Eman Dow 2 Reserch

You might also like

Download as pdf or txt
Download as pdf or txt
You are on page 1of 47

List of content:

Subject Page

Certification ii

List of content iii

List of tables iv

List of figures v

Abbreviation vi

Acknowledgment vii

Abstract viii

Introduction 1
Aim of study 16
Materials and methods 17
Result 18
Discussion 28
Conclusion and Recommendations 30
References 31
Arabic summary 36

iii
List of tables:
Table Title Page
number number
1 Age distribution of the mothers 18
2 Gravidity distribution of the patients 19
3 Parity distribution of the patients 20
4 Abortion distribution of the patients 21
5 Risk factors for PLROM 22
6 Mode of delivery 23
7 Maternal morbidity 24
8 Neonatal sex 25
9 Neonatal complications 26
10 Nursery admission 27

iv
List of figures:
Figure Title Page
number number
1 Age distribution of the mothers 18
2 Gravidity distribution of the patients 19
3 Parity distribution of the patients 20
4 Abortion distribution of the patients 21
5 Risk factors for PLROM 22
6 Mode of delivery 23
7 Maternal morbidity 24
8 Neonatal sex 25
9 Neonatal complications 26
10 Nursery admission 27

v
Abbreviations:

C/S: Caesarean section


PROM, PRLOM: Premature rupture of membranes
RDS: Respiratory distress syndrome
STD : Sexual transmitted disease
UTI: Urinary tract infection

vi
Acknowledgment

To “Allah “the Most Gracious and the Most Merciful, who directed us through the
way. To Dr. Maha Shinshin for her huge efforts of directing and supervising me to
achieve this adequate work. To Dr Taher Emahbes a biostatician who helped me a
lot in the result and discussion. To all my family and friends, they supported me
and encouraged me to finish this work, to all my staff members and my
colleagues, who helped me in my work. I thank all of them and wish you the best
in their lives.

Dr. Eman Daw Gayed

vii
viii
Summary

Background:
Preterm premature rupture of membranes (PPROM) is the main cause ofpreterm
delivery and is associated worldwide with increased rates of neonatal and
maternalmorbidity and mortality.
Aim of study:
To identify the maternal and fetal outcome in patients with PROM.
Materials and methods:
This was Retrospective case series study it was conducted in Tripoli Medical
Center during the year 2015-2016. One hundred patients with history of PLROM
were randomly selected from the hospital files. The following data was obtained
from the files: the age, gravidity, parity, history of previous abortion, risk factors,
maternal morbidity, mode of delivery, sex of the neonate, neonatal complications
and admission to the nursery.
Result:
The mean age for the patients was (30 ± 5 years). The maximum age of the patients
was 45 years and the minimum age was 20 years. Most of the age distribution of
the patients in this study was between 20 and 30 years. Most of the patients were
multigravidas and multiparous. The most prominent predisposing factor for
PLROM was UTI 44% followed by polyhydrominous (14%) then multiple
pregnancy (12%).
In respect to maternal morbidity, about 4% of the patients had chorioaminitis, 13%
had pyrexia, 5% had wound infection and only 3% had UTI. With regard neonatal
complications, around 12% of the neonates had RDS, 8% had septicemia, 3% had
jaundice, and 3% had conjunctivitis.
Conclusion:

ix
In summary, patients who had PROM were young, multigravidas and multiparous.
The main risk factors that cause PROM were UTI, polyhydraminous and multiple
pregnancy. Maternal morbidity showed that the most prominent maternal
morbidity was puerperal pyrexia while the most prominent neonatal morbidity was
RDS.

x
Introduction:
PROM refers to rupture of the membranes prior to the onset of labor and prior to
the onset of clinically apparent labour contractions [1, 2]. PROM can occur at any
gestational age and is classified as “preterm PROM” if the event occurs before 37
weeks of gestation or “term PROM” if the event occurs after 37 weeks of gestation
[3-5]. A number of issues are associated with PROM including infection, anatomic
and pregnancy-related factors [6]. PROM is related to number of adverse maternal
and neonatal outcomes. The most frequent maternal consequences associated with
PROM are chorioamnionitis, endomyometritis, wound infection, pelvic abscess,
bacteremia and postpartum haemorrhage [7, 8]. One of the most serious
consequences of PROM-related maternal infection is Early Onset Neonatal
Infection (EONI). EONI is often acquired prenatally in pregnancies with PROM
and is associated with increased neonatal morbidity and mortality. 9 Another
adverse outcome of prelabour rupture of membranes is the increased use of
operative procedures which can increase the likelihood of a cesarean section.II.
Review Of Literature History:
The foetal membranes are made of thin layer of amnion and thick outer layer of
chorion that is directly opposed to maternal decidual tissues. Between amnion and
chorion is connective tissue layer, which is rich of collagen. By 26 weeks of
gestation the amnion composed of single layer of cuboidal epithelium. The chorion
is four to six cells layers in thickness and the amnion has greater tensile strength
than the chorion, although thinner than the chorion. The membranes together with
stand the greater bursting pressure then they do separately. The amount of physical
stress tolerated by the membranes decreases as pregnancy progress, as the
pregnancy advances, the relative concentration of the collagen decreases. Collagen
maintenance and degradation are regulated in foetal membranes by interaction of
matrix metaloproteinases and specific tissues inhibitors of metalo proteinases.

1
Imbalance in action of this system may be associated with premature rupture of the
membranes, both collagenase and proteinase activity are increased in patients with
PROM.(10) Premature rupture of membranes is defined as spontaneous rupture of
membranes before onset of labour regardless of gestational age or duration of
ruptured to onset of labour, the latent period, which is duration between PROM
and onset of uterine contractions. When PROM occurs preterm is called preterm
premature rupture of membranes. When it occurs at term is called premature
rupture of membranes at term. PROM occurs in 4 – 8% of all pregnancies and
related to about 10% of perinatal deaths.(11) In early pregnancy the amniotic fluid
surrounding the developing foetus is produced from umbilical cord transfer and
transudation of fluid from foetal skin.(12) By the 20th week gestation the skin
loses its permeability, and from this time on wards the foetal kidneys play an
increasing role in the production of amniotic fluid. By term about 500 ml per day is
secreted as foetal urine and 200 ml from tracheal fluid. Disposal of fluid is partly
by absorption through the amnion into maternal plasma and partly by foetal
swallowing and absorption from foetal intestine into foetalplasma.(13) Amniotic
fluid is important for development of foetal lungs, limbs movement, head exchange
and protection of unbiblical cord and foetus from compression. If the membranes
rupture these protective functions may be compromised and portal is established
for entry of bacteria from the vagina to the uterus leading to chorioamnionitis and
foetalinfection.(13)
Aetiology of premature rupture of membranes:
Aetiology of premature rupture of membranes is usually not understood. There are
howeve,r many coexisting variables including.(12)
i- Cervical incompetence.
ii- Over distension of uterus like polyhydramnios and multiple pregnancy.
iii- Coitus. iv- Also Danforth(13) mention that the following risk factors play a

2
role in aetiology of PROM.
iv- History of preterm PROM in previous pregnancies.
v- History of first and second trimesteric vaginal bleeding.
vi- Two or more elective termination of pregnancy also increase the risk.
vii- A short cervical length of 2 cm or less diagnosed with transvaginal
ultrasound is best predictor of preterm PROM.
viii- Mother smoking is associated with increase risk of PROM.
ix- There is a controversial issue whether a routine digital examination plays a
role in aetiology of PROM.
x- Weekly digital vaginal examination increases the incidence of PROM.
Infectious causes: Lower genital tract infection with group -BStreptococci,
Chlamydia trachomatous, Neiseria gonorrhea, Bacterial vaginosis is associated
with increase risk of PROM. Effect of group-Bstreptococci on PROM seem to be
related to the number of bacteria present in the vagina, but the presence of group-
B-streptococci in the vagina does not increase the incidence of PROM. Heavy
vaginal colonization and group-Bstreptococcibacteriuria have been associated with
PROM. There are conflicting data about the role of chlamydia on PROM. Women
positive for gonorrhea are more likely to develop PROM, but there was no
increased risks for women with chlamydia.(13) Other genital tract pathogens that
alter vaginal environment and pH like Bactreiodsfragilis, Trichomonousvaginalis,
play a role in aetiology of PROM mainly via change in pH of the vagina. Example,
if the pH of vagina is equal to 4.0 or less, the incidence of PROM is 8%, but if the
vaginal pH is greater than 4.5 the incidence of PROM is 47%.(13) There are other
several mechanisms by which bacteria could increases the incidence of PROM.
Bacteria can produces proteases and phospholipases which may weaken the
membranes. Activated neutrophils have been shown in vitro to reduce the bursting
tension and elasticity of the membranes, in addition the host mediated response of

3
the cytokines may play an etiologic factor.(13)
Definition
The diagnosis was established whenever spontaneous rupture occurs prior to the
onset of labour.[14] PROM has been applied to rupture of the membranes at any
time before the onset of labour irrespective of the duration of gestation[15] .
PROM was defined as rupture of membranes prior’ to the establishment of regular
uterine contractions.[16] PROM was diagnosed only when a specified latent period
has elapsed following Amniorrhexis occurring at anytime prior to the onset of
labour; regardless of the length of gestation.[17] ROM was defined as rupture of
membranes occurring atleast one hour before onset of labour[18,19] . PROM was
defined as rupture of membranes with atleast 2 hours latent period before active
labour, latent period being the time elapsing from the time of rupture of
membranes to the onset of labour [20,21] . One of the main problems in diagnosing
PROM is the difficulty in accurately timing the onset of labour. This problem is
especially true in primigravida where regular uterine contractions may not result in
cervical diltation and where cervical effacement usually precedes the onset of true
labour. Spontaneous rupture of foetal membranes occurring prior to the onset of
uterine contractions, which result in progressive cervical dilation [22]
This definition permits the following:
1. It defines the onset of labour more accurately.
2. It usually allows the physician to establish the diagnosis as soon as the patient is
seen as to formulate an initial plan of management and
3. It tends to avoid the inherent in accuracy of a retrospective diagnosis after a
specified latent period has elapsed.
The definition is in agreement with that established by the American College of
Obstetrics and Gynaecology. Prolonged rupture of the membranes is defined as a
latency period of 24 hours or longer between the time of membrane rupture and

4
delivery. High leak is a term used to describe loss of amniotic fluid caused by a
tear in the membranes located above the lower uterine segment.
Latent Period: It is the time interval between rupture of the membranes and the
onset of regular uterine contraction.
Incidence Of PROM:
It is difficult to obtain an accurate determination of the incidence of PROM by
reviewing the literature because of the various definitions used in establishing the
diagnosis. The incidence as 6.6-13.9% of all patients with spontaneous rupture of
the membranes at least one hour prior to the onset of labour near term or earlier.22
The range of incidence as 2.7-17% with the majority falling between 7 to 12%
while in Gunn’s own series the incidence of spontaneous PROM was 10.7% of
total number of deliveries.21 Occurrence of spontaneous PROM in 12% of all the
pregnancies. Labour occurred spontaneously with in the first 24 hours after
spontaneous rupture of the foetal membranes in 51-95% of the cases reported in
the literature but most authors reported figures between 80-90%. When the
premature birth weight infants alone were considered, the incidence of spontaneous
labour in the first 24 hours dropped to approximately 35-50%. Management of
PROM is facilitated with an understanding of the events responsible for its
occurrence. Therefore it is appropriate to review the development, anatomy and
histology of the foetal membranes.
Diagnosis
In obstetric practice, cases often present before the onset of labor. with leaking
membrane. In some cases it is easy to diagnose ruptured membranes by a vaginal
examination when liquor is seen coming out or the presenting part is felt without
the covering membrane. But in some cases it is not easy if the os is closed or when
it is open and the bag of membrane is present with the possibility of a small, rent in
the membrane is higher. Diagnosis of ruptured membrane can be established

5
clinically or by laboratory methods. Most often the diagnosis is obvious by history
of leak and direct demonstration of leaking through cervical os carefully performed
per speculum examination.
History:
History of sudden passage of fluid from vagina in a gravid patient is strongly
suggestive of ruptured membrane, occasionally a single bolus of fluid has been
passed without further leakage or intermittent leakage of fluid has been noted.
These patients frequently have a so called second rupture of the membrane during
labor as do those with fluids accumulation between amnion and chorion.
Visualization Of Amniotic Fluid In The Vagina:
A sterile speculum is introduced into the vagina and observe for amniotic fluid
flowing from the cervix; copious fluid pouring out of the speculum is
pathognomonic of rupture of membranes. Amniotic fluid is colourless and may
contain white flecks (vernix). If no fluid is immediately seen, ask the patient to
cough and observe for a gush of fluid per vagina or applying slight fundal pressure
over the uterus may provoke leaking.
Laboratory Diagnosis: In clinical practice many times pregnant women present
with the history of watery vaginal discharge and physical examination may not
reveal the diagnosis of PROM. This is particularly so when cervical os is closed or
flat membrane felt over the presenting part on account of high leak. Other
discharges like urine, excessive vaginal discharge and inflammatory exudates may
also obscure the clinical diagnosis. In such conditions laboratory diagnosis helps.
They are:
1. Nitrazine Test: The vaginal PH is normally 4.5-5.5. Amniotic fluid, usually has
a pH of 7-7.5. Nitrazine paper quickly will turn deep blue if the vaginal fluid has
an alkaline pH. The membranes probably are intact if the color of the paper
remains yellow or changes to olive yellow. Antiseptic solutions, urine, blood and

6
vaginal infections alter the vaginal pH and cause false positive result. This test is
simple, rapid, inexpensive and fairly reliable method. The nitrazine test produce
12.7% false negative and 16.2% false positive results 23 .
2. Fern Test:Ferning results from the drying out of salts contained in the amniotic
fluid. The ferning is due to crystallization of sodium chloride derived from the
amniotic fluid. To perform the test, a sample of fluid is placed on a glass slide and
allowed to dry. The preparation is observed under microscope, looking for a
crystallization pattern that resembles a fern, The accuracy of the test is affected by
blood or meconium, the test may produce false positive results if the sample is
obtained from the cervix, because dry cervical mucus forms an arborization pattern
that may be confused with PROM. The fern test gives 4.8% false negative and
4.4% false positive results( 24). The diagnosis of PROM is close to 100% reliable
if the vaginal fluid gives both positive nitrazine and positive fern test
Ultrasound Examination: USG should not be used as the primary means of
diagnosis of PROM. False positive findings may occur in patients with
oligohydramnios resulting from causes other than PROM, and false negative
results may occur in patients with discrete amniotic fluid losses. However it should
be assumed that PROM has occurred if ultrasound examination shows little or no
fluid in the uterus. In contrast, the presence of a normal amount of fluid makes the
diagnosis of PROM unlikely.
Intra-Amniotic Fluorescein: Injection of fluorescein into the amniotic cavity is
rarely indicated for the diagnosis of PROM. This procedure may be performed
when PROM cannot be confirmed with non invasive technique. In these cases 1 ml
of sterile solution of 5% sodium fluorescein is injected into the amniotic cavity. A
tampon is placed in the vagina and examined with a long wave, ultraviolet light 1
or 2 hours later. The detection of fluorescent material is equivalent to a positive
diagnosis of PROM, one ml of sterile indigo carmine may be used instead of

7
fluorescein and the tampon is inspected for the presence of a blue discolouration.
Amnioscopy:Amnioscopy is an invasive procedure rarely indicated in the
diagnosis or management of PROM. It requires a dispensible cervix to introduce a
metallic or plastic cone for direct visualization of the membranes and the AF.
Amnioscopy may cause PROM in patients with intact membranes and may carry a
large bacterial inoculation into the amniotic cavity in patients with PROM.
Diamine Oxidase Test:Diamine oxidase is an enzyme produced by decidua,
which diffuses into the amniotic fluid, measurement of diamine oxidase by paper
strips placed in contact with the vagina is an accurate way to diagnose PROM. The
test requires relatively elaborate laboratory procedure and is not ready for general
use. Fetal Fibronectin: Fetal fibronectin is a large molecular weight glycoprotein
present in large amounts in the amniotic fluid. This substance can be detected in
the endocervix or the vagina of patients with PROM by means of an enzyme linked
immuosorbent assay. The test seems to be highly accurate and is not affected by
blood, but meconium may interfere.
Alpha Fetoprotein Test (AFP): AFP is present in high concentration in AF, but
does not exist in vaginal secretions or in the urine. Therefore determination of this
substance in the vaginal secretion is an accurate test for the diagnosis of PROM. A
study using a rapid calorimetric monoclonal antibody AFP test found a sensitivity
of 98% for AEP, 77% for nitrazine and 62% for ferning. Specificity was 100% for
AFP test. Maternal blood contamination affects the accuracy of test.
Identification Of Lanugo: This is a microscopy technique for detecting rupture of
fetal membranes. Lanugo and uric acid crystals in vaginal fluid can be identified.
The findings of fetal hair was specific, yet the process was time consuming,
requiring preparation of multiple slides. Fetal hair was present in scanty quantity
and identification of mate crystals was non specific. Because of these difficulties,
the technique was abandoned. Staining For Lipid: Nile blue sulfate staining was

8
introduced for the identification of desquamated fetal epithelial cells.
Oxazonepresent in nile blue sulfate stains, the fetal cells orange brown (25)
How should women with term PROM be assessed?
Initial assessment of women presenting with term PROM should include
confirmation of the diagnosis, gestational age, fetal presentation and assessment of
maternal and fetal wellbeing. Nitrazine (pH based) tests or Amnisure (detecting
placental alpha microglobulin-1 protein in vaginal fluid) may be used where there
is diagnostic uncertainty. Digital vaginal examination should be avoided unless
immediate induction is planned as this has been shown to increase the rate of
neonatal infection.
How should women with term PROM be managed?
Active management
Active management of term PROM with induction is associated with reduced
maternal infective morbidity and increased maternal satisfaction without increasing
caesarean section or operative vaginal birth. Fewer infants are admitted to NICU
and fewer infants require postnatal antibiotics. Nevertheless, following preliminary
assessment, some women and/ or clinicians may reasonably elect for a short trial of
expectant management (e.g. for up to 24/24) in highly selected and well supervised
cases.
Expectant management
Criteria for expectant management includes:
• Term PROM with fixed cephalic presentation.
• Group B streptococcus (GBS) negative.
• No signs infection (maternal tachycardia, fever, uterine tenderness).
• Normal CTG.
• No history of digital vaginal exam, cervical suture.
• Adequate resource/staffing to provide support as an outpatient or inpatient.

9
• Commitment to 4 hourly maternal temperature, evaluation of vaginal loss and
assessment of fetal well-being.
Recommendation
1 Grade and reference Initial assessment of women presenting with term PROM
should include confirmation of the diagnosis, confirmation of gestation and
presentation and assessment of maternal and fetal wellbeing. Nitrazine (pH based)
tests or Amnisure (detecting placental alpha microglobulin-1 protein in vaginal
fluid) may be used where there is diagnostic uncertainty.
(26) Digital vaginal examination should be avoided unless immediate induction is
planned as this has been shown to increase the rate of neonatal infection.
Consensus-based recommendation
1 Term Prelabour Rupture of Membranes (Term PROM)
What is the role of antibiotics in term PROM?
a) Women who are known to be GBS positive In women known to have
vaginal Group B streptococcus (GBS) colonisation, prophylactic antibiotics and
early administration of oxytocin is recommended.
Screening and Treatment for Group B Streptococcus in Pregnancy for further
detail.
b) Women known to be GBS negative Available evidence comes from a
Cochrane review involving 838 women, and a recent trial of 161 women.(27, 28 )
4 Collectively, these studies suggest that the use of antibiotics reduces the risk of
maternal infectious morbidity (chorioamnionitis and endometritis), with the
Cochrane review reporting RR of 0.43 (95% CI 0.23-0.82) for maternal infectious
morbidity, and NNT 25. The trial of Passos et al. was confined to women known to
be GBS negative and still found lower rates of infection among women receiving
intravenous ampicilinn and gentamicin (2.6% compared to 13.2%; RR 0.89 (0.81-
0.98), although the risks of this approach need to be considered given the recently

10
highlighted risks of vestibulotoxicity(29) particularly with repeated or prolonged
gentamicin dosing. The study of Passos also confirmed that all cases of maternal
infection occurred in women with ROM for >12 hours, underscoring the
importance of timely induction in reducing infectious morbidity. Whilst neither of
these studies reported a statistically significant difference in neonatal morbidity,
these trials are under-powered to assess this outcome
Should women with term PROM be managed at home or in hospital?
A sub-analysis of term PROM concluded that expectant management at home was
associated with a further increase in the risk of maternal need for antibiotics (OR
1.52) and neonatal infection (OR 1.97) (30) In preterm PROM, women managed as
an outpatient face additional risks associated with rapid delivery.(31) . Women
being managed expectantly at home must therefore be carefully selected to ensure
that they not only meet the criteria in 4.5.2, but also live close to the hospital, have
adequate support at home and dependable transport.
Recommendation 2 Grade and reference In women known to have vaginal Group
B streptococcus (GBS) colonisation, prophylactic antibiotics and early induction of
labour is recommended. Consensus-based recommendation Recommendation 3
Grade and reference Antibiotic use in term PROM appears to be associated with a
reduced risk of maternal infectious morbidity. Consensus-based recommendation
32, 33 Term Prelabour Rupture of Membranes (Term PROM) Should induction
of labour be undertaken with oxytocin or vaginal prostaglandins? The available
evidence on prostaglandins (Prostin, Cervidil or misoprostol) versus oxytocin for
induction following term PROM is limited, and has failed to show a clear benefit.
The previous Cochrane meta -analysis, suggested an increased risk of
chorioamnionitis and neonatal infection with administration of prostaglandins.33
Concerns regarding the risk of hyperstimuation and tachysystole may be part of the
reason that drug information on commonly used prostaglandin preparations

11
(Prostin and Cervidil) lists ruptured membranes as a contraindication to use. This
complication was not reported more frequently in the meta-analysis examining
misoprostol use for induction with term PROM, but doses greater than 25 µg have
been associated with increased risks of hyperstimulation and should be avoided.)34
(For these reasons, oxytocin remains the method of choice for most RANZCOG
fellows, but in the sub set of women with an unfavourable cervix, prostaglandins
may have an important role( 28). This has been evaluated in one small trial where
dinoprostone followed by oxytocin 6 hours later in women with a Bishop score of
6
Complications Of PROM Maternal Complications:
1) Chorioamnionitis: Infection occurs frequently in patients with PROM. The
early diagnosis and prompt treatment are essential. The overall evidence of
chorioamnionitis ranges from 4.2% 10.5%. The diagnosis of chorioamnionitis is
clinical. It requires the presence of fever 38°C and atleast 2 of the following
conditions – Maternal tachycardia, fetal tachycardia, uterine tenderness, foul
smelling amniotic fluid; maternal leukocytosis. Amniotic fluid cultures are
valuable for identifying the bacteria causing infection and their antibiotic
sensitivity. The amniotic cavity generally is sterile. The term microbial invasion of
the amniotic cavity refers to Maternal and foetal outcome in premature rupture of
membranes
the presence of a positive amniotic fluid for microorganisms cultures, regardless
of the presence or absence of clinical signs or symptoms of infection. Pathologic
chorioamnionitis refers to the presence of acute inflammatory lesions in placenta
and membranes, varying degrees of polymorphonuclearleukocytic infiltration of
the chorioamnion is found more frequently than the clinical disease. The
determination of C-reactive protein (CRP) in blood a substance that increases
markedly in patients with infection. The median CRP concentration during

12
pregnancy ranges from 0.7 to 0.9 mg/dI. The gram stain of AF is valuable for
confirming the diagnosis of amnionitis. Another valuable AF test is the leukocyte
estrase assay. A positive assay has a 91% sensitivity and 95% positive predictive
value for the diagnosis of chorioamnionitis. The incidence of chorioamnionitis
infection is more if the latent perod is more than 24 hours. 1.7% of his patients
developed fever within 24 hours after PROM, 7.5% between 24-48 hours and 8.6%
beyond 48 hours10 . The patients may have endometritis, parameteritis,
pyelonephritis. In rare cases of extensive infection with uterine necrosis multiple
abscess or clostridial infection, a life saving hysterectomy may be necessary.
Occasionally uncontrolled infection may lead to septicemia, shock, DIC and adult
RDS and maternal death. Unless the patient is grossly neglected maternal mortality
should not occur due to PROM. Maternal mortality and morbidity are primarily
related to sepsis and complications arising from efforts to affect delivery such as
oxytocin induction or caesarean section.
2) Abruptio Placenta: Patients with PROM have an incidence of abruption placenta
approximately 6%. Abruptio usually occurs within the setting of prolonged and
severe oligohydroamnios. ( 35) Nelson et al in a retrospective analysis of all
patients with prolonged PROM, estimated the risk of abruption during expectant
management to be 4%. The reason for the high incidence of abruption in patients
with PROM is the progressive decrease in intrauterine surface area causing
detachment of the placenta.
3) Cord Prolapse
If it is associated with malpresentation
4) Dry Labor
It continuous escape of liquid for long duration
Fetal And Neonatal Complications:
1) Neonatal Sepsis: PROM increases the risk of infection in the neonate to around

13
1.3% following prolonged rupture of membrane and 8.7% of neonatal sepsis
following prolonged rupture of membrane and 8.7% of neonatal sepsis following
prolonged and clinical amnionitis. Significant predictive risk factors were
histologic evidence of inflammation in the placental chorionic plate, gestational
age less than 34 weeks, male sex, apgar score of less than 6 in 5 minutes and
clinical amnionitis. Perinatal mortality is due to sepsis and respiratory distress. In
recent study of PROM, the neonatal mortality was reported as 6.7% of which 55%
was due to infection. Volume of AF remaining after PROM is of importance as it
possess antibacterial activity. Neonatal infection may manifest as septicemia,
meningitis pneumonia, pyoderma, umbilical sepsis and conjunctivitis. The first
manifestation of impending fetal infection are non reactive NST and the absence of
fetal breathing movements. The overall incidence of a perinatal mortality reported
in the literature ranges from 2.6 to 11%. According to Hassan et al(36) incidence
of neonatal mortality is 4.6%
2) Neonatal Rds: Gluck et al(37) (1973) explained the acceleration of pulmonary
maturity documenting following observations
1) PROM of more than 24 hours duration with a more matute L/s ratio of amniotic
fluid than normally expected for gestation
2) phosphatidyl glycerol apprared in the amniotic fluid at earlier period in gestation
following PROM.
3) tracheal or pharyngeal aspirates from preterm infants following PROM of more
than 24 hours showed a mature phospholipid pattern at gestation ranging from 29
to 33weeks. Jones reviewed 16000 births and concluded that there was no
association between decreased incidence of RDS and prolongation of latent period
after PROM. Aktar et al(38) reported 11.1% of incidence of RDS in study of
PROM
Oligohydromnia: When PROM is managed conservatively, most patients have

14
oligohydranmios to a greater or lesser degrees as a result of continuous leakage of
amniotic fluid. Neonates delivered from pregnancies complicated by
oligohydranmios sometimes have anomalies such as pulmonary hypoplasia or
retarded growth or both 39 .
The absence of amniotic fluid allows the uterus to exert continuous pressure
against the fetus resulting in abnormal fetal growth and development.
Fetal breathing movements have been shown to be critical for normal lung
development. Increase in the incidence of caesarean section of fetal distress
because of intrapartum fetal heart rate patterns consistent with umbilical cord
compression. There is increased incidence of skeletal deformities due to pressure
effect by oligohydramnios.
Perinatal Mortality: The perinatal mortality rate is 10.1% according to
collaborative perinatal study. Perinatal mortality after PROM near term ia
associated with infection and in preterm due to RDS. Perinatal mortality is 19%
according to Tanir et al40

15
Aim of study:
To identify the maternal and fetal outcome in patients with PROM.

16
Materials and methods:
Study design: Retrospective case series study
Study setting: This study was conducted in Tripoli Medical Center
Study period: during the year 2015-2016
Study population: One hundred patients with history of PLROM were randomly
selected from the hospital files. The following data was obtained from the files: the
age, gravidity, parity, history of previous abortion, risk factors, maternal morbidity,
mode of delivery, sex of the neonate, neonatal complications and admission to the
nursery.
Statistical analysis:
Statistical analysis was computerized using the Statistical Program for Social
Sciences (SPSS version 21) that used for data entry and analysis. Descriptive
statistics were used and all results are presented as frequencies, means ± standard
deviation and percentages. Categorical data were compared using the Chi-square
test and Fisher's exact test if appropriate. A P-value of less than or equal to
0.05was considered statistically significant.

17
Result:
Age distribution of the mothers:
The mean age for the patients was (30 ± 5 years). The maximum age of the patients
was 45 years and the minimum age was 20 years. Most of the age distribution of
the patients in this study was between 20 and 30 years, which account for 54%.
About 41% were between 31 and 40 yearsand only 5% were more than 40 years.
Table 1: Age distribution of the mothers
Age distribution No(%)
20 – 30 years 54 (54%)
31 – 40 years 41 (41%)
> 40 years 5 (5%)

60
54

50
41
40

30

20

10
5

0
20 – 30 years 31 – 40 years > 40 years

Figure 1: Age distribution of the mothers

18
Gravidity:
Regarding the gravidity, the result was as following; about 40% of the patients
were PG, 45% were between gravida 2 and gravida 4, 12% were between gravida 5
and gravida 7, and only 3% had more than gravida 7.
Table 2: Gravidity distribution of the patients
Gravidity distribution No (%)
PG 40 (40%)
2–4 45 (45%)
5–7 12 (12%)
>7 3 (3%)

50
45
45
40
40
35
30
25
20
15 12
10
5 3

0
PG 2– 4 5– 7 >7

Table 2: Gravidity distribution of the patients

19
Parity distribution:
In respect to the parity of the patients, about 72% of the patients were between
para 1 and para 3, about 20 % of the patients were between para 4 and 6 Only 8%
had more than 6 children. The parity ranged between 1 and 8. The percentage of
primiparitywas 32%.
Table 3: Parity distribution of the patients
Parity No(%)
1–3 72 (72%)
4–6 20 (20%)
>6 8 (8%)

80
72
70

60

50

40

30
20
20
8
10

0
1– 3 4– 6 >6

Figure3: Parity distribution of the patients

20
Abortion distribution:
The majority of the patients in the present study (76%) had no history of abortion
before. The percentage of patients who had previous abortion was 24%.
Table 4: Abortion distribution of the patients
Abortion distribution No (%)
Yes 24 (24%)
No 76 (76%)

24

76

Yes No

Figure4: Abortion distribution of the patients

21
Risk factors for PLROM:
In this study the most prominent predisposing factor for PLROM was UTI 44%
followed by polyhydrominous (14%) then multiple pregnancy (12%). About 3%
had vaginal infection, 5% had malpresentation. No risk was found in about 22% of
the patients
Table 5: Risk factors for PLROM
Predisposing factors No (%)
Polyhydrominos 14 (14%)
UTI 44 (44%)
Multiple pregnancy 12 (12%)
Vaginal infection 3 (3%)
Malpresentation 5 (5%)
No risk factors 22 (22%)

50
44
45

40

35

30

25 22
20
14
15 12
10
5
5 3

0
Polyhydrominos UTI Multiple pregnancy Vaginal infection Malpresentation No risk factors

Figure 5: Risk factors for PLROM

22
Mode of delivery:
With regards the mode of delivery, approximately 66% of the patients underwent
Normal vaginal delivery, about 29% had C/S and only 5% had Instrumental
delivery
Table 6: Mode of delivery
Mode of delivery No (%)
NVD 66 (66%)
C/S 29 (29%)
Instrumental 5 (5%)

29

66

NVD C/S Instrumental

Figure6: Mode of delivery

23
Maternal morbidity:
In respect to maternal morbidity, about 4% of the patients had chorioaminitis, 13%
had pyrexia, 5% had wound infection and only 3% had UTI
Table 7: Maternal morbidity
Maternal morbidity No (%)
Chorioaminitis 4 (4%)
Puerperal pyrexia 13 (13%)
Wound infection 5 (5%)
UTI 3 (3%)
No complications 75 (75%)

80 75

70

60

50

40

30

20
13
10 4 5 3
0
Chorioaminitis Puerperal pyrexia Wound infection UTI No complications

Figure 7: Maternal morbidity

24
Neonatal sex:
Regarding the neonatal sex, about 48% of the neonates were male and about 40%
were female. Twin pregnancies were as following; 5% (both male) and 7% (both
females).
Table 8: Neonatal sex
Neonatal sex No (%)
Male 48 (48%)
Female 40 (40%)
Twins (both male) 5 (5%)
Twins (both female) 7 (7%)

60

50 48

40
40

30

20

10 7
5

0
Male Female Twins (both male) Twins (both female)

Figure 8: Neonatal sex

25
Neonatal complications:
With regard neonatal complications, around 12% of the neonates had RDS, 8% had
septicemia, 3% had jaundice, and 3% had conjunctivitis. The majority of the
neonates (74%) do not have any complications.
Table 9: Neonatal complications
Neonatal complications No (%)
Respiratory distress syndrome 12 (12%)
Septicemia 8 (8%)
Jaundice 3(3%)
Conjunctivitis 3 (3%)
No complication 74 (74%)

80 74
70

60

50

40

30

20
12
8
10 3 3
0
Respiratory Septicemia Jaundice Conjunctivitis No complication
distress
syndrome

Figure 9: Neonatal complications

26
Admission to nursery:
The result showed that about 37% of the newborn babies admitted to the nursery
and about 63% of the newborn babies were healthy and did not admitted to the
nursery.
Table 10:Admission to nursery
Admission to nursery No(%)
Yes 37 (37%)
No 63 (63%)

37

63

Yes No

Figure 10:Admission to nursery

27
Discussion:
Premature rupture of membranes (PROM) refers to a patient who is beyond 37
weeks' gestation and has presented with rupture of membranes (ROM) prior to the
onset of labor. Patient with PROM presents withleakage of fluid, vaginal discharge
and pelvic pressure, but they are not having contraction. It occurs in 3 percent
ofpregnancies and is the cause of approximately one third of preterm deliveries. It
can lead to significant perinatalmorbidity, including respiratory distress syndrome,
neonatal sepsis, umbilical cord prolapse, placental abruption, andfetal death.
Appropriate evaluation and management are important for improving neonatal
outcomes. The risk ofintrauterine infection increases with the duration of ROM.
Evidence supports the idea that induction of labor, asopposed to expectant
management, decreases the risk of chorioamnionitis without increasing the
cesarean deliveryrate. (41)
The purpose of the current study was to identify the maternal and fetal outcome in
patients with PROM. The study reported that the mean age for the patients was (30
± 5 years).Most of the age distribution of the patients in this study was between 20
and 30 years, which account for 54%.The study of Gandhi M et al showed similar
result with most of the cases of PROM was between 21 and 30 years. (42) The
study of Lee C et al showed different result regarding the age with mean of 26
years and most of the cases were between 25 and 35 years. (43) The majority of the
patients were multigravidas, multiparous and had no previous abortion. Most of the
studies showed that the percentage of PROM were nulliparous women. (42-44)
The result of Shehla N et al study reported similar result regarding the parity with
most of the PROM patients were between para 1 and para 4. (45)
In respect to the risk factors for PROM, the result demonstrated that the most
common risk factor was UTI followed by polyhydrominous then multiple
pregnancy. Patil S study showed that the most important risk factors for PROM

28
were malpresentation followed by UTI then previous history of PROM. (47) In
other study by Newton ER, the result stated that genetic factors as well as possible
vaginal/ cervical infection could be the main causative factors. (48) The study of
Revathi V et al showed that the majority of the cases of PROM were due to
idiopathic cause followed by anemia, UTI and polyhydraminos. (44)
With regards the mode of delivery, about two third of the patients delivered
virginally and only 29% delivered by C/S. Studies showed that the rate of C/S in
patients with PROM was ranged between 14% to 58%. (45,47,49) Maternal
morbidity or complication in the current study showed that the most prominent
maternal morbidity was Puerperal pyrexia followed by wound infection then
Chorioaminitis. The result of Dars S et al study witch reported that premature
labour and chorioaminitis were the major complications of PROM. (45) The result
of Revathi V et al showed that the most common maternal complication of PROM
was chorioamnionitis followed by abruption placenta. (44)
With regard neonatal complications, the present study showed that RDS was the
most common complication followed by septicemia, jaundice and conjunctivitis.
The result of Gandhi M et al study reported similar result with the majority of the
neonates had no complications and only 1% and 5% had sepsis and RDS
respectively. (42)

29
Conclusion and Recommendations:
In summary, patients who had PROM were young, multigravidas and multiparous.
The main risk factors that cause PROM were UTI, polyhydraminous and multiple
pregnancy. Maternal morbidity showed that the most prominent maternal
morbidity was puerperal pyrexia while the most prominent neonatal morbidity was
RDS. PROM is a high risk obstetric condition which is a common problem among
pregnant women and a big challenge to the neonatologists. Evaluation of risks of
PROM and timely diagnosis is essential to reducematernal and perinatal morbidity
and mortality. Antibiotic administration to women with PROM
significantlyreduces maternal and neonatal morbidity. Active management is
needed to enable delivery within 24 hrs ofPROM and it offers better maternal and
neonatal outcome. The main objective of the obstetrician should beearly screening
, adequate antenatal visits and improvement of general condition of the mother ,
identifying riskfactors , treating associated complications ,correct diagnosis of
rupture of membranes and induction of deliverythat gives a high rate of successful
vaginal deliveries without a rise in neonatal and maternal infections. Ahealthy
neonate as well as a healthy satisfied mother are natural aims for the obstetrician.

30
References:
1. Caughey AB, et al. Contemporary diagnosis and management of preterm
premature rupture of membranes. Rev Obstet Gynecol. 2008;1(1):11–22.
[PubMed]
2. Keirse MJ, Ohlsson A, Treffers PE, Kanhani HHH. Prelabour rupture of the
membranes preterm. In: Chalmers I, Enkin M, Keirse MJ, editors. Effective care in
pregnancy andchildbirth. Oxford: Oxford University Press; 1989. p. 666.
3. Verber IG, Pearce JM, New LC, Hamilton PA, Davies EG. Prolllonged rupture
of the fetal membranes and neonatal outcome. J Perinat Med. 1989;17:469–
76.[PubMed]
4. Mercer BM. Preterm premature ruptures of the membranes. Obstet Gynecol.
2003;101:178–93. [PubMed]
5. Tamsen L, Lyrenas S, Cnattingius S. Premature rupture of the membranes–
intervention or not. GynecolObstet Invest. 1990;29:128–31. [PubMed]
6. Current Clinical Practice:Obstetrics in Family Medicine:A Practical Guide.
Totowa:New Jersey: P. Lyons © Humana Press Inc; 2006.
7. Rouse DJ, Landon M, Leveno KJ, et al. The Maternal-Fetal Medicine Units
cesarean registry:chorioamnionitis at term and its duration-relationship to
outcomes. Am J Obstet Gynecol. 2004;191:211. [PubMed]
8. Mark SP, Croughan-Minihane MS, Kilpatrick SJ. Chorioamnionitis and uterine
function. Obstet Gynecol. 2000;95:909. [PubMed]
9. Cohen-Wolkowiez M, et al. Early and late onset sepsis in late preterm infants.
The Pediatric Infectious Disease Journal. 2009;28(12):1052–1056. [PMC free
article][PubMed]
10. Polzin WJ, Brady K. The etiology of premature rupture of membranes.
ClinObstetGynaecol 1998 Dec; 41(4): 810 –6.

31
11- Belfort P, Pinott JA, Ab TK. Definition of premature rupture of membranes
pregnancy and labour. AdvanGynaecolObstet 1988; 5(1): 5-7.’
12- James R, Scott Philip J, Disuia CB, Hammond WN. Etiology of premature
rupture of membranes. In: James R, Scott Philip J, Disuia CB, Hammond WN
(editors) Danforth’s obstetrics and Gynaecology. 8th ed. New York: Lippncott
Williams and Wilkins; 2000. P. 269-70.
13. Stuart Campbell, Cristoph Lees. Amniotic fluid. In: Stuart Campbell, Cristoph
Lees (editors) Obstetrics by ten teachers. 17th ed. London: Arnold; 2000. P. 65 -
66.
14. Stedman CM, Crawford S, Stalen E, Cherney WB. Management of premature
rupture of membranes assessing amniotic fluid in the vagina for phosphatidyl
glycerol. Am J ObstetGynecol 1981; 140: 34.
15. Pritchard IA, McDonald PC. New York Appleton Century Craft, 1980. [9].
Mead PB. Management of the patient with premature rupture of membranes.
Clinics Perinatol 1980; 7: 243-355.
16. Burchell RC. Premature spontaneous rupture of the membranes. Am J
ObstetGynec 1964; 88: 251. 17. Aktar MS, Degan JS, Aktar UA, D Sharam.
PROM: Study of 300 cases and review of literature. J Obstet&Gynecol of India.
1980; 30: 81.
18. Webster A. Management of premature rupture of fetal membranes.
ObstetgynecolSurv 1969; 24: 485.
19. Longlee S, LEE JN. Fetal weight and PROM IN preterm delivery. Asia
Oceania.JObstet and GynecolSurv 1986; 21: 400.
20. Nelson, Arias Fernando. Study of premature rupture of membranes.
ObstetGynaecolSurv 1986; 21: 400. [15]. Kappy Kenneth A, Cetrulo Curtis,
Robert LK. A premature rupture of membranes. A conservative approach. Am J
ObstetGynecol 1979; 134(6): 655-661.

32
21. Gunn GC, Mishell DR, Morton DG. Premature of membranes, a review: Am J
ObstetGynec 1970; 106: 469.
22. Friedman ML, McElin TW. Diagnosis of ruptured fetal membranes. Am J
ObstetGynecol 1969; 104: 545-550. [18]. Bourne et al. Management of premature
rupture of membranes. Obstet and Gynecol 1976; 153: 37-40. [19]. Grant John,
Keirse Marc JNC. Prelabour rupture of membranes. Effective care in pregnancy
and childbirth. Oxford: Oxford university Press, 1989; 1112-1117
23. Baptisti A. Clinical test for the determination of ruptured membranes. Am J of
Obstet Gynecol. 1938; 24 : 688. [33]. Anjanayulur et al. Jr of ObstGynecol of India
1970; 17: 170.
25. Brosens I, Gorden H. J Obstet&Gynecol by Commonwealth. 1965; 72: 342
26. Neil PR, Wallace EM. Is Amnisure(R) useful in the management of women
with prelabour rupture of the membranes? Aust N Z J ObstetGynaecol.
2010;50(6):534-8.
27. Flenady V, King J. Antibiotics for prelabour rupture of membranes at or near
term. Cochrane Database Syst Rev. 2002(3):CD001807.
28 .Passos F, Cardoso K, Coelho AM, Graca A, Clode N, Mendes da Graca L.
Antibiotic prophylaxis in premature rupture of membranes at term: a randomized
controlled trial. Obstet Gynecol. 2012;120(5):1045-51
29. Ahmed RM, Hannigan IP, MacDougall HG, Chan RC, Halmagyi GM.
Gentamicin ototoxicity: a 23- year selected case series of 103 patients. MJA.
2012;196(11):701-4.
30. Hannah ME, Hodnett ED, Willan A, Foster GA, Di Cecco R, Helewa M.
Prelabor rupture of the membranes at term: expectant management at home or in
hospital? The TermPROM Study Group. Obstet Gynecol. 2000;96(4):533-8.

33
31. Ellestad SC, Swamy GK, Sinclair T, James AH, Heine RP, Murtha AP.
Preterm premature rupture of membrane management--inpatient versus outpatient:
a retrospective review. Am J Perinatol. 2008;25(1):69-73.
32. Tan BP, Hannah ME. Prostaglandins versus oxytocin for prelabour rupture of
membranes at term. Cochrane Database Syst Rev. 2000(2):CD000159.
33. Lin MG, Nuthalapaty FS, Carver AR, Case AS, Ramsey PS. Misoprostol for
labor induction in women with term premature rupture of membranes: a meta-
analysis. Obstet Gynecol. 2005;106(3):593-601
34. Tan BP, Hannah ME. Prostaglandins versus oxytocin for prelabour rupture of
membranes at term. Cochrane Database Syst Rev. 2000(2):CD000159.
35. Nelson, Arias Fernando. Study of premature rupture of membranes.
ObstetGynaecolSurv 1986; 21: 400.
36. Hassan Boskabadi, GholamaniMaamonei, ShahinMaFinejad. Macedonian
Journal of Medical Sciences 2011 March 15; 4(1): 93- 98.
37. Gluck L, Kulorich MV. Lecithin/ sphingomyelin ratio in amniotic fluid in
normal and abnormal pregnancy. Am J Obstet& Gynecol. 1979; 135: 64.
38. S Akhter, M Rasihd, R Akter et al. Journal of Bangladesh College of Physician
Singoel. 2010; 28: 1.
39. Danforth DN et al. Am J ObstetGynecl. 1953; 65: 480.
40. Tanir HM, Sener T, Tekin N, Aksit A, Ardic N. PROM & Neonatal Outcome
prior to 34 weeks of Gestation. Int J GynaecolObstet 2003; 82(2): 167-72.
41. Nagaria T, Diwan C, Jaiswal J. A study on feto-maternal outcome in patients
with premature rupture of membranes. Nagaria T et al. Int J Reprod Contracept
Obstet Gynecol. 2016 Dec;5(12):4123-4127
42. M Gandhi, F Shah, C Panchal. Obstetric Outcomes In Premature Rupture Of
The Membrane (Prom). The Internet Journal of Gynecology and Obstetrics. 2012
Volume 16 Number 2.

34
43. Lee C, Taylor D, Kaufman H. Maternal and Fetal outcomes of Spontaneous
Preterm Premature Rupture of Membranes. JAOA. 2004;104(12):537-542.
44. Revathi V, Sowjanya R, Lavanya S. Maternal and Perinatal Outcome in
Premature Rupture of Membranes at Term. IOSR-JDMS. 2015;14(4):12-15.
45. Shehla N, Fawwad A, Shahzad H, Sultana R. FOETOMATERNAL
OUTCOME IN PATIENTS WITH OR WITHOUT PREMATURE
RUPTURE OF MEMBRANES. J Ayub Med Coll Abbottabad.
2016;22(1):164-167.
46. Dars S, Malik S, Samreen E, Kazi R. MATERAL MORBIDITY AND
PERINATAL OUTCOME IN PRETERM PREMATURE RUPTURE OF
MEMBRENS BEFORE 37 WEEKS GESTATION. Pakistan Journal of
Medical Sciences. 2014;30(3).
47. Patil D, Patil D. Maternal and Foetal Outcome in Premature Rupture of
Membranes. IOSR Journal of Dental and Medical Sciences. 2014;13(12):56-
83.
48. Newton ER, Prithoda TJ, Gibbs RS. Logistic regression analysis of risk
factors for intra-amniotic infection. Obstet Gynecol 1984; 73: 571-5
49. Tahir S, Aleem M, Aziz K. Incidence of outcome of PROM. Pak T Med Sci
2002; 18(1): 26-32

35
‫نتائج األم والجنين في المرضى الذين يعانون من تمزق غشاء الحمل المبكر‬

‫ملخص البحث‬
‫خلفية‪:‬‬
‫تمزق قبل األوان لألغشية قبل الوالدة هو السبب الرئيسي للوالدة المبكرة ويرتبط في جميع أنحاء العالم مع‬
‫زيادة معدالت المرض و الوفيات لألطفال حديثي الوالدة واألمهات‪.‬‬
‫الهدف من الدراسة‪:‬‬
‫لتحديد نتائج األم والجنين في المرضى الذين يعانون من التمزق المبكر لغشاء الحمل‪.‬‬
‫المواد واألساليب‪:‬‬
‫وقد تم إجراء دراسة لسلسلة الحاالت في مركز طرابلس الطبى فى الفترة‪ .2015-1016‬تم اختيار مائة‬
‫مريض لديهم تاريخ تمزق مبكر في غشاء الحمل‪ .‬وتم االختيار عشوائيا من ملفات المستشفى‪ .‬تم الحصول‬
‫على البيانات التالية من الملفات‪ :‬العمر‪ ،‬تاريخ الحمل السابق‪ ،‬عوامل الخطر‪ ،‬اعتالل األمهات‪ ،‬طريقة‬
‫الوالدة‪ ،‬جنس الوليد‪ ،‬مضاعفات حديثي الوالدة والدخول في الحضانة‪.‬‬
‫نتيجة‪:‬‬
‫وكان متوسط عمر المرضى (‪ 5 ± 03‬سنوات)‪ .‬وكان الحد األقصى لسن المرضى ‪ 55‬عاما والحد األدنى‬
‫للسن هو ‪ 03‬عاما‪ .‬كان معظم التوزيع العمري للمرضى في هذه الدراسة بين ‪ 03‬و ‪ 03‬عاما‪ .‬وكان معظم‬
‫المرضى متعددي الحمل و الوالدة‪ .‬أهم عامل مسبب لتمزق الغشاء المبكر كان التهاب المسالك ‪ ٪55‬تليها‬
‫زيادة ماء الجنين (‪ )٪45‬ثم تعدد الحمل (‪.)٪40‬فيما يتعلق بمراضة األمهات‪ ،‬كان حوالي ‪ ٪5‬من المرضى‬
‫يعانون من التهاب المشيمية‪ ،‬و ‪ ٪40‬لديهم حمى بعد الحمل‪ ،‬و ‪ ٪5‬لديهم عدوى الجرح و ‪ ٪0‬فقط لديهم‬
‫التهاب المسالك البولية‪ .‬وفيما يتعلق بمضاعفات حديثي الوالدة‪ ،‬كان لدى ‪ ٪40‬من الولدان صعوبة تنفس‪ ،‬و‬
‫‪ ٪8‬لديهم تسمم الدم‪ ،‬و ‪ ٪0‬لديهم الصفير‪ ،‬و ‪ ٪0‬لديهم التهاب الملتحمة‪.‬‬
‫استنتاج‪:‬‬
‫باختصار‪ ،‬كان المرضى الذين عانوا من تمزق غشاء الحمل المبكرمتعددي الحمل و الوالدة‪ .‬عوامل الخطر‬
‫الرئيسية التي تسبب تمزق غشاء الحمل المبكر هي التهاب المسالك البولية‪ ،‬زيادة ماء الجنين ومتعددة الحمل‪.‬‬
‫وأظهرت اعتالل األمهات أن اعتالل األمهات األبرز كان حمى النفاس في حين كانت أبرز األمراض الوليدية‬
‫ضيق في التنفس ‪.‬‬

‫‪36‬‬

You might also like