Janus F. Diel

Post Graduate Intern

San Pedro Hospital

1. Hemorrhage2. Infection3. Hypertension

When BP:Systolic of >140 mm HgDiastolic > 90 mm HgDelta Hypertension: patient with bp

1-Gestational hypertension 2-Preeclampsia3-Eclampsia4-Chronic hypertension5-Preeclempasia superimposed on chronic hypertension

BP 140/90 mm Hg for the first time during pregnancyNo proteinuriaBP returns to N < 12 Wk postpartumFinal Dx made only postpartumMay have other signs of PET eg. Headache, epigastric discomfort or thrombocytopenia

Half of this patient subsequently develop preeclampsia syndrome.

*

Preganancy specific syndrome that affects all organ.

Minimum criteria

BP 140/90 mm Hg after 20 Wk gestationProteinuria 300 mg/24 hrs or 1+ dipstick persistent or protein: Creatinine ratio >0.3

Increased certainty of PET

Serum creatinine > 1.1 mg/or doubling of baselinePlatelets < 100 000/mmPulmonary edemaCerebral: headache, visual disturbance, convulsionSerum Transaminase level twice normal

Ominous Signs

Microangiopathic hemolysis (increased LDH)Elevated ALT or ASTPersistant headache or other cerebral/ visual disturbancePersistant epigastric pain

ECLAMPSIA

Seizures (generalized) pre-during-post labor not be attributed to other causes

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT OBGYN

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT OBGYN

CHRONIC HYPERTENSION

BP 140/90 mm Hg before pregnancy or Dx before 20 Wk gestationHPT first Dx after 20 Wk gestation & persistant after 12 Wk postpartum

PET SUPERIMPOSED ON CHRONIC HYPERTENSION

New onset proteinuria 300 mg/24 hrs in hypertensive women but no proteinuria before 20 Wk gestation A sudden increase in proteinuria or BP or

Plt count < 100 000/ mmin women with HPT & proteinuria before 20 Wk gestation

RISK FACTORS

Young and Nulliparity PreeclampsiaOldies: CH and SuperimposedBlack race and hispanicsHx of PET in a 1st degree female relativeHx of PET in prior pregnancyDMChronic renal diseaseCh HPTMultiple pregnancy twins 13 vs 6%Hydatidiform moleNonimmune hydrops fetalisObesity 4.3% BMI < 19.8 kg/m

13.3% BMI 35 kg/m

Smoking risk of HPT

Exposed to chorionic villi for the first time

Superabundance of chorionic villi as with twins or H mole

Preexisting conditions of endothelial cell activation or inflammation, DM or CVD

Genetics predisposition

Placental implantation with abnormal tropho invasion of uterine vessels

Immunologic maladaptive tolerance between maternal and paternal and fetal tissue

Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy

Genetics fators including inherited predisposing genes and epigenetic influnces

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT OBGYN

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT OBGYN

Loss of tolerance or dysregulationImmunization from previous pregnancyImpaired blocking AbPaternal antigenic loadMolar pregnancyTrisomy Immune maladaptation

Endothelial cell injury prostacyclin & thromboxaneA2Rejection phenomenon (inadequate matenal Ab response)Compromised placental perfusionAltered vascular reactivity sensitivity to vaspressin EPN, NEPN & angiotensin GFR with retention of salt & water intravascular volume CNS irritabilityDICUterine muscle stretch & ischemiaDietary factors Genetic factors

Summary of current hypothesis:

Immunological disturbance abnormal placental

implantation placental perfusion production of

substances that activate or injure endothelial cells of the

blood vessels multiple organ system involvement

MULTIPLE ORGAN SYSTEM INVOLVMENT

Similar to hypertensive encephalopathyPetechial HgGross hemorrhages due to ruptured arteriesThrombosis of the arteriolesMicroinfarctsFibrinoid necrosis in the walls of blood vesselsCerebral edema confusion, blurred vision / comaBrain stem herniation is a serious complication of cerebral edema death

MECHANISM cerebral hyperperfusion ,vasospasm &forced dilation

CT Scan of the pt focal hypodensities in the white matter / post half of the cerebral hemisphere & occasionally in the grey matter may represent petechial HgSevere cases IV Hg or subarachnoid HgMRI Abnormalities in the cortical & subcortical white matter of the occipital & parietal areasEEG nonspecific changes

Pulmonary edema

May occur with sever PET OR ECUsually postpartumMay be due to excessive fluid administration with crystalloids + plasma colloid pressure due to proteinuria in Pt with ch HPT & hypertensive cardiac disease

Aspiration of gastric content with EC

Plasma volume is reduced, the cause is unknown theories:

1-Generalized vasoconstriction with vascular permeability Advocate the use of vasodilators2-1ry hypovolemia hypoperfusion of the uterus release of pressor substances HPT

Advocate the use of volume expanders & avoidance of diuretics

High systemic vascular resistance & hyperdynamic ventricular function avoid aggressive fluid adminstrationLoss of the normal refractoriness to angiotensin II

HemoconcentrationThrombocytopenia < 150 000 15-20% of PTFibrinogen Thrombin time in 1/3 of the Ptwith ECFDP 20% of the PtDIC 5%Microangiopathic hemolytic anemia 5%HEELP hemolytic anemia, liver enzymes, low Plt

-LDH > 600 U/L

-T bilirubin >1.2 mg/dl

-AST > 70U/L

-Plt < 100 000/mm

Found in 10% of the Pt with severe PET

5-KIDNEY

Characteristic lesion glomeruloendotheliosis swelling of the gromelular capillary endothelium GFR creatinine clearance/ plasma creatinine uric acidProteinuriaRenal tubular necrosis &renal failure

6-Eyes

Visual disturbances due to retinal artery vasospasmRetinal detachment Cortical blindness occipital lobe ischemia infarction or edema lasting hrs up to 8 days

Minimal involvement with fibrin depositionPeriportal hemorrhagic necrosis serum liver enzymesBleeding from these lesions Subcapsular hematoma hepatic ruptureHepatic infarctionHEELP SYNDROME

plasma renin, angiotensin II & aldosterone to the normal prepregnancy valuesVasopressin levels are NAtrial natriuretic peptide

Volume expansion in PET ANP COP & periephal vascular resistance

Expansion of the extracellular fluid volume (edema) Proteinuria plasma oncotic pressure displacement of intravascular fluid to interstitium

Vasospasm compromised placental perfusion perinatal morbidity & mortalityDoppler velocimetry (systolic /diastolic velocity ratio of umbilical& uterine arteries )20% N

15% N Umbilical / Abnormal uterine

40% Both Abnormal

Histological changes in placental bed

Defective trophoblastic invasion of spiral arteries / decidual vessels but not myometrial vessels are invaded by trophoblastCharecteristic lipid rich lesions in the uteroplacental arteries

Calcium supplementation??Fish oil ineffectiveLow dose aspirin selective supression of throboxane synthesis by the plt & sparing endothelial prostacyclin production Not effective in preventing PETAntioxidants Vit C & E supplementation significant reduction in PET

BPProteinuriaEdema of the face & hands ( but it has been dropped of the definition due to poor predictive value)Headache Visual disturbance Epigastric painExaggerated reflexes

Fetal

IUGROligohydramnios Placental infarctsPlacental abruptionPrematurityUteroplacental insufficiencyPerinatal death

Maternal

CNS seizures & strokeDIC CSRenal failureHepatic failure or ruptureDeath

SEVERE PET

Systolic BP >160 mmHg or diastolic >110 mmHg on two occasions at least 6 hrs apartProteinuria 5 g/24 hrs Oliguria < 500 cc /24 hrsCerebral or visual symptomsEpigastric or Rt upper quadrant painPulmonary edema or cyanosisLow PLt liver enzymesIUGR

MILD PET any PET that is not considered severe

OBJECTIVES

Terminaton of pregnancy with the least possible trauma to the mother & fetusBirth of an infant who subsequently thrivesComplete restoration of health to the mother

1- Hospitalization

Women with new onset BP 140/90Worsening BP Development of proteinuria in addition to existing BP

Observe for headache , visual disturbance, epigastric pain & rapid wt gainWt dailyAnalysis for proteinuria every 2 days / dailyBP in sitting position every 4 hrs except during sleepBlood investigations Hct, Plt, S creatinine, liver enzymesFrequent evaluation of fetal size & AF Reduced physical activity but not absolute bed restN diet & fluid intake

Depends on:

Severity of PET Duration of gestationCondition of the CxComplete resolution of the signs & symptoms does not occur till after delivery

Lines of management

Termination of pregnancyAntihypertensive therapyAnticonvulsant therapyHome health care if BP improved within few days Pt can be managed as outpatient Home BP & urine protein monitoring . Instruction to come to hospital if she has waning symptoms . Rest at home

Indications

Term pregnancy with mild or severe PETSevere PET regardless of the gestational age

Warning signs headache , visual disturbance, epigastric pain, oliguria

Eclampsia Pt must be stabilized & delivered immediately

Preterm with mild PET Assess fetal wellbeing by NST, BPP, Doppler

Methods of termination

IOL with prostaglandines to ripen the Cx followed by IV oxytocinElective CS Severe PET with unfavorable Cx

Mild PET

There is no benefit of antihypertensive therapy Reduction in the maternal BP with labetalol or nifedipine IUGRACI contraindicated IUGR, boney malformations, limb contracture, PDA, pulmonary hypoplasia, RDS, hypotension &death

Severe PET

Antihypertensive therapy is used to control BP untill the Pt delivers or in preterm for 48 hrs to allow time for glucocorticoid administration for fetal lung maturity then delivery

Hydralazine

IV infusion or IV 5-10 mg bolus at 15-20 min interval

when diastolic BP 100-110 mm Hg or systolic BP 160 mmHg

Nifedipine 10 mg po repeated in 30 min Labetalol 10 mg IV / 20 mg after 10 min/ 40mg after 10min/80 mg (not to exceed 220 mg)Nitroprusside used only in PT not responding to other drugsDiuretics not recommended because intravascular volume depletion already exists in PET

Hyperosmotic agents not recommended because intravascular influx of fluid subsequent escape of fluid to vital organs pulmonary edema & cerebral edemaLR 60-120 ml/hr Excessive fluid administration pulmonary edema & cerebral edema

Magnesium sulfate IV infusion 4 gm loading dose in 100 ml of IV fluid over 20 min 2 gm /hr maintenanceMeasure serum MG level at 4-6hrs maintain at 4-7 mEq /LD/C 24 hrs after delivery25% of seiz occur post partumAvoid toxicity by :

-monitoring patellar reflexes

-respiratory rate

-urine output

Antidote calcium gluconate 1gm IVMgS myometrial contractilityCompared to phenytoin or diazepam 50% in maternal mortality ,67% in convulsionsInfants were less likely to be admitted to NICU/ intubation

Maternal death rare due to cerebral Hg, aspiration pneumonia, hypoxic encephalopathy, thromboembolism, hepatic rupture, renal failure, ansthesiaRecurrence 25-33% primipara

70% multipara

PG, PET before 30 wk 40%

HEELP 5%

Incidence of ch HPT 0.5-4%80% essential HPT20% due to renal disease

Symptoms & signs

risk in Age > 30, obese, multipara, DM, renal disease, black race, family Hx Difficult to deffirentiate HPT with superimposed PET from HPT with renal disease both have proteinuria

INVESTIGATIONS

Chest x ray cardiomegalyECG Lt vent hypertrophy serum creatinine, creatinine clearance & proteinuria 5-10%

MATERNAL COMPLICATIONS

Superimposed PET in 1/3 of Pt risk of abruptio placentae 0.4-10% DIC, acute tubular & cortical necrosisIf renal function is well creatinine < 1.5 mg/dl pregnancy does not change the coarse of renal diseaseIf renal function is affected prior to pregnancy deterioration of renal function occur more rapid in pregnancy

FETAL COMPLICATIONS

Prematurity 25-30%IUGR 10-15%Stillbirth & fetal distress due to abruptio placentae or ch intrauterine asphyxia

No benefit of treating mild CH HPT ( 140-179/90-109)

in pregnancy should be monitered for worsening HPT or superimposed PET

Pt with severe CH HPT should have their BP controlled before pregnancy & continue Rx in pregnancy Methyle DopaCalcium channel blockersB blockers can be used but IUGRLabetalol

Serial U/S for fetal growth. BPP, NST34wkFollow up every 2 wks till 30 then weeklyWarn the mother about symptoms of superimposed PETInvestigations Renal function test,uric a , calcium ,LFT, 24hrs urine for creatinine clearance & protein, CBC, Urinalysis, ECG.GTTEarly U/S for dating of pregNot allowed to continue past 40wksIOL at40 wksRegular diet no salt restrictionIOL for superimposed PET,IUGR, fetal distress, worsening renal function