Preterm Labor

Adapted from dr. Eric Edwin SpOG(K)

Learning Objectives

 Define preterm labor

 Appreciate risk factors and morbidity/mortality associated with preterm labor

 Learn diagnosis for preterm labor

 Learn management of PTL : corticosteroids, tocolytics, and GBS prophylaxis,

DEFINITION OF PRETERM

 Preterm birth  delivery before 37 completed weeks

 Preterm labor  regular contraction before 37 weeks AND associated with cervical
change including dilatation, effacement, or both.

 Preterm Birth :
 Preterm birth before 336/7 weeks  early preterm
 Preterm birth between 34 and 36 completed weeks  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

 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

 4 main direct reasons for preterm births in the United States :

 (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

 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 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 sufficient 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 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 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-for- gestational 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.

 Symptoms :
 Painful or painless uterine contractions, symptoms such as pelvic pressure, menstrual like cramps, watery vaginal
discharge, and lower back pain

 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.
 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. 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 use—up to 48 hours.
Thank You