Record of Investigation into Death (Without Inquest)

Coroners Act 1995
Coroners Rules 2006
Rule 11

These findings have been de-identified by direction of the Coroner pursuant to S.57(1)(c) of Coroners Act 1995

I, Rod Chandler, Coroner, having investigated the death of

‘Mr H’



(a) The ‘deceased’, was aged 46, was married and self employed as an electronic technician;

(b) ‘Mr H’ died as a result of an hypoglycaemic episode;

(c) the cause of his death was hypoglycaemia due to the combined effects of poor oral intake and oral hypoglycaemic treatment for diabetes;

(d) ‘Mr H’ on 11 January 2009 at his residence in North West Tasmania.


In about 1995 ‘Mr H’ was diagnosed with Type II diabetes which he managed with diet and medication. He self-tested his blood sugar levels and had not previously suffered a hypoglycaemic episode. He was morbidly obese weighing in excess of 150 kg.

In the course of its investigation of this death Tasmania Police obtained a statement from ‘Mr H’s’ wife. In that document ‘Mrs H’ describes events in the months preceding her husband’s death in these terms:

"Over the six months before my husband passed away I noticed that he was getting a bit more run down and seemed more tired than usual. My husband was not working more than usual. About two weeks before Christmas he told me that he had a sore throat. He did not go to the doctor but told me that he thought that he might have a "quinsy" which is an old form of tonselitis which had had many years ago.

At about this time my husband went off his food because of the sore throat and was only eating small amounts of foods such as one wheet-bix, a quarter of a peace of toast and half a cup of tea. He wasn't hungry and was not eating regular meals because he felt generally unwell. He would try and drink but couldn't.

I told him repeatedly to go and see a doctor but he would not.

About two weeks before my husband died he was coughing up gunk and crap and often would not get out of bed until late in the afternoon. If he got up he would shower and shave and then sit on the couch in the lounge and do nothing which was unusal for him. My husband was still not eating a lot at this time. He did have some days where he appeared a bit brighter and you thought that he was getting a bit better. My husband was not leaving the house much at all.

I remember him saying that once before he had a "quinsy" and it had ruptured and that he thought that the same thing was happening this time. He still did not go and see a doctor.


After New Years my husband was not eating well still, he was having icecream, soft eggs or a cup of soup. He could not have juice because he said that the juice upset his stomach. He was still not having regular round meals just small bits and pieces. He wasn’t one to eat if he didn’t want to. I again told him to go and see the doctor but he didn’t.

About four or five days before my husband died he started vomiting and have diohera. He said to me that he felt like he had picked up a bug on top of what he already had. On Wednesday 7 January 2009 he said that he wanted to go with us when we went to Burnie to do some shopping. We went to the K-Mart complex and I left him in the car because he didn't think that he could walk down whilst I lay-byed the kids school bags. When I came back to the car, he was leaning out of the car vomiting into a bag. I took my husband straight home and told him that I wanted to take him to the hospital but he refused.

The vomiting and diohera was fairly constant with a lot of dry reaching when he wasn't vomiting. This was going on, on and off throughout the day and the night. As far I know my husband was still taking his medications whilst he was sick.

My husband's condition did not get better or worse over the next few days. On Saturday 10 January 2009 at approximately 3am we were in bed when I woke up because I heard my husband making noises. His eyes were fixed and staring into nothing and he looked at me really stupid. I tried to get him to roll over and he vomited. I helped him out to the lounge and he slept out there. I asked him if we could go to the hospital or see the doctor but he did not want to."

On Saturday 10 January 2009 at about 5.00pm the Tasmanian Ambulance Service ("TAS") was called to ‘Mr H’s residence after he was found by his children ‘making stupid noises.’ ‘Mr H’s’ blood sugar level (BSL) was 1.5 mmol/L which is considered to be very low, (normal levels are in the range of 3.5 to 8mmol/L). He responded to treatment with intramuscular glucagon and intravenous dextrose (50%) and was then transported to the North West Regional Hospital (NWRH) at Burnie.

On arrival at the NWRH ‘Mr H’ was able to walk into the Emergency Department ("the ED"). His initial BSL was 6.5 mmol/L. His medical records indicate that he had three sets of clinical observations taken at 5.52pm, 6.35pm & 6.40pm. Throughout ‘Mr H’s’ blood pressure remained low, initially being recorded at 95/53 and later at 93/50 after a re-test when it showed 87/53.

‘Mr H’ was seen by Dr Behdin Abed-Haghighi. Dr Brian Doyle was the Director of the ED and Dr Abed-Haghighi was working under his supervision. ‘Mr H’ was considered to have suffered an hypoglycaemic episode, most likely related to poor oral intake combined with his oral anti-diabetic medication. He was provided with sandwiches to eat which he tolerated. He was observed for an hour and remained well.

‘Mr H’ was discharged home at 7.00pm. At this time his BSL was recorded at 4.2 mmol/L. ‘Mrs H’ was instructed to return her husband to hospital if any further problems arose and to follow up with his general practitioner should his other symptoms (cough and diarrhoea) not settle. She was also advised to take her husband’s BSL at regular intervals.

‘Mrs H’ reports that when they arrived home her husband was very lethargic and he took about ten minutes to exit the car. At 10.00pm she tested her husband’s BSL and it recorded 2 mmol/L. ‘Mr H’ was then given some sugar on a spoon and some jelly beans. He refused to eat a sandwich and went to bed.

‘Mrs H’ awoke at about 12.34am. Her husband was making unusual sounds and ‘breathing funny.’ He could not be roused. He was blue in colour and his skin was clammy. His BSL was recorded at 1.0 mmol/L. ‘Mr H’ was given some sugar and juice which he appeared to swallow. ‘Mrs H’ telephoned the hospital for advice. TAS was summoned. However, when the ambulance personnel arrived ‘Mr. H’ was in cardiac arrest. Resuscitation efforts were unsuccessful and he was declared deceased at 1.45am.

Pathologist, Dr Terry Brain carried out a post-mortem examination. His report was reviewed by State Forensic Pathologist, Dr Christopher Lawrence. Dr Lawrence has reported;

"Dr Terry Brain performed the autopsy. He found a man with a body mass index of around 40 kg/m2 which is in the morbid obese range. There was moderate cardiomegaly…..

Based on the information supplied to me by the records and by Dr Brain's report I would conclude that the cause of death is 1(a) Hypoglycaemia I (b) Due to combined effects of poor oral intake and oral hypoglycaemic treatment for the diabetes...

In my opinion the hypoglycaemia has played a central role in the death and it is likely that the prolonged hypoglycaemia was a consequence of both his poor oral intake and the medications, in particular the sulfonylurea which has long lasting effects and the Metformin which appears to have been present in higher than normal therapeutic levels.

I recommend that this case be reviewed by an experienced diabetic physician to ascertain whether the medical treatment, particularly the decision to allow him to go home played a significant role in the death and what could have been done to prevent this outcome."

Associate Professor Tim Greenaway is the Clinical Director of Diabetes and Endocrine Services at the Royal Hobart Hospital. He has provided reports incorporating his opinion upon ‘Mr H’s’ management by NWRH. Those reports include these comments;

"…… way of introduction it is important to note that an episode of severe hypoglycaemia (such as that suffered by ‘Mr H’ prior to his death) is a clinical red flag and mandates careful assessment, further investigation and adjustment of the patient's treatment regime. In particular, the likelihood of further significant hypoglycaemia is high and careful screening for this is mandatory

At a minimum, ‘Mr H’ should have had investigations performed to exclude conditions significantly associated with an increased risk of hypoglycaemia. In particular, as indicated in my initial report, I believe it highly likely that his intercurrent illness had resulted in acute deterioration in his renal function (known to be impaired secondary to diabetic nephropathy) which would have resulted in altered pharmacokinetics of glimepiride and increased likelihood of hypoglycaemia. A screen of his renal and liver function together with investigations to exclude sepsis, such as a full blood count, blood and urine cultures, should have been performed. These investigations are widely available and the results with the exception of the final blood and urine cultures could have been accessed with minimal delay. Whilst the oral ingestion of rapidly acting carbohydrate (approximately 20 g) followed by complex carbohydrate (for example the ingestion of a sandwich) is appropriate in a conscious patient with hypoglycaemia, ‘Mr. H’'s continued hypotension and falling blood sugar at the time he was allowed to leave hospital should have resulted in action by the Emergency Department staff. I believe that intravenous access should have been obtained and parenteral fluid therapy (possibly including glucose) commenced pending the results of the investigation listed above. At the very minimum, specific instructions should have been given to ‘Mr. H’ and his family with respect to his increased risk of further hypoglycaemic episodes and the importance of avoiding these. His management regime should have been altered. Glimepiride should have been ceased and a protocol for regular blood glucose monitoring by the patient instituted. Early physician review of his treatment regime should have been arranged. It would also have been appropriate to instruct his wife regarding parenteral glucagon administration should further severe hypoglycaemia have occurred.

These measures could and should have been implemented by the Medical Staff of the (NWRH’s Emergency Department). Such investigation and treatment is standard practice and not the province of tertiary referral centres."

As part of this investigation reports were also sought from Dr Doyle and from Dr Dean Powell, the Acting Director of Emergency Medicine at the Royal Hobart Hospital. Dr Doyle’s reports include these observations;

"It was thought that (‘Mr. H’s) hypoglycaemic episodes related to his decrease in oral intake. We did consider his other symptoms and did not feel that further diagnostic testing was indicated at the time in the ED. In the department, he demonstrated ability to tolerate oral intake. He was observed for about 1 hour and remained well. Prior to discharge, his BSL was 4.2. It was thought that this should actually increase since he had just ingested two sandwiches."

"There are a multitude of prospective clinical decisions made in the Emergency Department every day. It is not possible, feasible nor in the best interests of patients to perform formal investigations regarding every clinical decision made. By definition, clinical decisions are fallible but should be judged in the prospective clinical context keeping in mind what constitutes standard practice."

"I very much respect and appreciate the expertise provided by Associate Professor Greenaway…..but I have highlighted some concerns about what constitutes standard practice in Emergency Departments. ….. overall, the vast majority of patients presenting to an ED with severe hypoglycaemia do well and are discharged home… Specific protocols and policies regarding the mandated management of patients with hypoglycaemia do not exist in the major public ED’s in Tasmania.

"…..unrecognised renal failure was the most likely the (sic) contributing factor" and "In retrospect and knowing the ultimate outcome, I would have made different decisions..."

Dr Powell, having reviewed the relevant material has concluded that had ‘Mr. H’ been his patient he would have taken the decision either to admit him or at least to have observed him for a longer period. In his opinion ‘Mr. H’s profoundly low BSL’s for a person being treated with only oral hypoglycaemics and his persistently low blood pressure were matters of concern which warranted further investigation. However, he tempers his opinion with these comments;

"The above outline is of the considerations I believe I would have had if this patient had been mine. However, neither of the doctors looking after Mr. Heazlewood should be compared against this as a standard. Dr. Abed-Haghighi is not an emergency specialist, and likely not even training to be an emergency specialist. While he had the most information about this man, he does not yet have the training and experience to apply it in the way that I would. Dr. Doyle, whilst being an emergency specialist, was also not in possession of the knowledge that I have in looking through the notes and had to base all his decisions upon what he was told by the junior doctor and the patient in a brief contact. It has taken several specialists some hours of considered opinion, with access to results from sources other than those available at the time, to determine a "right" way to manage this man, but doubtless Dr. Doyle, as the single Emergency specialist on for that shift, was trying to make the safe decisions for several junior doctors, all seeing many patients simultaneously on a Saturday afternoon. He had several minutes only to come to what he felt was a safe plan, and probably had several other things on his mind at the same time. There is simply not time in modern Emergency Departments to search out all available information prior to a decision, and often as the most senior clinician, disposition decisions come to us. This is not our only priority among the many tasks, so the time available is short and we are largely dependent on the information we are told.

Lastly, I have surveyed other colleagues in Emergency practice here in Hobart regarding their approach to hypoglycaemic adults, and those approaches vary. Some would have done some basic investigation and observed, others would simply have observed longer and others would have allowed him to go with family once he was feeling well and had a normal level."

Comments & Recommendations:

It is self evident from the history that I have set out above that ‘Mr. H’ was permitted to prematurely leave NWRH’s Emergency Department and return home in the evening of 10 January. Had he remained in hospital for a longer period and been subject to close monitoring and to more intensive investigations then it is likely in my view that the seriousness of his condition would have become evident and life-saving treatment put in place. These matters give rise to the question whether the decision to permit ‘Mr. H’ to go home without further monitoring and/or investigation was, in all the circumstances, a reasonable one?

‘Mr. H’ presented to the Emergency Department with a history of having been unwell for at least the previous two weeks. During his time at hospital ‘Mr. H’ had ongoing hypotension and declining blood sugar levels. These factors together, in my view, required a cautious approach to be taken to his management and care. This necessitated, in the least, ‘Mr. H’ being monitored in hospital until the decline in his blood sugar levels was reversed and stabilised. Had he stayed a little longer in hospital it would have soon become apparent that the expected elevation in the blood sugar levels as a consequence of the ingestion of the sandwiches was not going to occur thus firmly establishing the need for his admission and further investigation. In these circumstances the decision to permit ‘Mr. H’ to go home at about 7.00pm on 10 January 2009 was a regrettable misjudgement.

It is clear from the evidence of ‘Mrs. H’ that her husband had been suffering from declining health over an extended period, most particularly in the two weeks prior to his death. It is clear too that ‘Mr. H’ resisted his wife’s repeated advice to seek medical help. Had he done so it is likely, in my view, that his deteriorating renal condition would have been detected and treatment commenced which in all probability would have avoided his later hypoglycaemia and its tragic consequences. ‘Mr. H’’s death is a reminder of the need for sufferers of diabetes in particular to seek timely medical treatment when signs or symptoms of unwellness present.

I conclude by conveying my sincere condolences to ‘Mr. H’s family.

DATED : 17 December 2010 at Hobart in Tasmania.


Rod Chandler