Key words
placenta previa - placenta accreta - pregnancy
Schlüsselwörter
Placenta praevia - Placenta accreta - Schwangerschaft
Introduction
Placentation disorders are disorders which occur during attachment of the placenta
to the uterine wall; their incidence depends on the week of gestation. The incidence
of placentation disorders in the 20th week of gestation (GW) is estimated to be around
5 in 100 pregnancies. At delivery, the incidence is only around 0.3 %, as uterine
growth in pregnancy often leads to migration of the placenta away from the internal
os [1], [2].
There are different forms of placentation disorders and they occur with varying degrees
of severity, depending on the underlying pathophysiological process. Placentation
is a complex process, mediated by prostaglandins, sexual hormones, cytokines and immunological
factors [3]. It occurs in the early days after fertilization of the ovum. The fertilized ovum
or zygote reaches the uterine cavity around 4 days after fertilization. The zygote
divides repeatedly, developing into a blastocyst consisting of two layers. The outer
layer of the blastocyst is made up of trophoblast cells which will form the placenta
and the fetal membranes. The inner cell layer, the embryoblast, will later develop
into the embryo. Physiologically, invasion of the endometrium by the trophoblast is
limited to the decidua basalis. Placenta accreta is present when there is excessive
invasion during placentation extending beyond the decidua basalis. If invasion by
the placenta extends into the uterine myometrium, this is known as placenta increta.
If the placental villa penetrate the myometrium and reach the uterine serosa or even
invade neighboring organs such as the bladder, this is known as placenta percreta
[4]. Rosen has suggested that placentation is regulated by the degree of oxygen saturation
of the tissue, with local hypoxia promoting invasion by placental villi. This would
explain why scar tissue resulting from previous uterine surgical procedures contributes
to placentation disorders [5].
In addition to faulty invasion by placental villi, placental disorders include low-lying
placenta (placental edge closest to the cervix < 2 cm from the inner os), marginal
placenta previa (placenta extends to the edge of the cervix), partial placenta previa
(a portion of the cervix is covered by the placenta), and total placenta previa (inner
os completely covered by the placenta) [4].
Case Report
We report here on a 39-year-old woman, gravida 8, para 4, who was transferred to our
department from another hospital on November 12, 2014 in the 18 + 3 week of pregnancy
because of suspicion of placenta percreta and total placenta previa. The woman had
been admitted to the other hospital 3 days earlier for antepartum bleeding and lower
abdominal pain. A diagnosis of total placenta previa was made following examination
on admission. Doppler sonography raised the suspicion of placenta percreta with involvement
of the bladder. The suspicion of placenta percreta was confirmed by an MRI of the
pelvis. After 3 daysʼ expectant management which included bed rest, oral magnesium
substitution and rhesus prophylaxis (blood group 0, rhesus negative), the patient
was transferred to our department.
Medical History
On admission the patient complained of dragging lower abdominal pain and a feeling
of abdominal pressure (“bloated abdomen”). She had not had any further bleeding since
three days. She had been suffering from diffuse lower abdominal pain since several
weeks. Outpatient examinations had not yielded any findings and parameters had always
been within normal ranges. The patient had previously given birth to four children.
The first delivery was by primary cesarean section for breech presentation in 1997.
In 2000 she gave birth to a girl by forceps-assisted vaginal delivery performed in
the expulsion period for obstructed labor. Three years later she gave birth to a boy
by secondary cesarean section, performed for nuchal cord. She last gave birth in 2006
by primary cesarean section (her third cesarean section) for breech presentation.
The possibility of bilateral tubal ligation was discussed at the time, but the patient
opted to take oral contraceptives. The patient had had 3 further surgical uterine
procedures: 2 terminations in 2001 and 2005, respectively, and one abortion curettage
in the 8th week of gestation in May 2014. The patient reported smoking between 8–10
cigarettes daily. The patient did not consume alcohol. She was allergic to nickel
and perfume. When asked about her social history, the patient reported having worked
as a shop assistant in a bakery but that she was currently not employed.
Clinical Findings
No vaginal bleeding was found on examination at admission. Vaginal pH was 4.0. A routine
vaginal smear test was performed. The pathogen Enterococcus faecalis was found with
no resistances. On palpation the cervix was sacral, medium soft and closed. Abdominal
sonography showed an intact singleton pregnancy appropriately developed for age. Cervical
length on vaginal sonography was 35 mm without funneling. The placenta covered the
inner os. Doppler sonography was suspicious for placenta percreta with placental vessels
invading the bladder ([Fig. 1]).
Fig. 1 Doppler sonography image showing vessels pointing in the direction of the bladder
wall. White arrow: bladder, red arrow: placenta, star: fetal head.
Course after Admission
We admitted the 39-year-old, gravida 8, woman as an inpatient in our gynecological
department and continued oral magnesium substitution (200 mg 3 × per day). Because
of the suspicion of placenta percreta she additionally received prophylactic oral
antibiotics with metronidazole (400 mg 3 × per day). On November 13, 2014 she underwent
ultrasound for detailed diagnosis. After imaging clearly showed pronounced vasculature
between the scarred uterine wall and the maternal bladder, a tentative diagnosis of
placentation disorder in the 19th week of pregnancy following 3 cesarean sections,
total placenta previa and placenta percreta was made ([Fig. 2]). A residual myometrium thickness of 4 mm was measured at the anterior uterine wall.
Fig. 2 Detailed ultrasound imaging done on November 13, 2014: placental villi appear to
be invading the bladder, confirming a diagnosis of placenta percreta and demonstrable
total placenta previa. White arrow: bladder, yellow arrow: placenta.
After an extensive and detailed discussion of the diagnosis with the patient and careful
weighing up of the pros and cons of continuing the pregnancy (giving birth to a fifth
child on the one hand, maternal and fetal risk from infiltration of the bladder, uterine
rupture or threatening miscarriage on the other) the decision was taken to perform
planned abdominal hysterectomy without adnexectomy. During the consultation we also
discussed expectant management as another potential option in this specific situation
and explained the difficulties of obtaining a precise preoperative diagnosis of placentation
disorders. The patient ultimately opted for hysterectomy to forestall potential serious
injuries to organs and prevent strong hemorrhaging.
The surgical intervention was performed on November 14, 2014 in GW 18 + 5. Intraoperatively,
the bladder was found to be stretched cranially across the uterus. The preoperative
suspicion of placental invasion of the bladder was not confirmed. However, the lower
uterine segment was massively overextended, extremely thin and very soft. The uterus
measured around 10 × 12 cm. After the bladder had been dissected caudally, the extent
of the defect in the uterine wall became clear. The entire lower anterior uterine
wall consisted only of a thin translucent layer of peritoneum with the placenta clearly
visible through it ([Fig. 3]). These clinical findings led to a diagnosis of placenta accreta. Coverage of the
defect would not have been possible as the defect was the size of the palms of two
hands. The patient received 2 erythrocyte concentrations intraoperatively after losing
1000 ml of blood and presenting with an intraoperative Hb of 5.9 mmol/l (preoperative
Hb was 8.1 mmol/l). A male fetus weighing 210 g without morphological anomalies was
found in utero. The uterus and placenta weighed 400 g ([Fig. 4]). It was sent for histological examination. Histopathological workup resulted in
a diagnosis of placenta accreta, total placenta previa and concealed uterine rupture.
Fig. 3 Surgical site with thin, extended, lower anterior uterine wall and partially visible
placenta. Black arrow: concealed rupture of the anterior uterine wall; white arrow:
bladder extended across the uterine wall.
Fig. 4 Uterus with placenta after hysterectomy. Thin white arrow: placenta in the uterus;
thick white arrow: uterine body; black arrow: uterine cervix.
The patientʼs postoperative course was uneventful. After 24-hour monitoring in the
recovery room, the patient was transferred to a regular ward on November 15, 2014.
A detailed postoperative discussion was held with the patient who was also offered
pastoral care at the bedside. The patient did not want a postmortem autopsy of the
fetus. On November 21, 2014 (7th postoperative day) the 39-year-old patient was discharged
home after findings at final examination were unremarkable.
Discussion
This clinical case report describes a case of placentation disorder which took the
form of placenta accreta and total placenta previa after 3 previous cesarean sections.
The case additionally presented with concealed uterine rupture. This clinical case
illustrates the potential complications which may appear after repeated cesarean sections.
The status post cesarean section is one of the main risk factors for the development
of placentation disorders in the next pregnancy. The largest study on this issue to
date, published in 2006, was carried out by Silver et al. and investigated the association
between cesarean section and later maternal complications in 30 132 women. The study
found a risk of 0.24 % for placenta accreta in the subsequent pregnancy after cesarean
section. The risk after 6 cesarean sections was 6.47 % [6]. Endometrial scarring of other provenance, for example after curettage or endometritis,
also increased the incidence of impaired placentation. Other risk factors for placentation
disorders include maternal age > 35 years, multiparity, submucous fibroids, and deposition
of the embryo close to the cervix during embryo transfer with assisted reproductive
technology [7].
Ultrasound, potentially combined with Doppler sonography, is the gold standard for
the diagnosis of placentation disorders. The placenta is located during the first
ultrasound examination performed between GW 9–12. A low-lying placenta or a placenta
covering all or part of the inner os are still fairly common at this point as the
uterus has not grown much yet [1]. If a second ultrasound examination performed sometime in the 19th to the 22nd week
of pregnancy again raises the suspicion of placentation disorder and it is not possible
to confirm or disprove the suspicion, then – as was done with our patient – MRI is
recommended [8]. The 2010 DGGG guideline recommends that pregnant women with impaired placentation
after previous cesarean section contact their maternity hospital early on, preferably
before the start of the 30th week of pregnancy, to plan the birth [9].
Management of placentation disorders depends, in the first instance, on the extent
of the disorder as well as on the patientʼs wish to have a child. Co-morbidities and
clinical presentation of the impaired placentation must also be considered. The standard
management of pregnancy in women with placental invasion of the myometrium is cesarean
hysterectomy [10]. Another therapy option for patients with placenta accreta, increta or percreta
who wish to have further children consists of leaving the part of the placenta adhering
to the uterine wall in situ after performing cesarean section. This option must then
be followed by non-surgical treatment such as interventional radiology for uterine
artery embolization and/or the administration of methotrexate. Treatment with the
folic acid antagonist methotrexate was first proposed in 1986 by Arulkumaran. He reported
on a patient who had received intravenous methotrexate for a period of 2 weeks after
cesarean section for placenta accreta. At the end of this period there were no signs
of the placenta on ultrasound examination, and the patient was discharged 15 days
postpartum [11], [12]. Khan et al. described performing uterine artery embolization within 2 hours of
cesarean section in a patient with placenta accreta in whom the placenta remained
in utero, followed by the administration of methotrexate 50 mg by weekly intramuscular
injection for 3 weeks with folic acid. Beta HCG in this patient after 5 months was
less than 5 mIU/ml. However, in their review, the authors noted that this conservative
therapy cannot yet be considered the standard treatment [13]. Potential risks of a conservative approach which leaves the placenta in utero include
hemorrhage, clotting disorders and septicemia [14]. The consensus is that in cases with total placenta previa, delivery should be by
primary cesarean section after the pregnancy has been prolonged under close monitoring.
In cases with partial placenta previa the choice of delivery can be an individual
decision between vaginal delivery and cesarean section; however, vaginal delivery
should be the delivery method of choice for women with marginal placenta previa [15].
If placenta accreta, increta or percreta is only recognized in labor, the lack of
uterine tone can result in life-threatening hemorrhage. Welsch et al. collected data
on cases of fatal postpartum hemorrhage due to placentation disorders in women who
were status post cesarean section from the Bavarian Perinatal Survey. There were 11
deaths between 1983 and 2007 in Bavaria, but there have been no cases of fatal uterine
rupture since 1987 [16]. Because ultrasound imaging in our patient was suspicious for placenta percreta
with invasion of the bladder and the patient considered prolonging the pregnancy to
be of secondary importance in view of the potential health risks to herself, we agreed
with her that we would terminate the pregnancy by performing a hysterectomy. The aim
was to prevent maternal risks such as hemorrhage, clotting disorder or infection with
its threat of subsequent sepsis. The intraoperative findings proved to be less complex,
and a diagnosis of placenta accreta was made. This clearly illustrates the limitations
of ultrasound in the prenatal diagnosis of impaired placentation. The case report
demonstrates that it is not possible to make a definitive diagnosis of placentation
disorder with the available prenatal diagnostic methods, meaning that it is important
to be cautious when deciding on further measures. In a recently published retrospective
cohort study, Hall et al. reported that cases of placenta accreta not diagnosed prenatally
on ultrasound tended to be less complex and that maternal and neonatal outcomes in
patients with prenatally undiagnosed placenta accreta were statistically similar to
outcomes where impaired placentation had been diagnosed prenatally. This raises questions
about the diagnostic accuracy of ultrasound for the detection of this entity. Ultrasound
was found to be more accurate for the diagnosis of placenta percreta compared to placenta
accreta [17].
As the prenatal diagnosis was not confirmed in our case, the decision to terminate
the pregnancy in the 19th week of pregnancy must, in hindsight, be considered critically.
Retrospectively it is possible to say that the hysterectomy might have been avoided.
It must also be noted that continuing the pregnancy would have been possible despite
the prenatal findings, but this would have involved incalculable maternal and fetal
risks. This is made very clear by the intraoperative finding of concealed uterine
rupture. After detailed discussions in which the patient was informed of the pros
and cons of the various options in her specific situation, the mother of 4 children
opted to terminate the pregnancy. This shows how much therapy decisions for placentation
disorders are based on the individualʼs specific circumstances, particularly when
definitive clinical evidence is lacking.
Conclusion
Placentation disorders can present with heterogeneous symptoms of varying severity
and clinical findings can differ. Placentation disorders should be considered in the
differential diagnosis of woman who have previously had several uterine surgical interventions.
Diagnosis is made using imaging techniques, primarily ultrasound, complemented by
MRI where necessary. The therapy depends, in the first instance, on the type of placentation
disorder and on whether the patient wishes to have children. In addition to expectant
management and a number of experimental drug therapies, in most cases treatment consists
of primary cesarean section, often performed early on, curettage and even hysterectomy.
Our case report emphasizes the difficulty of making a definitive diagnosis of placentation
disorder prenatally. It also illustrates the far-reaching consequences of cesarean
sections and, above all, the impact repeated cesarean sections can have for affected
women. This underlines how strict the indications for cesarean section should be.
Nevertheless, the numbers of medically indicated cesarean sections have continued
to increase in the last decades. Timely diagnosis of impaired placentation can help
reduce the risk for affected women.
