Update on Prediction & prevention of Preeclampsia
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Transcript of Update on Prediction & 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
IntroductionPredictionPrevention
Cochrane Systematic ReviewGold 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 PEpreexisting vas dispreexisting 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: SimpleNoninvasiveRapidInexpensiveEasy to perform early in pregnancyHighly sensitivity & predictive.
I. Preconception factors1st 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 FactorsRates of preeclampsia depend on: severity of underlying
complications & combinations of risk
factors . Risk% Risk factors
15-40 Chronic hypertension/renal disease10-35 Pre gestational DM10-20 Connective tissue disease (lupus, rheumatoid
arthritis) 10-40 Thrombophilia (acquired or congenital) 10-15 Obesity/insulin resistance 10-20 Age older than 40 y10-35 Limited sperm exposure10-15 Family history of preeclampsia/ cardiovascular
disease1.5 fold Woman born as SFGA
2-3 fold
Adverse outcome in a previous pregnancy: IUGR, ab placentae, IUFD
II. Pregnancy-Related FactorsRegular antenatal care is mandatory for the prevention & early detection of PE .Risk factors: Magnitude of risk depends on the
number of factorsHydrops/hydropic degeneration of the placenta
Multifetal gestationUnexplained FGRGestational hypertensionUTIPeriodontal infectionMarkersBiophysicalBiochemical
Markers Many Based on: pathophysiological abnormalities
• SCREENING TESTS FOR PE (WHO, 2004)
I. Placental perfusion & vascular resistance dysfunctionMean arterial blood pressureRoll 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 dysfunctionHuman 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
Platelet countPlatelet activation and endothelial cell adhesion moleculesProstacyclinCytokinesIsoprostanes, Antiphospholipid antibodies, Placenta growth factorHematocritAntithrombin IllCalciumTransferrinAtrial natriuretic peptide
Fibronectin Endothelin Thromboxane Homocysteine Serum lipids Insulin resistance Plasminogen activator inhibitor Leptin Total proteins Magnesium Ferritin Haptoglobin microglobulin Genetic markers
IV. Endothelial& oxidant stress dysfunction
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 sphygmomanometereffect 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 testNot of value in predicting PE
II. Biochemical Markers Angiogenic factors before & after the onset of PE(Barton& Sibai, 2008). Serum placental growth factor: reducedSoluble fms-like tyrosine kinase: elevatedEndoglin: elevated
Conclusion•BP remains the cornerstone of early diagnosis
•MarkersReliability is inconsistentMany 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)
PrimarySecondary
Prevention of PE
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 pharmacologicalII. Nutritional III. Pharmacological
I. Non pharmacological1. Daily Bed restRest for 4-6 h/dMay 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 growthReduction of oxidative stressReversal of maternal endothelial dysfunction}. • Insufficient evidenceModerate 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 factorEffects of nicotine on angiogenic proteins}. Smoking: abnormal fetal growthpreterm birthAbruptionAdverse effects on maternal health.
II. Nutritional1. 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
2006 3: 006Cochrane Library Issue CD065
)
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. Pharmacological1 .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 deliveryHigher 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 hypertensionNo 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
2 level evidence ( 2008 Cochrane Library Issue 1: 004227CD)
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 PElevel 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 PECochrane Library 2007 Issue 2:CD006490
12. Progesterone Insufficient evidence for preventing PE Cochrane review, 2006
ConclusionRegular antenatal care is mandatory for the prevention & early detection of PE. For prevention of PEBed restReduction of job stressHigh dietary fiber intake Low dose aspirinLow dose aspirin/heparinCa 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%