Record of Investigation Into Death
Coroners Act 1995
Coroners Regulations 1996
I, Rod Chandler, Coroner, having investigated the death of
Clement Bernard Kilby
WITHOUT HOLDING AN INQUEST
Find That :
Clement Bernard Kilby ("Father Kilby") died on 6 February 2009 in the Calvary Hospital ("Calvary") at Lenah Valley.
Father Kilby was born in Launceston in Tasmania on 5 February 1930 and was aged 79 years. He was single and a retired Catholic Priest.
I find that Father Kilby died as a result of the combined effects of mixed drug toxicity (tramadol, oxycodone, morphine, propofol) and atherosclerotic and hypertensive cardiovascular disease. Significant contributing factors were recent surgical general anaesthesia and emphysema.
Circumstances Surrounding the Death :
Father Kilby resided in Mount Stuart having retired from active work as a Catholic Priest, a role he had undertaken since being ordained in 1954. He was instrumental in establishing the Catholic welfare organization now known as Centacare. Father Kilby was a recipient of the Order of Australia Medal and was also a former Tasmanian Citizen of the Year.
In September 2008 general practitioner, Dr Dimitrios Klonaris referred Father Kilby to orthopaedic surgeon Mr John Mills because of osteoarthritic change in both knees. Mr Mills attended Father Kilby on 13 November 2008 and it was agreed, after discussion, that Father Kilby’s condition would be treated surgically with bilateral and simultaneous knee joint replacement.
The surgery was undertaken at Calvary by Mr Mills on 4 February. It commenced at 9.20 am and concluded at 11.07 am. Mr Mills reports that the procedure was uncomplicated but comments that the bilateral femoral nerve catheters which had been inserted as part of the anaesthetic management were "less than ideal and (Father Kilby) required additional intramuscular analgesia as well as oral medication for pain."
Dr Andrew Ottaway was Father Kilby’s attending anaesthetist. In the recovery room he commenced local anaesthetic infusions consisting of 0.2% ropivacaine at 5mls per hour to be delivered via each of the femoral nerve catheters. Dr Ottaway prescribed these to continue until 8.00 am two days later. In addition, whilst in recovery, Father Kilby was given 100 mg tramadol intravenously for mild discomfort in the knees. Otherwise, his period in recovery was described as uneventful and Father Kilby was returned to the ward shortly after 12.00 noon.
Father Kilby’s pain increased in the evening of 4 February requiring further analgesia. He had been prescribed regular paracetamol four times a day and regular oxycontin 10 mg twice a day. In addition, tramadol and oxycodone were available as required. At 6.40 pm Father Kilby was given paracetamol 1,000 mg and tramadol 100 mg intravenously. At 7.20 pm oxicontin 10 mg was given orally as prescribed together with a dose of oral oxycodone. (the amount of this dose was unrecorded) At about 10.30 pm Dr Ottaway was contacted by telephone because Father Kilby was still suffering significant pain. At this time he was prescribed an immediate dose of intramuscular morphine 10 mg. The available dose of oxycodone was also increased to 20 mg as required, maximum 3 hourly. Father Kilby continued to have a difficult night with ongoing significant pain.
At about 7.30 am on 5 February Dr Ottaway reviewed Father Kilby. At this time he was alert and orientated but appeared tired. He felt that his pain was improving and that he was comfortable at rest. Local anaesthetic infusions continued as prescribed via each femoral nerve catheter. All recorded observations at this time were within normal limits. Dr Ottaway increased the regular oxycontin from 10 mg to 20 mg twice a day in order to improve analgesia but otherwise made no changes to Father Kilby’s management regime.
Later in the morning of 5 February Father Kilby suffered a significant increase in pain following physiotherapy. Dr Ottaway was contacted and at about 11.25 am he ordered that Father Kilby be given an immediate dose of morphine 10 mg intramuscularly as well as boluses of infusion solution (0.2% ropivacaine) via each femoral nerve catheter with an increase in the rate of infusion to 8 mls per hour. Dr Ottaway reports that these measures appeared to have had good effect as Father Kilby required no further tramadol that day and only two further doses of oxycodone in the 20 hours to 8.00 am on 6 February. Father Kilby did continue with regular paracetamol and oxycontin as prescribed.
At about 11.00 am on 6 February clinical nurse educator, Anne-Marie Alomes received a telephone call for Father Kilby from a relative. She transferred the call to Father Kilby’s room and then went to his room to make sure he was able to reach the ‘phone. She saw that Father Kilby was sleeping. She advised the caller of this and suggested that he/she call back at a later time. Ms Alomes says that at this time Father Kilby appeared to be sleeping with regular breathing patterns and no changes in his colour. She did not note any audible breath sounds.
At about 11.15 that morning Dr Ottaway visited Father Kilby in his room. Dr Ottaway reports, "I found him sleeping peacefully. His breathing appeared normal and there were no signs to arouse suspicion of an impending clinical event. I reviewed his chart and noted his observations to be satisfactory. I also noted the Ropivacaine infusions via the femoral nerve catheters were continuing despite being prescribed to cease earlier that morning. In view of the difficult preceding 48 hours the patient had endured, I thought it best not to disturb the patient but decided to review him again another time." Dr Ottaway then left the room and shortly afterwards instructed Ms Alomes to cease the ropivacaine infusions and remove the femoral nerve catheters. Ms Alomes recorded this direction in the progress notes at 11.20 am.
At about 11.45 am hospital staff found Father Kilby unresponsive. Attempts to resuscitate him were unsuccessful and he was declared deceased at 12.10 pm.
Forensic Pathologist, Dr Donald Ritchey undertook a post-mortem examination. An associated toxicology report indicates multiple drugs within Father Kilby’s blood including the following:
Ropivacaine (46 mg/L)
Tramadol (1.1 mg/L2)
Oxycodone (0.1 mg/L)
Morphine (less than 0.03 mg/L)
Propofol (less than 0.06 mg/L)
Metoclopramide (less than 0.05 mg/L paracetamol (26 mg/L2).
The levels of ropivacaine, tramadol and paracetamol are all described as greater than therapeutic and the oxycodone is described as being high therapeutic. However, the analyst’s report includes this comment, "Although some drugs are present at apparently greater than therapeutic levels, the drug levels determined may be entirely consistent with specialist medical treatment (eg surgical/intensive care/emergency)."
In Dr Ritchey’s opinion, the cause of Father Kilby’s death was "the combined effects of mixed drug toxicity (tramadol, oxycodone, morphine, propofol) and atherosclerotic and hypertensive cardiovascular disease. Significant contributing factors were recent surgical general anaesthesia and emphysema."
Dr Ritchey’s post-mortem report includes these comments:
"The autopsy revealed a well developed, well nourished elderly Caucasian man with moderately severe natural disease including atherosclerotic and hypertensive cardiovascular disease, emphysema and diabetes. Toxicology testing of post-mortem femoral vein blood revealed multiple opioid analgesic medications at therapeutic and greater than therapeutic concentrations; as detailed in the forensic toxicology report….. In addition, there was residual propofol (used in general anaesthesia) at a sub-therapeutic concentration and a markedly elevated ropivacaine concentration (discussed below).
"This complex set of anatomical and toxicological findings is interpreted by me to suggest that Mr. KILBY has died due to the synergistic effects of multiple central nervous system depressants acting by different pharmacologic mechanisms. Elderly individuals, especially those with heart and lung disease are at increased risk of the CNS depressant effects of medications as are individuals having recent general anaesthesia."
Specific to the level of ropivacaine detected in Father Kilby’s blood Dr Ritchey comments:
"Ropivacaine (and related local anaesthetic drugs) are frequently used to provide regional anaesthesia by infusion of the drug adjacent to a peripheral nerve (in the present case the femoral nerve) producing a local, "nerve block" providing pain relief after the bilateral knee replacement surgery. In the peripheral blood, excessive ropivacaine can cause death by inducing lethal cardiac arrhythmias. Although the concentration of ropivacaine was markedly elevated in the post-mortem sample; it is my opinion that this likely resulted from the phenomenon called post-mortem redistribution (PMR). PMR occurs when, after death, drugs diffuse from areas of high concentration (in this case the deep soft tissues adjacent to the femoral nerve) to areas of lower concentration (including into the nearby femoral vein-the standard source of blood for post-mortem toxicology sampling;………). It is my opinion that ropivacaine toxicity did not contribute to Mr. KILBY’S death."
Findings and Comments :
I am satisfied that a full and detailed investigation has been conducted in relation to the death of Father Kilby and that there are no suspicious circumstances.
I accept the opinion of Dr Ritchey upon the cause of death and therefore find that Father Kilby died as a result of the combined effects of mixed drug toxicity (tramadol, oxycodone, morphine, propofol) and atherosclerotic and hypertensive cardiovascular disease. I accept too that significant contributing factors were recent surgical general anaesthesia and emphysema.
I observe that Dr Ottaway’s direction for the ropivacaine infusions to cease at 8.00am on 6 February had not been complied with by the time of Father Kilby’s death about 4 hours later. However, Dr Ritchey has opined that the elevated levels of ropivacaine indicated by toxicology were the likely result of post-mortem redistribution and hence, I infer, could not be attributable to an "overdose" of this drug via the femoral nerve catheters. Dr Ritchey has further opined that ropivacaine toxicity was not a factor which contributed to Father Kilby’s death. I accept these opinions.
It is noted that this investigation has identified an instance occurring on 4 February where hospital staff has not fully completed the entry in the drug charts to show the dosage administered to Father Kilby. Further, it is not clear from the records whether the dose of morphine prescribed for Father Kilby in the morning of 5 February was delivered in the manner directed. Although these matters did not play any role in Father Kilby’s death they nevertheless lead me, particularly when coupled with the nursing staff’s failure to promptly cease the administration of the ropivacaine, to recommend that Calvary undertake a comprehensive review of its drug administration processes with a view to eliminating errors of this nature.
Father Kilby’s death was both unexpected and unfortunate. It occurred, in my view, despite him receiving appropriate and reasonable medical care.
I conclude by conveying my sincere condolences to Father Kilby’s family.
DATED: Monday 17 January 2011 at Hobart in the State of Tasmania.