Medical Board of Queensland v Broadbent
[2010] QCAT 280
•10 June 2010
QUEENSLAND CIVIL AND ADMINISTRATIVE TRIBUNAL
CITATION:
Medical Board of Queensland v Broadbent [2010] QCAT 280
PARTIES:
Medical Board of Queensland
(Applicant)v
Michael Russell Mark Broadbent
(Registrant)FILE NO/S:
2962 of 2007, 976 of 2008 and 1189 of 2008
PROCEEDING:
Disciplinary Hearing
DELIVERED ON:
10 June 2010
DELIVERED AT:
Southport
HEARING DATES:
27 Aug, 7 – 11, 15 – 18 Sep and 23 Nov 2009 (Health Practitioners Tribunal) and 24 – 26 Feb, 1 – 5 Mar and 11 Mar 2010 (Queensland Civil and Administrative Tribunal)
JUDGE:
Judge C.F. Wall Q.C. assisted by Dr P Richardson, Dr G Powell and Ms G Bolland
ORDER:
Unsatisfactory professional conduct established
CATCHWORDS:
HEALTH PRACTITIONERS (PROFESSIONAL STANDARDS) ACT – DISCIPLINARY PROCEEDINGS – Unsatisfactory professional conduct – biliary pancreatic diversion (BPD) by-pass surgery – whether pre-operative nutritional advice to patient was sufficient – whether registrant should have involved a dietician – post-operative management and treatment of patient – whether registrant arranged appropriate cover and pain management co-ordination for patient during registrant’s absence interstate – whether anastomotic leak recognised – whether appropriate to perform gastrointestinal endoscopy – whether registrant’s management of patient contributed to patient’s death.
LEGISLATION:
Health Practitioners (Professional Standards) Act 1999 Section 124(1)(a)
CASES:
Coleman v Kinbacher (2003) QCA 575
Fletcher v Queensland Nursing Council [2009] QCA 364
Briginshaw v Briginshaw (1938) 60 CLR 336
Besser v Medical Board of Victoria (1981) VR 953COUNSEL:
Applicant: Mrs K McMillan SC and Mrs J Farr
Registrant: Mr P Hackett
SOLICITORS:
Applicant: Sparke Helmore (2009), then Moray and Agnew
Registrant: O'Keefe Mahoney Bennett
NATURE OF PROCEEDINGS
There are disciplinary proceedings against Dr Michael Russell Mark Broadbent, a retired medical practitioner and general surgeon relating to his pre-retirement treatment of two patients, Mrs Ursula MacLeod and Mrs Margaret Pearce.
It is alleged by the Medical Board of Queensland (MBQ) that in the case of each patient and in a number of respects Dr Broadbent behaved in a way that constitutes unsatisfactory professional conduct (s 124(1)(a)) Health Practitioners (Professional Standards Act 1999 (the Act).
The Act defines “unsatisfactory professional conduct” as including
(a) professional conduct that is of a lesser standard than that which might reasonably be expected of the registrant by the public or the registrant’s professional peers
(b) professional conduct that demonstrates incompetence or a lack of adequate knowledge, skill, judgment or care, in the practise of the registrant’s profession, and
(f) providing a person with health services of a kind that are excessive, unnecessary or not reasonably required for the person’s wellbeing.
Mr Hackett, counsel for Dr Broadbent agreed that it is not necessary that all of the factual allegations against Dr Broadbent be established before an adverse finding could be made against Dr Broadbent. See Coleman v Kinbacher (2003) QCA 575 at para [14] and Fletcher v Queensland Nursing Council [2009] QCA 364 at para [74]-[76].
The onus of proof is on MBQ and the standard of proof required is in accordance with Briginshaw v Briginshaw (1938) 60 CLR 336 at 361-362. See also Besser v Medical Board of Victoria (1981) VR 953 at 967.
REFERRAL NOTICES
As amended before and during the hearing the Referral Notice in relation to Mrs Ursula MacLeod (ex 1 dated 10 November 2008) is in the following terms:
Grounds for Disciplinary Action:
Pursuant to section 124(1)(a) of the Act, the Registrant has behaved in a way that constitutes unsatisfactory professional conduct in that the Registrant has engaged in:
· Professional conduct that is of a lesser standard than that which might reasonably be expected of the Registrant by the public or the Registrant’s professional peers; and
· Professional conduct that demonstrates incompetence, or lack of adequate knowledge, skill, judgment or care, in the practise of the registrant’s profession.
Facts and circumstances forming the basis for the grounds
Background
(a) On 16 June 2003 Mrs Ursula MacLeod underwent a biliary pancreatic diversion bypass procedure, performed by Dr Broadbent, at the Allamanda Private Hospital (“the Hospital”). Mrs MacLeod was discharged from the Hospital on 26 June 2003.
(b) Mrs MacLeod was readmitted to the Hospital, under the Care of Dr Broadbent, during the following periods:
(1) 28 June 2003 to 30 June 2003 (“the June admission”);
(2) 13 September 2003 to 25 September 2003 “the September admission”);
(3) 2 October 2003 to 15 October 2003 (“the October admission”).
(c) Mrs MacLeod died at 1935 hours on 15 October 2003.
Dr Broadbent failed to adequately manage and treat Mrs Ursula MacLeod’s renal function during the period 13 September 2003 to 25 September 2003.2.
2.3 Dr Broadbent;
(a) prescribed in the period 13 – 25 September 2003 Voltaren to Mrs MacLeod;
(b) such medication was inappropriate in light of her renal impairment.
3.Dr Broadbent failed to investigate or cause to be investigated, Mrs Ursula MacLeod’s symptoms of vomiting and diarrhoea.
Particulars
3.1 Mrs MacLeod suffered vomiting (and) diarrhoea during the period 16 June 2003 to 13 October 2003.
3.2 The nature and extent of the diarrhoea suffered by Mrs MacLeod was suggestive of additional pathology.
3.3 During August, September and October 2003, Mrs Macleod suffered frequent diarrhoea despite:
(a) the absence of fat in her diet;
(b) inadequate fluid intake; and
(c) the continued ingestion of codeine;
for which no cause was sought to be identified.
3.4 Dr Broadbent failed to investigate;
(a) in the September and October admissions by any means, the cause of Mrs MacLeod’s unexplained diarrhoea leading up to and during the admissions for example with contrast meal, CT scan, sigmoidoscopy, colonoscopy, or other process.
(b) in the September and October admissions the cause of Mrs MacLeod’s ongoing vomiting when she self-presented to the emergency department at the Allamanda Hospital on 13 September 2003 complaining of a three week history of vomiting.
For the purposes of paragraph 3 the Medical Board of Queensland (MBQ) provided the following particulars (ex 57): Dr Broadbent failed to investigate – that is, take appropriate steps to enquire into the cause or aetiology of or cause appropriate steps to be taken to enquire into the cause or aetiology of Mrs Ursula MacLeod’s symptoms of vomiting and diarrhoea.
4.Dr Broadbent failed to provide or prescribe appropriate and adequate nutritional advice, management and treatment.
Particulars
4.1The advice provided by Dr Broadbent with respect to the meal size following biliary pancreatic diversion surgery was inappropriate, as follows:
(a) The pre-operative consent form utilised by Dr Broadbent stipulated for consumption of no more than 3 meals per day at a size of 50mls during the “weight loss phase”;
(b) The food consumption/meal size recommended in the consent form by Dr Broadbent was insufficient to provide for adequate nutrition.
4.2Dr Broadbent failed to ensure that Mrs MacLeod was provided with adequate nutrition during the June admission, as follows:
(a) Mrs MacLeod consumed only simple carbohydrates and fluids during the period of hospitalisation;
(b) Mrs MacLeod’s consumption of protein, during the period 28 June 2003 to 30 June 2003, was:
(1) negligible; and
(2) insufficient for someone recovering from major surgery.
4.3Dr Broadbent failed to ensure that Mrs MacLeod was provided with adequate nutrition during the September admission, as follows:
(a) During the entirety of the September admission the records reveal that negligible food and or fluid were provided to and/or consumed by Mrs MacLeod;
(b) Mrs MacLeod was not prescribed by Dr Broadbent vitamin, iron or calcium supplements during the September admission;
(c) Mrs MacLeod’s consumption of protein, during the September admission, was inadequate.
4.4Dr Broadbent failed to ensure that Mrs MacLeod was provided with adequate nutrition during the October admission, as follows:
(a) Mrs MacLeod’s oral food intake during the period of hospitalisation was inadequate to sustain long term health;
(b) Dr Broadbent failed to institute an adequate oral feeding regime and/or nasoenteral feeds;
(c) Dr Broadbent failed to institute adequate parenteral nutrition – lipids and fat-soluble vitamins being withheld;
(d) Dr Broadbent failed to assay and replace Mrs MacLeod’s vitamins and minerals.
4.5Dr Broadbent failed to investigate, adequately or at all, Mrs MacLeod’s poor oral food intake and/or her inability to tolerate adequate oral food intake, at any time during the October admission prior to her admission to the Intensive Care Unit on 13 October 2003.
4.6Dr Broadbent failed to monitor (by assaying or ordering and considering an appropriate number of tests) during the period 13 June to 13 October 2003, the following levels for Mrs MacLeod:
(a) Vitamin A;
(b) Vitamin D;
(c) Zinc; and
(d) Parathyroid hormone levels.
4.7Dr Broadbent failed to recognise that by the September admission Mrs MacLeod was malnourished.
4.8Dr Broadbent failed to recognise, during the course of the September and October admissions, that Mrs MacLeod’s malnutrition was a possible cause of her oedema, skin condition and diarrhoea.
5.Dr Broadbent failed to facilitate appropriate cover for Mrs Ursula MacLeod for the period 11 October 2003 to 12 October 2003 whilst he was absent in Sydney.
Particulars
5.1At the material times Mrs MacLeod was admitted under Dr Broadbent’s care.
5.2Dr Broadbent was responsible for the co-ordination of Mrs MacLeod’s health care.
5.3Dr Broadbent:
(a)attended on Mrs MacLeod at 0630 hours on 10 October 2003;
(b)next attended on Mrs MacLeod at 2000 hours on 12 October 2003;
5.4During the period 11 October 2003 to 12 October 2003 Dr Broadbent attended a conference in Sydney.
5.5There is no record in Mrs MacLeod’s medical file, to the effect that Dr Broadbent had arranged to hand over to an appropriately qualified medical practitioner the co-ordination of Mrs MacLeod’s medical care for the period 11 October 2003 to 12 October 2003.
5.6No written directive or order was given to the nursing staff by Dr Broadbent to the effect that he had arranged for another appropriately qualified medical practitioner to co-ordinate Mrs MacLeod’s medical care in his absence.
5.7By virtue of 5.5 to 5.6, no appropriate handover of Mrs MacLeod’s care occurred prior to his absence.
5.8Dr Kay attended on Mrs MacLeod on 11 and 12 October 2003 and Dr Renton attended on Mrs MacLeod on 12 October 2003.
5.9Both doctors attended in a consultative capacity only, neither having been asked to or consented to assume a co-ordinating role in relation to Mrs Macleod’s health care.
5.10Mrs MacLeod’s pathology result of 10 October 2003 indicated the presence of sepsis by revealing a falling platelet count (80), neutrophilia, toxic granulation and presence of band forms.
5.11Dr Broadbent failed to consider Mrs MacLeod’s pathology results and identify in a timely manner the onset of septicaemia, as follows:
(a) full blood tests conducted on 6 October 2003 and 7 October 2003 showed band neutrophils suggestive of sepsis; and
(b) urinalysis of 8 October 2003 showed leukocytes suggestive of sepsis.
5.12By the October admission:
(a) Dr Broadbent was aware, or ought to have been aware, that Mrs MacLeod was immunocompromised and/or susceptible to bacterial and fungal infections.
(b) Mrs MacLeod’s pathology results of 10 October 2003 indicated the presence of sepsis by revealing a falling platelet count (80), neutrophilia, toxic granulation and presence of band forms.
5.13Dr Broadbent failed to undertake any, or any adequate, investigation and treat [sic] with respect to the cause of septicaemia until 12 October 2003.
6.Dr Broadbent failed to co-ordinate Mrs Ursula MacLeod’s pain management during his absence in Sydney.
Particulars
6.1At the material times during the October admission Dr Broadbent was responsible for the co-ordination of Mrs MacLeod’s health care.
6.2Dr Broadbent:
(a)attended on Mrs MacLeod at 0630 hours on 10 October 2003;
(b)next attended on Mrs MacLeod at 2000 hours on 12 October 2003;
6.3Nursing notes during the period 11 October 2003 to 12 October 2003 indicate constant complaints of pain by Mrs MacLeod and requests for analgesia.
6.4Nursing notes of 0700 hours on 11 October 2003 record that Mrs MacLeod wished to speak to a doctor regarding pain relief however there is no record of such an opportunity being afforded to Mrs MacLeod until 2000 hours on 12 October 2003.
6.5Nursing notes of 1545 hours on 12 October 2003 state “… patient requesting analgesia and Dr Broadbent contacted. Not for analgesia until reviewed by Dr Broadbent this evening…”.
6.6Dr Broadbent failed to:
(a)adequately monitor or cause to be monitored, Mrs MacLeod’s deteriorating condition during the period 10 October 2003 to 12 October to ensure that Mrs MacLeod was provided adequate pain relief during the period 10 October 2003 to 12 October 2003;
(b)investigate the causes of Mrs MacLeod’s increasing levels of pain during the period 10 October 2003 to 8.00pm 12 October 2003;
(c)organise or request, following the telephone call of 1545 hours on 12 October 2003, another practitioner to review Mrs MacLeod’s pain management in his absence;
(d)afford Mrs MacLeod the opportunity to discuss with him her condition and the management of her pain.
7.Dr Broadbent failed to arrange referrals when necessary to other specialists to assist in the investigation of Mrs Ursula MacLeod’s deterioration.
Particulars
7.2Dr Broadbent failed to seek an opinion from a gastroenterologist, or another bariatric surgeon, with respect to the cause and treatment of Mrs MacLeod’s diarrhoea, abdominal pain, vomiting and inability to tolerate oral intake.
7.4Dr Broadbent failed to seek advice from a dietician or nutritionist with respect to the adequacy of Mrs MacLeod’s nutritional intake.
As amended before and during the hearing the Referral Notice in relation to Mrs Margaret Pearce (ex 8 dated 10 November 2008) is in the following terms:
Grounds for Disciplinary Action:
Pursuant to section 124(1)(a) of the Act, the Registrant has behaved in a way that constitutes unsatisfactory professional conduct in that the Registrant has engaged in:
· Professional conduct that is of a lesser standard than that which might reasonably be expected of the Registrant by the public or the Registrant’s professional peers; and
· Professional conduct that demonstrates incompetence, or lack of adequate knowledge, skill, judgment or care, in the practise of the registrant’s profession.
· Providing a person with health services of a kind that are excessive, unnecessary or not reasonably required for a person’s wellbeing.
Facts and circumstances forming the basis for the grounds
Background
(a)On 27 March 2000 Mrs Margaret Pearce underwent a biliary pancreatic diversion bypass procedure with sleeve gastrectomy, cholecystectomy and division of adhesions, performed by Dr Broadbent, at the Allamanda Private Hospital (“Allamanda”) (“Mrs Pearce’s first admission”). Mrs Pearce was discharged from hospital on 4 April 2000.
(b)Mrs Pearce was readmitted to Allamanda, under the care of Dr Broadbent, on 10 April 2000 (“Mrs Pearce’s second admission”).
(c)On 17 April 2000, during her second admission, Mrs Pearce underwent an upper gastrointestinal endoscopy, performed by Dr Broadbent.
(d)Mrs Pearce died on 17 April 2000 during the upper gastrointestinal endoscopy.
14.Dr Broadbent failed to diagnose and treat Mrs Pearce’s anastomotic leak.
Particulars
14.1At the material times Dr Broadbent was responsible for the co-ordination of Mrs Pearce’s health care;
14.2During her surgery of 27 March 2000 Mrs Pearce underwent two (2) anatomoses;
14.3 Mrs Pearce’s post-operative symptoms included failure to progress, progressive weight loss, anorexia, nausea, vomiting, abdominal discomfort and a high fever, all symptoms consistent with anastomotic leak;
14.4Dr Broadbent:
(a) did not give, and/or did not document that he gave, any consideration to a diagnosis of anastomotic leak;
(b) failed to undertake, or cause to be undertaken, any investigations to exclude anastomotic leak and/or establish the cause of Mrs Pearce’s symptoms, namely:
(1) Dr Broadbent failed to undertake chest x-rays, abdominal x-rays or CAT scans of the abdomen.
16Dr Broadbent failed to diagnose and treat Mrs Pearce’s sepsis.
Particulars
16.1 At the material times Dr Broadbent was responsible for the co-ordination of Mrs Pearce’s health care.
16.2 During the period 11 April 2000 to 17 April 2000 Mrs Pearce exhibited signs and symptoms indicative of sepsis:
(a)Mrs Pearce:
(1) failed to progress;
(2) continued to lose weight;
(3) suffer intermittent fevers with temperatures ranging up to 39.2°c of a hectic nature that could otherwise not be explained;
(b)a Pathology Report of 15 April 2000 indicated a possible growth of pathogens from a swab taken from Mrs Pearce’s abdominal drain site;
16.3Dr Broadbent:
(a)–
(b)failed to undertake any, or any adequate, investigation to exclude sepsis and/or establish the cause of Mrs Pearce’s symptoms, namely:
(1) Dr Broadbent failed to undertake blood films, sputum cultures, urine cultures, or cultures of aspiration of the subphrenic collection.
(c) failed, despite the presence of factors strongly suggestive of sepsis, to institute any, or any adequate, treatment for sepsis.
19.Dr Broadbent carried out an upper gastrointestinal endoscopy when it was inappropriate to do so.
Particulars
19.1Mrs Pearce was suffering with symptoms consistent with anastomotic leak and/or small bowel perforation and/or intra abdominal abscess formation:
(a) the Registrant’s Board repeats and relies on the matters set out in paragraphs 14.2 and 14.3 herein.
19.2Upper gastrointestinal endoscopy is contraindicated for persons suffering anastomotic leak and/or small bowel perforation and/or intra abdominal abscess formation as it carries with it the risk of further rupture of the bowel and/or the rupture of the abscess into the peritoneal cavity.
20.Dr Broadbent’s management of Mrs Pearce contributed to her death.
Particulars
20.1 The Registrant’s Board repeats and relies on the matters set out at paragraphs 14, 16 and 19 herein.”
EXPERT WITNESSES
On the 28th of July 2009, the Tribunal then constituted by the Chief Judge, made the following order:
“3.The experts of both parties are to confer and prepare joint reports on MacLeod and Pearce, to be provided to the Tribunal on 18 August 2009. The joint reports are to identify:
(a) Each matter on which agreement can be reached;
(b) Each matter on which agreement has not been reached; and
(c) Reasons for the differences between the experts in their approach to each matter on which agreement has not been reached.”
The experts in the case of each patient were:
MacLeod
Assoc. Prof. Simon Woods, General Surgeon, experienced in bariatric surgery – MBQ
Ms Trudy Williams, Dietician – MBQ
Dr Leon Cohen – Physician and General Surgeon – Broadbent
Dr Picard Marceau – General Surgeon – Broadbent
Dr Marceau did not give evidence and references to him have been removed from the joint report, ex 2. Ms Williams did not participate in discussions about the allegations in paragraphs 5 – 7 of the amended Referral Notice “as she felt (those) were not in her area of expertise.”
Pearce
Dr Daryl Wall, General Surgeon – MBQ
Dr Leon Cohen, Physician and General Surgeon – Broadbent
Dr Matthew Carmody – Broadbent
Dr Carmody did not give evidence and references to him have been removed from the joint report, ex 3.
In relation to each of the allegations levelled against Dr Broadbent the experts (and other witnesses) gave evidence about
(a) the standard which might reasonably be expected of Dr Broadbent by his professional peers and whether his professional conduct fell below that standard (i.e. was of a lesser standard);
(b) whether his professional conduct demonstrated incompetence or a lack of adequate knowledge, skill, judgment or care in the practise of his profession; and
(c) in the case of the gastrointestinal endoscopy whether the provision of that procedure (an admitted health service) was excessive, unnecessary or not reasonably required for the wellbeing of the patient.
It was in this objective sense that Mr Hackett conceded, correctly, that if the allegations were “made out factually” it would be established that Dr Broadbent behaved “in a way that constitutes unsatisfactory professional conduct” (T18-71).
JOINT EXPERT WITNESS REPORTS
The joint report for MacLeod (ex 2) is in the following terms (the paragraph numbers are those in the amended Referral Notice):
2.3.1[sic]Dr Woods agrees that the prescription of Voltaren to a patient with acute renal failure was inappropriate. Dr Cohen believed it should be used with caution and noted that it was not cancelled by her renal physician in October. Drs Woods and Cohen concurred that it probably did not materially affect her outcome long term. Ms Williams declined to comment.
3.Dr Cohen was of the opinion that the vomiting did not necessarily require radiological or endoscopic investigation, provided she could tolerate oral fluids. Dr Woods believed she should have had at least a contrast X-Ray to exclude mechanical obstruction in the stomach or at the duodenal anastomosis. Ms Williams declined to comment.
Drs Woods and Cohen concurred that the diarrhoea was more than would be expected 3 months after the surgery. Drs Woods and Cohen agreed it was not reasonable to assume it was related to fat intake, especially during her time in hospital as she was not consuming fat. A faecal culture had been performed and was negative. Dr Woods felt further investigation should have been undertaken. Ms Williams declined to comment.
4.1All agreed that if the dietary advice provided by Dr Broadbent was to consume no more than 3 meals per day of no more than 50 ml during the “weight loss phase”, then adequate nutrition, particularly the provision of protein was impossible. The advice was such that it would inevitably lead to malnutrition if it were adhered to. Furthermore, all agreed that the advice to avoid all animal products was inappropriate and would make provision of adequate nutrition even more difficult.
4.2All agreed that the amount of nutrition provided during her initial admission in June 2003 was low, but reasonable at this point in time, provided there was a plan for it to be increased over the weeks ahead. Dr Woods and Ms Williams would have recommended protein enriched drinks in the early phase, Dr Cohen would not necessarily have done so.
4.3All agreed that the patient was not provided with adequate nutrition during the September admission, in particular she received virtually no protein and there is no documentation that (she) received vitamin supplements, notwithstanding Dr Broadbent’s assertion that she was self medicating with vitamins.
4.4(a)All agreed that Mrs MacLeod failed to receive adequate nutrition during the October admission until TPN was commenced.
4.4(b)All agreed that Dr Broadbent failed to institute an adequate enteral feeding regimen during the October admission. He had been planning to institute parenteral nutrition, but this was delayed by 3 days due to her coagulopathy on the advice of the TPN service.
4.4(c)All agreed that when the patient eventually began parenteral nutrition it was not “total” parenteral nutrition as lipids were withheld, apparently at the direction of Dr Broadbent. This was considered inappropriate. However, all agreed that parenteral or enteral nutrition should have been phased in gradually to avoid refeeding syndrome. Dr Cohen believed that the intravenous feeding regime was the responsibility of the TPN team.
4.4(d)All agreed that Dr Broadbent should have assayed a range of vitamin and minerals prior to her October admission. Any deficiencies should have been treated prior to that time. Appropriate tests were ordered on October 1st.
4.5This has been answered in (3) above.
4.6All agreed that at least Zinc, Vitamin A, Vitamin D and Parathyroid Hormone Levels should have been assayed prior to the October admission. Dr Woods and Ms Williams would have recommended additional tests but there was variation in their testing regimes.
4.7All agreed that the patient was developing malnutrition by the time of the September admission and that Dr Broadbent appeared not to realise this.
4.8All agreed that Mrs MacLeod’s malnutrition was a possible cause of her oedema, skin condition and diarrhoea. However, there may have been other causes for the diarrhoea specifically, including the apparent self administration of a “herbal” remedy said to contain Senna.
5.1All agreed that the patient was under the care of Dr Broadbent on October 11th and 12th 2003.
5.2All agreed that he was responsible for the coordination of her health care.
5.3All agreed that the records showed that he attended Mrs MacLeod on October 10th at 06.30 hours and October 12th at 20.00 hours.
5.4All agreed that it appeared that Dr Broadbent was in Sydney during the time stated.
5.5All agreed that there was no record in the patient’s file to indicate that Dr Broadbent had handed over her medical care during that time. We cannot say with certainty that no such record existed “elsewhere”.
5.6All agreed that there was no apparent written directive to the nursing staff to the effect that he had arranged another medical practitioner to coordinate her care during his absence.
5.7We cannot state with certainty whether a handover did, in fact occur as it may have been verbal or written elsewhere.
5.8All agreed that Dr Kay attended the patient on October 11th and 12th and Dr Renton saw her on October 12th.
5.9We cannot know with certainty whether Drs Kay and Renton had agreed to work in any capacity other than a consulting one. However, all agreed that even so, it would have been appropriate for them to respond to the patient’s condition.
5.10All agreed that the pathology results on October 10th indicated the presence of sepsis.
5.11We believe that the tests in question on October 6th and 7th were ordered by the renal physicians and the responsibility for checking the results and responding to them lay, at least in part, with those doctors. At a minimum they should have alerted Dr Broadbent to the results and liaised re a management plan.
5.11(a)We agreed that the blood tests on October 6th and 7th were indicative of sepsis.
5.11(b)We agree that the presence of leukocytes in the urine on October 8th was suggestive of sepsis.
5.12(a)We agree that by the October admission Dr Broadbent should have been aware that the patient was immunocompromised due to malnutrition. We cannot know whether he was aware.
5.12(b)We agree that the pathology results on October 10th indicated sepsis (as stated above in 5.10).
5.13 We agree that Dr Broadbent failed to undertake adequate investigation and treatment with respect to the cause of septicaemia until October 12th. However, we would like to highlight the fact that she was seen by the renal physicians on October 11th and 12th and question why they took no action as they were physically present whilst Dr Broadbent was not.
6.1 As stated above in 5.5, we cannot know with certainty whether Dr Broadbent had handed over care whilst he was in Sydney, but agree that, from the information available, he appeared to be co-ordinating her health care throughout the October admission.
6.2 We agree with the statement relating to the times that Dr Broadbent attended the patient.
6.3 We agree that the nursing notes indicate constant complaints of pain by Mrs Macleod on October 11th and 12th and that she requested analgesia.
6.4 We agree that there is no record of Mrs MacLeod speaking to a doctor about her pain relief from 07.00 on October 11th until Dr Broadbent saw her at 20.00 hours on October 12th.
6.5 We note the request by Dr Broadbent to withhold analgesia pending his review on October 12th. Whilst this is not something Dr Cohen or Woods would do, they acknowledge that this is an accepted practice by some doctors who are concerned that analgesia may mask the signs of intra-abdominal pathology. Dr Woods noted that it would be more than 4 hours from the request until Dr Broadbent saw the patient, so there was little point in withholding analgesia at the time of the request at 15.45 hours.
6.6(b)We agree that no investigations of her increasing pain were undertaken by either Dr Broadbent or the attending physicians.
6.6(c)We are unsure whether another practitioner was requested to attend his absence as Dr Broadbent maintains that he requested Dr Lee Rutherford did so [sic].
6.6(d)We don’t believe it was practicable for the patient to speak to Dr Broadbent about her pain during the time he was away.
The joint report for Pearce (ex 3) is in the following terms (again the paragraph numbers are those in the amended Referral Notice):
Patient background – Paragraphs (a) to (d)
The expert panel agrees on all matters.
14.Dr Broadbent failed to diagnose and treat Mrs Pearce’s anastomotic leak.
The expert panel is in agreement that Dr Broadbent failed to diagnose or treat Mrs Pearce’s anastomotic leak. There was agreement that the nature of this leak was a contained leak alongside the duodeno-ileal anastomosis in the supracolic compartment and is in keeping with the findings at endoscopy. It is the panel’s agreement that Dr Broadbent failed to undertake the appropriate radiological investigations to exclude the critically important diagnosis of an anastomotic leak or establish the cause of Mrs Pearce’s symptoms.
16.Dr Broadbent failed to diagnose and treat Mrs Pearce’s severe sepsis.
It is the panel’s agreed opinion that Dr Broadbent did make efforts to investigate the patient’s signs and symptoms. It is the panel’s opinion that the term “severe sepsis” (NB: the Referral Notice now refers to “sepsis” and not “severe sepsis”) does not entirely accurately reflect the patient’s state as the hallmarks of this state, hypotension, low urine output and the development of systemic inflammatory response syndrome were not manifested. There is also some evidence based on her observation chart and white cell count, that her septic state was improving by the time of her endoscopy. The panel recognises that Dr Broadbent instituted blood cultures and it appears in the hospital notes that a request for further blood cultures should the temperature rise again be taken. A swab was also taken of the drained fluid from the abdominal drain site. The experts agree that Dr Broadbent did likely give consideration to the possible diagnosis of sepsis. The experts agree that for a comprehensive diagnosis or exclusion thereof, radiological visualisation and exclusion of a leak from the gastro-intestinal tract would be agreed practice.
19.Dr Broadbent carried out an upper endoscopy when it was inappropriate to do so.
It is the expert panel’s opinion that in the absence of a radiological exclusion of a leak from the gastro-intestinal tract, that a non-therapeutic endoscopy was contraindicated. It is therefore in the panel’s opinion inappropriate to have carried out an upper endoscopy.
20.Dr Broadbent’s management of Mrs Pearce contributed to her death.
It is the expert panel’s opinion that the patient died as a complication of her endoscopy. It is the expert panel’s opinion that Dr Broadbent’s recommendation to perform an endoscopy led to the complication resulting in the patient’s death. It is the expert panel’s opinion that this complication is exceedingly rare and it is unlikely to have been foreseen prior to the procedure. The expert panel agrees that this would have been avoidable had an alternative pathway of diagnosis been undertaken.
NATURE OF SURGERY
Each patient underwent biliary (bilio) pancreatic diversion (BPD) by-pass surgery with duodenal switch and a cholecystectomy performed by Dr Broadbent. Essential details of this surgery are described by Dr Cohen in ex 49, LC-5, pg 25. See also ex 51, LC-8, pg 20, ex 54 and ex 64 paras 301-312, 464-469 and 479-493. No complaint is made about how these operations were performed.
This procedure was performed for the treatment of refractory morbid obesity and is different from gastric banding. It was major surgery. It involved reducing the effective size of the stomach as well as by-passing the normal process for digesting food. This was achieved by transforming the stomach essentially into a tube. The size depended on the surgeon’s preference, with the stomach being stapled down its entire length to the lesser curvature using a bougie as the template to guide the suture line. This clearly created a stomach of a very small size with only a volume of 50 ml, limiting the quantity and consistency of food that could be tolerated. In contrast, some of the early BPD procedures (in particular the Scopinaro), allowed for the creation of a stomach with a much larger size, such that relatively speaking, large quantities of food could still be introduced and tolerated.
During surgery the small bowel was divided creating 2 limbs. The first limb was then attached to the first part of the duodenum and ran its natural course down the caecum. This was named the alimentary limb and was fundamental to this procedure as it allowed food to by-pass the mixing that normally would occur in the 3rd part of the duodenum, with bile from the gall bladder that is essential for the digestion particular of fats.
The other limb began when the duodenum had been divided at its first part but its distal end was surgically attached to the lower end of the alimentary limb. This meant that bile that still would be produced only had the opportunity to mix with food coming down the alimentary limb at this connection limiting any meaningful digestion of fats in the diet, the consequence being that even small amounts of fatty foods consumed would not be digested, and would transit through the bowel at an accelerated rate creating a loose offensive stool.
In addition during this procedure, the gall bladder was removed if it was still in situ. Although the gall bladder is the usual reservoir for bile, the latter is produced by the liver and continues to be made despite the absence of the gall bladder itself.
Dr Broadbent had performed approximately 50 of these procedures prior to operating on Mrs MacLeod.
MACLEOD ALLEGATIONS
Mrs MacLeod underwent the operation on 16 June 2003 at Allamanda Private Hospital. Her weight at the time of surgery was most likely 126kg, despite the anaesthetic sheet and nursing admission note indicating her weight as 110kg. 110kg is almost certainly an error judging from Dr Broadbent’s notes.
Her post-operative course was complicated by 3 admissions:
First, on 28 June 2003 (June Admission) for 2 days and 12 days post operatively. Her weight then was recorded as 110kg.
Second, on 13 September for 12 days and 3 months post operatively. Her weight was recorded as 92.8kg at this time.
Third, on 2 October for 13 days until her death on 15 October. Her weight on admission was recorded as 94kg.
At the time of Mrs MacLeod’s death, the last recorded weight was 102.9kg on 12 October 2003, the day prior to her admission to the I.C.U with overwhelming sepsis.
No post mortem examination was performed (one was performed on Mrs Pearce).
Expected weight loss in the first 2 weeks can be quite dramatic with at least 10 kg to be expected. Following this, the loss on average is around 4kg per month. So by the June admission she had lost 16kg – perhaps a little more than expected.
By the September admission she had lost 31kg. Using the average as a guide her weight loss could have been expected to be at least 20kg.
Mrs MacLeod’s issues that precipitated each admission related to complaints of vomiting and diarrhoea. Her actual relevant medical problem in both the September and October admission was significant, unexplained renal impairment. In the October admission, additional significant malnutrition was treated parenterally. The October admission was finally complicated by overwhelming infection for which patients like Mrs MacLeod are at serious and potential threat, given her morbid obesity, the fact she was on TPN and the fact she was being treated with steroids.
2.3 Voltaren and whether inappropriate
I am satisfied that Dr Broadbent prescribed Voltaren for Mrs MacLeod between 13 and 25 September 2003.
Voltaren is a non-steroidal anti-inflammatory drug.
The nursing history taken on her admission to hospital on 13 September 2003 records her as currently taking Voltaren, see ex 15, Vol 2, pg 169. Dr Broadbent is recorded as ordering Voltaren for her on 15 September; the order is signed by him and the chart indicates she continued to take Voltaren until her discharge on 24 September 2003, see ex 15, Vol 2, pg 213.
In his evidence Dr Broadbent admitted prescribing Voltaren in the September admission. He said “I continued what she was already taking. She’d been taking that substance or something similar to that since 2000” (T16-88).
Her prior history is summarised in ex 71, tab 1, paras 3-6.
Mrs MacLeod was suffering from renal failure. Voltaren is now known to be contraindicated in renal failure because it could compromise kidney function; it could have a deleterious effect on the kidneys (Woods T3-26, 6-43 and Cohen T13-13). In evidence Professor Woods maintained his view that prescribing Voltaren in 2003 to a patient with renal impairment was, for the same reasons, inappropriate and contrary to good practice (T6-42, 43). I felt though that he was to an extent influenced by hindsight. I also felt that at least for the September admission he may have been prepared to defer to the opinion of a renal physician (T6-45) even though the admitted fact that Mrs MacLeod’s renal function improved notwithstanding her continued taking of Voltaren did not cause him to alter his opinion (T6-42).
Dr Cohen departed from the view he expressed in ex 2. In evidence he said he was “warned off” Voltaren in 2005 (T13-13, 14). He said it’s possible impact on renal function “really only started to be appreciated from about 2005” and that “may not have been widely understood in 2003”. He also said that some people respond negatively to Voltaren if given in the presence of renal failure and for others it has very little impact. In the present case it seemed to have no impact at all on the renal function of Mrs MacLeod because she continued to take it and her renal function improved (T13-14).
Even though Dr Cohen said (T13-14) that from the point of view of knowledge in 2003 both he and Professor Woods considered that Dr Broadbent did not, by prescribing Voltaren, fail to manage and treat Mrs MacLeod, he really, in my view, only meant himself because Professor Woods was adamantly of the contrary view.
Dr Broadbent in evidence said he was not aware at the time that Voltaren was inappropriate or contraindicated because of Mrs MacLeod’s renal condition. He also referred to the improvement in her renal function during her admission and the absence of adverse effects on her renal function (T16-89).
I accept the view of Dr Cohen including his reasons for apparently departing from the view he appeared to express in ex 2. Dr Broadbent’s evidence is consistent with that. I have, as I have said, some reservations about the dogmatism of Professor Woods in relation to the state of medical knowledge in this respect in 2003. In these circumstances this allegation against Dr Broadbent has not been made out.
3. Diarrhoea and vomiting
September Admission
On 6 September 2003 Mrs MacLeod complained to her general practitioner of diarrhoea off and on since the operation aggravated by medication (ex 15, Vol 2, pg 339).
She complained of persistent diarrhoea to Dr Broadbent’s secretary on 12 September 2003. Dr Broadbent refers also to “long episodes of diarrhoea”. On 13 September 2003 she complained to Dr Broadbent of “persisting diarrhoea”. He arranged her admission to hospital (ex 65, paras 205-210).
She did not complain of diarrhoea on admission. Her admission details state “vomiting post-op” and “vomiting 3/52” i.e. for three weeks, see ex 15, Vol 2, pgs 161,164 and 165. The discharge summary for the September admission states her presenting problem as “admitted with vomiting” (ex 15, Vol 2, pg 162). The nursing history for 13 September 2003 refers to diarrhoea concerns but not vomiting (ex 15, Vol 2, pg 170). On 13 September 2003 after admission no diarrhoea was noted or recorded and no vomiting is noted or recorded (ex 15, Vol 2, pg 198 “no BO”).
On 14 September 2003 she had “nil complaints of nausea or vomiting” (ex 15, Vol 2, pg 171). No complaint of vomiting on any day of her admission other than the history she gave on admission is noted or recorded.
During her admission excessive bowel movements were recorded on only two days (15 September – 12, 22 September – 7) neither of which were sighted/signed off by nursing staff, see ex 15, Vol 2, pgs 186-197. On all other days where it is recorded the number of bowel motions do not appear excessive. In this respect I agree with Dr Broadbent that Mrs MacLeod’s “actual diarrhoea” in hospital was non existent and the records “clearly show that”. He said any pre-existing diarrhoea or vomiting “ceased on her admission to hospital” (T16-39).
In evidence Dr Broadbent, when referred to Mrs MacLeod’s persisting complaint of vomiting for three weeks, said “I don’t think she reported a three week history of vomiting to me. She reported a three week history of diarrhoea… What she complained to me about was diarrhoea” (T16-31). He also said “she underwent a period of observation to see if her symptoms of vomiting and diarrhoea could be reproduced and on the basis of that we may be able to then make further investigations as necessary. But following her admission and observation period neither vomiting nor diarrhoea were observed and gradually as we introduced fluids orally and then food there was still no sign of the reported vomiting or diarrhoea and those observations continued right through that admission” (T-16-35,36). He said that investigations into the cause of any vomiting or diarrhoea by Mrs MacLeod were not indicated (T16-109,110).
Dr Broadbent also said “what the patient interprets as diarrhoea and what is diarrhoea are often separate things” (T16-26). I think Professor Woods may, to some extent, have elevated reported diarrhoea to actual diarrhoea or overlooked dietary factors as the most likely cause of Mrs MacLeod’s vomiting and diarrhoea. I think he also overestimated the extent of any diarrhoea suffered by Mrs MacLeod. There is no evidence of “constant liquid diarrhoea” or of “serious persistent diarrhoea in the absence of any dietary fat” (ex 11, SW-4, paras 6 and 17).
I also think he is mistaken when he says (ex 11, SW-4, para 44) that Mrs MacLeod’s ongoing vomiting “was never investigated”. There is no evidence of any possible mechanical problem which needed correction.
Upon admission “basic investigations” were undertaken. Any symptoms of diarrhoea which Mrs MacLeod may have had resolved on admission and Dr Broadbent saw no reason to conduct the investigations suggested by MBQ and in fact Mrs MacLeod instructed him not to perform a colonoscopy (ex 65, paras 221, 222 and 216-43).
Her recovery was “straightforward and uneventful” (para 226).
None of the results of tests were, Dr Broadbent said, “consistent with serious intra-abdominal pathology, gut sepsis or anything other than simple dehydration” (para 230).
He said that in hospital there was no diarrhoea or vomiting to investigate (T16-41) and that would appear to be so. He said that after “introduction of food slowly over a period of a few days Mrs MacLeod returned to exactly what one would expect a patient to be doing” (T16-42). Had she not settled in hospital he would have conducted investigations such as suggested by MBQ (T16-42).
Dr Broadbent said the most common cause of her presenting symptoms is over-eating, eating too quickly and eating food with excessive fat; and that BPD surgery does not cause diarrhoea. Excessive fats, food and fluids could cause both the vomiting and diarrhoea she complained of (T16-42, 48).
He said her symptomatology fitted that pattern exactly because in the controlled hospital environment all of her symptoms ceased “and when a normal diet was reintroduced there was no vomiting” (T16-48).
Professor Woods conceded that diarrhoea is an inevitable consequence of BPD if the patient consumes fat in any significant quantity (ex 11, para 6). That, I think is in fact the most likely cause of diarrhoea in this case. Professor Woods has assumed or accepted that Mrs MacLeod in fact suffered more diarrhoea than was to be expected three months after surgery and that what she suffered was in fact diarrhoea. I am unable to reach the same conclusion but if that was the case the cause in my view was most likely dietary. In my view the September admission proved quickly, for the reasons given by Dr Broadbent, that tests such as MBQ suggest were not necessary. In these circumstances I think Professor Woods was being overly cautious.
Ms Williams said she would first have looked at dietary factors (T4-6) but this is perhaps not surprising as she is a dietician. In evidence Ms Williams said (T4-8):
“If the person has got really really bad diarrhoea then you would withdraw the fat out of their diet, tell them to withdraw the fat out of their diet, and you should get improvement in their bowel output.”
and (T4-21):
“If someone increases their intake too dramatically or too suddenly then that make cause vomiting but the solution is to reduce the pace and the volume and that will resolve that vomiting”
Ms Williams also said (T4-9):
“You can’t rely on what someone tells you in terms of what they’re eating. I think that’s very important step 1. We know that people who are obese are very very bad reporters. So we can’t make an assumption that what they tell us is actually true about what they’re eating.”
What Dr Broadbent said in his affidavit, ex 64, paras 561-5, 567-570, 607, 611 and 612 was to a similar effect:
“561 The greatest risk however in Obesity Surgery is after the first week when the patient leaves hospital and when left to their own devices for a few days.
562.Despite all the indoctrination, training and warnings, a non- compliant episode can effectively ruin an otherwise good operation and lead to a serious complication and lengthy hospital stay.
563.For example overeating and overdrinking in the first three weeks after leaving hospital seems to be the problem in early gastric leaks. Eating excess fats is the most common cause of diarrhoea.
564.In explaining risks to the patient I explain that their conduct will be the great unknown with the operation and that non-compliant conduct can lead to severe complications.
565.Even with those warnings, it is human nature to explore and test the boundaries of what they can and cannot do, often driven by life long life-style habits that can at times inadvertently be almost reflexly carried out – such as habitually chug-a-lugging a glass of water or fizzy drink.
567.The other “patient factor” which is explained eloquently by Dr Scopinaro (see “RB-5”) is ‘what the patient eats after surgery’.
568.Whilst this is important at all times after surgery it is particularly important in the first few weeks (as described above) and in the first year or two throughout the weight loss phase as the subject is literally on a ‘nutritional tightrope’. One wobble or indiscretion can precipitate a chain of catastrophic events.
569.Compliance, or ‘patient factors’ as Dr Scopinaro refers to them, are paramount hence the importance of pre-operative education and practical understandable explanations from those who know and have experienced the pitfalls (our ‘counsellor’) and the close follow-up programme.
570.One can anticipate that those who fail to attend for follow up adequately will inevitably experience troubles as they do not get reinforcement and gradually become complacent and slip into old established habits. Overeating and eating fatty foods in the first 4 to 6 weeks after surgery is hazardous and thus has to be restricted.
607.The subject is on the nutritional tightrope as described. If there is too much energy intake the operation becomes a failure. If too little energy intake, the candidate may lose too much weight, but more importantly become seriously nutritionally depleted-particularly in protein.
611.The phenomenon of ‘non-compliance’ is endemic in any way of life.
612.The same occurs with patient non-compliance with dietary and other instructions after bariatric surgery. Such can be very dangerous and have serious consequences for the subject. It is the opinion of most authors that patient factors or compliance usually precipitates the HAL-PEM state and are not operation factors.”
In evidence Dr Cohen again departed from ex 2 – this time in relation to diarrhoea. This was he said because he had since examined in more detail the hospital records and concluded that he erred in concluding that Mrs MacLeod had diarrhoea which was more than expected. He said he agreed with the approach taken by Dr Broadbent (T13-14, 16, T14-24). He agreed no vomiting was recorded in the hospital records (which indicated any pre-existing vomiting had not persisted) (T14-28,29) and as to diarrhoea he said he “would have been concerned about what food she was having” (T13-17).
He said that after Dr Broadbent admitted Mrs MacLeod to hospital and observed, that under more controlled dietary conditions that diarrhoea was not in fact present, he was correct to assume that was all that needed to be done at that stage and that investigations of the type suggested by MBQ were not necessary (T13-18, T17-27).
On 25 September 2003 Dr Broadbent wrote in the following terms to Dr Reynolds, Mrs MacLeod’s General Practitioner:
“Dear Dr Reynolds,
Just to let you know that Ursula was discharged from Allamanda Private Hospital today. She has been an inpatient for two weeks with a variety of problems.
She was admitted after she was supposedly vomiting with diarrhoea for two weeks. She was quite dehydrated on arrival, there were difficulties finding IV sites. We did manage to get a fair bit of fluid into her. As you are perhaps aware, we had planned a colonoscopy because of bleeding she had reported a couple of weeks earlier and this was deferred, of course, until things settled. Her bowels settled very quickly, I believe this is because we started her onto the correct food regime. Her vomiting also settled, particularly once we stopped her over eating. Ursula needs to be constantly reminded that her stomach is particularly small, anything more than 50-60mls at one time will cause her to vomit at this stage. Things will improve as the months go by, but during the weight loss phase it is absolutely important for her to minimise her food intake and measure it. The same goes for her fluid intake. Failure to do this and the stomach will just reject it. Ursula also needs to be constantly reminded about the quality of the food that she is unable to tolerate, at this stage any form of fats. It will cause instant diarrhoea. There were a couple of episodes of this whilst in hospital that she somehow managed to get the wrong food from the kitchen (easy to do as the patients are responsible for filling in their own menus) and considerable diarrhoea insued.
At this stage things are reasonably settled, she still has a little bit of ankle oedema, which is caused by fluid retention and perhaps slight hyperalbuminaemia despite having some IV albumin. I believe there is perhaps more than a slight compliance problem here. I will be reviewing her in a weeks time.”
I see no reason to doubt what Dr Broadbent said in this letter.
In ex 64, para 340, Dr Broadbent said:
“340. Diarrhoea following a BPD operation can be caused by many means, but primarily it is caused by ingestion of fatty food. Given that only 25% of ingested fat is absorbed in the common limb of the bypass, 75% of ingested fats will proceed into the large bowel and create an effect like Castor Oil.”
In evidence Dr Cohen said that as a BPD surgeon he didn’t fear fat.
“My view is that the short common channel is going to produce the malabsorption of fat if they choose to take it, and the patient will then get diarrhoea and foul wind, and that will make them not eat it, and what I fear is a lack of protein, and so I encourage my patients to have a protein hit with every meal, because the body can do without most of its fat, but it can’t do without protein.” (T13-20)
In relation to vomiting and diarrhoea Dr Reynolds said in evidence (T9-55):
“Doctor Reynolds, the times you saw Mrs MacLeod, post-operatively, do you recall whether vomiting or diarrhoea was a significant feature or did she complain of those things? -- No, she had - she complained of the mild diarrhoea for which I prescribed Imodium. She’d had no vomiting. She was very well and very happy and quite delighted with her progress.”
Leesa MacLeod, Mrs MacLeod’s daughter, did not in her letter to Dr Broadbent dated 27 August 2004 (ex 72, LM-3) refer to or complain about vomiting or diarrhoea before and during either the September or October admissions.
Dr Broadbent has raised herbal tea with senna as a possible cause of Mrs MacLeod’s diarrhoea. Herbal tea with senna is a laxative (see ex 5, para 345-351 and T16-83, 84). Dr Parnham, one of the renal physicians who treated Mrs MacLeod during part of her October admission, agreed that herbal tea can be a laxative (T9-42, 43). In his letter to Leesa MacLeod dated 14 September 2004 Dr Broadbent said (ex 72, LM-5, pgs 4-6):
“I became concerned that the symptoms she developed almost 3 months after surgery might have been related to the operation. The evidence eventually showed this was not the case. As soon as Ursula was restored to the very low fat diet she was supposed to be adhering to, her diarrhoea settled. As soon as the volume of food she was eating was reduced to the amount her stomach could accommodate her vomiting ceased… She was on a low calorie dietary regime that included essential daily supplements of vitamins and minerals. Ursula knew that if she ate excessive (for her) amounts of food she would regurgitate and vomit. Ursula knew that if she ate excessive fats she would get diarrhoea. If this happened she would mal-absorb her essential nutrients. Compliance to the regime exactly as instructed was essential to her on going well being…
It became apparent after her discharge and after a couple more weeks at home that Ursula’s kidneys were failing again and she was readmitted back to Allamanda Hospital. The cause or reason for her problem was obscure but eventually after my persistent questioning Ursula about things she might have taken Ursula told me she had been regularly taking a herbal drink every day for some weeks just before she fell ill. This self administration of the herbal drink ceased during he first readmission to hospital because the herbal ingredients were left at home but Ursula said she resumed taking the herbal drink as soon as she got back home. Ursula could not or would not advise me the details of what it was, where she got it, nor who gave it to her. Ursula was convinced though it was not the herbal drink that made her ill but the several courses of antibiotics that had made her worse and affected her kidneys and indeed such may have been the case. Among the many causes of kidney failure are the toxic effects of chemicals, herbs and even drugs like antibiotics. However I believe the cause was the herbal drink. I told Ursula then she was not to have any more of that substance whatever it was…”
In his letter to the Health Rights Commission dated 2 November 2004 (ex 72, LM-7, Pg 3) Dr Broadbent said, in relation to Mrs MacLeod’s admission to hospital on 13 September 2003:
“It was at that admission to hospital that Mrs MacLeod eventually revealed to me that she had been taking herbal remedies regularly for a few weeks. These were not listed on the medications she volunteered on admission.”
In evidence Dr Broadbent said that Mrs MacLeod told him “she’d been regularly taking a herbal drink every day for some weeks just before she fell ill. This self-administration of the herbal drink ceased during her first re-admission to hospital because the herbal ingredients were left at home but she said she resumed taking the herbal drink as soon as she got back home.” He also said (T16-90) that he thought Mrs MacLeod didn’t understand the effects of what she was taking. See also T17-29.
In relation to the period after the September admission, Dr Cohen said (T13-19):
“…there was something else going on in her home environment which was causing another deterioration.
Now, could that have been herbal tea with senna? – Well, my answer is absolutely, yes. If I knew that a patient was taking senna, which is a strong purgative laxative, it would have caused not only diarrhoea, but a wash through of protein and other nutrients too rapid for there to be effective absorption, and it would have very significantly precipitated a malnourished crisis.”
Nurse Judith Bryceson, in her affidavit (ex 38) said:
“23.I recollect Mrs MacLeod because she was a difficult patient, she was never in her room, roamed the hospital, helped herself to kitchen facilities, things in the refrigerator, and made her own tea. Mrs MacLeod would also visit the pharmacy, where they sold sweets and chocolate, and the canteen which sold food and drink.
24.She had drips which needed to be resited frequently because of her constant movement. Her movements and lack of compliance with instructions regarding intake of fluid and measuring output, meant fluid balance and stool charts were unreliable. As a consequence nursing measurements and observations were not fully accurate, and not a true record – just an indication.”
In evidence she said that she saw some of these things herself. She said she didn’t know what type of tea Mrs MacLeod was taking but said she was allowed to make her own tea (T10-34).
Mrs MacLeod told Lee Kvist that she used Chinese herbal tea prescribed by a Fortitude Valley herbalist before and after the operation. She said it “would hasten her weight loss.” She showed Ms Kvist a box in which the tea was packaged. Photographs of such a box are ex LQ1 to ex 41. The ingredients are stated to include Follium Sennae. Mrs MacLeod said she had not at that stage told Dr Broadbent but intended to (see ex 40, paras 48-57 and ex 41, paras 1-9). Ms Kvist also overheard advice by Dr Broadbent to patients that for the first 12 months they weren’t to eat anything that “ever walked, swam or flew, in other words nothing that contained fat” because that would cause “the most awful bout of diarrhoea” (T10-60).
I accept the evidence of Ms Kvist. It is supported by other evidence which I also accept.
Christine Warby was Dr Broadbent’s receptionist/secretary from July 2003 until September 2008. After a consultation with Dr Broadbent following her operation Mrs MacLeod told Ms Warby she was taking herbs and herbal tea. Dr Broadbent may have overheard this because he told Mrs MacLeod not to take anything other than what he had told her (ex 39 paras 9 & 10).
Mrs MacLeod’s attitude may also be apparent from what she said to Melanie Woodward soon after her operation, namely:
“Now I’ve had the operation there is nothing more I have to do.”
and
“Everything will be alright because the operation will do everything for me.”
(ex 48 paras 17 & 18).
This may be reflective of a casual attitude to compliance with Dr Broadbent’s dietary regime.
Leesa MacLeod describes as “complete rubbish” suggestions that her mother was “taking any herbal remedy” (T2-39) but I consider the preponderance of evidence, which I accept, is to the contrary.
October Admission
In evidence Dr Broadbent said Mrs MacLeod advised him on about 1 October 2003 that her vomiting and diarrhoea were back.
At admission on 2 October 2003 Mrs MacLeod reported diarrhoea (ex 15, Vol 2, pg 368).
The hospital records do not indicate persistent diarrhoea. The Fluid Balance Summary records five bowel motions on 8 October 2003 (ex 15, Vol 2, pg 557, see also pg 551) and two on 9 October 2003 (pg 552). The progress notes (ex 15, Vol 2, pg 369-390) do not suggest persistent diarrhoea. The note by Dr Parnham (Renal Physician) of 6 October 2003 (ex 15, Vol 2, pg 377) that he was told Mrs MacLeod was experiencing “very severe diarrhoea, up to 100 episodes a day” was based on what Mrs MacLeod said without any supporting objective or nursing evidence (T9-8) and is not meant to state the position in hospital. In evidence Dr Parnham said Mrs MacLeod described diarrhoea up to 100 times a day in the months before coming to hospital but that had “slowed down recently” (T9-37). He also said that whenever he went to see her (presumably in hospital) she was always in the toilet (T9-37). Other hospital records do not however support this or his note of 9 October 2003 of “ongoing severe diarrhoea” (ex 15, Vol 2, Pg 383). It is likely that Mrs MacLeod was also the source of this note. There is no supporting objective or nursing evidence either.
I agree with what Dr Broadbent said in exhibit 65, para 312. He also correctly summarised the hospital records as follows in para 343 of exhibit 65:
“343. The records show Mrs MacLeod’s bowels did not open on 4, 5 and 6 October 2003, moved once on 7 October 2003, 5 times on 8 October 2003, twice on 9 October 2003, little on 10 October 2003 and not on 11, 12 or 13 October 2003, although flatus was passed on 11 October 2003”.
After two or three days in hospital there was no vomiting or diarrhoea and she could tolerate food (T16-62).
I am not satisfied that what Dr Broadbent was faced with required anything other than the conservative steps he took to monitor and control her presenting symptoms. I am not satisfied that Dr Broadbent acted inappropriately after Mrs MacLeod’s presenting complaints of vomiting and diarrhoea generally appeared to settle, in concluding, as he did in September 2003, that it had been caused by dietary non-compliance on the part of Mrs MacLeod (T16-83). Circumstances did not, in my view, then call for tests such as contended for by MBQ and Professor Woods.
Dr Broadbent said that Dr Parnham advised a continuation of the present line of treatment (T16-84). Dr Broadbent was the last witness to give evidence. Dr Parnham gave evidence some time before him. Dr Broadbent said that Dr Parnham assured him that Mrs MacLeod “was going to get better and all we need to do was continue the present line of treatment”. Dr Parnham was not asked whether he gave this assurance to Dr Broadbent but he did say that between 6 and 10 October 2003, when he last saw Mrs MacLeod, he thought her treatment in hospital was appropriate (T9-39). In these circumstances I accept what Dr Broadbent says.
Dr Cohen said (T13-18) that he agreed with the decisions taken by Dr Broadbent. He also said that he didn’t understand that her diarrhoea was a major feature of the October admission, at least after the first few days of her admission. The pressing priority was perceived to be the re-establishment of nutrition to stabilise her situation and the main reason Dr Broadbent admitted her then was for the insertion of a TPN central line.
4.Nutritional advice, management and treatment
4.1 Pre-operative consent form
In the consent form (ex15, Vol 1, pg 37) the patient agreed to consume food only as follows:
(1) 50mls per meal during the weight loss phase and 100mls thereafter.
(2) no more than 3 meals per day.
(3) only fat free food during the weight loss period and reduced fat thereafter.
Dr Broadbent said the “weight loss phase” (which for Mrs MacLeod extended to September 2004 over which time it was expected she would progressively lose weight, T16-18, 61, 110) was in two parts:
(1) the immediate post-operative 4-6 weeks period (the “inevitable phase applying to all patients (T17-39,40)
(2) the 6 weeks – 9 months period (the “dependent on patient” phase) during which period meal size would change with time depending on the patient’s compliance. Weight loss after the “inevitable” phase would depend on compliance by the patient with the diet and exercise program (T17-40).
The consent form did not differentiate between these phases and therefore literally provided inadequate nutritional advice. To this extent it was wrong and misleading. Clearly, according to the experts, no more than 3 meals per day, each limited to 50mls, for up to 9 months would not provide adequate nutrition and the advice in the form was incorrect.
Dr Cohen said (T13-21) he doesn’t have differential weight loss phases for his surgery and didn’t know what the weight loss phase was in Dr Broadbent’s program.
In fact though, Mrs McLeod was consuming more than 50mls per meal 3 times per day in the immediate post-operative period and in the June, September and October admissions. See also ex 65 paras 271 (as to the advice given to Mrs McLeod) and 273 (as to the fact that the consent form is said not to be reflective of all the nutritional “information” given to a patient). See also Dr Broadbent’s evidence at T17-12.
Mr Hackett’s submission is that the “advice” in the consent form is “limited to the immediate post-operative period of weight loss that would extend 4-6 weeks”. I cannot agree; the form speaks for itself.
4.2 June admission
The fluid balance charts (ex 15, Vol 2, paras 236-238) indicate an oral intake of fluids in excess of 50mls 3 times a day.
The experts agree that the nutrition Mrs MacLeod received, while low, was reasonable.
I am unable in the face of this evidence to conclude that Dr Broadbent failed in the June admission to ensure the provision of adequate nutrition to Mrs McLeod.
4.3 September admission
The fluid balance summary (Ex 15, Vol 2, para 211) indicates the oral fluid intake ranged from 530mls to 1,585mls [sic] per day. This, Dr Cohen said (T13-25), the experts agreed in ex 2, was an “inadequate amount of nutrition”.
Food intake is difficult to assess as there appears to be no oral food/fluid balance charts for the June and September admissions; only in the October admission is the food separately recorded. This is the reason for another change of view on the part of Dr Cohen. In ex 2 he agreed that Mrs McLeod was not provided with adequate nutrition, in particular proteins and, in the absence of records, vitamins. In evidence he said (T13-26, 27, 14-18, 19) that a more detailed review of the clinical charts (ex 15, Vol 2, paras 172-175, 178-180) shortly before giving evidence (which however were available in the first place T14-19) indicates that the patient was having “free amounts of fat-free” food and was getting enough nutrition.
Dr Broadbent agreed (T17-16) that the hospital records indicate the provision of negligible food and/or fluid to Mrs McLeod but maintained she received appropriate amounts of food and fluids. He agreed that she wasn’t, in hospital, prescribed vitamins.
I am not satisfied that the facts are as materially different as Dr Cohen sought to portray in his evidence such that I should depart from the views (still maintained) of Prof Woods and Ms Williams as expressed in ex 2. Nor can I accept Dr Cohen’s attempt to include Prof Woods and Ms Williams in his conversion (T13-25). Neither in fact departed from the views they expressed in ex 2 and in fact Mrs McMillan correctly objected to his attempt to include them. In these circumstances this allegation has been made out. The preponderance of the evidence supports it.
It is important though to recognise the limitations associated with the allegations made in para 4.3 namely:
· they depend upon an absence of records rather than records in support; and to this extent assume that because there are no records the contrary is established
· the failure of Dr Broadbent to prescribe vitamins, iron or calcium supplements does not mean that Mrs McLeod was not taking her own vitamins, which he understood her to be doing.
4.4 October admission - malnutrition
Mrs McLeod was admitted on 2 October in a malnourished state. She was “admitted because of her nutritional needs” (T10-38 Bryceson). TPN (total parenteral nutrition) was commenced on 5 October. Dr Broadbent intended that TPN commence on admission (it was not intended that the patient’s nutritional needs be provided orally) but the central line could not be inserted until 5 October due to coagulopathy (see T7-25, T16-61). The oral food/fluid balance charts for this admission indicate minimal oral food intake (ex15, Vol 2, pgs 434-441) but while waiting for the central line to be placed Dr Broadbent said (T16-67) a peripheral intravenous line was inserted and the patient was commenced on intravenous fluids and a clear fluid diet. Nasoenteral feeding was not instituted. Whether this should have occurred depends on when the patient’s coagulopathy was expected to be resolved – sooner rather than later. Be that as it may Mrs McLeod should have, but wasn’t, provided with adequate nutrition between 2 and 5 October. Dr Cohen said (T13-29) that it was during this period that the experts considered (ex 2) that Mrs McLeod was not getting enough nutrition. In evidence (T14-42, 43) he initially agreed that there were alternative ways to provide nutrition while awaiting the start of TPN. This was also the view Dr Woods expressed in evidence. I cannot accept Dr Broadbent’s contention (T17-18) that “an adequate oral feeding regime” was in place. I cannot accept his evidence (T16-66, 67) that by not starting TPN because of the patient’s coagulopathy the intensivists “assessed her nutritional situation as not being desperate or really serious.” They did nothing of the sort. Their decision was only that TPN could not be started on admission because of coagulopathy.
TPN was commenced on 5 October by the intensivists. In ex 65 Dr Broadbent said:
“301As the co-ordination of the management of Mrs MacLeod was accepted by the Intensivists, my role was now considerably reduced, however I continued to monitor progress during my daily rounds and as and when I was provided with results by ICU and other doctors.
305On 5 October 2003 I referred Mrs MacLeod to Dr Allan Parnham, Consultant Nephrologist for the management of incipient renal failure and Dr Parnham accepted that role, assessed Mrs MacLeod and annotated the chart. The involvement of a second managing physician further reduced my involvement.
399.Dr Broadbent's co-ordinating role was taken over by Intensivists on 2 October 2003 and they were further assisted by Dr Parnham on 5 October 2003.
400.ICU Intensivists and Nephrologists were in a treating capacity – hence they initiated investigations, charted drugs and fluids, inserted catheters and replaced them, and gave general orders regarding Mrs MacLeod’s treatment.”
The intensivists did not in fact become involved until TPN began on 5 October.
In the period before the intensivists took over Dr Broadbent maintained there was an adequate oral feeding regime and nasoenteral feeding was not required (T17-17). I am unable to agree that this was so nor can I accept the “revised evidence” Dr Cohen later gave. The preponderance of evidence suggests inadequate provision of nutrition.
Dr Cohen said (T13-28) that he did not think a delay of about 3 days before TPN was commenced “made any difference at all to her outcome”. He also said that it was not Dr Broadbent’s fault that TPN had to be delayed and that is so. He agreed though (T13-29) that ex 2 contained a “statement of fact” that before TPN was commenced Mrs MacLeod “was not getting enough nutrition”.
When TPN was commenced lipids were withheld. Lipids would normally be included in parenteral nutrition. The hospital notes give the impression that this was at the direction of Dr Broadbent (ex 15, Vol 2, pg 376). Dr David Stephens, one of the intensivists, said this occurred “by consultation” and “she was on some oral intake anyway” (T12-40). Dr Broadbent said (T16-12,13) that he “asked the intensivists to consider omitting lipids from the mixture” and discussed why; the intensivists made their own decision. It is not necessarily the case that this meant that Mrs MacLeod’s nutritional intake was, as a result, inadequate.
There is no evidence that Dr Broadbent specifically directed that fat-soluble vitamins be withheld but he agreed they were withheld “but that was quite adequate” (T17-18).
So far as assaying vitamins and minerals is concerned some tests were ordered on 1 October prior to the patient’s admission. (Dr Broadbent said “they were assayed and what needed to be replaced was replaced” and “that’s all we could do” (T17-18). The suggestion in ex 2 (paras 4.4(d) and 4.6) is that the tests should have been assayed before 1 October. MBQ’s complaint however relates to a failure to assay after admission on 2 October.
During the period referred to in para 4.6 of the Referral Notice it is the case that Dr Broadbent did not assay parathyroid hormone levels but there is no evidence that the TPN with which she was provided did not contain all the necessary vitamins and minerals.
During the October admission Mrs MacLeod received Intravite (multivitamins) vitamins A and K, folic acid and trace elements (ex 15, Vol 2, pg 559).
4.5 Oral food intake issues
These allegations have been dealt with in paras 4.1, 4.2, 4.3 and 4.4.
4.6 Failed to monitor levels
Dr Broadbent assayed vitamin A and zinc only on 10 October (ex 15, Vol 1, pg 77, Vol 2, pg 323). Vitamin D was assayed pre-operatively and then again only on 1 October. There is no record of Dr Broadbent assaying parathyroid hormone levels at any time. The experts agreed (ex 2) that all four should have been assayed prior to the October admission.
In evidence Dr Cohen again changed tack. He seemed to say that the views in ex 2 were based on a “standard post operative testing regime” and he said the experts couldn’t ascertain what Dr Broadbent’s testing regime was leading up to the October admission (T13-33). He then said (T13-33, 34) that by 2 October Dr Broadbent had requested “an appropriate panel of tests” (zinc and vitamin A) and vitamin D and parathyroid hormone were not required at that time (even though vitamin D had in fact been assayed on 1 October) – they were more related to low metabolism, rather than renal or liver function. He did say though that he himself would, at the September admission, have ordered “a panel of nutritional indices including vitamin A and zinc and vitamin D”. This is consistent with what Prof Woods said (T3-19, 20). Prof Woods conceded some variation between individual doctors as to exactly what is assayed and the frequency of it. As to vitamin D he said that in addition to its role in controlling calcium levels it is also necessary for the immune system and along with vitamin A is vital “for good health”. He also said (T3-18) that parathyroid hormone levels were assayed
“in an effort to ensure that the patient is not, if you like, cannibalising her bones for calcium.”
Ms Williams also said that given Mrs MacLeod’s symptoms post-surgery, testing only in October would not have been adequate; she would have arranged for tests about 2 months post-operatively (T4-20).
Dr Broadbent’s response (T17-18) that assaying vitamins and minerals on 2 October was “all we could do” is not sufficient.
In my view the opinion expressed in ex 2 more accords with what I consider should have been done. Monitoring only on one occasion and then only of vitamins A and D and zinc was not sufficient.
4.7 Failure to recognise that patient was malnourished by September admission
The experts agreed she was developing malnutrition by this time and that Dr Broadbent appeared not to realise this.
Prof Woods said (T3-41) that by the time of her September admission she was “grossly protein deficient” and her rate of weight loss was “double what one would expect”. Also her albumin level on 13 September (requested by Dr Broadbent) was low (ex 15, Vol 2, pg 218, T6-55, 56).
Dr Cohen agreed (T13-3, 39) that her low protein state “probably reflected a patient who was not getting adequate protein, particularly nutrition” and she was probably developing malnutrition by the September admission and this was not then appreciated or recognised by Dr Broadbent. He further said that on the available evidence presented to him Dr Broadbent should not have recognised it.
Prof Woods said the basis of the opinion expressed in ex 2 was that a dehydrated patient with low albumin (which Dr Broadbent “set about supplementing intravenously) and a history of 2 - 3 weeks vomiting pre-admission was likely to be malnourished (T6-54, 55, 56).
In my view it is implicit in Prof Wood’s evidence that when he said the experts agreed Dr Broadbent appeared not to realise this, they meant also that he should have and I am unable to accept the different view expressed by Dr Cohen in evidence. In my view the objective evidence more supports the view expressed in ex 2 and the evidence of Prof Woods.
Dr Broadbent’s statement (T16-110) that Mrs MacLeod was not malnourished was not really responsive to the allegation that she was then developing malnutrition and in any event I am satisfied that she was at least developing malnutrition, if not malnourished in fact, and that he should have recognised this.
4.8 September and October – Possible consequences of malnutrition
Prof Woods said (T3-42, 43) that at the October admission a combination of her appearance (grossly oedematous), her low protein levels and low vitamin A levels indicated she had not been receiving adequate nutrition between the September and October admissions.
The experts agreed that Mrs MacLeod was suffering from malnutrition and that this was a possible cause of her oedema, skin condition and diarrhoea. They did not, in ex 2, express a view as to whether Dr Broadbent failed to recognise these matters.
I have already concluded that the patient was malnourished at her September admission and that Dr Broadbent should have realised this. The same applies with even more force to the October admission – she was then admitted by Dr Broadbent for TPN because she was malnourished.
The fact that malnutrition was a possible cause of Mrs MacLeod’s rash and skin condition (certainly in October but less certain for September) oedema and diarrhoea does not necessarily exclude
· dietary factors including herbal tea as a cause of her diarrhoea
· a low platelet count as a cause of her skin condition - certainly at the time of her October admission (Dr Cohen T13-38)
· low plasma proteins, a protein deficiency, as a cause of her oedema which Dr Broadbent said he treated (T16-110 and ex 15, Vol 2, pg 369).
The fact that Mrs Pearce in fact did exhibit the symptoms outlined in para 14.3 is referred to in the report of Prof Wall dated 26 February 2008 (ex 42) and in his evidence (T11-9). It was not put to him that she did not exhibit those symptoms.
Dr Cohen agreed that the chief clinical signs raising the possibility of a leak were the proximity of symptoms so close to surgery, the development of a fever, a tachycardia and a high white cell count and possibly vomiting (T13-70).
Prof Wall said in evidence:
· the symptoms exhibited by Mrs Pearce post operatively were such as to require Dr Broadbent to consider the possibility of an anastomotic leak (T11-9)
· quite clearly Mrs Pearce’s progress was inferior, she fell off the clinical pathway and there needed to be an explanation; she didn’t fit the post-operative pattern of BPD surgery (T11-9,10)
· the presence of bile in a drain tube “is extremely alarming for a clinician… and immediately raises issues of a surgical failure or misadventure;… it’s a flag of distress for the patient and the surgeon;… it is a recognised symptom of an anastomotic leak”;… it’s a shocking event for the patient and the surgeon; the surgeon should immediately then look for the source and that can be done by either an x-ray or putting contrast down the bile to see where the hole is and once found it may be possible to repair it (T11-10, 11, 12 and 13)
· the “discharge of the bile was alarming and the fact that it didn’t continue was more alarming… in the sense that it was probably collecting inside;… if it doesn’t keep coming you’ve got to say to yourself why – has it healed or is it collected inside (T11-14, 15)
· interpreting physical signs at the bedside of a patient such as Mrs Pearce is “inherently dangerous;… the way to exclude a leak is either an x-ray, a CT or a gastrografin meal study” (T11-18, 20)
· a diverticulum adjacent to the anastomosis line is very suspicious (T11-20)
· there was “a leak of some kind in this patient;… the observations of Dr Broadbent, the history of the patient progress and the appearance of discharge from the abdominal drain which contained a large number of pathogens all add up to evidence to support the leak from the abdominal track. These phenomena don’t occur spontaneously from the abdomen;… they are indicators or evidence supporting a leak, they could be supportive of something else but you need to at least give her the dye or something like that just to see what it is” (T11-21)
· “in this instance there were two possibilities, one a generalised leak and the second a localised leak” (T11-27).
I accept this evidence; it is supported by the fact, as I have found, that there was in fact an anastomotic leak. For the same reasons I accept the following opinions of Prof Wall in his report dated 26 February 2008 (ex 42):
“Dr Broadbent failed to diagnose the anastomotic leak following a bilio pancreatic diversion for obesity. Mrs Pearce underwent a complex operation of division of adhesions, cholecystectomy and bilio pancreatic diversion on the 27/03/2000. Post operatively Mrs Pearce presented to Dr Broadbent with the features of failure to progress, progressive weight loss, anorexia, nausea, vomiting, abdominal discomfort and a high fever of 39.3°. While these features may have been consistent with a urinary tract infection or a subphrenic abscess it is obligatory of the surgeon to consider a post operative anastomotic leak given that the patient underwent 2 anastomoses during the recent operation. Mrs Pearce should have undergone chest x-ray, erect and supine, abdominal x-ray and blood cultures followed by a CAT scan of the abdomen when the diagnosis of contained anastomotic leak or localised perforation of small bowel would have been confirmed. The safest expedient pathway in the care of Mrs Pearce would be an immediate referral to an interventional radiologist to carry out percutaneous drainage of the collection under anaesthetic with the patient supported by blood transfusion, antibiotics and with intensive care follow up. Such intervention would have confirmed the diagnosis and provided a means of improving Mrs Pearce. In turn, this would have provided an opportunity for a safe operation to be carried out at a later date to formally manage the fistula.”
The presence of bile in the drain in the gall bladder bed may or may not be indicative of an anastomotic leak. I cannot accept Dr Cohen’s evidence that it cannot be indicative of such a leak. In any event I consider that the presence of bile or bile stained fluid coupled with the failure of Mrs Pearce to progress warranted investigations of the nature suggested by Prof Wall and if they had been carried out I am satisfied that they would have indicated a leak at the duodeno-ileal anastomosis. The fact is that bile stained fluid was observed. Prof Wall said “she did have a bile leak” and that “bile stain is intestinal content” (T11-16, 17) and Dr Cohen conceded that if it were in fact bile then a leak of bile would be coming from somewhere. He agreed with Prof Wall that this would raise a red flag for the surgeon and the patient (T13-70). He did though say that the bile stained colour of the discharge “would warrant some assessment”. An investigation may be part of that assessment. He had also previously agreed that a discharge of 800 mls “is a fair bit” (T13-71). I prefer the evidence of Prof Wall conceding the possibility that the fluid leak may not have been bile but rather bile-stained fluid from some other source but stating that “if it keeps coming then we must take our clinical acumen and focus on the dangerous possibility” (T11-13, 14). Dr Broadbent admitted that Mrs Pearce was exhibiting some “abnormal signs” – “a fluctuant temperature and a bile stained discharge”. He said he “considered they were connected and were from the same pathology, namely a persisting bile leak in the gall bladder bed of the liver” (ex 66, para 71) but in my view he could not, without tests, exclude an anastomotic leak. In other words he could not, without tests, be certain of the source of the discharge. The fine line dividing possible causes because of the physical proximity of intestinal parts to each other was described by Prof Wall as follows (T11-11, 12) (and this in my view supports tests of the nature referred to by Prof Wall rather than a gastroscopy):
“The analysis was quite well put by Dr Broadbent in retrospect when he outlined that the bile could have come from the gall bladder bed, it could have come from where the cystic duct was cut because a gall bladder has to be separated from the bile duct. It could have come from a bit of bowel which was cut across and then stitched over the so-called dural stump or the bile could have come from where the join was fashioned by Dr Broadbent. Statistically, the leak of bile would run the risk of about one per cent but a leak from an anastomosis might double that rate in any major gastrointestinal surgery. Overall, major gastrointestinal surgery is associated with re-operation rate of three per cent in the best of hands.”
Dr Broadbent also appeared to agree that there may in fact have been a leak of bile. In para 74, ex 66 he said
“74. Admittedly Mrs Pearce was not as well and advancing as quickly as other BPD patients have. The bile leak itself could have been responsible for the mild leucocytosis and fluctuating temperature. It is, and was, a very likely explanation.”
Without tests this “explanation” was at best speculative only.
Dr Broadbent conceded it is reasonable to adopt an approach of continued suspicion and important that opportunities to help be not missed (T17-10). Relevant investigatory mechanisms were available on the Gold Coast at the time (see also T16-106). If there were a leak he agreed with the evidence of Prof Wall as to how to treat it (T16-104). 800 mls of bile stained fluid is recorded as having “oozed from the site” on 11 April 2000 (ex 16, pg 63) Dr Broadbent conceded that if that were so “it would be of concern” (T16-93).
Dr Broadbent agreed only that if what was observed was in fact bile further investigations should be carried out (T16-96, 97, 100 and 17-7, 18). He said the discolouration could come from other sources (T16-98). I am unable to accept that it is only in circumstances where the fluid was in fact bile that further investigations should be carried out. I prefer the evidence of Prof Wall, supported to the extent that it is, by Dr Cohen. I think that Dr Broadbent may have closed his mind to the possibility of an anastomotic leak. Mrs Pearce was the 30th or 40th case he’d “done of this type” and he’d only had one leak in that time. He said leaks occurred in only about 1 in every 25 cases (4% of patients) (T16-105, 106). It may have been because Mrs Pearce may not have in all respects exhibited the same symptoms as the previous case that he did not investigate the possibility of a leak (T16-106). Prof Wall referred to a complication rate of around 3% - “3 out of 100 patients might have to go back to theatre” (T11-27). Dr Broadbent agreed (T16-104). Additional, but similar statistics are referred to in ex 64, paras 500-504, 506, 508, 519 and 526-532. Prof Wall recognised that Mrs Pearce was not in all respects observed to exhibit the continuous symptoms ordinarily expected of a patient with an anastomotic leak but said this didn’t cause him to alter his opinions because these “observations do happen clinically”. He said “she still did have a bile leak” and “bile-stained is intestinal content” (T11-15, 16, 17).
The result is that I accept the submission of MBQ (ex 70, para 171) that:
“it was incumbent on the Registrant to attempt to exclude the critical diagnosis of anastomotic leak utilising the least invasive investigations available before submitting Mrs Pearce to not only an invasive procedure requiring anaesthesia but one which was contraindicated in the presence of (possible) anastomotic leak.”
This is based on the evidence of Prof Wall. In addition to what I have already referred to he said:
•“the important burden on the surgeon is to disprove a leak and I don’t believe that pathway was taken, another pathway was taken to find the mechanism of blockage in the upper gastrointestinal tract” (T11-22)
•“In Mrs Pearce’s situation, I believe she was progressing. I believe we would have not operated. We would have imaged and repeatedly checked for collections inside her abdomen which were making her sick and then intermittently drained those. We might have even done a small operation to facilitate the drainage... I believe that the conservative management was appropriate… I believe in view of her strength, her good quality renal function and her response to the initiatives that Dr Broadbent carried out, there were very positive and I believe that we could have got by without any surgical intervention, with confidence. Yes.” (T11-27, 28)
16Failed to diagnose and treat sepsis
Para 16.2(a) Dr Broadbent recorded on 17 April 2000 (ex 16, pg 70) that Mrs Pearce “had failed to make progress after BPD procedure”. She had lost weight (weight at operation 70.9kg (ex 16, pg 165) – down to 65.4kg on 27 March 2000 (ex 16, pg 87)) but she had undergone a procedure to lose weight and weight loss would normally be expected following such a procedure. She also suffered intermittent fevers (ex 16, pg 86). Also a swab taken from her abdominal drain site indicated a possible growth of pathogens (15 April 2000 pathology report). Collectively these factors were indicative of sepsis (see Prof Wall ex 42, report dated 26 February 2008) but, according to the experts “her septic state was improving by the time of her endoscopy”.
Dr Broadbent said he did not consider antibiotics necessary in the circumstances and was content with observation and the investigations ordered (ex 66, para 76). I do not consider this approach was inappropriate in circumstances where, as the experts state, “her septic state was improving”. The allegations in para 16 have, for these reasons not been made out.
The statement in the last sentence of the experts report in relation to para 16 relates more to investigations into the possibility of an anastomotic leak than to the diagnosis and treatment of sepsis.
Para 16.3 As to the allegations in sub paras (b) and (c) of a failure to undertake investigations and treat Mrs Pearce for sepsis (Prof Wall ex 42, report dated 26 February 2008 suggested blood cultures, blood film, sputum culture, urine culture and culture of aspiration of the subphrenic collection) the experts concluded (ex 3) that Dr Broadbent “did make efforts to investigate the patient’s signs and symptoms”; he instituted blood cultures and requested further cultures should the patient’s temperature rise again; and a swab was taken of the drained fluid from the abdominal site. They agreed that he did “likely give consideration to the possible diagnosis of sepsis”.
MBQ submitted (ex 70, paras 187, 191 and 192) that Dr Broadbent should have treated the sepsis with antibiotics. Having regard to the opinion of the experts I think the course adopted by Dr Broadbent as outlined in ex 66, para 76 is a sufficient response:
“76. I did not consider antibiotics necessary in these circumstances and it is not good practice to give antibiotics blindly. One needs to know what you are treating, and that was the purpose of the period of observation and subsequent investigation.”
To a similar effect is ex 67, paras 101 and 102 and Dr Broadbent’s evidence at T16-101.
19. Carrying out a gastrointestinal endoscopy when it was inappropriate to do so.
By reason of the evidence referred to in para 14 I am satisfied that Mrs Pearce was suffering symptoms consistent with an anastomotic leak or a small bowel perforation. Even if there was no anastomotic leak the connection of the pseudodiverticulum at the peritoneum constitutes a small bowel perforation. The gastroscopy carried out by Dr Broadbent confirmed a pseudodiverticulum at the duodeno-ileal anastomosis which connected with the peritoneum.
There is no dispute that an upper gastrointestinal endoscopy is contra-indicated in a patient who has an anastomotic leak in which case it would be inappropriate to carry out such a procedure. This was the conclusion of the experts. Dr Cohen confirmed this is so when giving evidence (T13-69). What Prof Wall said to the same effect (in the case of an anastomotic leak, a small bowel perforation and an intra abdominal abscess) in his report dated 26 February 2008 (ex 42) was not challenged by Dr Broadbent and Dr Broadbent (at T16-109) agreed that such a procedure is contra-indicated for persons suffering an anastomotic leak or a small bowel perforation. This allegation has been made out.
20. The endoscopy contributed to the death of Mrs Pearce.
It is not entirely clear why Dr Broadbent performed a gastroscopy.
In the hospital records for 17 April 2000 Dr Broadbent wrote (ex 66, pg 70):
“Patient taken to theatre for diagnostic gastroscopy as the patient had failed to make progress after bilio pancreatic diversion on 27/3/00.”
In his affidavit (ex 66) he said:
“46. I was concerned that the few vomits that Mrs Pearce had might have been because of stomach pathology or had caused stomach pathology, so on the morning of 17 April 2000 I considered some investigations were warranted and that a gastroscopy should be carried out.”
See also ex 67, paras 71 and 72.
In his evidence he said:
“I was looking for gastric pathology related to her oral thrush which was causing her to be reluctant to eat and which caused the occasional vomit” (T16-104, 105).
and
“not all of her symptoms abated. The residual symptoms were that she had persistent oral thrush. She had difficulties swallowing and she was reluctant to eat her meals for that reason. And in my mind, I was concerned that the oral thrush continuing down her oesophagus and into her stomach and there may be other pathology there and furthermore, it is always possible and we’d just done a further blood culture, at that stage, that she may even be developing a systemic candidiasis not just orally, and so, looking at the extent of this was quite important” (T17-11).
Prof Wall said (T11-19) he thought
“Dr Broadbent precipitated the endoscopy because she was nauseated and vomiting, and he thought there might’ve been a mechanical factor and he thought he might’ve been able to find evidence of why the food wasn’t going down”.
He continued
“HIS HONOUR: And a mechanical factor could be an anastomotic ---? Could’ve been, yes. Or a kink. And I think that the concern that Dr Broadbent had about the passage of food through the anastomoses is logical, understandable – because she’s now 20 days after the operation. That’s reasonable. But the manoeuvre of looking inside is more hazardous than having somebody swallow a radio opaque material and following it through.
All right. Well, what you’re saying is – correct me if I’m wrong – is that if he had at an early stage carried out inquiries to see whether there was such a leak and then discovered there was, and then repaired it, there would be no need for the procedure that he was carrying out when she died? -- I believe that’s true.”
He also said (T11-28, 29) that alternative “conservative management” such as a contrast
“would have been a procedure which did not have an anaesthetic and did not have stress of the magnitude of an endoscopy. I believe the contrast would have shown a little, fine pathway which ran from the bowel to the surface of the skin or into the region and may or may not have been a collection. But even finding that, it would have been reasonable for them – for Dr Broadbent to say, ‘right, we know what to do. We’re going to manage you conservatively. We’ll make you nil by mouth and we’ll give you Octreotide and we’ll give you antibiotics and we’ll build you up and that should heal.’”
Non-invasive tests to exclude an anastomotic leak, not a gastroscopy, should in my view have been carried out. In the circumstances as they existed Mrs Pearce was placed at considerable risk by undergoing a gastroscopy.
In his report dated 26 February 2008 (ex 42) Prof Wall said:
“With respect to the role of the upper GI endoscopy in the presence of an anastomotic or small bowel perforation and intra abdominal abscess formation, upper gastrointestinal tract endoscopy involves inflation of the gastrointestinal tract. The inflation is highly likely to cause further rupture of the bowel and possibly also rupture of the abscess into the peritoneal cavity proper. Only a small increase in the pressure of the gas within the lumen of the bowel will be responsible for sudden catastrophic events during the endoscopy. The possible catastrophic events are:
1. Rupture of the toxic fluid into the peritoneal cavity leading to rapid onset of severe widespread peritonitis and the onset of septic shock.
2. The introduced gas may dissect into the surrounding tissues and then in turn into a major vein which would lead to a sudden onset of circulatory instability due to massive air embolus.
3. Upper gastrointestinal tract endoscopy can precipitate death through introduction of the gas into the lumen of the bowel causing increased intra-abdominal pressure. This raised pressure can then displace clots in the pelvis which can lead to pulmonary embolus. There is a case for screening such seriously ill patients prior to carrying out such a procedure. This would allow the placement of a caval filter if major thrombosis was detected.”
In his earlier report (also in ex 42) he said:
“Mrs Pearce suffered an early post operative complication associated with failure to progress, severe infection and subsequently sudden death under anaesthesia. Dr Broadbent recommended and carried out an upper GI endoscopy to assess the patient’s status. Dr Broadbent failed to diagnose an anastomotic leak. He failed to diagnose serious sepsis and he carried out an upper gastrointestinal endoscopy which was contra indicated. The patient’s management contributed to her death. The failure to diagnose an anastomotic leak is responsible through causation (that is, the limiting of the patient’s clinical pathways) for the patient’s death. Dr Broadbent’s care of Mrs Pearce was incompetent.”
Dr Broadbent conceded “some risks” undergoing a general anaesthetic.
The experts concluded (ex 3) that Mrs Pearce died as a result of an “exceedingly rare” complication of the endoscopy which is “unlikely to have been foreseen prior to the procedure.” Her death, they said, “would have been avoidable had an alternative pathway of diagnoses been undertaken”. I assume the “complication” is her death from ischemic heart disease and coronary atherosclerosis. It does not appear to have been any of the 3 “possible catastrophic events” referred to by Prof Wall.
The anaesthetic record for the endoscopy (ex 16, pg 84) shows no serious concerns in her vital signs indicative of any serious physiological disturbance such as to have raised concerns prior to the procedure. She was administered a “light general anaesthetic” (T16-98) but was breathing spontaneously. Towards the end of the procedure there was a sudden unexpected deterioration in her condition following which resuscitation was unsuccessful (ex 16, pg 72).
The post-mortem report indicated Mrs Pearce had moderate coronary artery disease (ex 44) which would have been present at the time of her BPD surgery which occurred uneventfully.
In his report dated 26 February 2008 (ex 42) Prof Wall said the “safest pathway” for Mrs Pearce would have been percutaneous drainage by an interventional radiologist under anaesthetic. (Dr Broadbent referred to “sedation” T17-41). This may have exposed her to the same risk of sudden death as in fact occurred during the endoscopy, but at an earlier time. (Notwithstanding the evidence of Dr Broadbent at T17-41 (which is not particularly clear) it was not put to Prof Wall that such a procedure could not have been undertaken at the time and I am prepared to accept that it was then available as an option).
Notwithstanding this, the fact is that a gastroscopy was, for the reasons given by Prof Wall in his report dated 26 February 2008 (ex 42), fraught with catastrophic risk and even though the risks referred to by Prof Wall do not appear to have caused her death, in my view it is likely Mrs Pearce would not have died had she not undergone the endoscopy. In short I do not think she would have suffered cardiac arrest (see T14-54, ex 66, para 53 and ex 71, para 52(a “cardiac event” – Prof Wall T11-18)) had she not undergone the endoscopy. Prof Wall said (T11-18):
“we have to recognise that maybe she wouldn’t have had an infarct if she hadn’t have been subjected to the gastroscopy.”
He also said (T11-29) that given the post-mortem findings of the atherosclerosis, death would have been likely given that she died during the procedure. She died whilst undergoing the gastroscopy but Dr Broadbent wasn’t to know that she had such a heart condition as placed her at risk of a heart attack during such a procedure.
RESULT
MACLEOD ALLEGATIONS
I am satisfied that in the respects alleged in paras 4 (sub paras 4.1, 4.3, 4.4, 4.6 and 4.7 only), 5 (sub paras 5.1-5.9 only) 6.6 (sub paras (a)-(d)) and 7.4 of the Amended Referral Notice Dr Broadbent behaved in a way that constitutes unsatisfactory professional conduct by engaging in professional conduct
• that was of a lower standard than that which might reasonably be expected of him by the public and his professional peers and
• that demonstrated a lack of adequate knowledge, skill, judgment or care, in the practise of his profession.
PEARCE ALLEGATIONS
I am satisfied that in the respects referred to in paras 14.4 (sub-paras (a) and (b)), 19 and 20 of the Amended Referral Notice Dr Broadbent behaved in a way that constitutes unsatisfactory professional conduct by engaging in professional conduct
• that was of a lower standard than that which might reasonably be expected of him by the public and his professional peers
• that demonstrated a lack of adequate knowledge, skill, judgment or care, in the practise of his profession and
• that involved the provision of a health service (the gastroscopy) of a kind that was excessive, unnecessary and not reasonably required for the patient’s wellbeing.
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