Record of Investigation Into Death

Coroners Act 1995
Coroners Regulations 1996
Regulation 14
Form 4

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 M

WITHOUT HOLDING AN INQUEST

Find That :

Mr M died in December 2007 at the Royal Hobart Hospital ("the RHH") in Hobart.

Mr M was born in Hobart and was aged 36 years. At the time of his death he was divorced and on a Disability support pension.

I find that Mr M died as a result of the combined effects of mixed drug toxicity (propranolol, venlafaxine, nortriptyline) and an aberrant cardiac conduction pathway.

At the time of his death Mr M was in the care of medical practitioners at the RHH.

Events on the day of death

Mr M was at the time of his death staying with his mother and her husband at their residence in southern Tasmania. Mrs M reports that in the late morning of 26 December her son called out for her and her husband "to come and hold him down because he was shaking uncontrollably." They both attended him in his room. When the shaking eased an ambulance was called. It arrived promptly. Mr M as conveyed to the Department of Emergency Medicine (DEM) at the RHH.

The ambulance arrived at DEM at 1.22 pm. The ambulance officers were Damian Crump and Simon Butterley. Mr M was wheeled into DEM on a stretcher. Mr Butterley spoke to the triage nurse and the decision was taken for Mr M to wait in the waiting room. At this time Mr Crump was observing Mr M on the stretcher. He reports; "At this stage he was pretending to be asleep. While I was watching him I noticed that he would glance from time to time to check what was going on. This further convinced me that this was a behavioural problem, rather than neurological in nature." Mr Crump told Mr M that he would need to walk to the waiting room and Mr M accepted this. Mr Crump then went to assist him to sit up on the stretcher at which time he "forcefully (threw) himself on to the floor." Mr Crump reports that Mr M landed heavily but appeared unhurt. He then "began jerky movements on the floor" which Mr Crump considered to be a "pseudo seizure." After a discussion with the medical officer in charge the decision was taken to place Mr M in the seclusion room. A mattress was obtained and Mr M was helped onto it. It was then dragged into the seclusion room. This was at 1.36 pm. Mr M was then left. His vital signs had not been taken contrary to a direction of the medical officer.

The DEM's seclusion room is monitored by CCTV cameras. Initial footage shows Mr M raising his head and moving his feet on several occasions. However, at about 1.42 pm he is shown to be motionless and face down on the mattress. At 1.53 pm a doctor, nurse and security guard all entered the room to check on him. It is at this point that Mr M is discovered to be in cardiac arrest. Attempts were made to resuscitate Mr M but they were unsuccessful. He was declared deceased at 2.23 pm.

Post mortem examination

A post mortem examination was undertaken by Forensic Pathologist, Dr Donald Ritchey. It did not indicate an apparent anatomic cause of death. Toxological testing of blood samples revealed the presence of propranolol, nortriptyline and venlafaxine, all in greater than therapeutic concentrations, plus a sub-therapeutic level of diazepam. Forensic Scientist, Andrew Griffiths makes these specific comments upon the toxological findings;

Dr Ritchey also reviewed Mr M's medical records from the RHH and noted "multiple electrocardiograms from 2004 that demonstrate an aberrant re-entrant pathway between the upper and lower chambers of the heart. These aberrant pathways can cause cardiac arrhythmias leading to sudden death." Dr Ritchey also comments that "propranolol and nortriptyline are especially cardiotoxic in individuals susceptible to cardiac arrhythmias" and "the combination of nortriptyline and venlaxafine may produce the serotonin syndrome, an adverse drug reaction producing mental status changes, autonomic hyperactivity and neuromuscular abnormalities."

After his consideration of all the relevant material Dr Ritchey has expressed the opinion that the cause of Mr M's death was the combined effects of mixed drug toxicity (propranolol, venlafaxine, nortriptyline) and aberrant cardiac conduction pathway, with the mechanism of his death being cardiac arrhythmia.

Mr M's personal and medical history

Mrs M has provided a detailed personal history of her son. His secondary schooling was undertaken at New Town High. He was then trained as a baker at Banjos Bakery. He first married in 1989 when he was aged 18. The marriage was short-lived and its ending coincided with Mr M having a brief admission to the psychiatric unit at the RHH. In about 1992 Mr M married again but the marriage ended in late 1996. There were children from the marriage. From 1997 to 2005 Mr M held various positions as a baker in the Northern Territory and King Island. During this period he suffered a broken ankle and also complained of back pain. He was noted to have "a drinking problem." In about 2005 Mr M operated a "hobby shop" at Mangalore. His mother was aware that at this time he was continuing to drink and was "taking a cocktail of medication for his back complaint." She believes that it was also about this time that she became aware that her son was consulting a psychiatrist for a psychiatric condition which was being treated with medication. Too, she became aware that "S was having blackouts."

In December 2006 Mr M went to King Island to stay with friends. In November 2007 Mrs M received a phone call from one of those friends saying that her son had been suffering "bad seizures" and was in hospital. She travelled to King Island and "brought him home." She says that a doctor in King Island had arranged for Mr M to see a medical specialist in Burnie later in December and also separate arrangements were in place for him to have an MRI in Hobart in the New Year.

A review of Mr M's records reveals a complex medical history. From about 2001 he complained of chronic back pain. In September 2005 he began consulting psychiatrist, Dr David Weidmann. He was described at this time to have "severely depressed mood, highly distressing global insomnia, anergia, anhedonia, thoughts of suicide, poor appetite (in the face of weight gain), severe chronic pain." It was noted that "There was a past history of amphetamine abuse and steroid abuse. There was a current history of alcohol abuse." Some time in early 2006 Dr Weidmann prescribed nortriptyline at doses of 200mg per day and later that year he added venlafaxine, initially 150mg per day then increasing to 300mg per day. In late August 2006 Mr M was admitted to the Department of Psychological Medicine at the RHH for suicidal thoughts. Seizure activity was noted at this time but was described as "more histrionic tantrums, ? Attention seeking." Mr M had his last consultation with Dr Weidmann on 15 December 2006 when his treatment with venlafaxine and nortriptyline was confirmed.

In January 2006 Mr M had been diagnosed with Type 2 Diabetes.

After moving to King Island Mr M's medical care was overseen by Dr Anil Cheeti. He had multiple admissions to the King Island District Hospital. He first was admitted for hypoglycaemia and later for depression and alcohol abuse. Beginning in November 2007 he had several admission for seizures. These admissions followed an examination by Neurologist, Dr Stan Seijka in August 2007 when an EEG examination was normal. It was queried at this time whether Mr M's seizures were related to his medication. This led to Dr Cheeti referring him to psychiatrist, Dr Catherine Stringer. She reported to Dr Cheeti that she did not consider there was a need to change the medications although she made the suggestion that the serum nortriptyline level should be checked to ensure that the dose was not too high. Dr Stringer again saw Mr M on 6 December 2007 after he'd been admitted to hospital following a seizure at home. In her assessment made at that time Mr M "had suffered a seizure as a combined result of having stopped high dose Gabapentin medication suddenly and consumed alcohol with his other medications." Of relevance is this comment made by Dr Stringer in her report; "Of more concern was Mr M's tendency to take medications in ways other than those prescribed, as suggested by his history of drug abuse, his self reported sudden cessation of gabapentin, his continued alcohol use, his drug seeking behaviour and his lack of openness in giving the history. Mr M also reported suicidal ideation and had a history of self injury. He denied any active suicidal intent when I interviewed him. However, his behaviour fluctuated, and it is possible that self destructive impulses may have resulted in him taking higher than the prescribed doses of his medications."

Before Mr M left King Island Dr Cheeti had made an appointment for him to see consultant physician, Mr Raymond Wilson in Burnie. That appointment was later in December. Mr Wilson subsequently reported to Dr Cheeti that Mr M's "main concern is unusual turns or seizures which became troublesome one month ago, possibly because he had ceased Gabapentin 1200mg TDS which he has for low back pain." Mr Wilson concluded; "I have requested an MRI scan to be performed at Hobart……..He was advised to continue with Gabapentin and I hope he can avoid alcohol and other substance abuse."

Investigation post death

At the time of Mr M's death Clinical Professor Anthony Bell was the Deputy Director of Medical Services at the RHH. He reviewed the medical records and has provided two reports which incorporate a clinical history of Mr M and an explanation of the probable cause of his death. The following matters are highlighted in the clinical history:

• "Review of the medical records from June 2004 revealed repetitive themes of admission. Mr M had long-standing psychological and psychiatric problems, usually diagnosed as bipolar disorder. This was complicated by drug and alcohol abuse. The alcohol abuse appears to have resolved by 2006."
• "Mr M suffered from Charcot-Marie-Tooth syndrome. This syndrome is an hereditary motor sensory neuropathy (HMSN), also known as Charcot-Marie-Tooth (CMT) disease. The disease is a spectrum of disorders caused by a specific mutation in one of several myelin genes resulting in defects in myelin structure, maintenance, and formation…….Affected patients typically present in the first decade or early second decade, but infants may be symptomatic. Early complaints may include frequent sprained ankles caused by distal muscle weakness or difficulty running and keeping up with peers."
• "Mr M suffered chronic back pain and was under the treatment of the chronic pain team at the RHH. He was diagnosed as a diabetic in 2006 and was under the care of the endocrinology team."
• "Possible seizure activity was thought to be either the serotonin syndrome or seizure activity related to the drugs for treatment of his psychological condition."
• "Serotonin syndrome is a potentially life-threatening condition associated with increased serotonergic activity in the central nervous system (CNS). It is seen with therapeutic medication use, inadvertent interactions between drugs, and intentional self-poisoning."
• "On the presentation to the RHH Emergency Department on 26/12/2007, Mr M presented with typical complaints as per previous admissions."

Clinical Professor Bell has also offered the following comments relevant to the cause of death:

• "I have examined the medical records and electrocardiograms from 8/6/2004 and 24/2/2005. These electrocardiograms, were strongly suggestive that Mr M had Wolff-Parkinson-White (WPW) syndrome."
• "Both Wolff-Parkinson-White (WPW) syndrome and other forms of supraventricular tachycardia (SVT) can cause sudden cardiac death (SCD)."
• "In this case the patient may have had the seratonin syndrome associated with autonomic nervous system dysfunction. This may have precipitated the arrhythmia that lead to Mr M's death. This appears to be the most likely cause of his death."

Following Mr M's death a Serious Incident Panel was convened by the RHH to investigate its circumstances. I am informed that this investigation led to the following recommendations:

1. "That a complete review of the use of the Emergency Department (ED) seclusion rooms is undertaken;
2. Formulation of clear guidelines outlining the responsibility of security staff in providing direct supervision for any patient placed in a seclusion room in the Emergency Department. In particular patients under Initial Order.
3. Development of guidelines for the handover of patient information by Tasmanian Ambulance Service (TAS) Officers to the primary ED nurse/s allocated to a patient, prior to the TAS leaving the ED."

I am further informed that the following action has been taken in respect of the Panel's recommendations:

"Recommendation 1: Guidelines are now in place for seclusion of patients in the ED under the Mental Health Act. Orientation provided by Clinical Nurse Educators now informs new staff of the need to undertake vital signs on patients in seclusion rooms (where possible). Implementation of a Mental Health Nurse in the ED…has improved the safety of patients managed in seclusion rooms - one of the core skills is a set of vital signs on all patients in the seclusion rooms. It has become accepted standard practice by all nursing staff.

After patients are sedated in the seclusion cubicles, they are subsequently managed as medical patients, including transfer to a general cubicle, close observation and full monitoring.

Physical layout - Facilities Management were consulted about potential changes to layout of seclusion rooms. The development of guidelines has removed the need for structural changes.

New mattresses have been installed which are higher off the ground, making patients more visible from door/windows.

Recommendation 2: Changes have been made to operating procedures for security staff - they initially watched CCTV screens to observe areas in the ED. They are now stationed outside the seclusion rooms and have direct sight of patients in seclusion rooms.

A survey was completed to audit ED and security staff knowledge.

In addition, there are clear guidelines for nursing for management of patients secluded under the Mental Health Act in seclusion rooms (i.e. Initial Order.)

Recommendation 3: The TAS and ED staff were consulted through the process of the National Clinical Handover Initiative. As a result, we have developed a clinical handover form, which is used for all patients in the ED. There is a section on this form for ambulance staff to sign when handover has been given to ED staff. This information is on the form and accessible throughout the patient¡¦s stay in ED and ultimately forms part of the patient record.

The process has been clarified between TAS and ED - all parties acknowledge that clinical handover occurs when TAS hand over to the responsible nursing staff member in the main area (triage does not indicate clinical handover). The exception to this rule (in case of need for urgent release of TAS staff prior to formal handover) is covered in the ED Overload Policy."

Professor Gregory Petersen is the Professor of Pharmacy and Head of School of Pharmacy at the University of Tasmania. He has provided an opinion upon the pharmacological aspects surrounding Mr M's death, most notably his prescribed dosages of nortriptyline (200 mg per day) combined with venlafaxine (300 mg per day). Professor Petersen makes these observations:

• Mr M was receiving high dosages of both nortriptyline and venlafaxine. He notes that doses of the former drug greater than 100 to 150 mg per day are generally not recommended. Further, most guidelines do not recommend doses of the latter drug greater that 225 m/g per day although others acknowledge that a dose greater than 350-375 mg per day may be needed for the severely depressed.
• That antidepressants aren't recommended for patients with a history of seizures.
• That antidepressants should be used with caution for patients with a known history of cardiac disease or cardiac arrhythmias.
• That the levels of nortriptyline and venlafaxine reported after toxicology could not be explained by the high prescribed dosages alone and raise the possibility "that there has been an overdose, either intentionally or by mistake."
• That Mr M's history of seizures represented "significant alarm signs" and warranted a reconsideration of his medications by all health professionals involved in his care.
• That while there is a risk of serotonin syndrome when nortriptyline and venlafaxine are combined, "I believe that serotonin syndrome is not the major issue in this case."
• That "it is very likely, as concluded in the Forensic Pathologist¡¦s report, that the cause of death was cardiac arrhythmia in someone with a pre-existing conduction abnormality and exposed to very high blood levels of nortriptyline, in particular, and venlafaxine."

Findings and Comments :

I am satisfied that a thorough and detailed investigation has occurred into the death of Mr M and that there are no suspicious circumstances.

I accept the opinion of Dr Ritchey and find that Mr M died as a result of the combined effects of mixed drug toxicity (propranolol, venlaxafine, nortriptyline) and aberrant cardiac conduction pathway.

It is clear upon the evidence that Mr M, for all of his adult life, suffered from a range of medical ailments, both psychological and physiological. I accept that his medical management presented a significant challenge for all of his treaters.

It is my opinion that this investigation has revealed a number of factors which have conspired to bring about this unfortunate death.

First is the high levels of nortriptyline and venlafaxine detected in Mr M's post-mortem blood, levels which I am satisfied exceeded the levels which could have been anticipated if the prescribed dosages only had been taken. These elevated drug levels, in my view, increased the likelihood of cardiac arrhythmia. I need to observe at this point that there is no evidence that Mr Mx took additional quantities of these drugs with the intention of causing himself self harm and I conclude that the overdosing was accidental on his part.

A second factor was the failure to recognise that Mr M was suffering from a cardiac condition, probably Wolff-Parkinson-White syndrome, which made him vulnerable to cardiac arrhythmia. If Dr Weidmann had been aware of this condition it is unlikely that he would have prescribed the venlafaxine and nortriptyline as these drugs are contra-indicated for patients with cardiac ailments.

Another factor was the failure to cease Mr M's use of both venlaxafine and nortriptyline when his seizures began to present and to desist from using these drugs until the cause of the seizures was clearly established. However, I recognise that the decision to cease using these drugs had to be weighed against the need to maintain Mr M's psychological health and that the ongoing use of these drugs may have been the best of two evils.

A fourth contributing factor was the failure to check Mr M's vital signs prior to him being placed in the seclusion room at the RHH. It is possible that this check would have indicated a cardiac irregularity which required immediate medical attention.

The final factor relevant to this death was the failure to attend Mr M in the seclusion room in the eleven minute period after he became motionless. More timely attention at this time would have increased the prospect of successful resuscitation.

I acknowledge the steps taken by the RHH in response to the recommendations of its Serious Incident Panel and accept that they are likely to reduce the risk of other deaths occurring in the seclusion room.

I conclude by conveying my sincere condolences to Mr M's family.

DATED : 29 August 2011 at Hobart in the State of Tasmania.

Rod Chandler
CORONER