3. INTRODUCTION
Incidence is 5-10%.
The most frequent cause of iatrogenic
prematurity.
Preterm delivery
Intrauterine growth restriction (IUGR)
Perinatal death
Maternal cerebrovascular accidents (
CVA).
Placental abruption.
4. NORMAL BLOOD PRESSURE CHANGES
IN PREGNANCY
Decreases during the first
trimester,
Reaching its lowest point at 20
weeks,
Returns to pre-pregnancy levels
during the third trimester.
6. Pregnancy induced
Hypertension
Gestational
HTN
● BP ≥ 140/90mmHg
●No evidence of underlying
cause of HTN
●No associated symptoms
●Comes to normal within 6
wks of delivery
Pre-
eclampsia
Non Severe Severe
Eclampsia
PreEclamsia
+
Convulsion
±
Coma
N.B: Grades of proteinuria (in g/L): Trace=0.1, 1+=0.3, 2+=1, 3+=3, 4+=10
7. GESTATIONAL
HYPERTENSION
Blood Pressure ≥ 140/90mmHg on two
or more occasions
- in a previously normotensive patient
- after 20 weeks gestation
- without proteinuria
- returning to normal 6 weeks after
delivery
• Almost half of these develop preeclampsia
syndrome
9. CRITERIA FOR GESTATIONAL HYPERTENSION
Blood Pressure > 140 to < 160 mm Hg, systolic
> 90 to < 110 mm Hg, diastolic
Proteinuria < 300 mg per 24-hr collection
Platelet count > 100,000/mm3
Liver enzymes Normal
Maternal symptoms Absent
IUGR / Oligohydramnios Absent
10. PREECLAMPSI
A
• It is defined as hypertension of at
least 140/90mm Hg recorded on
two separate occasions at least 4
hours apart and in the presence
of at least 300mg protein in a 24
hour collection of urine, arising
after the 20th week of gestation in
a previously normotensive
woman and resolving completely
by the 6th postpartum week.
11. DEFINATION OF
PRE ECLAMPSIA
Blood pressure >140/90 mm of Hg with
proteinuria
- >30 mm of Hg or more in SBP.
- >15 mm of Hg or more in DBP.
This rise of BP is observed at interval of 4
hrs.
12. DEGREE OF HYPERTENSION
Systolic BP Diastolic BP
Mild Hypertension 140-149 90-99
Moderate
Hypertension
150-159 100-109
Severe Hypertension ≥ 160 ≥ 110
14. Genetic
Genetic
Predisposition
Family History
Race & Ethnicity
More Common in
black & Asians
Pregnancy by
ovum donation
Age
&Parity
Teenage
pregnancy <18 yrs
Age>35 yrs
Long interval
between
pregnancy >10
years
Nulliparity
Partner
Factors
Change of partner
Limited sperm
exposure
Pregnancy by
donor
insemination
Partner fathered
an eclamptic
pregnancy
18. MECHANISMS
Stage 0
3-8 weeks
Stage 1
8-18 weeks
Stage 2
20 weeks to
birth
Poor Immunoregulation
Inadequate tolerance to feto-paternal
antigens during conception and implantation
Poor Placentation
Deficient trophoblast invasion and
spiral artery remodeling
Clinical manifestation
Over activation of maternal
endothelium and systemic
inflammatory network
Oxidative
Stress
Endoplasmic reticulum
Stress
Inflammatory
Stress
19. MECHANISMS
Invasive cytotrophoblasts of
fetal origin invade the
maternal spiral arteries
Transforms them from small-
caliber resistance vessels to
high-caliber capacitance
vessels
Capable of providing placental
perfusion adequate to sustain
the growing fetus
Normal
Pregnancy
20. PREECLAMPSIA
cytotrophoblasts fail to adopt an
invasive endothelial phenotype
invasion of the spiral arteries is shallow
and they remain small caliber, resistance
vessels
placental ischemia
28. C O M P L I C AT I O N S
- M AT E R N A L :
Convulsions and coma (eclampsia).
Cerebral haemorrhage.
Renal failure.
Heart failure.
Liver failure.
Disseminated intravascular coagulation.
Abruptio placentae.
Residual chronic hypertension in about 1/3 of cases.
Recurrent pre-eclampsia in next pregnancies.
29. COMPLICATIONS – FOETAL:
a. Intrauterine
growth
retardation
(IUGR).
b. Intrauterine
foetal death.
c. Prematurity
and its
complications.
30. PREDICTION OF PRE ECLAMPSIA
• Prediction of pre-eclampsia depends on variety of biochemical and
biophysical markers based on rationale implicated in the pathology
and pathophysiology
35. PREVENTIO
N
Regular Antenatal checkup:
• rapid gain in weight
• rising blood pressure
• edema
• proteinuria/deranged liver or renal profile
Low dose Aspirin in High risk group: ↑PGs
and↓TXA2
Calcium supplementation: no effects unless
women are calcium deficient
Antioxidants- Vitamin C and E
Nutritional supplementation: zinc, magnesium,
fish oil, low salt diet
37. ANTI HYPERTENSIVE DRUGS
Drug Starting dose Maximum dose
Methyldopa 250 mg TDS/QID 4 g / day
Labetalol 100 mg BD 2400 mg/ day
Nifedipine 10 mg BD 120 mg / day
38.
39. • Blood pressure ≥
140/90 before 20
weeks of gestation.
OR
• persistence of
hypertension beyond
6 weeks after
delivery.
CHRONIC HYPERTENSION
42. M AN A G E M E N T
O F C H R O N I C
H Y P E R T E N S I O N
Antihypertensive meds
(if B.P >100 mm Hg diastolic)
Labetalol is drug of choice
Serial ultrasounds (increase risk of
IUGR >30 weeks )
Serial B.P and urine protein
(watch for superimposed preeclampsia)
Induce labour at term
43. SU PER IMPOSED
PR EEC LA MPSIA
( ON C H R ON IC
HYPERTENSION
)
New-onset proteinuria > 300
mg/24 hrs in hypertensive women
but no proteinuria before 20 wks
gestation.
A sudden increase in proteinuria
or blood pressure or platelet count
< 100,000/ cu mm in women with
hypertension and proteinuria
before 20 wks gestation.
45. MANAGEMENT
IV MgSO4 – To prevent convulsions
( continue 24 hrs post-partum )
LOWER B.P ( hydralazine or
labetalol)
INDUCE LABOR (IV oxytocin and
amniotomy )
46. HELLP SYNDROME
• HTN patients with hemolysis (H),
elevated liver enzymes (EL), low
platelet count (LP)
• 5-20% of pt. with severe
preeclampsia and eclampsia develop
HELLP syndrome
47. HELLP SYNDROME
• Cardiovascular stabilization, correction of
coagulation abnormalities, and delivery
• PLT transfusion before or after delivery if PLT
count is <20,000/mm3 (advised at
<50,000/mm3 before cesarean)
• <32 weeks gestation; steroid therapy may
help stabilize maternal PLT count
49. ECLAMPSIA
• New onset of seizures or unexplained coma during
pregnancy in patients with pre-existing preeclampsia and
without pre-existing neurological disorder.
50. ECLAMPSIA
• Addition of convulsions in a woman with preeclampsia
• Occurs in 0.5-4% of deliveries
• 38% antenatlly 18% intrapartum, and 44% post partum.
Eclampsia Preeclampsia
Seizure/
Convulsion/
Coma
52. RECOMMENDED REGIME FOR MGSO4
• Loading dose for IV is 4g. i.e. 8 ml diluted in 12ml
normal saline. This 20 ml is given in 20 minutes.
• Maintenance dose is 20 g i.e. 40ml diluted in 60ml
normal saline and given at rate of 1g/hr.
53. DELIVERY IN ECLAMPSIA
• Unless contraindicated: Eclamptic women should undergo normal
vaginal delivery
Indications for caesarean section:
• Fetal distress
• Placental abruption
• Unfavourable cervix
• Failed induction of labour
• Recurrent seizures
Editor's Notes
It complicates
Gest hypertendion is the most benign part of the spectrum
N.B: Pre-eclampsia is principally a syndrome of signs and when symptoms appear it is usually late.
Gestational hypertension is most benign side of spectrum
It has Vast presentation pt may be asymptomattic with unremakable examination
The main goals in the initial evaluation of pregnant women with newly developed hypertension are to distinguish gestational hypertension from preeclampsia, which has a different course and prognosis, and to determine whether hypertension is mild or severe, which affects management and outcome
A women who is already hypertnsive I rise of blood pressure
According to the severity devided into mild moderate and severe
Its more common ib elderly primi patints
Can occur in molar pregnancies where fetus absent
Can also occur in abdominal pregnancy (pregnancy not in uterus
Abnormal placentation (stage 1), particularly lack of dilatation of the uterine spiral arterioles, is the common starting point in the pathogenesis of pre-eclampsia, which compromises blood flow to the maternal–fetal interface. Reduced placental perfusion activates placental factors and induces systemic hemodynamic changes. The maternal syndrome (stage 2) is a function of the circulatory disturbance caused by systemic maternal endothelial cell dysfunction resulting in vascular reactivity, activation of coagulation cascade and loss of vascular integrity. Pre-eclampsia has effects on most maternal organ systems, but predominantly on the vasculature of the kidneys, liver and brain.
process of vascular invasion, the cytotrophoblasts differentiate from an epithelial phenotype to an endothelial phenotype, a process referred to as "pseudovasculogenesis"
Hypo perfused placentation leading to manifestation of maternal hypertension protein uria and endothelial dysfunction
As we know its multi organ dysfunctuion RENal system glomerular endotheliosis which leads to excretion of moderate size protein molecule hepatic Cardiovascular System
Increased cardiac after load caused by-Hypertenison,
endothelial injury,
extravasation- especially in lungs (pulm edema)
Haemodynamic Changes
Marked reduction in cardiac output
Increased peripheral resistance
Blood Volume
Haemoconcentration
Increased vascular permeability
Patients is sensitive to vigorous fluid therapy, even sensitive to blood loss at delivery.
In pre eclampsia both mother and fetuse are effected
Most common cause of maternal death is cerebro vascular hemorrhage
Although it’s a most common and serious complication but there is no screening test
There is no screening test now a days interst is growing in FMS LIKE increases before pre eclampsia mani fest
at 24 weeks of pregnancy: Flow velocity waveform from the uterine artery at 24 weeks of gestation in a pregnancy with impaired placentation; in early diastole there is a notch (yellow arrow) and in late diastole there is decreased flow (orange arrow). Increased impedance to flow in the uterine arteries as indicated by:
Diastolic Notch in uterine artery waveform
Increase in uterine artery pulsatility index .
is associated with increased risk of preeclampsia
How we prevent this MOST COMMON AN D MOST SERIOUIS COMPLICATION
ONLY LDA has some benificial effevts other are in research process
How the already existing htn effects athe pregnency and vice versa
If there is only hypertension with of mild cetagory then its usually have good prognosis
If there is already end organ demage then prognosis is poor
How the already existing htn effects athe pregnency and vice versa
If there is only hypertension with of mild cetagory then its usually have good prognosis
If there is already end organ demage then prognosis is poor
Maternal mortality 1%
Fetal mortality 10. to 60
Menagement depends upon gestational age and fetal complication
38 have eclamptic seizures before labour, 18% during labour, and 44% after delivery.
uusually 48 hrs
Initiated with onset of labor till 24h postpsrtum.
For caesarean, started 2hrs before the section till 12hrs postpartum
Calcium gluconate is antagonist for MgSO4.it is usually given as 10 ml of 10% Calcium gluconate in 10 minutes