Record of Investigation Into Death (Without Inquest)
Corners Act 1995
Coroners Rules 2006
Rule 11
I, Rod Chandler, Coroner, having investigated the death of Ian Douglas Johnson.
Find:
(a) the deceased is Ian Douglas Johnson born 21 September 1958 and aged 52 years;
(b) Mr Johnson died on 8 May 2011 at Smithton; and,
(c) the cause of his death was pulmonary thromboembolism. Other significant contributing factors were ischaemic heart disease and recent coronary artery angioplasty and stenting.
Circumstances:
1. Mr Douglas was married to Patricia Annette Johnson. They had 2 children. They resided at 18 Carnac Court in Smithton.
2. In December 2010 Mr Johnson became unwell. He was breathless and had a persistent tickle in his throat. He consulted his general practitioner and was prescribed antibiotics for a presumed chest infection. He was also given asthma medication for use via a puffer. He continued to periodically consult his doctor. On 11 January 2011 he had a chest x-ray which was normal. An electrocardiogram (ECG) on 18 February was also normal. On 30 April 2011 he again saw his doctor with shortness of breath on exertion and associated with pressure across his chest. He was referred for admission to the Smithton Hospital. At this time his ECG was abnormal and his troponin level consistent with myocardial injury. When reviewed the following day his episodic shortness of breath with chest tightness was ongoing. His troponin level was still elevated and the ECG remained abnormal. It was decided to transfer him by air ambulance to the Launceston General Hospital (‘the LGH’).
3. Mr Johnson arrived at the LGH at 8.12pm on 1 May 2011. He was admitted to the Coronary Care Unit. The treating cardiologist was Dr George Koshy. A diagnostic coronary angiogram was undertaken on 2 May 2011. It disclosed severe coronary artery disease with left ventricular dysfunction. An angioplasty was performed and 2 stents were placed in the right coronary artery. A further angioplasty was undertaken on 4 May 2011 and more stents were placed. On the same day Mr Johnson had a bedside echocardiogram. It revealed a dilated and hypertrophied right ventricle with marked hypokinesis, a dilated right atrium and right ventricular systolic pressure estimated at 70mmHg.
4. On 5 May Mr Johnson was ‘trialled’ off supplemental oxygen and his oxygen saturations dropped to 82-88%. He became anxious so supplemental oxygen was again administered. Later in the day nursing staff noted Mr Johnson to be short of breath on exertion. The following day he was again noted by nursing staff to still be short of breath on exertion. He was reviewed by the cardiology team. It was considered that his underlying heart condition was possibly cardiomyopathy and required follow-up in 2 to 3 months. He was discharged home in the afternoon of 6 May 2011.
5. On the following day Mr Johnson experienced chest pain after some exertion when helping a friend try to start a chain saw. He was taken by ambulance to the North West Regional Hospital where he was assessed and then transferred by ambulance to the LGH. He arrived at about 11.00pm. He was kept in the Emergency Department (‘the ED’) overnight where his clinical observations were monitored and were basically stable although it was noted that his oxygen saturation level was low at 89% on room air. ECG monitoring showed widespread T wave inversion and it was queried whether Mr Johnson’s presentation was due to an episode of ischaemic chest pain the day before. There is no report of further chest pain while in the ED.
6. 8 May was a Sunday. Mr Johnson was reviewed by the cardiology team at about 11.00am. It was noted that Mr Johnson had had no further chest pain and his ECG was unchanged. Although his troponin level was abnormal it had not elevated. It was determined that he would be discharged.
7. Mrs Johnson collected her husband from the hospital and took him home in the early afternoon. They arrived home at about 4.30pm. Not long afterwards Mr Johnson sat down in a chair and suddenly became unresponsive. Mr Johnson’s son performed CPR until paramedics arrived. However, the resuscitation attempts were unsuccessful and Mr Johnson died.
Post-Mortem Examination:
8. A post-mortem examination was conducted by the State Forensic Pathologist, Dr Christopher Lawrence. Dr Lawrence found a very large saddle pulmonary thrombo-embolus blocking both pulmonary arteries and that this was the cause of Mr Johnson’s death. His examination revealed evidence that suggested a smaller pulmonary thrombo-embolus may have been present for some days. According to Dr Lawrence, whose findings I accept, the breathing difficulties experienced by Mr Johnson prior to his death were probably due to the unrecognised pulmonary thrombo-embolus and not to cardiac ischaemia.
Investigation And Its Outcome:
9. The investigation of Mr Johnson’s death has included the following:
a) An inspection and summary of Mr Johnson’s hospital records carried out by Research Nurse, Ms Libby Newman;
b) Inspection of Mr Johnson’s general practice records;
c) Obtaining affidavits from Mrs Johnson;
d) The consideration of a report by Dr Koshy;
e) The consideration of a report made by cardiologist, Dr Shruti Kapila and supplied by Mrs Johnson’s legal advisers; and,
f) A comprehensive review undertaken by Dr A J Bell as medical consultant to the coroner.
10. Mrs Johnson is understandably concerned by the circumstances of her husband’s death, most particularly the failure to diagnose and treat his pulmonary embolism. It is this subject which has been the focus of my investigation.
11. It is plain that at the time of his first admission to the LGH Mr Johnson was suffering from significant coronary artery disease as shown by the coronary angiogram of 2 May. This was successfully treated by stenting, the final stents being placed on 4 May. However, it is also plain that despite this treatment Mr Johnson remained unwell. Why was this so? Was it because of his cardiac condition or was it because of a contemporaneous but unrelated condition?
12. Dr Bell advises me that in his view it was clear that at the time Mr Johnson was being treated for his coronary artery disease he was also suffering from pulmonary arterial hypertension. It is his further advice that this diagnosis should have been made by 4 May as there was ample information available by this time to unambiguously support the diagnosis. He points to the following:
• On 18 February 2011 Mr Johnson had an ECG, seemingly carried out by his General Practitioner which was reported as normal. (Dr Bell has sighted the ECG and confirms this interpretation.) However, subsequent ECGs taken at the Smithton Hospital on 30 April and in the days following at the LGH are all abnormal in two respects. Firstly, they show a right axis deviation well outside the normal range. For example the axis deviation shown on the ECG of 30 April is 124 degrees. This compares with the 64 degrees shown on 18 February and which is within the normal range. These contrasting readings are, Dr Bell advises, suggestive of right heart strain and are consistent with a diagnosis of either pulmonary arterial hypertension or pulmonary embolism. Secondly, those ECGs post 18 February consistently indicate a S1, Q3 and T3 pattern which again is suggestive of either pulmonary arterial hypertension or pulmonary embolism.
• That despite the treatment of his diseased coronary arteries Mr Johnson remained exertion intolerant and had oxygen saturation levels significantly below normal. These were signs suggestive that Mr Johnson was suffering a condition separate from his cardiac disease. They are also consistent with a diagnosis of either pulmonary arterial hypertension or pulmonary embolism.
• The bedside echocardiogram performed on 4 May reports a right ventricular systolic pressure estimated at 70mmHg, (the norm is 15 to 30 mmHg). This reading, on the advice of Dr Bell, is clear evidence of pulmonary arterial hypertension and by itself permits the diagnosis. This diagnosis is consistent with Mr Johnson’s ongoing symptomatology and explains the changes in the ECGs which are referred to above.
13. I accept the advice of Dr Bell and find that at the time of his first admission to the LGH Mr Johnson was suffering from pulmonary arterial hypertension. I accept too his advice that this diagnosis should have been made, at least by 4 May, when the echocardiogram results were known. It follows that in my view Mr Johnson should not have been discharged from the LGH without his pulmonary arterial hypertension being fully investigated and an appropriate treatment regime being put in place.
14. The diagnosis of pulmonary arterial hypertension mandates the investigation of its cause. This should ordinarily involve a ventilation perfusion lung scan and/or a CT scan pulmonary angiogram. Either procedure would, in all likelihood, have revealed that Mr Johnson was suffering from pulmonary arterial thromboembolism.
15. A diagnosis of pulmonary arterial thromboembolism necessitates immediate treatment with full-dose anticoagulation and monitoring in a hospital setting. I am advised by Dr Bell that absent anticoagulation a patient suffering from pulmonary arterial thromboembolism has a 30% risk of death. However, that risk significantly and quickly reduces so that after 72 hours of anticoagulation the risk of death is within the range of 2 to 6%.
16. It is regrettable that Mr Johnson was discharged home on 6 May without the diagnosis of pulmonary arterial thromboembolism having been made and treatment commenced. However, his re-presentation at the LGH the following day should, in my view, have alerted his treaters to the real possibility that his persisting signs and symptoms were not explained by his coronary disease, as previously believed, and that his diagnosis required a thorough reconsideration. Again regrettably this did not occur and he was sent home. In the result Mr Johnson was denied the final opportunity of the correct diagnosis being made and the benefit of anticoagulation, which even at that late stage may have avoided his death.
17. I am advised by the LGH that the circumstances of Mr Johnson’s death were the subject of review by its Department of Cardiology’s Mortality and Morbidity Committee and it was resolved that in future patients presenting with dyspnoea; ie respiratory distress on exertion, would undergo a CT pulmonary angiogram if clinically appropriate. This, in my view, is an appropriate resolution.
Comments & Recommendations:
18. It is not the function of a coroner under the Coroners Act 1995 to attribute moral or legal blame or responsibility for the death of a person. The coroner’s principal function is to investigate and find facts relevant to determining identity of a deceased person, when and where a death occurred, how a death occurred and the cause of death. I have decided not to hold an inquest into Mr Johnson’s death because the investigation which I have undertaken has sufficiently disclosed the identity of the deceased, the time, place, cause of death, relevant circumstances concerning the death and the particulars needed to register the death under the Births, Deaths and Marriages Registration Act 1999. I do not consider that the holding of an inquest would elicit any information further to that disclosed by the enquiries conducted. The circumstances of the death do not require me to make any further comment or to make any recommendations.
I convey my sincere condolences to Mr Johnson’s family.
DATED: 30 June 2014 at Hobart in Tasmania.
Rod Chandler
CORONER