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Shaken Baby/Impact Syndrome:

Flawed Concepts and Misdiagnoses

(Based on a Review of Twenty-Two Cases)

Harold E Buttram, M.D.

September 3, 2002

Introduction:

The following article represents a review of twenty-two cases of shaken baby syndrome (SBS) accusations and/or convictions over a period of approximately three and a half years. Its primary purpose is to offer a composite of information gained from study of these cases to parents or caretakers who have been accused and/or convicted of child abuse in the form of SBS, information which may be of value in their defense. Every effort has been made to maintain simplicity and clarity in the organization of the material. Each section is designed to be complete in itself, and for this reason some portions are repetitious.

Among the many adversities and difficulties facing the American family today, there is a relatively new and growing hazard in which a parent or caretaker may be falsely accused of murdering or injuring an infant by the shaken baby syndrome, when the true cause of death of injury arises from other sources. Very tragically, child abuse does occur and deserves appropriate punishment. However, it is equally tragic when a family, already grieving from the death of their infant, finds a father or mother unjustly accused, convicted, and imprisoned for murder of the infant, a murder of which he or she is innocent. I know of an attorney, an anesthesiologist, a Mormon mother, an Amish mother, and others accused and/or imprisoned (many believe falsely) on charges of injuring or murdering an infant by SBS. It could happen to anyone regardless of race, sex, educational, financial, or social status. It has happened and is happening to more than a few.

Very early in my work with SBS cases I learned of the work of Dr. Archivedes Kalokerinos of Australia who has testified in defense of parents in thirty SBS cases, as well as of others in Australia and New Zealand who have been working in this field for many years. From the experiences of these veteran physicians and researchers, as well as my own, in many cases there has been a time-related onset of signs and symptoms mimicking the diagnostic criteria of SBS following the administration of vaccines. Most other doctors will dismiss this association as coincidental, but this is not reasonable. Coincidental occurrences might be expected occasionally, but not in the high incidence being observed by some. If a large portion of SBS accusations and convictions are the result of misdiagnosis, then we are witnessing a rapidly growing reign of terror against home and family. There is no other term for it.

Medical-Legal Facets of Shaken Baby Syndrome:

By the inherent nature of SBS cases, where a caretaker or parent is alone with an infant at the time of collapse or accidental injury of the infant, it is rarely if ever possible to prove the innocence of parent or caretaker, there being no witnesses to corroborate the stories of the accused person in maintenance of his or her innocence. Defense of these cases, therefore, must be based on evidence showing a likelihood that death or injury of the infant arose from causes other than child abuse. This is done by a careful analysis of the clinical history and findings supported by scientific and medical literature, together with bringing to light the fallibility of current concepts and doctrines surrounding SBS.

It is also done by finding (as one often does) unreserved and vehement support of the innocence of the accused by family or friends.

No one is capable of remaining entirely unbiased in these cases, but I can honestly claim that I have tried to remain objective in evaluation of each of the twenty-two cases. For most I was convinced of the innocence of the accused from the first. There have been several for whom, at first, I held a margin of doubt as to their innocence, but as I probed deeper into the cases, I also became convinced of the innocence of these cases as well. At the present time, in my own mind, I have not the slightest doubt of the innocence of each and all of the cases.

One of the main reasons for my opinion as to the their innocence is a rather strange pattern that often takes place in hospital emergency rooms, where once a suspicion of SBS or non-accidental injury arises, all thought of further diagnostic investigation ceases. I know of no other situation in medicine where the usual diagnostic thoroughness one finds in such centers is abandoned. For this and other reasons, I have not seen a single case where, in my opinion, the prosecution has met the standards of “proof beyond a reasonable doubt,” standards which are supposed to apply in criminal cases. Most do not even come close.

Acknowledgements:

Most of the material and scientific references included in this article has come from other sources. Chief among these has been Alan R Yurko, with whom I have been in constant communication since February, 1999. Other sources of material include friends and colleagues in Australia and New Zealand including Dr. A Kalokerinos, Dr. Viera Scheibner, George Wilson, and Hilary Butler. Contributors of invaluable medical references in the United States include retired pediatrician, FE Yazbak, M.D., Susan Kreider, R.N., Catherine Diodate, B.A., M.A., and Rita Hoffman.

Current Concepts and Assumptions in Diagnosis of SBS – Shaky Foundations:

SBS, sometimes also referred to as nonaccidental injury (NAI) commonly describes a combination of subdural hematoma (brain hemorrhage), retinal hemorrhage, and diffuse axonal injury (diffuse injury of nerve cells in brain and/or spinal cord) as the triad of diagnostic criteria. In some, the presence of rib or other fractures is also taken as sign of child abuse (1-4) These basic concepts, which originated approximately 30 years ago, remain a basis for most SBS accusations and convictions today in spite of newer scientific publications which promise to revolutionize these older concepts.

At the present time the following assumptions concerning SBS/NAI usually prevail in both hospitals and the courts:

- That the severity of shaking force required to produce injuries (retinal and subdural hemorrhages, etc) is such that it cannot occur in any normal activity but is of such violence that untrained observers would immediately recognize it as dangerous and intentional; (5)

- that such central nervous system (brain) injury on an accidental basis can only

be associated with a massive force equivalent to a motor vehicle accident or a fall from a second story building;

- that such injury is immediately symptomatic and cannot be followed by a lucid interval, so that from this reasoning, the last caretaker with the injured child is automatically considered guilty of abusive injury, especially if the incident is unwitnessed; (1, 6-8)

- that changing symptoms in a child with prior head injury is due to newly inflicted injury and not just a rebleed; (9-13)

- that the presence of retinal/subdural hemorrhages in the absence of known disease or accident (as described) above are exclusively diagnostic of SBS.

In a comprehensive review of ethical issues in radiological diagnosis of child abuse, Patrick D Barnes, MD, with the radiology department of Stanford University Medical Center, Palo Alto, California, wrote the following concerning difficulties of diagnosing NAI/SBS in the absence of witnessed or admitted violent shaking:

“This problem is magnified further by the lack of consistent and reliable criteria for the diagnosis of NAI/SBS, and that the vast body of literature on child abuse is composed of anecdotal care series, case reports, reviews, opinion, and position papers…From an evidence-based medicine perspective, quality of evidence ratings for diagnostic criteria regarding the literature on SBS reveal that few published reports merit a rating above class IV (any design where the test is not applied in blinded evaluation, where evidence is provided by expert opinion alone, or in descriptive case series without controls). Such quality of evidence hardly earns a diagnostic criteria recommendation level of “optional,” much less as a “guideline” or a “standard.” (14)

In the remainder of this article various major problem areas will be reviewed showing that not only can there be other causes of the findings now thought to be exclusively diagnostic of SBS, but that these other causes may well comprise a majority

of cases now being diagnosed as SBS. These categories include residual effects of birth trauma, vaccine reactions, respiratory paralysis from accidental (nonviolent) whiplash of the infant’s neck, Barlow’s Disease (rediscovered subclinical scurvy), and a variety of old and newly recognized metabolic disorders:

Residual Effects of Birth Trauma:

One of the cases that I recently reviewed typifies this type of problem where a probable residual subdural or brain hemorrhage from birth trauma was later misdiagnosed as SBS or child abuse. The mother was known to have uterine fibroids from ultra sound exams taken during her pregnancy. Her labor started following spontaneous rupture of the membranes, but after several hours of limited progression, she was started on pitocin drip. In spite of hard labor which went on for several hours there was little progression, and a Cesarian section was performed. The baby died two months later from a massive acute subdural hematoma, but at autopsy an older or chronic subdural hematoma was also found, in my opinion almost certainly the result of birth trauma. The father, who was attending the baby at time of his collapse, was convicted of child abuse and is now serving a prolonged prison sentence.

In analysis of this case, the combination of outlet obstruction from fibroid tumors along with pitocin intravenous drip, must have generated much greater pressures on the fetal head than would take place in normal labor, and so by definition such a birth could be considered traumatic. This is indicated by a survey of retinal hemorrhages conducted at Tel Aviv University Medical Center of 100 newborns following labor induced by intravenous oxytocin (pitocin) or oral dinoprostone, following which retinal hemorrhages were found in 40% of the neonates in the dinoprosone group and 28% in the oxytocin

treatment group. (16)

As stated in Nelson Textbook of Pediatrics, 16^th Edition:

“Traumatic epidural, subdural, or subarachnoid hemorrhage is especially likely when the fetal head is large in proportion to the size of the mother’s pelvic outlet; when for other reasons the labor is prolonged as in malposition…..” (17)

In an article published in Archives of Neurology in 1994, Fenichel and colleagues identified 22 term newborns with intracranial hemorrhage by computerized tomography in an intensive care unit for newborns. Primary subarachnoid hemorrhage was the most common type of hemorrhage, caused either by traumatic deliver or severe hypoxic-ischemic encephalopathy…(18) In a three-year survey at the Southwestern medical Center, Dallas, Texas, 26 near-term and term nonasphyxiated infants were found to have small subdural hematomas on computed tomography. It was concluded that the presence of subdural hematoma is not necessarily always indicative of birth trauma and may occur as sequelae of an otherwise uncomplicated delivery. (19) Patrick D Barnes also commented that “birth trauma may persist beyond the neonatal period and mimic

Abuse.” (14)

Acute Brain Hemorrhage from Pre-Existing Chronic Subdural Hematoma or Malformations such as Hydrocephalus:

In rebuttal to the current SBS doctrine that changing symptoms in a child with head injury is due to newly inflicted injury and not to a rebleed, as outline above, Joseph Piatt reported on a case of retinal hemorrhages and bilateral subdural hematomas in a child with external hydrocephalus following a minor fall. In discussion of the case he wrote:

“The presence of craniocerebral disproportion that develops from any cause – external hydrocephalus, internal hydrocephalus, arachnoid cyst, or chronic subdural hematoma – makes the patient exceptionally susceptible to subdural hemorrhage after what would otherwise be inconsequential trauma….as a result of the vulnerability of the bridging veins.” (20)

Other authors have also reported on similar findings, including the proneness of a chronic hematoma to rebleed with minimal trauma. (21-23, 73)

The Controversy of the Lucid Interval:

In rebuttal to another of the standard SBS doctrines, that an ultimately fatal head injury cannot be followed by a lucid interval (an interval between trauma and onset of symptoms), a retrospective study of 76 children who died from head injuries was done by M.G.F. Gilliland. The children were divided into those who died from shaking, those who died from impact, and those who died from combined of the two. It was found that 20 % of the shaken children and 25% of the impact children had lucid intervals over 24 hours. In the latter groups there were four children for whom the interval was over 72

hours. (56) Similarly in a retrospective report by J Plunkett of 18 fall-related head injury fatalities from distances of 2 to 10 feet, 12 of the 18 children had a lucid interval.(57)

The Vaccine Issue:

Since 1999 there have been ongoing hearings in the U.S. Congress concerning growing concerns about vaccine safety. Primarily these hearings have dealt with concerns about a possible link between the MMR vaccine and the growing epidemic of childhood autism in the U.S.A. Out of these hearings there is now an emerging background pattern of deficiencies in basic science in vaccine testing. As a result of these deficiencies, large numbers of unrecognized vaccine reactions may be taking place, especially reactions of a delayed nature.

Based on these hearings, as a general statement scientific evidence does not support the safety of immunizations in that safety studies on vaccinations are limited to short periods only: several days to several weeks. There are no long-term (months or years) safety studies on any childhood vaccine in use today. In addition, there have been no systematic before-and-after studies on the effects of vaccines on immune parameters and brain function of babies, studies which should be considered indispensable information of a basic science for the vaccines. Inadequate consideration has been given to the additive or synergistic adverse effects of multiple simultaneous vaccines, although in cases of toxic chemicals, two chemicals together may be 10 times more toxic than either separately, or 3 chemicals 100 times more toxic. (24-25)

As one example of the deficiencies in basic science among the vaccines, in 1994 the Institute of Medicine, a federal government advisory board, published a comprehensive review of the safety of the hepatitis B vaccine. When the committee, which carried the responsibility for determining the safety of vaccines by Congressional Mandate, investigated five possible and plausible adverse effects, they were unable to come to conclusion for four of them, because they found that relevant safety research had not been done. Furthermore, they found that serious “gaps and limitations” exist in both the knowledge and infrastructure needed to study vaccine adverse events. Among the 76 types of vaccine adverse events reviewed by the IOM, the basic science evidence was inadequate to assess definitive vaccine causality for 50 (66%). The IOM also noted that “if research,,,(is) not improved, future reviews of vaccine safety will be similarly handicapped.” (26)

Several examples of before-and-after studies from older medical literature will be cited as examples of these deficiencies.

Vaccines and Immune Paralysis:

The first example involves a study reported in 1984 in the New England Journal of Medicine (27) which involved the testing of T-lymphocyte subpopulations (white blood cells which help govern the immune system) in eleven healthy adults before and after routine tetanus booster immunizations. The results showed a significant though temporary drop in T-helper lymphocytes. Special concern rests in the fact that in 4 of the subjects the T-helper lymphocytes dropped to levels found in active AIDS patients. If this was the result of a single vaccine in healthy adults, it is sobering to think of the immune consequences of the multiple vaccines with their immature and vulnerable immune systems. And yet, as far as I am aware, this test has never been repeated.

Comment: In my mind, until this study is repeated and disproved, it would be both folly and insupportable to claim that vaccines are not having an effect in contributing to the increasing patterns of sickness now seen as a matter of common observation in today’s children. In point of fact, reports are now appearing from widely separated geographic areas in which vaccinated children were found to have more allergic disorders (and patterns of sickness) than children with limited or no vaccines. (28-31) (Also see Appendix entitled, “Vaccines and Allergy Citations”)

Vaccines and Seizure Disorders:

For the second example, in 1955 AL Low of Chicago published a study in which he performed electroencephalograms (EEGS) on 83 children before and after pertussis immunization. (32) In two of the children he found that the EEGs turned abnormal following the immunizations without other signs or symptoms of abnormal reactions. In his report he commented:

“This study suggests that mild but possibly significant cerebral reactions may occur in addition to the reported very severe neurological changes.”

Careful search of the literature has disclosed only one similar before-and-after immunization study, one from Japan in which it was found that 61 children with epilepsy or a history of febrile seizures showed significant increases in “epileptic spikes” on EEGs following DTP, DT, or BCG vaccines. (33)

Comment: Both of these studies, the only studies of their kind as far as I am aware, show strong evidence that subclinical brain damage may be taking place on a far larger scale than has been officially recognized.

The Controversy of the Latent Period:

Continuing further with our analysis, there is an admitted problem with the prolonged latent period of about two and a half months between the last series of vaccines on 25 January, 2001 and the seizure which occurred 8 May. For this reason, as an appendix to this report, I am also sending an article entitled “The Controversy of the Latent Period following Immunizations,” which explores this issue in some depth. I will state here, however, that several leading authorities who formerly held positions in the regulation and licensing of medicines in the United Kingdom have published statements that pre-licensing observation periods for vaccines (in this case the MMR vaccine) have been too short to include the onset of delayed neurological (emphasis mine) or other adverse events, (34) one of the former health officers stating that pre-licensing observation periods should have been extended to a year rather than several weeks.

In my opinion the fundamental flaw in current medical legal standards in the U.S.A. for the latent period, and probably also in other English-speaking countries, is that their time limitations allow only for immediate or anaphylactic-type of reactions, by inference denying the possibility or even the existence of delayed-type reactions. This is clearly unrealistic, as delayed-type hypersensitivity directed against the nervous system has been demonstrated by BCG vaccine in the laboratory. (35)

In this regard, two of the vaccines routinely given to children, the Pertussis and Haemophilus influenza vaccines, are known to be potent in causing hypersensitivity reactions. (36,37)

Vaccine Reactions Mimicking the Diagnostic Criteria of Shaken Baby Syndrome:

As previously reviewed, (1-4) shaken baby syndrome commonly describes a combination of subdural hematoma (brain hemorrhages), retinal hemorrhages, and diffuse axonal injury (diffuse injury of nerve cells in brain and spinal cord) as a sign of child abuse. In the absence of known accidental or disease causes, these findings in a child are considered as diagnostic of non-accidental injury or SBS. The following information, however, will show that there may be other causes, among which may be unrecognized vaccine reactions.

In medical research it is standard procedure to develop an animal model of a disease for experimentation before proceeding into human studies. In the case of shaken baby syndrome, these animal models already exist in publications involving pertussis toxin reactions mimicking the diagnostic criteria of SBS.

Studies by Iwasa stressed the finding of brain edema as a feature of pertussis-induced encephalopathy. (38) It is also of interest to point out that there are anecdotal human reports of infants which developed increased intracranial pressure with bulging fontanelles following DTP immunization which tend to support these animal findings. (39-41) In addition, in 1972 Galazka reviewed a series of autopsies on children whose deaths followed the pertussis vaccine/ Although autopsies were limited in number, findings included brain edema, hyperemia, and soft meninges. (42) As will be reviewed in the next section, studies of J Geddes have shown that brain edema in and of itself may result in retinal and brain hemorrhages.

Munoz in turn conducted mice studies with pertussigen, an endotoxin derivative of the pertussis bacteria, in which he found (inflammatory) infiltrates of lymphocytes surrounding blood vessels in the brain and spinal cord, findings compatible with an autoimmune encephalitis. (43)

It is noteworthy that vaccines such as pertussis have been used to induce allergic encephalomyelitis in laboratory animals since 1973, (44) characterized by brain swelling and hemorrhages similar to those caused by mechanical injuries. As another example, in 1982 Steinman and coworkers described mice studies following pertussis immunization as follows:

“Post-mortem examination of the brain (in experimental mice) after immunization revealed diffuse vascular congestion and parenchymal haemorrhage in both the cortex and white matter. Cortical neurons showed ischaemic changes. Occasional areas of hypercellularity were evident in the meninges…B pertussis has a wide range of physiological effects including increased IgE production, increased sensitivity to anaphylactic shock, lymphocytosis, and hyperinsulinaemia. Its ability to induce increased vascular permeability may account for the tendency to produce haemorrhage. (45)

In terms of human studies, I have available a list of 109 references involving reports of adverse reactions from hepatitis B vaccine, a vaccine which appears to be especially prone to be followed by hemorrhagic complications. Among these reactions various forms of vasculitis (inflammation of blood vessels) appear with special frequency, which may contribute to hemorrhagic complications because of greater fragility and friability of blood vessels and consequently may mimic both cutaneous and cerebral hemorrhagic findings now considered to be diagnostic of SBS.

In regard to the issue of retinal hemorrhages, in the text Ocular Differential Diagnosis by Frederick Hampton Roy, M.D., papilledema (swelling in the retinal area) and increased intracranial pressure (from any cause) are listed as possible causes of retinal hemorrhages. (46) DPT vaccine is also listed as a possible cause, along with other routine childhood immunizations (OPV, MMR).

Comment: As stated previously, animal models for vaccine reactions mimicking the diagnostic features of SBS exist for each of the major criteria of SBS. In my opinion, it is only from the lack of basic science in the vaccine field that these reactions very frequently are not being recognized for their true nature and therefore misdiagnosed as SBS.

New Findings that May Change the Diagnostic Criteria of SBS:

As reported in the medical journal, Brain, in a study which may revolutionize current concepts of SBS, Jennian F Geddes, a neuropathologist at Royal London Hospital and colleagues examined the brains of 53 children suspected of dying from deliberate injury. (47) Of the 53 children, 37 were less than a year old.

In the past, brain damage in such circumstances has been blamed on the brain banging against the skull as a baby is violently shaken or struck. It has been thought that this direct assault causes a characteristic kind of damage to the axons of the nerves known as diffuse axonal injury (DAI). However, the researchers found evidence of DAI in only two of the 37 babies. Instead they found that three-quarters of the 37 babies had died because they stopped breathing as a result of previously unseen and undescribed pathology that was focused on the cranio-cervical junction, the area which controls breathing, where the brain meets the spinal cord. When babies stop breathing as a result of this injury, subsequent lack of oxygen causes the brain to swell dramatically, which in turn causes hemorrhagic complications and brain damage formerly attributed to violent shaking or blows.

The cranio-cervical junction is uniquely vulnerable in very young babies, the authors explained, because their neck muscles are weak and their heads relatively large and heavy.

The researchers found subdural hemorrhages in 72% of the 53 cases, although most were too superficial to cause death. Also, retinal hemorrhages were found in 71% of the 38 cases in which the eyes were examined, but the authors felt that these resulted from a lack of oxygen to the brain (and the brain edema or swelling) rather than trauma.

There are scenarios in which such nonviolent, unintentional injuries might take place, as in an accidental fall of a parent or caretaker while holding an infant, the infant in turn receiving a whiplash of the neck and secondary injury to the respiratory center at the base of the brain, or a parent awakening in the night to sooth a crying infant, and the parent still not being fully awake, rocking the baby without adequate head support.

Although vaccines were not mentioned in the Geddes study, it would be very interesting to know how many of these adverse events occurred in a time-related fashion following vaccines.

The Issue of Retinal Hemorrhages:

Based on my own review of medical records involving SBS accusations and convictions, ophthalmologists are always called to examine infants for retinal hemorrhages following hospitalization where there is suspected non-accidental trauma or SBS. Without exception in each of the cases I have seen, the finding of retinal hemorrhage has been considered diagnostic of non-accidental trauma from violent shaking or impact. However, it would appear from the medical literature that others disagree as to the diagnostic specificity of retinal findings. John Plunkett in the American Journal of Forensic Medicine and Pathology made the following statements concerning this issue:

“I do not understand the ‘retinal hemorrhage’ litmus test for shaken infant. No one knows what causes retinal hemorrhage, although it is highly correlated with rotational deceleration injury/subdural hemorrhage in children, but retinal hemorrhage indistinguishable from that found in rotational deceleration may be found in association with ruptured vascular malformations , arachnoid cysts, and CNS (central nervous system) infections. (48)

AC Tongue mentions that “hemorrhages in all layers of the retina occur in a number of nontraumatic disorders associated with changes in cerebrovascular dynamics such as central retinal vein occlusion, high altitude retinopathy, and subarachnoid hemorrhage secondary to ruptured intracranial aneurysms.” (49) Also there is a report of retinal hemorrhages after near drowning (50) and three reports following CPR resuscitation. (51-53) Patrick Barnes reported that retinal hemorrhages may be seen with a variety of conditions including accidental trauma, resuscitation, increased intracranial pressure, increased venous pressure, subarachnoid hemorrhage, sepsis, coagulopathy, certain metabolic disorders, and systemic hypertension. (14)

Diffuse Axial Injury (DAI), the Third Diagnostic Criteria for SBS:

There is no doubt that diffuse axonal (nerve injury) may take place in head trauma. The question is whether or not the pathologic findings described on histologic slides of the brain in the present case, with widespread B-amyloid precursor protein deposits and axonal spheroids, are specific for non-accidental injury or whether these findings are also present in other, non-head injured conditions, including vaccine injury.

Based on the work of F.E. Sherriff and associates, this question can be answered, (54) as described in the following:

“Severe non-missile head injury commonly results in a form of brain damage known as diffuse axonal injury (DAI). The histological diagnosis of DAI is made by silver staining for the presence of axonal retraction balls…We have used immunocytochemistry for the B-amyloid precursor protein (BAPP) as a marker for axonal injury in formalin-fixed, paraffin-imbedded sections of human brain. Axonal BAPP was present in all (23 cases of head injury) that survived for 3 hours or more…...BAPP immunoreactivity was also found in some (5 of 13) non-head injury cases and so cannot to considered to be a specific marker for trauma.” (Emphasis mine)

In a survey conducted at the department of forensic medicine, University of Sheffield, UK, GN Rutty and associates studied sections from a series of brains comprised of four groups: those showing evidence of hypoxia with no history of head trauma, those with head trauma but no evidence of hypoxic change, those with history of head trauma and hypoxic change, and four controls originally described as “diffuse axonal injury.” Using the same staining technique as described above in the Sherriff study, it was found that axonal bulbs may occur from hypoxia in the absence of head injury. It was concluded that “the presence of axon bulbs cannot necessarily be attributed to shearing forces alone.” (55)

Barlow’s Disease (Subclinical Scurvy) Rediscovered:

Physicians and the lay-public alike generally think of scurvy as an historical disease of the days of wooden sailing ships, which was eliminated by the introduction of limes or other citrus fruit into the diet. However, as the younger generations in industrialized nations turn increasingly to commercially processed “fast foods” as a major part of their diets, subtle forms of scurvy may be returning and contributing to the hemorrhagic complications now thought to be exclusively diagnostic of SBS.

In the early 1970s Dr. Archivedes Kalokerinos, then stationed as a medical officer among the Australian aborigines, was troubled by a very high child mortality rate, in some areas approaching 50%. Having observed signs of scurvy in some of the children, and noticing that they often died following immunizations, especially if they had colds or minor respiratory infections, the thought occurred to him that there might be a connection between vitamin C deficiency and deaths following vaccines. With improved nutrition, oral vitamin C supplements, avoidance of vaccines during minor illnesses, and injectable vitamin C during crises, infant mortality was virtually abolished. (58) As a result of this work he was awarded the Australian Medal of Merit in 1978.

One of the primary roles of vitamin C in the body being that of producing and maintaining connective tissue, Dr. Kalokerinos hypothesized that with minor viral infections further depleting an already marginal store of vitamin C, the administration of toxin-bearing vaccines would sweep away the small residual traces of vitamin C, somewhat like a flash-fire, provoking fulminating scurvy with hemorrhagic complications from the weakening of blood vessels. Does such a theory have a foundation in the scientific literature? Based on the following, I believe that it does.

Basic Facts about Vitamin C:

- Vitamin C deficiency still does occur in the Western World. The plasma vitamin C status was found to be depleted, between 0.2 and 0.5 mg/100 ml (or 11 to 28 micromol/L) in 30 %, and to be deficient, below 0.2 mg/100 ml in 6% of people attending a Health Maintenance Organization (HMO clinic) in Tempe, Arizona in 1998. (59)

- The blood leukocyte ascorbic acid concentration is further reduced by infection. Even the common cold causes a fifty per cent reduction of the leukocyte ascorbic acid concentration within 24 hours. (60) Moreover, E coli endotoxin has been shown to inhibit the uptake of vitamin C by mouse fibroblasts in tissue culture. (61)

- When the human plasma ascorbic acid level falls below 0.2 mg/100 ml, the whole blood histamine level is doubled or quadrupled. (62) Ascorbic acid is needed for the conversion of histamine to hydantoin-5-acetic acid and on to aspartic acid in vivo. (63)

- The whole blood histamine level is also increased by vaccines or toxoids, by stresses such as heat or cold, and by various drugs in guinea pigs. (63) Sleep-lack more than doubles the blood histamine levels of resident physicians. (64) Ascorbic acid supplementation rapidly reduces the blood histamine levels of ascorbate-depleted subjects. (62)

- Blood histamine concentration begins to rise when the plasma ascorbic acid level falls below the normal level of 1 mg/100 ml and rises exponentially when it falls below 0.7 mg/100 ml. (62)

- Vitamin C impairs the hydroxylation of proline and lysine, which are essential building blocks for the synthesis of collagen, which forms the foundation for fibrous tissue, cartilage, bone and teeth. (65)

- It is the increased blood histamine, or histaminemia, that causes separation of the endothelial cells from one another in scurvy, (66) which causes the capillary fragility and bleeding of scurvy.

- Humans are vulnerable to vitamin C deficiency as we lack the enzyme, L-gulono-gamma-lactone oxidase, needed to synthesize this essential substance, making us totally dependent on dietary vitamin C from our diet. This is in contrast to most other mammals which are able to manufacture their own vitamin C from simple sugars in the liver.

- Vitamin C protects against diphtheria toxin, (67-68), tetanus toxin, (69) and typhoid endotoxin. (70)

- In 1932 a report on the hemorrhagic complications of scurvy stated that these occurred most commonly beneath the periosteum of the long bones and into joint spaces, but frequently also involved the skin, mucous membranes (gums), orbits (eyes), and serous cavities of the body. (71) One of the most characteristic signs of adult scurvy was swollen bleeding gums, but this is never seen in edentulous infants. It is the bacteria in the crevice between the tooth and the gum that cause local infection and bleeding gums.

With the foregoing information as a background, it is now appropriate to site an unpublished series of cases involving accusations or convictions for SBS largely collected by attorney and jury counselor Toni Blake of San Diego, California (personal communication, 2000), which had the following features: 1) All occurred in fragile infants born from complicated pregnancies. Problems included prematurity, low birth weights, drug/alcohol problems, diabetic mothers, or other maternal complications. 2) All infants were 6 months of age or less. 3) Onset of signs and symptoms occurred at about 2, 4, or 6 months of age, within 12 days of vaccines. 4) All infants had subdural hematomas. 5) Some infants had multiple fractures. In 2000 the series included 25 cases, but I understand it is now much larger.

It is probably in the situations of fragile infants described above that one finds a final common pathway for most major risk factors for vaccine reactions with 1) sub-optimal nutrition including vitamin C deficiency, 2) immature liver and kidneys, where most body detoxification takes place, and 3) in those instances where the baby is on formula instead of breast feeding, increased intestinal Escherica coli colonization. (E coli is a gram negative bacteria with a toxic component in its outer coating). (72) In such situations, the toxins from diphtheria, tetanus, and pertusis vaccines may overwhelm the liver’s marginal detoxification system, sweep away the small vitamin C reserve, and potentially lead to catastrophic vaccine reactions. In my view this is probably the common scenario in which parents are being blamed and accused of death or injury from SBS, when the true causes arose from vaccine reactions.

Among the 22 cases that I have reviewed, infant fatalities, or survivals with residual brain damage, took place in a time-related fashion following routine childhood vaccines, two taking place within hours of vaccines, most others within 11 to 12 days, and one with a delay of six weeks. In most instances the plot was the same: a parent or caretaker was alone with the infant when the infant abruptly went into respiratory arrest and stopped breathing. After initial clumsy attempts at resuscitation, 911 was called, the baby taken to a local hospital emergency room where retinal and subdural hemorrhages were found along with rapidly increasing cerebral edema, invariably followed by a diagnosis of SBS and accusation of child abuse.

What actually happened in each and every instance, in my opinion, was that each infant suffered a vaccine-related encephalitis with onset of brain edema (brain swelling) and secondary depression of the respiratory center. Once breathing ceased, severe brain hypoxia (lack of oxygen) rapidly accelerated the brain edema, followed in turn by retinal and brain hemorrhages.

Acute Autoimmune Hemolytic Anemia from DTP Vaccine:

In 2001 KA Downes and colleagues reported on a 4-month old child admitted to the hospital with fever and increasing lethargy a few days following the second series of routine immunizations, which included the DTP vaccine. By the third hospital day the hemoglobin had dropped to 2.3 grams%. The child subsequently died, but careful evaluation before death identified an acute autoimmune hemolytic anemia from the DTP vaccine. (74) In a review of the literature, 7 other reports of autoimmune hemolytic anemia following DTP vaccines. (If this reaction were routinely sought in hospitals, as it was in the present case, probably the numbers would be much greater).

In my own case reviews there were several admitted to hospitals with hemoglobin levels in the 6s and 7s. One child was admitted with an hematocrit of 6% and a hemoglobin of 2 grams %, dying within hours of admission. In not one of these cases, including the latter, was there mention in the medical records or investigation into a possible hemolytic process.

Bleeding Diatheses from Coagulopathy

In his medical review of the death of Baby Alan Yurko, Dr. Michael D Innis, MBBS, DTM&H, FRCPath, Honorary Consultant Haematologist, Princess Alexandra Hospital, Brisbane, Australia, diagnosed death from intracranial hemorrhage and a bleeding diathesis following a coagulopathy resulting from failure of the liver to synthesize clotting factors in adequate amounts.

Liver failure was diagnosed by significant elevations of liver enzymes and significant lowering of serum albumen, cholesterol, and creatinine, from which it was concluded that there was inadequate liver production of coagulation factors II, VII, IX, and X. (74)

The presence of a coagulopathy, in turn was reflected by an elevated prothrombin time, high D Dimer test, and high fibrin spit products. (Fibrinogen not done) Marked platelet elevation ruled out disseminated intravascular coagulopathy. (75)

In my opinion, bleeding studies of the types described above should be done in all infants or children with retinal/brain hemorrhages before entertaining a diagnosis of SBS. According to Dr. Innis’s report, coagulopathies can result in subdural bleeding, intracerebral bleeding, retinal hemorrhages, bleeding into the spinal cord and into the skin in the form of bruising. (76)

Skeletal Fractures:

Skull fractures:

In cases of suspected child abuse where skull or rib fractures are found in addition to retinal and brain hemorrhages, medical-legal difficulties are greatly increased for the accused parent or caretaker and his or her defenders. Two examples will be given here, one with bilateral skull fractures and the other with four rib fractures. Both infants had fatal outcomes. Both fathers are now imprisoned.

Regarding the former case, the baby with skull fractures, at roughly seven months age the baby was taken to the pediatrician by the parents because of an ongoing intestinal virus infection with a two-week history of recurrent vomiting. In spite of the illness the baby was given DTP, Hib, OPV, and Hep B vaccines during the office visit. (Later investigation revealed that the vaccines contained exceptionally large amounts of mercury in the form of thimerosal). Soon following the vaccines the baby went into a pattern of inconsolable crying. Hours later, while alone with the father, the baby abruptly became apneic (stopped breathing). Resuscitation efforts were futile, and the baby died soon afterwards. Bilateral skull fractures of the parietal bones were demonstrated by CT scans and confirmed at autopsy.

Aside from an accidental fall from a car seat in the home, the skull fractures were unexplained, and the father was accused of violent child abuse and is now in prison.

Present defense of the father now rests primarily on the finding of extremely thin skull bones at autopsy, as reported by the medical examiner during her testimony. On this basis there are several possible and plausible explanations for the fractures other than violent child abuse:

- In the German scientific journal Z Rechtsmed, 1990: 103(4):311-313, W Weber performed postmortem biomechanical fragility tests on infant skulls. As reported in the article abstract, “skulls were dropped from 82-centimeter heights onto (A) stone, (B) carpet, and (c) foam-backed linoleum. 35 further falling tests were carried out onto softly cushioned ground. In 10 cases (D) a 2-cm thick foam rubber mat was chosen and in 25 further cases (E) a double-folded (8-cm-thick) camel hairblanket. Hence the results of altogether 50 tests could be evaluated. In test groups A-C on a relatively hard surface, skull fractures of the parietals were observed in every case; in test group D this fracture was seen in one case and in test group E in four cases. Measurements along the fracture fissures showed bone thickness of 0.1-0.4 mm. The fracture injuries originated in paper-thin single-layerbone areas without diploe, which can also be considered the preferred regions for skull fractures of older infants following falls from low heights. These results indicate that it is no longer possible to assume that the skull of infants is not damaged after falls from table height.”

- In a report entitled, “Fatal Head Injuries from Short Distance Falls,” J Plunkett reported on 18 fall-related fatalities taken from the U.S Consumer Product Safety Commission database for head injury associated with playground equipment. The youngest child was 12-months old, the oldest 13 years. The falls were from 2 to 10 feet. (78)

- Metabolic conditions subject to spontaneous fractures, or to fractures with minimal trauma include scurvy, (vitamin C deficiency), rickets (vitamin D deficiency), osteogenesis imperfecta (79-80), and temporary brittle bone disease (TBBD). (81-82) In regard to the latter, Miller and Hangartner described the condition characterized by transient bone weakness and presenting as multiple unexplained fractures during the first year of life. For this reason it has often been confused with child abuse. In a study involving 26 infants with TBBD it was found that 25 had a history of decreased fetal movement or confinement in limited uterine space during the mother’s pregnancies. Plain X-ray films were normal in all cases, but osteopenia was confirmed by bone densitometry studies. (82)

- In a report by Kirschner in 1985 entitled, “The Mistaken Diagnosis of Child Abuse,” a number of cases were presented in which mistaken diagnosis of child abuse was confirmed. (83) One of these was a case with pseudo fractures from atypical parietal suture lines. An attempted search of the literature on the subject revealed very little, but in the paper-thin bone of the present case, any line of weakness (as with the course of a blood vessel) would be easily separated by the immense hydrostatic pressures generated by the massive brain edema that took place in this case, thus giving an appearance of fractures.

Rib Fractures:

The case with the rib fractures was the infant Alan R Yurko, whose case is thoroughly reviewed on the Yurko website (see reference 77), so that there is no need for confidentiality.

In brief summary of the case, the mother had had almost constant nausea during her pregnancy, initially lost 10 pounds, and barely regained her initial weight by time of childbirth. Birth was premature. Due to this and other complications both before and following birth, it is highly probable that the baby was born with multiple nutritional deficiencies, including deficiencies in vitamin C and vitamin D, and delayed organ development as previously mentioned.

It is very interesting that during the father’s trial, when the medical examiner was giving his testimony to the jury about autopsy findings, when he accidentally dropped one of the baby’s ribs that he was demonstrating, the rib broke on hitting the floor. This alone indicates that there must have been extreme deficiencies of bone connective tissue and calcification.

Be this as it may, explanation for the rib fractures was one of the most difficult aspects of until a voluminous report on the case was received from Dr. Archivedes Kalokerinos of Australia (previously mentioned). In his previous writings Dr. Kalokerinos referred to a previous case with similar findings to those of the Yurko child including, retinal and brain hemorrhages and rib fractures. (84) In this report Dr. Kalokerinos referred to a 1920 text on classical scurvy, which described a vulnerability to fractures at costochondral junctions (areas of connections of ribs to the spine) in the following words:

“Scurvy disrupts these areas (costochondral junctions), the bone breaks down and the ribs ‘overide,’ forming in typical cases ‘beads.’ The healing commences with new born formation looking just like true healing fractures. Furthermore, not all the ribs may be involved in this process and the changes will not all occur at the same time – giving the impression of multiple fractures of different ages.” (85)

This interpretation by Dr. Kalokerinos tends to be corroborated by a report from Hiller in 1972, which states that metaphyseal (costochondral junction) slippage (fragility) could be the result of either rickets or scurvy, and that such findings are of doubtful validity in diagnosis of battered child syndrome. (86)

As another possible explanation for the rib findings, it is known that subperiosteal bleeding (bleeding under the fibrous covering of the bone) is the commonest form of bleeding in scurvy. In the subsequent healing and calcification of the subperiosteal blood clots, X-ray appearances may closely resemble those of healing fractures.

Are There Lessons To Be Learned?

In my opinion, unless doctors become more thoughtful and objective in evaluation of these cases as they come into hospital emergency rooms, the casual diagnostic evaluations commonly seen until now may become grounds for malpractice.

As a very minimum, the following should be added to the usual hospital procedures as routine screening tests when there is suspicion of SBS:

1. With findings of retinal and subdural hemorrhages, check plasma ascorbate and serum histamine, to rule out subclinical scurvy; check prothrombin and partial prothrombin times, fibrinogen level, fibrin split products, and D Dimer test to rule out coagulopathy.

2. In cases of skeletal fractures, test plasma ascorbate and serum histamine along with appropriate textbook tests for rickets; bone densitometry should be done to rule out temporary brittle bone disease.

3. When there is significant lowering of hemoglobin, hematology consult should be requested and the patient evaluated for hemolysis.

4. At the present time there are no officially recognized laboratory tests for diagnosis of vaccine reactions. In my opinion this is largely or entirely due to historical deficiencies in safety testing and scientific infrastructure in the vaccine field. Very sadly, there does not appear to be any official inclination to remedy these deficiencies at time of this writing. We can only hope that new and wiser heads will realize these needs and act upon them.

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76. Ibid, page 1475

77. The Innis report can be found on the Yurko website: http://www.freeyurko.bizland.com

78. Plunkett J, Fatal head injuries caused by short-distance falls, Am J Forens Med Path, 2001; 22(1):1-12.

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81. Miller ME, Temporary brittle bone disease: a true entity?, Seminars in Perinatology, April, 1999, 23(2):174-182.

82. Miller ME, Hangartner, Temporary brittle bone disease: associated with decreased fetal movement and osteopenia, Calcif Tissue Int, 1999; 64:137-143.

83. Kirschner RH, Stein RJ, the mistaken diagnosis of child abuse, AJDC, September, 1985; 139, 873-875.

84. A Kalokerinos, Autobiography, publication pending,

85. Scurvy, Past and Present, Alfred F Hess, M.D., J.B. Lippincott Co., Philadelphia, 1920.

86. Hiller HG, Battered or not – a reappraisal of metaphyseal fragility, Am J Roent Rad Ther & Nucl Med, 1972; 114(2):241-246.

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