understanding is impossible. This is because
of the extreme complexity of the medical issues
involved. To be able to firmly and logically
withstand questioning in court, when faced
with 'experts' in various fields, one would
need to have ten times the power of Einstein
and be an expert (and I mean, a 'real' expert)
in every branch of science, chemistry, biochemistry,
anatomy, physiology, pathology, microbiology,
bacteriology, virology, immunology, radiology,
forensic medicine, and whatever. Such a person
does not exist. It is important, therefore,
that I explain how I became involved in the
issue of 'shaken babies', and why I do not
accept the views held by a vast proportion
of medical authorities.
It began because I made some clinical observations
(note that the word is 'observations') that
needed to be explained. These observations
involved sudden, unexpected deaths; sudden,
unexpected unconsciousness; and sudden, unexpected
shock—in infants that were either apparently
previously well or suffering from a 'trivial'
complaint (such as a mild upper respiratory
tract infection). Autopsies failed to offer
a satisfactory explanation
I found, first, that, provided I began treatment
early, I could reverse sudden, unexplained
unconsciousness, and sudden, unexplained shock
(remember that I am not discussing infants
with conditions such as meningitis) by administering
huge amounts of Vitamin C by injection. An
important detail was that, previous to the
sudden collapse, all infants had been supplemented
with more than the recommended daily allowances
of vitamin C.
Something, obviously, was responding to vitamin
C, administered by injection, when it would
not respond to orally administered vitamin
C. And the response was, indeed, dramatic
in its rapidity.
Publicity surrounding my work eventually brought
me into contact with an American research
veterinarian (the late Robert Reisinger, from
Baltimore) who introduced me to endotoxin.
There was no doubt that Vitamin C, when used
in big doses, and administered by injection,
'detoxified' endotoxin. And that was the reason
for its extremely rapid action.
Another major advance in understanding came
when a microbiologist colleague in Australia
(Dr. Glen Dettman) gave me a copy of a book
(Scurvy Past and Present) written in 1920
by Professor Hess, a pediatrician in America.
Many of the references in this report come
directly from this book. However, when Hess
wrote his book, little was known about endotoxin.
Furthermore, the main method of production
of endotoxin, in the body, has been changed
• The use of antibiotics
• The use of vaccines
This has led to new understanding of the nature
of scurvy and the coagulation/bleeding problems
associated with it. Now it is common to see
cases where the patient's problems are a combination
of endotoxemia and scurvy. And each of these,
endotoxin and scurvy, when existing in combination,
makes the clinical situation much worse. The
result is an extremely powerful and dangerous
synergism with a complex variety of clinical
'Scurvy' is now, because it is likely to be
mixed with endotoxemia, not a good word to
use. It is, with modern knowledge, not a specific
disease. In fact, it was never a specific
disease. And that is why the recognition of
the multitude of variations in its presentation,
is difficult. Rather than use the word 'scurvy'
one should use 'reduced intake of vitamin
C and/or increased utilization'. Then it is
necessary to consider the pathological effects
of whatever causes the increased utilization.
CLINICAL HISTORY OF BABY ALAN
Date of birth: September 16, 1997. Second
baby. Mother had gestational diabetes, and
labor was induced at 35 weeks because of oligohydramnios
(reduced fluid surrounding the fetus). The
nature of this was not clearly defined. There
was no specific history of loss of amniotic
fluid. Usually, with gestational diabetes,
there is a degree of hydramnios (excessive
fluid surrounding the fetus).
There are several known 'causes' for oligohydramnios—placental
insufficiency (e.g., preclampsia and post-term
pregnancy), and renal malfunction. The amniotic
fluid and blood of smokers is high in cadmium
(a toxic element), and low in zinc (which
tends to be 'protective). Furthermore smokers
who have oligohydramnios have a considerably
larger number of still births and babies with
central nervous system disorders (Milnerowlez
et al, Int J Occup Med Environ Health 2000;13(3):185-93.
Oligohydramnios is associated with an inflammatory
response in fetal, amniotic and maternal compartments—Yoon
et al Am J Obstet Gynecol 1999 Oct;181(4):784-8.
The significance of this, in this case, could
be questioned, but it points to problems that
could add to, or initiate, the disorders later
Diabetes, that is, a high blood sugar, interferes
with the cellular uptake and utilization of
Vitamin C. It is not possible to definitely
associate this with what was to follow but,
at the least, it had to be an added form of
stress to the unborn baby. In addition, the
mother had a urinary tract infection, and
she was a smoker—two known risk factors.
At birth there were marked respiratory problems.
Ampicillin and gentamycin were administered.
These antibiotics can be lifesaving, and I
am not going to state that they should not
have been administered. But, sometimes, there
is a price to pay for the benefits of their
use. One is the overproduction of endotoxin
resulting from a direct 'killing' of certain
bacteria and the liberation of endotoxin that
is stored in the bacterial walls. Another
involves disturbances in gut flora, which
also tends to result in an overproduction
of endotoxin and disturbances in gut immunology.
Respiratory problems persisted for some days
after birth. This never cleared to a satisfactory
At the age of 8 weeks, six vaccines were administered.
Satisfactory counselling was not provided.
For example, no warning was given about the
rare, but well documented complication, central
retinal vein thrombosis, that can follow the
administration of Hepatitis B vaccine. This,
obviously, involves a coagulation disorder.
The day after the vaccine administrations,
the mother noticed increasing lethargy and
feeding problems. Ten days later there was
a high-pitched cry (which can exist when there
are some cerebral problems, such as encephalopathy).
On November 24, while under the care of the
father, Alan Yurko, the baby began to wheeze
and then stopped breathing. There was apparently
up to 5 minutes of a degree of apnea.
The Transport Team noted mottling of the skin.
This may have various causes. One cause I
will never forget, because, in the days before
I used Vitamin C injections, whenever I saw
that in an infant who had suddenly collapsed
for no recognized reason, no matter what I
did, that infant would die. And autopsies
failed to explain why. That one memorable
cause is endotoxemic shock. Several shaken
baby cases that I have investigated exhibited
skin mottling during the initial phase of
Hospital tests revealed bilateral pulmonary
infiltrates, what were diagnosed as rib fractures,
and subdural and cerebral hemorrhages. Death
occurred 75 hours after admission.
THE AUTOPSY REPORT
Cause of death, as recorded by the autopsy
team: Subdural hemorrhages due to shaken baby
A. Contusions, minor, on both temporal areas
of the head.
B. Periorbital ecchymosis, right lower eyelid.
C. Subdural hemorrhage, fresh, right and left
cerebral hemispheres, predominately right
D. Hemorrhage at the base of the brain
E. Subarachnoid hemorrhage, thin layer, biparietal
F. All cranial bones intact
G. Subdural hemorrhage, lumbar and lumbothoracic
region of the spinal cord.
H. Vertebral arteries and dissection of the
Force Injury of the Chest
A. Healing contusion, left lateral chest
B. Fractures of left ribs, partially healing
5, 6 ,7 and 10 posteriorly.
Lungs—mildly hemorrhagic. Air passages
No hemorrhages at the thoracic, lumbar or
Buttocks—no superficial or deeper contusions
Description of External
Right, lower eyelid - a thin rim of ecchymosis.
Pinkish in color and measures 1 x 0.2 cms.
On the left temporal area, slightly above
and in front of the tragus of the left ear,
there is a very pale area of contusion measuring
12x16mm. Its edges are irregular and appear
diffuse. There is no change in coloration
from pink to green to yellow, etc. The color
in general appears a very pale, pink.
On the right temporal area there is a very
pale contusion, of similar appearance, measuring
10 x 9 mm. The auricle of the right ear shows
similar pale appearance, which is diffuse,
and measures 15x4 mm. Its distribution is
more towards the posterior surface of the
middle portion of the right auricle. On the
parieto-occipital regions of the head bilaterally,
the scalp shows a slightly pinkish discoloration
of the skin. On the right side there appears
to be a small impression mark from some medical
On the left lateral surface of the chest there
is a very pale, slightly pinkish, ovoid, healing-type
contusion measuring 10x8 mm. It is located
in the region of rib 7. Palpation of the chest
does not reveal any evidence of subcutaneous
On the left side of the chest, the following
ribs showed irregular swelling, probably resulting
from healed fractures: left rib 5, 6, 7 and
10. The fractures are located on the posterior
and posterolateral surfaces of these ribs.
X-rays are taken and confirm the presence
and positions of these healing fractures.
Multiple sections are taken for histopathological
Both lungs appear congested and show irregular
areas of hemorrhagic appearance.
Examination of the Body
Subdural hemorrhage, prominently seen on the
right cerebral hemisphere, is noted. This
hemorrhage is in liquid as well as clotted
form, total weight is about 10 grams. There
is subdural hemorrhage on the left cerebral
hemisphere posteriorly. This hemorrhage is
relatively less prominent as compared to the
right. The dura mater of the cortex of the
cerebral hemispheres shows thickened and slightly
clotted blood adherent to the dura mater.
At places the thickness of this clotted material
is between 2-4 mm. The entire surface of the
dura mater appears wet, and as mentioned previously
there is liquid and clotted blood.
The brain is edematous, shiny and symmetrical.
There are minor areas of subarachnoid hemorrhage
seen in the cerebral hemispheres. One area
of hemorrhage is located on the medial aspect
of the parietal lobe measuring 3x2 cm. A similar
small area of subarachnoid hemorrhage is also
seen on the right cerebral hemisphere on the
posterior parietal lobe.
Note by Dr. Kalokerinos:
At this stage, without further knowledge/information
it is not possible to state how significant
(if, indeed, it is significant) the finding
of liquid blood in the intracranial haemorrhages
is. If it can be regarded as more than normal
it could signify the presence of a coagulation
disturbance such as has been documented in
some cases of SIDS.
Goldwater, et al, The Medical Journal of Australia,
Vol 153 July 2, 1990, quotes levels of a fibrin
degradation product ('D-dimer') in some SIDS
cases. The mean level was 1792. The mean level
in control cases was 56.6. This is an astonishing
figure, given the fact that no other clear-cut
clinical signs of coagulation/bleeding disturbances
in SIDS cases exist. One factor that stimulated
Goldwater's research was the finding of 'liquid
blood' in some SIDS cases.
The finding: 'the dura mater of the cortex
of the cerebral hemisphere shows thickened
and slightly clotted blood adherent to the
dura' requires discussion. It could indicate
that at least some of the clot was 'old'.
This should be considered later with the evidence
of Dr. Shanklin.
Brain Examination with
The brain appears very edematous, shiny and
fluffy. There are areas of subdural hemorrhage
which appear relatively fresh. There are minor
areas of subarachnoid hemorrhage on the left
parietal lobe. Serial cut sections of the
brain do not show any internal hemorrhage
in the brain parenchyma grossly. Cerebral
edema is confirmed. Differentiation of the
cortex and medulla appears poor. The ventricles
are slightly reduced in size and the cerebrospinal
fluid appears clear. The eyeballs are examined
and these are also sectioned for confirming
the presence of retinal hemorrhages.
It is noted that there is a small quantity
of hemorrhage in the subdural space of the
spinal cord representing the areas of thee
lower thoracic, lumbar and sacral regions.
At the base of the brain on the right side
middle cranial fossa and the major part of
the posterior cranial fossa on the right side
contain a small quantity of blood. On the
left side a very small portion of the left
middle cranial fossa and the posterior cranial
fossa show presence of blood.
Note by Dr. Kalokerinos
Subdural hemorrhages in the spinal area have
been documented in scurvy cases. Hess, page
93, states 'Hemorrhage may occur into the
brain substance, into the cord or the membranes
Organs of the Thoracic
Both lungs are congested. Externally, the
lobes of the lungs show evidence of hemorrhages.
On serial cut section, both lungs show irregular
areas of hemorrhages.
Organs of the Abdominal
The kidneys show fetal lobulations, and on
serial cut section appear very pale.
A few very pale contusions are noted on the
bitemporal regions of the head. A very faint
contusion is also noted on the left lateral
side of the chest.
The left 5th, 6th, 7th and 10th ribs show
old healing or partially healed fracture sites.
These fracture sites appear as globular masses
of cartilaginous tissue. Cut sections of these
healing fractures show normal appearance of
Lungs: The alveolar spaces
are uniformly inflated with evidence of a
few red blood cells and clumps of inflammatory
cells. The inflammatory cell infiltrates are
scattered throughout one section. There is
no evidence of bronchopneumonia or lobar pneumonia.
This picture appears somewhat similar to interstitial
Kidneys: The tubules show
minimal vacuolation of the cells, consistent
with an early degenerative change but no acute
tubular necrosis is noted.
Brain: There is no evidence
of inflammatory cellular infiltration. The
two sections which are stained with H and
E show presence of very minute parenchymal
One section of the cerebellum shows evidence
of shearing type injury with multiple foci
of minute hemorrhages.
Eyeball sections: The right
shows definite evidence of minute retinal
Spinal cord: Minute epidural
hemorrhages are seen on the cord at C5 and
C6 corresponding areas.
Heart: Dr. Gore testified
that he 'removed the heart, the lungs, and
all the organs.' He also stated that there
was a microscopic examination of the heart.
This contradicts what appears to be a fact;
that the organs were harvested for transplantation.
Conclusion (by the pathologist):
This 2 month old black (should be 'white')
male infant died as a result of Shaken Baby
Syndrome. There are old healing fractures
of the left ribs. Subdural hemorrhage is recent.
Discrepancies exist between what was documented
before death and what was documented after
death. Therefore, there is no evidence that
contusions existed before death and it follows
that the nature of the lesions, and their
ages must be carefully considered. By definition,
a contusion is an injury where the skin is
not broken. A bruise is defined as an injury
producing hemorrhage beneath unbroken skin.
These definitions are not absolutely specific,
because the word injury suggests just that—an
injury. Hemorrhage beneath unbroken skin can
be caused by a great variety of conditions
apart from injuries—such as coagulation/bleeding
disturbances. Bruises and contusions can overlap
in nature. Unfortunately, when these words
are used in reports it is natural, for many
non-medically trained, and some medically
trained individuals, to immediately and totally
imagine that the cause of the pathology is
an injury. So there are two things to consider:
1. The ages of the lesions and
2. Is there any evidence that suggests the
presence of a coagulation/bleeding disorder
and/or an inflammatory process?
Mason's text book Paediatric Forensic Medicine
and Pathology ISBN 0 412 29160 6, page 275,
The age of bruises is a vital observation
in child abuse, as the repetitive nature of
the injuries is often the essence of the differentiation
from accident. The colour changes of bruising
are not a reliable guide as to their absolute
age but the well-known sequence is useful
in a relative way; bruises of widely differing
hues cannot have been caused by the same 'accident'
- as is often alleged by parents. The rate
of colour change depends upon the size of
bruise, its depth in the tissues and other
idiosyncratic factors which differ from child
to child. A small fingertip-sized bruise may
pass through the spectrum of blue-red-brown-green-yellow
to complete fading in 4-5 days, but more extensive
collections of blood can last for two or three
times that period.
Histology may assist, but many of the claims
of exact dating by cellular content cannot
be substantiated. Bruises which are obviously
of very recent origin may not require histological
examination, but older lesions showing colour
changes should be sampled: microscopic examination
may, at least, show if the cell population
is broadly similar or divergent in different
bruises if dating becomes a controversial
issue. Faint or doubtful bruises seen on the
skin should be incised to confirm or exclude
bleeding in the subcutaneous tissues. In the
case of Alan Yurko none of this was done.
evidence, though not totally conclusive, may
have been significant. Furthermore, because
most of the lesions were not observed when
baby Alan was admitted and during the period
he was alive in hospital, one cannot exclude
the possibility that the lesions developed
after admission. There are other issues involved.
careful, microscopic examination (and, even
better, an electron microscope study) may
have revealed evidence of scurvy—such
as changes in the blood vessel walls and connective
tissue. One detail is certain. That is the
possibility that the lesions were scorbutic
in nature. If one does not look, then one
will not find this. In view of other evidence
that strongly suggests that scurvy was a factor
the failure to look becomes an important issue.
This was very marked - the Hb level being
6.3 on 11/24/97. Certainly, this was not due
to hemorrhage. The amount of blood in the
hemorrhages was not sufficient to explain
the Hb level. So one is left to make what
is known as a 'differential diagnosis'. Unfortunately,
because extensive iron studies etc. were not
done, one is left unable to issue a clear,
indisputable diagnosis. It is necessary to
understand that this denies, once more, what
could be vital evidence for the defense.
There are many possible explanations for the
anemia. Baby Alan was certainly a sick infant
from the time of birth—prematurity,
respiratory difficulties, infections, antibiotic
administration, and vaccine administrations.
It is known that scurvy, in infants and adults
can be associated with anemia.
• Eisele et al, Lab Anim Sci 1992
June;42(3):245-9: Skeletal lesions and anemia
associated with ascorbic acid deficiency in
juvenile rhesus macaques. Anemia was a consistent
• Von Muhlendahi, Monatsschr Kinderheilkd
1984 Apr;132(4):240-1 Infantile scurvy can
be diagnosed either by recognition of a characteristic
constellation of clinical features, or on
the correct interpretation of nearly pathognomonic
radiological signs: anemia, costochondral
swelling, and subperiosteal hemorrhage are
important diagnostic clues.
None of these references proves that, in the
case of baby Alan, scurvy was the cause of
the anemia. However, they demonstrate that
scurvy is a possible diagnosis. What is quite
clear is the fact that baby Alan was not well
from day one. There were many serious, and
obvious problems (anemia being one) that cannot
be ignored and are not consistent with a diagnosis
of shaken baby.
Rib and acromion pathology
I use the word 'pathology' rather than 'fractures'
because there is no clear evidence that what
was found were fractures. That is, there is
an explanation for the pathology that does
not include trauma. Furthermore, there are
reasons to consider that the pathology began
before, or shortly after birth. There appears
to be doubt that the acromion was actually
involved in any pathological process.
Hess, in Scurvy Past and Present, stated,
In perusing the literature but one study has
been noted on the effect of a scorbutic diet
on the foetus. This investigation was carried
out on a large series of guinea-pigs by Ingier
(1915).in these experiments intra-uterine
fractures, premature births and still-born
litters are frequently mentioned.
Obviously, in this study, the author is referring
to scurvy bone changes and not true traumatically
induced fractures. Ribs can be affected in
several ways by scurvy.
• Subperiosteal hemorrgages
• Costochondral changes
• Changes in one or more of the epiphyseal
areas, including those in the posterior portion
of the ribs.
Subperiosteal hemorrhages occur under the
periostium; that is, the 'skin' of the bone.
The blood is quickly ossified (changed to
bone - in the same manner that a blood clot
surrounding a fracture is changed to bone
as healing progresses). The appearance, on
a scan or X-ray is similar to what is seen
when ribs are broken. This is what was seen
in the case under discussion.
Costochondral changes were noted by a radiologist.
These areas are where the front ends of the
ribs join the sternum, and can be recognized
as swellings, called 'beading'. Bone changes
occur where there is rapid bone growth—where
the ribs joins onto the cartilages in the
front near the breast-bone There are several
smaller ones at the back of each rib near
the spine the spine. Another area lies under
the 'periosteum', the membranous covering
of bones. The periosteum becomes elevated
from the bone surface by a collection of blood.
If one is not aware of this pathology an incorrect
diagnosis of trauma-induced injury can be
Hess, page 95, states:
The susbperiosteal hemorrhage has long been
recognized as a lesion characteristic of scurvy.
Hess, page 108, states:
The most typical site of hemorrhage is beneath
the periosteum, a lesion widely known because
of its clinical significance.
Richard H. Follis, Departments of Pathology
and Pediatrics, the Johns Hopkins Medical
School, Journal of Pediatrics, Vol. 20, Number
3, 1942, pp.347-351, referring to "Sudden
Death In Infants With Scurvy," states:
...the periosteum stripped from the cortex
with a fair amount of ease (case 1) ...there
was hemorrhage beneath the periostium (case
2) ...the periostium stripped from the cortex
with extreme ease (case 3).
Thus, the subperiosteal hemorrhages and increased
ease of periosteal stripping can be used as
guides to the diagnosis of scurvy. In the
Yurko case, no note was made of the ease of
periosteal stripping, and this, unfortunately
means that this issue is not available (as
it should be) to the defense. The rib pathology
does not always involve every rib. Only one,
or more, may be involved and there may be
only subperiosteal hemorrhage, or costochondral
changes, or there may be both types of lesions.
Hess, page 91, referring to rib pathology,
These changes are not found in every specimen,
so that in order to exclude scurvy definitely,
it is necessary to examine a considerable
number of ribs, several may be normal, only
one or two showing the characteristic microscopic
Here Hess is, of course, referring to microscopic
changes. In more obvious cases the lesions
are visible to the naked eye.
The changes seen in the acromion process of
the left scapula can also be explained by
scurvy. That is; if there was any pathology
in that area.
page 12, referring to experimental scurvy
in monkeys, states:
Subperiosteal hemorrhages of the cranial bones
were constantly seen, and not infrequently
involvement of the scapula. (The acromion
is part of the scapula.)
I could not find, in the notes provided to
me, any mention of a microscope examination
of the acromion process of the scapula after
the autopsy. That is disturbing for three
• The lesion was not found in the first
X-rays taken. It was seen in films taken two
• So the age of the lesion is important
• A proper macroscopic and microscopic
examination may have provided evidence of
scorbutic changes, rather than trauma-initiated
changes. Once again, because this was not
done, this information will never be available
and the obtaining of evidence that may have
supported the case for the defense is denied.
Another feature of scurvy bone changes is
that they can, and do, occur at different
times. This gives rise to the incorrect conclusion
that the lesions represent multiple acts of
trauma—a feature of some of the cases
I have investigated.
On page 219 of the court proceedings, Dr.
Gore answered a question:
Q. Were these ribs in different stages of
A. I feel that because I looked at the swellings,
they are different. It means they probably
occurred at different intervals, maybe a few
days. So one occurs say about three weeks
ago. Then the second occurred maybe after
four or five days later. And that's why there
is variability in the reaction. You can see
a big knot and so forth.
This is both incorrect and misleading. The
size of the callus is not a clear indication
of the age of the fracture because a host
of variables is involved. In Paediatric Forensic
Medicine and Pathology, edited by J.K. Mason,
Regis Professor (Emeritus) of Forensic Medicine,
Faculty of Law, Old College, University of
Edinburgh, pages 303-304, are the following
Dating of fractures on the basis of radiological
features is an inexact science. Neither radionuclitide
studies or computer tomography have been found
helpful in establishing the age of fractures.
Reports should be cautious [author's
emphasis] when it comes to assessing the age
of fractures and suggesting the mechanism
by which injuries were sustained.
The rib pathology may have developed before
birth, or shortly after birth. Experimental
evidence demonstrates that scurvy bone changes
can be found (in experimental animals) before
Hess, referring to experimental scurvy in
animals, page 126, states:
In these experiments intrauterine fractures,
premature births and still-born litters are
The 'fractures' mentioned, of course, refer
to scurvy changes and not traumatically induced
fractures. A more recent document is as follows:
Landman et al, Rib fractures as a cause of
immediate neonatal tachypnoea. Eur L Pediatr
Two macroscopic term neonates are described
who presented with uncomplicated apneoea immediately
following vaginal delivery. The tachypnoea
was not associated with lung injury, metabolic,
endocrine or cardio-respiratory disease but
with multiple unilateral posterior rib fractures.
Dr. Seibel, page 159, was asked:
Dr. Seibel, can this rib fracture be caused
It is not described in the medical literature
as being a result of birth trauma.
Obviously, Dr. Seibel did not review the literature
in a thorough manner. Nor had he investigated
possible reasons for rib fractures at birth.
These include varieties of brittle bone disease,
including temporary brittle bone disease and
scorbutic changes. It is important to note
that osteoporosis may not be obvious on ordinary
X-rays and bone density measurements provide
The problem in the Yurko case lies in the
fact that the manner by which Dr.Seibel answered
the question would imprint in the minds of
judges and juries the impression that the
rib pathology could not have existed from
birth, and that it was caused by trauma alone,
at a later date. When all the evidence of
the case of baby Alan is considered, there
is, of course, many reasons to deduce that
one very possible cause is scurvy.
Osteoporosis, brittle bones, and scurvy
Hess, page 128 states:
The osseous tissue itself shows marked changes,
corresponding to the rarification and brittleness
noted on gross examination. It is important
to note that the so-called 'classical' X-ray
finding seen in scurvy bones—the 'white
line' sometimes seen near the ends of long
bones, is not always present.
Hess, page 199, states:
It is best seen at the lower end of the radius
and femur, and appears as a white, transverse,
somewhat irregular band. Its diagnostic value
has been greatly exaggerated as it is frequently
not present when the disease is advanced.
Nearly one hundred years ago intense interest
in osteoporosis and brittle bones was generated
by the observation of a connection with scurvy.
First, it was necessary to differentiate between
the bone changes in scurvy and rickets—not
an easy task, because sometimes the two conditions
existed together. Then osteogenesis imperfecta
and osteomalacia had to be clearly separated
from scurvy. Now, it is known that osteoporosis
is, sometimes, a specific feature of scurvy.
John Caffey, who was a pioneer in the nonaccidental
trauma pathology published and article in
Pediatric X-ray Diagnosis, 4th edition, Year
Book Medical Publishers, Chicago. Under a
reproduction of an X-ray he states:
Early skeletal changes in an infant, scorbutic
bones showing osteoporosis.
The issue of osteoporosis and spontaneous
fractures in infants has resurfaced recently
because of controversy surrounding so-called
'temporary brittle bone disease'. This has
been raised in at least one shaken baby case
and dismissed as 'not proven' or something
meaning the same. However, the subject has
been reconsidered in a manner that demands
Miller, Department of Pediatrics, Wright State
University School of Medicine and the Children's
Medical Center, Dayton, OH, Seminars in Perinatology,
Vol 23, No 2 (April) 1999: pp174-182, states:
The author feels that temporary brittle bone
disease is a real entity, and the use of bone
density measurements can be helpful in making
The infant who presents with multiple, unexplained
fractures poses a difficult diagnostic dilemma.
If no apparent medical explanation can be
found, then a parent or caregiver may be accused
of intentionally injuring the child, even
though they may deny it. In some instances,
criminal proceedings may be filed against
a parent that could result in incarceration
The natural history of temporary brittle bone
disease (TBBD) was one of multiple unexplained
fractures during the first year of life, and
no unexplained fractures thereafter. The hallmark
of TBBD was a lack of cutaneous injury at
the time of injury. Paterson et al found that
there were certain features associated with
TBBD including twinning, prematurity, apnea,
colic anemia, and a family history of hyperextensibility.
He postulated that a copper deficiency might
be the basis. Most individuals in child abuse
work do not accept Patterson's TBBD. Understandable,
because the acceptance as a true entity challenges
several dogmas of radiological features of
bone in the infant with multiple unexplained
fractures that are thought to be pathognomonic
of child abuse. However, there are some features
of TBBD that would suggest that intentional
injury is unlikely.
Bone density measurements by computerised
tomography or radiographic absorptiometry
Bone densities were low in eight of the nine
TBBD infants studied, indicating an increased
susceptibility to fracture. Noteworthy is
that these infants had low bone density measurements
in spite of apparent normal bone density on
I believe that there has heretofore been an
unchallenged acceptance of three radiological
features of bone in infants with multiple
fractures that have been called pathognomonic
of child abuse. These three features are (1)
the finding of apparent normal bone density
on the plain radiographs, (2) metaphyseal
(shaft of long bones) fractures, and (3) posterior
rib fractures. However, these features can
be seen in intrinsic bone diseases of infancy—TBBD,
osteogenesis imperfecta, and the bone disease
of prematurity. Bone strength
is assumed to be closely related to bone density.
It is widely accepted that if there is normal
whiteness of the bones on the plain radiograph,
then the bones are of normal density and therefore
have normal strength. These assumptions are
not correct. The
second radiographic finding is that metaphyseal
fractures (corner fractures or bucket handle
fractures) are diagnostic of child abuse.
However, there is a differential diagnosis
for metaphyseal fractures that includes many
of the other bone diseases of infancy that
can cause unexplained fractures, such as osteogenesis
imperfecta, TBBD, copper deficiency, scurvy,
In the case under consideration (Alan Yurko)
bone density studies were not performed. Therefore,
a potentially critical piece of evidence is
not available for the defense (note: bone
density studies in infants can be difficult
and confusing because of the rapid turnover
of tissues during normal rapid growth).
Beyers et al, S Afri Med J 1986 Sept 27;70(7):407-413,
Small preterm infants often develop osteopenia
with or without rickets and with or without
fractures. Whether these bone abnormalities
are all or part of the same disease process
with a wide spectrum of presentation or whether
each abnormality represents a different disease
is as yet unclear.
There is a multitude of reasons, reading the
article just quoted, why scurvy should play
a critical role in many cases of TBBD. It
is important to note two critical facts:
• The enormous variability of the presentations
• When the precipitating factor (an
infection and/or endotoxin, for example) spontaneously
clears, as it can, then there may be a spontaneous
cure of the scurvy. On the other hand, scurvy,
and/or its causes, may persist and, without
treatment, death may result. Therefore, Dr.
Gore's evidence cannot be considered as proof
of guilt. The rib and acromion pathology,
as a stand-alone feature, is consistent with
a diagnosis of scurvy. And the dating of the
pathology is not proof of trauma.
A standard radiology textbook by Keats and
Anderson, Atlas of Normal Roentgen Variants
That May Simulate Disease, Seventh Edition,
figure 5-174, states:
Simulated cupping of the anterior ends of
the ribs produced by lordotic projection.
That is, a 'false' impression of enlargement
due to the angle of projection of the X-rays
can be mistaken for enlargement or abnormality.
The same textbook shows 'large anterior ends
of the ribs simulating extrapleural (outside
the pleural linings of the lungs and chest
wall). This needs to be taken into account
when reading X-rays. However, during an autopsy,
it should not be a factor, because physical
examination of the ribs, followed by histology,
should clarify the differences between 'a
normal variant' and something that is abnormal.
If periosteal elevations are also found, one
would need to be extremely careful before
excluding a diagnosis of scurvy-type changes.
Keats and Anderson list under a heading of
'Multiple Symmetrical Anterior Rib Enlargement'
the following list:
1. Asphyxiating thoracic dysplasia
3. Leukaemia (chloromas)
6. Thanatophoric dwarfism
The statement that enlargement can be 'normal'
opens up a minefield. A better description
would be 'cause not known'. The pathology
cannot, for example, follow acute suffocation
because the bone tissue changes take time
to develop. When there is chronic anoxia,
endotoxin becomes involved and this causes
an increased utilization of Vitamin C. The
anterior rib enlargements (costochondral junctions)
should be regarded as being caused by Vitamin
C deficiency and endotoxin. The other conditions
noted, apart from scurvy, need not be considered
here. Apparently, one rib broke during the
autopsy. Just what force caused this (if any)
needs to be clarified.
The so-called 'chest contusion'—on
the left side, in the region of the 7th rib.
This is an important, indeed, vital, issue
that requires careful study. Dr. Gore, the
pathologist who performed the autopsy reports
"On the left lateral surface of the chest
there is a very pale, slightly pinkish, ovoid,
healing type of contusion measuring 10 x 8
mm. It is located in the region of rib # (fracture)
A 'contusion' is defined (Blakiston's Pocket
Medical Dictionary, 4th Edition,) as 'an injury,
usually caused by a blow, in which the skin
is not broken'. Therefore, the intent of this
portion of Dr. Gore's report is to convey
a meaning of a blow or 'trauma'. Furthermore,
because it is over one of the so-called 'rib
fractures', the intent is to convey to a reader,
including a judge or jury, that this represents
proof of a blow, or trauma of some sort, causing
the contusion. There are several serious omissions
and deliberate misrepresentations in the report.
• There is no record of a 'contusion'
in the area under discussion in the hospital
notes compiled while the infant was in hospital
• No attempt was made to cut into the
area to see if there was blood, new or old,
in the tissues
• No sections were prepared for microscopic
Mason's book, Paediatric Forensic Medicine
and Pathology, pages 270-271 states:
The police will attend [the autopsy] and will
take their own photographs when criminal charges
are in prospect; the direction of the pathologist
as to the most appropriate pictures to take
will usually be accepted. Photographs are
often taken both in monochrome and colour—many
police forces now also take Polaroid or 'instant'
photographs and may even use videotape recordings.
The pathologist is almost always able to obtain
copies for his own use, but may prefer to
take his own pictures, especially in the form
of colour transparencies.
photography is far superior to black-and-white
reproduction for the recording of skin bruising
and other lesions. Care should be taken to
obtain correct exposure, as over-exposed or
'highlighted' frames may fail to capture faint
Mason's book, page 274-275 goes on to state:
When a very faint lesion is present or there
is doubt as to whether a discoloured area
is due to a bruise or hypostasis (special
attention should be paid to this) an incision
should be made into the skin in order to examine
the subcutaneous tissues, and histology may
be useful. Faint or doubtful bruises seen
on the skin should be incised to confirm or
exclude bleeding in the subcutaneous tissues.
The problems just discussed on the so-called
'chest contusion' apply to the 'contusions,
minor, on both temporal areas of the head',
and elsewhere. Finally, on this issue, it
is necessary to stress that scurvy can cause
skin bruises. And there are some specific
differences between bruising due to trauma
and bruising due to scurvy.
Hess, page 96-97, states:
Skin.- As pointed out by Aschoff and Kock,
examination of skin which to gross appearance
was the seat of small hemorrhages, showed
various lesions. In some, perhaps, the most
typical forms there had been an extravasation
of red blood cells. This condition is found
usually in the subepidermal layers, especially
in the papillary stratum. Many round cells
may be seen in these areas lying between the
connective tissue strands or around the blood
vessels. Rheindorf, as quoted by Tuechler,
has called attention to this round-celled
reaction, which in many instances gives a
picture analogous to the granulomas, which
leads him to infer an infectious origin for
these lesions. Aschoff and Kock have found
that suitably-stained preparations show a
loss of elastic fibers, which Rheindorf states
constitutes one of the earliest signs of the
It is highly likely that electron microscope
examinations will reveal even more details
that would aid in the differential diagnosis
between trauma induced skin bruises and scurvy
skin bruises. Since histology was not performed
on the area of so-called 'contusion' one will
never know its true nature. Therefore, under
no circumstances must this be permitted to
be admitted as evidence of guilt.
In the notes provided to me, I could find
no reference to a whole-body scan, being performed
after death before the autopsy was commenced.
et al, Radiologe 1982 Aug;22(8):342-351, states:
The diagnosis of the Battered-Child Syndrome
(BCS) is made by the pediatrician and the
radiologist.The skeletal changes are illustrated
by X-ray pictures and bone scans.
Dr. Gore, pages 279-280, gave evidence
Q. Dr. Gore, in looking at the fact that this
child had diffuse axonal injury, you determine
the child would have shown signs of this injury
within how much time?
A. These are immediate
Q. And in looking at that, could the child
have received the subdural hemorrhages at
the same time as the diffuse axonal injury?
Q. In the professional literature is diffuse
axonal injury easier to narrow when it occurred
or recognize it in a narrower time frame than
a subdural hemorrhage?
A. Well the injuries both are actually of
the same motion, producing two different types
of scenarios. One you get subdural hemorrhage.
Other you get axonal types of injuries. These
are at the same time and as a result of the
Q. So in your professional opinion, these
injuries occurred at the exact same time?
A. That is correct.
Following this, on page 280:
Well diffuse axonal injury is nothing but
minute hemorrhages and these we cannot show
Further evidence given stressed that motion,
through shaking, produces a shearing type
injury and this is responsible for the axonal
There is no doubt that axonal injury can follow
head trauma. However, it can also follow a
period of cerebral anoxia that can result
from factors different to trauma. It is inaccurate
and misleading to infer, through neglect to
mention the role of nontraumatically induced
anoxia, and state that trauma is the sole
• Geddes et al, Neuro Pathol Appl. Neurobiol
2000 April 26 (2):105-16. Department of Histopathology
and Morbid Anatomy, St Bartholomew's and the
Royal London School of Medicine and Dentistry,
London, U.K: Department of Pathology, University
of Auckland, New Zealand and Department of
Neuropathology, Institute of Neu, in an article
titled, Traumatic axonal injury; practical
issues for diagnosis in medicologal cases,
In the 25 years or so after the first clinicopathlogical
descriptions of diffuse axonal injury (DAI)
the criterion for diagnosing recent traumatic
white matter damage was the identification
of swollen axons ('bulbs') on routine silver
stains, in the appropriate clinical settings.
In the last decade, however, experimental
work has given us greater understanding of
the cellular events initiated by trauma to
axons, and this in turn has led to the adoption
of immunocytochemical methods to detect markers
of axonal damage in both routine and experimental
These methods have shown that traumatic axonal
injury (TAI) is much more common than previously
realized, and that what was originally described
as DAI occupies only the most severe end of
the spectrum of diffuse trauma initiated brain
injury. They have also revealed a whole new
field of previously unrecognized white matter
pathology, in which axons are diffusely damaged
by processes other than head injury; this
in turn led to some terminological confusion
in the literature. Neuropathologists are often
asked to assess head injuries in a forensic
setting: the diagnostic challenge is to sort
out whether the axonal damage detected in
the brain is indeed trauma, and if so, to
decide what - if anything - can be inferred
from it. The lack of correlation between well-documented
histories and neuropathological findings means
that in the interpretation of assault cases
at least, a diagnosis of 'TAI" or 'DAI'
is likely to be of limited use for medicolegal
• Shjerriff et al, Laboratory of Neuropathology,
Academic Unit of Pathology, Department of
Clinical Medicine, University of Leeds LS2
9JT, U.K, Acta Neuropathologica, ISSN:1432-0533
(electronic version) Abstract Volume 87, Issue
1 (1994) pp55-62, states:
Severe nontraumatic head injury commonly results
in a lot of brain damage known as diffuse
axonal injury (DAI). The histological diagnosis
of DAI is made by silver staining for the
presence of axonal retraction balls. This
feature takes about 24 hours to develop and
does not allow for the early histological
diagnosis of DAI. We have used immunocytoreactivity
for the beta-amyloid precursor protein (beta
APP) as a marker for axonal injury in formalin-fixed
paraffin-embedded sections of human brain.
beta APP immunoreactivity was present in all
cases which had survived for 3 h or more.
This was true even where the degree of head
injury did not appear to be severe, supporting
the theory that DAI in a severe form of a
more common phenomenon of axonal injury which
occurs after cerebral trauma beta APP immunoreactivity
was also found in some non-head injury cases
and so cannot be considered to be a specific
marker for trauma. The results show that beta
APP immunocytoreactivity may be useful in
the detection of traumatic injury in its early
stages, before the formation of retraction
balls, provided care is taken to exclude other
causes such as immunoreactivity.
• Stys PK, Ottawa Civic Hospital Loeb
Medical Research Institute, University of
Ottawa, Ontario, Canada, J Cereb Blood Flow
Metab 1998:Jan 18(1):2-25. Anoxic and ischaemic
injury of myelinated axons in CNS white matter:
from mechanistic to therapeutics, states:
White matter of the brain and spinal cord
is susceptible to anoxia and ischemia. Irreversible
injury to this tissue can have serious consequences
for the overall function of the CNS through
disruption of signal transmission. Myelinated
axons of the CNS are critically dependent
on a continuous supply of energy largely generated
through oxidative phosphorylation. Anoxia
and ischemia cause rapid energy depletion,
failure of the Na(+)-K)-ATPase, and accumulation
of axoplasmic Na+ through noninactivating
Na= channels, with concentrations approaching
100 mmol/L after 60 minutes of anoxia. Coupled
with severe K+ depletion that results in large
membrane depolarization, high (Na+)I stimulates
reverse Na(+)-Ca2+ exchange and axonal Ca2+
overload. A component of Ca2+ in turn activates
various Ca(2+)-dependent enzymes, such as
calpain, phospholipases, and proteinkinase
C, resulting in irreversible injury. The later
enzyme may be involved in "utoprotection",
triggered by release of endocenous gamma-aminobuteric
acid and adenosine, by modulation of certain
elements responsible for deregulation of iron
Glycolytic block, in contrast to anoxia alone,
appears to preferentially mobilize internal
Ca2+ stores; as control of internal Ca+ pools
is lost, excessive release from this compartment
may in itself contribute to axonal damage.
Reoxygenation paradoxically accelerates injury
in many axons, possibly as a result of severe
mitachondrial Ca+ overload leading to secondary
failure of respiration (referring to cellular
respiration). Although glia are relatively
resistant to anoxia, oligodendrocytes and
the myelin sheath may be damaged by glutamate
released by reverse NA9+)-glutamate transport.
Use-dependent Na+ channel blockers, particularly
charged particles such as QX-314, are highly
neuroprotective in vitro, but only agents
that exist partially in a neutral form, such
as mexiletine and tocainide, are effective
after systemic administration, because charged
species can penetrate the blood-brain barrier
These concepts also apply to other white matter
disorders, such as spinal cord injury or diffuse
axonal injury in brain trauma. Moreover, whereas
many events are unique to white matter injury,
a number of steps are common to both gray
and white matter anoxia and ischemia. Optimal
protection of the CNS as a whole will therefore
require combination therapy aimed at unique
steps in gray and white matter regions, or
intervention at common points in the injury
• Kaur et al, Department of Forensic
Pathology, University of Sheffield. U.K.,
J Clin Pathol 1999 Mar;52(3):203-9, state:
AIMS: To assess the possible
role of hypoxia in the formation of axonal
METHODS: Study material comprised
sections from 28 brains showing evidence of
cerebral hypoxia with no history of head injury,
four with a history of head trauma but no
evidence of hypoxic change, eight with a history
of head trauma and hypoxic change, and four
from control brains originally described as
'diffuse axonal injury'.
CONCLUSIONS: Axonal bulbs
staining positively for beta 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 ventilation support in the formation of
axonal bulbs is discussed. The presence of
axonal bulbs cannot necessarily be attributed
to shearing forces alone.