NSW Coronial Inquest into the death of David Dungay
Deaths in Custody
Day 4 Wesnesday 07/03/2019
- Dungay died of Asystole (loss of oxygen eventually leads to the heart stopping beating and leads to cardiac arrest). He was depleted of oxygen primarily (rather than ventricular fibrillation or genetic causes) and there were numerous contributory factors to his premature death.
- There is no basis of a genetic predisposition relation to oxygen nor heart function
- Blood sugar levels swung to very high just before he died. Hypoglycemia can be life-threatening and can significantly add as a compounding deleterious effects to asystole.
- Death caused by asystole is confirmed ie heart stops due to lack of oxygen, and this occurred after he struggled with CSO
- ‘Chemical storm’ of three medications not the cause, but was likely to have affected his premature death by cardiac arrest as can increase cardiac dysrhythmia
- Medazolam as a substance was unlikely cause of death
- Clear signs that Dungay maintained a struggle, and the sudden nature of his death included hypoxia/asphyxia
- Head Concussion has not been ruled out was a possible factor – Neuro-pathologist report?
- Dungay’s neck being placed on the edge of the bed could have contributed to his death
- Autopsy Report confirmed ‘quite marked congestion to the head’ that is due to some kinds of pressure- cant report why . This congestion pertains to head/chest pressure stopping blood flow, that then stops heart beating and person dies of cardiac arrest.
- Autopsy Report considers cause as cardiac arrest due to hypoxia, and summarized as that any single, isolation of factors is not indicative of cause of death, however in combination, concluded is ‘maybe, uncertain’.
- Autopsy Report isolated various negative factors that may have caused or contributed to Hypoxia such as: pressure to body areas like the neck, bruising and haemmorages, dehydration, if he was beaten up, Ketone Acidosis.
Witness 1 – Consultant Cardiologist, Associate Professor Adams
Causes of death
Dr Adams presented his evidence in relation to the factors that may have been related to or caused the premature death of David Dungay. This included analysing ECG data, wthe effect of medication he was on, the timing of when hypoxia (the heart stopped beating) was likely to have happened. In particular, he considered the factors that could potentially have deleterious effect on the electrical conductivity of his heart and caused asystole to occur. The QT Interval is the normal expected time rhythm of the heart to contract and pump blood through, and the effect of some dysfunction of the heart is marked by an increase of the QT Interval .
Key matters related to the presence or likelihood of damaging effects to Dungay’s health with regard to his QT Interval including the likelihood of effects of: stress, and either internal – such as a genetic disposition, or medically induced causes – or externally induced hypoxia (reduced or insufficient oxygen)1.
He stated that the QT Interval can vary with Blood Sugar Levels, and that at 7 am on the day he died, BSL was 6.3 which is low but in OK limits. He noted there was a BSL swing from high to very high just before he died up to 20-25. It is ‘quite possible’ that his QT Interval would have increased with this swing.
He considered the potential of any genetic factors impacting, but concluded there were no indications of this in his or his family history, nor of him having any “Long QT Syndrome’, stating ‘Not suggesting at all that he had a genetic disposition – we don’t know’. ECG’s show he is unlikely to have had a genetic disposition.
Based on the 2 ECG’s he said we may have increased QT Interval simply from what we understand about the medications Dungay was on, and this was likely to have affected his premature death.
He summed up that rather than any initial problem of ventricular fibrillation, Dungay most likely suffered asystole (the heart stops beating) seconds before he loses consciousness. He noted a consistency in that when Mr Ma had found a ‘very weak pulse’ it was probably a short time to asystole.
Dr Adams explained why he thought it was likely that the arrhythmia did not start when Dungay was in the first cell but rather at a later stage, an important sign being his capacity to struggle eg sustaining a struggle with five guards, his labored breathing and shortness of breath as he said ‘I can’t breathe’, getting out of the leg lock, showing ‘amazing strength’. This indicated that the asystole occurred after the struggle, as he could not have had the capacity to struggle if it came beforehand.
Dr Adams also referred to the additive effects on increasing QT Interval due to medication, and described it as a ‘chemical storm’ that significantly would have increased the QT Interval, thus the struggle and the medication he received would have had a compounding effect.
He noted that there was food in the lungs indicative of aspiration of the stomach contents during resuscitation.
Also, he noted that congestion was in the lungs, rather than in the head. The Autopsy report showed ‘petachial haemorrages’ that can be present with prolonged straining, caused by some way that produced increased thoracic pressure that can stop the blood flow, such as congestion to the head and upper chest. These haemorrages can be caused by compression being applied to body during CPR, but he said there was no such resultant congestion was relevant to his thinking.
10:40 AM: Professor Adams in court
- Kept stuttering when talking about his death
- He had two theories for his death.
- Shortness of breath in first cell
- Shortness of breath started significantly later
- He had little doubt he was exerting himself and after one minute he was breathing differently
- Professor Adams thought that there were pre-disposing factors that led to David Dungay’s passing. He thinks it was side effects from psychosis medicine.
- Whilst there was no clear cause of death (according to the autopsy), Professor Adams thinks that David Dungay had heart arrhythmia as his death was sudden and not slow (From observation that David Dungay turned blue from lack of oxygen quickly not slowly like hypoxia)
- Professor Adams stated restraining or struggling against someone stops the blood return.
- Professor Adams stated the two psychosis medications together with diabetes increased the likelihood of this.
- Professor Adams observed and stated prolonged congestion in the head, shoulders however, has no comment.
- He stated food on the lungs from the autopsy orbited from the stomach in resuscitation.
Witness 2 – Forensic Pharmocologist Consultant, Mr John Farrah
Mr Farrah had listened to the evidence above by Professor Adams, as well as attended to the Autopsy Report . He analysed the chemical substances and their potential involvement in Dungay’s death, including the injection of Medazolam, and the three antipsychotic drugs he was treated with therapeutically.
Mr Farrah concluded that he can make a good estimate regarding the rapid sedative, Medazolam (forced medication delivered as a intramuscular injection of a rapid sedative): that while found in the body was negligible and under the reportable level, and at a sub-therapeautic level. If Dungay’s collapse did occur within 1-2 minutes after receiving the intramuscular injection, it would have had a negligible effect.
The three anti-psychotic treatments were all at therapeutic levels or a bit higher. One drug Chlorpromosine (?) would have had a sedation effect. Zoopathixol (??) had no sedative effect but we could expect would increase QT elongation (ie adversely affect heart rhythm, as per Professor Adam report above, to which he would defer to). Mr Farrah concluded that the three antipsychotics were unlikely to be a cause of Dungay’s death.
Also, that the antipsychotic drugs taken alone would have not increased the QT Interval (ie on their own, affected his heart beat). [Noted discrepancy: Prof. Adams stated a likely deleterious effect of these chemicals, adversely compounding on his QT Interval. However, Mr Farrah noted, he did not have a PhD nor the expertise Prof. Adams has, thus to defer to Adam’s opinion.)
It was noted that at autopsy compared to when Dungay was alive, substance levels were likely to register as slightly up, not down.
12:04 PM: Dr. John Farrah in court
- Stated that he has seen a media report showing the video after he prepared the toxicology part of the autopsy report
- Toxicology segment showed that:
- David Dungay had antipsychotic medication at therapeutic levels (level administered is really dependent on the circumstances could be administered in. For example, a person can be administered a higher than “normal” dosage for something if the person would be under strict supervision)
- Dungay was injected with 10MG(?) of Midazolam > This dosage is considered to be on the higher end of the therapeutic range (even for David Dungay’s weight)
- First usage of defibrillator was 5 minutes after David Dungay’s death.
- Note : He was stuttering when questioned.
- Dr. Farrah believes that:
- The amount of midazolam administered contributed to Dungay’s death
- Believes that little midazolam entered his blood (low bioavailability), due to being injected in the gluteus muscle. The midazolam may not have entered the bloodstream properly but entered into fatty tissue instead. S response was 2 minutes.
- Dr Farrah stated that Dungay would have a built up tolerance to Midazolam and that it would have no significant sedative effect on Dungay. Dr Farrah suggested Chlorpromazine is known to cause this effect.
- He also stated he didn’t have access to the video or much information in allegations to restraint.
- Stated an average response is 45 minutes however Dungay’s was 2 minutes.
Witness 3 – Pathologist who conducted the Autopsy, Dr Bailey
Dr Bailey considered a range of factors in her Autopsy Report, including for example, bruising of the head, which was unidentified, but where concussion was a possible effect. She summarized that in isolation factors she considered where not indicative of cause of death, however in combination, that her conclusion was that the factors considered were ‘maybe, uncertain’.
Dr Bailey detailed any noticeable damage on various regions of the body that indicate compression or damage such as bruising or haemorraging. She was unclear – ‘cant say’ – of any evidence of blood in the mouth, but there was lots of vomit, despite prolonged resuscitation. There was a small amount of haemorraging that may have occurred if head turned, but not significant enough to say was neck compression of injury. There was ‘quite marked congestion to the head’. The head and neck showed minor injuries.
Diabeties related Ketoacidosis2 was excluded as a cause of death, as [unspecified what level] levels were below cases she has seen.
Autopsy findings were of no pathology or ‘unascertained cause of death with several attributions’. She can see mechanical chest and neck compression, and that increased blood pressure that led to rupture, causing haemorraging. Compression can cause blood failure to drain from out of the head, but no conclusive evidence as she can’t conclude if compression of neck was due to prone position.
She can see that compression is evident but can’t say why – eg CPR or prone position. Congestion of scalp corroborates with petechial haemmorages that blood into head but whether it is because of prone position, restraint, cardiogenic (?) shock, or maybe a combination of the above.
She noted the CSO/IAT use of the knee ride was a potential mechanism, but can’t confirm that this was a cause of death.
Dr Bailey summarized important aspects when considering cause of death: heightened agitation as a signal of some kind of dysfunction, some obesity, diabetic, held face down, and that the effects could be cumulative. Such cumulative effects cold be where: blood oxygen level was down, plus possibly some dehydration (if had high BSL then dehydration can add to physical distress), plus placed under higher metabolic challenge.
Adding to the above, the combination of antipsychotic medication, many of which can increase cardiac dysrhythmia. She recommended we refer to the Cardiologist for this matter [and if we check above, Prof Adams did state this could have compounded and had a likely deleterious effect on heart beat rhythm].
Dr Bailey stated that the path to hypoxia with metabolic demand is already high ie affecting oxygen levels. Also, we cannot exclude that the cardiac arrest was induced by hypoxia. [See Emergency Specialist, Prof. Brown’s July 2018 evidence where he stated this as the cause of death.]
By way of summary, Dr Bailey concluded that the combination with the heightened agitation and the altercations he had with CSO, these numerous effects would have contributed to his heart going into further strain, with ‘lots of small things in combination can have an effect in this case’.
She added that Dungay’s neck being placed on the edge of the bed ‘could be contributory’.
Considering whether Dungay was beaten up, she said there are small, minor effects, but she can’t say if they were inflicted by another person in altercations, and if they were she didn’t see any signs of this as a significant contribution.
She asked herself if the police report matched with her inquiries with a neuropathologist to see if there was any brain damage/trauma – however her conclusion was not clear. She made note of rib fractures that may be common with standard CPR delivery [however positive CPR delivery was not adhered to for Dungay].
Dr Bailey said she could ‘not see serious injury at post-morteum’, and that there were far too many contributing factors to the causes of death. She is in no doubt that cardiac arrhythmia occurred, when being aspiration, in hypoxia or atoxia, and that she cant give certainty to know why he suddenly collapsed.
For a non-diabetic person the normal rate of ketones is between 55 – 150, as the upper limit of fasting level. She reported that the biochemical analysis of Dungay’s Ketone Acidosis shows 151 micros and concluded this was below level of Diabetic Ketosis.
1:45 PM: Dr. Kendal Bailey in court
- Viewed the footage prior to post mortem however, didn’t have access to CPR footage of what happened before conducting autopsy. The video was provided to her by the police so she could corroborate the events that happened in the video with the injuries that were showed in the autopsy.
- Note: Bruising on the head makes you concerned about concussions
- Note: Injuries to the mouth might reflect compression to the nose and mouth
- Note: Bruising is very difficult to date
- The injuries that were shown in the autopsy report were:
- Y shaped Laceration between the eyebrows → minor skin injury, occurred when entering the first cell where his head came into contact with a shield
- Lesions on the forehead with bleeding on the right side
- Purple discolouration on left eyebrow → acute bruising
- Red-purple abrasion (scrapte type injury) on left eyebrow
- Superficial scratch marks on the right cheekbone
- Intramuscular hemorrhage on the jaw muscle
- Multifocal hemorrhage to the muscle from the sternum to the neck (which helps a person turn their head)
- Scrape injury → some skin loss to the medial surface of the right forearms
- Both wrists showed bruising → may be due to handcuffs
- Pink bruise on the back of the left hand
- Bruising on both knees
- She considers these injuries as “minor injuries if they were in isolation”
- Dr. Bailey thinks that he passed because:
- Heightened agitation/stress = Increased heart rate → can lead to cardiac death
- Blood oxygen level went down = due to being compressed (abdominal organs compressed → harder for blood to drain from the head)
- Those two were compounded by his diabetes and obesity
- These then led for him to have a cardiac arrhythmia
- Whilst giving her thoughts as to what the causes of David Dungay’s death, she uses the words “possibly”, “could have”, “maybe”, “not conclusive”, to demonstrate that she really isn’t sure what the causes are and doesn’t want her word to make her accountable to conclusively determine the cause/causes. For example, “the bruises on his knee could have been due to compression, but I don’t want to conclude it as that as people get bruises on their knees all the time”
- She stated injuries don’t exclude the possibility of minor altercation with another person.
- Dr. Bailey was asked how does an autopsy take place. She stated:
- That the autopsy took place a day after his death
- Steps included:
- Medical imaging through CT scans
- External examinations: to find evidence of cuts, bruises, any injury that could be found on the surface of the skin.
- Internal examination: involves looking at evidence of injuries on the organs and muscles of the body. She would take a sample of each tissue and look at it through a microscope
- She stated that she needed legal permission from the coroner to perform the autopsy
Conclusions from the observation:
- If David Dungay wasn’t physically restrained, he wouldn’t have a cardiac arrest.
- Seems like the lawyers want ONE conclusive cause for his death (most likely lack of oxygen), but if there are a multiple amount of causes compounded, then that should be utilised as well
- However, a death by one thousand cuts is still a death
- Currently, the family thinks the causes were: External pressure, cardiac arrhythmia (can’t determine the cause of this)
- Observation : Family prepared statements and media application however opessission are trying to delay by requesting to see it first. The coroner previously stated the family can provide a statement as long as they don’t use defamatory language and pin point names.
- Questions to think about:
- Why didn’t they show the photos from the autopsy?
- Why are they unable to settle on the cause/causes of death?
- Why was the evidence inconclusive?
- Why wasn’t the Aboriginal liaison officer called to speak?
- Why did the correctional officer breach the protocol of cell transfer (usually need permission and need to document that the cell transfer for an inmate would occur but it didn’t)?
Court adjourned 3:06pm on the 7th March 2019.
Hypoxia (medical), a pathological condition in which the body or a region of the body is deprived of an adequate oxygen supply