Early Accreta and Uterine Rupture in The Second Trimester: Open Access Case DOI: 10.7759/cureus.2904
Early Accreta and Uterine Rupture in The Second Trimester: Open Access Case DOI: 10.7759/cureus.2904
Early Accreta and Uterine Rupture in The Second Trimester: Open Access Case DOI: 10.7759/cureus.2904
1. Internal Medicine, Texas Tech University Health Sciences Center of the Permian Basin, Odessa, USA 2. MS3/Ross
University School of Medicine, California Hospital Medical Center, Los Angeles, USA 3. MS4/Ross University School of
Medicine, California Hospital Medical Center, Los Angeles, USA
Abstract
The differential diagnosis of third trimester bleeding can range from placenta abruptia to placenta previa to
uterine rupture and the placenta accreta spectrum (PAS). However, patients with risk factors such as multiple
cesarean sections (c-sections), advanced maternal age (AMA), grand multiparity, and single-layer uterine
closure are at greater risk of developing these complications earlier than we would traditionally expect.
This case recounts a 38-year-old gravida 6 preterm 3 term 1 abortus 1 live 4 (G6P3114) at 23 weeks and five
days gestational age (GA) with a past medical history of preterm pregnancy, pre-eclampsia, chronic abruptia,
three previous c-sections, and low-lying placenta who presented to the emergency department (ED) with
vaginal bleeding. Initial workup revealed placenta accreta and possible percreta. The patient was placed on
intramuscular (IM) corticosteroids in anticipation of preterm delivery. As soon as the patient was stable, she
was discharged home. She presented to a different hospital the next day with the same complaints. Imaging
was consistent with accreta and her presentation with abruption. During the hospital stay, the patient went
into threatened preterm labor (PTL). At first, we suspected preterm premature rupture of membranes
(PPROM) due to apparent pooling of amniotic fluid in the vaginal canal. Upon further work up, the diagnosis
was consistent with chronic abruption oligohydramnios sequence (CAOS). Before this could be investigated,
her hospital course was complicated by acute abruption and Category III/nonreassuring fetal heart rate
(FHR) tracing. The patient underwent an emergency c-section at 26 weeks GA as well as a planned
supracervical hysterectomy for desired permanent sterilization. During the operation, the patient suffered a
postpartum hemorrhage (PPH) of 4500 mL. She was later discharged home on postoperative day (POD)
eight.
Patients who are at the highest risk for placenta accreta are those with a placenta previa affecting their
current pregnancy and they have a history of multiple c-sections. Placenta previas—placentas overlying the
internal cervical os in varying degrees—are also included in the spectrum of differential diagnoses of third
trimester bleeding. Prospective studies have examined the incidence of placenta accreta in patients with
concurrent underlying previas. Resnick et al. explain that these studies found the frequency of placenta
accreta to be increased commensurately with the number of previous c-sections after the first from three to
up to 67% (in one c-section to five to six or more c-sections, respectively) in such expectant mothers. First
suspicion of placenta accreta is about obstetrical ultrasound (US) when the patient is asymptomatic. No
single modality can establish the prenatal diagnosis of placenta accreta with absolute certainty although the
diagnosis is more likely between 18 and 20 weeks gestational age (GA) (with imaging evidence of abnormal
Uterine ruptures are often associated with a trial of labor after the cesarean delivery (TOLAC), especially if
the prior cesarean delivery involved a classical incision. TOLAC refers to attempted labor during a vaginal
birth after (a prior delivery by) c-section (VBAC). As per Landon et al., incidence rates of uterine rupture at
term for TOLAC are even higher than in women who undergo elective repeat cesarean delivery (ERCD), 78%
versus 22%, respectively [3]. Uterine rupture is a life-threatening pregnancy complication for both the
mother and the fetus. All uterine layers are disrupted including the serosa, ultimately leading to decline in
maternal and fetal status. The patient will present with vaginal bleeding, sudden or worsening abdominal
pain, hemodynamic instability secondary to hemopertioneum, and nonreassuring fetal heart rate
(FHR) tracing (Category II or Category III) due to deterioration of fetal status. Clinicians should note that
placental abruption is actually the leading diagnosis in pregnant women with acute abdominal pain,
bleeding, and Category II or III tracing. It may not be distinguishable from uterine rupture before exploratory
laparotomy.
Case Presentation
This case describes a 38-year-old G6P3114 at 23 weeks and five days GA with chronic abruptia and low-lying
placenta who presented to the ED with vaginal bleeding. Her past medical history was significant for
preterm pregnancy, preeclampsia, and three previous c-sections. Initial workup revealed placenta accreta
and possible percreta (Figure 1) [4]. The patient was placed on IM corticosteroids in anticipation of preterm
delivery. As soon as the patient was stable, she was discharged home. She presented to a different hospital
the next day with the same complaints.
Key:
*Accreta: anchoring placental villi attach to the myometrium instead of the decidua
The maternal fetal medicine (MFM), neonatal intensive care unit (NICU), and anesthesia teams were
consulted on her case due to the concern of placenta accreta. A magnetic resonance imaging (MRI) was done
and was significant for loss of the decidual line along the right lateral anterior uterus with myometrial
thinning along the region of her previous c-section scar. There was no evidence of percreta on the MRI. Of
note, her bedside transvaginal ultrasound (TVU) showed placenta accreta with low-lying anterior placenta
with a short cervix and funneling, but ruled out placenta previa. Still, the patient continued to have vaginal
bleeding presumably from chronic abruption (Figure 2) [5]. She was transferred back and forth between labor
and delivery (L&D) unit and the maternal fetal care unit (MFCU) with threatened PTL.
A few days later, the patient was complaining of leakage of fluid and while on sterile speculum examination
(SSE), there was vaginal pooling. Standard diagnostic strategies (nitrazine blue testing and presence of
ferning on microscopy of fluid) were used to determine whether the fluid was indeed amniotic and came up
positive. Treatment for PPROM was started which included antibiotics as well as rescue steroids. Upon
further assessment, it was found that amniotic fluid index (AFI) >7 cm. Subsequent amniotic fluid exam
via repeat US the next day was consistent with oligohydramnios. It was thought that her low-lying placenta
could have also caused retroplacental blood to accumulate. But, based on the finding of oligohydramnios,
chronic abruptia oligohydramnios sequence (CAOS) was more likely the diagnosis than PPROM. Before any
further evaluation could be done, the patient went into PTL that night, which ultimately was spontaneously
arrested. Her PTL was then complicated by presumed uterine rupture at the site of her previous c-section, as
indicated by deterioration of her FHR tracing to Category III.
The patient received general anesthesia for an emergent c-section in the setting of uterine rupture at 26
weeks GA. She then underwent a planned supracervical hysterectomy. The surgery was complicated by
PPH as the patient's estimated blood loss (EBL) was about 4500 mL. She received one unit of packed red
blood cells (pRBCs) preoperatively the night before, seven units intraoperatively, and two units
postoperatively. She was also given four units of fresh frozen plasma (FFP), one unit of platelets, and one
unit of cyroprecipitate. She was stable postoperatively and was discharged on POD eight in stable condition.
The diagnosis of placenta accreta is typically made in the second trimester around 18-20 weeks, prior to the
onset of symptoms in the third trimester. To make the diagnosis, imaging modalities and blood tests can be
used. Elevated maternal serum alpha fetoprotein (msAFP) in the second trimester (>2.0-2.5 multiples of the
median) supports an US-based diagnosis of placenta accreta but is not useful on its own. The imaging
modalities typically used include two-dimensional transabdominal and transvaginal US, color Doppler US,
three-dimensional power Doppler, and magnetic resonance imaging (MRI) (Figures 3-4) [2, 6-7]. While usage
of any of these imaging modalities has its own benefits, Resnick et al. highlight transabdominal and
transvaginal US as the most sensitive (90.7%) and specific (96.7%) studies to evaluate placental position and
implantation [2]. The accuracy of first trimester sonographic diagnosis of placenta accreta is still unclear,
but second trimester findings include anechoic areas and an irregular placental-myometrial interface.
Additional second and even third trimester sonographic findings, touted to be the most common, include
loss of placental homogenicity which is replaced by intraplacental sonolucent spaces such as venous lakes or
placental lacunae adjacent to the involved myometrium as well as hypervascularity of the serosa-bladder
wall interface (disruption of the "bladder line") (Figure 4) [7].
Transitioning to uterine rupture, incidence is higher in women with previous c-sections (who undergo
induction) than in those with spontaneous delivery. Due to the fact that the rupture is increased by the use
of prostaglandins, Landon et al. states that the American College of Obstetrics and Gynecologists
(ACOG) has advised against the use of misoprostol in women with previous history of c-sections [4]. The risk
of rupture is 2.45%. Oxytocin presents a 1.1% risk of rupture yet is not contraindicated when compared to
misopristol. He goes on to explain how possible risk factors for uterine rupture include advanced maternal
age (AMA), GA > 40 weeks, birth weight >4000 g, single-layer uterine closure, and more than one previous c-
section [4]. Measurement of the thickness of the residual myometrium in the lower segment of the uterus at
the site of previous c-section can help to determine the risk of uterine rupture. Clinical signs of rupture, as
per Landon, et al., include hemodynamic instability, vaginal bleeding, abdominal pain, weakening
contractions, loss of station of the fetal presenting part, and FHR abnormalities [4]. Intrapartum FHR
tracings help assess the status of fetal cardiovascular well-being. The FHR abnormalities refer to sudden
development of consistently Category II or III tracings. A Category I tracing indicates reassuring fetal status
while a Category III tracing (Figure 5) indicates nonreassuring fetal status and increased risk of fetal
acidemia, necessitating expeditious c-section [8]. Patients with Category II tracings should be managed
expectantly and preparations should be made for urgent delivery. As a diagnosis of placental abruption
This figure was used from The Female Patient with consent.
Given the patient’s history of chronic placental abruption, equivocal testing for PPROM with Amnisure and
SSE, and reduction in AFI, she was given the diagnosis of CAOS. According to Elliott et al., the condition is
defined by the following criteria: (1) clinically significant vaginal bleeding in the absence of placenta previa
or other identifiable source of bleeding; (2) amniotic fluid volume initially documented as normal; (3)
oligohydramnios with an AFI less than or equal to five eventually developing without concurrent evidence
of ruptured membranes [9]. The CAOS occurs in pregnancies complicated by placenta abruptia and if it
develops, the mean GA at delivery is 28 weeks (i.e., preterm). Attending physicians should be aware that
although this condition is rare, according to Kurata et al. it does present risk of lung injury to the infant,
which is a major clinical concern [10]. The MRI studies describe CAOS pathophysiology as chronic separation
of the placenta, exposing its peripheral veins thus resulting in a marginal hematoma distributed extensively
along the decidua. There were no blood-derived products in the amniotic fluid on the patient’s imaging
results, which would otherwise show high signal intensity and help confirm the diagnosis on T1-weighted
imaging. As Kurata et al. goes on to explain, however, as a consequence of the chronic venous bleeding from
the placenta, blood-derived products can leak into the amniotic fluid and the fetus can aspirate them
consequently yielding lung injury [10].
The MFM specialists still agree that there are several risk factors that increase the risk for placental abruption
alone: substance abuse (cocaine/tobacco), AMA, uncontrolled hypertension (HTN)/preeclampsia, prior
history of abruption (7x), asthma (1.2x), and blunt abdominal trauma (6x). Previous abruption confers
the strongest risk for future occurrence with recurrence risks at 10 up to 93 times higher according to prior
studies. Smoking increases risk by 2.5 times (40% for each pack per day smoked) and has a synergistic effect
with HTN while HTN alone increases risk by five times [11]. Epidemiologically, Kurata et al. explain that
abruptia occurs in 1% of pregnancies with two-thirds of cases being severe. Some 40%-60% occur <37 weeks
GA and 14% <32 weeks GA [10]. The diagnosis of placenta abruptia is reserved for pregnancies over 20 weeks
GA. It is a common cause of mild to moderate third trimester bleeding and characterized by complete or
partial premature placental detachment prior to the delivery of the fetus. The FHR tracings will become
nonreassuring (Category II or III) and the patient will also experience bleeding and abdominal/back pain as
well as uterine tenderness. As per Ananth et al. the perinatal mortality rate appears to be declining, but it is
still 20 times higher in comparison to pregnancies without abruption (12% versus 0.6%) [11]. Nonetheless,
10%-20% of abruptia cases end up being preterm births either from PTL or PPROM with scant or no vaginal
Pathogenesis of placenta abruptia as pictured in Figure 2 involves rupture of maternal vessels in the decidua
basalis where they interface with anchoring villi of the placenta—blood accumulates and splits the decidual-
placental interface leading to complete or near complete placental separation. This is evidenced by findings
of retroplacental hematoma on transabominal US (sensitivity 25%-60%, PPV 88%) [11]. Ananth et al. note
that the presence of the following findings in symptomatic patients can improve pretest probabilities in
favor of the diagnosis: subchorionic collections of fluid, echogenic debris in the amniotic fluid, and
thickened placenta that shimmers with maternal movement ("jello" sign) [11]. Note that the absence of the
hematoma does not exclude acute severe abruption because blood may not collect behind the uterus. The
consequence of such pathophysiology, however, is uteroplacental insufficiency (and subsequent growth
restriction if chronic) to the fetus, excessive blood loss, microangiopathic hemolytic anemia (MAHA), and
disseminated intravascular coagulation (DIC) in the mother (if the abruptia is severe). More than 50% of
fetal demise cases are stillborn due to intrauterine asphyxia in such settings [11]. These abnormalities,
including elevation of msAFP or hCG and decreased PAPPA-A or unconjugated estriol (E1) (10-fold increased
risk of subsequent abruption), strongly support the clinical diagnosis as per Ananth et al. [11]. Patient
mortalityl depends on the severity of the placental separation, and whether it becomes severe and exceeds
50%. Oyelese et al. caution that laboratory findings suggestive of mild DIC need to be interpreted with
caution as normal pregnancy is a hypercoagulable state—there is an increase in concentration of almost all
of the coagulation factors and a mild decline in the platelet count [12]. Sections of the placenta that remain
attached cannot compensate for the surface area of gas exchange that has been lost in the sections that have
separated, thus the FHR tracing will inevitably show late decelerations (Figure 6) [8]. If missed, prolonged
late decelerations can result in fetal bradycardia and fetal demise. Nonetheless, Ananth et al. have identified
that DIC occurs in 10%-20% of severe abruptions with the death of the fetus [11]. All in all, MFM specialists
believe that placenta abruptia is one of the most common causes of fetal demise itself.
*Late decelerations indicate uteroplacental insufficiency, poor circulation of oxygen, nutrients, and metabolic
byproducts between the mother and fetus in utero . Fetuses exhibiting prolonged late decelerations warrant
expeditious delivery via caesarean section to circumvent maternal and fetal morbidity.
This figure was used from The Female Patient with consent.
Management
The primary aim of placenta accreta is to reduce the risk of massive hemorrhage, which is the most common
complication. The first step in management is to have a multidisciplinary care team on board, retrieve
informed consent early on, and have a scheduled delivery around 34-35 weeks GA at a well-equipped facility.
The probability of complications over the hospital course can be decreased by having a planned c-section
In anticipation of an increasing amount of blood loss, clinicians should be wary of imminent deterioration of
a reassuring FHR tracing (Category I) as well as extravasation of blood into the myometrium (Couvelaire
uterus). Studies show in this particular setting that decision-to-delivery time of less than 20 minutes is
associated with better outcomes than a 30-minute interval. Category II tracings should be managed
expectantly. As such tracing is at risk of worsening to a Category III (Figure 5) in the setting of acute
abruption, close monitoring should be prioritized and preparations should be made for urgent delivery of the
fetus [8]. The determination for delivery is made based on GA, cervical dilation, and the current maternofetal
condition. Should the mother become hemodynamically unstable or develop signs and symptoms of
significant coagulopathy, immediate c-section has the greatest mortality benefit. If the abruption was severe
enough and a Couvelaire uterus develops, Oyelese et al. warn that the uterus can become atonic and the risk
of PPH rises significantly [12]. Intravenous oxytocin and manual uterine massage can be used acutely in this
scenario. Nevertheless, the patient is at risk of DIC [fibrinogen < 200 mg/dL, elevated fibrinogen degradation
products (FDP), and elevated d-dimer] and exsanguination which can result in multisystem organ failure
(MSOF) if the uterine atony is not aggressively managed. Delivery should be scheduled for 37-38 weeks
Management of uterine rupture in patients who are not in labor includes undergoing imaging studies [US,
MRI, and/or computed tomography (CT)]. They may be done as part of the routine follow-up in patients
at risk or during a trauma evaluation. These studies may show disruption of the myometrium, extrauterine
fluid-distended fetal membranes, free peritoneal fluid, anhydraminos, an empty uterus, fetal parts outside of
the uterus, fetal demise, or pneumoperitoneium (signs of visceral perforation). While these imaging studies
may guide management, Landon et al. emphasize that FHR abnormalities, maternal hemodynamic
instability, and severe abdominal pain usually require urgent delivery [4]. Hemodynamically unstable
patients are stabilized with fluids and blood transfusions and are then prepared for c-section. Abdominal
incision options include Pfannenstiel (lower uterine/bikini line) and midline (classical) incision. Pfannanstiel
incision has limitations as it only provides good exposure to the lower uterine segment and pelvis while the
midline incision provides better exposure for a more thorough abdominal exploration. Midline incision
exposes the uterine fundus which will extend above the umbilicus by late second trimester. In the event
uterine rupture is discovered during laparotomy, Landon et al. explain that the uterus may be saved through
rapid primary single or double-layer closure with a delayed absorbable suture [4]. If the uterine defect
cannot be repaired in the setting of uncontrollable hemorrhage, hysterectomy is indicated. With subsequent
pregnancies, a scheduled c-section is highly recommended before the onset of labor. Although early rupture
of the uterus is rare, Faguer and Endres et al. emphasize that it should not be discounted [14-15]. Faguer
recounts the case of a patient at the 22nd week of her third pregnancy who presented with internal
hemorrhage that required immediate exploratory laparotomy and subsequent hysterectomy to achieve
hemostasis. Faguer concludes that ruptures are more likely to occur in a uterus with an anterior scar from a
prior c-section [14]. In Faguer's defense, Endres et al. believe that uterine rupture should be considered in
the differential diagnosis of severe abdominal pain in the early second trimester, especially if the patient
underwent prior c-sections involving classical incision [15].
Conclusions
Early detection, diagnosis, and proper management are critical in the setting of placenta accreta and/or
uterine rupture to decrease the likelihood of clinical deterioration and maternofetal morbidity and
mortality. Adverse outcomes in similar cases have included neonatal periventricular leukomalacia, stillbirth
secondary to intrauterine asphyxia, and preterm delivery (<37 weeks GA). To help reduce morbidity and
mortality in the setting of placenta accreta, abruption, and/or uterine rupture, MFM and obstetrical
specialists should continue to carry a high index of suspicion in patients presenting with similar findings
suggestive of any of the aforementioned diagnoses especially during the second trimester.
Additional Information
Disclosures
Human subjects: Consent was obtained by all participants in this study. Conflicts of interest: In
compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services
info: All authors have declared that no financial support was received from any organization for the
submitted work. Financial relationships: All authors have declared that they have no financial
relationships at present or within the previous three years with any organizations that might have an
interest in the submitted work. Other relationships: All authors have declared that there are no other
relationships or activities that could appear to have influenced the submitted work.
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