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4 Acute Abdomen-Induced Preterm Labor
ab
Fig. 4.7 (a) Uteroplacental apoplexy means extravasa-
tion of blood into the uterus myometrium, and serosa. (b)
Blood clots adherent to the placenta (arrows) indicates
4.3.3.3 Trauma-induced Preterm Labor
Placental Abruption
See Sect. 25.3.6.1.
Traumatic Uterine Contractions
Uterine contractions induced by uterine trauma
are the result of two processes. First is when a
traumatic uterine injury destabilizes lysosomal
enzymes that can initiate prostaglandin production. Second, thrombin produced by actively clotting blood interacts with the protease-activated
receptors in the myometrium, resulting in robust
uterus contractions, even without prostaglandin
production [118]. Thrombin at concentrations
1–100U/mL represents less thrombin generated
by 1mL of clotting blood and stimulates myometrial contractions in a dose-dependent fashion.
Thrombin activates the phosphatidylinositol signaling pathway and generates cytosolic calcium
oscillations [119].
Maternal demographic factors, presence of
uterine contractions, maternal clinical conditions
(abdominal pain, abdominal tenderness, vaginal
bleeding), hematologic and coagulation studies,
US ndings, fetal heart rate tracing category, AIS
score for abdomen, and ISS score do not predict
preterm delivery or other secondary outcomes
[120].
abruptio placentae caused by uteroplacental apoplexy.
(Reproduced with permission from [111])
4.3.4 Maternal Nutritional Status
Many causes of fetal morbidity, in addition to
PTL, are due to the loss of adequate maternal
nutrition during pregnancy. A low prepregnancy
BMI is associated with a high risk of spontaneous
PTB, whereas obesity can be protective [121].
Women with low serum iron, folate, or zinc have
more PTB [122, 123]. Maternal thinness is associated with decreased blood volume and reduced
uterine blood ow, increasing the rate of PTL
[124].
The acute abdomen during pregnancy results
in three scenarios of prolonged maternal starvation as follows:
• recurrent or persistent symptomatology of
underlying disease such as symptomatic
cholelithiasis/cholecystitis, acute/chronic pan-
creatitis, adnexal torsion, etc.,
• postoperative catabolism with inadequate IV
supplementation,
• protracted posttreatment sepsis/septic shock.
Peroral nutrition is inadequate mainly due to a
higher basal metabolism in systemic inammation leading to body mass loss in all these scenarios. Due to blood redistribution in sepsis,
uterine blood ow can further be decreased.

Preterm Labour: Pathogenesis & Maternal Complications
4.4 Clinical Presentation
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89
Cervical
Procedures
Removing part of
the cervix
Ex. Cone biopsy,
cervical LEEP
cervical
stroma &
cervical
scarring
tensile
strength
and
plasticity
Cervical Insufficiency
effacement (thinning)
Authors: Skye Russell
Reviewers: Danielle Chang,
Crystal Liu, Yan Yu*, Nicholas
Papalia*
*MD at time of publication
Legend:
cervical
glands
mucous
production
risk of infection
inflammation
prostaglandins
Cervical collagen
degradation
Pathologic cervical
dilation and/or
Genitourinary
Infections
E.g. Urinary tract
infection, bacterial
vaginosis,
chorioamnionitis,
abnormal vaginal
flora
bacterial
colonization
of fetal
membrane
bacterial
enzymes and
immune
reactions
Rupture of Membranes
Antepartum
Hemorrhage
risk
placental
abruption
decidual
tissue
factor
release
Activates
coagulation
cascade
thrombin
proteases
Digest and weaken
amniotic membrane
Preterm Premature
Uterine contractions and cervical change occurring <37wk gestational age
Risk of future preterm labour and preterm birth
Substance
Use
Smoking or
cocaine
use
Vasoconstriction
in uterine
circulation,
endothelial
dysfunction
Placental
hypoperfusion
and ischemia
fetal ACTH
placental
prostaglandins
myometrial
sensitivity to oxytocin
Uterine contractions
Preterm Labour
ComplicationsSign/Symptom/Lab Finding MechanismPathophysiology
Maternal
Stress
Malnutrition,
depression,
traumarelated
disorders,
work-related
stress
cortisol
placental
corticotropin
releasing
hormone
Uterine
Abnormalities
Mullerian duct anomalies:
congenital abnormalities in
uterine shape
Septate uterus: ridge of tissue
dividing uterus into two horns
Intracavitary leiomyoma:
benign mass inside uterus
Rapid growth
exceeds blood
supply
lschemia & necrosis
of fetal tissue
prostaglandins
and cytokines
Uterine
volume
functional
volume of
uterine cavity
Uterine stretch
Upregulation of
oxytocin receptors
Abbreviations:
• LEEP – Loop electrosurgical
excision procedure
• ACTH – adrenocorticotropic
hormone
Multifetal
pregnancy,
poly-
hydramnios
Maternal
Genome
Family hx or
personal hx of
preterm birth,
previous
preterm
premature
rupture of
membrane
Genes for
risk
Mechanism
unknown
Fig. 4.8 Pathogenesis of preterm delivery. (Reproduced with permission from [129])
4.3.5 Final Common Pathway
inammation, abruption, and excess stretch
occurring before 24weeks present as “incomThe generation of prostaglandins and proteases
reects the nal common delivery pathway,
preterm or at term. Prostaglandin levels
increase in reproductive tract tissues, maternal
plasma, and amniotic uid immediately before
petent cervix” with or without subsequent
PPROM and not PTL.Figure4.8 presents the
discrete pathogenic processes leading to pre-
maturity and their nal common biochemical
pathway.
and during parturition [125, 126]. Concurrent
with rising prostaglandin levels is the upregulation of myometrial prostaglandin receptors
4.4 Clinical Presentation
before labor onset [127, 128]. Prostaglandins
induce functional progesterone withdrawal,
enhance sensitivity to estrogens, and increase
MMP and IL-8 expression. Moreover, all the
pathways of prematurity described above also
directly trigger MMP and IL-8 expression to
mediate cervical change and fetal membrane
rupture. The myometrium is quiescent before
20weeks’ gestation because of the high PR-B,
low ER-α, low circulating estrogen levels, and
inhibition of CAP gene expression. Therefore,
Clinical presentation of acute abdomen warrants
a search of its cause and other potential causes of
PTL. For pregnant patients with abdominal
trauma, maternal hemodynamic status should be
checked rst (see Chap. 25), then the cause of
acute abdomen and PTL should be evaluated.
Sometimes a clinical picture is challenging to
establish due to attenuated inammatory
response. Several authors observed this in the late
nineteenth century [130].

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4 Acute Abdomen-Induced Preterm Labor
One-third of all patients with PTL have intact
membranes, one-third present with PPROM, and
one-third result from indicated delivery (delivery
in response to maternal or fetal complications)
[131].
Diagnosis of ROM is made by sterile vaginal
examination by speculum in women presenting
with a suspicious clinical history or US detected
oligohydramnios. Conrmation of vaginal lacerations or bony fragments may indicate pelvic
fractures. Evident uid passing through the cervical os is diagnostic.
For the presentation of traumatic placental
abruption, see Sect. 25.3.6.1.
4.5 Diagnosis
4.5.1 Prediction ofPreterm Labor
4.5.1.1 Uterine Contractions
Intrauterine infection is associated with uterine
contraction frequency or PTL [132–134].
However, uterine contractions do not predict PTL
well in singletons because of the wide variation
in frequency in normal pregnancy and PTL [134].
Similar results were found in twins [135]; however, women admitted with a diagnosis of PTL, if
they do not deliver, remain at increased risk of
subsequent PTL and PPROM.
4.5.1.2 Laboratory Findings
A marked correlation of elevated CRP and ALP
in women with non-acute abdomen PTL was
observed compared to women without PTL,
whereas the best cut-off values of CRP >20–
27mg/L and ALP >300–399IU/L were the best
values in the prediction of PTL [136, 137].
Currently, no studies predict PTL in pregnant
patients with acute abdomen.
Most patients with acute abdomen have
elevated CRP values and are at increased
risk for PTL.
4.5.1.3 Transvaginal Ultrasound
Transvaginal US has shown that a short cervix
(cervical length ≤25mm) is associated with IAI
and an increased risk of adverse pregnancy outcomes [83, 138]. Women with a cervical length
of ≤15mm between 22 and 30weeks of gestation have a higher rate of microbial invasion of
the amniotic cavity and are more likely to deliver
spontaneously before 35 weeks of gestation
[139]. Therefore, the US cervical length may be a
valuable predictor of the risk of microbial invasion of the amniotic cavity and IAI [83].
Unfortunately, there are no studies in patients
with localized/diffuse peritonitis or abdominal
trauma when PTL develops quickly, in hours or
days.
4.5.2 Preterm Premature Rupture
ofMembranes
The presence of vaginal bleeding outside the rst
trimester has been associated with a sevenfold
increase in the risk of PROM and a 2.9-fold
increased risk of PTB [96].
An alkaline vaginal pH (6.0–6.5) and a “ferning” pattern on microscopic examination of dried
vaginal secretions are supportive (normal vaginal
secretions have a pH of 5.0, whereas amniotic
uid has a pH of 7.0) when visual inspection is
equivocal. False-positive ndings are due to cervical mucus, blood, semen, alkaline antiseptics,
or bacterial vaginosis. False-negative results are
from prolonged leakage and oligohydramnios.
Repeat speculum examination after prolonged
bed rest may provide diagnostic information if
initial testing is negative despite a suspicious history. In the absence of fetal growth restriction or
urogenital abnormalities, US evidence of
oligohydramnios is suggestive but not diagnostic
of ROM. The diagnosis can be conrmed by
indigo carmine amnioinfusion with the transvaginal passage of dye. A search for concomitant
maternal and fetal injuries is mandatory, and prolonged continuous fetal monitoring is advocated.

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4.5.3 Placental Pathology
Placental pathology has a better predictive value
for IAI than clinical signs and symptoms.
Placental histology has a high negative predictive
value (97%) and reasonable positive predictive
value (79%) for diagnosing IAI compared with
uid cultures [140]. Placental pathology has a
twofold improvement in positive predictive value
compared with the clinical signs and symptoms
of IAI [141]. Unfortunately, placental pathology
can be obtained when the patients’ management
has been completed without inuencing the
immediate therapeutic process.
4.6 Treatment
With extrauterine intra-abdominal infection, the
underlying cause and the PTL should be treated
simultaneously. With maternal abdominal
trauma, the mother should be stabilized rst (see
Chap. 25), then PTL treated.
The vast majority (70–80%) of the women
with symptoms of all-cause spontaneous PTL do
not deliver preterm even without intervention.
The most common criteria for PTL are uterine
contractions (≥4/20 min or ≥8/h) and cervical
change with intact membranes at 20–36 weeks
6days.
Women without cervical change do not
have PTL and should not receive tocolysis.
Women with PTL but negative fFN and
TVU CL ≥30 mm have a less than 1%
chance of delivering within 1week and a
more than 95% chance of delivering
≥35 weeks without therapy [142] and
should not receive tocolysis.
The complete diagnostic-therapeutic algorithm is presented in Fig.4.9.
In infection-induced PTL prevention, therapeutics should ideally eliminate the microorgan-
Fig. 4.9 Suggested
algorithm for evaluating
and managing
threatened preterm labor.
(−) negative, (+)
positive, CL cervical
length, fFN fetal
bronectin, PTB preterm
birth. (Reproduced with
permission from [143])
CL <20 mm
Admit for tocolysis,
steroids. magnesium
sulfate for
neuroprotection, etc.
Shortening >5mm
Consider admission,
tocolysis and steroids,
especially if prior PTB
Threatened
preterm labor
0/7
6/7
23
-33
weeks
Obtain fFN prior to digital
exam and vaginal CL
TransvaginalCL
CL >20 – 30 mm
fFN + fFN -
Repeat CL in 2-6
hours if persistent
contractions
-Stable CL and no prior PTB routine care
-Stable CL <25mm and/or prior PTB
consider vaginal proge sterone, repeat CL
in 1 week
(repeat CL for
persistent/recurrent
CL >30 mm
Discharge
contractions)

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4 Acute Abdomen-Induced Preterm Labor
isms from the amniotic cavity and block the
ensuing cytokine cascade that drives the release
of PGs and matrix metalloproteinases (MMPs),
prevent the onset of PTL, and minimize the risk
of FIRS.
Thirty-four weeks of gestation is a threshold at which perinatal morbidity and mortality are too low to justify the potential
maternal and fetal complications and costs
associated with the inhibition of labor and
short-term delivery delay [144, 145].
Tocolytics are not indicated before viability (23–24weeks of gestation) since these
drugs do not delay delivery for more than a
few days [146].
One explanation for the inefcient longer
delay of PTB is that most interventions are
directed on only one of many perplexing pathways of the complex process of parturition (see
Sect. 4.2).
4.6.1 Nontocolytic Treatment
4.6.1.1 Bed Rest
Bed rest has never been tested in singleton gestations complicated by PTL or PPROM. In twin
pregnancies with cervical dilatation, bed rest in the
hospital has not been shown to decrease PTL [147].
4.6.1.2 Antibiotics
The lack of antibiotic effectiveness in all-cause
PTB may be the result of (1) a therapeutic application long after the infection is established
[148], (2) the difculties in identifying the specic pathogens and prescription of the pathogenspecic therapy, (3) an increase in PTB in some
subgroups [149], and 4) potential adverse effects
on neonatal outcomes.
Intrauterine Infection
Antibiotics are given to women with intrauterine
infection-induced PTL. However, it is not the
infection but the subsequent inammation that
initiates PTL and is primarily responsible for
adverse neonatal outcomes. An exception is an
improvement in women with PPROM with antibiotics such as erythromycin. These results
include increased latency before labor and
improved neonatal outcomes [150, 151].
Compared with metronidazole, clindamycin
has similar activity against anaerobes. However,
it is far superior concerning broad-spectrum
activity, group B streptococcus (associated with
PTL when present as heavy colonization), and
many other bacterial vaginosis-related organisms, particularly fastidious organisms such as
M. hominis [152, 153]. Also, clindamycin has
anti-inammatory properties [154, 155]. There
is merit in oral and intravaginal administration
of clindamycin to eradicate abnormal genital
tract ora/bacterial vaginosis in pregnancy.
Vaginal administration delivers the highest concentration of antibiotics to the site of the heaviest bacterial load. On the other hand, bacterial
vaginosis could be associated with subclinical
endometritis [156], so if vaginal organisms have
already gained access to the choriodecidua,
these organisms may not be accessible to vaginal administration. Therefore, systemic therapy
may provide benets. There are no studies on
the combined use of oral and vaginal clindamycin. Even if this reverts to normal, abnormal
genital tract ora in early pregnancy is still
associated with LM and PTB.This suggests that
whatever damage is done by infection/inammation occurs early and persists [157]. Suppose
antibiotics are used late in pregnancy when
inammatory tissue damage may have already
occurred, with irreversible changes in the cervix, myometrium, decidua, placenta, and extraplacental membranes. In that case, antibiotics
are unlikely to be benecial [158, 159].
Unfortunately, some of these studies were not
adequate.
The immune system is primed in utero and
modied after birth. Accordingly, antibiotics during pregnancy or the neonatal period may disrupt
the developing neonatal gut microbiome, failing
immune response maturation, resulting in asthma,
allergy, and atopic disease [160–163]. This has
led to new diets and gut microora treatments for
newborns.

4.6 Treatment
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93
Acute Abdomen
Studies on antibiotic prevention of infectioninduced PTL did not include pregnant patients
with extrauterine intra-abdominal infection (IAI).
The general recommendations are:
• removal of the infective source with
dosage and duration of antibiotic therapy as indicated by guidelines for the
treatment of the primary infective cause,
not for the prevention of uterine contractions and PTL,
• IV clindamycin, in addition to other
antibiotics indicated for patients with
acute abdomen or abdominal trauma
with unknown group B Streptococcus
culture status (especially before
32 weeks of pregnancy), should be
administered.
Abdominal trauma patients are a specic
subgroup because infection-induced PTL is not
the primary mechanism. Antibiotic treatment
of all women with threatened PTL to prevent
neonatal infection with group B streptococcus
is recommended because preterm infants have
an increased risk of this infection [164]. Rates
of neonatal group B streptococcus infection
and corresponding mortality rates have
declined since this strategy was adopted in the
USA [164]. Preterm infants with traumatic
injuries and possible hemodynamic instability
(due to maternal hemorrhagic shock) or blood
loss are particularly susceptible to neonatal
infections.
4.6.1.3 Antioxidants
In vitro studies indicate that vitamins C and E
can prevent tissue damage to chorioamniotic
membranes inicted by hypochlorous acid, a
reactive oxygen species produced by host cells
during infection and inammation [165].
Although the dose-response relationship
between the plasma ascorbic acid concentration
and the prevalence of PPROM has been shown,
ascorbic acid concentrations may have only
reected the general nutritional status of patients
[166]. The issue is that studies focused on single, for example, hypochlorous acid-induced
damage [165], whereas in vivo infectioninduced damage could occur via nonoxidative
pathways (e.g., elastase, protease). The diet
alone could be an inadequate source of vitamins
C and E during pregnancy, and supplementation
may reduce PPROM [167]. Supplemental intake
of vitamins C and E to prevent preeclampsia did
not lower PTB and PPROM rates, but respiratory morbidity was reduced [168]. The role of
antioxidants in preventing PTL in acute settings
(i.e., peritonitis/intra-abdominal trauma) is
unknown.
4.6.1.4 Inhibitors ofThrombinmediated Contractions
Uterine trauma can cause nonplacental abruption
uterine bleeding that activates thrombin.
Thrombin causes uterine contractions even without prostaglandin synthesis (see Sect. 4.3.3.3). IV
hirudin, a direct thrombin inhibitor, was used for
other emergent indications in pregnancy and
should be evaluated for this indication [169].
Another consideration is whether to administer
r-hirudin as prophylactic therapy or only when
uterine contractions are present and other causes
for uterine contractions are excluded. The oral
direct thrombin inhibitor, ximelagatran, was
withdrawn due to potential hepatotoxicity [170].
This therapy could be contraindicated in traumainduced uterine bleeding.
Thrombin-stimulated myometrial contractions could be suppressed with inhibitors of the
phosphatidylinositol signaling pathway [171].
4.6.1.5 Vitamin D
Maternal circulating 25-OHD deciency could
increase overall PTL risk, and vitamin D supplementation alone during pregnancy could reduce
PTB risk. The effect was signicant with maternal serum 25-OHD <50nmol/L [172]. Although
not analyzed for pregnant patients with acute
abdomen, vitamin D supplementation in the
perioperative period could decrease the likelihood of PTL.

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4 Acute Abdomen-Induced Preterm Labor
4.6.2 Tocolytic Treatment
Seventy years ago, it was stated that, when peritonitis is present, CS is mandatory [173–175],
and cesarean hysterectomy in more severe cases
of abscess formation may prove lifesaving.
Although preterm contractions caused by uterine
irritation from peritonitis occur in up to 83% of
the cases, PTL and delivery occur in only 5–14%.
However, >50% of these patients in the third trimester deliver preterm [176]. True PTL can be
dened as uterine contractions with transvaginal
CL <20 mm, or CL 20–29 mm with a positive
fetal fFN [177]. Threatened PTL is when a
woman has symptoms of PTL, such as contractions or cramping, but no cervical change, for
example, a transvaginal CL ≥30mm.
Women with true PTL should receive
tocolysis and corticosteroids. Despite
symptoms, there is no need for therapy in
threatened PTL, including tocolysis [177].
For patients with true PTL, tocolytic therapy
can temporarily abolish contractions. However, it
does not remove the underlying stimulus that initiated the process of parturition or reverse parturition changes in the uterus and cervix.
Prematurity is associated with adverse neonatal
outcomes, while tocolytic agents can cause
adverse neonatal effects. Between 23 and 26
completed weeks of gestation, each day of prolongation of pregnancy increases the survival rate
by 3% [178].
Prostaglandin inhibitors and calcium chan-
nel blockers are the tocolytics with the best
probability of 48h delay in all- cause PTL,
respiratory distress syndrome, neonatal
mortality, and maternal side effects [179].
The probability of postponed delivery for
48was highest with prostaglandin inhibitors (OR
5.39), followed by magnesium sulfate (OR 2.76),
calcium channel blockers (OR 2.71), betamimetics (OR 2.41), and the oxytocin receptor blocker
atosiban (OR 2.02) [179].
Tocolytic treatment after the onset of contractions could not prevent PTL and should be
ordered for patients with delayed presentation
and advanced gestational age to prevent PTL and
fetal loss [180]. Tocolysis only delays PTD for
several days, but PTD is not prevented [181].
No study has documented positive effects on
the outcome. The current recommendation is that
using these agents is a matter of choice
[182–184].
SAGES and EAES guidelines recommend
tocolytics only if uterine contractions are
present.
Tocolytics could calm the uterus from the
insult of the acute abdomen and the intraoperative uterine manipulation, but their benet is
equivocal [185, 186]. There is no signicant difference in the efcacy of different tocolytics or
outcomes with or without tocolytics (Fig.4.10)
[187]. Also, tocolytics have severe maternal and
fetal side effects, which could contraindicate
their use, especially ritodrine and prostaglandin
synthetase inhibitors.
Ritodrine causes maternal and fetal tachycardia, nausea, and vomiting [188, 189], impairing
important signs of the acute abdomen. Unlike
ritodrine and prostaglandin synthetase inhibitors,
nifedipine is safer and does not alter the disease
symptomatology [185]. Nifedipine causes insignicant hypotension [189, 190]. The evidence for
teratogenicity [191] is not conclusive [192], and
no malformations were reported [188].
Nearly 26% with symptomatic cholelithiasis
developed preterm contractions requiring tocolysis [193]. Tocolysis is used only if uterine contractions are present [194].
Maintenance Tocolysis: While acute tocolysis
delays delivery of >48h and enables completion
of antenatal corticosteroid administration and

35
Number of cases
prostaglandin
4.6 Treatment
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Fig. 4.10 No
statistically signicant
difference between
different tocolytics with
their effect on the
duration of pregnancy
and prevention of
preterm labor in the
acute abdomen.
(Reproduced with
permission from [188])
95
30
25
20
15
Te rm Labor
Preterm Labor
Abortion
19
17
10
5
0
7
6
Ritodrine
5
2
1
Progesterone
patient’s transfer to a tertiary perinatal center,
maintenance tocolysis is still controversial. So
far, maintenance of tocolysis is a case-by-case
decision outweighing its benets and harms
(Table4.1).
4.6.2.1 Magnesium Sulfate
Magnesium is not metabolized, and elimination
of the drug is conducted mainly through renal
excretion. Therefore, the difference in clearance
during and after pregnancy likely reects modications in renal clearance. Pregnant women
receiving magnesium sulfate for nonpreeclamptic indications (i.e., neuroprotection
and tocolysis) have an increased clearance of the
drug compared with preeclamptic women [196].
Abdominal Trauma
Maternal trauma can cause PPROM and PTB, but
is seldom an isolated event. At <24weeks of gestation, ROM may predispose the fetus to pulmonary hypoplasia or orthopedic deformities if the
amniotic uid volume does not return to normal.
With the injury to the placenta, bleeding may
result in fetal anemia, hypovolemia, or both.
Management is usually not different from spontaneous ROM in the absence of maternal or fetal
compromise.
2
1
1
Calcium Channel
Anti-
5
1
1
All Tocolytics No Drug
8
5
5
6
The use of tocolysis to treat PTL after blunt
abdominal trauma is limited. Tocolysis is not recommended because regular uterine activity after
a traumatic event could result from a uterine contusion or placental abruption and these two diagnoses are indistinguishable [197]. There are cases
of placental abruption with <1 uterine contraction every 10min. In that population, almost 20%
with frequent contractions had placental abruption [197]. In noncatastrophic abdominal trauma
in pregnancy, tocolysis for persistent contractions
is reassuring after the maternal and fetal testing
results [198].
Magnesium sulfate is the tocolytic agent of
choice for pregnant patients with abdomi-
nal trauma, with the added effect of fetal
neuroprotection to decrease the risk of
cerebral palsy. Minimal dose includes 4g
loading dose + 1 g/h maintenance dose
over 12h.
The PTL group received more magnesium
sulfate tocolysis than the term birth group (31%
vs. 7%, respectively). However, there were no
differences in the gestational age at abdominal

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Side effect
risk Recommendation
Improvement of
neonatal outcome
PTB
rate- reduction
decision
4 Acute Abdomen-Induced Preterm Labor
decision
No No Low Not recommended
Terbutaline, fenoterol, ritodrine No No High Not recommended
bolus, pump
Oral Nifedipine No No Intermediate Case-by-case
Oral/rectal/vaginal Indomethacin No No Intermediate Case-by-case
Substance class Administration route Substance
Beta-sympathomimetics Oral, parenteral:
Calcium-channel
blockers
Cyclooxygenase
inhibitors
Magnesium Oral/parenteral Magnesium sulfate No No Intermediate Not recommended
Table 4.1 Classes and substances for maintenance tocolysis
Nitric oxide donors Transdermal Nitroglycerine No No Intermediate Not recommended
Micronized progesterone,
17α-hydroxyprogesterone caproate
Parenteral Atosiban No No Low Not recommended
Oxytocin receptor
intramuscular
antagonists
Progesterone Oral/vaginal
Reproduced with permission from [195]

8
Time (hours)
Magnesium concentration (mg/dL)
Wt
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trauma and the interval between trauma and
delivery between groups. In abdominal trauma,
patients with PTB had a closed and no effaced
cervix at the time of abdominal trauma [198].
Magnesium sulfate in non-acute abdomen PTL is
neuroprotective. It improves long-term neonatal
health outcomes, despite maternal side effects
(decreases respiratory efforts and, in high doses,
may lead to hypotension, respiratory collapse, or
cardiac arrhythmias). While magnesium sulfate
has not signicantly improved cognition and
behavior outcomes at school age, it prevents
cerebral palsy at 2years [199]. The most benecial dosing regimen for neuroprotection remains
unknown [196]. Magnesium readily crosses the
placenta, with an almost 1:1 ratio of magnesium
in the pregnant mother and umbilical cord [200].
Magnesium levels increase in fetal serum within
1h and amniotic uid within 3h after maternal
IV administration [200]. Among pregnant women
with preeclampsia, serum magnesium levels
were signicantly greater during magnesium sulfate infusion than non-preeclamptic women
receiving the same magnesium sulfate dosing.
Women with the greatest body weight had lower
serum magnesium levels after the bolus administration of magnesium sulfate than women with
the lowest body weight (Fig.4.11).
Several classes of tocolytic agents are not recommended in abdominal trauma. Betamimetics
(β2-adrenergic agonists) cause maternal and fetal
tachycardia. They can mask the clinical signs of
hypovolemia in both the mother and the fetus,
leading to a delay in the institution of the appropriate intervention. NSAIDs/Indomethacin affect
platelet function and are contraindicated in
patients with head injury or occult bleeding.
Calcium channel blockers may produce hypotension. Such vital sign changes mimic those seen in
occult hemorrhage, mandating close monitoring.
Renal Colic
Although controversial, magnesium sulfate could
have combined benecial effects in patients with
renal colic or renal collecting system rupture
[201, 202]:
• tocolysis,
• ureteric muscle relaxation,
• direct pain relief,
• decreased formation and progression of some
forms of renal stones.
Ureteric muscle relaxations relieve pain and
magnesium sulfate directs pain relief on the
molecular level. It is a noncompetitive antagonist
of N-methyl-d-aspartate (NMDA) glutamate
receptors that participate in pain feeling and persistence. These pain relief effects can result in
lesser use of other analgesics. Magnesium is a
urinary stone inhibitor because it competes with
calcium for oxalate, thus forming a magnesium-
Fig. 4.11 Magnesium
serum concentration
after 4g loading dose of
magnesium sulfate,
followed by 2g/h
infusion among pregnant
women with and without
preeclampsia and
women of lowest
(55kg), mean (88kg),
and greatest (157kg)
body weights.
(Reproduced with
permission from [196])
7
6
5
4
3
2
1
0510 15 20 25
Low Wt
Mean Wt
High Wt
Preeclampsia Low Wt
Preeclampsia Mean
Preeclampsia High Wt
30 35 40 45 50 55 60
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