5.6 Pre-Eclampsia Flashcards
How do you define preeclampsia
Preeclampsia is described as
hypertension (> 140/90 mmHg)
+
significant proteinuria*
that develops after 20 weeks of gestation;
although preeclampsia can develop without proteinuria
and eclamptic fits can occur
with a minimally elevated blood pressure.
oedema is no longer part of the definition although it is often present.
*Significant proteinuria ?
- Urine Protein: Creatinine (PCR) > 30 mg/mmol (oR)
- Total protein excretion ≥ 300 mg per 24-hr collection of urine (oR)
- Two specimens of urine collected ≥ 4 hours apart
with ≥ 2+ on the protein reagent strip.
24-hour proteinuria is difficult to measure and
has been replaced by PCR
(protein creatinine ratio).
Where does the morbidity lie
What is important is the fact that preeclampsia is linked to
eclampsia,
HELLP
(haemolysis, elevated liver enzymes, and low platelet count)
most probably AFLP (acute fatty liver disease of pregnancy).
Some statistics
- Preeclampsia occurring before 30 weeks of pregnancy
is associated with severe morbidity
- Preeclampsia occurring before 30 weeks of pregnancy
- Up to 30% can occur after delivery (up to 6 weeks post-delivery)
- Occurs in 5%–6% of pregnancies overall
and up to 25% of hypertensive mothers
- Occurs in 5%–6% of pregnancies overall
- 1%–2% women with PET will develop eclampsia
Could you explain the pathophysiology?
A two-stage process into the pathogenesis has been explained.
- An abnormal placentation along
with endothelial dysfunction gives rise to the
spectrum of the disease. - Preeclampsia is linked to a failure of placentation,
which occurs early in pregnancy and
results in the placenta becoming hypoxic. - This leads to an immune reaction
with secretion of upregulated inflammatory mediators
from the placenta causing vascular endothelial
cell damage and dysfunction.
stage 1
Abnormal placentation and vascular remodeling
=
decreased placental perfusion
Maternal factors
* Genetic
* Behavioral
* Environmental
Stage 2
Maternal syndrome of preeclampsia
with endothelial dysfunction
Resulting endothelial dysfunction produces
an imbalance of pro- and antiangiogenic factors,
with an increase in anti-angiogenic factors.
It should be noted that these biomarkers
do not have sufficiently high positive predictive
value when used alone.
The typical hypertension which is the cardinal diagnostic feature of pre-eclampsia is a
result of the production of endogenous vasoconstrictors as a means of ensuring that
uteroplacental perfusion is sustained. It is mediated by circulating vasoactive humoral
compounds (these have been identified in blood, placenta and amniotic fluid)
Pro-angiogenic factors
Anti-angiogenic factors
+
Vascular Endothelial Growth Factor (VEGF)
Placental Growth Factor (PlGF)
Placental protein 13 (PP-13)
Pregnancy-associated plasma protein A (PAPP-A)
-
Soluble fms-like tyrosine kinase-1 receptor (sFlt-1)
Soluble Endoglin (sEng)
Asymmetric Dimethylarginine (ADMA)
Sequelae of disease
The maternal syndrome of preeclampsia is
characterised by decreased perfusion
due to vasospasm and activation of coagulation cascade with
microthrombi formation and end organ damage.
- Fluid shift:
Leaky capillaries together with a low oncotic pressure
result in a low intravascular volume and
fluid shift into the interstitial compartment
- Fluid shift:
- Vasoconstriction:
The generalised vasoconstriction will mean increased
systemic vascular resistance
- Vasoconstriction:
and in severe preeclampsia increased pulmonary pressure;
also renal, hepatic, and pancreatic dysfunction.
Vasospasm in the cerebral vasculature causes seizures and intracerebral
bleeds.
- Decreased placental blood flow:
The compromised placental blood flow
will result in IUGR (intrauterine growth retardation),
fetal distress,
the high blood pressure increases the risk of placental abruption
What risk factors are associated with the development of preeclampsia?
- Pregnancy associated factors
First pregnancy
Multiple pregnancy
Donor insemination
Molar pregnancy
Chromosomal abnormalities
___________________________
- Maternal factors
> 35 years
< 25 years
Family history of preeclampsia
Prior history of preeclampsia
(20% will develop PET in subsequent pregnancy,
2% eclampsia)
Booking diastolic blood pressure of 80 mmHg or more
Associated diabetes, obesity, chronic hypertension, and renal disease
Antiphospholipid antibodies/factor V Leiden
___________________________
Paternal factors
First-time father
Previous history of preeclampsia
How would you manage a preeclamptic woman?
Preeclampsia requires multidisciplinary team management,
and effective communication with midwives and obstetrician is crucial.
The mother should be reviewed regularly
by the whole team and the treatment plan clearly
written in the notes.
Aim
The aim is to stabilise the blood pressure until the decision to deliver is taken
whilst monitoring for signs of severe preeclampsia.
Before 34 weeks, two doses of steroids are given
to the mother to improve fetal lung maturity.
__________________________________________
Monitoring
* BP, RR, SpO2, urine output recorded on a MEoWS chart
- Strict input/output chart (fluid balance)
- Fetal monitoring in the form of cardiotocography
Vigilance
Clinical examination looking for photophobia, headache, epigastric pain,
hyperreflexia and other signs and symptoms of eclampsia
__________________________________________
Treatment
* Control of hypertension
- Prevention and control of eclamptic seizures
The Royal College of obstetricians and Gynaecologists (Green top guideline
10A) and National Institute for Health and Care Excellence (NICE CG 107)
have produced guidelines setting specific criteria for the treatment of
preeclampsia including the method for measuring blood pressure.
Discuss the medical management of hypertension in pregnancy.
The evidence base for treatment of mild to moderate chronic hypertension
in pregnancy resides in maternal benefit rather than clear evidence of
an enhanced perinatal outcome for the baby.
NICE suggests treating only moderate and severe hypertension (BP > 150 mmHg systolic and
100 mmHg diastolic pressure) and recommends
- Labetalol as the first line.
- Methyldopa
- Nifedipine
- Hydralazine
- Alpha Blockers
- Beta Blockers
- Diuretics
- Magnesium Sulphate
- Labetalol
Route and dose:
Oral—200–1600 mg in divided doses;
IV—50 mg bolus followed by titrated infusion
Mode of action:
Combined specific α1 and nonspecific β adrenoceptor antagonist.
The ratio of α:β blocking effects depend on
the route of administration—
1:3 for oral and 1:7 for intravenous
Side effects:
Bradycardia, fatigue, bronchospasm, gastrointestinal disturbances
Contraindication and caution:
Asthma, cardiac disease, phaeochromocytoma
- Methyldopa
Route and dose:
Oral only—250 mg–3 g/day in divided doses
Mode of action:
Acts as false neurotransmitter to norepinephrine
Side effects:
Postural hypotension, bradycardia, headache, haemolytic anaemia
Contraindication and caution: Liver disease, risk of postnatal depression
Nifedipine
Route and dose:
Oral only—20–90 mg od (Avoid sublingual route)
Mode of action:
Calcium channel antagonist.
Blocks the entry of calcium ions
through the L-type channels.
Side effects:
Headache, tachycardia, flushing, and visual disturbances
Contraindication and caution:
Aortic stenosis, liver disease
