HYPERTENSIVE DISORDER OF PREGNANCY

HYPERTENSIVE DISORDER OF PREGNANCY

• FIRST YEAR STUDENT

• JIVANYOG NURSING HOME

• VISNAGAR

• FIRST YEAR STUDENT

• JIVANYOG NURSING HOME

• VISNAGAR

DR. SUMAIYA KHARODIA DR. SUMAIYA KHARODIA

IntroductionIntroduction

• Disease of many theories, known from centuries back, PIH is an enigmatic condition of pregnancy, can’t predict, can’t prevent, can’t treat absolutely.

• Disease of many theories, known from centuries back, PIH is an enigmatic condition of pregnancy, can’t predict, can’t prevent, can’t treat absolutely.

IntroductionIntroductionWorld 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• 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

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• 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

IncidenceIncidence• Preelampsia 5 to 10 %

• Eclampsia (Developed countries) 1 : 2000Eclampsia (Developed countries) 1 : 2000 In India 1:30 to 1:500In India 1:30 to 1:500

• Maternal Mortality in US 17.6 % Maternal Mortality in US 17.6 % In India 25.5 %In India 25.5 % Walker JJ, Lancet:2000;356:1260-Walker JJ, Lancet:2000;356:1260-

6565

Sawhney H et al, JOGR 2000

• Three fold increase in Perinatal MortalityThree fold increase in Perinatal Mortality

• Preelampsia 5 to 10 %

• Eclampsia (Developed countries) 1 : 2000Eclampsia (Developed countries) 1 : 2000 In India 1:30 to 1:500In India 1:30 to 1:500

• Maternal Mortality in US 17.6 % Maternal Mortality in US 17.6 % In India 25.5 %In India 25.5 % Walker JJ, Lancet:2000;356:1260-Walker JJ, Lancet:2000;356:1260-

6565

Sawhney H et al, JOGR 2000

• Three fold increase in Perinatal MortalityThree fold increase in Perinatal Mortality

Perinatal OutcomePerinatal OutcomeUK 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 1994 Shah DS, FOGSI Perinatal Survey, 1994 Sardesai Jr Obstet Gynecol 2003

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.

• PIH 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)

• Hypertension that develops de novo as a consequence of pregnancy after 20th week of gestation, returning to normal after 6 weeks of delivery.

• PIH 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)

National High Blood Pressure Education Program Classification ( NHEP) 2000

• Gestational hypertension.

• Preeclampsia (mild, severe).

• Eclampsia.

• Superimposed preeclampsia upon chronic hypertension.

• Chronic hypertension with pregnancy.

Definitions• Gestational hypertension:

– Hypertension for first time after 20 w, without Proteinuria. BP returns to normal before 12 weeks postpartum.

• Chronic hypertension with pregnancy: – Hypertension antedates pregnancy and detected

before 20 w, & lasts more than 12 weeks postpartum.

Definitions– Preeclampsia:

• The development of hypertension and Proteinuria after 20 w

• May occur earlier in vesicular mole or twins.

– Eclampsia (in Greek= Flash of light): • The occurrence of tonic-clonic convulsions (without

any neurological disease) in a woman with pre-eclampsia.

Definitions

• Superimposed pre-eclampsia: ¤ It is the new development of Proteinuria

after 20 weeks gestation in a patient with chronic hypertension

Definitions• Proteinuria:

• ≥ 300mg/24 hours urine.– ≥ +1 dipstick.

• Heavy Proteinuria :–= ≥ 2gm/24 hours

– or ≥ +2 in dipstick.

Preeclampsia

Epidemiology of preeclampsia

Incidence: • Is a disease of humans only.• Is the most common medical disorder complicating

pregnancy 5-15%• Is the most common hypertensive disorder in

pregnancy.• More common in primigravidas and elderly

multipara.• More common in winter.• More in black races.

14

Etiology

• Basic concepts– Exposed to chorionic villi for the first time

– Exposed to a superabundance of chorionic villi, as with twins or hydatidiform mole

– Have preexisting vascular disease

– Genetically predisposed to hypertension developing during pregnancy

15

• Vascular endothelial damage with vasospasm, transudation of plasma, and ischemic and thrombotic sequelae.

• Currently plausible potential cause (2003, Sibai)– Abnormal trophoblastic invasion of Uterine vessels

– Immunological intolerance between maternal and fetoplacental tissues

– Maternal maladaptation to cardiovascular or inflammatory changes of normal pregnancy

– Diatary deficiencies

– Genetic influences

16

Abnormal Trophoblastic Invasion

• In normal implantation, endovascular trophoblasts invade the uterine spiral arteries.

17

18

• In preeclampsia– Incomplete trophoblastic invasion– The magnitude of defective trophoblastic invasion of the

spiral arteries correlated with the severity of the hypertensive disorder (2000, Madazli)

• Using electron micorscopy– Endothelial damage– Insudation of plasma constituents into vessel walls– Proliferation of myointimal cells– Medial necrosis– Lipid and macrophage accumulates in myointimal cells

Abnormal Trophoblastic Invasion

Etiology= theories

• Genetic Predisposition.

• Free Radicals Theory• In pre-eclampsia the levels of free radicals

are higher than normotensive women leading to endothelial damage.

Oxidative stress

Antioxidant capacity

ROS synthesis

O2._

H2O2

ONOO_

Vitamin CSOD

Etiology= theoriesEndothelial injury:

• Endothelin 1(potent vasoconstrictors).

• Nitric Oxide ( vasodilator action).

• Vascular Endothelial Growth Factor (VEGF).

Etiology= theories

Prostaglandins:• There is decrease in prostacyclin

/TX A2 ratio leading to :• vasoconstriction and tendency to

thrombosis.

Etiology= theoriesInflammatory Factors:• Pre-eclampsia is considered an inflammatory

disease due to increased number of activated leukocytes in the maternal circulation.

• Immunological Factor: • primigravidas• Multipara with 1st pregnancy from a

new husband. • Abundant trophoblast ( vesicular mole

and multiple pregnancy.

The Central Players (Hemostats) in PET

1. The Endothelium 2. Neutrophils3. Platelets 4. Coagulation system. Once one is triggeredCo- Workers are released (NO, PGs, ROS,

Homosystein, etc)

The Constant Pathophysiological Changes

IsVascular endothelial:

Damage +Dysfunction + Spasm

PathologyPET is the clinical ice-berg

tip manifestation of the disturbances in the maternal homeostasis, involving many systems and organs.

Multisystem Features Of Preeclampsia

Hypertension Proteinuria

Eclampsia HELLP syndrome

Intra-uterine growth restriction

Multi-organ disease

Cerebral vessels

Fetus

Liver

Systemic blood vessels Kidneys

PATHOPHYSIOLOGY

MULTIPLE ORGAN SYSTEM INVOLVMENT

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT

OBGYN

1- CNS • Similar to hypertensive encephalopathy

• Petechial Hg

• Gross hemorrhages due to ruptured arteries

• Thrombosis of the arterioles

• Microinfarcts

• Fibrinoid necrosis in the walls of blood vessels

• Cerebral edema confusion, blurred vision / coma

• Brain stem herniation is a serious complication of cerebral edema death

MECHANISM cerebral hyperperfusion ,vasospasm &forced dilation

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT

OBGYN

1- CNS

• CT Scan ½ of the pt focal hypodensities in the white matter / post half of the cerebral hemisphere & occasionally in the grey matter may represent petechial Hg

• Severe cases IV Hg or subarachnoid Hg

• MRI Abnormalities in the cortical & subcortical white matter of the occipital & parietal areas

• EEG nonspecific changes

2-PULMONARY SYSTEM

Pulmonary edema

• May occur with sever PET OR EC

• Usually postpartum

• May be due to excessive fluid administration with crystalloids + ↓ plasma colloid pressure due to proteinuria

• ↑ in Pt with ch HPT & hypertensive cardiac disease

Aspiration of gastric content with EC

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT

OBGYN

3-CVSPlasma volume is reduced, the cause is unknown

theories:

• 1-Generalized vasoconstriction with ↑ vascular permeability Advocate the use of vasodilators

• 2-1ry hypovolemia hypoperfusion of the uterus release of pressor substances HPT

Advocate the use of volume expanders & avoidance of diuretics

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT

OBGYN

3-CVS• High systemic vascular resistance &

hyperdynamic ventricular function avoid aggressive fluid adminstration

• Loss of the normal refractoriness to angiotensin II

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT

OBGYN

4-BLOOD• Hemoconcentration• Thrombocytopenia < 150 000 15-20% of PT• Fibrinogen ↑• Thrombin time ↑ in 1/3 of the Ptwith EC• FDP ↑ 20% of the Pt• DIC 5%• Microangiopathic hemolytic anemia 5%• HEELP hemolytic anemia, ↑↑ liver enzymes, low Plt -LDH > 600 U/L -T bilirubin >1.2 mg/dl -AST > 70U/L -Plt < 100 000/mm³Found in 10% of the Pt with severe PET

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT

OBGYN

5-KIDNEY

• Characteristic lesion glomeruloendotheliosis swelling of the gromelular capillary endothelium ↓↓GFR

• ↓↓ creatinine clearance/ ↑↑plasma creatinine • ↑↑ uric acid• Proteinuria• Renal tubular necrosis &renal failure

6-Eyes

• Visual disturbances due to retinal artery vasospasm• Retinal detachment • Cortical blindness occipital lobe ischemia infarction or

edema lasting hrs –up to 8 days

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT

OBGYN

7-Liver

• Minimal involvement with fibrin deposition

• Periportal hemorrhagic necrosis ↑↑ serum liver enzymes

• Bleeding from these lesions Subcapsular hematoma hepatic rupture

• Hepatic infarction

• HEELP SYNDROME

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT

OBGYN

8-Endocrine & metabolic changes

• ↓↓ plasma renin, angiotensin II & aldosterone to the normal prepregnancy values

• Vasopressin levels are N• Atrial natriuretic peptide ↑↑

Volume expansion in PET ↑ ANP ↑ COP &↓ periephal vascular resistance

• Expansion of the extracellular fluid volume (edema) Proteinuria ↓↓ plasma oncotic pressure displacement of intravascular fluid to interstitium

DR SALWA NEYAZI ASS. PROF.KSU CONSULTANT

OBGYN

9-Uteroplacental perfusion

• Vasospasm compromised placental perfusion ↑↑ perinatal morbidity & mortality

• Doppler velocimetry (systolic /diastolic velocity ratio of umbilical& uterine arteries )20% N

15% N Umbilical / Abnormal uterine

40% Both Abnormal

Histological changes in placental bed• Defective trophoblastic invasion of spiral arteries / decidual

vessels but not myometrial vessels are invaded by trophoblast• Charecteristic lipid rich lesions in the uteroplacental arteries

High Risk FactorsHigh Risk Factors

Primigravida : Extremes of reproductive age (young and elderly) Socio economic (status) : Disadvantaged Ethnicity : African American Family history : Hypertension, pre-eclampsia,

(First degree relatives) eclampsia Placental abnormalities : Molar pregnancy

Hyperplacentosis – multiple pregnancy Placental ischaemia

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

Thrombophilias : Anti-phospholipid syndrome, Protein C, S deficiency, Factor V LeidenGenetic : History of pre-eclampsia in sister, mother (Multi-factorial inheritance) Immunological

PredictionPrediction Roll-over Test Second Trimester Mean Arterial Pressure Urinary Calcium Uric acid Fibronectin Homocysteine level Cytokines Coagulation factors Placental peptides Doppler Ultrasound Fetal DNA

Roll-over Test Second Trimester Mean Arterial Pressure Urinary Calcium Uric acid Fibronectin Homocysteine level Cytokines Coagulation factors Placental peptides Doppler Ultrasound Fetal DNA

Tests for Prediction

• Roll over test is positive (rise of diastolic blood pressure 20 mmHg or more after turning from left lateral to dorsal position).

• Increased pressor response.

• Uric acid: is elevated.

• Hypercalciuria.

• Doppler velocimetry to detect Uteroplacental hypo perfusion.

Diagnosis Of PET

Hypertension + Proteinuria =

Two facets of a complex pathophysiological process

A): Signs: :

it is a disease of signs :

2 cardinal signs + or - Edema:

• Hypertension: – usually precedes Proteinuria,

• Proteinuria: detected by – Boiling test.– Quantitative assay.– Dipstick test.

+ or - Edema• occult or manifest:

» The lower extremities.

» Abdominal wall, vulva or may be generalized anasarca.

• usually after hypertension.

Peripheral edema is not a useful diagnostic criterion

  1) it is common in normal pregnancy.

2) PET can occur without edema (dry type).

so its presence does not ensure a poor prognosis and its absence not ensure a favorable outcome.

B) Symptoms (non specific):

• Headache.

• Blurring of vision.

• Nausea and vomiting.

• Epigastric pain (distension of the liver capsule)

• Oliguria or anuria

Severity Of Pre-eclampsia

• The severity of pre-eclampsia is assessed by:

–The frequency and intensity of the signs and symptoms.

–The more the severity of PET, the more likely is the need to terminate pregnancy.

DD ,mild & severe PET

Abnormality Mild SevereDiastolic blood pressure < 100 mg Hg 110 mm Hg or higher

Proteinuria Trace to 1+ Persistent 2+ or more

Headache Absent Present

Visual disturbances Absent Present

Upper abdominal pain Absent Present

Oliguria Absent Present

Convulsion Absent Present (eclampsia)

Serum creatinine Normal Elevated

Thrombocytopenia Absent Present

Liver enzyme elevation Minimal Marked

Fetal growth restriction Absent Obvious

Pulmonary edema Absent Present

4) Diagnosis Of Eclampsia:

• Eclamptic fit stages ( 4 stages):– Premonitory stage (1/2 minute):

» Eye rolled up.» Twitches of the face and hands.

– Tonic stage (1/2 minute): » Generalized tonic spasm with

episthotonus.» Cyanosis.» Tongue may be bitten between the

clenched teeth.

4) Diagnosis Of Eclampsia:

• Clonic stage (1-2 minutes): » Convulsions .

» Tongue may be bitten.

» face is congested and cyanosed.

» conjunctival congestion.

» blood stained froth from the mouth,

» Stertorous breathing,

» temperature may rise.

» involuntary passage of urine or stool.

» Gradually convulsions stop.

4) Diagnosis Of Eclampsia:

• Coma: – Variable duration due to respiratory and

metabolic acidosis.– Deep coma may occurs (cerebral hemorrhage). – Labor usually starts shortly after the fit.– Sometimes labor does not start and convulsions

recur again the so called ‘intercurrent eclampsia’ and carries a bad prognosis.

Classifications of Eclampsia

–Intercurrent Eclampsia: eclampsia in which the eclamptic fits recur in the same pregnancy.

–Recurrent Eclampsia: eclampsia that recurs in subsequent pregnancy.

Classifications of Eclampsia 1)Mild

2) Severe (Eden's criteria):• Coma > 6 hours.• Temperature > 39 (pneumonia or pontine

hge)• Systolic Bp > 200 (risk of cerebral hge)• Pulse > 120/min ( acute heart failure).• Anuria or Oliguria( renal failure).• Respiratory rate > 40/min( pneumonia)• More than 10 fits (status eclampticus).

PreventionPrevention

• 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.

• 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.

PreventionPrevention

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

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

PreventionPrevention

• 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

• 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

Criteria for diagnosis of Preeclampsia

Criteria for diagnosis of Preeclampsia

• Blood pressure of 140 mm Hg systolic or higher or 90 mm Hg diastolic or higher that occurs after 20 wks of pregnancy in a woman with previously normal BP

• Proteinuria as urinary excretion of 0.3 g protein or higher in a 24 hrs specimen

Am J Obstet Gynecol 2000;183:S1-S22

• Blood pressure of 140 mm Hg systolic or higher or 90 mm Hg diastolic or higher that occurs after 20 wks of pregnancy in a woman with previously normal BP

• Proteinuria as urinary excretion of 0.3 g protein or higher in a 24 hrs specimen

Am J Obstet Gynecol 2000;183:S1-S22

PROTEINURIAPROTEINURIA

Develops late in the disease processInfluenced by exercise and posture24 hour estimation is better than randomHypertension with proteinuria is a reliable indicator of fetal jeopardy

Proteinuria alone PNM unchangedHT alone PNM 3 fold riseHT + proteinuria PNM 8 fold rise(PNM: perinatal mortality rate)

EDEMAEDEMA

• Early but non specific sign• Rapid weight gain• Edema of PIH 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

• Early but non specific sign• Rapid weight gain• Edema of PIH 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

ManagementManagement

AIMS• Control of hypertension• Prevention of eclampsia• Prevention of accidental hemorrhage

and DIC• Prevention of renal damage• Maintenance of placental perfusion• Monitoring of fetal growth and well-

being• Planning timely delivery• Care in puerperium• Follow up.

AIMS• Control of hypertension• Prevention of eclampsia• Prevention of accidental hemorrhage

and DIC• Prevention of renal damage• Maintenance of placental perfusion• Monitoring of fetal growth and well-

being• Planning timely delivery• Care in puerperium• Follow up.

Out Patient ManagementOut Patient Management

Gestational Hypertension less than160/100 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

Gestational Hypertension less than160/100 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.

• 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 (Severe

Preeclampsia)

Indications for Hospitalization from Day Care Unit (Severe

Preeclampsia)

• 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

• 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 SURVEILLANCEMaternal SURVEILLANCE

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

BIOCHEMICAL MONITORINGBIOCHEMICAL MONITORING

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

Fetal Well-beingFetal 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 HypertensionControl 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

• 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

Indications for Antihypertensive Therapy

• Role of antihypertensive therapy in Mild to Moderate Hypertension is unclear.

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

• Persistent rise of BP in mild to moderate cases

• Severe preeclampsia• Hypertensive crisis• Chronic hypertension

• Role of antihypertensive therapy in Mild to Moderate Hypertension is unclear.

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

• Persistent rise of BP in mild to moderate cases

• Severe preeclampsia• Hypertensive crisis• Chronic hypertension

Oral Antihypertensive for Control of Mild to Moderate Hypertension in

Pregnancy

Oral Antihypertensive for Control of Mild to Moderate Hypertension in

Pregnancy

• 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

• 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

Antihypertensive for Control of Acute or Severe Hypertension in

Pregnancy

Antihypertensive for Control of Acute or Severe Hypertension in

PregnancyShort Acting Antihypertensive agents :• Hydralazine : 5 mg IV repeated after 20 min• 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 mgOther Antihypertensive agents :Diazoxide : 30 to 50 mg IV, repeated every 10to 15 min or by continuous infusion.Sodium Nitroprusside : IV infusion 0.5 to 10 mg/kg/min

Short Acting Antihypertensive agents :• Hydralazine : 5 mg IV repeated after 20 min• 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 mgOther Antihypertensive agents :Diazoxide : 30 to 50 mg IV, repeated every 10to 15 min or by continuous infusion.Sodium Nitroprusside : IV infusion 0.5 to 10 mg/kg/min

Drugs used to lower blood pressure during pregnancyDrugs used to lower blood pressure during pregnancy

Planning DeliveryPlanning Delivery

PlaceMultidisciplinary team and high dependency care availableNeonatal care facilities

RouteAim for vaginal deliveryLSCS required for obstetric indication or maternal or fetal compromiseTo avoid general anaesthesia

TimeConservative v/s Early intervention

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

Criteria for delivering patient with Severe Preeclampsia

Criteria for delivering patient with Severe Preeclampsia

• 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

• 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

Labour Management• IV access

• Repeat haematological investigations

• Fluid management

• Seizure prophylaxis and anti

hypertensives

• Electronic fetal monitoring

• Analgesia and Anaesthesia

• No ergometrine

Period of gestation convulsions occur

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.

• Eclampsia • Epilepsy • Cerebral malaria in tropics • Encephalitis • Meningitis • Intracranial tumors • Peripheral cerebral

thrombosis • Poisoning • Hysteria

Differential Diagnosis

• 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

• Cerebral haemorrhage

• Anoxia

• Cardiac failure

• Pulmonary oedema

• Aspiration pneumonia

• Pulmonary embolism

• Postpartum shock

• Puerperal sepsis

Causes of maternal / Perinatal 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.

• General management

• To control convulsions using MgSO4

• To control Hypertension

• To avoid Diuretics

• To limit IV fluids unless excessive fluid loss

• To investigate

• To terminate the 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

Specific managementTo control seizures and to prevent its recurrenceMagnesium sulfate: the drug of choice

Regimens Loading dose Maintenance dose

Pritchard 4gm IV over 3 to 4 min 5gm buttock 4 hrly 10gm 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%

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%

Phenytoin therapy

10mg/kg IV followed by 5mg/kg 2 hrs later

Sedatives can be used with above regimen

To control hypertensionInspite of sedative if BP >160/110mg then antihypertensive drugs are administered

Hydralazine

- 5mg iv slowly

- rate 10mg every 20 minutes

-Monitoring BP every 5 minutes

- Repeat the dose when diastolic BP >110mmHg labetalol - 20 mg i.v., repeated every 30 min & can be doubled maximum upto 80 mgNifedepine : 5 to 10 mg every 15 min to maximum upto 30 mg

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.

Planning the delivery

• Delivery is the ultimate cure

•Vaginal.

•LSCS is done for obstetric reasons, or before 32 weeks of gestation.•Anesthesia – •General to be avoided, as it increases blood pressure during intubation and extubation.•Epidural is better than spinal.

Route of delivery• Probability of achieving vaginal

delivery after induction through an unripe cervix are below 20%

Hall DR et al, BJOG 2000Haddad B et al, AJOG 2004

• Prolonged labor can be detrimental for mother and fetus

• Caesarean delivery is preferableSibai BM et al, COG 2005

HemolysisSchistocytes in the blood smearS.Bilirubin > or equal to 1.2 mg%Absent Plasma hapatoglobinElevated Liver EnzymesSGOT > 72 IU/LLDH > 600 IU/LLow Platelet Count

Diagnosis of HELLP Syndrome

HELLP Syndrome.

• 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.

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 %.

Conclusion.• PIH 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.

TOGETHER WE CAN MAKE IT A REALITY

Motherhood … .

.. A dream of every woman