Transcript Lecture 10 – Fetal distress. IUFD

Lecture 10
FETAL DISTRESS
DEFINITION
•Fetal distress is the term commonly used to describe
fetal hypoxia
•It is a clinical diagnosis made by indirect methods and
should be defined as:
Hypoxia that may result in fetal damage / death if not
reversed or the fetus delivered immediately
•It includes acute distress and chronic distress
ETIOLOGY
Maternal:
 poor placental perfusion
 hypovolaemia
 hypotension
 myometrial hypertonus
• prolonged labor
• excess oxytocin
ETIOLOGY
Fetal:
 cord compression
• oligohydramnios
• entanglement
• prolapse
 pre-existing hypoxia or growth retardation
 infection
 cardiac
MECHANISM
• There are potentially limitless causes for fetal
distress, but several key mechanisms are usually
involved
• Contractions reduce temporarily placental blood
flow and can compress the umbilical cord
• If a women is in labor longer then this can cause
fetal distress via the above mechanism
MECHANISM
• Acute distress can be a result of:
 placental abruption
 prolapse of the umbilical cord (especially with
breech presentations)
 hypertonic uterine states
 use of oxytocin
• Hypotension can be caused by either epidural
anesthesia or the supine position, which reduces
inferior vena cava return of blood to the heart
• The decreased blood flow in hypotension can be a
cause of fetal distress
SIGNS AND SYMPTOMS
Acute fetal distress
SIGNS AND SYMPTOMS
•
Cardiotocography signs:
 Increased / decreased fetal heart (tachycardia and
bradycardia), especially during and after a
contraction decreased varibility in the fetal heart
rate
 Abnormal fetal heart rate (< 120 or > 160 bpm)
• A normal fetal heart rate may slow during a contraction
but usually recovers to normal as soon as the uterus
relaxes
• A very slow fetal heart rate in the absence of
contractions or persisting after contractions is
suggestive of fetal distress
SIGNS AND SYMPTOMS
• A rapid fetal heart rate may be a response to:
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maternal fever
drugs
hypertension
amnionitis
• In the absence of a rapid maternal heart rate, a
rapid fetal heart rate = a sign of fetal distress
• For a diagnosis of fetal distress to be made, one or
more of the following must be present:
 persistent severe variable deceleration
 persistent and non-remediable late declarations
 persistent severe bradycardia
SIGNS AND SYMPTOMS
• Amniotic fluid is contaminated by meconium
• There are 3 degrees about contaminated
 I - slight contamination
• The color of the amniotic fluid = slight green
 II - mild contamination
• Color of the amniotic fluid = dark green
 III - severe contamination
• Color of the amniotic fluid is dark yellow.
• If the amniotic fluid is severely contamination, it
suggests the, fetal distress - it must be managed as
soon as possible
SIGNS AND SYMPTOMS
• Decreased fetal movement felt by the mother
• Biochemical signs - assessed by collecting a small
sample of baby‘s blood from a scalp prick through
the open cervix in labor:
 Fetal acidosis elevated fetal blood lactate levels
 A fetal scalp pH < 7.2 , Po2 >60mmHg suggests
fetal distress
Chronic Fetal Distress
SIGNS AND SYMPTOMS
• Decreased or disappear fetal movement:
 < 10 times per 12 hours is regarded as decreased
 With the first effect of hypoxia, the fetal movement
is increased
 If the hypoxia persists, the fetal movement is
decreased, and may disappear
 If the fetal movement lost, the fetal heart beat will
be disappearing within 24 hours
Cautions: Dangerous for the fetus if the fetal
movement disappear. Management immediately!!
SIGNS AND SYMPTOMS
• Abnormal cardiotocography signs:
 Slow fetal heart rate(<120bpm) or rapid
fetal heart rate (>180bpm) last more than
10 min in the absence of contractions is
suggestive of fetal distress
 The fetal heart rate > 160 bpm , especially
> 180 bpm, it suggests early hypoxia,
unless the maternal heart rate is faster
SIGNS AND SYMPTOMS
• FHR < 120bpm, typically less than 100bpm
 It is very danger for fetus
• The fetal heart rate normally show continuous
minor variations, with a range of about 5 bpm,
loss of base line variability implies that the
cardiac reflexes are impaired, either from the
effect of hypoxia or of drugs such as valium
 It may be serious
SIGNS AND SYMPTOMS
• Early deceleration: with each contraction the rate
often slows, but it returns to normal soon after
removal of the stress
• The early deceleration in the heart rate start within
30 seconds of the onset of the contraction and
return rapidly to the baseline rate
• It is not of serious significance as a rule and
indicate that while the fetus is undergoing some
stress the cardiac control mechanisms are
responding normally
EARLY DECELERATION
SIGNS AND SYMPTOMS
• Variable deceleration: no consistent relationship
with uterine contraction.
• It is sometimes caused by compression of the
umbilical cord between the uterus and the fetal
body, or because it is looped round some part of
the fetus
• Provided that it does not persist for more than a
few minutes it may have little significance, but
persistence for more than 15 minutes would call for
treatment
VARIABLE DECELERATION
SIGNS AND SYMPTOMS
• The most serious pattern of heart rate changes is
fetal bradycardia with loss of baseline variability
and late decelerations
• Decrease (defined as onset of deceleration to nadir
=30 seconds) and return to baseline FHR
associated with a uterine contraction.
• The deceleration is delayed in timing, with the
nadir of the deceleration occurring after the peak
on the contraction
LATE DECELERATION
BIOPHYSICAL PROFILE
• Biophysical Profile:
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Amniotic Fluid Volume Normal = 2 Points
Non-Stress Test Result Positive = 2 Points
Fetal Breathing Movements Active = 2 Points
Fetal Extremity/Trunk Movements Active = 2 Points
Fetal Movements Active= 2 Points
• If Biophysical Profile scores < 4 suggest fetal
distress
• Placental Insufficiency: Low estriol levels, E3 in
urine < 10mg/24h
TREATMENT
• Reposition patient: left-side-lying position
• Administer oxygen by mask
• Perform vaginal examination to check for
prolapsed cord
• Ensure that qualified personnel are in attendance
for resuscitation and care of the newborn
 Note: each institution shall define in writing the
term qualified personnel for resuscitation and
care of the newborn
TREATMENT
• Each of the following actions should be performed
and documented prior to starting a Cesarean
section for fetal distress:
 Perform vaginal exam to rule out imminent
vaginal delivery
 Initiate preoperative routines
 Monitor fetal heart tones (by continuous fetal
monitoring or by auscultation) immediately prior
to preparation of the abdomen
TREATMENT
• Ensure that qualified personnel are in
attendance for resuscitation and care of the
newborn (each institution shall define in
writing the term qualified personnel for
resuscitation and care of the newborn)
• STOP using oxytocin !
 Oxytocin can strengthen the contraction of
uterine which affects the baby's heart rate
DEFINITIONS MUST GRASPED
• Baseline FHR:
 approximate mean FHR rounded to increments
of 5 bpm during a 10-minute segment,
excluding periodic or episodic changes, periods
of marked FHR variability, and segments of the
baseline that differ by > 25 bpm
 In any 10-minute window, the minimum
baseline duration must be at least 2 minutes or
the baseline for that period is indeterminate
DEFINITIONS MUST GRASPED
• Baseline FHR variability:
 Fluctuations in the baseline FHR =2 cycles / min
 These fluctuations are irregular in amplitude and
frequency, and are visually quantitated as the
amplitude of the peak to the trough in beats per
minute as follows:
• amplitude range undetectable, absent FHR
variability;
• amplitude range greater than undetectable but =
5 bpm, minimal FHR variability;
• amplitude range 6 bpm to 25 bpm, moderate FHR
variability;
• amplitude range >25 bpm, marked FHR variability
DEFINITIONS MUST GRASPED
• Bradycardia:
 a baseline FHR <120 bpm
• Tachycardia:
 a baseline FHR >160 bpm
DEFINITIONS MUST GRASPED
• Early deceleration:
 a visually-apparent, gradual decrease (defined
as onset of deceleration to nadir =30 seconds)
and return to baseline FHR associated with a
uterine contraction
 The decrease is calculated from the most
recently determined portion of the baseline
 It is coincident in timing with the nadir of the
deceleration occurring at the same time as the
peak of the contraction
 In most cases the onset, nadir, and recovery of
the deceleration are coincident with the
beginning, peak, and ending of the contraction,
respectively
DEFINITIONS MUST GRASPED
• Variable deceleration:
 a visually-apparent, abrupt decrease in FHR
below the baseline
 The decrease is calculated from the most
recently determined portion of the baseline
 The decrease in FHR below the baseline is =15
bpm, lasting =15 seconds and =2 minutes from
onset to return to baseline
DEFINITIONS MUST GRASPED
• Late deceleration:
 a visually-apparent, gradual decrease (defined
as onset of deceleration to nadir = 30 seconds)
and return to baseline FHR associated with a
uterine contraction
 The decrease is calculated from the most
recently determined portion of the baseline
 The deceleration is delayed in timing, with the
nadir of the deceleration occurring after the
peak on the contraction
INTRAUTERINE FETAL DEATH (IUFD)
DEFINITION:
• dead fetuses or newborns weighing > 500g or > 20
wks gestation
4.5/ 1000 total births
DIAGNOSIS:
Absence of uterine growth
Serial ß-hcg
Loss of fetal movement
Absence of fetal heart
Disappearance of the signs & symptoms of pregnancy
X-ray Spalding sign
Robert’s sign
U/S 100% accurate Dx
CAUSES OF IUFD
Fetal causes 25-40%
•Chromosomal anomalies
•Birth defects
•Non immune hydrops
•Infections
Placental 25-35%
•Abruption
•Cord accidents
•Placental insufficiency
•Intrapartum asphyxia
•P Previa
•Twin to twin transfusion S
•Chrioamnionitis
Maternal 5-10%
•Antiphospholipid antibody
•DM
•HPT
•Trauma
•Abnormal labor
•Sepsis
•Acidosis/ Hypoxia
•Uterine rupture
•Postterm pregnancy
•Drugs
•Thrombophilia
•Cyanotic heart disease
•Epilepsy
•Severe anemia
Unexplained 25-35%
A systematic approach to fetal death is valuable in
determining the etiology
B-Maternal History
I-Maternal medical conditions
1-HISTORY
•VTE/ PE
A-Family history
•DM
•Recurrent abortions •HPT
•Thrombophilia
•VTE/ PE
•Congenital anomalies •SLE
•Abnormal karyptype •Autoimmune disease
•Hereditary conditions •Severe Anemia
•Epilepsy
•Developmental delay
•Consanguinity
•Heart disease
II-Past OB Hx
•Baby with congenital anomaly / hereditary
condition
•IUGR
•Gestational HPT with adverse sequele
•Placental abruption
•IUFD
•Recurrent abortions
1-HISTORY
Current Pregnancy Hx
Specific fetal conditions
•Nonimmune hydrops
•IUGR
•Infections
•Congenital anomalies
•Chromosomal abnormalities
•Complications of multiple gestation
•Maternal age
•Gestational age at fetal death
•HPT
•DM/ Gestational D
•Smooking , alcohol, or drug abuse
•Abdominal trauma
•Cholestasis
Placental or cord complications
•Placental abruption
•Large or small placenta
•PROM or prelabor SROM
•Hematoma
•Edema
•Large infarcts
•Abnormalities in structure , length
or insertion of the umbilical cord
•Cord prolapse
•Cord knots
•Placental tumors
2-EVALUATION OF STILL BORN INFANTS
Infant description
•Malformation
•Skin staining
•Degree of maceration
•Color-pale ,plethoric
Umbilical cord
•Prolapse
•Entanglement-neck, arms,
legs
•Hematoma or stricture
•Number of vessels
•Length
Amniotic fluid
•Color-meconium, blood
•Volume
Placenta
•Weight
•Staining
•Adherent clots
•Structural abnormality
•Velamentous insertion
•Edema/hydropic changes
Membranes
•Stained
•Thickening
3-INVESTIGATIONS
Maternal investigations
•CBC
•Bl Gp & antibody screen
•HB A1 C
•Kleihauer Batke test
•Serological screening for Rubella
•CMV, Toxo, Sphylis, Herpes &
Parovirus
•Karyotyping of both parents (RFL,
Baby with malformation
•Hb electrophorersis
•Antiplatelet anbin tibodies
•Throbophilia screening
(antithrombin
Protein C & S , factor IV leiden,
Factor II mutation, , lupus
anticoagulant,
anticardolipin antibodies)
•DIC
Fetal investigations
•Fetal autopsy
•Karyotype
(specimen taken from cord
blood, intracardiac blood,
body fluid, skin, spleen,
placental wedge, or amniotic
fluid)
•Fetography
•Radiography
Placental investigations
•Chorionocity of placenta in
twins
•Cord thrombosis or knots
•Infarcts, thrombosis,
abruption
•Vascular malformations
•Signs of infection
•Bacterial culture for E.coli,
Listeria, gp B strpt.
IUFD COMPLICATIONS
• Hypofibrinogenemia  4-5 wks after IUFD
• Coagulation studies must be started 2 wks after
IUFD
• Delivery by 4 wks or if fibrinogen  < 200mg/ml
PSYCHOLOGICAL ASPECT & COUNSELING
• A traumatic event
• Post-partum depression
• Anxiety
• Psychotherapy
• Recurrence 0-8% depending on the cause of IUFD