Gyneco. D. Ezdehar L5 Fetal Assessment in Labor.pptx

obstetric

1. Fetal assessment in labour Dr . Izdihar Nsaif Ali

2. Objectives: The objective of fetal monitoring during labour is the prediction & diagnosis of fetal asphyxia before fetal / newborn morbidity with particular reference to brain damage has occurred . How we can improve the outcome, by intra-uterine resuscitation , and by using the secondary fetal-well-being tests . Decrease the operative delivery by using secondary fetal-well being tests .

3. A healthy term fetus is usually able to withstand the demands of a normal labour . However, with each contraction, placental blood flow and oxygen transfer are temporarily interrupted and a fetus that is compromised before labour starts will become increasingly so. Insufficient oxygen delivery to the fetus causes a switch from aerobic to anaerobic metabolism and results in the generation of lactic acid and hydrogen ions. a metabolic acidosis, which if prolonged and severe, can cause neuronal damage and permanent neurological injury, even intrapartum fetal death. .

4. Hypoxia and acidosis cause a characteristic change in the fetal heart rate (FHR) pattern, which can be detected by auscultation and cardiotocography (CTG). Meconium (fetal stool) is often passed by a healthy fetus at or after term as a result of maturation of the gastrointestinal tract , it is usually thin and a very dark green or brown color . However, it may also be expelled from a fetus exposed to marked intrauterine hypoxia or acidosis.

5. Fetal distress Fetal distress’ is a condition of significant impairment of oxygen transport resulting in progressive fetal hypoxia, acidosis, and asphyxia. In labour it should thought of as hypoxia which if allowed to persist may result in fetal death or permanent damage . Factors that cause fetal distress during labour : I ) Maternal causes : 1. Hypotension 2. Seizures 3. Hypertension . II ) Fetal causes : 1. Fetal blood loss 2.Meconium aspiration III ) Uterine causes : 1. Tetanic contractions of the uterus IV ) Umbilical cord causes : 1. Single umbilical artery 2. Vasa – praevia 3.Cord prolapse. 4. Short-cord 5 . True-knots in umblical cord V ) Placental causes : 1. placenta abruption . 2. Post mature placenta.

6. Fetal assessment in labour : Is performed in all labour Inspection of amniotic fluid – fresh meconium staining, absence of fluid, and heavy blood-stained fluid or bleeding are markers of potential fetal compromise. Intermittent auscultation of the fetal heart using a Pinard stethoscope or a handheld Doppler ultrasound. (Low risk labour ) Continuous external electronic fetal monitoring (EFM) using CTG.(High risk labour ) Continuous internal electronic fetal monitoring using a fetal scalp electrode (High risk labour )

7. Secondary Tests of fetal well - being 1. Vibroacoustic stimulation 2. Fetal blood sampling 3. Scalp stimulation 4. Fetal electrocardiogram 5. Fetal pulse oximetry

8. What is a high risk labour : Maternal risk factor 1. Hypertention /Pre-eclampsia 2.Diabetes mellitus 3.Ante partum hemorrhage 4.Maternal fever

9. Fetal conditions 1. Intrauterine growth restriction 2. Oligohydramnias . 3.Post term pregnancy 4. Multiple pregnancy . 5. Abnormal Doppler arterial velocimetry . 6. Breech presentation

10. Labour 1.Significant meconium staining of the amniotic fluid. 2.Abnormal FHR detected by intermittent auscultation. 3.Maternal pyrexia 4.Augmentation of contractions with an oxytocin infusion. 5.Maternal request. 6.Previous caesarean section

11. Intermittent auscultation of FHR : Intermittent auscultation ,early on in the initial assessment. It should be listened to for at least one minute immediately after a contraction. This should be repeated every 15 minutes in first stage of labour , if abnormal FHR : shift to CTG. This should be repeated every every 5 min in second stage of labour , if abnormal FHR : shift to CTG.

12. Continuous FHR monitoring 1-External machine (Cardiotocography) Is a continuous tracing of the fetal heart rate used to assess fetal wellbeing, together with an assessment of uterine activity. The CTG recording is obtained with the pregnant woman positioned comfortably in a left lateral or semi-recumbent position to avoid compression of the maternal vena cava. An external ultrasound transducer for monitoring the fetal heart , and measures the interval between successive beats, thereby allowing a continuous assessment of fetal heart rate and a tocodynometer (stretch gauge) for recording uterine activity are secured overlying the uterus. Recordings are then made for at least 30 minutes with the output from the CTG machine producing two ‘lines’, one a tracing of fetal heart rate and a second a tracing of uterine activity.

13. The cardiotocography (CTG)

14. 2. Internal machine : More invasive ,and more accurate , but they need rupture of membranes . The electrode should not be applied to a malpresentation ,when placenta previa or excessive vaginal bleeding is present, and genital infection.

15. Important CTG features Fetal cardiac behavior is regulated through the autonomic nervous system and by vasomotor, chemoreceptor, and baroreceptor mechanisms. Features which are reported from a CTG to define normality & identify abnormality and potential concern for fetal well-being include the: • Baseline rate; • Baseline variability; • Accelerations; • Decelerations;

16. 1-Baseline fetal heart rate The normal fetal heart rate at term is 110–150 beats per minute (bpm). Higher rates are rates are defined as fetal tachycardia and lower rates as fetal bradycardia . The baseline fetal heart rate falls with advancing gestational age as a result of maturing fetal parasympathetic tone and, prior to term, 160 bpm is taken as the upper limit of normal. The baseline rate is best determined over a period of 5–10 minutes. Fetal tachycardias ; can be associated with maternal or fetal infection, acute fetal hypoxia , prematurity, fetal anaemia , and drugs such as adrenoceptor agonist e.g. ritodrine . Fetal bradycardia; can be associated with fetal hypoxia (as a late sign) ,oxytocin ,maternal hypotension , cord prolapse and epidural anesthesia .

17. 2-Baseline variability Under normal physiological conditions, the interval between successive heart beats (beat-to-beat) varies. This is called ‘ short-term variability’ and increases with increasing gestational age .It is not visible on a standard CTG but can be measured with computer –assisted analysis. In addition to these beat- to- beat variations in heart rate, there are longer-term fluctuations in heart rate occurring between two and six times per minute . This is known as ‘ baseline variability’. Normal baseline variability reflects a normal fetal autonomic nervous system. Baseline variability is considered abnormal when it is less than 10 beats per minute (bpm).

18. Baseline variability It is measured by estimating the difference in beats per minute between the highest peak and the lowest trough of fluctuation in a one minute segment of the trace.

19. Causes of decreases fetal variability Fetal metabolic acidosis. Fetal sleep cycles; as fetuses display deep sleep cycles of 20–30 minutes at a time. Drugs suppressing the fetal central nervous system, ( opioids, and hypnotics). Congenital abnormalities. Fetal infection.

20. 3-Fetal heart rate accelerations These are increases in the baseline fetal heart rate of at least 15 bpm, lasting for at least 15 seconds. The presence of two or more accelerations on a 20–30-minute antepartum fetal CTG defines a reactive trace and is indicative of a non-hypoxic fetus (i.e. they are a positive sign of fetal health). 4-Fetal heart rate decelerations These are transient reductions in fetal heart rate of 15 bpm or more, lasting for more than 15 seconds. Decelerations can be indicative of fetal hypoxia or umbilical cord compression. There is a higher chance of fetal hypoxia being present if there are additional abnormal features such as reduced variability or baseline tachycardia.

21. Types of deceleration 1.Early deceleration Begins at or after the onset of a contraction & returns to the baseline rate by the time the contraction has finished & produces a mirror image of the contraction .it not sign of fetal problem , It's due to vagal nerve stimulation .

22. 2. Late decelerations Transitory reduction in FHR caused by utero-placenta insufficiency . Begins after the onset of the peak or middle of the contraction & ends after the contraction . This results from direct myocardiac depression secondary to hypoxemia .The presence of late deceleration , justify secondary testing .

23. 3.Variable decelerations If repetitive & fall < 90 bpm and last > 60 second ,and late recovery to the base line .

24. Management The principle goal of management of late decelerations is to : Replenish utero placental blood flow by correcting the underling cause. Increase fetal PO2 Prevention or correction of fetal academia The resuscitative measures: 1. Stop oxytocin 2 . Oxygen 3. Maternal repositioning to lateral position. 4 .Intravenous hydration 5. pre vaginal examination to exclude cord prolapse & to determine the progress of labour 6. Expeditious operative vaginal delivery or cesarean delivery .

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