PREECLAMPSIA & ECLAMPSIA

ENIS RAHMANIK 09-187FLORIDA SIREGAR 09-189LEONARD EVAN 09-199 KHARISMA PERTIWI 10-168

NADIA VINKA LISDIANTI 10-189ILHAM SURYO W. 10-190

ARGRACIA AMAHORU 10-192

HypertensionSustained BP elevation of 140/90 or greater

PIH

MildHELLP Synd

Impending eclampsia

Preeclampsia

Gestasional

Effect

Chronic

Severe

Eclampsia

Hypertensive Disease Associated with PregnancyChronic HypertensionGestational HypertensionPreeclampsiaEclampsiaHELLP Syndrome

Hypertensive Disease Associated with PregnancyChronic Hypertension

Diagnosed before the 20th week or present before the pregnancy

Mild hypertension > 140-180 mmHg systolic > 90-100 mmHg diastolic

Gestational Hypertension

Preeclampsia

Eclampsia

HELLP Syndrome

Hypertensive Disease Associated with Pregnancy Chronic Hypertension

Gestational Hypertension Criteria

Develops after 20 weeks of gestation Proteinuria is absent Blood pressures return to normal postpartum

Morbidity is directly related to the degree of hypertension Preeclampsia

Eclampsia

HELLP Syndrome

Overlap/Disease Progression

E leva te d B P a bo vefirs t trim e s ter

le ve ls5 5 -7 5%

G e sta tion a l h yp erte ns ionN o p ro te in u ria

5 -1 0% o f s in g le to ns3 0 % o f m u lt ip les

P re e c la m p s iaH yp e rte n s ion

P ro te in u ria5 -8 % o f p ro gn a nc ies

P a tien t w ith H yp e rten s ion

25%

Hypertensive Disease Associated with Pregnancy Chronic Hypertension

Gestational Hypertension

Preeclampsia Criteria

Develops after 20 weeks Blood pressure elevated on two occasions at least 6 hours apart Associated with proteinuria and edema

May occur less than 20 weeks with gestational trophoblastic neoplasia

Eclampsia

HELLP Syndrome

Preeclampsia vs. Severe Preeclampsia

Criteria for Preeclampsia

Previously normotensive woman

> 140 mmHg systolic> 90 mmHg diastolicProteinuria > 300 mg in

24 hour collectionNondependent edema

Criteria for Severe Preclampsia

BP > 160 systolic or >110 diastolic > 5 gr of protein in 24 hour urine or >

3+ on 2 dipstick urines greater than 4 hours apart

Oliguria < 500 mL in 24 hours Cerebral or visual distrubances

(headache, scotomata) Pulmonary edema or cyanosis Epigastric or RUQ pain Evidence of hepatic dysfunction Thrombocytopenia Intrauterine growth restriciton (IUGR)

Risk Factors for Preeclampsia

Nulliparity Multifetal gestationsMaternal age over 35Preeclampsia in a

previous pregnancyChronic hypertensionPregestational diabetes

Vascular and connective tissue disorders

NephropathyAntiphospholipid

syndromeObesityAfrican-American race

Hypertensive Disease Associated with Pregnancy Chronic Hypertension

Gestational Hypertension

Preeclampsia

EclampsiaDiagnosis of preeclampsiaPresence of convulsions not explained by a neurologic

disorder Grand mal seizure activity

Occurs in 0.5 to 4% or patients with preeclampsia HELLP Syndrome

Hypertensive Disease Associated with Pregnancy Chronic Hypertension

Gestational Hypertension

Preeclampsia

Eclampsia

HELLP Syndrome◦ A distinct clinical entity with:

Hemolysis, Elevated Liver enzymes, Low Platelets◦ Occurs in 4 to 12 % of patients with severe preeclampsia

Microangiopathic hemolysis Thrombocytopenia Hepatocellular dysfunction

Morbidity and Mortality from Hypertensive DiseaseHypertension affects 12 to 22% of pregnant

patients Hypertensive disease is directly responsible for

approximately 20% of maternal mortality in the United State

Mississippi Classification:Class 1 : Platelet count : <= 50.000 / ml LDH >= 600 IU / l AST and/or ALT >= 40 IU / lClass 2 : Platelet count : >50.000 <= 100.000 / ml LDH >= 600 IU / l AST and/or ALT >= 40 IU / lClass 3 : Platelet count : >100.000 <= 150.000 / ml LDH >= 600 IU / l AST and/or ALT >= 40 IU / l

PathophysiologyVasospasmUterine vesselsHemostasisProstanoid balanceEndothelium-derived factorsLipid peroxide, free radicals and antioxidants

Pathophysiology Vasospasm

◦ Predominant finding in gestational hypertension and preeclampsia

Uterine vessels

Hemostasis

Prostanoid balance

Endothelium-derived factors

Lipid peroxide, free radicals and antioxidants

Pathophysiology Vasospasm

Uterine vessels◦ Inadequate maternal vascular response to

trophoblastic mediated vascular changes◦ Endothelial damage

Hemostasis

Prostanoid balance

Endothelium-derived factors

Lipid peroxide, free radicals and antioxidants

Pathophysiology Vasospasm Uterine vessels

Hemostasis Increase platelet activation resulting in consumption Increased endothelial fibronectin levels Decreased antithrombin III and α2-antiplasmin levels Allows for microthrombi development with resultant

increase in endothelial damage Prostanoid balance Endothelium-derived factors Lipid peroxide, free radicals and antioxidants

Pathophysiology Vasospasm

Uterine vessels

Hemostasis

Prostanoid balance◦ Prostacyclin (PGI2):Thromboxane (TXA2) balance shifted to

favor TXA2 ◦ TXA2 promotes:

Vasoconstriction Platelet aggregation

Endothelium-derived factors

Lipid peroxide, free radicals and antioxidants

Pathophysiology 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

Pathophysiology Vasospasm

Uterine vessels

Hemostasis

Prostanoid balance

Endothelium-derived factors

Lipid peroxide, free radicals and antioxidants◦ Increased in preeclampsia◦ Have been implicated in vascular injury

Pathophysiologic ChangesCardiovascular effectsHematologic effectsNeurologic effectsPulmonary effectsRenal effectsFetal effects

Pathophysiologic Changes Cardiovascular effects

◦ Hypertension◦ Increased cardiac output◦ Increased systemic vascular resistance

Hematologic effects

Neurologic effects

Pulmonary effects

Renal effects

Fetal effects

Pathophysiologic Changes Cardiovascular effects

Hematologic effects◦ Volume contraction/Hypovolemia◦ Elevated hematocrit◦ Thrombocytopeniz◦ Microangiopathic hemolytic anemia◦ Third spacing of fluid◦ Low oncotic pressure

Neurologic effects Pulmonary effects Renal effects Fetal effects

Pathophysiologic Changes Cardiovascular effects

Hematologic effects

Neurologic effects◦ Hyperreflexia◦ Headache◦ Cerebral edema◦ Seizures

Pulmonary effects

Renal effects

Fetal effects

Pathophysiologic Changes Cardiovascular effects

Hematologic effects

Neurologic effects

Pulmonary effects◦ Capillary leak◦ Reduced colloid osmotic pressure◦ Pulmonary edema

Renal effects

Fetal effects

Pathophysiologic Changes Cardiovascular effects

Hematologic effects

Neurologic effects

Pulmonary effects

Renal effects◦ Decreased glomerular filtration rate◦ Glomerular endotheliosis◦ Proteinuria◦ Oliguria◦ Acute tubular necrosis

Fetal effects

Renal EffectsDecreased glomerular filtration rateGlomerular endotheliosisProteinuriaOliguriaAcute tubular necrosis

Pathophysiologic Changes Cardiovascular effects

Hematologic effects

Neurologic effects

Pulmonary effects

Renal effects

Fetal effects◦ Placental abruption◦ Fetal growth restriction◦ Oligohydramnios◦ Fetal distress◦ Increased perinatal morbidity and mortality

ManagementThe ultimate cure is deliveryAssess gestational ageAssess cervixFetal well-beingLaboratory assessmentRule out severe disease!!

Gestational HTN at TermDelivery is always a reasonable option if termIf cervix is unfavorable and maternal disease is

mild, expectant management with close observation is possible

Mild Gestational HTN not at TermRule out severe diseaseConservative managementSerial labsTwice weekly visitsAntenatal fetal surveillanceOutpatient versus inpatient

Indications for DeliveryWorsening BPNonreassuring fetal conditionDevelopment of severe PIHFetal lung maturityFavorable cervix

Unfavorable CervixNo contraindication to prostaglandin agentsIf < 32 weeks, consider cesareanWhen favorable, oxytocin

Hypertensive EmergenciesFetal monitoringIV accessIV hydrationThe reason to treat is maternal, not fetalMay require ICU

Criteria for TreatmentDiastolic BP > 105-110Systolic BP > 200Avoid rapid reduction in BPDo not attempt to normalize BPGoal is DBP < 105 not < 90May precipitate fetal distress

Characteristics of Severe HTNCrises are associated with hypovolemiaClinical assessment of hydration is inaccurateUnprotected vascular beds are at risk, eg, uterine

Key Steps Using Vasodilators250-500 cc of fluid, IVAvoid multiple doses in rapid successionAllow time for drug to workMaintain LLD positionAvoid over treatment

Acute Medical TherapyHydralazineLabetalolNifedipineNitroprussideDiazoxideClonidine

HydralazineDose: 5-10 mg every 20 minutesOnset: 10-20 minutesDuration: 3-8 hoursSide effects: headache, flushing, tachycardia,

lupus like symptomsMechanism: peripheral vasodilator

LabetalolDose: 20mg, then 40, then 80 every 20 minutes,

for a total of 220mg Onset: 1-2 minutesDuration: 6-16 hoursSide effects: hypotensionMechanism: Alpha and Beta block

NifedipineDose: 10 mg po, not sublingualOnset: 5-10 minutesDuration: 4-8 hoursSide effects: chest pain, headache, tachycardiaMechanism: CA channel block

ClonidineDose: 1 mg poOnset: 10-20 minutesDuration: 4-6 hoursSide effects: unpredictable, avoid rapid withdrawalMechanism: Alpha agonist, works centrally

NitroprussideDose: 0.2 – 0.8 mg/min IVOnset: 1-2 minutesDuration: 3-5 minutesSide effects: cyanide accumulation, hypotensionMechanism: direct vasodilator

Seizure ProphylaxisMagnesium sulfate4-6 g bolus1-2 g/hourMonitor urine output and DTR’sWith renal dysfunction, may require a lower dose

Magnesium SulfateIs not a hypotensive agentWorks as a centrally acting anticonvulsantAlso blocks neuromuscular conductionSerum levels: 6-8 mg/dL

ToxicityRespiratory rate < 12DTR’s not detectableAltered sensoriumUrine output < 25-30 cc/hourAntidote: 10 ml of 10% solution of calcium

gluconate 1 v over 3 minutes

Treatment of EclampsiaFew people die of seizuresProtect patientAvoid insertion of airways and padded tongue

bladesIV accessMGSO4 4-6 bolus, if not effective, give another 2 g

THE FIRST THING TO DO AT A SEIZURE IS TO TAKE YOUR OWN PULSE!

Alternate AnticonvulsantsHave 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 IVSodium Amytal 100 mg IVPentobarbital 125 mg IVDilantin 500-1000 mg IV infusion

After the SeizureAssess maternal labsFetal well-beingEffect deliveryTransport when indicatedNo need for immediate cesarean delivery

Other ComplicationsPulmonary edemaOliguriaPersistent hypertensionDIC

Pulmonary EdemaFluid overloadReduced colloid osmotic pressureOccurs more commonly following delivery as

colloid oncotic pressure drops further and fluid is mobilized

Treatment of Pulmonary EdemaAvoid over-hydrationRestrict fluidsLasix 10-20 mg IVUsually no need for albumin or Hetastarch

(Hespan)

Oliguria25-30 cc per hour is acceptableIf less, small fluid boluses of 250-500 cc as neededLasix is not necessaryPostpartum diuresis is commonPersistent oliguria almost never requires a PA cath

Persistent HypertensionBP may remain elevated for several daysDiastolic BP less than 100 do not require

treatmentBy definition, preeclampsia resolves by 6 weeks

Disseminated Intravascular CoagulopathyRarely occurs without abruptionLow platelets is not DICRequires replacement blood products and delivery

Anesthesia IssuesContinuous lumbar epidural is preferred if

platelets normalNeed adequate pre-hydration of 1000 ccLevel should always be advanced slowly to avoid

low BPAvoid spinal with severe disease

HELLP SyndromeHe-hemolysisEL-elevated liver enzymesLP-low platelets

HELLP SyndromeIs a variant of severe preeclampsiaPlatelets < 100,000LFT’s - 2 x normalMay occur against a background of what appears

to be mild disease

Conservative ManagementControversialSteroidsRequires tertiary careMust have stable labs and reassuring fetal statusMay use antihypertensives

PreventionLow dose ASA ineffective in patients at low

riskCalcium supplementation is ineffective (2.0

g of calcium gluconate per day)No compelling evidence that either are

harmfulRecent study done with antioxidant

(1,000mg VitC and 400mg VitE). Small study that needs to be confirmed.