1. Fetal distress and intrauterine death
DR. Dan Mihalcea MD, PHD.

2. Fetal distress
Def: metabolic derangements (hypoxia and acidosis) that affect the functions of vital organs to the point of temporary or permanent injury or death
Type: - chronic (during pregnancy)
- acute (usualy during labor and delivery)

3. Etiology Maternal causes:
- vascular abnormality (HBP, preeclampsia, eclampsia) or diabetes with pelvic vascular complications
- inadequate systemic circulation- congenital or aquired heart disease
- inadequate oxygenation of the blood ( chronic respiratory diseases or high altitude)

4. Etiology Placental abnormalities :
-abnormal insertion – placenta praevia
- PSNIP
- placental insufficiency
- diabetes
- premature placental ageing

5. Placenta 3-rd degree

6. Placenta praevia

7. PSNIP= abruptio

8. Etiology -cord compression (oligohydramnios, prolapse) Fetal factors:
- multiple gestation (prematurity or twin to twin transfusion)
- erythroblastozis fetalis
- postmaturity
- congenital anomalies
- infections
- IUGR

9. Nucal cord

10. Twin to twin syndrome

11. Erythroblastozis fetalis

12. Umbilical cord knot

13. Etiology of acute fetal distress
Excessive uterine contractions ( iatrogenic! )
Hypotonic uterine disfunction
Maternal causes(HTA , shock, sudden heart failure)
Placenta and cord pathology ( prolapse, abruptio)
Obstetrical maneuvers ( forceps, versions, vacuum)
Inappropriate use of drugs

15. Cord prolapse

16. Forceps

17. Physiopathology
The factors can induce 3 types of abnormal phenomena to the fetus:
- chemical injury (hypoxia)
- mechanical injury
- infectious injury

18. Fetal hypoxia
The fetal oxygen supply can be reduced by any of the following:
- reduction in blood flow through the maternal vessels (HBP)
- reduction in blood flow through the uterine sinuses (hypertonia or prolonged uterine contractions)
- reduction of the oxygen content of maternal blood (anemia of the mother or severe hemorage)
- alterations of fetal circulation
- placental infarction or separation ( abruptio)

19. Mechanical injury Birth trauma may cause intracranial hemorrage
Severe molding or marked overlap of the parietal bones
Fetal infection
Bacteria, viruses or parasites may gain access transplacentally or they may cross the membranes, even trough intact.
Rubella , lues, CMV, toxoplasmosis, group B streptoccocus
Bacteria may colonize and infect the fetus during delivery (ROM) + after 6 hours start AB!

20. Molding

21. Diagnosis A) During pregnancy: - Complete anamnesis for risk factors
- Fetal heart tones (tahicardia/bradicardia)
Heart rate variability
Fetal movement
Meconium appearence after ROM
Size of the uterus < we expect
During labor FHR should be recorded every 30 min.

22. Paraclinical tests Ultrasound Biopysical profile - FHR acceleration
- Fetal breathing
- Fetal movements
- Fetal tone
- Amniotic fluid volume
Amniocentesis
- L/S ratio and phosphaditilglicerol – lung maturity of the fetus
Percutaneous umbilical blood sampling
– alpha FP – elevated levels suspect the possibility of neural-tube deffect
- E3- low concentration = IUGR, High concentration- evaluation of posterm
- Human placental lactogen < 4um/ml after 30 weeks = reduced placental function

23. Umbilical blood sampling

24. Paraclinical tests
The most commonly used tests in antepartum fetal surveillance are:
Contraction stress test – response of the fetal heart rate to uterine contractions
Non stress test- is based on the premise that the heart rate of the fetus will temporarily accelerate with fetal movement
Biophysical profile 8-10 normal
6 equivocal
<4 abnormal

25. Cardiotocography ( CTG)
B) During labor
Clinical recognition
- auscultation of tachycardia, bradicardia or cardiac arrithmia
- passage of meconium by the fetus in vertexpresentation
- fetal movement modification
Laboratory tests – evaluation of acid/base status –fetal scalp blood sampling- Ph- normal 7,25-7,35
- border line: 7,20-7,25
- abnormal: <7,20
Fetal heart rate pattern - Cardiotocography

26. Normal pattern

27. Variability
Baseline variability refers to the variation of foetal heart rate from one beat to the next
Variability occurs as a result of the interaction between the nervous system, chemoreceptors, barorecptors & cardiac responsiveness.
Therefore it is a good indicator of how healthy the foetus is at that moment in time.
This is because a healthy foetus will constantly be adapting it’s heart rate to respond to changes in it’s environment.
Normal variability is between bpm³

28. Variability Variability can be categorised as: 4 Reassuring ≥ 5 bpm
Non-reassuring < 5bpm for between minutes
Abnormal < 5bpm for >90 minutes

29. Variability Reduced variability can be caused by:
Foetus sleeping - this should last no longer than 40 minutes – most common cause
Foetal acidosis (due to hypoxia) – more likely if late decelerations also present
Foetal tachycardia
Drugs – opiates, benzodiazipine’s, methyldopa, magnesium sulphate
Prematurity – variability is reduced at earlier gestation (<28 weeks)
Congenital heart abnormalities

31. Accelerations
Accelerations are an abrupt increase in baseline heart rate of >15 bpm for >15 seconds
The presence of accelerations is reassuring
Antenatally there should be at least 2 accelerations every 15 minutes¹
Accelerations occurring alongside uterine contractions is a sign of a healthy foetus

32. Accelerations

33. Early decelerations
Early decelerations start when uterine contraction begins & recover when uterine contraction stops
This is due to increased foetal intracranial pressure causing increased vagal tone
It therefore quickly resolves once the uterine contraction ends & intracranial pressure reduces
This type of deceleration is therefore considered to be physiological & not pathological

34. Early decelerations

35. Late decelerations
Late decelerations begin at the peak of uterine contraction & recover after the contraction ends.
This type of deceleration indicates there is insufficient blood flow through the uterus & placenta
As a result blood flow to the foetus is significantly reduced causing foetal hypoxia & acidosis
Reduced utero-placental blood flow can be caused by: 
Maternal hypotension
Pre-eclampsia
Uterine hyper-stimulation
The presence of late decelerations is taken seriously & foetal blood sampling for pH is indicated
If foetal blood pH is acidotic it indicates significant foetal hypoxia & the need for emergency C-section

36. Late decelerations

37. Variable decelerations
Variable decelerations are seen as a rapid fall in baseline rate with a variable recovery phase
They are variable in their duration & may not have any relationship to uterine contractions
They are most often seen during labour & in patients with reduced amniotic fluid volume
Variable decelerations are usually caused by umbilical cord compression
Variable decelerations can sometimes resolve if the mother changes position
The presence of persistent variable decelerations indicates the need for close monitoring

38. Variable decelerations

39. Sinusoidal pattenr Sinusoidal Pattern
This type of pattern is rare, however if present it is very serious
It is associated with high rates of foetal morbidity & mortality  .
It is described as:
A smooth, regular, wave-like pattern
Frequency of around 2-5 cycles a minute
Stable baseline rate around bpm
No beat to beat variability
A sinusoidal pattern indicates:
Severe foetal hypoxia
Severe foetal anaemia
Foetal/Maternal Haemorrhage
Immediate C-section is indicated for this kind of pattern.
Outcome is usually poor

41. MECONIUM ASPIRATION SYNDROME

42. SIGNS & SYMPTOMS INTRA PARTUM PERIOD Tachycardia & Bradycardia
especially during contractions
Decreased variability in FHR
FHR should be recoreded every 15 minutes
Meconium in the amniotic fluid
Fetal acidosis – fetal scalp pH <7.2
Elevated fetal blood lactate levels – lactic acidosis

43. pH fetal blood From the scalp after ROM pH normal 7.25-7.35
Borderline
Abnormal below 7.20

44. Doppler ultrasound Ombilical artery MCA * medium cerebral artery
DV ductus venosus
Uterine arteries

45. Doppler ombilical artery = normal

46. Doppler ombilical artery= abnormal diastolic flow =0

47. Doppler of umbilical artery abnormal reversed diastolic flow

48. Management of fetal distress
Acute fetal distress: emergency treatment
Chronic fetal distress: management plan depends on severity of the pregnancy complications, gestational age, fetal maturity, fetal distress condition

49. Management of acute fetal distress
Give oxygen: face mask or nasal prong continuous oxygen at 10L/min flow
Search for cause, active management: if patient has supine hypotensive syndrome, lie the patient on left lateral position; if excessive oxytocin leading to uterine hyperstimulation, stop oxytocin immediately, use tocolytics when necessary /

50. Management of acute fetal distress
Terminate pregnancy soonest possible:
If cervix is not fully dilated with the following conditions => Immediate caesarean section:
(1)fetal heart rate <120bpm or >180bpm, accompanied by meconium stained amniotic fluid;
(2) meconium stained amniotic fluid, with low
amniotic fluid amount;
(3) frequent late decelerations or severe variable decelerations;
(4) fetal scalp blood pH <7.20

51. Management of acute fetal distress
If fully dilated cervix:
fetal biparietal diameter, has descend below
ischial spines, perform assisted vaginal delivery
FORCEPS/ VACUUM DELIVERY
Prepare for newborn resuscitation

53. Management of chronic fetal distress
Routine management: left lateral position, give oxygen regularly (30mins, 2-3times/day)
Active treatment of pregnancy complications
Terminate pregnancy: pregnancy near term with less fetal movement or late decelerations, severe variable decelerations, or biophysical profile <= 3 score, caesarean is indicated

54. Management of chronic fetal distress
Expectant treatment: early gestation, low chance of survival if delivered, prolong pregnancy while inducing fetal lung maturation
Must explain to the family that during the process of expectant treatment, there is risk of sudden fetal death, poor placental function might affect fetal growth, poor outcome.

55. Intrauterine death Definition Missed abortion < 28 weeks
Stillbirth > 28 weeks
NOW LIMIT IS 24 WEEKS
Maceration is a distructive aseptic process wich first reveals itself by blistering and peeling of the fetal skin.
Macerated stillbirth nearly always indicates death in pregnancy and not in labor and in most cases in caused by anoxia

57. Maternal pathology includes
Etiology
Maternal pathology includes
Prolonged pregnancy (>42 weeks)
Diabetes
Systemic lupus erythematosus
Antiphospholipid syndrome
Infection
Hypertension
Preeclampsia
Eclampsia
Hemoglobinopathy
Rh disease
Uterine rupture
Maternal trauma or death
Inherited thrombophilias

58. Etiology Fetal pathology includes Placental pathology involves
Multiple gestations * TWIN TO TWIN TRANFUSION
Intrauterine growth restriction IUGR
Congenital abnormality
Genetic abnormality
Infection
Hydrops
Placental pathology involves
Cord accident ( prolapse, true knot)
Abruptio
Premature rupture of membranes /Vasa previa
Placental insufficiency

59. Vasa praevia

60. Prolapse of cord

61. Fetal malformations Trisomy 18, 21 Anencephalia Potter sdr.
Severe cardiac malformations
FETAL INFECTION
Rubella
Lues
Toxoplasmosis

62. Anencephalia

63. Symptoms
Certain signs and symptoms make a doctor guess a possible intrauterine death.
A mother who notices the baby has stopped moving for a long period of time
A uterus or womb that fails to get bigger over time
An inability to hear the baby's heartbeat with a special heart monitor
Lack of movement of the baby or no heartbeat during a pregnancy ultrasound

64. Diagnosis
History and physical examination are of moderate value in the diagnosis of intrauterine death. In most patients, the only symptom is diminished fetal movement. An inability to obtain fetal heart modulates upon examination suggests intrauterine death; however, this is not diagnostic and death must be confirmed by ultrasonographic examination.
Intrauterine death is confirmed by visualization of the fetal heart and the absence of cardiac activity.

65. ultrasound

66. Hydrops

68. Problems 1. infection – rare if membranes are intact
2. maternal psychological distress
3. coagulopathy : release of thromboplastin from the dead fetus = fibrinogen consumption
coagulopathy appears if retention is prolonged ex. 2=3 weeks- 1 month

69. Treatment
Once the intrauterine death has been confirmed, the patient should be informed of her condition.
Often, allowing the mother to see the lack of cardiac activity helps her to admit the examination.
Labor induction should be rendered after examination. .
Induction may be carried out with preinduction cervical ripening with prostaglandins followed by intravenous oxytocin.
Early intrauterine death may be managed with laminaria insertion followed by dilatation and evacuation. In women with intrauterine death before 28 weeks' gestation, induction may be carried out using misoprostol vaginally or orally (400 mcg q4-6h), and/or oxytocin. In women with intrauterine death after 28 weeks' gestation, lower doses should be used.

70. Prostaglandin gel

71. laminaria

72. Treatment Evacuation of pregnancy
Correction of coagulation defect : heparin
Treatment of active hemorrhage: blood, coagulation factors

73. Treatment
In women with no uterine scar, misoprostol (25 mcg q4-6h) may be dispensed for ripening after 28 weeks’ gestation.
In the presence of a dead fetus, C section may be indicated in:
- placenta praevia
- severe cephalo-pelvic disproportion
- previous c-section
- transverse presentation and no conditions to perform version
In some cases hysterectomy is mandatory

74. Thank you !