INTRAUTERINE FETAL DEATH
PREPARED BY DR KAMILYA
OUTLINE
 INTRODUCTION
 AETIOLOGY
 RISK FACTORS AND CLINICAL FEATURES
 INVESTIGATIONS
 MANAGEMENT
 COMPLICATIONS
 REFERENCES
2
Introduction
 intrauterine fetal death (IUFD) embraces all fetal
deaths weighing 500 g or more occurring
 both during pregnancy (antepartum death) or during
labor (intrapartum). But death of a fetus weighing
 less than 500 g (before 22 weeks) has got a distinct
etiology and is usually termed as abortion.
 antepartum death occurring beyond the period of
viability is termed as intrauterine death.
AETIOLOGY
A. Maternal (5–10%)
 Infections ,chorioamnionitis).
 Rh-incompatibility
 Non-immune hydrops
 Growth restriction
 Hypertensive disorders in
pregnancy
 Diabetes in pregnancy
 Maternal infections (malaria,
hepatitis, in uenza,
 toxoplasma, syphilis
 Hyperpyrexia (temp > 39.4°C)
 Antiphospholipid syndromes
 Thrombophilias: Factor V
Leiden, protein C, protein
 S-de ciency,
hyperhomocysteinemia
 Abnormal labor (prolonged
or obstructed labor,
 ruptured uterus)
 Post-term pregnancy
 Systemic lupus
erythematosus
b. Fetal (25–40%) C. Placental (20–35%)
 Chromosomal
abnormalities
 Major structural anomalies
 Infections (virus,
bacteria
 chorioamnionitis).
 Rh-incompatibility
 Non-immune hydrops
 Growth restriction
 Antepartum hemorrhage
Both placenta previa and
abruptio placentae can cause
fetal death by producing
acute placental insu ciency .
 Cord accident (prolapse,
true knot, cord round the
 neck)
 Twin transfusion
syndrome (TTTS) .
 Placental insu ciency .
AETIOLOGY CONT….
 D. Iatrogenic
 External cephalic version (p. 663)
 Drugs (quinine beyond therapeutic doses
 E. Idiopathic (25–35%)
 Cause remains unknown even with thorough clinical
 examination and investigations
PATHOLOGY
 The dead fetus undergoes an aseptic degenerative process
called maceration.
 The epidermis is the first structure to undergo the process,
whereby blistering and peeling off of the skin
 occur. It appears between 12 hours and 24 hours after
death. The fetus becomes swollen and looks dusky red.
Gradually, aseptic autolysis of the ligamentous structure
and liquefaction of the brain matter and other viscera take
place.
 The changes vary in degree and are responsible for the
characteristic radiological signs.
DIAGNOSIS
 SYMPTOMS—Absence of
fetal movements which were
previously noted by the patient.
 SIGNS: Retrogression of the
positive breast changes that
occur during pregnancy is
evident after variable period
following death of the fetus
 Per abdomen
 Gradual retrogression of the
fundal height and it becomes
smaller than the period of
gestation.
 Uterine tone is diminished
and the uterus feels fl accid.
Braxton-Hicks contraction is
not easily felt.
 Fetal movements are not felt
during palpation.
 Fetal heart sound is absent.
 Cardiotocography (CTG):
Flat trace
 Egg-shell crackling feel of
the fetal head is a late feature
INVESTIGATION
Sonography
 (a) Lack of all fetal motions (including cardiac) during a
10-minute period
(b) Oligohydramnios and collapsed cranial bones
Straight X-ray abdomen
 Spalding sign Th e irregular overlapping of the cranial
bones on one another is due to liquefaction of the brain
matter and softening of the ligamentous structures
supporting the vault. It usually appears 7 days after death.
 .
Investigation cont…
 Hyperfl exion of the spine is more common. In some
cases hyperextension of the neck is seen.
 Crowding of the ribs shadow with loss of normal
parallelism. Appearance of gas shadow (Robert’s sign) in
the chambers of the heart and great vessels may appear as
early as 12 hours but diffi cult to interpret.
 BLOOD—To estimate the blood fibrinogen level and
partia thromboplastin time periodically, when the fetus is
retained for more than 2 weeks
INVESTIGATION CONT…
 Hematological examination
consists of ABO and Rh grouping,
Kleihauer-Betke test, VDRL,
postprandial blood sugar, HbA1C,
urea, creatinine estimations,
thyroid profile, viral serology, lupus
anticoagulant,
 anticardiolipin antibodies and
thrombophilia studies. Urine
examination for casts and pus
cells.
 Thorough examination of the infant
and placenta should be done:
 Infant—for malformations
(skeletal X-ray) umbilical cord for
entanglement, number of
vessels (, placenta for
meconium staining,
 Malformations and the respective
weights are to be recorded
 Autopsy and chromosome
studies are done for fetuses with
anomalies and dysmorphic
features. It is
 also done if there is history of
recurrent stillbirths or if either
parent is a carrier for balanced
translocation.
 Fetal skin, blood are usually taken
for aneuploidy and single gene
disorder study. For cytogenetic
studies
 tissues must contain some viable
cells.
(Spalding sign) and hyperfl
exion of the spine
MANAGEMENT
 EXPECTANT ATTITUDE (NONINTERFERENCE):
 The patient and her relatives are likely to be upset
 psychologically but they should be assured of safety of
noninterference.
 In about 80% of cases, spontaneous expulsion occurs
within 2 weeks of death. The woman with intact
membranes, no evidence of DIC or sepsis may remain at
home with the advice to come to the hospital for delivery.
 Fibrinogen estimation should be done twice weekly.
Methods of delivery
 —The delivery should always be done by medical
induction:
 (a) A combination of mifepristone and a prostaglandin . A
single dose (200 mg) of oral mifepristone and misoprostol
 (PGE1) intravaginal 25 μg 4 hourly are safe, effective and
of low cost. Induction delivery interval was 8 hours.
Mifepristone (600 mg daily for 2 days) alone can be used
for induction .
 (b) Misoprostol (PGE1) 25–50 μg either vaginally or
orally is also found effective every 4hrs
MANAGEMENT CONT….
 Induction of labor in women with previous LSCS: PGE2
gel may be used safely in women with previous one
LSCS, but for women with previous two LSCS, risk
(rupture uterus) is slightly more.
 Place of cesarean section in a case with IUD is limited.
Previous cesarean section (two or more), major degree
placenta previa and transverse lie are the rare conditions.
 Postpartum suppression of lactation: Cabergoline
(dopamine agonist), single dose (1 mg), is found
 effective. It should not be given to women with
preeclampsia or hypertension
INDICATIONS OF EARLY INTERFERENCE
 Psychological upset of the patient—common
 Manifestations of uterine infection
 Tendency of prolongation of pregnancy beyond 2 weeks
 Falling fibrinogen level (rare)
COMPLICATION
 (1) Psychological upset often becomes a problem.
 (2) Infection—As long as the membranes are intact,
infection is unlikely but once the membranes
 rupture, infection, especially by gas forming organisms
like Clostridium welchii may occur. The dead
tissue favors their growth with disastrous consequences.
COMPLICATION CONT…..
 (3) Blood coagulation disorders are rare. If the fetus is
retained for more than 4 weeks (10–20%), there is a
possibility of defibrination from “silent” disseminated
intravascular coagulopathy (DIC). It is due to gradual
absorption of thromboplastin, liberated from the dead
placenta and decidua, into the maternal circulation.
 (4) During labor—Uterine inertia, retained placenta and
postpartum hemorrhage
PREVENTION
 Preconceptional counseling and care is essential to
prevent its occurrence in the high-risk group.
 Prenatal diagnosis —CVS or amniocentesis in selected
cases .
 To screen the “at-risk mothers” during antenatal care
 Careful assessment of fetal well-being and to terminate
pregnancy with the earliest evidences of fetal compromise
REFERENCES
Dutta
THANKS FOR LISTENING

INTRAUTERINE FETAL DEATH_1.pptx

  • 1.
  • 2.
    OUTLINE  INTRODUCTION  AETIOLOGY RISK FACTORS AND CLINICAL FEATURES  INVESTIGATIONS  MANAGEMENT  COMPLICATIONS  REFERENCES 2
  • 3.
    Introduction  intrauterine fetaldeath (IUFD) embraces all fetal deaths weighing 500 g or more occurring  both during pregnancy (antepartum death) or during labor (intrapartum). But death of a fetus weighing  less than 500 g (before 22 weeks) has got a distinct etiology and is usually termed as abortion.  antepartum death occurring beyond the period of viability is termed as intrauterine death.
  • 4.
    AETIOLOGY A. Maternal (5–10%) Infections ,chorioamnionitis).  Rh-incompatibility  Non-immune hydrops  Growth restriction  Hypertensive disorders in pregnancy  Diabetes in pregnancy  Maternal infections (malaria, hepatitis, in uenza,  toxoplasma, syphilis  Hyperpyrexia (temp > 39.4°C)  Antiphospholipid syndromes  Thrombophilias: Factor V Leiden, protein C, protein  S-de ciency, hyperhomocysteinemia  Abnormal labor (prolonged or obstructed labor,  ruptured uterus)  Post-term pregnancy  Systemic lupus erythematosus
  • 5.
    b. Fetal (25–40%)C. Placental (20–35%)  Chromosomal abnormalities  Major structural anomalies  Infections (virus, bacteria  chorioamnionitis).  Rh-incompatibility  Non-immune hydrops  Growth restriction  Antepartum hemorrhage Both placenta previa and abruptio placentae can cause fetal death by producing acute placental insu ciency .  Cord accident (prolapse, true knot, cord round the  neck)  Twin transfusion syndrome (TTTS) .  Placental insu ciency .
  • 6.
    AETIOLOGY CONT….  D.Iatrogenic  External cephalic version (p. 663)  Drugs (quinine beyond therapeutic doses  E. Idiopathic (25–35%)  Cause remains unknown even with thorough clinical  examination and investigations
  • 7.
    PATHOLOGY  The deadfetus undergoes an aseptic degenerative process called maceration.  The epidermis is the first structure to undergo the process, whereby blistering and peeling off of the skin  occur. It appears between 12 hours and 24 hours after death. The fetus becomes swollen and looks dusky red. Gradually, aseptic autolysis of the ligamentous structure and liquefaction of the brain matter and other viscera take place.  The changes vary in degree and are responsible for the characteristic radiological signs.
  • 8.
    DIAGNOSIS  SYMPTOMS—Absence of fetalmovements which were previously noted by the patient.  SIGNS: Retrogression of the positive breast changes that occur during pregnancy is evident after variable period following death of the fetus  Per abdomen  Gradual retrogression of the fundal height and it becomes smaller than the period of gestation.  Uterine tone is diminished and the uterus feels fl accid. Braxton-Hicks contraction is not easily felt.  Fetal movements are not felt during palpation.  Fetal heart sound is absent.  Cardiotocography (CTG): Flat trace  Egg-shell crackling feel of the fetal head is a late feature
  • 9.
    INVESTIGATION Sonography  (a) Lackof all fetal motions (including cardiac) during a 10-minute period (b) Oligohydramnios and collapsed cranial bones Straight X-ray abdomen  Spalding sign Th e irregular overlapping of the cranial bones on one another is due to liquefaction of the brain matter and softening of the ligamentous structures supporting the vault. It usually appears 7 days after death.  .
  • 10.
    Investigation cont…  Hyperflexion of the spine is more common. In some cases hyperextension of the neck is seen.  Crowding of the ribs shadow with loss of normal parallelism. Appearance of gas shadow (Robert’s sign) in the chambers of the heart and great vessels may appear as early as 12 hours but diffi cult to interpret.  BLOOD—To estimate the blood fibrinogen level and partia thromboplastin time periodically, when the fetus is retained for more than 2 weeks
  • 11.
    INVESTIGATION CONT…  Hematologicalexamination consists of ABO and Rh grouping, Kleihauer-Betke test, VDRL, postprandial blood sugar, HbA1C, urea, creatinine estimations, thyroid profile, viral serology, lupus anticoagulant,  anticardiolipin antibodies and thrombophilia studies. Urine examination for casts and pus cells.  Thorough examination of the infant and placenta should be done:  Infant—for malformations (skeletal X-ray) umbilical cord for entanglement, number of vessels (, placenta for meconium staining,  Malformations and the respective weights are to be recorded  Autopsy and chromosome studies are done for fetuses with anomalies and dysmorphic features. It is  also done if there is history of recurrent stillbirths or if either parent is a carrier for balanced translocation.  Fetal skin, blood are usually taken for aneuploidy and single gene disorder study. For cytogenetic studies  tissues must contain some viable cells.
  • 12.
    (Spalding sign) andhyperfl exion of the spine
  • 13.
    MANAGEMENT  EXPECTANT ATTITUDE(NONINTERFERENCE):  The patient and her relatives are likely to be upset  psychologically but they should be assured of safety of noninterference.  In about 80% of cases, spontaneous expulsion occurs within 2 weeks of death. The woman with intact membranes, no evidence of DIC or sepsis may remain at home with the advice to come to the hospital for delivery.  Fibrinogen estimation should be done twice weekly.
  • 14.
    Methods of delivery —The delivery should always be done by medical induction:  (a) A combination of mifepristone and a prostaglandin . A single dose (200 mg) of oral mifepristone and misoprostol  (PGE1) intravaginal 25 μg 4 hourly are safe, effective and of low cost. Induction delivery interval was 8 hours. Mifepristone (600 mg daily for 2 days) alone can be used for induction .  (b) Misoprostol (PGE1) 25–50 μg either vaginally or orally is also found effective every 4hrs
  • 15.
    MANAGEMENT CONT….  Inductionof labor in women with previous LSCS: PGE2 gel may be used safely in women with previous one LSCS, but for women with previous two LSCS, risk (rupture uterus) is slightly more.  Place of cesarean section in a case with IUD is limited. Previous cesarean section (two or more), major degree placenta previa and transverse lie are the rare conditions.  Postpartum suppression of lactation: Cabergoline (dopamine agonist), single dose (1 mg), is found  effective. It should not be given to women with preeclampsia or hypertension
  • 16.
    INDICATIONS OF EARLYINTERFERENCE  Psychological upset of the patient—common  Manifestations of uterine infection  Tendency of prolongation of pregnancy beyond 2 weeks  Falling fibrinogen level (rare)
  • 18.
    COMPLICATION  (1) Psychologicalupset often becomes a problem.  (2) Infection—As long as the membranes are intact, infection is unlikely but once the membranes  rupture, infection, especially by gas forming organisms like Clostridium welchii may occur. The dead tissue favors their growth with disastrous consequences.
  • 19.
    COMPLICATION CONT…..  (3)Blood coagulation disorders are rare. If the fetus is retained for more than 4 weeks (10–20%), there is a possibility of defibrination from “silent” disseminated intravascular coagulopathy (DIC). It is due to gradual absorption of thromboplastin, liberated from the dead placenta and decidua, into the maternal circulation.  (4) During labor—Uterine inertia, retained placenta and postpartum hemorrhage
  • 20.
    PREVENTION  Preconceptional counselingand care is essential to prevent its occurrence in the high-risk group.  Prenatal diagnosis —CVS or amniocentesis in selected cases .  To screen the “at-risk mothers” during antenatal care  Careful assessment of fetal well-being and to terminate pregnancy with the earliest evidences of fetal compromise
  • 21.
  • 22.