Labor Abnormalities
Timely onset of labor and delivery has an important
role in pregnancy outcome. Both preterm and postterm births are at higher risk
for poor outcomes than pregnancies delivered at term.
Preterm labor
Preterm labor is the onset of labor
before 37 weeks’ gestation. It is the final common pathway for a number of
conditions that induce uterine contractions at a time when the uterus is
normally quiescent.
Preterm labor complicates 7–10% of
all pregnancies and is a very large contributor to perinatal morbidity and
mortality. Although over half the cases of preterm labor occur without warning, some
factors do carry an identifiable risk: multiple gestation, uterine anomalies,
third trimester bleeding, intrauterine infection, excessive amniotic fluid
volume, maternal smoking and a history of prior preterm delivery. There have
been many unsuccessful attempts to use risk scoring, close clinical observation
and home uterine contraction moni toring to predict women at high risk for
preterm labor. Several bio chemical markers suggest increased risk of preterm
labor: raised salivary estriol, which reflects activation of the fetal
hypothalamic pituitary adrenal axis, and cortisol releasing hormone, which is
syn thesized by the placenta (Chapters 19 and 22). Fetal fibronectin is
normally restricted to the fetal compartment but will appear in vaginal
secretions of women who are at risk for preterm delivery. Therefore the absence
of fetal fibronectin in maternal vaginal secretions is highly predictive of
women who will not experience preterm labor.
Potential mechanisms for preterm
labor
The normal
mechanisms involved in labor (Chapter 22) predict the pathways for stimuli that
start labor prematurely. For instance, intrauterine infection is associated
with an elevation in the amniotic fluid levels of the cytokines interleukin-1β,
interleukin-6 and tumor necrosis factor α (TNF-α). Products of the
cyclo-oxygenase and prostaglandin pathways are also elevated in patients with
intrauterine infections. Cytokines and prostaglandins act synergistically to
stimulate the myometrium. Their premature
elevation with intrauterine infection could activate the uterus prematurely.
Recently, thrombin has been shown to be an extremely potent uterotonic agent.
The increase in thrombin production that accompanies bleeding in pregnancy may
cause preterm labor. Multiple gestations and excessive amniotic fluid
excessively stretch the myometrial syncytium. While this may stimulate muscle
activity, it is unclear how fiber stretching produces the regular, coordinated
contractions of labor.
Pharmacologic interventions
In some
cases of preterm labor, contractions represent an attempt by the uterus to
expel the fetus from a hostile intrauterine environment. This may be the goal
when premature labor accompanies intrauterine infection. It is usually not
prudent to intervene by attempting to stop labor in these clinical situations.
When the cause of preterm labor does not independently place the fetus in
danger, pharmacologic attempts to stop the premature contractions may be used
(Fig. 37.1). Several agents, called tocolytics, are available to inhibit
premature uterine contractions. Tocolytics work by interrupting one of four
processes: (i) intracellular Ca2+ homeostasis; (ii) myosin phosphorylation;
(iii) prostaglandin synthesis; and (iv) oxytocin binding to its receptors (Fig.
37.1). Calcium ions are required for normal myometrial contractions. Magnesium sulfate
(MgSO4) acts as a competitive antagonist for Ca2+ and is a
commonly used tocolytic. High extracellular magnesium concentrations inhibit Ca2+
entry into myometrial cells via voltage operated channels. In addition, intracellular
magnesium competes with Ca2+ for binding sites on calmodulin. Decreased
calcium calmodulin binding decreases the activity of myosin light chain kinase and
muscle contraction. Nifedipine and
nitrendipine are type II (dihydropyridine) calcium channel blockers. They
prevent Ca2+ influx through the cell membrane into the myometrial
cells via the voltage-operated Ca2+ channels. Beta-adrenergic
agonists, such as ritodrine, salbutamol, iso xsuprine and terbutaline, bind to β2-adrenergic
receptors on the myo- metrial cell membrane, activate G proteins and increase
intracellular cAMP levels. An increase in cAMP levels activates protein kinase
A. Activated protein kinase A inhibits myosin light chain phosphoryla- tion.
Prostaglandins E and F2α stimulate uterine contractions. The
tocolytic, indomethacin, reduces prostaglandin production. It competi tively
inhibits cyclo-oxygenases that are necessary for conversion of arachidonic acid
to prostaglandins. Oxytocin antagonists bind to the oxytocin receptor but do
not activate it. Antagonist-binding blocks activation by the agonist oxytocin.
Progesterone prophylaxis has been shown to reduce the rate of preterm birth
among women with a history of spontaneous preterm delivery. The mechanism of
action of the supplemental progesterone is not known.
Postterm pregnancy
Postterm pregnancy refers to a
pregnancy that has extended to or beyond 42.0 weeks’ gestation or 294 days from the
first day of the last normal menstrual period. About 2% of pregnancies dated by
first trimester ultrasound go postterm. The cause of postterm pregnancy is
largely unknown. Risk factors include first pregnancy, male fetus, obesity,
prior postterm pregnancy and maternal postterm birth. The latter two factors
suggest that maternal genetic factors may have a role. Interesting recent data
indicate that paternal genes expressed in the fetus may also be involved. Early
reports that placental sulfatase deficiency and fetal anencephaly are
associated with postterm pregnancy have not been corroborated.
Postterm pregnancy is linked to
increased maternal and fetal risk. Labor abnormalities and cesarean deliveries
increase because of fetal overgrowth and placental dysfunction. Fetal risks include
stillbirth, asphyxia and birth injury from overgrowth. Management of the
postterm pregnancy may include induction at 41.0 weeks’ gestation or expectant
management with close fetal surveillance.
Placental abnormalities
Placental abruption is defined as
premature separation of the placenta prior to delivery of the fetus. Typical symptoms of
placen- tal abruption are vaginal bleeding and abdominal pain that are often
accompanied by frequent prolonged uterine contractions, uterine tenderness and
fetal distress. Placental abruption complicates about 1% of all births. Severe
abruptions can result in stillbirth (Chapter 36).
Risk factors
for placental abruption that precedes labor include maternal trauma,
hypertension, uterine anomalies, inherited and acquired clotting disorders,
abruption or pre-eclampsia in a prior pregnancy, poor fetal growth, cocaine
use, cigarette smoking and acute intrauterine infection. Rupture of the fetal
membranes, either prior to the onset of labor or during labor in the presence
of excess amniotic fluid, is also associated with increased risk for placental
abruption.
Most
commonly, the cause of the placental separation is the rupture of maternal
vessels in the decidua basalis next to the placental villi. Rupture of vessels
may result from acute trauma, high intravascular pressures or from chronic
inflammation and/or necrosis. Maternal blood infiltrates into the decidua and
lifts it off of the placenta. The resulting hematoma may stay small or it may
enlarge to completely separate the placenta from the uterine wall. Thrombin, an
important component of the clotting cascade, is released from the decidua in response
to the local hypoxia that accompanies abruption. Thrombin is a very potent
uterotonic agent; its release likely produces the exaggerated uterine
activity seen with abruption. Thrombin also induces expression of inflammatory
cytokines, leading to additional vascular disruption. The detached portion of
the placenta cannot exchange gases or deliver nutrients for the duration of the
pregnancy. Pregnancy outcome is largely dependent on the size of the
separation.
The amount
of vaginal bleeding from a placental abruption is not a good indicator of the
extent of the separation because some or all of the bleeding can be concealed
within the uterus. In cases of abruption severe enough to kill the fetus,
maternal disseminated intravascular coagulation can develop due to consumption
of available clotting factors by the massive amounts of released thrombin.
Management of placental abruption depends on severity and gestational age.
Placenta previa refers to the
presence of placental tissue overlying or extremely close to the internal os
of the cervix. It occurs in 5–6% of first trimester gestations; however, placental
migration away from the cervix results in an incidence of 0.5% in the third
trimester. The diagnosis is made by ultrasound examination of the pregnancy
within the uterus. Risk factors for placenta previa include prior cesarean
delivery and uterine curettage, advancing maternal age and parity, cigarette
smoking, multiple gestation and male fetal gender. Conditions associated with
placenta previa include placenta accreta, velamentous umbilical cord
insertion, vasa previa and abnormal fetal lie. Placenta accreta occurs
when the placenta traverses the decidua and invades the myometrium. Velamentous
insertion of the umbilical cord occurs when the fetal blood vessels do not
insert on the disc of the placenta, presumably as a result of abnormal
placental migration. Vasa previa is a rare condition in which the umbilical
blood vessels insert onto the fetal membranes instead of the placenta and a
fetal vessel lies over the internal os of the cervix.
Placenta
previa is thought to occur when an embryo fails to implant in the upper segment
of the uterus. Reasons for the abnormal implantation include scarring of the
uterus from cesarean deliveries, uterine curettage and prior pregnancies, a
need for increased placental surface area to compensate for a reduction in
uteroplacental nutrient or oxygen delivery such as occurs with maternal smoking
or multiple gestation, and delayed implantation associated with later
fertilization in male embryos. An abnormal fetal lie may result from the large
volume of placenta in the lower portion of the uterine cavity with a placenta
previa.
Abnormal fetal lie and presentation
The term “lie” refers to the
orientation of the fetus in the uterus. By far the most common fetal lie is longitudinal.
Transverse lie means the fetus is lying sideways in the uterus. Occasionally,
the fetal and maternal axes will cross at a 45° angle, forming an oblique lie.
Oblique lies are unstable and will usually convert to a longitudinal lie in
labor. Only longitudinal lies can safely be delivered vaginally.
Presentation refers to the fetal
part that is in closest proximity to the birth canal. The most common fetal
presentation is head-down (cephalic or vertex); 95% of fetuses are vertex at
term. The second most common presentation is breech, in which the fetal legs or
buttocks are just above the cervix. A shoulder typically presents when the
fetus is lying transverse.
The major
risk factor for abnormal fetal lie and presentation is prematurity. Other risk
factors include fetal malformations, congenital neuromuscular disorders,
multiple gestation, uterine malformations and high maternal parity (number of
prior births).
