This document discusses pregnancy induced hypertension (PIH), including definitions, classifications, risk factors, pathophysiology, diagnosis, and management. PIH is a multisystem disorder characterized by new onset hypertension after 20 weeks of gestation. It includes gestational hypertension, preeclampsia, and eclampsia. Management involves monitoring for signs of worsening disease and delivering after 37 weeks if mild or earlier if severe to prevent maternal and fetal morbidity and mortality. Treatment includes antihypertensives, magnesium sulfate to prevent seizures, and delivery.

1. Pregnancy Induced Hypertension
Dr. Ayshwarya Revadkar
OBGY UNIT 3, YCMH

2. INTRODUCTION
 Multisystem
disorder with
varied and still
unknown
etiology with
unpredictable
outcome, with
increase in
maternal & fetal
morbidity and
mortality.

3. Intro conti…
 Also known as “Toxaemia of pregnancy”
 Major cause of maternal mortality in India.
 Asso with poor outcome of pregnancy if
uncared for.
 It affects 7 – 15 % of all pregnancies.

4. 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 atleast 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)

5. 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.

6. 4) Preeclampsia : Gestational HTN asso
with proteinuria .
5) Eclampsia : Convulsions occuring 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 elavated liver enzymes (AST>70,
U/L, LDH>600 U/L)

7. Physiological changes in pregnancy :
 Normal pregnancy is char 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.

8. 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.

9. 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
3. Systolic HTN :
Thyrotoxicosis, hyperkinetic circulation.

10. 2 categories :
 First one responding to medications &
without complications, good outcome of
pregnancy
 Second one : HTN difficult to control,
require multiple drugs, fetal hazards or
end organ damage, demanding delivery,
 Risk factors : severe HTN (HTN crisis, risk
of stroke and abruption), superimposed
PIH, IUGR, abruptio placenta.

11. Important points to note :
 Difficult to differentiate from PIH as Pts
came for ANC mainly after 20th week &
very few pts diagnosed in pre-pregnant
state.
 Pre-conceptional counseling : for
determination of cause, organ functions,
exercise & weight loss, salt restriction
 Change of medications : eg omit ACE
inhibitors & ARBs
 Daily self monitoring of BP twice at home
 Don’t lower BP rapidly: harm to fetus

12. Antihypertensives used in Pregnancy :
1. Diuretics :
Furosemide, chlorthiazide
2. Vasodilators :
Labetalol, Nifedipine, Prazosin,
Hydralazine.
3. Drugs that decrease CO : Beta blockers,
Propanalol
4. Centrally acting : Methyldopa

13.  30% pts have chance to develop
super-imposed preeclampsia.
 If this happens, PIH is very severe,
occurs early in pregnancy, responds
poorly to bed rest.
 How to differentiate aggrevated HTN
from superimposed PIH ?
 Proteinuria, Urinary Ca excretion,

14. High risk factors indicating poor outcome
 Diastolic BP 85 or greater, MAP 95 or
greater, in repeated observations 6hrs apart
after 14weeks of GA.
 H/O severe HTN in previous pregnancies.
 h/o abruption
 h/o stillbirth or unexplained neonatal death.
 h/o IUGR
 AGE > 35yrs or chronic HTN of >15yrs
duration
 Marked obesity
 Secondary HTN

15. Management
 Many pts will have mild disease &
progress to term.
 ANC visits every 2 weekly until 32 wks
& then every weekly.
 Variables to monitor : BP, uterine
growth, preterm labor, DFMC,
maternal weight
 Pts with other high risk factor develop
complication resulting in preterm
delivery.

16. Gestational HTN
 Prevalence 6-15% in nulliparas & 2-4% in
multiparas.
 Early : before 30wks, frequently severe,
advances to preeclampsia and has a
guarded perinatal prognosis.
 Late : after 30wks, frequently in obese
women and multiple pregnancies, due to
poor maternal adaptation to physiological
changes in pregnancy.

17. Conti..
 Criteria to identify high risk women
with gestational HTN :
1. BP > 150/100 mm Hg.
2. GA < 30wks
3. Evidence of end organ damage
4. Oligohydramnios
5. Fetal growth restriction
6. Abnormal CD.
7. Nullipara, Age > 35yrs, BMI > 35 kg/m2

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

19. 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
 Thrombophilias : APLA, deficiency of
protein C/S, factor 5 leiden,

20. 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).

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

23. 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

24. 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

25. 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.

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

27. Laboratory findings :
 Haemoconcentration leads to false
Hb.
 Thrombocytopenia
 RFTs: Serum Uric Acid >4.5mg/dl,
BUL, serum creatinine- derrange only
in severe cases.
 LFTs : raised liver enzymes in severe
cases
 Incresed fibrinogen, it is decreased in

28. Abnormal fetal growth
 IUGR of 2-4 wks in PIH commonly
seen.
 Demands uterine, umbilical & MCA
doppler.
 UA utero-placental circulation
 Umb A : Placento-umbilical circulation.
 Doppler weekly in moderate to severe
PIH.
 NST & MBBP twice weekly to assess
fetal wel-being.

29. Management of mild PIH
 GA > 37 weeks : Deliver.
 GA b/w 32 & 36 wks : periodic
evaluation by NST, Lab, USG & CD.
In-hospital management to avoid
complications.
 GA < 32wks :
 IPD, continuous assessment: daily BP,
Weight, daily urine dipstick, LFT &
Platelets twice wkly, DFMC, NST twice
wkly, doppler wkly,

30. Conti..
 If only pt. is stable : continue
pregnancy.
 If unstable : may require early delivery.
 Indication for delivery in k/c/o mild
PIH: BP>160/110, proteinuria > 5gm in
24hrs urine.
 Trying to conserve pregnancy in
severe PIH by giving antihypertensive
: invitation for disaster.

31. Anti hypertensive
 Drug of choice: Labetalol orally in
dose of 100-400 mg every 8-12hrly.
 Others :
 Methyl dopa 250mg-500mg 6-8 hrly.
 Nifedipine 10-20mg bd - tds.
 Hydralazine : 10-25mg 12hrly.
 Iv or oral furosemide, oral thiazide:
only after delivery.
 If s/o severity devlop : MgSO4.

32. Management Of Severe PIH
 Criteria for diagnosis of severe
preeclampsia :
 Systolic BP > 160 / Diastolic > 110 on 2
occasions 6hrs apart while pt is in bed
rest.
 Proteinuria of 5 g or higher in 24hr urine
or 3+ or greater in 2 samples 4hrs apart.
 Oliguria of less than 5oo ml urine in 24
hrs.
 IUGR
 Cerebral or visual disturbances

33. Conti..
 Pulmonary oedema or cyanosis
 Epigastric or right uppaer quadrant
pain
 Impaired liver function
 Thrombocytopenia
 Very imp : s/o impending eccampsia

34. Management of severe PIH
 GA > 34 wks :
 MgSO4 to prevent seizures
 Antihypertensive to control BP
 Delivery : if Cx ripe Induction or
Caesarean section.
 Don’t try to lower BP suddenly, it will
impair organ perfusion and result in
maternal & fetal morbidity

35. Hypertnsive crisis BP> 160/110
 Labetalol 10-20mg iv every 10min,
max upto 300mg iv, maintenance dose
40mg/hr
 Hydralazine : 5mg iv every 30min,
max 30mg iv, maint dose 10mg/hr
 Nifedipine : 10-20mg oral, max up to
240mg in 24hrs, for maint 4-6 hrly
 Nitroglycerine : 5microgm/min iv or
 Sod nitroprusside 0.25-5
microgm/kg/min iv short term therapy
only when other drugs failed.

36. Regimes of MgSO4
1. Intra-muscular (PRITCHARD)
2. Intra-venous (zuspan or Sibai)
6 gm(25%) iv over 20min f/b maint
dose of 2 gm(50%) /hr or 100ml/hr iv
infusion.
• Therapeutic level 4-7 meq/L.
• 4 Actions. Toxicity. Antidote.

37. Severe PIH :
 GA 28-33 wks :
 Postpone delivery for 24-48hrs for
action of steroids.
 GA 24-28 wks : Indivisualised for pt
acc to severity.

38.  Guidelines for expectant management
:
Bed rest
Daily weight
Daily input & output
Antihypertensive t/t
Steroids
Lab on alternate days
Daily NST
DFMC
CD twice a week
AFI twice a week
USG to see for fetal growth every 2 weeks

39. GA < 24 weeks:
 Severe maternal morbidity if
pregnancy conserved
 Perinatal mortality, IUDs.
 Only t/t is Delivery.

40. Ecampsia
 It is the extremely severe form of PIH char by
sudden onset of generalized tonic clonic
convulsions.
 Higher frequency in developing countries.
 Occurs antepartum in 35-45%, intrapartum in
15-20%,
postpartum in 35-45%.
 Preceded by impending signs & aura.
 In 15 % of patients, HTN & protenuria are
absent.
 Preventable in 70% cases.
 No any long term neurological deficit.

41. Pathophysiology :
 In mild HTN or normotension : abnormal
autoregulatory response consisting of
severe arterial vasospasm with rupture
of endothelium & pericapillary
haemorhages with development of
abnormal electric foci causing
convulsion.
 In severe HTN, limit of autoregulation
exceeded, vasodialatation occurs with
hyperperfusion causing endothelial
capillary damage and interstitial
vasogenic edema.

42. Management of Eclampsia
 Place pt in lateral decubitus.
 Mouth gag
 Suction oral secretions
 O2 by mask
 Elevate bedside rails to avoid injury
 Switch off lights, keep quite environment
surrounding pt.
 Pulse oxymeter, foley’s catheter, iv access
 MgSO4
 Start IV fluids at low rate 100ml/hr.
 Antihypertensive : 1st drug of choice in severe
HTN is iv Labetalol.
 Deliver the pt.

43. Conti..
 Continue MgSO4 till 24hrs postpartum to avoid
convusion.
 Nimodepine 60 mg oral 4hrly: drug of choice in
mild elevated BP with impending signs/
eclampsia.
 Phenytoin :
loading dose 10-15 mg/kg slow iv f/b maint
dose 100mg iv every 6-8hrly.
For prophylaxis 100mg iv/im 4hrly.
 Oral phenytoin should be continued in
postpartum period.
 Postpartum i.v. Furosemide should be given
aggresively for early recovery.

44. Fetal Response To Maternal Seizures
 In majority of cases: transient fetal
distress during seizure, normalizes as
seizure is over.
 Occasionaly the tetanic uterine
contraction is severe enough to cause
abruption & IUD.
 Thus if fetal distress continues for more
than 5 min after end of seizure & despite
giving O2, abruption should be
suspected & LSCS should be done. In
these case both maternal & fetal

45. Increase in LSCS for eclampsia
in modern OBs :
 Due to
 Unripe Cx, poor progress in labor
 IUGR, preterm baby
 Inadequate control of BP
 Mainly to avoid adverse maternal &
fetal effects of pregnancy continuation.

46. Postparum care :
 MgSO4 for atleast 24hrs after delivery
 Aggressive diuresis & maintained
several days
 Antihypertensive until BP normalizes.
 Approximately 35% pts will have PIH
in subsequent pregnancy.

47. HELLP SYNDROME
 Criteria for diagnosis :
1) Haemolysis (microangiopathic H.A.)
Burr cells, schistocytes on PBS
bilirubin > 1.2mg/dl
absent plasma haptoglobin
2) Elevated liver enzymes
AST > 72 IU/L
LDH > 600 IU/L
3)Low platelets
< 1 lakh/mm3

48. Conti..
Maternal morbidity :
 Abruption
 DIC
 Pulmonary oedema
 ARF
 ARDS
 Hepatic rupture leading to DIC & death
 Death in 1%

49. Management
 Immediate delivery is indicated once
diagnosis of HELLP established.
 Vaginal or LSCS
 Platelets if count < 50000 or if s/o
altered hemostasis.
 Plasmapheresis is lifesaving if
deterioration in course of disease.
 Better to err by delivering preterm
fetus than to conserve for further
harm.

50. Other severe complications of PIH
 Pulmonary oedema (d/t fluid overload,
oligouria & LVF)
 ARF
 Abruption
 Intra-cranial bleeding
 Visual disorders.
 Recurrence in next pregn 30%
 High risk of chronic HTN.

51. Post natal care
 Daily BP monitoring till pt is indoor.
 Once discharged, BP on alt days till
normal value settles in.
 Continue antihypertensive till
normalization of BP postpartum.
 Repeat lab after 48hrs.
 If abnormal monitor weekly.
 Do reagent strip for proteinuria at 6wks
follow up. If abn, repeat at 3months.
 Counselling of pt about recurrence of
PIH and risk of chronic HTN.

52. Prevention
 Research going on without effective
solution
 Low dose aspirin
 Ca supplementation: cheap & effective
 ? Anti-oxidants, ? Fish oil
supplementation
 No role of salt restricted diet in PIH
 Predictive tests.

53.  “Let us understand PIH better for
managing patients more efficiently.”
“THANK YOU…”