This document discusses pregnancy induced hypertension (PIH), also known as preeclampsia. PIH is a multisystem disorder characterized by high blood pressure and protein in the urine that develops during pregnancy. It can lead to serious complications for both the mother and baby if untreated. The document covers the definition, classification, signs and symptoms, risk factors, pathogenesis, diagnosis, and management of mild and severe cases of PIH.

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
 Haemoconcentration

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.  “Neverneglect 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
abruption.

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 prognosis is poor.

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…”