*Hypertensivedisordersinpregnancy

Hypertension in Pregnancy
 Systolic B.P. > 140 mmHg
 and/or
 Diastolic B.P. > 90 mmHg
 Documented on two occasions
 At least 6 hours apart
 Not more than 7 days apart
 Other Criteria (Not part of definition currently)
 SBP increased by 30mmHg
 DBP increased by 15mmHg
 Mean Arterial Pressure increased by 20mmHg
2

Outline
 Classification of hypertensive
disorders of pregnancy
 Physiology and pathophysiology
 Blood pressure et al
 Specific hypertensive disorders
of pregnancy
 Antihypertensive
pharmacotherapy
 Management principles

Why care about hypertension
(HTN) in pregnancy?
 HTN is common (10% of 1st pregnancies, 8% of
all pregnancies)
 18% of maternal mortality in the US
 Development of pre-eclampsia(PE):
 Increased maternofetal mortality
 Preterm delivery, IUGR/LBW
 Increased HTN when these babies become
adults
 Pre-existing hypertension:
 Increased PE, IUGR/PE, fetal mortality

Definitions and classification

Classification
Hypertension in
Pregnancy
Gestational Hypertension
Preeclamsia-Eclampsia
Chronic Hypertension
Preeclamsia superimposed
on Chronic Hypertension6

Classification of hypertensive disorders of
pregnancy
1. Vesna D. Garovic Hypertension. 2012;59:555-557
2. National High Blood Pressure Education Program Working
Group on High Blood Pressure in Pregnancy. Am J Obstet Gynecol.
2000 Jul. 183(1):S1-S22
<20GW with
trophoblastic
disease

Updated Classification of Hypertensive
disorders of pregnancy
1. Preeclampsia (PE)-eclampsia (BP elevation
after 20 weeks of gestation with proteinuria or
any of the severe features of preeclampsia)
2. Chronic hypertension (CHTN, of any cause that
predates pregnancy)
3. Chronic hypertension with superimposed
preeclampsia (chronic hypertension in
association with preeclampsia)
4. Gestational hypertension (GH: BP elevation >20
weeks of gestation in the absence of
proteinuria or any of the severe features of
preeclampsia)
Obstetrics & Gynecology, Vol. 122, No. 5, November
2013

The New vs the Old
classifications
 Pre-eclampsia does not require the presence of
proteinuria for Dx
 Pre-eclampsia may be diagnosed if HTN +
 Thrombocytopenia (PLTs<100k)
 Liver injury (ALT/AST > x2 UNL)
 Renal dysfunction (S.Cr>1.1 or x2 from baseline*)
 Pulmonary edema
 New onset cerebral or visual disturbances
2013
*in the absence of other renal
disease

Normal Blood Pressure changes in
Pregnancy
10

What is Significant Proteinuria in
Pregnancy?
 Total protein in 24 hours urine >
300mg
 Protein : Creatinine ratio in random
sample > 0.1
11

Gestational Hypertension
 New onset of hypertension after 20
weeks of gestation without
proteinuria, followed by return of
B.P. to normal within 12 weeks post-
partum.
12

Preeclamsia
 New onset of hypertension after 20
weeks of gestation along with
properly documented proteinuria,
followed by return of B.P. to normal
within 12 weeks post-partum.
Preeclamsia Gestational
Hypertension Proteinuria
13

PREECLAMPSIA
Incidence : 5-15%
In primigravida: 10%
In Multigravida 5%

Risk factors for Preeclampsia :
 Primi : younger or elderly
 Family history of PIH, HTN, DM
 H/O PIH in previous pregnancy
 Hyperplacentosis as in molar pregnancy, twins, DM
 Obesity, Chronic HTN, pre-existing vascular or Renal
disease, DM
 New paternity
 Thrombophilia : APLA, deficiency of protein C/S,
factor 5 Leiden,

ETIOLOGY & PATHOGENESIS
 Basic etiology is abnormal placentation : failure of
trophoblast invasion
 Failure of second wave of endovascular trophoblast
migration resulting in reduction of blood supply to
fetoplacental unit.
 2 main things we should remember :
Endothelial Dysfunction due to oxidative stress and
inflammatory mediators, Vasospasm due to
imbalance b/w vasodilators(PGI2, NO) &
vasoconstrictors (TxA2, angiotensin 2, endothelin).

Eclampsia
 Generalized tonic-clonic seizure in a
patient with Preeclampsia not attributed
to any other cause.
Eclampsia Preeclampsia
Seizure/
Convulsion/
Coma
17

Chronic Hypertension in Pregnancy
 Hypertension before pregnancy /
Diagnosed before 20 weeks of pregnancy
not due to gestational trophoblastic
disease.
 Hypertension diagnosed after 20 weeks
but persistent after 12 weeks postpartum
18

Chronic HTN & Pregnancy :
 Etiology :
1. Most common : Essential HTN
2. Secondary HTN :
1. Renal : parenchymal or renovascular
2. Endocrine : pheochromocytoma, prim
aldosteronism, cushings syndrome.
3. Neurogenic : increased ICT
4. Vascular : Aortic coarctation
5. Genetic: Glucocorticoid remediable aldosteronism,
Liddle Syndrome (Pseudoaldosteronism)
3. Systolic HTN :
Thyrotoxicosis, hyperkinetic circulation.

Superimposed Preeclampsia On
Chronic Hypertension
 New onset proteinuria in hypertensive
women but no proteinuria before 20
weeks' gestation
 A sudden increase in proteinuria or blood
pressure or platelet count < 100,000/L in
women with hypertension and
proteinuria before 20 weeks' gestation
20

Hypertension In Pregnancy
 Definition (ACOG) :
Diastolic BP of 90mm Hg or higher or systolic BP of
140mm Hg or higher after 20wks of gestation in a
woman with previously normal BP.
It should be documented on at least 2 occasions
measured 4hrs apart.
 Proteinuria : It is defined as the urinary excretion of
300mg/L or more of protein in a 24hr urine
collection. (correlates with reagent strip >1+ i.e.
>30mg/dl)

CLASSIFICATION OF HYPERTENSION IN PREGNANCY
1) Chronic HTN : HTN present before the 20th week of
pregnancy or that present before pregnancy.
2) Chronic HTN with superimposed Preeclampsia :
defined as proteinuria developing for first time
during pregnancy in a woman with known chronic
HTN.
3) Gestational HTN : HTN without proteinuria
developing after 20wks of gestation during labor or
the peurperium in previously normotensive non
proteinuric woman.

4) Preeclampsia : Gestational HTN asso with
proteinuria .
5) Eclampsia : Convulsions occurring in a pt with
preeclampsia.
* HELLP Syndrome : Severe form of preeclampsia char
by hemolysis (abnormal PBS, bil > 1.2mg/dl),
thrombocytopenia (platelets<1lakh/mm3) and
elevated liver enzymes (AST>70 U/L, LDH>600 U/L)

Physiological changes in pregnancy :
 Normal pregnancy is characterised by :
1. Increase in plasma volume(preload), starts to
increase by 6th wk, & plateaus at 30wks. (+50%) so
fall in haematocrit.
2. Increase in CO, starts to increase in 5th week, peak
at 30-34 weeks then remains static till term,
increases further in labor & immediately following
delivery.
3. Decrease in PVR
4. So results in a physiological decrease in mean BP
during 2nd trimester but it rises to normal value as
pregnancy advances.

Conti..
 Hypercoagulable state :
 Increase (50%) in fibrinogen to 300-600
 Fall in platelets (15%)
 Raised ESR 4 times of normal. (so no diagnostic value)
 Decreased fibrinolytic activity
 Increase in clotting factors 1 7 9 10 but others
decreased so difference in CT.
 All these help to effectively control blood loss &
achieve hemostasis after placental separation.

Risk Factors
Genetic
Age & parity
Partner factors
Pregnancy Factors
Underlying Medical
Conditions
Others
Risk Factors: Preeclampsia
26

Risk Factors: Cont.
Genetic
Genetic
Predisposition
Family
History
Race & Ethnicity
More Common in black
& Asians
Pregnancy
by ovum
donation
Age &Parity
Teenage
pregnancy
Age>35 yrs
Long
interval
between
pregnancy
Nulliparity
Partner Factors
Change of
partner
Limited
sperm
exposure
Pregnancy by
donor
insemination
Partner
fathered an
eclamptic
pregnancy
27

Risk Factors: Cont.
Pregnancy Factors
Multiple
pregnancy
Hydatiform
mole
Hydrops
fetalis
Fetal
chromosomal
anomaly
(trisomy 13)
Underlying Medical
Disease
Chronic hypertension
Diabetes mellitus
Renal Disease
Cardiovascular disease
Hyperthyroidism
Sickle cell disease
Others
Obesity
Psychological
stress &
strain
Previous
history of
preeclamsia
28

Two stage model for
preeclampsia
Stage 2
Maternal
syndrome
(HTN, proteinuria,
Endothelial
dysfunction)
Stage1
Reduced placental
implantation ???
30

Reduced placental
implantation –Stage-1
 PREDISPOSING FACTORS:
 Abnormal implantation
 Association with microvascular diseases
(diabetes, hypertension etc.)
 Association with large placentas
(hydrops, multiple gestation,
hydatidiform mole)
31

NORMAL ENDOMETRIAL VASCULARITY

35
Net effect
Replacement of endothelial lining & muscular
arterial wall by fibrinoid formation
Distended tortuous spiral arteries
Low resistence, low pressure high flow system in normal
pregnancy

ETIOLOGICAL FACTORS
 Placental hypoxia
 Immunological factors
 Placental enzymes
 Genetic factors (MTHFR, F5,)
 Oxidative stress
 ???????????????????
36

What causes maternal
syndrome?
Stage 2
Maternal
syndrome
(HTN,
proteinuria,
Endothelial
dysfunction)
Stage1
Reduced
placental
implantation
???
What gets into maternal circulation??????37

Maternal Syndrome
stage-II
 not just hypertension and
proteinuria
 But also involves different end
organs
38

Physiology of maintain
uteroplacental flow in Normal
pregnancy
 Placenta releases angiotensinase 
destruction of angiotensin-II(a potent
vasoconstrictor) BP stabilized
 Vascular synthesis of PGI-2 and NO in
excess  vasodilation  BP stabilized &
uteroplacental flow maintains
 Release of VEGF  restores
uteroplacental flow
39

Normal balance of agonist &
anta-agonistic factors:
1.vasodialator &
vasoconstrictor
2. angiogenic and
antiangiogenic factors
40

1.vasodialator & vasoconstrictor
vasodialator
NO
PGI-2
vasoconstrictor
Angiotensin-
II
Endothelin-I
placenta
Syncytiotrophoblast
& endothelium
41

2. angiogenic and
antiangiogenic factors
Angiogenic
factor
•VEGF
•TFG-beta
•PlGF
Antiangiogenic
factor
• sFlt-1
• sEng
42

Conti..
 All of above result in :
 Increased vasoconstriction
 Decreased organ perfusion : utero-placental –
IUGR, Kidneys- glomerular endotheliosis,
oliguria, liver ischemia, HELLP, CNS seizures.
 Increased endothelial dysfunction – capillary
leak, oedema, Pulmonary oedema,
proteinuria.
 Activation of coagulation: DIC, low platelets
 Haemoconcentration

Cardiovascular physiology,
and pathophysiology

Hemodynamic changes during pregnancy
Kidney International (1998) 54, 2056–2063
Circulatory
Parameters
Renal
Hemodynamics

Uteroplacental & maternal hemodynamics
in hypertensive disorders of pregnancy
Kaplan: Clinical Hypertension, 2010,
p414

Pathogenesis of pre-eclampsia:
a renal perspective
Kidney International (2005) 67, 2101–2113
Glomerular endotheliosis

Glomerular endotheliosis.
 (A) Normal human glomerulus (hematoxylin and eosin stain).
 (B) Human preeclampsia glomerulus (hematoxylin and eosin stain). A
33-year-old woman with twin gestation and severe preeclampsia at 26
weeks' gestation with urine protein/creatinine ratio of 26 at the time of
biopsy.
 (C) Electron microscopy of glomerulus of the above patient described in
(B). Note occlusion of capillary lumen cytoplasm and expansion of the
subendothelial space with some electron-dense material. Podocyte
cytoplasms show protein resorption droplets and relatively intact foot
processes (original magnification 1500).
 (D) Control rat glomerulus (hematoxylin and eosin stain). Note normal
cellularity and open capillary loops.
 (E) Soluble Flt-1–treated rat (hematoxylin and eosin stain). Note
occlusion of capillary loops by swollen cytoplasm with minimal increase
in cellularity.
 (F) Electron microscopy of sFlt-1–treated rat. Note occlusion of capillary
loops by swollen cytoplasm with relative preservation of podocyte foot
processes (original magnification 2500). All light micrographs taken at
identical original magnification of 40).
50

Theories about pathogenesis
are too numerous to count
 Placentation
 Immune theory
 Placental debris hypothesis syncytiotrophoblast
(SCT) shedding
 Theories are not mutually exclusive and are
likely complimentary (see renal perspective)

Pathogenesis of pre-eclampsia: theories too numerous to count or
different converging pathways based on placenta derived biomarkers?
Anne Cathrine Staff et al. Hypertension. 2013;61:932-942
Copyright © American Heart Association, Inc. All rights reserved.

Pathogenesis of pre-eclampsia
 A model of extended definition of preeclampsia on the
basis of placenta-derived biomarkers.
 The figure illustrates the main alternative pathways
during pregnancy leading to same diagnosis of
preeclampsia, with or without fetal growth restriction
(FGR), or to development of FGR without preeclampsia.
 The pathways are differentiated by maternal circulating
placenta growth factor (PlGF) as a biomarker of
placental dysfunction.
 At present, it is not clear whether the addition of other
placenta-derived biomarkers (such as soluble fms-like
tyrosine kinase-1 and soluble endoglin), or even
maternally derived biomarkers (such as inflammatory
cytokines), should be added to this flow-chart to
improve the definition and sub classification of
preeclampsia types.

Schematic representation of the proposed initiating
events and factors in the pathophysiology of PE
preeclampsia.
Junie P. Warrington et al. Hypertension. 2013;62:666-673
Copyright © American Heart Association, Inc. All rights reserved.

Pathophysiology for different
organ damage:
55

Basic mechanism of different organ
damage:
 Increased vasoconstriction
 Decreased organ perfusion :
 Increased endothelial dysfunction – capillary
leak, oedema, Pulmonary oedema,
proteinuria.
 Activation of coagulation: DIC, low platelets
 Haemoconcentration
56

Organ damage
utero-placenta IUGR
Hematological Epistaxis, DIC like features,
hemoconcentration
CNS Cerebral edema, cerebral hge seizures
Heart Subendothelial hge , focal necrosis & hge,
cardiomyopathy, heart failure
Lungs Pulmonary edema, hemorrhagic
brochopneumonia
Kidneys glomerular endotheliosis, oliguria
liver Subcapsular hge, ischaemiaperiportal
necrosis, HELLP
58

CVS involvement:
• ↑afterload
↑ed peripheral
resistance
• ↓preload
↓ed pregnancy
induced
hypervolumia
•Pulmonary leak edema
alveolar
endothelial
damage & ↓ed
plasma oncotic pr
• hemoconcentration
& ↑ed hematocrit
↓ed blood volume
than normal
pregnancy
(16% vs 50%):
Heart
failure
↓cardiac
output
59

Hematological system
Thrombocytopenia
& other PL
abnormality:
• ↑ed PL
activation &
degranulation,
• ↓ed life span.
• Corelates well
wth disease
severity.
Intravascular
hemolysis
• endothelial
damage & altered
fluidity of
erythrocyte
membrane d/t
change in serum
lipid content →
↑ed LDH,
spherocytosis,
reticulocytosis
• microangiopathic
hemolysis
↑ed coagulation &
fibrinolysis
• Feature like DIC
• Release of
thromboplastin
• ↓fibrinogen
• AT-III
• plasminogen
60

Renal system involvement:
 ↓ed renal perfusion :(d/t ↓ed blood volume & ↑ed
afferent arteriolar pr.)
 ↓ed GFR : d/t
 glomerular capillary endotheliosis
 Endothelial dysfunction + mesangial swelling + BM
disruption
 (but podocyte disruption minimal)
 Oliguria
 ↑ed creatinine level
 ↑ed uric acid 61

Hepatic involvement:
Periportal
hemorrhage
hematoma
formation
Rupture
epigastric pain
62

Brain involvement:
Acute severe HTN
cerebrovascular
overregulation
Vasospasm
Parenchymal
ischemia
Cytotoxic edema
sudden ↑↑SBP
exceeds normal range of
cerebrovascular
autoregulation
Forced vasodilation
+ hyperperfusion
Vasogenic edema
63

Lungs involvement:
High SBP
↑ed arteriolar pr
↑ed extravasation of blood into
alveoli + rupture of arteriole
Pulmonary edema, hemorrhagic
brochopneumonia
64

Diagnosis of
Hypertensive
Disorders of
Pregnancy

Diagnostic criteria for pre-eclampsia
2013
*

Diagnosing Preeclampsia-Eclampsia:
• Blood pressure ≥ 140/90 mm of Hg (at
or after 20 weeks of gestation) on 2
occasions at least 6 hours apart during
bed rest. (≥ 160/90 mm of Hg is
severe disease)
• accompanied by one or more of:
* significant proteinuria
-urinary dipstick 2+
-random urinary
protein/creatinine
ratio ≥ 30 mg/mmol
-24 hour urine excretion ≥300
mg/24 hrs
* renal involvement
-serum creatinine ≥ 90 mmol/L
or
-oliguria (<400 ml in 24 hrs)
* haematological involvement
-platelet count<1 lakh
* liver involvement
-raised AST, ALT (>70 IU/l)
-severe upper abdominal pain
* neurological involvement
-severe headache
-persistent visual disturbances
-hyperreflexia with sustained
clonus
-convulsions (eclampsia)
-stroke
* pulmonary oedema
* fetal growth restriction
* placental abruption

Risk factors for Pre-eclampsia
Clinical factor Risk Ratio
Renal Disease 20:1
Chronic hypertension 10:1
Antiphospholipid syndrome 10:1
Previous pre-eclampsia 7:1
Family history 5:1
Twin gestation 4:1
Nulliparity 3:1
Age >40 3:1
Diabetes 2:1
African American 1.5:1

Diagnosis
 BP > 140/90 mmHg
(NICE gudelines mild 140/90 to 149/99,
Moderate150/100 to 159/109 & severe 160/110)
 Proteinuria :
24hr urinary protein >300mg, (>5gm severe PIH)
dipstick method > 1+ (30mg/dl)
 Urinary Protein/creatinine ratio > 30mg/mmol

Other :
 Pathological oedema
 Excessive weight gain : is > 0.5kg in one week
or >2kg in one month in later months of
pregnancy.
 Clinical e/o vasoconstriction by fundoscopy

Definition of Albuminuria
Method Normal
Micro-
albuminuria
Overt/Macro-
albuminuria
24 hour excretion <30 mg/day 30-300 mg/day >300 mg/day
Timed urine specimen <20 g/min 20-200 g/min >200 g/min
Spot-urine albumin
specific dipstick
(screening)
<3 mg/dl >3 mg/dl N/A
Spot urine albumin/
creatinine ratio (ADA)
< 30 mg/g 30-300 mg/g >300 mg/g
Spot urine albumin/
creatinine ratio
(gender specific)
(K/DOQI)
<17 mg/g (men)
<25 mg/g (women)
17-250 (men)
25-355 (women)
>250 (men)
>355 (women)
K/DOQI and ADA

Proteinuria
Clinical Sample Cutoff
24 hour collection > 300mg
Timed collection Extrapolated* > 300mg
Spot Protein/Creatinine > 0.3
(both in mg/dl)
Spot Dipstick > 1+
Not recommended unless
other approaches not
available
*24/duration of collection in hrs x protein
2013
Massive proteinuria (>5g) and fetal growth restriction were
eliminated from the diagnostic criteria of severe pre-eclampsia

s/o Impending Eclampsia :
 Headache
 Epigastric or rt upper quadrant pain :
particularly in HELLP S due to liver
dysfunction.
 Visual symptoms : scotomas progressing
to blurred vision, even blindness.
(abnormality lies in occipital cortex, not
in retina.) recovers faster post natally.
 Brisk DTRs : CNS irritabilty.

“Never neglect these
alarming signs….and u
will save a life or two…”

HELLP Syndrome:
-Hemolysis:
● LDH > 600 U per L
● Abnormal PBS showing schistocytes,
burr cells.
● Serum bilirubin ≥ 1.2 mg/dL
-Elevated Liver enzymes:
● AST and ALT >70 IU/l
-Low Platelet count:
● <1 lakh/cubic mm

Abnormal Peripheral Blood Smear
(PBS)

History -special points
• Patient Particulars: Age young or >35 yrs, nulliparity, low SES
-risk factors
• Chief Complaints: Swelling of legs or other parts of body
(face, abdominal wall, vulva, or whole body and tightness of
the ring on the finger.) Severe disease -Headache, visual
changes, nausea, vomiting, abdominal or epigastric pain, and
oliguria, insomnia, vaginal bleeding, seizures.
• Present Obstetric History: Onset, Duration, Severity of
Htn/Proteinuria and H/o drug intake
• Past Obstetric History: H/o any hypertensive disorder of
pregnancy with week of onset. Also note the interval since
last pregnancy, gestational age at delivery. Any foetal
complications.
• Past History: of pre-existing hypertension, renal disease,
diabetes, thrombophilia, or thyroid disorder.
• Family History: of Htn, Preeclampsia, Diabetes, CVD

Physical Examination:
● Obesity/BMI>35 kg/m2
● Weight (serial measurements): Gain in wt at the rate of >1 lb a week
or >5 lbs a month in the later months of pregnancy may be the
earliest sign of preeclampsia.
● Oedema (all sites): has to be pathological, meaning visible pitting
edema demonstratable over the ankles after 12 hrs bed rest.
● Pulse (in all 4 limbs)
● B.P.:
○ right arm, sitting/supine, arm at level of heart, cuff length=1.5
times of arm circumference, diastolic BP is the disappearance of
Korotkoff sounds (phase V)
○ taken on 2 occasions at least 6 hrs apart for confirmation of
diagnosis.
● CVS examination: auscultation for heart rate, rhythm, splitting of S2,
murmurs.
● Ophthalmic examination: retinal haemorrage, nicking of veins,
arteriole/vein ratio 3:1 from 3:2, papilloedema
● Deep tendon reflexes: hyperreflexia/presence of clonus

How to Measure Blood
Pressure?
 Sitting Position
 Patient Relaxed
 Arm well supported
 Measured in right arm
 Cuff at heart level
 Proper cuff size (80% of
arm circumference)
 Slow deflation of bladder
(2mmHg/s)
 From start of Korotkoff I to
end of Korotkoff V 79

How to measure blood pressure?
 Patient sit quietly with the back supported, the arm
bared (supported at heart level) and an empty bladder
 No caffeine or smoking 30 mins prior
 Bladder cuff >80% arm circumference and cover 2/3 of
the arm length
 Take 2 readings and average; if readings > 5 mmHg
keep taking until 2 are close (and then average)
 For diagnosis take 3 sets of measurement over 1 week
 Obtain BP in both arms; use the arm with the highest
blood pressure
 If arm pressure is elevated r/o coarctation by
measuring BP in one leg

Obstetric Examination:
Nothing special is found except features
of IUGR, oligohydramnios in some
cases.

Maternal Investigations:
Tests may be abnormal even when BP elevation is minimal.
• Urine dipstick testing for proteinuria
o Quantitation by laboratory methods if ≥ 2+ on dipstick testing
o Urinary ACR(albumin-creatinine ratio) to detect significant
proteinuria (≥30mg/mmol)
o 24 hour urine collection is not necessary in routine clinical
management
• Routine Blood Examination: TLC, DLC, Peripheral Smear, BT, CT,
Hb%
• Serum Urea, creatinine, electrolytes including lactate
dehydrogenase (LDH) and uric acid.
• Liver function tests (LFT) -AST, ALT >70 IU/l
 • Skiagram of chest –PA view, Pulmonary Capillary Wedge Pressure
(PCWP), Brain Natriuretic Peptide (BNP)  for detection of
pulmpnary oedema

Foetal Investigations:
• Cardiotocograph (CTG)
• Ultrasound scan (USS) assessment of:
o fetal growth
o amniotic fluid volume (AFV)
o umbilical artery flow (Doppler)

uterine artery DOPPLER
In preeclamptic mother:
Showing early diastolic NOTCH
Decreased EDF
(due to high resistance)
In normal mother
84

Differential Diagnosis
 Pre-existing hypertension,
 New/gestational hypertension
 Pre-eclampsia
 Eclampsia
 Exacerbation of underlying renal disease/Superimposed pre-
eclampsia-eclampsia
 SLE
 ΔΔ ECLAMPSIA
 -Epilepsy,
 -Intracranial haemorrhage/thrombosis,
 -meningitis,
 -cerebral malaria,
 -amniotic fluid embolism can mimic eclampsia. 85

Assessment of the severity of Gestational
Hypertensive Disorders
There are several
indicators used to
assess the severity of
PIH
Blood pressure
Proteinuria
Other associated
abnormalities
86

N.B: Grades of proteinuria (in g/L): Trace=0.1, 1+=0.3, 2+=1, 3+=3,
4+=10
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: Pre-eclampsia is principally a
syndrome of signs and when
symptoms appear it is usually late.
Assessment of the severity of pre-
eclampsia is given in the next
slide.
87

Indicators of severityof Pre-eclampsia
ABNORMALITIES NONSEVERE (mild) SEVERE
Blood pressure ≥140/90mmHg but
<160/110mmHg
≥160/110mmHg
Proteinuria ≤2+ ≥3+
Oliguria Absent <400ml/day
Headache Absent Present
Visual disturbances Absent Present
Platelet count Normal Thrombocytopenia
(100,000/mm3)
HELLP syndrome Absent May be present
ALT,AST >70 IU/L
LDH>600 IU/L
Bilirubin >1.2g/L
Serum transaminases(AST,ALT) Normal (<40 IU/L) Elevated
Epigastric pain Absent Present
Fetal growth restriction Absent Obvious
Pulmonary oedema Absent present

COMPLICATIONS OF PRE-ECLAMPSIA
IMMEDIATE REMOTE
MATERNAL FETAL
● IUGR
● IUD
● Asphyxia
●Prematurity
During Pregnancy During Labour During
puerperium●Eclampsia(2%) (more in acute cases)
●Accidental hemorrhage
●Oliguria
●Diminished vision
●HELLP Syndrome
●Cerebral hemorrhage
●ARDS
● Eclampsia
● Postpartum
hemorrhage
●Eclampsia( in
< 48hrs of
delivery)
●Shock
●Sepsis
●Residual hypertension
●Recurrent pre-eclampsia
●Chronic Renal Disease
• Abruptio placentae
89

COMPLICATIONS OF ECLAMPSIA
MATERNAL FETAL
●Asphyxia
●Prematurity
●Hypoxia & IUD
Injuries Systemic
●Tongue bite
●Injuries due
to fall
●Bed sore
●PULMONARY: edema,
pneumonia, ARDS,
embolism
●CARDIAC: acute left
ventricular failure
●RENAL: renal failure
●HEPATIC: necrosis,
subcapsular hematoma
●CNS: cerebral
hemorrhage,
edema(vasogenic)
Vision
●Diminished
vision due to
retinal
detachment or
occipital lobe
ischemia
Hematology
●Low platelet
count
●Disseminated
Intravascular
Coagulation
Postpartum
●Shock
●Sepsis
●Psychosis
90

HELLP Syndrome
This is an acronym for Hemolysis (H), Elevated Liver
enzymes (EL), and Low Platelet count (LP).
It is a rare multisystem disorder that complicates
pregnancy with lab evidences of micro-angiopathic
hemolysis, hepatic dysfunctioning &
thrombocytopenia.
It is a complication mostly associated with Pre-
eclampsia but can also be diagnosed (rarely though) in
the absence of these disorders.

HEMOLYSIS
(due to
passage of
RBCs
through
partially
obstructed
vessel)
s)HEPATIC
DYSFUNCTI
ON (due to
intravascula
r fibrin
deposition &
sinosoidal
obst.)
Decreased
Liver blood
flow
HELLP
Syndrome
THROMBO-
CYTOPENIA
(due to
platelet
aggregation
& diposition
in the sites of
endothhelial
damage)
P
A
T
H
O
G
E
N
E
S
I
S
92

Diagnosis OF HELLP Syndrome
Hemolysis (Hallmark
of the triad)
Elevated Liver
Enzymes
Low Platelet Count
 LDH>600IU/L  Liver Enzymes  (<100,000/cu.mm)
 Low serum
haptoglobin
 High serum bilirubin
(>1.2 mg/dl)
High ALT & AST
(>70 IU/L)
 Abnormal PBS
(Schistocytes, burr
cells)
 Later-low Hb%
• ●Epigastric /Right Upper Quadrant pain
• ●Nausea, Vomiting1. Clinical Features:
2. Lab Investigation:

Usual Time of Onset
Relation to delivery Percentage
Antepartum 72
Post_partum 28
 ≤48 hours 80
 >48 hours 20
Gestational Age
(Weeks)
21-27 10
28-36 70
>37 20

Can we predict whether a pregnancy would be
complicated with Hypertensive disorders?
Endothelial
Dysfunction/Oxidant Stress
Feto-Placental unit Endocrine
Dysfunction
Renal Dysfunction Misc
Placental Perfusion/ Vascular
Resistance related Tests
Uterine Artery Doppler
Velocimetry
AT- III
ANPFree fetal DNA
Indirectly, YES…

How effective are they???
• is most promising, but currently, none of them
is completely suitable for clinical use.
• As a result of these trials, some methods to
prevent Preeclampsia have been theorized…
Uterine Artery Doppler Velocimetry
(abnormal flow resistance/ diastolic notch in
2nd/ 3rd trimester)

Trials of different preventive methods and their outcomes
Sibai et al. Lancet 365:785-99, 2005.

The efficacy of the preventive
methods is questionable
too…
The investigative procedures are
cumbersome,
time-consuming and
expensive…

MANAGEMENT OF
PREECLAMPSIA & PIHAfter early diagnosis, further management
depends on …
Severity of disease
Fetal maturity
Condition of cervix

What is EXPECTANT MANAGEMENT?
NO
YES
Neither forced nor
restricted

Management
• Goal: delivery to balance maternal and fetal
risks
• Maintain the safety of the mother
• Expectant v.s. immediate delivery:
– Disease severity
– Fetal maturity
– Maternal condition
– Fetal condition
– Cervical status

Pre-eclampsia without severe features
• >37 weeks gestation: deliver
• <37 weeks gestation: expectant management
until term or maternal/fetal indication for
delivery
– Bedrest no longer “suggested”
– Serial maternal assessment (BP, symptoms, labs,
weight gain)
– Serial fetal assessment (NST/BPP, fetal kick count,
serial US for AFI and growth)
– Oral antihypertensives

Severe Pre-eclampsia
• >34 weeks: deliver
• 33-34 weeks: steroids and deliver after 48
hours if maternal/fetal status allows
• 22-32 weeks: antihypertensive meds(oral/IV),
steroids, extensive counseling, close
surveillance deliver for maternal/fetal
indications or 34 weeks gestation
• <22 wk: expectant mgmt not recommended
Start MgSO4 upon diagnosis

Other issues
Prevention of pre-eclampsia
• Smoking cessation
• Do’s:
– Low dose ASA before 16GW
(high risk populations)
– Moderate exercise
• Don’t’s:
– Calcium supplement
– Anti-oxidants
– Low salt diet
– Bed rest
Long term sequeale
• Mothers have a higher risk:
– Diabetes
– Hypertension
– Kidney Disease
– Obesity
– Cardiovascular disease
– Future pre-eclampsia

Gestational hypertension (PIH) is a
transient diagnosis
1. Vesna D. Garovic Hypertension. 2012;59:555-557
2. National High Blood Pressure Education Program Working Group on High
Blood Pressure in Pregnancy. Am J Obstet Gynecol. 2000 Jul. 183(1):S1-S22

Management of GH
SBP < 160/110
• Managed as outpatients
• Twice weekly BP monitoring
• Weekly assessments of proteinuria,
PLTs, LFTs
• ASA? after 20wk
• Activity:
– Individualize decision to put
patient at bed rest
– Advise against strength
training/isometric exercises
– In the absence of data re: BP
response to aerobic exercise,
avoid such exercise
• No BP meds unless end organ
damage
• Delivery: at term
SBP>160/110 (severe)
• Treat with
antihypertensives
(<160/110 vs <140/90 with
end organ damage)
• Deliver ≥ 34 wk
• MgSO4 for peripartum
seizure prophylaxis
• Offer ASA in subsequent
pregnancies to reduce risk
of pre-eclampsia

CHRONIC HYPERTENSION WITH OR W/O
SUPERIMPOSED PRE-ECLAMPSIA

Diagnostic criteria for Chronic
Hypertension
• Hypertension:
– Before pregnancy
– Before 20 GW
– Persisting > 12 wk post-partum
• Severity:
– Mild: BP > 140/90
– Severe: BP > 160/110

When to suspect secondary causes of
hypertension?
• Resistant hypertension (various definitions: 3-
4 drugs, at least one diuretic)
• Hypokalemia
– Off treatment with diuretics
– Suggests a hyper(aldo/renin) state
– Renal disease
• Family history of renal dz (genetic s., RAS)
• Board exam patient histories: thyroid dz, pheo,
Cushing, aortic coarctation, hypokalemia
Obstetrics & Gynecology, Vol. 122, No. 5, November 2013

Risk Factors in Chronic HTN
– Maternal age >40 years old
– HTN for >15 years
– BP > 160/110 mmHg early in gestation
– Diabetes
– Renal disease
– Cardiomyopathy
– Connective tissue disease
– Presence of lupus anticoagulant
– Previous pregnancy with perinatal loss
– Secondary causes of HTN (pheo/renovascular)

Preconception counseling
• Risks associated with CHTN
• Education about the signs and symptoms of
pre-eclampsia
• Meds adjustment:
Stop angiotensin enzyme inhibitors (the
“prils”),angotensin receptor blockers (the
“sartans”) and mineralocorticoid blockers
BEFORE CONCEPTION
Statins (due to conflicting evidence about fetal
effects)

Antepartum management
• Assess early or before pregnancy
 Level of blood pressure & treatment targets
Evaluation for end organ damage: LVH,kidney
Rule out secondary causes
Baseline labs: creatinine/eGFR,electrolytes, uric
acid, urine protein
Evaluate glucose tolerance

Lifestyle modifications help lower blood
pressure in the general population
References: Chobanian et al. J Am Med Assoc 2003; 289(19):2560–2571;
Neter et al. Hypertension 2003; 42(5):878–884; Dietary Guidelines, 2010
Modification Recommendation Lowers Systolic Blood
Pressure by (Range)
Weight reduction •Maintain normal body weight
•Body mass index (BMI) 18.5–24.9
kg/m2
5–20 mm Hg /  10 kg
 4 mm Hg /  5 kg
DASH •Increase potassium (fruits and
vegetables) and calcium (dairy)
•DASH may be too high in protein,
potassium and phosphorus for CKD
8–14 mm Hg
Physical activity •At least 30 minutes most days 4–9 mm Hg
Moderate alcohol
consumption
•Women: ≤ 1 drink per day
•Men: ≤ 2 drinks per day
2–4 mm Hg
Sodium restriction •2,300 mg per day
•1,500 mg per day for hypertension,
diabetes, and CKD
2–8 mm Hg
Modification Recommendation Lowers Systolic Blood
Pressure by (Range)
Weight reduction •Maintain normal body weight
•Body mass index (BMI) 18.5–24.9
kg/m2
5–20 mm Hg /  10 kg
 4 mm Hg /  5 kg
DASH •Increase potassium (fruits and
vegetables) and calcium (dairy)
•DASH may be too high in protein,
potassium and phosphorus for
CKD
8–14 mm Hg
Physical activity •At least 30 minutes most days 4–9 mm Hg
Moderate alcohol
consumption
•Women: ≤ 1 drink per day
•Men: ≤ 2 drinks per day
2–4 mm Hg
Sodium restriction •2,300 mg per day
•1,500 mg per day for
hypertension, diabetes, and CKD
2–8 mm Hg

Superimposed PE and CHTN
• Suspect superimposed pre-eclampsia when:
– Sudden increase in BP, or need to escalate Rx
– New onset of proteinuria or worsening of
proteinuria
– Symptoms of non-proteinuric pre-eclampsia
• Evaluate in a hospital environment to:
– Confirm diagnosis, evaluate maternal-fetal status
and monitor for disease progression
– Obtain pre-eclampsia/HELLP labs (including uric
acid level)

Management of blood pressure in
CHTN with superimposed PE
• Lack of clinical trials
• Extrapolation from CHTN/pre-eclampsia literature
• Same targets/thresholds as isolated CHTN
• Same meds as isolated CHTN
• Women at risk for premature delivery: fetal lung
maturity
• MgSO4 is good for seizure prophylaxis but not a good
anti-hypertensive medication in CHTN+PE
• Delivery decisions: GW (>37 v.s. <37, PE manifestations,
lung maturity: 34 GW (severe pre-eclampsia), 37 GW
without severe features)

Management of CHTN in the
postpartum period
• Blood pressure will gradually decline (first 2
weeks may be higher than > 2wk)
• BP targets: <160/90
• AVOID NSAIDS!!!
• Considerations for breast feeding:
– Methyldopa is safe (low conc)
– Atenolol/metoprolol (high conc)
– Propranolol/labetalol (low conc)
– Low dose ACEi (low conc)
– Calcium channel blockers (generally safe)

For mild - controlled disease :
Thereafter induction may be done at
term depending on cervical condition
Can be managed expectantly till term at
home/hospital and continued till term.

Hospitalisation???
• Gestational HTN : only if
severe HTN
• Preeclampsia :
 If diastolic pressure≥ 100mm of Hg OR,
there is proteinuria OR, there is fetal
compromise.
37 completed weeks of gestation.

When should we use antihypertensive
to control the BP???
• Acute management of
severe hypertension
(BP > 160/110: to
prevent stroke)
which may require
parenteral therapy.

Principles of antihypertensive
pharmacotherapy in pregnancy

Antihypertensives for urgent (inpatient) blood
pressure control
Cochrane Database Syst Rev. 2013 Jul 31;7:CD001449.
Inadequate evidence to
choose among hydralazine,
labetalol or calcium
blockers
Theoretical concern for
neuromuscular blockade when
using MgSO4+nifedipine
Nimodipine or MgSO4:
higher incidence of
persistent HTN

Antihypertensive regimens for urgent
hypertension in pregnancy
Drugs. 2014 Mar;74(3):283-96. doi: 10.1007/s40265-014-0187-7.

Antihypertensives for outpatient blood
pressure control
Cochrane Database Syst Rev. 2013 Jul 31;7:CD001449.
For women of reproductive age,
ACEi/ARB/DRIs/aldo-antagonists not
recommended unless compelling reason:
proteinuric renal dz
In CHTN who are at risk for pre-eclampsia,
initiation of low dose ASA 60-80 mg, will ↓
risk by ~25%

Diuretics in pregnancy
Practice implications
• Concerns that diuretics will
adversely effect IUGR due to
reductions in plasma volume
• Plasma volume may be
reduced but IUGR risk is
theoretical
• Women on diuretics before
pregnancy may be continued
on them
• May have to adjust the dose to
reduce the risk of hypoK
• Particularly useful in women
with Na-sensitive HTN
Meta-analyses
Outcome OR 95% CI
Pre-eclampsia 0.68 0.45-1.03
Perinatal death 0.72 0.40-1.27
Pre-term death 0.67 0.32-1.41
BW 139 gm -484.20 to
762.40
Nausea
vomiting
5.81 1.04-32.46
Discontinuation 1.85 0.81-4.22
C-section 1.00 0.26 – 3.81
Cochrane Database Syst Rev. 2007 Jan 24;(1):CD004451
Drugs. 2014 Mar;74(3):283-96. doi: 10.1007/s40265-014-0187-7.

Management Options for CHTN
Drugs. 2014 Mar;74(3):283-96.
doi: 10.1007/s40265-014-0187-7.

What are the
options???
Acute
Hydralazine inj.:
now available
Labetalol
Injection
Nifedipine
capsule/Tablet
Long
term
Methyl Dopa
250 mg Tab.
Labetalol Tablet
100 mg
Nifedipine
5,10,20 mg

But wait…can antihypertensives be used in
expectant management???
• In non-severe Pregnancy hypertension – No clear
Evidence of benefit other than to reduce
The Frequency of Episodes of Severe
hypertension
• May Adversely Effect Fetal Growthvelocity

For severe-uncontrolleddisease:
LUCS OR In case of very severe uncontrolled disease elective LUCS
may be done without induction
Preinduction
Cervical ripening with prostaglandin/osmotic dilators followed by
induction
Termination is considered
If failed

For early onset severe preeclampsia:
• Controversy regarding termination in
early onset disease
• But there is no beneficial role for
mother, as well as perinatal mortality is
also high instead of conservative
management
• So…
termination is seriously considered

Fetal
considerations
Prematurity
Stillbirth
Newborn
asphyxia
Maternal
considerations
– Worsening
of disease
Complications

DELIVERY CARE
• For any HDP, vaginal delivery should be
considered unless a CS is required for the
usual obstetric indications.
• Antihypertensives : continued throughout
labour to maintain BP < 160/110 mmHg .
• 3rd Stage : actively managed with oxytocin 5
units IV or 10 units IM, particularly in the
presence of thrombocytopenia or
coagulopathy. (I-A)
• Ergometrine should NOT be given

Management of Eclampsia :
Prompt delivery of fetus to achieve cure
Avoidance of diuretics & hyper osmotic agents
Limitation of I.V fluid
Intermittent antihypertensive to control BP judiciously
Control of convulsion by MgSO4 (IM/IV route)
Protection & supporting care during convulsion
Protection in a railed cot
Protection of airway &
prevention of tongue bite
Correction of hypoxia &
acidosis
Managed in Eclampsia room.

to control convulsion
“It is the most effective drug
to control even recurrent
seizures without any central
nervous system depression to
mother & fetus”
Magnesium
sulphate

Dosages
→Paralysing agent & Intubation
→Amobarbital 250mg I.V over 3 min
In case of uncontrolled recurrent seizure (10-15%) : →additional 2-4g of 20%
solution IV @ <1g/min
→4gm of 20% solution IV slowly(@ <1g/min) + 10g of 50% solution deep
IM in upper & outer quadrant of buttock by a wide bore needle then 5g
of 50% solution IM 4hrly similarly
IM regime (Pritchard protocol):1955
→4 gm loading in 100ml of IVF over 15-20 min followed by
2-3g/hr in 100 ml IVF as maintenance
I.V regime (Sibai protocol):1990
IM doses are as active as IV doses in controlling seizures

Some more about Magnesium
• Duration : 24 hrs from last convulsion or from delivery which one is
longer.(This is called Magnesium sulphate prophylaxis in severe
preeclampsia.)
• Features of toxicity:
i> Impaired breathing(@8-10meq/L)
ii>Arrythmia and Asystole ( @10-13 mEq/L)
iii>Decreased/absent deep tendon reflex
(Hyporeflexia at 4 mEq/L, loss of patellar reflex at 7-10 mEq/L)
iv> Shock (>13 mEq/L)
• For a maintenance dose following must be present -
Serum Mg level 4-7meq/l(twice daily)
Having Patellar reflex
Urine output >30ml/hr
RR>12/min

WHAT If magnesium toxicity is suspected???
Administration of 10mL of 10% calcium gluconate (1 g in total) as
a slow intravenous push.
Serum magnesium level obtained.
Magnesium infusion should be discontinued, supplemental oxygen
administered,

Eclampsia
 Characterized by convulsions and/or
coma
 Women has PIH
 Types antepartum, intrapartum and
postpartum.
 No lower limit of B.P. for eclampsia can
even occur at 120/80 mmHg
139

140
Maternal Mortality
Major causes of maternal mortality are
• PIH
• Eclampsia
• APH
• PPH
• Puerperal sepsis
• Obstructed labour
• Unsafe abortions

Fulminating Eclampsia
Symptoms :
 Severe headache
 Drowsiness
 Mental confusion
 Visual distrubances
 Epigastric pain
 Nausea, vomiting
 Decreased urinary output 142

Signs
A sharp rise in B.P.
Increased proteinuria
Exaggerated knee jerk
143

Status Eclampticus
Continuous convulsions
Dangerous for mother and fetus
Can lead to fetal and maternal
mortality
144

Stage of Eclampsia
Premonitory
Tonic
Clonic
Coma
145

Eclampsia
 Can occur regardless of severity of hypertension
 Difficult to predict
 Tonic clonic
 Rapid sequence
 Can occur in the absence of hyper-reflexia,
headache and visual disturbances.
146

D/D of Eclampsia
 Epilepsy
 Cerebral malaria
 Meningitis
 Encephalitis
 Tetanus
 Head injury
147

Effect on Mother
 Asphyxia
 Aspiration
 Pulmonary edema
 Bronchopneumonia
 Cardiac failure
 Brain hemorrhage
 Cerebral thrombosis
 Cerebral edema
148

Effect on Mother
 ARF
 HELLP
 DIC
 Temporary blindness
 Injuries
 Tongue bite
149

Effect on Fetus
Hypoxia
* IUGR
* Stillbirth
150

High risk for Eclampsia
 Teenagers / elderly primi.
 Essential HT
 Twins
 Women with DM, polyhydramnios, V. mole
 H/o eclampsia
 Obese women
151

Eclampsia
Six major steps :
1. Maintain airway
2. Control fits
3. Control B.P.
4. Deliver the pt.
5. Maintain fluid balance
6. Give after care of delivery
152

Eclampsia
Maintain airway :
1. LLP
2. Gentle section
3. Oxygen
4. Place padded tongue blade in her mouth to
prevent aspiration and tongue bite
DO NOT ATTEMPT THIS DURING
CONVULSIONS
153

Eclampsia
Control fits :
MAGSULF THERAPY
 Dose – Inj. MgSo4 – 4 gm (20 ml of 20%
sol.) slow I.V. at the rate of 1 ml / min.
NOT TO BE GIVEN AS BOLUS
 Maintenances dose 5 gm deep I.M. every
4 hrly.
154

Eclampsia
 If convulsions recur give additional 2
gm magsulf (10 ml of 20% sol.) I.V. over
20 min.
 Wait for 15 min.
 If still convulsions recur – give
diazepam
155

Eclampsia
Monitoring of MgSo4 therapy
1. Output atleast 100 ml/4 hrs.
2. Knee jerk present
3. Respiratory rate 16 breath/min
POSTPONE THE NEXT DOSE IF
ABOVE CRITERIA NOT MET
156

Eclampsia
Precautions :
Do not give
1. 50% MgSo4 without diluting it to 20%
2. Rapid I.V. infusion as it may cause respiratory
failure and death
If respiratory depression occurs (RR < 16/min)
1. Discontinue MgSo4
2. Give calcium gluconate - 1 gm I.V. (10 ml of
10% solution) over a period of 10 min.
157

Eclampsia
Other options available are :
1. Diazepam (10 mg I.V. slowly over 2
min.)
2. Phenytoin sodium
3. Largactil
MgSO4 IS SUPERIOR TO ALL
ABOVE DRUGS IN ECLAMPSIA
158

Eclampsia
Controlling the B.P.
Tab. Depine – 10 mg t.d.s.
Tab. Labetelol – 50 mg b.d.
Other drugs available – Hydralazine
159

Eclampsia
Controlling fluid balance :
1. Intake output chart
2. Output 100 ml/4 hrs.
3. 60 ml /hr fluid intake
4. Extra fluid if vomiting, excessive blood loss or
diarrhoea.
PROPER MAINTENANCE OF FLUID BALANCE
TO PREVENT WATER INTOXICATION,
DEHYDRATION, HYPONATREMIA OR
PULMONARY EDEMA.
160

Eclampsia
DIURETICS SHOULD NOT BE
USED, IT IS DANGEROUS
161

Eclampsia
Delivering the baby
1. If PIH deliver within 24 hrs.
2. If eclampsia deliver within
12 hrs.
3. If vg. Delivery is not
anticepated or Cx is
unfavourable or S/o fetal
distress,
> C/S
162

Eclampsia
Delivery
1. Before labour
- Control B.P.
- Control fits
2. Late 1st stage / 2nd stage
- Carry out Vg. delivery
163

Eclampsia
Difficult deliveries :
1. Labour not progressing quickly
2. Big size baby
GIVE MgSO4
> C/S
164

Rule of Thumb
 Pt. with severe PIH comes early 1st
stage of labour –
> C/S
 Pt. comes in late labour or 2nd stage –
conduct delivery, give MgSO4 – C/S
165

Eclampsia – Postpartum
Care
1. Refer pt. After one hr. of delivery
after ruling out PPH
2. If pt. Has fits, observe for 48 hrs.
after convulsions.
3. Closely observe her
consciousness, output
4. Monitor B.P. every hrly.
5. Given anti-hypertensives till B.P.
comes down to 100 mmHg
diastolic 166

Eclampsia – Postpartum Care
 Do not give excessive IV fluid
 If after 72 hrs. there are no
convulsions, output is good, and
B.P. is 100 mmHg diastolic –
discharge the pt.
 Arrange for follow-up – 7 to 10
days after delivery.
167

Eclampsia – Postpartum Care
Following Eclampsia B.P. may :
1. Return to normal within 48-72
hrs.
2. Return to normal after a few wks.
May remain high permanently.
168

Through a team approach all of the
skills of the health care members
involved can be combined to provide
the best possible approach to meet the
pregnancy’s need. The role of patient
education can not be over emphasized.
Incorporating the mother as an active
member in her health care is an
investment in time and effort that is
cost effective both during pregnancy
and labour.
169

*Hypertensivedisordersinpregnancy

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