A STUDY OF MATERNAL AND PERINATAL

OUTCOME IN PREECLAMPSIA

Dissertation submitted to

The Tamilnadu Dr. M.G.R. Medical University,

Chennai – 600032

with partial fulfillment of the regulations

for the award of degree of

M.S – BRANCH - II

OBSTETRICS AND GYNAECOLOGY

K.A.P.Viswanatham Government Medical College

Tiruchirappalli

The Tamilnadu Dr.M.G.R.Medical University

Chennai.

April 2016.

CERTIFICATE

This is to certify that this dissertation titled “A STUDY OF

MATERNAL AND PERINATAL OUTCOME IN PREECLAMPSIA” IN

MAHATMA GANDHI MEMORIAL HOSPITAL, TIRUCHIRAPPALI”

is a bonafide work of DR.PADMA. K., Postgraduate M.S.Obstetrics and

Gynaecology, Department of Obstetrics and Gynaecology,

K.A.P.Viswanatham Government Medical College, Trichy and has been

prepared by her under our guidance. This has been submitted in partial

fulfillment of regulations of The Tamilnadu Dr. M.G.R. Medical University,

Chennai -32 for the award of M.S. Degree in Obstetrics and Gynaecology.

Prof.Dr.D.PARIMALADEVI,M.D.D.G.O

Professor & Head

Department of Obstetrics and Gynaecology

K.A.P.V. Govt.Medical College,

Trichy

Dr.D. UMA.,M.D., D.G.O.,

Associate Professor

Department of Obstetrics and

Gynaecology

K.A.P.V. Govt. Medical College,

Trichy

Prof.Dr.M.K .MURALIDHARAN,M.S.,M.ch (Neurosurgery)

Dean

K.A.P.Viswanatham Govt.Medical College, Trichy

DECLARATION

I Dr.Padma. K., solemnly declare that this dissertation titled, A STUDY

OF MATERNAL AND PERINATAL OUTCOME IN PREECLAMPSIA

IN MAHATMA GANDHI MEMORIAL HOSPITAL, TRICHY” is a

bonafide work done by me at K.A.P.Viswanatham Government Medical

College, Trichy, during 2012-2015 under the guidance and supervision of Head

of the Department , Department of Obstetrics and Gynaecology

PROF.Dr.D.PARIMALADEVI, M.D,D.G.O. The dissertation is submitted to

The Tamilnadu Dr. M.G.R. Medical University, towards the partial fulfillment

of university rules and regulations for the award of M.S.Degree(Branch-II) in

Obstetrics and Gynaecology.

PLACE : TRICHY.

DATE :

Dr. PADMA.K.

ACKNOWLEDGEMENT

I am extremely grateful to The Dean, Prof.Dr.B.MURALIDHARAN,

M.S.,M.ch. K.A.P.Viswanatham Government Medical College,

Tiruchiraappalli for granting me permission to undertake the study and to avail

the facilities needed for my dissertation work.

It gives me immense pleasure to express my gratitude and thanks to my

respected Prof. Dr. D. PARIMALA DEVI , M.D.,D.G.O. Professor and Head

of the Department, Obstetrics and Gynaecology who gave immense support

and encouragement and all the facilities to complete thiswork.

I sincerely express my gratitude and thanks to my respected

Prof. Dr. D.UMA, M.D.,D.G.O Associate Professor, Obstetrics and

Gynaecology Department.

I am particularly grateful for Prof. Dr. Vidhyaravi.M.D., D.G.O., and

Prof. Dr.S. Bama.,M.D.,D.G.O.,DNB.O.G., for their valuable guidance and

help during the study.

I sincerely thank my teacher, guide and mentor Senior Assistant Prof.

Dr. P.Backiavathy.M.D.,O.G.. for her valuable guidance and support.

My heartfelt thanks to all my assistant professors for their guidance in my

study.

I owe my thanks to Dr. Selvam.,M.D., Assistant Professor.,Department

of community Medicine.

I am grateful to the patients without whom the study would have not

been possible.

CONTENTS

S. NO.

TITLE

PAGE

NO.

1. INTRODUCTION 1

2. AIM OF THE STUDY 2

3. REVIEW OF LITERATURE 3

4. MATERIALS AND METHODS 45

5. RESULTS AND ANALYSIS 47

6. DISCUSSION 80

7. SUMMARY 82

8. CONCLUSION 84

9 BIBLIOGRAPHY 85

.

ANNEXURES

PROFORMA

CONSENT

MASTER CHART

ABBREVATIONS

INTRODUCTION

INTRODUCTION

Pre-eclampsia is a multisystem disorder specific to pregnancy and

puerperium, it manifests by onset of hypertension and proteinuria after

twenty weeks of gestation .It occur earlier with gestational trophoblastic

diseases or multiple pregnancies and resolves by twelve weeks postpartum.

Hypertension During pregnancy is diagnosed when the systolic pressure is

140mmHg or more and Diastolic pressure of 90mmHg or more measured

on two occasions at least 6 hours apart within seven days. A single

reading of diastolic above 110mmHg in a pregnant woman is considered as

hypertension.

In 1916, Zweifel first called the toxaemia ―the disease of

theories‖.1 This was recognised as clinical entity since time of Hippocrates.

Pre-eclampsia remained a significant public health threat in both developed

and developing countries, contributing to maternal and perinatal

morbidity and mortality globaly the incidence of preeclampsia among

hospital patients about 7 to 10% of antenataladmissions. The dangers of

Eclampsia, Intrauterine growth restriction & Intrauterine fetal death, etc.

dependent on the degree of pre-existing pre-eclampsia .They can be

mitigated by good obstetric care. In this study, an attempt has been made

to study effect of Preclampsia & the severity on pregnancy & on

maternal & fetal outcome.2

AIM OF THE STUDY

AIMS OF THE STUDY

To study about the prevalence of preeclampsia in relation to

1)age

2)parity

3)unregistered and registered

To study the incidence of various maternal complication of pre

eclampsia. To study the fetal outcome in pregnancies complicated by pre

eclampsia.

REVIEW

OF

LITERATURE

REVIEW OF LITERATURE

SIMILAR STUDIES:

1) Study of maternal and perinatal outcome in preeclampsia by Ankita

Gawde ,U. T. Bhosale dept of obs and gynae , Bharathi Vidhyapeeth ,

Deemed University, Medical college and hospital Sangli , Maharashtra

,INDIA.

2) Maternal and perinatal outcome associated with eclampsia in a teaching

hospital Sukkur, BY Aisha Abdullah , Altaf Ahmed Shakik ,

Bahawaldin Jamro , Dept of obs and gynaecol, medicine, and

paediatrics . Ghulam Mohamed mahar medical college sikkur.

3) Risk factors for preeclampsia and its perinatal outcome. By Sultana and

Aparna.j The Shadan institute of medical sciences , Himayatsagar,

Hyderabad.

4) Maternal and perinatal outcome in pregnancy induced hypertension –

Hospital based study .By Dr. P.Meshram , Dr. Y.H. Chavan G.M.C

Nanded India.

Hypertension is the most common medical problem encountered in

pregnancy .Incidence is seen around 5-10% of all pregnancies.Preeclampsia is

the second common cause of maternal mortality in India & major cause of

perinatal mortality & morbidity.According to International society for the study

of Hypertension in pregnancy(ISSHP).Hypertension is defined as a Systolic

blood pressure morethan 140 mmhg or Diastolic blood Pressure morethan 90

mmhg atleast 2 occations taken 6 hours apart.

MEAN ARTERIAL PRESSURE:

Mean arterial pressure calculated by following formula.

MAP=Diastolic pressure+1/3 Pulse pressure

MAP morethan 105 is significant.In normal pregnancy diastolic Blood

pressure begins to fall in early pregnancy and continues to fall in the second

trimester and reach a nadir at 22-24 weeks .The fall is Due to reduced vascular

tone .Blood pressure should be measured in Woman sitting at 45 degree angle,

cuff should be appropriate size placed at the level of Heart .Multiple readings

should be taken. Korotkoff sound phase 5 is the appropriate measurement of

diastolic blood pressure .Preferably Right arm should be used.

CLASSIFICATION OF HYPERTENSIVE DISORDERS IN

PREGNANCY:

GESTATIONAL HYPERTENSION Hypertension first time

during pregnancy.

No proteinuria

BP returns normal twelve

weeks postpartum.

PRE-ECLAMPSIA & ECLAMPSIA Hypertension diagnosed after

20 weeks of Gestation

Proteinuria

Associated with other signs

& symptoms of pre-eclampsia

Eclampsia associated with

seizures that cannot be

attributed to other causes like

space occupying lesions

,seizure disorders, head injury

and electrolyte imbalance.

PRE-ECLAMPSIA

SUPERIMPOSED ON CHRONIC

HYPERTENSION

New onset proteinuria in

hypertensive women after

twenty weeks gestation

CHRONIC HYPERTENSION Hypertension before

pregnancy

Hypertension diagnosed

before twenty weeks of

pregnancy not attributable to

trophoblastic disease or

multible pregnancy.

Hypertension diagnosed 1st

diagnosed after twenty weeks

gestation &persistent beyond

12 weeks postpartum.

CRITERIA FOR DIAGNOSIS OF PREECLAMPSIA;

Blood pressure of >140/90 mmhg occurring after 20 weeks of Gestation,

presence of proteinuria >300mg per day or 1+ in urine dipstick

examination.24 hours protein measurement is the best method to

quantify proteinuria3.Urinary protein creatinine ratio 0.3 or more is

significant. Edema is little value as an objective sign.

RISK FACTORS: 4

Couple

related

Primi parity

Limited

sperm

exposure

Paternal

Factors

Maternal risk

facors:

Extremes of age

Prior history of

pre eclampsia

Renal diseases

Infection

Susceptible

history

Pregnancy related

Multi fetal

gestation

Hydropic

degeneration of

placenta

Hydatidiform

mole& triploidy

Genesis of pre eclampsia as a two stage disorder

Maternal factors

1.genetic

2.underlying medical disorders

(thrombophilia ,diabetes,

hyperhomocysteinemia,

obesity,hypertension,etc.)

3.immune-maladaptations to

pregnancy.

Placental factors

1.shallow trophoblast invasion in

spiral arteries(abnormal

placentation)

2. placental ischaemia

Connecting

link

Endothelial dysfunction Stage 2

Pre-eclampsia

Good endothelium Bad endothelium

Mild disease Severe disease

Balanced tilted in

favour of oxidative

stress markers

OXIDATIVE STRESS

Free Radicals

Anti oxidants

AETIOPATHOGENESIS:

Exact aetiology of preeclampsia is unknown. Preeclampsia is a two

stage disorder.Theory was propounded by Redman and collegues. 4

According

to this stage one is preclinical and characterised by poor placentation or faulty

endovascular trophoblastic remodelling of Uterine arteries which cause

placental hypoxia. Stage two caused by oxidative stress which causes release

of placental factors into maternal circulation .This inturn causes systemic

inflammatory response and endothelial activation results in clinical syndromes

of preeclampsia and intra uterine growth restriction.

ABNORMAL TROPHOBLASTIC INVASION:

In normal pregnancy, spiral arteries of placenta are invaded by

cytotrophoblast and the elastic and muscular layers are replaced by fibrinoid .In

second trimester second wave of cytotrophoblastic invasion transforms the

myometrial segments of spiral arteries into wide mouthed vessels unresponsive

to vasomotor stimuli .Blood supply is transformed from high resistence low

flow system to low resistence high flow system inorder to increase

uteroplacental flow and meet the needs of the fetus. In preeclampsia primary

wave of trophoblastic invasion is impaired and secondary wave fails to occur.

ABNORMAL ANGIOGENESIS:

Angiogenesis and Antiangiogenesis factors5 involved in placental

vascular development .There is imbalance in these factors. There excess

antiangiogenic factors produced as a result of hypoxia. Trophoblast produces

atleast two antiangiogenic peptides in the circulation . Soluble fms like

tyrosinekinase [sflt -1] and soluble endoglobulin. Decrease in angiogenic

factors like vascular endothelial growth factor [VEGF].

Endothelial cell dysfunction and vasospasm

Endothelial cell dysfunction is the most important factor in

preeclampsia .AntiAngiogenic and metabolic factors and other inflammatory

factors provoke endothelial cell injury .Another one theory is lipid peroxidation

stimulated by Free oxygen radicals because of oxidative stress .Cytokines like

tumour necrosis factor and interleukins also contribute to preeclampsia .It

causes endothelial cell injury, modify the nitricoxide production and interfere

with prostaglandin balance.Increased capillary permeability manifests as

oedema and proteinuria. 4

ETIO PATHO GENESIS

CLINICAL FEATURES OF PRE ECLAMPSIA

ALTERATION IN NITRICOXIDE AND PROSTOGLANDINS:

Protacyclin is a Prostoglandin produced by the vascular endothelium 5. It

is a powerful vasodilator and inhibitor of platelet aggregation. Nitric oxide is

an another potent vasodilator produced by the endothelium .Thromboxane is

produced by platelets and causes vasoconstriction and platelet aggregation. In

normal pregnancy there is an increased production of prostacyclin resulting in

vasodilatation. 6

Damaged endothelial cell lead to reduced production of

nitricoxide. So in preeclampsia vasospasm and platelet activation and adhesion

occurs and activation of coagulation system also occurs.

COAGULATION SYSTEM AND PLATELETS:

Endothelial dysfunction will lead to activation of platelets and

coagulation system by the tissue factor on the endothelium .Results in

widespread disseminated intravascular coagulation . So clotting factors are

used. This results in subclinical to frank DIC. This results in consumption

coagulopathy lead to thrombocytopenia.

METABOLIC FACTORS :

Central obesity and insulin resistance are risk factors for preeclampsia.

Dramatic Increase in free fatty acids and triglycerides in preeclamsia. Calcium

deficiency also a risk factor for preeclampsia.

GENOTYPE AND PHENOTYPE:

There is a definite inherited maternal component in preeclampsia.

Phenotypes will differ among genotypes depending on interaction with

environmental factors.

IMMUNOLOGICAL FACTORS:

Invasion of trophoblast into myometrium and decidua is controlled by

the immune mechanism7. The decidua contains lymphoid tissue,

predominantly natural killers .The NK cells express KIR receptors ,which

recognise the LA class1 molecules. The NK cells VEGF, PLGF, and

Angiotensin 2 which bring about maternal placental bed vascular changes.

MOFFET KING and collegues studied the HLA C-NKcell receptor

Interaction. They state that each pregnancy is unique because of the NKcell

KIR –HLA C interaction .Mothers with absent or decreased KIRs which

interact with HLA C group have increased propensity towards preeclampsia6

PATHOPHYSIOLOGY

Changes because of vasospasm and endothelial dysfunction.

PLACENTA

The typical vascular lesion is termed acute atherosis of the decidual

arteries. Leads to fibrinoid necrosis, macrophages and mononuclear

infiltration. Result in intra uterine growth restriction oligohydraminios,

placental abruption and ultimately fetal demise.

KIDNEY

Main pathology in kidney is glomerular and tubular dysfunction and

glomerular endotheliosis Swollen endothelial cells due to fibrin

deposition.Glomerular dysfunction lead to reduced glomerularFiltration rate

and creatinine clearance. Acute renal failure usually due to acute tubular

necrosis which is reversible. Rarely it lead to irreversible due to acute cortical

necrosis. Tubular dysfunction manifest as hyperuricaemia. Proteinuria due to

increased capillary permeability.

LIVER

Periportal thrombosis and fibrin deposition, haemarrhages and necrosis

seen in liver. There is an increase in enzyme levels [SGOT,SGPT] and clinical

jaundice can occur. 7 Liver changes are responsible for nausea and vomiting.

Small haemorrhages may coalesce to form a sub scapsular haematoma. Which

cause stretching of Glisson’s capsule, and epigastric pain.Catastrophic rare

complication is liver rupture. The typical vascular lesion is termed acute

atherosis of the decidual arteries Lead to fibrinoid necrosis, macrophages and

mononuclear infiltration.

Result in intra uterine growth restriction,

oligohydraminios, placental abruption and uiltimately fetal demise.

PATHOPHYSIOLOGY :

CARDIOVASCULAR SYSTEM.

Three major changes in the cardio vascular system

1.Increased cardiac afterload caused by hypertension .

2Dimnished cardiac preload due to the diminished hypervolaemia of

pregnancy in preeclamsia .

3 Endothelial cell activation with increased capillary permeability Which

causes extravasation of fluid from the intravascular to extravascular space and

into The lungs resulting in pulmonary edema. Haemoconcentration is the

hallmark preeclamsia.so women with preeclamsia and eclampsia sensitive to

fluid therapy and easily can develop pulmonary edema .Also sensitive to even

normal blood loss at delivery.

BLOOD AND COAGULATION

Endothelial dysfunction lead to activation of platelets and the

coagulation System. By activation of tissue factor on the endothelium ,Results

in subclinical to frank DIC. Resulting in consumption coagulopathy result in

throbocytopaenia.This can be demonstrated by the presence of schistiocytes,

Burr cells and fragmented red cells in peripheral blood and also by elevated

lactate dehydrogenase levels.

BRAIN.

In the brain main pathology is cerebral vasospasm .Small cerebral

haemarrhages , thrombosis and fibrinoid necrosis can occur. 9

Cerebral edema

also occur8. Massive cerebral haemorrhage may be the rare complication in

severe hypertension .In CT imaging may show localised hyper intense lesions

are seen at the gray- white matter junction ,primarily in the occipital lobes. This

is known as PRES OR POSTERIOR REVERSIBLE ENCEPHALOPATHY

SYNDROME.

EYES

Retinal vasospasm is the most common finding .Haemorrhage and

Papilloedma Rarely seen in severe hypertension.Visual disturbances are

common and are due to edema of the occipital lobe. Cortical blindness rarely

due to occipital edema . It is temporary. Blindness can also occur due to

involvement of Lateral geniculate nuclei and retina.In Retina ischaemia

,infarction, or retinal detachment can occur. Prognosis is usually good and

reversible following delivery.

CLINICAL EVALUATION.

Most women with hypertension during pregnancy may or may not

present with symptoms and signs of hypertension and related disorders. Raised

blood pressure may be noticed during routine antenatal checkups.Detailed

history is important .

Blood pressure in early pregnancy or in the booking visit Blood

pressure in the prior pregnancy

Is there any palpitation, chestpain pallor?

Is there any history of Headache or epigastric pain orvisual

disturbances?

Is there any history of kidney disease?

Had she noticed any weakness of limbs?

Is there any history of nocturia, polyuria, ?

Is there any history of reduced urine output?

Is there any family history of hypertension

Is there any history of oral contraceptive pills prior to pregnancy?

CLINICAL MANIFESTATIONS :

Hypertension in pregnancy is generally asymptomatic and diagnosed

during antenatal check up.sudden onset and excessive weight gain ,generalized

edema affecting the face ,hands and ankles, particularly non-dependent

oedema, epigastric or right upper quadrant pain, headache and visual

complaints like scotomata,blurred vision or rarely,blindness in a woman with

hypertension are features of severe pre-eclampsia. Symptoms of blurred vision

and severe generalized or occipital headache are suggestive of accelerated

hypertension and impending eclampsia. Physical examination On physical

examination,particular attention should be paid to the apex beat; the second

sound at the aortic area may be accentuated .Ophthalmoscopic examination is

an essential part in the examination .In most women with mild and moderate

pre-eclampsia,fundus is normal.women with long standing pre-existing

hypertension, silver – wiring and tortuosity of the arterioles .In more severe

cases , arterio venous nipping is seen.The grave sign is the development of

papilledema.

Laboratory investigations:

In addition to the routine test in the pregnancy , platelet count ,liver

enzymes ,serum uric acid , lactate dehydrogenase level ,24 hour urine analysis

and culture ,Creatinine clearance should be done.patients with history of poor

compliance to blood pressure ,target organ damage must be detected by ECG ,

ECHO to rule out left ventricular hypertrophy.

Complete blood count and blood film:

Low haemoglobin with increased reticulocytes and abnormally shaped

red blood cells (schistocytes and spherocytes ) indicates microangiopathic

haemolytic anemia. Blood urea and serum creatitine levels are usually lower in

pregnancy due to increased glomerular filteration and hemodilution. Acute rise

may indicate acute renal injury . Serum uric acid is also lowered in pregnancy

due to increased renal clearance. It is more specific especially in women with

super imposed preeclampsia. A rising level in the last trimester indicates

impaired fetal prognosis.

URINE ANALYSIS:

It is usually examined by dip stick method on random sample of urine .if

positive , 24 hour urine collection is done for the quantification of the

albuminuria. Infection gives a false positive results. So culture and sensitivity

must be done to exclude it.

SEVERITY OF PRE-ECLAMPSIA

Pre-eclampsia is classified into mild and severe according to blood

pressure and Proteinuria.

SEVERITY OF PRE-ECLAMPSIA

Diastolic blood pressure 110mmhg and above .

Systolic blood pressure 160mmhg and above

Proteinuria 5gm in 24 hours or more [3+proteinuria or more]

Headache ,visual disturbances or epigastric pain

Oliguria or urine output <than 500ml in 24 hours.

Intra uterine growth restriction

Pulmonary edema

Thrombocytopaenia <than 1,00,000/mm3

Increased liver enzymes[>50IU/L]

PREDICTION OF PRE- ECLAMPSIA.

Previous h/o pre-eclampsia ,antiphospholipid antibodies, and pre-

existing medical conditions. Advanced maternal age in first pregnancy,

multiple pregnancy, interpregnancy interval>10years And booking blood

pressure 130≥systolic ,80mmhg ≥ diastolic historical markers .It will Help us to

screen the women for high risk of pre-eclampsia. At present no single

screening test That can be considered reliable and cost effective for predictive

of pre-eclampsia. BMI>than 35kg/m2, alfa fetoprotein , fibronectin , and

uterine artery Doppler [bilateral notching ]were all Found to have specificities

above 90%,but poor sensitivity.Uterine artery Doppler pulsatility Index

combined with bilateral notching shows the best predictive value.

UTERINE ARTERY DOPPLER VELOCIMETRY

In normal pregnancy, impedence to uterine artery blood flow is

markedly reduced. Failure to undergo physiological trophoblastic invasion

reflected by high impedence flow in the uterine arteries. Increased resistance

to flow and presence of a diastolic notch associated with pre-eclampsia.

PREVENTION.

Low dose aspirin in women at high risk for developing disease.Dietary

supplements like magnesium, antioxidants, marine oils ,and folic acid,do not

reduce the incidence of preeclampsia.Low Serum zinc levels may be

associated with suboptimal level of outcome of pregnancy.

COCHRANE REVIEW (2012) which included over 15,000 women

did not reveal any evi dence of improvement of pregnancy.L-arginine calcium

supplementation ,vitC ,vitE β carotene however the studies investigating

so far having conflicting results.

REST: COCHRANE REVIEW (2006) showed that there was a

significant reduction in the relative risk of pre-eclampsia.

EXERCISE AND PHYSICAL ACTIVITY

Prospective study failed to show the reduction in the relative risk of

pre-eclampsia.

REDUCED DIETARY SALT

Two trials conducted them showed no correlation was observed.

ASPIRIN AND PLATELET AGENTS

Aspirin is an antiplatelet aggregator so improves blood flow by

preventing the formation of micro thrombi within the vessels .A large

randomised control trial ,the Collaborative Low Dose Aspirin Study in

Pregnancy (CLASP) .It showed a non significant reduction of 12%in pre-

eclampsia. Significant reduction of proteinuric pre-eclampsia in a group of

women who were at high risk of Developing early onset pre-eclampsia

leading to preterm delivery, when aspirin was started early in the 2nd trimester.

The study showed that low dose aspirin was generally safe for the fetus and

neonate.

MANAGEMENT OF PRE-ECLAMPSIA.

Natural course of preeclampsia is blocked at the secondary and tertiary

level of prevention. Early detection and treatment according to severity

reduces the complications ,thereby reduce the morbidity and mortality, better

maternal and neonatal outcome9 .Evidence based practice and setting a

protocol in the management of acute onset, severe Hypertension in

preeclampsia and eclampsia improve an immense outcome.10

NICE

guidelines state that intravenous or oral labetalol,oral nifedipine and

intravenous hydralazine May be the 1st line of management of severe pre-

eclampsia. Magnesium sulphate regimen to be considered in case of eclampsia

and imminent eclampsia. 11

Incase of severe pre-eclampsia after 34 weeks of

gestation induction of labour shoud be Considered.The patient is delivered by

induction or caesarean section depending on the Obstetric and fetal indications

benefits of termination weighed against potential risk of continuation of

Pregnancy.

If pregnancy is less than 34 weeks betamethasone 12mg 2 doses 24hours

apart for the Benefit of baby.It will accelerate lung maturity , reduce the

incidence of intra ventricular haemorrhage Necrotising enterocolitis.12

Likewise patients with gestation of ≤34weeks with imminent symtoms, Signs

of multiorgan failure, non reassuring fetus, and eclampsia are delivered,

similarly. A recent review states expectant management in a patients with

pre-eclampsia at a gestational age between 24 and 33 weeks is a safe and a

better practice and is said to bring prolongation of pregnancy for 7 to 10

days. Criteria for termination of pregnancy for patients on expectant

management are as follows;

Uncontrolled blood pressure

Imminent signs and symptoms of pre –eclampsia

Nonreassuring fetal cardiac status

Oligohydraminios

Elevated liver enzymes

Oliguria

Elevated liver parameters especially serum creatinine concentration

Elevated liver enzymes

Development of Hellp syndrome

Pulmonary edema

Pre eclampsia is an unpredictable disorder, only definite cure is

termination of pregnancy. Management depends upon the severity of disease

and period of gestation.IF the pregnancy is 37 weeks are more elective

induction of labour may be performed when Particularly if association of

proteinuria. Time of delivery depends upon the gestational age ,fetal lung

maturity,and most importantly Severity of disease.

MANAGEMENT ACCORDING TO GESTATIONAL AGE

<Than 24weeks ;Stabilise the patient and terminate the pregnancy. 25 to

33 weeks ;Expectant management with intensive maternal and fetal

monitoring.

Indication>34 weeks ;Stabilise the patient with strict fetal surveillance

and deliver Surveillance, steroid therapy for fetal lung maturity, and deliver,if

maternal or fetal compromise.

MATERNAL SURVEILLANCE

Blood pressure should be checked at least 4 times a day. Urine

albumin once a day. Biochemical parameters including full blood count,

kidney function test ,electrolytes, Liver enzymes,and serum bilirubin two to

three times a day . ophthalmic examination to be done On admission to be

repeated if required.

FETAL SURVEILLANCE

Fetel well being by NST and BIOPHYSICAL PHYSICAL (BPP)

.NST is performed usually twice a week .In severe cases twice daily.BPP

can be done weekly.Fetal growth must be monitored by ultrasonagraphy and

sonography wise Amniotic fluid volume is assessed periodically. DOPPLER

studies are useful,in case of Intrauterine growth restriction .It helps in deciding

the frequency of monitoring and optimal time of delivery. DOPPLER is

velocimetery started at 28 and 30 weeks .Repeated at 2 to 4 weeks intervals.

MODE OF DELIVERY.

Preferred mode of delivery for pre eclampsia is vaginal. Caesarean

section may be indicated in Fetal distress , malpresentation, placental

abruption or placenta previa . In case of severe pre eclampsia Remote from

term , caesarean section may be advisable due to the chances of prolonged

and Unsuccessful induction and fetal compromise .

INTRA PARTUM MANAGEMENT.

Blood pressure should be measured every two hours. Aim is to maintain

the diastolic BP below 110mmhg and systolic BP below 160mmhg .Urine

output and signs of impending Eclampsia to be monitored

carefully.Eclampsia prophylaxis to be given in case of severe precclampsia

and Impending pre eclampsia. Continuous fetal monitoring should be

done.Adequate pain relief by Epidural anaesthesia avoids the risk of aspiration

and difficult intubation due to edema of the Airway.Ergometrine to be avoided

because it will cause intense vasoconstriction may lead to Hypertensive crisis.

MATERNAL COMPLICATIONS

Eclampsia

Cerebro vascular accident

Hemiplegia ,Dysphasia

Visual disturbances

Placental abruption

HELLP syndrome [Haemolytic anaemia,Elevated liver

enzymes,low platelets]

Pulmonary edema with or without left ventricular failure

Acute renal failure

Microangiopathic haemolytic anaemia

Side effects of drug therapy.

FETAL COMPLICATIONS

Intrauterine growth restriction related to duration of hypertension

Oligohydraminios

Prematurity

Ante partum and Intrapartum asphyxia

Intrauterine death

Fetal side effects of antihypertensive drugs.

HELLP SYNDROME

Hellp syndrome is an acronym which was coined by Louis Weinstein in

1982 .It includes Haemolysis ,Elevated liver enzymes, and Low platelets.Well

recognised complication of severe pre eclampsia, it can occur in the absence of

Hypertension and proteinuria.Incidence about 0.2 to o.6 % of all pregnancies

and in 10 to 20 %0f cases with severe pre eclampsia .About 2/3 of patients

present antepartumly and the rest in the postpartum period, usually within 48

hours of delivery.

DIAGNOSIS.

The syndrome generally presents in the third trimester. When it occurs

earlier ,particularly in association with early onset pre-eclampsia , Anti

phospholipid antibody syndrome. Symptoms of Malaise ,nausea, vomiting ,

epigastric pain and headache.Because of vague symtoms diagnosis May be

missed until laboratory investigations are performed.The diagnosis of Hellp

requires the Presence of elevated liver enzymes (ALT and AST), and low

platelet count Haemolysis can be documented by examination of a peripheral

blood smear (schistocytes ,echinocytes , and burr cells).Elevated indirect

bilirubin ,Low serum haptoglobulin level, a low haematocrit, and serum LDH

greater than 600IU/L.The coagulation profile is usually normal unless DIC

supervenes.Positive D –dimer test ,which indicates subclinical

coagulopathy.Differential diagnosis for hellp syndrome

1)Acute fatty liver of pregnancy

2)Thrombotic thrombocytopenic purpura

3)Haemolytic uremic syndrome.

CLASSIFICATION

Classified into three categories based on the platelet counts.

Class 1] ,<50,000/mm3.

Class2] _50,000 to <1,00,000/mm3.

Class 3}more than 1,00,000.

Another system of classification based on number of abnormalities

present , I,e. haemolysis, elevated liver enzymes and low platelets.when 2 or 3

present this known as Partial Hellp , When all are present this is known as

complete or full Hellp syndrome.

MANAGEMENT.

Maternal mortality and morbidity increase with increasing disease

severity and worsening laboratory parameters.Perinatal mortality and morbidity

depends on the gestational age associated complications like Intra uterine

growth restriction or placental abruption rather than the severity of Hellp

syndrome.LDH Platelet will be the best marker to follow the Hellp syndrome ,

disease progression, which start to normalize by 72 hours follow the

delivery.Anti hypertensive treatment and anticonvulsant trearment are

administered as indicated.High dose corticosteroid treatment has to be

proposed to improve maternal prognosis of HELLP Syndrome10

. COCHRANE

review, ELEVEN TRIALS were included comparing the corticosteroids with

placebo or no treatment . There was no difference in the risk of maternal

death or maternal morbidity . or perinatal morbidity. Therefore good evidence

to support corticosteroids therapy in the management of Hellp

syndrome.Termination of pregnancy is planned according to the gestational

age, the favorability of cervix and severity of condition. When gestational age

34 weeks or more , prompt delivery as soon as the maternal condition is

stabilised .

At 27 to 34 weeks , corticosteroid should be given to promote the fetal

lung maturity prior to delivery. Expectant management before 34 weeks

seems to be rational approach to increase fetal maturity and survival .There

is no clinical trials to compare with conservative management and immediate

delivery.The potential benefits have to be outweighed against the risks of

expectant management, which include abruption placentae, acute renal

failure, pulmonary edema DIC, perinatal and maternal morbidity and

mortality.Patients more than 34 weeks of gestational age may be induced

unless there is no other contraindication.Women have past history of HELLP

syndrome carry on increased risk of atleast 20% developing some form of

gestational hypertension in the future pregnancy.

ANTI HYPERTENSIVE THERAPY

A wide of variety drugs available with various modes of administration

.The most commonly used drugs are Labetalol, Nifedipine, Alpha methyl

dopa, and Hydralazine.Gradual and prompt reduction of blood pressure in

severe pre –eclampsia is warranted by administration of intermittent dosage of

drugs or by a continuous monitored infusion .Combination of drugs not

advisable because of their compound effect may lead to hypotensive episode.

Maintenance of Blood pressure at 140 to 160 mmhg systolic and 90 to 105 mhg

of Diastolic range during the treatment of hypertension in pregnancy .A

sudden decline of Blood pressure will compromise the uteroplacental flow

and thereby the fetus. The patient should be monitored for antihypertensive

effect of the drug and occurrence of adverse effect s in mother and the fetus.

The dosage to be monitored according to the response. Many studies

comparing the antihypertensive effect of Hydralazine with Labetalol in acute

blood pressure control.Hydralazine is associated with poor outcomes namely

increased caesarean sections , placental abruption , and fetal heart

abnormalities ,so the use of Hydralazine is not recommended . Many studies

show the efficacy and rapidity of action of oral and intravenous Labetalol in

mild to moderate hypertension and acute severe hypertension of pregnancy.

Use of intravenous Labetalol and oral nifedipine has found its place in the

Tertiary care protocol in the management of severe pre-eclampsia and

eclampsia in our India.

LABETALOL.

Labetalol is a alfa and beta adrenergic blocker. Chemical formulation

four sterioisomers With distinct action profiles on the receptor subtype. The

available commercial preparation is Racial mixture of two pairs of chiral

isomers. The ration of alfa to beta blockade is 1:7 following intravenous

administration .The systolic and diastolic fall in blood pressure is due to both

alfa 1 and beta1 blockade. Vasodilatation is due to beta2 weak agonistic

activity. The reduction in systemic vascular resistance with no change heart

rate and cardiac output is by alfa blockade. It reduces the Bood pressure

smoothly and rapidly. There is a decrease in cardiac index following both oral

and Intravenous administration .Labetalol is a category C drug .It crosses the

placenta small amounts secreted in the breast milk .Sibai in his study prefers

the use of Labetalol.The protocol by the NHBPEP Working group (2000) and

American College of Obstetricians and Gynaecologists (2002)Recommends

the usage of 20mg initial intravenous dose in the management of acute

severe hypertension in pregnancy.

The dose is doubled every ten minutes if there is no desired reduction

of blood pressure till the total dose infusion of 220mg per episode.The use of

20mg initial dose of labetalol is preferred since target concentration is reached

more rapidly.100% bioavailability following iv administration.Onset of action

following i.v is 2.5minutes .Peak action at 5minutes.Target concentration is

0.1mg/dl .Labetalol was about 50% plasma protein bound.T1/2 is

4.9hours.Metabolized in liver via conjugation to glucuronide metabolites.

Various studies conducted by Mabie and collegues12

and Vigil-De13

Gracia

and collegues high light the rapid action , better maternal and neonatal

outcomes and minimal side effect profile of intravenous labetalol in

comparison with hydralazine in antepartum and postpartum period

accordingly.Hydralazine needs lower dose to control but associated with higher

maternal and fetal adverse effects. Labetalol is a safe and effective

alternative drug ,when compared to Hydralazine.

ADVERSE EFFECTS.

Most common side effect is dizziness reported in 20% of the patients.

Nausea fatigue and light headedness .since postural hypotension is common

Left lateral position is advisable during Intravenous administration.

CONTRAINDICATIONS.

1] Patients with obstructive airway diseases including bronchial asthma

2] Cardiac failure and heart block

3] Impaired liver function

4] Diabetes mellitus and cardiac failure

The drug does not have any adverse impact on the maternal symptoms ,

neonatal outcome ,mode of Delivery ,and further complications disease per se.

NIFEDIPINE.

This drug was discovered as early as 1800 that calcium influx is an

essential part in smooth muscle contraction. L type calcium channel blockers

are used in various indications. Nifedipine , a prototype of dihydropyridine

group of calcium channel blocker12

has been studied for its utility in

hypertensive disorders of pregnancy. This drug has been used both in mild to

moderate hypertensive disorders of pregnancy and severe pre-eclampsia for

acute blood pressure control .Calcium channel had 4sub types of receptor ,

Nifedipine is said to block the α1 subtypes of receptor And thus reduce s the

transmembrane calcium current , thereby producing a long lasting smooth

muscle relaxation14

.

PHARMACOKINETICS OF NIFEDEPINE.

It has 45 t0 70% bioavailability .Metabolized in the liver.Onset of action

in 20 minutes .peak action in 0.5 to 1 hour.T1/2 is 4 hours duration is 4 to8

hours .excreted through renal 20% .No need for dose reduction in renal

disorders. Nifedipine effectively dilates the arterioles in preference to veins

thus producing an effective vasodilatation without producing postural

hypotension.It also reduces the total peripheral resistance so reduces the

afterload. It may produce inconsequential amount of reflex tachycardia. There

is a small increase in cardiac index . It has rapid onset of action by oral route.

The drug is available in immediate release, and extended release tablets and

capsules.The oral route provides an ease of administration without

compromising the efficacy. The site of absorption of oral Nifedipine is at the

duodenum and jejunum. The gastric emptying time of pregnant women is

found to be the same as in the non pregnant. However there is a delay in the

gastric emptying in labour most often due to the use of analgesics. The

elimination half life of Nifedipine is said to be shortened with pregnant women

implying a frequent dosing for a better Antihypertensive effect.so oral route of

administration is adequate enough to give a prompt onset of Action in the

Blood pressure control. Sublingual route is not recommended, since it produce

Rapid fall of blood pressure .

NICE guidelines recommends the use of oral nifedipine in blood

Pressure control in eclampsia and pre-eclampsia.The antihypertensive effect

was compared with Placebo in a trial by Ismail et al 15

. which shows that the

Mean arterial pressure was effectively reduced in nifidepine group and the

drug brought about the increased urine output because of vasodilatory effect.

This is a category C drug .The drug crosses the placenta. There in reported

change in the uteroplacental blood flow.About 5% of the drug secreted in

breast milk , producing little or no neonatal hypotension.

ADVERSE REACTIONS and CONTRAINDICATIONS.

a]Ankle edema 10 to 30%

b]Flushing 10 t0 20%

c]Dizziness25% Headache10 to 20%[34]

The only contraindication for this drug is hypersensitivity reactions.

Theoriticaly some interaction between magnesium sulphate has been

demonstrated.both the Drugs exhibit pharmacodynamic synergism when

administered together producing hypotension neuromuscular blockade and

warranted close monitoring. 16

Magpie trial involving 10141women with pre –

eclampsia had 3029 women with concominant magnesium sulphate and

ifidepine administration .There was no hypotension or neuromuscular blockade

reported in this study.

ALPHA METHYL DOPA.

Methyi dopa with an established long term safety, 17

is an effective drug

as a Monotherapy in mild to moderate hypertension reducing the progression to

severe Pre-eclampsia .This is not useful in severe hypertension.Mechanism of

action is by reduction of overall sympathetic flow. Onset of action is in 4 to 6

hours.It is metabolized in the liver and excreted through kidney.The most

common side effect is postural hypotension; excessive sedation and depression.

HYDRALAZINE.

It acts by direct peripheral vasodilatation.It was the drug of choice in

hypertensive Emergencies in the past. The onset of action is 10 to 20

minutes.It produces significant hypotension producing non reassuring fetal

cardiac status and fetal distress.18

DIAZOXIDE.

Diazoxide is a benzothiazine derivative that acts by direct vasodilataion

Producing arapid and long lasting effect.Since its usage is associated with

maternal cerebral Ischaemia , maternal death and fetal distress.Recently the use

of mini bolus doses of diazoxide Constituting 15mg has not associated with

profound maternal hypotension.

SODIUM NITROPRUSSIDE.

It has been used as a last resort in reducing high blood pressure. It acts

by release of nitric oxide .It has vasodilator effect. It has rapid onset of

action.Associated with rebound hypertension Cyanide toxicity is reported in the

fetus following its use.

NICARDIPINE.

A calcium channel blocker, nicardipine is evaluated as asecond line drug

antihypertensive agent in pregnancy. The drug needs monitoring for possible

renal shut down.

DIURETICS AND OTHER DRUGS.

Diuretics can compromise placental blood flow, 20

the usage is solely

limited to pulmonary edema. It reduces the already depleted intravascular

volume.19

FLUID MANAGEMENT.

Pre-eclampsia is intravascular fluid depleted condition .The knowledge

of fluid management comes from invasive hemodynamic monitoring in pre-

eclampsia and in compromised states such as pulmonary edema, cardiac

failure, and renal shut down. The state of volume depletion with decreased

cardiac output coupled with low oncotic pressure And capillary damage

predisposes to pulmonary edema. The condition is further deteriorated By the

injudicious use of volume expanders .The American College of Obstetrics and

gynaecologist recommends invasive hemodynamic monitoring in severe

cardiac diseases , renal disorders renal shut down, refractory hypertension and

pulmonary edema.Central venous pressure. Monitoring and Swan Ganz

catheter insertion provide information regarding right ventricular pressure

monitoring is validated in the correction of hypovolaemia prior to

antihypertensive therapy.

Crystalloids are recommended in comparison to 125ml per hour in

volume dpleted states. Swan Ganz catheter is useful in conditions like

pulmonary edema , uncontrolled hypertension ,Severe oliguria and multi organ

dysfuntion Both the procedure associated with risk of cardiac arrhythmias,

pulmonary infarction, and pulmonary haemorrhage.

ANASTHETIC CONSIDERATION.

General practice principles recommend early involvement of

anaesthetists in patients With pre –eclampsia the issues in consideration are

anaesthetic risk assessment control of blood Pressure, fluid management

,seizure prophylaxis and anasthetic or or analgesic considerations.

Patients with organ failure require high dependency setting .Epidural

anaesthesia serves as a good adjunct to vaginal delivery by improving the

renal and uteroplacental blood supply.

The drugs to be avoided are ergometrine ketamine and NSAIDS

.Regional anaesthesia is used in Preference to general anaesthesia.platelet count

of less than 50,000/cu.mm is a contraindication for regional anaesthesia .

POSTPARTUM MANAGEMENT.

Seizure prophylaxis should be considered for 24 hours post partum

period.Antihypertensives drugs should be continued in the post partum period

according to blood pressure .The dosage to the titrated according to the blood

pressure control.Fluid balance monitoring, evaluation of hepatic renal function

and neurological status is validated .Since preeclampsia Is a risk factor for

thrombosis ,throboprophylaxis is administered unless surgically

contraindicated. In hospital stay, obesity, nephritic range proteinuria and

operative delivery predispose to thrombosis.

FOLLOW UP.

Patients requiring medication for the control of blood pressure should be

frequently Reviewed .Since these patients are at an increased risk for adverse

cardiovascular events, They should be under surveillance.21

Preconception

counselling should be advised in the next pregnancy. Early onset severe

disease should be evaluated for the presence of Antiphospholipid . Antibody

syndrome and further screening for thrombophilia if indicated20

Contraceptive

advice Should also be provided.

ECLAMPSIA.

Eclampsia is defined as the development of seizures that cannot be

attributed to other Causes and unexplained coma during pregnancy or

puerperium in a women with pre-eclampsia.1 in 2000 deliveries in developed

countries21

, whereas the incidence in developing countries , varies from 1 in

100 to 1 in 1700 cases.Incidence and mortality and morbidity of maternal and

perinatal has come down because of better antenatal care.23

PATHOPHYSIOLOGY OF ECLAMPSIA.

Loss of cerebral vascular autoregulation lead to either overdilatation or

vasospasm. As part of the autoregulatory response to severe hypertension ,

cerebral vasoconstriction occurs which leads to ischaemia ,cytotoxic edema

and infarction. When the autoregulatory mechanism fails at some point ,

dilatation of vessels occurs resulting in hyper perfusion and vasogenic edema.

Autopsy studies showed edema, cortical and white matter microinfarcts

, pericapillary And parenchymal bleeding and vascular lesions predominantly

in the occipital and watershed Areas.

SYMTOMS AND SIGNS OF IMPENDING ECLAMPSIA.

1] Headache -Persistent occipital or Frontal

2]Visual disturbances - Blurred vision and photophobia

3Restless ness and Agitation

4Epigastric and or Right upper guardant pain

5]Nausea and vomiting

6]Oliguria

7]Laboratory evidence of disseminated intra vascular coagulation

CLINICAL COURSE OF ECLAMPSIA.

Stage of invasion:

(a)The patient become unconscious. There is twitching of muscles of the

face, tongue and limbs which lsats for about 30 seconds.

(b)Stage of contration: whole body goes into a tonic spasm . Cyanosis

appears .this last for about 30 seconds.

(c)Stage of convulsion: All voluntary muscles undergo alternate

contraction and Relaxation.Biting of the tongue occurs.This will last for 1 to 4

Minutes.

(d) Stage of coma: Following the convulsions , the patient passes on to

the stage of coma which usually lasts for a brief period.

DIFFERENTIAL DIAGNOSIS.

Epilepsy, Hysteria, Encephalitis, Meningitis, Puerperal cerebral

thrombosis, cerebral malaria in trophics, Cysticercosis , Intracranial tumour.

COMPLICATIONS OF ECLAMPSIA.

1]Maternal injuries

2]Placental abruption(10%)

3]Neurological deficit(7%)

4]Aspiration pneumonia(7%)

5]Pulmonary edema(5%)

6]Disseminated intravascular coagulation(3%)

7]Cardio pulmonary arrest(5%)

8]HELLP syndrome(4%)

9]Acute renal failure(4%)

10]Maternal death(1%)

FETAL COMPLICATIONS

The perinatal morbidity and mortality rate is very high to the extent of

about 30 to 50%.24

THE CAUSES ARE;

1]IUGR due to chronic placental insufficiency

2]Prematurity either spontaneous or induced.

3]Intra uterine asphyxia

4]Effects of the drugs used to control convulsions.

5]Increased operative deliveries.

GENERAL MANAGEMENT.

It plays on important role in the management of eclampsia. The patient

is nursed in a quiet room with a medical or nursing attendant always present .

Pulse rate, respiration, blood pressure , oxygen saturation, restlessness, urine

output, must be constantly observed . A mouth gag , airway ,and O2 must be

available .Patient is put in left lateral position in a railed cot .Throat is cleared

of secretions and vomitus by intermittent suctioning .A soft firm mouth gag

introduced in time will save injury to the Tongue. An indwelling catheter in

the bladder will give an accurate assessment of the urine output and will also

prevent restlessness due to a full bladder.Blood pressure is measured half

hourly till it is controlled and then second hourly .A record of grade of

consciousness is maintained.Nutrition and hydration are maintained

parenterally.

MEDICAL MANAGEMENT.

ANTICONVULSANT THERAPY.

The drug of choice for control and prevention of convulsions is

magnesium sulphate. PRITCHARD’S Regime.This has been conclusively

proven by the collaborative eclampsia trial in 1995.which was large

multicenteric trials comparing magnesium sulphate and phenytoin in

eclampsia.Previously used anticonvulsants for eclampsia include Krishna

Menon’s regime (lytic cocktail of pethidine chlorpromazine and Phenergan)

phenytoin sodium ,and diazepam.

MAGNESIUM SULPHATE(Mgso4).

In 1955 , Pritchard initiated a standardized treatment regimen at

Parkland hospital. In 1964 , Zuspan initiated the intravenous magnesium

sulphate regimen.

PHARMACOKINETICS OF MAGNESIUM SULPHATE.

Magnesium sulphate USP is Mgso4 .7H2O. Molecular weight about

24.3 1gm of magnesium sulphate has 98mg of elemental magnesium.

DISTRIBUTION AND PLASMA LEVELS.

40% of plasma magnesium is protein bound . Un bound magnesium ion

diffuses into the extra vascular , extracellular space , into bone and across the

placenta and fetal membrane and into the fetus and amniotic fluid . In pregnant

women , apparent volumes of distribution usually reach constant values

between the third and fourth hour after administration.

EXCRETION.

Magnesium is excreted by the kidneys. 50% of the infused dose is

excreted after 4 hours in urine .90% of the bolus intravenous dose is excreted

within 24 hours.

MECHANISM OF ACTION.

Mainly peripheral at the neuromuscular junction with minimal central

effects. Calcium entry into the neurons is regulated by specific excitatory

amino acid linked channels like L _ glutamate and L _ aspartate are the major

neurotransmitters in mammalian central nervous system.NMDA receptor has

its channel blocked by magnesium ion and thus blocking the calcium influx.

Magnesium sulphate is a potent vasodilator especially in cerebral vasculature

thus relieving cerebral vasospasm which is thought to be a cause for

eclampsia.

OTHER ACTIONS .

Increased uterine bood flow

Vasodilatation in vascular beds

Increased prostacyclin release by endothelial cells

Increased renal blood flow

Bronchodilatation

Attenuation of vascular response to pressor substances

Decreased angiotensin converting enzyme levels

Decreased plasma renin activity

Reduced platelet aggregation

PHARMACOLOGICAL EFFECTS .

Mild decrease in frequency of uterine contractions , no change in

the intensity of contractions.

Anticonvulsant action

Transient hypotensive action

No change in long term variability of fetal heart rate or fetal heart

rate acclerations.

Insignificant decrease in short term variability of fetal heart rate.

Duley et al .(1995 ) in his study he proved clinical evaluation alone is

enough , there is no need to check the serum magnesium levels routinely

PRITCHARD REGIMEN 33

Loading dose Maintenance Dose

4gm of 20% Mgso4 IV at a rate not

exceeding

1gm /minute

Every 4 hours there after , 5gm of

50%Mgso4 as

IM on alternate buttocks after ensuring

10gm of 50% Mgso4 as deep IM ,

5gm in each buttock through a 3inch

long _20 gauge needle

a)Patellar reflex is present

b)Respiration rate >16/minute

c)urine output >100ml in the

preceding 4 hours.

IF convulsions persists after 15 minutes ,2gm of Mgso4 IV is given at

a rate not exceeding 1gm/minute.Mgso4 is continued for 24 hours after

delivery or the last episode of convulsion Whichever is later.

Monitoring to be done .If there is any abnormality urine output less than

30ml/min or there is any abnormality in respiratory rate and patellar reflex

the next dose to be skipped. Loading dose. To be given to all cases irrespective

of urine output. If patellar reflex absent the blood level of Magnesium

sulphate is about 10MEq/L.IF there is respiratory arrest the level of Magnesium

sulphate is about 12MEq/L. The therapeutic range is about 4 to 8MEq/L. This

is the narrow therapeutic index drug.So close monitoring is needed.

TREATMENT FOR MAGNESIUM TOXICITY.

If there is magnesium toxicity respiratory depression will occur. In that

case infusion Should be discontinued.O2 should be given and 10ml of 10%

calcium gluconate to be given. If respiratory arrest cardio pulmonary

resuscitation should be started and the patient should be intubated. Recurrent

seizures. Further bolus of 2g magnesium sulphate to be considered.Midazolam

or lorazepam may be given.

FETAL EFFECTS OF MAGNESIUM.

Neonatal depression will occur it may be clinically insignificant. Beat to

beat variability may occur. Magnesium sulphate have a protective effect

against cerebral palsy in very low birth weight infants.

ABSOLUTE CONTRAINDICATIONS.

1]Myasthenia gravis

2]Recent myocardial infarction.

ANTIHYPERTENSIVE AND FLUID MANAGEMENT.

Like pre –eclampsia the antihypertensive drug should be given

according to blood Pressure. Strict fluid intake and output chart to be

maintained because these patients are more Prone for pulmonary edema.

OBSTETRIC MANAGEMENT.

Immediate termination of pregnancy after controlling of seizures and

stabilization of the patients. Principles of obstetric management and

postnatal care will be the same like pre-eclampsia There is contraindication for

vaginal delivery, delivery is not within 6 to 8 hours of induction from the

clampsia caesaerean section to be considered. The anaesthetist should be

informed about the magnesium sulphate and this drug should be continued

throughout labour and 24hours postpartum or occurrence of fits whichever is

later.

STATUS ECLAMPTICUS.

In these cases , Midazolam , lorazepam , or even Thiopentone sodium

may be given under supervision of anaesthetist. If it persist even after the

above measurement patient may be intubated and connected to ventilator in

intensive care unit.

MATERIALS AND

METHODS

MATERIALS AND METHODS

METHODS

This is a prospective observational study done from August 2013 to

August 2015 (22 months) at K.A.P.V. Medical College &

M.G.M.GOVERNMENT HOSPITAL, Tiruchirapalli . It consists of analysis

of maternal and fetal outcome in preeclampsia. pregnant women with more

than 20 weeks of pregnancy with systolic B.P >140 mmHg & diastolic

>90mmHg in two separate readings taken 6 hrs apart. any patient fulfilling the

inclusion criteria to be explained the type of study and after taking her

writtenconsent patients were assessed on the basis of history, clinical

examination, ultra sound & laboratory investigations were done according to

the severity of pre eclampsia

INCLUSION CRITERIA :

(i) BP Systolic >140mmHg and diastolic >90mmHg

(ii) Urine albumin>1+ on dipstick single test

(iii) Edema may or may not be present

EXCLUSION CRITERIA :

(i) Chronic hypertension diagnosed before 20 weeks of gestations,

(ii) Patients Having hepatitis

(iii) Heart disease

(iv) DM

(v) Reno vascular HT

(vi) Cushing syndrome

(vii) Pheochromocytoma

(viii) Thyrotoxicosis

(ix) SLE

(x) Glomerulonephritis

PROTOCOL

Patients having mild PE, with gestation age group >37 weeks were

induced & delivered, and <37 weeks were advised in patient or out patients

according to their Bloood pressure. Severe pre eclampsia patients were

admitted to hospital . Within 1st 24 hours of admissions all patients with GA

<34 wks should be received 2 doses of beta methasone 12 mg each 24 hrs

apart.noted and any NICU admissions indications and duration of admission

were recorded.

DATA COLLECTION AND METHODS

Detailed history is taken. Clinical evaluation of the patient is done.

Investigations are recorded. Patients with imminent ecclampsia should be

received mgso4 prophylactically as per criteria laid down in MAGPIE trial and

were intensively monitored. For Hypertension labetalol, nifedepine were

commonly used , dose was adjusted according to the severity of hypertension.

Monitoring to be done depending on severity and Gestational age. Mode of

termination depends on the periods of gestation, favourability of cervix &

urgency of termination. Fetal outcome assessed by APGAR SCORE at birth.

In preeclampsia. To study the prevalence of preeclampsia in relation to

A) Unregistered or registered age &parity

B) To study the incidence of various maternal complication of

preeclampsia.

C) To study the fetal outcome in pregnancies complicated by

preeclampsia

RESULTS AND

ANALYSIS

RESULTS AND ANALYSIS

OBSTETRIC-CODE

CATEGORY FREQUENCY

Primi 46

Multi 54

Total 100

In our study group 46 members belongs to Primi gravida

and 54 members belongs to Multi gravid.

*These cases are referal from Periphery

46

54

42

44

46

48

50

52

54

56

Primi Multi

Obstetric _ code

BOOKING STATUS

CATEGORY FREQUENCY

No 9

Yes 91

Total 100

In this study 9 were unbooked and 91 were booked.

9

91

0

10

20

30

40

50

60

70

80

90

100

No Yes

Booking status

HYPERTENSION- STATUS

CATEGORY FREQUENCY

Severe 32

Mild 68

Total 100

In this study 32 were severe hypertensive and 68 were mild

hypertensive.

32

68

0

10

20

30

40

50

60

70

80

Severe Mild

Hypertension_ status

ANTI HYPERTENSIVE DRUGS

CATEGORY FREQUENCY

No anti

hypertensive 6

Labetalol 64

Nifedipine 9

Combined 21

Total 100

IN our study 64 patients were on labetalol ,9 patients were on

nifedipine,21 patients on both drugs,

6 patients not started any drugs.

6

64

9

21

0

10

20

30

40

50

60

70

No anti hypertensive

Labetalol Nifedipine Combined

ANTI HYPERTENSIVE DRUGS

"LFT" AND "RFT" RESULTS

RESULTS LIVER FUNCTION

TEST

RENAL FUNCTION

TEST

Increased 29 17

Normal 71 83

Total 100 100

29% of patients had increased liver function test values and 17%

patients had renal function test values.71% of patients had normal liver

function tests,83% of patients had normal renal function tests.

29

17

71

83

0

10

20

30

40

50

60

70

80

90

LIVER FUNCTION TEST

RENAL FUNCTION TEST

Increased

Normal

"LFT & RFT " Results

CATEGORY FREQUENCY

Labour Natural 55

LSCS

Maternal Indication 30

Fetal Indication 15

Total 100

In our study 55% patients had labour natural,45% patients had lscs

among them 30% were maternal indication,15% were fetal indication.

LABOUR CATEGORY

55

30

15

0

10

20

30

40

50

60

Maternal Indication Fetal Indication

Labour Natural LSCS

ECLAMPSIA

CATEGORY FREQUENCY %

No 85 85.00

Antepartum 8 8.00

Intrapartum 3 3.00

Postpartum 4 4.00

Total 100 100

In our study in 100 patients 15 patients were developed eclampsia among them

8 patients were developed antepartum eclampsia&3 patients were developed

intrapartum& 4 patients developed Postpartum eclampsia.

85

8

3 4

0

10

20

30

40

50

60

70

80

90

No Antepartum Intrapartum Postpartum

ECLAMPSIA

ABRUPTION ,HELLP,CVT

CATEGORY

FREQUENCY

%

PRESENT ABSENT

Abruption 14 86 100

Hellp 15 85 100

CVT 10 90 100

Among 100% patients 14% were developed abruption,15% patients

developed HELLP,10% patients were developed CVT.

14 15

10

86 85

90

0

10

20

30

40

50

60

70

80

90

100

Abruption Hellp CVT

FREQUENCY PRESENT

FREQUENCY ABSENT

ABRUPTION HELLP CVT

RENAL FAILURE ,PULMONARY EDEMA & MATERNAL DEATH

CATEGORY

FREQUENCY

%

PRESENT ABSENT

Renal failure 8 92 100

Pulmonary Edema 13 87 100

Maternal death 2 98 100

8 % OF patients were developed renal failure,13% of patients were

developed pulmonary edema.2 % of patients were died and they were belongs

to severe preeclampsia category.

813

2

9287

98

0

20

40

60

80

100

120

Renal failure Pulmonary Edema Maternal death

FREQUENCY PRESENT

FREQUENCY ABSENT

RENAL FAILURE PAULMONARY EDEMA& MATERNAL DEATH

APGAR - NEW BORN AT 1 MINUTE

CATEGORY FREQUENCY

1[0 >3] 5

2[3 to5] 36

3[more than 6] 59

Total 100

APGAR new born at one minute,5%were under 0-3 ,36% were under3-

5,59% were under>6.

0

10

20

30

40

50

60

70

1[0 >3] 2[3 to5] 3[more than 6]

APGAR -NEW BORN AT 1MINUTE

PERINATAL OUTCOME

CATEGORY FREQUENCY %

NICU Admission 49 49

IUGR 20 20

IUD 3 3

Neonatal death 7 7

Normal Neonates 21 21

49% of new born admitted in NICU,20% of developed IUGR,3% died

inutero,7% died in neonatal period.

PERINATAL OUTCOME

49

20

3

7

21

0

10

20

30

40

50

60

NICU Admission IUGR IUD Neonatal death Normal Neonates

BOOKING STATUS vs ABRUPTION

Abruption %

Statistical

significance

Present Absent

No 4 5 9

0.006

44.40% 55.60% 100.00%

Yes 10 81 91

11.00% 89.00% 100.00%

Total 14 86 100

14.00% 86.00% 100.00%

9% were unbooked &91 were booked.P Value in this study is 0.006

which is highly significant.44.4% of unbooked cases developed Abruption.

4

44

.40

% 10

11

.00

%

14

14

.00

%

5

55

.60

%

81

89

.00

%

86

86

.00

%9

10

0.0

0%

91

10

0.0

0%

10

0

10

0.0

0%

0

20

40

60

80

100

120

No Yes Total

Abruption Present

Abruption Absent

%

BOOKING STATUS VS ABRUPTION

HYPERTENSION STATUS vs ECLAMPSIA

Hyper tension status Eclampsia

Absent Antepartum Intrapartum Postpartum

Severe 21

65.60%

7

21.90%

1

3.10%

3

9.40%

Mild 64

94.10%

1

1.50%

2

2.90%

1

1.50%

Total 85

85.00%

8

8.00%

3

3.00%

4

4.00%

Statistical

significance 0.001

In this study 32 patients were severe preeclamptic&68 patients were mild

preeclamptic.P Value between this group is 0.001 which is highly

significant.21.9% of severe preeclamptic group developed antepartum

eclampsia,94.1%of mild preeclamptic patients not developed any type of

eclampsia.so severity of hypertension highly influence the occurance of

eclampsia.

21

65

.60

%

64

94

.10

%

85

85

.00

%

7

21

.90

%

1 1.5

0% 8

8.0

0%

1 3.1

0%

2 2.9

0%

3

3.0

0%

3

9.4

0%

1 1.5

0%

4

4.0

0%

05

1015202530354045505560657075808590

1 2 3 4 5 6

Hyper tension status

Eclampsia Absent

Eclampsia Antepartum

Eclampsia Intrapartum

Eclampsia Postpartum

HYPERTENSION STATUS vs ECLAMPSIA

URINE ANALYSIS vs ABRUPTION

Category Abruption

% Present Absent

Nil 1 22 23

Trace 1 24 25

1+ 6 33 39

2+ 5 6 11

3+ 1 1 2

Total 14 86 100

Statistical significance 0.004

23% of patients with no proteinuria among them only 1% developed

abruption .Among 77%of patients with proteinuria 13% of patients developed

abruption.P value is highly significant.so proteinuria significantly differs

between this two groups.So severity of proteinuria significantly correlates with

occurrence of abruption.

1 1

6

5

1

22

24

33

6

1

0

5

10

15

20

25

30

35

Nil Trace 1+ 2+ 3+

Abruption Present

Abruption Absent

URINE ANALYSIS VS ABRUPTION

URINE ANALYSIS vs HELLP

Category Hellp

% Present Absent

Nil 2 21 23

Trace 2 23 25

1+ 3 36 39

2+ 6 5 11

3+ 2 0 2

Total 15 85 100

Statistical significance 0.000

Among 23% of patients with no proteinuria 2% developed HELLP.

Among 77% of patients with proteinuria 13% developed HELLP.P value in this

study is 0.000 which is highly significant. So severity of proteinuria has

significant impact on occurance of HELLP.

2 2

3

6

2

21

23

36

5

0

0

5

10

15

20

25

30

35

40

Nil Trace 1+ 2+ 3+

Hellp Present

Hellp Absent

URINE ANALYSIS VS HELLP

OBSTETRIC CODE vs COMPLICATION

Abruption %

Statistical

significance

Hellp %

Statistical

significance Present Absent Present Absent

Primigravida 5 41 46

0.405

3 43 46

0.028

10.90% 89.10% 100.00% 6.50% 93.50% 100.00%

Multigravida 5 45 54 12 42 54

10.90% 83.30% 100.00% 22.20% 77.80% 100.00%

Total 14 86 100 15 85 100

14.00% 86.00% 100.00% 14.00% 86.00% 100.00%

In comparison of parity and the occurance of abruption and HELLP ,P value is 0.4,which is not significant. 10.9 % of the

multi gravida developed abruption. 22.2 % of muti gravida developed HELLP.

5

10

.90

%

5

10

.90

%

14

14

.00

%

41

89

.10

%

45

83

.30

%

86

86

.00

%

46

10

0.0

0%

54

10

0.0

0%

10

0

10

0.0

0%

0

20

40

60

80

100

120

Abruption Present

Abruption Absent

%

OBSTETRIC CODE VS ABRUPTION

OBSTETRIC CODE vs HELLP

DISCUSSION

DISCUSSION

Pre-eclampsia is more prevalent in both developed and developing

countries contributing to maternal and and perinatal morbidity and mortality. It

will produce maternal syndrome.It includes Hypertension , proteinuria and

with or without edema.Fetal syndrome includes fetal growth restriction,reduced

amniotic fluid,and abnormal placentation.OUT of 100 cases 32 cases were

severe and 68 cases were mild pre –celampsia.Some patients had irregular

antenatal check up and followup. This is the reason why incidence of pre

eclampsia and related complications more in developing countries . In our

study 9% cases were unbooked and 91%of patients were booked .

Unbooked cases were developed more complication than booked cases. Study

cases are referral cases from the periphery.

In the study age < 20years 9 cases among them 3 cases had

eclampsia, and age 20 to 29 83 cases among them 10 patients had

eclampsia , and age more than 30 years 8 cases among them 2cases were

developed eclampsia .Similar incidence was found in SIBAI BH IN 1997.

Least incidence was found in age group above 30 years.It positively correlates

with vitthal Kulchake study in 2010. Out of 100 cases 46 patients were

primigravida, and 54 patients were multigravida.26

Urinary proteins are directly

correlates with severity of pre eclampsia .urinary protein also correlates with

severity of Maternal morbidity like onset of HELLP syndrome, and

abruptioplacenta. In our study 29% percentage of patients had

elevated liver enzymes and 71% of patients had normal liver parameter.17%

of patients had altered [elevated liver parameters]and 83% patients had normal

renal function. Out of 100 patients 54 patients had labour natural, 44 patients

had lscs. 1patient Had hystrotomy.Among lscs 30% had maternal indications

like mal presentation ,cephalo pelvic Disproportion and failure of

induction .15% had lscs because of fetal indications like fetal distress, Intra

uterine growth restriction.27

ECLAMPSIA.

Eclampsia is the preventable condition31

by means of regular ante natal

visits and control of Blood pressure.Eclampsia means flashes of light.It may

develop antepartum , intrapartum And postpartum. Postpartum eclampsia

unlikely to be after 4 days, but it may occur up to 6 weeks Postnatally.Out of

100 patients 85% patients didn’t had eclampsia episode. 8% had ante partum

Eclampsia, 3% had intrapartum eclampsia, and 4% patients had post partum

eclampsia. 5 patients belongs to primigravida and 10 patients belongs to

multigravida. Abruption is the one the dreadful complications of servere pre-

celampsia.14% of patients had Abruption.booking status had highly significant

relation with abruption .Among 9patients of Unbooked 4 had {44.4% }

developed abruption. Abruption strongly correlates with severity of

preeclampsia and severity of urine proteinuria.

A study done by Conde Agadelo A, 2000 and Noreen Akmal and Gul

E , Raanian 2006 revealed urinary protein levels are directly related to

severity of preeclampsia , in turn increase the morbidity and mortality. In this

study among 23% of patients with no proteinuria 2% were developed HELLP

among 77% of patients with proteinuria 13% developed HELLP.P value in

this study is 0.000. which is highly significant.so severity of proteinuria has

significant impact on Occurance of HELLP syndrome.

Mode of delivery depends on the severity of the disease .Induced

vaginal delivaries were higher in severe preeclampsia. Similar study by

Vitthal kuchake deliveries by caesarean section were around 61% . In this

study caesarean section rate was 45% . labour by induction by various

methods were about 55%.Incidence of maternal mortality 1% a study

conducted by who in2002. In this study the maternal mortality was 2% . , and

they were belong to severe preeclampsia and multigravida and they had

Irregular antenatal visit.

Acute renal failure. Study of maternal and fetal outcomes in pregnancy

induced hypertension A Hospital based study by Dr.D.P . Meshram ARF was

found in only 2 cases of preeclampsia .No case was found in

eclampsia.incidence found to be 2.2%. In this study 8%developed renal

failure. 2% were irreversible belongs to severe preeclampsia. 6% were

recovered from renal failure later.Leduc et al 1n 1992 reported significant

association between Thrombocytopenia and maternal complications and

reported that platelet nadir is the best predictor of maternal outcome. . 20%

had reduced platelet count In this study 15% patients developed HELLP. 80%

were normal platelet count.

Comparing the APGAR score at 1minute and severity of disease

there was statistically significant correlation .Study done by Odegard et al

showed pregnancies complicated by severe preeclampsia had infant birth

weight less than 12% lower than expected .

Doppler study, Study done by Sulthana and Aparna J, on Risk factors

for preeclampsia and its perinatal outcome28

showed increased resistance on

Doppler in 10 cases of preeclampsia when compared to without any high risk

cases. This data shows significance of abnormal Doppler finding sin relation to

perinatal morbidity and mortality in preeclampsia and need for early

termination of pregnancy in high risk cases managed through abnormal

Doppler. In this study Doppler abnormalities were found in 26 cases and those

cases were strictly followed and delivered accordingly.

IUGR29

babies were more common in severe Preeclampsia .study by

Attiya Ayaz, Taj Muhammad, neonatal outcome in preeclamptic patients

IUGR were about 10% .

APGAR new born at one minute,5%were under 0-3 ,36% were under3-

5,59% were under>6 49% of new born admitted in NICU,20% of developed

IUGR,3% died inutero,7% died in neonatal32

period. Main factor determining

the perinatal mortality was the lack of regular antenatal checkups,

complicated caes of preeclampsia and lack of awareness regarding significance

of symptoms like decreased fetal movements and late arrival at hospital, all

contributing to stillbirth and Intra uterine death and early neonatal death.

SUMMARY

SUMMARY

In this study, 46 were primi gravida and 54 were multi gravid In this

study 9 were unbooked and 91 were booked.In this study 32 were severe

hypertensive and 68 were mild hypertensive IN our study 64 patients were on

labetalol ,9 patients were on nifedipine,21 patients on both drugs,6 patients not

started any drugs In this study,29% of patients had increased liver function test

values and 17% patient had renal function test values.71% of patients had

normal liver function tests,83% of patients had normal renal function tests. In

our study 55% patients had labour natural,45% patients had lscs among them

30% were maternal indication,15% were fetal indication In our study in 100

patients 15 patients were developed eclampsia among them 8 patients Were

developed antepartum eclampsia&3 patients were developed intrapartum& 4

patients developed Postpartum eclampsia.

Among 100% patients 14% were developed abruption,15% patients

developed HELLP,10% patients were developed CVT.8 % OF patients were

developed renal failure,13% of patients were developed pulmonary edema.2 %

of patients were died and they were belongs to severe preeclampsia category.

APGAR new born at one minute,5%were under 0-3 ,36% were under3-

5,59% were under>6 49% of new born admitted in NICU,20% of developed

IUGR,3% died inutero,7% died in neonatal period 9% were unbooked &91

were booked.P Value in this study is 0.006 which is highly significant.44.4% of

unbooked cases developed Abruption.In this study 32 patients were severe

preeclamptic&68 patients were mild preeclamptic. P Value between this group

is 0.001 which is highly significant.21.9% of severe preeclamptic group

developed antepartum eclampsia,94.1%of mild preeclamptic patients not

developed any type of eclampsia.so severety of preeclampsia highly influence

the occurance of eclampsia. 23% of patients with no proteinuria among them

only 1% developed abruption .

Among 77%of patients with proteinuria 13% of patients developed

abruption.P value is highly significant.so proteinuria significantly differs

between this two groups Among 23% of patients with no proteinuria 2%

developed HELLP. Among 77% of patients with proteinuria 13% developed

HELLP.P value in this study is 0.000 which is highly significant. So severity of

proteinuria has significant impact on occurance of HELLP.

In comparison of parity and the occurance of abruption and HELLP ,P

value is 0.4,which is not significant. 10.9 % of the multi gravida developed

abruption. 22.2 % of muti gravida developed HELLP.

CONCLUSION

CONCLUSION

Life threatening complications like Eclampsia , Abruption, HELLP,

DIC, and pulmonary edema were more common in unbooked and Severe

preeclampsia category. 2% Maternal death occured in multigravida and

severe preeclampsia. Preterm deliveries and IUGR, more common in severe

pre eclampsia cases.The natural course of preeclampsia is blocked at the

secondary and tertiary levels of prevention.while early detection and prevention

of occurrence of the disease per se is called for,the allying of the severity of the

disease and thereby reducing the complications prompt the mainstay in the

present times.

The morbidity and mortality of the preeclamptic mother and the neonate

is considerably reduced with effective management. Evidence based practice

and setting up of a protocol in the management of acute onset ,severe

hypertension in preeclampsia and eclampsia bring about an immense

encouraging outcome.

BIBLIOGRAPHY

BIBLIOGRAPHY

1) Zweifel P. Eklampsiein: Dorlain A (ed) Handbuch Der Gerburtshilfe,

ii Wiesbandin; Bergman 1916;672-676

2) Cunningham F ,Leveno KJ, Bloom SL ,Hauth JC ,Rouse DJ ,Spong CY.

Pregnancy hypertension. In: Dashe JS ,Hoffman BL,editors. Williams

Obstetrics.23 rd ed .NewYork: McGraw-Hill.2010.706-7.

3) Mabie WC , Gonalez AR, Sibai BM, et al .Acomparative trial of

labetalol and hydralazine in the management Of severe hypertension

complicating pregnancy .Obstet Gynecol. 1987;70

4) Gant NF, ChandS, Worley RJ, et al .Aclinical test useful for predicting

the development of acute hypertension in pregnancy.AM J Obstet

Gynaecol. 1974:120.

5) Lam ,Chun, Kee hak Lim and S.Ananth Karumanchi.Circulating

angiogenic factors in the pathogenesis and prediction of

preeclampsia.Hypertension 2005;46.5:1077-85.

6) Morris NH: Nitric oxide, the endothelium pregnancy and preeclampsia

7) Br J Obstet Gynecol 166:224,1992. Moffett king , Ashley. Natural

killer cells and pregnancy .Nature Reviews immunology.2002:2. 9 656

_63

8) Martin Jr,J.N..,Rinehart, B.K.,May. W .L., Magann, E . F., Terrone, D

.A.,& Blake. P.G. The spectrum of severe preeclampsia: comparative

analysis by HELLP(hemolysis,elevated liver enzymes levels and low

platelet count)syndrome classification.American journal of obstetrics

and gynaecology.1999;180.6:1373-84.

9) Port, J. D., Beauchamp, N. J. Reversible intracerebral pathologic entities

mediated by vascular autoregulatory dysfunction. Radiographics.

1998;18.2:353-67 National Institute of Health and Clinical

Excellence. Hypertension in pregnancy. Clinical guidelines CG107

Issued: August 2010.

10) Sibai, BM. Diagnosis and management of gestational hypertension

and preeclampsia. Obstetrics & Gynaecology.2003;102.1:181-92.

11) Sibai, B.M., Mercer, B.M., Schiff, E., & Friedman, S. A. Aggressive

versus expectant management of severe preeclampsia at 28 to 32 weeks

gestation:a randomized controlled trial. American journal of obstetrics

and gynaecology.1994;171(3):818-22.

12) Mabie WC , Gonalez AR, Sibai BM, et al .Acomparative trial of

labetalol and hydralazine in the management Of severe hypertension

complicating pregnancy .Obstet Gynecol. 1987;70:328

13) Vigil -De Gracia P, Ruiz E, Lopez JC, et al .management of severe

hypertension in the postpartum Period with intravenous hydralazine or

labetalol :A randomized clinical trial. Hypertens pregnancy .2007

;26(2);163.

14) Katzung B, Barton JR, SherifAKL, SarinogluC, MercerBM,

.Arandomized prospective comparison of nifedipine And bed rest versus

bed rest alone in the management of preeclampsia remote from term .

1992 ;/167:879 _884

15) Ismail AA, Medhat I , Tawfic TA , Kholeif A , Evaluation of calcium

antagonist s (nifedipine) in the management of preeclampsia. Snyder

SW, Cardwell MS, Neuromuscular blockade with magnesium sulphate

and nifedipine Am J Obstet Gynecol 1987 ;/161:35 -36.

16) Cockburn J , Moar V.A , Ounstead M, Redman CWG. Final report of

study on hypertension during pregnancy . Lancet. 1982 :I 647 -9

17) Report of the National High Blood Pressure Education Program

Working Group on High Blood pressure In Pregnancy. Am J Obstet

AND Gynaecol .Jul 2000;183 (1)S1_ S22.

18) Zeeman GG, Cunningham FG, Pritchard JA;The magnitude of

haemoconcentration with eclampsia. Hypertens pregnancy 2009 :28

(2):127.

19) De Groot C.J. B loemenkamp , K. W. , Duvekot , E. J . H

elmerhorst, F .M Bertina , R. M . Oei , S , Rosendaal , F. R .

Preeclampsia and genetic risk factors for thrombosis; Case control sudy

American journal Of obstetrics and gynaecology . 1999; 181(4):975 -

80.

20) Cotton DB, Hallak M. Central anticonvulsant effect of Magnesium

sulphate on N- Methyl D aspartate induced seizures AM J Obstet

Gynaecol 1993 :168 :974 -8

21) Du1. Zweifel P. Eklampsiein: Dorlain A(ed) Handbuch der

Gerburtshilfe,ii Wiesbandin: Bergman 1916:672-676.

22) World Health Organization. Global Program to Conquer

Preeclampsia/Eclampsia.2002.

23) Dolcea C. AbouZahr C. Global burden of hypertensive disorders of

pregnancy in year 2002. In: Global Burden of Diseases;2000; World

Health Organisation.

24) Shah A, Fawole B, M’ Imunya JM, et al. Cesarean delivery outcomes

from the WHO global survey onmaternal and perinatal health in.

25) Africa. International Journal of Gynecology and Obstetrics.

2009;107(3): 191-197.

26) MoodleyJ.South Africa Med.j.CME-1991;9:72. XXVIII. Sibai BH,

Ewel m, et al, Risk factors associated with preeclampsia in healthy

multiparous women, AM. J.Obstetrics and Gynaecology 1997;177:1003.

27) Vitthal et al.,IJPSR, 2010;vol.1(11):74-82.

28) Voto LS, Illia R, Darbon-Grosso HA, Imaz FU, Margulies M. Uric Acid

levels: a useful index of the severity of preeclampsia and perinatal

prognosis. JPerinat Med. 1988;16:123-6.

29) C lam et al uric acid and preeclampsia 25:56 60 2005(cum lam).

30) R. A. Odegard, L. J. Vatten, S.T. Nilsen, K.A. Salvesen, and R.

Austgulen, ―Preeclampsia and fetal growth,‖ Obstetrics and

Gynecology, Vol. 96,no. 6, pp.950-955, 2000.

31) World Health Organisation. Global Program to conquer

Preeclampsia/Eclampsia.2002.

32) L.L. Simpson, ―Maternal medical disease: risk of antepartum fetal

death,‖ Seminars in Perinataologyley DB, Berman EF , anticonvulsant

effect of Magnesium sulphate on Hippocampal seizures :Am , J Obstet

Gynaecol 1992 :166; 1127—36 .

APPENDIX

PROFORMA

PROFORMA

MATERNAL AND PERINATAL OUTCOME IN PREECLAMPSIA

NAME: AGE: IP NO:

HUSBAND NAME: GRAVIDA: PARA:

MISCARRIAGE:

BOOKED/UNBOOKED:

PRESENTING COMPLAINTS:

MENSTRUAL HISTORY:

MARITAL HISTORY: OBSTETRICAL HISTORY:

LMP EDC

PAST SURICAL HISTORY: PAST MEDICAL HISTORY:

FAMILY HISTORY: PERSONAL HISTORY:

SOCIO-ECONOMIC HISTORY

GENERAL EXAMINATION:

BUILT : SENSORIUM: ANEMIA: ICTERUS:

EDEMA : BMI:

TEMPERATURE : PULSE : BP : RR :

SYSTEMIC EXAMINATION: CVS: RS: CNS:

OBSTETRICAL EXAMINATION:

Fundal height:

Acting

Presenting part

FETAL HEART SOUND

ESTIMATED FETAL WEIGHT:

PELVIC EXAMINATION:

ADMISSION CTG:

DIAGNOSIS:

INVESTIGATIONS: Urine albumin: Hb%: Blood Group and Rh typing :

Others :

Serum uric acid: clotting time: platelet count:

24hrs urine protein: RFT: LFT:

Fundus examination:

ULTRASOUND :

Previous USG

Malformation

AFI

LABOUR:

Induced / Spontaneous :

Induction-Delivery interval:

Appearance of amniotic fluid: Clear / Thick Meconium / Thin Meconium

Intrapartum CTG:

MATERNAL OUTCOME:

Mode of delivery:

Delivery notes:

Operative Notes:

Indication for LSCS:

Post op complications:

FETAL OUTCOME:

Apgar score : 1 min 5min

Birth weight :

Admission to neonatal ward:

Maternal morbidity :

Maternal mortality:

Perinatal morbidity:

Perinatal mortality :

MASTERCHART

CONSENT

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ABBREVIATIONS

ABBREVIATIONS

BMI : Body mass index.

Baby wt : Baby weight.

CPD : Cephalo pelvic disproportion.

DIC : Disseminated intra vascular coagulation.

F/D : Fetal distress

F/I : Failed induction.

Gel : Cerviprime gel.

IUGR : Intra uterine growth restriction.

IUD : Intra uterine death.

MSAF : Meconium stained amniotic fluid.

Nife : Nifedipine.

NICU : Neonatal intensive care unit

PROM : Premature rupture of membrane.

Pre lscs : Previous lower segment caesarean section.

RF : Renal failure.

RFT : Renal function test.

SSM : Sweeping and stipping of membrane.

SYS bp : Systolic blood pressure.

24 Hours UP : 24 H ours urine protein.

CVT : Cortical vein thrombosis.

DIA BP : Diastolic blood pressure.

LAB : Labetalol.

LFT : Liver function test.

OBST CODE : Obstetric code.

GA IN WKS : Gestational age in weeks.

CT BRAIN : COMPUTED TOMOGRAPHY.

HELLP : HAEMOLYSIS, ELEVATED LIVER ENZYMES,

LOW PLATELET COUNT.

DOP : DOPPLER STUDY OF UMBILICAL ARTERIES.

S/D ratio

ECLAMP : Eclampsia

ABRUP : Abruption

PUL EDEMA : Pulmonary Edema

MAT DEATH : Maternal death

HT : Hypetension

DM : Diabetes Mellitus

- : Absent

+ : Present