Hypertensive disorders in pregnancy -I

2.  Commonest medical disorders during
pregnancy.
 Being the major cause of maternal and
perinatal morbidity and mortality.
INCIDENCE
 Hypertensive disorders complicate 5-10 % of
all pregnancies.
 Incidence of eclampsia is reduced due to
adequate and better antenatal care.
 GHTN : 6-17% in nullipara
 Pre eclampsia – 3-10% in nullipara

3. CARDIOVASCULAR SYSTEM :
-Cardiac output
-Blood pressure
BP = CO * SVR
CO increases ; SVR decreases
BP
overall Diastolic BP & M.A.P

4.  BP can be recorded either in sitting
or lateral recumbent posture.
 Brachial artery and mercury
manometer should be at the level of heart.
 Appropriate sized cuff should be used.
 DISAPPEARANCE OF KOROTKOFF PHASE V
Diastolic BP

5.  By NHBPEP (2000)
GESTATIONAL HYPERTENSION
PRE ECLAMPSIA & ECLAMPSIA
PRE ECLAMPSIA SUPER IMPOSED ON CHRONIC
HYPERTENSION
CHRONIC HYPERTENSION

6.  BP ≥ 140/ 90 mmHg for first time during
pregnancy after 20 weeks of gestation
 No proteinuria
 Returns to normal before 12 weeks
postpartum
 With / without other symptoms of pre
eclampsia

7. Abnormality Mild Severe
Diastolic BP <110 mmHg ≥110 mmHg
Systolic BP <160 mmHg ≥160 mm Hg
Proteinuria ≤2+ ≥3+
Headache - +
Visual disturbances - +
Epigastric pain - +
Oliguria _ +
Convulsion - +
Serum creatinine normal
Thrombocytopenia _ +
Serum transaminase minimal marked
Growth restriction - obvious
Pulmonary edema - +

8. ECLAMPSIA :
Seizures that cannot be attributed to other causes
in a women with pre eclampsia.
CHRONIC HYPERTENSION :
BP ≥140/ 90 mmHg before pregnancy or
diagnosed first before 20 wks of gestation
or
Hypertension diagnosed after 20 wks and persists
after 12 wks postpartum

9. SUPER IMPOSED PRE ECLAMPSIA ON
CHRONIC HTN :
New onset proteinuria ≥ 300mg/24 hrs in a
hypertensive women but no proteinuria
before 20 wks of gestation
or
Sudden in proteinuria / BP / in platelet
count in hypertensive women with
proteinuria before 20 wks.
TRANSIENT HYPERTENSION :
GHTN reclassified if pre eclampsia
doesnot develop and BP returns to normal by
12 wks postpartum.
ATYPICAL PRE ECLAMPSIA :
Without hypertension/ proteinuria/
both

10. Clinical findings Chronic HTN GHTN Pre eclampsia
Time of onset of
hypertension
<20 wks 3rd trimester ≥20 wks
Degree of
hypertension
Mild / severe Mild Mild/ severe
Proteinuria --- --- +
S.Uric acid >5.5 --rare -- +
hemoconcentration - - Severe
Thrombocytopenia - - „
Hepatic dysfunction - - „

11. Incidence : 6-17% in nullipara
CRITERIA FOR MILD GHTN :
BP <160/110mmHg
Proteinuria <300mg/24 hrs
Platelet count > 100000
Normal liver enzymes
Absent maternal symptoms
Absent IUGR & OLIGO by
USG

12. INCIDENCE – 3-10% IN NULLIPARA
Occurs before 20 wks in trophoblastic diseases.
Clinical findings of pre eclampsia can manifest
either as maternal or fetal syndrome.
RISK FACTORS
1.AGE AND PARITY :
Young primigravida
Elderly > 40yrs
Long interval between pregnancies
Nulliparity
2.MATERNAL OBESITY
BMI > 35kg/m2 – 13.3%

13. 3.Genetic :
Family h/o pre eclampsia
Genetic predisposition
Race and ethnicity
By ovum donation
4. OBSTERIC :
Prev h/o pre eclampsia
Multifetal gestation
Hydrops
Hydatiform mole
Congenital & chromosomal fetal anomalies
5.PARTNER RELATED FACTORS
Change of partner
Partner who fathered a pre eclamptic preg
Limited sperm exposure
By donor Insemination

14. 6. UNDERLYING MEDICAL DISORDERS
Chronic hypertension
Renal diseases
Type I diabetes mellitus
Thrombophilia
Factor V leiden deficiency
Sickle cell disease or trait
Collagen vascular diseases
PCOS
Uncontrolled hyperthyroidism
Migraine
Autoimmune diseases

15.  CAUSES :
 ESSENTIAL ( IDIOPATHIC / PRIMARY )
 SECONDARY :
 RENAL DISEASE
 Renal artery stenosis
 Glomerulonephritis
 Pyelonephritis
 Interstitial nephritis
 Polycystic disease
 TB
 Neoplasm
 ADRENAL DISEASE
 Phaeochromocytoma
 Cushing syndrome
 Conn’s syndrome
 CONNECTIVE TISSUE DISORDER
 Polyarteritis nodosa
 SLE
 Scleroderma
 COARCTATION OF AORTA

16. POOR PLACENTATION
PLACENTAL OXIDATIVE STRESS
FETAL
GROWTH RESTRICTION
RELEASE OF PLACENTAL
FACTORS
SYSTEMIC
INFLAMMATORY
RESPONSE
ENDOTHELIAL
ACTIVATION
STAGE I
STAGE II

17. Placental implantation with
abnormal trophoblastic
invasion
Immunological maladaptive
tolerance between
maternal,paternal and
fetal tissues.
Maternal maladaptation to
CVS / inflammatory
changes of normal
pregnancy
Genetic factors – inherited
predisposing genes &
epigenetic influences
Coagulation abnormalities
Dietary deficiency

18. Incomplete trophoblast invasion
Shallow invasion upto decidual
segments
Abnormally narrow spiral arteriolar
lumen
Impairs blood flow
Diminished placental perfusion
Hypoxia
Release of placental debris
Systemic inflammatory response

19.  uNK cells with HLA class I in extravillous
cytotrophoblasts control invasion.
 Reduced expression of HLA-G by extravillous
trophoblasts messenger RNA
 Defective placental vascularisation

20. Defective
placentation
Placental
ischemia /
hypoxia
Inflammatory
mediators-
Il.TNF
Xanthine
oxidase
activation
Oxidative
stress
Free radical
Placenta
Maternal
endothelium
leucocytes
CEC
Platelet
aggregation
fibrin ,thrombin
Lipid peroxides
&
Foam cells

21. NUTRITIONAL FACTORS :
ascorbic acid < 85mg - incidence
GENETIC FATORS :
- Multifactorial & Polygenic Disorder
WARD AND LINDHEIMER (2009)
20-40 % for daughters of pre eclampsia mothers
11-37 % for sisters of pre eclampsia women
22-47 % in twins
CANDIDATE GENES :
Genome wide linkage studies
OUDEJANS Susceptibility loci on 10q22.1
2p12
2p25
9p13

22. GENETIC CONFLICT THEORY :
nutrients transfer limit the transfer
INCREASE BP REDUCE BP
INADEQUATE UTEROPLACENTAL BLOODFLOW
FETAL RESCUE STRATEGY TO INCREASE
NON PLACENTAL RESISTANCE
ENDOTHELIAL DYSFUNCTION
FETAL GENES
MATERNAL
GENES

23. VASOSPASM :
Vascular constriction increase in resistance
ENDOTHELIAL CELL ACTIVATION :
Placental factors activation & dysfunction
CEC of endothelial cells
NO synthesis
INCREASED PRESSOR RESPONSES - Sensitivity to AG II
NITRIC OXIDE – vasodilator
from L-arginine & fetal endothelium
synthesis
ENDOTHELINS – vasoconstrictor
human endothelium

24. PROSTAGLANDINS
prostacyclin thrombaxene A2
Vasodilatation & vasoconstriction
Inhib plt aggregation plt aggregation
In pre eclampsia:
PGI2 production
TXA2 Vasoconstriction
PGI2 : TXA2
endothelium
Renal cortex
Platelet
Trophoblast

25. sFlt-1 reduced
free VEGF & PLGF
endothelial
dysfunction
sEng
inhibits TGF- b
binding to
endothelial
receptors - NO dep
vasodilatation

26. CVS :
Preload affected
Extravasation of fluid
BLOOD VOLUME :
Hemoconcentration
BLOOD & COAGULATION :
Endothelial activation plt activation & aggreg
plt exhaustion thrombocytopenia
HEMOLYSIS :
LDH
Schizocytosis,reticulocytosis, spherocytosis

27. COAGULATION :
INCREASED Factor VIII consumption
fibrinopeptides & FDP
DECREASED regulatory protein level
VOLUME HOMEOSTASIS :
ENDOCRINE CHANGES
PLASMA NORMAL PRE ECLAMPSIA
Renin
Angiotensin II
Aldosterone
INCREASES DECREASES
Deoxycorticosterone INCREASES NO CHANGE
Vasopressin Same Same
ANP -/ Increases Increases

28. FLUID AND ELECTROLYTE CHANGES :
Oncotic pressure Pathological fluid retention
LIVER :
Periportal hemorrhage
Subcapsular hemorrhage
stretching of glisson’s cap
Proteinuria Edema

29.  Can be unruptured or
ruptured.
 DD for unruptured :
Acute FLP, Ruptured
uterus, abruption with
DIC, TTP.
 Presents with shoulder
pain, shock, massive
ascites, pleural
effusion or respiratory
difficulty.

30. BRAIN :
VISUAL CHANGES AND BLINDNESS :
SCOTOMA, BLURRED VISION, DIPLOPIA
BLINDNESS – Visual cortex of occipital lobe --AMAUROSIS
Lateral geniculate nuclei
Retina ---PURTSCHER RETINOPATHY
RETINAL DETACHMENT
Acute and severe hypertension cerebrovascular over regulation
Vasospasm
Diminished cerebral flow – ischemia-cytotoxic edema-tissue infarction
Sudden in systemic BP exceed the normal cerebrovascular auto
regulatory capacity
Posterior reversible encephalopathy syndrome

31. KIDNEY :
- Renal Perfusion & GFR
- Due to renal afferent arteriolar
resistance
- Glomerular capillery endotheliosis blocking
the filtration barrier.
Pre renal
Urine osmolality
Urine :plasma
creatinine
Excretion of sodium
sr.creatinine-
filtration
Uric acid -
tubular
reabsorption

33.  Onset : Insidious
 Symptoms :
 MILD : Swelling over ankles, face, abdominal wall, vulva
 ALARMING :
-Headache
- Disturbed sleep
- Diminished urine output
- Epigastric pain
- Visual disturbances
Signs :
-Abnormal weight gain
-Rise of blood pressure
-Oedema
-Pulmonary edema
-Abdominal examination

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