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Preeclampsia
1.
2.
3. The National High Blood Pressure Education Program (NHBPEP) Working
Group defines HYPERTENSION in PREGNANT WOMAN:
systolic blood pressure (BP) of 140 mmHg or higher
diastolic BP of 90 mmHg or higher
on more than 1 occasion
5. Primiparity Immunologic factors Previous pregnancy complicated by
Preeclampsia/Eclampsia/HELLP
Family history of Preeclampsia BMI Pregnancy related conditions
7. Stage 0
3-8 weeks
Stage 1
8-18 weeks
Stage 2
20 weeks to
birth
Poor Immunoregulation
Inadequate tolerance to feto-paternal antigens
during conception and implantation
Poor Placentation
Deficient trophoblast invasion and spiral artery
remodelling
Clinical manifestation
Over activation of maternal endothelium and
systemic inflammatory network
Oxidative Stress
Endoplasmic reticulum Stress
Inflammatory Stress
8. invasive cytotrophoblasts
of fetal origin invade the
maternal spiral arteries
transforms them from
small-caliber resistance
vessels to high-caliber
capacitance vessels
capable of providing
placental perfusion
adequate to sustain the
growing fetus
Normal Pregnancy
9. cytotrophoblasts fail to adopt an invasive
endothelial phenotype
invasion of the spiral arteries is shallow and they
remain small caliber, resistance vessels
placental ischemia
Preeclampsia
10. Soluble Flt-1 (sFlt-1) causes endothelial
dysfunction by antagonizing vascular
endothelial growth factor (VEGF) and
placental growth factor (PlGF)
In normal pregnancy, the placenta
produces modest concentrations ofVEGF,
PlGF, and soluble Flt-1
In preeclampsia, excess placental soluble
Flt-1 binds circulatingVEGF and PlGF and
prevents their interaction with endothelial
cell-surface receptors
decreased prostacyclin
nitric oxide production
release of procoagulant
proteins
ENDOTHELIAL
DYSFUNCTION
13. Gestational HPN
• Previously normal BP
• Elevated BP without proteinuria
• Develops after 20 weeks of gestation and BP normalizes 12 weeks postpartum
Preeclampsia
• Previously normal BP
• Elevated BP with proteinuria
• Develops after 20 weeks of gestation and BP normalizes 12 weeks postpartum
Eclampsia
• Hypertension in pregnancy with proteinuria along with convulsions
• Preeclampsia with occurrence of grand mal seizures
14. Chronic HPN
• Previously elevated BP
• Use of antihypertensive medications before pregnancy
• Develops before 20 weeks of gestation and
• BP elevation persists longer than 12 weeks postpartum
Chronic HPN with
Superimposed
Preeclampsia
• Previously elevated BP or persists postpartum with associated signs and symptoms of
preeclampsia
• Develops before 20 weeks of gestation with new-onset proteinuria
• Development of HELLP syndrome
15. Ideal: mercury manometer
• Alternative: aneroid, digital, or other automated devices
• Cuff should cover: 2/3 of arm or at least 80% of pt’s arm circ
Position: seated, supine, or left lateral recumbent position
• Should be rested at least 5-10 minutes
• Not smoked or ingested caffeine 30 min. before measurement
Bladder is inflated 30 mmHg above point of radial pulse
extinction
• Deflation: 2 mmHg per beat
16. Systolic BP: 1st clear tapping sound (Korotkoff phase I)
• Diastolic BP: disappearance of tapping sounds (Korotkoff phaseV) OR
• Present near 0: softening of sounds (Korotkoff phase IV)
If BP taken for the 1st time: take BP of both arm, subsequent
determination is done on the arm with higher BP
• Arm with the higher values will be used for all BP measurements
For white coat HPN: ambulatory BP monitoring
• Instruct proper BP monitoring if BP monitoring is done at home
17. Screening maneuvers
• Mean Arterial Pressure
• Roll over test
• MAP-2 with Roll over test
• 48 hour BP monitoring
• 24 hours ambulatory BP
with heart rate
• Hyperbaric Index
Laboratory Test
• Doppler Velocimetry
• Fibronectin
• Hematocrit
• Proteinuria
• Serum uric acid
LaboratoryTest
• Hemoglobinuria
• Masternal Serum AFP
• Hypocalciuria
• Glucose intolerance
• Inhibin A
Others:
biochemical markers
18.
19. Calcium Supplementation
Dose: 1.5 to 2 g per day before 32 weeks AOG until delivery
Antiplatelet agents
ASA or dipyridamole: reduce risk of preeclampsia by 17%
Insufficient evidence on others
Antioxidants, nitric oxide, rest, exercise, diuretics, ↓ed salt intake, marine oil, prostaglandin
20. PREECLAMPSIA
MILD No manifestations of any of severe preeclampsia
SEVERE
BP SBP ≥ 160 or
DBP ≥ 110
Laboratories
Elevated serum creatinine
Thrombocytopenia
Hepatocellular dysfunction (↑ed AST and ALT)Pulmonary edema
Microangiopathic hemolysis
Urine
≥5 g/24h or ≥ 3 in 2 random urine sample (q4h)
Oliguria <500ml/24h
IUGR or Oligohydramnios
Symptoms of End-organ involvement
Headache
Visual disturbances
Epigastric pain or RUQ pain
21. Criteria for home health care
Ability to comply with recommendation
Diastolic BP <100 mm Hg
Systolic BP <140 mm Hg
Proteinuria < 1,000 mg/24 hr OR < 2+ on dipstick
Platelet count > 120,000/mm
Normal fetal growth and testing
No indications for delivery
22. TimingofDelivery Gestational Age
≥ 40 weeks
• Bishop score > 5
• Fetal weight < 10th percentile
• Non-reactive non-stress test (NST)
Gestational Age
≥ 37 weeks with:
• Labor
• Rupture of membranes
• Vaginal bleeding
• Abnormal biophysical profile
• Criteria for severe preeclampsia
Gestational Age
≥ 34 weeks with:
DELIVER
Expectant management: remote from term with mild preeclampsia
23. Maternal and fetal well-being at least once weekly
• BP each visit
• Platelet count and liver enzymes at regular intervals
• NST at regular interval
• Fetal growth every 2 to 3 weeks
MEDICATIONS
Anti-HPN meds will be given only if there is an increase in
BP reading.
Not recommended:
• Magnesium sulfate and other anti-convulsants
• Low-dose aspirin and high dose calcium for prevention
of progression to severe preeclampsia
24. 5-6% of all pregnancies worldwide
5-10% - severe
Local incidence: 2-5%
2nd most common cause of maternal death
High perinatal mortality and morbidity rate: Iatrogenic prematurity
Definitive treatment: Delivery of fetus and placenta
25. CNSDysfunction
• Blurred
vision
• Scotomata
• Altered
mental
status
• Severe
headache
Livercapsuledistentionor
rupture
• Persistence
right
quadrant
pain
• Epigastric
pain
Bloodpressurecriteria
• Sitting
SBP ≥160
mm Hg
• DBP ≥110
mm Hg
• * On 2 separate
occasions at rest or
at least 6 hours
apart
Eclampsia
• Generalized
seizure
• Unexplained
coma in
setting of
preeclampsia
in absence of
neurologic
d/o
26. Pulmonaryedemaorcyanosis
• Excessive
fluid
accumu-
lation in
the lungs
Cerebrovascularaccident(CVA)
• Acute loss
of brain
function
• Altered
mental
status
• coma
CorticalBlindness
• Partial or
total loss of
vision in
normal
appearing
eye
IUGR
• EFW < 5
percentile for
gestational
age
• EFW <10
percentile for
gestational
age with
evidence of
fetal
compromise
CoagulopathyandThrombocytopenia
• Prolonged
prothrombin
time: >1.4s
• Low
fibrinogen:
<300 mg/dl
• Low
platelet:
<100,000
mm3
Due to disturbance
of vasculature that
supplies the brain
Damage to the
visual region of
occipital cortex
27. Proteinuria
• >5 g per 24h
or ≥3+ on 2
random
urine
samples
collected at
least 4 hours
apart
Oliguriaand/orRenalFailure
• Urine output
<500 ml per
24h
• Serum
creatinine:
>1.2 mg/dl
HELLPSyndrome
• Hemolysis:
• Abnormal
peripheral smear
• total bilirubin >1.2
mg/dl
• LDH >600 U/L
• Elevated liver
enzyme:
• ALT > 70 U/L
• LDH > 600 U/L
• Low platelet:
• Platelet <100,000
mm3
Hepatocellularinjury
• Serum
transaminase
≥ 2x the
normal
29. Objectivesofmanagement Reduce severity or prevent progression of disease process
Prevent convulsions
Control severe hypertension
Deliver the fetus at the optimum time and with the least trauma
Detect and appropriately treat end-organ damage
Completely restore the health of the mother
30. •Safety of mother
and fetus
Main objective
• Stabilization of mother’s
condition
• Confirmation of gestational age
• Assessment of fetal well-being
Initial
34. Drug of choice for prevention of seizures
Drug is considered when women is at risk for eclampsia: moderate to severe
preeclampsia (at least BP 150-160/100-110 mm Hg)
Can be given in 2 ways:
(2) intermittent intramuscular injections
(1) continuous intravenous infusions
When given, regularly assess:
Maternal reflexes
Urine output
Oxygen saturation
Respiratory rate
35. Continuous intravenous infusion
• Loading dose: 4-6 g dose of MgSO4 diluted in 100 ml of IVF administered over 15-20 min
• Begin 2 g/h in 50 ml of IV maintenance infusion
• Measure serum Mg level at 4-6 h and adjust infusion to maintain levels between 4 and 7 mEq/L
• MgSO4 is discontinued 24 h after delivery
Intermittent intramuscular injections
• Give 4 g MgSO4 as 20% solution of intravenous at a rate not to exceed 1 g/min
• Follow with 10 g of 50% MgSO4 solution:
• 5 g (one-half) injected deep in the upper outer quadrant of both buttocks through a 3-inch-long, 20 gauge
needle.
• If convulsion persists after 15 min, give up to 2 g more IV as 20% solution at a rate not to exceed 1 g/min. (if the
woman is large up to 4 g may be given slowly)
• Every 4 h thereafter: 5 g of 50% solution of MgSO4 deep IM upper outer quadrant of alternate buttocks, assuring
that:
• Patellar reflex is present
• Respirations are not depressed
• Urine output during the previous 4 h exceeded 100 ml
• MgSO4 is discontinued 24 h after delivery
36.
37. SBP: 140-155 mm Hg
DBP: 90-105 mm Hg
Labetolol
Hydralazine
Nifedipine
IV Nicardipine
Methyldopa
Second line agent:
• Labetolol
• Nifedipine
• Hydralazine
• Beta-receptor blocker
• Hydrochlothiazide
ACE-I
ARB
Diuretics
Given if BP >150/100
mm Hg PP:
Drugs used during
antepartum
Diuretics
Avoid NSAIDs PP
38. Labetalol (C)
> 10 to 20 mg IV, then 20 to 80 mg every
20 to 30 minutes
> maximum of 300 mg;
> for infusion: 1 to 2 mg/min
> Lower incidence of maternal hypotension and
other adverse effects, displaces hydralazine;
> Avoid in women with asthma or congestive
failure.
> Not available locally
Hydralazine (C)
> 5 mg IV or IM, then 5 to 10 mg every 20
to 40 minutes; once BP controlled repeat
every 3 hours;
> for infusion: 0.5 to 10.0 mg/hr; if no
success with 20 mg IV or 30 mg IM,
consider another drug
A drug of choice according to
NHBEP; long experience of
safety and efficacy
Nifedipine (C) >Tablets recommended only: 10 to 30 mg
PO, repeat in 45 minutes if needed Should be used with caution if
concomitantly used with MgSO4
IV Nicardipine
> D5W 90 mL + Nicardipine 10 mg in
soluset
Concentration = 0.1 mg/mL
> Start drip at 10 ugtts/min (equivalent to
1 mg/hr).
> Maximum dose 10mg/hr
*Note:The IV infusion site must be
changed every 12 horus
Should be used with caution if
concomitantly used MgSO4
DRUG Dose and Route Precautions andAdverse Effects
39. Methyldopa (B)
Secondlineagents
Preferred agent:
0.5 to 3.0 g in 2 divided dosage
Labetolol (C)
Nefidipine (C)
Hydralazine (C)
Beta Blockers (C)
Drug Dose Concerns
Drug of choice (NHBEP)
Safety after 1st trimester
200 to 1200 mg/d in 2-3 divided dose
30 to 120 mg/d slow release prep
May be assoc. with fetal growth restriction
May inhibit labor and synergistic
action with MgSO4 in lowering BP
Useful in combination with
sympatholytic agents
May cause neonatal thrombocytopenia
May ↓ uteroplacental blood flow
May impair fetal response to hypoxia
Risk of IUGR when start 1st or 2nd Tri (Atenolol)
Associcated with neonatal hypoglycemia
50 to 300 mg/d in 2-4 divided doses
Depends on specific agent
40. Hydrochlothiazide (C)
Contraindicated
Second line agents:
12.5 to 25.0 mg/d
ACE-I
ARB
Drug Dose Concerns
Can cause volume contraction and
electrolyte d/o
Useful in combination with Methyldopa and
vasodilator to mitigate fluid retention
Leads to fetal loss in animals
Human use is associated with:
1. Cardiac defects
2. oligohydramnios
3. Fetopathy
4. Growth restriction
5. Renal agenesis
6. Neonatal anuric renal failure
41. Controlof
seizures
MgSO4 For prevention and reduction of recurrence
Diazepam Loading dose: 10
mg IV over 2 min
Followed by: IV infusion
40 mg in 500 ml Normal
saline for 24 h
After 24 h: 20 mg
in 500 ml NS,
slowly reduced
Phenytoin
Only for seizure
prevention
Dose: initial - 1 g slow IV d by 100 mg every 6 hours for the next 24 hours
Anti-HPN
Therapy
Hydralazine Drug of choice
IV boluses of 5 to 10 mg at 20-30 min interval until
desired BP attained
Clonidine Next recommended drug IM: 75-150 mcg
Nifedipine 5-10 mg orally NOT sublingual
Labetalol Initial dose: 20 mg IV bolus
If desired BP not attained w/in 10 min, give 40
mg then 80 mg every 10 minutes
42. > 34 weeks
Deliver
Mode: vaginal
delivery
< 34 weeks
Defer delivery
Give corticosteroids
(24-34 weeks)
<32 weeks: CS
Eclampsia
Deliver after seizure
is controlled
CS is done if:
Anticonvulsant therapy
continued atleast 24 hours after
deliver
Betamethasone: 12 mg IM every 24 h for 2 doses
Dexamethasone: 6 mg IM every 12 h for 4 dosesGiven between 23-34 weeks for
fetal lung maturity
Corticosteroids
Vaginal delivery is
not easy and
imminent
Failure of
progress after
induction
Fetal compromise
45. Most widely used for assessment of fetal well
being
Hypothesis: HR of non-acidotic fetus temporarily
increase in response to movement
Normal or reactive:
≥2 accelerations of ≥15 bpm lasting for ≥15 sec
within 20 min
Nonreactive:
Does not contain at least 2 accelerations
Uteroplacental insufficiency:
Absent acceleration during 80-min period with variability or late
deceleration following spontaneous uterine contractions
47. NST
2
≥2 accelerations of ≥15 bpm
lasting for ≥15 sec within 20
min
0 0 or 1 acceleration in 20-
40 min
Fetal
Breathing
2 ≥1 ep rhythmic breathing
lasting ≥30 sec w/in 30 min
0 <30 sec of breathing in 30
min
Fetal
mov’t
2 ≥3 discrete or body limb
movement w/in 30 min
0 <3 discrete
movements
Fetal
tone
2
≥1 ep of ext and flex of
extremity OR
opening/closing of hand
w/in 30 min
0 No movement or no
extension/felxion
AF
volume
2 Single vertical
pocket >2cm
0 Largest single vertical
pocket <2cm
49. Biophysical
Score
Interpretation Recommended management
10 Normal, nonasphyxiated
No fetal indication for intervention
Repeat test weekly
Repeat 2x weekly for postterm and diabetic
8
Normal fluid
Normal, nonasphyxiated
fetus
No fetal indication for intervention
Repeat test per protocol
8
oligohydramnios
Chronic fetal asphyxia
suspected
Deliver if ≥37 weeks, otherwise repeat test
6 Possible fetal asphyxia
IF:
AF is abnormal: deliver
Norma AF >36 weeks w/ favourable cervix: deliver
Repeat test <6: deliver
Repeat test >6: observe and repeat per protocol
4 Probable fetal asphyxia Repeat test on same day: if ≤6 - deliver
0-2
Almost certain fetal
asphyxia
Deliver
50. Non-invasive way to assess blood flow characterizing downstream impedance
Umbilical artery systolic/diastolic ratio is commonly used Doppler index
Ratio compares max systolic flow with end-diastolic flow: evaluate downstream impedance to
flow
Consider abnormal if elevated above 95th percentile OR if diastolic flow is absent or reversed
Doppler of the uterine and uteroplacental arteries at 24 weeks is an effective test to predict
Preeclampsia
53. ABNORMALITY BPS FREQUENCY DECISION TO DELIVER (FETAL)
Elevated Indices
Only
Weekly
Abnormal BPS orTerm or >36
weeks with no fetal growth
AEDV Twice weekly
Abnormal BPS or >34 weeks
proven maturity or conversion to
REDV
REDV Daily
Any BPS < 10/10 or >32 weeks
dexamethasone given
REDV-UVP Three times daily
Any BPS < 10/10 or >28 weeks
dexamethasone given
Notas del editor
Primiparity: the risk of preec in 1st pregnancy is 3% whereas 1% in the second
Immunologic: immunological tolerance involving cytokines through the tolerance network- TH2 reaction. Preeclampsia caused by failure of trophoblast invasion can be considered as a type of rejection
Previous pregnancy-increased risk of recurrence in subsequent pregnancies
- recurrence rate is as high as 50%
Family history of Preclampsia
BMI – relationship between maternal weight and risk of preeclampsia is progressive
- increases from 4.3% for women with BMI less than 19.8 kg/m2 to 13.3% to those with BMI >35 kg/m2
Underlying medical condition – related to vaascular, connective and renal implications
Pregnancy related conditions – conditions such as hydrops fetalis, multifetal gestation, twin gestation are at increased risk secondary to increased trophoblast mass
Primipaternity – immunogentic factors – immunological habituation to paternal antigens: having new sexual partners will expose the mother to a new paternal antigens – paternal genes in fetus may therefore contribute to woman’s risk of preeclampsia
Sexual co-habituation – aka disease of new couples, the longer the duration of co-habituation before conception (w/o barriers to contraception) the lower the risk of preeclampsia <within the first 4 months: the risk is 40% compared to 3-5% over 12 months>
Maternal infection – there is a direct relationship, in which a maternal infection increases the risk of preeclampsia, infections such as UTI and periodontal diseases
Gestational age at delivery in first pregnancy – risk of recurrent preeclampsia is INVERSELY related to gestational age at the first delivery. <it can be implicated: that a previous preterm delivery and SGA newborn increases rhe risk of preeclampsia in subsequent pregnancies
Socioeconomic status – there is a similar risk. Therefore, this disease is NOT associated with poor social status
Smoking – IRONICALLY, it is consistently associated with a reduced risk of hypertension during pregnancy
Abnormal placentation (stage 1), particularly lack of dilatation of the uterine spiral arterioles, is the common starting point in the genesis of pre-eclampsia, which compromises blood flow to the maternal–fetal interface. Reduced placental perfusion activates placental factors and induces systemic hemodynamic changes. The maternal syndrome (stage 2) is a function of the circulatory disturbance caused by systemic maternal endothelial cell dysfunction resulting in vascular reactivity, activation of coagulation cascade and loss of vascular integrity. Pre-eclampsia has effects on most maternal organ systems, but predominantly on the vasculature of the kidneys, liver and brain.
process of vascular invasion, the cytotrophoblasts differentiate from an epithelial phenotype to an endothelial phenotype, a process referred to as "pseudovasculogenesis"
> release of procoagulant proteins such as von Willebrand factor, endothelin, cellular fibronectin, and thrombomodulin.
MAP= DBP + 1/3 PP where PP= SBP-DBP
Inc incidence of preec:
MAP-(2nd Tri >90)
MAP-3rd Tri >105
Immune factors (such as AT1-AA), oxidative stress, NK cell abnormalities, and other factors may cause placental dysfunction, which in turn leads to the release of anti-angiogenic factors (such as sFlt1 and sEng) and other inflammatory mediators to induce hypertension, proteinuria, and other complications of preeclampsia.
Natural killer (NK) cells at the maternal/fetal interface are also thought to play an important role in the pathogenesis of preeclampsia. They are thought to be important in modulating immune tolerance required for normal placental development as well as the induction of angiogenic factors and vascular remodeling
4-7 meq/l or 4.8-8.4mg/dl or 2.0-3.5 mmol/L
AFI – calculated by dividing the pregnant uterus into 4 quadrants and placing the transducer on the maternal abdomen along the longitudinal axis
Vertical diameter of largest amniotic of in each quadrant is measured with the transducer held perpendicular to the floor.
Several factors may modulate amniotic fluid index:
Attitude
Maternal fluid restriction
dehydration
This vessel normally has forward flow throughout the cardiac cycle, and the amount of flow during diastole increases as gestation advances. Thus the S/D ratio decreases, from about 4.0 at 20 weeks to 2.0 at term. The S/D ratio is generally less than 3.0 after 30 weeks (Fleischer and associates, 1986). Umbilical artery Doppler may be a useful adjunct in the management of pregnancies complicated by fetal growth restriction.
Umbilical artery Doppler is considered abnormal if the S/D ratio is above the 95th percentile for gestational age. In extreme cases of growth restriction, end-diastolic flow may become absent or even reversed (Fig. 16–20). These are ominous findings and should prompt a complete fetal evaluation—almost half of cases are due to fetal aneuploidy or a major anomaly (Wenstrom and associates, 1991). In the absence of a reversible maternal complication or a fetal anomaly, reversed end-diastolic flow suggests severe fetal circulatory compromise and usually prompts immediate delivery. Sezik and colleagues (2004) recently reported that fetuses of preeclamptic women who had absent or reversed end-diastolic flow were more likely to have hypoglycemia and polycythemia.
AEDV is not stable and will progress to REDV over time
•AEDV is not stable and will progress to REDV over time
• Many fetuses with AEDV also have altered brain blood flow with increased diastolic velocities-”brain-sparing phenomenon”
• Indication to prepare for delivery, appropriate referral, administartion of antenatal steroids, and detailed maternal evaluation
• 20% of fetuses with AEDV have malformations or overt aneuploidy so a congenital anomaly scan is indicated and in some cases, even fetal karyotyping. (