What causes fetal growth restriction?

From the Guidelines

Fetal growth restriction is primarily caused by suboptimal perfusion of the maternal placental circulation, accounting for 25-30% of all cases, as well as chromosomal disorders and congenital malformations, which are responsible for approximately 20% of FGR cases. The causes of fetal growth restriction can be multifactorial, including maternal, fetal, and placental conditions. Maternal conditions such as hypertension, preeclampsia, diabetes, chronic kidney disease, and autoimmune disorders can contribute to FGR 1. Placental problems, including placental insufficiency, abnormal placental development, or placental infarction, can significantly impact nutrient and oxygen transfer to the fetus. Maternal behaviors, including smoking, alcohol consumption, drug use, and poor nutrition, can also severely restrict fetal growth. Infections during pregnancy, particularly TORCH infections, may contribute to FGR. Genetic factors, such as chromosomal abnormalities and genetic syndromes, play a role in approximately 5-20% of cases. Multiple gestations can result in growth restriction as fetuses compete for limited resources, and environmental factors like high altitude, exposure to toxins, and maternal stress can further impact fetal development.

Some key points to consider in the management of FGR include:

• Early diagnosis and optimal fetal surveillance are crucial in managing FGR 1.
• The use of umbilical artery Doppler in the surveillance of FGR has been shown to be beneficial 1.
• A standardized protocol for diagnosis and management of FGR can lead to more favorable outcomes 1.
• The decision to deliver is typically guided by maternal factors, such as the presence of maternal hypertension, and by fetal comorbidities, such as the degree of growth restriction and the severity of abnormal fetal surveillance results 1.
• The cerebroplacental ratio, calculated by dividing the middle cerebral artery pulsatility index by the umbilical artery pulsatility index, has emerged as a predictor of adverse outcome among those fetuses with FGR 1.

In terms of prevention, there are currently no proven strategies or treatments for FGR that have been shown to be effective, although the use of prophylactic low-dose aspirin has been suggested to provide a modest risk reduction in FGR and SGA in some studies 1. However, the American College of Obstetricians and Gynecologists recommends against the use of low-dose aspirin for the sole indication of FGR prevention due to conflicting evidence. Management of FGR is based on early diagnosis, optimal fetal surveillance, and timely delivery that reduces perinatal mortality and minimizes short- and long-term morbidity.

From the Research

Causes of Fetal Growth Restriction

Fetal growth restriction (FGR) is a complex condition with multiple causes. The main causes can be summarized as follows:

• Impaired placental development and dysfunction, leading to reduced nutrient and oxygen supply to the fetus 2, 3, 4, 5
• Uteroplacental dysfunction, resulting in inadequate supply of nutrients and oxygen to support normal fetal growth 4
• Placental insufficiency, leading to progressive deterioration in placental function and a decrease in transplacental transfer of oxygen and nutrients to the fetus 3
• Malperfusion of the placenta, inducing cell stress and reducing villous volume and surface area for maternal-fetal exchange 5

Risk Factors

Several risk factors contribute to the development of FGR, including:

• Pre-existing medical conditions, such as hypertension and diabetes
• Pregnancy complications, such as preeclampsia and placental abruption
• Uterine and placental abnormalities
• Fetal chromosomal anomalies and structural anomalies

Pathophysiology

The pathophysiology of FGR involves a complex interplay of factors, including:

• Impaired placental development and function
• Reduced uteroplacental blood flow
• Increased placental resistance
• Decreased villous volume and surface area for maternal-fetal exchange
• Dysregulation of imprinted and nonimprinted gene expression
• Activation of proinflammatory and apoptotic pathways within the syncytiotrophoblast 5

Diagnostic Challenges

Diagnosing FGR can be challenging, and current surveillance modalities, such as fetal Doppler ultrasound and fetal heart rate monitoring, may not detect all cases of FGR 2. Therefore, improving detection and effective monitoring of FGR is critical for the management of complicated pregnancies.