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[2019] ZAKZPHC 13
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A.D obo K.L.O v MEC for Health for the Province of KwaZulu-Natal (8700/2013) [2019] ZAKZPHC 13 (13 March 2019)

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IN
THE HIGH COURT OF SOUTH AFRICA
KWAZULU-NATAL
DIVISION, PIETERMARITZBURG
CASE
NO: 8700/2013
13/3/2019
In
the matter between:
A
D
Plaintiff
(and
on behalf of K L O)
and
MEC
FOR HEALTH FOR THE PROVINCE
Defendant
OF
KWAZULU-NATAL
ORDER
(a)
The defendant is directed to
compensate the plaintiff, in her representative capacity as mother
and as natural guardian of K, a
boy born on the 14
th
of May 2009, and in her personal capacity, for the damages claimed in
this action, either as proved or agreed;
(b)
The defendant is directed to
pay the plaintiff’s taxed or agreed party and party costs on
the High Court scale, such costs
to include:
(i)
the costs of the plaintiff’s attorney attending upon any
consultations with witnesses
in preparation for trial, including the
consultations with the under-mentioned expert witnesses;
(ii)
the costs of senior and junior counsel where employed, including the
reasonable and necessary
costs of their preparation for trial, and
for their attendance upon consultations with the under-mentioned
expert witnesses and
the plaintiff;
(iii)      the
qualifying fees of the under-mentioned expert witnesses, including
the costs of the preparation
of their reports, their attendance fees,
and the fees to qualify themselves to testify at the trial and for
any necessary consultations
with the plaintiff’s attorney and
counsel (with the quantum of fees, and expenses, to be determined by
the taxing master),
namely:
(aa) Dr Y Kara, the specialist
paediatrician;
(bb) Dr D McLynn, the obstetrician and
gynaecologist;
(cc) Prof J Lotz, the professor of
radiology; and
(c)
The proceedings are otherwise adjourned sine die.
JUDGMENT
Koen
J
Introduction
[1]
This is an action in which the plaintiff, in her personal capacity
and in her representative
capacity as guardian of her minor child, K
L O (‘K’), a boy born on 14 of May 2009, claims damages
from the defendant.
The damages are alleged to arise as a consequence
of the defendant’s medical personnel’s negligence in
treating the
plaintiff and her unborn foetus whilst she was an
in-patient at the Wentworth Hospital (’the hospital’)
prior to, during
and/or immediately after K’s birth. The
negligence is alleged to have resulted in K suffering birth asphyxia,
resulting in
hypoxic ischemic encephalopathy (‘HIE’) with
consequent brain damage.
[2]
At the commencement of the trial the issue of liability, including
causation, was
separated for determination before all other issues.
This judgment deals only with those separated issues.
Background
facts
[3]
The following background facts are common cause:
(a) At all material times
the defendant administered and operated the hospital. In 2009, the
hospital contained a midwife run obstetric
unit which functioned as a
community health centre. It was not staffed with an obstetrician who
could carry out caesarean section
deliveries. It was only able to
deal with low risk births. High risk labours and patients who
required caesarean section deliveries
would generally be referred to
the King Edward VIII Hospital (“the King Edward Hospital”).
(b) The medical and
nursing personnel at the hospital at all material times acted within
the course and scope of their employment
with the defendant;
(c) The plaintiff was
admitted to the hospital, pursuant to the agreement
[1]
pleaded by her, at
approximately 02h00 on 14 May 2009 for the purposes of giving birth
to her first child. She was examined by the
defendant’s medical
personnel and admitted to the labour ward;
(d)
The defendant’s medical personnel were under a legal duty to
ensure that the rendering of medical care, treatment and
advice to
the plaintiff and her unborn child, would be done with the skill,
care and diligence that can reasonably be expected
of medical
practitioners and/or nursing staff in similar circumstances;
(e)
K was born at the hospital at 19h10 on 14 May 2009.
The
pleadings
[4]
The plaintiff alleges that the defendant’s medical personnel
were negligent
in treating her and K, resulting in his condition, in
one or more of the following respects:
(a)
they failed to diagnose bloodstained liquor
observed after the plaintiff’s membranes had ruptured,
as being abnormal and failed to report that fact to a doctor on duty;
(b)
they failed to observe and record the foetal heart rate with a
cardio-tachograph (‘CTG’) machine half hourly, or
at all,
after 16h00;
(c)
they failed to continuously monitor the foetal heart rate with a
cardio tachograph (‘CTG’) after decelerations in
the
foetal heart rate were recorded;
(d)
they failed to diagnose foetal compromise from the CTG readings, or
otherwise;
(e)
they failed to recognise timeously that the foetus was in distress
and  to arrange for a caesarean section delivery;
(f)
they applied fundal pressure during the second stage of the
plaintiff’s labour when they ought reasonably to have known

that it was dangerous to do so; and
(g)
they accordingly failed to provide the plaintiff and K with
appropriate medical treatment as would reasonably be required in
the
circumstances for their well-being;
(h)
as a result of such negligence K was born severely mentally and
physically handicapped, and has irreparable brain damage.
[5]
The defendant in his plea denies these allegations of negligence on
the part of the
medical personnel. Initially the defendant contended
that K was born in a healthy state, as an MRI scan performed on him
at the
King Edward Hospital subsequent to his birth yielded a normal
result.
[2]
But the defendant pleaded over that even if K was not born in a
healthy state, the medical personnel at the hospital had provided
all
reasonable and necessary medical care and treatment to the plaintiff
and K. Specifically it is pleaded that:
(a)
the bloodstained liquor observed, on its own, is not an abnormal
event during the birthing process indicative only of a placental

abruption, but is generally caused by the patient pushing against a
not fully dilated cervix;
(b)
the plaintiff did not have a retro placental clot subsequent to K’s
delivery and therefore, did not suffer from a placental
abruption;
(c)
the defendant’s personnel had reasonably and appropriately
observed and recorded K’s foetal heart rate during the
birthing
process;
(d)
it is not uncommon for decelerations in the foetal heart rate to
occur during the birthing process;
(e)
there were no clinical signs demonstrating that the foetus was in
distress which required immediate invasive medical intervention;
(f)
at no stage was fundal pressure applied;
(g)
K was provided with emergency resuscitation upon his birth;
(h)
the second stage of labour was not prolonged.
[6]
The defendant pleaded in the alternative that in the event of it
being found that
K presents with cerebral palsy, such cerebral palsy
was not caused by any negligence on the part of the defendant’s
employees,
but was a direct and natural consequence of one or more of
the following factors:
(a)
the exposure by the plaintiff of K to the risks associated with the
plaintiff being afflicted with syphilis;
(b)
the plaintiff smoking cigarettes during the course of her pregnancy;
(c)
that K suffered from a perinatal ischaemic stroke/neonatal stroke and
not from any perinatal asphyxia.
[7]
In further amplification of his denials, the defendant pleaded that:
(a)
pethidine was administered to the plaintiff during the course of her
labour, which would account for the lower Apgar scores
which were
recorded in respect of K shortly after his birth;
(b)
K demonstrated no meconium stained liquor at birth;
(c)
If it is found that K suffered from seizures, that these seizures
occurred during a period which indicates that he suffered
an insult
ante-natally and prior to the plaintiff’s admission to the
hospital;
(d)
K could not have suffered from a partial prolonged hypoxic ischaemic
insult during the plaintiffs labour as there were no signs
of foetal
distress, her labour was not prolonged, and accordingly there was
insufficient time for the foetus to have suffered such
an insult to
the brain during labour;
(e)
K’s symptoms failed to meet the criteria stated by the American
Academy of Obstetrics and Gynaecology (ACOG) and therefore
cannot be
held to be as a result of intrapartum hypoxaemia;
(f)
If it is found that K suffered from an acute profound hypoxic insult,
it would have made no difference to the ultimate outcome
and sequela
suffered by him, as the midwives would have had insufficient time to
transfer him to King Edward Hospital for a caesarean
section to be
performed;
[3]
(g)
If it is found that K suffers from cerebral palsy, then it was caused
by a perinatal stroke.
The
witnesses
[8]
In order to discharge the burden of proof upon her, the plaintiff
testified and the
following expert witnesses were called on her
behalf:
(a)
Prof Lotz, a professor in radiology attached to the University of
Stellenbosch;
(b)
Dr Kara, a specialist paediatrician who practices for his own
account;
(c)
Dr McLynn, a specialist gynaecologist and obstetrician in private
practice.
[9]
The defendant adduced the evidence of inter alia:
(a)
Dr Moran, a specialist gynaecologist and obstetrician employed by the
defendant;
(b)
Dr Naidoo, a family physician employed by the defendant;
(c)
Dr V Govender, a paediatric neurologist employed by the defendant,
(d)
Dr R Singh, a neonatologist employed by the defendant;
(e)
Ms MF Adams, a midwife employed by the defendant at the hospital, at
the material time, and who attended to the plaintiff;
(f)
Mr Neville Padayachee, an ambulance attendant employed by EMRS;
(g)
Dr Reitz, a radiologist employed by the defendant.
Assessing negligence
[10]
The question of reasonableness and negligence is for the court to
decide on the basis of the
evidence and various and often conflicting
expert opinions presented. As a general rule, this determination does
not primarily
involve considerations of credibility, but the
examination by the court of the opinions and essential reasoning of
the experts
before reaching its own conclusion on the issues raised.
What is required in evaluating evidence is a determination of
whether,
and to what extent the opinions advanced are reasonably
justified as being founded on logical reasoning.
[4]
[11]
However, the fact that the defendant’s experts are all employed
by the defendant and could
therefore have some loyalty to or sympathy
for their employer, cannot be ignored altogether either. Specifically
in the case of
Ms Adams, there is the additional factor that she was
attending to the plaintiff during the crucial final stages of her
pregnancy
and labour, and that any culpable omissions or conduct on
her part will reflect negatively on her professional proficiency. In
this regard it was quite surprising that although Ms Adams testified
some nine years after the event, she claimed to still have
an
independent recollection of what period a specific recordal of the
foetal heart rate related to, although this was not recorded
on the
available hospital records, and notwithstanding that evidence prima
facie being in conflict with other evidence. I shall
return to this
aspect below.
K’s
cerebral palsy
[12]
Although initially disputed on the pleadings, it became
common cause that K has cerebral palsy.
[5]
What is in dispute is the nature and cause thereof. Regarding the
nature thereof, Dr Kara testified that K suffers from ‘dyskinetic

cerebral palsy with some spastic quadriparesis (a mixed type of
cerebral palsy)’, whereas Dr Govender is of the view that
K has
‘spastic hemiparetic cerebral palsy’ with a gross motor
classification of four (4), impaired speech and communication
skills
and poor hand function, the spasticity being particularly on the
right side. The nature of the cerebral palsy is not just
simply a
matter of terminology and academic interest, but significant in
considering the more important issue for the purpose of
this
judgment, namely the cause of K’s cerebral palsy and
specifically whether it can be attributed to any negligence on
the
part of the defendant’s medical personnel in their treatment of
the plaintiff prior to K’s birth.
The
possible causes of K’s cerebral palsy
[13]
Although the defendant specifically pleaded that K’s cerebral
palsy ‘was a direct
and natural consequence of one or more’
of the following exposures of K, by the plaintiff, to the risks
associated with her
being afflicted with syphilis, the plaintiff
smoking cigarettes during the course of her pregnancy, and K
suffering a stroke, Dr
Moran and Dr Singh, both called by the
defendant, conceded that the plaintiff’s smoking
[6]
and the syphilis could be excluded as the cause of K’s
condition. They however persisted with the view that these factors

might have made K more vulnerable to injury.
[7]
[14]
The only causes, amongst the possible causes for K’s cerebral
palsy suggested by the expert
witnesses that remained were whether,
as a matter of probability, K’s condition was consequent upon
him suffering brain damage
as a result of being distressed at some
stage or stages during the birthing process (as contended for by the
plaintiff and which
was alleged to be due to negligence on the part
of the defendant’s employees), or whether his condition is as a
consequence
of him having suffered a perinatal ischaemic
stroke/neonatal stroke (as contended for by the defendant). I turn
then to consider
the probability of these respective causes
accounting for K’s condition and whether these resulted from
any negligence on
the part of the defendant’s personnel.
Negligence
and the standard of care
[15]
In
Van
Wyk v Lewis
[8]
it was stated, with
reference to
Mitchell
v Dixon
,
[9]
‘
. . . that “a
medical practitioner is not expected to bring to bear upon the case
entrusted to him the highest possible degree
of professional skill,
but he is bound to employ reasonable skill and care.” And in
deciding what is reasonable the court
will have regard to the general
level of skill and diligence possessed and exercised at the time by
the members of the same profession
in the circumstances. . . .  The
ordinary medical practitioner should . . . exercise the same degree
of skill and care, whether
he carries on his work in the town or the
country. . . .  The fact that several incompetent or careless
practitioners happen
to settle at the same place cannot affect the
standard of diligence and skill which local patients have a right to
expect.’
[16]
The standard of care which the defendant’s employees were
required to provide inter alia
had to meet the defendant’s
Guidelines for Maternity Care.
The
defendant’s ‘Guidelines for Maternity Care in South
Africa 2007’
[17]
According to the defendant’s ‘
Guidelines
for Maternity Care in South Africa 2007’
[10]
(‘the guidelines’):
(a)
‘labour’ is diagnosed if there are persistent painful
uterine contractions accompanied by at least one of the following:
(i)
cervical effacement and dilatation;
(ii)
rupture of the membranes; or
(iii)
a show.
(b)
the first stage of labour comprises:
(i)
the latent phase, commencing when ‘the woman is in labour and
the cervix is less than 4 cm dilated or more than 1 cm long’;

and
(ii)
the active phase, commencing when ‘the woman is in labour and
the cervix is 4cm or more dilated and less than 1 cm long’;
[11]
(c)
As regards the first stage of labour, the latent phase of labour is
said to be prolonged when it ‘exceeds 8 hours’
and
the active phase of labour is said to be prolonged if ‘the
cervix dilates at a rate of less than 1 cm/hour’;
[12]
(d)
the second stage of labour commences when the ‘cervix reaches
full dilation (10 cm)’;
[13]
(e)
the second stage of labour is prolonged if:
(i)
the fetal [foetal] head has not descended into the pelvic floor
within two hours of full dilation; or
(ii)
delivery has not occurred after 45 minutes of pushing in a
nullipara
,
or 30 minutes of pushing in a
multipara
;
[14]
(f)
the fetal [foetal] heart rate ought to be monitored:
(i)
two hourly during the latent phase of labour; and
(ii)
half hourly (before, during and after contractions) during the active
phase of labour;
(g)
a cardio tachograph (CTG)  is used ‘for high risk labour
only’;
[15]
(h)
fetal [foetal] distress is suspected when the following signs are
observed:
(i)
a baseline fetal [foetal] heart rate of more than or equal to 160
beats per minute (bpm);
(ii)
a baseline fetal [foetal] heart rate of less than 110 bpm;
(iii)
variability persistently less than 5 bpm on the CTG, in the absence
of sedating drugs;
(iv)
late decelerations of the fetal [foetal] heart rate;
[16]
(i)
problems requiring referral to a hospital during labour, before
delivery, include:
(i)
suspected fetal [foetal] distress; and
(ii)
poor prognosis in the latent phase of labour (more than or equal to 8
hours).
[17]
The
hospital records
[18]
[18]
Regrettably, the clinical and obstetrical records relating to the
plaintiff’s labour are
incomplete in certain crucial and
material respects, notably the CTG’s reflecting the foetal
heart rate during the plaintiff’s
labour, and specifically from
16h00/16h20 onwards, assuming those entries to be accurate. This has
impacted on the adjudication
of this matter. It is a disturbing fact
that in more than one of these medical negligence cases that have
come before this court,
involving the current defendant, incomplete
records are produced in respect of a crucial stage of the labour of
plaintiffs. The
only possibly inference to be drawn is either that no
records were kept, or if there is some evidential basis for
concluding this,
that whatever records there might have been, have
been lost or otherwise became unavailable.
[19]
At the outset of the trial it was said that these records had been
lost. That is however assuming
they ever existed. Ms Adams was
probably the only one who could give direct evidence on whether there
were additional records kept,
specifically monitoring the foetal
heart rate as there should have been. She testified, but nine years
after the event, of alleged
ongoing monitoring of the plaintiff and
the heart rate of her unborn foetus until 16h50. There was however no
mention made of CTG
monitoring thereafter. CTG printout strips should
form part of a continuous record retained in the same record storage
location
as the other printouts, and would therefore be unlikely to
be lost separately if they existed. No CTG printouts of the latter
stages
of the plaintiff’s labour were produced. Although it was
indicated that these records have been lost, it is probably more

correct to conclude that they never existed.
[20]
The defendant and his staff are under a duty to properly monitor the
plaintiff’s condition and keep records of their
attendance to
the plaintiff and her unborn child. They failed to do so. Dr Moran,
called by the defendant, conceded that there
ought to have been
further monitoring after the last CTG recording produced in evidence.
He also agreed that the lack of monitoring
by the midwives amounted
to substandard care and that foetal distress might have occurred at
some time during that period. That
constitutes negligence. Further,
K’s cerebral palsy was consistent with having resulted, as a
matter of probability, from
a HIE, unless another clear credible
cause was demonstrated.
[21]
The maternity records that were produced in court reveal that:
(a)
when the plaintiff was admitted to the hospital at 02h00
,
she was recorded to be already two (2) cm dilated and experiencing
‘contractions moderate x 2 palpable’;
[19]
(b)
at 06h00 her cervix was three (3) cm dilated and one (1) cm long;
(c) the plaintiff’s
condition was reassessed by Ms Adams at 08h00. This assessment
revealed that she was coping with labour
pains, the foetal heart rate
was between 142 to 151 bpm via the CTG, which was reactive, and her
cervix was still three (3) cm
dilated;
(d)
the plaintiff’s membranes apparently ruptured at 10h30
while she was in the shower. This was
reported by the plaintiff to the nursing staff;
(e) the plaintiff’s
labour was assessed at 12h00 on the 14
th
of May 2009 by Ms Adams. This assessment revealed that she was coping
with labour pains, that the foetal heart rate was between
129 to 134
bpm, and that her cervix was four (4) cm dilated.
[20]
It was however
queried,
[21]
whether the plaintiff’s
membranes had ruptured at 10h30 whilst she was in the shower;
(f) the plaintiff’s
labour was again assessed at 14h00 and it was recorded that she was
not coping with labour pains, the
foetal heart rate was 136 bpm, her
cervix was five (5) cm dilated with the presenting part being 3/5
above the pelvic brim. The
plaintiff’s liquor was blood
stained;
(g) Pethidine 50 mg and
Maxolon IMI were administered to the plaintiff at 14h25;
(h) she was once more
assessed by Ms Adams at 16h00 which assessment revealed that she was
coping with labour pains, but her liquor
was blood stained. She was
experiencing strong contractions. Her management was to continue with
CTG monitoring, and monitoring
of her vital signs and she was
encouraged to mobilise;
(i) the plaintiff’s
cervix was found to be fully dilated at 18h00 when it was recorded
that she was 10 cm dilated;
[22]
(j) K was born at 19h10.
He weighed 3.5 kg, had a length of 53 cm, and had an Apgar score of
3/10 at one (1) minute and 5/10 at
five (5) minutes. He was provided
with oxygen via nasal prongs and naloxone to reverse the effects of
the pethidine administered
to the plaintiff during her labour;
(k) K suffered a seizure
within the first six (6) hours of birth.
[22]
From the above records it emerges that the only
record of foetal heart rate monitoring during the latent
phase of
labour was at:
(a)
02h00, when it was 120 bpm;
(b)
06h00, when it was 130 bpm;
(c)
08h00, when it was 142 - 151 bpm;
The
only record of foetal heart rate monitoring during the active phase
of labour was at:
(a)
12h00, when it was 129 - 134 bpm;
(b)
13h00, when it was 129 bpm;
(c)
14h00, when it was 136 bpm;
(d)
14h25
(determined by having
reference to the time pethidine was administered, as recorded on the
CTG trace);
[23]
(e)
16h00, when it was recorded at 118 bpm, and a second recording
(allegedly at 16h20) of 130 - 135 bpm.
Discussion
[23]
The mere
fact
that the medical
treatment administered was either unsuccessful or not as successful
as it might have been, or that the treatment
administered did not have the desired effect, does not on its own
necessarily justify the inference of a lack of diligence, skill
or
care on the part of a health care practitioner.
[24]
The question is whether the care received was substandard. Dr Moran,
as already indicted above, conceded that the care given to
the
plaintiff during the latter stages of her labour had been
substandard.
[24]
Dr Moran and Dr McLynn agreed that the plaintiff was post-date by one
(1) week when she presented
in labour at the hospital. Nothing
material appears to turn on that fact alone. What additionally was
known, or should have been
known, to the nursing staff shortly after
the plaintiff’s admission at the hospital over and above her
being post date by
one week is however material, namely that she was
a
primigravida
, smoked and had been treated for syphilis.
Although these factors did not causing K’s cerebral palsy, they
individually and
collectively were risk factors which, even on the
evidence of the defendant’s experts, would have made K more
vulnerable
to injury.
Cephalo-pelvic
disproportion
[25]
Dr McLynn raised the possibility of the plaintiff suffering from
cephalo-pelvic disproportion
(‘CPD’), stressing that it
is the disproportion of the size of a big baby, compared to the
pelvic area of a mother
with a smaller frame in relative terms, that
is important, rather than the actual size of either the baby or the
mother in isolation.
He expressed the view that there was
cephalo-pelvic disproportion.
[26]
That view was not shared by Dr Moran. Indeed he was not challenged
thereon during his cross-examination.
If there was CPD, the total
duration of the plaintiff’s labour would probably not have been
within the normal time limits
as agreed in the joint minute executed
between Dr Moran and Dr McLynn. But in any event, Dr McLynn’s
opinion was that the
plaintiff’s labour was prolonged by ten
minutes
in
the second stage which would seem to be of little consequence as no
caesarean section delivery could have been offered to her
within
those ten minutes. The plaintiff did have an episiotomy but this was
described by Dr Moran, although he did not attend to
her, as just a
cutting of soft tissue at the vaginal entrance which would be done
even if there was no CPD. In his opinion had
there been CPD, the
foetal head would have never descended into the pelvis and there
would not have been a need to do an episiotomy.
Accordingly, the
episiotomy demonstrated that the foetus successfully negotiated its
way into the pelvis of the plaintiff, thus
confirming that there was
no CPD.
[27]
In my view CPD can probably be excluded on the probabilities.
The progression of
the plaintiff’s labour and non-compliance with the guidelines
[28]
The plaintiff’s pregnancy should have from the time of her
admission been viewed as a pregnancy
with at least a moderate to
higher risk. It becomes necessary then to consider whether the
guidelines were observed.
[29]
According to the maternity records, the latent first stage extended
from her admission at 02h00,
when the plaintiff was already
experiencing contractions and was two (2) cm dilated, to the latest
12h00, when it was reflected
that she was already four (4) cm
dilated. The foetal heart rate should have been monitored two hourly
during that time. That notwithstanding,
there was no recordal of the
foetal heart rate at 04h00 or at 10h00. The guidelines inter alia
require that ‘poor prognosis
in the latent phase of labour
(more than or equal to 8 hours)’
[25]
require referral to a hospital.
[30]
The active phase extended from 12h00 until the plaintiff was fully
dilated at 18h00, which is
six hours. Monitoring during this period
had to have taken place half hourly. There were no regular half
hourly recordals of the
foetal heart rate during the active stage.
[31]
Based on the summary of labour:
(a) the plaintiff’s
first stage of labour had lasted more than eight (8) hours, and was
therefore prima facie prolonged. There
are no records of monitoring
K’s foetal heart rate after 16h20;
(b) The plaintiff’s
second stage of labour lasted one (1) hour and 10 minutes.
[32]
The neonatal records indicated that K was admitted inter alia for
severe birth asphyxia and respiratory
distress, had an abnormal
neurology with convulsions, and had raised cardiac enzymes (CK 1238).
That recorded observation
is consistent with prolonged labour
and foetal distress. These are clinical impressions recorded by
experienced attending staff,
and are significant.
[33]
In evidence the defendant however maintained, contrary to the
impressions noted and recorded
by his staff, that the labour was not
prolonged and that there was no indication of foetal distress.
[34]
Dr Moran testified that in his view the labour was not prolonged. Dr
McLynn however expressed
a contrary view. Prima facie, having regard
to the guidelines, the labour was prolonged. That should have
prompted considerable
more vigilance and more regular monitoring,
particularly in the light of the plaintiff’s history of being
primigravida
, a smoker and having required treatment for
syphilis. It would suggest a referral to a hospital with full
obstetric facilities.
The failure to have done so, in my view,
constitutes sub-standard care and hence negligence. Such substandard
care was compounded
by the lack of regular monitoring and no
monitoring (no records of monitoring being available) after 16h20.
[35]
Considerations of prolonged labour apart, the monitoring to determine
any possible foetal distress
was not conducted in accordance with the
guidelines and prima facie constitutes negligence. Proper monitoring
was not done at the
prescribed intervals. Given that the plaintiff’s
pregnancy should have alerted staff as being a risky one, and that
monitoring
was not done regularly in accordance with the guidelines,
proper care required that even more care should have been devoted to
proper monitoring.
[36]
The defendant submitted that the entry by the nursing staff of their
observations of K was erroneous,
and that the CTG strips which
reflect the monitored foetal heart rate until approximately 16h20,
even if not at half hourly intervals,
did not indicate foetal
distress and hence not the possibility of hypoxic brain injury during
the process of the plaintiff’s
labour.
[37]
One does however not know what manifested itself after approximately
16h20.
[38]
The proper monitoring of the foetal heart rate in correlation with
the uterine contractions is
vital, particularly during the active
phase of labour in order to diagnose potential foetal distress. This
was not disputed. Accurate
monitoring is particularly relevant to
identify and determine whether there are ‘type)’
decelerations, as explained
by Dr McLynn and confirmed by Dr Moran
under cross examination.  The active phase of labour, as
defined, was from 12h00 until
the plaintiff was fully dilated
allegedly at 18h00. The foetal heart rate was not monitored and
recorded half hourly during this
active phase as required by the
guidelines.
[26]
[39]
In reviewing the available CTG recordings, Dr McLynn and Dr Moran, in
their joint minute, however
agreed that they were normal, suggesting
a healthy foetus during labour. That agreement did not however extend
to the last section
of the active phase, which included variable
decelerations which Dr McLynn found alarming. The obstetricians were
in agreement
that there was no monitoring for at least two (2) hours
and 40 minutes, from 16h00 (and not from 16h20).
[40]
There is no written evidence in the medical notes or on the
partograph of any foetal monitoring
after 16h20, that is for the last
two (2) hours and some 50 minutes of labour. Accordingly, one does
not know what the foetal condition
was during the last two (2) hours
and 50 minutes of labour (from 16h20 until 19h10 when K was born),
particularly whether or not
the foetus was stressed.
[41]
Ms
Adams disputed that time
interval, suggesting that there was at worst no foetal heart rate
monitoring from 16h50 until K’s
birth at 19h10. Her viva voce
evidence was to the effect that she made the entry in the records at
16h20 but that it was in respect
of monitoring of the foetal heart
rate which had commenced at 16h20 when she recorded the time of the
monitoring, but that the
reading recorded against 16h20 related to
the monitoring for half an hour from 16h20, taking the monitoring to
approximately 16h50.
[42]
This evidence came at the end of the trial and after a number of
adjournments, and well after
the joint minute of the obstetricians
had been concluded recording that there was monitoring (albeit
inadequate) only until 16h20.
The defendant, having investigated the
relevant factual background to this matter, would presumably not have
agreed to the terms
of the join minute covering the period until
16h20 only, if Ms Adams had always disclosed that she had conducted
continuous monitoring
for half an hour after 16h20, that is until
16h50.
[43]
It also seems improbable that the foetal heart rate would have been
recorded at 16h00 at the
end of the half hour monitoring period, from
presumably 15h30 to 16h00, but that the next entry relating to a
monitoring period
would be identified with reference to the start of
the monitoring period, but the result be inserted at a later stage at
the end
of that monitoring period against the starting time of the
monitoring period. That would of course mean that if the previous
monitoring
period had been completed at 16h00, that the next half an
hour monitoring period could not have been completed at 16h20. But
that
potential complication would not arise, if the result recorded
at 16h20, was of a shorter monitoring period.
[44]
The timing intervals on the incomplete CTG tracings that are
available, are unhelpful in identifying
real time, except by a fairly
unreliable reconstruction with reference to the time recorded when
pethidine was administered to
the plaintiff. The recording does not
seem to accord with the timeline evidenced by the CTG tracings, if
one accepts the administration
of pethidine recorded thereon and
accepts that it is a continuous recording divided into ten (10)
minute segments.
[27]
[45]
It is highly improbable that Ms Adams, after the lapse of time from
the birth of K until she
testified, would still have an independent
recollection (seemingly in conflict with the practice relating to the
recordal of monitoring
results up to then, and prima facie in
conflict with what was agreed between the obstetricians), that what
was recorded as the
foetal heart rate at 16h20 was in fact the heart
rate covering the 30 minutes post 16h20. Her evidence in this regard
must be viewed
with suspicion, and as possibly representing what she
believed might have happened based on a retrospective reconstruction,
or
alternatively, having regard to the fact that it is her conduct
which is under scrutiny, representing a biased, probably untruthful

and improbable account to try and distance herself from any
culpability or criticism. This must inevitably casts doubt also on

the reliability of the heart rate recorded by her.
[46]
I agree with the submission by the plaintiff that this ‘second
recording’ of the
foetal heart rate must be viewed with
suspicion.
Should the
plaintiff have been transferred earlier?
[47]
Instead the defendant has sought, with reference to the CTG’s
that are available, to suggest
that the foetal heart rate recorded
indicated a healthy foetus. However the recordings were not done in
accordance with the guidelines
and are open to conflicting
interpretation.
[48]
With regard to the last recording, Dr McLynn cautioned that it
revealed three decelerations that
were greater than 15 bpm, which
ought to have been viewed with ‘suspicion’.
[49]
In that respect, Dr Moran testified that the foetal heart rate was
normal throughout the labour
until 16h00 when it was 118 bpm, which
was probably because the plaintiff had been administered pethidine
which would have depressed
the foetal heart rate. He further pointed
out that when the foetal heart rate was rechecked thereafter, it went
to normal limits
and was reactive and had improved to 130 - 135 bpm
at 16h30. Accordingly, in his view the foetus was healthy during the
period
of the last variable decelerations as there were also
accelerations.
[50]
Dr Naidoo stated that for a CTG to be suspicious and non-reassuring
relating to variable decelerations,
the decelerations must drop to
less than 60 bpm and must occur for at least 90 minutes and must
occur in at least 50 per cent of
contractions. Dr Naidoo concluded,
looking at the available trace containing the variable decelerations,
that one can see they
did not occur for 90 minutes and in 50 per cent
of the contractions. Dr Naidoo accordingly opined that the CTG with
variable decelerations
is not a non-reassuring trace and not
suspicious.
[51]
That might be so having regard to the available CTG, but these were
still decelerations which
should have been monitored continuously to
determine whether there was cause for concern, particularly in the
light of the plaintiff’s
history. There were clearl
y
indicators which required further careful and continuous monitoring,
rather than one simply concluding that because there are no
records
after that time, that the start of decelerations which were noticed
were innocuous.
[52]
The incomplete CTG records must also not be viewed in isolation.
Regard must also be had to whether
any risk indicating factors had
developed during the labour process.
[53]
Dr McLynn referred to the following factors which would have
persuaded him to have opted for
a caesarean section delivery
[28]
earlier:
(a)
Blood
stained liquor in the first stage of labour;
(b)
An abnormal
CTG;
(c)
Post
maturity;
[29]
(d)
A positive
VDRL and signs of borderline CPD; and
(e)
A high
head.
None of these in
isolation might have been sufficient to require a caesarean section
delivery, but they had to be viewed in totality.
It appears to me
that his opinion in this regard is reasonable and that the evidence
does not detract from his opinion.
[54]
Ms Adams, who had monitored the plaintiff’s labour and recorded
that the plaintiff’s
liquor was blood stained, stated, again
apparently on pure mental recollection, that the plaintiff was not
bleeding, the implication
being that this did not represent an
obstetric emergency.
[55]
I view this evidence, as I did with other aspects of her evidence
relating to the monitoring
of the foetal heart rate at the critical
stage, with suspicion. It seems highly improbable that she, being
employed as a midwife
in busy hospitals, could have a detailed
independent recollection of the peculiar facts of this matter, having
dealt with numerous
births since that of the plaintiff over the last
eight plus years.
[56]
Dr Moran, in seeming support of Ms Adams’ evidence, testified
that the tissues in the vagina
are fragile and bleed easily, and
therefore that during the process of examination, it is not uncommon
to cause a little bit of
contact bleeding. He was however not
present, does not have personal knowledge of the plaintiff’s
condition, and expressed
a general view. He drew attention to the
fact that Ms Adams had recorded that the liquor was blood stained and
not that the plaintiff
was ‘bleeding’.
[57]
If what Ms Adam observed as blood in the liquor was simply a common
consequence of conducting
an examination, then she would hardly have
considered it sufficiently significant to record it specifically. It
should have been
a factor of serious concern.
[58]
The same sentiment applies in respect of Dr Naidoo’s evidence
that the blood stained liquor
could be contact bleeding. The presence
of blood in the liquor should have been treated as a cause for
concern. More significantly,
is the further opinion of Dr Naidoo that
the blood stained liquor could be as a result of the plaintiff not
coping well with labour
pains, and she would have pushed against her
undilated cervix which would have caused trauma and a bit of
bleeding, even if not
active bleeding (even if there was no evidence
to suggest that the plaintiff was suffering an intrapartum
haemorrhage which would
constitute an obstetric emergency). It is
correct that in retrospect that there might not be evidence of an
intrapartum haemorrhage,
but this would not necessarily have been
known at the time, should not have been assumed to be absent, and
should have given rise
to heightened caution.
[59]
At the very least, even if the blood stained liquor might not have
suggested an immediate obstetric
emergency requiring an immediate
caesarean section delivery, it was an important indicator of risk at
an early stage, as Dr McLynn
rightly maintained.
[60]
Dr McLynn expressed the view that it was inappropriate for the
plaintiff’s labour to be
managed at the hospital and that there
were signs which were misinterpreted by the defendant’s
employees which indicated
that the plaintiff should have been
transferred to a level two (2) facility which had an obstetrician in
the theatre. These signs
included the plaintiff’s
primigravida
status, her smoking and the diagnosis of syphilis.
[61]
That view was however contradicted by Dr Moran and Dr Naidoo who
maintained that the plaintiff’s
primigravida
status did
not render her labour a high risk one which warranted referral to a
secondary or tertiary hospital such as the King
Edward Hospital. Dr
Moran stated that if every
primigravida
mother is a high risk
patient, every first pregnancy would be one and should be referred to
a high level of care, which was inappropriate.
That argument however
elevates the plaintiff’s
primigravida
status to being
the only factor. It was only one factor, in the opinion of Dr McLynn
of at least three factors, and they should
be viewed holistically and
cumulatively.
[62]
Dr Moran further testified that although the fact that the plaintiff
smoked was a known risk
factor to the foetus, it was not a risk
factor which warranted the plaintiff’s referral to a level two
(2) hospital for her
labour. Nor in his view was the fact that the
plaintiff was treated for syphilis via an effective form of treatment
a risk factor
which warranted her labour being referred to a high
level of care. He pointed out that the positive test could indeed
have been
a false positive for syphilis.
[63]
Again I am of the view that it is incorrect to consider the smoke and
syphilis issues in isolation.
They are factors which would make K
more vulnerable to injury. It is reasonable to expect that they
collectively contributed to
an increased risk as Dr McLynn stated,
which required increased monitoring and intervention.
[64]
Dr Naidoo, the defendant’s expert physician, also opined that
the plaintiff’s labour
was not a high risk as she only smoked
one (1) cigarette a day, which she had stopped. Further, she was
treated for syphilis and
her
primigravida
status did not
render her pregnancy a high risk one, but a pregnancy routinely
managed by a midwife run obstetric unit. In my view
however, these
factors did point to and required more vigilance in monitoring.
[65]
The question that however remains is whether on a totality of all the
evidence, it is established
on a preponderance of probability that a
HIE, as opposed to some other cause, for example a peri-natal stroke,
is the cause of
K’s cerebral palsy, the defendant’s
aforesaid negligence notwithstanding. If a stroke presents as the
probable cause
of his condition then, the defendant argued, the
plaintiff’s action must fail.
Did
K’s cerebral palsy on a balance of probability arise from a
hypoxic ischemic injury
or
a peri-natal stroke?
The
radiological evidence
[66]
Radiological evidence often provides an objective conclusive answer
to this question. Prof Lotz
confirmed that there was no doubt that
K’s brain suffered an infarct.
[67]
Prof Lotz outlined the following during his evidence with reference
to a slide presentation:
(a)
although the brain consists of several parts, the basal ganglia,
which he referred to as the ‘reptilian brain’,
and the
neocortex, which he referred to as the ‘human brain’,
require to be considered in the context of K’s
condition;
(b)
the reptilian brain is essential to ‘sustain life’ at the
time of birth, whilst the human brain is ‘essentially
asleep’
during this time, being only needed once the child develops;
(c)
accordingly, if there are any problems at birth, resulting in a lack
of oxygen supply to the reptilian brain, the body’s
‘auto
regulatory system’ will ‘steal’ blood and oxygen
from those areas of the brain not essential at birth,
in order to
maintain life;
(d)
this, he describes, often happens during the first stage of labour
when the mother and foetus start developing some kind of
distress and
the oxygen supply ‘is not what it should be’.  He
emphasised that this will take place over a period
of hours when the
‘salvage team’ will set up a system to redirect blood
away from those areas not needed, namely the
human brain, to the
reptilian brain;
(e)
he describes two processes that can occur, one is described as a
‘prolonged partial’ process and the other is described
as
an ‘acute profound’ process. The prolonged partial
process is when tacuteneocortex to the basal nuclei. This leaves
a
‘specific footprint’ that can be identified. In this
process one does not see an injury to the reptilian brain, because
it
has not been compromised as blood flow has been redirected to it.
However, the human brain would be compromised by this process
and one
would then see an injury in the periphery. This is the ‘hallmark
of the prolonged partial’ process. The auto
regulatory system
will initially endeavour to ‘steal’ blood from the
‘watershed’ areas of the brain. Consequently,
if injury
can be identified within the watershed areas of the brain it suggests
a partial prolonged process;
(f)
The acute profound injury occurs when there is ‘an acute
obstetrical emergency’. Here there is insufficient or no
time
for a redirection of blood as in the partial prolonged process. One
can recognise the mechanism by looking at the pattern
of injury. If
the injury is outside the reptilian brain, it is a prolonged partial
injury, and if inside, it is more likely an
acute profound injury. In
an acute profound injury, one would also expect to see injury to the
‘motor strip’, which
is the portion of the brain which
controls the essential functions immediately after birth, as this
area is also already activated
during the birthing process. The basal
ganglia and the motor strip ‘go together’. The motor
strip is extremely sensitive
to injury in an acute profound scenario
for the simple reason that it is the only area in the neocortex that
is active during birth.
(g)
With reference to the MRI scan taken of K’s brain on the 3
rd
of February 2016, Prof Lotz concluded that K had sustained an acute
profound hypoxic ischaemic injury by virtue of an injury to
the
central part of the brain, as well as his motor strip being
‘completely destroyed’. K also sustained a ‘second

infarct’, being an injury which was ‘slap bang within the
watershed territory’, which extended further along
into the
‘true arterial territory’. The injury was of a partial
prolonged process by virtue of the ‘mushroom
shaped’
gyrus in this area, but it was not a complete infarction of the gyrus
but only a partial infarction. This he testified
is indicative of the
gyrus being ‘undermined’, as there was still blood
‘coming through’ and the ‘injury
pattern is a sort
of excavation of the gyrus’. In his view, the MRI features ‘are
diagnostic of an acute profound and
partial prolonged hypoxic
ischaemic injury in the term brain at a chronic stage of evolution’,
which he referred to as a
‘mixed pattern’. Under
cross-examination he described this mixed pattern as ‘classically’
occurring when
there is a long stage of labour, with the partial
prolonged occurring initially and the acute profound occurring during
the second
stage of labour when ‘there is a crisis on hand’.
(h)
Under cross-examination, Prof Lotz stated that the MRI scan mitigated
against a conclusion that K had suffered from an isolated
arterial
occlusion, or stroke, because:
(i)
if there is such an arterial occlusion, the brain tissue dies
in
toto
by virtue of there being no blood supply, whereas there are
features of the injury being due to a partial prolonged hypoxic
ischaemic
injury by virtue of the presence of ulegyria;
(ii)
the arteries supplying the motor strip are the anterior cerebral
artery and the middle cerebral artery. Accordingly, for the
motor
strip to have been damaged, there would have had to have been two
arterial infarctions.  The injury in the motor strip
is partly
in the middle cerebral artery territory and partly in the anterior
cerebral artery territory.  There would therefore
had to have
been one in the middle cerebral artery territory and one in the
anterior cerebral artery territory, which he believed
was ‘hugely
unlikely’.
[68]
Much of the radiological evidence is not in dispute between Prof Lotz
and the radiologist called
by the defendant, Dr Reitz. In a joint
minute they agreed that:
(a)
a generic disorder was unlikely to have caused K’s brain
damage;
(b)
there were bilateral sonic abnormalities, bilateral subcortical and
periventricular white matter abnormalities, and that these
findings
are compatible with a mixed pattern of hypoxic ischaemic injury to a
term brain;
(c)
the MRI findings of hypoxic ischaemic injury to the term brain
indicate that a hypoxic-ischaemic injury occurred at some point
after
36 weeks of gestation;
(d)
additionally, there is asymmetrical focal atrophy of the left
posterior parietal region , including the left sensorimotor cortex;
(e)
asymmetrical damage has been described as part of the spectrum of
prolonged partial hypoxic ischaemic injuries, although Dr
Reitz
maintains that it is relatively rare; and
(f)
a final determination of the probable cause and probable timing of
the injury would also involve a consideration of the clinical
and
obstetrical records.
[69]
Dr Kara, the paediatrician called by the plaintiff, in a joint minute
with Dr Singh, the defendant’s
neonatologist and Dr Govender,
the defendant’s paediatric neurologist, also expressed the view
that the likely cause of the
minor child’s cerebral palsy was
a
n
intrapartum hypoxic ischemic injury
based on one or more of the following:
(a) a prolonged second
stage of labour;
(b) no record of foetal
monitoring for three hours prior to delivery;
(c) caput and moulding;
(d) depression at birth
with resuscitation, respiratory distress, and encephalopathy;
(e) an admission
diagnosis of HIE;
(f) normal head size at
birth, with no foetal growth restriction; and
(g) an MRI scan showing
features of HIE.
[70]
The defendant’s reply to the individual indicators relied upon
by Dr Kara (referred to
in the preceding paragraph) in brief, is as
follows:
(a) Dr Moran was of the
view that the plaintiff’s labour was not prolonged (he said the
total duration was 11 hours and 30
minutes) but normal including the
latent phase as well;
(b) The failure to
monitor and/or to record the foetal heart rate during the two (2)
hours 40 minutes prior to birth was conceded.
However it was
contended that this was not conclusive as the foetal heart rate was
not alarming prior to that, and because the
defendant believes that
K’s condition was cause
d
by a
peri-natal stroke and not HIE;
(c) Dr Moran testified
that there was no caput and no moulding, which would certainly have
been signs of a prolonged labour and
foetal distress;
(d) As regards depression
at birth with resuscitation, and respiratory distress, Dr Singh
stated that neurological depression at
birth may have been due to the
maternal sedation with pethidine;
(e) A normal head size at
birth with no foetal growth restriction would also not be
inconsistent with a peri-natal stroke, as opposed
to one earlier in
the pregnancy. Dr Kara confirmed that if K suffered a stroke after 36
or 37 weeks, his brain is 80 to 90 per
cent developed and therefore,
one would not get microcephaly (a small head) at birth;
(f) The MRI scan showing
features of HIE is not conclusive, as the MRI scan also has features
consistent with a perinatal stroke.
[71]
Dr Singh, a neonatologist, concluded that K’s cerebral injury
was due to a perinatal stroke,
which being a vascular event left
predominant lesion on the left. This it was said, is evidenced on the
MRI which also did reveal
also
a left middle
cerebral artery territory infarct.
[72]
Dr Govender concluded K suffered a neonatal stroke based on the MRI
findings which revealed this
left middle cerebral artery territory
infarct. Dr Govender suggested that K may have been predisposed
thereafter to HIE as a result
of the stroke, and/or that the HIE
could have also been caused by seizures after the peri-natal stroke.
Dr Govender assessed K
on two separate occasions and found,
consistent with the notion of a stroke, that:
(a) K predominantly uses
the left side of his body and that the right side of his body showed
spasticity resulting in right sided
hemiparesis;
(b) K had a contracture
at his right elbow joint which was fibrosed from disuse, indicating
that he suffered right sided hemiparesis
as his left side and other
elbow joint did not have any contractures;
(c) K’s right lower
limb had decreased power and a contracture of the right ankle, which
indicated that he suffered from hemiparesis
as he suffered no such
contracture to his left ankle;
(d) The right side of K’s
body had a power grade of 4/5 and his injury was predominantly on the
right side, and therefore
he is classified as a hemiplegic;
(e) The MRI scan of K’s
brain showed a left MCA infarct which predominantly affected the left
side of his brain with encephalomalacia.
The left side of the brain
controls the right side of the body, and therefore K suffered from
hemiparesis, as the predominant injury
is on the left side of his
brain which confirms that the minor child suffered a stroke and not
HIE, as with HIE one would get dual
affectation;
(f) There is significant
asymmetry with regards to the minor child’s brain which is very
remarkable.
Dr Govender accordingly
was of the view that the clinical examination is consistent with the
left middle cerebral artery territory
artery infarction on K’s
MRI scan as he displays right sided contractures and hemiparesis
which in her view confirms a stroke.
Dr Kara agreed that if there is
affectation of the right side of K’s brain, that this could
also happen with a stroke and
that his circumstances could be such a
case. But he also confirmed that strokes sometimes mimic HIE.
[73]
The findings during the clinical examination are supported by the
following evidence of the plaintiff
herself, namely:
(a) K has weakness only
on the right side of his body and has good use of his left arm and
leg;
(b) K is able to use his
right arm and is able to grasp, but not hold onto something;
(c) K is able to throw
with his left hand and kick with his left leg but is unable to do so
with the right side.
[74]
Dr Govender testified that there are many factors which could have
caused a stroke during the
plaintiff’s pregnancy. A pregnancy
state is a pro-coagulant state during which a lot of clotting factors
are present, including
from infections such as syphilis. During the
last three days of pregnancy, there is statistically a 34 fold
increase in the risk
of clots occurring which could cause a stroke.
Dr Kara confirmed that there is a high risk of stroke in pregnancy.
[75]
Dr McLynn conceded that smoking may be a risk factor which can cause
a stroke in a minor child.
[76]
Insofar as the causality and timing of the insult is concerned, Dr
Kara relied on the following
factors as being relevant, which they
indeed are at the level of determining the probable cause of K’s
condition:
(a)
that there were no pre-conceptual risk factors;
[30]
(b)
the comments in the medical records recorded by the defendant’s
staff that the labour was prolonged;
[31]
(c)
the lack of proper foetal heart rate monitoring during the last vital
hours of labour;
[32]
(d)
the alleged application of fundal pressure and the delivery being
facilitated by an episiotomy;
[33]
(e)
the neurological depression at birth, with low Apgar scores,
[34]
resuscitation being performed with oxygen, suction and naloxone;
(f)
that there was adequate evidence to confirm a moderate severe
encephalopathy where K had tone disturbances, depressed reflexes
and
convulsions soon after birth, poor suck and he did not cry for
several days;
(g)
that there were no major antenatal factors that affected the
placental circulation, or infections or injuries that could cause

encephalopathy;
(h)
that the neonatal records indicated that K was admitted for severe
birth asphyxia and respiratory distress, was obviously compromised
at
birth and had an abnormal neurology with convulsions, had raised
cardiac enzymes (CK 1238)
,
had no biochemical suspicion of
infection, had a relatively normal spinal puncture (no meningitis)
and that there was a normal CT
scan and cranial ultrasound, which
were done seven days after the birth;
(i)
there did not appear to be any other cause of the neonatal
encephalopathy other than hypoxic ischaemic injury; and
(j)
there is no documented evidence or history of any postnatal event
that could have caused the cerebral palsy.
[77]
With reference to the authoritative work of
Dr Volpe: Neurology of
the Newborn, 2008,
Dr Kara was of the opinion that the criteria
set for a diagnosis of intrapartum insult had been met and that, on
probability, K
had suffered such an insult.
[78]
With reference to the American Congress of Obstetrics and Gynaecology
(ACOG) criteria, Dr Kara
was of the opinion that the most probable
conclusion was that ‘there was acute intrapartum hypoxic injury
of sufficient severity
to cause cerebral palsy’, that
probability being indicated by:
(a)
the lowered Apgar scores;
(b)
the MRI scan showing features consistent with acute profound hypoxic
injury and prolonged partial injury at term;
(c)
the respiratory compromise and probable cardiac compromise/muscle
injury experienced by K at birth;
(d)
the absence of a sentinel  hypoxic event occurring before
delivery or during labour being recorded;
(e)
the lack of foetal monitoring immediately prior to birth;
(f)
there being no evidence of other proximal or distal factors that
could be considered as contributing; and
(g)
the development of spastic quadriplegia or dyskinetic cerebral palsy.
He
testified that the new criteria (2014) consider all potential
contributing factors and, even where all criteria might not be
met,
if the probability favours intrapartum hypoxia, then that is likely.
He concludes that the probable cause of K’s dyskinetic
cerebral
palsy was an intrapartum hypoxic injury.
[79]
Dr Singh agreed that the neonatal stroke contended for by the
defendant could not have happened
after K’s birth, and that if
that was the cause for his condition, that it had to have occurred
shortly prior to his birth.
Yet there was no sentinel event.
[80]
The defendant’s contention that K suffered a perinatal
ischaemic stroke/neonatal stroke
rather than birth asphyxia, is
premised upon the assumption that the injury to K’s brain was
asymmetrical, and confined to
the left middle cerebral artery
distribution, rather than being bilateral. A stroke would involve an
occlusion. Dr Singh was adamant
that the occlusion would have been in
the left middle cerebral artery, that the artery would have been
totally occluded for some
time (even weeks) and that the tissue
immediately adjacent to the occlusion would have died. She accepted
that, for her version
to be correct, the damage would have been to
the left-hand side of K’s brain given the paralysis
predominantly to his right
side.
[81]
That notion is however largely dispelled by the joint minute of the
radiologists Prof Lotz and
Dr Reitz who found the injury to be
bilateral, albeit with an additional asymmetrical focal atrophy in
the left posterior parietal
region. The question arising then is
whether there was anything that could have contributed to the
bilateral injury observed but
would also be compatible with K’s
condition being caused by a perinatal ischaemic stroke/neonatal
stroke which would account
for the asymmetry.
[82]
Dr Singh proffered that the bilateral damage might be accounted for
by K’s brain having
been more susceptible to the rigours of
birth, due to him having suffered a stroke shortly prior to his
birth. That hypothesis
was however only suggested by Dr Singh under
cross-examination, when faced with the fact that there was bilateral
damage to K’s
brain. It was not mentioned in the summary of her
expert opinions, not put to any of the Plaintiff’s witnesses
(the inference
being that she had also not mentioned it to the
defendant’s counsel), and was not supported by other evidence
adduced by
the defendant. She conceded that this hypothesis had not
been offered in her report.
[35]
[83]
Although Dr Singh initially contended that the stroke could have
occurred between the 20
th
week of foetal life through to the 28
th
post-natal day, she confined the occurrence of such a stroke in the
case of K to after the 36
th
week of gestation until birth. There was however no evidence of any
event recorded in the plaintiff’s medical history that

supported this notion.  Indeed, even the first stage of labour
indicated a seemingly healthy foetus. The CT and ultrasound
scans
conducted seven days after K’s birth, although contended not to
be definitive, also did not demonstrate that K had
in fact suffered a
stroke. Dr Singh conceded under cross-examination that there is no
evidence of a stroke on the scans conducted
of K’s brain. She
explained this on the basis that the occlusion must have dissolved.
There is however no evidence of this.
In the final analysis of her
evidence, Dr Singh conceded that there was bilateral damage to K’s
brain and she accepted that
this would have occurred during labour.
The explanation, at best for the defendant, she could advance was
that his brain was more
susceptible during birth by virtue of the
stroke.
[36]
[84]
As regards the timing of the infarct, Prof Lotz could only state that
it was after 36 weeks.
Dr Govender stated that with the 500 odd
babies that she has treated, seizures which occur within the first
six (6) hours of birth,
indicate that the insult had occurred in the
antenatal period, and not the intrapartum period. K suffered seizures
within the first
six hours of birth. She therefore contended that he
had suffered a stroke in the antenatal period but after 36 weeks of
gestation.
This
conclusion it was said,
was further confirmed in an article by
Philan
et al
which found that seizures within the first 12 hours of birth are
likely to be indicative of an antenatal insult. Dr Govender testified

that with a HIE, seizures occur later, after 12 hours from her
clinical experience with children in the nursery who have HIE,
because the damage does not occur immediately.
[85]
Prof Lotz accepted that the injury seen on the left of K’s
brain could be as a result of
a stroke, and that the injury is
predominantly on the left hemisphere. There are two arteries which
supply blood to the brain,
namely the left carotid artery and the
right carotid artery. With a HIE during labour in the majority of
cases, one usually finds
that there is a decreased blood flow in both
arteries, and therefore one would get global cerebral insult and not
usually the degree
of asymmetry observed in K’s brain. Global
hypoxic insult in most cases affects both arteries. Prof Lotz
conceded that in
less than 10 per cent of cases would one find one
sided encephalomalacia with global hypoxic ischemic insult. That
would on probability
make a HIE rare or unlikely in the present case.
He maintained however that although K’s set of circumstances
would be rare,
he found support for his conclusion that K had not
suffered a stroke but HIE in an article that was published in 2008
titled
Parasagittal Lesions and Ulegyria in Hypoxic Ischemic
Encephalopathy, Neuroimaging Findings and Review of Pathogenesis.
[86]
Doubt was sought to be cast on the reliability of that study and
whether it is reasonable, sound
and logical. The study apparently
considered only 14 patients, which is a relatively small statistical
group. The 14 patients further
all had suffered HIE and none a stroke
and only four (4) patients presented with the ulegyria. Prof Lotz
could not give evidence
regarding the remainder of the patients who
did not present with ulegyria.
[87]
Dr Reitz’s conclusion was that K had suffered a stroke and an
infarct in a specific area
of the brain which is supplied by a
specific blood vessel, namely the left carotid artery, which explains
the damage predominantly
to the left hemisphere of K’s brain.
It was argued that a perinatal stroke after 36 weeks’ of
gestation would have
predisposed K to suffer injury and not withstand
the rigours of labour.
[37]
Such a conclusion, it was
said was, corroborated by the MRI findings which confirm limited
damage to the right side of K’s
brain, which would have
occurred during the birthing process as his brain would be
susceptible to the rigours of labour, as confirmed
by both Dr Singh
and Dr Govender.
[38]
Dr Singh, the defendant’s
neonatologist, opined that the limited damage to the right side of
the minor child’s brain
on the MRI could have been caused by
the collateral supply to the right side of K’s brain, which
supply originates from the
left side of the brain, and is supplied by
the left carotid artery, which could also explain the limited
affectation on the right
side of the minor child’s brain.
[88]
The defendant was in my view not able to dispel the opinion of Prof
Lotz that a strong probability
factor is the presence of uligyria in
the affected area, which mitigates against K having suffered a stroke
and suggests as a more
probable conclusion that there was a partial
prolonged hypoxic ischaemic event.  The defendant could also not
dispel Prof
Lotz’s opinion that there would have to have been
an occlusion of two arteries to cause the bilateral damage seen on
the
MRI scan. Dr Govender was not able to provide any positive
evidence to dispel this evidence of Prof Lotz as a matter of
probability.
[89]
In my view K’s condition was caused by the negligence of the
defendant’s employees.
Was
the injury in any event unavoidable?
[90]
The defendant argued in the alternative, that even if K suffered a
HIE resulting in his cerebral
palsy, which was caused
by the negligence of the defendant’s employees at the level of
factual causation,
that
it should nevertheless be excused from legal liability as such
injury, and the damages arising there from, would have occurred
in
any event.
Such
a defence is in the nature of a confession and avoidance.
[39]
[91]
There is no onus on a plaintiff to adduce evidence to prove, on a
balance of probabilities, what
the lawful non-negligent conduct of
the defendant should have been. All that is required, is the
substitution of a hypothetical
course of lawful action, and posing
the question as to whether upon such hypothesis, the plaintiff’s
loss would have ensued
or not.
[40]
[92]
The argument is based on the hypothesis that if it is found that the
foetus only displayed signs
of foetal distress after 16h50 / 16h20,
which should have been detected but were not, that the procedure by
which the plaintiff
would have had to have been transferred to the
King Edward Hospital for an emergency caesarean section delivery,
would have resulted
in same only being offered to her after a period
in excess of two (2) hours, during which time the foetus in any event
and already
have suffered foetal distress. Accordingly, it is argued
that the failure to monitor the foetus after 16h20 but prior to
delivery,
made no difference in the outcome of the foetus, as a
caesarean section delivery could never timeously have been performed
upon
her at a referral hospital.
[93]
The factual basis for that argument was developed as follows in the
evidence of Dr Moran, who
contended that even
if
there was
documented foetal monitoring from the period 16h30 to 19h10 it would
have made no difference in the outcome of the minor
child for the
following reasons:
(a) The last documented
foetal monitoring at 16h20 / 16h50 (according to Ms Adams) indicated
that the foetal condition was good.
If the CTG had ran for the 90
minutes as mandated and required in terms of the guidelines and if
one were to have discovered variable
decelerations at this point,
only then would the nurses have been justified in assuming that it
was a suspicious CTG;
(b) Thereafter, the
nurses at 18h00 (90 minutes after 16h30) would have to reassess the
plaintiff to determine how her labour was
progressing. If foetal
distress was diagnosed, the nurses at the hospital would have to
contact the doctors at the King Edward
Hospital. Once contact with
the doctor was established, the doctor would have to be advised of
the plaintiff’s condition;
(c) If the doctor, after
being informed of the CTG, determined that the plaintiff was a
candidate for transferal, the doctor would
have to provide
instructions to transfer the plaintiff to the King Edward Hospital,
unless the plaintiff was ‘fully dilated
at the time’. If
she was fully dilated, the advice would have been to extract the
minor child at the hospital and resuscitate
him depending on how far
the plaintiff progressed in labour. As the plaintiff was fully
dilated at 18h00 it was unlikely that a
doctor would have performed a
caesarean section delivery to extract the foetus thereafter, as the
delivery was imminent.
(d) If the plaintiff was
not yet fully dilated, the doctor may have called for an ambulance
for her transfer to the King Edward
Hospital. The hospital would then
have to contact the ambulance services for transfer of the plaintiff
which is a laborious process.
The EMRS services would have dispatched
an ambulance in accordance with their transfer system, and the
plaintiff would have been
categorized as a ‘red code’.
The ambulance would have to travel from town to the hospital to
transfer the plaintiff,
which would take time. On arrival at the
hospital, the EMRS services would have to evaluate the plaintiff and
thereafter obtained
a handover from the hospital staff. The plaintiff
would have to be trolleyed out to the ambulance and transported to
the King Edward
Hospital. The process of the ambulance arriving and
the plaintiff being transferred to the King Edward Hospital would
have taken
at the very least, according to Dr Moran, one and a half
hours.
[41]
If it was decided at the
King Edward Hospital that the plaintiff required a caesarean section
delivery, this could not be done immediately.
Consent would have to
be obtained, tests would have to be done, and an anaesthetist would
have to assess the plaintiff to make
sure she is fit for anaesthetic.
Dr Moran stated that the pre-surgery safety checklist, draping the
plaintiff, cleaning the plaintiff
and putting the plaintiff on
anaesthetic, would have taken more time before the plaintiff actually
underwent a caesarean section
delivery. Accordingly, Dr Moran was of
the view that it was highly unlikely that the plaintiff would have
been able to get a caesarean
section delivery prior to the birth of
the minor child.
(e) Based on the evidence
of Ms Adams, the midwife monitoring the plaintiff’s condition
who had testified that she had commenced
the CTG at 16h30 (in fact
she had said 16h20 being the time of the entry) and ended same at
approximately 16h50, and that the foetal
heart rate was reactive,
indicating a normal foetus, and that Ms Adams testified that the
plaintiff was fully dilated at 18h00,
and if the King Edward Hospital
had to have been contacted for the transfer of the plaintiff, Dr
Moran argued that if foetal distress
should have been detected after
16h50, it would have made no difference in the outcome of the minor
child as he would have already
suffered hypoxic ischemic insult to
the brain even on the plaintiff’s version of events. The harm
would have in any event
occurred.
[94]
The aforesaid hypothesis however proceeds on the premise that the
last CTG monitoring ended at
16h50, that no greater or more vigilant
monitoring was required prior to that (notwithstanding Dr Moran
conceding that the level
of care received by the plaintiff prior to
that was substandard
)
, and that the
labour was not one with risk factors to which more attention had not
been given, all of which are incorrect as I
have endeavoured to show
above.
[95]
Having regard to my findings earlier in this judgment, the transfer
of the plaintiff to King
Edward hospital or a similar institution was
indicated earlier that day, at a stage which would have left
sufficient time for the
plaintiff to have been afforded proper care.
In my view the alternative argument advanced by the defendant has
therefore also not
been established.
Conclusion
[96]
As sought to be demonstrated above, the probabilities favour the
conclusion that K suffered a
mixed pattern of a partial prolonged
albeit of shorter duration, and acute profound hypoxic ischaemic
injury prior to his birth,
which became acute during the period when
there is no record of his condition.
[97]
The hypoxic-ischaemic insult, as described by Prof Lotz, and agreed
to by Dr Reitz, would accord
with the fact that the foetus was in
some distress during the active phase of labour (approximately 12h00
to 16h20), probably as
a consequence of it being partially starved of
both blood flow and oxygen, by virtue of the placenta being ‘squeezed
off’
during the plaintiff’s contractions immediately
prior to birth, and the foetus being slow to recover from such
contractions.
[98]
The plaintiff has accordingly discharged the burden of proving that
the defendant’s medical
personnel were negligent in their
treatment of or their failure to treat the plaintiff prior to K’s
birth and that the injury
to his brain, and subsequent cerebral
palsy, was caused as a consequence of that negligence.
Costs
[99]
The plaintiff has been successful. In the exercise of my discretion
on costs,
it is appropriate that the defendant be directed to pay the
plaintiff’s legal costs to date on the High Court scale,
including
the costs of the experts, in accordance with the terms of
the order set out below.
Order
[100]
The following order is made:
(a)
The defendant is directed to
compensate the plaintiff, in her representative capacity as mother
and as natural guardian of K, a
boy born on the 14
th
of May 2009, and in her personal capacity, for the damages claimed in
this action, either as proved or agreed;
(b)
The defendant is directed to
pay the plaintiff’s taxed or agreed party and party costs on
the High Court scale, such costs
to include:
(i)
the costs of the plaintiff’s attorney attending upon any
consultations with witnesses
in preparation for trial, including the
consultations with the under-mentioned expert witnesses;
(ii)
the costs of senior and junior counsel where employed, including the
reasonable and necessary
costs of their preparation for trial, and
for their attendance upon consultations with the under-mentioned
expert witnesses and
the plaintiff;
(iii)      the
qualifying fees of the under-mentioned expert witnesses, including
the costs of the preparation
of their reports, their attendance fees,
and the fees to qualify themselves to testify at the trial and for
any necessary consultations
with the plaintiff’s attorney and
counsel (with the quantum of fees, and expenses, to be determined by
the taxing master),
namely:
(aa) Dr Y Kara, the specialist
paediatrician;
(bb) Dr D McLynn, the obstetrician and
gynaecologist;
(cc) Prof J Lotz, the professor of
radiology; and
(c)
The proceedings are otherwise adjourned sine die.
_____________________
Koen J
APPEARANCES
Plaintiff’s
Counsel:
ADV. I L TOPPING SC with
M SIBISI
INSTRUCTED BY:

FRIEDMAN & ASSOCIATES
C/O

MACGREGOR ERASMUS ATTORNEYS
Ref.:  CC
Smythe/Cathy/FR12/0005
Tel.:  031 389
0433
Defendant’s
Counsel:         ADV S NANKAN
INSTRUCTED
BY:
STATE ATTORNEY (KWAZULU-NATAL)
Ref.:
24/3958/13/D/P12-CW BAILEY
Tel.:  031 265
2560
C/O

CAJEE SETSUBI CHETTY INC
Ref: Mr Essa
Tel.:  033 345
6719
[1]
In order to succeed with
a claim for damages based on medical negligence, a patient has to
allege and prove the contract, negligence,
and that such negligence
caused damages –
Blyth
v Van den Heever
1980 (1) SA 191 (A).
[2]
This contention has subsequently been
reviewed, as will appear below.
[3]
Briefly stated, the
argument in this regard is that the plaintiff was fully dilated at
18h00 and K was born at 19h10. Consequently,
even if he suffered
from an acute intrapartum hypoxic event during this period, a
caesarean section delivery would not have been
performed on the
plaintiff to extract the minor child as she was ready to deliver at
the hospital.
[4]
Michael & another
v Linksfield Park Clinic (Pty) Ltd & another
2001 (3) SA 1188
(SCA);
Medi
-Clinic Ltd v Vermeulen
2015 (1) SA 241 (SCA).
[5]
Per the joint minute of
Dr Singh, the defendant’s neonatologist, Dr Govender, the
defendant’s paediatric neurologist
and Dr Kara, the
plaintiff’s paediatrician. The joint minute further recorded
inter alia that K has severe cerebral palsy,
which Dr Kara contended
was dyskinetic and spastic, while Dr Govender indicated that it was
spastic hemi-paretic with a gross
motor functional classification of
four (4), impaired speech and communication skills and poor hand
function. K’s vision
and hearing appears to be reasonable and
he has microcephaly. There are no dysmorphic or syndromic features.
K was born at term
and was appropriate for gestation. His head size
was normal at birth. K had Apgar scores of three (3) and five (5),
and he was
resuscitated at birth and had convulsions soon after
birth. Dr Kara noted that the minor child had a mixed type of
cerebral palsy,
while Dr Govender indicated that the minor child was
predominantly hemiplegic with spasticity especially on the right
side and
his power on the right side was of a grade three (3) and he
had contractures of the right elbow and wrist and used his left hand

predominantly. Dr Govender contended that the minor child had
bilateral short Achilles tendons. Dr Kara submitted that these

findings by Dr Govender did not describe hemiplegia but rather
described asymmetric spastic quadriplegia. Dr Kara noted the joint

minute by Dr Reitz and Prof Lotz which commented on acute profound
and partial prolonged hypoxic ischemic injury which is asymmetrical

and involved with the left hemisphere more than the right one. Dr
Govender disagreed.
[6]
Prior to the plaintiff
discovering that she was pregnant, she had smoked approximately one
(1) cigarette a day. She stopped after
she went to her second visit
to the antenatal clinic.  The plaintiff had her second
antenatal visit to the clinic on the
7
th
of October 2009.
[7]
It was inter alia
maintained that pregnancy is a hyper co-aguable state and the fact
that the plaintiff smoked during her pregnancy
further increased the
risk of coagulation which could cause a stroke.
[8]
Van Wyk v Lewis
1924
AD 438
at 444.
[9]
Mitchell v Dixon
1914 AD at 525.
[10]
Available at :
http://www.kznhealth.gov.za/family/Maternity_care_guidelines_2007.pdf
,
accessed 20 February 2019
[11]
The guidelines at 34.
[12]
The guidelines at 44.
[13]
The guidelines at 40.
[14]
The guidelines at 52.
[15]
The guidelines at 51.
[16]
The guidelines at 55.
[17]
The guidelines at 65.
[18]
These are clinical and obstetrical
records.
[19]
The plaintiff was admitted to the
hospital on the 14
th
of May 2009 at 02h00 complaining of lower abdominal pain and a
‘show’. On assessment at 02h00 on the 14
th
of May 2009, it was revealed that her BP was 134/79, she was 38/40
weeks pregnant via palpation and 40/40 via sonar, presented
with a
SFH of 37 cm, the presentation of the foetus was cephalic with a
longitudinal lie and posterior, she experienced moderate
X 2
contractions which were palpable, on PV examination her cervix
admitted one (1) finger and was two (2) cm long posteriorly
and her
membranes were intact with the presenting part of the foetus being
4/5 above the pelvic brim. The plan formulated for
her treatment was
to carry out CTG monitoring which revealed a reactive foetal
baseline heart rate of 120 bpm. She was to be
monitored and assessed
within four (4) hours at 06h00. The plaintiff was in labour and
according to the guidelines the foetal
heart rate should thereafter
be monitored two hourly.
[20]
According to the guidelines the
foetal heart rate should thereafter be monitored half hourly.
[21]
It is not clear on what basis, but
presumably because the nursing staff had not observed it for
themselves.
[22]
The plaintiff had now entered the
second stage of labour.
[23]
The first CTG is
labelled with the plaintiff’s name and the date of 14
th
May 2009. The CTG’s appeared to be a progressive series of
records in time but the exact time when they were recorded is
not
documented on any of them, and therefore there is uncertainty as to
what stage of labour the last CTG was done.
[24]
Louwrens
v Oldwage
2006 (2) SA 161 (SCA).
[25]
The guidelines at 65.
[26]
The defendant’s
medical personnel did not follow the defendant’s own
guidelines, as the foetal heart rate was not
monitored every half
hour during the active phase of the first stage of labour. The
experts agreed that this is necessary to
assess the condition of the
foetus and to ensure that there are no ‘late decelerations’.
It is common cause that
the ‘mechanism’ of late
decelerations can cause a hypoxic ischaemic injury to the foetus’
brain. Dr Singh agreed
that late decelerations could have caused
hypoxic ischaemic injury to the brain. With proper monitoring of
late decelerations,
or any similar problems which could cause or
contribute to a hypoxic ischaemic injury, hypoxic ischaemic injury
could be determined
timeously in advance before such injury occurs.
The lack of proper monitoring during this later phase of K’s
birth indicates
that the defendant’s medical personnel did not
monitor whether the foetus was in distress with the level of care
the defendant
himself  requires of his staff, which accordingly
resulted in them failing to diagnose that the foetus was distressed.
This
failure by the defendant’s professional nursing staff to
adhere to the general level of skill and diligence possessed and

exercised in the same circumstances by members of the same
profession constitutes negligence.
[27]
Exhibit "C" at 19-21, if
one calculates the ten (10) minute time segments from 14h30, the
tracings end at 15h20
[28]
The defendant has raised
the fact that caesarean section deliveries themselves carry risks,
including deaths due to bleeding during
and after the delivery,
surgical complications in terms of damage to the bladder and other
tissues, anaesthetic complications,
and longer term complications as
many women with previous caesarean section deliveries are at a
higher risk for future pregnancies.
Dr Moran expressed the view that
there were no indications which warranted the plaintiff’s
exposure and that of the foetus
with which she was pregnant, to the
inherent risks associated with a caesarean section delivery. Dr
Naidoo also testified that
the National Committee For Confidential
Enquiries Into Maternal Deaths released in 2011 to 2013 had found
that caesarean section
deliveries were associated with a 2.8 per
cent increase in the chance of maternal death compared to normal
vaginal deliveries.
The risk of a caesarean section does not arise
in this case, although it is not an insignificant matter. If the
need for a caesarean
was indicated, then the plaintiff should have
at least been given that option after a full explanation of the
risks. The fact
of the matter is that she was not given that option.
The issue is whether the need therefore was indicated.
[29]
The plaintiff being
post-mature does not feature as a material aspect of her case and
correctly so, and stands to be discounted.
She was post-date only by
approximately one (1) week as confirmed in the joint minute executed
between Dr McLynn and Dr Moran.
Dr McLynn conceded that K did not
have any vernix cream left on his skin, nor did he have red, dry,
peeling or wrinkled skin
at birth and long nails, which are all
characteristics of post-maturity.
[30]
Smoking and syphilis were in his view
unlikely causal factors (Exhibit "B": report of Dr Kara
para 9.1 at 235; Dr Kara's
evidence at 419-421).
[31]
Exhibit "B": report of Dr
Kara para 9.2 at 235. This comment is recorded in exhibit D":
the neonatal records at
14.  The plaintiff is recorded as being
two (2) cm dilated and having moderate contractions at 02h00 and
only being four
(4) cm dilated at 12h00 - see exhibit "C"
at 4 and 22.  This would equate to at least 10 hours in the
latent phase
of labour.  The summary of the plaintiff’s
labour records her first stage as being 10 hours and 10 minutes in
duration
- exhibit "C" at 23.
[32]
Exhibit "B" report of Dr
Kara para 9.2 at 235.
[33]
Exhibit "B" report of Dr
Kara para 9.2 at 236.
[34]
Even accepting the effects of
pethidine having been administered.
[35]
Cross-examination of Dr Singh at 936.
[36]
Cross-examination of Dr Singh at
922-923.
[37]
A normal baby going through the
normal stresses of labour will react normally, but a baby who has an
abnormal brain, in that the
blood supply is affected, might not
respond to hypoxia or hypercarbia similarly like a normal baby, and
will come out with low
Apgar scores as was the case with K.
[38]
The opinions of Dr Singh
and Dr Govender are further confirmed by medical articles which are
reflected in exhibit F.  F33
refers to a study by Karen B.
Nelson which confirms that K’s clinical features at birth did
not exhibit signs of asymmetrical
hemiplegia, and that he presented
with neonatal seizures and hypotonia at birth. F34 confirms that a
CT scan is not sensitive
enough to detect a stroke, contrary to the
opinion of Dr Kara. A stroke may cause children to present with
neonatal depression,
suggestive of birth asphyxia. Normal pregnancy
is a pro-coagulant and pro-inflammatory condition and a risk of a
stroke is higher
in pregnancy than in a non-pregnant state. F91
confirms that a baby with a pre-existing cerebral insult reacts
differently to
the stresses of labour, referred to as brain priming,
which would result in a baby not reacting appropriately to the
stresses
of labour, recognised also in Volpe’s standard
textbook.
[39]
Johannesburg
City Council v Television and Electrical Distributors
1997 (1) SA 157
(A).
[40]
Lee
v Minister of Correctional
Services
2013
(2) SA 144
(CC)
.
[41]
Mr Padayachee who was in
charge of the EMRS services testified that the ambulance could have
taken approximately two (2) to three
(3) hours before the plaintiff
was transported to the King Edward Hospital.