Baby Syndrome was originally defined to include
4. Other injuries not explained by a clear and witnessed
(by so-called ‘reliable witnesses’) history of accidental
injury. That is; what is regarded as ‘nonaccidental injury’
It was later defined by intracranial and/or retinal haemorrhages alone.
Then it was claimed that gentle shaking alone could initiate
still, the definition was extended to include some cases of the ‘Sudden
Infant Death Syndrome’. Reasons for this included the idea
that shaking a baby could upset the brain stem and result in cessation
of breathing. Support for this was generated by the fact that, sometimes
in the brain stem ‘diffuse axonal injury’ is found, and cervical
spinal ‘injuries’, such as haemorrhages, are sometimes found
that diffuse axonal injury does not necessarily mean that an inflicted
injury is always the cause. The term is misleading because cerebral anoxia
can result in similar pathology – and this, obviously, is not always
precipitated by inflicted injuries.
so-called ‘diffuse axonal injury’ was added to the list of
‘baddies,’ paediatricians and forensic scientists became totally
overcome by what they saw as the ultimate crime - someone loosing control,
grasping an infant firmly around the chest, and shaking it violently for
several seconds. Animated videos were produced to demonstrate how the
brain moved inside the skull and ‘tore’ the axons apart. Animal
experiments were performed and the results appeared to support the shaking
hypothesis. The matter was therefore declared closed. Those who were accused
appeared to have no defence. In America several individuals are on death
like so many other aspects of medicine, it was not simple. There are reasons
to believe that shaking is not always the cause of the pathologies found.
That is: there are explanations that do not involve inflicted trauma.
HUNT FOR THE REAL CRIMINAL
A true ‘whodunit’ detective story
search began some years ago when I was asked to investigate one particular
shaken baby case. There was a mountain of paperwork. To make matters difficult,
I was not involved in the case until a Thursday and the long trial was
due to end a few days later.
At the time I was also investigating another case. Deep within myself
I sensed that I was missing something, but I could not determine what
it was. This obsessed me, it bothered me, and I could not rest. Then suddenly,
it appeared like a gift from heaven. In both cases there were ‘fractures’
of the costochondral junctions—caused, according to the prosecutors,
when the infants were roughly gripped around the chest. These, I realised,
were not inflicted injuries. They were similar to the changes that occur
in the costochondral junctions in scurvy!
All this happened on the Friday night. Excited, almost beyond measure,
I faxed the information to the lawyers. On the Monday I contacted them
by phone. But that is where I came down to earth. A ‘confession’
had been extracted—as part of a ‘plea bargain’. The
case was closed.
However, I was not closed. With the help of Dr. Ian Dettman, an extremely
extensive literature search, and my own clinical experience, I was able
to piece together a picture that was remarkable in its clarity and significance.
Words and terms that previously had no meaning to me now became a part
of me. I had, from the medical libraries of the world unearthed a treasure
of medical knowledge and understanding. And to think that it had been
there, documented by many medical researchers, for many years. It was
also exploding in size every day.
I was left to wonder why so many of my colleagues could not see the glitter
of the gems that so obviously confronted me.
ALTERNATIVE EXPLANATION FOR THE PATHOLOGIES FOUND IN ‘SHAKEN BABIES’
THAT DOES NOT INVOLVE INFLICTED TRAUMA
of the complexities of the issues, it is best to initially consider, separately,
the various pathologies found:
2. Haemorrhages, including intracranial, and retinal haemorrhages
There are some important common causes and features in each of these pathologies.
However, because of differences in physiology and biochemistry, responses
and, therefore, pathologies, will vary in many ways according to which
organ is involved. For example, a haemorrhage in the brain, can progress
towards complications that cannot occur in a skin haemorrhage.
fundamental cause of all the pathologies
There is an increased utilization of Vitamin C precipitated (mostly) by
endotoxin or other bacterial toxins. This, in turn, results in two pathologies:
1. Due to Vitamin C deficiency
2. Due to endotoxaemia.
Usually there is a combination of these two factors, with special complications
that can occur in the brain because of its unique physiology. Taking this
one step further, one can then move on to understand how:
1. Vitamin C deficiency can, in itself, cause haemorrhages.
2. Vitamin C deficiency can, in itself, cause spontaneous fractures.
3. Endotoxin can in itself, cause coagulation/bleeding disorders.
4. Endotoxin uses vast quantities of Vitamin C while being ‘detoxified’
(involving free radical reactions).
can specifically target the brain by:
1. specifically, and selectively, damaging the endothelial linings of
cerebral blood vessels
2. breaking the blood-brain barrier
3. seeping into the cerebral tissue
4. causing anoxia by a direct effect on the respiratory centre
5. initiating a rapid series of biochemical disturbances, including free
radical reactions, leading to an extremely rapid onset of cerebral oedema—with
a host of possible complications
6. causing coagulation/bleeding disturbances.
Lacroix, Brain Pathol 1998 Oct:8(4):625-40 states:
" …a direct role of endotoxin on specific cell populations
of the central nervous system, which is likely to be responsible for the
transcription of proinflammatory cytokines, first within accessible structures
from the blood vessels and thereafter through scattered cells."
Mayer, Medicina (B Aires) 1998;58(4):377-85, states:
" Lipopolysaccharide affects the permeability of the blood-brain
The cerebral capillaries are particularly sensitive to endotoxin damage.
Because of this the cerebral circulation can quickly cease—either
in a localised area, or totally. Because the respiratory centre is damaged,
respiration may cease—either forever, or for a period. This has
the same effect as anoxia due to cardiac or respiratory arrest. In other
words, there is no need to have cardiac or respiratory arrest for the
initiation of cerebral oedema, although cardiac and/or respiratory arrest
may sometimes occur. Failure to understand this is the reason why, in
some very high profile cases, the prosecution has attempted to add an
element involving suffocation, even though no evidence existed.
Thus, there can be two separate, but sometimes related, mechanisms responsible.
Both involve a breakdown of the blood-brain barrier. The first involves
a direct effect of endotoxin on the respiratory centre. The second involves
a breakdown of cerebral circulation and, indirectly, a cessation of function
of the respiratory centre.
The rapid effects of hypoxia on certain blood coagulation factors and
fibrinolysis is well known. A coagulation/bleeding disorder follows on
Immediately, one can understand that there are features in the developing
pathology of so-called ‘shaken babies’ that are similar to
what is found following obvious cerebral trauma—for example, disseminated
intravascular coagulopathy complicating cerebral trauma.
How does one separate the ‘spontaneous’ causes (via endotoxin/
excessive vitamin C utilization) from somewhat similar pathologies found
The answer lies in:
1. the case history – sometimes a difficult issue
2. the presence of pathologies (outside the brain, such as scurvy type
bone changes) suggestive of increased utilization of Vitamin C
3. factors that can lead to, or cause, endotoxaemia.
INCREASED UTILIZATION OF VITAMIN C
is known that requirement for Vitamin C may vary from one individual to
another by a factor of 1,000 - or even more. Furthermore, there are many
conditions that may respond to Vitamin C only when this is administered,
in a large dose, by injection.
Dr Sherry Lewin, in Vitamin C. Its Molecular Biology and Medical Potential,
pages 182-183, states:
"It follows that the variation in vitamin C requirements by different
individuals allowing for the various parameters noted, is of the order
of a hundred – to a thousand fold…the range is likely to lie
between the very approximate limits of 0.2 to 10 g daily."
Scurvy can occur when an infant is supplemented with the recommended daily
allowance of Vitamin C – or more.
Hess, page 228-229, states:
"We have met two cases of recurrences in infants, one of which is
of particular interest as it happened in spite of giving lemon juice in
the intervening period…It improved, but during the winter had bronchitis,
otitis, enteritis, and later furunculosis. In spite of the fact that it
had been receiving an antiscorbutic for almost this entire period it developed
scurvy once more."
This matches my own experience – infants, under my care, developed
scurvy (usually following infections) despite being supplemented with
more than the recommended daily allowances of Vitamin C. The use of Vitamin
C, administered by injection, was a dramatic ‘discovery’ by
myself in 1967 – or so I thought, because I later found that other
practitioners, in other parts of the world, had beaten me to it by many
Endotoxin is often the precipitating factor for an increased utilization/need
for Vitamin C. Furthermore, an intramuscular or intravenous injection
of Vitamin C can almost instantly ‘detoxify’ endotoxin; and
free radical reactions, set in train, are quickly quenched.
There is no standard, typical, presentation of scurvy.
Certainly, some presentations have been highlighted, but the absence of
all the signs of typical scurvy does not negate a diagnosis.
Furthermore because of:
1. The administration of antibiotics.
2. The administration of vaccines
3. Failure to exclusively breast-feed
4. The role played by endotoxin
infantile scurvy is presenting at an earlier age than it did 75-100 years
And the mode of presentation and the nature of the pathologies, are different,
in many respects, to what is usually described in the literature as ‘classical’
infantile scurvy is mainly a mixture of scurvy and endotoxaemia. Scurvy
and endotoxaemia cause haemorrhages by different mechanism, although the
two, more often than not, combine.
From a purist’s point of view, scurvy is a disease caused by Vitamin
C deficiency and affecting collagen formation. Certainly, Vitamin C is
necessary for more than one of the stages involved in the synthesis of
the complex triple helix that is a feature of the four types of collagen.
Faulty collagen formation—the feature of scurvy.
This affects many tissues, including bone and blood vessels. The result
1. Bruises and haemorrhages.
2. Some complex bone pathologies that, to the uninitiated, look like trauma-induced
Bruises and haemorrhages can occur anywhere – including:
2. Other intracranial areas
There is no typical area for bruising and haemorrhaging. And there is
no typical distribution.
1. Periosteal elevations with underlying haemorrhages that quickly ossify
in a manner similar to ossification that occurs in haemorrhages that surround
2. Epiphyseal disorders, primarily due to breakdown of collagen formation,
complicated by haemorrhages. There may be separation of the epiphyses
– resulting in ‘pathological’ fractures.
3. Weakening of bone structure, due to faulty collagen formation.
A ‘favourite’ site for epiphyseal changes is the costochondral
junctions—the so-called ‘scorbutic rosary’, or ‘beading’.
This, in individual cases, may involve only one, or several ribs. The
areas involved quickly heal with callus formation. The bone pathologies
can occur in any bone, in one bone (or area of a bone) at a particular
time, and in another area at a different time. This ‘reinforces’
the impression that an infant has been physically abused on multiple occasions.
One overseas case that I am investigating at the moment had 32 ‘fractures’
of various ages.
The fractures may be painless and not detected by a clinical examination.
Much depends on how quickly the scorbutic process proceeds. Relatively
slow onset of a scorbutic bone pathology may not present with signs typical
of inflicted injury (pain or tenderness). Yet, X-rays may show many fractures.
The so-called ‘frog-leg posture’, with pain and tenderness
(due to haemorrhages) does exist. However, mechanisms involved are complex,
and the posture can present, together with pain and tenderness, without
haemorrhages – and be relieved quickly, and dramatically, in a matter
of minutes, by administering Vitamin C by injection.
I do not understand the mechanisms involved. But there is a striking resemblance
to some of the features found in acute poliomyelitis. Because of the dramatic
response to injections of Vitamin C I suspect that endotoxin is involved.
is necessary to highlight several details.
1. Coagulation factors are not fully understood – despite the
presence of an enormous amount of knowledge that has been instrumental
in the saving of many lives.
2. Standard coagulation profiles may be normal but the patient may bleed
3. Extensive coagulation profiles may reveal a problem not revealed
by standard profiles.
4. Platelet function tests should always be a part of extensive profiles
despite known difficulties that exist with infants..
5. In typical scurvy, standard coagulation profiles can be normal.
6. In typical scurvy, capillary fragility tests are abnormal.
7. Endotoxaemia (a ‘cause’ of scurvy) can disturb coagulation/bleeding
factors and result in bleeding.
8. In shaken baby cases a diagnosis of ‘shaking’ is usually
made at an early stage, and it is then not considered necessary to search
for signs of endotoxaemia, or anything else.
9. Strangely, cost has been advanced as a reason for failure to thoroughly
10. One ‘authority’ demanded that I produce retinal haemorrhages
‘with retinal haemorrhages due to scurvy written all over them’
[my words]. What he really asked for were features of scurvy-induced
retinal haemorrhages that differentiated them from other retinal haemorrhages.
This was quite absurd. Retinal haemorrhages due to scurvy can occur
anywhere in the retina. They are, simply, haemorrhages, and have no
specific features – unless one uses technologies like electron
11. It is of interest to note that during autopsies on SIDS cases liquid
(uncoagulated blood) is sometimes found. This demonstrates the presence
of a coagulation disturbance – confirmed by extremely high D-dimer
12. Platelet functions may be abnormal in some cases of scurvy, but
it is difficult to separate scurvy and endotoxin as causes. The two
interact together in many cases.
Sushkevick et al, Vopr Pitan, 1969 Sept-Oct;28(5):23-7. state:
" Experiments were staged on 25 healthy and 38 guinea pigs with vitamin
C deficiency. The blood platelets count, their adhesiveness, thrombocytogram,
factor X111 activity, thrombotic test, bleeding time and the volume of
blood lost were determination the 18-22nd day of keeping the animals on
a scorbutogenic diet, parallel with analogous determinations in controls.
In animals suffering from C-avitaminosis the number of blood platelets
dropped, thrombocytograms demonstrated a decrement of mature forms of
blood platelets and an increase in degenerative forms. This was attended
by reduced adhesiveness of blood platelets and factor X111 activity and
also by deranged structure and properties of the fibrin clot. Hence, disrupted
formation of full-fledged thrombocyte plugs and fibrin clots with impaired
vessels which in scurvy have reduced mechanical strength, this resulting
in lengthening of the bleeding time and in increased volume of blood lost."
This does not mean that every case of infantile scurvy presents with all
these features. However, it is a very significant report. Obviously, coagulation
factors should be intensely investigated in all shaken baby cases. The
extreme example of haemorrhage complicating a viral infection is seen
in Ebola fever. With an extremely short time of presentation, most patients
‘bleed from everywhere’. I never cease to wonder why intravenous
Vitamin C is not used to treat this awful disease—and used early.
use of italics for the word ‘injury’ is deliberate because
the pathology involved is not always caused by an ‘inflicted injury’.
Kaur et al, J Clin Pathol. 1999;52::203-209, state:
" Conclusions – Axonal bulbs staining positively for _APP may
occur in the presence of hypoxia and in the absence of head injury. The
role of hypoxia, raised intracranial pressure, oedema, shift effects,
and ventilatory support in the formation of axonal bulbs is discussed.
The presence of axonal bulbs cannot necessarily be attributed to shearing
Rosomoff et al, Crit Care Med, 1996, Feb;24(2 Suppl):S48-56,
"Severe traumatic brain injuries are extremely heterogenous. At least
seven of the secondary derangements in that have been identified as occurring
after most traumatic brain injuries also occur after cardiac arrest."
Geddes et al, Neuropathol Appl Neurobiol 2000 Apr:26(2):105-16,
"The lack of correlation between well-documented histories and neuropathological
findings means that in the interpretation of assault cases at least, a
diagnosis of traumatic axonal injury or diffuse axonal injury is likely
to be of limited use for medicolegal purposes."
Little more needs to be said about this except to state that, in many
cases, diffuse axonal injury is presented as clear evidence of shaking.
The animated video showing how the brain is supposed to move inside the
skull when a baby is shaken, and ‘tear’ the axons apart, certainly
impresses the judge and the jury. The effect of that video is, indeed,
dramatic. Attempting to counter that, even with extensive references from
the best medical literature, is difficult—particularly when the
video is presented by authorities with impeccable qualifications.
can have extremely rapid actions – and, often, this is virtually
instantaneous. Although, in this paper, I refer to ‘endotoxin’,
other toxins of bacterial origin can have somewhat similar actions. It
is possible to estimate the amount of endotoxin in blood and CSF –
during life and during an autopsy. Endotoxin can specifically ‘target’
the brain via mechanisms involving specific sensitivity of the cerebral
capillaries to endotoxic damage. This allows endotoxin to seep into the
brain tissue. Cerebral anoxia can follow. Anoxia can, of course, by itself
cause a breakdown of the blood-brain barrier. Free radical reactions are
immediately initiated and accelerate violently. The result is cerebral
haemorrhage, retinal haemorrhage and/or cerebral oedema that can begin
and accelerate with dramatic rapidity.
to look for endotoxaemia
1. Can be measured directly.
2. Look for ‘toxic’ strains of intestinal bacteria.
3. The administration of vaccines can result in changes in the nature
of intestinal bacteria and excessive endotoxin formation.
4. The administration of antibiotics can result in excessive endotoxin
5. Failure to exclusively breast-feed has already been mentioned.
6. Culture blood and CSF, during life and during the autopsy. Cultures
should include viral cultures, which can, by indirect mechanisms result
in excessive endotoxin production by gut bacteria.
7. Check for otitis media – which is sometimes associated with
endotoxaemia. In the Australian Nanny case there was no sign of otitis
media when the baby was first admitted to hospital following the final
collapse. Yet during the autopsy , a few days later, ‘muco-purulent’
material was found in both middle ears.
8. Check liver and kidney functions – which can be disturbed by
9. Check liver and kidney histology – including electron microscope
10. Electron microscope studies of several parts of the gastrointestinal
tract may show signs of endotoxin damage or abnormal adhesion of bacteria
to the gut wall.
11. Electron microscope, and light microscope, studies of blood vessels
(including capillaries in the brain) may reveal signs of endotoxin damage.
* Note that it is not necessary to have a raised leucocyte count to
have raised levels of endotoxin.
ROLE PLAYED BY VACCINE ADMINISTRATION
would like to avoid this subject but cannot do so.
It is not a matter of whether vaccines should or should not be used.
It is a matter of – "Is there a role for vaccines in the pathogenesis
of the Shaken Baby Syndrome?"
In several cases (probably a significant number) the final collapse followed
within a very short period of a vaccine administration. In the Sally Clarke
case, this happened with her two babies. She refused to have her third
baby (born after she was charged) vaccinated.
There is no doubt, in my mind (and this is based on long experience) that
despite advice to the contrary it is not wise to administer vaccines to
sick infants—including infants with ‘colds’. This is
because, with infections (including ‘colds’), endotoxin is
likely to be produced in the gut in excessive amounts, and liver detoxification
processes are likely to be stressed. Immediately, some practitioners are
going to state that in many situations some infants ‘always have
colds’. This applies particularly to groups such as Australian Aborigines.
The answer to that is to supplement, first, with Vitamin C and zinc. Risks
will then be reduced enormously (but not completely).
Mechanisms involved with vaccine administration include excessive endotoxin
formation. Knowing this allows one to follow the remainder of the pathway
towards the development of the pathologies found in so-called ‘shaken
PSYCHOLOGY THAT LEADS DOCTORS TO IGNORE IMPORTANT DETAILS IN ORDER TO
MAKE A GUILTY VERDICT APPEAR MORE LIKELY
are several aspects to this:
1. Infants are said to have been ‘healthy and normal’ before
the final collapse despite a long history of medical problems, such as
repeated infections and the administration of multiple courses of antibiotics.
2. Many infants were hospitalised several times before the final collapse.
One infant, for example, was on an intravenous drip for several days,
for what was called (by specialists) ‘a trivial illness’.
3. The inappropriate administration of medications.
One case, being investigated at the moment, was given (inappropriately)
frequent doses of promethazine.
Parry EW. Inflamm Res 1996 Jul;45(7):354-6, states:
" The three drugs (dexamethasone, promethazine and nordihydroguauaretic
acid) have the ability to inhibit powerfully the synthesis of tumour necrosis
factor-alpha in response to lipopolysaccharide [endotoxin] …it is
the three drugs act by impairing the hepatic mechanism which normally
removes portal vein-borne endogenous lipopolysaccharide leading to systemic
distribution of lipopolysaccharide."
One problem, demonstrated here, is that many practitioners are too busy
and cannot find the time to study everything. I have a ‘bone to
pick’ with this issue, because, for 30 years I have been trying
to interest my colleagues about the potential dangers involved when antihistamines
are administered to infants. The response has been one of extreme hostility.
THE GOALPOSTS AND IT IS POSSIBLE TO PROVE ANYTHING
shaken babies this is done in several ways:
1. By ‘declaring’ that certain pathologies are ‘diagnostic’,
when there are serious doubts about the logic involved.
2. By accepting that ‘convictions’ are certain evidence
of guilt, and the features found in these cases are therefore diagnostic
of the shaken baby syndrome.
3. By the process of ‘plea bargaining’ – where it
is made clear to the defendant that to plead innocent will result in
a charge of murder and a long jail term (or even execution), and a guilty
plea will result in a lesser charge (such as involuntary manslaughter)
and a short sentence.
4. Many of those charged have limited financial resources and cannot
afford good lawyers.
5. Publishing what are called ‘position papers’ and ‘a
consensus’, that generates an impression of ‘finality’.
That is; the matter is settled and there is no need to examine it further.
6. By deliberately withholding important information from the defence
in order to strengthen the case for the prosecution.
The ‘Australian Nanny’ (Louise Sullivan) case was one of the
first where lack of knowledge (and an absolute determination to achieve
a conviction) generated disturbing responses. It was felt that Louise
had ‘killed’ the child, but lacking was an important piece
of evidence. The prosecution could not understand what initiated the rapid
onset of cerebral oedema. It was, of course, cerebral anoxia, caused by
endotoxin, but the prosecution did not know this. So it was deduced that
Louise not only shook the infant but suffocated it as well.
In order to win a conviction, it was decided that if Louise was 'psychologically
softened' first, then hit with an invented piece of evidence, she would
‘confess.' I will not detail how the ‘softening’ was
carried out—but it was not nice. Then Scotland Yard said to Louise,
"We have re-examined the lungs and can prove that you suffocated
the infant as well as shook it. Plead guilty to a lesser charge of involuntary
manslaughter and your sentence will be light. Plead innocent and you will
be charged with murder and spend many years in jail." Louise accepted
the plea in order to save her sanity. She was allowed to go home.
I then asked to see the reports of the lung examination. Clearly stated
was: "The lungs are normal. No evidence of anoxia." Unfortunately,
that ‘little’ detail was omitted from the book that was later
written about the case.
The recently finalised Sally Clarke case (England) demonstrated the existence
of the strange psychology involved in the last (number 6) factor, in a
dramatic manner—after Sally had spent more than 3 years in jail
for ‘killing’ two of her babies.
The first died, and an autopsy resulted in a diagnosis of ‘cot death’.
Later, a second baby died, and the authorities claimed that this was because
it was ‘shaken’. Then the first death was ‘reconsidered’
and the authorities said that this, also, was ‘shaken’. Paediatrician,
Professor Sir Roy Meadow, stated that the likelihood of having two cot
deaths in one family were one in 73 million. This certainly impressed
the court. Then the Home Office Pathologist, Dr Alan Williams, withheld
vital evidence from the court. This concerned the fact that cultures were
taken from the blood and CSF from the second baby—and these showed
that the baby was ‘riddled with potentially lethal organisms’
After more than 3 years, Sally’s husband was finally able to obtain
the full medical records to which the defence had previously been denied
access. And a ‘proper statistician’ showed that the chances
of having two cot deaths in one family could be as low as one hundred
to one. Sally was freed.
Now the two ‘experts’ who gave false/wrong evidence are in
real trouble. The question that should be asked is - Why did the eminent
doctors behave in such a fashion? It appears that they were hell-bent
on achieving a prosecution and cared little about how this was achieved.
In another case an eminent paediatrician was asked to comment about a
detail in my report to the court, where I stated that the infant concerned
‘had endotoxaemia’. He declared something to the effect that
this could not be so because ‘the infant was not sick’. Some
time later he was asked why he did not transfer the infant to another
hospital (as recommended by an ophthalmologist) in order to have the retinas
photographed for evidence. He answered with something like ‘We could
not, because he was too sick’.
I have no doubt that this ‘shaken baby’ business will eventually
be recorded as one of the worst pages in the history of paediatrics. And
the saddest part of it all concerns the fact that, while important doctors
are busy collecting ‘evidence’ for the prosecution, vital
issues that can save many lives are being not only ignored but destroyed
with intense hostility.
During one trial, the prosecution stated that infantile scurvy was no
longer seen. I replied with ‘Yes it is. But it is not called ‘scurvy’
it is called the ‘shaken baby syndrome’.
Failure to properly consider the case history.
Usually, the prosecution attributes all problems suffered by an infant
previous to the final collapse as caused by abuse. For example, if an
infant has ‘colic’ this is diagnosed as being due to abuse.
Crying is also considered to be due to abuse. Of particular concern is
the tendency to disregard concern expressed by parents, and then claim
that the parents were negligent. Frequent admissions to hospital (for
infections or undiagnosed problems), and frequent examinations by doctors
(including paediatricians) are usually, in retrospect, after the final
collapse, left unexplained or considered to be part of the chronic abuse
If a premature infant, while still in hospital after birth, develops intracranial
haemorrhages or periosteal haemorrhages the diagnosis is usually considered
to be ‘a normal risk that all premature babies are exposed to’.
However, if one of these infants is diagnosed with one or more of these
disorders soon after being allowed home the chances are that someone will
be charged with abuse. Radiologists
report the presence of periosteal elevations in premature infants as ‘a
normal variant’. Mechanisms responsible are rarely considered.
When the findings, either before or after death, cannot be explained by
a carer, this is regarded as ‘an inconsistency’ consistent
with abuse. It is considered by authorities to be a diagnostic feature
In many ways this is like the ‘witch hunts’ of old.
Because of knowledge that is now available, prosecutors (including doctors)
who provide evidence suggestive of guilt, without considering the factors
stated in this lecture, possibly, later, may be charged with criminal
negligence. Furthermore, the issues involved are extremely complex. No
single doctor can possibly claim to be an ‘authority’ on every
aspect of every factor involved in the genesis of the pathologies found
in shaken babies. However, sufficient knowledge exists to enable one to
at least cast serious doubt on the inflicted trauma hypothesis of the
pathologies found in some so-called ‘shaken babies’.
For those of you who want to investigate the subject of shaken babies
in greater detail I suggest that you connect onto PubMed, and Google.
Type in endotoxin, vitamin C, blood-brain barrier, coagulation/bleeding
disorders, platelets, Factor X111, axonal injury, shaken babies, collagen,
and free radicals. Be prepared to spend a few years doing so, because
there is an enormous amount of literature available. [Don't forget the
considerable collection of information on this website also - ed.]
do not doubt that it is possible to shake a baby to death. However, in
the 35 cases I have extensively investigated, there were substantial reasons
to conclude that shaking was not the cause of the pathologies found.