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[2012] ZAGPJHC 217
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Makgomarela v Premier of Gauteng and Another (2011/35273) [2012] ZAGPJHC 217 (1 November 2012)
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NOT REPORTABLE
SOUTH GAUTENG HIGH COURT
JOHANNESBURG
CASE NO: 2011/35273
DATE:01/11/2012
In the matter between:
MAKGOMARELA, VIRGINIA ITUMELENG
…....................................
Plaintiff
(on behalf of KM)
and
THE PREMIER OF
GAUTENG
.............................................................
First
Defendant
MEC FOR
HEALTH
................................................................................
Second
Defendant
J U D G M E N T
LAMONT, J
:
[1] The plaintiff instituted
proceedings against the two defendants in her personal and
representative capacity as guardian and
mother of her minor child.
The plaintiff claimed damages arising out of alleged negligent
conduct on the part of the defendants
which resulted in the baby
being born with cerebral palsy.
[2] The parties agreed to
separate the questions of merits and quantum and I will make the
relevant order.
[3] The plaintiff after a normal
pregnancy was admitted to hospital on 8 December 2005 at 17h30. The
plaintiff remained overnight.
The next morning at approximately 11h00
she was examined. During that examination she disclosed that she was
approximately 42 weeks
pregnant. Various tests were conducted
including a CTG (Cardiotachograph). A decision was made to
administer four Prostin tablets
to induce labour. The tablets were
administered during approximately 11h00. The plaintiff was next
monitored at 20h10 at which
time she was moved to the labour ward.
At 20h45, 21h45 and 22h45 she was again monitored. There was no
further monitoring until12h50
by which time the plaintiff was in the
second stage labour. The time of the delivery was 01h00 with the end
of the third stage
at 01h10. After birth the baby was examined by a
doctor; the baby was resuscitated, a drip was inserted, oxygen was
administered
and the baby was transferred to the neonatal intensive
care unit. One minute after birth the baby’s Apgar was 6; 5
minutes
after birth it remained at 6; 10 minutes after birth it
became 7. The baby at birth was floppy, sucked poorly and did not
cry.
The baby was sent to the radiology unit within the hospital with
a note reflecting that the clinical findings were that birth asphyxia
had occurred. At 01h28 the baby’s pH was 7.178 and acid base
status -19.8 mmol/L.
[4] Until the baby was
discharged the symptoms persisted; the baby from time to time
received oxygen, had fits continued not to
suck well and was
distressed. On the day of discharge it was recorded that the baby was
well recovered, but neurological state
and sucking were to be
followed up.
[5] During May 2006 the baby
fitted. An examination revealed that the baby was suffering from
cerebral palsy. This was the first
time cerebral palsy was diagnosed.
PROSTIN
[6] The plaintiff was given four
0,5 mg Prostin tablets to induce labour. The guidelines published
during March 2002 which reflect
the standard treatment read as
follows:
“
Ripening of the cervix
This is necessary when the cervix is unfavourable for induction
(unaffected or difficult to rupture membranes or by bishop scoring).
Establish foetal well-being with a CTG tracing before starting
cervical ripening.
Give intravaginal prosteglandin E² 1 mg (e.g. tablets),
repeated after six to twelve hours.
If possible, run a CTG tracing 30 to 60 minutes after inserting
prostaglandin.
When the cervix is ripe (favourable for induction), induce
labour.
”
The aforegoing represents the treatment to be applied by the medical
staff.
[7] The reference to prostaglandin is a reference to a hormone
contained within the Prostin tablets.
7.1 Prostin may only be administered to patients who are not in
labour. The plaintiff was in labour at the time she was given Prostin
and she should not have been treated in this way.
7.2 The plaintiff having been given four tablets was given double the
dose which should have been administered (2 mg instead of
1 mg). The
dose represents four times the dosage recommended by the manufacturer
of the drug (0.5mg).
7.3 The danger inherent upon treating patients with Prostin is that
there can be hyperstimulation. An excessive dosage can result
in the
patient having too many contractions which are too strong too close
together and which occur too quickly. The consequence
of the
excessive number of strong contractions occurring too quickly is that
the baby is unable to recover between the contractions.
The mechanism
causing the baby distress is the reduction of blood flow to the baby
during each contraction. In consequence of the
reduced blood flow the
heart of the baby slows down (known as a deceleration). The oxygen to
the baby is carried in the blood.
If the blood flow reduces the
oxygenation of the baby reduces. If the baby is affected and does not
recover the baby can become
hypoxic. Hypoxia is a state of
inadequate oxygenation. The excessive administration of Prostin
accordingly can result in the
baby being under-oxygenated and in
consequence suffering harm. This is particularly so if Prostin is
administered when labour has
already begun.
MONITORING
[8] Hypoxia is a recognised side
effect of the administration of Prostin to a patient. It is for this
reason that the procedure
set out above requires an initial CTG
reading and subsequent readings to be taken 30 to 60 minutes after
the Prostin has been inserted.
If CTG tracings are taken then it is
possible to determine whether or not the baby is in distress and
accordingly take steps to
deal with such distress. If no CTG reading
can be taken the monitoring must be manually done.
[9] The view of the expert Dr
Pistorius called on behalf of the plaintiff was that it is common
practice for the manual readings
to be taken at 30 minute intervals.
[10] The Department of Health
March 2002 Guidelines for Maternity Care which is referred to above
sets out additional requirements
insofar as monitoring is concerned.
Routine monitoring of the first stage of labour requires in respect
of the foetal condition
that the foetal heart rate be measured
half-hourly before, during and after each contraction (para 6).
[11] The same document requires
that if the pregnancy is post-dates (i.e. the pregnancy exceeds 40
weeks gestation) that additional
monitoring take place. That
monitoring includes monitoring the foetus during labour with CTG if
it is available (it was available
and was not used save as set out
above). At the time of the admission of the plaintiff to the hospital
the height of fundus was
measured at 38 weeks. This indicates a two
week premature foetus. On the next day however the plaintiff
furnished information
that she believed she was 42 weeks pregnant.
Accordingly the treating doctors from that time forward had reason to
suspect that
the plaintiff was post-dates and should have been put on
guard that they were dealing with a post-dates pregnancy. They should
have taken steps to deal with the worst scenario namely that
plaintiff was 42 weeks pregnant. The monitoring which was required
should have been performed every 30 minutes to an hour by way of each
monitoring occasion requiring three readings being taken
and
considered.
[12] The only labour partogram
monitoring took place at 20h45, 21h45 and 22h45. That labour
partogram reflects a normal baby.
No monitoring took place between
22h45 and birth at 00h50 to 01h00.
HYPOXIA
[13] It is probable that the baby
was hypoxic at birth:
She was diagnosed as such.
She was administered treatment to resuscitate her. That
treatment included administration of oxygen and fluids.
She was floppy.
She had poor sucking reflex.
She was blue in her extremities.
She did not cry.
She was sickly and was immediately sent to the intensive care
unit (indicating that the treating doctor regarded her condition
as
requiring that treatment).
BLOOD GAS READINGS
[14] The baby’s blood gas measured 28 minutes after birth,
measured at a pH of 7.178 and a base deficit of 19.8 mmol/L. These
measurements are relevant to demonstrate hypoxia. If a baby is
hypoxic it burns glucose to produce energy. This burning of glucose
produces acid. This is the reason why the more hypoxic the child the
more acidic the blood gas and acid base status.
[15] The readings were taken 28 minutes after birth. The readings are
accurate as to the baby’s condition at that time. They
do not
reflect the baby’s blood gas at birth as they reflect the
improved state of the baby after treatment and the lapse
of 28
minutes. The treatment of the baby between the time of birth and the
time of taking the test, including giving the baby
oxygen and fluids.
The effect of this treatment is to raise the pH level and reduce the
negative acid base level. Accordingly
although the exact reading
cannot be established the pH level at the time of birth prior to
treatment was lower than reflected
in the blood gas tests.
[16] In the morning after the birth at 09h53 tests were taken and the
pH of the baby’s blood gas had improved to 7.36 (indicating
that the baby had been hypoxic at birth) and the baby’s acid
base status had reduced to -9,4 mmol/L. An acid base status
of
between -12mmol/L indicates asphyxia depending on which experts view
is followed. An acid base level of -19.8 mmol/L reflects
that the
baby was hypoxic at birth on any experts approach. It is possible to
determine what the levels were at birth i.e. prior
to the treatment
slightly more accurately by considering the acid base level rate of
change as the acid base level changes more
slowly than the pH reading
rate of change. Hence the later reading of the acid base level will
more accurately reflect the extent
of the hypoxia at birth. The acid
base level was extreme even 28 minutes post birth and after treatment
hence the pH level must
have been much lower than reflected. It is
impossible to scientifically accurately perform any calculation.
[17] On the probabilities the
baby suffered hypoxia in consequence of the treatment administered
during the course of the birth.
On the probabilities the pH level
was less than is reflected at 28 minutes after birth as the baby’s
condition would have
improved in between. It was much closer to 7 and
could well have been less than 7.
EFFECT OF POOR MONITORING
[18] Had the mother and baby
been monitored as required the monitoring would have yielded data
which would have enabled the medical
team to intervene at an early
stage so as to prevent hypoxia occurring. A CTG could have been used
to effect tracings on a continuous
basis as such was available at the
hospital.
[19] Had the baby and mother
been monitored and managed in accordance with the standard required
the hypoxia would not have occurred
as the deceleration in the heart
rate (reflecting lower blood supply) would have been noticed. The
rate and extent of the baby’s
recovery after each contraction
would have been known. This data would have enabled the treating
staff to make and timeously act
on informed decisions. They disabled
themselves from being able to do so due to their poor monitoring.
[20] The experts are
ad
idem
that the
management of the labour was not in accordance with practice and that
the decision to administer Prostin was incorrectly
made.
[21] Even after the baby had been treated with oxygen and its oxygen
levels were restored the baby suffered from fits and/or convulsions
and poor sucking reflexes; it remained floppy; was mildly distressed
and on the day before discharge was administered oxygen. The
discharge document reflects the baby as being in a stable condition.
It is apparent that notwithstanding that note that the baby
was still
being treated by use of phototherapy and had recently been treated
oxygen supply indicating a poor respiration. The
expert called by
the plaintiff indicated that he was of the view that the baby had not
recovered on discharge. The expert called
by the defendants indicated
that the baby had recovered fully and was in a stable condition. It
is my view that the defendants’
expert failed to have regard to
the proximity of other treatment and the fact that the baby was not
well. In choosing to rely on
the recordal being stable and
disregarding this evidence he erre.
[22] Subsequent to discharge and during May 2005 the baby again
commenced suffering from fits. It appears that the fitting of
the
baby was controlled at the time of the discharge but that fitting
re-appeared during May/June 2005.
[23] Subsequent tests revealed that the baby suffered from cerebral
palsy.
[24] It was common cause between the experts that the fact that
cerebral palsy was not diagnosed until May/June 2005 is not
indicative
of the fact that cerebral palsy did not exist at the time
of birth or before.
[25] “Cerebral palsy which is characterised by non-progressive
abnormal control of movement or posture may not be diagnosed
until
months or years after birth. Retrospective review of the pregnancy
records often cannot show any obvious antenatal cause
because foetal
brain development and function cannot currently be routinely
visualised or monitored. Complications occurring in
the antepartum
period common and important causes of cerebral palsy.
Epidemiological studies suggest that in about 90% of cases
intrapartum hypoxia could not be the cause of cerebral palsy and that
in the remaining 10% intrapartum signs is compatible with
damaging
hypoxia may have had antenatal or intrapartum origins. These studies
show that a large proportion of cases are associated
with maternal
and antenatal factors such as prematurity, intrauterine growth
restriction, intrauterine infection, foetal coagulation
disorders,
multiple pregnancy, antepartum haemorrhage, bridge presentation and
chromosomal or genital anomalies”. See the
article headed
Education and Debate
BMJ 8 August 2006 page 1055. In the
article it is recognised that in individual cases it is very
difficult to identify retrospectively
whether or not there were
antenatal causes of cerebral palsy. Damaging hypoxia occurring
during labour can be suspected from any
clinical signs none of which
are specific to the damaging hypoxia and which could therefore
reflect other conditions of the foetus.
Clinical science and
objective investigations need to be considered to attempt to
ascertain more reliably what caused the hypoxia.
[26] The timing of the cause of the neuropathology causing the
cerebral palsy could take place pre-birth, during the birth or
subsequent to the birth. The mother gave evidence and excluded any
cause which may have arisen subsequent to the birth of the child.
The
child was well fed, did not choke and suffered no injury. Whatever
the cause was it is not occur subsequent to birth.
[27] Prior to birth the baby suffered no injury, there was no
relevant infection (such infection as there appears to have been
was
a urinary tract infection which does not cross the placenta). The
only possible cause which there could have been prior to
birth was
intrauterine growth restriction. The evidence which it was submitted
demonstrated intrauterine growth restriction was
the rate of change
of weight of the mother during the pregnancy as recorded in the
charts of the clinic, as also the rate of change
of the fundus
height. The fundus height should grow at a rate of 1 cm per week.
DATE
WEIGHT
HEIGHT
WEEKS
5 June 2005
50 kilograms
8 July 2005
50 kilograms
4 weeks
5 August 2005
52 kilograms
28 weeks
26 August 2005
55 kilograms
2 September 2005
55 kilograms
33 weeks
23 September 2005
55 kilograms
33 weeks
7 October 2005
54 kilograms
34 weeks
28 October 2005
56 kilograms
35 weeks
4 November 2005
55 kilograms
36 weeks
2 December 2005
60 kilograms but weeks
queried (referred for gestational age)
38 weeks
28 October 2005
35 weeks
[28] The submission was that the
weight change reflected a poor rate of growth of the baby. The poor
growth could be occasioned
so the submission went by intrauterine
restriction. The submission was that the rate the baby grew as
represented by the height
of fundus was not constant, did not
increase at the correct rate and was an indication that there could
have been intrauterine
restriction.
[29] The evidence against the
submission and facts which founded it consists of the following:
29.1 There was never any attention drawn to an abnormal rate of
change of the baby as to height or weight when the plaintiff attended
the clinic which she regularly did as and when required.
29.2 The records themselves appear to be inaccurate in a number of
respects particularly for example with regard to the transposition
of
the numbers from a number to a graph. This is indicative in my view
of potential inaccuracies relating to the taking of the
data and is
generally a warning that the document is to be approached cautiously.
29.3 An examination of the brain of the baby at approximately the
time of birth indicates no abnormalities. If any abnormalities
had
been occasioned during the pregnancy such should have evidenced in
the test.
29.4 At the time the cerebral palsy was discovered a scan of the
brain reflected a nature and extent of deterioration of the brain
consonant with the injury being occasioned approximately at the time
of birth.
[30] The suggestion that there was pre-existing injury to the baby
at the time of birth is in my view highly speculative and appears
on
analysis of the facts on their own relating to likelihood of the
event occurring to be unlikely.
[31] The likelihood of damages prior to birth cannot be excluded if
one has regard to the postulates. The facts relating thereto
when
considered alone are unlikely to have caused the cerebral palsy.
[32] It remains to consider the probability of the cerebral palsy
having been sustained during the hypoxic incident at birth.
The
scientific opinion is that cerebral palsy caused by an intrapartum
hypoxic event is established if three essential criteria
are present.
The essential criteria are:
Evidence of a metabolic acidosis in intrapartum foetal umbilical
arterial cord or very early neonatal blood.
Early onset of severe or moderate neonatal encephalopathy in infants
of greater than 34 weeks’ gestation.
Cerebral palsy of the spastic quadriplegic or dyskinetic type.
[33] “All three of the essential criteria are necessary before
an intrapartum hypoxic cause of cerebral palsy can begin
to be
considered. If any one of the essential criteria is not met it
strongly suggests that intrapartum hypoxia was not the cause
of the
cerebral palsy. If blood gas data are not available it cannot be
assumed from other signs that hypoxia was present at birth
since
these signs lack specificity either individually or as a group. When
all three essential criteria are met it is then necessary
to
determine whether the hypoxia was acute or chronic. If evidence for
some of criteria 4 to 8 is missing or contradictory the
timing of the
onset of the neuropathology becomes increasingly in doubt.
Individually, these latter criteria are only weekly associated
with
an acute intrapartum damaging hypoxic event because … they may
be caused by other factors such as infection. Logically
most of the
final five criteria would have to be present for the balance of
probabilities to suggest an acute timing to the hypoxic
event.
Contrary evidence rather than missing evidence – for example a
normal Apgar score at 5 minutes – would weigh
against a serious
acute event”. See Article labelled
Education and Debate
British Medical Journal
1999 319: 1054-9.
[34] The criteria which together suggest an intrapartum timing but
by themselves are non-specific include:
“
4. A signal hypoxic event occurring immediately before or
during labour.
5. A sudden rapid and sustained deterioration of the foetal heart
rate pattern usually after the hypoxic signal event where the
pattern
was previously normal.
6. Apgar scores are 0 to 6 for longer than five minutes.
7. Early evidence of multi-system involvement.
Early imaging evidence of acute cerebral abnormality.
”
[35] Of the criteria which are essential to define acute event items
1, 2 and 3 are all present save in respect of the pH. The
pH level
was found to be as set out above at 7.178, 28 minutes after birth.
The acid base deficit far exceeded requirement and
was at -19.8
mmol/L. The question which arises is whether or not one of the
criteria is missing in that the pH level was above
the level of 7.00
as required. The pH level was only above the level required some 28
minutes after birth and after oxygen and
other resuscitation had been
administered to the baby. The base deficit indicates a severe hypoxia
even after treatment. The base
deficit changes more slowly than the
pH. Not only is the pH reading inaccurate in that it measures the
state of the baby’s
blood after treatment but it is ineffective
in that it is taken at the wrong time. It is not possible to
extrapolate backwards
with any degree or certainty. The expert
evidence was limited to a suggestion that the pH was less than what
was found.
[36] As to the criteria which would suggest an intrapartum timing
for the hypoxia item four was present, item five was not measured,
item six was present, item seven was present and item eight was
established at the time the brain was examined in 2006. (During
June
2006 the radiology of the brain reflected bilateral hypodensities
involving mainly grey matter in parietal globes indicating
atrophy).
[37] The approach of a court to evidence of opinions expressed by
experts is set out in
Michael and Another v Linksfield Park Clinic
(Pty) Ltd and Another
2001 (3) SA 1188
(SCA) at 1200.
“
[36] That being so,
what is required in the evaluation of such evidence is to determine
whether and to what extent their opinions
advanced are founded on
logical reasoning. That is the thrust of the decision of the House of
Lords in the medical negligence case
of Bolitho v City and Hackney
Health Authority
[1997] UKHL 46
;
[1998] AC 232
(HL (E)). With the relevant dicta in
the speech of Lord Browne-Wilkinson we respectfully agree.
Summarised, they are to the following
effect.
[37] The Court is not bound
to absolve a defendant from liability for allegedly negligent medical
treatment or diagnosis just because
evidence of expert opinion,
albeit genuinely held, is that the treatment or diagnosis in issue
accorded with sound medical practice.
The Court must be satisfied
that such opinion has a logical basis, in other words that the expert
has considered comparative risks
and benefits and has reached a
defensible conclusion (at 241G - 242B).
[38] If a body of
professional opinion overlooks an obvious risk which could have been
guarded against it will not be reasonable,
even if almost universally
held (at 242H).
[40] . . . This essential
difference between the scientific and the judicial measure of proof
was aptly highlighted by the House
of Lords in the Scottish case of
Dingley v The Chief Constable, Strathclyde Police 200 SC (HL) 77 and
the warning given at 89D
– E that
"(o)ne cannot entirely
discount the risk that by immersing himself in every detail and by
looking deeply into the minds of
the experts, a Judge may be seduced
into a position where he applies to the expert evidence the standards
which the expert himself
will apply to the question whether a
particular thesis has been proved or disproved - instead of
assessing, as a Judge must do,
where the balance of probabilities
lies on a review of the whole of the evidence.'
It is well established that
what is expected of a medical practitioner is the general level of
skill and diligence possessed and
exercised at the time by members of
the branch of the profession to which he belongs. Van Wyk v Lewis
1924 AD 438
at 444”.
[38] A court is required to assess all the evidence which it has
before it with a view to establishing whether it is possible
to
assess what probably caused the event.
[39] There is no probable evidence founding any of the suggestions
made by the defendant as to the cause. I have dealt with this
issue
supra
. In considering the evidence of whether or not the
hypoxic event was sufficient to cause the cerebral palsy it appears
to me that
in all probability notwithstanding scientific evidence
that the pH was less than 7 that it was either in fact less than 7,
or else
in this particular case the pH was sufficiently low for the
criteria to have been sufficiently present.
[40] The only event which occurred which probably could have resulted
in the cerebral palsy was the hypoxic event at birth.
[41] The treating personnel did not maintain the general level of
skill and diligence possessed and exercised at the time by the
members of the branch of the professions to which they belonged (see
Van Wyk v Lewis
1924 AD 438
at 444).
[42] The monitoring was substandard. Had the monitoring taken place
as is required the distress of the baby would have become
apparent
and other procedures could have been adopted. The insertion of
Prostin was ill-advised and not in accordance with general
practice
in that the administration was not called for at all and inasmuch as
the dose exceeded the recommended dosage. The treating
staff ware
faced with a patient and baby which required special attention. There
was reason to believe that the baby was post-dates.
Having
administered Prostin, special management and observation were
required during the course of the delivery monitoring which
could and
should have taken place did not take place. The treatment was so
inadequate that the relevant data required to assess
the acidity at
the time of birth was not taken.
[43] In my view negligence has been established. In consequence of
that negligence the baby suffered a hypoxic event at birth
causing
the cerebral palsy.
[44] I accordingly find that the plaintiff has established liability.
[45] I make the following orders.
The issue of liability and quantum are separated.
The defendants are liable to pay damages to the plaintiff in such
amount as the plaintiff is able to establish at the resumed
hearing.
The balance of the trial is postponed sine die.
The defendants are to pay the costs of the action including the
qualifying fees of Dr. Pistorius.
_____________________________
C.G. LAMONT
JUDGE OF THE SOUTH GAUTENG
HIGH COURT, JOHANNESBURG
COUNSEL FOR THE PLAINTIFF: GARY AUSTIN
PLAINTIFF’S ATTORNEYS: GARY
AUSTIN INC
COUNSEL FOR THE DEFENDANTS: P.M. MTSHAULANA SC
DEFENDNANTS ATTORNEYS: THE STATE
ATTORNEY
DATE/S OF HEARING: 12
October 2012
DATE OF JUDGMENT: 1
November 2012