!

Intrapartum assessment
During labor, CTG is a good indicator of fetal
compromise, particularly if used in conjunction with fetal
blood sampling - Murphy et al 1990

Great Expectations
Intrapartum Assessment: Fetal Emergencies

Electronic fetal heart rate monitoring provided accurate Whats the problems in
information. intrapartum
The information was of value in diagnosing fetal distress. assessment?
It would be possible to intervene to prevent fetal death
or morbidity.
Continuous electronic fetal heart rate monitoring was
superior to intermittent methods.
3.3. Cerebral palsy and intrapartum events

A recent international consensus statement attempted to define a causal

2 4 0 raju
relationship between acute intrapartum events and cerebral palsy.2 That
document was not aiming to examine the failings of intrapartum monitoring
techniques but to highlight the rarity with which acute intrapartum events Development of fetal monitoring
were associated with cerebral palsy.
Epidemiological data suggest that only 10% of cases of cerebral palsy have IIa
potential intrapartum causes and, even in some of these there may have In the first study, there was a significant increase in the odds of developing IIa
been an antenatal component.1 neonatal encephalopathy in the presence of an abnormal CTG in the first or
The document concluded that for a diagnosis of cerebral palsy to have been III last 30 minutes of labour.25 Abnormal was defined as either suspicious or
the result of intrapartum hypoxia certain criteria should be fulfilled (see ominous patterns as defined by the International Federation of Gynecology
Appendix 1). These included evidence of metabolic acidosis, moderate to and Obstetrics (FIGO) classification,11 (first 30 minutes: OR 2.89, 95% CI
severe neonatal encephalopathy and the presence of specific types of 1.077.77; last 30 minutes: OR 7.5; 95% CI 2.1426.33). However, no
cerebral palsy. Similarly, the authors thought that there needed to be association with neonatal encephalopathy was seen if a different CTG
evidence of a sentinel hypoxic event (see Appendix 1). In the absence of scoring system was used.43
any of the essential criteria, an intrapartum cause could be assumed. The In the second study, the definition of an ominous CTG was based on the IIa
absence of any of the five remaining criteria similarly would cast doubt on classification used in the Dublin RCT.34 This included any marked
the diagnosis of an intrapartum cause of cerebral palsy. tachycardia or bradycardia (limits not defined), a moderate
tachy/bradycardia with minimal variability, late decelerations or severe
variable decelerations. A significant association with an ominous CTG was
3.4. EFM as a screening test seen with both first- and second-stage traces (first stage: OR 10.2, 95% CI
2.936.4; second stage: OR 7.2, 95% CI 2.124.4).42
As highlighted above, EFM was introduced with an aim of reducing perinatal In the last of these studies, an abnormal CTG (which was reported as those IIa
mortality and cerebral palsy. This reduction has not been demonstrated and, interpreted by the attending clinician as abnormal) was associated with a
in turn, an increase in maternal intervention rates has been shown in significant increase in the odds of neonatal encephalopathy (OR 1.98; 95%
systematic reviews and RCTs. However, the the lack of improvement in CI 1.263.10). However, as these are casecontrol studies, caution is needed
neonatal outcome and also the increase in intervention rates should be F i g . 1 ( continued
in ascribing a causal relationship to the) . observed effect.
viewed with caution, givenF i g . the low ) .incidence of the outcomes EFM seeks to IIa
r e s o l v e t o h The e l p h relationship
i m s e l f a n d o between t h e r s w i t h neonatal d i s a b i l i t encephalopathy
i e s . A f t e r s t u d y i and n g F r subsequent
2 ( continued

reduce. e n c h a t th e
disability has been examined in a systematic review of five cohort studies
s y l v a n i a i n P h i l a d e l p h i a i n 1 8 8 4 [ 2] 1 ,2 2 . B a s e d o n th e e x p er ie n c e o f s e e in g c e l e b r a t e d J e s u i t C o l l e g e i n S t . O 44 m e r , h e d e c i d e d t o b e c o m e a d o c t o r . T w o y e a r s
Current
1 5 1 c h i l prevalence
d r e n w i t h n e u r o l rates o g i c d e f for
o r m i t perinatal
i e s a t t h e P h i l mortality,
a d e l p h i a I n f i r mneonatal
a r y f o r N e r - encephalopathy IIa (see Evidence Table 4). All the studies used a similar grading/staging system
andChildren cerebral palsy are shown below (Table
v o u s D i s e a s e s , O s l e r p u b l i s h e d a m o n o g r a p h e n t i t l e
3.1). Of these, only a small
d The Cerebral Palsies of o f a p p r e n t i c for e w definingo r k u n d the e r grade
J a m e s ofS neonatal
e q u e i r a , encephalopathy
a l o c a l s u r g e o n and , a n therefore
d 3 m o r e data y e a from
rs o f
( F ig . 2 B ] ) [ 2 3 . A v i s i o n a r y w o r d s m i t h , O s l e r i n tr o d u c e d t h e p h r a s e s t u d y a t t h e each L o n d can o n be H o compared.
s p i t a l q u a l The i f i e d results
h i m t suggest
o b e c o m e a the s u rlikelihood
g e o n . H e ofo b death t a i n e dor a
proportion
cerebral palsy aret o d thought
e s c r i b e t h i s to n o n be
p r o g r attributable
e s s i v e n e u r o m u s c to u l a r intrapartum
d i s e a s e i n c h i l d r e n causes,
. hence the that
trueI n preventable
h i s m o n o g r a p h , O prevalence
s l e r r e p o r t e d 1 2 0 for c h i l d these
r e n w h o conditions
h a d h e m i p l e g i a is a n d also
2 0 o t h shown.
er s l i c e n t i a t e f r o developing
m t h e S o c isevere e t y o f handicap
A p o t h e c a was r i e s proportional
o f L o n d o n i to n 1 the 8 3 1 grade
, a n d ort h e severity
n e x t y eofa r
With
w h o h a d b i l a t e r a l h e mi p l e g i a s . B e s i d e s t h e u s u a l o s l e r i a n w i t a n d c l a r i t y , t h i s
w o r k the
a l s o lowp r o v i d e prevalence
s a n e x c e l l e n t c l a of s s i f i these
c a t i o n o f conditions,
c e r e b r a l p a l s y . any screening test would
w a s a d m i t t e neonatal
d t o t h e encephalopathy
R o y a l C o l l e g e (Table o f L o 3.2).n d o n.
require a specificity above 99% to avoid numerous unnecessary L i t t l e c o nOne t i n u ofe d thes u rlimitations
g i c a l t r a i of n i n theg studies
i n L o n examining
d o n , B e r l neonatal
i n , L e i p z encephalopathy
i g , a n d D r e s d as e n.
interventions. W h i l e i n B e an r l i outcome
n , h e p e rmeasure s u a d e d has D r . been L o u i thes S t absence
r o m e y e r oft o anp agreeder f or m definition
s u b c u t a ofn e the
o u s
t e n o t o m y , gradinga n e w s of u r g babies
i c a l p r witho c e d u encephalopathy.
r e o f i n c i s i n g t An h e Aoutline
c h i l l e s oft e an d recommended
o n s to re le a s e
system for grading is presented in Appendix 3.
Table 3.1 Overall and intrapartum prevalence rates for perinatal mortality, neonatal c o n tr a c t u r e s . R e p o r t e d l y , t h e p r o c e d u r e c o m p l e t e l y c u r e d L i t t l e s f o o t d e f o r m i t y .
encephalopathy and cerebral palsy
Table 3.2 Likelihood ratios of death and severe disability in relation to grade of
Condition Prevalence Prevalence of intrapartum causes neonatal encephalopathy
Perinatal mortality6 8 per 1000a 0.8 per 1000a Grade of neonatal Likelihood ratiosa for Likelihood ratiosa for severe
Neonatal encephalopathy25 7 per 1000b encephalopathy death(95% CI) disability (95% CI)
Cerebral palsy26 1.1 per 1000c 0.1 per 1000c
1: Mild 0.09 (0.030.30) 0.10 (0.030.28)
a
per 1000 live births 2: Moderate 0.39 (0.210.71) 1.51 (1.191.52)
b
includes all grades of encephalopathy 3: Severe 10.98 (7.5615.94) 16.60 (6.8535.70)
c
per 1000 children who survived to three years of age (includes all birthweights) a
refer to glossary for definition

19 3.6.5. Umbilical cord blood acid-base status

A single RCT (see Evidence Table 5) has found that EFM was significantly Ib
more sensitive in detecting both respiratory and metabolic acidosis in
comparison with intermittent auscultation.45 However, the specificity was
poor (detection of all acidosis: EFM: sensitivity 97%, specificity 84%;
intermittent auscultation: sensitivity 34%, specificity 91%).
A number of studies have examined the relationship between acidaemia with IIa
both short-4648 and long-term4952 complications (see Evidence Table 6). In the
 JM Roberts et al, SGI Meeting 2008 JM Roberts et al, SGI Meeting 2008

Identification of "fetal distress" The terms fetal distress

based upon fetal heart rate and birth asphyxia are too
patterns is imprecise and broad and vague to be
controversial. applied with any precision
to clinical situations

ACOG, 2004 ACOG, 2004

MODEL FOR FETAL RESPIRATORY
STATUS AND INJURIES

NORMAL OXYGENATION

HYPOXIA

ACIDOSIS

TISSUE DAMAGE/DEATH

Why is the diagnosis of fetal A large proportion of asphyxial damage

distress based on heart rate begins before labor and may not benefit
patterns so tenuous? from electronic FHR monitoring-
prompted interventions occurring during
labor.

Williams 23rd, 2011 ACOG, High-Risk Pregnancy

Series 2002
 binations of maternal factors and MAP in the detection

Table 2Pearson correlation between log10 uterine artery L-PI MoM, log10 MAP MoM and log10 PAPP-A MoM i
of late PE. There was also prediction from the combi-

Log10
nation of maternal factors, uterine artery L-PI and MAP

Unaffected

<0.0001
(Poon et al., 2009b) but this was not improved by the

0.103
0.067

0.018

addition of PAPP-A.

1
Y = 0.273 + 2.469 log10 maternal factor-derived a
Work on Pregnancy
Prenatal diagnosis
priori risk for late PE 0.964 log10 PAPP-A MoM;
Nagelkerke R 2 = 0.135, p < 0.0001.

0.911
0.010

0.030
0.727
Y = 0.447 + 2.580 log10 (risk for late PE based

GH

Log10 uterine artery L-PI MoM
on maternal factor and MAP) 0.941 log10 PAPP-A

1
MoM; Nagelkerke R 2 = 0.207, p < 0.0001.
But for a variety of reasons, many aspects of

<0.0001
0.890
0.011

0.286
Gestational hypertension

PE

human health and disease remain very dicult to

1
study and, consequently, are poorly understood.
Logistic regression analysis demonstrated that there was
Pregnancy is a prime example.

Unaffected
no significant additional contribution from PAPP-A and

<0.0001

<0.0001
- Susan J Fisher

0.067

0.159
combination of maternal factors, MAP and uterine artery

L-PI in the prediction of GH (Poon et al., 2009b).

1
The areas under the ROC curves and detection rates
of early PE, late PE and GH for different false-positive
rates in screening by the combinations of maternal

Pearson correlation
Pearson correlation

Pearson correlation
factor, MAP, uterine artery L-PI and PAPP-A are given
in Table 3. The ROC curves for the prediction of early
PE by combinations of maternal factor, MAP, uterine

p
artery L-PI and PAPP-A are shown in Figure 2. The
performance of screening for early PE, late PE and GH
by risks generated by the specific prediction algorithm
Sequential Screening Log10 uterine artery L-PI MoM for early PE based on maternal factors, MAP, uterine
artery L-PI and PAPP-A is given in Table 4.
hypertension (GH) groups

Example
individual risk = Log10 PAPP-A MoM
For example, in a Black woman in her first pregnancy,
Log10 MAP MoM

a priori risk x test1-LR x cfactor with no family history of PE, who is 28 years old, has
a BMI of 20 kg/m2 , does not smoke and is at 12 weeks
x test2-LR x cfactor x test3-LR gestation (CRL 65 mm), a uterine artery L-PI of 1.6, her
x cfactor MAP is 85 mmHg, her PAPP-A is 1.0 MoM, the risks
of developing early PE, late PE and GH are 0.20, 2.17
and 1.37%, respectively.

Copyright 2010 John Wiley & Sons, Ltd. Prenat Diagn 2010; 30: 216223.
DOI: 10.1002/pd
(PE), late PE and gestational hypertension (GH) by risks gener- MoM) = 4.280
Y = 0.468 + 2.272 1.699 (log maternal factor- Odds = eY = 0.014
ated by the specific prediction algorithm for early PE based on
maternal factors, mean arterial pressure, lowest uterine artery derived factor-derived
Maternal a priori risk afor late risk
priori + early
PE) for 21.147PE: 0.021 Risk for late PE = 0.014 = 1.37%.
pulsatility index and pregnancy-associated plasma protein-A (log MAP MoM) + 3.537 0.023 (log uterine artery
L-PI MoM) = 3.806
Y = 5.674 + 1.267 (Black race) + 0 (history of If the same woman had had a previous pregnancy with
Detection rates (%) PE, a BMI of 35 kg/m2 , her lowest uterine artery PI is
chronic
Odds = eY = 0.022+ 0 (spontaneous conception)
hypertension)
+Risk for late PE==4.406
0 (nulliparous) 0.023 = 2.17%. 2.2, her MAP is 100 mm Hg and her PAPP-A is 0.9
Risk (%) False-positive rate (%) Early PE Late PE GH
MoM, her risks for early PE, late PE and GH would be
1.0 6.5 86.5 40.0 17.9 A posteriori risk for GH based on biophysical mark-16.48, 38.29 and 12.48%, respectively.
1.5 4.8 81.1 33.6 16.4 Odds= eY = 0.012
ers:
2.0 3.8 78.4 32.8 12.9 A priori = odds/(1 + odds) = 0.012 = 1.21%.
2.5 3.0 75.7 28.0 10.0 Y = 0.357 + 2.251 1.936 (log maternal factor- DISCUSSION
5.0 1.6 51.4 18.4 6.4 derived factor-derived
Maternal a priori risk for + 18.953
GH) risk
a priori for latePE:
0.021 (log
10.0 0.7 35.1 12.8 3.6 MAP MoM) + 1.869 0.023 (log uterine artery L-PI
= 4.280 The findings of this study have confirmed the results
Y MoM)
= 7.856 + 0.034 28 (age in years) + 0.096 of several previous studies that low-maternal serum
Odds
20 (BMI= eY = in 0.014
kg/m2 ) + 1.089 (Black race) + PAPP-A concentration at 1113 weeks is associated
Maternal factor-derived a priori risk for early PE: 0 Risk for late
(womans PE = had
mother 0.014 PE) =+ 1.37%.
0 (nulliparous) = with increased risk for subsequent development of PE
3.892
Y = 5.674 + 1.267 (Black race) + 0 (history of Odds If the=same woman had had a previous pregnancy with(Ong et al., 2000; Smith et al., 2002; Yaron et al., 2002;
eY = 0.020 2 Dugoff et al., 2004; Spencer et al., 2005, 2007; Pilalis
chronic hypertension) + 0 (spontaneous conception) PE,
+ 0 (nulliparous) = 4.406 2.2,
a BMI
A priori
her
= of
MAP
35 kg/m
odds/(1
is 100
, her=lowest
+ odds)
mm Hg
0.020 =
and
uterine
her PAPP-A is 0.9 The recently recognized contribution of
2.00%.artery PI iset al., 2007). The results demonstrated that the levels
MoM, her risks for early PE, late PE and GH would beof PAPP-A are substantially lower in those developing
Maternal
EARLY SCREENING FOR PREECLAMPSIA
16.48, factor-derived
38.29 and 12.48%, a priori risk for GH:
respectively. 221 early PE rather than late PE. infection producing a fetal inflammatory
Y
Odds= e = 0.012
A priori = odds/(1 + odds) = 0.012 = 1.21%. Y =7.532
Copyright 2010 John+ 0.040
Wiley 28
& Sons, Ltd. (age in years) + 0.098 response may be responsible for a large
Prenat Diagn 2010; 30: 216223.
20 (BMI in kg/m2 ) + 0 (womans mother had PE) +
0 (nulliparous) = 4.446 DISCUSSION percentage of patients who have
DOI: 10.1002/pd

Maternal factor-derived a priori risk for late PE: Y

Odds= e = 0.012 abnormal electronic FHR monitoring
Y = 7.856 + 0.034 28 (age in years) + 0.096
The
A priori = odds/(1
findings of this +study
odds)have = 0.016 = 1.16%.
confirmed
of several previous studies that low-maternal serum
the results
patterns and later develop cerebral palsy.
20 (BMI in kg/m2 ) + 1.089 (Black race) +
0 (womans mother had PE) + 0 (nulliparous) =
A posteriori risk for early PE based
PAPP-A concentration at 1113 weeks is associated
markers:
with increased risk for subsequent development of PE
on biophysical
It is unknown if there is a benefit from
3.892
Y
Odds = e = 0.020
(Ong et al., 2000; Smith et al., 2002; Yaron et al., 2002;
Y = 3.657 + 1.593 1.919 (log maternal factor-
Dugoff et al., 2004; Spencer et al., 2005, 2007; Pilalis
earlier intervention in such cases.

A priori = odds/(1 + odds) = 0.020 = 2.00%. derived a priori risk for early PE) + 31.396 0.021
et al., 2007). The results demonstrated that the levels ACOG, High-Risk Pregnancy
(log MAP MoM) + 13.322 0.023 (log uterine artery
of PAPP-A are substantially lower in those developing Series 2002
L-PI MoM) = 5.755
Maternal factor-derived a priori risk for GH: early
OddsPE = rather than late PE.
eY = 0.003
Risk for early PE = 0.003 = 0.32%.
Copyright 2010 John Wiley & Sons, Ltd. Prenat Diagn 2010; 30: 216223.
DOI: 10.1002/pd
A posteriori risk for early PE based on biophysical
and biochemical markers:
Y = 0.154 + 2.546 2.501 (log risk for early PE
based on maternal factor, MAP and uterine artery L-
Figure 2Receiver operating characteristics curves for the prediction PI) 2.603 0 (log PAPP-A MoM) = 6.213
of early preeclampsia in screening by maternal factors only ( . . . . . . ),
maternal factors with biophysical tests (- - - - - -) and maternal factors
Odds = eY = 0.002
with biophysical and biochemical tests ( ) Risk for early PE = 0.002 = 0.20%.

A posteriori risk for late PE based on biophysical 1. Evidence of metabolic acidosis in intrapartum fetal umbilical
Table 4Performance of screening for early preeclampsia markers:
(PE), late PE and gestational hypertension (GH) by risks gener- arterial cord or very early neonatal blood samples (pH < 7.00 and
Y = 0.468 + 2.272 1.699 (log maternal factor-
ated by the specific prediction algorithm for early PE based on
maternal factors, mean arterial pressure, lowest uterine artery derived a priori risk for late PE) + 21.147 0.021 base deficit 12 mmol/L)
pulsatility index and pregnancy-associated plasma protein-A (log MAP MoM) + 3.537 0.023 (log uterine artery
L-PI MoM) = 3.806
2. Early onset of severe or moderate neonatal encephalopathy in
Detection rates (%)
Odds = eY = 0.022 infants of 34 weeks' gestation

Risk (%) False-positive rate (%) Early PE Late PE GH Risk for late PE = 0.023 = 2.17%.
3. Cerebral palsy of the spastic quadriparetic or dyskinetic type
1.0 6.5 86.5 40.0 17.9 A posteriori risk for GH based on biophysical mark-
1.5 4.8 81.1 33.6 16.4 ! ers:
2.0
2.5 Because the amount of Yderived
3.8
3.0
78.4
75.7 asphyxia
32.8
28.0
12.9
= 0.357 + 2.251
10.0 required
1.936 (log maternal factor-
Criteria that together suggest an intrapartum timing but by themselves
5.0
to cause permanent neurological
1.6 51.4 18.4 6.4
damage
a priori risk for GH) + 18.953 0.021 (log are nonspecific

10.0 0.7 35.1 12.8 3.6
MAP MoM) + 1.869 0.023 (log uterine artery L-PI
4. A sentinel (signal) hypoxic event occurring immediately before
is very near the amount MoM) that
= 4.280
Odds = e = 0.014
causes fetal
Y
or during labor

death,
Maternal factor-derived a priorithe
risk fornumber
early PE: ofRisk patients
for late PE = 0.014who
= 1.37%.
5. A sudden, rapid, and sustained deterioration of the FHR pattern
Y = 5.674 + 1.267develop
(Black race) +cerebral
0 (history of palsy
If the samecaused
woman had hadbya previous pregnancy with
usually after the hypoxic sentinel event where the pattern was
intrapartum+ 0 (spontaneousasphyxia is probably quite
2
chronic hypertension) conception) PE, a BMI of 35 kg/m , her lowest uterine artery PI is
2.2, her MAP is 100 mm Hg and her PAPP-A is 0.9 previously normal

+ 0 (nulliparous) = 4.406
small.

MoM, her risks for early PE, late PE and GH would be
16.48, 38.29 and 12.48%, respectively. 6. Apgar scores of 0-6 for longer than 5 minutes

Odds= eY = 0.012
A priori = odds/(1 + odds) = 0.012 = 1.21%. ACOG, High-Risk Pregnancy
Series 2002
7. Early evidence of multisystem involvement

Maternal factor-derived a priori risk for late PE:
DISCUSSION 8. Early imaging evidence of acute cerebral abnormality
The findings of this study have confirmed the results Essential criteria for defining an acute intrapartum hypoxic event sufficient to
Y = 7.856 + 0.034 28 (age in years) + 0.096 of several previous studies that low-maternal serum cause permanent neurological impairment

20 (BMI in kg/m2 ) + 1.089 (Black race) + PAPP-A concentration at 1113 weeks is associated ACOG, High-Risk Pregnancy Series 2002
0 (womans mother had PE) + 0 (nulliparous) = with increased risk for subsequent development of PE
3.892 (Ong et al., 2000; Smith et al., 2002; Yaron et al., 2002;
Odds = eY = 0.020 Dugoff et al., 2004; Spencer et al., 2005, 2007; Pilalis
A priori = odds/(1 + odds) = 0.020 = 2.00%. et al., 2007). The results demonstrated that the levels
of PAPP-A are substantially lower in those developing
 for variety of reasons many aspects of
early pregnancy remain very difficult to
study and are consequently poorly
understood

Apgar scores have a poor correlation to

!abnormal FHR patterns

ACOG, High-Risk Pregnancy

Series 2002
Susan J Fisher

Factors influence FHR

Medical conditions in the mother, e.g. Diabetes mellitus,
Renal disease.
Any pregnancy-related diseases, e.g. pregnancy-
induced hypertension, Rhesus incompatibility.
Identified risk factors occurring in pregnancy, e.g.
intrauterine growth retardation Fetal abnormality,
Antepartum haemorrhage.
Gestational period.
Progress in labor.
Drugs e.g. MgSO4
Posture of the mother throughout the CTG lying supine
causes a decrease in uterine blood flow, and a decrease
JM Roberts et al, SGI Meeting 2008
in oxygen transfer to the fetus.
!
!
 %$*
,
,$) ,$# %$* "./

LC:9M&B2N@;H:;O 3&89:;2<$0==>:;5

FG--$%&'(+/
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?8'*-/-3'-/@
&'
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!

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& $B-,'1,)138/3+'1-<),8)/6)6

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Insufficient oxygen is transferred from the mother to the

C1%DC2EB@@F
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fetus through the placenta. ('

01)*+,-.%&'(+/ V1%W(22222228;@A2(29@2(7

If the transfer of oxygen is adequate, but the fetus is #

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unable to utilize it due to, e.g. impaired circulation. & 6 &7 ----------------------- C
# #$%# :)8?D6+'1-E-<),8)/6)6

?@;A&B 222222222222222222222222222 Z

C1%DC2EB@@F
1%2KJ>>BU236[2Z2V1%W&5 Y1%
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Despopoulos/Silbernagl, Color Atlas of Physiology, 6th Edition. All rights reserved. 2009 Thieme Publishers

Plate 5.13 Internal (Tissue) Respiration, Hypoxia 131

0G--;"-6D&&9%H-I8'4.J6-,%9+1<)8-*'<)9

5 Respiration
!--A'8*/9 R=88JK=@H2F=K9&HN:2S
01%2340&5
+ )$* !$- , %.* "$- #$+
/$- #$+

"$-
"#$*
"% + )$* !$- , -$!
!

Normal CTG
G;9:;=&B2:HF
T&>=BB&;U
PJ>>B=:F23M@A@Q:H:@JK529=KKJ: I:H@JK2:HF
The baseline heart rate is 120-160 b.p.m.
01%2340&5
"--$%&'()*+,-.%&'(+/ The variability is 5-15 b.p.m.
Accelerations may or may not occur in response to
"$- #
%$" #

%$*
, uterine contractions or fetal movements.
No decelerations occur.
,$) ,$# %$* "./

!
LC:9M&B2N@;H:;O 3&89:;2<$0==>:;5

FG--$%&'(+/
& 083)8+/9-:;"-/1<-=;">/--<),8)/6)
! #$%#
?8'*-/-3'-/@
&'
?@;A&B
1%DC2EB@@F

#$"# (
V1%W(22222228;@A2(29@2(7
$%&'()*+,-.%&'(+/
 !

Early Deceleration
The onset of the deceleration is at the onset of the
contraction.
The heart rate reaches its lowest point at the peak of the
contraction and has recovered to the baseline by the end
of the contraction.
!
!
 !

Late Deceleration
Any deceleration whose lowest point occurs more
than 15 seconds after the peak of the contraction is
said to be late
!

Cord Compression
The effect of variable decelerations upon the fetus varies
depending upon the duration and degree of cord occlusion
that occurs during a contraction
!
 delivery by caesarean section were significantly increased with the use of
EFM in comparison with intermittent auscultation (Table 3.3). This effect was
more pronounced if only those deliveries for presumed fetal distress were
considered. The increase in intervention rates was less pronounced in those
trials using FBS as an adjunct to EFM.62

Table 3.3 Operative delivery rates comparing electronic fetal monitoring with
intermittent auscultation Electronic fetal monitoring
Consideration should be given to maternal preference and priorities
Outcome Event rate in Event rate in Relative risk NNT
EFM group (%) IA group (%) (95% CI) (risk difference) Admission assessment
Intermittent auscultation Abnormal FHR on auscultation
Are any of the following risk factors present?
LSCS (Thacker) 464/9398 (4.9) 327/9394 (3.5) 1.41 (1.231.61) 71 (1.4) (this list is not exhaustive) For full minute after a contraction Baseline <_ 110 bpm or >_ 160 bpm
No But at least every: 15 minutes in the first stage
Any decelerations
LSCS (Vintzilleos) 484/9398 (5.1) 344/9163 (3.75) 1.31 (1.151.50) 74 (1.35) Maternal problems
Previous caesarean section
5 minutes in the second stage
Pre-eclampsia
LSCS for FD 129/8778 (1.4) 47/8506 (0.6) 2.49 (1.783.49) 118 (0.8) Post-term pregnancy (> 42 weeks)
Prolonged membrane rupture (> 24 hours)
(Vintzilleos) Induced labour
Diabetes
Cardiotograph (CTG) Classification
Instrumental 1156/9276 (12.5) 965/9270 (10.4) 1.20 (1.111.30) 48 (2.1) Antepartum haemorrhage NORMAL A CTG where all four features fall into the reassuring category
Other maternal medical disease
delivery (Thacker) SUSPICIOUS A CTG whose features fall into one of the non-reassuring categories and the remainder of the
Fetal problems features are reassuring
Instrumental 1147/9398 (12.2) 889/9163 (9.7) 1.22 (1.131.33) 40 (2.5) Fetal growth restriction PATHOLOGICAL A CTG whose features fall into two or more non-reassuring categories or one or more

Continuous electronic fetal monitoring

Prematurity
delivery Oligohydramnios
abnormal categories

Abnormal Doppler artery velocimetry

(Vintzilleos) Multiple pregnancies Fetal heart-rate feature classification
Meconium-stained liquor
Instrumental 246/7679 (3.2) 96/7403 (1.3) 2.45 (1.933.10) 105 (1.9) Breech presentation
Baseline
(bpm)
Variability
(bpm)
Decelerations Accelerations

delivery for FD >_ 5

Yes Reassuring 110160 None Present
(Vintzilleos) Non-reassuring 100109 < 5 for 40 but Early deceleration
Offer and recommend continuous EFM 161180 < 90 minutes Variable decelerations The absence of
LSCS 270/7482 (3.6) 218/7507 (2.9) 1.24 (1.051.48) 143 (0.7) Single prolonged deceleration accelerations
up to 3 minutes with an otherwise
(EFM + FBS vs. Intrapartum risk factors normal CTG
Abnormal <100 < 5 for >_ 90 Atypical variable decelerations
IA (Thacker)) Oxytocin augmentation >180 minutes Late decelerations
is of
uncertain
Epidural analgesia Sinusoidal Single prolonged deceleration significance
LSCS 194/1916 (10.1) 109/1887 (5.8) 1.72 (1.382.15) 23 (4.3) Vaginal bleeding in labour
Yes pattern for greater than 3 minutes
Maternal pyrexia >_ 10 minutes
(EFM FBS vs. Fresh meconium-stained liquor
CTG ! cardiotograph
IA (Thacker)) EFM ! electronic fetal monitoring
FBS ! fetal blood sample
This algorithm should, where necessary, be interpreted with reference to the full Guideline (The Use of Electronic Fetal Monitoring) FHR ! fetal heart rate
CI = confidence interval, EFM = electronic fetal monitoring, FD = fetal distress, IA = intermittent FSE ! fetal scalp electrode

auscultation, LSCS = lower segment caesarean section, NNT = number needed to treat

3.7.2. Maternal response

Maternal response, measured as expressions of levels of maternal
satisfaction or anxiety related to methods of intrapartum fetal monitoring, is
an important outcome by which to measure the impact on women of EFM
and ofintermittent
Ensure adequate quality recording
auscultation.
both FHR and contraction pattern Ensure thatMeasures
of satisfaction and anxiety are
mother is informed of concerns and included in management plan

Inadequate quality CTG

necessarilyUterine subjective yet can be measured
hypercontractility
usefully. Satisfaction
Maternal tachycardia/pyrexia
andfactors
Other maternal anxiety
Poor transducer? EFM
contact from external with and intermittent
Is the mother receiving oxytocin? Maternal
auscultation can be affected
infection?
byIs the a number
What is the maternal position?
of
FSE not working or detached?variables including: Has the mother recently received vaginal Tocolytic infusion?
mother hypotensive?
examination? had a vaginal
prostaglandins? Dehydrated? Has the mother just

Has the mother just used a bedpan?

Has
Suspicious CTG

the mother been vomiting or had a

issues of mobility vasovagal episode?
Check maternal pulse
maternal control of events during labour Has the mother just had an epidural sited
Check position of transducer/FSE Stop oxytocin infusion
If temperature >_ 37.8C consider screening or topped up?
Consider applying FSE 0.25 mg subcutaneous terbutaline
Consider tocolysis and treatment
IfCheck
pulse >_ 140 bpm reduce tocolytic infusion
crystalloid
blood pressure, give 500 ml
if appropriate
Ensure that the mother is not lying supine
Encourage mother to adopt left lateral
position 25
Check blood pressure, give 500 ml
crystalloid if appropriate

If trace remains suspicious continue to observe for further suspicious FHR features and taking into consideration other clinical factors

Fetal blood Subsequent action

sample result (pH)

Fetal blood Encourage mother to adopt left

lateral position
>_ 7.25 FBS should be repeated if the FHR abnormality persists
Pathological CTG

sampling 7.217.24 Repeat FBS within 30 minutes or consider delivery if rapid fall since last sample

indicated
Check blood pressure, give 500 ml
crystalloid if appropriate
<_ 7.20 Delivery indicated
All scalp pH estimations should be interpreted taking into account the previous pH measurement, the rate of progress in
labour and the clinical features of the mother and baby

Fetal blood Encourage mother to adopt left

Expedite Call anaesthetist and paediatrician
lateral position Urgency of delivery should take into account the severity of the FHR abnormality
sampling Check blood pressure, give delivery and relevant maternal factors
inappropriate 500 ml crystalloid if appropriate The accepted standard has been that ideally this should be accomplished within 30
minutes

Following delivery, paired umbilical cord samples should be taken and 1- and 5-minute Apgar scores calculated and all results recorded in the mothers notes

 Noproblemcan besolvedfrom
thesame levelof consciousness
that created it

Acknowledgements

Showa Univ. : Akihiko Sekizawa, Keiko Koide, Masamitsu Nakamura,

Asami Fukuda, Hiroshi Chiba, Hanako Shimizu, Ryu Matsuoka,
Kiyotake Ichizuka, Junichi Hasegawa,Takashi Okai

Kanazawa Med. Univ. : Haruo Takabayashi, Miki Kita, Kazuo Kanasaki

Thank you Kings College: Kypros Nicolaides, Tylki Eliza, Walter Ventura
Laveriano

If it doesn't kill the cat, curiosity is a luxury Univ. Indonesia : Noroyono Wibowo, Handaya, Azen Salim, Damar
Prasmusinto, Bambang Karsono, Ali Sungkar, Yudianto BS, Aria
Wibawa, Rima Irwinda, Edwina FrisdianVny

Bologna Univ: Antonio Farina, Nicola Rizzo

NCCHD, Tokyo: Michihiro Kitagawa, Satoshi Hayashi, Hirohiko Sagou