practice, I used a specially devised instrument
called a 'petechaeometer'. This was like a
small bicycle pump, with a domed cup at one
end. A piston produces a vacuum in the cup,
which is held in contact with the skin. The
vacuum 'sucks' up the skin, and it is possible
to count the number of petechial spots in
the area occupied by the suction cup, in a
selected period of time. There is no doubt
that this is a useful test when one is attempting
to clinically diagnose scurvy when other,
classical signs, are absent or difficult to
assess. I must stress that the test is not
specific. To a degree it measures 'capillary
fragility' which is disturbed in Vitamin C
deficiency and endotoxemia.
The high platelet counts
The first specimen of blood examined after
admission following the acute collapse, showed
a significantly high platelet count. This
is another complex issue and open to discussion
and debate. However, what is known about it
must be considered in this case. One well
documented coagulation/bleeding disorder following
cranial trauma is called 'disseminated intravascular
et al, the New England Journal of Medicine,
August 19, 1999, pages 586-592, state:
Disseminated intravascular coagulation is
characterized by the widespread activation
of coagulation. At the same time, the use
and subsequent depletion of platelets and
coagulation proteins resulting from ongoing
coagulation may induce severe bleeding. Bleeding
may be the presenting symptom.
Associated clinical conditions: It is an acquired
disorder that occurs in a wide variety of
conditions...the most important of which are
listed: sepsis, trauma, head injury, serious
tissue injury, fat embolism, cancer, obstetrical
complications, vascular disorders, reactions
to toxins, immunologic disorders.
Diagnosis. There is no single laboratory test
that can establish or rule out the diagnosis.
In clinical practice the disorder can be diagnosed
on the basis of the following findings: an
underlying disease known to be associated
with DIC, an initial platelet count of less
than 100,000 per cubic millimeter or a rapid
decline in the platelet count.
Obviously, baby Alan did not have DIC. But
he did have a coagulation/bleeding disorder.
Kuhne et al, Division of Oncology/ Haematology,
University Children's Hospital, Postfach,
Basel, Switzerland; Eur J Pediatr Feb;157(2):87-94,
Platelets contribute to primary haemostatic
events and are closely linked to plasmatic
coagulation. Their function is highly dependent
not only on their number but also on their
integral physiology. In comparison with adults
or children, the haemostasis of newborn infants,
although physiological, is characterized by
reduced functional reserve capacity leading
to rapid occurrence of bleeding disorders
especially in the presence of additional risk
factors such as prematurity, asphyxia, or
infection. Morphological and biochemical differences
reflect an immature cellular stage which results
in platelet hyporeactivity and contributes
to the reduce capacity of the neonatal haemostatic
acquired and inherited platelet disorders
markedly affect platelet function. Hence assessment
of neonatal platelet physiology may supply
important information; however, no adequate
screening tests are currently available, and
technical difficulties of blood sampling limit
the value of laboratory testing. Evaluation
of the neonatal platelet functions highly
dependent on individual laboratory results
and it advisable to perform complex diagnostic
procedures with the collaboration of specialists
experienced in neonatal haematology. With
the advent of new technology such as platelet
flow cytometry more adequate tools are available,
although still reserved for specialized laboratories,
thus awaiting their clinical significance.
The role of maternal influences on neonatal
platelet function must always be considered.
Thus, neonatal platelet physiology and pathophysiology
is complex and requires more studies and experience.
During the acute collapse, baby Alan was not
neonatal, which usually means 'under the age
of one month'. However, he:
• was premature
• was a 'sick' baby from day one
• had respiratory distress syndrome
• had 'sepsis' at birth and later.
The reference just quoted shows:
• the extraordinary complexity of the
issue (as stated previously)
• that laboratory tests are difficult
to perform and do not always display a problem
that may be present.
The problem of coagulation screening tests
is again noted in the following article:
Br Med J (Clin Res Ed) 1982 Jul 10;285(6335):133-134:
Severe bleeding disorders in children with
normal coagulation screening tests.
What came first—the cerebral hemorrhage,
which can trigger coagulation disturbances,
or did abnormal coagulation/bleeding factors
cause the hemorrhage? This is a critical issue,
and the case history is of prime importance.
• The tests performed cannot exclude
a primary coagulation/bleeding disorder
• The article by Goldwater et al, in
The Medical Journal of Australia (already
quoted) does provide some evidence for a primary
coagulation/bleeding disorder. This article
was initiated by the observation that 'Liquid
(unclotted) blood is an almost invariable
finding in the sudden infant death syndrome'.
It considers the extraordinarily high levels
of D-dimer in SIDS cases compared with infants
and children who died following, for example,
from motor vehicle accidents.
already stated in this report, the D-dimer
levels in the case of baby Alan were >8.00.
That is 'greater' than 8.0. Most hospital
laboratories do not estimate how much above
8.0 the levels are. There is enormous controversy
surrounding the significance of high D-dimer
levels in infants. I present it here as a
positive point that, at the very least, cannot
• The rib and acromion pathology are
consistent with infantile scurvy.
• Reasons for a problem involving the
utilization of vitamin C have been discussed.
• The role of endotoxin has been discussed.
• The role of vaccines has been discussed.
• There were abnormal liver function
tests, which sometimes, can indicate endotoxemia.
• 'Sepsis' was present at birth and
• Antibiotics were administered at various
stages. This can result in the liberation
of excessive amounts of endotoxin.
Unfortunately, some tests that may have confirmed
the presence of excessive amounts of endotoxin
were not done:
• direct assays in the blood during
life or at autopsy
• microscopic (and careful) examination
of the small intestine for signs of damage
(for example, minute ulceration) due to endotoxin
• some tests for endotoxin induced disturbances
of platelet and other coagulation disturbances
• full examination of the cerebrospinal
fluid for cells and culture (viral and bacterial).
I understand, of course, that some of these
tests are not routine. But in cases like the
Yurko one they should be done.
Then there is the evidence of Dr. Shanklin.
There are many features in the intracranial
pathology that suggest the existence of 'inflammation'.
Dr.Shanklin could clarify some differences
between injury and inflammation. In view of
what is known about endotoxin/vitamin C utilization/coagulation/bleeding
factors, his evidence should be reconsidered.
The hemoglobin was very low—7.9, on
11/26/97 (normal - 12.1-17.3), and while this
can be interpreted in various ways (for example,
due to 'sepsis') it can logically be attributed
to scurvy. On that date, the MCH (mean corpuscular
hemoglobin) was 29.6, which is near the low
end of 'normal' (normal 28.0-40). It is not
possible to explain this very low hemoglobin,
etc., by saying that it was 'sepsis'. The
sepsis was not severe enough. Certainly, one
could state that the low hemoglobin had existed
for a long period, and that is possible. But
an explanation is still required. Nor is it
logical to say that the low hemoglobin was
due to the cerebral hemorrhages because the
amount of blood lost in the cranium is not
sufficient to explain the low level. Hess
provides a possible explanation.
page 209, referring to scurvy he states:
The hemoglobin is greatly diminished.
This 'anaemia' was a common finding in scurvy
cases before and during the time when Hess
wrote his book. With modern knowledge there
is no doubt that the nature of the anemia
is complex. In some cases it appears to be
more or less 'specific'. In others the presence
of infections (and endotoxin), with gastrointestinal
disturbances, influences the picture. When
scurvy alone is the specific cause, the response
to vitamin C administration can be dramatic.
Oral doses may be sufficient, but when infections
and gastrointestinal disturbances are major
factors it is necessary to administer vitamin
C by injection and to deal with the underlying
FAILURE TO LOOK FOR TOXIGENIC STRAINS OF E.COLI
Although there is certainly no guarantee that
such strains existed in baby Alan's gut, failure
to look for them denies access to what may
have been important evidence. In SIDS cases,
for example (and there is no need here to
directly prove an association with SIDS in
Alan Yurko's case) the following reference
illustrates what is involved.
Bettelheim et al, Department of Clinical Pathology,
Fairfield Hospital, Victoria, Australia; Scand
J Infect Dis 1990;22(4):467-76, state:
This high incidence of toxigenic E.coli among
the SIDS infants versus the low incidence
in controls, together with the general rarity
of finding such toxigenic E.coli in the community
made us conclude that there may be a causal
relationship between toxigenic E.coli and
SIDS. The O and H serotypes of the toxigenic
E.coli associated with SIDS infants tended
not to be those normally considered to be
toxigenic. This toxigenicity appeared to be
relatively labile. It is suggested that SIDS
may be associated with the infant either acquiring
these unusual types of E.coli or more likely
that its normal resident E.coli acquire the
plasmids to produce these toxins.
It must be stressed again that it is not necessary
to accept or refute the theory relating the
toxic E.coli strains to SIDS. It is merely
necessary to recognize that the toxigenic
strains exist. And they do produce endotoxin.
Failure to look for the strains denies important
evidence to the defense.
Stephen A. Levine, PhD and Paris M. Kidd,
PhD, in a book, Antioxidant Adapation, ISBN;0-9614360-0-7,
define free radicals: (page 14)
Free radicals are atomic or molecular species
which are extremely reactive by virtue of
having unpaired electrons.
Levine and Kidd state (page 15):
It is this unpaired electron that is responsible
for the instability and reactivity characteristics
of all free radicals. Simply by losing or
gaining an electron, any nonradical compound
can be converted to a free radical form and
thereby undergo dramatic changes in its physical
and chemical properties.
Once initiated, free radicals tend to propagate,
by taking part in chain reactions with other,
usually less reactive species. These chain
reaction compounds generally have longer half-lives
and therefore extended potential for cell
damage. Thus the toxicity of a single radical
species may be amplified in subsequent reactions.
The stages of initiation and propagation are
followed by the stage of termination, at which
the free radicals are neutralized either by
nutrient-derived antioxidant species, by enzymatic
mechanisms, or by recombination with each
Referring to brain disorders, Levine and Kidd
, state: (pages 189-190)
Neural tissue is particularly sensitive to
oxidative (free radical) stress ... ischemic
or traumatic injuries damage the brain and
spinal cord more extensively than other organs.
Oxygen is seven to eight times more soluble
in nonpolar compartments such as the hydrophilic
lipid bilayers of biological membranes; thus
cellular membranes are at considerably greater
risk of peroxidative attack by activated oxygen
species. Neuronal membrane systems, especially
mitochondria and myelin sheath membranes,
are especially rich in polyunsaturated fatty
acids, so also will be particularly prone
to peroxidative attack
Neurones due to their high mitochondrial content
have an unusually high rate of oxidative phosphorlation,
presumably to support their large complement
of iron pumps (note; the word is 'ion', not
'iron'). Neurones are therefore enriched in
ubiquinone (Coenzyme Q), a lipid soluble component
of the respiratory electron transfer chain
which can readily autoxidize in low oxygen
tensions to produce superoxide anion.
A number of studies have established that
neural tissue is preferentially susceptible
to oxidative stress.
Thus atoms of iron, once freed from sequestration
in biological complexes (i.e., bound in enzymes
or transport proteins) can potentially cause
severe tissue damage. Initiation of lipid
peroxidation. Redox-active metals, especially
iron and copper, are often present on or in
cell membranes as obligate cofactors of membrane
enzymes. They can also become available in
relatively unbound forms from dietary sources
or damaged tissues.
Vessel hemorrhages in the CNS may result in
free radical-mediated damage. Blood escaping
from the vascular system introduces free (unbound)
iron, and sometimes also copper, into the
extravascular fluids, as metaloenzymes are
destroyed by ltsosomal proteases. These metals
are particularly good catalysts for free radical
reactions, even at low concentrations, and
would tend to exacerbate lipid peroxidation.
agent that can cause direct damage to the
cell membrane, or to the membranes of critical
cell organules (for example, intracellular
mitochondria which are the genetically controlled
'chemical factories' in the cell), can trigger
a sequence of events which, in the end, may
mimic those occurring in hypoxia.
It should be noted here that, following brain
injury, following the breakdown of the blood-brain
barrier from endotoxin, endotoxin enters the
brain structure, destroys some brain tissue
and releases what was previously bound iron
and initiated free radical reactions. Some
parts of the brain are particularly rich in
Following this initial initiation of free
radical reactions, when red blood cells that
escape into the tissues break down they release
their content of iron and copper which accelerate
further free radical reactions. Unfortunately,
because the cerebral circulation is impaired
(either wholly or in parts) antioxidants,
such as vitamin C, and nutrients are unable
to enter the damaged tissue and reverse the
Clemetson, in Vitamin C, Volume 1, on pp 240-241,
It seems that all patients with cerebral hemorrhage,
whether or not they have cerebrovascular ascorbate
deficiency before the hemorrhage, will susbsequently
have local ascorbate deficiency due to hemolysis.
One can try to correct the increase in the
oxidation-reduction potential by chelating
of iron, by administration of cortisone, or
by administration of ascorbic acid. Indeed
Ohimoto et al reported encouraging results
in the treatment of delayed vasospasm following
subarachnoid hemorrhage in two out of five
patients by intrathecial administration of
ascorbic acid (200-1000 mg.)
This introduces into this discussion the role
of vasospasm and the possibility of it being
involved in mechanisms causing cerebral anoxia.
Thus, following endotoxin or anoxic initiation
of brain damage, two stages of free radical
reactions occur—one commences immediately
and the other commences when red blood cells
break down. Further, endotoxin and free radical
reactions accelerate the breakdown of red
blood cells, which means that the time taken
INTRACRANIAL HEMORRHAGES - TRAUMA
The important issues are:
• what precipitates the hemorrhage
• what, if any, special tests can differentiate
between the two
• what, if any, are the macroscopic
and microscopic differences.
Obviously, one looks for:
Signs of endotoxemia
Are factors leading to excessive endotoxin
production and/or failure to detoxify endotoxin
Is the history suggestive?
Are there physical findings suggestive?
Are there pathological findings, either macroscopically
Signs of scurvy
Is the history suggestive?
Factors responsible for increased vitamin
Pathological findings - macroscopic and microscopic
Blood and tissue levels of vitamin C, including
the cerebrospinal fluid
An important issue concerns complexities surrounding
the differentiation between inflammation and
trauma. There are several major problems involved:
• Very little research has been published
in this field.
• Interpreting what is known is a nightmare.
• There are many common features.
• In many cases the end result, particularly
in the brain, is the same. That is; there
are hemorrhages and brain tissue destruction.
It is therefore necessary, indeed vitally
important, to carefully consider all factors
involved, including the history.
Unfortunately, in every shaken baby case that
I have investigated (more than 30) vital evidence
has not been collected. This particularly
applies to special investigations before death,
failure to examine some tissues and body fluids
during the autopsy, macroscopic and microscopic
examinations of important tissues, and the
collection of cerebrospinal fluid during autopsy
for cells and viral and bacterial cultures.
The 'gold standard', particularly when an
individual is charged with a serious crime,
is to collect, during autopsy, about 40 specimens
from various tissues and organs.
John Emery, Emeritis Professor of Paediatric
Pathology, University of Sheffield, in Paediatric
Forensic Medicine and Pathology, edited by
What tissues to block (referring to paraffin
blocks, for microscopic examination). My own
necropsies entail about 40 completely standardized
blocks that include all organs and tissues
and then extra blocks taken as related to
any lesions seen naked eye. A further seven
bblocks are used for frozen sectioning (brain,
two blocks, liver right and left, heart kidney,
In the Yurko case, special reasons were advanced
for not taking many important blocks, apparently
because some organs were to be used for transplants.
However, there is no record in the notes sent
to me of any cultures that may have been performed
and there is no record of what happened to
the recipients, if any, of the various organs.
This information could provide vital evidence—particularly
cultures, if done. One could hardly imagine
that cultures were not performed before organ
transplant procedures were carried out, even
if the results were not immediately available.
Regarding the cerebrospinal fluid: it was
stated during evidence that this could not
be examined because of the danger of complications.
This is only a partial truth. Certainly, during
autopsies there is a special technique that
permits this to be done with minimal risk
of contamination, when cultures and the presence
of inflammatory cells would possibly provide
Professor Emery, in Paediatric Forensic Medicine
and Pathology, page 78, states:
For this reason we have for many years inspected
the brain through the foramen magnum (the
hole in the base of the skull through which
the spinal cord emerges) before opening the
cranial cavity. To do this place the child
face down with the body mass supported on
a block and open the skin at the back of the
head with a 'question mark' incision. It is
important that the incision is carried fairly
well back behind the ears and over the back
of the skull: the line of the incision must
be out of sight when the skin is replaced
after the necropsy but, at the same time,
the line across the skull must be far enough
forward to enable the scalp to be pulled forward.
Having produced the skin flap, remove the
muscles attached to the occiput and clean
the rami of the upper cervical vertebrae.
Then, using a small bone forceps, snip off
the back of the atlas and, possibly, of the
second or third cervical vertebrae leaving
the dura (the membrane surrounding the brain
and spinal cord) exposed beneath. Make sure
that the area is free of blood, hold the skull
level with the body and incise the dura carefully,
(the dura can be be incised without cutting
the arachnoid so that the cerebral fluid does
not escape). At this point, perforate the
arachnoid using an ordinary glass pipette
with a rubber teat and remove a sample of
cerebral spinal fluid.
In the case of Scott Walters, Sydney, 1898
(the defendant was found not guilty) cultures
were taken during the autopsy.
Dianne Little, pediatric forensic pathologist,
in a report dated July 3, 1996, states:
Bacteriology. Blood cultures grew Streptococcus
oralis. Cultures of a swab of the right lung
grew scanty E. coli. These results likely
represent postmortem bacterial overgrowth
and/or contamination. Cultures of the left
lung grew no bacteria.
Virology, cytomegalovirus was isolated from
a nasal swab.
Cultures of pancreas, salivary gland, bowel,
heart, lung and a throat swab isolated no
The interpretation of these cultures is a
problem in itself, but the fact is that they
were done because it is necessary to obtain
as much information as possible.
Another issue in the Yurko case concerns the
failure to do stool cultures—for viruses
and bacteria. Although I could find no record
of bouts of diarrhoea, the fact that baby
Alan suffered from infections and was given
antibiotics increases chances for the development
of 'mutant' strains of E.coli, or the 'overgrowth'
of certain strains. Or viruses of various
types may have been present. Specifically,
one should look for toxic strains of E. coli.
DR. SHANKLIN'S EVIDENCE
This showed clearly that inflammatory processes
were present, and these cannot be explained
by the 'shaken baby' theory. It also demonstrates
the extreme complexity of the factors involved.
For reasons that I do not fully understand,
much of this evidence was ignored. I assume
that the combination of so-called 'rib fractures',
intracranial hemorrhages, and retinal hemorrhages,
was interpreted as 'shaken baby', and the
complexities involved were conveniently ignored.
My understanding of murder trials is that
guilt must be established beyond reasonable
doubt. It is apparent that this 'rule' did
not apply in this case.
Dr. Shanklin's evidence should be carefully
analyzed and reasons for disagreement listed
and considered. This will provide a basis
for the consideration of factors important
for a logical defense. One detail, that is
possibly important, can be found in the evidence.
It relates to what Dr. Shanklin said (page
“While looking at various blood clots,
I found this particular area. If memory serves,
it was near the back part of the brain within
the skull and not the spinal cord. It did
have this inner structure here which is pale
in this photograph surrounded by this recent
bleeding. When this was greatly magnified,
I'd see in it and you can see in these dark,
purplish brown dots which are some kind of
organism, either a fungus or a bacteria. This
was not tested further and I was not in a
position to make specific tests on this. Its
called destructive testing and I did not do
that, in terms of understanding what the process
is, the bacteria or fungus, whichever it is
here. Some of this growth may have occurred
after death. But the growth is not the key.
The presence of it is the key. It gets there
as a matter of disease process.”
Q. So some of those bacteria or fungus would
have been present in this child prior to death?
A. Exactly. And there is no reaction to it.
In other words, this is quite recent as well.
Now there are many possible explanations for
this. One can be found in the book by Hess,
who states, page 133:
In the study by Jackson and Moore on experimental
scurvy in guinea-pigs, the histology of the
blood-vessels is carefully considered. 'Marked
thinning of the wall' was found and depicted,
'the wall as a whole had partially melted
away, leaving few traces'. These parts of
the walls contained many small round bodies
resembling cocci, [spherical bacteria-like
structures, obviously of unknown nature] which
were stained a deep blue by the Wright and
the Giemisn method. These bodies were present
also in the lumen of the vessel and in the
inner layers of the more normal portions of
the wall. As a result of this pathology the
authors are of the opinion that they may have
been dealing with a mild infection. This is
quite possible because scurvy tends to render
the tissues less resistant to the entrance
of bacteria. We believe, however, that even
if such were the case, the phenomenon must
be regarded merely as secondary in its relation
to the pathogenesis of scurvy.
Following the study on the pathology of experimental
scurvy, Jackson and Moore undertook to determine
primarily whether the small stained bodies
seen in the sections of the scurvy lesions
were bacteria. This investigation has been
cited frequently as presenting cogent evidence
in favor of the infectious nature of scurvy,
so that it will be necessary to consider it
fully: the general question of whether scurvy
is a bacterial infection is discussed under
the consideration of etiology.
There is a long discussion in the book by
Hess on this subject. Page 31:
Jackson and Moody cultivated a diplococcus
from the tissues of scorbutic animals after
death, reproduce hemorrhages by inoculating
cultures of these microorganisms in to the
circulation, and recovered the bacteria from
the tissues some weeks later. Their results
are open to critism that bacteria were found
only after death, and that all blood cultures
during life proved negative.
The matter was never clearly settled, and
it remains so to this day. However, the observation
by Shanklin cannot be totally ignored. It
also remains as an item placed in the 'too-hard
basket'. I can only state that, if anything,
it is a positive finding, supporting the defense.
There are many details revealed in the evidence
provided by Dr. Shanklin that require attention
because they cannot be explained by assuming
that shaking was the cause of the pathology
found during autopsy and by microscopic examinations
of some of the tissues. On page 22 he states:
“This child died of natural causes.
In specific, the child died from the latent
consequences of probably perinatal events
of a hypoxic nature. There are some features
of this case that are strongly suggestive
of either a concurrent or a supplanting general
infection due to viruses. The brain slides,
in particular, the spinal cord are most strongly
suggestive of a hypoxic occurring some ten
weeks before death.”
The history of the baby during the time from
birth to the time of the final collapse is
evidence that serious problems existed, but
that the true nature of these was not diagnosed.
In many ways this is understandable because
intracranial problems in infants may not be
clinically obvious even to a trained observer.
On page 24-25, Dr. Shanklin, referring to
microscopic examinations of the cerebral cortex
and parts of the spinal cord, states:
“We are looking at overt necrosis of
brain material, which is quite old, as witnessed
by the penetration of the area by new blood
vessels of an extremely vigorous nature. There
are many nerve cells, which are what we call
red neurons. They do not constitute all of
the neurons in the spinal cord, but there
has been insufficient loss there that the
capacity of this brain to function normally
would be seriously compromised.”
The origin of this needs to be explained,
and it would be possible to do this by considering
the role of anoxia occurring a long time before
the final collapse. However, it is of interest
and possible importance to note what Hess
has to state and illustrate on pages 104-105:
In a case of fatal scurvy in an infant a "focal
degeneration of the cord" has been described,
extending for a distance of a quarter of an
inch (Hess). The lesion differed from that
of poliomyelitis in the absence of round-celled
infiltration and the characteristic changes
in the anterior horn cells (Fig.3 and 4).
The outstanding feature was a loss of cells
in the lateral groups of the left anterior
horn; there were also fewer nerve fibres in
this region, but this diminution was less
striking. No definite interpretation can be
made as the data are insufficient to permit
a conclusion as to whether the lesion was
truly scorbutic or the result of an associated
It would be foolish to dogmatically associate
this lesion with what Dr. Shanklin found but,
at least some consideration should be given
Furthermore, it is important to note, again,
that scurvy is not a pure disease and endotoxemia
and/or infections (bacterial or viral) can
complicate the clinical picture. Thus, mixtures
of so-called 'scurvy' and inflammatory process
can coexist. Added to this is the almost endless
variety and combinations of lesions found—if
one searches diligently.
Dr. Shanklin, page 25-26, states:
“The changes in the spinal cord and
in parts of the brain also include the infiltration
of certain types of inflammatory cells into
the blood vessels and surrounding the blood
vessels. And one can see elements very clearly
in these sections of the process of these
vessels assisting in the process of repair.
This is a sufficiently advanced lesion that
there is no way it could have occurred during
the seventy-five hours or, indeed, during
the interval of an equivalent period of time
prior to admission. It is clearly many weeks
old and is fully consistent with a perinatal
incident of some sort.”
The mechanisms involved in causing these lesions
could be debated, but one detail is certain;
and that is that the lesions were old. It
is possible that the differences between what
was noted by Hess and Dr. Shanklin are mainly
due to age differences. That is, differences
in the ages of the pathologies.
On page 28, Dr. Shanklin notes that:
“Coagulation determinations were stopped
in the afternoon of 25th November, which left
over forty-eight hours for further changes
to occur which could have led to spontaneous
Also, on page 28, Dr. Shanklin states:
“The chemical studies done on the child
show that the liver function is greatly disturbed.
One realistic contributing factor for this
would be the presence of endotoxin in amounts
exceeding the capacity of the liver to detoxify.”
Dr. Shanklin then considers, further, the
spinal cord changes and continues with (page30):
“Babies can be born with essentially
no brain and have Apgars of eight and nine.
The Apgar is a test of the biochemical status
at the time of birth.”
This can only be described as an issue of
prime importance. Many physicians and forensic
pathologists overlook it. In the case under
consideration, it cannot be ignored. It is
apparent that baby Alan was never a well baby.
Had extensive tests, including scans and extensive
coagulation factors been carried out after
birth and during the weeks that followed,
there is no doubt that something serious and
abnormal may have been revealed.
Dr. Shanklin then offers an explanation for
some of the changes found in the brain and
spinal cord (page 32):
“It's the kind of distribution which
occurs with generalized hypoxia, as I have
suggested, in the alternative, a generalized
It is possible that endotoxin and/or an increased
utilization of Vitamin C played a role.
Dr. Shanklin, comments on the eye pathology
“There is actually some chronic inflammation,
which I note particularly in the left retina,
which is both consistent with a virus etiology
as well as hypoxic injury to the eyes at the
time of birth or around the time of birth.”
This clearly demonstrates the complexities
of the issues involved. To state categorically
that the only cause is shaking is to ignore
the obvious evidence.
Dr. Shanklin then discusses the so-called
rib fractures. I have already dealt with this
Dr. Shanklin raises another vital issue on
“The appearance of the hemorrhage itself.
It is pure red cell. There is no essential
clotting going on indicating that there may
have been a bleeding problem at this point
in time. There is a pattern of a few trapped
cells, which are incidental to the hemorrhage.
I mean when we bleed, we loose white blood
cells as well as red blood cells, of course.
There is absolutely no reaction to this whatsoever.
And seventy-vive hours is more than enough
given a child who has clearly got good marrow
and who is producing large numbers of white
blood cells. There would have been a very
distinct and fairly precisely datable inflammatory
reaction at the edges of this hemorrhage had
it been in place at the time of admission.”
When asked “What in the body caused
a spontaneous subdural hemorrhage?”
Dr. Shanklin replied (pages 51-52):
“This is a brain which is undergoing
the longer-term effects of a long-standing
series of infarctions. Part of the response
to this is a development in the subarachnoid
tissues, in the so-called leptomeninges, of
numerous small blood vessels. They are very
thin walled. They are very fragile. If a child
ceases to breath and then is resuscitated
and the blood pressure is restored to near
normal, then you have the possibility of these
many vessels damaged by the incident which
led to the necessity for resuscitation . It
leads them to leak.”
Dr. Shanklin then continues with a discussion
about another vital issue (pages 52-53):
“Fibrinogen is the protein in the blood
which is principally responsible for blood
clotting. It has to be converted to fibrin.
And then fibrin starts breaking down over
a period of hours to days, and the product
can be measured in the blood. It's called
fibrin split products. The test was one hundred
and sixty micrograms per milliliter. The upper
limit of normal is ten. So this is a dramatic
rise. So we know that on the afternoon of
the 25th, that the coagulation is going on
and breaking down rapidly.”
It is necessary, at this point to consider
what I have written earlier in this report
split products) and coagulation
Dr. Shanklin, during the court session on
February 24, 1999, gave evidence. On page
358, he states:
“Cause of death was natural, that there
was a disease state, actually two disease
states within the tissues, which indicate
to me that either of them alone, certainly
both of them working together, was sufficient
to have caused the death of the child.”
Dr. Shanklin, notes the elevated white blood
cell count and confirms the fact that (page
...the child was essentially fighting off
Furthermore, (page 369):
...consistent with a long-standing infection
of some kind.
Dr. Shanklin highlights the old nature of
the pathology (Page 374):
“These structures have been largely
destroyed in this brain by very old process
and they have been replaced by the presence
of hundreds of small blood vessels, which
are these thick-walled, rounded and slit-like
structures. This is the normal reaction of
a damaged brain and spinal cord tissue to
a low order, long standing problem. None of
this is consistent with recent shaking.”
Dr. Shanklin repeatedly details evidence pointing
to old pathology, which is inconsistent with
recent shaking. He details some factors that
can cause blood clots (page)382):
“Clots can come from a variety of causes
and mechanisms. They can be trauma. There
can be a problem with blood clotting. There
can be a reaction to medication. There could
be infection or a combination of these.”
I elaborate on some of these issues this report.
Dr. Shanklin then discusses another vital
issue. In answer to a question (page 383-384):
“So we are not talking about a situation
where had this child been shaken or injured
by Mr. Yurko on the 24th you would expect
to see what injuries, had it occurred at that
Dr. Shanklin answered:
“I would expect to see that the red
blood cells which make up the hemorrhage would
have lost some of their pigment, which they
have not. I would expect to see an inflammatory
reaction, which is beginning to convert to
a more chronic form of response, neither of
which is present.”
Then, when asked (page 384):
“Why would this child continue to bleed
while in hospital?”
Dr. Shanklin replied:
“...so that anyone who's vulnerable
and being maintained in the sepsis is still
going or becomes worsened. Then small blood
vessels will break down and start to bleed.
As they do, they tear, and more blood follows.
A person in the late stage of serious illness
may have trouble clotting blood so that bleeding
This is a precise and accurate description
of what can happen and I elaborate on this
in earlier sections of this report.
Dr. Shanklin, page 396, highlights another
vital issue when asked:
“The fact that there was no culture
done, though, you can still diagnose meningitis?”
“Yes. Meningitis is the cellular reaction
independent of the agent or organism which
got it started.”
There are two issues involved here. First:
bacteremia or septicemia need not be present
when endotoxemia exists, and endotoxemia produces
an inflammatory response. Second; since no
cultures were taken we will never know if
a viral or a bacterial infection did exist.
Viral infections can precipitate the excessive
formation of endotoxin. They can cause pneumonic
changes that are consistent with what was
found during the autopsy. The absence of cultures
denies vital evidence to the defense.
Dr. Guedes, page 45, referring to the intracranial
“Those have to be acute injuries because
you wouldn't have - you wouldn't have tolerated
them. They wouldn't have looked like that.
If you had an injury at birth, it would have
been healed long before, you might see some
abnormal brain from such an injury but it
would be healed leaving some scarring or something
This is contrary to what Dr. Shanklin found
when he carefully examined sections under
the microscope. That is; the oral evidence
of Dr.Guedes on this vital issue must not
be accepted as fact, because he did not perform
proper microscopic examinations.
Dr. Guedes, when questioned about subdural
hemorrhages and intercranial bleeding, in
an infant the age of baby Alan, states (page
“Not this late in the game. No. Premature
children are more susceptible to bleeds, but
those are a different type and they occur
in children more premature than this, usually
choroid plexus bleeds and they occur in premature
infants. In other words bleeds into the brain
substance itself, not subdural bleeds.”
is very misleading and fundamentally not true,
as the following references demonstrate.
• Nelson, Textbook of Pediatrics,
11th edition, page 419, states:
Some of the membrane-enclosed subdural effusions
observed in later infancy may have their origin
in subdural hemorrhage at birth.
• Hayashi, et al, Childs Nerv Syst
199987;3(1):23-29. Neonatal subdural hematoma
secondary to birth injury. states:
In order to evaluate the treatment and prognosis
of subdural hematoma in neonate, we analyzed
48 survivors. There were 36 mature and 12
premature infants. The mothers were primiparous
in 27 cases....fetal presentation was cephalic
in 38 cases 10 of which suction delivery was
performed, and breech in 11. Retinal hemorrhage
was noted in 12 cases.
• Hanigan et al, J Neurosurg 1985
A case is presented of subdural hemorrhage
diagnosed in utero at 31 weeks of gestation.
• Margalith et al, Surg Neurol,
1981 Dec;14(6):405-409, state:
A large subdural hematoma of the posterior
fossa was diagnosed by computerized tomography
in a normally delivered, full-term newborn.
• King et al, Br J Radiol 1998 Feb;71(842):233-238,
.to demonstrate the imaging features of a
range of cranial injuries associated with
birth at term. ..Intracranial injuries include
extradural, subdural and subarachnoid hemorrhage.
Seibel, was asked a question (page 170):
“If the child were to have pneumonia,
would that cause the type of brain injury
that you saw.”
This is not absolutely true. As already demonstrated,
infections can precipitate scurvy by a variety
of mechanisms—one of which is an increased
utilization of Vitamin C. Another is by an
overproduction of endotoxin. 'Sepsis', as
already documented in this report, can disturb
coagulation factors and precipitate hemorrhages.
References have already been provided in this
Dr. Hanna, page 135-136, stated:
“Something happened to one or more of
those veins to cause them to bleed, or to
cause hemorrhage from those veins.”
He was then asked:
“A subdural hemorrhage, is that something
caused by a spontaneous bleeding in a person?”
He answered with:
“Not usually. That would be very uncommon.
Usually it is trauma of some type.”
This answer is misleading, because, to provide
the court with information that is available,
a differential diagnosis should have been
provided. Then, reasons should have been advanced
for the decision made.
Dr. Seibel, page 161 discusses the theories
regarding the injuries in so-called 'shaken
babies'. He states:
“The axon or the nerve cell itself becomes
injured or damaged.”
This is misleading because, as already referenced,
anoxia can result in similar pathologies.
This fact should have been brought to the
attention of the court.
Dr. Seibel also stated, page 161:
“The symptoms associated with severe
brain injury occur within a very few number
of minutes after the brain injury.”
There are two errors in this statement. First,
it assumes that the cause of the pathology
is an injury. Second, it assumes that "within
a very few minutes after the injury"
is beyond dispute.
Nashelsky, Am J Forensic Med Pathol 1995 June;16(20;154-157,
Many health care professionals believe that
there is a very short interval between an
act of ultimately lethal shaking and the onset
of symptoms. The medical literature contains
minimal data that substantiate or contradict
the contention that is stated here.
Lund et al, Ugeska Laeger 1998 Nov (46):6632-7,
A combination of subdural haematomas and retinal
haemorrhages with minimal or no trauma and
no coagulopathy is almost pathognomonic of
the syndrome (shaking).
Note that one must know that no coagulopathy
exists. In this case that is not so.
Dr. Seibel, page 172, when asked:
“Did you make any attempts to get this
child's prior medical records, prenatal record,
anything like that?”
“No sir, I did not.”
In view of the seriousness of the charges
it is difficult to understand why this fundamental
rule in the practice of medicine was not obeyed.
Dr. Seibel, page 174-175, was asked:
“What you're telling us is because of
what you found you made the determination
that this (shaking) was the cause of death
in this child's case and didn't look any further?”
“No, I didn't make determinations as
to cause of death. That's done by the attending
physician and the person at the medical examiner's
He was then asked:
“Didn't you just testify, doctor, that
this child died from shaken baby syndrome?
Dr. Seibel answered:
In my opinion, yes sir.”
I find this difficult to understand or explain.
Dr. Seibel, page 177, when asked about brittle
bones answered with:
“We would see markedly diffuse demineralized
bone, which we do not see in this case.”
This is misleading because it is not always
possible to determine the degree of mineralization
in a plain film. That is why special machines
have been devised to measure bone density.
Dr. Gore, page 238, was asked:
“Is there any way that a subdural hemorrhage
can just be caused spontaneously, the child's
body starts to bleed in the subdural?”
The response was:
This answer is difficult to understand, because
subdural hemorrhages can occur spontaneously
at any age. A variety of coagulation/bleeding
disorders can result in spontaneous subdural
Mitrakul et al, J Trop Pediatr Environ Child
Health 1977 Oct;23(5):226-35, state:
Spontaneous subdural hemorrhage is commonly
associated with bleeding diathesis of obscure
etiology in Thai infants.
Then there is the Vitamin C/scurvy/endotoxin
combinations already detailed.
Ms Wilkinson (prosecutor) Page 476, states:
“You have to look at the diffuse axonal
injury, which is the clincher in this case.”
It is interesting and frustrating when reporting
on a 'shaken baby' case to be faced with this
type of comment. Sometimes retinal hemorrhages
are highlighted, sometimes it is fractures,
and sometimes something else. Apparently,
different investigators regard different factors
as the vital issues. The issue of axonal injury
has already been dealt with in this report.
CAUSE OF DEATH - after considering the evidence,
applying my clinical experience, and considering
what is documented in the medical literature.
Two things need to be considered - the final
cause of death and factors that led to the
pathology that caused death. There is, no
simple way of expressing this. Furthermore,
factors involved interrelate with each other
and this interrelationship extends over a
period commencing before conception—taking
into account genetic and other features that
have influences on the final outcome.
When considering the pathology one cannot
separate one issue from another. For example,
genetic factors, though initially strong in
parents, can be influenced by environmental
and other factors. This can disturb immune
responses and set in motion a cascade of events
that may, months after birth, result in death.
When arriving at a final cause of death it
is necessary to be able to explain all the
important pathologies found and associate
this with the clinical history. To ignore
aspects of the evidence because they cannot
be explained by the person reporting is a
fundamental error. On the other hand, because
present knowledge is incomplete, it is an
obvious error to assume that knowledge is
complete. A final decision, therefore, is
a balance of what is known and what is not.
The most fundamental error, in most of the
so-called 'shaken baby' cases that I have
investigated is clearly demonstrated by the
fact that, early in the case, a diagnosis
of 'shaking' is made and this becomes entrenched.
From then on no attempt to make a proper differential
diagnosis is made and many vital issues are
ignored. This is compounded by the failure
to carry out proper investigations. The result
is not only incorrect verdicts of guilty,
but continuing failure to understand mechanisms
and prevent future deaths. This is the real
issue, and the reason why studies like the
ones in this report should be carefully considered.
It is not a question of opinion or the expression
of a particular theory. It is a matter of
looking at what is recorded in the literature
and matching this with what is found in each
Cause of death
Intracranial hemorrhages, wth cerebral edema
and brain tissue damage. Precipitating factors
include endotoxin, vaccine administration,
excessive utilization of vitamin C, antibiotic
administrations, and failure to be able to
exclusively breast feed. Associated pathology
includes, scurvy bone changes in some ribs
and the acromion process of one scapula, disturbed
coagulation factors, disturbed liver functions,
and the effects of anoxia—all of which
interrelated with each other. The age of the
intracranial hemorrhages date back to before,
during or shortly after birth. Rebleeding
Any other cause/causes for death would need
to fit what was documented in the clinical
history and the pathologies found.