http://www.debbiewadle.org/research/Twenty%20Eight%20Case%20Review%20April%2013.pdf
Shaken Baby/Impact Syndrome: Flawed Concepts and Misdiagnoses
(Based on Review of a Series of Cases)
Harold E Buttram, M.D.
August 18, 2003
Introduction:
The following article represents a review of over 30 cases of shaken
baby syndrome
(SBS) accusations and/or convictions over a period of approximately
four years. Its
primary purpose is to offer a composite of information gained from study
of these cases
to parents or caretakers who have been accused and/or convicted of child
abuse in the
form of SBS, information which may be of value in their defense. Although
effort has
been made to maintain simplicity and clarity in the organization of
the material, there is
unavoidably some technical complexity due to the nature of the material.
Each section is
designed to be complete in itself, and for this reason some portions
may be repetitious.
Among the many adversities and difficulties facing the American family
today, there is a
relatively new and growing hazard in which a parent or caretaker may
be falsely accused
of murdering or injuring an infant by the shaken baby syndrome, when
the true cause of
death or injury arises from other sources. Very tragically, child abuse
does occur and
deserves appropriate punishment. However, it is equally tragic when
a family, already
grieving from the death of their infant, finds a father or mother unjustly
accused,
convicted, and imprisoned for murder of the infant, a murder of which
he or she is
innocent. I know of an attorney, an anesthesiologist, a Mormon mother,
an Amish
mother, and others accused and/or imprisoned (many believe falsely)
on charges of
injuring or murdering an infant by SBS. It could happen to anyone regardless
of race, sex,
educational, financial, or social status. It has happened and is happening
to more than a
few.
Medical-Legal Facets of Shaken Baby Syndrome:
By the inherent nature of SBS cases, where a caretaker or parent is
alone with an infant at
the time of collapse or accidental injury of the infant, it is rarely
if ever possible to prove
the innocence of parent or caretaker, there being no witnesses to corroborate
the stories of
the accused person in maintenance of his or her innocence. Defense of
these cases,
therefore, must be based on evidence showing a likelihood that death
or injury of the
infant arose from causes other than child abuse. This is done by a careful
analysis of the
clinical history and findings supported by scientific and medical literature,
together with
bringing to light the fallibility of current concepts surrounding SBS.
It is also done by
finding (as one often does) unreserved and vehement support of the innocence
of the
accused by family or friends.
One of the main reasons for my opinion as to the their innocence of
many accused
parents or caretakers is a rather strange pattern that often takes place
in hospital
emergency rooms, where once a suspicion of SBS or non-accidental injury
arises, in
many instances all thought of further diagnostic investigation ceases.
I know of no other
situation in medicine where the usual diagnostic thoroughness one finds
in such centers is
abandoned. For this and other reasons, I have not seen a single case
where, in my
opinion, the prosecution has met the standards of “proof beyond
a reasonable doubt,”
standards which are supposed to apply in criminal cases.
Current
Concepts and Assumptions in Diagnosis of SBS – Shaky Foundations:
SBS, sometimes classified as nonaccidental injury (NAI) commonly describes
a
combination of subdural hematoma (brain hemorrhage), retinal hemorrhage,
and diffuse
axonal injury (diffuse injury of nerve cells in brain and/or spinal
cord) as the triad of
diagnostic criteria. In some, the presence of rib or other fractures
is also taken as sign of
child abuse (1-4) These basic concepts, which originated approximately
30 years ago,
remain a basis for most SBS accusations and convictions today in spite
of newer
scientific publications which promise to revolutionize these older concepts.
At the present time the following assumptions concerning SBS/NAI
usually prevail in
both hospitals and the courts:
- That
the severity of shaking force required to produce injuries (retinal
and
subdural hemorrhages, etc) is such that it cannot occur in any normal
activity
but is of such violence that untrained observers would immediately recognize
it as dangerous and intentional; (5)
- that such central nervous system (brain) injury on an accidental basis
can only
be associated with a massive force equivalent to a motor vehicle accident
or a
fall from a second story building;
- that such injury is immediately symptomatic and cannot be followed
by a
lucid interval, so that from this reasoning, the last caretaker with
the injured
child is automatically considered guilty of abusive injury, especially
if the
incident is unwitnessed; (1, 6-8)
- that changing symptoms in a child with prior head injury is due to
newly
inflicted injury and not just a rebleed; (9-13)
- that the presence of retinal/subdural hemorrhages in the absence of
known
disease or accident (as described) above are exclusively diagnostic
of SBS.
- That bone callus seen radiologically is exclusively indicative of
traumatic/abusive fracture.
In the case of retinal hemorrhages, as an example, the present
conventional doctrine is
that findings of both intraretinal hemorrhage (hemorrhage with the substance
of the
retina) and preretinal hemorrhage (on the surface of the retina) are
exclusively diagnostic of shaken baby syndrome. (96-101) This
is based largely on studies of Buys and
Duhaime, (100, 101) which reported on a total of 148 children under
three years of age,
with suspected
child abuse, the remainder with accidental injury, who were
specifically examined for retinal hemorrhage. As interpreted by a professor
of
ophthalmology, testifying as a prosecution witness in one of the cases
I have reviewed,
retinal hemorrhage was found in only one case among accidental injuries,
a high speed
car accident. In contrast, retinal hemorrhages were found in 12 of 28
cases of suspected
child abuse.
The professor went on to say, “it has been assumed that the shaking
has to be fairly
vigorous” (to bring sufficient shearing forces to cause retinal
hemorrhage). Parenthetically, the professor’s use of the term,
“it has been assumed,” is interesting in that it infers
that current concepts of SBS may be based more on assumption than on
basic science. A recently published review of this controversy by Patrick
D Barnes, MD (see next page) brings strong evidence that this is the
case.
As will be reviewed in the remainder of this paper, the conventional
view that diagnostic
criteria for SBS are exclusively diagnostic, miss a key point: that
the accidental cases
reported by Buys and Duhaime were presumably among healthy children,
whereas the
large majority of infants and children suffering death or injury and
subsequently diagnosed as SBS either came from problem pregnancies,
or had been ill before death or injury, or perhaps most important of
all, had recently had routine childhood immunizations from which they
were suffering reactions. In other words they differed from the accident
cases in being largely a fragile population.
Consequently these children could have had smoldering hemorrhagic vasculitis
from vaccines, poor connective tissue formation with fragile blood vessels,
or multiple nutrient deficiencies, one example being subclinical scurvy.
I have yet to see a case in which these possibilities were taken into
consideration.
In a comprehensive review of ethical issues in radiological diagnosis
of child abuse, Patrick D Barnes, MD, with the radiology department
of Stanford University Medical Center, Palo Alto, California, wrote
the following concerning difficulties of diagnosing NAI/SBS in the absence
of witnessed or admitted violent shaking: “This problem is magnified
further by the lack of consistent and reliable criteria for the diagnosis
of NAI/SBS, and that the vast body of literature on child abuse is composed
of anecdotal case series, case reports, reviews, opinion, and position
papers…From an evidence-based medicine perspective, quality of
evidence ratings for diagnostic criteria regarding the literature on
SBS reveal that few published reports merit a rating above class IV
(any design where the test is not applied in blinded evaluation, where
evidence is provided by expert opinion alone, or in descriptive case
series without controls). Such quality of evidence hardly earns a diagnostic
criteria recommendation level of “optional,” much less as
a “guideline” or a “standard.” (14) Perhaps
the most definitive work disclosing the fallacies of SBS theories comes
from University of California’s (at Berkeley) Werner Goldsmith,
co-author of the only book on the subject of impacts, (123, 124) as
well as author of over 50 papers on the biomechanics of head and neck
injury. As reported in a Berkeley Campus News Release of November
27, 2001,
Goldsmith made the following observations, quoted in part: “I
am absolutely convinced that in order to do serious or fatal damage
to an infant by shaking you have to have soft tissue neck damage, yet
in 95 % of cases, medical examiners do not look at the neck in autopsy…Though
most doctors look for brain edema, subdural hematoma and retinal hemorrhaging,
(as diagnostic of shaken baby syndrome) many other types of trauma produce
similar symptoms,” Goldsmith said. “In fact, bleeding in
the brain normally increases pressure, leading to swelling and retinal
bleeding, so anything that causes intracranial bleeding, in particular
falls, can display this trio of symptoms.
{Comment: The work of JF Geddes and coworkers, reviewed
on pages 10 to 12 below, is in accord with Goldsmith’s comments,
in which Geddes et al showed that nonviolent stretch injuries to the
neck, involving the respiratory center at the base of the brain, may
result in respiratory arrest, cerebral edema, and hemorrhagic complications
involving the brain and retina, thereby inferring that this type injury
may comprise a large portion of cases now being misdiagnosed as
shaken baby syndrome.} “A fall backwards from three feet onto
a hard surface, like concrete,” Goldsmith continued, “can
produce nearly 180 Gs of acceleration – 180 times the force of
Earth’s gravity – enough to cause a subdural hematoma…Shaking
a child once a second through a range of one foot produces only 11 Gs,
at the most…There is an order of magnitude difference between
shaking and falling. From the point of view of the brain, shaking is
a much, much milder form of braking than a fall.
“One dogma often espoused by doctors is that short distance
falls do not cause serious harm. However, videotapes demonstrate that
falls from as little as 32 inches can cause fatal brain damage in infants
and toddlers. To complicate matters, between 5 and 10 percent of children
are born with undiagnosed subdural hematomas, and 30 percent are born
with retinal bleeding…If you get a rebleed, you may get something
that looks like shaken baby syndrome.”
A more recent study by Ommaya, Goldsmith, and Thibault (2002) supports
the 1987 findings of Duhaime in revealing that impact creates 50-100
times the Gravity (G) force created by shaking, and that shaking alone
in an otherwise healthy infant did not create enough force to cause
subdural hematomas and retinal hemorrhages. (132)
More
recent still, a study by Prange, Coats, Duhaime, and Margulies (Journal
of Neurosurgery, 2003) entitled “Anthropomophic simulations
of falls, shakes, and inflicted impacts in infants,” an anthropomorphic
surrogate of a 1.5 month-old human infant was constructed and used to
simulate falls from 1 ft, 3 ft, and 5 ft, as well as vigorous shakes
and inflicted head impact. During falls, the surrogate experienced occipital
contact against a concrete surface, carpet pad, or foam mattress. Values
of rotational velocity were recorded directly, and the values of the
maximum peak change in angular velocity and the peak angular acceleration
were calculated. The conclusions of the study were that vigorous shakes
produced rotational responses similar to those resulting from minor
falls, but inflicted impacts produced responses that were significantly
higher than even a 5 foot fall onto concrete.
Although
the study did not directly address the issue of whether or not vigorous
shaking without impact could generate sufficient force to cause brain
hemorrhages and injury, it did find that forces resulting from shakes
were equivalent to those from minor falls, an area which still remains
controversial (as reviewed in this article). It is reasonable to conclude,
therefore, that the current hypothesis on which
many shaken baby syndrome accusations are based, that shaking alone
is capable of causing brain injury and brain hemorrhages, remains unproven.
Continuing next into the main body of discussion, the remainder of this
article will
review major problem areas showing that not only can there be other
causes of the
findings now thought to be exclusively diagnostic of SBS, but that these
other causes
may well comprise a majority of cases now being diagnosed as SBS. These
categories
include residual effects of birth trauma, vaccine reactions, respiratory
paralysis from
accidental (nonviolent) whiplash of the infant’s neck, Barlow’s
Disease (rediscovered
subclinical scurvy), and a variety of old and newly recognized metabolic
disorders:
Residual Effects of Birth Trauma:
One of the cases that I recently reviewed typifies this type of problem
in which a probable residual subdural or brain hemorrhage from birth
trauma was later misdiagnosed as SBS or child abuse. The mother was
known to have uterine fibroids from ultra sound exams taken during her
pregnancy.
Her labor started following spontaneous rupture of the membranes, but
after several hours with limited progression, she was started on pitocin
drip. In spite of hard labor which went on for several hours there was
still little progression, and a Cesarian section was performed. Under
these circumstances it can be assumed that the increased force of uterine
contractions generated by the pitocin drip, together with outlet obstruction
within the uterine cavity, would have generated much greater mechanical
pressure on the fetal head than would have taken
place during normal labor. This is indicated by a survey of retinal
hemorrhages
conducted at Tel Aviv University Center of 100 newborns following labor
induced by
intravenous pitocin or oral dinoprostone, following which retinal hemorrhages
were
found in 40% of the neonates in the dinoprosone group and 28% of the
pitocin
group. (16) Almost by definition this could have been considered a traumatic
birth for the
fetus with significant risk for brain hemorrhage.
As
it turned out, it is highly probable that this is what did happen. The
baby died two
months later from a massive acute subdural hematoma, but at autopsy
an older or chronic
subdural hematoma was also found, in my opinion almost certainly the
result of birth
trauma. Instead of considering the possibility of a rebleed from a birth-related
chronic
subdural hematoma, the father, who was attending the baby at time of
his collapse, was
accused and convicted of child abuse and is now serving a prolonged
prison sentence.
(Refer to next page for additional information on chronic subdural hematomas
as a risk
factor for rebleeds).
As stated in Nelson Textbook of Pediatrics, 16 th Edition: “Traumatic
epidural, subdural, or subarachnoid hemorrhage is especially likely
when the fetal head is large in proportion to the size of the mother’s
pelvic outlet; then for other reasons the labor is prolonged as in malposition…..”
(17)
In an article published in Archives of Neurology in 1994, Fenichel and
colleagues identified 22 term newborns with intracranial hemorrhage
by computerized tomography in an intensive care unit for newborns. Primary
subarachnoid hemorrhage was the most common type of hemorrhage, caused
either by traumatic deliver or severe hypoxic- ischemic encephalopathy…(18)
In
a three-year survey at the Southwestern medical Center, Dallas, Texas,
26 near-term and term nonasphyxiated infants were found to have small
subdural hematomas on computed tomography. It was concluded that the
presence of subdural hematoma is not necessarily always indicative of
birth trauma and may occur as sequelae of an otherwise uncomplicated
delivery. (19) In 1989 Demir reported on an atraumatic antepartum subdural
hematoma causing fetal death. (105) In addition, prenatal ultrasound
examinations have revealed the existence of unexplained subdural hemorrhages
in utero. (106) Patrick D Barnes also commented that “birth trauma
may persist beyond the neonatal period and mimic abuse.” (14)
In 2003 MK Tauscher et al reported on brain hemorrhages in preterm infants
associated with histologic chorioamnionitis (inflammation of the placenta).
(128) Since these hemorrhages may later be mistaken for child abuse,
reason would indicate that an histologic exam of the placenta should
be routine in premature infants.
Acute Brain Hemorrhage (Rebleeding) from Pre-Existing Chronic Subdural
Hematoma or Malformations such as Hydrocephalus:
In rebuttal to the current SBS doctrine that changing symptoms in a
child with head injury is due to newly inflicted injury and not to a
rebleed, as outlined on page 3, Joseph Piatt reported
on a case of retinal hemorrhages and bilateral subdural hematomas in
a child with external hydrocephalus following a minor fall. In
discussion of the case he wrote: “The presence of craniocerebral
disproportion that develops from any cause – external hydrocephalus,
internal hydrocephalus, arachnoid cyst, or chronic subdural hematoma
– makes the patient exceptionally susceptible to subdural hemorrhage
after what would otherwise be inconsequential trauma….as a result
of the vulnerability of the bridging veins.” (20) Other authors
have also reported on similar findings, including the proneness of a
chronic hematoma to rebleed with minimal trauma. (21-23, 73) In an article
by Hymel et al published in November, 2002, the authors reviewed the
pathophysiology of subdural hematomas and the mechanisms by which chronic
subdural hematomas may brebleed spontaneously or with minimal trauma.
(112) In addition, in a table extending nearly four pages the authors
provided a list of possible differential diagnoses for subdural hematomas.In
my opinion, even this list was incomplete, as it did not include scurvy
or childhood vaccines.
Once established, chronic subdural hematomas may take on lives of their
own. Very often, as a result of tears in the tissue-paper thin subarachnoid
membrane which separates the subdural space from the brain, there is
a leakage of cerebrospinal fluid into the subdural hematoma. This in
turn tends to thin the clot converting it into a consistency similar
to “crankcase oil.” Also, after a period of two weeks or
so, a thin healing membrane begins to form around the clot. However,
because of the fragility of this membrane, it is very prone to have
off and on capillary oozing of blood into the clot area.
Because of these and other variables, subdural clots may sometimes resolve
spontaneously, they may continue active but stable for months, or even
in one documented case for years, or they may slowly grow and potentially
end in catastrophy. (112) The bridging veins, which are located in the
subdural space, may play a key role in this, as experiments have shown
that they tend to rupture when stretched more than 40%. In such instances
acute, massive rebleeds may take place with minimal or no trauma. (113)
The propensity of chronic subdural hematomas/hygromas for secondary
rebleeding is further supported by study by Kawakami et al in which
19 patients with chronic subdural hematomas had venous blood taken at
the time of surgical aspiration from the chronic subdural hematomas.
Both the venous blood and surgical aspirate were then tested and compared
for various coagulation factors with the following results: “Compared
with coagulation results for venous blood the hematoma contents demonstrated
marked prolongation of the recalcification time, prothrombin time, and
activated partial thromboplastin time, and marked reduction of clotting
factor V, the hepaplastin test, prothrombin, and fibrinogen… These
finding indicate excessive activation of the clotting system, thrombin
generation, and increased fibrinolytic activity occurring in the hematomas…fibrin
and fibrinogen degradation products were increased in the hematomas…From
these results, excessive activation of both the clotting and fibrinolytic
systems is emphasized to be the possible etiological factor for the
origin and development of chronic subdural hematoma. (114) (And for
the proneness for rebleeding).
(Editorial comment). The Controversy of the Lucid Interval:
In rebuttal to another of the standard SBS doctrines, that an ultimately
fatal head injury
cannot be followed by a lucid interval (an interval between trauma and
onset of symptoms), a retrospective study of 76 children who died from
head injuries was done by M.G.F. Gilliland. The children were divided
into those who died from shaking, those who died from impact, and those
who died from combined of the two. It was found that 20 % of the shaken
children and 25% of the impact children had lucid intervals over 24
hours. In the latter groups there were four children for whom the interval
was over 72 hours. (56) Similarly in a retrospective report by J Plunkett
of 18 fall-related head injury fatalities from distances of 2 to 10
feet, 12 of the 18 children had a lucid interval.(57)
The Vaccine Issue:
Since 1999 there have been ongoing hearings in the U.S. Congress concerning
growing concerns about vaccine safety. Primarily these hearings have
dealt with concerns about a possible link between the MMR vaccine and
the growing epidemic of childhood autism in the U.S.A. Out of these
hearings there is now an emerging background pattern of deficiencies
in basic science in vaccine testing. As a result of these deficiencies,
it is a virtual certainty that large numbers of unrecognized vaccine
reactions are taking place, especially reactions of a delayed nature.
Based on these hearings, scientific evidence does not support the safety
of immunizations
in that safety studies on vaccinations are limited to short periods
only: several days to
several weeks. There are no long-term (months or years) safety studies
on any
childhood vaccine in use today. In addition, there have been no systematic
before-and-
after studies on the effects of vaccines on the immune, hematologic,
brain and neurologic
systems of babies, studies which should be considered indispensable
for any ongoing
medical intervention. Inadequate consideration has been given to the
additive or
synergistic adverse effects of multiple simultaneous vaccines, although
in cases of toxic
chemicals, two chemicals together may be 10 times more toxic than either
separately, or
3 chemicals 100 times more toxic. (24-25) As one example of the deficiencies
in basic science among the vaccines, in 1994 the Institute of Medicine,
a federal government advisory board, published a comprehensive review
of the safety of the hepatitis B vaccine. When the committee, which
carried the responsibility for determining the safety of vaccines by
Congressional Mandate, investigated five possible and plausible adverse
effects, they were unable to come to conclusion for four of them, because
they found that relevant safety research had not been done. Furthermore,
they found that serious “gaps and limitations” exist in
both the knowledge and infrastructure needed to study vaccine adverse
events. Among the 76 types of vaccine adverse events reviewed by the
IOM, the basic science evidence was inadequate to assess definitive
vaccine causality for 50 (66%). The IOM also noted that “if research…(is)
not improved, future reviews of vaccine safety will be similarly handicapped.”
(26) Several examples of before-and-after studies from older medical
literature will be cited as examples of these deficiencies.
Vaccines and Immune Paralysis:
The first example involves a study reported in 1984 in the New England
Journal of
Medicine (27) which involved the testing of T-lymphocyte subpopulations
(white blood
cells which help govern the immune system) in 11 healthy adults before
and after routine
tetanus booster immunizations. The results showed a significant though
temporary drop
in T-helper lymphocytes. Special concern rests in the fact that in 4
of the subjects the T-
helper lymphocytes dropped to levels found in active AIDS patients.
If this was the result of a single vaccine in healthy adults, it is
sobering to think of the immune consequences of the multiple vaccines
given to infants with their immature and vulnerable immune systems.
And yet, as far as I am aware, this test has never been repeated.
Comment: In my mind, until this study is repeated and
disproved, it would be both folly
and insupportable to claim that vaccines are not having an effect in
contributing to the
increasing patterns of sickness now seen as a matter of common observation
in today’s
children. In point of fact, reports are now appearing from widely separated
geographic
areas in which vaccinated children were found to have more allergic
disorders (and
patterns of sickness) than children with limited or no vaccines. (28-31)
(Also see
Appendix entitled, “Vaccines and Allergy Citations”)
Vaccines and Seizure Disorders:
For the second example, in 1955 AL Low of Chicago published a study
in which he
performed electroencephalograms (EEGS) on 83 children before and after
pertussis
immunization. (32) In two of the children he found that the EEGs turned
abnormal
following the immunizations without other signs or symptoms of abnormal
reactions. In
his report he commented:
“This study suggests that mild but possibly significant cerebral
reactions may
occur in addition to the reported very severe neurological changes.”
Careful search of the literature has disclosed only one similar before-and-after
immunization study, one from Japan in which it was found that 61 children
with epilepsy
or a history of febrile seizures showed significant increases in “epileptic
spikes” on EEGs
following DTP, DT, or BCG vaccines. (33)
Comment: Both of these studies, the only studies of
their kind as far as I am aware,
show strong evidence that subclinical brain damage may be taking place
on a far larger
scale than has been officially recognized.
Lack of Safety Studies for the Mercury-Containing Vaccine Additive,
Thimerosal
In June, 1999 the US Congress passed a mandate requiring the Food &
Drug
Administration (FDA) to reveal the mercury content in all prescribed
medications.
Formerly unknown, it was then revealed that children had been receiving
large amounts
of mercury in their vaccines in the additive, Thimerosal, which consists
of 49% ethyl
mercury, with children commonly receiving more than 50 or even 100 times
the dose of
mercury in a single day than considered safe by current US Environmental
Protection
Agency (EPA) standards. When Dan Burton, chairman of the Congressional
Committee
of Government Reform, questioned a panel of FDA officials whether or
not there had
been any safety testing for Thimerosal, he could learn of only one study
done in 1929, the
results of which were uniformly bad.
What Toxins and Foreign Substances Do Vaccines Contain?
In addition to live virus vaccines and the bacterial endotoxins inherent
in bacterial
vaccines, foreign substances in vaccines may include formaldehyde, mercury,
aluminum
phosphate, antibiotics, phenols, alcohols, mineral oils, animal serums,
animal DNA,
chicken embryo, aborted fetal tissue (in measles, mumps, rubella, and
chicken pox
vaccines), Simian Cytomegalic Virus (CMV, in oral polio vaccines), and
Mycoplasma.
(This list of ingredients has been compiled from annual Physicians’
Desk Reference
manuals and from reports in the medical literature in the cases of Simian
CMV and
Mycoplasma).
The Controversy of the Latent Period:
Several leading authorities who formerly held positions in the regulation
and licensing of
medicines in the United Kingdom have published statements that pre-licensing
observation periods for vaccines (in this instance referring to the
MMR vaccine) have
been too short to include the onset of delayed neurological (emphasis
mine) or other
adverse events, (34) one of the former health officers stating
that pre-licensing
observation periods should have been extended to a year rather than
several weeks, as
was the case with the MMR vaccine.
In my opinion the fundamental flaw in current medical legal standards
in the U.S.A. for
the latent period, and probably also in other English-speaking countries,
is that their time
limitations allow only for immediate or anaphylactic-type reactions,
by inference denying
the possibility or even the existence of delayed-type reactions. This
is clearly unrealistic,
as delayed-type hypersensitivity directed against the nervous system
has been
demonstrated by BCG vaccine in the laboratory. (35)
In this regard, two of the vaccines routinely given to children, the
Pertussis and
Haemophilus influenza vaccines, are known to be potent in causing hypersensitivity
reactions. (36,37) In addition the mercury-containing vaccine additive,
Thimerosal, has
been found to be potentially sensitizing. (141)
Vaccine Reactions Mimicking the Diagnostic
Criteria of Shaken Baby Syndrome:
As previously reviewed, (1-4) shaken baby syndrome
commonly describes a combination
of subdural hematoma (brain hemorrhages), retinal hemorrhages, and diffuse
axonal
injury (diffuse injury of nerve cells in brain and spinal cord) as a
sign of child abuse. In
the absence of known accidental or disease causes, these findings in
a child are
considered as diagnostic of non-accidental injury or SBS. The following
information,
however, will show that there may be other causes, among which may be
unrecognized
vaccine reactions.
It is also of interest to point out that there are anecdotal human reports
of infants which
developed increased intracranial pressure with bulging fontanelles following
DTP
immunization which tend to support these animal findings. (39-41) In
addition, in 1972
Galazka reviewed a series of autopsies on children whose deaths followed
the pertussis
vaccine. Although autopsies were limited in number, findings included
brain edema,
hyperemia, and soft meninges. (42) In 1983 Levin et al described ten
cases of what they
thought was a new syndrome of hemorrhagic shock and encephalopathy (HSE).
(131)
Although vaccines were not mentioned in the article, some of these incidences
occurred
in ages when vaccines were routinely given and, conversely, in no case
was trauma
implicated as a cause of the syndrome. Most of the early literature
in the 1930s and 1940s
on vaccine reactions surrounded the DTP vaccine, as reviewed by Scheibner
(148) and
Wilson. (149) However, human medical reports on vaccine-induced encephalitis,
rare at
any time, have virtually ceased since the early 1990s when a series
of articles appeared in
major medical journals attempting to dismiss encephalitis-like events
following the
pertussis vaccine as coincidental. (150-152) This is difficult to understand
considering
that vaccines like pertussis have been used to induce encephalitis (experimental
allergic
encephalomyelitis) in laboratory animals, as reviewed below:
In medical research it is standard to develop studies of animal models
before proceeding
with human studies, and such studies do exist for the vaccines. In a
publication in 1985
Iwasa stressed the finding of brain edema as a feature of Pertussis-induced
encephalitis.
(38) Munoz in turn conducted mice studies with pertussigen, an endotoxin
derivative of
the pertussis bacteria, in which he found (inflammatory) infiltrates
of lymphocytes
surrounding blood vessels in the brain and spinal cord, findings compatible
with an
autoimmune encephalitis. (43)
It is noteworthy that vaccines such as pertussis
have been used to induce allergic
encephalomyelitis in laboratory animals since 1973, (44) characterized
by brain swelling
and hemorrhages similar to those caused by mechanical injuries. As another
example, in
1982 Steinman and coworkers described mice studies following pertussis
immunization
as follows:
“Post-mortem examination of the brain (in experimental mice)
after immunization
revealed diffuse vascular congestion and parenchymal haemorrhage in
both the
cortex and white matter. Cortical neurons showed ischaemic changes.
Occasional areas of hypercellularity were evident in the meninges…B
pertussis
has a wide range of physiological effects including increased IgE production,
increased sensitivity to anaphylactic shock, lymphocytosis, and
hyperinsulinaemia. Its ability to induce increased vascular permeability
may
account for the tendency to produce haemorrhage.” (45)
In terms of human studies, I have available a list of 109 references
involving reports of
adverse reactions from hepatitis B vaccine, a vaccine which appears
to be especially
prone to be followed by hemorrhagic complications. Among these reactions
various
forms of vasculitis (inflammation of blood vessels) appear with special
frequency, which
may contribute to hemorrhagic complications because of greater fragility
and friability of
blood vessels and consequently may mimic both cutaneous and cerebral
hemorrhagic
findings now considered to be diagnostic of SBS. In addition, Burton
Waisbren has
reported on 3 cases of severe meningoencephalitis following hepatitis
B vaccine, as well
as 58 cases of acquired autoimmunity following this vaccine. (87)
In 1979 Hennessen and Quast reported on adverse reactions following
the pertussis
vaccine in 149 children including 13 deaths and 59 severe reactions
involving fever
followed by convulsions, shock, persistent screaming, and various involvements
of the
central nervous system. (144) In 1983 M Levin et al reported 10 infants
admitted to the
hospital with hemorrhagic shock and encephalopathy, which the authors
described as a
previously unrecognized disorder. (145) Seven of the infants died. Coagulation
was
severely deranged in the infants with prolonged prothrombin and partial
thromboplastin
times, low fibrinogen, and elevated fibrin-degradation products. Ages
ranged from 3 to 8
months. Although vaccines were not mentioned in the article, these of
course were the
ages during which 2, 4, and 6-months series of vaccines were routinely
given.
In regard to the issue of retinal hemorrhages, in the text Ocular Differential
Diagnosis by
Frederick Hampton Roy, M.D., papilledema (swelling in the retinal area)
and increased
intracranial pressure (from any cause) are listed as possible causes
of retinal
hemorrhages. (46) DPT vaccine is also listed as a possible cause, along
with other
routine childhood immunizations (OPV, MMR).
Comment: As stated previously, animal models for vaccine
reactions mimicking the
diagnostic features of SBS exist for each of the major criteria of SBS.
In my opinion, it
is only from the lack of basic science in the vaccine field that these
reactions very
frequently are not being recognized for their true nature and therefore
misdiagnosed as SBS.
New Findings that May Change the Diagnostic Criteria of SBS:
As reported in the medical journal, Brain, in a study which may revolutionize
current
concepts of SBS, Jennian F Geddes, a neuropathologist at Royal London
Hospital and
colleagues examined the brains of 53 children suspected of dying from
deliberate injury.
(47) Of the 53 children, 37 were less than a year old.
In the past, brain damage in such circumstances has been blamed on the
brain banging
against the skull as a baby is violently shaken or struck. It has been
thought that this
direct assault causes a characteristic kind of damage to the axons of
the nerves known as
diffuse axonal injury (DAI). However, the
researchers found evidence of DAI in only
two of the 37 babies. Instead they found that three-quarters of the
37 babies had died
because they stopped breathing as a result of previously unseen and
undescribed
pathology that was focused on the cranio-cervical junction, the area
which controls
breathing, where the brain meets the spinal cord. When babies stop breathing
as a result
of this injury, subsequent lack of oxygen causes the brain to swell
dramatically, which in
turn causes hemorrhagic complications and brain damage formerly attributed
to violent
shaking or blows.
The cranio-cervical junction is uniquely vulnerable in very young babies,
the authors
explained, because their neck muscles are weak and their heads relatively
large and
heavy.
The researchers found subdural hemorrhages
in 72% of the 53 cases, although most were
too superficial to cause death. Also, retinal hemorrhages were found
in 71% of the 38
cases in which the eyes were examined, but the authors felt that these
resulted from a
lack of oxygen to the brain (and the brain edema or swelling) rather
than trauma.
In a subsequent publication in Neuropathology and Applied Neurobiology
(2003), JF
Geddes et al reported on a histological review of the dura mater taken
from a post-
mortem of 36 pediatric cases aging up to 5 months with fresh bleeding
in the dura, in
which severe hypoxia had been documented clinically in 27 of the 36
cases. (120) The
subdural bleeding in these infants differed from that seen in older
children or adults in
that it was characteristically spread over both hemispheres in thin
films which did not
require neurosurgical intervention. Because stretch injury to the craniocervical
junction
“need not involve either violence or impact”
(emphasis mine), the authors offered the
following hypothesis regarding the intradural bleeding:
“It has been calculated that the maximal forces involved in shaking
a baby,
derived from experimental work (123,124) do not reach the threshold
necessary to
rupture the bridging veins if there is no (accompanying) impact of the
head…The
question arises: if the assumed circumstances of the incident (severe
shaking with
or without impact, the force equivalent to a fall from a two story window,
or
involvement in a high speed road traffic accident) do not fit the observed
neuropathology in many of the infants, could there be another source
(and
mechanism) of bleeding for this uniqute form of subdural hemorrhage?
“Our observations in the present series indicate that, in the
immature brain,
hypoxia both alone (from respiratory arrest following craniocervical
junction
injuries) and in combination with infection is sufficient to activate
the
pathophysiological cascade which culminates in altered vascular permeability
and
extravasation of blood within and under the dura. In the presence of
brain
swelling and raised intracranial pressure, vascular fragility and bleeding
would be
exacerbated by additional haemodynamic forces, such as venous hypertension,
and the effects of both sustained systemic arterial hypertension and
episodic
surges in blood pressure…Cerebral venous hypertension occurs when
there is an
obstruction to flow, which is the situation where there is cerebral
swelling…Similarly, retinal haemorrhages can be explained by rises
in
intracranial and central venous press, with and without hypoxia.(120)
In summary, the authors concluded: “We propose that, in such
infants, a
combination of severe hypoxia, brain swelling and raised central venous
pressure
causes blood to leak from intracranial veins into the subdural space,
and that the
cause of the subdural bleeding in some cases of infant head injury is
therefore not
traumatic rupture of bridging veins, but a phenomenon of immaturity.
Hypoxia
with brain swelling would also account for retinal haemorrhages.”
(120)
Comment: The authors suggested that inadvertent, nonviolent
neck stretch injuries
together with infection could have resulted in depression of the respiratory
center and
subsequent respiratory collapse in this series of infant deaths. It
is possible that neck
stretch injuries could have played a role in some instances, but in
my opinion the authors
were misinterpreting their own findings, which in time may come to be
recognized as a
classic description of the pathogenesis of vaccine reactions. Unfortunately,
the authors
never mentioned a possible role of vaccines, leaving this issue loose-ended
and
unresolved. As a result, the studies are of little help in preventing
injustices to many
parents and caretakers now being falsely accused of child abuse.
The
Issue of Retinal Hemorrhages:
Based on my own review of medical records involving SBS accusations
and convictions,
ophthalmologists are always called to examine infants for retinal hemorrhages
following
hospitalization where there is suspected non-accidental trauma or SBS.
Without
exception in each of the cases I have seen, the finding of retinal hemorrhage
has been
considered 100 % diagnostic of non-accidental trauma from violent shaking
or impact,
the basis of which has been previously reviewed. (96-101) However, it
would appear
from the medical literature that others disagree as to the diagnostic
specificity of retinal
findings. John Plunkett in the American Journal of Forensic Medicine
and Pathology
made the following statements concerning this issue:
“I do not understand the ‘retinal hemorrhage’
litmus test for shaken infant. No
one knows what causes retinal hemorrhage, although it is highly correlated
with
rotational deceleration injury/subdural hemorrhage in children, but
retinal
hemorrhage indistinguishable from that found in rotational deceleration
may be
found in association with ruptured vascular malformations , arachnoid
cysts, and
CNS (central nervous system) infections." (48)
AC Tongue mentions that “hemorrhages in all layers of the
retina occur in a number of
nontraumatic disorders associated with changes in cerebrovascular dynamics
such as
central retinal vein occlusion, high altitude retinopathy, and subarachnoid
hemorrhage
secondary to ruptured intracranial aneurysms.” (49)
Also
there is a report of retinal hemorrhages after near drowning, (50) three
reports following CPR resuscitation. (51- 53), and a
report in which retinal hemorrhages appeared in a healthy adult from
central retinal vein occlusion following hepatitis B vaccine.
(137) Retinal hemorrhage may be caused by ligating the central retinal
vein or its tributaries, or by suddenly increasing
intracranial venous pressure. (88,89) In reality, any sudden increase
in intracranial
pressure may cause a retinal hemorrhage. (90,91) Furthermore, retinal
and optic nerve
sheath hemorrhages associated with a ruptured vascular malformation
are due to an
increase in venous pressure, not extension of blood along extravascular
spaces.
(88,89,92,93) Patrick Barnes reported that retinal hemorrhages may be
seen with a
variety of conditions including accidental trauma, resuscitation, increased
intracranial
pressure, increased venous pressure, subarachnoid hemorrhage, sepsis,
coagulopathy,
certain metabolic disorders, and systemic hypertension. (14) In 1999
in the American
Journal of Forensic Medicine and Pathology GN Rutty et al listed the
following possible
alternate causes of retinal hemorrhages other than child abuse: natural
and assisted birth,
prematurity, raised intracranial venous pressure, abnormal intracranial
blood vessels, and
vitamin deficiencies, including vitamin B and K deficiencies. (129)
In the text, Ocular
Differential Diagnosis, Frederick H Roy listed the DTP, influenza, measles,
mumps, and
rubella vaccines (the latter three given individually or combined) as
causing retinal
hemorrhages, and that bleeding could be intraretinal, preretinal, or
subretinal. (46) Roy
also listed papilledema (swelling in the retinal area) and increased
intracranial pressure
from any cause as potential causes of retinal hemorrhages.
{Comment: Among the conditions listed above associated
with retinal hemorrhages, that
of brain edema (swelling) is by far the most common finding in found
in shaken baby
syndrome cases. It certainly constitutes a large majority of cases that
I have reviewed.
What then would be the mechanism by which brain swelling could produce
retinal
hemorrhages? The answer may be found in the fact that much of the venous
outflow from
the brain takes place through bridging veins transversing the subdural
space between the
outer surface of the brain and the inner surface of the skull, this
narrow space in turn
containing cerebrospinal fluid. Since venous flow is purely passive,
it would not take
much brain swelling to obstruct the outflow of blood from the brain,
this in turn resulting
in increased central venous pressure which, as outlined above, has been
shown to cause
retinal hemorrhages. (88-91)}
Vaccines,
Disseminated Intravascular Coagulation, and Brain Hemorrhages
In an unpublished series of cases involving accusations or convictions
of inflicted trauma
in the form of “shaken/impact baby syndrome,” largely collected
by attorney and jury
counselor Toni Blake of San Diego, California (personal communication,
2000), the
cases had the following features in common: 1) All occurred in fragile
infants born from
complicated pregnancies; problems included prematurity, low birth weights,
drug/alcohol
problems, maternal toxemia, diabetic mothers, or other maternal complications;
2) all
infants were 6 months age or less; 3) onset of signs and symptoms occurred
at about 2, 4,
or 6 months of age, within 12 days of vaccines; 4) all infants had subdural
hematomas; 5)
some infants had multiple fractures. In the year 2000 the series included
25 cases, but I
understand that it is now much larger.
Common experience has shown an unmistakable time-related onset of many
types of
health complications in infants following immunizations. Brain hemorrhages
are among
these complications, as demonstrated by the above-series. As already
stated, animal
models for vaccine reactions exist for each of the diagnostic criteria
now considered
exclusively diagnostic of SBS. The one large area still remaining virtually
untouched and
unknown in the basic science of vaccines is that of systematic before-and-after
human
tests on the effects of childhood vaccines on the neurologic, immunologic,
hematologic,
and other systems of the body.
In the case of brain hemorrhages, we know that they happen following
vaccines because
we see them, but we do not know the mechanism. Not knowing the mechanism,
we are
unable to prove a causal relationship between vaccines and brain hemorrhages
so that, in
my opinion, many parents and caretakers are being falsely accused and/or
convicted of
violent child abuse, of which the present case is an example. This is
the heart of the
problem. We have no positive means of diagnosing vaccine reactions other
than
observation, which is usually discounted in the courts and dismissed
as coincidental.
Turning now to the subject of disseminated intravascular
coagulation (DIC) as a plausible
common denominator for brain hemorrhages following
vaccines, in Williams
Hematology, Sixth Edition,(105) DIC is described as a condition brought
about by the
introduction of procoagulants (clotting factors) into the blood circulation
which overcome
the normal anticoagulant (teflon-like) endothelial lining of blood vessels
and cause
widespread thrombin (clotting-factor) generation with microthrombi (clots)
involving
multiple organ systems. Bleeding manifestations are caused by consumption
of platelets,
fibrinogen, coagulation factors V and VIII, as well as secondary fibrinolysis.
Major
clinical causes of DIC include two major categories. The first takes
place when blood is
exposed to “tissue factor,” a clot-inducing substance present
in the cell membranes of
most body tissues, as may occur with trauma, burns, malignant metastasis,
or amniotic
fluid embolism. The second category, more germane to our purposes here,
can result
from systemic viral, fungal, or bacterial infections in which the invading
organisms
activate tissue factors from monocytes and endothelial cells, which
may then activate a
pro-coagulant cascade.
The Williams text does cite experiments in which tissue factor was activated
in primates
(monkeys) by injection of live E coli bacteria, and in humans by injection
of low-dose
bacterial endotoxin. Hemorrhagic encephalopathy (hemorrhagic brain inflammation)
with
DIC has also been described clinically in 6 patients suffering from
Gram-negative
septicemia. (106) If the cascade of DIC can be initiated by a common
bacterial endotoxin,
why not expect the same result from injections of potentially virulent
diphtheria and
pertussis endotoxins? Unfortunately for a generation of children and
for many parents
now embattled with accusations of violent child abuse, this is where
research has
stopped. We know nothing about the potential activity of endotoxin-bearing
vaccines or
viral vaccines in bringing about harmful procoagulant reactions and
hemorrhagic
complications simply because it has never been tested. If this cannot
be proven at this
time due to deficiencies in research, by the same taken it cannot be
disproved. Proof of
safety of vaccines should rest on the prosecutors in cases in cases
such as these and not
on the parent, as often occurs in our courts; on the contrary, should
not the burden of
proof should rest on prosecutors to provide scientific reasons why vaccine-related
coagulopathy and DIC should be not be considered as a valid possibility
in the
differential diagnosis of brain hemorrhages?
As a practical note relating to initial screening
tests in cases of suspected child abuse, it is
of utmost importance to perform most or all of the standard coagulation
tests including
prothrombin time (PT), activated partial prothrombin time (APTT), fibrinogen,
d-dimer,
fibrinogen degradation products, and the examination of a red blood
film to check for
fragmented red cells. The purpose is to differentiate between acute
and chronic DIC.
ACUTE DIC: low PT, low APTT, and low or falling platelets. The fibrinogen
may be
normal but falls with time. D-dimer levels and fibrinogen degradation
products may be
elevated. CHRONIC DIC: PT AND APTT may be normal, while fibrinogen degradation
products, and d-dimer are usually elevated. Fragmented red blood cells
are commonly but
not universally present. (105)
Comment: The differentiation between acute and chronic
DIC is of utmost importance in
the courts, as it places the initial events causing brain hemorrhage
in entirely different
time frameworks. Acute DIC of course reflects a recent event, on which
basis most
shaken/impact baby accusations are made, but chronic DIC would tend
to implicate other
causes of earlier origin.
In an unpublished paper by Frank Hartman entitled, “Vaccination
Toxicity, Infection and
Science,” which will be submitted with this report, Hartman
proposed a very plausible
theory implicating aluminum toxicity as one of the prime agents in vaccines
leading to
intravascular coagulation. There are over 7000 references to the toxicity
of aluminum, he
noted. In regards to its procoagulant effects, he quoted a simple experiment
of making a
mixture of flour and water (in which the flour readily goes into solution).
When one drop
of an antiperspirant (contains aluminum) is added, the flour immediately
clumps and
settles to the bottom. Touching on areas of physics, Hartman went on
to explain:
“All trace minerals, metals, inorganic materials, proteins
and amino acids are held
in suspension in liquids as microscopic and submicroscopic particles
like dust
particles in the air. The very small particles are called colloids…Colloids
are held
in suspension via a very slight electro-negative charge on the surface
of each
particle. This charge is called a Zeta Potential. The ability of a liquid
to carry
material in suspension is a function of these minute electrical charges.
As the
electro-negative charge increases, more material can be carried in suspension.
As
the charge decreases, the particles move closer to each other and the
liquid is
unable to carry the same amount of materials. Calcium and heavy metals
drop out
first adhering to the vessel wall or organ surface.
“The quantity of positive and negative charges from chemical elements
in
suspension as colloids has a major effect on carrying capacity. Electropositive
ions decrease carrying capacity while electronegative ions increase
it. Elements
with only one excess positive or one excess negative ion have little
effect on
suspensions. Elements with two positive or two negative ions (divalent)
such as
magnesium and beryllium (+2) and selenium (-2) have 3,000 times more
effect on
coagulation or dispersion than elements with single ions. Elements with
a valence
of 3, such as aluminum (+3) and nitrogen and phosphorus (-3) have 6,000
times
more effect on carrying capability due to the three extra positive charges.
Vaccines contain aluminum salts which greatly exacerbate coagulation.”
The importance of Hartman’s observations about the adverse effects
of aluminum
additives in vaccines is underscored by other reports. In the journal
Brain (2001), in an
article entitled “Macrophagic Myofasciitis Lesions Assess Long-term
Persistence of
Vaccine-Derived Aluminium Hydroxide in Muscle,” RK Gherardi et
al reported studies
showing both long-term persistence of aluminium hydroxide and an ongoing
local
immune reaction in patients with systemic symptoms which appeared subsequent
to
vaccination. (125) In an earlier article in the journal Vaccine, (1991)
by RK Gupta and
EH Relyveld, the authors pointed out that reactions from the DPT vaccine
ordinarily
attributed to bacterial endotoxins in the vaccine may be also due to
other factors, such as
sensitization induced by aluminium adjuvants and other impurities. (147)
As a further observation on this subject, in an article entitled “Activation
of the
Coagulation System in the Gulf War Illness: a Potential Pathophysiologic
Link with
Chronic Fatigue Syndrome; a laboratory approach to diagnosis,”
by KL Hannon et al
(2000), the authors reported on a controlled study of 33 veterans with
the Gulf War
Illness which confirmed hypercoagulability states in the veterans as
compared with
controls. (117) In discussing these findings the authors pointed out
that there appears to
be significant overlap in the symptoms of Gulf War Illness, chronic
fatigue, and
fibromyalgia, each having in common an activation of the clotting cascade
with fibrin
deposition in the circulatory system and reduced flow of oxygen and
nutrients to the
nerves and muscles of the body. In addition to a variety of toxic chemical
exposures, the
authors listed live virus vaccines such as smallpox or polio, vaccine
adjuvants (additives),
vaccine toxins and contaminants among various possible causes of the
syndrome. The
common denominator, according to the authors, was that of “immune
complexes”
consisting of a foreign chemical or biological agent (vaccines) combining
with the body’s
own antibodies, these immune complexes in turn attacking the endothelial
surfaces of
blood vessels and converting them from their normal Teflon-like anticoagulant
surfaces
to procoagulant surfaces with cobweb-like fibrin deposits. It is precisely
this
procoagulant effect of vaccines which, as an initiating event, may in
some instances lead
to hemorrhagic complications from disseminated intravascular coagulation,
almost
always now being misdiagnosed as SBS.
Late Onset Hemorrhagic Disease of the Newborn
In addition to disseminated intravascular coagulation, hemorrhagic disease
of the
newborn is another possible cause of brain and retinal hemorrhages in
infants, as
reviewed in a comprehensive report on the subject by GN Rutty et al.
(129) According to
the authors, the classical form of hemorrhagic disease of the newborn
(HDN) is usually a
self-limiting, acquired, hemorrhagic disorder that occurs as a result
of vitamin K
deficiency and takes place within 24 to 72 hours after birth. Late-onset
HDN, in contrast,
is defined as cases occurring after the first week of life, with most
presenting between 4
to 6 weeks after birth, though rarely occurring as late as 6 months
age. Intracranial
bleeding may occur in up to 100% of late-onset case (emphasis mine);
retinal
hemorrhages may also take place; other common sites of bleeding may
include the
oronasal, gastrointestinal, and urogenital tracts.
Late-onset HDN is usually associated with breast-fed babies who did
not receive
prophylactic vitamin K at birth, although other risk factors (even when
vitamin K is
given) include prematurity, being small for gestational age, birth asphyxia,
traumatic
delivery, antibiotic therapy in the neonatal period (reduces
vitamin K production by
intestinal flora), drugs taken by the mother (including warfarin,
dilantin, barbiturates,
isoniazid, some Chinese medications), infective gastroenteritis (with
vomiting and/or
diarrhea), malabsorption, and liver disease.
Normal full-term babies, the authors continued, have vitamin K-dependent
factors
between 25% and 70% of adult levels and do not achieve adult levels
until 2 to 12
months of age. Sponteneous hemorrhage, however, does not occur until
levels of these
factors fall below 25% of adult levels. Prophylactic vitamin K given
intramuscularly at
birth is reported to protect the infant from HDN for up to 8 weeks.
Vitamin K is required
for carboxylation of glutamic acid residues on the precursors of the
vitamin K-dependent
coagulation factors (factors II, VII, IX, and X) for their normal function.
Failure of
carboxylation (from Vitamin K deficiency) results in the production
of nonfunctioning
proteins which appear in the blood. These are known as proteins induced
by vitamin K
absence (PIVKA). Laboratory diagnosis of HDN is characterized by elevated
PIVKA,
prolonged prothrombin and thromboplastin times, normal thrombin time
and normal
fibrinogen time (the latter differentiating from disseminated intravascular
coagulation, in
which the fibrinogen level will be diminished).
Diffuse Axonal Injury (DAI), the Third Diagnostic Criteria for
SBS:
There is no doubt that diffuse axonal (nerve injury) may take place
in head trauma. The
question is whether or not the pathologic findings with widespread B-amyloid
precursor
protein deposits and axonal spheroids, are specific for non-accidental
injury or whether
these findings are also present in other, non-head injured conditions,
including vaccine
injury.
Based on the work of F.E. Sherriff and associates, this question can
be answered, (54) as
described in the following:
“Severe non-missile head injury commonly results in a form 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…We
have used
immunocytochemistry for the B-amyloid precursor protein (BAPP) as a
marker
for axonal injury in formalin-fixed, paraffin-imbedded sections of human
brain.
Axonal BAPP was present in all (23 cases of head injury) that survived
for 3
hours or more…...BAPP immunoreactivity was also found
in some (5 of 13) non-
head injury cases and so cannot be considered to be a specific marker
for
trauma.” (Emphasis mine)
In a survey conducted at the department of forensic medicine, University
of Sheffield,
UK, GN Rutty and associates studied sections from a series of brains
comprised of four
groups: those showing evidence of hypoxia with no history of head trauma,
those with
head trauma but no evidence of hypoxic change, those with history of
head trauma and
hypoxic change, and four controls originally described as “diffuse
axonal injury.” Using
the same staining technique as described above in the Sherriff study,
it was found that
axonal bulbs may occur from hypoxia in the absence of head injury. It
was concluded
that “the presence of axon bulbs cannot necessarily be attributed
to shearing forces
alone.” (55)
Barlow’s Disease (Subclinical Scurvy) Rediscovered:
Physicians and the lay-public alike generally think of scurvy as an
historical disease of
the days of wooden sailing ships, which was eliminated by the introduction
of limes or
other citrus fruit into the diet. However, as the younger generations
in industrialized
nations turn increasingly to commercially processed “fast foods”
as a major part of their
diets, subtle forms of scurvy may be returning and contributing to the
hemorrhagic
complications now thought to be exclusively diagnostic of SBS.
In contrast to classical scurvy of earlier times which was characterized
by a total lack of
vitamin C in the diet, “subclinical scurvy” describes a
condition with marginal dietary
deficiencies of vitamin C (apparently very common today) where an additional
stress,
such as a viral infection, further drains away the already lowered levels
of vitamin C, thus
predisposing to serious or catastrophic consequences should additional
stresses be placed
on the body. The credit for clinical recognition of sublinical
scurvy should be attributed
to Dr. Archivedes Kalokerinos of Australia.
In the early 1970s Dr. Kalokerinos, then stationed as a medical officer
among the
Australian aborigines, was troubled by a very high child mortality rate,
in some areas
approaching 50%. Having observed signs of scurvy in some of the children,
and noticing
that they often died following immunizations, especially if they had
colds or minor
respiratory infections, the thought occurred to him that there might
be a connection
between vitamin C deficiency and deaths following vaccines. With improved
nutrition,
oral vitamin C supplements, avoidance of vaccines during minor illnesses,
and injectable
vitamin C during crises, infant mortality was virtually abolished. (58)
As a result of this
work he was awarded the Australian Medal of Merit in
1978.
One of the primary roles of vitamin C in the body being that of producing
and
maintaining connective tissue, Dr. Kalokerinos hypothesized that with
minor viral
infections further depleting an already marginal store of vitamin C,
the administration of
toxin-bearing vaccines would sweep away the small residual traces of
vitamin C,
somewhat like a flash-fire, provoking fulminating scurvy with encephalitis
(brain
inflammation) and hemorrhagic complications from the weakening of blood
vessels.
In Vienna in the 1840s, long before recognition of the importance of
sanitation and the
role of microbes in causing disease, an obstetrician by the name of
Ignaz Semmelweis
was assigned to a birthing center in Vienna which was notorious for
its high maternal
mortality rates. Based on simple observation, Semmelweis deduced that
doctors and
nurses were carrying the infection from one patient to another and subsequently
required
that they wash their hands between patients. As a result, the mortality
rate among
maternity patients under his care was reduced from nearly 30% in some
of the hospital
wings to less than 2%.
Was Semmelweis honored by his peers for this discovery? No,
at least not at that time.
Instead he was dismissed from the hospital staff because his procedures
did not conform
with the medical thinking of the time. In the case of Dr. Archivedes
Kalokerinos, could
history be repeating itself?
Basic Facts about Vitamin C:
- Vitamin C deficiency still does occur in the Western World. The plasma
vitamin
C status was found to be depleted, between 0.2 and 0.5 mg/100 ml (or
11 to 28
micromol/L) in 30 %, and to be deficient, below 0.2 mg/100 ml in 6%
of people
attending a Health Maintenance Organization (HMO clinic) in Tempe, Arizona
in
1998. (59)
- The blood leukocyte ascorbic acid concentration is further reduced
by infection.
Even the common cold causes a fifty per cent reduction of the leukocyte
ascorbic
acid concentration within 24 hours. (60) Moreover, E coli endotoxin
has been
shown to inhibit the uptake of vitamin C by mouse fibroblasts in tissue
culture. (61)
- When the human plasma ascorbic acid level falls below 0.2 mg/100 ml,
the whole
blood histamine level is doubled or quadrupled. (62) Ascorbic acid is
needed for
the conversion of histamine to hydantoin-5-acetic acid and on to aspartic
acid in
vivo. (63)
- The whole blood histamine level is also increased by vaccines or toxoids,
by
stresses such as heat or cold, and by various drugs in guinea pigs.
(63) Sleep-lack
more than doubles the blood histamine levels of resident physicians.
(64)
Ascorbic acid supplementation rapidly reduces the blood histamine levels
of
ascorbate-depleted subjects. (62)
- Blood histamine concentration begins to rise when the plasma ascorbic
acid level
falls below the normal level of 1 mg/100 ml and rises exponentially
when it falls
below 0.7 mg/100 ml. (62)
- Vitamin C impairs the hydroxylation of proline and lysine, which are
essential
building blocks for the synthesis of collagen, which forms the foundation
for
fibrous tissue, cartilage, bone and teeth. (65)
- It is the increased blood histamine, or histaminemia, that causes
separation of the
endothelial cells from one another in scurvy, (66) which causes the
capillary
fragility and bleeding of scurvy.
- Humans are vulnerable to vitamin C deficiency as we lack the enzyme,
L-gulono-
gamma-lactone oxidase, needed to synthesize this essential substance,
making us
totally dependent on dietary vitamin C from our diet. This is in contrast
to most
other mammals which are able to manufacture their own vitamin C from
simple
sugars in the liver.
- Vitamin C protects against diphtheria toxin, (67-68), tetanus toxin,
(69) and
typhoid endotoxin. (70)
- A 1932 report on the hemorrhagic complications of scurvy stated that
these
occurred most commonly beneath the periosteum of the long bones and
into joint
spaces, but frequently also involved the skin, mucous membranes (gums),
orbits
(eyes), and serous cavities of the body. (71) One of the most characteristic
signs
of adult scurvy was swollen bleeding gums, but this is never seen in
edentulous
infants. It is the bacteria in the crevice between the tooth and the
gum that cause
local infection and bleeding gums.
- Lund and Kimble of Madison, Wisconsin in 1943 reported that “Hyperemesis
Gravidarum may lead to dangerously low levels of vitamin C. Clinical
scurvy may
appear. The retinal hemorrhages of severe hyperemesis gravidarum are
a
manifestation of vitamin C deficiency and are similar to petechial hemorrhages
seen elsewhere. The hemorrhages cease after adequate therapy with vitamin
C;
henceforth they are not necessarily an indication for the use of therapeutic
abortion. (107)
- Sanford et al (1942) drew attention to the low blood vitamin C values
obtained in
6 neonatal infants with cerebral hemorrhage (0.03 to 0.25 mg/100 ml)
and
emphasized the need for vitamin C. (121) {Comment: Histamine is removed
by
vitamin C-activated conversion to hydantoin-5-acetic acid and on to
aspartic acid
in the body. When the rate of accumulation of histamine in the blood
exceeds the
rate of its removal by vitamin C, the blood histamine levels rises,
causing
capillary and venous fragility, leading to bleeding. The blood escaping
from the
blood vessels slowly undergoes hemoylsis. With release of pro-oxidant
iron from
the blood cells, this causes further vitamin C depletion}
- In his classic 3-volume work on vitamin C, (64) Dr. AC Clemetson included
a
chapter entitled “Subclinical Scurvy.” In contrast to classical
scurvy of earlier
times, which was characterized by a total lack of dietary vitamin C,
Clemetson
described subclinical scurvy as a condition with marginal dietary deficiency
of
vitamin C where additional stresses of many kinds including lack of
sleep,
exposure to cold, viral infections, and vaccines could throw the subject
into an
acute scurvy with potentially catastrophic consequences. Another important
and
unique contribution of Dr. Clemetson was his research showing a reciprocal
relationship between plasma ascorbate and serum histamine levels and
of the role
of increased serum histamine in the hemorrhagic features of scurvy.
Thus we have
a newly described variant of classical scurvy of historical importance,
recognized
clinically by A Kalokerinos, (122) and described academically by AC
Clemetson. (64)
Vaccine-Induced Hemorrhagic Encephalitis: an Hypothetical Model
Based on
Clinical Observations
Toni Blake, an attorney in San Diego who specializes in defending parents
and caretakers
accused of shaken baby syndrome, has described a pattern of fragile
infants with the
following characteristics: 1) All babies came from problem pregnancies
including
prematurity, low birth weight, maternal diabetes or toxemia, maternal
drugs or alcohol,
and other problems; 2) all had subdural hemorrhages; 3) many had fractures;
4) infant
complications occurred in clusters around 2 months, 4 months, and 6
months of age; 5)
most infant complications and collapses occurred within 11 or 12 days
of vaccinations.
(Personal communications 2000 and 2002)
In my opinion, the observations of attorney Toni Blake may hold a key
to what is
happening in many of these infants now being (mis)diagnosed as victims
of
shaken/impact baby syndrome; that is, the ill-advised vaccination of
fragile infants as
described above, and/or vaccination in the presence of viral infections,
which are known
to increase the consumption of vitamin C. The combination of viral infection
and vaccine
toxins in turn may precipitously plunge the infant’s vitamin C
to critically low levels.
One of the prime roles of vitamin C in the body is its role as an antioxidant
in donating
electrons to quench free-radical inflammatory damage from infections
and/or vaccine
toxins. However, once the level of vitamin C is reduced to the point
that it can no longer
protect the brain, which is unduly susceptible to toxic or infectious
damage, it (the brain)
may become subject to free-radical damage. In explanation, the same
as with harmful
radiation exposures, toxins cause their damage by creating “free-radicals”
which, by
definition, consist of oxygen molecules with unpaired electrons. When
uncontrolled, free-
radical generation can become harmful and destructive to the cells of
the body. Vitamin
C is critically important in protection against free-radical proliferation
because of its
ability to donate electrons to neutralize the unpaired electrons on
the oxygen molecules.
For these reasons, the combinations of ill-advised vaccines given to
fragile infants in the
presence of viral and/or bacterial infections is, in my opinion, an
invitation to disaster,
with the brain being potentially subjected to a firestorm of free-radical
inflammatory
damage. Once this is set in motion there is a variable latent period
with gradual
progression of inflammatory brain edema (swelling). As the brain continues
to swell, the
breathing center at the base of the brain may become herniated into
the spinal canal
resulting in respiratory arrest and collapse. The resultant brain hypoxia,
in turn, may
further accelerate the brain swelling (edema) as described by J Geddes
above. (120)
Among the cases that I have reviewed, I have found this to be a common
pattern, too
frequent to be coincidental.
As described in his autobiography, Dr. Kalokerinos describes the mechanisms
involved
in the production of brain and retinal hemorrhages in much the same
fashion: (122)
“1. Endotoxin (endogenous and/or from vaccines) damages the endothelial
linings
of the brain blood vessels.
2. Endotoxin then ‘leaks’through to the surrounding brain
tissue. This includes the
retina that is an extension of the brain.
3. The brain tissue is damaged.
4. The blood supply to the portions of the brain involved is reduced.
5. Insufficient oxygen, glucose, and Vitamin C follows.
6. Parts of the brain are ‘rich’ in ‘bound’(controlled)
iron. This is released.
7. Violent free radical reactions result, and these cannot be controlled
because of a
lack of immediately available Vitamin C and other antioxidants.
8. So further, and rapid, brain tissue damage results, with more free
radical
reactions.
9. Hemorrhages occur in the area/areas involved.
10. After a variable period (depending on a host of factors) some of
the red blood
cells in the hemorrhages break down and release their stores of iron
and copper.
11. This results in a further cascade of free radical reactions and
tissue
destruction.
12. Cerebral edema (brain swelling) occurs.”
One final question remains: Why is the brain uniquely susceptible to
this chain of events?
The answer probably rests in the fact that the brain is made up of at
least 60% fatty
material, with the highest fat content of any vital organ in the body.
In addition, a large
portion of this fatty (lipid) material is made up of Omega-3 polyunsaturated
fatty acids,
which are highly vulnerable to peroxidation when exposed to uncontrolled
oxidative
stresses from endotoxins.
Acute Autoimmune Hemolytic Anemia from DTP Vaccine:
In 2001 KA Downes and colleagues reported on a 4-month old child admitted
to the
hospital with fever and increasing lethargy a few days following the
second series of
routine immunizations, which included the DTP vaccine. By the third
hospital day the
hemoglobin had dropped to 2.3 grams%. The child subsequently died, but
careful
evaluation before death identified an acute autoimmune hemolytic anemia
from the DTP
vaccine. (74) In a review of the literature the authors found 7 other
reports of
autoimmune hemolytic anemia following DTP vaccines. (If this reaction
were routinely
sought in hospitals, as it was in this case report, probably the numbers
would be much
greater).
In my own case reviews there were several admitted to hospitals with
hemoglobin levels
in the 6s and 7s. One child was admitted with a hematocrit of 6% and
a hemoglobin of 2
grams %, dying within hours of admission. In none of these cases was
there mention or
investigation in the medical records of a possible hemolytic process,
at least none that I
could find.
Bleeding Diatheses from Coagulopathy
In his medical review of the death of Baby Alan Yurko, Dr. Michael D
Innis, MBBS,
DTM&H, FRCPath, Honorary Consultant Haematologist, Princess Alexandra
Hospital,
Brisbane, Australia, diagnosed death from intracranial hemorrhage and
a bleeding
diathesis following a coagulopathy resulting from failure of the liver
to synthesize
clotting factors in adequate amounts.
Liver failure was diagnosed by significant elevations of liver enzymes
and significant
lowering of serum albumen, cholesterol, and creatinine, from which it
was concluded that
there was inadequate liver production of coagulation factors II, VII,
IX, and X. (74)
The presence of a coagulopathy, in turn was reflected by an elevated
prothrombin time,
high D Dimer test, and high fibrin spit products. (Fibrinogen not done)
Marked platelet
elevation ruled out disseminated intravascular coagulopathy. (75)
In my opinion, bleeding studies of the types described above should
be done in all infants
or children with retinal/brain hemorrhages before entertaining a diagnosis
of SBS.
According to Dr. Innis’s report, coagulopathies can result in
subdural bleeding,
intracerebral bleeding, retinal hemorrhages, bleeding into the spinal
cord and into the skin
in the form of bruising. (76)
Post-Vaccinal Bruises Mistaken for Inflicted Trauma
Post-vaccinal bruises were studied by Krause et al (1996) who found
that they were the
result of perivascular infiltrates of polymorphonuclear cells containing
various immune
deposits such as IgA, so that they were not real bruises. (140) In 1993
a similar case was
reported of a previously healthy woman who developed cutaneous vasculitis,
confirmed
by biopsy, and pulmonary problems following inoculation with recombinant
Hepatitis B
vaccine. (142) In another case in which vaccines were not mentioned,
a 2-1/2 year old
black boy was seen in an emergency room with unexplained “swelling
and bruising “ all
over his body. The father was accused of child abuse, but upon hospitalization,
further
evaluation revealed that the child was suffering from post-Streptococcal
hypersensitivity
vasculitis. Although the authors could find only two similar
cases of misdiagnosis in the
period of 1970 to 1978, they suspected that it occurred frequently.
(143)
Skeletal Fractures:
In cases of suspected child abuse where skull, rib, or long bone fractures
are found in
addition to brain and retinal hemorrhages, medical-legal difficulties
are greatly increased
for the accused parent or caretaker and defenders. It is therefore important
to point out a
variety of known conditions in which fractures can take place spontaneously
or with
minimal trauma. When fractures are found from any of these conditions
in infants, birth
trauma should be considered as a possible source.
Skull fractures:
In a postmortem study of infant skulls reported by S Margulies and K
Thibault with ages
ranging up to 6 months at time of death, skull thicknesses were reported
as 3 to 5 mm,
(94) so that from this it can be assumed that a normal skull thickness
for a 7-month-old
child would have been greater than 5 mm. On this basis we have a standard
for
measurement of excessive thinness of the skull, which can carry increased
risk of fracture
with minimal trauma, as indicated by the following study from Germany:
- In the German scientific journal Z Rechtsmed, 1990: 103(4):311-313,
W Weber
performed postmortem biomechanical fragility tests on infant skulls.
As reported
in the article abstract, “skulls were dropped from 82-centimeter
heights onto (A)
stone, (B) carpet, and (c) foam-backed linoleum. 35 further falling
tests were
carried out onto softly cushioned ground. In 10 cases (D) a 2-cm thick
foam
rubber mat was chosen and in 25 further cases (E) a double-folded (8-cm-thick)
camel hairblanket. Hence the results of altogether 50 tests could be
evaluated. In
test groups A-C on a relatively hard surface, skull fractures of the
parietals were
observed in every case; in test group D this fracture was seen in one
case and in
test group E in four cases. Measurements along the fracture fissures
showed bone
thickness of 0.1-0.4 mm. The fracture injuries originated in paper-thin
single-
layerbone areas without diploe, which can also be considered the preferred
regions for skull fractures of older infants following falls from low
heights. These
results indicate that it is no longer possible to assume that the skull
of infants is
not damaged after falls from table height.”
- Prange, Coats, Duhaime, and Margulies (J Neurosurg, 2003)
designed an
anthropomorphic surrogate of a 1.5 month-old human infant used to simulate
falls
from 1 foot, 3 feet, and 5 feet as well vigorous shaking and inflicted
impact. They
concluded that vigorous shakes produced rotational responses similar
to those
resulting from minor falls, but inflicted impacts produced responses
that were
significantly higher than even a 5 foot fall. (146)
- As noted above on page 2, common doctrine on which shaken/impact baby
syndrome charges are based holds that injuries, such as skull
fractures, can only
be caused by forces equivalent to a fall from a second story building.
However, it
would appear that this doctrine is based more on supposition than fact,
as
indicated by the following representative articles: In a report entitled,
“Fatal Head
Injuries from Short Distance Falls,” J Plunkett reported
on 18 fall-related fatalities
taken from the U.S Consumer Product Safety Commission database for head
injury associated with playground equipment. The youngest child was
12-months
old, the oldest 13 years. The falls were from 2 to 10 feet. (78) In
an article entitled
“The Mortality of Childhood Falls,” JR Hall et all reported
on a survey of
pediatric deaths due to falls of the Cook County Medical Examiner’s
office
(Chicago) from January, 1983 through December, 1986, in which it was
found
that falls were the third leading cause of death in children less than
4 years of age
(mean age 2.3 years); and among these falls forty-one percent of deaths
occurred
from minor falls such as falls from furniture or while playing. (118)
Also there is
the report of a freak accident in which an eight-month old boy received
a parietal
skull fracture when his sister dropped or tossed a toy airplane (480
gms) which
landed on the boy’s head. (119) Other reports have shown that
short falls can
cause brain and retinal hemorrhages and sometimes fatalities. (133-135)
- Metabolic conditions subject to spontaneous fractures, or to fractures
with
minimal trauma include scurvy, (vitamin C deficiency), rickets (vitamin
D
deficiency), osteogenesis imperfecta (79-80), and temporary brittle
bone disease
(TBBD). (81-82) In regard to the latter, Miller and Hangartner described
the
condition characterized by transient bone weakness and presenting as
multiple
unexplained fractures during the first year of life. For this reason
it has often been
confused with child abuse. In a study involving 26 infants with TBBD
it was
found that 25 had a history of decreased fetal movement or confinement
in limited
uterine space during the mother’s pregnancies. Plain X-ray films
were normal in
all cases, but osteopenia was confirmed by bone densitometry studies.
(82)
- In a report by Kirschner in 1985 entitled, “The Mistaken Diagnosis
of Child
Abuse,” a number of cases were presented in which mistaken diagnosis
of child
abuse was confirmed. (83) One of these was a case with pseudo fractures
from
atypical parietal suture lines. An attempted search of the literature
on the subject
revealed one reference on parietal pseudosutures. (95)
Spontaneous Rib Fractures; Alternate Explanations other than
Child Abuse:
There is a general consensus in the medical community that spontaneous
fractures can
occur where there is: (1) Brittle bone disease; (2) scurvy with imperfect
connective tissue
formation in fetal or infant skeletal tissue; (3) osteomalacia; (4)
traumatic birth situations;
(5) during cardiopulmonary resuscitation; (6) rickets; (7) osteogenesis
imperfecta, and
prematurity.
Rib Fractures and Other Long Bone Skeletal Fractures; Due to
Epiphyseal Slippages and
Not Due to Trauma:
According to a study by V.F. Garcia et al (1990) published in Journal
of Trauma titled,
“Rib fractures in children: a marker for severe trauma,”
(104) of the 2080 children
studied in trauma centers in Australia, 33 had multiple rib fractures.
Among these 33, the
injuries were accompanied by severe (emphasis mine) internal thoracic
injuries in 85% of
the cases. (It will be recalled that no thoracic injuries were reported
in the present case).
Comment: {If severe internal chest injuries took place in 85% of cases
with multiple
traumatic rib fractures, this represents a 15% margin for error for
a single occasion of
trauma sufficiently severe to cause rib fractures. In cases with multiple
rib fractures (or
apparent rib fractures), which appear to be in different phases of healing,
the parents
often became subject to charges of repeated acts of violent squeezing
or trauma.
However, if one thinks about it, this scenario would be virtually impossible
without
causing severe internal chest injuries, in that the partially healed
fractures from the first
act of violence, scarcely beginning to heal, would become easily dislodged
and act as
shards or spears pointing and plunging into the thoracic cavity with
a second or third
incident of violent squeezing or battering. The odds that this could
happen repeatedly
without causing severe injuries in the thoracic cavity are extremely
unlikely, quickly
reaching the vanishing point. One of the basic issues/questions in such
cases concerns the
length of time required for firm healing and reattachment, and the elimination
of
vulnerability to re-fracture. According to the text, Forensic Pathology
by Vincent and
Dominick DiMaio, in healing of fractures in children, a callus is visible
radiologically
within 2 weeks of the fracture, the bone is consolidated in 4 to 6 weeks,
though it usually
takes 2 to 3 months to heal solid. (139)
{Also considering the matter of pain, in the cases I have reviewed,
if there had been fresh
rib fractures at various times, unmistakable pain would have been observed
such as when
picking up the baby or changing diapers, and lasting up to a week or
more following each
fresh incident of fractures, and reported by family members. I have
never seen this
happen in a single instance in babies with multiple rib fractures.}
Page 28
28
We now come to an anomaly in many instances if not a majority of rib
fractures, in that
they occur near or within the anterior or posterior costochondral junctions
between ribs
and cartilage attached to the sternum (breast bone), at the junction
of ribs and spine if
posterior, or in the epiphyseal plates of the long bone. These are unusual
locations for
traumatic fractures, as reviewed in a study by HG Hiller entitled, “Battered
or Not – a
Reappraisal of Metaphyseal Fragility.” (111) In this study a group
of 145 children
admitted to a pediatric trauma center for traumatic fractures were reviewed.
Not one case
of metaphyseal plate (costochondral junction) type was found. The study
also looked at
five cases of metaphyseal plate fractures from another hospital, where
in all five cases the
bones had a chalky appearance on X-rays. Of the two cases available
for microscopic
evaluation and bone scan, both revealed abnormal bone formation and
were ruled non-
traumatic. In his discussion the author observed that this type of trauma
is common in
scurvy (emphasis mine) without undue trauma to the child, and that green
stick fractures
are equally common in rickets. Hiller interpreted these findings as
causing doubt on the
advisability of accepting multiple epiphyseal plate fractures as definite
roentgenologic
evidence of battering, and that they are in need of close reappraisal.
Additional reports
have pointed out that rib fractures may occur with traumatic births,
(108 – 110)
prematurity, (126) and chest physiotherapy. (127) Each of these causes
may be mistaken
for child abuse unless carefully investigated.
In addition to scurvy, there is another situation in which spontaneous
fractures are prone
to take place: temporary brittle bone disease as described by Marvin
Miller, M.D., Ph.D.
In his publications he showed that unusually close uterine confinement
with reduction of
fetal movement resulted in increased fetal bone fragility and vulnerability
to spontaneous
fracture. As outlined by C.R. Paterson and cited by Miller, reduced
movement in such
instances delays fetal neo-ossification, which is controlled by a bone
“mechanostat”
mechanism. Dr. Miller stressed that TBBD could not be diagnosed by plain
X-rays but
required bone densitometry for diagnostic confirmation. (81,82) Merck
Manual, Seventeenth Edition, states that both rib fractures and costochondral
separations can take place with cardiopulmonary resuscitation (CPR)
(Page 1748).
Returning to the subject of bone changes in scurvy, in a book by AF
Hess entitled,
“Scurvy, Past and Present,” published in 1920, one finds
the following quotations: (85)
- As described by Hess, scurvy disrupts these areas, (epiphyseal plates)
the bone
breaks down, and the ribs may over-ride, forming in typical cases “beads.”
Then
healing commences with new bone formation (looking just like true healing
fractures). Furthermore, not all the ribs may be involved in this process,
and the
changes will not all occur at the same time – giving the appearance
of multiple
fractures of different ages. (Pages 94-95)
- Several illustrations provided in the Hess text showed separations
of the
epiphyses of the head of the humerus, and both partial and complete
separation of
the lower ends of the femora. Hess commented that this was a frequent
lesion of
fully-developed scurvy in infants, children, and even in young adults,
being most
frequent at the lower end of the femur, the upper end of the tibia,
the head of the
humerus, and the costochondral junctions. Very significantly as applied
to the
present case Hess stated, “it is to these epiphyseal separations
that the term
fracture or infraction usually refers,” (Page 198)
- In perusing the literature a single 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. (Page 126)
- The most typical site of hemorrhage is beneath the periostium, a lesion
widely
known because of its clinical significance. (Subperiosteal hemorrhages
occur
under the periostium; that is, the ‘skin’ of the bone).
The blood is quickly ossified,
and the appearance on X-ray is similar to what is seen when ribs are
broken.
(Pages 95, 108)
- Speaking of the classical X-ray finding seen in scurvy bones, the
‘white line’
sometimes seen near the ends of long bones, Hess 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. (page 199)
- These changes (subperiosteal hemorrhage, costochondral 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 changes. (page 91)
As another source of references on bone changes in scurvy, the 5th
chapter, volume II of Dr. Clemeton’s books on vitamin C, a chapter
entitled “Bone Changes,” (64) begins with the following
introduction:
“One of the most basic defects in scurvy is the inability
of connective tissue cells
to form mature extracellular materials; the fibroblasts, the chondroblasts,
the
odontoblasts, and the cementoblasts are all connective which are related
to one
another and are responsible for the secretion of collagen fibers which
are the
foundation of fibrous tissue, bone, cartilage, dentin, and tooth cement
respectively. In scurvy, it seems that they continue to secrete a semiliquid
protocollagen, but the ability to form mature collagen fibers is
lacking…Consequently the extracellular tissues lack the framework
of collagen
on which to grow.”
Clemetson went on to comment that retarded growth, multiple fractures,
and severe pain
due to periosteal hematomas may lead to a suspicion of child abuse,
especially if there are
accompanying bruises and ecchymoses. Bruises of the thighs and even
spontaneous
fractures of both femurs have been recorded from the gentle act of raising
the legs of an
infant to change diapers.
Clemetson concluded the chapter with the following comments:
“The bone pathology of acute scurvy was described in detail by
Wolbach (1937)
and by Dalldorf (1938), but the changes observed in protracted moderate
scurvy,
as produced in guinea pigs by Ham and Elliott (1938) are much more relevant
to
the human condition than is total ascorbate deficiency. Not only did
these workers
observe osteoporosis, profound changes at the epiphyseal plates, slipped
epiphyses, and the fractures which are so well documented in acute scurvy,
they
also observed a marked diminution in the amount of epiphyseal bone,
resulting in
loss of support for the articular cartilage.”
Prematurity, a Risk Factor for Vaccines
In the New Complete Medical and Health Encyclopedia, (25) prematurity
has been listed
as a contraindication to vaccines during early infancy because of the
relative immaturity
of kidneys, liver, and other detoxification systems of the body, necessary
for buffering
and detoxification of the bacterial endotoxins and other toxic substances
in the vaccines,
these in turn bringing greater risk of vaccine reactions. A separate
paper entitled
“Multiple Studies Show Increased Hazard of Vaccines in Premature
Infants” is available
providing additional information on this subject for those who are interested.
Thimerosal, the Mercury Issue:
As result of a US Congressional mandate, in June, 1999 the Food &
Drug Administration
(FDA) revealed the mercury content in childhood vaccines. Formerly generally
unknown,
it then came to be realized that children had been receiving far greater
amounts of
mercury in their vaccines in the form of the additive, thimerosal, than
were considered
safe. Up until that time many or most brands of DTP, DTaP, hepatitis
B, and Hib
vaccines contained mercury so that, depending on the combinations of
vaccines used,
children were receiving as much as 25 or 50 or even a 100-fold the amounts
of mercury
in a single day than were considered safe according to US Environmental
Protection
Agency standards. (102)
For over 200 years mercury has been known as a potent neural (brain)
toxin and one of
the most toxic of the heavy metals. Recent animal studies have shown
that exposures to
mercury vapors produce retrograde degeneration of neuronal (brain) membranes
producing molecular lesions similar to those seen in the brains of patients
dying with
Alzheimer’s disease. (103)
Apparently as an offshoot of the Congressional hearings on vaccine safety,
the Institute
of Medicine (IOM) issued a report on October 1, 2001 entitled, “Thimerosal-Containing
Vaccines and Neuro-developmental Outcomes.” The IOM report states:
Page 10:”The committee concludes that although the hypothesis
that exposure to
thimerosal-containing vaccines could be associated with neuro-developmental
disorders is not established and rests on indirect and incomplete information,
primarily from analogies with methylmercury and levels of maximum mercury
exposures from vaccines given in children, the hypothesis is biologically
plausible.” (emphasis--the writer)
Strong evidence indicating that mercury-containing vaccines have elevated
the risk of
neurological damage in infants and children comes a report by Mark and
David Geier
(2003) which showed a six-fold increase in autism and mental retardation,
and two-fold
increase in speech disorders in children receiving Thimerosal (mercury)-containing
DTaP
vaccines compared with children receiving mercury-free DTaP vaccines.
(136) Although
this report does not deal with the shaken baby syndrome, it does strongly
undermine the
positions sometimes assumed by prosecutors that vaccines are irrelevant
in shaken baby
syndrome cases.
Are There Lessons To Be Learned?
In my opinion, unless doctors become more thoughtful and objective in
evaluation of
these cases as they come into hospital emergency rooms, the casual diagnostic
evaluations commonly seen until now may become grounds for malpractice.
At a very minimum, the following should be added to the usual hospital
procedures as
routine screening tests when there is suspicion of SBS:
- With findings of retinal and subdural hemorrhages,
check plasma ascorbate and
serum histamine, to rule out subclinical scurvy; check prothrombin and
partial
prothrombin times, fibrinogen level, fibrin split products, D Dimer
test, and blood
smears to check for fragmented red blood cells to rule out coagulopathy,
and if
DIC presence is indicated, to differentiate between acute and chronic
DIC. With
elevated prothrombin and thromboplastin times, a PIVKA test should be
done
along with thrombin time and fibrinogen to test for late-form hemorrhagic
disease
of the newborn. In addition to the more standard blood tests including
blood
counts and chemistries, there should be a serum iron, triglycerides,
and absolute
neutrophil count in instances with low white blood cell counts. A metabolic
screening by tandem mass spectronomy would desirable to test for inherited
disorders of fatty acid oxidation, sometimes a cause of unexpected infant
deaths.
(Refer to dhchace@neogenscreening.com, or Neo Gen Screening, PO Box
219,
Bridgeville, PA 15017)
- In cases of skeletal fractures, test plasma ascorbate and serum histamine
along
with appropriate textbook tests for rickets; bone densitometry should
be done to
rule out temporary brittle bone disease. If there are skull fractures
and the baby
comes to autopsy, specific measurements of skull thickness should be
required.
- When there is significant lowering of hemoglobin, hematology consult
should be
requested and the patient evaluated for hemolysis.
- At the present time there are no officially recognized laboratory
tests for diagnosis
of vaccine reactions. In my opinion this is largely or entirely due
to historical
deficiencies in safety testing and scientific infrastructure in the
vaccine field. Very
sadly, there does not appear to be any official inclination to remedy
these
deficiencies at time of this writing. We can only hope that new and
wiser heads
will realize these needs and act upon them.
The same standards as those listed above should also apply in the courtroom
in that:
- Prosecution attorneys and their witnesses should be held to standards
of “proof of
guilt beyond a reasonable doubt” in shaken/impact baby (SBS) cases,
a standard
which is or should be applied in all criminal cases. Since SBS is a
diagnosis of
exclusion, this proof should include the exclusion of alternate diagnostic
possibilities.
- Juries should be made aware of the gross deficiencies in safety testing
of
vaccines, and of the likelihood that large-scale adverse reactions are
taking place
unrecognized as to their true nature. Among these, in many instances,
may be
vaccine reactions mimicking the current diagnostic criteria of SBS and
a being
source of many misdiagnoses. Deficiencies in safety testing of vaccines
include:
1) a total lack of long-term surveillance of any vaccine in use today,
and 2) gross
deficiencies in systematic before-and-after testing of vaccines for
possible adverse
effects on the brain and nervous system as well as hematologic and immunologic
systems of the body; and on finding adverse reactions, to seek for safer
methods.
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Creek Publishing, PO Box 1448, Lismore, NSW 2480, Australia.
(150)
Cherry JD et al, Pertussis immunization and characteristics related
to
first seizures in infants and children, J Pediatrics, 1993; 122(6):900-
903.
(151)
Camfield P, Brain damage from pertussis immunization, AIDC, 1992;
146:327-331.
(152)
Blumberg DA et al, Severe reactions associated with diphtheria-
tetanus-pertussis vaccine: detailed study of children with seizures,
hypotonic-hyporesponsive episodes, high fevers, persistent crying,
Pediatrics, June, 1993; 91(6): 1158-1165.
(153)
Forensic Pathology, Second Edition, Vincent J DiMaio, Dominick
DiMaio, CRC Press, Boca Raton, 2001, pages 177-179.
ORIGINAL
ARTICLE (Top article is a revised, updated version)
http://www.woodmed.com/Shaken%20Baby%20Web%202002.htm
Woodlands Healing Research Center
Family, Environmental & Preventive Medicine
5724 Clymer Rd. Quakertown, PA 18951
215-536-1890 * 800-517-9545
Fax 215-529-9034 * Email: foffice@woodmed.com
Web Page- http://www.woodmed.com
Shaken Baby/Impact Syndrome:
Flawed Concepts and Misdiagnoses
(Based on a Review of Twenty-Two Cases)
Harold E Buttram, M.D.
September 3, 2002
Introduction:
The following article represents a review of twenty-two cases of shaken
baby syndrome (SBS) accusations and/or convictions over a period of
approximately three and a half years. Its primary purpose is to offer
a composite of information gained from study of these cases to parents
or caretakers who have been accused and/or convicted of child abuse
in the form of SBS, information which may be of value in their defense.
Every effort has been made to maintain simplicity and clarity in the
organization of the material. Each section is designed to be complete
in itself, and for this reason some portions are repetitious.
Among the many adversities and difficulties facing the American family
today, there is a relatively new and growing hazard in which a parent
or caretaker may be falsely accused of murdering or injuring an infant
by the shaken baby syndrome, when the true cause of death of injury
arises from other sources. Very tragically, child abuse does occur and
deserves appropriate punishment. However, it is equally tragic when
a family, already grieving from the death of their infant, finds a father
or mother unjustly accused, convicted, and imprisoned for murder of
the infant, a murder of which he or she is innocent. I know of an attorney,
an anesthesiologist, a Mormon mother, an Amish mother, and others accused
and/or imprisoned (many believe falsely) on charges of injuring or murdering
an infant by SBS. It could happen to anyone regardless of race, sex,
educational, financial, or social status. It has happened and is happening
to more than a few.
Very early in my work with SBS cases I learned of the work of Dr. Archivedes
Kalokerinos of Australia who has testified in defense of parents in
thirty SBS cases, as well as of others in Australia and New Zealand
who have been working in this field for many years. From the experiences
of these veteran physicians and researchers, as well as my own, in many
cases there has been a time-related onset of signs and symptoms mimicking
the diagnostic criteria of SBS following the administration of vaccines.
Most other doctors will dismiss this association as coincidental, but
this is not reasonable. Coincidental occurrences might be expected occasionally,
but not in the high incidence being observed by some. If a large portion
of SBS accusations and convictions are the result of misdiagnosis, then
we are witnessing a rapidly growing reign of terror against home and
family. There is no other term for it.
Medical-Legal Facets of Shaken Baby Syndrome:
By the inherent nature of SBS cases, where a caretaker or parent is
alone with an infant at the time of collapse or accidental injury of
the infant, it is rarely if ever possible to prove the innocence of
parent or caretaker, there being no witnesses to corroborate the stories
of the accused person in maintenance of his or her innocence. Defense
of these cases, therefore, must be based on evidence showing a likelihood
that death or injury of the infant arose from causes other than child
abuse. This is done by a careful analysis of the clinical history and
findings supported by scientific and medical literature, together with
bringing to light the fallibility of current concepts and doctrines
surrounding SBS.
It is also done by finding (as one often does) unreserved and vehement
support of the innocence of the accused by family or friends.
No one is capable of remaining entirely unbiased in these cases, but
I can honestly claim that I have tried to remain objective in evaluation
of each of the twenty-two cases. For most I was convinced of the innocence
of the accused from the first. There have been several for whom, at
first, I held a margin of doubt as to their innocence, but as I probed
deeper into the cases, I also became convinced of the innocence of these
cases as well. At the present time, in my own mind, I have not the slightest
doubt of the innocence of each and all of the cases.
One of the main reasons for my opinion as to the their innocence is
a rather strange pattern that often takes place in hospital emergency
rooms, where once a suspicion of SBS or non-accidental injury arises,
all thought of further diagnostic investigation ceases. I know of no
other situation in medicine where the usual diagnostic thoroughness
one finds in such centers is abandoned. For this and other reasons,
I have not seen a single case where, in my opinion, the prosecution
has met the standards of “proof beyond a reasonable doubt,”
standards which are supposed to apply in criminal cases. Most do not
even come close.
Acknowledgements:
Most of the material and scientific references included in this article
has come from other sources. Chief among these has been Alan R Yurko,
with whom I have been in constant communication since February, 1999.
Other sources of material include friends and colleagues in Australia
and New Zealand including Dr. A Kalokerinos, Dr. Viera Scheibner, George
Wilson, and Hilary Butler. Contributors of invaluable medical references
in the United States include retired pediatrician, FE Yazbak, M.D.,
Susan Kreider, R.N., Catherine Diodate, B.A., M.A., and Rita Hoffman.
Current Concepts and Assumptions in Diagnosis of SBS – Shaky Foundations:
SBS, sometimes also referred to as nonaccidental injury (NAI) commonly
describes a combination of subdural hematoma (brain hemorrhage), retinal
hemorrhage, and diffuse axonal injury (diffuse injury of nerve cells
in brain and/or spinal cord) as the triad of diagnostic criteria. In
some, the presence of rib or other fractures is also taken as sign of
child abuse (1-4) These basic concepts, which originated approximately
30 years ago, remain a basis for most SBS accusations and convictions
today in spite of newer scientific publications which promise to revolutionize
these older concepts.
At the present time the following assumptions concerning SBS/NAI usually
prevail in both hospitals and the courts:
- That the severity of shaking force required to produce injuries (retinal
and subdural hemorrhages, etc) is such that it cannot occur in any normal
activity but is of such violence that untrained observers would immediately
recognize it as dangerous and intentional; (5)
- that such central nervous system (brain) injury on an accidental
basis can only
be associated with a massive force equivalent to a motor vehicle accident
or a fall from a second story building;
- that such injury is immediately symptomatic and cannot be followed
by a lucid interval, so that from this reasoning, the last caretaker
with the injured child is automatically considered guilty of abusive
injury, especially if the incident is unwitnessed; (1, 6-8)
- that changing symptoms in a child with prior head injury is due to
newly inflicted injury and not just a rebleed; (9-13)
- that the presence of retinal/subdural hemorrhages in the absence
of known disease or accident (as described) above are exclusively diagnostic
of SBS.
In a comprehensive review of ethical issues in radiological diagnosis
of child abuse, Patrick D Barnes, MD, with the radiology department
of Stanford University Medical Center, Palo Alto, California, wrote
the following concerning difficulties of diagnosing NAI/SBS in the absence
of witnessed or admitted violent shaking:
“This problem is magnified further by the lack of consistent
and reliable criteria for the diagnosis of NAI/SBS, and that the vast
body of literature on child abuse is composed of anecdotal care series,
case reports, reviews, opinion, and position papers…From an evidence-based
medicine perspective, quality of evidence ratings for diagnostic criteria
regarding the literature on SBS reveal that few published reports merit
a rating above class IV (any design where the test is not applied in
blinded evaluation, where evidence is provided by expert opinion alone,
or in descriptive case series without controls). Such quality of evidence
hardly earns a diagnostic criteria recommendation level of “optional,”
much less as a “guideline” or a “standard.”
(14)
In the remainder of this article various major problem areas will be
reviewed showing that not only can there be other causes of the findings
now thought to be exclusively diagnostic of SBS, but that these other
causes may well comprise a majority
of cases now being diagnosed as SBS. These categories include residual
effects of birth trauma, vaccine reactions, respiratory paralysis from
accidental (nonviolent) whiplash of the infant’s neck, Barlow’s
Disease (rediscovered subclinical scurvy), and a variety of old and
newly recognized metabolic disorders:
Residual Effects of Birth Trauma:
One of the cases that I recently reviewed typifies this type of problem
where a probable residual subdural or brain hemorrhage from birth trauma
was later misdiagnosed as SBS or child abuse. The mother was known to
have uterine fibroids from ultra sound exams taken during her pregnancy.
Her labor started following spontaneous rupture of the membranes, but
after several hours of limited progression, she was started on pitocin
drip. In spite of hard labor which went on for several hours there was
little progression, and a Cesarian section was performed. The baby died
two months later from a massive acute subdural hematoma, but at autopsy
an older or chronic subdural hematoma was also found, in my opinion
almost certainly the result of birth trauma. The father, who was attending
the baby at time of his collapse, was convicted of child abuse and is
now serving a prolonged prison sentence.
In analysis of this case, the combination of outlet obstruction from
fibroid tumors along with pitocin intravenous drip, must have generated
much greater pressures on the fetal head than would take place in normal
labor, and so by definition such a birth could be considered traumatic.
This is indicated by a survey of retinal hemorrhages conducted at Tel
Aviv University Medical Center of 100 newborns following labor induced
by intravenous oxytocin (pitocin) or oral dinoprostone, following which
retinal hemorrhages were found in 40% of the neonates in the dinoprosone
group and 28% in the oxytocin
treatment group. (16)
As stated in Nelson Textbook of Pediatrics, 16th Edition:
“Traumatic epidural, subdural, or subarachnoid hemorrhage is
especially likely when the fetal head is large in proportion to the
size of the mother’s pelvic outlet; when for other reasons the
labor is prolonged as in malposition…..” (17)
In an article published in Archives of Neurology in 1994, Fenichel
and colleagues identified 22 term newborns with intracranial hemorrhage
by computerized tomography in an intensive care unit for newborns. Primary
subarachnoid hemorrhage was the most common type of hemorrhage, caused
either by traumatic deliver or severe hypoxic-ischemic encephalopathy…(18)
In a three-year survey at the Southwestern medical Center, Dallas, Texas,
26 near-term and term nonasphyxiated infants were found to have small
subdural hematomas on computed tomography. It was concluded that the
presence of subdural hematoma is not necessarily always indicative of
birth trauma and may occur as sequelae of an otherwise uncomplicated
delivery. (19) Patrick D Barnes also commented that “birth trauma
may persist beyond the neonatal period and mimic
Abuse.” (14)
Acute Brain Hemorrhage from Pre-Existing Chronic Subdural Hematoma
or Malformations such as Hydrocephalus:
In rebuttal to the current SBS doctrine that changing symptoms in a
child with head injury is due to newly inflicted injury and not to a
rebleed, as outline above, Joseph Piatt reported on a case of retinal
hemorrhages and bilateral subdural hematomas in a child with external
hydrocephalus following a minor fall. In discussion of the case he wrote:
“The presence of craniocerebral disproportion that develops from
any cause – external hydrocephalus, internal hydrocephalus, arachnoid
cyst, or chronic subdural hematoma – makes the patient exceptionally
susceptible to subdural hemorrhage after what would otherwise be inconsequential
trauma….as a result of the vulnerability of the bridging veins.”
(20)
Other authors have also reported on similar findings, including the
proneness of a chronic hematoma to rebleed with minimal trauma. (21-23,
73)
The Controversy of the Lucid Interval:
In rebuttal to another of the standard SBS doctrines, that an ultimately
fatal head injury cannot be followed by a lucid interval (an interval
between trauma and onset of symptoms), a retrospective study of 76 children
who died from head injuries was done by M.G.F. Gilliland. The children
were divided into those who died from shaking, those who died from impact,
and those who died from combined of the two. It was found that 20 %
of the shaken children and 25% of the impact children had lucid intervals
over 24 hours. In the latter groups there were four children for whom
the interval was over 72
hours. (56) Similarly in a retrospective report by J Plunkett of 18
fall-related head injury fatalities from distances of 2 to 10 feet,
12 of the 18 children had a lucid interval.(57)
The Vaccine Issue:
Since 1999 there have been ongoing hearings in the U.S. Congress concerning
growing concerns about vaccine safety. Primarily these hearings have
dealt with concerns about a possible link between the MMR vaccine and
the growing epidemic of childhood autism in the U.S.A. Out of these
hearings there is now an emerging background pattern of deficiencies
in basic science in vaccine testing. As a result of these deficiencies,
large numbers of unrecognized vaccine reactions may be taking place,
especially reactions of a delayed nature.
Based on these hearings, as a general statement scientific evidence
does not support the safety of immunizations in that safety studies
on vaccinations are limited to short periods only: several days to several
weeks. There are no long-term (months or years) safety studies on any
childhood vaccine in use today. In addition, there have been no systematic
before-and-after studies on the effects of vaccines on immune parameters
and brain function of babies, studies which should be considered indispensable
information of a basic science for the vaccines. Inadequate consideration
has been given to the additive or synergistic adverse effects of multiple
simultaneous vaccines, although in cases of toxic chemicals, two chemicals
together may be 10 times more toxic than either separately, or 3 chemicals
100 times more toxic. (24-25)
As one example of the deficiencies in basic science among the vaccines,
in 1994 the Institute of Medicine, a federal government advisory board,
published a comprehensive review of the safety of the hepatitis B vaccine.
When the committee, which carried the responsibility for determining
the safety of vaccines by Congressional Mandate, investigated five possible
and plausible adverse effects, they were unable to come to conclusion
for four of them, because they found that relevant safety research had
not been done. Furthermore, they found that serious “gaps and
limitations” exist in both the knowledge and infrastructure needed
to study vaccine adverse events. Among the 76 types of vaccine adverse
events reviewed by the IOM, the basic science evidence was inadequate
to assess definitive vaccine causality for 50 (66%). The IOM also noted
that “if research,,,(is) not improved, future reviews of vaccine
safety will be similarly handicapped.” (26)
Several examples of before-and-after studies from older medical literature
will be cited as examples of these deficiencies.
Vaccines and Immune Paralysis:
The first example involves a study reported in 1984 in the New England
Journal of Medicine (27) which involved the testing of T-lymphocyte
subpopulations (white blood cells which help govern the immune system)
in eleven healthy adults before and after routine tetanus booster immunizations.
The results showed a significant though temporary drop in T-helper lymphocytes.
Special concern rests in the fact that in 4 of the subjects the T-helper
lymphocytes dropped to levels found in active AIDS patients. If this
was the result of a single vaccine in healthy adults, it is sobering
to think of the immune consequences of the multiple vaccines with their
immature and vulnerable immune systems. And yet, as far as I am aware,
this test has never been repeated.
Comment: In my mind, until this study is repeated and disproved, it
would be both folly and insupportable to claim that vaccines are not
having an effect in contributing to the increasing patterns of sickness
now seen as a matter of common observation in today’s children.
In point of fact, reports are now appearing from widely separated geographic
areas in which vaccinated children were found to have more allergic
disorders (and patterns of sickness) than children with limited or no
vaccines. (28-31) (Also see Appendix entitled, “Vaccines and Allergy
Citations”)
Vaccines and Seizure Disorders:
For the second example, in 1955 AL Low of Chicago published a study
in which he performed electroencephalograms (EEGS) on 83 children before
and after pertussis immunization. (32) In two of the children he found
that the EEGs turned abnormal following the immunizations without other
signs or symptoms of abnormal reactions. In his report he commented:
“This study suggests that mild but possibly significant cerebral
reactions may occur in addition to the reported very severe neurological
changes.”
Careful search of the literature has disclosed only one similar before-and-after
immunization study, one from Japan in which it was found that 61 children
with epilepsy or a history of febrile seizures showed significant increases
in “epileptic spikes” on EEGs following DTP, DT, or BCG
vaccines. (33)
Comment: Both of these studies, the only studies of their kind as far
as I am aware, show strong evidence that subclinical brain damage may
be taking place on a far larger scale than has been officially recognized.
The Controversy of the Latent Period:
Continuing further with our analysis, there is an admitted problem
with the prolonged latent period of about two and a half months between
the last series of vaccines on 25 January, 2001 and the seizure which
occurred 8 May. For this reason, as an appendix to this report, I am
also sending an article entitled “The Controversy of the Latent
Period following Immunizations,” which explores this issue in
some depth. I will state here, however, that several leading authorities
who formerly held positions in the regulation and licensing of medicines
in the United Kingdom have published statements that pre-licensing observation
periods for vaccines (in this case the MMR vaccine) have been too short
to include the onset of delayed neurological (emphasis mine) or other
adverse events, (34) one of the former health officers stating that
pre-licensing observation periods should have been extended to a year
rather than several weeks.
In my opinion the fundamental flaw in current medical legal standards
in the U.S.A. for the latent period, and probably also in other English-speaking
countries, is that their time limitations allow only for immediate or
anaphylactic-type of reactions, by inference denying the possibility
or even the existence of delayed-type reactions. This is clearly unrealistic,
as delayed-type hypersensitivity directed against the nervous system
has been demonstrated by BCG vaccine in the laboratory. (35)
In this regard, two of the vaccines routinely given to children, the
Pertussis and Haemophilus influenza vaccines, are known to be potent
in causing hypersensitivity reactions. (36,37)
Vaccine Reactions Mimicking the Diagnostic Criteria of Shaken Baby
Syndrome:
As previously reviewed, (1-4) shaken baby syndrome commonly describes
a combination of subdural hematoma (brain hemorrhages), retinal hemorrhages,
and diffuse axonal injury (diffuse injury of nerve cells in brain and
spinal cord) as a sign of child abuse. In the absence of known accidental
or disease causes, these findings in a child are considered as diagnostic
of non-accidental injury or SBS. The following information, however,
will show that there may be other causes, among which may be unrecognized
vaccine reactions.
In medical research it is standard procedure to develop an animal model
of a disease for experimentation before proceeding into human studies.
In the case of shaken baby syndrome, these animal models already exist
in publications involving pertussis toxin reactions mimicking the diagnostic
criteria of SBS.
Studies by Iwasa stressed the finding of brain edema as a feature of
pertussis-induced encephalopathy. (38) It is also of interest to point
out that there are anecdotal human reports of infants which developed
increased intracranial pressure with bulging fontanelles following DTP
immunization which tend to support these animal findings. (39-41) In
addition, in 1972 Galazka reviewed a series of autopsies on children
whose deaths followed the pertussis vaccine/ Although autopsies were
limited in number, findings included brain edema, hyperemia, and soft
meninges. (42) As will be reviewed in the next section, studies of J
Geddes have shown that brain edema in and of itself may result in retinal
and brain hemorrhages.
Munoz in turn conducted mice studies with pertussigen, an endotoxin
derivative of the pertussis bacteria, in which he found (inflammatory)
infiltrates of lymphocytes surrounding blood vessels in the brain and
spinal cord, findings compatible with an autoimmune encephalitis. (43)
It is noteworthy that vaccines such as pertussis have been used to
induce allergic encephalomyelitis in laboratory animals since 1973,
(44) characterized by brain swelling and hemorrhages similar to those
caused by mechanical injuries. As another example, in 1982 Steinman
and coworkers described mice studies following pertussis immunization
as follows:
“Post-mortem examination of the brain (in experimental mice)
after immunization revealed diffuse vascular congestion and parenchymal
haemorrhage in both the cortex and white matter. Cortical neurons showed
ischaemic changes. Occasional areas of hypercellularity were evident
in the meninges…B pertussis has a wide range of physiological
effects including increased IgE production, increased sensitivity to
anaphylactic shock, lymphocytosis, and hyperinsulinaemia. Its ability
to induce increased vascular permeability may account for the tendency
to produce haemorrhage. (45)
In terms of human studies, I have available a list of 109 references
involving reports of adverse reactions from hepatitis B vaccine, a vaccine
which appears to be especially prone to be followed by hemorrhagic complications.
Among these reactions various forms of vasculitis (inflammation of blood
vessels) appear with special frequency, which may contribute to hemorrhagic
complications because of greater fragility and friability of blood vessels
and consequently may mimic both cutaneous and cerebral hemorrhagic findings
now considered to be diagnostic of SBS.
In regard to the issue of retinal hemorrhages, in the text Ocular Differential
Diagnosis by Frederick Hampton Roy, M.D., papilledema (swelling in the
retinal area) and increased intracranial pressure (from any cause) are
listed as possible causes of retinal hemorrhages. (46) DPT vaccine is
also listed as a possible cause, along with other routine childhood
immunizations (OPV, MMR).
Comment: As stated previously, animal models for vaccine reactions
mimicking the diagnostic features of SBS exist for each of the major
criteria of SBS. In my opinion, it is only from the lack of basic science
in the vaccine field that these reactions very frequently are not being
recognized for their true nature and therefore misdiagnosed as SBS.
New Findings that May Change the Diagnostic Criteria of SBS:
As reported in the medical journal, Brain, in a study which may revolutionize
current concepts of SBS, Jennian F Geddes, a neuropathologist at Royal
London Hospital and colleagues examined the brains of 53 children suspected
of dying from deliberate injury. (47) Of the 53 children, 37 were less
than a year old.
In the past, brain damage in such circumstances has been blamed on
the brain banging against the skull as a baby is violently shaken or
struck. It has been thought that this direct assault causes a characteristic
kind of damage to the axons of the nerves known as diffuse axonal injury
(DAI). However, the researchers found evidence of DAI in only two of
the 37 babies. Instead they found that three-quarters of the 37 babies
had died because they stopped breathing as a result of previously unseen
and undescribed pathology that was focused on the cranio-cervical junction,
the area which controls breathing, where the brain meets the spinal
cord. When babies stop breathing as a result of this injury, subsequent
lack of oxygen causes the brain to swell dramatically, which in turn
causes hemorrhagic complications and brain damage formerly attributed
to violent shaking or blows.
The cranio-cervical junction is uniquely vulnerable in very young babies,
the authors explained, because their neck muscles are weak and their
heads relatively large and heavy.
The researchers found subdural hemorrhages in 72% of the 53 cases,
although most were too superficial to cause death. Also, retinal hemorrhages
were found in 71% of the 38 cases in which the eyes were examined, but
the authors felt that these resulted from a lack of oxygen to the brain
(and the brain edema or swelling) rather than trauma.
There are scenarios in which such nonviolent, unintentional injuries
might take place, as in an accidental fall of a parent or caretaker
while holding an infant, the infant in turn receiving a whiplash of
the neck and secondary injury to the respiratory center at the base
of the brain, or a parent awakening in the night to sooth a crying infant,
and the parent still not being fully awake, rocking the baby without
adequate head support.
Although vaccines were not mentioned in the Geddes study, it would
be very interesting to know how many of these adverse events occurred
in a time-related fashion following vaccines.
The Issue of Retinal Hemorrhages:
Based on my own review of medical records involving SBS accusations
and convictions, ophthalmologists are always called to examine infants
for retinal hemorrhages following hospitalization where there is suspected
non-accidental trauma or SBS. Without exception in each of the cases
I have seen, the finding of retinal hemorrhage has been considered diagnostic
of non-accidental trauma from violent shaking or impact. However, it
would appear from the medical literature that others disagree as to
the diagnostic specificity of retinal findings. John Plunkett in the
American Journal of Forensic Medicine and Pathology made the following
statements concerning this issue:
“I do not understand the ‘retinal hemorrhage’ litmus
test for shaken infant. No one knows what causes retinal hemorrhage,
although it is highly correlated with rotational deceleration injury/subdural
hemorrhage in children, but retinal hemorrhage indistinguishable from
that found in rotational deceleration may be found in association with
ruptured vascular malformations , arachnoid cysts, and CNS (central
nervous system) infections. (48)
AC Tongue mentions that “hemorrhages in all layers of the retina
occur in a number of nontraumatic disorders associated with changes
in cerebrovascular dynamics such as central retinal vein occlusion,
high altitude retinopathy, and subarachnoid hemorrhage secondary to
ruptured intracranial aneurysms.” (49) Also there is a report
of retinal hemorrhages after near drowning (50) and three reports following
CPR resuscitation. (51-53) Patrick Barnes reported that retinal hemorrhages
may be seen with a variety of conditions including accidental trauma,
resuscitation, increased intracranial pressure, increased venous pressure,
subarachnoid hemorrhage, sepsis, coagulopathy, certain metabolic disorders,
and systemic hypertension. (14)
Diffuse Axial Injury (DAI), the Third Diagnostic Criteria for SBS:
There is no doubt that diffuse axonal (nerve injury) may take place
in head trauma. The question is whether or not the pathologic findings
described on histologic slides of the brain in the present case, with
widespread B-amyloid precursor protein deposits and axonal spheroids,
are specific for non-accidental injury or whether these findings are
also present in other, non-head injured conditions, including vaccine
injury.
Based on the work of F.E. Sherriff and associates, this question can
be answered, (54) as described in the following:
“Severe non-missile head injury commonly results in a form 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…We have used immunocytochemistry for the B-amyloid
precursor protein (BAPP) as a marker for axonal injury in formalin-fixed,
paraffin-imbedded sections of human brain. Axonal BAPP was present in
all (23 cases of head injury) that survived for 3 hours or more…...BAPP
immunoreactivity was also found in some (5 of 13) non-head injury cases
and so cannot to considered to be a specific marker for trauma.”
(Emphasis mine)
In a survey conducted at the department of forensic medicine, University
of Sheffield, UK, GN Rutty and associates studied sections from a series
of brains comprised of four groups: those showing evidence of hypoxia
with no history of head trauma, those with head trauma but no evidence
of hypoxic change, those with history of head trauma and hypoxic change,
and four controls originally described as “diffuse axonal injury.”
Using the same staining technique as described above in the Sherriff
study, it was found that axonal bulbs may occur from hypoxia in the
absence of head injury. It was concluded that “the presence of
axon bulbs cannot necessarily be attributed to shearing forces alone.”
(55)
Barlow’s Disease (Subclinical Scurvy) Rediscovered:
Physicians and the lay-public alike generally think of scurvy as an
historical disease of the days of wooden sailing ships, which was eliminated
by the introduction of limes or other citrus fruit into the diet. However,
as the younger generations in industrialized nations turn increasingly
to commercially processed “fast foods” as a major part of
their diets, subtle forms of scurvy may be returning and contributing
to the hemorrhagic complications now thought to be exclusively diagnostic
of SBS.
In the early 1970s Dr. Archivedes Kalokerinos, then stationed as a
medical officer among the Australian aborigines, was troubled by a very
high child mortality rate, in some areas approaching 50%. Having observed
signs of scurvy in some of the children, and noticing that they often
died following immunizations, especially if they had colds or minor
respiratory infections, the thought occurred to him that there might
be a connection between vitamin C deficiency and deaths following vaccines.
With improved nutrition, oral vitamin C supplements, avoidance of vaccines
during minor illnesses, and injectable vitamin C during crises, infant
mortality was virtually abolished. (58) As a result of this work he
was awarded the Australian Medal of Merit in 1978.
One of the primary roles of vitamin C in the body being that of producing
and maintaining connective tissue, Dr. Kalokerinos hypothesized that
with minor viral infections further depleting an already marginal store
of vitamin C, the administration of toxin-bearing vaccines would sweep
away the small residual traces of vitamin C, somewhat like a flash-fire,
provoking fulminating scurvy with hemorrhagic complications from the
weakening of blood vessels. Does such a theory have a foundation in
the scientific literature? Based on the following, I believe that it
does.
Basic Facts about Vitamin C:
- Vitamin C deficiency still does occur in the Western World. The plasma
vitamin C status was found to be depleted, between 0.2 and 0.5 mg/100
ml (or 11 to 28 micromol/L) in 30 %, and to be deficient, below 0.2
mg/100 ml in 6% of people attending a Health Maintenance Organization
(HMO clinic) in Tempe, Arizona in 1998. (59)
- The blood leukocyte ascorbic acid concentration is further reduced
by infection. Even the common cold causes a fifty per cent reduction
of the leukocyte ascorbic acid concentration within 24 hours. (60) Moreover,
E coli endotoxin has been shown to inhibit the uptake of vitamin C by
mouse fibroblasts in tissue culture. (61)
- When the human plasma ascorbic acid level falls below 0.2 mg/100
ml, the whole blood histamine level is doubled or quadrupled. (62) Ascorbic
acid is needed for the conversion of histamine to hydantoin-5-acetic
acid and on to aspartic acid in vivo. (63)
- The whole blood histamine level is also increased by vaccines or
toxoids, by stresses such as heat or cold, and by various drugs in guinea
pigs. (63) Sleep-lack more than doubles the blood histamine levels of
resident physicians. (64) Ascorbic acid supplementation rapidly reduces
the blood histamine levels of ascorbate-depleted subjects. (62)
- Blood histamine concentration begins to rise when the plasma ascorbic
acid level falls below the normal level of 1 mg/100 ml and rises exponentially
when it falls below 0.7 mg/100 ml. (62)
- Vitamin C impairs the hydroxylation of proline and lysine, which
are essential building blocks for the synthesis of collagen, which forms
the foundation for fibrous tissue, cartilage, bone and teeth. (65)
- It is the increased blood histamine, or histaminemia, that causes
separation of the endothelial cells from one another in scurvy, (66)
which causes the capillary fragility and bleeding of scurvy.
- Humans are vulnerable to vitamin C deficiency as we lack the enzyme,
L-gulono-gamma-lactone oxidase, needed to synthesize this essential
substance, making us totally dependent on dietary vitamin C from our
diet. This is in contrast to most other mammals which are able to manufacture
their own vitamin C from simple sugars in the liver.
- Vitamin C protects against diphtheria toxin, (67-68), tetanus toxin,
(69) and typhoid endotoxin. (70)
- In 1932 a report on the hemorrhagic complications of scurvy stated
that these occurred most commonly beneath the periosteum of the long
bones and into joint spaces, but frequently also involved the skin,
mucous membranes (gums), orbits (eyes), and serous cavities of the body.
(71) One of the most characteristic signs of adult scurvy was swollen
bleeding gums, but this is never seen in edentulous infants. It is the
bacteria in the crevice between the tooth and the gum that cause local
infection and bleeding gums.
With the foregoing information as a background, it is now appropriate
to site an unpublished series of cases involving accusations or convictions
for SBS largely collected by attorney and jury counselor Toni Blake
of San Diego, California (personal communication, 2000), which had the
following features: 1) All occurred in fragile infants born from complicated
pregnancies. Problems included prematurity, low birth weights, drug/alcohol
problems, diabetic mothers, or other maternal complications. 2) All
infants were 6 months of age or less. 3) Onset of signs and symptoms
occurred at about 2, 4, or 6 months of age, within 12 days of vaccines.
4) All infants had subdural hematomas. 5) Some infants had multiple
fractures. In 2000 the series included 25 cases, but I understand it
is now much larger.
It is probably in the situations of fragile infants described above
that one finds a final common pathway for most major risk factors for
vaccine reactions with 1) sub-optimal nutrition including vitamin C
deficiency, 2) immature liver and kidneys, where most body detoxification
takes place, and 3) in those instances where the baby is on formula
instead of breast feeding, increased intestinal Escherica coli colonization.
(E coli is a gram negative bacteria with a toxic component in its outer
coating). (72) In such situations, the toxins from diphtheria, tetanus,
and pertusis vaccines may overwhelm the liver’s marginal detoxification
system, sweep away the small vitamin C reserve, and potentially lead
to catastrophic vaccine reactions. In my view this is probably the common
scenario in which parents are being blamed and accused of death or injury
from SBS, when the true causes arose from vaccine reactions.
Among the 22 cases that I have reviewed, infant fatalities, or survivals
with residual brain damage, took place in a time-related fashion following
routine childhood vaccines, two taking place within hours of vaccines,
most others within 11 to 12 days, and one with a delay of six weeks.
In most instances the plot was the same: a parent or caretaker was alone
with the infant when the infant abruptly went into respiratory arrest
and stopped breathing. After initial clumsy attempts at resuscitation,
911 was called, the baby taken to a local hospital emergency room where
retinal and subdural hemorrhages were found along with rapidly increasing
cerebral edema, invariably followed by a diagnosis of SBS and accusation
of child abuse.
What actually happened in each and every instance, in my opinion, was
that each infant suffered a vaccine-related encephalitis with onset
of brain edema (brain swelling) and secondary depression of the respiratory
center. Once breathing ceased, severe brain hypoxia (lack of oxygen)
rapidly accelerated the brain edema, followed in turn by retinal and
brain hemorrhages.
Acute Autoimmune Hemolytic Anemia from DTP Vaccine:
In 2001 KA Downes and colleagues reported on a 4-month old child admitted
to the hospital with fever and increasing lethargy a few days following
the second series of routine immunizations, which included the DTP vaccine.
By the third hospital day the hemoglobin had dropped to 2.3 grams%.
The child subsequently died, but careful evaluation before death identified
an acute autoimmune hemolytic anemia from the DTP vaccine. (74) In a
review of the literature, 7 other reports of autoimmune hemolytic anemia
following DTP vaccines. (If this reaction were routinely sought in hospitals,
as it was in the present case, probably the numbers would be much greater).
In my own case reviews there were several admitted to hospitals with
hemoglobin levels in the 6s and 7s. One child was admitted with an hematocrit
of 6% and a hemoglobin of 2 grams %, dying within hours of admission.
In not one of these cases, including the latter, was there mention in
the medical records or investigation into a possible hemolytic process.
Bleeding Diatheses from Coagulopathy
In his medical review of the death of Baby Alan Yurko, Dr. Michael
D Innis, MBBS, DTM&H, FRCPath, Honorary Consultant Haematologist,
Princess Alexandra Hospital, Brisbane, Australia, diagnosed death from
intracranial hemorrhage and a bleeding diathesis following a coagulopathy
resulting from failure of the liver to synthesize clotting factors in
adequate amounts.
Liver failure was diagnosed by significant elevations of liver enzymes
and significant lowering of serum albumen, cholesterol, and creatinine,
from which it was concluded that there was inadequate liver production
of coagulation factors II, VII, IX, and X. (74)
The presence of a coagulopathy, in turn was reflected by an elevated
prothrombin time, high D Dimer test, and high fibrin spit products.
(Fibrinogen not done) Marked platelet elevation ruled out disseminated
intravascular coagulopathy. (75)
In my opinion, bleeding studies of the types described above should
be done in all infants or children with retinal/brain hemorrhages before
entertaining a diagnosis of SBS. According to Dr. Innis’s report,
coagulopathies can result in subdural bleeding, intracerebral bleeding,
retinal hemorrhages, bleeding into the spinal cord and into the skin
in the form of bruising. (76)
Skeletal Fractures:
Skull fractures:
In cases of suspected child abuse where skull or rib fractures are
found in addition to retinal and brain hemorrhages, medical-legal difficulties
are greatly increased for the accused parent or caretaker and his or
her defenders. Two examples will be given here, one with bilateral skull
fractures and the other with four rib fractures. Both infants had fatal
outcomes. Both fathers are now imprisoned.
Regarding the former case, the baby with skull fractures, at roughly
seven months age the baby was taken to the pediatrician by the parents
because of an ongoing intestinal virus infection with a two-week history
of recurrent vomiting. In spite of the illness the baby was given DTP,
Hib, OPV, and Hep B vaccines during the office visit. (Later investigation
revealed that the vaccines contained exceptionally large amounts of
mercury in the form of thimerosal). Soon following the vaccines the
baby went into a pattern of inconsolable crying. Hours later, while
alone with the father, the baby abruptly became apneic (stopped breathing).
Resuscitation efforts were futile, and the baby died soon afterwards.
Bilateral skull fractures of the parietal bones were demonstrated by
CT scans and confirmed at autopsy.
Aside from an accidental fall from a car seat in the home, the skull
fractures were unexplained, and the father was accused of violent child
abuse and is now in prison.
Present defense of the father now rests primarily on the finding of
extremely thin skull bones at autopsy, as reported by the medical examiner
during her testimony. On this basis there are several possible and plausible
explanations for the fractures other than violent child abuse:
- In the German scientific journal Z Rechtsmed, 1990: 103(4):311-313,
W Weber performed postmortem biomechanical fragility tests on infant
skulls. As reported in the article abstract, “skulls were dropped
from 82-centimeter heights onto (A) stone, (B) carpet, and (c) foam-backed
linoleum. 35 further falling tests were carried out onto softly cushioned
ground. In 10 cases (D) a 2-cm thick foam rubber mat was chosen and
in 25 further cases (E) a double-folded (8-cm-thick) camel hairblanket.
Hence the results of altogether 50 tests could be evaluated. In test
groups A-C on a relatively hard surface, skull fractures of the parietals
were observed in every case; in test group D this fracture was seen
in one case and in test group E in four cases. Measurements along the
fracture fissures showed bone thickness of 0.1-0.4 mm. The fracture
injuries originated in paper-thin single-layerbone areas without diploe,
which can also be considered the preferred regions for skull fractures
of older infants following falls from low heights. These results indicate
that it is no longer possible to assume that the skull of infants is
not damaged after falls from table height.”
- In a report entitled, “Fatal Head Injuries from Short Distance
Falls,” J Plunkett reported on 18 fall-related fatalities taken
from the U.S Consumer Product Safety Commission database for head injury
associated with playground equipment. The youngest child was 12-months
old, the oldest 13 years. The falls were from 2 to 10 feet. (78)
- Metabolic conditions subject to spontaneous fractures, or to fractures
with minimal trauma include scurvy, (vitamin C deficiency), rickets
(vitamin D deficiency), osteogenesis imperfecta (79-80), and temporary
brittle bone disease (TBBD). (81-82) In regard to the latter, Miller
and Hangartner described the condition characterized by transient bone
weakness and presenting as multiple unexplained fractures during the
first year of life. For this reason it has often been confused with
child abuse. In a study involving 26 infants with TBBD it was found
that 25 had a history of decreased fetal movement or confinement in
limited uterine space during the mother’s pregnancies. Plain X-ray
films were normal in all cases, but osteopenia was confirmed by bone
densitometry studies. (82)
- In a report by Kirschner in 1985 entitled, “The Mistaken Diagnosis
of Child Abuse,” a number of cases were presented in which mistaken
diagnosis of child abuse was confirmed. (83) One of these was a case
with pseudo fractures from atypical parietal suture lines. An attempted
search of the literature on the subject revealed very little, but in
the paper-thin bone of the present case, any line of weakness (as with
the course of a blood vessel) would be easily separated by the immense
hydrostatic pressures generated by the massive brain edema that took
place in this case, thus giving an appearance of fractures.
Rib Fractures:
The case with the rib fractures was the infant Alan R Yurko, whose
case is thoroughly reviewed on the Yurko website (see reference 77),
so that there is no need for confidentiality.
In brief summary of the case, the mother had had almost constant nausea
during her pregnancy, initially lost 10 pounds, and barely regained
her initial weight by time of childbirth. Birth was premature. Due to
this and other complications both before and following birth, it is
highly probable that the baby was born with multiple nutritional deficiencies,
including deficiencies in vitamin C and vitamin D, and delayed organ
development as previously mentioned.
It is very interesting that during the father’s trial, when the
medical examiner was giving his testimony to the jury about autopsy
findings, when he accidentally dropped one of the baby’s ribs
that he was demonstrating, the rib broke on hitting the floor. This
alone indicates that there must have been extreme deficiencies of bone
connective tissue and calcification.
Be this as it may, explanation for the rib fractures was one of the
most difficult aspects of until a voluminous report on the case was
received from Dr. Archivedes Kalokerinos of Australia (previously mentioned).
In his previous writings Dr. Kalokerinos referred to a previous case
with similar findings to those of the Yurko child including, retinal
and brain hemorrhages and rib fractures. (84) In this report Dr. Kalokerinos
referred to a 1920 text on classical scurvy, which described a vulnerability
to fractures at costochondral junctions (areas of connections of ribs
to the spine) in the following words:
“Scurvy disrupts these areas (costochondral junctions), the bone
breaks down and the ribs ‘overide,’ forming in typical cases
‘beads.’ The healing commences with new born formation looking
just like true healing fractures. Furthermore, not all the ribs may
be involved in this process and the changes will not all occur at the
same time – giving the impression of multiple fractures of different
ages.” (85)
This interpretation by Dr. Kalokerinos tends to be corroborated by
a report from Hiller in 1972, which states that metaphyseal (costochondral
junction) slippage (fragility) could be the result of either rickets
or scurvy, and that such findings are of doubtful validity in diagnosis
of battered child syndrome. (86)
As another possible explanation for the rib findings, it is known that
subperiosteal bleeding (bleeding under the fibrous covering of the bone)
is the commonest form of bleeding in scurvy. In the subsequent healing
and calcification of the subperiosteal blood clots, X-ray appearances
may closely resemble those of healing fractures.
Are There Lessons To Be Learned?
In my opinion, unless doctors become more thoughtful and objective
in evaluation of these cases as they come into hospital emergency rooms,
the casual diagnostic evaluations commonly seen until now may become
grounds for malpractice.
As a very minimum, the following should be added to the usual hospital
procedures as routine screening tests when there is suspicion of SBS:
1. With findings of retinal and subdural hemorrhages, check plasma
ascorbate and serum histamine, to rule out subclinical scurvy; check
prothrombin and partial prothrombin times, fibrinogen level, fibrin
split products, and D Dimer test to rule out coagulopathy.
2. In cases of skeletal fractures, test plasma ascorbate and serum
histamine along with appropriate textbook tests for rickets; bone densitometry
should be done to rule out temporary brittle bone disease.
3. When there is significant lowering of hemoglobin, hematology consult
should be requested and the patient evaluated for hemolysis.
4. At the present time there are no officially recognized laboratory
tests for diagnosis of vaccine reactions. In my opinion this is largely
or entirely due to historical deficiencies in safety testing and scientific
infrastructure in the vaccine field. Very sadly, there does not appear
to be any official inclination to remedy these deficiencies at time
of this writing. We can only hope that new and wiser heads will realize
these needs and act upon them.
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77. The Innis report can be found on the Yurko website: http://www.freeyurko.bizland.com
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