About SAFLII
Databases
Search
Terms of Use
RSS Feeds
South Africa: Supreme Court of Appeal
SAFLII
>>
Databases
>>
South Africa: Supreme Court of Appeal
>>
2018
>>
[2018] ZASCA 141
|
|
AM obo KM v Member of the Executive Council for Health, Eastern Cape (699/17) [2018] ZASCA 141 (1 October 2018)
SAFLII
Note:
Certain
personal/private details of parties or witnesses have been
redacted from this document in compliance with the law
and
SAFLII
Policy
THE SUPREME COURT OF
APPEAL OF SOUTH AFRICA
JUDGMENT
Not
reportable
Case
no: 699/17
In
the matter between:
A.
M. obo K.
M.
APPELLANT
and
MEMBER
OF THE EXECUTIVE COUNCIL FOR HEALTH,
EASTERN
CAPE
RESPONDENT
Neutral
citation:
M. v MEC for Health, Eastern Cape
(699/17)
[2018] ZASCA 141
(1 October 2018)
Coram:
Ponnan, Tshiqi, Majiedt, Swain and Zondi JJA
Heard:
3 September 2018
Delivered:
1 October 2018
Summary:
Delict – medical
negligence – child suffering cerebral palsy as a result of
acute profound hypoxic ischaemic event during
labour – hypoxia
developing and catastrophic event ensuing – delictual liability
not established on the facts.
ORDER
On
appeal from:
Eastern Cape Division of the High Court, Mthatha
(Nhlangulela DJP, sitting as court of first instance):
The
appeal is dismissed with costs.
JUDGMENT
Majiedt
JA (Tshiqi JA concurring):
[1]
The appellant, Ms A M, claimed delictual damages in the High Court,
Mthatha, on behalf of her minor child, K. M. (K.) against
the
respondent, the Member of the Executive Council for Health, Eastern
Cape Province (the MEC). The claim emanated from the child
suffering
cerebral palsy as a consequence of a hypoxic ischaemic event during
the birth process. Nhlangulela DJP who, by agreement
between the
parties, was called upon to decide only the question of liability,
dismissed the claim. The learned Judge found that
Ms M. did not
succeed in proving negligence and causation. This appeal is with his
leave.
The
factual matrix
[2]
The facts set out below were either common cause or not seriously
disputed. It became common cause that the hospital records
relating
to Ms M.’s treatment were altered in material respects. More
will be said about that later. Ms M. was admitted to
the All Saints
hospital at Engcobo on 4 May 2010 at around 12h40, when she presented
with labour pains. All Saints is a level one
state hospital. For
present purposes that classification entails that the hospital has
properly trained and qualified staff (doctors
and nurses), medical
equipment and a theatre to provide proper obstetric care. Ms M. was
17 years old at that time and it was her
first pregnancy. She
attended antenatal care at her local clinic from the 32nd week of her
pregnancy. The antenatal care was uneventful.
[3]
At admission Ms M. was 40 weeks pregnant, ie full term. Good foetal
movements were reported and vital observations were normal.
She
appeared generally in good health, although her blood pressure rate
was recorded as marginally high at 141/71. The foetal heart
rate
(FHR) was recorded to be 138/min which is within the normal range of
110 – 160 per minute. The records reflect that
Ms M. refused to
undergo a vaginal examination. No assessment or plan for further
management appear in the records.
[4]
The next entry in the medical records is at 23h45, some 12 hours and
45 minutes later. Mild contractions were noted and a FHR
of 135/min
was recorded. Another inordinate time lapse ensued before the next
entry at 08h20 on the following day, 5 May 2010.
The entries reflect
that Ms M. was uncooperative, experienced weakness of the knees and
refused to get onto the bed. The Partogram,
a document which is meant
to chart the progress of labour, was said to have been started at
this point by the attending nurse.
It charted the foetal head as 4/5
above the pelvic brim and the FHR was 140/min. The following
contractions were noted: two moderate
contractions in 10 minutes at
08h20 and precisely the same contractions at 08h50 and at 09h20.
[5]
According to the records the foetal head was showing at 09h50 when Ms
M. pushed. The Partogram showed that the foetal head was
at 2/5 at
this time and there were three moderate contractions. The FHR was
recorded as normal at intervals of half an hour on
four occasions
between 08h20 and the time of delivery.
[6]
Ms M. delivered her baby at 10h00 by face to pubis delivery. This is
a risky manner of delivery, since it is usually delayed
because of
the difference in angle and size of the baby’s head, compared
to a normal delivery. A face to pubis delivery often
requires
assistance, such as ventouse (vacuum extraction) or by forceps. The
Agpar score, which is a basic, general assessment
of a newborn baby’s
general health, was assessed to be five at one minute and seven at
five minutes after birth. These scores
were later overwritten to
eight and eight respectively. Agpar scores are out of 10, with a
score of 10 indicating optimal health
and well-being.
[7]
The medical records noted no visible abnormalities with the placenta,
umbilical cord or membranes. It also recorded an absence
of meconium
staining of the amniotic fluid (which is usually indicative of a
healthy newly born baby). Ms M. sustained a severe
third degree
perineal tear in the delivery process. The tear was sutured in
surgery some seven hours later.
[8]
It was common cause that K. suffered
an acute profound hypoxic event during labour.
[1]
The experts were agreed that all
indications point to a global hypoxic ischaemic injury of a
catastrophic nature which resulted
in spastic dystonic quadriplegic
cerebral palsy.
[2]
A hypoxic ischaemic event can be
described as lack of oxygen and inadequate perfusion of oxygen
through the blood to the brain which
causes damage to the brain.
Despite initial vigorous contestation on behalf of the MEC, it became
common cause by the end of the
trial that the cerebral palsy was
caused by an acute, profound hypoxic ischaemic injury (the injury).
The consensus was brought
about by the conclusions contained in the
admitted expert report of Professor Van Toorn, a paediatric
neurologist. His conclusions
were supported by the findings of
Professor Savvas Andronikou, a radiologist who performed a magnetic
resonance imaging (MRI) scan
on Kangwa. His radiology report was
admitted as evidence by agreement. In that report, Professor
Andronikou concluded as follows:
‘
Features are those of a chronic
evolution of a global insult to the brain due to hypoxic ischaemic
injury, of the acute profound
type, most likely occurring at term’.
Professor
Van Toorn concurred with the radiology report that ‘K.’s
MRI changes are consistent with a global hypoxic
ischaemic injury, of
a catastrophic nature, at or around term’.
[9]
A brief explanation of the cause and development of hypoxic ischaemia
which injures the brain is necessary. The foetus is completely
dependent upon the mother for nutrition and oxygen, transmitted
through the umbilical cord from the mother’s placenta. During
the onset of labour the contractions of the uterus (commonly known as
‘labour pains’) affect the placenta. As the contractions
increase in strength, the blood vessels in the placenta become
constricted and the blood supply to the foetus via the umbilical
cord
contains increasing levels of carbon dioxide and less oxygen.
Monitoring of the foetal heart rate occurs by means of a
cardiotocograph
(CTG), which also measures the uterine contractions.
CTG readings will convey to nursing staff monitoring the patient
three important
facets of heart normality: (
a
) the average
(baseline) heart rate which, as stated, should be between 110 –
160 beats per minute; (
b
) the baseline variability of the
heartbeat which normally should be between 5 – 10 beats per
minute; and (
c
) accelerations in the heartbeat. Early and late
decelerations of the heartbeat are related to contractions of the
uterus. Late
decelerations occur after the commencement of uterine
contractions and recovers some time after the contractions had
ceased. A
foetal heart rate below 90 bpm and a series of late
decelerations of the heartbeat are cause for concern, as they may
suggest that
the foetus is in distress. They are referred to in
medical parlance as ‘non-reassuring foetal heart rate’.
Depending
on the severity of the foetal distress, it may be necessary
to expedite the delivery by performing an urgent caesarean section.
Absent timeous intervention, the increasing levels of reduced oxygen
supply to the foetus (hypoxia) will result in brain damage.
[10]
The central issues at the trial, as in this court, were the
reliability of the records, whether the hospital staff was negligent
in their treatment of Ms M. and, if so, whether their negligence
caused the injury and resultant cerebral palsy. Nhlangulela DJP
found
in favour of the MEC on all these issues. He found that the hospital
records were admitted by consent. The learned Judge
held further
that, absent forewarning of a non-reassuring foetal condition
ex
facie
the medical records, the hospital staff were not negligent
in their treatment of Ms M.. There had not been suboptimal monitoring
of the patient which amounted to negligence. On the applicable legal
principles, ‘the hypothetical non-negligent monitoring
would
not have produced a better labour outcome’, thus factual
causation had not been proved. Before deliberating on the
cogency of
these findings, it is necessary to consider briefly the evidence. A
key factor in that consideration is the effect of
the altered
records. At the end of the trial there was consensus on virtually all
aspects of the expert evidence. The essential
dispute between the
parties related to the conclusions to be drawn from the evidence.
The
evidence
[11]
Ms M. did not testify, nor did any of the hospital staff. Two
obstetric and gynaecology experts, Professor Smith of Tygerberg
Children’s Hospital and Stellenbosch University, and Dr Hulley,
a practising obstetrician and gynaecologist of more than
30 years’
experience, testified on behalf of Ms M. As stated, Professor Van
Toorn’s expert report was admitted into
evidence by agreement.
The same occurred in respect of the expert reports of Mr Irving, a
forensic document examiner (who also
testified), and Professor
Andronikou. On behalf of the MEC the only oral evidence presented was
that of Professor Buchmann of the
Department of Obstetrics and
Gynaecology of the University of Witwatersrand. There were several
reports of other medical specialists
before the trial court, but the
ones which I have mentioned formed the main evidential material on
the three central issues.
[12]
The common cause facts were as follows:
(a) There was no dispute that the
medical records were tampered with, as detailed in Mr Irving’s
report.
(b) The management and care afforded
to Ms M. by the medical staff at All Saints hospital was below
standard. Professor Buchmann
agreed that Ms M. was not managed and
cared for properly in the following important respects:
(i)
She should have undergone a full vaginal assessment every four hours
after admission.
(ii)
In the face of her alleged refusal to be vaginally examined a doctor
should have been called in to assist.
(iii)
Ms M. had a prolonged latent phase of
labour (ie poor progress of labour). She ought therefore to have been
monitored continuously
and an epidural
[3]
and analgesia
[4]
should have been offered to her.
(iv)
She should generally have been checked properly and ought to have
received proper medical treatment.
(v)
Lastly and conclusively, when asked under cross-examination whether
he agreed ‘that the staff of the hospital did not
comply with
the duty and neglected to treat and monitor [Ms M.] as is required in
a hospital, Prof Buchmann replied that ‘yes
according to the
guidelines they fell short of that’. When pressed further as to
whether that conduct in fact fell short
of the guidelines as
practised, he stated: ‘[t]hat’s reasonable to state
that’.
(c) The absence of proper monitoring
would create a risk to both Ms M. and the foetus in the process of
labour.
(d)
K.’s
brain injury was caused by a hypoxic ischaemic injury (also at times
referred to as ‘intrapartum ashpyxia’
[5]
during the trial) which caused the
cerebral palsy.
The
medical records
[13]
At issue was whether those parts of the hospital records disputed on
behalf of Ms M., in particular the Partogram, were admissible
as
evidence. The authors of those records were not called to testify.
Absent agreement between the parties, they would ordinarily
constitute inadmissible hearsay. The trial Judge held that the
records were admissible on the basis that ‘the plaintiff.
. .
agreed to the introduction and use of the hospital records before and
during the commencement of the trial without demur’.
That
finding flies in the face of the basis upon which it was agreed on
behalf of Ms M. in the pre-trial minute that documents
may be
admitted without proof at the trial. The minute noted that the
parties agreed that hospital records ‘will be admitted
as
evidence without formal proof, subject to the entitlement of any
party to dispute any aspect thereof’. The finding is
also
controverted by the evidence on behalf of Ms M. as adduced by Prof
Smith and Dr Hulley. Both of them, particularly Dr Hulley,
were
adamant in disputing the correctness of the records. Moreover, Mr
Irving’s report and testimony became undisputed. He
demonstrated persuasively that the hospital records were extensively
altered. Absent any explanation by those who effected the
alterations, it must be accepted that the alterations were made to
falsify the records.
[14]
The trial Judge invoked the provisions of
s 3(1)(a)
and (c)(vi) of
the
Law of Evidence Amendment Act 45 of 1988
in support of this
finding. The section reads as follows:
‘
Hearsay evidence
(1) Subject to the provisions of any
other law, hearsay evidence shall not be admitted as evidence at
criminal or civil proceedings,
unless –
(a)
each party against whom the evidence is to be adduced agrees to the
admission thereof as evidence at such proceedings;
. . .
(c)
the court, having regard to –
(i) the nature of the proceedings;
(ii) the nature of the evidence;
(iii) the purpose for which the
evidence is tendered;
(iv) the probative value of the
evidence;
(v) the reason why the evidence is not
given by the person upon whose credibility the probative value of
such evidence depends;
(vi) any prejudice to a party which
the admission of such evidence might entail; and
(vii) any other factor which should in
the opinion of the court be taken into account,
is of the opinion that such evidence
should be admitted in the interests of justice. ’
[15]
The high court’s reliance on this section to rule that the
records were admitted by consent is flawed in the following
respects.
First, the MEC did not seek their admission on this basis and the
parties were not afforded an opportunity to address
the court on it.
Secondly, the learned Judge disregarded the factors listed in
s
3(1)(
c
)(ii) – (v) and failed to have adequate regard to
s 3(
c
)(vi). The tampering of the records had become common
cause at the trial. The only possible inference is that the tampering
had
as its sole purpose the falsification of the records. A proper
application of the provisions of
s 3(1)(
c
) would have
compelled the high court to a conclusion that the provisions do not
find application here.
[16]
The evidence constituted crucial documentary evidence which
purportedly tracked Ms M.’s labour progress which culminated
in
a catastrophe upon delivery of her baby. The documentary evidence has
a material impact on the question of liability, more particularly
the
hospital staff’s alleged negligent conduct. Had the records in
fact been a true, accurate recordal of Ms M.’s labour
progress,
they would be of great probative value and perhaps even decisive in
adjudicating the dispute between the parties. No
reason at all was
proffered why the authors of the records, upon whose credibility the
probative value of the records depended,
were not called to testify
in respect of the numerous instances where the correctness of the
records were disputed. And, lastly,
the prejudice to Ms M. is
self-evident – falsified hospital records distorted the true
picture of how her labour progressed
and of the well-being of her and
the foetus.
[17]
For these reasons I find that the high court erred in its ruling
regarding the admissibility of the disputed parts of the hospital
records. The correct approach to the records is to accept the
undisputed parts and to exclude the disputed parts which were
falsified.
The latter are simply too unreliable to be considered as
part of the evidence. This is particularly true of the Partogram. As
stated,
the compelling deduction is that the Partogram was written up
afterwards, at the time of the falsification of the rest of the
hospital
records. Again, the only reasonable inference is that the
Partogram was drawn up as part of the reprehensible scheme to falsify
the records. For that reason, the Partogram cannot be relied upon in
instances of disputed facts.
Liability
[18]
Ms M. had to prove that her damages
were caused by the hospital staff’s negligence. A negligent
omission is unlawful only
in circumstances which ‘the law
regards as sufficient to give rise to a legal duty to avoid
negligently causing harm’.
[6]
Professional persons such as doctors
and nurses are required to adhere to the level of skill and diligence
exercised by members
of the profession to which they belong,
[7]
failing which they would be negligent.
The sole ground of negligence advanced before us on behalf of Ms M.,
was the failure by the
nursing staff to adequately monitor and treat
her during labour. Counsel was driven to concede that the postnatal
neglect initially
relied upon was not pleaded and that it would in
any event be superfluous in the case of a favourable finding on the
main ground
of negligence.
[19]
With regard to the sole ground of negligence ultimately relied upon,
it became common cause through the evidence of Professor
Buchmann
that (a) the monitoring and treatment were not in accordance with the
guidelines as practised in hospitals; and (b) the
absence of proper
monitoring would create a risk to both mother and foetus. The crux of
the dispute pertains to the question what
had caused the injury. The
argument advanced on behalf of Ms M. was that the lack of proper
monitoring and care and the failure
to intervene timeously, created a
risk of damage to the foetus which then, as a fact, materialised into
cerebral palsy. Factual
causation was to be found in the creation of
the risk, so the argument went. But, when pressed, counsel correctly
conceded that
inadequate monitoring and treatment, without more,
would not constitute a negligent omission. I consider next the
crucial enquiry
– what caused the injury?
[20]
It was contended on behalf of the MEC
that because this was an acute, profound injury of a catastrophic
nature, inadequate treatment
and monitoring played no role in its
occurrence. The determination of this decisive aspect requires first
a discussion of the relevant
medical concepts and then an evaluation
of the evidence. The terms ‘hypoxia’ and ‘ischaemia’
have been
explained above. Counsel for the MEC advanced various
dictionary meanings in respect of the medical concepts. As stated,
Professor
Andronikou did not testify – his radiology report was
admitted by agreement. Absent oral evidence, regard must be had to
these dictionary meanings for a proper understanding of the medical
terms. Stedman’s Medical Dictionary (Stedman’s)
[8]
defines ‘acute’ as
‘referring to a disease of sudden onset and brief course, not
chronic’.
[9]
The Concise Oxford Dictionary
[10]
defines it as ‘coming sharply to
a crisis; severe. Often contrasted with chronic’. It defines
‘chronic’
as ‘persisting for a long time or
constantly recurring’. ‘Profound’ means ‘very
great or intense,
severe’
[11]
and ‘catastrophic’ is
defined as ‘involving or causing sudden great damage or
suffering’.
[12]
Reference was made on several
occasions to a ‘sentinel event’. Stedman’s defines
it as follows:
‘
Nursing – any unexpected
occurrence resulting in death, serious injury (eg. physical,
psychological, or other), or risk to
the patient.’
[13]
Some
of the experts who testified gave examples of sentinel events such as
the abruption of the placenta or umbilical cord, uterine
rupture and
a prolapse of the umbilical cord (where the cord slips forward or
down). The MEC’s case is that a sentinel event
has in fact
occurred here, namely a sudden onset (‘acute’),
unexpected profound event which caused sudden great damage
(‘catastrophic’).
[21]
It will be immediately apparent that the conclusion in Professor
Andronikou’s radiology report appears to be confusing
and, on
the face of it, contradictory. It mentions a ‘
chronic
evolution
of a global insult to the brain’ which was caused
by a ‘hypoxic ischaemic injury, of the acute profound type’.
The conclusion suggests in the same breath a condition which
developed over a long period of time (‘chronic evolution’),
but which is said to be ‘acute’ and ‘profound’.
As appears from the preceding paragraph, the term ‘acute’
is defined by both Stedman’s and the Oxford Dictionary as an
antonym to ‘chronic’. Both Professor Smith and Professor
Buchmann placed much reliance on the findings in the radiology
report. I regard their evidence, read with the radiology findings,
as
decisive in determining the question of liability.
[22]
The diametrically opposing positions
adopted by the parties are on the one hand that there was a gradual
development of hypoxia
(referred to in the evidence as a ‘partial
prolonged event’), unnoticed by the hospital staff due to
inadequate monitoring,
which later resulted in the catastrophic
hypoxic ischaemia. On this argument there would have been ample
forewarning of the impending
catastrophe had the hospital staff acted
properly and in accordance with what was required of them in
practice. The lack of adequate
monitoring constitutes a negligent
omission. And factual causation, on this argument, is to be found in
the creation of a situation
where the foetus was placed at risk of,
amongst others, hypoxia, which could have been averted by proper,
adequate monitoring.
In this regard reliance was placed on
Lee
v Minister of Correctional Services.
[14]
[23]
On the other hand, the MEC’s case is that no negligent conduct
has been proved, since inadequate monitoring in itself
would not have
averted the sudden, catastrophic outcome of hypoxic ischaemia. On the
well-established principles of delict, liability
has not been
established and
Lee
does not apply here, so the argument went.
[24]
On the common cause facts there was no monitoring of Ms M. for
extraordinarily lengthy periods: from 12h40 until 23h45 on 4
May 2010
and from 23h45 until 08h20 on the following day. The undisputed parts
of the hospital records bear this out. Professor
Buchmann conceded
that this was inadequate and contrary to not only the guidelines, but
also to standard practice. It would appear
that Ms M.’s
apparent refusal to co-operate may have caused this apathy towards
her monitoring and care. As Professor Buchmann
pointed out, the
hospital staff should in those circumstances have called in a doctor
to assist. On the common cause facts the
inadequate monitoring placed
both Ms M. and the foetus at risk. In an article co-authored by
Professor Buchmann the following conclusion
appears:
‘
A labour related Intrapartum
Hypoxia is a common and avoidable cause of perinatal death in South
Africa, and the majority of these
deaths occur in no risk situations
where labour appears to be normal.
The
overwhelming problem seems to be failure to detect evidence of foetal
distress. To prevent these unnecessary deaths the emphasis
in labour
and care should be close and careful monitoring of all women in
labour, with particular attention to detail in foetal
heart rate
monitoring
.’ (my
emphasis).
Counsel
for the MEC correctly contended that Professor Smith and Dr. Hulley
gave inadmissible hearsay evidence regarding Ms M.’s
treatment
and care in hospital. As stated, Ms M. did not testify. But the
undisputed parts of the hospital records bear testimony
to this fact.
The next enquiry is – when on the probabilities did the hypoxia
start developing?
[25]
Professor Smith’s conclusion in
his report was that ‘the foetus suffered acute profound
intrapartum asphyxia and hypoxic
ischaemic injury to his brain which
developed into an early onset neonatal encephalopathy
[15]
which ultimately manifested as
cerebral palsy. These outcomes would probably have been preventable
had proper obstetric care been
provided to the patient and delivery
of the child been expedited.’ He explained under
cross-examination that with proper
monitoring there would have been
forewarning of abnormal heart rate during uterine contractions and a
caesarean section could have
been performed urgently to expedite
delivery. It was common cause that the active phase of labour
commenced at around 08h20 on
5 May. During this second, active phase
of labour in the hour before delivery (ie between 09h00 and 10h00 on
5 May 2010), a caesarean
section would not have been appropriate, in
the event of an abnormal foetal heart rate having been detected at
that time. A caesarean
section would have taken too long to avert a
catastrophe.
[26]
Reference was made by Professor Smith
to an article by Murray and others
[16]
where the authors discuss the timing
of injury in hypoxic ischaemic encephalopathy, a key question in this
case. One of the observations
made in the article is that ‘infants
with acute sentinel events had the worst encephalopathy. This
suggests that the mechanism
of insult may be as important as the
timing in determining the extent of the cerebral insult.’
[27]
With reference to the opinions
expressed in the article, which he endorsed
[17]
,
Professor Smith indicated that where the FHR was normal upon
admission but gradually deteriorated, warning signs would have
started
some 145 minutes prior to delivery. In the present case, that
would translate into a time of approximately 07h35 on 5 May 2010.
The
article shows, however, that where an acute sentinel event occurs,
the duration between that event and delivery is only 22
minutes, ie
around 09h38 on the 5th. It can therefore be accepted that the period
between 07h35 and 09h38 was the window during
which an opportunity
existed for urgent intervention by the hospital staff. This period is
narrowed down in the article to 90 minutes
prior to delivery. The
authors say that ‘the narrow window of 90 minutes prior to
delivery could theoretically offer an opportunity
for intensive
monitoring and intervention’, but they express no final view on
it. They do make the point though, that in
instances of pre-admission
brain injuries or acute sentinel events ‘obstetric intervention
may not be possible or beneficial’.
[28]
From the above it is plain that the crucial time when the outcome
could no longer be averted was after around 09h38. But Professor
Smith stated in re- examination that the acute insult can arise in
the period between 10 to 46 minutes before delivery, ie between
09h14
– 09h50. Given the periods of forewarning and of the acute
insult occurring as outlined above, the hospital records
of 5 May
2010 assume particular importance. The disputed Partogram shows that
the FHR was normal at 142 bpm at 08h20 on 5 May.
As stated, the FHR
was recorded as normal at half-hourly intervals on four occasions
between 08h20 and the time of delivery, 10h00.
And two moderate
contractions in 10 minutes were noted at 08h20, 08h50 and 09h20.
Three moderate contractions were recorded at
09h50. All these notes
emanate from the Partogram and the falsified clinical notes.
[29]
Professor Buchmann conceded under cross-examination that the heart
rates, contractions and Agpar scores (which it will be recalled
were
altered to 8 at 1 minute after birth and 8 at 5 minutes after birth)
on these records incorrectly paint a picture of a healthy,
normal
baby having been delivered. Even with the falsification, there is an
inconsistency between the FHR measured at 08h20 as
it appears on the
Partogram (134 bpm) and the altered clinical records (142 bpm) which
Professor Buchmann conceded. It was common
cause that Ms M.’s
first blood pressure reading during admission at 12h40 on 4 May 2010
was changed from 140/71 to 120/80.
The Partogram reflects the
subsequently altered reading of 120/80. The ineluctable conclusion is
that the Partogram was drawn up
at the same time as the falsified
clinical notes. Professor Buchmann conceded as much. He also conceded
that his assessment and
conclusions were squarely based on the
Partogram. The exchange under cross-examination went as follows
(‘witness’ refers
to Professor Buchmann):
‘
Mr Wessels
:
That’s the point I am making thank you. You see Professor you
and your colleagues as you had to do, you have got to use
whatever
you have, to come to your opinion rightly or wrongly, but having
regard to the fact that this Partogram, such as it is,
with the
deficient entries, or in the sense that it doesn’t help you
much to first get a heart rate, the fact that they would
have known,
that there was what the cervical dilation was, because they wouldn’t
have been able to do a test of the moulding
without assessing that,
with the blood pressure recording which is inconsistent with the
problems identified, this tells you that
this Partogram, cannot be
relied upon at all, and that unfortunately puts all of your doctors
in the position that there is nothing
there that reliable to base
your opinion on. You have any comment?
Witness
: All I have is a
Partogram which has been completed, and we have to use it as the
record, because there isn’t anything else.
. .
Witness
: I go with the record
that’s in front of me, and I, I have nothing else and that’s
what I have to follow, if someone
has been tampering I don’t
know whose been tampering and why that I cannot get into that
discussion, all I know is there
is a record, and I look at it, and I
try my best, to judge not to judge but to work out what went on.
Mr
Wessels
: And if the basis of your opinion being the records fall
away, then obviously your opinion is not based on fact.
Witness
:
If there is no
Partogram I cannot make any of this assessment
.
Mr Wessels
: Yes.
Witness
: But there is a
Partogram and its in front of me, and that’s what I used to
work out what had happened.’ (My emphasis).
[30]
These concessions must self-evidently adversely impact upon Professor
Buchmann’s conclusions insofar as they differ from
the
objective, undisputed facts as they appear in the hospital records.
On the important aspects of inadequate monitoring and its
effect,
however as stated, he was
ad idem
with Professor Smith and Dr
Hulley.
[31]
In developing the argument on behalf of the MEC, much reliance was
placed on the normal FHR of 142 bpm at 08h20 on 5 May 2010.
That
information came from the questionable Partogram and was disputed by
both Professor Smith and Dr Hulley. Apart from its unreliability,
there is a further problem with the recording of the heart rates
between the critical period of 08h00 to 10h00 on 5 May. Both
Professor Smith and Professor Buchmann stated that the weakness in
the Partogram recordings is that they do not indicate whether
the
recorded heart rates were before, during or after a uterine
contraction. This is an important aspect, since foetal distress
can
only be properly determined through an indication of when exactly a
deceleration in the foetal heart rate occurs. All the Partogram
showed was a normal baseline heart rate. When asked about this
inadequacy in the Partogram recordings, Professor Buchmann conceded
the point as follows:
‘
Mr Wessels
:
But the indications for Hypoxia is not in, not necessarily in the
base line heart rate it is in the decelerations?
Witness
: Yes.’
[32]
Professor Buchmann explained the mechanics of a late deceleration as
follows:
‘
Witness
:
Now what happens when a woman is in labour, is the contractions
sometimes deprive the baby of oxygen, either by compressing the
cord,
or just being strong, and the baby reacts to low oxygen, by slowing
down the foetal heart. This can happen during a contraction,
which is
not a big worry, because as long as it recovers, at the end of the
contraction, it means the baby is compensating for
the lack of
oxygen. If the slowing of the heart rate persists, past the
contraction. Now the uterus is no longer contracting, its
soft, but
the deceleration is still there, then we call it a late deceleration,
and that suggests that the baby is becoming more
severely Hypoxic.
The last stage is when the heart rate goes right down, below the
normal limit of 110, and it stays there, or
it goes even lower, and
that’s called a Bradycardia that’s slowing of the heart
rate without recovery at all.’
[33]
On the common cause facts, three moderate uterine contractions are,
absent a placental disease or sentinel event, unlikely
to cause
foetal distress. While the frequency of contractions were recorded
after 08h20, there is no indication of either the strength
or
duration of contractions prior to 08h20. These measurements are
important, since they could be indicative of foetal distress
which
would manifest itself in a deceleration and slow recovery of the
heart rate. Absent proper monitoring and assessment, these
warning
signs may be missed altogether.
[34]
A further area of neglect and inadequate care and treatment was, as
Professor Buchmann confirmed, Ms M.’s poor progress
of labour
which manifested in her prolonged latent phase (or first phase) of
labour. While there was some debate as to whether
the national
guidelines of eight hours or the international standard of 20 hours,
should be used in determining whether Ms M. had
a prolonged latent
phase of labour, ultimately it makes no difference. At best for the
MEC, by 08h40 on 5 May 2010 Ms M. was in
that phase. On the evidence
nothing was done to address this concern. Although Professor Buchmann
subscribed to the international
standard, he agreed that eight hours
in hospital should have raised the hospital staff’s concern.
The exchange under cross-examination
went as follows:
‘
Witness
:
Yes I have explained the rationale for the South African guidelines,
it doesn’t change the internationally recognised 20
hour cut
off as prolonged latent phase of labour, the eight hours is for the
woman to be checked to see what’s going on,
because eight hours
in hospital is of concern.
Mr Wessels
: Precisely she
should have been checked eight hours because the South African norm
says, there is prolonged latent phase after
eight hours.
Witness
: I have said as much in
my report’.
[35]
In my view the acute, profound hypoxic
ischaemia was not a sentinel event as understood in the medical
profession and as defined
in Stedman’s
[18]
.
Instead, there was, as Professor Andronikou’s radiology report
suggest, hypoxia and foetal distress which developed, undetected
due
to the lack of monitoring, over some time. The catastrophic insult
followed thereafter, probably after 09h38 on 5 May 2010.
Professor
Smith explained it as follows: ‘. . . . we have what I inform
the Court about the likelihood that there was forewarning,
foetal
heart rate abnormalities, because there was probable intermittent
Hypoxia, which depleted the reserves and then that was
followed by an
acute decompensation profound insult and the child developed this
brain injury as per MRI.
Mr De Bruyn
: Professor, I am
not going to go over and over the so-called warnings that you find
somewhere. All I am saying to you is, we have
an acute Hypoxia in
this case, not so?
Witness
: Yes but I don’t
want the Court to get the impression that it was ten minutes, and its
all over, and it couldn’t have
been prevented. That’s why
I am repeating myself, as long as the Court understand my point of
view and I also initially Counsel
and I debated this in human studies
with acute sentinel events, when its clear cut catastrophic was fine
and then boef, last anything
between 10 and 46 minutes, so there is a
wider timeframe we are looking at. We are not just talking about 22
minutes medium.
Mr De Bruyn
: We are looking at
anything between 22 and 145 minutes that is what you told us.
Witness
: That’s the
forewarning I am now talking about just.
Mr De Bruyn
: The incident.
Witness
: The incident yes.
Mr De Bruyn
: But the incident
normally occurs close to birth?
Witness
: No.
Mr De Bruyn
: If its an acute
incident.
Witness
: Well as I said yes, it
occurs within the timeframe, I have now again put that 10 to 46
minutes.
Mr De Bruyn
: Yes.
Witness
: But.
Mr De Bruyn
: It could have
occurred in this case at 9h30 for instance.
Witness
: No I don’t, the
final incident could have occurred then but the forewarning I state
to the Court must have been there based
on the analysis of
probability.
Mr De Bruyn
: But you don’t,
nobody can say when it started, if at all?
Witness
: We know that those
that develop the acute insult, have a 22 to a 146 Counsel just said
it 146 minutes before birth, that’s
when it starts occurring.’
[36]
The outcome could have been prevented through proper, adequate
monitoring. Had there been proper monitoring, the forewarning
of
foetal heart abnormalities, which must on the probabilities have been
present from approximately 07h35 on 5 May 2010, could
have been
heeded. Urgent intervention would in all likelihood have followed,
most probably by way of an emergency caesarean section.
[37]
Professor Buchmann agreed that there
was no placental disease, nor sentinel event in this case. In
reliance on the Partogram, he
opined that ‘at 08h20 it would
seem unlikely given the absence of those factors, that two moderate
contractions could cause
significant hypoxemia’
[19]
.
I have already alluded to the discrepancy in the heart rate of the
foetus at 08h20 as recorded in the Partogram on the one hand
and the
clinical notes on the other. This raises some doubt as to the
correctness of Professor Buchmann who, as stated, based his
opinions
squarely on the medical records.
[38]
As far as the key question under discussion is concerned, Professor
Smith was adamant in his view that hypoxia developed gradually
over
some time, unnoticed, and the acute, profound hypoxic ischaemic
insult ensued thereafter. I have already referred to Professor
Andronikou’s conclusions. Professor Buchmann relied on the
latter conclusions in expressing an opinion that there was no
partial, prolonged event, but an acute, profound event which occurred
suddenly. It is necessary, given the importance of this aspect,
to
recount the evidence verbatim:
‘
Mr Wessels
:
In most cases. In some cases it develops slowly over a period of
time, the foetus compensates, and when the next contraction come,
it
happens again that the foetus compensates, but so, so it goes on, and
it may wear the foetus down, the coping mechanisms get
worn down is
that correct?
Witness:
It is correct, you,
Counsel is describing the evolution of a partial prolonged event.
Mr Wessels
: Yes.
Witness
: It’s that
evolution of compensation to decompensation is very good with an
acute profound event.
Mr Wessels
: But Professor that
acute profound event, is when you have abruption placenta one of
those factors that you dealt with here, that
are not present,
correct?
Witness
: You don’t have to have.
Mr Wessels
: Cord compression,
abruptio placenta, one of those type of things?
Witness
: Those
are examples of acute profound events, but even an abruptio can give
you a partial prolonged, even a cord prolapse can do
that, and even
none of those can the absence of any can result in an acute profound
event. One of the possibilities, and I think
we may have discussed in
the, in the course of proceedings, was what was called an occord
cord, an umbilical cord that is, that
is partially wrapped around the
baby and gets compressed, and as the baby delivers its released and
you can’t see that it
was there. These are things that can
happen which are not obvious, hence I say there was no obvious cause.
Mr Wessels
: Yes, but what I
want to suggest to you is, what could possibly have happened here,
was that there was indications of Hypoxia which
you would only find
if you observed the woman properly and check the foetal heart rate
during contractions, and eventually when
the contractions became very
strong, there was an exacerbation of all of it, that you have warning
of and that is what caused this
acute profound event.
Witness
:
yes, yes, M’Lord, we don’t know if the midwives listened
before during and after contractions, they simply recorded
normal
heart rates, as samples of the heart rate measurement at that time.
So it, I don’t know if it was properly monitored
in that way,
in that sense.’
[39]
As I have said, in my view, the
radiology report supports the contentions advanced on behalf of Ms M.
that what had occurred was
an unmonitored and undetected gradual
evolution of hypoxia, followed by the acute, catastrophic hypoxic
ischaemia. The lack of
adequate monitoring and care constitutes in my
view negligence. It was common cause (conceded by Professor Buchmann)
that this
neglect was contrary to the professional guidelines and
practice. Such a ‘failure of a professional person to adhere to
the
general level of skill and diligence possessed and exercised at
the same time by members of the branch of the profession to which
he
or she belongs would normally constitute negligence’.
[20]
[40]
This court has held that the nursing
profession is a distinct profession and nurses are expected to
perform their duties with the
requisite skill and diligence exercised
by members of that profession.
[21]
The negligent lack of monitoring and
care for the extraordinarily long periods, as set out above, resulted
in the risk of,
inter alia
,
hypoxia developing unnoticed. Was this, however, adequate for factual
causation to have been established on a preponderance of
probabilities? For the reasons that follow, I am of the view that the
answer should be in the affirmative.
[41]
In this case there is no clear, direct
evidence of when exactly the catastrophic event occurred. In drawing
inferences from the
proved facts, a plaintiff need only prove that
the inference that she propounds, is the most readily apparent and
acceptable inference
from a number of possible inferences.
[22]
The most plausible explanation is in
my view the one advanced on behalf of Ms M.. And I agree that this
case falls squarely within
the ambit of
Lee
[23]
.
In
Lee
the
plaintiff sued the Minister for Correctional Services for his
department’s failure to adopt adequate measures to prevent
contamination in prisons. Mr Lee contracted tuberculosis while
incarcerated in prison. His difficulty in proving factual causation
was that the incident or source of his tuberculosis infection was
unknown. In applying the ‘but for test’, this court
found
against Mr Lee. The Constitutional Court, however, overturned that
decision. The majority applied a more flexible approach
in
determining factual causation. It held that the question of factual
causation should have been approached as the high court
correctly did
‘by asking whether the factual conditions of Mr Lee’s
incarceration were a more probable cause of his
tuberculosis, than
that which would have been the case had he not been incarcerated in
those conditions.’
[24]
[42]
The majority furthermore cautioned
that it is wrong to reason that factual causation can never be proved
where the specific incident
or source of infection cannot be
identified’
[25]
It concluded that ‘it would be
enough . . . to satisfy probable factual causation where the evidence
establishes that the
plaintiff found himself in the kind of situation
where the risk of contagion would have been reduced by proper
systemic measures’.
[26]
On this basis, the majority found for
Mr Lee on factual causation.
[43]
Here, too, Ms M. was unable to locate the source and time of the
hypoxic ischaemia, largely due to the poor and deceitful record
keeping by the hospital staff. On Professor Buchmann’s
testimony the absence of proper monitoring would create a risk for
Ms
M. and the foetus. On this basis, factual causation had been proved
on a balance of probabilities. K.’s injury would not
have
occurred on the probabilities, had his mother been properly
monitored. That, in my view, is the most plausible inference on
the
available evidence.
Conclusion
[44]
For these reasons, I would have upheld the appeal with costs. As this
is a minority judgment, there is no need to formulate
an order. What
remains is to seriously deprecate the abhorrent conduct of those who
falsified the medical records. It is conduct
unbecoming to persons
employed to serve all citizens.
______________________
S
A Majiedt Judge of Appeal
Ponnan JA (Swain and Zondi JJA
concurring):
[45]
I accept that the interaction between the law and medicine can, and
usually does, present complex challenges, particularly
where, as
here, a minor suffers a hypoxic ischaemic (HI) event during the birth
process. What occupied the attention of the high
court were two
issues: first, whether the medical staff in the employ of the MEC
were negligent and second, whether that negligence
is causally
connected to the permanent brain damage and consequent cerebral palsy
sustained by the appellant’s minor child,
K. M..
[46]
In dismissing the claim of the appellant, Ms M., the high court held:
‘On the probabilities emerging from the facts of
this case it
is not likely that the improper monitoring of plaintiff’s
labour caused the HI that led to the cerebral palsy.
The evidence
does not show that the hypothetical negligent monitoring of the
foetus in the absence of warning signs would have
prevented [the]
insult from occurring.’ Majiedt JA takes the view that the
reasoning and conclusion of that court cannot
be supported and
consequently he would allow the appeal with costs. I regret, I cannot
agree.
[47]
A peculiar feature of this case is that, despite the appellant being
available and there having been an intimation by her counsel
to the
trial court that she would be called as a witness, she did not
testify. Her failure to testify means that there are significant
gaps
in the factual narrative. Thus, to the extent that there were matters
that were peculiarly within her knowledge, which were
not placed
before the court, this must count against her.
[48]
The appellant’s failure to testify also meant that in certain
important respects the evidence of her experts, Dr Hulley
and
Professor Smith, constituted inadmissible hearsay. That was made
plain by counsel for the MEC during the course of the trial.
In that
regard he cautioned:
‘
Mr de Bruyn: M’Lord, I am
so sorry to interrupt, I forgot to put something on record, before
when Mr Hulley was called. Your
Lordship, will remember Mr Hulley
gave a lot of hearsay evidence as to what the plaintiff would have
told him. We did not object
at that stage, because we assumed
plaintiff is going to be called. We still do not object to any
hearsay evidence, as to what the
plaintiff told him provided, that
the plaintiff be called to confirm. If plaintiff be not called, then
all that evidence must be
ignored. Its hearsay evidence, and I just
want to place that on record. I did put to Professor Smith that his
evidence is actually
double hearsay, from plaintiff to Dr Hulley,
from Dr Hulley to Professor Smith, thank you, M’Lord.’
[49]
Moreover, absent Ms M.’s testimony, all too often the opinions
expressed by the experts lacked a proper factual foundation
and
amounted to no more than speculative or conjectural hypotheses. This
had the effect of the trial becoming an unnecessarily
protracted one.
One, conducted as if the parties were engaged in an abstract,
theoretical exercise. In the result, an unwieldy
record in excess of
2600 pages came to be generated and filed with this court on appeal.
[50]
It must be noted that according to the joint pre-trial minute between
the parties, the appellant sought consent for - and the
respondent
agreed to - the medical records being ‘admitted as evidence
without formal proof’. It was the appellant
who sought the
admission of the medical records into evidence. The alteration of the
hospital records, however suspicious, does
not constitute proof
positive of negligence on the part of the hospital staff. Nor, can
one, without more, infer negligence from
such conduct. My colleague
postulates accepting the undisputed parts and excluding the disputed
parts. However, it is unclear where
the one ends and the other
begins. What is more, such an approach may conduce to conflating
admissibility with evidential weight.
On the view that I take of the
matter, the issue need hardly detain us, because as I shall endeavour
to show, whilst the falsification
of the hospital records must
obviously be deprecated, that the records were altered is a neutral
factor in this case.
[51]
On appeal, the appellant’s case of negligence came to be
restricted to alleged substandard monitoring by the MEC’s
employees. She was admitted to the hospital at 12h40 on 4 May 2010.
Upon admission, the foetal heart rate was normal and the condition
of
the foetus was reassuring. Of course, that may not have been the time
of onset of labour. In the absence of the appellant’s
testimony, one simply does not know when that was. As Dr Hulley
observed ‘the patient is the best indicator of [when] she
start
feeling contractions, and labour. . . .’
[52]
It is so that there is no record of her having been re-assessed at 4,
and thereafter 8 hours, after admission in compliance
with the
National Guidelines but, as Professor Smith accepted, she could have
been sleeping in that period. Dr Hulley acknowledged
that ‘most
women, 85 percent, manage by therapeutic rest, sleep soundly for six
to ten hours, and awaken in advanced active
labour.’ In that
regard, Dr Hulley testified that there are four stages of labour. The
first stage consists of two phases
- the first phase or the latent
phase is from the onset of labour until 3 to 4cm dilation; whilst,
the second phase is from 3 to
4cm dilation, until fully dilated. The
second stage is from full dilation until delivery. The third stage is
from the delivery
of the foetus until delivery of the placenta.
[53]
Professor Buchmann’s evidence was to the effect that ‘if
the woman is truly in labour and there are no complications,
then up
to 20 hour latent phase is normal.’ He further testified that
it is very difficult to establish an occipital posterior
position.
This is the case even if a vaginal examination had been performed and
even for doctors who specialise in this area. Dr
Hulley agreed that
in this regard the staff treating the appellant were not negligent.
The evidence was that even had an examination
revealed the foetus to
have been in that position, unless there are warning signs, nature
should be allowed to take its course.
That is because it may still be
possible for the foetus to turn.
[54]
All of this however fades into insignificance because as Professor
Smith accepted at 8h20 the next morning the foetus was still
in a
re-assuring condition. Professor Buchmann agreed. The latter opined
that if the foetal heart rate was normal at 8h20 one would
expect
that it would also have been normal prior thereto and that any
monitoring before 8h20 am would also have shown normality.
[55]
After 8h20 the appellant’s condition changed. Professor Buchman
explained:
‘
I would certainly agree that
she was in the active phase of labour at 08h20 and that is because
her demeanour changed, she was feeling
weak at the knees, she didn’t
want to get up on the bed, the typical posture of a woman, who is in
the active phase of labour,
she is no longer walking around like the
latent phase. She likes to lean against something like this.
. . .
But certainly her demeanour changed,
so she probably had moved into, what we would call in a more lay term
strong labour, she was
feeling strong pains, probably in the active
phase, probably not yet in the second stage, because there were only
two contractions
in ten minutes, and the head was four fifths up. We
certainly know she was in the second stage at 09h50, because that’s
where
the head showed, and that’s how normally women
demonstrate second stage of labour, they say I feel something, I want
to push,
and she did that at ten to ten, 09h50.’
According to Professor Smith, once
‘the active phase started at 08h20 then there was rapid
progression . . . The baby’s
head crowned with bearing down
efforts at 9h50 and it was now evident that the presentation was
abnormal in that it was an occipital
posterior position.’
[56]
In this regard, an important piece of the mosaic is the report of the
radiologist, Professor Andronikou. Professor Andronikou,
who
performed an MRI scan on K., concluded:
‘
Features are those of a chronic
evolution of a global insult to the brain due to hypoxic ischaemic
injury, of the acute profound
type, most likely occurring at term’.
Majiedt
JA, after referring to various authoritative dictionaries, states
(para 21) that the report ‘appears to be confusing
and, on the
face of it contradictory’. With that, I feel constrained to
disagree. There is simply nothing to gainsay Professor
Andronikou’s
conclusion. The report was admitted into evidence by consent. Counsel
for the appellant placed on record then:
‘
Furthermore the radiology
opinion was not that the minor suffered a brain injury as a result of
global Hypoxic Ischemic Encephalopathy
but that it is due to Hypoxic
Ischemic injury of the acute profound type’.
[57]
Whilst lexical research is useful and
at times indispensable, occasionally it is not.
[27]
As pointed out in
Fundstrust
(Pty) Ltd (in Liquidation) v Van Deventer
(at
726H -727B):
[28]
‘
Recourse to authoritative
dictionaries is a permissible and often helpful method available to
courts to ascertain the ordinary meaning
of words. . .but judicial
interpretation cannot be undertaken. . . by ‘excessive peering
at the language to be interpreted
without sufficient attention to the
contextual scene.’’
[58]
The experts, who testified during the trial, did not express any
reservations about Professor Andronikou’s report. None
suggested that it was confusing, much less contradictory. Nor, do I
understand that to have been the appellant’s case either
in
this court or the one below. Indeed, Professor Smith accepted:
‘
. . . There’s no doubt,
and I’ll get to that, there is no doubt that this baby suffered
an acute, profound intrapartum,
that is during labour, hypoxic
ischemic brain injury. The MRI of this child’s brain is one of
the two classic or prototypes
of the types of injuries babies suffer
during labour which result in cerebral palsy. There is no other
condition that repeatedly
and reliably can give this MRI injury
pattern in a newborn baby.
[59]
Later, Professor Smith added:
‘
The process of – this
child’s injury occurred in utero by the nature of the MRI scan
which reveals an acute profound
type injury, the injury probably
occurred within the last hour of birth. . . .’
In that, Professor Buchman was at one
with Professor Smith, when he stated: ‘We know from the
subsequent findings that it
was an acute profound incident that it
was short and severe, and that it, and we also know that the
contractions are strongest
at the end of labour.’
The
‘subsequent findings’ were in fact the MRI scan and
Professor Andronikou’s report. Professor Buchmann testified
that because contractions tend to strengthen as labour progresses, it
is unlikely that foetal hypoxia could have occurred before
09h20,
because at that time the contraction frequency was still two in ten
minutes. He explained that ‘two contractions in
ten minutes,
which are moderate, cannot possibly deprive the baby of oxygen to a
point that it has a Hypoxic Ischemic injury and
that was the case up
to 09h20.’
[60]
Importantly, Professor Smith was alive to the distinction between, on
the one hand, an acute profound injury as alluded to
by Professor
Andronikou and, on the other, a partial prolonged type brain injury.
He explained:
‘
This type of injury pattern,
the acute profound, is established within less than an hour. And my
statement is based on the literature.
. . .
That could be hours, but the final
picture suggests very strongly that the final insult occurred over a
short period of time.
. . .
No, I disagree, M’Lord. It
definitely times it as hours. If it’s a partial prolonged type
brain injury it will be hours.
If it is an acute profound injury, as
in this case, it is less than 60 minutes.
. . .
And we know that the likelihood of
this type of brain injury to have occurred was during the last hour
of labour.’
[61]
According to Professor Smith, ‘[t]he foetal condition changed
from reassuring to non-assuring, in that 22 to 145 minute
period
before delivery, which is in accordance with scientific evidence.’
He elaborated under cross examination:
‘
Mr de Bruyn: Just to come back
to your evidence again, as I put it in my unscientific medical way,
as a build up something that
happened, you can’t time it, you
cannot say when that would’ve occurred, how close to birth, how
close to delivery,
is that correct? Smith: The timeframes that I’ve
given in my summary of my evidence is what is recorded in the
literate,
and that is 22 to a 145 minutes before birth.
Mr de Bruyn: So 22 minutes before
birth – or let us say 25 minutes before – or 30 minutes
before birth it could’ve
happened?
Smith: Up to a 145 minutes, yes.
Mr de Bruyn: Yes-yes. (Pause). Apart
from these two articles that you so kindly referred us to, normally,
if I understand it correctly,
the cause of HI is normally unknown,
unless there was this cord prolapse or the abruptio placentae, or
something like that, but
that you will see?
Smith: Yes, that you will see. And in
most of these cases where the placenta is not examined and where
there’s no clear evidence
for a catastrophic event, it’s
related to the umbilical cord, but that you can’t find after
the – because if
there’s not knot in the cord or anything
like that, that you won’t pick up because the intermittent
pressure will not
leave on the cord and impression or a footprint so
to speak, you will just have the cord.’
[62]
Later, Professor Smith added:
‘
It is more likely, M’Lord,
these articles, and the times now I am going to refer to, tells you
that anything between 22 minutes
and a 146 minutes before the baby is
born, during that period, the foetal heart will then show changes of
a baby who developed
a non-reassuring condition. We then debated also
shorter periods, because we were talking about acute and profound
Hypoxic Ischemic
injury to the brain. That type of injury follows
closer to birth, and that period that I initially when I first
appeared in court
earlier this year, showed, or told the Court that
that acute insult can take from then minutes, to 46 minutes before
the baby is
born. So within that warning period of 22 minutes to 146
minutes, and that 10 to 46 minutes is in the range that Counsel for
the
defendant took me yesterday where we discussed this 22 minutes
period that you require for such an acute and a profound injury to
occur. I hope I made myself clear.’
[63]
On this aspect Professor Buchman’s evidence ran thus:
‘
. . . [O]ne would search for a
sentinel event, that could have caused the Hypoxia in a case of AM,
there is no evidence of any sentinel
event. No cord prolapse, no knot
in the cord, no placental abruption, no ruptured uterus and no
difficult delivery. On the abovementioned
premise, one is left with a
possibility that the baby suffered a Hypoxic event immediately before
delivery. That could have been
related to uterine contractions, but
it must be pointed out, that unless there are obvious sentinel events
and the placenta has
not been examined, the cause of Hypoxia Ischemia
is normally unknown.’
[64]
It thus came to be accepted that baby K. suffered a HI event
immediately before delivery. At such a late stage in labour,
according to Professor Buchmann, the staff would not have been able
to make a difference to the outcome. That is because if foetal
distress had been detected at that stage, a caesarean section would
have taken about an hour to arrange and the appellant would
have
delivered spontaneously before then as she in fact did at 10 o’clock.
Professor Smith agreed. He testified: ‘Between
09:00 and 10:00
if you pick up an abnormal foetal heart rate at that point in time
expediting delivery with a caesarean section
is not going to be of
assistance because it will take much longer to perform a caesarean
section.
[65]
It was for the appellant to prove on a
balance of probabilities that the conduct complained of caused the
harm.
[29]
Assuming in the appellant’s
favour that the MEC’s employees negligently failed to: (i)
re-examine the appellant on the
4 and 8 hour mark after her admission
and (ii) properly monitor the appellant between 23h45 and 8h20, such
failure could have had
no causal effect on what happened after 8h20
on 5 May 2010. Whilst such failure may well have been relevant had we
been concerned
with what has been described as ‘a partial
prolonged type brain injury’ that occurs over hours, it is not
for ‘an
acute profound type’, as in this case.
[66]
It follows that the appeal must fail and I would accordingly dismiss
it with costs.
The
following order issues:
The
appeal is dismissed with costs.
_____________________
V
M Ponnan Judge of Appeal
APPEARANCES:
For
First Appellant: J J Wessels SC
Instructed
by: Nonxuba Inc, Rivonia Webbers, Bloemfontein
For
Second Respondent: P J de Bruyn SC (with him V Kunju)
Instructed
by: The State Attorney, Mthatha
The
State Attorney, Bloemfontein
[1]
Hypoxia is a prolonged reduction in
oxygen supply to the brain.
[2]
Ischaemia is a restriction in blood
supply which leads to a shortage of oxygen.
[3]
A pain relieving injection
administered in the area of the spinal cord.
[4]
Pain relieving medication.
[5]
Oxygen deprivation during labour.
[6]
Minister of Safety and Security v Van
Duivenboden 2002(3) All SA 741 (SCA); 2002(6) SA 431 (SCA) para 12.
[7]
Van Wyk v Lewis
1924 AD 438
at 444.
[8]
Stedman’s Medical Dictionary
for the Health Professions and Nursing 7ed (2012).
[9]
Id at 28.
[10]
The Concise Oxford English Dictionary
12ed (2011).
[11]
Id.
[12]
Id.
[13]
Supra at 1524.
[14]
Lee v Minister of Correctional
Services [2012] ZACC 30; 2013 (2) SA 144 (CC).
[15]
A general term describing brain
disease or brain damage.
[16]
Deidre M. Murray and others ‘Fetal
heart rate patterns in neo-natal hypoxic-ischaemic encephalopathy:
relationship with
early cerebral activity and neurodevelopmental
outcome’ 2009 American Journal of Perinatology, 605 –
612.
[17]
And thus became his own opinion: R v
Mofokeng & another
1928 AD 132
at 136, as cited in R v Harris
1965 (2) SA 340
(A) at 344 D – H.
[18]
See para 20 above.
[19]
An abnormally low level of oxygen in
the blood which could lead to hypoxia. The term is also sometimes
used interchangeably with
‘hypoxia’.
[20]
Goliath v MEC for Health, Eastern
Cape
[2014] ZASCA 182
;
2015 (2) SA 97
(SCA) para 8.
[21]
Van Wyk v Lewis, supra, at 458-459.
[22]
A A Onderlinge Assuransie Assosiasie
Bpk v De Beer 1982 (2) SA 603 (A).
[23]
See footnote 14 above.
[24]
Lee v Minister of Correctional
Services, supra, para 55.
[25]
Lee, para 63.
[26]
Paragraph 60.
[27]
Aktiebolaget Hässle and Another
v Triomed (Pty) Ltd
2003 (1) SA 155
(SCA) para 9.
[28]
Fundstrust (Pty) Ltd (in Liquidation)
v Van Deventer
1997 (1) SA 710
(A);
[1997] 1 All SA 644
at
726H–727B.
[29]
Lee v Minister of Correctional
Services
2013 (2) SA 144
CC para 39.