Hypertensive Disorders in Pregnancy

Dr. Jograjiya G.R.

Post Graduate Student

ESI-PGIMSR, Basaidarapur, New Delhi.

INTRODUCTION

It is associated with severe maternal obstetric

complications.

Incidence is 5-10%.

The most frequent cause of iatrogenic

prematurity.

Preterm delivery

Intrauterine growth restriction (IUGR)

Perinatal death

Maternal cerebrovascular accidents

Placental abruption

Hypertension in Pregnancy

Systolic B.P. ≥ 140 mmHg

and/or

Diastolic B.P. ≥ 90 mmHg

Documented on two occasions

At least 6 hours apart

Not more than 7 days apart

Readings should be confirmed using appropriate

measurement technique, and should be remeasured after

10-15 minutes of rest.

Other Criteria (Not part of definition currently)

SBP increased by 30mmHg

DBP increased by 15mmHg

Mean Arterial Pressure increased by 20mmHg

SEVERITY HYPERTENSION

Non-severe hypertension: SBP

140-159 mmHg or DBP 90-109

mmHg.

Mild: SBP 140-149 mmHg or

DBP 90-99mmHg.

Moderate: SBP 150-160 mmHg

or DBP 100-110 mmHg.

Severe hypertension: SBP >

160 mm Hg or DBP > 110 mmHg

or both.

How to Measure Blood

Pressure

Sitting Position

Patient Relaxed

Arm well supported

Measured in right arm

Cuff at heart level

Proper cuff size (80% of arm

circumference)

Slow deflation of bladder

(2mmHg/s)

From start of Korotkoff I to end

of Korotkoff V

Normal Blood Pressure

changes in Pregnancy

• Decreases during the first

trimester,

• Reaching its lowest point at 20

weeks,

• Returns to pre-pregnancy

levels during the third

trimester.

What is Significant

Proteinuria in Pregnancy

Total protein in 24 hours urine

> 300mg

Protein : Creatinine ratio in

random sample > 0.1

Calcification and

Definitions

Classification

2. Pre-eclampsia

4. Eclampsia

3. Preeclampsia superimposed

on chronic hypertension

5. Chronic hypertension

with pregnancy

1. Gestational hypertension

GESTATIONAL HYPERTENSION

New onset of hypertension after

20 weeks of gestation without

proteinuria or other features of

preeclampsia, followed by return

of B.P. to normal within 12

weeks post-partum.

This terminology replaces the term

“Pregnancy Induced Hypertension.”

Gestational HTN:

DIAGNOSIS

Determine the severity of

hypertension

Measure protein excretion

24-hour urine collection

Evaluate for signs/symptoms of

severe preeclampsia

Perform laboratory evaluation

+/- end - organ

involvement

Gestational HTN: DIAGNOSIS

CRITERIA FOR MILD GESTATIONAL HYPERTENSION

Blood Pressure > 140 to < 160 mm Hg, systolic

> 90 to < 110 mm Hg, diastolic

Proteinuria < 300 mg per 24-hr collection

Platelet count > 100,000/mm3

Liver enzymes Normal

Maternal symptoms Absent

IUGR / Oligohydramnios Absent

Gestational HTN: MANAGEMENT

Mild Gestational HTN

Managed as outpatients (weekly antepartum

visits)

Daily fetal movement/kick counting

NST + AFI OR BPS

Fetal growth monitoring every 3-4 weeks

No antihypertensive therapy

No antenatal corticosteroids

Deliver patients no later than their EDD

Gestational HTN: MANAGEMENT

Severe Gestational HTN

SBP ≥160 mmHg or DBP

≥110 mmHg is treated with

antihypertensive agents

> 34 wks AOG DELIVER!

< 34 wks AOG give

steroids

Gestational HTN:

Risk of Progression to Preeclampsia

15-25% risk

Women with early onset of

gestational hypertension

are more likely to progress

to preeclampsia than

women with late onset

Gestational HTN:

RECURRENCE

Prevalence: 22 - 47 % (2nd

pregnancy)

tends to recur with

subsequent pregnancies

Gestational HTN:

LONG-TERM PROGNOSIS

associated with

development of HTN later

in life

associated with

development of diseases

related to hypertension

(CVD, CKD,DM)

PREECLAMSIA

New onset of hypertension after 20

weeks of gestation along with properly

documented proteinuria or end-organ

dysfunction symptoms, followed by

return of B.P. to normal within 12

weeks post-partum.

Preeclamsia Gestational Hypertension Proteinuria

Note it……………………..

Preeclampsia can also occur

without proteinuria, with end-

organ dysfunction manifestations.

Edema is no longer considered a

specific diagnostic criterion for

preeclampsia.

Risk Factors

Genetic

Age & parity

Partner factors

Pregnancy Factors

Underlying Medical Conditions

Others

Risk Factors

Risk Factors: Cont.

Genetic

Genetic Predisposition

Family History

Race & Ethnicity

More Common in black & Asians

Pregnancy by ovum donation

Age &Parity

Teenage pregnancy <18 yrs

Age>35 yrs

Long interval between

pregnancy >10 years

Nulliparity

Partner Factors

Change of partner

Limited sperm exposure

Pregnancy by donor

insemination

Partner fathered an eclamptic pregnancy

Risk Factors: Cont.

Pregnancy Factors

Multiple pregnancy

Hydatiform mole

Hydrops fetalis

Fetal chromosomal anomaly

(trisomy 13)

Underlying Medical Diseae

Chronic hypertension

Diabetes mellitus

Renal Disease

Cardiovascular disease

Hyperthyroidism

Metabolic Syndrome

Others

Obesity BMI> 35 kg/m2

Psychological stress & strain

Smoking

Previous history of preeclamsia

• Hyperhomocysteinemia ,

• Autoimmune disease

• Antiphospholipid antibodies,

• Thrombophilia

PATHOPHYSIOLOGY

2 stage model for

preeclampsia

Stage 2

Maternal syndrome

(HTN, proteinuria,

Endothelial dysfunction)

Stage1

Reduced placental implantation ???

Reduced placental

implantation –Stage-1

PREDISPOSING FACTORS:

Abnormal implantation

Association with microvascular

diseases (diabetes,

hypertension etc.)

Association with large

placentas (hydrops, multiple

gestation, hydatidiform mole)

Net effect

Replacement of endothelial lining & muscular arterial wall by trophoblast cells

Distended tortuous spiral arteries

Low resistence, low pressure, high flow system

ETIOLOGICAL FACTORS

Placental hypoxia

Immunological factors

Placental enzymes

Genetic factors (MTHFR, F5,)

Oxidative stress

What causes maternal

syndrome

Stage 2

Maternal syndrome

(HTN, proteinuria,

Endothelial dysfunction)

Stage1

Reduced placental implantation

What gets into maternal circulation

Maternal Syndrome

stage-II

Not just hypertension and

proteinuria

But also involves different end

organs

Physiology of maintain

uteroplacental flow in

Normal pregnancy Placenta releases angiotensinase

destruction of angiotensin-II(a

potent vasoconstrictor) BP

stabilized

Vascular synthesis of PGI-2 and

NO in excess vasodilation BP

stabilized & uteroplacental flow

maintains

Release of VEGF restores

uteroplacental flow

Normal balance of agonist &

anta-gonistic factors:

1.vasodialator &

vasoconstrictor

2. angiogenic and

antiangiogenic factors

1.vasodialator & vasoconstrictor

vasodialator

NO

PGI-2

vasoconstrictor

Angiotensin-II

Endothelin-I

Thromboxane A2

placenta

Syncytiotrophoblast

& endothelium

2. angiogenic and

antiangiogenic factors

Angiogenicfactor

• VEGF

• TFG-beta• PlGF

Antiangiogenicfactor

• sFlt-1

• sEng

Gestational Hypertension

Basic mechanism of different

organ damage

Increased vasoconstriction

Decreased organ perfusion

Increased endothelial dysfunction –

capillary leak, oedema, Pulmonary

oedema, proteinuria.

Activation of coagulation: DIC, low

platelets

Haemoconcentration

Multisystem Features

Of Preeclampsia

Hypertension Proteinuria

Eclampsia HELLP syndrome

Intra-uterine growth restriction

Multi-organ disease

Cerebral

vessels

Fetus

Liver

Systemic blood vessels Kidneys

Organ Damage

utero-placenta IUGR

Hematological Epistaxis, DIC like features,

hemoconcentration

CNS Cerebral edema, cerebral hge seizures

Heart Subendothelial hge , focal necrosis & hge,

cardiomyopathy, heart failure

Lungs Pulmonary edema, hemorrhagic

brochopneumonia

Kidneys glomerular endotheliosis, oliguria

liver Subcapsular hge, ischaemiaperiportal

necrosis, HELLP

CVS involvement:

• ↑afterload↑ed peripheral resistance

•↓preload ↓ed pregnancy induced

hypervolumia

•Pulmonary leak edemaalveolar endothelial damage & ↓ed plasma

oncotic pr

•hemoconcentration & ↑edhematocrit

↓ed blood volume than normal pregnancy(16%

vs 50%):

Heart failure

↓cardiac output

Hematological system

Thrombocytopenia & other PL

abnormality:

• ↑ed PL activation & degranulation,

• ↓ed life span.

• Corelates well wthdisease severity.

Intravascular hemolysis

• endothelial damage & altered fluidity of erythrocyte membrane d/t change in serum lipid content →↑ed LDH, spherocytosis, reticulocytosis

• microangiopathichemolysis

↑ed coagulation & fibrinolysis

• Feature like DIC

• Release of thromboplastin

• ↓fibrinogen

• AT-III

• plasminogen

Renal system involvement:

↓ed renal perfusion :(d/t ↓ed blood volume & ↑ed

afferent arteriolar pr.)

↓ed GFR : d/t

glomerular capillary endotheliosis

Endothelial dysfunction + mesangial swelling + BM

disruption

(but podocyte disruption minimal)

Oliguria

↑ed creatinine level

↑ed uric acid

Hepatic involvement:

Periportalhemorrhagic

necrosis

hematoma formation

Stretch/Rupture

epigastric pain

Brain involvement:

Acute severe HTN

cerebrovascular overregulation

Vasospasm

Parenchymal ischemia

Cytotoxic edema

sudden ↑↑SBP

exceeds normal range of cerebrovascular autoregulation

Forced vasodilation + hyperperfusion

Vasogenic edema

Lungs involvement:

High SBP

↑ed arteriolar pr

↑ed extravasation of blood into alveoli + rupture of arteriole

Pulmonary edema, hemorrhagic brochopneumonia

PREECLAMPSIA PREDICTION

There are many test during early pregnancy—

or across pregnancy—of various biological,

biochemical, and biophysical markers

implicated for preeclampsia prediction.

The most predictive investigative procedures

are cumbersome, time-consuming and with

poor sensitivity and with poor positive

predictive value for preeclampsia.

The efficacy of the preventive methods is

questionable too

Currently, no screening tests are predictably

reliable, valid, and economical

(Kleinrouweler, 2012).

Endothelial Dysfunction/Oxidant Stress

Feto-Placental unit Endocrine Dysfunction

Renal Dysfuntion Misc

Placental Perfusion/ Vascular Resistance related Tests

Uterine Artery Doppler Velocimetry

AT- III

ANPFree fetal DNA

Adapted from Conde-Agudelo and associates (2009)

Trials of different preventive methods and their outcomes

Sibai et al. Lancet 365:785-99, 2005.

Provocative

Pressure Tests

Three tests have been extensively

evaluated to assess the blood pressure

rise in response to a stimulus.

1.Roll-over test

After resting in the left lateral

position turning to a supine

position induces a rise in

diastolic pressure of 20 mmHg

or more is a positive test

indicative of tendency to

develop pre-eclampsia.

Perform at 28 to 32 weeks

pregnancy.

2.Hand-grip test

Isometric (sustained) contraction of

striated muscles is known to cause

general sympathetic activation and hence

increase systemic arterial pressure in

healthy adults. The patient compresses

an inflated sphygmomanometer cuff for a

3-minutes period at maximal and then at

50% of maximal voluntary contraction. An

increase in diastolic pressure >20 mmHg

at 28-32 weeks’ gestation is associated

with an increased incidence of GHTN and

eclampsia.

3. Angiotensin II sensitivity

Sensitivity to infused angiotensin II: is

increased may be due to alteration in

vascular smooth muscle A II receptors.

Sensitivities of all above three tests to

range from 55 to 70 percent, and

specificities approximated 85 percent.

(metaanalysis, Conde-Agudelo and

associates 2014)

• is most promising, but currently, none of them is completely suitable for clinical use. (Conde-Agudelo, 2014; Kleinrouweler, 2012; Myatt, 2012a).

• These have value for fetal-growth restriction but not preeclampsia (ACOG, 2013a).

• As a result of these trials, some methods to prevent Preeclampsia have been theorized…

Uterine Artery Doppler Velocimetry (abnormal flow resistance/ diastolic notch in

2nd/ 3rd trimester)

uterine artery DOPPLER

In preeclamptic mother:

Showing early diastolic NOTCH

Decreased EDF

(due to high resistance)

In normal mother

Urinary assays

a. Micro-albuminuria: detected by

radioimmunoassay before albuminuria can

be detected by the ordinary methods. The

drawback is that not all proteinuric pre-

eclampsia are preceded by this phase.

Sensitivities ranging from 7 to 90% and

specificities between 29 and 97 % (Conde-

Agudelo,2014).

b. 24 hours urinary calcium excretion: is

lower in women with pre-eclampsia than

normotensive pregnant women.

Urinary assays

c.Kallikrein/creatinine ratio: is reduced

in patients who develop PIH later on

if compared to the increased ratio in

normal pregnancy. Kallikrein is a

blood pressure reducing agent.

d. Prostaglandins metabolites: The end

metabolite of prostacyclin is

decreased while thromboxane B2 (the

metabolite of thromboxane A2) is

increased in urine of pre-eclamptic

women.

Blood tests

a. Plasma urate: serial increase is a

warning of PIH before appearance

of other clinical features.

b.Platelet count: a reduction

occurs early in pre-eclampsia.

c. Anti-thrombin - III activity: begin

to decline as much as 13 weeks

prior to the development of clinical

manifestations of pre-eclampsia.

PREVENTION

Prepregnancy

• Weight loss to ideal BMI

• Control of glucose in diabetes

• Control of BP in CHTN (diet, exercise)

Low dose aspirin 75 mg in High risk patient (from 12 wks) once a day

Calcium 500mg twice a day.

Not recommended

• Vitamins C & E

• Dietary salt restriction

• Anti-HTN therapy to prevent preeclampsia

History -special points

• Patient Particulars: Age young or >35 yrs, nulliparity, low SES -risk factors

• Chief Complaints: Swelling of legs or other parts of body (face, abdominal wall, vulva, or whole body and tightness of the ring on the finger.) Severe disease -Headache, visual changes, nausea, vomiting, abdominal or epigastric pain, and oliguria, insomnia, vaginal bleeding, seizures.

• Present Obstetric History: Onset, Duration, Severity of Htn/Proteinuria and H/o drug intake

• Past Obstetric History: H/o any hypertensive disorder of pregnancy with week of onset. Also note the interval since last pregnancy, gestational age at delivery. Any foetal complications.

• Past History: of pre-existing hypertension, renal disease, diabetes, thrombophilia, or thyroid disorder.

• Family History: of Htn, Preeclampsia, Diabetes, CVD

Physical Examination:● Obesity/BMI >35 kg/m2

● Weight (serial measurements): Gain in wt at the rate of >500gs a week or

2.5kgs a month in the later months of pregnancy may be the earliest sign

of preeclampsia.

● Oedema (all sites): has to be pathological, meaning visible pitting edema

demonstratable over the ankles after 12 hrs bed rest.

● Pulse

● B.P.:

○ right arm, sitting/supine, arm at level of heart, cuff length=1.5

times of arm circumference, diastolic BP is the disappearance of

Korotkoff sounds (phase V)

○ taken on 2 occasions at least 6 hrs apart for confirmation of

diagnosis.

● CVS examination: auscultation for heart rate, rhythm, splitting of S2,

murmurs.

● Ophthalmic examination: retinal haemorrage, nicking of veins,

arteriole/vein ratio 3:1 from 3:2, papilloedema

● Deep tendon reflexes: hyperreflexia/presence of clonus

Obstetric Examination:

Nothing special is found except features of IUGR, oligohydramnios in some cases.

Maternal Investigations:

Tests may be abnormal even when BP elevation is minimal.

• Urine dipstick testing for proteinuria

o Quantitation by laboratory methods if ≥1+ on dipstick testing

o Urinary ACR(albumin-creatinine ratio) to detect significant

proteinuria (≥30mg/mmol)

o 24 hour urine collection is not necessary in routine clinical

management

• Routine Blood Examination: TLC, DLC, Peripheral Smear, BT, CT,

Hb%

• Serum Urea, creatinine, electrolytes including lactate

dehydrogenase (LDH) and uric acid.

• Liver function tests (LFT) -AST, ALT >70 IU/l

• Skiagram of chest –PA view, Pulmonary Capillary Wedge

Pressure (PCWP), Brain Natriuretic Peptide (BNP) for

detection of pulmpnary oedema

Diagnosing Preeclampsia-Eclampsia:• Blood pressure ≥ 140/90 mm of Hg (at

or after 20 weeks of gestation) on 2

occasions at least 6 hours apart during

bed rest. (160/90 mm of Hg is severe

disease)

• accompanied by one or more of:

o significant proteinuria

-urinary dipstick 1+

-random urinary

protein/creatinine

ratio ≥ 30 mg/mmol

-24 hour urine excretion ≥300

mg/24 hrs

o renal involvement

-serum creatinine ≥ 90 mmol/L

or

-oliguria (<400 ml in 24 hrs)

o haematological involvement

-platelet count <1 lakh

o liver involvement

-raised AST, ALT (>70 IU/l)

-severe upper abdominal pain

o neurological involvement

-severe headache

-persistent visual disturbances

-hyperreflexia with sustained

clonus

-convulsions (eclampsia)

-stroke

o pulmonary oedema

o fetal growth restriction

o placental abruption

Foetal Investigations:

• Cardiotocograph (CTG)

• Ultrasound scan (USS) assessment

of:

o fetal growth

o amniotic fluid volume (AFV)

o umbilical artery flow (Doppler)

Differential Diagnosis

Pre-existing hypertension

New/gestational hypertension

Pre-eclampsia

Eclampsia

Exacerbation of underlying renal disease/Superimposed pre-eclampsia-eclampsia

SLE

N.B: Grades of proteinuria (in g/L): Trace=0.1, 1+=0.3, 2+=1, 3+=3,

4+=10

Hypertensive Disorders in Pregnancy

Gestational HTN

● BP ≥ 140/90mmHg

●No evidence of underlying cause of HTN

●No associated symptoms

●Comes to normal within 12 wks of delivery

Pre-eclampsia

Non Severe Severe

Eclampsia

PreEclamsia

+

Convulsion

±

Coma

N.B: Pre-eclampsia is

principally a syndrome of

signs and when symptoms

appear it is usually late.

Indicators of severity of Pre-eclampsiaABNORMALITIES NONSEVERE SEVERE

Blood pressure ≥140/90mmHg but

<160/110mmHg

≥160/110mmHg

Proteinuria ≤2+ ≥3+

Oliguria Absent <400ml/day

Headache Absent Present

Visual disturbances Absent Present

Platelet count Normal Thrombocytopenia

(<100,000/mm3)

HELLP syndrome Absent May be present

ALT,AST >70 IU/L

LDH>600 IU/L

Bilirubin >1.2g/L

Serum transaminases(AST,ALT) Normal (<40 IU/L) Elevated

Serum Creatinine Normal Elevated

Epigastric pain Absent Present

Fetal growth restriction Absent Obvious

Pulmonary oedema Absent present

MANAGEMENT

Definitive treatment: DELIVERY!

Based on:

AOG

Severity of PE

Maternal / Fetal condition

NONSEVERE PE: MANAGEMENT

Deliver at ≥37 weeks of

gestation

Labor induction encouraged

For Nonsevere - controlled disease :

There after induction may be done at term depending on cervical condition

Can be managed expectantly till term at home/hospital and continued till term.

74

What is EXPECTANT MANAGEMENT?

NO

YES

Neither forced nor restricted

EXPECTANT ANTEPARTUM MANAGEMENT OF

NONSEVERE PREECLAMPSIA

Inpatient vs outpatient care

Close maternal monitoring upon diagnosis

of preeclampsia is important to establish

disease severity and the rate of

progression

Hospitalization is useful for making these

assessments and facilitates rapid

intervention in the event of rapid

progression

Outpatient care is a cost-effective option

for women with stable mild preeclampsia

after initial dx evaluation

EXPECTANT ANTEPARTUM MANAGEMENT

OF NONSEVERE PREECLAMPSIA

Laboratory follow – up

platelet count, serum creatinine,

serum AST

1-2x/wk, assess disease

progression

Assessment of fetal well-being

daily fetal movement count

twice weekly fetal NST with AFI

or

twice weekly BPS

UMA Doppler indices evaluation

EXPECTANT ANTEPARTUM MANAGEMENT

OF NONSEVERE PREECLAMPSIA

Assessment of fetal growth

Sonographic estimation of fetal weight

done to look for growth restriction and

oligohydramnios at the time of diagnosis

of PE , repeated every 3 weeks if the

initial examination is normal

Antenatal corticosteroids

< 34 weeks AOG

But wait…can antihypertensives be used in expectant management???

• In non-severe Pregnancy hypertension – No clear

Evidence of benefit other than to reduce

The Frequency of Episodes of Severe

hypertension

• May Adversely Effect Fetal Growth velocity

Fetal considerations

Prematurity

Stillbirth

Newborn asphyxia

Maternal considerations

Worsening of disease

Complications

Hospitalisation???

• Gestational HTN : only if severe HTN

• Preeclampsia : If diastolic pressure≥ 100mm of Hg OR, there is proteinuria OR, there is fetal compromise.37 completed weeks of gestation.

INTRAPARTUM MANAGEMENT

Intrapartum monitoring

Fluids

monitored closely to avoid

excessive administration,

since women with severe

disease are at risk of

pulmonary edema and

significant third-spacing

DELIVERY CARE

• For any HDP, vaginal delivery should be considered unless a CS is required for the usual obstetric indications.

• Antihypertensives : continued throughout labour to maintain BP < 160/110 mmHg .

• 3rd Stage : actively managed with 10 units IM, particularly in the presence of thrombocytopenia or coagulopathy. (I-A)

• Ergometrine should NOT be given

PES: MANAGEMENTDeliver regardless of gestational age

if proteinuria ( ≥5 grams) is the

only criteria for severe disease

managed as nonsevere PE

mild fetal growth restriction with

reassuring Doppler velocimetry

treat conservatively *

severe hypertension treat

conservatively *

NOTE: * remote from term

For early onset severe preeclampsia:

• Controversy regarding termination in early onset disease

• But there is no beneficial role for mother, as well as perinatal mortality is also high instead of conservative management

• So…

85

termination is seriously considered

suspected

severe

preeclampsia

at < 34 weeks

Acute Management of PESSet 1: Labetalol first protocol

•Notify OB provider when patient presents with severe HTN (systolic ≥ 160 mmHg or diastolic > 110 mmHg)

• Initiate appropriate fetal surveillance

• Labetalol 20 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then:

• Labetalol 40 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then:

• Labetalol 80 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then:

• Hydralazine 10 mg IV over 2 min; recheck BP in 20 min; if still above either threshold then:

• Emergency consultation with maternal fetal medicine (MFM), anesthesia, internal medicine, critical care specialist.

• Give additional antihypertensive medication per specific order.

• Once the aforementioned BP thresholds are achieved, repeat BP measurement every 10 minutes for 1 hour, then every15 minutes for 1 hour, then every 30 minutes for 1 hour, and then every hour for 4 hours.

• Institute additional BP timing per specific order.

Acute Management of PES

Set 2: Hydralazine first protocol

• Notify OB provider when patient presents with severe HTN (systolic ≥ 160 mmHg or diastolic ≥ 110 mmHg)

• Initiate appropriate fetal surveillance

• Hydralazine 5 or 10 mg IV over 2 min; recheck BP in 20 min; if still above either threshold then:

• Hydralazine 10 mg IV over 2 min; recheck BP in 20 min; if still above either threshold then:

• Labetalol 20 mg IV over 2 min; recheck BP in 10 min; if still above either threshold then:

• Labetalol 40 mg IV over 2 min and;

• Obtain emergency consultation with MFM, anesthesia, internal medicine, critical care specialist.

• Give additional antihypertensive medication per specific order.

• Once the aforementioned BP thresholds are achieved, repeat BP measurement every 10 minutes for 1 hour, then every 15 minutes for 1 hour, then every 30 minutes for 1 hour, and then every hour for 4 hours

• Institute additional BP timing per specific order.

TARGET BP

130 to 150 mm Hg systolic and 80 to 100

mm Hg diastolic OR reduce MAP by no

more than 25% over 2hrs

Cerebral or myocardial ischemia or

infarction can be induced by aggressive

antihypertensive therapy if the blood

pressure falls below the range at which

tissue perfusion can be maintained by

autoregulation.

WOMEN WHO FAIL TO RESPOND TO

FIRST LINE AGENTS

Emergent consultation with anesthesia, maternal

fetal medicine or critical care for second line

management decisions, which can include

labetalol or nicardipine by infusion pump, and

nitroprusside for extreme emergencies.(ACOG

2013)

Sodium nitroprusside to be used rarely when

other agents fail, at 0.25 μg/kg/min to a

maximum of 5 μg/kg/min. Nitroprusside should

be used for the shortest amount of time possible,

due to the risk of fetal cyanide poisoning and

increased intracerebral pressure with worsening

cerebral edema.

Seizure Prophylaxis

MgS04 given to mild / severe PE

Loading dose: 4-6 g, slow IV

push, over 15-20 mins

Continuous infusion: 1-2 g/hr

OR 5g IM into each buttock

(total 10 g) followed by 5 g IM,

alternate buttocks ever 4h

continued for 24 hours after last

convulsion or delivery.

MgS04 Toxicity

1. Impaired breathing(@8-10meq/L)

2. Arrythmia and Asystole ( @10-13 mEq/L)

3. Decreased/absent deep tendon reflex

(Hyporeflexia at 4 mEq/L, loss of patellar reflex at 7-10 mEq/L)

4. Shock (>13 mEq/L)

• For a maintenance dose following must be present -

Serum Mg level 4-7meq/l(twice daily)

Having Patellar reflex

Urine output >30ml/hr

RR>12/min

WHAT If magnesium toxicity is suspected???

Administration of 10mL of 10% calcium gluconate (1 g in total) as a slow intravenous push.

Serum magnesium level obtained.

Magnesium infusion should be discontinued, supplemental oxygen administered,

For severe-uncontrolled disease:

LUCS OR In case of very severe uncontrolled disease elective LUCS may be done without induction

Preinduction

Cervical ripening with prostaglandin followed by induction

Termination is considered

95

If failed

Postpartum Management

NSAIDs

for pain control should be avoided in

women with poorly controlled

hypertension, oliguria, renal

insufficiency, or thrombocytopenia

patient controlled fentanyl or

remifentanil analgesia or epidural.

Monitor VS q 2h while on MgS04

Treat PES

IMMEDIATE REMOTE

MATERNALFETAL

● IUGR

● IUD

● Asphyxia

●Prematurity

During Pregnancy During Labour During

puerperium●Eclampsia(2%) (more in acute cases)

●Accidental hemorrhage

●Oliguria

●Diminished vision

●HELLP Syndrome

●Cerebral hemorrhage

●ARDS

● Eclampsia

● Postpartum

hemorrhage

●Eclampsia(

in < 48hrs

of delivery)●Shock

●Sepsis

●Residual hypertension

●Recurrent pre-

eclampsia●Chronic Renal Disease

• Abruptio placentae

HELLP SyndromeThis is an acronym for Hemolysis, Elevated Liver

enzymes, and Low Platelet count.

It is a rare multisystem disorder that complicates

pregnancy with lab evidences of micro-

angiopathic hemolysis, hepatic dysfunctioning &

thrombocytopenia.

It is a complication mostly associated with Pre-

eclampsia but can also be diagnosed (rarely

though) in the absence of these disorders.

Incidence 20% of women with severe

preeclampsia.

HEMOLYSIS

(due to passage of

RBCs through partially

obstructed vessel)

s)HEPATIC

DYSFUNCTION(due to

intravascular fibrin

deposition & sinosoidal

obst.)

Decreased Liver blood

flow

HELLP

Syndrome

THROMBO-CYTOPENIA

(due to platelet

aggregation & dipositionin the sites of endothhelial

damage)

Diagnosis

Hemolysis (Hallmark of

the triad)

Elevated Liver Enzymes Low Platelet Count

LDH>600IU/L Liver Enzymes (<100,000/cu.mm)

Low serum haptoglobin

High serum bilirubin

(>1.2 mg/dl)

High ALT & AST

(>70 IU/L)

Abnormal PBS

(Schistocytes {helmet

cells} , burr cells

{Echinocytes})

Later-low Hb%

• ●Epigastric /Right Upper Quadrant pain

• ●Nausea, Vomiting1. Clinical Features:

2. Lab Investigation:

HELLP Syndrome

Initiate IV Dexamethasone:

Only for dangerously low platelet counts <50,000/uL

The 2013 Task Force does not recommend for HELLP syndrome

Antepartum: Dex 10mg q12 hrs

Postpartum: Dex 10+10+5+5

@ 0,12,24,36 hrs

Usual Time of Onset

Relation to delivery Percentage

Antepartum 72

Post_partum 28

≤48 hours 80

>48 hours 20

Gestational Age (Weeks) Percentage

21-27 10

28-36 70

>37 20

SUPERIMPOSED PREECLAMPSIA

ON CHRONIC HYPERTENSION

New onset proteinuria in

hypertensive women but no

proteinuria before 20 weeks' gestation

A sudden increase in proteinuria or

blood pressure or platelet count <

100,000/L in women with

hypertension and proteinuria before

20 weeks' gestation

ECLAMPSIA

Generalized tonic-clonic seizure in a

patient with Preeclampsia not attributed

to any other cause.

If seizures occur beyond 48-72 hours postpartum

causes may be more likely other than eclampsia.

occurs in 2 to 3 percent of severely preeclamptic

women not receiving anti-seizure prophylaxis

Eclampsia Preeclampsia

Seizure/

Convulsion/

Coma

D/D ECLAMPSIA

Epilepsy,

Intracranial

haemorrhage/thrombosis,

Meningitis,

Cerebral malaria,

Amniotic fluid embolism

can mimic eclampsia.

PATHOGENESIS OF SEIZURES

1. Cerebral overregulation in

response to high systemic blood

pressure

vasospasm of cerebral arteries

underperfusion of the brain

localizedischemia/infarction

cytotoxic (intracellular) edema

PATHOGENESIS OF SEIZURES

2. Loss of autoregulation of cerebral

blood flow in response to high systemic

pressure

E.g., hypertensive encephalopathy

Hyperperfusion

endothelial damage

vasogenic (extracellular) edema

MANAGEMENT

Iinitial Mx: Maintenance of airway

patency and prevention of

aspiration

Gravida rolled onto her left side

Protect from trauma

Supplemental O2 (8-10L/min via

face mask)

Management of severe hypertension,

if present

Prevention of recurrent seizures

Evaluation for prompt delivery

definitive treatment of eclampsia

is delivery, irrespective of

gestational age

Management of Eclampsia :

Prompt delivery of fetus to achieve cure

Avoidance of diuretics & hyper osmotic agents

Limitation of I.V fluid

Intermittent antihypertensive to control BP judiciously

Control of convulsion by MgSO4 (IM/IV route)

Protection & supporting care during convulsionProtection in a railed cot

Protection of airway & prevention of tongue bite

Correction of hypoxia & acidosis

Managed in Eclampsia room.

113

to control convulsion

“It is the most effective drug to control even recurrent seizures without any central nervous system depression to mother & fetus”

114

Magnesium sulphate

Dosages

→Paralysing agent & Intubation

→Amobarbital 250mg I.V over 3 min

In case of uncontrolled recurrent seizure (10-15%) : →additional 2-4g of 20% solution IV @ <1g/min

→4gm of 20% solution IV slowly(@ <1g/min) + 10g of 50% solution deep IM in upper & outer quadrant of buttock by a wide bore needle then 5g

of 50% solution IM 4hrly similarly

IM regime (Pritchard protocol):1955

→4 gm loading in 100ml of IVF over 15-20 min followed by 2-3g/hr in 100 ml IVF as maintenance

I.V regime (Sibai protocol):1990

IM doses are as active as IV doses in controlling seizures

115

• Duration : 24 hrs from last convulsion or from delivery which one is longer.

116

MATERNAL FETAL

●Asphyxia

●Prematurity

●Hypoxia & IUD

Injuries Systemic

●Tongue bite

●Injuries due

to fall

●Bed sore

●PULMONARY: edema,

pneumonia, ARDS,

embolism

●CARDIAC: acute left

ventricular failure

●RENAL: renal failure

●HEPATIC: necrosis,

subcapsular hematoma

●CNS: cerebral

hemorrhage,

edema(vasogenic)

Vision

●Diminished

vision due to

retinal

detachment or

occipital lobe

ischemia

Hematology

●Low platelet

count

●Disseminated

Intravascular

Coagulation

Postpartum

●Shock

●Sepsis

●Psychosis

CHRONIC HYPERTENSION IN

PREGNANCY

Hypertension before pregnancy /

Diagnosed before 20 weeks of

pregnancy not due to gestational

trophoblastic disease.

Hypertension diagnosed after 20

weeks but persistent after 12

weeks postpartum

Chronic HTN & Pregnancy

Etiology :

1. Essential HTN (Most Common)

2. Secondary HTN :

1. Genetic: Glucocorticoid remediable aldosteronism,

Liddle Syndrome

2. Renal : Parenchymal, Renovascular

3. Endocrine : Primary hyperaldosteronism, cushing

syndrome, Pheochromocytoma

4. Vascular : Aortic coarctation, Estrogen use

5. Others

Thank you…