INTRODUCTION
•
INTRODUCTION
Death though inevitable has never been accepted as 'Unchallenged'
by medical science, ever since the era of Charak or Hippocrates; the father of
various methods of medicines. Death of foetus in womb or snipping of life at its
budding stage (with in one week of birth) is undoubtedly the most moumful of all
deaths.
"Yet tears to human suffering are due" and mortal hopes defeated
and over thrown are moumed by men and by man alone.
'WORDS WORTH'
We now turn to consider the perinatal mortality (PNM) by which is
meant that mortality rate of the foetus in utero combined with that of the child
during the first week after the birth. The subject PNM is gaining importance in the
field of child health due to the fact that maximum loss of human life occurs in this
period.
"Childhood shows the man,
As morning shows the day".
(John Milton).
PNM serve as a sensitive index of maternal and neonatal care for an
area and also reflects the general health, and other socio-biological factors, of
mother and infant in that area. The term perinatal mortality was first coined by
'Peller' (1948) to mean the mortality in ante, intra and immediate postnatal period, 1.e. period around and including the time of birth. The PNM rate is a hybrid
of two rates, which are not strictly comparable.
The 'still birth rate' is an expression of number of stillbirths per
thousand total births, and 'Neonatal death rate' is derived from the number of
such death per thousand births within first week of life.
The international health organization in 1957 defined perinatal mortality; it is a composite term to include intra utenne deaths of the fetus after 28
week of gestation, and neonatal deaths during the first week of extra uterine life
per thousand viable births.
WHO ( 1976) differentiated perinatal mortality ratio from perinatal
mortality rate, according to it be reserved for those calculation where the denominator is a count of live birth, and the term 'pennata! mortality rate' should be
used when the denominator is count oflive births plus stillbirth (Total birth).
Late foetal death (28 week or more)+ Neonatal deaths
under one week
PNMR = - - - - - - : - : - : c - - - : - - : - - - : - - : - - - - - X 1000
Total live birth + still birth
The international conference for the ninth revision of the international classification of diseases 1975, has recommended a change of definition,
introducing birth weight as criterion instead of gestational age, which is notalways easy to determine. A birth weight of thousand grams is considered to be
achieved at gestational age of 28 weeks.So reYised definition of perinatal
mortality rate be
PNMR =
Late foetal death + deaths under one week & weighing over
1000 grams at birth
X
Total live birth + still birth weighing over I000 grams at birth
!000
Nevertheless, of these death result from the condition before or during birth, they are conveniently combined to give a useful yardstick of obstetric
achievements in regards to the child.
Long term studies by investigators in Europe and USA, have revealed
that PNMR has been falling steadily but not so in less developed countries.
With the decline in infant mortality. to low levels in many developed countries, PNM assumed importance as an index of the efficiency of mother
and child health services.
2
In India accurate figure for PNM are not available because the registration of still births is neither uniform nor accurate, consequently all studies on
PNM, in this country are based on hospital statistics, which shows this rate varies
from 60-150 /I 000 births or more (Park). Besides, because of marked paucity of
autopsy studies, most of the published reports in Indian literatures have been entirely clinical.
PNM continues to be a problem of challenging aspects. Thus inspite
of a sharp fall that has been recorded in well developed countries, it continues to
remain at an alarmingly high level in developing countries like India.
The important causes of PNM are intra uterine anoxia, (which may
be due to trauma and stress oflabour). Toxaemias of pregnancy, antepartum haemorrhage, anaemia with pregnancy, maternal and obstetrical complications, prematurity, pulmonmy lesions, congenital malformations, trauma and infections, merit
particular studies for high PNM figures in developing country like India. The
reason indicates a society, which is largely illiterate and comes from a relatively
low socio-economic strata which is strongly religious and still believes in the
right and wrong thought to them over the generations.
Perinatal death from these causes are almost entirely preventable by
proper effective antenatal care in its widest sense, coupled with good facilities
for delivery and resuscitation of newborn.
Experience has established the fact that efficient antenatal care is
preventive medicine, at its best. However, some conditions such as malformations, unexplained deaths could not have been helped even by the most strict medical supervision and treatment.
The object of all 'perinatal care' is to improve efficiency and to increase maternal well being during pregnancy age to help the foetus to reach the
stage of maturity, so that it may be able to withstand the normal stress and strains
of labour and adopt its self satisfactorily to extra uterine life.
3
Correction of the various defects noticed in the maternal services is
of the paramount importance. lfthe basic principles of medical care are satisfactorily applied, the corrigible omissions are corrected in time greater care is provided to pregnant woman and she herself is encouraged to cooperate more fully,
the efforts will be more rewarding.
4
AIMS AND OBJECTIVES:-
The present study has been proposed with the following aims.
1.
To ascertain the reason for perinatal mortality.
2.
To determine the avoidable and unavoidable factors responsible
for perinatal mortality.
3.
To attempt a reduction in perinatal deaths among the Hill Korwas.
4.
Evaluation of the utilization of the available maternal and child
care services with regard to perinatal mortality.
5.
To know their misconceptions, taboos and practices, care regarding
antenatal, natal and postnatal care and utilization of government
health facilities.
5
HISTORY OF PERINATAL MORTALITY STUDIESThe evidence of first scientific attempt to study the perinatal mortality dates back to 1928 when the national birthday of"trust fund" was founded to
discover the underlying causes of high rates of maternal and perinatal mortality
then prevailing.ln 1946, Dr. J.B.B. Douglas planned out this study in Great
Britain.
The tenn perinatal mortality was first coind by Peller ( 1948) to mean
mm1a!ity in ante, intra and immediately postnatal period, that is the period around
and including the time of birth.
Nixon in 1953 after attending a W.H.O symposium on perinatal mortality introduced pilot investigation program in the city of Morocco on the basis
of his conclusion steering committee of perinatal mortality survey was set up in
1953.
The term of reference to steering committee was "to explore the
possibility of carrying out a survey which may be expected to provide information
of value upon a number of aspects rotating to the safety and health of mother and
infant including the possible effect of place" confinement and with special reference to P.N.M. This work finally reached its culmination in the nation wise P.N.M.
(perinatal mortality) survey which was carried out in 1958.
Problems of cities in India were clearly projected by president's panel
on mental retardation. It pointed out that thousands of women oflow income families give premature birth at two or two and half times the normal rates, that these
women have higher rate of complications and that between Y. to Y:i of the total of
these women deliver, had either no parental or only a last minute attendance.
6
DEFINITION:Statistical analysis of still birth presents several difficulties. First
of all registration is incomplete, secondly, different countries have adopted different cnteria for defining still birth and live births. While in some countries
babies bam with heart beats but failing to breathe have been recorded as still birth,
in others they have been classed under live births.
Intemational standardization of definition of still births and live births
were first attempted by the international statistical of its I 0 15-session. It was
decided that the criteria for determining the presence of life or absence i.e. (still
birth) should be 'any sign of life'.
In 1925 league of nation health committee recommended that criteria should be breathing rather than any sign of life. For statistical purposes, still
birth rate means, the number of viable still birth i.e. still birth after 28 weeks of
gestation per thousand deliveries.
In 1940 United States bureau of census directed that "A foetus showing no evidence oflife after complete i.e. no action of heart, breathing or movements of voluntary muscles, if the 20 weeks of gestation has been reached should
be registered still birth.
In U.K., a still birth has been defined as any child which has been
issued forth from its mother after 28 weeks of pregnancy and which did not at any
time after being completely expelled from its mother, breathe or show any other
sign of life.
In 1950, the W.H.O defined foetal deaths and live births by specifying the perinatal mortality period that is as the period from 28 weeks of pregnancy until the end of the first week of life.
Baired and Thomson (1969) defined the PN.M as the number of
late fetal deaths where in 28 weeks gestation has been completed before delivery
and early neonatal death occurring within the last week of life per thousand live
7
and still birth. W.H.O. ( 1970) statistics defined perinatal mortality as late foetal
and early neonatal death, it covers all still birth and neonatal deaths occurring
during the first week of life per thousand live birth.
Brown (I 973) defined this as the number oflate fetal deaths where
in 28 weeks gestation has been completed before delivery and early neonatal deaths
occurring within the first week of life /I OOOiive and still births. Park ( I 9 7 7),
W.H.O ( 1976) differentiate perinatal mortality ratio from perinatal mortality rate.
According to it the terminology 'perinatal mortality ratio' be reserved for those
calculations where the denominator is a count of live birth, and the tem1 'perinatal
mortality rate' should be used when the denominator is count of live births plus
still births (Total birth);
The international conference for the ninth revision of the international classification of diseases 1975 has recommended a change of the definition introducing birth weight as criterion instead of gestational age which is not
always easy to determine. A birth weight of 1000 g is considered equivalent to
gestational age of 28 weeks.
INCIDENCES :Despite all the advances in well-developed countries, perinatal mortality still continues to be a great problem of challenging proportions in developing countries. It is still at an alarmingly high level in India.
Survey of literature and vital statistics from different parts of the
world reveals that thousands of still births and neonatal deaths occur every year
in every country. However, the statistical data in published reports are not exactly
comparable owing to the lack of uniformity in their definitions and classification
of causes of still birth and neonatal death.
Perinatal mortality reflects on the obstetrical and the neonatal services in the country. In all the developing countries, the perinatal loss is shockingly high.
8
Table- I
PNMR in India (Within 7 days)
Year
Rural
1970
28
20
28
1971
38
23
36
1972
35
22
33
1973
35
22
33
1974
37
24
35
1975
40
33
38
1976
58
27
49
1977
53
23
48
1978
52
47
1980
1986
-
-
1994
49.1
32.7
46
Urban
9
Total
56
48
Table 2
P.N.M. /1000 DELIVERIES IN DIFFERENT PARTS OF INDIA IN DIFFERENT YEAR
S.No.
NAME OF AUTHOR
YEAR
PLACE
P.N.M./1000
DELIVERY
I.
Kher eta!
1964-71
Nagpur
41.5
2.
Vlsaac
1968-72
Veil ore
53.8
3.
Dutta et al
1967-68
Calcutta
54.3
4.
AjitMehta
1975
Bombay
56.3
5.
Manson
1960-61
Madras
60.6
6.
Ghosh
1969-70
Delhi
63.9
7.
Mukherjee et. a!
1948-80
Calcutta
71.2
8.
AjitMehta
1963
Bombay
73.8
9.
Dutta et.al.
1956-58
Calcutta
74.0
I 0.
Dutta et.al
1972-73
Delhi
74.69
II.
Rao
1976
Madras
77.4
12.
Shah et.al.
1969
Palghar
83.5
13.
ParkJ.E.
1977
Sur at
86.0
14.
Sharma et. a!
1975
Aurangabad
86.9
15.
Shanti Indra et. a!.
1974
Calcutta
90.75
16.
Nair
1962-63
Cali cut
94.7
17.
Kusturilal
1973
Gulburga
112.6
18.
Raj Goplan
1964
Lucknow
114.0
19.
Engineer
1962
Lucknow
124.7
20.
Agrawal I.
1980
Raipur
94.49
21.
Bhargawa et.al
1989
Indifferent
30-80
States
I
22. !
Chandrashekhar et.al
1992
I
10
South Kanara
44.65
CLASSIFICATIONS:Various authors have tried to classify the causes of perinatal deaths.
Classifications were based on clinical, pathological or clinicopathological grounds
to know the causes of perinatal deaths. Earliest classifications were clinical (Halt
and Babbitt 191 5) MC Ananie, 1929, Holland and Lane Clarypon 1926, the death
rate of the baby being ascribed to maternal diseases obstetric complications
present.
I.
Classification of causes of neonatal death according to Browne ( 1922)
~
Traumatic:
a
Inh·anatal-Cerebral haemorrhage
b.
•
Supra renal haemorrhage
•
Other injuries
•
Craniotomy
Postnatal Injury during artificial respiration
•
Other injuries
~
Infective:
~
Toxaemia:
II.
Classifications according to Bhowmick and Datta (1956-60)
Due to diverse factors directly and indirectly involved, classifica-
tion of the factors in the etiogenesis is by no means an easy task.
Causes separately classified as fresh still birth or macerated and
mature or immature:
~
Causes of macerated still birth:
1.
Toxaemia of pregnancy
2.
Antepartum haemorrhage
( i)
Accidental haemorrhage
( i i)
Placenta previa
11
....
3.
Actual fever
4.
Anaemia in pregnancy
5.
Post maturity
6.
Rh. Incompatibility
7.
Syphilis
8.
Diabetes
9.
Congenital malformation
I 0.
l'vfiscellaneous
Causes of premature fresh still birth:
1.
Complications of pregnancy
(i)
Toxaemia of pregnancy
(ii) Accidental haemorrhage
(iii) Placenta preria
(iv)
2.
Anaemia in pregnancy
Complication of labour:
(i)
Premature rupture of membranes
(ii) Cord complications
(iii) Difficult labour
....
3.
Congenital malformation
4.
Causes unknown
Causes of Fresh Mature Still Birth:
I.
Complications of pregnancy
(1)
Toxaemiaofpregnancy
( i 1)
Accidental haemorrhage
(ii1) Placenta previa
!2
(iv) Anaemia m pregnancy
(\·)
2.
Postmaturity
Complications of labour
( 1)
Premature rupture of membranes
(ii) Cord complications
(iii) Difficult labour
Ill.
3.
Congenital malformation
4.
!\ Iisee llaneous
Classification of causes of PNM according to Browne et a! (1964 ):
The foetus may die before the onset of labour (antenatal death) or
during labour (Intranatal death) or within 7 days of birth (neonatal death).
~
Antenatal Death:
Foetus is born in a state of maceration.
Causes :
( 1)
Pre-eclamptic toxaemia
( i 1) Chronic hypertension - in both the cases the cause of death
is placental insufficiency.
( i1i) Postmortality.
(iY)
Diabetes Mellitus.
(Y)
Erythroblastosis
(n)
Accidental haemorrhage
(Yii) True Knots in the Cord
(Yiii) Syphilis
Pathology of maceration :\laceration is an aspetic process. The skin peerls in 12 hours after
death The brain is the first organ to show softening hence the spalding's sign
becomes positive by the end of the week
I3
~
Intranatal Death:
The foetus may or may not be born macerated depending upon how
long before death occurred.
Causes :a
Anoxia
Premature rupture of membrane
(i)
(ii) Clycky Uterus
In both these cases causes of death is due to interference with
placental circulation.
(iii) Prolapse of cord or cord round the neck.
(iv) Delay in the birth of after coming head in breech
delivery.
(v)
Placenta separation in placenta previa.
(vi)
Postmaturity
(vii) Morphia and other analgesics and anaesthetics
These act by depressing the respiratory center.
(viii) Aspiration of blood, mechanism, mucous, and
liquor into the lungs.
b.
Cerebral trauma and cerebral haemorrhage.
c.
Haemorrhage into other organs subcapsular
haemorrhage in liver and supra renal
d.
Congenital pneumoma
~
Neonatal Deaths:-
C~Jttct.,
Causes:
a
Prematurity
b.
Birth injury
c
Congenital deformities
d
Antenatal, Intranatal and postnatal infection e.g. Syphilis
14
VI
Classification according to Robert H. Usher (1967-1970)
Causes:
I.
Asphyxia
a
A.P.H.
b.
Abnormal labour
(i)
Cord loops and knots.
( ii) Prolapsed cord
(iii) Maternal pathology
(iv) Unexplained
2.
Malformations
3.
Respiratory distress syndrome
4.
Isoimmunisation
5.
Foetal malnutntion
6.
Infections
7.
Tramna
8.
Other causes
9.
Unexplained
V
Classification according to Mas am (1976 ):
Section - 1:
Foetal death may occur:
1.
Before the onset of labour
2.
During the labour
3.
During the first week of life
15
Before the onset of labour :
(a)
Severe toxaemia
(b)
Repeated small A. P.H. and severe bout of bleeding in placenta
previa.
(c)
Premature separations of pla-:enta .
(d)
Strangulation by loops of cord round the neck.
(e)
Diabetes
(f)
Rh. or ABO blood group in compatibility
(g)
Syphilis
(h)
Higher maternal age
(i)
1\lultiple pregnancies
During the labour : (a)
Intrapartum asphyxia
(b)
Stress of labour
(c)
RD.S.
Intrapartum Asphyxia:I.
Prolapse of cord
2.
Abruption placenta or intrapartum bleeding in placenta previa.
3.
Post maturity beyond 42 weeks.
4.
Prolonged labour for more than 24 hours.
5.
Breech presentation.
Trauma or stress of labour :Predisposing causes
(I)
Abnormal uterine action
( 2)
Breech delivery and extraction
( 3)
1\lalpresentations.
16
Respiratory distress syndrome (R.D.S.): They occur either singly or in combination :(I)
Hyaline membrane disease.
(2)
Massive intra-alveolar haemorrhage.
( 3)
Pulmonary oedema pulmonary syndrome commonly occur in
premature births.
Neonatal deaths during the first week of life.
(a)
Prematurity.
(b)
Congenital malformation.
(c)
Effects of intrapartum birth trauma or asphyxia.
(d)
R.D.S.
(e)
Massive intraventricular or pulmonary haemorrhage.
(f)
Pneumonia
(g)
Pulmonary infections
Congenital malformations :(a)
Anencephaly.
(b)
Hydrocephaly.
Section - II
II )
Socio - economical factors.
12)
Obstetric problems.
1
a)
Prematurity.
ib)
Post maturity.
I C)
Age and parity.
17
AREA AND PEOPLE
Chhattisgarh lies between 20° North -24'' North !attitude and 8011 east
- 84" east longitude represented by hills, valleys, plateaux, undulating plains, rocky
surface, open tracts, forests and low lands. The plateaux punctuated by undulating plains and forests are more numerous in the eastern region than the rest. The
northern part is mostly covered by open tracts and rocky surface and the southwestern portion is mosth· plain having low lands. :\ good number of large and
small rivers and their tributaries form the drainage system of the state. To name
the important among them are Narmada, Mahanadi, Sone, Rihand, Seonath,
Wainganga, Mand, Kanhar. Arpa, Mahanadi and Indravati. Temperature in the state
varies from one area to another. Undulating plains low lands and open tracts experience oppressive heat and dust sto1ms during summer and a mild winter. Plateaux
and hilly areas have mild surruner and a very cold wmter. The average maximum
and minimmn temperature recorded during smnmer are 43 .8°C and 27.8°C and in
winter 28.6 °C and 12.7'( respectively. The approxunate annual rainfall of the
state is 1400 mm.
The soil types of the state are varied according to landscape, like.
red, yellow, brown, yellowish clay and alluvial. Irrigation facilities are limited to
certain districts only. In other districts it is yet to be developed in the region and
as a result, a great majority of the cultivable fields, especially in the tribal dominated zones are under single crop.
CommunicatiOn and transport facilities m respect of mill roads and
metal roads are moderately developed in the central and southern part of the state
The North and north-eastern part roads are rather poorly developed. Interior villages of this part do not have all weather roads. In the north-eastern region the
roads get out of use during rains and it takes about a month after cessation of rains
for their return to usable state.
18
84 t.
CHHATTISGARH
ADMINISTRATIVE DIVISIONS 2001
'
N
1'
11.
rl
2G
I
0
I
20Km
I
10
DISTRICT BOUNDARIES
.
11
0
DIVISIONAL HEAD QRS
•
DISTRICT HEAD O.RS
si DRAWING:
STUDY AREA
C .R.RATAE
S. T.A.G!:OGAAPIIY
1 •
,,
Total population of Chhattisgarh was recorded as 176. I 5 lakhs ( 1991
census) out of which scheduled tribes, scheduled castes, other backward castes
and minority community constitute 32.45, 12. 19,34.36 and 03.97 percent respectively. The total area of the state is 13,133 Km. scheduled area measures 81,669.70
Km. and tribal sub-plan area extends to 88,000 Km. Important tribal groups inhab-
iting are Baiga, Binjhwar, Dhanwar, Gond, Halba, Kanwar, Nagesia, Oraon, Pando
and Pardhan. Important crops are paddy, wheat, gram, kodo (paspalum
scrobiculatum), kutki (panicum miliaceum), bajra (penicillaria spicata) and pulses.
Paddy is an important food crop here than any other grain. Some tribes used to
practice shifting cultivation. Subsistence agriculture is the economic way oflife
of most tribal communities.
BASIC SOCIO-DEMOGRAPHIC FEATURES OF CHHATTISGARHCarved out from the eastern part of Madhya Pradesh, the new state
of Chhattisgarh, came into existence on 1 NoYember 2000. Prior to the postindepencence reorganization of states in India in 1956, Chhattisgarh was included
in the Mahakaushal area and was part of the Central Provinces and Berar. At the
time of the 1991 Census when it was still a part of Madhya Pradesh, Chhattisgarh
comprised only seven districts; by the 2001 Census, it had 16 districts, 97 tehsils,
I 46 blocks. 20,378 villages, and 97 urban centres.
According to the provisional population total oflndia Chhattisgarh
has a population of20.8 million (Director of Census Operations, Chhattisgarh.
2001). The state contributes 2.03 percent of the total population of the country
and is ranked 1" among all the states and union territories of India in terms of
population size. With a total area 1,35, I 95, I 95km 2 , the state's share in the total
area of India is 4. I I percent. The population of Chhattisgarh increased from 4.2
million in I901 to 7.5 million in I951, 14.0 million in I98I, and 20.8 million in
200 I, but population growth has begun to decline in the state. The decadal population growth rate was I 8. I percent during 1991-200 I, lower than the growth rate
of 25 in the preceeding decade. The decadal growth rate during 1991-2001 in
Chhattisgarh was also lower than the corresponding growth rate for Madhya
19
Pradesh (24.3 percent), as well as for the country as a whole (2 I .3 percent). The
population density per km 2 is I 54, less than population density of Madhya Pradesh
( 196), and only about half the population density of India as a whole (324). In
terms of population density, the state is one of the more sparsely populated states
in India, ranking 26 among all the Indian states and union territories. The population density in Chhattisgarh increased from 130 in 199 I to !54 in 200 I. The
population sex ratio of 990 females per 1,000 males is not only higher than the
all India sex ratio (933), but is also some what higher than the state sex ratio in
1991 (985). The sex ratio of the child population (0-6 age group) is 975 girls per
1,000 boys, much higher than the corresponding all-India sex ratio of 927, but
lower than the corresponding sex ratio of 984 for the state in 1991. Raipur and
Durg are the largest districts in the state in terms of population size (Office of
the Registrar General and Census Commissioner, India 200la and Director of
Census Operations, Chhattisgarh 200 l ).
DISTRICT JASHPUR-HEALTH FACILITIES
Population
7.5 million
Village
764
Tola
2969
Civil Hospital
01
CHC
7
PHC
2
MiniPHC
23
Sub- centre
185
Medical Officers
41
Population
6,56,352
Geographical Area
6088 Km2
Male
3,28,054
Female
3,28,298
Tahsil
4, Bagicha,Jashpur
Patthalgaon, Kunkuri
8, Bagicha, Manora,
Block
Duldula, Kunkuri,
Jashpur,Pharsabahar,
Patthalgaon, Kansabel
2, J ash pur, Patthalgaon
Municipal
20
MAN
The physical features of Hill k0rwas have differentiated them from
maj.~war,khairwar ,bhuiyan, chhero pahanya and the other neighbouring tnbes. They
..•~aye. been compared with negroes too but there is very less similarities. They do
' not possess any important feature of the negr,,es . There is very negligible amount
of race mixture among the korwas and they are regarded as pure blooded wondering tribe migra-ted from pathar region of Chhota nagpur.
They are generally dark complexioned and tall statured.Their chest
is well developed and their built is compati'Qle with their physical fitness. They
have small eyes and eyelids are swollen. Ncse is flat and depressed at the root.
They have broad lips. Their chin is well de\' eloped as compared to the ~lundaris.
Women also are well built but generally look depressed. Dalton have described
themas "Short statured and dark brown in complexion, strongly built and active
with good muscular development but it appeared to be disproportionately short
legged (Russel &Hiralal 1916). Dalton meaured 20 korwas from Sarguja and
showed that the stature of male is 5 '3" and females is 4 '9".
D.N. Majumdar published his results in Man in India in 1929 ~ter
taking the measurements of 50 korwas. According to his data their cephalic index
is 72.9 which implies that they are dolichocephalic. The average cephalic index
reported by Risley was 74.5. Nasal index was 83. 7. Most of the korwas. possess
platyrrhine type of nose but few possess mesorrhine type also. These indices
indicate that they are related to Mundari branch of Austric .
According to Risley the anthropometric indices of korwas are the
following
Stature
Korwas
159
Cephalic index
74.4
Nasal index.
92.5
According to the survey conducttd by Majumdar the percentage of
blood group is 31. 97%and of 'B"is 40.6%.
21
F-01
HIH Korwa MUlder
11WB1. , _ Fn AliiRNMIMW U l ' , 1117/nD,.
, ,An,.,
I
The distribution of ABO blood group among the korwas is
0
31 97
A
B
AB.
20.58
40.64
7.81
The korwas of Palamau as discussed in the gazatteur is as follows
"they appear to be more closer to the African negroes as compared to the Mundas.
Round face, very thick skin ,broad face, very thick lips, broad and flat nose, broad
shoulders and deep chest are the characters which indicate that they are strong
and active. They are extremely poor farmer. They depend on minor forest produce, roots and tubers and herbs. At present they are a fast vanishing tribe who
have lost all hopes for bright future and strive hard to fetch a single meal a day.
(Cited from Shrivastava M.K. 1994).
KORWA
The Korwas belong to the kolarian family. The tribe is concentrated
mainly in Sarguja and Jashpur districts. They are also refferred to as Kodakus. The
Korwas inhabiting the Khudia tract of Jashpur are the typical of the tribe. The
korwas of Jashpur district are divided into two groups, the "Pahari Korwas" or the
Hill Korwas and "Diharia Korwas" or the plain Korwas. There is no commensality
between the two groups. In Sarguja also they are divided into two groups, namely
"Agaria Korwas" and "Bhadia Korwas".
The Pahari Korwas are divided into four classes; Hezda. Edikhar,
Somati and Madhikar. In all the kolarian tribes Hill korwas are the most savage
looking tribe. Korwa women have a good built but they appear ground down by
hard work. They do all the work in the house as well as in the fields. The average
Korwa woman does not put on much ornament; a pair of bangles a kardhan; worn
round the waist. a pair of angutha on the toes are all that Korwa woman is seen to
wear. Tattooing is practiced and every woman tattoos her arms, specially upper
arm, which is always kept exposed. The tattoo designs are most geometric figures, rarely of animals or plant and there is no totemic belief connected with the
marks Hill Korwas use minimum clothes. Males wear dhoti while women put on
san 5 yards long, which serves also to cover waist upwards.
22
BLOCK- WISE POPrLATION OF HILL KORWAS IN JASHPUR
DISTRICT
(Hill Korwas Development Agency 1998-1999)
Block
No. of\111ages
No. of family
Bagicha
72
2076
9053
Man ora
J:
129
531
Total
84
2205
9584
Total population
POPULATION CHART
Districts
No. of Families
Population
1975
1993
1975
1981
1993
Jashpur
1289
2195
15895
5394
9494
Sarguja
2193
3709
10361
1(1861
16477
Korba
117
23S
605
605
1138
ORIGIN OF KORWA
"The Hill Kornas" believed in myths and thought that the frrsthurnan
in Sarguja was Hill Korwas by Mahadeo. The stories told by them is that the first
human being that settled in Sarguja being very much troubled by the depredation
oi the wild beasts on their crops, put up scarecrows, in their fields, figures made
of bamboo dangling in the au, the most hidden caricatures of humanity that they
cculd devise to frighten the animals. When the great spint saw the scarecrows, he
hn on an expedient to save his votaries the trouble of reconstructing them. He
arumated the day ling figures thus bringing into existence creatures ugly enough
to frighten all the birds and beasts in creation and they were the ancestors ofthe
wild Korwas.
The word is also found in the alternative name Ho for the Kol tribe
and in the names of cognate korwa and korwa tribes. The principal tribes of the
Munda or Kolarian family in the Central Provinces are Kol, \1unda, Ho, Bhumij,
Santhal, Kharia, Korwa, Korku. Gadba, Khairwar, Binjhwar etc. The name Kol comes
23
from Santhali language means "similarly the name ofKorku tribe is simply a corruption of Korku, young man and that of the Korwa tribe is from the same root.
The dialect ofKorku and the Korwa tribe is closely approximate to Mundari.
Both the Korwa of Chhota Nagpur Plateau and Korkus of Satpura
hills were known as muasi. a term having the meaning of robber or raiders. The
korwas have also a subtribe called Koraku and some people think that they were
onginally the same tribe. The dialect of the Korwa tribe closely approximate to
mundari. In own language Korwas are called Arundha. Some other names such as
Vanala, Vangarie, Ghamala. Khadkiya are given by the neighbouring tribes.
Hill Korwas are originally from Chhota :-.lagpur and they were migrated to highlands ofRa1garh and Sarguja. In Chhattisgarh their habitat areas are
Sarguja, Jashpur and Korba districts. Hill Korwas come under the primitive tribe.
Madhya Pradesh Govt. has made "Pahari Korwa Vikas Abhikaran" for better development, which does all the development works for the Hill Korwas. Three
Tahsil of Sarguja viz . Samari, Ambikapur and Pal and one Bagicha Tahsil of
Jashpur comes under this \'ikas Abhikaran. This Vikas Abhikaran has two development blocks in Jashpur district, one development block in Korba district and tweh·e
development blocks in Sarguja district.
HJLL KORWA AREA
Hill korwa tribe is found in the north-eastern
tribal zone of
Chhattisgarh state in Jashpur, Sarguja and Korba districts. The history of this tribe
reYeals that they moved westwards into the old Khudia Jamindari (Present Sanna
& Bagicha of Jashpur district) from Chhota Nagpur Region. From Khudia they
further migrated to the adjacent parts of Sarguja district and settled there. From
Sarguja,a group of the community gradually migrated to Palamau high land and
further, into the hill of \'indhyachal and Dhudhi in \1irzapur district of Uttar
Pradesh.
24
In Chhattisgarh the "Hill Korwas" are concentrated in the north-west
of Jashpur district, they continue to extend to the north-west of Samari and further to the north-eastern area of Ambikapur Tahsil of Sarguja district. They are
also scattered in the south-east and south-west of Samari Tahsil and Ambikapur
Tahsil.
The major habitation of Pahari Korwa is found to spread over from
north -west of Jashpur district to the south-west of Samari and to north-east of
Ambikapur Tahsil. In Samari Tahsil of Sarguja district, they are concentrated in
two tribal development blocks namely, Shankargarh and Kusumi whereas in
Ambikapur Tahsil they are spread over eight tribal development blocks but their
major concentration is in two blocks i.e. Lundra and Rajpur.The population of the
tribe is very much scattered in Sarguja and Jashpur districts while not so in Korba
district.
TOPOGR-\.PHY OF HILL KORWAS
Hill Korwa habitant comes under the north eastern part of the tribal
zone of Chhattisgarh. The area of this zone is 3 8,282 square km, consisting of
numerous hills and undulating plateaus. The plateau is situated between 20-18
western lanitude.
Hill Korwas live in fastnesses of hills and forests of this zone and
this conditiOn is responsible for keeping them in the primitive age and the stage
of hunting Hill Korwa area comprises the J ashpur district, Sarnari Ambikapur and
Pal Tahsil of Sarguja district and Katghora Tahsil of Korba.
J ashpur district is divided into upper and lower ghats the upper ghat
previously under khudia Jamidari comprises Bagicha and Man ora tribal development blocks. This is an extensive plateau about 3600ft. above sea level and covered by the dense forest. The elevated plateau called "Pat" is the main habitant
area of hill Korwas. Ibb is the important river of this area. which has its source in
the Khudia high land. The main peak is Burjudih (3,390ft.)of Jashpur district
Sarguja district is the second biggest district of Chhattisgarh. Samari is separated
25
from adjoining tribal area by Kanhar River which is the main river of the Tahsil.
The south west region of the Tahsil Is almost hilly, undulating and is covered by
dense forest. The western region IS almost inaccessible and remains cut off
during the rainy seeason. Pal tahsil Ism the north-west while Ambikapur is in the
south-west of Samari tahsil. Ambikapur tahsil is not so hilly. The lofty plateau of
Mainpat lies on the southerh boundary of the tahsil. This is a big plateau which is
29km. in length and 12km. in width. the highest peak of plateau is 1,152 meter.
The other parts of this district are Lahson pat and Hamir pat in Shankargarh development block. The large area of korwa habitant comes under the north-eastern
region of the Katghora Tahsil which has irregular range of hills alternating with
small paleteau covered with dense forest. A number of nalas flow in this region.
The main tributaries of the Mahanadi are Hasdeo and Mand, which
rise respectively in Sonhat and Main pat plateaus ofSarguja, Jashpur and Sarguja
district fall under the drainage system of the sone. The Kanhar and Rihnd are the
main tributaries of Sone.
All the Hill Korwa area can be divided into three types of climatic
zones viz. hot,cold and moderate. The area which is not on the elevation and is on
the bottom have hot climate, the pat area which is on higher elevation has cold
climate and slopes of elevation has a moderate climate.
In winter, the temperature of the whole Sarguja except southern tip
varies between 7.5°C to IO'C. The Jashpur and Bilaspur area has IOoC to 12.5°C
temperatures. The summers are coolest in the central Sarguja and north Jashpur
with 35°( to 37.5°C temperatures.
The average rainfalls
111
elevated and pat areas are 1250mm and
150mm respectively. The average annual rainfali varies between l20cm to over
160cm.
26
SOILS
The entire zone comes under the red soil zone. In the whole of Jashpur
and East Sarguja, mixed black, red and yellow soil of Archean and Dharwarian ages
are predominant, while ,,·estern Sarguja is covered with red-brown sandy
soils. sandstone and shells.
The soil is laterite, in general it is not heavy and clayey. It is hilly
soil so it does not retain moisture welL The laterite has largely red soil with
sandy texture. Soil is classified into Matasi (yellowish clay soil), Kanhar (Black
soil), Dorsa (Mixture of Kannhar and Matasi) and Bhata (poor red soil with pebbles).
Matasi is good for paddy cultivation found in eastern half of Sarguja
district Mair is a blackish soil and crops such as padd~ and wheat can grow well
on it Dundia is a greyish soil on which paddy and wheat can grow but the soil
being inferior the yield is poor.
MINERAL RESOURCES
The whole zone is rich in mineral resources. In J ashpur, bauxite is
found at many places. Iron is produced in modular form, in the hilly tracts and is
smelted by the aboriginal tribes for domestic use and also for export Samri the
eastern most tahsil of SarguJa is rich in bauxite. This bauxite belt runs from Jashpur
tahsil to east Sarguja (Samri 1 Central Sarguja is known for its carboniferous coalfields. A small gold belt on the banks and bed of the riYer lbb, is reported.
FLORA
The tract in J ashpur and Sarguja is rich in forest Forest (all type)
accounts for in Sarguja, area under the forest (all type 1 accounts for 52.06 percent of district area. These are in general composed of a mixture of semi-evergreen and deciduous species The forest can broadly, be classified into two groups
i.e. Sal and mixed forest. Sal (Shorrea robusta) is the dominant species of the
area. The other important species found in area are Saja ITermanalia tourentosa),
27
Bija (Peterocarpus marsupium), Behra (Terminalia belerica), harra (Terminallia
chebula), Char (Buchanaria latifolia), Kusum (Chetcbera trigua). Some other trees
like Mango (mangifera indica), Amla (Phyllathus conplica), Imli (tamirindus) are
also found here. Fruits consumed by Hill Korwas are papaya, banana, jackfruit,
etc. Mahua (madhucaletic folia) is the main fruit item, which is frequently used
by the Hill korwas.
FAUNA
The forest of Hill Korwas settlement contain tigers, leopards, wolves,
bears, wild dogs, bison, etc. Main birds are parrot, green and blue pigeon, perki,
etc. But now they are reducing in number due to hunting and destruction of forest.
REPORT ON HILL KORWAS BY INDIAN COUNCIL OF MEDICAL
RESEARCH (ICMR) 1990-91
Hill Korwa community is still backward on the basis of literacy.
According to 1961 census, percentage ofliteracy among tribes in Sarguja, Korba
and Jashpur were 3 %, 6.9% and 7.9% percent respectively. ICMR report in
1990-91 among the Hill korwas of Sarguja district reveals the following facts
(Data based on 42 Villages, 819 families and 3527 individuals).
1.
2/3 of Hill korwas have nuclear type of family and the average
number per family is 4.3-4.4.
2.
The sex ratio of Hill Korwas is 945/1000 males (Abhikaran survey
reported 991.25/1000) three districts ofBilaspur division was also
included in the survey.
3.
The median age is 23.8 years which appears to be very high in
comparison to the other.
4.
Only 33.4% population comes under the age group of 15 years
which is lower in comparison to National Index. The percent of
dependency rates is also less.
5.
Index of longi..,;ty is high.
28
6.
Literacy rate is very low only 4.5% males and 1.6% females are
literate from 1975 onwards the literacy rate is 3.8% and from
the last 3 decades the literacy rate is constant, there is no change.
7.
The percent of working population in the 15-49 years age group
is 48.9%.31.6%are farmers. whose land is unirrigated. Only 0.5%
of the population is in service or other bussiness.
The fertility rate of korwa women is comparatively low. The total
fertility rate is 2.99, the maximum fertility is in the 15-20 years age group and
after which it goes on reducing .This trend is very unusual in Indian context. The
age at first conception is 2.4 years after the age at marriage (The interval between
the age of marriage and first conception is 2.4 years).
Family planning is prohibited amongst the Hill korwas but due to
financial gains they declare themselves Nagesia and get themselYes sterilized.
They are strictly endogamous and they marry outside their clans (exogamous). 'vfost of the marriages are consanguineous preferentialy. They follow
the cross- cousin marriage type. In villages endogamous is observed to be very
high. In 40 percent cases the age at marriage of males is 16.4 years and in females
it is 14.5 years which is quite unusual
Females were illiterate. in 1971, percentage of illiteracy had come
down to 96.27% and 99.35% for males and females respectively Literacy is not
satisfactory till now. Only 4.5% and 1.6% females are literate in both Jashpur and
Sarguja district. Education has not yet made any impact on the tribe. A Hill korwa
child becomes an economic entity at a fairly early stage and therefore sending the
child to school is a losing proposition. They are thus not motivated to send their
children to school and this is the biggest cause of illiteracy there.
29
HEALTil
Their low rate of literacy further adds to their ignorance and unawareness of surrounding environment, which continues to envelop them with deep
magi co- religious beliefs and taboos. The local traditional healer 'Guniya' provides them with traditional and herbal medicines. They do not want to go to primary health center for their treatment and mostly this facility is not available in
the deep forest surrounding Korwa area. Malaria and anaemia are the most found
diseaes in korwa area. Some other diseases like Diarrhoea, dysentry are also
seen in the rainy season due to consumption of unhygienic and unsafe water.
The normal health of tribal people cannot be said to be very bad, but
their condition are often chronic after repeated infections.The tribals suffer from
many chronic diseases but the the most prevalent taking heavy toll of them is
water supply, resulting into intestinal and skin diseases. Deficiency of certain
minerals and other elements is also one of the reasons for diseases.
The Korwas represent one of the weakest sections of primitive tribal
group. Their economic condition is precarious and they are unable to make their
both ends meet. There is a subsistence economy, mostly dependent on forest
With the passage of forest law, their rights have been severly curtailed. They had
little land for cultivation and now have no scope for claiming new lands. The land
they own is not sufficient for their survival and they are obliged to work in other
fields as 'Dhangars' .
The effect of all this is that they are not only losing cultural identity,
but also their existence,as it is evident in the ever-decreasing population in the
last four decades. Socio-cultural and economic factors are responsible for their
poor health status. Hill korwas inhabit isolated and difficult terrains of Sarguja
and Jashpur district and their natural habitat render them vulnerable to host of
exrringent factor, which have direct or indirect bearing on their health status.
30
F • 03
Rare Albino Case
1I.
REVIEW OF LITERATURE
(1)
GEOGRAPHICAL DISTRIBUTION:There are marked regional differences in PNM from place to place
and from one institute to other. Studies on P.J\.M. rates of different countries
give the following incidences.
In 1934 Brang studied marked differences between birth weight of
Negro and white races at the time there was considerable differences in the average birth weight of white infant in different parts of United States and a seasonal
difference of birth weight was also noted. Butler et.al.(l962) reported high incidence of foetal congenital malformations in the south and less incidence at
lower altitude level in eastern region of England and Wales.
Anaemia was highest in the north and west and lowest in south and
east. Toxaemia was most prevalent in southern region.
Mortality from intrapartum anoxia was highest in Wales, United
States ranked high m disease for the respiratory and digestive system and for
accidents and it has been reported that proportion of! ow birth weight infant 1;
~
about 82.2 percent m 1964. It appears to be higher than in Netherland, Sweeden
or any other Non-European countries.
Ghosh et. a!, ( 1969-70) reported the perinatal mortality of 63.9 per
thousand live births at Delhi while Kher et a!. ( 1964-71) reported 41.5/1000 Jiye
birth at Nagpur. Sharma eta!. (1975) reported the incidence of perinatal mortality
of 36.9/1000 live binhs at Aurangabad. While Agrawal I, (1980) reported 91.49/
1000 live births at Raipur.
(2) AGE AND PARITY:Baird ( 194 7) reported that the still birth rate was higher in I st than
in the 2nd pregnancy and the still birth rate, rises with maternal age in each parity.
Still birth rate rises more rapidly after fourth pregnancy.
31
In England and Wales mother aged 16-20 years 1 having 2nd and 3rd
baby had a high still birth rate.
(a)
Babies of young mothers are like]\· to be still born.
(b)
Where social conditions are poor still birth rates are higher in
each parity and age.
(c)
Recent social improvements have had a proportionately lesser
amongst high parity mothers who are mainly from poor social
classes
Baird also reported the perinatal mortality rate was about three times
high in social class (V) as compared to social class (I) and the foetal wastage
(still births and neonatal mortality) about twi.:e as much. Under such conditions
in which the women are healthy and have always lived in a good social environment have their first pregnancy before the age of 30 years, limit their families to
3 or 4 and in which skilled medical attention is available. Obstetric death rates
can be brought as low as 20 per thousand births.
Baird eta!, reported that still birth rate is the lowest in the age group
between 20 to 24 years and then it goes on rismg till it is highest in the age group
above 40 years.
Baird and Thomson in 1961 con.:luded the lowest P.N.M. rate was
found in second pregnancy and highest in 5th and subsequent pregnancy in all
parities.
The highest P.N.M. rates were found in oldest women and lowest in
the age of20-29 years. Highest P.N.M. rate was found in prim para.
- Nair et al, (1956) concluded that perinatal loss was higher in offsprings of primiparous women being low in 2nd ,3rd and 4th gravida. Nair et al,
(1965) reported that P.N.M. was more frequent under 20 years and over 3·) years
of age, being minimum in the age group 25 to 29 years which correspond to the
period of maximum fertility.
32
Johan stall worthy et al, ( 1966) reported that maximum P.N.M. was
in the patients under 20 years having their 3rd child in patient 20-24 years mortality ratio remains below I 00 until the Sth child and in patients between 25-29
years the first child has a mortality ratio as patients of 23 years having 5th child
(Cited from Agrawal!. 1979).
Nevile eta!, ( 1969) reported that parity has a high significant effect
on birth weight regardless of the associated effect of the maternal, age, social
class, height, presence or absence of eclamsia or other disease.
Isaac etal,(\968-72) concluded that P.N.M. was highest between age
group of20-24 i.e. 28.5%, 27.5% (25-29 years), 18.2%(30-34 years), 14.9% in
15-19 years and 10.7%(35 onwards) P.N.M. was highest in prirni i.e. 32.3 percent
and was again high in parity five onward i.e. 25.48 percent.
Gupta (J 971-73) reported highest P.N.M. in age group between 2030 (66.0%), 30 onwards (23.4%) and in age group between 15-19 (10.6%).
Kalavati S.Parikh (1973-74)reported P.N.M. 3.9% between age group
15-19 years 68.3% between 20-29 and 27.1% above 30 years and found highest
incidence ofP.N.M. in primi (34.4%) and in later 3 pregnancies i.e. 2nd,3rd and
4th it was 38.9% and it was again high in the parity 5 onwards (26.7%). (Cited
from Agarwal I. 1979).
Sankholkar, 1975 reported increased P.N.M. rate in primi pare as
compared with multipare at Bombay. Dutta (1975) reported that P.N.M. was high
in very young mothers 12.53% (below 20 years) and in the elderly 13.33% (31
years and above) also reported that P.N.M. was high in the primiparous 9.64% as
compared to the second para 4. 70% and was again high from 3rd para onwards.
High parity was mostly found among the lower socio-economic section.
Masani and Parikh (1976) reported that irrespective of parity the
mortality rate increases proportionately as maternal age advances. The highest
perinatal mortality rate was on primiparae. From parity five onwards the P.N.M.
rate nses.
33
Raman (1989) reported that mother's age below 20 and above 30
years are associated with h1gh early neonatal death rate. In poor socio-economic
groups 30% ofprimigravids are teenagers.
Chandra Shakar et al (1998) reported that P.N.M.R. in age group of
19 years was 52 and age groups> 30 was 59 in the rural area of south Kanara
district of south India.
Pandey et. al 12000) reported that total percentage of abortion and
still birth was higher while maternal age was above 30 years. Study was carried
out in four endogamous populations ofPur~ia, Bihar (India).
(3) PNMR IN RELATION TO SOCIO-ECONOMIC STATUS:In families with income below Rs. 100/month the perinatal mortality was 70.51 percent, while between 100 to 300 rupees per month the perinatal
mortality was 27.95 percent and above 300 rupees per month and perinatal mortality was 15.5 percent only. In 1959 Heady and Morris reported that in social
class V, the 6th and subsequent birth the still birth rate was 55.2 per thousand live
births.
Dass and Bhargava (1961) reported that about 70 percent of the cases
fall in the group with family income ofRs.lOO/-per month or below.
Butler et al. ( 1963) reported that women from poor socio-economic
ctrcumstances:
(a)
Withaheightabout5'2"
(b). Under 15yearsofage.
(c)
Having their second, third and fourth child.
(d)
Who did not smoke had perinatal mortality of9.8 per thousand
live births.
34
Nair et al 1965 also reported that there is increasing P.N.M with
poor socio-economic conditions. Thus the safest social class parity group is the
wife of professional man having her second baby. The most dangerous group is
the wife of unskilled worker having her fourth or subsequent baby.
John Stall worthy and Cordan Bourne (1966) reported that P.N.M.
rises as social class descends. In class I it is 69/1000 and rises to 128/1000 in
class IV. Browne et. a! ( 1966) reported that in social class I the still birth rate of
first birth was 20.4/1000 birth while in social class V it was 27.111000 live birth
14.7 and 22.7 and in live birth 16.4 and 25.3/1000 live births.
Baird and Thomson (1969) in British mortality study the lowest
perinatal mortality 2011000 rate was observed in all well built women of high
socio-economic group and highest mortality rate (above 50/1000) was observed
in short statured undernourished women mostly from low income group.
Robert H. Usher (1971) reported that the lower socio-economic
clsses have a higher frequency of still births and low birth rate; weak neonates
with in the poorest areas may combine to double the total P.N.M. over that
obtained amongst patients who are socio-economically greater with identical
obstetrical and neonatal health care. (Cited from Agrawal I. 1979).
Kalavati S.Parikh and Joshi in 1975 concluded that higher mortality
is seen in poor classes. Patients i.e. 92.6 percent in group IV, III and II and 7.4
percent in group I.
Sharma eta! in 1975 reported that mortality of the patient belong to
lower socio-economic strata which reflects inadequate antenatal care and
malnutritious deficiencies these factors along with orand multi parity affects
mothers health adversely. Major maternal disease further increase the incidence
of perinatal mortality.
Issac eta!. (1975) reported P.N.M. 7 times higher in the low income
group than the higher income group . 70 percent overall incidence of PNMR in
our country occur in socio-economic group IV and V.
35
Berendes ( 1989) reported that lower socio-economic classes have a
higher frequency of still birth and infant mortality in India.
NFHS (1992-93) in state of Madhya Pradesh, due to low literacy
rate and poverty infant mortality and maternal mortality exist high.
Chandrashekar et.al. ( 1998) reported that PNMR is 73/1000 live birth
in lower socio-economic group and 29/1000 live birth in upper socio-economic
group.
(4)
PLACE OF BOOKING AND DELIVERY:Dass and Bhargava (1961) reported that booked cases formed 37.5
per cent of the total admissions, out of these 20.4 per cent were still birth and in
most cases the chances of foetal death were obscure.
Butler et. al (1963) reported that 17.1 per cent of still births are
from high risk group of patients which were home delivered. About 49 per cent of
these cases were booked for the hospital, 42 per cent were booked for delivery at
home or to a general practitioner, 3.2 per cent of perinatal deaths had no prenatal
care and mortality rate for these patients was five times the over all average figures.
Eastman quoted that unhooked cases have higher perinatal mortality
as compared to booked cases
Gupta eta!. (1971-73) reported PNM higher in unhooked (75.5%)
than booked (74.5%) cases. Kasturi La! eta!. (1975) reported perinatal mortality
was four times higher in the infants where the mother had not sought antenatal
care as compared to booked cases. Isaac et.al ( 1975) reported that more perinatal
death occurred in the unhooked cases than booked cases at Veil ore.
Agrawal (1979) reported that PNMR is 73.8% in unhooked cases
while it is 26.2% in booked cases.
36
Das and Bhargava (I 961) in every pregnant mother blood groping
and Rh. typing, urine for albumin and sugar, B.P. and regular weight recording of
the patient should be done regularly at each antenatal visit so that any deterioration can be judged in time and treated energetically and thus reduce P.N.M.
If early toxaemia is diagnosed, the patient must be admitted to hospital, if anaemia is found the patient must be treated and the effective treatment
observed.
Walker et al. ( 1960) stated that frequent antenatal examinations are
worth less, however, unless the significance of the fmding is appreciated. Theobald
( 1962) has eliminated eclampsia by examining his patients weekly from the 24
weeks; concentrating more on the measurement ofB.P., weight ,Hb., oedema and
proteinuria than on abdominal palpation.
Abnormal presentations, associated maternal diseases, oedema from
local or systematic cause can be diagnosed in time by proper antenatal check up,
can be corrected in time and accordingly, mode of de-livery is planned and thereby
P.N.M. is reduced.
Special attention should be paid to high risk pregnancy during antenatal check up .~.e. in cases of previous bad obstetric history, over weight or under
weight, under 17 years of age, grand multipara, hy-pertensive diseases .
Apart from medical care available, which should include giving iron,
folic acid, ascorbic acid, vitamins etc. are given to improve nutrition of patient to
allow the foetus to reach the state of maturity. Nutritional supplement to be given
to the patients who are looking in the home diet. Lastly, every mother should be
made to realize the importance and advantage of early and sustained perinatal care
for herself and un-born child. Early hospitalization of high-risk pregnancy should
be done, so that any complication can be treated in time.
38
In 1975 Datta and Benik et a!., New Delhi ,reported that perinatal
deaths decreases with better ante-natal care. Perinatal deaths were nearly seven
times more (20.6 percent) in babies of mother's with irregular antenatal care in
comparison with those (2.68 %) born to the mothers who attended the antenatal
clinic regularly and were under proper medical supervision.
Park ( 19-7) stated that perinatal supervision of medical diseases;
complications of pregnancy will prevent premature labour in many cases.
In unmarried mothers along with above measures, psychological
treatment is also necessary. The benefits of antenatal care are reflected in the
reduction of perinatal mortality.
(7) AVOIDABLE H.CTOR5One happy conclusion that emerges from the fact that large number
of perinatal deaths are preventable.
The high mcidences of perinatal mortality are closely correlated with
adverse social and economical conditions, which tend to lower the standard maternal health. It is also an avoidable factor which gives rise to increased incidence
of perinatal mortality but there are certain cases in which no cause can be found.
Among the maternal conditions responsible, are the toxaemia of pregnancy, nephritis, severe anaemia and syphilis. Here we can check these conditions
by proper antenatal care and free supply of anti-anaemia medicines and other necessary medicines.
Platt has suggested that poor birth weight in some oriental communities is mainly due to poor nutrition.
Burke et al. recorded a rise in birth weight by 0.5llbs. with e\'ery
increase by I 0 grams in the protein content in maternal diet
Park ( 1977) stated that balanced diet during prenatal period is
utmost important from the point of view of reducing the perinatal wastage.
39
From above statements, it is evident that perinatal mortality can be
reduced by impro,1ng the nutrition of pregnant women, giving abundant iron,
protein, liver according to blood picture in antenatal period.
Majonry of foetal deaths are due to poor antepartum care, maternal
malnutrition and inadequate obstetric services. These are all preventable.
Roben H. Usher (1971) reported that abnormalities of labour and
delivery resulted in 42% of all perinatal deaths. The cause of death in all cases
were asphyxia such 1s in difficult breech, O.P. with vertex presentation, although
all such deaths are rotentially preventable.
They c:mtinue to occur with discouraging frequency, which should
be reduced with imrroved foetal monitoring.
There are certain other factors like endocrinal disturbances and local abnormalities oi uterus like bicornuate uterus, tumors like fibroid, incompetent OS and congerutal malformations, resulting rn premature births which forms
a large group responsible for perinatal mortality. These are partially avoidable by
proper operative tre 1tment at appropriate time.
Still there are other conditions in which premature labour is common occurrences fo; example in cases of accidental haemorrhage, diabetes, and
severe sensitization :o Rh. blood factor and severe hydramnios.
This shJws the magnitude of the role played by prematurity in causation of perinatal monality and should draw the attention of all concerns with the
welfare of the newborn. So, it is essential to consider all measures to lessen the
incidences of prema:urity.
Devi ( 1975) reported that identification of the high risk improved
services; both institutional and domiciliary to such groups is important. Certain
traditional procedures in working of antenatal clinics have to be modified or discarded, so that women with high risk get more attention from technically bettertrained staff Additional hospital beds for antenatal cases attending the clinics
would be required. (Cited from Agrawal!. 1979).
40
(8)
GESTATIONAL AGE:The period of pregnancy was shown to be of immense 1mportance to
the fetal out come.
\1c Clure Browne (I 973) reported that the lowest pennata] mortality occurs in pregnancies lasting from 39 to 4 I weeks. Birth before this or birth
after this carries increased risk to the foetus. Before 38 weeks, only 9.4% of
deliveries occur but46.2% of total perinatal death account for this :n England.
Birth weight and gestational age have a joint influence on P,N.M. A
number of factors are known to be associated with low birth weight account for
this in England.
Birth weight and gestational age have a joint influence on P.N.M. A
number of factors are known to be asso,iated with low birth weight. Low birth
weight is more common in low socio-ecvnomic groups, young motiers, women
above the age of 35 years, women without perinatal care and womerr with major
complications of pregnancy like toxaelllla, placenta praevis etc. (Hellen, 1970).
Gupta (1975) reported that P.N.M. is higher in gestaticn period less
than 36 weeks i.e. 61% and less in gestation period of more than :6 weeks (39
%).
Isaac eta!. (1975) reported that P.N.M. is higher where :he gestation
period was less than 38 weeks (55.6 %) and less where the gestatioJ. period was
more than 38 weeks i.e. 44.4% and Ajit l..lehta (I 967-74) 57.4%. In
~ases
where
gestation period is less than 39 weeks and 42.6% in cases where ges:ation period
was more than 37 weeks.
Sankholkar ( 1975) reported that the lesser the gestatioml age higher
is the P.N.M.
Devi (1975) reported that birth before term (258 da~; or less) is
associated with perinatal mortality which is 30 to 33 times higher tha."l for normal
gestation period i.e. between 259 to 293 days. (Cited from Agrawal I 1979).
41
(9) PREMATURITY:Prematurity is a common result of chronic glomerular nephritis,
maternal pre eclampsia and chronic hypertension.
Dead births are more common in the mature infant as compared to
premature infants.
Franck, A. Cravaffo ( 1948) reported that prematurity is responsible
for 54.6% of perinatal mortality. Datta eta!. (1955-60) reported that prematurity
is responsible for 61.3% of still births in premature labour and 22.2% of still
births in intranatal period . 2.2% were due to congenital malformations and in
14.3'1o the causes were unknown.
Dass and Bhargava (1961) reported that more premature the baby,
higher the incidence of stillbirth. The lowest percentage of still births is in between 5 to 8 lbs. Nair eta!. ( 1965) reported that perinatal mortality of 36% is due
to premature infants.
Stall worthy (1965) reported that high incidence of .IR..D.S. is associated with prematurity. In women of social class I only 3.6% of babies were premature and in women of social class V -7.2%.
According to Peal, 60% of all perinatal deaths occur in premature
infants. Sugai et al. reported 66% of perinatal death occurring in premature infant
in Japan. According to Sastman 84.56% of perinatal death, occur in infants weighing 2500 grams or Jess.
Purandare et a!. reported that prematurity accoUlllts for 62% of
perinatal deaths at K.E.M. Hospital, Bombay. Mas ani and Parikh ( 1976) reported
60% of all P.N. deaths occur in premature infants. Ajit Mehta ( 1977) reported
that prematurity which was responsible for 19.3% of all deaths. Bhargava (1989)
reported that P.N.M. was 45.3 due to prematurity in rural India.
42
( 10) POST MATURITY:-
Perinatal mortality is definitely found to be high in post dated pregnancy and this rise starts after 41 weeks of gestation and increases with further
prolongation.
Clayton ( 19-11) reported stillbirths in post mature infants as 6.!5~o.
Grenhill ( 1943) considered increased foetal mortality to be due to slow labour 0r
disproportion because of harder and bigger skull in prolonged pregnancy resulting in higher arrest and difficult forceps ex-tractions.
Mackiddi ( 1949) reported stillbirths as 4.2 per cent in post dated
pregnancy, while Racker et al. (1953) reported stillbirths as 8.72 per cent after
42 weeks of gestations, and Latto (1951) Baired (1955 to 1957), Arnot (1961 l
suggested that occipito posterior predisposes to prolonged pregnancy. Failure of
rotation and difficult operative delivery accounted for 2 neonatal (13.2 per cent)
deaths out of II perinatal deaths in post dated groups. (Cited from Agrawal L
1979).
Devi (1975) reported that prolonged pregnancy (294 days or oven
has roughly twice the mortality as at term (W.H.O., 1972).
According to Masani (197 4) perinatal mortality in first pregnancy
prolonged for more than -12 weeks is three times higher than the pregnancies
ending between 38 weeks to 42 weeks.
According to Browne (1973) P.N.M gets doubled by the end of 41
weeks. Ajit Mehta ( 1977 J reported that post maturity contribute 4.2 per cent to
total deaths. According to Bhargava ( 1989) prolonged pregnancy has high perinatal
mortality than normal pregnancy.
43
(11) PERINATAL MORTALITY IN RELATION TO SEX
OF THE FOETUS:Butler et al.(l963) reported higher mortality in male babies for all
gestation group except between 32 and 35 weeks, when a slightly greater death
rate in female could be due to relative excess of foetal C.N.S. malformation and
particularly to anencephalus and to myelocele complex. Apart from this, the ratio
of male to female mortality was 1.6: I between 28and 31 weeks. Male deaths exceed female except between I 00 I and 1500 grams.
It was confirmed that there is a heavy average birth rate in the male
than in the female inspite of similar gestation distribution within the sexes. In
general, all causes of death show a noticeable preponderance of males. The highest preponderance is seen in the first week deaths.
Robert H. Usher ( 1971) reported the mortality was I 0 per cent higher
among the male than the female. Vlsaac et al.(1968-72) concluded high P.N.M in
male in comparison to female i.e. 60.2per cent male and 39.4 per cent in female.
Agrawal (1979) reported that out ofP.N.M 63.1 per cent were males and 36.9 per
cent were female new born.
Rao (1989) reported that neonatal mortality was 56.2/1000 live births
among male sex while it is 41.3/1000 in case of female sex.
Chandrashekhar eta! (1998) concluded that out of total P.N.M 39
per thousand were female and 50 per thousand were male.
(12) BIRTH WEIGHT PATTERN IN PERINATAL DEATHS:There are number offactors which attribute to low birth weight for
example age, parity, height and weight of mother, period of gestation, multiple
pregnancy, social class,disease of mother and foetus, smoking, abnormalities of
placenta and cord and so on. In developing countries sometimes, malnutrition and
anaemia are the major causes responsible for low birth weight (Platt, 194 7).
44
According to Webster ( 1957) survival rate of premature infant
depends directly upon the birth weight. He reported that if baby weighs under
I 000 gm, the perinatal mortality was 9~.44 per cent, between thousand grams to
1499 grams It was 42.54 per cent while between 1500 to 2499 grams it was 6.81
per cent and between 2500 grams or oYer it was0.53 per cent ..
Isaac et al. concluded in their study ( 1968-72) at Yell ore that 66.2
per cent deaths in babies who weighed less than 2500gm. and 33. 7 per cent deaths
in babies who weighed more than 2500 gms. Gupta (1971-73} concluded P.N.M.
rate (76.3 per cent) in the birth weight below 2500 grams and (23. 7 per cent) the
birth weight above 2500 grams.
Dutta et al. concluded that low birth weight was associated with increased P.N .\'1. Sharma (1975) found that 83.5 per cent of perinatal death 92 percent of early neonatal deaths and 76.9 percent of the stillbirths had birth weight
of2.5 kg or below. Sankholkar (1975) reported in a population at Bombay that as
far as P.N.M is concerned the survival rate is higher in proportion to birth weight.
Kusturilal ( 1975) reported low birth weight is associated with increased risk to
the infants at M.R. Medical College, Gulburga also concluded birth weight below
IOOOgm. 100% P.N.M., 1001 to 1500g:m. 91.6%, 1510 to 2000gm. 30%, 2001
to 2500, 6.5°~ and 250 I and above 4.3° o perinatal deaths.
(13) MULTIPLE PREGNANCY:.-\ccording to Douglas, multiple pregnancies are more prone to give
premature b1rth.
Butler et al. ( 1963) reported the still births ( 17) and neonatal deaths
(32) out of 211 cases of multiple pregnancy. Nair et al. (I 965) commented that
multiple pregnancies are mostly associated with prematurity, toxaemia,
hydramnios. which further increases the foetal mortality in these deliveries. Dutta
and Bhowmik (1975) New Delhi reported the P.N.M. rate in multiple pregnancies
is about 4 times higher than singleton pregnancy.
45
Richard, L.N aerge et a!. ( 1978) concluded in 12 United cities and in
African city, that P.N.M. rate was 139/1000 for twins and 33/1000 for singleton
also reported for Addis Ababa 338/1000 for twin and 53/1000 for singleton.
(14) LABOUR AND DELIVERY:Frank, A. Craceffo (1946) revived the various causes of neonatal
mortality. The total mortality was found to be 4.26%; out of which 2.47%
occurred intrapartum, 1.49% occurred postpartum.
Dutta eta!. (1956-1960) reported causes related to labour like premature, rupture of membranes, cord complications and difficult labour accounted
for 22.2% stillbirths, 22.2% was due to congenital malformation and in 14.3%
cause was unknown.
Butler eta!. ( 1963) reported a low mortality ratio of 68 in spontaneous delivery as vertex (O.P.) de-livering face to pubes, had an appreciably higher
mortality ratio reported 93, but in face presentation mor-tality in faces presentation was due to high incidence of congenital malformation particularly
anencephalus.
Nair eta!. (1965) reported that the high frequency of perinatal
deaths in breech, face, brow, and compound presentations is hardly surprising.
Perinatal mortality reported in vertex presentation was 8%, in face 25%, in brow
3. 8%, in breech 22.65%, in compounds presentations 55% and in shoulder 28%.
Cord prolapse was observed in 23 cases of these 13 resulted in perinatal death i.e.
50% perinatal mortality.
Robert H. Usher (1971) reported that abnormalities of labour and
deliveries resulted in perinatal mortality of 0. 7per thousand births.
Cord loops and knots were considered to be the cause of death due
to asphyxia and the rate of this type of death is 1.1 (perinatal death) per thousand
births recorded.
46
Prolapse of umbilical cord-0.3 perinatal death per thousand births
or 2% perinatal death.
Eastman reported 4.2% perinatal mortality in occipita posterior position of vertex while 2.5';o peri-natal mortality in face presentation and 30%
perinatal mortality in cases oftransverse lie ending in vaginal delivery.
The perinatal mortality associated with prolapse of cord in 26.2%,
while in compound presentation perinatal loss of 13% is reported. Cox, Fanton
and Steer found that fetal distress was responsible for 5% perinatal loss.
(15) BREECH DELIVERY:According to \"art en ( 1945) perinatal mortality in breech delivery is
2.2% but Lloyd Wood Raw. Cox (1950) reported perinatal mortality 4-6% in primi
para and while in multipara it is 2.3%. Lloyd Wood Raw, Cox (1950) reported that
perinatal mortality in singleton breech presentation was four times more than
normal vertex presentation. William eta!. (1952) reported the foetal mortality
ior breech to be 3.82 to 4.2%.
Bhargava eta!. (1964) reported the P.N ..\1. in breech deliveries as
63.~%
P.N.M. in cases of internal pudalic version and S.B. rate of 3.5% in for-
-:eps delivery for after coming ahead, while Lahiri (1964) reported that forceps
ior after coming head in breech presentation carried a perinatal mortality of20%.
Sharma eta!. (I 975) reported that incidence of asphyxia and perinatal
mortality is more in complete breech presentation than in incomplete presentanon. Masani ( 1976) reported that perinatal mortality in breech as 8%.
According to Eastman perinatal mortality is 12% when the foetal
weight was over thousand grams.
Cellis ( 1976) reported neonatal mortality rate for infants born followmg breech presentation varies between 25-30%, which is 10-12 times the
mortality rate among non breech deliveries.
47
Maharban Singh et al. (1979) reported 19.5%neonatal mortality rate
following breech presentation. He also reported the evidence of birth trauma in
45 out of 157 cases, those delivered vaginally with breech presentation.
Agrawal (1979) reported that P.N.\1. was found to be highest in
normal vertex deliveries (55.6%), breech delivery was next in descending order
(14.2%).
Chandrashekhar et al. (I 998) reported that P.N.M.R. was lowest in
vertex deliveries (4 I/1 000), and highest in breech delivery (181/1 000).
(16) PERINATAL MORTALITY IN RELATIO~ TO DURATION
OF LABOUR:Perinatal mortality is 2.9% for 24 hours of duration P.N.M. 9.3%
and labour prolonged over 48 hours P.N.M. to be recorded 19%.
Stallworthy (I 956) a particularly rapid first stages carrier a high
perinatal mortality and this may be associated with prematurity. The mortality
ratio elevated to I 56 after 48 hours.
(17) TOXAEMIA AND BLEEDING IN PREGNANCY:Bhowmic eta! (I 956-1960) reported that 39 per cent ofP.N.M was
due to toxaemia, A.P H and anaemia of pregnancy. Dass et a!. ( 1961) reported
that perinatal mortality in antepartum haemorrhage was about 14.9 per cent.
Manson (I 962) admits that toxaemia of pregnancy and accidental
haemorrhage were common causes of premature
P.~.
fatalities.
Toxaemia pregnancy was the most important of the maternal diseases
responsible for increased perinatal death. The cause of death is the placental
ischaemia with or without infarction or retroplacental haemorrhage.
Contributory factors presumably mclude intrauterine growth
retardation and higher frequency of premature birth.
48
In eclampsia the anoxaemia which occurs with convulsive episodes
and sedative administered are contributory factors.
Toxaemia also results in low birth weight of the foetus, which is itself responsible for increasing perinatal mortality.
The perinatal loss was higher in placenta previa; prematurity was the
most significant factor in these cases.
Butler et a! ( 1963) reported that high perinatal loss is associated
with the presence of any forms of toxaemia as measured by hypertension or
proteinuria.
Toxaemic mothers gave birth to the babies with foetal congenital
malformation more often than non-toxaemia.
With increasing degree of toxaemia, the mortality rose sharply when
associated with albuminuria, mortality was three times of the average. The risk to
the baby from maternal toxaemia rose markedly after term and was higher at every
week of gestation than for non-toxaemic cases.
Babies of toxaemia mother were at increased risk of death before
labour, intrapartum asphyxia and death in the first week from hyaline membrane
disease, intraventricular haemorrhage or massive pulmonary haemorrhage.
Accidental haemorrhage had a very high risk to the foetus. The majority of cases included had massive retro-placental haemorrhage with a consequently very high foetal mortality.
Sharma eta!. (1975) reported that P.N.M. of27.5 per cent occurs in
cases associated with antepartum haemorrhage and 12.5 percent P.N. death
occurs in cases associated with toxaemia of pregnancy.
Mas ani stated that toxaemia and abruptioplacenta in combination is
associated with foetal loss of utmost I 00 per cent.
49
In placenta previa, 25 years ago, foetal loss during vaginal delivery
was 60 to 70 percent. Now in placenta previa with C.S. perinatal loss has reduced
to 30 percent.
According to M.C. Browne ( 1973) perinatal deaths in preeclampsia
is commonest in primigravidae and in women aged 5 or over. It is commoner in
short than in tall women and in social class IV and Vas opposed to social class I.
Virna! Parikh et a!. 1 197 5) reported perinatal mortality in toxaemia
of pregnancy 156/1000 while total P.N.M. rate 32/1000, also reported perinatal
loss was more when accidental haemorrhage appears preterrn with low birth weight
infants. The severe variety of accidental haemorrhage, the more is the perinatal
loss.
Helan Weightman et al. ( 1978) concluded that 7 out of I 0 perinatal
deaths were in the category of eclampsia.
Agrawal (1979) reported that due to toxaemia of pregnancy P.N.M.
was observed to be 13.3 percent m Raipur.
(18) DIABETES:Allen (193 9) reported that even properly controlled diabetes in pregnancy is accompanied by a foetal mortality much greater than normal.
Pederson eta!. (1956) reported that foetal monality was 38 percent
( 1926 to 1945) before introductwn of strict treatment. Since then mortality has
reduced to 27 percent (1946-1952) and 15 percent in 1953-1955.
Pederson eta!. ( 196-l) reported that congenital malformations seems
to be three times more common in infant of diabetic mother as compared to
normal, in whom incidence reported is 6.4 percent. The frequency of fatal and
multiple malformations is about six times higher than in general population.
50
Stallworthy et al. reported that long standing diabetics are more prone
to develop toxaemia of pregnancy. 25 percent of perinatal loss of all diabetic
patients have hypertension, chronic renal and vascular disease and are known to
cause placental infarction, foetal hypoxia, premature labour and in severe cases
intrauterine deaths. Inevitably, they must contribute the unavoidable foetal loss.
Overall P.N.M. in untreated cases reported 40 percent, 50 percent
while in properly treated cases perinatal mortality is decreased to IO-IS percent.
Briendstrup reported prophylactic treatment, making the babies more
like normal babies in different ways, especially as regards neonatal blood sugar
level, weight and length, volume of liquor amnii and foetal mortality.
(19) SYPHILIS:Browne (I 922) examined 35 cases in which causes of death was put
down as syphilis. They died within a week or some gasped only once or twice and
died soon after birth.
Browne et al. (I 964) reported that about one in every ten of all macerated foetal is syphilitic. The cause of death is the chronic inflammation of the
placental villi, which destroys the foetal vessels.
In syphilitic and in premature infant in which the vessels are particularly apt to give way under strains a fairly acute congestion of lungs occurs, the
capillaries in the alveolar walls may give way and suddenly flood the air passages
with blood, invariably causing sudden death, the only proceeding physical sign
being the blanching ofthe skin or epiataxis.
Agrawal (1979) reported that P.N.M. was 13.08% due to Syphilis.
Russell (I 989) reported that in a study in Zambia, Syphilis account
for 20% of spontaneous abortion, 40% of stillbirths and 30% of perinatal
mortality.
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51
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(20) RHESUS (Rh) INCOMPATIBILITY:Carld Henry Devis reported first pregnancy with maternal Rh
antibodies resulted in 7 to 8 per cent of still birth.
Women with Rh antibodies and previous still birth or severely
diseased newborn have 60 to 70 percent chances for a still birth in subsequent
pregnancy. Browne eta!. (1964) reported that 10 per cent oferythroblasttic infants die in utero and are born macerated.
Usher ( 1971) reported that immunization accounted for 5.2 percent
of all perinatal deaths and all these deaths were due to Rh. '0' isoimmunization.
Pathak (1972-74) reported P.N.M. due to Rh. incompatibility to be 1.2%.
Bro~ne eta!. reported that about I 0% of erythroblastic infants die
in utero and are macertated. Mollison (1975) reckoned that somewhere between
5 and 10% of all S.B. are due to haemolytic diseases. The foetus usually dies in
utero characteristically about 6 weeks before term. Ajit Mehta (1975) reported
P.N.M. due to Rh. incompatibility to be 1.4%.
(21) ABO BLOOD GROUP INCOMPATIBILITY AND FOETAL WASTAGE:The most different effects of selection on blood groups can be best
discerned by analysing the haemolytic diseases of newborns which result in still
births in some cases or in some cases baby dies shortly after birth or in some
cases it results at least in abortions or jaundice. Cohen and Sayre's (1968) study
in New York City shows that the risk offoetal death is greater in the ABO incompatibility than in the Rh. The blood group incompatibility influences the fertility
and mortality rates and also the viability of certain blood group phenotypes in
populations, (Hirszfeld and Zhorowsky, 1926; Levine, 1943 Waterhouse and
Hogben Levine ( !9-l3 and 1958). There is evidence which suggests that the sperms
carrying the A or B blood group genes tend to be eliminated because they are
serologically incompatible with the anti A or anti B antibody found in the cervical secretion of mother. Charkraverty and Chakravery ( 1977) observed that ABO
incompatibility manifests its harmful effects in early pregnancies. Satyanarayan
52
et. al ( 1978) also concluded that, there are more number of prenatal deaths in
ABO incompatible than ABO compatible mating. (Cited from Sharma and
Chakravery 2002).
(22) ANOXIA:By anoxia is meant interference of oxygen supply reaching the foetus, may be in the mother, in the placenta or in the umbilical cord (Porter Bound
et all958) and Mehdi et al. (1961).
Characteristic oflesions in foetus depends on the manner in which
the oxygen supply is interrupted.
On the other hand, fetus anoxia resulting from premature separation
of placenta does produce characteristic lesion.
Conditions of umbilical cord like prolapse of cord, cord around the
neck and true knots in the cord are often designated as casual factors in intrapartum
deaths (Bound eta!.).
Abnormal prolonged labour is also a cause responsible for anoxic
deaths.
Large majority of anoxic deaths are associated trauma and stress of
labour, toxaemia, A.P.H. maternal disease, such as C. C. F. anaemia, pyrexia, syphilis and diabetes-(Porter, 1952;Bound eta!. 1961 and Ghosh et al1971).
Kher eta!. (1972), Pathak (1972-74), Gupta (1975) reported P.N.M.
due to anoxia, as 29. 9%. 25.3%, 49.3% respectively.
Sharma et al. ( 1975) reported that the anoxic death accounted for
24. I% of perinatal deaths (S.B. and neonatal deaths).
Ajit Mehta ( 1975) reported that death due to anoxia was 38.42% of
perinatal deaths.
53
Agrawal (1979) reported that P.N.M. was very high due to anoxia
(52.9%). Bhargava (1988) reported that P.N.M. would be higher in case of anoxia.
(23) BIRTH TRAUMA:More than 50% of birth injuries are seen among breech and forcep
deliveries . Birth trauma in about 35% of cases was probably intracranial injuries
lie tentorial tears mvolving the unsupported sinus, were due to excessive
moulding and rupture of tributaries of the great vein ofCalen (Stoewene, 1959)
resulting into excess1ve venous engorgement.
In cases of difficult deliveries head is more often injured than other
region and severe mtracranial lesion are liable to cause death, as a result of
pressure exerted by extravasated blood on medulla.
Premature infants are more liable to suffer from intracranial
haemorrhage. The same degree oftraumamight have little or no influence on the
vessels of a full term infant (Stovowene, 1959).
Birth trauma was responsible for causing perinatal deaths in 10%
Claireaux (1958), 11% Bound et al. (1956) ,4.6% Kurilece and Downe (1956).
Agrawal (1979) reported that P.N.!\1. was 4% due to birth trauma.
Gupta ( 1997) et al. reported that P.K\.1. was 6.22% with birth trauma.
(24) RESPIRATORY DISTRESS SYNDR0:\IE :A)
Hyaline membrane diseases.
B)
Massive mtraalveolar haemorrhage.
C)
Pulmonary oedema.
These three may exist either singly or in combination.
Browne ( 1922) reported 26.25% perinatal deaths, the cause of death
was found to be pneumonia during the first week of life.
54
He claimed that premature infants are about 14 times as liable to die
from pneumonia as the infants born at full term.
I.
Atelectasis is a pre-disposing factor in the causation of pneumonia.
2.
Premature rupture of membranes can allow antenatal infection to
occur and that child may be bom suffering from pneumonia in an
advanced stage.
3.
Acute haemorrhagic pneumonia of infants form a distinct clinical and
pathological entity which gives rise to sudden death of infant who may
be apparently healthy either full term or premature.
Butler et a!. (1963) reported that first week deaths were associated
with high incidence of R.D.S., hyaline membrane
15%, intraventricular
haemorrhage 6.4% and neonatal deaths with no histological lesion 8. 7%.
Pulmonary syndrome commonly occurs in premature births, it is also
frequent association with caesarean section.
Usher (1971) reported that 7.5% of perinatal deaths over lOOOgm.
R.D.S. was a syndrome of pre-maturity, never responsible for deaths in infants
delivered beyond 36 weeks. Pathak (1972-1974) reported P.N.M. due to R.D.S.
0.8%. Maternal disease accounted for 10% perinatal deaths. These deaths are
mainly due to R.D.S. ( C',te,{
\-Ya}ct
f\ ....-«.vcJ 1-· \ '?t-~)
0
Browne (Cardiff) stated that pulmonary hyaline membrane disease
is important cause of many neo-natal deaths especially in premature babies and
those delivered abdominally especially from diabetes mothers was of endogenous
vascular origin.
Browne thought it was likely that early ligation of cord in the
presence of delayed onset of breathing was an etiological factor.
He concluded that newborn baby had considerable tolerance to
anoxia but very little to Ischaemia.
55
Agrawal (I 979) reported that P.N .M. was 1. 7 per cent due to
respiratory distress syndrome.
Bhargava (I989) reported that P.N.M. was 45.3 per cent due to
respiratory infection.
(25) INFECTION :It has been well documented that premature rupture of membranes,
obstructed labour, and long intervals between rupture of membranes and birth of
child have a deleterious influence on perinatal mortality.
Usher (I 97 I) claimed that infection accounted for I 3 percent of
neonatal and 6.1 per cent of peri-natal deaths. Deaths were due to acute infections. Lethal outcome is practically restricted to very premature infant dying soon
after birth from pneumonia acquired in utero after long rupture of membranes and
infant developing infection because of invasive instrumentation.
Mathur et al.(1950)reported 9.1 percent, Mehdi et al.(196I) 6 per
cent, Ghosh eta!.( I 969-70) 13.5 per cent, Sharma eta!. (I 971) 3.0 percent, Kher
et al.(l972) 7.2 percent, Pathak (1972-74) 3.9 percent, Ajit Mehta (1975) 8.2
percent, Russell (1989) 30 percent P.N.M. due to infection. (Cited from Agrawal
I.l979).
(26) CONGENITAL MALFORMATIONS:Available information indicates that congenital malformations are
more common among premature than among mature infants. Potter has said that
'In our experience about one half of all infant with major malformations are
delivered prematurely'. In addition, the rule that congenital malformations play in
causing deaths of premature infants is undeniable.
Warkany introduced his discussion of the causes of congenital
malformations as structural or functional defects present at birth. They may be
gross or microscopic, on the surface of the body or within it, familiar or
sporadic, hereditary or non-hereditary and single or multiple.
56
Nair et al.(l966) reported that there were 5.86 percent perinatal
deaths due to gross congenital malformation. These include anencephalic,
hydrocephalus, exemphalos and meningomyelocoele.
Robert H. Usher (1971) reported that unexplained S.B. prior to
labour, along with lethal malformations provide the largest residue of P.N. death
for which prevention seems to be impossible even with the optimum utilization of
modem techniques.
A certain amount of increase of the relative percentage of deaths
due to congenital defects has consequently been recorded (Sharma et al. 1972).
Kher eta!. (1972) Pathak (1972-74) and Gupta (1975) reported
P.N.M. due to congenital malformation 15.0 percent, 14.5 percent and 15
percent respectively
Sharma et a!. (1975) reported that congenital malformations
accounted for 15.7 percent perinatal deaths.
Brown eta!. in their study proved that congenital malformation were
responsible for one in every 30 infant deaths and today one in every five infant
deaths is due to these causes.
Wagh (1975) during his study on congenital malformation since last
8 years in Kamla Raja Hospital, Gwalior, reported the incidence of 5.7 percent
while in western countries the incidence of congenital malformations accounted
as 15 percent of total perinatal mortality.
Ajit Mehta (1977) reported 3.5 percent congenital malformation in
infants following breech presentation. Agrawal (1979) reported that due to
congenital malformation P.N. M. was 6.0 percent. Kaushik et al. ( 1998) reported
that neonatal mortality was 11.6 and 9. 7 due to congenital malformation in AIIMS
and PGl respectively.
57
(26) IRON DEFICIENCY ANAEMIA:Iron deficiency anemia of pregnancy is generally detected in the third
trimester and is responsible for high maternal and infant mortality rate (Shah &
Shah 1979). Data from hospital studies and the available mea,._-e informaJition
from community based surveys regarding the prevalence of anaemia in pregnancy
has remained uncluttered over the past three decades and remain the major nutritional problems associated with maternal and perinatal morbidity and mortality
(Hingorani and Kihara 1976, Mukherjee 1976). About 25 percent maternal death
have been attributed to anaemia of the pregnant women in the poor income group,
50-60 percent had haemoglobin level below I 0 g/dl during the last three months
of pregnancy (Rajlaxmi 1975). Widespread prevalence of iron deficiency
anaemia is also seen in several series of pregnant women of the poor socioeconomic groups according to the ICMR (1975).
The fall in maternal haemoglobin below llg/dl was associated with a
significant rise in perinatal mortality rate, which increased, by two to three folds
as maternal Hb level -fall below 8g/dl shows a significant decrease in the birth
weight due to increased prematurity rate and intrauterine growth retardation. A
steep rise of maternal mortality rate was a sequel to Hb level below 5 g/dl (Prema
et.al 1991 ).
Severe anaemia during pregnancy can lead to maternal morbidity, and
mortality, incidence of! ow birth weight (LBW). In pregnant women Hb level less
than 11 g/ dl and haematocrit value less than 3 3. 0 percent are considered as
anaemic (ICMR 2002).
58

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