Blood flow is selectively redirected to the myocardium, adrenal glands, and in particular to the brain in a brain-sparing effect.In late stage, the redistribution becomes ineffective, there is decrease in cardiac output, ineffective preload handling and elevation of central venous pressure. This deterioration in circulation may ultimately lead to tricuspid insufficiency and death of the fetus. Peripheral circulatory disturbances also accompany these central circulatory changes. Fetal behavioral changes
Chronic hypoxemia leads to delay in all aspects of CNS maturation. With worsening fetal hypoxemia, there is decline in fetal activity. With further hypoxemia, fetal breathing ceases. Gross body movements and tone decrease further. Fetal heart rate decreases due to spontaneous deceleration due to direct depression of cardiac contractility. This leads to intrauterine fetal death. Risk of later metabolic disease
According to the theory of thrifty phenotype, placental insufficiency triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment rich in food it may be more prone to metabolic disorders, such as obesity and type II diabetes.
Diagnosis
The following tests have been promoted as supposedly diagnosing placental insufficiency, but all have been unsuccessful at predicting stillbirth due to placental insufficiency:
Placental grading
Amniotic fluid index
Fetal biophysical profile test scoring
Doppler velocimetry
Routine ultrasound scanning
Detection and management of maternal diabetes mellitus
Antenatal fetal heart rate monitoring using cardiotocography
Vibroacoustic stimulation, fetal movement counting
Home vs. hospital-based bed rest and monitoring in high-risk pregnancy
In-hospital fetal surveillance unit
Use of the partograph during labor
Cardiotocography during labor with or without pulse oximetry

See also
Small for gestational age

References


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