“COMPARATIVE STUDY OF VAGINAL DELIVERY AND CAESAREAN ...

I

“COMPARATIVE STUDY OF VAGINAL DELIVERY AND

CAESAREAN SECTION IN ANTEPARTUM ECLAMPSIA IN

PRIMIGRAVIDA AFTER 32 WEEKS OF GESTATION”

BY

DR. SUDHARANI. C. N M.B.B.S., DGO,

Dissertation submitted to the

Rajiv Gandhi University of Health Sciences, Karnataka, Bangalore.

In partial fulfillment of the requirements for the degree of

MASTER OF SURGERY

IN

OBSTETRICS & GYNAECOLOGY

Under the guidance of

Dr. MUMTAZ BENDIGERI MD, Professor

DEPARTMENT OF OBG

VIJAYANAGAR INSTITUTE OF MEDICAL SCIENCES

CANTONMENT BELLARY-583104.

2012

II

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES,

KARNATAKA

DECLARATION BY THE CANDIDATE

I hereby declare that this dissertation / thesis entitled “COMPARATIVE STUDY OF

VAGINAL DELIVERY AND CAESAREAN SECTION IN ANTEPARTUM ECLAMPSIA

IN PRIMIGRAVIDA AFTER 32 WEEKS OF GESTATION” a bonafide and genuine

research work carried out by me under the guidance of DR. MUMTAZ BENDIGERI MD,

Professor OBG, Department of OBG, VIMS, Bellary.

Date: Signature of the Candidate Place: Bellary Name: Dr. SUDHARANI C.N

III

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA

CERTIFICATE BY THE GUIDE

This is to certify that this dissertation entitled “COMPARATIVE STUDY OF VAGINAL

DELIVERY AND CAESAREAN SECTION IN ANTEPARTUM ECLAMPSIA IN

PRIMIGRAVIDA AFTER 32 WEEKS OF GESTATION” is a bonafide research work done

by Dr. SUDHARANI. C. N, in partial fulfillment of the requirement for the degree of M.S

(OBG).

Date : Dr. MUMTAZ BENDEGERI. M.D Place: Bellary Professor, Dept. of OBG, Vijayanagar Institute of Medical Sciences, Bellary.

IV

RAJIV GANDHI UNIVERSITY OF HEALTH SCIENCES, KARNATAKA

ENDORSEMENT BY THE HOD, PRINCIPAL/ HEAD OF THE INSTITUTION

This is to certify that this dissertation entitled “COMPARATIVE STUDY OF

VAGINAL DELIVERY AND CAESAREAN SECTION IN ANTEPARTUM ECLAMPSIA

IN PRIMIGRAVIDA AFTER 32 WEEKS OF GESTATION” is a bonafide research work

done by Dr. SUDHARANI. C.N under the guidance of

Dr. Mumtaz Bendegeri, M.D, Professor, Department of OBG, VIMS Bellary.

Dr. A.A. KHAZI, M.D., DGO, Dr. A.SRINIVASA MURTHY MD Professor & HOD PRINCIPAL Department of OBG, Vijayanagar Institute of Medical Sciences, Vijayanagar Institute of Medical Sciences, Bellary. Bellary. Date : Place : Bellary

V

COPYRIGHT

DECLARATION BY THE CANDIDATE

I hereby declare that the Rajiv Gandhi University of Health Sciences, Karnataka shall

have the rights to preserve, use and disseminate this dissertation / Thesis in print or electronic

format for academic / research purpose.

Date: Signature of the Candidate Place: Bellary. Name: Dr. SUDHARANI. C.N

© Rajiv Gandhi University of Health Sciences, Karnataka

VI

ACKNOWLEDGEMENT

My sincere thanks to my guide Dr. Mumtaz Bendigeri M.D, Professor, Department of

OBG for her constant guidance and valuable suggestions.

I also express my heartfelt gratitude to Dr. Khazi. A. A., Professor and Head, all

Professors, Associate Professors & Assistant Professors for their valuable suggestions.

My sincere thanks to the Dr. Srinivasa Murthy Principal, V.I.M.S., Dr. B. Devanand

Director, V.I.M.S., and Dr. Vidyadhar Kinhal Medical Superintendent V.I.M.S., Bellary for

their unconditional help and support during my post-graduation and dissertation.

My also express my heartfelt gratitude to All- dept. of Anaesthesiology i.e., Prof. &

HOD, Dr. Devanand. B., Professors, Dr. Srinivasmurthy. A., Dr. Srinivasulu, Associate

Professors, Assistant Professors and postgraduates for their full co-operation during the study

period.

I am thankful to my Parents & Brother, & co postgraduate students for their full support

during this work.

I also acknowledge with gratitude, All the Patients who have co-operated for this study.

Finally I acknowledge the almighty.

Date: Signature of the Candidate Place: Bellary. Name: DR. SUDHARANI. C.N

VII

LIST OF ABBREVIATIONS USED

C.D. group....... Caesarean Delivery group

CPD................. Cephalopelvic Disproportion

DIC.................. Disseminated Intravascular Coagulation

IUD................. Intrauterine Death

IUGR............... Intrauterine Growth Restriction

MMR............... Maternal Mortality Rate

NICU............... Neonatal Intensive Care Unit

PND................. Post Natal Day

PNM................ Perinatal Mortality

PMR................ Perinatal Mortality Rate

PPH................. Postpartum Hemorrhage

V.D. group...... Vaginal Delivery group

HIE…………. Hypoxic Ischemic Encephalopathy

MAS………... Meconium Aspiration Syndrome

RDS………… Respiratory Distress Syndrome

NND………... Neonatal Death

VIII

ABSTRACT

Objective: To compare maternal and fetal outcome in pregnancies of primigravidae with more

than 32 weeks gestation complicated by antepartum eclampsia when terminated by caesarean

section and when terminated by vaginal delivery.

Material and Methods: 100 primigravidae with more than 32 weeks of gestation with

antepartum eclampsia were studied from admission to discharge or death.

Depending upon the mode of delivery, they were divided into two groups: C.D. group, where

caesarean section was performed and V.D. group, where vaginal delivery was carried out.

Maternal and perinatal outcomes were studied in the two groups and compared.

Results: Of the 100 cases, caesarean section was done in 41% of the cases, while vaginal

delivery was carried out in 59%. Maternal complications were seen in 13.4% of the cases in the

C.D. group and 29.2% of the cases in the V.D. group. Maternal deaths occurred in none of the

cases in the C.D. group and in 1.7% of the cases in the V.D. group.

The incidence of live births, still births and neonatal deaths was 92.3%, nil and 7.3% respectively

in the C.D. group, while it was 78%, 11.8% and 8.4% in the V.D. group. Apgar score less than 5

at 1 minute was seen in 9.7% cases in the C.D. group and 25.5% cases in the V.D. group. 21.9%

of the cases in the C.D. group and 32.2% of the cases in the V.D. group required NICU

admission.

IX

Conclusion: Timely caesarean section reduces maternal and perinatal mortality and improves

their outcome in antepartum eclampsia, especially in primigravidas with more than 32 weeks of

pregnancy.

Keywords: Primigravida; Antepartum eclampsia; Caesarean section.

X

TABLE OF CONTENTS

1. Introduction........................................................................... 01

2. Objectives ............................................................................. 03

3. Review of Literature ............................................................. 04

4. Methodology......................................................................... 35

5. Results................................................................................... 41

6. Discussion............................................................................. 65

7. Summary ............................................................................ 77

8. Conclusion............................................................................. 80

9. Bibliography ......................................................................... 82

10. Annexures

Proforma ............................................................................... 93

Master Chart.......................................................................... 96

XI

LIST OF TABLES

SL.

NO.

TITLE PAGE PAGE

NO.

1. Incidence of Eclampsia in Primis 14

2. Incidence of Unbooked Cases 14

3. Incidence of Different types of Eclampsia in Different Studies 18

4. Maternal Mortality figures in different Studies using different

Regimes

23

5. Perinatal Mortality in Different Studies 26

6. Age-wise distribution of study subjects 41

7. Religion-wise distribution of study subjects 42

8. Relation between number of convulsions and mode of delivery 43

9. Relation between consciousness b/w convulsions and mode of

delivery

44

10. Relation between ante natal checkup and mode of delivery 45

11. Relation between patient general condition and mode of delivery 45

12. Relation between conjunctiva status and mode of delivery 46

13. Relation between tongue condition and mode of delivery 46

14. Mode of delivery 47

15. Relation between gestational age and mode of delivery 48

XII

16. Indications for caesarean section 49

17. Incidence of IUD’S on admission 50

18. Relation between Modified bishop score finding and mode of

delivery

50

19. Bishop’s Preinduction Cervical Scoring System 51

20. Convulsion- delivery interval 52

21. Induction-delivery interval 52

22. Perinatal Morbidity 53

23. Comparison of birth weight, APGAR score and NICU stay 54

24. Perinatal Mortality 55

25. Analysis of causes of perinatal mortality with gestational age

>32 weeks

56

26. Comparison of pnm with respect to GA (excluding IUDS) 57

27. Comparison of pnm with respect to birth weight 58

28. Relation of pnm to total no convulsion 59

29. Maternal complications 60

30. Relation maternal complications to convulsion delivery interval 61

31. Relation maternal complications to induction delivery interval 62

32. Relation between cessation of proteinuria and mode of delivery 62

33. Maternal Mortality 63

XIII

34. Comparison of time between events 63

35. Comparison Blood Pressure 63

36. Comparison blood pressure during admission and delivery 64

37. Comparative incidence of caesarean section in eclampsia 66

38. Comparative incidence of PNM to mode of delivery 70

39. Comparative study of PNM to Convulsion-Delivery Interval

in Lopezllera Series

73

40. Comparative Incidence of Maternal Mortality to Mode of

Delivery

75

41. Relation of maternal Mortality to First Convulsion-Delivery

Interval

76

XIV

LIST OF FIGURES Sl.

No.

Figure Page No.

1. Age wise distribution 41

2. Religion wise distribution 42

3. Relation b/w no. of convulsions and mode of delivery 43

4. Relation b/w consciousness and mode of delivery 44

5. General condition and mode of delivery 45

6. Distribution of study subjects based on tongue status 46

7. Mode of delivery 47

8. Gestational age and mode of delivery 48

9. Indications for caesarean section 49

10. Perinatal morbidity 53

11. Birth weight of babies 54

12. APGAR score 54

13. Perinatal outcome 55

14. Causes of perinatal mortality with gestational age > 32 weeks 56

15. Comparison of PNM with respect to gestational age 57

16. Comparison of PNM with respect to birth weight 58

17. Relation between PNM and Convulsions 59

18. Maternal complications 60

19. Relation between maternal complications and convulsion delivery

interval

61

XV

20. Maternal mortality and mode of delivery 62

21. Systolic Blood Pressure during admission and delivery 64

22. Diastolic Blood pressure among study subjects 64

1

INTRODUCTION

The term eclampsia is derived from a Greek word, meaning "like a flash of

lightening"1.

The onset of convulsions in a woman with pre-eclampsia that cannot be

attributed to other causes is termed eclampsia2.

The incidence in India ranges from 1 in 500 to 1 in 30. It is more common in

primigravidae (75%), five times more common in twins than in singleton pregnancies

and occurs between the 36th week and term in more than 50%1.

Eclampsia is an obstetric enigma. Though it has almost been eradicated from

the developed world, it continues to be a major cause of maternal and fetal mortality

and morbidity in the developing countries. The real challenge of eclampsia has not

been met. In spite of considerable progress made in the field of obstetrics, the

incidence of eclampsia and its consequent complications has not decreased

significantly in our country over the past few decades. It is indeed sad that even today

antenatal care is available only to a fraction of our rural population. However, the

management of eclampsia still poses a fascinating challenge to the obstetrician,

requiring the greatest skill, judgement and patience3.

Eclampsia is essentially a disease of low socio economic status of

primigravida, a product of ignorance and neglect. Ideally, it is a preventable disease or

almost so. But unfortunately its incidence is still uncomfortably high in any hospital

accepting unbooked cases. Menon et al (1989) quoted an incidence of 0.83% to 1.6%

from leading centres of India.

Faced with this reality, a plan of management has to be evolved. Though the

exact pathophysiology leading to the occurrence of fits is still not understood, one

2

thing has been proved beyond doubt that termination of pregnancy, removes the basic

cause of the disease. Keeping this in view an attempt has been made in the present

study to ascertain if caesarean section has any distinct advantage over vaginal delivery

in lowering maternal and perinatal deaths4.

3

AIMS AND OBJECTIVES

1. To evaluate the role of termination of pregnancy by caesarean section and

termination by vaginal delivery in antepartum eclampsia occurring in

primigravidae with more than 32 weeks gestation, with reference to perinatal

morbidity and mortality and maternal morbidity and mortality.

2. To compare the results of termination of pregnancy by caesarean section with

those obtained by routine or induced vaginal delivery in primi with more than

32 weeks gestation with antepartum eclampsia, with reference to perinatal

morbidity and mortality and maternal morbidity and mortality.

4

REVIEW OF LITERATURE

Historical Aspects:

The oldest source for eclampsia literature starts from 2200 BC, when Kahun

Papyrus mentioned the use of a wooden stick to prevent the mother from biting her

tongue on the day of delivery.

Indian Atharvaveda described an amulet to be worn by the mother at her 8th

month of pregnancy for warding off convulsions during childbirth.

In Sushrutha Samhita, it has been mentioned that, 'the child moving in the

womb of a dead mother, who has just expired from convulsions, should be delivered

by cutting open the abdomen'.

Hippocrates, in his aphorisms section VI, No. 39, wrote convulsion take place

either from repletion or depletion. He noted that headaches, convulsions and

drowsiness represented omnious signs in postpartum period.

Rossilin (1513) listed unconsciousness with convulsions as the ominous sign

of eclampsia.

Gaebel Khouren (1596) stated that pregnant uterus causes convulsions

particularly if it contains a malformed fetus5.

Dexter and his associates mentioned that the term "eclampsia" first appeared

in a treatise on gynecology written by Varandaeus in 1619.

Pew (1694) described clonic spasms in association with pregnancy.

Mauriceau (1668) stated that convulsions often cease with delivery and

recommended prompt termination of pregnancy as the best treatment. He set forth

several aphorisms dealing with eclampsia. Among them were:

5

• The mortal danger to mother and fetus is greater when the mother does

not recover consciousness between convulsions.

• The primigravidae are at greater risk of convulsions than the

multigravidae.

• Convulsions during pregnancy are more dangerous than those

beginning after delivery.

• Convulsions are more dangerous if the fetus is dead.

Eclampsia has been a therapeutic problem since it was first recognized as a

definite disease. Its treatment has undergone an evolutionary process consisting of six

periods as described by Dieckmann;

The First Period: beginning in 1745 and lasting approximately 100 years, was

considered a non-operative era and had as its stalwarts purging, sweating and blood

letting.

The Second Period: began about 1845 and lasted approximately 50 years. This was

characterized by the initial introduction of veratrum viride as well as the more radical

trend toward immediate delivery by manual dilatation of the cervix.

The Third and Fourth Periods: Overlapped each other, beginning about 1895 and

terminating in 1915. They represented the era of ultra radicalism. During this period,

immediate delivery by caesarean section, vaginal hysterectomy, or accouchement

force (Boosidilator) was the treatment of choice.

The Fifth Period: Extended from 1915 to 1927 and brought into focus conservative

medical management utilizing intravenous hypertonic glucose solution, sedation,

elimination and parenteral magnesium sulphate, which was introduced by Titus

6

(1920). The slogan in the late 1920s thus became, "treat the eclampsia medically and

ignore the pregnancy".

The Sixth Period: Started in 1928 when Stroganoff advocated artificial rupture of

membranes for induction of labour in addition to profound sedation and narcosis to

prevent and control seizures. Stroganoff regime included:

• A darkened room

• Liberal use of chloroform, chloralhydrate and morphine

• Artificial rupture of membranes

• Magnesium sulphate

• Administration of oxygen during fits.

He reported a maternal mortality rate of 2.6% and uncorrected perinatal mortality of

16.6% with his regime.

All the periods as described were overlapping eras of therapy, which came

into existence after the discovery of a new drug, procedure, or method of treatment by

a noted person of the time. A wide variety of both operative and non-operative

methods was used in an attempt to lower the exceedingly high maternal mortality

rates. Some of these, such as:

• Retromammary injection of potassium iodide or air

• Radical mastectomy

• Renal decapsulation

• Trephining of the skull

• Massive venesection

7

• Lumbar puncture with withdrawal of large amounts of spinal fluid and

• Massive doses of thyroid undoubtedly seemed barbaric

When one also considers the radical procedures of the day for emptying the

uterus, however, it becomes quite obvious that the accoucheurs of that period were

desperate in their attempts to conquer a disease with a fantastically high mortality

rate6.

The following years (1929-1950) saw the use of varied drugs like veratone,

bromethanol caudal anesthesia with 15% solution of methycaine, tribromethanol,

sodium thiopentone, etc.

Morris and Dewar (1947) during their trials with rectal bromethal in eclampsia

recommended caesarean section in cases where prompt uterine responses to artificial

rupture of membranes was unlikely as judged by the nature of the cervix on vaginal

examination.

Then, followed a period of indecision, obstetricians all over the world began to

realize that the results could not be improved further by the conservative line of

treatment in whatever shape it is adopted. It was then that caesarean section came into

focus. Several authors started recommending caesarean section: prominent among

them were Dieckmann (1952) remarked "caesarean section is performed if there is

cephalopelvic disproportion or if the eclampsia is severe and the cervix is closed and

uneffaced7.

River Forest8 (1956) who commented further on the use of caesarean section

in eclampsia, that it should be selected primarily in patients in whom the cervix was

not ripe because of prematurity.

8

Corhill TF9 (1957) who stated that there was no place for caesarean section as

a last desperate measure in cases, which were rapidly deteriorating. He advocated

caesarean section whenever the eclampsia was severe and occurred earlier in

gestation.

Tenny and Dandrow10 (1961) who asserted that caesarean section is a life

saving procedure especially in the young primigravida with premature baby and an

unfavourable cervix.

Krishna Menon7 (1961) who studied 104 cases of eclampsia by subjecting

them to caesarean section. He was surprised when contrary to the heavy maternal

mortality reported earlier and because of which caesarean section was literally

contraindicated in the eclamptic state, he obtained a maternal mortality of 4.8% and

one death in his series was not attributable to operative procedure. He was convinced

that in properly selected cases under modernconditions, caesarean section did not

enhance the inherent maternal mortality. Menon made 2 pertinent observations:

• Firstly, that antepartum eclampsia has the maximum mortality

• Secondly, that in the severe type of eclampsia the longer the time

interval between the onset of fits and delivery, the greater the

mortality.

He advocated caesarean section in all severe cases of eclampsia in which

convulsions could not be controlled. From his study of caesarean section, two things

struck him"

1. Caesarean section in the eclamptic under modern condition is

not so very dangerous to the mother.

9

2. There is remarkable improvement in the patient within 24 hours

of section.

Derek Crichton11 (1962) who gave his firm belief that earlier recourse to

caesarean section would reduce the incidence of eclampsia in patients with severe pre-

eclampsia who were not responding satisfactorily to treatment. Similarly, he

considered that, caesarean section should play an important role in eclamptic patients,

whose onset or progress in labour was not rapid, who did not come into labour rapidly

after induction of labour, or who were unfavourable for induction.

Lokenath Bhose12 (1964) who remarked that none of the women with non

conclusive toxaemia developed convulsion after abdominal delivery.

Alan Alexander13 (1966) who obtained a low MMR of 4.2% and a low PNM

by rapid stabilization of patients and early delivery of the fetus. He found that those

delivered by caesarean section after stabilization, without an attempt to induce labour

had no PNM and none of the surviving babies showed any neurological sequelae,

whereas 50% babies born by caesarean section after an attempt at induction of labour

had neurological damage. Those delivered vaginally following successful induction

had a PNM of 33% and 33% of the surviving infants had neurological damage.

Brooks Ramney (1966) and Mario Lopezllera14 (1967) whose studies agreed

with Alan Alexander's studies. They noted that fetal hypoxia and increasing cerebral

pressure, resulting from strong uterine contractions of a difficult induction, would do

the toxaemic baby no good.

Lean TH, Ratnam SS, Sivasamboo R15 (1968) who reported MMR of 3.3%

and PMR of 11.1% with diazepam therapy. 2.2% was the incidence of recurrence of

fits after initiation of the therapy. Caesarean section was done in primigravidae who

10

were not in labour or with less than 5cms dilatation 1 hour after sedation and in multi

gravidae who were not in labour or whose cervix was unfavourable.

Derek Crichton, Morris Notelo Vitz and Heller16 (1968) who resorted to

caesarean section if the patient was not in labour or if fits could not be controlled.

Preliminary hypotensive and pethidine therapy was not given if immediate caesarean

section was to be carried out. The MMR was 4.2% to 4.8% in the caesarean section to

vaginal route delivery and the PMR was 27.6% to 45.7% in the caesarean section to

vaginal delivery route groups. They advocated prompt caesarean section unless easy

vaginal delivery could be anticipated within 4-6 hours and also if convulsions could

not be adequately controlled.

Villiers and Slabber17 (1970) who advocated an early termination by caesarean

section and the rate of caesarean section in their series was 76%. The overall fetal

mortality was 23.3% and the corrected PMR was 14.4%. Eclamptic patients recovered

smoothly from caesarean section, more smoothly than after vaginal delivery in 24-48

hours after the last fit. MMR was 4.3% to 12.7% in the caesarean section to vaginal

delivery groups.

Ajay Ghosh18 (1974) who reported favourably on caesarean section in ante

and intrapartum eclampsia. There was no mortality in his series and was impressed

with the dramatic recovery of the cases after caesarean section. He observed that early

operation when the patient was in good condition was much safer than delayed

operation after an unpredictable or failed conservative regime.

Chesley5 (1978) who has favoured caesarean section to reduce maternal and

perinatal mortality.

11

Nanda Smiti19 (1989) who studied 172 patients of eclampsia to analyze

perinatal mortality and stated that mortality increased with increase in blood pressure,

increase in first fit treatment interval and first fit delivery interval. This study,

perinatal mortality was lowest (20%) where caesarean section was performed.

Swain S20 (1993) who suggested that more frequent use of properly timed

caesarean section can improve the maternal outcome.

Arupkumar Majhi21 (2001) who found that the outcome of mother and fetus

was relatively better in cases who were actively managed delivered by caesarean

section than in those who waited deliveries by vaginal route, in his study of 877

eclamptic women.

Lee W Connell115 studied maternal and perinatal outcomes of eclampsia found

increased rates of caesarean section 79%. No maternal deaths, maternal complications

were 32%, perinatal mortality rate was 64 in 1000 deliveries112

Taj116 studied 100 patients of eclampsia, among them 71 patients were normal

vaginal delivery, 25 patients needed caesarean section. Maternal mortality was 2%

perinatal mortality was 38%. Perinatal mortality was higher in vaginal group 12%

than LSCS group 7%113.

Kamilya G, Bharracharyya SK, Mukherji J22 (2005) who analyzed maternal

and perinatal outcomes in eclampsia after the introduction of magnesium sulphate and

liberarization of caesarean section over a period from August 2002 to September

2004. They found that the caesarean section rate for eclampsia has increased from

near 10% to 49.7%. Both maternal mortality and perinatal mortality are lowest in the

caesarean section group.

12

Jamila117 study conducted on 254 cases found that maternal death is 0.4% that

is 1 and perinatal mortality was 11 % in caesarean section114.

Barret118 M discussed vaginal delivery is the optimum mode of delivery in

women with severe preeclampsia and eclampsia116.

M Khanum119 studied 100 cases of eclampsia out of which vaginal delivery

had better apgar than caesarean section group. Perinatal mortality was 38%118.

Incidence

The incidence of Pregnancy induced hypertension is between 5% to 15%. The

incidence of Eclampsia varies from country to cou'ntry. Incidence ranges from 0.02%

in United Kingdom (Douglas, Redman) 1994 to 2.3% in India (Arup Kumar Kanhi

1998)24.

The incidence in various University Hospital are24,25,26,27,28,29

1. National University Hospital Singapore 1990 0.1%

2. Women's Hospital, Madras 1990 0.5%

3. NRS Medical College Hospital, Calcutta 1990 1.2%

4. Collaborative Eclampsia Trial Group 1995 1.0%

5. Arup Kumar Kanhi 1998 2.3%

6. Nilesh Dalal 1998 1.59%

In a one year descriptive study, Dr. Suchita Mundle27 found the incidence to

be 1.13% Dr. Srinivas Gadappa in a prospective study of 175 cases over a 2 year

period (1995-1997) found the incidence to be 1.5%.

13

Age:

Most studies found Eclampsia27,30,31 to be high between 20-25 years of age

Some studies found Eclampsia to be more common in age less than 20 years.

14

Parity:

Eclampsia is very common in primigravidae as found out by most

studies24,29,30,32,33.

Table-l: Incidence of Eclampsia in Primis

Author Year Primis

Low 11 1995 64%

A.K. Kanhi 1998 88.6%

Vinita Bansal 1998 74.4%

Arati Srivastav 1998 70%

Srividya 1998 70%

Socioeconomic Status:

Eclampsia is found to be high in women with low socioeconomic

status24,27,28,32.

Arup Kumar Kanhi(l998) found 53% of the Eclamptic women to be in low

socioeconomic status.

Unbooked Status:

According to the following studies24,29,32,34. Unbooked status is found to be a

significant risk factor for development of Eclampsia.

Table-2: Incidence of Unbooked Cases

Author Year Percentage unbooked

A.K.Kanhi 1998 82.3%

Srividya 1998 70%

Arati Srivastav 1998 96%

Conde Aguedelo (1997)35 an Mwinyoglee Amoko 199636 were other authors

who found un booked status to be high.

15

Gestational Age:

The mean gestational age found out by various studies are as follows

Low JJ33 1995 35.9 weeks

S Mundle27 1998 29 to 36 weeks

Hungarga31 1998 33 to 37 weeks

Clinical Features:

The women with Eclampsia will have generalized tonic clonic convulsions,

mostly preceded by imminent signs like headache, vomiting, epigastric pain and

visual disturbances. The frequency of various signs and symptoms of impending

Eclampsia as found out by Sibai 198137 are as follows.

Symptoms Patients in whom present %

Headache 83%

Proteinuria 80%

Oedema 60%

Clonus 46%

Visual Signs 45%

Epigastric pain 20%

Low JJ in 199533 has found out that 40.7% patients were asymptomatic prior

to first fit. Headache was next common symptom.

Sibai et al (1992 to 1997)38 has studied the association between various

imminent signs and symptoms and development of Eclampsia. Only headache, deep

tendon reflexes and protenuria more than 3+ were found to be significantly associated

with development of Eclampsia. He has found no association between Eclampsia and

systolic, diastolic or Mean Arterial Pressure, epigastric pain, gestational age at

delivery or laboratory values including platelet count and Liver Function Tests.

16

Convulsions are of tonic clonic nature. Tonic phase lasts for 15 to 20 seconds.

Clonic phase lasts for 1 minute. Respiration is halted followed by deep stertorous

breathing. The woman usually recovers some degree of consciousness after each

attack. On general examination patient can be conscious, semiconscious, restless,

irritable or comatose.

Other clinical features are

• Increased respiratory rate due to hypercarbia Cyanosis

• Fever

• Proteinuria

• Decreased Urine output Edema

• Exaggerated deep tendon reflexes Increased Blood Pressure

Points to be remembered:

• Deep coma and fever more than 39°C are grave signs.

• The number of convulsions, interval between convulsions, convulsion

• delivery interval are important in influencing maternal and perinatal

out come.

• Once the convulsion occurs, prognosis becomes uncertain. Prognosis

depends on may factors and the ominous features are:

1. Long interval between fit and commencement of treatment.

2. Antepartum Eclampsia with long convulsion delivery interval.

3. Fits more than 10.

4. Coma in between fits.

5. Temperature more than 102° F with pulse rate more than 120 per minute.

6. Blood pressure more than 200 mm of Hg systolic.

7. Oliguria less than 400 ml per 24 Hours.

8. Proteinuria more than 5 grams per 24 Hours.

17

9. Non response to treatment 10. Jaundice.

Differential Diagnosis:

Though Eclampsia is easily diagnosed on clinical grounds, other conditions

have to be considered especially when Eclampsia is unresponsive to Magnesium

Sulphate therapy.

According to Friedman, Sibai (1997) the following are the differential diagnosis.

1. Status epilepticus

2. Head injury

3. Intra cranial bleeding

4. Cerebral tumors

5. Meningitis

6. Cerebral infarction

7. Cerebral aneurysms

Sejal V.Desai et. al., (I 998)40 conducted a retrospective study and found that

out of 84 cases 24.7% were non eclamptic convulsions. Non eclamptic causes of

convulsions were cerebral malaria, cortical venous thrombosis, encephalopathy,

tuberculosis, infarct, hemorrhage.

18

Type of Eclampsia:

Various authors have found the following incidence of different types of

Eclampsia in their studies.

Table-3: Incidence of Different types of Eclampsia in Different Studies

Name of the Author Type of Eclampsia Incidence

Sibai (I 981 )37 Antepartum Eclampsia

Intrapartum Eclampsia

Postpartum Eclampsia

46.3%

16.4%

37.3%

Mwinyoglee Amoko (I 996)36

Antepartum Eclampsia



77.3%

18.2%

4.50%

Leitch, Cameron(1997)41 Antepartum Eclampsia



77.3%

18.2%

4.50%

A. Srivastava (I998)32 Antepartum Eclampsia



48.0%

24.0%

28.0%

Leitch et al have conducted that due to decreased incidence in antepartum and

intrapartum Eclampsia, there is a relative increase in incidence of postpartum

Eclampsia in United Kingdom.

Laboratory Abnormalities in Eclampsia:

Laboratory values reflect the effects of Eclamptic process on kidney, liver,

hematological elements and fetoplacental unit. In complicated Eclampsia renal

parameters like serum creatinine, blood urea nitrogen and serum uric acid are

19

increased. Liver parameters like serum bilirubin, SGPT, SGOT and LDH are

increased.

Coagulation abnormalities:

Pritchard (1976)62 found thrombocytopenia in 29% of 95 cases, prolonged

prothrombin time in 50% and increase serum fibrin degradation products in 3%. Overt

hemolysis was seen in only less than 2%. Coagulation disorders in Eclampsia are rare

in the absence of abruption.

Thrombocytopenia can be induced acutely by preeclampsia and Eclampsia.

Leudec et al 199225 found that thrombocytopenia is more common in severe

preeclampsia/ eclampsia and depends upon the length of delay between the onset of

preeclampsia and delivery and the frequency with which platelet counts are

performed. Overt thrombocytopenia, defined by a platelet count less than one lakh is

an ominous sign.

Causes of thrombocytopenia in Eclampsia were investigated by Torres

associates, 199644 Pritchard of colleagues 197642 Samuels and colleagues 198745

Burrows and colleagues 198746 , Kelton and colleagues 198547, Kilby associates

199048 Weinstein 1982 referred to the combination of thrombocytopenia, elevated

liver enzymes and hemolysis as HELLP syndrome which is more ominous than

Eclampsia.

Dickmann 195249 Pritchard 198450 have found hemoconcentration and absent

hypervolemia in Eclampsia. Eclamptic women are unduly sensitive to vigorous fluid

therapy and tend to go for pulmonary edema easily (Lopez-Llera 1982)51

20

Pathology and Pathophysiology in Eclampsia:

Main pathology is in brain, which shows vasospasm. Sheehan 1950 52 in his

study observed edema, hyperemia, thrombosis and hemorrhage in 56% (in

histopathological examination). 75% of Eclamptic women show abnormal

electroencephalograms within .48 hours of seizures, which become normal by 3

months (Sibai 1985)53.

Brown and colleagues 198854 studied CT scans and found abnormal findings

in 50% of Eclamptic women. The most common findings in CT were hypodense

cortical areas corresponding to petechial hemorrhage. Moriss and colleagues 199755

showed changes especially in the area of posterior cerebral artery in MRI studies.

21

Pathophysiology:

Exact pathogenesis of Eclampsia remains unknown. It is possible that severe

arterial vasospasm causes rupture of the vascular endothelium and peri capillary

hemorrhage with the development of foci of abnormal electrical discharge that may

generalize and cause convulsions.

Horn and Filshie 199056 found that nimodipine, which is a selective cerebral

vasodilator, caused rapid reversal of symptoms in an Eclamptic patient. Donaldson in

198757, proposed that with acute severe hypertension the upper level of auto

regulation is reached producing a reactive vasospasm, leading to seizures. According

to this theory, upper limit of cerebral perfusion pressure varies among individuals.

Patient with chronic hypertension are capable of tolerating higher mean arterial

pressure than others. So a young preeclamptic patient may convulse with a systemic

blood pressure of 140/96 mm of Hg, where as a patient with chronic hypertension and

superimposed preeclampsia may

Tolerate pressure as high as 226/150mm of Hg or more without convulsions.

Retina:

Retinal artery vasospasm is associated with visual distrubances. Fundoscopy

shows focal or generalised vasospasm. Belfort and associates in 199258 showed that

Magnesium sulphate dilates retinal artery.

Liver:

Liver shows periportal hemorrhagic necrosis reflected by raised liver function

tests. Manas and colleagues59 have done CT scan study and found that 5 out of 7

women with preeclampsia and upper abdominal pain had hepatic hemorrhage. Smith

22

and coworkers 199160 reviewed 28 cases of spontaneous hepatic rupture associated

with preeclampsia and found the mortality rate to be 30%.

Kidney:

Renal perfusion and glomerular filtration rate are reduced with development of

preeclampsia/eclampsia. Plasma uric acid concentration is typically elevated

especially in women with more severe disease. The elevation of plasma creatinine is

likely due to intrinsic renal changes caused by severe vasospasm (Pritchard et al

198450 Lee and associates 1987)61 In the absence of underlying chronic renovascular

disease, complete recovery of renal function is anticipated after delivery. Sibai and

associates 199062 have concluded that if renal cortical necrosis supervenes, oliguria is

irreversible.

Maternal outcome is Eclampsia:

Eclampsia is one of the most dangerous conditions that can afflict a pregnant

women and her fetus. Fortunately maternal mortality due to Eclampsia has fallen in

the past 3 decades.

Given below are the maternal mortality figures in different studies, using

different treatment regimens, from 1960's to 1990's:

23

TABLE-4 MATERNAL MORTALITY FIGURES IN DIFFERENT STUDIES

USING DIFFERENT REGIMES

Sl.

No Study Year Treatment Mortality %

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20

Menon 7

Llewellyn Jones63

Byrant Fleming64

Zuspanos65

Lopez-Llerasl51

Lean and coworkers 15

Gedekoh and colleagues66

Pritchard and associates50

Bhalla and coworkers68

Eclampsia trail collaborative Group69

Frangieh and associates 70

Porapakkam 71

Harrison 72

Giri26

WH073

Mwinyoglee Amoko36

Saumundal B.K74

S. MundleD37

S. GadappaL28

Khanum119

1961 1961 1962 1964 1967 1970 1973 1976 1979 1968 1981 1984 1994 1995 1996 1979 1985 1991 1991 1996 1998 1998 1998 2004

Lytic cocktail Lytic cocktail Magnesium Sulphate Magnesium Sulphate Lytic cocktail Lytic cocktail Diazepam+Reserpine Furosemide+Reserpine+ Alb umin+antithrombotic Barbiturates+ MgSo4. 7H2O+ Resperpine Chlordiazepoxide MgS04.7H2O+ Hydrallazine MgS04.7H2O+Hydrallazine + standard regimen MgS04. 7H2O + nifedipine Lytic cocktail + nifedipine MgS04.7H2O; Diazepam MgS04.7H2O; Phenytoin MgS04.7H2O+ Hydrallazine Thailand Nigeria India Malaysia South Africa India India India Rajshahi

2.20 6.60 1.60 3.40 10.20 11.70 17.50 12.50 16.20 3.30 5.80 0.40 4:40 3.8; 5.1 2.6; 5.2 0.50 4.70 10.80 6.20 12.00 21.20 5.30 7.00 1.41 2.00

The maternal mortality has ranged from less than 1.0% to as much as 20% in

these studies.

Maternal Complications:

Cerebral haemorrhage:

Govan( 1961 )75 investigated the cause of death in 110 fatal cases of

Eclampsia and concluded that cerebral hemorrhage was responsible in 39 of them.

24

Coma:

Prognosis for comatose eclamptic women in guarded. Extreme cerebral edema

is documented in most of these cases. Sheehan and Lynch 197376 reported that 6 out

of 76 women with fatal Eclampsia had massive white matter hemorrhage that caused

coma and death. They also reported a high mortality rate with bleeding into basal

ganglia or pons.

Hellp Syndrome:

Liver involvement in preeclampsia/eclampsia is serious and is frequently

accompanied by evidence of other organ involvement especially kidney, brain along

with hemolysis and thrombocytopenia (DE Boer 199177 , Pritchard 195478 , Weinstein

1985 )79 Sibai and co. workers 199380 found the incidence to be 2.3% in eclampsia.

When HELLP syndrome occurs in Eclampsia, the incidence of other complications is

also increased (Audibert Associates 1996)81

Pulmonary Edema:

Eclamptic women are prone to develop left ventricular failure and pulmonary

edema in response to even minimal fluid overload (Lopez-Llera 198251, Gedekoh

198166 , Sibai 198782 ) Cinocotta and Ross A found the incidence of pulmonary

edema to be 3%. Bansal V 19986 found the incidence to be 4.6%.

Blindness:

The causes for visual disturbances in Eclampsia are retinal artery vasospasm,

retinal detachment, occipital lobe ischemia. Cunningham and associates 199583

described 15 women with severe preeclampsia or Eclampsia who also had blindness.

In all women it resolved between 4 hours to 8 days. Even with retinal detachment,

vision usually returns within a week.

25

Abruption:

Sibai38 found the incidence of abruption to be 16% in Eclampsia. Bansal V in

199830 found the incidence of abruption in her study to be 6.9%. Abruption in

Eclampsia increases the occurrence of complications like acute renal failure and Ole.

Acute Renal Failure:

Los Angeles country study 198384 implicated acute renal failure in 7 out of 67

maternal deaths (10.4%). Collaborative Eclampsia trial group 199569 found 5 cases of

renal impairment in 110 maternal deaths due to Eclampsia (4.5%). Sibai 1990

concluded that incidence of acute renal failure is high in Eclampsia complicated with

abruption.

Psychosis:

It rarely follows Eclampsia and it can last of several days to 2 weeks.

Perinatal outcome:

Perinatal outcome is compromised in eclampsia. Perinatal Mortality has been

evaluated in various studies.

26

TABLE-5 PERINATAL MORTALITY IN DIFFERENT STUDIES

SI. No.

Author

Year

Perinatal

Mortality Rate l. 2. 3. 4 5 6 7 8.

Sibai58

Douglas Redman23

Collaborative Eclampsia Trial Group69

Mwinyoglee Amoko36

S.Mundle27

V Bansal30

B.K.Saumadal25

Lee W Connell115

1983 1994 1995 1996 1998 1998 1998 2004

107/1000 56/1000 224 to 307/1000 477/1000 465/1000 348/1000 390/1 000 64/1000

Preeclampsia/eclampsia is associated with uteroplacental insufficiency, which

leads to various complications like intrauterine growth retardation, oligohydramnios,

acidosis, asphyxia, intrauterine death and still births.

Superimposed on this pathology, eclamptic seizure brings about further fetal

hypoxia, bradycardia and' decreased beat to beat variability. Fetal heart returns to

normal about 5 minutes after eclamptic seizure.

Non stress test and contraction stress tests are not much useful in eclampsia

because of the rapidly deteriorating maternal condition.

According to Ducey 198786, hypertensive pregnant patients with normal

umbilical and uterine velocimetry have fetal outcomes that are similar to those of

normal women. Patients with abnormal umblical and uterine Doppler wave forms

have poor outcomes.

Sibai 198385 has found prematurity to be 56% and small for gestational age

incidence to be 30%. Brazy, Lopez Llera 1982 found symmetric IUGR in early onset

eclampsia. Llera (1972)33 the incidence of small for gestational age to be 27%. Brazy

has found 27% of SGA babies in eclampsia.

27

Low JJ 199529 reported that mean birth weight in his study was 2.328 Kgs.

The incidence of prematurity and birth asphyxia were 51.9% and 29.6% respectively.

Srividya 199824 reported 42.6% of low birth weight babies in her 1 year study

of Eclampsia where as A.K Kanhi 1998 found 49.6% of low birth weight babies in his

study.

V.Bansal 199830 has found the following complications:

Intrauterine growth retardation 48.8%

Prematurity 69%

Still birth 74%

Birth asphyxia 13.9%

28

Management of Eclampsia:

Delivery is the definitive treatment of Eclampsia. The pathological changes

disappear after delivery and eventually are reversed completely.

Pritchard has applied standardized treatment uniformly to all access of

eclampsia at Parkland Memorial Hospital since 1955 to 1975 (1975) 88. This treatment

consisted to:

1. Control of convulsions with MgSO4 7H2O using an intravenous

administered loading dose and periodic intramuscular injections

standardized in dose and frequency of administration.

2. Intermittent intravenous injection of hydrallazine to lower blood pressure

whenever diastolic blood pressure is 110 mm Hg or more.

3. Avoidance of diuretics and hyperosmolar agents

4. Limitation of intravenous fluid administration

Lot of studies have been done to determine the best drug of choice for control

of convulsions, for improving maternal and perinatal outcome. The different drugs,

which have been studied and compared are:

i) Lytic cocktail (chlorpromazine, diethazine, pethidine) (Bhalla et a1

68 Menon77 , Llewellyn Jones63 , Chatterji & Mukherji 90, Lopez

Llera ).91

ii) Diazepam, Chloridazepoxide (Lean 15, 1968; Lopez Llera, 1973)91

iii) Veratrum alkaloids (Bryant Fleming64, 1962).

iv) Frusemide, Reserpine (Lopez Llera, 1976)

29

v) Nifedipine (Bhalla et a168, 1994)

vi) Phenytoin (Eclampsia Trail Group69, 1995).

vii) Magnesium sulphate (Bryant Fleming, 196264 Zuspan , 196465

Gedekoh, 198166 Pritchard, 198450 Bhlla, 199471 Eclampsia Trial

Collaborative Group, 1994)69 to 3.4% (Zuspan64, 1964) for

magnesium sulphate.

30

Mechanism of Action of Magnesium Sulphate:

• Magnesium exerts a specific anticonvulsant action on the cerebral

cortex (Borges Gucer, 1978).

• Cotton and associates (1992) proposed that N-methyl-O aspartate

receptor is implicated in Eclampsia seizures.

• Lipton and Rosenberg (1994) attribute the anticonvulsant effects

to

• Neuronal calcium influx blocking through the glutamate channel.

• Improved mitochondrial calcium buffering.

• Potentiation of adenosine action

MANAGEMENT OF ECLAMPSIA:

I. General Management:

• Eclamptic women are ideally nursed in a dark quiet room with no

bright light

• Suctioning of oropharynx to prevent aspiration.

• Oxygen supply to prevent hypoxia.

• Facilities for endotracheal intubation and ventilation.

• Mouth kept open by a soft gag.

• Nursed in left lateral position with head low to reduce the risk of

aspiration.

II. Medical Management:

1. Anticonvulsant therapy:

Administration of magnesium sulphate as per Pritchard's regime (1975).

31

2. Antihypertensive therapy:

The objective of antihypertensive treatment is to prevent intracranial bleeding

and left ventricular failure. Immediate reduction of blood pressure is desired if

systolic blood pressure is > 170 mm of Hg and diastolic blood pressure is >110 mm of

Hg.

Hydrallazine, diazoxide, sodium nitroprusside, sublingual nifedpine are the

most common antihypertensive drugs used. Pritchard 197588 in his series of 154

patients used intravenous hydrallazine. Sublingual nifedipine is extensively used in

most developing nations including India (Bhalla 68, 1994; Hangarga US , 1998)31.

According to Donaldson (1987)57 antihypertensive treatment may be useful in

avoiding the selective cerebral arterial vasospasm that causes eclamptic seizures.

III. Obstetric Management:

Delivery is the definitive treatment of eclampsia. Pritchard (1975)88 has

incorporated delivery as the essential part of his standardized treatment. Steps were

taken to effect the delivery once the woman regained consciousness to the extent that

she could be oriented to time and space. Once convulsions had been controlled and no

other obstetric complication coexisted without obstetric contraindication to vaginal

delivery, labour was induced with intravenous oxytocin in Pritchard's series.

Dewhurst in 198497 felt that if the fetus is viable and unless the mother is

already in labour with cervix more than 3 cm dilated, early caesarean section is ideal.

But Zuspan 198198 preferred vaginal mode of delivery in view of increased maternal

morbidity for operative delivery.

32

Cunningham and Pritchard (1984) reported 75% vaginal delivery rate out of

209 women with antepartum eclampsia. The following are the incidence for vaginal

delivery given by other

Authors:

Pritchard (1975)88................96.00%

Hangarga (1998)31...............90.62%

Bansal y (1998)30 ................65.00%

The caesarean section in different studies is as follows:

Mwinyoglee Amok036 (1996) 66.70%

Bansal y30 (1998) 9.00%

Kale Y 99 (1998) 21.00%

Kahni AK24 (1998) 8.00%

The modes of induction in these studies were extra amniotic ethacrydyl lactate

instillation, intravenous oxytocin, prostaglandins, amniotomy or the combination of

the above.

The maternal and perinatal prognosis depends directly on convulsion delivery

interval and induction delivery interval (Menon71961). The longer the duration, the

worse is the prognosis (Mundle S27, 1998).

The induction delivery interval in Pritchard88 1975 study ranged between 3

and 51 hours. In a study by Hangarga31 US (1998), the mean induction delivery

interval was 15.78 hours and 80% delivered within 24 hours of admission.

33

Anaesthesia and Analgesia in Eclampsia:

For labour analgesia intravenous pethidine and intravenous phenergan at 2

hours or longer (avoided 2 hours before delivery) was used by Pritchard 88(1975) in

his study.

Anaesthesia for Caesarean Section:

Spinal blockade produces hypotension and potential for pulmonary edema

following infusion of large volumes of crystalloid solutions. General anesthesia and

tracheal intubation may result in severe sudden hypertension further complicated by

pulmonary or cerebral edema or intracranial hemorrhage. Over the past two decades,

most obstetrical anesthesiologists have to come to favour epidural blockade for labour

and caesarean section in eclampsia (Cheek & Samuels, 1001991; Chadwick &

Easterling , 1011991; Ramanathan ,102 1991).

Neonatal Complications:

Sibai103 (1983) has found that neonatal complications in eclampsia were

related to prematurity and unrelated to maternal eclamptic process. There were no

differences between premature babies of eclampsia and premature babies of control

population.

Infant Follow-up:

Long-term follow-up data 4 years of age seems favourable according to Sibai

study (1983).

34

Postpartum Care:

Consists of fluid and electrolyte balance, input, output chart, continuation of

MgSO4.H2O for 24 hours and blood pressure monitoring.

Long term prognosis:

Recurrence rate of pre-eclampsia is 30% according to Sibai. Risk of

recurrence of eclampsia is 1.4%. Most of the complications are however completely

reversible.

35

METHODLOGY

The study period extended from October 2010 to September 2011 a period of

12 months. The study was done in VIMS, Bellary.

A total of 100 patients were studied. Patients with the following criteria were

studied.

1. Primigravida

2. Duration of gestation more than 32 weeks

3. Antepartum eclampsia

Exclusion criteria

1. Patients with pregnancy induced hypertension without eclampsia,

2. Patients with epilepsy or other causes of convulsions with pregnancy.

3. Multigravida with pregnancy induced hypertension with anaemia.

4. Patients with chronic hypertension with eclampsia.

5. Patients with connective tissue disorder with eclampsia.

100 Patients were studied by delivering them into two (2) groups for

comparative analysis.

The first group consisted of patients whom conservative obstetric management

& delivey per vaginum was carried and was called the “VD group”.

The second group consisted of patient in whom lower segment cesarean

section was carried out due to eclampsia & varied associated indications was called

“C D group”.

36

METHODS

On admission a detailed history was taken regarding

1. Name, age, socioeconomic status, religion and address of the patients

2. the antenatal check-up

3. the duration of gestation in terms of months of amenorrhoea

4. The time of onset of convulsion, total number of convulsion, interval

between convulsion, duration of each convulsion, the time of case

convulsion, history of loss consciousness & history of frothing longitude,

passing urine/stood during convulsion

5. Premonitory symptoms like headache epigastric pain nausea, vomiting and

blurred vision.

6. Any history pain abdomen trauma pervaginal leak or bleeding pervaginal.

7. Obstetric menstrual, past history, family history and personal history

8. Any nature of treatment before hospitalization

A rapid general examination was subsequently made noting the grade of

consciousness of patients, temperature, pulse rate blood pressure, presence

of edema, evidence of injuries, condition of heart, lungs & knee jerk

The second group consisted of patients in whom lower segment caesarean

section was carried out due to eclampsia and varied associated indications and was

called the "C.D. group".

37

Methods:

On admission, a detailed history was taken regarding:

1. The name, age, socioeconomic status, religion and address of the patient.

2. The antenatal checkups.

3. The duration of gestation in terms of months of amenorrhea.

4. The time of onset of convulsion, total number of convulsions, interval

between convulsions, duration of each convulsion, the time of last convulsion, history

of loss of consciousness and history of frothing, tongue bite, passing urine/ stools

during the convulsions.

5. Premonitory symptoms like headache, epigastric pain, nausea, vomiting and

blurred vision.

6. Any history of pain abdomen, trauma, per vaginal leak or bleeding

7. Obstetric, menstrual, past, family and personal history

8. Any nature of treatment taken before hospitalization.

A rapid general examination was subsequently made noting the grade of

consciousness of the patient, temperature, pulse rate, respiratory rate, blood pressure,

presence of edema, evidence of tongue bite, condition of the heart, state of the lungs

and knee jerk.

A detailed obstetric examination was conducted noting the height of the

uterus, presence, frequency and duration of uterine contraction, lie and presentation of

the fetus, relation of the presenting part to the brim and the rate and regularity of the

fetal heart.

Vaginal examination was done and the condition of the cervix - position,

consistency, dilatation, effacement and station of the presenting part i.e., Bishop's

score was noted. Presence of bag of membrane and adequacy of the pelvis was also

38

noted.

Bladder was catheterized and urine output was noted.

IV line was started and 1 pint of Ringer lactate was given for hydration.

Investigations were sent for complete hemogram, urine analysis, blood

grouping and Rh-typing, renal and liver function tests and coagulation profile.

Medical Management:

1. Anticonvulsants:

Magnesium sulphate as per single dose regime on admission, loading dose

4gm of MgSO4 (MgS04.7H20) as a 20% solution was given intravenously at the rate

of 1 gm per minute followed by 4gms of 50% MgS04 2 gm was injected deeply in the

upper outer quadrant of one buttock and another half (2gm) injected similarly in the

other buttock with a 3 inch long 20 gauge needle.

If the patient has recurrence then Pritchard’s regime was followed, 2gms of

50% MgS04 solution to each buttock was injected as above.

Maintenance dose: Every 4 hours thereafter, 5 g of 50% solution of MgS04 was given

in alternate buttocks but only after ascertaining the following:

a) The patellar reflex is present

b) Respiratory rate is more than 14/ minute

c) Urine output in the previous 4 hours was 100 ml or more

This was continued for 24 hours after delivery.

2. Antihypertensive; Nifedipine 10 mg

On admission, if diastolic blood pressure was more than 110 mm Hg,

39

nifedipine 10 mg was given orally. Thereafter, the dose was titrated as per blood

pressure response.

Labetolol, if diastolic blood pressure was more than 110 mm of Hg inj.

labetolol 20mg IV bolus is given. If blood pressure is not decreased to desirable level

in 10 minutes then 20mg, 40 mg upto 220mg is given

3. Antibiotics were given stat and continued for an average of 1 week.

Obstetric Management:

Due consideration was given to:

1. Age of the patient

2. Gestational age

3. Whether the patient was in labour or not

4. Rate and regularity of fetal heart

5. Bishop's score

Then, either induction was done with pervaginal misoprostol or dinoprostone

gel following conservative obstetric management or were taken up for caesarean

section directly with unfavourable cervix as the associated indication. Patients who

delivered per vaginum following successful induction (if not in labour), with

prostoglandins patients who were in labour (augmented with ARM or pitocin or both)

who also delivered per vaginum and those who were fully dilated and effaced on

admission and went for spontaneous delivery/outlet forceps, were all included under

the "V.D. group".

Caesarean section was also done in those cases wherein induction failed or

other varied associated obstetric indications were present. Thus, all the patients where

in caesarean section was done were included in the "C.D. group".

40

The associated indication for caesarean, induction delivery interval in induced

vaginal deliveries, total blood loss and intraoperative/intrapartum complications if any

were noted. Baby notes were noted.

Follow up : The mother and the neonate were followed till discharge at

hospital and then details noted in the proforma.

41

OBSERVATIONS

TABLE-6 AGE-WISE DISTRIBUTION OF STUDY SUBJECTS

Delivery Total Age group

Caesarean Vaginal

Up to 20 years 19 (46.3%) 24 (40.7%) 43 (43%)

21 – 24 years 20 (48.8%) 27 (45.8%) 47 (47%)

More than 24 years 02 (4.9%) 08 (13.6%) 10 (10%)

Total 41 (100%) 59 (100%) 100 (100%)

Chi-square – 2.05 df-2 p value – 0.35

Incidence of eclampsia found be high in primigravida between 21-24 years.

1. Age wise distribution

46.30% 48.80%

4.90%

40.70%45.80%

13.60%

0.00% 10.00% 20.00% 30.00% 40.00% 50.00% 60.00%

upto 20 yrs 21 - 24 yrs > 24 yrs Age group

Ceaserean Vaginal

42

TABLE.7 RELIGION-WISE DISTRIBUTION OF STUDY SUBJECTS

Delivery Age group

Caesarean Vaginal

Total

Hindu 37 (90.2%) 51 (86.4%) 88 (88%)

Muslims 03 (7.3%) 08 (13.6%) 11 (11%)

Christian 01 (2.4%) 00 01 (01%)

Total 41 (100%) 59 (100%) 100 (100%)


In my study Hindus were affected when other groups.

2. Religion wise distribution

90.20%

7.30%

2.40%

86.40%

13.60%

0.00%

0.00% 10.00 %

20.00%

30.00%

40.00%

50.00%

60.00%

70.00 %

80.00 %

90.00 %

100.00%

Hindu

Muslims

christian

Religion

Ceaserean Vaginal

43

TABLE-8 RELATION BETWEEN NUMBER OF CONVULSIONS AND MODE OF

DELIVERY

Delivery Convulsions

Caesarean Vaginal

Total

1 -3 34 (82.9%) 49 (83.1%) 83 (83%)

4 – 6 06 (14.6%) 10 (16.9%) 16 (16%)

More than 6 01 (2.4%) 00 01 (01%)

Total 41 (100%) 59 (100%) 100 (100%)

Chi-square – 1.52 df-2 p value – 0.46 p value insignificant

0.00% 20.00% 40.00% 60.00% 80.00%

100.00%

1 to 3 4 to 6 >6 Covulsions

3. Relation b/w no. of convulsions and mode of delivery

Ceaserean Vaginal

44

TABLE-9 RELATION BETWEEN CONSCIOUSNESS B/W CONVULSIONS AND

MODE OF DELIVERY

Delivery Consciousness

Caesarean Vaginal

Total

Yes 40 (97.6%) 57 (96.6%) 97 (97%)

No 01 (2.4%) 02 (3.4%) 03 (03%)

Total 41 (100%) 59 (100%) 100 (100%)

Fischer exact test p value – 0.46

97.60%

2.40%

96.60%

3.40%

0.00%

20.00%

40.00%

60.00%

80.00%

100.00%

Ceaserean Vaginal

Mode of delivery

4. Relation b/w consciousness and mode of delivery

YesNo

45

TABLE-10 RELATION BETWEEN ANTE NATAL CHECKUP AND MODE OF

DELIVERY

Delivery ANC

Caesarean Vaginal

Total

Yes 26 (63.4%) 36 (61%) 38 (38%)

No 15 (36.6%) 23 (39%) 62 (62%)

Total 41 (100%) 59 (100%) 100 (100%)


TABLE-11 RELATION BETWEEN PATIENT GENERAL CONDITION AND MODE OF

DELIVERY

Delivery Patient condition

Caesarean Vaginal

Total

Conscious 33 (80.5%) 47 (79.7%) 80 (80%)

Irritable 07 (17.1%) 06 (10.2%) 13 (13%)

Un conscious 01 (2.4%) 06 (10.2%) 07 (07%)

Total 41 (100%) 59 (100%) 100 (100%)


80.50%79.70%

17.10%10.20%

2.40% 10.20%

0.00% 20.00% 40.00% 60.00% 80.00%

100.00%

Conscious Irritable Unconscious

5. General condition and mode of delivery

Ceaserean Vaginal

46

TABLE-12 RELATION BETWEEN CONJUNCTIVA STATUS AND MODE OF

DELIVERY

Delivery Conjunctiva

Caesarean Vaginal

Total

Pink 36 (87.8%) 59 (100%) 95 (95%)

Pale 05 (12.2%) 00 05 (05%)

Total 41 (100%) 59 (100%) 100 (100%)

Fischer exact test p value – 0.01

TABLE-13 RELATION BETWEEN TONGUE CONDITION AND MODE OF DELIVERY

Delivery Tongue

Caesarean Vaginal

Total

Pink 30 (73.2%) 46 (78%) 76 (76%)

Pale 01 (2.4%) 01 (1.7%) 02 (02%)

Bite 10 (24.4%) 12 (20.3%) 22 (22%)

Total 41 (100%) 59 (100%) 100 (100%)


6. Distribution of study subjects based on tongue status

Pink76%

Pale2%

Bite22%

47

TABLE-14 MODE OF DELIVERY

Mode of delivery Frequency Percentage

CD 41 41%

VD 59 59%

Total 100 100%

Incidence of vaginal delivery is 59% caesarean section is 41%.

7. Mode of delivery

41%

59%

0% 10% 20% 30% 40% 50% 60% 70%

CD

VD

48

TABLE-15 RELATION BETWEEN GESTATIONAL AGE AND MODE OF DELIVERY

Delivery Gestational age

Caesarean Vaginal

Total

32 – 34 weeks 01 (2.4%) 17 (28.8%) 18 (18%)

34 – 36 weeks 03 (7.3%) 06 (10.2%) 09 (09%)

36 – 40 weeks 37 (90.2%) 36 (61.0%) 73 (73%)

Total 41 (100%) 59 (100%) 100 (100%)


8. GESTATIONAL AGE AND MODE OF DELIVERY

0

5

10

15

20

25

30

35

40

32 34 wk 34 ‐ 36 wk 36 ‐ 40 wk

Caesarean

Vaginal

It was found that there was increase in evidence of antepartum eclampsia with increase in gestational age the maximum incidence being 36 – 40 weeks in both the groups.

49

TABLE-16 INDICATIONS FOR CAESAREAN SECTION

Indications Frequency Percentage

Cervical factors

Unfavourable cervix

Failure to progress

Cervical dystocia

11

20

02

26.8%

48.8%

04.9%

Fetal distress

CPD

06

02

14.6%

04.9%

Total 41 100%

Failure to progress induction topped the list for caesarean section. Next common indication is fetal distress.

26.80%

48.80%

4.90%

14.60%

4.90% 0.00%

10.00% 20.00% 30.00% 40.00% 50.00%

Unfavourablecervix

Failure toprogress

Cervicaldystocia

Fetal distress CPD

Indications

16 Indications for caeserean section

50

TABLE-17 INCIDENCE OF IUD’S ON ADMISSION

VD group CD group Total FHR

No. of cases % No. of cases % No. of cases %

Present 58 98.3 41 100% 99 99%

Absent 1 1.7 _ _ 1 1%

Total 59 100 41 100% 100 100%

Fischer exact test p value – 1.00 P value is insignificant on admission There was no IUD’s in CD group only one VD group.

TABLE-18 RELATION BETWEEN MODIFIED BISHOP SCORE FINDING AND MODE

OF DELIVERY

Delivery Bishop score

Caesarean Vaginal

Total

0 11 (26.8%) 12 (20.3%) 23 (23%)

2 13 (31.7%) 15 (25.4%) 28 (28%)

3 06 (14.6%) 08 (13.6%) 14 (14%)

4 11 (26.8%) 23 (39%) 34 (34%)

5 00 01 (1.7%) 01 (01%)

Total 41 (100%) 59 (100%) 100 (100%)


P value is insignificant, Bishop’s score was unfavourable in all most all cases.

51

TABLE-19 BISHOP’S CERVICAL SCORING SYSTEM

Factors 0 1 2 3

Dilatation of cervix < 1cm 1-2 cm 2-4 cm > 4 cm

Length of cervix 4 cm 2-4 cm 1-2 cm < 1 cm

Consistency Firm average Soft

Position posterior Mid anterior

Station of presenting part -3 -2 -1/0 +1,+2

Bishop’s score was unfavourable in 90% of the cases in.

In CD group, Bishop’s score was 0.

In VD group also, Bishop’s score was 0 but vaginal delivery was opted.

Incidence of operative vaginal delivery

Outlet forceps was applied in all cases of 36-40 weeks gestation and ventouse was

applied in one case in vaginal delivery group.

Indications for application of forceps:

1. To cut short second stage of labour .

2. Fetal distress.

Indication for application of ventouse:

Poor maternal efforts.

Incidence of induced vaginal delivery

95% of cases who delivered vaginally were either not in labour or in latent phase of

labour. Those patients are induced with prostaglandins, that is misoprostol tablets and

dinoprostone gel.

TABLE-20

52

CONVULSION- DELIVERY INTERVAL

VD group CD group Convulsion-delivery interval

No. of cases % No. of cases %

0-6 hrs 2 3.4 6 14.6

6-12 hrs 18 30.5 11 26.8

12-18 hrs 20 32.2 11 26.8

18-24 hrs 12 20.3 9 21.9

>24 hrs 8 13.6 4 9.9

Total 59 100 41 100

P value 0.34 insignificant

Net convulsion delivery interval was less than 6 hrs in13.15% of cases in CD group

and 3.22% of cases in VD group.

70% of the cases CD group delivered within 18 hours of the first convulsion

TABLE-21

INDUCTION-DELIVERY INTERVAL

VD group Induction delivery interval

No. of cases %

0-6 hrs 1 1.5%

6-12 hrs 34 54.8%

12-18 hrs 20 32.3%

18-24 hrs 2 3.2%

> 24 hrs 2 3.2%

Perinatal outcome

VD group: No. of cases were 59 and no. of babies were 58

CD group: No. of cases were 41 and no. of babies were 41

53

TABLE-22 PERINATAL MORBIDITY

VD group CD group P value Perinatal outcome


Apgar < 5 at 1 min. 15 25.5 4 9.7 0.04

Need for resuscitation 8 13.5 2 4.9 0.19

Need for NICU 19 32.2 9 21.9 0.26

Mean duration of stay in NICU in CD group 5.78 days

Mean duration of stay in VD group 3 days

P value 3.8

Apgar < 5 at 1 min. p value significant

25.40%

9.70%13.50%

4.90%

32.20%

21.90%

0.00% 5.00%

10.00% 15.00% 20.00% 25.00% 30.00% 35.00%

APGAR < 5 at ! Min Need for resuciation need for NICU

10. Perinatal morbidity

VD CD

54

TABLE-23 COMPARISON OF BIRTH WEIGHT, APGAR SCORE AND NICU STAY

Delivery Parameters

Caesarean (mean+/-sd) Vaginal (mean+/-sd)

P value *

Birth weight (Kgs) 2.51 +/- 0.44 2.03 +/- 0.42 0.00

APGAR score 1 min 5.8 +/- 0.6 5.3 +/- 1.4 0.03

APGAR score 5 min 7.7 +/-0.9 7.1 +/-1.6 0.02

NICU stay (days) 5.78 +/- 0.85 3.00 +/- 1.37 0.16

* student‘t’ test

Birth weight of babies, Apgar score at 1minute & 5 minute was more in CD group than vaginal group

11. Birth weight of babies

2.51

2.03

0 0.5 1 1.5 2 2.5 3

Ceaserean

VaginalMode of delivery

Kgs

5.8 5.3

7.77.1

0

2

4

6

8

Score

At 1 min At 5 min

Time

12. APGAR score

Ceaserean Vaginal

55

TABLE-24 PERINATAL MORTALITY

VD group CD group Perinatal outcome


Live births 46/59 78 38/41 92.68

Still births 5/59 8.4 _ _

NND 7/59 11.4 3 7.3

IUD an admission 1/59 1.7 100

Corrected perinatal mortality was 7.35% in CD group than 18.6% vaginal group.

13. Perinatal outcome

78% 92.60%

8.40% 0%

11.40% 7.30% 1.70% 0%0%

20% 40% 60% 80%

100%

VD CD Delivery

Live births Still births NND IUD

56

TABLE-25 ANALYSIS OF CAUSES OF PERINATAL MORTALITY WITH

GESTATIONAL AGE >32 WEEKS

VD group CD group P value Cause


H I E 5 8.5 1 2.4 0.39

Septicemia 1 1.7 _ _

RDS 1 1.7 _ _

MAS 1 1.7 2 4.8 0.56

In CD group PNM was due to MAS in VD group HIE is commonest cause

P value is insignificant

8.50%

1.70%1.70%1.70%2.40%

0.00%0.00%

5%

0.00%

2.00%

4.00%

6.00%

8.00%

10.00%

VD CD

14. Causes of perinatal mortality with gestational age > 32 weeks

HIE Septicemia RDS MAS

57

TABLE-26 COMPARISON OF PNM WITH RESPECT TO GA (EXCLUDING IUDS)

VD group CD group P value Gestational

No. of

cases

PNM % No. of

cases

PNM %

32-34 17 5 29.2 1 _ _

34-36 7 4 57.2 3 _ _

36-40 35 3 8.6 37 3 8.10

Total 59 12 13.5 41 8.10 0.51

For both gestational ages between 36-40 PNM was lesser in CD group P value is insignificant

29%

57.20%

8.50%0.00% 0%

8.82%

0% 10% 20% 30% 40% 50% 60%

VD CD

Delivery

15. Relation of PNM with respect to gestational age

32 - 34 weeks 34 - 36 weeks 36 - 40 weeks

58

TABLE-27 COMPARISON OF PNM WITH RESPECT TO BIRTH WEIGHT

VD group CD group P value Birth weight

(KGs) No. of cases PNM % No. of cases PNM %

1.5-2 40 7 11.8 11 1 9.9 1.00

2-2.5 16 4 6.77 15 1 6.6 1.00

2.5-3 2 1 50 15 1 6.7 0.22

3-3.5 1

>3.5

Total 59 12 18.5 41 3 7.3

For all birth weights PNM was lesser CD group

P value is insignificant

12% 6.77%

50.00%

0.00%0%

9.90%7%6.60%0% 0%

0% 10% 20% 30% 40% 50%

VD CD

Delivery

16. Relation between PNM and Birth weight

1.5 - 2.0 Kgs 2.0 - 2.5 kgs 2.5 - 3.0 Kgs 3.0 - 3.5 Kgs > 3.5 Kgs

59

TABLE-28 RELATION OF PNM TO TOTAL NO CONVULSION

VD group CD group P value Total no

Convulsion No. of

cases

PNM % No. of

cases

PNM %

1-5 57 11 19.2 36 2 5.5 0.47

6-10 2 1 50 4 1 25 1.00

>10 _ _ _ _ _

Total 59 12 20.3 41 3 7.3

There was increase PNM with increase total no of convulsion in both the groups

P value is significant in 1 – 5 convulsions.

12.30%

50.00%

5.50%

20.00%

0.00%

10.00%

20.00%

30.00%

40.00%

50.00%

VD CD

17. Relation between PNM and Convulsions

1 to 56 to 10

60

TABLE-29 MATERNAL COMPLICATIONS

Delivery Maternal complications

Caesarean Vaginal

Total

Pulmonary edema 01 (2.4%) 01 (17.0%) 02 (02%)

Placental abruption/HELLP 00 03 (5.1%) 03 (03%)

UTI 03 (7.2%) 00 03 (03%)

PPH 01 (2.4%) 01 (1.7%) 02 (02%)

Cerebral infarction 01 (2.4%) 01 (1.7%) 01 (01%)

Cortical Blindness 01 (2.4%) 01 (1.7%) 02 (02%)

Nil 35 (84.0%) 52 (88.4%) 87 (87%)

Total 41 (100%) 59 (100%) 100

(100%)


There was progressive increase in maternal morbidity with increase in induction

delivery interval.

61

TABLE-30 RELATION MATERNAL COMPLICATIONS TO CONVULSION DELIVERY

INTERVAL

VD group CD group P value Time

interval in

hours

No

of

cases

With

complications

% No of

cases

With

complications

%

0-6 04 1 25 5 1 20 1

6-12 32 2 6.2 13 2 15.4 0.56

12-18 19 2 10.52 10 2 20 1

18-24 2 2 100 8 1 12.5 0.01

>24 2 5

P value is significant in 18-24 time interval in hours

There was progressive increase in incidence of maternal complication with increase in

convulsion delivery interval in both the groups. The incidence of maternal

complication was found to be higher in VD group.

25.00%20.00%6.20%

15.40% 15.80%20%

100.00%

12.50%

0.00% 20.00% 40.00% 60.00% 80.00%

100.00%

0 to 6 6 to 12 12 to 18 18 to 24 Time interval (hours)

19. Relation between maternal complications and convulsion delivery interval

VD CD

62

TABLE-31 RELATION MATERNAL COMPLICATIONS TO INDUCTION DELIVERY

INTERVAL

Time interval in hours

No of cases No of cases With

complications

%

0-6 10 1 7.1

6-12 14 1 7.1

12-18 10 2 20

18-24 2 2 20

>24 2

TABLE.32 MATERNAL MORTALITY AND MODE OF DELIVERY

Delivery Maternal mortality

CD VD

Total

Yes 00 01 (1.7%) 01 (1%)

No 41(100%) 58 (98.3%) 99 (99%)

Total 41(100%) 59 (100%) 100

(100%)

There was no maternal death in CD group, 1 in VD group

0%

100%

1.70%

98.30%

0%

20%40%60%80%

100%

Maternal mortality

CD VD

Delivery

20. Maternal mortality and mode of delivery

Yes No

63

TABLE-33 RELATION BETWEEN CESSATION OF PROTEINURIA AND MODE OF

DELIVERY

Delivery Proteinuria nil

Caesarean Vaginal

Total

Day 1 09 (22%) 20 (33.9%) 29 (29%)

Day 2 17 (40.8%) 19 (32.2%) 36 (36%)

Day 3 12 (29.6%) 16 (27.1%) 28 (28%)

Day 4 03 (7.6%) 04 (6.8%) 07 (07%)

Total 41 (100%) 59 (100%) 100 (100%)


Cesasation of proteinuria early in vaginal group then CD group

TABLE-34 COMPARISON OF TIME BETWEEN EVENTS

Delivery Time (hours)


P value *

Admission – convulsions 5.24 +/- 2.36 5.5 +/- 2.4 0.60

Convulsions - delivery 17.3 +/- 7.0 17.0 +/- 5.5 0.84

Admission - delivery 14.2 +/-9.0 13.0 +/-9.1 0.52

* student‘t’ test

TABLE-35 COMPARISON BLOOD PRESSURE

Delivery Blood pressure


P value *

SBP (admission) 159.27 +/- 16.15 152.75 +/- 13.35 0.03

SBP (delivery) 139.46 +/- 16.24 136.78 +/- 15.42 0.40

DBP (admission) 104.88 +/- 14.98 102.58 +/- 13.03 0.41

DBP (delivery) 92.20 +/- 7.89 92.03 +/- 7.61 0.91

* student ‘t’ test

64

TABLE-36 COMPARISON BLOOD PRESSURE DURING ADMISSION AND DELIVERY

Blood pressure Mean +/- sd P value*

SBP

Admission

Delivery

155.42 +/- 14.8

137.88 +/- 15.7

0.00

DBP

Admission

Delivery

103.52 +/- 13.83

92.10 +/- 7.56

0.00

*Paired ‘t’ test

21. Systolic Blood Pressure during admission and delivery

159.27

139.46

152.75

136.78

125 130 135 140 145 150 155 160 165

SBP(admission) SBP(delivery)

Mean (mmHg)

Ceaserean Vaginal

104.88102.58

92.2 92.03

85

90

95

100

105

Mean(mmHg)

DBP(admission) DBP(delivery)

22. Diastolic Blood pressure among study subjects

Ceaserean Vaginal

65

DISCUSSION

Eclampsia a dreaded complication in pregnancy is still associated with a great

deal of maternal and fetal loss.Some decades ago the conventional treatment of

eclampsia was conservative approach, with the use of sedatives anticonvulsants and

antihypertensives to be followed by induction or stimulation of labour after the fits are

controlled.

Caesarean section was considered to be extremely risky procedure and

reserved for highly selected cases.

Now in twenty first century with advancement in the field of anesthesiology

caesarean section in eclampsia is no more risky and promises reassuring maternal and

perinatal outcome.

In the present series 100 primigravidae with more than 32weeks gestation with

antepartum eclampsia were studied.

1. VD group where vaginal delivery was done.

2. CD group where caesarean section was performed.

Comparative incidence of CD vs VD Incidence of caesarean section was 41% and that of vaginal delivery was 59%.

This was comparable with study of MarioLopezllera series,out of 107 cases the

incidence of caesarean section was 40.4% .the incidence quoted by other authors are

66

TABLE-37 COMPARATIVE INCIDENCE OF CAESAREAN SECTION IN

ECLAMPSIA

Authors Year Percent

Mario Lopezellera104 1967 40.4%

Lean et al15 1968 63.3%

Sibai et al105 1981 49%

Abdullah AR106 1990 42.05%

Mondal RN4 1991 19.17%

Habeebullah S107 1995 28.70%

Hakerwadi AU108 1996 50.12%

Oladoken A et al109 2000 66%

Lee W Connell115 2004 79%

Kamilya G et al22 2005 49.70%

Present series 2011 41%

Age in both the groups the highest incidence was in age group 21-24 years

.this was comparable with the following studies who also found the highest incidence

between 20-25years.

• Hakerwadi108

• Suchita Mundle, Indrajit Mullik27

• Vinita Bansal30

Socioeconomic status: In both the groups 80% of cases belong to low

socioeconomic status. The incidence correlates well with the other studies24, 27 & 28,

which have found the incidence of eclampsia to be high in women of low

socioeconomic status due to poverty, illiteracy and lack of proper antenatal care.

Antenatal care:

Twenty six percent of cases in CD group and thirty six percent of cases in VD

group were booked. Here notable fact is that more than cases were booked, still had

67

eclamptic seizure. This was because in few cases there was no mid trimester fall of

blood pressure and this was overlooked by attending doctor. Infrequent antenatal

visits and refusal to get admitted when advised were instrumental in causing

eclampsia in these cases.

Gestational age:

The highest incidence was found between 36-40weeks. 90.2% in CD group

and 61.0% in VD group. Most studies found that the incidence to be high when the

age is less than 37weeks.

Low JJ33 found maximum incidence between 33-37 weeks (60%).

Mundle S27 found maximum incidence between 29-36weeks (70%).

Most of the referrals constituted term gestation with viable fetus and poor cervical

scores.

After 32weeks gestation - out of 100cases 59 were delivered vaginally because

• 1 was IUD

• 23 were preterm

• 25 were induced

• 10 cases did not give consen.

Condition at admission:

Most of the patients were admitted in a compromised state after throwing a

number of convulsions at home. However almost 80% of the cases in both the groups

had thrown less than 4 convulsions. None of cases in both the groups had more than

six convulsions. Most of them were conscious on admission. All three signs of

toxemia were seen in 78% of cases.

Bishop score on admission:

68

It was unfavourable in 72.5% of cases in CD group and 78% of cases in VD

group. All these 78% group who were otherwise not ideal candidates for vaginal

delivery were allowed to deliver vaginally either because of poor expectancy of fetal

salvage or refusal for caesarean section by the patient’s attender in view of poor fetal

salvage. To be more precise 59 cases with unfavourable cervix who were allowed

vaginal delivery one was IUD, 23 were preterm, 10 cases did not give consent.

Zuspan FP111 asserted that condition of cervix is a fetal prognostic indicator

and presents the obstetrician with the challenge as to how, when and what means of

delivery are most appropriate for best results.

Indications for caesarean section:

Eleven cases were operated for unfavourable cervix, cervical factors top the

list of indications for caesarean section 30. Next commonest indication was fetal

distress accounting for 6 cases.

In Mondal RN series4, 41 out of 62 cases (62.12%) CD was a deliberate

decision with the sole purpose of shortening the exposure to delivery.

Hakerwadi AV108 quoted fetal distess 36.18% of section patients followed by

failed induction in 20.6%.

Habebullah107 quoted fetal distress 34.7% of CD.

Incidence of operative vaginal delivery:

Outlet forceps was applied in almost all cases the commonest indication being

cut short second stage of labour followed by fetal distress. Ventouse was applied in

one case due to poor maternal efforts.

Induction delivery interval:

All the cases with VD were induced of which required more than twelve hours

for delivery.

69

Perinatal Mortality:

The incidence in the C.D. and V.D. group of live births was 92.3 and 73%

respectively, of still births was nil and 11.8% respectively and that of neonatal deaths

was 7.3% and 8.4% respectively. The striking difference in the incidence of live birth

and still births in the two groups could be partly attributed to the comparatively

increased rates of, low birth weight and preterm babies in the V.D. group. However,

still the difference was considerable. The corrected PNM figures in the C.D. and V.D.

groups were 7.3% and 18.6% respectively. This was comparable with Dandekar

LM113 series (1992).

70

TABLE-38 COMPARATIVE INCIDENCE OF PNM TO MODE OF DELIVERY

Authors Year PNM in CD VD

Derek Crichton

Morris11

1968 21.6% 45.70%

Dandekar L M112 1992 10% 40%

Taj116 2004 7% 12%

Present Series 2011 7.3% 18.6%

Comparison of Causes of PNM:

Between 32- 34 Weeks: In the C.D. group, there was 1 case no deaths. In the V.D.

group, out of 17 cases 7 had perinatal deaths, the predominant causes being

intrauterine hypoxia (where FHR was lost during the process of induction, and birth

asphyxia) resulting in fresh still births, accounting for 11.8% of the total deaths).

After 34 Weeks:, There were 3 perinatal deaths in the C.D. group of which 2 were

due to meconium aspiration syndrome and 1 each due to birth asphyxia and

intrauterine hypoxia. 4 of these had their C-D intervals more than 16 hours. Only 1

case had C-D interval of 8 hours but however it was a case of failed induction with

fetal distress. In the V.D. group, intrauterine hypoxia was the predominant cause

(13.4%).

Comparison of PNM with respect to gestational age (excluding IUDs): For all

gestational age, PNM was found to be lesser in the C.D. group, when compared with

the V.D. group.

71

In the V.D. group: There were 12 perinatal deaths of which:

• 24 were between 32 to 36 weeks, but were preterm IUGRs with poor fetal

expectancy and so were let to deliver vaginally, as a result of which, , 4 were fresh

stillbirths and 5 were neonatal deaths.

• 35 were more than 36 weeks gestation and were opted for vaginal delivery because

patients opted for vaginal delivery ,out of which 1 was fresh still birth 2 were

neonatal deaths, .

In the C.D. group: Of the 3 neonatal deaths, 1 was born in a bad state due to birth

asphyxia with and the other 2 were due to fetal distress (MAS).

Comparison of PNM with respect to birth weight (excluding IUDs):

For all birth weights, PNM was found to be lesser in the C.D. group, except 2 cases;

one baby 2kgs which was delivered by caesarean section when 11 hours of induction

failed and another baby of 2.5kgs, 2.7Kgs where caesarean section was done for failed

induction and fetal distress. Both the babies died in postnatal period.

In the V.D. group:

• Of the 40 babies between 1.5 to 2 Kgs,4 were stillborn due to birth asphyxia and 2

had neonatal death due to respiratory distress syndrome & HIE – they were let to

deliver vaginally as they were preterm babies.

• 16 babies between 2 to 2.5kgs were induced except 1 where consent for surgery was

not given – as a result, 3 were fresh stillborn and 2 had neonatal deaths.

• One baby of 2.5-3Kgs 1 was neonatal death. In the C.D. group: One baby died with birth weight 2.5kgs due to HIE.

72

• Two babies with birth weights 2.2 and 2.5kgs respectively had neonatal deaths due

to meconium aspiration syndrome, both the babies being taken for caesarean section

with fetal distress in utero.

Factors affecting PNM:

1. Number of convulsions: PNM increased in proportion to increase in the number of

convulsions. Similar finding was observed by Mundle S27. (1998) and Swain S20

(1993). Dutta DC1 quotes bad prognosis for mother and fetus if number of

convulsions are more than 10.

2. Induction delivery interval: PNM increased progressively with increase in the

induction delivery interval beyond 24 hours. Nanda S19 (1989) also asserted that

increased induction delivery interval is associated with adverse perinatal outcome

because of increased duration

of exposure to fetal asphyxia.

3. Convulsion delivery interval: PNM also increased proportionately as the first

convulsion-delivery interval increased in both the groups. Similar finding was

observed by Lopezllera et al104 (1967), Nanda Smiti19 (1989) and Swain S20

(1993).73.

73

TABLE-39 COMPARATIVE STUDY OF PNM TO CONVULSION-DELIVERY

INTERVAL IN LOPEZLLERA SERIES104 (1967)

Convulsion – delivery interval hours PNM %

< 6 Hours 14%

6 – 12 Hours 19%

12 – 24 Hours 62%

> 24 Hours 53%

4. Time when caesarean section was performed: PNM was decreased when

caesarean section was performed within 6 hours and was when

performed after 6 hours of admission. So, early decision for caesarean

section when delivery is not anticipated within 6 hours of admission helps

in improving fetal outcome.

Maternal Outcome:

Maternal Complications:

Maternal complications were encountered in 14% of the cases in the C.D. group and

27.2% of the cases in the V.D. group. The complications were:

1. Postpartum hemorrhage was seen in 1.75% of the cases in the V.D. group,

all of which were controlled with oxytocin and carboprost .two bottles of blood was

transfused.on the other hand one case in CD group had postpartum haemorrhage.

intraoperatively but was controlled with B-lynch sutures.

2. Abruptio placenta was seen in 5.1% of the cases in the V.D. group.

However, they improved after component therapy. Hakerwadi AV108 (1995) quoted an

incidence of 19.6% and Sibai et. al.,38 (1993) quoted an incidence of 20% in

eclampsia.

74

3.Cerebral infarction: One case in the C.D. group, on third postoperative day

developed cerebral infarction in occipitoparietal region. Other case in VD group on

4th postnatal day developed cerebral infarction. Both the patients recovered

uneventfully with conservative treatment.

Los Angeles Country study84 (1983) found a case fatality rate of 10.4% for cerebral

infarction in eclampsia.

4. Pulmonary edema was seen in one case in the V.D. group (17%) and did not

respond to medical line of therapy. Patient died on second post natal day. Bansal V6

(1998) found the incidence to be 4.6%.

5. Cortical blindness was encountered in both VD and CD group. They however

regained back their vision within 4 days in VD group and 5 days in CD group.

6. Urinary tract infection was seen in 7.2% of the cases in the C.D. group for which

cases are treated according to culture and sensitivity.

Maternal Mortality:

Maternal deaths occurred in 1.7% of the cases in the V.D. group while there were no

maternal deaths in the C.D. group.77

75

TABLE-40 COMPARATIVE INCIDENCE OF MATERNAL MORTALITY TO MODE OF

DELIVERY MATERNAL MORTALITY (%)

Authors Year Maternal mortality VD CD

Mario Lopezllera104 1967 12 12

RatnamSS8

Sivasamboo5 1968 6 1.7

Derek Crichton16 1968 4.8 4.2

Villiers&Slabber17 1970 12.7 4.3

MondalRN4 1991 15.48 8.06

HabeebullahS103 1995 7.10 4.30

Present series 2011 1.7% -

Cause for Maternal Deaths:

1 Women out of total 59 in the V.D. group died, accounting for a maternal mortality

of 1.7%.

One woman had pulmonary edema following induction of labour. Induction delivery

interval was ten hours. She delivered dead male baby. Her pulmonary edema did not

respond to oxygen inhalation. Diuretic therapy. Later developed acute respiratory

distress syndrome died 22hours following delivery.

Relation of Maternal Mortality to First Convulsion-Delivery Interval:

In the present series, the mother who died had an induction-delivery interval more

than 10 hours and convulsion-delivery interval more than 14 hours.

Menon7 (1961) observed that maternal mortality increased with increase in the first

convulsion-delivery interval. His results were:

76

TABLE-41

RELATION OF MATERNAL MORTALITY TO FIRST CONVULSION-DELIVERY INTERVAL

First Convulsion-delivery

interval (hours)

Maternal Mortality (%)

0 – 2 7

2 – 4 13

4 – 8 19

8 – 12 22

12 – 18 25

18 – 24 32

>24 42

Thereby, we infer, that both the maternal and perinatal outcome may be considerably

improved in primigravid eclamptics if an early decision for caesarean section is taken,

in cases where delivery is not anticipated within 6 hours of adminssion or 12 hours of

the first fit, whichever is earlier.

77

SUMMARY

1. The study period extended from October 2010 to September 2011, a period of

12 months.

2. 100 primigravidas with more than 32 weeks gestation with antepartum

eclampsia were studied by dividing them into two groups for comparison.

• The C.D. group consisted of patients in whom caesarean section was

performed.

• The V.D. group consisted of patients who delivered vaginally.

3. The incidence of caesarean section was 41% and that of vaginal delivery was

59%.

4. Highest incidence of antepartum eclampsia was seen in the age group of 20-24

years in both the groups.

5. Majority of the cases in both the groups were Hindus of low socioeconomic

status from rural areas with improper antenatal care.

6. Maximum incidence of antepartum eclampsia was seen between 36-40 weeks

in both the groups.

7. Most of the cases had thrown less than 5 convulsions and were conscious on

admission in both the groups.

8. Pedal edema was predominant in both groups but the V.D. group had

comparatively more number of cases with nil edema.

9. Most of the patients presented with all the 3 signs of toxaemia in both the

groups.

10. Bishop’s score was unfavorable the C.D. group and the V.D. group.

78

11. Almost all the vaginal deliveries were induced. Outlet forceps was applied in

all cases and ventouse was applied in 1 case in the V.D. group.

12. 11 of the cases were taken for caesarean section for unfavourable. Cervical

factor were responsible for 80.2% of cases in the C.D. group.

13. 11 of the cases were operated within 6 hours and 31 cases were operated

within 24 hours of admission in the C.D. group.

14. 26.8% of the cases in the C.D. group were delivered within 12 hours of

admission, while in the V.D. group only one case delivered within 6 hours.

15. 41.4% of the cases in the C.D. group was delivered within 12 hours of the first

fit, while 33.9% of the cases in the V.D. group did so.

16. 88.6% of the cases in the V.D. group required more than 18 hours for delivery

after the start of induction.

17. Live birth rate was 92.23% in the C.D. group and 78% in the V.D. group.

18. Corrected perinatal mortality rate was 7.35% in the C.D. group and 18.64% in

the V.D. group.

19. NICU admission rate was 21.9% in the C.D. and 32.2% in the V.D. group.

20. Mean duration of stay in NICU in the C.D. group was 5.75 days and in the

V.D. group was 3 days.

21. The predominant cause for PNM was intrauterine hypoxia in the V.D. group

while it happened to be the second commonest cause in the C.D.

22. PNM was lesser in the C.D. group irrespective of the gestational age and birth

weight.

23. PNM increased with increase in the total number of convulsions, admission-

delivery, induction-delivery and convulsion-delivery intervals.

79

24. Both PNM and incidence of NICU admission were lesser when caesarean

section was performed within 6 hours of admission.

25. Incidence of maternal complications was 84% in the C.D. and 88.6% in the

V.D. group.

26. The incidence of maternal complications increased with increase in the total

number of convulsions, convulsion-delivery and induction-delivery intervals.

27. Maternal mortality was 1.7% in the V.D. group and nil (0%) in the C.D group.

28. Maternal deaths had their induction delivery interval more than 6 hours and

convulsion-delivery interval more than 12 hours.

29. Both perinatal morbidity and mortality and maternal morbidity and mortality

were found to be lesser in the C.D. group in comparison with the V.D. group.

30. Thus, early decision for caesarean section especially when delivery is not

anticipated with 6 hours of admission is detrimental in improving the perinatal

as well as maternal outcome in eclampsia in primigravidas with more than 32

weeks pregnancy.

80

CONCLUSION

“In antepartum eclampsia in primigravidas with more than 32 weeks gestation with

unfavourable cervix on admission with expected fetal weight >1.5 kgs, an early

decision for caesarean section either within 6 hours of admission or 12 hours of first

fit whichever is earlier is detrimental in improving the fetomaternal outcome”.

Prompt termination of pregnancy by caesarean section reduces maternal and

perinatal mortality, improves maternal outcome by reducing complications and also

improves perinatal outcome with better one minute Apgar scores and reduced NICU

admission.

With advanced expert surgical and anaesthetic techniques in modern

obstetrics, caesarean section is not unsafe as seen in previous years.

Both maternal and perinatal outcome can be improved by taking an early

decision for caesarean section when on admission cervix is unfavourable or delivery

is not anticipated within 6 hours. In severe antepartum eclamptic with a closed

uneffaced cervix and unengaged presenting part, it might give better results if

onservative treatment is supplemented by timely caesarean section instead of

withholding it.

As this study comprised of young primigravidae, it was seen that most had

unfavourable cervix and induction failure and moreover the duration of labour was

more in comparison with multigravidae patients.

81

Therefore, from my study of a small number of cases, I have come to a

conclusion that caesarean section if done promptly leads to more favourable outcome

than conservative obstetric management with vaginal delivery in eclampsia in

primigravidae after 32 weeks of pregnancy with unfavourable cervix on admission.

“Caesarean section should be done at the optimum time and not as a last resort when

conservative management has failed in eclampsia especially in primigravidas after32

weeks of pregnancy”.

82

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93

PROFORMA

NAME I.P.NO.

AGE

DATE OF ADMISSION

HUSBAND DATE OF DISCHARGE

OCCUPATION DATE OF DELIVERY

SE STATUS BOOKED/UNBOOKED

RELIGION

ADDRESS

CHIEF COMPLAINTS WITH PERIOD OF AMENORHOEA

H/O CONVULSIONS

NUMBER OF CONVULSIONS BEFORE ADMISSION

AFTER ADMISSION

LAST CONVULSION

DURATION OF EACH CONVULSION

CONSCIOUSNESS BETWEEN ATTACKS

H/O FROTHING/TONGUE BITE/INCONTINENCE OF URINE/STOOLS

PREMONITORY SYMPTOMS : H/O HEADACHE1 / EPIGASTRIC PAIN2 /

NAUSEA3 / VOMITING4 / BLURRED VISION5

OBSTETRIC HISTORY : M.L. CONSANGINOUSC/

NONCONSANGINOUSN

ANTENATAL I

II

III

ANC YESY/NON

DATE OF LAST/B.P.RECORDING

MENSTRUAL HISTORY: AGE OF MENARCHE

CYCLES

FLOW

PAST HISTORY : HTN/DM/TB/HEART DISEASES/LIVER &RENAL /ANY

MAJOR ILLNESS

FAMILY HISTORY:HTN/DM/TB/ECLAMPSIA IN MOTHER OR SISTER

94

PERSONAL HISTORY:

GENERAL PHYSICAL EXAMINATION

CONSCIOUS1/IRRITABLE2/UNCONSCIOUS3

EYE : CONJUNCTIVA :PINK1/PALE2/ICTERIC3

TONGUE : PINK1/PALE2/BITE3

NECK : THYROID/LYMPH NODES

BREAST

EDEMA: PEDALa/VULVALb/ABDOMENc/GENERALISEDd

VITALS : TEMP

PULSE

BP

RR

PUPILS-NORMAL1 / SLUGGISH REACTING2

KNEE JERK – NORMAL1 / EXAGGERATED2

SYSTEMIC EXAMINATION

C.V.S

R.S

C.N.S

OBSTETRIC EXAM

P/A – 32 – 34 WEEKS1, 34 – 36, WEEKS2, 36 – 403 WEEKS

P/S

P/V - BISHOP’S SCORE

INVESTIGATIONS :

HAEMOGRAM

LFT – SGOT/STPT/LDH /S.BILIRUBIN

RFT – BLOOD UREA/SERUM CREATININE/SERUM URIC ACID

USG

FUNDOSCOPY – Y/N

BLOOD GROUPING AND TYPING

HBsAG HIV I & II

COAGULATION PROFILE

CT BRAIN IF NECESSARY

95

MANGEMENT

SEDATION -

ANTIHYPERTESIVES - NIFIDEPINEN

ANTICONVULSANT - LABETOLOLL

ANTIBIOTICS

MODE OF DELIVERY : VAGINAL/LSCS

DELIVERY NOTES

BABY NOTES LBW/SFG/NND

GA/SEX/PLACENTA

ADMISSION TO NICU : DURATION OF STAY

DIAGNOSIS – HIE1/SEPTICAEMIA2/RDS3/MAS4

OBSERVATIONS

1. B.P AT ADMISSION

2. PROTEINURIA AT ADMISSION

3. TIME B/N ADMISSION AND CONVULSION (HOURS)

4. TIME B/N CONVULSION AND DELIVERY (HOURS)

5. TIME B/N ADMISSION AND DELIVERY (HOURS)

6. IMMEDIATE POST DELIVERY B.P.

7. URINE ALBUMIN NIL FOLLOWING DELIVERY

8. MATERNAL COMPLICATIONS

• PULMONARY EDEMA6

• PLACENTAL ABRUPTION/HELLP1

• CEREBRAL INFARCTION3

• UTI2

• PPH4

• CORTICAL BLINDNESS5

9. DURATION OF STAY IN HOSPITAL

10. CONDITION OF MOTHER AND BABY AT DISCHARGE

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format.

PROFORMA

NAME I.P.NO.

AGE

DATE OF ADMISSION

HUSBAND DATE OF DISCHARGE

OCCUPATION DATE OF DELIVERY

SE STATUS BOOKED/UNBOOKED

RELIGION

ADDRESS

CHIEF COMPLAINTS WITH PERIOD OF AMENORHOEA

H/O CONVULSIONS

NUMBER OF CONVULSIONS BEFORE ADMISSION

AFTER ADMISSION

LAST CONVULSION

DURATION OF EACH CONVULSION

CONSCIOUSNESS BETWEEN ATTACKS

H/O FROTHING/TONGUE BITE/INCONTINENCE OF URINE/STOOLS

PREMONITORY SYMPTOMS : H/O HEADACHE1 / EPIGASTRIC PAIN2 /

NAUSEA3 / VOMITING4 / BLURRED VISION5

OBSTETRIC HISTORY : M.L. CONSANGINOUSC/

NONCONSANGINOUSN

ANTENATAL I

II

III

ANC YESY/NON

DATE OF LAST/B.P.RECORDING

MENSTRUAL HISTORY: AGE OF MENARCHE

CYCLES

FLOW

PAST HISTORY : HTN/DM/TB/HEART DISEASES/LIVER &RENAL /ANY

MAJOR ILLNESS

FAMILY HISTORY:HTN/DM/TB/ECLAMPSIA IN MOTHER OR SISTER

PERSONAL HISTORY:

GENERAL PHYSICAL EXAMINATION

CONSCIOUS1/IRRITABLE2/UNCONSCIOUS3

EYE : CONJUNCTIVA :PINK1/PALE2/ICTERIC3

TONGUE : PINK1/PALE2/BITE3

NECK : THYROID/LYMPH NODES

BREAST

EDEMA: PEDALa/VULVALb/ABDOMENc/GENERALISEDd

VITALS : TEMP

PULSE

BP

RR

PUPILS-NORMAL1 / SLUGGISH REACTING2

KNEE JERK – NORMAL1 / EXAGGERATED2

SYSTEMIC EXAMINATION

C.V.S

R.S

C.N.S

OBSTETRIC EXAM

P/A – 32 – 34 WEEKS1, 34 – 36, WEEKS2, 36 – 403 WEEKS

P/S

P/V - BISHOP’S SCORE

INVESTIGATIONS :

HAEMOGRAM

LFT – SGOT/STPT/LDH /S.BILIRUBIN

RFT – BLOOD UREA/SERUM CREATININE/SERUM URIC ACID

USG

FUNDOSCOPY – Y/N

BLOOD GROUPING AND TYPING

HBsAG HIV I & II

COAGULATION PROFILE

CT BRAIN IF NECESSARY

MANGEMENT

SEDATION -

ANTIHYPERTESIVES - NIFIDEPINEN

ANTICONVULSANT - LABETOLOLL

ANTIBIOTICS

MODE OF DELIVERY : VAGINAL/LSCS

DELIVERY NOTES

BABY NOTES LBW/SFG/NND

GA/SEX/PLACENTA

ADMISSION TO NICU : DURATION OF STAY

DIAGNOSIS – HIE1/SEPTICAEMIA2/RDS3/MAS4

OBSERVATIONS

1. B.P AT ADMISSION

2. PROTEINURIA AT ADMISSION

3. TIME B/N ADMISSION AND CONVULSION (HOURS)

4. TIME B/N CONVULSION AND DELIVERY (HOURS)

5. TIME B/N ADMISSION AND DELIVERY (HOURS)

6. IMMEDIATE POST DELIVERY B.P.

7. URINE ALBUMIN NIL FOLLOWING DELIVERY

8. MATERNAL COMPLICATIONS

• PULMONARY EDEMA6

• PLACENTAL ABRUPTION/HELLP1

• CEREBRAL INFARCTION3

• UTI2

• PPH4

• CORTICAL BLINDNESS5

9. DURATION OF STAY IN HOSPITAL

10. CONDITION OF MOTHER AND BABY AT DISCHARGE

1 2 3 4 5 6 7 8 9 10 11 13 14 15 16 17 18 19 20 21 22 23 24 25 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48

Sl. No.

Name AgeOccupat

ion

SE Status

Religion

Address

I.P. No DOA DO Del DOD

No Convulsi

ons Before/After

Consciousness

between attacks

Premonitory

symptoms a/b/c/d

Married Life Year

Consanginous/ nonconsanginous

Antenatal

I/II/III

Anc yes/no

BP Recordi

ng

GPE 1/2/3

Eye Conjunctiva 1/2/3

Tongue

1/2/3

Edema a/b/c/d

Vitals/ pulse

RRKJ a/b

Pupils

PA 1/2/3

PV bishop’s score

Haemogram

LFT 1/2/3 USGRFT 1/2

Serum Uric acid

Fundoscopy

VIMSAntihypertesives N/L

VD/CD

B/W ApgarNICU

Diagnosis/Stay

Diagnosis

1/2/3/4

Proteinuria A/D

Admission &

Convulsion

Admission & Deliver

y

Convulsion &

delivery

Complications 1/2/3/4/5/6

Dead

Systole Diastole

1 Jaidunissa 22 Cooli Low M Bellary 500872 1.7.11 2.7.11 8.7.11 3 Y a 1 C N N N 1 1 1 a 82 22 a 2 2 2/10Hb 9.6 Plt.1.6 lacs

26, 30, 429 IU/L

N0.6, 28 DL

4.6 Y Y N CD 2kg6/10 8/10

7dys 21+/Nil 4day

4hrs 24 hrs 26 hrs160 140

100 90

3 Renuka 19 Cooli Low H Bellary 501026 3.7.11 3.7.11 6.7.11 3 Y ab 3 C N N N 3 1 1 a 92 20 b 2 3 2/10Hb 11.2 Plt.2 lacs

60, 67 498 IU/L

N18 0.7

5 Y Y N VD 2kg4/10 6/10

3dys 14+/Nil 4day

6hrs 10 hrs 18 hrs150 130

110 90

4 Kavitha 22 Cooli Low H Bellary 501644 8.7.11 9.7.11 10.7.11 4/1 Y a 3 N Y Y Y 1 1 1 a 80 18 b 2 3 2/10Hb 12.2 Plt.3.8 lacs

28, 19 340 IU/L

Y20 0.6

4.2 Y Y N VD 2.8kg6/10 8/10

‐ ‐3+/Nil 3day

2hrs 6 hrs 6 hrs160 100

140 90

5 Basamma 22 Cooli Low H Bellary 502344 14.7.11 14.7.11 20.7.11 1 Y a 2 N Y Y Y 1 1 1 a 92 20 b 2 3 0/10Hb 11.6 Plt.2.4 lacs

56, 48 378 IU/L

Y22 1

3 Y Y N CD 2.5kg6/10 8/10

3dys 23+/Nil 5day

6hrs 12hrs 18 hrs170 150

120 100

4

6 Honnuramma 30 Cooli Low H Bellary 502999 17.7.11 19.7.11 22.7.11 4/1 Y ab 2 C Y Y Y 1 1 3 a 98 20 b 2 3 2/10Hb 10 Plt.1.6 lacs

21, 16 460 IU/L

Y20 .9

5.6 Y Y N VD 2.5kg6/10 8/10

‐ ‐3+/Nil 5day

5hrs 16hrs 22 hrs170 150

110 100

7 Fathima 18 Cooli Low M Bellary 503865 26.7.11 28.7.11 30.7.11 2 Y a 2 N Y Y Y 1 1 3 a 92 18 a 2 2 0/10Hb 9.5 Plt.2.8 lacs

34, 28 300 IU/L

Y20 .6

6 Y Y N VD 1.5kg ‐ ‐ ‐1+/Nil 2day

4hrs 20hrs 24 hrs140 120

90 80

8 lacshmi 22 Cooli Low H Bellary 504685 2.8.11 3.8.11 6.8.11 2 Y abc 1 N Y Y Y 1 1 1 82 22 a 2 1 2/10Hb 9.6 Plt.1.8 lacs

10, 15 310 IU/L

Y20 .8

7 Y Y N VD 1.7kg6/10 8/10

3dys 32+/Nil 2day

5hrs 18hrs 26 hrs130 128

80 80

9 Maremma 20 Cooli Low H Durga 505803 11.8.11 13.8.11 15.8.11 2 Y ad 2 C Y Y Y 2 1 3 ab 82 20 b 1 1 0/10Hb 9 Plt.1.4 lacs

18, 15 676 IU/L

N20 .8

3.8 Y Y N VD 2kg6/10 8/10

‐ ‐2+/Nil 3day

5hrs 28hrs 30 hrs160 158

100 90

10 Shabana 20 Cooli Low M Hospet 505803 15.8.11 17.8.11 21.8.11 2 Y a 1.6 C Y Y Y 1 1 1 ac 80 22 a 1 3 3/10Hb 12.7 Plt.2.9 lacs

22, 40 520IU/L

N20 .8

4.2 Y Y N VD 2.25kg ‐ ‐ ‐4+/Nil 5day

4hrs 16hrs 20 hrs170 170

110 100

2

11 Kavitha 19 Cooli Low H Bellary 490849 31.3.11 9.4.11 01.4.11 4 Y ac 1 N Y Y Y 2 1 3 a 90 22 b 1 3 4/10Hb 10 Plt.1.5 lacs

30, 34 510IU/L

Y10 1

5.2 Y Y N VD 2.5kg4/10 6/10

3dys 32+/Nil 6day

4hrs 16hrs 20 hrs140 130

100 90

12 Fathima 20 Cooli Low M Bellary 481970 3.1.11 4.1.11 6.1.11 2 Y ac 1 C Y Y Y 1 1 1 a 98 20 b 1 3 4/10Hb 9.3 Plt.1.9 lacs

32, 20 320IU/L

N20 .6

6.7 Y Y N VD 2.5kg6/10 8/10

‐ ‐2+/Nil 4day

6hrs 10hrs 18 hrs150 140

90 90

13 Yashodamma 20 Cooli Low H Bellary 481975 5.1.11 6.1.11 8.1.11 2 Y ac 2 N Y Y Y 1 1 3 a 90 22 a 1 1 3/10Hb 9.8

Plt.1.2lacs20, 40 610IU/L

N20 .1

4.6 Y Y N VD 1.5kg2/10 4/10

5dys1

Death3+/Nil 4day

5hrs 10hrs 20 hrs170 160

110 910

2

14 PusHbalatha 20 Cooli Low H Bellary 482036 4.1.11 5.1.11 8.1.11 2 Y ad 2 N N N N 1 1 1 a 90 20 b 1 1 2/10Hb 9.8 Plt.1.4 lacs

40, 30 610IU/L

N20 .9

3.9 Y Y N VD1.5kg death

‐ 5dys ‐3+/Nil 5day

6hrs 8hrs 16 hrs160 140

100 100

15 Renuka 22 Cooli Low H Bellary 482196 6.1.11 7.1.11 15.1.11 2 Y ac 10m C Y Y Y 3 1 3 ac 100 20 b 1 3 3/10Hb 1.8

Plt.2 lacs20, 28 490IU/L

Y20 .6

4.7 Y Y L CD 2kg 6/10 8/10

28dys 24+/Nil 8day

5hrs 18hrs 24 hrs180 170

110 90

1

16 Sunitha 22 Cooli Low H Bellary 482297 6.1.11 6.1.11 9.1.11 4 Y ab 1.6 N Y Y Y 3 1 1 abd 90 28 b 1 1 3/10Hb 10 Plt.1.8 lacs

20, 35 549IU/L

N 20 5.2 Y Y L VD 1.6kg2/10 2/10

6hous1 death of 6hrs

3+/Nil 4day

5hrs 10hrs 18 hrs170 160

110 100

17 Manjamma 22 Cooli Low H Bellary 482505 9.1.11 10.1.11 13.1.11 2 Y ad 1 N N N N 3 1 1 a 90 20 b 1 1 0/10Hb 11 Plt.1.8 lacs

20, 24 680IU/L

N 20 .6 5.9 Y Y N VD 1.5kg6/10 8/10

‐ ‐1+/Nil 3day

6hrs 10hrs 18 hrs160 140

100 100

18 Sunitha 22 Cooli Low H Bellary 482515 8.1.11 9.1.11 15.1.11 3 Y a 2 N N N Y 1 1 1 ab 92 20 a 1 2 0/10Hb 9.8 Plt.1.6 lacs

40, 20 688IU/L

N 20 .9 4.9 Y Y N VD 1.6kg2/10 4/10

3dys 13+/Nil 6day

5hrs 10hrs 18 hrs170 150

104 100

2

19 Eramma 22 Cooli Low H Bellary 482514 8.1.11 9.1.11 12.1.11 3 Y ac 2 C Y Y Y 1 1 1 ac 90 22 a 1 3 3/10Hb 12 Plt.1.6 lacs

22, 18 688IU/L

Y 24 .1 3.9 Y Y N VD (F) 2.5kg4/10 6/10

‐ ‐1+/Nil 3day

6hrs 8hrs 14 hrs140 130

90 90

20 Shahena Banu 20 Cooli Low M Bellary 482524 9.1.11 10.1.11 13.1.11 2 Y ad 2 N N N N 1 1 1 a 90 20 a 1 2 2/10Hb 10 Plt.2.8 lacs

20, 18 432IU/L

N 24 .9 4.8 Y Y N VD1.5kg death

‐ ‐ ‐4+/Nil 3day

10hrs 6hrs 8 hrs140 130

90 90

21 lacshmidevi 19 Cooli Low H Hospet 480014 17.12.1018.12.1

024.12.10 5/1 Y ac 2 C Y Y Y 1 1 3 abc 92 20 b 1 3 3/10

Hb 10 Plt.1.6 lacs

34, 26 412IU/L

N 20 .9 4.6 Y Y N CD 2.5kg 6/10 8/10

‐ ‐2+/Nil 5day

6hrs 12hrs 16 hrs160 140

100 100

4

22 Kavitha 22 Cooli Low H Bellary 479985 16.12.1018.12.1

027.12.10 2 Y a 2 C N N N 1 1 1 a 90 24 b 1 3 3/10

Hb 9.8 Plt.3.8 lacs

20, 28 786IU/L

N24 1.1

5.1 Y Y N CD 3kg 6/10 8/10

‐ ‐2+/Nil 5day

8hrs 30hrs 34 hrs150 140

100 90

23 Gangamma 19 Cooli Low H Bellary 480025 16.12.1019.12.1

028.12.10 1 Y a 2 C Y Y C 1 1 1 a 92 22 b 1 3 0/10

Hb 13 Plt.1.8 lacs

40, 20 554IU/L

Y20 1.1

3.7 Y Y N CD 3kg 6/10 8/10

2 2 5day4+/Nil 8day

10hrs 36hrs 38 hrs160 140

100 90

24 Kavitha 20 Cooli Low HAnanth pur

482764 11.1.11 12.1.11 14.1.11 2 Y a 1 N Y Y Y 1 1 1 a 92 20 b 1 3 4/10Hb 936 Plt.1.6 lacs

24, 40 436IU/L

Y30 1.0

3.9 Y Y N VD 2kg 6/10 8/10

‐ ‐2+/Nil 3day

6hrs 12hrs 14 hrs160 140

100 90

25 Geetha 22 Cooli Low H Bellary 483032 13.1.11 14.1.11 16.1.11 2 Y a 2 N Y Y Y 1 1 1 a 92 18 b 1 3 0/10Hb 11 Plt.1.4 lacs

30, 20 430IU/L

Y 20 .8 4.8 Y Y N VD 2kg 6/10 8/10

‐ ‐1+/Nil 3day

6hrs 18hrs 20 hrs160 140

100 90

26 Bhagyamma 22 Cooli Low H Bellary 473126 16.10.10 17.10.10 23.10.10 O2 Y a 2 N N N N 1 1 1 a/c 92 22 a 1 3 4/10HB 9.8 PLT 1.8

26,34, 612

Y20, 1.1

5.2 Y Y N CD 2.2Kg7/10, 9/10

‐ ‐2+/1+, 7day

4hrs 18hrs 24 hrs150 140

100 90

27 Rathnamma 21 Cooli Low HAnanth pur

475077 31.10.10 01.11.10 7.11.10 2 Y a 2 C Y Y Y 3 1 3 a/b 92 22 a 1 3 4/10HB 12.8 PLT 2.7

35,28, 465

N21,0.9

4.7 Y Y N VD 1‐75Kg4/10,6/10

2 3days3+/NIL, 4day

3.5hrs 24hrs 26 hrs160 130

90 80

MASTER CHART

BP Admision & Delivery

28 Mahadevi 19 Cooli Low H Bellary 475009 2.11.10 3.11.10 7.11.10 1 Y a 1 N Y Y Y 1 1 1 c 92 20 a 1 1 4/10Hb 10.5 plt 2.66

16,12, 500

y15,0.9

5.6 y n N VD 2.25Kg6/10,7/10

0 03+/NiL, 3days

30min 16hrs 12 hrs150 130

100 80

29 Rahimbee 20 Cooli Low H Bellary 475328 2.11.10 3.11.10 6.11.10 1 Y a 2 C Y Y Y 1 1 1 a 80 20 a 1 3 0/10Hb 10 plt

1.830,20, 310 N

20,0.9

4.6 Y Y N VD 2Kg7/10,9/10

0 0 0 8hrs 12hrs 18 hrs140 110

90 80

30 Shwetha 20 Cooli Low H Hospet 475325 2.11.10 3.11.10 1O.11.10 1 Y a 1 C Y Y Y 1 1 1 a 80 20 b 1 3 4/10Hb 10 PLT 2 iaks

42,33,215 Y20, 0.9

4.3 Y Y N CD 2.5Kg6/10,8/10

0 0 0 30min 10hrs 6 hrs200 160

120 100

31 Wahida 23 Cooli Low M Bellary 476299 11.11.10 12.11.10 15.11.10 1 Y a/c/d 2 N Y Y Y 1 1 1 a 82 18 a 1 3 0/10Hb 9.6 plt

2.4721,25, 390

y19, 0.7

4.8 Y Y N VD 2.5Kg7/10,9/10

0 01+/nil 3day

3hrs 10hrs 14 hrs130 120

90 90

32 Vedavathi 25 Cooli Low H Bellary 476576 16.11.10 17.11.10 19.11.10 2 Y a 7 N Y Y Y 1 1 1 a 82 20 a 1 3 4/10Hb 9 plt 2.1

43,26, 315

y19, 0.7

3.9 N Y N VD 1.5Kg7/10,9/10

2 41+/NIL 3DAY

3hrs 10hrs 20 hrs148 110

100 80 5

33 Banu 25 Cooli Low m Bellary 476879 16.11.10 17.11.10 20.11.10 2 Y a 1 C Y Y N 1 1 3 a/b 80 20 a 1 3 4/10Hb 12 plt

1.840,30, 162

y27, 1.1

3.7 Y Y N VD 2Kg7/10,9/10

0 01+/nil 3day

10hrs 18hrs 26 hrs160 140

100 90

34 Huligamma 25 Cooli Low H Bellary 479162 8.12.10 9.12.10 13.11.10 1 Y a 6 C N N N 1 1 1 a 82 22 a 1 3 4/10Hb 12.8 PLT 2 iak

30,38, 728

n13. 0.9

5.1 Y Y N VD 1.75Kg7/10,9/10

1 43+/NIL 4day

2hrs 10hrs 16 hrs150 130

100 80

35 Sarita 25 Cooli Low H Bellary 479088 7.12.10 8.12.10 12.12.10 1 Y a 2 N Y Y Y 1 1 1 a/b 82 22 a 1 1 4/10Hb 9.4 plt

3.218,14,3 52

Y21, 0.9

5.1 Y Y N VD 2Kg7/10,9/10

0 03+/NIL 6day

10hrs 18hrs 18 hrs180 134

100 90

36 Radha 19 cooli low H Bellary 479304 9.12.10 9.12.10 12.12.10 1 Y abc 2 c N N N 1 1 1 ab 92 20 a 1 1 4/10Hb 13

plt2.11,21,16.

1,21,16614, 0.7

4.9 Y Y n VD 2Kg6/10 8/10

1+/nil 4day

4 hrs 6hrs 16 hrs140 100

140 100

37 Nagveni 23 cooli low H Bellary 485159 3.2.11 4.2.11 7.2.11 1 Y a 1 N N N N 1 1 1 a 80 22 a 1 2 0/10Hb10.4plt1.093634

490

30,20, 520

n20 0.9

4.5 Y y n VD 1.5Kg6/10, 8/10

3+nil 3day

5hrs 24hrs 28 hrs170 150

100 90

38 Jayamma 22 cooli low H Bellary 485341 5.2.11 6.2.11 13.2.11 1 Y a 2 c N N N 1 1 1 a 92 20 b 1 3 4/10Hb10.4plt3.235,34,

5.8

20,10, 500

y20, 1.1

5.2 Y y L CD 2.5Kg6/10 8/10

3+nil 5day

6 hrs 24hrs 28 hrs190 100

160 100

39 Priyanka 22 cooli low H Hospet 485610 8.2.11 8.2.11 10.2.11 4 Y a 2 N Y Y Y 1 1 3 a 5 20 b 1 2 4/10Hb9plt1.836,20,62

10,10, 200

n24 1.1

5.1 Y y N VD 1.5 IUD1+nil 2day

3hrs 6hrs 10 hrs150 140

110 90

40 Huligemma 23 cooli low H Bellary 486132 13.2.11 13.2.11 15.2.11 1 Y a 2 c Y Y Y 1 1 3 a 90 22 b 1 3 4/10Hb9.2plt2.3,70,72,6

20

30,40, 360

n20 0.8

4.6 Y N N VD 2.8Kg7/10 9/10

2+nil 3day

1hr 6hrs 6 hrs160 140

110 90

41 Honnamma 24 cooli low H Bellary 486402 15.2.11 16.2.11 18.2.11 2 Y a 3 N Y Y Y 1 1 1 ab 80 18 b 1 1 4/10Hb9.1plt80000,28,19,396

20,30, 400

y21 0.8

4.7 Y Y N VD 1.5Kg6/10 8/10

2 42+nil 4day

6hr 18hrs 22 hrs174 160

110 90

42 Gangamma 19 Cooli Low H Bellary 486469 16.02.11 16.02.11 23.02.11 1 Y a 2 N Y Y Y 1 1 1 a 80 22 b 1 3 3/10Hb 9 plt 1.2lac

63,51, 490

Y20, 0.9

3.9 Y Y N CD 2.5Kg4/10 6/10

4 NND3+/Nil 5day

2hrs 6hrs 10 hrs140 140

90 90

43 Jayamma 22 Cooli Low H Bellary 486448 16.2.11 16.2.11 24.2.11 2 Y a 2 C N N N 1 1 3 a 90 20 a 1 3 4/10Hb 9 plt 1.9

30,20, 257

n20, 0.9

3.6 Y Y N CD 2Kg6/10 7/10

0 02+/NIL 3DAY

3hrs 16hrs 12 hrs146 130

96 90

44 Yasmeen 20 Cooli Low M Bellary 486896 21.2.11 22.2.11 1.3.11 2 Y a/d 2 N N N N 1 1 1 a 82 20 a 1 3 4/10Hb 10.8 plt 2lacs

13,14, 310

n22, 0.8

4.7 Y Y N CD 2Kg6/10 8/10

0 02+/Nil 4day

6hrs 16hrs 10 hrs144 140

90 90

45 lacshmamma 22 Cooli Low h Bellary 487884 2.3.11 3.3.11 10.3.11 1 Y a/d 3 C Y Y Y 1 1 1 a 90 22 a 1 3 4/10Hb9.2 plt 2.3lac

42,32, 525

y30, 1.1

4.2 Y Y N CD 2.5Kg6/10 8/10

0 03+/Nil 4day

4hrs 6hrs 12 hrs150 130

110 100

46 Mallamma 22 Cooli Low h Bellary 488674 4.3.11 5.3.11 12.3.11 2 Y a 2 C Y Y Y 1 1 1 a 82 22 a 1 2 4/10Hb 9.9 plt

1.829,31, 512

Y26,0.2

3.9 Y Y N CD 1.5kg6/10,8/10

2 43+/6da

y2hrs 6hrs 10 hrs

150 148

90 80

47 Yellamma 22 Cooli Low H Bellary 487924 3.3.11 4.3.11 10.3.11 1 Y a 2 C Y Y Y 1 1 1 a 80 20 a 1 2 4/10Hb 9.2 plt 1.8lac

42,40, 752

y28, 1.1

3.9 Y Y N CD 2Kg6/10,8/10

0 02+/nil6day

6hrs 8hrs 20 hrs150 130

110 90

48 Shanthamma 25 Cooli Low h Bellary 488267 6.3.11 6.3.11 10.3.11 1 Y a 1 C Y Y Y 1 1 1 a 82 20 b 1 1 0/10Hb 9 plt 2lac

30,26, 567

y20, 0.9

3.7 Y Y N VD 1.75Kg6/10 7/10

5 22+/NIL4day

6hrs 10hrs 18 hrs160 150

90 90

49 Pavithra 20 Cooli Low H Bellary 488533 8.3.11 9.3.11 11.3.11 1 Y a 3 N Y Y Y 1 1 1 a 90 20 b 1 3 4/10Hb 9 plt 2lac

15,30, 423

Y22, 0.9

3.8 Y Y N VD 2.5Kg6/10 8/10

0 01+/nil 2day

8hrs 12hrs 18 hrs170 150

100 90

50 Lagmavva 19 Cooli Low h Belgaum 488598 9.3.11 9.3.11 12.3.11 2 Y a/d 1 N N N N 1 1 1 a 90 20 b 1 1 4/10HB 9.1 plt 1.3lac

30,35, 875

y20, 1.2

5.8 Y Y N VD 1.5Kg6/10 8/10

2 NND 3day2+/nil 3day

3hrs 8hrs 10 hrs150 150

100 100

51 Ambujakshi 23 Cooli Low H Tumkur 488774 11.3.11 12.3.11 19.3.11 2 y a 2 c Y Y Y 1 1 1 a/b/d 82 22 a 1 3 4/10Hb 8.8 ply 2.8lac

20,26, 4800

y24, 0.6

4.9 Y Y N CD 2.5Kg6/10 8/10

0 02+/NIL 6day

6hrs 12hrs 18 hrs150 140

100 90

52 Sunitha 18 Cooli Low H Bellary 489509 18.3.11 19.3.11 26.3.11 1 Y a 1 N Y Y Y 1 1 1 a/c 80 18 b 1 3 4/10Hb 10.3 plt 1.2

30,20, 504

Y20, 1.1

5.1 Y Y N CD 2kg6/10 8/10

0 02+/nil 5day

6hrs 18hrs 20 hrs160 160

100 90

53 Rathnamma 18 Cooli Low H Bellary 489129 13.3.11 14.3.11 19.3.11 2 Y a 1 C Y Y Y 1 1 1 a 92 20 b 1 3 0/10Hb 8.2 plt 2.6lac

16,22, 420

Y20, 04

4.7 Y Y N VD 2Kg4/10 6/10

2 12+/nil 5day

4hrs 6hrs 10 hrs140 130

90 80

54 Shaheen 22 Cooli Low M Bellary 489174 20.3.11 20.3.11 24.3.11 4 Y a 1 C N N N 1 1 1 a 80 20 b 1 3 4/10Hb 11 plt 1.5lac

53,47, 490

Y24, 0.8

5.1 Y Y N VD 2Kg dead 0 02+/nil 3day

10hrs 8hrs 18 hrs150 150

100 100

55 Radhamma 25 Cooli Low H Bellary 489310 16.3.11 16.3.11 22.3.11 6 Y a 10m N Y Y Y 3 1 3 a/b/c 90 20 b 1 3 4/10HB 9.8 PLT 1.8

20,24, 512

N20, 0.9

4.9 Y Y N VD 2KgSTILL birth

0 03+/nil 8day

4hrs 6hrs 10 hrs150 140

110 110

56 Deenakumari 23 Cooli Low C Bellary 488122 10.3.11 11.3.11 18.3.11 6 Y a/d/e 2 C Y Y Y 1 1 3 a/d 92 18 a 1 3 0/10Hb 9.2 plt 1.5lac

18,20, 600

Y16, 0.9

3.9 Y Y N CD 2Kg6/10 8/10

0 02+/NIL 4day

2hrs 10hrs 14 hrs150 160

100 100

57 Gouramma 22 Cooli Low H Bellary 490246 25.3.11 26.3.11 29.3.11 2 Y a 1 C N N N 3 1 3 a/d 92 18 a 2 2 40818Hb 9.8 plt

1.630,10, 600

N20, 0.9

3.7 Y Y N VD 1.5kg dead 0 0 2+ 6hrs 14hrs 16 hrs150 160

110 110 1 Y

58 Manjula 22 Cooli Low H Bellary 490188 24.3.11 28.3.11 1.4.11 2 Y a 1 N N N N 1 1 3 a 82 20 b 1 1 0/10Hb 9.2 plt 1.7lac

34,24, 400

N20, 0.8

3.6 Y Y N VD 1.8Kg4/10 6/10

4 12+/nil 3day

2hrs 72hrs 30 hrs140 120

90 80

59 Manjamma 22 Cooli Low H Koppal 491052 3.4.11 4.4.11 6.4.11 2 Y a/b 4 N Y Y Y 1 1 1 a 90 20 a 1 1 0/10Hb 8.8 plt 1.6lac

21,16, 520

Y28, 1.1

4.5 Y Y N CD 1.5Kg 2 22+/NIL 4day

6hrs 12hrs 11 hrs160 140

100 100

60 Gangamma 22 Cooli Low h Bellary 491142 3.4.11 4.4.11 11.4.11 10 Y a/b/c/d 4 N Y Y Y 1 1 3 a/b 82 20 a 2 3 0/10Hb 10.7 plt 1.7

20,18, 510

Y18, 0.6

4.8 Y Y N CD 2.5Kg6/10 8/10

0 02+/nil 7day

6hrs 12hrs 18 hrs160 150

110 100

61 Hanumanthi 21 Cooli Low H Lingasur 491748 9.4.11 10.4.11 13.4.11 6 Y a/b 1 C Y Y Y 1 1 1 a/d 82 20 a 1 3 4/10Hb 11.2 plt 1.4lac

20,28, 560

Y18, 0.8

4.1 Y Y N VD 2.5Kg6/10 6/10

2 NND1+/nil 3day

13hrs 12hrs 18 hrs120 120

90 90

62 Sharada 20 Cooli Low H Hospet 482305 15.1.11 21.1.11 2.1.11 1 Y a/b 2 C N N N 2 1 1 a 90 24 b 1 1 2/10Hb 9.8 plt 1.8 lac

30,50, 478

Y20, 0.9

4.2 Y Y N VD 2.Kg6/10 8/10

1+/nil 5day

6hrs 18hrs 20 hrs120 120

90 90

63 Mahalacshmi 22 Cooli Low H Bellary 484211 25.1.11 26.1.11 29.1.11 4 Y a/c 2 C Y Y Y 1 1 1 a/b 92 22 b 1 3 4/10Hb 9.8 plt 1.6 lac

38,30, 485

Y20, 0.8

5.1 Y Y L VD 2.Kg6/10 8/10

1+/nil 2day

6hrs 8hrs 10 hrs180 140

110 100

64 Nagavani 20 Cooli Low H Bellary 484003 23.1.11 23.1.11 30.1.11 2 Y a/c 2 C Y Y Y 2 1 2 a/c 92 20 b 1 3 0/10Hb 9.6 plt 3.3 lac

30,28, 390

Y20, 0.9

4.7 Y Y L CD 3 Kg6/10 5/10

3+/nil 6day

6hrs 6hrs 12 hrs170 100

120 90

65 Mallamma 20 Cooli Low H Bellary 484043 23.1.11 21.1.11 28.1.11 1 N a/b 2 C N N N 2 1 1 a 90 20 a 1 3 3/10Hb 9.2 plt 1.3 lac

36, 30, 516

Y28, 0.9

4.6 Y Y N VD 2.5 Kg1/10 6/10

2 23+/nil 5day

10hrs 12hrs 24 hrs150 150

108 100

66 Kamalamma 25 Cooli Low H Bellary 484024 23.1.11 24.1.11 30.1.11 2 Y a/c 1 C N N N 1 1 1 a/c 96 20 b 1 3 2/10Hb 9.8 plt 2.1 lac

30, 20, 400

Y20, 0.9

3.9 Y Y N CD 3 Kg6/10 8/10

2+/nil 5day

4 hrs 10 hrs 16 hrs140 130

100 90

67 Gangamma 22 Cooli Low H Bellary 484430 27.1.11 28.1.11 02.2.11 3 Y a/b 2 N Y Y Y 1 1 1 a 92 20 b 1 3 4/10Hb 10 plt 2.1 lac

40, 40, 502

Y20, 0.8

3.2 Y Y N VD 2.5 Kg2/10 4/10

1+/nil 4day

2 hrs 10 hrs 12 hrs140 130

100 80

68 Sujatha 23 Cooli Low H Bellary 484415 27.1.11 27.1.11 30.1.11 2 Y a/c 2 N Y Y Y 1 1 1 a 88 20 b 1 3 3/10Hb 9.8 plt 2.1 lac

20, 30, 586

Y20, 0.9

3.7 Y Y N VD (F) 2.4 Kg6/10 8/10

1+/nil 4day

6 hrs 10 hrs 18 hrs140 130

100 100

69 Mallamma 20 Cooli Low HAnanth pur

484378 26.1.11 27.1.11 30.1.11 2 N a 2 N Y Y Y 1 1 1 a 90 20 b 1 3 2/10Hb 11 plt 1.8 lac

20, 40, 410

Y21, 1.0

3.8 Y Y N VD 2.2 Kg6/10 5/10

2+/nil 3day

6 hrs 10 hrs 18 hrs150 140

100 100

70 Gayathri 20 Cooli Low H Bellary 484553 28.1.11 08.1.11 04.1.11 4/1 N a/b/c/d 1.6 N Y Y Y 2 1 3 a 96 22 a 1 3 0/10Hb 10 plt 2.4 lac

20, 72, 1000

Y28, 1.2

4.1 Y Y N CD 3 Kg6/10 8/10

3+/nil 10day

4 hrs 6 hrs 12 hrs170 160

100 100

71 lacshmi 18 Cooli Low H Bellary 479247 09.12.10 10.02.10 13.12.10 3 Y a 1 N N N N 1 1 1 a 90 20 a 1 1 2/10Hb 9.8 plt 1.4 lac

20, 28, 510

Y20, 0.9

4.6 Y Y N VD 1.6 kg4/10 6/10

3 23+/nil 10day

6 hrs 12 hrs 16 hrs150 130

100 90

72 lacshmi 18 Cooli Low H Bellary 480689 22.12.10 23.02.10 1.1.11 3 Y a 1 N N N N 1 1 1 a 90 20 b 1 3 2/10Hb 10 plt 1.8 lac

30, 20, 600

Y30, 0.9

4.5 Y Y N CD 2 kg6/10 8/10

2NND3+/nil 7day

8 hrs 18 hrs 24 hrs160 150

100 100

73 Shanthamma 20 Cooli Low H Bellary 510201 17.09.11 17.09.11 25.09.11 1 Y a 1 N Y Y Y 2 1 1 a 92 20 a 1 3 0/10Hb 12.6 plt 2.97 lac

22, 17, 439

Y60, 0.9

4.9 Y Y N CD 2.5 kg6/10 8/10

3+/nil 7day

4 hrs 8 hrs 13 hrs160 130

100 90

74 Sujatha 18 Cooli Low H Bellary 510285 18.09.11 19.09.11 27.09.11 5 Y a/b 1 C Y Y Y 2 1 1 a 80 20 b 1 3 2/10Hb 8.9 plt 3.3 lac

28, 19, 1330

Y12, 0.6

5.1 Y Y N CD 3 kg6/10 8/10

1+/nil 3day

4 hrs 12 hrs 12 hrs170 160

100 100

5

75 Jyothi 18 Cooli Low H Bellary 509383 11.09.11 11.09.11 19.09.11 2 Y a 1 C Y Y Y 2 1 3 a 90 22 b 1 3 2/10Hb 10.8 plt 1.6 lac

20, 30, 420

Y20, 0.9

5.2 Y Y N CD 2 kg4/10 4/10

3 NND2+/nil 7day

6 hrs 6 hrs 12 hrs160 110

100 70

76 Anitha 22 Cooli Low H Bellary 511372 26.09.11 26.09.11 03.10.11 2 Y a/d 1 C Y Y Y 1 1 1 a 80 18 b 1 3 4/10Hb 10 plt 4.1 lac

12, 10, 1099

Y20, 1.4

5.8 Y Y N CD 3 kg6/10 8/10

1+/nil 4day

2 hrs 6 hrs 8 hrs140 130

94 90

77 Nagalacshmi 19 Cooli Low H Bellary 480600 22.12.10 22.12.10 24.12.10 2 Y a/c 2 N N N N 1 1 1 a 84 20 a 1 3 2/10Hb 10 plt 1.26 lac

20, 10, 560

N20, 1.9

3.8 Y Y N VD 1.5kg4/10 4/10

2 NND2+/nil 1day

8 hrs 12 hrs 18 hrs150 150

100 100

78 lacshmi 18 Cooli Low H Bellary 480681 22.12.10 23.12.10 30.12.10 2 Y a 1 C Y Y Y 2 1 1 a/d 90 20 a 1 3 2/10Hb 10 plt 1.26 lac

16, 20, 612

N 28, 1 3.9 Y Y N CD 2 kg6/10 8/10

2+/nil 7day

6 hrs 12 hrs 16 hrs170 100

160 100

79 Vedavathi 18 Cooli Low H Bellary 480693 24.12.10 24.12.10 02.01.11 2 Y a/d 1.6 C Y Y Y 1 1 1 a 90 22 a 1 3 2/10Hb 9.8 plt 1.6 lac

30, 28, 420

Y20, 1.9

5.6 Y Y N CD 3 kg6/10 8/10

3+/nil 8day

4 hrs 6 hrs 12 hrs160 140

100 90

80 Varalacshmi 19 Cooli Low H Bellary 480712 25.12.10 26.12.10 03.01.11 2 Y a/c 1 C N N N 2 1 1 a/d 92 22 b 1 3 2/10Hb 10 plt 1.8 lac

18, 30, 850

N32, 1.1

4.7 Y Y N CD 3 kg6/10 8/10

4+/nil 7day

4 hrs 16 hrs 18 hrs170 150

100 90

3

81 Shanthi 19 Cooli Low H Bellary 471385 01.01.10 02.10.10 05.10.10 2 Y b 1 N Y Y Y 1 1 2 a 90 20 a 1 3 2/10Hb 10.8 plt 1.8 lac

36, 24, 133

Y28, 0.1

5.7 Y Y N VD 2.5 kg6/10 8/10

3 hrs 12 hrs 16 hrs160 130

110 100

82 lacshmi 19 Cooli Low H Bellary 473910 24.10.10 24.10.10 28.10.10 2 Y a/c 1 N Y Y Y 1 1 1 a 88 22 a 1 3 5/10Hb 10 plt 1.8 lac

25, 18, 460

Y18, 0.7

5.1 Y Y N VD 2.5 kg7/10 9/10

1+/nil 3day

4 hrs 10 hrs 16 hrs160 130

110 90

83 Asma 22 Cooli Low M Bellary 473137 17.10.10 18.10.10 21.10.10 1 Y a/c 2 N Y Y Y 1 1 1 a 82 18 a 1 3 4/10Hb 10.2 plt 1.7 lac

30, 45, 610

Y20, 1.1

5.4 Y Y N VD 2.5 kg6/10 8/10

2+/nil 4day

4 hrs 8 hrs 13 hrs150 140

110 90

84 Pavithra 24 Cooli Low H Bellary 473090 16.10.10 17.10.10 20.10.10 2 Y a 1.6 N N N N 1 1 1 a 82 20 a 1 3 3/10Hb 10 plt 2.5 lac

20, 80, 342

N20, 0.8

3.6 Y Y N VD 2 kg6/10 8/10

2+/nil 4day

4 hrs 12 hrs 16 hrs150 140

96 90

6

85 Shantha 24 Cooli Low H Bellary 472145 08.10.10 09.10.10 12.10.10 1 Y a 1 C N N N 1 1 1 a 82 18 a 1 1 2/10Hb 9 plt 1.6 lac

35, 30, 500

N25, 0.6

4 Y Y N VD 2 kg6/10 8/10

1+/nil 3day

6 hrs 12 hrs 16 hrs160 140

90 90

86 Rudramma 22 Cooli Low H Bellary 492024 12.4.11 13.04.11 16.04.11 1 Y a 2 C N N N 1 1 1 a/d 80 20 b 1 1 0/10Hb 10.08 plt 2.33 lac

22, 70, 479

N11, 0.7

3 Y Y N VD 1.6 kg4/10, 6/10

1+/nil 4day

6 hrs 8 hrs 10 hrs140 130

94 90

87 Neelamma 28 Cooli Low H Bellary 492312 13.4.11 14.04.11 16.04.11 2 Y a 3 N N N N 1 1 1 a/b 82 22 a 1 3 2/10Hb 13.2 plt 1.8 lac

32, 28, 400

N22, 1.2

4.5 Y Y N VD 2 kg4/10, 6/10

3+/nil 5day

6 hrs 12 hrs 16 hrs140 140

100 90

88 Chandramma 22 Cooli Low H Bellary 494107 01.05.11 02.05.11 05.05.11 1 Y a/c 2 C Y Y Y 1 1 1 a 92 22 a 1 3 2/10Hb 9.2 plt 1.67lac

30, 20, 300

Y38, 0.8

4.7 Y Y N VD 2 kg6/10, 8/10

1+/nil 3day

8 hrs 10 hrs 18 hrs170 100

160 100

3

89 Honnur Bee 22 Cooli Low H Bellary 494642 07.05.11 08.05.11 12.05.11 1 Y a/d 2 C Y Y Y 1 1 1 a 90 22 a 1 3 3/10Hb 10.3

plt 2.15lac

33, 28, 858

N20, 0.6

3.6 Y Y N CD 2.8 kg6/10, 8/10

3+/nil 8day

4 hrs 6 hrs 6 hrs200 140

120 90

90 Jayashree 25 Cooli Low H Bellary 496247 21.05.11 22.05.11 28.05.11 2 Y a/d 2 N Y Y Y 1 1 1 a 92 20 a 1 3 0/10Hb 10.3 plt 2.8lac

25, 40, 223

N20, 0.6

5.1 Y Y N CD 2.5 kg6/10, 8/10

1+/nil 2day

6 hrs 12 hrs 18 hrs140 130

90 80

91 Huligemma 20 Cooli Low H Bellary 496061 19.05.11 20.05.11 27.05.11 5 Y a/d 2 N Y Y Y 1 2 1 a 82 20 a 1 3 2/10Hb 11.3 plt 2.8lac

24, 32, 380

N22, 0.8

4.9 Y Y N CD 3 kg6/10, 8/10

3+/nil 5day

4 hrs 6 hrs 26 hrs150 140

90 90

92 Rekhamma 19 Cooli Low H Bellary 498028 06.06.11 07.06.11 07.06.11 3 Y a 1.6 N N N N 1 1 1 a 82 20 a 1 3 2/10Hb 11.4 plt 2.4lac

27, 21, 605

N21, 0.7

3.8 Y Y N CD 2.5 kg6/10, 8/10

2+/nil 7day

10 hrs 16 hrs 18 hrs150 140

120 90

93 Thippamma 20 Cooli Low H Bellary 498933 09.06.11 09.06.11 13.06.11 1 Y a 1 N N N N 1 1 1 a 90 18 a 1 3 4/10Hb 9.8 plt 1.6 lac

20, 30, 340

N26, 0.7

5.7 Y Y N VD 2.5 kg6/10, 8/10

1+/nil 4day

6 hrs 12 hrs 6 hrs150 140

100 90

1

94 Ademma 20 Cooli Low H Bellary 498930 09.06.11 10.06.11 17.06.11 2 Y c 1 N Y Y Y 1 1 1 a 82 20 b 1 3 0/10Hb 8.8 plt 2.9 lac

23, 70, 761

N28, 0.7

3.9 Y Y N CD 2.5 kg6/10, 8/10

12 hrs 18 hrs 18 hrs190 160

110 100

95 Sudha 22 Cooli Low H Bellary 498619 11.06.11 11.06.11 15.06.11 2 Y a/d 1 N N N N 1 1 1 a/d 82 20 b 1 3 3/10Hb 11 plt 1.8 lac

31, 24, 300

N20, 0.1

3.7 Y Y N CD 2.5 kg6/10, 8/10

1+/nil 5day

10 hrs 6 hrs 16 hrs150 140

100 100

96 Ananthamma 22 Cooli Low H Hospet 499320 17.06.11 18.06.11 20.06.11 5 Y a/b/c 1 N N N N 2 1 1 a 82 20 b 1 3 2/10Hb 9 plt 1.8 lac

31, 40, 520

N28, 0.1

4.5 Y Y N VD 2 kg6/10, 8/10

3+/nil 5day

10 hrs 12 hrs 16 hrs160 160

110 100

97 Rajamma 21 Cooli Low H Hospet 484881 31.01.11 01.02.11 04.02.11 2 Y a/b 1 N N N N 2 1 1 a 92 20 b 1 3 3/10Hb 10.2 plt 1.9 lac

36, 30, 610

N20, 0.9

4. Y Y N VD 2.5 kg7/10, 9/10

6 hrs 12 hrs 18 hrs150 150

110 100

98 Kuchamma 20 Cooli Low HChitradurga

472475 13.10.10 14.10.10 21.10.10 6/1 Y a/b/c/d/e 1 N N N N 1 2 3 a 96 22 a 1 3 2/10Hb 10.4 plt 1.33 lac

32, 25, 680

N20, 1.3

5.1 Y Y N CD 2.5 kg4/10, 6/10

11+/nil 4day

4 hrs 10 hrs 26 hrs170 150

100 90

99 Shahida 22 Cooli Low M Bellary 495565 15.5.11 17.5.11 24.5.11 2 y a/c 1 N N N N 1 2 1 a 90 20 a 1 3 0/10Hb 10 Plt 1.8 lac

15,20,450 N 20,1 3.2 Y Y N CD 3 kg 6/10, 8/10

2+/nil 6day

6 hrs 18 hrs 22 hrs170 150

110 90

100 RAthnamma 22 Cooli Low H Bellary 495913 18.5.11 20.5.11 28.5.11 3 Y a/c 1 N N N N 1 2 3 a 88 18 a 1 3 2/10Hb 9.8 plt 1.8 lac

15,14,520 N 18,.9 4 Y Y N CD 3 kg 6/10, 8/10

1+/7 day

4 hrs 40 hrs 18 hrs140 130

100 90

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“COMPARATIVE STUDY OF VAGINAL DELIVERY AND CAESAREAN ...

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