Shaken Baby/Impact Syndrome: Flawed Concepts and Misdiagnoses
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Shaken Baby/Impact Syndrome: Flawed Concepts and Misdiagnoses
(Based on a Review of Twenty-Eight Cases)
by
Harold E Buttram, M.D.
February 5, 2003
Introduction:
The following article represents a review of twenty-eight 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. 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.
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, 28 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 sick 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 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)
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, 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) 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)
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
catastrophe. (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, 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 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.
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 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
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 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, 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)
and three reports following CPR resuscitation. (51-53) 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)
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 large area still remaining virtually untouched and unknown in the
safety testing and basic science of vaccines is two-fold: 1) lack of
long-term surveillance following vaccines and 2) systematic before-and-after
human tests on the effects of childhood vaccines on the neurologic,
immunologic, hematologic, and other systems of the body. Because of these
lacks it is predictable that unknown numbers of vaccine reactions are taking
place, unrecognized as to their true nature, as previously reviewed.
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. 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,(115) 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, bacterial infections, or bacterial toxins in which the
invading organisms (or toxins) activate tissue factors from monocytes and
endothelial cells, which may then activate a pro-coagulant cascade.
The Williams text did 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. (116) 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 human
research and surveillance has stopped. We know little or nothing about the
potential activity of endotoxin-bearing vaccines or viral vaccines in
bringing about harmful procoagulant reactions and hemorrhagic complications
simply because this area has been largely neglected (some believe purposely
avoided) in research circles. 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 (apt), 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. (115)
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 > sub microscopic
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."
Older medical literature does include vaccines as a potential cause of
"Haemorrhagic and perivenous encephalitis." (117) Louis Reik Jr (1980)
outlined a hypothetical mechanism for post-vaccine brain hemorrhages in the
following statements:
"Common to all the postinfectious and postvaccinal complications affecting
the nervous system is the initial introduction of a foreign antigen, through
either invasion or inoculation, followed by a variable free of nervous
system symptoms and then clinical nervous system involvement. During this
asymptomatic period, antibodies could form and combine with the foreign
antigen to form circulating immune complexes. If such complexes are of
appropriate size and contain the correct proportion of antigen to antibody,
they can cause systemic liberation of vasoactive substances. An increase in
vascular permeability results, complexes are trapped in vessel walls in a
focal fashion, complement is activated, and inflammatory cells accumulate
and release proteolytic enzymes, causing tissue injury. (118)
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. (119)
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. 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. Current laboratory tests available for hypercoagulatility
``include fibrinogen, fibrin monomer, prothrombin fragment, and
thrombin-antithrombin complex.
Comment: The only missing link in this chain of evidence that vaccines may
be causing brain edema, retinal hemorrhages, and brain hemorrhages in large
numbers of children now being misdiagnosed as shaken baby syndrome is the
final mechanism provoking brain hemorrhages. As a scientist Reik stopped
short of stating this, this being an area with very limited research.
However, it is easily imagined how hemorrhagic complications may follow the
vascular injuries from immune-complexes with increased local release of
vasoactive substances and proteolytic enzymes, these in turn acting
destructively on the blood vessels of the brain.
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 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 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 probably
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 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)
-
- 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. (122) {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 level rises, causing capillary and venular fragility, leading to
bleeding. The blood escaping from the blood vessels slowly undergoes
hemolysis, and this causes further vitamin C depletion.}
With the foregoing information as a background, it may now be timely to cite
a personal communication (2000) with Toni Blake, Attorney and Jury Counselor
of San Diego, who told of a series of 25 cases in which a parent had been
accused of shaken baby syndrome in which the babies had the following
features in common:
1) All came from problem pregnancies including
prematurity, low birth weight, maternal drug/alcohol problems, maternal
toxemia of pregnancy, or other prenatal risk factors;
2) All were 6 months or less of age;
3)All had subdural hemorrhages;
4) complications interpreted as shaken baby syndrome occurred at 2, 4, or 6 months of age, within 11 or
12 days of vaccines.
5) Many also had fractures. A recent communication from Attorney Blake informed me that
this series is now much larger.
It is probably in situations of fragile infants, as described above, that
one finds a final common pathway for most major risk factors for vaccine
reactions with
1) sub-optimal nutrition, including marginal vitamin C
deficiency;
2) immature liver and kidneys, where most body detoxification
takes place;
3) ongoing minor viral infections, which further deplete
vitamin C levels (pediatricians commonly ignore the presence of viral
infections in administrations of vaccines);
4) formula feeding rather than
breast feeding (breast milk has four times the level of vitamin C as the
mother's blood level of vitamin C). 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 a common scenario in which parents are being blamed and accused of
death or injury from SBS, when the true causes arose from vaccine reactions.
This series of reactions, in which disseminated intravascular coagulapthy
(DIC) may also be involved, might be thought of as a variant of classical
scurvy, or Barlow's Disease.
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)
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."
-
- 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. (120) 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.
(121)
-
- 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) and osteogenesis imperfecta.
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.
{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.}
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
and may be mistaken for child abuse. (108-110)
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 but one study as 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
Before concluding, I wish to place special emphasis on what I believe to
have been ill-advised vaccines in a premature infant. If this had not been
evident with the first series November 17, 2001, it certainly should have
been on December 17 when the second series was administered to an ill child.
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.
As an addendum to this report I am enclosing a series of selected published
studies showing increased hazards of vaccine reactions in premature infants.
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 mine)
It is true that thimerosal is now being withdrawn from childhood vaccines, a
process which reportedly should be complete by the year 2003. However,
considering that mercury has been used in vaccines since the 1930s, it is
both possible and plausible that vaccine reactions, which result in part
from mercury toxicity, have gone largely unrecognized for well over half a
century by medical authorities. As a result, many conditions, including
misdiagnosed cases of shaken baby syndrome, are not being traced to their
true origins: vaccine reactions.
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.
-
- 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, the nervous and immune systems, as well as
other systems of the body; and in finding adverse reactions, to seek for
safer methods.
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SBS and SIDS Index of Articles on Vaclib site
A longer article on only the 'latent period' by Dr. Buttram:
The Controversy of the Latent Period Following Immunizations
http://www.mercola.com/2001/dec/1/immunizations.htm
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