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![The Aim of Obstetrics
Healthy mum
Healthy babe(s)
[happy family]
NOT a vaginal
delivery at any cost](https://image.slidesharecdn.com/48569bbf-1073-4015-bea4-f355b0e88b60-160226093320/85/The-DVH-MasterClass-Course-one-day-2016-5-320.jpg)
The DVH MasterClass Course - one day 2016
- 1. The Darent Valley CTGMasterClass Course Bringing order to Chaos Mark Waterstone Consultant Obstetrician
- 3. Why this course? •Provide physiological basis for CTG interpretation • Offer tools and solutions to improve fetal outcomes • Illustrate with case studies • Suggest interface language to communicate with others
- 4. Timetable • Introduction -fetal monitoring in the wider context • Physiology and pathophysiology • The four features • Acid-base analysis • Use of ultrasound • Required documentation (NICE & CNST) • NICE or FIGO? • CTGs: Stories they could tell … • Case studies
- 5. The Aim ofObstetrics Healthy mum Healthy babe(s) [happy family] NOT a vaginal delivery at any cost
- 6. Obstetrics is notscience but art based on science
- 7. “The major correctableerror for avoidance of intra- partum related deaths was the interpretation of EFM traces” Mary MacIntosh J Roy Soc Med 2001 94:14-16
- 8. Fetal “monitoring” Antepartum – Nuchal/ combined testing – Anomaly scans – Fetal activity (objective / subjective) – Ultrasound: • Growth • Dopplers • Liquor Volume • Biophysical Profile – CTG (non-stress test)
- 9. Fetal Movement • Asudden change in fetal movements should always be followed by CTG • Second presentation should have CTG + USS (within 48 hours)
- 10. Fetal monitoring Intrapartum – Auscultation •Intermittent (Pinard / electronic) – CTG • Continuous (EFM – electronic fetal monitoring) • +/- FBS (fetal blood sample) • +/- FSS (fetal scalp stimulation) – STAN • Fetal ECG – Liquor • quantity and quality (meconium/blood)
- 11. Intermittent Auscultation Duration: forat least 60 seconds during and at least 30 seconds after a contraction for 3 contractions if the FHR is not always in the normal range Baseline (as a single counted number in bpm) presence or absence of accelerations and decelerations. Interval: Every 15 minutes in the active phase of the first stage of labour. Every 5 minutes in the second stage of labour. Uterine contractions: Before and during FHR auscultation, in order to detect at least two contractions. Fetal movements: at the same time as evaluation of contractions Maternal heart rate: At the time of FHR auscultation. FIGO 2015
- 12. Fetal heart rate: externalprobes susceptible to recording maternal rate (esp second stage) Internal probes more invasive Uterine activity: External pressure transducer susceptible to maternal interference Continuous CTG
- 13. Continuous CTG • Neversubjected to randomised controlled trials • PPV 40-60 % • NPV 99 % • Associated with a reduction in neonatal seizures, but … • No significant differences in cerebral palsy, infant mortality, etc
- 14. CTG R. W. Beard,et al. The significance of the changes in the continuous foetal heart rate in the first stage of labour. J Obstet Gynaecol Br Commonw 78:865-881, 1971.
- 15. Postpartum Apgar Score SIGN SCORE 0 12 Heart rate Absent < 100 bpm > 100 bpm Respiratory rate Absent Weak, irregular Good, crying Muscle tone Flaccid Arms and legs flexed Well flexed Reflex irritability No response Grimace Cough or sneeze Skin colour Blue / pale Hands and feet blue Completely pink
- 16. Acidosis - pH <7.1 BD> 13 mmol/l RELATIONSHIP OF APGAR SCORES WITH ACIDOSIS Apgar score < 7 Apgar score > 7 Acidosis No acidosis Apgar score at one min <7 Sykes et al (1982) Lancet i 494 - 496 73% 79%
- 17. Alternative postnatal • Measuretime to first gasp • Measure time to regular respiration • Heart rate at delivery • Time to regular rate > 100 bpm
- 18. Fetal blood –cord or scalp • pH • Base deficit • pCO2 pH Lactate (mmol/l) Interpretation >7.25 < 4.2 Normal 7.20-7.25 4.2-4.8 Intermediate <7.20 > 4.8 Abnormal • Hb • Lactate
- 19. Fetal ECG • Analyses30 cycles to construct average ECG • Analyses ST segment • Changes similar to adult angina • Machine needs to be told baby not hypoxic at start • Requires significant teaching • Allows less intervention
- 20. Fetal ECG Fewer severelyacidotic babies (pH < 7.05, BE > -12): RR 0.64; CI 0.41-1.00 Fewer HIE: RR 0.33, CI 0.11-0.95 (but only 17/8108 in total) Fewer FBS: RR 0.76; CI 0.67-0.86 Fewer Op Dels: 0.87; CI 0.78-0.96 No diff in c/s, SCBU or low Apgar scores Overall, advantages must be balanced with disadvantages
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- 22. Biphasic ST gradeI Biphasic ST grade II Biphasic ST grade III
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- 27. The Darent Valley CTGMasterClass Course Bringing order to Chaos Physiology / Pathophysiology of fetal heart rate regulation
- 28. Basic principle All afetus wants to do is maintain its blood pressure stable BP ≡ HR x SV
- 29. Placenta = fetallungs Single vein from mum to baby with oxygenated blood Two arteries from babe to mum with deoxygenated blood (and more CO2 ↓pH) Placenta is low pressure system
- 30. Remember – The heartis a muscle - if overworked it will become tired and fail Myocardium blood flow only occurs in diastole
- 31. Somatic system: fetalmovement → rise in FH Autonomic system: Sympathetic – fight / flight / freeze Parasympathetic – rest / relaxation / restore Two systems control the heart rate
- 33. Control of FetalHeart Rate Pressure - Baroreceptors • Carotid sinus & aortic arch • Quick response • ‘early’ decelerations, i.e. synchronous
- 34. Chemical - Chemoreceptors •Central • Peripheral: aortic and carotid bodies • “Slow” response • late / hypoxic decelerations Control of Fetal Heart Rate
- 35. Control of FetalHeart Rate • Stress - maternal – Adrenaline – Cortisol • Others – Drugs • pethidine, methyl dopa etc… – pyrexia • Stress – Fetal – Adrenaline – Cortisol
- 36. Labour is stressful thebaseline rate will always increase before hypoxic changes appear e.g. Non-physiological decelerations or reduction in variability
- 37. The Four Features •Baseline Rate – Reduces with increasing gestation because of increasing parasympathetic influence • Baseline Variability (‘bandwidth’) – Battle of sympathetic with parasympathetic • Accelerations – Increase of 15 by 15. – “If you have to count it, it ain’t there” Waterstone 2009 • Decelerations – Decrease of 15 by 15, but not if variability reduced
- 38. Baseline Rate • Meanlevel of the most horizontal and less oscillatory segments • Normal range 110-160 bpm (NICE: 100-160) • Reduces with advancing gestation with greater parasympathetic influence • Rises with maternal pyrexia (usually 1 hour before ↑ temp) • First sign of hypoxic stress is increase in baseline = normal physiologic response • Will not reduce unless intra-uterine environment improves (e.g. reduce contractions, change position, ↑ BP)
- 39. Variability • The rangeof rate above and below the baseline (‘bandwidth’) over 1 minute • Normal range 5-25 bpm • Single most important feature indicating fetal well being • Physiological cycling (sleep/wake pattern) indicates good health, even with reduced variability • Beware reduction during labour
- 40. Variability Silent: 0-3 bpm Reduced:3-5 bpm Normal: 5-25 bpm Saltatory: > 25 bpm
- 41. Accelerations • Abrupt increasesof 15 bpm from the baseline lasting at least 15 secs • “Should be visible from the end of the room” • Usually in response to fetal activity • Must be present in antenatal trace • Do not normally occur during contractions in the second stage (think maternal instead) • May incorporate cord compression (biphasic acceleration)
- 42. Decelerations • Reduction inthe baseline of 15 bpm lasting at least 15 seconds • With a tired myocardium the decelerations may be shallow (<15 bpm) and are more sinister – usually associated with reduced variability • May be a physiological response by the fetus to its environment • Head compression – early (synchronous) • Cord compression – classic appearance with shouldering
- 43. but…. do not forgetcontractions
- 44. Acute hypoxia –saltatory / saw-tooth (>25 bpm for more than 30 minutes)
- 45. Chronic anaemia -sinusoidal Regular smooth undulating signal, resembling a sine wave, with an amplitude of 5-15 bpm and a frequency of 3-5 cycles/min for longer than 30 minutes
- 47. Types of deceleration •Early – Synchronous with and mirroring the contraction – Mediated by baroreceptors – Caused by head compression – Not associated with hypoxia
- 48. Types of deceleration •Late – The nadir of the deceleration occurs after the peak of contraction – The recovery of the deceleration occurs after the end of the contraction – Mediated by chemoreceptors
- 49. Variable decelerations Standard teaching •Typical • Atypical CTG MasterClass • Typical • Atypical • Others – unnamed as yet – usually / almost always in labour therefore: LABOUR VARIABLES
- 50. Basic principle All afetus wants to do is maintain its blood pressure stable BP ≡ HR x SV
- 52. Cord Compression –Step 1 Decreased blood flow from placenta to baby = haemorrhage Reduced blood volume Systemic hypotension Reactive tachycardia BP ≡ HR x SV
- 53. Cord Compression –Step 2 Total occlusion Sudden increase in peripheral resistance Hypertension Compensatory deceleration BP ≡ HR x SV
- 54. Reversal of Compression- Step 3 Recoil of umbilical arteries Normalisation of peripheral resistance Relief of systemic hypertension No parasympathetic stimulation Recovery of the deceleration to normal baseline BP ≡ HR x SV
- 55. Post-Compression – Step4 Decreased blood flow from the placenta to the baby Reduced blood volume Systemic hypotension Reactive and reflex tachycardia BP ≡ HR x SV
- 56. Post-Compression – Step5 Normalisation of blood flow blood volume re-established BP normalises Return to baseline BP ≡ HR x SV
- 57. Typical and atypicalvariables
- 58. Types of variabledecelerations Normal shouldering, usually with variability Loss of shouldering (pathological) Late recovery * (pathological) Overshoot shouldering +/- variability (pre- pathological) Smoothing at trough (pathological) Biphasic deceleration * (pathological) * = also Labour Variable
- 60. The Darent Valley CTGMasterClass Course Bringing order to Chaos Fetal acid-base status
- 65. Hypoxia Acute (total) hypoxia –Baby can survive 10 minutes before permanent brain damage Sub-acute (chronic partial) hypoxia – Baby can sustain 60 minutes before permanent brain damage Chronic ‘hypoxia’ (technically hypoxaemia) – PET / IUGR
- 66. Acute Total Hypoxia Completecessation in flow through cord No gas exchange Increasing fetal acidosis Increasing hypoxia Base deficit will increase by 1 mmol per min Increasing damage to basal ganglia between 10 and 25 minutes Most dead after 25 minutes
- 67. Prolonged Partial Hypoxia Heartrate below baseline > at baseline Fetal hypotension Cerebral hypoperfusion Reduced pressure “sprinkler effect” Damage to the watershed areas
- 70. Respiratory acidaemia andmetabolic acidosis
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- 74. Fetal Blood SamplepH> 7.30 = repeat pH 7.25-7.29 = repeat pH 7.20-7.24 = consider delivery pH < 7.20 deliver BUT… beware the normal pH with a high base deficit Also consider pCO2
- 75. Normal range –cord gases
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- 79. Cord Bloods • Essentialto differentiate between – Acute hypoxia – Chronic hypoxia – Acute on chronic hypoxia • Requires both venous and arterial samples with pH and base deficit • Arterial pH ALWAYS lower than venous
- 81. The Darent Valley CTGMasterClass Course Bringing order to Chaos markwaterstone@obstetricexpert.co.uk Use of Ultrasound in Fetal Monitoring
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- 86. Doppler Christian Doppler The firstfetal doppler was invented by Dr. Edward H. Hon in 1958
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- 88. Fetal Doppler • RoutineDoppler USS in low risk / unselected pregnancies does not confer benefit • The use of Doppler USS in high risk pregnancies appears to improve a number of obstetric care outcomes and appears promising in reducing PND (OR 0.71)
- 89. High-Risk Doppler • FewerIOL (OR 0.83; 0.74-0.93) • Fewer TCIs (OR 0.56; 0.43-0.72) but no difference in … • Fetal “distress” in labour (OR 0.81; 0.59-1.13) • Caesarean delivery (OR 0.94; 0.82-1.06)
- 90. An early stagein fetal adaptation to hypoxaemia • Central redistribution of blood flow (brain- sparing reflex) • Increased blood flow to protect the brain, heart and adrenals • Reduced flow to the peripheral and placental circulations
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- 97. Doppler wave formof early stage of fetal hypoxaemia • Increased end-diastolic flow (EDF) in the middle cerebral artery – ↓MCA pulsatility index (PI) / resistance index (RI) • Decreased end-diastolic flow in the umbilical artery – ↑umbilical artery RI
- 98. MCA – fetalanaemia
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- 100. Uterine Artery Dopplers a. non-pregnant b.1st trimester c. 2nd trimester d. 3rd trimester e. Abnormal with ↑resistance
- 101. Biophysical Profile (BPP) ComponentDefinition Fetal movements 3 body or limb movements Fetal tone One episode of active extension and flexion of the limbs; opening and closing of hand Fetal breathing movement episode of > 30 seconds in 30 minutes Hiccups are considered breathing activity. Amniotic fluid volume single 2 x 2 cm pocket is considered adequate. Non-stress test (i.e. CTG) 2 accelerations > 15 beats per minute of at least 15 seconds duration.
- 102. PNM and theBPP Score Score Perinatal Mortality/1000 8-10 1.86 6 9.76 4 26.3 2 94.0 0 285.7
- 103. BPP - Cochrane •Not enough evidence to support use in high-risk pregnancies • Associated with significantly increased use of induction and caesarean section • Recommended by NICE for monitoring of twins in late pregnancy
- 104. USS - Summary USShas a central place in fetal monitoring Caution regarding predictions Cannot be used in isolation
- 105. Progress in placentalfailure ↓ umbilical artery EDF ↑ MCA flow ↓ aortic flow Mod-severe redistribution ↓ growth Abnormal venous flow ↓ FM ↓ LV Abnormal CTG
- 107. The Darent Valley CTGMasterClass Course Bringing order to Chaos markwaterstone@obstetricexpert.co.uk NICE / CNST
- 108. NICE provides...... ... thealphabet blocks from which words are made It is not the words themselves
- 109. NICE Guidance does notapply to antenatal traces only intrapartum
- 110. Issue date: September2007 NICE clinical guideline 55 Developed by the National Collaborating Centre for Women’s and Children’s Health Intrapartum care Care of healthy women and their babies during childbirth 2001
- 112. Classification of FHRtrace features NICE 2007
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- 115. Rule of 3s 0:bradycardia commences 3: bradycardia confirmed and help called 6: help (reg) arrives 9: decision to deliver taken and transferred 12: anaesthesia commences 15: delivery of baby
- 116. Hinshaw K (1996)ALSO course manual DR C BRAVADO D determine R risk C contractions B baseline R rate A and V variability A accelerations D decelerations O overall impression and plan
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- 119. REMEMBER CTGs are aSCREENING tool... not a DIAGNOSTIC tool Fetal Blood Sampling is a DIAGNOSTIC tool NICE: CTGs should be backed up by fetal blood sampling
- 120. Not so NICE… •No mention of contractions • Does not allow for shallow decelerations • No upper limit for variability • Does not take into account changes in CTG within the normal range • Does lead to ‘jobsworths’ waiting for 90 minutes before reporting a flat trace as pathological
- 121. All very NICE,but...
- 122. All very NICE,but...
- 124. Need to retaincommon sense And remember ... It’s only a guidance
- 126. CNST Standard 2– Criterion 1 Care of women in labour • Observations to be carried out on admission and in 1st, 2nd and 3rd stages as per NICE • Documentation of observations as per NICE
- 127. CNST Standard 2– Criterion 3 Continuous EFM • Date and time checks on CTG machines as per NICE • Minimum data on tracing: – Name & hospital number – Date & time – Any intrapartum event, recorded at time of event, signed and timed – Any review documented on trace as well as notes – End of trace documentation as per NICE • Hourly systematic assessment of trace as per NICE
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