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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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

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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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