8.1 Placental Failure Flashcards by tzeyee yeo

The human placenta receives ~500mL/min of blood at term, with an ~11m2 total surface area for gas and nutrient exchange:
• Optimal placental function and development are needed for optimal foetal growth
• Abnormal placentation occurs due to ___________________
• Causes a small placenta with morphological changes (e.g. infarcts, basal haematomas)

total/patchy failure of trophoblast invasion of myometrial segments of spiral arteries:

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what is the presentation of acute placental failure?

Placental abruption (abruptio placentae)

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What is the presentation of chronic placental failure?

Intrauterine growth restriction (IUGR), hypertensive disorders of pregnancy (e.g. gestational hypertension, pre-eclampsia)

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what are causes of placental abruption?

Poor trophoblastic invasion (e.g. in pre-eclampsia)
Direct abdominal trauma (e.g. road traffic accidents, assault)
External cephalic version (manually turn baby from breech to cephalic presentation)
Uterine overdistension and sudden decompression (e.g. polyhydramnios, multiple gestation)
Other causes: cocaine use, anticoagulant therapy

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what is the presentation of placental abruption?

The classical presentation of placental abruption is severe constant abdominal pain, and may or may not include vaginal bleeding and uterine contractions:

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why is there abdominal pain during placental abruption?

extravasation of blood into the myometrium

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what is the presentation of silent/ unusual placental abruption?

Nausea, restlessness, backache, diarrhoea, urge to defecate, feeling faint (hypovolaemia); no blood loss per vaginum, bleeding not seen externally (blood hidden behind placenta /within amniotic cavity)

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what is the presentation of major placental abruption?

Signs of hypovolaemic shock, tachycardia, hypotension, signs of peripheral vasoconstriction

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What would qualify as grade 0 of placental abruption?

Asymptomatic with diagnosis made retrospectively/postnatally; finding on delivered placenta of organised retroplacental blood clot or depression on maternal surface of placenta (retroplacental centre → haematoma)

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What would qualify as grade 1 of placental abruption?

Absent/minimal vaginal bleeding with no foetal/maternal compromise

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What would qualify as grade 2 of placental abruption?

Absent/moderate vaginal bleeding with some maternal evidence of blood loss (hypotension, tachycardia) and may be associated with foetal distress

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What would qualify as grade 3 of placental abruption?

Absent/severe vaginal bleeding with maternal symptoms (hypovolaemic shock) and compromise and intrauterine foetal death

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how does placental abruption feel like on palpation?

On palpation: classical finding of ‘woody hard’/firm abdomen and tender to touch (blood seeping into the myometrium)
Uterus may be large for gestation (due to blood inside) and the foetus is often difficult to palpate

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what are the maternal effects of placeta abruption?

Postpartum haemorrhage (PPH): due to poorly contracting Couvelaire uterus and coagulation failure (DIC)
• Predisposing: multiparity, multiple gestation, polyhydramnios
Hypovolaemic shock: occurs in major abruptions
• Shock may be disproportional to haemorrhage in concealed form
• Associated with tachycardia, hypotension, maternal collapse
• DIC occurs in 0.1% of cases (secondary phenomenon following trigger to generalised activation of coagulation system)
Acute renal failure: hypovolaemia, hypotension, DIC → poor perfusion
• Prognosis is extremely good with adequate/prompt resuscitation
Maternal death (rare event with appropriate management)
Risk of recurrence in future pregnancies (~6 – 17% after a single episode; increases to 25% after 2 episodes)

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What are the foetal effects of placental abruption?

Feto-maternal haemorrhage: small amount of foetal and maternal cells travel across placental barriers in normal pregnancy
• Large volume of foetal blood transferred into maternal circulation in abruption → foetal movement anaemia and foetal death
• Loss of ≥ 20% of foetal blood volume → fatal hypovolaemia
• Rhesus isoimmunisation in Rh-negative mothers
Hypoxic ischaemic encephalopathy (HIE) → cerebral palsy and death
• Hypovolaemia and reduced oxygenation (secondary to poor gas exchange at placental surface) → hypoxic injury to foetal brain
Intrauterine growth restriction (IUGR):
• Inadequate trophoblast invasion of maternal decidua and spiral arteries → pre-eclampsia
• Chronic/recurrent small abruption → reduction of functional placenta → IUGR (reduced foetal growth)
Foetal death (4 – 67% depending on the severity of abruption, interval to delivery, gestational age, reserves of foetus)

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what is the effect of prostacyclin on myocyte contractility and platelet aggregation?

Vasodilatory → reduces myocyte contractility and performance and inhibits platelet aggregation

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what is the effect of thromboxane of prostacyclin on myocyte contractility and platelet aggregation?

Vasoconstrictive → affects myocyte contractility and stimulates platelet aggregate (promotes clot formation)

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Chronic placental failure is associated with _____________ (aetiology is not clearly understood) leading to local alteration of _____________
• Prostacyclin produced by trophoblasts decreases → ratio favours thromboxane → local vasoconstriction and platelet agglutination on the undilated spiral arteries

In normal pregnancy, the utero-placental circulation has a high flow, low impedance and thin walls → poses extremely low resistance to flow and exchange:
• Continuous narrowing/clotting of abnormal vessels causes further increase in _______________ and _____________ → compromises foetal growth
• Commonly results in _____________________

defective trophoblastic invasion;

prostacyclin : thromboxane ratio;

peripheral resistance (hypertension);

uteroplacental ischaemia;

intrauterine growth restriction (IUGR) and pre-eclampsia

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what happens to blood pressure from early pregnancy to 2nd trimester?

Decrease (nadir/lowest point reached by 22 – 24 weeks)

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what happens to blood pressure from 2nd trimester to term?

Steady rise to pre-pregnancy levels

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what happens to blood pressure postpartum?

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Decreases immediately → rises (peaks at day 3 – 6)
• Period of vasomotor instability while non-pregnant vaso-regulation is re-established
• Normotensive women may be transiently hypertensive post-delivery due to return of normal vascular tone

what is the time frame of pre-existing/ chronic hypertension?

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HTN predating/presents < 20 weeks gestation OR persists > 12 weeks postpartum; no proteinuria

what is the time frame of pregnancy induced/ gestational hypertension?

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New onset of mild HTN > 20 weeks gestation and resolves < 12 weeks postpartum; no proteinuria or other signs of PE

what is the time frame of preclempsia?

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New onset of HTN & proteinuria (± other signs of organ damage) > 20 weeks gestation → pregnancy-specific multisystem disorder
• May arise de novo or superimposed on chronic HTN or gestational HTN

Pre-eclampsia (PE) is a hypertensive disorder caused by impaired placentation leading to inactivation/dysfunction of vascular endothelial cells and co-existent platelet activation: • Defined as _____________________ (if PE < 20 weeks, suspect molar pregnancy) • Alternatively defined as ___________________ (thrombocytopenia, renal insufficiency, impaired liver function, pulmonary oedema, cerebral/visual symptoms)

new onset of HTN and proteinuria > 20 weeks gestation; HTN in absence of proteinuria (rare) with new onset of signs of organ damage

PE presents with the classic triad of hypertension, proteinuria, and oedema (but absence of any of the 3 does not preclude diagnosis): Hypertension: Elevation of BP ___________ (systolic) and/or ____________ (diastolic) on 2 occasions at least 6 hours apart or BP > _______________ on single occasion: • Device (gold standard): ____________________ o Phase V (disappearance) rather than phase IV (muffling) of Korotkoff sounds should be taken as diastolic reading • Posture: woman sitting/ __________________ with correct cuff size *BP taken supine during the late 2nd/3rd trimesters will be lower due to _________________

≥ 140 mmHg; ≥ 90 mmHg; 160/110 mmHg; mercury sphygmomanometers; lying on her side (30° tilt) with upper arm at the same level as the heart; decreased venous return to the heart (pressure from gravid uterus)

PE presents with the classic triad of hypertension, proteinuria, and oedema (but absence of any of the 3 does not preclude diagnosis): Proteinuria: Indicates glomerular damage (almost always occurs after hypertension): • Gold standard: ___________________ (proteinuria usually 1 – 3g daily; 50 – 60% being albumin → severe cases may exceed 15g of protein) • ______________ (PCR) with cut-off of 30mg/mmol is recommended for confirmation or exclusion of proteinuria when PE is suspected • Dipstick is not accurate to confirm/exclude significant proteinuria Oedema: Weight gain of ________ in any one week OR ______ in any one month: • Clinical oedema is present in ~2/3 of patients with pregnancy-induced HTN (but 2/3 of pregnant women with clinical oedema do not develop hypertension) • Oedema is a less specific symptom for pre-eclampsia

urinary protein > 0.3g (> 300mg) in 24h collection; Spot urine protein/creatinine ratio; > 1kg; > 2.25kg

Pathogenesis of Pre- eclempsia 1. Abnormal placentation: Abnormal __________ → spiral arteries in placental bed do not undergo the normal vascular remodelling → fail to adapt to become ______________ vessels: • Invading placenta is unable to optimise its blood supply from the maternal uterine vessels • ____________ is the common feature in PE 2. Maternal response: Normal pregnancy is associated with systemic inflammatory response which is exacerbated in PE (higher levels of pro-inflammatory cytokines associated with endothelial dysfunction): • Endothelial cell activation → increased _________ + increased endothelial expression of _______________ + platelet activation, increased vascular tone • Reduction in prostacyclin synthesis and increase in thromboxane A2 (TXA2) synthesis → ______________→ platelet activation and vasoconstriction → widespread microvascular damage and dysfunction → HTN, proteinuria, hepatic disturbance

trophoblastic invasion; high capacitance and low resistance; Uteroplacental ischaemia ; capillary permeability; adhesion molecules and prothrombotic factors' reversed prostanoid balance

What are angiogenic factors that are present in physiologic conditions and normal pregnancy: maintain endothelial health by interacting with their endogenous endothelial receptors

VEGF and TGF-β1

What are anti angiogenic factors that are present weeks before onset of PE

Weeks before onset of PE: ↑ sFlt1 & sEng, ↓ platelet growth factor (PlGF) in maternal circulation

What are anti angiogenic factors that are present during PE

sFlt1 & sEng secreted by placenta in excess → antagonise VEGF & TGF-β1 signalling → systemic endothelial dysfunction

What are the effects of PE on the kidneys?

1. Glomerular capillary endotheliosis: endothelial cell swelling, loss of fenestrations, occlusion of capillary lumen • Proteinuria (due to glomerular damage) • Reduced GFR → reduced uric acid clearance, increased plasma creatinine levels, oliguria (reduced urine output) 2. Acute renal failure

What are the effects of PE on the liver?

1. HELLP syndrome (Haemolysis, Elevated Liver Enzymes, Low Platelet Count) • Subendothelial fibrin deposits + periportal haemorrhages + ischaemic patches → elevated liver enzymes

What are the effects of PE on the blood?

1. Disseminated intravascular coagulation (DIC): from increased thromboxane A2 levels → platelet aggregation & clumping → thrombocytopenia * Dilutional anaemia of pregnancy is not seen in pre-eclampsia

What are the effects of PE on the brain?

1. Cerebral oedema & vasospasm (secondary to endothelial cell dysfunction → may progress to eclampsia in severe forms) 2. Hashimoto’s thyroiditis (HT) encephalopathy (encephalopathy, thyroid autoimmunity, good clinical response to steroids) 3. Ischaemia & infarction 4. Haemorrhage

What are the effects of PE on the placenta & foetus?

1. Characteristic placental bed vasculature lesions: atherosis of spiral arteries (fibrinoid necrosis of vessel wall, lipid macrophages, mononuclear infiltrate) with platelet microaggregates and larger thrombosis → placental failure → IUGR 2. Preterm delivery 3. Placental abruption

What are the effects of PE on the CVS ?

1. Reduced plasma volume + increased systemic vascular resistance & arterial pressure 2. Decreased/unchanged pulmonary capillary wedge pressure (measures LA pressure) 3. Decreased central venous pressure 4. Usually unchanged contractility

What are the effects of PE on the lungs?

1. Pulmonary oedema (leaky capillaries) → ARDS

what is the ultrasonographic definition of IUGR?

expected birth weight (EBW) < 10th percentile OR EBW < 2SD of the mean OR ponderal index (PI → index of weight in relation to height/length) < 10th percentile

what is the period in which growth of foetus is via hyperplasia (rapid mitosis)?

4-20 weeks

what is the period in which growth of foetus is via hyperplasia (mitosis is slower) + hypertrophy (cells become larger?

20-28 weeks

what is the period in which growth of foetus is via hypertrophy?

28-40 weeks

what is the cause of a small symmetric baby at 4- 20 weeks? what is the treatment? what are the foetal parameters?

- Congenital malformations, intrauterine infections - usually not corectable - Weight, HC, AC, FL < 10th centile*

what is the cause of a small asymmetric baby after 28 weeks? what is the treatment? what are the foetal parameters?

- Maternal, foetal, placental factors - Normal HC & FL but reduced AC (brain-sparing effect): Reduced O2 transfer to the foetus and impaired CO2 excretion → chemoreceptor response in foetal carotid body → vasodilation in foetal brain, myocardium, adrenals; vasoconstriction in kidneys, splanchnic vessels, limbs → brain-sparing with reduced abdominal girth and oligohydramnios - May be treatable (e.g. HTN)

what is the cause of a small combined baby early 2nd trimester? what is the treatment? what are the foetal parameters?

- Chronic maternal disorders (severe chronic HTN, lupus nephritis, vascular disease) - Usually not correctable (worst prognosis) - Initially symmetric → later asymmetric

what is a gravidogram?

serial measurement of symphysis-fundal height (SFH) to gestational age in weeks

How is symphysis fundal height measured?

SFH is measured using tape from the upper border of the pubic symphysis to the uterine fundus (normal SFH: increase by ~1cm/week between 14 – 32 weeks; normal is ± 2cm of the week from 24 weeks) o Lag of 2 – 4cm in SFH may suggest IUGR (less than expected for gestational age)

where is blood flow measured to assess uteroplacental and fetoplacental circulations in IUGR?

• Absent end-diastolic (ED) umbilical artery flow: foetal hypoxia (likely indicates high placental pressure blocking flow) • Reversed ED umbilical artery flow: worsening foetal status and impending demise • MCA: detecting the brain-sparing effect of asymmetric IUGR

what are the complications of IUGR?

IUGR presents with the antepartum risks of oligohydramnios, chronic foetal hypoxia and intrauterine foetal demise.

What is the management of IUGR?

There is currently no therapy available to reverse IUGR → only intervention possible in most cases is delivery of the foetus (via induced delivery or C-section): • Principle: when the risk of intrauterine existence > risk of extrauterine existence → deliver the baby • If there is foetal growth (even along the 3rd centile), continue weekly foetal surveillance until 38 weeks then deliver the baby • Substantial increase in perinatal morbidity (3x) and mortality (8x) in IUGR neonates

8.1 Placental Failure Flashcards

(50 cards)