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 Table of Contents  
ORIGINAL ARTICLE
Year : 2022  |  Volume : 35  |  Issue : 2  |  Page : 788-795

Predictors of placental abruption during expectant management of premature preterm rupture of membranes


Department of Obstetrics and Gynecology, Faculty of Medicine, Menoufia University, Menoufia, Egypt

Date of Submission18-Nov-2021
Date of Decision14-Dec-2021
Date of Acceptance19-Dec-2021
Date of Web Publication27-Jul-2022

Correspondence Address:
Mohamed Safwat Mohamed Mostafa
Department of Obstetrics and Gynecology, Faculty of Medicine, Menoufia University, Menoufia
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/mmj.mmj_250_21

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  Abstract 


Objective
To predict the risk factors of placental abruption during expectant management of preterm rupture of membranes.
Background
A frequency of abruption of 4.0%–6.8% has been reported in patients with preterm premature rupture of membranes (PPROM). Antepartum vaginal bleeding occurs during the period of expectant management, the associated risk of developing placental abruption is high. It may be possible to approximate the risk for placental abruption based on these simple prepregnancy risk factors.
Patients and methods
An observational study was conducted on 100 pregnant women. The patients were randomly selected from those attending labor ward at Menoufia University Hospital and Shebin EL-Kom Teaching Hospital. All women included in this study are with PPROM, divided into group I that included 79 without placental abruption and group II included 21 with placental abruption. Full analysis of detailed history and examination and primarily samples are taken during the study period from January 2019 to December 2020.
Results
There were statistically significant differences among patients with placental abruption than those without placental abruption regarding antepartum or intrapartum fetal distress requiring urgent cesarean section and gestational age. The majority of patients with placental abruption had gestational age more than 32 weeks (P < 0.05). Most of the patients with placental abruption had latency to its occurrence more than 48 h since the time of admission with PPROM with a percentage of 85.71%.
Conclusion
Placental abruption is a complex disease. Although several risk factors are known, the etiopathogenesis is not fully understood and its occurrence often remained unpredictable or unpreventable. Placental abruption was absent in 79% of our patients.

Keywords: placenta, placental abruption, predictors, preterm, risk factors


How to cite this article:
Salama HF, Omara MA, Mostafa MS, Fathey AA. Predictors of placental abruption during expectant management of premature preterm rupture of membranes. Menoufia Med J 2022;35:788-95

How to cite this URL:
Salama HF, Omara MA, Mostafa MS, Fathey AA. Predictors of placental abruption during expectant management of premature preterm rupture of membranes. Menoufia Med J [serial online] 2022 [cited 2024 Mar 28];35:788-95. Available from: http://www.mmj.eg.net/text.asp?2022/35/2/788/352174




  Introduction Top


Preterm premature rupture of membranes (PPROM) complicates 1%–3% of all pregnancies and is associated with maternal and perinatal morbidity and mortality. The optimal management of pregnancies complicated by PPROM remains unclear. Specifically, the issue of expectant management vs. immediate delivery, especially in cases of PPROM occurring at ≥32 weeks of gestation, is controversial[1]. During recent years, there has been an increased interest in expectant management. Among the large amount of data on the topic of PPROM, only a limited number of studies have reported the incidence and associated increased risk of placental abruption. A frequency of abruption of 4.0%–6.8% has been reported in patients with PPROM[2]. Moreover, none of these studies has addressed the issue of whether there is an increased risk of placental abruption by decreasing gestational age (GA) at the time of PROM. However, if antepartum vaginal bleeding occurs during the period of expectant management, the associated risk of developing placental abruption (even so if the bleeding occurred after the first trimester but prior to rupture of membranes) is high[3]. Placental abruption is defined as the complete or partial premature separation of the placenta before delivery with hemorrhage into the decidua basalis. The diagnosis of placental abruption is clinical. It should be suspected in women who present with vaginal bleeding or abdominal pain or both, a history of trauma, and in those who present with unexplained preterm birth. The symptoms of abruption vary from none, in which the diagnosis is made only on placental inspection, to massive abruption, leading to fetal death and maternal morbidity[4]. Abruption results from a rupture of maternal decidual artery causing dissection of blood at the decidual–placental interface, around the placental margin, or behind the membranes. Acute vasospasm of small vessels may be one event immediately preceding placental separation[5]. Immunological defects may well play a role in the origin of placental abruption. These defects may lead to maternal inflammatory response with cytokine release, resulting in a chain of events such as shallow trophoblast invasion, defective spiral artery remodeling, placental infarctions, and thrombosis[6]. Placental abruption may also be a manifestation of acute or chronic inflammation. Infection or inflammation and tissue injury can cause a rapid release of various bioactive mediators at the maternal–fetal interface, which may predispose to abruption. Normal placentation requires trophoblast invasion of maternal spiral arteries, and development of a high-flow, low-resistance uteroplacental circulation[7]. Vascular remodeling occurs under the influence of several proangiogenic and antiangiogenic factors. Proangiogenic placental growth-factor deficiency and antiangiogenic soluble FMS-like tyrosine-kinase 1 excess may result from placental hypoxia associated with incomplete remodeling of maternal spiral arteries[8]. Therefore, we performed an observational study to predict the risk factors of placental abruption during expectant management of preterm rupture of membranes.


  Patients and methods Top


An observational study was conducted on 100 pregnant women. The patients were randomly selected from those attending labor ward at Menoufia University Hospital and Shebin EL-Kom Teaching Hospital during the study period from January 2019 to December 2020. All women were included in this study with PPROM, divided into group I that included 79 without placental abruption and group II that included 21 with placental abruption. Ethical consideration: all participants were volunteers. All of them signed a written informed consent with explaining the aim of the study before the study initiation. Approval of the study protocol was obtained by Ethical Scientific Committee for human research at Menoufia University Hospital and Shebin EL-Kom Teaching Hospital.

Inclusion criteria included patients with singleton pregnancy and premature rupture of membranes in pregnant women with GA more than 28 weeks and less than 36 weeks. Exclusion criteria included patients with multiple gestations and patients in active labor, preeclampsia and chorioamnionitis, fetal distress, or any cause that requires immediate termination of pregnancy and congenital anomalies, respiratory infection at the time of admission, and any long-standing diseases, such as rheumatoid arthritis, patient with heart disease, diabetic or gestational, and chronic hypertension, were excluded. All selected women included in this study were subjected to the following: full detailed history to detect risk factors. Full general examination of the patient, including vital signs: pulse, blood pressure, and temperature, abdominal examination, including fundal level and abdominal tenderness, and local examination: Cusco speculum examination to detect fluid pooling. Laboratory examination: complete blood count every 72 h, erythrocyte-sedimentation rate (ESR), and C-reactive protein (CRP) every 48 h and urine analysis weekly. Ultrasound examination: done twice weekly using CHISON ECO 1 device to detect presentation, amniotic fluid index (AFI), and GA in weeks and to ensure fetal viability. Biophysical profile twice weekly, and manual count of uterine contractions twice daily. Medications, essential third-trimester medications, including oral iron and oral calcium and a single course of corticosteroids of 24 mg divided into three doses 12 h apart[9]. Centers for Disease Control and Prevention (CDC) recommendations 2018, for prophylaxis of chorioamnionitis in the case of PPROM: 2 g of ampicillin/8 h for 48 h, then azithromycin 500-mg tab once daily for 5 days, and then follow-up[10]. According to the World Health Organization and CDC recommendations, no tocolytics were given to patients with PPROM. Follow-up of the patient was done from the time of admission till delivery and recording of the latency period till placental-abruption occurrence and mode of delivery. Appearance, Pulse, Grimace, Activity, and Respiration.” In the test, five things are used to check a baby's health APGAR Score was recorded after delivery of the baby at 5 and 10 min. Outcome measures: detection of the incidence of abruptio placenta between pregnant women with premature preterm rupture of membranes and their risk factors. Sample size was calculated based on an expected incidence of placental abruption in PPROM of 5%[11]. It was calculated through N=(t2 × p (1 − p))/m2. Description: N = required sample size, t = confidence level at 95% (standard value of 1.96). P = estimated the incidence of abruption in PPROM. m = margin of error at 5% (standard value of 0.05). Sample size = N/[1+(N/Population)]. Assuming = 0.05, we calculated that we would need 100 participants to estimate the incidence of 5% with 5% precision, to achieve a power of 80% (=0.8), and an alpha level of 0.05 and beta 0.2.

Statistical analysis

The results were collected, tabulated, and statistically analyzed by IBM personal computer and Statistical Package SPSS version 22 (IBM Corp., 2013, Armonk, NY). Descriptive statistics included percentage (%), mean (x), and SD, and analytic statistics included χ2 test, Student's t-test, intergroup comparison, Fisher's exact test, and Mann–Whitney test. P value < 0.05 was considered statistically significant.


  Results Top


Our study showed that the mean age and body mass index of the studied patients were 27.11 ± 4.65 years and 25.84 ± 1.88 (kg/m2), respectively. Also, most of the patients (86%) were multipara. The majority of them had no previous history of PPROM, vaginal bleeding, placental abruption, chorioamnionitis, and cesarean-section delivery with percentages of 85%, 93%, 91%, 53%, and 89%, respectively. They all did not smoke or drink alcohol and most of them had coitus in the last month and with no history of trauma with percentages 80% and 94%, respectively [Table 1].
Table 1: Demographical and historical data of the patients in this study

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As regards to general examination of the studied patients, our study showed that the mean systolic blood pressure, diastolic blood pressure, pulse, and temperature of the studied patients were 114.00 ± 10.00, 76.00 ± 11.00, 83.50 ± 5.02, and 37.12 ± 0.15, respectively. Most of the patients (84%) had fundal level less than the period of amenorrhea. All of the patients had no uterine tenderness and fluid pooling was present [Table 2].
Table 2: General, abdominal, and local examination of the patients in this study

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As regards to laboratory investigations, our study revealed that the mean ESR at the 1st and 2nd hour of the studied patients were 32.08 ± 6.25 and 52.11 ± 13.45, respectively. Also, the mean positive CRP, total leukocyte count (TLC), hemoglobin (HB), platelet (PLT), pus cells, and red blood cells (RBCs) in urine were 7.86 ± 16.57, 8.39 ± 2.82, 11.01 ± 1.08, 186.26 ± 66.79, 7.74 ± 5.54, and 4.36 ± 4.21, respectively. The mean GAs by ultrasound and AFI of the studied patients were 32.02 ± 2.28 and 4.00 ± 2.00, respectively. Most of the studied patients (86%) had cephalic presentation. Most of the patients (79%) had no placental abruption and 21% had placental abruption [Table 3].
Table 3: Laboratory investigations and ultrasound examination of the patients in this study

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In our study, there was a high statistically significant difference between the two groups regarding parity, past history of PPROM, history of vaginal bleeding, or early bleeding in this pregnancy, past history of placental abruption, previous cesarean section (CS), and past history of chorioamnionitis occurring in previous pregnancy (P ≤ 0.05), whereas there was no statistically significant difference between the studied groups regarding their age, body mass index, past history of urinary-tract infection (UTI), history of trauma, and coitus in the last month (P > 0.05) [Table 4].
Table 4: Demographic and historical data among patients with and without placental abruption

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Our study showed that there was no statistically significant difference between patients with and without placental abruption regarding systolic blood pressure, diastolic blood pressure, pulse, and temperature (P > 0.05), whereas there was a statistically significant increase among patients with placental abruption than those without placental abruption regarding ESR at 1st and 2nd hours, positive CRP, and TLC (P ≤ 0.05). There was no statistically significant difference between the studied groups regarding HB, PLT levels, pus cells, and RBCs in urine (P > 0.05). Also, there was a statistically significant difference between the studied groups regarding AFI and GA. The majority of patients with placental abruption had GA more than 32 weeks. Most of the patients with placental abruption had AFI levels less than 5 with a significant difference between the two groups. Also, there was a statistically significant difference between the two groups regarding presentation (P ≤ 0.05) [Table 5].
Table 5: General examination, laboratory investigations, gestational age, AFI, and presentation among patients with and without placental abruption

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Our study revealed that there was a statistically significant difference between patients with and without placental abruption regarding latency to placental-abruption occurrence (P ≤ 0.003). Most of the patients with placental abruption had latency to its occurrence more than 48 h since the time of admission with PPROM with a percentage of 85.71%. Also, there was a statistically significant difference among patients with placental abruption than those without placental abruption regarding antepartum or intrapartum fetal distress requiring urgent CS and APGAR score lower than 6 (P ≤ 0.05) [Table 6].
Table 6: Latency to placental-abruption occurrence, fetal distress requiring urgent CS, and low APGAR score among patients with and without placental abruption

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  Discussion Top


Among the large amount of data on the topic of PPROM, only a limited number of studies have reported the incidence and associated increased risk of placental abruption[2],[3],[6]. A frequency of abruption of 4.0%–6.8% has been reported in patients with PPROM. Antepartum vaginal bleeding occurs during the period of expectant management, the associated risk of developing placental abruption is high. It may be possible to approximate the risk for placental abruption based on these simple prepregnancy risk factors[7]. Therefore, our study was designed to predict the risk factors of placental abruption during expectant management of preterm rupture of membranes. Our study showed that the mean age and body mass index of the studied patients were 27.11 ± 4.65 years and 25.84 ± 1.88 kg/m2, respectively. Also, most of the patients (86%) were multipara. The majority of them had no previous history of PPROM, vaginal bleeding, placental abruption, chorioamnionitis, cesarean-section delivery, and UTI with percentages of 85%, 93%, 91%, 53%, and 89%, respectively. Our results were in accordance with Fahmy et al.[12], who found that the mean age of their cases was 27.67 ± 5.94. The correlation of PPROM in pregnant women >25 years of age can be explained by endogenous changes in the fetus and its annexes, as the occurrences of fetal aneuploidy with growing maternal age are greater. PPROM was common in multigravidas 70% due to possible long-standing infection, previous trauma to the cervix, and patulous. Discussing maternal morbidities, they found a significantly increased rate of antepartum hemorrhage due to placental separation by 20%. Also, Hackenhaar et al.[13] reported that the lack of correlation between PPROM and urinary infections in pregnancy may be due to the complete treatment of UTI in most cases. On the other hand, Surekha et al.[14] and Assefa et al.[15] found that 28% of cases had past history of PPROM and then 16% had UTI. The CS was set to be a remarkable risk factor. Cases with previous CS were 3.15 times more prone to developing PPROM and abruptio placenta. Our study showed that mean Systolic blood pressure (SBP), Diastolic blood pressure (DBP), pulse, and temperature of the studied patients were 114 ± 10.00, 76.00 ± 11.00, 83.50 ± 5.02, and 37.12 ± 0.15, respectively. Our study revealed that the mean ESR at the 1st and 2nd hour of patients were 32.08 ± 6.25 and 52.11 ± 13.45, respectively. Also, the mean positive CRP, TLC, HB, PLT, pus cells, and RBCs were 7.86 ± 16.57, 8.39 ± 2.82, 11.01 ± 1.08, 186.26 ± 66.79, 7.74 ± 5.54, and 4.36 ± 4.21, respectively. The current findings were in accordance with Fahmy et al.[16], who found that the mean value of white blood cells (WBCs) was 11.73 ± 2.75 and ranged 7.4–19.4. The mean value of CRP was 10.6 ± 9.03. Normal CRP does not exclude infection and a raised CRP is not specific and should not be depended upon to determine if pregnancy should be terminated, it should be used to identify early subclinical infection in addition to other parameters. Similar results were reported by Giles et al.[17], who reported that the median CRP (range 8–56 mg/l) was 9 mg/l. CRP was presented with a mean initial value of 15.96 mg/l, which is very close to the value of 14.80 mg/l reported in a Turkish study by Kurdoglu et al.[18]. In disaccordance with Pratiwi et al.[19], who revealed that maternal anemia in women had a significant association with PROM occurrence. Pregnancy with anemia will have three-times higher risk than those without anemia. Meanwhile, Pusparini[20] mentioned that 59.6% of anemic mothers experience premature rupture of membranes, which showed a significant relationship between anemia status and premature rupture of membranes, pregnant women with anemia had 2.4-times greater risk compared with nonanemic pregnant women. Our study showed that mean GA and AFI of the studied patients were 32.02 ± 2.28 and 4.00 ± 2.00, respectively. These were in accordance with Fahmy et al.[12], who found that the most common GA group was between 32 and 36 weeks by 60% that peaked at 34 weeks by 20%. Agreeing with Rodrigo and Kannamani[21], who found that the peak GA group complicated by PPROM and subsequent abruptio placenta was between 34 and 36 weeks of gestation by 20%. Similar results were reported by Fahmy et al.[16], who reported that GA at the time of presentation was 31.04 ± 1.72 (28–34), and the majority (68.49%) was 29–32 weeks and 23.29% of them aged 33–34 weeks. Similar results were reported by Giles et al.[17]. On the other hand, Galletta et al.[22] found that the mean initial AFI was 8.1 cm. Also, a total of 27.9% of their patients had oligohydramnios at the initial evaluation. Also, Shweta and Patil[23] found that the most affected GA group was between 35 weeks and 36 weeks + 6 days of gestation by 75% among the total analyzed patients. In our study, there was no statistically significant difference found between the studied groups regarding their age, body mass index, past history of UTI, history of trauma, and coitus in the last month, whereas there were statistically significant differences between the two groups regarding past history. This agreed with Nath et al.[24] and Ananth et al.[25] who reported that PPROM is a common obstetric complication occurring in ~1%–2% of pregnancies, and it is one of the important risk factors for placental abruption. Also, Holmgren and Olofsson[26] found a frequency of placental abruption of 78%, that is, in good agreement with previous reports: 69% by Major et al.[11] and 63% by Gonen et al.[27]. In addition, Hoa and Tuyen[28] found that nearly all cases had vaginal bleeding, abdominal pain and/or uterine tenderness, hypertonic contractions, and possibly fetal heart-rate abnormalities, as well as presentation of acute abruption rather than chronic abruption.

In this study, there was a statistically significant increase among patients with placental abruption than those without placental abruption regarding ESR at the 1st and 2nd hours, positive CRP, and TLC. Also, Shah et al.[29] found that the admission of WBC count may also be useful in assessment for placental abruption. The white count (WBC × 103/mm3) has been found to be significantly elevated in patients with abruption vs. those without, along with the band count. Therefore, a WBC more than 20 000/mm3 on admission should raise one's suspicion of the possibility of abruptio placentae. Conversely, a WBC of 20 000/mm3 or less may be associated with a very small, if any, risk for abruption, because the negative predictive value is 100%, whereas our study revealed that there was no statistically significant difference between the studied groups regarding HB, PLT levels, pus cells, and RBCs in urine.

The current study demonstrated that there was a statistically significant increase among patients without placental abruption than those with placental abruption regarding GA and AFI. Also, there was a statistically significant difference regarding presentation and latency to placental-abruption occurrence. Another agreement with Nelson et al.[30] found a three-to-eight-fold increased risk for abruption in patients who were followed up expectantly after prolonged PPROM. In their case reports, patients had significantly decreased amniotic fluid. This agreed with Saquib et al.[31], who found that preterm premature rupture of the membranes before 37 weeks of gestation leads to 4%–12% of cases of placental abruption. Our study revealed that there were statistically significant differences among patients with placental abruption than those without placental abruption regarding antepartum or intrapartum fetal distress requiring urgent CS. Saquib et al.[31] revealed that placental abruption leading to fetal and neonatal morbidity and mortality is mainly associated with preterm birth and low birth. About 40% of cases had fetal distress during the intrapartum period. Also, Salihu et al.[32] reported that adverse fetal outcomes like intrauterine growth restriction, preterm birth, low birth weight, fetal distress, low APGAR score, transfer to neonatal intensive-care unit, stillbirth, congenital anomalies, and perinatal death ranging from 4.4% to 67.3% are also observed in cases of placenta abruption.


  Conclusion Top


Placental abruption is a complex disease. Although several risk factors are known, the etiopathogenesis is not fully understood and its occurrence often remained unpredictable or unpreventable. Most of the patients who had PROM in our study had no placental abruption (79%), and we found that there was a statistically significant difference between the two groups regarding past-history risk factors, parity, ESR at the 1st and 2nd hours, positive CRP, TLC, GA, AFI, and antepartum or intrapartum fetal distress requiring urgent CS and APGAR score lower than 6. Also, most of the patients with placental abruption had latency to delivery more than 48 h. So, doctors should be increasingly aware of the association between preterm premature rupture of membranes and the subsequent risk of developing placental abruption.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Lorthe E, Torchin H, Delorme P, Ancel PY, Marchand-Martin L, Foix- L'Hélias L, et al. Preterm premature rupture of membranes at 22–25 weeks' gestation: perinatal and 2-year outcomes within a national population-based study (EPIPAGE-2). Am J Obstet Gynecol 2018; 219:3.  Back to cited text no. 1
    
2.
Ekmekci E, Gencdal S. Placental abruption and preterm premature rupture of membranes: how much frequent. J Clin Mol Med 2018; 1:2.  Back to cited text no. 2
    
3.
Brennan K. Placental pathology: a review of placenta previa, placental abruption and placenta accreta. https://pennstate.pure.elsevier.com/en/publications/placental-pathology-a-review-of-placenta-previa-placental-abrupti”Update in Anaesthesia. 2019; 34:51-55.  Back to cited text no. 3
    
4.
Fadl SA, Linnau KF, Dighe MK. Placental abruption and hemorrhage review of imaging appearance. Emerg Radiol 2019; 26:1.  Back to cited text no. 4
    
5.
Gonen N, Levy M, Kovo M, Schreiber L, Noy LK, Volpert E, et al. Placental histopathology and pregnancy outcomes in 'early' vs. 'late' placental abruption. Reprod Sci 2020; 18:1.  Back to cited text no. 5
    
6.
Levy M, Gonen N, Kovo M, Schreiber L, Marom O, Barda G, et al. Does macroscopic estimation of the extent of placental abruption correlate with pregnancy outcomes. Eur J Obstet Gynecol Reprod Biol 2020; 254:188–194.  Back to cited text no. 6
    
7.
de Moreuil C, Hannigsberg J, Chauvet J, Remoue A, Tremouilhac C, Merviel P, et al. Factors associated with poor fetal outcome in placental abruption. Pregnancy Hypertension 2021; 23:59–65.  Back to cited text no. 7
    
8.
Müller A, Horvat V, Vulin M, Mandić S, Seric V, Vidosavljevic D. The soluble fms-like tyrosin kinase-1 (sFLT-1) to placental growth factor (PIGF) ratio as a possible indicator for the severity of preeclampsia-single institution experience. Med Glas 2019; 16:1.  Back to cited text no. 8
    
9.
Antenatal Corticosteroid Clinical Practice Guidelines Panel. Antenatal corticosteroids given to women prior to birth to improve fetal, infant, child and adult health: Clinical Practice Guidelines. Auckland, New Zealand: Liggins Institute, The University of Auckland; 2015.  Back to cited text no. 9
    
10.
O'Brien JM, Santolaya JL, Palomares K, Blitzer D, Santolaya-Forgas J. Association of histological chorioamnionitis and magnesium sulfate treatment in singleton and dichorionic twin pregnancies with preterm premature rupture of membranes: preliminary observations. J Perinat Med 2018; 46:8.  Back to cited text no. 10
    
11.
Major CA, de Veciana M, Lewis DF, Morgan MA. Preterm premature rupture of membranes and abruptio placentae: is there an association between these pregnancy complications. Am J Obstet Gynecol 1995; 172:2.  Back to cited text no. 11
    
12.
Fahmy AM, Ait-Allah AS, Fattah LE. Pregnancy outcomes in cases of preterm prelabor rupture of membranes at Aswan University Hospital. Egypt J Hosp Med 2020; 78:2.  Back to cited text no. 12
    
13.
Hackenhaar AA, Albernaz EP, da Fonseca TM. Preterm premature rupture of the fetal membranes: association with sociodemographic factors and maternal genitourinary infections. J Pediatr (Rio J) 2014; 90:2.  Back to cited text no. 13
    
14.
Surekha S. Mohan, Chamaraja Thippeveeranna, Naorem N. Singh, Laiphrakpam R. Singh. analysis of risk factors, maternal and fetal outcome of spontaneous preterm premature rupture of membranes: a cross sectional study. IJRCOG 2017; 6 (9): 3781-3787.  Back to cited text no. 14
    
15.
Assefa NE, Berhe H, Girma F, Berhe K, Berhe YZ, Gebreheat G, et al. Risk factors of premature rupture of membranes in public hospitals at Mekele city, Tigray, a case control study. BMC Pregnancy Childbirth 2018; 18:1.  Back to cited text no. 15
    
16.
Fahmy AM, Mohamed MA, Nour El-dien M, Rasheed S. Management of premature rupture of membranes at Sohag University Hospital: a clinical audit. Sohag Medical Journal 2020; 24(2): 204-212.  Back to cited text no. 16
    
17.
Giles M, Garland S, Oats JJ. Management of preterm pre-labour rupture of membranes: an audit. How do the results compare with clinical practice guidelines?. Aust N Z J Obstet Gynaecol 2005; 45:3.  Back to cited text no. 17
    
18.
Kurdoglu M, Kolusari A, Adali E, Yildizhan R, Kurdoglu Z, Kucukaydin Z, et al. Does residual amniotic fluid after preterm premature rupture of membranes have an effect on perinatal outcomes? 12 years-experience of a tertiary care center. Arch Gynecol Obstet 2010; 281:4.  Back to cited text no. 18
    
19.
Pratiwi PI, Emilia O, Kartini F. The effect of anemia on the incidence of premature rupture of membrane (prom) in kertha usada hospital, singaraja, bali. Belitung Nursing Journal 2018; 4.(3):336-342.  Back to cited text no. 19
    
20.
Pusparini NL. Status anemia dengan Kejadian Ketuban Pecah Dini. Jurnal Genta Kebidanan.journal health quality.2014; 5(1): 1-66.  Back to cited text no. 20
    
21.
Mamusha Aman Hussen. Maternal and fetal outcomes in term premature rupture of membrane. “https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4905872/”World J Emerg Med. 2016; 7(2): 147–152.  Back to cited text no. 21
    
22.
Galletta MA, Bittar RE, Agra I, Guerra EC, Francisco RP, Zugaib M. Epidemiological profile of patients with preterm premature rupture of membranes at a tertiary hospital in São Paulo, Brazil. Clinics. 2019; 74: e1231.  Back to cited text no. 22
    
23.
Koothan U. T., Nina V. Kate, Anuradha V.A study of feto-maternal outcome in cases of pre-labour rupture of membranes.IJRCOG 2017;6 (10): 4329-4333.  Back to cited text no. 23
    
24.
Nath CA, Ananth CV, Smulian JC, Shen-Schwarz S, Kaminsky L. New Jersey–Placental Abruption Study Investigators. Histologic evidence of inflammation and risk of placental abruption. Am J Obstet Gynecol 2007; 197:3.  Back to cited text no. 24
    
25.
Ananth CV, Oyelese Y, Srinivas N, Yeo L, Vintzileos AM. Preterm premature rupture of membranes, intrauterine infection, and oligohydramnios: risk factors for placental abruption. Obstet Gynecol 2004; 104:1.  Back to cited text no. 25
    
26.
Holmgren PÅ, Olofsson JI. Preterm premature rupture of membranes and the associated risk for placental abruption. Inverse correlation to gestational length. Acta Obstet Gynecol Scand 1997; 76:8.  Back to cited text no. 26
    
27.
Gonen R, Hannah ME, Milligan JE. Does prolonged preterm premature rupture of the membranes predispose to abruptio placentae? Obstet Gynecol 1989; 74: 347–50.  Back to cited text no. 27
    
28.
Hoa NH, Tuyen NT. Unpredictable placental abruption: case series. Case Reports in Clinical Medicine 2020; 9, 165-175.  Back to cited text no. 28
    
29.
Shah S, Miller PR, Meredith JW, Chang MC. Elevated admission white blood cell count in pregnant trauma patients: an indicator of ongoing placental abruption. Am Surg 2002; 68:644-7.  Back to cited text no. 29
    
30.
Nelson DM, Stempel LE, Zuspan FP. Association of prolonged, preterm premature rupture of the membranes and abruptio placentae. J Reprod Med 1986; 31:4.  Back to cited text no. 30
    
31.
Saquib S, Hamza LK, AlSayed A, Saeed F, Abbas M. Prevalence and its feto-maternal outcome in placental abruption: a retrospective study for 5 years from Dubai Hospital. Dubai Med J 2020; 3:1.  Back to cited text no. 31
    
32.
Salihu HM, Bekan B, Aliyu MH, Rouse DJ, Kirby RS, Alexander GR. Perinatal mortality associated with abruptio placenta in singletons and multiples. Am J Obstet Gynecol 2005; 193:1.  Back to cited text no. 32
    



 
 
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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]



 

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