Placental Development

Placentation begins with the trophoblast's invasion of the endometrium. By day 9, lacunae form within the syncytiotrophoblast, which later fuse and fill with maternal blood from eroded spiral arteries. Chorionic villi develop in three stages: 1) Primary villi: cytotrophoblast cores grow into the syncytiotrophoblast. 2) Secondary villi: mesoderm grows into the cores. 3) Tertiary villi: fetal blood vessels develop within the mesoderm. By the end of the 4th month, the placenta has two parts: the fetal portion (chorion frondosum) and the maternal portion (decidua basalis). The villi are bathed in maternal blood within the intervillous spaces. The 'placental barrier' consists of the syncytiotrophoblast, cytotrophoblast, connective tissue, and the endothelium of the fetal capillaries. As pregnancy advances, this barrier thins to improve exchange efficiency. The placenta also acts as an endocrine organ, producing Human Placental Lactogen (hPL) to increase maternal glucose availability for the fetus and progesterone to maintain the pregnancy.

The 'remodelling' of maternal spiral arteries is a crucial physiological step. Cytotrophoblasts migrate into the walls of the spiral arteries, replacing the muscular and elastic tissue with fibrinoid material. This converts high-resistance vessels into low-resistance, high-capacity vessels to ensure adequate blood flow to the placenta. Failure of this process is the underlying cause of pre-eclampsia. The umbilical cord, containing two arteries (deoxygenated blood) and one vein (oxygenated blood), connects the fetus to the placenta, surrounded by Wharton's jelly.

Placental dysfunction leads to fetal growth restriction (FGR) and pre-eclampsia. Placenta praevia (low-lying placenta) and placental abruption (premature separation) are major causes of third-trimester haemorrhage. Placenta accreta occurs when villi attach too deeply into the myometrium. Clinicians must examine the placenta after birth to ensure it is complete, as 'retained products of conception' can cause postpartum haemorrhage (PPH) and sepsis. Rhesus disease involves maternal antibodies crossing the placenta and attacking fetal RBCs.

Ultrasound is used to assess placental position (rule out praevia) and morphology. Doppler ultrasound of the uterine and umbilical arteries assesses placental resistance and fetal well-being in suspected growth restriction.

Placenta praevia requires delivery via C-section if the placenta covers the os. Pre-eclampsia is managed with antihypertensives (e.g., Labetalol) and delivery of the placenta (the only definitive cure). Anti-D is given to Rhesus-negative women to prevent sensitisation.