NKM (obo BM) v Member of the Executive Council for Health: Eastern Cape (413/2017) [2024] ZAECBHC 10 (15 March 2024)

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[2024] ZAECBHC 10
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NKM (obo BM) v Member of the Executive Council for Health: Eastern Cape (413/2017) [2024] ZAECBHC 10 (15 March 2024)

IN
THE HIGH COURT OF SOUTH AFRICA
(EASTERN
CAPE DIVISION, BHISHO)
NOT
REPORTABLE
CASE
NO. 413/2017
In
the matter between:
NKM
(obo BM)
Plaintiff
and
THE
MEMBER OF THE EXECUTIVE COUNCIL
FOR
HEALTH: EASTERN CAPE
Defendant
(in re the
negligence of the staff at the Livingstone and Dora Nginza Hospitals,
Gqeberha)
JUDGMENT
IN RESPECT OF MERITS
HARTLE
J
Introduction:
[1]
The plaintiff claims damages in her representative capacity on behalf

of her minor son, BM, who was born at the Dora Nginza Hospital in
Gqeberha (“
DNH
”) on 19 August 2007.
[2]
BM, presently 16 years of age, suffers from asymmetrical cerebral

palsy with one side more affected than the other. Although this is
not the typical spastic or dyskinetic cerebral palsy, it nevertheless

renders him permanently disabled and is a significant injury.
[3]
The plaintiff alleges negligent intrapartum care on the part of the

staff who attended to her during her hospitalization, latterly at the
Dora Nginza Hospital where BM was delivered, and in the few
days
preceding his birth, at the Livingstone Hospital.
[4]
In essence the plaintiff’s case is premised on BM having
suffered
a hypoxic ischaemic brain injury during a prolonged and
stressful labour that was due to the claimed negligent care.  The
injury is validated by an MRI brain scan showing a picture consistent
with an acute intrapartum event compatible with the allegations
of
substandard management during this interlude.
[5]
The plaintiff
exhaustively pleaded a history of relevant events relating to her
care (or alleged lack of it) at each hospital and
several grounds of
negligence.
[1]
Both aspects of
the history relied upon by her, and the claimed negligence, were
denied by the defendant in her plea.
[6]
Apart from denying
the essential elements of the plaintiff’s claim, the defendant
differed with the plaintiff about dates,
her supposed presentation at
each hospital, the nature of the care administered to her (or not),
the maternal and foetal well-being
(or not) of her and her then
unborn foetus, the nature of and whether her labour was prolonged (or
not) and, significantly, whether
BM was born in a poor state of
health and exhibited signs of neonatal encephalopathy (“
NE
”
)
at birth, which is one of the accepted early markers for cerebral
palsy sustained intrapartum according to a professional Consensus

Statement.
[2]
[7]
Although on the pleadings BM’s condition of cerebral palsy
was
not acknowledged, the defendant yet denied that she was responsible
for his “
condition
”.  In giving a context to
her denial of causal negligence, the opinion formed by the experts
relied upon by her to assist
the court in getting to the bottom of
the unfortunate outcome, is that BM probably suffered the brain
injury which he did as a
result of a meningitis infection, thus
contending for a non-negligent cause for his condition.
Background:
[8]
The plaintiff was 25 years old when she delivered BM who according
to
antenatal records was expected to be born on a date in September
2007.  This was her first pregnancy.
[9]
She is HIV
positive, a factor that was confirmed by a blood test undertaken in
the second month of her pregnancy at the Marselle
Clinic in Bushman’s
River where she initially booked to receive antenatal care.  The
plaintiff in her testimony clarified
that her HIV status (which she
has lived with since 2002) was clearly endorsed on her “
green
passbook
”
(clinic card) that
accompanied her after her initial visit at the Marselle Clinic on 15
January 2007 once she relocated to Gqeberha,
from whence she
continued to receive antenatal care at the “
Dwesi
Clinic
”
.
[3]
[10]
By all accounts her antenatal care was unremarkable and she was
relatively healthy despite
her HIV status.
[11]
On 13 August 2007
she was collected by ambulance and taken to DNH at her request
because she was in abdominal pain and had passed
vaginal mucous.
She recalls that this happened on the same day as her last routine
visit at the “
Dwesi
”
clinic that
morning.  She was assessed and told that she was not yet due to
deliver and was thus sent home.  On 14 August
2007 she was still
in continuous pain and reported again to the DNH via ambulance.
[4]
She was examined vaginally and similarly returned home on the basis
that her baby was not yet coming.  On 16 August
2007, with
worsening pain, she hired private transport to the Livingstone
Hospital where she was admitted
inter
alia
with
high blood pressure.  On the afternoon of the 17 August 2007 she
was transferred to DNH
[5]
whose
staff took over her obstetrical management.  Although the reason
for the transfer was flagged as being due
inter
alia
to
her raised blood pressure, she was only given medication for her
gestational hypertension at the DNH from 18 August 2007.
[12]
By 16h00 on 18 August 2007 she was diagnosed as being in prolonged
labour (latent phase).
Despite this no intervention was
undertaken to birth BM by caesarean section despite her also being
preeclamptic and HIV positive.
Her labour was instead augmented
with Syntocinon with trial of labour continuing even though there
were indications of foetal distress.
[13]
BM was ultimately
born at 15h35 on 19 August 2007 by a difficult forceps delivery after
the delivery of his head was delayed in
the plaintiff’s birth
canal.
[6]
[14]
By all accounts he
was born in a “
significantly
compromised neurological condition
”
.
[7]
The
plaintiff’s testimony:
[15]
The plaintiff related her own experience of the delivery and focused
in her testimony on
the key events leading up to it and how BM
presented at birth. It is necessary to advert to aspects of her
testimony (both relating
to the management of her care and BM’s
condition) to give a context to the opinions offered by the experts
and to close some
of the gaps left wanting in the records of DNH that
were self-evidently deficient and mostly unreliable.
[16]
The fact of the plaintiff being HIV positive was a known entity.
She was first diagnosed
in 2002 but despite this was healthy and not
taking any medication for her condition.  She was advised upon
her first visit
to the Marselle Clinic that it would not be necessary
to take any medication during her pregnancy for the disease but the
anticipation
was that she would receive Nevirapine at the time of her
baby’s birth.
[17]
She learnt upon
her admission at the Livingstone Hospital that she had high blood
pressure although it was the abdominal pain that
had driven her to
DNH twice before to seek care.  She could not recall how they
treated her for this but remembers being especially
informed as to
such a diagnosis.  The hospital staff put a red sticker on her
file and told her that she was a high risk,
hence the need to
transfer her to DNH.  She acknowledged that the staff at
Livingstone Hospital had put a strap around her
stomach to check her
baby’s heart rate
[8]
which
they did “
all
day
”
.
They were however more focused on her raised blood pressure.
[18]
Her recall, upon
being transferred to DNH and after being initially examined, is of
being dizzy but told to ambulate with about
eight other expectant
mothers.  She was not assigned to a bed, but fellow patients
recognized that she should be lying down
and made a place for her on
one of the three beds available in this ward, which she could at best
describe as a waiting room although
not an admission waiting
room.
[9]
[19]
She slept until the Saturday morning when she was again examined.
This was around
9 – 10am.  During this assessment some
water ran out on her legs which she thought was urine, but the
examining doctor
told her that her water was breaking.  She says
that was transferred to the labour ward at 6pm.
[20]
Until her transfer to the labour ward she waited in a chair.
According to her neither
she nor her then foetus were checked at all
and her move to the labour ward was coincidentally contemporaneous
with another patient’s
whose water was said to have broken, a
nursing sister complaining at the time: “
Yoh it is the two
now and I must take the other one and go to the labour ward
”.
Here for the first time she was given a bed in a ward with the other
patient.    They were also asked
individually about
their status.  She informed the nursing sister that she was HIV
positive.
[21]
Her next
recollection was of waking up the following morning on Sunday 19
August
2007.  A nursing sister was shouting at her saying: “
Do
not sleep, you must wake up and walk because the head of your
child…must come out.  If you are lying down like that

your child is not coming out
”
.
[10]
She attempted to reason that she was dizzy yet was urged to “
wake
up and walk
”
.
She tried to walk.  Her next recall is of the nurse
telling her conversely not to push because her baby’s
head was
coming out.  At this time she claims that she started to fit.
This was around 4pm.  She described the
sensation as being
conscious but hearing voices from afar.
[22]
She was assured
that she should not panic.  An oxygen mask was put over her
mouth and a doctor was called to help her.
Three doctors came
to her bedside.  One of them pushed on her stomach just below
her sternum.
[11]
Another
arranged her legs in stirrups and the third one put something cold in
her vagina.  BM was delivered. He was
momentarily given to her
but was instantly spirited away to the nursery.   She heard
them say as if their voices were
far away: “
Nursery,
Nursery, Nursey”
.
She gleaned that her baby was a boy. In the brief moment of
holding him she noticed that he was not crying.  She was

brusquely informed after a while that the nurse would be stitching
her because the doctor is “
leave
it like that
”
which is when she
learnt that they had made a cut in her vagina to get her baby’s
head out.
[12]
[23]
Asked how she knew she had fitted during labour she explained that a
nurse had told her
afterwards that she had fitted when the head of
her baby was coming down.
[24]
Later that afternoon in the ward she fitted again whilst coming from
the toilet and was
similarly informed by the nursing sisters that she
had had a fit.  On this occasion she had felt weak and dizzy and
was cautioned
to rather remain in bed.
[25]
She only saw her baby again on the ensuing Monday, 20 August 2007.
In the nursery
he was in an incubator.  It was then that the
nurse told her that she had had a fit during the delivery and added
that it
was her fault that BM had also fitted.
[26]
BM had a tube coming out of both his nostrils.  She could only
hold him for brief
moments out of the incubator.  He could not
latch on when she tried to feed him at her breast.  He was
otherwise fed
by tube.
[27]
She related that
she had seen a special doctor at BM’s cot who told her that he
was not breastfeeding, or at least could not
suck, because of
something inside his mouth on the tongue that had to first be
cut.
[13]
[28]
BM remained in the
hospital nursery for ten days.  He was discharged from the
nursery together with her.  She remembered
that this was on the
same day that she received a blood transfusion.
[14]
[29]
She noticed soon after his birth that BM was different than other
children and not meeting
the regular milestones in growing up.
He was for example two years and nine months old before he started to
walk and that
was with the dedicated assistance of a Dr. Baker at a
hospice in Hamburg who administered physiotherapy to him to get him
mobile.
[30]
It is opportune to state here that although counsel for the defendant
in closing submissions
contended that the plaintiff was a poor
witness, this was certainly not my impression.  She was
exhaustively cross examined
in English (which is not her primary
language) and consistently maintained a narrative that she had
earlier repeated to the specialist
experts who she had consulted with
in the course of litigating in the same minute detail.  Although
certain minor aspects
escaped her recall, not surprisingly given BM’s
delivery fourteen years before the trial, her version of the material
events
was also coincidentally corroborated by notes in the DNH
Maternity Case Record (“
MCR
”) and other medical
records some of which were only made available to her legal team
after she had testified.  Moreover
her account is neither
improbable nor implausible and the unique vignette, for example, of
her having “
fitted
” (which detail was not written
in DNH’s MCR) is entirely consistent with her having been
diagnosed with preeclampsia
at least in circumstances where she was
not pre-emptively given any medication to avoid seizures after her
blood pressure became
seriously elevated. A random note alluded to by
Dr. Chimusoro, specialist obstetrician and gynaecologist who
testified on her behalf,
also co-incidentally referenced an isolated
entry dated 17 February 2017 in BM’s Marselle Clinic card (made
before the issue
of summons) in which it is deduced, after a history
taken contemporaneously from the plaintiff, that “
Mom had
eclamptic seizures at delivery
”.  I mention finally
that the plaintiff’s insistence of this minutiae is rendered
credible by her amplification
that subsequently she was advised by a
nurse that her fitting had caused the injury to BM, a disclosure
which made her very emotional
at the telling when she gave her
testimony.
The
medical records:
[31]
It
is necessary to give a brief exposition of the medical records that
were discovered by the defendant and to correlate these with
the
plaintiff’s evidence. The records, such as they are, also
constitute the foundation for the expert opinions tendered
in this
matter.
[15]
Antenatal care:
[32]
Firstly the records of the Marselle Clinic carried
forward to the “
Dwesi
”
Clinic reflect that regular antenatal visits were
maintained by the plaintiff and that nothing abnormal was noted to
suggest any
problems with her pregnancy.  The uterine growth
evolved as it should have and there was no suggestion of any earlier
hypertension.
The plaintiff’s last menstrual period was
loosely reflected as “
11/06
”
but her expected delivery date was anticipated
towards the end of September 2007. This is obvious from the
indication recorded at
her last routine visit that she should come
again (“
TCA
”
)
on “
27/09/7
”
.
[33]
Despite
the wrong indication aforesaid, the staff at DNH did not believe that
the plaintiff’s baby was premature when she
presented to
deliver him.
[16]
Livingstone
Hospital (16 – 17 August 2007):
[34]
The
single page of clinical notes from the LH (which reflect a “
PTO
”
at
their foot but with nothing following) confirms the plaintiff’s
admission there on 16 August 2007 at “
34
weeks
”
(
sic
).
[17]
[35]
They
note that the plaintiff had a “
history
”
of
lower backache and abdominal pains since 16h00 that day and that she
had been treated “
at
DNH for the same problem with oral antibiotics.  Course
finished
”
.
(This coincides with the plaintiff’s testimony that she had
presented herself at the DNH with abdominal pain twice
before her
admission to LH.)
[18]
[36]
They
record an estimated gestational age of “
34
weeks
”
(sic),
[19]
foetal movement felt, vaginal discharge and cervical os closed and
uneffaced on the night of the 16
th
,
but by 13h00 on 17
th
August
2007 allowing the tip of a finger in (without any contractions
though), a single recording of a reactive CTG on the 13
th
,
an indication of trace protein in the plaintiff’s urine, and
most significantly, a blood pressure that was rising (from
152/83 on
admission to 159/94 upon her transfer to DNH the following day).
The last entry recording the plaintiff’s
leaving for DNH by
official transport at 16h30 indicates the reasons for this as being
“
slow
progress and raised blood pressure
”
.
DNH (17 August
2007):
[37]
A
single page of clinical notes appears in the DNH MCR for 17 August
2007.  They acknowledge the plaintiff’s referral
for the
said reasons at 17h20 with an opening blood pressure reading of
146/94 recorded and an indication that a medical officer
is to see
her.
[20]
They further
note the first assessment of her by a Dr. Lamprecht at 18h00.
The doctor puts the gestational age
at 38 weeks (with reference to
fundal height because the plaintiff was unsure of dates). She is
assessed to be in “
early
latent labour
”
(mild
contractions are palpable) with gestational hypertension (“
GPH
”
).
The plan indicates that she is to have bloods taken and is to be put
on CTG with a review after 6 – 8 hours.
A random note at
the foot of the page indicates that she is transferred “
to
the
side
wards
”
at
17h00.
[21]
DNH (18 August
2007):
[38]
As
testified to by the plaintiff, there is no assessment of her again
until the next morning on 18 August 2007.
[22]
At 07h00 there is a question mark indicated in the notes over whether
she is in early latent labour, but she is found to
be 1cm dilated
with her membranes intact.  Blood results are interpreted for
example haemoglobin of 7.5 G/dl (low –
anaemic), white cell
count was 12 (normal) and platelets 290 (normal).  The urea and
electrolytes were normal.  Uric
acid was 0.19 (low).  Liver
enzymes were not suggestive of HELLP syndrome.
[23]
The plan is to repeat CTG and to start anti-hypertensive
medication (evidently only if her blood pressure remains on the

increase). (Notably there is no indication of what the blood pressure
is at this stage.) There is no rupture of her membranes yet
at this
point.
[39]
At
16h00 she is assessed by the same Dr. Lamprecht again who examined
her upon her admission.  She is still found to be 1cm
dilated
“
since
16/08/07
”
and
complaining of labour pains.  The gestational hypertension is
again recognized and there is a comment that there are “
contractions
on CTG
”
.
There
is a random note that ward “
BG
3 will not take patient
”
which
gives credence to the plaintiff’s testimony that she was not in
a ward but left in a chair until that evening.
[24]
A
diagnosis of “
prolonged
latent phase
”
is
made by the doctor in addition to the hypertension.  The plan is
to monitor her by CTG, to give her 50mg Pethidine (notes
endorsed to
say “
given
”
),
[25]
and to transfer her to the labour ward.  Augmentation is
proposed (possibly with “
Miso
”
)
[26]
and the doctor acknowledges a discussion with a consultant, Dr.
Blignaut, in this regard.  The concluding remark is that the

plaintiff is having regular (painful) contractions.
[40]
At
the foot of the page, but with no time indicated, Dr. Blignaut
ostensibly has recorded his/her review of the plaintiff.
She is
noted to be asymptomatic re “
IE
”
(imminent
eclampsia).  Blood pressure is recorded as 178/105.
[27]
The cervix is 4cm dilated.
[28]
Fully effaced. The presenting part is at 3/5 (above brim).  Her
membranes are noted to be intact. The plan is to sedate her

intravenously and see her in two hours.  CTG is to be repeated.
75mg of Pethidine is to be given immediately.
[41]
To return to the period in-between the plaintiff’s
morning and late afternoon assessments, there are three entries made.
[42]
The
first at 08h53 records a blood pressure reading of 155/105, an
assessment of no ROM (rupture of membranes) and a 1cm dilation.

The plan (with regard to the diagnosis of GPH) is that she is to be
admitted into ward BG 3 (which ward did not take her and with
no
explanation forthcoming from the defendant as to why that was the
case), to be given Aldomet 500mgs,
[29]
to do CTG and, “
if
reactive
[30]
to
administer Pethidine 75mg stat
”
.
A urine dip stick is also indicated in the plan.
[43]
A
note at 10h55 records that the plaintiff is “
attached
to CTG FHR is 150 bpm.  Cervix 2cm dilated
(written
over an obvious “4”).
Cervix
thick.  Membranes ruptured at 10.10
”
(the
ten minutes written over a figure “
30
”
).
[31]
[44]
The
next consequential entry made at 13h38 (before the plaintiff is
reviewed again by Dr. Lamprecht two hours and twenty-two minutes

later) surprisingly records that she is 1cm dilated again.
Again a diagnosis of GPH is reflected (but with no reference to

gestational proteinuria hypertension) and a plan is framed to admit
her to the ward that would not take her.
[32]
[45]
The
plaintiff was ostensibly admitted to the labour ward at 20h10
according to the notes, denoted by an appropriate entry that
indicates that she is having strong and regular contractions and is
attached to CTG with FHR of 120-160 bpm.  Dr. Chimusoro

especially noted his concern regarding the fact that the plaintiff’s
blood pressure at this point was severely elevated and
needed
consideration for “
MGS04
”
to
prevent seizures.
[33]
Her pulse was 109.  (It is fair comment that nothing is written
to indicate what steps, if any, were taken contemporaneously
with
this elevated BP reading.)
[46]
Co-incidentally the remark that the plaintiff is having strong and
regular contractions
may have been made at 23h45.  If it was
intended to concern events just before midnight (and that this is
possibly the time
when she moved to the first stage of labour), the
person making the entry has written it over the 20h10 entry which is
when the
plaintiff moved to the labour ward with the markedly
elevated blood pressure reading. (It is disconcerting that a reader
cannot
really fathom when exactly the plaintiff’s first stage
of labour commenced.)
DNH (19 August
2007):
[47]
At 01h45 an entry is made that “
CTG
reactive (Signed).  Pethidine 75mg given intramuscularly as
ordered.
”
[48]
At 03h45, randomly written at the foot of a blank
“
Forceps Delivery/Vacuum
Extraction
”
page, is “
Rpt
CTG – FHR 120 – 140 Strong contractions”
and
“
(P) RPT. GPH bld
.”
[49]
At
5h10, written on the same page ostensibly by the same hand is: “
PV
CX fully effaced.  Os 4cm dilated.  BP 129/106, membranes
intact, AROM done - clear liquor.”
The
plan indicated is to do “
5U
of Syntocinon infusion stat and a CTG at 6h00”.
[34]
[50]
At 6h00 an entry is recorded that the plaintiff is
“
attached to CTG machine
”
and that the FHR is “
ranging
between 135 – 129 bpm
”
.
[51]
At 6h15 it is acknowledged that she is given 75mg
of Pethidine intramuscularly for pain.
[52]
At
8h10 there is a substantial entry to the effect that the plaintiff
“
is
sleeping, no contractions, (having short contractions on
augmentation) PV – fully effaced, still 4 -5 cm dilated, caput

+, clear liquor draining, CTG reactive.”
The
plan indicated is to do GPH Bloods, short/10 U duration of
augmentation, review in two hours – if no progress then for

caesarean section (“CS”).  Prepare for CS in the
meantime.  Discussed (handover) with Dr. Blignaut –
For
CS. The Blood results are interpreted and then follows a review by
Dr. Sipuka with a plan to do a short trial of augmentation.
[35]
CTG is noted to be reactive. A review in 2 hours is expected to
happen.
[53]
A
further entry appears at 8h45 recording that the dilation has
progressed to 6cm. There is a caput++, with no moulding. CTG is
said
to be reactive. The plan is to give Pitocin 10 U
[36]
(as a bolus or as an infusion in the drip),
[37]
to empty bladder, and review in 2 hours.
[54]
At 8h50 a note indicates that the plaintiff’s
bladder has emptied (100ml) and that she has felt foetal movements.
[55]
At
09h30 she is “
attached
to the CTG.  Heart ranges between 100 – 160 bpm.
Foetal movements felt by mother
”
.
The next annotation is “
nursed
left lateral position 02 per mask
”
.
[38]
No implication is provided for this significant event.
[56]
At 10h50 a review is recorded to the effect that
the plaintiff’s cervix is fully effaced and 8cm dilated. A
caput of ++ is
noted.  Clear liquor.  CTG reactive.
The plan is to continue augmentation. Repeat CTG and review in an
hour.
[57]
At
11h36 the plaintiff is noted to be attached to CTG with foetal heart
ranges between 100 – 160 bpm.
[39]
[58]
At 12h30 it is noted that the plaintiff’s
cervix is 9cm dilated, and well effaced.  A caput of ++ is
observed.
The plan is that the patient is to “
sit
up
”
and to review her case again
at 13h30.  Nothing is said about the foetal condition despite
the drop in range mentioned in the
last note an hour before.
[59]
The next entry records a review only at 15h00.
The plaintiff is by now noted to be fully dilated, having a caput ++,
no moulding,
and the head is said to be at the “
spines
”
.
CTG is said to be reactive.  Bladder is empty.  The
reviewing clinician questions whether there is a malposition
but
affirms that the pelvis feels adequate.  The plan is to continue
augmentation if undelivered in 30 minutes for CS.
[60]
At
15h20 an entry is made to the effect that an episiotomy is performed
and that there was a struggle to apply forceps.  The
note goes
on to say that Dr. Sipuka was called and at 15h40 a live male is
recorded as having been delivered.  APGAR scores
of 5/10 and
8/10 are written down.
[40]
[61]
A separate entry is made at 15h35 on a different
page regarding delivery.  It confirms the forceps delivery of a
live male
infant however with APGAR scores of 1/10 and 3/10 and seen
by Dr. Titus.  Dr. Sipuka appears to have signed “
pp
”
on the latter’s behalf.
[62]
At 16h05, a retrospective note is made (evidently
by Dr. Lamprecht) regarding the plaintiff’s labour and the
condition of
BM as follows:
“
Called
to labour ward. “Flat baby”
Apgar’s 1/ 10, 3/
10.
Forceps delivery (with)
delay + difficulty of delivering head.
Analgesia (Pethidine)
given in morning only.
Initial assessment
Apgar 6/ 10
-
good pulse, HR ˂ than 100
-
no spontaneous respiration
-
some flexion
-
peripherally pink
-
Baby
bagged. 0.4mg Naloxone given IM
[41]
Baby responded slowly;
Nasopharynx suctioned = clear fluid
Spontaneous respiration
only after +- 15 minutes
O/E:
+++Caput
pink – (no signs)
of respiratory distress
No obvious (signs) of
dysmorphism
Baby cold to touch”
Postnatal records:
[63]
It is unnecessary
to go into minute detail regarding BM’s condition after birth
given the parties’ agreement that there
were classic indicators
for a diagnosis of NE.  It is relevant to mention however that
Dr. Lamprecht immediately recorded
an assessment after delivery of
birth asphyxia and “
?
HIE
”
.
[42]
The doctor further references cycling and lip smacking as noted by
the sisters and that BM is feeding via nasogastric (“
NGT
”
)
tube.  On examination the baby is said to be lethargic, pink,
and comfortable in the room air.  There are no signs of

respiratory distress.
[43]
The
assessment at this point is of a Grade II HIE and he is to start on
“
Phenobarb
”
(probably
Phenobarbital).
[44]
[64]
It is also noted in the clinical notes that BM had convulsions on the
20
th
, after which a cervical spinal fluid (“
CSF
”)
sample was taken.
[65]
On 22 August 2007
a provisional diagnosis of meningitis was made which was repeated
over the next few days and pursuant to which
BM was treated with an
antibiotic for 9 days.
[45]
I deal with this below.
[66]
It is also worth repeating the initial nursing note made at 16h40
after BM’s admission
to the ward, which is as follows:
“
A
live baby boy born by forceps delivery. Flat. Apgar 1/10, 3/ 10.
Admitted in for observations. On admission baby …colour
pale
Caput +++ cold and clammy to touch. Subcostal recession but not in
distress. Lethargic with some poor muscle tone- HGT 7.9
G/dl. Put
into a closed incubator attached to the... and SA O2 .94- 99% on room
air.  HR 133 beats/ minute RR 58 beats per
minute. Stable awaits
review by doctor. Oxygen not administered baby stable.”
Miscellaneous
other entries in the DNH MCR:
[67]
Other
indications appear in the Newborn Care Record which confirm that Dr.
Sipuka delivered BM at 15h35 by forceps. The birth weight
is 3.80kg,
length is 53cm, head circumference 36cm.  The APGAR here is also
reflected as 1/10 at one minute and 3/10 at ten
minutes.
For
the first time the MCR notes the plaintiff’s positive HIV
status but other vital information about the labour and
resuscitation,
distress indicators and neonatal treatment of the baby
is lacking on this form.
The
part especially indicated for APGAR scoring has been left blank and
unsigned.
[46]
Under the
discharge part “
check
and plan
”
of
the same page (with no problems noted and no plan indicated) the
indication is given, contrary to the plaintiff’s evidence
and
inconsistent with what has become known about BM’s condition
after the fact, that the baby is “
breastfed
”
and
“
feeding
well
”
.
[68]
The Summary of Labour form has some details
recorded, some of which I have already related above.  Only two
features of the
APGAR rating criteria have been scored but indicate a
total of 1/10 at one minute and 3/10 at five minutes.
[69]
The first stage of labour is said to have
commenced on 19 August 2007 at 00h03 for a duration of 14h25, second
stage on 19 August
at 14h30 (for 1 hour 5 minutes) and the third
stage on the same date at 15h35 – 15h45 (for ten minutes).
The total
duration of labour is given as 15h40. These periods are
self-evidently incorrect (and inconsistent with other clinical notes)
and
Dr. Chimusoro went so far as to suggest (not unfairly in my view)
that the person recording them was probably trying to gloss over
the
prolonged labour.
[70]
The forceps delivery report (elsewhere indicated
as being a difficult procedure) is completely blank and leaving one
to surmise
what about it caused the concern for the staff involved
and how they dealt with whatever challenges they were faced with.
[71]
The
partogram is similarly incomplete but reflects supposedly normal
foetal heart rates at every half hour from 8h10 to 15h40 on
19 August
2007 (the only period chartered),
[47]
the last one and time coinciding with the comment “
delivered
”
as
if the writer (all in the same handwriting) knew when he/she started
recording the data that the birth would happen within half
an hour of
the penultimate check.  The contractions shaded in on the
partogram are designated as having been moderate in nature
contrary
to clinical notes appearing elsewhere suggesting strong contractions.
[72]
Dr. Chimusoro ventured his view (again not implausibly) that it
looked like a person had
in a single sitting sat and wrote all the
times in on the partogram at once. He pointed out that the stroking
of the purported
contractions (the shading-in referred to above)
contradict what the notes say as do some of the supposed heart rates
recorded on
the graph. One looks in vain for example to find on the
partogram the two so called non reassuring CTG reports referenced in
the
clinical notes at 9h30 and 11h36 in that interlude.
[73]
There is indeed in my view nothing in this vital document that a
court is able to rely
upon that gives comfort that it is authentic
and responsibly made.
The
lack in the medical records and the perspective offered by DNH:
[74]
The clinical
records kept by the DNH were appallingly deficient and haphazard.
No original documentation was produced in evidence.
The copies passed
off as true copies of the originals bear annotations or comments
written all over them.  As I have already
remarked, the records
of the plaintiff’s assessments at DNH before she presented
herself at LH were not made available at
the trial and some notes
only came to the party after the trial had commenced.
[48]
Several critical templates were not completed at all.  Some
reflected bare entries here and there. Clinical notes were scribbled

indiscriminately in places where one would not look, foiling the
objective of note keeping which is to maintain a continuous record
of
critical events both to appreciate what has gone before and to plan
going forward on the premise of a reliable consequential
thread
especially at handovers.   Some entries were not timed. In
the one instance I have already referred to above there
was evidently
an overwriting of the extent of the plaintiff’s cervical
dilation so obviously out of sync with the foregoing
and subsequent
entries. If not careless the only inference to be drawn from this is
that the writer was deliberately obfuscating
the reality or seeking
to paint it in a better light after the fact.
[75]
Another critical discrepancy or confusion which arises from the notes
is whether there
was a rupture of the plaintiff’s membranes as
early as 10h10 on 18 August 2007 already given the inconsistency with
a later
note as to the supposed defining moment of AROM indicated.
This detail is important because of the plaintiff’s HIV status

and danger of ascending infections and transmission of the virus to
the baby.  (According to Dr. Chimusoro’s evidence
the
standard operating procedure at the time would have required the
delivery to have been within 4 hours of the rupture because
of the
plaintiff’s positive HIV status even if the early entry related
to hind-waters only coming down.)
[76]
I am further satisfied that the information on the partogram was
probably reconstructed
as a reality after the fact. This was
ostensibly to give a picture of what supposedly pertained during the
plaintiff’s labour
and to create an impression of compliant
step-taking and recordkeeping.  This can in my view be plausibly
inferred because
the on-the-half-hour times and foetal heart rates
written down do not align with separate entries written down in the
clinical
notes as to foetal heart rate checks or CTG interpretations.
The strength of the plaintiff’s contractions are also as I have

said above inconsistent with what is written in the clinical notes.
[77]
Odd CTG tracings were made available but the full picture was left to
everyone’s
surmise.  Intermittent notes appear regarding
fetal heart rate monitoring in a highly complicated labour in
circumstances
where the foetus was supposed to be subjected to
continuous surveillance by cardiotocography.  The trend of her
blood pressure
readings was evidently not captured on a graph
anywhere.
[78]
Not only are the records such as were made available tainted with
suspicion, but the staff
fell horribly short of their legal
obligation to keep a proper maternity case record and/ or to have
ostensibly taken every measure
they were supposed to take in the
management of the plaintiff’s labour at the requisite
intervals, which steps were consequently
required to be reported on
in the official maternity case record.
[79]
If I accept the plaintiff’s evidence that she fitted, for
example (as I do since
it appears plausible and consistent with all
the features of her labour taken wholistically), this vital
information was not recorded
in her MCR. There is further an absence
of her vital statistics taken at each regulated interval such as her
blood pressure, this
despite her gestational hypertension being one
of the most serious risk factors that threatened her health and life
as well as
the well-being of her foetus going in to labour.
[80]
Despite every indication being that those who were involved in the
oversight of the plaintiff’s
labour and who could have filled
in the obvious gaps were available to testify, the defendant chose to
present her impression of
what went down in this critical period
solely with reference to the testimony of the experts who reviewed
the inadequate or slanted
MCR on her behalf.  How these notes
could have been defended by Dr. Janowski as reliable in showing a
supposedly properly
managed labour is frankly concerning.
[81]
Mr. Kincaid who
appeared on behalf of the plaintiff appropriately drew my attention
to the dictum of Lord Brooke in the matter of
Ratcliffe
v Plymouth & Torbay Health Authority
,
[49]
cited with approval and applied in
M
obo M v MEC Health and Social Development; Gauteng Provincial
Department
,
[50]
in which the following realism is expressed:
“
It
is likely to be a very rare medical negligence case in which the
defendants take the risk of calling no factual evidence, where
such
evidence is available to them, of the circumstances surrounding a
procedure which led to an unexpected outcome for a patient.
If
such a case should arise, the judge should not be diverted away from
the inference of negligence dictated by the plaintiff’s

evidence by mere theoretical possibilities of how that outcome might
have occurred without negligence: the defendants’ hypothesis

must have the ring of plausibility about it.”
[82]
I am grateful to all the experts who assisted in making sense of the
entries that were
made in the plaintiff’s hospital records put
at the court’s disposal.
Issues
for determination:
[83]
As is the expectation in matters such as these involving a review by
specialist experts
of the medical records and data giving flesh to
the relevant clinical setting, some of the points of difference
raised in the pleadings
were resolved by the time the trial
commenced.  Certain basic premises were accepted which were
recorded in joint minutes
of the radiologists, obstetricians, and
paediatricians filed in preparation for and during the trial. I deal
with these below.
[84]
I also made an order at the onset of the matter separating quantum
from merits and the
trial proceeded on the issue of liability only.
[85]
Although the parties seemed to have accepted in the Joint Practice
Note filed pursuant
to the case management processes that the
obstetric management of the plaintiff was sub-standard leaving only
the issue of causal
negligence to be determined, it became evident to
me from the tenor of Dr. Janowski’s evidence that only aspects
of the management
were conceded to have been below the professional
standard. For example it was accepted that the failure to have
treated the plaintiff’s
GHT before 18 August 2007 was
substandard but the defendant resisted the implication that this
could have led to the unfortunate
outcome.  It was also accepted
that the record keeping was exceptionally poor but again any causal
connection with BM’s
condition thereby was eschewed. As for the
augmentation administered and the decision not to deliver BM by
caesarean section, the
contention was that the standard of management
adopted was perfectly in line with the Maternity Healthcare
Guidelines applicable
at the time and beyond reproach. The defendant
differed with the plaintiff that her labour was prolonged or that
there was any
cephalopelvic disproportion. Whatever challenges came
in her obstetric management as from the 18
th
, so the
defendant’s case went, these were met properly and
professionally. Negligence in her treatment, such as there may
have
been, was in any event abjured on the basis that BM’s condition
more probably arose along a different pathway than intrapartum
NE or,
conversely put, the supposed hypoxia and ischemia were not the unique
initiating causal mechanism for the neurological outcome
in
contention here.
[86]
I set out below the allegations of negligence relied upon by the
plaintiff in her particulars
of claim to understand her starting
point.
The
alleged negligent intrapartum care:
[87]
In summary the
claimed basis for the defendant’s negligence is premised on the
failure on the part of the hospital staff to
have pre-empted that BM
would be especially at risk from suffering asphyxia and HIE during
labour, a hypoxic- centric event all
on its own,
[51]
because of the high risk factors that pertained to her situation.
[88]
Firstly, she was a
prima gravida
(cephalopelvic disproportion
always being a concern with a first pregnancy) and is HIV positive.
[89]
Additionally she ostensibly developed gestational hypertension
which was not diagnosed
by DNH at her earlier presentations when she
reported complaining of abdominal pain.
[90]
Although her hypertension was recognized at LH, she was not given any
anti-hypertension
treatment for her condition before being
transferred to DNH.
[91]
Even once transferred to DNH, which is a tertiary institution geared
to deal with complicated
cases, however, treatment for the added on
risk factor was delayed.
[92]
The failure to bring her blood pressure in check put the plaintiff at
risk of suffering
from fits.
[93]
The hospital staff failed to take steps to deliver BM by caesarean
section despite the
indications for this step as a necessity being
recognized by the staff because of the plaintiff’s delayed
labour.
[94]
Instead her labour was augmented whereas the plaintiff was having
strong, normal and regular
contractions.
[95]
The hospital staff
also failed to take note of documented signs of foetopelvic
disproportion.
[52]
[96]
They failed to promote intrapartum resuscitation by causing the
plaintiff to lie on her
side rather than instructing her to sit up
which would further have conduced to a hypoxic environment rather
than ameliorating
the challenge for BM’s delayed delivery.
[97]
They failed to take regular CTG recordings prior to delivery, missing
a valuable opportunity
to have detected foetal distress and to have
acted upon it.
[98]
They were ill-prepared, in the sense that there was no doctor on hand
when her labour went
awry warranting an ultimate delivery by forceps,
and also failed in any event, when the plaintiff’s foetus’
condition
deteriorated, to diagnose and react properly to meet this
emergency.
[99]
In general the contention is that the hospital staff failed to take
reasonable precautions
and to exercise the requisite level of skill
as professionals to ensure BM did not suffer from birth asphyxia or
HIE.
BM’s
condition:
[100]
It is opportune to begin with what BM’s condition is as this is
not in dispute, and to reflect on the agreement
between the parties
concerning what the neuroimaging reveals about the injury sustained
by him.
[101]
According to the clinical assessment, he has gross motor function
classification system (GMFCS) level 1 (
the grading looks at
movements such as sitting, walking and use of mobility devices
);
manual ability classification systems (MACS) level 1 (
the grading
looks at handling objects
); and communication function
classification system (CFCS) level 2 [
the grading looks at
everyday communication
].
[102]
The joint minute of the radiologists, which embodies the accepted
premise for how BM’s brain scan image
(taken 10 years 11 months
after his birth) presents, or ought to be interpreted, indicates as
follows:
“
1.
This joint minute has been prepared between Dr D Alheit (
BA
)
and Dr Z Zikalala (
ZZ
).
This joint agreement is presented as a constructive attempt to
present to the Court the imaging features of the MRI brain
scan and
to advance a diagnosis for the described pattern.
2.
BA refers to the body and comment of ZZ’s report.
3.
BA
agrees with
ZZ
that the MR study displays features
of hypoxic ischaemic injury
of the
brain
.
4.
BA
submits that
the MR findings make the diagnosis, in the appropriate clinical
context, the peri-partum
*PBGT/Central
hypoxic ischaemic injury of the brain
highly
probable.
[53]
5.
The experts agree that the findings of the MRI study suggests that
genetic disorders
as a cause of the child’s brain are unlikely
but not excluded in the light of the signal changes of the Dentate
nuclei and
posterior Pons.  Further, clinical, genetic and
metabolic assessment is advised.
6.
The
experts agree
that there is no evidence of current or
previous infective or inflammatory disease on the various MRI
sequences and agree that
inflammatory or infective conditions are
unlikely as causes of the child’s brain damage.
7.
The
experts agree
that a review of the clinical and
obstetrical records by appropriate specialists in the field of
Neonatology and Obstetrics to
be essential in determining the cause
and probable timing of this hypoxic ischemic injury.”
[103]
The parties agreed
that the reports of the expert radiologists could be admitted into
evidence.
[54]
[104]
The diagnosis of “
PBGT
” as indicated above is what
the radiologist previously used to refer to as an “
acute
profound (central) hypoxic ischaemic injury of the brain
”.
[105]
In the field of radiology this pattern of injury would be consistent
with a history of an intrapartum sentinel
event.
[106]
It is common cause
that no obstetric emergency sentinel event is in contention here, but
Dr. Alheit qualified in his report that
the injury pattern seen on
the MRI image should be interpreted in the context of an article by
Smith
et
al
.
[55]
[107]
This article
postulates that more recent scientific evidence indicates that short
or relatively short incremental hypoxic insults
play a significant
role in the eventual outcome of an injury pattern.
[56]
[108]
In this context, a
“
PBGT
”
injury, if not one
that develops over a short period of time during an obstetric
emergency (read classical sentinel event), can
also result from final
circulatory collapse in a neonate exposed to subacute or subthreshold
hypoxia over a period of time.
[57]
This type of injury in the nature of an terminal insult is juxtaposed
with a “
prolonged
partial injury
”
that develops over
a period allowing compensatory redistribution of blood flow to occur,
resulting in a different pattern of injury.
[109]
The kind of injury
pattern advocated for here (where there are documented warning signs
in the form of a non-reassuring foetal status
- in some instances
even hours before delivery) are preventable as opposed to classical
sentinel events that are not, for obvious
reasons.
[58]
[110]
An image shown on the scan typically reflects the structural pattern
description and severity, rather than it
implies a causative
mechanism of the brain injury.  It can for example be accepted
that if the clinical context or history
supports the premise of a
non-reassuring foetal status developing during the labour in question
and is prolonged, a BGT pattern
may result in the absence of a
perinatal sentinel event
.
[111]
I add that the 2019 ACOG update referenced in the report of Dr.
Alheit states that “
Deep gray nuclear injury commonly occurs
(25 – 75% of cases) following severe partial insult of
prolonged duration or combined
partial with profound terminal
insult”.
[112]
But this is where the assistance to this court ends from the
radiological perspective.  The timing and pathogenic
mechanism
of the injury falls outside the field of radiological imaging
according to the experts and must be informed by obstetricians
and
paediatric experts, hence the concluding remark in paragraph 7 of the
joint minute above in which the radiologists fairly defer
these
issues to the other experts.
[113]
Regarding the
reservation expressed in paragraph 5 of the joint minute above,
although Dr. Alheit pointed out that the differential
diagnosis
suggested by the increased signal and some loss of volume in the
dentate nuclei and posterior pons seen on BM’s
scan included
the likelihood of congenital/genetic/hereditary and metabolic
conditions, this was definitively ruled out by Prof.
Denis Viljoen, a
specialist in medical genetics.
[59]
[114]
Prof. Viljoen did not testify, but his opinion was accepted that:
“
From both the
negative family trees and clinical histories of this child’s
birth and subsequent obstetric/neonatal complications,
(supported by
MRI brain scans), hypoxic ischaemic cerebral palsy is the most
probable diagnosis.
Genetic
causes for his clinical findings are very unlikely
.
Similarly, syndromic or metabolic cause for the epilepsy, development
delays and cerebral palsy are also unlikely.”
(Emphasis
added.)
[115]
Notwithstanding
the common opinion expressed in paragraph 6 of the joint minute that
there is no evidence on the MRI picture of
previous infective or
inflammatory disease and that such conditions are unlikely as causes
of BM’s brain damage (in effect
putting paid to the defendant’s
hypothesis of neonatal meningitis being the cause of BM’s brain
injury), the professional
view held by the defendant’s
paediatric neurologist expert, Dr. Yavini Reddy, who was initially
expected to testify on the
defendant’s behalf and who put up a
summary foreshadowing such opinion,
[60]
is that BM’s confirmed neonatal encephalopathy
post-delivery was “
most
likely due to neonatal meningitis
”
.
To give a context to the picture seen on the MRI scan, Dr. Reddy
stood poised to state that neonatal meningitis can cause
neonatal
encephalopathy and bilateral basal ganglia or thalamic infarcts on
MRI.
[61]
(The defendant in the
end led the evidence of Prof. Bolton, paediatric neurologist, who
also sought to present such a hypothesis.)
[116]
With this agreed premise of the expert radiologists in mind, the
issue arising is whether the originating cause
for BM’s
cerebral palsy in this case can, on a balance of probabilities, be
ascribed to intrapartum birth events.
[117]
If the answer to this question is in the affirmative, a causal
connection between the alleged negligence (if established)
and BM’s
injury can then in my view plausibly be inferred.
The
timing of the damage causing event:
[118]
It is often repeated in our courts by specialists in the fields of
neonatal and obstetrics in matters such as
these (as was the case
here), that the timing of the HIE injury, at least from a clinical
perspective, is hard to gauge unless
some sentinel event in the
classical sense of an obstetric emergency has occurred. In all other
cases and in the absence of direct
evidence on the obstetric
management or other indications that there was fetal compromise at a
specific point in time, or a noticeable
“
bradycardia moment
”
in this instance as Mr. Kincaid who appeared for the plaintiff put
it, this is often left to inferential reasoning based
on the medical
records indicating the clinical setting and objective expert opinion
concerning the probabilities one way or the
other. The condition of
the baby at birth is also vital to this enquiry.
[119]
Since HIE suffered during labour is a recognized pathway in itself to
cerebral palsy (as discussed below) it is
already in my view
suggested as a cause for such a condition or having a natural
relationship with intrapartum birth events.
[120]
Before discussing
the criteria the specialists in the field commonly advert to in order
to determine the cause and probable timing
of a hypoxic ischaemic
injury, and more especially BM’s in this instance, it is
necessary firstly to outline certain basic
concepts and premises
referenced by the experts in this matter that are applicable to the
issues at hand.
[62]
[121]
Firstly neonatal encephalopathy 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.
[122]
HIE, in turn, is a subgroup of neonatal encephalopathy.  To
consider hypoxic ischaemic encephalopathy to
have occurred in the
intrapartum period, there has to be evidence of neonatal
encephalopathy.  This needs to be confirmed
to be a moderately
severe encephalopathy (grade 2), and to last at least 7 days.
[123]
A Table of Grades of Encephalopathy appears below:
Alertness
Muscle tone
Seizures
Pupils
Respiration
Duration
Grade
1 Mild
Hyperalert
Normal
or increased
None
Dilated,
reactive
Regular
˂24
Hours
Grade
II Moderate
Lethargy
Hypotonic
Frequent
Small,
reactive
Periodic
2 –
14 Days
Grade
III Severe
Coma
Flaccid
Uncommon
Variable,
fixed
Apnoea
Weeks
[124]
Further, before attributing intrapartum hypoxic injury to be the
cause of neonatal encephalopathy,
one has to consider the probability
of other conditions that may cause an encephalopathy such as for
example, meningitis, congenital
brain abnormalities; vascular
abnormalities; maternal infection or intrauterine infection or severe
neonatal sepsis; metabolic
or chromosomal disorder; obstetric cases
that affect blood flow to the foetal brain (for example placental
abruption; eclampsia,
maternal hypotension, umbilical cord
compression; prematurity; intrauterine growth retardation); maternal
drug use; and severe
neonatal jaundice.
[125]
Then, to the
question whether such an injury has occurred during labour, according
to Volpe
[63]
certain factors
need to be present before being able to make the diagnosis of an
intrapartum insult being the cause of neonatal
brain injury.
Firstly, there should be evidence of foetal distress and/or foetal
risk for hypoxia-ischaemia (FHR abnormalities,
sentinel event, foetal
acidaemia), secondly, there ought to be evidence that there was a
need for resuscitation of the baby and/or
low Apgar scores and,
thirdly an overt neurological syndrome in the first hours and day of
life should be indicated. If these criteria
can be confirmed, this
supports the probability of a relationship between intrapartum events
and cerebral injury further strengthened
by the injury picture shown
on the MRI scan where applicable.
[126]
The American Congress of Obstetrics and Gynaecology (“
ACOG
”)
stipulates its own criteria which all the experts who testified to in
this matter subscribe to.  In 2003 ACOG and
the American Academy
of Paediatrics (“
AAP
”) published guidelines that
had 4 essential criteria and 5 supplementary criteria to define an
acute intrapartum event as
sufficient to cause cerebral palsy.
These guidelines were revised in April 2014 and “
essential
criteria
” no longer exist.  Presently, in order to
determine the likelihood that an acute hypoxic ischaemic event that
occurred
in close proximity to labour and delivery contributed to
neonatal encephalopathy, the Consensus Report instead emphasizes the
weighting
of various risk factors.  It considers all potential
contributing factors including maternal medical history, obstetric
history,
intrapartum factors (foetal heart rate and issues relating
to delivery) and placental pathology.  The more factors present,

so it is suggested, the more likely it is that there was an
intrapartum event that conduced to the NE.
[127]
Indeed the second edition of the Consensus Statement recognizes that:
“
There are
multiple potential causal pathways that lead to cerebral palsy in
term infants.  A broader perspective is now necessary
before
attributing neonatal encephalopathy to an intrapartum event.  It
is now recommended 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.”
[64]
[128]
Prof. Bolton who came late to the party in filing an expert summary
applied the science through the filter of
the abovementioned
Consensus Report to determine if the features of the plaintiff’s
labour and the condition of BM immediately
after birth and in the
aftermath, culminating in him developing cerebral palsy, fitted the
template.  He thought not, or more
specifically that neonatal
meningitis was the more likely cause.  The same scientific
measure was applied by Dr. Kara, specialist
paediatrician, who
reached a different opinion, namely that the cause for BM’s
neurological outcome probably resided in an
intrapartum birth event.
[129]
As for the foetal heart rate monitoring patterns both Drs Kara and
Chimusoro were satisfied that there were at
least two foetal heart
rate tracings at 09h30 and 11h36 on the morning preceding BM’s
birth that indicated a non-reassuring
foetal status, coupled with the
significant event that the plaintiff was nursed on her side and given
oxygen by mask at 09h30.
Both specialists opined that this was
consistent with a concern for the wellbeing of the foetus at the
time.
[130]
That leads me to the type and timing of “
contributing
factors
” that are consistent with an acute peri-partum or
intrapartum event according to the Consensus Statement.
Concerning
the “
other significant factors
” that
might steer one in the direction of concluding that an acute
intrapartum event as the sole underlying pathogenesis
of NE becomes
“
much less likely
”, the experts accepted that
there were indeed proximal and distal factors in the offing, but Dr.
Kara disagreed in this instance
that the idea of infective causes
could lead one away from concluding that the acute intrapartum event
was the more probable causative
agent for BM’s cerebral palsy.
[131]
The Consensus Statement conceptualizes certain pathways to cerebral
palsy over various stages commencing with
conception and ending with
childhood.  In between these outer limits are the two stages of
pregnancy and labour (ante and
intrapartum respectively) followed by
the neonatal stage.
[132]
It recognizes that both distal and proximal risk factors straddling
this five stage period can exert a pathogenic
effect on foetal brain
development.  It is opportune to repeat these pathways envisaged
by the Consensus Statement as it will
give a context to Prof.
Bolton’s opinion that Pathway “
E
” pertains
in the current scenario:
A
B
C
D
E
Conception
+-DRF
+-DRF
+-DRF
+-DRF
↓
↓
↓
↓
Antepartum
+-DRF
+-PRF
+-PRF
+-DRF
↓
↓
↓
↓
Intrapartum
PRF
PRF
↓
PRF
DRF
↓
↓
↓
↓
↓
*
*
↓
*
*
↓
↓
↓
↓
↓
Neonatal
NE
NE
+-NE
NE
PRF
→*→NE
↓
↓
↓
↓
↓
Childhood
CP
CP
CP
CP
CP
FIGURE 1
Prenatal and perinatal
causal pathways to cerebral palsy in term infants.  Distal risk
factors exert a pathogenic effect on
fetal 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 exert
pathogenic effects on fetal brain
development at a time that closely predates or coincides with the
onset of irreversible brain
injury.  Examples include abruption
placentae, chorioamnionitis, and twin-twin transfusion.  There
are multiple potential
causal pathways that lead to cerebral palsy in
term infants, and the signs and symptoms of neonatal encephalopathy
may range from
mild to severe, depending on the nature and timing of
the brain injury. A.  Intrapartum brain injury that is due to a
proximal
risk factor may lead to neonatal encephalopathy and
subsequent cerebral palsy.  B. Intrapartum brain injury may be
the result
of both distal and proximal risk factors that predispose
the fetus to brain injury and cerebral palsy.  C.  Brain
injury
or anomaly may occur in the antepartum period as a result of
distal and proximal risk factors.  D.  Brain injury may
occur at multiple points during gestation.  E.  Proximal
risk factor and brain injury may occur in the neonatal period

following predisposing distal risk factors.  Abbreviations: DRF,
distal risk factor; PRF, proximal risk factor.”
[133]
It is appropriate to point out that the concepts
of “
distal
”
and
“
proximal
”
are
unique to the application of the professional Consensus Statement. Of
course its criteria implicating intrapartum hypoxia in
neonatal
encephalopathy has utility from an obstetric and pediatric
perspective and can and does assist the court in its

determination of the proof of a causal link between a defendant’s
claimed 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, but its application
is not a
substitute for the court’s own legal causation enquiry that it
must undertake.  There is a clear difference
between scientific
and judicial measure which a court is constrained to keep in mind.
The
legal requirements:
[134]
It is a trite
principle that a successful delictual claim entails the proof of a
causal link between a defendant’s claimed
culpable actions or
omissions, on the one hand, and the harm suffered by the plaintiff,
on the other hand.
[65]
This is
in accordance with the flexible “
but-for
”
test.
[66]
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 alleged wrongful conduct of the defendant.
Sometimes however this enquiry involves the mental
elimination of the
claimed wrongful conduct and the substitution of a hypothetical
course of lawful conduct and the posing of the
question as to whether
upon such hypothesis the plaintiff’s loss would have ensued or
not.
[67]
[135]
Legal causation is
required to be established on a balance of probabilities.
[68]
[136]
Given 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, the significant question
in this matter is
therefore whether, as a matter of probability, BM’s condition
would in any event have ensued even if the
defendant’s claimed
negligent intrapartum care had not occurred.
[69]
[137]
Dr. Kara opined
that all the indications in the multifactorial assessment supported
the probability of BM having sustained the injury
during the
intrapartum period. Prof. Bolton conversely offered his primary view
that the originating cause for BM’s cerebral
palsy is to be
found in the differential diagnosis of meningitis made by the staff
at DNH after his birth which he was comfortable
elevating to a
confirmed diagnosis as far as he was concerned.
[70]
Later however, as he was fleshing out his opinion and challenged by
Mr. Kincaid as to why he was quite resolute about postnatal

meningitis being causal of BM’s neurological outcome, a new
theory evolved that it was a “
foetal
meningitis
”
at
play, caused by a viral infection that later emerged as a sepsis and
inflammation of the placenta, in other words, a chorioamnionitis.
The
case for the paediatricians:
[138]
From the
paediatric perspective certain features of BM’s birth and
neonatal status were confirmed in the joint minutes of
Dr. Kara
(paediatrician) and Dr. Reddy (paediatrician neurologist)
[71]
that set the tone for the way forward.
[139]
It is firstly not
in dispute that BM has hemiparetic cerebral palsy with global
development delay and epilepsy. Despite this not
being the typical
spastic or dyskinetic cerebral, it is nonetheless cerebral palsy. (He
is also known with retroviral diseases
on treatment.)
[72]
[140]
Also not in dispute is the fact that BM was actively resuscitated at
birth and had spontaneous respiration only
at 15 minutes.  The
admitting concerns were birth asphyxia and HIE.  He had lip
smacking at 23h00 on19 August and documented
convulsions on 20 August
2007 at 09h00.  He was commenced on Phenobarbitone.
According to the experts there was no doubt
that he had at least a
moderate neonatal encephalopathy lasting several days after his
delivery.
[141]
There was certainly no concern over the foetal condition on admission
in labour.  There was poor progress
in labour and augmentation
of labour with Syntocinon. Despite the import of the notes in the MCR
that suggested that the CTGs were
generally reactive, there were
concerns of foetal distress and intrapartum resuscitation was
commenced at 09h30 on 19 August 2007,
in his view exactly to
ameliorate concerns of foetal compromise.
[142]
Dr. Reddy however
deferred to expert obstetric opinion regarding the management of
labour.   Her observation was that
there is no record
in
the notes
regarding
foetal distress at the time intrapartum resuscitation was commenced,
hence one of the
indiciae
required in the
Consensus Statement to confirm the presence of NE was lacking.
[73]
[143]
Ultimately the paediatricians differed (in the joint minute)
regarding the more probable cause of BM’s neonatal

encephalopathy, the defendant’s expert contending that neonatal
meningitis was a more likely cause, whereas on behalf of
the
plaintiff the theory promoted is that the injury shown in the
neuroimaging fits in with an intrapartum hypoxic event which
renders
infective, metabolic and genetic aetiologies less likely for this
appearance.
[144]
Applying the criteria of the Consensus Statement, according to Dr.
Kara. the confirmation of foetal compromise,
the prolonged
resuscitation at birth and the significant encephalopathy, together
with the MRI scan features, the abnormal renal
function suffered by
BM, the respiratory distress and the events in labour make it
probable that his cerebral palsy was due to
an intrapartum hypoxic
ischaemic injury.
[145]
Contrariwise the opinion proffered by Dr. Reddy was that although BM
had confirmed neonatal encephalopathy post-delivery,
this was most
likely due to neonatal meningitis.  This view seems to be
founded on her sub-view, if I can call it that, that
neonatal
meningitis can mimic the changes seen in hypoxic ischaemic
encephalopathy on neuroimaging.
[146]
Prof. Bolton when he testified on behalf of the defendant expounded
upon Dr. Reddy’s opinion that, in the
absence of a sentinel
event during labour and a supposed lack of evidence of negligence,
neonatal meningitis was the most likely
cause of BM’s clinical
condition.
[147]
His approach initially was to resolutely adopt
pathway “E” referred to in the Consus Statement which as
I point out
above differentiates from a clinical point of view
between distal and proximal risk factors. He found distal factors at
the conception
stage to include the plaintiff's HIV status. Since HIV
is a neurotrophic virus (that is likely to attack or affect the
nervous
system) he noted that the plaintiff’s status increased
the risk of infection within the amniotic cavity, the umbilical cord,

and the placenta - referred to as chorioamnionitis. Infection of the
placenta results in inflammation and impairs the foetal oxygenation

process. Chorioamnionitis is also associated with an inflammatory
cytokine storm according to his testimony, which directly damages
the
brain.
[148]
His conclusion was that the plaintiff's HIV
infection in itself predisposed BM to cerebral palsy. The mechanism
was probably placental
inflammation, the impairment of foetal
oxygenation during labour, and the production of inflammatory
cytokines which he opined
directly damaged the brain.
[149]
He added that the plaintiff’s hypertension
would also have contributed to the impairment of maternal-foetal
oxygen perfusion.
In his view these two factors predisposed BM to the
poor condition evidenced at birth and the subsequent development of
NE.
[150]
Under cross examination he conceded that a hypoxic
ischemic injury may have occurred
during
labour
but yet maintained that it was
most likely caused by placental damage or insufficient placental
perfusion as a result of the chorioamnionitis
and that the
possibility exists that the hypoxic ischemic injury could have been
further compounded by the onset of neonatal meningitis.
[151]
In essence his view is that the damage, manifested
at the neonatal stage, probably had its origins in the risk factors
which were
in existence as far back as conception and which remained
present throughout the ante and intrapartum development of the
foetus.
[152]
It goes without saying however that the
known existing risk factors referred to by Prof. Bolton were common
cause (this includes
the plaintiff status as a primigravida) and
impacted significantly on the labour management strategy that had to
be adopted as
a very result.  In this respect he deferred to the
obstetricians.
[153]
As Mr. Kincaid pointed out in his argument, if
Prof. Bolton was deferring to Dr. Jankowski’s assessment of the
plaintiff’s
labour management, the implication thereby is that
there was no fault whatsoever with the way in which the plaintiffs
labour was
managed, that there was no foetal distress recorded during
the labour, and that accordingly BM’s clinical condition at
birth
could not have had a hypoxic ischemic origin.
[154]
However, as I intend to demonstrate below, this was a very tenuous
ground on which to rest his theory as to the
more probable cause of
BM’s NE.
[155]
There further seems to be no basis to reject the accepted views of
the radiologists that BM’s brain injury
seen on the MRI scan
does not show any evidence of current or previous infective or
inflammatory disease, hence such a causal agent
for BM’s damage
is unlikely.
Obstetric
management:
[156]   As for
the plaintiff’s pregnancy and the management of her labour her
antenatal care was described by the
expert obstetricians generally as
“
no abnormalities detected
”. (Prof. Bolton
introduced the possibility that the infections that the plaintiff had
presented with during her pregnancy
closer to her labour were
“
relevant
”, suggestive of chorioamnionitis, and at
least constituted a distal factor in the whole scheme of things.)
[157]
They agree that upon the plaintiff’s earlier admission to the
Livingstone Hospital (between 16 and 17 August
2007), despite her
presenting with raised blood pressure, she was not given treatment
for her hypertension.  It was also commonly
accepted that no
treatment for gestational hypertension was administered at DNH on the
17
th
. Treatment only commenced on the 18
th
at
07h00, after a recordal of a blood pressure reading of 155/105. Dr.
Janowski readily conceded that up until the 18
th
this
constituted substandard care, but with no causal outcome. In his view
from the 18
th
everything was done in compliance with the
Maternity Care Guidelines “
on the dot
”, but was
it? And, from a causal perspective, what about possible insults from
before given his acknowledgement of the risks
posed by the
plaintiff’s raised blood pressuring during contractions?
[158]
The latent phase of labour commenced at the very latest at 7h00 on 18
August 2007 at the DNH, this after the plaintiff’s
transfer
from LH.  Dr. Chimusoro explicated that based on pain and
cervical changes that the plaintiff suffered on the 17
th
already that this denoted that the latent phase of labour had
commenced earlier but was prepared to accept that it was later as

suggested by his counterpart.  But by the standards set out in
the Maternity Care Guidelines, the plaintiff’s labour
was way
prolonged and Dr. Janowski’s approach of letting nature take
its course and adopting a wait-and-see approach with
all that was
going on with the plaintiff’s pregnancy and the peculiar risk
factors that pertained does not accord with the
expectation of a
reasonable clinician to be particularly concerned and more attentive
to the risk of hypoxia developing.  It
certainly makes practical
sense to have explored why after being more than forty weeks into her
pregnancy the plaintiff’s
labour was progressing
slowly by the hospital’s own normative standards of how long it
should reasonably have been taking.
[159]
A CGT was commenced on the plaintiff’s admission, but no
comments appear from the MCR that on arrival these
were moving to
Category II (ACOG) or suspicious. (FIGO).  (Dr. Kara
coincidentally referenced this as a measure to determine
that before
labour the foetus’ wellbeing was certainly not in contention.
This provided a further indication that the damage
causing event must
have been something that occurred during the plaintiff’s
labour, not before.)
[160]
At 16h00 on the 17
th
the plaintiff was diagnosed as being
in prolonged labour (latent phase) with recognized gestational
hypertension. From this point
on at least, according to Dr.
Chimusoro, a different, focused, management strategy, again guided by
the defendant’s own normative
guidelines, ought to have been
put in place. Indeed after having identified the plaintiff as a code
red patient who was especially
required to be referred to a tertiary
hospital to deal with her complications, it was counterintuitive to
then have adopted a lackadaisical
approach one she got to DNH.
[161]
Digital foetal heart rate monitoring was purportedly in place and at
least twice abnormalities were recorded (tracings
interpreted by Dr.
Chimusoro as non-reactive), even though other recordings (in-between
and afterwards) were opportunistically
latched on to by the defendant
as being reassuring.  I have elsewhere adverted to the poor
standard of reporting and the criticism
that those that had commented
upon the foetal heart rate monitoring in the vaguest of terms fell
short of the ordinary standard
of reporting on the wellbeing of the
foetus that is an imperative during the course of a patient’s
labour.  But the
fact is that the writer of these two cryptic
reports indicated that the heartrate on those occasions came close to
the bradycardia
upper limit.  I will assume that this is what
was intended to be conveyed by the range indicated at these two
moments. At
least in respect of the 09h30 recording there is the
further entry as to the plaintiff’s intrapartum resuscitation
which
gives credence to a worrying concern for the foetus’
wellbeing at this juncture.
[162]
Despite the administering of anti-hypertension medication the
plaintiff’s blood pressure was raised even
further. Even if
asymptomatic (of imminent eclampsia) as written by a doctor, I accept
Dr. Chimusoro’s reasonable suggestion
that the management of it
should have been preventative and that the possibility of the
plaintiff fitting especially kept in mind.
[163]
The success or not of the argumentation is open to interpretation
because at the end of it the foetus became stuck
in the birth canal
and the plaintiff’s contractions were no longer effective to
push her baby out.  I accept the plaintiff’s
evidence that
she was also not conscious at critical moments when her effort was
required to assist with the expulsion, an outcome
that I should
imagine was quite inevitable given what medication was being
administered to her despite the fact that her contractions
had been
gathering a momentum on their own up to a point. (It is not clear
exactly when the stimulant was introduced but it appears
to have been
after she had progressed to the active stage of labour by her own
efforts.)
[164]
The Apgar scoring was open to different interpretation but this to my
mind is a mere red herring. I have dealt
with this elsewhere.
[165]
Clear liquor was in evidence at 5h10 on the 19
th
(although
Dr. Kara disagreed that this was indicative of the fact that the
foetus was not in a non-reassuring status). The defendant
did not
deal with the conflicting entry regarding the supposed rupture of the
plaintiff’s membranes at 10h10 on the 18
th
already.
I accept that this event on its own had adverse consequences for
placental perfusion given the plaintiff’s HIV status.
[166]
The caput ++
with no moulding
(in relation to the possible
existence of CPD against the background of an extremely protracted
labour) is open to interpretation.
Dr. Chimusoro’s observation
that it was strange to report “
no moulding
” given
the obvious challenges to the foetus coming out and thereafter having
to be extracted by forceps delivery commends
itself to me.
[167]
The fact that the plaintiff was given intrapartum resuscitation at
09h30 on the 19
th
is as I have said before entirely
consistent with foetal distress.  There is simply no reason
offered by the defendant as
to why a resuscitation would have been
necessary at all if it was not significant in relation to the
management of the plaintiff’s
labour at that point in time.
[168]
Dr. Janowski was of the view that trial of labour was appropriate and
that there was no indication for a caesarean
section.  The irony
is though that those involved in the management of the plaintiff’s
labour recognized the necessity
for such a procedure but dallied.
On any reading of the situation the concerns that brought them to
this conclusion were
not kept in check afterwards as a reasonable
practitioner ought to have done.
[169]
The experts across the board all described the impact of labour on a
foetus as hypoxic-centric.  This is
because when the womb
contracts the muscles of the uterus compress the blood vessels and
the blood supply to the placenta drops
at the time when this is
happening.  After the contraction wanes, there is reperfusion
and blood flows back into the placenta
making sure that the foetus
gets enough oxygen again.  Dr. Chimusoro explained that in the
latent phase very little harm is
expected to occur because the
contractions are mild and spaced out but even these stresses can
conduce to sub hypoxia if the labour
is protracted.  This is
because in the face of a continual constriction of the vessels the
foetus will ultimately run out
of oxygen but in the ordinary course a
foetus has adequate compensatory mechanisms to bounce back.  In
the active phase of
labour the mother’s contractions are
significantly ramped up in intensity, frequency and duration so the
uterine environment
becomes naturally more of an effort.
[170]
The situation becomes uniquely challenging, so Dr. Chimusoro
explicated, when the mother suffers from hypertension
which can cause
harm to both her and the foetus. In such a situation the blood flows
into the uterus under very low pressure.
The placenta has no
real arteries.  It is just a pool where the blood circulates
slowly so when the mother’s blood pressure
goes up that flow is
interfered with and the foetus stops getting enough oxygen perfusion.
Other complications may also arise such
as bleeding between the
placenta and the uterus which can compromise the foetus even further.
These factors need to be taken into
consideration and acted upon by
ameliorating the hypoxic risk to the foetus and ensuring that it is
delivered in defined times,
not as the staff chose to do on a
provisional wait and see basis.  For this reason, so Dr.
Chimusoro noted, the caesarean
threshold is lower for a patient who
has hypertension.
[171]
He added that challenges can also arise in the case of a patient who
is HIV positive because once the protective
membrane is ruptured and
delivery does not ensue promptly, ascending infections from the
mother’s vagina can on their own
cause damage to the placenta.
He added his opinion that the risk of hypoxia is three times higher
in a mother who is HIV
positive, a notable risk factor in the
plaintiff’s pregnancy that was also confirmed by Dr. Kara’s
evidence.
[172]
There would have been an imperative to have been aggressive in
preventing the plaintiff from fitting, so Dr. Chimusoro
observed,
because this would also have involved a significant drop in perfusion
for the foetus upon such an event. As it turns
out the plaintiff in
fact fitted and intrapartum resuscitation had to be implemented
forthwith, plausibly both suggesting that
the treatment of her
hypertension had not been inadequate and that the foetus had been
driven to the very point of distress that
should have been reasonably
contemplated.
[173]
It is accepted that the plaintiff’s labour (latent phase) was
protracted or “
very prolonged
”.  Dr. Janowski
was the only expert who thought it didn’t matter and that one
should let nature take its course.
The Maternity Care
Guidelines at the time suggested that the latent phase of labour for
someone in their first pregnancy should
not have been longer than 8
hours. In Dr. Chimusoro’s view the national tolerance at the
time was 12 hours.
[174]
In the plaintiff’s situation it seems that apart from
suggesting that a caesarean section might be indicated
there was no
real investigation into the reasons for the delay and no alacrity was
shown in moving the plaintiff’s delivery
along.  Indeed no
one seemed to be concerned that she was post term and had been
suffering from raised blood pressure (with
protein indicated in her
blood 3 days before).  The size of the foetus on its own should
also have raised concerns in the
context of the duration of the
latent phase of labour, the other presenting challenges, and the
known risk factors.
[175]
It is not clear that the plaintiff’s HIV status received
appropriate recognition in the planning and management
of her labour.
There are simply no notes that give such an assurance and even Dr
Janowski failed to factor it in as a consideration
in his expert
report.
[176]
Regarding the
issue of the plaintiff’s hypertension there is no consistent
recording of this and at one stage when bloods
were interpreted there
was a conflict in the numbers reading off the same blood report.
[74]
CTG monitoring was also inadequate especially closer to the delivery,
which means that a valuable opportunity was lost to detect
if the
foetus was tolerating the labour and from what point it began to
suffer compromises which it must have for the Grade II
neonatal
encephalopathy BM presented with at birth to have exhibited itself.
[177]
I accept for present purposes that there was no Misoprostol
administered to the plaintiff, but the MCR is lacking
in clarity
concerning what medication was given and when. Dr. Janowski proffered
the explanation that Pitocin would not have been
dispensed from the
pharmacy but from the midwife’s stock as it were, which is all
the more reason why detailed notes of its
administration should have
been in evidence to satisfy the court that the plaintiff’s
contractions (in effect being managed
through the use of a stimulant
and which at some point were said to have caused a tachysystole) was
handled appropriately and professionally.
[178]
Dr. Chimusoro found fault with inadequate monitoring according to
standard operating procedure of all the necessary
milestones and
markers to confirm maternal and foetal wellbeing in the circumstances
especially of the plaintiff’s high blood
pressure that
continued in an upward trend including the absence of prompt
treatment by medication
inter alia
implicating anti-seizure
management; the absence of continuous CTG monitoring to make sure
that there was no gap or window where the foetus
was left unobserved; the absence of management by a senior specialist
or a senior
consultant or dedicated medical officer for an admittedly
complicated case; the failure to have charted a proper partogram or
to
have taken any appropriate steps when on the supposed instrument
the action line had in any event been crossed; the failure to have

had a meaningful focussed strategy plan in place; the failure to have
ruptured the plaintiff’s membranes earlier to release
the
forewaters (by latest 17 Aug  or to augment labour timed earlier
in proximity to the rupture at 10h10 of the 18
th
);
the failure in any event to have treated the recorded rupture of the
plaintiff’s waters on the 18
th
by way of an antibiotic course when delivery was
not yet imminent; the giving of a bolus of Oxytocin  (because
flooding the
plaintiff’s veins would have had  the
opposite effect  of stimulating and making the contractions more
coordinated
and might have caused receptors in the uterus that cause
oxytocin to stop working to have been blocked off); the failure
commensurate
with the recognition of foetal distress registered at
9h30 on the 19
th
to
have taken steps to immediately get the foetus out of the hypoxic
environment or the taking of other appropriate steps; the failure
to
have recognized the further indication of the slowing down of the
foetal heart rate at 11h36 and thereupon to have redirected
the plan
regarding augmentation and again to have immediately removed the
foetus from the harmful environment; and the failure
of the staff  to
have recognized the  hyper stimulation of the plaintiff’s
uterus by the augmentation.
[179]
I have dealt elsewhere with the failure of the staff to have kept
adequate notes.
[180]
The opinion of Dr. Janowski by comparison is that the management of
the plaintiff’s labour was not substandard
except before the
17
th.
He was not concerned by the number of hours
added to the plaintiff’s labour because in his view the
condition of the
baby was not compromised.  Whilst acknowledging
all the risks posed by the plaintiff being pre-eclamptic and whatever
could
go wrong, he yet defended the treatment as being adequate and
according to the textbook.
[181]
Regarding the augmentation, he was similarly alive to the reality
that the plaintiff had to be strictly monitored,
agreeing that more
frequent contractions equals the risk of foetal distress and/or
compromise.
[182]
He acknowledged that the labour graph is incomplete and filled in
incorrectly as well as the absence of CTGs to
have given a picture
after the fact of whether the monitoring ought to have raised any
alarm bells. He appreciated that the value
in these records is for
the staff to have had a graphic recording to hand of foetal heart
rates and uterine contractions exactly
with a view to acting
appropriately upon these results where necessary to promote the
wellbeing of the foetus. Concerning the manner
in which the staff
reported on the CTGs he assumed that they were appropriately trained
to say what they did (that is by only reporting
a curt conclusion)
despite the reporting not conforming to the normative standard
required for this.
[183]
For the rest, and despite the reservation expressed by him in his
summary at the outset that the incomplete records
made it difficult
for him to give a fair report he yet defended the actions of the
hospital staff as having been beyond reproach,
causing Mr. Kincaid to
contend, not unfairly in my view, that he failed to meet the high
standards required for an objective and
independent review of the
labour management.
[184]
Not only that, but he also seemed prepared to put his head on a block
that the plaintiff had as a fact not fitted
because there was nothing
in the records to this effect.  Despite the standard of the
recordkeeping which he noted in superlative
terms to be poor, he went
so far as to suggest that her evidence on his feature of her labour
experience was contrived. When it
became evident that this was a
serious consideration that the court might accept, he failed to offer
any opinion on the subject
as if it were true.
[185]
He was further adamant that the lower Apgar scores (as opposed to the
lone recording by a doctor that purported
to signal that BM was well
at birth contrary to every other indication), fell to be rejected.
[186]
This is certainly one of those instances in which the staff of the
hospital should have been called to expound
upon their treatment of
the patient, rather than leaving it to an expert to make speculative
submissions about whether they met
the requisite standard of
reasonable care predicated on a very tenuous basis.
[187]
I am satisfied
that both Drs Kara and Chimusoro’s evidence meets the required
logical reasoning standard
[75]
(the same cannot be said of Dr. Janowski’s views) and that
their views accord with generally accepted medical norms.
[188]
I add that the alternative hypotheses put forward by Prof. Bolton as
to the cause of BM’s condition (at
least the primary view that
Pathway “E” pertained based on the hospital staff’s
differential diagnosis of meningitis)
was also speculative and in
fact contraindicated by the objective MRI brain injury pattern and
the views of the expert neuro-radiologists
expressed in this regard.
Conclusion:
[189]
The failure of a
professional person to adhere to the general level of skill and
diligence possessed and exercised at the same time
by the member of
the branch of the profession to which he or she belongs would
normally constitute negligence.
[76]
[190]
Concerning the
approach to be adopted in determining the issue of negligence the
court in
Goliath
v MEC for Health
[77]
noted with reference to Lord Justice Hobhouse’s
dictum
in
Ratcliffe
that:
“
At the end of
the trial, after all the evidence relied upon by either side has been
called and tested, the judge has simply to decide
whether as a matter
of inference or otherwise he concludes on the balance or
probabilities that the defendant was negligent and
that such
negligence caused the plaintiff’s injury.  That is the
long and short of it.
”
[78]
[191]
The court noted further in this connection that:
“…
it is
important to bear in mind that in a civil case it is not necessary
for a plaintiff to prove that the inference that she asked
the court
to draw is the only reasonable inference.  It suffices for her
to convince the court that the inference that she
advocates is the
most readily apparent and acceptable inference from a number of
possible inferences (AA Onderlinge Assuransie
Assosiasie Bpk v De
Beer
1982 (2) SA 603
(A); see also Cooper & another NNO v
Merchant Trade Finance Ltd
2003 SA 1009
SCA)
”
.
[79]
[192]
I am satisfied that BM’s brain injury that predisposed him to
cerebral palsy was caused by the negligent
intrapartum care on the
part of the hospital as contended for in the plaintiff’s
particulars of claim which had a deleterious
effect on his foetal
wellbeing, leading to the final acute insult that caused the damage.
[193]
A plaintiff is not
required to establish the causal link with certainty, but only to
establish that the wrongful conduct was probably
a cause of the
loss.
[80]
[194]
When the factual premise is considered in its entirety, that is the
plaintiff’s protracted labour, the negligent
monitoring, the
failure to have properly assessed the evident risks, and the failure
to have implemented the necessary and appropriate
interventions in
proper time as the exigencies dictated, all logically in my view
contributed to and have a sufficiently close
connection with the
damage to BM that resulted.
Order:
[195]
In the result I issue the following order:
1.    The
defendant is declared liable for all such damages as the plaintiff
may prove on behalf of her minor child
who was delivered at the Dora
Nginza Hospital, Gqeberha, on 19 August 2007.
2.    The
defendant is liable to pay the plaintiff’s costs of suit to
date, which costs shall include the qualifying
and related travelling
and appearance fees of the expert witnesses retained by the
plaintiff, as well as the costs of two counsel.
B
HARTLE
JUDGE
OF THE HIGH COURT
DATES
OF HEARING
23-25
February    ,
1-2
August  & 28-29 November 2022 ,
31
January  -2 February  &
12
April 2023
DATE
OF JUDGMENT
15
March 2024
Appearances:
For
the plaintiff:
Mr.
J Kincaid together with Mr. X C Stemela, instructed by Gqeba Inc.,
East London (ref. Mr. Gqeba.).
For
the defendant:
Mr.
N D Ngadlela instructed by the State Attorney, East London (ref.
Mr M Maqambayi).
[1]
Although the particulars of claim are drawn on the basis of 3
separate distinct claims, at the commencement of the trial
plaintiff’s
counsel indicated the intention to pursue only
plaintiff’s claim founded in delict, described as claim B in
the particulars
of claim.
[2]
Neonatal
Encephalopathy and Neurological Outcome, 2
nd
Edition,
Report on the American College of Obstetricians and Gynaecologists
Task Force on Neonatal Encephalopathy (2014).
[3]
Probably
Kwadesi in Gqeberha.
[4]
No
records were available in respect of these visits.
[5]
It
is common cause that DNH is a tertiary hospital that
inter
alia
deals
with complicated obstetric cases.  According to the applicable
Guidelines for Maternity Care in South Africa issued
by the
Department of Health, 3
rd
Edition,
2007, (“
Maternity
Care Guidelines
”
)
it would have been recognized as a Level 3 hospital at the time.
[6]
This
is evidenced by a note in the DNH Maternity Case Record (“
MCR
”
)
to the effect that the person making the entry “
struggled
to apply forceps
”
.
[7]
Dr.
Kara who testified on behalf of the plaintiff described BM’s
condition in his manner.  Prof. Bolton who testified
on behalf
of the defendant agreed with this assessment adding that: “
I
could not have said it better myself
”
.
[8]
It
was assumed that this was monitoring by cardiotocograph (“
CTG
”
),
a technique used to monitor foetal heartbeat and uterine
contractions during pregnancy and labour.
[9]
This
was possibly a triage ward.
[10]
The
plaintiff expressed herself quite quaintly in English which is not
her first language.
[11]
This
action suggests the use of fundal pressure which is controversial.
It was one the grounds of negligence relied upon
by the plaintiff in
her particulars of claim but its significance (or not) was not a
focus in the expert testimony.
[12]
It
is common cause that an episiotomy was performed.
[13]
No
clinical justification emerged from this explanation given to her,
leaving the impression that the full extent of her baby’s

condition was probably withheld from her.
[14]
The
records reveal that this must have happened on 28 August 2007.
[15]
The
records were admitted into evidence on the customary basis that they
are what they purport to be.
[16]
Dr.
Janowski, paediatrician, who gave evidence on behalf of the
defendant, believed that the plaintiff was in fact “
post-dates,
”
that
is beyond her expected date of delivery upon admission to the LH.
Dr. Kara, specialist paediatrician who testified on behalf
of the
plaintiff, assumed a delivery date of 18 August 2007 and opined that
the plaintiff was post term. By all accounts the
expectation that
the plaintiff should come back on 27 September 2007 to birth her
baby was unrealistic. The gestational age was
fortunately
responsibly reassessed by a member of staff at the DNH upon the
plaintiff’s transfer there to be approximately
38 weeks based
on the fundal height of the foetus. An ultrasound scan during her
pregnancy would have put the uncertainty of
her delivery date beyond
the pale but unfortunately no scan was undertaken. It was not
suggested that the plaintiff ought to
have had a scan during her
labour, but the criticism all round was that the gestational age
assessed at the antenatal clinic
was inaccurate. This may have been
the reason why she was turned back by DNH twice before when she
presented with abdominal pain
on the basis that her baby was not yet
due to be born.
[17]
See
footnote 16. The last entry in the antenatal records on the same
date record a “
HOF
”
of
34cm.  This could perhaps have been misread as the gestational
age by the person making the opening entry at the Livingstone

Hospital.  It is coincidentally evident from the same entry in
the records of the Marselle Clinic dated 17 February 2017
referenced
in paragraph 30 above that the plaintiff herself believed that BM
had been born “premature” consistent
no doubt with what
she had been made to believe by the “
Dwesi
”
clinic
was her expected date of delivery.
[18]
The
notes of this treatment did not surface during the trial. The
plaintiff in giving the exposition of the dates may have been

confused.  She says that her first visit to DNH was on the same
day as her last routine visit but on the antenatal records
this date
was cut off in the photocopying so could not be verified. (The
original antenatal records were not provided). There
was also a
suggestion that between her second visit to DNH and her reporting to
LH a week had passed.  This too could not
be checked with
reference to formal records which ought to exist but were not made
available by the defendant. The earlier DNH
records were certainly
relevant given the plaintiff’s claim (at least in the
particulars of claim) that the hospital staff
were negligent in
failing to diagnose that she was post term and suffering with
hypertension when she presented there with lower
abdominal pain not
once but twice before going to LH.  The fact that she took
private transport to get to LH after having
been treated
dismissively by the staff at DNH who informed her that it was not
yet her time to deliver indicates the level of
the plaintiff’s
concern that something was wrong with her pregnancy as well as her
determination to have done something
about it. It was thus an
important aspect of the history for the hospitals treating her to
have taken into consideration.
(Dr. Janowski coincidentally
believed that the comment about the plaintiff’s prior
treatment related to the two occasions
during her pregnancy when she
was treated with antibiotics by the “
Dwesi
”
clinic.)
[19]
See
footnote 16.
[20]
Dr.
Chimusoro clarified that a normal blood pressure would be 140/90 and
that anything outside of this range would make the pregnancy
a
complicated one.
[21]
The
nature of this ward or relevance of the transfer was not given any
context.  If it was for special management one would
imagine
that the notes would confirm as much but since according to the
plaintiff’s testimony she was not given any treatment
there
overnight it follows logically that she was not sent there for any
meaningful objective. Dr. Chimusoro formed the view
that it appeared
that she had been cast to one side. Further and in any event she was
only scheduled for a review in 6-8 hours
which was an unacceptable
wait given her raised blood pressure and the suggestion recorded by
LH that she was slow to progress
in her labour.
[22]
Her
alarm expressed at the fact that she had received no treatment
overnight after her transfer from LH with a specific concern
having
been noted that she was hypertensive was not misplaced.  The
examining doctor upon her arrival had also indicated
that her case
should only be reviewed within 6 – 8 hours. As it turned out
13 hours lapsed before she was checked again.
[23]
These
results were gratefully expounded upon by the experts.  The
tests obviously implicate the battery of tests that would
monitor
the concern of the plaintiff’s raised blood pressure.
HELLP syndrome is a complication of high blood pressure
during
pregnancy.  The acronym stands for haemolysis, elevated liver
enzymes, low platelet count.
[24]
It
is worrying that a ward would not take the plaintiff and one is left
to surmise that this might have been because of her HIV
positive
status.
[25]
The
medication chart in the MCR confirms that Pethidine was dispensed on
the 18
th
but
no time is indicated.
[26]
This
is explained as a reference to Misoprostol which Dr. Chimusoro said
was being used off licence for induction or augmentation
and was not
recommended by its manufacturer for use in pregnancies with viable
foetuses.  Dr. Janowski, specialist obstetrician
and
gynaecologist, who testified on behalf of the defendant pointed out
that the DNH MCR does not support any suggestion that
the pharmacy
ever dispensed it.
[27]
The
blood pressure reading here coincides with the entry made at 20h10
so probably times the review entry by Dr. Blignaut to have
been made
at this juncture.
[28]
According
to the 2007 Maternity Care Guidelines this would have heralded the
start of the active phase of labour for the plaintiff.
[29]
The
expert evidence suggested that this is standard treatment for
gestational hypertension, well at least for moderate cases and
that
the medication is slow acting. Dr. Chimusoro explicated that Adalat
was more rapid acting.  He thought it more appropriate
that the
plaintiff be treated as if her blood pressure was veering toward the
severe range.  He noted that the highest he
has seen was
150/105 which was still in the “
upper
moderate range
”
but
was concerned by the “
unconfirmed
issue
”
in
the clinical notes that she had fitted.  The medication chart
in the MCR coincidentally references a script for Adalat,
also dated
17 August 2007, if a certain (illegible) contingency materializes,
but it does not appear that this medication was
in fact given to the
plaintiff.
[30]
The
evidence established that a CTG referred to as reactive is one that
suggests no compromise to the foetus after a contraction.
It
is reassuring in its nature.
[31]
This
entry was noted by Dr. Chimusoro to be inconsistent with the next
entry.  Also confusing is the indication that the
plaintiff’s
membranes were ruptured because elsewhere it is noted that the
artificial rupture occurred only on the 19
th
.
The plaintiff did suggest in her testimony that around this time
some waters leaked out which she was informed meant that her
water
had broken. Dr. Chimusoro explained that this may have been hind
waters but the timing was important because there was
a risk to her
foetus by any kind of rupture which would have meant that it was no
longer in a sterile sac.  Indeed it would
by the breach of its
safe environment from that point have been rendered vulnerable to
ascending infections in the plaintiff’s
vagina, and to the
risk of transmission of the HIV virus. He proposed that two steps
were not taken that would have made a difference.
The first is
that the plaintiff should have been treated with antibiotics
(assuming a pre-screening for infection(s)) and the
second is that
counting from that moment, augmentation should have commenced to get
the baby out or put another way, the decision
to deliver ought to
have been contemplated right then and there.
[32]
There
are two conflicting times indicated in respect of this entry. The
second time written opposite the same entry is “
23:45
”
.
The handwriting is different but what is written also encroaches on
to the entry of Dr. Lamprecht and overwrites his/her signature

suggesting that it may have been made after the fact and was
squeezed into a gap between entries.  (Prof. Bolton does not

reference these entries in his report which may suggest that his
copy of the MCR did not have these two entries on the page at
all.)
[33]
This
is a reference to Magnesium Sulphate (commonly known as Epsom Salts)
which Dr. Chimusoro explained is the standard international

medication used to prevent fits in pregnant women when they are in
labour or when they get hypertension.  He emphasized
the point
that it is given preventatively and not when the patient is fitting
already.
[34]
Dr.
Chimusoro opined that whilst on the Syntocinon infusion the
plaintiff ought to have been on
continuous
CTG.
[35]
Dr.
Chimusoro remarked that the Syntocinon infusion had been running
from 5h10 already.
[36]
Dr.
Chimusoro suggested that Pitocin and Oxytocin were one and the same
stimulant.
[37]
In
his view this was not the correct way to administer the stimulant as
something squirted into the plaintiff’s vein.
Instead it
is supposed to be a slow infusion.
[38]
The
evidence revealed that this CTG and the one referenced in paragraph
57 above were non reassuring.  Dr. Chimusoro’s
opinion
was that the event recorded at 09h30, taken together with the drop
in the foetal heart rate range between “
100
– 160
”
,
should have raised concerns that there was foetal distress at this
juncture.
[39]
See
footnote 36.  This is the second indication according to Dr.
Chimusoro’s opinion that the foetal condition was
non
reassuring.
[40]
Dr.
Janowski was the only specialist to suggest that these scores might
be authentic whereas everyone else agreed that they were
unrealistic
and inconsistent not only with what the nurses had recorded but also
with the fact that the baby was said to have
been flat and only
resuscitated after about 15 minutes. In my view a discussion of them
is unnecessary.  If the defendant
wished to make out a case
that the doctor’s inconsistent entry should have any cogency
she should have adduced this person’s
testimony.
[41]
Evidence
suggested that this medication would be given to reverse the opioid
effect of the Pethidine given.  It is hard to
make sense of the
entries regarding when Pethidine was dispensed and how much exactly.
The medication chart in the MCR indicates
a single dose of 75mg stat
given on the 18
th
and
nothing else. It was supposed to have been given 8 hourly. Dr.
Chimusoro proffered his view that the plaintiff was probably
not
sleeping on the morning of the 19th but that she was “
woozy”
from
Pethidine because by then she was already in the active stage of her
latent phase of labour and 4-5 cm dilated so would hardly
have been
naturally sleepy or inclined to want to sleep at this juncture.
[42]
This
assessment was repeated on the 20
th
.
[43]
Dr.
Kara testified that it was hugely unlikely that there were no signs
of respiratory distress if there was also at the same
time
“
subcostal
recession
”
recorded
by the nurses upon BM’s admission to the ward. See par [66].
[44]
This
is a drug used for anti-seizure management.
[45]
By
all accounts this was for a shorter than usual period of 14 days
applicable at the time.
[46]
See
page 51 of the medical records, Bundle B1.
[47]
There
are 16 entries recorded.
[48]
The
two pages of notes of the 18
th,
for
example.
[49]
[1998]
EWCA Civ 2000
(11 Feb 1998) at para 48
[50]
2018
ZAGPPH JHC 513 (1 October 2018) SAFLII.
[51]
Each
of the experts testified to the hypoxic strain placed on a foetus in
utero during contractions. See further par [169] explaining
the
unique features and risks that pertain during labour especially.
[52]
This
would have been with reference to the baby’s size and weight
and the fact that the plaintiff was probably beyond her
date for
delivery.
[53]
The
acronym means Peri Rolandic, Basal Ganglia & Thalamus.
[54]
Mr.
Kincaid placed on record before closing the plaintiff’s case
that there was “
no
controversy
”
in
respect of the joint minute of the radiologists and that their
respective reports and recorded agreement could go in as a
reflection of the evidence that they would have testified to at the
trial.
[55]
“
Intrapartum
Basal Ganglia – Thalamic Pattern Injury and Radiologically
Termed “Acute Profound Hypoxic-Ischemic Brain
Injury”
Are Not Synonymous
”
Johan
Smith
et
al,
PubMed
(Dec 2020), also accepted for publication in the American Journal of
Perinatology.
[56]
Dr.
Kara explained that an “
insult
”
is
the event that occurs that can lead to an injury, but that it may
not.
[57]
This
is in my view exactly the kind of scenario in contention here.
[58]
See
Smith
et
al
,
Supra
,
where the following is stated: “
This
paper supports the notion that with appropriate intrapartum care and
timeous reaction to FHR abnormalities and action in
the form of
intrapartum resuscitation and expedited delivery, in the majority of
cases adverse BGT pattern injury would have
been prevented.”
[59]
Mr.
Kincaid at a point before closing the plaintiff’s case placed
on record that he was awaiting the defendant’s instructions
in
respect of Dr. Viljoen’s report (to which there had been no
corresponding report from the defendant).  When the
matter
resumed after a long break I was informed from the bar that Dr.
Viljoen would not be testifying so I assumed that the
contents of
his report was no longer in contention. With hindsight though I did
not enquire from Mr. Ngadlela, who appeared for
the defendant, as to
the status of the report in the evidentiary context.  There was
however no countervailing evidence
adduced by the defendant that the
causal potentiate for BM’s brain injury was generic or
hereditary or congenital.
[60]
Prof.
Bolton stepped into the breach.
[61]
I
clarify that the parties agreed in the pre-trial processes that the
reports of the experts who could not avail themselves to
testify for
varying reasons would not amount to evidence, but the joint minute
already finalised as between the paediatric specialists
by then
obviously bound the parties to their agreement.
[62]
The
ensuing detail is derived from the expert reports of the
corresponding obstetricians which in turn reference the summary of

the ACOG Consensus Statement and the standard textbook on the
neurology of the newborn by Volpe.
[63]
Neurology
of the Newborn, 2017, Sixth Edition.
[64]
This
quote is referenced from Dr. Kara’s expert report.
[65]
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].
[66]
Lee,
supra at
para
[37] – [58]
[67]
Mashongwa
v PRASA
2016
(3) SA 528
(CC) at [65];
AN
v MEC for Health, Eastern Cape
[2019]
ZASCA 102
at
[8]
.
[68]
Lee
supra
at
[39]
[69]
Oppelt,
supra
,
at [35];
Mashongwa,
supra
at
[65]
[70]
This
view was based solely on his interpretation of the blood report even
though there was no culture of the organisms done that
would have
definitively clarified the issue. It is common cause that specimen
extracted from BM’s spine had traces of blood
in it and that
it was not adequate for its purposes.
[71]
As indicated
elsewhere Dr. Reddy was not called to testify and Prof. Bolton
stepped into the breach. The agreement recorded by
her with Dr. Kara
however bound the parties and dictated the premise going forward.
[72]
This
diagnosis pertains to the plaintiff’s separate claim for
damages arising from the hospital staff’s failure to
have
prevented the mother to child transmission of HIV (Claim C). This
has no bearing for present purposes.
[73]
It
is common cause that there were only two CTG tracings leaning toward
an indication of foetal compromise at 09h30 contemporaneously
with
the intrapartum resuscitation, and shortly afterwards at 11h36, but
I have elsewhere stated that these recordings (at least
according to
the plaintiff’s experts) support an inference that there was
foetal distress at these moments.
[74]
The
blood reports themselves were not provided at the trial.
[75]
Michael
and Another v Linksfield Park Clinic (Pty) Ltd and Another
2001
(3) SA 1188
at [36]
[76]
Goliath
v MEC for Health, Eastern Cape
2015
(2) SA 97
SCA.
[77]
Supra
at
para 8.
[78]
Supra
at
par 18.
[79]
Supra
at
par 19.
[80]
Minister
of Safety and Security v Duivenboden
2002
(6) SA 431
(SCA) at par [25].