Janus F. Diel
Post Graduate Intern
San Pedro Hospital
Half of this patient subsequently develop preeclampsia syndrome.
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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 >0.3Increased certainty of PET
Serum creatinine > 1.1 mg/or doubling of baselinePlatelets < 100 000/mmPulmonary edemaCerebral: headache, visual disturbance, convulsionSerum Transaminase level twice normalOminous Signs
Microangiopathic hemolysis (increased LDH)Elevated ALT or ASTPersistant headache or other cerebral/ visual disturbancePersistant epigastric painECLAMPSIA
Seizures (generalized) pre-during-post labor not be attributed to other causesDR 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 postpartumPET 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 orPlt 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/m13.3% BMI 35 kg/m
Smoking risk of HPTExposed 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
Summary of current hypothesis:
Immunological disturbance abnormal placentalimplantation placental perfusion production of
substances that activate or injure endothelial cells of the
blood vessels multiple organ system involvement
MULTIPLE ORGAN SYSTEM INVOLVMENT
MECHANISM cerebral hyperperfusion ,vasospasm &forced dilation
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 diseaseAspiration 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 HPTAdvocate the use of volume expanders & avoidance of diuretics
-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 failure6-Eyes
Visual disturbances due to retinal artery vasospasmRetinal detachment Cortical blindness occipital lobe ischemia infarction or edema lasting hrs up to 8 daysVolume expansion in PET ANP COP & periephal vascular resistance
Expansion of the extracellular fluid volume (edema) Proteinuria plasma oncotic pressure displacement of intravascular fluid to interstitium15% 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 arteriesFetal
IUGROligohydramnios Placental infarctsPlacental abruptionPrematurityUteroplacental insufficiencyPerinatal deathMaternal
CNS seizures & strokeDIC CSRenal failureHepatic failure or ruptureDeathSEVERE 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 enzymesIUGRMILD 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 mother1- Hospitalization
Women with new onset BP 140/90Worsening BP Development of proteinuria in addition to existing BPDepends on:
Severity of PET Duration of gestationCondition of the CxComplete resolution of the signs & symptoms does not occur till after deliveryLines 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 homeIndications
Term pregnancy with mild or severe PETSevere PET regardless of the gestational ageWarning signs headache , visual disturbance, epigastric pain, oliguria
Eclampsia Pt must be stabilized & delivered immediatelyPreterm 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 CxMild 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 &deathSevere 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
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-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/ intubation70% multipara
PG, PET before 30 wk 40%
HEELP 5%
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 proteinuriaINVESTIGATIONS
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 pregnancyFETAL COMPLICATIONS
Prematurity 25-30%IUGR 10-15%Stillbirth & fetal distress due to abruptio placentae or ch intrauterine asphyxiain 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 IUGRLabetalolTop Related