Teresa G Berg MD MaternalFetal Medicine University Medical Associates M3 Lecture Materials Be able to define hypertension in relationship to pregnancy Be able to classify hypertensive diseases in pregnant women ID: 682674
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Slide1
Hypertension in Pregnancy
Teresa G. Berg, M.D.
Maternal-Fetal Medicine
University Medical Associates
M3 Lecture MaterialsSlide2
Be able to define hypertension in relationship to pregnancy
Be able to classify hypertensive diseases in pregnant women
Be able to list criteria for the diagnosis of preeclampsiaBe able to list criteria for the diagnosis of severe preeclampsia/HELLP syndromeBe able to discuss current management considerationsUnderstand and discuss the effects of hypertension on the mother and fetus
OBJECTIVESSlide3
Sustained BP elevation of 140/90 or greaterProper cuff size
Measurement taken while seated
Arm at the level of the heartUse 5th Korotkoff soundHypertensionSlide4
Four Categories based on ACOG Executive SummaryPreeclampsia
-
eclampsiaSevere featuresHEELPChronic hypertensionChronic hypertension with superimposed preeclampsiaGestational hypertensionHypertensive Disease Associated with PregnancyACOG Executive Summary: Obstet Gynecol 2013; 122: 1122-31.Slide5
Preeclampsia
Associated with:
Proteinuria. Thrombocytopenia. Impaired liver function.New onset renal insufficiency.Pulmonary edema.
New onset cerebral or visual
distrubances
.
Hypertensive Disease Associated with PregnancySlide6
Chronic Hypertension
Predates the pregnancy.
Diagnosed before the 20th week or present before the pregnancy.Hypertensive Disease Associated with PregnancySlide7
Chronic Hypertension with Superimposed Preeclampsia
Hypertension p
redates the pregnancy.Features of preeclampsia noted after 20 weeks.Hypertensive Disease Associated with PregnancySlide8
Gestational Hypertension
Hypertension after 20 weeks.
Absence of proteinuria.Absence of systemic findings noted with preeclampsia.Hypertensive Disease Associated with PregnancySlide9
Preeclampsia vs. Severe Preeclampsia
Criteria for Preeclampsia
Criteria for Preeclampsia with Severe FeaturesPreviously normotensive woman> 140 mmHg systolic> 90 mmHg diastolic
Proteinuria:
>
300
mg in 24 hour
collection
Protein/creatinine ratio of 0.3 mg/
dL
.
Dipstick protein discouraged.
BP
>
160 systolic or
>
110 diastolic
Thrombocytopenia <100,000
Impaired liver function (LFT’s 2X normal) severe RUQ pain or epigastric pain or both
Progressive renal insufficiency (serum creatinine >1.1 mg/
dL
or doubling of serum creatinine
in the absence of renal disease)
Pulmonary edema
New onset cerebral
or visual
disturbancesSlide10
Overlap/Disease Progression
25%Slide11
Risk Factors for Preeclampsia
Nulliparity
Multifetal gestationsMaternal age over 35Preeclampsia in a previous pregnancyChronic hypertensionPregestational diabetesVascular and connective tissue disorders
Nephropathy
Antiphospholipid
syndrome
Obesity
African-American raceSlide12
FACTOR
RISK RATIO
Nulliparity
3:1
Age
>
40
3:1
African American
1.5:1
Chronic hypertension
10:1
Renal disease
20:1
Antiphospholipid syndrome
10:1
Risk FactorsSlide13
Hypertension affects 12 to 22% of pregnant patients Hypertensive disease is directly responsible for approximately 20% of maternal mortality in the United State
Morbidity and Mortality from Hypertensive DiseaseSlide14
VasospasmUterine vesselsHemostasis
Prostanoid balance
Endothelium-derived factorsLipid peroxide, free radicals and antioxidantsPathophysiologySlide15
Vasospasm
Predominant finding in gestational hypertension and preeclampsia
Uterine vesselsHemostasis
Prostanoid
balance
Endothelium-derived factors
Lipid peroxide, free radicals and antioxidants
PathophysiologySlide16
Vasospasm
Uterine vessels
Inadequate maternal vascular response to trophoblastic mediated vascular changesEndothelial damageHemostasis
Prostanoid
balance
Endothelium-derived factors
Lipid peroxide, free radicals and antioxidants
PathophysiologySlide17
Vasospasm
Uterine vessels
HemostasisIncrease platelet activation resulting in consumptionIncreased endothelial fibronectin levels
Decreased
antithrombin
III and
α
2
-antiplasmin levels
Allows for
microthrombi
development with resultant increase in endothelial damage
Prostanoid
balance
Endothelium-derived factors
Lipid peroxide, free radicals and antioxidants
PathophysiologySlide18
Vasospasm
Uterine vessels
HemostasisProstanoid balance
Prostacyclin
(PGI
2
):
Thromboxane
(TXA
2
) balance shifted to favor TXA2
TXA2 promotes:
Vasoconstriction
Platelet aggregation
Endothelium-derived factors
Lipid peroxide, free radicals and antioxidants
PathophysiologySlide19
Vasospasm
Uterine vessels
Hemostasis
Prostanoid
balance
Endothelium-derived factors
Nitric oxide is decreased in patients with preeclampsia
As this is a vasodilator, this may result in vasoconstriction
Lipid peroxide, free radicals and antioxidants
PathophysiologySlide20
Vasospasm
Uterine vessels
Hemostasis
Prostanoid
balance
Endothelium-derived factors
Lipid peroxide, free radicals and antioxidants
Increased in preeclampsia
Have been implicated in vascular injury
PathophysiologySlide21
Cardiovascular effectsHematologic effects
Neurologic effects
Pulmonary effectsRenal effectsFetal effectsPathophysiologic ChangesSlide22
Cardiovascular effects
Hypertension
Increased cardiac outputIncreased systemic vascular resistanceHematologic effectsNeurologic effectsPulmonary effects
Renal effects
Fetal effects
Pathophysiologic
ChangesSlide23
Cardiovascular effects
Hematologic effects
Volume contraction/HypovolemiaElevated hematocritThrombocytopeniaMicroangiopathic hemolytic anemia
Third spacing of fluid
Low
oncotic
pressure
Neurologic effects
Pulmonary effects
Renal effects
Fetal effects
Pathophysiologic
ChangesSlide24
Cardiovascular effects
Hematologic effects
Neurologic effectsHyperreflexiaHeadacheCerebral edema
Seizures
Findings of PRES on radiologic imaging
Pulmonary effects
Renal effects
Fetal effects
Pathophysiologic
ChangesSlide25
Cardiovascular effects
Hematologic effects
Neurologic effectsPulmonary effectsCapillary leak
Reduced colloid osmotic pressure
Pulmonary edema
Renal effects
Fetal effects
Pathophysiologic
ChangesSlide26
Cardiovascular effects
Hematologic effects
Neurologic effectsPulmonary effectsRenal effects
Decreased
glomerular
filtration rate
Glomerular
endotheliosis
Proteinuria
Oliguria
Acute tubular necrosis
Fetal effects
Pathophysiologic
ChangesSlide27
Decreased glomerular filtration rateGlomerular endotheliosis
Proteinuria
OliguriaAcute tubular necrosisRenal EffectsSlide28
Cardiovascular effects
Hematologic effects
Neurologic effectsPulmonary effects
Renal effects
Fetal effects
Placental abruption
Fetal growth restriction
Oligohydramnios
Fetal distress
Increased
perinatal
morbidity and mortality
Pathophysiologic
ChangesSlide29
The ultimate cure is deliveryAssess gestational age
Assess cervix
Fetal well-beingLaboratory assessmentRule out severe disease!!ManagementSlide30
>39 0/7 weeksChronic hypertension
>
37 0/7 weeksGestational hypertensionPreeclampsia without severe features>34 0/7 weeks Preeclampsia with severe featuresTiming of Delivery Slide31
< 34 0/7 weeks
Deliver immediately
for preeclampsia with severe features with unstable maternal or fetal conditionsThis recommendation is made without regard to gestational ageTiming of DeliverySlide32
< 34 0/7 weeks (Viable Fetus)
Give steroids but do not delay delivery for preeclampsia with severe features complicated by any of the following:
Uncontrollable severe hypertensionEclampsiaPulmonary edemaAbruptio placentaDisseminated intravascular coagulationEvidence of non-reassuring fetal status Intrapartum fetal demiseTiming of DeliverySlide33
< 34 0/7 weeks (Viable Fetus)
Deliver after steroid administration (48 hour delay) for preeclampsia with severe features with stable maternal and fetal condition and the following:
PPROM LaborThrombocytopeniaPersistently abnormal LFT’sIUGR (<5%) OligohydramniosReverse end-diastolic flow on umbilical artery Doppler studiesNew-onset renal dysfunction or increasing renal dysfunctionTiming of DeliverySlide34
Determined by:Gestational age
Fetal presentation
Cervical statusMaternal conditionFetal conditionRoute of DeliverySlide35
Magnesium sulfateRecommended for patients with preeclampsia with severe features
Not universally recommended for patients without severe features
Seizure ProphylaxisSlide36
Is not a hypotensive agentWorks as a centrally acting anticonvulsant
Also blocks neuromuscular
conduction4-6 g bolus1-2 g/hourMonitor urine output and DTR’sWith renal dysfunction, may require a lower doseSerum levels: 6-8 mg/dL are considered therapeutic Magnesium SulfateSlide37
Respiratory rate < 12DTR’s not detectable
Altered sensorium
Urine output < 25-30 cc/hourAntidote: 10 ml of 10% solution of calcium gluconate 1 v over 3 minutesToxicitySlide38
Few people die of seizuresProtect patient
Avoid insertion of airways and padded tongue blades
IV accessMGSO4 4-6 bolus, if not effective, give another 2 gTreatment of EclampsiaSlide39
THE FIRST THING TO DO AT A SEIZURE IS TO TAKE YOUR OWN PULSE!Slide40
Have not been shown to be as efficacious as magnesium sulfate and may result in sedation that makes evaluation of the patient more difficultDiazepam 5-10 mg IV
Sodium Amytal 100 mg IV
Pentobarbital 125 mg IVDilantin 500-1000 mg IV infusionAlternate AnticonvulsantsSlide41
Assess maternal labsFetal well-being
Effect delivery
Transport when indicatedNo need for immediate cesarean deliveryAfter the SeizureSlide42
Fetal monitoringIV accessIV hydration
The reason to treat is maternal, not fetal
May require ICUHypertensive EmergenciesSlide43
Diastolic BP > 105-110Systolic BP > 160
Avoid rapid reduction in BP
Do not attempt to normalize BPGoal is DBP < 105 not < 90May precipitate fetal distressCriteria for TreatmentSlide44
Crises are associated with hypovolemiaClinical assessment of hydration is inaccurate
Unprotected vascular beds are at risk, eg, uterine
Characteristics of Severe HTNSlide45
250-500 cc of fluid, IVAvoid multiple doses in rapid succession
Allow time for drug to work
Maintain LLD positionAvoid over treatmentKey Steps Using VasodilatorsSlide46
HydralazineLabetalol
Nifedipine
Acute Medical TherapySlide47
Dose: 5-10 mg every 20 minutesOnset: 10-20 minutes
Duration: 3-8 hours
Side effects: headache, flushing, tachycardia, lupus like symptomsMechanism: peripheral vasodilatorHydralazineSlide48
Dose: 20mg, then 40, then 80 every 20 minutes, for a total of 220mg Onset: 1-2 minutes
Duration: 6-16 hours
Side effects: hypotensionMechanism: Alpha and Beta blockLabetalolSlide49
Dose: 10 mg po, not sublingual
Onset: 5-10 minutes
Duration: 4-8 hoursSide effects: chest pain, headache, tachycardiaMechanism: CA channel blockNifedipineSlide50
Pulmonary edemaOliguriaPersistent hypertension
DIC
Other ComplicationsSlide51
Fluid overloadReduced colloid osmotic pressure
Occurs more commonly following delivery as colloid oncotic pressure drops further and fluid is mobilized
Pulmonary EdemaSlide52
Avoid over-hydrationRestrict fluids
Lasix 10-20 mg IV
Usually no need for albumin or Hetastarch (Hespan)Treatment of Pulmonary EdemaSlide53
25-30 cc per hour is acceptableIf less, small fluid boluses of 250-500 cc as needed
Lasix is not necessary
Postpartum diuresis is commonPersistent oliguria almost never requires a PA cathOliguriaSlide54
BP may remain elevated for several daysDiastolic BP less than 100 do not require treatment
By definition, preeclampsia resolves by 6 weeks
Persistent HypertensionSlide55
Rarely occurs without abruptionLow platelets is not DIC
Requires replacement blood products and delivery
Disseminated Intravascular CoagulopathySlide56
Continuous lumbar epidural is preferred if platelets normalNeed adequate pre-hydration of 1000 cc
Level should always be advanced slowly to avoid low BP
Avoid spinal with severe diseaseAnesthesia IssuesSlide57
He-hemolysisEL-elevated liver enzymes
LP-low platelets
HELLP SyndromeSlide58
Is a variant of severe preeclampsiaPlatelets < 100,000
LFT’s - 2 x normal
May occur against a background of what appears to be mild diseaseHELLP SyndromeSlide59
Low dose ASA (60-80 mg daily) is recommended in patients with a history of early-onset preeclampsia and delivery less than 34 0/7 weeks or preeclampsia in more than one prior pregnancy.
PreventionSlide60
Low dose ASA ineffective in patients at low riskCalcium, Vitamin C and Vitamin E supplementation
is ineffective
No compelling evidence that any of these are harmfulPreventionSlide61
Criteria for diagnosisLaboratory and fetal assessment
Magnesium sulfate seizure prophylaxis
Timing and place of deliverySUMMARY