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Janus F.

Diel
Post Graduate Intern
San Pedro Hospital

1. Hemorrhage
2. Infection
3.

Hypertension

When BP:
Systolic of >140 mm Hg
Diastolic > 90 mm Hg

Delta Hypertension: patient with bp <140/90


but has substantially increased blood
pressure. Some of this women will develop
eclamptic seizure or HELLP sydrome.

1-Gestational hypertension

2-Preeclampsia

3-Eclampsia

4-Chronic hypertension

5-Preeclempasia superimposed on chronic


hypertension

BP 140/90 mm Hg for the first time


during pregnancy
No proteinuria
BP returns to N < 12 Wk postpartum
Final Dx made only postpartum
May have other signs of PET eg.
Headache, epigastric discomfort or
thrombocytopenia

Preganancy specific syndrome that affects all


organ.
Minimum criteria

BP 140/90 mm Hg after 20 Wk gestation

Proteinuria 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 baseline

Platelets < 100 000/mm

Pulmonary edema

Cerebral: headache, visual disturbance,


convulsion

Serum Transaminase level twice normal

Ominous Signs
Microangiopathic hemolysis (increased
LDH)
Elevated ALT or AST
Persistant headache or other cerebral/
visual disturbance
Persistant epigastric pain
ECLAMPSIA
Seizures (generalized) pre-duringpost labor

not be attributed to other causes

DR SALWA NEYAZI ASS. PROF.KSU


CONSULTANT OBGYN

CHRONIC HYPERTENSION

BP 140/90 mm Hg before pregnancy or Dx


before 20 Wk gestation
HPT 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


Preeclampsia

Oldies: CH and
Superimposed

Black race and


hispanics

Hx of PET in a 1st
degree female relative

Hx of PET in prior
pregnancy

DM

Chronic renal disease

Ch HPT

Multiple pregnancy
twins 13 vs 6%
Hydatidiform mole
Nonimmune hydrops
fetalis
Obesity 4.3%
BMI < 19.8 kg/m
13.3%
BMI 35 kg/m
Smoking risk of
HPT

1.

2.

3.

4.

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

1.

2.

3.

4.

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

Loss of tolerance or dysregulation


Immunization from previous pregnancy
Impaired blocking Ab
Paternal antigenic load
Molar pregnancy
Trisomy
Immune maladaptation

Endothelial cell injury prostacyclin &


thromboxaneA2
Rejection phenomenon (inadequate matenal Ab
response)
Compromised placental perfusion
Altered vascular reactivity sensitivity to
vaspressin EPN, NEPN & angiotensin
GFR with retention of salt & water
intravascular volume
CNS irritability
DIC
Uterine muscle stretch & ischemia
Dietary 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 encephalopathy


Petechial Hg
Gross hemorrhages due to ruptured arteries
Thrombosis of the arterioles
Microinfarcts
Fibrinoid necrosis in the walls of blood vessels
Cerebral edema confusion, blurred vision /
coma
Brain 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 Hg

Severe cases IV Hg or subarachnoid Hg

MRI Abnormalities in the cortical &


subcortical white matter of the occipital &
parietal areas

EEG nonspecific changes

Pulmonary edema

May occur with sever PET OR EC


Usually postpartum
May 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
vasodilators

2-1ry 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 adminstration

Loss of the normal refractoriness to


angiotensin II

Hemoconcentration

Thrombocytopenia < 150 000 15-20% of PT

Fibrinogen

Thrombin time in 1/3 of the Ptwith EC

FDP 20% of the Pt

DIC 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 acid
Proteinuria
Renal tubular necrosis &renal failure

6-Eyes

Visual disturbances due to retinal artery


vasospasm
Retinal detachment
Cortical blindness occipital lobe ischemia
infarction or edema lasting hrs up to 8 days

Minimal involvement with fibrin deposition


Periportal hemorrhagic necrosis
serum liver enzymes
Bleeding from these lesions
Subcapsular hematoma hepatic rupture
Hepatic infarction
HEELP SYNDROME

plasma renin, angiotensin II &


aldosterone to the normal prepregnancy
values
Vasopressin levels are N
Atrial 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 & mortality

Doppler 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 trophoblast

Charecteristic lipid rich lesions in the


uteroplacental arteries

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

BP
Proteinuria
Edema of the face & hands ( but it has
been dropped of the definition due to
poor predictive value)
Headache
Visual disturbance
Epigastric pain
Exaggerated reflexes

Fetal

IUGR

Oligohydramnios

Placental infarcts

Placental abruption

Prematurity

Uteroplacental
insufficiency

Perinatal death

Maternal

CNS seizures &


stroke

DIC

CS

Renal failure

Hepatic failure or
rupture

Death

SEVERE PET

Systolic BP >160 mmHg or diastolic >110


mmHg on two occasions at least 6 hrs apart

Proteinuria 5 g/24 hrs

Oliguria < 500 cc /24 hrs

Cerebral or visual symptoms

Epigastric or Rt upper quadrant pain

Pulmonary edema or cyanosis

Low PLt

liver enzymes

IUGR
MILD PET any PET that is not considered severe

OBJECTIVES

Terminaton of pregnancy with the least


possible trauma to the mother & fetus

Birth of an infant who subsequently thrives

Complete restoration of health to the mother


1- Hospitalization

Women with new onset BP 140/90

Worsening BP

Development of proteinuria in addition to


existing BP

Observe for headache , visual disturbance,


epigastric pain & rapid wt gain
Wt daily
Analysis for proteinuria every 2 days / daily
BP in sitting position every 4 hrs except during
sleep
Blood investigations Hct, Plt, S creatinine,
liver enzymes
Frequent evaluation of fetal size & AF
Reduced physical activity but not absolute bed
rest
N diet & fluid intake

Depends on:

Severity of PET

Duration of gestation

Condition of the Cx

Complete resolution of the signs & symptoms


does not occur till after delivery
Lines of management

Termination of pregnancy

Antihypertensive therapy

Anticonvulsant therapy

Home 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 PET

Severe 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 oxytocin

Elective CS Severe PET with unfavorable Cx

Mild PET

There is no benefit of antihypertensive therapy

Reduction in the maternal BP with labetalol or


nifedipine IUGR

ACI 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 drugs
Diuretics 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
edema

LR 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 maintenance
Measure serum MG level at 4-6hrs maintain at 4-7 mEq
/L
D/C 24 hrs after delivery25% of seiz occur post
partum
Avoid toxicity by :
-monitoring patellar reflexes
-respiratory rate
-urine output
Antidote calcium gluconate 1gm IV
MgS myometrial contractility
Compared to phenytoin or diazepam 50% in
maternal mortality ,67% in convulsions
Infants 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, ansthesia
Recurrence 25-33% primipara
70% multipara
PG, PET before 30 wk 40%
HEELP 5%

Incidence of ch HPT 0.5-4%


80% essential HPT
20% 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 cardiomegaly

ECG 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 necrosis

If renal function is well creatinine < 1.5


mg/dl pregnancy does not change the
coarse of renal disease

If 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 ( 140179/90-109)


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 Dopa

Calcium channel blockers

B blockers can be used but IUGR

Labetalol

Serial U/S for fetal growth. BPP, NST34wk


Follow up every 2 wks till 30 then weekly
Warn the mother about symptoms of
superimposed PET
Investigations Renal function test,uric a ,
calcium ,LFT, 24hrs urine for creatinine
clearance & protein, CBC, Urinalysis, ECG.GTT
Early U/S for dating of preg
Not allowed to continue past 40wks
IOL at40 wks
Regular diet no salt restriction
IOL for superimposed PET,IUGR, fetal distress,
worsening renal function

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