preterm infants pose various complex medical,
Preterm Birth
Lourdes R. Abeleda,MD
June 16, 2014
I. INTRODUCTION
Birthweight
 Low birthweight = neonates who are born too
small
o Births 500 to 2500 g
 Very low birthweight
o Births 500 to 1500 g
 Extremely low birthweight
o Births 500 to 1000 g
Preterm or premature births:
Define neonates who are born too early
Respect to size:
 Appropriate for gestational age (AGA)
o Weight is between the 10th and 90th
percentiles
 Small for gestational age (SGA)
o Categorize newborns whose birthweight
is usually below the 10th percentile for
gestational age
o Fetal-growth restriction or intrauterine
growth restriction
 Large for gestational age (LGA)
o Categorize newborns whose birthweight
is above the 90th percentile for
gestational age.
Preterm birth
 Delivery before 37 completed weeks
 Prematurity responsible for incomplete
development of various organ system
Early Preterm
 Births 37 6/7 weeks through 38 6/7 weeks
Term
 39 weeks to 40 6/7 weeks
Late preterm births
 Delivery between 34 to 36 weeks' gestation
 70% of all preterm birth
II. MORBIDITY IN PRETERM INFANT
 Largely due to system immaturity
 Very small infants suffer disproportionately not
only the immediate complications of prematurity
but also long-term sequelae such as
neurodevelopmental disability.
 After achieving a birthweight of ≥1000 g or a
gestational age of 28 weeks females to 30 weeks
males: survival rates reach 95%
Mortality & Morbity at extremes of prematurity
 There has been uncertainty and controversy as to
the lower limit of fetal maturation compatible
with extrauterine survival.
 Resulted in continual reassessment of the
threshold of viability.
 Births before 26 weeks are generally considered
at the current threshold of viability, and these
social, and ethical considerations.
 Infants now considered to be at the threshold of
viability are those born at 22, 23, 24, or 25
weeks (ACOG, 2012a,b). These infants have
been described:
o As fragile and vulnerable because of
their immature organ systems.
o High risk for brain injury from hypoxic-
ischemic injury and sepsis.
 Cesarean delivery at the threshold of viability is
controversial.
Policy for threshold of viability at Parkland hospital
 At 25 weeks
o All fetal indications for cesarean
delivery in more advanced pregnancies
 At 23 weeks
o Cesarean delivery is not offered for fetal
indications
 At 24 weeks
o Cesarean delivery is not offered unless
fetal weight is estimated ≥750 g
o Growth restriction: aggressive
obstetrical management
Late preterm birth
 Infants 34-36 weeks : approximately 75% of all
preterm births
 Late preterm births accounted for 3/4 of all
preterm births
 Approximately 80 percent of these were due to
idiopathic spontaneous preterm labor or
prematurely ruptured membranes
 Complications such as hypertension or placental
accidents were implicated in approximately 20%
of cases
III. REASONS FOR PRETERM DELIVERY
Four Main Reason for Preterm Delivery
 Spontaneous unexplained preterm labor with
intact membranes
 Idiopathic preterm premature rupture of
membranes (PPROM)
 Twins and higher-order multifetal births.
 Maternal or fetal indication
Basic Science of SPONTANEOUS LABOR.
 Pregnancies with intact fetal membrandes and
spontaneous preterm labor must be distinguished
from those complicated by PPROM.
 More common associated findings are multifetal
pregnancy, intrauterine infection, bleeding,
placental infarction, premature cervical
dilatation, cervical insufficiency, hydramnios,
uterine fundal abnormalities
 Severe maternal illness as a result of infections,
autoimmune diseases, and gestational
hypertension also increases preterm labor risks.
Major causes of spontaneous preterm labor
 Uterine distension
 Maternal-fetal stress
 Premature cervical changes
 Infection
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Uterine distension
 Multifetal pregnancy and hydramnios
 Acts to initiate expression of contraction
associate proteins in the myometrium
 CAP genes- influenced by stretch include those
coding for gap-junction proteins such as
connexion 43, for oxytocin receptors and
prostaglandin synthase.
 Gastrin-releasing peptides (GRP’s)- increase
with stretch to promote myometrial contractility
 GRP antagonists can inhibit uterine contractility
 Stretch induced potassium channel—TREK-1—
that is upregulated during gestation and
downregulated in labor.
 Excessive uterine stretch causes premature loss
of myometrial quiescence.
 Leads to early activation of the placental-fetal
endocrine cascade
o 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.
Maternal-fetal stress
 Stress is defined as a condition or adverse
circumstance that disturbs the normal
physiological or psychological functioning of an
individual.
 Complexities of measuring ―stress‖.
 Maternal psychological stress and the placental–
adrenal endocrine axis that provides a potential
mechanism for stress-induced preterm birth.
 Last trimester- rising maternal serum levels of
placentalderived corticotropin-releasing
hormone (CRH) works with
adrenocorticotropic hormone (ACTH) to
increase adult and fetal adrenal steroid hormone
production, including the initiation of fetal
cortisol biosynthesis.
 Rising CRH Cortisol stimulate fetal
adrenal dehydroepiandrosterone sulfate (DHEA-
S) biosynthesis, which acts as substrate to
increase maternal plasma estrogens, particularly
estriol.
 Premature rise in cortisol and estrogen early
loss of uterine quiascent and accelerate cervical
ripening.
Infection
 Some cases – histological evidence of
inflammation in the fetal membrances, deciduas
or umbilical cord
 Other cases – ―sublinical‖
 Microbial invasion of the reproductive tract is
sufficient to induce infection-mediated preterm
birth- more specifically, there is ongoing
―subcinical‖ infection.
 Women with amnionic fluid bacteria are more
likely to develop clinical chorioamnionitis and
preterm ruptured membranes compared with
women with sterile cultures.
 The earlier the onset of preterm labor the greater
the likelihood of documented infection
 In preterm pregnancies – bacteria represent an
important cause of labor
o Data that associayte chorioamnionitis
with preterm labor
 The microbes may invaded
maternal tissue only and not
amniotic fluid.
 Endotoxins can stimulate
amnionic cells to secrete
cytokines that enter amnionic
fluid.
Sources of infection
 Bacteria can gain access intrauterine tissues
through
o Transplacental transfer of maternal
systemic infection
o Retrograde flow of infection into the
peritoneal cavity via the fallopian tubes
o Ascending infection with bacteria ffrom
the vagina and cervix – MOST
COMMON.
4 Stages of microbial invasion
 Bacterial vaginosis
 Decidual infection
 Amniotic infection
 Fetal systemic infection
**progression of these stages is thought to increase rates
of preter birth and neonatal morbidity.
Ascending microorganisms colonize the cervix,
decidua, and possibly the membranes, where they then
may enter the amnionic sac. Lipopolysaccharide (LPS)
or other toxins elaborated by bacteria induce immune-
cell recruitment into the reproductive tract and cytokine
production by immune cells and by cells within the
cervix, decidua, membranes, or fetus itself.
LPS and cytokines then provoke prostaglandin
release from the membranes, decidua, or cervix. These
may influence both cervical ripening and loss of
myometrial quiescence.
Microbes Associated with preterm birth
 Garnerella vaginalis, Fusobacterium,
Mycoplasma hominis, and Ureaplasma
urealyticum
 Fusobacteria – more capable of burrowing
through these tissues.
 Initial inflammatory response – specific
receptors on mononuclear phagocytes, dicidual
cells, cervical epithelia, and trophoblast.
 Toll-like receptors represent a family that has
evolved to recognize pathogen-associated
molecules.
 Influence of ligands such as bacterial LPS
influence of ligands such as bacterial LPS, these
receptors increase chemokine, cytokine, and
prostaglandin release as part of an inflammatory
response. (Interleukin 1β).
Intrauterine inflammatory response.
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  Interleukin 1β (IL-1β) promote a series of
responses.
o Increased synthesis of others, that is, IL-
6, IL-8, and tumor-necrosis factor alpha
(TNF-α);
o Proliferation, activation, and migration
of leukocytes;
o Modifications in extracellular matrix
proteins;
o Mitogenic and cytotoxic effects such as
fever and acute-phase response.
**IL-1 promotes prostaglandin formation in many
tissues, including myometrium, decidua, and amnion.
 Prostaglandin inhibitors can reduce the rate of
LPS-induced preterm birth in both the mouse
and nonhuman primate.
 Inhibition of cyclooxygenase-2 prevents
inflammation-mediated preterm labor in the
mouse.
 Immunomodulators plus antibiotics delay
preterm delivery after experimental
intraamnionic infection in a nonhuman primate
model.
Origin of cytokines
 Transfer of cytokines such as IL-1 from decidua
across the membranes into amnionic fluid
appears to be severely limited.
 Cytokines produced in maternal decidua and
myometrium will have effects on that side
 Cytokines produced in the membranes or in cells
within the amnionic fluid will not be transferred
to maternal tissues.
 (+) infection leukocytes - mainly neutrophils,
macrophages and T lymphocytes- infiltrate the
cervix, lower uterine segment fundus, and
membranes at the time of labor.
 Term labouring uterus have shown that both
invading leukocytes and certain parenchymal
cells produce cytokines
o Leukocytes appear to be the primary
source of myometrial cytokines,
including IL-1, IL-6, IL-8, and TNF-α.
o IL-8 is considered a critical cytokine in
cervical dilation, and it is produced in
both cervical epithelial and stromal
cells.
 Amniotic fluid – secreted by mononuclear
phagocytes or neutrophils activated and
recruited into amniotic fluid.
o Amount of amnionic fluid IL-1 would
be determined by the number of
leukocytes recruited, their activational
status, or the effect of amnionic fluid
constituents on their IL-1 secretion rate.
PRETERM PREMATURE RUPTURE OF
MEMBRANES (PPROM)
Spontaneous rupture of the fetal membranes
before 37 completed weeks and before onset of labor.
Risk Factor
 Intrauterine infection
 Low socioeconomic status
 Body mass index <19.8
 Nutritional deficiencies
 Cigarette smoking
 Prior PPROM
Molecular Changes
 Related to increased apoptosis of membrance
cellular components and to increased levels of
specific proteases in membranes and amniotic
fluid.
 Tensile strength of the membranes – provided by
the amniotic extracellular matrix and interstitial
amniotic collagens – primarily type I and III-
which are produced in mesenchymal cell.
 Matrix metalloproteinase (MMP) family is
involved with normal tissue remodeling and
particularly with collagen degradation.
 MMP-1, MMP-2, MMP-3, and MMP-9
members of this family are found in higher
concentrations in amnionic fluid from
pregnancies with preterm prematurely ruptured
membranes.
 MMP activity is in part regulated by tissue
inhibitors of matrix metalloproteinases—TIMPs.
 The expression of MMPs can be increased by
treatment with IL-1, TNF-α, and IL-6.
 The amnion exhibits a higher degree of cell
death and more apoptosis markers than that in
term amnion.
 PPROM cases result from collagen degradation,
altered collagen assembly, and cell death, which
all lead to a weakened amnion.
Infection
 Inflammatory-induced premature rupture of
membrane
 Inflammatory response that leads to membrane
weakening.
 Research is focused on mediators if this process
with a goal to identify early risk for PPROM.
Multifetal Gestation
 Increased rate of multifetal births is due to the
increased number of women having babies after
the age of 30 at which time the risk to conceive
multiples rise.
 Use of fertility treatments has contributed to the
elevated rates of multifetal pregnancies
 Effect of uterine stretch.
Myriad genetic and environment factors affect the
frequency of preterm labor.
 Threatened Abortor
o Vaginal bleeding in early pregnancy (6-
13 weeks) preterm labor, placental
abruption, and subsequent pregnancy
loss before 24 weeks
 Lifestyle Factors
o Cigarette smoking, inadequate maternal
weight gain and illicit drug use.
o Overweight and obese mothers
o Young or advanced maternal age,
poverty, short stature, and vitamin C
deficiency.
o Psychological factors such as
depression, anxiety and chronic stress.
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 o Working long hours and hard physical
labor are probably associated with
increased risk of preterm birth
 Genetic Factors
o Recurrent, familial, and racial nature of
preterm birth
o Immunoregulatory genes in potentiating
chorioamnionitis in cases of preterm
delivery due to infection
 Birth Defects
o First- and Second-Trimester Evaluation
of Risk (FASTER) Trial
 Found that birth defects were
associated with preterm birth
and low birthweight
 Periodontal defects
o Gum inflammation is a chronic
anaerobic inflammation
 Treatment during pregnancy
improved periodontal disease
and that it is safe. However,
treatment failed to significantly
alter preterm birth rates
 Interval between pregnancies
o Short intervals between pregnancies
have been known for some time to be
associated with adverse perinatal
outcomes.
o Intervals < 18 months and > 59 months
were associated with increased risks for
both preterm birth and smallfor-
gestational age newborns.
 Prior Preterm Birth
o Major risk factor
o 1st delivery is preterm-3fold risk
o 1st & 2nd delivery are preterm – 1/3 of
women will deliver preterm
o 70% occurred within 2weeks of the
gestational age of the prior preterm
delivery
o Causes of prior preterm delivery also
recurred.
 Infection
o Intrauterine infections are believed to
trigger preterm labor by activation of the
innate immune system.
o Microorganisms elicit release of
inflammatory cytokines such as
interleukins and TNF-α, which in turn
stimulate the production of
prostaglandin and/or matrix-degrading
enzymes.
o Prostaglandins stimulate uterine
contractions, whereas degradation of
extracellular matrix in the fetal
membranes leads to preterm rupture of
membranes.
Symptoms
Causes of Preterm birth
 Infection
o Antimicrobial treatment has been given
to prevent preterm labor due to
microbial invasion. Based on available
data, these strategies especially targeted
mycoplasma species.
o Given in the second trimester may
prevent subsequent preterm birth.
o Study placebo or metronidazole plus
erythromycin between 20 and 24 weeks’
gestation followed by ampicillin plus
metronidazole during labor.
 This antimicrobial regimen did
not reduce the rate of preterm
birth or that of histological
chorioamnionitis.
 Bacterial Vaginosis
o Normal, hydrogen peroxide-producing,
lactobacillus-predominant vaginal flora
is replaced with anaerobes that include
Gardnerella vaginalis, Mobiluncus
species, and Mycoplasma hominis
o Using Gram staining, relative
concentrations of the bacterial
morphotypes characteristic of bacterial
vaginosis are determined and graded as
the Nugent score.
o Bacterial vaginosis has been associated
with spontaneous abortion, preterm
labor, PPROM, chorioamnionitis, and
amnionic fluid infection.
o Environmental factors appear to be
important in bacterial vaginosis
development. Exposure to chronic
stress, ethnic differences, and frequent
or recent douching have all been
associated with increased rates of the
condition
o Gene-environment interaction
 Susceptible TNF-α genotype
had a ninefold increased
incidence of preterm birth.
IV. DIAGNOSIS
 Early differentiation between true and false
labor is difficult
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  Braxton hicks contraction – irregular,
nonrhythmical and either, and either painful or
painless
 ACOG 2012, define preterm labor to be regular
contractions before 37 weeks that are associated
with cervical change.
 Pelvic pressure, menstrual-like cramps, watery
vaginal discharge, and lower back pain have
been empirically associated with impending
preterm birth.
Cervical Change
 Dilation
o Asymptomatic cervical dilatation after
midpregnancy is suspected to be a risk
factor for preterm delivery.
o Cervical examination were not related to
preterm membrane rupture
o Prenatal cervical examination are
neither beneficial nor harmful.
 Length
o Vaginal-probe sonographic cervical
assessment
 Not affected by maternal
obesity, cervix position, or
shadowing from the fetal
presenting part.
o Safe, highly reproducible, and more
predictive than transabdominal
sonographic screening
o Mean cervical length at 24 weeks was
approximately 35mm and those women
with progressively shorter cervices
experienced increase rates of preterm
birth.
o The risk of spontaneous preterm birth
increase as the length of the cervix
decrease across the entire range if
cervical length.
o Cervical Length and Funnelling
 T shaped cervix - best
 Y shaped cervix
 V shaped cervix
 U shaped cervix – poor,
associated with cervical
dilatation
Ambulatory Uterine Monitoring
 An external tocodynamometer belted around the
abdomen and connected to an electronic waist
recorder allows a woman to ambulate while
uterine activity is recorded.
 Women are educated concerning signs and
symptoms of preterm labor, and clinicians are
kept apprised of their progress.
 ACOG does not recommend home uterine
activity monitoring.
Fetal fibronectin
 Glycoprotein is produced in 20 different
molecular forms by various cell types, including
hepatocytes, fibroblasts, endothelial cells, and
fetal amnion.
 High concentrations in maternal blood and in
amnionic fluid, it is thought to function in
intercellular adhesion during implantation and in
maintenance of placental adherence to uterine
deciduas.
 Detected in cervicovaginal secretions in women
who have normal pregnancies with intact
membranes at term.
 It appears to reflect stromal remodeling of the
cervix before labor.
 Detection in cervicovaginal secretions before
membrane rupture was a possible marker for
impending preterm labor.
 (+) > 50ng/ml (ELISA)
 ACOG does not recommend screening with fetal
fibronectin tests.
o fetal fibronectin screening in
asymptomatic women have not
demonstrated improved perinatal
outcomes.
V. PRETERM BIRTH PREVENTION
Prevention of preterm birth has been an elusive goal.
Recent reports, however, suggest that prevention in
selected populations may be achievable.
 Cervical cerclage
There are at least three circumstances when
cerclage
o Prophylactic cerclage is used in women
who have a history of recurrent
midtrimester losses and who are
diagnosed with cervical insufficiency
o Prophylactic cerclage is for women
identified during sonographic
examination to have a short cervix.
o ―rescue‖ cerclage, done emergently
when cervical incompetence is
recognized in women with threatened
preterm labor.
o Owen (2009) - Women with a cervical
length < 15 mm delivered before 35
weeks significantly less often following
cerclage compared with women with no
cerclage—30 versus 65 percent.
 Recurrent preterm birth can be
prevented in a subset of women
who have a history of prior
preterm births.
o To and associates (2004) - 253 women
with cervices < 15 mm to cerclage or no
cerclage.
 The frequency of preterm
delivery < 33 weeks was not
significantly different between
the treatment groups.
 Cerclage for sonographically
detected short cervix alone has
not been found to be beneficial.
 Women with a very short
cervix, that is, < 15 mm, and a
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 history of prior preterm birth
may benefit.
Prophylaxis with progestin Compounds
 Progesterone levels in most mammals fall
rapidly before the onset of labor.
 Parturition-triggering event – progesterone
withdrawal.
 Human parturition involves functional
progesterone withdrawal mediated by decreased
progesterone activity of progesterone receptors.
 Administration of progesterone to maintain
uterine quiescence may block preterm labor.
VI. MANAGEMENT OF PPROM
 History of vaginal leakage of fluid, either as
continous stream or as a gush.
 Speculum exam to visualize gross vaginal
pooling of amniotic fluid, clear fluid from the
cervical canal
 Sonographic exam to assess amniotic fluid
volume, to identify the presenting part, and if not
previously determined, to estimate gestational
age
 Amniotic fluid is slightly alkaline (pH 7.1-7.3)
compared with vagina (pH 4.5-6.9)
Hospitalization
 Most clinicians hospitalize women with
PPROM.
 Carlan & co-workers (1993)-No benefits were
found for hospitalization.
 Concern regarding the cost of lengthy
hospitalization.
Intentional Delivery
 1970s, labor was usually induced in women with
preterm ruptured membranes because of fear of
sepsis.
 Reduced the length of maternal hospitalization
and also reduced infection rates in both mothers
and neonates.
Expectant Management
 Despite extensive literature concerning
expectant management of PPROM, tocolysis has
been used in few studies.
o Investigators concluded that active
interventions did not improve perinatal
outcomes
 Use of digital cervical examination and cerclage.
o Women who were examined had a
rupture-to-delivery interval of 3 days
compared with 5 days in those who were
not examined. This difference did not
worsen maternal or neonatal outcomes.
 114 women with cerclage in place who later had
ruptured membranes before 34 weeks. They
were compared with 288 controls who had not
received a cerclage.
o Pregnancy outcomes were equivalent in
both groups.
 Management is controversial
Risks of Expectant Management
 Maternal and fetal risks vary with the gestational
age at membrane rupture.
 Neurologic abnormality, oligohydramnios,
pulmonary hypoplasia, limb compression
deformities, infectious morbidity, umbilical cord
prolapsed.
 23 weeks or less is the threshold for
development of lung hypoplasia
Clinical Chorioamnionitis
 Prolonged membrane rupture: increased fetal
and maternal sepsis
 Chorioamnionitis is diagnosed, prompt efforts to
effect delivery, preferably vaginally.
 Fever is the only reliable indicator for this
diagnosis, and temperature of 38°C (100.4°F) or
higher accompanying ruptured membranes
implies infection.
 Maternal leukocytosis alone has not been found
to be reliable
 WOF- maternal or fetal tachycardia, for uterine
tenderness, and for a malodorous vaginal
discharge.
 Increase incidence of sepsis, RDS, early onset
seizures, intraventricular hemorrhage and
preventricular leukomalacia
 Neurological injury, cerebral palsy.
Accelerated Pulmonary Maturation
 Various clinical events—some well defined—
were once proposed to accelerate fetal surfactant
production
 Chronic renal or cardiovascular disease,
hypertensive disorders, heroin addiction, fetal-
growth restriction, placental infarction,
chorioamnionitis, and preterm ruptured
membranes.
Antimicrobial Therapy
Mercer & associates (1995) reviewed 13 randomized
trials performed before 35 weeks.
 3 out of 10 outcomes were possibly benefited.
o Fewer women developed
chorioamnionitis
o Fewer newborns developed sepsis,
o more often prolonged 7 days in women
given antimicrobials.
 Neonatal survival, however, was
unaffected, as was the incidence
of necrotizing enterocolitis,
respiratory distress, or
intracranial hemorrhage.
 7-day treatment with ampicillin, amoxicillin plus
erythromycin, or placebo. The women had
membrane rupture between 24 and 32 weeks.
 Efficacy of shorter treatment lengths and other
antimicrobial combinations.
 Amoxicillin-clavulanate regimen was NOT
recommended,
 Increase risk of resistant bacteria
Corticosteriods to accelerate fetal lung maturity
National Institute of Health (NIH) (200)
 Single course of antenatal corticosteroids for
women with preterm membrane rupture before
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 32 weeks and in whom there was no evidence of
chorioamnionitis.
ACOG (2013d)
 Single-dose therapy is recommended from 24 to
32 weeks.
 No consensus regarding treatment between 32
and 34 weeks.
 Corticosteroid therapy is not recommended
before 24 weeks.
VII. MANAGEMENT OF PRETERM
LABOR WITH INTACT MEMBRANE
Women with signs and symptoms of preterm
labor with intact membranes are managed much the
same as described above for those with preterm
ruptured membranes. If possible, delivery before 34
weeks is delayed.
Amniocentesis to detect infection
 Test have been used to diagnose intraamniotic
infection
o Elevated leukocyte count
o Low glucose content
o High IL-6 concentration
o Positive gram stain result
 Amniocentesis to diagnose infection does not
improve pregnancy
 ACOG (2012a) has concluded that there is no
evidence to support routine amniocentesis to
identify infection.
Corticosteriods for fetal lung maturity
 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.
o 12mg Betamethasone every 24 hrs for 2
doses
o 6mg Dexamethasone every 12 hrs for 4
doses.
Corticosteroid Rescue Therapy
 Administration of a repeated corticosteroid dose
when delivery becomes imminent and more than
7 days have elapsed since the initial dose.
 2000 NIH Concensus
o Should not be routinely used and that it
should be reserved for clinical trials.
 ACOG (2012a) S
o Single rescue course of antenatal
corticosteroids should be considered in
women before 34 weeks whose prior
course was administered at least 7 days
previously.
Antimicrobials
 Given in an attempt to arrest preterm labor.
 ORACLE Collaborative Group study of 6295
women with spontaneous preterm labor, intact
membranes, but without evidence of infection.
o Primary outcomes of neonatal death,
chronic lung disease, and major cerebral
abnormality were similar in both groups.
o Not recommended.
 ORACLE II trial
o That fetal exposure to antimicrobials in
this clinical setting was associated with
an increased cerebral palsy rate at age 7
years compared with that of children
without fetal exposure.
Bed Rest
 Most often prescribed interventions during
pregnancy, yet one of the least studied.
 Insufficient evidence to support the use of bed
rest and found several studies showing harm
with its use
Cervical Pessaries
 To support the cervix in women with a
sonographically short cervix.
Emergency or Rescue Cerclage
 Risk of infection and pregnancy loss
 Althuisius and colleagues (2003)
o Delivery delay was significantly greater
in the cerclagegroup
 Terkildsen and co-workers (2003)
o Significantly decreased chance of
pregnancy continuation to 28 weeks or
beyond.
Tocolysis to treat preterm labor
ACOG(2012) - tocolytic agents do not markedly
prolong gestation but may delay delivery in some
women for up to 48 hours.
 Allow transport to a regional obstetrical center
 Permit time for corticosteroid therapy.
ACOG recommends that women with preterm
contractions without cervical change, especially those
with cervical dilation of less than 2 cm, generally should
not be treated with tocolytics.
 β- adrenergic receptor agonist
o Reduce intracellular ionized calcium
levels and prevent activation of
myometrial contractile proteins.
o Ritodrine and terbutaline
 SE: maternal tachycardia,
hypotension and pulmonary
edema
 Magnesium SO4
o Calcium antagonist
o Dose: 4g IV initially then continous
infusion of 2g/hr
o SE: pulmonary edema & respiratory
depression
o FDA (2013) - warned against prolonged
use of magnesium sulfate given to arrest
preterm labor due to bone thinning and
fractures in fetuses exposed for more
than 5 to 7 days.
 Attributed to low Ca levels
 Prostaglandin inhibitors
o Act by inhibiting prostaglandin
synthesis or by blocking their action on
target organs.
o Group of enzymes collectively termed
prostaglandin synthase is responsible for
the conversion offree arachidonic acid to
prostaglandins
o Acetylsalicylate and indomethacin
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 o SE: oligohydramnios, intraventricular
hemorrhage, PDA, sepsis, necrotizing
enterocolitis or neonatal death.
 Calcium channel blockers
o Myometrial activity is directly related to
cytoplasmic free calcium, and a
reduction in its concentration inhibits
contractions
o Nifedipine
o No clear superiority of either to delay
delivery was identified, and otherwise,
neonatal morbidity was equivalent.
o Combination of nifedipine with
magnesium for tocolysis is potentially
dangerous.
 Atosiban
o Nonapeptide oxytocin analogue is a
competitive antagonist of oxytocin-
induced contractions.
o fFailed to improve relevant neonatal
outcomes and was linked with
significant neonatal morbidity.
o FDA- denied approval - because of
concerns regarding efficacy and fetal–
newborn safety.
 Nitric Oxide Donors
o Potent smooth-muscle relaxants affect
the vasculature, gut, and uterus.
o Nitroglycerin administered orally,
transdermally, or intravenously was not
effective or showed no superiority to
other tocolytics.
o SE: maternal hypotension

VIII. LABOR
 Monitor FHR and uterine contraction
 Continuous electronic monitoring
 Fetal tachycardia, intrapatum acidosis (
umbilical artery pH less than 7.0 )
 Group B strep infections – prophylaxisshould be
provided.

IX. DELIVERY
 Vaginal delivery and episiotomy
 NO to routine forceps delivery to protect the
―fragile‖ fetal head
 Importance if specialized personnel and facilities
for preterm newborn care.

X. PREVENTION OF NEONATAL
INTRACRANIAL HEMORRHAGE
 Preterm newborn frequently have intracranial
germinal matrix bleeding that can extend to
more serious intraventricular hemorrhage
 Vaginal delivery vs C section
 MgSO4 for fetal neuroprotection
o Maternal MgSO4 therapy had a fetal
neuroprotective effect
o Parkland Hospital
 Provide MgSO4 for threatened
preterm delivery from 24 6/7 to
27 6/7 weeks
 6g loading dose is followed by
an infusion of 2g/hr for at least
12 hr
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