“evaluation of role of non-stress test (nst) in

i

“EVALUATION OF ROLE OF NON-STRESS TEST (NST) IN

HIGH RISK PREGNANCY”

BY

Dr. DEVARASETTI ANURUPA

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 AND GYNECOLOGY

Under the guidance of

Dr. GEETA J DOPPA

HOD AND PROFESSOR

DEPARTMENT OF OBSTETRICS & GYNECOLOGY

KVG MEDICAL COLLEGE SULLIA

2018

vi

ACKNOWLEDGEMENT

I derived great pleasure and satisfaction in preparing this dissertation and I would like

to take this opportunity to thank everyone who has made it possible.

I convey my heartfelt gratitude and sincere thanks to my guide Dr. GEETA J DOPPA,

M.B.B.S.,M.D, Professor, HOD Department of Obstetrics and Gynecology,

K.V.G. Medical College and Hospital, Sullia, who with her knowledge and experience

has provided able guidance and constant encouragement throughout the course of my

postgraduate studies and residency and in the preparation of this dissertation.

It gives me immense pleasure to thank Dr. RAVIKANTH.G.O, M.D., D.G.O.,

Associate Professor, Department of Obstetrics and Gynecology, for his valuable

guidance during this study and throughout my PG course and residency in Sullia.

My sincere thanks to Dr. ANIL BAIPADITHAYA Associate Professor, Dr. U.S.

BORKAR, Dr. VEENA for their valuable guidance and encouragement during my

study period.

I am indebted to my loving PARENTS, my father Mr. D. MOHANA KRISHNA and

my mother Mrs. D. SARADA and my sister Mrs. ANUPAMA D, for their constant

encouragement and support, without whom I wouldn’t have achieved what I’m today.

I would like to convey my thanks to my friends for their help and guidance. I also extend

my thanks to my beloved seniors Dr. VIDYASHREE, Dr. PALLAVI

GANGATKAR, Dr. ASHA RANI, Dr. ASMA RAFIQUE and my juniors Dr.

LALITYA, Dr. SHAKUNTALA, Dr. SARADA and Dr. NIYAF, Dr.

AKSHATHA, Dr. ARAVINDA.

vii

I thank Sri. SHASHIDHAR KOTIAN., Assistant Professor, Department of Preventive

and Social Medicine, K.M.C .Mangalore, for his help in statistical analysis of this

dissertation.

I thank all my PATIENTS, who formed the backbone of this study without whom

this study would not have been possible.

LIST OF ABBREVATIONS USED

ACOG - American College of Obstetricians & Gynaecologists

AFI - Amniotic Fluid Index

AFV – Amniotic Fluid Volume

ANS – Autonomic nervous system

BBV - Beat to Beat Variability

BOH - Bad Obstetric History

Bpm – Beats per minute

BPP - Bio Physical Profile

CF – Cord Factor

CNS – Central nervous system

CPD - Cephalopelvic disproportion

CST - Contraction Stress Test

CTG - Cardio Tocogram

DFMC – Daily Fetal Movement Count

EDD – Expected Date of Delivery

EFM – Electronic Fetal Monitoring

EFW – Estimated Fetal Weight

FAST – Fetal Acoustic Stimulation Test

FBM - Fetal Breathing Movement

FD – Fetal Distress

FH – Fetal Heart

FHR - Fetal Heart Rate

FI – Failed Induction

FIGO – Federation of International Gynaecological and Obstetrical Society

FM - Fetal Body Movement

FT - Fetal Tone

GA – Gestational Age

GDM - Gestational Diabetes Mellitus

IUGR - Intra Uterine Growth Retardation

LMP – Last Menstrual Period

LQ – Liquor Quantity

LSCS - Lower Segment Caesarean Section

MBBS - Bachelor of Medicine & Bachelor of Surgery

MBPP - Modified Bio Physical Profile

Mod – Mode of delivery

MS - Master of Surgery

MSAF – Meconium Stained Amniotic Fluid

MVP - Maximum Vertical Pocket

NICU - Neonatal Intensive Care Unit

NPV – Negative Predictive Value

NR – Non Reactive / Non Reassuring

NST - Non Stress Test

OCT – Oxytocin Challenge Test

OBG - Obstetrics & Gynaecology

Obs&Gyn - Obstetrics & Gynaecology

PIH - Pregnancy Induced Hypertension

PNM – Perinatal Mortality

PPV – Positive Predictive Value

R – Reactive / Reassuring

RhNeg - Rhesus Negative

USG - Ultra Sonogram

VAST - Vibroacoustic Stimulation Test

VD – Vaginal Delivery

Wt - Weight

viii

LIST OF TABLES

Table No TABLES Page No.

1 Showing Distribution of the patients in different age group 73

2 Age wise comparison between Low risk & High risk 74

3 Mean age for high risk and low risk groups 75

4 Showing distribution of the patients with their gravid state 76

5 Showing gravida wise comparison between Low risk &

High risk

77

6 Distribution of study participants with High Risk cases 78

7 Distribution of Patients based on NST results 79

8 Comparison of Mean Gestational age with the two groups 80

9 Distribution of cases in low risk and high risk groups based

on mode of delivery

81


on induction of labour

82


on mode of delivery and NST result

83

12 Distribution of cases in low risk and high risk groups who

underwent LSCS based on NST results

84


on Intra Partum Fetal Distress (IPFD)

85

14 Distribution of cases who underwent cesarean section in

low risk and high risk group for IPFD

86

15 Comparison of mean birth weight between two groups 87

ix

16 Comparison of Meconium Stained Amniotic Fluid (MSAF)

between two groups

88

17 Distribution of patients in low risk and high risk groups

based on MSAF and NST results

89

18 Comparison of APGAR scores among both groups 89

19 Distribution of cases who had NICU admission in low risk

and high risk group based on NST results

90

20 Comparison of Perinatal Mortality in low risk and high risk

group

91

21 Predictive accuracy of NST for perinatal mortality 92

x

LIST OF FIGURES

Fig.No Figure Name

Page No

1 Showing Distribution of the patients in different age group 72

2 Age wise comparison between Low risk & High risk 73

3 Mean age for high risk and low risk groups 74

4 Showing distribution of the patients with their gravid state 75

5 Showing gravida wise comparison between Low risk &

High risk

76

6 Distribution of study participants with High Risk cases 77

7 Distribution of Patients based on NST results 78

8 Comparison of Mean Gestational age with the two groups 79


on mode of delivery

80


on induction of labour

81


on mode of delivery and NST result

82

12 Distribution of cases in low risk and high risk groups who

underwent LSCS based on NST results

83


on Intra Partum Fetal Distress (IPFD)

84

14 Comparison of Mean birth weight between two groups 86

15 Comparison of MSAF between two groups 87

16 Distribution of cases who had NICU admission in low risk

and high risk group based on NST results

89

xi

17 Comparison of Perinatal Mortality in low risk and high risk

group

90

18 Predictive accuracy of NST for perinatal mortality 91

ABSTRACT

“EVALUATION OF ROLE OF NON-STRESS TEST (NST) IN HIGH RISK

PREGNANCY”

Background and Objectives:

In developing countries, maternal mortality has been significantly decreased so

now modern obstetricians are focusing more on fetal health. Initially fetus was

considered only as an outcome of pregnancy but now-a-days the fetus is considered as

second patient. So it also requires as much surveillance as the health of mother. In

modern obstetrics methods for fetal risk determination have shifted from less specific

biochemical methods (e.g. maternal estriol determination) to more specific fetal

biophysical methods. Non stress test is one of the biophysical techniques, which is

widely used in the management of high risk pregnancies. With the acceptance of ‘ small

family norm’, it has become necessary that every wanted conception should

successfully end in birth of a viable healthy baby. The non stress test can identify the

fetus in jeopardy in utero.

Objective of the Study:

1. To evaluate the efficacy of NST for antenatal surveillance.

2. To correlate the test results with mode of delivery.

3. To correlate the test results with perinatal morbidity and mortality.

Methods:

This clinical study was conducted at KVG Medical College and Hospital, on

patients attending outpatient department or admitted as in patient in department of

Obstetrics and Gynaecology over a period of 1.5 years from November 2016 - April

2018.

50 High Risk pregnant women (study group-selected based on inclusion and

exclusion criteria) and 50 Low Risk pregnant women (control group) will be

randomly enrolled into study and were evaluated by NST from 32 weeks of gestation

onwards or whenever risk factor was identified and repeated at appropriate intervals

as per subjective results in cases of high risk group.

Results:

NST results shows that in low risk group 76% were reactive and 24% was non

reactive. In high risk group it was 66% in Reactive and 34% non reactive. Most of the

subjects were normal in low risk group (74%) whereas in high risk group 50 % were

normal and 50% were under LSCS. In low risk group, 18.4% cases of reactive NST

underwent LSCS and 50% of cases with non-reactive NST underwent LSCS. In high

risk group, 42.4% of cases with reactive NST underwent LSCS where as 64.7% of cases

with non reactive NST underwent LSCS. The mean NICU admission in reactive of low

risk is 2.579 and that of non reactive is 3.25 . But in High risk group the NICU

admission days in reactive group is 4.67 and that of non reactive is 5.882.

Conclusion:

The potential advantage of NST is that, a decrease in decision to delivery time

can be made for those patients with fetal distress so that a major improvement in the

outcome among parturients can be achieved with abnormal (non-reactive) NST results.

In conclusion NST is a valuable screening test for detecting fetal compromise

in both HR and LR fetuses that may have poor perinatal outcome. But, larger

randomised controlled trials are needed to know if the use of NST in HR and LR

pregnancies for antenatal surveillance, benefit by reduction in the incidence of adverse

perinatal outcome

Keywords:

Non Stress Test, Reactive /Reassuring, Non-Reactive / Non Reassuring

1

INTRODUCTION

The antepartum evaluation of fetal well being has now turned into an essential.

Part of management of all pregnancies. To accomplish this assessment different

biochemical, biophysical systems have been devised. The basic role of different

antepartum assessment systems is to recognize fetal distress in order to forestall fetal

death.

Generally, obstetricians have a tendency to arrange pregnant ladies as "low"

and "high" risk. Although some efficient strategies are accessible for dealing with the

high-risk, we need more efficient methods for identifying pregnant women in distress

in the low-risk group. Even in low risk mothers, fetal acidosis can occur with equal

frequency as in high risk group.

Routine electronic monitoring is accepted in high risk women, but low risk

women too require some reliable objective assessment to optimize the outcome.

In developing countries, maternal mortality has been fundamentally

diminished so now current obstetricians are concentrating more on fetal wellbeing.

Initially fetus was viewed as just as a result of pregnancy however now-a-days the

fetus is considered as second patient. So it also requires as much reconnaissance as

the wellbeing of mother

In modern obstetrics methods for fetal risk determination have shifted from

less specific biochemical methods (e.g. maternal estriol determination) to more

specific fetal biophysical methods. Non stress test is one of the biophysical

techniques, which is widely used in the management of high risk pregnancies. With

the acceptance of “small family norm”, it has become necessary that every wanted

conception should successfully end in birth of a viable healthy baby. For this, close

2

monitoring for assessment of fetal wellbeing is required, especially for high risk

pregnancies. The non stress test can identify the fetus in jeopardy in utero.1

Non stress test (NST) is a graphical recording of fetal heart rate reactivity

to fetal movements. It is one of the most widely used primary testing methods for

antepartum surveillance. It is simple, inexpensive, non-invasive, easily performed and

interpreted. NST was repeated weekly or biweekly according to indication. Cases

were followed up till the delivery and data regarding mode of delivery and perinatal

outcome were noted.2

High risk pregnancies require sophisticated maternal and fetal surveillance.

Fetal morbidity and mortality are greater in high risk women, such as those with

prolonged pregnancy, intrauterine growth restriction (IUGR), hypertension or other

risk factors.3

For detecting high risk fetus, NST is a simple screening procedure and

is helpful in decreasing perinatal morbidity and mortality.4

3

OBJECTIVES

To evaluate the efficacy of NST for antenatal surveillance.

To correlate the test results with mode of delivery.

To correlate the test results with perinatal morbidity and mortality.

4

REVIEW OF LITERATURE

HISTORICAL DEVELOPMENT

In 1818, Franscois-Isaac Mayor of Geneva, a surgeon reported the fetal heart

sound while placing his ear on the maternal abdomen.5

In 1821 Kergaradec – using Laennec’s 1806 invention, the stethoscope

listened to the fetal heart and wondered if variations in the fetal heart rate revealed the

fetus’s state of health.

In 1833, Kennedy published the first book suggesting that there was great

value in listening to the fetal heart and proposing that fetal heart rate changes were

indicative of fetal distress, urging physician intervention in labor with forceps.

Anton Freidrich Hohi was first to describe fetal stethoscope in 1834.

In 1876, Pinard modified this stethoscope which was widely used. The

obstetrics started with the discovery of fetal heart auscultation by who used the

stethoscope for monitoring FHR.7

Winkelet al in 1893, empirically set the limits of normal fetal heart rates of

120-160 b/min.6

“The rate of fetal heart is subjected to considerable variation which afford a

fairly reliable means of judging as to the well being of the child. As a general rule, its

life should be considered in danger when the heart beats fall below 100 or exceed

160”5,7

Whitride Williams. J – This was the comment on judging fetal well being in

1903 – 1st edition of William’s obstetrics.

5

Phillipe-le-Goust6 first described the fetal heart in his poetry. He was a

colleague of Marsac who had claimed to have heard FHR in 1950.

In 1960, Caleyro Barcia and Hon pioneered intrapartum fetal monitoring54.

Kubli first employed antepartum fetal heart rate monitoring as a means of evaluating

the fetal satus of high risk pregnancy.55

Hon and Quilligan, in 1967 noted characteristic fetal heart rate patterns

correlated with neonatal outcome.8

Various patterns of fetal heart rate ( FHR ) was used to interpret as indicators

of fetal risk beat to beat variation was described as a marker of fetal well being in

1968. 9,10

In mid 1970s, the correlation between fetal well-being and acceleration of the

heart rate in response to movement was noted by many authors.11,12

Specific description of significance of accelerations in FHR as a good

prognostic sign for perinatal outcome is attributable to Ruttegers and associates in

1972.

Sadovsky and Waffe et al, in 1973 quantitated fetal activity on patients at risk

of uteroplacental insufficiency.13

Lee et al, in 1976 suggested that FHR acceleration in response to movements

i.e. non-stress test could be relied upon as prediction.14

Hammacher focused primarily on FHR characteristics in those patients with

no exogenous stress factors imposed. Specific attention was directed towards the FHR

response associated with spontaneous uterine contractions, fetal movement and a

6

“silent pattern” (<5 bpm) or a smooth FHR. In addition, he advised that “an acoustic

or mechanical stimulus: should be used when the fetus exhibited a “silent” or

“narrowed undulatory pattem” (5-10 bpm)-toensure that the fetus is not asleep.15

Keegan KA et al tested the feasibility of NST as an office approach and found

it practical in screening at risk patients and it required a minimum of time to

perform.40

Freeman (1975) and Lee and Colleagues (1975) introduced to non-stress test

to describe the FHR acceleration in response to fetal movement as a sign of fetal

health.’

Read and Miller et al, in 1977 utilized acoustic stimulation to evoke

accelerations.16

Barret and associates in 1981 conducted the twice weekly testing with non-

stress test and felt it was necessary in certain high-risk pregnancies to avoid fetal

death within 7 days following a normal reactive test results.17

lngemarsson I et al (1986), admission test can detect fetal distress already

present at admission and unnecessary delay in intervention can be avoided in such a

case.Admission test seems to have some predictive value for fetal well being for the

next few hours of labor.The test is simple to perform. A reactive test with two

accelerations in first ten minutes probably makes extension of recording unnecessary.

Such a short test makes screening convenient.18

Leveno KJ et al 1986, In conclusion the results of this clinical trial indicate that

universal fetal monitoring changed obstetrical practices but did not significantly

improve perinatal outcome. Abnormalities in fetal heart rate were observed more

7

frequently in low-risk pregnancies during universal monitoring, and this observation

was associated with the performance of more caesarean sections because of fetal

distress. We conclude that not allpregnancies, particularly not those at low risk of

complications, need continuous electronic fetal monitoring during labor.’7

Arulkumaran S et al (2001), for patients who are considered as low risk, a

short l5-20 minutes external EFM on admission in labour has been suggested as a

screening ‘admission test’. If no FHR changes are observed with early labour

contractions and the trace is normal and reactive, the chances of fetal hypoxia due to

causes other than acute events are unlikely in the next few hours of labour. ln a study

of over 1,000 low risk women conducted in Singapore, 40% of women with an

ominous AT developed fetal distress, compared to 1.4% in those with a reactive AT.

Thus, AT helps to identify a subgroup of foetuses who would benefit from more

intensive monitoring, while others can be monitored with intermittent auscultation.9

EVOLUTION OF NST

Trierweilcr observed during the process of CST-the relationship between the

fetal movement and FHR accelerations during the observation period preceding the

CST. Such observations in which fetal movement and FHR acceleration were noted

precluded subsequent observations of an abnormal CST results.

Retrospective evaluation of the potential for NST clearly defined the

relationship between repetitive accelerations and the absence of positive CST

results.19

Evertson and Associates found a reactive NST as predictive of good outcome

as was a negative CST. Also two or more accelerations were not associated with

8

abnormal CST. Although CST or “oxytocin challenge test" (OCT) is useful in

evaluating fetal condition, it is time consuming (60-90minutes), needs intravenous

access, high incidence of suspicious/equivocal CST results.’ An excellent alternative

for intrapartum fetal heart rate testing was NST.20

Keane MWD et al in 1980 found that there was excellent correlation between

a reactive NST and a negative CST (99.4%) whereas that between a non reactive NST

and a positive CST was poor (24.8%).21

Nochimson DJ et al evaluated 421 patients with a total of 812 tests (NSTs)

utilizing NST as the primary screening device and concluded that NST was a reliable,

in expensive, convenient and time saving screening procedure which can be made

available to a greater number of patients than the CST alone.38

BASIS OF NON STRESS TEST AND FETAL CARDIAC PHYSIOLOGY

The Non Stress Test is seemingly more logical approach to Antepartum fetal

heart rate testing as a screening device. It has proved successful in screening large

number of patients (Martin and Schifrin 1977).

The rationale for use of Non Stress Test for antepartum evaluation is that the

presence of acceleration of FHR associated with fetal movement indicate intact

responsive CNS mechanisms that are reflected by these FHR changes. Depression of

normal FHR fluctuations and fetal movements have been seen with fetal sleep,

hypoxia, acidosis, fetal anamolies and certain narcotic and sedative drugs (Sterman

and Hoppen Browers, 1971; Keegan et al., 1979).

9

Acceleration in the fetal heart rate may be periodic or not related to

contraction. Those acceleration accompanying uterine contractions may occur during

the contractions phase of uterine pressure wave or may follow or precede a periodic

fetal heart rate pattern. The acceleration is fairly rapid and the return to baseline is

equally abrupt. Cause is partial occlusion of umbilical vein, which produces

hypovolemia, hypotension and increase FHR via physiologic mechanism of the

baroreceptor.

Non periodic fetal heart rate accelerations are the most common form of the

pattern observed and are associated with fetal movement. These are typically in the

range of 15-25bpm and last 10 to 30 seconds.

The mechanisms underlying these accelerations may be either a transient

decrease in vagal tone or increase in sympathetic tone or both.

The presence of non periodic acceleration signifies an intact nervous system

and a responsive myocardium.

Pillai and James (1990) studied the development of fetal heart rate

acceleration patterns during normal pregnancy. The percentage of body movements

accompanied by acceleration and the amplitude of these accelerations increased with

gestational age.56

Chemoreceptors in the carotid arteries and the aorta may be stimulated by

arterial O2 tension. Acute hypoxia produced increased variability whereas chronic

hypoxia results in decreased variability of the heart rate.

10

PHYSIOLOGY OF FHR ACCELERATION

Fetal cardiac response normally is affected by neural and humoral factors.

Sympathetic cardiac accelerator nerve fibres arise in the upper thoracic segments of

the spinal cord and function as a cardioacceleration center which is subordinate to

higher centers in the hypothalamus.

During early fetal development, sympathetic dominance appears to influence

baseline rate, with maturation there is general slowing of the fetal heart and a more

even balance is effected between sympathetic and parasympathetic systems. Both

central and peripheral nerve stimulation can produce acceleration of fetal cardiac rate.

Thus normal human fetal cardiac development is characterised by progressive

dominance of the parasympathetic system as maturation proceeds.

Fetal heart rate is normally increased or decreased on a beat-to-beat basis by

autonomic influences mediated by sympathetic or parasympathetic impulses from the

brain stem centers. Thus, fetal heart rate acceleration is believed to be an indication of

fetal intact autonomic function. “Beat-to-beat variability is also under the control of

autonomic nervous system (Matsuura and Colleagues 1996). Consequently,

pathological loss of acceleration may be seen in conjunction with significantly

decreased beat-to beat variability of fetal heart rate.

Smith and Colleages (1988) observed a decrease in the number of

accelerations in preterm human fetuses. Subsequently found to have lower umbilical

artery blood Po2 values compared with those fetuses who had normal fetal heart rate

characteristics. Thus, non stress testing is considered to reflect the chronic condition

of the fetus.57

11

The fetal heart rate is modulated by a number of stimuli, central nervous

system influence is important with cortisol and subcortical influences which are not

under voluntary control. We cannot alter our heart rate at will. The cardioregulatory

centre in the brain stem also plays a part. Other physiological factors regulate the

heart rate are circulatory catecholamines, chemoreceptors, baroreceptors and their

interplay with the autonomic nervous system (ANS).

Cortical nerve cells associated with motor function and cardiovascular

response are located in close proximity in the fetal brain. The center for NST matures

only at about 28weeks and is most sensitive to asphyxia, it is located in the posterior

hypothalamus and medulla oblongata.

12

Guinn and colleagues (1998) studies NST results between 25 and 28 weeks

in 188 pregnancies that ultimately had normal outcomes. Only 70% of these normal

fetuses demonstrated the required 15 bpm or more of heart rate acceleration. Lesser

degrees of acceleration i.e., l0bpm occurred in 90% of the tested pregnancies.58

The National Institute of Child Health and Development Fetal

Monitoring Workshop 2 (1997) has defined accelerations based on gestational age.

The acme of acceleration in 15bpm or more above the baseline heart rate and the

accelerations lasts 15 seconds or larger for <2 minutes in fetuses at or beyond 32

weeks. Before 32 weeks, accelerations are defined as having an acme l0bpm or more

for 10 seconds or longer.59

Fetal reactivity appears between 28 and 30 weeks and it is a function of

posterior hypothalamus and nucleus in the upper medulla. Fetal breathing movements

begin at 20 to 2l weeks while fetal tone and the movements appears between 7 and 9

weeks of intrauterine life.22

Menning FA et al stated that the sensitivity of each of these biophysical

variables to hypoxia is different and those that becomes functional earlier in fetal

development and more resistant to acute changes in the fetal oxygenation.60

DevoeLD has reported that the actual FHR pattems that first signal cellular

hypoxia and acidosis depends on the duration and severity of these biochemical

abnormalities. All the compromised fetuses may not uniformly express these pattems.

FHR patterns associated with pre-terminal fetal asphyxia may exhibit relatively fixed

FHR baselines, loss of FHR variation, disappearance of accelerations or the

appearance of spontaneous late FHR decelerations.23

13

Nijhuis and colleagues studied FHR patterns, general body movements and

eye movements and described four fetal behavioural states.61

Weibgold AB et al concluded that as the gestation advances, the FHR

decreases and variability increases.62

Sheldon RE et al showed that acute fetal hypoxernia may cause sudden and

profound decrease in fetal movements and acceleration frequencies whereas

chronically reduced placental functions leads to gradual decline in fetal movements

and acceleration frequencies as compensatory circulatory shunting occurs.63

Visser GHA et al concluded from their study that episodes of low variability

and decrease movements signaling quiet sleep states, recur with a mean duration of

20min and may last as long as 2 hours in normal term fetuses. These states alternate

with episodes of increased fetal breathing and FHR variability, rapid eye movements

and occasionally body movements, the so called active sleep state.64

Active sleep state may occupy nearly half the entire day. Brief episodes of

“wakefulness” account for approximately 10-15% of the total day when most of the

reactive FHR accelerations are observed.

Different findings have been found by different authors as the early indicators

of fetal compromise. Freeman RK et al found that late deceleration was earlier

warning sign of decreased uteroplacental function than was a loss of fetal reactivity fr

om their study. They also found that the non-reactive NST or positive CST correlates

with the highest mortality rate.34

Weingold AB et al found progressive loss of baseline variability and

decreasing frequency of accelerations to be early signs of fetal compromise.62

14

Rochard F et al reported that in the human fetus during the last trimester,

the balance of autonomic response appears to shift from sympathetic predominance

early to vagal dominance by 38th week with a gradual slowing in the baseline heart

rate of the fetus. He also demonstrated that, progressive decrease in variability and

frequency of accelerations was the earliest indicator of fetal distress.24

Kubli and associates found that the presence of late decelerations was a most

consistent sign of severe fetal hypoxia and impending death. Baseline tachycardia is

neither a reliable nor a consistent sign of severe fetal hypoxia or impending fetal

death. Persistent bradycardia has been the least commonly observed of all monitoring

patterns. In serial tracings prior to death, the most consistent feature has been a

progressive loss of baseline beat- to-beat variability in FHR pattern.55

According to Devoe LD, sequential studies of NST in the same fetus

suggests that fetal compromise may be signaled by a gradual decrease in the

acceleration counts, a subsequent decrease in the incidence of fetal movements,

decoupling of accelerations with fetal movements and finally the disappearance of

both accelerations and movements.65

Higher centres in the brain

There are influences on the cardioregulatory centre from higher centres in the

brain. It is this input that is thought to be responsible for the so called fetal rest

activity cycle.

During fetal rest cycle the fetus is apparently sleeping in utero with no fetal

body and limb movements, electroencephalogram activity and FHR variability all

decreased. A fetal rest cycle normally lasts about 20minutes, following which there is

a return to normal fetal movements and FHR variability.

15

Baroreceptors –

Situated in the arch of aorta and carotid sinus. In response to increasing BP ,

impulses from those receptors are sent to the cardioregulatory centre resulting in an

increase in vagal activity which slow heart rate.

Chemoreceptors –

Situated in the carotid and aortic bodies and responds to changes in oxygen and

carbondioxide tension.

Fall in oxygen tension is detected by the carotid aortic bodies and would result

in a sympathetic discharge from the cardioregulatory centre causes an increase in

FHR and thus blood pressure.

Adrenal medullary response –

In response to stress, adrenal medulla releases hormones, adrenaline and

noradrenaline which result in an increase in both FHR and the force of cardiac

contraction.

The intrinsic FHR is therefore under the complex influence of many

physiological factors and is modulated by the parasympathetic and sympathetic

nervous systems.

Synchronus acceleration of the fetal heart rate coincidental with body

movement suggests a coordination of both functions.The more premature fetuses were

less capable of reacting to stimuli with sufficient heart rate accelerations because of

neuromotor immaturity.

16

The Physiologic Basis of Fetal Monitoring

Clinical FHR monitoring is actually an ongoing observation of human

physiology. The question being asked of the fetal monitor by the clinician is, what is

the adequacy of fetal oxygenation? Because the FHR pattern appears to assume

certain characteristics under the influence of various hypoxic and non hypoxic

stresses, it becomes important for the clinician to have a understanding of the

physiology of fetal respiratory exchange and the physiologic control of FHR.

Anatomy of Maternal-Fetal Exchange

The placenta is an organ that functions as the fetus extracorporeal life support

system. The placenta serves as the fetal lung (respiration). Kidney (excretion),

gastrointestinal tract (nutrition) and skin (heat exchange), and as a barrier against

certain susbstances dangerous to fetus. In addition, it is an endocrine organ that

produces steroid ( oestrogen, progesterone) and protein ( HCG, HPL ) hormones very

early in gestation, the blastocyst implants in the decidualised endometrium and the

trophoblast cells invade the maternal circulation, creating a lake of maternal blood

that baths the trophoblast and developing embryo. As the gestation grows a number of

spiral arteries that supply blood to the endometrium are penetrated and provide the

basic architecture as the placenta develops, with villi forming cotyledons arranged

around these cspiral arteries. This maternal blood occupies an area referred to as the

intervillous spaces and it between this space and the fetal capillary (contained within

the chorionic villi) that maternal-fetal and fetal-maternal exchange occurs.21

The human placenta is thus referred to as a hemochorial type because the

mother’s blood comes into direct contact with the fetal chorionic villus, oxygen,

carbon dioxide, nutrients, waste products, water and heat are exchanged at this level

17

and must cross two layers of fetal trophoblasts, the fetal connective tissue with in the

villus, and the fetal capillary wall.

Physiologic features of change in FHR

Myer and co-workers found two physiologic mechanisms for late

deceleration autonomic reflex mechanism occurs in fetuses during early mild hypoxia.

As prolonged hypoxia occurs, metabolic acidosis develops in the fetus. This activates

a second mechanism of direct myocardial depression. In pronounced asphyxia, this

mechanism causes shallow late decelerations such decelerations are shallow because

the heart is less efficient at decreasing its own rate, Because most fetuses are being

tested before such marked level of fetal compromise, the reflex mechanism is

responsible for most late decelerations.19

In fetus with normal oxygen reserve periodic decrease in oxygen during

contraction do not go below the ‘so-called “critical level”. This level is 17-18mm Hg,

and indicates when the chemo receptors in the carotid arteries are stimulate, fetuses

with diminished oxygen reserves reach this critical level during contractions and

activate the chemo receptors. As a reflex, the stimulated chemoreceptors must cross

two layers of fetal trophoblasts, the fetal connective tissue within the villus, and the

fetal capillary wall.

The uterine blood flow is supplied principally from the uterine arteries, but

anastomosis occurs between these vessels, other branches of the hypogastric arteries,

and ovarian arteries. Significantly, the spiral arteries must traverse the full thickness

of the myometrium in order to reach the intervillous space, anything that effects

maternal cardiac output will, of course, affect the flow through the spiral arteries.

Additionally, as the uterus contracts, the intramyometrial pressure, may exceed the

18

intra arterial pressure causing occlusion of these vessels and resulting in cessation of

blood flow to the intervillous space.25

Fetal metabolism continues during such interruptions and as a result, the

arterial oxygen supply to the fetus is decreased. Therefore, uterine contractions

routinely cause a periodic decrease in fetal oxygen levels, causes the autonomic

nervous system to send a message to the brainstem to direct blood to the vital area of

the body. The brainstem responds with alpha sympathetic stimulation that constricts

the low resistance peripheral arterial beds in the hind limbs. This results in systemic

arterial hypertension that diverts blood to the brain and heart. The baroreceptor

respond with an afferent link to the brainstem and causes and efferent vagal response.

The vagal stimulation slows the FHR and is seen as a late deceleration fetal heart race

tracing.26

This bradycardia persists until fetal oxygen increases to levels at which the

chemo receptors are no longer stimulated at the end of contraction. When the fetal

pO2 consistently decreases to less than the “critical level”, the late decelerations

become persistent. This causes the CST result to be positive. If the oxygen level is

fluctuating between normal and low, the late decelerations are intermittent and test is

equivocal.

The combination of the two mechanisms, explain the clinical observations of

three stages of late deceleration with progressive uteroplacental insufficiency.

Initially, mild stimulation of the brainstem mechanism causes late decelerations. As

hypoxia progresses, the stimulus increases, causing progressively deeper

Decelerations. As anaerobic metabolism occurs, the fetus becomes acidotic. Once

acidotic, the brainstem is less responsive and the autonomic reflexes are blunted. The

19

reflex mechanism stops functioning at this point. The second mechanism of direct

myocardialdepression begins, causing shallow late decelerations.27

Fetal Hypoxia

A pathological condition characterised by a decreased concentration of oxygen

in the tissue and in the blood( Arias, 1998 ). Severe foetal hypoxia can result in death,

cerebral palsy and lesser degree of neurological damage.28

Foetal hypoxia can result from:

• Insufficiency of uterine blood flow.

• Decrease in maternal arterial oxygen content.

• Other causes including foetal anemia or increased foetal demand for oxygen.

Fetal oxygen supply depends upon maternal ventilation, uterine perfusion and

adequate placental and fetal circulation. The oxygen tension in maternal arterial blood

reaching the intervillous space is high and foetal blood, reaching the villi through the

umbilical arteries, has a low oxygen tension. Umbilical venous blood, returning

directly to the foetal heart, carries oxygen from the placenta for distribution to the

fetal tissues. The placenta also uses oxygen for its metabolic processes and so

umbilical venous oxygen tension never reaches the same level as uterine venous

oxygen tension.

Two main factors contribute to the adequacy of foetal oxygenation despite the

low oxygen tension. First, foetal haemoglobin is present in higher concentration than

in the adult and has a greater affinity for oxygen. Second, the foetus normally supplies

more oxygen to its tissues than required, with the result that the fetus is relatively

resistant to mild/moderate hypoxia.29

20

A reduction in uteroplacental perfusion results initially in a greater extraction

of oxygen by the fetus with a consequent reduction in the oxygen concentration of the

uterine veins. Subsequently, there is a reduction in umbilical venous oxygen

concentration but fetal hypoxemia does not produce tissue hypoxia as long as the

oxygen supply exceeds the needs of fetal tissues for aerobic metabolism.

Normal fetus, faced with an acute hypoxic insult will usually develop some

degree of neurological depression. This is manifested by a significant reduction in

most types of fetal movements. By doing this, oxygen consumption is reduced and

therefore oxygen availability to the brain is increased. As fetal activity returns, fetal

swallowing may then be occurring while renal blood flow and thus urine output is

decreased. This unbalanced situation can lead to the development of oligohydramnios

in the following days. Hence, the finding of oligohydramnios is a fetus with intact

membranes and normal kidneys is suggestive of chronic hypoxia. A fetus in this

situation has a limited capacity to respond to further acute hypoxic stress. Ultimately,

fetal tissue hypoxia occurs and the fetus changes to anaerobic metabolism with a build

up of lactic acid.30

Fetal Acidosis

A pathological condition characterised by an increased concentration of

hydrogen ions in the tissues and in the blood.

Besides redistributing blood to vital organs ‘the brain sparing effect’, the fetus

can switch from aerobic to anaerobic metabolism in situations of hypoxia. Glucose is

broken down to lactic acid, which in the presence of oxygen is converted to carbon

dioxide releasing energy. CO2 is transported to the placenta and diffuses into the

maternal circulation for elimination. When the transfer is interrupted such as by cord

21

compression or reduced uterine perfusion, CO2 accumulates and forms excess of

carbonic acid. The subsequent formation of hydrogen ions results in fetal acidosis.

This respiratory acidosis usually accompanies the hypoxia that results from any

mechanism that interferes with feto-maternal gas exchange and constitutes the

physiological definition of asphyxia. Initially, base deficit remains normal or is

slightly increased; this acidosis can be readily reversed if CO2is eliminated.

With more severe hypoxia, respiratory acidosis progresses to a mixed

respiratory and metabolic acidosis. With longer hypoxia, the later increases in

significance. As lactic acid accumulates, PH will begin to fall further and the base

deficit will rise.

A continuing or worsening of the situation leads to an acidosis dominated by

the metabolic component, with a further fall in PH and increase of base deficit. In

contrast to problems in transporting CO2 across the placenta, metabolic acidosis

cannot be reversed unless oxygenation of the fetus can be re established. The fetal

tissues will accumulate acid metabolites, which will not be removed until the fetal

circulation is re established upon correction of the hypoxia. Fetal brain injury is likely

if the hypoxia is prolonged or severe. Although the fetus can cope with respiratory or

mild mixed acidosis for some hours, an acute fall in oxygen supply will produce a

rapid shift to metabolic acidaemia and would not be tolerated for long. Faced with

hypoxic insult, the normal fetus will respond predictably with:

• Changes in heart rate.

• Alterations in biophysical activity.

22

Changes in fetal heart rate

Acute hypoxia produces an immediate reflex mediated fall in FHR

secondary to chemoreceptor stimulation of the vagus nerve. However, if hypoxia is

prolonged, adrenal stimulation produces an elevation of catecholamines that can

overcome the vagal drive. If hypoxia is corrected then reflex parasympathetic reduces

immediately leaving the elevated catecholamine level to produce tachycardia which

settles over a period of 30-60 minutes. The fetal response to reduction in oxygen

supply depends on factors such as speed of onset, degree and duration. When acute

and severe, such as with cord prolapse or placental abruption, the fetal heart rate

response is prolonged bradycardia recurrent, prolonged decelerations. If fetal hypoxia

evolves slowly, the fetal response will be modified by compensatory mechanisms,

which depends upon the reserve capacity of fetoplacental unit (intervillous space).

Initially, the FHR may not change but variability becomes reduced and accelerations

disappear. Braxton Hicks contractions may provoke late decelerations in such

circumstances.31

Changes in fetal biophysical activity

Biophysical activities like fetal breathing movements, fetal body movements,

fetal tone, amniotic fluid volume and FHR reactivity are dependent on the integrity of

the Central Nervous System for which adequate fetal cerebral oxygenation is

necessary. Studies have shown that hypoxic fetuses lose certain behavioral parameters

in the reverse order in which they were acquired in the course of fetal development.

Fetal neurodevelopment and sequence of fetal deterioration (Fetal

Neurodevelopment)

• Tone (Cortex/Sub cortex) - 7.5 to 8.5 weeks.

• Movement (Cortex/nuclei) - 9 weeks.

23

• Breathing (Ventral surface of fourth ventricle) - 20 to 21 weeks.

• Fetal heart rate reactivity (posterior hypothalamus/medulla) - 24 weeks.

Sequence of fetal deterioration

• Late decelerations (CST).

• Accelerations disappears (NST, BPP, CST).

• Fetal breathing stops (BPP).

• Fetal tone absent (BPP).

• Amniotic fluid decreases (Chronic hypoxia resulting in redistribution of

cardiac output away from the kidneys towards the brain).

Methods of surveillance

Although controversy remains over which surveillance technique is

preferable in the pregnancy risk biophysical methods have definitely replaced the

biochemical methods.

Biochemical Methods

Biochemical methods have little value in the management of complicated

pregnancies.They serve more as a screening device rather than for picking finer

details as seen with the biophysical methods:

Two biochemical methods performed were:

1. Estimation of urinary or plasma oestriol.

2. Estimation of Human Placental Lactogen (HPL) (Benet, 1977 Sadovsky and

Yaffe, 1982).

24

Basis of Biochemical Tests

During pregnancy oesriol is synthesized in the placenta but the

precursor is derived from the foetus. As such the estimation of oestriol or HPL in

the mother can take as an index of placental function and indirectly of foetal

well being.

Oestrodiol Estimation

At term, the oestriol level is about 40-50 mg in 24 hours urine but there is

considerable variation f rom patient to patient. An acute fall of 40-50% from the

mean of three previous values or a single value of less than 12 mg in 24 hours urine

is considered critical and significant. A value of 4 mg signifies impending foetal

death.

A plasma level is measured by RIA or less than 10mg/ 100ml in the last

4weeks of pregnancy indicates a foetus at risk.

HPL Estimation

Values less than 4 µg/ml in plasma after 30 weeks of gestation is

significance.

These tests are of value in post term pregnancy complicated with

Hypertensive disorders and IUGR, but are of little significance in Diabetes, Multiple

pregnancy and Rh-isoimmunization. These biochemical markers represent foetal

h e a l t h in the immediate past not in the present as the results are those due to

foetal metabolism in the past few days. A wide range of values is observed for

the same gestation making serial measurements necessary to derive meaningful

conclusions. The period of gestation should known for the interpretation of results.

In addition to these, the problem of sample collection. The need for laboratory

25

technology and personnel and of all the poor predictive value of these tests

have made biochemical methods of foetal monitoring less favourable.

Biophysical methods

They comprise the tests based on biophysical activity to determine foetal well

being. Foetal biophysical activity is a reflection of an intact central nervous system of

the foetus and their use requires understanding of the foetal response to hypoxemia

and acidaemia. The foetal CNS is very much sensitive to diminished foetal

oxygenation. Hypoxia-CNS cellular dysfunction metabolic acidosis-CNS depression-

changes in biophysical activity.

A) Tests of Placental Dysfunction: Placental hypoxia lead to foetal hypoxemia

which can lead to anaerobic metabolism and acidosis leading to the alteration of

biophysical activity.

(1) Placental Grading - was described by Grannum. He described essentially the

textural qualities of placenta and graded 0 to 3, on real time USG and linked their

appearance with pulmonary maturity. Subsequently the appearance of Grade 3 in the

early third trimester was linked with pregnancies complicated by IUGR and

Hypertensive diseases. This led to the consideration of the use of this USG finding as

a screening test for pregnancies at risk. But the correlation between USG signs of

placental maturity and the functional capacity of the placental is poor. The correlation

between Grade 3 placental and foetal pulmonary maturity is excellent in pregnancies

near term.

(2) Foetal Growth: Although not strictly a test, measures of foetal growth are an

index of placental function in the absence of foetal malformation or infection. The

26

question as far as monitoring the foetus is concerned; it is not necessarily the size but

the linear growth pattern, which is more important. Documented foetal growth

failure is a potent indicator of severe placental dysfunction.

(3) Amniotic Fluid Volume: is a dynamic product of foetal, placental and maternal

metabolism. In the late second and third trimester, amniotic fluid volume is

empirically taken as an indirect measure of foetal urine output.Increased liquor

volume should not be ignored as a monitoring tests as in Rh isoimmunization and

Diabetes. Hydramnios may be an important determiner of illness. However, it is

reduced liquor volume, which is the most sought after finding in foetal monitoring

programmes.

The rationale behind the use of liquor volume is derived from animal models.

Hypoxia in foetal sheep results in the redistribution of blood towards brain, heart and

adrenals with reduction in renal blood flow. Colour Doppler has confirmed this

possible aetiology in the human foetus with IUGR and chronic hypoxia. Moore

et al 1990, claimed that Amniotic Fluid Index was superior to single pocket

diameter whereas others (Fischer et al 1993) have failed to show significant

differences. A four quadrant vertical pocket measurement in excess of 5 cm has

correlated well with good perinatal outcome.

B) Tests of foetal hypoxia

1) Foetal Movement Counts: The basis of most antepartum evaluation test is the

evaluation of foetal movements. The rationale behind all these is that alternation in

foetal activity will predate foetal heart rate changes and reduced foetal activity.

27

Prolonged absence of foetal movement is not physiologic and has been shown to

precede foetal death.

Passive unstimulated foetal activity starts as early as 7 weeks and becomes

more sophisticated and coordinated b y the end of pregnancy (Vindla and James

1995).

In the third trimester, foetal movement maturation continues until about 36

weeks when behavioral states are established in 80 percent of normal fetuses.

Although several foetal movement counting protocols have been used neither

the optimal number of movements nor the ideal duration for counting them has been

defined and they seem to be acceptable.32

Cardiff ‘count -10’ formula: The patient counts foetal movements starting

at 9 am. The counting comes to an end as soon as 10 movements are perceived.

She is instructed to report to the physician if i) Less than 10 movements occur

during 12 hours on two successive days or ii) no movements is perceived even

after 12 hours in a single day.

Daily foetal movement count (DFMC): The count each of one hour duration

(morning, afternoon and evening) are recommended. The total COUIIU multiplied

by four give the daily (12 hour) foetal movement count (DFMC). If there i s

diminution i n the number of "kicks" to less than 10 in 12 hours, at indicates

failing placental funct ion .

2) Non-Stress Test (NST) : Freeman (1975) and Lee and Colleagues (1975)

introduced the Non-Stress Test to describe foetal heart rate acceleration in response

to foetal movement, as a sign of foetal health. This test is based on the hypothesis

28

that the heart rate of a foetus who is not acidotic as a result of hypoxia or

neurological depression, will temporarily accelerate in response to foetal

movement. A possible explanation for this acceleration caused by foetal movement

may be provided by partial occlusion of the umbilical vein caused by foetal

movement. This occlusive event may precipitate a decrease in foetal blood pressure

and acute hypoxia that results in reflex stimulation of the autonomic nervous system.

The NST is non-invasive, easily performed and interpreted and readily

accepted by patients. This test involves the use of Doppler detected foetal heart rate

acceleration coincident with foetal movements perceived by the mother.

The variables that must be evaluated are:

1) Baseline foetal heart rate.

2) Variability of foetal heart rate.

3) Presence or absence of acceleration.

4) Presence or absence of deceleration.

Definition and Interpretation

The International Federation of Obstetricians and Gynecologists (FIGO)

recommended a classification with three patterns of FHR, normal, suspicious and

pathological (Rooth et al 1987) while the classification adopted by the American

College of Obstetricians and Gynecologists (ACOG) Committee on Obstetric

Practice uses the terms reassuring and non-reassuring to describe patterns of FHR

on CTG 9ACOG 1994, 1998).

Recently, the National Institute of Clinical Excellence (NICE) and the Royal

College of Obstetricians and Gynecologists (RCOG) of the United Kingdom have

defined these parameters (NICE 2001).9,10

29

There are no intrapartum diagnostic tests of fetal condition that may

give an indication of the eventual outcome in terms of neurological deficit. The

responses of a fetus before the onset of labour, the magnitude and duration of

intrapartum stress and the intervention of carers. Fetuses exhibit different outcomes

to the same apparent circumstances and FHR patterns.

CATEGORIZATION OF FHR FEATURES AND TRACES

(From ACOG 1994, 1998/NICE 2001)

Features Baseline

( bpm )

Variability

( bpm)

Decelerations Accelerations

Reassuring 110-160 >5 None Present

Non-

reassuring

100-109

161-180

<5 to >40 for

<90 minutes

Early

Deceleration

Variable

Deceleration

Single

prolonged

Deceleration

Upto 3min.

The absence of

Accelerations

with an

otherwise CTG

is of uncertain

significance.

Abnormal <100

>180

Pattern

Sinusoidal

Pattern

> 10 minutes

<5 for >90

minutes

Atypical

variable

Decelerations.

Late

decelerations

Single

prolonged

deceleration

> 3minutes

Abnormal patterns seen in fetuses that subsequently develop untoward

outcomes are also seen in fetuses with normal outcomes (Nelson, 1999).

30

Despite the shortcoming of CTG and the controversies surrounding its

application in clinical practice, it remains in widespread use because of lack of

adequate alternatives

(Haggerty, 1999; Thacker and Stroup. 1999)

Some useful guidelines regarding EFM are ( Arulkumaran et al 1995):

Accelerations and normal baseline variability are hallmarks of fetal health.

Accelerations without baseline variability should be considered suspicious.

Periods of decreased variability without decelerations may represent quiet

fetal sleep.

Hypoxic fetuses may have a normal baseline FHR of 110-160 bpm with no

accelerations and baseline variability of <5 bpm for >40 minutes.

In the presence of baseline variability <5 bpm even shallow late decelerations

<15 bpm are ominous in a non reactive trace.

Abruption, cord prolapsed, and scar rupture can cause acute hypoxia and

should be suspected clinically (may give rise to prolonged deceleration?

bradycardia).

Fetal hypoxia and acidosis may develop faster with an abnormal trace when

there is scanty thick meconium, intrauterine growth restriction, intrauterine

infection with pyrexia and/ or pre or post term labour.

In preterm fetuses (especially < 34weeks), hypoxia and acidosis can increase

the likelihood of respiratory distress syndrome and may contribute to

intraventricular hemorrhage, warranting early intervention in the presence of

an abnormal trace.

31

Hypoxia can be made worse by oxytocin, epidural analgesia and difficult

operative deliveries.

During labour, if decelerations are absent, asphyxia is unlikely although it

cannot be completely excluded.

Abnormal patterns may represent the effects of drugs, fetal anamoly, fetal

injury or infection, not only hypoxia.

3) CONTRACTION STRESS TEST (CST):

The contraction stress test is based on the response of fetal heart rate to uterine

contractions. Uterine contraction result in brief episodes of decreased uteroplacental

blood flow causing impaired oxygen exchange. Therefore, uterine contractions causes

a hypoxic stress that normal healthy fetus can tolerate without difficulty. In contrast a

fetus with chronic or acute hypoxia elicit fetal heart rate decelerations. Depending on

them the contraction is brought about, CST can be classifies into two types as follows:

A) Oxytocin Challenge Test (OCT)

Contraction are induced using intravenous oxytocin, a dilute intravenous

infusion is initiated at a rate of 0.5 mu/min and doubled at an interval of 15-20minutes

until atleast three uterine contractions each lasting for 40 to 60 seconds are present in

10minutes period.

Criteria for interpretation of CST (ACOG Bulletin, 1999)5

Negative: No late or significant variable decelerations.

Positive: Late deceleration following 50% or more of contractions

(even if the contraction frequency is fewer than three in 10 minutes).

32

Equivocal – suspicious: Intermittent late deceleration or significant

variable deceleration.

Equivocal – hyperstimulatory : Fetal heart deceleration that occur in

the presence of contractions more frequent than every 2 minutes or

lasting longer than 90 seconds.

Unsatisfactory: Fewer than three contractions in 10 minutes or an

uninterruptible tracing.

Relative contraindications to CST are those associated with an increased risk

of preterm labour and delivery, uterine rupture or uterine bleeding. Because of long

duration of the test, the requirement of continuous supervision by trained personnel,

and the existence of risks and contraindications associated with its performance, CST

is nowadays used infrequently for primary fetal surveillance, rather as the test to

follow a ‘non-reactive’.33

This test involves the use of Doppler detected fetal heart rate accelerations

coincident with fetal movement perceived by the mother.

A) Nipple Stimulation Stress Test ( NSST )

Nipple stimulation in lieu of Oxytocin induced contractions has been reported

to be usually successful contraction stress testing (Huddleston et al, 1984).

Advantages include reduced cost and shortened testing times.

4) Biophysical Profile (BPP):

Manning and colleagues (1980) proposed the combined use of five fetal

biophysical variables as a more accurate means of assessing fetal health than any one

used to alone. Required equipments include a real time ultrasound device and Doppler

33

ultrasound to record fetal heart rate. Typically, these tests require 30 to 60 minutes of

examination time.34

The five biophysical components assessed are:

1. Fetal heart rate acceleration.

2. Fetal breathing.

3. Fetal movements.

4. Fetal tone.

5. Amniotic Fluid Volume.

Normal variables were assigned a score of two each abnormal variable a score

of zero. Thus, the highest score possible is 10.

Score of 8 – 10: associated with normal pH.

Score of 6: Equivocal.

Score <4 Abnormal.

Components and their scores for the biophysical profile (ACOG, 1999)

Component Score 2 Score 0

Non-stress test >2 accelerations of >15 bpm for

>15 sec in 20- 40 min

0 or 1 accelerations in

20-40min

Fetal Breathing >1 episode of rhythmic breathing

lasting >30sec within 30 min

<30 sec of breathing in

30 min

Fetal Movement >3 discrete body or limb

movements within 30min

< 2movements in 30min

Fetal Tone >1 episode of extension of a fetal

extremely with return to flexions

or opening or closing hands

No movement or no

extension/flexion

Amniotic Fluid

Volume

Single vertical pocket >2cm Largest vertical

pocket<2cm

34

Interpretation of the BPP results should be made by separate analysis of each

of the individual component of the test.

5) Modified Biophysical Profile (MBPP)

Vintzileous et al, 1987 were the first to propose a modification of the

biophysical profile for evaluation of fetal well being. The MBPP combines the

observation of an index of acute fetal hypoxia, the amniotic fluid index (AFI). The

MBPP is considered normal if the NST is reactive and the AFI is greater than 5cm

and abnormal if the NST is non reactive or the AFI is 5cm or less.

The MBPP has the advantage of excellent negative and positive predictive

values but requires expensive equipment and a trained sonologist.

6) Doppler Ultrasonography

A recent development in feto-maternal medicine is the Doppler waveform

analysis of the fetoplacental and uteroplacental circulations. It is used to assess the

haemodynamic components of vascular impedance. The umbilical artery

systolic/diastolic ratio (S/D), the most commonly used index is considered abnormal

if it is elevated above the 95th percentile for gestational age or if diastolic flow

signifies increased impedance and is usually associated with intrauterine growth

restriction ( ACOG, 2000).

Recently, the Middle Cerebral Artery has received particular attention because

of observation that the hypoxic fetus compensates by ‘brain sparing effect’ via

reduced impedance-increased blood in cerebral vessels.

35

7) Fetal Actogram/ Actocardiogram

Full activity of the fetus (Actography) is monitored including its limb

movements, trunk movements and breathing movement during Antepartum period

along with continuous recording of its FHR pattern.

This method was the ‘low frequency content’ of Doppler USG signals of FHR

transducer of a CTG machine to pick up fetal movements and represented in the form

of a graph.

The investigation in conjuction with AFI gives a very reliable assessment of

fetal health.

8) Vibro acoustic stimulation tests (VAST) :

In 1935 Sontag and Wallace35 reported that the fetus responds to sound.

External low frequency sounds of <125Hz are enhanced, but sounds of greater

frequency are attenuated with maximum attenuation of 4000Hz. Loud sounds have

been used to startle the fetus, provoking accelerations of fetal heart rate. To perform

acoustic stimulation, an artificial larynx is positioned on the maternal abdomen and a

stimulus of 1-2 seconds is applied. This may be repeated upto 3 times for upto 3

seconds (ACOG, 1999).

Read and Miller (1977) were the first to suggest that acoustic stimulation

could be used to examine fetal health.

Marden D et al reported that the fetal acoustic stimulation test evokes

significantly more palpated or visualised fetal movements than in controls. Palpated

or visualised fetal movement after acoustic stimulation was almost always

accompanied by a reactive NST. VAST may not only reduce false positive and

36

worrisome non-stress tests but also reduces the testing time. Smith CV et al found that

the incidence of non-reactive test was 14% in control group and 9% in the study

group (using transabdominal acoustic stimulation). A significant reduction in testing

time was also observed. The fetal acoustic stimulation test offers advantages over the

transabdominal NST by lower incidence of non-reactive NST (by 50%) and reducing

the testing time.36

FALSE NORMAL NST:

False normal NST means – reactive NST in a fetus who is actually in

distress. Smith and associates (1987)37 performed a detailed analysis of the cause of

fetal death within 7 days of normal non-stress tests. The most common indication for

testing was post term pregnancy. The mean interval between testing and the death was

4days with a range of 1-7 days. The single most common autopsy finding was

meconium aspiration, often associated with some type of umbilical cord abnormality.

They concluded that an acute asphyxia insult had provoked fetal gasping. They also

concluded that non-stress testing was inadequate to preclude such an acute asphyxial

event and that other biophysical characteristics might be beneficial adjunct like AFI

estimation.

INTERVAL BETWEEN TESTING:

Nochism DJ et al reported that the still birth rate within 7 days of a reactive

NST was 6.4 / 1000 with the still births occurring either in patients with diabetes

mellitus or IUGR.38

Weekly non stress testing is effective in preventing still births in most of the

risk groups is not adequate in patients with Diabetes mellitus or IUGR. The interval

between tests originally, rate arbitrarily set at 7 days appears to have been shortened

37

as experience evolved with non stress testing. According to ACOG (1999) more

frequent testing was advocated by some investigators for women with post term

pregnancies, type 1 DM, IUGR and PIH. In these conditions, some investigators

perform biweekly tests. Some clinicians perform NSTs daily or even more frequently.

The once a week testing method was chosen empirically and was associated

with a varied perinatal outcome.39,40 The rate of still birth with reactive NSTs was

reduced to 1.9 / 1000 by biweekly NSTs compared to 6.1 / 1000 when NST were

done weekly. It was suggested that the patients who are at risk for fetal stress should

be evaluated on a twice a week basis when NSTs is used as a primary test.

NST is most useful for antenatal surveillance of a wide range of high risk

pregnancies. For all practical purposes, the NST has supplanted. The CST is used as

the primary screening tool to determine the risk for uteroplacental insufficiency

conditions associated with IUGR. Such fetuses display progressive deterioration of

fetal reactivity and variability concurrent with the development of academia.41

Optimal screening strategies for this population must include other biophysical

observations such as AFV/ (Amniotic fluid volume) measurements or Umbilical

Artery Doppler velocimetry.

Weekly non stress testing is effective in preventing still birth in most risk

groups is not adequate in patients with IUGR or Diabetes mellitus. A significantly

higher incidence of SGA ( small for gestational age ) infants was found when the high

risk women had the accelerations : fetal movements ratio of < 10 % in last weeks

before birth.42 There was 38% incidence of SGA babies born to mothers with an

abnormal ratio, only 4% of the mothers having normal ratio over 10% delivered

38

growth retarded fetuses. It was noted 13 out 0f 45 patients with PIH in this study had

acceleration: Fetal movement ratio below 10% and 3 perinatal death occurred in them.

Ingardia CJ et al showed that the growth retarded non reactive fetuses differed

from the fetuses born adequate for gestational age by number of accelerations more

than 15beats/ min and the number of accelerations lasting for 30 seconds.43

A greater problem associated with the use of antenatal FHR testing as a sole

screening method of identifying compromised fetuses in post datism was that the

intrapartum period carries high risk for perinatal damage. Previous work has shown

the poor sensitivity of FHR testing to adverse outcomes in this group supporting a

combined screening approach that incorporates some regular assessment of AFV.

Although this approach enhances the screening of infants at risk of intrapartum

complications, it does not obviate the need for close intrapartum assessment of post

dated fetuses with otherwise normal antenatal testing.

Arias JW et al noted that most of the diabetic females had normal NSTs.

Infants of diabetic mothers were delivered at or near term if serial NSTs remain

normal. Only 6 fetuses out of 37 had acceleration: fetal movement ratio below 10% in

this group and all of them survived.42

Devoe L.D. has observed that in diabetic pregnancy fetal breathing activity is a

reassuring finding when breath rates are in the normal range (<60/min).44

Rh isoimmunisation may produce a sinusoidal FHR pattern characterised by

repetitive low amplitude uniform oscillations without reactive accelerations. Fetuses

exhibiting this pattern are at high risk of morbidity and mortality.45

39

AUTOMATED ANALYSIS OF NST COMPUTERISED SYSTEMS:

Pit falls in the use of FHR test may reflect the differences among the

observers, differing interpretative criteria and uncontrolled testing conditions and on

occasion inappropriate clinical responses to the test results.46 Computers and fetal

monitoring devices have been linked for two decades. Several proprietary systems

have been developed for computerised analysis of continuous FHR signal. Eg:- NST

Analysis System ( Augusta, GA), Oxford-Sonicaid system 8000, Chinchesta UK.

These systems designed to be consistent and objective and could be useful in

primary screening in the absence of experts. An additional benefit of these system in

their virtual elimination of inter observer and intra observer variability.47

Another approach to intelligent analysis of FHR tests comes from neural

network development.48 These programmes which are based on establishing

association between facts or ‘in puts’ and answers or ‘out put’ can provide solution to

FHR test analysis. Devoe LD et al used neural network trained with 2500 cases to

predict pregnancy outcome which correctly predicted 249 of 250 cases (99.5%)

compared with an accuracy of 85% using conventional test assessment.49

New portable devices have become available for home monitoring of FHR.

These devices have the potential to immediately transmit these tracings to a medical

facility. Self non stress testing50 (performed by the mother) is a reliable and accurate

method of antepartum FHR testing compared to associated NST (done by professional

medical personnel). This will significantly reduce the medical cost without

compromising to the result of fetal testing.

40

TEST RELIABILITY AND STUDIES OF NST EFFECTIVENESS:

NST was significantly better at predicting the absence of fetal compromise

than its presence and an abnormal NST should be supported by other clinical data

before obstetric intervention could be undertaken. The best screening performance

(sensitivity > 70%) was obtained for NST when indicated for IUGR or maternal

hypertension.51

Adverse perinatal outcomes following normal or reassuring NST occurs

rarely. A cumulative review of available literature shows that an abnormal test confers

a corrected antenatal mortality of 0.3/1000 births and a perinatal death rate of 2.3 per

1000 births.

BASIC FHR PATTERN

Baseline FHR is taken as the mean FHR over a period and should be arrived

at by observing a tracing of at least 10 minutes duration. It is deduced from continues

FHR record by imaging a line passing horizontally, roughly, through the middle of the

way line of the FH tracing.52,53

Normal baseline FHR at various periods of gestation:

12-30 weeks – 140-180 bpm

30-40 weeks - 120-160 bpm

40+ weeks lowest up to 110 bpm may be considered as normal.

Progressive vagal dominance occurs as the fetus approaches term results in a

gradual decrease in the baseline FHR.

Types of baseline abnormality:

Tachycardia

Bradycardia

41

Baseline variability

Tachycardia

Tachycardia means sustained (not transient) increase in FHR to above 160

bpm (Only after observing the tracing for a minimum period of 10 minutes).

Degree of Tachycardia

Mild: 160 to 180bpm.

Severe: greater than 180bpm.

If the rate exceeds 200 bpm the risk of fetal heart decompensation is very

high.

Causes of Baseline Tachycardia

Stress

Adrenaline and nor adrenaline released by mother or fetus in response to

stressful stimuli have a powerful effect on FHR causing tachycardia.

However, if the stress is severe causing release of a very high quantity of

catecholamines, it may cause constriction of uterine blood vessels, interfering with the

placental blood supply leading to hypoxic bradycardia (Steer, 1986).

Mother in severe pain with resultant increase in her sympathetic tone may also

excite fetal tachycardia which usually settles on giving adequate analgesia

(Ingemarsson et al, 1993)

Hypoxia

In case of gradually developing hypoxia, the baseline FHR gradually rises in

order to increase the cardiac output so as to maintain oxygenation of vital centres. As

42

the fetus has limited capacity of increasing the stroke volume, it increases its heart

rate to maintain adequate cardiac output (Arulkumaran, 1992).

Baseline tachycardia is often the first clinical sign of fetal hypoxia (distress) on

ordinary auscultation.

Infection

Both maternal and fetal infection may result in tachycardia as the temperature

rises above 38c / 100.4 F.

Epidural analgesia

This occurs in response to maternal hypotension.

Pre term Fetus

Due to immaturity of the parasympathetic system, pre term fetus may manifest

some tachycardia. Such a tachycardia may be considered physiological, provided all

potentially ominous aetiologies have been ruled out.

Drug Treatment

Drugs used to arrest premature labour e.g.: beta adrenergic agents like

salbutamol, ritodrine etc, can produce tachycardia because of excessive sympathetic

activity. Administration of atropine to the mother has been shown to induce fetal

tachycardia by vagolysis.

Anemia

Severe maternal and fetal anemia may result baseline tachycardia.

Cardiac Failure

Maternal cardiac failure has been known to produce baseline tachycardia.

43

Fetal heart Tachyarrhythmia

Obviously this would be associated with fetal tachycardia ( Ingemarsson et al,

1993)

Incidental Tachycardia

This short term tachycardia is seen usually after a period of vigorous or

prolonged fetal movement and is normal. In such instances, baseline variability is not

affected.

This pattern is often seen when the fetus wakes up and makes lot of

environment after a period of quiet sleep of fetus.

Complicated Baseline Tachycardia

Any baseline tachycardia complicated by other untoward features such as –

loss of baseline variability and/or deceleration of any type is extremely ominous and

is associated with highest incidence of acidosis (Steer,1986). This pattern calls for

fetal blood sampling and PH estimation or immediate delivery.

Bradycardia

Baseline bradycardia means sustained (not transient) decrease in FHR to below

120 bpm.

Mild bradycardia - 100-120

Moderate bradycardia - 80-100bpm is a nonreassuring pattern, occurs in

fetuses with congenital heart abnormalities or myocardial conduction defects.

Severe bradycardia - less than 80bpm is an ominous finding indicating severe

hypoxia. The causes include maternal hypoperfusion, uterine hyperactivity,

44

rapid descent, prolonged cord compression, cord prolapsed, placental

abruption, uterine rupture, paracervical block, epidural and spinal anesthesia.

Hypoxemia – Fall in Po2 in fetal blood stimulated chemoreceptors present in

cardiac and aortic bodies and causes baseline bradycardia.

Tissue Hypoxia – This develops as the hypoxia gets more severe and

prolonged and causes more severe baseline bradycardia. Tissue hypoxia which

leads to metabolic acidosis is responsible for this severity. In such cases, in

addition to baseline brachycardia there also occurs reduced baseline variability

and deceleration.

It has been found that fetal acidosis develops if bradycardia lasts for more than

20minutes. ( Ingemarsson et al, 1993).

Local Anaesthetic Agent: Bradycardia which is sometimes seen after

epidural block or paracervical block may be due to direct action of local

anaesthetic agents on fetal myocardium as the drug passes from mother to

fetus. Such bradycardia usually doesnot last more than 20 minutes

(Ingemarsson et al 1993).

Narcotic Drugs : They may reduce the baseline by 10 – 20 bpm due perhaps

to reduction in fetal activity ( Ingemarsson et al 1993).

Mild (partial) Umbilical Cord Compression : Trapping of cord e.g: between

fetal limbs can possibly cause temporary baseline bradycardia which usually

gets corrected by itself as the fetus moves under the stress of the

cardiovascular disturbance caused by partial compression. On turning the

patient from one side to another relieves such compression and consequent

bradycardia. Such happenings are more common with oligohydramnios and

45

postdated cases. Incidental tight stretching of the cord over fetal trunk can also

cause such, more than transient bradycardia.

Post dated Fetus (40 plus weeks): According to Steer (1986), at this fetal

age, rates between 100-120 bpm can be considered as normal provided there

are no other abnormality. These cases must be monitored closely not by CTG

alone but also by ultrasound, i.e. by Amniotic fluid index (AFI) and

Biophysical profile (BPP).

Head Compression : Persistent bradycardia especially in the second stage of

labour in the range of 100-120 bpm has been reported to be associated with

occipito – transverse position with very rare incidence of acidosis and also

invariable good neonatal outcome (Cunningham et al, 1989). However such

bradycardia may happen late in labour even with normal presentation if the

descent of head through the birth canal is very rapid ( Ingemarsson et al 1993).

This pressure related bradycardia is thought to be caused by sustained basal

centre stimulation resulting from raised intracranial pressure occasioned by

mild fetal head compression.

Heart Block : Congenital atrioventicular block obviously would present as

baseline bradycardia.

Fetal heart rate variability

Variability has been defined as FHR fluctuations in the baseline over 1

minute. These fluctuations are variable in amplitude and frequency and are usually

identified as the amplitude of the peak to through in beats per minute between the

highest peak and lowest trough of fluctuation in a one-minute segment of the trace.

46

FHR variability reflects a healthy nervous system, chemoreceptors,

baroreceptors and cardiac responsiveness. Prematurity decreases variability.

Variability should be normal after 32weeks.

Normal baseline variability is greater than or equal to 5 bpm between

contractions.

Beat to beat or short term variability reflects the instantaneous change in FHR

from one beat to the next. This is a measure of the time interval between cardiac

systole. This can be accurately measured with direct electronic monitoring.

Long term variability is a somewhat slower oscillation in heart rate and has a

frequency of 3 to 6 cycles per minute. If amplitude is not detectable, but less than 5

bpm, then it is defined as decreased FHR variability; if amplitude ranges from 5 to 25

bpm, then it is defined as normal; if amplitude is greater than 25bpm, then it is

increased FHR variability.

Absent or decreased FHR variability may be an ominous sign, associated with

fetal hypoxia, acidosis and low Apgar scores. Clinically, loss of beat to beat

variability is more significant than loss of long term variability. The combination of

late or severe variable decelerations with loss of variability is particularly ominous.

Fetal sleep cycles or medications may also decrease the FHR variability. The

development of decreased variability in the absence of decelerations is unlikely to be

due to hypoxia.

Increased variability (salutatory pattern) is usually caused by acute hypoxia or

mechanical compression of umbilical cord. This pattern is most often seen during the

second stage of labor. The presence of a salutatory pattern, especially when paired

47

with decelerations, should warn the physician to look for and try to correct possible

causes of acute hypoxia. Although it is a nonreassuring pattern, it is usually not an

indication for immediate delivery.

The sinusoidal pattern is a regular, smooth and undulating from typical of

a sine wave that occurs with frequency of two to five cycles per minute and an

amplitude range of 5 to 15 bpm. It is also characterised by a stable baseline heart rate

of 120 to 160bpm and absent beat to beat variability. The sinusoidal pattern is rare but

ominous and is associated with high rates of fetal morbidity and mortality.

Clinical correlation of sinusoidal pattern

Main underlying cause severe fetal anemia, as occurs in cases of Rh disease

or severe hypoxia.

Massive fetal hemorrhage from whatever cause e.g: maternal anticoagulant

therapy (Aspirin, Warfarin etc), bleeding from vasapraevia, cordocentesis etc

has been found to be associated with sinusoidal pattern.

Transient sinusoidal rhythm has been reported even during normal labour.

(Cunningham et al, 1989, Mishell et al, 1993).

It should be differentiated from the ‘pseudosinusoidal’ pattern, which is a

benign, uniform long term variability pattern. A pseudosinusoidal pattern

shows less regularity in the shape and amplitude of the variability waves and

the presence of beat to beat variability, compared with the true sinusoidal

pattern.

48

Transient changes in FHR

Accelerations

Accelerations are transient increases in the FHR of 15 bpm or more from the

baseline rate and lasting 15 seconds or more.

Cause:

Primary cause: Associated with fetal movement.

There are two exceptions to above explanation,

Fetal heart rate acceleration may occur in absence of perceived movement by

the mother.

Acceleration may not occur with every small movement that can be seen

during ultrasonography.

Other causes:

Uterine contractions,

Vaginal examinations,

Fetal scalp stimulation or external acoustic stimulation.

The presence of accelerations is considered a reassuring sign of fetal well

being.

Acceleration coinciding with uterine contraction

a) This phenomenon is called periodic acceleration. Two reasons have been

ascribed to this.

b) Uterine contraction provokes fetal movement which in turn causes fetal heart

acceleration. Acceleration may be an early sign of partial cord compression. In

the specific situation fetal heart acceleration is compensatory in nature and

49

follows ‘immediately’ an episode of transient hypoxia caused by cord

compression during the contraction. As the degree of compression increases –

this pattern gradually takes the shape of variable deceleration.

Acceleration in response to fetal stimulation

Incidental stimulation: This included abdominal palpation and manipulation and

vaginal manipulation like exploratory palpation to find the position of occiput in

relation to pelvis, fetal manipulation associated with artificial rupture of membranes,

scalp electrode application, fetal blood sampling etc.

Investigative stimulation: This include acoustic stimulation and purposeful scalp

stimulation as a part of scalp stimulation test.

Significance

Beard et al (1971) found that when FHR pattern exhibited accelerations the

incidence of fetal acidosis was nil. Arulkumaran (1992) found that even in the

presence of suspicious or abnormal traces, accelerations induced by external stimuli

were indicative of non acidotic state and this constitutes the basis of Vibroacoustic

Stimulation test – VAST and scalp stimulation test.

So, overall conclusion is presence of qualifying acceleration signifies healthy

state of the fetus. However, absence of acceleration is not a reliable indicator of fetal

hypoxaemia and such cases should be monitored for longer period and be investigated

further to arrive at a decision.

50

Decelerations

From the baseline rate a sudden decrease in FHR by more than 15 bpm lasting

for more than 15seconds but less than two minutes is considered as deceleration (

Ingemarsson, et al 1993).

During antepartum period, decelerations are usually of pathological

significance, whereas in labour, they are quite commonly associated with uterine

contractions.

Classifications

A-Hon’s Classification (1968)

Early deceleration

Late deceleration

Variable deceleration

Cladeyro – Barcia et al (1996)

Type 1 dips correspond to Hon’s early or variable deceleration or a

combination of both.

Type 2 dips corresponds to Hon’s late deceleration.

Early deceleration (Type 1 dip)

This is also called ‘synchronous deceleration’ because it exactly synchronizes

with uterine contraction. The other term used for it is reflex deceleration because here

the bradycardia has been proved to be due to reflex stimulation of the vagal centre by

the compression of fetal head during contraction.

51

Pressure on fetal head

Altered cerebral blood flow

Central vagal stimulation

FHR Deceleration

Classical Features

The dip in FHR is ‘V’ shaped with a ‘sharp’ lowest point.

The apex of V coincides with the peak (apex) of uterine contraction.

Deceleration starts very shortly after the beginning of contraction, hence it is

called early.

Deceleration recovers fully by the end of the contraction.

Deceleration is short lived.

Baseline FHR and baseline variability of FHR remain normal in between

contraction.

Degree of Early Deceleration

Small Depth of the dip is less than 40 bpm.

Large Depth of the dip is more than 40 bpm. Rarely the rate falls to below 100

bpm.

Causes of Early Deceleration

Head Compression: Early Deceleration indicates that patient is at the end of

first stage or in second stage of labour, with head deep in the pelvis which is

getting compressed during contraction.

Partial Cord Compression: This is how cord compression causes transient

deceleration through mechanical stress. Cord compression - constriction of

52

arterial outflow in the cord damming back the fetal blood into aorta – rise of

blood pressure in aorta – triggering of stretch receptors in aorta – stimulation

of vagal centre slowing heart (deceleration) restoration of BP to normal (Steer,

1986).

Significance of Early Deceleration: Early deceleration, if ‘uncomplicated’,

does not signify hypoxia or acidosis and hence immediate intervention is

usually not necessary in these cases. However, it has been suggested that it is

possible for co existent mild hypoxia to potentiate the effect of early

deceleration shape. Hence, tracing should be continued in these cases right up

to delivery.

Management of Early Deceleration

A. A prompt vaginal examination is to be done :

i. To know the state of progress of labour (i.e. dilatation and descend)

ii. To exclude any obstruction in the passage causing the compression

iii. To exclude cord prolapsed.

B. Tracing must be continued to watch whether other ominous features are making

their appearances or not, and one has to act accordingly.

Late Deceleration (Type 2 dip):

It is that type of ‘contraction associated’ deceleration of FHR, which starts

only late in contraction and does not return to normal baseline until after the

contraction is over.

Occurrence of late deceleration on the face of artificially induced uterine

contraction forms the basis of Contraction Stress Test ( CST ), Oxytocin Challenge

Test (OCT), and Nipple Stimulation Stress Test ( NSST ).

53

According to FIGO (1987): There must be three or more late decelerations

following ‘consecutive’ contraction for a diagnosis of late deceleration to be made.

Classical Features

The dip FHR trace is somewhat wide mouthed ‘U’ shaped with round bottom.

The lowest point of ‘U’ does not coincide with the peak of uterine contraction.

It comes after a ‘time lag’ of minimum of 15 seconds.

Deceleration starts ‘late’ in contraction and hence it is called late deceleration.

Deceleration does not recover by the end of contraction. It outlasts the

contraction.

This type of deceleration is much more prolonged than early decoration.

Late deceleration can occur even during antenatal period probably in response

to Braxton-Hicks Contraction. This may be seen in the cases of gross intrauterine

growth retardation specially those which result from chronic placental insufficiency

54

like those associated with long standing pregnancy induced hypertension, recurrent

small abruption of placenta etc.

Mechanism

It is generally agreed that late decelerations occur as a result of contraction

when the fetus is already significantly hypoxic (acute or chronic fetal hypoxia). Steer

(1986) has shown that late decelerations make their appearance only when the PO2 in

the fetus falls below 10 mmHg. Clinical studies show that late decelerations are

associated with fetal acidaemia in approximately 40% of cases. A normal fetus is

capable of reacting to stimulations like abnormal uterine activity, maternal

hypotension, epidural block etc with late decelerations. In this situation, late

deceleration will disappear after correcting the cause (stopping the oxytocin infusion,

correcting the maternal supine position, restoration of maternal blood pressure and

increasing circulatory volume.

Degree of Late Deceleration

This can be classified in two major ways as follows (Ingemarsson et al, 1993)

A. Degree of drop in rate

Moderate: Upto 100 bpm level.

Severe – below 100 bpm level.

B. Magnitude of beats lost

Less than 15 bpm

Between 15 – 45 bpm

Greater than 45 bpm

55

Clinical causes of Late Deceleration

A. Preuterine

Maternal Hypotension

Supine Hypotension

Following Epidural Block

Severe Anemia

B. Uterine

Uterine Hyperactivity

Oxytocin infusion given for induction or acceleration of labour

Prostaglandin induction

C. Intrauterine

Placental insufficiency

Management

Patient should be turned on her side to relieve venacaval compression.

If the patient has been on Oxytocin drip it should be stopped.

Tocolysis in case the uterine contraction are too frequent.

Oxygen inhalation.

Rehydration correct hypovolaemia if present.

Case to be reassessed and decision for delivery taken accordingly.


Variable Deceleration means decelerations which are variable in their relation

to uterine contraction which means:

May come (variably) during any phase of contraction – not typically ‘early’ or

‘late’.

56

May or may not come with each and every uterine contraction.

The decelerations usually vary in degree of fall of FHR and also in duration.

However, these deceleration have not been found to be related to the intensity

of uterine contractions.

Degree of Variable Deceleration

Mild: Drop up to 80 bpm level.

Moderate: Drop upto 70 bpm level.

Severe: Drop to lower than 70 bpm level.

Causes of variable deceleration

1. Cord Compression: The main cause is due to disturbance in blood flow through

the umbilical cord due to its compression of varying degrees.

The course of vascular events in variable deceleration has been described by Steer

(1986) as follows:

57

Milder degree of cord compression

Only the venous flow is obstructed which leads to decrease venous return to

fetal heart – a situation which is compensated by tachycardia in order to maintain

blood pressure.

Severe degree of cord compression:

In the later stages, arterial blood flow is also obstructed leading to increased

peripheral resistance and rise of blood pressure.

Rise of blood pressure activates aortic stretch receptor, which in turn leads to

activation of vagal centre to produce bradycardia.

Once cord compression is over, reactive tachycardia occurs. Thus, a typical M

shaped heave is formed acceleration before and acceleration after a deep deceleration.

2. Rapid descent of head through birth canal.

3. Fetal head compression in normal second stage of labor

In last two conditions, Fetal heart variability in between episodes of

decelerations remains quite normal ( Ingemarsson et al 1993).

Predisposing Factors

Both Short Cord (Less than 35 cm) and long cord (more than 80cm) have

been found to be associated with higher incidence of variable deceleration

(Ingemarsson et al 1993).

Oligohydramnios .

Deficiency of Wharton’s Jelly as in IUGR ( Ingemarsson et al 1993).

Breech presentation.

Occipital-posterior position.

58

Face position.

Prognosis of Variable Deceleration

Frequency of deceleration: Risk of hypoxia is high if decelerations come in

quick succession.

Duration of deceleration: Longer the deceleration higher is the risk of hypoxia.

Shape of deceleration: ‘V’ shaped dips are of short duration and carries almost

no risk. But ‘U’ shaped dips which are long duration dips carry higher risk of

hypoxia.

Presence of initial acceleration: Is a reassuring sign.

Rebound tachycardia: If after the end of each deceleration the baseline settles

at a higher level, it should be considered as a sign of approaching hypoxia.

FHR pattern in between episodes of variable deceleration. Baseline

tachycardia and absence of baseline variability are considered ominous.

Mixed pattern: If variable deceleration shows an element of late deceleration

specially with ‘U’ shaped bottom – it should be taken as a sign of hypoxia.

Management

Positioning of the patient – Patient should be immediately turned to her left

side – if that does not work – even the knee chest position may be tried.

Oxygen inhalation.

Continous monitoring and analysis of tracing.

Amnioinfusion.

Fetal Blood Sampling: In moderate degree of variable deceleration, it is done

only specially where normal delivery is not likely to occur soon to see whether

more time can be allowed or not.

59

Severe cases should be delivered immediately.

Combined Deceleration

Definition: When tracing shows more than one type of deceleration.

It can be of two types:

Early + Late Deceleration

Variable + Late deceleration

Shape: There is no typical shape.

Cause: Ingemarsson et al (1993) found highest association of this type of tracing with

oxytocin over stimulation. However it can also happen with spontaneous labour.

Significance: It is same as late deceleration i.e., indicates fetal hypoxic state.

Management: Stop Oxytocin drip.

Rest of the management is same as late deceleration.

Tracing Character Sequence and Degree of Hypoxia

Normal Trace

Early Hypoxia -Disappearance of acceleration with FM

-Disappearance of acceleration with uterine contraction

Further Hypoxia -Rising baseline FHR – Baseline tachycardia

Further Hypoxia -Reduction in baseline variability to less than 5 bpm i.e, almost

straight line CTG.

Further Hypoxia -Late deceleration with Braxton-Hicks contraction or labour

contraction ( Arulkumaran, 1992, Debdas, 1993).

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Abnormal FHR Tracing – Acidosis Interval

Fleischer et al (1982), demonstrated that with an averagely grown fetus at

term with clear amniotic fluid, 50% of foetuses took the following time duration to

become acidotic after an abnormal or suspicious trace-

With repeated late deceleration – 115 min (2 hours).

With repeated variable deceleration – 145 min (2 1/2 hours).

With flat trace (baseline variability – 185 min (3 hours) of less than 5 bpm).

Fetal Sleep, Rest, Activity

Four levels of fetal activity has been recognized in third trimester specially in

last four intra-uterine weeks (Ingemarsson et al 1993) comprising of two sleep like

levels (Steer, 1986) and two levels of wakefulness. They are as follows:

1. Deep Sleep State: This is like sleep ‘without rapid eye movement’ (REM) as

can be observed in a neonate. In this fetal state, mother does not feel any fetal

movement. This period shows very low baseline variability (around 5 bpm

even less) and no FH acceleration.

2. Light Sleep – Like State: This sleep is comparable to neonatal REM sleep. In

this sleep, state mother may feel only rare occasion fetal movement. This

period shows normal baseline variability but rare fetal movement acceleration.

3. Quiet Awake State: S the term implies, this state is comparable with neonatal

quiet awake state. In this period there will be normal baseline variability and at

least two fetal movement acceleration in twenty minutes.

4. Active Awake State: This is usually seen at the end of deep sleep or after

stimulation. This period shows good acceleration with fetal movements.

This cycle of sleep and wakefulness continues even during labour.

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How to exclude Fetal Sleep

In a case where the baseline variability ‘ of less than 5 bpm’ has lasted for

more than 20 minutes (assumed fetal sleep) the following should be done:

A. The clinical situation of the case should be critically reviewed to exclude the

following:

Any factor which could cause fetal hypoxia e.g: IUGR, Oligohydramnios

etc.

Any possibility of fetal CNS malformation.

Any sedation given to mother and for a case in labour.

Whether the liquor is meconium stained or not.

B. Then the patient may be given an acoustic stimulation and fetal heart rate and

fetal movement response observed or alternatively the monitoring session may

extended up to 50-90 minutes to see whether and when the active cycle returns

(Debdas AK).

62

INSTRUMENTATION AND TECHNIQUE

While using electronic fetal monitoring to interpret the fetal monitor tracings,

it is necessary to understand the process involved in acquisition and proceeding of

fetal heart rate and uterine activity data.

This basically works using the ultrasound Doppler principle

a) Ultrasonic signals will penetrate human tissues.

b) When the ultrasonic beam encounters an interface with increased density to

the transmission of the signal will be reflected at 90 degrees angle to the

surface and a portion will be transmitted to the next interface.

c) The reflected signal will undergo a frequency change (Doppler Shift) as the

reflecting interface is moving.

The frequency will increase if the reflecting interface is moving towards the

signal source and will decrease if the reflecting interface is moving away

from the signal source.

The instrument used for recording NST is called cardiotocogram.

Cardiotocogram

It essentially consists of a central unit with attatchments. A central unit

processes the signals from the sensors and prints them in the form of a trace.

Fetograph – Teksonic Fetal Monitor

The teksonic fetal monitor is a complete monitoring system used for

antepartum as well as intrapartum fetal monitoring. It is used during the antepartum

period for Non-stress test using ultrasound and external toco facilities. In addition to

plotting a graph of uterine activity against Fetal heart rate with special event marker

63

(which is patient operated hand held switch) for maternally sensed fetal movements, it

has facility of data logging. It logs all the data in real time like date, time, patiemt

identification no, FHR, uterine activity, maternally sensed fetal movements etc.

Depending on where the sensors are placed, these monitors are of two kinds:

1. External monitors: Have sensors placed on the surface of the maternal

abdomen.

2. Internal monitors: Sensors are placed by the vaginal route.

External monitors are used for antepartum assessment and during early labour.

Internal monitors are used during labour after rupture of the membranes.

Following is a list of various features of a standard NST machine under broad

headings:

1. Machine on/off switch.

2. Features concerned with fetal heart rate monitoring

a. Socket for ultrasonic FH transducer plug.

b. Digital display of FHR.

c. Flashing light display of FHR.

d. FHR signal quality display window.

e. FHS audio volume control knob.

f. FHR abnormality alarm bell/ light.

g. Socket for direct fetal ECG.

h. FHR tracing on/off switch.

3. Features concerned with uterine contraction monitoring

a. Socket for toco transducer.

b. Toco baseline setter knob or zeroing knob.

64

c. Toco amplitude.

d. Toco tracing on/off switch.

4. Switches for the records (paper drive).

5. Switches for annotation including Event Marker Button.

6. LCD display facility.

7. Memory.

8. Home/ Distance monitoring.

9. CTG tracing paper.

10. Arrangement for alarm.

Printer (Epson LX – 300)

It plots a graph of FHR together with uterine activity (UA) on two separate

scales. FHR and UA are depicted on the vertical axis with time on the horizontal axis.

The fetal movement perceived by the mother are printed in the middle of UA and

FHR scale on the graph.

Paper speed is the distance ( in cm ) the chart paper advances in a certain

period of time. The speed employed is 3cm/min.

Paper size – 8’ to 12’’

FHR range 60 – 220 bpm, 20 bpm/ Div.

Time – 60 sec/Div.

Paper single sheet ( manual insertion )

The tocotransducer

This is a process gauge that picks up the uterine activity and is fixed onthe

maternal abdomen at the level of fundus of the uterus. The change in the shape and

hardness of the uterus with contraction depresses a plunger on the tocotransducer,

65

which moves a slight distance and causes a change in voltage of small electric current

that is passing through. These voltage changes are proportional to the uterine activity

and are represented quantitatively by the fetal monitor as contractions.

Aquasonic gel

Ultrasound waves travel very poorly through air and extremely easily through

liquids. Gel is applied to eliminate air between transducer and mother’s abdomen.

Abdominal belt

Two types of belt: Disposable belt and Reusable belt (good).

Methods

Patient preparation

At first counselling of the patient is done regarding the procedure.

Detailed history is taken and through clinical examination done.

Bladder should be emptied.

The test is done after patient had taken a proper meal.

Position of the patient

The patient is laid on bed in 15 degree left lateral tilt, which can be achieved

by placing a pillow underneath the right hip. The objective is to displace the uterus

from the inferior vene cava minimizing aortocaval compression.

Procedure

The ultrasound (fetal heart rate) transducer is belted on the lower abdomen at

a site from where the FHS is most distinctly audible after applying an aquasonic jelly.

The Toco transducer is belted on the upper abdomen over the uterine fundus so that it

can easily detect the anterior deflection of the uterus that occurs during a contraction.

66

The belts should fit snugly and comfortable. The event marker is held by the patient

and she is instructed to press the button with each fetal movement.

Non stress test

This test was performed in patients, admitted to wards or labour room for a

period of 20 minutes.

If a reassuring test failed to occur within this 20 minutes, extended upto 40

minutes for non reactive traces.

The NSTs were classified into 3 groups based on the presence or absence of

atleast 2 FHR accelerations of 15 bpm lasting for 15 seconds in a 20 minutes

reading into

o Reactive or normal test or reassuring test.

o Non reactive or abnormal test or non reassuring test.

o Suspicious or Equivocal test.

Points considered in reading a graph

a) Baseline fetal heart rate.

b) Beat to beat variability.

c) Qualifying acceleration.

d) Any deceleration if present.

The following definitions were followed in this study:

Definition of a reassuring NST

[American College of Obstetricians and Gynaecologists (1999)]

i. Two or more accelerations that peak at 15 bpm or more, each lasting for 15

seconds or more, and all occurring within 20 minutes of beginning the test.

67

ii. It was also recommended that acceleration with or without fetal movement can

be accepted, and that a 40 minute or longer tracing ( to account for fetal sleep)

should be performed before concluding that there was insufficient reactivity.

Definition of a non-reassuring NST

At the end of 40 minutes if there are:

i. No qualifying accelerations.

ii. Baseline variability less than 5 bpm.

iii. Late decelerations with spontaneous uterine contractions.

iv. Variable decelerations, repetitive and lasting for more than 30 seconds.

The patients were then followed up for the mode of delivery and the different

variables of the perinatal outcome. At the time of delivery following data variables

were collected like perinatal mortality, fetal distress during labour, 5 min Apgar score

of >7, meconium stained amniotic fluid (MSAF),decreased liquor and the cord factor.

The end points used to judge the perinatal outcome includes the following

1. Perinatal death defined as the death of a fetus whose birth weight was 500

grams or more/ whose gestational age at death was 28 weeks or more within

the first 28 days of life.

2. Fetal distress during labour – defined as an abnormal FHR (FHR < 100 OR >

160) irregular FHR, post contraction bradycardia FHR takes > 30 seconds to

come back to normal.

3. 5 minutes Apgar score of <7 – judged by an independent observer – a

Pediatrician. A 5 min Apgar score of < 7 was considered as abnormal.

68

4. Meconium stained amniotic fluid (MSAF) – The colour of liquor during the

labour was looked for and meconium staining of the liquor was noted.

5. Decreased liquor quantity – the reduction in the amount of liquor appropriate

for gestational age as noted by routine antenatal ultrasound examination and /

or observed clinically during delivery.

6. Cord factor – Any nuchal cords or cord presentations or abnormalities were

noted.

69

Persistent nonreassuring decelerations with normal FHR variability and

absence of tachycardia usually indicate no fetal acidosis.

Persistent late decelerations or severe variable decelerations associated with

absence of variability are nonreassuring and generally require prompt intervention

unless they spontaneously resolve or can be corrected rapidly with conservative

measures (oxygen, hydration, maternal repositioning).

In the presence of nonreassuring decelerations, a fetal scalp electrode should

be placed. In cases of suspected or confirmed fetal compromise, delivery should be

accomplished as soon as possible, accounting for the severity of the FHR abnormality

and relevant maternal factors. The accepted standard has been that ideally this should

be accomplished within 30 minutes.

Measures that improve fetal oxygenation and placental perfusion

• In the supine position, the vene cava and aortoiliac vessels are compressed by

the gravid uterus. This results in reduced return of blood to the

70

METHODOLOGY

This clinical study will be conducted at KVG Medical College and Hospital, on

patients attending outpatient department or admitted as in patient in department of

Obstetrics and Gynaecology over a period of 1.5 years from November 2016 - April

2018.

50 High Risk pregnant women (study group-selected based on inclusion and

exclusion criteria) and 50 Low Risk pregnant women (control group) will be

randomly enrolled into study and were evaluated by NST from 32 weeks of gestation

onwards or whenever risk factor was identified and repeated at appropriate

intervals as per subjective results in cases of high risk group.

Inclusion criteria:

1. Patients of all age groups who give written informed consent.

2. Singleton, non-anomalous pregnancies of 32 weeks or more weeks of gestation.

3. Patients with clinically suspected or diagnosed cases of IUGR or Pre eclampsia or

chronic hypertension or diabetes mellitus or previous fetal demise or decreased

fetal movements or severe anemia or third trimester bleeding or post-dated

pregnancy or Rh isoimmunization or PROM or advanced maternal age (>35 yrs)

are included in the study

Exclusion Criteria:

1) Sedative usage in the mother 24 hours before testing

2) Gestational age of < 32 weeks.

3) Multiple gestation.

4) Malpresentations, cephalo pelvic disproportion and patients with previous LSCS.

5) Major congenital anomaly of the fetus detected by routine antenatal ultrasound

scanning.

71

Procedure of study:

For all the pregnant ladies above 32 weeks of gestation detailed history

and examination will be done. Informed consent will be taken.

Women with high risk pregnancies will be randomly enrolled into study and will

be followed up with NST (non-stress test) from 32 weeks of gestation onwards and

repeated at appropriate intervals. 50 high risk patients (study group) and 50 low risk

patients (control group) will be studied.

72

OBSERVATION AND RESULTS

Table No. 1: Showing Distribution of the patients in different age group

Age group No. of Patients Percentage

18 -20 7 7.0

21 - 25 32 32.0

26 - 30 43 43.0

31 - 35 16 16.0

>35 2 2.0

Total 100 100.0

Fig. 1: Showing Distribution of the patients in different age group

18 -20

7%

21 - 25

32%

26 - 30

43%

31 - 35

16%

>35

2%

AGE DISTRIBUTION

18 -20 21 - 25 26 - 30 31 - 35 >35

73

Table no. 2: Age wise comparison between Low risk & High risk

group Total

Low risk High risk

18 -20 No. of subjects 3 4 7

% 6.0% 8.0% 7.0%

21 - 25 No. of subjects 17 15 32

% 34.0% 30.0% 32.0%

26 - 30 No. of subjects 23 20 43

% 46.0% 40.0% 43.0%

31 - 35 No. of subjects 6 10 16

% 12.0% 20.0% 16.0%

>35 No. of subjects 1 1 2

% 2.0% 2.0% 2.0%

Total No. of subjects 50 50 100

% 100.0% 100.0% 100.0%

In the low risk group most of them were in 21- 25 and 26 -30 with 34% and 46%

respectively. But in the high risk also same proportion of the subjects were in the age

group of 21-25 and 26 -30 having 30% & 40% respectively.

Fig. 2: Age wise comparison between Low risk & High risk

0

5

10

15

20

25

18 -20 21 - 25 26 - 30 31 - 35 >35

3

17

23

6

1

4

15

20

10

1

Nu

mb

er o

f s

ub

ject

s

Agewise comparison

Low risk High risk

74

Table no. 3: Mean age for high risk and low risk groups

Group N Mean Std. Deviation t

Age

Low risk 50 26.360 3.927 .870

High risk 50 27.080 4.337 p=0.386

Mean age n the low risk group was 26.36 and that of High risk group was 27.08.

The difference was not significant (p=0.386).

Fig. 3: Mean age wise distribution of study participants in high and low risk groups

26

26.2

26.4

26.6

26.8

27

27.2

Low risk High risk

26.36

27.08Mean Age

75

Table no. 4: Showing distribution of the patients with their gravid state

Fig. 4: Showing distribution of the patients with their gravid state

Among 100 cases, 57 were primigravida, 43 were multigravida. The maximum

number of cases were primigravida.

Primi

57%

Multi

43%

GRAVIDA

Primi Multi

Gravid state No. of Patients Percentage

Primigravida 57 57%

Multigravida 43 43%

Total 100 100%

76

Table no. 5: Showing gravida wise comparison between Low risk & High risk

group Total

Low risk High risk

gravida

Primi Number 30 27 57

% 60.0% 54.0% 57.0%

Multi Number 20 23 43

% 40.0% 46.0% 43.0%

Total Number 50 50 100

% 100.0% 100.0% 100.0%

Fig. 5: Showing gravida wise comparison between Low risk & High risk

60% of the Low risk groups were seen in Primi gravida whereas 54% of high risk

were on the same . Multi gravida were more in high risk groups 46% compare to low risk

groups 40%. The assocaiton between the groups with the gravid is not significant

(p=0.545)

0

5

10

15

20

25

30

Low risk High risk

30

27

20

23

Nu

mb

er o

f su

bje

cts

GRAVIDA WISE COMPARISON

Primi Multi

77

Table no 6: Distribution of study participants with High Risk cases

High Risk Case Frequency Percentage

Premature Rupture of Membranes(PROM) 14 28

Pregnancy Induced Hyprtention(PIH) 06 12

Gestational Diabetes Mellitus(GDM) 05 10

Oligohydramnios 13 26

Rh Negative 05 10

Severe Anemia 02 4

Intra Uterine Growth Retardation(IUGR) 03 6

Antepartum Haemorrhage(APH) 01 2

GDM with Cardiomyopathy 01 2

Total 50 100

Table 6 shows that 28% of the study participants had premature rupture of

membranes. About 26% were having oligohydrioamnios, 12% were PIH. GDM was

observed in 10% of the study participants while Rh negative was seen in 10% of study

participants. Intra Uterine Growth Retardation was seen in 6%, Severe Anemia in 4% of

them. Antepartum haemorrhage was seen in 2% of study participants.

Fig. 6: Distribution of study participants with High risk cases.

2812 10

2610 4 6 2 2

100High Risk Cases

78

Table no. 7: Distribution of Patients based on NST results

group Total

Low risk High risk

Reactive Number 38 33 71

% 76.0% 66.0% 71.0%

Non reactive Number 12 17 29

% 24.0% 34.0% 29.0%


% 100.0% 100.0% 100.0%

Fig. 7: Distribution of Patients based on NST results

NST results shows that in low risk group 76% were reactive and 24% was non

reactive. In high risk group it was 66% in Reactive and 34% non reactive.

0

5

10

15

20

25

30

35

40

Low risk High risk

38

33

12

17

Nu

mb

er o

f su

bje

cts

NST RESULTS

Reactive Non reactive

79

Table no. 8: Comparison of Mean Gestational age with the two groups

Group N Mean Std. Deviation t 95% Confidence Interval

Lower Upper

Low risk 50 38.062

1.796

7.372

-3.492

-2.011

High risk 50 35.310 1.935

p<0.001

vhs

Fig. 8: Comparison of Mean Gestational age with the two groups

Mean gestational age was seen in the low risk group was 35.31 where as in high

risk group it was 38.062 and the difference was found to be very highly significant.

35.31

38.062

0

5

10

15

20

25

30

35

40

high Rish Low risk

80

Table no. 9: Distribution of cases in low risk and high risk groups based on mode of

delivery

group Total

Low risk High risk

Normal Number 37 25 62

% 74.0% 50.0% 62.0%

LSCS Number 13 25 38

% 26.0% 50.0% 38.0%


% 100.0% 100.0% 100.0%

Fig. 9: Distribution of cases in low risk and high risk groups based on mode of

delivery

Most of the subjects were normal in low risk group (74%) whereas in high risk

group 50 % were normal and 50% were under LSCS. The association between mode of

delivery and the type of the risk is statistically significant (p=0.013)

0

5

10

15

20

25

30

35

40

Low risk High risk

37

25

13

25

Nu

mb

er

of

sub

ject

s

MODE OF DELIVERY

Normal LSCS

81

Table no. 10: Distribution of cases in low risk and high risk groups based on

induction of labour

Group Total

Low risk High risk

Induction

Induced Number 12 16 28

% 24.0% 32.0% 28.0%

Non

induced

Number 38 34 72

% 76.0% 68.0% 72.0%


% 100.0% 100.0% 100.0%

Fig. 10: Distribution of cases in low risk and high risk groups based on induction of

labour

0

5

10

15

20

25

30

35

40

Low risk High risk

12

16

38

34

Nu

mb

er o

f su

bje

cts

INDUCTION

Induced Non induced

82

Table no. 11: Distribution of cases in low risk and high risk groups based on mode

of delivery and NST result

Mode of Delivery Low Risk group High Risk group

R (%)

( n=38 )

NR (%)

(n=12)

R (%)

(n=33)

NR (%)

(n=17)

Vaginal 31(81.6%) 6(50%) 19 (57.6%) 6(35.3%)

LSCS 7 (18.4%) 6(50%) 14(42.4%) 11(64.7%)

Fig. 11: Distribution of cases in low risk and high risk groups based on mode of

delivery and NST result

In low risk group, 18.4% cases of reactive NST underwent LSCS and 50% of

cases with non reactive NST underwent LSCS.

In high risk group, 42.4% of cases with reactive NST underwent LSCS where

as 64.7% of cases with non reactive NST underwent LSCS.

81.6

50

57.6

35.3

18.4

50

42.4

64.7

0

10

20

30

40

50

60

70

80

90

R NR R NR

Low Risk group High Risk group

Vaginal LSCS

83

Table no. 12: Distribution of cases in low risk and high risk groups who underwent

LSCS based on NST results

NST Result

Low Risk group (%)

( n= 13)

High Risk group (%)

( n= 25)

NR 6 (46.1) 11 (44)

R 7 (53.8) 14 (56)

Fig. 12: Distribution of cases in low risk and high risk groups who underwent LSCS

based on NST results

In low risk group, out of 13 cases who underwent LSCS, 46.1% of them had non

reactive NST and 53.8% of them had reactive NST.

In high risk group, out of 25 cases who underwent LSCS, 44% of them had non

reactive NST and 56% of them had reactive NST.

0

10

20

30

40

50

60

70

80

90

100

Non Reactive Reactive Total

46.1

53.8

100

44

56

100

Low Risk

High Risk

NST & Risk Group

84

Table no 13: Distribution of cases in low risk and high risk groups based on Intra

Partum Fetal Distress (IPFD)

IPFD

Low Risk group

(%)

High Risk group

(%)

Total

Present 3 (6%) 5 (10%) 8

Absent 47 (94%) 45 (90%) 92

Total 50 (100%) 50 (100%) 100 (100%)

Fig. 13: Distribution of cases in low risk and high risk groups based on IPFD

In low risk group 6% of cases found to have FD and among high risk group 10%

of cases had FD.

0

5

10

15

20

25

30

35

40

45

50

Low risk High risk

3 5

47 45

Nu

mb

er o

f su

bje

cts

FD

Absent Presemt

85

Table no 14: Distribution of cases who underwent cesarean section in low risk

and high risk group for IPFD

IPFD LR –NST Result HR – NST Result

R (n= 38) NR (n=12) Total R (n=33) NR(n=17) Total

Present 2 (5.26) 1(8.3) 3 2 (6) 3 (17.6) 5

Absent 36(94.7) 11(91.6) 47 31(93.9) 14 (82.3) 45

Total 38(100) 12(100) 50 (100) 33(100) 17(100) 50 (100)

In low risk group 8.3% of cases with non reactive NST developed IPFD when

compared to 5.26% of cases with reactive NST who had IPFD for which they underwent

LSCS.

In high risk group 17.6% of cases with non reactive NST developed IPFD when

compared to 6% of cases with reactive NST who had IPFD for which they underwent

LSCS

86

Table no 15: Comparison of mean birth weight between two groups

Group N mean birth

weight

SD t value P value

Low Risk 50 2.948 .474 2.274 0.025

High Risk 50 2.696 .622

Fig. 14: Comparison of mean birth weight between two groups

The mean birth weight of the subjects in low risk group is 2.948 whereas that of

high risk group is less 2.696. The difference between the mean birth weights between the

groups was significant.

0

0.5

1

1.5

2

2.5

3

Low risk High risk

2.948

2.696

Mea

n v

alu

e

BIRTH WEIGHT

87

Table no. 16: Comparison of Meconium Stained Amniotic Fluid (MSAF) between

two groups

MSAF Group Total

Low risk High risk

Present Count 6 9 15

% 12.0% 18.0% 15.0%

Absent Count 44 41 85

% 88.0% 82.0% 85.0%

Total Count 50 50 100

% 100.0% 100.0% 100.0%

Fig. 15: Comparison of MSAF between two groups

Meconium stained amniotic fluid was present in 12% of low risk group and 18%

in High risk group.

0

5

10

15

20

25

30

35

40

45

50

Low risk High risk

69

4441

Nu

mb

er o

f su

bje

cts

MECONIUM

Absent Presemt

88

Table no 17: Distribution of patients in low risk and high risk groups based on

MSAF and NST results

Group MSAF NST Results Total


Low risk

Present Count 4 2 6

% 10.5% 16.7% 12.0%


% 89.5% 83.3% 88.0%


% 100.0% 100.0% 100.0%

High risk

Present Count 4 5 9

% 12.1% 29.4% 18.0%


% 87.9% 70.6% 82.0%


% 100.0% 100.0% 100.0%

Meconium was seen in 10.5% of the reactive group of low risk whereas it is

present in 12.1% at high risk group. But in non reactive, 16.7% in the low risk and

29.4% in the high risk group But the association between Meconium with NST results

were not significant.in both low risk and high risk groups.

Table no. 18: Comparison of APGAR scores among both groups

Low risk High risk Low Risk High Risk

6.00

Count 0 2 0 0

% 0.0% 4.0% 0% 0%

7.00

Count 34 19 11 13

% 68.0% 38.0% 22.0% 26%

8.00

Count 16 29 17 13

% 32.0% 58.0% 34.0% 26%

9.00

Count 50 50 22 24

% 100.0% 100.0% 44.0% 48%

50(100%) 50(100%) 50(100%) 50(100%)

89

Table no 19: Distribution of cases who had NICU admission in low risk and high

risk group based on NST results

Group NST Results N Mean SD t

Low risk

Reactive 38 2.579 1.368 1.484

Non reactive 12 3.250 1.357 p-=0.144 ns

Highrisk

Reactive 33 4.667 1.339 2.604

Non reactive 17 5.882 1.933 p=0.012 sig

Fig. 16: Distribution of cases who had NICU admission in low risk and high risk

group based on NST results

The mean NICU admission in reactive of low risk is 2.579 and that of non

reactive is 3.25 and the difference between these two is found to be snon significant. But

in High risk group the NICU admission days in reactive group is 4.67 and that of non

reactive is 5.882 and that difference was found to be significant (p=0.012)

0

1

2

3

4

5

6

Low risk High risk

2.579

4.667

3.25

5.882

Me

an v

alu

e

NICU ADMISSION


90

Table no. 20: Comparison of Perinatal Mortality in low risk and high risk group

group Total

Low risk High risk

Perinatal

Mortality

Yes

Count 1 5 6

% 2.0% 10.0% 6.0%

No

Count 49 45 94

% 98.0% 90.0% 94.0%

Total

Count 50 50 100

% 100.0% 100.0% 100.0%

A total of 6 perinatal mortality was seen in the study in which 1(2%) was in low

risk group and 5(10%) were in high risk group.

Fig. 17: Comparison of Perinatal Mortality in low risk and high risk group

0

10

20

30

40

50

60

70

80

90

100

Low Rsik High Risk

210

98

90

Yes

No

91

Table no. 21: Predictive accuracy of NST for perinatal mortality

Perinatal Mortality Rate

Low risk (%) High risk(%) P value

Sensitivity 100 80 <0.001

Specificity 77.6 71.1 0.425

Poistive predictive value 8.3 23.5 0.002

Negative Predictive value 100 96.9 0.645

Accuracy rate 78 72 0.086

Fig. 18: Predictive accuracy of NST for perinatal mortality

The predictive accuracy of NST with regard to perinatal mortality rate was seen.

In the Low risk there is 100 % sensitivity and 77.6% specificity was seen. Whereas in

High risk group the sensitivity was 80% and specificity was 71.1%. The accuracy rate at

high risk is 72% whereas in Low risk it was 78%.

0

10

20

30

40

50

60

70

80

90

100

Sensitivity Specificity Poistive

predictive

value

Negative

Predictive

value

Accuracy rate

100

77.6

8.3

100

7880

71.1

23.5

96.9

72

Per

cen

tag

e

Perinatal mortality rate with NST results

Low risk High risk

92

DISCUSSION

Among the various antenatal surveillance modalities used for high risk

pregnancies such as NST, CST, BPP, modified BPP, Doppler Velocimetry etc., NST

is one of the easiest test to perform and cost effective. There are considerable number

of clinical literatures that support the use of NST in the management of high risk

pregnancies.

The present study conducted in the Dept. of Obstetrics and Gynaecology, at

KVG Medical College and Hospital, Sullia from November 2016 to April 2018.

In the present study, observation correlate shows that the maximum number

of patients ( 43%) were from the age group 26 - 30 , followed by 32% from the age

group 21- 25.

In the present study, among low risk group 76% had reactive NST and 24%

had non reactive NST. Among high risk group 66% had reactive NST and 34% had

non reactive NST, which is similar to study by Nochimson D J et al.

In a study conducted by Himabindu P and Tripura Sundari M et al (2015) ,

70% had reactive NST and 30% had non reactive NST . The results are comparable

with our study.66

Further evaluation of non-reactive NST:

Some studies suggest that a reactive test encouraged continuation of

pregnancy. On the other hand, Lenstrup C and Hasse N concluded that a pathological

NST was not an indication for immediate delivery but it was rather an indication for

closed observation and should be considered in conjuction with the other clinical data

of the particular pregnancy.67

93

Evaluation of NST predictability has classically been based on the single last

test usually within 7 days prior to delivery. The concept of serial comparison of test

results was applied by Devoe et al in a series of 148 patients who had atleast 4 NSTs

prior to delivery, percentage acceleration time (PAT) was calculated and the fetus was

used as its own control in sequential NSTs. Test sensitivity improved from 30% to

75% using PAT, compared to conventional NST interpretation while the specificity

was 100%, PPV 100% and NPV 96.2%.65

Grace LM et al and Gelman SR et al have repeated non-reactive NST within

24 hours after glucose drink or meal and have found an inconsistent effect on NST

reactivity while Keegan K A et al have suggested eliminating the possibility of drug

ingestion.68

Richardson B et al found an inconsistent effect of external physical

stimulation like suprapubic and fundal pressure on fetal heart rate while Lenovo KJ et

al immediately extended the NST recording to 80 minutes to improve the reactivity of

NST.69

LSCS Rates:

In our study , 71 patients having reactive NST 29.5 % underwent caesarean

section , while out of 29 patients having non reactive NST , 58.6% had caesarean

section. This shows that a significant number of patients underwent caesarean section

when NST is non reactive.

In the study done by Patel S et al LSCS rate was 14.84% in Reactive group

and 66.66% in Non reactive group.70 It was similar to the study done by Verma A,

Bhide AA where Reactive NST had less intervention.71,72

94

Phelan J.P. et al studied 3000 NST s done on 1452 high risk patients and

observed that 14% tests were NR and in these women, there was a significant increase

in LSCS rate, the rate of LSCS for fetal distress and the perinatal mortality rate.73

Operative delivery was more common in non reactive NST in the study done

by Hafizur R74 and Ingemarsson I.75

In our study, the rate of LSCS for fetal distress in high risk group was quite

high, it was 17.6% in non-reactive group and 6% in reactive group with 71.1%

specificity, while Kidd et al in their study found LSCS rate to be 29% in their series of

77 patients. Bhinde A et al studied non-reactive NST in 143 cases and found that the

false positive rates for LSCS to be as high as 74.36%.

Study group

Incidence of fetal distress

Reactive Non Reactive

Ingemarsson (1986) 0.9% 50%

Aparna Hegde (2001)80 3.6% 75%

Present study 6% 17.6%

In our study, among low risk group MSAF was seen in 10.5% of the reactive

cases and 16.7% of non reactive cases. Among high risk group, MSAF was seen in

12.1% of reactive cases and 29.4% of non reactive cases.

In the study done by Patel S et al 7.7% of reactive NST and 44.4% of

nonreactive NST had meconium stained liquor.70 This was also similar to the study

done by Lohana et al.76

95

In our study, incidence of NICU admission is higher in non reactive group as

compared to babies of reactive group. Similar findings were noted in the study

conducted by Kamal Buckshee et al (1999).77

Perinatal mortality

Abhijit Biswas

et al77

Himabindu

P et al

Devangi

Munshi et al78

Present

study

Sensitivity 72.7% 82.3% 71.4% 80%

Specificity 72.7% 80.7% 67.7% 71.1%

Positive Predictive Value 30.7% 46.6% 60% 23.5%

Negative Predictive Valuev 94.1% 95.7% 70% 96.9%

In our study, perinatal mortality occurred among 5 cases in high risk group

and 1 case in low risk group. Hence the sensitivity of NST in low risk group was

100% in predicting perinatal mortality while the sensitivity in high risk group was

80%. The specificity and NPV of NST in high risk group for perinatal mortality in our

study are 71.1% and 96.9% respectively while in low risk group it is as high as 77.6%

and 100% respectively. On the other hand, the sensitivity and PPV is found to be 80%

and 23.5% respectively in high risk group and 100% and 8.3% in low risk group. This

shows that a reactive test is an excellent indicator of a healthy fetus especially in the

low risk group.

NST associated with other surveillance modalities

Nochimson DJ et al concluded that additional discriminatory evaluation was

required for non-reactive NST. For this purpose, the CST was used but it appeared

that a more discriminatory test which will better indicate the loss of fetal well being

96

may be required. The need for a better test is based on the reports indicating a false

positive rate of CST which was approximately 25%.37 Devoe LD et al have reported

on the use of NST, amniotic fluid assessment and umbilical artery Doppler

velocimetry in 1000 high risk patients.50

Each had specificity of > 90% and sensitivities ranged from 69 % (NST) to

21% (Doppler velocimetry). Negative predictive value of each method exceeded 85%.

Amniotic fluid measurements or Doppler velocimetry compared with NST, appeared

to be less powerful screening test when used alone.

Miller DA et al used the modified BPP in which NST serves as an

immediate indicator of fetal well being and AFI reflects the long term adequacy of

placental function. The false negative rate of the modified BPP is lower than that of

NST and compares favourably with false negative rates of CST and complete BPP.79

Schifrin BS38 et al and Kubli F54 et al have demonstrated good results with the

use of NST in screening low risk pregnancy as shown similarly in our study. In our

study the predictive value of NST for mortality was higher in low risk group

compared to high risk group ( but not statistically significant). But the use of NST for

low risk patients will lead to an even greater number of false positive results because

of lower incidence of abnormality in low risk population, but may increase

inappropriate intervention.

97

CONCLUSION

The antenatal surveillance of high risk pregnancies with NST can

effectively screen for identification of high risk fetuses and segregate the population

that is at risk for perinatal mortality and morbidity.

The potential advantage of NST is that, a decrease in decision to delivery time

can be made for those patients with fetal distress so that a major improvement in the

outcome among parturients can be achieved with abnormal (non-reactive) NST

results.

The use of NST in monitoring high risk pregnancies may result in an increase

in incidence of operative delivery as seen in our study ( 50% LSCS rate in high risk

pregnancies when compared to 26% in low risk pregnancies) and hence, associated

high LSCS rates has to be considered in such pregnancies.

In high risk group there was statistical significance of increased NICU

admission, low apgar score and decreased mean birth weight between the 2 groups

(reactive and non reactive). Though the incidence MSAF, perinatal mortality was not

statistically significant but it appears clinically significance.

NST can be effectively used in both high risk and low risk pregnancies. This is

because a reactive NST result has a high negative predictive value for mortality and

morbidity hence, can reliably identify a healthy fetus. NST effectively identified all

the perinatal mortality cases in low risk group and hence had high sensitivity in low

risk group when compared to high risk group. On the other hand, a non-reactive test

has high false positive rate, hence does not reliably identify a compromised fetus in

both HR and LR groups. Hence an abnormal (non-reactive) NST should alert the

98

clinician to consider the possibility of fetal compromise and has to be followed up by

other biophysical tests.

In conclusion NST is a valuable screening test for detecting fetal compromise in

both HR and LR fetuses that may have poor perinatal outcome. But, larger

randomised controlled trials are needed to know if the use of NST in HR and LR

pregnancies for antenatal surveillance, benefit by reduction in the incidence of

adverse perinatal outcome.

99

SUMMARY

50 high risk and 50 low risk pregnant women were enrolled into a study

conducted between November 2016 to April 2018 at K.V.G. Medical College and

Hopsital ,Sullia, to evaluate the role of NST as a means of antepartum surveillance

and in predicting perinatal outcome. All the pregnancies were followed up by non-

stress tests from 32weeks onwards till the delivery, either done weekly or biweekly

for a period of 20 minutes and for non reactive tests tactile stimulation was done or

test repeated after food. The NST done within 7 days of delivery was used for

correlation with the perinatal outcome. The mode of delivery, perinatal morbidity and

mortality were studied in all the women. The two groups were well matched in age

distribution and parity.

The incidence of non-reactive NST result was 34% in high risk group and

24% in low risk groups. The LSCS rate was higher in HR group (50%) when

compared to LR group (26%).Among low risk group MSAF was seen in 10.5% of the

reactive cases and 16.7% of non reactive cases. Among high risk group, MSAF was

seen in 12.1% of reactive cases and 29.4% of non reactivecases.Incidence of NICU

admission is higher in non reactive group as compared to babies of reactive group.

Perinatal mortality occurred among 5 cases in high risk group and 1 case in

low risk group. Hence the sensitivity of NST in low risk group was 100% in

predicting perinatal mortality while the sensitivity in high risk group was 80%. The

specificity and NPV of NST in high risk group for perinatal mortality in our study are

71.1% and 96.9% respectively while in low risk group it is as high as 77.6% and

100% respectively. On the other hand, the sensitivity and PPV is found to be 80% and

23.5% respectively in high risk group and 100% and 8.3% in low risk group. This

100

shows that a reactive test is an excellent indicator of a healthy fetus especially in the

low risk group.

101

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109

PARTICIPANT’S INFORMED CONSENT FORM

Name of the Institution: KVG Medical College and Hospital

Name of the Principal (Co) Investigator: DR. Devarasetti Anurupa

I ............................................................................... have been told in a language that I understand about the aims, objectives, methods and duration of the study, the benefits, foreseeable risks,

or discomfort resulting from participation has been explained by the investigator. I have been told that

I/he/she have/has the full right to claim for free treatment for research related injury, if any by the

investigator and compensation for disability/death, resulting from such an injury. I have been told that the

study is a research procedure, that my/his/her participation is voluntary, and I/HE/SHE reserve(s) the full

right to withdraw from the study at my/his/her own initiative at any time without penalty, or loss of

benefits, or giving any reason, and that the right to participate or withdraw from the study at any stage

will not prejudice my/his/her rights and welfare. I have also been assured that confidentiality will be

maintained and only be shared for academic purposes. I hereby give consent to participate in the aforesaid study. I am aware that I can withdraw

this consent at any later date if I wish to. This consent form is being signed voluntarily by indicating my agreement to participate in the study, until I decide otherwise. I understand that I will receive a signed and dated copy of this form. If I have any doubts/ questions pertaining to the aforesaid study, I have been asked to contact DR. Devarasetti Anurupa Department of General medicine, KVG Medical College and Hospital, Sullia. Mobile no. 9618133610

Name of the Research Subject/ Guardian:

Signature:

Date:

Place:

Name of the Witness:

Signature:

Date:

Place: I have signed this consent form before my participation in this study.

Signature of the research subject :

Date : Place :

Signature of witness :

Date : Place :

I hereby state that the study procedures in detail were explained to the study subject and

all questions were fully and correctly answered to the above mentioned participants/his/her relatives.

Investigator signature:

Date : Place :

Contact address :

111

PROFORMA

Name : IP NO. :

Age : DOA :

W/o :

Address :

Socioeconomic status:

Chief Complaints :

HOPI :

Obstetrics History : ML - yrs Consanguinous/ Non -consanguinous

Obstetric score. : G P L A

LMP :

EDD :

Period of Gestation :

Previous Menstrual cycles :

Age of menarche-

. Regular/ Irregular, days cycle, days flow, pads/day.

Clots, dysmenorrhea - present/absent

Past h/o Medical / Surgical Illness :

H/o HTN/DM/TB / Asthma/epilepsy /Drug Allergy

H/o previous surgery / blood transfusion

Family History :

Personal History : Diet :

Sleep :

Appetite :

Bowel an Bladder habits :

Addictions :

GPE :

Built : Nourishment :

Pallor : Height :

Icterus : Weight :

Cyanosis :

Clubbing :

Lymphadenopathy:

Edema :

BP : mm Hg

Pulse : bpm

112

LOCAL EXAMINATION :

Thyroid

Breast

Spine

SYSTEMIC EXAMINATION:

CNS :

CVS :

RS :

PA :

Uterus weeks size

Diagnosis :

Investigations:

HB % - gm/dl. RBS - mg/dl

Blood grouping & Rh typing

Urine

HIV -

HbsAg -

VDRL -

Others ( investigations done depending on the type of risk factor )

Ultrasound. :

Gestational age :

Liquor ( AFI ) :

EFW. :

Presentation. :

Congenial anamolies:

Non Stress test.

Date and Time

Position of patient

Duration

Basal heart rate

Beat to beat variability

Accelerations

Deccelerations

Impression - Reactive / Non reactive

In case of NR -NST

Extended recording

Change of position

Repeat NST after food intake

Interpretation :

Decision to terminate pregnancy was based on -

NST alone

NST and other factors

113

Mode of Delivery :

Vaginal - spontaneous, forceps, vaccum

LSCS - Induced

Placenta:

Weight

Infarcts

Retroplacental clots

Baby :

Date of birth and time

Sex

Birth weight

MSAF

Apgar scores at 1 minute and 5 minutes

Any admission to NICU

Perinatal morbidity / mortality

112

KEY TO MASTER CHART

Primi – Primigravida

H – High risk

PROM- Premature rupture of membranes

GDM- Gestational Diabetes Mellitus

Oligo – Oligohydramnios

PIH – Pregnancy Induced Hypertension

IUGR – Intra Uterine growth restriction

Rh neg – Rh negative

APH – Antepartum Hemorrhage

FM – Fetal movements

R – Reactive

NR- Non reactive

FD- Fetal distress

W- weeks

MSAF – Meconium stained amniotic fluid

MOD – Mode of delivery

LSCS- Lower segment caesarean section

ND – Normal delivery

112

113

112

114

112

115

116

ANNEXURES

Monitor

Recording a Trace

117

Reactive NST

Non-Reactive NST

118

Base Line Tachycardia

Base line Variability

119

Early deceleration

Early deceleration


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