Preterm Labor

dr. Eric Edwin SpOG(K)

DEFINITION OF PRETERM
Preterm birth defned 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 signifcantly 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
Tere 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
 Maternal–Fetal Stress
 Infection
Spontaneous Preterm Labor
Uterine Distention
Tere 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 placental–fetal endocrine cascade
resulting early rise in maternal corticotropinreleasing 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.
Maternal–Fetal 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 .
Infection
Current data suggest that microbial invasion of the reproductive tract is sufcient to induce infection-
mediated preterm birth—more specifcally, there is ongoing “subclinical” infection. However,
microorganisms certainly are not ubiquitous in the amnionic fluid 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 flow of infection into the peritoneal cavity via the fallopian tubes, or
(3) ascending infection with bacteria from the vagina and cervix.
Some microorganisms—examples include Gardnerella vaginalis, Fusobacterium, Mycoplasma
hominis, and Ureaplasma urealyticum—are detected more frequently than others in amnionic fluid
of women with preterm labor (Gerber, 2003; Hillier, 1988; Yoon, 1998)
Preterm Premature Rupture of Membranes
This term defnes 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 fluid.
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 effacement.
Accordingly, the American Academy of Pediatrics and the American College of Obstetricians and
Gynecologists (2012) defne 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 effective 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 effective. Te 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 use—up to 48 hours.
Thank You