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Wendy McLean, retired home
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Since there is no dispute that some cot deaths are not due to abuse it is important to discover their cause. Lead is now known to be released from the maternal skeleton and transmitted to babies during pregnancy and lactation. It has been suggested (1,2) that lead is related to SIDS but there appears to have been little investigation. Lead is known to be related to low birthweight, levels are higher in smokers and there are seasonal variations - all factors in SIDS. Lead levels are declining but levels in very young children are higher than in the population generally. Further research is needed. 1. Drasch GA et al Eur J Pediatric 1988 Jan 147(1) 79-84 2. Erickson M Med AI Pediatr Res 1983 Oct 17(10)779-84 |
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Brian Morgan, Freelance journalist Cardiff
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Ordinarily one would welcome any new points being made on the cot death issue - but these letters were published just days before a new definitive report from the CESDI team appears (scheduled for Wednesday February 2nd 2000), with only one of the authors of the letters being privy to the contents. They are premature and possibly redundant. Emery and Waite are very respected figures in the cot death world, and their principal point that parents must not be victimized is a good one. But to say that an earlier CESDI report confirms their own estimate that 10% of cot deaths were technically filicide is at odds with that particular CESDI report's findings. These were that deliberate action by a parent or carer was a probable major contributory factor in 18 of the 228 deaths originally registered as Sudden Infant Death. This is 8%, not 10% and there is no suggestion that all of these were murdered only that their carer's actions contributed in some way. However, exaggeration of the only best estimates currently around - to as much as 25% by one by eminent paediatrician - serves the 'think dirty' campaign and fuels the trawling of past cot death records, particularly multiple deaths in the same family, for cases to prosecute in the criminal court. All three correspondents press for better quality investigations of all sudden unexplained infant deaths, and that is truly to be desired. It cannot be glossed over that many unexplained deaths were never properly investigated to the standard expected today. This makes defence of a criminal charge very difficult. It ought to make prosecution difficult too, but as has been recorded in the BMJ juries may be influenced by high profile and forcefully stated opinions, not the hard facts which are absent anyway. Professor Emery may recall a case which was my first investigation of a false allegation of deliberate killing. I reported this in the Independent in 1992 and in Dispatches in 1994. The child died suddenly after experiencing breathing difficulties. The mother was accused of causing the death. Her surviving children were taken from their beds at midnight on a Police Protection Order, the parents kept in custody. It took four pathologists to ascertain the true cause of death and it was the only the fourth who found that overwhelming polymyositis in the muscles of the diaphragm was responsible - and had that effort not been put in - the final call to a muscle expert, the mother might have been convicted or been open to further criminal investigations had a later child died. This was one of the most controversial cases of false allegation of Munchausen Syndrome by Proxy that I have reported, and to my knowledge has never been reported by the medical profession. The distress caused to this family is inestimable. The BMJ has asked what fuels my desire to see a full investigation of the impact of false MSBP allegations, which of course covers the cot death arena, and it is cases like this which are part of the answer. Every case of cot death should be given this level of pathology. The true abusers will be found but equally importantly innocent parents will not be victimized. |
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John P Heptonstall, Director of the Morley Acupuncture Clinic and Complementary Therapy Centre West Yorkshire
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Editor Although there are likely to be a number of causes of SIDS, a neonate being a delicate rapidly developing individual and therefore at risk of many factors, could Vitamin K Deficiency Bleeding (VKDB) be one of them? Mark Powell writes (BMJ 1999;319:77(10 July) of "Suboptimal care implicated in many infant deaths in UK" describing the annual report of the confidential enquiry into still births and deaths in infancy published last year. Looking at 573 randomly selected infant deaths a panel judged suboptimal care was provided in 28% of cases for which a different approach 'might have made a difference to the outcome'. A further 22% of cases 'would reasonably have been expected to make a difference to the outcome'. The strongest link was for neonates (61%). Suboptimal care was described as - failure to act apppropriately, failure to recognise problems, failure of communication, shortfall in fetal surveillance, poor record keeping in a THIRD of neonatal and stillbirth deaths. Does this provide a scenario for misdiagnosis of VKDB as some staff merely "go thro' the motions" either injecting or providing orally Vitamin K and then fail to follow-up the neonate whose Vit K status drops dramatically at around 8 to 12 weeks for intramuscular injection and 3 to 4 weeks for oral administration(1)(2)(3)(4). Are all SIDS cases checked for Vit K levels, and are mothers assessed for having had eg. anticoagulant, antiepileptic or antibiotic therapy during gestation which are contributing factors to neonatal VKDB (5)(6)? Sutor AH et al, March 1999, Zeitschriften, Thrombosis, "Vitamin K Deficiency Bleeding in Infancy; On behalf of the ISTH Pediatric/Perinatal Subcommittee" say ..."The incidence of intracranial bleeding VKDB can be reduced by early recognition of the signs of predisposing conditions (prolonged jaundice, failure to thrive) and by prompt investigation of 'warning bleeds'....VKDB can be classified by age at onset into early (<24h), classical (days 1-7) and late (>1week, <6months) and by aetiology into idiopathic and secondary. In secondary VKDB, in addition to breast feeding, other predisposing factors are apparent such as poor intake or absorption of Vit K. Oral and intramuscular VK (one dose of 1mg) protect equally well against classical VKDB but intramuscular VK is more effective in preventing late VKDB.....protection against bleeding should be achievable with lower peak VK levels by using repeated (daily or weekly) small oral doses rather than using one intramuscular dose." In West Yorkshire typically a neonate is given an oral dose of Vitamin K at birth and then at 6 days. That's all. After this the will be in the hands of parents and perhaps a community midwife or health visitor. If a child is particularly, (and rarely), predisposed to VKDB or has an undiagnosed hepatobiliary problem (running a risk of VKDB) can the system ensure he/she does not become a victim of late-onset VKDB and, if the infant does suffer haemorrhage due to VKDB, is medical surveillance sufficiently powerful and objective enough to prevent such children being labelled with SIDS? If it is not, the probability of two children developing VKDB in a family will be higher after the first and hence a second 'SIDS death' more likely. Is Professor Roy Meadow's call for doctors to 'think dirty' where SIDS is concerned likely to confuse an investigation (typically involving police, social services and medical 'experts') and would it not be more prudent for Prof. Meadows to call for doctors to 'think scientific' and leave the police to 'think dirty'? Similarities and aspects of neonate SIDS and VKDB:- 1. Maximum occurrence in 1 to 3 months old children
Some of this knowledge is very new which explain the requirements for, and processes involved in, Vitamin K metabolism. Suspected dangers associated with Vit K injections - leukaemia and tumours - may have induced more oral Vit K supplementation than the more protective intramuscular route, leaving particular children at risk of VKDB - are these some of the SIDS cases we're seeing? Would a predisposition to VKDB be familial and therefore likely to affect more than one child in any family? Is VKDB initially ruled out at autopsy? Would medical strategies adopted in SIDS cases identify and admit to failing to maintain needy neonates' Vit K levels during the 'dangerous' first few months of life? Do vaccination schedules pose dangers to such children? If these questions cannot be answered one must question medical knowledge, opinion, and surveillance strategies in SIDS cases. Regards John H. Refs. 1. von Kries R, Drug Saf 1999 Jul;21(1):1-6 2. Muntean W, Z Geburtshilfe Perinatol 1986 May-Jun;190(3):107-13 3. Cornelissen EA et al, Arch Dis Child 1992 Oct;67(10):1250-4 4. Loughnan PM, McDougall PN, J Paediatr Child Health 1996 Jun;32(3):251-4 5. Astedt B, Semin Thromb Hemost 1995;21(4):364-70 6. Prescrire Int 1998 Aug;7(36):125-7 7. Koshihara Y, Nippon Rinsho 1999 Oct;57(10):2247-53 8. Weber P, Int J Vitam Nutr Res 1997;67(5):350-6 9. Kolb E, Z Gesamte Inn Med 1981 Nov 1;36(21):801-6 10. Matsuzaka T et al, Arch Dis Child 1993 Mar;68(3 Spec No):297-302 |
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J H Edwards
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EDITOR - The second surprising judgment, from the Court of Appeal, on the case of a solicitor whose two children died suddenly has now been reported (Daily Telegraph, 3.10.00) but has yet to receive the attention of your columns. In the first judgment odds of 73 million to one against were offered by the prosecution and apparently not challenged by the defence. They were calculated by assuming that all cases of sudden death in infancy from natural causes have the same cause and that brothers do not share any inborn similarity. The incidence in the population was squared. The definitive article by the late Professor Emery et al. (1) found a recurrence risk of almost 1% (44/500) and 'at least 20 of the second deaths in these families were due to natural causes'. These estimates were wrong in both logic and the nature of the disorders presenting in this way. The risk figure relevant to a conviction is the risk after an event has happened once. There are many causes of sudden infant death: some rare forms would be expected to have a recurrence risk of a quarter. The second judgment implied that even if wrong the figures were irrelevant and that 'the evidence was of overwhelming similarities between the two deaths'. It is these rare inborn errors of metabolism that would be expected to die at similar ages under similar circumstances. The published evidence on which both judgments were made is disturbing. It seems the second judgment accepted that the figures presented in the first were wrong but considered them irrelevant and confirmed the judgment on the basis of facts which were right but irrelevant. As both parents are solicitors we can assume all procedures were correct. The husband conceded that the three judges were 'eminent, respected, with intellect beyond ours'. If his hopes that 'sense has a way of seeping even through these walls' are to be realised he may need the help of better informed medical comment than I can offer and an editorial on what should be learned from this case. In view of the instant guilt which will be assumed by those involved in the investigation of further cases of recurrent sudden infant death without evident cause the implications of go far beyond the personal tragedy of a single family. J H Edwards
1) Debate on cot death J L Emery, Alison J Waite, C J Bacon, Peter Reder, and Sylvia Duncan BMJ 2000; 320: 310. |
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Ken Norman, Chairman, Portia Campaign The Croft, Bowness-on-Solway, Cumbria CA7 5AG
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Within the medical profession it is good that so many differing viewpoints are being made known concerning SIDS/abuse/manslaughter/murder. No doubt each reader forms the personal opinion that bats may be present in the belfrey. But there is huge danger when child deaths lead to prosecution. Judges and jurors have no means of assessing the evidence, and the forensic exidence presented with most conviction almost inevitably succeeds. We in the Portia Campaign believe that the consequence is a catastrophic (and increasing) number of false convictions of parents and carers. Is there a need for the defence, in these cases, to have the right to demand medication qualifications for judge and jurors? The law is very reluctant to make changes of this magnitude Could there be an informal group of medical experts (perhaps retired) who would consider the evidence before each such case comes to court, and present their own opinion, in as balanced a form as possible, for submission to the prosecution and to the defence? |
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Penny Mellor, Child Advocate Home 6 Coven Mill Close Coven WV9 5HX
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I too want full paediatric pathology done on any infant that dies. What astounds me that toxicology tests are not routinely done in cases of "sudden infant death". How can a true cause of death be established if the full range of tests have not been carried out in the first place? What if a baby was on medication at the point of death and the medication contributed to that death? What if the baby say had a reaction to fabric conditioners or air fresheners or other household products know commonly used? What if the baby had a toxic reaction to a vaccine? How can we either convict or clear a parent of "murder" when all the evidence hasn't been reviewed thoroughly with all possible explanations discounted? What if there are answers to the problem of SIDS in performing routine toxicology on these babies? Answers please, because I was under the impression that to be found guilty beyond a reasonable doubt meant just that and I fail to see that there can be a guilty verdict bought in when something so simple has not been performed. |
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