Estate of McQueen v Accident Compensation Corporation

IN THE DISTRICT COURT HELD AT HAMILTON Decision No. 190/2005 IN THE MATTER of the Accident Insurance Act 1998 AND IN THE MATTER of an appeal pursuant to Section 152 of the Act BETWEEN THE ESTATE OF ALBERT FRANCIS McQUEEN (AI 222/02) Appellant AND - ACCIDENT COMPENSATION CORPORATION Respondent HEARD at HAMILTON on 9 June 2005 APPEARANCES Mrs A De Jonge, Advocate for Appellant. Mr J Roberts, Counsel for Respondent. RESERVED JUDGMENT OF JUDGE M J BEATTIE [1] The issue in this appeal arises from the respondent’s decision of 14 January 2002, whereby it declined to extend cover to the appellant for the death of the deceased, Albert Francis McQueen, as having been caused by medical misadventure. [2] The decision now under appeal followed on from an earlier decision of the respondent of 22 November 2001, whereby it accepted that medical error had occurred on the part of a registered health professional and that that medical error had caused the hospitalisation of the deceased. Cover was granted for the treatment necessary to counteract the effects of a morphine overdose which had been brought about by medical error. [3] The representatives of the deceased have contended that the medical error, namely the dispensing of a grossly excessive strength of morphine, was a contributing 222.02 (pg) 2 cause of the death of the deceased, who died in hospital on 1 March 2000, two days after admission. [4] It is therefore the case that this appeal is not concerned with a determination of whether medical misadventure occurred or not, that issue having been determined and there being no questioning of that decision. The issue is whether the medical error so committed was a contributing cause of the death of the deceased. Again, there is no dispute that the excessive dose of morphine administered to the deceased caused injury for which treatment was necessary, and that again is the respondent’s first decision on cover. It is only the second decision of the respondent that the medical error was not causative of the deceased’s death that is in issue. [5] The background facts relevant to the determination of this issue may be stated as follows: • As at 27 February 2000, Albert Francis McQueen, was a 61 year old Maori residing at his home in Hamilton. • His background medical condition, as stated by his GP, Dr Bowen, was as follows: “This patient was under my care from 1974 to his death. Although he suffered from obesity, his general health was good until 1996 when he was admitted to Waikato Hospital with acute diabetic ketoacidosis brought on by an acute viral illness. Not long after this he started to develop signs of early renal failure and then in 1999 was admitted to Waikato Hospital with acute congestive heart failure. An echocardiogram at that stage showed poor ventricular function. After his admission it was concluded that he had a severe cardiomyopathy and also had early renal failure. His health from May 1999 onwards was not good and he was mostly house bound. From the end of (1999) he was more or less bed bound but could get around in a wheelchair. He suffered with severe oedema and was treated with massive doses of diuretics.” • On 27 February, the deceased developed acute leg pain and was visited by Dr Maplesden, a duty doctor at 11.00 a.m. Dr Maplesden had no previous knowledge of this patient. Dr Maplesden noted gross oedema (excessive accumulation of fluid) from mid-abdomen and down both legs. • Dr Maplesden considered the deceased’s overall condition and determined that a small dose of morphine would be the most suitable 222.02 (pg) 3 form of analgesia in the short term until review by his usual practitioner the next day. • Dr Maplesden prescribed morphine elixir in a strength of 1 mg/ml – 5 ml to be taken every six hours. • That prescription was presented to the Anglesea Clinic Pharmacy, where instead of dispensing morphine of 1 mg/ml strength, morphine of 10 mg/ml strength was dispensed. • 5 mls of 10 mg strength morphine was thereupon administered to the deceased. • The deceased’s wife soon noticed certain effects which the morphine was having on the appellant and from a description of symptoms she gave over the telephone to the dispensing pharmacist, it was determined that the appellant was suffering from a morphine overdose. • The deceased was admitted to Waikato Hospital in the afternoon of 27 February 2000. Immediately upon admission a narcotic antagonist Naloxone, was administered, which only had a temporary effect, and shortly after a second dose was administered. • The visible effects of the morphine overdose were determined as being reversed within five to six hours of the morphine being taken and within three to four hours of the side effects being noted. • The deceased remained hypertense and did not pass urine. He also displayed respiratory problems. • The deceased died in hospital on 1 March 2000. • A Death Certificate was signed by Dr Gemenis, one of the duty doctors at the hospital, and it showed the cause of death as being cardiac failure. • Members of the deceased’s family were concerned with that finding and contacted the Coroner, who instructed the Police to carry out an investigation. • In May 2001, representatives of the deceased lodged a claim for cover with the respondent in relation to his death. • The respondent investigated the claim and obtained a report from Dr Nunn, Cardiologist, of Waikato Hospital, who had been involved in the treatment of the deceased on his admission. 222.02 (pg) 4 • Dr Nunn advised that in his opinion the cause of death as stated in the Death Certificate was correct. He advised that morphine had not contributed to the patient’s death. • The Corporation sought further independent opinion from Dr Carl Burgess, Associate Professor of Clinical Pharmacology at the University of Otago. The essence of Dr Burgess’s report was that the morphine overdose had added insult to the deceased’s pre-morbid condition and was a contributing cause. • On 22 November 2001, the Corporation advised the appellant that it had cover for medical error for the treatment required as a consequence of the overdose of morphine but not for death. • The Corporation continued with consideration on the question of death but on 14 January 2002 it issued a formal decision declining to grant cover for the deceased’s death as having arisen from the morphine overdose. • The Coroner did not convene a hearing until 31 October 2003. Because there appeared to be a conflict in the opinions of Dr Nunn and Professor Burgess, the Coroner called for the hearing of evidence from those persons. • In his decision, dated 11 November 2004, the Hamilton District Coroner made a formal ruling that the cause of the deceased’s death was morphine overdose in a background of chronic heart and renal failure. An amended Death Certificate to that effect was thereupon issued. • A Review Hearing of the respondent’s decision of 14 January 2002 took place on 7 May 2002. • In a decision dated 8 May 2002 the Reviewer found that the evidence did not establish that the deceased had suffered death as a result of morphine overdose and the review application was therefore dismissed. • For the purposes of the appeal to this Court the respondent has obtained an opinion from Dr Peter Leslie, Honorary Consultant Cardiologist, and his report has been introduced in evidence. [6] As earlier noted, the sole inquiry with which the Court is concerned is whether the morphine overdose was a contributing cause of the deceased’s death. For assistance in that regard, the Court has received reports from Dr Chris Nunn, Cardiologist, Professor Carl Burgess and Dr Peter Leslie. In addition to those reports I have 222.02 (pg) 5 received a transcript of the evidence of Professor Burgess as given at the Coroner’s inquest as well as the evidence of Dr Nunn, given at that inquest, as it was noted in the Coroner’s decision. The Medical Evidence 1. Report from Dr Chris Nunn, Cardiologist, dated 5 June 2001. Dr Nunn is a cardiologist attached to the Cardiology Department at Waikato Hospital and he was on duty when the deceased was admitted. Dr Nunn stated as follows: “I understand there are two main questions being raised. The first pertains to the Morphine overdose that had been administered to him prior to his admission and its impact on his subsequent outcome. The second question pertains to his Death Certificate which had stated that he had died from heart failure. I will address these two questions in order. 1. Morphine had been administered to this patient on the day of his admission at a dose of 50mg orally. I understand this was administered to him because he was having severe pains, which in retrospect I believe were related to his excessive fluid accumulation secondary to heart failure. The fluid had resulted in significant swelling and distension of his abdomen which was clearly causing him pain. In addition I understand he was having severe pains from his limbs, which may have been unrelated to his heart. When he arrived at hospital he was clearly showing the signs of morphine overdose. He was immediately administered Narcan which reverses the effects of Morphine. Within a matter of minutes of receiving this he awoke and was able to converse normally. It was clear however, that the underlying condition, i.e. severe heart failure had deteriorated such that he required hospitalisation and intensive care. The Morphine itself had not caused heart failure and indeed is commonly used as a treatment for heart failure. I do not believe that the Morphine in any way contributed to this mans decompensation. As recorded in the hospital records the effect of the Morphine was reversed rapidly but this obviously did not influence his underlying heart function which for some time had been very poor. 2. The Death Certificate I understand listed heart failure, as the primary cause of this patient’s death. I believe this is accurate. As stated above, this man had severe heart disease for some considerable time and this had slowly deteriorated. Morphine was not listed on the Death Certificate, as it was not believed that this contributed to this patient’s death. In my opinion the Death Certificate is a true and accurate reflection of the cause of this patient’s death.” 222.02 (pg) 6 2. Report from Professor Carl Burgess dated 19 October 2001. After noting the history leading up to the deceased’s admission to Waikato Hospital and the administration of the morphine antagonist, Dr Burgess then stated as follows: “There were major problems during his time in hospital as Mr McQueen remained hypotensive and did not pass urine. He became more hypotensive and short of breath, and did not pass urine at all. He died on 1 March of renal failure. The pharmacy admitted that they did dispense the wrong dose of morphine. The question is whether the morphine resulted in an adverse event that caused the death of Mr McQueen. This matter is currently being investigated by the Hamilton Police. There is no doubt that medical error occurred in this particular case. The wrong dose of morphine was dispensed and the Late Mr McQueen took the morphine in good faith. Although there was some reversal of the morphine overdose when he was in hospital, plainly the fact that he did not pass urine would suggest that the half-life of morphine would have been prolonged. With the ongoing degree of hypotension, it is likely that he developed acute tubular necrosis which caused renal failure and his death. Unfortunately, a post-mortem was not performed, nor were blood levels for morphine taken. Prior to this man receiving the morphine, although he had severe cardiac failure, he was conscious and alert. The morphine seems to have played a crucial role in this particular case. The symptoms that he developed after taking the morphine, namely nausea and vomiting, sweating, the signs of pinpoint pupils, and decreased level of consciousness and hypotension, are all due to the morphine. It is likely that this added insult on his pre-morbid condition was the probable cause of his eventual demise. My opinion is that there has been medical error in this particular case, and has resulted in a physical disorder which unfortunately in this case has gone on to cause death. My finding would be for medical error. The individual responsible is the pharmacist who dispensed the morphine.” 3. Evidence given by Professor Burgess at the Coroner’s Inquest on 31 October 2003. This evidence included extensive cross-examination from Counsel for the interested parties. The relevant passages of that evidence is reproduced in the Coroner’s decision and these passages of evidence are as follows: “There is clear medical error in this particular case in that the wrong dose of morphine was dispensed. The excessive morphine is highly likely to have caused the hypertension which would have been exacerbated by vomiting; this in turn in a patient with pre existing renal disease and marked cardio respiratory failure, proceeded on to cause an acute on chronic renal failure. Unfortunately 222.02 (pg) 7 despite all the treatment that Mr McQueen was given, his kidneys did not turn to functioning and it is because of this that his heart did not compensate and he died. I believe that his treatment at Waikato Hospital was appropriate, and in particular I concur with their opinion that Mr McQueen was far too ill to consider dialysis.” At pages 16,17 and 19 of the Notes of Evidence, Professor Burgess stated as follows: Page 16: “Now to move on to the next statement there are also statements that the morphine was reversed with the use of Niloxone (sic). There is evidence that that is the case and that the patient from my reading of the notes was given two doses of Niloxone which initially reversed the toxicity and he was then put on an infusion of Niloxone for approximately 12 hours. It is claimed that his blood pressure fell and rose remained low and because it remained low the morphine could not have been the cause of the eventual outcome here. This may or may not be true however, there is clear evidence from the clinical notes that anyone can look at that he in fact remained hypotensive from the 27th with no evidence of a reversal at all whilst he was receiving this infusion right up until the following morning when there was reversal in a change in his blood pressure. His blood pressure rose. It is not also clear to me why the patient required ongoing respiratory support with BIPAP when he did not require such support at home. It is known that morphine depresses respiration that is one of its cardinal effects. There is clear evidence here that this man had respiratory failure. This is shown by the blood gases that were recorded during his stay at the Waikato Hospital. It is likely that the morphine in its derivatives were responsible or at least responsible for that. Morphine is handled in the body by being broken down to a number of break down products, the most important of which is called M6G. This substance is approximately 10 times as potent as morphine on a weight basis. It is excreted exclusively by the kidney, there is no evidence in the notes that I had that Mr McQueen passed any urine in his stay therefore the M6G would have persisted. There is evidence in the literature that individuals that do not pass urine may have this substance in their body for 20 days after a dose of morphine thus I do not doubt that the deterioration in his cardiac function played a role in his death. I also do not doubt that the morphine and its derivatives would also have played a major role and would have been present.” At page 17. “In answer to your question, although I don’t doubt that heart failure played a role here and I had no doubt that Mr McQueen had been a fairly healthy man that he would have got over the morphine, I believed it played a significant role here and although the signs of fluid retention can occur with heart failure and do occur with heart failure they can also occur with renal failure and can be very difficult to distinguish . . . this man had a low blood pressure to start we know that from Dr Bowan’s notes in 1999. He was obviously a patient sitting on a borderline between life and death any added insult is likely to have been harmful to him. The excessive dose of morphine is likely to have been that insult.” 222.02 (pg) 8 At page 19. “ . . .I don’t think either of us would disagree that Mr McQueen had fluid overload, neither of us would disagree that Mr McQueen had severe heart failure we don’t disagree on that, what we disagree on I think is that the morphine played a significant role in his deterioration Dr Nunn doesn’t he believes that the morphine was antagonised by the antagonist and thereafter played no further role, have I got that right, because that is the crunch, to me that is what he saying, I am saying the opposite I am saying the morphine was still in the man’s body and continued to play a role and I think that is where we differ, we don’t differ that this man died from fluid overflow or whether the cause of death was cardiac or renal failure is neither here nor there it’s the underlying cause that where we differ, I think that’s the difference whereas when he answered one of the questions from somebody that he did not believe that the morphine played a significant role and I think that it did play a significant role.” 4. Evidence given by Dr Nunn at the Inquest. Dr Nunn is in effect responding to the opinion expressed by Professor Burgess and it is he who is the person referred to in the evidence. Dr Nunn stated as follows: “He has stated that all the organs have failed simultaneously and that he felt the cause of death was kidney failure not a heart attack or heart failure, I disagree to the extent that the organs have failed altogether they both have failed but one has led to failure of the other. My opinion is that the heart condition led to the kidney failure. He in particular stated or answered the question could his kidneys have stopped because his heart had just given up. He responded this is correct and we are in agreement in that regard. He has stated that the reasons for his opinion that the kidneys were the primary problem with the absence of heart failure and seeing Mr McQueen when he arrived in hospital, the features he exhibited were all consistent with heart failure. He very much had symptoms and signs as I have described earlier of heart failure and therefore if Dr Burgess’s feelings were that the kidneys could have stopped because of his heart and, if his reasoning for not feeling that the heart was a cause of the kidney failure or the absence of symptoms and in fact there were symptoms, and I would agree with that comment”. 5. Report from Dr Peter Leslie, Honorary Consultant Cardiologist, dated 29 March 2005 to Respondent’s Counsel. Dr Leslie noted the background, including the progress of the appellant’s twin problems of heart disease and renal failure. Dr Leslie provided his opinion from all the medical records which had been made available to him. He stated as follows: 222.02 (pg) 9 “There is no doubt that there was a dispensing error in the strength of oral morphine that was prescribed for pain relief and he took 50 mg at 1300 hrs on 27 Feb. 2000, instead of the 5 mg intended by Dr Maplesden, in his clear script. Equally, it is beyond doubt that that he had respiratory depression and loss of consciousness, from the effects of morphine, but these were rapidly relieved by the repeated use of Naloxone, a morphine antagonist. Despite this, Mr McQueen subsequently deteriorated, with low blood pressure, no urine output, rising serum creatinine and potassium as a result and died 3 days later. The potassium had reached a potentially dangerous level the day before death and may have caused a fatal heart rhythm disturbance, but the terminal event is not recorded. Authorities differ on the appropriate first oral dose of morphine for those who have never had it before. It is an agent which is not absorbed fully when taken by mouth and acts more slowly than when administered by injection. A first dose of 5 to 30 mg. Is suggested by different authors for adults over 50 kg in weight. The point is that 50 mg. Is not likely to be a fatal dose, other things being equal, in such a person. However, the serum concentration reached and the duration of effect are greater in those with impaired renal function. On the face of it, the visible effects of morphine overdose in this case were reversed within 5 to 6 hours of the drug being taken and within 3 to 4 hours of side effects being noted. His blood pressure, immediately after being given Naloxone was as high as when measured at his home earlier in the day before morphine was taken. The respiratory rate, previously slow, had become rapid and his conscious level and conversation had returned to normal. Investigations included a chest x-ray which showed a large pleural fluid collection, occupying most of the right thoracic cavity. Renal function had deteriorated markedly compared with 8 months earlier, with the creatinine level having reached 0.295 mmo1/litre. An ECG showed no evidence of acute heart muscle damage and this was supported by a normal level of the serum enzyme, creatine kinase. Four hours later, his blood pressure dropped and remained very low despite medication to raise it and repeat doses of Naloxone. Some respiratory support maintained his blood oxygen at a reasonable level, but carbon dioxide measurements remained persistently high. No urine was passed at any stage. Divergent opinions have been expressed about the ultimate cause of death here and in particular, the contribution of the accidental morphine overdose. All of those giving opinions have touched on one or more of the contributory causes of death. Those contributory factors were:- severely impaired cardiac function for at least 2 years, with resistant congestive heart failure, diabetes, anaemia and acute on chronic renal failure. There are some unknowns, specifically his renal pathology, since an autopsy was not performed. As already stated, in someone with impaired renal function, morphine can have prolonged, adverse effects. These include lowering of blood pressure and respiratory depression. Each of these may be more serious in a patient with heart and/or kidney failure. The major, obvious side effects of morphine, on respiration, consciousness and blood pressure here appeared to be reversed within 3 hours or so of those effects appearing. By then his kidney function, judged by the high creatinine level, had deteriorated markedly from 8 months earlier. It is unlikely that such a great 222.02 (pg) 10 deterioration would have occurred in only 3-4 hours. There is a comment in the records, 24 hours after admission, that he had not passed urine for 36 hours. If that is correct, his kidneys had failed completely before morphine was given. Even when the respiratory effects of morphine appeared to have been completely reversed by Naloxone, he was hypoventilating as shown by high blood carbon dioxide levels, despite some respiratory support. The “stiff” lungs from his poor heart function and the very large amount of fluid in his right chest cavity, would have contributed to this and added to the adverse metabolic burden, but longer term, unrecognised, effects of morphine could have played a part. It cannot be denied that unmeasurable side effects of morphine may persist or recur in a patient with renal failure, for several days, despite using Naloxone repeatedly. The drug has a half life of only an hour or so. In all this complex tapestry, the actual, quantitative contribution of morphine to his terminal decline, can be debated endlessly. That apart, the over all (sic) picture makes it clear that he was very near life’s end. The analysis and practise of medicine often involves handling uncertainties. In this case, if the complete renal failure occurred before morphine was given, and there is some suggestion of that, then death was inevitable from cardio-renal causes, probably within the time frame of his final hospital admission. Having said that, the possibility cannot be excluded, as analysed above, that morphine was a contributory factor, whether major, or in only a minor, terminal fashion. In that case, it seems to me, that natural justice should give the patient the benefit of any doubt and some cause and effect relationship between morphine overdose and the exact time of death, be admitted.” DECISION [7] This is an extremely difficult case to determine and I make no apology for saying so. The medical evidence makes it clear that the deceased’s condition up to the point of, but prior to, the taking of the morphine was one of significant deterioration and he was suffering from both congestive heart failure and renal failure. [8] An analysis of Dr Nunn’s evidence identifies that his opinion rests on the premise that the effects of the morphine overdose were arrested and reversed by the administration of the morphine antagonist Naloxone. Dr Nunn said that the deceased appeared to come out of the respiratory distress, depression and loss of consciousness which had been the principal visible effects and that he was able to engage in conversation. [9] On the other hand, both Professor Burgess and Dr Leslie noted that there is a distinction between the visible effects of the morphine and the underlying effects. In the case of Professor Burgess, he considered that the morphine brought about 222.02 (pg) 11 respiratory failure which proceeded to cause acute on chronic renal failure. Dr Burgess then identified that one of the products created in the body from morphine, namely M6G, would have remained in the deceased’s body as he did not pass any urine during his stay, and that this substance caused a deterioration in his cardiac function as well as contributing to the renal failure. [10] This same observation was made by Dr Leslie, and despite the fact that he too was of the view that the deceased was very near life’s end when the morphine was administered, the morphine nevertheless did contribute to the actual timing of death by reason of an acceleration of the loss of functions of the heart and kidneys respectively. [11] It is the case that a causative link needs to be established on the balance of probabilities, a possible link is insufficient. In that regard, were the Court to have only the opinion of Dr Leslie, and when that is balanced against the opinion of Dr Nunn, then at best it could be said that the morphine possibly contributed to the deceased’s earlier than expected demise. [12] However, there is the reasoned and extensive opinion provided by Professor Burgess, and I have no doubt that his opinion is expressed in terms of a high degree of probability that the morphine was a causative factor or influence on the death of the deceased on the day that it occurred. [13] I am attracted to the reasoning provided by Professor Burgess for coming to his opinion, he has not simply made a statement to that effect, but rather he has explained in considerable detail why he has come to the view that he has. No evidence has been presented which would show that his reasoning is flawed. [14] In my view, the opinion of Professor Burgess tips the scales in favour of the test of the balance of probabilities as being satisfied, and that the morphine overdose was a contributing causative factor in the death of the deceased on 1 March 2000. The temporal connection cannot be overlooked and it must be recognised that the deceased died within 48 hours of the taking of that overdose. [15] In all the circumstances, I find that the deceased is entitled to cover for his death, it having been caused in some material measure by the medical misadventure which had been committed by the pharmacist in dispensing the wrong strength morphine for the purposes of his treatment. 222.02 (pg) 12 [16] The effect of this decision is that the respondent’s decision of 14 January 2002 is quashed and cover is hereby granted to the appellant as stated above. The appellant is entitled to costs which I fix at $1,250. DATED at AUCKLAND this 28th day of June 2005 M J Beattie District Court Judge 222.02 (pg)