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Woman's Health > 8.1 Placental Failure > Flashcards

8.1 Placental Failure Flashcards

1
Q

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)

A

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

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2
Q

what is the presentation of acute placental failure?

A

Placental abruption (abruptio placentae)

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3
Q

What is the presentation of chronic placental failure?

A

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

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4
Q

what are causes of placental abruption?

A
  • 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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5
Q

what is the presentation of placental abruption?

A

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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6
Q

why is there abdominal pain during placental abruption?

A

extravasation of blood into the myometrium

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7
Q

what is the presentation of silent/ unusual placental abruption?

A

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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8
Q

what is the presentation of major placental abruption?

A

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

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9
Q

What would qualify as grade 0 of placental abruption?

A

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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10
Q

What would qualify as grade 1 of placental abruption?

A

Absent/minimal vaginal bleeding with no foetal/maternal compromise

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11
Q

What would qualify as grade 2 of placental abruption?

A

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

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12
Q

What would qualify as grade 3 of placental abruption?

A

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

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13
Q

how does placental abruption feel like on palpation?

A
  • 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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14
Q

what are the maternal effects of placeta abruption?

A
  1. Postpartum haemorrhage (PPH): due to poorly contracting Couvelaire uterus and coagulation failure (DIC)
    • Predisposing: multiparity, multiple gestation, polyhydramnios
  2. 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)
  3. Acute renal failure: hypovolaemia, hypotension, DIC → poor perfusion
    • Prognosis is extremely good with adequate/prompt resuscitation
  4. Maternal death (rare event with appropriate management)
  5. Risk of recurrence in future pregnancies (~6 – 17% after a single episode; increases to 25% after 2 episodes)
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15
Q

What are the foetal effects of placental abruption?

A
  1. 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
  2. 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
  3. 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)
  4. Foetal death (4 – 67% depending on the severity of abruption, interval to delivery, gestational age, reserves of foetus)
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16
Q

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

A

Vasodilatory → reduces myocyte contractility and performance and inhibits platelet aggregation

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17
Q

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

A

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

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18
Q

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 _____________________

A

defective trophoblastic invasion;

prostacyclin : thromboxane ratio;

peripheral resistance (hypertension);

uteroplacental ischaemia;

intrauterine growth restriction (IUGR) and pre-eclampsia

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19
Q

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

A

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

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20
Q

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

A

Steady rise to pre-pregnancy levels

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21
Q

what happens to blood pressure postpartum?

A

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

22
Q

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

A

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

23
Q

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

A

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

24
Q

what is the time frame of preclempsia?

A

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

25
Q

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)

A

new onset of HTN and proteinuria > 20 weeks gestation;

HTN in absence of proteinuria (rare) with new onset of signs of organ damage

26
Q

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 _________________

A

≥ 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)

27
Q

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

A

urinary protein > 0.3g (> 300mg) in 24h collection;

Spot urine protein/creatinine ratio;

> 1kg;

> 2.25kg

28
Q

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
A

trophoblastic invasion;

high capacitance and low resistance;

Uteroplacental ischaemia ;

capillary permeability;

adhesion molecules and prothrombotic factors’

reversed prostanoid balance

29
Q

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

A

VEGF and TGF-β1

30
Q

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

A

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

31
Q

What are anti angiogenic factors that are present during PE

A

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

32
Q

What are the effects of PE on the kidneys?

A
  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
33
Q

What are the effects of PE on the liver?

A
  1. HELLP syndrome (Haemolysis, Elevated Liver Enzymes, Low Platelet Count)
    • Subendothelial fibrin deposits + periportal haemorrhages + ischaemic patches → elevated liver enzymes
34
Q

What are the effects of PE on the blood?

A
  1. Disseminated intravascular coagulation (DIC): from increased thromboxane A2 levels → platelet aggregation & clumping → thrombocytopenia
    * Dilutional anaemia of pregnancy is not seen in pre-eclampsia
35
Q

What are the effects of PE on the brain?

A
  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
36
Q

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

A
  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
37
Q

What are the effects of PE on the CVS ?

A
  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
38
Q

What are the effects of PE on the lungs?

A
  1. Pulmonary oedema (leaky capillaries) → ARDS
39
Q

what is the ultrasonographic definition of IUGR?

A

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

40
Q

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

A

4-20 weeks

41
Q

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

A

20-28 weeks

42
Q

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

A

28-40 weeks

43
Q

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

A
  • Congenital malformations, intrauterine infections
  • usually not corectable
  • Weight, HC, AC, FL < 10th centile*
44
Q

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

A
  • 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)
45
Q

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

A
  • Chronic maternal disorders (severe chronic HTN, lupus nephritis, vascular disease)
  • Usually not correctable (worst prognosis)
  • Initially symmetric → later asymmetric
46
Q

what is a gravidogram?

A

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

47
Q

How is symphysis fundal height measured?

A

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)

48
Q

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

A

• 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

49
Q

what are the complications of IUGR?

A

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

50
Q

What is the management of IUGR?

A

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

Woman's Health (29 decks)

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