1. Lecture 10 FETAL DISTRESS

2.   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

3. ETIOLOGY Maternal: poor placental perfusion hypovolaemia hypotension
myometrial hypertonus
prolonged labor
excess oxytocin

4. ETIOLOGY Fetal: cord compression oligohydramnios
entanglement
prolapse
pre-existing hypoxia or growth retardation
infection
cardiac

5. 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

6. 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

7. SIGNS AND SYMPTOMS Acute fetal distress

8. 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 

9. SIGNS AND SYMPTOMS A rapid fetal heart rate may be a response to:
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

10. SIGNS AND SYMPTOMS I - slight contamination II - mild contamination
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

11. 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

12. Chronic Fetal Distress

13. 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!!

14. 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

15. 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

16. 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

18. EARLY DECELERATION

19. 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

20. VARIABLE DECELERATION

21. 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

22. LATE DECELERATION

23. BIOPHYSICAL PROFILE Biophysical Profile:
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

24. 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

25. 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

26. 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

27. 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

28. 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

29. DEFINITIONS MUST GRASPED
Bradycardia:
a baseline FHR <120 bpm
Tachycardia:
a baseline FHR >160 bpm

30. 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

31. 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

32. 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

33. 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

34. CAUSES OF IUFD 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%
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

35. A systematic approach to fetal death is valuable in
determining the etiology
B-Maternal History
I-Maternal medical conditions
VTE/ PE DM
HPT
Thrombophilia
SLE
Autoimmune disease
Severe Anemia
Epilepsy
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
A-Family history
Recurrent abortions
VTE/ PE
Congenital anomalies
Abnormal karyptype
Hereditary conditions
Developmental delay

36. 1-HISTORY Maternal age Gestational age at fetal death HPT
Specific fetal conditions
Nonimmune hydrops
IUGR
Infections
Congenital anomalies
Chromosomal abnormalities
Complications of multiple gestation
Current Pregnancy Hx
Maternal age
Gestational age at fetal death
HPT
DM/ Gestational D
Smooking , alcohol, or drug abuse
Abdominal trauma
Cholestasis
Placental abruption
PROM or prelabor SROM
Placental or cord complications
Large or small placenta
Hematoma
Edema
Large infarcts
Abnormalities in structure , length or insertion of the umbilical cord
Cord prolapse
Cord knots
Placental tumors

37. 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

38. 3-INVESTIGATIONS Fetal investigations Fetal autopsy Karyotype
(specimen taken from cord
blood, intracardiac blood,
body fluid, skin, spleen,
placental wedge, or amniotic
fluid)
Fetography
Radiography
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
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.

39. 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

40. PSYCHOLOGICAL ASPECT & COUNSELING
A traumatic event
Post-partum depression
Anxiety
Psychotherapy
Recurrence 0-8% depending on the cause of IUFD

41. THANK YOU !