Conduct and Competence Committee
Substantive hearing
7 – 18 December 2015 and 6 – 8 January 2016
Nursing and Midwifery Council, 114 – 116 George Street, Edinburgh
Name of
Registrant Nurse:
Kirsteen Jane Stewart
NMC PIN:
83H0529S
Part(s) of the register:
Registered Nurse – Sub Part 1
Adult – October 1986
Registered Midwife – March 1989
Area of Registered Addresses:
Scotland
Type of Case:
Misconduct
Panel members:
Anne Booth (Chair, lay member)
Julie Tindale (Registrant member)
John Liddington (Lay member)
Legal Assessor:
Gerard Coll
Panel Secretary:
Sebastian Harrison/Julia Wanless
Nursing and Midwifery Council:
Represented by Michael Collis, case presenter,
instructed by the Nursing & Midwifery Council
Regulatory Legal Team
Mrs Stewart:
Not present and not represented
Facts proved:
1 and 2 in relation to 15 service users listed in
schedule 1
Fitness to practise:
Impaired
Sanction:
Striking-off order
Interim Order:
18 month interim suspension order
Page 1 of 96
Charges:
That you, while employed by NHS Grampian as a registered midwife working at
Aberdeen Maternity Hospital:
1.
Between 4 October 2007 and 13 March 2010 administered a bolus dose of an
oxytocic drug to one or more of the service users listed in schedule 1.
2.
Your actions at charge 1 above caused or contributed to the fetuses of one or
more of the service users listed in schedule 1 experiencing bradycardia.
AND, in light of the above, your fitness to practise is impaired by reason of your
misconduct.
Schedule 1
A.
Mother A, date of delivery 4 October 2007 – not proved
B.
Mother B, date of delivery 3 November 2007 – proved
C.
Mother C, date of delivery 8 November 2007 – proved
D.
Mother D, date of delivery 17 November 2007 – not proved
E.
Mother E, date of delivery14 June 2009 – proved
F.
Mother F, date of delivery 17 June 2009 – proved
G.
Mother G, date of delivery 2 August 2009 – not proved
H.
Mother H, date of delivery 19 September 2009 – proved
I.
Mother I, date of delivery 20 September 2009 – not proved
J.
Mother J, date of delivery 16 October 2009 – proved
K.
Mother K, date of delivery 30 October 2009 – proved
L.
Mother L, date of delivery 3 November 2009 – proved
M.
Mother M, date of delivery 15 November 2009 – proved
Page 2 of 96
N.
Mother N, date of delivery 23 November 2009 – proved
O.
Mother O, date of delivery 23 November 2009 – proved
P.
Mother P, date of delivery 28 November 2009 – not proved
Q.
Mother Q, date of delivery 5 February 2010 – proved
R.
Mother R, date of delivery 6 March 2010– proved
S.
Mother S, date of delivery 11 March 2010 – proved
T.
Mother T, date of delivery 13 March 2010 – proved
Decision on Service of Notice of Hearing:
The panel was informed at the start of this hearing that Mrs Stewart was not present
and was not represented.
In the light of the information available, the panel was satisfied that notice had been
served, as advised by the legal assessor, in compliance and accordance with Rules 11
and 34 of The Nursing and Midwifery Council (Fitness to Practise) Rules Order of
Council 2004 (as amended February 2012) (The Rules):
11.— (2) The notice of hearing shall be sent to the registrant—
(b) in every case, no later than 28 days before the date fixed for the hearing.
34.—(1) Any notice of hearing required to be served upon the registrant shall be
delivered
by sending it by a postal service or other delivery service in which delivery or receipt is
recorded to,
(a) her address in the register
(b) where the practitioner is represented by a professional body or trade union, at the
business address of that professional body or trade union; or
(c) In any other case –
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(i) her address in the register, or
(ii) where this differs, and it appears more likely to reach her at her last known
address, the registrant’s last known address
Notice of this hearing was sent to Mrs Stewart, at her registered address, on 9
September 2015 by recorded delivery. The panel came to the conclusion that this
complied with the rules of service.
Proceeding in the absence
The panel then considered continuing in the absence of Mrs Stewart. The panel heard
the submissions made by Mr Collis, on behalf of the Nursing and Midwifery Council
(NMC), and accepted the legal assessor’s advice.
The panel was mindful that, whether to proceed in absence or not, was a discretion that
must be exercised with the utmost care and caution as referred to in the case of R. v
Jones (Anthony William), (No.2) [2002] UKHL 5.
In deciding whether to proceed in the absence of Mrs Stewart the panel weighed its
responsibilities for public protection and the expeditious disposal of the case with her
right to a fair hearing.
The panel was advised by the case presenter that there had been various
correspondence received from Mrs Stewart including a recent log of a telephone call
between the NMC and the case officer on 26 November 2015. In this log Mrs Stewart is
recorded as saying that she confirmed that she would not attend the hearing by reason
of ill-health. The panel also had sight of some letters which outlined Mrs Stewart’s
health condition.
Furthermore, Mrs Stewart sent in correspondence on the day of the hearing itself in the
form of an email with two documents attached, which outline Mrs Stewart’s response to
the charges. It was evident from these documents that Mrs Stewart had only received
the hearing bundle on Friday (4 December 2015). Mr Collis conceded that the NMC had
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not complied with directions given at an earlier pre-meeting in this case on 1 September
2015 which specified that the hearing bundle was to be sent to Mrs Stewart by no later
than 13 October 2015.
The panel noted that, although the situation with the hearing bundles was unfortunate
and indeed regrettable, Mrs Stewart had not been taken by surprise by any of the
documents contained therein. She had already received copies of all of the NMC papers
in other proceedings, and incrementally in these proceedings. The panel was informed
that Mrs Stewart had given extensive written responses to the charges and, in the
panel’s judgement, she was keenly aware of the case against her. In the light of this, the
panel reminded itself of the Rule 22(3)(d) of the 2004 Rules: it would be in a position to
test the witnesses’ evidence by ensuring her case is put in a way that would prevent any
prejudice.
The panel, furthermore, noted that Mrs Stewart had not applied for an adjournment. She
was contacted today and offered the possibility of participating by telephone, which she
declined on account of her health. With respect to her medical condition the panel
considered that there was currently no date set as to when Mrs Stewart would be able
to attend a hearing.
The charges in this case date as far back as 2007. There have been two judicial
reviews and substantial delays. The panel also considered the nature and severity of
the charges and observed that there are a number of interested families and members
of the public who are waiting the resolution of this case. There are also five witnesses
scheduled to attend who would be caused significant inconvenience should the hearing
be adjourned today.
In the panel’s view there is a profound public interest in the expeditious disposal of this
hearing. It would also be in Mrs Stewart’s own interests for this hearing to be concluded
within the next two weeks, not least because of her medical condition which those
treating her say is exacerbated by the stress of these proceedings.
Page 5 of 96
Having weighed the interests of Mrs Stewart with those of the NMC and the public
interest in an expeditious disposal of this hearing, the panel has determined that it
would be in the interest of justice to proceed in Mrs Stewart’s absence.
Decision and Reasons on applications under Rule 31:
The panel were informed by Mr Collis that Mrs Stewart made an application under Rule
31 of the Nursing and Midwifery (Fitness to Practise) Rules Order of Council 2004 (the
Rules) to exclude the police statement of Dr 1. She stated, in her response to the
charges, dated 21 August 2014:
“Objection is taken to evidence from this witness in the absence of the evidence being
based at least partly on statistical reports. This witness has previously advised that prior
to properly assessing whether there is a case to answer relevant sttatiscal [sic]
information must be available. In the event that this stat[istical] information is not
available he should not be offering an opinion.”
Mr Collis, on behalf of the NMC, submitted that the objections raised by Mrs Stewart do
not bear upon relevance or fairness but rather the weight or the strength of the
evidence. He submitted that Dr 1 will give evidence before the panel and it will be open
for the panel to question him on the issue of further statistical analysis.
Mr Collis also made a separate application under Rule 31 to exclude the evidence of
Professor 2. He observed that Professor 2 would not be called to give evidence by Mrs
Stewart and pointed out a number of irrelevant aspects of his report relating to other
proceedings. Professor 2 also only refers to a small sample of cases over a reduced
timeframe, he has not seen any of the patient notes and observations are made
regarding the strength of the NMC’s case. He pointed out that the hearsay report made
reference to statements of persons who were not witnesses and whose statements are
not available, and so contains multiple hearsay.
On the latter point Mr Collis submitted that the assessment of the evidence was the
preserve of the panel and any such observations are not relevant to proceedings. He
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also questioned the relevance of the parts of the report which pertained to an interim
order. With respect to fairness Mr Collis submitted that the NMC would be put at a
disadvantage as it could not challenge the contents of the report in cross-examination.
The panel heard and accepted the legal assessor’s advice on the issues it should take
into consideration in respect of this application. This included that Rule 31 provides that
so far as it is ‘fair and relevant’ a panel may accept evidence in a range of forms and
circumstances and whether or not it is admissible in civil proceedings.
With respect to Mrs Stewart’s application to exclude the police statement of Dr 1, the
panel noted that he will be attending to give evidence. There will be, therefore, an
opportunity to explore the reasons behind the omission or inclusion of any statistical
evidence and the precise objection which is elaborated by Mrs Stewart in her standard
directions form of August 2014.
In the panel’s judgment the report of Dr 1 was relevant and, in light of the opportunity to
test the evidence fully, would also be fair to admit into evidence. Therefore the panel
determined to refuse Mrs Stewart’s application to exclude the evidence of Dr 1.
The panel noted that Professor 2 had provided an expert witness report in support of
Mrs Stewart’s case. In general terms, it offered alternative explanations to central issues
to be determined by this panel.
The panel accepted that criticisms could be made of the comprehensiveness of this
report. Professor 2 did not have sight of any contemporaneous case notes relating to
the five incidents that he considered, including Cardiotocography tracing (‘CTG’s),
medical administration charts (‘MAR’s’) and multidisciplinary continuation notes. In
addition he had no access to protocols and policies at the time.
The panel considered the opinion he offers with respect to an interim order decision
made by a previous panel of the NMC is not relevant to this fact-finding exercise.
Page 7 of 96
The panel noted that Professor 2 would not be called to give evidence. The panel
considered that although there may be unfairness to the NMC, as it would be unable to
ask questions of Professor 2, the NMC would be able to challenge his opinions by
putting these to other NMC witnesses and indeed Dr 1.
There was also, in the panel’s view, public interest in the issues being explored fully
which supported the admission of this evidence into the proceedings. In these
circumstances the panel came to the view that it would accept into evidence the report
of Professor 2 but would give what it deemed appropriate weight once the panel had
heard and evaluated all the evidence before it.
With respect to matters which were not relevant, such as the observations of Professor
2 in respect of the interim order decision, the panel would exclude these observations
from its deliberations and would hold in mind that the report does not deal with the
entirety of matters now before the panel.
In receiving and considering expert reports the panel was mindful that these are
opinions only, and that in resolving conflicts of evidence and in deciding on facts, the
panel is the judge.
Prior to announcing the decision on facts, the hearing adjourned part-heard due to a
lack of time.
Determination on Interim Order
Pursuant to Rule 32 (5) of the Nursing and Midwifery Council Fitness to Practise Rules
2004 the panel is required to consider the imposition of an interim order upon
adjourning the hearing.
Article 31 of the Nursing and Midwifery Order 2001 outlines the criteria for the
imposition of an interim order. The panel may only make an interim order if it is satisfied
that it is necessary on one or more of three grounds; for the protection of the public,
Page 8 of 96
otherwise in the public interest or in the registrant’s own interest. The panel may make
an interim conditions of practice order or an interim suspension order for a maximum of
18 months.
Mr Collis submitted, on behalf of the NMC, that he was not applying for an interim order.
The panel heard and accepted the advice of the legal assessor.
The panel considered that no decision has been reached in relation to the facts in this
matter and therefore the position is as it was prior to the hearing. The panel was
informed that Mrs Stewart is not under an interim order at present and was satisfied that
no issues of public protection or public interest arose which merited the imposition of an
interim order.
Resumed hearing dates January 2015
Mrs Stewart was not present or represented at the resumed hearing.
Decision on Service of Notice of Hearing:
The panel was informed that Mrs Stewart was sent notice of the resumed hearing dates
on 23 December 2015. The Royal Mail track and trace service showed that the notice
was successfully delivered on 29 December 2015.
In the light of the information available, the panel was satisfied that notice had been
served, in compliance and accordance with Rule 32 of the Rules which states:
(3) Where the proceedings have been adjourned, the Practice Committee shall, as soon
as practicable, notify the parties of the date, time and venue of the resumed hearing.
Proceeding in the absence
Page 9 of 96
The panel then considered continuing in the absence of Mrs Stewart. The panel heard
the submissions made by Mr Collis, on behalf of the Nursing and Midwifery Council
(NMC), and accepted the legal assessor’s advice in relation to Rule 21 of the Rules.
The panel was mindful that, whether to proceed in absence or not, was a discretion that
must be exercised with the utmost care and caution as referred to in the case of Jones.
The panel held in mind the case of Tait v RCVS [2003] UKPC 34 and the risk of coming
to the wrong conclusion on the merits of the case without the account of a registrant.
In deciding whether to proceed in the absence of Mrs Stewart the panel weighed its
responsibilities for public protection and the expeditious disposal of the case with her
right to be present and contribute to a fair hearing.
The panel was advised by the case presenter that there had been no correspondence
from Mrs Stewart in relation to the resumed hearing dates nor has she provided any
further information including up to date medical reports.
The panel noted that Mrs Stewart had been informed of the resumed hearing dates but
had not applied for an adjournment. It was satisfied that she had voluntarily absented
herself from the hearing.
The panel considered the nature and severity of the charges and observed that there
are a number of interested families and members of the public who are awaiting the
resolution of this case. In the panel’s view there remains a profound public interest in
the expeditious disposal of this hearing.
Having weighed the interests of Mrs Stewart with those of the NMC and the public
interest in an expeditious disposal of this hearing, the panel has determined that it
would be in the interest of justice to proceed in Mrs Stewart’s absence.
Decision on Facts
Background:
Page 10 of 96
At the time of the allegations Mrs Stewart was employed by NHS Grampian as a Band 6
midwife working at Aberdeen Maternity Hospital (‘the Hospital’) on the Labour Ward
(‘the Ward’). The Ward was comprised of 13 delivery rooms, a theatre and procedure
room, a three bed recovery area, a birthing pool room and an admission room. Over a
period of one year at NHS Grampian there are approximately 5,000 births, which
equates to around 400 births per month.
Within the Ward there were approximately 60 midwives, of Band 5 (newly qualified) and
Band 6 (normal banding for a midwife) seniority, who were in turn line-managed by
Band 7 Ward Sisters. The midwives were expected to provide one to one care to
mothers with a diverse range of health issues who were expecting to give birth.
Mrs Stewart trained as a midwife at the Hospital between 1987 and 1989, and worked
there since completing her training. From 2004, she worked 30 hours a week as a Band
6 midwife. Mrs Stewart was placed in a non-clinical role between September 2006 and
April 2007 in relation to periods of absence. On 1 April 2007 she returned to clinical
practice in other departments of the Hospital, and on 16 September 2007 returned to
work on the Labour Ward.
The NMC received a referral about Mrs Stewart on 15 April 2010 from the Local
Supervisory Authority Midwifery Officer (LSAMO) for the North of Scotland.
On 13 March 2010 an alleged incident occurred concerning Mother T, who was under
the care of Mrs Stewart. Mother T was transferred from the Westburn ward at 00:45
hours for continuing induction of labour as her pregnancy was 15 days overdue. A
cardiotocograph (CTG) was commenced and Mrs Stewart sited a venflon, for
intravenous administration of medication and to obtain blood samples that were routine
in the circumstances.
According to the maternity progress notes for Mother T, Mrs Stewart performed a
vaginal examination and an amniotomy (amniotomy is a procedure where the midwife
ruptures the bag of waters that surround the fetus in the womb). A partograph, a
Page 11 of 96
composite graphical record of key labour progress data was also commenced at this
stage.
At 01:30 Mrs Stewart recorded that she commenced intravenous (‘IV’) Syntocinon at
1ml/hour. Syntocinon is an oxytocic drug, an artificial form of a natural hormone
produced by women which makes their uterus contract, pushing the baby out. At 01:55
Mrs Stewart recorded a reassuring fetal heart rate within normal limits.
At 02:00 Mrs Stewart recorded that she increased the dose of Syntocinon, as per the
Hospital induction of labour (IOL) policy, to 2 mls/hour. The fetal heart rate continued to
be reassuring. At 02:30 the decision is taken, by Mrs Stewart, to increase the dose of
Syntocinon again to 4mls/hour according to the IOL policy and at 03:00, Mrs Stewart
was relieved by another midwife who continued to monitor the progress of the labour.
At 03:39, a significant deterioration was recorded; the fetal heart rate dropped to 60bpm
and at this point Mrs Stewart and Sister 4 answered the emergency buzzer. At this point
the Syntocinon was stopped.
At 03:45 the prolonged deceleration of the fetal heart rate recovered and Mother T was
to be reviewed again in 30 minutes. By 04:00 the CTG was again reassuring and had
stabilised.
Mrs Stewart recorded that at 04:03 IV Syntocinon had been recommenced at 4mls/hour.
At 04:07 Mrs Stewart recorded a deep deceleration of the fetal heart rate to 60 – 70
bpm. The emergency buzzer was pulled and at 04:15 Mother T was transferred to
theatre and the baby was later delivered by Caesarean section.
The panel noted that the prolonged fetal bradycardia (where the fetal heart rate
decelerated to 60 bpm) occurred within minutes of the recommencement of the IV
Syntocinon.
Following this incident with Mother T, concerns were raised about the similarity between
this case and the care which Mrs Stewart provided to another mother, Mother S, two
Page 12 of 96
days previously on 11 March 2010. There were initial concerns that something untoward
had occurred and the pump that had been used to administer the Syntocinon was
retained.
On 11 March 2010, Mother S was transferred to the Ward from the Westburn ward, at
14:45 for induction of labour. Mrs Stewart assumed responsibility for her care.
A CTG was commenced. It is further recorded in the notes that at 15:25 Mrs Stewart
conducted a vaginal examination and then performed an artificial rupture of the
membranes (‘ARM’) (also known as an amniotomy) with the consent of Mother S. Mrs
Stewart recorded that she had sited a venflon.
At 15:42 Mrs Stewart recorded that there had been a fetal heart rate deceleration from
70 to 80 Beats per Minute (‘BPM’) (the normal fetal heart rate being 110 to160 BPM).
The emergency buzzer was activated and, after turning Mother S, it is recorded that the
heart rate had fallen further to 60 bpm.
The multi-disciplinary team answered the emergency buzzer and Mother S was
transferred to theatre at 15:50. Mother S then underwent a Caesarean section under
general anesthetic. The baby was born in a poorly condition and taken to the neonatal
unit.
On Monday 15th March 2010, Miss 1a asked Ms 5 and Professor 1 (then a Consultant
Midwife and a Supervisor of Midwives, now a Clinical Professor of Midwifery at Robert
Gordon University) to undertake the management and midwifery supervisory
investigations into the concerns that had been raised about Mrs Stewart.
Professor 1 approached Ms 6, the Risk Management Midwife, and was advised that
three further cases should be examined; those of Mothers R, Q and F. Professor 1
identified that the five cases she reviewed (Mothers R, S, T, Q and F) all involved Mrs
Stewart as the midwife providing direct care to the women, and that all the women had
a prolonged fetal bradycardia that required the birth to be accelerated.
Page 13 of 96
Professor 1 requested records from PROTOS (the electronic maternity database at
NHS Grampian) of all Category 1 Caesarean sections (performed to save the life of the
baby and/or the mother, and often carried out under general anaesthetic) that had
occurred at the Hospital between April 2009 and March 2010. This revealed that there
were 10 further incidents of a Category 1 Caesarean section due to fetal compromise
where Mrs Stewart was the allocated midwife.
Of these three were discounted as they contained no commonalities to the cases
involving Mothers T, S, R, Q and F. The remaining seven, however, all shared
similarities; there was a prolonged fetal bradycardia, a Category 1 Caesarean section
and Mrs Stewart was the allocated midwife.
Professor 1 provided the twelve sets of records to Dr 3 (Consultant Obstetrician at
Aberdeen Maternity Hospital) for her opinion. Dr 3 was able to identify a pattern of a
reassuring CTG immediately prior to an intravenous or intramuscular injection or
infusion on and very shortly afterwards a prolonged fetal bradycardia necessitating
urgent birth, usually by Caesarean section, with no cause for the prolonged fetal
bradycardia identified at birth.
Dr 3’s view was that the intravenous or intramuscular injection or infusion may have
been the administration of an oxytocic drug to produce a prolonged uterine contraction.
On 13 April 2010, Mrs Stewart was interviewed by Professor 1 in relation to the first five
identified cases (Mothers R, S, T, Q and F).
Mrs Stewart was able to provide a detailed account of the incident involving Mother T.
She stated that Mother T received IV Syntocinon infusion from about 02:30 to 04:00,
Syntocinon infusion was increased until there were three to four contractions in five
minutes. Mrs Stewart confirmed that she had administered the Syntocinon, but asserted
that Ms 7 (Staff Midwife) would have checked the 3 ampules of Syntocinon observed
the fluid being drawn into the syringe, note the expiry dates on the products and that the
3ml of solution in the syringe was added to the 500ml bag of saline as verified in the
notes.
Page 14 of 96
Mrs Stewart accepted that she returned to the patient’s room and administered the
infusion unsupervised. When Mrs Stewart subsequently returned from her break, the
fetal heart rate had dropped and the Syntocinon infusion was switched off and a fetal
scalp electrode was applied. This process helped monitor the fetal heart rate. Mother T
was reviewed by a doctor, and an instruction was given to re-start the Syntocinon at the
rate of 4ml per hour. A short time later, the fetal heart rate dropped again, when Mrs
Stewart was the only person in room. Assistance was called for and a doctor eventually
took the decision to move Mother T to theatre for an emergency Caesarean under
general anaesthetic.
Mrs Stewart was able to provide a similar level of detail for the births involving Mothers
R and S, but was unable to remember many details for Mothers Q and F. When asked
about the frequency of the events she had been involved with, Mrs Stewart replied that
she did not know what to think, and wondered if it was just bad luck on her part.
On the same day as that interview, the Executive Team at NHS Grampian took the
decision to inform the police regarding the concerns that had been identified. On 16
April 2010, NHS Grampian was instructed by the police to cease any internal
investigation into Mrs Stewart and Professor 1 concluded her report on 19 April 2010.
Prior to the police requesting NHS Grampian to cease their investigation, Miss 1a asked
Mrs 1b to participate as an independent and external reviewer of records. Mrs 1b was a
Consultant Midwife employed by NHS Ayrshire and Arran.
Mrs 1b was provided with 27 sets of maternity records relating to Mothers A-T, Z and
AA (cared for by Mrs Stewart) and five further mothers (relating to care given by other
midwives).
Mrs 1b concluded that cases involving Mrs Stewart showed a worrying trend of
unexplained, sudden severe fetal bradycardia. She noted that the majority of these
cases of fetal bradycardia appeared to correlate with an intravenous intervention by Mrs
Stewart and sent a summary of her findings to Miss 1a in May 2010.
Page 15 of 96
In relation to the Police investigation, the police requested assistance with their
investigation from a number of individuals who had already contributed to the NHS
Grampian inquiries; Miss 1a, Professor 1, Mrs 1b and Dr 3.
Miss 1a reviewed the maternity records for Mothers A-T, Z and AA as part of the police
investigation, and provided statements detailing her findings. This included, “There
appears to be a pattern in these cases where the Midwife had done something such as
siting a venflon or starting infusion, or giving an intramuscular injection just prior to the
fetal bradycardia. A possible reason for this could be that the Midwife has administered
a drug inappropriately to cause the fetal bradycardia”.
Professor 1’s police statement commented on the Mother’s notes she inspected, and
she remarked, “The thing I found about the 27 cases I reviewed was that I could not for
the vast majority of them find a plausible clinical explanation for the fetal bradycardia. In
my experience, and using the knowledge that I have got, I wouldn’t expect any midwife
to encounter the frequency of fetal bradycardias that she encountered in that time
frame.”
The police also obtained a witness statement from Dr 1, a Consultant Obstetrician and
Gynaecologist with the Greater Glasgow and Clyde Health board. He commented, “The
trend is that this individual sites a venflon for venflon access, a fetal bradycardia occurs,
usually within ten minutes, without an obvious clinical event such as cord prolapse or
placental abruption. The nature of the bradycardia is that of a sudden onset with a steep
slope and slow, but usually complete recovery. The length of the bradycardia was
prolonged and specifically longer than the forty to sixty second declarations that can
occur in labour, usually from cord compression. The CTG pattern was not typical of a
cord compression event. I noted that the fetal bradycardia was not explained by findings
at caesarean section or vaginal delivery, if this occurred immediately following the
event.”
Dr 1 went on in his statement to remark, “…in the vast majority of cases there is a
pattern/sequence of events that cannot be readily explained and led me to conclude
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that there is a reason to be suspicious that some voluntary action has led to the fetal
bradycardia events.”
NHS Grampian undertook a comparison exercise. Three comparator midwives were
identified, with a similar length of experience, who had worked on the labour ward and
who worked similar hours to Mrs Stewart. 1,609 cases from deliveries that these three
midwives were involved in were inspected, spanning from 2001 to 2010.
Of these cases, four criteria were established to trigger a further medical review: (a) a
reassuring CTG; (b) an intervention being performed, such as IV access or medication
administration; (c) a profound fetal bradycardia following the intervention; and (d) no
recorded cause for the fetal bradycardia in the records. Only seven of the 1,609 cases
matched these criteria and were medically reviewed. It emerged that all seven of these
cases differed from those involving Mrs Stewart in that the fetal issues could be
explained.
In 2011, the Procurator Fiscal requested that further comparisons were conducted by
NHS Grampian. This time, seven comparators were used, spanning the timeframe of
January 2007 to March 2010. Of the 1,237 reviewed cases for these seven additional
comparators, only one matched the index cases involving Mrs Stewart, namely it
involved a profound, prolonged fetal bradycardia that could not be explained as being
caused by a recognised obstetric cause.
In April 2012, NHS Grampian received permission from the police to resume their
internal investigation. This investigation was carried out by Miss 1a. Focus was placed
on cases from 2007 until 2010. The case of Mother AA was discounted due to the
suspicious CTG for a significant period of time prior to birth.
Miss 1a interviewed Mrs Stewart on the 2nd and 3rd July 2012. Mrs Stewart denied
providing a bolus dose of an oxytocic drug to the mothers she was asked about, but
was unable to account for why she had been involved with so many cases involving a
prolonged, unexplained fetal bradycardia.
Page 17 of 96
Miss 1a also interviewed Dr 3, Professor 1 and Mrs 1b as part of the investigation. The
panel had sight of extracts of their interviews.
A decision was reached that the case involving Mother Z would not be considered
during the Trust’s investigation on the basis that her circumstances could provide an
explanation for the fetal bradycardia. The 20 cases identified in Schedule 1, and
considered by NHS Grampian’s investigation, however all involved unexplained
episodes of fetal bradycardia, where Mrs Stewart was involved in the care of the
mothers.
Mrs Stewart was further interviewed by Miss 1a on the 31st October 2012. She again
denied all allegations that were put to her, but offered no explanation as to why she had
such a high rate of unexplained fetal bradycardia.
The panel heard evidence from the following witnesses:
•
Miss 1a, the Head of Midwifery at NHS Grampian
•
Dr 3, the obstetric lead for the Ward and for risk management
•
Mrs 1b, consultant Midwife with NHS Ayrshire and Arran
•
Professor 1, the clinical lead for midwifery practice throughout NHS Grampian
and also a clinical professor of midwifery at Robert Gordon University
•
Dr 1, Consultant Obstetrician and Gynaecologist with the Greater Glasgow and
Clyde Health board
The panel also had sight of written responses and supporting documentation from Mrs
Stewart in which she denied all of the allegations against her.
Findings:
The panel has given careful consideration to all the evidence, including the oral
evidence, the statements and the other documentary exhibits adduced in this case. The
panel was aware that the burden of proof rests with the NMC to prove each of the facts
alleged and that the standard of proof is the balance of probabilities. There is no burden
on Mrs Stewart to disprove the allegations.
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The panel has considered each allegation and the evidence relating to it separately.
At the conclusion of the evidence, the panel heard submissions from Mr Collis. It
received the advice of the legal assessor, which it accepted.
The panel found the NMC witnesses it heard to be consistent, credible and reliable.
The panel noted that it was not in dispute that Mrs Stewart cared for all the mothers
listed in Schedule 1.
The panel checked with each witness their findings in relation to every mother listed in
the schedule by cross referencing the expectant mothers' unique hospital numbers. All
the witnesses confirmed their findings to be correct and true to their recollection.
Miss 1a’s evidence was, “There appears to be a pattern in these cases where the
Midwife had done something such as siting a venflon or starting infusion, or giving an
intramuscular injection prior to the fetal bradycardia. A possible reason for this could be
that the Midwife has administered a drug inappropriately to cause the fetal bradycardia."
Professor 1’s evidence was, "The thing I found about the 27 cases I reviewed was that I
could not for the vast majority of them find a plausible clinical explanation for the fetal
bradycardia. In my experience, and using the knowledge that I have got, I would not
expect any midwife to encounter the frequency of fetal bradycardias that she
encountered in that time frame".
Dr 3 on reviewing 12 sets of records provided by Professor 1 was able to identify a
pattern of a reassuring CTG immediately prior to apparent intravenous or intramuscular
intervention and very shortly afterwards a prolonged fetal bradycardia necessitating
urgent birth, usually by Caesarean section, with no cause for the prolonged fetal
bradycardia being identified at birth. Dr 3's view was that the intervention may have
been the administration of an oxytocic drug to produce a prolonged uterine contraction.
Page 19 of 96
Dr 1 commented, "The trend is that this individual sites a venflon access, a fetal
bradycardia occurs, usually within 10 minutes, without obvious clinical event such as
cord prolapse or placental abruption. The nature of the bradycardia is that of a sudden
onset with a steep slope and slow, but usually complete recovery. The length of the
bradycardia was prolonged and specifically longer than the forty to sixty second
deceleration that can occur in labour, usually from cord compression. The CTG pattern
was not typical of a cord compression event. I noted that the fetal bradycardia was not
explained by findings at Caesarean section or vaginal delivery, if this occurred
immediately following the event".
Dr 1 further evidence was that, " ....in the vast majority of cases there is a pattern/
sequence of events that cannot be readily explained and led me to conclude that there
is reason to be suspicious that some voluntary action has led to the fetal bradycardia
events".
The panel found that each witness understood the words "bolus dose" to mean the
administration of a dose of a drug which, could be given to an expectant mother in a
variety of ways whether intravenously or intramuscularly.
Miss 1a and Professor 1 both worked on the Ward at the Hospital. Miss 1a knew Mrs
Stewart by name but worked days, where Mrs Stewart worked regular night shifts.
Professor 1 knew Mrs Stewart professionally throughout her career and worked with
Mrs Stewart as a midwifery peer or as her senior at the Hospital.
Both Miss 1a and Professor 1 described working on the Ward at the time, the protocols
in place and the accessibility of oxytocic drugs.
The panel accepted the evidence of Dr 1 that these drugs "can rapidly lead to fetal
bradycardias by causing the uterine contraction to be too strong or prolonged in time,
leading to hypertonus [a sustained contraction].... Oxytocin is rapidly metabolised and
its actions will be short lived, typically around eight to ten minutes duration, if a bolus is
given".
Page 20 of 96
The panel found Syntocinon, an oxytocic drug, was commonly used for the induction of
labour. It was easily accessible, being kept in an unlocked fridge in a room centrally
located near the nurses’ station. Midwives frequently entered this room as, in addition to
drugs, it contained equipment regularly used. Miss 1a told the panel no one would have
noticed if a midwife was entering this room more than usual or removing more ampules
of Syntocinon than prescribed. There was no audit of the quantity of Syntocinon used.
Both Miss 1a and Professor 1 confirmed that it was best practice for another midwife to
be present when a prescribed dose of Syntocinon was added to a saline infusion bag in
preparation for infusion and, for that midwife to counter sign its administration. However,
on a busy ward this often did not happen. Professor 1 told the panel that it was
common practice for a midwife to gather the drug and equipment necessary, then to
quickly show the drug to be infused to another midwife for checking. The mixing
procedure and setting up of the infusion would be done alone in the labour room with
the expectant mother, unobserved.
Both witnesses confirmed Syntocinon is a clear liquid so it would not be noticeable if a
bolus dose was being infused. They advised the panel that the infusion bag requires
agitation to mix correctly. They agreed it was possible for a high concentration of
Syntocinon to pool in the bottom of an infusion bag if not agitated. However, they
thought this unlikely to happen as the process of placing the bag in position should be
sufficient to mix the drug and saline solution.
The panel noted that when concerns were raised in relation to Mother T's care the
infusion pump utilised was retained and found to be in working order. The pump's data
did not reveal an excessive rate of dose. Mother T was not tested to see if there was an
excess of an oxytocic drug in her system at the time. The panel was advised that unless
there was an immediate blood test, Syntocinon would have metabolised within a few
hours and thus, be untraceable.
Dr 1 advised the panel that there were various ways in which a bolus of a drug could be
administered. One would be by increasing the speed of dose via the infusion pump (this
was not the case with Mother T). Alternatively, an additional dose could be injected
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through the second port in the venflon cannula sited for intra venous infusion. Such a
dose would pass directly into a mother's vein avoiding the infusion pump and bag. A
bolus dose could also be administered by intravenous or intramuscular injection. It was
also possible to tamper with the infusion tubes resulting in a concentrated dose being
administered.
Dr 3 explained that because of the ready supply of the Syntocinon a midwife could
administer a bolus dose unchecked and unobserved.
The panel was informed that other oxytocic drugs were also readily available for
administration on the labour ward including Ergometrine and Syntometrine.
Mrs Stewart volunteered during her interview with Miss 1a and Professor 1 that it was
her practice to carry Ranitidine in her pocket just in case it was needed. This is not an
oxytocic drug but is usually administered prior to surgery to prevent gastric reflux and
does not effect uterine contractions. Professor 1 confirmed it was not an approved or
safe practice to have any drugs in one’s pocket.
The administration of Ranitidine should have been checked, administration observed
and the medication administration record countersigned by another midwife. The panel
noted that this protocol was not always observed.
Professor 1 described Mrs Stewart as a "theoretical midwife" who liked the technical
aspects of midwifery and being in theatre. She regarded Mrs Stewart as competent and
that she would have been well aware of the effect a bolus dose of Syntocinon on a
woman in labour. Miss 1a also described Mrs Stewart as a competent and experienced
midwife.
None of the witnesses could explain why a midwife would want to give an unprescribed
dose of an oxytocic drug to these mothers in these circumstances. Professor 1’s
evidence was that Mrs Stewart did not like spending long periods of time in a labour
room waiting with an expectant mother and her partner. She described this aspect of
the job as potentially very lonely. Doctors and other members of staff would only enter a
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labour room when called to assist by the assigned midwife. According to Professor 1's
personal observation Mrs Stewart was in and out of the labour rooms, far more often
than she would have expected. She thought Mrs Stewart had difficulty in building a
rapport with patients. In her opinion Mrs Stewart may have wanted to speed up a
woman's time in labour.
The panel found Professor 1's theory a plausible explanation however it was unable to
put this to Mrs Stewart for comment. In her investigatory meeting Mrs Stewart offered
no explanation for what had occurred other than to say it was bad luck.
During their investigation both Miss 1a and Professor 1 became aware that it had
become a "joke" amongst other members of staff that if Mrs Stewart was on duty there
was likely to be an emergency Caesarian Section (CS1).
Caesarian Sections are categorised depending on the degree of risk to the expectant
mother and fetus. A CS1 was described as being a true emergency instigated in a life
threatening situation to both expectant mother and fetus. A rapid response is required
from a multi-disciplinary team to deliver the baby as quickly as possible in no longer
than 30 minutes.
The majority of women listed in the schedule to these charges underwent emergency
Caesarian sections categorised as CS1 and their babies were delivered on average
between 15 and 20 minutes.
Professor 1 speculated that Mrs Stewart may have enjoyed the attention such
emergencies brought.
All the witnesses thought unexplained prolonged fetal bradycardia (drop in the fetal
heart rate below acceptable levels for more than 3 minutes) resulting in an emergency
CS1 to be an extremely rare event in their experience. Usually there would be an
explanation for the fetal bradycardia such as placenta abruption or cord prolapse
necessitating emergency surgery. If there was any possible explanation for the fetal
Page 23 of 96
bradycardia in the many cases reviewed as part of the investigation, these cases were
eliminated as being of concern.
Upon discovering Mrs Stewart was involved in numerous cases where there was no
apparent explanation for the prolonged fetal bradycardia Miss 1a and Professor 1
undertook a comparator survey.
The panel considered the criteria for this survey as described in the background above
was appropriate and relevant. In particular the panel noted that if there were other
explainable outside influences, the witnesses would have expected to see similar
scenarios occurring with other midwives working at the Hospital. This was not the case.
In 2011, the Procurator Fiscal requested that further comparisons were conducted by
the Trust. As a result, the electronic data for a further 7 midwives using the above four
criteria was reviewed over the timescale 2001 to 2010. In all 1,237 cases were looked
at. Of note to the panel was that only one case of unexplained prolonged fetal
bradycardia leading to an emergency CS1 was found. No other such cases were found
in relation to that particular midwife.
The panel accepted the witness evidence that unexplained prolonged fetal bradycardia
was a very unusual event. This was rare, in the witness’ own personal experience and
in relation to other midwives working at the Hospital.
Professor 1 told the panel she would have expected Mrs Stewart to discuss her practice
with her own supervisor of midwives and/or colleagues. The panel accepted that Mrs
Stewart must have been aware of the recurring events. It was her responsibility to
enquire whether there was any identifiable cause or error in her practice. This does not
appear to have happened. In Mrs Stewart’s written response to this panel she states
she did raise an issue with her mentor (who was not her supervisor of midwives). She
did not elaborate what was discussed or when. The panel was provided with no
evidence to suggest that Mrs Stewart instigated a review of her practice.
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Dr 3 told the panel she acted as Chair of the risk management committee for the Trust
from late 2009. This primarily considered clinical risk with the aim of making
improvements in practice. From 2007 to 2010 there was no automatic referral to risk
management if a CS1 occurred. Reviews only took place if a baby was delivered in poor
condition. As a result, the number of expectant mothers cared for by Mrs Stewart in the
labour ward for induced labour who underwent emergency CS1 surgery was not
identified. Dr 3 advised the panel that the Trust has now extended its automatic referral
policy.
The panel noted that there were no alleged incidents after November 2007 and before
June 2009. The panel has ascertained from the documentary evidence before it that
during this time Mrs Stewart was absent from work on several occasions for health
reasons. In particular she was absent from work between June 2008 and April 2009.
The panel was also informed that in early 2008 Mrs Stewart did not work on the Ward
but rotated between Westburn antenatal ward and working in theatre.
The panel then reviewed the evidence in relation to each mother listed in the schedule
of charges.
In relation to the charges:
That you, while employed by NHS Grampian as a registered midwife working at
Aberdeen Maternity Hospital:
1.
Between 4 October 2007 and 13 March 2010 administered a bolus dose
of an oxytocic drug to one or more of the service users listed in
schedule 1.
2.
Your actions at charge 1 above caused or contributed to the fetuses of
one or more of the service users listed in schedule 1 experiencing
bradycardia.
AND, in light of the above, your fitness to practise is impaired by reason of your
misconduct.
Page 25 of 96
Schedule 1
A.
Mother A, date of delivery 4 October 2007
Mother A
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother A and the CTG tracings of Mother A. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3, the obstetric lead for the Ward and for risk management, commented on the
midwifery progress notes of Mother A as part of the police investigation. She describes
the clinical actions taken with respect to Mother A on the 4 October 2007, noting that
Mother A was transferred to the Ward for induction of labour at 13:15 hours on this day.
She observes that an IV was started at 16:50 hours for an antibiotic. She said:
“At 1745 hours, following a normal CTG she has a fetal bradycardia. She is taken for
delivery by caesarean section and has a live male infant in good condition. There is a
knot found in the cord at section which is not unusual and babies are usually fine with
this. This does not explain the fetal bradycardia and no other cause was found.
“This case is slightly different in that the administration of drugs was almost an hour
before the (fetal) bradycardia but some blood tests were taken immediately before the
(fetal) bradycardia which could have provided an opportunity for the administration of
Syntocinon.”
Professor 1, the clinical lead for midwifery practice throughout NHS Grampian and also
a clinical professor of midwifery at Robert Gordon University, conducted the
management and midwifery supervisory investigations into the initial concerns which
had been raised by Mrs Stewart. As part of the police investigation into this matter,
Professor 1 was invited to comment on the case of Mother A. She stated:
“…Kirsty [Mrs Stewart] broke her [Mother A’s] waters and her cervix was 3 centimetres
dilated. Intravenous Penicillin is given due to Group B strep and intramuscular
Page 26 of 96
Ranitidine given. 50 (Fifty) minutes after this there is a prolonged fetal bradycardia
lasting for 7 minutes.
“Mother A was transferred to theatre for emergency caesarean. There is no
documented medicine administered immediately prior to bradycardia…There was a true
knot found in the cord at caesarean section which may have caused (the) bradycardia.
The CTG, however, was normal prior to (the) bradycardia and I would have expected
some cord compressions.”
Miss 1a, the Head of Midwifery at NHS Grampian, was informed of the initial concerns
with Mrs Stewart’s practice. She was also asked, as part of the police investigation, to
comment on the midwifery progress notes and records of Mother A. She gives a very
brief outline, within her police statement, of the circumstances of Mother A’s labour. She
states:
“…At 17:45 hours, fetal bradycardia occurred. She was turned on her side, oxygen
given and Kirsty buzzed for assistance…The plan was for Caesarean Section (CS1),
which occurred under general anaesthetic. The baby was fine with a true knot in the
cord. If the knot was tight, this could cause the fetal bradycardia, but I do not know if it
was tight or not.”
Mrs 1b, consultant Midwife with NHS Ayrshire and Arran, conducted an initial review
into the concerns surrounding Mrs Stewart. She was asked by Miss 1a to participate as
an independent and external reviewer of records. Mother A was one of the 27 cases
that she was asked to review. With respect to Mother A she also outlined the
progression of labour and the clinical interventions carried out by Mrs Stewart. She
stated:
“…On the partogram I do see at 1650 hours that antibiotics was (were) administered
intravenously which would mean a cannula was sited…At 1745 hours Midwife K.Stewart
notes a drop in (the) fetal heart rate. The care at this point, and as documented, is
appropriate…Although a true knot was recorded at birth I would have expected for fetal
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distress to be shown on the CTG tracing. It is possible, however, that if this was a
rapidly descending birth but you would again expect some dips in the tracing.”
Dr 1, Consultant Obstetrician and Gynaecologist with the Greater Glasgow and Clyde
Health board, was asked for a witness statement by the police and he provided an
opinion regarding Mother A’s case. He had access to the midwifery progress notes and
provides the following comments on Mother A’s labour:
“This patient had a medical complication that limited the obstetric options. She was high
risk, given that she had a previous caesarean section. The sudden onset of fetal
bradycardia follows the previous established pattern. The bradycardia could (be)
explained by the presence of a true knot in the umbilical cord, found at the delivery,
however there is an absence of cord compression type variable decelerations prior to
the bradycardia during contractions and the good condition of the baby at birth goes
against the knot as (being) causative, ie if the umbilical cord was tightly compressed
then I would have expected the bradycardia to be unremitting and the baby to be born in
poor condition, which it was not.”
The panel also had regard to the additional report written by Dr 1 which is an expert
opinion commissioned by a law firm on behalf of the NMC. He was asked to consider
and provide an opinion on cases A to T and in relation to Mother A he elaborated upon
his prior conclusion:
“…However the CTG and contemporaneous clinical context had no abnormalities to
indicate cord compression was occurring or that there was deteriorating fetal condition
prior to the bradycardia event. Had the knot been so acutely tightened to cause an
acute bradycardia I would have expected a severely asphyxiated infant, perhaps
stillborn, as it is so unlikely to believe this degree of knot tightness could loosen given
the nature of the structure of the cord.”
The panel also considered the submissions of Mrs Stewart who writes: “if I had given a
bolus of syntocinon then two injections would have been need[ed], a vacutainer for
Page 28 of 96
getting the bloods than a syringe to give bolus. There was also a true knot in the cord
which could have been tight.”
The panel noted that Mother A suffered an unexplained, prolonged and profound fetal
bradycardia at 17:45, which resulted in compromise of the fetal heart rate for a period of
seven minutes. It is also not disputed that the CTG trace prior to this event was normal
and, indeed, reassuring which is borne out by the actual CTG tracings of Mother A’s
labour.
With respect to Mrs Stewart’s contention that this particular bradycardia could have
been caused by a tight cord knot, the panel paid careful regard to the evidence of the
NMC witnesses. The panel had regard to the fact that the baby was born in a healthy
condition at birth and that there was an absence of what Dr 1 describes as cord
compression type variable decelerations on the CTG. Both of these factors, and the
evidence of the NMC witnesses, led the panel to conclude that a tight cord knot was not
a possible explanation of the fetal bradycardia in Mother A’s case.
The panel observed, however, that there is no actual record, on the records before it, of
Syntocinon (or any other oxytocic drug) being administered, although it is clear that
there was a plan in place for its administration and it was also used post-operatively.
There was merely an opportunity to administer a bolus dose of an oxytocic drug as
Intravenous Penicillin had been administered, as prescribed, at 16:50 by Mrs Stewart.
This would have necessitated a venflon being sited which would, in turn, have provided
potential access for Mrs Stewart to administer a drug. The panel considered that this
fetal bradycardia was suspicious, following as it did after an IV administration of
antibiotics. However, the panel did not form the view that it fitted the alleged pattern,
identified by the NMC witnesses, of Mrs Stewart inserting a venflon followed by a fetal
bradycardia with the CTG not being typical of a cord event and no reason found at
delivery.
Furthermore, the panel noted the timings of the intravenous medication which was
administered at 16:50 hours. The fetal bradycardia in the case of Mother A did not occur
until 17:45. In the panel’s judgement there was a lack of a close temporal association
Page 29 of 96
between the two events which rendered the possibility of Mrs Stewart administering a
bolus dose of an oxytocic drug to be more remote.
The panel was not satisfied on the balance of probabilities that Mrs Stewart had
administered a bolus dose of an oxytocic drug to Mother A on 4 October 2007. It
followed that the panel was also not satisfied that Mrs Stewart’s actions caused or
contributed to the fetus of Mother A developing a bradycardia.
The panel accordingly found Charges 1 and 2 not proved with respect to Mother A.
Schedule 1
B.
Mother B, date of delivery 3 November 2007
Mother B:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother B and the CTG tracings of Mother B. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3, commented on the midwifery progress notes of Mother B as part of the police
investigation. She identified that Mrs Stewart took over the care of Mother B at 01:30
hours and then sited a venflon. She stated:
“Syntocinon was commenced at 02:35 hours and the CTG had been normal before this.
There was a profound fetal bradycardia at 02:37 hours. This recovered after seven to
eight minutes and the baby was delivered by normal delivery at 03:35 hours, a male
infant in good condition.
“This case again follows the pattern of a normal CTG followed by an intervention and
then a fetal bradycardia and very rapid progress in labour. A possible explanation of this
is a bolus (dose) of an oxytocin agent around 02:35 hours.
Page 30 of 96
“…At the time of delivering the cord was slipped from around the neck and over the
head and (was) unlikely to have caused the (fetal) bradycardia. No other cause for the
(fetal) bradycardia was found.”
Professor 1, conducted the management and midwifery supervisory investigations into
the initial concerns which had been raised regarding Mrs Stewart. As part of the police
investigation into this matter, Professor 1 was invited to comment on the case of Mother
B. She stated:
“…A venous cannula was sited and IV Syntocinon started. Two minutes later (a)
profound, prolonged fetal bradycardia (occurred) for 5 minutes. Syntocinon was stopped
and (the) fetal heart rate recovered, and within half an hour (she) progressed to a
normal birth. This is suspicious because of (the) rapid progress and (the) bradycardia
within a couple of minutes of Syntocinon.”
Miss 1a, was informed of the initial concerns with Mrs Stewart’s practice. She was also
asked, as part of the subsequent police investigation, to comment on the midwifery
progress notes and records of Mother B. She gives an account, within her police
statement, of the circumstances of Mother B’s labour. She remarks that Mrs Stewart
continued Mother B’s care. At 02:35, Miss 1a notes that Mrs Stewart commenced IV
Syntocinon infusion at 1ml/minute and goes on to state:
“At 02:37 hours, the fetal heart rate dropped to 60. Kirsty buzzed for assistance and
discontinued the IV Syntocinon…At 02:40 hours Kirsty performed a vaginal
examination. At 02:45 hours, Kirsty gave 50ml [sic – should be milligrams]
Ranitidine…The labour progressed to a spontaneous vaginal delivery. The notes do not
indicate a reason for the fetal bradycardia.”
Mrs 1b, conducted an initial review into the concerns surrounding Mrs Stewart. She was
asked by Miss 1a to participate as an independent and external reviewer of records.
Mother B was one of the 27 cases that she was handed. With respect to Mother B she
outlined the progress of Mother B’s labour and Mrs Stewart’s documented interventions.
She stated:
Page 31 of 96
“…On the whole the CTG is fine and only after Syntocinon is administered, and very
quickly after this, there is a fetal bradycardia which recovers and is a very good trace for
second stage labour…There is a natural birth and although it is noted as cord being
round the neck but was loose and would not be a likely causation factor for bradycardia.
This case is extremely unusual in that to have a fetal bradycardia immediately after
Syntocinon administered along with normal tracing before and after.”
Dr 1, was asked for a witness statement by the police and he provided an opinion
regarding Mother B’s case. He had access to the midwifery progress notes and
provides the following comments on Mother B’s labour:
“This is the twentieth case reviewed and follows the now obvious pattern. There is an
unprovoked bradycardic event lasting four minutes which might be attributed to rapid
progress in labour, however, the normality of the CTG before and after the bradycardia
is somewhat surprising if a rapid labour was a factor.”
The panel also had regard to the additional report written by Dr 1 which is an expert
opinion commissioned by a law firm on behalf of the NMC. He was asked to consider
and provide an opinion on cases A to T and in relation to Mother B he elaborated upon
his prior conclusion:
“…The CTG was entirely normal before the unprovoked bradycardia event and returned
to normal following its resolution. Thereafter the CTG pattern was entirely reassuring
until delivery. The baby was appropriately grown, tolerated the labour process without
difficulty and was born with very reassuring Apgar scores.
“Blood stained Liquor (BSL) can be associated albeit weakly with premature separation
of the placenta (abruption) but there is no evidence of this or any other cause for a
bradycardia event in this case. This was a potentially vulnerable infant who coped
extremely well with the extra stress of an induced labour and had no[…] specific
reasons for a bradycardia.
Page 32 of 96
“Importantly there were no recurrences of bradycardia (Which might have suggested
cord vulnerability). Acute fetal bradycardia can occur at amniotomy as a result of cord
prolapse (not an issue here), cord trauma (not an issue here), placental abruption (see
above), the effect of increasing the baby’s intracranial pressure by it’s head descending
into the pelvis (The head was deeply engaged at one fifth palpable therefore this is very
unlikely) and if the liquor volume had meant the cord was vulnerable to compression.
Even if the liquor volume had been low this did not manifest as a problem thereafter
therefore this is unlikely to have been the case…For the reasons above I have
concluded this was an unanticipated bradycardia hence my surprise it happened at all.”
The panel also considered written responses of Mrs Stewart: “? Precipitate labour. Have
to be careful with syntocinon in parous women, can be very sensitive to it. 4cms to fully
in 100minutes.”
The panel noted that a prolonged fetal bradycardia occurred at 02:37, which lasted for a
period of 6 minutes until 02:43. Just two minutes previously, at 02:35, Mrs Stewart had
documented that she had commenced an IV Syntocinon infusion at 1ml/hour. The fetal
heart rate was severely compromised, falling to 60 bpm. The panel also observed that
the CTG was reassuringly normal up until the Syntocinon was administered by Mrs
Stewart.
The panel accepted the evidence of Dr 1, who ruled out the common causes of fetal
bradycardia: cord prolapse, cord trauma, placental abruption, the unborn baby’s head
descending rapidly or deeply into the pelvis or cord compression or lack of liquor. The
panel concluded that the evidence before it demonstrated a clear, documented
intervention relating to IV Syntocinon in relation to Mother B which, if administered as a
bolus dose, would result in a fetal bradycardia such as occurred in relation to the fetus
of Mother B.
This explanation, bearing in mind the rarity of unexplained fetal bradycardias is the only
plausible one in the circumstances and is more likely than not to have occurred.
Page 33 of 96
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother B.
Schedule 1
C.
Mother C, date of delivery 8 November 2007
Mother C:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother C and the CTG tracings of Mother C. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3, commented on the midwifery progress notes of Mother C as part of the police
investigation. She remarks that Mother C was transferred to the Ward at 10:00 hours on
7 November 2007. At this juncture Mrs Stewart took over the care for Mother C. Dr 3
stated:
“A decision was made to give her Syntocinon and it was commenced at 10:30 hours.
The CTG had been normal to this point. At 1032 hours, she had a prolonged fetal
bradycardia and was taken for an emergency caesarean section. She had a live born
male infant in good condition and no cause was found for the fetal bradycardia. In my
opinion the most likely explanation for this was a bolus (dose) of Syntocinon or similar
(agent) at 1030 hours.”
Professor 1, conducted the management and midwifery supervisory investigations into
the initial concerns which had been raised regarding Mrs Stewart. As part of the police
investigation into this matter, Professor 1 was invited to comment on the case of Mother
C. She stated:
“Mother C was a first time mother and kept well in pregnancy and had a spontaneous
labour at term. She had a slow progressing labour so was transferred to Aberdeen
Maternity Hospital from Peterhead. She was admitted by Kirsty…who examined her and
Page 34 of 96
found her cervix to be 7 centimetres dilated. Kirsty documents starting IV Syntocinon
and two minutes later a prolonged and unexpected fetal bradycardia (occurred).
“Mother C was taken to theatre for an emergency caesarean which was performed
under general anaesthetic. (The) baby was born in good condition and no cause for
bradycardia found. This was suspicious due to (the) CTG being normal and (the)
bradycardia occurring after Syntocinon.”
Miss 1a, was informed of the initial concerns with Mrs Stewart’s practice. She was also
asked, as part of the subsequent police investigation, to comment on the midwifery
progress notes and records of Mother C. She gives an account, within her police
statement, of the circumstances of Mother C’s labour. She also observes that Mrs
Stewart took over Mother C’s care upon transfer to the Ward and that an IV Syntocinon
infusion at 1ml per hour was commenced at 10:30:
“At 1032 hours, Kirsty notes the fetal heart rate was down to 60 and not picking up. She
turned the woman on her side and buzzed for assistance…At 10:50 hours, she was
transferred to theatre for CS1 under general anaesthetic. The operation notes give no
indication for the cause of the fetal bradycardia.”
Mrs 1b, conducted an initial review into the concerns surrounding Mrs Stewart. She was
asked by Miss 1a to participate as an independent and external reviewer of records.
Mother C was one of the 27 cases that she was handed. With respect to Mother C she
outlined the progress of Mother C’s labour and Mrs Stewart’s documented interventions.
She stated:
“This patient was admitted from Peterhead due to a delay in progress in (the) first stage
(of) labour and (the) cervix had stopped dilating. She would have needed some form of
intervention. Upon being admitted to Labour Ward by K.Stewart…the contractions had
stopped so (it) was decided to commence Syntocinon…
K.Stewart notes some deceleration on the CTG which recovers but 2 minutes after
Syntocinon there is a fetal bradycardia which is documented as lasting 8 minutes…The
Page 35 of 96
baby is delivered by CS1 and again this case I would class as very strange and, going
on documentation unexplained.”
Dr 1 was asked for a witness statement by the police and he provided an opinion
regarding Mother C’s case. He had access to the midwifery progress notes and
provides the following conclusion on Mother C’s labour and fetal bradycardia:
“The CTG trace is of poor quality but sufficient to be suspicious of a hypertonic event
leading to a fetal bradycardia. No explanation for this was found at delivery.”
The panel also had regard to the additional report written by Dr 1 which is an expert
opinion commissioned by a law firm on behalf of the NMC. He was asked to consider
and provide an opinion on cases A to T and in relation to Mother C he notes that he was
unable to read the CTG trace but nonetheless comments:
“…In this case there is a clear temporal association with the commencement of IV
Syntocinon and the bradycardia…In this case delivery was by caesarean section. The
bradycardia was prolonged and the liquor now meconium stained. This was a new
finding and therefore accorded higher status as a sign of acute fetal stress. At the
caesarean section no direct explanation for a bradycardia was identified. The baby was
born in excellent condition.”
The panel also considered the response of Mrs Stewart who writes: “Obstructed labour.
10 hours at 7cms. Meconium stained liquor noted by medical staff but nil of note at
delivery???”.
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 10:32am, just two minutes after Mrs Stewart documented in the progress
notes that IV Syntocinon was commenced. The fetal heart rate was severely
compromised, falling to 60 bpm. The CTG trace is illegible but, nevertheless, the
sudden precipitous drop in heart rate, as clearly recorded by the progress notes, is
highly suspicious.
Page 36 of 96
The panel concurred with the opinion of Dr 1 who justifiably pointed out the close
association between the IV Syntocinon infusion and the bradycardia. There is also, in
the panel’s view, no other explanation advanced for the fetal bradycardia, such as cord
compression or entanglement, and the panel concluded that the most likely explanation
was an intervention by Mrs Stewart.
The panel bore in mind the rarity of unexplained fetal bradycardias. In this case the IV
Syntocinon was already set up and the panel concluded that it was more likely than not
that Mrs Stewart administered a bolus dose of an oxytocic drug which was a direct
cause of the fetal bradycardia suffered by the fetus of Mother C.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother C.
Schedule 1
D.
Mother D, date of delivery 17 November 2007
Mother D:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother D and the CTG tracings of Mother D. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3, commented on the midwifery progress notes of Mother D as part of the police
investigation. She observes that Mother D was transferred to the Ward and looked after
by another midwife at 09:50 hours. She goes on to identify that Mrs Stewart relieved the
other midwife at 11:25 hours and stated:
“…The CTG had been showing occasional typical decelerations but was otherwise reassuring. At 11:50 hours Kirsteen commenced IV Syntocinon and at 11:55 hours there
was a fetal bradycardia. The fetal heart recovered although there continued to be
decelerations on the CTG from this point and the baby was delivered at 12:51 hours by
forceps.
Page 37 of 96
“The baby was initially in poor condition at birth but responded well to resuscitation, but
required a later admission to the neonatal ward after a colour change. There was no
cause for the fetal bradycardia. It is possible that the change in CTG following the (fetal)
bradycardia at 11:55 hours could have been attributed to a bolus (dose) of Syntocinon
or similar drug.”
Professor 1, conducted the management and midwifery supervisory investigations into
the initial concerns which had been raised regarding Mrs Stewart. As part of the police
investigation into this matter, Professor 1 was invited to comment on the case of Mother
D. She noted that when Mother D was transferred to the Ward, her cervix was 7cm
dilated. Professor 1 stated:
“An hour and a half later, Kirst Stewart…is documented as going into room to relieve for
(a) staff break. Twenty five minutes later she starts IV Syntocinon and five minutes after
there is a fetal bradycardia which is prolonged and lasts 7 minutes. Syntocinon is
stopped and (the) fetal heart rate returns to 135 heart beats per minute, and thirty
minutes later there is a further fetal bradycardia.”
Miss 1a, was informed of the initial concerns with Mrs Stewart’s practice. She was also
asked, as part of the subsequent police investigation, to comment on the midwifery
progress notes and records of Mother D. She gives an account, within her police
statement, of the circumstances of Mother D’s labour. She stated:
“At 11:50 hours, Kirsty commenced IV Syntocinon at 1ml per hour. At 11:55 hours Kirsty
noted the fetal heart rate had dropped to 80 to 90 beats per minute…the woman
continued to have an abnormal CTG and progressed to a forceps delivery at 12;51
hours. There is nothing in the notes to indicate a reason for the fetal bradycardia.”
Mrs 1b, conducted an initial review into the concerns surrounding Mrs Stewart. She was
asked by Miss 1a to participate as an independent and external reviewer of records.
Mother D was one of the 27 cases that she was handed. With respect to Mother D she
Page 38 of 96
outlined the progress of Mother D’s labour and Mrs Stewart’s documented interventions.
She stated:
“A short time after Syntocinon was administered the CTG shows a fetal bradycardia for
eight minutes which recovers to a similar pattern as before bradycardia. The Syntocinon
was stopped at (the) first bradycardia…in my opinion this is more difficult to provide (an)
explanation for as there was (an) abnormal trace in the Maternity Ward and admission
to Labour Ward. It is, however, strange how the bradycardia occurred just after
Syntocinon was switched on.”
“The second bradycardia occurs when there is no Syntocinon documented as being
used. Between bradycardias there is a period of hyperstimulation uterus tension with 5
contractions in (a) 8 minute period.”
Dr 1 was asked for a witness statement by the police and he provided an opinion
regarding Mother D’s case. He had access to the midwifery progress notes and
provides the following conclusion on Mother D’s labour and fetal bradycardia:
“This case of bradycardia follows the now established pattern. There is questionable
use of Syntocinon to augment what appears to be a progressive labour. Once again the
steep slope of the deceleration is notable.”
The panel also had regard to the additional report written by Dr 1 which is an expert
opinion commissioned by a law firm on behalf of the NMC. He was asked to consider
and provide an opinion on cases A to T and in relation to Mother D he notes that the
patient was in active progressive labour, that there had been CTG anomalies, that the
Obstetric Registrar had recorded ‘no further decelerations’ and that the Syntocinon was
being administered ‘as per protocol.’ He stated:
“I consider Syntocinon administration at this stage questionable but it was a medical
decision. Thereafter a familiar patter[n] of decelerations and resolution occurs
associated with KS however a bradycardia could have been physiological. The
Page 39 of 96
subsequent vaginal delivery of a baby in good condition suggests that Sytonicon was
unnecessary…”
The panel also considered the responses of Mrs Stewart who writes: “Descent of fetal
vertex. No sign of hyperstimulation, decelerations continue. ? Second stage trace.”
The panel noted that Mrs Stewart took over from another midwife at 11:25 hours. Mrs
Stewart recorded in the labour progress notes that the CTG baseline was 120 bpm and
that there were occasional early decelerations. At 11:35 hours she recorded that Mother
D was contracting four moderate in 10 minutes and that a medical review is expected to
happen.
In the progress notes a Dr 8 then makes an entry at 11:40 hours. He notes that the
contractions are occurring irregularly and makes a plan which is “Syntocinon as per
protocol, Review CTG 30 mins ? FBS [Fetal Blood Sampling]”. After this entry Mrs
Stewart records at 11:50 that IV Syntocinon infusion is commenced at 1ml/hour. Mother
D felt rectal pressure: a sign of the second stage of labour.
At 11:55 the fetal heart rate drops down to 80/90 bpm and Mrs Stewart recorded that
the IV Syntocinon has been stopped. At 12:05 hours the panel noted that Mrs Stewart
records that another doctor has said that he does not wish for Syntocinon to be
recommenced. Nevertheless at 12:40 hours Mrs Stewart records that the fetal heart rate
has again dropped to 80 – 90 bpm and that the doctor is present in the room for an
instrumental delivery.
The panel considered that the first bradycardic event occurred shortly after a doctor
made a clinical decision to start Syntocinon at 11:40 following a review. The panel noted
that Mother D was also in active labour.
The panel noted that there was evidence in the labour progress notes that Mother D
was experiencing rectal pressure which could have been a potential factor in a fetal
bradycardia. Furthermore, the Syntocinon infusion at 1ml/hour, while a low dose, may
have been a factor in the fetal bradycardia which occurred.
Page 40 of 96
The second bradycardic event did not present an obvious opportunity, based on the
records before the panel, for Mrs Stewart to administer a bolus dose of an oxytocic
drug. Prior to 12:40 hours, when the second bradycardic episode occurred, Dr 9 reviews
the situation (recorded in Mrs Stewart’s notes at 12:30 hours) and it is recorded that
Mother D is fully dilated.
Dr 1 notes that the bradycardia could have been physiological and the panel came to
the conclusion that a positive intervention by Mrs Stewart was not the sole possible
explanation for either bradycardic event. In these circumstances, the panel was not
satisfied that the NMC had discharged its burden of proof and found Charges 1 and 2
not proved with respect to Mother D.
Schedule 1
E.
Mother E, date of delivery 14 June 2009
Mother E:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother E and the CTG tracings of Mother E. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother E as part of the police
investigation. She observes that Mother E was transferred to the Ward at 23:43 hours,
whereupon Mrs Stewart took over responsibility for her care. Dr 3 identifies that the
CTG trace is normal at this stage. She then stated:
“At 0030 hours, IV Syntocinon was commenced. At 0035 hours, there is a fetal
bradycardia which recovers. At 0105 hours, an epidural is sited and (she) has a further
short (fetal) bradycardia at 0112 hours but this is immediately following the siting of the
epidural and is likely to be associated with this.
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“At 0159 hours, there is a note to say fetal heart (is) down to 79 (bpm). She has (had) a
ventouse delivery to (of) a live male infant with some bleeding after the delivery of the
placenta. No cause is found for the (fetal) bradycardia.
“In this case I feel it is the first (fetal) bradycardia that is suspicious and it follows the
pattern of the other case(s), being after the administration of an IV drug. And what
happens thereafter is, there is very frequent uterine activity on the CTG which could
account for the ongoing fetal distress and rapid cervical progress (which) could be
explained by a bolus (dose) (dose) of Syntocinon or similar substance around 00:30
hours.”
Professor 1 conducted the management and midwifery supervisory investigations into
the initial concerns which had been raised regarding Mrs Stewart. As part of the police
investigation into this matter, Professor 1 was invited to comment on the case of Mother
E. She refers to the circumstances of Mother E’s labour and stated:
“IV Syntocinon was commenced and 5 minutes later a profound, prolonged fetal
bradycardia which lasts for 7 minutes. Syntocinon was switched off and (the) fetal heart
rate recovers. (An) Epidural is sited then (her) cervix (is) found to be fully dilated and
another fetal bradycardia is recorded. It lasts for 5 minutes. Nothing is recorded to
suggest the Syntocinon has started again.”
In Professor 1’s opinion both of the bradycardias are suspicious as Mother E was only
contracting 1 in 10 minutes prior to the Syntocinon being administered. Upon the
Syntocinon being administered, she states, “she becomes immediately hypertonic and
has these bradycardias.”
Miss 1a observes, in her police statement, that IV Syntocinon is commenced at 00:30
hours at 1ml per hour. She states that another midwife, at 00:35, records that the fetal
heart rate dropped to 60bpm. She notes that Mrs Stewart then makes an untimed entry
which confirms the drop in the fetal heart rate following the IV Syntocinon
administration.
Page 42 of 96
Mrs 1b similarly describes the circumstances of Mother E’s labour in identical terms to
the other NMC witnesses. She concludes that “This case is suspicious due to a normal
trace prior to bradycardia. It could be explained by an placental abruption, but there is
nothing (in the) symptoms suggestive of abruptions until immediately prior to delivery.”
Dr 1 was asked for a witness statement by the police and he provided an opinion
regarding Mother E’s case. He had access to the midwifery progress notes and
provides the following conclusion on Mother E’s labour and fetal bradycardia:
“…The two events of fetal bradycardia are not explained by the subsequent delivery
findings. There is a “terminal” bradycardia prior to delivery which may be explained by
the presence of cord loops around the fetal neck and an active antepartum
haemorrhage. I believe the two early events are suspicious.”
The panel also had regard to the additional report written by Dr 1 which is an expert
opinion commissioned by a law firm on behalf of the NMC (June 2012). He was asked
to consider and provide an opinion on cases A to T and in relation to Mother E he
elaborates upon his earlier conclusion:
“My suspicious are entirely based on the close temporal association of the introduction
of Syntocinon and the major change in the stability of the fetal heart on the CTG, the
rapid recovery and the return to the established CTG pattern…At 0030 Syntocinon is
introduced and there is a bradycardia. Nothing else had changed other than the
commencement of Syntocinon.”
The panel also considered the responses of Mrs Stewart who writes: “I was not in room
when bradycardia arose. Quick dilatation for prim 3cms to fully in 2 hours. If bolus given
at 00.30 then FH would have taken longer to recover and hyperstimulation would have
been noted.”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 00:35, resulting in the fetal heart rate being severely compromised at 60
bpm. This occurred just five minutes after IV Syntocinon was commenced by Mrs
Page 43 of 96
Stewart and happened in the context of a reassuring CTG which was, in the accepted
opinion of the NMC witnesses, entirely normal and not indicative of any other problems.
The panel noted that the circumstances of the second fetal bradycardia could be
explained by a placental abruption. Mrs 1b records that there is a fresh PV blood prior to
delivery accompanied by a large gush of fresh blood upon the delivery of Mother E’s
baby. The panel also noted that there was a 100ml retroplacental clot which was
discovered when the placenta was examined.
Furthermore, the panel considered that Mrs Stewart was not present during the second
bradycardia as she had been buzzed into the room, as recorded in the labour progress
notes. The panel concluded that the second bradycardia could be explained by other
causes and Mrs Stewart did not have an obvious opportunity to administer a bolus
dose.
With respect to the first bradycardia, however, the panel considered that there was, as
Dr 1 noted, a close temporal association between the administration of Syntocinon and
the fetal bradycardia. There is also, in the panel’s view, no other explanation advanced
for the first fetal bradycardia, such as cord compression or entanglement, and the panel
concluded that the most likely explanation was an intervention by Mrs Stewart.
The panel bore in mind the rarity of unexplained fetal bradycardias, their common
causes and the record of care documented by Mrs Stewart in relation to Mother E. Mrs
Stewart had an opportunity to administer a bolus dose of Syntocinon and the panel
concluded that it was more likely than not that Mrs Stewart administered a bolus dose of
an oxytocic drug which was a direct cause of the first fetal bradycardia suffered by the
fetus of Mother E.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother E.
Schedule 1
F.
Mother F, date of delivery 17 June 2009
Page 44 of 96
Mother F:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother F and the CTG tracings of Mother F. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother F as part of the police
investigation. She observes that Mother F was transferred to the Ward for induction of
labour at term plus seven (days) due to a prolonged rupture of membrane. Mother F
arrived on the Ward at 1220 hours and Mrs Stewart assumed responsibility for her care.
Dr 3 then describes the circumstances of Mother F’s labour, observing:
“At 13:10 hours, IV Syntocinon was commenced and up to this point the CTG was
normal. At 1312 hours, there was a profound fetal bradycardia. I see the on call
Registrar, [Dr 10], has noted the abdomen was tense, rigid and tender.
“There is also evidence on the CTG, on the topography of what could be a tonic uterine
contraction. The Registrar thought this was due to an abruption and took her for an
emergency caesarean section. She was delivered by section and had a male live infant
in good condition.
“…In my opinion the most likely explanation of the finding from 1310 hours onwards is
that a bolus (dose) of Syntocinon or similar agent was given.”
Professor 1 conducted the management and midwifery supervisory investigations into
the initial concerns which had been raised regarding Mrs Stewart. As part of the police
investigation into this matter, Professor 1 was invited to comment on the case of Mother
F.
She identified that at 12:20 hours that day Mrs Stewart sited a venous cannula. She
also observes that the CTG is normal, as recorded by Mrs Stewart at 13:10 and then
she confirms the evidence of Dr 3 in that a fetal bradycardia occurs at 13:12, two
minutes after Syntocinon is commenced. She stated:
Page 45 of 96
“[Mother F] was taken to theatre and a CS1 was carried out under general anaesthetic.
It was recorded by [Dr 11] in the labour and birth notes that there was no clinical
explanation and no evidence of abruption.”
Miss 1a and Mrs 1b similarly describes the circumstances of Mother F’s labour in
identical terms to the other NMC witnesses. Miss 1a concludes that there is no
documented evidence of abruption or cord involvement and Mrs 1b’s opinion is similar
in that on delivery there is no evidence of placental abruption despite some suggestive
signs during labour. Mrs 1b states that, “This was a very swift and painful reaction to the
administration of Syntocinon. I would not expect to see such a reaction for such [a] low
dose.”
Dr 1 was asked for a witness statement by the police and he provided an opinion
regarding Mother F’s case. He had access to the midwifery progress notes and
concludes that there is no other explanation for the fetal bradycardia other than the
Syntocinon commenced by Mrs Stewart.
The panel also had regard to the additional report written by Dr 1 which is an expert
opinion commissioned by a law firm on behalf of the NMC (June 2012). He was asked
to consider and provide an opinion on cases A to T and in relation to Mother F he
elaborates upon his earlier conclusion:
“…At the caesarean birth 17 minutes later the consultant found no evidence of
abruption or cord involvement. Profuse bleeding noted at the section was secondary to
the surgical procedure, the mother was not hypotensive. The fetal condition in this case
was satisfactory because of rapid action by the attending staff, a short decision to
delivery interval, the cessation of Syntocinon and the administration of Terbutaline. The
baby was a normal size with no evidence of fetal growth restriction. The patient’s past
history of precipitate labour is irrelevant here as this was not a case of rapid labour. It
can be concluded that no cause for the fetal bradycardia other than the possibility of
Syntocinon inducted hyperstimulation is likely.”
Page 46 of 96
The panel also considered the written responses of Mrs Stewart who writes: “Para 2
Response to syntocinon have seen very quick reactions in my career.”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 13:12 hours and resulted in a significant drop in the fetal heart rate from a
baseline of 130bpm to 80 bpm, at 13:12 hours, and then 60 bpm at 13:15 hours. This
occurred just 2 minutes after Mrs Stewart had recorded in the labour progress notes
that she commenced IV Syntocinon at 1ml/hour. The panel also noted that the CTG up
to the point of IV Syntocinon being commenced was reassuring.
With respect to the first bradycardia the panel considered that there was a close
association between the administration of Syntocinon and the fetal bradycardia. In the
panel’s judgement, there is no other explanation advanced for the fetal bradycardia,
such as cord compression or entanglement, and the panel concluded that the most
likely explanation was an intervention by Mrs Stewart.
The panel bore in mind the rarity of unexplained fetal bradycardias. Mrs Stewart had an
opportunity to administer a bolus dose of Syntocinon, via the IV which she set up shortly
before the fetal bradycardia occurred, and the panel concluded that it was more likely
than not that Mrs Stewart administered a bolus dose of an oxytocic drug which was a
direct cause of the fetal bradycardia suffered by the fetus of Mother F.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother F.
Schedule 1
G.
Mother G, date of delivery 2 August 2009
Mother G:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother G and the CTG tracings of Mother G. The panel also noted the
response of Mrs Stewart concerning this case.
Page 47 of 96
Dr 3, commented on the midwifery progress notes of Mother G as part of the police
investigation. She observes that Mother G was transferred to the Ward for induction of
labour at 00:40 hours and her care was taken over by Mrs Stewart. She stated:
“On the CTG there are atypical decelerations prior to the (fetal) bradycardia. She was
fully dilated at 02:30 hours and reviewed at 04:25 hours due to lack of progress and a
decision (was) made to commence Syntocinon. At 04:35 hours, she was given an
intramuscular injection and at 04:40 hours IV Syntocinon was commenced.
“At 04:43 hours, a fetal bradycardia commenced. She was transferred to theatre and the
(fetal) bradycardia recovered and she progressed to a normal delivery of an infant
female who was fine. There were no causes found for the (fetal) bradycardia.
“In this case, because of the pre-existing abnormality in the CTG it is more likely this
baby would have had a spontaneous (fetal) bradycardia, however, the CTG immediately
preceding the (fetal) bradycardia was normal and the fact that the (fetal) bradycardia
occurred following administration of intramuscular and intravenous drugs and that no
cause for the (fetal) bradycardia was found following delivery and (that) it follows the
pattern of the other case makes it suspicious in my opinion”.
Professor 1 conducted the management and midwifery supervisory investigations into
the initial concerns which had been raised regarding Mrs Stewart. As part of the police
investigation into this matter, Professor 1 was invited to comment on the case of Mother
G.
With respect to Mother G, Professor 1 observed that a venous cannula was sited by Mrs
Stewart and IV fluids started because Mother G had a raised temperature and was not
passing urine at the time. She also identifies that Mrs Stewart commenced IV
Syntocinon at 04:40 hours and there is, in her words, an “immediate, profound,
prolonged fetal bradycardia.”
Page 48 of 96
Miss 1a and Mrs 1b describe the progress of the labour and of Mother G and states that
there is no reason for the bradycardia within the progress notes of Mother G. Mrs 1b,
however, provides more detail on the decision to commence IV Syntocinon:
Mrs 1b states, in her opinion, the Syntocinon commenced at 8ml per hour was “strange
based on the circumstances and very high”. Dr 1 also makes reference to this unusually
high starting dose for Syntocinon:
“There is the established pattern of K Stewart’s involvement, however, the rapid onset
prolonged fetal bradycardia may have been due to commencing Syntocinon at a higher
starting dose as instructed by an Obstetrician (witness [Dr 12].)…There is a benefit of
the doubt in this particular case.”
In his supplementary report, Dr 1 identifies the medical advice, as well as the unit policy,
as being crucial here, “hence my conclusion given the evidence available that the
benefit of doubt was appropriate.”
The panel also considered the written responses of Mrs Stewart who writes: Fully
dilated synt commenced at 8mls!!! An hour not1iml as protocol, doctor’s instructions.
Reaction to amount of synt being given. High dose started in 2nd stage.
The panel considered that there was a profound and prolonged fetal bradycardia which
occurred at 04:43 and resulted in the fetal heart rate dropping down to 60 – 70 bpm.
This occurred only eight minutes after IV Syntocinon was commenced. This close
temporal association led the panel to conclude that this is the most likely cause of the
fetal bradycardia.
The panel accepted Mrs 1’s and Dr 1’s concerns that an 8ml per hour dose of
Syntocinon was a higher starting dose than usual, but Mrs Stewart acted on a doctor’s
instruction and at a time when Mother G was fully dilated. The panel concluded there
could be a clinical reason for administering such a high dose.
Page 49 of 96
In these circumstances the panel accepted that Mrs Stewart administered a high dose
of Syntocinon by way of infusion on the instruction of a doctor. It concluded that it was
unlikely that an additional bolus dose was administered by Mrs Stewart in such
circumstances.
The panel therefore determined that the NMC had not discharged its burden of proof
and found Charges 1 and 2 not proved with respect to Mother G.
Schedule 1
H.
Mother H, date of delivery 19 September 2009
Mother H:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother H and the CTG tracings of Mother H. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother H as part of the police
investigation. She observes that Mother H was transferred to the Ward on 19
September 2009, initially under the care of a different midwife. At the change of shift, at
19:10 hours, Mrs Stewart then assumes responsibility for the care of Mother H. Dr 3
notes that Mrs Stewart suggested that Mother H be transferred to the Ward and
connected to a CTG, which occurs at 19:45 hours. Dr 3 stated:
“…The trace [CTG] shows typical variable decelerations but is largely re-assuring.
Midwife Stewart had unsuccessfully tried to site a venflon and requested medical staff
site it. No-one was available so at 20:20 hours Midwife Stewart managed to site the
venflon.
“At 20:30 hours, there was a profound fetal bradycardia down to fifty beats per minute.
[Mother H] progress to caesarean section although fully dilated and had a live born
female (infant) in good condition.
Page 50 of 96
“The combination of the venflon being sited and the fetal bradycardia and the rapid
progress following previously slow progress makes a bolus (dose) (dose) of Syntocinon
a possible explanation for these events. The notes indicate cord around the neck but no
other explanation of (fetal) bradycardia.”
Professor 1 conducted the management and midwifery supervisory investigations into
the initial concerns which had been raised regarding Mrs Stewart. As part of the police
investigation into this matter, Professor 1 was invited to comment on the case of Mother
H and the fetal bradycardia which occurred. Her conclusion, based on the
circumstances of Mother H’s labour, is that “This is suspicious due to a normal CTG
prior to the event and a short time after a cannula (was) sited.”
Miss 1a and Mrs 1b, describe the circumstances of Mother H’s labour in identical terms
to the other NMC witnesses. Miss 1a concludes that “There is nothing in the notes to
indicate a reason for the fetal bradycardia.”
Mrs 1b agrees with this conclusion, observing that “Apart from the fact that the
bradycardia occurred just after (the) venflon was sited there is nothing else to suggest
what happened around that time to cause it. Although the cord was round the neck it
does not always cause (a) profound bradycardia but would cause decelerations.”
Dr 1, in his statement to the police, was asked to comment on Mother H’s midwifery
notes. He stated: “The character of the bradycardic episode and the circumstances
around this event are highly suspicious even although this case has a number of
obstetric complexities.”
In his supplementary statement, Dr 1, elaborated upon this conclusion. He observed,
like the other NMC witnesses, that the cord was tight around the fetal neck and
excluded other causes of the acute bradycardia such as descent of the head, abruption
and cord prolapse. He made reference to occasional deep and wide variable
decelerations during the CTG prior to the bradycardia event but nonetheless concludes:
Page 51 of 96
“Not withstanding the above complexities of the case itself, the findings following the
bradycardia events indicate this fetus was remarkably tolerant of significant stress
challenges and a number of causes of bradycardia can be confidently excluded. The
‘highly suspicious’ conclusion was drawn from the recognisable pattern of KS
involvement, venous access, sudden profound bradycardia with a typical CTG change
and recovery seen when there is fetal hypertension or transient profound restriction of
usual placental oxygen/nutrient transfer presumably due to hypertonus.”
The panel also considered the written responses of Mrs Stewart who writes: “Bandles
ring present sign of obstructed labour. Cord tight round neck. Rapid dilatation 3cms in
an hour. Medical staff sited venflon, usually brought own equipment. How could I have
given bolus?”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 20:30 hours and resulted in a significant drop in the fetal heart rate to 50 –
60 bpm. This occurred within a short space of time after Mrs Stewart recorded in Mother
H’s notes that she had sited a venflon. The precise time is unknown but both events are
recorded within the same timed entry in the labour progress notes. The evidence of the
NMC witnesses, which the panel accepted, all point out that the CTG was reassuring up
until the venflon is sited.
No Syntocinon was prescribed or recorded as being administered in the case of Mother
H but the panel considered that the venflon provided an opportunity for a bolus dose of
an oxytocic drug to be administered. The other potential explanations for an acute
bradycardic episode such as occurred in this instance have been discounted (such as
cord prolapse for example) by the NMC witnesses. The panel noted complications in the
second stage of labour with a failed forceps delivery and signs of obstructed labour
(Bandles ring) which caused no further apparent fetal stress.
Dr 1 does make reference to the deep variable decelerations prior to the bradycardic
event. He states that in retrospect this could have been caused by the obstructed labour
or nuchal cord found at the Caesarean section, but discounts these as a cause for the
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bradycardia because of the reassuring CTG prior to and following the bradycardic event
which occurred following the venflon being sited.
The panel considered that the specific circumstances of venous access followed by
sudden profound bradycardia with a previously reassuring CTG trace strongly
suggested that it was more likely than not that Mrs Stewart administered a bolus dose of
an oxytocic drug which was a direct cause of the fetal bradycardia.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother H.
Schedule 1
I.
Mother I, date of delivery 20 September 2009
Mother I:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother I and the CTG tracings of Mother I. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3, commented on the midwifery progress notes of Mother I as part of the police
investigation. She observed that Mother I was a self-referral from home on 19
September 2009. Mother I was admitted to the Ward at 22:38 hours and was cared for
by Mrs Stewart. She stated:
“A plan is made for an IV access (venflon/cannula) to be sited at 23:55 hours, and for
Syntocinon to be commenced at 00:20 hours. However, there are no notes documented
if or when these events occurred.
“At 00:55 hours there is a profound fetal bradycardia, although the CTG earlier is hard
to interpret due to loss of contact and may show some earlier decelerations, the CTG
immediately preceding the (fetal) bradycardia is normal.
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“Fetal heart recovers after 7 – 8 minutes but (the) decision is made to deliver the baby
by Caesarean section. A live female infant is delivered in good condition.”
Dr 3 goes on to discuss the presence of meconium found during the Caesarean section.
She argues that the meconium would most likely have been a result of the fetal
bradycardia or another event. She concludes by saying that, “…Due to the lack of
documentation of the IV access etc, it is difficult to speculate as to the cause of (fetal)
bradycardia, although a bolus dose of Syntocinon or other oxytocin agent could have
been a cause.”
Professor 1 also reviewed Mother I’s notes and observed, like Dr 3, that the CTG was
normal prior to the fetal bradycardia. She stated:
“A CS1 [caesarean section] was carried out and no cause found for (the) fetal
bradycardia. APGAR scores for baby was normal but no arterial PH was recorded.
“This case is suspicious in my opinion as the CTG is perfectly normal until the
bradycardia. There is no clinical explanation. Although no Syntocinon was administered
a venous cannula was inserted.”
Miss 1a and Mrs 1b also describe the circumstances of Mother I’s labour. Miss 1a
concludes that there is no “indication of a cause for fetal bradycardia,” while Mrs 1b
concluded:
“In summary I think that the Midwife ... should have been writing more. There is nothing
documented of a venflon being sited or Syntocinon being administered. I cannot see
any cause for the fetal bradycardia other than there was abnormal trace and there was
meconium.”
Dr 1, in his statement to the police, was asked to comment on Mother I’s midwifery
notes. He states: “This is a case of (an) unexplained, profound bradycardia of rapid
onset.” Within his supplementary report, Dr 1 elaborated upon this conclusion. He noted
that she had an assisted conception and pregnancy induced hypertension. This was her
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first pregnancy which was, in his view, a risk factor for adverse outcomes. He excluded
other obstetric complications such as fetal growth restriction or placental abruption.
The panel also considered the written responses of Mrs Stewart who writes: “No venous
access, bloods taken or drugs given prior to brady. How could a bolus be given. Thick
meconium noted at 2cms.
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 00:55 hours and resulted in a significant drop in the fetal heart rate to 50 –
60 bpm. This occurred 55 minutes after Mother I was transferred to the Ward under the
care of Mrs Stewart. There was, however, no oxytocic drug which was recorded as
being administered to Mother I preceding the fetal bradycardia.
There was also a lack of an opportunity to administer a bolus drug through, for example,
an IV cannula or a venflon. Dr 3’s evidence was that it was difficult to speculate as to
the cause of the fetal bradycardia in the absence of documentation regarding IV access.
She did advance a bolus dose of an oxytocic drug as a possible cause.
In the absence of a written record of an IV venflon being sited or other intravenous or
intramuscular injection the panel regarded this a significant deviation from the pattern
with which the fetal bradycardias have occurred under the care of Mrs Stewart. In these
circumstances, the panel was not satisfied that, on the balance of probabilities, Mrs
Stewart had administered such a bolus dose to Mother I.
The panel accordingly concluded that the NMC had not discharged its burden of proof
and found Charges 1 and 2 not proved in relation to Mother I.
Schedule 1
J.
Mother J, date of delivery 16 October 2009
Mother J:
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The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother J and the CTG tracings of Mother J. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother J as part of the police
investigation. She observes that Mother J was admitted at 18:00 hours on 16 October
2009. She also notes that Mrs Stewart takes over the care of Mother J from 19:05 hours
who commenced a CTG. Dr 3 describes this CTG as entirely reassuring. She then
points out that a venflon is sited by a Senior House Officer (SHO) and goes on to state:
“At 2012 hours, there is a fetal bradycardia but the CTG had been normal to this point.
Like similar cases there may be evidence on the tocograph of a prolonged tonic uterine
contraction. Patient is delivered by emergency caesarean section and has a live male
infant in good condition. The Surgeon, [Dr 13] documented there was no cause for the
(fetal) bradycardia found at section. These findings would be in keeping with a bolus
(dose) of Syntocinon or other uterotonic agent given at 2010 hours.”
Professor 1, Miss 1a and Mrs 1b also reviewed the midwifery notes of Mother J.
Professor 1 stated that it was her opinion that, “that it was unexplained clinically but
followed the general pattern of Kirsty starting shift, venous access and a sudden
deterioration.” Professor 1 told the panel she would have anticipated a normal labour
and birth with a good outcome in this particular case.
Miss 1a stated that Dr 13 has documented that there was no cause for the fetal
bradycardia to be found. Mrs 1b placed emphasis on the CTG trace being fine which
was immediately followed by a “sudden bradycardia that is unexplained.” In her view
this is highly unusual and she states that “I can’t ever recall ever seeing a totally normal
trace that suddenly plummets.”
Dr 1, in his statement to the police, was asked to comment on Mother J’s midwifery
notes. He stated: “This is a case of a rapid onset deep and prolonged unexplained
unprovoked deceleration event lasting twelve to thirteen minutes.”
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In his supplementary report, Dr 1, elaborated upon this conclusion. He notes that
Mother J was a primigravida (first birth) and was born by Caesarean section by election
of the patient. He also describes the nature of the fetal bradycardia and comes to the
following conclusion:
“The CTG is as close to a perfect intrapartum trace as possible…until the unprovoked,
unexplained acute bradycardia. The tocograph changes significantly and raises the
possibility of hypertonus as a cause. As the CTG improves the tocograph elevation
decreases again highly suggestive of a hypertonic event.”
The panel also considered the written responses of Mrs Stewart who writes: “Again
medical staff sited venflon, usually brought own equipment. FH recovered and options
discussed patient decided for LUSCS”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 20:12 hours and resulted in a significant drop in the fetal heart rate to 80
bpm (check). This occurred within a short space of time after Mrs Stewart recorded in
Mother J’s notes that a SHO had sited a venflon. The precise time that the venflon was
sited is unknown as Mrs Stewart’s entry is untimed but it follows chronologically within
her notes. The evidence of the NMC witnesses, which the panel accepted, all point out
that the CTG was reassuring up until the venflon is sited and indeed Dr 1 refers to the
CTG trace as being a textbook reassuring trace.
No Syntocinon or other oxytocic drug was prescribed or recorded as being administered
in the case of Mother J but the panel considered that the venflon, instigated by Mrs
Stewart for IV fluids, provided an opportunity for a bolus dose of an oxytocic drug to be
administered. The other potential explanations for an acute bradycardic episode have
been discounted (such as placental abruption or cord prolapse) by the NMC witnesses.
The panel also noted the evidence of Dr 1 who, interpreting the tocograph, said that it
was a hypertonic event which suggests the involvement of an oxytocic drug.
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The panel also bore in mind the rarity of unexplained fetal bradycardias, their common
causes, the pattern of cases which have occurred whilst Mrs Stewart was in care of a
patient, the accessibility of oxytocic drugs on the Ward and the record of care
documented by Mrs Stewart in relation to Mother J. Mrs Stewart had an opportunity to
administer a bolus dose of an oxytocic drug, via the venflon, and the panel concluded
that it was more likely than not that Mrs Stewart administered a bolus dose of an
oxytocic drug which was a direct cause of the fetal bradycardia suffered by the fetus of
Mother J.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother J.
Schedule 1
K.
Mother K, date of delivery 30 October 2009
Mother K:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother K and the CTG tracings of Mother K. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother K as part of the police
investigation. She observes that Mother K was admitted at 19:13 hours following
spontaneous labour. Mother K was transferred to the Ward at 20:00 hours and Mrs
Stewart assumed responsibility for Mother K’s care.
Dr 3 identifies from the records that at 20:15 hours Mrs Stewart sites a venflon and at
20:25 hours it is recorded that a fetal bradycardia occurred, with the mother becoming
distressed. A further vaginal examination revealed that Mother K was fully dilated and
active pushing was commenced. The CTG then returns to normal. With regard to the
care given to Mother K, Dr 3 concluded:
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“In this case a combination of the fetal bradycardia and extremely rapid progress in a
primagravida makes the administration of a bolus (dose) (dose) of oxytocive a possible
explanation.”
Professor 1, Miss 1a, and Mrs 1b also reviewed the midwifery notes of Mother K.
Professor 1 comments on the fact that Mrs Stewart sited a venflon and then 10 minutes
later a fetal bradycardia occurs which lasts for twelve minutes. She also notes that
Mother K’s uterus is hypertonic and concludes “The fetal bradycardia does not appear
to have any explanation for it and it is very unusual for someone in spontaneous labour
to be hypertonic and progress so rapidly.” She states, “As in the previous cases there
seems to be very little uterine activity before the fetal bradycardia but a strong tonic
contraction during it (recorded almost off the scale of the tocograph). Again this lady is a
primigravida who progresses extremely quickly from 4.5 cm at 19:30 to fullt at 20~:20
when previously her progress had been slow taking twelve hours to progress from 3cm
to 4.5 cm. It would be unusual for someone who takes so long to establish in labour to
then progress so rapidly. Although there are discrepancies in the timing this case does
seem to follow the pattern of a normal CTG, IV access being obtained or an IV or IM
injection given, a profound fetal bradycardia with evidence of a marked increase in
uterine active, very quick progress for a primigravida, and no cause found for the fetal
bradycardia at birth”.
Mrs 1b concluded along similar lines: “This is an unexplained bradycardia and (there is)
a significant discrepancy in times documented. The mother was low risk and no obvious
reason. A venflon was sited.” Miss 1a only confirms the details of the event within her
police statement.
Dr 1 in his statement to the police, was asked to comment on Mother K’s midwifery
notes. He stated: “This is a case of a prolonged sustained bradycardia of thirteen
minutes of sudden onset in a previously completely normal CTG. The tocopgraph
suggests hypertonus, however, this is not mentioned in the clinical notes.”
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In his supplementary report, Dr 1, elaborated upon this conclusion. He observed that
other possibilities could be discounted such as cord prolapse or nuchal cord (tight cord
around neck of fetus). He also suggests that “Rapid descent of the fetal head can cause
acute bradycardia but would not cause a change in tocography”. He was of the view
that no rapid descent occurred.
The panel also considered the written responses of Mrs Stewart who writes: “Rapid
dilatation Cx 4-5cms to fully in 50 mins. If bolus given surely the FH would have reacted
to it sooner than 10 minutes.”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 20:25 hours and resulted in a significant drop in the fetal heart rate to75
bpm. This occurred within ten minutes of Mrs Stewart recording in Mother K’s notes that
she had sited a venflon. The evidence of the NMC witnesses, which the panel accepted,
all point out that the CTG was reassuring up until the venflon is sited which is borne out
by the CTG trace notes of Mother K.
No Syntocinon or other oxytocic drug was prescribed or recorded as being administered
in the case of Mother K but the panel considered that the venflon, sited by Mrs Stewart,
provided an opportunity for a bolus dose of an oxytocic drug to be administered. The
other potential explanations for an acute bradycardic episode such as occurred in this
instance have been discounted (such as cord prolapse for example) by the NMC
witnesses. The panel also noted the evidence of Dr 1 who, interpreting the tocograph,
said that it was a hypertonic event which suggests the involvement of an oxytocic drug.
Mother K was also a primigravida and was low risk which makes her rapid progress of
labour all the more unusual and suggestive of an outside influence.
The panel also bore in mind the rarity of unexplained fetal bradycardias, their common
causes, the pattern of cases which have occurred whilst Mrs Stewart was in care of a
patient, the accessibility of oxytocic drugs on the Ward and the record of care
documented by Mrs Stewart in relation to Mother K. Mrs Stewart had an opportunity to
administer a bolus dose of an oxytocic drug, via the venflon, and the panel concluded
that it was more likely than not that Mrs Stewart administered a bolus dose of an
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oxytocic drug which was a direct cause of the fetal bradycardia suffered by the fetus of
Mother K.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother K.
Schedule 1
L.
Mother L, date of delivery 3 November 2009
Mother L:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother L and the CTG tracings of Mother L. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother L as part of the police
investigation. She observes that Mother L came to the Ward at 11:30 hours on 3
November 2009 due to prolonged rupture of membrane for induction of labour. She
identifies that Mrs Stewart assumed responsibility for the care of Mother L and stated:
“She had a venflon sited at 1130 hours and at 1140 hours, there is a fetal
bradycardia…the fetal heart began to recover at 11:52 hours and terbutaline was given
as a subcutaneous injection on the instructions of Dr 16…
“…At 14:00 hours, it is documented that the plan is to commence IV Syntocinon. At
1415 hours, IV Syntocinon is commenced and it is increased in dose from 1ml to 2ml
per hour. At 1450 hours, there is a further fetal bradycardia and (the) decision is made
to deliver the baby by caesarean section.”
“…Apart from the two episodes of (fetal) bradycardia the CTG is entirely normal. It is
possible that the first episode of (fetal) bradycardia is due to a bolus (dose) of
Syntocinon or other oxytocin agent at the time the venflon was sited. The Terbutaline
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that was given could have counter-acted the effect and allow the fetal heart to return to
normal. It is difficult to comment on the cause of the second episode of (fetal)
bradycardia but a similar explanation may be appropriate.”
Professor 1, Miss 1a and Mrs 1b also reviewed the midwifery notes of Mother L.
Professor 1 concludes that “In my opinion the fetal bradycardias are suspicious. The
first cannot be explained and the second does not follow the normal pattern for
intravenous Syntocinon with a sustain(ed) uterus (uterine) contraction.” Miss 1a, in her
police statement, cannot identify from the records a reason for the fetal bradycardia and
Mrs 1b observes:
“The cause of [the] first bradycardia was a sustained hypertonic uterus contraction but
the cause of this symptom is unknown. The cause of the second bradycardia appears to
have been as a result of the Syntocinon increase…This case is off as I cannot
understand why a PRIM would have a hypertonic uterus contraction without Oxytocic
intervention or abruptions.”
Dr 1 in his statement to the police, was asked to comment on Mother L’s midwifery
notes. He stated that both bradycardic events with respect to Mother L were highly
suspicious. He points out that hyperstimulation “was diagnosed and treated by Medical
Staff after the first event.” In his supplementary report Dr 1 excludes other possible
causes of the first bradycardic event and the “second episode has a clear temporal
association with Syntocinon use.”
The panel also considered the written responses of Mrs Stewart who writes: “Reaction
time between supposed bolus an FH dropping 10 mins.”
The panel considered that there were two prolonged and profound fetal bradycardias
which occurred at 11:40 and 14:50 hours. Both events resulted in a significant drop in
the fetal heart rate to 60 – 70 bpm and 60 bpm respectively. The first bradycardia
occurred against the background of a reassuring CTG trace up to the point that venflon
is sited by Mrs Stewart. 10 minutes after Mrs Stewart sites the venflon, the first fetal
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bradycardia occurred. The exact timing of the siting of the venflon being sited is difficult
to determine. Although Mrs Stewart points out that there is a 10 minute time gap the
panel formed the view that some kind of untoward intervention could have occurred at
any point during those 10 minutes.
The second fetal bradycardia occurred 5 minutes after Mrs Stewart had increased the
dose of IV Syntocinon to 2 mls per hour and also occurred against the background of a
reassuring CTG trace. The panel also had regard to the CTG readings and what
Professor 1 called the “sustained uterine” contractions which occurred following this
incident. Dr 1 was of the opinion that this could not have been caused by the 2ml dose
of Syntocinon. In the panel’s judgement his opinion is justified given the low nature of
the prescribed dose. The panel considered that Mrs Stewart may have had the
opportunity to administer a bolus dose of an oxytocic drug whilst the 2ml infusion was
running.
The panel accepted the evidence of Dr 1 who stated that both events feature a
tocograph which strongly suggests hypertonus as the baseline “sharply rises as the fetal
heart falls”. The panel noted his conclusion that “The length of time for fetal heart rate
recovery is typical of a response to an episode of Syntocinon induced hypertonicity.”
Although Syntocinon was not in use during the first fetal bradycardia the panel formed
the view that it represented an opportunity to administer a bolus dose of an oxytocic
drug. The second bradycardic episode features a close temporal association between
the use of Syntocinon and the fetal bradycardia.
The panel also noted that the other potential explanations for an acute bradycardic
episode such as occurred in these two instances have been discounted by the NMC
witnesses. The panel also bore in mind the rarity of unexplained fetal bradycardias, the
pattern of cases which have occurred whilst Mrs Stewart was caring for the patient, the
accessibility of oxytocic drugs on the Ward and the record of care documented by Mrs
Stewart in relation to Mother L.
With respect to the first bradycardia, the panel considered it more likely than not to have
occurred that Mrs Stewart administered a bolus dose of an oxytocic drug, via the
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venflon. The panel also concluded that it was more likely than not that another bolus
dose of Syntocinon was administered to Mother L by Mrs Stewart by the already
established IV route causing the second bradycardia.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother L.
Schedule 1
M.
Mother M, date of delivery 15 November 2009
Mother M:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother M and the CTG tracings of Mother M. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother M as part of the police
investigation. She observes that Mother M was transferred to the Ward for induction of
labour at 23:00 hours, whereupon Mrs Stewart was assigned to care for her. She
stated:
“At 23:25 hours, a venflon was sited but at 2327 or 2328 hours from the CTG, as it’s not
documented in the notes, there is a fetal bradycardia. The CTG prior to this could
appear as fetal tachycardia but with reference to the immediately preceding CTG (this)
is normal.
“The (fetal) bradycardia lasts for eleven minutes and recovers but CTG thereafter is felt
to be abnormal and a decision is made to go for caesarean section. She delivers a live
female infant in good condition. No cause is found the fetal bradycardia. These events
could be explained by a bolus (dose) of Syntocinon or other agent when the venflon
was sited.”
Professor 1 and Mrs 1b also reviewed the midwifery notes of Mother M.
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Professor 1 concludes that “My opinion of this case is that it is suspicious and cannot be
clinically explained. There are no contractions noted by Kirsty or CTG preceding the
bradycardia.” Miss 1a observed that Mrs Stewart was the only midwife in the room when
this occurred and Mrs 1b concluded:
“I don’t know what was the cause of the fetal bradycardia although there was a
pathological trace. The only significant thing is a venflon (was) sited immediately prior to
(the) bradycardia.”
Dr 1, in his statement to the police, was asked to comment on Mother M’s midwifery
notes. He concluded: “This is a case of unexplained, profound, prolonged bradycardia
over eleven minutes. The contraction pattern appears to increase over the period of the
bradycardia.”
In his supplementary report Dr 1 elaborated upon this conclusion. He described the
CTG trace prior to the bradycardic event was being within normal limits and also
identified that Mrs Stewart had sited a venflon. He commented:
“Ten minutes after the vaginal examination there is an unprovoked very rapid onset
deceleration lasting ten minutes with reduced variability. I have not seen a more
alarming bradycardia in my career to date…No explanation for this bradycardia event is
found at the caesarean section, the baby was born in excellent condition, was of
appropriate size and no resuscitation was required. This bradycardia episode is
completely unexplained.”
The panel also had regard to Mrs Stewart’s written response. She stated: “Grade 2
meconium noted in Westburn ward. Nil of note???? Dr’s notes.”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 23:38 hours and resulted in a significant drop in the fetal heart rate to 50
bpm. This lasted for 10 minutes and occurred 13 minutes after a venflon was sited by
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Mrs Stewart. The CTG trace, as analysed by the NMC witnesses, was reassuring prior
to this event and there was also strong uterine contractions.
No Syntocinon or other oxytocic drug was prescribed or recorded as being administered
in the case of Mother M but the panel considered that the venflon, sited by Mrs Stewart,
provided an opportunity for a bolus dose of an oxytocic drug to be administered. The
other potential explanations for an acute bradycardic episode such as occurred in this
instance have been discounted (such as placental abruption) by the NMC witnesses
and the panel noted that the baby was born in excellent condition.
The panel also bore in mind the rarity of unexplained fetal bradycardias, the pattern of
cases which have occurred whilst Mrs Stewart was in care of a patient, the accessibility
of oxytocic drugs on the Ward and the record of care documented by Mrs Stewart in
relation to Mother M.
Mrs Stewart had an opportunity to administer a bolus dose of an oxytocic drug, via the
venflon, and the panel concluded that it was more likely than not that she did do so.
This administration of a bolus dose was also, in the panel’s view, a direct cause of the
fetal bradycardia suffered by the fetus of Mother M.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother M.
Schedule 1
N.
Mother N, date of delivery 23 November 2009
Mother N:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother N and the CTG tracings of Mother N. The panel also noted the
response of Mrs Stewart concerning this case.
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Dr 3 commented on the midwifery progress notes of Mother N as part of the police
investigation. She stated that Mother N was transferred to the Ward at 10:45 hours for
induction of labour due to recurring antepartum haemorrhage. Mrs Stewart took over
responsibility for her care at 11:10 hours. She stated:
“She had a venflon sited by Kirsteen. Up until this time the CTG was normal. There is
no documented time on the notes but from the CTG, at 11:12 hours there was a fetal
bradycardia and the lady was taken for delivery by emergency caesarean section.
“She had a live male infant and although his cord PH was low at birth he seemed to be
in good condition. No cause was found for the (fetal) bradycardia and section.
“…on the CTG at the time of the (fetal) bradycardia there appears on the topography
(tocograph) what appears to be a tonic uterine contraction. I think the most likely cause
of the (fetal) bradycardia is a bolus (dose) (dose) of Syntocinon or similar (agent) when
the venflon was sited.”
Professor 1, Miss 1a, and Mrs 1b also reviewed the midwifery notes of Mother N.
Professor 1 notes that Mother N was primigravida and she identifies that at 11:10 hours
Mrs Stewart sites a venous cannula whereupon a fetal bradycardia occurs. She
observes that no cause was found for this at emergency Caesarean and concludes:
“My opinion of this case, given her obstetric history, you might have expected there to
have been an abruption of the placenta but I would have expected evidence of this at
the section, but there wasn’t. Again there is no clinical explanation but it follows the
same pattern as the others.”
Miss 1a also is of the view that there is nothing in the notes which can explain the fetal
bradycardia and Mrs 1b similarly concludes that “In summary there was no obvious
cause for the bradycardia. The bleeding could have come from the placenta but nothing
was noted on delivery.”
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Dr 1, in his statement to the police, was asked to comment on Mother N’s midwifery
notes. He concluded: “This is a case of unexplained, unprovoked fetal bradycardia of
rapid onset over seven minutes. The CTG may indicate hypertonus but there is potential
movement artefact.”
In his supplementary report Dr 1 elaborated upon this conclusion. He observed that
Mother N was in her first term pregnancy having previously lost an early pregnancy
before. He identified that the CTG was reassuringly normal prior to the fetal bradycardia
and also commented on potential hypertonus:
“No explanation for the bradycardia was identified at the section. This was a normally
grown baby delivered in excellent condition. Given the previous recurrent APH history
there was an increased risk of abruption (premature separation of the placenta) but
there was no evidence for this whatsoever at the caesarean section indeed the placenta
required delivery by controlled cord traction…No normal practice or obstetric pathology
explains why this fetal bradycardia occurred.”
The panel also had regard to Mrs Stewart’s written response. She stated: “several
APH’s. Blood only at ARM? Small abruption? Medical staff documentation.”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 11:12 hours and resulted in a significant drop in the fetal heart rate to 60
bpm. This occurred three minutes after a venflon was sited by Mrs Stewart. The CTG
trace, as analysed by the NMC witnesses, was reassuring prior to this event and there
was also evidence of strong uterine contractions.
No Syntocinon or other oxytocic drug was prescribed or recorded as being administered
in the case of Mother N but the panel considered that the venflon, sited by Mrs Stewart,
provided an opportunity for a bolus dose of an oxytocic drug to be administered. The
other potential explanations for an acute bradycardic episode such as occurred in this
instance have been discounted (such as placental abruption) by the NMC witnesses
and the panel noted that the baby was born in excellent condition. Dr 1 notes that there
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is an increased risk of placental abruption (in light of the obstetric history of Mother N)
but “there was no evidence for this whatsoever at the caesarean section”.
The panel also bore in mind the rarity of unexplained fetal bradycardias, the pattern of
cases which have occurred whilst Mrs Stewart was in care of a patient, the accessibility
of oxytocic drugs on the Ward and the record of care documented by Mrs Stewart in
relation to Mother N.
Mrs Stewart had an opportunity to administer a bolus dose of an oxytocic drug, via the
venflon, and the panel concluded that it was more likely than not that she did do so in
light of the circumstances of Mother N’s labour. This administration of a bolus dose was
also, in the panel’s view, a direct cause of the fetal bradycardia suffered by the fetus of
Mother N.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother N.
Schedule 1
O.
Mother O, date of delivery 23 November 2009
Mother O:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother O and the CTG tracings of Mother O. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3, commented on the midwifery progress notes of Mother O as part of the police
investigation. She notes that Mother O was transferred to the Ward having gone into
spontaneous labour at 08:00 hours. Mrs Stewart assumes responsibility for Mother O’s
care. Dr 3 stated:
“The CTG is re-assuring at 08:10 hours and Kirsteen gives an intramuscular antacid
injection. Again there is a discrepancy between the times on the records and the CTG.
Page 69 of 96
Two minutes after the injection there is a profound unrecovering fetal bradycardia, Once
again there is evidence on the CTG topography (tocograph) of what could be a tonic
uterine contraction.
“The lady was delivered by emergency caesarean section and had a live male infant
who was born in poor condition but recovered quickly. No cause was found at
caesarean section for the (fetel) bradycardia.
“…I think the most likely explanation for these events in (is) the use of some uterotonic
agent, (which) was given instead of the Ranitidine at 08:10 hours.”
Professor 1, Miss 1a and Mrs 1b also reviewed the midwifery notes of Mother O.
Professor 1 identified that Mother O had a previous Caesarean and therefore that there
was a risk present of acute scar rupture. However, she observes that the scar was
intact. She concludes that the “fetal bradycardia is suspicious and cannot be explained.”
Miss 1a also identifies the potential for scar rupture but concludes the operation notes
from the Caesarean under general anaesthetic “do not indicate any problems or reason
for fetal bradycardia.” Mrs 1b concludes:
“In summary there is no obvious cause and (it) is an unexplained bradycardia. Looking
at the recorded blood gases of (the) baby it was obvious it was being affected by
something.”
Dr 1, in his statement to the police, was asked to comment on Mother O’s midwifery
notes. He concluded: “This patient had a medical condition that limited obstetric
interventions. K Stewart’s notes are retrospective. This was a profound unprovoked and
unexplained bradycardia with a steep descent from a normal heart rate and evidence of
hypertonus on the CTG.”
In his supplementary report Dr 1 elaborated upon this conclusion. He identified that
Mother O had a number of obstetric risk factors including a previous Caesarean section,
Group B Streptococcus infection risk and low platelets. He notes that the CTG was
Page 70 of 96
entirely reassuring beforehand although he comments that it is not clear when venous
access “was achieved”. He also analyses the CTG trace which shows that there are
strong uterine contractions at the same time as the “unheralded” fetal bradycardia. He
concludes:
“No cause for the acute bradycardia was found. In particular, there was no abruption,
cord problem and the uterine scare was intact (i.e. no rupture). There was no evidence
of fetal infection…the bradycardia remains unexplained. The clinical course and the
CTG are suspicious of a hypertonic event.”
The panel also had regard to Mrs Stewart’s written response. She stated: “Ranitidine
would have been brought in by and checked with another midwife.”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 08:12 hours and resulted in a significant drop in the fetal heart rate to 80
bpm. This occurred two minutes after Ranitidine was administered to Mother O by Mrs
Stewart. Furthermore, the CTG trace, as analysed by the NMC witnesses, was
reassuring prior to this event and there was also evidence of strong uterine
contractions, constituting a hypertonic event.
The other potential explanations for an acute bradycardic episode such as occurred in
this instance have been discounted (such as a scar rupture) by the NMC witnesses. No
Syntocinon or other oxytocic drug was prescribed or recorded as being administered in
the case of Mother O but the panel considered that administration of Ranitidine provided
an indirect opportunity for a bolus dose of an oxytocic drug to be administered.
On the evidence before it the panel considered that the only plausible explanation was
that Mrs Stewart administered a bolus dose of an oxytocic drug at the same time as the
Ranitidine. The panel also bore in mind the rarity of unexplained fetal bradycardias, the
accessibility of oxytocic drugs on the Ward and the accepted fact volunteered by Mrs
Stewart that she routinely carried an ampoule of Ranitidine in her pocket.
Page 71 of 96
The panel concluded that it was more likely than not that Mrs Stewart administered a
bolus dose of an oxytocic drug to Mother O. This administration of a bolus dose of an
oxytocic drug was also, in the panel’s view, a direct cause of the fetal bradycardia
suffered by the fetus of Mother O.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother O.
Schedule 1
P.
Mother P, date of delivery 28 November 2009
Mother P:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother P and the CTG tracings of Mother P. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother P as part of the police
investigation. She notes that Mother P was transferred to the Ward for induction of
labour, as she had ruptured membranes, at 02:30 hours and her care was taken over by
Mrs Stewart. She stated:
“At 02:45 hours, she had a vaginal examination and was 4cm dilated. She was given IV
Penicillin at 03:15 hours and at 03:18 hours there was a fetal bradycardia. Prior to that
time the CTG was entirely normal.
“At 03:20 hours, she had a further vaginal examination and (was) found to be fully
dilated. At 03:34 hours, she had a natural delivery with no cord found round the neck or
any other cause of the (fetal) bradycardia.
“In this case there was a normal CTG, antibiotics were given and there was a (fetal)
bradycardia. Along with (the) rapid delivery it is possible a uterotonic was given similar
to Syntocinon instead of, or and with the antibiotics.”
Page 72 of 96
Professor 1, Miss 1a, and Mrs 1b also reviewed the midwifery notes of Mother P.
Professor 1 concluded that “No cause (was) found at birth for (the) fetal bradycardia. It
is suspicious due to rapid progress and (the) fetal bradycardia after (the) administration
of the Penicillin.” Miss 1a stated that there was a Caesarean section at 22:46 hours and
there was no “obvious cause for the fetal bradycardia”. Mrs 1b also identifies that no
cause for the bradycardia is identified at the Caesarean and concludes that “in summary
there is no obvious cause for bradycardia.”
Dr 1, in his statement to the police, was asked to comment on Mother P’s midwifery
notes. He concluded: “This patient rapidly delivered and the fetal bradycardia might be
due to this. The length of the bradycardia at eight minutes is somewhat prolonged and
the established pattern of K Stewart’s ... involvement is present. On this occasion
intravenous antibiotics have apparently been administered. I would give the benefit of
the doubt that this bradycardia may have been due to physiology (head compression).”
In his supplementary report Dr 1 elaborated upon this conclusion. He comments that
while the CTG pattern is suspicious, “there appears to have been some uterine activity
which may not have been appreciated by either the patient or the midwife. The cervical
stimulation might have stimulated endogenous PG release and a precipitate labour is
often associated with head compression bradycardia. There is therefore a plausible
clinical explanation for the events hence the benefit of doubt is given.”
The panel also had regard to Mrs Stewart’s written response. She stated: “precipitate
labour para 2. Rapid delivery. Antibiotics checked by 2 midwives.”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 03:18 hours and resulted in a significant drop in the fetal heart rate. This
occurred within three minutes of IV Penicillin being given and the CTG trace was normal
prior to the episode.
Page 73 of 96
In this instance, however, the fetal bradycardia had a potential explanation other than
the administration of a bolus dose of an oxytocic drug. The panel noted the evidence of
Dr 1 regarding precipitate labour, as noted by Mrs Stewart, could be a cause for a fetal
bradycardia owing to head compression.
The panel concluded that while the CTG was suspicious and there was a potential
indirect opportunity to administer a bolus dose of an oxytocic drug, the possibility of a
clinical cause for the events, head compression due to the precipitate labour, was
plausible in light of the opinion of Dr 1. In addition the panel took into account Mrs 1b’s
finding that she found nothing unusual in this case.
The panel accordingly was not satisfied that the NMC had discharged its burden of
proof and found Charges 1 and 2, in relation to Mother P, not proved.
Schedule 1
Q.
Mother Q, date of delivery 5 February 2010
Mother Q:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother Q and the CTG tracings of Mother Q. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3, the obstetric lead for the Ward and for risk management, commented on the
midwifery progress notes of Mother Q as part of the police investigation. She
commented that Mother Q was transferred to the Ward at term plus two days for
induction of labour (at 21:15 hours). Her care was taken over by Mrs Stewart. Dr 3
stated:
“At 21:30 hours, Kirsteen tried and failed to site a venflon and documented she would
ask the medical staff to do it. At 22:00 hours, she documented the venflon was sited but
not by whom. At 22:20 hours, IV Syntocinon was commenced and the CTG is reassuring at this point.
Page 74 of 96
“At 22:40 hours, there is a profound unrecovering fetal bradycardia. She was taken for
emergency caesarean section and delivered a live female infant in very poor condition,
with very abnormal cord PH’s. The baby required to be incubated (intubated) and
ventilated and transferred to the Neonatal Unit. There was no cause found for the (fetal)
bradycardia at caesarean section.”
Professor 1, Miss 1a and Mrs 1b also reviewed the midwifery notes of Mother Q.
Professor 1 observes that the CTG trace was normal up until the fetal bradycardia and
that “no reason (was) found for fetal bradycardia at caesarean section.”
Miss 1a also concludes there is no obvious explanation for the fetal bradycardia. Mrs
1b, however, notes that CTG is unclear and concludes:
“There is no cause recorded for (the) bradycardia at delivery. The baby was born in
poor condition and the CTG tracing is open to interpretation. It is difficult to make a
judgement because of this as the baby may have been in distress prior to (the)
bradycardia.”
Dr 1, in his statement to the police, was asked to comment on Mother Q’s midwifery
notes. He observed that Mother Q was a low risk mother and concluded that the
episode was: “…an unexplained and apparently unprovoked fetal bradycardia within
twenty minutes of K Stewart ... initiating Syntocinon. There was severe fetal
compromise present at the subsequent caesarean section.”
In his supplementary report Dr 1 elaborated upon this conclusion. He notes that the
tocograph is not helpful in establishing a contraction pattern but does note that the CTG
was entirely reassuring before the bradycardic episode. He concludes that “No
explanation for the fetal bradycardia was identified therefore Syntocinon
hyperstimulation is the most likely reason.”
The panel also had regard to Mrs Stewart’s written response. She stated: “Again if bolus
given at 22.20 then again Fh would have reacted sooner than 10 mins.”
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The panel noted that in the maternity progress notes Mrs Stewart has altered the time of
the fetal bradycardia contrary to the NMC record keeping guidelines. The original time
recorded appears to be 22:30 and the apparent amendment is overwritten and not
countersigned.
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred recorded at 22:30 and amended to 22:40 hours and resulted in a significant
drop in the fetal heart rate to 50 – 60 bpm. This occurred 10 to 20 minutes after a
venflon was sited by Mrs Stewart. The CTG trace, as analysed by the NMC witnesses,
was reassuring prior to this event.
Syntocinon was recorded by Mrs Stewart as being given at 22:20 hours. This was, in
the panel’s view, an opportunity for Mrs Stewart to administer a bolus dose at some
time prior to 22:30/22:40 which would have accounted for the fetal bradycardia. No
other explanations for the fetal bradycardia are discovered at the Caesarean section
which happened. Dr 1 specifically excludes cord prolapse and justifiably concludes that
there is no explanation other than a positive act by Mrs Stewart.
The panel also bore in mind the rarity of unexplained fetal bradycardias, the pattern of
cases which have occurred whilst Mrs Stewart was caring for the patient, the
accessibility of oxytocic drugs on the Ward and the record of care documented by Mrs
Stewart in relation to Mother Q.
Mrs Stewart had an opportunity to administer a bolus dose of an oxytocic drug, via the
venflon, and the panel concluded that it was more likely than not that she did do so in
light of the circumstances of Mother Q’s labour. This administration of a bolus dose was
also, in the panel’s view, a direct cause of the fetal bradycardia suffered by the fetus of
Mother Q.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother Q.
Page 76 of 96
Schedule 1
R.
Mother R, date of delivery 6 March 2010
Mother R:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother R and the CTG tracings of Mother R. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother R as part of the police
investigation. She commented that Mother R was transferred to the Ward at 21:00
hours as she was in established labour. Mrs Stewart assumed responsibility for her
care. She also comments that Mother R had wanted to use the birthing pool but
tachycardia (increased heart rate) led to her giving birth in a delivery room. She was
transferred at 22:40 hours to room 3 on the Ward and a CTG was commenced. Dr 3
observes:
“At 23:25 hours she had a venflon sited by Kirsteen Stewart. At 23:27 hours there was a
profound, non-recovering fetal bradycardia. Prior to the (fetal) bradycardia the CTG was
re-assuring. She was transferred to theatre for delivery by caesarean section and had a
live born female infant in poor condition and very (with) abnormal cord PH’s. The baby
was transferred to the Neonatal Unit intensive care. There was no cause found for the
(fetal) bradycardia at caesarean section.
“Again a possible explanation for these findings is that a bolus (dose) or Syntocinon or
other uterotonic agent was given when the venflon was sited at 23:25 hours.”
Professor 1, Miss 1a and Mrs 1b also reviewed the midwifery notes of Mother R.
Professor 1 and Miss 1a both observed that no cause was found for the fetal
bradycardia.
Mrs 1b stated: “In summary the traces are abnormal in parts but nothing to suggest a
bradycardia. The only intervention was a venflon sited prior to (the) bradycardia”.
Page 77 of 96
Dr 1, in his statement to the police, was asked to comment on Mother R’s midwifery
notes. He concluded: “This (is) an unexpected, unprovoked, unexplained bradycardia
leading to emergency caesarean section with a baby with a very abnormal cord PH. The
CTG prior to the event was reassuring. In this particular case there appears to be at
least eight minutes of an apparently hypertonic event although this was not specifically
mentioned in the notes.”
In his supplementary report Dr 1 elaborated upon this conclusion. He notes the potential
risk factor of sepsis, as the mother experienced spontaneous rupture of membranes
over 24 hours before delivery and thereby being a route of infection to reach the unborn
baby, but points out that the infection could not have caused the acute bradycardia
event. During the Caesarean section there was no explanation, evident, for the acute
bradycardia.
The panel also had regard to Mrs Stewart’s written response. She stated: “Deceleration
already happening prior to venflon. Mother pyrexic and tachcardic. Had been in pool
difficult to know how long FH had been dropping.”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 23:27 hours and resulted in a significant drop in the fetal heart rate to 75
bpm initially and then dropped to 60 bpm shortly thereafter. This occurred two minutes
after a venflon was sited by Mrs Stewart. The CTG trace, as analysed by the NMC
witnesses, was reassuring prior to this event.
Syntocinon was not recorded as being prescribed or administered in the case of Mother
R. The siting of the venflon by Mrs Stewart, however, presented an opportunity to
administer a bolus dose of an oxytocic drug and fit the established pattern which has
already been found by the panel. No other explanations for the fetal bradycardia was
discovered at the subsequent Caesarean section and the NMC witnesses all confirmed
that this bradycardia was unexplained.
Page 78 of 96
The panel bore in mind the rarity of unexplained fetal bradycardias, the pattern of cases
which have occurred whilst Mrs Stewart was in care of a patient, the accessibility of
oxytocic drugs on the Ward and the record of care documented by Mrs Stewart in
relation to Mother R.
Mrs Stewart had an opportunity to administer a bolus dose of an oxytocic drug, via the
venflon sited two minutes before the fetal bradycardia, and the panel concluded that it
was more likely than not that she did do so in light of the circumstances of Mother R’s
labour. This administration of a bolus dose was also, in the panel’s view, a direct cause
of the fetal bradycardia suffered by the fetus of Mother R.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother R.
Schedule 1
S.
Mother S, date of delivery 11 March 2010
Mother S:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother S and the CTG tracings of Mother S. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother S as part of the police
investigation. She commented that Mother S was transferred to the Ward at 14:45 hours
on 11 March 2010 for induction of labour. Mrs Stewart assumed responsibility for her
care. Dr 3 identifies that Mrs Stewart sited a venflon, performed a vaginal examination
and an ARM between 15:25 and 15:42 hours.
Dr 3 stated: “At 15:40 hours there was a profound fetal bradycardia that failed to
recover. She [Mother S] was delivered by caesarean section of a live male infant in
extremely poor condition and with very abnormal cord PH’s.
Page 79 of 96
“Again there was thick meconium recorded at section but (this) was likely a result of the
(fetal) bradycardias, rather than the cause. No cause was found for the (fetal)
bradycardia. In fact the surgeon, [Dr 2], has specifically noted there was no clot or
nuchal cord found”.
Dr 3 stated “no clot indicates t me that the placenta had not separated prior to birth, and
no nuchal cord refers to the cord not being aound the neck. These two factors, if
present, may have been a reason for the fetal bradycardia but they were not present”.
“The CTG prior to the (fetal) bradycardia was normal. Once again it is very difficult to
find a logical explanation for these events but one explanation could be a bolus (dose)
of a uterotonic agent when the venflon was sited.”
Professor 1, Miss 1a and Mrs 1b also reviewed the midwifery notes of Mother S.
Professor 1 agreed with Dr 3 in that she says that the meconium was more likely to be a
symptom of the fetal bradycardia rather than a cause. She also notes the evidence of a
sustained and prolonged contraction at the time and states, “In my experience this does
not occur in normal natural labour or using our induction regime.”
Mrs 1b stated, “In summary this is an unexplained bradycardia although meconium
(was) found on delivery. There was no sign of abruption and tracings appear normal to
the point of bradycardia.”
Dr 1, in his statement to the police, was asked to comment on Mother S’s midwifery
notes. He concluded: “This case has an unexplained acute fetal bradycardia with no
clear causative factor. This event was unexpected given the entirety of the clinical
picture and the baby was profoundly compromised at birth.”
In his supplementary report Dr 1 elaborated upon this conclusion. He specifically notes
that placental abruption or cord problems are excluded by the operating surgeon at
Caesarean. He states that CTG is entirely reassuring prior to the fetal bradycardia
although he notes that the tocograph is of poor quality. In his conclusion, “The
bradycardia could not be physiological and is unexplained.”
Page 80 of 96
The panel also had regard to Mrs Stewart’s written response. She stated: Thick
Meconium. If bolus given it took 17 minutes for FH to react, surely reaction time would
have been sooner.”
The panel considered that there was a prolonged and profound fetal bradycardia which
occurred at 15:40 hours and resulted in a significant drop in the fetal heart rate to 70
bpm for four minutes. This occurred shortly after a venflon was sited by Mrs Stewart
although the precise time is unknown as the relevant entry is untimed. The CTG trace,
as analysed by the NMC witnesses, was reassuring prior to this event.
Syntocinon was not recorded as being prescribed or administered in the case of Mother
S. The siting of the venflon by Mrs Stewart, however, presented an opportunity to
administer a bolus dose of an oxytocic drug and fit the established pattern which has
already been found by the panel. No other explanations for the fetal bradycardia are
discovered at the Caesarean section which happened and the NMC witnesses all affirm
that this bradycardia is unexplained. The panel also noted that the CTG indicates that
there was a hypertonic uterine contraction which is consistent with a bolus dose of an
oxytocic drug being administered.
The panel bore in mind the rarity of unexplained fetal bradycardias, the pattern of cases
which have occurred whilst Mrs Stewart was in care of a patient, the accessibility of
oxytocic drugs on the Ward and the record of care documented by Mrs Stewart in
relation to Mother S.
Mrs Stewart had an opportunity to administer a bolus dose of an oxytocic drug, via the
venflon sited shortly before the fetal bradycardia, and the panel concluded that it was
more likely than not that she did do so in light of the circumstances of Mother S’s labour.
This administration of a bolus dose was also, in the panel’s view, a direct cause of the
fetal bradycardia suffered by the fetus of Mother S.
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother S.
Page 81 of 96
Schedule 1
T.
Mother T, date of delivery 13 March 2010
Mother T:
The panel had regard to the oral and written evidence of Dr 3, Professor 1, Dr 1, Mrs 1b
and Miss 1a. It also considered the midwifery progress notes completed by Mrs Stewart
with respect to Mother T and the CTG tracings of Mother T. The panel also noted the
response of Mrs Stewart concerning this case.
Dr 3 commented on the midwifery progress notes of Mother T as part of the police
investigation. She commented that Mother T was transferred to the Ward at 04:45 hours
for the induction of labour at term plus fifteen (days) and her care was taken over by
Mrs Stewart. Dr 3 states:
“At 00:55 hours, she had a venflon sited and Syntocinon was commenced at 01:30
hours and (the) CTG was normal at this point. Syntocinon was escalated and [Midwife
14] took over for a break at 03:05 hours. At 03:39 hours, there was a deceleration on
the CTG lasting three minutes. This would be termed a short (fetal) bradycardia.
“At 03:50 hour, Kirsteen made a note that she answered the buzzer on her return from
(her) break and the fetal heart was down to sixty beats per minute. It recovered and the
CTG was normal until 04:00 hours. At 04:03 hours Kirsteen re-commenced the
Syntocinon.
“At 04:07 hours, there was a profound and unrecovering fetal bradycardia. She [Mother
T] had a live female infant by (caesarean) section who very abnormal cord PH’s but
appeared to be in good condition. No cause was identified for the fetal bradycardia at
section.
“Due to the previous short episode of (fetal) bradycardia it is more difficult to be certain
regarding the likely cause of the second (fetal) bradycardia. I (it) could however have
Page 82 of 96
been explained by a bolus (dose) (dose) of Syntocinon or other similar agent when
given the Syntocinon was re-commenced at 04:03 hours.”
Professor 1, Miss 1a, and Mrs 1b also reviewed the midwifery notes of Mother T.
Professor 1 concluded from her own review of the notes that “…there does not appear
to be any clinical explanation for the fetal bradycardia.”
Miss 1a agrees that there is no obvious cause of the fetal bradycardia and Mrs 1b
identifies that the CTG tracing is normal up to the first and second bradycardias. Her
conclusion is that this is an “unexplained bradycardia.”
Dr 1, in his statement to the police, was asked to comment on Mother T’s midwifery
notes. He concluded: “This is a case of sustained unprovoked (ie no appropriate
medical intervention or pathological event) unexplained fetal bradycardia. The CTG
pattern is highly suspicious because of the lack of subsequent pathology.”
In his supplementary report Dr 1 elaborated upon this conclusion. He places emphasis
on the second bradycardic event (Mrs Stewart was not present during the first), stating
that it is “of critical importance the Syntocinon was commenced at 4mls per hour by KS
and 4 minutes later there was an acute fetal bradycardia.”
He concludes that “…the profound fetal bradycardic terminal event leading to the GA
[general anaesthetic] caesarean section is unexplained by any pathology other than
hyperstimulation. This might have been due to the commencement of Syntocinon at a
higher dose in a fetus already stressed but the length of the sustained bradycardia and
the degree of fetal acidosis here (by cord PH) is highly unusual.”
The panel also had regard to Mrs Stewart’s written response. She stated: “Not present
when CTG became suspicious and FH dropped. From notes I made at time [Dr 15] was
still in room when synto restarted.”
The panel considered that there were two significant events. The first episode is what
Dr 3 termed a short fetal bradycardia at 03:39 hours. This resulted in the fetal heart rate
Page 83 of 96
dropping to 60bpm for a period of three minutes with good recovery. The second fetal
bradycardia was prolonged and profound. It started at 04:07 hours and the fetal heart
rate dropped to 60 – 70 bpm.
With respect to the first incident the panel noted that Mrs Stewart was out of the room
when this occurred as she answered the emergency buzzer. In the panel’s view,
therefore, it was unlikely that she would have had an opportunity to administer a bolus
dose of an oxytocic drug.
With respect to the second bradycardia, however, the panel considered that there was
either an extreme reaction to the 4mls per hour of Syntocinon which Mrs Stewart
administered or another cause. While Dr 1 conceded that it was possible this dose
could cause the bradycardia, in light of a fetus already recently stressed due to the
earlier bradycardia. He concluded the second fetal bradycardia was unexplained by any
pathology other than hyperstimulation.
The panel considered that there was clearly an opportunity for Mrs Stewart to
administer a bolus dose of Syntocinon as the IV had already been set up and was
established. The other explanations for the second fetal bradycardia are convincingly
refuted by the NMC witnesses. The panel also considered that the decision by the
doctor to make a clinical decision to restart Syntocinon indicated that the fetus was
coping well prior to the second bradycardia.
The panel bore in mind the rarity of unexplained fetal bradycardias, the pattern of cases
which have occurred whilst Mrs Stewart was caring for the patient, the accessibility of
oxytocic drugs on the Ward and the record of care documented by Mrs Stewart in
relation to Mother T.
Mrs Stewart had an opportunity to administer a bolus dose of Syntocinon, via the IV
cannula, shortly before the fetal bradycardia, and the panel concluded that it was more
likely than not that she did do so in light of the circumstances of Mother T’s labour. This
administration of a bolus dose was also, in the panel’s view, a direct cause of the fetal
bradycardia suffered by the fetus of Mother T.
Page 84 of 96
The panel accordingly concluded that the NMC had discharged its burden of proof and
found Charges 1 and 2 proved in relation to Mother T.
Determination on impaired fitness to practise
Having announced the facts the panel has now considered whether on the basis of the
facts found proved, Mrs Stewart’s fitness to practise is currently impaired. This is a two
stage process. The panel must first determine if Mrs Stewart’s actions amounted to
misconduct. If misconduct is found, the panel must consider whether that misconduct
amounts to current impairment of her fitness to practise.
When coming to its decision the panel has taken into account the facts found proved. It
has taken account of all the evidence before it and Mr Collis’ submissions on behalf of
the NMC. The panel has accepted the legal assessor’s advice.
Mr Collis submitted that the panel must exercise its own professional judgement as
there is no standard or burden of proof that is applied at this stage in the process. He
directed the panel to the case of Roylance v GMC (no. 2) [2000] 1 AC 311 which
defines misconduct as ‘a word of general effect, involving some act or omission which
falls short of what would be proper in the circumstances. The standard of propriety may
often be found by reference to the rules and standards ordinarily required to be followed
by a medical practitioner in the particular circumstances.’
In relation to the relevant standards Mr Collis referred the panel to The NMC code of
professional conduct: standards for conduct, performance and ethics (the 2004 code);
the code: Standards of conduct, performance and ethics for nurses and midwives 2008
(the 2008 code) and the Midwives rules and standards (2004), which were in force at
the relevant times. He highlighted a number of standards which were, in the NMC’s
view, breached. He submitted that the charges found relate to 15 separate incidents
over a 28 month period and that it was clear the fetuses would have been put at risk of
harm. He emphasised that a number of the mothers involved underwent Caesarean
sections as a result of Mrs Stewart’s actions, which they may not have otherwise
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needed. Mr Collis submitted that Mrs Stewart acting in such a manner, for what
appeared to be her own purposes, must amount to misconduct.
In relation to current impairment Mr Collis referred the panel to the remarks made in the
case of CHRE v The Nursing and Midwifery Council and Grant, [2011] EWHC 927
(Admin), including the fundamental public interest that must be taken into account at
this stage. He submitted that the mothers and babies were put at unwarranted risk of
harm and that Mrs Stewart prioritised her own interests over those in her care thereby
breaching fundamental tenets of the profession and bringing the profession into
disrepute. He invited the panel to consider any insight and remorse that may have been
demonstrated and highlighted Mrs Stewart’s steadfast denials over a six year period. He
invited the panel to find nature and significance of the charges is such that public
confidence would be undermined if a finding of impairment were not made.
The panel heard and accepted the advice of the legal assessor. In relation to
misconduct he referred the panel to the case of Roylance and also to the case of Mallon
v GMC [2007] CSIH 17 and Nandi v GMC [2004] EWHC 2317 (Admin). He advised that
it was a matter for the panel whether Mrs Stewart’s actions in relation to the charges
that have been found proved, amounted to misconduct.
In relation to impairment, the legal assessor made reference to the cases of Cheatle vs
GMC [2009] EWHC 645 Admin and of Yeong v GMC [2009] EWHC 1923 (Admin). He
made further reference to the remarks made in the case of Grant. He emphasised that
the public interest which must be taken into account included public protection and the
wider public interest: the need to maintain proper professional standards and whether in
the particular circumstances of this case, public confidence in the profession and in the
NMC as a regulatory body would be undermined if a finding of impairment were not
made.
Decision on whether the facts found proved amount to misconduct:
When determining whether the facts found proved amount to misconduct the panel was
satisfied that Mrs Stewart was in breach of the following standards;
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The 2004 code (which applied to Mothers B and C):
As a registered nurse, midwife or specialist community public health nurse, you
are personally accountable for your practice. In caring for patients and clients,
you must:
•
respect the patient or client as an individual
•
obtain consent before you give any treatment or care
•
act to identify and minimise risk to patients and clients.
1.2 As a registered nurse, midwife or specialist community public health nurse, you
must:
•
protect and support the health of individual patients and clients
•
protect and support the health of the wider community
•
act in such a way that justifies the trust and confidence the public have in
you
•
uphold and enhance the good reputation of the professions.
1.4 You have a duty of care to your patients and clients, who are entitled to receive safe
and competent care
2.1 You must recognise and respect the role of patients and clients as partners in their
care and the contribution they can make to it. This involves identifying their preferences
regarding care and respecting these within the limits of professional practice, existing
legislation, resources and the goals of the therapeutic relationship.
7.1 You must behave in a way that upholds the reputation of the professions. Behaviour
that compromises this reputation may call your registration into question even if is not
directly connected to your professional practice.
The 2008 code (which applied to the remaining 13 mothers):
The people in your care must be able to trust you with their health and wellbeing
To justify that trust, you must:
• make the care of people your first concern, treating them as individuals and
respecting their dignity
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• work with others to protect and promote the health and wellbeing of those in
your care, their families and carers, and the wider community
• provide a high standard of practice and care at all times
• be open and honest, act with integrity and uphold the reputation of your
profession.
As a professional, you are personally accountable for actions and omissions in your
practice, and must always be able to justify your decisions.
13 You must ensure that you gain consent before you begin any treatment or
care.
15 You must uphold people’s rights to be fully involved in decisions about their
care.
21 You must keep your colleagues informed when you are sharing the care of
others.
22 You must work with colleagues to monitor the quality of your work and
maintain the safety of those in your care.
35 You must deliver care based on the best available evidence or best practice.
42 You must keep clear and accurate records of the discussions you have, the
assessments you make, the treatment and medicines you give, and how effective
these have been.
61 You must uphold the reputation of your profession at all times.
Midwives rules and standards (which applied to all the mothers):
Rule 6
1. A practising midwife is responsible for providing midwifery care, in accordance
with such standards as the council may specify from time to time, to a woman
and baby during the antenatal, intranatal and postnatal periods.
2. Except in an emergency, a practising midwife shall not provide any care, or
undertake any treatment, which she has not been trained to give.
Rule 7
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A practising midwife shall only supply and administer those medicines, including
analgesics, in respect of which she has received the appropriate training as to use,
dosage and methods of administration.
Rule 9
1. A practising midwife shall keep, as contemporaneously as is reasonable,
continuous and detailed records of observations made, care given and medicine
and any form of pain relief administered by her to a woman or baby.
The panel reflected on its finding of fact. In each case the fetal heart rate was severely
compromised and there were no other explanations other than Mrs Stewart, an
experienced and competent midwife, administering a bolus dose of an oxytocic drug.
The mothers were in a vulnerable position and had placed their trust in Mrs Stewart as
their midwife. She did not provide safe care but administered an unnecessary bolus
dose of an oxytocic drug, without the mothers’ consent and knowledge. The panel found
it plausible that she did so to speed up the labour process for her own purposes.
It was clear to the panel that at the point at which she administered the bolus of oxytocic
drug, she did not make the Mother and their unborn babies her first concern. The panel
was satisfied from the evidence available that she performed a deliberate act which
increased the risk of serious harm to the mothers and their unborn babies, the
consequences of which could have been life-threatening. Through her actions she
created an emergency situation which affected the whole running of the Ward. The
mothers involved required intervention by the multi-disciplinary team, who were involved
in other tasks. This would have had a direct effect on the care of other service users in
the Ward and the Maternity Hospital.
Furthermore, the panel was concerned at Mrs Stewart’s record keeping which was of an
inconsistent standard. At times her records appeared substandard in relation to
contemporaneousness of record keeping of events, the timings of insertion of venflons
and in not recording administration of bolus doses of oxytocic drugs which the panel has
found she must have administered.
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Given the seriousness of facts found proved in relation to misconduct, the panel
considers that Mrs Stewart’s conduct is a very serious departure from the standards
expected of a Registered Midwife and as such she did not uphold the reputation of the
profession at the relevant times. The panel has found that she demonstrated reckless
behaviour at times, which other Registered Midwives would find deplorable, and she
has brought the profession into disrepute.
Therefore for all of the above reasons the panel determined that the facts found proved
do amount to misconduct.
Decision on impairment:
Having found misconduct, the panel had to decide whether Mrs Stewart’s fitness to
practise is currently impaired. The NMC defines fitness to practise as a registrant’s
suitability to remain on the register unrestricted, and in this regard the panel took into
account the following;
The panel had in mind the remarks in the case of Grant in relation to the appropriate
guidance identified by Dame Janet Smith in the Fifth Shipman report:
“Do our findings of fact in respect of the doctor's misconduct, deficient
professional performance, adverse health, conviction, caution or
determination show that his/her fitness to practise is impaired in the sense
that s/he:
a. has in the past acted and/or is liable in the future to act so as to put
a patient or patients at unwarranted risk of harm; and/or
b. has in the past brought and/or is liable in the future to bring the
medical profession into disrepute; and/or
c. has in the past breached and/or is liable in the future to breach one
of the fundamental tenets of the medical profession; and/or
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d. has in the past acted dishonestly and/or is liable to act dishonestly
in the future”
The panel was satisfied that limbs a, b and c were engaged in this case.
The panel summarises the recurring pattern following Mrs Stewart’s care as: a low risk
pregnancy requiring induction in which Mrs Stewart is providing care to the mother on
her own; a venflon is sited; there is a prolonged fetal bradycardia; and an emergency
situation ensues. The panel has found that Mrs Stewart inappropriately administered a
bolus of a powerful oxytocic drug to mothers, causing a sustained tonic contraction of
the uterus which caused the fetal heart rate to decrease due to reduced oxygen supply
via the umbilical cord. The panel was satisfied that this prolonged unexplained
bradycardia was indicative of actual harm to the fetuses. The panel consider that the
emergency interventions must have caused considerable psychological stress and fear
to the mothers. In a majority of cases the mothers underwent major and potentially
unnecessary surgery under general anaesthetic. The panel was very concerned about
the incidents which increased in frequency over time. In November 2009 there were four
incidents, two of which occurred on the same day, and in March 2010 there were three
incidents within one week.
The panel has considered the evidence before it and notes that at no time has Mrs
Stewart expressed consideration for the distress that the mothers must have been
caused. The panel was satisfied that her actions were deliberate and determined that
she therefore breached fundamental tenets of the profession and brought the profession
into disrepute.
The panel next considered any insight or remorse that may have been forthcoming. Mrs
Stewart has continued to maintain her denials and the panel has no evidence of insight
into the facts now found proved. The panel was satisfied that Mrs Stewart must have
known that there was a recurring pattern for those under her care and she has not
provided evidence to suggest that she took steps to address this by raising concerns
with her supervisor of midwives or other colleagues and only said it was “bad luck”
when questions during NHS Grampian’s investigation. The panel considered that this
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was demonstrative of a deep seated attitudinal behaviour. It formed the view that there
is a high risk of repetition if Mrs Stewart’s practice were not to be restricted.
The panel also formed the view that other Registered Midwives and members of the
public would be appalled by Mrs Stewart’s actions.
The panel has therefore determined that Mrs Stewart’s fitness to practise is currently
impaired by reason of her misconduct. To find otherwise would not protect patients and
would undermine public confidence in the profession and in the NMC as a regulatory
body.
Determination on sanction:
Having determined that Mrs Stewart’s fitness to practise is impaired, the panel has now
considered what sanction, if any, it should impose. The panel can dispose of the case
by taking no action, imposing a caution order for one to five years, a conditions of
practice order for no more than three years, a suspension order for a maximum of one
year or a striking-off order. In reaching its decision, the panel has considered all the
evidence that has been placed before it. It has accepted the advice of the legal
assessor.
Mr Collis submitted that the appropriate sanction was a matter for the panel and
referred the panel to the Indicative Sanctions Guidance (ISG).
The legal assessor advised the panel to take account of the ISG and to employ the
principles of proportionality, weighing the interests of patients and the public with Mrs
Stewart’s own interests. He also referred the panel to the case of Dr S v GMC [2007]
EWHC 3257 (Admin) in relation to sanction considerations where a risk of repetition has
been identified.
The panel has considered the least restrictive sanctions first, before moving on to
consider more restrictive sanctions. It has borne in mind that the purpose of a sanction
is not to be punitive, though it may have a punitive effect. The panel has had regard to
both the public interest and Mrs Stewart’s own interest and has considered whether
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there are any mitigating and aggravating factors in this case. The panel has borne in
mind that the public interest includes the protection of patients, the maintenance of
public confidence in the profession and declaring and upholding proper standards of
conduct and behaviour.
[PRIVATE]
The panel determined that the aggravating factors are:
•
Very serious departure from the expected professional behaviour of a Registered
Midwife
•
Repeated behaviour over a long period
•
15 mothers and their unborn babies were subjected to unsafe care
•
An increasing frequency of incidents
•
No remorse or apology has been offered to the service users involved
•
Actual harm to the unborn babies who experienced a slowing of their heart rates
and actual harm to the mothers, whether psychological or physical because of
enduring emergency situations, most going on to have emergency surgery
•
Repeated lack of insight into pain, distress and anxiety for the mothers and their
families
•
Increased pressures on the function of the Ward and the Maternity Hospital staff
during the emergency events, which may not have been necessary
•
Although Mrs Stewart in her written response asserts that she discussed her
practice with her mentor in the period 2009 -2010, she has provided no evidence
of the content of this discussion. Nor has she provided any evidence that she
raised concerns relating to her practice with her supervisor of midwives or other
colleagues to address any concerns
•
No acceptance of any responsibility for what occurred
•
Mrs Stewart has portrayed herself as a victim in her written responses
•
Poor and inconsistent record keeping at the relevant times
The panel determined that the mitigating factors are:
•
Some engagement with this process
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Mrs Stewart has not provided the panel with any references or testimonials regarding
her practice or her current circumstances.
The panel noted that the Ward and the Hospital had inconsistent practices of auditing
some drugs and untoward or serious incidents during the time in question. The pattern
of Mrs Stewart’s behaviour may have been identified earlier.
The panel first considered whether to take no action but concluded that this would be
inappropriate in view of the seriousness of Mrs Stewart’s actions as reflected in the
panel’s findings of fact and impairment. The panel decided that to take no action would
not take into account the need to protect the public nor would it take into account the
need to uphold confidence in the profession and to maintain the standards expected of
a Registered Midwife.
Next, in considering whether a caution order would be appropriate, the panel took into
account that a caution order does not restrict a nurse or midwife’s ability to practise. The
panel, having made a finding at the impairment stage that Mrs Stewart’s practice ought
to be restricted to ensure there is no repetition of her behaviour, was satisfied that for
the same reasons as given above a caution order is neither appropriate nor
proportionate.
The panel next considered a conditions of practice order. Mrs Stewart was described as
an experienced and competent midwife and, in the panel’s view, the incidents appeared
to be deliberate acts. It therefore determined that conditions of practice could not be
formulated which could address such conduct. The panel was satisfied that a conditions
of practice order would not be sufficient to protect patients and the public. In any event
the panel considered that such a sanction would not be proportionate in the public
interest given the very serious nature of the facts found proved.
The panel next considered a suspension order. The panel considered that this case was
a serious departure from what is expected of a Registered Midwife. This was not a
single incident of misconduct. The conduct occurred over a protracted time and involved
15 mothers and their unborn babies. The panel has identified evidence of a harmful
deep seated attitudinal behaviour. Mrs Stewart has not provided the panel with any
evidence of insight nor has she demonstrated any active steps she took, at the time, to
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minimise the risk to service users under her care. Mrs Stewart has accepted no
responsibly for the serious situations faced by the mothers nor has she shown any
remorse. The panel therefore formed the view that there would be a continued risk to
patient safety if she were allowed to practice. It therefore determined that temporary
removal from the register would not be appropriate or proportionate.
The panel therefore concluded that the seriousness of this case is incompatible with
ongoing registration. A Registered Midwife is in a special position of trust in the eyes of
the public and the panel has found that Mrs Stewart abused that trust. Mrs Stewart did
not provide safe care, in-labour mothers are particularly vulnerable as are their unborn
babies. The panel reflected on the aggravating factor it has identified in relation to
patient harm above. The panel regarded Mrs Stewart’s breach of trust to be equally
relevant to practising as a registered nurse as well as a registered midwife.
The panel concluded that striking-off is the only sanction which is sufficient to protect
the public interest and to maintain the standards expected of a Registered Midwife. It
determined that public confidence in the profession and the NMC will only be sustained
if Mrs Stewart is removed from the register.
The striking-off order results in the removal of Mrs Stewart’s name from the register,
thus preventing her from working as a Registered Midwife or as a Registered Nurse.
She may not apply for restoration until a period of five years has elapsed since the
striking-off order was made. An application for restoration will not be granted unless a
panel is satisfied that Mrs Stewart meets the requirements for admission to the register
and in addition, is a fit and proper person to practise as a nurse or midwife.
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Decision on Interim Order and reasons:
The striking-off order will not take effect until the end of the appeal period (28 days after
the date on which the decision letter is served) or, if an appeal has been lodged, before
the appeal has concluded.
The panel therefore considered the submissions made by Mr Collis that an interim
suspension order should be made to cover the appeal period.
The panel accepted the advice of the legal assessor and took account of the guidance
issued to panels by the NMC when considering interim orders and the appropriate test
as set out at Article 31 of The Nursing and Midwifery Order 2001. It may only make an
interim order if it is satisfied that it is necessary for the protection of the public, is
otherwise in the public interest or in Mrs Stewart’s own interest.
The panel is satisfied that an interim order is necessary for the protection of the public
and in the public interest to uphold the reputation of the profession. The panel has had
regard to the seriousness of this case as detailed in the reasons set out in its decision
for the substantive order. The panel has identified a risk of repetition and determined
that Mrs Stewart’s practice must be restricted by removal from the register. The panel
has therefore decided to impose an interim suspension order. To do otherwise would be
incompatible with its earlier findings.
The period of this order is for 18 months to allow for the possibility of an appeal to be
made and determined.
If no appeal is made then the interim suspension order will be replaced by the strikingoff order 28 days after Mrs Stewart is sent the decision of this hearing in writing.
That concludes this hearing.
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