Preterm Labor

dr. Eric Edwin SpOG(K)

DEFINITION OF PRETERM
Preterm birth defined as delivery before 37 completed weeks
Preterm birth before 336/7 weeks are labeled early preterm
and those occurring between 34 and 36 completed weeks are labeled
late preterm
MORBIDITY IN PRETERM
INFANTS
Various morbidities, largely due to organ system immaturity, are
significantly increased in infants born before 37 weeks gestation
compared with those delivered at term .
Threshold of Viability
Births before 26 weeks are generally considered at the current threshold of
viability, and these preterm infants pose various complex medical, social,
and ethical considerations.
Infants now considered to be at the threshold of viability are those born at
22, 23, 24, or 25 weeks (American College of Obstetricians and
Gynecologists, 2012a,b).
These infants have been described as fragile and vulnerable because of
their immature organ systems. Moreover, they are at high risk for brain
injury from hypoxic-ischemic injury and sepsis.
Because active brain development normally occurs throughout the second
and third trimesters, those infants born at 22 to 25 weeks are believed
especially vulnerable to brain injury.
CAUSES OF PRETERM DELIVERY
There are four main direct reasons for preterm births in the
United States. These include:
(1) spontaneous unexplained preterm labor with intact membranes,
(2) idiopathic preterm premature rupture of membranes (PPROM),
(3) delivery for maternal or fetal indications, and
(4) twins and higher-order multifetal births.
Of all preterm births, 30 to 35 percent are indicated, 40 to 45 percent
are due to spontaneous preterm labor, and 30 to 35 percent follow
preterm membrane rupture (Goldenberg, 2008).
Spontaneous unexplained preterm
labor with intact membranes
Uterine Distention
MaternalFetal Stress
Infection
Spontaneous Preterm Labor
Uterine Distention

There is no doubt that multifetal pregnancy and hydramnios lead to an

increased risk of preterm birth. It is likely that early uterine distention acts
to initiate expression of contraction-associated proteins (CAPs) in the
myometrium.
Excessive uterine stretch also leads to early activation of the placentalfetal
endocrine cascade resulting early rise in maternal corticotropin releasing
hormone and estrogen levels can further enhance the expression of
myometrial CAP genes
Prematurely increased stretch and endocrine activity may initiate events
that shift the timing of uterine activation, including premature cervical
ripening.
Spontaneous Preterm Labor
MaternalFetal Stress
The last trimester is marked by rising maternal serum levels of placental-
derived corticotropin-releasing hormone (CRH). This hormone works with
adrenocorticotropic hormone (ACTH) to increase adult and fetal adrenal
steroid hormone production, including the initiation of fetal cortisol
biosynthesis. Rising levels of maternal and fetal cortisol further increase
placental CRH secretion, which develops a feed-forward endocrine cascade
that does not end until delivery. Rising levels of CRH further stimulate fetal
adrenal dehydroepiandrosterone sulfate (DHEA-S) biosynthesis, which acts
as substrate to increase maternal plasma estrogens, particularly estriol.
It has been hypothesized that a premature rise in cortisol and estrogens
results in an early loss of uterine quiescence. A number of studies have
reported that spontaneous preterm labor is associated with an early rise in
maternal CRH levels and that CRH determination may be a useful biomarker
for preterm birth risk assessment.
Spontaneous Preterm Labor
Infection
Current data suggest that microbial invasion of the reproductive tract is sufficient to
induce infection-mediated preterm birthmore specifically, there is ongoing
subclinical infection. However, microorganisms certainly are not ubiquitous in the
amnionic uid of all women with preterm labor, and indeed, positive cultures are
found in only 10 to 40 percent (Goncalves, 2002).
It has been suggested that bacteria can gain access to intrauterine tissues through:
(1) transplacental transfer of maternal systemic infection,
(2) retrograde ow of infection into the peritoneal cavity via the fallopian tubes, or
(3) ascending infection with bacteria from the vagina and cervix.
Some microorganismsexamples include Gardnerella vaginalis, Fusobacterium,
Mycoplasma hominis, and Ureaplasma urealyticumare detected more frequently
than others in amnionic uid of women with preterm labor (Gerber, 2003; Hillier,
1988; Yoon, 1998)
Spontaneous Preterm Labor
Preterm Premature Rupture of Membranes
This term defines spontaneous rupture of the fetal membranes before
37 completed weeks and before labor onset (American College of
Obstetricians and Gynecologists, 2013d).
Such rupture likely has various causes, but intrauterine infection is
believed by many to be a major predisposing event. Preterm membrane
rupture pathogenesis may be related to increased apoptosis of
membrane cellular components and to increased levels of specifc
proteases in membranes and amnionic uid.
ANTECEDENTS AND
CONTRIBUTING FACTORS
Threatened Abortion
Lifestyle Factors
Cigarette smoking, inadequate maternal weight gain, and
illicit drug
Genetic Factors
Birth Defects
Periodontal Disease
Interval between Pregnancies
Intervals < 18 months and > 59 months were associated
with increased risks for both preterm birth and small-forgestational age
newborns.
Prior Preterm Birth
Infection
DIAGNOSIS
Preterm labor is primarily diagnosed by symptoms and physical
examination.
Sonography is used to identify asymptomatic cervical dilation and
eacement.
Accordingly, the American Academy of Pediatrics and the American
College of Obstetricians and Gynecologists (2012) define preterm labor
to be regular contractions before 37 weeks that are associated with
cervical change.
In addition to painful or painless uterine contractions, symptoms such
as pelvic pressure, menstrual-like cramps, watery vaginal discharge, and
lower back pain have been empirically associated with impending
preterm birth.
Cervical Change
Dilatation
Asymptomatic cervical dilatation after midpregnancy is suspected to be
a risk factor for preterm delivery

Length
The mean cervical length at 24 weeks was approximately 35 mm, and
those women with progressively shorter cervices experienced increased
rates of preterm birth
MANAGEMENT OF PRETERM PREMATURELY
RUPTURED MEMBRANES
MANAGEMENT OF PRETERM LABOR WITH
INTACT MEMBRANES
Corticosteroids for Fetal Lung Maturation
Corticosteroid therapy was eective in lowering the incidence of
respiratory distress syndrome and neonatal mortality rates if birth
was delayed for at least 24 hours after initiation of betamethasone.
Antimicrobials
Bed Rest
Tocolysis to Treat Preterm Labor
Tocolysis to Treat Preterm
Labor
Although several drugs and other interventions have been used to
prevent or inhibit preterm labor, none has been shown to be completely
eective. The American College of Obstetricians and Gynecologists
(2012a) has concluded that tocolytic agents do not markedly prolong
gestation but may delay delivery in some women for up to 48 hours.
Beta-adrenergic agonists, calcium-channel blockers, or indomethacin
are the recommended tocolytic agents for such short-term useup to
48 hours.
Thank You