Data has indicated adverse maternal and neonatal outcomes from placental conditions, alongside a high risk of recurrence in subsequent pregnancies.
In a recent review, investigators described the pathological findings of the placenta and how communication should be performed between obstetricians, neonatologists, and pathologists diagnosing placental disorders.1
Placental function may be impacted by a variety of conditions, including genetic, metabolic, maturation, and circulatory disorders. Understanding the pathology of the placenta is crucial for proper treatment, with multiple organizations publishing guidelines for placental examination.
During placental investigation, maternal or fetal diseases that were previously unsuspected may be identified. Many current guidelines are based on unique health care systems, highlighting the need for increased variety toward examination standards.2
Investigators published a review to highlight clinical indications for placental pathological examinations and provide standardized recommendations.1 The review began with recommendations for weighing the placenta with the membranes while still in the delivery room to achieve a fresh weight.
The umbilical cord should also be measured, including placental and newborn components. Placenta undergoing histopathological examination should be fresh and untrimmed when sent to the pathology department, where it will be weighed without the membranes or umbilical cord.
In 2016, a group of placental and perinatal pathologists published criteria for diagnosing placental lesions. A normal placenta has low-velocity, high-volume blood flow, which changes to accelerated villous maturation during maternal vascular malperfusion. This presents as increased syncytial knots and intervillous fibrin causing villous paucity.
Patients with abruptio placentae are at an increased risk of preeclampsia caused by arteriopathy, with abruption occurring following rupture of the maternal veins at the placenta’s periphery. The course of abruptio placentae may be acute or chronic.
Delayed villous maturation is another placental condition, presenting as a monotonous villous population. Patients may also present with fetal vascular malperfusion, characterized by scattered small foci of avascular villi.
The placenta is also at an increased risk of infection and immune-mediated allograft-type responses. This includes acute inflammation, as well as chronic cellular inflammation of the villous stroma in patients with villitis of unknown etiology.
Patients with maternal and obstetrics disorders are more likely to experience severe maternal vascular malperfusion, which may be an indicator of maternal autoimmune disease. Therefore, maternal cardiovascular status, glucose tolerance, thrombophilia, and renal function must be assessed in these patients.
Potential adverse outcomes of severe maternal vascular malperfusion include intrauterine growth restriction, fetal and neonatal demise, and neonatal neurocompromise. The odds of recurrence range from 34% to 100%, highlighting the need for preventative measures to improve fetal and maternal outcomes in subsequent pregnancies.
Investigators recommended acetylic salicylic acid, uterine artery Doppler, and early third-trimester placental ultrasound to reduce the risk in subsequent pregnancies. Neonatal antibiosis may be recommended in patients with histologic chorioamnionitis.
Mothers should be tested for autoimmune diseases if they present with villitis of unknown etiology, maternal floor infarction, or chronic histiocytic intervillositis. There is also an association between chronic histiocytic intervillositis and alloimmune thrombocytopenia in fetuses and neonates, indicating a need for a respective hematologic workup of the child.
Placental circulation disorders may also impact fetal brain lesions. Fetoplacental lesions significantly impact fetoplacental physiology in infants with cerebral palsy, highlighting this association.
In placental membranes, certain organisms may create an inflammatory response known as chorioamnionitis, which is the most common cause of preterm birth. Examinations for this inflammation include a swab from the placenta in premature children and cases of prolonged membrane rupture.
Notably, 75% to 90% of subsequent pregnancies face recurrent chronic histiocytic intervillositis. Other high recurrence rates include 40% to 60% for massive perivillous fibrin deposition, 25% to 50% for high-grade villitis, 25% to 30% for placenta accreta, 10% to 25% for severe maternal malperfusion, and 10% to 25% for preterm birth with chorioamnionitis.
This data highlights the adverse outcomes associated with placental pathology and the need for investigation. Investigators concluded standardized guidelines and reproducible nomenclature are needed to help clinicians prioritize patient health.
Reference
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