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Fetal Assessment

Fetal Assessment. دكتر عليه مرتضوي اسفند ماه 1395 گروه هدف: ماماهاي بيمارستان بنت الهدي. Screening for high risk pregnancy. History * Age *Social burden *Smoking *Past medical conditions e.g D.M, HTN *Past Obstetric history. Fetal assessment.

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Fetal Assessment

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  1. Fetal Assessment دكتر عليه مرتضوي اسفند ماه 1395 گروه هدف: ماماهاي بيمارستان بنت الهدي

  2. Screening for high risk pregnancy History • * Age • *Social burden • *Smoking • *Past medical conditions e.g D.M, HTN • *Past Obstetric history

  3. Fetal assessment Aim: Ensure fetal wellbeing ( Identify patients at risk of fetal asphyxia) To prevent prenatal mortality & morbidity

  4. When to start fetal Assessment ** Risk assessed individually ** uncomplicated D.M. :start from 32 weeks onward ***If complicated D.M. :start at 24 weeks onward **For Post date pregnancy start at 40 weeks **For any patient with decrease fetal movement start immediately ** Fetal assessment is done once or twice weekly

  5. FETAL AND NEONATAL COMPLICATIONS OF ANTEPARTUM ASPHYXIA Fetal Outcomes Neonatal Outcomes Stillbirth Mortality Metabolic acidosis Hypoxic renal damage Necrotizing enterocolitis Intracranial haemorrhage Seizures Cerebral palsy

  6. CONDITIONS ASSOCIATED WITH INCREASED PERINATAL MORBIDITY/MORTALITY WHEREANTENATAL FETAL TESTING MAY HAVE AN IMPACT SGA Decreased FM Postdates pregnancy (>294 days) Pre-eclampsia/chronic HTN Overt DM GDM A2 PPROM Chronic (stable) abruption

  7. Fetal Assessment Fetal movement counting Non stress test Contraction stress test Ultrasound fetal assessment Umbilical Doppler Velocimetry

  8. METHODS OF ANTENATALTESTING Fetal movement Selective counting ↑ risk + Standard inquiry FM Routine counting Cardiff Sadovsky No difference in  mortality

  9. Fetal movement counting Cardiff technique: *Done in the morning, patient should *calculate how long it takes to have 10 fetal movement **10 movements should be appreciated in 12 hours

  10. Fetal movement counting Sadovsky technique: -For one hour after meal the woman should lie down and concentrate on fetal movement -4 movement should be felt in one hour -If not , she should count for another hour -If after 2 hours four movements are not felt, she should have fetal monitoring

  11. Non stress test *Done using the cardiotocometry with the patient in left lateral position **Record for 20 minutes

  12. The Nonstress Test Ultrasound Probe Pressure Transducer

  13. Interpretation of the Fetal Heart Tracing The interpretation of the fetal heart rate tracing should follow a systematic approach with a full qualitative and quantitative description of the following: Baseline fetal heart rate (FHR) variability Presence of accelerations Periodic or episodic decelerations Changes or trends of FHR patterns over time Frequency and intensity of uterine contractions

  14. Baseline Fetal Heart Rate The baseline FHR is the heart rate during a 10 minute segment rounded to the nearest 5 beat per minute increment excluding periods of marked FHR variability, periodic or episodic changes, and segments of baseline that differ by more than  25 beats per minute. The minimum baseline duration must be at least 2 minutes.  If minimum baseline duration is < 2 minutes then the baseline is indeterminate.(wandering base line)

  15. Baseline Fetal Heart Rate Two Minutes

  16. Interpretation of CTG Normal Baseline FHR 110–160 bpm – Moderate bradycardia 100–109 bpm – Moderate tachycardia 161–180 bpm – Abnormal bradycardia < 100 bpm – Abnormal tachycardia > 180 bpm

  17. Non stress test *The base line 120-160 beats/minute *Reactive: At least two accelerations from base line of 15 bpm for at least 15 sec within 20 minutes Non reactive: No acceleration after 20 minutes- proceed for another 20 minutes

  18. Non stress test If non reactive in 40 minutes---proceed for contraction stress test or biophysical profile The positive predictive value of NST to predict fetal acidosis at birth is 44%

  19. NST

  20. NST

  21. Bradycardia Mean FHR < 110 BPM A rate of 100-119 BPM in the absence of other non reassuring patterns is not usually a sign of compromise Causes Heart block (little or no  variability) Occiput posterior or transverse position Serious fetal compromise. Patients with new onset bradycardia should be transferred to Labor and Delivery for further observation and physician notified

  22. Tachycardia Mean FHR>160 BPM In the presence of good variability tachycardia is not a sign of fetal distress Causes: SVT (200-240 BPM) Fetal heart failure Drugs Beta sympathomimetics Vistaril Phenothiazines Rebound transient tachycardia following a deceleration accompanied by decreased variability) Maternal fever Fetal hypoxia Fetal anemia Amnionitis Normal variant Fetal tachyarrhythmia (usually > 200 BPM with abrupt onset little to no variability)

  23. Tachycardia

  24. TachycardiaHypoxia ChorioamnionitisMaternal fever B-Mimetic drugsFetal anaemia,sepsis,ht failure,arrhythmias

  25. FHR Variability Fluctuation in baseline FHR > 2 cycles per minute. No distinction is made between short-term variability (or beat-to-beat variability or R-R wave period differences in the electrocardiogram) and long-term variability.

  26. Development of FHR Variability Early in gestation the fetal heart rate is predominately under the control of the sympathetic nervous system and arterial chemoreceptors.  As the fetus develops its heart rate decreases in response to parasympathetic (vagal stimulation) nervous system maturation and variability becomes more pronounced.

  27. FHR Variability Grades of fluctuation are based on amplitude range (peak to trough) • A sinusoidal pattern has regular amplitude and frequency and is excluded in the definition of variability. • The tracing to the right shows an amplitude range of ~ 10 BPM (moderate variability).

  28. FHR Variability

  29. Reduced Variability

  30. The Presence of Moderate FHR Variability is Reassuring . • Persistently minimal or absent FHR variability appears to be the most significant intrapartum sign of fetal compromise. • On the other hand  the presence of good FHR variability may not always be predictive of a good outcome (such as may occur with an abruption).

  31. Causes of Decreased Variability • Fetal metabolic acidosis • CNS depressants • Fetal sleep cycles • Congenital anomalies • Prematurity • Fetal tachycardia • Preexisting neurologic abnormality • Normal variant • Betamethasone

  32. Sinusoidal and Pseudosinusoidal Patterns Sinusoidal pattern: A smooth, undulating pattern, lasting at least 10 minutes with a fixed period of three to five cycles per minute and an amplitude of 5-15 bpm. Pseudosinusoidal: Usually caused by drugs such as Nubain or Stadol.

  33. Accelerations An acceleration is an abrupt increase in FHR above baseline with onset to peak of the acceleration less than < 30 seconds and less than 2 minutes in duration. The duration of the acceleration is defined as the time from the initial change in heart rate from the baseline to the time of return to the FHR to baseline. • <32 weeks' : >10 BPM above baseline for >10 seconds [3] • >32 weeks' : >15 BPM above baseline for > 15 seconds[3]. • Prolonged acceleration: Increase in heart rate lasts for  2 to 10 minutes. • The absence of accelerations for more than 80 minutes correlates with increased neonatal morbidity.

  34. Reactivity A NST is considered reactive when two or more fetal heart rate accelerations peak (but do not necessarily remain) at least 15 beats per minute above the baseline and last 15 seconds from baseline to baseline within a 20 minute period with or without fetal movement discernible by the woman.

  35. Acceleration

  36. Vibroacoustic stimulation (VAS) If the pattern is nonreactive after 20 minutes of observation then vibroacoustic stimulation (VAS), using an artificial larynx, may be performed. The acoustic stimulator should be positioned on the maternal abdomen and a stimulus of 3 seconds or less applied near the fetal head. If the NST remains nonreactive, the stimulus is repeated at 1-minute intervals up to three times.

  37. How Reassuring is a Reactive NST? • A reactive NST has been associated with a perinatal mortality of approximately 5/1,000. • The false-positive rate (the test indicates fetal compromise when the fetus is actually O.K.) associated with the nonreactive NST is approximately 75 to 90 percent • Malformed fetuses have a higher incidence of nonreactive NSTs.

  38. Likelihood of a Nonreactive NST • A nonreactive NST is one that lacks sufficient fetal heart rate accelerations as described above over a 40-minute period. Overall, on initial testing, 85 percent of NSTs will be reactive and 15 percent will be nonreactive Most fetuses exhibiting a nonreactive NST will not be compromised but will simply fail to exhibit heart rate reactivity during a 40-minute period of testing . ~50 percent of NSTs are nonreactive between 24 and 28 weeks' gestation. ~15 percent of NSTs remain nonreactive between 28 and 32 weeks.

  39. A non‑reactive NST requires that a biophysical profile be done.

  40. METHODS OF ANTENATALTESTING CTG Non stress test Stress test +ve -ve Non reactive Reactive Suspecious Continue Another 20 Min BPP Perinatal Mortality Within 1wk 1.2/1000 birth 50% of N fetus <28 Non reactive

  41. Periodic or Episodic Decelerations • Episodic patterns are those not associated with uterine contractions • Periodic patterns are those associated with uterine contractions. • Early and late decelerations (with some exceptions-i.e., supine hypotension) are periodic. • Variables can also be periodic. • Quantitated by the depth of the nadir in BPM below the baseline. • Duration is quantitated in minutes and seconds from the beginning to the end of the deceleration. • (Accelerations are quantitated similarly.)

  42. Decelerations • The type of the deceleration is distinguished on the basis of its waveform. • Abrupt (variables) decrease in FHR below baseline with onset to nadir < 30 seconds. • Gradualdecrease and return to baseline with time from onset of the deceleration to nadir >30 seconds. • Further subclassified based on their relation to the contraction. • Early decelerations:The nadir occurs with the peak of a contraction. • Late decelerations:The nadir occurs after the peak of a contraction.

  43. Deceleration • EARLY : Head compression • LATE : U-P Insufficiency • VARIABLE : Cord compression Primary CNS dysfunction

  44. Variable Deceleration Abrupt  decrease in FHR of > 15 beats per minute measured from the most recently determined baseline rate.  The onset of deceleration to nadir is less than 30 seconds. The deceleration lasts   > 15 seconds and less than 2 minutes. A shoulder, if present, is not included as part of the deceleration. Variable decelerations may be observed in up to 50% of NSTs. If nonrecurrent and <30 seconds, they are of no clinical significance.

  45. Variable Deceleration

  46. Early Deceleration Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. The nadir occurs with the peak of a contraction.

  47. Early deceleration

  48. Late Deceleration Gradual decrease in FHR with onset of deceleration to nadir >30 seconds. The nadir of the deceleration occurs after the peak of the contraction

  49. Late Decelerations Late Decelerations associated with preservation of beat-to beat variability • These decelerations appear to be mediated by arterial chemo receptors in mild hypoxia. • Below a pO2 of 15-20 mm Hg chemoreceptors are triggered causing reflex alpha adrenergic stimulation leading to hypertension. • The hypertension stimulates a baroreceptor mediated vagal response (deceleration) • The onset of reflex late decelerations typically precedes the loss of accelerations

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