- Placenta, Umbilical Cord and Membranes
- Amniotic Fluid
- Multiple Pregnancy
- Uterus and Adnexae in Pregnancy
- Other disorders of Pregnancy
Placenta, Umbilical Cord and Membranes
The blastocyst embeds into the endometrium, sends out finger-like chorionic villi projections, with the entire endometrial lining undergoing decidual proliferation/reaction. Most villi and decidua atrophy by mid-late 1st T, but chorion frondosum and decidua basalis along the gestational sac proliferate forming the placenta. Mature placenta has maternal blood entering intervillous spaces via endometrial/spiral arteries. Blood circulates around villi, allowing for gas and nutrient exchange through the thinned syncytio-trophoblast and cytotrophoblast. Deoxygenated blood flows from intervillous spaces to decidua and endometrial veins. Foetal blood enters the villi as chorionic arteriess (via 2 umbilical arteries), forming extensive branching of capillaries. Drainage is via the single umbilical vein.
Initially the placenta is a rounded disc with umbilical insertion at centre, trophoblastic proliferation at areas of better blood supply and atrophy in poorer vascularity (usually lower uterine segment, areas of scarring, near large fibroids). This causes trophotropism (remodelling) where eccentric cord insertion may occur (marginal at edge, velamentous if outside placenta), unusual placental shapes (bilobed, succenturiate lobe if separate from main body), resolution of placenta previa.
Normal placenta seen at ~8/40 as focal thickening at peripheral gestational sac -> disclike at 12/40 -> granular, homogeneous, smooth covering chorion at 18/40 -> heterogeneous with focal echolucent venous lakes (maternal intervillous connections) and fibrin deposits, septations and undulations, calcifications. Placental thickness usually measured subjectively, or perpendicular from chorionic plate to beginning of basilar-myometrial layer, 20-40mm (thins with time); thicker associated with diabetes, anaemia, hydrops (immune and nonimmune), chronic uterine infections; thinner associated with preeclampsia, placental insufficiency, IUGR, trisomy 13 and 18, marked polyhydramnios (stretched and compressed). Chorionic plate – chorioamnionic membranes on inner aspect of placenta, is bright specular reflector when beam perpendicular. Basilar-myometrial layer – uterine wall attachment, hypoechoic band. Serosal and juxtrauterine veins are prominent, conforming to uterine wall without mass efect.
- Grade 0 – Normal uniform echogenicity.
- Grade 1 – Small diffuse intraplacental speckled calcifications, normal >30/40.
- Grade 2 – Larger calcifications along basilar plate, normal >32/40.
- Grade 3 – Thicker more extensive calcification also along cotyledons, normal >34/40 (if before then IUGR in 50%).
Circumvallate placenta – placental margin and membranes elevated; partial or complete; margin calcifies with time. Marginal shelf is band of tissue attaching to edge of the placenta mimicing synechia. Increased risk of abruption, PROM, IUGR, preterm labour. Circummarginate placenta – only membranes involved (usually not seen on US).
Placental membranes include outer chorion and inner amnion, commonly separated by fluid until fusion at 14-16/40. Occasional persistence of chorioamnionic separation into 3rd T is thought to be of no clinical significance.
Myometrial contractions occur at any time, more likely focal in 1st and 2nd T, more generalised (Braxton-Hicks contractions) towards term. Anywhere in uterine wall, typically round ‘mass’ bulging into amniotic space, rarely bulges outer uterine contour, may bow placenta into amniotic space (may falsely place over cervix if low-lying), usually homogeneous, changes over time rarely lasting >1hr.
Clinical diagnosis at time of delivery, with part or all of the placenta covering the dilated and effaced cervix, in 0.3-0.6% at term. Cannot be diagnosed <20/40 as ~45% will have low placenta from low implantation, filling of bladder distorts lower uterus and cervix, trophotropism (change in shape/position of placenta due to better growth in better blood supply, atrophy in poor blood supply); over time muscular cervix elongates increasing distance of margin from os. Those ~<20mm from os (‘low lying placenta’) after 20/40 should be followed up at ~32/40 (more often if symptomatic), in 3rd T low lying is ~<40mm from os. Variable definitions with marginal/partial extending to edge but not crossing over os or complete totally covering os (asymmetric complete when placenta eccentric over os, central when central placenta over os). Painless PV bleeding in 3rd T, from effacement of cervix and dilation of os disrupting vascular bed. Increased risk with lower uterine segment scarring (previous C-section, placenta previa or surgery), multiple previous pregnancies. 5% associated with placenta accreta/percreta. Best seen translabially or transvaginally.
Normal cord has 2 arteries and 1 vein surrounded by Wharton jelly. Normal diameter is 10-20mm, thickened with excessive normal Wharton’s jelly, DM, foetal hydrops (oedema), foetal urachal/urine extravasation. Two-vessel cord in 10% (more common in multiple gestations, DDx normal 3 vessel with 2nd artery reconstituting closer to foetus), of which 10-20% are associated with congenital malformations (cardiac, urinary tract, CNS, omphalocoele, aneuploidy). If entire cord can be seen in one projection it is too short. An untwisted cord has a higher risk of perinatal morbidity and mortality. Nuchal cord – location adjacent to foetal neck in 20%, if indents soft tissues of neck then may be potential strangulation.
Normal placental insertion if remains within substance. Marginal insertion (Battledore placenta) is within 20mm of edge, all branching vessels within placenta. Velamentous if beyond margin, arteries and veins not anchored, but connected via pedicle covered only by chorioamnionic membrane (not protected by Wharton jelly) hence increased risk of bleeding. Obligate cord presentation if near internal os with prolapse potentially causing loss of foetal circulation. Vasa previa if foetal vessels cross over the internal os (eg umbilical insertion of vessels extending between succenturiate and main lobes of placenta), cervical dilatation may tear these causing foetal demise.
Cord masses usually arise closer to foetal insertion, including allantoic cysts, urachal remnant, Wharton’s jelly cyst (associated with omphalocoele), haematoma, haemangiomas, teratomas, remnant of blighted twin.
(Placental abruption). Haemorrhage within or around placenta; spontaneous, from direct trauma or iatrogenic (biopsy/transfusion/amniocentesis). Increased risk with maternal HTN, smoking, cocaine, previous abruption. Acute phase hypoechoic/anechoic; subacute (clots within minutes) hyperechoic heterogeneous; chronic lyses to hypoechoic/anechoic. May recur with PV bleeding, pain/tenderness. Haemorrhage cannot be excluded as appearances vary as it dissects into other areas, may shrink extensively if expelled. May extend into amniotic cavity creating floating echoes.
- Subchorionic haematoma (marginal abruption) – Common at margin of placenta from venous maternal bleeding, between chorioamnionic membrane and uterus. Equivalent to SDH, extending parallel to uterine wall. Normal outcome except when large in 1st T (foetal loss), but probable increased risk of preterm labour and growth restriction.
- Retroplacental haemorrhage (central abruption) – Between the placenta and uterine wall, usually arterial. Equivalent to EDH with lentiform shape.
- Implantation bleeding – Small collections of blood at attachment of chorion to endometrium early in pregnancy, ie small areas of subchorionic haemorrhage. US followup.
Attachment of placenta to part of uterus deficient in endometrial decidua increases risk of invasion to (accreta), into (increta) or through (percreta) the myometrium. Placenta is difficult to separate from uterus causing maternal haemorrhage, may require hysterectomy. Increased risk with previous C-section, previous placenta accreta/praevia; scarring -> malformation of decidua. Associated with placenta previa in 60%. Lack of hypoechoic basilar-myometrial margin. Low anterior placenta over uterine scar. Thinned/interrupted myometrium. Absent normal vascular channels in retroplacental region with increased retroplacental echogenicity. Irregular vascular spaces. Retroplacental vessels within bladder lumen. Difficult to differentiate between accreta/increta/percreta.
Insufficient foetal nutrition and oxygenation. From maternal systemic vascular abnormalitity (IDDM, collagen vascular disease, severe HTN) causing placental microinfarcts. Thinned placenta <20mm. Increased risk of foetal growth restriction and hypoxia. Placental infarcts are usually too small to be detected, when seen are usually hypoechoic 10-20mm, indistinguishable from venous lake or fibrin deposition. If more than 50% of placenta is affected then may cause placental insufficiency.
May occur via ascending infeection (more common) or haematogenous (transplacental) routes. Localised infection of the membranes (chorioamnionitis) causes PROM, premature delivery. May have purulent exudate within the amniotic fluid, vasculitis within the umbilical and foetal chorionic vessels with insufficiency.
Benign vascular placental mass from foetal circulation. Solid hypoechoic round/oval, occasionally septated placental mass. Usually close to chorionic plate, bulging into amniotic fluid, arterial waveforms at FHR is diagnostic. Vascular shunting may -> foetal high-output cardiac failure, hydrops esp with increased arterial flow.
Amniotic Band Syndrome
Early <10/40 disruption of amnion, enabling foetus to enter chorionic cavity. Foetus may entangle in fibrous bands crossing chorionic cavity with entrapment of parts. Mild to severe asymmetric and unusual patterns of deformities, including asymmetric absence of cranium, encephalocoeles, gastroschisis, truncal defects, spinal deformities, extremity amputations, tissue swelling, strangulation. Amniotic membrane not always seen. No increased risk with subsequent pregnancy.
(Uterine synechia). Shelf-like >2mm thick multilayered membranes projecting into uterine cavity with bulbous-free edge (characteristic), thinner midportion and thickened base, may have Y-shaped split at endometrial margin. Foetus can move freely about the sheet with no associated deformities. From folding of chorioamnionic membranes over an intrauterine adhesion. Increased risk with previous D&C, therapeutic abortion, endometritis. Increased risk of foetal malpresentation -> C-section.
Gestational Trophoblastic Disease (GTD)
(Hydatiform mole). Abnormal placental tissue with trophoblast proliferation, oedematous vesicular villi resembling bunch of grapes with inadequate vascularisation, variable degrees of hyperplasia/anaplasia. Hyperemesis gravidarum, HTN/preeclampsia, PV bleed, markedly elevated Î²hCG (>100,000 mIU/L), occasional thyrotoxicosis. 1:1,000-2,000 of pregnancies, higher in Asia/Latin America, young (teens) and old (40-50yo). Theca lutein cysts – large septated bilateral cysts massively enlarging ovaries in 50%, caused by ovarian hyperstimulation from Î²-hCG. DDx hydropic degeneration of placenta after spontaneous abortion (lower Î²hCG, no theca letein cysts, no live foetus), twins with separate sacs (one may contain a mole). 10% have persistent or invasive mole after curettage, hence HCG monitoring required.
- Noninvasive hydatiform mole (85%) – Usually benign, but potentially malignant. Uterus enlarged (50%), normal (35%) or small (15%) for dates. Usually diagnosed in 2nd T. May appear as anechoic fluid (mimics anembryonic pregnancy), echogenic or solid with through transmission (cystic villi from hydropic change).
- Complete/classic mole (70%) – Involves entire placenta, diploid 46 karyotype (all paternal genes from fertilisation of an empty ovum). Uterus filled with innumerable tiny cysts in 1st T, snowstorm of multiple echogenic foci. In 2nd T vesicles are larger at 2-30mm. Rarey contains foetal vessels/parts (embryo dies very early). 2.5% risk of choriocarcinoma.
- Partial mole (30%) – Involves a portion of the placenta, abnormal foetus (lethal), triploid 69 karyotype (fertilisation of ovum by two sperm). Vesicular change in portion of placenta. Multiple anomalies in triploid foetus. May not be obvious in 1st T. Increased risk of persistent molar disease, but less risk of choriocarcinoma.
- Invasive mole (chorioadenoma destruens, 13%) – Invasion of molar tissue into, but usually not beyond myometrium. Usually evident after treatment. Hydropic villi may embolise to lungs/brain etc, but do not grow in these organs and regress.
- Choriocarcinoma (2%) – Highly aggressive from trophoblasts without any villous structure. From trophoblastic cells derived 50% from hydatiform moles, 25% from abortions, 22% from normal pregnancies (intraplacental choriocarcinoma); rarely nongestational from germ cells in ovaries or even mediastinum. Rapid growth with extensive areas of haemorrhage, ischaemic necrosis, cystic softening. Doesn’t produce chorionic villi, mixture of syncytiotrophoblasts and cytotrophoblasts. Local invasion to myometrium, parametrium; haematogenous metastases to anywhere in body. Î²-hCG rising or plateua at 8-10/52 following molar pregnancy surgery suggests invasion or metastatic disease. US insensitive, myometrial nodules suggestive (but overlaps with degenerating fibroids and ovarian dysgerminomas). CT and MR shows an enlarged uterus, focal myometrial mass.
- Placental-site trophoblastic tumour (PSTT, <2%) – Tumour of extravillous (intermediate) trophoblast, normally found at nonvillous sites (implantation, islands within placenta, chorionic plate, membranes; cf syncytiotrohpoblast and cytotrophoblasts on chorionic villi). Moderately elevated Î²hCG. Diffuse infiltration of the endomyometrium. 1/2 from arise in normal pregnancy, 1/6 spontaneous abortion, 1/5 hydatiform mole.
Liquor in early pregnancy is dialysate of maternal serum; later is mostly foetal urine with a small amount of transudate from lungs. Turnover every 3hrs, foetus swallowing ~450mL/day. Water crosses membranes via osmosis. Fluid essential for normal development and maturation of lungs. Suspended particles in fluid is normal vernix (desquamated foetal skin), blood or meconium.
Subjective assessment of volume is as accurate as the objective/quantitative approach. Amniotic fluid index (AFI) is summation of vertical diameter of deepest pockets in the four quadrants, strictly perpendicular, not including pockets with foetal parts or umbilical cord. Normal 5-20cm (maximal in early 2nd T). In multiple gestations, the deepest pocket is used rather than AFI.
Excessive fluid >2L. Measured subjectively, AFI >20cm, deepest pocket >8cm, failure of foetal abdomen to contact anterior and posterior uterine walls after 24/40, may thin the placenta if severe, foetal parts too well seen. Associated with preterm labour, PROM, maternal discomfort. 33% idiopathic (usually mild), 25% associated with maternal disease (diabetes, preeclampsia, anaemia, obesity), 10% multiple gestation, 20% associated with foetal anomalies (1/2 of all anomalies are associated with polyhydramnios; eg anencephaly, encephalocoele, GI obstruction, abdominal wall defect, anchondroplaisa), 12% hydrops.
Fluid pockets small or absent, foetal parts crowded, surface features eg face difficult to visualise, AFI <5cm. Deepest pocket <1cm is severe. Causes include premature rupture of membranes (PROM), IUGR, GU anomalies (bilateral renal dysfunction/obstruction, bladder or outflow obstruction), foetal death >/= 5/7, ecclampsia, incorrect dates. Cx pulmonary hypoplasia (fluid required for normal development), esp when present in 2nd T.
Twins in 1/85 births. Increased morbidity and mortality including prematurity, polyhydramnios, congenital anomalies, discordant growth, cord accidents. Increased risk with monochorionic twins. Fraternal/nonidentical/dizygotic twins (from two ova) in 80%, may be different gender; identical/monozygotic twins in 20%. Dichorionic twins (Di-Di, 85%) have their own placentas (but fused in 1/2), are dizygotic or monozygotic with separation of blastomere within 1st day (20-30% of monozygotes). Monochorionic-diamniotic twins (Mono-Di, 70-75% of monozygotic with separation at 1-7 days’) share a placenta; usually have vascular anastomoses, hence at risk of twin-twin transfusion and embolisation syndromes. Monoamnionic (Mono-Mono, 1-3% of monozygotics with late separation at 7-13 days’) share a single amniotic cavity. Differentiation between types of twinning best performed in 1st T, include placental number (Di-Di if two), genders, interposed membranes (Di-Di is >/=2mm thick but may be falsely stretched by fluid, may have unfused amnion and chorion; Mono-Di thin and whispy ~1mm like spiderweb), twin-peak/lambda/triangle sign (Di-Di), volume of amniotic fluid, separate gestational sacs in 1st T (Di-Di). Fluid in each sac remains normal, AFI inacurrate so deepest pocket used. Foetal age can be estimated by averaging measurements between twins, picking the foetus age closed to menstrual dates or assigning dates from the larger foetus. Normal twins (any type) should parallel each other in size and growth (BPD within 5mm and interval growth within 3mm, HC within 15mm, AC limited by crowding, FL least affected by crowding and should be within 5mm), parallel singletons until 30/40 after which normal slowing should not go below 10th percentile of singletons.
- Twin-twin transfusion syndrome (TTS) – All monochorionic twins have vascular interconnections in placenta, most small and inconsequential. Significant shunting in 15-30% may cause minor discordance in growth to severe IUGR/anaemia in one twin, hydropic fluid overload in the other. Can occur any time after 1st T, usually not apparant until late 2nd/3rd T. Disparity in fluid volumes with larger twin polyhydramnios and the other virtually anhydramniotic (‘stuck twin’ with limited movement and membranes very close, compressed against uterine wall by amnion), persistent empty bladder. The other twin has increased fluid with persistent distended bladder and pelvicalyceal systems. Mortality up to 70%, worse in smaller twin, frequent follow-up required. Tx therapeutic amniocentesis in polyhydramnionic sac which may also permit reaccumulation in oligohydramnionic sac, laser ablation of placental vascular interconnections.
- Twin-twin embolisation syndrome – Uncommon Cx of one twin death in utero with dead twin blood products shunted to live twin -> DIC and multifocal tissue infarction. Risk reduces with time, but DIC may not be apparant until birth. Tx ablation of dead twin cord.
- Conjoined twins (<1%) separate >13 days. Most commonly thoracopagus (joined at chest), but can be anywhere from head to hips. If at abdomen, the combined umbilical cord may contain two sets of vessels.
- Acardiac twining – Twin reversed arterial perfusion (TRAP) similar to fetus in fetu, with the acardiac twin fed deoxygenated blood by umbilical-cord structure from other twin, blood supply is reversed (a->a, v->v). The acardiac twin has undeveloped head, upper extremities, thorax down to heart, marked skin thickening. Reversed flow through umbilical arteries and aorta, absent cardiac Doppler flow. Increased cardiac burden on the normal foetus can cause failure.
- Umbilical cord entanglement.
- Severe polyhydramnios of otherwise normal pregnancy of unknown aetiology.
Embryonic loss most common in 1st T, 20-25% in one twin, rarely in both. Many go undetected, vanishing twin sign (usually Di-Di) – in 1st T a second abnormal/distorted sac is seen, which disappears with time leaving singleton gestation. In the 2nd/3rd T foetal material less likely to disappear, with small thin remnant of bone/soft tissue at margins (papyraceus = ‘like paper’). In late 2nd/3rd T foetus undergoes autolysis and maceration, clearly visible and may obstruct delivery.
Uterus and Adnexae in Pregnancy
(Fibroids). Most common solid pelvic mass in pregnancy. Commonly enlarges and undergoes cystic degeneration from hormonal stimulation. Associated with malposition of gestational sac, miscarriage, bleeding, premature contractions, malpresentation, mechanical obstruction during labour; especially if in lower segment (hence should be followed). Compared to contractions which are transient (up to ~1hr), fibroids are more heterogeneous, persistent, bulge outer margin of uterine wall (as well as inner), splay myometrial vessels.
Corpus Luteal Cysts
Most common cystic pelvic lesions. Most corpus lutea are <30mm and resolve by mid 2nd T. Haemorrhage -> enlargement up to 100-150mm, internal echoes, septation. Most regress by 16-18/40. DDx benign cystic teratoma, cystadenoma, hydrosalpinx, paraovarian cyst.
Theca Lutein Cyst
From exaggerated corpus luteum response to Î²-hCG. Bilateral multicystic enlarged ovaries. Occur with gestational trophoblastic disease, multiple gestation, ovulation-inducing drugs.
Painless preterm cervical dilatation in absence of contractions. Congenital or secondary to cervical lacerations, excessive cervical dilatation, therapeutic abortion. Incapable of retaining pregnancy to term. Recurrent loss of pregnancy in 2nd T. US measures shortest closed endocervical length (best TV or translabially) with empty bladder in sagittal between internal os (V-shaped notch) and external os (triangular echogenicity). Normal cervical length is 30-50mm after 20/40, pathologically shortened if <25mm indicating incompetence. Endocervical canal dilatation with funneling (% = length of open portion / total length). Excessive probe pressure or full bladder may falsely increase length or reduce funelling. Cervical dilatation (between anterior and posterior canal) >8mm indicates incompetence. If complete, amniotic fluid, foetal parts or umbilical cord may descend with ‘hourglass deformity’ representing membranes bulging into vagina (suggets imminent pregnancy loss; notify Drs immediately and place patient in Trendelenburg position). TV scaning is not contraindicated, but should be inserted cautiously. Tx bedrest, tocolytics, cervical cerclage (through vagina around proximal 1/3 of cervix, unable to be done if foetal parts or cord already within canal).
Postpartum the uterus is large, spongy and easily compressible. Involution takes 6-7 weeks, most in 3-4 weeks. If too large, measurements from fundus to sacral angle then to cervix can be added. Normal postpartum endometrium is thin <15mm. Complications include:
- Endometritis – Tenderness, may have contain fluid or gas (but gas seen in 15% in normal 1st 3-4/52).
- Retained placenta.
- Ovarian vein thrombosis – Usually R-sided.
- Haematomas – Hypoechoic mass in anterior abdo wall or bladder flap (betw bladder and uterus) after C-section, if infected may not change until gas present.
Other disorders of Pregnancy
Preeclampsia is systemic maternal endothelial dysfunction with vasoconstriction (causing hypertension) and increased vascular permeability (oedema and proteinuria). Onset usually >34/40, earlier with hydatiform moles. 3-5% of women, increased risk with primiparas. Probably mediated by systemic release of a placenta derived factor, induced by abnormal placental trophoblastic implantation and lack of materal physiologic alterations (persistent small calibre spiral arteries) to adequetely perfuse the bed. This causes defective vascular development in the placenta and placental insufficiency. Hypercoagulable state. Improves with removal of the placenta. 20% of women develop HTN and microalbuminuria within 7 years, 2x increased risk of long-term vascular diseases of the heart and brain. Complications include:
- Retroplacental haemorrhages
- Eclampsia – Hyper-reflexia, convulsions, coma.
- Haemolysis, elevated liver enzymes and low platelets (HELLP syndrome) – In 10%, may be the primary manifestation of preeclampsia. Subclinical elevation of transaminases, bilirubin. Advanced disease may cause dysfunction and coagulopathy. Fibrin deposits within the periportal sinusoids with haemorrhage into the space of Disse, causing peirportal coagulative necrosis. Blood may coalesce forming a hepatic haematoma under Glisson’s capsule. This may rupture with catastrophic bleeding. Tx for severe disease is TOP.
- Kidneys – Fibrin within glomeruli and capillaries, when advanced may cause bilateral renal cortical necrosis.
- Brain – Microscopic haemorrhages, small vessel thromboses. Also seen in the heart and anterior pituitary.
Pre-existing insulin dependent diabetes increases risk of foetal anomalies, no increased risk in gestational onset diabetes. Increased subcutaneous fat, perinephric fat, glycogen stores (enlarged liver, thickened interventricular septum >5mm measured during diastole which may -> obstructive cardiomyopathy).