L P v Bloy (2658/2014) [2020] ZAGPJHC 185 (28 May 2020)

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[2020] ZAGPJHC 185
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L P v Bloy (2658/2014) [2020] ZAGPJHC 185 (28 May 2020)

SAFLII
Note:
Certain
personal/private details of parties or witnesses have been
redacted from this document in compliance with the law
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SAFLII
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IN
THE HIGH COURT OF SOUTH AFRICA
(GAUTENG LOCAL
DIVISION,JOHANNESBURG)
REPUBLIC OF SOUTH AFRICA
Case
number: 2658/2014
In
the matter between:
P,
L.
F.
Plaintiff
and
DR
B. M
BLOY
Defendant
JUDGMENT
BHOOLA
AJ:
Introduction
[1]
The plaintiff claims damages from the defendant arising from the
standard of care and treatment rendered to her from February
2011 to
September 2012, which she alleges resulted in her suffering various
sequelae
. At the commencement of the trial an order was
granted in terms of Rule 33(4) separating the issue of liability from
the determination
of quantum, and postponing the determination of
quantum
sine die.
The matter proceeded on the issue of
liability only.
The
plaintiff's pleaded case
[2]
The plaintiff, who was 43 years old at the time and employed as a
credit controller at Servest Landscaping, pleads that she
was
admitted to the Flora Clinic under the care of Dr Becker on 4
February 2011 after having presented with atypical chest pain.
This
was investigated and she underwent a coronary angiogram, the results
of which were normal. She was discharged on 24 February
2011.
[3]
The plaintiff alleges that she was under the care of the defendant
during this period. It is common cause that she was diagnosed
with
Addison's disease (“Addisons”
)
by the defendant
during this time. Addisons is an adrenocortical insufficiency due to
dysfunction of the adrenal gland, which does
not produce enough of
the hormones cortisol and aldosterone, and is a life threatening
condition. She alleges that the diagnosis
was made without proper
investigation, and purportedly on the results of two blood tests
performed on her at the defendant's request.
After the defendant
diagnosed her with Addisons he placed her on corticosteroidal
medication (commonly referred to as "steroids")
called
Covocort (a hydrocortisone) and Florinef (a fludrocortisone). This
medication will be referred to herein as "steroid
medication"
or "steroid therapy". The defendant explained to the
plaintiff that Addisons is a life threatening condition
and that she
will require lifelong steroid replacement therapy.
[4]
The plaintiff alleges that after she commenced the steroid therapy
her condition in general gradually deteriorated. She was
medically
boarded in May 2012 following the defendant's declaration of her as
medically unfit to continue in her employment. She
alleges that she
was on the prescribed steroid medication for approximately 18 to 19
months.
[5]
The plaintiff alleges in her particulars of claim that she complied
with the medication regime prescribed by the defendant until

September 2012. She further alleges that the steroid medication
interfered with her immune system thus disposing her, over the

prolonged period that she took the medication, to the development of
certain infections, with tuberculosis ("TB
"
) being
one of them.
[6]
On 6 September 2012 the plaintiff attended the Chris Hani Baragwanath
Hospital ("CHB") as a result of elevated blood
pressure. At
this stage she was no longer on a medical aid scheme and could not go
to a private hospital. She had stopped taking
the steroid medication
prescribed by the defendant about approximately a month before her
visit to CHB.  At CHB, under the
care of Professor Huddle, a
Long Synacthen Stimulation Test (“Synacthen test”) was
performed on her.  This test
is known as the gold standard test
for purposes of diagnosing Addisons.  The results were
negative.  Professor Huddle
directed that the plaintiff should
gradually be withdrawn from the steroid medication.
[7]
According to the plaintiff, she was then referred to the Rheumatology
Clinic where all her symptoms were diagnosed as being
secondary to
the steroid usage and not to any other underlying rheumatological
condition. The plaintiff was given Zolmeta infusion
for osteoporosis.
A magnetic resonance imaging ("MRI") scan of her brain was
performed and was found to be normal apart
from periventricular
changes but an MRI scan of her cervical spine revealed degenerative
changes.
[8]
In November 2013 the plaintiff attended the Helen Joseph Hospital.
She was found to have cervical lymphadenopathy on the
right hand side
that on biopsy proved to be secondary TB. She alleges that she was
also diagnosed with neurological symptoms in
her lower limbs and with
TB of the spine. She was placed on anti-TB treatment on 4
November 2013. The plaintiff alleges that the diagnosis of TB
was most likely a direct result of her having been on the steroid
medication prescribed by the defendant for 19 months.
[9]
The plaintiff alleges that the diagnosis of Addisons in February 2011
was incorrect and negligent, and that the defendant was
negligent in
that:
9.1 He relied solely on two blood
tests and failed to do any other appropriate tests;
9.2 He failed to avoid the
misdiagnosis when by the exercise of reasonable care he should have
done so; and
9.3 He failed to perform the long
Synacthen stimulation test to confirm the diagnosis when he could and
should have done so.
[10]
The plaintiff pleads that as a result of the misdiagnosis by the
defendant she received steroid medication for the period February

2011 to September 2012 when same was not indicated. As a result she
suffered the following
sequelae:
10.1 She developed symptoms and
complications associated with long term steroid therapy;
10.2 Her immune system was suppressed
resulting in her acquiring infectious diseases and making her more
susceptible to infectious
disease;
10.3 She developed tuberculosis,
alternatively aggravation of any pre-existing tuberculosis;
10.4 She developed tuberculosis in the
spine, alternatively aggravation of any pre-existing tuberculosis of
the spine;
10.5 She developed osteoporosis,
alternatively aggravation of any pre-existing osteoporosis;
10.6 She developed aggravation of any
pre-existing hypertension;
10.7 She developed depression,
alternatively aggravation of any pre-existing psychological problem;
10.8 She suffered increased risk from
factors associated with coronary artery disease;
10.9 She developed significant
coronary artery disease, alternatively aggravation of any coronary
artery disease, resulting in cardiac
surgical procedures;
10.10 She developed increased risk for
developing left ventricular hypertrophy; and
10.11 She developed increased risk for
cataract.
[11]
The plaintiff pleaded that she currently suffers from a range of
problems inclusive of cervical lymph node and spinal TB, upper
and
lower limb dysfunction, brain damage and psychological problems.
Before her admission to the Flora Clinic on 4 February
2011 and
before her treatment under the care of the defendant commenced, her
medical history presented only with hypertension and
periodic
headaches, and hence her current medical problems are due to her
being placed on steroid therapy by the defendant.
The
Defendant's pleaded case
[12]
The defendant admitted the following facts:
12.1 That the plaintiff was under his
care during the period 4 to 24 February 2011 but that she was not
continuously at Flora Clinic
during this period.
12.2 That he diagnosed the plaintiff
with Addisons based on two blood tests and that he prescribed
Covocort and Florinef.
12.3 That the diagnosis of Addisons
was incorrect but he denies that he was negligent in making it as it
was based on her low cortisol
levels.
[13]
The defendant pleaded that the plaintiff was diagnosed with a
compression fracture at level T12, reactive depression and
hypertension
during her stay at the Flora Clinic between 4 and 24
February 2011.
[14]
The defendant denied that the plaintiff suffered from the
sequelae
as alleged, alternatively denied that the alleged
sequelae
were a result of the medication prescribed by him on the basis of
his incorrect diagnosis.
[15]
The defendant pleaded that he had no knowledge of the allegations of
the damages suffered by the plaintiff and accordingly
denied same.
The
issues
[16]
It is common cause that the defendant’s diagnosis of Addisons
was incorrect and that the defendant did not perform the
Synacthen
test at any stage prior to making the diagnosis. Hence, wrongfulness
is not in issue and the first issue is whether the
defendant was
negligent in making the diagnosis of Addisons. If he was negligent, I
am required to determine whether the 20 mg
of Covocort he prescribed
following his diagnosis is causally linked to the plaintiff's alleged
sequelae.
[17]
It also became common cause, as a result of a concession by
plaintiff's counsel in his closing submissions, that the evidence
of
the plaintiff's expert that the combined dosage of corticoids
prescribed by the defendant was supraphysiological or a high dose
was
incorrect. The plaintiff therefore accepts that the dosage was
physiological, in other words the normal dose produced by the
body,
which is also referred to as a low dose.
Expert
evidence
Plaintiff's
expert: Dr Promnitz
[18]
The plaintiff relied on five reports prepared by Dr Promnitz a
specialist physician, in terms of Rule 36(9) (a) and (b). In
his
evidence Dr Promnitz explained that Addisons is a rare condition in
which the adrenal glands fail for a variety of reasons
to produce
cortisone and another hormone called aldosterone. The clinical
presentations are that the patient is often fatigued,
has poor
appetite, experiences weight loss, muscle aches and joint pains and
often presents with low blood pressure. The plaintiff
however had
normal cortisone secretion from her adrenal glands. He was informed
that the defendant prescribed Covocort and Florinef
for 19 months
after diagnosing the plaintiff with Addisons. He agreed with the
defendant's expert, Dr Kok that the defendant prescribed
20mg of
Covocort, which is equivalent to 5mg of prednisone.
First
report of Dr Promnitz: 24 December 2013
[19]
Dr Promnitz prepared his first report prior to the plaintiff
instituting action in 2014. He noted that the plaintiff had
underlying
medical problems and suspected that she had long standing
depression that may account for her many problems. He noted that she
was given Protos for treatment of osteoporosis. According to him
exogenous cortisone would have aggravated her existing osteoporosis

despite her being on Protos and she would have to undergo treatment
to reverse the osteoporosis as she is at greater risk for fractures.

He stated that the use of exogenous cortisone would also have
aggravated her pre-existing depression and pre-existing hypertension.

The report noted further that the use of cortisone for a period of 19
months when it was not indicated would have aggravated her

hypertension and it appears that when she was admitted to CHB her
blood pressure was not well controlled. This would predispose
her to
the development of left ventricular hypertrophy and an increased risk
for cerebral vascular incidents. He also noted that
the clinical
notes from CHB indicate that the doctor who attended to her
considered that she might have proximal myopathy, and
according to
him this is a complication of long-term steroid therapy that would
result in muscle weakness. Furthermore, she would
have been at a
higher risk of developing infections. Importantly, he stated that it
is not apparent from the clinical notes whether
the plaintiff
developed any infections
while she was on steroids,
but in his
view the suppression of her immune system would continue for some
time despite her being off steroids. His view was that
the steroid
therapy would not have interfered with her ability to continue to
perform her occupation and that her inability to
work at the time was
probably related to her depression. However, while she was on the
high dose of steroids
, her existing depression would have been
aggravated.
Second
report of Dr Promnitz: 27 December 2013
[20]
Dr Promnitz deals in this report with an email about the plaintiff's
admission to Helen Joseph Hospital in October and November
2013. He
records that the plaintiff was found to have cervical lymphadenopathy
on the right hand side, which on biopsy proved to
be secondary TB.
She was investigated for neurological symptoms in her lower limbs and
a diagnosis of TB of the spine was made.
This, he concludes, is most
likely a direct result of her having been on corticosteroids for 19
months. He stated that corticosteroids
interfere with the immune
system and predispose the patient receiving glucocorticoids for
prolonged periods to certain infections,
with TB being one of them.
In his view this might have been secondary reactivation of latent TB,
which is common in South Africa
where people are exposed to TB at a
young age. The primary infection remains dormant until reactivation
occurs under certain circumstances.
He concluded that it was
well
accepted
that patients on long-term steroids are at a greater
risk of developing primary or secondary TB. He did not refer to the
dosage
actually prescribed by the defendant.
Third
report of Dr Promnitz: 12 August 2015
[21]
Dr Promnitz deals, for this first time, with the dosage prescribed by
the defendant, and confirms that she was placed on Covocort
10mg
morning, 5mg noon and 5 mg night as well as on Florinef. He states
that when the plaintiff was informed in October 2013 that
she had TB
of the cervical node, she was also told that she had TB of the
thoracic spine. He also confirmed that in October 2014
she presented
with chest pains at the Helen Joseph Hospital and was diagnosed with
a myocardial infarct, had an angioplasty performed
and went back for
insertion of a stent on 18 November 2014. He further confirmed that
in April 2015 she collapsed and was referred
to Helen Joseph Hospital
for further investigations. She was told that she has ongoing
ischaemic heart disease and required a coronary
bypass graft. He
records the plaintiff's current complaints as being the following:
generalised body pain; headaches and dizziness;
weakness in both
limbs with the left being more pronounced; paraesthesia in both limbs
with the left being worse than the right;
depression; episodes of
chest pain; ischaemic heart disease; calcification of her brain; and
blackouts that had not been adequately
investigated at the time and
might present as epilepsy since she was already on low dosages of
Epilim. Dr Promnitz also records
that she informed him that prior to
her treatment at the Flora Clinic in February 2011 she had only
suffered from hypertension
and periodic headaches (this was
subsequently shown in evidence to be incorrect). He also recorded
that on examination the plaintiff
had pigmentation on her face in the
malar distribution, which she explained resulted from her treatment
for TB.  Dr Promnitz
further noted evidence of left ventricular
myopathy, and importantly that she had a T12 compression fracture. He
stated that this
was subsequently diagnosed as secondary TB for which
she was still on treatment. He again classified the dosage prescribed
by the
defendant as a
high dose
of Covocort, which in his
opinion would have aggravated the TB of the spine. The steroids would
also have resulted in development
of osteoporosis, which would in
turn aggravate her spinal problem. These two factors, he explained,
have undoubtedly resulted in
the plaintiff having a permanent
neurological deficit in her lower limbs.
[22]
In relation to ischaemic heart disease, Dr Promnitz stated that he
had sight of the angiogram Dr Becker performed in February
2011 when
there was no evidence of coronary artery disease, but four years
later the plaintiff required a coronary artery bypass
graft. This
suggests to him that she developed ischaemic heart disease since
2011. He stated that it is documented that long-term
steroid use
might influence the risk factors associated with coronary artery
disease such as lipids and hypertension adversely
and this might be
contributing factor. He went further to state that in his opinion the
steroid therapy she was incorrectly placed
on had predisposed the
plaintiff to developing significant coronary artery disease requiring
a coronary artery bypass graft. She
had also been left with what
appears to be impaired left ventricular function following her
development of ischaemic heart disease
and this will not improve over
time.
Fourth
report of Dr Promnitz: 31 January 2016
[23]
Dr Promnitz responds in this report to the report prepared by Prof
Richards on behalf of the defendant. He agreed that in the
literature
20mg of Covocort is equivalent to 5mg prednisone. However, he states
that in replacement therapy for Addisons one uses
hydrocortisone
rather than prednisone as the latter has an 8 to 12 hour duration and
has a mineralocorticoid effect as well. He
confirmed that the
plaintiff was also on a fludrocortisone (Florinef), which is
classified as a steroid with a mineralocorticoid
effect, but he does
not state the dosage that the defendant prescribed. Despite this he
is of the opinion that the plaintiff received
a higher dosage of
steroids than that referred to by Prof. Richards. He questioned Prof
Richards's opinion that the plaintiff's
use of Covocort of 20mg for
approximately 19 months would not have predisposed her to the
development of TB as this is alluded
to in most articles with
reference to steroid usage and the risk of TB. He referred to an
article dealing with meta-analysis of
controlled trials in which
glucocorticoids or placebo were given to patients, and which reported
that infection occurred more significantly
with steroid therapy. He
stated that "the infection rates were significantly increased
only in patients given an average dose
of prednisone of more than
10mg per day or an accumulative dose per day of 700mg".
According to him, the plaintiff received
a cumulative dose of
approximately 2800g (he corrected this in cross examination to
milligrams) of prednisone over the period that
she was taking
Covocort. This in his view placed her at
greater risk of
reactivation of TB
, and is evident from the fact that she was
diagnosed with TB of the cervical gland. He referred to the existence
of considerable
literature on the immune effect of prolonged steroid
usage and in his opinion the fact that the plaintiff received
steroids for
a long period of 19 months predisposed her to
reactivation of TB. In regard to TB of the spine he did not have
sight of the x-rays
from Helen Joseph Hospital but assumed that it
was fair that the orthopaedic surgeon would have found some or other
evidence to
suggest TB involvement of the spine.
Fifth
report of Dr Promnitz: 15 February 2016
[24]
Dr Promnitz noted from an x-ray report dated March 2011 that the
plaintiff had a compression fracture at T12; that there was
gibbus
formation in the area and the comment on the report was that this has
the appearance of post-traumatic compression fracture.
It was also
recorded that this was an old injury and there is no mention of
osteopenia or osteoporosis. He noted that the right
hip showed a
T-score of minus 1.4 which represents some osteopenia and the x-ray
report notes some osteopenic changes in the right
hip and right femur
but no other areas. Dr Promnitz notes that he would not have treated
the plaintiff for osteoporosis (as the
defendant did) because it is
only indicated where there is a T-score of minus 2. There was in his
opinion no indication for prescribing
Protos on these results. He
also noted that the bone density scan of 30 January 2012 indicated no
evidence of osteoporosis, which
implies that her condition had
improved on the Protos, but he still stated there was no reason for
prescribing Protos. He confirmed
that the plaintiff undoubtedly does
not have osteoporosis based on the information supplied to him.
Defendant's
expert: Professor Richards
[25]
Prof. Richards, a specialist physician, agreed that the diagnosis of
Addisons was incorrect and inappropriate. He confirmed
that a T11 and
T12 disc protrusion would cause pain the chest region, in other
words, in the lower chest and upper abdomen area.
He confirmed his
agreement with Dr Promnitz that the plaintiff's diagnosis of cervical
lymph node TB in November 2013 was probably
a reactivation of
pre-existing exposure to TB.  He testified that most people have
been exposed to TB at some time, but that
it could remain latent for
long periods of time without it ever manifesting as infection, or one
could develop overt infection,
which is most frequent in the lungs.
He confirmed that the use of corticoids could re-activate latent TB
but that this could only
occur when supraphysiological doses were
administered.
[26]
Prof. Richards confirmed that it is well known that the dose of
Covocort given to the plaintiff was less than the physiological
dose,
and this dose does not result in suppression of the immune system. He
repeatedly stated that side effects only occur when

supraphysiological doses are administered, and that if the plaintiff
had been given an immuno-suppressive dose, the TB would have

manifested during the period she was still on steroid therapy. In
cross-examination he confirmed, when referred to the medical

literature, that the risks from steroid medication occur
during
use
and the immune system reconstitution occurs rapidly
thereafter. In the plaintiff's case, she developed TB long after the
cessation
of the steroid use and hence in his opinion there was no
association with the steroid use.
Defendant's
expert: Professor Greeff
[27]
Prof. Greeff is a registered pharmacologist. He explained that
corticosteroids are synthetic analogues of the natural hormones

produced by the body's adrenal cortex. There are two types of
corticosteroids: mineralocorticoids, which are primarily involved
in
the regulation of electrolytes and water balance and can cause the
retention of sodium and water in the body; and glucocorticoids,
which
are predominantly involved in carbohydrate, fat and protein
metabolism. Glucocorticoids have an anti-inflammatory,
immunosuppressive
and vasoconstrictive effect. In other words, they
have an ability to suppress the body's immune system. According to
him the defendant
prescribed Florinef in a dosage of 0.1mg and this
is a mineralocorticoid with no appreciative glucocorticoid effect at
usual daily
dosages of 0.05mg to 0.2mg. This reference was made
relying on the Goodwin and Gilman textbook. He therefore confirmed
that the
defendant prescribed a physiological dose of steroids to the
plaintiff, in combining Covocort and Florinef. This has since been

conceded by plaintiff's counsel.
[28]
Prof Greeff explained the difference between a physiological and
supra-physiological dose as follows:
"Supra-physiological means
higher concentration that the body normally has in its own right, so
if you add to that, more than
what the body needs and this is why
with hydrocortisone the 20mg is a physiological dosage. It's less
than what the body normally
produces on a daily basis and it's not
too much. If you administer too much the HPA axis will be suppressed
and you will stop secretion
and if you do that for a long time, you
will suppress the adrenal gland and when you stop using, you won't be
able to produce the
hormones anymore and that’s a danger of
this and that’s why you have to stay within your dosages to
make sure that
you don’t get total suppression of the adrenal
glands so that when you discontinue treatment the [Indistinct] can
re…
If you will re-secrete its own hormones in the normal way.
That’s why we are cautious not to give high dosages or
supra-physiological
doses."
[29]
Prof Greeff's evidence was that due to the different pharmacological
actions of the Florinef and the Covocort, Florinef at
the dosage
given to the plaintiff could not have had any appreciable additive
glucocorticoid effect on the plaintiff and hence
could not have
contributed to the plaintiff's alleged
sequelae.
He explained that Florinef could not
increase the serum levels of cortisone in the body. Cortisone is
relatively available in the
body at a concentration of 60 nanomole
per millilitre.
Once the body needs
cortisol, the cortisone is converted to cortisol by an enzyme in the
kidney, and then it can have a pharmacological
action or an action in
the body. Thus, there is a fine balance and there is enough cortisone
if the body needs it to convert into
cortisol. His evidence was that
if there is too much cortisol in the body its negative feedback
mechanism will kick in and the
pituitary gland will not secret any
more steroid hormones, so there will be less glucocorticoids secreted
by the body. The body
therefore keeps the balance of what it needs,
depending on circumstances. Hence the ideal glucocorticoid
replacement therapy would
mirror the normal physiological state of
the patient as closely as possible. He confirmed that the defendant
prescribed 20 mg of
hydrocortisone to the plaintiff and this is the
acceptable daily dose in two or three divided doses.  According
to him the
long-term effects of all drugs are dose dependent and
evidence of long-term side effects must be evaluated in the context
of the
doses of the glucocorticoid preparations administered.
[30]
Prof. Greeff explained that a physiological dose is the normal
acceptable dosage in replacement therapy, and it will not suppress

the adrenal glands. However, it was put to him that the plaintiff was
not on a replacement dose because her steroid hormone concentration

levels were normal. He replied:
"
[t]he tests that … [the defendant] has done, showed low
concentrations, which clinically in his judgment was inadequate
and
that’s why he started replacement therapy. So we cannot say
that she's had enough, so we've added the two and now she's
had too
much. The body will secrete less if you add more to the body."
[31]
With regard to the suppression of the immune system, which the
plaintiff alleges contributed to the plaintiff acquiring or
having
aggravated infectious diseases such as TB, he testified that where
patients receive more than 15 mg of prednisone (equivalent
to 80 mg
of cortisone) daily, there was an increased risk of contracting TB
whilst on long term glucocorticoid therapy. This does
not apply to
the plaintiff. The defendant's prescription of 20mg of hydrocortisone
daily is equivalent to 5mg of prednisone, and
this dosage did not put
the plaintiff at a higher risk of developing TB especially 14 months
after the cortisone was discontinued.
In relation to the academic
article by Jick
et al
which calculated the ratio for people not exposed to glucocorticoids
and those on recent and past glucocorticoid therapy to be
a ratio of
1 and 1.4 respectively, he commented that although a trend of
increased risk was observed even with a physiological
dose, the
association did not reach statistical significance and it therefore
cannot be said that the plaintiff was at a higher
risk of contracting
TB or any other infectious disease. The article also confirmed that
there was no clear effect of duration or
cumulative dose on the risk
of TB.
[32]
Prof. Greeff confirmed that he saw the entry in the CHB records dated
4 November 2013 that the plaintiff experienced severe
back pain
radiating to the whole back from the cervical spine. He also saw the
entries dated 26 and 27 March 2012 indicating that
the plaintiff
received physiotherapy for her neck and back.
[33]
In regard to osteoporosis, his evidence was that the plaintiff's bone
mineral density ("BMD") improved on glucocorticoid
therapy
prescribed by the defendant over one year (from 16 February 2011 to
30 January 2012) as seen on the radiology reports.
[34]
In relation to ischaemic heart disease, Prof Greeff referred to a
report by Liu
et al
on a population base study comparing 68781
glucocorticoid users and 82282 non-users which found the rate of
cardiovascular events
to be significantly higher in patients
prescribed high glucocorticoid dosages (greater than 7.5mg per day of
prednisone or greater
than 30 mg of cortisol). According to him
cardiovascular risk was not increased in patients using less than
7.5mg per day of prednisone
or less than 30 mg of cortisol, which was
the dosage applicable to the plaintiff. Prof. Greeff also referred to
another large retrospective
case control study which found that
current
glucocorticoid use was associated with significantly
increased risk and cardiovascular risk was found to be greater with
higher glucocorticoid doses
and with current use.
[35]
In regard to depression, Prof. Greeff stated that the plaintiff was
diagnosed with reactive depression on her first admission
to hospital
(in 2011) and before she received cortisone treatment. He stated
further that most patients with psychiatric reactions
to
corticosteroids usually recover from their symptoms with dose
reduction or upon cessation of therapy.
[36]
In concluding his testimony Prof. Greeff stated that given the lower
dose of cortisol that was prescribed and the time span
between
treatment and the development of clinical conditions, it was highly
unlikely that any of the alleged
sequelae
were caused by the
cortisol therapy. In support of his opinions and reasoning, Prof.
Greeff referenced (in addition to the literature
referred to by Dr
Promnitz), further articles and studies on the impact of
glucocorticoids.
[37]
When it was suggested to Prof. Greeff in cross-examination that he
could not exclude the possibility that if a low dose of
cortisol is
administered to a patient that it could cause the
sequelae
exhibited by the plaintiff, he replied that “
anything is
possible in medicine”
. He added that in his opinion the
probability is very low and unlikely albeit “
not improbable
to really happen”
and that "
different patients
react differently to drugs".
Defendant's
expert: Dr Kok
[38]
Dr Kok is a specialist physician. She testified that although the
defendant found two borderline levels of cortisol, there
were no
other features of Addisons clinically and she confirmed that the
diagnosis was incorrect. She stated that the defendant
could have
confirmed the diagnosis with a more robust test and assessed the
plaintiff's response to the proposed treatment. However,
given the
plaintiff's initial presentation at the Flora Clinic, including
fatigue, low blood pressure in normally hypertensive
patient and
borderline levels of cortisol it would have been reasonable for the
defendant to treat the plaintiff as an Addison's
disease patient.
[39]
In her view the dosage prescribed by the defendant was not of such
magnitude that any metabolic or bony
sequelae
would follow. There was evidence of a T12 fracture, which had
occurred in 2007, but this was four years before the defendant saw

the plaintiff. Her view was also that the subsequent lymphadenitis
due to TB was remote from any possible influence by the defendant's

treatment. Dr Kok confirmed that she could not find any biopsy of the
spine that confirmed the diagnosis of TB of the spine or
that showed
that TB of the spine was presumed after the lymphadenitis was
diagnosed. What is important is that she stated that
the reports of
the chest radiographs did not reveal any evidence of TB or Ghon focus
(lesions in the lung) indicating a risk of
TB or past exposure to TB.
Her evidence was that the plaintiff had a normal full blood count on
several occasions and there was
no anaemia or chronic disorder, which
if present, would be in keeping with TB. Furthermore the plaintiff's
erythrocyte sedimentation levels
("ESL") were never elevated, which would
have indicated inflammation.
[40]
Dr Kok also stated that the likely cause of the spinal insufficiency
fracture would have been osteoporosis and that this preceded
any
treatment by the defendant. She further stated that the plaintiff
received treatment for pain neuropathic systems and muscle
weakness
throughout the entire period and this was not due to the defendant's
treatment. It is also significant to note her evidence
that the
defendant attempted to improve the plaintiff's symptoms with
appropriate treatment when he saw her and these symptoms
are
unrelated to the Covocort and Florinef subsequently prescribed by
him. The defendant's treatment of her with Protos as well
as vitamin
D and calcium supplementation was appropriate as reflected by a
subsequent bone density scan in 2012 which confirmed
an improvement
in her bone mineral density.
[41]
In relation to the plaintiff’s low cortisol levels, Dr Kok
confirmed that on both July 2012 and August 2012 when the
plaintiff
was at the Garden City Clinic her blood levels for cortisol showed
"not detectable".
[42]
In regard to heart disease, Dr Kok stated that she could find any
link or association between the plaintiff's ischaemic heart
disease
and the defendant's treatment. In her opinion the defendant's
treatment did not cause or contribute to the plaintiff's
alleged
diagnosis of heart disease.
The
plaintiff's evidence
[43]
The plaintiff testified that prior to February 2011, she was
relatively healthy and could walk about 3km a day to work, and
was
only chronic medication for high blood pressure. Her general
practitioner, Dr Bodhania, had arranged an appointment with the

defendant for 7 February 2011 for syncope (collapsing and fainting).
She initially denied that that was the reason she had been
referred
to the defendant, but conceded this in cross-examination. Prior to
the appointment and on 4 February 2011 she had to be
admitted to the
Flora Clinic with complaints of chest pain and high blood pressure.
She was admitted under the care of Dr Becker,
a cardiologist, who did
an angiogram on 7 February 2011, the results of which were normal.
[44]
The defendant also attended to her during this time and he ran some
tests and diagnosed her with Addisons. The diagnosis of
Addisons came
as a shock to her and she was unable to cope because the defendant
advised her that it was a lifelong disease and
she would have to take
chronic medication. The defendant called in a psychiatrist to consult
with her at the Flora Clinic in order
to cope with the diagnosis. It
was put to her in cross-examination that she consulted with a
psychiatrist, Dr Magnus, at the clinic
prior
to the diagnosis
of Addisons, but she could not recall this. The plaintiff had sadly
had many traumatic life experiences including
the murder of her
husband, relocation from one province to another, as well as being a
single parent of three children. She could
not recall being involved
in a car accident in 2007 or having x-rays taken as a result.
[45]
Before her discharge from the Flora Clinic on 24 February 2011 after
this first admission, and after the steroid treatment
commenced, she
experienced symptoms of weakness in her knees and fatigue. She was
treated by a physiotherapist for neck and back
pain at the clinic but
denied that she complained about back pain prior to her admission to
the clinic. She also received acupuncture
treatment in the hospital.
She said she was "
just getting more and more sick
"
and she left the hospital in a wheelchair although she was fully
ambulant when she was admitted. The defendant told her that
this was
the nature of the illness and informed her to take the cortisone
medication daily as she had a life-threatening illness.
He prescribed
20 mg Covocort which she was required to take three times a day (in
three divided doses of 10 mg, 5 mg and 5 mg)
and Florinef 0.1 mg,
which she was instructed by the defendant to take each morning.
[46]
She was also given a prescription to be filled at the pharmacy for
the same medication for a further six months. Later that
year, in
November 2011, the defendant gave her a second prescription for
another six months of repeat medication. She complied
with the
treatment regime and took the medication daily because of the warning
she had received from the defendant about the seriousness
of her
condition.
[47]
After her first hospital admission she had episodes of collapsing at
home and her children often had to rush her to the hospital.
She
experienced severe back pain, tiredness and her legs were weak. Her
children gave her a walking frame to assist her with walking.
After
yet another episode of passing out her children took her to the
Garden City clinic instead of Flora Clinic. She was placed
in a
psychiatric ward where a physician told her she does not have
Addisons because it is not associated with high blood pressure.
She
insisted on returning to the defendant for treatment and she informed
him of the advice given to her at Garden City to the
effect that she
does not have Addisons.
[48]
She confirmed that the defendant completed a form for the purpose of
her claiming disability benefits in March 2011. The form
indicated
that the diagnosis had been made on 5 February 2011. She also
confirmed that she suffered from all the symptoms that
the defendant
listed on the form including: impossible to perform seated/sedentary
tasks; impossible to climb, walk on uneven terrain;
difficulty with
bending, lifting, pushing and pulling, operate light and heavy
machinery, and working with weights.  The defendant
had
indicated on the form that these symptoms had appeared a few months
prior to that date. She confirmed this in cross-examination.
She
confirmed that he also completed a certificate for her employer, at
her request, booking her off from work "
till further notice
"
and as a result she was medically boarded from her employment in May
2012. Her last visit to the defendant was in April 2012
when he told
her to continue with her medication. She was fully compliant with
taking her medication until 15 April 2012 but by
August 2012 she was
very sick. She stopped taking the steroid medication and her daughter
in fact threw them away.
[49]
She attended the endocrine clinic at CHB in September 2012 where
Professor Huddle informed her that she does not have Addisons.
She
testified that he was very upset about her being diagnosed with
Addisons. He told her she had to be weaned off the medication
as a
result of which she was kept in hospital for approximately six weeks
for that purpose.
[50]
In May 2013 she developed painful lumps in her neck and was referred
by her clinic to the Helen Joseph hospital where a biopsy
was
performed. She started to feel better but still had to receive
physiotherapy as her legs were still weak. She returned to Helen

Joseph hospital in October 2014 where she was informed of her
diagnosis with TB. In October 2014 she was admitted to the Helen

Joseph Hospital presenting with chest pain and was diagnosed with a
myocardial infarct. She was transferred to the Charlotte Maxeke

Hospital where a coronary angiogram and angioplasty was performed on
her and a stent was inserted on 18 November 2014. In April
2015 she
collapsed and was taken to the Helen Joseph Hospital where a coronary
artery bypass was performed on her on 14 May 2015.
In July 2015 she
again had a syncopal (fainting) attack.
The
plaintiff's medication regime
[51]
On the dispute as to whether the defendant prescribed steroid therapy
for 12 or 19 months, the plaintiff testified that she
was given a
third prescription by the defendant on 13 April 2012 for a further
six months' steroid medication. It was put to her
in cross
examination that this was not a prescription but rather an admission
order because she was being admitted to the Flora
Clinic that day and
the defendant was placing an order for the medication to be
administered to her during her stay as well as
for various tests to
be conducted. She accepted that this was not a prescription for
medication for her to obtain from the pharmacy
and take at home.
[52]
The plaintiff then suggested that she would still have had repeats
for medication remaining from the November 2011 prescription,
because
during her hospital admissions she was given medication from the
hospital and upon discharge she would be given medication
to take at
home. Under cross examination, however, she was shown that none of
the discharge forms after the first six months script
in March 2011
recorded any take home Covocort or Florinef and the plaintiff then
confirmed that she did not receive any Covocort
or Florinef to
administer at home upon discharge.
[53]
The plaintiff’s evidence was that but for the periods when she
was admitted to hospital from 10 February 2011 until 15
April 2012
(when she was discharged from Flora Clinic in respect of her last
admission on 13 April 2012) when Covocort and Florinef
was
administered to her during her hospital stay, she only received and
used the two six month prescriptions that were issued by
the
defendant.
[54]
For the period 24 February 2011 (when the plaintiff was discharged
from the Flora Clinic) until 18 March 2011, the defendant
placed on
record before the Court that he accepts that during this period the
plaintiff took 20 mg of Covocort and 0.1 mg Florinef
per day. This
would comprise a total of 23 day. From 18 March 2011 (the first
prescription) and 9 May 2012 (when the last prescription
would have
finished) the plaintiff was in hospital for 34 days when she received
hospital medication. This means that the steroid
medication
prescribed by the defendant would have ended in mid-June 2012.
Defendant's counsel submitted that this inference can
be drawn from
the undisputed and admissible evidence of the plaintiff that she took
her medication every day; that during the periods
she was in hospital
she was not taking her own medication and she would in addition get
"take home" medication prescriptions;
and her concession
that during 18 March 2011 to April 2012 she did not receive any
additional Covocort or Florinef from the hospitals
as "take
home" medication. It appears therefore on the probabilities that
the plaintiff stopped taking the Covocort and
Florinef prescribed by
the defendant in June 2012 and had not been on the steroids
prescribed by the defendant for 19 months as
was pleaded.
[55]
Plaintiff’s counsel informed the court during his opening
address that her evidence would be that she stopped taking
the
prescribed medication a month before her admission to CHB in
September 2012 because she could no longer afford the medication.
He
however stated that he subsequently consulted with her and her
evidence will be that she stopped taking the medication because
her
daughter told her to stop because her condition was not improving but
that she still had some cortisone medication. Counsel
took
responsibility for the discrepancy. In her evidence the plaintiff
indeed confirmed that she stopped the medication in August
2012, but
this had been based on her incorrect version of the so-called third
prescription issued by the defendant on 13 April
2012.
[56]
Defendant's counsel submitted that the only reason why the plaintiff
would still have steroid medication left after August
2012 would be
that she was not fully compliant with taking her medication daily, as
she had testified. As a matter of logic if
she was fully compliant
she would not have had any leftover medication after June 2012. This
is confirmed by the two
"not detectable"
cortisol
levels taken at Garden City Clinic in July 2012 and August 2012 as
testified by Dr Kok. The plaintiff would not have had
such negligible
cortisol levels if she was still taking Covocort and more so if Dr
Promnitz's additive theory was correct.
[57]
It must also be accepted, as was submitted by defendant's counsel,
that the plaintiff took 20 mg Covocort and 0.1 mg Florinef
daily
during this period. The plaintiff testified that she took the dosages
prescribed on the bottle, which was 20 mg. There were
three instances
when it appears in hospital records that 25 mg was administered to
her, but this would seem to be an error.
Events
post treatment
[58]
The plaintiff disputed that she took any other form of steroid
therapy other than that prescribed by the defendant. However,
on her
admission to CHB the admission form reflects that she was on
"Meticorton". She testified that she did not know
what this
referred to. Dr Promnitz (who testified before she did) said that at
the time of her admission to CHB she was on Meticorton
according to
the hospital records, and that this was a high dose of prednisone.
This was based on his incorrect understanding that
the defendant had
issued a third prescription for Covocort and Florinef on 13 April
2012. When it was put to him that the defendant's
version would be
that the 13 April 2012 document was not a prescription, Dr Promnitz's
evidence about the Meticorton changed. He
then no longer relied on it
being a high dose of prednisone, but said it was a less potent
version of Covocort sold when a pharmacy
does not have stock of
Covocort. This evidence was not substantiated.
[59]
The plaintiff testified that after she was informed at CHB that the
Addisons diagnosis was incorrect, she took a decision not
to go to
any doctors or hospitals again. However, in May 2013 she developed
lumps on her neck and was diagnosed with TB of the
cervical glands at
the Helen Joseph hospital. This version was not put to Dr Promnitz
since the plaintiff gave evidence after he
did and this was the first
time this version was given by the plaintiff. In 2015 she had
continuous angina pains and had to have
heart surgery.
Dr
Bodhania
[60]
Dr Bodhania, the plaintiff's general practitioner, confirmed in his
testimony (based on the notes in his patient file), that
the
plaintiff did not complain of or receive treatment at his practice
prior to 4 February 2011 for TB, myopathy, general weakness,

cardiovascular problems or psychiatric difficulties. She was treated
for syncope as she had symptoms of collapsing and fainting,
as well
as for headaches and back pain in 2010 (the plaintiff initially
denied consulting him for back pain but in cross examination

indicated that she would defer to him). He confirmed that in July
2012 she received an injection for pain. She was also treated
for
insomnia (a sleeping tablet was prescribed for anxiety and not
sleeping well at night), myalgia (muscle or soft tissue pain),

non-specific muscle pain (28 February 2011) which led to a referral
to a rheumatologist, a type of infection (3 March 2011), abdominal

pain (January 2012 with symptomatic treatment for ulcers and cramps),
and vomiting and fever (2 July 2012). The plaintiff submits
that this
confirms she was only treated after her steroid treatment commenced
for some the new or steroid related complications.
Defendant's
evidence
[61]
The defendant is a specialist physician and nephrologist. He
testified that he received a call from the plaintiff's general

practitioner, Dr Bodhania, prior to the plaintiff's admission to the
Flora Clinic on 4 February 2011. Dr Bodhania informed him
that the
plaintiff had pre-existing hypertension and had a syncope (fainting)
episode, and that he required a specialist to examine
her. An
appointment was made for the plaintiff to see him but a week before
the scheduled appointment she was admitted to the Flora
Clinic with
chest pain. She was under the care of Dr Becker but the defendant was
asked to consult with her when she told staff
she had a scheduled
appointment with him.
[62]
The defendant testified that although the plaintiff complained of
pain, she was unable to localise the pain. The medical team
at some
point considered whether the plaintiff was exaggerating her pain
since they were unable to find the cause. Two x-rays were
conducted
to establish the cause because Dr Becker's investigations did not
reveal a cause for the pain. The tests revealed that
the plaintiff
had a fracture on the T12 vertebra of her thoracic spine and a
significant wedge compression. According to the defendant
this was
one of the worst fractures he had seen and the medical team could not
understand why she had not been in severe pain from
this fracture
prior to her admission. They provided the plaintiff with a back brace
on the understanding that the T12 fracture
was a recent fracture and
that it would take eight weeks to heal. The plaintiff could not
recall how she had sustained the fracture.
Under cross examination
the plaintiff agreed that she had subsequently been informed by a
pain management clinic that what she
thought was chest pain was
actually pain radiating from her back. The defendant also confirmed
that when he saw the plaintiff in
court she was using crutches and a
back brace.
[63]
The defendant was concerned about her history of syncope
(collapsing), hyperpigmentation on her face, low blood pressure,
chronic fatigue, depression, pain, weakness and chest pain and he
ordered blood tests to establish her cortisol levels. Her symptoms

suggested underlying adrenal gland issues. The first test yielded a
low result (her cortisol level was 96 when it should have been

between 101 and 535). He wanted to identify if she had Addisons or
another underlying disease.
[64]
Once the low cortisol results came back he tried to obtain Synacthen
to perform a test to confirm the diagnosis but Synacthen
was not
available.
[1]
As an alternative, on 10 February 2011 he ordered a second cortisol
test to confirm whether her cortisol levels were consistently
low and
also ordered a course of Covocort to be administered subject to the
second test results. When he found out that the nurses
had already
administered a dose of Covocort before obtaining the second test
results, he instructed the nursing staff to
"omit"
the administration of Covocort for the next three days. The results
indicated that her cortisol level was just above normal (in
other
words it was borderline), but together with the plaintiff's other
symptoms he considered a clinical diagnosis of Addisons
to be
appropriate. He prescribed the lowest possible dose of steroids,
being 20mg Covocort and 0.1mg Florinef. He could not recall
the
discussion he had with the plaintiff when he informed her of the
diagnosis but he would have informed her that she had to take
the
medication daily and strictly since it is a chronic condition.
[65]
He testified that the plaintiff requested him to complete more than
one form for disability claims from her insurance and he
did so. He
got a sense that all she wanted was to submit a claim for disability
benefits.
[66]
He confirmed that he only issued two six month repeat prescriptions
to the plaintiff and that the so called third prescription
of 13
April 2012 was in fact an admission note which contained all the
tests (including blood tests) which had to be done as well
as well as
the medication to be administered during the plaintiff's hospital
admission.
[67]
The defendant testified that during the plaintiff's repeated
admissions to hospital she would arrive with elevated blood pressure

but as soon as she was given pain medication her blood pressure would
normalise as depicted by the various readings taken during
her
admissions.
[68]
His evidence was that the plaintiff's complaints during the various
hospital admissions were always related to her back or
chest pain.
Her chest pain was later identified as back pain radiating from the
T12 fracture. He said that despite having placed
the plaintiff on
treatment for the fracture, including a brace, Protos, Vitamin D,
calcium and multiple analgesics for months he
was unable to determine
why she still complained of severe pain. Plaintiff's counsel
submitted that this made it imperative to
obtain certainty about the
Addisons diagnosis, which he had failed to do.
[69]
He conceded that his diagnosis of Addisons was incorrect, but
testified that her symptoms at the time were in his opinion
consistent with Addisons. The defendant was referred to the
agreements between Dr Promnitz and Dr Kok and Dr Promnitz and Prof
Richards to the effect that the diagnosis of Addisons was incorrect
and the appropriate tests to confirm the diagnosis were not
done, and
he conceded this. His testimony was that the gold standard for
testing for Addisons was the Synacthen test as well as
the insulin
induced hypoglycaemia test. He confirmed in cross-examination that
although he could not obtain Synacthen from the
hospital pharmacy he
did not even perform the insulin induced hypoglycaemia test. He
testified that he continued to treat the plaintiff
with
corticosteroids as he was
"fairly convinced
" that
his diagnosis was correct. He accepted that this was his
"best
inconclusive shot at diagnosing Addison's disease”.
Evaluation
of expert evidence
[70]
The
approach to be taken by a court in evaluating expert opinion has been
set out by the Supreme Court of Appeals in
Bee
v Road Accident Fund
[2]
as follows:
"[22]
It is trite that an expert witness is required to assist the court
and not to usurp the function of the court. Expert
witnesses are
required to lay a   factual basis for their conclusions and
explain their reasoning to the court. The court
must satisfy itself
as to the correctness of the expert’s reasoning. In Masstores
(Pty) Ltd v Pick ‘n Pay Retailers
(Pty) Ltd
[2015] ZASCA 164
;
2016 (2) SA 586
(SCA) para 15, this court said '[l]astly, the expert
evidence lacked any reasoning. An expert’s opinion must be
underpinned
by proper reasoning in order for a court to assess the
cogency of that opinion. Absent any reasoning the opinion is
inadmissible'.
In Road Accident Appeal Tribunal & others v
Gouws & another
[2017] ZASCA 188
;
[2018] 1 ALL SA 701
(SCA) para
33, this court said '[c]ourts are not bound by the view of any
expert. They make the ultimate decision on issues on
which experts
provide an opinion'. (See also Michael & another v
Linksfield Park Clinic (Pty) Ltd & another
[2002] 1 All SA
384
(A) para 34.)
[23]
The facts on which the expert witness expresses an opinion must be
capable of being reconciled with all other evidence
in the case. For
an   opinion to be underpinned by proper reasoning, it must be
based on correct facts. Incorrect facts militates
against proper
reasoning and the correct analysis of the facts is paramount for
proper reasoning, failing which the court will
not be able to
properly assess the cogency of that opinion. An expert opinion which
lacks proper reasoning is not helpful to the
court. (See also Jacobs
v Transnet Ltd t/a Metrorail
[2014] ZASCA 113
; 2015 (1)
SA (SCA) paras 15 and 16; see also Coopers (South Africa)
(Pty) Ltd v   Deutsche
Gesellschaft
Für Schädlingsbekämpfung mbH
1976
(3
) SA
352 (A) at 371F.
[71]
In
Michael
and Another v Linksfield Park Clinic (Pty) Limited and Another
[3]
the
court noted "
....it
is perhaps as well to re-emphasise that the question of
reasonableness and negligence is one for the court itself to
determine
on the basis of the various, and often conflicting, expert
opinions presented. As a rule that determination will not involve
considerations
of credibility but rather the examination of the
opinions and the analysis of their essential reasoning, preparatory
to the court’s
reaching its own conclusion on the issues
raised."
[72]
The court held (at [36]) that what a court is required to do is
evaluate the evidence of experts 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
(H.L) 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” (at241 G - 242
B)....
[39] A defendant
can properly be held liable, despite the support of a body of
professional opinion sanctioning the conduct in issue,
if that body
of opinion is not capable of withstanding logical analysis and is
therefore not reasonable. However, it will very
seldom be right to
conclude that views genuinely held by a competent expert are
unreasonable. The assessment of medical risks and
benefits is a
matter of clinical judgment which the court would not normally be
able to make without expert evidence and it would
be wrong to decide
a case by simple preference where there are conflicting views on
either side, both capable of logical support.
Only where expert
opinion cannot be logically supported at all will it fail to provide
“the benchmark by reference to which
the defendant’s
conduct falls to be assessed” (at 243 A-E).
[40] Finally, it
must be borne in mind that expert scientific witnesses do tend to
assess likelihood in terms of scientific certainty.
Some of the
witnesses in this case had to be diverted from doing so and were
invited to express the prospects of an event’s
occurrence, as
far as they possibly could, in terms of more practical assistance to
the forensic assessment of probability, for
example, as a greater or
lesser than fifty per cent chance and so on. 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 89 D-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.”
[73]
In evaluating the expert
evidence, regard must also be had to the medical literature Dr
Promnitz provided which he asserted supported
his opinion that the
Covocort and Florinef prescribed by the defendant as a result of his
incorrect diagnosis of Addisons was the
cause of the plaintiff's
alleged
sequelae
.
The
high dosage theory
[74]
Dr Promnitz testified with reference to an academic article that the
Florinef prescribed, (which he incorrectly stated as being
1 mg
instead of 0.1mg), had a glucocorticoid potency of 5 times that of
the 20mg Covocort prescribed and the two together had a
high or
supraphysiological
potency. In his opinion,
in addition to this exogenous cortisol the plaintiff's body was still
producing its natural levels of physiological
cortisol. Thus, there
was an additive effect. He persisted in this view despite it being
put to him in cross examination that the
hypothalamic pituitary
adrenal ("HPA") axis meant that the body's negative
feedback loop would kick in and the hypothalamus
would ensure that
the adrenal gland stops releasing cortisol when cortisol levels in
the blood get high. Both Dr Kok and Prof.
Greeff disputed Dr
Promnitz's assertion, which they stated was biologically and
scientifically incorrect. The plaintiff has now
accepted this by way
of the concession made in closing argument and no longer relies upon
the evidence of Dr Promnitz that the
plaintiff received
supraphysiological doses of corticosteroids. This was a concession Dr
Promnitz refused to make when it was put
to him in cross-examination,
i.e. that not only that he had made a mathematical error in
calculating the dosage of the prescribed
steroids and that his
opinion of a supraphysiological dosage was not supported by the
literature.
[75]
Dr Promnitz testified however that even though the plaintiff might
have been given physiological or low doses of corticoids,
the drugs
would still have had an influence on her pituitary adrenal axis
resulting in suppression and side effects from the combination
of the
Covocort and Florinef she was prescribed. In his opinion, a patient
who is given steroids for no indication (a normal patient,
apart from
hypertension in the plaintiff's case), is subjected to the additive
effect of the “
two drugs”
on suppressing the adrenal gland.
In his
opinion the combined use of these agents exhibit glucocorticoid
activity, and hence it was recorded at CHB that the plaintiff
had a
cushingoid appearance and steroid induced proximal myopathy. He
testified that although a dosage of 5mg to 10mg a day of
steroids was
considered a low dose, there are trials that have concluded that even
low doses cause many adverse events such as
osteoporosis, myopathy,
cardiovascular disease, cataracts and increased risk of infections.
His counsel, to the extent that it
resulted in supraphysiological
doses, correctly rejected his additive effect theory, and his
generalised assumption that all steroids
have adverse effects added
no probative value to proving a link between the treatment
administered to the plaintiff and her alleged
sequelae.
[76]
I agree with defendant's counsel that without the high dosage theory
none of the findings of Dr Promnitz are supported.
Hence, when
this was in fact put to him in cross-examination he refused to make
the concession because it would have been an error
fatal to the
plaintiff's case. He eventually conceded that he was wrong, but
persisted without providing a basis for his reasoning
that Florinef
0.1mg had a glucocorticoid potency level of more than 20mg of
Covocort. This was despite the fact that the table
he had himself
provided and the extract from the Goodman and Gillman textbook
indicated that at the dosage prescribed by the defendant
there was no
appreciable glucocorticoid effect. The table in fact is supportive of
Prof Greeff's evidence that that Florinef (as
a fludrocortisone) has
no appreciable glucocorticoid potency at the dosage prescribed by the
defendant.
Tuberculosis
[77]
In his second report Dr Promnitz stated the lymphadenopathy on the
right-hand side proved was secondary TB and the diagnosis
of TB of
the spine were most likely the
direct result
of the plaintiff
having been on corticosteroids for 19 months. This is because
corticosteroids interfere with the immune system
thus predisposing
the patient to the development of certain infections, with TB being
one of them. His opinion was that the plaintiff's
TB might have been
a reactivation of latent TB and went further to say that it is
well
accepted
that patients on long-term steroids are at a greater
risk of reactivation of TB or primary TB infection. This evidence was
again
based on the incorrect assumption of a high dosage and, very
significantly, he did not deal with the actual and correct dosage of

the steroids prescribed by the defendant.
[78]
TB is the main
sequelae
the plaintiff relies on, and in this regard the academic article
relied on by Dr Promnitz (the Nicolaides article) fails to support
Dr
Promnitz's conclusions of the link between steroids and the
plaintiff's
sequelae
when regard is had to the sources the article he relied upon. The
source articles, which Prof Greeff testified about, confirm that
Dr
Promnitz's conclusions are scientifically unsupported. As one
example, the article Dr Promnitz refers to a study by Dickson
as
stating that patients receiving 5mg prednisolone continuously for the
last three months, six months or three years had a 30%,
46% or 100%
increased risk of serious infection respectively. However, it
excludes reference to the fact that this increased risk
applies to
current users
of
prednisolone. The plaintiff was not in the category of a current user
as she had been diagnosed with TB of the cervical gland
in November
2013, more than a year after she stopped taking the medication
prescribed by the defendant. Hence, the conclusions
would not apply
to her, and accordingly Dr Promnitz, in relying on the article to
support his proposition that the plaintiff was
more susceptible to TB
because of the cortisol prescribed by the defendant, would have been
relying on misleading information.
Also, the article Dr Promnitz
relied upon does not state (which the source Dickson article does),
that discontinuing a two-year
course of 10mg prednisolone, six months
ago halved the risk compared to ongoing use. It should also be noted
that 10mg prednisolone
is double the dosage of cortisol prescribed by
the defendant and a two-year course is longer than the period the
plaintiff was
on the steroid medication prescribed by the defendant.
Prof. Greeff alerted the court to the fact that he
had considered the Dickson article (which was not provided by the
plaintiff),
and the Dickson article does not contain the information
and figures that are attributed to it. The article relied upon by Dr
Promnitz
clearly contained incorrect information upon which he
relied.
[79]
Dr Promnitz's opinion that the steroid therapy led to the plaintiff
developing TB more than a year after she stopped the steroid
therapy,
was moreover not supported with reference to any evidence. In the
joint minute prepared by Dr Promnitz and Dr Kok both
agreed that the
plaintiff was diagnosed with
possible
spinal tuberculosis at Helen Joseph Hospital and that they did not
have sight of the x-rays on which the diagnosis was based.
Notwithstanding the absence of a bone biopsy (Dr Promnitz held the
view that it was inappropriate to perform a bone biopsy), Dr
Promnitz
attempted to elevate the possible spinal TB to that of a definitive
diagnosis with reference to a handwritten note questioning
the
presence of spinal TB. The TB diagnosis was made by way of a needle
biopsy on 29 August 2013. On the plaintiff's version in
evidence in
chief and without the concessions made in cross-examination, she
stopped using the Covocort and Florinef prescribed
by the defendant a
year before her lymph node TB diagnosis. Furthermore, Dr Promnitz's
evidence on the existence of spinal TB was
that the Helen Joseph
Hospital records have an entry referring to the plaintiff’s T11
“
end plate eroded”
being highly suggestive of TB of the spine or what is called “
POT
spine,”
which in his view is
consistent with TB of the spine. Previously there was no such erosion
only the T12 fracture diagnosed in 2011.
[80]
Dr Promnitz continued to rely on literature which is not relevant to
the facts in this matter because it applies to high dosage
and also,
in respect of the causal criteria, states that the effects were not
present for past users, such as the plaintiff.
Another
misleading or incorrect reference to the academic article relied upon
by Dr Promnitz arose in regard to the conclusion
that an
epidemiological study of patients with TB showed they were nearly
five times more likely to have been using glucocorticoids
at the
time of their diagnosis
. When the source article is consulted it
qualifies the five-fold reference by stating that patients who were
currently
exposed to a glucocorticoids had an approximately
five fold increased risk of developing
new
TB. The plaintiff
had subclinical or dormant TB not new TB and hence these conclusions
are not applicable to her. Furthermore,
the article states that the
magnitude of association was larger with the prednisone equivalent
dose than with a physiological dosage
(i.e. 7.5 mg daily) and was
larger with more than one prescription for a glucocorticoid. When
this was put to Dr Promnitz in cross-examination
his response was
that the articles were only provided for guidance purposes.
[81]
Dr Promnitz's reliance on a second academic article in his report of
31 January 2016 was also shown in cross-examination to
be wholly
incorrect and misleading. According to him the article refers to
infection rates from a meta-analysis of control trials
in which
glucocorticoids were given, and this supported his opinion that the
plaintiff was at a greater risk of reactivation of
TB as a result of
the Covocort prescribed by the defendant. The reference in his report
that infection rates were significantly
increased
only
in
patients given an average dose of prednisone of more than 10mg/day
(which is not applicable to the plaintiff) or an accumulative
dose of
700mg (which would be applicable to the plaintiff if it was correct)
is the converse of what was actually stated in the
article. It said :
"
The rate
was not
increased in patients
given a daily dose of less than 10mg [which includes the plaintiff]
or accumulative doses of less than 700mg
of prednisone".
This contradicts Dr Promnitz's testimony. He interpreted the article
to mean that the converse would apply i.e. if the rate is
not
increased in patients given a daily dose of less than 10mg a day then
it must mean that it does increase with a daily dose
of more than
10mg a day. As matter of logic this reasoning is flawed. The
plaintiff was given a dose of 5mg prednisone daily and
hence her rate
of risk was not increased because her dosage was below 10mg
prednisone daily. The use of the word "or"
makes it clear
that the article finds that in either category i.e. a daily dose of
10mg daily or accumulative doses of less than
700mg, the risk is not
increased. Since the plaintiff fell into the first category i.e. her
daily dose was less than 10mg, she
could not as a matter of logic
have also fallen into the second category as well. Dr Promnitz
interpreted this to mean that she
would have been in both categories
and in relation to the second category she would be at higher risk of
infection. Reference to
the article makes it clear that this cannot
be the correct interpretation. The article also goes further than
this and provides
a graph which makes it clear that even at a
duration of 1000 days (i.e. more than double the duration for which
the plaintiff was
prescribed the medication by the defendant)
provided the prednisone daily dosage is less than 10 mg, there was no
increased risk
of infection. This was confirmed by Prof Greeff in his
evidence.
[82]
The experts for the defendant thus testified that, unlike the
articles referred to by Dr Promnitz, the literature clearly shows

that the increased risk of developing TB associated with
glucocorticoid therapy is increased for those who are
current
users and on a high daily dose
, but not for past users such as
the plaintiff.
[83]
There is no support in the literature for Dr Promnitz's opinion,
particularly when she was already off steroid therapy at the
time of
her diagnosis of TB and even earlier when she noticed the lump in her
neck. Thus, defendant's counsel submitted, plaintiff
cannot advance a
case that she contracted TB whilst on the treatment prescribed by the
defendant. This would be in direct contradiction
of the proven facts
and the plaintiff's own version that she developed the lumps on her
neck in May 2013, which is 11 months after
she stopped the steroid
therapy. In order for her allegation to be true, this court would
have to find that throughout the time
she was on steroid therapy from
February 2011 until June 2012 and she was in and out of hospitals and
examined by various doctors,
they all ignored signs of TB which would
have been present had she developed the infection whilst on the
treatment, which was the
testimony of Dr Kok. This also disposes of
the submission by plaintiff's counsel that the lymphadenitis must
have started developing
or reactivating during the period that she
was on the steroid therapy. This is not an inference that can
correctly be drawn from
the facts.
Ischaemic
heart disease
[84]
The academic article that Dr Promnitz relied upon stated that the
relative risk for cardiovascular events in patients receiving
high
dose
glucocorticoids (more than 7.5 mg of prednisolone) was 2.5.6
after adjustment for covariates. The article also states that
current
use
of glucocorticoids was associated with increased risk of
heart failure and a smaller risk of ischaemic heart disease.  In
the joint minute of Dr Promnitz and Dr Kok, Dr Promnitz admits there
is no direct link of steroid usage causing coronary artery
disease
but stated that there are indirect effects on lipids and blood
pressure, which may contribute to its development. He again
relied on
the high dose theory, which has since been rejected by his legal
representatives. This confirms there is no scientific
or reasonable
basis for the statement that the steroid therapy contributed to the
plaintiff's ischaemic heart disease.
[85]
In his third report Dr Promnitz states that the plaintiff appears to
have been left with impaired left ventricular function
following her
development of ischaemic heart disease. However, under cross
examination, when he was referred to the report of Dr
Kalk prepared
after the plaintiff's 2015 procedure which indicated that the
plaintiff had no left ventricular hypertrophy, Dr Promnitz
conceded
that he did not actually conduct any tests to establish whether the
plaintiff in fact had impaired left ventricular function.
This once
again confirms, as was submitted by defendant's counsel, that Dr
Promnitz did not properly apply his mind to whether
or not
glucocorticoid therapy had any causal link to the plaintiff's
ischaemic heart disease and which occurred three years after
she
stopped the steroid treatment.
[86]
In relation to the acute myocardial infarct suffered by the plaintiff
in October 2014, Dr Promnitz stated that the fact that
in 2011 she
had normal coronary arteries, rendered it very
unusual
[4]
that a person her age would suddenly develop significant coronary
artery disease. He confirmed however that there was no direct
link
between steroid therapy and ischaemic heart disease. He said that the
plaintiff had been left with what appeared to be impaired
left
ventricular function following her development of ischemic heart
disease. However, he confirmed that when he examined the
plaintiff
subsequently, he did not find any evidence of left ventricular
hypertrophy.  Hence his only conclusion was that
he found it
difficult to account for someone who had normal coronary arteries in
2011 to have required a bypass three to four years
later.
Osteoporosis
[87]
In the academic article that Dr Promnitz relied upon, a study showed
that therapy with
high doses
of oral glucocorticoids caused
significant decease in bone mineral density ("BMD") even in
the first two months of therapy.
As a result, there is an increased
risk of osteoporotic fractures and it has been estimated that
fractures may occur in up to 30
to 50% of patients on glucocorticoid
therapy but fortunately there is a
rapid decrease
on the risk
on cessation of therapy. Similar findings are observed in a more
recent study showing that low daily dose prednisone
(less or equal to
7.5 mg per day) with high accumulative doses increases the risk for
fractures. The article continues to say that
the risk declines
rapidly, with the decrease beginning three months after cessation of
therapy.
[88]
Dr Promnitz conceded that the plaintiff does not have osteoporosis.
He confirmed that he and Dr Kok compiled a joint minute
in which they
agreed that the plaintiff had osteopenia not osteoporosis. This was
based on the bone density scan done on 16 February
2011. The
plaintiff produced no contemporaneous bone density scores to
establish that she has osteoporosis, and despite having
examined the
plaintiff and having stated in an earlier report that the plaintiff
is at high risk of developing osteoporosis, Dr
Promnitz did not
himself perform the necessary bone density tests.
[89]
Dr Promnitz criticised the fact that the defendant prescribed Protos
for the plaintiff, even though the plaintiff's bone density
scores
increased considerably while she was on the glucocorticoid therapy
together with the Protos and vitamin supplements prescribed
by the
defendant. In fact, the academic article that the plaintiff relies
upon indicates that the plaintiff, at the time she saw
the defendant
and he diagnosed her with osteoporosis, was in the higher risk
category for osteoporosis, as she is over 40, has
a previous
osteoporotic fracture and a T-score of minus 2.5. The article
recommends that adults with a moderate to high risk should
be treated
with calcium and Vitamin D as well as an oral bisphosphonate. This
was the treatment the defendant prescribed upon making
the diagnosis
of osteoporosis in 2011.
[90]
Dr Promnitz indicated in his report that a diagnosis of osteoporosis
could only be made where there is a T-score of minus 2.
The Helen
Joseph Hospital diagnosed the plaintiff with osteoporosis in
September 2012 based on T-scores of minus 1.2 and minus
1.5, and
based on Dr Promnitz's evidence this is also incorrect. Therefore,
other than criticising the defendant for treating the
plaintiff for
osteoporosis when in his opinion there was no basis for doing so, Dr
Promnitz was unable to support the allegation
that there is a link
between the steroid therapy prescribed by the defendant and any
possible osteoporosis diagnosis.
Other
relevant symptoms and complications associated with long-term steroid
use: cushingoid features and hypertension
[91]
The plaintiff does not strongly rely on the other symptoms and
complications associated with long-term steroids except for

cushingoid features and hypertension. These are dealt with below.
Cushingoid
features
[92]
The only inference that can be drawn from the fact that the plaintiff
was recorded as being on Meticorton is that she had been
taking
Meticorton without a prescription after she stopped the treatment
prescribed by the defendant, and this caused the cushingoid
features.
This is consistent with the literature. Dr Promnitz conceded that the
plaintiff did not have Cushing’s or Cushing
Syndrome and Dr Kok
was in agreement. Dr Promnitz testified that when plaintiff was
admitted to CHB it was recorded upon her admission
that she was on
Meticorton 10mg three times a day, and that this is 30mg of
prednisone daily (i.e. a high dose). This was at the
point where the
plaintiff relied upon the April 2012 admission note as the third
prescription, the implication being that the defendant
had prescribed
the Meticorton. Dr Promnitz's version changed in cross examination
when it was put to him that the document was
not a prescription but
an admission sheet and he then downplayed Meticorton as simply a
generic of Covocort, which he said is administered
when a pharmacy
cannot supply Covocort. However, Dr Kok's evidence was that
Meticorton is a powerful glucocorticoid far more potent
than the
hydrocortisone prescribed by the defendant. Dr Kok testified that if
the plaintiff was taking 10mg Meticorton prior to
her admission to
CHB and after her last repeat script from the defendant finished,
even for a short period of time, this would
account for her
cushingoid features. This was consistent with Dr Promnitz's evidence
in chief. The cushingoid features therefore
cannot on the
probabilities be attributed to the treatment prescribed by the
defendant.
Aggravation
of pre-existing hypertension
[93]
The Nicolaides article relied upon by Dr Promnitz states that
increased glaucoma, depression and increased blood pressure were

observed in patients receiving dosages of more than 7.5mg per day of
prednisone. It is common cause that the plaintiff's dosage
was less
than this threshold. Dr Promnitz's reliance on this article was based
on his mistaken belief that the plaintiff was on
a higher dose than
that which the defendant had actually prescribed.
[94]
In his evidence in chief Dr Promnitz relied upon a package insert for
Florinef, which was confirmed by Prof Greeff to list
every possible
adverse reaction that could occur and to have no probative value in
this matter. It is accordingly disregarded.
[95]
In the absence of any material evidence that establishes that the
plaintiff's risk of hypertension increased after glucocorticoid

therapy ceased, there is no causal link established pre the
defendant's misdiagnosis of Addisons and post the steroid therapy
prescribed by defendant. In order to establish that the steroid
therapy aggravated plaintiff's pre-existing hypertension, the
plaintiff
was required to show that prior to the commencement of the
therapy the plaintiff's hypertension was under control, but no
evidence
to this effect was led. Secondly, the plaintiff would have
had to show that post her cessation of the steroid therapy the
hypertension
was under control. Thirdly, the plaintiff would have had
to show that while on the steroid therapy her hypertension was more
elevated
than it was before she was put on the steroid therapy. The
plaintiff was unable to do so.
Has
negligence been established?
[99]
It is trite that he who asserts must prove and it is therefore the
plaintiff who bears the onus of proving that the defendant
was
negligent, and that his negligence caused the damage suffered.
Negligence involves an enquiry into whether the conduct of the

defendant measured up to the standard expected of a reasonable person
in the particular circumstances:
Kruger
v Coetzee.
[5]
This has been elevated in medical negligence cases to the reasonable
medical practitioner. The court held that for the purposes
of
liability
culpa
arises if - (a) a
diligens
pater
familias
in the position of the defendant - (i) would foresee the reasonable
possibility of his conduct injuring another in his
person or property
and causing him patrimonial loss; and (ii) would take reasonable
steps to guard against such occurrence; and
(b) the defendant failed
to take such steps.
[100]
In
Meyers
v
MEC Department of Health, Eastern Cape
[6]
Plasket JA
reminded us that more than a 100 years ago, in
Mitchell
v Dixon
[7]
the
then Appellate Division held in relation to the standard of care
expected of medical practitioners that :
"a
medical
practitioner is not expected to bring to bear upon the case entrusted
to him the highest possible degree of professional
skill, but he is
bound to employ reasonable skill and care; and he is liable for the
consequences if he does not."
[101]
Thus
the approach taken by the courts
[8]
is that the standard that is required is not based on what can be
expected of the exceptionally able doctor, but on what can be

expected of the ordinary or average doctor in view of the general
level of knowledge, ability, experience, skill and diligence

possessed and exercised by the profession, bearing in mind that a
doctor is a human being and not a machine and that no human being
is
infallible. Furthermore, an error of clinical judgment will not
constitute negligence if the doctor has adhered to the requisite

standard of reasonable care. Defendant's counsel referred the court
to
Pringle
v Administrator Transvaal
[9]
where the court considered whether a surgeon committed an error of
clinical judgment and referred with approval to
Whitehouse
v Jordan
[10]
and stated the following:
"The true
position is that an error of judgment may, or may not, be negligent;
it depends on the nature of the error. If it
is not one that would
have been made by a reasonable professional professing to have the
standard and type of skill that the
defendant
held himself out as having, and acting with ordinary care, then it is
negligent.
If on the other hand,
it is an error that a man, acting with ordinary care might have made,
then it is not negligence.
(Counsel's emphasis).
[102]
The plaintiff pleaded three bases for alleging that the defendant was
negligent in making the diagnosis of Addisons: he relied
solely on
two blood tests and failed to do any other appropriate tests; he
failed to avoid the misdiagnosis when by the exercise
of reasonable
care he should have done so; and he failed to perform the long
Synacthen stimulation test to confirm the diagnosis
when he could and
should have done so.
[103]
In determining whether the defendant's conduct in incorrectly
diagnosing Addisons involved the application of reasonable skill
and
care of a physician in the circumstances, I accept the defendant's
evidence that the low cortisol levels and clinical presentation
of
the plaintiff in February 2011 led to him to suspect she had
Addisons. She reported symptoms that he recorded on the disability

claim form he completed on her behalf. Notwithstanding his exercise
of clinical judgment, in my view he ought to have foreseen,
as
reasonable physician, that without following up with appropriate
tests (the insulin hypoglaecemic or the Synacthen test) to
confirm
the Addisons diagnosis, there was a reasonable possibility that the
diagnosis was wrong.  The link between his diagnosis
and her
high blood pressure also indicated that he was incorrect. A
reasonable physician would in my view have taken steps to guard

against an incorrect diagnosis in circumstances where a test is
available to confirm the diagnosis.  Insofar as the defendant's

counsel does not rely on Synacthen being unavailable at the time the
diagnosis was made, there was no explanation why he did not
even
administer the insulin hypoglaecemic test to confirm his diagnosis.
The defendant conceded that he relied on two tests indicating
normal
(the first albeit just under normal) cortisol levels. He conceded
that his diagnosis was incorrect and that he did not do
the necessary
tests.
[104]
The experts called by the defendant were understandably careful to
avoid reference to negligence, instead referring to the
treatment
and/or diagnosis without a follow up test being "
inappropriate"
.
The expert consensus in relation to the issue of negligence includes
the joint minute of Dr Promnitz and Prof Richards in which
they agree
that the diagnosis of Addisons was inappropriate and the appropriate
tests were not performed by the defendant to make
the diagnosis, as a
result of which the plaintiff was placed on Covocort and Florinef
medication for a period of approximately
19 months. In the joint
minute of Dr Promnitz and Dr Kok they agree that the diagnosis of
Addisons by the defendant was incorrect
and it was imperative that a
Synacthen test should have been performed before placing the
plaintiff on lifelong replacement therapy
(although it became common
cause he had only issued prescriptions for one year).
[105]
I am therefore in agreement with the submission by plaintiff's
counsel that the common cause facts and the expert consensus
in
relation to the issue of negligence in making the Addisons diagnosis
based purely on his clinical judgment and the two blood
tests, limits
the dispute between the parties to that of causation. In other words,
in failing to conduct follow up tests to confirm
his incorrect
diagnosis of Addisons and in prescribing steroid therapy as a result,
the defendant did not employ the reasonable
skill and care of a
physician in the circumstances. He ought to have foreseen that the
plaintiff might suffer adverse consequences
if his diagnosis was
incorrect and failed to take adequate steps to prevent this.
Has
causation been established?
[106]
It follows that the issue to be determined is whether the negligent
diagnosis of Addisons, and the consequent administration
of low doses
of steroid therapy for a period of 12 months, caused the series of
sequelae
the plaintiff allegedly suffered.
[107]
It is trite that
res
ipsa loquitur
(the facts speak for themselves) is not applicable in medical
negligence matters both in respect of negligence and causation. This

has been confirmed in the
locus
classicus
of medical negligence cases,
Van
Wyk v Lewis.
[11]
In
Goliath
v MEC for Health, Eastern Cape
[12]
the Supreme Court of Appeal reconsidered the relevance of the
doctrine and referred to the reluctance of the courts to apply the

maxim as being
"....because,
as Lord Denning MR observed in Hucks v Cole
[1968] 118 New LJ 469
([1993]
4 Med LR 393)
‘with the best will in the world things
sometimes went amiss in surgical operations or medical treatment. A
doctor was not
to be held negligent simply because something went
wrong’. For to hold a doctor negligent simply because something
had gone
wrong, would be to impermissibly reason backwards from
effect to cause (Medi-Clinic Limited v Vermeulen (504/13)
[2014]
ZASCA 150
(26 September 2014) para 27).
The
court confirmed however that (at [12]) , "
in
every case, including one where the maxim res ipsa loquitur is
applicable, the enquiry at the end of the case is whether the

plaintiff has discharged the onus of resting upon her in connection
with the issue of negligence ..."
[108]
The plaintiff is thus required to prove on a balance of probabilities
that a causal link was established between her alleged
sequelae
and the negligent diagnosis of Addisons in February 2011 and
subsequent 20mg cortisol prescribed which ceased (at the latest on

her own version) in August 2012 (but on the probabilities on June
2012)
.
[109]
Causation comprises of two components to establish liability. The
first is factual causation, which requires the question
of whether a
negligent act or omission caused the harm giving rise to the claim.
The second is legal causation, which requires
a consideration of
whether the negligent act or omission linked to the harm giving rise
to the claim is sufficiently close or directly
connected for legal
liability to occur. If the link on the facts between the negligent
act and the consequences is at best tenuous
then the plaintiff fails
at proving factual causation and legal causation does not even become
relevant.
[110]
The test for factual causation as set out in
Lee
v Minister for Correctional Services
[13]
is
still the "
but-for
"
test, as counsel for the defendant submitted, since the plaintiff is
not relying on an omission but an act by the defendant,
being the
misdiagnosis of Addisons and the consequent prescription of steroids.
This requires a plaintiff to establish that the
wrongful and
negligent conduct was probably a cause of the loss, which calls for a
sensible retrospective analysis of what would
probably have occurred,
based upon the evidence and what can be expected to occur in the
ordinary course of human affairs: see
Mashongwa
v Passenger Rail Agency of South Africa (PRASA) t/a Metrorail.
[14]
This court
is thus required to determine whether, but for the defendant's
wrongful conduct in diagnosing Addisons and prescribing
steroids, the
plaintiff's alleged
sequelae
would not have occurred. The plaintiff must therefore prove that it
is more likely than not, but for the defendant's wrongful and

negligent conduct, the harm she suffered would not have occurred. In
other words, but for the low dose steroids prescribed by the

defendant following his negligent diagnosis of Addisons she would not
have suffered further problems resulting in her being medically

boarded in 2012 and had further
sequelae
that manifested in 2013 and 2014, most importantly cervical gland TB
(which plaintiff suggests must have started in 2011 - 2012),
and
cardiac disease.
[111]
Plaintiff's counsel submitted in regard to causation, that neither
the defendant nor anyone else forwarded any other possible
cause for
the conglomerate of complications that the plaintiff experienced and
which are common to steroid use. Furthermore, counsel
submitted that
it was not helpful that defendant's case is that the complications
only arise with supraphysiological doses of steroids,
because the
literature does refer to adverse effects in consequence of low,
normal or high doses. Counsel accepts that the risk
is higher with
higher dosages but submits that the adverse effects can manifest even
at low or normal dosages.  In this regard,
he relied on the key
concession made by Prof Greeff that the effect of steroids is not the
same on all individuals, and that different
patients respond
differently to steroid use. The plaintiff thus submits that she fell
into a category of those who are more susceptible
even though the
dosages prescribed for her were not high but normal. The balance of
probabilities therefore strongly favour her
on causation in that the
impact of the steroids on her showed up very shortly after the
administration of the steroid therapy in
February 2011. She was
discharged on 8 February and the next day collapsed and had to be
wheeled back into hospital and she spent
the next year in and out of
hospital with the defendant not knowing what was causing her
symptoms. Thus, it is clear that her complications
are linked to the
steroid therapy, and the evidence that stands firm is that post
February 2011 the plaintiff presented with a
conglomeration of
complications which are common to steroid use. Plaintiff's counsel
accepts that her chest pain in February 2011
was in all probability
caused by the old T12 compression fracture. However, in his
submission the fracture was a red herring and
hence the plaintiff
does not rely on anything related to the old fracture.
[112]
Plaintiff's counsel also submitted the defendant did not contest the
lymph node TB in cross examination but merely suggested
that if the
plaintiff first noticed the lump in her neck in 2013 and her steroid
therapy ceased in 2012, there could be no link.
However, this misses
the point because both Dr Promnitz and Prof Richards suggest that it
was reactivation of latent TB, and the
court is bound by their
opinion as the Supreme Court of Appeal made it clear in
Bee
v Road Accident Fund
[15]
that when
experts agree on facts or opinions it becomes common cause unless a
party repudiates the agreement. Hence, plaintiff's
counsel submitted
that it was cast in stone that firstly, plaintiff presented with
lymph node TB in 2013 and tested positive for
it. It is not clear,
counsel submitted, when the latent TB began to reactivate but it is
common sense that it would not appear
overnight. Also, her heart was
normal in February 2011 but within two to three years she started to
develop serious problems, which
led to a heart attack and a stent
being inserted. Thus, it was submitted that there can be only one
cause for heart disease and
the TB and that is the steroids, and the
defendant has proffered no other cause. This is with respect not an
inference I can correctly
draw on the facts in evidence. It calls for
a conclusion, that it was necessary to “
individualise”
patients and the plaintiff was more susceptible to steroids than
other patients might be. There were no facts established in this

regard. Hence we have only Dr Promnitz's opinion that since
corticosteroids have different effects on different patients, one can

never predict what effect it will have on a patient. He was unable to
provide the court with any other possible causes for the
series of
complications the plaintiff presented with, except to suggest that
the medical literature reveals a definite association
with
corticosteroids and an increased risk of certain diseases and
conditions, because steroids work on the immune system and this

affects the inflammatory process. However, the evidence led by
defendant's experts, and based on the literature, was that only
high
doses have an effect on suppressing the immune system and hence Dr
Promnitz's evidence on this issue falls to be rejected.
[113]
It is also clear from the literature and documentary evidence
discussed above that the literature relied upon by Dr Promnitz
in
preparing his reports and in his testimony does not support his
conclusions. In this regard, I am in agreement with the defendant's

counsel that a careful consideration of the literature, as was done
in cross examination, shows that he in most instances did not

consider the literature in its entirety but rather cherry picked
aspects that supported his theories and opinion and in some instances

as indicated above, often misinterpreted the literature to support
his opinion. This is why Prof Greeff's evidence demonstrated
that the
very literature Dr Promnitz relied upon did not support his opinion.
It is clear that because Dr Promnitz had made the
fatal error of
classifying the plaintiff's dosage as high dose, he was inevitably
going to fall into the trap of referring to the
aspects of the
literature that related to high doses and not the low dose the
plaintiff was on that became common cause at the
end of the trial.
For the first time in his third report in August 2015 he referred to
the dosage actually prescribed by defendant.
Up to this point his
generalisations regarding the link between Covocort and the
plaintiff's alleged complaints could be excused
on the basis that he
did not know what dosage was prescribed. In this report he noted that
the dosage was Covocort 10mg, 5mg at
be administered at noon and 5 mg
at night. He stated further that the plaintiff was also prescribed
Florinef. He then explained
that this still led to a
supraphysiological dose because this exogenous dose of synthetic
steroids would have had an additive effect
given her body's own
physiological dose.  This theory came crumbling down in cross
examination and he refused to concede a
basic issue of maths and
logic and it was left to his legal team to refuse to deal with his
evidence in their heads of argument.
Hence I agree with the
submission made by defendant's counsel that having regard to the
circumstances of the matter, and the proven
and common cause facts
between the parties, it is evident that there is no support in the
scientific and medical literature or
on the facts for the contention
that the dosage prescribed by the defendant placed the plaintiff at
higher risk of infection and
caused her symptoms.
[114]
The experts for the defendant, Prof Greeff, Prof Richards and Dr Kok,
based their evidence on the facts and the scientific
and medical
literature. Their opinions were logical and reasoned. Prof Greeff's
extensive knowledge based on his experience as
a clinical
pharmacologist of was immense benefit to the court despite the
plaintiff's suggestion that his evidence should be disregarded
as he
was not involved in the development of steroids and did not have
experience with treating patients. His evidence was based
on the
facts, literature and logic and when an issue fell outside his area
of expertise he elected not to comment and deferred
to the relevant
experts. In contrast, when Dr Promnitz was faced with the absurdity
of his suggestion that Florinef at the dosage
prescribed by the
defendant had a glucocorticoid effect, he refused to make the
concession despite the fact that there was no support
for this view.
He persisted with his outlier view until his legal representatives
were forced to make the concession during closing
argument.
[115]
Prof Greeff was of great assistance to the court in explaining how
medical trials are conducted and the importance of determining
the
risk to benefit ratio in this process. He explained that
glucocorticoids are dangerous drugs but at the dosage prescribed by

the defendant they were not dangerous. His evidence was that dosage
is a material factor determining at what stage a drug is considered

to be dangerous and thus not worth the benefits it may yield. His
evidence was also helpful in explaining that the pamphlets inserted

by manufacturers into drugs packing has to list all possible side
effects and cannot be understood to be a concession as to the

probabilities of such side effects manifesting when the drug is
administered. Dr Kok's evidence was similarly of assistance to
the
court and despite the plaintiff's submissions as to her subjectivity,
her inexperience and somewhat naive approach as a first-time
witness
in court lent to her objectivity. She made the necessary concessions
about the inaccuracy of certain facts she relied upon
for her
conclusions and adequately explained why she had asked for a second
joint minute to be signed.
Conclusion
[116]
In my view therefore, if one has regard to the fact that the
plaintiff's osteopenia was improved while on the steroid therapy
with
Protos, vitamin D and calcium supplements prescribed by the
defendant; the plaintiff was diagnosed with TB of the cervical
glands
a year after she ceased the steroid therapy; and she experienced the
cardiac event three years after she ceased the steroid
therapy, the
probabilities do not favour a causal link. Nor is there a close
enough connection, as was required by the Constitutional
Court in
Mashongwa
v Passenger Rail Agency of South Africa (PRASA) t/a Metrorail
.
[16]
The
Court cautioned against the conflation of wrongfulness and causation,
and held that the wrongfulness element - the normative
consideration
based on social and policy considerations - should not be used to
contaminate the factual dimension of the causation
enquiry. If this
approach were to be accepted then the net of liability would be cast
too wide. The Court stated
[17]
:
"
no
legal system permits liability without bounds. It is universally
accepted that a way must be found to impose limitations on the

wrongdoer's liability. The imputation of liability to the wrongdoer
depends on whether the harmful conduct is too remotely connected
to
the harm caused or closely connected to it. When proximity has been
established, then liability ought to be imputed to the wrongdoer,

provided public policy considerations based on the norms and values
of our Constitution and justice also point to the reasonableness
of
imputing liability to the defendant".
[117]
In applying this approach to the facts in evidence it is clear there
is no causal link between the low dose Covocort and Florinef
and the
plaintiff's alleged
sequelae
. It was not established that the
steroid therapy predisposed the plaintiff to developing significant
coronary artery disease. All
that was left of the plaintiff's version
in the end was Dr Promnitz's opinion that he found it difficult to
account for her coronary
surgery in 2015 after her coronary arteries
were found to be normal in 2011, and the need for an
"individualised"
approach. Dr Promnitz also conceded that she did not have
osteoporosis and hence the link between the steroid therapy
prescribed
by the defendant and any osteoporosis diagnosis was not
proven. It was also not shown on a balance of probabilities that the
degenerative
changes in the plaintiff's spine were due to the steroid
therapy. Dr Promnitz testified that the T12 fracture could not be
disregarded
but then simply dismissed it as a red herring. It was in
addition not established that TB of the spine was a definitive
diagnosis.
The evidence of the defendant's experts established that
the reactivation of latent TB could only occur when
supraphysiological
doses were administered, as such doses result in
suppression of the immune system. Given that it became common cause
that the plaintiff
was not placed on an immuno-suppressant dose
prescribed by the defendant, any proximate cause between the steroid
therapy the defendant
prescribed (the Meticorton issue and her
evidence on leftover medication indicates the plaintiff may have been
on medication other
than that prescribed by the defendant) and her
alleged
sequelae
were not proven.
[118]
It must follow then that the negligent act committed by the defendant
in failing to perform any test to confirm his diagnosis
of Addisons,
as a result of which he placed the plaintiff on the low dose steroid
therapy for a year, is not causally linked to
the plaintiff's alleged
sequelae
. Insofar as it was submitted on behalf of the
plaintiff that the defendant failed to point to another cause of the
medical consequences,
it is not for the defendant to do so but for
the plaintiff, as a matter of logic and reasoning, to prove factual
and/or legal causation.
The high dosage theory contended for by the
plaintiff was proven to be a fallacy and the concession from the
plaintiff at the end
of the trial was fatal to the plaintiff's case.
In any event, having considered the evidence on each of the alleged
sequelae
, it was clearly established that none of the
sequelae
were suffered while the plaintiff was on the steroid treatment
and the evidence does not support a conclusion that
sequelae
suffered one to three years after steroid treatment ceased is
causally linked to the treatment.
[119]
The task of this court is to decide, at the conclusion of the trial,
whether, on all the evidence and the probabilities and
the inferences
to be drawn, the plaintiff has discharged the onus of proof resting
upon her on a preponderance of probabilities.
Despite my immense
sympathy for the plaintiff, I must find, for the reasons set out
above, that she has not done so.
Order
[120]
In the result, I make the following order:
The
plaintiff's claim is dismissed with costs.
________________________________
U. BHOOLA
Acting Judge of the High Court of
South Africa
Gauteng Local Division, Johannesburg
Appearances:
For
the Plaintiff: Adv G. J. Strydom SC
For
the Defendant: Adv L. Segeels - Ncube
[1]
The
defendant does not rely on the alleged stock outage of Synacthen as
part of its defence. When it was put to the defendant
in cross
examination that his reliance on the stock outage was a concoction
and would have been pleaded as a defence had he disclosed
it to his
legal representatives, his counsel placed it on record that their
case was that he did not do the test, and that they
do not intend
raising his inability to obtain the Synacthen as a defence.
[2]
Bee v
Road Accident Fund
(093/2017)
[2018] ZASCA 52
;
2018 (4) SA 366
(SCA) (29 March 2018)
[3]
Michael
and Another v Linksfield Park Clinic (Pty) Limited and Another
2001
(3) SA 1188
(SCA) (at
[34])
[4]
The
transcription suggests that Dr Promnitz used the word “
usual”
in the context, which is
incorrect.
[5]
Kruger v
Coetzee
1966 (2) SA 428
(A) at 430 E.
[6]
Meyers
v
MEC Department of Health, Eastern Cape
(1010/2018)
[2020] ZASCA 3
(4 March 2020) at [1].
[7]
Mitchell
v Dixon
1914
AD 519
at 525.
[8]
Castell
v De Greef
1993
(3) SA 501
(C),
1994 (4) SA 408
(C).
Michael
v Linksfield Park Clinic
(Pty) Ltd
2001 (3) SA 1188
(SCA) at 1192.
Goliath
v MEC for Health Eastern Cape 2
015
(2) SA 97
(SCA) at para 8.
Mitchell
v Dixon
1914 AD 519
at 525.
[9]
Pringle
v Administrator Transvaal
1990 (2) SA 379
(W)
.
[10]
Whitehouse
v Jordan
1981
(1) All ER 267
at 276H.
[11]
Van Wyk
v Lewis
1924 AD 438.
[12]
Goliath
v MEC for Health, Eastern Cape
2015
(2) SA 97
(SCA) at [9].
[13]
Lee v
Minister for Correctional Services
2013 (2) SA
144
CC.
[14]
Mashongwa
v Passenger Rail Agency of South Africa (PRASA) t/a Metrorail
2016 (3) SA
528 (CC).
[15]
Bee v
Road Accident Fund
(093/2017)
[2018] ZASCA 52
;
2018 (4) SA 366
(SCA) (29 March 2018)
[16]
Mashongwa
v Passenger Rail Agency of South Africa (PRASA) t/a Metrorail
2016 (3) SA
528
(CC) at [64].
[17]
At [64].