This document discusses Rh isoimmune disease, which occurs when a pregnant woman has Rh-negative blood and her baby has Rh-positive blood. It begins by explaining the differences between isoimmune and autoimmune diseases. It then covers blood group systems like ABO and Rh, how they are inherited, and the importance of compatibility for transfusions. The majority of the document focuses on Rh incompatibility during pregnancy, how it can harm the fetus, diagnosis, and treatments like intrauterine transfusions, early delivery, and phototherapy or exchange transfusions for the newborn. It emphasizes the need for Rh-negative mothers to receive Rh immunoglobulin injections during and after pregnancy to prevent sensitization.

1. PRESENTED BY
MS. SANCHAYEETA DEY
ISO-IMMUNE
DISEASE

2. • Iso - immune – Means immune disease
in which the antibodies are produced as
a result of antigens from another person.
• Autoimmune – in which the antigens
come from the same person.

4. •The differences in human blood are due to the
presence or absence of certain protein molecules
called antigens and antibodies.
•The antigens are located on the surface of the
RBCs and the antibodies are in the blood plasma.
•Individuals have different types and
combinations of these molecules.
•The blood group you belong to depends on what
you have inherited from your parents.

5. •There are more than 20 genetically determined
blood group systems known today
Eg. ABO System,Rh-System, MNS System, Kell
System, Lewis System
•The AB0 and Rhesus (Rh) systems are the most
important ones used for blood transfusions.
•Not all blood groups are compatible with each other.
Mixing incompatible blood groups leads to blood
clumping or agglutination, which is dangerous for
individuals.

6. Major Blood Grouping System:
⚫ ABO blood group system
⚫ Rh blood group system because they cause
major transfusion reaction.
Minor Blood Grouping System:
⚫ MNS blood group system
⚫ Blood group system because they cause minor
transfusion reaction.
Familial Blood Grouping System:
⚫ Kell, Daffy, Lutheran, Lewis, Deigo, and Many
more.

7. According to the ABO blood
typing system there are four
different kinds of blood types: A,
B, AB or O (null).

8. • It was given by Karl Landsteiner in 1900.
• It states that ; If an agglutinogen is
present on the RBC of an individual, the
corresponding agglutinin must be absent
in the plasma of that individual and vice-
versa.
• This law is only applicable to ABO blood
grouping system.

9. Blood group A
If you belong to the blood
group A, you have A
antigens on the surface of
your RBCs and B
antibodies in your blood
plasma.
Blood group B
If you belong to the blood
group B, you have B
antigens on the surface of
your RBCs and A
antibodies in your blood
plasma.

10. Blood group AB
If you belong to the blood group AB,
you have both A and B antigens on
the surface of your RBCs and no A
or B antibodies at all in your blood
plasma.
Blood group O
If you belong to the blood group O
(null), you have neither A or B
antigens on the surface of your RBCs
but you have both A and B antibodies
in your blood plasma.

12. Blood
Group
Antigens Antibodies Can give
blood to
Can receive
blood from
AB A and B None AB AB, A, B, O
A A B A and AB A and O
B B A B and AB B and O
O None A and B AB, A, B, O O

13. Blood group O is called
"universal donor"
because it has no antigens
on RBC.
Blood group AB are called
"universal
receivers“ because it has
no anti- bodies in the
plasma.

15. • The Rhesus factor gets its name from
experiments conducted in 1937 by scientists
Karl Landsteiner and Alexander S. Weiner.
• Their experiments involved rabbits which,
when injected with the Rhesus monkey's red
blood cells, produced an antigen that is
present in the red blood cells of many
humans.

16. •The genotype is determined by the inheritance of 3
pairs of closely linked allelic genes situated on
chromosome 9 named as
D/d,
C/c,
E/e
……….. (Fisher- Race theory)

17. • A condition that occurs during pregnancy if
a blood and her blood. Mother’s body
create Rh antibodies against the baby’s
blood.
• Also known as haemolytic disease of the
fetus and newborn(HDFN).
18

18. • First demonstrated in rhesus monkey
• Blood groups are classified as Rh
positive and Rh negative

19. •The Rh factor , Rh+ and Rh- usually refers
specifically to the presence or absence of antigen-
D
•There are two alleles, or genetic variants , of this
antigen: D and d.
•A person who is Rh- has two recessive traits, dd.
Anyone who has at least one D-DD or Dd-is Rh+

20. • A person's Rh type is generally most relevant
with respect to pregnancies
• If the pregnant woman and her husband are
Rh negative, there is no reason to worry about
Rh incompatibility

21. •If she is Rh negative and her husband is Rh
positive,the baby will inherit the father's blood
type ,creating incompatibility between mother
and her fetus.
•If some of the fetal blood gets into mother's
blood stream, her body will produce antibodies.
•These antibodies could pass back through the
placenta and harm the developing baby's red
blood cells, causing very mild to very serious
anemia in the fetus.

22. 23
1.Rh-ve mothercarryingRh+ve
fetus
2.Entry of fetus Rh+ve RBC into
maternalcirculation
3.Development of Rh antibodies
by the mother

23. •Usually placenta acts as barrier to fetal blood entering
maternal circulation. However, sometimes during
pregnancy or birth,fetomaternal haemorrhage (FMH)
can occur. The woman’s immune system reacts by
producing anti-D antibodies that cause sensitisation

25. •In subsequent pregnancies antibodies can cross placenta
and destroy fetal erythrocytes. The haemolytic disease of
fetus and new born caused by Rh isoimmunisation can
occur during the first pregnancy, but usually sensitisation
during the first pregnancy or birth leads to extensive
destruction of fetal RBC during subsequent pregnancies

26. • Miscarriage
• Abortion
• Feto-maternal haemorrage

27. • Rh incompatibility can cause symptoms ranging
from very mild to fatal.
• Mildest form- Rh incompatibility:
1-Hemolysis (Destruction of the red blood cells)
with the release of free hemoglobin into the
infant's circulation.
2- Jaundice (Hemoglobin is converted into,bilirubin
which causes an infant to become yellow.

30. 1- Hydrops fetalis (Massive fetal
red blood cell destruction).
It causes
anemiaFetal heart
failure Death of the infant
shortly after delivery.

31. 3 Respiratory distress (if the infant has been delivered)
4 Circulatory collapse.
5 Kernicterus. (Neurological syndrome in extremely
jaundiced infants)
6 It occurs several days after delivery and is
characterized initially by...
A)Loss of the Moro reflex.
B)Poor Feeding.
C) Decreased activity

32. • At last it may lead to death of the child
immediately after its birth

34. 1 There are no any physical symptoms can be seen
in rh incompatibility.
2 If the woman just found out she is pregnant,she
should undergo blood-type test. This test
determines her blood type and Rh factor.
3 Blood test that will determine whether she is Rh
positive or Rh negative

35. • Intrauterine transfusion
• Elect time of delivery
• Exchange transfusion after delivery
• Phototherapy after delivery
• Top-up transfusion
(Hb falls below 7g/dl, prophylactic :oral folate)
36

36. • The fetus can die in utero from severe anaemia and
hydrops before he can be delivered.
• An intrauterine transfusion can prolong the life in
utero of a fetus to a gestation where the risks of
prematurity are estimated as being less than those
of the Rh disease. This can be done by an:
1.Intraperitoneal transfusion guidedby ultrasound.
2.Umbilical veintransfusion guided by ultrasound.
37

37. Rh-negative
blood
is either transfused
under ultrasoundcontrol. Repeat as
necessary, accordingto amniotic optical
density, or fetal haematocrit. The
intravenous route is becoming increasingly
the preferred method.

38. Choose time of induction and best
method of delivery
• Balance the risks of prematurity (too soon) with
that of worsening Rh disease (too late).
• Consider the risks of vaginal delivery and be
prepared for a lower segment Caesarean section
(LSCS).
• Usually done only after 34 weeks of gestation.
• The paediatric team should be in close and a
senior paediatrician present at the delivery
• Fresh Rh-negative blood available.
39

39. • Good resuscitation is
essential. In an anaemic.
premature infant, lung
disease is common. It can
be due to:
 Surfactant deficiency at
very early delivery.
 Pulmonary oedema from
anaemia and
hypoproteinaemia.
 Hypoplastic lungs
secondary to pleural
effusions.
• In severe Rh haemolytic
disease of the newborn, an
umbilical artery catheter
should be inserted as soon
as possible to assess and
control PaO2 and pH.
• Central venous pressure
should be measured.
 Drain pleural effusions and
ascites at resuscitation.
40

40. Indication for exchange
Transfusion:
1. Early: Decisionmainly based
oncord
(in addition consider history of
previously affected babies).
• Cord haemoglobin <12g/dl.
• Strongly positive Coombs’ test.
• Cord bilirubin >85mmol/l.
2.HaemoglobinLate:
Usually donefor
hyperbilirubinaemia.
• The aims:
 Treat anaemia.
 Washes out IgG antibodies.
 Decreases degree of
haemolysis.
 Removes bilirubin.
 Prevents kernicterus.

41. • Placing newborn baby under a halogen or
fluorescent lamp with their eyes covered.
• Lowers the bilirubin levels in the baby’s blood
through photo-oxidation.
• During phototherapy, intravenous hydration is
required.
42

43. • Anti-D immunoglobulin to all Rh-negative women
at 28 and 34 weeks routinely-RAADP Or give anti-
D immunoglobulin
if she has a:
 Therapeutic abortion.
Spontaneous abortion/ectopic pregnancy.
 Amniocentesis.
 Any bleeding in pregnancy/threatened miscarriage.
 External Cephalic Version.
 After delivery at any gestation within 72Hours.
44

44. DIAGNOSIS
Risk for injury from breaking down products of RBCs
in greater numbers than normal and functional
immaturity of the liver.
Goals
• Will receive appropriate therapy to accelerate
bilirubin excretion.
• Will experience no complications from phototherapy.
• Will experience no complications from exchange
transfusin.

45. • Interrupted family process R/T infant with
potentially adverse physiologic response.
• Family will receive emotional support.
• Family will be prepared for home care of the
neonate.

46. • NURSING CARE for Rh incompatibility DURING
PHOTOTHERAPY
1.Remove clothing to proper skin exposure.
2.Turn infant frequently to expose all skin area.
3.Record and report jaundice and blood levels of
bilirubin.
4.Record and report if any change in body
temperature

47. -Be sure the eyes close before applying eye patch
to prevent corneal irritation.
-Should be loose enough to avoid pressure.
-Eye patches should be changed every 8houly and
eye care given.
6.Nurse should expect the infant’s stools to be
green and the urine dark because of photo
degradation products.

48. 7. Serum bilirubin and hematocrit should be
monitored during therapy and for 24 hours
following therapy.
8. In case of breast milk jaundice stop breast
feeding temporarily.
9. Maintain feeding intervals to prevent
dehydration.

51. Oct-15 Rhesus Incompatibility 53

54. • In addition to cases in which a fetus dies during
delivery as
deprivation
a result of asphyxia
if the umbilical cord
(oxygen
becomes
twisted) or difficult labor.
• Others can die in utero before labor starts.
followed by expulsion of the fetus from the
uterus within a few days.
• However, in rare instances the dead fetus is not
expelled from the uterus at once, but is retained
for several weeks.

55. • Fetal death refers to the spontaneous death of
a fetus at any time during pregnancy, although
the term is often used interchangeably with
‘stillbirth’.
• A stillbirth is a death that occurs after 20
weeks of gestation.

56. Intrauterine fetal death: is the clinical term for
the death of a baby in the uterus, during
pregnancy and before birth. The term is
usually used for pregnancy losses that
happen after the 20th week of gestation.

57. •In the present investigation the epidemiological
factors responsible for intrauterine fetal deaths
after 20 week of gestation were studied.
•A retrospective study
registered and managed
of 16882 pregnancies
in the Department of
Obstetrics and Gynecology, in united state

58. One hundred and three cases of intrauterine
fetal deaths were registered and treated
expectantly out of 16882 total pregnancies
registered during the four year study period.

59. Pregnancy complications:
- Pre-eclamptic toxemia
- Antepartum haemorrhage : placenta previa,
abruptio placentae
Pre- existing medical disease and acute
illness:
- Chronic hypertension
- Chronic nephritis
- Diabetes
- Severe anemia
- Hyperpyrexia
- Syphilis, Hepatitis, toxoplasmosis etc.
Hyperpyrexia

60. • Fetal
- Congenital malformation
- Rh-incompatibility
- Post maturity
• External version
• Idiopathic 20 –30%

61. • Maternal Complications
• Decreased platelets
• Decreased fibrinogen
• Increased PT/PTT (Clotting times)
• Clinical bleeding / oozing from all sites
RX involves DELIVERY, pRBC’s, FFP, PLATELETS,
Supportive Management

62. • Depression, Anxiety, Psychosocial
• Anxiety with future pregnancies
• May have repeat losses (depending on causes)
• Bleeding ---> can lead to DIC but may only
require blood product replacement
• Pain, Infection (similar to any other delivery)

63. •Multiple pregnancy
•Advanced maternal age
•History of fetal demise (IUFD)
•Maternal infertility
•Maternal haemoconcentration
•Maternal colonization with certain pathogens
•Small for gestational age infant
•Obesity
•Paternal age
•African American race

64. • Absence of fetal movement
• Vaginal bleeding
• Abdominal pain
• Small uterus than the duration of pregnancy
• Sometimes secretion of colostrum occur few
days after death of fetus in uterus.

65. • In most patients, the only symptom is decreased
fetal movement. An inability to obtain fetal heart
tones upon examination suggests fetal demise;
however, this is not diagnostic and death must be
confirmed by diagnostic tests .
• Labor should be induced as soon as possible after
diagnosis. Patient responses vary in regard to this
recommendation; some wish to begin induction
immediately, while others wish to delay induction
for a period of hours or days until they are
emotionally prepared.

66. • Blood test because it comes negative within a
week after the death of the fetus.
• The secretion of estriol it is a type of estrogen
produced by an active placenta in the
mother’s urine falls sharply.

67. • Explain the problem to the woman and her
family. Discuss with them the options of
expectant or active management.
• Medical induction of labor: Medicine is used
to start labor and fetus delivered naturally.

69. • Pain management in patients undergoing
induction of labor for fetal death is usually easier
to manage than in patients with live fetuses.
• Higher doses of narcotics are available to the
patient and often a morphine is sufficient for
successful pain control. Should a patient desire
superior pain control to intravenous narcotics,
epidural anesthesia should be offered.

71. Diagnosis
Anticipatory grieving related to fetal loss
Intervention
• To give the patient time to gather support
from her family and to fathom the reality of
the situation.
• Provide psychological support.
• Provide counseling to the mother as well as
family.

72. Nursing health care guidelines at home
• Teach the patient to be aware of the signs and
symptoms that could indicate postpartum
complications:
• Pain in the calf of the leg; increase in vaginal
bleeding; foul odor of vaginal discharge; fever;
burning with urination; persistent mood charge;
or a hard, reddened area on the breast.

73. • Explain that the patient
intercourse or drive a car until
should not have
after the
postpartum check.
• Encourage participation in a bereavement
support group, even if the patient and
significant other seem to be coping with the
loss.
• They may be able to help other couples cope.

77. SGA

78. • Cellular hyperplasia
• Hyperplasia and hypertrophy
• Hypertrophy

79. • Stage I (Hyperplasia)
- 4 to 20 weeks
- Rapid mitosis
- Increase of DNA content

80. • Stage II (Hyperplasia & Hypertrophy)
- 20 to 28 weeks
- Declining mitosis.
- Increase in cell size.

81. • Stage III ( Hypertrophy)
- 28 to 40 weeks
- Rapid increase in cell size.
- Rapid accumulation of fat, muscle and
connective tissue.
• 95% of fetal weight gain occurs during last 20
weeks of gestations.

82. • Maternal factors
• Fetal factors
• Placental factors
• Environmental factors

83. •Medical disease
•Malnutrition  BMI < 19 twice the risk of
IUGR
•Multiple pregnancy
•Smoking (460 gm < then none smoker)

84. •Alcohol
•Drugs
second
 12-fold increase risk of IUGR
 Beta- Blockers(Atenolol in
trimster, Anticoagulants,
Anticonvulsants( phenytoin)
•Hypoxemia
•Infections  UTI, Malaria,
Infections
TB, Genital

85. • Small stature/ low pre-pregnancy weight
• Teen pregnancy
• Primi gravida
• Grand multiparity

86. • A Chromosome Defect-
 In second trimester 20% SGA fetuses
have chromosomal abnormality



Triploid is most common under 26 wks.
Trisomy-18 is common after 26 wks .
Other are 21(Down’s syndrome), 16, 13,
xo (turner’s syndrome).

87. • Exposure to an infection-
• German measles (rubella), cytomegalovirus,
herpes simplex, tuberculosis, syphilis, or
toxoplasmosis, TB, Malaria, Parvo virus

88. • birth defects
• (cardiovascular, renal, anencephally, limb
defect, etc).
• A primary disorder of bone or cartilage.
• A chronic lack of oxygen during development
(hypoxia
• Placenta or umbilical cord defects.

89. • Uteroplacental Insufficiency Resulting
From -.
–Improper / inadequate trophoblastic
invasion and placentation in the first
trimester.
–Lateral insertion of placenta.
–Reduced maternal blood flow to the
placental bed.

90. • Fetoplacetal Insufficiency Due To-.
–Vascular anomalies of placenta and cord.
–Decreased placental functioning mass-.
• Small placenta, abruptio placenta,
placenta previa, post term pregnancy

93. • High altitude - lower environmental oxygen
saturation
• Toxins

94. •Symmetric IUGR (33
% of IUGR Infants)
•Asymmetric IUGR
(55 % of IUGR)
•Combined type IUGR
(12 % of IUGR)

95. • Height, weight, head circ proportional
• Early pregnancy insult:
• Commonly due to congenital infection, genetic
disorder, or intrinsic factors
• Reduced no of cells in fetus
• Normal ponderal index
• Low risk of perinatal asphyxia
• Low risk of hypoglycemia

96. • The ponderal index is used determine those
infants
normal
whose
for
soft tissue mass is
their
below
stage of skeletal
development.
Ponderal Index = birth weight x 100
crown-heel length

97. • Typical values are 20 to 25.
• Those who have a ponderal index below the
10th % can be classified as SGA
• PI is normal in symmetric IUGR.
• PI is low in asymmetric IUGR

98. • Later in pregnancy:
• Commonly due to utero placental
insufficiency, maternal malnutrition, hypoxia,
or extrinsic factors
• Low ponderal index
• Cell number remains same but size is small
• Increased risk of asphyxia
• Increased risk of hypoglycemia

99. • Growth restriction in the stage of hypertrophy
• Brain sparing effect
• Head growth remains normal but abdominal
girth slows down

103. 1. Normal Small Fetuses-
• Have no structural abnormality,
umbilical artery & liquor but wt., is
less.
normal
• They are not at risk and do not need any special
care.

104. Growth Restricted Fetuses- are due to impaired
function. Appropriate & timely
or termination can improve
placental
treatment
prospects.

106. Dry wrinkled skin
Large head circumference
Old man look
Cartilaginous ridges on pinna

107. Open eyes
Thin umbilical cord
Well defined creases
Normal reflexes
Alert and active
Normal cry

108. • Scaphoid abdomen

109. • Signs of recent wasting
- soft tissue wasting
- diminished skin fold thickness
- decrease breast tissue
- reduced thigh circumference
• Signs of long term growth failure
- Widened skull sutures, large fontanelles
- shortened crown – heel length
- delayed development of epiphyses

110. • History
• Risk factors
• Last menstrual period - most precise size of
uterus
• Time of quickening (detection of fetal
movements)
• Examination
• Maternal serum screening

111. - Notching of the waveform /reduce EDF
associated 3-fold increase in risk of FGR.
• Combination of un-explain elevated maternal AFP
is powerful predictor of adverse perinatal
outcome (FGR)
• Increase AFP combine with echogenic bowel is
strong predictor of FGR

112. • DOPPLER OF THE UMBILICAL ARTERY
• Reduced end diastolic flow.
• Absent end diastolic flow
• Reversed end diastolic flow( severe cases)

116. • Hypoxia
- Perinatal asphyxia
- Persistent pulmonary hypertension
- meconium aspiration
• Thermoregulation
-Hypothermia due to diminished
subcutaneous fat and elevated
surface/volume ratio

117. - Hypoglycemia
- result from inadequate glycogen stores.
- diminished gluconeogenesis.
- increased BMR
- Hypocalcemia
- due to high serum glucagon level, which
stimulate calcitonin excretion

118. • Hematologic
-hyperviscosity and polycythemia due to
increase erythropoietin level sec. to hypoxia
• Immunologic
-IUGR have increased protein catabolism and
decreased in protein, prealbumin and
immunoglobulins, which decreased humoral
and cellular immunity.

119. • Fetal distress,
• Hypoxia, Acidosis and Low Apgar Score at
birth.
Increased perinatal morbidity and mortality
• Grade 3-4 intraventricular haemorrhage
• Necrotizing enterocolitis

120. • BIOPHYSICAL
• HC:AC
• Brfore 32 wks
• 32—34 wks
more than 1
app 1
• FEMUR LENGTH
• FL:AC IS 22at all gest wks from 21 wks to term
• More than 23.5 indicate IUGR

121. • AFI
• <2 Suggest IUGR
• PI

122. • MUMMIFICATION
• KMC
• NESTING
• DELAY BATH
• WARMER

123. • VENTILATOR
• C PAP
• 02 SUPPLEMENTATION

124. • <30– IV FLUIDS, NG ,KATORI, BREAST FEEDS
• 30—34 NG ,KATORI, BREAST FEEDS
• >34 KATORI, BREAST FEEDS

125. • Vital signs
• Activity and behaviour.
• Color; Pink, pale, grey, blue, yellow.
• Tissue perfusion
• Fluids, electrolytes and ABG's.

128. • Bronchopulmonary dysplasia
• Metabolic disturbances and hypoglycemia
• Polycytemia
• Hypothermia
• Impaired cognitive function and cerebral
paresis

129. • ASPIRIN THERAPY
• Other forms of treatment that have been
studied are
• nutritional supplementation,
• zinc supplementation,
• fish oil,
• hormones and
• oxygen therapy

130. Diagnosis
• Impaired nutritional status less then body
requirement related to malnutrition.
Intervention
• To correct malnutrition by providing balanced
diet.
• To take extra calories from normal i.e. 300
calories extra.
• To provide nutritious foods, juices, fruits etc.

131. Diagnosis
• Decreased uteroplacental circulation related
to reduced blood flow to maternal surface or
placental cause.
Intervention
• Adequate bed red in left lateral position.
• Provide low dose of aspirin i.e. 50 mg daily.
• Prove o2 to mother at the rate of 2.5 L/min by
nasal prong for short term for prolongation of
pregnancy.

132. Diagnosis
• Decreased knowledge status of mother
related to IUGR, its complication to baby.
Intervention
• Provide knowledge to the mother.
• Provide health education to mother related to
self care as well as related to diet.
• Provide detailed information about her
condition of baby as well as complication for
baby.

133. Risk for infection related to poor immunity
Goal
Care at neonatal intensive care unit
Intervention
• The NICU should be warm, free from excessive sound
smoothing light.
• Protection from infection should be ensured by aseptic
measures and effective hand washing.
• Rough handling and painful procedure should be
avoided.
• Baby should be placed on soft comfortable, “nestled”
and cushioned bed.
• Continuous monitoring of the baby’s clinical status are
vital aspects.

134. Decreased body temperature related to IUGR
Goal
Maintenance of stable body temperature
Intervention
• Baby should be received in a pre warmed radiant
warmer or incubator. Environmental temperature
should be maintained according to baby’s weight
and age.
• Baby’s skin temperature should be maintained 36.5
to 37.5 degree celcious.
• Baby birth weight of less than 1200gm should be
cared in the NICU incubator with 60 to 70 %
humidity, oxygen and thermo nutral environment
for better thermal control and prevent heat loss.

135. Decreased body weight of baby related to IUGR.
Goal
Maintenance of nutrition and hydration
Intervention
• Caloric needs of non-growing LBW babies during first
week of life are 60 kcal/ kg/ day on 7th is to be
stepped up gradually to 100 on 14th day and about
120-150 on 21st day, to maintain satisfactory
growth.
• Human milk is the first choice of nutrition for all LBW
babies. Colostrums, hind milk, foremilk, and preterm
milk help faster growth of baby.
• If breast milk is not available cows milk in proportion
of 1:1 (milk: water) for 1st month and 2:1 during
second month is an alternative substitute.

136. AND
SUMMARY

137. TITLE - Study of causes and complications of intra
uterine fetal death (IUFD)
OBJECTIVES - This study were to study the causes of
Intra Uterine Fetal Death (IUFD), associated
complications and to suggest preventive measures.
METHODS - Study design: retrospective observational
study. This study was carried out over a period of 3
months (April 2014- June 2014) at a tertiary care
hospital. Inclusion criteria was all IUFD >20 weeks of
gestation.

138. Out of 1850 total births during the study period
80 IUFD occurred. Hence proportion of IUFD
was 4.3%. In this study, Still Birth Rate (SBR) as
per WHO criteria (28 weeks) was 22.1 per 1000.
Registered patients were 24 (30%) whereas 56
(70%) were emergency admissions. Majority of
cases, 48 (60%) were multigravidae with past
obstetric history of abortion and IUFD in 13
(16.2%) and 9 (11.2%) respectively. In 31
(38.7%) no identifiable cause of IUFD was found
whereas cause was identified in 49 (61.3%).

139.  who
had
who had
 care.A significant proportion of IUFD is
Anemia, PIH, accidental haemorrhage were
leading causes of IUFD. Majority of women
IUFD were emergency admission
not received adequate antenatal
preventable by health education to patients
and community for regular antenatal care,
about warning signs during antenatal period,
hospital delivery and early referral.