About SAFLII
Databases
Search
Terms of Use
RSS Feeds
South Africa: Eastern Cape High Court, Makhanda
SAFLII
>>
Databases
>>
South Africa: Eastern Cape High Court, Makhanda
>>
2024
>>
[2024] ZAECMKHC 56
|
|
T.Y obo M.Y v MEC for Health, Gauteng Province (CA18/2022) [2024] ZAECMKHC 56 (1 March 2024)
NOT
REPORTABLE
IN
THE HIGH COURT OF SOUTH AFRICA
(EASTERN
CAPE DIVISION, MAKHANDA)
CASE
NO. CA18/2022
In
the matter between:
TY
(obo MY)
Appellant
and
MEC
for Health, Gauteng Province
Respondent
(in
re the negligence of the staff at the Natalspruit Hospital)
APPEAL
JUDGMENT
HARTLE
J
[1]
The appellant appeals, with the leave of
the Supreme Court of Appeal, against the judgment and order of the
East London Circuit
Local Division of this court (“
the
trial court
”) dated 13 October
2020
dismissing her action for delictual
damages which she had sought to claim in her representative capacity
as mother and natural guardian
of her minor child, M, who was born at
the Natalspruit Hospital (“
the
hospital
”) on 5 March 2014.
[2]
In her claim she contended for negligent
intrapartum care on the part of the hospital staff responsible for
M’s safe delivery.
[3]
In essence her case came down to the fact
that the respondent’s employees failed to adequately monitor
her and her foetus
during her labour which led to a missed
opportunity to detect foetal distress and to appropriately act upon
it to prevent him from
suffering a hypoxic-ischaemic injury to his
brain. The latter injury was the fore runner to the mixed spastic
cerebral palsy condition
that he was diagnosed with in early
childhood.
[4]
The appellant initially instituted the
action in the Gauteng Local Division but the matter was transferred
to this court by order
of the latter division in 2018.
[5]
The respondent’s plea at first read
as a bare denial of the claimed negligent treatment of the appellant
or that the staff
at the hospital were responsible for M’s
cerebral palsy, but was amended almost three years later, ostensibly
just before
the trial commenced.
[6]
To the allegations going to the specific
grounds of negligence pleaded by the appellant, the respondent
countered that the hospital
staff had kept her under constant and
meticulous observation and that the treatment and advice given to her
was rendered to her
with such skill and diligence as could reasonably
be expected “
in the circumstances
of a pregnant woman presenting in labour with pyrexia and a urinary
tract infection and a foetus with fetal
tachycardia.
”
[7]
Regarding
causal negligence, the defendant denied that M’s condition was
as a result of the negligent actions of the hospital’s
employees. Instead he claimed that the child’s cerebral palsy
arose rather as a result of certain factors set out in the
amended
plea.
[1]
[8]
These
factors, alluded to in the trial court’s judgment “
as
the so-called proximal and or distal factors as the probable causes
of the cerebral palsy
”
(sic) entailed: (1) the appellant’s illness during pregnancy
which resulted in her losing weight in the third trimester;
(2) the
pyrexia and urinary tract infection that she presented with at the
hospital upon her admission in labour; (3) the foetal
tachycardia
which the foetus presented with; and (4) the “
congenital
neonatal encephalopathy
”
(sic).
[2]
[9]
The matter proceeded to trial on the merits
only after the trial court ordered a separation of the issues in
terms of rule 33 (4)
of the Uniform Rules of Court.
[10]
The appellant testified that she fell
pregnant during the year 2013. At the time she was residing in
Engcobo, Eastern Cape Province,
and initially accessed antenatal care
at the local community clinic (Sinqumeni). She relocated to Gauteng
during her pregnancy
and also obtained further antenatal care at the
Greenfield Clinic.
[11]
On
the face of it her antenatal care raised no concerns with the clinic
staff although it appears that she suffered a weight loss
of 9 - 10kg
during her pregnancy over a significantly short period. The appellant
herself confirmed that she was not ill at all
during her pregnancy,
but the defendant sought through expert testimony to persuade the
trial court that her significant weight
loss (the assumption being
that it was as a result of illness)
[3]
had probably redounded or contributed to M’s cerebral palsy.
[12]
On
4 March 2014 the appellant experienced labour pains and attended the
Phola Park Clinic in Ekurhuleni where she expected to deliver.
[4]
She was examined and treated there. She was admitted to a bed and a
drip was inserted. Her stay was brief and for a few hours only.
Ultimately she was conveyed by ambulance to the hospital. She
testified that she was told that the referral was necessary because
they were “
not
able to make me to give birth at the clinic
”.
Although there are no records of her treatment at the clinic the
surmise (from all the experts who testified) is that the
appellant
was probably treated for the infection for there to have been an
absence of any reference to it again in the hospital
records after
she was admitted.
[5]
The
appellant herself seemed oblivious to the fact that there was any
concern around her having had a fever or her foetus having
been in
any kind of distress. Indeed according to her testimony the reason
she presented herself at the clinic is that she
felt she was in labour
which, so it was confirmed by the hospital records, was in fact the
case.
[13]
She arrived at the hospital in the late
afternoon. The maternity case hospital records (these and others
admitted into evidence
at the trial on the customary basis that they
are what they purport to be without either party admitting the
correctness of the
content thereof), indicate in a note made
contemporaneously with her admission at 16h45 that she had presented
at the referring
clinic “
clinically
not well
” with a fever and a
temperature of 38.5°C, a urinary tract infection (leucocytes in
her urine), and the foetus with foetal
tachycardia, vouched for by
CTG tracings provided to the hospital by the clinic. Indeed this
accords with the premise pleaded by
the respondent upon which he
avers the appellant presented at the hospital with her foetus, and
which maladies the respondent contended
were among the factors that
gave rise to M’s condition.
[14]
I
should add that the appellant had volunteered to the hospital staff
upon her admission that she had drunk “
church
water
”
for eight months. This was evidently not of any concern to the staff
as nothing further was noted in the records about it.
I mention it
however as the defendant latched on to this at the trial as a further
factor possibly contributing to M’s condition.
[6]
[15]
The appellant testified that at the
hospital she was not initially referred to a bed. She was told
(commensurate with the hospital
notes that record that she was still
in the latent phase of labour upon her admission between 1 - 2cm
dilation) that she was not
yet to give birth and had to sit on a
bench where she remained until 3am the following morning when she was
referred to a ward
once her labour pains became severe. An earlier
assessment at 12pm that night had forecast that she would be checked
again in the
labour ward once in active labour.
[16]
At 3am on 5 March 2014 a doctor arrived at
her bedside and broke her water but still it remained “
hard
”
for her to give birth.
[17]
She
answered positively to various questions posed to her under cross
examination that she was continuously checked and examined
intermittently by a nurse. According to questions elicited by the
trial court, this entailed both vaginal examinations and foetal
heart
rate checks.
[7]
[18]
Eventually at 5.15am she gave birth to M.
[19]
Significantly, she testified that her baby
came out not crying. The staff took him away telling her that he was
not breathing well.
In fact she formed the belief that he was not
even alive but was later apprized that he was in the ward.
[20]
She saw him the following morning having
gone to find out where he was. (The staff did not bring him to her
bed.) He was in the
“
ward of the
sick children
”, on a drip, and
“
needed oxygen
”
administered to him by something “
inserted
in him
(in his nostrils)
and
also he was covered on his head only the lower part of his body ….
was seen
”.
[21]
She
noticed that he was different from how she remembered seeing her
first two children in the hospital.
[8]
He was not breathing well. He was not crying. He was not showing
movement in his arms or legs and was foaming at the mouth and
having
fits. She was also told by the doctor that M was fitting.
[22]
Despite how the appellant had presented at
the hospital on the morning of 4 March 2014, she was discharged the
following day but
M remained in hospital for three weeks after his
delivery. During this period he was fed through a tube. She did try
unsuccessfully
to feed him at her breast. Once he was discharged into
her care, she fed him by spoon.
[23]
At the age of three months she noticed that
he was definitely not on par with other children development-wise. He
could not sit
or engage. He was not using his hands which both
remained clenched in the formation of a fist. His toilet habits were
not normal.
He was (later) unable to walk or talk.
[24]
She
returned from Gauteng to Engcobo where she took him back to the
Sinqumeni clinic for immunization and in 2015 was referred to
the Red
Cross Children’s Hospital in Cape Town for him to be examined
(the records indicate for suspected neonatal encephalopathy
based on
the history that she had given them).
[9]
[25]
The
appellant’s experience of the birth of M was largely confirmed
by the medical records of the hospital to the extent that
the staff
bothered to complete the template documents that comprise all the
relevant stages of a patient’s confinement and
delivery of a
baby and their joint care but significantly there was an absence of
clinical notes detailing the treatment administered
to him
neonatally.
[10]
The experts
advising the parties and seeking to assist the trial court in
determining the vital issues upon trial had therefore
to piece
together what information they could from the negligible records
available and reason inferentially where applicable.
[26]
I do not intend to repeat all the salient
features of the appellant’s labour or the obstetric care
rendered to her as recorded
in the hospital’s maternity records
(again very negligibly) save that which is relevant to determine the
issue of factual
causation, which is at the core of the present
appeal.
[27]
The trial court found that the appellant
had established sub-standard monitoring on the part of the staff who
attended to her at
the hospital whilst in their care and leading up
to the birth of M. The expert obstetricians who reviewed the
management of the
appellant’s labour and testified at the trial
indeed conceded that the proper monitoring of the appellant by CTG in
all the
circumstances, especially having regard to the acknowledged
risk factors that she and her unborn foetus had presented with at
admission,
had been substandard. It was also accepted that M’s
birth could have been assisted if with proper monitoring his foetal
distress
(given the prior non-reassuring CTG traces) had been
recognized in time and acted upon.
[28]
There is no cross-appeal with regard to the
aspect of negligence.
[29]
What prompted the present appeal however is
the trial court’s failure to have found that the appellant had
established a causal
link between the accepted substandard monitoring
during her labour and the harm suffered by her in her representative
capacity
as a result of M developing cerebral palsy. Rather the
court’s judgment in this respect concluded that the evidence
suggested
in all probability that “
the
harm could have arisen due to the cumulative effect of the so-called
proximal or distal factors
”.
[30]
In getting to this conclusion the trial
court rejected the appellant’s case, underpinned by the expert
testimony adduced on
her behalf, that M’s cerebral palsy was
more probably related to birth events having a causal connection with
the established
negligence than the factors referenced by the
respondent in his plea.
[31]
Alluding to a professional Consensus
Statement referenced by the experts concerning the issue whether M
had exhibited neonatal encephalopathy
supportive of an intrapartum
birth event, the trial court observed as if this was the test that “
a
comprehensive multidimensional assessment
(had)
to be performed taking into account all
potential contributing factors
”
but suggested that such an assessment had not been undertaken
vis-à-vis
M and, more especially couldn’t, because there was a dearth of
hospital records concerning his treatment after birth against
which
the relevant Consensus Statement template could be tested.
[32]
With
regard to the factors relied upon by the respondent as constituting
either distal or proximal factors as the probable cause(s)
of the
cerebral palsy it found that their existence (each of the pleaded
bases found proven)
[11]
had
simply not been excluded. It found further that the opinions of the
appellant’s experts relied upon to gainsay or refute
that the
factors contended for by the respondent were causal of M’s
cerebral palsy rather than negligent intrapartum care,
were
“
unacceptable
”
to it.
[33]
The reasons for this according to the trial
court’s judgment relate to a perceived lack of cogency in the
opinions expressed
by them on the contentious issues. Indeed the
trial court concluded in this respect that:
“
It
would seem to me that the expert evidence led on behalf of the
plaintiff, on the triable issues, is argumentative, not authoritative
and not persuasive. It simply fails to take account of all the facts
and does not exclude the proximal and distal factors as the
cause for
the harm
.”
[34]
What
the contentious issues were was not clearly identified in the
judgment but the trial court’s starting premise cannot
be
criticized.
Remarking
upon the fact that there were “
a
lot of peripheral issues relating to
(the)
matter
,”
the “
true
issue
”
delineated by it was “
simply
whether or not the cerebral palsy was caused by a hypoxic ischemic
injury which was not detected or prevented by the defendant's
employees and…that
(it)
ultimately
caused the cerebral palsy
.”
[12]
[35]
Before adverting to an evaluation of the
expert testimony, it is necessary to highlight that the concepts of
“
distal
”
and “
proximal
”
are unique to the application of a professional Consensus Statement
developed by the experts in the field of obstetrics
and gynaecology
that was referenced by the experts in the trial. Although its
criteria implicating intrapartum hypoxia in neonatal
encephalopathy
have utility from an obstetric perspective and can and do assist the
court in its determination of the proof of
a causal link between a
defendant’s actions or omissions (read negligent intrapartum
care), on the one hand, and the harm
suffered by the plaintiff
(cerebral palsy in this instance), on the other hand, its application
is not a substitute for the court’s
own legal causation enquiry
that it must undertake.
[36]
It
is a trite principle that a successful delictual claim entails the
proof of a causal link between a defendant’s actions
or
omissions, on the one hand, and the harm suffered by the plaintiff,
on the other hand.
[13]
This is
in accordance with the “
but-for
”
test.
[14]
As is indicated by
the authorities, in order to apply this test one must make a
hypothetical enquiry as to what probably would
have happened but for
the wrongful conduct of the defendant. Sometimes however this enquiry
involves the mental elimination of
the wrongful conduct and the
substitution of a hypothetical course of lawful conduct (in this
instance the proper monitoring of
the plaintiff and her then unborn
foetus) and the posing of the question as to whether upon such
hypothesis the plaintiff’s
loss would have ensued or not.
[15]
[37]
Legal
causation must be established on a balance of probabilities.
[16]
[38]
The
vital question in this matter was whether, as a matter of
probability, M’s condition would in any event have ensued even
if the Respondent’s negligent intrapartum care had not
occurred,
[17]
given (this
confirmed by the common testimony of the paediatric experts) the
accepted premise underscored by the Consensus Statement
that cerebral
palsy has its pathogenesis in multifactorial pathways and is not
necessarily the direct result of an adverse event
during labour that
could have been prevented.
[39]
In evaluating the expert testimony, it
would have been necessary to glean if the other concerns raised by
the respondent as being
supposedly causal of M’s cerebral palsy
presented non-negligent
alternatives to
absolve the respondent from directional liability. But even before
getting to that inquiry it was also important
to establish, with the
assistance of the relevant experts, whether there was evidence of
neonatal encephalopathy as this, according
to the Consensus
Statement, if present soon after birth, favours an intrapartum insult
compared to an early antenatal insult. (Confusingly
the trial court's
judgment suggests that there was, yet accepted the respondent’s
expert’s view that neonatal encephalopathy
was contraindicated
because of M’s good Apgar scores in place at 10 minutes.)
[40]
For
the appellant to have succeeded it was sufficient for her to have
established that the inference she sought to have drawn in
this
respect, namely that the outcome was probably caused by birth events,
was the most apparent and acceptable inference from
a number of
possible inferences.
[18]
A
court is expected by balance of probability to select a conclusion
from amongst several conceivable ones even though that conclusion
is
not the only reasonable one
.
[19]
[41]
Firstly, on the issue of the non-negligent
alternatives contended for by the respondent, distal risk factors,
according to the Consensus
Statement, entail those that exert a
pathogenic effect on foetal brain development starting at a time that
is remote from the onset
of irreversible brain injury. Examples
include genetic abnormalities, environmental and sociodemographic
factors, and some placental
abnormalities. Proximal risk factors are
those that exert pathogenic effect on foetal brain development at a
time that closely
predates or coincides with the onset of
irreversible brain injury. Examples include
abruptio
placentae
, chorioamnionitis and twin to
twin transfusions.
[42]
The template put forward by the Task Team
of the American College of Obstetricians and Gynecologists (“
ACOG
”)
on Neonatal Encephalopathy was according to the common expert
testimony designed (and evolved over the past fifteen years)
to
examine the causal relationship between intrapartum hypoxic events
and cerebral palsy, particularly so it seems to provide guidelines
in
forensic settings.
[43]
The second edition of the Consensus
Statement recognizes that there are multiple causal pathways that
lead to cerebral palsy in
term infants and that a broader perspective
(by the consulting specialists) is now necessary before attributing
neonatal encephalopathy
to an intrapartum event. Thus, it recommends
presently that:
“
a
comprehensive multidimensional assessment be performed of neonatal
status and all potential contributing factors including maternal
medical history, obstetric antecedents, intrapartum factors and
placental pathology.”
[44]
The
paediatricians who testified (Dr. Kara on behalf of the appellant and
Prof. Bolton on behalf of the respondent) deferred to
the updated
Consensus Statement published by the American College of
Obstetricians and Gynecologists (the Second Edition)
[20]
both regarding what ought to be taken into consideration before
ascribing an intrapartum event as the likely cause for neonatal
encephalopathy as well as the warning sounded that the specialists
need to go beyond the radiological perspective by comprehensively
assessing the relevant clinical context.
[45]
Neonatal encephalopathy according to the
Consensus Statement is a clinically defined syndrome of disturbed
neurological function
in the earliest days of life in the term
infant, manifested by difficulty with initiating and maintaining
respiration, depression
of tone and reflexes, sub normal level of
consciousness and often seizures, usually affecting the full term
infant.
[46]
The term “
neonatal
encephalopathy
” is preferred to
hypoxic ischemic encephalopathy (HIE) as it is not always possible to
document a significant hypoxic-ischemic
insult and also because there
are potentially several other causes for it like metabolic disease,
infection, drug exposure, nervous
system malformation etc.
Investigation depends on the clinical presentation.
[47]
HIE is a subgroup of neonatal
encephalopathy. To consider HIE to have occurred in the intrapartum
period, there has to be evidence
of neonatal encephalopathy, but
before attributing the cause of neonatal encephalopathy, one has also
to consider the probability
of other conditions that may cause an
encephalopathy. Other indiciae of HIE relate to Apgar scoring,
umbilical artery cord PH,
the presence of multisystem organ failure
consistent with the condition, fetal heart rate patterns,
neuroimaging studies, developmental
outcome etc.
[48]
In the present matter the experts were
divided on the question of whether the Consensus Statement template
was a fit for M to implicate
intrapartum hypoxia having a causal
connection with the harm suffered by him.
[49]
The
correct approach to the evaluation of conflicting experts opinions
offered to a court to assist it in determining an issue does
not
involve considerations
of
their credibility but rather entails an examination of the opinions
presented and the analysis of their
essential
reasoning
,
preparatory to the court reaching its own conclusion on the issues
raised.
[21]
[50]
What
is further required in such evaluation is to determine whether and to
what extent the opinions advanced are founded on logical
reasoning.
[22]
[51]
The
Supreme Court of Appeal in
Oppelt,
[23]
with reference to
Micheal,
[24]
summarised the general thrust of the approach to be adopted in
medical negligence cases (adopted from English law) as follows:
“
The court is
not bound to absolve a defendant from liability for allegedly
negligent medical treatment or diagnosis just because
evidence of
expert opinion, albeit genuinely held, is that the treatment or
diagnosis in issue accorded with sound medical practice.
The court
must be satisfied that such opinion has a logical basis, in other
words that the expert has considered comparative risks
and benefits
and has reached ‘a defensible conclusion’ (at 241G-242B).
If a body of professional opinion overlooks
an obvious risk which
could have been guarded against it will not be reasonable, even if
almost universally held (at 242H).
A defendant can
properly be held liable, despite the support of a body of
professional opinion sanctioning the conduct in issue,
if that body
of opinion is not capable of withstanding logical analysis and is
therefore not reasonable. However, it will very
seldom be right to
conclude that views genuinely held by a competent expert are
unreasonable. The assessment of medical risks and
benefits is a
matter of clinical judgment which the court would not normally be
able to make without expert evidence and it would
be wrong to decide
a case by simple preference where there are conflicting views on
either side, both capable of logical support.
Only where expert
opinion cannot be logically supported at all will it fail to provide
‘the benchmark by reference to which
the defendant’s
conduct falls to be assessed’ (at 243A-E).
…
.
This essential
difference between the scientific and the judicial measure of proof
was aptly highlighted by the House of Lords in
the Scottish case of
Dingley v The Chief Constable, Strathclyde Police 2000 SC (HL) 77 and
the warning given at 89D-E that:
‘
[O]ne cannot
entirely discount the risk that by immersing himself in every detail
and by looking deeply into the minds of the experts,
a judge may be
seduced into a position where he applies to the expert evidence the
standards which the expert himself will apply
to the question whether
a particular thesis has been proved or disproved – instead of
assessing, as a judge must do, where
the balance of probabilities
lies on a review of the whole of the evidence
.”
[25]
[52]
The authorities referenced above recognize
that there is at play both clinical judgement on issues within the
expert’s peculiar
domain and the court’s own independent
judgement on what must be established for a delictual claim on the
appropriate standard
of proof. It goes without saying that an opinion
of an expert does not necessarily bind a court but its value is in
assisting it
to come to an informed view, particularly in a
specialized field where the court lacks the necessary expertise.
[53]
In
VN
obo PN v MEC for Health, Eastern Cape
[26]
the court in this Division also noted the following warnings
regarding the evaluation of expert testimony when there is a conflict
of opinions:
“…
the
evaluation of expert opinion in determining its probative value and
the considerations relevant thereto, are determined by the
nature of
the conflict in the opinion, and the context provided by all the
evidence and the issues which the court is asked to
determine. In
general, it is important to bear in mind that it is ultimately the
task of the court to determine the probative value
of expert evidence
placed before it and to make its own finding with regards to the
issues raised.
[27]
Faced with a conflict in the expert testimony of the opposing
parties, the court is required to justify its preference for one
opinion over another by a careful evaluation thereof. Further, the
primary function of an expert witness is to guide the court
to a
correct decision on questions which fall within that expert’s
specialised field. To that extent, the expert witness
has a duty to
provide the court with abstract or general knowledge concerning his
or her discipline, and the criteria, necessary
to enable the court to
form its own independent judgment by the application of the criteria
to the facts proved in evidence.
[28]
Accordingly, the mere “… pitting of one hypothesis
against another does not constitute the discharge of the functions
of
an expert.”
[29]
Finally, it is not the function of the court to develop its own
theory or thesis and to introduce on its own accord evidence that
is
otherwise founded on special knowledge and skill.
[30]
”
[54]
The trial court deviated from the standard
approached indicated above when the opinions of the two experts who
testified on behalf
of the appellant were dismissed by the broad
statement that they were not of any value or failed to take account
of all the facts
or because they “
excluded
”
the distal and proximal factors.
[55]
There is further an absence in the trial
court’s judgment for any real justification for its preference
for the respondent’s
experts’ opinions over the
appellant’s regarding the respondent’s theory that M’s
cerebral palsy was more
likely the cause of something other than a
hypoxic ischemic injury that had occurred perinatally.
[56]
There was no real dispute between the
experts as to the underlying factual bases forming the premise for
their application of the
accepted criteria.
[57]
Where their variance lay was instead in
their views on the impact of the relevant events or happenstances
pertaining to the question
of the timing of the insult that would
inform the question of causal negligence.
[58]
It was not in issue, for example, firstly
that the appellant suffered a significant weight loss (between 9-10
kgs) in the third
trimester of her pregnancy.
[59]
Further, even though the appellant seemed
to have been nescient of this, it was not in contention that she
presented in labour with
pyrexia and her foetus with foetal
tachycardia. Indeed, this was the pleaded premise on which the
respondent acknowledged it became
seized of the management of the
appellant’s labour.
[60]
Also,
it was not in dispute that the recorded measurement of M’s head
circumference at birth was 32cm, this being the only
perinatal
indicia
in the hospital records referencing his head size.
[31]
[61]
The
significance of M’s head measurement ties in with a related
aspect which is the last date of the appellant’s menstrual
cycle before her pregnancy commenced. This speaks to the period of
gestation and laterally to the question whether M’s head
was in
fact small in relation to how far along the appellant was in her
pregnancy at the time she birthed M. Testifying on behalf
of the
respondent, Prof. Bolton’s view that M’s head was
microcephalic for a
term
pregnancy which he put at 40 weeks - even though this was
inconsistent with her last menstrual period and expected date of
delivery
noted in the appellant’s antenatal records,
[32]
and could have accounted for a brain injury suffered before his
birth, underpinned his opinion that an earlier pathway existed
for
M’s cerebral palsy.
[33]
Dr. Kara was more inclined to opine that M was born at 36 weeks
(based on the same antenatal records that the respondent’s
experts referenced) and that the size of his head at birth, if it had
been measured correctly, was therefore not abnormal, neither
indicative of an earlier insult to his brain.
[62]
Even though there was some contention about
the appellant’s expected date of delivery (which would speak to
M’s gestational
age at birth) that might give a more probable
indication whether there was congenital microcephaly, I point out
that Dr. Kara readily
conceded that M might well have been born at
term and that his head would in that case then obviously have been
smaller than expected.
He also readily conceded the possibility of M
having suffered an earlier injury (manifest in the possibility of a
small brain that
had stopped growing) but explained why and how that
injury must have been survived by M up to the date of his delivery.
[63]
In the light of Dr. Kara’s
willingness to go along with the respondent’s very firm
contention that M was born microcephalic,
there was no real factual
“
dispute
”
that fell to be resolved about the date of the appellant’s last
menstrual cycle (translated to M’s gestational
age) and whether
M’s head was smaller than was to be expected when he was born.
[64]
The court correctly noted that the weight
of the appellant’s case concerned the experts’ reliance
on the existence of
neonatal encephalopathy for the contention that
there was a perinatal hypoxic ischemic injury. The answer to the
question whether
such encephalopathy was present in this instance (at
least from a scientific perspective) involved an application of the
accepted
data or information (as provided by the appellant and
supplemented by the maternity records such as they spoke to the
clinical
context) tested against the Consensus Statement template.
[65]
The respondent’s experts accepted M’s
ultimate diagnosis of mixed cerebral palsy (spastic with some
dyskinesia) and
blindness yet resisted the appellant’s experts’
opinion that his condition could be ascribed to birth related events
(that would causally implicate the negligent intrapartum care
contended for) rather than the other causes contended for on behalf
of the respondent.
[66]
In this respect Dr. Kara especially relied
on the existence of neonatal encephalopathy for the contention that
the hypoxic ischaemic
injury had occurred perinatally, this borne out
by the appellant’s history supplemented by the hospital’s
maternity
case records where they were completed and by reasoning
inferentially where the records were negligible or deficient.
[67]
It is necessary to recap some of the
features of the hospital records that concern our present enquiry.
The Summary of Labour confirms
that on natural vaginal delivery, M
required resuscitation. He was suctioned and given oxygen by
Ambu-bag. Afterwards he was admitted
to the ward due to “
respiratory
distress
”. In the ward he
received oxygen, but as indicated above there was an absence of any
notes regarding his treatment for the
next 23 days. The First
Examination of Neonate form amongst the hospital’s maternity
records indicates that M was “
well
”
but this is evidently contrasted by the assessment at the footnote of
the sheet that he “
didn’t
cry at birth
” and that he was
admitted “
at ward O2 for RD
”,
meaning that oxygen was administered to him for respiratory distress.
[68]
He was also noted under the category of
“
sick
”
(in contradiction to the note that he was “
well
”)
to have had “
caput ++
”
concerning the shape of his head. (Dr Kara explained that the
swelling would have been occasioned to M’s head as he
descended
into the birth canal. This would have been due to pressure and
accumulation of fluid on the head. In his view it indicates
relative
difficulty in the delivery although this is not always abnormal.)
[69]
According to the Assessment of Newborn
form, at birth M weighed 3.28 kilograms. His length was 49cm and his
head circumference 32cms.
(It is the later observation and
after-the-fact diagnosis of microcephaly that underpins the
respondent’s contention that
his brain damage was congenital
rendering it less likely that the injury had happened perinatally
and, by obvious implication,
as a result of intrapartum negligence).
[70]
M’s APGAR scores were recorded as
6/10, 7/10 and 8/10 at one, five and ten minutes respectively.
[71]
The
related APGAR assessment records that M had a “
a
vigorous cry”
at
10 minutes
[34]
in response to
stimulation. Respiration and muscle tone were scored at “
1
”
at ten minutes, indicative of “
slow
or irregular
”
breathing and “
slight
flexion
”
as far as his tone was concerned.
[72]
The interpretation of these scores in
relation to M’s birth was contentious as between the experts. I
will return to this
aspect later as it has a peculiar bearing on the
issue of whether M could be said to have exhibited neonatal
encephalopathy according
to the criteria postulated by the Consensus
Statement.
[73]
The Summary of Labour also records that the
feeding of M was not initiated at birth because he was admitted at
the ward, on oxygen,
for “
RD
”,
meaning respiratory distress.
[74]
After birth M remained in hospital for
three weeks. It is common cause though that the treatment
administered to him during this
period is not accounted for in the
hospital records.
[75]
In M’s Road to Health Chart (“
RTHC
”)
the Sinqumeni Clinic noted on 16 October 2014 that M was not growing
well, that he was not reaching his development milestones
and that
his head circumference was not normal. The appellant had also
reported to the staff a history of him having fits after
delivery.
For this reason the appellant was referred to the Red Cross Hospital
for further management and assessment of M.
[76]
On 29 January 2015 the Red Cross Hospital
Clinic, with reference to the appellant’s history leaning
toward neonatal encephalopathy
at birth (including seizures, two
weeks in hospital, one in the intensive care unit), made a diagnosis
that M had features of evolving
spastic quadriparesis. A CT scan was
scheduled to review the extent of injury noted
.
[77]
The ensuing CT scan confirmed his injuries
to have been “
cystic
encephalomalacia with profound volume loss in keeping with a
perinatal insult.
”
[78]
The nature and extent of M’s injuries
was professionally assessed at the instance of the respondent in the
course of preparing
for trial by a radiologist, Dr. Tracy
Westgarth-Taylor on whose findings both parties relied. Dr.
Westgarth-Taylor confirmed the
initial assessment by the appellant’s
radiologist, Dr. Thina Twetwa, of gross hypoxic ischaemic
encephalopathy (“HIE”),
although the latter opined that
the HIE’s sequelae was in keeping with a prolonged partial
insult to M’s brain.
[79]
Dr. Westgarth-Taylor recorded the following
comment with reference to the radiological picture upon analysis of
the MRI scan of
M’s brain:
“
Finding
suggests previous hypoxic ischemic injury in a term infant, most
likely a combination of partial prolonged hypoxic ischemic
injury and
acute profound hypoxic ischemic injury. The associated occipital and
extensive thalamic involvement may indicate super
added neonatal
hypoglycaemia.
”
[80]
Thus, the starting premise at the trial was
that the picture of the brain injury as indicated on the MRI scan was
in keeping with
an injury sustained during the labour process. It
also by necessary implication suggested a known pathway for cerebral
palsy. As
for the mechanism of the injury the scan shows that there
was first a gradual reduction in oxygen and a terminal sudden drop
that
happened after a partial injury occurred.
[81]
Further, and quite significantly, the MRI
scan, which was accepted by the parties, contra-indicates any other
cause for M’s
cerebral palsy. It notes that there is no
evidence of previous infection in the radiological picture of M’s
brain and, significantly,
no congenital abnormality is identified.
(Indeed, the expert paediatricians confirmed in a joint minute that
the MRI scan did not
record any neurocutaneous feature or features of
dysmorphology.)
[82]
The next question concerns the presence of
neonatal encephalopathy.
[83]
Prof. Bolton reluctantly conceded
ultimately that there were signs of neonatal encephalopathy yet when
he testified, he maintained
that the Apgar scores were to be
interpreted in favour of an argument against a compromised baby at
birth. He also referenced an
absence of any clinical notes
underscoring the appellant’s case that M was unwell after being
birthed.
[84]
Dr. Kara questioned whether the “
good
”
Apgar scoring in the hospital’s maternity
properly reflected the true situation given their appearance that
there was neurological
impairment at birth noting that M was
resuscitated, had slow and irregular respiration and abnormal tone at
10 minutes after birth
following resuscitation by manual ventilation.
(That M was neurologically depressed at birth was also drawn from the
history given
by the appellant.) Prof Bolton conversely insisted that
the Apgar score at 10 minutes “
speak
for itself
”. That is, the score
was 8/10 (1/2 for respiration and tone) which he considered to be a
satisfactory one customarily predictive
of a favourable outcome in
85% of babies.
[85]
Dr. Kara was careful to note that the Apgar
scoring is not a reliable basis upon which to confirm the presence or
absence of neonatal
encephalopathy because the scoring is subjective.
This is confirmed by the Consensus Statement itself that warns that:
“
The
Apgar scores are known to be subjective, are affected by
resuscitation and are in itself not to be used to confirm or refute
the presence or absence of intrapartum hypoxic ischemic injury. When
a Category I (normal) or Category II (indeterminate) fetal
heart rate
tracing is associated with Apgar scores of 7 or higher at 5 minutes,
a normal umbilical cord arterial blood pH (+_1
standard deviation),
or both, it is not consistent with an acute hypoxic-ischemic event.
(REF 3).
[86]
Dr. Kara opined that M’s Apgar score
of <7 did not predict that an acute hypoxic ischemic event was
unlikely without evidence
of normal foetal heart rate traces and
without evidence of normal blood gases. (It is common cause that
these were not available
but the evidence suggested that M must have
been in foetal distress to have come out as he did and if blood gases
were done given
all the other indiciae it would probably have been
reflective of the fact that M was not breathing at birth and had
respiratory
distress.)
[87]
Prof. Bolton disagreed, relying for his
opinion that M was relatively well after birth on an assertion in the
Consensus Statement
that “
if the
Apgar score at 5 minutes is greater than or equal to 7, it is
unlikely that
peri-partum
hypoxia-ischemia played a major
role in causing neonatal encephalopathy
”.
[88]
Notwithstanding Prof. Bolton’s
reservation aforesaid, he ultimately conceded that there was reason
to suspect that a moderately
severe neonatal encephalopathy had
existed with reference at least to the appellant’s history of M
having suffered convulsions
at birth, poor suck, poor cry, and a
twenty-three day admission to the hospital. Prof. Bolton’s only
qualification in this
respect is that no contemporaneous neonatal
records were available to speak to the clinical context, a feature of
the case perfectly
known to all concerned.
[89]
I digress briefly to deal with the issue of
M’s microcephaly which the respondent’s experts sought to
persuade the trial
court pointed away from the hypoxic ischemic
insult having been sustained intrapartum.
[90]
The evidence of Prof. Christianson, a
pediatrician with a sub-specialty in genetics who testified on behalf
of the respondent, was
somewhat of a damp squib. The expectation was
that he would say that M’s abnormal head circumference (first
commented on
16 October 2014 when M was examined at the Sinqumeni
Clinic seven months after his birth) warranted a diagnosis of
“
congenital microcephaly
”
(based on the premise that he was born at full term) but even before
giving his testimony, he had foreshadowed that coming
to a
comprehensive opinion “
was
frustrated by the absence of a medico-legal report on the MRI
”.
He noted in his expert summary that the lack of such a report meant
that it could not be confirmed that M had suffered
a hypoxic ischemic
injury, its nature or if there are other cerebral abnormalities.
[91]
However, a look at the report of Dr.
Westgarth-Taylor, which the parties accepted at the trial, indeed
confirms the radiologist’s
view that the injury seen on the MRI
scan was one probably sustained during the labour process.
[92]
Prof. Christianson in his testimony
ultimately was obliged to defer to the opinion of the radiologists
and at best could suggest
that the cause for M’s small head
premised on a birth at term was that microcephaly was present during
the applicant’s
pregnancy. But even accepting this as a
premise, he agreed that this could have been a cause of some of M’s
clinical problems
or a distal risk factor for him developing hypoxic
ischemic injury in the labour and delivery, in other words that such
earlier
compromise contended for would have rendered him more
susceptible to intrapartum asphyxia. Thus, the congenital
microcephaly, assuming
it to have established itself at a time before
M’s birth was less probably a
cause
(sic) for the cerebral palsy, although it could have been a
contributing factor in priming M’s brain for the ultimate
insult.
[93]
With reference to the history of
encephalopathy after birth, M’s prolonged hospital admission,
his spastic quadriplegia, the
reasonable exclusion of other causes of
encephalopathy at birth and the lack of evidence of intrauterine
growth restriction, Dr.
Kara noted that it is probable that the
injury recorded on the scan occurred during the intrapartum period.
Prof. Bolton disagreed
that these features reasonably timed the brain
injury to have occurred at birth.
[94]
Regarding the so-called antenatal or
maternity factors, Dr. Kara noted that the weight loss of the
appellant in pregnancy did not
concern those treating her at the
clinic. Prof. Bolton agreed that they treated her routinely despite
her obvious decrease in body
mass. Further, not only did they not
note any concern about it but they made no onward referral because of
it. The foetal growth
rate was also recorded as normal on 12 February
2014 when the appellant’s 9kg weight loss was recorded. I add
that although
the appellant testified that it worried her that she
was losing weight, she stated that she experienced a normal pregnancy
and
was not unwell.
[95]
Dr. Kara reasoned that although there had
been a significant weight loss, he was satisfied that by taking a
measurement of the appellant’s
upper arm circumference, the
clinic had ruled out that she was malnourished. In any event, so he
assured the trial court, M was
born at a normal weight of 3.2kg.
[96]
Concerning the appellant’s
presentation on admission in labour, both experts noted that there is
no record of any treatment
given by the hospital for the pyrexia or
infection first diagnosed at the Phola Clinic (the ostensible reason
for the referral
of the appellant to the hospital), but both assumed
that the appellant had probably been treated for the infection and
the high
temperature she had initially presented with. Dr. Kara
acknowledged that both these features posed significant risk factors
in
the birth process but contended that they were not likely to have
been a
causal
factor for the cerebral palsy. Prof. Bolton on the other hand
contended that fever in labour is
associated
with a variety of poor outcomes for a foetus including poor
neurological outcomes, but again the MRI picture excluded any
infective
cause for M's cerebral palsy.
[97]
The trial court appeared to fallaciously
equate the absence of the neonatal records with there have been no
comprehensive assessment
undertaken as if that were the end of the
matter for the appellant, missing the obvious implication that the
informed views of
the experts purported to stand in substitution of
that lack. Further, whilst noting the appreciable help that was to be
expected
of the opinion from a skilled witness, the trial court
instead resorted to its own speculation concerning the imponderables
and
boundless possibilities as to what could have caused M’s
cerebral palsy including the ingestion of the appellant of church
water during her pregnancy, in the process also in my view losing
sight of the fact that there was no obligation on the appellant
to
prove the exact cause of the cerebral palsy but rather to establish
the element of causal negligence on a balance of probabilities.
[98]
Dr. Kara, although himself lamenting the
pithy state of the hospital records (which the
National Health
Act, No. 61 of 2003
behooves its staff to have
kept) and qualifying that one generally cannot time a hypoxic
ischemic injury to a specific period in
labour except in the event of
a sentinel event (a principle often repeated in our courts in these
matters) yet went on to reason,
in my view to the contrary quite
cogently, why he believed that the insult to M’s brain
(accounted for on the MRI scan) was
probably causally connected to
the hospital’s staff failure to have monitored the appellant by
CTG on a continuous basis
until M was born.
[99]
I find myself constrained to mention the
main features of his opinion which, far from falling to be rejected
as lacking in reason
or logic, in my view presents coherently,
comprehensively and takes account of the array of concerns that were
pleaded by the respondent
as non-negligent alternatives for M’s
cerebral palsy.
[100]
In acquitting himself of his mandate to identify what caused
M’s injury and its timing in the context of all the evidence,
Dr. Kara’s essential reasoning is that M was born in a
compromised condition and required significant support. Firstly the
resuscitation was not routine, but a vigorous one. Secondly, M was
admitted into the neonatal unit for respiratory distress rather
than
given to his mother and breastfeeding was not initiated as it would
with a baby that was well.
[101]
He did not consider the Apgar score of eight at 10 minutes to
be an accurate reflection of M’s condition because he had slow
or irregular respiration at 10 minutes that was inconsistent with him
having had a “
vigorous cry
”. He also questioned
whether the first examination of neonate form indicating that M was
“well” could be accurate.
This is because M had Caput ++
and was admitted to the ward for respiratory distress consistent with
the single entry in the notes
12 hours after he was born that he was
in the ward on oxygen. As for M’s long admission in hospital
until 28 March 2014 he
opined that this strongly supported the
probability of some serious event having occurred in the neonatal
period.
[102]
He pointed out that M’s CT scan confirmed a finding in
keeping with a perinatal assault. He added his view that the
commonest
cause by far for cystic encephalomalacia noted on the scan
is a hypoxic injury. He explained that these cysts in this picture
arise
in the soft fluid areas in the brain where the tissue is dead
because of a lack of oxygen or blood supply to those tissues. He
reasoned that although the causes for a lack of oxygen to a foetal
brain is multifactorial, the commonest cause is hypoxic ischaemia
given that labour is a hypoxic-centric event.
[103]
He confirmed that M’s earlier diagnosis of spastic
quadriplegia CP together with the results of the CT scan was in line
with
his own clinical diagnosis of mixed cerebral palsy that followed
a natural evolution of M’s condition. This, together with
the
CT scan findings and the history of events at birth, all tied in to
link the injury to one sustained during the labour process.
[104]
On the issue of other causes of encephalopathy at birth or
altered neurological status after birth, he ruled out meningitis
because
this is not consistent with the radiological picture shown on
the MRI scan. He also confirmed the absence of any brain abnormality
as in a congenital brain abnormality. He further alluded to the
absence of any evidence that M had a severe overwhelming infection
that could cause shock (sepsis) and have damaged the brain. He
pointed out additionally that there was no evidence that M had a
chromosomal abnormality or a syndrome or metabolic condition that
could have caused his brain to be damaged. There was also an
absence
of any record of obstetric events affecting the appellant’s
placenta because M was not born growth restricted.
[105]
He dismissed the chance that the appellant’s consumption
of church water could have entailed the ingestion of toxins because
M
was normally grown at birth at a weight of 3.2 kgs. In his view a
severe maternal sepsis was unlikely given that the appellant
was
discharged from hospital the day after M was born.
[106]
He exhaustively dealt with every other probable cause for the
cerebral palsy as contended for by the respondent. He pointed out
that the appellant had no known genetic or predisposing risk factors
for cerebral palsy. As for her fever upon admission he noted
that
this was not going to cause fetal brain injury of the hypoxic
ischemic variety.
[107]
He readily acknowledged however that it might obviously have
increased the risk of asphyxia during labour but was not the cause
for M’s cerebral palsy. This is exactly why in his view the
obstetrician had to adequately manage her labour in the light
of this
risk factor.
[108]
As for the possibility that M was born with microcephaly, Dr.
Kara opined that it was unlikely that his brain had been injured
prior
to delivery. He explained firstly that a newborn with a head
size of about 32 centimetres is the average head size for a baby of
about 34 to 35 weeks gestation. Therefore, assuming a birth at 38 to
40 weeks, this would hypothetically mean that the brain injury
would
have happened prior to 36 or 37 weeks, thus two or three weeks
earlier than M’s delivery. If this had happened, he
opined that
M would not have come out in a condition of encephalopathy. Further,
if he had survived the brain injury (meaning that
certain brain areas
would not have been compromised at the time of delivery) there was no
reason why he would not have been born
in a reasonable, normal
condition. Instead, all the indications were of a neonatal
encephalopathy which is the commonest injury
occurring during labour.
[109]
As for the extent of M’s neonatal encephalopathy he
graded it as moderately severe that lasted several days noting poor
feeding
and poor cry on history.
[110]
Adverting to the MRI scan he emphasised that both experts had
found that it shows features of a hypoxic ischemic brain injury,
making
it fair to argue that M’s cerebral palsy was caused by
such injury rather than any other.
[111]
He added that the further finding of Dr. Westgarth-Taylor that
there was a hypoglycaemic injury to the brain (which was a
probability
that he had pre-empted upon examining M even before
seeing the MRI report in this regard) accorded with the more probable
scenario
that M had suffered the injury during labour. He explained
that when a baby is born with hypoxic ischemia, the stores of the
baby’s
glucose is exceptionally low. If after birth that
glucose is not rapidly replenished, there is ongoing brain damage
from HIE together
with further brain damage from low sugar. You would
not get the radiological picture on M’
s
MRI scan, so he pointed out, in a baby whose brain was damaged a few
weeks earlier. Indeed, this feature present in his MRI scan
helped
further in timing the injury.
[112]
Asked by the trial court to venture a time when the injury
occurred, he put this at a juncture between the appellant’s
admission
and before delivery of M, based on the fact that the foetal
condition was satisfactory on admission to the hospital. Earlier he
had explained that the CTG tracings taken at the time, although
suggestive of a non-reassuring foetal heart rate, had not prompted
an
immediate delivery of M by caesarean section. For the rest, he
deferred to the obstetricians who might further be able to narrow
down the period.
[113]
On the issue of the existence of
encephalopathy, Dr. Kara’s opinion that the hospital notes are
not a fair reflection of M’s
condition based on the appellant’s
history and the contra indications that he was well when admitted to
the ward where he
was hospitalized for an extensive period thereafter
is preferable to one that rigidly assumes a position based on a
subjective
Apgar score. In any event the Consensus Statement
postulates a wholistic view of all the clinical features rather than
a formalistic
approach.
[114]
Prof. Bolton remained adamant when he
testified that M had been birthed at full term and that his head
circumference was below the
3
rd
percentile for a full term infant, assessed as a microcephalic head.
He adverted to a chart and an elaborate process to assess
gestational
age to demonstrate how he got to this complicated conclusion, in the
process eschewing the plain old way of accepting
the entries in the
appellant’s antenatal records concerning when she had her last
menstrual period and what her expected
date of delivery was.
[115]
This informed his view that M’s head
growth was abnormal at birth and presumably before birth.
[116]
Put to him that the appellant’s last
menstrual period was in fact recorded in her antenatal records he
conceded as much:
“
Yes,
that was true and I looked at that again and thought why would I have
said that and I realised that I said it because I could
not read what
was written there, it has been crossed out, so it is incorrect, it
was recorded, but it was illegible, i am sorry.”
[117]
Expecting that he would then concede that M
was “before term” at birth he latched on to the
appellant’s testimony
that he had overheard her give in court
that her last menstrual period was in June 2014. Asked by the trial
court to instead focus
on what the medical records provide and put to
him that Dr Ebrahim’s opinion was that the appellant was not
full term when
she gave birth to M, he said; “
yes,
I presume that is true
” but added
that he could not now work it out in the absence of his “
wheel
”
that he uses for these purposes. Finally referred to the appellant’s
gestation window provided for in her antenatal
records, he relented
and deferred to the obstetricians. He conceded, as was put to
him in conclusion by counsel on this issue
that his evidence of the
gestation was “
on a different
plane
.”
[118]
He was equivocal too about the impact of
the appellant’s weight loss on her pregnancy:
“
What
concerned me here was that it got less. And all I think this was
indicative of was that the weight loss that was recorded by
the
scales was probably correct, something was going on, but I think
beyond that I would not make anything of it. I'm not going
to say but
that told me that the mother was malnourished, or she was not. She
went from 28 to 24 and I think as I recall both of
those, 24 is just
above the normal limit where they diagnose malnutrition. If I’m
right it is 23 where they say that it is
the indicator of
malnutrition, what concerned me and I tried to put it in the report
was that it dropped and so that it indicated
to me that perhaps
something had happened, but beyond that I would not be able to
comment.”
[119]
His rigid approach to identifying distal
and proximal events on a trajectory towards cerebral palsy is not of
any real assistance
to a court engaging with a factual causation
enquiry on a balance of probabilities. Ultimately, he appeared
to accept that
fetal priming (read both distal and proximal risk
factors according to the Consensus Statement) can predispose a fetus
in labour
to become hypoxic because the foetus is not set up to be
able to tolerate (the stresses of labour) properly:
“
But
there were also significant proximal and distal risk factors which
played a role in the causation of the brain damage and I
thought B
was the more likely thing, that there were distal factors and
proximal risk factors. We haven't talked about her weight
loss in
pregnancy. That was very unusual period that possibly played a role,
was probably a distal risk factor. Then the infection
during the
labour, the fever during the labour, that was a proximal risk factor.
Then there may well have been an intrapartum event,
i.e. that a
normal baby going through labour became hypoxic. It's absolutely
normal, but this baby was set up to not be able to
tolerate it
properly. So from that other risk factors and that's what happened.
So that's why I said there would be these various
possible- and it’s
just possible and probable ways and I thought the probability that
they were multiple risk factors, distal
and proximal, which then set
the baby up for hypoxic event- or not an event, but that the
hypoxemia during the labour- the normal
hypoxia during labour, was
working on a sensitised brain that had these things as risk factors.
And that's the multi-dimensional
factors of cerebral palsy.
…
But
if you've got a baby who's got- who set up by perhaps a damage to the
developing brain during the pregnancy, when she has a
weight loss,
I'm postulating, plus an infection, plus an inflammatory- a
temperature, now a normal contraction, not something that
was
abnormal, it's got to happen to push the baby out, might have
affected the baby whose brain was set up and that's the complex
issues.”
[120]
Having regard to the factors that he
perceived played a role in M’s condition he watered down some
of his starting premises.
Regarding the appellant’s weight loss
during pregnancy, for example, he acknowledged that she had not been
sick and then
equivocated:
“…
.
that
10 kg’ worries me, so I looked at it and thought was this an
event, whatever it was which may have affected fetal growth
including
fetal brain growth. And I speculated and it is speculation but that
is a possible cause for the microcephaly.”
[121]
Asked under cross examination about the
findings of Dr. Westgarth-Taylor’s findings he agreed that her
additional comment
about the hypoglycemic damage was not in line with
the features of microcephaly. He appeared to concede though that the
cause of
the microcephaly could be represented in the picture seen on
the MRI scan, adding that the radiologist was “
probably
right”
that it looks more like
the damage of hypoxic ischemia than anything else as the cause for
it. He then went on to suggest that
the injury could be the effect of
an acute profound injury on an abnormal brain that is vulnerable but
turned the order of things
around, suggesting that it was unlikely
that this (the already injured brain manifest in the small head) was
“
not contributed to by hypoxic
ischemia in the perinatal period
”.
This is simply another way of saying that a supposed prior injury
would render an already compromised foetus susceptible
to a hypoxic
ischemic injury during labour. It also presupposes that appropriate
monitoring may prevent further injury from happening.
[122]
I mention finally that the respondent’s
obstetrician expert, Dr. Marishana, accepted that M had presented as
one in respiratory
distress and also that his cerebral palsy was
caused by a hypoxic ischaemic event one way or another.
[123]
It is ironic in my view that the very risk
factors contended for by the respondent would have elevated the need
for closer monitoring
of the appellant during her labour given the
after-the-fact MRI finding of M having sustained a combination
partial prolonged and
acute profound injury. This radiological
picture suggests that there was some damage before the acute injury
occurred and the experts
were all in agreement that an infection in
the mother does make the foetus more susceptible to hypoxia.
[124]
It is exactly the cumulative consequence of
the factors at play in this matter as foetal priming as it were that
would have rendered
M more susceptible to asphyxia during labour.
There was no pushback from the appellant’s experts that all of
these contenders
(at least those that she presented with upon
admission) were significantly at play during her labour.
[125]
In my view the evidence establishes on the
requisite standard of proof that the history of M was one of being
neurologically depressed
at birth with all the related indications
suitably pointing to a neonatal encephalopathy (including the
findings of the MRI scan
showing features of a partial prolonged and
acute injury resulting from a cumulative deprivation of oxygen over
time) and that
the intrapartum negligence is causally connected with
his cerebral palsy.
[126]
This outcome, so it appears to have been
agreed between the expert obstetricians, was foreseeable because it
all came down to monitoring
and preventable in the sense that the
early signs of foetal distress could have been detected and acted
upon appropriately by expediting
the vaginal delivery.
[127]
In the premises the appeal should succeed
and the appellant should be entitled to her costs of the action as
well.
[128]
In the result I make the following order:
1.
The appeal succeeds with costs including
the costs of second counsel.
2.
The order of the trial court is set aside
and replaced with the following order:
“
1.
It is declared that the negligent conduct of the defendant’s
employees was the cause of the minor child’s condition
and the
defendant is ordered to pay to the plaintiff in her representative
capacity her agreed or proven damages.
2.
The defendant is ordered to pay the
plaintiff’s costs of suit, such costs to include the fees of
the experts employed for
purposes of the trial together with the
costs of second counsel.
”
B
HARTLE
JUDGE
OF THE HIGH COURT
I
AGREE,
N
W GQAMANA
JUDGE
OF THE HIGH COURT
I
AGREE,
I
BANDS
JUDGE
OF THE HIGH COURT
DATE
OF APPEAL
:
9 October 2023
DATE
OF JUDGMENT
:
1 March 2024
Appearances:
For
the Appellant: Mr. H van der Linde SC together with Mr. M James
instructed by Mgweshe Ngqeleni Inc, East London (ref. MN/Y06/16)
For
the Respondent: Mr. P L Mokoeana SC together with Mr. Y Malunga
instructed by State Attorney, Makhanda (ref. Mr. Maqambayi)
[1]
Implicit
in the respondent’s plea in response to the appellant’s
claim of causal negligence, is the suggestion that
proper monitoring
and detection and acting appropriately on the results would have not
made an iota of difference because the
cerebral palsy arose by
virtue of a different pathway than hypoxic ischaemic encephalopathy.
[2]
Gathering
from the context the defendant intended to refer to “
congenital
microcephaly
”.
[3]
The
evidence did not establish that the appellant was ill during her
pregnancy.
[4]
The
appellant stated in her evidence that the clinic is “
meant
for … to give birth
”
which accords with the respondent’s policy that a patient will
first report to a primary healthcare facility that
will refer her to
a hospital in appropriate circumstances. This was such a case, the
referral ostensibly necessitated by M’s
“
foetal
tachycardia
”.
This confirms the critical risk factors at play when the appellant
presented in labour.
[5]
The
notes of the Phola Clinic were not adduced at the trial.
[6]
T
his
was in my view a mere red herring. Whatever its implications, if
any, it was not pleaded by the respondent that the church
water was
toxic, that the appellant’s ingestion of it made her ill, or
in the end was supposedly a causal factor for M’s
cerebral
palsy. The trial court gave the appellant’s mention of the
ingestion of this water misplaced significance surprisingly
after
having agreed with counsel during closing arguments that it was a
bit of “nonsense”. Further, whilst cautioning
itself
that it should not enter into speculation as to the contents of the
water, it nonetheless took “
judicial
notice of the notorious fact that some churches are and have been
administering various toxins to congregants as published
in recent
times
”.
The consequence of elevating unwarranted concern to the appellant’s
throw away comment noted by the hospital in
its clinic notes as a
feature of the causality enquiry at the trial resulted in the
appellant being unfairly criticized for failing
to make any
“
meaningful
attempt
”
to “
discharge
the evidential burden resting upon her
”
to “
meaningfully
deal with the nature and effect of the water, if any, on her and
possibly the foetus
”.
The inevitable conclusion reached by the trial court along this
trajectory is that “(t)
his
proximal factor too
(was)
not
… excluded
”.
[7]
The evidence indicated the lack to be in continuous CTG monitoring
despite how the appellant presented on admission (and the
results of
earlier foetal heart rate tracings that were not assuring), as well
as the failure to have monitored her high temperature
which by all
accounts would have had an impact on the foetus. The joint minute
between the obstetricians for example recorded
that no temperature
checks were done whilst the appellant was in hospital though she had
been admitted on this premise by the
referring clinic. There was
also no specific cause for her pyrexia documented. The records
reflected no treatment given for her
fever and likely infection.
CTG’s were only done for short periods after her admission
which showed persistent foetal tachycardia
and several episodes of
reduced variability. Even though the experts agreed that the foetal
heart rate recordings, such as were
obtained, were not indicative of
significant foetal hypoxia, they concluded that they were neither
normal and at best were equivocal.
There was one check on the fetal
heart rate at 8.50 pm and no fetal heart rate monitoring in labour
from about 11pm until birth.
The experts agreed that in view of
their equivocal nature CTG monitoring ought to have been continued
in the ward at least on
an intermittent basis, which was not done at
all.
[8]
Co-incidentally
this was her fourth pregnancy, but she miscarried in her third
pregnancy. M was her third child.
[9]
The
history provided by the appellant was given without any inkling that
M suffered from cerebral palsy. She repeated it to the
medical
experts who consulted with her even before the hospital’s
maternity records were made available to the plaintiff’s
attorneys. To the extent that the records were completed, her
contemporaneous account of M being neurologically depressed at
birth
happened to coincide with what the records state.
[10]
There
were a few notes made at M’s birth concerning aspects of his
condition but certainly nothing in the ward later on
for the 23 days
that he remained under the care of the hospital. There was no
reference in the evidence as to what the Maternity
Guidelines
required of the hospital at the time concerning the requisite
recordkeeping, but it is fairly common knowledge in
matters of this
kind that there are Guidelines that prescribe how health records are
to be maintained. Section 13 of the National
Health Act, No. 61 of
2023 (“
NHA
”)
creates the obligation for the person in charge of a health
establishment to ensure that a health record “
containing
such information as may be prescribed
”
is created and maintained at health establishments (including public
institutions) for every user of health services.
Section 17 (2(d) of
the NHA under the captain “
Protection
of Health Records
”
provides that any person who “
fails
to create a record when properly required to do so
”
commits a criminal offence.
[11]
The
trial court added its finding that the appellant had ingested toxic
church water as one of the bases.
[12]
A proper reading of this conclusion suggests that there was no
confusion that M suffered a hypoxic ischaemic injury, the injury
qualified by the observations that it was one that was missed
because of a lack in the monitoring and further not prevented by
the
respondent’s employees.
[13]
International
Shipping Co (Pty) Ltd v Bentley
1990 (1) SA 680
(A) at 700F-I;
Siman
& Co (Pty) Ltd v Barclays National Bank Ltd
1984 (2) SA 888
(A) at 915B-H; Minister of Police v Skosana
1977 (1)
SA 31
(A) at 35C-E;
Lee
v Minister of Correctional Services
2013 (2) SA 144
(CC) at para
[37]
– 58];
Oppelt
v Head: Health, Department of Health Provincial Administration:
Western Cape
2016 (1) SA 325
(CC) at [35].
[14]
Lee,
supra at
para
[37] – [58]
[15]
Mashongwa
v PRASA
2016 (3) SA 528
(CC) at [65];
AN
v MEC for Health, Eastern Cape
[2019] ZASCA 102
at
[8]
.
[16]
Lee
supra
at [39]
[17]
Oppelt,
supra
,
at [35];
Mashongwa,
supra
at [65]
[18]
AA
Onderlinge Assuransie Bpk v De Beer
1982
(2) SA 603
(A
);
Cooper v Merchant Trade Finance Limited
2000 (3) SA 1099
SCA at [7];
Minister
of Safety and Security v Van Duivenboden
2002 (6) SA 431
(SCA) at para 25; and
Minister
of Finance and Others v Gore NO
2007 (1) SA 111
(SCA) at para 33.
[19]
Govan v
Skidmore
1952 (1) SA 732
(N) at 734 C-E.
[20]
ACOG/AAP,
Neonatal encephalopathy and neurological outcome, Second Edition,
Pediatrics 2014
[21]
Michael
and Another v Linksfield Park Clinic (Pty) Ltd and Another
2001
(3) SA 1188
at [34] – [40]
and
Oppelt supra
at [36].
[22]
Michael
supra
at
[36]
[23]
Supra
[24]
Supra
[25]
At [36].
[26]
[2021] ZAECPHC 50 (31 August 2021) at para [34].
[27]
Van
Wyk v Lewis
1924
AD 438
at 447 and S v Gouws
1967 (4) SA 527
(E) at 528D. See also
Schmidt
and Rademeyer op cit
at page 17 – 16.
[28]
See
the authorities referred to in
Stacey
supra
at 348 to 359 F. See also
AM
and Another v MEC for Health
supra
at para [17].
[29]
Stacey
supra
at
350 G-H.
[30]
MEC
for Health, Eastern Cape v ZM obo LM
(576/2019)
ZASCA 160 (14 December 2020) at paras [12] and [13].
[31]
The
first suggestion of a concern that his head was abnormally small was
only noted in M’s Road to Health Chart (“
RTHC
”),
months after his birth.
[32]
He conceded in his testimony that the antenatal records did not
support a 40 week gestation. He was however in court when the
appellant testified and heard her say that she had delivered at 9
months. The trial court had questioned the appellant about
this when
she testified and although she was certain that she must have been
at full term in the end she relented that she might
have been
mistaken in this respect. The appellant’s credibility was
never an issue at the trial.
[33]
Microcephaly
is a condition that pertains when a baby’s head is
significantly smaller than expected, often due to abnormal
brain
development. Causes of microcephaly include infection, malnutrition,
or exposure to toxins.
[34]
This
is not a factual assertion, namely that he had a vigorous cry, but a
prepopulated answer to the question how he responded
to stimulation.
On the APGAR scoresheet “
no
response
”
would score a zero point, a “
grimace
”
a score of one point, and a “
vigorous
cry
”
two points.