PIH : Etiology, Clinical features & Management

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…”