The Case of Alan Yurko (Florida, USA)
—an introduction and explanation
Revised - Page 3


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In practice, I used a specially devised instrument called a 'petechaeometer'. This was like a small bicycle pump, with a domed cup at one end. A piston produces a vacuum in the cup, which is held in contact with the skin. The vacuum 'sucks' up the skin, and it is possible to count the number of petechial spots in the area occupied by the suction cup, in a selected period of time. There is no doubt that this is a useful test when one is attempting to clinically diagnose scurvy when other, classical signs, are absent or difficult to assess. I must stress that the test is not specific. To a degree it measures 'capillary fragility' which is disturbed in Vitamin C deficiency and endotoxemia.

The high platelet counts

The first specimen of blood examined after admission following the acute collapse, showed a significantly high platelet count. This is another complex issue and open to discussion and debate. However, what is known about it must be considered in this case. One well documented coagulation/bleeding disorder following cranial trauma is called 'disseminated intravascular coagulopathy' (DIC).

Levi et al, the New England Journal of Medicine, August 19, 1999, pages 586-592, state:
Disseminated intravascular coagulation is characterized by the widespread activation of coagulation. At the same time, the use and subsequent depletion of platelets and coagulation proteins resulting from ongoing coagulation may induce severe bleeding. Bleeding may be the presenting symptom.

Associated clinical conditions: It is an acquired disorder that occurs in a wide variety of conditions...the most important of which are listed: sepsis, trauma, head injury, serious tissue injury, fat embolism, cancer, obstetrical complications, vascular disorders, reactions to toxins, immunologic disorders.

Diagnosis. There is no single laboratory test that can establish or rule out the diagnosis. In clinical practice the disorder can be diagnosed on the basis of the following findings: an underlying disease known to be associated with DIC, an initial platelet count of less than 100,000 per cubic millimeter or a rapid decline in the platelet count.

Obviously, baby Alan did not have DIC. But he did have a coagulation/bleeding disorder.

Kuhne et al, Division of Oncology/ Haematology, University Children's Hospital, Postfach, Basel, Switzerland; Eur J Pediatr Feb;157(2):87-94, state:
Platelets contribute to primary haemostatic events and are closely linked to plasmatic coagulation. Their function is highly dependent not only on their number but also on their integral physiology. In comparison with adults or children, the haemostasis of newborn infants, although physiological, is characterized by reduced functional reserve capacity leading to rapid occurrence of bleeding disorders especially in the presence of additional risk factors such as prematurity, asphyxia, or infection. Morphological and biochemical differences reflect an immature cellular stage which results in platelet hyporeactivity and contributes to the reduce capacity of the neonatal haemostatic system.

Additionally acquired and inherited platelet disorders markedly affect platelet function. Hence assessment of neonatal platelet physiology may supply important information; however, no adequate screening tests are currently available, and technical difficulties of blood sampling limit the value of laboratory testing. Evaluation of the neonatal platelet functions highly dependent on individual laboratory results and it advisable to perform complex diagnostic procedures with the collaboration of specialists experienced in neonatal haematology. With the advent of new technology such as platelet flow cytometry more adequate tools are available, although still reserved for specialized laboratories, thus awaiting their clinical significance. The role of maternal influences on neonatal platelet function must always be considered. Thus, neonatal platelet physiology and pathophysiology is complex and requires more studies and experience.

During the acute collapse, baby Alan was not neonatal, which usually means 'under the age of one month'. However, he:
• was premature
• was a 'sick' baby from day one
• had respiratory distress syndrome
• had 'sepsis' at birth and later.

The reference just quoted shows:
• the extraordinary complexity of the issue (as stated previously)
• that laboratory tests are difficult to perform and do not always display a problem that may be present.

The problem of coagulation screening tests is again noted in the following article:

Br Med J (Clin Res Ed) 1982 Jul 10;285(6335):133-134:
Severe bleeding disorders in children with normal coagulation screening tests.

What came first—the cerebral hemorrhage, which can trigger coagulation disturbances, or did abnormal coagulation/bleeding factors cause the hemorrhage? This is a critical issue, and the case history is of prime importance.
• The tests performed cannot exclude a primary coagulation/bleeding disorder
• The article by Goldwater et al, in The Medical Journal of Australia (already quoted) does provide some evidence for a primary coagulation/bleeding disorder. This article was initiated by the observation that 'Liquid (unclotted) blood is an almost invariable finding in the sudden infant death syndrome'. It considers the extraordinarily high levels of D-dimer in SIDS cases compared with infants and children who died following, for example, from motor vehicle accidents.

As already stated in this report, the D-dimer levels in the case of baby Alan were >8.00. That is 'greater' than 8.0. Most hospital laboratories do not estimate how much above 8.0 the levels are. There is enormous controversy surrounding the significance of high D-dimer levels in infants. I present it here as a positive point that, at the very least, cannot be ignored.
• The rib and acromion pathology are consistent with infantile scurvy.
• Reasons for a problem involving the utilization of vitamin C have been discussed.
• The role of endotoxin has been discussed.
• The role of vaccines has been discussed.
• There were abnormal liver function tests, which sometimes, can indicate endotoxemia.
• 'Sepsis' was present at birth and again later.
• Antibiotics were administered at various stages. This can result in the liberation of excessive amounts of endotoxin.

Unfortunately, some tests that may have confirmed the presence of excessive amounts of endotoxin were not done:
• direct assays in the blood during life or at autopsy
• microscopic (and careful) examination of the small intestine for signs of damage (for example, minute ulceration) due to endotoxin
• some tests for endotoxin induced disturbances of platelet and other coagulation disturbances
• full examination of the cerebrospinal fluid for cells and culture (viral and bacterial).

I understand, of course, that some of these tests are not routine. But in cases like the Yurko one they should be done.

Then there is the evidence of Dr. Shanklin. There are many features in the intracranial pathology that suggest the existence of 'inflammation'. Dr.Shanklin could clarify some differences between injury and inflammation. In view of what is known about endotoxin/vitamin C utilization/coagulation/bleeding factors, his evidence should be reconsidered.

The hemoglobin was very low—7.9, on 11/26/97 (normal - 12.1-17.3), and while this can be interpreted in various ways (for example, due to 'sepsis') it can logically be attributed to scurvy. On that date, the MCH (mean corpuscular hemoglobin) was 29.6, which is near the low end of 'normal' (normal 28.0-40). It is not possible to explain this very low hemoglobin, etc., by saying that it was 'sepsis'. The sepsis was not severe enough. Certainly, one could state that the low hemoglobin had existed for a long period, and that is possible. But an explanation is still required. Nor is it logical to say that the low hemoglobin was due to the cerebral hemorrhages because the amount of blood lost in the cranium is not sufficient to explain the low level. Hess provides a possible explanation.

On page 209, referring to scurvy he states:
The hemoglobin is greatly diminished.

This 'anaemia' was a common finding in scurvy cases before and during the time when Hess wrote his book. With modern knowledge there is no doubt that the nature of the anemia is complex. In some cases it appears to be more or less 'specific'. In others the presence of infections (and endotoxin), with gastrointestinal disturbances, influences the picture. When scurvy alone is the specific cause, the response to vitamin C administration can be dramatic. Oral doses may be sufficient, but when infections and gastrointestinal disturbances are major factors it is necessary to administer vitamin C by injection and to deal with the underlying causes.

Although there is certainly no guarantee that such strains existed in baby Alan's gut, failure to look for them denies access to what may have been important evidence. In SIDS cases, for example (and there is no need here to directly prove an association with SIDS in Alan Yurko's case) the following reference illustrates what is involved.

Bettelheim et al, Department of Clinical Pathology, Fairfield Hospital, Victoria, Australia; Scand J Infect Dis 1990;22(4):467-76, state:
This high incidence of toxigenic E.coli among the SIDS infants versus the low incidence in controls, together with the general rarity of finding such toxigenic E.coli in the community made us conclude that there may be a causal relationship between toxigenic E.coli and SIDS. The O and H serotypes of the toxigenic E.coli associated with SIDS infants tended not to be those normally considered to be toxigenic. This toxigenicity appeared to be relatively labile. It is suggested that SIDS may be associated with the infant either acquiring these unusual types of E.coli or more likely that its normal resident E.coli acquire the plasmids to produce these toxins.

It must be stressed again that it is not necessary to accept or refute the theory relating the toxic E.coli strains to SIDS. It is merely necessary to recognize that the toxigenic strains exist. And they do produce endotoxin. Failure to look for the strains denies important evidence to the defense.


Stephen A. Levine, PhD and Paris M. Kidd, PhD, in a book, Antioxidant Adapation, ISBN;0-9614360-0-7, define free radicals: (page 14)
Free radicals are atomic or molecular species which are extremely reactive by virtue of having unpaired electrons.
Levine and Kidd state (page 15):
It is this unpaired electron that is responsible for the instability and reactivity characteristics of all free radicals. Simply by losing or gaining 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 species. These chain reaction compounds generally 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 antioxidant species, by enzymatic mechanisms, or by recombination with each other.

Referring to brain disorders, Levine and Kidd , state: (pages 189-190)
Neural tissue is particularly sensitive to oxidative (free radical) stress ... ischemic or traumatic injuries damage the brain and spinal cord more extensively than other organs.
Oxygen is seven to eight times more soluble in nonpolar compartments such as the hydrophilic lipid bilayers of biological membranes; thus cellular membranes are at considerably greater risk of peroxidative attack by activated oxygen species. Neuronal membrane systems, especially mitochondria and myelin sheath membranes, are especially rich in polyunsaturated fatty acids, so also will be particularly prone to peroxidative attack
Page 190:
Neurones due to their high mitochondrial content have an unusually high rate of oxidative phosphorlation, presumably to support their large complement of iron pumps (note; the word is 'ion', not 'iron'). Neurones are therefore enriched in ubiquinone (Coenzyme Q), a lipid soluble component of the respiratory electron transfer chain which can readily autoxidize in low oxygen tensions to produce superoxide anion.

A number of studies have established that neural tissue is preferentially susceptible to oxidative stress.

Page 29:
Thus atoms of iron, once freed from sequestration in biological complexes (i.e., bound in enzymes or transport proteins) can potentially cause severe tissue damage. Initiation of lipid peroxidation. Redox-active metals, especially iron and copper, are often present on or in cell membranes as obligate cofactors of membrane enzymes. They can also become available in relatively unbound forms from dietary sources or damaged tissues.
Page 143:
Vessel hemorrhages in the CNS may result in free radical-mediated damage. Blood escaping from the vascular system introduces free (unbound) iron, and sometimes also copper, into the extravascular fluids, as metaloenzymes are destroyed by ltsosomal proteases. These metals are particularly good catalysts for free radical reactions, even at low concentrations, and would tend to exacerbate lipid peroxidation.

Any agent that can cause direct damage to the cell membrane, or to the membranes of critical cell organules (for example, intracellular mitochondria which are the genetically controlled 'chemical factories' in the cell), can trigger a sequence of events which, in the end, may mimic those occurring in hypoxia.

It should be noted here that, following brain injury, following the breakdown of the blood-brain barrier from endotoxin, endotoxin enters the brain structure, destroys some brain tissue and releases what was previously bound iron and initiated free radical reactions. Some parts of the brain are particularly rich in iron.

Following this initial initiation of free radical reactions, when red blood cells that escape into the tissues break down they release their content of iron and copper which accelerate further free radical reactions. Unfortunately, because the cerebral circulation is impaired (either wholly or in parts) antioxidants, such as vitamin C, and nutrients are unable to enter the damaged tissue and reverse the reactions.

Clemetson, in Vitamin C, Volume 1, on pp 240-241, states:
It seems that all patients with cerebral hemorrhage, whether or not they have cerebrovascular ascorbate deficiency before the hemorrhage, will susbsequently have local ascorbate deficiency due to hemolysis. One can try to correct the increase in the oxidation-reduction potential by chelating of iron, by administration of cortisone, or by administration of ascorbic acid. Indeed Ohimoto et al reported encouraging results in the treatment of delayed vasospasm following subarachnoid hemorrhage in two out of five patients by intrathecial administration of ascorbic acid (200-1000 mg.)

This introduces into this discussion the role of vasospasm and the possibility of it being involved in mechanisms causing cerebral anoxia. Thus, following endotoxin or anoxic initiation of brain damage, two stages of free radical reactions occur—one commences immediately and the other commences when red blood cells break down. Further, endotoxin and free radical reactions accelerate the breakdown of red blood cells, which means that the time taken is shortened.

The important issues are:
• what precipitates the hemorrhage
• what, if any, special tests can differentiate between the two
• what, if any, are the macroscopic and microscopic differences.

Obviously, one looks for:

Signs of endotoxemia
Are factors leading to excessive endotoxin production and/or failure to detoxify endotoxin present?
Is the history suggestive?
Are there physical findings suggestive?
Are there pathological findings, either macroscopically or microscopically?

Signs of scurvy
Is the history suggestive?
Factors responsible for increased vitamin C utilization
Physical findings
Pathological findings - macroscopic and microscopic
Blood and tissue levels of vitamin C, including the cerebrospinal fluid

An important issue concerns complexities surrounding the differentiation between inflammation and trauma. There are several major problems involved:
• Very little research has been published in this field.
• Interpreting what is known is a nightmare.
• There are many common features.
• In many cases the end result, particularly in the brain, is the same. That is; there are hemorrhages and brain tissue destruction.
It is therefore necessary, indeed vitally important, to carefully consider all factors involved, including the history.

Unfortunately, in every shaken baby case that I have investigated (more than 30) vital evidence has not been collected. This particularly applies to special investigations before death, failure to examine some tissues and body fluids during the autopsy, macroscopic and microscopic examinations of important tissues, and the collection of cerebrospinal fluid during autopsy for cells and viral and bacterial cultures. The 'gold standard', particularly when an individual is charged with a serious crime, is to collect, during autopsy, about 40 specimens from various tissues and organs.

Professor John Emery, Emeritis Professor of Paediatric Pathology, University of Sheffield, in Paediatric Forensic Medicine and Pathology, edited by Mason, states:
What tissues to block (referring to paraffin blocks, for microscopic examination). My own necropsies entail about 40 completely standardized blocks that include all organs and tissues and then extra blocks taken as related to any lesions seen naked eye. A further seven bblocks are used for frozen sectioning (brain, two blocks, liver right and left, heart kidney, adrenals).

In the Yurko case, special reasons were advanced for not taking many important blocks, apparently because some organs were to be used for transplants. However, there is no record in the notes sent to me of any cultures that may have been performed and there is no record of what happened to the recipients, if any, of the various organs. This information could provide vital evidence—particularly cultures, if done. One could hardly imagine that cultures were not performed before organ transplant procedures were carried out, even if the results were not immediately available.

Regarding the cerebrospinal fluid: it was stated during evidence that this could not be examined because of the danger of complications. This is only a partial truth. Certainly, during autopsies there is a special technique that permits this to be done with minimal risk of contamination, when cultures and the presence of inflammatory cells would possibly provide critical evidence.

Professor Emery, in Paediatric Forensic Medicine and Pathology, page 78, states:
For this reason we have for many years inspected the brain through the foramen magnum (the hole in the base of the skull through which the spinal cord emerges) before opening the cranial cavity. To do this place the child face down with the body mass supported on a block and open the skin at the back of the head with a 'question mark' incision. It is important that the incision is carried fairly well back behind the ears and over the back of the skull: the line of the incision must be out of sight when the skin is replaced after the necropsy but, at the same time, the line across the skull must be far enough forward to enable the scalp to be pulled forward. Having produced the skin flap, remove the muscles attached to the occiput and clean the rami of the upper cervical vertebrae. Then, using a small bone forceps, snip off the back of the atlas and, possibly, of the second or third cervical vertebrae leaving the dura (the membrane surrounding the brain and spinal cord) exposed beneath. Make sure that the area is free of blood, hold the skull level with the body and incise the dura carefully, (the dura can be be incised without cutting the arachnoid so that the cerebral fluid does not escape). At this point, perforate the arachnoid using an ordinary glass pipette with a rubber teat and remove a sample of cerebral spinal fluid.

In the case of Scott Walters, Sydney, 1898 (the defendant was found not guilty) cultures were taken during the autopsy.

Dr. Dianne Little, pediatric forensic pathologist, in a report dated July 3, 1996, states:
Bacteriology. Blood cultures grew Streptococcus oralis. Cultures of a swab of the right lung grew scanty E. coli. These results likely represent postmortem bacterial overgrowth and/or contamination. Cultures of the left lung grew no bacteria.
Virology, cytomegalovirus was isolated from a nasal swab.
Cultures of pancreas, salivary gland, bowel, heart, lung and a throat swab isolated no viruses.

The interpretation of these cultures is a problem in itself, but the fact is that they were done because it is necessary to obtain as much information as possible.

Another issue in the Yurko case concerns the failure to do stool cultures—for viruses and bacteria. Although I could find no record of bouts of diarrhoea, the fact that baby Alan suffered from infections and was given antibiotics increases chances for the development of 'mutant' strains of E.coli, or the 'overgrowth' of certain strains. Or viruses of various types may have been present. Specifically, one should look for toxic strains of E. coli.

This showed clearly that inflammatory processes were present, and these cannot be explained by the 'shaken baby' theory. It also demonstrates the extreme complexity of the factors involved. For reasons that I do not fully understand, much of this evidence was ignored. I assume that the combination of so-called 'rib fractures', intracranial hemorrhages, and retinal hemorrhages, was interpreted as 'shaken baby', and the complexities involved were conveniently ignored. My understanding of murder trials is that guilt must be established beyond reasonable doubt. It is apparent that this 'rule' did not apply in this case.

Dr. Shanklin's evidence should be carefully analyzed and reasons for disagreement listed and considered. This will provide a basis for the consideration of factors important for a logical defense. One detail, that is possibly important, can be found in the evidence. It relates to what Dr. Shanklin said (page 373):
“While looking at various blood clots, I found this particular area. If memory serves, it was near the back part of the brain within the skull and not the spinal cord. It did have this inner structure here which is pale in this photograph surrounded by this recent bleeding. When this was greatly magnified, I'd see in it and you can see in these dark, purplish brown dots which are some kind of organism, either a fungus or a bacteria. This was not tested further and I was not in a position to make specific tests on this. Its called destructive testing and I did not do that, in terms of understanding what the process is, the bacteria or fungus, whichever it is here. Some of this growth may have occurred after death. But the growth is not the key. The presence of it is the key. It gets there as a matter of disease process.”

Q. So some of those bacteria or fungus would have been present in this child prior to death?
A. Exactly. And there is no reaction to it. In other words, this is quite recent as well.

Now there are many possible explanations for this. One can be found in the book by Hess, who states, page 133:

In the study by Jackson and Moore on experimental scurvy in guinea-pigs, the histology of the blood-vessels is carefully considered. 'Marked thinning of the wall' was found and depicted, 'the wall as a whole had partially melted away, leaving few traces'. These parts of the walls contained many small round bodies resembling cocci, [spherical bacteria-like structures, obviously of unknown nature] which were stained a deep blue by the Wright and the Giemisn method. These bodies were present also in the lumen of the vessel and in the inner layers of the more normal portions of the wall. As a result of this pathology the authors are of the opinion that they may have been dealing with a mild infection. This is quite possible because scurvy tends to render the tissues less resistant to the entrance of bacteria. We believe, however, that even if such were the case, the phenomenon must be regarded merely as secondary in its relation to the pathogenesis of scurvy.

Following the study on the pathology of experimental scurvy, Jackson and Moore undertook to determine primarily whether the small stained bodies seen in the sections of the scurvy lesions were bacteria. This investigation has been cited frequently as presenting cogent evidence in favor of the infectious nature of scurvy, so that it will be necessary to consider it fully: the general question of whether scurvy is a bacterial infection is discussed under the consideration of etiology.

There is a long discussion in the book by Hess on this subject. Page 31:

Jackson and Moody cultivated a diplococcus from the tissues of scorbutic animals after death, reproduce hemorrhages by inoculating cultures of these microorganisms in to the circulation, and recovered the bacteria from the tissues some weeks later. Their results are open to critism that bacteria were found only after death, and that all blood cultures during life proved negative.

The matter was never clearly settled, and it remains so to this day. However, the observation by Shanklin cannot be totally ignored. It also remains as an item placed in the 'too-hard basket'. I can only state that, if anything, it is a positive finding, supporting the defense.

There are many details revealed in the evidence provided by Dr. Shanklin that require attention because they cannot be explained by assuming that shaking was the cause of the pathology found during autopsy and by microscopic examinations of some of the tissues. On page 22 he states:
“This child died of natural causes. In specific, the child died from the latent consequences of probably perinatal events of a hypoxic nature. There are some features of this case that are strongly suggestive of either a concurrent or a supplanting general infection due to viruses. The brain slides, in particular, the spinal cord are most strongly suggestive of a hypoxic occurring some ten weeks before death.”

The history of the baby during the time from birth to the time of the final collapse is evidence that serious problems existed, but that the true nature of these was not diagnosed. In many ways this is understandable because intracranial problems in infants may not be clinically obvious even to a trained observer.

On page 24-25, Dr. Shanklin, referring to microscopic examinations of the cerebral cortex and parts of the spinal cord, states:
“We are looking at overt necrosis of brain material, which is quite old, as witnessed by the penetration of the area by new blood vessels of an extremely vigorous nature. There are many nerve cells, which are what we call red neurons. They do not constitute all of the neurons in the spinal cord, but there has been insufficient loss there that the capacity of this brain to function normally would be seriously compromised.”

The origin of this needs to be explained, and it would be possible to do this by considering the role of anoxia occurring a long time before the final collapse. However, it is of interest and possible importance to note what Hess has to state and illustrate on pages 104-105:

In a case of fatal scurvy in an infant a "focal degeneration of the cord" has been described, extending for a distance of a quarter of an inch (Hess). The lesion differed from that of poliomyelitis in the absence of round-celled infiltration and the characteristic changes in the anterior horn cells (Fig.3 and 4). The outstanding feature was a loss of cells in the lateral groups of the left anterior horn; there were also fewer nerve fibres in this region, but this diminution was less striking. No definite interpretation can be made as the data are insufficient to permit a conclusion as to whether the lesion was truly scorbutic or the result of an associated process.

It would be foolish to dogmatically associate this lesion with what Dr. Shanklin found but, at least some consideration should be given to it.

Furthermore, it is important to note, again, that scurvy is not a pure disease and endotoxemia and/or infections (bacterial or viral) can complicate the clinical picture. Thus, mixtures of so-called 'scurvy' and inflammatory process can coexist. Added to this is the almost endless variety and combinations of lesions found—if one searches diligently.

Dr. Shanklin, page 25-26, states:
“The changes in the spinal cord and in parts of the brain also include the infiltration of certain types of inflammatory cells into the blood vessels and surrounding the blood vessels. And one can see elements very clearly in these sections of the process of these vessels assisting in the process of repair. This is a sufficiently advanced lesion that there is no way it could have occurred during the seventy-five hours or, indeed, during the interval of an equivalent period of time prior to admission. It is clearly many weeks old and is fully consistent with a perinatal incident of some sort.”

The mechanisms involved in causing these lesions could be debated, but one detail is certain; and that is that the lesions were old. It is possible that the differences between what was noted by Hess and Dr. Shanklin are mainly due to age differences. That is, differences in the ages of the pathologies.

On page 28, Dr. Shanklin notes that:
“Coagulation determinations were stopped in the afternoon of 25th November, which left over forty-eight hours for further changes to occur which could have led to spontaneous hemorrhage.”
Also, on page 28, Dr. Shanklin states:
“The chemical studies done on the child show that the liver function is greatly disturbed.
One realistic contributing factor for this would be the presence of endotoxin in amounts exceeding the capacity of the liver to detoxify.”

Dr. Shanklin then considers, further, the spinal cord changes and continues with (page30):
“Babies can be born with essentially no brain and have Apgars of eight and nine. The Apgar is a test of the biochemical status at the time of birth.”

This can only be described as an issue of prime importance. Many physicians and forensic pathologists overlook it. In the case under consideration, it cannot be ignored. It is apparent that baby Alan was never a well baby. Had extensive tests, including scans and extensive coagulation factors been carried out after birth and during the weeks that followed, there is no doubt that something serious and abnormal may have been revealed.

Dr. Shanklin then offers an explanation for some of the changes found in the brain and spinal cord (page 32):
“It's the kind of distribution which occurs with generalized hypoxia, as I have suggested, in the alternative, a generalized infection.”

It is possible that endotoxin and/or an increased utilization of Vitamin C played a role.

Dr. Shanklin, comments on the eye pathology (page 38).
“There is actually some chronic inflammation, which I note particularly in the left retina, which is both consistent with a virus etiology as well as hypoxic injury to the eyes at the time of birth or around the time of birth.”

This clearly demonstrates the complexities of the issues involved. To state categorically that the only cause is shaking is to ignore the obvious evidence.

Dr. Shanklin then discusses the so-called rib fractures. I have already dealt with this issue.

Dr. Shanklin raises another vital issue on page 48:
“The appearance of the hemorrhage itself. It is pure red cell. There is no essential clotting going on indicating that there may have been a bleeding problem at this point in time. There is a pattern of a few trapped cells, which are incidental to the hemorrhage. I mean when we bleed, we loose white blood cells as well as red blood cells, of course. There is absolutely no reaction to this whatsoever. And seventy-vive hours is more than enough given a child who has clearly got good marrow and who is producing large numbers of white blood cells. There would have been a very distinct and fairly precisely datable inflammatory reaction at the edges of this hemorrhage had it been in place at the time of admission.”

When asked “What in the body caused a spontaneous subdural hemorrhage?” Dr. Shanklin replied (pages 51-52):
“This is a brain which is undergoing the longer-term effects of a long-standing series of infarctions. Part of the response to this is a development in the subarachnoid tissues, in the so-called leptomeninges, of numerous small blood vessels. They are very thin walled. They are very fragile. If a child ceases to breath and then is resuscitated and the blood pressure is restored to near normal, then you have the possibility of these many vessels damaged by the incident which led to the necessity for resuscitation . It leads them to leak.”

Dr. Shanklin then continues with a discussion about another vital issue (pages 52-53):
“Fibrinogen is the protein in the blood which is principally responsible for blood clotting. It has to be converted to fibrin. And then fibrin starts breaking down over a period of hours to days, and the product can be measured in the blood. It's called fibrin split products. The test was one hundred and sixty micrograms per milliliter. The upper limit of normal is ten. So this is a dramatic rise. So we know that on the afternoon of the 25th, that the coagulation is going on and breaking down rapidly.”

It is necessary, at this point to consider what I have written earlier in this report on D-dimer (1)  D-dimer (2)  (coagulation split products) and coagulation disorders.

Dr. Shanklin, during the court session on February 24, 1999, gave evidence. On page 358, he states:
“Cause of death was natural, that there was a disease state, actually two disease states within the tissues, which indicate to me that either of them alone, certainly both of them working together, was sufficient to have caused the death of the child.”

Dr. Shanklin, notes the elevated white blood cell count and confirms the fact that (page 368):
...the child was essentially fighting off an infection.
Furthermore, (page 369):
...consistent with a long-standing infection of some kind.

Dr. Shanklin highlights the old nature of the pathology (Page 374):
“These structures have been largely destroyed in this brain by very old process and they have been replaced by the presence of hundreds of small blood vessels, which are these thick-walled, rounded and slit-like structures. This is the normal reaction of a damaged brain and spinal cord tissue to a low order, long standing problem. None of this is consistent with recent shaking.”

Dr. Shanklin repeatedly details evidence pointing to old pathology, which is inconsistent with recent shaking. He details some factors that can cause blood clots (page)382):
“Clots can come from a variety of causes and mechanisms. They can be trauma. There can be a problem with blood clotting. There can be a reaction to medication. There could be infection or a combination of these.”

I elaborate on some of these issues this report.

Dr. Shanklin then discusses another vital issue. In answer to a question (page 383-384):
“So we are not talking about a situation where had this child been shaken or injured by Mr. Yurko on the 24th you would expect to see what injuries, had it occurred at that time?”
Dr. Shanklin answered:
“I would expect to see that the red blood cells which make up the hemorrhage would have lost some of their pigment, which they have not. I would expect to see an inflammatory reaction, which is beginning to convert to a more chronic form of response, neither of which is present.”

Then, when asked (page 384):
“Why would this child continue to bleed while in hospital?”
Dr. Shanklin replied:
“ that anyone who's vulnerable and being maintained in the sepsis is still going or becomes worsened. Then small blood vessels will break down and start to bleed. As they do, they tear, and more blood follows. A person in the late stage of serious illness may have trouble clotting blood so that bleeding becomes profuse.”

This is a precise and accurate description of what can happen and I elaborate on this in earlier sections of this report.
Dr. Shanklin, page 396, highlights another vital issue when asked:
“The fact that there was no culture done, though, you can still diagnose meningitis?”
Answered with:
“Yes. Meningitis is the cellular reaction independent of the agent or organism which got it started.”

There are two issues involved here. First: bacteremia or septicemia need not be present when endotoxemia exists, and endotoxemia produces an inflammatory response. Second; since no cultures were taken we will never know if a viral or a bacterial infection did exist. Viral infections can precipitate the excessive formation of endotoxin. They can cause pneumonic changes that are consistent with what was found during the autopsy. The absence of cultures denies vital evidence to the defense.

Dr. Guedes, page 45, referring to the intracranial bleeding states:
“Those have to be acute injuries because you wouldn't have - you wouldn't have tolerated them. They wouldn't have looked like that. If you had an injury at birth, it would have been healed long before, you might see some abnormal brain from such an injury but it would be healed leaving some scarring or something like that.”

This is contrary to what Dr. Shanklin found when he carefully examined sections under the microscope. That is; the oral evidence of Dr.Guedes on this vital issue must not be accepted as fact, because he did not perform proper microscopic examinations.

Dr. Guedes, when questioned about subdural hemorrhages and intercranial bleeding, in an infant the age of baby Alan, states (page 50):
“Not this late in the game. No. Premature children are more susceptible to bleeds, but those are a different type and they occur in children more premature than this, usually choroid plexus bleeds and they occur in premature infants. In other words bleeds into the brain substance itself, not subdural bleeds.”
This is very misleading and fundamentally not true, as the following references demonstrate.

• Nelson, Textbook of Pediatrics, 11th edition, page 419, states:
Some of the membrane-enclosed subdural effusions observed in later infancy may have their origin in subdural hemorrhage at birth.
• Hayashi, et al, Childs Nerv Syst 199987;3(1):23-29. Neonatal subdural hematoma secondary to birth injury. states:
In order to evaluate the treatment and prognosis of subdural hematoma in neonate, we analyzed 48 survivors. There were 36 mature and 12 premature infants. The mothers were primiparous in 27 cases....fetal presentation was cephalic in 38 cases 10 of which suction delivery was performed, and breech in 11. Retinal hemorrhage was noted in 12 cases.
• Hanigan et al, J Neurosurg 1985 Dec;(6):977-9, states:
A case is presented of subdural hemorrhage diagnosed in utero at 31 weeks of gestation.
• Margalith et al, Surg Neurol, 1981 Dec;14(6):405-409, state:
A large subdural hematoma of the posterior fossa was diagnosed by computerized tomography in a normally delivered, full-term newborn.
• King et al, Br J Radiol 1998 Feb;71(842):233-238, state:
.to demonstrate the imaging features of a range of cranial injuries associated with birth at term. ..Intracranial injuries include extradural, subdural and subarachnoid hemorrhage.

Dr. Seibel, was asked a question (page 170):
“If the child were to have pneumonia, would that cause the type of brain injury that you saw.”
Answered with:
“Absolutely not.”

This is not absolutely true. As already demonstrated, infections can precipitate scurvy by a variety of mechanisms—one of which is an increased utilization of Vitamin C. Another is by an overproduction of endotoxin. 'Sepsis', as already documented in this report, can disturb coagulation factors and precipitate hemorrhages. References have already been provided in this report.

Dr. Hanna, page 135-136, stated:
“Something happened to one or more of those veins to cause them to bleed, or to cause hemorrhage from those veins.”
He was then asked:
“A subdural hemorrhage, is that something caused by a spontaneous bleeding in a person?”
He answered with:
“Not usually. That would be very uncommon. Usually it is trauma of some type.”
This answer is misleading, because, to provide the court with information that is available, a differential diagnosis should have been provided. Then, reasons should have been advanced for the decision made.

Dr. Seibel, page 161 discusses the theories regarding the injuries in so-called 'shaken babies'. He states:
“The axon or the nerve cell itself becomes injured or damaged.”
This is misleading because, as already referenced, anoxia can result in similar pathologies. This fact should have been brought to the attention of the court.

Dr. Seibel also stated, page 161:
“The symptoms associated with severe brain injury occur within a very few number of minutes after the brain injury.”
There are two errors in this statement. First, it assumes that the cause of the pathology is an injury. Second, it assumes that "within a very few minutes after the injury" is beyond dispute.

Nashelsky, Am J Forensic Med Pathol 1995 June;16(20;154-157, states:
Many health care professionals believe that there is a very short interval between an act of ultimately lethal shaking and the onset of symptoms. The medical literature contains minimal data that substantiate or contradict the contention that is stated here.

Lund et al, Ugeska Laeger 1998 Nov (46):6632-7, state:
A combination of subdural haematomas and retinal haemorrhages with minimal or no trauma and no coagulopathy is almost pathognomonic of the syndrome (shaking).

Note that one must know that no coagulopathy exists. In this case that is not so.
Dr. Seibel, page 172, when asked:
“Did you make any attempts to get this child's prior medical records, prenatal record, anything like that?”
Answered with:
“No sir, I did not.”
In view of the seriousness of the charges it is difficult to understand why this fundamental rule in the practice of medicine was not obeyed.

Dr. Seibel, page 174-175, was asked:
“What you're telling us is because of what you found you made the determination that this (shaking) was the cause of death in this child's case and didn't look any further?”
Answered with:
“No, I didn't make determinations as to cause of death. That's done by the attending physician and the person at the medical examiner's office.”
He was then asked:
“Didn't you just testify, doctor, that this child died from shaken baby syndrome?
Dr. Seibel answered:
In my opinion, yes sir.”
I find this difficult to understand or explain.

Dr. Seibel, page 177, when asked about brittle bones answered with:
“We would see markedly diffuse demineralized bone, which we do not see in this case.”
This is misleading because it is not always possible to determine the degree of mineralization in a plain film. That is why special machines have been devised to measure bone density.

Dr. Gore, page 238, was asked:
“Is there any way that a subdural hemorrhage can just be caused spontaneously, the child's body starts to bleed in the subdural?”
The response was:
This answer is difficult to understand, because subdural hemorrhages can occur spontaneously at any age. A variety of coagulation/bleeding disorders can result in spontaneous subdural hemorrhage.

Mitrakul et al, J Trop Pediatr Environ Child Health 1977 Oct;23(5):226-35, state:
Spontaneous subdural hemorrhage is commonly associated with bleeding diathesis of obscure etiology in Thai infants.

Then there is the Vitamin C/scurvy/endotoxin combinations already detailed.

Ms Wilkinson (prosecutor) Page 476, states:
“You have to look at the diffuse axonal injury, which is the clincher in this case.”
It is interesting and frustrating when reporting on a 'shaken baby' case to be faced with this type of comment. Sometimes retinal hemorrhages are highlighted, sometimes it is fractures, and sometimes something else. Apparently, different investigators regard different factors as the vital issues. The issue of axonal injury has already been dealt with in this report.

CAUSE OF DEATH - after considering the evidence, applying my clinical experience, and considering what is documented in the medical literature.

Two things need to be considered - the final cause of death and factors that led to the pathology that caused death. There is, no simple way of expressing this. Furthermore, factors involved interrelate with each other and this interrelationship extends over a period commencing before conception—taking into account genetic and other features that have influences on the final outcome.

When considering the pathology one cannot separate one issue from another. For example, genetic factors, though initially strong in parents, can be influenced by environmental and other factors. This can disturb immune responses and set in motion a cascade of events that may, months after birth, result in death. When arriving at a final cause of death it is necessary to be able to explain all the important pathologies found and associate this with the clinical history. To ignore aspects of the evidence because they cannot be explained by the person reporting is a fundamental error. On the other hand, because present knowledge is incomplete, it is an obvious error to assume that knowledge is complete. A final decision, therefore, is a balance of what is known and what is not.

The most fundamental error, in most of the so-called 'shaken baby' cases that I have investigated is clearly demonstrated by the fact that, early in the case, a diagnosis of 'shaking' is made and this becomes entrenched. From then on no attempt to make a proper differential diagnosis is made and many vital issues are ignored. This is compounded by the failure to carry out proper investigations. The result is not only incorrect verdicts of guilty, but continuing failure to understand mechanisms and prevent future deaths. This is the real issue, and the reason why studies like the ones in this report should be carefully considered. It is not a question of opinion or the expression of a particular theory. It is a matter of looking at what is recorded in the literature and matching this with what is found in each case.

Cause of death
Intracranial hemorrhages, wth cerebral edema and brain tissue damage. Precipitating factors include endotoxin, vaccine administration, excessive utilization of vitamin C, antibiotic administrations, and failure to be able to exclusively breast feed. Associated pathology includes, scurvy bone changes in some ribs and the acromion process of one scapula, disturbed coagulation factors, disturbed liver functions, and the effects of anoxia—all of which interrelated with each other. The age of the intracranial hemorrhages date back to before, during or shortly after birth. Rebleeding occurred.

Any other cause/causes for death would need to fit what was documented in the clinical history and the pathologies found.


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