CASE TEMPLATE

 Multiple Placental Abruption with Fetal Loss: Case Report and Review of the Literature

AUTHORS: Figueroa, J; Berutti, O; Pulido, N; Le, N; Maceri, A; Shakil, A

AFFILIATION:

American University of the Caribbean Medical School, Sint Maarten

Ross University School of Medicine, Barbados

ABSTRACT:

The risk for negative outcomes in a pregnancy increases substantially when the placenta disconnects from the endometrial lining too soon before birth. This serious complication in obstetrics is known as placental abruption. We present a 39-year-old G5P4003 patient at 32 weeks of gestation who went to the emergency department complaining of absent fetal movement and abdominal pain. Her medical history included gestational hypertension, a past placental abruption with fetal demise requiring cesarean delivery at 39 weeks, eclampsia during the surgery, and myocardial infarction following the delivery. She stated she followed her prescribed antihypertensive medication but failed to attend her last prenatal appointment. The emergency ultrasound confirmed a placental abruption, and found no heart rate in the fetus, making a cesarean delivery necessary.

The patient in this case had many risk factors for placental abruption, including gestational hypertension, preeclampsia and eclampsia, advanced maternal age and her last pregnancy also resulted in an abruption with fetal demise. High-risk patients such as this need to work closely with their medical team and follow the current monitoring guidelines to have the best chance of a healthy delivery. Still, this case exposes weaknesses in the current recommended protocols for delivery timing and monitoring of high-risk pregnancies, as well as highlighting the importance of a thorough patient education and strong relationship between the patient and their physician. Placental abruption remains a major cause of morbidity and death even with improvements in obstetric treatment. Further research is needed to develop improved evidence-based recommendations for the best management practices, delivery schedules, and risk stratification in high-risk pregnancies.

INTRODUCTION:

Placental abruption is a dangerous complication as it disrupts the essential blood supply of the fetus (Cindrova-Davies 2022) and can cause serious bleeding in the mother (Brandt 2023). It complicates 0.6% and 1.2% of pregnancies (Oyelese 2006, Tikkanen 2013), and once a patient experiences one abruption, they now have a higher risk of experiencing another (Ananth 1996, KÅREGÅRD 1986). When paired with other risk factors for abruption such as advanced maternal age, hypertension, and preeclampsia or eclampsia, the risk for abruption increases even further.

Yet, despite the established risk factors, there is not an evidence-based consensus on the suitable policies for handling these high-risk pregnancies. By presenting a patient with multiple risk factors who experienced recurrent placental abruption that led to intrauterine fetal demise, this case adds to the literature by contributing in three ways: (1) by demonstrating how risk factors can compound to influence adverse outcomes; (2) by highlighting inadequacies in the frequency and timing of current monitoring protocols for high-risk pregnancies; and (3) by emphasizing the need for a strong doctor-patient relationship and thorough patient education regarding the risks of recurrence and warning signs that require immediate attention. By pursuing this case, we hope to promote the development of more comprehensive management protocols and awareness for this vulnerable population.

CASE PRESENTATION:

At 32 weeks’ gestation, a 39-year-old G5P4003 woman arrived at the emergency department complaining of abdominal pain and no fetal movement. Her medical history included gestational hypertension, a past placental abruption with fetal demise requiring cesarean delivery at 39 weeks, eclampsia during the surgery, and myocardial infarction following the delivery. She took her antihypertensive medication as prescribed (aspirin 81 mg QD and nifedipine 30 mg BID), but she failed to appear at her most recent prenatal visit 1 week prior. She did not reschedule the missed appointment. Reported having constant abdominal pain for two hours and no fetal movement for three hours at the time of presentation. She did not smoke, drink or use illegal drugs.

On physical exam she was an afebrile patient with tachypnea, severe hypertension (BP 214/113 mmHg), and obvious distress. An examination of the uterus showed a closed, long, and high cervix with tight contractions. An emergency ultrasound showed an abnormal placenta without localized fluid collection in the placental bed (Image 1), consistent with placental abruption, and verified the absence of fetal heart activity (Image 2). Initial laboratory studies revealed hemoglobin 9.3 g/dL, hematocrit 29.6%, platelets 208×10³/μL, prothrombin time 16.8 seconds, partial thromboplastin time 28 seconds, and fibrinogen 107 mg/dL, indicating early coagulopathy.

Prior to the emergency cesarean delivery, the patient received four units of packed red blood cells (PRBCs) and one unit of fresh frozen plasma (FFP). Two more units of PRBCs, two units of FFP, and one unit of cryoprecipitate were administered intraoperatively. Laboratory tests conducted five hours after surgery showed creatinine 3.2 mg/dL, eGFR 15 mL/min/1.73 m2 and hemoglobin 6.9 g/dL indicating acute kidney injury and worsening anemia. Nephrology consultation diagnosed oliguric acute kidney injury superimposed on chronic kidney disease secondary to hypoperfusion and hemorrhage. She had increased bilateral cortical echogenicity on renal ultrasonography, which revealed underlying renal disease. She received stabilization and inpatient treatment for four days before being sent home. Later, she was diagnosed with a surgical site infection and complex hematoma, which were confirmed by CT imaging, when she returned to the emergency department a week later with bleeding from her surgical incision. She was treated with antibiotics and monitored closely as an outpatient.

DISCUSSION:

Risk Factors

In pregnancy, the placenta attaches itself to the uterine endometrial epithelium and grows into a special organ which maintains embryonic development by eliminating waste products from metabolism and delivering essential nutrients (Cindrova-Davies 2022). When this vital exchange system is prematurely separated, the mother can experience severe bleeding, and the fetus becomes endangered (Brandt 2023) leading to possible morbidity and demise. This serious complication in obstetrics is known as placental abruption.

Abruption complicates 0.6% to 1.2% of pregnancies (Oyelese 2006, Tikkanen 2013), and among the many risk factors, prior placental abruption is one of the most significant. Patients with a history of one prior abruption have a 10-fold increased risk of another, while two previous abruptions carry a remarkable 25-fold increased risk (Ananth 1996, KÅREGÅRD 1986). Similarly, the risk for abruption is increased in patients with chronic hypertension, which is 3- to 4-fold higher. Patients with preeclampsia face an increased risk of 4- to 6-fold, while there is an even greater danger in pregnancies with severe preeclamptic manifestations or hypertension compounded with pre-existing conditions (Williams 1991, Ananth 2016, Tikkanen 2006, Ananth 2007).

Another important risk factor for abruption is tobacco use, which is linked to a 1.7–2 fold increase (Kramer 1997, Ananth 2007, Kaminsky 2007). In an analysis of more than 1.3 million pregnancies, smoking during pregnancy was linked to a 90% increase in odds (OR 1.9, 95% CI 1.8–2.0), and tobacco exposure was linked to 25% of all abruptions (Ananth 1999). Additionally, the risk of abruption is increased by the use of illegal drugs, specifically cocaine and marijuana (McDonald 2007, Hoskins 1991).

Psychological factors also play a role in abruption, with research showing that maternal stress or depression raises the risk, particularly in later pregnancy (Laszlo 2014, Sanchez 2010). It was discovered that elevated plasma cortisol, β-endorphin, corticotropin-releasing hormone, and serotonin concentrations in pregnant women contributed to placental inflammation, though the precise mechanism is still unclear (Laszlo 2014).

Lastly, maternal age exceeding 35 years, also known as Advanced Maternal Age (AMA) is a growing trend in today’s socioeconomic environment and is quickly becoming another significant contributor to placental abruption risk. Centers for Disease Control and Prevention data show an increase in births among women aged >35 years over three decades, with rates for women aged 35–39 years rising from 45.9 per 1000 women in 2010 to 52.7 in 2019 (Martin 2012, Hamilton 2020). Pregnancy in this population has an increased risk of maternal health challenges such as gestational diabetes, blood pressure abnormalities, and cesarean deliveries. There are associated fetal and neonatal adverse outcomes as well, such as genetic anomalies, spontaneous pregnancy loss, premature birth, postnatal intensive care requirements, and pregnancy loss (Frederiksen 2018, Pinheiro 2019). Intrauterine fetal demise, especially when occurring beyond 20 weeks of gestation, shows a statistical association with advanced maternal age, although the exact relationship is under investigation. Research demonstrates a two-fold increased risk in women with AMA and a 3.4-fold increase in those with very advanced maternal age (95% CI 1.7–2.4 and 2.8–4.2, respectively) (Salihu 2008). A comprehensive meta-analysis encompassing 44 studies and over 44 million births confirmed this association (OR 1.75, 95% CI 1.62–1.89), and proposed accelerated placental aging with progressive vascular dysfunction as the underlying mechanism (Glick 2021).

Clinical Presentation

Placental abruption has both an acute and chronic form clinically. Sudden onset vaginal bleeding is seen in the acute form, whereas recurrent episodes of mild to moderate hemorrhage over time is seen in the chronic form. Also, the severity is primarily dependent on which maternal vessels are involved. Peripheral venous bleeding does not manifest as severe hemorrhage, yet it still needs to be closely monitored with appropriate delivery timing to prevent complications. While arterial bleeding that is centrally located is known to cause significant hemorrhage and immediate fetal compromise, thus requiring urgent intervention (Ananth 2022).

The triad of vaginal bleeding, abdominal pain and uterine contractions are commonly seen in abruption, though it’s important to note not all of these symptoms are present in every case. Also, though abruption is frequently accompanied by uterine contractility, this finding is not a precise diagnostic indicator. The most frequent cause of bleeding is maternal decidual hemorrhage, though fetal vessels can occasionally be the cause. The diagnosis is primarily clinical and requires ruling out alternative causes such as placenta previa or cervical changes brought on by active labor (Brandt 2023).

Concealed abruption is a particularly difficult variation to diagnose, which is characterized by uterine irritability and abdominal pain without vaginal bleeding on physical exam. Its presentation appears mild, but concealed hemorrhage can cause serious coagulopathy, fetal compromise, or even death (Sylvester 2017). Imaging may present with insignificant findings, yet clinicians should remain highly suspicious when they observe spontaneous tachysystole or unusually rapid labor progression. In fact, research suggests that underlying concealed abruption processes may be responsible for around 10% of all spontaneous preterm labor deliveries (Ananth 1999). Proving regardless of the diagnostic difficulty, clinicians should remain vigilant and take extra precautions in pregnancies with these seemingly minor symptoms.

Imaging and Histology

When placental abruption is clinically suspected, ultrasonography is the first imaging modality used to detect abnormal blood collections inside or next to placental tissue (Figures 1-3) (Elsasser 2010). However, the similar acoustic characteristics of placental tissue and blood products present diagnostic challenges, especially in advanced gestation when visualization is limited. Thirty patients with confirmed abruption were examined by Shinde et al., and they found that ultrasound imaging had an excellent positive predictive value (100%, CI 79.4–100.0) but a poor negative predictive value (14.0%, CI 1.8–42.8). They also determined ultrasonography to have a perfect specificity (100%, CI 15.8–100.0) but moderate sensitivity (57.0%, CI 37.2–75.6); concluding that a positive result can confirm abruption with good reliability, but a negative study cannot completely rule it out.

A different investigation by Yeo and colleagues reported higher sensitivity approaching 80% and cataloged seven characteristic sonographic patterns associated with abruption: preplacental collections, “jello-like” undulation of the chorionic plate during fetal movement, retroplacental collections, marginal hemorrhage, subchorionic blood accumulation, placentomegaly with abnormal echogenicity, and intra-amniotic hematoma formation. Recognition of these patterns improves diagnostic accuracy, though clinicians should remain aware that ultrasonography may still miss a substantial proportion of abruptions.

Once the placenta has been delivered, physical observation of its fetal surface may reveal clots, indicating an abruption (Chen 2017). In cases where an intraplacental hematoma has formed and contained the bleeding, clinicians may observe an organized hematoma within an infarcted region of the placenta. Histologically, hemorrhage in the decidua basalis with underlying parenchymal indentation is the finding most strongly correlated with acute abruption (Hall 2009). When this indentation is absent, such as in acute abruptions where blood exits vaginally or enters the amniotic fluid or in chronic abruptions, pathologic evaluation may reveal other less specific features.  For instance, decidual inflammation, early trophoblastic necrosis, and intravillous and intervillous hemorrhage may be observed (Chen 2017). Also, clear variations can be seen based on gestational age, according to a retrospective analysis of 305 cases of abruption. When compared to abruptions that occurred prior to 34 weeks, those that occurred at or after that time showed a lower incidence of placental hemorrhages, maternal inflammatory response lesions, and maternal vascular malperfusion lesions (Gonen 2021).

Pathophysiology

The underlying pathophysiology of placental abruption involves interactions between acute events and chronic disease processes (Ananth 2006). For example, processes of thrombosis, inflammation, infection, and uteroplacental vasculopathy result in multiple vascular and structural abnormalities. As a result, there is inadequate placental perfusion, compromised spiral artery development, areas of placental infarction, and insufficient trophoblastic penetration of maternal tissues (Tikkanen 2010). Also, in reaction to hemorrhage within the decidual layer, the resulting tissue hypoxia causes vascular endothelial growth factors to be up regulated, altering the body’s regular response to bleeding (Krikun 2007). These pathophysiological alterations lead to a complex interrelated syndrome of placental dysfunction, which not only predisposes to placental abruption, but other pathologies such as fetal growth restriction and preeclampsia (Ananth 2006).

A major player involved in these processes is the hemostatic protein thrombin, as it interacts with inflammatory and vascular pathways. Once decidual cells detect bleeding, they release tissue factor, causing thrombin to begin the process of hemostasis (Mackenzie 1996-2001, Buhimschi). This activation also upregulates vascular endothelial growth factors, producing a positive feedback loop, and creating more tissue factor and thrombin (Krikun 2007). In juxtaposition, there is an increased breakdown of extracellular matrix, that results in endothelial injury due to the expression of matrix metalloproteinases and pro-inflammatory cytokines such as interleukin-8 (Mackenzie 1996-2001, Lockwood 2005). The combination of these activities ultimately drives placental dysfunction, resulting in abruption and other serious complications.

Furthermore, thrombin’s role extends beyond local tissue effects, as it has pro-uterotonic properties which promote myometrial contractions and can result in premature membrane rupture (Elovitz 2000). When substantial quantities of thrombin enter the maternal circulation, disseminated intravascular coagulation and consumptive coagulopathy can also develop, initiating one of the most dangerous systemic complications of abruption, and dramatically increasing the risk of maternal morbidity and mortality (Thachil 2009). All in all, these complex interactions between disease processes proves the difficultly clinicians face when determining effective management and delivery timing for placental abruption. Cases such as these require further attention and investigation to develop optimal management protocols for pregnant women who are at risk.

Current Management Guidelines

Stabilizing the mother first and then initiating delivery immediately after is the standard procedure for acute placental abruptions at or near term, regardless of their severity. This intervention strategy aims to prevent further maternal hemorrhage and reduce the risk of fetal compromise or death. The initial laboratory evaluation should include a complete blood count and coagulation profile that measures fibrinogen levels, activated partial thromboplastin time, and prothrombin time. Additionally, arterial blood gas analysis, thromboelastography, and rotational thromboelastometry provide fast results which aid in vital transfusion management and resuscitation efforts. Clinicians will commonly use the Advanced Trauma Life Support (ATLS) classification of hypovolemic shock as a general guide when treating an abruption. However, it is important to keep in mind that this system has limitations when it comes to obstetric patients because it does not account for the unique physiological compensatory mechanisms that pregnant women have, and it hasn’t been validated for use in pregnancy. Despite these limitations, the ATLS procedure provides a useful theoretical framework for guiding clinical judgment during resuscitation (Brandt 2023).

With regard to chronic abruption, guidelines for optimal delivery timing also remain limited (ACOG 2013), and evidence supporting specific management protocols, whether inpatient or outpatient care, is insufficient for these high-risk pregnancies. After initial diagnosis and stabilization in the hospital, clinicians may choose the route of outpatient management. Yet this approach requires patients to follow intensified monitoring protocols for fetal surveillance, performed once or twice weekly, using non-stress testing and biophysical profile techniques (ACOG 2021). Multivessel Doppler velocimetry should also be implemented for cases with fetal growth restriction (FGR) or fetal anemia (Martins 2020, Mari 2000). These high-risk pregnancies need to be closely monitored for episodes of vaginal bleeding, and current guidelines recommend delivery between weeks 36 and 37 (Brandt 2023).

Standard intrauterine interventions, such as repositioning the mother or providing supplemental oxygen, generally show minimal effectiveness in placental abruption cases. When gestational age is below 36 6/7 weeks and delivery is expected within a week, clinicians may administer antenatal corticosteroids to enhance fetal pulmonary development. However, physicians should not postpone delivery to complete steroid administration when managing late preterm cases (34 0/7 to 36 6/7 weeks) (Reddy 2021). Additionally, while magnesium sulfate is not recommended for fetal neuroprotection in these circumstances, it remains a critical intervention for preventing seizures in patients experiencing preeclampsia with severe features (Brandt 2023).

In cases of newly presenting vaginal hemorrhage at advanced gestational ages, clinicians should assess the severity through thorough history-taking and gather an estimation of blood loss. Since concealed bleeding can make hemorrhage difficult to quantify accurately, evaluation must also include an assessment of vital signs, urine output, and mental status. The Advanced Trauma Life Support (ATLS) classification of hemorrhagic shock offers a framework of clinical findings associated with varying hemorrhage levels; however, this system has limitations when applied during pregnancy. It has not been scientifically validated in this population and might not account for physiological compensatory changes unique to pregnant patients. The ATLS classification may understate the amount of intravenous fluids and blood products needed for proper resuscitation, especially in cases with concomitant hypertension or preeclampsia (Brandt 2023). Therefore, there is a need for improved guidelines for abruption, especially when there are multiple compounding factors such as gestational hypertension, a history of preeclampsia or eclampsia, and/or a history of a prior abruption.

CONCLUSION:

In pregnancy, if the placenta separates from the uterine wall too soon, fetal blood supply becomes compromised, and there is significant maternal hemorrhage; this is known as placental abruption and is a serious obstetric emergency. Currently, clinical recommendations are limited for the management of this complication. Clinicians frequently use the Advanced Trauma Life Support (ATLS) classification of hypovolemic shock; however, this system has limitations because it has not been validated for pregnancy and does not account for the unique physiological compensatory mechanisms of pregnant women. Also, the evidence that is available and supports specific management protocols for inpatient and outpatient care, is insufficient for these high-risk pregnancies.

This case is a prime example of placental abruption recurrence in patients with several compounding risk factors, including advanced maternal age, chronic hypertension during pregnancy, preeclampsia and eclampsia, and history of abruption. Despite partial risk factor management, the patient experienced a second abruption that led to another fetal loss, highlighting the severity of this complication. Although the patient reported medication compliance, the missed follow-up appointment preceded the development of an abruption one week later, emphasizing the critical importance of consistent prenatal monitoring in high-risk pregnancies. This case reveals several opportunities for improved research and better clinical care, for example:

1. Development of comprehensive but understandable patient education regarding the compounding effects of several risk factors and recognition of warning signs requiring immediate medical attention.
2. Creation of evidence-based delivery and management protocols for high-risk pregnancies.
3. Implementing automated appointment reminder systems with escalation procedures for high-risk cases involving missed appointments.

All in all, further research is necessary to develop evidence-based recommendations for the best management practices, delivery schedules, and risk stratification in high-risk pregnancies. Placental abruption is a complex condition with high maternal and fetal morbidity and mortality, despite advancements in obstetric care. As such, it demands proactive management with evidenced-based guidelines, as well as clear communication and seamless collaboration between the patient and medical team.

Images:

(Image 1) Ultrasonographic visualization demonstrating placental separation from the uterine wall, consistent with abruption.

 (Image 2) Fetal demise was confirmed via ultrasonography demonstrating absence of cardiac activity.

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Placental Abruption Case Report Final Draft