Labor is considered “normal” when the woman is at or near term, no

complications exist, as single fetus presents by vertex and labor is completed within
24 hrs. The course of labor has 4 stages:

First Stage of Labor

The first stage of labor is the longest. There are three phases within the first
stage: Early or latent phase, Active phase and Transition phase. At the end of the
first stage, the cervix is dilated to 10 centimeters. In mothers having their first child,
this stage usually lasts 12 to 16 hours. For women having second or subsequent
children, the first stage lasts around 6-7 hours.

Early/Latent

During the early or latent phase, the cervix dilates to 4 centimeters.

The duration of the first phase is the longest, averaging around 8 hours. Your
contractions may be irregular, progressing to rhythmic and methodical. The
pain felt at this early stage may be similar to menstrual pain: aching, fullness,
cramping and backache. You will still be able to walk. Walking is usually more
comfortable than sitting. Most women spend these hours at home, or they
may be checked at the hospital and sent home until labor becomes more
active. You may feel eager, excited and social. It is important that you
conserve your energy for the work of labor.

 Active

Active labor is marked by regular contractions that become longer,

stronger and closer together over time. Most providers recommend that you
go to the hospital when your contractions are five minutes apart, lasting more

~1~
 then 60 seconds for at least an hour.
If you have had previous deliveries, the active phase of labor can proceed
more quickly. When you are in active labor, you will be concentrating on the
task at hand, and will not feel like doing anything else. Contractions are
growing stronger, longer and closer together. Contractions will be about 3-4
minutes apart, lasting 40 to 60 seconds. You may have a tightening feeling in
your pubic area and increasing pressure in your back. If you have learned
breathing techniques, begin using them now. Pain medication is often given
at this stage. If you have chosen to have an epidural anesthetic, it is usually
given at this stage.

 Transition

Transition is the most difficult phase of labor, and fortunately, the

shortest, lasting from 30 minutes to two hours. The cervix is opening the last
few centimeters, from 7 to 10 centimeters. The pain may be intense, as the
cervix stretches and the baby descends into the birth canal. All of your energy
is concentrated on doing the work of labor. At the end of transition, you may
feel a strong urge to push the baby out. The baby is ready to be born.

Second Stage of Labor

The second stage begins from the time the cervix is fully dilated(10 cm) until
the baby is born. This stage of labor lasts anywhere from one contraction up to two
hours. The baby's head stretches your vagina and perineum (the skin between the
vagina and rectum). This may cause a burning sensation. Some women may feel as
if they are having a bowel movement, and feel the urge to push, or bear down. The
labor nurse or physician will tell you when it is time to push. It is important that you
not push until instructed. Pushing too early will cause the cervix to become
edematous, or swollen. "Crowning" occurs as the widest part of the head appears at

~2~
the vaginal opening. In the next few pushes, the baby is born. Mucous and amniotic
fluid will be removed from the baby's mouth and nose with a bulb syringe. The baby
will take its first breath, and may begin to cry. Immediately after birth, the baby is still
connected to the placenta by the umbilical cord. The cord is clamped and cut.

Third Stage of Labor

The third stage of labor, or the placental site, begins with the birth of the infant
and ends with the delivery of the placenta. Two separate phases are involved:
placental separation and placental separation and placental expulsion. Signs of
placental separation includes: calkin’s sign, uterus becomes mobile, sudden gushing
of blood and lengthening of umbilical cord. The types of placental delivery or
presentation includes: schultze’s mechanism, which is the shiny “clean” side first
bluish side and duncan’s mechanism, appears to be rough, ”dirty”, reddish maternal
side out first.

After birth of the infant, the uterus can be palpated as a firm, round mass just
inferior to the level of the umbilicus. After few minutes of rest, uterine contractions
begin again, and the organ assumes a discoid shape. It retains this new shape until
the placenta has separated, approximately 5 minutes after the birth of the infant.

Fourth Stage of Labor

This stage is really more about getting back to normal than anything else --
the hour or two after delivery when the tone of the uterus is established and the
uterus contracts down again expelling any remaining contents. These contractions
are hastened by breast-feeding, which stimulates production of the hormone
oxytocin. Your blood pressure, temperature and heart rate will stabilize in much the
same way a marathon runners does: a little at a time during the hour after the
placenta is delivered. Contractions will cease. Your uterus will harden, doing its job

~3~
to tighten around the blood vessels that had supplied the placenta and your baby
with nutrients. Your midwife or doctor will keep an eye on you, make sure the entire
placenta was expelled and take a look at the umbilical cord. If you had an
episiotomy, this is when you'll get a few sutures.

Postpartal hemorrhage is usually defined as the loss of more than 500 ml of

blood during or after delivery. It is one of the leading causes of maternal mortality.
Hemorrhage may occur early, within the first 24 hr after delivery, or late, up to 28
days postpartum (the end of the puerperium).

Causes of postpartum hemorrhage

4 categories, commonly called "The Four T's":

• Trauma from the delivery may tear tissue and vessels leading to significant
postpartum bleeding.
• Uterine atony (Tone) refers to the inability of the uterus to contract and may
lead to continuous bleeding. Retained placental tissue and infection may
contribute to uterine atony.
• Tissue refers to any cellular debris from the placenta or fetus that may be left
in the uterus, causing the uterus to not contract.
• Thrombin refers to some failure of clotting, such as with diseases known as
coagulopathies.

Complications from postpartum hemorrhage include orthostatic hypotension,

anemia, and fatigue, which may make maternal care of the newborn more difficult.

~4~
Postpartum anemia increases the risk of postpartum depression. Blood transfusion
may be necessary and carries associated risks. In the most severe cases,
hemorrhagic shock may lead to anterior pituitary ischemia with delay or failure of
lactation (i.e., postpartum pituitary necrosis).

Tone

Uterine atony is the most common cause of postpartum hemorrhage.

Because hemostasis associated with placental separation depends on myometrial
contraction, atony is treated initially by bimanual uterine compression and massage,
followed by drugs that promote uterine contraction.

Figure 1. Technique of bimanual massage for uterine atony. Bimanual uterine

compression massage is performed by placing one hand in the vagina and pushing
against the body of the uterus while the other hand compresses the fundus from
above through the abdominal wall. The posterior aspect of the uterus is massaged
with the abdominal hand and the anterior aspect with the vaginal hand.

~5~
Uterine Massage. Brisk blood flow after delivery of the placenta should
alert the physician to perform a bimanual examination of the uterus. If the
uterus is soft, massage is performed by placing one hand in the vagina
and pushing against the body of the uterus while the other hand
compresses the fundus from above through the abdominal wall (Figure 1).
The posterior aspect of the uterus is massaged with the abdominal hand
and the anterior aspect with the vaginal hand.

Uterotonic Agents. Uterotonic agents include oxytocin, ergot alkaloids,

and prostaglandins. Oxytocin stimulates the upper segment of the
myometrium to contract rhythmically, which constricts spiral arteries and
decreases blood flow through the uterus. Oxytocin is an effective first-line
treatment for postpartum hemorrhage; 10 international units (IU) should be
injected intramuscularly, or 20 IU in 1 L of saline may be infused at a rate
of 250 mL per hour. As much as 500 mL can be infused over 10 minutes
without complications.

Figure 2. Reduction of uterine inversion (Johnson method). (A) The

protruding fundus is grasped with fingers directed toward the posterior
fornix. (B, C) The uterus is returned to position by pushing it through the
pelvis and into the abdomen with steady pressure towards the umbilicus.
 Misoprostol is another prostaglandin that increases uterine tone
and decreases postpartum bleeding. Misoprostol is effective in the
treatment of postpartum hemorrhage, but side effects may limit its use. It
can be administered sublingually, orally, vaginally, and rectally. Higher
peak levels and larger doses are associated with more side effects,
including shivering, pyrexia, and diarrhea.

Trauma

Lacerations and hematomas resulting from birth trauma can cause

significant blood loss that can be lessened by hemostasis and timely repair.
Sutures should be placed if direct pressure does not stop the bleeding.

Hematomas can present as pain or as a change in vital signs

disproportionate to the amount of blood loss. Small hematomas can be managed
with close observation. Patients with persistent signs of volume loss despite fluid
replacement, as well as those with large or enlarging hematomas, require
incision and evacuation of the clot. The involved area should be irrigated and the
bleeding vessels ligated. In patients with diffuse oozing, a layered closure will
help to secure hemostasis and eliminate dead space.

Uterine Inversion. Uterine inversion is rare, occurring in 0.05 percent of

deliveries. Active management of the third stage of labor may reduce the
incidence of uterine inversion. Fundal implantation of the placenta may
lead to inversion; the roles of fundal pressure and undue cord traction are
uncertain. The inverted uterus usually appears as a bluish-gray mass
protruding from the vagina. The Johnson method of reduction begins with
grasping the protruding fundus with the palm of the hand and fingers
directed toward the posterior fornix. The uterus is returned to position by
lifting it up through the pelvis and into the abdomen. Once the uterus is
 reverted, uterotonic agents should be given to promote uterine tone and to
prevent recurrence.

Uterine Rupture. Although rare in an unscarred uterus, clinically

significant uterine rupture occurs in 0.6 to 0.7 percent of vaginal births
after cesarean delivery in women with a low transverse or unknown
uterine scar. The risk increases significantly with previous classical
incisions or uterine surgeries, and to a lesser extent with shorter intervals
between pregnancies or a history of multiple cesarean deliveries,
particularly in women with no previous vaginal deliveries. Compared with
spontaneous labor, induction or augmentation increases the rate of uterine
rupture, more so if prostaglandins and oxytocin are used sequentially.

Before delivery, the primary sign of uterine rupture is fetal

bradycardia. Tachycardia or late decelerations can also herald a uterine
rupture, as can vaginal bleeding, abdominal tenderness, maternal
tachycardia, circulatory collapse, or increasing abdominal girth.
Symptomatic uterine rupture requires surgical repair of the defect or
hysterectomy. When detected in the postpartum period, a small
asymptomatic lower uterine segment defect or bloodless dehiscence can
be followed expectantly.

Tissue

Classic signs of placental separation include a small gush of blood with

lengthening of the umbilical cord and a slight rise of the uterus in the pelvis.
Placental delivery can be achieved by use of the Brandt-Andrews maneuver,
which involves applying firm traction on the umbilical cord with one hand while
the other applies suprapubic counterpressure. The mean time from delivery until
placental expulsion is eight to nine minutes. Longer intervals are associated with
an increased risk of postpartum hemorrhage, with rates doubling after 10
minutes. Retained placenta (i.e., failure of the placenta to deliver within 30
minutes after birth) occurs in less than 3 percent of vaginal deliveries. One
management option is to inject the umbilical vein with 20 mL of a solution of 0.9
percent saline and 20 units of oxytocin. This significantly reduces the need for
manual removal of the placenta compared with injecting saline alone.

Figure 3. Brandt-Andrews maneuver for cord traction. Firm traction is

applied to the umbilical cord with one hand while the other applies suprapubic
counterpressure.

Thrombin

Coagulation disorders, a rare cause of postpartum hemorrhage, are

unlikely to respond to the measures described above. Most coagulopathies are
identified before delivery, allowing for advance planning to prevent postpartum
hemorrhage. These disorders include idiopathic thrombocytopenic purpura,
thrombotic thrombocytopenic purpura, von Willebrand's disease, and hemophilia.
Patients also can develop HELLP (hemolysis, elevated liver enzyme levels, and
low platelet levels) syndrome or disseminated intravascular coagulation. Risk
factors for disseminated intravascular coagulation include severe preeclampsia,
amniotic fluid embolism, sepsis, placental abruption, and prolonged retention of
fetal demise. Abruption is associated with cocaine use and hypertensive
disorders. Excessive bleeding can deplete coagulation factors and lead to
consumptive coagulation, which promotes further bleeding. Coagulation defects
should be suspected in patients who have not responded to the usual measures
to treat postpartum hemorrhage, and in those who are not forming blood clots or
are oozing from puncture sites.

Lab Studies

• In the antenatal period, a CBC is performed. Findings alert caregivers to

women with anemia and indicate interventions to attempt to improve the
hemoglobin level. Hemoglobin levels below 10-10.5 g/dL have been
associated with adverse pregnancy outcome, and the rare patient with
thrombocytopenia will be identified (Xiong, 2000). Women admitted to
labor and delivery units should have a CBC performed if one has not been
performed recently. All women experiencing antepartum bleeding should
have a CBC.
• Blood typing and antibody screening tests may also have been performed
in the antenatal period. If the results are known and no blood group
antibodies were present, then the test may not need to be repeated upon
admission. However, many facilities routinely repeat this test (or at least
draw a sample to be held in the blood bank) in case blood is urgently
needed. The time frame between a request for blood products of various
types and their availability should be known. In a patient at high risk of
PPH, crossmatching of 2-6 U of blood before delivery is prudent.
Examples include previous severe PPH, placenta previa, possible
placenta accreta, multiple previous cesarean deliveries, known
coagulation disorders, or severe thrombocytopenia. The American
Association of Blood Banks currently recommends retesting women at
high risk every 72 hours for the development of antibodies.
 • Coagulation studies are no longer routinely performed in pregnant women,
including those about to undergo cesarean delivery. Instead, history is
relied on to uncover previous episodes suggesting preexisting hemostasis
disorders.

Placenta Previa is the abnormal implantation of the placenta in the lower

uterine segment, partially or completely covering the internal cervical os.

CLASSSIFICATION:
 Total placenta previa – implantation that totally obstructs the cervical os
 Partial placenta previa – implantation that occludes a portion of the
cervical os
 Marginal placenta previa - placenta edge approaches the cervical os
 Low-lying placenta – implantation in the lower rather than in the upper
portion of the uterus

PATHOPHYSIOLOGY AND ETIOLOGY

 The cause is unknown.
 One possible theory states that the embryo will implant in the lower uterine
segment if the decidua in the uterine fundus is not favorable or delayed
implantation.
 About 80% of placenta previa episode occur in multiparas.
 Seen more often with history of abortion, cesarean section, uterine
scarring or prior placenta previa.
 Age greater than 35 years of age.
  Conditions that yield abnormally large placentas such as multifetal
gestation or Rh isoimmunization.

CLINICAL MANIFESTATIONS:
 Cardinal sign is painless vaginal bleeding, which usually appears near the
end of the second trimester or later. Bleeding appears without warning.
 Initial episode is rarely fatal and usually stops spontaneously, with
subsequent bleeding episodes occurring spontaneously; each episode is
more profuse than the previous one.
 Bleeding from placenta may not occur until cervical dilation occurs and the
placenta is loosened from the uterus.
 With a complete placenta previa, the bleeding will occur earlier in
pregnancy and be more profuse.

DIAGNOSTIC EVALUATION
 Transabdominal ultrasound is the method of choice to show location of the
placenta.
 If findings are questionable, transvaginal ultrasound can improve the
accuracy of the diagnosis.
 Sterile speculum examination can also confirm placenta previa.

MANAGEMENT
 Conservative management with bed rest and hospitalization until fetus is
mature and delivery can be accomplished.
 If woman is discharged, she needs availability of immediate transport for
recurrent bleeding.
 IV access and at least 2 units of blood should be available at all times.
 Continuous maternal and fetal monitoring.
 Cesarean section is often indicated if the degree of previa is >30% or if
there is excessive bleeding.
  Vaginal delivery may sometimes be attempted in a marginal previa without
active bleeding.
 A pediatric specialty team may be needed at delivery due to prematurity
and other neonatal complications.

COMPLICATIONS
 Fetal mortality resulting from hypoxia in utero and prematurity.
 Immediate hemorrhage, with possible shock and maternal death.
 Postpartum hemorrhage resulting from decreased contractility of uterine
muscle.

NURSING ASSESSMENT
 Determine the amount and type of bleeding; also, review any history of
bleeding throughout this pregnancy.
 Inquire as to the presence or absence of pain in association with the
bleeding.
 Record maternal and fetal vital signs.
 Palpate for the presence of uterine contractions.
 Evaluate laboratory data ion hemoglobin and hematocrit status.


NURSING DIAGNOSIS INTERVENTION RATIONALE

Altered Tissue o Frequently monitor o Serves as a guide
Perfusion, Placental, mother and fetus. in determining
related to excessive underlying
bleeding causing fetal complications.
compromise o Administer IV Fluids o Restores
as prescribed. circulating volume
to maintain
adequate tissue
perfusion
o Position on side. o To promote
placental perfusion.
o Maximizes
o Administer oxygen available oxygen
 by face mask. for myocardial
uptake to reduce
cardiac workload
and cellular
hypoxia.
o Serves as an
o Prepare for immediate
emergency delivery, intervention to
as needed. prevent
complications
resulting from
hypoxia and fetal
death.

HEALTH TEACHINGS
 Educate the woman and her family about the etiology and treatment of
placenta previa.
 Educate the woman to inform medical personnel about her diagnosis and
no to have vaginal examinations.
 If discharged, inform the woman to:
o Avoid intercourse or anything per vagina.
o Limit physical activity.
o Have an accessible person in the event of an emergency.
o Go to the hospital immediately for repeat bleeding or uterine
contractions >6 per hour.

Abruption placenta is the premature separation of the normally

implanted placenta from the uterus. It may be classified as:
o Partial
o Complete
o Marginal
Hemorrhage can be either:
 o Occult – the placentaS separates centrally and a large amount of
blood is accumulated under the placenta.
o Apparent – the separation is a long margin and blood flows under
the membranes and through the cervix

PATHOPHYSIOLOGY AND ETIOLOGY

 The etiology is unknown.
 Women at risk for developing abruption placenta include those with history
of hypertension or previous abruption placenta; those who have rapid
decompression of the uterine cavity, short umbilical cord or presence of a
uterine anomaly or tumor; preterm premature rupture of membranes
(PROM) at <34weeks gestation, increased parity or multiple gestation.
 Additional risks occur in existing pregnancies complicated by blunt
abdominal trauma, supine hypotension, PIH, alcohol, cigarette smoking
and cocaine use.
 Hemorrhage occurs into the decidua basalis. Then forms a hematoma.
 This hematoma can expand as the bleeding increases, causing the
hematoma to increase in size and further detach the placenta from the
uterine wall.

CLINICAL MANIFESTATIONS:
 Sudden onset, intense, localized, uterine pain/tenderness with (external)
or without (occult) vaginal bleeding.
 Uterine contractions may be low amplitude and high frequency.
 FHR may change depending on the degree of hemorrhage; increased
FHR, late decelerations and decreased viability.
 Abdominal pain is often present due to increased uterine activity.
 Abruptio placenta grades:
o Grade 0 (mild) – small retroplacental clot or small rupture of
marginal sinus; <100 ml blood
 o Grade 1 (moderate) – small retroplacental clot; detachment <50%;
>100 ml but <500 ml blood
o Grade 2 (moderate to severe) – significant retroplacental clot;
detachment approaches 50%; blood loss approaches 500 ml
o Grade 5 (moderate to severe) – significant retroplacental clot;
detachment >50%; >500 ml

DIAGNOSTIC EVALUATION
 Ultrasound is done but is not always sensitive enough to rule out
diagnosis.
 Laboratory screen for APT on mother’s blood to check for fetal
hemoglobin.

MANAGEMENT
This depends on the maternal and fetal status and degree of bleeding.
 Mild – conservative management with bed rest, tocolytics and evaluation
of fetus with fetal assessment methods until fetal lung maturity can be
established and delivery accomplished.
 Moderate – augment labor if stable and decreased blood loss. Vaginal
delivery is accomplished if cervix dilates. If fetal or maternal status
deteriorates and blood loss excessive, cesarean delivery is performed.
 Moderate to severe – restore and maintain maternal physiologic status;
IV/blood replacement.
 A pediatric specialty team may be needed at delivery due to prematurity
and other neonatal complications.

COMPLICATIONS
 Maternal shock
 DIC
 Amniotic fluid embolism
  Postpartum hemorrhage
 Prematurity
 Maternal/fetal death
 Rapid labor and delivery

NURSING ASSESSMENT
 Determine the amount and type of bleeding and the presence or absence
of pain.
 Monitor maternal and fetal vital signs.
 Palpate the abdomen for contractions.
 Measure and record fundal height.
 Prepare for possible delivery.

NURSING DIAGNOSIS INTERVENTION RATIONALE

Altered Tissue o Frequently monitor o Serves as a guide
Perfusion, Placental, mother and fetus. in determining
related to excessive underlying
bleeding causing fetal complications.
compromise o Administer IV Fluids o Restores
as prescribed. circulating volume
to maintain
adequate tissue
perfusion
o Position on side. o To promote
placental perfusion.
o Maximizes
o Administer oxygen available oxygen
by face mask. for myocardial
uptake to reduce
cardiac workload
and cellular
hypoxia.
o Serves as an
o Prepare for immediate
emergency delivery, intervention to
as needed. prevent
complications
resulting from
hypoxia and fetal
 death.

HEALTH TEACHINGS
 Provide information to the woman and her family regarding etiology and
treatment for abruptio placenta.
 Encourage involvement from the neonatal team regarding education
related to fetal/neonatal outcome.
 Teach high risk women the signs and symptoms of placental abruption
and increased uterine activity.
 Instruct woman to report immediately if excessive bleeding and pain occur
at home.

Periodic changes

Periodic changes or fluctuations in FHR occur in response to contractions

and fetal movement and are described in terms of acceleration or deceleration.
Four such responses are acceleration, early deceleration, late deceleration and
variable deceleration. A deceleration (drop) of the fetal heart rate usually
indicates that the fetus is under some sort of stress, which may be a good
healthy sign if it corresponds with movement or uterine contractions, but may be
a bad sign if it happens apart from movement of uterine contractions.

Periodic FHR Changes

Accelerations

Accelerations are transient increases in the FHR (Figure 4). They

are usually associated with fetal movement, vaginal examinations, uterine
contractions, umbilical vein compression, fetal scalp stimulation or even
external acoustic stimulation. The presence of accelerations is considered
a reassuring sign of fetal well-being. An acceleration pattern preceding or
 following a variable deceleration (the "shoulders" of the deceleration) is
seen only when the fetus is not hypoxic. Accelerations are the basis for
the nonstress test (NST). The presence of at least two accelerations, each
lasting for 15 or more seconds above baseline and peaking at 15 or more
bpm, in a 20-minute period is considered a reactive NST.

FIGURE 4. Early deceleration in a patient with an unremarkable course of labor.

Notice that the onset and the return of the deceleration coincide with the start and the
end of the contraction, giving the characteristic mirror image.

Early Decelerations

Early decelerations are caused by fetal head compression during

uterine contraction, resulting in vagal stimulation and slowing of the heart
rate. This type of deceleration has a uniform shape, with a slow onset that
coincides with the start of the contraction and a slow return to the baseline
that coincides with the end of the contraction. Thus, it has the
characteristic mirror image of the contraction (Figure 5). Although these
decelerations are not associated with fetal distress and thus are
 reassuring, they must be carefully differentiated from the other,
nonreassuring decelerations.

FIGURE 5. Nonreassuring pattern of late decelerations with preserved beat-to-

beat variability. Note the onset at the peak of the uterine contractions and the return to
baseline after the contraction has ended. The second uterine contraction is associated
with a shallow and subtle late deceleration

Late Decelerations

Late decelerations are associated with uteroplacental insufficiency and are

provoked by uterine contractions. Any decrease in uterine blood flow or placental
dysfunction can cause late decelerations. Maternal hypotension and uterine
hyperstimulation may decrease uterine blood flow. Postdate gestation,
preeclampsia, chronic hypertension and diabetes mellitus are among the causes
of placental dysfunction. Other maternal conditions such as acidosis and
hypovolemia associated with diabetic ketoacidosis may lead to a decrease in
uterine blood flow, late decelerations and decreased baseline variability.

A late deceleration is a symmetric fall in the fetal heart rate, beginning at

or after the peak of the uterine contraction and returning to baseline only after the
contraction has ended (Figure 5). The descent and return are gradual and
smooth. Regardless of the depth of the deceleration, all late decelerations are
considered potentially ominous. A pattern of persistent late decelerations is
nonreassuring, and further evaluation of the fetal pH is indicated. Persistent late
decelerations associated with decreased beat-to-beat variability is an ominous
pattern (Figure 6).

FIGURE 6. Late deceleration with loss of variability. This is an ominous pattern, and
immediate delivery is indicated.

Variable Decelerations

Variable decelerations are shown by an acute fall in the FHR with a rapid
downslope and a variable recovery phase. They are characteristically variable in
duration, intensity and timing. They resemble the letter "U," "V" or "W" and may
not bear a constant relationship to uterine contractions. They are the most
commonly encountered patterns during labor and occur frequently in patients
who have experienced premature rupture of membranes and decreased amniotic
fluid volume. Variable decelerations are caused by compression of the umbilical
cord. Pressure on the cord initially occludes the umbilical vein, which results in
an acceleration (the shoulder of the deceleration) and indicates a healthy
response. This is followed by occlusion of the umbilical artery, which results in
the sharp downslope. Finally, the recovery phase is due to the relief of the
compression and the sharp return to the baseline, which may be followed by
another healthy brief acceleration or shoulder (Figure 7).
FIGURE 7. Variable deceleration with pre- and post-accelerations ("shoulders"). Fetal heart rate
is 150 to 160 beats per minute, and beat-to-beat variability is preserved.

Variable decelerations may be classified according to their depth and

duration as mild, when the depth is above 80 bpm and the duration is less than
30 seconds; moderate, when the depth is between 70 and 80 bpm and the
duration is between 30 and 60 seconds; and severe, when the depth is below 70
bpm and the duration is longer than 60 seconds. Variable decelerations are
generally associated with a favorable outcome. However, a persistent variable
deceleration pattern, if not corrected, may lead to acidosis and fetal distress and
therefore is nonreassuring. Variable decelerations indicating hypoxemia are
shown in Figures 8 and 9. Nonreassuring variable decelerations associated with
the loss of beat-to-beat variability correlate substantially with fetal acidosis and
therefore represent an ominous pattern.
 FIGURE 8. Severe variable deceleration with overshoot. However, variability is preserved.

FIGURE 9. Late deceleration related to bigeminal contractions. Beat-to-beat variability is

preserved. Note the prolonged contraction pattern with elevated uterine tone between the peaks
of the contractions, causing hyperstimulation and uteroplacental insufficiency. Management
should include treatment of the uterine hyperstimulation. This deceleration pattern also may be
interpreted as a variable deceleration with late return to the baseline based on the early onset of
the deceleration in relation to the uterine contraction, the presence of an acceleration before the
deceleration (the "shoulder") and the relatively sharp descent of the deceleration. However, late
decelerations and variable decelerations with late return have the same clinical significance and
represent nonreassuring patterns. This tracing probably represents cord compression and
uteroplacental insufficiency.
Pregnancy-Induced Hypertension

Pregnancy-induced hypertension (PIH) is a form of high blood pressure in

pregnancy and excess protein in the urine after 20 weeks of pregnancy. It occurs
in about 5 percent to 8 percent of all pregnancies. Pregnancy-induced
hypertension is also called preeclampsia. Originally it was called toxemia
because researchers pictured a toxin of some kind being produced by the
woman in response to the foreign protein of the growing fetus, the toxin leading
to the typical symptoms. No such toxin has ever been identified. It occurs most
often in young women with a first pregnancy.

Sign and symptoms

Usually, there are three primary characteristics of this condition, including the
following:

• high blood pressure (a blood pressure reading higher than 140/90 mm Hg,
or a significant increase in one or both pressures)

• proteinuria (protein in the urine)

• edema (swelling)

Other signs and symptoms of preeclampsia — which can develop gradually or

strike suddenly, often in the last few weeks of pregnancy — may include:

 Severe headaches
 Changes in vision, including temporary loss of vision, blurred vision or
light sensitivity
 Upper abdominal pain, usually under the ribs on the right side
 Nausea or vomiting
  Dizziness
 Decreased urine output
 Sudden weight gain, typically more than 2 pounds a week.

Pathophysiology Events

Vasospasm

Vascular effects Kidney effects Interstitial effects

Vasoconstriction Decreased glomeruli

filtration rate and
increased permeability
of glomeruli membranes

Diffusion of fluid from

blood stream into
interstitial tissue

Poor organ Increased serum blood

perfusion urea nitrogen, uric acid,
and creatinine

Increased blood Decreased urine Edema

pressure output and
proteinuria
Causes

The cause of PIH is unknown. Some conditions may increase the risk of
developing PIH, including the following:

• pre-existing hypertension (high blood pressure)

• kidney disease
• diabetes
• PIH with a previous pregnancy
• mother's age younger than 20 or older than 40
• multiple fetuses (twins, triplets)

Classification
PIH is classified as gestational hypertension, mild preeclampsia, severe
preeclampsia, and eclampsia, depending on how far advanced it has become.

Gestational Hypertension
A woman is said to have gestational hypertension when she
develops an elevated blood pressure (140/90 mmHg) but has no
proteinuria or edema.

Mild Preeclampsia
A woman is said to be mildly preeclamptic when her blood pressure
rises to 140/ 90 mmHg, taken on two occasions at least 6 hours apart.
With mild preeclampsia, in addition to the hypertension the woman has
proteinuria ( 1+ or 2+ on a reagent test strip on a random sample). Edema
also may present. This develops, as mentioned, because of the protein
loss, sodium retention, and lowered glomerular filtration rate. Edema
begins to accumulate in the upper part of the body, rather than just the
ankle edema of pregnancy. A weight gain of more than 2lb/wk in the
second trimester or 1lb/wk in the third trimester usually indicates abnormal
tissue fluid retention.
 Severe Preeclampsia
A woman has passed from mild to severe preeclampsia when her
blood pressure has risen to 160/110 mmHg or above on at least two
occasions 6 hours apart at bed rest or her diastolic pressure is 30 mm Hg
above the prepregnancy level. Marked proteinuria, 3+ or 4+ on a random
urine sample or more than 5g in a 24-hour sample, and extensive edema
are also present.

Eclampsia
This is most severe classification of hypertension of pregnancy.
Convulsion or coma accompanied by signs and symptoms of
preeclampsia.

Nursing Management

Nursing Diagnosis Intervention Rationale

1. Fluid volume
deficient related to a. Monitor vital signs a. With PIH, increased
altered intake during every hour. blood pressure may
labor. occur.
b. Monitor intake and b. These measures help
output strictly; notify ensure adequate
health care provider hydration.
if urine output is less c. To aid kidney
than 30ml/hour. perfusion and
increase cardiac and
c. Position the patient urine output.
on her left side d. Decreased urine
output, increased
d. If urine output is
blood pressure,
reduced, carefully
hyperreflexia, and
assess the patient for
peripheral edema
peripheral edema,
may indicate
hyperreflexia,
intrapartal PIH.
increased blood
Proteinuria may result
pressure, and
from dehydration,
presence of urine
exhaustion, or
protein.
preeclampsia.
 2. Ineffective tissue a. To promote placental
perfusion: fetal perfusion
cardiac and cerebral
related to altered a. Position to side
placental blood flow c. To determine fetal
b. Monitor fetal activity
caused by status
vasospasm and c. Evaluate NST d. To replace protein lost
thrombosis. through kidneys.
d. Increased protein
intake

Medical Management

Drugs used in pregnany-induced hypertension

• Hydralazine and Labetalol- hypotensive drug to reduce hypertension.
These drugs act to lower blood pressure by peripheral dilatation without
interfering with placental circulation.
• Magnesium Sulfate- drug of choice to prevent eclampsia. It acts as
anticonvulsant.
• Cathartic- reduces edema by causing a shift in fluid from the extracellular
spaces into the intestine. It has a central nervous system depressant
action which lessens the possibility of seizures.
• Calcium gluconate- antidote for magnesium toxicity.

Multiple births occur when multiple fetuses are carried during one
pregnancy. Since 1970, the prevalence of multiple births has been increasing
because of more widespread use of assisted reproductive technologies to treat
infertility. Multifetal pregnancies are high-risk pregnancies with numerous
associated fetal and neonatal complications. Researchers have studied twins in
an attempt to separate the influence of genetic and environmental factors on both
fetal and postpartum development.

Pathophysiology

Multiple births include twins and higher-order multiples (eg, triplets,

quadruplets). The 2 types of twins are monozygotic and dizygotic.

Dizygotic twins, which sometimes are called fraternal twins, are produced
when 2 sperm fertilize 2 ova. Separate amnions, chorions, and placentas are
formed in dizygotic twins (see Media file 1). The placentas in dizygotic twins may
fuse if the implantation sites are proximate. The fused placentas can be easily
separated after birth.

Monozygotic twins develop when a single fertilized ovum splits during the
first 2 weeks after conception. Monozygotic twins are also called identical twins.
An early splitting (ie, within the first 2 d after fertilization) of monozygotic twins
produces separate chorions and amnions (see Media file 1). These dichorionic
twins have different placentas that can be separate or fused. Approximately 30%
of monozygotic twins have dichorionic/diamniotic placentas.

Later splitting (ie, 3-8 d after fertilization) results in

monochorionic/diamniotic placentation (see Media file 2). Approximately 70% of
monozygotic twins are monochorionic/diamniotic. If splitting occurs even later (ie,
during 9-12 d after fertilization), monochorionic/monoamniotic placentation
occurs (see Media file 3). Monochorionic/monoamniotic twins are rare; only 1%
of monozygotic twins have this form of placentation.
Monochorionic/monoamniotic twins have a common placenta with vascular
communications between the 2 circulations. These twins can develop twin-to-twin
transfusion syndrome (TTTS). If twinning occurs more than 12 days after
fertilization, then the monozygotic pair only partially split, resulting in conjoined
twins.
 Triplets can be monozygotic, dizygotic, or trizygotic. Trizygotic triplets
occur when 3 sperm fertilize 3 ova. Dizygotic triplets develop from one set of
monozygotic cotriplets and a third cotriplet derived from a different zygote.
Finally, 2 consecutive zygotic splittings with one split results in a vanished fetus
and monozygotic triplets.

Although the evaluation of the placenta or placentas after the birth is

important in all multifetal pregnancies, the examination may not always help
determine zygosity, as in the case of monozygotic twins, in which 30% have a
dichorionic/diamniotic placentation.

Etiology

Mortality/Morbidity

Multifetal pregnancies are high-risk pregnancies. The fetal mortality rate

for twins is 4 times the fetal mortality rate for single births. The neonatal mortality
rate for twins is more than 5 times greater than the neonatal mortality rate for
single births. Higher-order multiple births have even greater mortality rates than
twin and single births.

A high prevalence of low birth weight infants, due to prematurity and

intrauterine growth retardation (IUGR) and their associated complications,
contribute to this problem. Twins have increased frequency of congenital
anomalies, placenta previa, abruptio placenta, preeclampsia, cord accidents, and
malpresentations, as well as asphyxia/perinatal depression, group B
streptococcal (GBS) infections, hyaline membrane disease (HMD), and TTTS.

Race

The frequency of naturally occurring twin births varies by race. Black

women have the highest birth rate of twins, followed by white and Hispanic
women. Asian women have the lowest birth rate of twins. A racial disparity
between black and white twin stillbirths is observed in the United States. Risk of
stillbirth is elevated in black fetuses compared with white fetuses among twins
but not among triplets.

Age

Maternal age has no effect on monozygotic twin births. Advanced

maternal age (>35 y) is associated with increased risk of dizygotic twins.
Prevalence of naturally occurring twin births has increased recently because of
the trend to delay childbearing to later years.

CLINICAL

History

Most multifetal pregnancies are prenatally diagnosed. Maternal complaints

of excessive weight gain, hyperemesis gravidarum, and/or sensation of more
than one moving fetus; use of ovulation-inducing drugs; or family history of
dizygotic twins should alert caregivers to the possibility of a multifetal pregnancy.

Physical

Women with multifetal pregnancies may have a uterine size that is

inconsistently large for dates and may experience accelerated weight gain. Upon
auscultation, more than one fetal heart rate may be heard.

Causes

Risk factors for multifetal pregnancy can be divided into natural and
induced. Risk factors for natural multifetal pregnancy include advanced maternal
age, family history of dizygotic twins, and race. Induced multifetal pregnancies
occur following infertility treatment via the use of ovulation-inducing agents or
gamete/zygote transfer.
WORKUP

Lab Studies

• CBC count: In TTTS, the donor twin is frequently anemic at birth. The
recipient twin is polycythemic at birth.
• Calcium level: Hypocalcemia is common in premature infants, especially
the donor twin in TTTS.
• Glucose level: Hypoglycemia is common in premature infants, especially if
TTTS is present.
• Bilirubin level: Hyperbilirubinemia due to TTTS may develop in
polycythemic infants.

Imaging Studies

• Maternal ultrasonography: This study confirms most multifetal

pregnancies.
• Neonatal head ultrasonography: Premature infants from multifetal
pregnancies have a higher incidence of intraventricular hemorrhage and
periventricular leukomalacia than singleton infants of the same gestational
age.

TREATMENT

Medical Care

Medical care of the woman with multifetal pregnancy is beyond the scope
of this article.

• The specific medical care required by infants from multifetal births varies
and is dictated by whatever complications may be present. Many require
only routine newborn care, whereas those with significant prematurity or
 other complications may require high-level intensive care in specialized
centers.
• The usual method of delivery for higher-order multiple births (eg, triplets,
quadruplets) is cesarean delivery. Cesarean delivery is also the usual
method of delivery for twins in the following situations:
•
o Breech/vertex presentation with the possibility of interlocking twins
o Monoamniotic twins
o Conjoined twins
o Congenital anomalies that threaten increased neonatal morbidity in
a twin
o Delayed interval delivery: Delayed interval delivery of remaining
fetuses in multifetal pregnancies at the border of viability is
becoming more common. Before 30 weeks’ gestation, delayed
delivery for 2 or more days is associated with improved survival in
the second twin.
• Delivery room management of infants from multifetal pregnancies requires
adequate personnel skilled in neonatal resuscitation. Infants from
multifetal pregnancies are at increased risk of birth asphyxia and
respiratory distress syndrome (RDS). Such infants may require bag mask
ventilation and endotracheal intubation in the delivery room.
• Partial exchange transfusion may be necessary in donor or recipient twins
from TTTS.
•
o Partial exchange transfusions are used to increase hemoglobin
concentrations in anemic donor twins while maintaining euvolemia.
Small aliquots (5-15 mL) of packed RBCs are infused (usually via
an umbilical venous catheter) following removal of an equal volume
of the infant's blood until a desired hemoglobin is attained. The
transfused packed RBCs should be appropriately cross-matched,
cytomegalovirus (CMV) negative, and irradiated.
 o Partial exchange transfusions are used to decrease hemoglobin
concentrations in polycythemic recipient twins while maintaining
euvolemia. Small aliquots (5-10 mL) of either a colloid such as
fresh frozen plasma or a crystalloid such as a 0.9% saline solution
are infused (usually via an umbilical venous catheter) following
removal of an equal volume of the infant's blood until a desired
hemoglobin level is attained.

Consultations

A woman with multiple gestation pregnancy may benefit from a

consultation with a perinatologist. A neonatologist may be involved in the
postnatal care of multiple birth infants, particularly if the births are premature or if
congenital anomalies are present.

MEDICATION

Medication requirements vary depending on specific comorbidities. Refer

to the eMedicine topics for the specific complication.

FOLLOW-UP

Complications

• Prematurity: Infants from multifetal pregnancies are more likely to be born

prematurely and are more likely to require neonatal intensive care.
Approximately 50% of twin deliveries occur before 37 weeks' gestation.
The length of gestation inversely decreases with the number of fetuses
present. Infants from multifetal pregnancies represent 20% of very low
birth weight infants.
• Hyaline membrane disease: Twins born at fewer than 35 weeks' gestation
are twice as likely to develop HMD as single birth infants born at fewer
than 35 weeks' gestation. The prevalence of HMD is greater in
monozygotic twins than in dizygotic twins. The concordance rate for HMD
(ie, both twins have HMD) is greater in monozygotic twins than in dizygotic
twins. If only one of a pair of twins develops HMD, then the second twin is
more likely to develop HMD than the first twin.
• Birth asphyxia/perinatal depression: Newborns from multifetal pregnancies
have an increased frequency of perinatal depression and birth asphyxia
due to various causes. Umbilical cord entanglement, locked twins, a
prolapsed umbilical cord, placenta previa, and uterine rupture can occur
and result in asphyxiation of an infant. Cerebral palsy is 6 times more
common in twin births and 30 times more common in triplet births than in
single births. Monochorionic/monoamniotic twins are at highest risk for
cord entanglement. The second-born twin is at greatest risk for birth
asphyxia/perinatal depression.
• Group B streptococcal infections: Early onset GBS infections in low birth
weight infants are nearly 5-fold greater than in average weight singletons.
• Vanishing twin syndrome: Early ultrasonography diagnosis has revealed
that as many as one half of all twin pregnancies result in the delivery of
only a single fetus; the second twin vanishes. Intrauterine demise of one
twin can result in neurologic sequelae in the surviving twin. Acute
exsanguination of the surviving twin into the relaxed circulation of the
deceased twin can result in intrauterine CNS ischemia.
• Congenital anomalies, acardia, twin reversed arterial perfusion sequence:
Congenital anomalies are more common in twins than in a single fetus.
CNS, cardiovascular, and GI defects occur with increased frequency.
Monozygotic twins have increased prevalence of deformations secondary
to intrauterine space constraints. Common deformations in twins include
limb defects, plagiocephaly, facial asymmetry, and torticollis. Acardia is a
rare anomaly unique to multifetal pregnancy. In this condition, one twin
 has an absent or rudimentary heart. Twin reversed arterial perfusion
(TRAP) sequence occurs when an acardiac twin receives all of the blood
supply from the normal "pump" twin. This only occurs in monochorionic
twins. Blood enters the acardiac twin in a reversed perfusion manner.
Blood enters this fetus via an umbilical artery and exits via the umbilical
vein. The excessive demands on the normal "pump" twin can cause
cardiac failure in that twin.
• TTTS: This syndrome occurs in monochorionic/monoamniotic or
monochorionic/diamniotic twins. Vascular anastomoses in the
monochorionic placenta result in transfusion of blood from one twin (ie,
donor) to the other twin (ie, recipient). Polyhydramnios develops in the sac
of the recipient twin because of volume overload and increased fetal urine
output. Oligohydramnios develops in the sac of the donor twin because of
hypovolemia and decreased urine output. Severe oligohydramnios can
result in the stuck twin phenomena, in which the twin appears in a fixed
position against the uterine wall.
• Conjoined twins
•
• Incomplete late division of monozygotic twins produces conjoined
twins.
• Conjoined twins are connected at identical points and are classified
according to site of union, as follows:
•

• Thoracopagus - Joined at chest (40%)

• Xiphopagus/omphalopagus - Joined at abdomen (34%)
• Pygopagus - Joined at buttocks (18%)
• Ischiopagus - Joined at ischium (6%)
• Craniopagus - Joined at head (2%)
• IUGR: The birth weights are smaller in infants from multifetal pregnancies
than weights in corresponding singletons. However, when combined, birth
weights of twins are greater than weights of corresponding singletons.
 Most of the deficit of birth weight occurs in the final 8-11 weeks of
pregnancy. Average birth weights are similar between twins and
singletons until 32 weeks’ gestation. Average birth weights are similar
between triplets and singletons until 29 weeks’ gestation. Birth weight
discrepancies of more than 20-25% are considered discordant. Discordant
birth weights occur in 10% of twins. The cause of discordant birth weight
among twins is the difference between each twin's placental surface area
or TTTS. Discordant birth weights among triplets are more common than
discordant birth weights between twins. Approximately 30% of
pregnancies with triplets have a birth weight discordance of more than
25%.

Prognosis

The prognosis of infants born from multifetal pregnancies depends on the

complications that develop. Some studies have reported that the risks of death,
chronic lung disease, and grade III/IV intracranial hemorrhage were similar in
twins and singletons. Other studies have reported a higher prevalence of
complications such as necrotizing enterocolitis, retinopathy of prematurity, and
patent ductus arteriosus in infants from multifetal pregnancies versus singletons.

MISCELLANEOUS

Medical/Legal Pitfalls

• Most problems that could result in medical legal action against the health
professional involve prenatal and intrapartum care issues.

Special Concerns

• Multiple births have significant economic implications. Twins and triplets

have more frequent and longer duration hospitalizations than singletons.
Multiple births contribute disproportionately to inpatient hospital costs in
the first 5 years of life.
MULTIMEDIA
Diamniotic/dichorionic placentation.

Diamniotic/monochorionic placentation.

Monoamniotic/monoamniotic placentation.
Preliminary Signs of Labor
Before labor, a woman often experiences subtle signs that signal the
onset of labor. All pregnant women should be taught these signs so that they can
recognize when labor is beginning.
• Lightening
This changes a woman’s abdominal contour, because the uterus
becomes lower and more anterior. Lightening gives a woman relief from a
diaphragmatic pressure and shortness of breath that she has been
experiencing and in this way “lightens” her load. As the fetus sinks lower in
the pelvis, the mother may experience shooting leg pains from the
increased pressure on the sciatic nerve, increased amounts of vaginal
discharge, and urinary frequency from pressure on the bladder.

• Increased in Level of Activity

A woman may awaken on the morning of labor full of energy, in
contrast to her feelings of chronic fatigue during the previous month. This
increase in activity is related to an increase in epinephrine release that is
initiated by a decrease in progesterone produced by the placenta.
Additional epinephrine prepares a woman’s body for the work of labor
ahead.

• Braxton Hicks Contractions

Also known as false labor or practice contractions. Braxton Hicks
are sporadic uterine contractions that actually start at about 6 weeks,
although one will not feel them that early. Most women start feeling them
during the second or third trimester of pregnancy. Braxton Hicks
contractions are a tightening of the uterine muscles for one to two minutes
 and is thought to be an aid to the body in its preparation for birth. Not all
expectant mothers have these contractions. They are thought to be part of
the process of effacement, the thinning and dilation of the cervix.

• Ripening of the Cervix

Ripening of the cervix is an internal sign seen only on pelvic
examination. Throughout pregnancy, the cervix feels soften that normal,
similar to the consistency of an earlobe (Goodell’s sign) at term, the cervix
becomes still softer, and it tips forward. Ripening is an internal
announcement that labor is very close at hand.

Signs of True Labor

Signs of true labor involve uterine and cervical changes. The more a
woman knows about true labor signs, the better, because then she will be better
able to recognize them. This is helpful both to prevent preterm birth and for the
woman to feel secure knowing what is happening during labor.

• Uterine Contractions
The surest sign that labor begun is productive uterine contractions.
Because contractions are involuntary and come without warning, their
intensity can be frightening in early labor.

• Show
As the cervix softens and ripens, the mucus plug that filled the
cervical canal during pregnancy (operculum) is expelled. The exposed
cervical capillaries leak blood as a result of pressure exerted by the fetus.
The blood, mixed with mucus, takes on a pink tinge and is referred to as
“show” or “bloody show.”

• Rupture of Membranes
 Labor may begin with rupture of the membranes, experienced
either as a sudden gush or as scanty, slow seeping of clear fluid from the
vagina. Early rupture of membranes can be advantageous if it causes the
fetal head to settle closely into the pelvis, this can actually shorten labor.

Two risks associated with ruptured membranes are intrauterine

infection and prolapse of the umbilical cord, which can cut off the oxygen
supply to the fetus.

DIFFERENTIATION BETWEEN TRUE

AND FALSE LABOR CONTRACTIONS
Type of Change True Labor False Labor
 Occur at regular  Often occur at irregular
Timing of
intervals. intervals.
Contractions  Interval between  Interval between
contraction decreases. contractions remains
the same or increases.
 Increase in  Do not increase in
duration, frequency duration, frequency and
and intensity. intensity.

Location of Contractions  Felt first in the lower  Felt first abdominally

back and sweep and remain confined to
around to the the abdomen and groin.
abdomen in wave
Change with movement  Generally intensified  Generally unaffected by
by walking. walking.
 Continue regardless of  Often disappear with
a woman’s level of ambulation and sleep
activity.
Effects on the Cervix  Results in progressive  Do not result in cervical
 cervical dilatation and dilatation and
effacement effacement.
Response to Sedation  Not affected by mild  Generally relieved by
sedation. mild sedation

BIBLIOGRAPHY
Book Sources:

Pillitteri, Adele. Maternal and Child Health Nursing: Care for the
Childrearing and Childbearing Family. 4th Edition. Volume 1.

Smeltzer, Suzanne and Brenda Bare. Textbook of Medical-Surgical

Nursing. 10th Edition.

Williams and Wilkins. The Lippincott: Manual of Nursing Practice.

8th Edition. Page 1174 – 1269.

Internet Sources:

http://www.emedicine.com/ped/TOPIC2599.HTM

http://www.fetalmonitorstrips.com/learn_more.html

http://www.moondragon.org/pregnancy/truefalselabor.html
http://www.riverwalk-obgyn.com/obcorner/tflabor.html