SWAM (Scientific Article Writing Management)

No Author Title Name of Journal Year Volume

1 Shree, R.,Short interpregnancy interval
The journal of increases the risk of&
maternal-fetal preterm premature2018
neonatal rupture of membranes
31 and early de
medicine : the official journal of the European
Association of Perinatal Medicine, the
Federation of Asia and Oceania Perinatal
Societies, the International Society of Perinatal
Obstetricians

2 Halimi AslEpidemiolEmergency (Tehran, Iran) 2017 5

3 Gezer, A.,Neonatal
Parafit-Yalciner,
m
J ObstetE.,
Gynaecol
Guralp, O., Yedigoz, V., Altinok, T., Madazli, R.
2013 33
4 FIGO Com Good cliniInternational Journal of Gynecology & Obstetrics 2019 144
5 Romero, R.,
Preterm
Dey, S.K.,
l Science
Fisher, S.J. 2014 345
6 Rubens, C.E.,
Prevention
Sadovsky,
Sci
ofTransl
preterm
Y., Muglia,
Med
birth:L.,
Harnessing
Gravett, M.G.,
science
Lackritz,
to address
E., Gravett,
the global
C.epidemic.
2014 6

7 Menon, R.Preterm prSeminars in perinatology 2017 41

8 Castillo-CChoriodeciAm J Reprod Immunol 2014 71
9 Vora, S., Nuclear faReprod Biol Endocrinol 2010 8
10 Castillo-CChoriodeciAm J Reprod Immunol. 2014 71
11 Kumar, D.,The physiology
Placenta
of fetal membrane weakening and rupture: Insights 2016gained from
42 the determination
12 Moco NP,Gene
M expre Eur J Obstet Gynecol Reprod Biol 2013 171
13 PuthiyachThrombinPlacenta
weakens the amnion extracellular matrix (ECM) directly 2013 rather than
34 through protease a
14 Murtha APRegulationAm J Obstet Gynecol 2015 213
15 Klebanoff,Epidemiology:
M.A. andClinics
Keim,
theinS.A.
changing
Perinatology
face of preterm birth. 2011 38
16 Langridge,Social
A.T., and
Nassar,
Paediatric
racial
N.,inequalities
Li,and
J., and
Perinatal
in
Stanley,
preterm
Epidemiology
F.J.births in Western Australia,
20101984 to 2006.
24
17 Taylor, H.G.,
Learning
Klein,pAN.,
rchives
Anselmo,
of Pediatrics
M.G., Minich,
and Adolescent
N., Espy,Medicine
K.A., and Hack,2011
M. 165
18 Kerstjens,Developmen
J.M., De Journal
Winter, A.F.,
of Pediatrics
Bocca-Tjeertes, I.F., Ten Vergert, E.M.J., 2011
Reijneveld,159S.A., and Bos, A.F.
19 Baldwin, E.A.,
Persistent
Walther-Antonio,
microbial dysbiosis
M., MacLean,
in preterm
A.M.,premature
Gohl, D.M.,
rupture
Beckman,
2015K.B., Chen, J., White, B., Cre
20 O'Hara, S.Cervical length
Australas
for predicting
J Ultrasound preterm
Med birth and a comparison of 2013
ultrasonic measurement
16 techniqu
21 Suman, V.,Preterm Labor 2019
22 Derakhshi,Risk factoIranian journal of public health 2014 43
23 Kozinszky,Severe mid Curr Opin Obstet Gynecol 2014 26
24 Tchirikov,Mid-trimes Journal of Perinatal Medicine 2017 46
25 Goebel, S.Continuous Prenat Diagn 2016 36
Number Pages Doi Link https
22 3014–30210.1080/14767058.2017.1362384 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5984161/

1 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5325899
1 38-42 https://www.researchgate.net/publication/233973179_Neonatal
3 340-346 https://obgyn.onlinelibrary.wiley.com/doi/full/10.1002/ijgo.12744
760-765 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4191866/
262sr5 https://www.researchgate.net/publication/268233125_Prevention
1.
7 409-419 10.1053/j.semperi.2017.07.012. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5659934/
1 86-93 https://doi.org/10.1111/aji.12179
8 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2845583/
1 86-93 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4000259/
59-73 https://www.ncbi.nlm.nih.gov/pubmed/27238715
1 012-017 https://www.ejog.org/article/S0301-2115(13)00343-6/fulltext
10 924-931 https://www.ncbi.nlm.nih.gov/pubmed/23953865
4 447-448 https://www.ajog.org/article/S0002-9378(15)00744-9/fulltext
339-350 https://www.perinatology.theclinics.com/article/S0095-5108(11)00057-1/fulltext
352-362 https://www.ncbi.nlm.nih.gov/pubmed/20618725
819-825 https://europepmc.org/backend/ptpmcrender.fcgi?accid=PMC329
92-98 https://assets.ncj.nl/docs/vroeggeboorte-ses-jped2013.pdf
https://www.researchgate.net/publication/284770971_Persistent
3 124-134 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5029998/pdf/AJ
https://www.ncbi.nlm.nih.gov/books/NBK536939/
4 499-506 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4433732/pdf/IJP
67-76 https://www.researchgate.net/publication/260682457_Severe_m
5 465-488 https://www.degruyter.com/downloadpdf/j/jpme.2018.46.issue-5
S1 75 www.researchgate.net/publication/306301058_Continuous_amni
 Significant Contribution Important Quotes
h.gov/pmc/articles/PMC5984161/ Preterm rupture of the premature membrane (PPROM) contributes significantly to overal

h.gov/pmc/articles/PMC5325899 Premature birth not only causes financial and emotional stress on the family, but can also
te.net/publication/233973179_Neonatal The most common neonatal morbidity in PPROM cases is respiratory distress syndrome
ary.wiley.com/doi/full/10.1002/ijgo.12744 Premature birth (PTB) is the main cause of death among newborns and the second cause,
h.gov/pmc/articles/PMC4191866/ Preterm birth (PTB) is a clinical manifestation of many different and different antecedent
te.net/publication/268233125_PreventionThe main etiology of spontaneous PTB is likely to be an infectious infection from the lower genit

h.gov/pmc/articles/PMC5659934/ Preterm prelabor rupture of the membranes (PPROM) remains a significant obstetric prob
The amnion is constantly bathed in amniotic fluid, signifying its importance as a primary
h.gov/pmc/articles/PMC2845583/ The chorion is in close proximity to maternal decidua and maintains the immune tolerance at th
h.gov/pmc/articles/PMC4000259/ The development of amnion and chorion begins with embryogenesis, although they do no
h.gov/pubmed/27238715 Contrary to the placenta, fetal membranes are not involved in transport of nutrients or oth
ticle/S0301-2115(13)00343-6/fulltext and immune protection and acts as a barrier for microbial access. This protective role is s
h.gov/pubmed/23953865 and membrane weakening predisposing the membranes to pPROM. Abruption associated
ticle/S0002-9378(15)00744-9/fulltext Clearly, the dysfunctional status of fetal membranes is more evident in pPROM than sPT
e/S0095-5108(11)00057-1/fulltext Preterm birth is defined as the birth of an infant prior to 37 weeks gestation. Its rates have
h.gov/pubmed/20618725 Preterm birth is linked with a number of adverse outcomes and is thought to account for 2
including respiratory and gastro-intestinal conditions and long-term developmental disord
backend/ptpmcrender.fcgi?accid=PMC3298457&blobtype=pdf
s/vroeggeboorte-ses-jped2013.pdf and behavioural disorders such as learning difficulties
te.net/publication/284770971_Persistent Approximately 45–50% of preterm births are idiopathic, 30% are related to preterm ruptu
h.gov/pmc/articles/PMC5029998/pdf/AJ If cervical dilatation is noted to be at least 2 or 3 cm at less than 34 weeks, then the patien
h.gov/books/NBK536939/ Diagnosis of Preterm Birth due to PPROM involves a speculum examination to visualize
h.gov/pmc/articles/PMC4433732/pdf/IJPHPremature rupture of membranes (PROM) is a major factor causing infection in pregnanc
te.net/publication/260682457_Severe_midOne third of preterm births in the USA are associated with PPROM.
om/downloadpdf/j/jpme.2018.46.issue-5 After clinical assessment, a management strategy should be developed, which will clarify
publication/306301058_Continuous_amnioThe repetitive or continuous intraamniotic infusion of any saline solutions, which are suf
 ntributes significantly to overall preterm birth (PTB) and increases neonatal morbidity and mortality

ress on the family, but can also cause permanent disability (physical or nerve damage) to the infant. Preterm birth is a major obst
respiratory distress syndrome (RDS), sepsis, and intraventricular hemorrhage (IVH)
newborns and the second cause, after pneumonia, during the first 5 years of life. PTB prediction and associated premature membr
fferent and different antecedent conditions.
ous infection from the lower genital tract in the sterile uterus that attacks the decidua, chorioamniotic membrane, amniotic fluid and, in so

mains a significant obstetric problem that affects 3-4% of all pregnancies and precedes 40% to 50% of all preterm births. PPROM
ing its importance as a primary responder to changes in the amniotic cavity.
ntains the immune tolerance at the maternal-fetal interface. Lastly, the presence of stem cells in fetal membranes further depicts the likely
ryogenesis, although they do not participate directly in the formation of the embryo or fetus. Like the fetus, early growth of the a
d in transport of nutrients or other materials. One of the major functions of fetal membranes is to protect the fetus during its grow
access. This protective role is supported by the biomarkers that are produced by fetal membranes during gestation and parturition
pPROM. Abruption associated thrombin, matrix metalloproteinase (MMP) activation and collagenolytic processes have also be
re evident in pPROM than sPTB with no ROM. Thus, pPROM is considered as a disease of the fetal membranes and likely a sep
7 weeks gestation. Its rates have increased may in part be due to older maternal age and higher numbers of multiple births
s and is thought to account for 20–27% of all neonatal deaths in high-income countries. Gestation <37 weeks is also linked to po
long-term developmental disorder include poorer cognitive function, and neurodevelopmental delays in coordination, communic

30% are related to preterm rupture of membranes (PROM) and another 15–20% are attributed to medically indicated or elective p
s than 34 weeks, then the patient is highly likely to deliver preterm. Another indicator is short cervix as assessed by transvaginal
culum examination to visualize amniotic fluid passing from the cervical canal and pooling in the vagina. Fern and pH testing of t
or causing infection in pregnancy. Based on this it can be estimated that intauterin infection due to PROM can cause premature bi
h PPROM.
be developed, which will clarify the question, whether to prolong the pregnancy vs. delivery because of signs of chorioamnionitis
saline solutions, which are sufficiently differ from physiologic amniotic fluid, could irreversibly change the fetal programming a
 t. Preterm birth is a major obstetric and pediatric challenge because it is a common, persistent, and often devastating condition w

d associated premature membrane rupture (PPROM) are actually based on the detection of risk factors and specific markers. The

mbrane, amniotic fluid and, in some cases, also the fetus. Infection is responsible for inflammatory reactions that trigger myometrial contra

of all preterm births. PPROM arises from complex, and multifaceted pathways. Human fetal membranes, also referred as placen

branes further depicts the likely important role of fetal membranes during in utero fetal life.
he fetus, early growth of the amnion and chorion layers is rapid and independent of each other. The formation of amniochorion a
rotect the fetus during its growth and development in utero. Specifically, the fetal membrane functions to provide mechanical
uring gestation and parturition21. Compromise in the immune and mechanical properties of the fetal membranes allows for micr
nolytic processes have also been reported in fetal membrane weakening and pPROM
al membranes and likely a separate entity from sPTB with no ROM. Current research on this disease of the fetal membranes is f
mbers of multiple births
<37 weeks is also linked to poorer ongoing child health
ys in coordination, communication, and social interaction

edically indicated or elective preterm deliveries. PPROM is responsible for one third of all preterm births. It is thought that subcl
ix as assessed by transvaginal ultrasound. Normal cervical length is 35-48 mm. The definition of a short cervix is cervical length
agina. Fern and pH testing of the pooled vaginal secretions can indicate rupture of membranes. The PH of amniotic fluid is 7.1 to
PROM can cause premature birth. In the literature it is mentioned that efforts to avoid premature rupture of membranes are to avo

se of signs of chorioamnionitis and/or fetal inflammatory response syndrome (FIRS). The short-term benefit of conservative man
hange the fetal programming and/or damage some fetal organs, especially the fetal kidney, skin, eyes, gut and bronchopulmonary
often devastating condition with considerable medical, economic, emotional, and social impact. It is thought to be a syndrome in

tors and specific markers. The prediction of this event is important to allow women to be moved to a higher level center for safe

s that trigger myometrial contractions, premature rupture of membranes, and cervical maturation (through several mediators), leading to P

branes, also referred as placental membranes or amniochorionic membranes, is the inner lining of the pregnant intrauterine cavity

e formation of amniochorion as a unit structure is complete by the 12th week of gestation. The composition of the membrane and
ons to provide mechanical
al membranes allows for microbial invasion from genital tract

se of the fetal membranes is focused on addressing three major questions: 1) what are the initiators of proteolytic activity in the f

births. It is thought that subclinical infection is a crucial factor in the pathophysiology of PPROM because 25–40% of patients p
short cervix is cervical length <25mm at 16-24 weeks of gestation. Of note, a transvaginal ultrasound can help to distinguish cer
PH of amniotic fluid is 7.1 to 7.3. Fetal fibronectin gets released as a result of the breakdown of the cervical extracellular matrix
pture of membranes are to avoid heavy work and sexual relations in the last months of pregnancy, maintain general hygiene / rep

m benefit of conservative management of PPROM with antenatal corticoids and maternal systemic antibiotic treatment are well e
es, gut and bronchopulmonary system. We would avoid the use of solutions, which deviate from the composition of human amni
is thought to be a syndrome initiated by multiple mechanisms, consisting of infection or inflammation, uteroplacental ischaemia

a higher level center for safe confinement because intensive nursery/neonatal care is very important for premature infants. Prete

h several mediators), leading to PTB

he pregnant intrauterine cavity. These fetal tissues are distinct from placenta and serves as a barrier between the feto-placental an

position of the membrane and its ability to produce a broad spectrum of biomarkers at different stages of gestation illustrate the p

of proteolytic activity in the fetal membranes resulting in pPROM, 2) what are the effectors (biochemicals) of proteolysis, mem

because 25–40% of patients present signs of chorioamnionitis on amniocentesis. Assessment of bacterial content of the vagina a
nd can help to distinguish cervical effacement due to cervical insufficiency versus due to active labor
he cervical extracellular matrix is also an indicator of preterm labor though, it is a specific but not a sensitive test. If the result is n
maintain general hygiene / reproductive organs because of the rupture of the amniotic skin sometimes preceded by cervicitis or a

antibiotic treatment are well established. Corticosteroids administration for the lung maturation between 24/0 (23/0) and 34/0 w
e composition of human amniotic fluid. The positive effect of continuous amnio-infusion “flush out” method through the subcut
ion, uteroplacental ischaemia or haemorrhage, uterine overdistension, stress, and other immunologically mediated processes. Ho

nt for premature infants. Preterm premature rupture of membranes (PPROM) are the largest identifiable causes of preterm birth. A

r between the feto-placental and the maternal compartments. Fetal membranes are comprised of the amnion (innermost layer of t

ges of gestation illustrate the possible role of the fetal membrane's influence on the growing fetus, as well as in adverse pregnanc

hemicals) of proteolysis, membrane weakening/ rupture and can these biochemicals serve as markers to predict risk of pPROM a

cterial content of the vagina and leaking amniotic fluid of subjects at presentation, throughout treatment and up until delivery be

sensitive test. If the result is negative, it is strongly indicative of an intact membrane, but if positive, it does not necessarily indic
mes preceded by cervicitis or amnionitis. PROM was a common causes of preterm labor (35.5%)

etween 24/0 (23/0) and 34/0 weeks’ gestation is the gold standard. First line of antibiotic therapy is a lactam group and macrolide
ut” method through the subcutaneously implanted perinatal port system with amniotic fluid-like hypo-osmotic solution in “classic
ically mediated processes. However, a defined mechanism cannot be established in most cases.

iable causes of preterm birth. At present there is no optimal screening test for PPROM in asymptomatic low risk patients. An acc

e amnion (innermost layer of the intraamniotic cavity) and the chorion (fetal tissue connected to maternal decidua), and are conne

as well as in adverse pregnancy outcomes. In addition, fetal membrane cells continue to divide throughout pregnancy and its gro

rs to predict risk of pPROM and 3) how can we reduce the risk of pPROM prior to its occurrence and minimize the impact on m

ment and up until delivery being needed, in order to search for common pathogens, microbiota changes, and microbial response

ve, it does not necessarily indicate premature rupture of membranes. Finally, laboratory evaluation can assist in eliciting the etiolo

a lactam group and macrolides, erythromycin or clarithromycin. However, the very low trans-placental transfer of erythromycin
po-osmotic solution in “classic PPROM” <28/0 weeks’ gestation with oligo/anhydramnion shows promise, but must be proved in
matic low risk patients. An accurate diagnosis of PPROM is very important for patient management. The traditional approach to d

ternal decidua), and are connected by collagen-rich extra cellular matrix (ECM). ECM, which is made up of fibrous proteins alo

oughout pregnancy and its growth plateaus at term, retaining the capacity for DNA replication

and minimize the impact on maternal-fetal wellbeing

anges, and microbial response to latency antibiotic treatment. The vaginal microbiome of PPROM subjects is highly variable and

can assist in eliciting the etiology of preterm labor and guide management. These include a rectovaginal group B streptococcal cu

ental transfer of erythromycin should be evaluated in future studies. Probably, the best choice will be a combination of antibiotic
promise, but must be proved in future prospective randomized studies before it can be recommended as part of the standard of ca
. The traditional approach to diagnosis of fetal membrane rupture is now supported by scientific progress: biomarkers and the se

ade up of fibrous proteins along with various types of collagen, provides the architectural and structural framework of the fetal m

subjects is highly variable and displays significant changes to treatment. However, the unchanging deficiency of Lactobacillus, a

ginal group B streptococcal culture. If not performed within the previous 5 weeks, then antibiotic prophylaxis would be required

be a combination of antibiotics. The antibiotic therapy perhaps should be tailored to address the results of amniotic fluid and/or c
d as part of the standard of care treatments for classic PPROM
ogress: biomarkers and the search for accurate tests are in dynamic evolution. PPROM occurs in about 3% of all pregnancies an

ctural framework of the fetal membranes. The amnion and chorion are fetal tissues in origin and play major roles in maintaining

deficiency of Lactobacillus, and persistence of known pathogenic species, such as Prevotella and Peptoniphilus from presentatio

prophylaxis would be required. A urine culture, since asymptomatic bacteriuria has associations with an increased risk of preterm

ults of amniotic fluid and/or cervical smear bacteriologic investigation and the presence of bacterial resistance. Tocolysis may be
bout 3% of all pregnancies and 30% of all preterm births. It is estimated that 20% –25% of pregnancies show suspicion of PPRO

ay major roles in maintaining pregnancy by providing multi-level protection to the growing fetus. Fetal membranes accommodat

Peptoniphilus from presentation, through antibiotic treatment and up until delivery, highlights the persistent dysbiosis and warran

h an increased risk of preterm labor and birth. In patients with substance abuse, a urine drug screen would be beneficial as there

al resistance. Tocolysis may be an option for initial treatment, at least to allow completion of course of corticosteroids for RDS pr
ncies show suspicion of PPROM; Of these, 40% did not have a clear leak of fluid from the cervical os and 47% of doctors were n

Fetal membranes accommodate constant challenges (immune, structural, mechanical and endocrine) during pregnancy; continue

ersistent dysbiosis and warrants further investigation into mitigating approaches.

n would be beneficial as there is a link between cocaine use and placental abruption. Fetal fibronectin testing is necessary for wom

e of corticosteroids for RDS prevention. Neuroprotection with magnesium sulfate approximately 24–32/0 weeks could be consid
 os and 47% of doctors were not sure about the diagnosis based solely on physical examination.

) during pregnancy; continue to grow and mechanistically, as well as biochemically, maintains elasticity to the stretch forces exp

in testing is necessary for women <34 weeks gestation, cervical dilation of <3 cm and with a cervical length of 20-30mm on tran

4–32/0 weeks could be considered. Close monitoring for signs of chorioamnionitis (CRP, leucocytes, IL-6, procalcitonine, tempe
ticity to the stretch forces experienced during fetal growth. Despite the fact that membranes overlaying the placenta and cervix fa

cal length of 20-30mm on transvaginal ultrasound. Testing for sexually transmitted infections as they can contribute to preterm la

s, IL-6, procalcitonine, temperature, CTG, in some cases amniotic fluid examinations) is necessary to avoid neonatal and matern
ying the placenta and cervix face distinctly different environments and insults during pregnancy, the membranes still maintain th

ey can contribute to preterm labor etiology. It is important to familiarize preterm birth with PPROM. Membrane rupture can be p

y to avoid neonatal and maternal complications, associated with infection.

 e membranes still maintain the homeostatic balance necessary to sustain fetal growth without interruption. This companionship b

M. Membrane rupture can be physiologic or pathologic. The intra-amniotic infection has been most commonly associated with PP
ruption. This companionship between the fetus and the membranes continues until term when the fetus reaches maturity and the

commonly associated with PPROM, especially at earlier gestational ages. Other causes contributing to PPROM include short ce
etus reaches maturity and the membranes reach longevity. activation of host inflammatory response leading to collagenolysis me

ng to PPROM include short cervical length, second and third trimester bleeding, low BMI, low socioeconomic status, cigarettes,
e leading to collagenolysis mediated mechanical disruption. PPROM is a disease of the fetal membranes where the inflammation

ioeconomic status, cigarettes, and illicit drug use. Typically, about half of mothers with PPROM deliver within a week of ROM.
ranes where the inflammation-oxidative stress axis plays a major role in producing pathways that can lead to membrane weaken

eliver within a week of ROM. The main concern with PPROM is prematurity. The most common complication of preterm birth is
can lead to membrane weakening through a variety of processes. Recent data provide molecular evidences for aging of fetal mem

omplication of preterm birth is respiratory distress. However, one must consider sepsis, intraventricular hemorrhage, and necrotiz
idences for aging of fetal membranes in response to oxidative stress (OS) (physiologically at term and pathologically at preterm)

cular hemorrhage, and necrotizing enterocolitis. PPROM with intrauterine inflammation can lead to neurodevelopmental impairm
and pathologically at preterm) can cause a telomere dependent, p38MAPK signaler driven senescence activation of the fetal mem

o neurodevelopmental impairment, and early gestational age at membrane rupture has an association with an increased risk of neo
nce activation of the fetal membranes. Senescence, a mechanism contributing to aging of fetal membranes, produce sterile inflam

n with an increased risk of neonatal white matter damage. Infection and umbilical cord accidents contribute to 1-2% risk of anten
mbranes, produce sterile inflammation that can cause further damage to fetal membranes leading to weakening and or rupture. In

ontribute to 1-2% risk of antenatal fetal demise after preterm PROM.

weakening and or rupture. In addition, we report microfractures in fetal membranes that are likely sites of tissue remodeling duri
sites of tissue remodeling during gestation; however, increase in number and morphometry (width and depth) of these microfract
and depth) of these microfractures in PPROM membranes suggests reduced remodeling capacity of membranes. In addition, thes
f membranes. In addition, these fractures can act as channels for amniotic fluid leak, and inflammatory cell and microbial migrat