Transcript Electronic Fetal Monitoring CTG CASES

Electronic Fetal Monitoring
HISTORY 
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EFM
1818-Francios Major in Geneva-DDx between FH and
Maternal Pulse
1827- John C Ferguson –described FHR sounds.
1849-Killian indicated FHr parameters requiring interventions.
1876-Pinard produced his design for a fetal stethoscope.
1893-Winkel set normal FHR120-169 bpm.
1958-Hon in USA and Hammacher in Europe introduced first
EFM.
1964- Doppler ultrasound scan replaced phonocord.
1966- Saling in Berlin introduced FBS.
1968-Hamacher and Hewitt-Packard developed first fetal
monitor.
1985- Dublin RCT changed terminology for the CTG
interpretation.
Electronic Fetal Monitoring
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Pioneered in 1958 by Hon.in USA and
Hammacher in Europe
Commercially available 1968
Continues monitoring of FH in low risks
pregnant -lacks evidence
Needs to be viewed in conjunction with
other assessment e.g. FBS and clinical
situation.
Should be used for the right reason and
with appropriate degree of skill.
EFM-ISSUES
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Detect fetal hypoxia i.e reduce and avoid harm to
the fetus and improve fetal and baby out-come.
Severe acidosis may result in FHR changes.
Could occur in Normal physiological response in
labor.
Misunderstanding the physiological and
pathphysiological CTGs will improve the Mx.
EFM Problems and Realities
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Electronic Intra-partum FHR Monitoring is now considered
mandatory for high-risk pregnancies.
Difficulties with interpretation include over confidence and not-only
difference in opinion between practitioners but, also when the
same practitioner examines the same CTG twice.
Increases CS rates 1.41%rr.
Increases operative vaginal delivery 1.20%rr.
And no change in incidence of C Palsy.
Reduction in Neonatal seizures rates 0.51%
No difference in APGAR scores.
? About the efficacy.
EFM- Facts
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Reliability of interpretation-50-75% are
false positive .
False positive Dx reduces to 105 with FBS.
FBS 93% sensitivity, 6% false positive.
PH Vs Lactate -39% Vs 2.3(rr 16.7).
Electronic Fetal MonitoringIndications
Indications for the
continuous EFM
 High risk
pregnancies
 IOL and
Augmentation of
Labour.
 Reduced FM.
 Premature
labour/TPL.
 APH/IPH
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Oligohydramnios
Hypertension.
Abnormal FHR
detected.
Malpresentation and in
labour.
DM,Multiple Gestation.
Previous CS.
Abdominal Trauma.
Prolonged ROM.
Meconium Liq.
EFM- Interpretation
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Consider :
Intrapartum/antepartum trace.
Stage of labour.
Gestation.
Fetal presentation, ?Malpresentation.
Any augmentation,?IOL Medications
Direct or indirect monitoring/
EFM- 4 Basic Features of FH
Trace
EFM-4 Basic Features.
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Baseline FHR - Mean level of FHR when this is stable,
excluding Accelerations and Decelerations (110-160
bpm)
-Tachycardia
-Bradycardia
Baseline Variability-5 bpm or greater than or equal to
5bpm, between contractions
-Normal
-Non-reassuring-Less than 5 bpm or less but less than
30 min
-Abnormal-less than 5 bpm for 90 min or more.
Baseline variability
Baseline variability
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The minor fluctuations on baseline
FHR at 3-5 cycles p/m produces
Baseline variability.
Examine imin segment and estimate
highest peak and lowest trough.
Normal is more than or equal to 5
bpm.
Factors affecting Baseline
variability.
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Para-Sympathetic affects short term
variability whilst Long Term is more
Symp.
CNS ,Drugs reduce Variability
High gestation increases variability
Mild Hypoxia may cause both S and
para S stimulation.
Non-reassuring Baseline
variability.
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NRCTGs- reduced or less than 5 bpm for 40
min or more but less than 90 mins..
B-B or short Term V is varying intervals
between successive heart beats .
Long Term v is irregular waves on the CTG
3-5 bpm.
Normal is 5-25 bpm– this indicates N-CNS.
EFM-Accelerations
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Accelerations- transient increase in FHR of 15 bpm or
more lasting for 15 sec.
Absence of accelerations on an otherwise normal
CTG remains un clear.
Presence of FHR Accelerations have Good outcome.
EFM Decelerations
Decelerationstransient slowing of
FHR below the
baseline level of
more than 15 bpm
and lasting for 15 sec.
Or more.
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Electronic Fetal Monitoring
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a) Early Decelerations (fig 3)
 Head compression
 Begins on the onset of contraction
and returns to baseline as the
contraction ends.
 Should not be disregarded if they
appear early in labor or Antenatal.
 Clinical situation should be r/v
Fig 3 Early Decelerations
Late Decelerations.
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Uniform periodic slowing of FHR with
the on set of the contractions .
Repetitive late decels increases risk of
Umbilical artery acidosis and Apgar
score of less than 7 at 5 mins and
Increased risk of CP.
Electronic Fetal Monitoring
b) Late Decelerations (Fig 4)
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Due to acute and chronic feto-placental
vascular insufficiency
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Occurs after the peak and past the length of uterine
contraction, often with slow return to the baseline.
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Are precipitated by hypoxemia
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Associated with respiratory and metabolic acidosis
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Common in patients with PIH, DM, IUGR or other
form of placental insufficiency.
Fig 4 Late Decelerations
Late Decelerations
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Reduces Baseline variability together
with Late Decelerations or Variable
Decelerations is associated with
increased risk of CP.
EFM- Variable Decelerations
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Variable intermittent periodic slowing of FHR with rapid onset
recovery and isolation.
They can resemble other types of deceleration in timing and
shape.
Atypical VD are associated with an increased risk of umbilical
artery acidosis and Apgar score less than 7 at 5 min
Additional components:
Loss of 1 degree or 2 degree rise in baseline Rate
Slow return to baseline FHR after and end of contraction.
Prolonged secondary rise in Base FHR
Biphasic deceleration
Loss of variability during deceleration
Continuation of base line at a lower level.
Electronic Fetal Monitoring
c) Variable Deceleration (Vagal activity) (Fig 5)
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Inconsistent in configuration,
No uniform temporal r-ship to the onset of contraction, are
variable and occur in isolation.
Worrisome when Rule of 60 is exceeded (i.e. decrease of
60 bpm,or rate of 60 bpm and longer than 60 sec)
Caused by cord compression of the umbilical cord
Often associated with Oligo-hydroaminos with or without
ROM
Can cause short lived RDS if they MILD
Acidosis if prolonged and Recurrent.
Fig 5 Variable Decelerations
EFM Prolonged deceleration
Prolonged Deceleration (Fig 6)
 Drop in FHR of 30 bpm or More lasting for at
least 2 min
 Is pathological when crosses 2 contractions i.e 3
mins.
 Reduction in O2 transfer to placenta.
 Associated with poor neonatal outcome.
EFM- Prolonged Decelerations
CAUSES
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Cord prolapse.
Maternal hypertension
Uterine Hypertonia
Followed by a VE or ARM or SROM
with High PP.
Fig 6 Prolonged Deceleration
EFM Mx Prolonged
Deceleration
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Maternal position
IV fluids
V.E to exclude cord prolapse
Assess BP
FBS if cx dilated and well applied PP
Mx Depending on the clinical situation.
Baseline Bradycardia
FH below 110bpm(FIGO ).
 less than 100bpm (RANZCOG).
Causes.
Postdates, Drugs, Idiopathic,
Arrythmias, hypothermia(increased Vagal
Tone)
Cord Compression (Acute Hypoxia, congenital
H/disease and Drugs).
Mx depends on the clinical situation.(FBS,VE
Observation or expedite delivery)
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Types
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Moderate Bradycardia 100-109 bpm
Abnormal bradycardia less than
100bpm.
Tachycardia 161-180 bpm
Abnormal Tachycardia more than 180
bpm
Ranzcog Australian more than 170
bpm
Baseline tachycardia and
Bradycardia.
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Uncomplicated baseline tachycardia
161-180 bpm or bradycardia 101-109
do not appear to be associated with
poor NN outcome.
Causes of B Tachycardia.
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Asphyxia
Drugs
Prematurity
Maternal Fever
Maternal thyrotoxicosis
Maternal Anxiety
Idiopathy
Mx depends on the clinical situation
Electronic Fetal Monitoring
Baseline Bradycardia
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FH Rate below 110bpm (FIGO Recommended)
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Postdates
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Drugs
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Idiopathic
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Arrhythmia's
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Hypothermia.(Increased Vagal tone),
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Cord compression(Acute Hypoxia,Congenital
H/disease, and drugs)
Mx depends on the clinical situation. (FBS, VE,
Observation or expedite Delivery).
Electronic Fetal Monitoring
Baseline Tachycardia
 Asphyxia
 Drugs
 Prematurity
 Maternal fever
 Maternal thyrotoxicosis
 Maternal Anxiety
 Idiopathy
Mx depends on the clinical situation
Interpretation of the CTG
EFM-Sinusoidal Pattern
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Regular Oscillation of the Baseline longterm Variability resembling a Sine wave
,with no B-b Variability (Fig 2),
Has fixed cycle of 3-5 p min. with amplitude
of 5-15 bpm and above but not below the
baseline.
Should be viewed with suspicion as poor
outcome has been seen (eg Feto-maternal
haemorrhage)
Electronic Fetal Monitoring
Sinusoidal pattern - distinctive smooth undulating
Sine-wave baseline with no B-b variability ( Fig 2 )
 0.3 % (Young 1980)
 cord compression
 hypovolemia
 ascites
 idiopathic(fetal thumb sucking)
 Analgesics
 Anaemia
 Abruption
 Mx r/v clinical situation
EFM- Saltatory pattern
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Seen During Fetal thumb sucking.
Could be associated with Hypoxia.
See slide 11.
NR CTGs
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Difficult to interpretation,leads to
Increased rate of C Section.
50% CTG in Labour have 1 abnormal
feature
15-20% Nr CTGs (pathological).
?? To reduce CS….
FOREMOST
Feta oximetry randomised
evaluation Multi Oxygen saturation Trial
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To evaluate the role of F Sats P02
Had a Multicentre Randomised trialRWB Brisbane
MMH Brisbane
RWH Melbourne
RWH Sydney
Endpoints
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To reduce Operative deliveries for the Nr CTG by
1/3
The Sample size was 600 participants.
Secondary EndpointInvestigate the incidence of Dystocia
F/up outcomes
Low Umbilical arterial PH
NICu admissions
HIE (Enchelopathy)
Maternal perception of monitoring
Clinician perception of sensor placement.
NR CTG (Foremost)
Any of the following for more than 15minPersistent Late decelerations
Sinusoidal pattern
Variable decels
Less than 70 bpm for more than 60 sec
Persistent slow return to the baseline
Long term variability less than 5 bpm
Tachycardia more than 160 bpm.
Recurrent prolonged deceleration 2 or more in15 min and less
than 70bpm for 90 sec .
Any on of the following for more than 60 min
Tachycardia with variability less than 5bpm
Persistent reduced baseline variability less than 5 bpm for more
than 60min.
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Inclusion Criteria
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NR CTG
Consent
Gest age more than 36 k
Early or active labour
ROM or eligible for
Exclusion criteria
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Multiple gestation
Non-Vertex
Pl Praevia
APH
Fetal anomaly
HIV other
Thrombocytopenia.
Clinical Mx Protocol
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CTG Only
Reassuring –continue labour unless
otherwise indicated
NR CTG –Evaluate and manage NR
CTG
Suspicious CTG
Deliver for NR Fetal Status.
CTG and Oximetry
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Reassuring CTG Continue
NR CTG Continue unless otherwise
indicated( FSp02 Reassuring) If FSp02
less than 30%- Further Evaluation and
MX
Suspicious CTG -Deliver
Conclusion
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R/v NR CTG Mx tools & decision
making
Responsibility to assess new
technology before widespread
introduction
Overview of Multicentre RCT
Case presentation.
Reliability of CGT
Interpretation
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50%-75% false positive
False Positive Dx is reduced to 10%
with FBS
PH Vs lactate 39% Vs 2.3%(rr16.79).
Fetal Blood Sampling
information on the acid base balance
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Has 6%-20% false- normal
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8-10% False Low values
Why and when to doPersistent Abnormal CTG after reversible factors have been
corrected, Persistent late decels and 2 abnormal other
features e.g baseline tachycardia or reduced B-B variability or
just difficult to interpret the CTG
Rom, PP accessible and well applied Cx dilatation at least 3 cm or
more
Left lateral maternal position
Sterile environment and good light and equipment.
Good analgesia
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FBS-PH
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Introduced by Sailing –fairly reliable
predictor of fetal PH in presence of
abnormal FHR
Has an error of 15% falsely low and 5
% falsely increased, however in
presence of abnormal FHR a scalp PH
of less 7.2 is pathologonomic of fetal
asphyxia.
FBS-Cord PH
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FBS-Arterial
Normal-7.25-7.35 Normally good agreement
between Apgar,cord PH .
Less than 7.20-significant asphyxia
Values between 7.2 and 7.24 need further
evaluation
Low –normal PH should be repeated in 30
min
Less than 7.20- eminent delivery
FBS- Lactate
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FBS easier to interpret, difficult to perform
Anaerobic metabolism can lead to metabolic
acidosis
Lactate is major end product of metabolic
acidosis
Lactate levels more specific for degree of
metabolic acidosis than Ph
Lactate rises quicker takes longer to resolve
than Ph.
FBS Contraindications
Fetal
Premature –less than 34 ks
Active Herpes
Known HIV,Hep B,C positive status.
Thrombocytopenia.
MaternalUnfavourable Cx
Mobile PP
Malpresentation(face etc) uncertain??
Pl Praevia or APH
Sepsis
FBS-Sampling errors
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Between decelerations if possible
Avoid Excess pressure on PP reduces
perfusion
Do not sample on the caput.
Failure of scalp to bleed –due to
peripheral shut down.
EFM-Summary
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Normal - CTG with all 4 Features
Suspicious -one non reassuring category
and reminder are reassuring
Pathological -2 or more non-reassuring
categories or one or more abnormal
categories.
At Birth
Need to Consider
Cord PH if CTG suspicious
Preterm labour
Mec Liquor
FBS intrapartum
Flat baby at delivery
Operative or instrumental delivery.
Mx of FBS Results
If PH /Lactate normal –Observe
 Pre-acidotic were CTG remains to be
Suspicious –Rpt after 30 min.
 Acidotic-eminent delivery
 Instrumental or CS depending on the clinical
situation.
Lactate
 4.8 upper limit-average 2.8 in 1st stage–
changes in labour
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Electronic Fetal Monitoring
Education and training
 Improves Knowledge for all staff
 Improves clinical skills
 Training should include instruction on
documenting traces and storage
 Training should include appropriate clinical
responses to suspicious or pathological traces
 Training should include local guidelines
relating to fetal monitoring both intermittent and
EFM
EFM-Legal Issues
CTG in Litigation
 Unsatisfactory or Missing
 Abnormal CTG ignored or not recognized
 Traces not done.
Risk Mx
 EFM traces should be kept up to 25 years.
 If removed for teaching purposes or etc,
should be easily located
 Minimize incidence of adverse outcome
Legal Issues
In the U.K
 70% of cases are due to EFM.
 In U S A 45.8% involve E F M,
3.8% more $1Million payouts and
only17% are due to delay or failure to
diagnose fetal distress.
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What Influences Litigation
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Consumer Expectation
The profession –education
The employer (policies/procedures)
Legislation (duty of care/scope of
practise/ registration)
Legal issues- Consumer
expectation
Are for a good outcome (healthy
baby/mother)
Bad outcome
 Someone to blame
 Someone must pay
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Professional Responsibility
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To act within scope of practise.
To seek support and guidance
Work within organisational standards
Duty of care to the woman and
employer
Maintain knowledge and skills
(evidence Based Practise)
Be prepared to defend ones practise.
When EFM is the focus of
Malpractice
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Comparison of consistency of
documentation contained on the trace and in
the chart will be made
Lapse in documentation may leave doubt
about the quality of care.
Hospital policy and procedure manuals will
be examined
Competency levels will be evaluated expert
witness (plaintiff/defence)-to determine if
acceptable standards were applied.
Major Omission in Liability
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Failure to appropriately monitor the
mothers and fetus status
In appropriate Syntocinon monitoring
Failure to notify the physician in a
timely manner.
Initiation of procedures without
adequate client information or consent
Elements of successful
Malpractice Action
The clinician had a duty to the woman
 The clinician had committed a breach
of duty
 The woman suffered damages
 There was a casual connection
between the clinician’s actions and the
woman's damage.
(MacRae,1993)
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Legal issues
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If you are going to use the CTG You
must be able to Interpret the trace and
respond accordinglyIt’s a permanent record
One that is scrutinized in litigation case
May be pivotal in determining liability
Legal issues
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A normal CTG can be used to indicate that
that were no abnormalities and no indication
for intervention.
An abnormal CTG or suspicious trace may
provide evidence that inappropriate or lack
of treatment may give rise to litigation,whilst
CTGs could be viewed as part of “defensive
medicine”, litigation is reported to be on the
increase but there is not enough data
reporting system in Australia to support this.
References
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Manual Obs and Gyn. by Niswander,
MD
Fetal Monitoring RCOG UK
CTGs RANZCOG
Literature review articles American
Family Physician
CTG Made Easy