Hypertensive Hypertensive Hypertensive Hypertensive Disorders Disorders Disorders Disorders

of of of of PregnancyPregnancyPregnancyPregnancy

Joshi Suyajna D.Professor of OBG,

VIMS- Bellary

HYPERTENSIVE DISORDERS OF PREGNANCYHYPERTENSIVE DISORDERS OF PREGNANCYHYPERTENSIVE DISORDERS OF PREGNANCYHYPERTENSIVE DISORDERS OF PREGNANCY

• PIH also known as preeclampsia

• Eclampsia present when seizures superimposed on preeclampsia

• HELLP syndrome:

(H) hemolysis, (EL) elevated liver enzymes, (LP) low platelet count

Definition of HYPERTENSION

a. One measurement of

DIASTOLIC BLOOD PRESSURE (DBP) more than 110 mm Hg

b.TWO consequestive measurement of DBP more than 90 mm Hg –

4 hours apart.

ISSHP 1986

JNC 6 & JNC 7JNC 6 & JNC 7JNC 6 & JNC 7JNC 6 & JNC 7

HYPERTENSION IN PREGNANCY

Classification (ACOG):

• Pregnancy Induced Hypertension

Pre-eclampsia

Eclampsia

• Chronic Hypertension

• PIH superimposed on chronic hypertension

• Transient hypertension

• Unclassified hypertensive disorders

National Institute of Health (National High Blood Pressure Education Program Working

Group- NHBPEPNHBPEPNHBPEPNHBPEP 2000)

�1. Chronic Hypertension

�2. Preeclampsia

�3. Preeclampsia superimposed on chronic hypertension

�4. Gestational Hypertension. (Transient

hypertension of pregnancy or chronic hypertension identified in the latter half of pregnancy).

International Society for the Study of Hypertension in Pregnancy (ISSHP)

Classification (ISSHP)

Known hyper-tension prior topregnancy or at

booking (<20 weeks)

Chronichypertension,renal disease

Hypertension(without proteinuria)

arising inpregnancy

Gestationalhypertension

Gestationalhypertension

plus proteinuria

Pre-eclampsia

Compulsionsassociated with

pregnancy

Eclampsia

No information onpre-pregnancy

or pre-20weeks GP

Unclassifiablehypertension

HypertensiveDisorders ofPregnancy

Introduction

World wide each year

• 1,500,000 to 1,800,000 women develop Preeclampsia

• Upto 1,50,000 women have eclamptic convulsions

• 90% of these women are from developing countries

MATERNAL MORTALITYMATERNAL MORTALITYMATERNAL MORTALITYMATERNAL MORTALITY

• Hypertensive disorders particularly severe hypertension of preeclampsia is the leading cause of maternal and perinatal mortality and morbidity.

Lewis G et al RCOG Press –2001

Perinatal Outcome

UK India

Overall Perinatal Mortality

(per 1000 live births) 15 34%

Proportion due to

Hypertensive disease 18% 18%

Increased risk with

Hypertensive disease 2.3 4.76

Douglas KA et al, BMJ 1994Shah DS, FOGSI Perinatal Survey, 1994

Sardesai Jr Obstet Gynecol 2003

Zweifel …. 1916

Pre-eclampsia

Disease of many theories

Chesley Chesley Chesley Chesley …………. 1978. 1978. 1978. 1978

The most common definitions :The most common definitions :

• Hypertension that develops de novo as a consequence of pregnancy after 20th

week of gestation, returning to normal after 6 weeks of delivery.

• PE is present when diastolic BP> 90 mmHg or Systolic >140 or a systolic BP rises at least 30 mm Hg over base line values or diastolic BP rises at least 15 mm Hg over base line value at least at two different occasions and at least 6 hours apart (ACOG)

Acog bulletin 2002

Pre-eclampsia

Hypertension associated with

proteinuria.

INCIDENCE

• PRE-ECLAMPSIA 5 to 10%

• Eclampsia

• Developed countries 1 : 2000

• INDIA 1:30 TO 1: 500

• MATERNAL MORTALITYMATERNAL MORTALITYMATERNAL MORTALITYMATERNAL MORTALITY:

• U.S.A 17.6%

• INDIA 25.5%Walker JJ, Lancet:2000;356:1260Walker JJ, Lancet:2000;356:1260--6565

Sawhney H et al,

CHICAGO-LYING-IN-HOSPITAL

Broughton- Pipkin….1985

Pregnancy in a

Non-Pregnant state

(Failure of normal physiological changes)

Some observations

�‘PRIMI’…Mac Gillivray..1958

�‘PRIMIPATERNITY’…Feeny & Scott…1980

�‘SINGLE GENE DISORDER’

Chesley and Cooper…1986

Pathogenesis

‘unknown’ (Barton& Sibai, 2008).

�Impaired trophoblast differentiation& invasion

�Placental & endothelial dysfunction

�Immune maladaptation to paternal Ags

�Exaggerated systemic inflam. response.

Normal trophoblast differentiation & invasion

Impaired trophoblast differentiation & invasion (second phase)

Robertson and Khong …1986

Placental and endothelial

dysfunction: multisystemic disorder

‘Hypertensive Disorders in Pregnancy’, published in 1978

Leon Chesley

“The Remote Prognosis of Eclamptic Women: Sixth Periodic Report,"

1908-2000

Leon Chesley's death on March 29, 2000,Leon Chesley's death on March 29, 2000,Leon Chesley's death on March 29, 2000,Leon Chesley's death on March 29, 2000,marked the end of an era in academic obstetrics and gynecology. It is doubtful that anyone in the second half of the 20th century equaled his depth and breadth of influence on the intellectual life of our discipline.

Leon Chesley

SIBAI BAHA MOHAMMED

Sibai B.M.

�Magnesium sulfate is

the ideal anticonvulsant in preeclampsia-eclampsia. Am J Obstet

Gynecol. 1990; 162: 1141–1145

� Sibai BM. Eclampsia VI. Maternal-perinatal

outcome in 254254254254 cases. Am J Obstet Gynecol.

1990; 163: 1049–1055JOSHI SUYAJNA D.

High Risk Factors

Primigravida : Extremes of reproductive age (young and elderly)

Socio economic (status) : DisadvantagedEthnicity : African AmericanFamily history : Hypertension, pre-eclampsia, (First degree relatives) eclampsia

Placental abnormalities : Molar pregnancyHyperplacentosis – multiple pregnancyPlacental ischaemia

Associated medical conditions : Obesity, Diabetes, Renal disease,Collagen vascular disease

Thrombophilias : Anti-phospholipid syndrome, Protein C, S deficiency, Factor V Leiden

Genetic : History of pre-eclampsia in sister, mother (Multi-factorial inheritance)

Immunological

Preconceptional Risk Factors

Rates of preeclampsia depend on: severity of underlying complications &combinations of risk factors.

Risk %Risk factors

15-40Chronic hypertension/renal disease

10-35Pre gestational DM

10-20Connective tissue disease (lupus, rheumatoid arthritis)

10-40Thrombophilia (acquired or congenital)

10-15Obesity/insulin resistance

10-20Age older than 40 y

10-35Limited sperm exposure

10-15Family history of preeclampsia/ cardiovascular disease

1.5 foldWoman born as SFGA

2-3 foldAdverse outcome in a previous pregnancy: IUGR, ab placentae, IUFD

DEGREE OF PE

• DEPENDS ON:

1. Degree of impairment of trophoblastic invasion

2. Time of detection of

continuous process

SYMPTOMS

�HEADACHE- vascular origin

�VISUAL DISTURBANCES-

retinal vascular spasm…..detachment

• Blurring

• Diplopia

• Scotoma

MacGillivary 1983

EPIGASTRIC PAIN

RUQ PAIN:

Stretching of the Liver capsule

Subcapsular haematoma

DISTENSION OF LIVER

Arias & Mancilla – Jimenez 1976

EDEMA

• Early but non specific sign

• Rapid weight gain

• Edema of PE is due to sodium retention and thus not limited to dependent edema

• Edema of hands and face more reliable than dependent edema

• Parasthesia due to medial or ulnar nerve compression

EDEMA

• 1. Persistent ankle edema

• 2. Rapidly progressing edema

• 3. Edema of the Upper part of body

EDEMA SUBSIDES ON RESTEDEMA SUBSIDES ON RESTEDEMA SUBSIDES ON RESTEDEMA SUBSIDES ON REST----

GOOD PROGNOSISGOOD PROGNOSISGOOD PROGNOSISGOOD PROGNOSIS

Occult edema

ABNORMAL WEIGHT GAINABNORMAL WEIGHT GAINABNORMAL WEIGHT GAINABNORMAL WEIGHT GAIN

Mudaliar & Krishna Menon

SIGNSSIGNSSIGNSSIGNS

HYPERTENSION

�MILD:

140/90 mm Hg – 150/100 mm Hg

�MODERATE: 150/100 to 160/110

�SEVERE:

160-180/110 and more

Drugs and Therapeutics Bulletin 1993

OLIGURIA & ANURIA

• LATE FEATURE – SEVERE DISEASE

ROBERTS AND REDMAN 1993

FUNDOSCOPY

• ARTERIOLAR CONSTRICTION

• RETINAL EDEMA

• HAEMORRHAGES & EXUDATES –

NOT COMMON

MacGillivary 1983

INVESTIGATIONS

• PROTEINURIA:

300mg. Or more in 24 hours

300 mg/dl – 2 random samples

6 hours apart

PERINATAL MORTALITY DOUBLED

Cowles et al 1994

PLATELET COUNT

• Thrombocytopenia- ≤ 150000/ml

20% of PE

Mild PE:Mild PE:Mild PE:Mild PE: 7%7%7%7%

Severe PE: 50%Severe PE: 50%Severe PE: 50%Severe PE: 50%

Giles and Inglis 1981

SERUM URIC ACID

• MORE THAN – 330 mmol/l:

• 1. Foetal Distress-

• 2. Low Birthweight Foetus

• 3. PNM-

Varma 1982

LIVER FUNCTION TESTSLIVER FUNCTION TESTSLIVER FUNCTION TESTSLIVER FUNCTION TESTS

• SERUM GLUTAMIC OXALOACETIC TRANSAMINASE

• ASPARATE TRANSAMINASE

• LDH

Magann and Martin 1995

STEROID PROPHYLAXISSTEROID PROPHYLAXISSTEROID PROPHYLAXISSTEROID PROPHYLAXIS

• ACCELERATED LUNG MATURITY X

SAME PROBABILITY

HMDGluk and Kulovich 1973

Carvalho 1997

Out Patient Management

Gestational Hypertension less than

160/100 mm Hg

• Bed rest at home (controversial)

• Home BP monitoring, weight and urine protein.

• Referred for Day Assessment Unit (DAU) for evaluation like NST and USG

DAU managementDAU management

• 4 to 6 hourly BP recording.

• Mid stream urine analysis.

• Proteinuria, protein creatinine ratio.

• CTG

• Hb, platelets, creatinine, liver function tests (enzymes, AST/ALT), uric acid.

• Review.

Indications for Hospitalization from Day Care Unit

• BP equal to or more than 160/100 mm Hg

• Uric acid equal to or more than 450 mmol/L

• Platelets less than 1,50,000

• Proteinuria equal to or more than 5 gm in 24 hrs

• Oliguria

• S creatinine more than 1 mg%

• Cerebral or visual disturbances

• Impaired liver function

• Non reactive CTG

• IUGR/Oligohydramnios

Maternal SURVEILLANCE

Bed restVital parametersBP measurement 6 hourly Daily weightInput /output chartingUrine protein estimation dailyPremonitory symptomsDeep tendon reflexesFundoscopy

BED REST

MILD PE : NO BENEFIT

MODERATE & SEVERE: BENEFICIAL

Mathews et al 1982

BIOCHEMICAL MONITORING

CBCUrine routine and microscopy24 hour urineRFT, BUN, Creatinine, uric acid, creatinine cleareanceLFT: enzymes, bilirubin, proteinsPlatelet countCoagulation profile

Fetal Well-being

•Delay the delivery if mother is safe•Prematurity is the most important determinant of perinatal outcome•Antenatal Corticosteroids

Fetal Surveillance

- Daily Fetal Movement Count- Fetal growth clinically and by USG- Amount of liquor- Cardiotocogram- Doppler velocimetry of the

umbilical artery

Control of Hypertension

• Aims of antihypertensive therapy

- To increase renal perfusion

- To increase uteroplacental perfusion

- To prevent intracranial bleeding

- To prevent Left ventricular failure

- To prevent the selective cerebral

arterial vasospasm that causes

eclamptic seizures

Indications for Antihypertensive Therapy

Role of antihypertensive therapy in Mild to Moderate Hypertension is

unclear.

Drugs and therapy Perceptive 2001,17(18),11-15

INDICATIONS FOR ANTI-HYPERTENSIVES IN

PEPEPEPEGROUP ‘A’

1.Persistent rise of BP in mild to moderate PE

2.Severe preeclampsia-EXPECTANT

GROUP ‘B’

Hypertensive crisis

Antihypertensive for mild PE

• Methyldopa : A drug of First Choice

• Labetalol : A reasonable Alternative

• Atenolol : To be avoided

• Nifedipine : Calcium channel blocker in late

pregnancy

• Propranolol : can be used in late pregnancy

• Hydralazine : add on therapy to Methyldopa

• ACE inhibitors : To be avoided

• Diuretics : not to be used as

antihypertensive

Following are the criteria for delivery in mild preeclampsia

1) Gestational age >/ = 40 weeks

2) Gestational age >/ = 37 weeksa) Fetal weight < 10th percentile b) Bishop score >/= 6 c) Non reactive NST pattern

3) Gestational age >/ = 34 weeks witha) Laborb) Rupture of membranesc) Vaginal bleedingd) Imminent symptoms

4) Abnormal biophysical profile.5) Criteria for severe preeclampsia met

DIURETICS IN PE:NO

1. GROSS ANASARCA

2. 2. PULMONARY EDEMA

• No reduction in the incidence of PE or perinatal mortality

• May have deleterious effects: • reduced renal & placental perfusion. • (Cochrane Library 2007 Issue 1:CD004451

Diagnostic criteria for

severe preeclampsia –ACOG PRACTICE BULLETIN

• Blood pressure >160-180 mm Hg systolic or >110 mm Hg diastolic

• Proteinuria >5g per 24 hr

• Oliguria defined as <500 mL per 24 hr

• Cerebral or visual disturbances• Pulmonary edema • Epigastric or right upper quadrant pain

• Impaired liver function of unclear etiology• Thrombocytopenia• Fetal intrauterine growth retardation or oligohydramnios• Elevated serum creatinine

• Grand mal seizures (eclampsia)

SEVERESEVERESEVERESEVERE----PEPEPEPEHYPERTENSION

� MILD:

140/90 mm Hg – 150/100 mm Hg

� MODERATE: 150/100 to 160/110

�SEVERE:

160-180/110 and moreDrugs and Therapeutics Bulletin 1993

Antihypertensive for Control of Acute or Severe

Hypertension in Pregnancy

Labetalol : 20 mg IV, repeated every 30 min & can be doubled maximum

upto 80 mg

Nifedipine : 5 to 10 mg every

15 min to maximum upto 30 mg

Antihypertensive for Control of Acute or Severe Hypertension in Pregnancy

Short Acting Antihypertensive agents :

• Hydralazine : 5 mg IV repeated after 20 min

Other Antihypertensive agents :

Diazoxide : 30 to 50 mg IV, repeated every 10

to 15 min or by continuous infusion.

Sodium Nitroprusside : IV infusion 0.5 to 10

mg/kg/min

Drugs used to lower blood pressure during pregnancy

Nifedepine

Labetalol

‘EXPECTANTEXPECTANTEXPECTANTEXPECTANT’ MANAGEMENTFETAL WELLBEING

�CTG: DAILY

�USGUSGUSGUSG---- FETAL WEIGHTFETAL WEIGHTFETAL WEIGHTFETAL WEIGHT

– GROWTH PROFILEGROWTH PROFILEGROWTH PROFILEGROWTH PROFILE---- ONCE IN 2 WksONCE IN 2 WksONCE IN 2 WksONCE IN 2 Wks

�AFI: TWICE WEEKLY

�UMBILICAL ARTERY DOPPLER –

TWICE WEEKLY

DAVID CHURCHILL 2000

DAVID CHURCHILL 2000

‘EXPECTANTEXPECTANTEXPECTANTEXPECTANT’ MANAGEMENTMATERNAL WELLBEING

�BLOOD PRESSURE: 4 HOURLY

�URINE FOR PROTEIN LOSS: DAILY

�PLATELET COUNT,

SERUM URIC ACID:TWICE WEEKLY

�LFT: WEEKLY

Criteria for delivering patient withEXPECTANT MANAGEMENT-PE

• BP persistently 160/110 or more inspite of treatment

• Urine output < 400 ml in 24 hrs

• Platelet count < 50,000/mm3

• Progressive increase in S. Creatinine

• LDH > 1000 IU/L

• Repetitive late decelaration with poor variability

• Severe IUGR with Oligohydramnios

• Reversed umbilical diastolic blood flow

Decision making in severe preeclampsia

Gestational Age Course

More than 34 weeks Delivery

Less than 26 weeks Delivery

26 to 34 weeks Expectant management v/s

Delivery

Planning Delivery

PlaceMultidisciplinary team and high dependency care availableNeonatal care facilities

Route

�Aim for vaginal deliveryLSCS required for obstetric indication or

maternal or fetal compromise�AVOID GENERAL ANAESTHESIA

TimeConservative v/s Early intervention

Labour Management• IV access

• Repeat haematological investigations

• Fluid management

• Seizure prophylaxis and anti hypertensives

• Electronic fetal monitoring

• Analgesia and Anaesthesia

• No ergometrine

•““““Like A Flash Of LighteningLike A Flash Of LighteningLike A Flash Of LighteningLike A Flash Of Lightening””””

• Acute Convulsive Disorder Acute Convulsive Disorder Acute Convulsive Disorder Acute Convulsive Disorder ––––

• Cause Cause Cause Cause –––– Hypertension Induced Or Induced Or Induced Or Induced Or Aggravated By PregnancyAggravated By PregnancyAggravated By PregnancyAggravated By Pregnancy.

BP may be normal !BP may be normal !BP may be normal !BP may be normal !

Treat all women with convulsions in pregnancy as

eclampsia until proven otherwise.

ECLAMPSIA

According to ACOG eclampsia is defined as convulsions occurring in a

patient with preeclampsia.

OR

Preeclampsia complicated with convulsion and /

or coma is called eclampsia. It can also occur in patients who have preeclampsia superimposed on essential hypertension or chronic nephritis

ECLAMPSIAECLAMPSIAECLAMPSIAECLAMPSIA

Pathogenesis of eclampsia - Unknown

- Severe arterial vasospasm

Rupture of the vascular endothelium

Pericapillary hemorrhage

Development foci of abnormal electrical discharge that may generalized

Convulsions

Period of gestation – convulsions

In 50% of cases >36 wks of gestation

Antepartum - 46.3%

Intrapartum - 16.4%

Postparum - 37.3%

usually within 48 hrs of delivery

Sibai BM et al Obstet Gynaecol 1981, 58 : 609.

HYPERTENSION IN ECLAMPSIAHYPERTENSION IN ECLAMPSIAHYPERTENSION IN ECLAMPSIAHYPERTENSION IN ECLAMPSIA

�Severe htn………..54%

�Mild htn…………..30%

�NORMAL BP…….16%

Temporary Blindness Temporary Blindness Temporary Blindness Temporary Blindness (amaurosis)(amaurosis)(amaurosis)(amaurosis)

Petechial hemorrhage

Focal vasogenic edema in the occipital cortex

cortical blindness …. 1 to 3%Cunningham, 1995

PERMANENT BLINDNESS

� cerebral infarction cerebral infarction cerebral infarction cerebral infarction

� retinal artery ischemia and retinal artery ischemia and retinal artery ischemia and retinal artery ischemia and infarction infarction infarction infarction

Lara-Torre and associates, 2002;

Moseman and Shelton, 2002.

• Eclampsia

• Epilepsy

• Cerebral malaria in tropics

• Encephalitis

• Meningitis

• Intracranial tumors

• Peripheral cerebral thrombosis

• Poisoning

• Hysteria

Differential Diagnosis

• General management

• To control convulsions using MgSO4

• To control Hypertension

• To avoid Diuretics

• To limit IV fluids unless excessive fluid loss

• To investigate

�TERMINATION OF PREGNANCY

• Care in puerperium

• Follow up.

Principles of Management of Eclampsia

General management

• To place in a railed cot in an isolated place

• To maintain airway

– To administer oxygen

– To take detail history from relatives

– After proper sedation quick examination

– Catheterization and check for proteinuria

– ½ an hourly Pulse, Temp, RR, BP, uterine contraction, FHS.

– 1 hrly urine output

– Maintain fluid balance with CVP monitoring

– To administer antibiotics

Management of Eclampsia

Cure for severe PreCure for severe PreCure for severe PreCure for severe Pre----eclampsia/ eclampsia/ eclampsia/ eclampsia/ Eclampsia is delivery of fetus & placenta Eclampsia is delivery of fetus & placenta Eclampsia is delivery of fetus & placenta Eclampsia is delivery of fetus & placenta

Treat with

anticonvulsants &

antihypertensives

Stabilize

Deliver

Rushed delivery in an unstable patient is dangerous

Transfer if necessary

Lytic cocktail regimen

On admission

25mg chlorpromazine +100mg pethidine in 20ml of

5% solution iv followed by 50mg chlorpromazine +

25 mg promethazine im.

Later on

Promethazine 25mg and chlorpromazine 50mg given alternately lM till

24 hr of last fit or

IV 500ml containing 100mg pethidine drip rate adjusted to 20-30

drops/min till 24 hrs of last fit and not to exceed 300 mg /day.

Maternal Mortality (MM): 2.2%

Diazepam regimen:

Initial drug of 100mg iv further 40mg in

500ml of Ringer lactate i. v. at 30 drops/min

M.M. 5%

LEAN’S regimen

Lean T.H. Et al 1968

RYAN’ REGIMEN

• Phenytoin therapy :

• 10mg/kg IV followed by 5mg/kg 2

hrs later

• Sedatives can be used with above

regimen

Ryan G. et al 1989

MgSO4 is the drug of choice For

preventing & treating Eclampsia.

Best Anticonvulsive

is the drug of choice for routine anti- convulsant management of women with eclampsia, when compared to Diazepam & Phenytoin.

Evidence from the Collaborative Eclampsia Trial.Evidence from the Collaborative Eclampsia Trial.Evidence from the Collaborative Eclampsia Trial.Evidence from the Collaborative Eclampsia Trial.

• Lancet. 1995 Jun 10. 345(8963). pp 1455Lancet. 1995 Jun 10. 345(8963). pp 1455Lancet. 1995 Jun 10. 345(8963). pp 1455Lancet. 1995 Jun 10. 345(8963). pp 1455----1463.1463.1463.1463.

Specific management

control seizures and to prevent its recurrence

Regimens Loading dose Maintenance dose

Pritchard 4gm IV over 3 to 4 min 5gm buttock 4 hrly10gm deep IM

Zuspan 4gm IV over 5 to 10 min 1-2gm hrly IV infu

Sibai 6gm IV over 20 min 2gm hrly IV infusion

Sardesai 4 gm IV or IM 2 gm 3 hrly IV or IM

Therapeutic level of MgSO4 – 4 to 7mRQ/litre

Monitor

Presence of patellar reflex (8 to 10mEQ/litre ���� diagnose)

Respiratory rate >16 (>12mEQ /litre ���� depression)

Urinary output 30ml/hr

Continuation for 24 hrs after the last seizure

M.M. 0.4%

Serum levels of Magnesium Serum levels of Magnesium Serum levels of Magnesium Serum levels of Magnesium toxicity toxicity toxicity toxicity

Normal therapeutic level 4-6 mEq/L

• Loss of patellar reflex 8-12 mEq/ L

• Feelings of warmth, flushing 9-12 mEq/L

• Somnolence 10-12 mEq/L

• Slurred speech 10-12 mEq/L

• Muscular paralysis 15-17 mEq/L

• Respiratory difficulty 15-17 mEq/L

• Cardiac arrest 30-35 mEq/L

Thinking…..

Delay in MgSo4 treatment-

referred to tertiary hospitals with

no or wrong treatement

13.9% maternal deaths..admitted in moribund state…

Lopez and LleraLopez and LleraLopez and LleraLopez and Llera

Early and –’PROPER” referral

is the is the is the is the cornerstone

in the success of in the success of in the success of in the success of

saving the mother saving the mother saving the mother saving the mother

in eclampsia.in eclampsia.in eclampsia.in eclampsia.

Adetoro reported 14.4% of Adetoro reported 14.4% of Adetoro reported 14.4% of Adetoro reported 14.4% of maternalmortality..referral maternalmortality..referral maternalmortality..referral maternalmortality..referral

without treatmentwithout treatmentwithout treatmentwithout treatment…………....

SEIZURESEIZURESEIZURESEIZURE -FREETRANSPORTATIONTRANSPORTATIONTRANSPORTATIONTRANSPORTATION

‘‘‘‘MgSO4’’’’ before referral’

CONVENTIONAL WESTERN CONVENTIONAL WESTERN CONVENTIONAL WESTERN CONVENTIONAL WESTERN REGIMENS:

• can not be given outside

• ‘‘‘‘obstetric care unitsobstetric care unitsobstetric care unitsobstetric care units’’’’

JOSHI SUYAJNA D.

Longerduration

Cost ineffective

TrainedHealth prof

More sideeffects

RequiresIns.therapy

Costantsupervision

High dose

Conv.mgso4regimen

DIFFERENT MgSO4 REGIMENS DIFFERENT MgSO4 REGIMENS DIFFERENT MgSO4 REGIMENS DIFFERENT MgSO4 REGIMENS …………

� Eastman. Eastman. Eastman. Eastman.

� Pritchard.Pritchard.Pritchard.Pritchard.

� Chesley & Teppers.Chesley & Teppers.Chesley & Teppers.Chesley & Teppers.

� Hall, Anderson, Hall, Anderson, Hall, Anderson, Hall, Anderson, Harbert.Harbert.Harbert.Harbert.

� Flowers.Flowers.Flowers.Flowers.

� Zuspan.Zuspan.Zuspan.Zuspan.

� Cruik Shant.Cruik Shant.Cruik Shant.Cruik Shant.

� Sibai.Sibai.Sibai.Sibai.

� SardesaiSardesaiSardesaiSardesai

� Leens.Leens.Leens.Leens.

etc etc etc etc JOSHI SUYAJNA D.

Low-Dose Regimen…………

‘‘‘‘Newer Innovations in the treatment Newer Innovations in the treatment Newer Innovations in the treatment Newer Innovations in the treatment

of of of of …………. . . . ECLAMPSIAECLAMPSIAECLAMPSIAECLAMPSIA……………………SINGLESINGLESINGLESINGLE----DOSEDOSEDOSEDOSE

Joshi Suyajna D.Joshi Suyajna D.Joshi Suyajna D.Joshi Suyajna D.

Professor of OBG,

VIMS- Bellary

JOSHI SUYAJNA D.

SINGLE DOSESINGLE DOSESINGLE DOSESINGLE DOSEMgSO4

SUYAJNA JOSHI1998

MgSOMgSOMgSOMgSO4 4 4 4 DOSAGE SCHEDULEDOSAGE SCHEDULEDOSAGE SCHEDULEDOSAGE SCHEDULE

VIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMENVIMS REGIMEN

4 gm of 50% MgSO4 in 20% dilution 4 gm of 50% MgSO4 in 20% dilution 4 gm of 50% MgSO4 in 20% dilution 4 gm of 50% MgSO4 in 20% dilution

to be given slow iv over to be given slow iv over to be given slow iv over to be given slow iv over

10 10 10 10 –––– 15 min , followed by 4 gm IM 15 min , followed by 4 gm IM 15 min , followed by 4 gm IM 15 min , followed by 4 gm IM

....

CLOSE MONITORINGCLOSE MONITORINGCLOSE MONITORINGCLOSE MONITORING

No need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levelsNo need to monitor MgSO4 levels

Antidote: If patient develops respiratory rate Antidote: If patient develops respiratory rate Antidote: If patient develops respiratory rate Antidote: If patient develops respiratory rate

<16 min administer <16 min administer <16 min administer <16 min administer

Calcium gluconate 1G IV over 10 min. Calcium gluconate 1G IV over 10 min. Calcium gluconate 1G IV over 10 min. Calcium gluconate 1G IV over 10 min.

(10ml of 10 % solution(10ml of 10 % solution(10ml of 10 % solution(10ml of 10 % solution))))

control hypertension

Labetalol - 20 mg i.v., repeated every 30 min & can be doubled maximum

upto 80 mg

Nifedepine : 5 to 10 mg every 15 min maximum upto 30 mg

FLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENTFLUID MANAGEMENT

PE PE PE PE –––– Hypovolaemia Hypovolaemia Hypovolaemia Hypovolaemia –––– Intravascular Intravascular Intravascular Intravascular

with fluid overload with fluid overload with fluid overload with fluid overload ---- Extra vascular Extra vascular Extra vascular Extra vascular

Do not give IV fluids rapidlyDo not give IV fluids rapidlyDo not give IV fluids rapidlyDo not give IV fluids rapidly

Fluid infusionFluid infusionFluid infusionFluid infusion---- Crystalloids 80ml/hrCrystalloids 80ml/hrCrystalloids 80ml/hrCrystalloids 80ml/hr

No colloidsNo colloidsNo colloidsNo colloids

NO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICSNO ROLE FOR DIURETICS

INVESTIGATIONSINVESTIGATIONSINVESTIGATIONSINVESTIGATIONS

FBC FBC FBC FBC ---- peripheral smear peripheral smear peripheral smear peripheral smear

If platelets < 1,00,000 If platelets < 1,00,000 If platelets < 1,00,000 If platelets < 1,00,000 ---- > Coagulation study> Coagulation study> Coagulation study> Coagulation study

LFTLFTLFTLFT----S. bilirubin, SGOT, SGPT, LDHS. bilirubin, SGOT, SGPT, LDHS. bilirubin, SGOT, SGPT, LDHS. bilirubin, SGOT, SGPT, LDH

S. CreatinineS. CreatinineS. CreatinineS. Creatinine

U. albuminU. albuminU. albuminU. albumin

S. Uric acidS. Uric acidS. Uric acidS. Uric acid

Minimum investigationsMinimum investigations-- Hb, platelets, SGOT, SGPT Hb, platelets, SGOT, SGPT UrineUrine--alb alb

Planning the delivery

Delivery is the ultimate cureVaginal.

•LSCS : only for obstetric reasons

•Anesthesia –•General to be avoided, as it increases blood pressure during intubation and extubation.•Epidural is better than spinal.

LABOURLABOURLABOURLABOURLABOURLABOURLABOURLABOUR

Severe / fulminant PE deliver within 24hours

Eclampsia - deliver within 12hours

Precautions during labour

I stage- Close monitoring, avoid fluid overload

II stage- Shorten second stage

III stage- only oxytocin for 3rd Stage Avoid- Ergometrine, PGF2

Route of delivery

• Probability of achieving vaginal delivery after induction through an unripe cervix are below 20%

Hall DR et al, BJOG 2000

Haddad B et al, AJOG 2004

• Prolonged labor can be detrimental for mother and fetus

• Caesarean delivery is preferableSibai BM et al, COG 2005

Status eclampticus

• Phenytoin sodium 0.5gm dissolve in

20mg of 5% dextose iv given slowly

• If no response then complete

anesthesia, muscle relaxant, assisted

ventilation and C. Section is done.

• Injuries

• Pulmonary edema

• Pneumonia

• Acute LVF

• Cerebral

hemorrhage

• Renal failure

• Pulmonary

embolism

• Hyperpyrexia

• Hepatic necrosis

• DIC

• Postpartum shock

• Puerperal sepsis

• Disturbed vision

• Psychosis

Complications of eclampsia

HELLP syndromeHELLP syndromeHELLP syndromeHELLP syndromeWeinstein, 1982

• Recommended criteria for HELLP syndrome

•

• 1) Hemolysis (at least two of the following)

• a) Peripheral smear(schistocytes,burr cells)

• b) Serum bilirubin (>1.2mg/dL)

• c) Low serum haptoglobin

• d) Severe anemia unrelated to blood loss

• 2) Elevated Liver enzymes

• a) ALT or AST >/= twice upper level of normal

• b) LDH >/= twice upper level of normal

• 3) Low platelets < 100.000/mm3

Pritchard et al in 1954

Hemolysis

Schistocytes in the blood smear

S.Bilirubin > or equal to 1.2 mg%

Absent Plasma hapatoglobin

Elevated Liver Enzymes

SGOT > 72 IU/L

LDH > 600 IU/L

Low Platelet Count

Diagnosis of HELLP Syndrome

Classificationon the basis of platelet

count

class I, less than 50,000 per mm3less than 50,000 per mm3

class II, 50,000 to less than 100,000 per mm350,000 to less than 100,000 per mm3

class III, 100,000 to 150,000 per mm3100,000 to 150,000 per mm3

MISSISSIPPI

ClassificationClassificationClassificationClassification

full HELLP syndrome

partial HELLP syndrome

based on the number of abnormalities

Audibert F, Friedman SA, Frangieh AY, Sibai BM. Am J Obstet Gynecol 1996; 175:460-4.

considered for delivery within 48 hours

candidates for more conservative management

MEMPHIS

HELLP

• Prompt delivery , if it develops beyond 34 weeks.

• Dilemma- Before 34 weeks, administrations of corticosteroid for 48 hrs for both maternal and fetal benefits. But the results are variable in different studies.

• Cerebral haemorrhage

• Anoxia

• Cardiac failure

• Pulmonary oedema

• Aspiration pneumonia

• Pulmonary embolism

• Postpartum shock

• Puerperal sepsis

Causes of maternal mortality

Causes of perinatal mortality :

• Prematurity • Intrauterine asphyxia • Effects of drugs used to control convulsion • Trauma during delivery • Perinatal mortality 30 to 50% •• Sibai BM et al American Journal of Obstet Gynaecol 1983; 146 : 307.

Recurrent PE & EclampsiaRecurrent PE & EclampsiaRecurrent PE & EclampsiaRecurrent PE & Eclampsia

Subsequent to ECLAMPSIA

Chesley Sebai

Eclmapsia 1% 1.9%

Preeclampsia 23% 22%

Post Partum Care

• Over 40% of maternal deaths occur postpartum

• Post delivery a relative oliguria is not uncommon,

occuring in 30% of patients with severe disease

• Continued close monitoring is required in a

suitable environment

• Taper antihypertensive agents

• Contraception Counseling and Follow up

Long term prognosis.

• PE and Eclampsia is a forerunner of later life cardiovascular risk

• It is more in early onset PE.

• Does not affect long term renal function.

• No long term residual hepatic disease.

• Recurrence Risk-20 to 50 %.

• HELLP-2 to 6 %.

LONG TERM SEQUELE

Prevalence of remote hypertension:

� increased in Multiparas who develop pre-eclampsia,

�

�women with severe early onset disease of any parity

Working Group Report on High Blood Pressure in Pregnancy Working Group Report on High Blood Pressure in Pregnancy Working Group Report on High Blood Pressure in Pregnancy Working Group Report on High Blood Pressure in Pregnancy 2001.2001.2001.2001.

Conclusion.

• PE is the leading cause of Maternal and Perinatal Mortality and Morbidity

• Maternal and neonatal outcome is good in gestational hypertension and with antihypertensive drugs they can go up to term.

• But PE is enigmatic, an unique syndrome, dangerous for both mother and fetus, no absolute preventive measure are available and does not respond well to treatment.

• Multidisciplinary approach with close medical supervision, timely delivery and management at tertiary center are the corner stones for good maternal and fetal outcomes.

•Suggested reading;Suggested reading;Suggested reading;Suggested reading;

1) Pregnancy induced hypertension by Harshalal R Seneviratne

and Chandrika by Orient Longman

• 2) Progress in Obstetrics and Gynecology , 17th edition

• 3) Williams Obstetrics 23rd edition

• 4) RCOG guidelines for management of severe preeclampsia/eclampsia

• 5) Critical care Obstetrics by Steven L Clarke et al

• 6) Obstetrics -normal and abnormal pregnancies by Steven G. Gabbe et al

• 7) Management of high risk pregnancy- an evidence based approach by John T.Queenan et al

• 8) Ian Donald’s practical obstetrics problems.

•

•

THANK YOU

• Joint Secretary FOGSI - 2009

• Consultant Obstet. & Gynecologist, Mumbai

• Ex. Associate Professor, GMC, Mumbai

• Member Managing Council, MOGS

• Chairperson Medico-legal committee, MOGS

DR. (MRS.) MADHURI A. PATEL

TO CONTACT ME

suyajna@yahoo.comsuyajna@yahoo.comsuyajna@yahoo.comsuyajna@yahoo.com

www.suyajna.comwww.suyajna.comwww.suyajna.comwww.suyajna.com

Why prediction is important:

1. The risk for recurrent PE can be as high as 65% (Barton& Sibai, 2008).

2. PE is associated with substantial

maternal& perinatal

complications

Prediction� Roll-over Test

� Second Trimester Mean Arterial Pressure

� Urinary Calcium

� Uric acid

� Fibronectin

� Homocysteine level

� Cytokines

� Coagulation factors

� Placental peptides

� Doppler Ultrasound

� Fetal DNA

SCREENING TESTS FOR PE (WHO, 2004)

I. Placental perfusion & vascular resistance dysfunctionMean arterial blood pressureRoll over test Doppler ultrasound Isometric exercise test Intravenous infusion of angiotensin II Platelet angiotensin II binding Platelet calcium response to arginine vasopressin Renin 24-hour ambulatory blood pressure monitoring II. Fetoplacental unit dysfunctionHuman chorionic gonadotropin Alpha fetoprotein Estriol Inhibin A Pregnancy-associated plasma protein A Activin A Corticotropin release hormone

Roll-Over Test

• GANT… ‘Roll – Over test’

Position of BP cuff….Nisell et al 1985

Gant NF, Daley GL, Chand S, Whalley PJ, MacDonald PC. A study of angiotensin II pressor responsiveness throughout primigravid pregnancy. J Clin Invest.1973;52:2682–2689

III. Renal dysfunction Serum uric acid Microalbuminuria Urinary calcium excretion Urinary kallikrein Microtransferrinuria N-acetyl- glucosarninidase

Platelet countPlatelet activation and endothelial cell adhesion moleculesProstacyclinCytokinesIsoprostanes, Antiphospholipid antibodies, Placenta growth factorHematocritAntithrombin IllCalciumTransferrinAtrial natriuretic peptide

Fibronectin Endothelin Thromboxane Homocysteine Serum lipids Insulin resistance Plasminogen activator inhibitor Leptin Total proteins Magnesium Ferritin Haptoglobin microglobulin Genetic markers

IV. Endothelial& oxidant stress dysfunction

II. Biochemical Markers

Angiogenic factors before & after the onset of PE(Barton& Sibai, 2008).

Serum placental growth factor: reducedSoluble fms-like tyrosine kinase: elevatedEndoglin: elevated

‘Angiotension-II infusion…’Gant…1973

Gant NF, Chand S, Worley RJ, Whalley PJ, Crosby VD, MacDonald PC. A clinical test useful for predicting the development of acute hypertension in pregnancy. Am J Obstet Gynecol. 1974;120:1–7

MDP

2nd trimester MD BP ≥ 90 mm Hg

Chesley LC, Sibai BM.

Clinical significance of elevated mean arterial pressure in the second trimester.

Am J Obstet Gynecol. 1988;159:275–279.[

Biophysical

Mean arterial pressure(2DBP+SBP)/3

•Better predictor of PE than S& DBP(BMJ 200817;336:111; Meta-analysis of 34 RCT)

•BP remains the cornerstone of early diagnosisalthough it has limitations:

….measurement errors associated with sphygmomanometer..(effect of maternal posture on BP in pregnant women).

Uterine artery Doppler ultrasound

‘Diastolic Notch’

�Impaired trophoblastic invasion of the spiral arteries: reduction in uteroplacental blood flow.

�High pulsatility index and/or Notch in 1st & 2nd

trimesters: poor predictor of PE(Papgeorghiou & Leslie, 2007)

Repeated routine urinalysis

throughout pregnancy NOT useful for predicting PE

(JAMA 2003: 12;289(10):1220)

Prevention

Aspirin-19% reduction in risk of PE.

-16 % reduction in fetal and neonatal death.

- 8 % reduction in the incidence of small for gestational age infants.

Updated chrochane review-2000. Systemic review 2003.

The controversy is when to start treatment.

Prevention

Calcium• Protective effect in women with low calcium intake.

Cochrane data base 2005

• Supplementation with 1.5 gm calcium /day did not result in statistically significant decrease in the overall incidence of PE, but there is significant decrease risk of the more serious complications which included maternal and neonatal morbidity and mortality and preterm delivery .

WHO-2006

Prevention

• Antioxidants • Antioxidants like Vit C, E, and lycopene found to be effective in smaller trials but VIP Trial demonstrated no decrease in risk of PE.

Lancet-2006, 367,1145-54.

• In the other large multicentric trial, the supplementation did not decrease the incidence of preeclampsia, IUGR or the risk of death or other serious outcomes.

N. Eng. J .of Med. 2006, 354, 1796-806

II. Pregnancy-Related FactorsRegular antenatal care is mandatory for the prevention & early detection of PE.

�Risk factors: Magnitude of risk depends on the number of factors

�Hydrops/hydropic degeneration of the placenta

�Multifetal gestation�Unexplained FGR�Gestational hypertension�UTI�Periodontal infection�Markers�Biophysical�Biochemical

•Currently: There is no clinically useful screening test to predict PE (WHO, 2004)

Conclusion•BP remains the cornerstone of early diagnosis•MarkersReliability is inconsistentMany suffer from poor specificity & predictive values.None provided a cutoff value that could be clinically useful for the prediction of PE (Widmer et al, 2007).

Secondary•Breaking off the disease process before emergence of obvious clinical disease•{Etiology of the disease is unknown} •To correct theoretical pathophysiology

I. Non pharmacologicalII. Nutritional III. Pharmacological

Primary

Secondary

Prevention of PE

Primary prevention•Avoiding occurrence of the disease•Obese:achieve an ideal b wt before conception (Villamor& Cnattingius, 2006)

No RCT•Ch hypertension:Control BP before conception. No RCT

I. Non pharmacological1. Daily Bed restRest for 4Rest for 4Rest for 4Rest for 4----6 h/d6 h/d6 h/d6 h/d

May reduce risk of PE for women with normal BP (level 2 evidence)(Cochrane Library 2006 Issue 2:CD005939)

2. Life-style changes •High job stress: greater risk of PE(Sharma& Mittal, 2006)

•Reducing job stress may be beneficial in the prevention of PE

•Stretching exercises are more effective at reducing the risk of PE than walking(University of North Carolina,2008)

3. Regular prenatal exercise•May prevent or oppose progression (Weissgerber et al, 2004)

•{Stimulation of placental growthReduction of oxidative stressReversal of maternal endothelial dysfunction}. •Insufficient evidenceModerate intensity regular aerobic exercise(Cochrane Library 2006 Issue 2:CD005942) Aerobic exercise =cardiovascular exercise=any sustained rhythmic activity that involves large muscle groups: makes the lungs work harder as the body's need for oxygen is increased.

�Smoking: Reduced risk for PE (Sibai et al, 2005).

{Nicotine inhibition of interleukin-2 & tumor necrosis factorEffects of nicotine on angiogenic proteins}. Smoking: abnormal fetal growthpreterm birthAbruptionAdverse effects on maternal health.

II. Nutritional1. Higher total dietary fiber intake in early pregnancymay reduce risk for PE(level 2 evidence)Prospective cohort study Am J Hypertens 2008 Aug;21(8):903

2. Increasing dietary protein & energy intake RCT: no benefit

•5 or more servings of chocolate/w in 3rd trimester:40% reduction(Triche, 2008; Epidemiology .19:459-464), Yale University

{Chocolate, especially dark chocolate, is rich in theobromine: stimulates the heart, relaxes smooth muscle & dilates blood vessels, and has been used to treat chest pain, high blood pressure}

3. Garlic Insufficient evidence to recommend for preventing PECochrane Library 2006

)Issue3:CD006065

4. Dietary sodium restriction • No significant differences (Cochrane Library 2005 Issue 4:CD005548)

5. Weight Reduction •Although obesity is a known risk factor, there is no evidence that limiting wt gain during pregnancy; reduces its occurrence.•Wt reduction is not recommended during pregnancy even in obese women (Kramer, 2004)

6. Fish Oil Supplementation •Observational studies: beneficial effects •{inhibition of platelet thromboxane A2 without affecting prostacyclin: shifting the balance toward a reduced platelet aggregation and increased VD}. •RCT: No benefit (Olsen et al, 2000)

•High doses: increase the risk of PIH(Olafasdottir et al, 2006).

•Not recommended for the prevention of PE

III. Pharmacological

1. Low-dose Aspirin•{inhibits biosynthesis of platelet thromboxane A2 with little effect on vascular prostacyclin production: altering the balance in favor of prostacyclin}. •(50-150 mg/day) For women with a previous history of hypertension or PE (n=6,107):Small to moderate benefits, safe. level 2 evidence(Cochrane Library 2007 Issue 2:CD004659)

2. Low-dose Aspirin/Heparin•History of severe preterm PE & LBW infants.(Sergio et al, 2006)

•Lower incidence of PE (3Vs 30%) Greater gestational age at deliveryHigher birth wt

3. Calcium Supplementation •Reduces the risk of PIH, particularly in populations that have diets deficient in calcium level 1 evidence (Cochrane Syt review , 2006)

•The relationship between cal & risk of PIH is inconsistent& inconclusiveThe relationship between cal & the risk of PE is highly unlikely.Evidence-based review by FDA (2007)

4. Antihypertensive Drugs •Mild to moderate hypertension: Halving in the risk of developing severe hypertensionNo difference in the risk of developing PE or proteinuria (Cochrane syst review, 2007)

5. Diuretics •No reduction in the incidence of PE or perinatal mortality•May have deleterious effects: reduced renal & placental perfusion. (Cochrane Library 2007 Issue 1:CD004451)

6. Antioxidant supplementation may not affect risk of PE or clinical outcomes level 2 evidence

)1:CD004227Cochrane Library 2008 Issue (

7. Concomitant Vit C& E supplementation•{PET: imbalance of oxidant & antioxidant activity: multiorgan endothelial dysfunction}. •Vit C (1,000 mg/d) plus vit E (400 IU/ d)•Did not prevent PElevel 2 evidence (Obstet Gynecol 2007 Dec;110(6):1311)•May increases rate of LBW infants& might be associated with higher rate of SBlevel 2 evidence (Lancet 2006 Apr 8;367(9517):1145

8. Magnesium •{Mg is beneficial for the prevention & tt of severe PE & EDecreased intracellular Mg in PE} •No effect•(365 mg& 500 mg).Cochrane syst review, 2004

9. Folic acid& other B-vits •{Deficiency of vit B2 may cause biochemical changes simulating abnormalities of PE}•No evidence that any of B vits can prevent PE (Shrama& Mittal, 2006).

10. Zinc supplementation •{Zinc concentrations are reduced in PE}•RCT: No benefit(Jonsson et al, 1996)

11. Nitric oxide Insufficient evidence for preventing PECochrane Library 2007 Issue 2:CD006490

12. Progesterone Insufficient evidence for preventing PE Cochrane review, 2006

The Roll over testNot of value in predicting PE(Mahomed &Lasiende,1990)

MCQ

1. Predictive tests for PIH are considered as positive when there is increase in all except

a) Maternal Serum Inhibin A level

b) Fibronectin level

c) Maternal Plasma Endothelium I level

d) Calcium / Creatinine ratio

Answer: d)Answer: d)Answer: d)Answer: d)

Explanation : This is considered a predictor test, with a lower calcium excretion in PIH. It has a sensitivity of 70% and specificity of 95%. Calcium – creatinine ratio of less than 0.04 is significant.

MCQ2. Maternal complications due to severe preeclampsia

includes all except

a) Convulsions

b)HELLP Syndrome

c) Abruptio Placenta

d) Placenta Previa

Ans. :Ans. :Ans. :Ans. : d)d)d)d)

Explanation : Vascular constriction in results in hypoperfusion in brain, liver and placenta and causes convulsion, HELLP Syndrome and abruptio placenta respectively but not placenta previa

MCQ3. PIH causes decrease in followings except :

a) Antithrombin III

b) Tissue Plasminogen activator

c) Protein S

d) Platelet count

Answer: bAnswer: bAnswer: bAnswer: b

Explanation : PIH is associated with altered coagulation, fibrinolysis, platelet and vascular endothelial function . The fall in the platelet count is most common , probably due to increased consumption (low grade DIC). Platelets are in an activated state. There is also reduction in anticoagulants .

MCQ4. Antihypertensives usually recommended in pregnancy

are all except

a) Methyldopa

b) Labetalol

c) Atenolol

d)Nifedipine

Ans. :Ans. :Ans. :Ans. : c)c)c)c)

Explanation : use of Antenolol, a β adrenergic blocker in pregnant women with chronic hypertension resulted in significantly lower birth-weight compared with other antihypertensive agents. Many studies also indicated that treatment with atenolol associated IUGR was dose and duration related, hence, should be avoided throughout pregnancy.

Acknowledgement

• Dr. C. N. Purandare

• Dr. S. N. Tripathy

• Dr. Parikshit Tank

Thank You