Prediction and prevention of Preeclampsia
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Transcript Prediction and prevention of Preeclampsia
UPDATE ON
PREDICTION & PREVENTION
OF PREECLAMPSIA
Assist. Prof. S. Rouholamin
HYPERTENSION IN PREGNANCY
Etiology & Definition
Complicates 10-20% of pregnancies
Elevation of BP ≥140 mmHg systolic and/or
≥90 mmHg diastolic, on two occasions at
least 6 hours apart.
Categories
Chronic Hypertension
Gestational Hypertension
Preeclampsia
Preeclampsia superimposed on Chronic
Hypertension
Chronic Hypertension
“Preexisting Hypertension”
Definition
Systolic pressure ≥ 140 mmHg, diastolic pressure
≥90 mmHg, or both.
Presents before 20th week of pregnancy or persists
longer then 12 weeks postpartum.
Causes
Primary = “Essential Hypertension”
Secondary = Result of other medical condition (ie:
renal disease)
Prenatal Care for Chronic
Hypertensives
Electrocardiogram should be obtained in women
with long-standing hypertension.
Baseline laboratory tests
Urinalysis, urine culture, and serum creatinine,
glucose, and electrolytes
Tests will rule out renal disease, and identify
comorbidities such as diabetes mellitus.
Women with proteinuria on a urine dipstick should
have a quantitative test for urine protein.
Treatment for Chronic
Hypertension
Avoid treatment in women with uncomplicated
mild essential HTN as blood pressure may
decrease as pregnancy progresses.
May taper or discontinue meds for women with
blood pressures less than 120/80 in 1st trimester.
Reinstitute or initiate therapy for persistent
diastolic pressures >95 mmHg, systolic pressures
>150 mmHg, or signs of hypertensive end-organ
damage.
Medication choices = Oral methyldopa and
labetalol.
Preeclampsia
Definition = New onset of hypertension and
proteinuria after 20 weeks gestation.
Systolic blood pressure ≥140 mmHg OR diastolic
blood pressure ≥90 mmHg
Proteinuria of 0.3 g or greater in a 24-hour urine
specimen
Preeclampsia before 20 weeks, think MOLAR
PREGNANCY!
Categories
Mild Preeclampsia
Severe Preeclampsia
Eclampsia
Occurrence of generalized convulsion and/or coma in
the setting of preeclampsia, with no other
neurological condition.
Preeclampsia
Severe Preeclampsia must have one of the
following:
Symptoms of central nervous system dysfunction = Blurred vision,
scotomata, altered mental status, severe headache
Symptoms of liver capsule distention = Right upper quadrant or
epigastric pain
Nausea, vomiting
Hepatocellular injury = Serum transaminase concentration at least
twice normal
Systolic blood pressure ≥160 mm Hg or diastolic ≥110 mm Hg on two
occasions at least six hours apart
Thrombocytopenia = <100,000 platelets per cubic milimeter
Proteinuria = 5 or more grams in 24 hours
Oliguria = <500 mL in 24 hours
Severe fetal growth restriction
Pulmonary edema or cyanosis
Cerebrovascular accident
Preeclampsia superimposed on
Chronic Hypertension
Affects 10-25% of patients with chronic HTN
Preexisting Hypertension with the following
additional signs/symptoms:
New onset proteinuria
Hypertension and proteinuria beginning prior to
20 weeks of gestation.
A sudden increase in blood pressure.
Thrombocytopenia.
Elevated aminotransferases.
Treatment of Preeclampsia
Definitive Treatment = Delivery
Major indication for antihypertensive therapy
is prevention of stroke.
Diastolic pressure ≥105-110 mmHg or systolic
pressure ≥160 mmHg
Choice of drug therapy:
Acute – IV labetalol, IV hydralazine, SR Nifedipine
Long-term – Oral methyldopa or labetalol
Gestational Hypertension
Mild hypertension without proteinuria or other
signs of preeclampsia.
Develops in late pregnancy, after 20 weeks
gestation.
Resolves by 12 weeks postpartum.
Can progress onto preeclampsia.
Often when hypertension develops <30 weeks
gestation.
Indications for and choice of antihypertensive
therapy are the same as for women with
preeclampsia.
Risk Factors for
Hypertension in Pregnancy
Nulliparity
Preeclampsia in a previous pregnancy
Age >40 years or <18 years
Family history of pregnancy-induced hypertension
Chronic hypertension
Chronic renal disease
Antiphospholipid antibody syndrome or inherited thrombophilia
Vascular or connective tissue disease
Diabetes mellitus (pregestational and gestational)
Multifetal gestation
High body mass index
Male partner whose previous partner had preeclampsia
Hydrops fetalis
Unexplained fetal growth restriction
Evaluation of Hypertension in
Pregnancy
History
ID and Complaint
HPI (S/S of Preeclampsia)
Past Medical Hx, Past
Family Hx
Past Obstetrical Hx, Past
Gyne Hx
Social Hx
Medications, Allergies
Prenatal serology, blood
work
Assess for Hypertension in
Pregnancy risk factors
Physical
Vitals
HEENT = Vision
Cardiovascular
Respiratory
Abdominal = Epigastric
pain, RUQ pain
Neuromuscular and
Extremities = Reflex,
Clonus, Edema
Fetus = Leopold’s, FM, NST
Evaluation of Hypertension
in Pregnancy
Laboratory Tests
CBC (Hgb, Plts)
Renal Function (Cr, UA, Albumin)
Liver Function (AST, ALT, ALP, LD)
Coagulation (PT, PTT, INR, Fibrinogen)
Urine Protein (Dipstick, 24 hour)
Management of Hypertension
in Pregnancy
Depends on severity of hypertension and
gestational age!!!!
Observational Management
Restricted activity
Close Maternal and Fetal Monitoring
BP Monitoring
S/S of preeclampsia
Fetal growth and well being (NST, and U/S)
Routine weekly or biweekly blood work
Management of Hypertension
in Pregnancy
Medical Management
Acute Therapy = IV Labetalol, IV Hydralazine, SR
Nifedipine
Expectant Therapy = Oral Labetalol, Methyldopa,
Nifedipine
Eclampsia prevention = MgSO4
Contraindicated antihypertensive drugs
ACE inhibitors
Angiotensin receptor antagonists
Management of Hypertension
in Pregnancy
Proceed with Delivery
Vaginal Delivery VS Cesarean Section
Depends on severity of hypertension!
May need to administer antenatal corticosteroids
depending on gestation!
Only cure is DELIVERY!!!
•Prediction:
Routine urine analysis
•Prevention:
Chocolate
Outline
Introduction
Prediction
Prevention
Cochrane Systematic Review
Gold Standard' for high-quality
systematic reviews
•Preeclampsia:
Hypertension
associated with
proteinuria.
•Pathogenesis:
•unknown (Barton& Sibai, 2008).
Impaired trophoblast differentiation& invasion
Placental & endothelial dysfunction
Immune maladaptation to paternal Ags
Exaggerated systemic inflam response.
•Pathogenesis:
•Differs with various risk factors:
PG Vs MG with previous PE
preexisting vas dis
preexisting DM or
multifetal gestation.
In PE:
Impaired trophoblast
differentiation &
invasion
Placental and
endothelial
dysfunction
PREDICTION OF PE
• Why prediction is important?
• The ideal screening test
• Methods
I. Preconception factors
II. Pregnancy-Related Factors
1. Risk factors
2. Markers
Why prediction is important:
1. The risk for recurrent PE can be
as high as 65% (Barton& Sibai, 2008).
2. PE is associated with substantial
maternal& perinatal
complications
The ideal Screening test:
Simple
Noninvasive
Rapid
Inexpensive
Easy to perform early in pregnancy
Highly sensitivity & predictive.
I. Preconception factors
st
1
step in the management of a
woman with a history of PE is to
conduct a detailed evaluation of
potential risk factors (Barton& Sibai, 2008).
Preconceptional Risk Factors
Rates of preeclampsia depend on: severity of underlying complications&
combinations of risk factors.
Risk factors
Risk %
Chronic hypertension/renal disease
15-40
Pre gestational DM
10-35
Connective tissue disease (lupus, rheumatoid arthritis)
10-20
Thrombophilia (acquired or congenital)
10-40
Obesity/insulin resistance
10-15
Age older than 40 y
10-20
Limited sperm exposure
10-35
Family history of preeclampsia/ cardiovascular disease
10-15
Woman born as SFGA
1.5 fold
Adverse outcome in a previous pregnancy: IUGR, ab placentae,
IUFD
2-3 fold
II. Pregnancy-Related Factors
Regular antenatal care is mandatory for the prevention & early detection
of PE.
Risk factors: Magnitude of risk depends on the number of factors
Hydrops/hydropic degeneration of the placenta
Multifetal gestation
Unexplained FGR
Gestational hypertension
UTI
Periodontal infection
Markers
Biophysical
Biochemical
Markers
Many
Based on: pathophysiological abnormalities
•SCREENING TESTS FOR PE (WHO, 2004)
I. Placental perfusion & vascular resistance dysfunction
Mean arterial blood pressure
Roll over test
Doppler ultrasound
Isometric exercise test
Intravenous infusion of angiotensin II
Platelet angiotensin II binding
Platelet calcium response to arginine vasopressin
Renin
24-hour ambulatory blood pressure monitoring
II. Fetoplacental unit dysfunction
Human chorionic gonadotropin
Alpha fetoprotein
Estriol
Inhibin A
Pregnancy-associated plasma protein A
Activin A
Corticotropin release hormone
III. Renal dysfunction
Serum uric acid
Microalbuminuria
Urinary calcium excretion
Urinary kallikrein
Microtransferrinuria
N-acetyl- glucosarninidase
IV. Endothelial& oxidant stress dysfunction
Platelet count
Platelet activation and endothelial cell
adhesion molecules
Prostacyclin
Cytokines
Isoprostanes,
Antiphospholipid antibodies,
Placenta growth factor
Hematocrit
Antithrombin Ill
Calcium
Transferrin
Atrial natriuretic peptide
Fibronectin
Endothelin
Thromboxane
Homocysteine
Serum lipids Insulin resistance
Plasminogen activator inhibitor
Leptin
Total proteins
Magnesium
Ferritin
Haptoglobin
microglobulin
Genetic markers
I. Biophysical
•Mean arterial pressure
•(2D BP+S BP)/3
•Better predictor of PE than S& D BP (BMJ
200817;336:111; Meta-analysis of 34 RCT)
2nd trimester MA BP ≥ 90 mm Hg had +ve LR 3.5
and –ve LR 0.46
•BP remains the cornerstone of early diagnosis
although it has limitations:
measurement errors associated with sphygmomanometer
effect of maternal posture on BP in pregnant women}.
•Repeated routine urinalysis
throughout pregnancy NOT useful for
predicting PE
(JAMA 2003: 12;289(10):1220)
Uterine artery Doppler ultrasound
•}impaired trophoblastic invasion of the spiral arteries:
reduction in uteroplacental blood flow}
•High pulsatility index and/or Notch in 1st & 2nd
trimesters: poor predictor of PE(Papgeorghiou & Leslie, 2007)
Uterine artery Doppler plus biochemical markers
•Promising results
•Current data do not support this combination for
routine screening for PE (Barton& Sibai, 2008).
Diastolic Notch in
uterine artery waveform
The Roll over test
Not of value in predicting PE
II. Biochemical Markers
Angiogenic factors before & after
the onset of PE
(Barton& Sibai, 2008).
Serum placental growth factor:
reduced
Soluble fms-like tyrosine kinase:
elevated
Endoglin: elevated
Conclusion
•BP remains the cornerstone of early
diagnosis
•Markers
Reliability is inconsistent
Many suffer from poor specificity &
predictive values.
None provided a cutoff value that could
be clinically useful for the prediction of
PE
(Widmer et al, 2007).
•Currently:
There is no clinically useful
screening test to predict PE (WHO,
2004)
Prevention of PE
Primary
Secondary
Primary prevention
•Avoiding occurrence of the disease
•Obese:
achieve an ideal b wt before conception
(Villamor& Cnattingius, 2006)
No RCT
•Ch hypertension:
Control BP before conception.
No RCT
•Pregestational DM:
-Complete her family as early as possible &
before vascular complications develop
-Control DM before conception & throughout
pregnancy
Secondary
•Breaking off the disease process before emergence
of obvious clinical disease
•{Etiology of the disease is unknown}
•To correct theoretical pathophysiology
•I. Non pharmacological
II. Nutritional
III. Pharmacological
I. Non pharmacological
1. Daily Bed rest
Rest for 4-6 h/d
May reduce risk of
PE for women with normal BP
(level 2 evidence)
(Cochrane Library 2006 Issue 2:CD005939)
2. Life-style changes
•High job stress: greater risk
of PE(Sharma& Mittal, 2006)
•Reducing job stress may be
beneficial in the prevention of
PE
3. Regular prenatal exercise
•May prevent or oppose progression (Weissgerber et al, 2004)
•{Stimulation of placental growth
Reduction of oxidative stress
Reversal of maternal endothelial dysfunction}.
•Insufficient evidence
Moderate intensity regular aerobic exercise
(Cochrane Library 2006 Issue 2:CD005942)
Aerobic exercise =cardiovascular exercise=any sustained rhythmic activity that
involves large muscle groups: makes the lungs work harder as the body's need for
oxygen is increased.
•Stretching exercises are more effective at reducing the
risk of PE than walking
(University of North Carolina,2008)
Smoking:
Reduced risk for PE (Sibai et al, 2005).
{Nicotine inhibition of interleukin-2 & tumor
necrosis factor
Effects of nicotine on angiogenic proteins}.
Smoking:
abnormal fetal growth
preterm birth
Abruption
Adverse effects on maternal health.
II. Nutritional
1. Higher total dietary fiber
intake in early pregnancy may
reduce risk for PE
(level 2 evidence)
Prospective cohort study
Am J Hypertens 2008 Aug;21(8):903
2. Increasing dietary protein & energy intake
RCT: no benefit
•5 or more servings of chocolate/w in
3rd trimester:40% reduction
(Triche, 2008; Epidemiology .19:459-464), Yale University
{Chocolate, especially dark chocolate, is rich
in theobromine: stimulates the heart, relaxes
smooth muscle & dilates blood vessels, and
has been used to treat chest pain, high blood
pressure}
3. Garlic
Insufficient evidence
to recommend for
preventing PE
Cochrane Library 2006 Issue3:CD006065)
4. Dietary sodium restriction
• No significant differences
(Cochrane Library 2005 Issue 4:CD005548)
6. Fish Oil Supplementation
•Observational studies: beneficial effects
•{inhibition of platelet thromboxane A2 without affecting
prostacyclin: shifting the balance toward a reduced platelet
aggregation and increased VD}.
•RCT: No benefit
(Olsen et al, 2000)
•High doses: increase the risk of PIH
(Olafasdottir et al, 2006).
•Not recommended for the prevention of PE
5. Weight Reduction
•Although obesity is a known risk
factor, there is no evidence that limiting
wt gain during pregnancy; reduces its
occurrence.
•Wt reduction is not recommended during
pregnancy even in obese women (Kramer, 2004)
III. Pharmacological
1. Low-dose Aspirin
•{inhibits biosynthesis of platelet thromboxane A2
with little effect on vascular prostacyclin production:
altering the balance in favor of prostacyclin}.
•(50-150 mg/day)
For women with a previous history of
hypertension or PE (n=6,107):
Small to moderate benefits, safe.
level 2 evidence
(Cochrane Library 2007 Issue 2:CD004659)
2. Low-dose Aspirin/Heparin
•History of severe preterm PE &
LBW infants.
(Sergio et al, 2006)
•Lower incidence of PE (3Vs
30%)
Greater gestational age at
delivery
Higher birth wt
3. Calcium Supplementation
•Reduces the risk of PIH, particularly in
populations that have diets deficient in
calcium
level 1 evidence (Cochrane Syt review , 2006)
•The relationship between cal & risk of PIH is
inconsistent& inconclusive
The relationship between cal & the risk of PE
is highly unlikely.
Evidence-based review by FDA (2007)
4. Antihypertensive Drugs
•Mild to moderate hypertension:
Halving in the risk of developing severe
hypertension
No difference in the risk of developing PE or
proteinuria
(Cochrane syst review, 2007)
5. Diuretics
•No reduction in the incidence of PE or
perinatal mortality
•May have deleterious effects:
reduced renal & placental perfusion.
(Cochrane Library 2007 Issue 1:CD004451)
6. Antioxidant supplementation
may not affect risk of PE or
clinical outcomes
level 2 evidence
(Cochrane Library 2008 Issue
1:CD004227)
7. Concomitant Vit C& E supplementation
•{PET: imbalance of oxidant & antioxidant activity:
multiorgan endothelial dysfunction}.
•Vit C (1,000 mg/d) plus vit E (400 IU/ d)
•Did not prevent PE
level 2 evidence (Obstet Gynecol 2007 Dec;110(6):1311)
•May increases rate of LBW infants& might be
associated with higher rate of SB
level 2 evidence (Lancet 2006 Apr 8;367(9517):1145
8. Magnesium
•{Mg is beneficial for the prevention &
tt of severe PE & E
Decreased intracellular Mg in PE}
•No effect
•(365 mg& 500 mg).
Cochrane syst review, 2004
9. Folic acid& other B-vits
•{Deficiency of vit B2 may cause
biochemical changes simulating
abnormalities of PE}
•No evidence that any of B vits
can prevent PE
(Shrama& Mittal, 2006).
10. Zinc supplementation
•{Zinc concentrations are reduced in
PE}
•RCT: No benefit
(Jonsson et al, 1996)
11. Nitric oxide
Insufficient evidence for preventing
PE
Cochrane Library 2007 Issue 2:CD006490
12. Progesterone
Insufficient evidence for preventing
PE
Cochrane review, 2006
Conclusion
Regular antenatal care is mandatory for
the prevention & early detection of PE.
For prevention of PE
Bed rest
Reduction of job stress
High dietary fiber intake
Low dose aspirin
Low dose aspirin/heparin
Ca supplementation
PREECLAMPSIA
PREECLAMPSIA
Hypertensive disorder specific to pregnancy
affects nearly 6% of all pregnancies
a major cause of maternal and neonatal mortality
and morbidity
15 to 20 % of maternal mortality in developed
countries
PREECLAMPSIA
Severity ranges from:
a mild disorder (transient hypertension in the later
part of the pregnancy) to
a life-threatening disorder with seizures, HELLP
syndrome, fetal hypoxia, and growth retardation
more severe disease: 0.56 per 1000 deliveries
PREECLAMPSIA
Predisposes women to other serious
complications:
placental abruption
acute renal failure
cerebral hemorrhage
disseminated intravascular coagulation
circulatory collapse
PREECLAMPSIA
The etiology is unknown
believed to be involved:
immune maladaptation
placental ischemia
oxidative stress
genetic susceptibility
PREECLAMPSIA
Classification of hypertension in pregnancy
Gestational hypertension
Preeclampsia / eclampsia
Chronic hypertension
Preeclampsia superimposed on chronic
hypertension
PREECLAMPSIA
Definition of hypertension
a systolic blood pressure of 140 mmHg or above,
or a diastolic blood pressure of 90mmHg or above,
on two occasions 6 hours apart
Abnormal proteinuria
the excretion of 300 mg or more of protein in 24
hours
PREECLAMPSIA
Criteria for severe preeclampsia
Blood pressure: > 160 mmHg systolic or
> 110
mm Hg diastolic
Proteinuria: > 5 g in 24 hours
Persistent and severe cerebral or visual
disturbances (headache, scotoma, blurred vision)
Persistent and severe epigastric pain or right
upper quadrant pain
PREECLAMPSIA
Criteria for severe preeclampsia
Pulmonary edema or cyanosis
Oliguria (< 500 mL of urine in 24 hours)
Eclampsia (grand mal seizures)
HELLP syndrome
PREECLAMPSIA
Screening tests for gestational hypertension
routine components of antepartum care trimester
early detection of vasoconstriction
early detection of altered renal function
early detection of altered hemodynamics
detection of placental hypoperfusion / ischemia
detection of endothelial activation or injury
detection of an activated coagulation / fibrinolytic
system
PREECLAMPSIA
Prevention of preeclampsia
women at risk: multifetal gestation, vascular or renal
disease, previous severe preeclampsia-eclampsia,
abnormal uterine artery Doppler velocimetry
antihypertensive drugs
magnesium
zinc
fish oil
calcium
low-dose aspirin
PREECLAMPSIA
Mild preeclampsia - management
< 37 weeks gestation
inpatient or outpatient management
worsening disease: delivery, magnesium sulfate
> 40 weeks gestation
delivery, magnesium sulfate
37 - 39 weeks gestation
inducible cervix: delivery, magnesium sulfate
cervix not inducible: inpatient or outpatient
management
PREECLAMPSIA
Severe preeclampsia - expectant
management
gestational age: not recommended for < 24 weeks
or > 34 weeks gestation
hospitalization: tertiary care center
antenatal testing: daily
PREECLAMPSIA
Severe preeclampsia - guidelines for
expedient delivery
maternal indications
eclampsia, thrombocytopenia, pulmonary edema,
acute renal failure
persistent severe headache or visual changes
elevated liver enzymes with persistent severe
epigastric pain or right upper quadrant tenderness
labor or rupture of membranes
vaginal bleeding, abruptio placenta
PREECLAMPSIA
Severe preeclampsia - guidelines for
expedient delivery
fetal indications
repetitive severe variables or late decelerations
biophysical profile < 4 on two occasions 4 hours
apart
amniotic fluid index < 2 cm
intrauterine growth restriction
fetal death
> 34 weeks gestation
PREECLAMPSIA
Severe preeclampsia - management protocol
admission to labor and delivery for 24 hours
magnesium sulfate IV for 24 hours
antihypertensives if diastolic blood pressure
110 mmHg
meet guidelines for expedited delivery?
yes? delivery
>
PREECLAMPSIA
Severe preeclampsia - management protocol
Expedited delivery? no?
< 23 weeks: counseling for termination of pregnancy
23-32 weeks: steroids, antihypertensive
medications, daily maternal and fetal evaluation,
delivery at 34 weeks
32-33 weeks: amniocentesis
immature fluid - steroids, delivery in 48 hours
PREECLAMPSIA
HELLP syndrome - diagnosis
10% before 27 weeks
20% after 37 weeks
70% between 27 and 37 weeks
slow initial phase with accelerated final phase
versus secondary expression of sepsis, ARDS,
renal failure
PREECLAMPSIA
HELLP syndrome
parameters used to diagnose preeclampsia are
not reflective of disease severity
target organ systems
liver
brain
kidneys
coagulation system
increased maternal and perinatal risk
PREECLAMPSIA
HELLP syndrome - diagnostic criteria
hemolysis
abnormal peripheral smear
lactate dehydrogenase > 600 U/L
elevated liver enzymes
serum aspartate aminotransferase > 70 U/L
lactate dehydrogenase > 600 U/L
low platelets
platelet count < 100,000/mm3
PREECLAMPSIA
HELLP syndrome - differential diagnosis
acute fatty liver of pregnancy
appendicitis
diabetes insipidus
gallbladder disease
gastroenteritis
glomerulonephritis
hemolytic uremic syndrome
hepatic encephalopathy
PREECLAMPSIA
HELLP syndrome - differential diagnosis
idiopathic thrombocytopenia
kidney stones
pancreatitis
pyelonephritis
systemic lupus erythematosus
thrombotic thrombocytopenia purpura
viral hepatitis
PREECLAMPSIA
HELLP syndrome - antepartum management
assess and stabilize the maternal condition
correct coagulopathy if DIC is present
give intravenous magnesium sulfate to prevent
seizures
provide treatment for severe hypertension to
prevent stroke
transfer to tertiary center if appropriate
if subcapsular hematoma of liver, computed
tomography or ultrasound of the abdomen
PREECLAMPSIA
HELLP syndrome - antepartum management
evaluate fetal well-being
non stress test
biophysical profile
timing of delivery
if > 34 weeks gestation, deliver
if < 34 weeks gestation, administer corticosteroids,
then deliver in 48 hours
PREECLAMPSIA
HELLP syndrome - management for
cesarean birth
use general anesthesia if platelet count is
<
75,000 / mm3
transfuse 5 to 10 units of platelets before surgery
if platelet count is < 50,000 / mm3
leave vesicouterine peritoneum open
install subfascial drain
PREECLAMPSIA
HELLP syndrome - management for
cesarean birth
schedule secondary closure of skin incision or
subcutaneous drain
administer postoperative transfusions as needed
perform intensive monitoring for at least 48 hours
postpartum
consider dexamethasone (10 mg IV every 12
hours) until postpartum resolution of disease
occurs
PREECLAMPSIA
HELLP syndrome - management of women
with a subcapsular liver hematoma
general considerations - blood bank aware for
potential need of many units of blood
general or vascular surgeon consultation
avoid direct and indirect manipulation of liver
closely monitor hemodynamic status
management of hematoma depends on whether
it is ruptured or not
PREECLAMPSIA
Eclampsia
occurrence of convulsions or coma unrelated to
other associated conditions
all new onset seizures during pregnancy eclampsia until proven otherwise
incidence: 1 in 500 pregnancies
3% in multiple gestations
PREECLAMPSIA
Eclampsia
precise cause unknown
theories
vasospasm
ischemia
edema
multisystem organ failure
PREECLAMPSIA
Eclampsia
seizures usually occur without aura
hypertension not severe in 20%
edema absent in 30%
proteinuria absent in 20%
hyperreflexia is not predictive of seizure
headache or visual changes - most common
precipitating event
PREECLAMPSIA
Eclampsia
80% of convulsions occur before or during the
delivery
1/3 of cases may be not preventable
atypical
less than 20 weeks gestation
more than 48 hours postpartum
PREECLAMPSIA
Eclampsia - risk factors
low socioeconomic status
extremes in childbearing age
African-American
no prenatal care
substance abuse
PREECLAMPSIA
Eclampsia - management
control convulsions
correction of hypoxia and acidosis
blood pressure control
delivery after maternal stabilization
PREECLAMPSIA
Eclampsia - anticonvulsant therapy
magnesium sulfate
mechanism of action - smooth muscle relaxation by
displacement of calcium
dosage - 4-6 g intravenous loading dose, followed
by 2 g per hour
may be given intramuscularly
PREECLAMPSIA
Eclampsia - magnesium sulfate
side effects:
maternal hypotonia
respiratory depression
cardiac arrest
neonatal depression
contraindicated in myasthenia gravis
use with caution in renal insufficiency
PREECLAMPSIA
Eclampsia - anticonvulsant therapy
phenytoin
used extensively in Europe
may be used in myasthenia gravis
mechanism of action - may increase gamma
aminobutyric acid-mediated chloride conduction in
postsynaptic membranes
may inhibit neurotransmitter inhibitory systems
PREECLAMPSIA
Eclampsia - phenytoin
dosage - 1 g loading dose over 1 hour
cardiac monitoring during administration
side effects
arrhythmias with rapid administration
hepatitis
Steven-Johnson syndrome
PREECLAMPSIA
Eclampsia - anticonvulsant therapy
diazepam
useful for status seizures
mechanism of action - facilitate the binding of GABA
to its receptor
benzodiazepine receptors
dosage - 10 mg at a rate of 5 mg per min
may be repeated at 10 to 15 minute intervals
PREECLAMPSIA
Eclampsia - diazepam
side effects - loss of consciousness, hypotension,
respiratory depression
caution - may increase risk of aspiration
causes prolonged depression of the neonate
sodium thiopentotal
long acting barbiturate
used when sedation, paralysis and intubation
needed
PREECLAMPSIA
Eclampsia - which anticonvulsant to use?
magnesium is associated with decreased
recurrence risks of seizures when compared with
diazepam or phenytoin
diazepam is associated with increased need for
mechanical ventilation
PREECLAMPSIA
Eclampsia - management of fetus
fetal bradycardia during seizure
~ 5 minutes after the onset of the seizure
may be associated with rebound tachycardia
recovery phase may show late decelerations
monitor for uterine hypertonicity
allow for fetal recovery
monitor for signs of abruption
PREECLAMPSIA
Eclampsia
delivery is indicated regardless of gestational age
immediate cesarean delivery is not necessary
PREECLAMPSIA
Eclampsia - radiographic evaluation
should be reserved for women with neurological
deficit, recurrent seizures, or atypical presentation
abnormal CT findings - 50%
edema, hemorrhage, infarction
cerebral angiography has limited use
90% of EEG evaluations may be abnormal
PREECLAMPSIA
Eclampsia - management
allow patient to have seizure
use bite block as needed to prevent maternal injury
establish airway
administer magnesium sulfate as soon as possible
obtain arterial blood gases
monitor urine output
control hypertension
PREECLAMPSIA
Eclampsia - management
rebolus with magnesium sulfate if repeat seizure
occurs
do not intervene for fetal status while mother is
unstable
if seizure continues, paralyze and intubate.
PREECLAMPSIA
Counseling regarding future pregnancies -
HELLP syndrome
information available varies
recurrent risk of preeclampsia: 43% (19%)
recurrent risk of HELLP syndrome: 19-27% (3%)
If HELLP syndrome < 32 weeks
recurrent risk of preeclampsia / eclampsia is 61%