SHAKEN BABY SYNDROME: CONTROVERSY

http://www.freemendez.org/dispute.html

The Shaken Baby Syndrome theory is a source of controversy in the medical field. Here we have the medical establishment debating its very existance.

* The evidence base for shaken baby syndrome; we need to question the diagnostic criteria
By J F Geddes, MD; J Plunkett, MD
British Medical Journal - Editorial (3-27-04)
* Physicians as well as the falsely-accused weigh in on the matter
BMJ - Rapid Responses published (3-26-04 through present)
o Retinal haemorrhages remain an important physical sign in the diagnosis of non accidental injury
By Michael P Clarke, et al (Members of Ophthalmology Child Abuse Working Party)
BMJ - Rapid Response (4-11-04)
* Retinal haemorrhages and SBS. Fact or Fantasy?
By Michael D. Innis FRCPath; FRCPA
Rebuttal: BMJ - Rapid Response (4-13-04)
* Re: Retinal haemorrhages remain an important physical sign in CONJECTURING the diagnosis of non accidental injury
By L. Travis Haws, Dentist
Rebuttal: BMJ - Rapid Response (4-13-04)
* Perimacular retinal folds from childhood head trauma
By P E Lantz, MD et al, Wake Forest University School of Medicine
British Medical Journal - Case Report (3-27-04)
* A falling television is cited as an example of accidental injury
BMJ - Rapid Responses published (3-26-04 through present)
* Shaken Baby Syndrome; pathological diagnosis rests on the combined triad, not on individual injuries
By Brian Harding, MD; R. Anthony Risdon, MD; Henry F Krous, MD
British Medical Journal - Editorial (3-27-04)
* The SBS Myth
By Michael D. Innis, MD
Rebuttal: BMJ - Rapid Response (4-4-04)
* Changes of Season
By L. Travis Haws, Dentist
Rebuttal: BMJ - Rapid Response (3-30-04)
* SBS Articles - Quality Research or Dogma?
By Tracy L. Emblem, Attorney
Rebuttal: BMJ - Rapid Response (3-29-04)
* Pathological diagnosis based on the triad, but where is the scientific evidence to back it up?
By Heather J Lohr, Parent
Rebuttal: BMJ - Rapid Response (3-28-04)
* Patterns of presentation of the shaken baby syndrome; four types of inflicted brain injury predominate
By Robert A Minns, MD; Anthony Busuttil, MD
British Medical Journal - Letter (3-27-04)
* Proposed Name Change of Shaken Baby Syndrome.
By Michael D. Innis FRCPath; FRCPA
Rebuttal: BMJ - Rapid Response (4-17-04)
* Patterns of presentation of the "shaken baby" syndrome may not be caused by trauma at all
By Viera Scheibner, PhD
Rebuttal: BMJ - Rapid Response (4-2-04)
* Parents demand gag on cot death doctor's lectures
Outrage at international acclaim for Meadow
UK Guardian (3-24-04)
* Shaken to Death?
BBC News - UK Edition (3-24-04)
* Shaken Baby Syndrome or Medical Malpractice?
By Mohammed Ali Al-Bayati, PhD, DABT, DABVT Toxicologist & Pathologist
www.freeyurko.bizland.com/ (3-13-04)
* We Can't Reunite Thousands of Mothers With Children Wrongly Taken From Them
By Melissa Kite, Deputy Political Editor
www.telegraph.co.uk/news (1-18-04)
* Responsible Medical Testimony and the GMC
By John Plunkett, MD Laboratory and Medical Education Director, and Forensic Pathologist
bmj.bmjjournals.com/ (11-24-03)
* Shaken Baby / Impact Syndrome:
By Harold E. Buttram, MD, FAAEM, Diplomat of the American Academy of Environmental Medicine
Flawed Concepts and Misdiagnoses (8-18-03)
* Go Tell It on The Mountains
By Michael D. Innis FRCPath; FRCPA
bmj.bmjjournals.com/ (6-4-03)
* Surveillance Should Include All Adverse Affects
By Michael D. Innis FRCPath; FRCPA
bmj.bmjjournals.com/ (5-17-03)
* A case in point – this family practitioner prevents a miscarriage of justice
Harold Buttram, MD, FAAEM
Misdiagnosis of SBS
* Iatrogenic Misadventure
By Michael D. Innis FRCPath; FRCPA
bmj.bmjjournals.com/ (4-5-03)
* Politically Incorrect But....
By Michael D. Innis FRCPath; FRCPA
bmj.bmjjournals.com/ (3-25-03)
* Misdiagnosis of SBS
By Michael D. Innis FRCPath; FRCPA
bmj.bmjjournals.com/ (3-22-02)
* Shaken Baby Syndrome (SBS) & Non-Accidental Injuries (NAI)
By Dr. Mark Donohoe
SBS & NAI (8-20-01)

http://news.bbc.co.uk/1/hi/programmes/real_story/3566127.stm
Last Updated: Wednesday, 24 March, 2004, 19:18 GMT
Shaken to death?
Cases of 'shaken baby syndrome' are increasing

Some experts say that when a baby suffers bleeds to the brain and the eye it must have been violently shaken.

But fresh research challenges the science behind Shaken Baby Syndrome, so that some doctors now think that the syndrome doesn't even exist.

No-one doubts that people do abuse, even kill their children, but what disturbs some doctors are those "shaken baby" cases where there is no evidence of previous abuse: no broken bones, no bruises, no scars.

Reporter John Sweeney and the Real Story team that helped free cot death mother Angela Cannings investigate how the courts and the police may be bringing "shaken baby"cases on disputed medical opinion - raising the possibility that people have gone to prison for murders that never actually happened.

Reporter John Sweeney writes about the programme:
My life has turned upside down

Real Story: BBC One, Monday 29 March 2004, 1930 BST and live on the Real Story website.

Responsible medical testimony and the GMC

John Plunkett
Laboratory and Medical Education Director, and Forensic Pathologist
Regina Medical Center, Hastings, MN 55033
John Stephenson, Thomas Carlstrom, Jennian F. Geddes, Lawrence E. Thibault, Dimitri Contostavlos, Patrick Barnes, Thomas Bohan, Marvin Miller, Julie Niedermier, Ron Uscinski

Send response to journal: Re: Responsible medical testimony and the GMC
24 November 2003

Editor,

Child abuse prevention is a laudable goal with which none of us would disagree. However, child abuse prevention has become an industry. The Web site for the National Center on Shaken Baby Syndrome, a non- governmental corporation in Salt Lake City, lists 13 professional employees (1). The Center co-sponsored the European Conference on Shaken Baby Syndrome this past May in Edinburgh. Government and private grants totaling millions of dollars have been granted to individuals and institutions to "study" and prevent child abuse. However, the grants have done little more than to increase the number of child abuse "specialists" with dubious qualifications, and almost none has been spent to research infant injury mechanisms.

Failure to understand injury mechanisms and the limitations of medical findings in infant injury evaluation is a critical problem (2). This failure has led to an unknown number of unsubstantiatable charges and unsafe convictions in the US, UK, Canada and Australia (3-7). Belief systems appropriate to social intercourse have been held to be scientific truths by many in medicine, the public, and the law (8-10). When these belief systems are questioned (11-13) or disproved (14-16), where is the outcry from medical practitioners, the public, and the law to correct these past wrongs?

Many infants suffer unexplained fractures. It is not sufficient to conclude that these fractures "must" be due to abuse based solely on the radiographic characteristics. A diagnosis of abuse should be based on total evaluation of a child, including his/her signs and symptoms, objective evidence for injury, and social/environmental circumstances. A diagnosis of abuse is made by evaluating the child, not by looking at a radiograph (17). The scientifically appropriate conclusion many times will be "I don’t know".

Dr. Paterson has made observations concerning a pattern of skeletal injuries in infants. He has formed a hypothesis based on his observations. His basic hypothesis is that there are infants with multiple fractures in whom the cause is unknown, but in which they may be due to factors other than abuse (18). Many in the US and Canada accept a similar although not identical hypothesis as "osteopenia of prematurity". This latter hypothesis was based on the observation that some premature infants were suffering fractures while in the neonatal ICU. It was assumed that the fractures were not due to abuse by the family or staff, and therefore must be due to some other cause. Dr. Paterson’s hypothesis deserves funding for research, not an appearance before the GMC.

For the GMC to invite and potentially accept testimony from a physician (19) with no qualifications in radiography, pathology, or metabolic bone disease is not merely a deviation from accepted UK standards (20) for expert testimony in civil if not criminal proceedings. It is frightening.

John Plunkett, et al.

References:

1. http://www.dontshake.com/
2. Plunkett J. Recognizing abusive head trauma in children. JAMA 1999;282:1421-22.
3. Coghlan A. The New Scientist 2002;173:11-13.
4. Dyer C. Sally Clark freed after appeal court quashes her conviction. BMJ 2003;326:304.
5. Milroy C. Medical experts and the criminal courts. BMJ 2003;326:294-95.
6. R. v. Lee. Supreme Court of the Australian Capital Territory. Nov - Dec 2001. Canberra. 2002 WL 14350.
7. Andrews v. Maryland. Court of Appeals of Maryland. 14 Nov 2002. 2002 WL 31521212 (Md.).
8. Chadwick DL, Kirschner RH, Reece RM, Ricci LR, Alexander R, et al. Shaken baby syndrome - a forensic pediatric response. Pediatr 1998;101:321-23.
9. Committee on child abuse and neglect. Shaken baby syndrome: rotational cranial injuries - technical report. Pediatr 2001;108:206-10.
10. Case ME, Graham M, Handy TC, Jentzen J, Monteleone J. Position Paper on Fatal Abusive Head Injuries in Infants and Young Children. Am J Forens Med Pathol 2001;22:112-22.
11. Donohoe M. Evidence-based medicine and shaken baby syndrome: Part I: Literature review, 1966-1998. Am J Forens Med Pathol 2003;24:239-42.
12. Geddes JF, Whitwell HL. Neuropathology of fatal infant head injury. J Neurotr 2003;20:905.
13. Geddes JF, Whitwell HL. New thoughts on inflicted head injury. For Sci Int 2003;in press.
14. Plunkett J. Fatal pediatric head injuries caused by short- distance falls. Am J Forens Med Pathol 2001;22:1-12.
15. Geddes JF, Hackshaw AK, Vowles GH, Nickols CD, Whitwell HL. Neuropathology of inflicted head injury in children: I. Patterns of brain damage. Brain 2001;124:1290-98.
16. Geddes JF, Vowles GH, Hackshaw AK, Nickols CD, Scott IS, Whitwell HL. Neuropathology of inflicted head injury in children: II. Microscopic brain injury in infants. Brain 2001;124:1299-1306.
17. Barnes PD. Ethical issues in imaging nonaccidental injuries: Child abuse. Top Mag Res Imag 2002;13:85-94.
18. Miller ME. The lesson of temporary brittle bone disease: all bones are not created equal. Bone 2003;33:466-74.
19. http://www.news.scotsman.com/archive.cfm?id=1255102003
20. The Law & You - Civil Procedure Rules 1998. Expert Witness Institute. http://www.ewi.org.uk/procedures.asp#35_1.

Competing interests: A number of us have given testimony at the request of defense council in cases of suspected child abuse.
[Return]
Shaken Baby / Impact Syndrome:
Flawed Concepts and Misdiagnoses

(Based on Review of a Series of Cases)
Privileged material, not to be copied except with permission of the author
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, 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 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, 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) 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 ith 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 food" 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:

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. (122)

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.}

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 mine)

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.

References:

1. David TJ, Shaken baby (shaken impact) syndrome: non-accidental head injury in infancy, Royal Soc Med, Nov.,1999; 99:556-561
2. Weston IT, The pathology of child abuse, in: Heifer RE, Kempe CH Eds, The Battered Child, University of Chicago Press, 1968, Pp 77-100.
3. Caffey J, On the theory and practice of shakng infants: its potential residual effects of permanent brain damage and mental retardation, Am J Dis child, 1972; 124:161-169.
4. Guthkelch AN, Infantile subdural hematoma and its relationship to whiplash injury, Brit Med J, 1971; 11:430-431.
5. Joint Statement on Shaken Baby Syndrome, Minister of Public Works and Government Services, Ottawa, 2001.
6. Brown J, Minns R, Non-accidental head injury, with particular reference to whiplash shaking injury and medical legal aspects, Dev Med Child Neurol, 1993; 35:849-869.
7. Plunkett J, Shaken baby syndrome and the death of Matthew Eapen: A forensic pathologist’s response, Am J Forensic med Pathol,1999; 20:17-21.
8. Wilkin B, Head injury - abuse or accident? Arch Dis child, 1997; 76:393-397.
9. Kemp AM, Investigating subdural hemorrhage in infants, Arch Dis Child, 2002; 86:98-102.
10. Kleinman PK, Barnes, PD, Head Trauma in, Kleinman PK, ed, Diagnostic Imaging of Child Abuse, 2nd edition, St Louis, MosbyYearbook, 1998:285-342.
11. Jenny C, Hymnel KP, Ritzen A et al, Analysis of missed cases of abusive head trauma, JAMA, 1999; 281:621-626.
12. Levitt CJ, Smith, WL, Alexander RC, Abusive head trauma, In Reece RM, ed: Child Abuse; Medical Diagnosis and Management, Philadelphia, Lea & Febiger, 1994: 1-22.
13. Shannon P, Becker L, Mechanisms of brain injury in infantile child abuse, (commentary), Lancet, 2001; 358:686-687.
14. Chester AC, Levine PH, Concurrent sick-building syndrome and chronic fatigue syndrome: epidemic neuromyasthenia revisited, Clin Infect dis, (Suppl 1), 1996;18:S43-S48.
15. Barnes PD, Ethical issues in imaging nonaccidental injury: child abuse, Topics in Magnetic Resonance Imaging, 2002; 13(2):85-94. (Lippincott, Williams, & Wilkins, Inc., Philadelphia)
16. Schoenfeld A, Buckman G, Cohen S et al, Retinal hemorrhages in the newborn following labor induced by oxytocin or dinoprostone, Arch Ophthalmol, July, 1985; 103:932-934.
17. Nelson Textbook of Pediatrics, 16th Edition, Behrman RE, Kliegman RM, Jenson HB (editors), WB Saunders Co, 2000, Page 489.
18. Fenichel GM, Webster DL, Wong WKT, Intracranial hemorrhage in the term newborn, Arch Neurol,Jan., 1984; 41:30-34.
19. Chamnanvanakij S, Rollins N, Perlman JM, Subdural hematoma in term infants, Pediatr Neurol, 2002; 26:301-304.
20. Piatt, JH, A pitfall in the diagnosis of child abuse: external hydrocephalus, subdural hematoma, and retinal hemorrhages, Neurosurg Focus, 1999; 7(4): Article 4
21. Parent AD, Pediatric chronic subdural hematoma: A retrospective comparative analysis, Pediatr Neurosurg, 1992; 18: 266-271.
22. Hwang SK, Kim SL, Infantile head injury with special reference to the development of chronic subdural hematoma, Child Nerv Syst,2000; 16:590-594.
23. Kim KA, Wang MY, Griffith PM, et al, Analysis of pediatric head injury from falls, Neurosurg Focus, 2000; 8:1-8.
24. Arnold SF et al, Synergistic activation of estrogen receptor with combinations of environmental chemicals, Science, 1996; 272:1489-1492.
25. Abou-Donia AB et al, Neurotoxicity resulting from exposure to Pyridostigmine bromide, DEET, and permitrin; implications of Gulf War chemical exposures, J Tox & Environ Health, 1996; 48:35-36.
26. Stratton KR, CJ Howe, and RB Johnston, Jr, Editors, Adverse events associated with childhood vaccines; evidence bearing on causality, Institute of Medicine, National Academy Press, Washington DC;, 1994: 211-236.
27. Eibl M et al, Abnormal T-lymphocyte subpopulations in healthy subjects after tetanus booster immunization, (letter) NEJM, 1984; 310(3): 198-199.
28. Shaneen SO et al, Measles and atopy in Guinea-Bissau, Lancet, June 19, 1996: 347:1792-1796. Odent MR, Pertussis vaccination and asthma; is there a link? JAMA, 1994; 271:229-231.
29. Alm JS et al, Atopy in children of families with anthroposophic lifestyle, Lancet, 1 May, 1999; 353:1485-1488.
30. Kemp T et al, Is infant immunization a risk factor for childhood asthma or allergy? Epidemiology; November, 1997; 8(6): 678-680.
31. Low AL, Electroencephalographic studies following Pertussis immunization, J Pediatrics, 1955; 47:35-39.
32. Nouno S et al, Adverse effects on EEG and clinical condition after immunizing children with convulsive disorder, Acta Paediatr Japan, Aug., 1990; 32(4):357-360.
33. Hurley DR, Vere DW, Fletcher AP, Referee 1, 2, 3 & 4, Adverse Drug React Toxicol Review, 2001; 19(4): 1-2.
34. Newman TA, Wooley ST, Hughes PM et al, T-cell and macrophage-mediated axon damage in the absence of a CNS-specific immune response: involvement of metalloproteinases, Brain, 2001; 124: 2203-2214.
35. Kosecka U et al, Pertussis adjuvant prolongs intestinal hypersensitivity, Int Arch Allergy Immunol, July, 1999, 119(3):205-211.
36. Terpstra GK, Comparison of vaccination of mice and rats with Haemophilus influenzae and Bordetella pertussis as models of atopy, Clin Exp Pharmacol Physiol, March-April, 1979; 6(2): 139-149.
37. Iwasa S, Ishida S, Akama K, Swelling of the brain caused by pertussis vaccine: its quantitative determination and the responsible factors in the vaccine, Japan Med J Sci Biol, April, 1985; 38(2):53-65.
38. Jacob J, Manning F, Increased intracranial pressure after diphtheria, tetanus, pertussis immunization, J Dis Child, Feb.., 1979; 133:217-218.
39. Gross TP et al, Bulging fontanel after immunization with diphtheria-tetanus-pertussis vaccine and diphtheria-tetanus vaccine, J Pediatr, March, 1989; 114(3):423-425.
40. Mathur R, Kamuri S, Bulging fontanel following DPT, Indian Pediatr, June, 1981; 18(6):417-418.
41. Galazka A, Kardymowiez BA, Complications and reactions after vaccination with pertussis, Epidemiol Rev, 1972; 26:411-424.
42. Munoz JJ et al, Elicitation of experimental encephalomyelitis in mice with the aid of pertussigen, Cellular Immunology, 1984; 83(1): 92-100.
43. Levine S, Lowinski R, Hyperacute encephalomyelitis, Am J Pathol, 1973; 37:247-250.
44. Steinman L, Sriram S, Adelman NE, et al, Murine model for pertussis vaccine encephalopathy: Linkage to H-2, Nature, 21 October, 1982, 2
45. Ocular Differential Diagnosis, Sixth Edition, Frederick Hampton Roy, Williams & Wilkins Publ., Philad., 1997:527-532.
46. Geddes JF, Hackshaw AK, Vowles GH et al, Neuropathology of inflicted head injury in children, 1. Patterns of brain damage, Brain, July, 2001, 124(7):1290-1298.
47. Plunkett J, Shaken baby syndrome and other mysteries, Am J Forens Med Path, Letter submitted spring, 1998.
48. Tongue AC, Discussion, Ophthalmology, 1986; 93:624-625.
49. Goetting MG, Sowa B, Retinal hemorrhage after cardiopulmonary resuscitation in children: an etiologic reevaluation, Pediatrics, 1990; 85:585-588.
50. Weeden VW et al, Retinal hemorrhage following CPR, Am J Forens Med Path, 1990; 11:79-82.
51. Kirschner RH, Stein RJ, The mistaken diagnosis of child abuse, Am J Dis Child, 1985; 139:873-875.
52. Kramer K, Goldstein B, Retinal hemorrhage following CPR, Clin Pediatr, 1993; 32:366-368.
53. Sherriff FE, Bridges LR, Sivaloganathan S, Acta Neuropathol, 1994; 87:55-62.
54. Kaur B, Rutty GN, Timberley WR, The possible role of hypoxia in the formation of axonal bulbs, V Clin Pathol, March, 1999; 52(3):302-209.
55. Gilliland, MGF, Interval duration between injury and severe symptoms in nonaccidental head trauma in infants and young children, J Forensic Science, 1998; 43(3):723-725.
56. Plunkett J, Fatal pediatric head injuries caused by short-distance falls, Am J Forens Med Pathol, 2001; 22(1):1-12.
57. Kalokerinos A, Every Second Child, Thomas Nelson, Australia, 1974.
58. Johnston CS, Thompson MS, Vitamin C status of an out-patient population, J Amer Col Nutr, 1998; 17:366-370.
59. Hume R, Weyers E, changes in the leucocyte ascorbic acid concentration during the common cold, Scot Med J, 1973; 18:3.
60. Aleo JJ, Padh H, Inhibition of ascorbic acid uptake by endotoxin, Proc Soc Exper Biol Med, 1985; 179:128-131.
61. Clemetson CAB, Histamine and ascorbic acid in human blood, J Nutr, 1980; 110:662-668.
62. Chatterjee IB, Majumder AK, Nandi BK et al, Synthesis and some major functions of vitamin C in animals, Ann NY Acad Sci, 1975; 258:24-47.
63. Clemetson CAB, Vitamin C, (Volume I of 3-volume set), CRC Press, Boca Raton, Florida, 1989, Pp 215-221.
64. Stone N, Meister A, function of ascorbic acid in the conversion of proline to collagen hydroxyproline, Nature, (London), 1962; 194:555.
65. Gore I, Tanaka Y, Fujinamik T et al, Endothelial changes produced by ascorbic acid deficiency in guinea pigs, Arch Pathol, 1965; 80:371-376.
66. King CG, Menten ML, The influence of vitamin C level upon resistance to diphtheria toxin, J Nutr, 1935; 10:129-140.
67. Jungblut CW, Zwemer RL, Inactivation of diphtheria toxin in vivo and in vitro by crystalline vitamin C (ascorbic acid), Proc Soc Exper Biol Med, 1935; 32: 1229-1234.
68. Dey PK, Efficiency of vitamin C in counteracting tetanus toxin toxicity, Naturwissenschaften, 1966; 53:310.
69. Fukada T, Koyama T, Prevention by ascorbic acid of liver glycogen depletion in endotoxin intoxication, Nature (London), 1963; 200:1327.
70. Gilman BB, Tanzer RC, Subdural hematoma in infantile scurvy, JAMA, September 17, 1932; 99(12): 989-991.
71. Butler, H, Position Paper on the Role of Vaccines in SIDS (Draft Version), 25 Harrisville road, Tuakau 1982, New Zealand (a portion of this 33 page report reviews the importance of breast feeding, as reflected in the higher incidence of Sudden Infant Death Syndrome (SIDS) in bottle fed babies as compared with those that are breast-fed). Presumably the same relationship applies with vaccine reactions.
72. Kawakami S, Chikama M, Tamiya T et al, Coagulation and fibrinolysis in chronic subdural hematoma, J Neurosurgery, 1989; 25:25-29.
73. Downes KA, Domen RE, McCarron, KF, Bringelsen, KA, Acute autoimmune hemolytic anemia following DTP vaccination: report of a fatal case and review of the literature, Clin Pediatr, 2001; 40:355-358
74. Williams Hematology, Sixth Edition, E Beutler, BS Coller, U Seligsohn, MA Lichtman, TJ Kpps, Ed., McGraw-Hill Medical Publ Division, New York, 2001, page 1673
75. Ibid, page 1475
76. The Innis report can be found on the Yurko website: http://www.freeyurko.bizland.com
77. Plunkett J, Fatal head injuries caused by short-distance falls, Am J Forens Med Path, 2001; 22(1):1-12.
78. Pozzati E, Poppi M, Gaist G, Acute bilateral extradural hematomas in a case of osteogenesis imperfecta congenital, Neurosurgery, 1983; 13:66-68.
79. Tokoro K, Nakajima F, Yamataki A, Infantile chronic subdural hematoma with local protrusion of the skull in a case of osteogenesis imperfecta, Neurosurgery, 1988; 22:595-598.
80. Miller ME, Temporary brittle bone disease: a true entity?, Seminars in Perinatology, April, 1999, 23(2):174-182.
81. Miller ME, Hangartner, Temporary brittle bone disease: associated with decreased fetal movement and osteopenia, Calcif Tissue Int, 1999; 64:137-143.
82. Kirschner RH, Stein RJ, the mistaken diagnosis of child abuse, AJDC, September, 1985; 139, 873-875.
83. A Kalokerinos, Medical Pioneer of the 20th Century, an Autobiography, Dr. Archie Kalokerinos, Biology Therapies Publishing, Braeside, Melbourne, Victoria, Australia, Fax (61) 39587 1720, published year 2000, Page 417.
84. Scurvy, Past and Present, Alfred F Hess, M.D., J.B. Lippincott Co., Philadelphia, 1920.
85. Hiller HG, Battered or not - a reappraisal of metaphyseal fragility, Am J Roent Rad Ther & Nucl Med, 1972; 114(2):241-246.
86. The Hepatitis B Vaccination Program in the United States - Lessons for the Future, Burton A waisbren, Sr, M.D., Delzer Lithograph Company, PO Box 679, Waukesha, WI 53186-0679, Copyright Pending, pages 34-36. The 58 case reports of acquired autoimmunity following hepatitis B vaccine were provided in a supplemental report accompanying the book.
87. Smith DC, Kearns TP, Sayre GP, Pre-retinal and optic nerve sheath hemorrhage: pathologic and experimental aspects in subarachnoid hemorrhage, Trans Am Acad Opthalmol Otolaryngol, 1957; 61:201-211.
88. Lehman RAW, Krupin T, Podos SM, Experimental effect of intracranial hypertension upon intraocular pressure, J Neurosurgery, 1972; 36:60-66.
89. David DB, Mears T, Quinlan MP, Ocular complications associated with bungee jumping, Brit J Ophthalmol, 1994; 78:234-235.
90. Jain BK, Talbot EM, Bungee jumping and intraocular hemorrhage, Br J Opthalmol, 1994: 78:236-237.
91. Vanderlinden RG, Chisolm LD, Vitreous hemorrhages and sudden increased intracranial pressure, J Neurosurg, 1974; 41:167-176.
92. Edlow JA, Caplan LR, Avoiding pitfalls in the diagnosis of subarachnoid hemorrhage, New Engl J Med, 2000; 342:29-36.
93. Margulies SS, Infant skull and suture properties: measurements and implications for mechanisms of pediatric brain injury, Transactions of the ASME, August, 2000; 122:364-371.
94. Fenton LZ, Sirotnak AP, Handler MH, Parietal pseudofracture and spontaneous intracranial hemorrhage suggesting nonaccidental trauma: report of 2 cases, Pediatric Neurosurgery, 2000; 33:318-322.
95. Ophthalmology Child Abuse Working Party, Child abuse in the eye, Eye, 1999; 13:3-10.
96. Green, Ocular and cerebral trauma in nonaccidental injury in infancy: underlying mechanisms and implications for pediatric practice. Brit J Ophthalmol, 1996; 80:282-287.
97. Taylor D, Unnatural injuries, Eye, 2000; 14:123-150.
98. Duhaime, AC, Nonaccidental head injury in infants - the shaken baby syndrome, New Eng J Med, 1998; 338:1822-1828.
99. Duhaime AC, Alario AJ, Lewander WJ et al, Head injury in very young children: mechanisms, injury types, and ophthalmologic findings in 100 hoepitalized patients younger than 2 years of age, Pediatrics, 1992; 90(2):179-185.
100. Buys, Retinal findings after head trauma in infants and young children, J ophthalmology, 1992; 99:1718-1723.
101. Halsey NA, Limiting infant exposure to thimerosal in vaccines and other sources of mercury, JAMA, 1999; 282:1763-1766. (According to current Environmental Protection Agency (EPA) standards, the maximum safe mercury exposure in a single day should be 0.1 micrograms per kilogram of body weight).
102. Leong CCW, Naweed IS, Lorscheiderae FL, Retrograde degeneration of neurite membrane structural integrity of nerve growth cones following in vitro exposure to mercury, NeuroReport, Accepted for publication Dec. 12, 2000; 12(4):0733-0737.
103. Garcia VF, Gotschall CS, Martin MA et al, Rib fractures in children: a marker of severe trauma, J Trauma, 1990; 30(6):695-700.
104. Demir RH, Gleicher N, Myers SA, Atraumatic antepartum subdural hematoma causing fetal death, Am J Obstet Gynecol, 1989; t160:619-620.
105. Gunn TR, Subdural hemorrhage in utero, Pediatrics, Oct. 1985; 76(4):606-609.
106. Lund CJ, Kimble MS, Some determinants of maternal and plasma vitamin C levels, Am J Obstet Gyn, 1943; 46:635.
107. Hartmann RW Jr, Radiological case of the month; Rib fractures produced by birth trauma, Arch Pediatr Adolesc Med, 1997; 151(9):947-948.
108. Rizzolo PJ, Coleman PR, Neonatal rib fracture; birth trauma or child abuse? J Fam Pract; 1989; 29(5):561-563.
109. Cumming WA, Neonatal skeletal fractures, Birth trauma or child abuse? J Canad Asso Radiol, 1979; 30(1):30-33.
110. Hiller HG, Battered or not: a reappraisal of metaphyseal fragility, Am J Roentgen Radiotherapy & Nucl Med, 1972; 114(2):241-246.
111. Hymel KP, Jenny C, Block RW, Intracranial hemorrhage and rebleeding in suspected victims of abusive head trauma: addressing the forensic controversies, Child Maltreatment, November, 2002; 7(4):329-348.
112. Personal communication, Jan E Leestma, MD, board certified in Neuropathology and Anatomic Pathology, 2002.
113. Kawakami Y, Chikama M, Tamiya T, Shimamura Y, Coagulation and fibrinolysis in chronic subdural hematoma, Neurosurgery, 1989; 25:25-29.
114. Williams Hematology, Sixth Edition, Beutler E, Coller BS, Seligsohn U, Lichtman MA, Kipps TJ, Editors; McGraw-Hill Publishing, New York, 2001, Pages 1677-1695.
115. Graham DI, Behan PO, More AR, Brain damage complicating septic shock, J Neurol, Neurosurgery, Psychiatry, 1979; 42:19-28.
116. Hannon KI, Berg DE, Baumzweiger W et al, Activation of the coagulation system in Gulf War Illness: A potential pathophysiologic link with the chronic fatigue syndrome; a laboratory approach to diagnosis, Blood Coagulation and Finbrinolysis, 2000; 11:673-678.
117. Hall JR, Reyes HM, Horvat M, et al, The mortality of childhood falls, J Trauma, 1989; 29(9):1273-1275.
118. Blumenthal I, Skull fracture - child abuse or an accident? Lancet, July 15, 2000; 356:258. Geddes JF, Tasker RC, Hackshaw CD et al, Dural haemorrhage in nontraumatic infant deaths: does it explain the bleeding in ‘shaken baby syndrome’? Neuropathol & Applied Neurobiol, 2003;29:14-22.
119. Sanford HN et al, JAMA, 1942; 118:697.
120. Medical Pioneer of the 20th Century, an Autobiography, Dr. Archie Kalokerinos, biology Therapies Publishing, Braeside, Melbourne, Victoria, Australia, Fax (61) 39587 1720, published 2000, page 417.
121. Monson KL, Goldsmith W, Barbaro NM et al, Static and dynamic mechanical and failure properties of human cerebral vessels, in Crashworthiness. Occupant Protection and Biomechanics in Transport Systems, Eds HF Mahmmod, SD Barbat, MR Baccouche, New York: ASME, AMD v 246/BED v 49, 2000:255-265.
122. Duhaime AC, Gennarelli TA, Thibault LE et al, The shaken baby syndrome. A clinical, pathological, and biomechanical study, J Neurosurgery, 1987; 66:409-415.
123. Gherardi RK, Coquet M, Cherin P et al, Marcophagic myofasciitis lesions assess long-term persistence of vaccine-derived aluminium hydroxide in muscle, Brain, 2001; 124:1821-1831.
124. Chalumeau M, Foix-Helias L, Scheinmann P et al, Rib fractures after chest physiotherapy for bronchiolitis or pneumonia in infants, Pediat Radiol, 2002; 32:644-647.
125. Amir J, Katz K, Grunebaum M et al, Fractures in premature infants, J Pediatr Orthop, 1988; 8:41-44.
126. Tauscher MK, Berg D, Brockmann M et al, Association of histologic chorioamnionitis, increased levels of cord blood cytokines, and intracerebral hemorrhage in preterm neonates, Biol Neonate, 2003; 83:166-170.
127. Rutty GN, Smith CM, Malia RG, Late-form hemorrhagic disease of the newborn, Amer J Forensic Med Pathol, 1999; 20(1): 48-51.
128. Vaccines, Autism and Childhood Disorders, Neil Z Miller, New Atlantean Press, PO Box 9638, Santa Fe, NM 87504, 2003. (Note: this book gives an excellent chronicle of US Congressional hearings on questions of childhood vaccine safety, a large portion of which have involved question of a suspected connection between vaccines and the growing epidemic of autism).
129. Levin M, Kay JDS, Gould JD et al, Haemorrhagic shock and encephalopathy: a new syndrome with a high mortality in young children, Lancet, 1983, ii: 64-47.
130. Ommaya, Goldsmith, and Thibault, Biomechanics and neuropathology of adult and pediatric head injury, British J Neurosurgery, 2002; 16(3):220-242.
131. Aoki N & Masuzawa H, Infantile subdural hematomas, Neurosurgery, 1984; 61: 273-280 Chapter: Neuropathology 13.
132. Reiber G, Fatal falls in childhood, Am J Forens Med Path, 1993; 14(3): 201-207.
133. Root I, Head injuries from short falls, Am J Forens Med Path,1992; 13(1):85-87.
134. Geier MR & Geier DA, Pediatric MMR vaccine safety, International Pediatrics, 2003; 18(2):108-113.
135. Devin F, Roques G, Disdier P, et al, Occlusion of central retinal vein after hepatitis B vaccination, Lancet, 1996; 147:1626.
136. Ocular Differential Diagnosis, Sixth Edition, Frederick Hampton Roy, Williams & Wilkins, Philadelphia, 1997, pages 526-529.
137. Forensic Pathology, Second Edition, Vincent J DiMaio & Dominick DiMaio, CRC Press, Boca Raton, Florida 2001, Page 114-115.
138. Krause I, Lazerov A, Rachmel A et al, Acute haemorrhagic oedema of infancy, a benign variant of leucocytoclastic vasculitis, Acta Paediatr, 1996; 85:114-117.
139. Patrizi A, Rizzoli L, Vincenzi C et al, Contact Dermatitis, 1999; 40:94-97.
140. Allen MB, Cockwell P, Page RL, Pulmonary and cutaneous vasculitis following hepatitis B vaccination, Thorax, 1993; 48: 580-581.
141. Waskerwitz S, Christoffel KK, Hauger S, Hypersensitivity vasculitis presenting as suspected child abuse: case report and literature review, Pediatrics, Feb., 1981, 67(2):283-284.
142. Hennessen W, Quast U, Adverse reactions after pertussis vaccination, International Symposium on Immunization: Benefit Versus Risk Factors, Brussels 1978, Development of Biological Standard, 1979; 43:95-100, (S Karger, Basel).
143. Levin M, Kay JD, Gould JD et al, Haemorrhagic shock and encephalopathy: a new syndrome with a high mortality in young children, Lancet, July 9, 1983; pages 64-67.
144. Prange MT, Coats B, Duhaime AC, Margulies SS, J Neurosurg, July, 2003, 99: 143-150.
145. Gupta RK, Relyveld EH, Adverse reactions after injection of adsorbed diphtheria-pertussis-tetanus (DPT) vaccine are not due only to pertussis organisms or pertussis components in the vaccine, Vaccine, Oct., 1991; 9:699-702.
146. Vaccination, 100 Years of Orthodox Research Shows that Vaccines Represent a Medical Assault on the Immune System, Viera Scheibner, PhD, 1993, available from New Atlantean Press, PO Box 9638-925, Santa Fe, New Mexico 87504.
147. Vaccination and Behavioral Disorder, Greg Wilson, 2000, Tuntable Creek Publishing, PO Box 1448, Lismore, NSW 2480, Australia.
148. Cherry JD et al, Pertussis immunization and characteristics related to first seizures in infants and children, J Pediatrics, 1993; 122(6):900-903.
149. Camfield P, Brain damage from pertussis immunization, AIDC, 1992; 146:327-331.
150. Blumberg DA et al, Severe reactions associated with diphtheria-tetanus-pertussis vaccine: detailed study of children with seizures, hypotonic-hyporesponsive episodes, high fevers, persistent crying, Pediatrics, June, 1993; 91(6): 1158-1165.
151. Forensic Pathology, Second Edition, Vincent J DiMaio, Dominick DiMaio, CRC Press, Boca Raton, 2001, pages 177-179.

[Return]
GO TELL IT ON THE MOUNTAINS

Michael D Innis,
Director Medisets International
Home 4575

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email British Medical Journal 'Rapid Responses'
Re: GO TELL IT ON THE MOUNTAINS
4 June 2003

Editor,

"Perth man found not guilty in 'baby shaking' case." http://www.abc.net.au/news/newsitems/200306/s871014.htm

At long last the medical myth, which has plagued young families around the world, that the combination of retinal bleeding, with or without retinoschisis, associated with cerebral swelling and subdural haemorrhages is pathognomonic of severe acceleration/deceleration injury has been put to rest by Justice Graeme Scott of the Supreme Court in Australia.

The Prosecution relied on the above findings to accuse a father of shaking his 10 month old son to death

The "Patterns of Presentation of Shaken Baby Syndrome" [1] into hyperacute, acute encephalopathic and subacute should all now be considered examples of anoxic brain damage resulting from respiratory arrest following an 'Apparent Life Threatening Event' (ALTE).

The Medical Profession, especially Paediatricians, Radiologists, Ophthalmologists and Forensic Pathologists, should be aware of the predisposing causes, manifestations and consequences of ‘Apparent Life Threatening Events’ and seek to eliminate any possibility of such an occurrence before declaring death due to ‘Shaken Baby Syndrome’.

They should take particular care to exclude:

1. Congenital disorders of coagulation and metabolism
2. Infections
3. Haemorrhagic Disease of the Newborn also known as Vitamin K Deficiency Bleeding (VKDB)
4. Malabsorption Syndromes
5. Malnutrition especially in children that are not being breast fed.
6. Liver disease
7. Drug and Vaccine hypersensitivities
8. Barlow’s Disease
9. Kawasaki Disease

And perhaps most importantly they should seek the opinion of a Haematologist, or someone capable of correctly interpreting laboratory results, rather than that of a Police Officer, before committing an innocent person to prison and destroying a family.

It is time the cultures of 'think dirty’ and Munchausen Syndrome By Proxy to explain the unexplained are relegated to the scrap heap of history.

Michael Innis FRCPath; FRCPA
email Michael D Innis: micinnis@ozemail.com.au

Reference: 1. Minns RA; Minns AB eBMJ Rapid Response 26th March 2003.
Competing interests: I gave evidence for the Defense.
[Return]
Surveillance should include all Adverse Effects

Michael D Innis,
Director Medisets International
Home 4575

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Re: Surveillance should include all Adverse Effects
17 May 2003

Editor,

"Studies on human subjects have reported decreased levels of vitamin C in plasma, leukocytes, and in urine during various infections, including pneumonia, which suggests that infections affect vitamin C metabolism."[1]

This being so there is every reason to be believe that other forms of antigenic stimulation such as the administration of vaccines are also capable of decreasing levels of Vitamin C even to the extent of causing an adverse reaction.[2]

Hopefully in their "post-marketing surveillance," which they consider essential, Dr Elliman and Dr Bedford will include surveillance of adverse reactions to the vaccines especially those occurring within 3 weeks of administration.

Among the adverse reactions they could, or rather should, include evidence of acute Vitamin C deficiency:

1. Anorexia, vomiting and diarrhoea
2. Weight loss
3. Irritability
4. Seizure
5. Apparent Life Threatening Event (apnoea followed by gagging, cyanosis, muscle weakness and limpness)
6. "Fractured ribs" reported by radiologists who label any rib callus (healing subperiosteal haemorrhage from any cause including Vitamin C deficiency) a "fracture."
7. Haemorrhage anywhere including intracranial, intraspinal, pulmonary and subcutaneous.
8. Death

Some Pathologists could no longer say "beyond reasonable doubt" that "fractured ribs" were evidence of child abuse but could offer no alternative explanation. g.rayner@dailymail.co.uk

Perhaps the pathologists, and for that matter the whole medical profession, should consider Barlow’s Disease (Vitamin C deficiency in infants) a reasonable explanation of these "fractures."

Michael Innis FRCPath; FRCPA;
email Michael D Innis: micinnis@ozemail.com.au

References:

1. Hemila H. Vitamin C and SARS eBMJ 16th May 2003
2. Kalokerinos A. Every Second Child. Foreword by Linus Pauling. Thomas Nelson (Australia) Limited 1981 Keats Publishing Inc

Competing interests: Advising accused
[Return]
Misdiagnosis of SBS

NEW MEXICO, USA - Dr. Harold E. Buttram, MD, FAAEM, director of Woodlands Medical Center in Quakertown, PA in a sweeping victory, single-handedly prevented a terrible travesty of justice. A parent charged with manslaughter after being accused of shaken baby syndrome had all charges immediately dismissed after Buttram's report and record review revealed that purported "skull fractures" were mistakenly diagnosed by prosecution "experts". In fact, these alleged fractures were actually separated sutures of skull formation.

Buttram also linked the brain swelling responsible for the separation of the suture lines to the vaccines administered to the child. The vaccines administered checked out to be from "hot lots", which are batches of vaccines that have high incidence of adverse reports to the governments Vaccine Adverse Event Reporting System (VAERS). Harold E. Buttram, MD, FAAEM can be reached at hbuttram@woodmed.com or 1-800-517-9545.
Dr. Buttram candid photo
Candid photograph of Dr. Buttram in his office, November 19, 2003 from his patient's perspective.
[Return]
IATROGENIC MISADVENTURE?

Michael D Innis,
Director Medisets International
Home 4575

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Re: IATROGENIC MISADVENTURE?
5 April 2003

Editor,

Some members of the Medical Profession are misdiagnosing Barlow’s Disease (Vitamin C deficiency in infants) and labelling it "Shaken Baby Syndrome" provoking a response such as this from one aggrieved member of the public.

"Our experience has enlightened us, that all children who sustain injuries or die, and whose caretakers or parents could not provide explanations to fit exactly, the theories of medical practitioners are regarded as liars and "abusers"... it is equally extremely unscientific for physicians to assume that the coexistence of subdural haematoma and retinal haemorrhages in every infant is virtually an indicative that child abuse has occurred." (help@ourhealthtoday.com, The National Health Service).

The physicians alluded to appear to be unaware of two important clinical facts:

1. Barlow’s Disease resembles "battered baby."[1]
2. The dangerous effects of vaccines in children who have borderline low levels of Vitamin C.[2.3]

Two important haematological facts are also ignored by these physicians:

1. The prothrombin time (PT), activated partial thromboplastin time (APTT), and fibrinogen are usually within the normal range in overt Vitamin C deficiency. These tests are measures of the adequacy of the coagulation factors and Vitamin K. They do not address problems associated with vascular integrity -- the site of the defect in Vitamin C deficiency.
2. Vitamin C levels in the serum and/or urine should be examined in all instances where bleeding in a child is unexplained.

Currently the profession, in general, seems to imagine that scurvy disappeared with the sailing ships. They are unable to comprehend it has resurfaced in the form of infantile scurvy due to their unrestrained enthusiasm for vaccinating children in unfavourable circumstances.

Malnutrition and infection increase the body’s need for Vitamin C.[2.3] Learned professors in the profession believe that the current breast milk substitutes provide enough Vitamin C for the infant’s needs under all circumstances -- a totally false belief for which I have documentary evidence (unpublished).

Statements such as " ...and after haematological and rare causes are excluded trauma remains the likely cause"[4] should not go unchallenged. What was the haematological evidence that excluded a disorder of haemostasis? What was the serum Vitamin C level? What was the level of the von Willebrand factor antigen? Was a platelet function test done? If the answer to any of these questions is "I don’t know" then a haematological cause has not been excluded.

Another misconception flourishes among the shaken baby syndrome advocates who claim... "However research confirms that the commonest cause of SDH in a baby is child abuse, some of these children have been shaken."[5] What research? Was the vaccination history recorded? Was the nutritional status of the child assessed. What were the levels of the serum albumin, calcium, magnesium, essential amino acids? Were the appropriate haematological investigations done? If not, who but the advocates of MSbP would place any credence on the evidence?

Following the report of Geddes et al;[6] it is time to re-evaluate the problem of infants who suffer intracranial bleeding, retinal haemorrhages, bruises and what radiologists call "fractures." They even apply this term to what every 3rd year medical student in the East would recognize as the "scorbutic rosary."

The history of these children is fairly typical. The child is immunized with number of vaccines and by the next day is ill with vomiting, irritability, lassitude, anorexia followed by weight loss, bruising, seizures coma and death. CT scans and X-Rays show intracranial haemorrhages and rib fractures. The ophthalmologist announces retinal haemorrhages with retinoschisis and the Child Protection Servicea spring into action and a unsuspecting 'perpetrator' is nominated. Proper investigation is seldom or never carried out once the diagnosis of Non-accidental Injury is proclaimed.

I propose a new diagnosis and to establish a new concept one must nail it with a name • iatrogenic misadventure is a valid designation, but Kalokerinos Syndrome (malnutrition, vaccination, acute Vitamin C deficiency and a haemorrhagic diathesis) may be less confronting to a sensitive profession already buffeted by the winds of change.

Michael Innis MBBS; DTM&H; FRCPA; FRC
Path Honorary Consultant Haematologist
Princess Alexandra Hospital Brisbane
email Michael D Innis: micinnis@ozemail.com.au

Reference:

1. Oxford Text Book of Medicine Second Edition Vol 1 Edited by Weatherall, Ledingham IGG, Warrell DA. Ch 17 page 36
2. Kalokerinos A. Every Second Child. Foreword by Linus Pauling. Thomas Nelson (Australia) Limited 1981 Keats Publishing Inc
3. Clemetson CAB Vaccinations, Inoculations and Ascorbic Acid Jour Orthomolecular Med; (1999) 14:137-142
4. Minns RA, Bussittil A. Patterns of Presentation of Shaken Baby Syndrome BMJ Rapid Response 26th March 2003
5. Kemp A et al; Experts must guide the courts to a clear understanding of the context of medical research BMJ Rapid Response 27th March 2003
6. Owen Dyer, Brain haemorrhage in babies may not indicate violent abuse BMJ 2003;326:616

Competing interests: Advising • pro bono
[Return]
Re: Re: Politically incorrect but....

Michael D Innis,
Director Medisets International
Home 4575

Send response to journal:
email British Medical Journal 'Rapid Responses'
Re: Re: Politically incorrect but....
25 March 2003

Editor,

Dr Philip Stowell has drawn attention to the work of Dr A.Kalokerinos [1] who more than twenty years ago documented the dangerous effects of vaccines in children who have borderline low levels of Vitamin C.

And in the 21st century the medical profession is still persecuting parents for what is essentially an Iatrogenic disorder which they call Shaken Baby Syndrome. How much longer is this deception to continue?

Michael Innis
email Michael D Innis: micinnis@ozemail.com.au

Reference:

1. Kalokerinos A. Every Second Child. Foreword by Linus Pauling. Thomas Nelson (Australia) Limited 1981 Keats Publishing Inc

Competing interests: None declared
[Return]
Misdiagnosis of 'Shaken Baby Syndrome'

Michael D Innis,
Director Medisets International
Home 4575

Send response to journal:
email British Medical Journal 'Rapid Responses'
Re: Misdiagnosis of 'Shaken Baby Syndrome'
22 March 2002

Editor,

Michael Innis
email Michael D Innis: micinnis@ozemail.com.au

Reference:

1. Kalokerinos A. Every Second Child. Foreword by Linus Pauling. Thomas Nelson (Australia) Limited 1981 Keats Publishing Inc

Competing interests: None declared
[Return]
Shaken Baby Sybdrome (SBS) and Non-Accidental Injuries (NAI)

by Dr. Mark Donohoe

THE SHAKEN BABY SYNDROME
It is not possible to address the specifics of any particular case without addressing the general medical and scientific literature regarding the so-called shaken baby syndrome (SBS). I have performed such a review of the medical literature in order to assess the quality of evidence related to the diagnosis of SBS, and include this as Appendix I, along with the references reviewed. The question which needs to be answered is not: 'could this be a case of shaken baby syndrome?' because this is clearly one possibility. The questions which need to be answered would appear to be:

1. does this case represent anything other than SBS?; and the related question
2. how certain are we that this was a case of SBS, as opposed to anything else?

Historical Issues and Evidence for SBS
For doctors dealing with potentially abused children, the error of assuming abuse, even when none has occurred, is acceptable and (some would argue) necessary. It is certainly preferable to the alternative of failing to identify abuse which has occurred. In the past, the medical profession seems to have failed to identify cases of abuse, resulting in tragic outcomes for families and for the children not identified in particular.

In the last decade or so, a concerted effort has been made to address this historical blind-spot, and a number of advocacy groups for the rights of the child have emerged. Public educational campaigns have arisen, bringing the risks of shaking to the attention of the public, and the medical profession, particularly in hospital emergency settings, tends to scrutinise all cases of childhood injury or unexplained illness for evidence of abuse. On the whole, this has been a positive change, and may have resulted in decreases in death or injury of babies and children, although this has yet to be demonstrated.

As with all 'swings of a pendulum', however, there are associated dangers of such increased surveillance for abuse. The most obvious risk is that cases not associated with abuse will be incorrectly assumed to be abuse, and that the totality of evidence in cases will be ignored in favour of apparently incriminating evidence. I say this because it is, even in theory, impossible to attain perfection in the correct attribution of cause of injury. In the past, actual abuse cases were missed as a result.

Now, cases unrelated to abuse are occasionally incorrectly attributed to abuse. The medical tests which are supportive of the diagnosis of non-accidental injury (NAI) have been pushed by many advocates as being proof of NAI generally, and SBS in particular. The diagnosis of NAI and SBS rests on a number of factors, including medical and social history, family circumstances, medical examination, a wide range of test results, and the results of investigations and interviews by experienced multi-disciplinary teams. The diagnosis of NAI or SBS cannot ever rest upon the results of a few isolated investigations alone, as has been the case in recent years.

There are two main reasons for pursuing suspected NAI vigorously, namely: identifying and punishing any perpetrator, should the person be found; and decreasing further risk to the abused child and other children in the family. While the medical profession may well be acting in the interests of the child by assuming NAI even when it has not occurred, one must recognise the potential for harm to the family and child where such assumptions prove to be incorrect. The decision on whether or not NAI has occurred, and who is responsible for it if it has occurred, must be made by the legal process, and such judgements must be dispassionate and based on evidence, rather than assertion by those wishing to protect the child.

While it is self-evident that the safety and rights of the child must be protected in every case, the rights of the parents and carers cannot be ignored or forgotten in so doing. There is a clear risk in assuming that abuse has occurred in cases where the evidence is weak, and where alternative opinions have not been adequately pursued and excluded. The cases which I have so far reviewed would never have been investigated for potential abuse had it not been for the medical findings, as there was no evidence of or suggestion of abuse. In such cases, NAI has been assumed where other alternative explanations not only exist, but are arguably more likely than NAI.

Finally, the tendency of the medical profession to ignore the possibility of adverse reactions to vaccines, especially those containing thiomersal (a mercury preservative), is important. In more than half of the cases I have reviewed, there is an apparent temporal relationship between the injury and prior vaccination with thiomersal-containing polyvalent vaccines or multiple simultaneous vaccinations. The vaccine typically leads to pyrexia and crying immediately following vaccination, and the infant is given paracetamol (acetaminophen) at increasing doses for control of crying and pyrexia in the following days. In most of these cases, a broad spectrum antibiotic has also been prescribed in the same period.

It has been suggested that the alternative explanation should be preferred, namely that the vaccination itself caused no injury, but induced crying which lasted for days, leading to frustration and eventual shaking by a parent or carer. Even if this is accepted, it raises a most interesting issue of ultimate causation. Had the vaccine(s) not been administered, the adverse reaction and crying would not have occurred, and there would have been no risk or likelihood of shaking or injury of any type. The acceptance of such crying and pyrexia as a "normal and expected" consequence of polyvalent vaccinations in up to 20% of infants does nothing to address the consequences of the crying and the increased risk of injury to the child from such a common event.

It is disingenuous to argue that "the disease would have been worse" than the vaccination, because the disease may or may not have occurred, and is a part of normal life of a child, whereas vaccination is a procedure requiring informed consent. If one identifiable risk of vaccination is that of shaking and injury following prolonged crying (assuming that shaking did occur as a result of the vaccine-induced crying), then this needs to be conveyed to parents of children being vaccinated as part of the informed consent. If they are made aware of the potential for prolonged crying and pyrexia, and are told of the risks associated with shaking which may be a consequence of this crying, then the risk itself may be reduced.

Thus, it is arguable that vaccination is an independent predictor (or risk factor) for neurological injuries in infants, whether it is directly causative or predisposes to other outcomes which are causative. A recognition of the association (direct or indirect) may allow for action and warnings which may decrease the likelihood of adverse outcomes.

Axioms and Assumptions Regarding Allegation of SBS
The case for this infant being the victim of intentional shaking rests upon certain axioms and assumptions, which may be reduced to the following:

1. Subdural haemorrhage (SDH) does not occur in a normal, healthy infant;
2. SDH combined with retinal haemorrhage (RH) is pathognomonic of non-accidental injury (NAI);
3. In the absence of identifiable external trauma, SDH and RH are only caused by violent "acceleration/deceleration" actions caused by an adult, otherwise known as 'shaken baby syndrome';
4. SBS must be intentional, or at least they would appear intentional and excessive to any dispassionate observer;
5. The diagnosis of 'shaken baby syndrome' can be made with absolute certainty on the basis of ophthalmological and radiological assessment alone;
6. The severity of shaking required to cause these findings would have been obvious, and was unrelated to any shaking or corporal punishment admitted to by family members.

I shall address each of these statements separately, and attempt to assess the evidence for and against each statement.

Spontaneous subdural haemorrhage (SDH) does not occur in a normal, healthy infant
Clearly, SDH should not occur in a 'normal healthy infant', although there is no medical or scientific evidence to back this assertion one way or the other. There is a logical difficulty, of course, in that any such cases which did occur in a 'normal healthy infant' would almost certainly be attributed to NAI, whether or not there was other evidence to support such an attribution. This is a part of a broader defect of logic in NAI cases, that all unexplained injuries can be assumed to be NAI, which has been allowed to continue in an effort to protect the child. There is evidence that SDH does occur in normal, healthy neonates as a result of birth trauma, and even in cases of normal, uncomplicated vaginal delivery. There is clear evidence that SDH can be caused by anatomical, infectious and biochemical disorders which cause no obvious symptoms prior to the intracranial bleeding. In such circumstances, the infant appears 'normal and healthy' (although probably not robustly healthy) despite the underlying, predisposing pathology.

Such disorders, predisposing to SDH, include:

1. arteriovenous malformations (AVM) or shunts (AVS);
2. certain infections such as malaria, hepatitis, septicaemia;
3. intravascular coagulopathy due to bacterial endotoxin;
4. certain malignancies, such as leukaemia;
5. clotting disorders;
6. accidental or intentional poisoning;
7. liver disease, such as microvesicular steatosis, hepatitis, etc;
8. gastrointestinal disorders, causing malabsorption, affecting trace elements, ascorbate or fat soluble nutrients (esp vitamins E and K);
9. metabolic disorders, such as Reye's syndrome, diabetes, disorders of energy metabolism;
10. inherited disorders, such as enzyme defects or chromosomal defects;
11. vascular and connective tissue disorders.

This list is not intended to be exhaustive. It is also possible that more than one predisposing factor existed, and that it was a combination of factors which led to the intracranial haemorrhage. For example, a mild factor XIII deficiency, when combined with malabsorption or Reye's Syndrome, would be likely to result in a greater risk of intracranial bleeding than would any one of these factors alone. In an infant under six months, such disorders may be asymptomatic, or may simply result in a non-specific failure to thrive. In some of these diseases, the first presentation is that of an intracranial bleed. It is only possible to exclude these other causes by careful history taking, examination, appropriate and extensive testing, including assessment of nutritional status, enzyme levels, and assessing pathology of the liver, gut, kidneys, muscle, brain and heart. It is my view, based on the cases I have reviewed, that there is a tendency to assume that NAI has occurred in infants with SDH and RH, and as a consequence of that assumption, there is a general failure in the first instance to pursue other potential causes or contributions to the injury as vigorously as would be expected.

Further, once the allegation of abuse has been made, and police or welfare services have become involved, there is a general unwillingness to consider any other plausible causes of the injury. In a sense, the parents or carer are assumed to be guilty, and have no logical way of "proving" their innocence. Investigations are continued, even if the infant dies, but those investigations are usually directed at building a stronger case for NAI (such as bone scan, MRI, autopsy), rather than identifying alternative causes or contributory factors.

SDH combined with retinal haemorrhage (RH) is pathognomonic of "non-accidental injury" (NAI)

This is frequently the claim made by medical experts involved in the prosecution of SBS cases. Unless this relationship is proven, there is reasonable doubt that anyone shook or otherwise injured this infant. The term "pathognomonic" implies a two-way relationship between the symptoms and signs on one hand, and the disease in question on the other hand. Pathognomonic symptoms or signs not only allow recognition of a disease, but differentiate it from all other diseases or disorders. Technically, it implies 100% specificity for the tests establishing the diagnosis. The combination of SDH and RH strongly support a diagnosis of NAI, but in no way constitute proof that NAI occurred. The value of the diagnosis of SDH and RH is that their presence can markedly increase the confidence of a diagnosis of NAI, given other circumstances or findings which may indicate NAI. Even if we assume that all non-accidental injuries involving shaking or blunt trauma to the head of babies cause subdural haemorrhage and retinal haemorrhage, it does not follow that all cases of SDH and RH are caused by NAI.

One must know what other diseases or circumstances may cause SDH and RH. Since the mechanism of RH is unknown (Riffenburgh 1991), it is important that the specific hallmarks of NAI be delineated, as proposed recently (Rohrbach 1997). Rohrbach (1997) has stated, "Intraretinal haemorrhages alone are typical, though not pathognomonic for the "battered-child syndrome". According to Rohrbach, the combination of the following provides increased certainty of NAI, although there are clearly shortcomings in this single case study:

1. retinal haemorrhage;
2. crater-like appearance of central retina;
3. haemorrhagic retinoschisis; and
4. intrascleral haemorrhages in the area of the circle of Zinn-Haller. The ophthalmologists examining the infant needs to be questioned as to whether the changes seen in the particular case match these proposed criteria.

Conditions apart from NAI which may result in SDH and RH include: bleeding disorders; meningitis; septicaemia; leukaemia; galactosaemia; hypertension; and Henoch-Schonlein purpura. RH may also occur simply as a consequence of the intracranial bleeding. A number of papers which deal with the mechanism of the RH have suggested that the increasing intracranial pressure and subarachnoid haemorrhage lead to retinal haemorrhages (Jacobi 1986), and these may be accompanied by SDH.

In fact, this association is known as "Terson's Syndrome". A number of papers (Giangiacomo 1985, Weingeist 1986, Jacobi 1986, Keithahn 1993, Poepel 1994) point out the similarities between Terson's Syndrome and the retinopathy of shaken baby syndrome, with some suggesting that SBS should be considered in the differential diagnosis of Terson 's Syndrome. Thus, there are other plausible and reasonable explanations for the combination of SDH and RH in an infant. Any of the factors listed above as potential causes of SDH must be considered a plausible cause of the RH as well. The presence of SDH and RH is insufficient to prove any particular cause. It is likely that the majority of cases in which SDH and RH are found in infants under one year of age are NAI, but this is a statistical association. In any given case, these findings are only supportive of NAI. The case must stand or fall on other factors which would lead one to suspect NAI.

In the absence of evidence of identifiable external trauma, SDH AND RH are only caused by violent "acceleration/deceleration" actions caused by an adult, known as 'shaken baby syndrome"

Most studies show a high proportion of NAIs are associated with other signs of trauma or abuse, either in the damaged infant or in other family members. In a recent British retrospective study (Jayawant 1998), about 60% showed signs of other trauma (bruising, fractures, resolving old SDH, etc). Other authors have suggested similar or higher percentages as showing signs of trauma or abuse, especially in cases of severe cerebral damage and death (Alexander 1990, Duhaime 1987, Lancon 1998).

As noted above, factors which may cause or contribute to SDH or SAH in an infant are likely to cause RH as well. A recent study (Jayawant 1998) noted an 80% association between SDH and RH, suggesting that RH is not an independent risk predictor, but a marker of severity and extensiveness of intracranial bleeding.

A number of authors (Duhaime 1987, Lancon 1998, Closset 1992) have suggested that shaking without impact does not generate sufficient forces to cause the types of injuries seen in SBS cases. Many others disagree, holding that shearing forces tend to rupture the fragile veins across the dural space. These other authors propose ways in which shaking with a rotatory component, possibly at particular frequencies, or with rapid deceleration caused by soft impact (eg pillow, etc), could cause such shearing. In fact, if this view of rotation at particular frequencies is correct, it is likely that the forces required to cause the damage observed may be less important than had previously been thought.

There is no case definition for SBS, and this tends to cause problems in deciding if a particular case is one of SBS. Many authors have taken the view that any unexplained presentation of SDH and RH in an infant is NAI until proven otherwise. While useful as a medical 'rule of thumb,' it should be noted that this leads to a reversal of the burden of proof if applied in a legal setting, and can result in the assumption of guilt in blameless carers. If all unexplained cases are defined as NAI or SBS, then the circular definition results in carers having to prove their innocence, which is logically impossible for this condition. The essential ingredient of SBS would appear to be strong evidence of shaking and NAI. The majority of studies, however, assume that all unexplained cases of SDH and RH are SBS and NAI, and do not determine the degree of confidence that the assumption is correct.

In addition, the actions said to be required to cause NAI have changed over time from fore-aft shaking with impact, to severe and prolonged fore-aft shaking without impact, to rotatory acceleration-deceleration without impact, and more recently to rotatory acceleration-deceleration with soft object impact. Without a clear case definition, and without a means of proving whether an unobserved carer performed the particular actions required, the attribution of unexplained SDH and RH to SBS is neither provable nor disprovable. It is not a question which can be scientifically decided with current knowledge and techniques, and does not meet Popper's test of a valid scientific hypothesis (that an experiment can be defined which could disprove the hypothesis, were it to be incorrect). The diagnosis rests on the presence of sufficient 'other factors' which would raise suspicion of NAI, and the clinical, ophthalmological and radiographic findings become supportive, rather than diagnostic, in such circumstances.

SBS must be intentional, or at least they would appear intentional to any dispassionate observer
This is, again, neither provable nor disprovable. Any concept of intention is not a medical or scientific issue, as it can only be decided by the person accused of shaking. As such, this becomes a matter for determination through the legal process. As the issue is one of degree (some degree of shaking and head movement in infants being an aspect of normal play and day to day life), the matter cannot be decided as it could for impact injuries, suffocation or penetrating injuries (which are not part of a continuum of normal life activities). There are few data or cases in which the precise actions or forces used to create the injuries have been determined or observed.

The lack of observational or experimental data make it impossible to determine what an independent, dispassionate observer would perceive. It may be a reasonable assumption that the rareness of the SBS-type injury (estimated incidence in Britain at less than one in 4,000 children per year - Jayawant 1998) would simply excessive force. This may be a false assumption, however, if the damage arises from a particular type of action, rather than simply being a function of applied force. Rhythmic rotation of the baby at a particular frequency, for example, would be expected to lead to an amplification of applied force and relative motion between brain and skull in the infant. Such shaking may appear to be benign, yet cause significant damage to the dural vessels.

The diagnosis of 'shaken baby syndrome' can be made with absolute certainty on the basis of clinical and X-ray assessment alone
As noted above, typical clinical and radiological changes seen in SBS cannot 'make the diagnosis,' but can strongly support the diagnosis made by other means. If the social and family circumstances are suggestive of NAI, then the medical investigations and clinical findings can increase the confidence that a NAI has occurred, and can help define the likely process of the NAI. The question arises as to how one goes about excluding a diagnosis which has no formal definition, and no unique defining characteristics.

A recent paper (Jayawant 1998) defines a number of characteristics of supposed and "proven" NAI in children in a retrospective study, and the findings of this would appear to suggest a set of criteria which, if applied, may increase the precision of the diagnosis.

Nine factors suggesting NAI are identified in children who have suffered SDH, namely:
Social and family issues

1. Sex of the child allegedly abused? (two thirds are male)
2. Sex of the alleged abuser? (four fifths are male)
3. Is there a past known history of abuse of this child or siblings by this alleged abuser? (about one eighth have previously abused)
4. Is the explanation/history internally consistent? (over half of carers change their stories two or three times)
5. Did the alleged perpetrator admit to shaking? (about half do, eventually)

Investigations and clinical findings

6. Haemoglobin at presentation less than 10 g/L (seen in half of NAI cases)
7. Skeletal survey (positive in 60% of NAI cases tested)
8. Evidence of some trauma or previous trauma (seen in about 60% of NAI)
9. Retinal haemorrhages (present in 80% of cases)

Of the nine proposed key factors in identification of NAI, the number found in any particular case may be important in determining likelihood of SBS/NAI.

The severity of shaking required to cause these findings would have been obvious, and was unrelated to any shaking or corporal punishment admitted to by family members

This can only be decided from an assessment of the social and family circumstances, and a knowledge of the family's past history and even around the time of the alleged injury. Evidence would be required that one of those with access to the infant in the period during which the injury is thought to have occurred had previously shaken or abused either the baby or another member of the family.

Additionally, the person would need to be proven to have the strength necessary to shake the child in the manner thought to be required to induce the injury. Without such evidence, and based solely upon the presence of subdural haemorrhage and retinal haemorrhage, it would seem that the attribution of the pathology to intentional abuse cannot be sustained

Dianne Jacobs Thompson Est. 2007
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