F430 LEADING ARTICLES

Umbilical cord blood gas analysis blood gas sample taken from the infant
.......................................................................................... soon after birth would be expected to
show marked acidosis if there had been

Use of umbilical cord blood gas analysis

cord obstruction.14
The umbilical vein is larger and easier

in the assessment of the newborn

to sample from than the umbilical artery,
and when only a single sample can be
obtained because of sampling difficulties
L Armstrong, B J Stenson it is likely to be venous. Even when paired
samples are obtained it cannot always be
......................................................................................
assumed that one is from an artery and
one from the vein. Because fetal carbon
Analysis of paired arterial and venous specimens can give insights dioxide is removed from the umbilical
into the aetiology of acidosis in the newborn arterial blood in the placenta, umbilical
venous blood should have a slightly
higher pH and lower PCO2 than umbilical

I
n 1958, James et al recognised that rendering them uninterpretable. It is also arterial blood. Westgate et al15 reported on
umbilical cord blood gas analysis can important to recognise that the umbilical 1798 supposedly paired umbilical arterial
give an indication of preceding fetal cord can become obstructed before birth. and venous blood samples. They found
hypoxic stress.1 It has since become Restriction of umbilical blood flow causes that in 350 (19.5%) cases the paired
widely accepted that umbilical cord blood a progressive widening of the difference samples were unreliable. In 169 (9.4%)
gas analysis can provide important infor- between umbilical arterial and venous cases the umbilical venous pH was lower
mation about the past, present and blood gas values. Martin et al showed that or PCO2 was higher than the correspond-
possibly the future condition of the term infants with nuchal cords have ing arterial value, suggesting that the
infant. Umbilical cord blood gas analysis larger differences in umbilical venous samples had been mixed up. In 181
is now recommended in all high-risk and arterial pH, PCO2 and PO2 than those (10.1%) cases, where the difference in
deliveries by both the British and without evidence of cord compression.10 pH between the two samples was ,0.02
American Colleges of Obstetrics and In contrast, arterial to venous differences units (5th centile) or the difference in
Gynaecology,2 3 and in some centres it is are small where there is impairment of PCO2 was less than 0.5 kPa (10th centile)
practised routinely following all deliv- the maternal perfusion of the placenta, they considered the two samples to be so
eries. It is therefore of increasing clinical such as in cases of abruption.11 In a similar that they must have been taken
and medicolegal importance that clini- comparative study between infants born from the same vessel. In the remaining
cians caring for newborn infants are after cord prolapse and those born after 1448 validated pairs, the median (range)
familiar with the principles and practice placental abruption, Johnson et al arteriovenous difference in pH was 0.09
of obtaining and interpreting cord blood observed veno-arterial differences in pH (0.02–0.49) units, and in PCO2 was 1.9
gas values, and with the underlying of up to 0.3 units, and showed that a (0.5–9.9) kPa. Tong et al had similar
evidence base. difference greater than 0.15 units could findings.16
be used to differentiate reliably between When paired cord blood gas samples
the two.11 Belai et al showed that in severe produce results that are so similar that it
SAMPLING PROCEDURE cases, where the cord arterial pH is less
Umbilical cord blood analysis is assumed is physiologically implausible and statis-
than 7.0, the magnitude of the difference tically unlikely that they came from an
to give a picture of the acid–base balance in PCO2 between the umbilical artery and
of the infant at the moment of birth when artery and a vein they should therefore be
vein predicts the risk of the infant interpreted in the same way if they were a
the umbilical circulation was arrested by developing encephalopathy.12 Because of
clamping of the cord. However, from this single vessel sample,17 and it is most likely
this it is imperative to sample both that they came from the umbilical vein.
moment onwards the umbilical cord arterial and venous blood, especially if
blood, if it remains in continuity with They do not then exclude the possibility
an infant is depressed at birth. In the of notable umbilical arterial acidosis,
placenta, will demonstrate progressive presence of cord obstruction, a normal
change in acid–base status due to particularly if the rest of the clinical
umbilical cord venous blood gas could picture points towards this.
ongoing placental metabolism and gas conceal severe mixed umbilical arterial
exchange. Small changes in umbilical pH acidosis in an infant with a high risk of
occur within 60 s of delivery,4 and over adverse outcome. If the obstruction to the WHAT IS A NORMAL CORD pH?
60 min cord arterial or venous pH can fall umbilical vessels was sudden and com- Many authors have studied normal umbi-
by more than 0.2 pH units.5 Similar plete and this persisted until the moment lical blood biochemistry and acid–base
changes occur in blood sampled from of delivery or until fetal death then the status. Most available data relate to
placental surface vessels except that they cord gases sampled at birth would give a infants born at full term. Parity,18 breech
are larger and less predictable.6 These snapshot of the fetal acid–base balance presentation,19 mode of delivery20 and
changes are not observed if the cord is prior to the obstruction. Both umbilical many other factors influence cord gas
doubly clamped at birth, isolating a arterial and venous gases could then be values. Reference ranges for term and
segment of cord blood from both the normal despite severe intrapartum preterm infants are summarised in table 1.
placenta and the environment.4 The pH of asphyxia.13 14 Fetal death with normal In a study of more than 15 000
the blood then remains relatively con- cord gases could also occur with fetal vigorous newborn infants, Helwig et al
stant at room temperature for an hour.5 7–9 cardiac arrest.13 In cases of intrapartum showed a stepwise reduction in mean
When there is considerable delay in stillbirth and in infants who are in very umbilical arterial pH for infants born
sampling, it is essential to know whether poor condition at birth and who require preterm, term and post term, respec-
the sample was taken from isolated cord considerable resuscitation, normal cord tively.22 They hypothesised that this trend
blood or whether ongoing placental venous and arterial pH do not therefore could be explained by the prevalence of a
metabolism may have altered the results, exclude acute intrapartum asphyxia. A shorter duration of labour in preterm

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LEADING ARTICLES F431

infants. However data by Nicolaides et al24 most commonly quoted figure, pH is not
and Weiner et al25 demonstrated a similar an ideal parameter for estimating the
trend in premature infants who had not cumulative exposure to hypoxia. Because

5
All gestations, all delivery types, Apgar .7
undergone labour. They hypothesised it is a logarithmic term it does not give a

Term, nulliparous, SOL, all delivery types

that this may reflect increased placental linear measure of acid accumulation. The

Term singleton infants, vaginal delivery

Preterm (24–36 weeks), normal CTG
oxygen consumption with advancing change in hydrogen ion concentration
gestational age. associated with a fall in pH from 7.0 to
Term non-anomalous singletons 6.9 is almost twice that which is asso-
OTHER FACTORS WHICH ciated with a fall in pH from 7.3 to 7.2.
INFLUENCE CORD BLOOD VALUES The base excess provides a more linear
Population studied

measure of the degree of accumulation of

Infants born by elective caesarean section
without labour20 have results which are metabolic acid and is adjusted for varia-
closer to normal adult values (higher pH, tion in Pco2.36
PO2, base excess and bicarbonate, and Uterine contraction during the second
lower PCO2), as do infants born of multi- stage of labour may impair placental flow,
parous mothers.18 The repeated uterine although periodic relaxation usually
allows restitution of gas exchange unless
20 456
15 073
1694a 1820v
3522
1393a 1526v

contractions of normal labour exert

appreciable metabolic stress on the fetus. placental function is already poor. In
Number

This effect is exaggerated in twin labour cases of excessive contraction such as

at full term, where the time-related during uterine hyperstimulation or pro-
deterioration of arterial cord pH is more longed second stage, incomplete restitu-
precipitous in the second twin.26 Regional tion may result in cumulative acidosis.
(0.93)
(0.97)
(1.02)
(1.29)

Interrupted placental perfusion also

Po2 (kPa)

anaesthesia, particularly spinal anaesthe-

sia is associated with increased incidence occurs during maternal hypotension, as
3.86
3.82
3.79
3.88

of cord blood acidosis.27 Sympathetic seen in acute blood loss, regional anaes-
blockade reduces uteroplacental perfu- thesia and systemic illness, as well as
during placental abruption and acute cord
(0.93)
(0.89)
(1.05)

sion. The resultant carbon dioxide reten-

PCO2 (kPa)

(1.1)

tion is manifest by predominantly compression.32

Uncomplicated labour changes base
5.45
5.83
5.41
5.77

respiratory acidosis, but there is no

evidence that this affects clinical out- excess by around 3 mmol/l overall.36 A
come.27 Although there seems to be a normal second stage of labour changes it
Base excess

(2.4)
(3.0)
(2.4)
(2.0)
(2.5)

weakly positive correlation between cord by around 1 mmol/l per h.37 In contrast,
(mmol/l)

pH and umbilical cord length, number of base excess changes by around 1 mmol/l
24.5
23.0
22.9
22.4
22.6

Data are presented as mean (SD). Arterial (a) and venous (v) sample numbers are given separately where available.

coils and number of vascular coils per per 30 min during prolonged periods
centimetre,28 umbilical cord morphology when there are repeated fetal heart rate
Umbilical vein

is of uncertain clinical importance. The decelerations.38 The most profound fetal

(0.06)
(0.06)
(0.06)
(0.06)
(0.07)

presence of true knotting of the cord compromise, such as that associated with
seldom seems to cause a problem.29 terminal bradycardia following acute
7.33
7.34
7.32
7.34
7.33
pH
Studies reporting umbilical cord values for term and preterm infants

Chorioamnionitis, with or without uterine rupture, changes base excess by

funisitis does not appear to influence 1 mmol/l per 2–3 min.36
CTG, cardiotocogram; SOL, spontaneous onset of labour; SVD, spontaneous vertex delivery.
(0.92)
(1.09)
(1.05)

cord blood pH or base excess.30 Although

(0.8)
Po2 (kPa)

placental infection is associated with CORD BLOOD P O 2 AND P CO 2

2.26
2.38
2.45
2.53

cerebral palsy in both term and preterm The blood gas analyser measures pH, PCO2
infants, the mechanism appears to be and PO2 and then calculates base excess
largely independent of hypoxia-ischae-
(1.33)
(1.14)
(1.48)
(1.33)

after normalising PCO2. The PO2 and PCO2

PCO2 (kPa)

mia.31 values can provide further clues to the

7.05
7.49
6.69
7.05

interpretation of the clinical picture and

Evaluation of fetal acidosis helps to exclude rogue results. From the
The pH of umbilical cord blood is deter- data series in table 1, the upper 95%
Base excess

(3.0)
(3.0)
(2.7)
(2.8)
(2.9)

mined by presence of respiratory and confidence level (mean + 2 SD) for

(mmol/l)

metabolic acids. Carbon dioxide diffuses umbilical arterial PO2 is 4.2 kPa and for
25.6
24.0
23.6
22.7
23.2

readily across the placenta. Fixed acids umbilical venous PO2 is 5.8 kPa.39 In
Umbilical artery

such as lactic acid and b-hydroxybuty- mothers breathing 60% mask oxygen
rate, which account for the majority of during uncomplicated delivery the upper
(0.07)
(0.07)
(0.07)
(0.07)
(0.08)

the metabolic load, have a relatively slow 95% confidence levels for PO2 were
5.0 kPa (umbilical artery) and 6.8 kPa
7.24
7.26
7.24
7.27
7.26

passage across the placenta.32

pH

It is important to evaluate both the (umbilical vein).40 In mothers ventilated

respiratory and metabolic components of with 100% oxygen during caesarean sec-
Riley and Johnson 1993

each sample. Isolated fetal respiratory tion the upper 95% confidence level for
Dickinson et al 1992

acidosis is usually the result of short- umbilical arterial PO2 was 4.9 kPa.41 These
Victory et al 2004
Helwig et al 1996
20
Thorp et al18 1989

lived impairment of the uteroplacental or data indicate that cord arterial samples
23

fetoplacental circulation and is seldom with PO2 greater than 5.0 kPa are likely to
21

22

associated with adverse outcome.33 have been affected by the presence of an

Table 1

Ongoing impairment results in progres- air bubble in the specimen. Because the
Author

sive metabolic acidosis due to anaerobic carbon dioxide content of air is very low,
glycolysis. Consequently most severe fetal this can be accompanied by a substantial
acidosis is mixed.34 35 Although it is the lowering of the PCO2 of the sample

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F432 LEADING ARTICLES
followed by a large rise in pH, with patterns becomes very strongly predictive measurement of acid–base status after
consequent risk of misinterpretation.42 of adverse sequelae. Perlman and Risser birth may be useful in prognosis. Casey et
These changes are likely to begin within showed that a combination of cord pH al found that infants in whom acidosis
a few minutes of exposure of the sample ,7.0, a requirement for intubation and a (pH ,7.20) persisted 2 h beyond delivery
to a bubble.43 The base excess should still 5-min Apgar score of (5 had an 80% had a poorer outcome than those in
provide a reliable measure of metabolic positive predictive value for the develop- whom acidosis had resolved.62 Recent
acidosis in the specimen but it may not be ment of seizures.53 Portman et al devel- data suggest that persisting lactic acidosis
possible to determine whether the speci- oped and validated a scoring system for is associated with severe encephalopathy
men is arterial or venous. predicting multiorgan impairment fol- and may be a reflection of the presence
The lower limit of carbon dioxide is less lowing perinatal asphyxia.54 They found and severity of seizures.63
informative because mothers can sponta- that a score combining a measure of cardio-
neously hyperventilate to low PCO2. In the tocographic abnormality, umbilical arterial PRETERM INFANTS
absence of compromise to the placental base excess, and low 5-min Apgar score The value of umbilical cord blood for
perfusion by mother and fetus there is a was much more strongly associated with predicting morbidity and mortality in
linear relationship between maternal and morbidity than any individual factor. In a preterm infants is less clear. As in term
fetal PCO2.44 However the changes in fetal separate study the score showed a positive infants, Victory et al demonstrated a
pH associated with brief hyperventilation predictive value of 73% and negative pre- relationship between increasing meta-
are small. Maternal hyperventilation low- dictive value of 99% for predicting impair- bolic acidosis and adverse outcomes in a
ers fetal PO2.44 45 ment of three or more organ systems.55 large cohort of preterm and very preterm
Goldaber et al studied the association infants (32–36 weeks and 25–32 weeks,
WHAT IS PATHOLOGICAL between umbilical arterial acidosis and respectively).64 Hibbard et al found that
ACIDOSIS? adverse neurological events among 3506 very low birthweight infants who sur-
It is unhelpful to define pathological term, singleton infants with cord arterial vived had higher umbilical arterial pH
acidosis statistically, using deviation from pH,7.20.56 Neonatal death was much than those who did not survive.65 Tejani
the normal population values. This is more likely at pH ,7.00. The cut-off at and Verma demonstrated similar findings
because acidosis is generally tolerated by which seizures became more likely was in low birthweight infants (,2000 g) for
the fetus without sequelae until it becomes pH ,7.05, and for unexplained seizures mortality, and also found a weak inverse
very severe. It is more clinically relevant to was pH ,7.00. They recommended that a association between umbilical artery pH
define pathological acidosis as the thresh- realistic value for defining pathological and risk of respiratory distress syn-
old at which the incidence of adverse acidaemia was pH ,7.00. Williams et al drome.66 Beeby et al found that any
clinical events starts to correlate strongly. also found that a threshold of pH ,7.00 association between umbilical artery pH
Serious adverse sequelae in the new- was the best independent predictor of and neonatal morbidity was negated
born period are rare after birth with neonatal seizures when compared with when adjusting for other risk factors such
umbilical cord pH greater than 7.0 or other indices.57 Low and colleagues stu- as gestation and birthweight.67
base excess less acidotic than minus died the association between metabolic In a retrospective study of extremely
12 mmol/l.34 35 46 Follow up of infants acidosis and multiorgan impairment. low birthweight infants, Gaudier et al
with cord pH above 7.0 suggests no Using a scoring system for renal, central showed that condition of the neonate at
adverse effect of acidosis on cognitive nervous system, respiratory and cardio- birth, evaluated by a low 1-min or 5-min
outcome.47 Even at pH below 7.0 most vascular morbidity they showed that both Apgar score (,4 and ,7, respectively)
infants will still recover fully without the presence and magnitude of metabolic was a better predictor of survival,
remarkable illness.48–50 In this respect cord disturbance was a good predictor of adjusted for gestation, than any indivi-
pH or base excess alone are poor pre- multiorgan involvement in both term dual cord blood measurement.68 This is
dictors of outcome.48 51 52 Most infants and preterm infants.33 58 They found that perhaps not surprising, as the Apgar
with evidence of intrapartum asphyxia the threshold of metabolic acidosis asso- scores are substantially influenced by
do not develop serious long-term seque- ciated with increased risk of newborn whether or not any resuscitative mea-
lae. In a series of around 14 000 newborn complications in term infants was a base sures are implemented and whether these
infants with routine cord blood gas excess of minus 12 mmol/l or worse.46 are performed effectively. However, in an
analysis, King et al identified pH ,7.0 in Once severe acidosis is present, the earlier study involving essentially the
58 (0.4%) infants who were born at likelihood of adverse sequelae rises shar- same cohort, the same authors demon-
35 weeks’ gestation or more.49 On the ply with worsening acidosis. Goodwin et strated that in those who survived, the
basis that they had birth weight .2100 g, al found that hypoxic-ischaemic encepha- risk of neurosensory impairment was
5-mim Apgar score >7 and an absence of lopathy occurred in 12% of infants with independently predicted by cord arterial
cardiopulmonary disturbance, 37 of these cord pH ,7.0, 33% with cord pH ,6.9, metabolic acidosis, when adjusted for
58 infants were triaged after birth to the 60% with cord pH ,6.8, and 80% with gestation, weight and other confounding
routine postnatal nursery. They were cord pH ,6.7.35 In a study of 69 000 term variables. The odds ratio (95% CI) of major
followed closely and none developed deliveries with cord blood gas measure- neurosensory impairment for pH ,7.05
clinical manifestations of hypoxic-ischae- ments, no infant was live born with pH was 6.48 (1.1 to 37.4) and for bicarbonate
mic injury. Two of the infants were ,6.6.35 Increasing morbidity with worsen- (14 mEq/l was 14.2 (1.8 to 112.8).69
admitted to the neonatal unit because of ing acidosis, once severe acidosis is present,
hypoglycaemia. This suggests that infants has also been noted in several other LACTIC ACID MEASUREMENT
who are in good clinical condition at birth studies.59–61 Collectively these data suggest Lactate is now routinely measured by
and are free of cardiopulmonary distur- that permanent neurologic injury from many blood gas analysers. Because it only
bance do not require neonatal unit intrapartum asphyxia occurs late in the sparingly crosses the placenta lactate
admission or detailed investigation purely course of the asphyxial insult in most of the measured in umbilical cord blood samples
on the basis of low cord pH. cases, once the fetus is close to death. is almost entirely fetal in origin.70
In contrast, the combination of low pH Whereas cord blood analysis pro- Umbilical cord lactate has been shown
at birth with other abnormal clinical vides a static measurement, longitudinal to correlate with both pH and base

www.archdischild.com
LEADING ARTICLES F433

excess.71 In a study of 4045 cord samples, Accepted 9 May 2007 22 Helwig JT, Parer JT, Kilpatrick SJ, et al. Umbilical
cord blood acid-base state: what is normal?
Westgren et al showed that lactate was Competing interests: B J Stenson is one of the Am J Obstet Gynecol, 1996;174:1807–12;
similar to both pH and base excess in its editors of Archives of Disease in Childhood. He discussion 1812–4.
ability to predict low Apgar scores, and has also acted as an expert witness in medico- 23 Dickinson JE, Eriksen NL, Meyer BA, et al. The effect
legal cases. of preterm birth on umbilical cord blood gases.
other selected short-term morbidities.72 A Obstet Gynecol 1992;79:575–8.
cut-off of the 95th centile (value not 24 Nicolaides KH, Economides DL, Soothill PW. Blood
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