Record of Investigation Into Death (Without Inquest)
Coroners Act 1995
Coroners Rules 2006
I, Rod Chandler, Coroner, having investigated the death of
WITHOUT HOLDING AN INQUEST
Find That :
Roger Steele ("Mr Steele") died at his residence in Lindisfarne at an unknown time but after 9.45pm on 14 November and before 5:30am on 15 November 2008.
Mr Steele was born in Hobart on 7 December 1944 and was aged 63 years at the time of his death. He was employed as a cleaner.
I find that Mr Steele died as a result of ischaemic heart disease due to triple vessel athersclerosis.
Circumstances Surrounding the Death :
Mr Steele resided with his de facto partner of 16 years, Noelene Helen Priest ("Ms Priest") at Lindisfarne.
At about 8.45pm on 14 November 2008 Mr Steele presented at the Emergency Department ("the ED") of the Royal Hobart Hospital ("the RHH") complaining of chest pain. At this time Registered Nurse, Ms Anne Barwick was the ED’s Nurse Co-ordinator. She reports:
"Mr Steele informed me he had ‘severe chest pain’ indicating his central chest, epigastric region through to the throat. I asked him what was the pain like, he again stated ‘severe’. I prompted him with words like dull/sharp/heavy etc. he told me ‘burning’, and he had had it for 2 days. I asked what he had been doing when the pain came on, he informed me ‘mowing the lawn’. I thought the pain was cardiac, I asked him if bending over made the pain worse as I was swayed by his description of ‘burning’, he immediately replied ‘yes’.
My opinion was the pain was reflux in nature; I informed the clerk I felt it would be okay to continue obtaining his details and to wait for the triage nurse. Mr Steele was pink, well perfused, he was not short of breath, he was not physically distressed, and his manner was calm. I did not take him aside and perform observations as I believed he was able to wait for the triage RN. I left the triage area and walked around the department to check on staff."
Approximately 15 minutes later Ms Barwick returned to the triage area and noted that Mr Steele had not been seen by the triage nurse. This concerned her. She then attempted to locate Mr Steele in and outside the ED. He had, however, left the premises.
Mr Steele had returned home. Ms Priest states that he arrived at their residence at between 9:00pm and 9:30pm. He told her of ‘the wait’ in the ED. He was complaining of indigestion and appeared very pale. He retired to bed at about 9:45pm.
At between 5.30 and 6.00am the following morning Ms Priest went to Mr Steele’s bedroom to deliver him a hot drink. However, she found him unresponsive in his bed. Ms Priest called for an ambulance and then commenced CPR which was maintained until the paramedics arrived. The attempts to revive Mr Steele were unsuccessful and he was declared deceased at 6:45am.
State Forensic Pathologist, Dr Christopher Lawrence carried out a post-mortem examination of Mr Steele. He reports that in his opinion the cause of death was acute myocardial infarction due to triple vessel atherosclerosis. Dr Lawrence’s examination made these findings specific to the heart:
"a. 50% stenosis of the left main coronary artery.
b. 70% stenosis of the left anterior descending coronary artery.
c. 90% stenosis of the circumflex artery with recannalisation.
d. 90% stenosis of the right coronary artery with recannalisation.
e. Pallor of the postero-lateral wall."
In his report Dr Lawrence makes these further comments:
"Autopsy reveals an enlarged heart (540 g) with severe triple vessel atherosclerosis…
In retrospect it would appear that he was having either unstable ischaemic heart disease or an early infarct when he attended the Department of Emergency Medicine and probably should have been admitted at that time. Given the radiation of the chest pain and the history that it was associated with mowing the lawn he should probably have been classified as a category 2 patient rather than a category 3 patient. He may have had some ischaemic symptoms when he saw Dr Welch.
It can be difficult to distinguish between pain due to heart disease and gastro-oesophageal reflux (heartburn). Mr Steele had evidence of both gastro-oesophageal reflux and severe narrowing of the coronary arteries. He had undergone a Sestamibi cardiac perfusion scan earlier this year which was negative. His earlier ECGs were normal as was an earlier gastroscopy."
Investigation of the circumstances of Mr Steele’s death has revealed that:
His general medical practitioner was Dr Michael Welch;
On 2 August 2007 Mr Steele attended Dr Welch with atypical chest pain in association with a history of severe work related stress. He was referred for an ECG monitored stress/rest sestimibi myocardial perfusion scan but he cancelled the appointment before the scan was performed;
When Mr Steele attended Dr Welch on 1 April 2008 with urinary symptoms he was re-encouraged to undergo the scan. It was carried out by Nuclear Medicine Physician, Dr Robert Ware on 9 April;
Dr Ware reported the results of the scan as follows;
"…this patient does not demonstrate significant myocardial perfusion reserve abnormality. Therefore his symptoms are very unlikely to be caused by significant areas of myocardial ischaemia and he is unlikely to have significant coronary artery disease. The study findings are also compatible with a favourable prognosis, a prognosis equivalent to that seen in patients with normal coronary arteries on coronary angiogram;"
At this time Dr Welch did not consider a coronary angiogram warranted given the report provided by Dr Ware and the fact that to this point Mr Steele had reported only one episode of chest pain and it had, in his opinion, been atypical for cardiac-related pain;
On 12 November 2008 Mr Steele attended Dr Welch complaining of several weeks of increasing lower retrosternal burning pain that radiated up retrosternally and increased especially when supine. Dr Welch did not record any typical cardiovascular ischaemic symptoms and his cardiovascular system was normal to clinical examination. A diagnosis of reflux oesophagitis was made and an appointment arranged for a gastroscopy. However, Mr Steele later cancelled this appointment without reference to Dr Welch.
The RHH reports that at the time of Mr Steele’s presentation to the ED it did not have in place a specific protocol for the management of patients attending with chest pain and Mr Steele was instead assessed by reference to general triaging guidelines. It further reports that the circumstances of Mr Steele’s death were the subject of investigation by a Serious Incident Panel. The Panel made these recommendations:
"1. The RHH ED undertake an education program which includes the assessment and documentation of patients presenting with chest pain;
2. A chest pain protocol will be developed, implemented and made available on the intranet; and
3. The chest pain protocol will be developed in consultation with the ED and the Department of Cardiology and General Medicine."
RHH has acted on the Panel’s recommendation and has devised and adopted a specific protocol for the management of patients presenting with chest pain. Had the protocol been in place at the time of Mr Steele’s attendance he could have expected an immediate medical assessment followed, within 10 minutes, by an electrocardiogram.
In the course of this investigation inquiry was made of Dr Ware concerning the apparent failure of the scan performed by him seven months prior to death to detect Mr Steele’s coronary artery disease. Dr Ware has advised in a written report:
"Myocardial Perfusion Scan is a very accurate diagnostic test in relation to coronary artery disease with a sensitivity for haemo-dynamically significant disease of the order of 90%, and a specificity of the order of 80%."
A colleague of Dr Ware’s undertook a review "in a blinded fashion" of Mr Steele’s scan results and she agreed with his interpretation of the data.
It appears highly probable that at the time of his scan Mr Steele had coronary heart disease and the "lack of significant perfusion abnormality at the time of this scan suggests that none of (sic) coronary lesions detected at the time of post mortem where(sic) causing significant net disturbance of myocardial perfusion" at the time of the scan.
"The limitations of current diagnostic technologies and therapies for coronary artery disease are significant, especially with regard to minimizing the possibility (sic) future adverse events. This emphasizes a need for caution especially when the clinical situation alters from the time of prior assessment."
Findings & Comments :
I am satisfied that a thorough and detailed investigation has been carried out into the death of Mr Steele and that there are no suspicious circumstances.
I accept the opinion of Dr Lawrence and find that Mr Steele died as a consequence of ischaemic heart disease due to triple vessel atherosclerosis.
It is regrettable that Mr Steele left the ED on 14 November 2008 before he was medically examined. Such examination, along with appropriate testing would, in all likelihood, have identified his underlying cardiac condition as the source of his symptoms and led to life-saving medical intervention.
It is also regrettable that the RHH did not have in place in November 2008 a specific protocol for the triaging and management of persons presenting with chest pain. It is noted that as a consequence of its own investigation into the circumstances of Mr Steele’s death that the RHH has devised and implemented an appropriate protocol thus minimising the prospect of future patients with chest pain "falling through the cracks" as occurred to Mr Steele.
The failure of the Myocardial Perfusion Scan undertaken by Dr Ware to identify the existence of Mr Steele’s coronary artery disease serves as a reminder that such scans and all other current diagnostic tests and procedures have their limitations and cannot be relied upon with certainty to detect disease or to form the basis for the prediction of future adverse events. This makes it imperative for treating practitioners not to be overly reliant upon test results and to be ever alert to changing clinical signs, especially when managing patients for whom cardiac disease is a possible diagnosis.
I conclude by conveying my sincere condolences to Ms Priest and to Mr Steele’s family.
DATED : Tuesday 19 May 2011 at Hobart in the State of Tasmania.