RISK MANAGEMENT
Birth asphyxia
Donald MF Gibb
NIL> MRCP FRCOG MEW1
A
spliyxia mcans literally stoppage o f t h e pulse and
is defined as the condition of suspended aninia-
tion produced by a deficiency of oxygen in the
blood; suffocation (Oxford English Dictionap9. Birth
asphyxia is an unsatisfactory termbecause it has come to
mean poor condition of the baby at birth irrespective of
cause; there are many causes of a txhy being in poor
condition at tirth. In common use it has implied asphyxia
caused by birth rather than asphyxia found at birth. This
has very important medicolegal implications.A preferable
concept is birth depression, depression at birth: which
demands consideration of various causes before treatment
can be logically and effectively undertaken. Theterm flat
baby should not be used: it has no scientific basis and is
used insensitively in the presence of parents and family. A
baby may be clepressed at hirth by causes as diverse as
diaphragmatic hernia. infection, maternal anaesthesia,del-
ivery problems as well as liypoxia and birth trauma.
Depressed babies have poor Apgar scores, but it should
be remembered that the Apgar score was devised as an
objective indicator of the condition of the neonate at hirth
and not as a marker of asphyxia. The term liypoxic
ischaemic encephalopathy should be avoided until
specific evidence for its origins becomes available.
Neonatal encephalopathy may not be asphyxia1 in origin.2
This revien7 considers birth depression due to hypoxia:
true birth asphyxia. The term brain damage is not
helpfiil in the neonatal period until the evolution of the
process is clear. Cerebral palsy is a non-progressive
disorder of movement o r posture not evident until
months or years after birth. It is clear that cerebral palsy
has multiple aetio1ogies.jThere are fen: countries where
there has been adequate follow-up of children relating
their subsequent condition to birth events. It is probable
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that only about 10Y0 of cases of cerebral palsy are related
to peripartum e\ ents, Our attention must turn to their
prevention, as n-omen are often in our care and under
supervision at this time
THE PROCESS OF BIRTH DEPRESSION
ASSOCIATED WITH HYPOXIA
The condition of a baby at birth is dependent on many
factors. To be healthy, the baby must be intact genetically
and constitutionally. Intrinsic fetal defects are important
contrihutors to l ~ h a v i o u rafter birth and t o later cerebral
palsy. The fetus mustbe provided witha supply of nutrients
and oxygen from the mother. Upstream deficienciesof
niaternal respiratory or cardiac function compromise supply
through the placental unit. It is uncommon for these to be
acutely interrupted befure latmur and there is more likely to
be a chronic interruption with chronicasphyxia Poor
placental function of long standing results in intrauterine
growth restriction and fetal compensation. In a different
scenario babies become asphyxiated in a period of time that
may be hours or days before birth. This is called chronic
partial asphyxia. The signs of this may be subtle, such as a
change in fetal movement, or theremay be no sign at all.
Such babies are usually well grown. Other babies suffer
severe acute compromise with conditionssuch as placental
abruption, umbilical cord prolapse or uterine rupture.
These babies behave in different way-s after birth. The
mechanisms that may leadto critical cerebral damage are
essentially hypoxaemia and ischaemia (poor perhsion),
resulting in tissue hypoxia and damage.
INTRAUTERINEGROWTH RESTRICTION
A clironically- asphyxiated fetus suffering from placental
dysfunction manifest as poor growth shows a reduction in
body movements and txeathing movements reducing
energy consumption and oxygen demand. There is a
redistribution of blood supply seen on Doppler examin-
ation. There is increased blood flow to the brain, myo-
cardium and adrenals. with reduced flow- through the
descending aorta to the viscera. Changes are integrated,
but loss of end-diastolic flow in the descending aorta
occurs in chronic hypoxia, and significant changes in
middle cerebral artery blood flow suggest acidosis. In
time, head growth slows. There is increased extraction of
o q g e n from the blood with hypercapnia, acidosis,
hyperlacticaemia and erythroblastosis.
These babies at birth may have superimposed acute
asphyxia, particularly if they have item exposed to
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RISK MANAGEMENT Donald Gibb
Donald MFMFGibb
labour. The Apgar scores will depend on this but may be
in the intermediate range. These babies in general do not
suffer from convulsions. Typically, they have temperature
regulation problems with hypotherrnia due to decreased
fat insulation, decreased stores of bron~nfat and glycogen
and poor lipid metabolism. They also have metabolic
problems such as hypoglycaemia, hypocalcaemia as nwll
as polycythaemia and hyperbilirubinaeinia. These babies,
when premature, may show periventricular leucomalacia
on brain imaging and? if they develop cerebral palsy, it is
of the spastic type.
CHRONIC PARTIAL ASPHYXIA
'These babies arc usually near term and show n o major
signs of compromise until there is an abnormal cardio-
tocogram (CTG). Included are fetuses identified as
compromised in pregnancy based on an abnormal
antenatal CTG. There rnay be subtle indicators, such as
vaginal bleeding o r reduced fetal movements, but not
enough concern to justify obstetric intervention. There
may IIC an unreactive C'lG with. poor baseline variability
from tlie start of labour.s The CTG may be unusual in
labour but not indicative o f progressive hypoxia. The
Apgar scores are reasonal-ile and in the neonatal period
convulsions occur late. These babies may have suffered
neurological injury prior to the start of labour.
ACUTE ASPHYXIA
An acutelp asphyxiated fetus tiehaves in a different way.
In monkeys stucliecl by Myers9 using total umbilical cord
occlusion, t h e fetal heart rate fell almost immediately at
the time of tlie asphyxia1 event; this was followed by a
transient rise in blood pressure which was short-lived and
t h e hlood pressure fell steadily from three minutes. The
blood oxygen was largely depleted in the firs1 tliree
minutes of total asphyxia. There was a rapid fall in pH but
this was initially a respiratory acidosis. If relieved of' the
insult at this point the animals sut-vived. The first evidence
f o r damage to the brain following resuscitation and
exterided survival in unanaesthetised term fetuses came
after ten minutes of total asphyxia. Tlie cerebral injui-y
appears to be clue to iscliaemia related to tlie period of
hypotension. Those fetirscs asphyxiated for longer than
25 minutes die in thc early hours in the intensive care unit
of progressive and intractable heart failure due to injury o f
the myocardium. The nervous system damage produced
by this asphyxia affects thaianiic, brainstem and spinal
cord structures. The focus is on the tlialamic structures
which are injured after 13 minutes of total asphyxia.
The liurnan fetus born after being exposed to acute
severe asphyxia will have a low lieart rate and delnyed
onset of respiration. The Apgar score at one minute will
be depressed. Aggressive resuscitation and artificial vent-
ilation are recluired. Umbilical artery 11load gas measure-
ments are important. An acidosis (pH c7.10, base deficit
>12 mmol/l) does not have a relationship with impaired
22 Il&eObstetrician & Gvnuecologist
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neurodevelopmental outcome at 4% years of age."'
However. there is evidence that a cluster of abnormal
perinatal signs, including acidosis, has a poor prognosis.'
These signs were umbilical arterial acidosis as defined
above, low Apgar scores and neonatal encephalopathy.
This suggests that the preceding events, severity and
cause of the acidosis were as important as the presence
of the acidosis itself. Neonatal enc:ephalopathy can he
due to hypoxia-ischaemia, infections. drugs, central
n e n o u s system malformations, intracranial liaemorrhage
and metabolic caciscs. A grading system has heen
intrciduccd to describe the neurological abnot-tnality."
Hypoxic ischaemic encephalopathy
0 Grade I: Irritability, staring with mild hypotonia and
poor sucking; these liabies d o not have seizures.
0 Grade 11: Lethargy, marked abnormalities o f tone, tube
feeding and seizures.
0 Grade 111: Conia, severely hypotonic. requiring artificial
ventilation and with prolonged seizures.
Grades TI and 111 hypmic ischaemic enceplialopathy confer
an increased risk of death or serious handicap.13 Infants
with a severe encephalopathy frequently have an adverse
outcome. The blood flow to vital organs is preserved during
acute asphyxia. Less vital organs arc deprived o f tilood
flow. Multi-organ dysfunction becc )mes apparent, with renal
failure, necrotising enterocolitis, persistent pulmonary
hypertension, disseminated intravascular coagulation and
various metabolic abnormalities. These abnormalities are
markers of hypoxic ischaemia.
If such a child has the misfortune t o develop ceret~ril
palsy then it will be of the spast.ic quadriplegia or a
dyskinetic (athetoid) type.14 However, spastic quadri-
plegia has other causes and only 24% of a series of cases
of children with moderate or severe quadriplegia were
considered to be related to intrapartuni events. li
BRAIN IMAGING
Great advances have heen made in imaging techniques in
recent years. Neonatal cranial ultrasound is now widely
available. Cranial ultrasound may reveal abnormalities of
txain structure or development that have been present
frorn early pregnancy. Cerebral oedema that is :i conse-
quence of asphyxia is recognised by an increase in echo-
density, a loss o f anatomical landmarks. indistinct sulci
ion of the ventricles. Later ultrasound find-
ings associated with a poor neurodevelopmental outcome
include bilateral uniformly echogenic thalami represent-
ing t>asaIganglia hypoxic ischaernic injury.16
Magnctic resonance imaging (MKI) is making an important
contriliution to understanding brain injuiy. In coiiiparison
with ultrasound, early MRI WIS found to be superior at
diagnosing cerebral arterial infarrts, cortical atrophy and
basal ganglia lesions, altliough ultrasound proved more able
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to detect periventricular luemorrhage.'7 Partial hypoxic
ischaemia acts on the heart, causing alteratiom in heart rate.
Bradycardia in the fetus and newborn reduces cardiac
output. Critical reduction of output lasting for more than one
hour beyond the capacity for regulation of die cerebral
blood flow in the term fetus (over 36 weeks of gestation)
causes ischaernic damage in the border zones between the
cortical distributions of the main cerebral arteries.
Profound hypoxic ischaemia as occurs with cardiac arrest or
severe bradycardia causes global lack of cerebral circulation.
This results in irreversible damage to cells as their metabolic
reserve becomes insufficient to maintain cell wall function.
Cell death occurs in proportion to the metabolic activity,
which varies with the mahirity of the fetus. In die term fetus,
active myelination is taking place in the basal ganglia, thalami
and pie- and post-central white nutter in which damage
commences after about ten minutes of profound asphyxia.
Asphyxia lasting for longer than 25 minutes usually results in
death or much more severe and diffuse brain damage.
Rctween about 26 and 34 weeks of gestation the o l i g -
dendroglia in the cerebral white matter are particularly
vulnerable to a variety of insults including hypoxic
ischaeinia and infection, particularly chorio-amnionitis. l'his
damage causes the typical clinical and imaging features of
periventricular leucomalacia. Leucomalacia is a much less
coininon reaction in the more mature fetus so that when it
is discovered in a baby who has been born near term it is
considered to be indicative of an earlier insult unless there
is oveim~helmingclinical evidence to the contrary:.
These changes on MRI persist and can be seen much later
in childhood and are considered in the rncdicolegal context.
Electroencephalograph), (EEG) may provide important
prognostic information. Term babies suffering from
asphyxia show reduced background activity, and the
more discontinuous the background t h e poorer the
associated outconie.lH
THE CONTINUUM OF HYPOXIA
In a medicolegal context there should be appreciation of
the continuing process of hypoxia. This has been
recognised by the American College of Obstetricians and
Gj7necologists.lo They have defined that a neonate who
has had severe hypoxia proximate t o delivery that is
severe enough to cause severe hypoxic ischaernic
encephalopathy will show other evidence of liypoxic
damage, including all of the following:
Profound metabolic or mixed acidaernia (pH <7.00)on
an umbilical arterial blood sample.
Persistent Apgar scores of 0-3 for five minutes or
longer.
Evidence of neonatal neurological sequelae (e.g.
seizures, coma, prolonged hypotonia and one or more of
the following: cardiovascukai-. gasti-ointestinal, haemato-
logical, pulmonary, or renal system dysfunction).
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AdamBalen RISK MANAGEMENT
The Perinatal Society o f Australia and New Zealand, in
collaboration with international experts, has published a
document trying to define the relationship between acute
intrapartum events and cerebral palsy.20 They suggest
essential criteria and additional criteria.
Essential criteria:
of a metabolic acidosis in intrapartum fetal,
arterial or very early neonatal cord samples
(pH <7.00, base deficit >12 mmol/l).
Early onset of severe or moderate encephalopathy in
infants >34 weeks of gestation.
Cerebral palsy of the spastic quadriplegic or dystonic
type.
Additional criteria:
A sentinel (signal) hypoxic event occurring immediately
before or during labour.
A sudden, rapid and sustained deterioration of the fetal
heart rate pattern usually following the hypoxic sentinel
event where the pattern was previously normal.
Apgar scores of 0-6 for longer than five minutes
Early evidence o f multi-system involvement.
Early imaging evidence of acute cerebral abnormality.
One problem with this document is the concept of a
sentinel event. There are events such as ruptured uterus,
abruption and cord prolapse that are fairly discrete. But it
also has to be recognised that there is a continuation of the
labour process which is a cumulative challenge, especially
when aided by oxytocin. Deterioration of the fetal ticart
rate pattern need not be sudden, rapid and sustained to be
seriously threatening to the fetus. Indeed, some of the
worst outcomes are seen when there is a final deterioration
to a bradycardia after some time of an abnormal Irace.
There appears to he a continuum from stress with
compensation to distress with time. This document is to he
reviewed as more information becomes available and will
need to address the important data becoming available
from imaging studies of the subjects' brains.
After reviewing the records of 210 singleton children
who had a diagnosis of cerebral palsy at five years of age,
35 (16.6%) were identified as those most likely to have
cerebral palsy of intrapartum origin. In 26 of these there
was evidence of suboptimal care in labour." A model was
constructed to identify potentially preventable causes of
intrapartum origin.
RISK MANAGEMENT ISSUES
While birth depression and later cerebral palsy may be
associated with poor care in labour, medical negligence
can only be proved when there is causation as well as
liability for the poor care. The jigsaw of hypoxia has to be
studied carefully. The umbilical arteq7 blood gases are the
best key we have. It cannot simply he a stand-alone pH
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 RISK MANAGEMENT Donald Gibb
Donald MFmfGibb
value because acidosis is common and relatively
innocuous. Respiratoi-y acidosis is particularly common
and benign. Tlie hlood gases tilust include a base deficit.
i t may not be cost-effective to perform umbilical artery
hlood gas estimation on all cases but tho American
College has proposed the following approach. which has
iiiuch to comiuend ir."
'Techfziyrie:Irninediatcly after de1ivery o f the neon;lte, a
segment of the umtiilical coi-ci should be doublj- claiiiped.
divided, and placed on the de1ivei-y table pending
assignrrient of the five-minute @gar score. Values froin the
uiiil)ilic;iI ~rtei-yprovide the most
rrgtlrtling fetal and nemhorn acici-base status. A claiuped
segment o f cord is stalile fur pII and Idood gas assessment
for at least 00 minutes. and a cord hlood sample in a syringe
flushed with heparin is stahle for LIPto hU minutes. IT the
five-minute Apgar bcore is satisfxtory and the infrint
appears stable and vigorous, the segment of umbilical cord
can lie discarded. If a serious abnorniality that arose in the
tielivery process. or a problem with the neonate's condition,
or Imth: persist a t o r lw).ond five minutes. blood can lw
w i t h d r m n from the cord ,segment and analysed for 131I and
gases. Soine txsic training will be required in .\rcuring an
arterial sample as it can sometimes be clifficult.'
Ideally, a sample should I x taken in all cases from both
artcry and vein to vedy by their discordancy that one is
arterial.23This may not be possihle in many hospitals. In the
important situation o f the delivery of' a gron-th-1-estrictecl
baby: with small cord vessels, it is iisefiil t o take the arterial
s;iniple while the cord is still att:ichcd to the placenta even
before the placenta is delivcrcd. Tlie sample may he
obtained froin the vesscls on the chorionic surf;ice o f ~ h c
placenta.
'l'he h p g a r scores, particularly at and after five minutes,
although crude, do provide a guide to the sevcrity of the
condition. The nced for transfer and treatrnenc of hypoxic
ischaeniic encephalopathy in the neonatal intensive unit is
also a marker of possible later prohlems. Early cranial
ultrasouIid and EEG are feasible in many units. MRT will
assume gre:it importancc in time and will become routine.
In o ~ day-today
r practice, obstetricians, iiiidwives and
paediatricians must not use the ternis fetd distress, birth
, flat loahy and brain damage. These terms have
led t o serious misiimlerstandings with families and
lawyers. We must strive t o prevent the portion of birth
asp1iyxi:i md subsequcnt brain injury due t o events in
labour ovcr which we may have some control.
Acknowledgements
'The author would like to acknowledge the advice
received froin Dr Janet Rennie, Consultant Yeonxal
Paecliatvichn at King's College Eiospitd, London, a n d nr
Brian iiendall, Consultant Radiologist a t the Royal Free
Hospital, London, in the preparation of this paper.
13
AUTHOR DETAILS
Donald MF Gibb h i n MRCP FRCOG h i k . a ~ , I m k p e m h t
C'o?zsu Itn t z t Obstetn L za I I Suite 207, Pa rliw ay Hou se ,
Sheen Lane, London SW14 8LS, L K
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