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Research Article: Hindawi Biomed Research International Volume 2018, Article Id 7162478, 6 Pages

Ruptura prematura de membrana

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Research Article: Hindawi Biomed Research International Volume 2018, Article Id 7162478, 6 Pages

Ruptura prematura de membrana

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Karla Ortiz
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© © All Rights Reserved
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Hindawi

BioMed Research International


Volume 2018, Article ID 7162478, 6 pages
https://doi.org/10.1155/2018/7162478

Research Article
A Retrospective Study on the Risk of Respiratory Distress
Syndrome in Singleton Pregnancies with Preterm Premature
Rupture of Membranes between 24+0 and 36+6 Weeks, Using
Regression Analysis for Various Factors

Anna NiesBuchowska-Hoxha,1 Wojciech Cnota,1 Bartosz Czuba,1 Aleksandra Ruci,1


Magdalena Ciaciura-Jarno,1 Agnieszka Jagielska,1 Dominik Wójtowicz,1 RafaB Kierach,1
Krzysztof Ddbrowski,1 Marcin Sidorowicz,1 Wioletta Skrzypulec-Plinta,2 Agata Wloch ,1
Dariusz Borowski,3 and Piotr Wwgrzyn4
1
Department of Obstetrics and Gynecology in Ruda Slaska, Medical University of Silesia, Ruda Slaska, Poland
2
Chair of Woman’s Health, Medical University of Silesia, Katowice, Poland
3
Department of Obstetrics and Gynecology, Collegium Medicum, Nicolaus Copernicus University, Torun, Poland
4
Department of Obstetrics and Perinatology, Faculty of Health Sciences, Medical University of Warsaw, Warsaw, Poland

Correspondence should be addressed to Agata Wloch; cornet@pron.pl

Received 30 April 2018; Revised 30 August 2018; Accepted 18 September 2018; Published 4 October 2018

Academic Editor: George J. Daskalakis

Copyright © 2018 Anna Niesłuchowska-Hoxha et al. This is an open access article distributed under the Creative Commons
Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is
properly cited.

Aim. This study aimed to investigate the cause of respiratory distress syndrome (RDS) in neonates from singleton pregnancies with
preterm premature rupture of membranes (pPROM) between 24+0 and 36+6 weeks by using regression analysis for various factors.
Methods. In 175 singleton pregnancies with pPROM, 95 cases of RDS (54,29%) were diagnosed. In all cases the following information
was collected: latency period of PROM, gestational age at birth, Umbilical Artery Pulsatility Index (UA PI), Middle Cerebral Artery
Pulsatility Index (MCA PI), fetal distress, antenatal steroids use, delivery type, pregnancy hypertension disease, gestational glucose
intolerance or diabetes, neonatal laboratory parameters, gender, weight, Apgar score, and other neonatal complications. Logistic
regression analysis was used to investigate the effect of variables on RDS. Results. The results of logistic regression analysis showed
that the following variables are closely correlated with RDS: female gender (OR=0.52; 95%CI:0.28-0,97), antenatal steroids use
(OR=0,46; 95%CI:0,34-0,64), abnormal UA PI and MCA PI (OR=2.96; 95%CI:1,43-6,12) (OR=2.05; 95%CI:1,07-3,95), fetal distress
(OR=2.33; 95%CI:1,16-4,71), maternal HGB (OR=0.69; 95%CI:0,5-0,96), and neonatal RBC, HGB (OR=0.32; 95%CI:0,19-0,55)
(OR=0.75; 95%CI:0,65-0,88). Conclusions. The main RDS risk factors in premature neonates are gender, abnormal fetoplacental
circulation, and fetal distress. The laboratory parameters such as lower RBC and HGB count are observed in infants with RDS.

1. Introduction after the 37th week of pregnancy referred to as term prema-


ture rupture of membranes (tPROM). pPROM complicates
Premature rupture of membranes (PROM) occurs in approx- approximately 2-4% of singleton pregnancies and about 7-
imately 3-10% of all pregnancies; it is defined as a rupture 20% of multiple pregnancies [1, 2]. This complication is a
of the membranes an hour before the start of uterine significant cause of an increased morbidity and mortality
contractions, regardless of gestational age [1, 2]. Taking into for both infants and mothers [3, 4]. pPROM occurs among
account the gestational age, PROM is divided into two 30-40% of all preterm births, which is still a significant
categories: before the 37th week of pregnancy defined as problem in perinatal medicine [5, 6]. Besides prematurity,
preterm premature rupture of membranes (pPROM) and neonatal complications include infection, sepsis, trauma,
2 BioMed Research International

fetal distress, intraventricular hemorrhage, and respiratory Other diagnostic criteria used in this study were [9–12]
distress syndrome [7, 8]. fetal distress as a significant abnormality in the fetal heart
Respiratory distress syndrome (RDS) is one of the most rate according to the result of fetal heart rate monitoring;
common causes of neonatal respiratory failure and neonatal congenital infection as fetal-neonatal infectious diseases
death. The underlying pathogenesis of RDS involves devel- such as pneumonia /septicemia caused by intra-amniotic
opmental immaturity of lungs, leading to inadequate pul- infection; neonatal anaemia as HGB lower than 18 g/dl; IVH
monary surfactant production [9]. It was previously believed was diagnosed using transfontanel ultrasonography; all IVH
that the most significant RDS factor is the prematurity. grades were included in the study.
Despite many studies, the reason for the occurrence of RDS Logistic regression analysis was used to investigate the
still remains unclear. effect of variables on neonatal RDS. Univariate and multi-
variate logistic regression models were created. A p<0.05 was
2. Objectives considered to be statistically significant.

This study aimed to investigate the cause of RDS in neonates 4. Results


from singleton pregnancies with pPROM between 24+0 and
36+6 weeks, using regression analysis for various factors, and From 9657 deliveries in the Department of Gynaecology
thus provide a useful reference for its prediction. and Obstetrics of the Municipal Hospital in Ruda Śląska
during the years 2011–2014, 175 cases (3,07%) met the pPROM
3. Material and Methods criteria. RDS was diagnosed in 95 cases, which represents
54.29% of the studied group. The median latency period of
This investigation is a retrospective study approved by pPROM was 19 hours and 48 minutes.
the bioethics committee of Silesian Medical University in We found that the lower Apgar score at 1st, 3rd, 5th, and
Katowice, Poland. In the Department of Gynaecology and 10th minute (respectively, (OR = 0.52; 95% CI 0,4-0,68; p
Obstetrics of the Municipal Hospital in Ruda Śląska from <0.001), (OR = 0, 46; 95% CI: 0,34-0,63; p <0.001), (OR = 0.37;
January 2011 to December 2014 a total of 175 singleton 95% CI: 0,24-0,56; p <0.001), and (OR = 0.4; 95% CI: 0,26-0,6;
pregnancies with pPROM were hospitalized. A consecutive p <0.001)); females sex (OR = 0.52; 95% CI: 0.28-0,97; p =
recruitment was used in this study. 0.039); antenatal steroid use (OR = 0,46; 95% CI: 0,34-0,64; p
The diagnosis of pPROM met the following criteria: (1) <0.001); abnormal Umbilical Artery Pulsatility Index (UA PI)
rupture of membranes based on the history, (2) leaking (OR = 2.96; 95% CI: 1,43-6,12; p = 0.003); abnormal Middle
amniotic fluid found in physical examination, (2) singleton Cerebral Artery Pulsatility Index (MCA PI) (OR = 2.05; 95%
pregnancies between 24 + 0/7 and 36 + 6/7 weeks of gestation. CI: 1,07-3,95; p = 0.031); fetal distress (OR = 2.33; 95% CI:
Cases with dubious diagnosis were excluded. 1,16-4,71; p = 0.018); lower maternal HGB (OR = 0.69; 95%
In all cases the following information was collected: CI: 0,5-0,96; p = 0.025); and lower neonatal RBC and HGB
latency period of PROM; gestational age at birth; Umbilical (OR = 0.32; 95% CI: 0,19-0,55; p <0.001) and (OR = 0.75; 95%
Artery Pulsatility Index (UA PI); Middle Cerebral Artery Pul- CI: 0,65-0,88; p <0.001) were the main risk factors of RDS in
satility Index (MCA PI); fetal distress; antenatal steroids use; premature neonates (Table 1) (Figure 1).
maternal age at pregnancy, maternal haemoglobin (HGB), A higher incidence of RDS resulted in newborns with
red blood cells (RBC), white blood cells (WBC) and platelets anaemia (OR = 8; 95% CI: 3,32-19,26; p <0.001); congenital
(PLT) count, maternal C-reactive protein (CRP) level, amni- infection (OR = 4.63; 95% CI: 1,8-11,94; p =0.001); and
otic fluid index (AFI), and delivery mode; pregnancy hyper- intraventricular hemorrhage (OR = 6.55; 95% CI: 1,44-29,82;
tension disease; gestational glucose intolerance or diabetes; p = 0.015).
neonatal sex; weight; Apgar score at 1st, 3rd, 5th, and 10th In the analysis using multivariate logistic regression
minute; RBC, WBC, HGB, and PLT count; CRP level; and model, gestational age at birth (OR = 0.93; 95% CI 0,9-0,96;
RDS, anaemia, congenital infection, and intraventricular p <0.001), neonatal HGB (OR = 0.77; 95% CI: 0.63-0.93; p
haemorrhage (IVH). = 0.007), and neonatal PLT (OR = 0.9912; 95% CI: 0,9857-
In 95 cases (54,29%) RDS was diagnosed based on the 0,9967; p = 0.002) were the risk factors of RDS in premature
following criteria: (1) acute onset; (2) representative clini- neonates (Table 2) (Figure 2).
cal manifestations including progressive respiratory distress In this study variables such as delivery type; maternal and
occurring shortly after birth, characteristic grunting respi- fetal WBC and CRP; maternal age; AFI; pregnancy hyper-
ration, retractions during inspiration, cyanosis, and reduced tension disease; gestational glucose intolerance; or diabetes
or absent breathing sounds; (3) typical chest x-ray findings, were not significant risk factors for RDS (p = ns) in preterm
including hypoexpansion and diffuse, fine granular densities neonates.
(grade I), air bronchograms caused by the atelectatic air
sacs (grade II), ground-glass appearance (grade III), or 5. Discussion
white lungs caused by diffuse bilateral atelectasis (grade IV);
(4) arterial blood gas analysis showing hypoxia, hypercap- The occurrence of PROM, regardless of gestational age, is
nia, and oxygen tension/fraction of inspired oxygen ratio at level of 3-10% [1, 2]; 2-18% [13–15]. pPROM complicates
(PaO2/FiO2) ≤ 26.7 kPa. approximately 2-4% of singleton pregnancies and 20-40%
BioMed Research International 3

Table 1: Univariate logistic analysis of various factors for preterm neonatal RDS.

Risk factor Odds ratios 95% CI p-value Nr. of cases


PROM latency period 1,0035 (1,0009;1,0061) 0,009 168
Gestational age at birth 0,9100 (0,88;0,94) <0,001 170
Abnormal UA PI 2,9600 (1,43;6,12) 0,003 169
Abnormal MCA PI 2,0500 (1,07;3,95) 0,031 169
Fetal distress 2,3300 (1,16;4,71) 0,018 170
Antenatal steroids use 0,4600 (0,34;0,64) <0,001 170
Maternal HGB 0,6900 (0,5;0,96) 0,025 153
Intraventricular hemorrhage 6,5500 (1,44;29,82) 0,015 167
Congenital infection 4,6300 (1,8;11,94) 0,001 169
Anaemia 8,0000 (3,32;19,26) <0,001 168
Neonatal PLT 0,9916 (0,9871;0,9961) <0,001 150
Neonatal HGB 0,7500 (0,65;0,88) <0,001 150
Neonatal RBC 0,3200 (0,19;0,55) <0,001 150
Gender (female) 0,5200 (0,28;0,97) 0,039 170
Apgar score at 10th min 0,4000 (0,26;0,6) <0,001 168
Apgar score at 5th min 0,3700 (0,24;0,56) <0,001 168
Apgar score at 3rd min 0,4600 (0,34;0,63) <0,001 168
Apgar score at 1st min 0,5200 (0,4;0,68) <0,001 168
Birth weight 0,9975 (0,9967;0,9983) <0,001 170

Table 2: Multivariate logistic analysis of various factors for preterm neonatal RDS.

Risk factor Odds ratios 95% CI p-value Nr. of cases


Gestational age at birth 0,9300 (0,9;0,96) <0,001 150
Neonatal HGB 0,7700 (0,63;0,93) 0,007 150
Neonatal PLT 0,9912 (0,9857;0,9967) 0,002 150

PROM latency period


Gestational age at birth
Abnormal UA PI
Abnormal MCA PI
Fetal distress
Antenatal steroids use
Maternal HGB count
Intraventricular hemorrhage
Congenital infection
Anaemia
Neonatal PLT
Neonatal HGB
Neonatal RBC
Gender (female)
Apgar score at 10th min
Apgar score at 5th min
Apgar score at 3rd min
Apgar score at 1st min
Birth weight

0 5 10 15 20 25 30
Odds Ratios

Figure 1: Odds ratios and confidence intervals for variables affecting the occurrence of preterm neonatal RDS–univariate logistic regression.
4 BioMed Research International

Gestational age at birth

Neonatal HGB

Neonatal PLT

0 0.2 0.4 0.6 0.8 1 1.2 1.4


Odds Ratios

Figure 2: Odds ratios and confidence intervals for variables affecting the occurrence of preterm neonatal RDS-multivariate logistic regression.

of all PROM cases [1, 2, 8, 13, 16]. In this study pPROM of preterm deliveries [28] while Laban M et al. find that
frequency was 3,07% which is similar to the one given in the measurement of fetal lung volume (FLV) or pulmonary artery
literature. resistance index (PA-RI) can help to predict RDS in preterm
According to Zanardo et al., RDS developed in 55.4% of fetuses [29].
the examined newborns from pregnancies complicated by The results of this study show that congenital infec-
pPROM [17], whereas JoonHo LEE et al. report that, in South tion and fetal distress are strong RDS factors. A similar
Korea, the RDS was diagnosed in 47% of the cases [18]. In correlation was observed in many studies [9, 18, 19, 26,
this study, RDS amounted 54.29% which is comparable to the 30]. Fetal distress may lead to birth asphyxia. Asphyxia
percentages mentioned above. together with congenital infection causes the direct injury
The results of this study show that gender; antenatal to the fetal lungs and alveolar type II cells, decreasing
steroid use; abnormal UA PI and MCA PI; fetal distress; the synthesis and releasing surfactant [9, 31, 32]. Fetal-
and congenital infection are the main risk factors of RDS in neonatal lung inflammation increases the permeability of the
preterm neonates from pPROM pregnancies. alveolar-capillary membrane to both fluid and solutes. This
This study shows that among female gender there is lower results in plasma proteins entering the alveolar hypophase,
incidence of RDS in preterm neonates. The relative risk of which further inhibits the function of surfactant [9, 31,
RDS is 0,52 times lower for females than males. These data 32].
are confirmed in the literature [9, 19–21]. It was found that In this study relationship between the lower count of
in gestation the female fetal lung produces surfactant earlier RBC, HGB, PLT, and RDS was found. Correct levels of
than the male one. The reasons for this may be as follows: RBC, HGB, and PLT vary depending on the gestational age
(1) androgens delay lung fibroblast secretion of fibroblast- and prematurity; i.e., the less mature the newborn is, the
pneumocyte factor, which can delay the development of lower the values are [33, 34]. Another factor affecting the
alveolar type II cells and reduce the release of surfactant; RBC, HGB, and PLT values was the increased percentage of
(2) androgens slow fetal lung development by adjusting newborns with IUI and prolongation of PROM latency, who
the signalling pathways of epidermal growth factor and are characterized by significantly lower count of RBC, HGB,
transforming growth factor-beta; (3) estrogen promotes the and PLT compared to noninfected newborns [34, 35].
synthesis of phospholipids, lecithin, and surfactant proteins A
There is also higher incidence of RDS in newborns
and B; and (4) estrogen also improves fetal lung development
affected by other complications such as anaemia, congenital
by increasing the number of alveolar type II cells and by
infection, and intraventricular hemorrhage. This was also
increasing the formation of lamellated bodies [9, 22–25].
reflected in the literature [2, 13, 16, 31, 36]. Furthermore,
Our study confirms that antenatal steroids' use reduces
in this study the occurrence of RDS was associated with
the risk for RDS. This fact results in the current international
lower PLT count; its deficiency leads to bleeding. Additional
recommendations of the Royal College of Obstetricians and
PLT reduction risk factors are prematurity and intrauterine
Gynaecologists (RCOG) in dealing with various accepted
infection [33]. This leads to the occurrence of both RDS and
dosage schemes of corticosteroids.
intraventricular hemorrhage [34].
Neonatal breathing disorders can be caused by circulatory
system diseases. The main factors in this group are congenital
heart disease, pulmonary hypertension, and congestive heart 6. Conclusions
failure [26, 27]. No reports were found regarding fetopla-
cental circulation in relation to the development of neonatal The main risk factors of RDS in premature neonates are
RDS. However, the abnormal UA PI, MCA PI correlates with gender, abnormal fetoplacental circulation, and fetal distress.
centralization of the cardiovascular system, which after the Other neonatal complications such as anaemia, congenital
birth is an additional risk factor for RDS on the background of infection, and intraventricular haemorrhage increase the risk
cardiovascular failure. Büke et al. concluded that pulmonary of RDS coexistence. The laboratory parameters abnormalities
artery acceleration time to ejection time ratio (PATET) such as lower RBC, HGB, and PLT count are observed in
is a promising noninvasive tool to predict RDS in cases infants with RDS.
BioMed Research International 5

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