The Shaken Baby Syndrome Myth
renamed "Abusive Head Trauma" or "Non-Accidental Injury"



* SBS began as an unproven theory and medical opinions, now discredited by biomechanical engineering studies
* No DIFFERENTIAL DIAGNOSIS done to eliminate other causes, abuse assumed without evidence
* Shaken Baby diagnostic symptoms not caused by shaking
* Child protective agencies snatch children, destroy families based on medical accusations without proof of wrong-doing
*Poor or deceptive police investigations, falsified reports, perjured testimony threaten legal rights, due process
* Prosecutors seek "victory", over justice; defense attorneys guilty of ineffective counsel, ignorance, lack of effort
* Care-takers threatened, manipulated, in order to force plea bargains, false confessions
* A fractured criminal justice system--a big piece for the rich, a small piece for the poor, and none for alleged SBS cases.



Related websites/ important people and projects ShakenBabySyndrome/Vaccines/YurkoProject
"Shaken Baby Syndrome or Vaccine Induced Encephalitis-- Are Parents Being Falsely Accused?" by Dr Harold Buttram, with Christina England (WEBSITE)
Evidence Based Medicine and Social Investigation:
EBMSI conferences, resources and information Articles and Reports
VacTruth: Jeffry Aufderheide; The SBS conection and other dangerous or deadly side effects of vaccination true, suppressed history of the smallpox vaccine fraud and other books:
Patrick Jordan
Sue Luttner, must-read articles and information on Shaken Baby Syndrome: her resources link
The Amanda Truth Project: Amanda's mother speaks out at symposium
Tonya Sadowsky


A report by Archie Kalokerinos, MD

RMB 218ZA Bournes Lane
Tamworth, NSW, 2340, Australia
Ph. 011 61 2 67608166
Fax. 015 61 2 67608344

Part 1……….A simplified study of the medical issues

Part 2……….How I became involved in this complex problem and an explanation why understanding is so difficult

Part 3……… The pathologies of so-called "shaken babies"

Part 4……….The autopsy

Part 6………..Clinical history of Baby Alan

Part 7………..The autopsy report3

Part 8………..Specific disorders requiring discussion [Missing and on request--ed]



This part of the study does not include references because I consider that to add these, at this stage, would make understanding difficult. However, throughout the body of the report, references are quoted in detail

To understand the complex medical issues involved in this case necessitates knowledge concerning several extremely involved issues:
1. Vitamin C
2. Free radical reactions
3. Endotoxin
4. The pathology of infantile scurvy, including the mechanisms responsible for:
A) Spontaneous hemorrhages
B) Bone disorders that, to the uninitiated, look like trauma-induced fractures.

Vitamin C

Vitamin C (also known as ascorbic acid, or ascorbate) is small molecule with a formula of C6H6O8. Its unique chemical properties are responsible for its use, by
nature, in an extraordinary number of complex reactions - where rapidity of action is essential.

Humans cannot live without obtaining supplies of Vitamin C in food. This is because, in common with only a few other species, humans do not have, built in to their biochemistry, the mechanism that allows for the synthesis of Vitamin C

Problems, in humans can arise when supplies of Vitamin C are insufficient for needs. This can occur when intakes are low, or when utilization is high. Individual humans, at various times, may need much more Vitamin C than others. This variation in utilization can, at times, reach a figure of 1,000 times more than the average.

But the problem does not stop there. There is a limit to the amount of Vitamin C that can be absorbed by the human intestine. This means that it is impossible, by consuming Vitamin C by mouth, to attain blood levels of Vitamin C that exceed a certain figure. Unfortunately, there are disease states that can be dealt with only when blood levels of Vitamin C are much higher than levels reached when Vitamin C is taken by mouth. Under these conditions, in order to achieve therapeutic blood levels, one must administer Vitamin C, in large amounts, by injection - either intramuscularly, or intravenously, depending on how rapid an effect must be, or how high the blood levels must be.

Vitamin C takes part in so many reactions, and its use in medicine is so extremely wide and varied, that it is difficult to draw just a few reactions out of the hat and not become involved in lengthy discussions on interrelationships with a vast host of important allied reactions. However, the following list provides the basis of understanding.

Vitamin C is involved in:
1. The production of collagen (connective tissue). This includes the
material that holds bones and blood vessels together. In other words; when
collagen is defective because of a lack of Vitamin C, bones can
break down in various ways and blood vessels can leak and bleed.
2. The control of coagulation/bleeding factors. When these factors are
Disturbed bleeding can occur.
3. The control of what are known as free radical reactions (to be described)
4. The detoxification of a wide range of toxic substances.
5. The control of infections.

Thus, there are two ways by which Vitamin C deficiency/excessive utilization can cause hemorrhages:
1. By resulting in a breakdown of blood vessel walls
2. By disturbing coagulation/bleeding factors

Infections, viral and bacterial, play an important role in this. Several mechanisms are involved.
1. Infections cause an increased utilization of Vitamin C
2. Through increased utilization (or simple Vitamin C deficiency) there is a breakdown in collagen structure.
3. Bleeding can then occur
4. Bleeding can also occur because coagulation/bleeding factors are disturbed.
5. Infections often result in an excessive production (by bacteria) of a toxin known as 'endotoxin'. While attempting to 'detoxify' this, vast quantities of Vitamin C are utilized. This creates what could be regarded as a secondary deficiency of Vitamin C
6. At the same time, the breakdown in collagen structure can alter bone structure and what look like 'fractures' can occur

One question that arises is, why do some infants suffer from these problems and others do not? This is answered in the body of the report.
Then, why do some changes take place in some infants and different changes take place in others? For example, in one infant there may be only intracranial hemorrhage. In another there may only be bone changes. The answer to this is also given in the body of the report.

Free radical reactions

Free radicals are atoms, or molecules (atoms joined together), that are extremely reactive chemically, and extremely toxic, because they have what are known as unpaired electrons.
Electrons orbit around the nucleus of atoms - just as the earth orbits around the sun.
Normally, there are paired electrons that orbit around the nucleus in opposite directions, and it so happens that this arrangement is stable.

A free radical, on the other hand, has an odd number of electrons, with a single unpaired electron in an outer orbit. It is this unpaired electron that is responsible for the instability and chemical reactivity characteristic of all free radicals. Simply by gaining or loosing an electron, any nonradical compound can be converted to a free radical form and thereby undergo dramatic changes in its physical and chemical properties.

Once initiated, free radicals tend to propagate, by taking part in chain reactions with other, usually less reactive compounds. These chain reactions have longer half-lives and, therefore, extended potential for cell damage. Thus the toxicity of a single radical species may be amplified in subsequent reactions.
The stages of initiation and propagation are followed by the stage of termination, at which the free radicals are neutralized either by nutrient derived (food) antioxidants, by enzymes, or by combination with each other. By joining together, the molecules, each of which originally had a single unpaired electron, now have created a larger molecule with paired (shared) electrons. The free radical has, therefore, been 'neutralized'.

The initiation and control of free radicals by free radical scavengers (also known as 'antioxidants') is, therefore, necessary for health and life. It so happens that Vitamin C plays a critical role (as an antioxidant) in the initial control of free radical reactions. Thus, a deficiency of Vitamin C, through any cause (dietary deficiency or excessive utilization) can have rapid and alarming effects. In the brain, in particular, the control of free radical reactions is absolutely critical.

The speed by which brain tissue destruction can be initiated is extreme.. Unfortunately, often, when free radical reactions accelerate in the brain there is a rapid breakdown of brain tissue - and this includes the blood vessels. Under these conditions fresh supplies of Vitamin C, and other nutrients (even when these are available in the blood) cannot reach the damaged brain tissue and recovery may be impossible.


Bacteria produce two types of toxins - exotoxins excreted actively by the organisms, and endotoxin, which normally resides in the walls of so-called 'Gram-negative' bacteria (named because of the staining characteristics). The most common Gram-negative organism is E.coli, which normally inhabits the gut.

Endotoxin is required, as a normal part of the relationship between humans and bacteria, for health. However, under some conditions endotoxin is produced in excessive amounts. These are documented in the body of this report. When this happens the endotoxin, is absorbed through the wall of the intestine (where it can do some damage) and is then carried in the blood stream to the liver where, normally, it is detoxified. However, if the liver detoxification systems are inadequate, some liver damage may occur and a quantity of endotoxin reaches the general circulation. What happens then depends on a variety of conditions.

There may be shock ('endotoxic' shock). There may be disturbances in coagulation/bleeding factors (coagulation problems and/or hemorrhages) excessive utilization of Vitamin C, scurvy bone changes, organ failure, and many others.

The stage is set, therefore, for what are apparently widely different pathologies - hemorrhages, bone changes, shock and others. Sometimes, one pathology may appear to dominate. Sometimes there are multiple pathologies occurring at the same time.

When one form of endotoxin (or toxin) is present alone there may not be, an apparent disease process. When two or more types of endotoxin (or toxin) are introduced together, the effects are multiplied enormously. That is; doses that would normally not cause much damage may be fatal. This, classically, occurs when endotoxin is present because of an infection and another type of endotoxin is introduced in a vaccine.

Worse still is the fact that a sudden extreme sensitivity to endotoxin can occur - somewhat like an extreme allergic response. Under these conditions a previously tolerated dose of endotoxin may cause death.

These pathologies can be very rapid in onset - within minutes or hours. This, unfortunately, is difficult for physicians to accept. They consider that scurvy is a slow onset condition (and, certainly, often, this can be so). But it can be extremely rapid in onset. Early writers, such as Professor Hess, describe how epidemics of scurvy occurred when infections swept through areas. And this did not take more than a few days. Some presentations of acute Vitamin C deficiency can appear within minutes of a deficiency (particularly in a particular organ) becoming established.

To add to this rapid onset of problems it is necessary to realize that endotoxin has an extremely rapid action. So, the combination of Vitamin C deficiency and endotoxemia can result in an extraordinarily rapid and dramatic onset of symptoms - even death.

Vitamin C can detoxify endotoxin. Sometimes, to obtain a worthwhile clinical result, it may be necessary to administer Vitamin C intravenously in big doses.

If the pathology is far advanced, or if a patient's immune responses are extremely poor (as in the terminal stagers of AIDS), then Vitamin C may not function effectively.

Also, as already discussed, particularly in the brain, endotoxin can disturb blood circulation and prevent Vitamin C reaching the damaged tissues.

Various factors can result in excessive endotoxin formation:
1. Failure to exclusively breast-feed - by disturbing the development of
'normal' gut organisms.
2. The use of antibiotics
3. Infections
4. Poor immune responses
5. The administration of vaccines

What to look for when investigating a 'Shaken Baby' case.

1. Signs of an increased utilization of vitamin C (including signs of scurvy and scurvy bone lesions)
2. Signs of free radical reactions
3. Signs of endotoxemia and factors leading to excessive production
4. Signs of coagulation/bleeding disorders.
5. Obviously, also, one does not ignore evidence pointing to guilt.

Only by doing this can a logical, and just, verdict - guilty or innocent - result.


Complete understanding is impossible This is because of the extreme complexity of the medical issues involved. To be able to firmly and logically withstand questioning in court, when faced with 'experts' in various fields, one would need to have ten times the power of Einstein and be an expert (and I mean, a 'real' expert) in every branch of science, chemistry, biochemistry, anatomy, physiology, pathology, microbiology, bacteriology, virology, immunology, radiology, forensic medicine, and whatever. Such a person does not exist. It is important, therefore, that I explain how I became involved in the issue of 'shaken babies', and why I do not accept the views held by a vast proportion of medical authorities.

It began because I made some clinical observations (note that the word is 'observations') that needed to be explained.These observations involved sudden unexpected deaths, sudden unexpected unconsciousness, and sudden unexpected shock, in infants that were either apparently previously well or suffering from a 'trivial' complaint (such as a mild upper respiratory tract infection). Autopsies failed to offer a satisfactory explanation

I found, first, that, provided I began treatment early, I could reverse sudden unexplained unconsciousness, and sudden unexplained shock (remember that I am not discussing infants with conditions such as meningitis) by administering huge amounts of vitamin C by injection. An important detail was that, previous to the sudden collapse, all infants had been supplemented with more than the recommended daily allowances of vitamin C. Something, obviously, was responding to vitamin C, administered by injection, when it would not respond to orally administered vitamin C. And the response was, indeed, dramatic in its rapidity.

Publicity, surrounding my work, eventually brought me into contact with an American research veterinarian (Robert Reisinger, from Baltimore) who introduced me to endotoxin. Endotoxin is a toxin produced by certain types of bacteria. It is necessary for survival of the organisms, and to an extent, for the survival of the bacterial hosts (for example; humans). Sometimes, however, excessive amounts of endotoxin can be produced and this can lead to 'toxic' disease states, or death. There was no doubt that vitamin C, when used in big doses, and administered by injection, 'detoxified' endotoxin. And that was the reason for its extremely rapid action.

Another major advance in understanding came when a microbiologist colleague in Australia (Dr Glen Dettman) gave me a copy of a book (Scurvy Past and Present) written by Professor Hess, in America, in 1920. Many of the references in this report come directly from this book. However, when Hess wrote his book, little was known about endotoxin. Furthermore the main method of production of endotoxin, in the body, has been changed because of:
· The use of antibiotics
· The use of vaccines
This has led to new understanding of the nature of scurvy and the coagulation/bleeding problems associated with it. Now it is common to see cases where the patient's problems are a combination of endotoxemia and scurvy. And each of these- endotoxin and scurvy- when existing in combination, makes the clinical situation much worse. The result is an extremely powerful and dangerous synergism with a complex variety of clinical presentations.

'Scurvy' is, because it is likely to be mixed with endotoxemia, not a good word to use. It is, with modern knowledge, not a specific disease.
In fact, it was never a specific disease. And that is why the recognition of the multitude of variations in its presentation, is so difficult for many clinicians to accept. Rather than use the word 'scurvy' one should use ' reduced intake of vitamin C and/or increased utilization'. Then it is necessary to consider the pathological effects of whatever causes the increased utilization (often, this is endotoxin).


There are two pathologies (abnormalities) that are regarded as 'typical' of the shaken baby syndrome. Other pathologies may be present but the two outstanding ones are:
1. Hemorrhages
2. Fractures

Obviously, hemorrhages and fractures may be caused by trauma.
However, causes may not be associated with trauma. Changes may develop in coagulation/bleeding factors and bone structure, leading to spontaneous bleeding and spontaneous fractures.
It is necessary, therefore, to understand how these changes occur and why coagulation/bleeding disturbances and bone changes are often found together.

Furthermore, bone changes are associated with disturbances in connective tissue structure. Connective tissue disturbances lead to weak blood vessels (the classical feature of scurvy) that add to the causes of hemorrhage. There may, therefore, be lesions of various types found in various internal organs, and these can be mistaken as 'proof'' of trauma. Worse still, the pathologies, often, are of different ages and this is wrongly assumed to indicate multiple acts of trauma.

It is usually possible, while investigating a 'shaken baby' case to determine, in a reasonable fashion, the pathway that ends in hemorrhages and/or fractures.
It is as follows: An increased utilization of Vitamin C, caused by excessive production of bacterial toxins, results in collagen breakdown. This may lead to spontaneous fractures.
At the same time coagulation/bleeding factors may be disturbed - contributing to bleeding.

Several factors contribute to this cascade. These include:
1. Individual susceptibility
2. The administration of antibiotics
3. The administration of vaccines
4. Failure to exclusively breast feed
5. Immune problems
6. Infections

Vitamin C is utilized while attempting to 'detoxify' endotoxin.

A second factor that may play a role in some cases, involves a sudden sensitivity to endotoxin.

Scurvy bone changes
Scurvy type bone changes resemble fractures, and in many cases, these changes actually result in spontaneous fractures.

In bones there are two types of changes that can be mistaken for fractures. The first involves the surface of long bones.
Overlying the surface of a long bone is a difficult to distinguish membrane called the 'periostium'. Normally, this is firmly attached to the bone so, when endeavors are made to strip this from the bone, considerable difficulty is experienced. In infants stripping of the periostium is easier. When scurvy exists the periostium strips abnormally readily - in adults and infants. It is a characteristic feature of scurvy and can be used as a diagnostic test.

In scurvy, the periostium can become detached, to a degree, over a variable area of bone surface. Blood accumulates under the detached periostium. If the patient survives, the collection of blood slowly ossifies. That is; it turns into bone.

This is the same mechanism that nature employs to heal fractures. Initially, there is a collection of blood around the fracture site. Then this gradually changes to bone and the fracture is united.

X-rays, taken during the healing process of the type of scurvy bone lesion under discussion, look like fractures, and during the healing process, look like healing fractures.

These scurvy bone changes may occur in one bone, or more than one bone. Furthermore the lesions may appear at different times so the appearance, on X-rays, is like that of multiple fractures of different ages. Thus accusations are made of multiple acts of traumatic abuse - or 'battering'.

The second type of scurvy bone change is found at the ends of bones where there are (in infants and children) growing plates known as 'epiphyseal plates'. In scurvy cases changes can occur in those areas- particularly where the front of a rib joins the breast-bone - the so-called 'costochondral junction'. This, mostly, appears as a swelling (known as 'beading'). Beading can occur in other conditions, such as rickets (Vitamin D deficiency) but the nature of beading is different to what is found in scurvy.
Sometimes, the area of beading can breakdown. The rib then appears to have been 'broken' and, unless the true nature is recognized, a diagnosis of a traumatic fracture is made. Sometimes all the ribs are involved in this process. Sometimes only one, or more, are involved.

Hemorrhages caused by scurvy
The excessive utilization of Vitamin C causes scurvy, and this can, by itself, cause hemorrhages.
Endotoxin disturbs coagulation/bleeding factors, resulting in hemorrhages in various organs, including the brain and retina - organs that are particularly susceptible to hemorrhages under these conditions.
This almost forgotten knowledge renders the understanding of what is found in so-called 'shaken baby' cases easier to follow.

It is important to know four facts -
1. These changes can occur with startling suddenness and without the
usual signs if 'classical' scurvy.
2. It is not necessary to have septicemia or bacteremia (bacteria in the
blood) to have endotoxemia (excessive blood levels of endotoxin). .
3. Scurvy can occur when the diet contains the recommended daily
allowances, or more, of Vitamin C.
4. All the so-called 'classical signs' of scurvy, as described many years ago,
are now rarely found in a particular case. One possible reason for this could
lie in the fact that the use of antibiotics, vaccines, and a more prominent role
as a result of these factors, of endotoxin, has altered the method of
presentation. A slow onset will present in a different way to a more acute

Recognizing the causes of the pathologies enables one to understand why coagulation/bleeding disturbances, and bone changes (the so-called 'fractures) are often associated together.

For reasons that I cannot understand most forensic and other medical witnesses refuse to accept the mechanisms described above. Each and every detail is substantiated by a vast amount of medical literature, and clinical experience - as this report to the court demonstrates.


This part of the report is without references - a strategy that is deliberate because a long list of references can be confusing to anyone who is unfamiliar with medical terminology and details. However, the detailed report, that follows, includes the necessary references.

The pregnancy

This was Francine's second pregnancy. It was complicated by oligohydramnios (insufficient amniotic fluid that surrounds the fetus in the uterus). At the same time there was gestational (pregnancy diabetes).
It is known that a high blood sugar level, in any diabetic, results in a difficulty in many tissues (including the fetus) of Vitamin C utilization., thus paving the way to potential problems.
Normally, with gestational diabetes the amniotic fluid is present in increased amounts. Some reasons for this include infections (which includes inflammatory responses).
Furthermore, Francine smoked. This is known to contribute to fetal problems.
Francine suffered from infections for which antibiotics were administered. It is known that antibiotics can result in excessive endotoxin production. This, in a pregnant mother can result in disturbances in the fetus.

Because of nausea Francine did not take the usual vitamin supplements. This, in the presence of the problems listed above, increased the chances of disturbances initiated by insufficient supplies of antioxidants - including Vitamin C.

At the 35-week stage, because of some of the problems just listed, the pregnancy was induced.
So there were problems, much more than one would desire, with the pregnancy, and potentially, with the fetus.

At birth

There were marked respiratory problems. Reasons for this, particularly in view of what happened later, were not satisfactorily explained.
Antibiotics were administered. It is known that this can disturb gut bacteria and pave the way for the excessive production of endotoxin.

While breast-feeding Baby Alan Francine was given more antibiotics. These are excreted into breast milk and can add to the production of endotoxin.

Respiratory problems, with Baby Alan, were never totally resolved. The nature of these was never clearly determined.

This concentration on endotoxin production is not just supposition. Baby Alan was never a 'well baby'. His clinical status, at all times, is certainly consistent with the excessive production of endotoxin. This view is reinforced with what happened later, the final collapse, and what was found during the autopsy and the microscope examinations of some tissues.

At the age of 8 weeks (3 weeks past the normal gestational age, because the birth was induced early) 6 vaccines were administered. No warning was given to Francine about certain adverse reaction that can follow the administration of vaccines. This is an issue that is difficult to understand because, for example, with a surgical procedure, a surgeon is obliged to warn about the possibility of even very rare complications.

One of the vaccines was for Hepatitis B. It is known that, sometimes, central retinal vein (the vein in the center of the retina) can become blocked by a thrombus- which is a coagulation/bleeding disorder. This simply illustrates the fact that these disorders can, and do, occur.

Immediately after the vaccines were administered Francine noticed that Baby Alan had a fever, which was followed by feeding/sleeping problems, diarrhea and lethargy. A high-pitched cry developed two days before the final collapse. All this is not consistent with shaking. It is consistent with serious intracranial pathology - including intracranial hemorrhage.

It is necessary, at this stage, to realize that serious intracranial pathology can exist and an examination, even by a trained neurologist, may not reveal an abnormality.

Baby Alan continued to be 'unwell'.

On November 24, while under the care of Mr. Yurko Baby Alan began to 'wheeze'. This was more like 'gasping' for air, with retraction of the chest. Then he stopped breathing. From the time of the collapse to revival in the emergency room there was, apparently, a period of 5 minutes when he did not breathe.

This could be sufficient time for the development of irreversible brain damage. During that time free radical reaction commence and accelerate. Particularly when there is endotoxemia, the brain circulation (almost entirely, or in part) ceases. Oxygen, glucose, and Vitamin C cannot reach the brain, so the free radical reactions cannot be reversed.

The transport team, called to attend Baby Alan, noted one important feature. There was 'mottling' of the skin. Defined as 'various colors without a distinct pattern' this, although not totally diagnostic, I have often observed, can be caused by endotoxic shock.

Unfortunately, at this stage, a diagnosis of 'shaken baby' was made. This became totally ingrained. No attempt was made to consider a 'differential diagnosis' where all possible causes are considered, reasons offered for the exclusion of some, and the inclusion of others. Often, it is necessary to perform special investigations, including laboratory tests, in order to clarify the issue and not overlook any other particular causes.

In this case, very few tests were performed. This included a failure to consider the case history and carry out extensive coagulation/bleeding disorder tests. In this way the possible existence of information that may have been critical for the defense, was not available.

X-rays of the lungs revealed 'bilateral pulmonary infiltrates' that are patches in the lungs where the air spaces are filled with fluid. These cannot be caused by shaking alone, in the absence of lung damage - and there is no evidence of that.

There were, what were diagnosed as 'rib fractures'. These are consistent with 'scurvy bone changes'. This diagnosis was not considered, as it should have been during a proper process of 'differential diagnosis'.

At that stage intracranial and retinal hemorrhages were diagnosed. This, with the rib changes just noted, was sufficient, in the eyes of the doctors, for a diagnosis of one cause, and one cause only - shaking.

Once again, no attempt was made to consider a differential diagnosis. That is; causes for spontaneous bleeding and spontaneous (scurvy) fractures, were not considered. Nor were some difficult to explain features involved with head injuries occurring in infants.

A head injury, even a serious one, in an infant does not necessarily end in a cascade of abnormal reactions - and death. Recovery can sometimes take place to a remarkable extent.

Sometimes there may be a rapid series of, for example, free radical reactions, leading to brain tissue destruction, and death. However, sometimes, remarkable recoveries occur. Some reasons for this are known. One involves the presence or absence of a period of apnea. That is a period where breathing ceases

There are two classical causes for apnea. The first is respiratory arrest, where the lungs cannot supply oxygen to the blood. The second is cardiac arrest, where the blood cannot circulate to provide oxygen to the tissues - including the brain.

The brain is particularly dependant on a continuous supply of oxygen and other nutrients - including Vitamin C. Even a short period of anoxia can result in permanent and irreversible brain damage.

An indirect form of cerebral anoxia can occur when part of, or the whole, of the circulation to the brain is disturbed. One obvious cause for this is strangulation.

Sometimes, there may be a blockage in a blood vessel in the brain - or there may be a burst blood vessel (a hemorrhage) and this can have the same effect.

Therefore if, following a head injury, there is a period when cerebral circulation is disturbed, the outlook is more likely to be serious. This can accelerate free radical reactions that are involved in brain tissue destruction. This is one fairly well understood mechanism, and is one of the reasons for recovery or death. There are other reasons, some of which are not well understood.

Endotoxin can have a specific effect on blood vessels - particularly in the brain. It can damage the lining of blood vessels (known as the 'endothelium'). This allows the endotoxin to leak through to the brain tissue. At the same time this leakage can result in a cessation of the circulation in the area supplied by the endotoxin-induced leakage. This prevents nutrients, and antioxidants reaching the area involved. What follows is a rapid series of free radical reactions - and brain tissue death.

At the same time, blood vessel destruction can result in bleeding. Two other factors then enter into the cascade of abnormal reactions and brain tissue destruction.

First, parts of the brain are rich in iron. Normally, this is 'stored' in a carefully controlled manner because it so happens that free iron is extremely chemically reactive and a powerful initiator of free radical reactions. When endotoxin leaks through to the brain tissue some of this iron is 'released' - and powerful free radical reactions are initiated.

This further damages brain tissue - and hemorrhages can result. This could be regarded as one stage.

Then, after a variable period that can be hastened by endotoxin, red blood cells in the hemorrhagic areas break down (rupture) and release stores of iron and copper. If ever a system was designed to accelerate free radical reactions then this is it. So a secondary, even more powerful series of reactions enter into the cascade.

What this amounts to is this. If, for example, in a serious motor vehicle accident involving brain hemorrhage, no endotoxin or a period of anoxia exists, there is a chance that recovery may take place. On the other hand, if there is a period of anoxia, and particularly if endotoxin is involved, there may be a rapid cascade of free radical reactions and brain death.

Attempts have been made to break this chain of free radical reactions using antioxidants of various sorts (including Vitamin C) but results generally have been disappointing - probably (in part at least) because the cessation of brain circulation prevents antioxidants reaching the damaged areas.

Therefore, while investigating an alleged shaken baby case it is vital to know two facts:
1. Is endotoxin involved
2. Has there been a period of cerebral anoxia
If endotoxin levels have not been estimated and/or the secondary effect, such as coagulation/bleeding disorders have not been investigated and/or problems involving scurvy have not been considered or investigated, it is impossible (without other compelling evidence) to make a diagnosis of shaken baby.

As the main body of this report shows it is possible to estimate endotoxin levels in blood and cerebrospinal fluid during life. And there are special techniques that permit this to be done during an autopsy. Failure to do this denies the defense access to what could be vital evidence.

The Anemia

Why this was present to such a marked degree was never satisfactorily explained. Certainly. It was not due to blood loss in the various hemorrhages because the amount involved is insufficient, by far, to explain it. One explanation, that is compatible with the theme of scurvy that I have considered is that the cause, directly, is scurvy.

Early medical writers document severe cases of anemia in scurvy cases. These references are included in the detailed section of this report. They must not be ignored.


Infections, leading to endotoxin formation, an increased utilization of Vitamin C, disturbances in coagulation/bleeding factors, scurvy type bone changes, and anemia

Any other diagnosis would need to consider all of the factors involved - and this cannot be done.


The autopsy is noteworthy not because of what was done and observed but for what was not done and observed. This was because, at an early stage in the investigation of this case, a diagnosis of shaking was made, ingrained, and, therefore, it was considered that nothing else needed to be considered or looked for.

Contusions and bruises
A very simplified description of what were called 'contusions and bruises' failed to document evidence of dating, There were unanswered (or ignored) questions about the failure to document what was observed before death and during the autopsy.

This failure does not explain why some of the bruises/contusions were not observed before death. So one is left to assume the possibility - indeed, the probability, that some of these lesions made their appearance only after Baby Alan was admitted to hospital. This is not consistent with shaking, or abuse, before, admission to hospital.

This issue may have been settled if a proper procedure for the examination of such lesions had been carried out - as documented in the main part of this report. At the very least, some attempt should have been made to do this. Once again, this failure denies, to the defense, what may have been vital information.

The rib pathology
Most aspects of this have already been discussed. There is a list of procedures that the pathologist failed to do:
1. Did not examine the periostium of the ribs to see how easily it stripped.
This may have produced evidence in favor of a scurvy type lesion.
3. No histology is available. That is; no microscope examinations. This, if
carefully carried out, and perhaps, included electron microscope studies,
may have revealed evidence of scurvy changes.
4. Then there is the matter of a rib that broke (apparently while being handled
normally). This could be because the bone was abnormally fragile. Since proper investigations were not carried out the facts will never be definitely known. Once again, this denies, to the defense, what could be important evidence.
5. Failed to test for bone density - which may have provided evidence of
reduced density, to a significant extent.

It must be remembered, here, that plain X-rays do not necessarily reveal reduced bone density. That is why special machines have been developed for this purpose.

The lungs
It is difficult to assess the pathology, as reported. I would like to leave this to Dr Shanklin -except for a few details.
1. The pathology is not consistent with shaking.
2. 'Mildly hemorrhagic' could mean several things. Hess, whose book on scurvy I constantly refer to, states that 'smaller or larger hemorrhages are described occasionally, which are considered truly scorbutic'. That is; caused by scurvy.

The subdural and other intracranial hemorrhages
The pathologist reported that 'thickened and slightly clotted blood adherent to the dura mater.
Just how adherent is not detailed. Nor, later, is there any record of a microscopic examination of the area where this adherence was observed.
The important issue is that, sometimes, there are what are known as 'neomembranes' in such areas. These consist of fibrous and other tissues that form around old clots. They indicate the existence of old clots and may not be visible to the naked eye. A microscope examination may be necessary before the existence of these membranes can be known. References for this are included in the main body of this report.
Old clots are not consistent with recent shaking - which is what Mr.Yurko was charged.
On the other hand, old clots, with new bleeding are consistent with an old, and ongoing, coagulation/bleeding disorders.

Cerebral (brain) edema and poor differentiation of cortex and medulla
'Edema' means 'excessive accumulation of fluid in the tissue spaces'. Various causes can be considered. Endotoxin damage, with free radical reactions, is a known cause.
The same cause can be applied to the poor differentiation of cortex (outer part of the brain0 and medulla (inner part). These changes are not specific and many forms of cerebral damage can result in these findings.

Failure to perform microscope examinations of the intestine.
This happened because the organs were harvested for transplant purposes. Unfortunately, a careful microscope examination (including, if necessary, an electron microscope examination) may have revealed evidence of endotoxin damage. So this is another potentially valuable piece of evidence that is not available for the defense.

Failure to perform a microscopic examination of the liver
This also denies to the defense what may have been important evidence of endotoxin damage.

Failure to assess the levels of endotoxin in the liver
This needs to be considered in two ways:
1. High endotoxin levels in a donor liver can lead to organ failure after a
2. High endotoxin levels would mean that endotoxemia was present
References for this important issue are included in the full report.
There are, in fact, three issues relating to this:
1. High endotoxin levels in a patient can be the cause of liver failure. This can be seen, sometimes, when, with chronic infections in the bowel, such as ulcerative colitis, excessive endotoxin formation disturbs liver functions and liver tissue to an extent where a transplant becomes necessary.
2. A donor liver containing high levels of endotoxin has a high chance of failing
3. If a transplant is carried out, and the recipient continues to produce excessive amounts of endotoxin (as can happen with ongoing ulcerative colitis) uncontrolled hemorrhage, postoperatively, is more likely to occur. Mechanisms involved include the endotoxin/Vitamin C utilization/coagulation/bleeding disorders in the so-called 'shaken baby' syndrome. So a consideration of this pathology is not just academic.

So, the failure to assess liver endotoxin levels, and to provide information about what happened to the donor liver are important issues.
If the liver transplant failed, or caused serious problems, the possibility is that this could indicate high endotoxin levels'

Apparently, it has not been possible to obtain this information, which could be of considerable value to the defense.

Brain microscope studies
Here, Dr Shanklin's evidence is of extreme importance. It is only necessary for me to highlight two facts:
1. The prime pathology is old
2. There is inflammation that is not consistent with recent shaking and is consistent with what is being considered in this report. That is; endotoxin initiated pathology.

The cause of death - (according to Dr Kalokerinos)
1. Excessive endotoxin formation
2. Excessive Vitamin C utilization
3. Various inflammatory processes in various organs initiated by infections/endotoxin, and the administration of vaccines
4. Scurvy type bone changes - as described
5. Coagulation/bleeding disorders initiated by endotoxin and excessive Vitamin C utilization.
6. Scurvy/endotoxin induced intracranial hemorrhages
Other signs of scurvy, such as anemia, are, of course, part of this picture.
So are the roles played by the administration of the vaccines, antibiotics, infections etc. - as detailed in the full report.


Date of birth: September 16, 1997. Second baby. Mother had gestational diabetes and labor was induced at 35 weeks because of oligohydramnios (reduced fluid surrounding the fetus). The nature of this was not clearly defined. There was no specific history of loss of amniotic fluid. Usually, with gestational diabetes, there is a degree of hydramnios (excessive fluid surrounding the fetus). Furthermore, with diabetes, the babies are usually large.

Therefore, there were two abnormal details here - the oligohydramnios, and the small baby. This suggests that there was present some problem not consistent with diabetes alone. It is possible that this was associated with an inflammatory process - as a reference shortly to be quoted states. The importance lies in what happened to the baby later. An inflammatory process may have set the stage for coagulation/bleeding disturbances, and the excessive utilization of Vitamin C..

There are several known 'causes' for oligohydramnios - placental insufficiency; preclampsia (once called toxemia of pregnancy), post-term pregnancy, and renal malfunctions. The amniotic fluid and blood of smokers is high in cadmium (a toxic element) and low in zinc (that tends to be 'protective). Furthermore smokers who have oligohydramnios have a considerably larger number of still births and babies with central nervous system disorders (Milnerowlez et al, Int j Occup Med Environ Health 2000;13(3):185-93.

Furthermore, oligohydramnios is associated with an inflammatory response in fetal, amniotic and maternal compartments - Yoon et al Am J Obstet Gynecol 1999 Oct;181(4):784-8. The significance of this, in this case, could be questioned, but it points to problems that could add to, or initiate, the disorders later found.

Diabetes (that is: a high blood sugar) interferes with the cellular uptake and utilization of Vitamin C. It is not possible to definitely associate this with what was to follow but, at the least, it had to be an added form of stress to the unborn baby. In addition, the mother had a urinary tract infection. And she was a smoker - another known risk factor. Francine smoked 3-5 cigarettes a day. She was told not to withdraw because this process could cause problems with the fetus. She was, apparently, not told about all the risks smoking subjected a fetus to.

At birth there were marked respiratory problems. Ampicillin and gentamycin were administered. These antibiotics can be lifesaving, and I am not going to state that they should not have been administered. But, sometimes, there is a price to pay for the benefits of their use. One is the overproduction of endotoxin. Another involves disturbances in gut flora, which also tends to result in an overproduction of endotoxin and disturbances in gut immunology. During the pregnancy Francine was also given antibiotics for urinary infections, and bronchitis. This, almost certainly, contributed to the overgrowth of abnormal gut organisms in Francine, including yeast, and the production of excessive amounts of endotoxin - that could have adverse effects on the fetus.

While breast-feeding Baby Alan, Francine was given more antibiotics, and this could contribute to gastrointestinal problems in Baby Alan - including to excessive endotoxin production.

Respiratory problems persisted for some days after birth. This never cleared to a satisfactory degree.

At the age of 8 weeks (which was only3 weeks past the normal gestational age) six vaccines were administered. Satisfactory counseling was not provided. For example, no warning was given about the rare, but well documented complication, central retinal vein thrombosis, that can follow the administration of Hepatitis B vaccine. This, obviously, is a coagulation disorder.

It is known that premature and infants with infections can suffer adverse responses to the administration of vaccines. There is some controversy about how severe an infection should be before vaccine administrations are delayed. But it is known that, even with a mild infection, risks are increased. Francine was not counselled about this, or provided with any information that would allow her to properly understand what risks were involved - particularly in view of the fact that not one but six vaccines were administered. With several factors that increase the risk of coagulation/bleeding disorders already present the addition of one more (hepatitis B vaccine) was obviously risky to an unacceptable degree.

Immediately after the vaccines were administered Francine noticed that Baby Alan had a fever, followed by feeding/sleeping problems, diarrhea, and lethargy. This worsened. A high-pitched cry followed for two days before the final collapse. All this is not consistent with shaking. It is consistent with a condition involving endotoxin, serious disturbances of many vital functions and, almost certainly, the onset of intracranial hemorrhages. It is necessary, here, to remind the court that quite substantial intracranial hemorrhages can exist and not be diagnosed, by a trained neurologist (see references later). Furthermore, there were 'regular' fever bouts from the time of birth to the time of death.

On November 24, while under the care of Mr.Yurko, the baby began to 'wheeze'. This was more like 'gasping' for air with retraction of the chest, and then Baby Alan stopped breathing. There was, apparently, up to 5 minutes of a degree of apnea - from the time of onset of the collapse to the emergency room 's successful revival.

This period of apnea, for 5 minutes, while the brain was denied oxygen, glucose, and other nutrients (including Vitamin C) is almost certainly critical. During that period free radical reactions can commence in the brain and, with the presence of endotoxin, the brain circulation can become irreversibly impaired. The result is a rapid cascade of free radical reactions. These cannot be reversed because the brain circulation (either locally or generally) is impaired and free radical scavengers (antioxidants, especially Vitamin C) cannot reach the site - nor can oxygen and glucose that must be always and immediately available for brain function.

The Transport Team, noted 'mottling' (defined as 'variability of coloring without distinct patterning') of the skin. Usually the skin, under those conditions, shows patches of paleness, redness and cyanosis. It is a sign of 'shock'. This may have various causes. One, I will never forget, because, in the days before I used Vitamin C injections, whenever I saw that in an infant who had suddenly collapsed for no recognized reason, no matter what I did, that infant would die. And autopsies failed to explain why. Now I know that one cause is endotoxemic shock. Several 'shaken baby' cases that I have investigated exhibited skin mottling during the initial phase of collapse. Endotoxin shock is caused by the excessive or uncontrolled production of endotoxin. Thus, anything that can cause endotoxemia can cause it. Shaking a baby will not cause endotoxic shock within minutes of the act of shaking..

There is, therefore, several reasons for concluding that the cause of the pathology found in Baby Alan was not shaking.

Tests revealed bilateral pulmonary infiltrates (patches where the air spaces in the lungs are filled with fluids of various types). These cannot be caused by shaking alone, unless ribs are fractured and during the fracture process the lungs are damaged. In such cases one would expect surface damage to the lungs. There was no such injury noted during the autopsy. Therefore, there must be another explanation for the infiltrates. Whatever it is, shaking was not responsible.

There were what was diagnosed as rib fractures, and subdural and cerebral hemorrhages.

Death occurred 75 hours after admission. This is consistent with a multitude of pathologies. It is certainly consistent with the 'endotoxin/Vitamin C/coagulation/bleeding disorders described above.

A head injury, in an infant, as a stand-alone factor does not necessarily result in death, even after (for example) a car accident with considerable brain damage and intracranial hemorrhages. What sometimes happens, following an accident with such injuries, is a series of free radical reactions leading to brain destruction. Death may then be inevitable. Often, the precipitating factor for brain tissue destruction is a period of apnea - respiratory or cardiac arrest. This allows the initiation of free radical reactions, and, if these reactions are not controlled by antioxidants etc., there will be rapid progress to brain death.

In some shaken baby cases it is assumed that shaking damages the brain in such a way that recovery cannot occur and free radical reactions are initiated. However, autopsies and microscope examinations do not always provide evidence for this. That is probably why, for example, in the Louise Sullivan (Australian Nanny), and other cases attempts were made to introduce an element of anoxia (lack of oxygen) - suffocation, even though the microscope reports clearly stated that the lungs were normal. That is; there was no evidence of suffocation.

Unfortunately, during Baby Alan's last few days of life, extensive coagulation/bleeding studies (beyond some standard profiles) were not performed. Nor were levels of endotoxin in the blood and cerebrospinal fluid carried out. Therefore, the possible existence of vital evidence was denied to the defendant.

It is apparent that, at an early stage, a diagnosis of 'shaken baby' was made and no effort was made to consider a 'differential diagnosis' where one considers the possible existence of factors responsible for the pathologies - apart from shaking. That is where the major error occurred. Further light will be cast on this aspect in the section dealing with the autopsy.

There are many details the must be examined and this includes a consideration of 'definitions' of various medical terms.

A 'contusion' is defined as 1' an injury usually caused by a blow in which the skin is not broken'.
One then needs to consider the definition of 'injury', which is 'any stress upon an organism that disrupts its structure or function, or both, and results in a pathological process. (2) The resultant hurt, wound, or damage'.
Therefore, if one states that the cause is an 'injury' then it is necessary to provide evidence as to why this is so, and to offer evidence why other explanations are not logical.
This is done, usually, by considering (1) the history provided. (2) the naked eye appearance and (3) the microscope findings (this may need to include electron microscope studies). But the issue does not stop there. For example, blood tests may reveal abnormalities that can spontaneously cause the problem. Genetic tests may reveal further abnormalities. And so can some biochemical tests.
In the case under consideration (Baby Alan) these procedures were not strictly adhered to.
Furthermore, in the autopsy report the term 'blunt force injury' is used by the pathologist. This is misleading for several reasons. First, it conveys to the court a distinct (and only) impression that the cause was a blow. And this is done without a consideration of other causes. (that will be detailed later in this report). Then the word 'force' follows 'blunt'. This also conveys something that means 'abuse'. Then, the word 'injury' immediately follows. Therefore, there is reinforcement of what has now become one, and only one, conclusion - that the cause is 'abuse'. If a proper differential diagnosis had been considered and scientific reasons offered for the exclusion of causes apart from abuse, proper scientific methodology would have been carried out. This was not done.

What was referred to as a 'healing contusion' on the left lateral (outer) side of the chest) is noted. Once again, there is no supporting evidence, and no differential diagnosis for this.

Fractures of left ribs, partially healing5, 6, 7 and 10 posteriorly are noted. There is no mention of the fact that the 10th rib broke while being handled. That this occurred is highly suggestive of excessive brittleness - a matter that is discussed at length later in this report. This detail needs to be considered at length because, if it is a fact, it amounts to define evidence for the existence of pathology in bone structure that not consistent with shaking and certainly consistent with a diagnosis of 'temporary brittle bone disease' which in turn is consistent with problems involving Vitamin C utilization/scurvy and, the association with endotoxin (as discussed later in this report).

The lungs were 'mildly hemorrhagic'. One cannot associate this with shaking. But it can be associated with some forms of pneumonia - in which case there would be microscopic (and bacterial or viral culture) evidence of infection. Or it can be associated with coagulation/bleeding disorders. Often, coagulation/bleeding disorders are associated with infections, and this is detailed later in this report.

During the autopsy it was noted that the kidneys were 'very pale'. This needs to be considered in connection with Dr Shanklin's comments regarding the kidneys and failure to thrive. It introduces pathology that, although not specific, is not consistent with shaking.

There was a thin rim of 'ecchymosis' (defined as (1) extravasation of blood into the subcutaneous tissue discoloring the skin (2) any extravasation of blood into soft tissue) in the right lower eyelid. No differential diagnosis is considered and no detailed examination performed to determine the cause. Therefore, particularly in view of facts supporting the existence of a coagulation/bleeding disorder, one cannot attribute this to trauma alone. Unfortunately, the manner by which it is mentioned in the autopsy, gives a distinct impression that there is one cause, and one cause only, and that is abuse.

The same comments can be made for other so-called 'contusions'.

Then there is the question of the age of some of the 'contusions'. During the court hearing it was stated that the contusions were fresh (within 24 hours of death). If this was so then they originated, not at home, but in the hospital. This important issue needs to be considered seriously and in detail. Dating bruises and contusions is, if one attempts to be dogmatic, extremely difficult and open to debate. Mason, in Pediatric Forensic Medicine and Pathology, page 275 states:
The aging of bruises is a vital observation in child abuse, as the repetitive nature of the injuries is often the essence of the differentiation from accident. The colour changes of bruising are not a reliable guide as to their absolute age but the well-known sequence is useful in a relative way, bruises of widely differing hues cannot have been caused in the same 'accident' as is often alleged by parents. The rate of colour change depends on the size of bruises, its depth in the tissues and other idiosyncratic factors which differ from child to child. A small fingertip-sized bruise may pass through the spectrum of blue-red-brown-green-yellow to complete fading in 4-5 days, but more extensive collections of blood can last for two to three times that period. Histology may assist, but many of the claims of exact dating by cellular content cannot be substantiated. Bruises which are obviously of very recent origin may not require histological examinations, but older lesions showing colour changes should be sampled; microscopic examination may, at least, show if the cell population is broadly similar or divergent in different bruises if dating becomes a controversial issue. Faint or doubtful bruises seen on the skin should be incised to confirm or exclude bleeding in the subcutaneous tissues
The issue, however, does not end there. Spontaneous bleeding/ bruises can occur when there are disturbances in coagulation/bleeding disorders and/or connective tissue disturbances - as seen in scurvy. If these conditions are not looked for they will not be found. Furthermore, it is likely, if these conditions exist, that bruises/contusions may originate on different parts of the body at different times - thus creating a false diagnosis of multiple acts of abuse.

What does matter, in the case of Baby Alan, is the failure to observe some of the bruises before death. That is, they were observed, first, during the autopsy. Therefore, it cannot be assumed that these bruises were present when Baby Alan was admitted. If that were so the bruises developed after admission. This means that Baby Alan was abused while in hospital or, more likely, the bruises developed after admission. This would be compatible with a coagulation/bleeding disorder. It is not compatible with shaking.

During the autopsy a note was made about lung congestion and the hemorrhagic appearance. Since Baby Alan was on life support it is possible that these findings were related to the conditions requiring that or to life support measures alone. However, it was known that during the few months of life Baby Alan suffered from respiratory problems and there is insufficient information, at this point, to permit an accurate opinion of the cause. The hemorrhagic appearance is, however, compatible with a bleeding/coagulation disorder.

During the autopsy the subdural hemorrhage showed liquid and clotted blood. At this stage there is insufficient information to enable one to clearly state the exact age of the bleeding. However, it was also noted that the clotted blood was slightly adherent to the dura. This could mean that the clot, in places was old and had formed what are known as 'neomembranes' - where a fibrous shell forms around the clot. This takes time to develop - certainly much longer than the period from the final collapse of Baby Alan and death. This issue is of prime importance. If neomembranes were present they demonstrate old hemorrhage - possibly dating from birth. Proper microscopic examination would cast some light on the age. It is known that these membranes may not be visible to the naked eye and may only be found with the aid of a microscope. A reference regarding this is quoted later in this report.

Once again, we are faced with a situation where the possible presence of evidence strongly supporting the defense was not looked for.

Failure to examine how easily the periostium strpped from the surface of long bones.
A serious omission, during the autopsy, involved the failure to examine the manner by which the periostium (what may be regarded as the 'skin' fixed to the surface of the bone) was attached to the bones. Normally this is not easily stripped (there is a variation in infants and adults). In scurvy it strips readily.
The reason for this lies in the fact that, in scurvy, collagen (connective tissue) is defective. So the normal strong bonds, which are a feature of collagen, are easily broken down. This also, of course, contributes to hemorrhages - when the walls of blood vessels readily break down.
Hess, page 95, summarizes the periostium abnormality:
The susbperiosteal hemorrhage has long been recognized as a lesion characteristic of scurvy…It may, however, involve almost any of the bones…It varies greatly in size, being confined to a small area or extending a long distance on the shaft of the bone…The periostium rarely becomes separated at the line of the junction of the epiphysis (growing end of the bone) and diaphysis (shaft of the bone). The underlying blood (that collects under the stripped periostium) coagulate rapidly (provided that a substantial coagulation/bleeding disorder (such as that caused by endotoxin) does not complicate the issue) and the periostium begins to calcify ('ossify or 'converted to bone') within a few weeks, as shown by the X-rays…
There seems to be some misconception as to the pathogenesis (cause) of the subperiosteal hemorrhage in scurvy. In most reports this lesion is described as if it resulted from a hemporrhage burrowing its way beneath the periostium and raising it from the adjacent bone. In point of fact, such an event is impossible, as will be fully realized when one experiences the great difficulty in separating periostium from normal bone. Scurvy involves a periostium which is not normal; it is insecurely attached to the shaft of the bone, so that it is readily stripped off by hemorrhage.
Sometimes, however, the epiphysis (growing end of the bone) is directly involved in scurvy. It can, in a fashion, 'fall, or break apart', or it may swell - as seen in the so-called 'beading' found, often, in the costochondral junctions (where the shafts of the ribs join the cartilages of the breastbone). There can be a substantial amount of hemorrhage involved in this process. If the periostium on the shaft is elevated at the same time, with underlying hemorrhage, the two hemorrhages coalesce, and as ossification proceeds, the entire area becomes involved in new bone formation. This can be easily mistaken as 'traumatically induced' - that is; as evidence of battering.

It is necessary, at this point, to note that other so-called 'classical' signs of scurvy bone changes need not be present when the pathologies, noted above, are found. That is; their absence does not exclude a diagnosis of scurvy. This great variability in the presentation of scurvy has been documented by Hess. Furthermore, much depends on precipitating factors, the length of time involved, and the possible involvement of endotoxin which was not seriously considered at the time that Hess made his studies.

Therefore, one cannot exclude a diagnosis of scurvy because all of the classical bone changes were not apparent.

Cause of death (according to the pathologist): Subdural hemorrhages due to shaken baby syndrome.

Comment, by Dr Kalokerinos, about this diagnosis of the cause of death
Without excluding causes of spontaneous hemorrhages, such as coagulation/bleeding disorders one is not entitled to arrive at this conclusion - unless there is clear evidence of shaking. That is; the existence of hemorrhages alone is not proof of shaking. It is necessary to demonstrate that a coagulation/bleeding disorder does not exist before a diagnosis of shaking can be established.
Lund et al, Ugeskr Laeger 1998 Nov;160(46):6632-7, states:
Shaken baby…A combination of subdural haematomas and retinal haemorrhages with minimal or no trauma is almost pathognomonic of the syndroma.
Note the word almost' is used - which means that other factors must be also considered.
Furthermore, as discussed later in detail, a normal standard coagulation profile does not totally exclude a coagulation/bleeding disorder. And it is possible for an infant to have a normal coagulation/bleeding profile and spontaneously bleed severely.
Br Med J (Clin Res Ed)1982) July 10;285(6335);133-134, states:
Severe bleeding disorders in children with normal coagulation screening tests.
Note that the word 'screening' is used. This is because only a limited number of tests are performed and those that are selected will detect the majority (and therefore, not all) of the abnormalities. Therefore, serious disorders may not be detected during screening tests.

This is the critical detail that one must understand before considering every other detail in this case. If this is not done it will be impossible to follow the evidence in a manner that will enable one to arrive at a logical verdict.
There will be a lengthy elaboration on this later in this report.

The autopsy report continues with some other findings:
A. Contusions, minor, on both temporal areas of the head.
B. Periorbital ecchymosis, (defined as 'an extravasation of blood into the subcutaneous tissues, discoloring the skin') right lower eyelid.
C. Subdural hemorrhage (defined as 'a collection of blood under the dura which is the outer layer, of three, coverings of the brain), fresh, right and left cerebral hemispheres, predominately right
D. Hemorrhage at the base of the brain
E. Subarachnoid hemorrhage (defined as 'blood under the arachnoid covering of the brain, which is the middle of the three coverings'), thin layer, biparietal (the right and left parts of the skull) areas minimal
F. All cranial bones intact
G. Subdural hemorrhage, lumbar and lumbothoracic region of the spinal cord.
H. Vertebral arteries and dissection of the neck - unremarkable.

Blunt force injury of the chest
The use of the word 'blunt' and the reasons why it is a misleading word have already been discussed.
A. Healing contusion, left lateral chest
B. Fractures of left ribs, partially healing 5,6,7 and 10 posteriorly.

Lungs - mildly hemorrhagic. Air passages clear.
Kidneys - very pale.
No hemorrhages at the thoracic, lumbar or sacral spine
Buttocks - no superficial or deeper contusions

Description of injuries (external)
Right, lower eyelid - a thin rim of ecchymosis. Pinkish in color and measures 1x0.2 cms.
On the left temporal area, slightly above and in front of the tragus of the left ear, there is a very pale area of contusion measuring 12x16mm. Its edges are irregular and appear diffuse. There is no change in coloration from pink to green to yellow, etc. The color in general appears a very pale, pink.
On the right temporal area there is a very pale contusion, of similar appearance, measuring 10x9 mm. The auricle of the right ear shows similar pale appearance, which is diffuse, and measures 15x4 mm. Its distribution is more towards the posterior surface of the middle portion of the right auricle. On the parieto-occipital regions (the parts of the head on the back of the sides) of the head bilaterally, the scalp shows a slightly pinkish discoloration of the skin. On the right side there appears to be a small impression mark from some medical monitoring device.

On the left lateral surface of the chest there is a very pale, slightly pinkish, ovoid, healing type contusion measuring 10x8 mm. It is located in the region of rib 7. Palpation of the chest does not reveal any evidence of subcutaneous emphysema.
Internal examination
On the left side of the chest, the following ribs showed irregular swelling, probably resulting from healed fractures: left rib 5, 6, 7 and 10. The fractures are located on the posterior and posterolateral surfaces of these ribs. X-rays are taken and confirm the presence and positions of these healing fractures. Multiple sections are taken for histopathological study.

Note that no report could be found in the notes provided to me about what was seen under the microscope when these ribs were examined. Nor was any attempt made to discover if the periostium (fibrous tissue 'skin over the bone surface) stripped easily - as it may do when scurvy is present.

Both lungs appear congested and show irregular areas of hemorrhagic appearance.

Systemic examination of the body.
Subdural hemorrhage, prominently seen on the right cerebral hemisphere, is noted. This hemorrhage is in liquid as well as clotted form, total weight is about 10 grams. There is subdural hemorrhage on the left cerebral hemisphere posteriorly. This hemorrhage is relatively less prominent as compared to the right. The dura mater of the cortex of the cerebral hemispheres shows thickened and slightly clotted blood adherent to the dura mater. At places the thickness of this clotted material is between 2-4 mm. The entire surface of the dura mater appears wet, and as mentioned previously there is liquid and clotted blood.
The brain is edematous, shiny and symmetrical. There are minor areas of subarachnoid hemorrhage seen in the cerebral hemispheres. One area of hemorrhage is located on the medial aspect of the parietal lobe measuring 3x2 cm. A similar small area of subarachnoid hemorrhage is also seen on the right cerebral hemisphere on the posterior parietal lobe.

Brain examination with Dr Pearl.
The brain appears very edematous, shiny and fluffy. There are areas of subdural hemorrhage which appear relatively fresh. There are minor areas of subarachnoid hemorrhage on the left parietal lobe. Serial cut sections of the brain do not show any internal hemorrhage in the brain parenchyma grossly. Cerebral edema is confirmed. Differentiation of the cortex and medulla appears poor. The ventricles are slightly reduced in size and the cerebrospinal fluid appears clear. The eyeballs are examined and these are also sectioned for confirming the presence of retinal hemorrhages.
It is noted that there is a small quantity of hemorrhage in the subdural space of the spinal cord representing the areas of thee lower thoracic, lumbar and sacral regions. At the base of the brain on the right side middle cranial fossa and the major part of the posterior cranial fossa on the right side contain a small quantity of blood. On the left side a very small portion of the left middle cranial fossa and the posterior cranial fossa show presence of blood.
Organs of the thoracic cavity.
Both lungs are congested. Externally, the lobes of the lungs show evidence of hemorrhages. On serial cut section both lungs show irregular areas of hemorrhages.

Comments (by Dr Kalokerinos)
The cause and nature of the lung hemorrhages need to be considered. One would expect, if the cause was trauma (fractured ribs) that there would be some damage to the pleura (covering of the lungs. And one would expect that the hemorrhages would be related to the ribs fractures. No evidence for this has been presented. Even if one assumes that a relationship with the rib fractures is 'apparent' then one must still exclude coagulation/bleeding disorders - particularly since it is known that spontaneous bone fractures, and elevations of the periostium with blood clots beneath the periostium, that became organized, then changed to bone, and resemble, in X-rays and scans trauma initiated fractures, are a feature of scurvy. Furthermore, the disturbances leading to scurvy (Vitamin C utilization and endotoxin) also may lead to coagulation/bleeding disorders. Therefore, the pathology under consideration need not be caused by shaking.

Organs of the abdominal cavity.
The kidneys show fetal lobulations and on serial cut section appear very pale.

Musculoskeletal system.
A few very pale contusions are noted on the bitemporal regions of the head. A very faint contusion is also noted on the left lateral side of the chest. The left 5th, 6th, 7th and 10th ribs show old healing or partially healed fracture sites. These fracture sites appear as globular masses of cartilaginous tissue. Cut sections of these healing fractures show normal appearance of the cartilage.

Comments (by Dr Kalokerinos)
Scurvy bone lesions heal in the same way that fractures heal. Furthermore, the note by the pathologist ('old and partially healed fracture sites) suggests to those who are not aware of other causes, very strongly, that this pathology represents multiple acts of abuse. To arrive at this conclusion one must exclude scurvy. The pathologist did not do that and, therefore, cannot justify his conclusion.

The pathologist detailed retinal hemorrhages. There is considerable confusion about these. Dr Gold stated (court records page 204), 'The right eye had diffuse scattered interretinal hemorrhages and preretinal hemorrhages meaning blood in the back of the eye. The left eye appeared to be normal.'
Dr Pearl stated (pag315), 'There was only one minute hemorrhage to the right eye only'.
Dr Gore stated (pages 271-272), 'There were minute hemorrhages in the retina…It was on the right eye.'.
Dr Shanklin noted one small retinal hemorrhage. More important was his observation of chronic inflammatory white cells - long standing in nature. He dates these changes to 'weeks, perhaps months'.
There is, therefore, room for controversy surrounding the nature of the retinal hemorrhages. This simply adds to the degree of difficulty when attempts are made to analyze the evidence.

Comments (by Dr Kalokerinos). These 'old' inflammatory changes are not characteristic of recent shaking. There are compatible with long standing inflammatory responses associated with infections (and almost certainly, endotoxin). It is also compatible with the diagnosis of infections, endotoxin, coagulation/bleeding disorders and scurvy.

Microscopic examination.
Lungs: The alveolar spaces are uniformly inflated with evidence of a few red blood cells and clumps of inflammatory cells. The inflammatory cell infiltrates are scattered throughout one section. There is no evidence of bronchopneumonia or lobar pneumonia. This picture appears somewhat similar to interstitial pneumonitis.

Comments(by Dr Kalokerinos). Interstitial pneumonitis is a complex condition. It is a diffuse (spread out) disease of the lungs and is a reaction to diverse 'irritations' that can be inflammatory in nature (for example, infections), but the cause is often obscure. The important issue is that the pathology is intraalvoar - that is there is infiltration (fluid or cells, for example) into the air sacs (alveolar spaces).
Causes are numerous. Included are infections, excessive fluid in the lungs, and hemosiderosis ( an iron containing substance, from broken down red blood cells), what is known as 'hypersensitive pneumonia' (allergic response). Whatever the cause, in Baby Alan, this represents an allergic/inflammatory response. It is not consistent with shaking.

Kidneys: The tubules show minimal vacuolation of the cells, consistent with an early degenerative change but no acute tubular necrosis is noted.

Brain: There is no evidence of inflammatory cellular infiltration. The two sections which are stained with H and E show presence of very minute parenchymal hemorrhages
One section of the cerebellum shows evidence of shearing type injury with multiple foci of minute hemorrhages.

Comment (by Dr Kalokerinos)
There is no detailed description of what is meant by 'evidence of shearing type injury'. The term, in itself, when used in this fashion can be misleading.
First; it assumes (and thus sows in the minds of those who are considering the evidence) a concept that dogmatically implies 'injury'. This is a serious error for several reasons:

1. The cause is not always an injury, (defining, 'injury', considered in this context, as 'something inflicted by a person').
2. Anoxia (lack of oxygen) can cause the condition
3. There is no detailed description of what was actually seen - just a 'diagnosis'.
4. The slides were not made available for examination in court.

Geddes et al, Neuro Pathol Appl, Neurobiol 2000, April 26 (2):105-16 states:
They have revealed a whole new field of previously unrecognized white matter (brain tissue) pathology, in which axons are diffusely damaged by processes other than head injury: this in turn led to some terminological confusion in the literature. This matter is detailed, further, later in this report.

Eyeball sections: The right shows definite evidence of minute retinal hemorrhage.
Spinal cord: Minute epidural hemorrhages are seen on the cord at C5 and C6 corresponding areas.

A serious omission
In the case notes provided to me I could find no reference to microscope reports on the rib fractures. A careful examination of the fractures may reveal evidence of scurvy-like changes. Many sections should be examined because the changes may be difficult to recognize. Related to this is the failure to examine the periostium of the ribs to see if it stripped easily, as it may do when scurvy is present. This has already been discussed.

CONCLUSION: (by the pathologist): This 2 month old black (should be 'white) male infant died as a result of Shaken Baby Syndrome. There are old healing fractures of the left ribs. Subdural hemorrhage is recent.

Comments (by Dr Kalokerinos).
The contusions - Discrepancies between what was documented before death and what was documented after death.
Therefore, there is no evidence that they existed before death, and it follows that the nature of the lesions and their ages must be carefully considered.
By definition, a contusion is an injury where the skin is not broken. A bruise is defined as an injury producing hemorrhage beneath unbroken skin.
These definitions are not absolutely specific because the word injury suggests just that - an injury. Hemorrhage beneath unbroken skin can be caused by a great variety of conditions apart from injuries - such as coagulation/bleeding disturbances. And bruises and contusions can overlap in nature.
Unfortunately, when these words are used in reports it is natural, for many non-medically trained, and some medically trained individuals, to immediately and totally imagine that the cause of the pathology is an injury.
So there are two things to consider -
1. The ages of the lesions and
2. Is there any evidence that suggests the presence of a coagulation/bleeding disorder and/or an inflammatory process?

Mason'stext book Paediatric Forensic Medicine and Pathology ISBN 0 412 29160 6, page 275, states:
"The age of bruises is a vital observation in child abuse, as the repetitive nature of the injuries is often the essence of the differentiation from accident. The colour changes of bruising are not a reliable guide as to their absolute age but the well-known sequence is useful in a relative way; bruises of widely differing hues cannot have been caused by the same 'accident' - as is often alleged by parents. The rate of colour change depends upon the size of bruise, its depth in the tissues and other idiosyncratic factors which differ from child to child. A small fingertip-sized bruise may pass through the spectrum of blue-red-brown-green-yellow to complete fading in 4-5 days, but more extensive collections of blood can last for two or three times that period. Histology may assist, but many of the claims of exact dating by cellular content cannot be substantiated. Bruises which are obviously of very recent origin may not require histological examination, but older lesions showing colour changes should be sampled: microscopic examination may, at least, show if the cell population is broadly similar or divergent in different bruises if dating becomes a controversial issue."

Faint or doubtful bruises seen on the skin should be incised to confirm or exclude bleeding in the subcutaneous tissues. In the case of Alan Yurko none of this was done. The evidence, though not totally conclusive, may have been significant.
Furthermore, because most of the lesions were not observed when Baby Alan was admitted, and during the period he was alive in hospital, one cannot exclude the possibility that the lesions developed after admission.
Since, from soon after admission, a diagnosis of 'abuse' (shaken baby) was made one would expect that a careful note would have been made of signs, such as bruising on parts of the body, that would (in theory) support the diagnosis. In other words, the fact that most of the bruises/contusions noted during the autopsy were not noted on admission is very significant.
There are other issues involved in this. A careful, microscopic examination (and, even better, an electron microscope study) may have revealed evidence of scurvy - such as changes in the blood vessel walls and connective tissue.
One detail is certain. That is; the possibility that the lesions were scorbutic in nature. If one does not look, then one will not find this. In view of other evidence that strongly suggests that scurvy was a factor the failure to look becomes an important issue.

Dianne Jacobs Thompson  Est. 2007
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