus is large (Gardberg,
rior shoulder appears under the symphysis pubis, and the 1994b). Poor contractions, faulty head flexion, or epidural
 444 Labor

analgesia, which diminishes abdominal muscular pushing

and relaxes pelvic floor muscles, may predispose to incom-
plete rotation. If rotation is incomplete, transverse arrest may
result. If no rotation toward the symphysis takes place, the
SECTION 7

occiput may remain in the direct occiput posterior position, a

condition known as persistent occiput posterior. Both persistent
occiput posterior and transverse arrest represent deviations
from the normal mechanisms of labor and are considered fur-
ther in Chapter 23.

■ Fetal Head Shape Changes

Caput Succedaneum
In vertex presentations, labor forces alter fetal head shape. FIGURE 22-19 Considerable molding of the head and caput suc-
In prolonged labors before complete cervical dilatation, the cedaneum formation in a recently delivered newborn.
portion of the fetal scalp immediately over the cervical os
becomes edematous (Fig. 33-1, p. 647). This swelling, known
Hicks contractions, some molding develops before labor.
as the caput succedaneum, is shown in Figures 22-18 and
Most studies indicate that there is seldom overlapping of the
22-19. It usually attains a thickness of only a few millimeters,
parietal bones. A “locking” mechanism at the coronal and
but in prolonged labors it may be sufficiently extensive to
lambdoidal connections actually prevents such overlapping
prevent differentiation of the various sutures and fontanels.
(Carlan, 1991). Molding results in a shortened suboccipi-
More commonly, the caput is formed when the head is in the
tobregmatic diameter and a lengthened mentovertical diam-
lower portion of the birth canal and frequently only after the
eter. These changes are of greatest importance in women
resistance of a rigid vaginal outlet is encountered. Because it
with contracted pelves or asynclitic presentations. In these
develops over the most dependent area of the head, one may
circumstances, the degree to which the head is capable of
deduce the original fetal head position by noting the location
molding may make the difference between spontaneous vagi-
of the caput succedaneum.
nal delivery and an operative delivery. Some older literature
Molding cited severe head molding as a cause for possible cerebral
trauma. Because of the multitude of associated factors, for
In addition to soft tissue changes, the bony fetal head shape
example, prolonged labor with fetal sepsis and acidosis, it is
is also altered by external compressive forces and is referred
impossible to link molding to any alleged fetal or neonatal
to as moldingg (see Fig. 22-19). Possibly related to Braxton
neurological sequelae. Most cases of molding resolve within
the week following delivery, although persistent cases have
been described (Graham, 2006).

CHARACTERISTICS OF NORMAL LABOR

The greatest impediment to understanding normal labor is rec-
ognizing its start. The strict definition of labor—uterine con-
tractions that bring about demonstrable effacement and dilatation
of the cervix—does
x not easily aid the clinician in determining
when labor has actually begun, because this diagnosis is con-
firmed only retrospectively. Several methods may be used to
define its start. One defines onset as the clock time when pain-
ful contractions become regular. Unfortunately, uterine activity
that causes discomfort, but that does not represent true labor,
may develop at any time during pregnancy. False labor often
stops spontaneously, or it may proceed rapidly into effective
contractions.
A second method defines the onset of labor as beginning at
the time of admission to the labor unit. In the United States,
admission for labor is frequently based on the extent of cervical
dilatation accompanied by painful contractions. If a woman
has intact membranes, then a cervical dilatation of 3 to 4 cm
FIGURE 22-18 Formation of caput succedaneum and head or greater is presumed to be a reasonably reliable threshold for
molding. the diagnosis of labor. In this case, labor onset commences
 Normal Labor 445

Descent
10
1959–1966
2002–2008
8

CHAPTER 22
Dilation (cm)

Dilatation
Dilatation
Preparatory division Pellvic
vic
2 division divissionn
0 1 2 3 4 5 6
Time (hour) Time
FIGURE 22-20 Average labor curves for women with singleton FIGURE 22-21 Labor course divided functionally on the basis
term pregnancies presenting in spontaneous labor with vaginal of dilatation and descent curves into: (1) a preparatory division,
delivery for nulliparas for 1959–1966 compared with 2002–2008. including latent and acceleration phases; (2) a dilatational divi-
(From Zhang, 2002.) sion, occupying the phase of maximum slope; and (3) a pelvic
division, encompassing both deceleration phase and second
stage concurrent with the phase of maximum slope of descent.
(Redrawn from Friedman, 1978.)
with the time of admission. This presumptive method obviates
many of the uncertainties in diagnosing labor during earlier
stages of cervical dilatation. Laughon and colleagues (2012)
compared the duration of spontaneous labor at term in nul- Latent Phase
liparas delivered in the United States between 1959 and 1966 The onset of latent labor, as defined by Friedman (1972), is
to that of those delivered from 2002 to 2008. As shown in the point at which the mother perceives regular contractions.
Figure 22-20, the length of labor increased by approximately The latent phase for most women ends once dilatation of 3 to
2 hours during those 50 years. 5 cm is achieved. This threshold may be clinically useful, for
it defines dilatation limits beyond which active labor can be
expected.
■ First Stage of Labor This concept of a latent phase has great significance in
Assuming that the diagnosis has been confirmed, what then understanding normal human labor, because labor is consider-
are the expectations for the progress of normal labor? A scien- ably longer when a latent phase is included. To better illustrate
tific approach was begun by Friedman (1954), who described
a characteristic sigmoid pattern for labor by graphing cervi-
cal dilatation against time. This graphical approach, based on
statistical observations, changed labor management. Friedman 10
Phase of maximum

developed the concept of three functional labor divisions to Deceleration

describe the physiological objectives of each division as shown phase
slope

in Figure 22-21. First, during the preparatory division, although 8

Cervical dilatation (cm)

the cervix dilates little, its connective tissue components change

considerably (Chap. 21, p. 410). Sedation and conduction anal- 6
gesia are capable of arresting this labor division. The dilatational
Acceleration

division, during which dilatation proceeds at its most rapid rate,

phase

is unaffected by sedation. Last, the pelvic division commences 4

with the deceleration phase of cervical dilatation. The classic
labor mechanisms that involve the cardinal fetal movements of
the cephalic presentation take place principally during this pel- 2
vic division. In actual practice, however, the onset of the pelvic Second
Latent phase Active phase
division is seldom clearly identifiable. 0
stage
As shown in Figure 22-21, the pattern of cervical dilata- 2 4 6 8 10 12 14
tion during the preparatory and dilatational divisions of normal Time (h)
labor is a sigmoid curve. Two phases of cervical dilatation are
defined. The latent phasee corresponds to the preparatory divi- FIGURE 22-22 Composite of the average dilatation curve for nul-
liparous labor. The first stage is divided into a relatively flat latent
sion, and the active phasee to the dilatational division. And as phase and a rapidly progressive active phase. In the active phase,
shown in Figure 22-22, Friedman subdivided the active phase there are three identifiable component parts that include an
into the acceleration phase, the phase of maximum slope, and the acceleration phase, a phase of maximum slope, and a decelera-
deceleration phase. tion phase. (Redrawn from Friedman, 1978.)
 446 Labor

10 Turning again to Friedman (1955), the mean duration of

9 active-phase labor in nulliparas was 4.9 hours. But the stan-
dard deviation of 3.4 hours is large, hence, the active phase
8
was reported to have a statistical maximum of 11.7 hours.
SECTION 7

7 Indeed, rates of cervical dilatation ranged from a minimum of

Dilatation (cm)

6 1.2 up to 6.8 cm/hr. Friedman (1972) also found that mul-

tiparas progress somewhat faster in active-phase labor, with a
5
minimum normal rate of 1.5 cm/hr. His analysis of active-phase
4 labor concomitantly describes rates of fetal descent and cervical
3 dilatation (see Fig. 22-21). Descent begins in the later stage of
2 active dilatation, commencing at 7 to 8 cm in nulliparas and
becoming most rapid after 8 cm.
1

Active-Phase Abnormalities. These have bee reported to

1 2 3 4 5 6 7 8 9 10 11 12 13 14
occur in 25 percent of nulliparous and 15 percent of mul-
Hours
tiparous labors (Sokol, 1977). Friedman (1972) subdivided
Hendricks, Brenner & Kraus Ledger active-phase problems into protraction and arrest disorders.
Studd Univ. of Michigan Protraction is defined as a slow ratee of cervical dilatation or
descent, which for nulliparas was < 1.2 cm dilatation per
Rodesch et al. Temple Univ.
T
hour or < 1 cm descent per hour. For multiparas, protrac-
Philpott & Castle Friedman tion was defined as < 1.5 cm dilatation per hour or < 2 cm
FIGURE 22-23 Progress of labor in primigravid women from the descent per hour. Friedman defined arrest as a complete cessa-
time of admission. When the starting point on the abscissa begins tion of dilatation or descent. Arrest of dilatation was defined
with admission to the hospital, a latent phase is not observed. as 2 hours with no cervical change, and arrest of descentt as
1 hour without fetal descent. The prognosis for protraction
this, Figure 22-23 shows eight labor curves from nulliparas in and arrest disorders differs considerably. Friedman found
whom labor was diagnosed beginning with their admission, that approximately 30 percent of women with protraction
rather than with the onset of regular contractions. When labor disorders had cephalopelvic disproportion (CPD). This
is defined similarly, there is remarkable similarity of individual compared with a 45-percent CPD rate for women in whom
labor curves. an arrest disorder developed. Abnormal labor patterns, diag-
nostic criteria, and treatment methods are summarized in
Prolonged Latent Phase. Friedman and Sachtleben (1963) Chapter 23 (p. 456).
defined this by a latent phase exceeding 20 hours in the nul- Hendricks and colleagues (1970) challenged Friedman’s
lipara and 14 hours in the multipara. These times corresponded conclusions about the course of normal human labor. Their
to the 95th percentiles. Factors that affected latent phase dura- principal differences included: (1) absence of a latent phase, (2)
tion include excessive sedation or epidural analgesia; unfavorable no deceleration phase, (3) brevity of labor, and (4) dilatation
cervical condition, that is, thick, uneffaced, or undilated; and at similar rates for nulliparas and multiparas after 4 cm. They
false labor. In those who had been administered heavy sedation, disputed the concept of a latent phase because they observed
85 percent of women eventually entered active labor. In another that the cervix dilated and effaced slowly during the 4 weeks
10 percent, uterine contractions ceased, suggesting that they had preceding labor. They contended that the latent phasee actually
false labor. The remaining 5 percent experienced persistence of progressed over several weeks. They also reported that labor was
an abnormal latent phase and required oxytocin stimulation. relatively rapid. Specifically, the average time from admission
Amniotomy was discouraged because of the 10-percent inci- to complete dilatation was 4.8 hours for nulliparas and 3.2
dence of false labor. Sokol and associates (1977) reported a 3- to hours for multiparas.
4- percent incidence of prolonged latent phase, regardless of par- There have been other reports in which investigators have
ity. Friedman (1972) reported that latent phase prolongation did reassessed the Friedman labor curves. Zhang and associates
not adversely influence fetal or maternal morbidity or mortality (2010) studied electronic labor records from 62,415 parturi-
rates. However, Chelmow and coworkers (1993) disputed the ents with spontaneous labor at term and vaginal birth. They
long-held belief that prolongation of the latent phase is benign. found that normal labor may take more than 6 hours to prog-
ress from 4 to 5 cm and more than 3 hours to progress from
Active Labor 5 to 6 cm dilation. Thereafter, labor accelerated much faster
The progress of labor in nulliparas has particular significance in multiparas. In a study performed at Parkland Hospital,
because these curves all reveal a rapid change in the slope of cer- epidural analgesia was found to lengthen the active phase of
vical dilatation rates between 3 and 5 cm (see Fig. 22-23). Thus, the Friedman labor curve by 1 hour (Alexander, 2002). This
cervical dilatation of 3 to 5 cm or more, in the presence of uterine increase was the result of a slight but significant decrease in the
contractions, can be taken to reliably represent the threshold for rate of cervical dilatation—1.4 cm/hr in women given epidu-
active labor. Similarly, these curves provide useful guideposts ral analgesia compared with 1.6 cm/hr in those without such
for labor management. analgesia. There are now several reports that maternal obesity
 Normal Labor 447

lengthens the first stages of labor by 30 to 60 minutes (Chin,

TABLE 22-2. Recommended Nurse/Patient Ratios for
2012; Kominiarek, 2011). Finally, Adams and coworkers
Labor and Delivery
(2012) found that maternal fear increased labor by approxi-
Ratio Clinical Setting

CHAPTER 22
mately 45 minutes.
1:2 Patients in labor
1:1 Patients in second-stage labor
■ Second Stage of Labor 1:1 Patients with medical/obstetrical complications
This stage begins with complete cervical dilatation and ends 1:2 Oxytocin induction/augmentation
with fetal delivery. The median duration is approximately 50 1:1 During epidural analgesia initiation
minutes for nulliparas and about 20 minutes for multiparas, 1:1 Circulation for cesarean delivery
but it is highly variable (Kilpatrick, 1989). In a woman of
higher parity with a previously dilated vagina and perineum,
two or three expulsive efforts after full cervical dilatation
may suffice to complete delivery. Conversely, in a woman of parity, if left unaided, will deliver within approximately 10
with a contracted pelvis, with a large fetus, or with impaired hours after admission for spontaneous labor. Insufficient uter-
expulsive efforts from conduction analgesia or sedation, ine activity is a common and correctable cause of abnormal
the second stage may become abnormally long. Robinson labor progress. Therefore, when the length of otherwise normal
and colleagues (2011) found that increasing maternal body labor exceeds the expected norm, interventions other than cesar-
mass index did not interfere with the second stage of labor. ean delivery—for example, oxytocin administration—must be
Abnormalities of this labor stage are described in Chapter first considered.
23 (p. 456).
MANAGEMENT OF NORMAL LABOR
■ Duration of Labor
The ideal management of labor and delivery requires two
Our understanding of the normal duration of labor may be
potentially opposing viewpoints on the part of clinicians. First,
clouded by the many clinical variables that affect conduct of
birthing should be recognized as a normal physiological process
labor in modern obstetrical units. Kilpatrick and Laros (1989)
that most women experience without complications. Second,
reported that the mean length of first- and second-stage labor
intrapartum complications, often arising quickly and unexpect-
was approximately 9 hours in nulliparous women without
edly, should be anticipated. Thus, clinicians must simultane-
regional analgesia, and that the 95th percentile upper limit
ously make every woman and her supporters feel comfortable,
was 18.5 hours. Corresponding times for multiparous women
yet ensure safety for the mother and newborn should compli-
were a mean of 6 hours with a 95th percentile maximum of
cations suddenly develop. Principles such as these are the basis
13.5 hours. These authors defined labor onset as the time
for a recent “Call to Action”” by seven national organizations
when a woman recalled regular, painful contractions every 3 to
intended to emphasize quality patient care in labor and deliv-
5 minutes that led to cervical change.
ery (Lawrence, 2012). The American Academy of Pediatrics
Spontaneous labor was analyzed in nearly 25,000 women
and the American College of Obstetricians and Gynecologists
delivered at term at Parkland Hospital in the early 1990s.
(2012) have collaborated in the development of Guidelines
Almost 80 percent of women were admitted with a cervical
for Perinatal Care. These provide detailed information on the
dilatation of 5 cm or less. Parity—nulliparous versus multipa-
appropriate content of intrapartum care, including both per-
rous—and cervical dilatation at admission were significant
sonnel and facility requirements. Shown in Table 22-2 are the
determinants of the length of spontaneous labor. The median
recommended nurse-to-patient ratios recommended for labor
time from admission to spontaneous delivery for all parturients
and delivery. Shown in Table 22-3 are the recommended room
was 3.5 hours, and 95 percent of all women delivered within
dimensions for these functions.
10.1 hours. These results suggest that normal human labor is
relatively short. Zhang and associates (2009a,b) described simi-
lar findings in their study of 126,887 deliveries from 12 United
States institutions.
TABLE 22-3. Recommended Minimum Room
Dimensions for Labor and Delivery
■ Summary of Normal Labor Function Net Floor Space (square feet)
Labor is characterized by brevity and considerable biological LDR 340
variation. Active labor can be reliably diagnosed when cervi- Intensive care 200
cal dilatation is 3 cm or more in the presence of uterine con- Vaginal delivery 340
tractions. Once this cervical dilatation threshold is reached, Cesarean delivery 440
normal progression to delivery can be expected, depending
LDR = labor, delivery, and recovery.
on parity, in the ensuing 4 to 6 hours. Anticipated progress
Data from American Academy of Pediatrics and American
during a 1- to 2-hour second stage is monitored to ensure fetal
College of Obstetricians and Gynecologists, 2012.
safety. Finally, most women in spontaneous labor, regardless
 448 Labor

■ Admission Procedures ■ Electronic Fetal Heart Rate Monitoring

Pregnant women should be urged to report early in labor rather As discussed in Chapter 24 (p. 473), electronic fetal heart rate
than to procrastinate until delivery is imminent for fear that monitoring is routinely used for high-risk pregnancies com-
SECTION 7

they might be experiencing false labor. Early admittance to the mencing at admission. Some investigators recommend moni-
labor and delivery unit is important, especially if during ante- toring women with low-risk pregnancies upon admission as
partum care the woman, her fetus, or both have been identified a test of fetal well-being—the so-called fetal admission test. If
as being at risk. no fetal heart rate abnormalities are detected, continuous elec-
tronic monitoring is replaced by intermittent assessment for
the remainder of labor. We are of the view that electronic fetal
■ Identification of Labor heart rate monitoring is reasonable in the preadmission evalu-
Although the differentiation between false and true labor is dif-f ation of women, including those who subsequently are dis-
ficult at times, the diagnosis usually can be clarified by contrac- charged. At Parkland Hospital, external electronic monitoring
tion frequency and intensity and by cervical dilatation. In those is performed for at least 1 hour before discharging the woman
instances when a diagnosis of labor cannot be established with who was ascertained to have false labor.
certainty, observation for a longer period is often wise.
Pates and associates (2007) studied the commonly used
recommendations given to pregnant women that, in the ■ Home Births
absence of ruptured membranes or bleeding, uterine contrac- A major emphasis of obstetrical care during the 20th cen-
tions 5 minutes apart for 1 hour—that is, ≥ 12 contractions tury was the movement to birthing in hospitals rather than in
in 1 hour—may signify labor onset. Among 768 women homes. In 2006, 98.9 percent of births in the United States
studied at Parkland Hospital, active labor defined as cervical took place in hospitals (Martin, 2011). Of the other 1.1 per-
dilatation ≥ 4 cm was diagnosed within 24 hours in three cent, 67.2 percent were in homes, and 27.6 percent were in
fourths of women with ≥ 12 contractions per hour. Bailit and birthing centers. Between 2004 and 2008, more than half of all
coworkers (2005) compared labor outcomes of 6121 women states had an increase in home births (MacDorman, 2011). As
who presented in active labor defined as uterine contractions discussed in Chapter 1 (p. 11) most studies suggest increased
plus cervical dilatation ≥ 4 cm with those of 2697 women risks with home deliveries (Berghella, 2008; Cheng, 2013; de
who presented in the latent phase. Women admitted during Jonge, 2013; Grunebaum, 2013). Indeed, Chervenak and col-
latent-phase labor had more active-phase arrest, more fre- leagues (2013) have questioned the ethics of physicians volun-
quent need for oxytocin labor stimulation, and higher rates tarily involved in home births.
of chorioamnionitis. It was concluded that physician inter-
ventions in women presenting in the latent phase may have
been the cause of subsequent labor abnormalities.
■ Initial Evaluation
Maternal blood pressure, temperature, pulse, and respira-
tory rate are recorded. The pregnancy record is promptly
■ Emergency Medical Treatment reviewed to identify complications. Problems identified or
and Labor Act—EMTALA anticipated during prenatal care should be displayed promi-
Congress enacted EMTALA in 1986 to ensure public access nently in the pregnancy record. Most often, unless there has
to emergency services regardless of the ability to pay. All been bleeding in excess of bloody show, a vaginal examination
Medicare-participating hospitals with emergency services must is performed. The gloved index and second fingers are then
provide an appropriate screening examination for any pregnant introduced into the vagina while avoiding the anal region
woman experiencing contractions and presenting to the emer- (Fig. 22-24). The number of vaginal examinations correlates
gency department for evaluation. with infection-related morbidity, especially in cases of early
The definition of an emergency condition makes specific membrane rupture.
reference to a pregnant woman who is having contractions.
Labor is defined as “the process of childbirth beginning with Ruptured Membranes
the latent phase of labor continuing through delivery of the The woman should be instructed during the antepartum period
placenta. A woman experiencing contractions is in true labor to be aware of fluid leakage from the vagina and to report such
unless a physician certifies that after a reasonable time of an event promptly. Rupture of the membranes is significant
observation the woman is in false labor.” A woman in true for three reasons. First, if the presenting part is not fixed in the
labor is considered “unstable” for interhospital transfer pur- pelvis, the possibility of umbilical cord prolapse and compres-
poses until the newborn and placenta are delivered. An unsta- sion is greatly increased. Second, labor is likely to begin soon
ble woman may, however, be transferred at the direction of if the pregnancy is at or near term. Third, if delivery is delayed
the patient or by a physician who certifies that the benefits after membrane rupture, intrauterine infection is more likely as
of treatment at another facility outweigh the transfer risks. the time interval increases (Herbst, 2007).
Physicians and hospitals violating these federal requirements Upon sterile speculum examination, ruptured membranes
are subject to civil penalties up to $50,000 and termination are diagnosed if amnionic fluid pools in the posterior fornix
from the Medicare program. or clear fluid flows from the cervical canal. Although several
 Normal Labor 449

thin as the adjacent lower uterine segment, it is completely, or

100-percent, effaced.
Cervical dilatation is determined by estimating the average

CHAPTER 22
diameter of the cervical opening by sweeping the examining
finger from the margin of the cervical opening on one side to
that on the opposite side. The diameter traversed is estimated
in centimeters. The cervix is said to be dilated fully when the
diameter measures 10 cm, because the presenting part of a
term-size newborn usually can pass through a cervix this widely
dilated.
The position of the cervix is determined by the relationship
of the cervical os to the fetal head and is categorized as poste-
rior, mid-position, or anterior. Along with position, the consis-
tencyy of cervix is determined to be soft, firm, or intermediate
between these two.
The level—or station—of the presenting fetal part in the birth
canal is described in relationship to the ischial spines, which are
halfway between the pelvic inlet and the pelvic outlet. When
the lowermost portion of the presenting fetal part is at the level
of the spines, it is designated as being at zero (0) station. In
the past, the long axis of the birth canal above and below the
ischial spines was arbitrarily divided into thirds by some and
into fifths (approximately 1 cm) by other groups. In 1989, the
FIGURE 22-24 To perform vaginal examination, the labia have
been separated with one hand, and the first and second fingers American College of Obstetricians and Gynecologists adopted
of the other hand are carefully inserted into the introitus. the classification of station that divides the pelvis above and
below the spines into fifths. Each fifth represents 1 cm above
or below the spines. Thus, as the presenting fetal part descends
from the inlet towardd the ischial spines, the designation
diagnostic tests for the detection of ruptured membranes is –5, –4, –3, –2, –1, then 0 station. Below the spines, as the
have been recommended, none is completely reliable. If the presenting fetal part descends, it passes +1, +2, +3, +4, and +5
diagnosis remains uncertain, another method involves pH stations to delivery. Station +5 cm corresponds to the fetal head
determination of vaginal fluid. The pH of vaginal secretions being visible at the introitus.
normally ranges from 4.5 to 5.5, whereas that of amnionic If the leading part of the fetal head is at 0 station or below,
fluid is usually 7.0 to 7.5. The use of the indicator nitra- most often the fetal head has engaged—thus, the biparietal
zinee to identify ruptured membranes is a simple and fairly plane has passed through the pelvic inlet. If the head is unusually
reliable method. Test papers are impregnated with the dye, molded or if there is an extensive caput formation or both, engage-
and the color of the reaction between these paper strips and ment might not have taken place although the head appears to be
vaginal fluids is interpreted by comparison with a standard at 0 station.
color chart. A pH above 6.5 is consistent with ruptured mem- In a study done at five teaching centers in Denver, residents,
branes. False-positive test results may occur with coexistent nurses, and faculty were surveyed to determine what definitions
blood, semen, or bacterial vaginosis, whereas false-negative were being used to describe fetal station (Carollo, 2004). Four
tests may result with scant fluid. different definitions were in use. Disturbingly, these investiga-
Other tests include arborization or ferning of vaginal tors found that few caregivers were aware that others were using
fluid, which suggests amnionic rather than cervical fluid. different definitions of station! Dupuis and colleagues (2005)
Amnionic fluid crystallizes to form a fernlike pattern due to tested the reliability of clinical estimations of station using the
its relative concentrations of sodium chloride, proteins, and position of the leading part in centimeters above or below the
carbohydrates (Fig. 4-2, p. 49). Detection of alpha-fetopro- spines as recommended by the American Academy of Pediatrics
tein in the vaginal vault has been used to identify amnionic and the American College of Obstetricians and Gynecologists
fluid (Yamada, 1998). Although rarely required, identifica- (2012). A birth simulator was used in which station could be
tion may also follow injection of indigo carmine into the precisely measured and compared with the vaginal examination
amnionic sac via abdominal amniocentesis. done by clinicians. They reported that the clinical examiners
were incorrect a third of the time.
Cervical Assessment These five characteristics: cervical dilatation, efface-
The degree of cervical effacementt usually is expressed in terms ment, consistency, position, and fetal station are assessed
of the length of the cervical canal compared with that of an when tabulating the Bishop score. This score is commonly
uneffaced cervix. When the length of the cervix is reduced by used to predict labor induction outcome and is discussed in
one half, it is 50-percent effaced. When the cervix becomes as Chapter 26 (p. 526).
 450 Labor

■ Laboratory Studies and qualitatively evaluated manually. With the palm of the
When a woman is admitted in labor, most often the hematocrit hand resting lightly on the uterus, the time of contraction onset
or hemoglobin concentration should be rechecked. The hema- is determined. Its intensity is gauged from the degree of firm-
ness the uterus achieves. At the acme of effective contractions,
SECTION 7

tocrit can be measured easily and quickly. At Parkland Hospital,

blood is collected in a standard collection tube with anticoagu- the finger or thumb cannot readily indent the uterus during a
lant. From this, a heparinized capillary tube is filled to spin in a “firm” contraction. The time at which the contraction disap-
microhematocrit centrifuge in the labor and delivery unit. This pears is noted next. This sequence is repeated to evaluate the
provides a hematocrit value within 3 minutes. The initial collec- frequency, duration, and intensity of uterine contractions.
tion tube is also sent to the hematology laboratory for evalua- Maternal Vital Signs
tion. Another labeled tube of blood is allowed to clot and sent
to the blood bank for blood type and antibody screen, if needed. Temperature, pulse, and blood pressure are evaluated at least
A final sample is collected for syphilis and human immuno- every 4 hours. If membranes have been ruptured for many
deficiency virus (HIV) serology. We obtain a urine specimen hours before labor onset or if there is a borderline tempera-
for protein determination in hypertensive women only (Chap. ture elevation, the temperature is checked hourly. Moreover,
40, p. 729). In some labor units, however, a clean-catch voided with prolonged membrane rupture, defined as greater than 18
specimen is examined in all women for protein and glucose. hours, antimicrobial administration for prevention of group B
Women who have had no prenatal care should be consid- streptococcal infections is recommended. This is discussed in
ered to be at risk for syphilis, hepatitis B, and HIV (Chap. 65, Chapter 64 (p. 1249).
p. 1265). In those with no prior prenatal care, these laboratory Subsequent Cervical Examinations
studies, as well as a blood type and antibody screen, should
be performed (American Academy of Pediatrics and American During the first stage of labor, the need for subsequent vaginal
College of Obstetricians and Gynecologists, 2012). Some states, examinations to monitor cervical change and presenting part
for example, Texas, require routine testing for syphilis, hepatitis position will vary considerably. When the membranes rupture,
B, and HIV in all women admitted to labor and delivery units, an examination to exclude cord prolapse should be performed
even if these were done during prenatal care. expeditiously if the fetal head was not definitely engaged at
the previous examination. The fetal heart rate should also be
checked immediately and during the next uterine contraction
■ Management of the First Stage of Labor to help detect occult umbilical cord compression. At Parkland
As soon as possible after admittance, the remainder of a gen- Hospital, periodic pelvic examinations are typically performed
eral examination is completed. Whether a pregnancy is nor- at 2- to 3-hour intervals to evaluate labor progress.
mal can best be determined when all examinations, including
record and laboratory review, are completed. A rational plan for Oral Intake
monitoring labor can then be established based on the needs of Food should be withheld during active labor and delivery.
the fetus and the mother. Because there are marked individual Gastric emptying time is remarkably prolonged once labor is
variations in labor lengths, precise statements as to its antici- established and analgesics are administered. As a consequence,
pated duration are unwise. ingested food and most medications remain in the stomach
and are not absorbed. Instead, they may be vomited and aspi-
Intrapartum Fetal Monitoring rated (Chap. 25, p. 519). According to the American Academy
This is discussed in detail in Chapter 24. Briefly, the American of Pediatrics and the American College of Obstetricians and
Academy of Pediatrics and American College of Obstetricians Gynecologists (2007), sips of clear liquids, occasional ice chips,
and Gynecologists (2012) recommend that during first-stage and lip moisturizers are permitted.
labor, in the absence of any abnormalities, the fetal heart rate
should be checked immediately after a contraction at least every Intravenous Fluids
30 minutes and then every 15 minutes during the second stage. Although it has become customary in many hospitals to estab-
If continuous electronic monitoring is used, the tracing is eval- lish an intravenous infusion system routinely early in labor,
uated at least every 30 minutes during the first stage and at least there is seldom any real need for this in the normal pregnant
every 15 minutes during second-stage labor. For women with woman, at least until analgesia is administered. An intravenous
pregnancies at risk, fetal heart auscultation is performed at least infusion system is advantageous during the immediate puer-
every 15 minutes during first-stage labor and every 5 minutes perium to administer oxytocin prophylactically and at times
during the second stage. Continuous electronic monitoring therapeutically when uterine atony persists. Moreover, with
may be used with evaluation of the tracing every 15 minutes longer labors, the administration of glucose, sodium, and water
during the first stage of labor, and every 5 minutes during the to the otherwise fasting woman at the rate of 60 to 120 mL/hr
second stage. prevents dehydration and acidosis. Shrivastava and associates
(2009) noted shorter labors in nulliparas delivering vaginally
Uterine Contractions who were provided an intravenous normal saline with dex-
Although usually assessed by electronic monitoring as also dis- trose solution compared with those given saline solution only.
cussed in Chapter 24, contractions can be both quantitatively Garite and coworkers (2000) randomly assigned 195 women in
 Normal Labor 451

labor to receive either 125 or 250 mL/hr of lactated Ringer or analgesia. Risk factors for retention were primiparity, oxyto-
isotonic sodium chloride solution. The mean volume of total cin-induced or -augmented labor, perineal lacerations, opera-
intravenous fluid was 2008 mL in the 125 mL/hr group and tive vaginal delivery, catheterization during labor, and labor
2487 mL in the 250 mL/hr group. Labor lasted > 12 hours in duration > 10 hours.

CHAPTER 22
significantly more (26 versus 13 percent) of the women given
a 125 mL/hr infusion compared with those given 250 mL/
hr—26 versus 13 percent, respectively. ■ Management of the
Second Stage of Labor
Maternal Position With full cervical dilatation, which signifies the onset of the
The normal laboring woman need not be confined to bed early second stage, a woman typically begins to bear down. With
in labor. A comfortable chair may be beneficial psychologi- descent of the presenting part, she develops the urge to def- f
cally and perhaps physiologically. In bed, the laboring woman ecate. Uterine contractions and the accompanying expulsive
should be allowed to assume the position she finds most com- forces may now last 1 minutes and recur at an interval no lon-
fortable—this will be lateral recumbency most of the time. She ger than 1½ minute. As discussed on page 447, the median
must not be restricted to lying supine because of resultant aor- duration of the second stage is 50 minutes in nulliparas and
tocaval compression and its potential to lower uterine perfusion 20 minutes in multiparas, although the interval can be highly
(Chap. 4, p. 60). Bloom and colleagues (1998) conducted a variable. Monitoring of the fetal heart rate is discussed on page
randomized trial of walking during labor in more than 1000 450, and interpretation of second-stage electronic fetal heart
women with low-risk pregnancies. They found that walking rate patterns is discussed in Chapter 24 (p. 487).
neither enhanced nor impaired active labor and that it was not
harmful. Lawrence and associates (2009) reached similar find- Expulsive Efforts
ings in their Cochrane database review. In most cases, bearing down is reflexive and spontaneous dur-
ing second-stage labor. Occasionally, a woman may not employ
Analgesia her expulsive forces to good advantage and coaching is desir-
This is discussed in detail in Chapter 25. In general, pain relief able. Her legs should be half-flexed so that she can push with
should depend on the needs and desires of the woman. The them against the mattress. When the next uterine contraction
American College of Obstetricians and Gynecologists (2009) begins, she is instructed to exert downward pressure as though
has specified optimal goals for anesthesia care in obstetrics. she were straining at stool. A woman is not encouraged to push
beyond the completion of each contraction. Instead, she and
Amniotomy her fetus should be allowed to rest and recover. During this
If the membranes are intact, there is a great temptation, even period of actively bearing down, the fetal heart rate auscultated
during normal labor, to perform amniotomy. The presumed immediately after the contraction is likely to be slow but should
benefits are more rapid labor, earlier detection of meconium- recover to normal range before the next expulsive effort.
stained amnionic fluid, and the opportunity to apply an elec- Several positions during the second stage have been rec-
trode to the fetus or insert a pressure catheter into the uterine ommended to augment pushing efforts. Eason and colleagues
cavity for monitoring. The advantages and disadvantages of (2000) performed an extensive review of various positions and
amniotomy are discussed in Chapter 26 (p. 531). Importantly, their effect on the incidence of perineal trauma. They found
the fetal head must be well applied to the cervix and not be dis- that the supported upright position had no advantages over
lodged from the pelvis during the procedure to avert umbilical the recumbent one. Upright positions include sitting, kneel-
cord prolapse. ing, squatting, or resting with the back at a 30-degree eleva-
tion. Conversely, in their systematic review, Berghella and
Urinary Bladder Function coworkers (2008) reported good-quality data that supported
Distention of the bladder should be avoided because it can the upright position. Fetal and obstetrical outcomes appear to
hinder descent of the fetal presenting part and lead to subse- be unaffected whether pushing is coached or uncoached during
quent bladder hypotonia and infection. During each abdomi- second-stage labor (Bloom, 2006; Tuuli, 2012). The maternal
nal examination, the suprapubic region should be inspected effects of coached pushing were reported by Schaffer and col-
and palpated to detect distention. If the bladder is readily leagues (2005), who performed urodynamic testing in primi-
seen or palpated above the symphysis, the woman should be gravidas 3 months following delivery. Women coached to push
encouraged to void. At times, those who may be unable to during second-stage labor had decreased bladder capacity and
void on a bedpan may be able to ambulate with assistance decreased first urge to void compared with women encouraged
to a toilet and successfully void. If the bladder is distended to push or rest as desired. The long-term effects of this practice
and voiding is not possible, catheterization is indicated. are yet to be defined.
Carley and coworkers (2002) found that 51 of 11,332 vagi- As the head descends through the pelvis, the perineum
nal deliveries (1 in 200) were complicated by urinary reten- begins to bulge and the overlying skin becomes stretched. Now
tion. Most women resumed normal voiding before discharge the scalp of the fetus may be visible through the vulvar opening.
from the hospital. Musselwhite and associates (2007) reported At this time, the woman and her fetus are prepared for delivery,
retention in 4.7 percent of women who had labor epidural which is described in Chapter 27 (p. 537).
 452 Labor

LABOR MANAGEMENT PROTOCOLS active phase starts at 3 cm dilatation, and progress should be
no slower than 1 cm/hr. A 4-hour wait is recommended before
An orderly and systematic approach to labor management intervention when the active phase is slow. Labor is graphed,
results in reproducible maternal and perinatal outcomes. This and analysis includes use of alert and action lines. Lavender
SECTION 7

was proven by Althabe and coworkers (2008), who randomized and colleagues (2006) randomized 3000 nulliparous women to
implementation of evidence-based care in 19 hospitals in labor interventions at 2 hours versus 4 hours as recommended
Argentina and Uruguay. Several labor management proto- by WHO. Their cesarean delivery rate was unaffected, and they
cols are subsequently presented. These include those from the concluded that interventions such as amniotomy and oxytocin
National Maternity Hospital in Dublin, the World Health were needlessly increased using the 2-hour time interval. After
Organization, and from Parkland Hospital. their Cochrane Database review, Lavender and associates (2008)
do not recommend use of the partograph for standard labor
■ Active Management of Labor management.
More than 30 years ago, O’Driscoll and associates (1984)
pioneered the concept that a disciplined, standardized labor ■ Parkland Hospital Labor
management protocol reduced the number of cesarean deliv- Management Protocol
eries for dystocia. Their overall cesarean delivery rate was Women are admitted if active labor—defined as cervical dila-
5 percent in the 1970s and 1980s with such management. tation of 3 to 4 cm or more in the presence of uterine contrac-
The approach is now referred to as active management of tions—is diagnosed or if ruptured membranes are confirmed.
labor. Two of its components—amniotomy and oxytocin— Management guidelines summarized in Figure 22-25 stipu-
have been widely used, especially in English-speaking coun- late that a pelvic examination be performed approximately
tries outside the United States. With this protocol, labor is every 2 hours. Ineffective labor is suspected when the cervix
diagnosed when painful contractions are accompanied by does not dilate within approximately 2 hours of admission.
complete cervical effacement, bloody “show,” or ruptured Amniotomy is then performed, and labor progress deter-
membranes. Women with such findings are committed to mined at the next 2-hour evaluation. In women whose labors
delivery within 12 hours. Pelvic examination is performed do not progress, an intrauterine pressure catheter is placed
each hour for the next 3 hours, and thereafter at 2-hour to assess uterine function. Hypotonic contractions and no
intervals. When dilatation has not increased by at least cervical dilatation after an additional 2 to 3 hours result in
1 cm/hr, amniotomy is performed. Progress is again assessed stimulation of labor using the high-dose oxytocin regimen
at 2 hours and high-dose oxytocin infusion, described in described in Chapter 26 (p. 530). The goal is uterine activ-
Chapter 26 (p. 530), is started unless dilatation of at least ity of 200 to 250 Montevideo units for 2 to 4 hours before
1 cm/hr is documented. Women are constantly attended by dystocia can be diagnosed.
midwives. If membranes rupture before admission, oxytocin
is begun for no progress at the 1-hour mark.
López-Zeno and colleagues (1992) prospectively compared
such active management with their “traditional” approach Admission:
to labor management at Northwestern Memorial Hospital cervix 4 cm
in Chicago. They randomly assigned 705 nulliparas with 2 to 3 hours
uncomplicated pregnancies in spontaneous labor at term. depending
The cesarean delivery rate was significantly lower with active on parity
versus traditional management—10.5 versus 14.1 percent, Amniotomy
respectively. Subsequent studies did not show this. Wei and
associates (2009) in a Cochrane database review found a mod- 2 hoursa
est reduction in cesarean delivery rates when active manage- 4 to 8 hours
Internal
depending
ment of labor was compared with standard care. Frigoletto contraction monitor
on parity
and coworkers (1995) reported another randomized trial with
3 hoursa
1934 nulliparous women at Brigham and Women’s Hospital
in Boston. Although they found that such management some-
Oxytocin
what shortened labor, it did not affect the cesarean delivery
2 to 4 hoursa
rate. These observations have since been reported by many
depending
others (Brown, 2008). on parity
Delivery
■ World Health Organization Partograph a
Depending on progress of cervical dilatation
A partographh was designed by the World Health Organization
(WHO) for use in developing countries (Dujardin, 1992). FIGURE 22-25 Schematic of labor management protocol in
According to Orji (2008), the partograph is similar for nullipa- use at Parkland Hospital. The total admission-to-delivery times
ras and multiparas. Labor is divided into a latent phase, which are shorter than the potential sum of the intervention intervals
should last no longer than 8 hours, and an active phase. The because not every woman requires every intervention.
 Normal Labor 453

Dilatation rates of 1 to 2 cm/hr are accepted as evidence of Friedman E: The graphic analysis of labor. Am J Obstet Gynecol 68:1568,
1954
progress after satisfactory uterine activity has been established Friedman EA: An objective approach to the diagnosis and management of
with oxytocin. This can require up to 8 hours or more before abnormal labor. Bull N Y Acad Med 48:842, 1972

CHAPTER 22
cesarean delivery is performed for dystocia. The cumulative time Friedman EA: Labor: Clinical Evaluation and Management, 2nd ed. New
York, Appleton-Century-Crofts, 1978
required to effect this stepwise management approach permits Friedman EA: Primigravid labor: a graphicostatistical analysis. Obstet Gynecol
many women to establish effective labor. This management 6:567, 1955
protocol has been evaluated in more than 20,000 women with Friedman EA, Sachtleben MR: Amniotomy and the course of labor. Obstet
Gynecol 22:755, 1963
uncomplicated pregnancies. Importantly, these labor interven- Frigoletto FD Jr, Lieberman E, Lang JM, et al: A clinical trial of active manage-
tions and the relatively infrequent use of cesarean delivery did ment of labor. N Engl J Med 333:745, 1995
not jeopardize the fetus-newborn. Gardberg M, Tuppurainen M: Anterior placental location predisposes for
occiput posterior presentation near term. Acta Obstet Gynecol Scand
73:151, 1994a
Gardberg M, Tuppurainen M: Persistent occiput posterior presentation—a
REFERENCES clinical problem. Acta Obstet Gynecol Scand 73:45, 1994b
Garite TJ, Weeks J, Peters-Phair K, et al: A randomized controlled trial of the
Adams SS, Eberhard-Gran M, Eskild A: Fear of childbirth and duration of effect of increased intravenous hydration on the course of labor in nullipa-
labour: a study of 2206 women with intended vaginal delivery. BJOG rous women. Am J Obstet Gynecol 183:1544, 2000
119(10):1238, 2012 Graham JM Jr, Kumar A: Diagnosis and management of extensive vertex birth
Alexander JM, Sharma SK, McIntire DD, et al: Epidural analgesia lengthens molding. Clin Pediatr (Phila) 45(7):672, 2006
the Friedman active phase of labor. Obstet Gynecol 100:46, 2002 Grunebaum A, McCullough LB, Sapra KJ, et al: Apgar scores of 0 at 5 minutes
Althabe F, Buekens P, Bergel E, et al: A behavioral intervention to improve and neonatal outcomes or serious neurologic dysfunction in relation to birth
obstetrical care. N Engl J Med 358:1929, 2008 setting. Am J Obstet Gynecol 209:323.e1, 2013
American Academy of Pediatrics and the American College of Obstetricians Handa VL, Blomquist JL, Knoepp LR, et al: Pelvic floor disorder 5–10 years
and Gynecologists: Guidelines for Perinatal Care, 6th ed. Washington, 2007 after vaginal or cesarean childbirth. Obstet Gynecol 118:777, 2011
American Academy of Pediatrics and the American College of Obstetricians Hendricks CH, Brenner WE: Cardiovascular effects of oxytocic drugs used
and Gynecologists: Guidelines for Perinatal Care, 7th ed. Washington, 2012 postpartum. Am J Obstet Gynecol 108:751, 1970
American College of Obstetricians and Gynecologists: Obstetric forceps. Herbst A, Källén K: Time between membrane rupture and delivery and septi-
Committee Opinion 71, August 1989 cemia in term neonates. Obstet Gynecol 110:612, 2007
American College of Obstetricians and Gynecologists: Optimal goals for anes- Kilpatrick SJ, Laros RK Jr: Characteristics of normal labor. Obstet Gynecol
thesia care in obstetrics. Committee Opinion No. 433, May 2009 74:85, 1989
Bailit JL, Dierker L, Blanchard MH, et al: Outcomes of women presenting in Kominiarek MA, Zhang J, VanVeldhuisen P, et al: Contemporary labor
active versus latent phase of spontaneous labor. Obstet Gynecol 105:77, 2005 patterns: the impact of maternal body mass index. Am J Obstet Gynecol
Berghella V, Baxter JK, Chauhan SP: Evidence-based labor and delivery man- 205:244.e1, 2011
agement. Am J Obstet Gynecol 199:445, 2008 Laughon SK, Branch W, Beaver J, et al: Changes in labor patterns over 50
Bloom SL, Casey BM, Schaffer JI, et al: A randomized trial of coached versus years. Am J Obstet Gynecol 206:419.e1.9, 2012
uncoached maternal pushing during the second stage of labor. Am J Obstet Lavender T, Alfirevic A, Walkinshaw S: Effect of different partogram action
Gynecol 194:10, 2006 lines on birth outcomes. Obstet Gynecol 108:295, 2006
Bloom SL, McIntire DD, Kelly MA, et al: Lack of effect of walking on labor Lavender T, Hart A, Smyth RM: Effect of partogram use on outcomes for
and delivery. N Engl J Med 339:76, 1998 women in spontaneous labour at term. Cochrane Database Syst Rev
Brown HC, Paranjothy S, Dowswell T, et al: Package of care for active man- 8:CD005461, 2008
agement in labour for reducing caesarean section rates in low-risk women. Lawrence A, Lewis L, Hofmeyr GJ, et al: Maternal positions and mobil-
Cochrane Database Syst Rev 8:CD004907, 2008 ity during first stage labour. Cochrane Database Syst Rev 2:CD003934,
Caldwell WE, Moloy HC, D’Esopo DA: A roentgenologic study of the mecha- 2009
nism of engagement of the fetal head. Am J Obstet Gynecol 28:824, 1934 Lawrence HC, Copel JA, O’Keeffe DF, et al: Quality patient care in labor and
Calkins LA: The etiology of occiput presentations. Am J Obstet Gynecol delivery: a call to action. Am J Obstet Gynecol 207(3):147, 2012
37:618, 1939 Leopold J: Conduct of normal births through external examination alone. Arch
Carlan SJ, Wyble L, Lense J, et al: Fetal head molding: diagnosis by ultrasound Gynaekol 45:337, 1894
and a review of the literature. J Perinatol 11:105, 1991 López-Zeno JA, Peaceman AM, Adashek JA, et al: A controlled trial of a pro-
Carley ME, Carley JM, Vasdev G, et al: Factors that are associated with clini- gram for the active management of labor. N Engl J Med 326:450, 1992
cally overt postpartum urinary retention after vaginal delivery. Am J Obstet Lydon-Rochelle M, Albers L, Gorwoda J, et al: Accuracy of Leopold maneuvers
Gynecol 187:430, 2002 in screening for malpresentation: a prospective study. Birth 20:132, 1993
Carollo TC, Reuter JM, Galan HL, et al: Defining fetal station. Am J Obstet MacDorman MF, Declerq E, Mathews TJ: United States home births increase
Gynecol 191:1793, 2004 20 percent from 2004 to 2008. Birth 38(3):185, 2011
Chelmow D, Kilpatrick SJ, Laros RK Jr: Maternal and neonatal outcomes after Martin JA, Hamilton BE, Ventura SJ, et al: Births: final data for 2009. Natl
prolonged latent phase. Obstet Gynecol 81:486, 1993 Vital Stat Rep 60(1):1, 2011
Cheng YW, Snowden JM, King TL, et al: Selected perinatal outcomes associ- Musselwhite KL, Faris P, Moore K, et al: Use of epidural anesthesia and the risk
ated with planned home births in the United States. Am J Obstet Gynecol of acute postpartum urinary retention. Am J Obstet Gynecol 196:472, 2007
209(4):325.e1, 2013 Nygaard I, Barber MD, Burgio KL, et al: Prevalence of symptomatic pelvic
Chervenak FA, McCullough LB, Brent RL, et al: Planned home birth: the floor disorders in US women. JAMA 300:1311, 2008
professional responsibility response. Am J Obstet Gynecol 208(1):31, 2013 O’Driscoll K, Foley M, MacDonald D: Active management of labor as an
Chin JR, Henry E, Holmgren CM, et al: Maternal obesity and contrac- alternative to cesarean section for dystocia. Obstet Gynecol 63:485, 1984
tion strength in the first stage of labor. Am J Obstet Gynecol 207:129. Orji E: Evaluating progress of labor in nulliparas and multiparas using the
e1, 2012 modified WHO partograph. Int J Gynaecol Obstet 102:249, 2008
de Jonge A, Mesman JAJM, Manniën J, et al: Severe adverse maternal out- Pates JA, McIntire DD, Leveno KJ: Uterine contractions preceding labor.
comes among low risk women with planned home versus hospital births in Obstet Gynecol 110:566, 2007
the Netherlands: nationwide cohort study. BMJ 346:f3263, 2013 Robinson BK, Mapp DC, Bloom SL, et al: Increasing maternal body mass
Dujardin B, De Schampheleire I, Sene H, et al: Value of the alert and action index and characteristics of the second stage of labor. Obstet Gynecol
lines on the partogram. Lancet 339:1336, 1992 118:1309, 2011
Dupuis O, Silveira R, Zentner A, et al: Birth simulator: Reliability of trans- Schaffer JI, Bloom SL, Casey BM, et al: A randomized trial of the effects of coached
vaginal assessment of fetal head station as defined by the American College vs uncoached maternal pushing during the second stage of labor on postpartum
of Obstetricians and Gynecologists classification. Am J Obstet Gynecol pelvic floor structure and function. Am J Obstet Gynecol 192:1692, 2005
192:868, 2005 Segel SY, Carreño CA, Weiner MS, et al: Relationship between fetal sta-
Eason E, Labrecque M, Wells G, et al: Preventing perineal trauma during tion and successful vaginal delivery in nulliparous women. Am J Perinatol
childbirth: a systematic review. Obstet Gynecol 95:464, 2000 29:723, 2012
 455

CHAPTER 23

Abnormal Labor

DYSTOCIA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 455 More simply, these abnormalities can be mechanistically sim-

plified into three categories that include abnormalities of the
ABNORMALITIES OF THE EXPULSIVE FORCES. . . . . . . . . 458 powers—uterine
s contractility and maternal expulsive effort; the
PREMATURELY RUPTURED MEMBRANES AT TERM . . . . 462 passenger—the
r fetus; and the passage—the
e pelvis. Common
clinical findings in women with these labor abnormalities are
PRECIPITOUS LABOR AND DELIVERY . . . . . . . . . . . . . . . 462 summarized in Table 23-1.

FETOPELVIC DISPROPORTION . . . . . . . . . . . . . . . . . . . . 463

■ Dystocia Descriptors
PELVIC CAPACITY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 463
Abnormalities that are shown in Table 23-1 often interact
FACE PRESENTATION . . . . . . . . . . . . . . . . . . . . . . . . . . 466 in concert to produce dysfunctional labor. Commonly used
expressions today such as cephalopelvic disproportion and fail- l
BROW PRESENTATION . . . . . . . . . . . . . . . . . . . . . . . . . 467 ure to progresss are used to describe ineffective labors. Of these,
cephalopelvic disproportion is a term that came into use before the
TRANSVERSE LIE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468
20th century to describe obstructed labor resulting from dispar-
COMPOUND PRESENTATION . . . . . . . . . . . . . . . . . . . . . 469 ity between the fetal head size and maternal pelvis. But the term
originated at a time when the main indication for cesarean deliv-
COMPLICATIONS WITH DYSTOCIA . . . . . . . . . . . . . . . . . 470 ery was overt pelvic contracture due to rickets (Olah, 1994).
Such absolute disproportion is now rare, and most cases result
from malposition of the fetal head within the pelvis (asynclit-
ism) or from ineffective uterine contractions. True dispropor-
DYSTOCIA tion is a tenuous diagnosis because two thirds or more of women
There are several labor abnormalities that may interfere with
the orderly progression to spontaneous delivery. Generally, TABLE 23-1. Common Clinical Findings in Women with
these are referred to as dystocia. Dystocia literally means difficult Ineffective Labor
laborr and is characterized by abnormally slow labor progress. It
arises from four distinct abnormalities that may exist singly or Inadequate cervical dilation or fetal descent:
in combination. First, expulsive forces may be abnormal. For Protracted labor—slow progress
example, uterine contractions may be insufficiently strong or Arrested labor—no progress
inappropriately coordinated to efface and dilate the cervix— Inadequate expulsive effort—ineffective pushing
uterine dysfunction. Also, there may be inadequate voluntary Fetopelvic disproportion:
maternal muscle effort during second-stage labor. Second, fetal Excessive fetal size
abnormalities of presentation, position, or development may Inadequate pelvic capacity
slow labor. Also, abnormalities of the maternal bony pelvis may Malpresentation or position of the fetus
create a contracted pelvis. And last, soft tissue abnormalities of
Ruptured membranes without labor
the reproductive tract may form an obstacle to fetal descent.
 456 Labor

TABLE 23-2. Abnormal Labor Patterns, Diagnostic Criteria, and Methods of Treatment
Diagnostic Criteria
Preferred
Labor Pattern Nulliparas Multiparas Treatment Exceptional Treatment
SECTION 7

Prolongation Disorder
Prolonged latent phase > 20 hr > 14 hr Bed rest Oxytocin or cesarean delivery
for urgent problems
Protraction Disorders
Protracted active-phase dilatation < 1.2 cm/hr 1.5 cm/hr Expectant and
Cesarean delivery for CPD
Protracted descent < 1 cm/hr < 2 cm/hr support
Arrest Disorders
Prolonged deceleration phase > 3 hr > 1 hr
Secondary arrest of dilatation > 2 hr > 2 hr Evaluate for CPD:
Arrest of descent > 1 hr > 1 hr Rest if exhausted
CPD: cesarean
Failure of descent No descent in deceleration Cesarean delivery
No CPD: oxytocin
phase or second stage

CPD = cephalopelvic disproportion.

Modified from Cohen, 1983.

undergoing cesarean delivery for this reason subsequently deliver the birth canal, must encounter a relatively thick lower uterine
even larger newborns vaginally. A second phrase, failure to prog-
g segment and undilated cervix. The uterine fundus muscle is
resss in either spontaneous or stimulated labor, has become an less developed and presumably less powerful. Uterine contrac-
increasingly popular description of ineffectual labor. This term tions, cervical resistance, and the forward pressure exerted by
reflects lack of progressive cervical dilatation or lack of fetal the leading fetal part are the factors influencing the progress of
descent. Neither of these two expressions is specific. Terms pre- first-stage labor.
sented in Table 23-2 and their diagnostic criteria more precisely As also shown in Figure 23-1B, after complete cervical dila-
describe abnormal labor. tation, the mechanical relationship between the fetal head size
and position and the pelvic capacity, namely fetopelvic propor-
■ Mechanisms of Dystocia tion, becomes clearer as the fetus descends. Because of this,
Dystocia as described by Williams (1903) in the first edition abnormalities in fetopelvic proportions become more apparent
of this text is still true today. Figure 23-1 demonstrates the once the second stage is reached.
mechanical process of labor and potential obstacles. The cervix Uterine muscle malfunction can result from uterine overdis-
and lower uterus are shown at the end of pregnancy and at the tention or obstructed labor or both. Thus, ineffective labor is gen-
end of labor. At the end of pregnancy, the fetal head, to traverse erally accepted as a possible warning sign of fetopelvic disproportion.

Ac
tiv
e

Pa
s siv
.
C.R

e
R. os
C. t.
s

In
.o

s
t. o
t. o
Int

Ex
Ex

A B

FIGURE 23-1 Diagrams of the birth canal. A. At the end of pregnancy. B. During the second-stage of labor, showing formation of the
birth canal. C.R. = contraction ring; Int. = internal; Ext = external. (Adapted from Williams, 1903.)
 Abnormal Labor 457

Although artificial separation of labor abnormalities into pure

TABLE 23-4. Duration of Active Phase Labor:
uterine dysfunction and fetopelvic disproportion simplifies clas-
Comparison in Contemporary Reportsa
sification, it is an incomplete characterization because these
Active Phase,

CHAPTER 23
two abnormalities are so closely interlinked. Indeed, according
to the American College of Obstetricians and Gynecologists Oxytocin Epidural 4–10 cm
(2013), the bony pelvis rarely limits vaginal delivery. In the Investigator (%) (%) Dilation
b
absence of objective means of precisely distinguishing these two 47 84 6 hr
causes of labor failure, clinicians must rely on a trial of laborr to Graseck (2012) 0 70 5 hr
determine if labor can be successful in effecting vaginal delivery. Alexander (2002) 44 100 7.4 hr
a
Includes nulliparous women at term with spontaneous
■ Revised Dystocia Diagnosis labor and cervical dilatation 4 cm.
b
In 2009, the total cesarean delivery rate for all births in the Safe Labor Consortium.
United States reached a record high of 32.9 percent (Martin,
2011). This was the 13th consecutive year in which the cesarean
rate increased, and it represented a nearly 60-percent increase results of the NICHD-sponsored Safe Labor Consortium and on
compared with 20.7 percent in 1996. The 2010 rate of 32.8 an NICHD-sponsored report on second-stage labor duration
percent could suggest that this long trend of increasing cesar- (Rouse, 2009; Zhang, 2010). Shown in Table 23-4 is a compar-
ean rates may now be moderating (Martin, 2012). Given that ison of active labor phase duration in the Safe Labor Consortium
many repeat cesarean deliveries are performed after primary compared with other contemporary reports. It is important to
operations for dystocia, it is estimated that 60 percent of all note that almost half of the Consortium cohort received oxytocin
cesarean deliveries in the United States are ultimately attribut- and 84 percent had received epidural analgesia—both factors
able to the diagnosis of abnormal labor (American College of associated with longer active-phase labor. Indeed, cases using
Obstetricians and Gynecologists, 2013). oxytocin and epidural analgesia in the studies of Graseck (2012)
To address this increasing cesarean delivery rate, a workshop and Alexander (2002) had similar active-labor phase durations
was convened by the National Institute of Child Health and to those from the Consortium. Importantly, all these reports
Human Development (NICHD) and the American College of were based on contemporary obstetrical practices.
Obstetricians and Gynecologists (Spong, 2012). The workshop The Safe Labor Consortium report by Zhang and associates
recommended new definitions for arrest of labor progress to (2010) was a multicenter retrospective study using abstracted
prevent unnecessary first cesarean deliveries. Specifically, it con- 2002 to 2008 data from electronic medical records in 19 hos-
cluded that “adequate time for normal latent and active phases pitals across the United States. One purpose of this study was
of the first stage and for the second stage should be allowed as to analyze labor patterns and develop contemporary criteria for
long as the maternal and fetal conditions permit. The adequate labor progress in nulliparas. Shown in Figure 23-2 is a synopsis
time for each of these stages appears to be longer than tradi- of the study cohort, which formed the basis of the proposed
tionally estimated.” The implication of this viewpoint is that new criteria for labor progress. Importantly, all women with
changing the diagnostic criteria of abnormal labor will reduce cesarean delivery were excluded as were all of those with com-
the excessive cesarean birth rate. Shown in Table 23-3 is a syn- promised newborn infants. Because of these major exclusions,
opsis of some of these workshop recommendations for revised the pattern of labor now defined as normal is problematic given
labor management criteria. According to the workshop, these that only women who achieved vaginal birth with a normal
definitions “vary somewhat from published criteria and are infant outcome were included. It is also problematic to con-
recommended in recognition of more recent findings regarding clude that these revised labor criteria will reduce the cesarean
labor progress that challenge our long-held practices based on rate when the overall rate in the Safe Labor Consortium was 30.5
the Friedman curve.” percent using the newly proposed first-stage labor intervals. The
These proposed new criteria listed in Table 23-3 for normal, authors of a report from the Maternal Fetal Medicine Units
and therefore also abnormal labor, were heavily dependent on Network of the NICHD analyzed labor management practices

TABLE 23-3. Evidence for Adequate and Arrested Labor

Arrest of labor: “. . . the diagnosis of arrest of labor should not be made until adequate time has elapsed.”
Adequate labor: “. . . includes greater than 6 cm dilation with membrane rupture and 4 or more hours of adequate
contractions (e.g., greater than 200 Montevideo units) or 6 hours or more if contractions inadequate with no
cervical change. . . .”
Second-stage labor: “. . . no progress for more than 4 hours in nulliparous women with an epidural, more than 3 hours in
nulliparous women without an epidural. . . .”
“No cesarean before these time limits . . . in the presence of reassuring maternal and fetal status.”

From Spong, 2012.

 458 Labor

women reaching 4 hours in the second stage had been given

Spontaneous onset epidural analgesia and were awaiting cesarean delivery that was
of labor, singletons, decided on at the 3-hour time point. Typically, oxytocin had
cephalic been discontinued, and they also had reassuring fetal heart rate
SECTION 7

n = 98,169 tracings that permitted temporization awaiting operative space.

Thus, such prolonged second stages were unintentionall in that
Excluded:
further efforts to effect vaginal delivery were not made. Despite
23,280 cesarean births these caveats, virtually every adverse infant outcome analyzed
increased significantly when the second stage exceeded 3 hours
in women with labor epidural analgesia (Table 23-5).
We conclude that at this time, an improved definition of
Vaginal delivery
V the adequacy of a trial of labor before diagnosing dystocia
n = 74,889 women
remains an elusive goal. The newly proposed criteria for first-
stage labor are already in use in contemporary practice, and
thus they are unlikely to have much impact on the cesarean
Excluded: delivery rate for abnormal labor. Importantly, the purported
5-min Apgar score < 7 (n = 632) safety of the proposed new criteria for second-stage labor man-
Birth injury (n = 645) agement should be viewed with caution until more published
NICU admission (n = 3033) experiences accrue.

Final study sample

ABNORMALITIES OF THE EXPULSIVE FORCES
n = 62,415
Cervical dilatation and propulsion and expulsion of the fetus
are brought about by contractions of the uterus, which are
reinforced during the second stage by voluntary or involuntary
FIGURE 23-2 Study cohort for the analysis of spontaneous labor muscular action of the abdominal wall—“pushing.” The diag-
in the Safe Labor Consortium. NICU = neonatal intensive care unit. nosis of uterine dysfunction in the latent phase is difficult and
(Data from Zhang, 2010.)
sometimes can be made only in retrospect (Chap. 22, p. 446).
Women who are not yet in active labor commonly are errone-
in 8546 women undergoing primary cesarean delivery for dys- ously treated for uterine dysfunction.
tocia in a wide cross section of hospitals in the United States Beginning in the 1960s, there have been at least three signif-
f
(Alexander, 2003). Approximately 92 percent of the cesareans icant advances in the treatment of uterine dysfunction. First is
for dystocia were performed in the active phase of labor defined the realization that undue labor prolongation may contribute to
as ≥ 4 cm cervical dilatation. The median admission to delivery maternal and perinatal morbidity and mortality rates. Second,
interval was 17 hours, and the median cervical dilation was dilute intravenous infusion of oxytocin is used for treatment of
6 cm before the dystocia diagnosis in women in active-phase certain types of uterine dysfunction. Last, cesarean delivery is
labor. Oxytocin was used in 90 percent of women diagnosed selected rather than difficult midforceps delivery when oxytocin
with dystocia. It was concluded that bona-fide efforts were fails or its use is inappropriate.
being made in contemporary practice to achieve active labor
before diagnosing dystocia leading to cesarean delivery.
The report by Rouse and colleagues (2009) on second-stage ■ Types of Uterine Dysfunction
labor was a secondary analysis of 4126 nulliparous women who Reynolds and coworkers (1948) emphasized that uterine con-
reached the second stage during a randomized trial to study fetal tractions of normal labor are characterized by a gradient of
pulse oximetry. Of the 360 women—9 percent—whose second myometrial activity. These forces are greatest and last longest at
stage was > 3 hours, 95 percent had received epidural analgesia. the fundus—considered fundal dominance—and e they diminish
A third of these 360 women—3.5 percent of the whole cohort— toward the cervix. Caldeyro-Barcia and colleagues (1950) from
had a second stage > 4 hours. The results of this study were inter- Montevideo, Uruguay, inserted small balloons into the myo-
preted as support for extending the duration of the second stage metrium at various levels (Chap. 24, p. 498). They reported
in nulliparas to beyond the current recommended 3 hours when that in addition to a gradient of activity, there was a time dif-
f
epidural analgesia is used (American College of Obstetricians and ferential in the onset of the contractions in the fundus, mid-
Gynecologists, 2013). The investigators concluded that a fetus zone, and lower uterine segments. Larks (1960) described the
born after a > 3-hour second stage had a higher—albeit still low— stimulus as starting in one cornu and then several milliseconds
neonatal intensive care unit (NICU) admission rate and a low risk later in the other. The excitation waves then join and sweep
for brachial plexus injury (Rouse, 2009). over the fundus and down the uterus. Normal spontaneous
These latter results are in contrast to those associated with contractions often exert pressures approximating 60 mm Hg
prolonged second-stage labors at Parkland Hospital (Bleich, (Hendricks, 1959). Even so, the Montevideo group ascertained
2012). This study included 21,991 women of whom 7 percent that the lower limit of contraction pressure required to dilate
had a second-stage labor > 3 hours. Most of the 2 percent of the cervix is 15 mm Hg.
 Abnormal Labor 459

TABLE 23-5. Neonatal Outcomes in Relation to Second-Stage Labor Duration

Second-Stage Duration

CHAPTER 23
< 3 hours 3–4 hours ≥ 4 hours p
Outcome n = 20,502 n = 1062 n = 427 value
Birthweight ≥ 4000 g 962 (5) 150 (14)a 71 (17)a < 0.001
pg scores ≤ 3 at 5 minutes
Apgar 14 ((0.1)) ( )a
3 (0.3) 2 ((0.5))a 0.002
Umbilical artery blood pH < 7.0 75 (0.4) 8 (0.8)a 4 (1)d 0.024
Resuscitation at delivery 120 (0.6) 18 (2)a 13 (3)a < 0.001
Admission to intensive care 150 (0.7) 22 (2)a 8 (2)a < 0.001
Seizuresb 23 (0.1) 18 (1.7)a 13 (3)a < 0.001
Sepsisc 32 (0.2) 7 (0.7)a 0 < 0.001
Erb palsy 67 (0.3) 15 (1.4)a 2 (0.5) < 0.001
Neonatal death 3 (0.02) 0 0 0.897

All data shown as n (%).

a
Significantly different compared to < 3 hours.
b
Seizure within the first 24 hours of life.
c
Sepsis defined as positive blood culture.
d
Significant compared to < 3 hours after adjustment for age, race, body mass index,
and epidural analgesia.
Data from Bleich, 2012.

From these observations, it is possible to define two types Hauth and coworkers (1986, 1991) reported that when
of uterine dysfunction. In the more common hypotonic uterine labor is effectively induced or augmented with oxytocin,
dysfunction, there is no basal hypertonus and uterine contrac- 90 percent of women achieve 200 to 225 Montevideo units,
tions have a normal gradient pattern (synchronous), but pres- and 40 percent achieve at least 300 Montevideo units. These
sure during a contraction is insufficient to dilate the cervix. In results suggest that there are certain minimums of uterine
the second type, hypertonic uterine dysfunction or incoordinate activity that should be achieved before performing cesarean
uterine dysfunction, either basal tone is elevated appreciably or delivery for dystocia. Accordingly, the American College of
the pressure gradient is distorted. Gradient distortion may result Obstetricians and Gynecologists (2013) has suggested that
from more forceful contraction of the uterine midsegment than before the diagnosis of first-stage labor arrest is made, spe-
the fundus or from complete asynchrony of the impulses origi- cific criteria should be met. First, the latent phase has been
nating in each cornu or a combination of these two. completed, and the cervix is dilated 4 cm or more. Also, a
uterine contraction pattern of 200 Montevideo units or more
■ Active-Phase Disorders in a 10-minute period has been present for 2 hours without
Labor abnormalities are divided into either a slower-than- cervical change. Rouse and associates (1999) have challenged
normal progress—protraction
— disorderr—or a complete cessation of the “2-hour rule” on the grounds that a longer time, that is,
progress—arrest disorder. A woman must be in the active phase at least 4 hours, is necessary before concluding that the active
of labor with cervical dilatation to at least 3 to 4 cm to be diag- phase of labor has failed. We agree.
nosed with either of these. Handa and Laros (1993) diagnosed
active-phase arrest, defined as no dilatation for 2 hours or more,
in 5 percent of term nulliparas. This incidence has not changed ■ Second-Stage Disorders
since the 1950s (Friedman, 1978). Inadequate uterine contrac- As discussed in Chapter 21 (p. 415), fetal descent largely fol-
tions, defined as less than 180 Montevideo units, calculated as lows complete dilatation. Moreover, the second stage incorpo-
shown in Figure 23-3, were diagnosed in 80 percent of women rates many of the cardinal movements necessary for the fetus
with active-phase arrest. to negotiate the birth canal. Accordingly, disproportion of the
Protraction disorders are less well described, and the time fetus and pelvis frequently becomes apparent during second-
necessary before diagnosing slow progress is undefined. The stage labor.
World Health Organization (1994) has proposed a labor Until recently, there have been largely unquestioned second-
management partograph in which protraction is defined as less stage rules that limited its duration. These rules were established
than 1 cm/hr cervical dilatation for a minimum of 4 hours. in American obstetrics by the beginning of the 20th century. They
Criteria for the diagnosis of protraction and arrest disor- stemmed from concerns about maternal and fetal health, likely
ders have been recommended by the American College of regarding infection, and led to difficult forceps operations. The
Obstetricians and Gynecologists (2013). These criteria were second stage in nulliparas was limited to 2 hours and extended to
adapted from those of Cohen and Friedman (1983), shown 3 hours when regional analgesia was used. For multiparas, 1 hour
in Table 23-2. was the limit, extended to 2 hours with regional analgesia.
 460 Labor

FHR 240 bpm FHR 240 bpm FHR 240 bpm

210 210 210
10 min
180 180 180
SECTION 7

150 150 150

120
1 20 120
1 20
0 12
120
12
20
0

90 90 90

60 60 60

30 30 30

100 100 100

1 75 75 75
2 3 4 5

50
5 0 50 50

25 25 25

mmHg
H UA mmHg UA mmHg
H UA mmHg
0 0 0
52 mm Hg 50 mm Hg 47 mm Hg 44 mm Hg 49 mm Hg

FIGURE 23-3 Montevideo units are calculated by subtracting the baseline uterine pressure from the peak contraction pressure for each
contraction in a 10-minute window and adding the pressures generated by each contraction. In the example shown, there were five contrac-
tions, producing pressure changes of 52, 50, 47, 44, and 49 mm Hg, respectively. The sum of these five contractions is 242 Montevideo units.

Cohen (1977) investigated the fetal effects of second-stage ity and morbidity rates were not related to the length of the
labor length at Beth Israel Hospital. He included 4403 term second stage.
nulliparas in whom electronic fetal heart rate monitoring was
performed. The neonatal mortality rate was not increased in Relationship between First- and
women whose second-stage labor exceeded 2 hours. Epidural Second-Stage Labor Duration
analgesia was used commonly, and this likely accounted for the It is possible that prolonged first-stage labor presages that
large number of pregnancies with a prolonged second stage. with the second stage. Nelson and associates (2013) studied
These data influenced decisions to permit an additional hour the relationships between the lengths of the first and second
for the second stage when regional analgesia is used. stages of labor in 12,523 nulliparous women at term delivered
Menticoglou and coworkers (1995a,b) challenged the pre- at Parkland Hospital. The length of the second stage signifi-
vailing dictums on second-stage duration. These arose because cantly increased concomitantly with increasing length of the
of grave neonatal injuries associated with forceps rotations to first stage. The 95th percentile was 15.6 and 2.9 hours for the
shorten second-stage labor. As a result, they allowed a longer first and second stages, respectively. Women with first stages
second stage to decrease the operative vaginal delivery rate. lasting longer than 15.6 hr (> 95th percentile) had a 16.3 per-
Between 1988 and 1992, second-stage labor exceeded 2 hours cent rate of a second-stage labor lasting 3 hr (95th percentile)
in a fourth of 6041 nulliparas at term. Labor epidural anal- compared with a 4.5-percent rate in women with first-stages
gesia was used in 55 percent. The length of the second stage, labors lasting less than the 95th percentile.
even in those lasting up to 6 hours or more, was not related to
neonatal outcome. These results were attributed to careful use
of electronic monitoring and scalp pH measurements. These
investigators concluded that there is no compelling reason to TABLE 23-6. Clinical Outcomes in Relation to the
intervene with a possibly difficult forceps or vacuum extraction Duration of Second-Stage Labor
because a certain number of hours have elapsed. They observed, Duration of Second Stage
however, that after 3 hours in the second stage, delivery by
< 2 hr 2–4 hr > 4 hr
cesarean or other operative method increased progressively. By Clinical Outcome (%) n = 6529 n = 384 n = 148
5 hours, the prospects for spontaneous delivery in the subse-
quent hour are only 10 to 15 percent. Cesarean delivery 1.2 9.2 34.5
Adverse maternal outcomes, however, are increased with Instrumented delivery 3.4 16.0 35.1
prolonged second-stage labor. Myles and Santolaya (2003) Perineal trauma 3.6 13.4 26.7
analyzed both the maternal and neonatal consequences of this Postpartum hemorrhage 2.3 5.0 9.1
in 7818 women in Chicago between 1996 and 1999. Adverse Chorioamnionitis 2.3 8.9 14.2
maternal outcomes in relation to the duration of second-stage
Adapted from Myles, 2003.
labor were increased as shown in Table 23-6. Neonatal mortal-
 Abnormal Labor 461

Maternal Pushing Efforts TABLE 23-7. Effect of Epidural Analgesia on the Progress
With full cervical dilatation, most women cannot resist the urge of Labor in 199 Nulliparous Women Delivered
to “bear down” or “push” each time the uterus contracts (Chap. Spontaneously at Parkland Hospital

CHAPTER 23
22, p. 451). The combined force created by contractions of the
Epidural Meperidine p
uterus and abdominal musculature propels the fetus downward.
Factora Analgesia Analgesia value
Bloom and colleagues (2006) studied effects of actively coach-
ing expulsive efforts. They reported that although the second Cervical dilatation at 4.1 cm 4.2 cm NS
stage was slightly shorter in coached women, there were no analgesia
other maternal advantages. Active phase 7.9 hr 6.3 hr .005
At times, force created by abdominal musculature is com- Second stage 60 min 48 min .03
promised sufficiently to slow or even prevent spontaneous vag- Fetal descent 4.2 cm/hr 7.9 cm/hr .003
inal delivery. Heavy sedation or regional analgesia may reduce a
Mean values are listed.
the reflex urge to push and may impair the ability to contract
NS = not stated.
abdominal muscles sufficiently. In other instances, the inherent
Data from Alexander, 1998.
urge to push is overridden by the intense pain created by bear-
ing down. Two approaches to second-stage pushing in women
with epidural analgesia have yielded contradictory results.
The first advocates pushing forcefully with contractions after
Chorioamnionitis
complete dilation, regardless of the urge to push. With the
second, analgesia infusion is stopped and pushing begun only Because of the association of prolonged labor with maternal
after the woman regains the sensory urge to bear down. Fraser intrapartum infection, some clinicians have suggested that
and coworkers (2000) found that delayed pushing reduced dif- f infection itself contributes to abnormal uterine activity. Satin
ficult operative deliveries, whereas Manyonda and associates and coworkers (1992) studied the effects of chorioamnionitis
(1990) reported the opposite. Hansen and colleagues (2002) on oxytocin stimulation in 266 pregnancies. Infection diag-
randomly assigned 252 women with epidural analgesia to one nosed late in labor was found to be a marker of cesarean deliv-
of the two approaches. There were no adverse maternal or ery performed for dystocia, whereas this was not a marker in
neonatal outcomes linked to delayed pushing despite signifi- women diagnosed as having chorioamnionitis early in labor.
cantly prolonging second-stage labor. Plunkett and coworkers Specifically, 40 percent of women developing chorioamnionitis
(2003), in a similar study, confirmed these findings. after requiring oxytocin for dysfunctional labor later required
cesarean delivery for dystocia. It is likely that uterine infection
in this clinical setting is a consequence of dysfunctional, pro-
■ Fetal Station at Onset of Labor longed labor rather than a cause of dystocia.
Descent of the leading edge of the presenting part to the level of
the ischial spines (0 station) is defined as engagement. Friedman Maternal Position During Labor
and Sachtleben (1965, 1976) reported a significant association Advocacy for recumbency or ambulation during labor has
between higher station at the onset of labor and subsequent dys- vacillated. Proponents of walking report it to shorten labor,
tocia. Handa and Laros (1993) found that fetal station at the time decrease rates of oxytocin augmentation, decrease the need for
of arrested labor was also a risk factor for dystocia. Roshanfekr analgesia, and lower the frequency of operative vaginal deliv-
and associates (1999) analyzed fetal station in 803 nulliparous ery (Flynn, 1978; Read, 1981). But other observations do not
women at term in active labor. At admission, the third with support this. According to Miller (1983), the uterus contracts
the fetal head at or below 0 station had a 5-percent cesarean more frequently but with less intensity with the mother lying
delivery rate. This is compared with a 14-percent rate for those on her back rather than on her side. Conversely, contraction
with higher stations. The prognosis for dystocia, however, was frequency and intensity have been reported to increase with sit-
not related to incrementally higher fetal head stations above the ting or standing. Lupe and Gross (1986) concluded, however,
pelvic midplane (0 station). Importantly, 86 percent of nullipa- that there is no conclusive evidence that upright maternal pos-
rous women without fetal head engagement at diagnosis of active ture or ambulation improves labor. They reported that women
labor delivered vaginally. These observations apply especially for preferred to lie on their side or sit in bed. Few chose to walk,
parous women because the head typically descends later in labor. fewer to squat, and none wanted the knee-chest position. They
tended to assume fetal positions in later labor. Most women
■ Reported Causes of Uterine Dysfunction enthusiastic about ambulation returned to bed when active
labor began (Carlson, 1986; Williams, 1980).
Epidural Analgesia Bloom and colleagues (1998) conducted a randomized trial
Various labor factors have been implicated as causes of uter- to study the effects of walking during first-stage labor. In 1067
ine dysfunction. Of these, epidural analgesia can slow labor women with uncomplicated term pregnancies delivered at
(Sharma, 2000). As shown in Table 23-7, epidural analgesia Parkland Hospital, these investigators reported that ambulation
has been associated with lengthening of both first- and second- did not affect labor duration. Ambulation did not reduce the
stage labor and with slowing of the rate of fetal descent. This is need for analgesia, nor was it harmful to the perinate. Because of
documented further in Chapter 25 (p. 515). these observations, we give women without complications the
 462 Labor

option to select either recumbency or supervised ambulation with ruptured membranes managed with labor stimulation
during labor. This policy is in agreement with the American compared with those expectantly managed.
College of Obstetricians and Gynecologists (2013), which has Subsequent research included that of Hannah (1996)
concluded that ambulation in labor is not harmful, and mobil- and Peleg (1999) and their associates, who enrolled a total
SECTION 7

ity may result in greater comfort. of 5042 pregnancies with ruptured membranes in a random-
ized investigation. They measured the effects of induction
Birthing Position in Second-Stage Labor versus expectant management and also compared induction
Considerable interest has been shown in alternative second- using intravenous oxytocin with that using prostaglandin E2
stage labor birth positions and their effect on labor. Gupta and gel. There were approximately 1200 pregnancies in each of
Hofmeyr (2004) in their Cochrane database review compared the four study arms. They concluded that labor induction
upright positions with supine or lithotomy positions. Upright with intravenous oxytocin was the preferred management.
positions included sitting in a “birthing chair,” kneeling, squat- This determination was based on significantly fewer intrapar-
ting, or resting with the back at a 30-degree elevation. With these tum and postpartum infections in women whose labor was
positions, they found a 4-minute shorter interval to delivery, less induced. There were no significant differences in cesarean
pain, and a lower incidence both of nonreassuring fetal heart rate delivery rates. Subsequent analysis by Hannah and coworkers
patterns and of operative vaginal delivery. There was, however, (2000) indicated increased adverse outcomes when expectant
an increased rate of blood loss > 500 mL with the upright posi- management at home was compared with in-hospital obser-
tions. Berghella and colleagues (2008) hypothesized that parity, vation. Mozurkewich and associates (2009) reported lower
less intense aortocaval compression, improved fetal alignment, rates of chorioamnionitis, metritis, and NICU admissions
and larger pelvic outlet diameters might explain these findings. for women with term ruptured membranes whose labors
In an earlier study, Russell (1969) described a 20- to 30-percent were induced compared with those managed expectantly.
increase in the area of the pelvic outlet with squatting compared At Parkland Hospital, labor is induced soon after admission
with that in the supine position. Finally, Babayer and associates when ruptured membranes are confirmed at term. The ben-
(1998) cautioned that prolonged sitting or squatting during the efit of prophylactic antibiotics in women with ruptured mem-
second stage may cause common fibular nerve neuropathy. branes before labor at term is unclear (Passos, 2012).

Water Immersion
PRECIPITOUS LABOR AND DELIVERY
A birthing tub or bath has been advocated as a means of relax-
ation that may contribute to more efficient labor. Cluett and Labor can be too slow, but it also can be abnormally rapid.
coworkers (2004) randomly assigned 99 laboring women at term Precipitous labor and deliveryy is extremely rapid labor and deliv-
in first-stage labor identified to have dystocia to immersion in ery. It may result from an abnormally low resistance of the soft
a birthing pool or to oxytocin augmentation. Water immersion parts of the birth canal, from abnormally strong uterine and
lowered the rate of epidural analgesia use but did not alter the abdominal contractions, or rarely from the absence of painful
rate of operative delivery. More infants of women in the immer- sensations and thus a lack of awareness of vigorous labor.
sion group were admitted to the NICU. These findings were According to Hughes (1972), precipitous labor terminates
similar to their subsequent Cochrane database review, except in expulsion of the fetus in < 3 hours. Using this definition,
that NICU admission rates were not increased (Cluett, 2009). 89,047 live births—2 percent—were complicated by precipi-
Robertson and associates (1998) reported that immersion tous labor in the United States during 2006 (Martin, 2009).
was not associated with chorioamnionitis or uterine infection. Despite this incidence, there is little published information
Moreover, Kwee and coworkers (2000) studied the effects concerning adverse effects.
of immersion in 20 women and reported that blood pressure
decreased, whereas fetal heart rate was unaffected. Neonatal com-
plications unique to underwater birth that have been described ■ Maternal Effects
include drowning, hyponatremia, waterborne infection, cord Precipitous labor and delivery seldom are accompanied by seri-
rupture, and polycythemia (Austin, 1997; Pinette, 2004). ous maternal complications if the cervix is effaced appreciably
and compliant, if the vagina has been stretched previously,
PREMATURELY RUPTURED and if the perineum is relaxed. Conversely, vigorous uterine
MEMBRANES AT TERM contractions combined with a long, firm cervix and a non-
compliant birth canal may lead to uterine rupture or extensive
Membrane rupture at term without spontaneous uterine con- lacerations of the cervix, vagina, vulva, or perineum. It is in
tractions complicates approximately 8 percent of pregnancies. these latter circumstances that the rare condition of amnionic-
Until recently, management generally included labor stimula- fluid embolism most likely develops (Chap. 41, p. 812).
tion if contractions did not begin after 6 to 12 hours. This Precipitous labor is frequently followed by uterine atony. The
intervention evolved more than 50 years ago because of mater- uterus that contracts with unusual vigor before delivery is likely to
nal and fetal complications due to chorioamnionitis (Calkins, be hypotonic after delivery. Postpartum hemorrhage from uterine
1952). Such routine intervention was the accepted practice atony is discussed in Chapter 41 (p. 784).
until challenged by Kappy and colleagues (1979). These inves- Mahon and colleagues (1994) described 99 pregnancies
tigators reported excessive cesarean delivery in term pregnancies delivered within 3 hours of labor onset. Short laborss were
 Abnormal Labor 463

defined as a rate of cervical dilatation of 5 cm/hr or faster for through an inlet that has an anteroposterior diameter of less
nulliparas and 10 cm/hr for multiparas. Such short labors were than 10 cm. Mengert (1948) and Kaltreider (1952), employ-
more common in multiparas who typically had contractions at ing x-ray pelvimetry, demonstrated that the incidence of dif- f

CHAPTER 23
intervals less than 2 minutes and were associated with placental ficult deliveries is increased to a similar degree when either the
abruption, meconium, postpartum hemorrhage, cocaine abuse, anteroposterior diameter of the inlet is < 10 cm or the trans-
and low Apgar scores. verse diameter is < 12 cm. As expected, when both diameters
are contracted, dystocia is much greater than when only one
is contracted.
■ Fetal and Neonatal Effects A small woman is likely to have a small pelvis, but she is
Adverse perinatal outcomes from precipitous labor may be also likely to have a small neonate. Thoms (1937) studied 362
increased considerably for several reasons. The tumultuous nulliparas and found that the mean birthweight of their off- ff
uterine contractions, often with negligible intervals of relax- spring was significantly lower—280 g—in women with a small
ation, prevent appropriate uterine blood flow and fetal oxygen- pelvis than in those with a medium or large pelvis. In veterinary
ation. Resistance of the birth canal may rarely cause intracranial obstetrics, in most species, maternal size rather than paternal
trauma. Acker and coworkers (1988) reported that Erb or size is the important determinant of fetal size.
Duchenne brachial palsy was associated with such labors in a Normally, cervical dilatation is aided by hydrostatic action
third of cases (Chap. 33, p. 648). Finally, during an unattended of the unruptured membranes or after their rupture, by direct
birth, the newborn may fall to the floor and be injured, or it application of the presenting part against the cervix (Fig. 21-7,
may need resuscitation that is not immediately available. p. 414). In contracted pelves, however, because the head
is arrested in the pelvic inlet, the entire force exerted by the
■ Treatment uterus acts directly on the portion of membranes that contact
the dilating cervix. Consequently, early spontaneous rupture of
Unusually forceful spontaneous uterine contractions are not
the membranes is more likely.
likely to be modified to a significant degree by analgesia. The
After membrane rupture, absent pressure by the head against
use of tocolytic agents such as magnesium sulfate is unproven
the cervix and lower uterine segment predisposes to less effective
in these circumstances. Use of general anesthesia with agents
contractions. Hence, further dilatation may proceed very slowly
that impair uterine contractibility, such as isoflurane, is often
or not at all. Cibils and Hendricks (1965) reported that the
excessively heroic. Certainly, any oxytocin agents being admin-
mechanical adaptation of the fetal passenger to the bony passage
istered should be stopped immediately.
plays an important part in determining the efficiency of contrac-
tions. The better the adaptation, the more efficient the contrac-
FETOPELVIC DISPROPORTION tions. Thus, cervical response to labor provides a prognostic view
of labor outcome in women with inlet contraction.
■ Pelvic Capacity A contracted inlet also plays an important part in the pro-
Fetopelvic disproportion arises from diminished pelvic capacity, duction of abnormal presentations. In normal nulliparas, the
excessive fetal size, or more usually both. Any contraction of the presenting part at term commonly descends into the pelvic cav-
pelvic diameters that diminishes its capacity can create dystocia ity before labor onset. When the inlet is contracted considerably
during labor. There may be a contraction of the pelvic inlet, the or there is marked asynclitism, descent usually does not take
midpelvis, or the pelvic outlet, or a generally contracted pelvis place until after labor onset, if at all. Cephalic presentations still
may be caused by combinations of these. Normal pelvic dimen- predominate, but the head floats freely over the pelvic inlet or
sion are additionally discussed in Chapter 2 (p. 32). rests more laterally in one of the iliac fossae. Accordingly, very
slight influences may cause the fetus to assume other presen-
Contracted Inlet tations. In women with contracted pelves, face and shoulder
The pelvic inlet usually is considered to be contracted if its presentations are encountered three times more frequently, and
shortest anteroposterior diameter is < 10 cm or if the greatest the cord prolapses four to six times more often.
transverse diameter is < 12 cm. The anteroposterior diameter
of the inlet is commonly approximated by manually measuring Contracted Midpelvis
the diagonal conjugate, which is approximately 1.5 cm greater This finding is more common than inlet contraction. It fre-
(Chap. 2, p. 33). Therefore, inlet contraction usually is defined quently causes transverse arrest of the fetal head, which poten-
as a diagonal conjugate < 11.5 cm. tially can lead to a difficult midforceps operation or to cesarean
Using clinical and at times, imaging pelvimetry, it is impor- delivery.
tant to identify the shortest anteroposterior diameter through The obstetrical plane of the midpelvis extends from the
which the fetal head must pass. Occasionally, the body of the inferior margin of the symphysis pubis through the ischial
first sacral vertebra is displaced forward so that the shortest dis- spines and touches the sacrum near the junction of the fourth
tance may actually be between this abnormal sacral promontory and fifth vertebrae (Chap. 2, p. 33). A transverse line theoreti-
and the symphysis pubis. cally connecting the ischial spines divides the midpelvis into
Before labor, the fetal biparietal diameter has been shown anterior and posterior portions. The former is bounded ante-
to averagee from 9.5 to as much as 9.8 cm. Therefore, it might riorly by the lower border of the symphysis pubis and laterally
prove difficult or even impossible for some fetuses to pass by the ischiopubic rami. The posterior portion is bounded
 464 Labor

dorsally by the sacrum and laterally by the sacrospinous liga- warrants careful review of previous radiographs and possibly
ments, forming the lower limits of the sacrosciatic notch. pelvimetry later in pregnancy.
Average midpelvis measurements are as follows: transverse,
or interischial spinous, 10.5 cm; anteroposterior, from the lower ■ Estimation of Pelvic Capacity
SECTION 7

border of the symphysis pubis to the junction of S4–5, 11.5 cm;

The techniques for clinical evaluation using digital examina-
and posterior sagittal,l from the midpoint of the interspinous
tion of the bony pelvis during labor are described in detail in
line to the same point on the sacrum, 5 cm. The definition of
Chapter 2 (p. 32). Briefly, the examiner attempts to judge the
midpelvic contractions has not been established with the same
anteroposterior diameter of the inlet—the diagonal conjugate,
precision possible for inlet contractions. Even so, the midpelvis
the interspinous diameter of the midpelvis, and the intertuber-
is likely contracted when the sum of the interspinous and pos-
ous distances of the pelvic outlet. A narrow pelvic arch of less
terior sagittal diameters of the midpelvis—normally, 10.5 plus
than 90 degrees can signify a narrow pelvis. An unengaged fetal
5 cm, or 15.5 cm—falls to 13.5 cm or less. This concept was
head can indicate either excessive fetal head size or reduced pel-
emphasized by Chen and Huang (1982) in evaluating possible
vic inlet capacity.
midpelvic contraction. There is reason to suspect midpelvic
The value of radiologic imaging to assess pelvic capacity
contraction whenever the interspinous diameter is < 10 cm.
has also been examined. First, with x-ray pelvimetry alone, the
When it measures < 8 cm, the midpelvis is contracted.
prognosis for successful vaginal delivery in any given pregnancy
Although there is no precise manual method of measuring
cannot be established (Mengert, 1948). Thus, the American
midpelvic dimensions, a suggestion of contraction sometimes
College of Obstetricians and Gynecologists (2009) considers
can be inferred if the spines are prominent, the pelvic sidewalls
x-ray pelvimetry to be of limited value in the management of
converge, or the sacrosciatic notch is narrow. Moreover, Eller
labor with a cephalic presentation.
and Mengert (1947) noted that the relationship between the
Advantages of pelvimetry with computed tomography (CT),
intertuberous and interspinous diameters of the ischium is suf-f
such as that shown in Figure 23-4, compared with those of con-
ficiently constant that narrowing of the interspinous diameter
ventional x-ray pelvimetry include reduced radiation exposure,
can be anticipated when the intertuberous diameter is narrow.
greater accuracy, and easier performance. With either method,
A normal intertuberous diameter, however, does not always
costs are comparable, and x-ray exposure is small (Chap. 46,
exclude a narrow interspinous diameter.
p. 934). Depending on the machine and technique employed,
Contracted Outlet fetal doses with CT pelvimetry may range from 250 to
1500 mrad (Moore, 1989).
This finding usually is defined as an interischial tuberous diam- Advantages of magnetic resonance (MR) pelvimetry include
eter of 8 cm or less. The pelvic outlet may be roughly likened to lack of ionizing radiation, accurate measurements, complete
two triangles, with the interischial tuberous diameter constitut- fetal imaging, and the potential for evaluating soft tissue dys-
ing the base of both. The sides of the anterior triangle are the tocia (McCarthy, 1986; Stark, 1985). Zaretsky and colleagues
pubic rami, and its apex is the inferoposterior surface of the (2005) used MR imaging to measure pelvic and fetal head
symphysis pubis. The posterior triangle has no bony sides but volume to identify those women at greatest risk of undergo-
is limited at its apex by the tip of the last sacral vertebra—not ing cesarean delivery for dystocia. Although significant asso-
the tip of the coccyx. Diminution of the intertuberous diameter ciations were found with some of the measures and cesarean
with consequent narrowing of the anterior triangle must inevita- delivery for dystocia, these researchers could not with accuracy
bly force the fetal head posteriorly. Floberg and associates (1987) predict which individual women would require cesarean deliv-
reported that outlet contractions were found in almost 1 percent ery. Others have reported similar findings (Sporri, 1997).
of more than 1400 unselected nulliparas with term pregnancies.
A contracted outlet may cause dystocia not so much by itself but
by an often-associated midpelvic contraction. Outlet contraction ■ Fetal Dimensions in Fetopelvic
without concomitant midplane contraction is rare. Disproportion
Although the disproportion between the fetal head and the Fetal size alone is seldom a suitable explanation for failed
pelvic outlet is not sufficiently great to give rise to severe dystocia, labor. Even with the evolution of current technology, a fetal
it may play an important part in perineal tears. With increased size threshold to predict fetopelvic disproportion is still elu-
narrowing of the pubic arch, the occiput cannot emerge directly sive. Most cases of disproportion arise in fetuses whose weight
beneath the symphysis pubis but is forced farther down upon is well within the range of the general obstetrical population.
the ischiopubic rami. The perineum, consequently, becomes As shown in Figure 23-5, two thirds of neonates who required
increasingly distended and thus exposed to risk of laceration. cesarean delivery after failed forceps delivery weighed less than
3700 g. Thus, other factors—for example, malposition of the
head—obstruct fetal passage through the birth canal. These
■ Pelvic Fractures include asynclitism, occiput posterior position, and face and
Vallier (2012) reviewed experiences with pelvic fractures and brow presentations.
pregnancy. Trauma from automobile collisions was the most
common cause. Moreover, they note that fracture pattern, Estimation of Fetal Head Size
minor malalignment, and retained hardware are not absolute Efforts to clinically and radiographically predict fetopelvic dis-
indications for cesarean delivery. A history of pelvic fracture proportion based on fetal head size have proved disappointing.
 Abnormal Labor 465

250.00 MM 250.00 MM

CHAPTER 23
A
1.00 MM

B
1.00 MM

FIGURE 23-4 A. Anteroposterior view of a digital radiograph. Illustrated is the measurement of the transverse diameter of the pelvic
inlet using an electronic cursor. The fetal body is clearly outlined. B. Lateral view of a digital radiograph. Illustrated are measurements of
the anteroposterior diameters of the inlet using the electronic cursor. C. An axial computed tomographic section through the midpelvis.
The level of the fovea of the femoral heads was ascertained from the anteroposterior digital radiograph because it corresponds to the
level of the ischial spines. The interspinous diameter is measured using the electronic cursor. The total fetal radiation dose using these
three exposures is approximately 250 mrad.

Mueller (1885) and Hillis (1930) described a clinical maneuver maneuverr and concluded that there was no relationship between
to predict disproportion. The fetal brow and the suboccipital dystocia and failed descent during the maneuver.
region are grasped through the abdominal wall with the fingers, Measurements of fetal head diameters using plain radio-
and firm pressure is directed downward in the axis of the inlet. graphic techniques are not used because of parallax distortions.
If no disproportion exists, the head readily enters the pelvis, The biparietal diameter and head circumference can be mea-
and vaginal delivery can be predicted. Thorp and coworkers sured sonographically, and there have been attempts to use
(1993) performed a prospective evaluation of the Mueller-Hillis this information in the management of dystocia. Thurnau and
 466 Labor

25
SECTION 7

20
Percent

15

10

0
9

9
79

09

39

69

99

39

59

89
–2

–3

–3

–3

–3

–4

–4

–4
00

00

00

00

00

00

00

00
25

28

31

34

37

40

43

46
Birthweight
FIGURE 23-5 Birthweight distribution of 362 newborns born
by cesarean delivery at Parkland Hospital (1989–1999) after a
failed forceps attempt. Only 12 percent (n = 44) of the newborns
weighed > 4000 g (dark bars).

colleagues (1991) used the fetal-pelvic indexx to identify labor

complications. Unfortunately, the sensitivity of such measure-
ments to predict cephalopelvic disproportion is poor (Ferguson, FIGURE 23-6 Face presentation. The occiput is the longer end of
1998). We are of the view that there is no currently satisfac- the head lever. The chin is directly posterior. Vaginal delivery is
impossible unless the chin rotates anteriorly.
tory method for accurate prediction of fetopelvic disproportion
based on head size.

Extended positions develop more frequently when the pel-

■ Face Presentation vis is contracted or the fetus is very large. In a series of 141
With this presentation, the head is hyperextended so that the face presentations studied by Hellman and coworkers (1950),
occiput is in contact with the fetal back, and the chin (men- the incidence of inlet contraction was 40 percent. This high
tum) is presenting (Fig. 23-6). The fetal face may present with incidence of pelvic contraction should be kept in mind when
the chin (mentum) anteriorly or posteriorly, relative to the considering management.
maternal symphysis pubis (Chap. 22, p. 436). Although some High parity is a predisposing factor to face presentation
mentum posterior presentations persist, most convert sponta- (Fuchs, 1985). In these cases, a pendulous abdomen permits
neously to anterior even in late labor (Duff, 1981). If not, the the back of the fetus to sag forward or laterally, often in the
fetal brow (bregma) is pressed against the maternal symphysis same direction in which the occiput points. This promotes
pubis. This position precludes flexion of the fetal head necessary extension of the cervical and thoracic spine.
to negotiate the birth canal. Thus, a mentum posterior presen-
tation is undeliverable except with a very preterm fetus. Diagnosis
Face presentations rarely deliver as such vaginally. Cruikshank Face presentation is diagnosed by vaginal examination and pal-
and White (1973) reported an incidence of 1 in 600, or 0.17 pation of facial features. As discussed in Chapter 28 (p. 560),
percent. As shown in Table 22-1 (p. 434), among more than it is possible to mistake a breech for a face presentation because
70,000 singleton newborns delivered at Parkland Hospital, the anus may be mistaken for the mouth and the ischial tuber-
approximately 1 in 2000 had a face presentation at delivery. osities for the malar prominences. The radiographic demon-
stration of the hyperextended head with the facial bones at or
Etiology below the pelvic inlet is characteristic.
Causes of face presentations are numerous and include con-
ditions that favor extension or prevent head flexion. Preterm Mechanism of Labor
infants, with their smaller head dimensions, can engage before Face presentations rarely are observed above the pelvic inlet.
conversion to vertex position (Shaffer, 2006). In exceptional Instead, the brow generally presents early and is usually con-
instances, marked enlargement of the neck or coils of cord verted to present the face after further extension of the head
around the neck may cause extension. Bashiri and associates during descent. The mechanism of labor in these cases consists
(2008) reported that fetal malformations and hydramnios were of the cardinal movements of descent, internal rotation, and
risk factors for face or brow presentations. Anencephalic fetuses flexion, and the accessory movements of extension and exter-
naturally present by the face. nal rotation (Fig. 23-7). Descent is brought about by the same
 Abnormal Labor 467

CHAPTER 23
45°
45°

45°
5

FIGURE 23-7 Mechanism of labor for right mentoposterior position with subsequent rotation of the mentum anteriorly and delivery.

factors as in cephalic presentations. Extension results from the Next, the chin rotates externally to the side toward which
relation of the fetal body to the deflected head, which is con- it was originally directed, and the shoulders are born as in
verted into a two-armed lever, the longer arm of which extends cephalic presentations.
from the occipital condyles to the occiput. When resistance is Edema may sometimes significantly distort the face. At the
encountered, the occiput must be pushed toward the back of same time, the skull undergoes considerable molding, mani-
the fetus while the chin descends. fested by an increase in length of the occipitomental diameter
The objective of internal rotation of the face is to bring the of the head.
chin under the symphysis pubis. Only in this way can the neck
traverse the posterior surface of the symphysis pubis. If the chin Management
rotates directly posteriorly, the relatively short neck cannot In the absence of a contracted pelvis, and with effective labor,
span the anterior surface of the sacrum, which measures about successful vaginal delivery usually will follow. Fetal heart rate
12 cm in length. Moreover, the fetal brow (bregma) is pressed monitoring is probably better done with external devices to
against the maternal symphysis pubis. This position precludes avoid damage to the face and eyes. Because face presentations
flexion necessary to negotiate the birth canal. Hence, birth of among term-size fetuses are more common when there is some
the head from a mentum posterior position is impossible unless degree of pelvic inlet contraction, cesarean delivery frequently
the shoulders enter the pelvis at the same time, an event that is is indicated. Attempts to convert a face presentation manu-
impossible except when the fetus is extremely small or macer- ally into a vertex presentation, manual or forceps rotation of
ated. Internal rotation results from the same factors as in vertex a persistently posterior chin to a mentum anterior position,
presentations. and internal podalic version and extraction are dangerous and
After anterior rotation and descent, the chin and mouth should not be attempted.
appear at the vulva, the undersurface of the chin presses
against the symphysis, and the head is delivered by flexion.
The nose, eyes, brow (bregma), and occiput then appear in ■ Brow Presentation
succession over the anterior margin of the perineum. After This rare presentation is diagnosed when that portion of the
birth of the head, the occiput sags backward toward the anus. fetal head between the orbital ridge and the anterior fontanel
 468 Labor

In transient brow presentations, the prognosis depends on

the ultimate presentation. If the brow persists, prognosis is poor
for vaginal delivery unless the fetus is small or the birth canal
is large. Principles of management are the same as those for a
SECTION 7

face presentation.

■ Transverse Lie
In this position, the long axis of the fetus is approximately per-
pendicular to that of the mother. When the long axis forms an
acute angle, an oblique liee results. The latter is usually only tran-
sitory, because either a longitudinal or transverse lie commonly
results when labor supervenes. For this reason, the oblique lie
is called an unstable liee in Great Britain.
In a transverse lie, the shoulder is usually positioned over the
pelvic inlet. The head occupies one iliac fossa, and the breech
the other. This creates a shoulder presentation in which the side
of the mother on which the acromion rests determines the des-
ignation of the lie as right or left acromial. And because in
either position the back may be directed anteriorly or poste-
riorly, superiorly or inferiorly, it is customary to distinguish
varieties as dorsoanterior and dorsoposterior (Fig. 23-9).
Transverse lie was found once in 322 singleton deliveries
(0.3 percent) at both the Mayo Clinic and the University of
Iowa Hospital (Cruikshank, 1973; Johnson, 1964). This is
remarkably similar to the incidence at Parkland Hospital of
FIGURE 23-8 Brow posterior presentation. approximately 1 in 335 singleton fetuses.

presents at the pelvic inlet. As shown in Figure 23-8, the fetal Etiology
head thus occupies a position midway between full flexion Some of the more common causes of transverse lie include: (1)
(occiput) and extension (face). Except when the fetal head is abdominal wall relaxation from high parity, (2) preterm fetus,
small or the pelvis is unusually large, engagement of the fetal (3) placenta previa, (4) abnormal uterine anatomy, (5) hydram-
head and subsequent delivery cannot take place as long as the nios, and (6) contracted pelvis.
brow presentation persists. Women with four or more deliveries have a tenfold inci-
dence of transverse lie compared with nulliparas. A relaxed and
Etiology and Diagnosis pendulous abdomen allows the uterus to fall forward, deflecting
The causes of persistent brow presentation are the same as the long axis of the fetus away from the axis of the birth canal
those for face presentation. A brow presentation is commonly and into an oblique or transverse position. Placenta previa and
unstable and often converts to a face or an occiput presentation pelvic contraction act similarly. A transverse or oblique lie occa-
(Cruikshank, 1973). The presentation may be recognized by sionally develops in labor from an initial longitudinal position.
abdominal palpation when both the occiput and chin can be
palpated easily, but vaginal examination is usually necessary. Diagnosis
The frontal sutures, large anterior fontanel, orbital ridges, eyes, A transverse lie is usually recognized easily, often by inspec-
and root of the nose are felt on vaginal examination, but neither tion alone. The abdomen is unusually wide, whereas the uter-
the mouth nor the chin is palpable. ine fundus extends to only slightly above the umbilicus. No
fetal pole is detected in the fundus, and the ballottable head
Mechanism of Labor is found in one iliac fossa and the breech in the other. The
With a very small fetus and a large pelvis, labor is generally easy, position of the back is readily identifiable. When the back is
but with a larger fetus, it is usually difficult. This is because anterior (Fig. 23-9, p. 469), a hard resistance plane extends
engagement is impossible until there is marked molding that across the front of the abdomen. When it is posterior, irregu-
shortens the occipitomental diameter or more commonly, until lar nodulations representing fetal small parts are felt through
there is either flexion to an occiput presentation or extension the abdominal wall.
to a face presentation. The considerable molding essential for On vaginal examination, in the early stages of labor, if the
vaginal delivery of a persistent brow characteristically deforms side of the thorax can be reached, it may be recognized by the
the head. The caput succedaneum is over the forehead, and it “gridiron” feel of the ribs. With further dilatation, the scapula
may be so extensive that identification of the brow by palpation and the clavicle are distinguished on opposite sides of the tho-
is impossible. In these instances, the forehead is prominent and rax. The position of the axilla indicates the side of the mother
squared, and the occipitomental diameter is diminished. toward which the shoulder is directed.
 Abnormal Labor 469

shoulder thus becomes the most depen-

dent part, appearing at the vulva. The
head and thorax then pass through the

CHAPTER 23
pelvic cavity at the same time. The fetus,
which is doubled upon itself and thus
sometimes referred to as conduplicato cor-
pore, is expelled.

Management
Active labor in a woman with a transverse
lie is usually an indication for cesarean
delivery. Before labor or early in labor,
with the membranes intact, attempts at
external version are worthwhile in the
absence of other complications. If the fetal
A B head can be maneuvered by abdominal
manipulation into the pelvis, it should be
held there during the next several contrac-
tions in an attempt to fix the head in the
pelvis.
With cesarean delivery, because neither
the feet nor the head of the fetus occupies
the lower uterine segment, a low trans-
verse incision into the uterus may lead
to difficult fetal extraction. This is espe-
cially true of dorsoanterior presentations.
Therefore, a vertical incision is typically
indicated (Chap. 30, p. 598).

■ Compound Presentation
C D Incidence and Etiology
FIGURE 23-9 Leopold maneuver performed on a woman with a fetal transverse In a compound presentation, an extremity
lie, right acromiodorsoanterior position. A. First maneuver. B. Second maneuver. prolapses alongside the presenting part,
C. Third maneuver. D. Fourth maneuver. and both present simultaneously in the
pelvis (Fig. 23-11). Goplerud and Eastman
(1953) identified a hand or arm prolapsed alongside the head
Mechanism of Labor once in every 700 deliveries. Much less common was prolapse
Spontaneous delivery of a fully developed newborn is impos- of one or both lower extremities alongside a cephalic presenta-
sible with a persistent transverse lie. After rupture of the mem- tion or a hand alongside a breech. At Parkland Hospital, com-
branes, if labor continues, the fetal shoulder is forced into pound presentations were identified in only 68 of more than
the pelvis, and the corresponding arm frequently prolapses 70,000 singleton fetuses—an incidence of approximately 1 in
(Fig. 23-10). After some descent, the shoulder is arrested by 1000. Causes of compound presentations are conditions that
the margins of the pelvic inlet, with the head in one iliac fossa prevent complete occlusion of the pelvic inlet by the fetal head,
and the breech in the other. As labor continues, the shoulder is including preterm labor.
impacted firmly in the upper part of the pelvis. The uterus then
contracts vigorously in an unsuccessful attempt to overcome the Management and Prognosis
obstacle. With time, a retraction ring rises increasingly higher In most cases, the prolapsed part should be left alone, because
and becomes more marked. With this neglected transverse lie, most often it will not interfere with labor. If the arm is pro-
the uterus will eventually rupture. Even without this complica- lapsed alongside the head, the condition should be observed
tion, morbidity is increased because of the frequent association closely to ascertain whether the arm retracts out of the way
with placenta previa, the increased likelihood of cord prolapse, with descent of the presenting part. If it fails to retract and if
and the necessity for major operative efforts. it appears to prevent descent of the head, the prolapsed arm
If the fetus is small—usually < 800 g—and the pelvis is should be pushed gently upward and the head simultaneously
large, spontaneous delivery is possible despite persistence of downward by fundal pressure. Tebes and coworkers (1999)
the abnormal lie. The fetus is compressed with the head forced described a tragic outcome in a newborn delivered spontane-
against its abdomen. A portion of the thoracic wall below the ously with the hand alongside the head. The infant developed
 470 Labor
SECTION 7

FIGURE 23-10 Neglected shoulder presentation. A thick muscular

band forming a pathological retraction ring has developed just
above the thin lower uterine segment. The force generated dur-
ing a uterine contraction is directed centripetally at and above
the level of the pathological retraction ring. This serves to stretch
further and possibly to rupture the thin lower segment below the
retraction ring.
ischemic necrosis of the presenting forearm, which required
amputation. In general, rates of perinatal mortality and mor-
bidity are increased as a result of concomitant preterm delivery,
prolapsed cord, and traumatic obstetrical procedures.

B
COMPLICATIONS WITH DYSTOCIA
FIGURE 23-11 Compound presentation. A. The left hand is lying
■ Maternal Complications in front of the vertex. With further labor, the hand and arm may
retract from the birth canal, and the head may then descend nor-
Dystocia, especially if labor is prolonged, is associated with an mally. B. Photograph of a small 34-week fetus with a compound
increased incidence of several common obstetrical and neonatal presentation that delivered uneventfully with the hand presenting
complications. Intrapartum chorioamnionitis and postpartum first. (Photograph contributed by Dr. Elizabeth Mosier.)
pelvic infection are more common with desultory and pro-
longed labors. Postpartum hemorrhage from atony is increased
with prolonged and augmented labors. There is also a higher
incidence of uterine tears with hysterotomy if the fetal head is Pathological Retraction Ring. Localized rings or con-
impacted in the pelvis. strictions of the uterus develop in association with pro-
longed obstructed labors that are seldom encountered
Uterine Rupture today. The pathological retraction ring of Bandll is associated
Abnormal thinning of the lower uterine segment creates a seri- with marked stretching and thinning of the lower uterine
ous danger during prolonged labor, particularly in women segment. The ring may be seen clearly as a uterine indenta-
of high parity and in those with a prior cesarean delivery tion and signifies impending rupture of the lower uterine
(Chap. 41, p. 790). When disproportion is so pronounced that segment.
there is no engagement or descent, the lower uterine segment Following birth of a first twin, a pathological ring may still
becomes increasingly stretched, and rupture may follow. In develop occasionally as hourglass constrictions of the uterus.
such cases, there is usually an exaggeration of the normal con- The ring can sometimes be relaxed and delivery effected
traction ringg shown in Figure 23-1. with appropriate general anesthesia, but occasionally prompt
 Abnormal Labor 471

cesarean delivery offers a better prognosis for the second twin American College of Obstetricians and Gynecologists: Dystocia and augmenta-
tion of labor. Practice Bulletin No. 49, December 2003, Reaffirmed 2013
(Chap. 45, p. 917). Austin T, Bridges N, Markiewicz M, et al: Severe neonatal polycythaemia after
third stage of labour underwater. Lancet 350 (9089):1445, 1997
Fistula Formation

CHAPTER 23
Babayer M, Bodack MP, Creatura C: Common peroneal neuropathy secondary
to squatting during childbirth. Obstet Gynecol 91:830, 1998
With dystocia, the presenting part is firmly wedged into the Bashiri A, Burstein E, Bar-David J, et al: Face and brow presentation: indepen-
pelvic inlet and does not advance for a considerable time. dent risk factors. J Matern Fetal Neonatal Med 21(6):357, 2008
Tissues of the birth canal lying between the leading part and Berghella V, Baxter JK, Chauhan SP: Evidence-based labor and delivery man-
agement. Am J Obstet Gynecol 199(5):445, 2008
the pelvic wall may be subjected to excessive pressure. Because Bleich AT, Alexander JM, McIntire DD, et al: An analysis of second-stage
of impaired circulation, necrosis may result and become evi- labor beyond 3 hours in nulliparous women. Am J Perinatol 29:717, 2012
dent several days after delivery as vesicovaginal, vesicocervical, Bloom SL, Casey BM, Schaffer JI, et al: A randomized trial of coached versus
uncoached maternal pushing during the second stage of labor. Am J Obstet
or rectovaginal fistulas. Most often, pressure necrosis follows a Gynecol 194; 10, 2006
very prolonged second stage. They are rarely seen today except Bloom SL, McIntire DD, Kelly MA, et al: Lack of effect of walking on labor
in undeveloped countries. and delivery. N Engl J Med 339:76, 1998
Buchmann EJ, Libhaber E: Sagittal suture overlap in cephalopelvic dispropor-
tion: blinded and non-participant assessment. Acta Obstet Gynecol Scand
Pelvic Floor Injury 87(7):731, 2008
During childbirth, the pelvic floor is exposed to direct com- Caldeyro-Barcia R, Alvarez H, Reynolds SRM: A better understanding of
uterine contractility through simultaneous recording with an internal and a
pression from the fetal head and to downward pressure from seven channel external method. Surg Obstet Gynecol 91:641, 1950
maternal expulsive efforts. These forces stretch and distend the Calkins LA: Premature spontaneous rupture of the membranes. Am J Obstet
pelvic floor, resulting in functional and anatomical alterations Gynecol 64:871, 1952
Carlson JM, Diehl JA, Murray MS, et al: Maternal position during parturition
in the muscles, nerves, and connective tissues. There is accu- in normal labor. Obstet Gynecol 68:443, 1986
mulating evidence that such effects on the pelvic floor during Chen HY, Huang SC: Evaluation of midpelvic contraction. Int Surg 67:516,
childbirth lead to urinary incontinence and to pelvic organ pro- 1982
Cibils LA, Hendricks CH: Normal labor in vertex presentation. Am J Obstet
lapse (Handa, 2011). As discussed in Chapter 27 (p. 548), the Gynecol 91:385, 1965
anal sphincter is torn in 3 to 6 percent of deliveries, and many Cluett ER, Burns E: Immersion in water in labour and birth. Cochrane
of these women report subsequent fecal or gas incontinence. Database Syst Rev 2:CD000111, 2009
Cluett ER, Pickering RM, Getliffe K, et al: Randomised controlled trial of
Many of these long-term sequelae have contributed to the cur- labouring in water compared with standard augmentation for management
rent trend of cesarean delivery on maternal requestt discussed in of dystocia in first stage of labour. BMJ 328:314, 2004
Chapter 30 (p. 589). Cohen W: Influence of the duration of second stage labor on perinatal outcome
and puerperal morbidity. Obstet Gynecol 49:266, 1977
Cohen W, Friedman EA (eds): Management of Labor. Baltimore, University
Postpartum Lower Extremity Nerve Injury Park Press, 1983
Wong and colleagues (2003) reviewed neurological injury involv- Cruikshank DP, White CA: Obstetric malpresentations: twenty years’ experi-
ence. Am J Obstet Gynecol 116:1097, 1973
ing the lower extremities in association with labor and delivery. Duff P: Diagnosis and management of face presentation. Obstet Gynecol
The most common mechanism is external compression of the 57:105, 1981
common fibular (fomerly common peroneal) nerve. This is usu- Eller WC, Mengert WF: Recognition of mid-pelvic contraction. Am J Obstet
Gynecol 53:252, 1947
ally caused by inappropriate leg positioning in stirrups, especially Ferguson JE, Newberry YG, DeAngelis GA, et al: The fetal-pelvic index
during prolonged second-stage labor. These and other injuries are has minimal utility in predicting fetal-pelvic disproportion. Am J Obstet
discussed in Chapter 36 (p. 676). Fortunately, symptoms resolve Gynecol 179:1186, 1998
Floberg J, Belfrage P, Ohlsén H: Influence of pelvic outlet capacity on labor:
within 6 months of delivery in most women. a prospective pelvimetry study of 1429 unselected primi-paras. Acta Obstet
Gynecol Scand 66:121, 1987
Flynn AM, Kelly J, Hollins G, et al: Ambulation in labour. BMJ 2:591, 1978
■ Perinatal Complications Fraser WD, Marcoux S, Krauss I, et al: Multicenter, randomized, controlled
Similar to the mother, the incidence of peripartum fetal sepsis trial of delayed pushing for nulliparous women in the second stage of labor
with continuous epidural analgesia. Am J Obstet Gynecol 182:1165, 2000
is increased with longer labors. Caput succedaneum and molding Friedman EA: Labor. Clinical Evaluation and Management, 2nd ed. New
develop commonly and may be impressive (Fig. 22-19, p. 444) York, Appleton-Century-Crofts, 1978
(Buchmann, 2008). Mechanical trauma such as nerve injury, Friedman EA, Sachtleben MR: Station of the fetal presenting part II: effect on
the course of labor. Am J Obstet Gynecol 93:530, 1965
fractures, and cephalohematoma are also more frequent and Friedman EA, Sachtleben MR: Station of the fetal presenting part IV: arrest of
discussed fully in Chapter 33 (p. 645). descent in nulliparas. Obstet Gynecol 47:129, 1976
Fuchs K, Peretz BA, Marcovici R, et al: The grand multipara—is it a problem?
Int J Gynaecol Obstet 73:321, 1985
REFERENCES Goplerud J, Eastman NJ: Compound presentation: survey of 65 cases. Obstet
Gynecol 1:59, 1953
Acker DB, Gregory KD, Sachs BP, et al: Risk factors for Erb-Duchenne palsy. Graseck A, Odibo AO, Tuuli M, et al: Normal first stage of labor in women
Obstet Gynecol 71:389, 1988 undergoing trial of labor after cesarean delivery. Obstet Gynecol 119:732, 2012
Alexander J: MFMU Cesarean Registry: Labor characteristics of women under- Gupta JK, Hofmeyr GJ: Position for women during second stage of labour.
going cesarean delivery for dystocia. Am J Obstet Gynecol 189(6):S138, 2003 Cochrane Database Syst Rev 1:CD002006, 2004
Alexander JM, Lucas MJ, Ramin SM, et al: The course of labor with and with- Handa VL, Blomquist JL, Knoepp LR, et al: Pelvic floor disorders 5–10 years
out epidural analgesia. Am J Obstet Gynecol 178:516, 1998 after vaginal or cesarean childbirth. Obstet Gynecol 118(4):777, 2011
Alexander JM, Sharma SK, McIntire DD, at el: Epidural analgesia lengthens Handa VL, Laros RK: Active-phase arrest in labor: predictors of cesarean deliv-
the Friedman active phase of labor. Obstet Gynecol 100:46, 2002 ery in a nulliparous population. Obstet Gynecol 81:758, 1993
American College of Obstetricians and Gynecologists: Guidelines for diagnos- Hannah ME, Hodnett ED, Willan A, et al: Prelabor rupture of the membranes
tic imaging during pregnancy. Committee Opinion No. 299, September at term: expectant management at home or in hospital? Obstet Gynecol
2004, Reaffirmed 2009 96:533, 2000
 473

CHAPTER 24

Intrapartum Assessment

ELECTRONIC FETAL MONITORING . . . . . . . . . . . . . . . . . 473 fetal monitoring has become the most prevalent obstetrical
procedure in this country.
OTHER INTRAPARTUM ASSESSMENT TECHNIQUES . . . . 488

FETAL DISTRESS . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 491

ELECTRONIC FETAL MONITORING
MECONIUM IN THE AMNIONIC FLUID . . . . . . . . . . . . . . 493
■ Internal (Direct) Electronic Monitoring
FETAL HEART RATE PATTERNS AND BRAIN DAMAGE . . 495
The fetus can be monitored electronically by direct or indi-
CURRENT RECOMMENDATIONS . . . . . . . . . . . . . . . . . . . 497 rect methods. Direct fetal heart measurement is accomplished
by attaching a bipolar spiral electrode directly to the fetus
INTRAPARTUM SURVEILLANCE OF UTERINE (Fig. 24-1). The wire electrode penetrates the fetal scalp, and
ACTIVITY . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 497
the second pole is a metal wing on the electrode. Vaginal body
fluids create a saline electrical bridge that completes the circuit
and permits measurement of the voltage differences between
the two poles. The two wires of the bipolar electrode are
Following earlier work by Hon (1958), continuous electronic attached to a reference electrode on the maternal thigh to elimi-
fetal monitoring (EFM) was introduced into obstetrical prac- nate electrical interference. The electrical fetal cardiac signal—P
tice in the late 1960s. No longer were intrapartum fetal sur- wave, QRS complex, and T wave—is amplified and fed into a
veillance and the suspicion of fetal distress based on periodic cardiotachometer for heart rate calculation. The peak R-wave
auscultation with a fetoscope. Instead, the continuous graph- voltage is the portion of the fetal electrocardiogram most reli-
paper portrayal of the fetal heart rate was potentially diagnos- ably detected.
tic in assessing pathophysiological events affecting the fetus. An example of the method of fetal heart rate process-
Indeed, there were great expectations: (1) that electronic fetal ing employed when a scalp electrode is used is shown in
heart rate monitoring provided accurate information, (2) that Figure 24-2. Time (t) in milliseconds between fetal R waves
the information was of value in diagnosing fetal distress, (3) is fed into a cardiotachometer, where a new fetal heart rate
that it would direct intervention to prevent fetal death or mor- is set with the arrival of each new R wave. As also shown in
bidity, and (4) that continuous electronic fetal heart rate moni- Figure 24-2, a premature atrial contraction is computed as a
toring was superior to intermittent methods. heart rate acceleration because the interval (t2) is shorter than
When first introduced, electronic fetal heart rate monitoring the preceding one (t1). The phenomenon of continuous R-to-R
was used primarily in complicated pregnancies, but gradually wave fetal heart rate computation is known as beat-to-beat vari-
became used in most pregnancies. By 1978, it was estimated ability. The physiological event being counted, however, is not
that nearly two thirds of American women were being moni- a mechanical event corresponding to a heartbeat but rather an
tored electronically during labor (Banta, 1979). Currently, electrical event.
more than 85 percent of all live births in the United States Electrical cardiac complexes detected by the electrode
undergo electronic fetal monitoring (Ananth, 2013). Indeed, include those generated by the mother. Although the maternal
 474 Labor

150 t1 t2 t3
Cardiotachometer −14
−1455
heart rate
140
SECTION 7

135

Fetal
R wave t1 t2 t3

Fetal ECG PAC

(scalp electrode)
FIGURE 24-2 Schematic representation of fetal electrocardio-
A graphic signals used to compute continuing beat-to-beat heart
rate with scalp electrodes. Time intervals (t1, t2, t3) in milliseconds
between successive fetal R waves are used by a cardiotachometer
to compute instantaneous fetal heart rate. ECG = electrocardio-
gram; PAC = premature atrial contraction.

is dead, the maternal R waves are still detected by the scalp

electrode as the next best signal and are counted by the cardio-
tachometer (Fig. 24-4).

■ External (Indirect) Electronic Monitoring

Membrane rupture may be avoided by use of external detectors
to monitor fetal heart action. External monitoring, however,
does not provide the precision of fetal heart rate measurement
afforded by internal monitoring (Nunes, 2014).
The fetal heart rate is detected through the mater-
nal abdominal wall using the ultrasound Doppler principle
(Fig. 24-5). Ultrasound waves undergo a shift in frequency
B
as they are reflected from moving fetal heart valves and from
pulsatile blood ejected during systole (Chap. 10, p. 209). The
FIGURE 24-1 Internal electronic fetal monitoring. A. Scalp elec- unit consists of a transducer that emits ultrasound and a sensor
trode penetrates the fetal scalp by means of a coiled electrode. to detect a shift in frequency of the reflected sound. The trans-
B. Schematic representation of a bipolar electrode attached to the
fetal scalp for detection of fetal QRS complexes (F). Also shown is
ducer is placed on the maternal abdomen at a site where fetal
the maternal heart and corresponding electrical complex (M) that heart action is best detected. A coupling gel must be applied
is detected. because air conducts ultrasound waves poorly. The device is
held in position by a belt. Care should be taken that maternal
arterial pulsations are not confused with fetal cardiac motion
electrocardiogram (ECG) signal is approximately five times (Neilson, 2008).
stronger than the fetal ECG, its amplitude is diminished when Ultrasound Doppler signals are edited electronically before
it is recorded through the fetal scalp electrode. In a live fetus, fetal heart rate data are printed onto monitor paper. Reflected
this low maternal ECG signal is detected but masked by the ultrasound signals from moving fetal heart valves are ana-
fetal ECG. If the fetus is dead, the weaker maternal signal will lyzed through a microprocessor that compares incoming sig-
be amplified and displayed as the “fetal” heart rate (Freeman, nals with the most recent previous signal. This process, called
2003). Shown in Figure 24-3 are simultaneous recordings of autocorrelation, is based on the premise that the fetal heart rate
maternal chest wall ECG signals and fetal scalp electrode ECG has regularity whereas “noise” is random and without regular-
signals. This fetus is experiencing premature atrial contractions, ity. Several fetal heart motions must be deemed electronically
which cause the cardiotachometer to rapidly and erratically acceptable by the microprocessor before the fetal heart rate is
seek new heart rates, resulting in the “spiking” shown in the printed. Such electronic editing has greatly improved the tracing
standard fetal monitor tracing. Importantly, when the fetus quality of the externally recorded fetal heart rate.
 Intrapartum Assessment 475

240 240
Scalp ECG
210 210

CHAPTER 24
180 180

150 150

120
120
0 12
120

90 90

60 60
20 per min
30 30
Scalp pH 7.35
100 100

80 80
Umbilical vein
60 pH
H 7.38
7 38 60

40 40

20
20 20
0

0 0

M F F F

M M PAC
Fetus 50 mm/sec 20 per min

II
Mother 50 mm/sec

FIGURE 24-3 The top tracing shows standard fetal monitor tracing of heart rate using a fetal scalp electrode. Spiking of the fetal rate
in the monitor tracing is due to premature atrial contractions. The second panel displays accompanying contractions. The bottom two
tracings represent cardiac electrical complexes detected from fetal scalp and maternal chest wall electrodes. ECG = electrocardiogram;
F = fetus; M = mother; PAC = fetal premature atrial contraction.

■ Fetal Heart Rate Patterns

240 240

210 210
It is now generally accepted that interpre-
180 180
tation of fetal heart rate patterns can be
150 150 problematic because of the lack of agree-
120 120
ment on definitions and nomenclature
(American College of Obstetricians and
90
Gynecologists, 2013b). In one example,
60 60 Blackwell and colleagues (2011) asked
30 30 three maternal-fetal medicine specialists
Dying fetus Maternal heart rate to independently interpret 154 fetal heart
100 100 rate tracings. Interobserver agreement was
80 80 poor for the most ominous tracings and
60 60 “moderate” for less severe patterns. The
40 40 authors cautioned that their results repre-
20 20
20 sented idealized circumstances that should
0 0 not be considered reflective of routine
FIGURE 24-4 Placental abruption. In the upper panel, the fetal scalp electrode first
clinical practice.
detected the heart rate of the dying fetus. After fetal death, the maternal electrocar- The National Institute of Child
diogram complex is detected and recorded. The second panel displays an absence of Health and Human Development
uterine contractions. (NICHD) Research Planning Workshop
 476 Labor

Thus, the choice of vertical and horizontal scaling greatly affects

the appearance of the fetal heart rate. Scaling factors recom-
mended by the workshop are 30 beats per minute (beats/min
or bpm) per vertical cm (range, 30 to 240 bpm) and 3 cm/
SECTION 7

min chart recorder paper speed. Fetal heart rate variation is

falsely displayed at the slower 1 cm/min paper speed com-
pared with that of the smoother baseline recorded at 3 cm/
min (Fig. 24-6). Thus, pattern recognition can be considerably
distorted depending on the scaling factors used.

■ Baseline Fetal Heart Activity

This refers to the modal characteristics that prevail apart
from periodic accelerations or decelerations associated with
uterine contractions. Descriptive characteristics of baseline
fetal heart activity include rate, beat-to-beat variability, fetal
arrhythmia, and distinct patterns such as sinusoidall or salta-
toryy fetal heart rates.
FIGURE 24-5 Ultrasound Doppler principle used externally to
measure fetal heart motions. Pulsations of the maternal aorta Rate
also may be detected and erroneously counted. (Adapted from
Klavan, 1977.) With increasing fetal maturation, the heart rate decreases. This
continues postnatally such that the average rate is 90 bpm by
age 8 (Behrman, 1992). Pillai and James (1990) longitudinally
(1997) brought together investigators with expertise in the field studied fetal heart rate characteristics in 43 normal pregnan-
to propose standardized, unambiguous definitions for interpre- cies. The baseline fetal heart rate decreased an average of 24
tation of fetal heart rate patterns during labor. This workshop bpm between 16 weeks and term, or approximately 1 beat/
was repeated in 2008. The definitions proposed and shown in min per week. This normal gradual slowing of the fetal heart
Table 24-1 as a result of this second workshop are used in this rate is thought to correspond to maturation of parasympathetic
chapter. First, it is important to recognize that interpretation (vagal) heart control (Renou, 1969).
of electronic fetal heart rate data is based on the visual pattern The baseline fetal heart rate is the approximate mean rate
of the heart rate as portrayed on chart recorder graph paper. rounded to increments of 5 bpm during a 10-minute tracing

240 240

210 210

180 180

150 150

120 120

90 90

60 60

30 30

Paper speed 1 cm/min Paper speed 3 cm/min

100 100

80 80

60 60

40 40

20 20

0 0

FIGURE 24-6 Fetal heart rate obtained by scalp electrode (upper panel) and recorded at 1 cm/min compared with that at 3 cm/min
chart recorder paper speed. Concurrent uterine contractions are shown (lower panel).
 Intrapartum Assessment 477

TABLE 24-1. Electronic Fetal Monitoring Definitions

Pattern Definition

CHAPTER 24
Baseline • The mean FHR rounded to increments of 5 bpm during a 10-min segment, excluding:
—Periodic or episodic changes
—Segments of baseline that differ by more than 25 bpm
• The baseline must be for a minimum of 2 min in any 10-min segment or the baseline for that time
period is indeterminate. In this case, one may refer to the prior 10-min window for determination of
baseline.
• Normal FHR baseline: 110–160 bpm
• Tachycardia: FHR baselines > 160 bpm
• Bradycardia: FHR baseline < 110 bpm
Baseline • Fluctuations in the baseline FHR that are irregular in amplitude and frequency
variability • Variability is visually quantified as the amplitude of peak-to-trough in bpm
—Absent: amplitude range undetectable
—Minimal: amplitude range detectable but ≤ 5 bpm or fewer
—Moderate (normal): amplitude range 6–25 bpm
—Marked: amplitude range > 25 bpm
Acceleration • A visually apparent abrupt increase (onset to peak in < 30 sec) in the FHR
• At 32 weeks and beyond, an acceleration has a peak of 15 bpm or more above baseline, with a
duration of 15 sec or more but less than 2 min from onset to return
• Before 32 weeks, an acceleration has a peak of 10 bpm or more above baseline, with a duration of
≥ 10 sec but < 2 min from onset to return
• Prolonged acceleration lasts ≥ 2 min, but < 10 min
• If an acceleration lasts 10 min, it is a baseline change
Early • Visually apparent usually symmetrical gradual decrease and return of the FHR associated with a
deceleration uterine contraction
• A gradual FHR decrease is defined as from the onset to the FHR nadir of ≥ 30 sec
• The decrease in FHR is calculated from the onset to the nadir of the deceleration
• The nadir of the deceleration occurs at the same time as the peak of the contraction
• In most cases the onset, nadir, and recovery of the deceleration are coincident with the beginning,
peak, and ending of the contraction, respectively
Late • Visually apparent usually symmetrical gradual decrease and return of the FHR associated with a
deceleration uterine contraction
• A gradual FHR decrease is defined as from the onset to the FHR nadir of ≥ 30 sec
• The decrease in FHR is calculated from the onset to the nadir of the deceleration
• The deceleration is delayed in timing, with the nadir of the deceleration occurring after the peak
of the contraction
• In most cases the onset, nadir, and recovery of the deceleration occur after the beginning, peak, and
ending of the contraction, respectively
Variable • Visually apparent abrupt decrease in FHR
deceleration • An abrupt FHR decrease is defined as from the onset to the FHR nadir of < 30 sec
• The decrease in FHR is calculated from the onset to the nadir of the deceleration
• The decrease in FHR is ≥ 15 bpm, lasting ≥ 15 sec, and < 2 min in duration
• When variable decelerations are associated with uterine contraction, their onset, depth, and duration
commonly vary with successive uterine contractions
Prolonged • Visually apparent decrease in the FHR below the baseline
deceleration • Decrease in FHR from the baseline that is ≥ 15 bpm, lasting ≥ 2 min but < 10 min in duration
• If a deceleration lasts ≥ 10 min, it is a baseline change
Sinusoidal • Visually apparent, smooth, sine wave-line undulating pattern in FHR baseline with a cycle frequency
pattern of 3–5 per minute which persists for 20 min or more

bpm = beats per minute; FHR = fetal heart rate.

Summarized from the National Institute of Child Health and Human Development Research Planning Workshop, 1997.
 478 Labor

segment. In any 10-minute window, the minimum inter- 240 240

pretable baseline duration must be at least 2 minutes. If the

210 210
baseline fetal heart rate is less than 110 bpm, it is termed
bradycardia. If the baseline rate is greater than 160 bpm, it is 180 180
SECTION 7

termed tachycardia. The average fetal heart rate is considered

the result of tonic balance between acceleratorr and decelerator 150 150

influences on pacemaker cells. In this concept, the sympa- 120 120

thetic system is the accelerator influence, and the parasym-
pathetic system is the decelerator factor mediated via vagal 9
90 90
slowing of heart rate (Dawes, 1985). Heart rate also is under
60 60
the control of arterial chemoreceptors such that both hypoxia
and hypercapnia can modulate rate. More severe and pro- 30 30
longed hypoxia, with a rising blood lactate level and severe
metabolic acidemia, induces a prolonged fall in heart rate
100 100
(Thakor, 2009).
80 80

Bradycardia. In the third trimester, the normal mean 60 60

baseline fetal heart rate has generally been accepted to range 40 40
between 120 and 160 bpm. The lower normal limit is dis-
20 20
puted internationally, with some investigators recommending
110 bpm (Manassiev, 1996). Pragmatically, a rate between 0 0
100 and 119 bpm, in the absence of other changes, usually is FIGURE 24-7 Fetal bradycardia measured with a scalp electrode
not considered to represent fetal compromise. Such low but (upper panel) in a pregnancy complicated by placental abruption
potentially normal baseline heart rates also have been attrib- and subsequent fetal death. Concurrent uterine contractions are
uted to head compression from occiput posterior or transverse shown in the lower panel.
positions, particularly during second-stage labor (Young,
1976). Such mild bradycardias were observed in 2 percent of with tachycardia seems to be concomitant heart rate decelera-
monitored pregnancies and averaged approximately 50 min- tions. Prompt relief of the compromising event, such as correc-
utes in duration. Freeman and associates (2003) have con- tion of maternal hypotension caused by epidural analgesia, can
cluded that bradycardia within the range of 80 to 120 bpm result in fetal recovery.
with good variability is reassuring. Interpretation of rates less
than 80 bpm is problematic, and such rates generally are con- Wandering Baseline. This baseline rate is unsteady and
sidered nonreassuring. “wanders” between 120 and 160 bpm (Freeman, 2003). This
Some causes of fetal bradycardia include congenital heart rare finding is suggestive of a neurologically abnormal fetus and
block and serious fetal compromise (Jaeggi, 2008; Larma, may occur as a preterminal event.
2007). Figure 24-7 shows bradycardia in a fetus dying from
placental abruption. Maternal hypothermia under general Beat-to-Beat Variability
anesthesia for repair of a cerebral aneurysm or during maternal Baseline variability is an important index of cardiovascular
cardiopulmonary bypass for open-heart surgery also can cause function and appears to be regulated largely by the autonomic
fetal bradycardia. Sustained fetal bradycardia in the setting of nervous system (Kozuma, 1997). That is, a sympathetic and
severe pyelonephritis and maternal hypothermia also has been parasympathetic “push and pull” mediated via the sinoatrial
reported (Hankins, 1997). These infants apparently are not node produces moment-to-moment or beat-to-beat oscillation
harmed by several hours of such bradycardia. of the baseline heart rate. Such heart rate change is defined as
baseline variability. Variability can be further divided into short
Tachycardia. Fetal tachycardia is defined as a baseline heart term and long term, although these terms have fallen out of
rate greater than 160 bpm. The most common explanation use. Short-term variabilityy reflects the instantaneous change in
for fetal tachycardia is maternal fever from chorioamnionitis, fetal heart rate from one beat—or R wave—to the next. This
although fever from any source can increase baseline fetal heart variability is a measure of the time interval between cardiac
rate. Such infections also have been observed to induce fetal systoles (Fig. 24-8). Short-term variability can most reliably be
tachycardia before overt maternal fever is diagnosed (Gilstrap, determined to be normally present only when electrocardiac
1987). Fetal tachycardia caused by maternal infection typically cycles are measured directly with a scalp electrode. Long-term
is not associated with fetal compromise unless there are associ- variabilityy is used to describe the oscillatory changes during 1
ated periodic heart rate changes or fetal sepsis. minute and result in the waviness of the baseline (Fig. 24-9).
Other causes of fetal tachycardia include fetal compromise, The normal frequency of such waves is three to five cycles per
cardiac arrhythmias, and maternal administration of parasym- minute (Freeman, 2003).
pathetic (atropine) or sympathomimetic (terbutaline) drugs. It should be recognized that precise quantitative analysis
The key feature to distinguish fetal compromise in association of both short- and long-term variability presents a number
 Intrapartum Assessment 479

t rates. This phenomenon presumably reflects less cardiovascular

physiological wandering as beat-to-beat intervals shorten due to
increasing heart rate.

CHAPTER 24
Decreased Variability. Diminished beat-to-beat variability
can be an ominous sign indicating a seriously compromised
fetus. Paul and coworkers (1975) reported that loss of vari-
FIGURE 24-8 Schematic representation of short-term beat-to-
ability in combination with decelerations was associated with
beat variability measured by a fetal scalp electrode. t = time fetal acidemia. They analyzed variability in the 20 minutes
interval between successive fetal R waves. (Adapted from Klavan, preceding delivery in 194 pregnancies. Decreased variabil-
1977.) ity was defined as 5 or fewer bpm excursion of the baseline
(see Fig. 24-10), whereas acceptable variability exceeded this
range. Fetal scalp pH was measured 1119 times in these preg-
of frustrating problems due to technical and scaling factors. nancies, and mean values were found to be increasingly aci-
For example, Parer and coworkers (1985) evaluated 22 math- demic when decreased variability was added to progressively
ematical formulas designed to quantify heart rate variability intense heart rate decelerations. For example, mean fetal scalp
and found most to be unsatisfactory. Consequently, most pH of approximately 7.10 was found when severe decelera-
clinical interpretation is based on visual analysis with sub- tions were combined with 5 bpm or less variability, compared
jective judgment of the smoothness or flatness of the base- with a pH of approximately 7.20 when greater variability was
line. According to Freeman and colleagues (2003), there is associated with similarly severe decelerations. Severe mater-
no current evidence that the distinction between short- and nal acidemia also can cause decreased fetal beat-to-beat vari-
long-term variability has any clinical relevance. Similarly, ability, as shown in Figure 24-11 in a mother with diabetic
the NICHD Workshop (1997) did not recommend differ- ketoacidosis.
entiating short- and long-term variability because in actual The precise pathological mechanisms by which fetal hypox-
practice they are visually determined as a unit. The workshop emia results in diminished beat-to-beat variability are not totally
panel defined baseline variability as those baseline fluctuations understood. Interestingly, mild degrees of fetal hypoxemia have
of two cycles per minute or greater. They recommended the been reported actually to increasee variability, at least at the out-
criteria shown in Figure 24-10 for quantification of variabil- set of the hypoxic episode (Murotsuki, 1997). According to
ity. Normal beat-to-beat variability was accepted to be 6 to Dawes (1985), it seems probable that the loss of variability is a
25 bpm. result of metabolic acidemia that causes depression of the fetal
brainstem or the heart itself. Thus, diminished beat-to-beat
Increased Variability. Several physiological and pathologi- variability, when it reflects fetal compromise, likely reflects aci-
cal processes can affect or interfere with beat-to-beat variabil- demia rather than hypoxia.
ity. Dawes and associates (1981) described increased variability A common cause of diminished beat-to-beat variability
during fetal breathing. In healthy infants, short-term variability is administration of analgesic drugss during labor (Chap. 25,
is attributable to respiratory sinus arrhythmia (Divon, 1986). p. 506). Various central nervous system depressant drugs can
Fetal body movementss also affect variability (Van Geijn, 1980). cause transient diminished beat-to-beat variability. Included
Pillai and James (1990) reported increased baseline variability are narcotics, barbiturates, phenothiazines, tranquilizers, and
with advancing gestation. Up to 30 weeks, baseline character- general anesthetics. Variability regularly diminishes within
istics were similar during both fetal rest and activity. After 5 to 10 minutes following intravenous meperidine adminis-
30 weeks, fetal inactivity was associated with diminished base- tration, and the effects may last up to 60 minutes or longer
line variability and conversely, variability was increased during depending on the dosage given (Petrie, 1993). Butorphanol
fetal activity. Fetal gender does not affect heart rate variability given intravenously diminishes fetal heart rate reactivity
(Ogueh, 1998). (Schucker, 1996). In a study performed at Parkland Hospital,
The baseline fetal heart rate becomes more physiologically Hill and colleagues (2003) found that 5 bpm or less variabil-
fixed (less variable) as the rate increases. Conversely, there is ity occurred in 30 percent of women given continuous intra-
more instability or variability of the baseline at lower heart venous meperidine compared with 7 percent in those given
continuous labor epidural analgesia.
Magnesium sulfate, widely used in the United States for
135 tocolysis as well as management of hypertensive women, has
130 been arguably associated with diminished beat-to-beat variabil-
ity. Hallak and associates (1999) randomly assigned 34 normal,
nonlaboring women to standard magnesium sulfate infusion
125 versus isotonic saline. Magnesium sulfate was associated with
FIGURE 24-9 Schematic representation of long-term beat-to- statistically decreased variability only in the third hour of the
beat variability of the fetal heart rate ranging between 125 and infusion. The average decrease in variability was deemed clini-
135 bpm. (Adapted from Klavan, 1977.) cally insignificant, however, because the mean variability was
 480 Labor

240 240 240

1 210 210
210

180 180 180

SECTION 7

150
0 150
0 150
1 50

120 120 120

90 90 90

60 60 60

30 30 30

240 240 240

2 210 210
210

180 180 180

150 150
0 150

120 120 120

90 90 90

60 60 60

30 30 30
240 240 240
3
210 210 210

180 180 180

150 150
0 150
1
150

120 120 120

90 90 90

60 60 60

30 30 30

240 240 240

4
210 210 210

180 180 180

150
50
0 150
0 150
15
50

120 120 120

90 90 90

60 60 60

30 30 30

240 240 240

5 210 210
210

180 180 180

150 150
5 150
0

120 120 120

90 90 90

60 60 60

30 30 30

1 min

FIGURE 24-10 Grades of baseline fetal heart rate variability shown in the following five panels. 1. Undetectable, absent variability.
2. Minimal variability, ≤ 5 bpm. 3. Moderate (normal) variability, 6 to 25 bpm. 4. Marked variability, > 25 bpm. 5. Sinusoidal pattern.
This differs from variability in that it has a smooth, sinelike pattern of regular fluctuation and is excluded in the definition of fetal heart
rate variability. (Adapted from National Institute of Child Health and Human Development Research Planning Workshop, 1997.)
 Intrapartum Assessment 481

240 240 240

210 210 210

CHAPTER 24
180 No variability 1 80
180 180

150 150
1 50 150

120
1 20
1200 120

90
90 90

60
A 60 Fetal intrapartum tracing 60

30

240

210

180

150
Neonatal ECG
Variability
120
FIGURE 24-12 Internal fetal monitoring at term demonstrated
90 occasional abrupt beat-to-beat fetal heart rate spiking due to
erratic extrasystoles shown in the corresponding fetal electrocar-
60 diogram. The normal infant was delivered spontaneously and had
B normal cardiac rhythm in the nursery.
30

FIGURE 24-11 A. External fetal heart recording showing lack of

long-term variability at 31 weeks during maternal diabetic keto- Cardiac Arrhythmia
acidosis (pH 7.09). B. Recovery of fetal long-term variability after When fetal cardiac arrhythmias are first suspected using elec-
correction of maternal acidemia. tronic monitoring, findings can include baseline bradycardia,
tachycardia, or most commonly in our experience, abrupt
baseline spikingg (Fig. 24-12). Intermittent baseline bradycardia
2.7 bpm in the third hour of magnesium infusion compared is frequently due to congenital heart block. As discussed in
with 2.8 bpm at baseline. Magnesium sulfate also blunted the Chapter 59 (p. 1172), conduction defects, most commonly
frequency of accelerations. complete atrioventricular (AV) block, usually are found in
It is generally believed that reduced baseline heart rate variabil-
l association with maternal connective-tissue diseases. An
ity is the single most reliable sign of fetal compromise. Smith and arrhythmia can only be documented, practically speaking,
coworkers (1988) performed a computerized analysis of beat-to- when scalp electrodes are used. Some fetal monitors can be
beat variability in growth-restricted fetuses before labor. They adapted to output the scalp electrode signals into an electro-
observed that diminished variability (4.2 bpm or less) that was cardiographic recorder. Because only a single lead is obtained,
maintained for 1 hour was diagnostic of developing acidemia analysis and interpretation of rhythm and rate disturbances are
and imminent fetal death. By contrast, Samueloff and associ- severely limited.
ates (1994) evaluated variability as a predictor of fetal outcome Southall and associates (1980) studied antepartum fetal
during labor in 2200 consecutive deliveries. They concluded cardiac rate and rhythm disturbances in 934 normal preg-
that variability by itself could not be used as the only indica- nancies between 30 and 40 weeks. Arrhythmias, episodes
tor of fetal well-being. Conversely, they also concluded that of bradycardia < 100 bpm, or tachycardia > 180 bpm were
good variability should not be interpreted as necessarily reas- encountered in 3 percent. Most supraventricular arrhythmias
suring. Blackwell and associates (2011) found that even experts are of little significance during labor unless there is coexis-
often disagreed as to whether variability was absent or minimal tent heart failure as evidenced by fetal hydrops. Many supra-
(< 5 beats per minute). ventricular arrhythmias disappear in the immediate neonatal
In summary, beat-to-beat variability is affected by various period, although some are associated with structural car-
pathological and physiological mechanisms. Variability has diac defects (Api, 2008). Copel and coworkers (2000) used
considerably different meaning depending on the clinical set- echocardiography to evaluate 614 fetuses referred for auscul-
ting. The development of decreased variability in the absence of tated irregular heart rate without hydrops. Only 10 fetuses
decelerations is unlikely to be due to fetal hypoxia (Davidson, (2 percent) were found to have significant arrhythmias, and
1992). A persistently flat fetal heart rate baseline—absent vari- all but one of these infants survived.
ability—within the normal baseline rate range and without Boldt and colleagues (2003) followed 292 consecutive
decelerations may reflect a previous insult to the fetus that has fetuses diagnosed with a cardiac arrhythmia through birth and
resulted in neurological damage (Freeman, 2003). into childhood. Atrial extrasystoles were the most common
 482 Labor

arrhythmia (68 percent), followed by atrial tachycardias characteristic of this pattern when due to narcotics is the sine
(12 percent), atrioventricular block (12 percent), sinus brady- frequency of 6 cycles per minute. A sinusoidal pattern also
cardia (5 percent), and ventricular extrasystoles (2.5 percent). has been described with chorioamnionitis, fetal distress, and
Chromosomal anomalies were found in 1.7 percent of the umbilical cord occlusion (Murphy, 1991). Young (1980a) and
SECTION 7

fetuses. Fetal hydrops developed in 11 percent, and 2 percent Johnson (1981) with their coworkers concluded that intrapar-
had intrauterine death. Fetal hydrops was a bad prognostic tum sinusoidal fetal heart patterns were not generally associated
finding. Overall, 93 percent of the study population was alive with fetal compromise.
at a median follow-up period of 5 years, and 3 percent— Modanlou and Freeman (1982), based on their extensive
seven infants—had neurological handicaps. Of the infants review, proposed adoption of a strict definition:
with atrial extrasystoles, 97 percent lived, and none suffered
1. Stable baseline heart rate of 120 to 160 bpm with regular
neurological injury. Only 6 percent required postnatal cardiac
oscillations,
medications. Lopriore and associates (2009) found low rates
2. Amplitude of 5 to 15 bpm (rarely greater),
of death and long-term neurological impairment in fetuses
3. Long-term variability frequency of 2 to 5 cycles per minute,
with supraventricular tachycardia or atrial flutter. In contrast,
4. Fixed or flat short-term variability,
higher mortality rates were noted in those with atrioventricu-
5. Oscillation of the sinusoidal waveform above or below a
lar block.
baseline, and
Although most fetal arrhythmias are of little consequence
6. Absent accelerations.
during labor when there is no evidence of fetal hydrops, such
arrhythmias impair interpretation of intrapartum heart rate Although these criteria were selected to define a sinusoi-
tracings. Sonographic evaluation of fetal anatomy and echocar- dal pattern that is most likely ominous, they observed that
diography may be useful. Some clinicians use fetal scalp sam- the pattern associated with alphaprodine is indistinguishable.
pling as an adjunct. Generally, in the absence of fetal hydrops, Other investigators have proposed a classification of sinusoi-
neonatal outcome is not measurably improved by pregnancy dal heart rate patterns into mild—amplitude 5 to 15 bpm,
intervention. At Parkland Hospital, intrapartum fetal cardiac intermediate—16 to 24 bpm, and major—25 or more bpm to
arrhythmias, especially those associate with clear amnionic quantify fetal risk (Murphy, 1991; Neesham, 1993).
fluid, are managed conservatively. Freeman and colleagues Some investigators have defined intrapartum sine wavelike
(2003) have extensively reviewed interpretation of the fetal baseline variation with periods of acceleration as pseudosinusoidal.
electrocardiogram during labor. Murphy and colleagues (1991) reported that pseudosinusoidal
patterns were seen in 15 percent of monitored labors. Mild
Sinusoidal Heart Rate pseudosinusoidal patterns were associated with use of meperi-
A true sinusoidal pattern such as that shown in panel 5 of dine and epidural analgesia. Intermediate pseudosinusoidal pat-
Figure 24-10 may be observed with fetal intracranial hemor- terns were linked to fetal sucking or transient episodes of fetal
rhage, with severe fetal asphyxia, and with severe fetal ane- hypoxia caused by umbilical cord compression. Egley and asso-
mia from Rh alloimmunization, fetomaternal hemorrhage, ciates (1991) reported that 4 percent of fetuses demonstrated
twin-twin transfusion syndrome, or vasa previa with bleeding sinusoidal patterns transiently during normal labor. These
(Modanlou, 2004). Insignificant sinusoidal patterns have been authors observed patterns for up to 90 minutes in some cases
reported following administration of meperidine, morphine, and also in association with oxytocin or alphaprodine usage,
alphaprodine, and butorphanol (Angel, 1984; Egley, 1991; or both.
Epstein, 1982). Shown in Figure 24-13 is a sinusoidal pattern The pathophysiology of sinusoidal patterns is unclear, in
seen with maternal meperidine administration. An important part due to various definitions. There seems to be general
agreement that antepartum sine wave baseline undulation
portends severe fetal anemia. Still, few D-alloimmunized
240 fetuses develop this pattern (Nicolaides, 1989). The sinusoi-
dal pattern has been reported to develop or disappear after
210
fetal transfusion (Del Valle, 1992; Lowe, 1984). Ikeda and
associates (1999) have proposed, based on studies in fetal
180
lambs, that the sinusoidal fetal heart rate pattern is related to
150 waves of arterial blood pressure, reflecting oscillations in the
baroreceptor-chemoreceptor feedback mechanism for control
120 of the circulation.
90

60
■ Periodic Fetal Heart Rate Changes
The periodic fetal heart rate refers to deviations from baseline
30 that are temporally related to uterine contractions. Acceleration
FIGURE 24-13 Sinusoidal fetal heart rate pattern associated with refers to an increase in fetal heart rate above baseline and decel-
l
maternal intravenous meperidine administration. Sine waves are eration to a decrease below the baseline rate. The nomencla-
occurring at a rate of 6 cycles per minute. ture most commonly used in the United States is based on the
 Intrapartum Assessment 483

timingg of the deceleration in relation to contractions—thus,

Onset Recovery
early, late, or variablee in onset related to the corresponding
uterine contraction. The waveform of these decelerations is also >30

CHAPTER 24
significant for pattern recognition. In early and late decelera- sec
tions, the slope of fetal heart rate change is gradual, resulting in
a curvilinear and uniform or symmetrical waveform. With vari-
able decelerations, the slope of fetal heart rate change is abrupt
and erratic, giving the waveform a jagged appearance. The 1997 Nadir
workshop proposed that decelerations be defined as recurrent
if they occur with 50 percent or more of contractions in any
20-minute period.
Another system now used less often to describe decelera-
Contraction
tions is based on the pathophysiological events considered most
likely to cause the pattern. In this system, early decelerations are
termed head compression, late decelerations are termed utero-
placental insufficiency, and variable decelerations become cord
compression patterns.
FIGURE 24-14 Features of early fetal heart rate deceleration.
Accelerations Characteristics include a gradual decline in the heart rate with
both onset and recovery coincident with the onset and recovery
These are visually apparent abrupt increases—defined as onset of the contraction. The nadir of the deceleration is 30 seconds or
of acceleration to a peak in less than 30 seconds—in the fetal more after the deceleration onset.
heart rate baseline (American College of Obstetricians and
Gynecologists, 2013b). At 32 weeks’ gestation and beyond, the
acceleration has a peak of 15 bpm with a duration of 15 sec- was first described by Hon (1958), who observed that there
onds or more but less than 2 minutes (see Table 24-1). Before was a heart rate drop with contractions and that this was
32 weeks, a peak of 10 bpm for 15 seconds to 2 minutes is related to cervical dilatation. He considered these findings to
considered normal. Prolonged acceleration was defined as be physiological.
2 minutes or more but less than 10 minutes. Freeman and associates (2003) defined early decelerations as
According to Freeman and coworkers (2003), accelerations those generally seen in active labor between 4 and 7 cm dilata-
most often occur antepartum, in early labor, and in association tion. In their definition, the degree of deceleration is generally
with variable decelerations. Proposed mechanisms for intra- proportional to the contraction strength and rarely falls below
partum accelerations include fetal movement, stimulation by 100 to 110 bpm or 20 to 30 bpm below baseline. Such deceler-
uterine contractions, umbilical cord occlusion, and fetal stimu- ations are common during active labor and not associated with
lation during pelvic examination. Fetal scalp blood sampling tachycardia, loss of variability, or other fetal heart rate changes.
and acoustic stimulation also incite fetal heart rate acceleration Importantly, early decelerations are not associated with fetal
(Clark, 1982). Finally, accelerations can occur during labor hypoxia, acidemia, or low Apgar scores.
without any apparent stimulus. Indeed, they are common in Head compression probably causes vagal nerve activation as
labor and are nearly always associated with fetal movement. a result of dural stimulation, and this mediates the heart rate
These accelerations are virtually always reassuring and almost deceleration (Paul, 1964). Ball and Parer (1992) concluded
always confirm that the fetus is not acidemic at that time. that fetal head compression is a likely cause not only of the
Accelerations seem to have the same physiological explana- deceleration shown in Figure 24-14 but also of those shown in
tions as beat-to-beat variability in that they represent intact Figure 24-15, which typically occur during second-stage labor.
neurohormonal cardiovascular control mechanisms linked to Indeed, they observed that head compression is the likely cause
fetal behavioral states. Krebs and colleagues (1982) analyzed of many variable decelerations classically attributed to cord
electronic heart rate tracings in nearly 2000 fetuses and found compression.
sporadic accelerations during labor in 99.8 percent. Fetal heart
accelerations during the first or last 30 minutes during labor, Late Deceleration
or both, was a favorable sign for fetal well-being. The absence The fetal heart rate response to uterine contractions can be
of such accelerations during labor, however, is not necessarily an index of either uterine perfusion or placental function. A
an unfavorable sign unless coincidental with other nonreassur- late deceleration is a smooth, gradual, symmetrical decrease
ing changes. There is an approximately 50-percent chance of in fetal heart rate beginning at or after the contraction peak
acidemia in the fetus who fails to respond to stimulation in the and returning to baseline only after the contraction has ended.
presence of an otherwise nonreassuring pattern (Clark, 1984; A gradual decrease is defined as 30 seconds or more from
Smith, 1986). the onset of the deceleration to the nadir. In most cases, the
onset, nadir, and recovery of the deceleration occur after the
Early Deceleration beginning, peak, and ending of the contraction, respectively
This consists of a gradual decrease and return to baseline asso- (Fig. 24-16). The magnitude of late decelerations is seldom
ciated with a contraction (Fig. 24-14). Such early deceleration more than 30 to 40 bpm below baseline and typically not more
 484 Labor

240 240

210
210
180
180
SECTION 7

150
150
15
5
120

120 90
C
90 60

B 30
60

100
30
80

60
100
40
80
20
60 0

40 FIGURE 24-17 Late decelerations due to uteroplacental insuf-

20
ficiency resulting from placental abruption. Immediate cesarean
delivery was performed. Umbilical artery pH was 7.05 and the
0 PO2 was 11 mm Hg.
FIGURE 24-15 Two different fetal heart rate patterns during
second-stage labor that are likely both due to head compression
(upper panel). Maternal pushing efforts (lower panel) correspond The lower the fetal Po2 before contractions, the shorter the lag
to the spikes with uterine contractions. Fetal heart rate decel- phase to onset of late decelerations. This lag period reflected
eration (C)
C is consistent with the pattern of head compression
the time necessary for the fetal Po2 to fall below a critical level
shown in Figure 24-14. Deceleration (B), however, is “variable” in
appearance because of its jagged configuration and may alterna- necessary to stimulate arterial chemoreceptors, which mediated
tively represent cord occlusion. decelerations.
Murata and coworkers (1982) also showed that a late decelera-
tion was the first fetal heart rate consequence of uteroplacental-
than 10 to 20 bpm. Late decelerations usually are not accom- induced hypoxia. During the course of progressive hypoxia
panied by accelerations. that led to death over 2 to 13 days, monkey fetuses invariably
Myers and associates (1973) studied monkeys in which they exhibited late decelerations before development of acidemia.
compromised uteroplacental perfusion by lowering maternal Variability of the baseline heart rate disappeared as acidemia
aortic blood pressure. The interval or lag from the contraction developed.
onset until the late deceleration onset was directly related to Numerous clinical circumstances can result in late decelera-
basal fetal oxygenation. They demonstrated that the length of tions. Generally, any process that causes maternal hypotension,
the lag phase was predictive of the fetal Po2 but not fetal pH. excessive uterine activity, or placental dysfunction can induce
late decelerations. The two most common causes are hypoten-
sion from epidural analgesia and uterine hyperactivity caused
Onset Recovery by oxytocin stimulation. Maternal diseases such as hyperten-
≥30 sion, diabetes, and collagen-vascular disorders can cause chronic
sec placental dysfunction. Placental abruption can cause acute late
decelerations (Fig. 24-17).

Variable Deceleration
Nadir The most common deceleration patterns encountered during
labor are variable decelerations attributed to umbilical cord
Contraction occlusion. Melchior and Bernard (1985) identified variable
decelerations in 40 percent of more than 7000 monitor tracings
when labor had progressed to 5 cm dilatation and in 83 percent
by the end of the first stage of labor. Variable deceleration is
defined as an abrupt decrease in the fetal heart rate beginning
with the onset of the contraction and reaching a nadir in less
FIGURE 24-16 Features of late fetal heart rate deceleration.
Characteristics include gradual decline in the heart rate with the than 30 seconds. The decrease must last between ≥ 15 seconds
contraction nadir, and recovery occurring after the end of the con- and 2 minutes and must be ≥ 15 bpm in amplitude. The onset
traction. The nadir of the deceleration occurs 30 seconds or more of deceleration typically varies with successive contractions
after the onset of the deceleration. (Fig. 24-18).
 Intrapartum Assessment 485

Variable <30 (beats/min)

onset sec 300

CHAPTER 24
Fetal heart rate

200

100
Nadir
Contraction

FIGURE 24-18 Features of variable fetal heart rate decelera- (mm Hg)
tions. Characteristics include an abrupt decline in the heart rate,
and onset that commonly varies with successive contractions. The 60 Blood pressure
decelerations measure ≥ 15 bpm for ≥ 15 seconds and have an
onset-to-nadir phase of < 30 seconds. Total duration is < 2 minutes.
50 Aorta
Umbilical
Very early in the development of electronic monitoring, 40 artery
Hon (1959) tested the effects of umbilical cord compression
on fetal heart rate (Fig. 24-19). Similar complete occlusion of 30
the umbilical cord in experimental animals produces abrupt,
jagged-appearing deceleration of the fetal heart rate (Fig. 24-20). 20
Concomitantly, fetal aortic pressure increases. Itskovitz and Umbilical
colleagues (1983) observed that variable decelerations in fetal 10 vein
lambs occurred only after umbilical blood flow was reduced by
at least 50 percent.
Two types of variable decelerations are shown in Figure 0 20 40 60 80 100 120
24-21. The deceleration denoted by “A” is very much like that Time (sec)
FIGURE 24-20 Total umbilical cord occlusion (arrow) in the
sheep fetus is accompanied by an increase in fetal aortic blood
240 pressure. Blood pressure changes in the umbilical vessels are also
200
shown. (Redrawn from Künzel, 1985, with permission.)
160
140
120
100
seen with complete umbilical cord occlusion in experimental
80
animals (see Fig. 24-20). Deceleration “B,” however, has a dif-
f
Fetal heart beats per minute

60
Cord compressed
ferent configuration because of the “shoulders” of acceleration
40 before and after the deceleration component. Lee and cowork-
ers (1975) proposed that this form of variable deceleration was
10 20 30 40 50 60 70 80 90 100 110 120 caused by differing degrees of partial cord occlusion. In this
240
physiological scheme, occlusion of only the vein reduces fetal
200 blood return, thereby triggering a baroreceptor-mediated accel-
160 eration. With increasing intrauterine pressure and subsequent
140
120 complete cord occlusion, fetal systemic hypertension develops
100 due to obstruction of umbilical artery flow. This stimulates a
80 baroreceptor-mediated deceleration. Presumably, the aftercom-
60 ing shoulder of acceleration represents the same events occur-
Cord compressed ring in reverse (Fig. 24-22).
40
Ball and Parer (1992) concluded that variable decelera-
10 20 30 40 50 60 70 80 90 100 110 120 tions are mediated vagally and that the vagal response may be
Seconds due to chemoreceptor or baroreceptor activity or both. Partial
FIGURE 24-19 A. The effects of 25-second cord compression or complete cord occlusion produces an increase in afterload
compared with those of 40 seconds in panel (B). (Redrawn from (baroreceptor) and a decrease in fetal arterial oxygen content
Hon, 1959, with permission.) (chemoreceptor). These both result in vagal activity leading to
 486 Labor

deceleration. In fetal monkeys, the baroreceptor reflexes appear

to operate during the first 15 to 20 seconds of umbilical cord
occlusion followed by decline in Po2 at approximately 30 sec- Fetal heart
onds, which then serves as a chemoreceptor stimulus (Mueller- rate
SECTION 7

Heubach, 1982).
Thus, variable decelerations represent fetal heart rate reflexes
that reflect either blood pressure changes due to interruption
of umbilical flow or changes in oxygenation. It is likely that Partial Complete Partial
occlusion occlusion occlusio
occlusion
most fetuses have experienced brief but recurrent periods of
hypoxia due to umbilical cord compression during gestation.
The frequency and inevitability of cord occlusion undoubtedly
have provided the fetus with these physiological mechanisms as
Uterine
a means of coping. The great dilemma for the obstetrician in
contraction
managing variable fetal heart rate decelerations is determining
when variable decelerations are pathological. According to the Umbilical vein
American College of Obstetricians and Gynecologists (2013a), Umbilical artery
recurrent variable decelerations with minimal to moderate vari-
Fetal
ability are indeterminate, whereas those with absent variability
systolic BP
are abnormal.l
Other fetal heart rate patterns have been associated with Umbilical
umbilical cord compression. Saltatoryy baseline heart rate cord
(Fig. 24-23) was first described by Hammacher and colleagues
(1968) and linked to umbilical cord complications during FIGURE 24-22 Schematic representation of the fetal heart
labor. The pattern consists of rapidly recurring couplets of rate effects with partial and complete umbilical cord occlusion.
acceleration and deceleration causing relatively large oscillations Uterine pressures generated early in a contraction cause cord
of the baseline fetal heart rate. We also observed a relation- compression predominantly of the thin-walled umbilical vein. The
ship between cord occlusion and the saltatory pattern (Leveno, resulting decrease in fetal cardiac output leads to an initial com-
1984). In the absence of other fetal heart rate findings, these pensatory rise in fetal heart rate. As cord compression intensifies,
umbilical arteries are then also compressed. The resulting rise
do not signal fetal compromise. Lambdaa is a pattern involv- in fetal systolic blood pressure leads to a vagal-mediated fetal
ing an acceleration followed by a variable deceleration with no heart rate deceleration. As the contraction abates and compres-
acceleration at the end of the deceleration. This pattern typi- sion is relieved first on the umbilical arteries, elevated fetal sys-
cally is seen in early labor and is not ominous (Freeman, 2003). tolic blood pressures drop and the deceleration resolves. A final
This lambda pattern may result from mild cord compression or increase in fetal heart rate is seen as a result of persistent umbili-
cal vein occlusion. With completion of the uterine contraction
and cord compression, the fetal heart rate returns to baseline.
BP = blood pressure. (Adapted from Lee, 1975.)

240 240

210 210

190 180
B
150
1 50 150
A
120 120
0

90 90

60 60

30 30

100 100

80 80

60 60

40 40

20 20
2 0
0
0

FIGURE 24-21 Varying (variable) fetal heart rate decelerations. FIGURE 24-23 Saltatory baseline fetal heart rate showing rapidly
Deceleration (B) exhibits “shoulders” of acceleration compared with recurring couplets of acceleration combined with deceleration.
deceleration (A). (Adapted from Künzel, 1985, with permission.)
 Intrapartum Assessment 487

stretch. Overshoott is a variable deceleration followed by accel- tenuous. Management of isolated prolonged decelerations
eration. The clinical significance of this pattern is controversial is based on bedside clinical judgment, which inevitably will
(Westgate, 2001). sometimes be imperfect given the unpredictability of these

CHAPTER 24
decelerations.
Prolonged Deceleration
This pattern, which is shown in Figure 24-24, is defined as an ■ Fetal Heart Rate Patterns During
isolated deceleration greater than 15 bpm lasting 2 minutes Second-Stage Labor
or longer but < 10 minutes from onset to return to baseline. Decelerations are virtually ubiquitous during the second
Prolonged decelerations are difficult to interpret because they stage. Melchior and Bernard (1985) reported that only
are seen in many different clinical situations. Some of the 1.4 percent of more than 7000 deliveries lacked decelera-
more common causes include cervical examination, uterine tions during second-stage labor. Both cord compression
hyperactivity, cord entanglement, and maternal supine hypo- and fetal head compression have been implicated as causes
tension. of decelerations and baseline bradycardia during second-
Epidural, spinal, or paracervical analgesia may induce pro- stage labor. The high incidence of such patterns minimized
longed deceleration of the fetal heart rate. For example, Eberle their potential significance during the early development
and coworkers (1998) reported that prolonged decelerations and interpretation of electronic monitoring. For example,
occurred in 4 percent of normal parturients given either epi- Boehm (1975) described profound, prolonged fetal heart
dural or intrathecal labor analgesia. Hill and associates (2003) rate deceleration in the 10 minutes preceding vaginal deliv-
observed prolonged deceleration in 1 percent of women given ery of 18 healthy infants. However, Herbert and Boehm
epidural analgesia during labor at Parkland Hospital. Other (1981) later reported another 18 pregnancies with similar
causes of prolonged deceleration include maternal hypoperfu- prolonged second-stage decelerations. There was one still-
sion or hypoxia from any cause, placental abruption, umbilical birth and one neonatal death. These experiences attest to
cord knots or prolapse, maternal seizures including eclampsia the unpredictability of the fetal heart rate during second-
and epilepsy, application of a fetal scalp electrode, impending stage labor.
birth, or even maternal Valsalva maneuver. Spong and associates (1998) analyzed the characteristics
The placenta is very effective in resuscitating the fetus if of second-stage variable fetal heart rate decelerations in 250
the original insult does not recur immediately. Occasionally, deliveries and found that as the total number of deceler-
such self-limited prolonged decelerations are followed by loss ations to < 70 bpm increased, the 5-minute Apgar score
of beat-to-beat variability, baseline tachycardia, and even a decreased. Put another way, the longer a fetus was exposed
period of late decelerations, all of which resolve as the fetus to variable decelerations, the lower the Apgar score was at
recovers. Freeman and colleagues (2003) emphasize rightfully 5 minutes.
that the fetus may die during prolonged decelerations. Thus, Picquard and coworkers (1988) analyzed heart rate pat-
management of prolonged decelerations can be extremely terns during second-stage labor in 234 women in an attempt
to identify specific patterns to diagnose fetal compromise.
Loss of beat-to-beat variability and baseline fetal heart rate
240 240
< 90 bpm were predictive of fetal acidemia. Krebs and associ-
210 210 ates (1981) also found that persistent or progressive baseline
bradycardia and baseline tachycardia were associated with low
180 180
Apgar scores. Gull and colleagues (1996) observed that abrupt
150
0 150 fetal heart rate deceleration to < 100 bpm associated with
loss of beat-to-beat variability for 4 minutes or longer was
120
0 120
predictive of fetal acidemia. Thus, abnormal baseline heart
90 90 rate—either bradycardia or tachycardia, absent beat-to-beat
variability, or both—in the presence of second-stage decel-
60 60
0
erations, is associated with increased but not inevitable fetal
30 30 compromise (Fig. 24-25).

100
0 100

80 80
■ Admission Fetal Monitoring
in Low-Risk Pregnancies
60 60
With this approach, women with low-risk pregnancies are mon-
40 40
itored for a short time on admission for labor, and continuous
20 20 monitoring is used only if fetal heart rate abnormalities are
0 0 subsequently identified. Mires and coworkers (2001) randomly
FIGURE 24-24 Prolonged fetal heart rate deceleration due to
assigned 3752 low-risk women in spontaneous labor at admis-
uterine hyperactivity. Approximately 3 minutes of the tracing are sion either to auscultation of the fetal heart or to 20 minutes of
shown, but the fetal heart rate returned to normal after uterine electronic fetal monitoring. Use of admission electronic fetal
hypertonus resolved. Vaginal delivery later ensued. monitoring did not improve infant outcome. Moreover, its use
 488 Labor

Second stage
240 240

21
2
210
10 21
21
10
210
SECTION 7

180 180
18
80

150 150
150

120 120
120

90 90
0

60 60

Tachycardia
T y Nuchal cord
30 30
Loss of variability pH 6.9

100 100

80 80

60 60
6 0

40
40 40
40

20 20

0 0

FIGURE 24-25 Cord-compression fetal heart rate decelerations in second-stage labor associated with tachycardia and loss of variability.
The umbilical cord arterial pH was 6.9.

resulted in increased interventions, including operative deliv- OTHER INTRAPARTUM ASSESSMENT

ery. Impey and associates (2003) performed a similar study TECHNIQUES
in 8588 low-risk women and also found no improvement
in infant outcome. More than half of the women enrolled ■ Fetal Scalp Blood Sampling
in these studies, whether they received admission electronic
monitoring or auscultation, eventually required continuous
Gynecologists (2009), measurements of the pH in capillary
monitoring for diagnosed abnormalities in the fetal heart
scalp blood may help to identify the fetus in serious distress.
rate.
That said, it also emphasized that neither normal nor abnormal
With the increasing rate of scheduled cesarean deliveries
scalp pH results have been shown to be predictive of infant
in the United States, clinicians and hospitals must decide
outcome. The College also indicated that the procedure is now
whether fetal monitoring is required before the procedure
used uncommonly and is not even available at some hospitals.
in low-risk women. The American College of Obstetricians
For completion, an illuminated endoscope is inserted
and Gynecologists (2010) has concluded that data are insuf- f
through the dilated cervix after membrane rupture so as to
ficient to determine the value of fetal monitoring under these
press firmly against the fetal scalp (Fig. 24-26). The skin is
circumstances.
wiped clean with a cotton swab and coated with a silicone
gel to cause the blood to accumulate as discrete globules. An
incision is made through the skin to a depth of 2 mm with a
■ Centralized Monitoring special blade on a long handle. As a drop of blood forms on
Technological advances have made it possible to observe fetal the surface, it is immediately collected into a heparinized glass
heart rate monitors from a remote, centralized location. Such capillary tube. The pH of the blood is measured promptly.
intrapartum monitoring equipment has become common The pH of fetal capillary scalp blood is usually lower than
in American labor and delivery units. The rationale behind that of umbilical venous blood and approaches that of umbili-
centralized monitoring is that the ability to monitor several cal arterial blood. Zalar and Quilligan (1979) recommended
patients simultaneously would lead to better outcomes. What a protocol to try to confirm fetal distress. If the pH is > 7.25,
is the evidence that this rationale is correct? To our knowl- labor is observed, and if between 7.20 and 7.25, the pH mea-
edge, only one study on centralized fetal monitoring has been surement is repeated within 30 minutes. If the pH is < 7.20,
reported. Anderson and colleagues (2011) measured the abil- another scalp blood sample is collected immediately, and the
ity of 12 individuals to detect critical signals in fetal heart rate mother is taken to an operating room and prepared for surgery.
tracings on one, two, or four monitors. The results showed Delivery is performed promptly if the low pH is confirmed.
that detection accuracy declined as the number of displays Otherwise, labor is allowed to continue, and scalp blood sam-
increased. ples are repeated periodically.
 Intrapartum Assessment 489

larynx placed approximately 1 cm from or directly onto the

maternal abdomen (Chap. 17, p. 341). Response to vibro-
acoustic stimulation is considered normal if a fetal heart rate

CHAPTER 24
acceleration of at least 15 bpm for at least 15 seconds occurs
within 15 seconds after the stimulation and with prolonged
fetal movements (Sherer, 1994). Lin and colleagues (2001)
prospectively studied vibroacoustic stimulation in 113 women
in labor with either moderate to severe variable or late fetal
heart rate decelerations. They concluded that this technique is
an effective predictor of fetal acidosis in the setting of variable
decelerations. The predictability for fetal acidosis, however, is
limited in the setting of late decelerations. Other investiga-
tors have reported that although vibroacoustic stimulation in
second-stage labor is associated with fetal heart rate reactivity,
the quality of the response did not predict neonatal outcome or
enhance labor management (Anyaegbunam, 1994).
Skupski and coworkers (2002) performed a metaanalysis
of reports on intrapartum fetal stimulation tests published
FIGURE 24-26 The technique of fetal scalp sampling using an
amnioscope. The end of the endoscope is displaced from the fetal between 1966 and 2000. Four types of fetal stimulation were
vertex approximately 2 cm to show the disposable blade against analyzed and included scalp puncture for pH testing, Allis
the fetal scalp before incision. (Adapted from Hamilton, 1974.) clamp pinching of the fetal scalp, vibroacoustic stimulation,
and digital stroking of the scalp. Results were similar for
all four methods. These investigators concluded that intra-
The only benefits reported for scalp pH testing are fewer partum stimulation tests were useful to exclude fetal acide-
cesarean deliveries for fetal distress (Young, 1980b). Goodwin mia. They cautioned, however, that these tests are “less than
and coworkers (1994), however, in a study of 112,000 deliv- perfect.”
eries, showed a decrease in the scalp pH sampling rate. The
rate dropped from approximately 1.8 percent in the mid-
1980s to 0.03 percent by 1992 but with no increased delivery ■ Fetal Pulse Oximetry
rate for fetal distress. They concluded that scalp pH sampling Using technology similar to that of adult pulse oximetry,
was unnecessary. Kruger and colleagues (1999) have advo- instrumentation has been developed that may allow assess-
cated the use of fetal scalp blood lactate concentration as an ment of fetal oxyhemoglobin saturation once membranes are
adjunct to pH. Wiberg-Itzel and associates (2008) random- ruptured. A unique padlike sensor such as shown in Figure
ized 1496 fetuses to scalp blood pH analysis and 1496 to scalp 24-27 is inserted through the cervix and positioned against
blood lactate analysis. They found either to be equivalent in the fetal face, where it is held in place by the uterine wall. A
predicting fetal acidemia. The advantage of lactate measure- transabdominal fetal pulse oximeter has also been described in
ment was that a smaller amount of blood was needed, which
led to a lower procedural failure rate compared with scalp
sampling for pH.

■ Scalp Stimulation
Clark and coworkers (1984) have suggested that scalp stimula-
tion is an alternative to scalp blood sampling. This proposal
was based on the observation that heart rate acceleration in
response to pinching of the scalp with an Allis clamp just before
obtaining blood was invariably associated with a normal pH.
Conversely, failure to provoke acceleration was not uniformly
predictive of fetal acidemia. Later, Elimian and associates
(1997) reported that of 58 cases in which the fetal heart rate
accelerated ≥ 10 bpm after 15 seconds of gentle digital stroking
of the scalp, 100 percent had a scalp pH of ≥ 7.20. Without an
acceleration, however, only 30 percent had a scalp pH < 7.20.

■ Vibroacoustic Stimulation
Fetal heart rate acceleration in response to vibroacoustic stimu-
lation has been recommended as a substitute for scalp sampling FIGURE 24-27 Schematic diagram of fetal pulse oximeter sensor
(Edersheim, 1987). The technique uses an electronic artificial placement.
624

CHAPTER 32

The Newborn

INITIATION OF AIR BREATHING . . . . . . . . . . . . . . . . . . 624 breathing movements both before and after birth (Dawes,
1974).
CARE IN THE DELIVERY ROOM . . . . . . . . . . . . . . . . . . . 625 • Thoracic compression—this occurs during pelvic descent,
EVALUATION OF NEWBORN CONDITION . . . . . . . . . . . . 627 following which vaginal birth forces fluid from the respira-
tory tract in volume equivalent to approximately a fourth
PREVENTIVE CARE. . . . . . . . . . . . . . . . . . . . . . . . . . . . . 631 of the ultimate functional residual capacity (Saunders,
1978).
ROUTINE NEWBORN CARE . . . . . . . . . . . . . . . . . . . . . . 632 • Aeration of the newborn lung does not involve the inflation
of a collapsed structure, but instead, the rapid replacement of
bronchial and alveolar fluid by air. After delivery, the residual
alveolar fluid is cleared through the pulmonary circulation
The American Academy of Pediatrics and the American
and to a lesser degree, through the pulmonary lymphatics
College of Obstetricians and Gynecologists (2012) recommend
(Chernick, 1978). Delay in fluid removal from the alveoli
attendance at delivery of at least one person whose primary
probably contributes to the syndrome of transient tachypnea
responsibility is the neonate and who is capable of initiating
of the newborn (TTN) (Guglani, 2008). As fluid is replaced
resuscitation that includes intubation, vascular access, and
by air, compression of the pulmonary vasculature is reduced
medication administration. This usually is a pediatrician, nurse
considerably, and in turn, resistance to blood flow is lowered.
practitioner, anesthesiologist, nurse anesthetist, or specially
With the fall in pulmonary arterial blood pressure, the ductus
trained nurse. However, in their absence, the responsibility for
arteriosus normally closes (Fig. 7-8, p. 136).
neonatal resuscitation falls to the obstetrical attendant. Thus,
obstetricians should be well versed in measures for immediate High negative intrathoracic pressures are required to
care of the newborn. bring about the initial entry of air into the fluid-filled
alveoli. Normally, from the first breath after birth, progres-
sively more residual air accumulates in the lung, and with
INITIATION OF AIR BREATHING each successive breath, lower pulmonary opening pressure is
required. In the normal mature newborn, by approximately
Immediately following birth, the infant must promptly con-
the fifth breath, pressure-volume changes achieved with each
vert to air breathing as the fluid-filled alveoli expand with air
respiration are very similar to those of the adult. Thus, the
and pulmonary perfusion is established. The newborn begins to
breathing pattern shifts from the shallow episodic inspira-
breathe and cry almost immediately after birth, which indicates
tions characteristic of the fetus to regular, deeper inhala-
establishment of active respiration. Some factors that appear to
tions (Chap. 17, p. 337). Surfactant, which is synthesized
influence the first breath include:
by type II pneumocytes and already present in the alveoli,
• Physical stimulation—examples include handling the neo- lowers alveolar surface tension and thereby prevents lung
nate during delivery. collapse. Insufficient surfactant, common in preterm infants,
• Oxygen deprivation and carbon dioxide accumulation— leads promptly to respiratory distress syndrome, which is
these serve to increase the frequency and magnitude of described in Chapter 34 (p. 653).
 The Newborn 625

CARE IN THE DELIVERY ROOM oxygen deprivation and asphyxia persist, however, the newborn
will develop deep gasping respirations, followed by secondary
Personnel designated for infant support are responsible apnea. This latter stage is associated with a further decline in

CHAPTER 32
for immediate care and for acute resuscitation initiation if heart rate, falling blood pressure, and loss of neuromuscular
needed. tone. Neonates in secondary apnea will not respond to stimu-
lation and will not spontaneously resume respiratory efforts.
Unless ventilation is assisted, death follows. Clinically, primary
■ Immediate Care and secondary apneas are indistinguishable. Thus, secondary
Before and during delivery, careful consideration must be apnea must be assumed and resuscitation of the apneic new-
given to several determinants of neonatal well-being includ- born must be started immediately.
ing: (1) maternal health status; (2) prenatal complications,
including any suspected fetal malformations; (3) gestational
age; (4) labor complications; (5) duration of labor and rup- ■ Resuscitation Protocol
tured membranes; (6) type and duration of anesthesia; (7) dif-
f The updated algorithm for newborn resuscitation recom-
ficulty with delivery; and (8) medications given during labor mended by ILCOR and the International Consensus on
and their dosages, administration routes, and timing relative Cardiopulmonary Resuscitation is shown in Figure 32-2. Many
to delivery. of its tenets follow below.

Basic Measures
■ Newborn Resuscitation
The vigorous newborn is first placed in a warm environment to
The International Liaison Committee on Resuscitation
minimize heat loss, the airway is cleared, and the infant dried.
(ILCOR) updated its guidelines for neonatal resuscitation that
Routine gastric aspiration has been shown to be nonbeneficial
are sanctioned by the American Academy of Pediatrics and the
and even harmful (Kiremitci, 2011). And although previously
American Heart Association (Biban, 2011; Perlman, 2010).
recommended, there is no evidence that bulb suctioning for
These substantially revised guidelines are incorporated into the
clear or meconium-stained fluid is beneficial, even if the new-
following sections.
born is depressed (Chap. 33, p. 638). With stimulation, the
Approximately 10 percent of newborns require some degree
healthy newborn will take a breath within a few seconds of
of active resuscitation to stimulate breathing, and 1 percent
birth and cry within half a minute, after which routine sup-
require extensive resuscitation. It is perhaps not coincidental
portive care is provided.
that there is a two- to threefold risk of death for newborns
delivered at home compared with those delivered in hospitals Assessment at 30 Seconds of Life. Apnea, gasping respira-
(American College of Obstetricians and Gynecologists, 2013b). tions, or heart rate < 100 bpm beyond 30 seconds after delivery
When deprived of oxygen, either before or after birth, neonates should prompt administration of positive-pressure ventilation
demonstrate a well-defined sequence of events leading to apnea with room airr (Fig. 32-3). Assisted ventilation rates of 30 to
(Fig. 32-1). With oxygen deprivation, there is a transient period 60 breaths per minute are commonly employed, and the per-
of rapid breathing, and if it persists, breathing stops, which is cent of oxygen saturation is monitored by pulse oximetry. At
termed primary apnea. This stage is accompanied by a fall in this point, supplemental oxygen can be given in graduated
heart rate and loss of neuromuscular tone. Simple stimulation increasing percentages to maintain oxygen saturation (Spo2)
and exposure to oxygen will usually reverse primary apnea. If values within a normal range (Vento, 2011). Adequate ventila-
tion is indicated by improved heart rate.

Rapid Irregular Assessment at 60 Seconds of Life. If the heart rate remains

breathing gasping < 100 bpm, then ventilation is inadequate. The head position
Primary Secondary should be checked as shown in Figure 32-3, secretions cleared,
apnea apnea and if necessary, inflation pressure increased. If the heart rate
persists below 100 bpm beyond 60 seconds, tracheal intuba-
tion is considered. A number of conditions may be the cause of
Heart rate (bpm) inadequate response, including the following:
200
150 • Hypoxemia or acidosis from any cause
MAP (mm Hg)
100 • Drugs administered to the mother before delivery
50 • Immaturity
0 • Upper airway obstruction
Time • Pneumothorax
• Lung abnormalities
FIGURE 32-1 Physiological changes associated with primary
and secondary apnea in the newborn. bpm = beats per minute; • Meconium aspiration
HR = heart rate; MAP = mean arterial pressure. (Adapted from • Central nervous system developmental abnormality
Kattwinkel, 2006.) • Sepsis syndrome.
 626 The Newborn

Birth is introduced at the side of the mouth and

Term Routine care:
Yes then directed posteriorly toward the oro-
Breathing/crying Warm
Good muscle tone Dry pharynx as shown in Figure 32-4. The
Clear airway laryngoscope is next moved gently into
SECTION 9

No Ongoing evaluation the vallecula—the space between the base

of the tongue and the epiglottis. Gentle
Warm elevation of the laryngoscope tip will raise
Dry the epiglottis and expose the glottis and
Stimulate No the vocal cords. The tube is then intro-
duced through the vocal cords. Gentle
cricoid pressure may be useful. Tube sizes
vary from 3.5 to 4.0 mm for term infants
30 sec HR < 100 bpm No Labored breathing down to 2.5 mm for those < 28 weeks or
Gasping, apnea Cyanosis < 1000 g.
Several steps are taken to ensure that
Yes Yes the tube is positioned in the trachea and
not the esophagus: observation for sym-
Positive-pressure ventilation Consider SpO2 monitoring metrical chest wall motion; auscultation
60 sec
SpO2 monitoring Consider CPAP for equal breath sounds, especially in the
axillae; and auscultation for the absence
of breath sounds or gurgling over the
stomach. Tracheal suctioning is no lon-
No
HR < 100 bpm ger recommended or discouraged. Using
an appropriate ventilation bag attached to
Yes the tracheal tube, puffs of air are delivered
into the tube at 1- to 2-second intervals
Confirm adequate ventilation Postresuscitation care
with a force adequate to gently lift the
Consider intubation chest wall. In term infants, pressures of
30 to 40 cm H2O typically will expand
the alveoli without causing barotrauma.
No
For preterm infants, pressures are 20 to
HR < 60 bpm 25 cm H2O. An increase in heart rate
and Spo2 levels within acceptable ranges
Yes reflect a positive response.

Chest compressions Chest Compressions

Positive-pressure ventilation If the heart rate remains < 60 bpm despite
adequate ventilation for 30 seconds,
chest compressions are initiated. These
are delivered on the lower third of the
HR < 60 bpm sternum at a depth sufficient to generate
a palpable pulse. A 3:1 compressions-
Yes to-ventilation ratio is recommended,
with 90 compressions and 30 breaths to
IV epinephrine achieve approximately 120 events each
Consider intubation
minute. The heart rate is reassessed every
FIGURE 32-2 Algorithm for resuscitation of the newborn. CPAP = continuous positive
30 seconds, and chest compressions are
airway pressure; HR = heart rate; IV = intravenous. (Adapted from Perlman, 2010.) continued until the spontaneous heart
rate is at least 60 bpm.

Tracheal Intubation Epinephrine and Volume Expansion

If bag-and-mask ventilation is ineffective or prolonged, tracheal Intravenously administered epinephrine is indicated when the
intubation is then performed. Other indications include the need heart rate remains < 60 bpm after adequate ventilation and chest
for chest compressions or tracheal administration of medications, compressions. Epinephrine may be given through the endotra-
or special circumstances such as extremely low birthweight or a cheal tube if venous access has not been established. The recom-
congenital diaphragmatic hernia. A laryngoscope with a straight mended intravenous dose is 0.01 to 0.03 mg/kg. If given through
blade—size 0 for a preterm infant and size 1 for a term neonate— the tracheal tube, higher doses are employed—0.05 to 0.1 mg/kg.
 The Newborn 627

Epiglottis

Vocal cord
Glottis

CHAPTER 32
Esophagus

Tongue
Laryngoscope blade
Vallecula
Epiglottis
Trachea
Esophagus

FIGURE 32-3 Correct use of bag-and-mask ventilation. The head

should be in a sniffing position with the tip of the nose pointing
to the ceiling. The neck should not be hyperextended.
FIGURE 32-4 Sagittal view of laryngoscope positioning during
intubation. The laryngoscope blade is inserted between the tongue
For infants with blood loss, early volume replacement with base and epiglottis. Upward tilting of the tongue also lifts the
crystalloid or packed red cells is indicated if they do not respond epiglottis. The endotracheal tube is then threaded below the epi-
to resuscitation. glottis and between the vocal cords (inset) to enter the trachea.

Discontinuation of Resuscitation assigned a value of 0 to 2. The total score, based on the sum
As expected, newborns with cardiopulmonary arrest who do of the five components, is determined in all neonates at 1 and
not respond promptly to resuscitation are at great risk for death, 5 minutes after delivery. In depressed infants, the score may
and if they survive, for severe morbidity (Haddad, 2000). The be calculated at further 5-minute intervals until a 20-minute
International Consensus Committee concluded that discontin- Apgar score is assessed.
uation of resuscitative efforts may be appropriate in a neonate The 1-minute Apgar score reflects the need for immediate
without a heartbeat for 10 minutes of continuous and adequate resuscitation. The 5-minute score, and particularly the change
resuscitative efforts (Perlman, 2010). This committee cites lack in score between 1 and 5 minutes, is a useful index of the
of data for more specific recommendations regarding the infant effectiveness of resuscitative efforts. The 5-minute Apgar score
whose heart rate remains < 60 bpm. also has prognostic significance for neonatal survival because
survival is related closely to the condition of the neonate in
the delivery room (Apgar, 1958). In an analysis of more than
EVALUATION OF NEWBORN CONDITION 150,000 infants delivered at Parkland Hospital, Casey and asso-
ciates (2001b) assessed the significance of the 5-minute score for
■ Apgar Score predicting survival during the first 28 days of life. They found
The scoring system described in 1953 by Dr. Virginia Apgar that in term neonates, the risk of neonatal death was approxi-
remains a useful clinical tool to identify those neonates who mately 1 in 5000 for those with Apgar scores of 7 to 10. This
require resuscitation and to assess the effectiveness of any risk compares with a mortality rate of 1 in 4 for term infants
resuscitative measures. As shown in Table 32-1, each of the with 5-minute scores of 3 or less. Low 5-minute scores were
five easily identifiable characteristics—heart rate, respiratory comparably predictive of neonatal death in preterm infants.
effort, muscle tone, reflex irritability, and color—is assessed and These investigators concluded that the Apgar scoring system

TABLE 32-1. Apgar Scoring System

Sign 0 Points 1 Point 2 Points
Heart rate Absent < 100 bpm ≥ 100 bpm
Respiratory effort Absent Slow, irregular Good, crying
Muscle tone Flaccid Some extremity flexion Active motion
Reflex irritability No response Grimace Vigorous cry
Color Blue, pale Body pink, extremities blue Completely pink

bpm = beats per minute.

Data from Apgar, 1953.
 628 The Newborn

is as relevant for the prediction of neonatal survival today as it Arterial blood is drawn from the isolated cord segment
was more than 50 years ago. into a 1- to 2-mL commercially prepared plastic syringe con-
There have been attempts to use Apgar scores to define taining lyophilized heparin or a similar syringe that has been
asphyxial injury and to predict subsequent neurological out- flushed with a heparin solution containing 1000 U/mL. Once
SECTION 9

come—uses for which the Apgar score was never intended. sampling is completed, the needle is capped and the syringe
Such associations are difficult to measure with reliability given transported, on ice, to the laboratory. Although efforts should
that both asphyxial injury and low Apgar scores are infrequent be made for prompt transport, neither the pH nor Pco2 val-
outcomes. For example, according to United States birth cer- ues change significantly in blood kept at room temperature
tificate records for 2010, only 1.8 percent of newborns had for up to 60 minutes (Duerbeck, 1992). Mathematical mod-
a 5-minute score below 7 (Martin, 2012). Similarly, in a els have been developed that allow reasonable prediction of
population-based study of more than 1 million term infants birth acid–base status in properly collected cord blood samples
born in Sweden between 1988 and 1997, the incidence of analyzed as late as 60 hours after delivery (Chauhan, 1994).
5-minute Apgar scores of 3 or less was approximately 2 per Also, Swedish investigators reported significant variances in
1000 (Thorngren-Jerneck, 2001). acid-base measurements with the use of different analyzers
Despite the methodological challenges, erroneous defi- (Mokarami, 2012).
nitions of asphyxia by many groups were established based
solely on low Apgar scores. These prompted the American
College of Obstetricians and Gynecologists and the American ■ Fetal Acid-Base Physiology
Academy of Pediatrics (2010) to issue a series of joint opin- The fetus produces both carbonic and organic acids. Carbonic
ions with important caveats regarding limitations of use of acid (H2CO3) is formed by oxidative metabolism of CO2. The
the Apgar score. One is that because certain elements of fetus usually rapidly clears CO2 through the placental circula-
the Apgar score are partially dependent on the physiologi- tion. If CO2 clearance is lowered, then carbonic acid levels
cal maturity of the newborn, a healthy preterm infant may rise. When H2CO3 accumulates in fetal blood and there is
receive a low score only because of immaturity (Catlin, no concurrent increase in organic acids, the result is termed
1986). Apgar scores may be influenced by a variety of factors respiratory acidemia. This often follows impaired placental
including, but not limited to, fetal malformations, maternal exchange.
medications, and infection. Therefore, it is inappropriate to In contrast, organic acids primarily include lactic and
use an Apgar score alone to diagnose asphyxia. A 5-minute β-hydroxybutyric acids. Levels of these increase with persis-
Apgar score of 3 correlates poorly with adverse future neuro- tent placental exchange impairment and result from anaero-
logical outcomes, and thus scores are measured also at 10, 15, bic glycolysis. These organic acids are cleared slowly from
and 20 minutes when the score remains 3 or less (Freeman, fetal blood, and when they accumulate without a concurrent
1988; Nelson, 1981). increase in H2CO3, the result is termed metabolic acidemia.
Importantly, the Apgar score alone cannot establish With the development of metabolic acidemia, bicarbonate
hypoxia as the cause of cerebral palsy. As discussed in Chapter (HCO3−) decreases because it is used to buffer the organic acid.
33 (p. 638), a neonate who has had an asphyxial insult proxi- An increase in H2CO3 accompanied by an increase in organic
mate to delivery that is severe enough to result in acute neu- acid reflected by decreased HCO3− causes mixed respiratory-
rological injury will demonstrate most of the following: (1) metabolic acidemia.
profound acidemia with cord artery blood pH < 7 and acid- In the fetus, respiratory and metabolic acidemia and ulti-
base deficit ≥ 12 mmol/L; (2) Apgar score of 0–3 persisting mately tissue acidosis are most likely part of a progressively
for 10 minutes or longer; (3) neurological manifestations such worsening continuum. This is different from the adult patho-
as seizures, coma, or hypotonia; and (4) multisystem organ physiology, in which distinct conditions result in either respi-
dysfunction—cardiovascular, gastrointestinal, hematologi- ratory acidosis—for example, pulmonary disease, or metabolic
cal, pulmonary, or renal (American College of Obstetricians acidosis—for example, diabetes. In the fetus, the placenta serves
and Gynecologists and the American Academy of Pediatrics, as both the lungs and to a certain degree, the kidneys. One
2003). principal cause of fetal acidemia is a decrease in uteroplacental
perfusion. This results in the retention of CO2, that is, respira-
tory acidemia, and if protracted and severe enough, a mixed or
■ Umbilical Cord Blood Acid–Base Studies metabolic acidemia.
Blood taken from umbilical vessels may be used for acid- Assuming that maternal pH and blood gases are normal,
base studies to assess the metabolic status of the neonate. the actual pH of fetal blood is dependent on the proportion
Blood collection is performed following delivery by imme- of carbonic and organic acids and the amount of bicarbonate,
diately isolating a 10- to 20-cm segment of cord with two which is the major buffer in blood. This can best be illustrated
clamps placed near the neonate and another two clamps by the Henderson–Hasselbalch equation:
nearer the placenta. The importance of clamping the cord is HCO3−
underscored by the fact that delays of 20 to 30 seconds can pH = pK + log [base] or, pH = pK + log
[acid] H2CO3
alter both the Pco2 and pH (Valero, 2012; White, 2012).
The cord is then cut between the two proximal clamps and For clinical purposes, HCO3− represents the metabolic com-
then the two distal clamps. ponent and is reported in mEq/L. The H2CO3 concentration
 The Newborn 629

represents the respiratory component and is reported as the normal pH. A base deficit occurs when HCO3− concen-
Pco2 in mm Hg. Thus: tration decreases to below normal levels, and a base excess
− occurs when HCO3− values are above normal. Importantly, a
pH = pK + log metabolic (HCO3 mEq/L)

CHAPTER 32
mixed respiratory–metabolic acidemia with a large base defi-
respiratory (Pco2 mm Hg)
cit and a low HCO3−, for example 12 mmol/L, is more often
The result of this equation is a pH value. Because pH is a associated with a depressed neonate than is a mixed acide-
logarithmic term, it does not give a linear measure of acid accu- mia with a minimal base deficit and a more nearly normal
mulation. For example, a change in hydrogen ion concentra- HCO3− level.
tion associated with a fall in pH from 7.0 to 6.9 is almost twice
that which is associated with a fall in pH from 7.3 to 7.2. For
this reason, the change in base, termed delta base, offers a more ■ Clinical Significance of Acidemia
linear measure of the degree of accumulation of metabolic acid Fetal oxygenation and pH generally decline during the course
(Armstrong, 2007). The delta base is a calculated number used of normal labor. Normal umbilical cord blood pH and blood
as a measure of the change in buffering capacity of bicarbonate gas values at delivery in term newborns are summarized in
(HCO3−). The formula for calculating the base excess (BE) is Table 32-2. Similar values have been reported for preterm
as follows: infants (Dickinson, 1992; Ramin, 1989; Riley, 1993). The
lower limits of normal pH in the newborn have been found
BE = 0.02786 × Pco2 × 10(pH – 6.1) × 13.77 × pH – 124.58
to range from 7.04 to 7.10 (Boylan, 1994). Thus, these val-
Shown in Figure 32-5 is a nomogram developed from ues should be considered to define neonatal acidemia. Even
which these can be calculated if only two parameters are so, most fetuses will tolerate intrapartum acidemia with a pH
known. For example, HCO3− concentration will be decreased as low as 7.00 without incurring neurological impairment
with a metabolic acidemia as it is consumed to maintain a (Freeman, 1988; Gilstrap, 1989). However, in a study of new-
borns with a pH < 7.0 from Parkland
Hospital, there were inordinate pro-
portions of neonatal deaths—8 per-
HCO3– PCO2
mEq/L mm Hg cent, intensive-care admission—39
Base excess percent, intubations—14 percent,
25 25
mEq/L and seizures—13 percent (Goldaber,
0
1991). And in a study from Oxford
0 of more than 51,000 term infants,
30
20 –5 the incidence of neonatal encepha-
pH lopathy with the pH < 7.0 was 3 per-
7.4 cent (Yeh, 2012).
35
Another important prognostic con-
–10 7.3 sideration is the direction of pH
15 40 change from birth to the immediate
7.2 neonatal period. For example, the risk
–15 of seizures during the first 24 hours of
7.1 life was reduced fivefold if an umbili-
50 cal artery cord pH below 7.2 nor-
7.0 malized within 2 hours after delivery
–20 (Casey, 2001a).
10 25 6.9 60
20 Respiratory Acidemia
g/100 mL

9
6.8 Acute interruption in placental gas
–25 15 70 exchange is accompanied by subse-
8
6.7 quent CO2 retention and respiratory
Hemoglobin

10
80 acidemia. The most common ante-
7 cedent factor is transient umbilical
6.6
5
cord compression. Generally, respira-
90
6 tory acidemia is not harmful to the
fetus (Low, 1994).
100
The degree to which pH is affected
110 by Pco2—the respiratory component
of the acidosis—can be calculated.
120 First, the upper normal neonatal
FIGURE 32-5 Nomogram for determining the delta base. (Adapted from Siggaard-Andersen, Pco2 of 49 mm Hg is subtracted
1963). from the cord blood gas Pco2 value.
 630 The Newborn

TABLE 32-2. Umbilical Cord Blood pH and Blood Gas Values in Normal Term Newborns
Ramin, 1989a
Spontaneous Riley, 1993b Kotaska, 2010b Kotaska, 2010e
SECTION 9

Delivery Spontaneous Delivery Spontaneous Delivery Cesarean Delivery

Values n = 1292c n = 3522c n = 303d n = 189d

pH 7.28 (0.07) 7.27 (0.069) 7.26 (7.01–7.39) 7.3 (7.05–7.39)

PCO2 (mm Hg) 49.9 (14.2) 50.3 (11.1) 51 (30.9–85.8) 54 (37.5–79.5)
HCO3− (mEq/L) 23.1 (2.8) 22.0 (3.6) — —
Base excess (mEq/L) −3.6 (2.8) −2.7 (2.8) — —
Venous Blood
pH — 7.34 (0.063) 7.31 (7.06–7.44) 7.34 (7.10–7.42)
PCO2 (mm Hg) — 40.7 (7.9) 41 (24.9–70.9) 44 (29.1–70.2)
HCO3− (mEq/L) — 21.4 (2.5) — —
Base excess (mEq/L) — –2.4 (2) — —
a
Infants of selected women with uncomplicated vaginal deliveries.
b
Infants of unselected women with vaginal deliveries.
c
Data shown as mean (SD).
d
Data shown as range with 2.5 or 97.5 percentile.
e
Cesarean delivery—labor not stated.

Each additional 10 mm Hg Pco2 increment will lower the Metabolic acidemia is associated with a high rate of mul-
pH by 0.08 units (Eisenberg, 1987). Thus, in a mixed respi- tiorgan dysfunction. In rare cases, such hypoxia-induced
ratory–metabolic acidemia, the benign respiratory component metabolic acidemia may be so severe that it causes subse-
can be calculated. As an example, acute cord prolapse during quent neurological impairment—hypoxic-ischemic encephalopathy
labor prompts cesarean delivery of an infant 20 minutes later. (Chap. 33, p. 639). In fact, a fetus without such acidemia
The umbilical artery blood gas pH was 6.95 and the Pco2 was cannot by definition have suffered recent hypoxic-induced
89 mm Hg. To calculate the degree to which the cord compres- injury. That said, severe metabolic acidosis is poorly pre-
sion and subsequent impairment of CO2 exchange affected the dictive of subsequent neurological impairment in the term
pH, the relationship given earlier is applied: 89 mm Hg minus neonate. Although metabolic acidosis was associated with
49 mm Hg = 40 mm Hg excess CO2. To correct pH: (40 ÷ 10) × an increase in immediate neonatal complications in a group
0.08 = 0.32; 6.95 + 0.32 = 7.27. Therefore, the pH before cord of infants with depressed 5-minute Apgar scores, there were
prolapse was approximately 7.27, well within normal limits, no differences in umbilical artery blood gas measurements
and thus the low pH resulted from respiratory acidosis. among infants who subsequently developed cerebral palsy
compared with those with normal neurological outcomes
Metabolic Acidemia (Socol, 1994).
The fetus begins to develop metabolic acidemia when oxy- In very-low-birthweight infants, that is, those < 1000 g,
gen deprivation is of sufficient duration and magnitude to newborn acid-base status may be more closely linked to long-
require anaerobic metabolism for cellular energy needs. Low term neurological outcome (Gaudier, 1994; Low, 1995). In the
and associates (1997) defined fetal acidosis as a base deficit study cited above, Casey and coworkers (2001b) described the
≥ 12 mmol/L and severe fetal acidosis as a base deficit ≥ 16 association between metabolic acidemia, low Apgar scores, and
mmol/L. In the Parkland study of more than 150,000 new- neonatal death in term and preterm infants. Regarding term
borns cited earlier, metabolic acidemia was defined using neonates, as shown in Figure 32-6, relative to newborns with
umbilical cord blood gas cutoffs that were 2 standard devia- a 5-minute Apgar score of at least 7, the risk of neonatal death
tions below the mean (Casey, 2001b). Thus, metabolic acide- was more than 3200-fold greater in term infants with metabolic
mia was an umbilical artery blood pH < 7.00 accompanied acidemia and 5-minute scores of 3 or less.
by a Pco2 of ≤ 76.3 mm Hg, with higher values indicat-
ing a respiratory component; HCO3− concentration ≤ 17.7
mmol/L; and base deficit ≥ 10.3 mEq/L. From the standpoint ■ Recommendations for Cord Blood Gas
of possiblee cerebral palsy causation, the American College of Determinations
Obstetricians and Gynecologists and the American Academy A cost-effectiveness analysis for universal cord blood gas mea-
of Pediatrics (2003), in their widely endorsed monograph, surements has not been conducted. In some centers, such as
defined metabolic acidosis as umbilical arterial pH < 7.0 and ours at Parkland Hospital, cord gas analysis is performed in all
a base deficit ≥ 12 mmol/L. neonates at birth. The American College of Obstetricians and
 The Newborn 631

3500 3204 intramuscularly or intravenously. Testing for both gonococ-

3000
cus and chlamydia should be obtained before treatment.

2500 Chlamydial Infection

CHAPTER 32
Relative risk

2000 Adequate neonatal prophylaxis against chlamydial conjunc-

1407 1460 tivitis is complex. Ideally, prenatal screening and treatment
1500
for Chlamydia trachomatiss obviates conjunctival infection
1000 708 (Hammerschlag, 2011). Of neonates delivered vaginally
500
of mothers with an active chlamydial infection, from 12 to
180 25 percent will develop conjunctivitis for up to 20 weeks
0 (Teoh, 2003). Prophylactic topical eye treatments do not
≤ 7.0 ≤ 6.9 ≤ 6.8 5-min 5-min Apgar
Apgar score score 0–3 reliably reduce the incidence of chlamydial conjunctivitis. In
Umbilical artery pH 0–3 and pH ≤ 7.0 a study from Kenya, 2.5-percent povidone-iodine solution
was reported to be superior to either 1-percent silver nitrate
FIGURE 32-6 Relative risk for neonatal death in term infants with
solution or 0.5-percent erythromycin ointment in preventing
low Apgar score or umbilical artery acidemia—or both. The rela-
tive risk is cited above each bar. (Data from Casey, 2001b.) chlamydial conjunctivitis (Isenberg, 1995). In another study
from Iran, povidone-iodine eye drops were twice as effective
in preventing clinical conjunctivitis as erythromycin drops—9
Gynecologists (2012) recommends that cord blood gas and pH versus 18 percent failure rate, respectively (Ali, 2007). In an
analyses be obtained in the following circumstances: Israeli study, tetracycline ointment was marginally superior to
povidone-iodine (David, 2011). For all of these reasons, con-
• Cesarean delivery for fetal compromise junctivitis in a newborn up to 3 months old should prompt
• Low 5-minute Apgar score consideration for chlamydial infection. Treatment for chla-
• Severe fetal-growth restriction mydial infection is with oral azithromycin for 5 days or eryth-
• Abnormal fetal heart rate tracing romycin for 14 days.
• Maternal thyroid disease
• Intrapartum fever
• Multifetal gestation. ■ Hepatitis B Immunization
Although umbilical cord acid-base blood determinations are Routine immunization of all newborns with thimerosal-free
poorly predictive of either immediate or long-term adverse neu- vaccine against hepatitis B before hospital discharge is stan-
rological outcome, they provide the most objective evidence of dard practice (American Academy of Pediatrics and American
the fetal metabolic status at birth. College of Obstetricians and Gynecologists, 2012). This vac-
cine does not appear to increase the number of febrile epi-
sodes, sepsis evaluations, or adverse neurological sequelae
PREVENTIVE CARE (Lewis, 2001). Some advocate treatment of high-risk or even
all seropositive women with antiviral nucleoside or nucleotide
■ Eye Infection Prophylaxis analogues during pregnancy to minimize transmission to the
fetus (Dusheiko, 2012; Tran, 2012). Certainly, if the mother
Gonococcal Infection is seropositive for hepatitis B surface antigen, then the neonate
Ophthalmia neonatorum is mucopurulent conjunctivitis should also be passively immunized with hepatitis B immune
of newborns. Some form of conjunctivitis affects 1 to 12 globulin as discussed in Chapter 55 (p. 1090).
percent of all neonates, and gonococcal and chlamydial
infections are some of the most common causes (Zuppa, ■ Vitamin K
2011). Blindness was previously common in children who This injection is provided to prevent vitamin K-dependent
developed Neisseria gonorrhoeaee infection. However, in hemorrhagic disease of the newborn, which is discussed in
1884, Credé, a German obstetrician, introduced a 1-percent Chapter 33 (p. 644). A single dose of 0.5- to 1-mg intra-
ophthalmic solution of silver nitrate that largely eliminated muscular vitamin K is given within 1 hour of birth (American
this. Various other antimicrobial agents have also proven Academy of Pediatrics and American College of Obstetricians
to be effective, and gonococcal prophylaxis is now man- and Gynecologists, 2012).
datory for all neonates (American Academy of Pediatrics
and American College of Obstetricians and Gynecologists,
2012). Recommendations for gonococcal eye prophylaxis ■ Newborn Screening
include a single application of either 1-percent silver nitrate State-based public-health newborn screening programs were
solution or 0.5-percent erythromycin or 1-percent tetracy- solidified when, in response to calls for a uniform national
cline ophthalmic ointment soon after delivery. Treatment policy, the Maternal and Child Health Bureau appointed a
of presumptive gonococcal ophthalmia, that is, conjuncti- committee of the American College of Medical Genetics to rec-
vitis in a neonate born to a mother with untreated gonor- ommend a panel of tests (Watson, 2006). Technical advances
rhea, is given with single-dose ceftriaxone, 100 mg/kg, either have made a large number of relatively simply performed mass
 632 The Newborn

TABLE 32-3. Newborn Screening Core Panel—Estimated Number of Children Shown in Parentheses Identified in the
United States in 2006
Acylcarnitine Disordersa
SECTION 9

Organic Acid Amino Acid Hemoglobin

Metabolism Fatty Acid Metabolism Metabolisma Disorders Others
Isovaleric (32) Medium-chain acyl-CoA Phenylketonuria SS disease Congenital hypothyroidism
Glutaric type I (38) dehydrogenase (239) (215) (1128) (2156)
3-Hydroxy-3-methyl Very long-chain acyl-CoA Maple syrup S-β-thalassemia Biotinidase (62)
glutaric (3) dehydrogenase (69) (urine) (26) (163) Congenital adrenal
Multiple carboxylase (3) Long-chain 3-OH acyl-CoA Homocystinuria SC disease (484) hyperplasia (202)
Methylmalonic mutase dehydrogenase (13) (11) Galactosemia (224)
(50) Trifunctional protein (2) Citrullinemia (24) Hearing loss (5073)
3-Methylcrotonyl-CoA Carnitine uptake (85) Arginosuccinic (7) Cystic fibrosis (1248)
carboxylase (100) Tyrosinemia I Critical congenital heart
Methylmalonic acid diseaseb
(cobalamine A, B) (12) Severe combined
Propionic (15) immunodeficiencyb
β-Ketothiolase (7)

a
Determined by tandem mass spectrometry.
b
Added after 2006.
From Centers for Disease Control and Prevention, 2012b; Watson, 2006.

screening tests available for newborn conditions, and many birthweight should be used to identify neonates at risk for
are mandated by various state laws (American College of complications (McIntire, 1999). For example, neonates who
Obstetricians and Gynecologists, 2011b). Since then, two have are either small or large for gestational age are at increased
been added to the original core panel of 29 congenital condi- risk for hypoglycemia and polycythemia, and measurements
tions, and all are shown in Table 32-3. of blood glucose and hematocrit are indicated (American
According to the Centers for Disease Control and Prevention Academy of Pediatrics and American College of Obstetricians
(2012b), the programs have been successful and cost effective. and Gynecologists, 2012).
For example, neonatal screening for hearing loss was shown in
a Dutch study to diagnose problems a mean of 6 months ear- ■ Care of Skin and Umbilical Cord
lier and improve long-term outcomes (Durieux-Smith, 2008). All excess vernix, blood, and meconium should be gently wiped
A successful screening program for medium chain acyl-CoA off at the time of delivery while keeping the infant warm. Any
dehydrogenase deficiency was described in a Danish study remaining vernix is readily absorbed and disappears within 24
(Anderson, 2012). The use of pulse oximetry to screen for hours. The first bath should be postponed until the neonate’s
severe congenital heart disease was reviewed by Thangaratinam temperature has stabilized.
(2012). Aseptic precautions should be observed in the immediate
Most states require that all tests in the core panel be per- care of the cord. The American Academy of Pediatrics and
formed. Supplemental conditions—secondary targets—are s also the American College of Obstetrics and Gynecologists (2012)
listed on the Maternal and Child Health Bureau website. Some have concluded that keeping the cord dry is sufficient care.
states require some of these 24 in addition to their mandated The umbilical cord begins to lose water from Wharton jelly
core panel. Each practitioner should be familiar with their indi- shortly after birth. Within 24 hours, the cord stump loses
vidual state requirements, which are available at http://genes-r- its characteristic bluish-white, moist appearance and soon
us.uthscsa.edu/resources/consumer/statemap.htm and http:// becomes dry and black. Within several days to weeks, the
www.hrsa.gov/advisorycommittee/mchbadvisory/heritabledis- stump sloughs and leaves a small, granulating wound, which
orders/recommendedpanel/index/html. after healing forms the umbilicus. Separation usually takes
place within the first 2 weeks, with a range of 3 to 45 days
(Novack, 1988). The umbilical cord dries more quickly and
ROUTINE NEWBORN CARE separates more readily when exposed to air. Thus, a dressing
is not recommended.
■ Gestational Age Estimation In resource-poor countries, prophylaxis is reasonable. Triple-
Newborn gestational age can be estimated very soon after dye applied to the cord was reported superior to soap and
delivery. The relationship between gestational age and water care in preventing colonization and exudate formation
 The Newborn 633

(Janssen, 2003). In a Nepalese study, cleansing the cord stump suggests a congenital defect, such as imperforate anus or a ure-
with 4-percent chlorhexidine reduced severe omphalitis by thral valve. After the third or fourth day, as a result of milk
75 percent compared with soap and water cleansing (Mullany, ingestion, meconium is replaced by light-yellow homogenous

CHAPTER 32
2006). Likewise, 0.1-percent chlorhexidine powder was supe- feces with a consistency similar to peanut butter.
rior to dry cord care (Kapellen, 2009).
Despite precautions, a serious umbilical infection—ompha-
litis—is sometimes encountered. In a German study of more ■ Icterus Neonatorum
than 750 newborns with aseptic cord care, 1.3 percent devel- Between the second and fifth day of life approximately one
oped omphalitis (Kapellen, 2009). The most likely offending third of all neonates develop so-called physiological jaundice
organisms are Staphylococcus aureus, Escherichia coli, and group of the newborn. It has special significance considering most
B streptococcus. Typical signs of cellulitis and stump discharge hospitals have policies for early discharge. Correspondingly, it
usually aid diagnosis. However, mild erythema and some bleed- has been the subject of several recent reviews and is discussed
ing at the stump site with cord detachment is common, and further in Chapter 33 (p. 644) (Dijk, 2012; Gazzin, 2011;
some cases may present no outward signs. Thus, the diagnosis Hansen, 2011; Lauer, 2011).
can be elusive.
■ Newborn Male Circumcision
■ Feeding and Weight Loss
Neonatal circumcision has been a controversial topic in the
According to the American College of Obstetricians and United States for at least 25 years. For centuries, newborn
Gynecologists (2013a), exclusive breast feeding is preferred male circumcision has been performed as a religious ritual.
until 6 months. In many hospitals, infants begin breast feeding Even so, scientific evidence supports several medical ben-
in the delivery room. Most term newborns thrive best when efits that include prevention of phimosis, paraphimosis, and
fed 8 to 12 times daily for approximately 15 minutes per epi- balanoposthitis. Circumcision also decreases the incidence of
sode. Preterm or growth-restricted newborns require feedings penile cancer and of cervical cancer among their sexual part-
at shorter intervals. ners. In 1999, the American Academy of Pediatrics concluded
One goal of Healthy People 20200 of the United States that existing evidence was insufficient to recommend routine
Department of Health and Human Services (2010) is to neonatal circumcision. It seems that this policy has had only a
increase the proportion of mothers who breast feed their negligible effect on practices in this country. Specifically, the
infants. Substantial progress toward this goal has been made. In Centers for Disease Control and Prevention (2011) estimated
2009, 77 percent of infants were initially breast fed, and 47 per- that the newborn male circumcision rate decreased during a
cent were still breast fed at 6 months and 26 percent at 1 year 12-year period from approximately 60 percent in 2009 to only
(Centers for Disease Control and Prevention, 2012a). Breast 55 percent in 2010.
feeding is discussed further in Chapter 36 (p. 673). Because Subsequent studies have again endorsed health benefits of
most neonates actually receive little nutriment for the first 3 circumcision. In two large randomized trials from regions of
or 4 days of life, they progressively lose weight until the flow Africa with a high prevalence of human immunodeficiency
of maternal milk has been established or other feeding is insti- virus (HIV), adult male circumcision was found to lower the
tuted. Preterm infants lose relatively more weight and regain risk of HIV acquisition by half (Bailey, 2007; Gray, 2007). And
their birthweight more slowly. Conversely, growth-restricted adult male circumcision was reported to decrease incidences
but otherwise healthy infants regain their initial weight more of HIV, HPV, and herpes infections (Tobian, 2009). These
quickly than those born preterm. With proper nourishment, and other studies were considered by the American Academy
birthweight of term infants usually is regained by the end of of Pediatrics Task Force on Circumcision (2012). In its pol-
the 10th day. icy statement, the Task Force concluded that health benefits
of newborn male circumcision outweigh the risks, and thus,
■ Stools and Urine access to the procedure is justified for families who choose it.
For the first 2 or 3 days after birth, the colon contains soft, Benefits cited include prevention of urinary infections, penile
brownish-green meconium. This consists of desquamated epi- cancer, and transmission of some sexually transmitted infec-
thelial cells from the intestinal tract, mucus, epidermal cells, tions, including HIV infection. The Task Force stopped short
and lanugo (fetal hair) that have been swallowed along with of recommending circumcision for alll newborns. The American
amnionic fluid. The characteristic color results from bile pig- College of Obstetricians and Gynecologists (2011a) endorses
ments. During fetal life and for a few hours after birth, the these views.
intestinal contents are sterile, but bacteria quickly colonize
the bowel. Anesthesia for Circumcision
Meconium stooling is seen in 90 percent of newborns The American Academy of Pediatrics Task Force (2012) rec-
within the first 24 hours, and most of the rest within 36 hours. ommends that if circumcision is performed, procedural anal-
Usually, newborns first void shortly after birth, but may not gesia should be provided. Various pain relief techniques have
until the second day. Meconium and urine passage indicates been described, including lidocaine-prilocaine topical cream,
patency of the gastrointestinal and urinary tracts, respectively. local analgesia infiltration, dorsal penile nerve block, or ring
Failure of the newborn to stool or urinate after these times block. Several studies attest to the efficacy of the dorsal penile
 634 The Newborn

nerve block (Arnett, 1990; Stang, 1988). Studies show that the that it is normal, (3) the inner preputial epithelium must be
dorsal penile nerve block or the ring block techniques are both freed from the glans epithelium, and (4) the circumcision
superior to topical analgesia (Hardwick-Smith, 1998; Lander, device must be left in place long enough to produce hemo-
1997; Taddio, 1997). The use of a pacifier dipped in sucrose is stasis before amputating the prepuce (Lerman, 2001). For a
SECTION 9

a useful adjunct to these methods (Kaufman, 2002). detailed description of surgical techniques, see the second edi-
After appropriate penile cleansing, the ring block technique tion of Operative Obstetricss (Mastrobattista, 2002).
consists of placing a wheal of 1-percent lidocaine at the base of
the penis and advancing the needle in a 180-degree arc around Circumcision Complications
the base of the penis first to one side and then the other to As with any surgical procedure, there is a risk of bleeding, infec-
achieve a circumferential ring of analgesia. The maximum dose tion, and hematoma formation. These risks, however, are low
of lidocaine is 1.0 mL. No vasoactive compounds such as epineph- (Christakis, 2000). Unusual complications reported as isolated
rine should ever be added to the local analgesic agent. cases include distal glans amputation, acquisition of human
immunodeficiency virus-1 (HIV-1) infection or other sexually
Surgical Technique transmitted diseases, meatal stenosis, penile denudation, penile
Newborn circumcision should be performed only on a destruction with electrosurgical coagulation, subsequent epider-
healthy neonate. Other contraindications include any geni- mal inclusion cyst and urethrocutaneous fistula, and ischemia
tal abnormalities such as hypospadias and a family history of following the inappropriate use of lidocaine with epinephrine
a bleeding disorder unless excluded in the infant. The most (Amukele, 2003; Berens, 1990; Gearhart, 1989; Neulander,
commonly used instruments are shown in Figure 32-7 and 1996; Nicoll, 1997; Pippi-Salle, 2013; Upadhyay, 1998).
include Gomco and Mogen clamps and the Plastibell device.
Compared with the Gomco procedure, Kaufman and col- ■ Rooming-In
leagues (2002) reported that the Mogen technique required
This model of maternity care place newborns in their moth-
less time to perform and was associated with less apparent
ers’ rooms instead of central nurseries. Termed rooming-in,
discomfort for the newborn. Regardless of the method used,
this approach first appeared in United States hospitals in the
the goal is to remove enough shaft skin and inner preputial
early 1940s (Temkin, 2002). In part, rooming-in stems from
epithelium so that the glans is exposed sufficiently to prevent
a trend to make all phases of childbearing as natural as pos-
phimosis. In all techniques: (1) the amount of external skin
sible and to foster early mother-child relationships. By 24
to be removed must be accurately estimated, (2) the prepu-
hours, the mother is generally fully ambulatory. Thereafter,
tial orifice must be dilated to visualize the glans and ensure
with rooming-in, she can usually provide routine care for
herself and her newborn. An obvious advantage is her
increased ability to assume full care of the infant when she
arrives home.

■ Hospital Discharge
Traditionally, the newborn is discharged with its mother,
and in most cases, maternal stay has determined that of the
neonate. Safe discharge for late preterm infants has special
concerns (Whyte, 2012). From 1970 to the mid-1990s, aver-
age maternal postpartum length of stay declined steadily, and
A many mothers were discharged in under 48 hours. Although
it is clear that most newborns can be safely discharged within
48 hours, this is not uniformly true. For example, using data
from the Canadian Institute for Health Information, Liu and
colleagues (2000) examined readmission rates in more than
2.1 million neonatal discharges. As the length of hospital stay
decreased from 4.2 days in 1990 to 2.7 days in 1997, the
readmission rate increased from 27 to 38 per 1000 births.
Dehydration and jaundice accounted for most of these read-
B
missions, and brain damage from icterus neonatorum is
discussed in Chapter 33 (p. 644). Using Washington state
neonatal discharge data, Malkin and coworkers (2000) found
that the 28-day mortality rate was increased fourfold and
the 1-year mortality rate increased twofold in newborns dis-
C charged within 30 hours of birth.
FIGURE 32-7 Three different tools used for circumcision. A. Mogen Because of the increased scrutiny regarding short hospital
clamp. The arms of the clamp open to a 3-mm maximum width. stays, federal legislation—The Newborns’ and Mothers’ Health
B. Gomco clamp, assembled. C. Plastibell device. Protection Act of 1996—was
6 enacted to prohibit insurers from
 The Newborn 635

restricting hospital stays for mothers and newborns to less Catlin EA, Carpenter MW, Brann BS, et al: The Apgar score revisited: influ-
ence of gestational age. J Pediatr 109:865, 1986
than 2 days for vaginal delivery or 4 days for cesarean delivery. Centers for Disease Control and Prevention: Breastfeeding report card—
As a result, the average length of hospital stay for childbirth United States, 2012. Available at: http://www.cdc.gov/breastfeeding/data/

CHAPTER 32
increased from 2.1 days in 1995 to 2.5 days in 2000. This reportcard2.htm. Accessed October 10, 2012a
Centers for Disease Control and Prevention: CDC grand rounds: newborn
increase reflected the reduced number of very short hospital screening and improved outcomes. MMWR 61(21)390, 2012b
stays following childbirth (Hall, 2002). Although Mosen and Centers for Disease Control and Prevention: Trends in in-hospital newborn male
associates (2002) found that implementation of the new legisla- circumcision—United States, 1999—2010. MMWR 60(34):1167, 2011
Chauhan SP, Cowan BD, Meydrech EF, et al: Determination of fetal acidemia
tion was associated with a 6-percent increase in cost, readmis- at birth from a remote umbilical arterial blood gas analysis. Am J Obstet
sion rates within 7 days of discharge decreased by nearly half. Gynecol 170:1705, 1994
In an analysis of more than 662,000 births in California, Datar Chernick V: Fetal breathing movements and the onset of breathing at birth.
Clin Perinatol 5:257, 1978
and Sood (2006) found decreased rates of readmission of 9, Christakis DA, Harvey E, Zerr DM, et al: A trade-off analysis of routine new-
12, and 20 percent, respectively, at 1, 2, and 3 years after the born circumcision. Pediatrics 105:246, 2000
legislation was implemented. Credé CSF: Die Verhütung der Augenenzündung der Neugeborenen. Berlin,
Hirschwald, 1884
Datar A, Sood N: Impact of postpartum hospital-stay legislation on newborn
length of stay, readmission, and mortality in California. Pediatrics 118:63, 2006
REFERENCES David M, Rumelt S, Weintraub Z: Efficacy comparison between povidone
iodine 2.5% and tetracycline 1% in prevention of ophthalmia neonatorum.
Ali A, Khadije D, Elahe A, et al: Prophylaxis of ophthalmia neonatorum Ophthalmology 118(7):1454, 2011
comparison of Betadine, erythromycin and no prophylaxis. J Trop Pediatr Dawes GS: Breathing before birth in animals or man. N Engl J Med 290:557,
53(6):388, 2007 1974
American Academy of Pediatrics and the American College of Obstetricians Dickinson JE, Eriksen NL, Meyer BA, et al: The effect of preterm birth on
and Gynecologists: Care of the newborn. In: Guidelines for Perinatal Care, umbilical cord blood gases. Obstet Gynecol 79:575, 1992
7th ed. Washington, 2012, p 265 Dijk PH, Hulzebos CV: An evidence-based view on hyperbilirubinemia. Acta
American Academy of Pediatrics, Task Force on Circumcision: Circumcision Paediatr Suppl 101(464):3, 2012
Policy Statement. Pediatrics 103:686, 1999 Duerbeck NB, Chaffin DG, Seeds JW: A practical approach to umbilical artery
American Academy of Pediatrics, Task Force on Circumcision: Circumcision pH and blood gas determinations. Obstet Gynecol 79:959, 1992
Policy Statement. Pediatrics 130(3):585, 2012 Durieux-Smith A, Fitzpatrick E, Whittingham J: Universal newborn hearing
American College of Obstetricians and Gynecologists: Breastfeeding: maternal screening: a question of evidence. Int J Audiol 47(1):12, 2008
and infant aspects. Committee Opinion No. 361, Reaffirmed 2013a Dusheiko G: Interruption of mother-to-infant transmission of hepatitis B: time
American College of Obstetricians and Gynecologists: Circumcision. to include selective antiviral prophylaxis? Lancet 379(9830):2019, 2012
Committee Opinion No. 260, October 2001, Reaffirmed 2011a Eisenberg MS, Cummins RO, Ho MT: Code Blue: Cardiac Arrest and
American College of Obstetricians and Gynecologists: Newborn screening. Resuscitation. Philadelphia, Saunders, 1987, p 146
Committee Opinion No. 481, March 2011b Freeman JM, Nelson KB: Intrapartum asphyxia and cerebral palsy. Pediatrics
American College of Obstetricians and Gynecologists: Planned home birth. 82:240, 1988
Committee Opinion No. 476, February 2011, Reaffirmed 2013b Gaudier FL, Goldenberg RL, Nelson KG, et al: Acid–base status at birth and
American College of Obstetricians and Gynecologists: Umbilical cord blood subsequent neurosensory impairment in surviving 500 to 1000 gm infants.
gas and acid–base analysis. Committee Opinion No. 348, November 2006, Am J Obstet Gynecol 170:48, 1994
Reaffirmed 2012 Gazzin S, Tiribelli C: Bilirubin-induced neurological damage. J Matern Fetal
American College of Obstetricians and Gynecologists and the American Neonatal Med 24(Suppl 1):154, 2011
Academy of Pediatrics: Neonatal encephalopathy and cerebral palsy: defin- Gearhart JP, Rock JA: Total ablation of the penis after circumcision with
ing the pathogenesis and pathophysiology. January 2003 electrocautery: a method of management and long-term follow-up. J Urol
American College of Obstetricians and Gynecologists and the American 142:799, 1989
Academy of Pediatrics: The Apgar score. Committee Opinion No. 333, May Gilstrap LC III, Leveno KJ, Burris J, et al: Diagnosis of birth asphyxia on the
2006, Reaffirmed 2010 basis of fetal pH, Apgar score, and newborn cerebral dysfunction. Am J
Amukele SA, Lee GW, Stock JA, et al: 20-year experience with iatrogenic Obstet Gynecol 161:825, 1989
penile injury. J Urol 170:1691, 2003 Goldaber KG, Gilstrap LC III, Leveno KJ, et al: Pathologic fetal acidemia.
Anderson S, Botti C, Li B, et al: Medium chain acyl-CoA dehydrogenase Obstet Gynecol 78:1103, 1991
deficiency detected among Hispanics by New Jersey newborn screening. Gray RH, Kigozi G, Serwadda D, et al: Male circumcision for HIV prevention
Am J Med Genet A 158A(9):2100, 2012 in Rakai, Uganda: a randomized trial. Lancet 369:657, 2007
Apgar V: A proposal for a new method of evaluation of the newborn infant. Guglani L, Lakshminrusimha S, Ryan RM: Transient tachypnea of the new-
Curr Res Anesth Analg 32:260, 1953 born. Pediatr Rev 29(11):e59, 2008
Apgar V, Holaday DA, James LS, et al: Evaluation of the newborn infant— Haddad B, Mercer BM, Livingston JC, et al: Outcome after successful resusci-
second report. JAMA 168:1985, 1958 tation of babies born with Apgar scores of 0 at both 1 and 5 minutes. Am J
Armstrong L, Stenson BJ: Use of umbilical cord blood gas analysis in the assess- Obstet Gynecol 182:1210, 2000
ment of the newborn. Arch Dis Child Fetal Neonatal Ed 92:430, 2007 Hall MJ, Owings MF: 2000 National hospital discharge survey. Adv Data
Arnett RM, Jones JS, Horger EO III: Effectiveness of 1% lidocaine dorsal penile 329:1, 2002
nerve block in infant circumcision. Am J Obstet Gynecol 163:1074, 1990 Hammerschlag MR: Chylamydial and gonococcal infections in infants and
Bailey RC, Moses S, Parker CB, et al: Male circumcision for HIV preven- children. Clin Infect Dis 53(3):S99, 2011
tion in young men in Kismu, Kenya: a randomized controlled trial. Lancet Hansen TW: Prevention of neurodevelopmental sequelae of jaundice in the
369:643, 2007 newborn. Dev Med Child Neurol 53(Suppl 4): 24, 2011
Berens R, Pontus SP Jr: A complication associated with dorsal penile nerve Hardwick-Smith S, Mastrobattista JM, Wallace PA, et al: Ring block for neo-
block. Reg Anesth 15:309, 1990 natal circumcision. Obstet Gynecol 91:930, 1998
Biban P, Filipovic-Grcic B, Biarent D, et al: New cardiopulmonary resusci- Isenberg SJ, Apt L, Wood M: A controlled trial of povidone-iodine as prophy-
tation guidelines 2010: managing the newly born in delivery room. Early laxis against ophthalmia neonatorum. N Engl J Med 332:562, 1995
Hum Dev 87 Suppl 1:S9, 2011 Janssen PA, Selwood BL, Dobson SR, et al: To dye or not to dye: a randomized
Boylan PC, Parisi VM: Fetal acid–base balance. In Creasy RK, Resnik R (eds): clinical trial of a triple dye/alcohol regime versus dry cord care. Pediatrics
Maternal–Fetal Medicine, 3rd ed. Philadelphia, Saunders, 1994 111:15, 2003
Casey BM, Goldaber KG, McIntire DD, et al: Outcomes among term infants Kapellen TM, Gebauer CM, Brosteanu O, et al: Higher rate of cord-related
when two-hour postnatal pH is compared with pH at delivery. Am J Obstet adverse events in neonates with dry umbilical cord care compared to
Gynecol 184:447, 2001a chlorhexidine powder. Results of a randomized controlled study to compare
Casey BM, McIntire DD, Leveno KJ: The continuing value of the Apgar score efficacy and safely of chlorhexidine powder versus dry care in umbilical cord
for the assessment of newborn infants. N Engl J Med 344:467, 2001b care of the newborn. Neonatology 96(1):13, 2009
668

CHAPTER 36

The Puerperium

INVOLUTION OF THE REPRODUCTIVE TRACT . . . . . . . . . 668 INVOLUTION OF THE REPRODUCTIVE TRACT

PLACENTAL SITE INVOLUTION . . . . . . . . . . . . . . . . . . . . 670
■ Birth Canal
URINARY TRACT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 671
vagina and its outlet gradually diminish in size but rarely regain
PERITONEUM AND ABDOMINAL WALL . . . . . . . . . . . . . 671
their nulliparous dimensions. Rugae begin to reappear by the
HEMATOLOGICAL PARAMETERS AND PREGNANCY third week but are less prominent than before. The hymen is
HYPERVOLEMIA . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 671 represented by several small tags of tissue, which scar to form
the myrtiform caruncles. Vaginal epithelium begins to prolifer-
BREASTS AND LACTATION . . . . . . . . . . . . . . . . . . . . . . 672 ate by 4 to 6 weeks, usually coincidental with resumed ovarian
MATERNAL CARE DURING THE PUERPERIUM . . . . . . . . 675 estrogen production. Lacerations or stretching of the perineum
during delivery may result in vaginal outlet relaxation. Some
HOME CARE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 678 damage to the pelvic floor may be inevitable, and parturition
predisposes to urinary incontinence and pelvic organ prolapse.
This is discussed in detail in Chapter 27 (p. 536).

■ Uterus
The massively increased uterine blood flow necessary to main-
The word puerperium is derived from Latin—puer,— child + tain pregnancy is made possible by significant hypertrophy and
parus, bringing forth. Currently, it defines the time following remodeling of pelvic vessels. After delivery, their caliber gradu-
delivery during which pregnancy-induced maternal anatomi- ally diminishes to approximately that of of the prepregnant
cal and physiological changes return to the nonpregnant state. state. Within the puerperal uterus, larger blood vessels become
Its duration is understandably inexact, but is considered to be obliterated by hyaline changes, are gradually resorbed, and are
between 4 and 6 weeks. Although much less complex compared replaced by smaller ones. Minor vestiges of the larger vessels,
with pregnancy, the puerperium has appreciable changes, some however, may persist for years.
of which may be either bothersome or worrisome for the new During labor, the margin of the dilated cervix, which cor-
mother. Importantly, several complications can develop, and responds to the external os, may be lacerated. The cervical
some are serious. opening contracts slowly and for a few days immediately after
The puerperium may be a time of intense anxiety for many labor, readily admits two fingers. By the end of the first week,
women. Some mothers have feelings of abandonment following this opening narrows, the cervix thickens, and the endocervical
delivery because of a newly aimed focus on the infant. Kanotra canal reforms. The external os does not completely resume its
and colleagues (2007) analyzed challenges that women faced pregravid appearance. It remains somewhat wider, and typi-
from 2 to 9 months following delivery. A third of these new cally, ectocervical depressions at the site of lacerations become
mothers felt the need for social support, and 25 percent had permanent. These changes are characteristic of a parous cervix
concerns with breast feeding (Table 36-1). (Fig. 36-1). The markedly attenuated lower uterine segment
 The Puerperium 669

TABLE 36-1. Pregnancy Risk Assessment Surveillance

System—PRAMS.a Concerns Raised
by Women in the First 2–9 Months

CHAPTER 36
Postpartum
Concerns Percent
Need for social support 32
Breast-feeding issues 24 A B
Inadequate education about newborn care 21
FIGURE 36-1 Common appearance of nulliparous (A) and parous
Help with postpartum depression 10
(B) cervices.
Perceived need for extended hospital stay 8
Need for maternal insurance coverage 6
postpartum ischemic compared with the reddish-purple hyperemic preg-
a nant organ.
Centers for Disease Control and Prevention, 2012b.
Myometrial involution is a truly remarkable tour de forcee of
Data from Kanotra, 2007.
destruction or deconstruction that begins as soon as 2 days after
delivery as shown in Figure 36-2. As emphasized by Hytten
(1995), studies that describe the degree of decreasing uterine
contracts and retracts, but not as forcefully as the uterine cor- weight postpartum are poor quality. Best estimates are that by
pus. During the next few weeks, the lower segment is converted 1 week, the uterus weighs approximately 500 g; by 2 weeks,
from a clearly distinct substructure large enough to accom- about 300 g; and at 4 weeks, involution is complete and the
modate the fetal head to a barely discernible uterine isthmus uterus weighs approximately 100 g. After each successive deliv-
located between the corpus and internal os. ery, the uterus is usually slightly larger than before the most
Cervical epithelium also undergoes considerable remodeling, recent pregnancy. The total number of myocytes does not
and this actually may be salutary. Ahdoot and associates (1998) decrease appreciably—rather, their size decreases markedly.
found that approximately half of women showed regression of
high-grade dysplasia following vaginal delivery. Kaneshiro and Sonographic Findings
coworkers (2005) found similar regression—about 60 percent Uterine size dissipates rapidly in the first week (Fig. 36-3).
overall—regardless of delivery mode. And the uterus and endometrium return to pregravid size by
Postpartum, the fundus of the contracted uterus lies slightly 8 weeks after delivery (Belachew, 2012; Steinkeler, 2012). In
below the umbilicus. It consists mostly of myometrium covered a study of 42 normal women postpartum, Tekay and Jouppila
by serosa and internally lined by basal decidua. The anterior (1993) identified fluid in the endometrial cavity in 78 percent
and posterior walls, which lie in close apposition, are each 4 to at 2 weeks, 52 percent at 3 weeks, 30 percent at 4 weeks, and
5 cm thick (Buhimschi, 2003). At this time, the uterus weighs 10 percent at 5 weeks. Demonstrable uterine cavity contents are
approximately 1000 g. Because blood vessels are compressed seen for up to 2 months following delivery. Belachew and col-
by the contracted myometrium, the uterus on section appears leagues (2012) used 3-dimensional sonography and visualized

17 days p.p.

At delivery

8 days p.p.

24 days p.p.

8 hrs p.p. 14 days p.p. 3 months p.p.

FIGURE 36-2 Cross sections of uteri made at the level of the involuting placental site at varying times after delivery. p.p. = postpartum.
(Redrawn from Williams, 1931.)
 670 The Puerperium

20 Lochia. Early in the puerperium, sloughing of decidual tissue

18 Uterine length results in a vaginal discharge of variable quantity. The discharge
16
15 15 is termed lochiaa and contains erythrocytes, shredded decidua,
15 14 13.5 epithelial cells, and bacteria. For the first few days after delivery,
SECTION 10

13
Centimeters

12 there is blood sufficient to color it red—lochia rubra. After 3

12.8 12.4
10 10 12 or 4 days, lochia becomes progressively pale in color—lochia
10 9 Cavity length
8 7.6 7.3 serosa. After approximately the 10th day, because of an admix-
7.0 6.7 8
6 ture of leukocytes and reduced fluid content, lochia assumes a
AP diameter 6.4
5 white or yellow-white color—lochia alba. The average duration
of lochial discharge ranges from 24 to 36 days (Fletcher, 2012).

1 2 3 4 5 6 7 8 9 ■ Placental Site Involution

Days postpartum Complete extrusion of the placental site takes up to 6 weeks
FIGURE 36-3 Sonographic measurements of uterine involu- (Williams, 1931). Immediately after delivery, the placental
tion during the first 9 days postpartum. AP = anteroposterior. site is approximately palm-sized. Within hours of delivery, it
(Data from Hytten, 1995.) normally consists of many thrombosed vessels that ultimately
undergo organization (see Fig. 36-2). By the end of the second
intracavitary tissue matter in a third on day 1, 95 percent on week, it is 3 to 4 cm in diameter.
day 7, 87 percent on day 14, and 28 percent on day 28. By Placental site involution is an exfoliation process, which is
day 56, the small cavity was empty. Sohn and associates (1988) prompted in great part by undermining of the implantation
described Doppler ultrasound results showing continuously site by new endometrial proliferation (Williams, 1931). Thus,
increasing uterine artery vascular resistance during the first involution is not simply absorption in situ. Exfoliation consists
5 days postpartum. of both extension and “downgrowth” of endometrium from
the margins of the placental site, as well as development of
Decidua and Endometrial Regeneration endometrial tissue from the glands and stroma left deep in the
Because separation of the placenta and membranes involves the decidua basalis after placental separation. Anderson and Davis
spongy layer, the decidua basalis is not sloughed. The remain- (1968) concluded that placental site exfoliation results from
ing decidua has striking variations in thickness, it has an irregu- sloughing of infarcted and necrotic superficial tissues followed
lar jagged appearance, and it is infiltrated with blood, especially by a remodeling process.
at the placental site (see Fig. 36-2).
Within 2 or 3 days after delivery, the remaining decidua Subinvolution
becomes differentiated into two layers. The superficial layer In some cases, uterine involution is hindered because of infec-
becomes necrotic and is sloughed in the lochia. The basal layer tion, retained placental fragments, or other causes. Such sub-
adjacent to the myometrium remains intact and is the source of involution is accompanied by varied intervals of prolonged
new endometrium. This arises from proliferation of the endo- lochia as well as irregular or excessive uterine bleeding. On
metrial glandular remnants and the stroma of the interglandu- bimanual examination, the uterus is larger and softer than
lar connective tissue. would be expected. Ergonovine (Ergotrate) or methylergono-
Endometrial regeneration is rapid, except at the placental vine (Methergine), 0.2 mg orally every 3 to 4 hours for 24 to
site. Within a week or so, the free surface becomes covered by 48 hours, is recommended by many, but its efficacy is question-
epithelium, and Sharman (1953) identified fully restored endo- able. Of these, only methylergonovine is currently available in
metrium in all biopsy specimens obtained from the 16th day the United States. If there is infection, antimicrobial therapy
onward. Histological endometritis is part of the normal repara- usually leads to a good response. In an earlier study, Wager
tive process. Moreover, microscopic inflammatory changes and coworkers (1980) reported that a third of these late cases
characteristic of acute salpingitis are seen in almost half of of postpartum metritis are caused by Chlamydia trachomatis.
women between 5 and 15 days, but these findings do not reflect Empirical therapy with azithromycin or doxycycline usually
infection (Andrews, 1951). prompts resolution regardless of bacterial etiology.
Another cause of subinvolution is incompletely remodeled
Clinical Aspects uteroplacental arteries (Andrew, 1989; Kavalar, 2012). These
Afterpains. In primiparous women, the uterus tends to remain noninvoluted vessels are filled with thromboses and lack an
tonically contracted following delivery. In multiparas, however, endothelial lining. Perivascular trophoblasts are also identified
it often contracts vigorously at intervals and gives rise to after-
r in the vessel walls, suggesting an aberrant interaction between
pains, which are similar to but milder than labor contractions. uterine cells and trophoblasts.
These are more pronounced as parity increases and worsen when
the infant suckles, likely because of oxytocin release (Holdcroft, Late Postpartum Hemorrhage
2003). Usually, afterpains decrease in intensity and become mild The American College of Obstetricians and Gynecologists
by the third day. We have encountered unusually severe and per- (2013b) defines secondary postpartum hemorrhagee as bleeding
sistent afterpains in women with postpartum uterine infections. 24 hours to 12 weeks after delivery. Clinically worrisome uterine
 The Puerperium 671

hemorrhage develops within 1 to 2 weeks in perhaps 1 percent of exercise. These may be started anytime following vaginal deliv-
women. Such bleeding most often is the result of abnormal invo- ery and as soon as abdominal soreness diminishes after cesarean
lution of the placental site. It occasionally is caused by retention delivery. Silvery abdominal striae commonly develop as striae

CHAPTER 36
of a placental fragment or by a uterine artery pseudoaneurysm. gravidarum (Chap. 4, p. 51). Except for these, the abdominal
Usually, retained products undergo necrosis with fibrin deposi- wall usually resumes its prepregnancy appearance. When mus-
tion and may eventually form a so-called placental polyp. As the cles remain atonic, however, the abdominal wall also remains
eschar of the polyp detaches from the myometrium, hemorrhage lax. Marked separation of the rectus abdominis muscles—dias-
may be brisk. As discussed in Chapter 56 (p. 1118), delayed tasis recti—may
— result.
postpartum hemorrhage may also be caused by von Willebrand
disease or other inherited coagulopathies (Lipe, 2011).
In our experiences, few women with delayed hemorrhage are HEMATOLOGICAL PARAMETERS AND
found to have retained placental fragments. Thus, we and others PREGNANCY HYPERVOLEMIA
do not routinely perform curettage (Lee, 1981). Another con-
cern is that curettage may worsen bleeding by avulsing part of ■ Hematological and Coagulation Changes
the implantation site. Thus, in a stable patient, if sonographic Marked leukocytosis and thrombocytosis may occur dur-
examination shows an empty cavity, then oxytocin, methylergo- ing and after labor. The white blood cell count sometimes
novine, or a prostaglandin analogue is given. Antimicrobials are reaches 30,000/μL, with the increase predominantly due to
added if uterine infection is suspected. If large clots are seen in granulocytes. There is a relative lymphopenia and an absolute
the uterine cavity with sonography, then gentlee suction curettage eosinopenia. Normally, during the first few postpartum days,
is considered. Otherwise curettage is carried out only if appre- hemoglobin concentration and hematocrit fluctuate mod-
ciable bleeding persists or recurs after medical management. erately. If they fall much below the levels present just before
labor, a considerable amount of blood has been lost (Chap.
41, p. 781).
URINARY TRACT By the end of pregnancy, there are many changes in labo-
ratory findings that assess coagulation (Kenny, 2014). These
Normal pregnancy-induced glomerular hyperfiltration persists
are discussed in Chapter 4 (p. 57) and listed in the Appendix
on the first postpartum day but returns to prepregnancy base-
(p. 1288). Many persist in the puerperium. One example is
line by 2 weeks (Hladunewich, 2004). Also, dilated ureters and
that the markedly increased levels of plasma fibrinogen are
renal pelves return to their prepregnant state during the course
maintained at least through the first week, and hence, so is the
of 2 to 8 weeks postpartum. Because of this dilated collect-
increase in sedimentation rate.
ing system, coupled with residual urine and bacteriuria in a
traumatized bladder, urinary tract infection is a concern in the
puerperium. ■ Pregnancy-Induced Hypervolemia
Bladder trauma is associated most closely with labor length
When the amount of blood attained by normal pregnancy hyper-
and thus to some degree is a normal accompaniment of vagi-
volemia is lost as postpartum hemorrhage, the woman almost
nal delivery. Funnell and colleagues (1954) used cystoscopy
immediately regains her nonpregnant blood volume (Chap. 41,
immediately postpartum and described varying degrees of sub-
p. 781). If less has been lost at delivery, it appears that in most
mucosal hemorrhage and edema. Postpartum, the bladder has
women, blood volume has nearly returned to its nonpregnant
an increased capacity and a relative insensitivity to intravesi-
level by 1 week after delivery. Cardiac output usually remains
cal pressure. Thus, overdistention, incomplete emptying, and
elevated for 24 to 48 hours postpartum and declines to non-
excessive residual urine are common. Their management is dis-
pregnant values by 10 days (Robson, 1987). Heart rate changes
cussed on page 676.
follow this pattern. Systemic vascular resistance and blood pres-
It is unusual for urinary incontinence to manifest during
sure rise (Fig. 36-4). Systemic vascular resistance remains in the
the puerperium. That said, much attention has been given to
lower range characteristic of pregnancy for 2 days postpartum
the potential for subsequent development of urinary inconti-
and then begins to steadily increase to normal nonpregnant val-
nence and other pelvic floor disorders in the years following
ues (Hibbard, 2014).
delivery. A fuller discussion is found in Chapter 30 (p. 588).
Normal pregnancy is associated with an appreciable increase
in extracellular sodium and water, and postpartum diuresis is
PERITONEUM AND ABDOMINAL WALL a physiological reversal of this process. Chesley and coworkers
(1959) demonstrated a decrease in sodium space of approxi-
The broad and round ligaments require considerable time to mately 2 L during the first week postpartum. This also cor-
recover from stretching and loosening during pregnancy. As a responds with loss of residual pregnancy hypervolemia. In
result of ruptured elastic fibers in the skin and prolonged dis- preeclampsia, pathological retention of fluid antepartum and
tention by the pregnant uterus, the abdominal wall remains soft its diuresis postpartum may be prodigious (Chap. 40, p. 768).
and flaccid. If the abdomen is unusually flabby or pendulous, Postpartum diuresis results in relatively rapid weight loss of
an ordinary girdle is often satisfactory. An abdominal binder 2 to 3 kg, which is added to the 5 to 6 kg incurred by delivery
is at best a temporary measure. Several weeks are required for and normal blood loss. Weight loss from pregnancy itself is
these structures to return to normal, and recovery is aided by likely to be maximal by the end of the second week postpartum.
 672 The Puerperium

125 Systolic
120 121 120
114 115 118
SECTION 10

100
90 91
mm Hg

88 89
MAP 86 M
86

75 72 76
71 74 75 73
Diastolic

A
0 1 2 3 4 5
Days postpartum

FIGURE 36-4 During the early puerperium, blood pressure nor-

mally rises toward nonpregnant values. MAP = mean arterial
pressure. D

It follows that any residual increased weight compared with D

prepregnancy values probably represents fat stores that will per- A
sist. According to Schauberger and associates (1992), women
approach their self-reported prepregnancy weight 6 months
after delivery but still retain an average surplus of 1.4 kg (3 lb).

BREASTS AND LACTATION

■ Breast Anatomy and Products

FIGURE 36-5 Schematic of the alveolar and ductal system dur-
25 lobes. They are arranged radially and are separated from one ing lactation. Note the myoepithelial fibers (M) that surround
another by varying amounts of fat. Each lobe consists of several the outside of the uppermost alveolus. The secretions from the
lobules, which in turn are composed of numerous alveoli. Each glandular elements are extruded into the lumen of the alveoli (A)
alveolus is provided with a small duct that joins others to form and ejected by the myoepithelial cells into the ductal system (D),
which empties through the nipple. Arterial blood supply to the
a single larger duct for each lobe as shown in Figure 36-5. These alveolus is identified by the upper right arrow and venous drain-
lactiferous ductss open separately on the nipple, where they may age by the arrow beneath.
be distinguished as minute but distinct orifices. The alveolar
secretory epithelium synthesizes the various milk constituents,
described next. impact on its quantity or quality (Institute of Medicine, 1990).
After delivery, the breasts begin to secrete colostrum, which Milk is isotonic with plasma, and lactose accounts for half of the
is a deep lemon-yellow liquid. It usually can be expressed from osmotic pressure. Essential amino acids are derived from blood,
the nipples by the second postpartum day. Compared with and nonessential amino acids are derived in part from blood
mature milk, colostrum is rich in immunological components or synthesized in the mammary gland. Most milk proteins are
and contains more minerals and amino acids (Ballard, 2013). unique and include α-lactalbumin, β-lactoglobulin, and casein.
It also has more protein, much of which is globulin, but less Fatty acids are synthesized in the alveoli from glucose and are
sugar and fat. Secretion persists for 5 days to 2 weeks, with secreted by an apocrine-like process. Most vitamins are found
gradual conversion to mature milk by 4 to 6 weeks. The colos- in human milk, but in variable amounts. Vitamin K is virtually
trum content of immunoglobulin A (IgA) offers the newborn absent, and thus, an intramuscular dose is given to the newborn
protection against enteric pathogens. Other host resistance (Chap. 33, p. 644). Vitamin D content is low—22 IU/mL.
factors found in colostrum and milk include complement, Thus, newborn supplementation is also recommended by the
macrophages, lymphocytes, lactoferrin, lactoperoxidase, and American Academy of Pediatrics (Wagner, 2008).
lysozymes. Wheyy is milk serum and has been shown to contain large
Mature milk is a complex and dynamic biological fluid that amounts of interleukin-6 (Saito, 1991). Human milk has a
includes fat, proteins, carbohydrates, bioactive factors, minerals, whey-to-casein ratio of 60:40, considered ideal for absorption.
vitamins, hormones, and many cellular products. The concen- Prolactin appears to be actively secreted into breast milk (Yuen,
trations and contents of human milk change even during a single 1988). Epidermal growth factor (EGF) has been identified in
feed and are influenced by maternal diet, as well as infant age, human milk. And because it is not destroyed by gastric pro-
health, and needs. A nursing mother easily produces 600 mL teolytic enzymes, it may be absorbed to promote growth and
of milk daily, and maternal gestational weight gain has little maturation of newborn intestinal mucosa (McCleary, 1991).
 The Puerperium 673

Other critical components in human milk include lactoferrin, milk T lymphocytes are almost exclusively composed of cells
melatonin, oligosaccharides, and essential fatty acids. that exhibit specific membrane antigens. These memory T cells
appear to be an avenue for the neonate to benefit from the

CHAPTER 36
■ Endocrinology of Lactation maternal immunological experience (Bertotto, 1990).
The precise humoral and neural mechanisms involved in lacta-
tion are complex. Progesterone, estrogen, and placental lacto- ■ Nursing
gen, as well as prolactin, cortisol, and insulin, appear to act Human milk is ideal food for neonates. It provides age-
in concert to stimulate the growth and development of the specific nutrients as well as immunological factors and anti-
milk-secreting apparatus (Porter, 1974). With delivery, there is bacterial substances (American College of Obstetricians and
an abrupt and profound decrease in the levels of progesterone Gynecologists, 2013a). Milk also contains factors that act as
and estrogen. This decrease removes the inhibitory influence biological signals for promoting cellular growth and differen-
of progesterone on α-lactalbumin production and stimulates tiation. The American Academy of Pediatrics (2012) has pro-
lactose synthase to increase milk lactose. Progesterone with- vided a list of dose-response benefits of nursing (Table 36-2).
drawal also allows prolactin to act unopposed in its stimula- For both mother and infant, the benefits of breast feeding are
tion of α-lactalbumin production. Serotonin is produced in long-term. For example, women who breast feed have a lower
mammary epithelial cells and has a role in maintaining milk risk of breast and reproductive cancer, and their children have
production. This may explain the decreased milk production in increased adult intelligence independent of a wide range of pos-
women taking selective serotonin-reuptake inhibitors—SSRIs sible confounding factors (Jong, 2012; Kramer, 2008). Breast
(Collier, 2012). feeding is associated with decreased postpartum weight reten-
The intensity and duration of subsequent lactation are con- tion (Baker, 2008). In addition, rates of sudden-infant-death
trolled, in large part, by the repetitive stimulus of nursing and syndrome are significantly lower among breast-fed infants.
emptying of milk from the breast. Prolactin is essential for lac- Last, in the Nurses’ Health Study, women who reported breast
tation, and women with extensive pituitary necrosis—Sheehan feeding for at least 2 cumulative years had a 23-percent lower
syndrome—do
— not lactate (Chap. 58, p. 1163). Although plasma risk of coronary heart disease (Stuebe, 2009). For all these
prolactin levels fall after delivery to levels lower than during preg- reasons, the American Academy of Pediatrics (2012) supports
nancy, each act of suckling triggers a rise in levels (McNeilly, the World Health Organization (2011) recommendations of
1983). Presumably a stimulus from the breast curtails the release exclusive breast feeding for up to 6 months, with avoidance of
of dopamine, also known as prolactin-inhibiting factor, from the exposure to cow milk proteins.
hypothalamus. This in turn transiently induces increased prolac- The Surgeon General of the U.S. Department of Health and
tin secretion. Human Services (2011) lists some barriers for breast feeding
The posterior pituitary secretes oxytocin in pulsatile fashion. and suggests practical means of overcoming them. Educational
This stimulates milk expression from a lactating breast by caus- initiatives that include father and peer counseling may improve
ing contraction of myoepithelial cells in the alveoli and small these rates (Pisacane, 2005; Wolfberg, 2004). The Baby Friendly
milk ducts (see Fig. 36-4). Milk ejection, or letting down, is Hospital Initiativee is an international program to increase rates
a reflex initiated especially by suckling, which stimulates the of exclusive breast feeding and to extend its duration. It is
posterior pituitary to liberate oxytocin. The reflex may even be based on the World Health Organization (1989) Ten Steps
provoked by an infant cry and can be inhibited by maternal to Successful Breastfeedingg (Table 36-3). Worldwide, almost
fright or stress. 20,000 hospitals are designated as “baby-friendly.” Forrester-
Knauss and coworkers (2013) described successful trends
■ Immunological Consequences of toward exclusive breast feeding in Switzerland during 9 years
Breast Feeding
Human milk contains several protective immunological sub-
stances, including secretory IgA and growth factors. The anti- TABLE 36-2. Advantages of Breast Feeding
bodies in human milk are specifically directed against maternal
environmental antigens such as against Escherichia colii (Iyengar, Nutritional
2012). As a result, breast-fed infants are less prone to enteric Immunological
infections than bottle-fed ones (Cravioto, 1991). Human milk Developmental
also provides protection against rotavirus infections, a major Psychological
cause of infant gastroenteritis (Newburg, 1998). Moreover, the Social
risks of atopic dermatitis and respiratory infections are reduced Economical
(Ip, 2009). Bartick and Reinhold (2010) calculated that signifi- Environmental
cant economic burdens from pediatric disease could be lessened Optimal growth and development
by improved breast-feeding rates. Decrease risks for acute and chronic diseases
Much attention has been directed to the role of maternal
Summarized from the American Academy of Pediatrics
breast-milk lymphocytes in neonatal immunological processes.
and the American College of Obstetricians and
Milk contains both T and B lymphocytes, but the T lympho-
Gynecologists, 2012.
cytes appear to differ from those found in blood. Specifically,
 674 The Puerperium

TABLE 36-3. Ten Steps to Successful Breast Feeding ■ Contraindications to Breast Feeding
Nursing is contraindicated in women who take street drugs or
1. Have a written breast-feeding policy that is regularly do not control their alcohol use; have an infant with galacto-
communicated to all health-care staff
SECTION 10

semia; have human immunodeficiency virus (HIV) infection;

2. Train all staff in skills necessary to implement this have active, untreated tuberculosis; take certain medications;
policy or are undergoing breast cancer treatment (American Academy
3. Inform all pregnant women about the benefits and of Pediatrics and American College of Obstetricians and
management of breast feeding Gynecologists, 2012; Faupel-Badger, 2013). Breast feeding has
4. Help mothers initiate breast feeding within an hour been recognized for some time as a mode of HIV transmission
of birth and is proscribed in developed countries in which adequate
5. Show mothers how to breast feed and how to nutrition is otherwise available (Chap. 65, p. 1282). Other viral
sustain lactation, even if they should be separated infections do not contraindicate breast feeding. For example,
from their infants with maternal cytomegalovirus infection, both virus and anti-
6. Feed newborn infants nothing but breast milk, bodies are present in breast milk. And although hepatitis B
unless medically indicated, and under no virus is excreted in milk, breast feeding is not contraindicated
circumstances provide breast milk substitutes, if hepatitis B immune globulin is given to the newborns of
feeding bottles, or pacifiers free of charge or at low affected mothers. Maternal hepatitis C infection is not a contra-
cost indication because breast feeding has not been shown to trans-
7. Practice rooming-in, which allows mothers and mit infection. Women with active herpes simplex virus may
infants to remain together 24 hours a day suckle their infants if there are no breast lesions and if particular
8. Encourage breast feeding on demand care is directed to hand washing before nursing.
9. Give no artificial pacifiers to breast-feeding infants
10. Help start breast-feeding support groups and refer
mothers to them ■ Drugs Secreted in Milk
Most drugs given to the mother are secreted in breast milk,
Adapted from the World Health Organization, 1989. although the amount ingested by the infant typically is small.
Many factors influence drug excretion and include plasma con-
centration, degree of protein binding, plasma and milk pH,
in which a Baby-Friendly Hospital Initiative was implemented. degree of ionization, lipid solubility, and molecular weight
However, in 2011 in the United States, fewer than 10 percent (Rowe, 2013). The ratio of drug concentration in breast milk to
of births in 43 states and the District of Columbia occurred that in maternal plasma is the milk-to-plasma drug-concentration
in “baby friendly” hospitals (Centers for Disease Control and ratio. Most drugs have a ratio of ≤ 1, approximately 25 per-
Prevention, 2012a). In a large population-based study, fewer cent have a ratio > 1, and about 15 percent have a ratio > 2
than two thirds of term neonates were exclusively breast fed at (Ito, 2000). Ideally, to minimize infant exposure, medication
the time of discharge (McDonald, 2012). selection should favor drugs with a shorter half-life, poorer oral
There are a variety of individual resources available for absorption, and lower lipid solubility. If multiple daily drug
breast-feeding mothers that include online information from doses are required, then each is taken by the mother afterr the
the American Academy of Pediatrics (http://www.aap.org) and closest feed. Single daily-dosed drugs may be taken just before
La Leche League International (http://www.lalecheleague.org). the longest infant sleep interval—usually at bedtime (Spencer,
2002).
There are only a few drugs that are absolutely contraindicated
■ Care of Breasts while breast feeding (Berlin, 2013; Bertino, 2012). Cytotoxic
The nipples require little attention other than cleanliness and drugs may interfere with cellular metabolism and potentially
attention to skin fissures. Fissured nipples render nursing pain- cause immune suppression or neutropenia, affect growth, and,
ful, and they may have a deleterious influence on milk produc- at least theoretically, increase the risk of childhood cancer.
tion. These cracks also provide a portal of entry for pyogenic Examples include cyclophosphamide, cyclosporine, doxorubi-
bacteria. Because dried milk is likely to accumulate and irritate cin, methotrexate, and mycophenolate. If a medication presents
the nipples, washing the areola with water and mild soap is a concern, then the importance of therapy should be ascer-
helpful before and after nursing. When the nipples are irritated tained. It should be determined whether there is a safer alter-
or fissured, it may be necessary to use topical lanolin and a native or whether neonatal exposure can be minimized if the
nipple shield for 24 hours or longer. If fissuring is severe, the medication dose is taken immediately after each breast feeding
infant should not be permitted to nurse on the affected side. (American Academy of Pediatrics and the American College
Instead, the breast should be emptied regularly with a pump of Obstetricians and Gynecologists, 2012). Data on individual
until the lesions are healed. Poor latching of the neonate to drugs are available through the National Institutes of Health
the breast can create such fissures. Proper technique for posi- website, LactMed, which can be found at: toxnet.nlm.nih.gov/
tioning the mother and infant during latch-on and nursing has cgi-bin/sis/htmlgen?LACT.
been reviewed by the American College of Obstetricians and Radioactive isotopes of copper, gallium, indium, iodine,
Gynecologists (2013a). sodium, and technetium rapidly appear in breast milk.
 The Puerperium 675

Consultation with a nuclear medicine specialist is recommended Galactocelee is a milk duct that becomes obstructed by inspis-
before performing a diagnostic study with these isotopes (Chap. sated secretions. The amount is ordinarily limited, but an excess
46, p. 934). The goal is to use a radionuclide with the short- may form a fluctuant mass—a galactocele—that may cause

CHAPTER 36
est excretion time in breast milk. The mother should pump pressure symptoms and have the appearance of an abscess. It
her breasts before the study and store enough milk in a freezer may resolve spontaneously or require aspiration.
for feeding the infant. After the study, she should pump her There are marked individual variations in the amount of milk
breasts to maintain milk production but discard all milk pro- secreted. Many of these are dependent not on general maternal
duced during the time that radioactivity is present. This ranges health but on breast glandular development. Rarely, there is
from 15 hours up to 2 weeks, depending on the isotope used. complete lack of mammary secretion—agalactia. Occasionally,
Importantly, radioactive iodine concentrates and persists in the mammary secretion is excessive—polygalactia
— .
thyroid. Its special considerations are discussed in Chapter 63
(p. 1231).
MATERNAL CARE DURING THE PUERPERIUM
■ Breast Engorgement
■ Hospital Care
This is common in women who do not breast feed and is typi-
For 2 hours after delivery, blood pressure and pulse should
fied by milk leakage and breast pain. These peak 3 to 5 days
be taken every 15 minutes, or more frequently if indicated.
after delivery (Spitz, 1998). Up to half of affected women
Temperature is assessed every 4 hours for the first 8 hours
require analgesia for breast-pain relief, and as many as 10 per-
and then at least every 8 hours subsequently (American
cent report severe pain for up to 14 days.
Academy of Pediatrics and American College of Obstetricians
Evidence is insufficient to firmly support any specific treat-
and Gynecologists, 2012). The amount of vaginal bleeding is
ment (Mangesi, 2010). That said, breasts can be supported
monitored, and the fundus palpated to ensure that it is well
with a well-fitting brassiere, breast binder, or “sports bra.” Cool
contracted. If relaxation is detected, the uterus should be mas-
packs and oral analgesics for 12 to 24 hours aid discomfort.
saged through the abdominal wall until it remains contracted.
Pharmacological or hormonal agents are not recommended to
Uterotonics are also sometimes required. Blood may accumu-
suppress lactation.
late within the uterus without external bleeding. This may be
Fever caused by breast engorgement was common before
the renaissance of breast feeding. In one study, Almeida and detected early by uterine enlargement during fundal palpation
in the first postdelivery hours. Because the likelihood of sig-
Kitay (1986) reported that 13 percent of postpartum women
nificant hemorrhage is greatest immediately postpartum, even
had fever from engorgement that ranged from 37.8 to 39°C.
in normal births, the uterus is closely monitored for at least
Fever seldom persists for longer than 4 to 16 hours. The inci-
1 hour after delivery. Postpartum hemorrhage is discussed in
dence and severity of engorgement, and fever associated with
Chapter 41 (p. 783). If regional analgesia or general anesthesia
it, are much lower if women breast feed. Other causes of fever,
was used for labor or delivery, the mother should be observed
especially those due to infection, must be excluded. Of these,
in an appropriately equipped and staffed recovery area.
mastitiss is infection of the mammary parenchyma. It is rela-
Women are out of bed within a few hours after delivery. An
tively common in lactating women and is discussed in Chapter
attendant should be present for at least the first time, in case
37 (p. 691).
the woman becomes syncopal. The many confirmed advantages
of early ambulation include fewer bladder complications, less
■ Other Issues with Lactation frequent constipation, and reduced rates of puerperal venous
With inverted nipples, lactiferous ducts open directly into a thromboembolism. Almost half of thromboembolic events
depression at the center of the areola. With these depressed associated with pregnancy develop in the puerperium. Jacobsen
nipples, nursing is difficult. If the depression is not deep, milk and colleagues (2008) reported that pulmonary embolism is
sometimes can be made available by use of a breast pump. If most common in the first 6 weeks postpartum. In a recent
instead the nipple is greatly inverted, daily attempts should audit of puerperal women at Parkland Hospital, the frequency
be made during the last few months of pregnancy to draw or of venous thromboembolism was found to be 0.008 percent
“tease” the nipple out with the fingers. after a vaginal birth and 0.04 percent following cesarean deliv-
Extra breasts—polymastia
— , or extra nipples—polythelia
— , may ery. We attribute this low incidence to early ambulation. Risk
develop along the former embryonic mammary ridge. Also factors and other measures to diminish the frequency of throm-
termed the milk line, this line extends from the axilla to the boembolism are discussed in Chapter 52 (p. 1029).
groin bilaterally. In some women, there may be vulvar breast There are no dietary restrictions for women who have been
tissue (Wagner, 2013). The incidence of accessory breast tis- delivered vaginally. Two hours after normal vaginal delivery, if
sue ranges from 0.22 to 6 percent in the general population there are no complications, a woman should be allowed to eat.
(Loukas, 2007). These breasts may be so small as to be mistaken With breast feeding, the level of calories and protein consumed
for pigmented moles, or if without a nipple, for lymphade- during pregnancy should be increased slightly as recommended
nopathy or lipoma. Polymastia has no obstetrical significance, by the Food and Nutrition Board of the National Research
although occasionally enlargement of these accessory breasts Council (Chap. 9, p. 178). If the mother does not breast
during pregnancy or engorgement postpartum may result in feed, dietary requirements are the same as for a nonpregnant
discomfort and anxiety. woman. It is standard practice in our hospital to continue oral
 676 The Puerperium

iron supplementation for at least 3 months after delivery and to she also is likely to have further trouble. An examination for
check the hematocrit at a first postpartum visit. perineal and genital-tract hematomas is made. With an overdis-
tended bladder, an indwelling catheter should be left in place
until the factors causing retention have abated. Even without
SECTION 10

■ Perineal Care a demonstrable cause, it usually is best to leave the catheter in

The woman is instructed to cleanse the vulva from anterior to place for at least 24 hours. This prevents recurrence and allows
posterior—the vulva toward the anus. A cool pack applied to recovery of normal bladder tone and sensation.
the perineum may help reduce edema and discomfort during When the catheter is removed, it is necessary subsequently
the first 24 hours if there is a laceration or an episiotomy. Most to demonstrate ability to void appropriately. If a woman can-
women also appear to obtain a measure of relief from the peri- not void after 4 hours, she should be catheterized and the urine
odic application of a local anesthetic spray. Severe discomfort volume measured. If more than 200 mL, the bladder is not
usually indicates a problem, such as a hematoma within the first functioning appropriately, and the catheter is left for another
day or so and infection after the third or fourth day (Chap. 37, 24 hours. If less than 200 mL of urine is obtained, the catheter
p. 689 and Chap. 41, p 790). Severe perineal, vaginal, or rectal can be removed and the bladder rechecked subsequently as just
pain always warrants careful inspection and palpation. Beginning described. Harris and coworkers (1977) reported that 40 per-
approximately 24 hours after delivery, moist heat as provided cent of such women develop bacteriuria, and thus a single dose
by warm sitz baths can be used to reduce local discomfort. Tub or short course of antimicrobial therapy is reasonable after the
bathing after uncomplicated delivery is allowed. The episiot- catheter is removed.
omy incision normally is firmly healed and nearly asymptom-
atic by the third week.
Rarely, the cervix, and occasionally a portion of the uterine ■ Pain, Mood, and Cognition
body, may protrude from the vulva following delivery. This is Discomfort and its causes following cesarean delivery are con-
accompanied by variable degrees of anterior and posterior vagi- sidered in Chapter 30 (p. 605). During the first few days after
nal wall prolapse. Symptoms include a palpable mass at or past vaginal delivery, the mother may be uncomfortable because of
the introitus, voiding difficulties, or pressure. Puerperal proci- afterpains, episiotomy and lacerations, breast engorgement, and
dentia typically improves with time as the weight of the uterus at times, postdural puncture headache. Mild analgesics contain-
lessens with involution. As a temporizing measure in those with ing codeine, aspirin, or acetaminophen, preferably in combina-
pronounced prolapse, the uterus can be replaced and held in tions, are given as frequently as every 3 hours during the first
position with a suitable pessary. few days.
It is fairly common for a mother to exhibit some degree
of depressed mood a few days after delivery. Termed postpar-
■ Bladder Function tum blues, this likely is the consequence of several factors that
In most delivery units, intravenous fluids are infused during include emotional letdown that follows the excitement and
labor and for an hour or so after delivery. Oxytocin, in doses fears experienced during pregnancy and delivery, discomforts
that have an antidiuretic effect, is typically infused postpartum, of the early puerperium, fatigue from sleep deprivation, anxiety
and rapid bladder filling is common. Moreover, both blad- over the ability to provide appropriate infant care, and body
der sensation and capability to empty spontaneously may be image concerns.
diminished by local or conduction analgesia, by trauma to the In most women, effective treatment includes anticipation,
bladder, by episiotomy or lacerations, or by operative vaginal recognition, and reassurance. This disorder is usually mild and
delivery. Thus, urinary retention and bladder overdistention is self-limited to 2 to 3 days, although it sometimes lasts for up
common in the early puerperium. Ching-Chung and associ- to 10 days. Should these moods persist or worsen, an evalu-
ates (2002) reported retention in 4 percent of women delivered ation for symptoms of major depression is done (Chap. 61,
vaginally. Musselwhite and coworkers (2007) reported reten- p. 1205). Suicidal or infanticidal ideation is dealt with emer-
tion in 4.7 percent of women who had labor epidural analgesia. gently. Because major postpartum depression recurs in at least a
Risk factors that increased likelihood of retention were primi- fourth of women in subsequent pregnancies, some recommend
parity, perineal lacerations, oxytocin-induced or -augmented pharmacological prophylaxis beginning in late pregnancy or
labor, operative vaginal delivery, catheterization during labor, immediately postpartum.
and labor duration > 10 hours. Last, postpartum hormonal changes in some women may
Prevention of bladder overdistention demands observation affect brain function. Bannbers and colleagues (2013) com-
after delivery to ensure that the bladder does not overfill and pared a measure of executive function in postpartum women
that it empties adequately with each voiding. The enlarged blad- and controls and observed a decrease in postpartum subjects.
der can be palpated suprapubically, or it is evident abdominally
indirectly as it elevates the fundus above the umbilicus. Van ■ Neuromusculoskeletal Problems
Os and Van der Linden (2006) have investigated the use of an
automated sonography system to detect high bladder volumes Obstetrical Neuropathies
and thus postpartum urinary retention. Pressure on branches of the lumbosacral nerve plexus dur-
If a woman has not voided within 4 hours after delivery, ing labor may manifest as complaints of intense neuralgia or
it is likely that she cannot. If she has trouble voiding initially, cramplike pains extending down one or both legs as soon as
 The Puerperium 677

the head descends into the pelvis. If the nerve is injured, pain
may continue after delivery, and there also may be variable
degrees of sensory loss or muscle paralysis. In some cases, there

CHAPTER 36
is footdrop, which can be secondary to injury at the level of
the lumbosacral plexus, sciatic nerve, or common fibular (pero-
neal) nerve. Components of the lumbosacral plexus cross the
pelvic brim and can be compressed by the fetal head or by for-
ceps. The common fibular nerves may be externally compressed
when the legs are positioned in stirrups, especially during pro-
longed second-stage labor.
Obstetrical neuropathy is relatively infrequent. Wong and
associates (2003) evaluated more than 6000 delivered women
and found that approximately 1 percent had a confirmed nerve
injury. Lateral femoral cutaneous neuropathies were the most
common (24), followed by femoral neuropathies (14). A motor
deficit accompanied a third of injuries. Nulliparity, prolonged
second-stage labor, and pushing for a long duration in the FIGURE 36-7 Bacterial osteitis pubis–osteomyelitis caused by
semi-Fowler position were risk factors. The median duration Streptococcus millerii in a woman with symptomatic symphyseal
of symptoms was 2 months, and the range was 2 weeks to separation.
18 months.
Nerve injuries with cesarean delivery include the iliohypo-
gastric and ilioinguinal nerves (Rahn, 2010). These are dis- vary widely from 1 in 600 to 1 in 30,000 deliveries (Reis, 1932;
cussed further in Chapter 2 (p. 17). Taylor, 1986). In our experiences, symptomatic separations are
uncommon. Their onset of pain is often acute during delivery,
Musculoskeletal Injuries but symptoms may manifest either antepartum or up to 48
Pain in the pelvic girdle, hips, or lower extremities may follow hours postpartum (Snow, 1997). Treatment is generally con-
stretching or tearing injuries sustained at normal or difficult servative, with rest in a lateral decubitus position and an appro-
delivery. Magnetic resonance (MR) imaging is often informa- priately fitted pelvic binder. Surgery is occasionally necessary
tive. One example is the piriformis muscle hematoma shown in some symphyseal separations of more than 4 cm (Kharrazi,
in Figure 36-6. Most injuries resolve with antiinflammatory 1997). The recurrence risk is > 50 percent in subsequent preg-
agents and physical therapy. Rarely, there may be septic pyo- nancy, and Culligan and associates (2002) recommend con-
myositis such as with iliopsoas muscle abscess (Nelson, 2010; sideration for cesarean delivery. In rare cases, fractures of the
Young, 2010). sacrum or pubic ramus are caused by even uncomplicated
Separation of the symphysis pubis or one of the sacroiliac deliveries (Alonso-Burgos, 2007). As discussed in Chapter 58
synchondroses during labor leads to pain and marked interfer- (p. 1159), the latter are more likely with osteoporosis associ-
ence with locomotion. Estimates of the frequency of this event ated with heparin or corticosteroid therapy (Cunningham,
2005). In rare but serious cases, bacterial osteomyelitis—osteitis
pubis—can
s be devastating (Fig. 36-7). Lawford and coworkers
(2010) reported such a case that caused massive vulvar edema.

■ Immunizations
The D-negative woman who is not isoimmunized and whose
infant is D-positive is given 300 μg of anti-D immune globu-
lin shortly after delivery (Chap. 15, p. 311). Women who are
not already immune to rubella or rubeola measles are excellent
candidates for combined measles-mumps-rubella vaccination
before discharge (Chap. 9, p. 184). Unless contraindicated, at
Parkland Hospital a diphtheria-tetanus toxoid booster injection
is also given to postpartum women.

■ Hospital Discharge
Following uncomplicated vaginal delivery, hospitalization is
seldom warranted for more than 48 hours. A woman should
FIGURE 36-6 Magnetic resonance image of a piriformis hema-
toma. A large inhomogeneous mass of the right piriformis muscle
receive instructions concerning anticipated normal physi-
consistent with a hematoma (yellow cursor measurements) ological puerperal changes, including lochia patterns, weight
is compared with the normal-appearing left piriformis muscle loss from diuresis, and milk let-down. She also should receive
(yellow arrow). instructions concerning fever, excessive vaginal bleeding, or leg
 678 The Puerperium

pain, swelling, or tenderness. Persistent headaches, shortness of 100

breath, or chest pain warrant immediate concern.
Hospital stay length following labor and delivery is now
regulated by federal law (Chap. 32, p. 634). Currently, the
SECTION 10

75
norms are hospital stays up to 48 hours following uncompli-
cated vaginal delivery and up to 96 hours following uncom-

Percent
plicated cesarean delivery (American Academy of Pediatrics
50
and the American College of Obstetricians and Gynecologists,
2012). Earlier hospital discharge is acceptable for appropriately
selected women if they desire it.
25

■ Contraception
During the hospital stay, a concerted effort should be made to 0
provide family planning education. Various forms of contra- 0 10 20 30 40 50 60 70
ception are discussed throughout Chapter 38 and sterilization Weeks postpartum
procedures in Chapter 39. FIGURE 36-8 Cumulative proportion of breast-feeding women
Women not breast feeding have return of menses usually who ovulated during the first 70 weeks following delivery.
within 6 to 8 weeks. At times, however, it is difficult clinically (Data from Campbell, 1993.)
to assign a specific date to the first menstrual period after deliv-
ery. A minority of women bleed small to moderate amounts by breast-feeding women. However, these are withheld until
intermittently, starting soon after delivery. Ovulation occurs at after the first 4 weeks because of their higher thromboembolic
a mean of 7 weeks, but ranges from 5 to 11 weeks (Perez, 1972). risk in puerperal patients. These hormonal methods are summa-
That said, ovulation before 28 days has been described (Hytten, rized in Table 36-4 and are discussed in Chapter 38 (p. 695).
1995). Thus, conception is possible during the artificially
defined 6-week puerperium. Women who become sexually active
during the puerperium, and who do not desire to conceive, should HOME CARE
initiate contraception. Kelly and associates (2005) reported that
by the third month postpartum, 58 percent of adolescents had ■ Coitus
resumed sexual intercourse, but only 80 percent of these were There are no evidence-based data concerning resumption of
using contraception. Because of this, many recommend long- coitus after delivery. It seems best to use common sense (Minig,
acting reversible contraceptives—LARC (Baldwin, 2013). 2009). After 2 weeks, coitus may be resumed based on desire
Women who breast feed ovulate much less frequently com- and comfort. Barrett and colleagues (2000) reported that almost
pared with those who do not, but there are great variations. 90 percent of 484 primiparous women resumed sexual activ-
Timing of ovulation depends on individual biological varia- ity by 6 months. And although 65 percent of these reported
tion as well as the intensity of breast feeding. Lactating women problems, only 15 percent discussed them with a health-care
may first menstruate as early as the second or as late as the provider.
18th month after delivery. Campbell and Gray (1993) analyzed Intercourse too soon may be unpleasant, if not frankly pain-
daily urine specimens to determine the time of ovulation in ful, due to incomplete healing of the episiotomy or lacerations.
92 lactating women. As shown in Figure 36-8, breast feeding Moreover, the vaginal epithelium is thin, and very little lubri-
in general delays resumption of ovulation, although as already cation follows sexual stimulation. This is due to the hypoes-
emphasized, it does not invariably forestall it. Other findings in trogenic state following delivery, which lasts until ovulation
their study included the following: resumes. It may be particularly problematic in breast-feeding
women who are hypoestrogenic for many months postpar-
1. Resumption of ovulation was frequently marked by return
tum (Palmer, 2003; Wisniewski, 1991). For treatment, small
of normal menstrual bleeding.
amounts of topical estrogen cream can be applied daily for
2. Breast-feeding episodes lasting 15 minutes seven times daily
delayed ovulation resumption.
3. Ovulation can occur without bleeding.
4. Bleeding can be anovulatory. TABLE 36-4. Some Hormonal Contraceptive Regimens
5. The risk of pregnancy in breast-feeding women was approxi- for Breast-Feeding Womena
mately 4 percent per year. Progestin-only “mini pill”
For the breast-feeding woman, progestin-only contracep- Intramuscular depot medroxyprogesterone acetate
tives—mini-pills, depot medroxyprogesterone, or progestin Progesterone-releasing implants
implants—do not affect the quality or quantity of milk. These Progesterone-releasing intrauterine systems
may be initiated any time during the puerperium. Estrogen- Combination oral contraceptives—low-dose estrogen
progestin contraceptives likely reduce the quantity of breast a
See also Chapter 38 (p. 695).
milk, but under the proper circumstances, they too can be used
 The Puerperium 679

several weeks to vulvar tissues. Additionally, vaginal lubricants REFERENCES

may be used with coitus.
Ahdoot D, Van Nostrand KM, Nguyen NJ, et al: The effect of route of deliv-
ery on regression of abnormal cervical cytologic findings in the postpartum

CHAPTER 36
■ Late Maternal Morbidity period. Am J Obstet Gynecol 178:1116, 1998
Almeida OD Jr, Kitay DZ: Lactation suppression and puerperal fever. Am J
Taken together, major and minor maternal morbidity are Obstet Gynecol 154:940, 1986
surprisingly common in the months following childbirth Alonso-Burgos A, Royo P, Diaz L, et al: Labor-related sacral and pubic frac-
tures. J Bone Joint Surg 89:396, 2007
(MacArthur, 1991). In a survey of 1249 British mothers fol- American Academy of Pediatrics: Breastfeeding and the use of human milk.
lowed for up to 18 months, 3 percent required hospital read- Pediatrics 129(3):e827, 2012
mission within 8 weeks (Glazener, 1995; Thompson, 2002). American Academy of Pediatrics and the American College of Obstetricians
and Gynecologists: Guidelines for Perinatal Care, 7th ed. Washington, AAP
Milder health problems during the first 8 weeks were reported and ACOG, 2012
by 87 percent (Table 36-5). Moreover, almost three fourths American College of Obstetricians and Gynecologists: Breastfeeding: maternal and
continued to have various problems for up to 18 months. infant aspects. Committee Opinion No. 361, February 2007, Reaffirmed 2013a
American College of Obstetricians and Gynecologists: Postpartum hemor-
Practitioners should be aware of these potential issues in their rhage. Practice Bulletin No. 76, October 2006, Reaffirmed 2013b
patients convalescing from birthing. Anderson WR, Davis J: Placental site involution. Am J Obstet Gynecol 102:23,
1968
Andrew AC, Bulmer JN, Wells M, et al: Subinvolution of the uteroplacental
■ Follow-Up Care arteries in the human placental bed. Histopathology 15:395, 1989
Andrews MC: Epithelial changes in the puerperal fallopian tube. Am J Obstet
By discharge, women who had an uncomplicated course Gynecol 62:28, 1951
can resume most activities, including bathing, driving, and Baker JL, Gamborg M, Heitmann BL, et al: Breastfeeding reduces postpartum
weight retention. Am J Clin Nutr 88(6):1543, 2008
household functions. Jimenez and Newton (1979) tabulated Baldwin MK, Edelman AB: The effect of long-acting reversible contraception
cross-cultural information on 202 societies from various inter- on rapid repeat pregnancy in adolescents: a review. J Adolesc Health 52
national geographical regions. Following childbirth, most (4 Suppl):S47, 2013
Ballard O, Morrow AL: Human milk composition: nutrients and bioactive
societies did not restrict work activity, and approximately half factors. Pediatr Clin North Am 60(1):49, 2013
expected a return to full duties within 2 weeks. Wallace and Bannbers E, Gingnell M, Engman J, et al: Prefrontal activity during response
coworkers (2013) reported that 80 percent of women who inhibition decreases over time in the postpartum period. Behav Brain Res
241:132, 2013
worked during pregnancy resume work by 1 year after deliv- Barrett G, Pendry E, Peacock J, et al: Women’s sexual health after childbirth.
ery. Despite this, Tulman and Fawcett (1988) reported that BJOG 107:186, 2000
only half of mothers regained their usual level of energy by Bartick M, Reinhold A: The burden of suboptimal breastfeeding in the United
States: a pediatric cost analysis. Pediatrics 125(5):e1048, 2010
6 weeks. Women who delivered vaginally were twice as likely Belachew J, Axelsson O, Mulic-Lutvica A, et al: Longitudinal study of the uter-
to have normal energy levels at this time compared with those ine body and cavity with three-dimensional ultrasonography in the puerpe-
with a cesarean delivery. Ideally, the care and nurturing of rium. Acta Obstet Gynecol Scand 91(10):1184, 2012
Berlin CM Jr, van den Anker, JN: Safety during breastfeeding: drugs, foods,
the infant should be provided by the mother with ample help environmental chemicals, and maternal infections. Semin Fetal Neonatal
from the father. Med 18(1):13, 2013
The American Academy of Pediatrics and the American Bertino E, Varalda A, Di Nicola P, et al: Drugs and breastfeeding: instructions
for use. J Matern Fetal Neonatal Med 25(Suppl 4):78, 2012
College of Obstetricians and Gynecologists (2012) recommend Bertotto A, Gerli R, Fabietti G, et al: Human breast milk T lymphocytes dis-
a postpartum visit between 4 and 6 weeks. This has proven play the phenotype and functional characteristics of memory T cells. Eur J
quite satisfactory to identify abnormalities beyond the immedi- Immunol 20:1877, 1990
Buhimschi CS, Buhimschi IA, Manlinow AM, et al: Myometrial thickness
ate puerperium and to initiate contraceptive practices. during human labor and immediately post partum. Am J Obstet Gynecol
188:553, 2003
Campbell OMR, Gray RH: Characteristics and determinants of postpartum
ovarian function in women in the United States. Am J Obstet Gynecol
169:55, 1993
TABLE 36-5. Puerperal Morbidity Reported by 8 Weeks Centers for Disease Control and Prevention: Breastfeeding Report Card—
United States, 2012a. Available at: http://www.cdc.gov/breastfeeding/data/
Morbidity Percenta reportcard.htm. Accessed May 18, 2013
Fatigue 59 Centers for Disease Control and Prevention: PRAMS, the Pregnancy Risk
Breast problems 36 Assessment Monitoring System. 2012b. Available at: http://www.cdc.gov/
prams/index.htm. Accessed May 18, 2013
Anemia 25 Chesley LC, Valenti C, Uichano L: Alterations in body fluid compartments
Backache 24 and exchangeable sodium in early puerperium. Am J Obstet Gynecol
Hemorrhoids 23 77:1054, 1959
Ching-Chung L, Shuenn-Dhy C, Ling-Hong T, et al: Postpartum urinary
Headache 22 retention: assessment of contributing factors and long-term clinical impact.
“Blues” 21 Aust N Z J Obstet Gynaecol 42:365, 2002
Constipation 20 Collier RJ, Hernandez LL, Horseman ND: Serotonin as a homeostatic regula-
tor of lactation. Domest Anim Endocrinol 43(2):161, 2012
Suture breakdown 16 Cravioto A, Tello A, Villafan H, et al: Inhibition of localized adhesion of
Vaginal discharge 15 enteropathogenic Escherichia colii to HEp-2 cells by immunoglobulin and
oligosaccharide fractions of human colostrum and breast milk. J Infect Dis
a 163:1247, 1991
At least one symptom was reported by 87 percent of all
Culligan P, Hill S, Heit M: Rupture of the symphysis pubis during vagi-
women. nal delivery followed by two subsequent uneventful pregnancies. Obstet
Data from Glazener, 1995. Gynecol 100:1114, 2002
728

CHAPTER 40

Hypertensive Disorders

TERMINOLOGY AND DIAGNOSIS . . . . . . . . . . . . . . . . . . 728 were caused by preeclampsia or eclampsia. The rate was similar
to that of 10 percent for maternal deaths in France from 2003
INCIDENCE AND RISK FACTORS. . . . . . . . . . . . . . . . . . . 731 through 2007 (Saucedo, 2013). Importantly, more than half of
ETIOPATHOGENESIS . . . . . . . . . . . . . . . . . . . . . . . . . . . 731 these hypertension-related deaths were preventable (Berg, 2005).

PATHOPHYSIOLOGY . . . . . . . . . . . . . . . . . . . . . . . . . . . 736
TERMINOLOGY AND DIAGNOSIS
PREDICTION AND PREVENTION . . . . . . . . . . . . . . . . . . . 746
In this country for the past two decades, pregnancy hypertension
MANAGEMENT . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 749 was considered using the terminology and classification pro-
mulgated by the Working Group of the National High Blood
LONG-TERM CONSEQUENCES . . . . . . . . . . . . . . . . . . . . 769
Pressure Education Program—NHBPEP (2000). To update
these, a Task Force was appointed by President James Martin
for the American College of Obstetricians and Gynecologists
(2013b) to provide evidence-based recommendations for clini-
How pregnancy incites or aggravates hypertension remains cal practice. The basic classification was retained, as it describes
unsolved despite decades of intensive research. Indeed, hyper- four types of hypertensive disease:
tensive disorders remain among the most significant and
intriguing unsolved problems in obstetrics. 1. Gestational hypertension—evidence for the preeclampsia
Hypertensive disorders complicate 5 to 10 percent of all syndrome does not develop and hypertension resolves by
pregnancies, and together they are one member of the deadly 12 weeks postpartum
triad—along with hemorrhage and infection—that contributes 2. Preeclampsia and eclampsia syndrome
greatly to maternal morbidity and mortality. Of these disorders, 3. Chronic hypertension of any etiology
the preeclampsia syndrome, either alone or superimposed on 4. Preeclampsia superimposed on chronic hypertension.
chronic hypertension, is the most dangerous. As subsequently Importantly, this classification differentiates the preeclamp-
discussed, new-onset hypertension during pregnancy—termed sia syndrome from other hypertensive disorders because it is
gestational hypertension—is followed by signs and symptoms of potentially more ominous. This concept aids interpretation
preeclampsia almost half the time, and preeclampsia is identi- of studies that address the etiology, pathogenesis, and clinical
fied in 3.9 percent of all pregnancies (Martin, 2012). management of pregnancy-related hypertensive disorders.
The World Health Organization (WHO) systematically
reviews maternal mortality worldwide, and in developed coun-
tries, 16 percent of maternal deaths were reported to be due to ■ Diagnosis of Hypertensive Disorders
hypertensive disorders (Khan, 2006). This proportion is greater Hypertension is diagnosed empirically when appropriately taken
than three other leading causes that include hemorrhage—13 per- blood pressure exceeds 140 mm Hg systolic or 90 mm Hg dia-
cent, abortion—8 percent, and sepsis—2 percent. In the United stolic. Korotkoff phase V is used to define diastolic pressure.
States from 1998 to 2005, Berg and colleagues (2010) reported Previously, incremental increases of 30 mm Hg systolic or 15
that 12.3 percent of 4693 pregnancy-related maternal deaths mm Hg diastolic from midpregnancy blood pressure values had
 Hypertensive Disorders 729

TABLE 40-1. Diagnostic Criteria for Pregnancy-Associated Hypertension

Condition Criteria Required
BP > 140/90 mmHg after 20 weeks in previously normotensive women

CHAPTER 40
Gestational hypertension
Preeclampsia—Hypertension and:
Proteinuria • ≥ 300 mg/24h, or
• Protein: creatinine ratio ≥ 0.3 or
• Dipstick 1+ persistenta
or
Thrombocytopenia • Platelets < 100,000/μL
Renal insufficiency • Creatinine > 1.1 mg/dL or doubling of baselineb
Liver involvement • Serum transaminase levelsc twice normal
Cerebral symptoms • Headache, visual disturbances, convulsions
Pulmonary edema —
a
Recommended only if sole available test.
b
No prior renal disease.
c
AST (aspartate aminotransferase) or ALT (alanine aminotransferase).
Modified from the American College of Obstetricians and Gynecologists, 2013b.

also been used as diagnostic criteria, even when absolute values “hypertension” in nonpregnant individuals. As discussed in detail
were < 140/90 mm Hg. These incremental changes are no longer in Chapter 50 (p. 1000), these levels were selected by insurance
recommended criteria because evidence shows that such women companies for a group of middle-aged men. It seems more real-
are not likely to experience increased adverse pregnancy outcomes istic to define normal-range blood pressures that fall between an
(Levine, 2000; North, 1999). That said, women who have a rise in upper and lower limit for blood pressure measurements for a par-
pressure of 30 mm Hg systolic or 15 mm Hg diastolic should be ticular population—such as young, healthy, pregnant women. A
observed more closely because eclamptic seizures develop in some schematic example is shown in Figure 40-1 using arbitrary blood
of these women whose blood pressures have stayed < 140/90 mm pressure readings. Data curves for both women show blood pres-
Hg (Alexander, 2006). A sudden rise in mean arterial pressure sure measurements near the 25th percentile until 32 weeks. These
later in pregnancy—also known as “delta hypertension”—may begin to rise in patient B, who by term has substantively increased
also signify preeclampsia even if blood pressure is < 140/90 mm blood pressures. However, her pressures are still < 140/90 mm
Hg (Macdonald-Wallis, 2012; Vollaard, 2007). Hg, and thus she is considered to be “normotensive.” We termed
this rather acute increase in blood pressure as “delta hyperten-
Concept of “Delta Hypertension” sion.” As discussed later, some of these women will develop
The systolic and diastolic blood pressure levels of 140/90 eclamptic seizures or HELLP (hemolysis, elevated liver enzyme
mm Hg have been arbitrarily used since the 1950s to define levels, low platelet count) syndrome while still normotensive.

Patient A ■ Gestational Hypertension

Patient B 95th This diagnosis is made in women whose blood pressures reach
140/90 mm Hg or greater for the first time after midpregnancy,
Blood pressure

but in whom proteinuria is not identifiedd (Table 40-1). Almost half

50th of these women subsequently develop preeclampsia syndrome,
which includes findings such as headaches or epigastric pain, pro-
5th teinuria, and thrombocytopenia. Even so, when blood pressure
increases appreciably, it is dangerous to both mother and fetus to
ignore this rise only because proteinuria has not yet developed.
As Chesley (1985) emphasized, 10 percent of eclamptic seizures
develop before overt proteinuria can be detected. Finally, gesta-
8 16 24 32 40 tional hypertension is reclassified by some as transient hyperten-
Weeks’ gestation sion if evidence for preeclampsia does not develop and the blood
FIGURE 40-1 Schematic shows normal reference ranges for pressure returns to normal by 12 weeks postpartum.
blood pressure changes across pregnancy. Patient A (blue) has
blood pressures near the 20th percentile throughout pregnancy. ■ Preeclampsia Syndrome
Patient B (red ) has a similar pattern with pressures at about the
25th percentile until about 36 weeks when blood pressure begins As emphasized throughout this chapter, preeclampsia is best
to increase. By term, it is substantively higher and in the 75th described as a pregnancy-specific syndrome that can affect virtually
percentile, but she is still considered “normotensive.” every organ system. And, although preeclampsia is much more than
 730 Obstetrical Complications

simply gestational hypertension with proteinuria, appearance of

TABLE 40-2. Indicators of Severity of Gestational
proteinuria remains an important diagnostic criterion. Thus, pro-
Hypertensive Disordersa
teinuria is an objectivee marker and reflects the system-wide endo-
thelial leak, which characterizes the preeclampsia syndrome. Abnormality Nonsevereb Severe
SECTION 11

Abnormal protein excretion is arbitrarily defined by 24-hour Diastolic BP < 110 mm Hg ≥ 110 mm Hg
urinary excretion exceeding 300 mg; a urine protein:creatinine Systolic BP < 160 mm Hg ≥ 160 mm Hg
ratio ≥ 0.3; or persistent 30 mg/dL (1+
+ dipstick) protein in random Proteinuriac None to positive None to positive
urine samples (Lindheimer, 2008a). None of these values is sacro- Headache Absent Present
sanct, and urine concentrations vary widely during the day, as do Visual disturbances Absent Present
dipstick readings. Thus, assessment may show a dipstick value of Upper abdominal Absent Present
1++ to 2+ from concentrated urine specimens from women who pain
excrete < 300 mg/day. As discussed on page 740, it is likely that Oliguria Absent Present
determination of a spot urine:creatinine ratio is a suitable replace- Convulsion Absent Present
ment for a 24-hour urine measurement (Chap. 4, p. 65). (eclampsia)
It is now appreciated that overt proteinuria may not be a Serum creatinine Normal Elevated
feature in some women with the preeclampsia syndrome (Sibai, Thrombocytopenia Absent Present
2009). Because of this, the Task Force (2013) suggested other (< 100,000/μL)
diagnostic criteria, which are shown in Table 40-1. Evidence of Serum transaminase Minimal Marked
multiorgan involvement may include thrombocytopenia, renal elevation
dysfunction, hepatocellular necrosis (“liver dysfunction”), cen- Fetal-growth Absent Obvious
tral nervous system perturbations, or pulmonary edema. restriction
Pulmonary edema Absent Present
Indicators of Preeclampsia Severity
a
The markers listed in Table 40-1 are also used to classify pre- Compare with criteria in Table 40-1.
b
eclampsia syndrome severity. Although many use a dichoto- Includes “mild” and “moderate” hypertension not
mous “mild” and “severe” classification, the Task Force (2013) specifically defined.
c
discourages the use of “mild preeclampsia.” It is problematic that Most disregard degrees of proteinuria as being
there are criteria for the diagnosis of “severe” preeclampsia, but nonsevere or severe.
the default classification is either implied or specifically termed BP = blood pressure.
as “mild,” “less severe,” or “nonsevere” (Alexander, 2003;
Lindheimer, 2008b). There are no generally agreed-on criteria
for “moderate” preeclampsia—an elusive third category. We partum approximates 10 percent (Sibai, 2005). In some reports,
use the criteria listed in Table 40-2, which are categorized as up to a fourth of eclamptic seizures develop beyond 48 hours
“severe” versus “nonsevere.” Importantly, while it is pragmatic postpartum (Chames, 2002). Our experiences from Parkland
that nonsevere classifications include “moderate” and “mild,” Hospital, however, are that delayed postpartum eclampsia con-
these have not been specifically defined. tinues to occur in about 10 percent of cases—similar to what we
Some symptoms are considered to be ominous. Headachess or first reported more than 20 years ago (Alexander, 2006; Brown,
visual disturbancess such as scotomataa can be premonitory symp- 1987). This lower percentage was also found in 222 women
toms of eclampsia. Epigastric or right upper quadrant pain fre- with eclampsia from The Netherlands (Zwart, 2008).
quently accompanies hepatocellular necrosis, ischemia, and edema
that ostensibly stretches Glisson capsule. This characteristic pain is
frequently accompanied by elevated serum hepatic transaminase ■ Preeclampsia Superimposed on
levels. Finally, thrombocytopeniaa is also characteristic of worsen- Chronic Hypertension
ing preeclampsia as it signifies platelet activation and aggregation Regardless of its cause, any chronic hypertensive disorder pre-
as well as microangiopathic hemolysis. Other factors indicative disposes a woman to develop superimposed preeclampsia syn-
of severe preeclampsia include renal or cardiac involvement and drome. Chronic underlying hypertension is diagnosed in women
obvious fetal-growth restriction, which also attests to its duration. with documented blood pressures ≥ 140/90 mm Hg before
As will be discussed, the more profound these signs and pregnancy or before 20 weeks’ gestation, or both. Hypertensive
symptoms, the less likely they can be temporized, and the disorders can create difficult problems with diagnosis and man-
more likely delivery will be required. A caveat is that differen- agement in women who are not first seen until after midpreg-
tiation between nonsevere and severe gestational hypertension or nancy. This is because blood pressure normally decreases during
preeclampsia can be misleading because what might be apparently the second and early third trimesters in both normotensive and
mild disease may progress rapidly to severe disease. chronically hypertensive women (Chap. 50, p. 1003). Thus, a
woman with previously undiagnosed chronic vascular disease
Eclampsia who is seen before 20 weeks frequently has blood pressures
In a woman with preeclampsia, a convulsion that cannot be within the normal range. During the third trimester, however,
attributed to another cause is termed eclampsia. The seizures are as blood pressures return to their originally hypertensive levels,
generalized and may appear before, during, or after labor. The it may be difficult to determine whether hypertension is chronic
proportion who do not develop seizures until after 48 hours post- or induced by pregnancy. Even a careful search for evidence of
 Hypertensive Disorders 731

preexisting end-organ damage may be futile, as many of these in the woman who was normotensive during her first pregnancy,
women have mild disease and no evidence of ventricular hyper- the incidence of preeclampsia in a subsequent pregnancy is much
trophy, retinal vascular changes, or renal dysfunction. lower than for a first pregnancy. In a population-based retro-

CHAPTER 40
In some women with chronic hypertension, their blood pres- spective cohort analysis, Getahun and colleagues (2007) studied
sure increases to obviously abnormal levels, and this is typically almost 137,000 second pregnancies in such women. The inci-
after 24 weeks. If new-onset or worsening baseline hypertension dence for preeclampsia in secundigravida white women was 1.8
is accompanied by new-onset proteinuria or other findings listed percent compared with 3 percent in African-American women.
in Table 40-1, then superimposed preeclampsia is diagnosed.
Compared with “pure” preeclampsia, superimposed preeclamp- Eclampsia
sia commonly develops earlier in pregnancy. It also tends to be Presumably because it is somewhat preventable by adequate prena-
more severe and often is accompanied by fetal-growth restric- tal care, the incidence of eclampsia has decreased over the years in
tion. The same criteria shown in Table 40-2 are also used to areas where health care is more readily available. In countries with
further characterize severity of superimposed preeclampsia. adequate resources, its incidence averages 1 in 2000 deliveries.
Ventura and associates (2000) estimated that the incidence in the
United States in 1998 was 1 in 3250 births. According to the Royal
INCIDENCE AND RISK FACTORS College of Obstetricians and Gynaecologists (2006), it approxi-
mates 1 in 2000 in the United Kingdom. Akkawi and coworkers
■ Preeclampsia Syndrome (2009) reported it to be 1 in 2500 in Dublin, Andersgaard and
Young and nulliparous women are particularly vulnerable to associates (2006) as 1 per 2000 for Scandinavia, and Zwart and
developing preeclampsia, whereas older women are at greater colleagues (2008) as 1 per 1600 for The Netherlands.
risk for chronic hypertension with superimposed preeclampsia.
The incidence is markedly influenced by race and ethnicity— ETIOPATHOGENESIS
and thus by genetic predisposition. By way of example, in
nearly 2400 nulliparas enrolled in a Maternal-Fetal Medicine Any satisfactory theory concerning the etiology and pathogen-
Units (MFMU) Network study, the incidence of preeclampsia esis of preeclampsia must account for the observation that ges-
was 5 percent in white, 9 percent in Hispanic, and 11 percent tational hypertensive disorders are more likely to develop in
in African-American women (Myatt, 2012a,b). women with the following characteristics:
Other factors include environmental, socioeconomic, and
even seasonal influences (Lawlor, 2005; Palmer, 1999; Spencer, • Are exposed to chorionic villi for the first time
2009). With consideration for these vicissitudes, in several • Are exposed to a superabundance of chorionic villi, as with
worldwide studies reviewed by Staff and coworkers (2014), twins or hydatidiform mole
the incidence of preeclampsia in nulliparous populations • Have preexisting conditions of endothelial cell activation or
ranged from 3 to 10 percent. The incidence of preeclampsia inflammation such as diabetes or renal or cardiovascular disease
in multiparas is also variable but is less than that for nullipa- • Are genetically predisposed to hypertension developing
ras. Specifically, population studies from Australia, Canada, during pregnancy.
Denmark, Norway, Scotland, Sweden, and Massachusetts indi- A fetus is not a requisite for preeclampsia to develop. And,
cate an incidence of 1.4 to 4 percent (Roberts, 2011). although chorionic villi are essential, they need not be intra-
There are several other risk factors associated with pre- uterine. For example, Worley and associates (2008) reported a
eclampsia. These include obesity, multifetal gestation, maternal 30-percent incidence in women with an extrauterine pregnancy
age, hyperhomocysteinemia, and metabolic syndrome (Conde- exceeding 18 weeks’ gestation. Regardless of precipitating eti-
Agudelo, 2000; Scholten, 2013; Walker, 2000). The relation- ology, the cascade of events leading to the preeclampsia syn-
ship between maternal weight and the risk of preeclampsia is drome is characterized by abnormalities that result in vascular
progressive. It increases from 4.3 percent for women with a endothelial damage with resultant vasospasm, transudation of
body mass index (BMI) < 20 kg/m2 to 13.3 percent in those plasma, and ischemic and thrombotic sequelae.
with a BMI > 35 kg/m2 (Fig. 48-5, p. 966). In women with
a twin gestation compared with those with singletons, the inci-
dence of gestational hypertension—13 versus 6 percent, and ■ Phenotypic Expression of
the incidence of preeclampsia—13 versus 5 percent, are both Preeclampsia Syndrome
significantly increased (Sibai, 2000). It is interesting that this The preeclampsia syndrome is widely variable in its clinical phe-
latter incidence is unrelated to zygosity (Maxwell, 2001). notypic expression. There are at least two major subtypes differ-
Although smoking during pregnancy causes various adverse entiated by whether or not remodeling of uterine spiral arterioles
pregnancy outcomes, ironically, it has consistently been asso- by endovascular trophoblastic invasion is defective. This concept
ciated with a reduced riskk for hypertension during pregnancy has given rise to the “two-stage disorder” theory of preeclampsia
(Bainbridge, 2005; Zhang, 1999). Kraus and associates (2013) etiopathogenesis. Ness and Roberts (1996) consider that the two-
posit that this is because smoking upregulates placental adreno- stage disorder includes “maternal and placental preeclampsia.”
medullin expression, which regulates volume homeostasis. According to Redman and coworkers (2014), stage 1 is caused by
Women with preeclampsia in the first pregnancy are at greater faulty endovascular trophoblastic remodeling that downstream
risk in a second pregnancy compared with women normotensive causes the stage 2 clinical syndrome. Importantly, stage 2 is sus-
during their first pregnancy (McDonald, 2009). And conversely, ceptible to modification by preexisting maternal conditions that
 732 Obstetrical Complications

are manifest by endothelial cell activation or inflammation. Such trophoblasts. The deeper myometrial arterioles do not lose their
conditions include cardiovascular or renal disease, diabetes, obe- endothelial lining and musculoelastic tissue, and their mean
sity, immunological disorders, or hereditary influences. external diameter is only half that of corresponding vessels in
Such compartmentalization is artificial, and it seems logical normal placentas (Fisher, 2014). In general, the magnitude of
SECTION 11

to us that preeclampsia syndrome presents clinically as a spec- defective trophoblastic invasion is thought to correlate with
trum of worsening disease. Moreover, evidence is accruing that severity of the hypertensive disorder (Madazli, 2000).
many “isoforms” exist as discussed below. Examples include Using electron microscopy, De Wolf and coworkers (1980)
differences in maternal and fetal characteristics, placental find- examined arteries taken from the implantation site. They reported
ings, and hemodynamic findings (Phillips, 2010; Valensise, that early preeclamptic changes included endothelial damage,
2008; van der Merwe, 2010). insudation of plasma constituents into vessel walls, proliferation of
myointimal cells, and medial necrosis. Lipid accumulated first in
myointimal cells and then within macrophages. These lipid-laden
■ Etiology cell changes, shown in Figure 40-3, were referred to as atherosiss by
Writings describing eclampsia have been traced as far back as Hertig (1945). Nelson and colleagues (2014) completed placental
2200 bc (Lindheimer, 2014). And, an imposing number of examination in more than 1200 women with preeclampsia. These
mechanisms have been proposed to explain its cause. Those investigators reported that vascular lesions including spiral arteriole
currently considered important include: narrowing, atherosis, and infarcts were more common in placentas
1. Placental implantation with abnormal trophoblastic inva- from women diagnosed with preeclampsia before 34 weeks.
sion of uterine vessels Thus, the abnormally narrow spiral arteriolar lumen likely
2. Immunological maladaptive tolerance between maternal, impairs placental blood flow. McMahon and colleagues
paternal (placental), and fetal tissues (2014) have provided evidence that decreased soluble anti-
3. Maternal maladaptation to cardiovascular or inflammatory angiogenic growth factors may be involved in faulty endo-
changes of normal pregnancy vascular remodeling. Diminished perfusion and a hypoxic
4. Genetic factors including inherited predisposing genes and environment eventually lead to release of placental debriss or
epigenetic influences. microparticless that incite a systemic inflammatory response
(Lee, 2012; Redman, 2012). Fisher and Roberts (2014) have
provided an elegant review of the molecular mechanisms
Abnormal Trophoblastic Invasion involved in these interactions.
Normal implantation is characterized by extensive remodel- Defective placentation is posited to further cause the suscep-
ing of the spiral arterioles within the decidua basalis as shown tible (pregnant) woman to develop gestational hypertension, the
schematically in Figure 40-2 (Chap. 5, p. 93). Endovascular preeclampsia syndrome, preterm delivery, a growth-restricted
trophoblasts replace the vascular endothelial and muscular lin- fetus, and/or placental abruption (Brosens, 2011; Kovo, 2010;
ings to enlarge the vessel diameter. The veins are invaded only McElrath, 2008; Nelson, 2014). In addition, Staff and cowork-
superficially. In some cases of preeclampsia, however, there may ers (2013) have hypothesized that acute atherosis identifies a
be incomplete trophoblastic invasion. With this, decidual vessels, group of women at increased risk for later atherosclerosis and
but not myometrial vessels, become lined with endovascular cardiovascular disease.

Anchoring villi

Synccytiotrophoblast
Cytottrophoblast

Extravillous trophoblastts

Interstitial extravillous
trophoblast

Endovascular extravillo
ous
trophoblast Spiral arteries

NORMAL PREECLAMPSIA
FIGURE 40-2 Schematic representation of normal placental implantation shows proliferation of extravillous trophoblasts from an
anchoring villus. These trophoblasts invade the decidua and extend into the walls of the spiral arteriole to replace the endothelium and
muscular wall to create a dilated low-resistance vessel. With preeclampsia, there is defective implantation characterized by incomplete
invasion of the spiral arteriolar wall by extravillous trophoblasts. This results in a small-caliber vessel with high resistance to flow.
 Hypertensive Disorders 733

Area of endothelial
disruption

CHAPTER 40
Lu
ume
menn

Fibrin/plasma
prootein

Endothelial ce
ells
A B
Lipid-laden macrophages
FIGURE 40-3 Atherosis in a blood vessel from a placental bed. A. Photomicrograph shows disruption of the endothelium that results
in a narrowed lumen because of subendothelial accumulation of plasma proteins and foamy macrophages. Some of the foamy macro-
phages are shown by curved arrows,s and straight arrows highlight areas of endothelial disruption. B. Schematic diagram of the photomi-
crograph. (Modified from Rogers, 1999, with permission.)

Immunological Factors Redman and colleagues (2014) reviewed the possible role
Maternal immune tolerance to paternally derived placental of immune maladaptation in preeclampsia pathophysiology. In
and fetal antigens is discussed in Chapter 5 (p. 97). Loss of this women destined to be preeclamptic, extravillous trophoblasts
tolerance, or perhaps its dysregulation, is another theory cited early in pregnancy express reduced amounts of immunosup-
to account for preeclampsia syndrome (Erlebacher, 2013). pressive nonclassic HLA G. Black women more commonly
Certainly, the histological changes at the maternal-placental have the 1597ΔC allele that further predisposes to preeclampsia
interface are suggestive of acute graft rejection. Some of the (Loisel, 2013). Zhou and coworkers (2012b) have shown this
factors possibly associated with dysregulation include “immu- to be associated with high levels of placental oxidative prod-
nization” from a previous pregnancy, some inherited human ucts. These changes may contribute to defective placental vas-
leukocyte antigen (HLA) and natural killer (NK)-cell receptor cularization in stage 1 of the preeclampsia syndrome (p. 732).
haplotypes, and possibly shared susceptibility genes with diabe- Recall that as discussed in Chapter 4 (p. 56), during normal
tes and hypertension (Fukui, 2012; Ward, 2014). pregnancy, T-helper (Th) lymphocytes are produced so that
Inferential data also suggest preeclampsia to be an type 2 activity is increased in relation to type 1—termed type 2
immune-mediated disorder. For example, the risk of pre- biass (Redman, 2012, 2014). Th2 cells promote humoral immu-
eclampsia is appreciably enhanced in circumstances in which nity, whereas Th1 cells stimulate inflammatory cytokine secre-
formation of blocking antibodies to placental antigenic tion. Beginning in the early second trimester in women who
sites mightt be impaired. In this scenario, the first pregnancy develop preeclampsia, Th1 action is increased and the Th1/Th2
would carry a higher risk. Tolerance dysregulation might also ratio changes. Contributors to an enhanced immunologically
explain an increased risk when the paternal antigenic load is mediated inflammatory reaction are stimulated by placental
increased, that is, with two sets of paternal chromosomes— microparticless and by adipocytes (Redman, 2012, 2014).
a “double dose.” Namely, women with molar pregnancies
have a high incidence of early-onset preeclampsia. Women
with a trisomy 13 fetus also have a 30- to 40-percent inci- ■ Endothelial Cell Activation
dence of preeclampsia. These women have elevated serum In many ways, inflammatory changes are believed to be a con-
levels of antiangiogenic factors, and the gene for one of tinuation of the stage 1 changes caused by defective placenta-
these factors, sFlt-1, is on chromosome 13 (Bdolah, 2006). tion as discussed above. In response to placental factors released
Conversely, women previously exposed to paternal anti- by ischemic changes or by any other inciting cause, a cascade of
gens, such as a prior pregnancy with the samee partner, are events begins (Davidge, 2014). Thus, antiangiogenic and meta-
“immunized” against preeclampsia. This phenomenon is not bolic factors and other inflammatory mediators are thought to
as apparent in women with a prior abortion. Strickland and provoke endothelial cell injury.
associates (1986) studied more than 29,000 pregnancies at Endothelial cell dysfunction may result from an extreme
Parkland Hospital. These investigators reported that hyper- activated state of leukocytes in the maternal circulation (Faas,
tensive disorder rates were decreased in women who previ- 2000; Gervasi, 2001). Briefly, cytokines such as tumor necro-
ously had miscarried compared with nulligravidas. However, sis factor-α (TNF-α) and the interleukins (IL) may contrib-
the difference, although statistically significant, was not ute to the oxidative stress associated with preeclampsia. This is
great—22 versus 25 percent. Other studies have shown that characterized by reactive oxygen species and free radicals that
multiparas impregnated by a new consort have an increased lead to formation of self-propagating lipid peroxides (Manten,
risk of preeclampsia (Mostello, 2002). 2005). These in turn generate highly toxic radicals that injure
 734 Obstetrical Complications

endothelial cells, modify their nitric oxide production, and

TABLE 40-3. Genes with Possible Associations with
interfere with prostaglandin balance. Other consequences of
Preeclampsia Syndrome
oxidative stress include production of the lipid-laden macro-
phage foam cells seen in atherosis and shown in Figure 40-3; Gene (Polymorphism) Function Affected
SECTION 11

activation of microvascular coagulation manifest by thrombo- MTHFR (C677T) Methylene tetrahydrofolate

cytopenia; and increased capillary permeability manifest by reductase
edema and proteinuria. F5 (Leiden) Factor VLeiden
These observations on the effects of oxidative stress in pre- AGT (M235T) Angiotensinogen
eclampsia have given rise to increased interest in the potential HLA (Various) Human leukocyte antigens
benefit of antioxidants to prevent preeclampsia. Unfortunately, NOS3 (Glu 298 Asp) Endothelial nitric oxide
dietary supplementation with vitamins E (α-tocopherol) and F2 (G20210A) Prothrombin (factor II)
C (ascorbic acid) to prevent preeclampsia has thus far proven ACE (I/DatIntron 16) Angiotensin-converting enzyme
unsuccessful (Task Force, 2013). This is discussed subsequently. CTLA4 Cytotoxic T-lymphocyte-
associated protein
LPL Lipoprotein lipase
■ Nutritional Factors SERPINE1 Serine peptidase inhibitor
John and colleagues (2002) showed that in the general pop-
ulation, a diet high in fruits and vegetables with antioxidant Data from Buurma, 2013; Staines-Urias, 2012; Ward, 2014.
activity is associated with decreased blood pressure. Zhang and
associates (2002) reported that the incidence of preeclampsia
was doubled in women whose daily intake of ascorbic acid was genes for Fas receptor, hypoxia-inducible factor-1α protein
less than 85 mg. These studies were followed by randomized (HIF-1α), IL-1β, lymphotoxin-α, transforming growth fac-
trials to study dietary supplementation. Villar and coworkers tor beta 3 (TGF-β3), apolipoprotein E (ApoE), and TNF-α
(2006) showed that calcium supplementation in populations have also been studied with varying results (Borowski, 2009;
with a low dietary calcium intakee had a small effect to lower Hefler, 2001; Jamalzei, 2013; Lachmeijer, 2001; Livingston,
perinatal mortality rates but no effect on preeclampsia inci- 2001; Wilson, 2009). Because of the heterogeneity of the pre-
dence (p. 748). According to the 2013 Task Force, in several eclampsia syndrome and especially of the other genetic and
trials, supplementation with the antioxidant vitamins C or E environmental factors that interact with its complex pheno-
showed no benefits. typic expression, it is doubtful that any onee candidate gene will
be found responsible. Indeed, Majander and associates (2013)
have linked preeclampsia predisposition to fetall genes on chro-
■ Genetic Factors mosome 18.
From a hereditary viewpoint, preeclampsia is a multifactorial,
polygenic disorder. In their comprehensive review, Ward and Other Genetic Variables
Taylor (2014) cite an incident risk for preeclampsia of 20 to An extensive list of other variables affect genotypic and pheno-
40 percent for daughters of preeclamptic mothers; 11 to 37 typic expression of the preeclampsia syndrome. Some include
percent for sisters of preeclamptic women; and 22 to 47 percent maternal and paternal genotypes, associated disorders, genomic
for twins. In a study by Nilsson and colleagues (2004) that ethnicity, gene-gene interactions, epigenetic phenomena, and
included almost 1.2 million Swedish births, there was a genetic gene-environmental interactions. Combinations of these are
component for gestational hypertension and for preeclampsia. infinite. Ethnoracial factors are important as discussed regard-
They also reported 60-percent concordance in monozygotic ing the high incidence of preeclampsia in African-American
female twin pairs. women. It may be that Latina women have a lower prevalence
The hereditary predisposition for preeclampsia likely is the because of interactions of American Indian and white race
result of interactions of literally hundreds of inherited genes— genes (Shahabi, 2013).
both maternal and paternal—that control myriad enzymatic
and metabolic functions throughout every organ system.
Plasma-derived factors may induce some of these genes in ■ Pathogenesis
preeclampsia (Mackenzie, 2012). Thus, the clinical manifesta-
tion in any given woman with the preeclampsia syndrome will Vasospasm
occupy a spectrum as previously discussed. In this regard, phe- The concept of vasospasm with preeclampsia was advanced
notypic expression will differ among similar genotypes depend- by Volhard (1918) based on his direct observations of small
ing on interactions with environmental factors (Yang, 2013). blood vessels in the nail beds, ocular fundi, and bulbar con-
junctivae. It was also surmised from histological changes seen
Candidate Genes in various affected organs (Hinselmann, 1924; Landesman,
Hundreds of genes have been studied for their possible associa- 1954). Endothelial activation causes vascular constriction with
tion with preeclampsia (Buurma, 2013; Ward, 2014). Several increased resistance and subsequent hypertension. At the same
of those that may have positive significant association with time, endothelial cell damage causes interstitial leakage through
preeclampsia are listed in Table 40-3. Polymorphisms of the which blood constituents, including platelets and fibrinogen,
 Hypertensive Disorders 735

are deposited subendothelially. Wang and associates (2002) is decreased in preeclampsia. This action appears to be medi-
have also demonstrated disruption of endothelial junctional ated by phospholipase A2 (Davidge, 2014). At the same time,
proteins. Suzuki and coworkers (2003) described ultrastruc- thromboxane A2 secretion by platelets is increased, and the

CHAPTER 40
tural changes in the subendothelial region of resistance arter- prostacyclin:thromboxane A2 ratio decreases. The net result
ies in preeclamptic women. The much larger venous circuit is favors increased sensitivity to infused angiotensin II and,
similarly involved, and with diminished blood flow because of ultimately, vasoconstriction (Spitz, 1988). These changes are
maldistribution, ischemia of the surrounding tissues can lead to apparent as early as 22 weeks in women who later develop pre-
necrosis, hemorrhage, and other end-organ disturbances char- eclampsia (Chavarria, 2003).
acteristic of the syndrome. One important clinical correlate is
the markedly attenuated blood volume seen in women with Nitric Oxide
severe preeclampsia (Zeeman, 2009). This potent vasodilator is synthesized from l-arginine by endo-
thelial cells. Withdrawal of nitric oxide results in a clinical picture
similar to preeclampsia in a pregnant animal model (Conrad,
■ Endothelial Cell Injury 1989). Inhibition of nitric oxide synthesis increases mean arte-
As discussed on page 733, during the past two decades, endo- rial pressure, decreases heart rate, and reverses the pregnancy-
thelial cell injury has become the centerpiece in the contem- induced refractoriness to vasopressors. In humans, nitric oxide
porary understanding of preeclampsia pathogenesis (Davidge, likely is the compound that maintains the normal low-pressure
2014). In this scheme, protein factor(s)—likely placental—are vasodilated state characteristic of fetoplacental perfusion (Myatt,
secreted into the maternal circulation and provoke activation 1992; Weiner, 1992). It also is produced by fetal endothelium,
and dysfunction of the vascular endothelium. Many of the fac- and here it is increased in response to preeclampsia, diabetes,
ets of the clinical syndrome of preeclampsia are thought to result and sepsis (Parra, 2001; von Mandach, 2003).
from these widespread endothelial cell changes. Grundmann The effects of nitric oxide production in preeclampsia are
and associates (2008) have reported that circulating endothelial unclear (Davidge, 2014). It appears that the syndrome is asso-
cell—CEC—levels
C are elevated fourfold in the peripheral blood ciated with decreased endothelial nitric oxide synthase expres-
of preeclamptic women. Similarly, Petrozella and colleagues sion, thus increasing nitric oxide inactivation. These responses
(2012) demonstrated increased levels of circulating endothelial may be race related, with African-American women producing
microparticles—EMPs—in preeclamptic women. more nitric oxide (Wallace, 2009).
Intact endothelium has anticoagulant properties, and endo-
thelial cells blunt the response of vascular smooth muscle to
agonists by releasing nitric oxide. Damaged or activated endo-
■ Endothelins
thelial cells may produce less nitric oxide and secrete substances These 21-amino acid peptides are potent vasoconstrictors,
that promote coagulation and increase sensitivity to vasopres- and endothelin-1 (ET-1) is the primary isoform produced by
sors (Gant, 1974). Further evidence of endothelial activation human endothelium (George, 2011). Plasma ET-1 levels are
includes the characteristic changes in glomerular capillary increased in normotensive pregnant women, but women with
endothelial morphology, increased capillary permeability, and preeclampsia have even higher levels (Ajne, 2003; Clark, 1992).
elevated blood concentrations of substances associated with According to Taylor and Roberts (1999), the placenta is not
endothelial activation. These latter substances are transferable, the source of increased ET-1 concentrations, and they likely
and serum from women with preeclampsia stimulates some of arise from systemic endothelial activation. Interestingly, treat-
these substances in greater amounts. It seems likely that mul- ment of preeclamptic women with magnesium sulfate lowers
tiple factors in plasma of preeclamptic women combine to have ET-1 concentrations (Sagsoz, 2003).
these vasoactive effects (Myers, 2007; Walsh, 2009).

Increased Pressor Responses ■ Angiogenic and Antiangiogenic Proteins

As discussed in Chapter 4 (p. 61), pregnant women normally Placental vasculogenesis is evident by 21 days after concep-
tion. There is an ever-expanding list of pro- and antiangio-
develop refractoriness to infused vasopressors (Abdul-Karim,
genic substances involved in placental vascular development.
1961). Women with early preeclampsia, however, have increased
The families of vascular endothelial growth factor (VEGF) and
vascular reactivity to infused norepinephrine and angiotensin II
angiopoietin (Ang) are most extensively studied. Angiogenic
(Raab, 1956; Talledo, 1968). Moreover, increased sensitivity to
imbalancee is used to describe excessive amounts of antiangio-
angiotensin II clearly precedes the onset of gestational hyperten-
genic factors that are hypothesized to be stimulated by wors-
sion (Gant, 1974).
ening hypoxia at the uteroplacental interface. Trophoblast of
Prostaglandins women destined to develop preeclampsia overproduces at least
two antiangiogenic peptides that enter the maternal circulation
Several prostanoids are thought to be central to preeclampsia
(Karumanchi, 2014):
syndrome pathophysiology. Specifically, the blunted pressor
response seen in normal pregnancy is at least partially due 1. Soluble Fms-like tyrosine kinase 1 (sFlt-1) is a variant of
to decreased vascular responsiveness mediated by endothelial the Flt-1 receptor for placental growth factor (PlGF) and
prostaglandin synthesis. For example, compared with nor- for VEGF. Increased maternal sFlt-1 levels inactivate and
mal pregnancy, endothelial prostacyclin (PGI2) production decrease circulating free PlGF and VEGF concentrations,
 736 Obstetrical Complications

1600 and hypoxia genes (Karumanchi, 2014). Clinical research is

PE directed at use of antiangiogenic proteins in the prediction and
sFlt-1
Concentration (pg/mL) diagnosis of preeclampsia. In a systematic review, Widmer and
NT
associates (2007) concluded that third-trimester elevation of
SECTION 11

1400 sFlt-1 levels and decreased PlGF concentrations correlate with

preeclampsia development after 25 weeks. These results require
verification in prospective studies. Subsequently, Haggerty and
coworkers (2012) reported that doubling of expressions of
1200 sFlt-1 and sEng increased the preeclampsia risk 39 and 74 per-
cent, respectively.

1000 PATHOPHYSIOLOGY
8–12 15–18 23–26
Although the cause of preeclampsia remains unknown, evidence
for its manifestation begins early in pregnancy with covert
400
pathophysiological changes that gain momentum across gesta-
PlGF NT
tion and eventually become clinically apparent. Unless deliv-
Concentration (pg/mL)

300 ery supervenes, these changes ultimately result in multiorgan

involvement with a clinical spectrum ranging from an attenu-
PE
ated manifestation to one of cataclysmic deterioration that is
200
life threatening for both mother and fetus. As discussed, these
are thought to be a consequence of endothelial dysfunction,
100 vasospasm, and ischemia. Although the many maternal conse-
quences of the preeclampsia syndrome are usually described in
terms of individual organ systems, they frequently are multiple,
0 and they overlap clinically.
8–12 15–18 23–26
Weeks’ gestation
FIGURE 40-4 Angiogenic and antiangiogenic factors in normoten- ■ Cardiovascular System
sive (NT) and preeclamptic (PE) women across pregnancy. Both Severe disturbances of normal cardiovascular function are com-
pairs of factors are significantly divergent by 23 to 26 weeks. mon with preeclampsia syndrome. These are related to: (1)
sFlt = soluble Fms-like tyrosine kinase 1; PlGF = placental growth increased cardiac afterload caused by hypertension; (2) cardiac
factor. (Data from Myatt, 2013.)
preload, which is affected negatively by pathologically dimin-
ished hypervolemia of pregnancy and is increased by intravenous
leading to endothelial dysfunction (Maynard, 2003). As crystalloid or oncotic solutions; and (3) endothelial activation
shown in Figure 40-4, sFlt-1 levels begin to increase in with interendothelial extravasation of intravascular fluid into
maternal serum months before preeclampsia is evident. the extracellular space and importantly, into the lungs.
Haggerty and colleagues (2012) observed that these high
Hemodynamic Changes and Cardiac Function
levels in the second trimester were associated with a dou-
bling of the risk for preeclampsia. This divergence from The cardiovascular aberrations of pregnancy-related hyperten-
normal levels appears to occur even sooner with early-onset sive disorders vary depending on several modifiers. These fac-
preeclampsia (Vatten, 2012). tors include hypertension severity, underlying chronic disease,
2. Soluble endoglin (sEng) is a placenta-derived 65-kDa mol- preeclampsia severity, and in which part of the clinical spectrum
ecule that blocks endoglin, which is a surface coreceptor these are studied. In some women, these cardiovascular changes
for the TGFβ family. Also called CD105, this soluble may precede hypertension onset (De Paco, 2008; Easterling,
form of endoglin inhibits various TGFβ isoforms from 1990; Khalil, 2012; Melchiorre, 2013). Nevertheless, with the
binding to endothelial receptors and results in decreased clinical onset of preeclampsia, cardiac output declines, due at
endothelial nitric oxide-dependent vasodilatation (Levine, least in part to increased peripheral resistance. When assess-
2006; Venkatesha, 2006). Serum levels of sEng also begin ing cardiac function in preeclampsia, consideration is given to
to increase months before clinical preeclampsia develops echocardiographic measures of myocardial function and to clini-
(Haggerty, 2012). cally relevant ventricular function.

The cause of placental overproduction of antiangiogenic Myocardial Function. Serial echocardiographic studies have
proteins remains an enigma. Concentrations of the soluble documented in preeclampsia evidence for ventricular remod-
forms are not increased in the fetal circulation or amnionic eling that is accompanied by diastolic dysfunction in 40 per-
fluid, and their levels in maternal blood dissipate after deliv- cent of women (Melchiorre, 2012). In some of these women,
ery (Staff, 2007). Research currently is focused on immuno- functional differences persisted up to 16 months after delivery
logical mechanisms, oxidative stress, mitochondrial pathology, (Evans, 2011). Ventricular remodeling was judged to be an
 Hypertensive Disorders 737

120 Ventricular function studies of preeclamptic women from

several investigations are shown in Figure 40-6. Although car-
110 Hyperdynamic diac function was hyperdynamic in all women, filling pres-

CHAPTER 40
100 sures were dependent on the volume of intravenous fluids.
Specifically, aggressive hydration resulted in overtly hyper-
90 dynamic ventricular function in most women. However, this
LVSWI (g·m·m–2)

80 Normal was accompanied by elevated pulmonary capillary wedge pres-

sures. In some of these women, pulmonary edema may develop
70 despite normal ventricular function because of an alveolar
endothelial-epithelial leak. This is compounded by decreased
60
oncotic pressure from a low serum albumin concentration
50 (American College of Obstetricians and Gynecologists, 2012b).
Depressed
Thus, increased cardiac output and hyperdynamic ventricu-
40 lar function is largely a result of low wedge pressures and not a
30
result of augmented myocardial contractility. By comparison,
women given appreciably larger volumes of fluid commonly
0 had filling pressures that exceeded normal, but their ventricu-
0 5 10 15 20 25 30
lar function remained hyperdynamic because of concomitantly
PCWP (mm Hg)
increased cardiac output.
FIGURE 40-5 Ventricular function in normally pregnant women From these studies, it is reasonable to conclude that aggres-
(striped area) and in women with eclampsia (boxed area) is sive fluid administration to otherwise normal women with
plotted on a Braunwald ventricular function curve. Normal values severe preeclampsia substantially elevates normal left-sided
are from Clark, 1989, and those for eclampsia are from Hankins, filling pressures and increases a physiologically normal cardiac
1984. LVSWI = left ventricular stroke work index; PCWP = pulmo-
nary capillary wedge pressure.
output to hyperdynamic levels.

Blood Volume
adaptive response to maintain normal contractility with the For nearly 100 years, hemoconcentration has been a hallmark
increased afterload of preeclampsia. In the otherwise healthy of eclampsia. This was not precisely quantified until Zeeman
pregnant woman, these changes are usually clinically incon- and colleagues (2009) expanded the previous observations
sequential. But when combined with
underlying ventricular dysfunction—for 120
example, concentric ventricular hypertro-
phy from chronic hypertension—further 110 Hyperdynamic Hyperdyna
Hy
ype
erd
rdy
yyna
namic
na
n
diastolic dysfunction may cause cardio-
genic pulmonary edema as discussed in 100
Chapters 47 (p. 943) and 49 (p. 990). 90
)

Ventricular Function. Despite the rela-

−2

80 Normal
Normal
LVSWI (g·m·m

tively high frequency of diastolic dysfunc-

tion with preeclampsia, in most women 70
clinical cardiac function is appropriate.
60
This has been shown by several studies in
L

which ventricular function was assessed 50

using invasive hemodynamic methods
Depressed Depressed
(Hibbard, 2014). Importantly, both nor- 40
mally pregnant women and those with
30
preeclampsia syndrome can have normal
or slightly hyperdynamic ventricular func- 0
tion (Fig. 40-5). Thus, both have a cardiac 0 5 10 15 20 25 30 0 5 10 15 20 25 30
output that is appropriate for left-sided PCWP (mm Hg) PCWP (mm Hg)
A B
filling pressures. Data from preeclamptic
women obtained by invasive hemody- FIGURE 40-6 Ventricular function in women with severe preeclampsia–eclampsia plot-
namic studies are confounded because ted on the Braunwald ventricular function curve. The pulmonary capillary wedge pres-
of the heterogeneity of populations and sures (PCWP) are lower in those managed with restricted fluid administration (striped
area in A) compared with women managed with aggressive fluid therapy (striped area
interventions that also may significantly in B). In those managed with aggressive fluid infusions, eight developed pulmonary
alter these measurements. Some of these edema despite normal to hyperdynamic ventricular function in all but one. LVSWI = left
are crystalloid infusions, antihypertensive ventricular stroke work index. (Data for A from Benedetti, 1980; Hankins, 1984; data for
agents, and magnesium sulfate. B from Rafferty, 1980; Phelan, 1982.)
 738 Obstetrical Complications

of Pritchard and associates (1984) and 6000 a

showed in eclampticc women that the nor- b c
mally expected hypervolemia is severely d
5000
curtailed (Fig. 40-7). Women of average
SECTION 11

b
d
size should have a blood volume of nearly

Blood volume (mL)

4500 mL during the last several weeks 4000 c Nonpregnant
a
of a normal pregnancy. In nonpregnant 1st pregnancy
Subsequent
women, this volume approximates only 3000
pregnancy
3000 mL. With eclampsia, however, much
or all of the anticipated normal excess 1500 2000
mL is lost. Such hemoconcentration results
from generalized vasoconstriction that fol-
lows endothelial activation and leakage of 1000
plasma into the interstitial space because
of increased permeability. In women with 0
preeclampsia, and depending on its sever- (n = 44) (n = 29) (n = 14)
ity, hemoconcentration is usually not as Normal Eclamptic women
marked. Women with gestational hyper- controls
tension, but without preeclampsia, usually FIGURE 40-7 The two bar graphs on the left compare mean blood volumes in non-
have a normal blood volume (Silver, 1998). pregnant and term normally pregnant women. On the right, graphs display values for a
For women with severe hemoconcen- group of 29 women with eclampsia and their nonpregnant values. The red bar reflects
tration, it was once taught that an acute values for a subset of 14 who had a subsequent normotensive pregnancy. Extensions
above bars represent one standard deviation. Comparison between values with identical
fall in hematocrit suggested resolution lowercase letters, that is, a-a, b-b, c-c, d-d, are significant p < .001. (Data from Zeeman,
of preeclampsia. In this scenario, hemo- 2009, with permission.)
dilution follows endothelial healing with
return of interstitial fluid into the intravascular space. Although defined by a platelet count < 100,000/μL—indicates severe dis-
this is somewhat correct, it is important to recognize that a sub- ease (see Table 40-2). In general, the lower the platelet count,
stantive cause of this fall in hematocrit is usually the consequence the higher the rates of maternal and fetal morbidity and mortal-
of blood loss at deliveryy (Chap. 41, p. 783). It may also partially ity (Leduc, 1992). In most cases, delivery is advisable because
result from increased erythrocyte destruction as subsequently thrombocytopenia usually continues to worsen. After delivery,
described. Vasospasm and endothelial leakage of plasma may the platelet count may continue to decline for the first day or
persist for a variable time after delivery as the endothelium so. It then usually increases progressively to reach a normal level
is restored to normalcy. As this takes place, vasoconstriction within 3 to 5 days. As discussed on page 768, in some instances
reverses, and as the blood volume increases, the hematocrit usu- with HELLP syndrome, the platelet count continues to fall after
ally falls. Thus, women with eclampsia: delivery. If these do not reach a nadir until 48 to 72 hours, then
preeclampsia syndrome may be incorrectly attributed to one of
• Are unduly sensitive to vigorous fluid therapy administered
the thrombotic microangiopathies (George, 2013). These syn-
in an attempt to expand the contracted blood volume to nor-
dromes are discussed in Chapter 56 (p. 1116).
mal pregnancy levels
• Are sensitive to amounts of blood loss at delivery that are Other Platelet Abnormalities
considered normal for a normotensive woman.
In addition to thrombocytopenia, there are myriad other plate-
let alterations described with the preeclampsia syndrome. These
■ Hematological Changes were reviewed by Kenny and coworkers (2014) and include
Several hematological abnormalities are associated with the platelet activation with increased α-degranulation produc-
preeclampsia syndrome. Among those commonly identified is ing β-thromboglobulin, factor 4, and increased clearance.
thrombocytopenia, which at times may become severe enough Paradoxically, in most studies, in vitro platelet aggregation is
to be life threatening. Occasionally, the levels of some plasma decreased compared with the normal increase characteristic
clotting factors may be decreased, and erythrocytes display of pregnancy. This likely is due to platelet “exhaustion” fol-
abnormal morphology and undergo rapid hemolysis. lowing in vivo activation. Although the cause is unknown,
immunological processes or simply platelet deposition at sites
Thrombocytopenia of endothelial damage may be implicated. Platelet-bound and
Decreased platelet concentrations with eclampsia were described circulating platelet-bindable immunoglobulins are increased,
as early as 1922 by Stancke. The platelet count is routinely mea- which suggest platelet surface alterations.
sured in women with any form of gestational hypertension. The
frequency and intensity of thrombocytopenia vary and are depen- Neonatal Thrombocytopenia
dent on the severity and duration of the preeclampsia syndrome Severe thrombocytopenia does not develop in the fetus or infant
and the frequency with which platelet counts are performed born to preeclamptic women despite severe maternal throm-
(Heilmann, 2007; Hupuczi, 2007). Overt thrombocytopenia— bocytopenia (Kenny, 2014; Pritchard, 1987). Importantly,
 Hypertensive Disorders 739

maternal thrombocytopenia in hypertensive women is not a fetal further complex shifts with the preeclampsia syndrome. In
indication for cesarean delivery. addition to blood volume changes shown in Figure 40-7, there
are many hormonal, fluid, and electrolyte aberrations.
Hemolysis

CHAPTER 40
Severe preeclampsia is frequently accompanied by evidence of Endocrine Changes
hemolysis as manifest by elevated serum lactate dehydrogenase Plasma levels of renin, angiotensin II, I angiotensin 1–7, aldoste-
levels and decreased haptoglobin levels. Other evidence comes rone, and atrial natriuretic peptidee are substantively increased
from schizocytosis, spherocytosis, and reticulocytosis in periph- during normal pregnancy. Deoxycorticosterone (DOC) is a
eral blood (Cunningham, 1985; Pritchard, 1954, 1976). These potent mineralocorticoid that is also increased remarkably in
derangements result in part from microangiopathic hemolysis normal pregnancy (Chap. 4, p. 71). This compound results
caused by endothelial disruption with platelet adherence and from conversion of plasma progesterone to DOC rather than
fibrin deposition. Sanchez-Ramos and colleagues (1994) described increased maternal adrenal secretion. Because of this, DOC
increased erythrocyte membrane fluidity with HELLP syndrome. secretion is not reduced by sodium retention or hypertension.
Cunningham and coworkers (1995) postulated that these changes This may explain why women with preeclampsia retain sodium
were due to serum lipid alterations, and Mackay and associates (Winkel, 1980). In pregnancy, the mineralocorticoid receptor
(2012) found substantively decreased long-chain fatty acid con- becomes less sensitive to aldosterone (Armanini, 2012).
tent in erythrocytes of preeclamptic women. Erythrocytic mem- Vasopressin levels are similar in nonpregnant, normally preg-
brane changes, increased adhesiveness, and aggregation may also nant, and preeclamptic women even though the metabolic
promote a hypercoagulable state (Gamzu, 2001). clearance is increased in the latter two (Dürr, 1999).
Atrial natriuretic peptide is released during atrial wall
HELLP Syndrome. Subsequent to reports of hemolysis and stretching from blood volume expansion, and it responds to
thrombocytopenia with severe preeclampsia, descriptions fol- cardiac contractility (Chap. 4, p. 61). Serum levels rise in
lowed that abnormally elevated serum liver transaminase levels pregnancy, and its secretion is further increased in women
were commonly found and were indicative of hepatocellular with preeclampsia (Borghi, 2000; Luft, 2009). Levels of its
necrosis (Chesley, 1978). Weinstein (1982) referred to this precursor—proatrial natriuretic peptide—are also increased in
combination of events as the HELLP syndrome—and this mon- preeclampsia (Sugulle, 2012).
iker now is used worldwide. Also, and as shown in Table 40-2,
facets of the HELLP syndrome are included in criteria that Fluid and Electrolyte Changes
differentiate severe from nonsevere preeclampsia. The HELLP
In women with severe preeclampsia, the volume of extracellu-
syndrome is discussed in further detail on page 742.
lar fluid, manifest as edema, is usually much greater than that
in normal pregnant women. The mechanism responsible for
■ Coagulation Changes pathological fluid retention is thought to be endothelial injury
Subtle changes consistent with intravascular coagulation, and (Davidge, 2014). In addition to generalized edema and pro-
less often erythrocyte destruction, commonly are found with teinuria, these women have reduced plasma oncotic pressure.
preeclampsia and especially eclampsia (Kenny, 2014). Some This reduction creates a filtration imbalance and further dis-
of these changes include increased factor VIII consumption, places intravascular fluid into the surrounding interstitium.
increased levels of fibrinopeptides A and B and of d-dimers, and Electrolyte concentrations do not differ appreciably in
decreased levels of regulatory proteins—antithrombin III and women with preeclampsia compared with those of normal
protein C and S. Except for thrombocytopenia discussed above, pregnant women. This may not be the case if there has been
coagulation aberrations generally are mild and are seldom clini- vigorous diuretic therapy, sodium restriction, or administration
cally significant (Kenny, 2014; Pritchard, 1984). Unless there of free water with sufficient oxytocin to produce antidiuresis.
is associated placental abruption, plasma fibrinogen levels do Following an eclamptic convulsion, the serum pH H and bicar-
not differ remarkably from levels found in normal pregnancy. bonatee concentration are lowered due to lactic acidosis and
Fibrin degradation products such as d-dimers are elevated only compensatory respiratory loss of carbon dioxide. The intensity
occasionally. Fibronectin, a glycoprotein associated with vascular of acidosis relates to the amount of lactic acid produced—
endothelial cell basement membrane, is elevated in women with metabolic acidosis—and the rate at which carbon dioxide is
preeclampsia (Brubaker, 1992). As preeclampsia worsens, so do exhaled—respiratory acidosis.
abnormal findings with thromboelastographyy (Pisani-Conway,
2013). Despite these changes, routine laboratory assessments ■ Kidney
of coagulation, including prothrombin time, activated partial
thromboplastin time, and plasma fibrinogen level, were found During normal pregnancy, renal blood flow and glomeru-
to be unnecessary in the management of pregnancy-associated lar filtration rate are increased appreciably (Chap. 4, p. 63).
hypertensive disorders (Barron, 1999). With development of preeclampsia, there may be a number
of reversible anatomical and pathophysiological changes. Of
clinical importance, renal perfusion and glomerular filtration
■ Volume Homeostasis are reduced. Levels that are much less than normal nonpreg-
The normal pregnancy-induced extra- and intracellular vol- nant values are infrequent and are the consequence of severe
ume increases that are accompanied by vasodilatation undergo disease.
 740 Obstetrical Complications

A small degree of decreased glomerular filtration may result protein:creatinine ratios that are below 130 to 150 mg/g,
from reduced plasma volume. Most of the decrement, however, that is, 0.13 to 0.15, indicate a low likelihood of proteinuria
is from increased renal afferent arteriolar resistance that may be exceeding 300 mg/day. Midrange ratios, that is, 300 mg/g or
elevated up to fivefold (Conrad, 2014; Cornelis, 2011). There 0.3 have poor sensitivity and specificity. Stout and colleagues
SECTION 11

are also morphological changes characterized by glomerular (2013) found that values < 0.08 or > 1.19 had negative- or
endotheliosiss blocking the filtration barrier. This is discussed positive-predictive values of 86 and 96 percent, respectively. At
further subsequently. Diminished filtration causes serum cre- this time, most recommend that with midrange ratio values,
atinine levels to rise to values seen in nonpregnant individuals, 24-hour protein excretion should be quantified.
that is, 1 mg/mL, and sometimes even higher (Lindheimer, There are several methods used to measure proteinuria,
2008a). Abnormal values usually begin to normalize 10 days or and none detect all of the various proteins normally excreted
later after delivery (Spaan, 2012a). (Nayeri, 2013). A more accurate method involves measurement
In most preeclamptic women, urine sodium concentration of albumin excretion. Albumin filtration exceeds that of larger
is elevated. Urine osmolality, urine:plasma creatinine ratio, globulins, and with glomerular disease such as preeclampsia,
and fractional excretion of sodium also indicate that a prerenal most of the protein in urine is albumin. There are test kits that
mechanism is involved. Kirshon and coworkers (1988) infused permit rapid measurement of urinary albumin:creatinine ratios
dopamine intravenously into oliguric women with preeclamp- in an outpatient setting (Kyle, 2008).
sia, and this renal vasodilator stimulated increased urine out- Although worsening or nephrotic-range proteinuria has been
put, fractional sodium excretion, and free water clearance. As considered by most to be a sign of severe disease, this does not
was shown in Figure 40-6, sodium-containing crystalloid infu- appear to be the case (Airoldi, 2007). Certainly, this concept
sion increases left ventricular filling pressure, and although oli- was not accepted by the 2013 Task Force. Finally, increasing
guria temporarily improves, rapid infusions may cause clinically proteinuria is more common in multifetal pregnancy compli-
apparent pulmonary edema. Intensive intravenous fluid therapy cated by preeclampsia (Zilberberg, 2013).
is not indicated as “treatment” for preeclamptic women with oli-
guria. Exceptions are diminished urine output from hemorrhage or Anatomical Changes
fluid loss from vomiting or fever. Sheehan and Lynch (1973) commonly found changes identifi-
Plasma uric acid concentration is typically elevated in pre- able at autopsy by light and electron microscopy in the kidneys
eclampsia. The elevation exceeds the reduction in glomerular of eclamptic women. Glomeruli are enlarged by approximately
filtration rate and likely is also due to enhanced tubular reab- 20 percent, they are “bloodless,” and capillary loops variably are
sorption (Chesley, 1945). At the same time, preeclampsia is dilated and contracted. Endothelial cells are swollen—termed
associated with diminished urinary excretion of calcium, glomerular capillary endotheliosiss by Spargo and associates (1959).
perhaps because of increased tubular reabsorption (Taufield, Endothelial cells are often so swollen that they block or partially
1987). Another possibility is from increased placental urate block the capillary lumens (Fig. 40-8). Homogeneous suben-
production compensatory to increased oxidative stress. dothelial deposits of proteins and fibrin-like material are seen.
Endothelial swelling may result from angiogenic factor “with-
Proteinuria drawal” caused by free angiogenic proteins complexing with the
As shown in Table 40-1, some degree of proteinuria will estab- circulating antiangiogenic protein receptor discussed on page
lish the diagnosis of preeclampsia syndrome. Proteinuria may 735 (Conrad, 2014; Eremina, 2007; Karumanchi, 2009). The
develop late, and some women may already be delivered or have angiogenic proteins are crucial for podocyte health, and their
had an eclamptic convulsion before it appears. For example, inactivation leads to podocyte dysfunction and endothelial swell-
10 to 15 percent of women with HELLP syndrome did not ing. One marker of this is excretion of podocyte proteins such as
have proteinuria at presentation (Sibai, 2004). In another nephrin, podocalyxin, and βig-h3 (transforming growth factor,
report, 17 percent of eclamptic women did not have protein- β-induced) (Wang, 2012b). Also, eclampsia is characterized by
uria by the time of seizures (Zwart, 2008). increased excretion of urinary podocytes, a phenomenon shared
Problematically, the optimal method of establishing abnor- by other proteinuric disorders (Garrett, 2013; Wagner, 2012).
mal levels of either urine protein or albumin remains to be Of interest, podocytes are epithelia, and thus renal pathology
defined. Chen and associates (2008) have shown that clean- involves both endothelial and epithelial cells (see Fig. 40-8).
catch and catheterized urine specimens correlate well. But
dipstick qualitative determinations depend on urinary concen- Acute Kidney Injury
tration and are notorious for false-positive and -negative results. Rarely is acute tubular necrosiss caused by preeclampsia alone.
For a 24-hour quantitative specimen, the “consensus” thresh- Although mild degrees are encountered in neglected cases, clin-
old value used is > 300 mg/24 h (Task Force, 2013). Tun and ically apparent renal failure is invariably induced by coexistent
colleagues (2012) have shown equivalent efficacy using protein hemorrhage with hypovolemia and hypotension (Chap. 41,
excretion of 165 mg in a 12-hour sample. Importantly, these p. 814). This is usually caused by severe obstetrical hemorrhage
values have not been irrefutably established. for which adequate blood replacement is not given. Drakeley
Determination of urinary protein:creatinine ratio may and coworkers (2002) described 72 women with preeclamp-
supplant the cumbersome 24-hour quantification (Ethridge, sia and renal failure. Half had HELLP syndrome, and a third
2013; Kyle, 2008; Morris, 2012). In a systematic review, had placental abruption. As discussed on page 742, Haddad
Papanna and associates (2008) concluded that random urine and colleagues (2000) reported that 5 percent of 183 women
 Hypertensive Disorders 741

Podocyte called shock liver (Alexander,

Foot process 2009).
Pedicel
Second, asymptomatic eleva-

CHAPTER 40
Narrow tions of serum hepatic transami-
interspace nase levels—AST and ALT—are
Endothelium also considered markers for severe
preeclampsia. Values seldom
Endothelial exceed 500 U/L, but have been
swelling reported to be greater than 2000
U/L in some women (Chap. 55,
p. 1085). In general, serum lev-
els inversely follow platelet levels,
Basement Endothelial and they both usually normalize
membrane fenestra Swollen fenestra within 3 days following deliv-
ery as previously discussed on
page 738.
NORMAL PREECLAMPSIA In a third example of liver
involvement, hemorrhagic infarc-
FIGURE 40-8 Schematic showing glomerular capillary endotheliosis. The capillary of the normal tion may extend to form a hepatic
glomerulus shown on the left has wide endothelial fenestrations, and the pedicels emanating hematoma. These in turn may
from the podocytes are widely spaced (arrow). The illustration on the right is of a glomerulus
with changes induced by the preeclampsia syndrome. The endothelial cells are swollen and their
extend to form a subcapsular
fenestrae narrowed, as are the pedicels that now abut each other. hematoma that may rupture. They
can be identified using computed
tomography (CT) scanning or
with HELLP syndrome had kidney injury. Half of these, how- magnetic resonance (MR) imaging as shown in Figure 40-10.
ever, also had a placental abruption, and most had postpartum Unruptured hematomas are probably more common than clini-
hemorrhage. Rarely, irreversible renal cortical necrosiss develops cally suspected and are more likely to be found with HELLP
(Chap. 53, p. 1064). syndrome (Carlson, 2004; Vigil-De Gracia, 2012). Although
once considered a surgical condition, contemporaneous manage-
ment usually consists of observation and conservative treatment of
■ Liver hematomas unless hemorrhage is ongoing. In some cases, however,
Hepatic changes in women with fatal eclampsia were described prompt surgical intervention may be lifesaving. Vigil-De Gracia
in 1856 by Virchow. The characteristic lesions were regions of and coworkers (2012) reviewed 180 cases of hepatic hematoma or
periportal hemorrhage in the liver periphery. In their elegant rupture. More than 90 percent had HELLP syndrome, and in 90
autopsy studies, Sheehan and Lynch (1973) described that percent, the capsule had ruptured. The maternal mortality rate was
some degree of hepatic infarction accompanied hemorrhage 22 percent, and the perinatal mortality rate was 31 percent. In rare
in almost half of women who died with eclampsia. These cor- cases, liver transplant is necessary (Hunter, 1995; Wicke, 2004).
responded with reports that had appeared during the 1960s Last, acute fatty liver of pregnancy is sometimes confused
describing elevated serum hepatic transaminase levels. Along with preeclampsia (Nelson, 2013; Sibai, 2007a). It too has
with the earlier observations by Pritchard and associates (1954), an onset in late pregnancy, and often there is accompanying
who described hemolysis and thrombocytopenia with eclamp-
sia, this constellation of hemolysis, hepatocellular necrosis,
and thrombocytopenia was later termed HELLP syndromee by
Weinstein (1985) to call attention to its seriousness (p. 742).
Lesions as extensive as those shown in Figure 40-9 are
unusual, even in the autopsy series by Sheehan and Lynch
(1973). From a pragmatic point, liver involvement with pre-
eclampsia may be clinically significant in several circumstances.
First, symptomatic involvement is considered a sign of severe
disease. It typically manifests by moderate to severe right-upper
quadrant or midepigastric pain and tenderness. In many cases,
such women also have elevated levels of serum aminotrans-
ferase, namely, aspartate aminotransferase (AST) or alanine
aminotransferase (ALT). In some cases, however, the amount
of hepatic tissue involved with infarction may be surprisingly
extensive yet still clinically insignificant. In our experiences, FIGURE 40-9 Gross liver specimen from a woman with preeclamp-
infarction may be worsened by hypotension from obstetrical sia who died from aspiration pneumonitis. Periportal hemorrhagic
hemorrhage, and it occasionally causes hepatic failure—so- necrosis was seen microscopically. (From Cunningham, 1993.)
 742 Obstetrical Complications

■ Pancreas
According to Sheehan and Lynch (1973), there are no con-
vincing data that the pancreas has special involvement with
SECTION 11

preeclampsia syndrome. If so, the occasional case reports

of concurrent hemorrhagic pancreatitis are likely unrelated
(Swank, 2012). That said, severe hemoconcentration may pre-
dispose to pancreatic inflammation.

■ Brain
Headaches and visual symptoms are common with severe pre-
eclampsia, and associated convulsions define eclampsia. The earliest
anatomical descriptions of brain involvement came from autopsy
specimens, but CT- and MR-imaging and Doppler studies have
added many important insights into cerebrovascular involvement.
Neuroanatomical Lesions
FIGURE 40-10 Abdominal CT imaging performed postpartum in Most gross anatomical descriptions of the brain in eclamptic
a woman with severe HELLP syndrome and right-upper quadrant
women are taken from eras when mortality rates were high.
pain. A large subcapsular hematoma (asterisk) is seen confluent
with intrahepatic infarction and hematoma (arrowhead). Numer- One consistent finding was that brain pathology accounted
ous flame-shaped hemorrhages are seen at the hematoma inter- for only about a third of fatal cases such as the one shown in
face (arrows). Figure 40-11. In fact, most deaths were from pulmonary edema,
and brain lesions were coincidental. Thus, although gross intra-
hypertension, elevated serum transaminase and creatinine lev- cerebral hemorrhage was seen in up to 60 percent of eclamp-
els, and thrombocytopenia (Chap. 55, p. 1086). tic women, it was fatal in only half of these (Melrose, 1984;
Richards, 1988; Sheehan, 1973). As shown in Figure 40-12,
HELLP Syndrome
other principal lesions found at autopsy of eclamptic women
There is no universally accepted strict definition of this syn- were cortical and subcortical petechial hemorrhages. The classic
drome, and thus its incidence varies by investigator. When microscopic vascular lesions consist of fibrinoid necrosis of the
it is identified, the likelihood of hepatic hematoma and rup- arterial wall and perivascular microinfarcts and hemorrhages.
ture is substantially increased. In a multicenter study, Haddad Other frequently described major lesions include subcortical
and colleagues (2000) described 183 women with HELLP edema, multiple nonhemorrhagic areas of “softening” through-
syndrome of whom 40 percent had adverse outcomes includ- out the brain, and hemorrhagic areas in the white matter. There
ing two maternal deaths. The incidence of subcapsular liver also may be hemorrhage in the basal ganglia or pons, often with
hematoma was 1.6 percent. Other complications included rupture into the ventricles.
eclampsia—6 percent, placental abruption—10 percent, acute
kidney injury—5 percent, and pulmonary edema—10 percent. Cerebrovascular Pathophysiology
Other serious complications included stroke, coagulopathy, Clinical, pathological, and neuroimaging findings have led
acute respiratory distress syndrome, and sepsis. to two general theories to explain cerebral abnormalities with
Women with preeclampsia complicated by the HELLP syn-
drome typically have worse outcomes than those without these
findings (Kozic, 2011; Martin, 2012, 2013). In their review
of 693 women with HELLP syndrome, Keiser and coworkers
(2009) reported that 10 percent had concurrent eclampsia. Sep
and associates (2009) also described a significantly increased
risk for complications in women with HELLP syndrome com-
pared with those with “isolated preeclampsia.” These included
eclampsia—15 versus 4 percent; preterm birth—93 versus
78 percent; and perinatal mortality rate—9 versus 4 percent,
respectively. Because of these marked clinical differences, these
investigators postulate that HELLP syndrome has a distinct
pathogenesis. Others have shown a difference in the ratio of
antiangiogenic and inflammatory acute-phase proteins in these
two conditions and have reached similar conclusions (Reimer,
2013). Given all of the variables contributing to the incidence
and pathophysiology of preeclampsia as discussed on page 736,
this is a reasonable conclusion. Sibai and Stella (2009) have
discussed some of these aspects under the rubric of “atypical FIGURE 40-11 This autopsy brain slice shows a fatal hyperten-
preeclampsia-eclampsia.” sive hemorrhage in a primigravida with eclampsia.
 Hypertensive Disorders 743

2004a). The most frequently affected region is

Pia-arachnoid the parietooccipital cortex—the boundary zone
of the anterior, middle, and posterior cerebral

CHAPTER 40
arteries. Also, in most cases, these lesions are
reversible (Cipolla, 2014).

Cortical Cerebral Blood Flow

Autoregulation is the mechanism by which
cerebral blood flow remains relatively constant
despite alterations in cerebral perfusion pres-
sure. In nonpregnant individuals, this mecha-
nism protects the brain from hyperperfusion
Subcortical when mean arterial pressures increase to as high
as 160 mm Hg. These are pressures far greater
than those seen in all but a very few women with
eclampsia. Thus, to explain eclamptic seizures,
it was theorized that autoregulation must be
Midbrain altered by pregnancy. Although species differ-
ences must be considered, studies by Cipolla and
FIGURE 40-12 Composite illustration showing location of cerebral hemorrhages colleagues (2007, 2009, 2014) have convincingly
and petechiae in women with eclampsia. Insert shows the level of the brain
shown that autoregulation is unchanged across
from which the main image was constructed. (Data from Sheehan, 1973.)
pregnancy in rodents. That said, some, but not
others, have provided evidence of impaired
eclampsia. Importantly, endothelial cell dysfunction that char- autoregulation in women with preeclampsia (Janzarik, 2014;
acterizes the preeclampsia syndrome likely plays a key role in van Veen, 2013).
both. The first theory suggests that in response to acute and Zeeman and associates (2003) showed that cerebral blood
severe hypertension, cerebrovascular overregulation leads to flow during the first two trimesters of normal pregnancy is
vasospasm (Trommer, 1988). This presumption is based on similar to nonpregnant values, but thereafter, it significantly
the angiographic appearance of diffuse or multifocal segmental decreases by 20 percent during the last trimester. These
narrowings suggestive of vasospasm (Ito, 1995). In this scheme, investigators also documented significantly increased cere-
diminished cerebral blood flow is hypothesized to result in bral blood flow in women with severe preeclampsia com-
ischemia, cytotoxic edema, and eventually tissue infarction. pared with that of normotensive pregnant women (Zeeman,
Although this theory was widely embraced for many years, 2004b). Taken together, these findings suggest that eclamp-
there is little objective evidence to support it. sia occurs when cerebral hyperperfusion forces capillary fluid
The second theory is that sudden elevations in systemic interstitially because of endothelial damage, which leads to
blood pressure exceed the normal cerebrovascular autoregu- perivascular edema characteristic of the preeclampsia syn-
latory capacity (Hauser, 1988; Schwartz, 2000). Regions of drome. In this regard, eclampsia is an example of the pos-
forced vasodilation and vasoconstriction develop, especially terior reversible encephalopathy syndrome as previously
in arterial boundary zones. At the capillary level, disruption discussed.
of end-capillary pressure causes increased hydrostatic pres-
sure, hyperperfusion, and extravasation of plasma and red cells Neurological Manifestations
through endothelial tight-junction openings. This leads to vaso- There are several neurological manifestations of the preeclamp-
genic edema. This theory is incomplete because very few eclamp- sia syndrome. Each signifies severe involvement and requires
tic women have mean arterial pressures that exceed limits of immediate attention. First, headache and scotomataa are thought
autoregulation—approximately 160 mm Hg. to arise from cerebrovascular hyperperfusion that has a predi-
It seems reasonable to conclude that the most likely mech- lection for the occipital lobes. According to Sibai (2005) and
anism is a combination of the two. Thus, a preeclampsia- Zwart and coworkers (2008), 50 to 75 percent of women have
associated interendothelial cell leak develops at blood pressure headaches and 20 to 30 percent have visual changes preced-
(hydraulic) levels much lower than those usually causing ing eclamptic convulsions. The headaches may be mild to
vasogenic edema and is coupled with a loss of upper-limit severe and intermittent to constant. In our experiences, they
autoregulation (Zeeman, 2009). With imaging studies, these are unique in that they do not usually respond to traditional
changes manifest as facets of the reversible posterior leukoen- analgesia, but they do improve after magnesium sulfate infu-
cephalopathy syndromee (Hinchey, 1996). This subsequently sion is initiated.
became referred to as the posterior reversible encephalopathy Convulsions are a second potential manifestation and are
syndrome—PRES. This term is misleading because although diagnostic for eclampsia. These are caused by excessive release
PRES lesions principally involve the posterior brain—the of excitatory neurotransmitters—especially glutamate; massive
occipital and parietal cortices—in at least a third of cases, depolarization of network neurons; and bursts of action poten-
they also involve other brain areas (Edlow, 2013; Zeeman, tials (Meldrum, 2002). Clinical and experimental evidence
 744 Obstetrical Complications

suggest that extended seizures can cause significant brain injury

and later brain dysfunction.
As a third manifestation, blindnesss is rare with preeclampsia
alone, but it complicates eclamptic convulsions in up to 15
SECTION 11

percent of women (Cunningham, 1995). Blindness has been

reported to develop up to a week or more following delivery
(Chambers, 2004). There are at least two types of blindness as
discussed subsequently.
Last, generalized cerebral edemaa may develop and is usually
manifest by mental status changes that vary from confusion
to coma. This situation is particularly dangerous because fatal
transtentorial herniation may result.

Neuroimaging Studies
With CT imaging, localized hypodense lesions at the gray-
and white-matter junction, primarily in the parietooccipital
lobes, are typically found in eclampsia. Such lesions may also FIGURE 40-14 Cranial magnetic resonance imaging performed
be seen in the frontal and inferior temporal lobes, the basal 3 days postpartum in a woman with eclampsia and HELLP syn-
ganglia, and thalamus (Brown, 1988). The spectrum of brain drome. Neurovisual defects persisted at 1 year, causing job dis-
ability. (From Murphy, 2005, with permission.)
involvement is wide, and increasing involvement can be iden-
tified with CT imaging. Edema of the occipital lobes or dif- f
fuse cerebral edema may cause symptoms such as blindness,
lethargy, and confusion (Cunningham, 2000). In the latter in women who have severe disease and who have neurological
cases, widespread edema shows as a marked compression or symptoms (Schwartz, 2000). And although usually reversible,
even obliteration of the cerebral ventricles. Such women may a fourth of these hyperintense lesions represent cerebral infarc-
develop signs of impending life-threatening transtentorial tions that have persistent findings (Loureiro, 2003; Zeeman,
herniation. 2004a).
Several MR imaging acquisitions are used to study eclamptic
women. Common findings are hyperintense T2 lesions—poste- Visual Changes and Blindness
rior reversible encephalopathy syndrome (PRES)—in the sub- Scotomata, blurred vision, or diplopia are common with
cortical and cortical regions of the parietal and occipital lobes severe preeclampsia and eclampsia. These usually improve with
(Fig. 40-13). There is also relatively common involvement of magnesium sulfate therapy and/or lowered blood pressure.
the basal ganglia, brainstem, and cerebellum (Brewer, 2013; Blindness is less common, is usually reversible, and may arise
Zeeman, 2004a). Although these PRES lesions are almost uni- from three potential areas. These are the visual cortex of the
versal in women with eclampsia, their incidence in women with occipital lobe, the lateral geniculate nuclei, and the retina. In
preeclampsia is less frequent. They are more likely to be found the retina, pathological lesions may be ischemia, infarction, or
detachment (Roos, 2012).
Occipital blindness is also called amaurosis—from
s the
Greek dimming. Affected women usually have evidence of
extensive occipital lobe vasogenic edema on imaging stud-
ies. Of 15 women cared for at Parkland Hospital, occipital
blindness lasted from 4 hours to 8 days, but it resolved com-
pletely in all cases (Cunningham, 1995). Rarely, extensive
cerebral infarctions may result in total or partial visual defects
(Fig. 40-14).
Blindness from retinal lesions is caused either by serous
retinal detachment or rarely by retinal infarction, which
is termed Purtscher retinopathyy (Fig. 40-15). Serous retinal
detachmentt is usually unilateral and seldom causes total visual
loss. In fact, asymptomatic serous retinal detachment is rela-
tively common (Saito, 1998). In most cases of eclampsia-
associated blindness, visual acuity subsequently improves,
but if caused by retinal artery occlusion, vision may be per-
manently impaired (Lara-Torre, 2002; Roos, 2012). In some
FIGURE 40-13 Cranial magnetic resonance imaging in a nullipara
women, these findings are additive. Moseman and Shelton
with eclampsia. Multilobe T2-FLAIR high-signal lesions are appar- (2002) described a woman with permanent blindness due to
ent. FLAIR = fluid-attenuated inversion recovery. (Image contrib- a combination of retinal infarctions and bilateral lesions in
uted by Dr. Gerda Zeeman.) the lateral geniculate nuclei.
 Hypertensive Disorders 745

CHAPTER 40
A B

FIGURE 40-15 Purtscher retinopathy caused by choroidal ischemia and infarction in preeclampsia syndrome. A. Ophthalmoscopy shows
scattered yellowish, opaque lesions of the retina (arrows). B. The late phase of fluorescein angiography shows areas of intense hyper-
fluorescence representing pooling of extravasated dye. (From Lam, 2001, with permission.)

Cerebral Edema rial systolic and diastolic velocity waveforms. By the completion
Clinical manifestations suggesting widespread cerebral edema of placentation, impedance to uterine artery blood flow is mark-
are worrisome. During 13 years at Parkland Hospital, 10 of edly decreased, but with abnormal placentation, abnormally high
175 women with eclampsia were diagnosed with symptomatic resistance persists (Everett, 2012; Ghidini, 2008; Napolitano,
cerebral edema (Cunningham, 2000). Symptoms ranged from 2012). Earlier studies were done to assess this by measuring
lethargy, confusion, and blurred vision to obtundation and peak systolic:diastolic velocity ratios from uterine and umbilical
coma. In most cases, symptoms waxed and waned. Mental arteries in preeclamptic pregnancies. The results were interpreted
status changes generally correlated with the degree of involve- as showing that in some cases, but certainly not all, there was
ment seen with CT and MR imaging studies. These women increased resistance (Fleischer, 1986; Trudinger, 1990).
are very susceptible to sudden and severe blood pressure eleva- Another Doppler waveform—uterine artery “notching”—
tions, which can acutely worsen the already widespread vasogenic has been reported to be associated with increased risks for
edema. Thus, careful blood pressure control is essential. In the preeclampsia or fetal-growth restriction (Groom, 2009). In
10 women with generalized edema, three became comatose the MFMU Network study reported by Myatt and colleagues
and had imaging findings of impending transtentorial hernia- (2012a), however, notching had a low predictive value except
tion. One of these three died from herniation. Consideration for early-onset severe disease.
is given for treatment with mannitol or dexamethasone. Matijevic and Johnson (1999) measured resistance in uterine
spiral arteries. Impedance was higher in peripheral than in cen-
Long-Term Neurocognitive Sequelae tral vessels—a so-called ring-like distribution. Mean resistance
Women with eclampsia have been shown to have some cogni- was higher in all women with preeclampsia compared with
tive decline when studied 5 to 10 years following an eclamptic that in normotensive controls. Ong and associates (2003) used
pregnancy. This is discussed further on page 770. MR imaging and other techniques to assess placental perfusion
ex vivo in the myometrial arteries removed from women with
preeclampsia or fetal-growth restriction. These investigators
■ Uteroplacental Perfusion confirmed that in both conditions myometrial arteries exhib-
Defects in endovascular trophoblastic invasion and placenta- ited endothelium-dependent vasodilatory response. Moreover,
tion germane to development of the preeclampsia syndrome other pregnancy conditions are also associated with increased
and fetal-growth restriction were discussed on page 732. Of resistance (Urban, 2007). One major adverse effect, fetal-
immense clinical importance, compromised uteroplacental growth restriction, is discussed in Chapter 44 (p. 874).
perfusion is almost certainly a major culprit in the increased Pimenta and colleagues (2013) assessed placental vascular-
perinatal morbidity and mortality rates. Thus, measurement ity using a three-dimensional power Doppler histogram. These
of uterine, intervillous, and placental blood flow would likely researchers described the placental vascularity index, which was
be informative. Attempts to assess these in humans have been decreased in women with any pregnancy-associated hyperten-
hampered by several obstacles that include inaccessibility of the sive disorders—11.1 percent compared with 15.2 percent in
placenta, the complexity of its venous effluent, and the need for normal controls.
radioisotopes or invasive techniques. Despite these findings, evidence for compromised uteropla-
Measurement of uterine artery blood flow velocity has been cental circulation is found in only a few women who go on
used to estimate resistance to uteroplacental blood flow (Chap. to develop preeclampsia. Indeed, when preeclampsia develops
17, p. 345). Vascular resistance is estimated by comparing arte- during the third trimester, only a third of women with severe
 746 Obstetrical Complications

disease have abnormal uterine artery velocimetry (Li, 2005). In Vascular Resistance Testing and
a study of 50 women with HELLP syndrome, only a third had Placental Perfusion
abnormal uterine artery waveforms (Bush, 2001). In general, Most of these are cumbersome, time consuming, and overall
the extent of abnormal waveforms correlates with severity of
SECTION 11

inaccurate.
fetal involvement (Ghidini, 2008; Groom, 2009).
Provocative Pressor Tests. Three tests have been exten-
sively evaluated to assess the blood pressure rise in response to a
PREDICTION AND PREVENTION stimulus. The roll-over testt measures the hypertensive response in
women at 28 to 32 weeks who are resting in the left lateral decu-
■ Prediction bitus position and then roll over to the supine position. Increased
Measurement during early pregnancy—or across pregnancy— blood pressure signifies a positive test. The isometric exercise test
of various biological, biochemical, and biophysical markers employs the same principle by squeezing a handball. The angioten-
implicated in preeclampsia syndrome pathophysiology has sin II infusion testt is performed by giving incrementally increasing
been proposed to predict its development. Attempts have been doses intravenously, and the hypertensive response is quantified.
made to identify early markers of faulty placentation, impaired In their updated metaanalysis, Conde-Agudelo and associates
placental perfusion, endothelial cell activation and dysfunction, (2014) found sensitivities of all three tests to range from 55 to
and activation of coagulation. For the most, these have resulted 70 percent, and specificities approximated 85 percent.
in testing strategies with poor sensitivity and with poor positive-
predictive value for preeclampsia (Conde-Agudelo, 2014; Uterine Artery Doppler Velocimetry. Faulty trophoblas-
Lindheimer, 2008b; Odibo, 2013). Currently, no screening tests tic invasion of the spiral arteries, which is depicted in Figure
are predictably reliable, valid, and economical (Kleinrouweler, 40-2, results in diminished placental perfusion and upstream
2012). There are, however, combinations of tests, some yet to increased uterine artery resistance. Increased uterine artery
be adequately evaluated, that may be promising (Dugoff, 2013; velocimetry determined by Doppler ultrasound in the first two
Kuc, 2011; Navaratnam, 2013; Olsen, 2012). trimesters should provide indirect evidence of this process and
The list of predictive factors evaluated during the past three thus serve as a predictive test for preeclampsia (Gebb, 2009a,b;
decades is legion. Although most have been evaluated in the first Groom, 2009). As described on page 745 and in Chapter 10
half of pregnancy, some have been tested as predictors of sever- (p. 220), increased flow resistance results in an abnormal waveform
ity in the third trimester (Chaiworapongsa, 2013; Mosimann, represented by an exaggerated diastolic notch. These have value for
2013; Rana, 2012). Others have been used to forecast recurrent fetal-growth restriction but not preeclampsia (American College
preeclampsia (Demers, 2014). Some of these tests are listed in of Obstetricians and Gynecologists, 2013a). Several flow velocity
Table 40-4, which is by no means all inclusive. Conde-Agudelo waveforms—alone or in combination—have been investigated
and coworkers (2014) have recently provided a thorough review for preeclampsia prediction. In some of these, predictive values
of many of these testing strategies. for early-onset preeclampsia were promising (Herraiz, 2012).

TABLE 40-4. Predictive Tests for Development of the Preeclampsia Syndrome

Testing Related To: Examples
Placental perfusion/ Roll-over test, isometric handgrip or cold pressor test, pressor response to aerobic exercise,
vascular resistance angiotensin-II infusion, midtrimester mean arterial pressure, platelet angiotensin-II binding,
renin, 24-hour ambulatory blood pressure monitoring, uterine artery or fetal transcranial
Doppler velocimetry
Fetal-placental unit Human chorionic gonadotropin (hCG), alpha-fetoprotein (AFP), estriol, pregnancy-associated
endocrine dysfunction protein A (PAPP A), inhibin A, activin A, placental protein 13, corticotropin-releasing
hormone, A disintegrin, ADAM-12, kisspeptin
Renal dysfunction Serum uric acid, microalbuminuria, urinary calcium or kallikrein, microtransferrinuria,
N-acetyl-β-glucosaminidase, cystatin C, podocyturia
Endothelial dysfunction/ Platelet count and activation, fibronectin, endothelial adhesion molecules, prostaglandins,
oxidant stress prostacyclin, MMP-9, thromboxane, C-reactive protein, cytokines, endothelin, neurokinin B,
homocysteine, lipids, insulin resistance, antiphospholipid antibodies, plasminogen activator-
inhibitor (PAI), leptin, p-selectin, angiogenic factors such as placental growth factor (PlGF),
vascular endothelial growth factor (VEGF), fms-like tyrosine kinase receptor-1 (sFlt-1), endoglin
Others Antithrombin-III(AT-3), atrial natriuretic peptide (ANP), β2-microglobulin, haptoglobin,
transferrin, ferritin, 25-hydroxyvitamin D, genetic markers, cell-free fetal DNA, serum and
urine proteomics and metabolomic markers, hepatic aminotransferases

ADAM12 = ADAM metallopeptidase domain 12; MMP = matrix metalloproteinase.

Adapted from Conde-Agudelo, 2014.
 Hypertensive Disorders 747

At this time, however, none is suitable for clinical use (Conde- Oxidative Stress. Increased levels of lipid peroxides coupled
Agudelo, 2014; Kleinrouweler, 2012; Myatt, 2012a). with decreased antioxidant activity have raised the possibility
that markers of oxidative stress might predict preeclampsia.
Pulse Wave Analysis. Like the uterine artery, finger arte-

CHAPTER 40
For example, malondialdehyde is a marker of lipid peroxida-
rial pulse “stiffness” is an indicator of cardiovascular risk. tion. Other markers are various prooxidants or their potentia-
Investigators have preliminarily evaluated its usefulness in pre- tors. These include iron, transferrin, and ferritin; blood lipids,
eclampsia prediction (Vollebregt, 2009). including triglycerides, free fatty acids, and lipoproteins; and
antioxidants such as ascorbic acid and vitamin E (Bainbridge,
Fetal-Placental Unit Endocrine Function
2005; Conde-Agudelo, 2014; Mackay, 2012; Powers, 2000).
Several serum analytes that have been proposed to help predict These have not been found to be predictive, and treatment to
preeclampsia are shown in Table 40-4. Newer ones are contin- prevent preeclampsia with some of them has been studied as
uously added (Jeyabalan, 2009; Kanasaki, 2008; Kenny, 2009). discussed on page 748.
Many of these gained widespread use in the 1980s to identify Hyperhomocysteinemia causes oxidative stress and endo-
fetal malformations and were also found to be associated with thelial cell dysfunction and is characteristic of preeclampsia.
other pregnancy abnormalities such as neural-tube defects and Although women with elevated serum homocysteine levels at
aneuploidy (Chap. 14, p. 289). Although touted for hyperten- midpregnancy had a three- to fourfold risk of preeclampsia,
sion prediction, in general, none of these tests has been shown these tests have not been shown to be clinically useful predic-
to be clinically beneficial for that purpose. tors (D’Anna, 2004; Mignini, 2005; Zeeman, 2003).
Tests of Renal Function Angiogenic Factors. As discussed on page 735, evidence
Serum Uric Acid. One of the earliest laboratory manifesta- has accrued that an imbalance between proangiogenic and
tions of preeclampsia is hyperuricemia (Powers, 2006). It likely antiangiogenic factors is related to preeclampsia pathogenesis.
results from reduced uric acid clearance from diminished glo- Serum levels of some proangiogenic factors—vascular endo-
merular filtration, increased tubular reabsorption, and decreased thelial growth factor (VEGF) and placental growth factor
secretion (Lindheimer, 2008a). It is used by some to define (PlGF)—begin to decrease before clinical preeclampsia devel-
preeclampsia, but Cnossen and coworkers (2006) reported that ops. And, recall as shown in Figure 40-4 that at the same time
its sensitivity ranged from 0 to 55 percent, and specificity was levels of some antiangiogenic factors such as sFlt-1 and sEng
77 to 95 percent. become increased (Maynard, 2008). In one study, these abnor-
malities were identified coincidentally with rising uterine artery
Microalbuminuria. As a predictive test for preeclampsia, Doppler resistance (Coolman, 2012).
microalbuminuria has sensitivities ranging from 7 to 90 percent Conde-Agudelo and colleagues (2014) reviewed the predic-
and specificities between 29 and 97 percent (Conde-Agudelo, tive accuracy of some of these factors for severe preeclampsia.
2014). Poon and colleagues (2008) likewise found unacceptable Sensitivities for all cases of preeclampsia ranged from 30 to 50 per-
sensitivity and specificity for urine albumin:creatinine ratios. cent, and specificity was about 90 percent. Their predictive accu-
racy was higher for early-onset preeclampsia. These preliminary
Endothelial Dysfunction and Oxidant Stress
results suggest a clinical role for preeclampsia prediction. However,
As discussed on page 733, endothelial activation and inflam- until this role is better substantiated, their general clinical use is
mation are major participants in the pathophysiology of the not currently recommended (Boucoiran, 2013; Kleinrouweler,
preeclampsia syndrome. As a result, compounds such as those 2012; Widmer, 2007). Automated assays are being studied, and
listed in Table 40-4 are found in circulating blood of affected the World Health Organization (WHO) began a multicenter trial
women, and some have been assessed for their predictive value. in 2008 to evaluate these factors (Sunderji, 2009).
Fibronectins. These high-molecular-weight glycoproteins are Cell-Free Fetal DNA
released from endothelial cells and extracellular matrix following
As discussed in Chapter 13 (p. 279), cell-free fetal DNA can
endothelial injury (Chavarria, 2002). More than 30 years ago,
be detected in maternal plasma. It has been reported that fetal-
plasma concentrations were reported to be elevated in women
maternal cell trafficking is increased in pregnancies complicated
with preeclampsia (Stubbs, 1984). Following their systematic
by preeclampsia (Holzgreve, 1998). It is hypothesized that cell-
review, however, Leeflang and associates (2007) concluded that
free DNA is released by accelerated apoptosis of cytotropho-
neither cellular nor total fibronectin levels were clinically useful
blasts (DiFederico, 1999). From their review, Conde-Agudelo
to predict preeclampsia.
and associates (2014) concluded that cell-free fetal DNA quan-
Coagulation Activation. Thrombocytopenia and platelet tification is not yet useful for prediction purposes.
dysfunction are integral features of preeclampsia as discussed
on page 738. Platelet activation causes increased destruction Proteomic, Metabolomic, and Transcriptomic
and decreased concentrations, and mean platelet volume rises Markers
because of platelet immaturity (Kenny, 2014). Although mark- Methods to study serum and urinary proteins and cellular
ers of coagulation activation are increased, the substantive over- metabolites have opened a new vista for preeclampsia predic-
lap with levels in normotensive pregnant women stultifies their tion. Preliminary studies indicate that these may become useful
predictive value. (Bahado-Singh, 2013; Carty, 2011; Liu, 2013; Myers, 2013).
 748 Obstetrical Complications

randomized trials conducted thus far have shown no such ben-

TABLE 40-5. Some Methods to Prevent Preeclampsia That
efits (Makrides, 2006; Olafsdottir, 2006; Olsen, 2000; Zhou,
Have Been Evaluated in Randomized Trials
2012a).
Dietary manipulation—low-salt diet, calcium or fish oil
SECTION 11

supplementation Exercise. There are a few studies done to assess the protective
Exercise—physical activity, stretching effects of physical activity on preeclampsia. In their systematic
Cardiovascular drugs—diuretics, antihypertensive drugs review, Kasawara and associates (2012) reported a trend toward
Antioxidants—ascorbic acid (vitamin C), α-tocopherol risk reduction with exercise. More research is needed in this
(vitamin E), vitamin D area (Staff, 2014).
Antithrombotic drugs—low-dose aspirin, aspirin/
dipyridamole, aspirin + heparin, aspirin + ketanserin Antihypertensive Drugs
Because of the putative effects of sodium restriction, diuretic
Modified from Staff, 2014. therapy became popular with the introduction of chlorothiazide
in 1957 (Finnerty, 1958; Flowers, 1962). In their metaanalysis,
Churchill and colleagues (2007) summarized nine randomized
trials that included more than 7000 pregnancies. They found
■ Prevention that women given diuretics had a decreased incidence of edema
Various strategies used to prevent or modify preeclampsia and hypertension but not of preeclampsia.
severity have been evaluated. Some are listed in Table 40-5. In Because women with chronic hypertension are at high
general, none of these has been found to be convincingly and risk for preeclampsia, several randomized trials—only a few
reproducibly effective. placebo-controlled—have been done to evaluate various anti-
hypertensive drugs to reduce the incidence of superimposed
Dietary and Lifestyle Modifications preeclampsia. A critical analysis of these trials by Staff and
A favorite of many theorists and faddists for centuries, dietary coworkers (2014) failed to demonstrate salutary effects.
“treatment” for preeclampsia has produced some interesting
abuses as chronicled by Chesley (1978). Antioxidants
There are inferential data that an imbalance between oxidant
Low-Salt Diet. One of the earliest research efforts to prevent
and antioxidant activity may play an important role in the
preeclampsia was salt restriction (De Snoo, 1937). This inter-
pathogenesis of preeclampsia (p. 747). Thus, naturally occur-
diction was followed by years of inappropriate diuretic therapy.
ring antioxidants—vitamins C, D, and E—might decrease
Although these practices were discarded, it ironically was not
such oxidation. Indeed, women who developed preeclampsia
until relatively recently that the first randomized trial was done
were found to have reduced plasma levels of these antioxi-
and showed that a sodium-restricted diet was ineffective in pre-
dants (De-Regil, 2012; Raijmakers, 2004). There have now
venting preeclampsia in 361 women (Knuist, 1998). Guidelines
been several randomized studies to evaluate vitamin supple-
from the United Kingdom National Institute for Health and
mentation for women at high risk for preeclampsia (Poston,
Clinical Excellence (2010) recommend against salt restrictions.
2006; Rumbold, 2006; Villar, 2007). The one by the MFMU
Calcium Supplementation. Studies performed in the 1980s Network included almost 10,000 low-risk nulliparas (Roberts,
outside the United States showed that women with low dietary 2009). None of these studies showed reduced preeclampsia
calcium intake were at significantly increased risk for gestational rates in women given vitamins C and E compared with those
hypertension (Belizan, 1980; López-Jaramillo, 1989; Marya, given placebo. The recent metaanalysis by De-Regil and col-
1987). Calcium supplementation has been studied in several leagues (2012) likewise showed no benefits of vitamin D sup-
trials, including one by the National Institute of Child Health plementation.
and Human Development (NICHD) that included more than The rationale for the use of statinss to prevent preeclampsia
4500 nulliparous women (Levine, 1997). In one recent meta- is that they stimulate hemoxygenase-1 expression that inhibits
analysis, Patrelli and coworkers (2012) reported that increased sFlt-1 release. There are preliminary animal data that statins
calcium intake lowered the risk for preeclampsia in high-risk may prevent hypertensive disorders of pregnancy. The MFMU
women. In aggregate, most of these trials have shown that Network plans a randomized trial to test pravastatin for this
unless women are calcium deficient, supplementation has no purpose (Costantine, 2013).
salutary effects (Staff, 2014).
Antithrombotic Agents
Fish Oil Supplementation. Cardioprotective fatty acids There are sound theoretical reasons that antithrombotic agents
found in some fatty fishes are plentiful in diets of Scandinavians might reduce the incidence of preeclampsia. As discussed on
and American Eskimos. The most common dietary sources page 734, the syndrome is characterized by vasospasm, endo-
are EPA—eicosapentaenoic acid, ALA—alpha-linoleic acid, thelial cell dysfunction, and inflammation, as well as activation
and DHA—docosahexaenoic acid. With proclamations that of platelets and the coagulation-hemostasis system. Moreover,
supplementation with these fatty acids would prevent inflam- prostaglandin imbalance(s) may be operative, and other
matory-mediated atherogenesis, it was not a quantum leap to sequelae include placental infarction and spiral artery throm-
posit that they might also prevent preeclampsia. Unfortunately, bosis (Nelson, 2014).
 Hypertensive Disorders 749

these small trials, evidence is insufficient to recommend these

TABLE 40-6. Maternal-Fetal Medicine Units Network
regimens to prevent preeclampsia (National Institute for
Trial of Low-Dose Aspirin in Women at
Health and Clinical Excellence, 2010; Staff, 2014).
High Risk for Preeclampsia

CHAPTER 40
Preeclampsia (%)a
Risk Factors No. Aspirin Placebo
MANAGEMENT
Normotensive, no proteinuria 1613 14.5 17.7 Pregnancy complicated by gestational hypertension is managed
Proteinuria plus hypertension 119 31.7 22.0 based on severity, gestational age, and presence of preeclamp-
Proteinuria only 48 25.0 33.3 sia. With preeclampsia, management varies with the severity of
Hypertension only 723 24.8 25.0 endothelial cell injury and multiorgan dysfunction.
Insulin-dependent diabetes 462 18.3 21.6 Preeclampsia cannot always be diagnosed definitively
Chronic hypertension 763 26.0 24.6 (p. 728). Thus, the Task Force of the American College
Multifetal gestation 678 11.5 15.9 of Obstetricians and Gynecologists (2013b) recommends
Previous preeclampsia 600 16.7 19.0 more frequent prenatal visits if preeclampsia is “suspected.”
Increases in systolic and diastolic blood pressure can be either
a
No statistically significant difference for any comparison normal physiological changes or signs of developing pathology.
between groups. Increased surveillance permits more prompt recognition of
Data from Caritis, 1998. ominous changes in blood pressure, critical laboratory find-
ings, and clinical signs and symptoms (Macdonald-Wallis,
2012).
The basic management objectives for any pregnancy compli-
Low-Dose Aspirin. In oral doses of 50 to 150 mg daily, cated by preeclampsia are: (1) termination of pregnancy with
aspirin effectively inhibits platelet thromboxane A2 biosyn- the least possible trauma to mother and fetus, (2) birth of an
thesis but has minimal effects on vascular prostacyclin pro- infant who subsequently thrives, and (3) complete restoration
duction (Wallenburg, 1986). However, clinical trials have of health to the mother. In many women with preeclampsia,
shown limited benefits. For example, results in Table 40-6 are especially those at or near term, all three objectives are served
from the MFMU Network, and none of the outcomes shown equally well by induction of labor. One of the most important
were significantly improved. Some reports are more favorable. clinical questions for successful management is precise knowledge
For example, the Paris Collaborative Group performed a meta- of fetal age.
analysis that included 31 randomized trials involving 32,217
women (Askie, 2007). For women assigned to receive antiplate-
let agents, the relative risk for development of preeclampsia, ■ Early Diagnosis of Preeclampsia
superimposed preeclampsia, preterm delivery, or any adverse
Traditionally, the frequency of prenatal visits is increased dur-
pregnancy outcome was significantly decreased by 10 percent.
ing the third trimester, and this aids early detection of pre-
Another review and metaanalysis reported marginal benefits for
eclampsia. Women without overt hypertension, but in whom early
low-dose aspirin and severe preeclampsia (Roberge, 2012). A
developing preeclampsia is suspected during routine prenatal vis-
recent small Finnish multicenter trial included 152 women at
its, are seen more frequently. The protocol used successfully for
high risk for preeclampsia (Villa, 2013). Although there were
many years at Parkland Hospital for women with new-onset
no benefits to low-dose aspirin, the accompanying metaanaly-
diastolic blood pressures > 80 mm Hg but < 90 mm Hg or
sis reported a lowering of risk. The 2013 Task Force recom-
with sudden abnormal weight gain of more than 2 pounds per
mended the use of low-dose aspirin in some high-risk women
week includes, at minimum, return visits at 7-day intervals.
to prevent preeclampsia.
Outpatient surveillance is continued unless overt hypertension,
Low-Dose Aspirin plus Heparin. In women with lupus proteinuria, headache, visual disturbances, or epigastric discom-
anticoagulant, treatment with low-dose aspirin and heparin fort supervene. Women with overt new-onset hypertension—
mitigates thrombotic sequelae (Chap. 59, p. 1175). Because either diastolic pressures ≥ 90 mm Hg or systolic pressures
of the high prevalence of placental thrombotic lesions found ≥ 140 mm Hg—are admitted to determine if the increase is
with severe preeclampsia, observational trials have been done due to preeclampsia, and if so, to evaluate its severity. Women
to evaluate such treatments for affected women. Sergis and with persistent severe disease are generally delivered, as discussed
associates (2006) reviewed effects of prophylaxis with low- subsequently. Conversely, women with apparently mild disease
molecular-weight heparin plus low-dose aspirin on pregnancy can often be managed as outpatients, although there should be
outcomes in women with a history of severe early-onset pre- a low threshold for continued hospitalization for the nullipara,
eclampsia and low-birthweight neonates. They reported better especially if there is proteinuria.
pregnancy outcomes in women given low-molecular-weight
heparin plus low-dose aspirin compared with those given
low-dose aspirin alone. Similar findings were reported in a ■ Evaluation
trial that included 139 women with thrombophilia and a his- Hospitalization is considered at least initially for women with
tory of early-onset preeclampsia (de Vries, 2012). Despite new-onset hypertension, especially if there is persistent or