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EDUCATION AND DEBATE: A W Craft and D M B Hall Munchausen syndrome by proxy and sudden infant death BMJ 2004; 328: 1309-1312 [Full text]

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Medicalisation

C Johnson   (29 May 2004)

Recurrent SIDS is not synonymous with homicide.

James A. Morris   (29 May 2004)

The SBS Myth

Michael Innis   (30 May 2004)

Differentiating MSbP from Infanticide

John J Plunkett   (31 May 2004)

Shot at dawn as an example to others

Mark Struthers   (31 May 2004)

Muddled terms cause further confusion

Richard Braithwaite   (1 June 2004)

Re: Differentiating MSbP from Infanticide

Penny Mellor   (1 June 2004)

Protecting children from the Child Protection system

Charles Pragnell   (3 June 2004)

Munchausen Syndrome by Proxy Can Inflame Needless Fears

Loren Pankratz   (6 June 2004)

Sudden unexpected death and covert homicide in infancy

Christopher J Bacon, Sara Levene   (8 June 2004)

SIDS family clusters: the neglected role of infection

Paul N. Goldwater, Karl A. Bettelheim   (17 June 2004)

Re: SIDS family clusters: the neglected role of infection

Hilary Butler   (18 June 2004)

The mathematics of multiple sudden infant deaths

Ray Hill   (27 June 2004)

Study first, judge later

Viera Scheibner   (29 June 2004)

Re: Study first, judge later

Clive Davies   (29 June 2004)

Re: Study first, judge later

Michael D Innis   (30 June 2004)

Re: Re: Study first, judge later

Lisa C Blakemore-Brown   (30 June 2004)

Comparative Child Mortality of Munchausen's By Proxy

Colin Pritchard   (2 July 2004)

Some Questions for Clive Davies or Anyone

L. Travis Haws   (3 July 2004)

Re: Study first, judge later

Viera Scheibner   (3 July 2004)

Mortality in Munchausen's By Proxy exaggerated.

Brian Morgan   (3 July 2004)

Re: Comparative Child Mortality of Munchausen's By Proxy

Michael D Innis   (3 July 2004)

Concerns about MSBP

Helen P Hayward-Brown PhD   (4 July 2004)

Re: Comparative Child Mortality of Munchausen's By Proxy

Charles Pragnell   (7 July 2004)

Re: Some Questions for Clive Davies or Anyone

Viera Scheibner   (23 July 2004)

Getting the facts right

Penny Mellor   (27 July 2004)

MSbP and sudden infant death: authors' reply

David M Hall, Alan Craft   (11 October 2004)

Re: MSbP and sudden infant death: authors' reply

C Johnson   (11 November 2004)

Re: Re: MSbP and sudden infant death: authors' reply

Dr John Rumbold   (12 November 2004)

Re: Re: Re: MSbP and sudden infant death: authors' reply

Penny Mellor   (13 November 2004)

Re: Re: Re: Re: MSbP and sudden infant death: authors' reply

Ed Cooper   (14 November 2004)

What is MSbP?

Brian Morgan   (14 November 2004)

Re: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply

Penny Mellor   (16 November 2004)

Re: Re: Re: Re: Re: MSbP and sudden infant death: authors' reply

C Johnson   (16 November 2004)

Defining FII

Ed Cooper   (18 November 2004)

MSBP/FII - science and facts are needed, not mythology.

Charles Pragnell   (21 November 2004)

Re: Defining FII

C Johnson   (23 November 2004)

Re: Munchausen syndrome‚ MSBP, and FII

Graeme Johnston   (23 November 2004)

Re: Defining FII

Ed Cooper   (23 November 2004)

FII - give us the science and not the mythology

Charles Pragnell   (26 November 2004)

Re: Re: Munchausen syndrome‚ MSBP, and FII

Michael O'Donnell   (26 November 2004)

Defining FII - WINDSCALE NOW SELLAFIELD - MSbP NOW FII

Clifford G. Miller   (26 November 2004)

Re: Defining FII

Michael D Innis   (27 November 2004)

Cauliflowers/cabbages

Mark Struthers   (27 November 2004)

Re: Re: Defining FII

Penny Mellor   (27 November 2004)

SIDS – Joining The Dots

Michael D Innis   (5 May 2007)

Sudden Infant Death - Revisited

Michael D Innis   (19 June 2007)

Medicalisation 29 May 2004
C Johnson, Parent LA9 Send response to journal: Re: Medicalisation	Is not MSbP/FII the medicalisation of deception simply because it occurs in a medical context? Here are four historical examples: 1 - is it a case of MSbP/FII if a mother falsely tells doctors her child is ill in order to get her husband released from jail on compassionate grounds? 2 - is it a case of MSbP/FII if CVS records a mother taking out her frustration at being stuck in hospital on her infant, then explains away the broken arm as accidental? 3 - is it a case of MSbP/FII if a mother, already convicted of cheque and credit fraud, falsely tells her neighbours her child has cancer in order to raise financial donations? 4 - is it a case of MSbP/FII if a father falsely tells his employer his child is sick in order to get time off work? Cases one, two and three involved the mother; case four involved the father. Cases one, two and three have all been identified as MSbP/FII by one expert or another. Case four has not. In cases one and four the parent perpetrated no physical acts upon the child; in cases two and three the parent did (violently in case two, not in case three). In cases three and four the parent did not approach healthcare workers; in cases one and two the parent did. Would it not be better to identify an act of abuse by its name - e.g. smothering, poisoning - and require evidence of the act before accusation, and proof in prosecution? Would it not be better to identify an act of deception by its name - e.g. fraud - and also prosecute it accordingly? Competing interests: None declared
Recurrent SIDS is not synonymous with homicide. 29 May 2004
James A. Morris, Consultant Pathologist Department of Pathology, Royal Lancaster Infirmary, Lancaster LA1 4RP. Send response to journal: Re: Recurrent SIDS is not synonymous with homicide.	Professors Craft and Hall state "we are concerned that everything we have learnt over the past 40 years about sudden infant death syndrome and the spectrum of child abuse seems to have been forgotten". This is a response to the intense media interest and comment following three recent high profile cases in which mothers were accused of murdering their infants. One problem is that much that is written about sudden infant death syndrome (SIDS) and child abuse is based on insecure foundations. For instance Craft and Hall state "Bleeding from the nose and mouth suggests deliberate suffocation, and the presence of haemosiderin laden macrophages in the lungs might signify previous episodes of suffocation". But there is no reliable information on the sensitivity nor on the specificity of either marker. Thus it is not possible to calculate positive and negative predictive values and use the results in a sensible and scientific manner. This would not be good enough for any other branch of medicine and should not be acceptable in a Court of Law. The authors go on to state "In a single case neither the autopsy findings nor other background information are likely to provide unequivocal evidence". With that I agree. My main concern, however, is their section on recurrent sudden infant death symdrome; in my opinion it is misleading. The risk of SIDS was close to 2 per 1000 live births in the mid 1980s but then gradually fell to approximately 0.5 per 1000 following the "back to sleep" campaign. The risk in a subsequent sibling of an index case was approximately 1 per 100 in the 1980s and is of the same order at the present time. Any study attempting to measure recurrent risk inevitably deals with low numbers and has wide confidence intervals but the several different estimates give similar results [1 - 4]. It is generally accepted that most cases diagnosed as SIDS are due to natural disease (90% or over) but a minority (10% or less) are a consequence of gentle smothering that leaves no marks of injury. All natural disease is a consequence of the environment interacting with genetic constitution and chance. The environment and genetics together set a level of risk that could be 1 in 10, 1 in 100, 1 in 1000, 1 in 10,000 and so on. Since our environments vary and our genetic constitutions vary then so will the risk between infants and between families. Let us assume, to simplify presentation and calculation, that the risk of SIDS is 1 per 1000 for the general population (midway between the 1985 and 1995 figures). If SIDS were due entirely to chance, with no environmental or genetic influence, and the risk was exactly the same in all infants then the risk of two deaths in a mother who had given birth to two infants would be 1 per million. The risk of two deaths in a mother who had had three infants would be 3 per million, and the risk of two deaths in a mother with four infants would be 6 per million. There are approximately 700,000 live births per annum in England and Wales; thus each year at least one mother would have a second case of SIDS. She would risk being accused of homicide and might be found guilty but she would be innocent. The risk of SIDS, however, is not constant. It varies because there are environmental influences that vary such as sleeoing position and exposure to tobacco smoke amongst others [3]. The CESDI SUDI study found that the average risk in families with no recognised environmental risk factors was 1 in 8543; in those with one factor it was 1 in 1616; in those with two factors it was 1 in 596; and in those with three it was 1 in 214. A consequence of this is that if the risk varies then the number of families with two deaths will rise. To illustrate this point consider a population in which the overall risk is 1 per 1000, but 90% have a very low risk and 10% have a risk of 1 per 100. This would in fact give a recurrence rate in siblings of 1 per 100. Mothers at risk in this population would have a 1 in 10,000 chance of two deaths if they had two infants and a 3 per 10,000 chance of two deaths if they had three infants. In a population the size of England and Wales there would be approximately 7 to 10 new cases each year in which a mother had a second case of SIDS. This is higher than the number actually observed (extrapolated from the CESDI study). Thus if risk varied to this degree all second deaths could be explained as natural disease. The CESDI study showed that the average risk in families with no recognised environmental risk factors was 1 in 8500. This does not mean that the actual risk in all those families is the same; some will have a lower risk and some a higher risk. This is because they will vary in hitherto unrecognised environmental risk factors and in genetic risk factors. If one of the families has a cot death then that family is more likely to be in the higher rather than the lower risk groups. The best estimate we have of the risk prior to the first death is 1 in 8500, but the best estimate after the first death is 1 per 100 i.e. the risk of death in a subsequent sibling. If a mother in this group has two infants following a first death then the risk of a second death is 1 in 50. Craft and Hall state "Chance has no memory, so a low risk family would have a 1 in 8500 risk of a second death". The first part of the sentence is correct, chance has no memory, but the second part is simply wrong. The prior risk is 1 in 8500 but the subsequent risk is much higher for reasons given above. This is a serious error in view of all the discussion that has followed the notorious quotation of "a one in 73 million chance" and indicates a major failure of the peer review process of the British Medical Journal. Craft and Hall go on to state, "There is little evidence of familial clustering of SIDS". This is misleading. All natural disease is influenced to some degree by genetics and the environment, as noted above. Siblings share a similar environment and have genes in common so that the risk of SIDS must be increased in families compared with the general population, and studies indicate that it is [1 - 4]; the risk rising from around 1 per 1000 to 1 per 100. If there are two deaths in a family then homicide is a possibility as is inherited disease. But if investigation of inherited disease draws a blank that does not mean that homicide is the most likely. At least one eminent paediatrician has argued that two deaths indicate homicide or some gentic disease unknown to medical science; a statement that is superficially plausible but deeply flawed. There are 30,000 genes in the genome and myriad ways in which deleterious mutations and neutral mutations could influence the risk of death. A failure to name the genes responsible is not a reason for doubting their influence. It is possible to do a similar analysis for three deaths in one family. If the risk is 1 per 1000 for all infants then the chance of a mother with three infants experiencing three deaths is 1 per billion. There haven't been a billion births in England since the Norman Conquest and that remote possibility can be ignored. But if 90% of the population have a low risk and 10% have a risk of 1 per 100 then a new family with three deaths would appear in England and Wales every ten years. If we then allow for the fact that the mother might have four or more children with just three deaths then the situation would occur every four years (approximate). A one per 100 risk is a low genetic risk and it is likely that there are a few families in which the risk is closer to 1 in 10. If that were the case then families with three deaths would arise at a rate of one per year or one every other year. That is approximately the rate at which they do occur and thus even three deaths don't indicate homicide. A mother should not be convicted of murder unless there is evidence, beyond reasonable doubt, that a crime has been committed. The medical evidence for smothering, in the absence of significant injury, is rarely enough. A conviction should not be based soley on the occurrence of two or three infant deaths in one family as natural disease is a more likely explanation. I agree with the authors that more research is required, particularly into the pathogenesis of SIDS. The sciences of genomics and proteomics can provide answers if the investment is made. References 1. Peterson DR, Chinn NM, Fisher LD. The sudden infant death syndrome. J Paediatr. 1980; 97: 265 - 270. 2. Irgens LM, Skjaerven R, Peterson DR. Prospective assessment of recurrence risk in sudden infant death syndrome siblings. J Paediatr. 1984; 104: 349 - 351. 3. Fleming PJ, Bacon CJ, Blair PS, Berry PJ. Sudden unexpected deaths in infancy - the CESDI SUDI studies 1993 - 1996. London: The Stationery Office, 2000. 4. Irgens LM. Recurrent death from natural causes : SIDS and non SIDS. Proceedings of 7th SIDS International Conference, Florence, 2002; 26 - 27. Competing interests: I was an expert witness, introduced by the defence,in two of the three cases mentioned in the above article. i am also involved in a further case in which the issues are similar.
The SBS Myth 30 May 2004
Michael Innis, Director Medisets International Home 4575 Send response to journal: Re: The SBS Myth	Editor, Professors Craft and Hall state, “Caffey described what was undoubtedly child abuse in 1946 but was reluctant to draw the obvious conclusions.” The constellation of subdural haematoma, brain injury and retinal haemorrhages in a child is what they are referring to. However, child abuse is not necessarily the way in which these lesions can be induced. From an analysis of 22 cases of alleged child abuse sent to me from the United Kingdom, United States of America, Australia and Iceland I conclude 1.Vaccines administered within 21 days of the onset of symptoms 2.Disorders of Haemostasis and 3.Nutritional disorders are the main causes of the condition commonly known as Shaken Baby Syndrome. Can Professor Craft or Professor Hall, or anyone of the 106 signatories [1] to the letter responding to the Editorial of Drs Geddes and Plunkett, document a SINGLE case in which the three causes mentioned above could be excluded? No they cannot. As Drs Geddes and Plunkett wisely conclude in their Editorial on the subject “We need to reconsider the diagnostic criteria, if not the existence, of shaken baby syndrome.” [2] I can only add the Shaken Baby Syndrome is a myth invented to hide ignorance and inadequate or improper investigation. Michael D Innis MBBS; DTM&H; FRCPA; FRCPath Reference: 1.Reece RM The evidence base for shaken baby syndrome BMJ 2004;328:1326-1317 2.Geddes JF, Plunkett J. The evidence base for shaken baby syndrome Editorial BMJ 2004; 328; 718 –720 Competing interests: Previously declared paid Court appearances
Differentiating MSbP from Infanticide 31 May 2004
John J Plunkett, Laboratory and Medical Education Director Regina Medical Center, Hastings, MN 55033 Send response to journal: Re: Differentiating MSbP from Infanticide	Infanticide: The intentional killing of an infant or child. It may be "serial". It is murder. I don't know the psychopathology. However, it is NOT MSbP. It does NOT present as an ALTE. It presents as a dead child. It may be impossible to detect or prove. MSbP: Factitious or induced illness in an infant or child with the intent to make oneself appear as the "savior". This MAY present itself as an ALTE. There is NO intent to kill. I, too, have seen the videos. When MSbP and infanticide are "lumped", both lose their meaning. Competing interests: As previously disclosed
Shot at dawn as an example to others 31 May 2004
Mark Struthers, GP Bedfordshire Send response to journal: Re: Shot at dawn as an example to others	This defensive paper by professors Craft and Hall is a sad reflection on paediatrics and child protection and the state they’re in. Amidst widespread confusion, threat and denial they’ve got it wrong again. The protagonists, both medical and legal, in this sorry saga should admit mistake, apologise and accept fair punishment for doing wrong. Then will come ‘closure’. Only then can we move forward to begin the process of restoring public faith in a child protection system that should befit a civilised society. There is no other way. Competing interests: None declared
Muddled terms cause further confusion 1 June 2004
Richard Braithwaite, Staff Grade Psychiatrist West Wight Community Mental Health Team, Chantry House, Pyle St, Newport, Isle of Wight, PO30 1JW Send response to journal: Re: Muddled terms cause further confusion	Editor, Professors Craft and Hall [1] add confusion to an already complex area by muddling various medical and legal terms surrounding the issue of homicide and sudden infant death syndrome (SIDS). Infanticide is a legal term, defined in the UK by the Infanticide Act of 1938. It specifically refers to death caused by a mentally unbalanced mother within the first year of life, the mental imbalance caused by the effects of childbirth or lactation [2]. Thus it does not include every homicide by a parent upon his or her infant. The other two legal categories of homicide are murder and manslaughter. With the exception of manslaughter, Craft and Hall appear to use all these terms interchangeably. Munchausen syndrome by proxy, as first described by Meadow, involves parents fabricating or faking symptoms in their children, thus seeking medical investigations and needless treatment [3]. It is classified in the tenth revision of the International Classification of Diseases (ICD-10) as a form of child abuse, rather than as a medical diagnosis. This is in contrast to the unrelated Munchausen syndrome, which is classified in ICD- 10 as a personality disorder [4]. The 10% of SIDS cases that may be due to foul play are not related to Munchausen syndrome by proxy. The parent is not seeking unnecessary investigations or treatment for the child; he or she has purely and simply killed the child. Craft and Hall are unable to provide any evidence that those who exhibit Munchausen syndrome by proxy behaviour during the first few months of parenthood go on to kill their babies, subsequently claiming “cot death”. They point out, in a section entitled “Is Munchausen’s the best label?” that “many UK paediatricians feel that the term [Munchausen syndrome by proxy] should be abandoned” [1]. They back up this view robustly with no counter-argument, yet use this very label in the title of their paper. There is ample research, cited in the paper, to suggest that a minority of child abusers do fit Meadow’s description of Munchausen syndrome by proxy; the term need not be abandoned in those circumstances. But it cannot be used when describing parents who kill their babies. The public outcry over this issue has been caused by misinformation about the frequency and causes of SIDS. Let us not continue this process by confusing sudden infant death, of whatever cause, with an unrelated form of child abuse that is serious but rarely lethal. References: 1. Craft AW, Hall DMB. Munchausen syndrome by proxy and sudden infant death. BMJ 2004;328:1309-1312. 2. Gelder M, Gath D, Mayou R, Cowen, P. Oxford Textbook of Psychiatry (3rd Edition) Oxford: Oxford University Press, 1996. 3. Meadow R. Management of Munchausen syndrome by proxy. Arch Dis Child 1985;60:385-93. Cited in [2] 4. World Health Organisation. The ICD-10 International Classification of Mental and Behavioural Disorders. Clinical Descriptions and Diagnostic Guidelines. Geneva: WHO, 1992. Competing interests: None declared
Re: Differentiating MSbP from Infanticide 1 June 2004
Penny Mellor, Advocate Home WV9 5HX Send response to journal: Re: Re: Differentiating MSbP from Infanticide	Craft and Hall go on to state, "There is little evidence of familial clustering of SIDS". Does that mean that the jury in the Patel trial were wrong? Does it also mean that Lord Deputy Chief Justice Judge is wrong when the court of appeal in Cannings stated in paragraph 177 "We recognise that the occurrence of three sudden and unexpected infant deaths in the same family is very rare, or very rare indeed, and therefore demands an investigation into their causes. Nevertheless the fact that such deaths have occurred does not identify, let alone prescribe, the deliberate infliction of harm as the cause of death. Throughout the process great care must be taken not to allow the rarity of these sad events, standing on their own, to be subsumed into an assumption or virtual assumption that the dead infants were deliberately killed, or consciously or unconsciously to regard the inability of the defendant to produce some convincing explanation for these deaths as providing a measure of support for the Prosecution's case. If on examination of all the evidence every possible known cause has been excluded, the cause remains unknown." (1) It is interesting that Dr Plunkett makes the comment that he has seen CVS tapes and states for the record that there was no intention to kill, unlike the paper by Sudden unexpected death and covert homicide in infancy S Levene, C J Bacon. (2) in which they assert "Suffocation may leave no external signs and noclear postmortem evidence.10 The significance of intra-alveolar haemorrhage and siderophages is still subject to debate.11 We know that mothers do sometimes suffocate their babies because a number have made very credible confessions,12 13 while others have been witnessed by video surveillance.14" The implication being that because in the UK parents/carers have been caught on camera, that this in turn would lead to death "covert homicides". Of course the reality is quite different. Intervention at 20 seconds (3) occurred and therefore there is no way of knowing whether or not the "smothering" would have continued. It is a presumption only that it would ultimately have led to death and furthermore there is no reference to a control group for this particular research, we have no idea how many parents/carers were filmed that did not harm their child in any way. We can't work out what percentage of parents may harm their child if we only have the one set of figures to study and in particular this research was not random the suspicion of abuse was already there which invalidates the whole thing as a scientific study to be relied upon. As to credible confessions, I question this ascertation, mothers who have had children die for no apparent reason feel incredibly guilty and further to that, if they have surviving infants and there is a prospect of their permanant removal if they don't "admit", there is a very strong motive to "confess" to something you haven't done and within the criminal arena even more so as a confessed infanticide does not lead to imprisonment. Far more research into how the confessions were obtained and under what circumstances needs to be done before such claims can be made. Or even references to research so that we can study this particular statement. I hope that forensic psychiatrists and psychologists contribute to this particular aspect of the debate. When all is said and done, this whole area has been confused by a label that does not look at evidence, just a cluster of events, which may or may not be sinister. The research into this area is at best inadequate, confusing and based mainly on suposition and anecdotal stories. That is not robust enough to remove children and incarcerate mothers. I maintain my stance that until we have a full public inquiry into this entire area, children can not and will not be adequately protected, because in pursuing a negative false allegation, resource is being drained from a child that really does need protecting and to falsley accuse a parent with surviving children is an abuse in itself. 1 http://www.bailii.org/ew/cases/EWCA/Crim/2004/1.html 2 http://press.psprings.co.uk/adc/may/443_ac36202.pdf. 3 http://medicine.ucsd.edu/peds/Pediatric%20Links/Links/General%20Pediatrics%20Inpatient/Covert%20Video%20Recordings%20of%20Life%20Threatening%20Child%20Abuse%20Pediatrics%20Nov%201997.htm. Competing interests: Campaigner against false allegations of child abuse
Protecting children from the Child Protection system 3 June 2004
Charles Pragnell, Expert Defence Witness - Child Protection U.K./Australasia Send response to journal: Re: Protecting children from the Child Protection system	Drs Craft and Hall are suggesting moving forward by preserving the status quo with only a few minor modifications to what has been exposed on many occasions as a child protection system which is deeply, flawed, erratic, and grossly dysfunctional that has been contributed to in large measure by the shortcomings and inadequacies of medical research and opinion. Craft and Hall “are concerned that everything we have learnt over the last 40 years about sudden infant death syndrome and the spectrum of child abuse seems to have been forgotten.” What the public and many professionals have not forgotten are the child protection scandals of the last 40 years of which recent events are just the latest episode. These child protection scandals have caused incalculable harm to many thousands of children and their families and to many care workers, teachers, and others, from false and wrongful accusations of child abuse. Many thousands of children have been wrongfully removed into state care and adoption and many hundreds of parents have been imprisoned. Yet on the other hand, many children have been killed or been horribly abused while agencies failed to act on the signs of abuse and abysmally failed “to communicate with each other”. After every one of these scandals the child protection agencies have made claims that lessons have been learned and procedures have been changed to prevent similar recurrences only for another scandal to occur within a few years if not months when another child has died or another family has been destroyed by false accusations. It is clear that lessons have not been learnt from any of these scandals, or at least only how better to protect agencies and individuals from the legal and financial consequences of their malpractices and misdeeds. Many of these scandals have involved the use of medical and other theories of child abuse which lacked scientific integrity and authenticity but have been zealously grasped by the child protection industry under a perverse pretext of protecting children whilst inflicting immense harm on children and families by their unnecessary and unwarranted interventions and with little thought or compassion for the innocents who suffer as a consequence of their ill-considered decision making based on those flawed theories. Even in those instances where only minor abuse of a child has occurred, the punishment far outweighs the offence and often results in children being separated for the rest of their lives from their genetic family and kinship groups. Those who administer and implement the child protection system seem not to know nor understand the devastating effects on children and families from false accusations of abuse. Of children who live in constant fear of being removed and extreme anxiety that they will be torn from their familiar world, never to return. Of parents who are stigmatized and persecuted in the communities in which they live, who are rejected by their extended families, neighbours and friends and are .paralysed with dread that every knock on the door may lead to their imprisonment and the destruction of their family. Research by Wexler (1991) and others has shown that, “the War against child abuse has become a War against Children” and that the incidence of false and wrongful accusations of child abuse has reached unconscionable levels. It is this research which appears to have been forgotten. The child protection industry now operates Craft and Hall are correct when they state that there is a desperate need to “restore the faith of the public and the professions in the child protection system that are vital for a civilized society”. But such faith, trust, and confidence will not be obtained by continuing to go into denial that there are very serious defects in the present child protection system which are leading to immense suffering by children and families from overzealous and unnecessary interventions and failures to intervene. Nor will it be achieved by paediatricians who are claiming victim status or that there is some kind of orchestrated campaign to discredit them. Such claims are as fanciful as the unproven theories on which they have based their assertions of child abuse. Such a campaign would be welcome if it eventually led to a root and branch reform of the present child protection system. I agree with Dr Mark Struthers that the child protection industry can only move forward when those responsible are able to admit their wrongdoings, apologies are given to those who have been harmed by the child protection system, and the wrongdoers are able to accept fair and just punishment for their misdeeds. The lessons which must now be learned are that a rigorous procedure of investigation and authentication must be introduced to prevent the introduction of medical theories of child abuse which have no basis in scientifically-conducted research and are no more than conjecture, speculation, and supposition. In the future children and families must be protected from a system which is terrorising and harming children and parents under a perverse pretext of protecting those children. Yet at the same time is ignoring those children where the signs of abuse are obvious and the children are dying as a consequence. And smug defensive comments of “damned if we do and damned if we don’t”, are no longer a valid excuse for incompetence and inaction. Competing interests: Concern to reform of the U.K. Child Protection system
Munchausen Syndrome by Proxy Can Inflame Needless Fears 6 June 2004
Loren Pankratz, Clinical Professor, Oregon Health & Sciences University 1525 SW Palatine St.. Portland, OR 97219 Send response to journal: Re: Munchausen Syndrome by Proxy Can Inflame Needless Fears	Craft and Hall(1) suggest that we must not forget everything we have learned over the past 40 years about child abuse. But do not forget that we fall off both sides of the horse. To his surprise, Roy Meadow(2) admitted in 1995 that Munchausen syndrome by proxy had become so popular that it was being overused and misunderstood by some social workers and legal professionals. Since then, many have tried to define the disorder in a way that avoids over-inclusion and diagnostic error. However, the medical literature does not convey the prevalence of these misunderstandings or the devastating consequences, especially as they unfold in juvenile courts across the country. In my experience, most of these mothers have problems that should have been solved clinically, but instead they became entangled in a confrontational legal system. I have written 22 reports on mothers accused of Munchausen syndrome by proxy, and I offer them to any institutionally approved committee investigating this disorder. Although some describe tragic child abuse, the majority illustrate how quickly this diagnosis can enflame needless fears. 1. Craft AW, Hall MB. Munchausen syndrome by proxy and sudden infant death syndrome. BMJ 328:1309-1312. 2. Meadow R. What is, and what is not, "Munchausen syndrome by proxy?" Arch Dis Child 1995;72:534-538. Competing interests: I provide consultations on MSbP.
Sudden unexpected death and covert homicide in infancy 8 June 2004
Christopher J Bacon, Medical adviser, Foundation for the Study of Infant Deaths Foundation for the Study of Infant Deaths, Artillery House, Artillery Row, London SW1P 1RT., Sara Levene Send response to journal: Re: Sudden unexpected death and covert homicide in infancy	We welcome this timely discussion of a very difficult subject, and particularly the recommendations for better procedures when parents are suspected of harming their children. However we should like to comment on two points of detail. First, the authors say it is estimated that around 10% of otherwise unexplained infant deaths may be caused by deliberate suffocation, citing our recent paper [1] as a reference. In fact in our paper we make it plain that the figure of 10%, which was derived from the CESDI SUDI studies [2], referred not just to deliberate suffocation, but to deaths arising from all kinds of maltreatment, ranging from deliberate smothering to negligence and poor care. Deaths due to deliberate suffocation were not separately identified, but they comprise only a proportion of the 10% in question. Second, we agree with Professor Morris [3] that the risk of a second case of SIDS in a family is not the same as the risk for the first death. Calculation of the risk of repeat SIDS from observational studies is complicated by the difficulty in identifying and excluding cases of familial disease and covert homicide. On theoretical grounds, however, SIDS, like most other conditions, arises from a combination of genetic and environmental factors, and if these stay constant, a family who has lost one baby by SIDS must have an increased risk of losing another. References 1. Levene S, Bacon C. Sudden unexpected death and covert homicide in infancy. Arch Dis Child 2004; 89: 443-7. 2. Fleming P, Bacon C, Blair P, Berry PJ. Sudden unexpected deaths in infancy: the CESDI SUDI studioes 1993-1996. London, Stationery Office 2000. 3. Morris JA. Recurrent SIDS is not synonymous with homicide. bmj.com 29 May 2004. Competing interests: Both the authors are or have been medical advisers to the Foundation for the Study of Infant Deaths
SIDS family clusters: the neglected role of infection 17 June 2004
Paul N. Goldwater, senior consultant clinical micr Women's & Children's Hospital, North Adelaide, South Australia 5006, Karl A. Bettelheim Send response to journal: Re: SIDS family clusters: the neglected role of infection	In the very interesting article by Craft & Hall (BMJ 328:1309- 1312), the authors discuss the argument that multiple deaths of infants in one family may indicate the possibility of infanticide, and point to "little evidence of familial clustering of sudden infant death syndrome". In cases where this clustering occurs they suggest two possibilities: homicide or inherited conditions. We would like to draw readers' attention to a third possibility, which has been neglected by many investigators of this condition, namely infection. Indeed, the non-random socioepidemiological factors listed by the authors apply even more to risk of infection than to risk of infanticide. In our researches on a possible infective agent responsible for sudden infant death syndrome, especially the possible role of Escherichia coli, we have noted cases where siblings who died of sudden infant death syndrome some time apart carried the same E. coli serotype, indicating infection from a common source. Karl A Bettelheim Paul N. Goldwater Competing interests: None declared
Re: SIDS family clusters: the neglected role of infection 18 June 2004
Hilary Butler, freelance journalist home 1892 NZ Send response to journal: Re: Re: SIDS family clusters: the neglected role of infection	Dear Sir, Paul Goldwater and Karl Bettelheim, indeed raise a very important point about endotoxemia and SIDS. I have followed all the literature on e -coli endotoxemia and endotoxemia in general as far back as I could trace. I would like the above authors to expand for the readers, on their comments. Drs Goldwater and Bettelheim mention one serotype of E.coli. However, I believe that this is misleading for the following reasons. It is clear from the medical literature from way back, that all serotypes of E.coli (and other bacteria) are capable of endotoxemia. This is not a function of ONE type of e.coli, but seems to be, rather, a function of a fragment of lipopolysaccharide which (for the lack of a better description) floats free off each bacteria, when it multiplies in the gut. The toxicity of the lipopolysaccharide doesn't appear to be dependant on the type. It appears to be a function of the reproductive nature of the bacteria itself. So how might this impact on babies? We all know that endotoxemia causes dysfunction in both the cardiac and respiratory system, that bradycardia is not uncommon..That bacterial endotoxins not detoxified by the liver injure blood platelets which then release large amounts of serotonin (as much as 100-fold). What is the result of this? The Bezold- Jarish reflex, leading to profound bradycardia, hypotension and vascular collapse. If rather less sudden, you would expect to see oedema and haemorrhage by diapedesis.. and after six hours of more, if the process is slower, you would expect to see fibrin platelet clots present as disseminated intravascular coagulation in lungs, kidneys and other organs and tissues. But DIC is not necessary for death by endotoxemia. It all depends on the baby, the health of the baby, feeding methods, medical interventions which have been "imposed" on the baby. So what might doctors be able to test to show the effects of endotoxemia? I have a letter on file from a Professor L. Joe Barry, in which he discusses the fact that Dr Henry Lardy reported finding low levels of the enzyme Phosphoenolypyruvate carboxykinase (PEPCK) in livers of human infants who died of SIDS. (I have this paper) In this letter Professor Barry then describes that he has in brief, proven that endotoxin blocks synthesis of PEPCK and since it has a half life of about two hours, results in changes soon after endotoxin is present. I notice also that a paper in Epidemiol Infect. 1993, 110, 507-617 discussed the role of toxigenic Staphylococcus aureaus likewise causing a potential form of endotoxemia in SIDS children. Having read all of Goldwater and Bettelheims’ papers, I am struck how little notice the rest of the medical world has taken of their vital work. In particular, it seems to me to be a relatively simple matter to test for endotoxemia, and perhaps for that reason, should be part of routine testing on all near SIDS and SIDS babies, yet who else does it, but Drs Bettelheim and Goldwater? In other letters such as Archives of disease in childhood, 1994; 70:252 (" Sudden infant death syndome" by JCK Wells, and PSW Davies), the point is made that heat production has been identified as a risk factor in SIDs. Yet no-one in the endotoxin field has made the point that bacteria such as E.coli literally go berserk when in the presence of heat, either heat by fever/infection, or overclothing.... Furthermore, anyone familiar with the various clinical scenarios and autopsies following SIDs can at times clearly see tell-tale signs of endotoxemia, yet, because it is not understood by clinicians not versed in its vast metabolic effects, these "signs" are considered to be “of unknown origin.” One of the earliest references that would have alerted doctors wanting to understand the role of endotoxin, was an article in Amer J. Dis Child 89:701-716, 1955 ("Hepatitis in Infants and Small Children by Richard Capps, et al) , which showed that inoculation of DPT and infection with other viral agents, caused liver dyfunction changes of shorter duration, which could be confused with hepatitis virus infection. This was later confirmed in mice ( as opposed to humans), in an abstract from the Sixth International Symposium on Pertussis (Dept of Health and Human Services, USPHS, FDA, 1990) on page 124 called "Alternations in Hepatic Drug Metabolism following Vaccine Administration to Mice", by Sherry Ansher and William Habig, who worked for the Center for Biologics Evaluation and Research, Bethesda Maryland. This abstract stated: "There have been several reports of inhibition of drug metabolism following administration of vaccines .... the relationship of these observations to the mechanism for the inhibition of drug metabolism is not known..." They then go on to describe what happened on the administration of DTP...; "DPT vaccine increased hexobarbital-induced sleep time in mice injected with a single human dose of vaccine. Measurement of barbiturate- induced sleep time (the time from injection of hexobarbital to return of the redressment or righting reflex) is a sensitive indicator of specific cytochrome P-450 enzyme function. A minimum of one single human dose was required to induce significant increases in hexobarbital-induced sleep time. Sleep time increased significantly 12 hours after DTP vaccine administration and reached a maximum increase of 2.2 - 2.4 fold above controls 7 - 10 days after a single injection. The effect declined rapidly to levels not significantly different from the controls by day 14. DPT vaccine caused dose and time dependent alterations in hexobarbital- induced sleep time and drug-metabolizing enzyme actitivies. Microsomal cytochrome P-450 and other microsomal and cytosolic enzyme activities were altered in a time dependent manner in mice injected with DTP vaccine. Spectrally assayed cytochrome P-450 was decreased by 50% for 7 days, and similar effects were observed in benzpyrene monooxygenase, benzphetamine demethylase, and ethylmorphine demethylase activity. Cytosolic glutathione transferases and quinone reductase activities were altered, but the time course was different than that observed with the microsomal enzyme activities." "the increased hexobarbital-induced sleep times were not limited to DTP vaccine. Other vaccines with Bordetella pertussis components caused alterations in drug metabolism. One common component of many vaccines is endotoxin, and its presence could enhance, or be responsible for, the observed effects on hepatic drug metabolism." Since this time, there has been little done in children. Though there is one study ( http://www.pediatrics.org/cgi/content/full/101/3/e3 ) Interleukin-6, C-Reactive Protein, and Abnormal Cardiorespiratory Responses to Immunization in Premature Infants”by Massroor Pourcyrous* et al, Clearly, for anyone with any clinical understanding of endotoxemia this study shows this phenomenon very clearly. Yet it appears the authors were stumped. E-coli and endotoxemia in general, in babies, is a grossly neglected, but blatantly obvious area, which has been disregarded, ….. and had it not been so neglected, parents would be better off today. So lets consider endotoxemia briefly in a broader context. A key article to understand this in a fuller context is "Role of the Intestinal Flora in Major Trauma" by P.W.H. Woodruff et al. in The Journal of infectious diseases, Vol 128, Supplement, July 1973. (The whole supplement is on endotoxemia, and is very good. Just because it is "early work", doesn't mean anyone should turn their nose up at it...) They took patients with septic and nonseptic dosorders in whom circulating endotoxin was demonstrated. Tthey also encountered additional patients who had clinical features suggesting persisting endotoxemia, but in whom the test was negative. This study looks at these patients in detail. This article clearly shows "Data indicated that the finding of endotoxin in the livers of these patients signified an endotoxemia consequent on a failure of the endotoxin-detoxifying mechanisms."....."Because of the extreme sensitivity of man to endotoxin, we suspected that clinical endotoxemia.... we undertook postmortem studies on a random series of patients having observed that in animals dying of endotoxic shock, the liver and spleen immediately after death contain considerably higher concentrations of endotoxin that the blood or other tissue..." Without quoting more, they found that some patients lost the ability to detoxify endotoxin, and that because postmortems showed that a septic process was absent, they assumed that the endotoxin was derived from the intestine. So why is this not looked at in babies? It is plain that not only CAN vaccines stop the liver detoxifying endotoxin in SOME babies, the risk to that particular baby is greatly increased if their gut flora have large amounts of E.coli as a result of bottlefeeding, or stress. But the fact is, that if the vaccine was NOT given, these baby’s livers would at least have a better chance to deal with both endogenous and vaccine endotoxin. In essence, in some babies, vaccines could be the equivalent of pulling a trigger, releasing a bullet. The key to survival for these babies, is a well functioning liver, and also nutritional adequacy. There is enough work now to show that adequate vitamin C is crucial in all the endotoxin pathways. I notice that from the very start of Dr Bettelheim and Goldwater's interest in endotoxin, they do not quote key historical information relating to either the overall clinical problem or the actual process. Perhaps that is because some of it, like J. Bendig and H Haenel's landmark paper, called "Gastrointestinal microecology in sudden unexpected death of infants" in "Proceedings of the Eighth International congress of Butrition, Prague, September 1969 is a bit old??? Or take one of the best papers around "The role of Endotoxin in Liver injury" by James P. Nolan in "Gastroenterology 69: 1346-1356 1975. Yes old. But sets it all in its proper context. To study a topic requires a foundation. Gut flora and endotoxemia is such a crucial topic, which even benefits from the studying of the 1905 - 8 works by M. Henry Tissier, and also the studies on the Intestinal Flora of Infants by Erik Olsen, 1949. Considered into this whole equation must ALSO be the blase way doctors prescribe antibiotics to babies without any thought as to its destructive effects on the beneficial gut flora needed to keep toxin producing gram negative bacteria at bay. There is also enough literature on this to suggest that antibiotics have a major down side for many babies. Now, we have these studies they are doing in this country to try to reduce allergies by giving babies a probiotic mix for the first two years of their life, to replace that which babies appear now, to be missing??? Why is that? Wouldn't it be better if the babies guts weren't messed up in the first place? The reality is that, as Dr Catherina Svanborg from Lund University has shown, the intestinal tract/gut flora, is really the seat of the immune system. Whatever is done, to mess that up, be it bottle feeding, or the overuse and abuse of antibiotics, vaccine which shut down the liver,…will all have far-reaching consequences. Naturally, breastfeeding is a must in this regard. Why? It has long since been proven that bottle-fed babies have far higher concentrations of e-coli in their gut. That can be found in the work of Dr Robert Reisinger (and others as well) , who also did extensive studies in other mammals, and proved the crucial protective nature of the right sort of gut flora. If you put this together with the fact that it has LONG BEEN KNOWN, both in humans and animals that vaccines can down-regulate key liver functions which process and eliminate the particles of the bacteria envelope which are the toxin,... and if you put that along side the fact that endotoxemia itself, causes disseminated vascular coagulation which in many cases, will result in haemorrhaging.... yes, perhaps even into the brain ... we start to see a more complete more complex picture. As Dr Michael Innis has stated repeatedly on this forum, there are other very specific haemotological markers which COULD be used in order to get correct diagnoses for parents who currently innocent, but who are in jail for SBS by spurious assertions by people who know nothing about the topic of endotoxemia, or those field in which Dr Innis is an “expert”. There are also other tests, which Dr Bettelheim and Goldwater know only too well, which should also be mandatory for any autopsy following any death of any baby. Where haemorrhaging and other related conditions are implicated, there is a lot more that could be done, than is being done right now. The shame is that prosecution "experts" don't appear to wish to look at anyone else's work. They appear to feel that their own, is the only valid expertise, and that no-one else has anything to offer. There is now enough work on the topic of E-coli to sink a ship. BUT.... most of it is not concerned with clinical practicalities. It is surrounding such topics like genetic typing, looking at the minutae of X factors, until the cows come home. It is time for this situation to be brought into balance. It is time for medical people to openly share expertise with people like Dr Goldwater, Bettelheim,...Dr Michael Innis - to work out exactly what blood tests will show what, and start to "own up" to the real meaning of science, and get their heads around the fact that SBS is not a valid diagnosis on present case histories. It is time for some decent medical studies to be done on the etiology of endotoxemias and related problems. I think here of Professor Clemetson.s CRC Press 3 volume text on Vitamin C in which he details why Vitamin C is so important when looking at infection and endotoxemia. The problem is that in order to do such a study, the researchers have to have a very broad and more complete understanding of all aspects of endotoxemia, haemorrhagic Diseases, Malabsorption or malnutrition, and infections. A broader understanding of the function of the liver in these disorders, particularly relating to endotoxin detoxification is crucial. But there is a problem. The minute the word "vaccine" comes into it, its almost as if any topic is dirty by association. We have this "lets talk about anything but vaccines" syndrome. Don't want to ruin our reputations, or our funding, by challenging the status quo. Why is the issue of vaccines crucial? Because the trend is towards combo vaccines with much larger numbers of vaccines in them. Already this month a bulletin was released showing that combo vaccine plans used in three injections instead of four, are resulting in more fevers, more antibiotic use. Why is that? Could it be that there is an endotoxin trigger here? Well, oops. No-one is either looking at, or thinking about that.... www2.epediatricnews.com/scripts/om.dll/serve?action=searchDB&searchDBfor=art&artType=full&id=aqp04038601d It is interesting that the vaccines concerned include pertussis, haemophilus and the 7 prevnar types. All bacteria capable of creating forms of endotoxemia, which of course, does not even factor in endogenous endotoxemia sources which might add as a co-factor. I can see nothing which studies just WHAT administering these vaccines does to either the PEPCK/liver, or resultant immunological parameters other than the Pourcyrous study above. But even then, while they state the "results", they plainly miss the "why".... When the medical profession starts to grapple with the clinical realities of the role of endotoxemia in SIDS, SBS and other childhood conditions, then maybe parents will have half a fair shot at justice. Until then, parents continue to be at the mercy of the arrogance of ignorance. Hilary Butler. Competing interests: None declared
The mathematics of multiple sudden infant deaths 27 June 2004
Ray Hill, Professor of Mathematics School of Computing, Science and Engineering, Newton Building, University of Salford, Salford M5 4WT Send response to journal: Re: The mathematics of multiple sudden infant deaths	Professors Craft and Hall state that “there is little evidence of familial clustering of SIDS”. To see three examples, they need look no further than the cases of Sally Clark, Angela Cannings and Trupti Patel (assuming that the authors now accept the innocence of these parents). Of course, to prove that two SIDS in a particular family are associated with a familial link is asking the impossible. To establish the link would necessitate establishing the causes of death, in which case the deaths would cease to be classified as SIDS. However, it would be astonishing if there were no familial clustering and, as Professor Morris [1] points out, there is plenty of statistical evidence that SIDS is significantly more likely to occur in a family which has had a previous SIDS. For example, in the CESDI study [2], among the 323 SIDS families studied there were 5 previous SIDS, while among the 1288 control families there were only 2 previous SIDS. This suggests that SIDS is about 10 times more likely in a family which has had a previous SIDS than in one which has not. Other studies, both in the UK and overseas, suggest an increased risk factor of at least 5. So Craft and Hall’s assertion that, in a low-risk family for which the chances of SIDS are 1 in 8,500, the chances of second SIDS (given a first) are also 1 in 8,500, is plainly wrong. Their preceding remark that “chance has no memory” should be reserved for truly random events such as the Lotto draw and the ineffectiveness of playing “hot” or “cold” numbers. As the authors themselves had earlier stated, “sudden infant deaths do not follow a random pattern”. Incidentally, the use of the figure of 1 in 8,500 for a first SIDS in a low-risk family has the potential to be misleading. It compares with a figure of 1 in 1,300 for an average-risk family and so it might be inferred (say, by a prosecution witness or a juror) that when a sudden death has occurred in a low-risk family, the chances of foul play are 6 times greater than would have been the case in an average-risk family. This would be a fallacy. The figures simply show that SIDS will come along in low-risk families rather less often than in high-risk families. When a case does come along, the very factors which make SIDS less likely (e.g. affluent parents in a stable relationship) also make murder less likely, and so there is no justification for any significant increase in suspicion. A more worrying feature of Craft and Hall’s article is that it appears to perpetuate the myth that a second or third sudden death in a family should be viewed with considerably more suspicion than a first. They quote a United States Court judgement that “there might be insufficient evidence in any one child death to prove murder or infanticide, but evidence of repeated incidents was admissible as evidence of non-accidental deaths”. So what are the relevant figures here? What is of no direct relevance is a figure such as 1 in 73 million (obtained by the invalid squaring of 8,543) or even a corrected figure for the chances of two SIDS in the same family. What is relevant is an estimate of the relative chances of double SIDS or double murder in cases where two or more sudden deaths have occurred. Obtaining reliable estimates, based on limited data, is fraught with difficulty. However, my own calculations [3] give the following rough estimates. Single cot deaths outweigh single murders by about 17 to 1, double cot deaths outweigh double murders by about 9 to 1, and triple cot deaths outweigh triple murders by about 2 to 1. So each successive death does give rise to some slightly increased suspicion, but to nothing like the extent that a dictum such as the so- called “Meadow’s Law” would imply. In particular, when multiple sudden infant deaths have occurred in a family, there is no initial reason to suppose that they are more likely to be homicide than natural. In the cases of Clark, Cannings and Patel, it seemed that the second or third death served in itself as the trigger for a criminal investigation and subsequent prosecution. Surely, if these cases are to teach us anything, it is that simplistic rules of thumb should have no place in our thinking, and that all sudden deaths, whether first, second or subsequent, should be thoroughly, but sympathetically, investigated. References Morris JA. Recurrent SIDS is not synonymous with homicide. bmj.com 29 May 2004. Fleming P, Bacon C, Blair P and Berry PJ. Sudden unexpected deaths in infancy: the CESDI studies 1993-1996. London, The Stationery Office, 2000. Hill R. Multiple cot deaths: coincidence or beyond coincidence? Paediatric and Perinatal Epidemiology, to appear. Competing interests: I wrote reports for the defence in two of the three cases mentioned above.
Study first, judge later 29 June 2004
Viera Scheibner, Principle Research Scientist (Retired) Blackheath, NSW 2785 Australia Send response to journal: Re: Study first, judge later	I would like to refer Craft and Hall to my Rapid Response dated 2 April 2004 (http://bmj.bmjjournals.com/cgi/eletters/328/7442/766#55368) which pointed out that Caffey was not a formally trained radiologist and made a real mess of the radiology of what are typical scurvy fractures, misinterpreting them as fractures caused by physical trauma inflicted by parents and other carers. One has to have studied in depth a great deal of medical research to correctly analyse and understand many medical issues. I urge Craft and Hall to do a great deal more study before they enter this foray and muddy the picture with many pieces of incorrect information, such as their claim that multiple cot deaths in one family are rare: quite to the contrary, the risk of another cot death in the same family is increased (2 per 100 of such families)(Gunteroth 1990. J Pediatrics; 116: 520-524) The accusations of parents causing what are typical vaccine injuries is not only reprehensible, it is an indictment of the ignorance of medical doctors about published facts. Medical doctors have a vitally important social, and indeed legal, responsibility to find the correct facts before cluttering medical literature with incorrect information which results in victimisation of innocent carers. Competing interests: None declared
Re: Study first, judge later 29 June 2004
Clive Davies, GP Wimpole Street, London W1 Send response to journal: Re: Re: Study first, judge later	Sheibner mentions Caffey in her rapid response from 26th March, not her one from 2nd April. Agreed, Caffey was not a formally trained radiologist -- but what would radiology training have consisted of in those days? Remember that Caffey was born in 1895 (the same year that Roentgen discovered x-rays). Caffey became professor of radiology at Columbia University, and University of Pittsburgh. Though he described the association between subdurals and limb fractures in 1946 ("Multiple Fractures in the Long Bones of Infants Suffering From Chronic Subdural Hematoma") he didn't jump to the conclusion that these were inflicted. This dawned on him years later. Competing interests: None declared
Re: Study first, judge later 30 June 2004
Michael D Innis, Director Medisets International Home 4575 Send response to journal: Re: Re: Study first, judge later	Editor, Accusing parents of ”causing what are typical vaccine injuries is not only reprehensible, it is an indictment of the ignorance of medical doctors about published facts” –Viera Scheibner. I agree entirely. “…but we are concerned that everything we have learnt over the past 40 years about sudden infant death syndrome and the spectrum of child abuse seems to have been forgotten” say Craft and Hall. I say ‘so much the better’. It’s time to learn the signs and symptoms of Infantile Scurvy (Barlow's Disease), induced by vaccines, and not further abuse children and their parents by perpetuating ignorance. Forget Caffey [1] he was mistaken, and get up to date with Kalokerinos [2] and Clemetson.[3] Michael Innis References: 1.Caffey J. Multiple fractures in long bones of infants suffering from subdural hematoma. Am J Roentgenol, 1946, 56: 163-73 2.Kalokeinos A. Every Second Child. Foreword by Linus Pauling.Keats Publishing, Inc. New Canaan Connecticut 3.Clemetson CAB. Barlow’s Disease. Medical Hypotheses (2002) 59(1).52 -56 Competing interests: I have declared SBS a myth.
Re: Re: Study first, judge later 30 June 2004
Lisa C Blakemore-Brown, Psychologist UK based Send response to journal: Re: Re: Re: Study first, judge later	Drs Innis and Kalokerinos restored my faith in the medical profession when we all spoke at a recent conference in Sydney, Australia. These caring, insightful and brilliant men personified how medics should behave. Stories about how a careful audit trail led them to very different conclusions in many cases of suspected child abuse, mapped onto my own experiences. Their highly detailed, careful work, including interweaving others' intelligent research into their own perceptions, led, for instance, to clear evidence of system failure in vulnerable infants and young children following multiple vaccinations. Dr Innis has outlined his findings on these pages in many Rapid Responses. Whilst prevention is the ideal, from this position of fully understanding what had happened to the children's systems, it was possible for some fortunate children to be given appropriate interventions. It was a joy to see `after` pictures of some children up and laughing after appropriate treatment - given the right diagnosis - but who looked as if they had cigarette burns all over them in the 'before' pictures and who had been at high risk of not surviving. Their form of Kawasaki Syndrome was triggered post vaccine. It should not be the case, in our so called advanced society, that the caring attitudes, highly detailed research and logical observations of these Doctors stand out as unusual. But they do. One day, what they know, what they do and what they say will be heard and appreciated. For the sake of all the children damaged, or likely to be, by vaccinations and experimental drugs, and all the parents falsely accused of causing that damage, or likely to be, given the current climate, may that day come very soon. Competing interests: Specialist and Expert in ASD and ADHD spectrum disorders
Comparative Child Mortality of Munchausen's By Proxy 2 July 2004
Colin Pritchard, Research Professor in Psychiatric Social Work Bournemouth University BH1 3 UH Send response to journal: Re: Comparative Child Mortality of Munchausen's By Proxy	Dear Editor, The over-simplistic media response to Muchausen's By Proxy [MBP] leads me to share new data which suggests that MBP people have a substantially higher child mortality rate than child homicide assailants [1] Based upon a decade of child homicides in a 5% sample of the General Population of England it was found that in terms of acutal numbers Mentally-Ill-Mothers were resonsible for 30% of deaths, Mothers on the `At Risk of Abuse Register' 22%, 15% respectively for Mentally-Ill-Fathers and Non-Blood Fathers with prior conviction for violence and the 19% `Extra Family' assailants were all `Multi-Criminal Violent-Child Sex-Abusers [MCVCSA]. However in epidemiological terms the Mentally-Ill-Mothers rate was 10 per 100,000 but the MCVCSA rate was 869 per 100,000.[2] These rates were juxtaposed [1] against a two-year cohort of 128 parents referred to a `paediatric survelleince unit', who included a substantial number thought to be possible MBP parents [3]. They had an annual child mortality of 6%, an epidemiological rate of 6,250 per 100,000, i.e. seven times the rate of the most dangerous MCVCSA. MBP is an imprecise condition and may well include atypical psychotics but it has been found in over 20 Western countries [4]. British Child Protection [social work, health visitors, general practitioners, police and paeditrics}, despite the media image, in terms of reducing child homicide over the past 25 years, is amongst the best in the world [5]. We must resist an ill-informed and scapegoating media, and rely upon the best evidenced based practice, otherwise the complaint that we are too active will swing if paediatrics are over cautious, and we shall be castigated for being too passive. We must avoid being driven by an irresponsible media to the detriment of the children we are charged to protect Yours truly Colin Pritchard Research Professor in Psychiatric Social Work [1] Pritchard C. The Child Abusers: Research & Controversy, Open University Press. 2004 [2] Pritchard C & Bagley C. Suicide and murder in child murdereres and child sex abusers Journal Forensic Psychiatry. 2001: 12: 269-286 [3] McClure R, Davies P, Meadows R & Sibert J. Epidemiology of Munchausen's Syndrome By Proxy: Non-accidental poisonings & suffocating. Archives Childhood Disease. 1996: 75: 57-61 [4] Feldman M & Brown R. Muchuasen's By Proxy in an interantional context. Child ABuse Neglect.2002: 26:509-524 [5] Pritchard C & Butler A . A comparative study of children's and adult homicide in the USA and the 2003: 18: 341-350major Western countries 1974-1999. Journal Family Violence Competing interests: None declared
Some Questions for Clive Davies or Anyone 3 July 2004
L. Travis Haws, Dentist Lakewood CO 80228 Send response to journal: Re: Some Questions for Clive Davies or Anyone	Editor: Clive Davies states that Caffey concludes the so called long bone fractures were inflicted. Here are some questions regarding; the so called proof of battering, inflicted abuse...? Let's take a journey back some 30 years to some of the original SBS research by Caffey. (1) This article is quoted frequently by SBS proponents as the ground-breaking "proof" of what we now know as SBS, non- accidental injury, inflicted trauma... In the paper, Caffey is describing what he calls injury evidence of whiplash shaking deaths. It appears Caffey's suspicions were confirmed when an infant nurse confessed to shaking, heavy handed burping... Caffey spends some time describing necropsies of two babies--babies H and K. To quote from the 1974 article: "Baby H, 12 days of age, premature girl was well until tonight, when she awakened crying as if in pain. There were no external signs of trauma. Nutrition good, respirations deep and gasping, anterior fontanel bulged slightly, diffuse hemorrhages in the ocular fundi...no history of trauma, no fracture of calvaria. Necropsy findings: skin normal, thymus large microscopic focal hemorrhages in the myocardium: pinkish cellular exudates in the pulmonary alveoli: small subcapsular laceration of the liver filled with fresh blood, liver capsule intact. Brain and head: bulging anterior fontanel, bilateral subdural hematomas, bilateral subarachnoid bleedings, subpial bleeding, lacerations of the cerebral parenchyma, pyknosis and death of ganglion cells and large perivascular bleedings...” "Baby K, girl 11 weeks of age. Chief complaint: bulging of anterior fontanel. Fell asleep well but awakened crying and lethargic; semicomatose on arrival, tachypneic, fontanel bulging, reflexes hyperactive, ocular fundi invisible (bleeding?), moderate generalized cyanosis. Cerebrospinal fluid was bloody, gross fresh blood. Infant turned greyish and died 2 hours after admission. No external signs of trauma on the face or head...No evidence of fractures. Several small foci of atelectasis in the lungs. Brain: no external signs of trauma to the head; bilateral subdural hematomas with subarachnoid hemorrhages...extensive bleedings at the sites of attachment of the bridging cerebral veins to the superior sagittal sinus...eyes not examined." It is important to note that Caffey, in his prior paper, discusses at length, traumatic "involucra" at the ends of long bones as eluded to by Dr. Davies. (2) Caffey concludes from these necropsies that "the findings in these two necropsies demonstrate that the manual whiplash shaking by an adult assailant was pathogenic, especially to the brains and eyes." A few more "supportive" examples discussed by Caffey: 1)--"An infant 2 months of age was treated for "sunken fontanelle" by his Mexican grandmother. Two days before admission to the hospital, she had attempted to raise the sunken fontanel by...holding the infant topsy- turvy by its ankles, and then shaking the infant up and down while an assistant slapped and pounded on the soles of its feet. The sunken fontanel did rise and had become bulgy...subhyaloid hemorrhages were found in the ocular fundi...clonic seizures developed and the cerebrospinal fluid from the cranial subdural space and the lumbar subarachnoidal space contained fresh blood." 2)--"the father at first attempted to "strangle the infant with a blanket," but when the infant convulsed during this assault and became stuporous, the father apparently repented, and then with the mother spent the rest of the night manually shaking the comatose infant in a belated effort to revive it...the infant was admitted to the hospital with extensive bruising of the skin and bilateral intraocular bleedings...necropsy findings included bilateral large subdural hematomas and widely scattered intraocular hemorrhages in the retinas." Caffey concludes at the end of the article that "the essential elements in the infantile whiplash shaking syndrome present an extraordinary diagnostic contradiction. They include intracranial and intraocular hemorrhages, in the absence of signs of external trauma to the head or fractures of the calvaria, and are associated with traction lesions of the periosteums of the long bones in the absence of fractures and traumatic changes in the overlying skin of the extremities." Questions: 1) In the description of Baby H, are "the hemorrhages in the myocardium: pinkish cellular exudates in the pulmonary alveoli: small subcapsular laceration of the liver filled with fresh blood" of significance? And how do they relate to whiplash shaking? What would be your list of differentials considering the above? What additional testing should have been done to eliminate or confirm differential diagnosis? 2) What of Baby H's going to bed well, but awakening as if in pain...and then proceeding to her demise? Did the nurse sneak in and shake the baby while it was sleeping/not crying? Don't the SBS "experts" tell us, depending on the day and case, that the "trauma" immediately precedes the ill infant? 3) In the description of Baby K: semi-comatose with hyperactive reflexes, several areas of atelectasis, no fractures, eyes not visible and/or not examined (?). Again, how does baby K relate to Caffey's whiplash shaking conclusions and the trio of proposed signs? I only see one of the signs. What of the atelectasis? What is your list of differentials? What further testing...could have been done according to the list of differentials? What of Baby K falling asleep well, but awakening crying and lethargic? Again, did the nurse sneak in and violently shake the well sleeping infant? Don't the SBS "experts" tell us, depending on the day and case, that the "trauma" immediately supercedes the ill infant? 4) Does the example of the Mexican grandmother support whiplash shaking? Or does it sound more like cervical compression/extension? Do you agree or disagree that increased intracranial blood pressure from topsy-turvy up and down shaking...may have played a significant role in the hemorrhages and edema as compared to acceleration/deceleration? Where are the accompanying long bone traumatic involucra? One certainly would think this case would show periosteal traction? 5) Does the strangling example support SBS or whiplash? Did the subsequent shaking/revival attempts have anything to do with the hemorrhages? Or does this case more adequately support hypoxic induced hemorrhages from the strangle attempt? Or, along the same lines, does this case also support increased intracranial blood pressure (strangling blocking cerebral venous return...) induced hemorrhages? In this case, how would one go about differentiating between these etiologies? 6) In general, what happened to the long bone lesions? The traumatic involucra? I thought that was part of the triad? Would you agree, or disagree, that bones grow at the epiphysis? Would you agree, or disagree, that such newly forming bone tissues/periosteum may stretch rather easily as compared to mature developed tissue? Perhaps during play, swinging a baby, picking one up by the legs or arms? Or does it require violent abusive forces? Would bone fractures from inflicted abuse/trauma commonly result in changes in the overlying skin...i.e. bruising, edema...? 7) This is a little off of Caffey's discussions, but do you agree or disagree that rib fractures, caused from inflicted non-accidental trauma/abuse, would result in significant pain upon respiration/expiration, physical palpation from a pediatric office visit, laughing, crying...? Or would the infant generally not have pain from the trauma? Would spontaneous fractures from poor nutrition, TBBD be more or less likely to exhibit pain than traumatic fractures? 8) Considering all the above, what do you think the internal validity of Caffey's paper is? Are the conclusions made from the available data valid or potentially mis-leading? 9) Considering all the above, what is the external validity of Caffey's paper? Can the conclusions be generalized to all infants with subdural hematoma and intraocular hemorrhage as pathognomonic of SBS or does thorough testing or history taking need to be carried out to eliminate other causes? Without thorough testing, what is the confidence of diagnosing SBS from Caffey's paper? 10) Do you think much more research should have been done, especially regarding tissue properties, tissue injurability thresholds, biomechanics...before drawing such bold conclusions? Especially in regards to the few, more recent biomechanical studies, that conflict with Caffey's conclusions? (3,4) 11) What are your feelings on the reliability of confessions? How might such confessions effect internal or external validity? How would coercion, threats, promises of leniency, the "immunity or right to keep your kids if you name your partner game"...effect the reliability of a confession, and thus, the reliability of such data? Believe me, there are many more similar questions regarding the rest of the "supportive" SBS literature. L. Travis Haws 1) Caffey J. The whiplash shaken infant syndrome: manual shaking by the extremities with whiplash-induced intracranial and intraocular bleedings, linked with residual permanent brain damage and mental retardation. Pediat 1974; 54:396-403. 2) Caffey J. On the Theory and Practice of Shaking Infants. American Journal of Diseases in Childhood 1972; 124:161-9. 3) Duhaime A. et al., The Shaken baby syndrome. A clinical, pathological, and biomechanical study. J Neurosurg 1987; 66:409-415. 4) Prange M. et al. Anthropomorphic simulations of falls, shakes, and inflicted impacts in infants. Journal of Neurosurgery 2003 99: 143-150. Competing interests: As previously disclosed
Re: Study first, judge later 3 July 2004
Viera Scheibner, Principle Research Scientist (Retired) Blackheath, NSW 2785 Australia Send response to journal: Re: Re: Study first, judge later	I will respond myself to the purported conflict of interest issue in a subsequent post, but in response to Clive Davies, the point of my response to the Craft and Hall article was that to this day medical doctors, radiologists and others dealing with child abuse are still influenced by Caffey (1946, 1965a,b, 1970, 1972a,b) papers which (yes) were based on ignorance and misinterpretations of the observed x-rays of the babies whose carers are still being accused of inflicted trauma. By saying: “…but what would radiology training have consisted of in those days? Remember that Caffey was born in 1985 (the same year that Roentgen discovered x-rays)” Dr Davies is actually supporting my argument that Caffey was not well qualified to make such judgments, as opposed to demonstrating that he was. The sad part is that even these days the formally trained radiologists still follow Caffey’s misinterpretations, or is Dr Davies going to tell us that their training also leaves much to desire? If so, he would appear to be right. Why otherwise would they still continue interpreting clear and typical scurvy fractures as traumatic? I juxtapose Caffey’s and his followers misinterpretations with the contemporary interpretation of Hiller (1972), a formally trained Australian radiologist who correctly pointed out already in Caffey’s time that what Caffey considers traumatic fractures are in fact scurvy-type structural changes to the trabecular pattern of the bone tissue resulting in typical and bizarre fractures of such affected bones. Our discussion is not only academic in its nature. The consequences of Caffey’s and others’ misinterpretations of x-rays of the children whose carers still continue being accused of inflicted trauma are horrendous injustices of medieval proportions, destroying children and their carers and whole families. Caffey and his followers do not deserve our sympathy and consideration for their ignorance: Hess (1920) in his ahead of its time almost 300 page volume on “Scurvy past and present” elegantly demonstrated the effect of scurvy on many organs of the human body and devoted a number of pages specifically to the scurvic changes to the bone structure resulting in bizarre fractures. There was no excuse for Caffey and his followers misinterpretations or ignorance since Hess’ work was well-known in their times. Just as Roy Meadow’s (and others’) flawed statistics and the Munchausen per proxy ‘diagnosis’ which caused injustices and unspeakable suffering to innocent carers deserve resounding rejection, so does Caffey and his followers‘ ignorant and incorrect interpretations of x-rays. There are further major problems with the diagnosis of shaken baby syndrome and Munchausen per proxy, such as devaluation of the rule evidence in law and in science (and medicine. Please note my distinction between science and medicine as mutually exclusive entities) by the proponents of NAI (non- accidental injury): there is no eye-witness evidence that anybody injured their babies by shaking. In many cases, the accused carers have been persuaded to illogically believe themselves that they injured or killed the babies in their care even though they shook them AFTER they found them unconscious or dead, in their effort to resuscitate them. This applies to the bulk of the SBS cases: there is no eye-witness account of such harmful activity. As one judge in the USA pointed out, such accusations represent a factitious diagnosis carefully fabricated by medical profession. This leads us to the real cause of this factitious diagnosis: vaccination. I urge medical doctors to study more of medical literature which has demonstrated that vaccines are capable and do cause symptoms such as brain and retinal haemorrhages and bizarre fractures which are automatically and incorrectly considered pathognomic of non-accidental indicted trauma. How come thousands of carers from all walks of life, all educational, cultural and religious backgrounds know how to exactly shake a child to get exactly the same injuries and (with very few exceptions such as birth injury) always after, and never before vaccina