Pregnancy Induced Hypertension

Dr. Ayshwarya RevadkarOBGY UNIT 3, YCMH

INTRODUCTION

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

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.

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)

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 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)

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 PVR4. 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 300-600Fall in platelets (15%)Raised ESR 4 times of normal. (so no

diagnostic value)Decreased fibrinolytic activityIncrease 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.

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 ICT4. Vascular : Aortic coarctation 3. Systolic HTN : Thyrotoxicosis, hyperkinetic circulation.

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.

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 homeDon’t lower BP rapidly: harm to fetus

Antihypertensives used in Pregnancy :

1. Diuretics : Furosemide, chlorthiazide2. Vasodilators : Labetalol, Nifedipine, Prazosin,

Hydralazine.3. Drugs that decrease CO : Beta

blockers, Propanalol4. Centrally acting : Methyldopa

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,

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 IUGRAGE > 35yrs or chronic HTN of >15yrs

durationMarked obesitySecondary HTN

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.

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.

Conti..Criteria to identify high risk women

with gestational HTN :

1. BP > 150/100 mm Hg.2. GA < 30wks3. Evidence of end organ damage4. Oligohydramnios5. Fetal growth restriction6. Abnormal CD.7. Nullipara, Age > 35yrs, BMI > 35 kg/m2

PREECLAMPSIA

Incidence : 5-15%

In primigravida: 10%

In Multigravida 5%

Risk factors for Preeclampsia :

Primi : younger or elderlyFamily history of PIH, HTN, DMH/O PIH in previous pregnancyHyperplacentosis as in molar

pregnancy, twins, DMObesity, Chronic HTN, pre-existing

vascular or Renal disease, DMNew paternityThrombophilias : 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).

Conti..All of above result in :Increased vasoconstrictionDecreased 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

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 oedemaExcessive weight gain : is >

0.5kg in one week or >2kg in one month in later months of pregnancy.

Clinical e/o vasoconstriction by fundoscopy

s/o Impending Eclampsia :

HeadacheEpigastric 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…”

Laboratory findings :

Haemoconcentration leads to false Hb.

ThrombocytopeniaRFTs: 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.

Abnormal fetal growth

IUGR of 2-4 wks in PIH commonly seen.Demands uterine, umbilical & MCA

doppler.UA utero-placental circulationUmb A : Placento-umbilical circulation.Doppler weekly in moderate to severe

PIH.NST & MBBP twice weekly to assess

fetal wel-being.

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,

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.

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.

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.IUGRCerebral or visual disturbances

Conti..Pulmonary oedema or cyanosisEpigastric or right uppaer

quadrant painImpaired liver functionThrombocytopenia Very imp : s/o impending

eccampsia

Management of severe PIH

GA > 34 wks :MgSO4 to prevent seizuresAntihypertensive to control BPDelivery : 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

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 orSod nitroprusside 0.25-5

microgm/kg/min iv short term therapy only when other drugs failed.

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.

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.

Guidelines for expectant management :

Bed restDaily weightDaily input & outputAntihypertensive t/tSteroidsLab on alternate daysDaily NSTDFMCCD twice a weekAFI twice a weekUSG to see for fetal growth every 2 weeks

GA < 24 weeks:

Severe maternal morbidity if pregnancy conserved

Perinatal mortality, IUDs.Only t/t is Delivery.

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.

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.

Management of Eclampsia

Place pt in lateral decubitus.Mouth gagSuction oral secretionsO2 by maskElevate bedside rails to avoid injurySwitch off lights, keep quite environment surrounding pt.Pulse oxymeter, foley’s catheter, iv accessMgSO4Start IV fluids at low rate 100ml/hr.Antihypertensive : 1st drug of choice in

severe HTN is iv Labetalol. Deliver the pt.

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.

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.

Increase in LSCS for eclampsia in modern OBs :

Due to Unripe Cx, poor progress in laborIUGR, preterm babyInadequate control of BPMainly to avoid adverse maternal

& fetal effects of pregnancy continuation.

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.

HELLP SYNDROME

Criteria for diagnosis :

1) Haemolysis (microangiopathic H.A.) Burr cells, schistocytes on PBS bilirubin > 1.2mg/dl absent plasma haptoglobin2) Elevated liver enzymes AST > 72 IU/L LDH > 600 IU/L3)Low platelets < 1 lakh/mm3

Conti..Maternal morbidity :

Abruption DIC Pulmonary oedema ARF ARDS Hepatic rupture leading to DIC &

death Death in 1%

Management Immediate delivery is indicated

once diagnosis of HELLP established.

Vaginal or LSCSPlatelets 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.

Other severe complications of PIH

Pulmonary oedema (d/t fluid overload, oligouria & LVF)

ARFAbruption Intra-cranial bleedingVisual disorders.Recurrence in next pregn 30%High risk of chronic HTN.

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.

Prevention

Research going on without effective solution

Low dose aspirinCa supplementation: cheap &

effective? Anti-oxidants, ? Fish oil

supplementationNo role of salt restricted diet in

PIHPredictive tests.

“Let us understand PIH better for managing patients more efficiently.”

“THANK YOU…”