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


Dr. Kalokerinos' Analysis of the Alan Yurko Case

The Case of Alan Yurko (Florida, USA)
—an introduction and explanation

Archie Kalokerinos , MD
20 Kennedy Close, Cooranbong, NSW, 2265, Australia
Ph. 011 61 2 49772957
Fax 015 61 2 49772958

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 (the late Robert Reisinger, from Baltimore) who introduced me to endotoxin. 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 in 1920 by Professor Hess, a pediatrician in America. 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 now, 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 difficult. 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.

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).

There are several known 'causes' for oligohydramnios—placental insufficiency (e.g., preclampsia and post-term pregnancy), and renal malfunction. The amniotic fluid and blood of smokers is high in cadmium (a toxic element), and low in zinc (which 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.

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—two known risk factors.

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 resulting from a direct 'killing' of certain bacteria and the liberation of endotoxin that is stored in the bacterial walls. Another involves disturbances in gut flora, which also tends to result in an overproduction of endotoxin and disturbances in gut immunology. Respiratory problems persisted for some days after birth. This never cleared to a satisfactory degree.

At the age of 8 weeks, six vaccines were administered. Satisfactory counselling 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, involves a coagulation disorder.

The day after the vaccine administrations, the mother noticed increasing lethargy and feeding problems. Ten days later there was a high-pitched cry (which can exist when there are some cerebral problems, such as encephalopathy). On November 24, while under the care of the father, Alan Yurko, the baby began to wheeze and then stopped breathing. There was apparently up to 5 minutes of a degree of apnea.

The Transport Team noted mottling of the skin. This may have various causes. One cause 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. That one memorable cause is endotoxemic shock. Several shaken baby cases that I have investigated exhibited skin mottling during the initial phase of collapse.

Hospital tests revealed bilateral pulmonary infiltrates, what were diagnosed as rib fractures, and subdural and cerebral hemorrhages. Death occurred 75 hours after admission.

Cause of death, as recorded by the autopsy team: Subdural hemorrhages due to shaken baby syndrome.
A. Contusions, minor, on both temporal areas of the head.
B. Periorbital ecchymosis, right lower eyelid.
C. Subdural hemorrhage, fresh, right and left cerebral hemispheres, predominately right
D. Hemorrhage at the base of the brain
E. Subarachnoid hemorrhage, thin layer, biparietal 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
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 External Injuries
Right, lower eyelid - a thin rim of ecchymosis. Pinkish in color and measures 1 x 0.2 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 10 x 9 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 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.

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.

Note by Dr. Kalokerinos:
At this stage, without further knowledge/information it is not possible to state how significant (if, indeed, it is significant) the finding of liquid blood in the intracranial haemorrhages is. If it can be regarded as more than normal it could signify the presence of a coagulation disturbance such as has been documented in some cases of SIDS.

Goldwater, et al, The Medical Journal of Australia, Vol 153 July 2, 1990, quotes levels of a fibrin degradation product ('D-dimer') in some SIDS cases. The mean level was 1792. The mean level in control cases was 56.6. This is an astonishing figure, given the fact that no other clear-cut clinical signs of coagulation/bleeding disturbances in SIDS cases exist. One factor that stimulated Goldwater's research was the finding of 'liquid blood' in some SIDS cases.
The finding: 'the dura mater of the cortex of the cerebral hemisphere shows thickened and slightly clotted blood adherent to the dura' requires discussion. It could indicate that at least some of the clot was 'old'. This should be considered later with the evidence of Dr. Shanklin.

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.

Note by Dr. Kalokerinos
Subdural hemorrhages in the spinal area have been documented in scurvy cases. Hess, page 93, states 'Hemorrhage may occur into the brain substance, into the cord or the membranes surrounding them'.

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.
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.
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.
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.
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.
Heart: Dr. Gore testified that he 'removed the heart, the lungs, and all the organs.' He also stated that there was a microscopic examination of the heart. This contradicts what appears to be a fact; that the organs were harvested for transplantation.

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.

The contusions
Discrepancies exist between what was documented before death and what was documented after death. Therefore, there is no evidence that contusions 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. 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's text 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. There are other issues involved.

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.

The anaemia
This was very marked - the Hb level being 6.3 on 11/24/97. Certainly, this was not due to hemorrhage. The amount of blood in the hemorrhages was not sufficient to explain the Hb level. So one is left to make what is known as a 'differential diagnosis'. Unfortunately, because extensive iron studies etc. were not done, one is left unable to issue a clear, indisputable diagnosis. It is necessary to understand that this denies, once more, what could be vital evidence for the defense.

There are many possible explanations for the anemia. Baby Alan was certainly a sick infant from the time of birth—prematurity, respiratory difficulties, infections, antibiotic administration, and vaccine administrations. It is known that scurvy, in infants and adults can be associated with anemia.

• Eisele et al, Lab Anim Sci 1992 June;42(3):245-9: Skeletal lesions and anemia associated with ascorbic acid deficiency in juvenile rhesus macaques. Anemia was a consistent finding.

• Von Muhlendahi, Monatsschr Kinderheilkd 1984 Apr;132(4):240-1 Infantile scurvy can be diagnosed either by recognition of a characteristic constellation of clinical features, or on the correct interpretation of nearly pathognomonic radiological signs: anemia, costochondral swelling, and subperiosteal hemorrhage are important diagnostic clues.

None of these references proves that, in the case of baby Alan, scurvy was the cause of the anemia. However, they demonstrate that scurvy is a possible diagnosis. What is quite clear is the fact that baby Alan was not well from day one. There were many serious, and obvious problems (anemia being one) that cannot be ignored and are not consistent with a diagnosis of shaken baby.

Rib and acromion pathology
I use the word 'pathology' rather than 'fractures' because there is no clear evidence that what was found were fractures. That is, there is an explanation for the pathology that does not include trauma. Furthermore, there are reasons to consider that the pathology began before, or shortly after birth. There appears to be doubt that the acromion was actually involved in any pathological process.

Hess, in Scurvy Past and Present, stated, page 125:
In perusing the literature but one study has been noted on the effect of a scorbutic diet on the foetus. This investigation was carried out on a large series of guinea-pigs by Ingier (1915).in these experiments intra-uterine fractures, premature births and still-born litters are frequently mentioned.

Obviously, in this study, the author is referring to scurvy bone changes and not true traumatically induced fractures. Ribs can be affected in several ways by scurvy.

• Subperiosteal hemorrgages
• Costochondral changes
• Changes in one or more of the epiphyseal areas, including those in the posterior portion of the ribs.

Subperiosteal hemorrhages occur under the periostium; that is, the 'skin' of the bone. The blood is quickly ossified (changed to bone - in the same manner that a blood clot surrounding a fracture is changed to bone as healing progresses). The appearance, on a scan or X-ray is similar to what is seen when ribs are broken. This is what was seen in the case under discussion.

Costochondral changes were noted by a radiologist. These areas are where the front ends of the ribs join the sternum, and can be recognized as swellings, called 'beading'. Bone changes occur where there is rapid bone growth—where the ribs joins onto the cartilages in the front near the breast-bone There are several smaller ones at the back of each rib near the spine the spine. Another area lies under the 'periosteum', the membranous covering of bones. The periosteum becomes elevated from the bone surface by a collection of blood. If one is not aware of this pathology an incorrect diagnosis of trauma-induced injury can be made.

Hess, page 95, states:
The susbperiosteal hemorrhage has long been recognized as a lesion characteristic of scurvy.

Hess, page 108, states:
The most typical site of hemorrhage is beneath the periosteum, a lesion widely known because of its clinical significance.

Richard H. Follis, Departments of Pathology and Pediatrics, the Johns Hopkins Medical School, Journal of Pediatrics, Vol. 20, Number 3, 1942, pp.347-351, referring to "Sudden Death In Infants With Scurvy," states:
...the periosteum stripped from the cortex with a fair amount of ease (case 1) ...there was hemorrhage beneath the periostium (case 2) ...the periostium stripped from the cortex with extreme ease (case 3).

Thus, the subperiosteal hemorrhages and increased ease of periosteal stripping can be used as guides to the diagnosis of scurvy. In the Yurko case, no note was made of the ease of periosteal stripping, and this, unfortunately means that this issue is not available (as it should be) to the defense. The rib pathology does not always involve every rib. Only one, or more, may be involved and there may be only subperiosteal hemorrhage, or costochondral changes, or there may be both types of lesions.

Hess, page 91, referring to rib pathology, states:
These changes are not found in every specimen, so that in order to exclude scurvy definitely, it is necessary to examine a considerable number of ribs, several may be normal, only one or two showing the characteristic microscopic changes.

Here Hess is, of course, referring to microscopic changes. In more obvious cases the lesions are visible to the naked eye.
The changes seen in the acromion process of the left scapula can also be explained by scurvy. That is; if there was any pathology in that area.

Hess, page 12, referring to experimental scurvy in monkeys, states:
Subperiosteal hemorrhages of the cranial bones were constantly seen, and not infrequently involvement of the scapula. (The acromion is part of the scapula.)

I could not find, in the notes provided to me, any mention of a microscope examination of the acromion process of the scapula after the autopsy. That is disturbing for three reasons
• The lesion was not found in the first X-rays taken. It was seen in films taken two days later.
• So the age of the lesion is important
• A proper macroscopic and microscopic examination may have provided evidence of scorbutic changes, rather than trauma-initiated changes. Once again, because this was not done, this information will never be available and the obtaining of evidence that may have supported the case for the defense is denied.

Another feature of scurvy bone changes is that they can, and do, occur at different times. This gives rise to the incorrect conclusion that the lesions represent multiple acts of trauma—a feature of some of the cases I have investigated.

On page 219 of the court proceedings, Dr. Gore answered a question:
Q. Were these ribs in different stages of healing?

A. I feel that because I looked at the swellings, they are different. It means they probably occurred at different intervals, maybe a few days. So one occurs say about three weeks ago. Then the second occurred maybe after four or five days later. And that's why there is variability in the reaction. You can see a big knot and so forth.

This is both incorrect and misleading. The size of the callus is not a clear indication of the age of the fracture because a host of variables is involved. In Paediatric Forensic Medicine and Pathology, edited by J.K. Mason, Regis Professor (Emeritus) of Forensic Medicine, Faculty of Law, Old College, University of Edinburgh, pages 303-304, are the following statements:
Dating of fractures on the basis of radiological features is an inexact science. Neither radionuclitide studies or computer tomography have been found helpful in establishing the age of fractures. Reports should be cautious [author's emphasis] when it comes to assessing the age of fractures and suggesting the mechanism by which injuries were sustained.

The rib pathology may have developed before birth, or shortly after birth. Experimental evidence demonstrates that scurvy bone changes can be found (in experimental animals) before birth.

Hess, referring to experimental scurvy in animals, page 126, states:
In these experiments intrauterine fractures, premature births and still-born litters are frequently mentioned.

The 'fractures' mentioned, of course, refer to scurvy changes and not traumatically induced fractures. A more recent document is as follows:

Landman et al, Rib fractures as a cause of immediate neonatal tachypnoea. Eur L Pediatr 1986 Feb;144(5):487-8.
Two macroscopic term neonates are described who presented with uncomplicated apneoea immediately following vaginal delivery. The tachypnoea was not associated with lung injury, metabolic, endocrine or cardio-respiratory disease but with multiple unilateral posterior rib fractures.

Dr. Seibel, page 159, was asked:
Dr. Seibel, can this rib fracture be caused at birth?
He answered:
It is not described in the medical literature as being a result of birth trauma.

Obviously, Dr. Seibel did not review the literature in a thorough manner. Nor had he investigated possible reasons for rib fractures at birth. These include varieties of brittle bone disease, including temporary brittle bone disease and scorbutic changes. It is important to note that osteoporosis may not be obvious on ordinary X-rays and bone density measurements provide better information.

The problem in the Yurko case lies in the fact that the manner by which Dr.Seibel answered the question would imprint in the minds of judges and juries the impression that the rib pathology could not have existed from birth, and that it was caused by trauma alone, at a later date. When all the evidence of the case of baby Alan is considered, there is, of course, many reasons to deduce that one very possible cause is scurvy.

Osteoporosis, brittle bones, and scurvy

Hess, page 128 states:
The osseous tissue itself shows marked changes, corresponding to the rarification and brittleness noted on gross examination. It is important to note that the so-called 'classical' X-ray finding seen in scurvy bones—the 'white line' sometimes seen near the ends of long bones, is not always present.

Hess, page 199, states:
It is best seen at the lower end of the radius and femur, and appears as a white, transverse, somewhat irregular band. Its diagnostic value has been greatly exaggerated as it is frequently not present when the disease is advanced.

Nearly one hundred years ago intense interest in osteoporosis and brittle bones was generated by the observation of a connection with scurvy. First, it was necessary to differentiate between the bone changes in scurvy and rickets—not an easy task, because sometimes the two conditions existed together. Then osteogenesis imperfecta and osteomalacia had to be clearly separated from scurvy. Now, it is known that osteoporosis is, sometimes, a specific feature of scurvy.

John Caffey, who was a pioneer in the nonaccidental trauma pathology published and article in Pediatric X-ray Diagnosis, 4th edition, Year Book Medical Publishers, Chicago. Under a reproduction of an X-ray he states:
Early skeletal changes in an infant, scorbutic bones showing osteoporosis.

The issue of osteoporosis and spontaneous fractures in infants has resurfaced recently because of controversy surrounding so-called 'temporary brittle bone disease'. This has been raised in at least one shaken baby case and dismissed as 'not proven' or something meaning the same. However, the subject has been reconsidered in a manner that demands attention.

Miller, Department of Pediatrics, Wright State University School of Medicine and the Children's Medical Center, Dayton, OH, Seminars in Perinatology, Vol 23, No 2 (April) 1999: pp174-182, states:
The author feels that temporary brittle bone disease is a real entity, and the use of bone density measurements can be helpful in making the diagnosis.

The infant who presents with multiple, unexplained fractures poses a difficult diagnostic dilemma. If no apparent medical explanation can be found, then a parent or caregiver may be accused of intentionally injuring the child, even though they may deny it. In some instances, criminal proceedings may be filed against a parent that could result in incarceration if convicted.

The natural history of temporary brittle bone disease (TBBD) was one of multiple unexplained fractures during the first year of life, and no unexplained fractures thereafter. The hallmark of TBBD was a lack of cutaneous injury at the time of injury. Paterson et al found that there were certain features associated with TBBD including twinning, prematurity, apnea, colic anemia, and a family history of hyperextensibility. He postulated that a copper deficiency might be the basis. Most individuals in child abuse work do not accept Patterson's TBBD. Understandable, because the acceptance as a true entity challenges several dogmas of radiological features of bone in the infant with multiple unexplained fractures that are thought to be pathognomonic of child abuse. However, there are some features of TBBD that would suggest that intentional injury is unlikely.

Bone density measurements by computerised tomography or radiographic absorptiometry
Bone densities were low in eight of the nine TBBD infants studied, indicating an increased susceptibility to fracture. Noteworthy is that these infants had low bone density measurements in spite of apparent normal bone density on plain radiographs.

I believe that there has heretofore been an unchallenged acceptance of three radiological features of bone in infants with multiple fractures that have been called pathognomonic of child abuse. These three features are (1) the finding of apparent normal bone density on the plain radiographs, (2) metaphyseal (shaft of long bones) fractures, and (3) posterior rib fractures. However, these features can be seen in intrinsic bone diseases of infancy—TBBD, osteogenesis imperfecta, and the bone disease of prematurity. Bone strength is assumed to be closely related to bone density. It is widely accepted that if there is normal whiteness of the bones on the plain radiograph, then the bones are of normal density and therefore have normal strength. These assumptions are not correct. The second radiographic finding is that metaphyseal fractures (corner fractures or bucket handle fractures) are diagnostic of child abuse. However, there is a differential diagnosis for metaphyseal fractures that includes many of the other bone diseases of infancy that can cause unexplained fractures, such as osteogenesis imperfecta, TBBD, copper deficiency, scurvy, and rickets.

In the case under consideration (Alan Yurko) bone density studies were not performed. Therefore, a potentially critical piece of evidence is not available for the defense (note: bone density studies in infants can be difficult and confusing because of the rapid turnover of tissues during normal rapid growth).

Beyers et al, S Afri Med J 1986 Sept 27;70(7):407-413, states:
Small preterm infants often develop osteopenia with or without rickets and with or without fractures. Whether these bone abnormalities are all or part of the same disease process with a wide spectrum of presentation or whether each abnormality represents a different disease is as yet unclear.

There is a multitude of reasons, reading the article just quoted, why scurvy should play a critical role in many cases of TBBD. It is important to note two critical facts:

• The enormous variability of the presentations of scurvy
• When the precipitating factor (an infection and/or endotoxin, for example)

spontaneously clears, as it can, then there may be a spontaneous cure of the scurvy. On the other hand, scurvy, and/or its causes, may persist and, without treatment, death may result. Therefore, Dr. Gore's evidence cannot be considered as proof of guilt. The rib and acromion pathology, as a stand-alone feature, is consistent with a diagnosis of scurvy. And the dating of the pathology is not proof of trauma.

A standard radiology textbook by Keats and Anderson, Atlas of Normal Roentgen Variants That May Simulate Disease, Seventh Edition, figure 5-174, states:
Simulated cupping of the anterior ends of the ribs produced by lordotic projection.

That is, a 'false' impression of enlargement due to the angle of projection of the X-rays can be mistaken for enlargement or abnormality. The same textbook shows 'large anterior ends of the ribs simulating extrapleural (outside the pleural linings of the lungs and chest wall). This needs to be taken into account when reading X-rays. However, during an autopsy, it should not be a factor, because physical examination of the ribs, followed by histology, should clarify the differences between 'a normal variant' and something that is abnormal.

If periosteal elevations are also found, one would need to be extremely careful before excluding a diagnosis of scurvy-type changes.

Keats and Anderson list under a heading of 'Multiple Symmetrical Anterior Rib Enlargement' the following list:

1. Normal
2. Rickets

1. Asphyxiating thoracic dysplasia
2. Hypophosphatasia
3. Leukaemia (chloromas)
4. Scurvy
5. Thalassemia
6. Thanatophoric dwarfism

The statement that enlargement can be 'normal' opens up a minefield. A better description would be 'cause not known'. The pathology cannot, for example, follow acute suffocation because the bone tissue changes take time to develop. When there is chronic anoxia, endotoxin becomes involved and this causes an increased utilization of Vitamin C. The anterior rib enlargements (costochondral junctions) should be regarded as being caused by Vitamin C deficiency and endotoxin. The other conditions noted, apart from scurvy, need not be considered here. Apparently, one rib broke during the autopsy. Just what force caused this (if any) needs to be clarified.

The so-called 'chest contusion'—on the left side, in the region of the 7th rib.
This is an important, indeed, vital, issue that requires careful study. Dr. Gore, the pathologist who performed the autopsy reports as follows:
"On the left lateral surface of the chest there is a very pale, slightly pinkish, ovoid, healing type of contusion measuring 10 x 8 mm. It is located in the region of rib # (fracture) 7."

A 'contusion' is defined (Blakiston's Pocket Medical Dictionary, 4th Edition,) as 'an injury, usually caused by a blow, in which the skin is not broken'. Therefore, the intent of this portion of Dr. Gore's report is to convey a meaning of a blow or 'trauma'. Furthermore, because it is over one of the so-called 'rib fractures', the intent is to convey to a reader, including a judge or jury, that this represents proof of a blow, or trauma of some sort, causing the contusion. There are several serious omissions and deliberate misrepresentations in the report.
• There is no record of a 'contusion' in the area under discussion in the hospital notes compiled while the infant was in hospital before death.
• No attempt was made to cut into the area to see if there was blood, new or old, in the tissues
• No sections were prepared for microscopic examination.

Mason's book, Paediatric Forensic Medicine and Pathology, pages 270-271 states:
The police will attend [the autopsy] and will take their own photographs when criminal charges are in prospect; the direction of the pathologist as to the most appropriate pictures to take will usually be accepted. Photographs are often taken both in monochrome and colour—many police forces now also take Polaroid or 'instant' photographs and may even use videotape recordings. The pathologist is almost always able to obtain copies for his own use, but may prefer to take his own pictures, especially in the form of colour transparencies.

Colour photography is far superior to black-and-white reproduction for the recording of skin bruising and other lesions. Care should be taken to obtain correct exposure, as over-exposed or 'highlighted' frames may fail to capture faint surface marks.

Mason's book, page 274-275 goes on to state:
When a very faint lesion is present or there is doubt as to whether a discoloured area is due to a bruise or hypostasis (special attention should be paid to this) an incision should be made into the skin in order to examine the subcutaneous tissues, and histology may be useful. Faint or doubtful bruises seen on the skin should be incised to confirm or exclude bleeding in the subcutaneous tissues.

The problems just discussed on the so-called 'chest contusion' apply to the 'contusions, minor, on both temporal areas of the head', and elsewhere. Finally, on this issue, it is necessary to stress that scurvy can cause skin bruises. And there are some specific differences between bruising due to trauma and bruising due to scurvy.

Hess, page 96-97, states:
Skin.- As pointed out by Aschoff and Kock, examination of skin which to gross appearance was the seat of small hemorrhages, showed various lesions. In some, perhaps, the most typical forms there had been an extravasation of red blood cells. This condition is found usually in the subepidermal layers, especially in the papillary stratum. Many round cells may be seen in these areas lying between the connective tissue strands or around the blood vessels. Rheindorf, as quoted by Tuechler, has called attention to this round-celled reaction, which in many instances gives a picture analogous to the granulomas, which leads him to infer an infectious origin for these lesions. Aschoff and Kock have found that suitably-stained preparations show a loss of elastic fibers, which Rheindorf states constitutes one of the earliest signs of the disorder.

It is highly likely that electron microscope examinations will reveal even more details that would aid in the differential diagnosis between trauma induced skin bruises and scurvy skin bruises. Since histology was not performed on the area of so-called 'contusion' one will never know its true nature. Therefore, under no circumstances must this be permitted to be admitted as evidence of guilt. In the notes provided to me, I could find no reference to a whole-body scan, being performed after death before the autopsy was commenced.

Greinacher et al, Radiologe 1982 Aug;22(8):342-351, states:
The diagnosis of the Battered-Child Syndrome (BCS) is made by the pediatrician and the radiologist. The skeletal changes are illustrated by X-ray pictures and bone scans.

Diffuse axonal injury
Dr. Gore, pages 279-280, gave evidence
Q. Dr. Gore, in looking at the fact that this child had diffuse axonal injury, you determine the child would have shown signs of this injury within how much time?
A. These are immediate
Q. And in looking at that, could the child have received the subdural hemorrhages at the same time as the diffuse axonal injury?
A. Yes
Q. In the professional literature is diffuse axonal injury easier to narrow when it occurred or recognize it in a narrower time frame than a subdural hemorrhage?
A. Well the injuries both are actually of the same motion, producing two different types of scenarios. One you get subdural hemorrhage. Other you get axonal types of injuries. These are at the same time and as a result of the similar motion.
Q. So in your professional opinion, these injuries occurred at the exact same time?
A. That is correct.
Following this, on page 280:
Well diffuse axonal injury is nothing but minute hemorrhages and these we cannot show you.
Further evidence given stressed that motion, through shaking, produces a shearing type injury and this is responsible for the axonal injury.

There is no doubt that axonal injury can follow head trauma. However, it can also follow a period of cerebral anoxia that can result from factors different to trauma. It is inaccurate and misleading to infer, through neglect to mention the role of nontraumatically induced anoxia, and state that trauma is the sole cause.

• Geddes et al, Neuro Pathol Appl. Neurobiol 2000 April 26 (2):105-16. Department of Histopathology and Morbid Anatomy, St Bartholomew's and the Royal London School of Medicine and Dentistry, London, U.K: Department of Pathology, University of Auckland, New Zealand and Department of Neuropathology, Institute of Neu, in an article titled,
Traumatic axonal injury;
practical issues for diagnosis in medicologal cases, state:

In the 25 years or so after the first clinicopathlogical descriptions of diffuse axonal injury (DAI) the criterion for diagnosing recent traumatic white matter damage was the identification of swollen axons ('bulbs') on routine silver stains, in the appropriate clinical settings. In the last decade, however, experimental work has given us greater understanding of the cellular events initiated by trauma to axons, and this in turn has led to the adoption of immunocytochemical methods to detect markers of axonal damage in both routine and experimental work.

These methods have shown that traumatic axonal injury (TAI) is much more common than previously realized, and that what was originally described as DAI occupies only the most severe end of the spectrum of diffuse trauma initiated brain injury. They have also revealed a whole new field of previously unrecognized white matter pathology, in which axons are diffusely damaged by processes other than head injury; this in turn led to some terminological confusion in the literature. Neuropathologists are often asked to assess head injuries in a forensic setting: the diagnostic challenge is to sort out whether the axonal damage detected in the brain is indeed trauma, and if so, to decide what - if anything - can be inferred from it. The lack of correlation between well-documented histories and neuropathological findings means that in the interpretation of assault cases at least, a diagnosis of 'TAI" or 'DAI' is likely to be of limited use for medicolegal purposes.

• Shjerriff et al, Laboratory of Neuropathology, Academic Unit of Pathology, Department of Clinical Medicine, University of Leeds LS2 9JT, U.K, Acta Neuropathologica, ISSN:1432-0533 (electronic version) Abstract Volume 87, Issue 1 (1994) pp55-62, states:

Severe nontraumatic head injury commonly results in a lot of brain damage known as diffuse axonal injury (DAI). The histological diagnosis of DAI is made by silver staining for the presence of axonal retraction balls. This feature takes about 24 hours to develop and does not allow for the early histological diagnosis of DAI. We have used immunocytoreactivity for the beta-amyloid precursor protein (beta APP) as a marker for axonal injury in formalin-fixed paraffin-embedded sections of human brain.

Axonal beta APP immunoreactivity was present in all cases which had survived for 3 h or more. This was true even where the degree of head injury did not appear to be severe, supporting the theory that DAI in a severe form of a more common phenomenon of axonal injury which occurs after cerebral trauma beta APP immunoreactivity was also found in some non-head injury cases and so cannot be considered to be a specific marker for trauma. The results show that beta APP immunocytoreactivity may be useful in the detection of traumatic injury in its early stages, before the formation of retraction balls, provided care is taken to exclude other causes such as immunoreactivity.

• Stys PK, Ottawa Civic Hospital Loeb Medical Research Institute, University of Ottawa, Ontario, Canada, J Cereb Blood Flow Metab 1998:Jan 18(1):2-25.

Anoxic and ischaemic injury of myelinated axons in CNS white matter: from mechanistic to therapeutics, states:

White matter of the brain and spinal cord is susceptible to anoxia and ischemia. Irreversible injury to this tissue can have serious consequences for the overall function of the CNS through disruption of signal transmission. Myelinated axons of the CNS are critically dependent on a continuous supply of energy largely generated through oxidative phosphorylation. Anoxia and ischemia cause rapid energy depletion, failure of the Na(+)-K)-ATPase, and accumulation of axoplasmic Na+ through noninactivating Na= channels, with concentrations approaching 100 mmol/L after 60 minutes of anoxia. Coupled with severe K+ depletion that results in large membrane depolarization, high (Na+)I stimulates reverse Na(+)-Ca2+ exchange and axonal Ca2+ overload. A component of Ca2+ in turn activates various Ca(2+)-dependent enzymes, such as calpain, phospholipases, and proteinkinase C, resulting in irreversible injury. The later enzyme may be involved in "utoprotection", triggered by release of endocenous gamma-aminobuteric acid and adenosine, by modulation of certain elements responsible for deregulation of iron hemostasis.

Glycolytic block, in contrast to anoxia alone, appears to preferentially mobilize internal Ca2+ stores; as control of internal Ca+ pools is lost, excessive release from this compartment may in itself contribute to axonal damage. Reoxygenation paradoxically accelerates injury in many axons, possibly as a result of severe mitachondrial Ca+ overload leading to secondary failure of respiration (referring to cellular respiration). Although glia are relatively resistant to anoxia, oligodendrocytes and the myelin sheath may be damaged by glutamate released by reverse NA9+)-glutamate transport. Use-dependent Na+ channel blockers, particularly charged particles such as QX-314, are highly neuroprotective in vitro, but only agents that exist partially in a neutral form, such as mexiletine and tocainide, are effective after systemic administration, because charged species can penetrate the blood-brain barrier easily.

These concepts also apply to other white matter disorders, such as spinal cord injury or diffuse axonal injury in brain trauma. Moreover, whereas many events are unique to white matter injury, a number of steps are common to both gray and white matter anoxia and ischemia. Optimal protection of the CNS as a whole will therefore require combination therapy aimed at unique steps in gray and white matter regions, or intervention at common points in the injury cascade.

• Kaur et al, Department of Forensic Pathology, University of Sheffield. U.K., J Clin Pathol 1999 Mar;52(3):203-9, state:

AIMS: To assess the possible role of hypoxia in the formation of axonal bulbs.

METHODS: Study material comprised sections from 28 brains showing evidence of cerebral hypoxia with no history of head injury, four with a history of head trauma but no evidence of hypoxic change, eight with a history of head trauma and hypoxic change, and four from control brains originally described as 'diffuse axonal injury'.

CONCLUSIONS: Axonal bulbs staining positively for beta APP may occur in the presence of hypoxia and in the absence of head injury. The role of hypoxia, raised intracranial pressure, oedema, shift effects, and ventilation support in the formation of axonal bulbs is discussed. The presence of axonal bulbs cannot necessarily be attributed to shearing forces alone.

Povlishock et al, Department of Anatomy, Virginia Commonwealth University, Richmond, Brain Pathol 1995 Oct;5(4):415-26, state:

Traumatic brain injury has long been thought to evoke immediate and irreversible damage to the brain parenchyma and its intrinsic vasculature. In this review we call into question the correctness of this assumption by citing two traumatically related brain parenchymal abnormalities that are the result of progressive, traumatically induced perturbation. In this context, we first consider the pathogenesis of traumatically induced axonal damage to show that it is a delayed consequence of complex axolemmal and/or cytoskeletal changes evoked by the traumatic episode which then lead to cytoskeletal collapse and impairment of axoplasmic transport, ultimately progressing to axonal swelling and disconnection.

Second, we consider the traumatized brain's increased neuronal sensitivity to secondary insult, evidence is provided that it is triggered by the neurotransmitter storm evoked by traumatic brain injury, allowing for sublethal neuro-excitation. Collectively, it is felt that both examples of the brain parenchyma's response to traumatic brain injury show that the resulting pathobiology is much more complex and progressive than previously envisioned, and as such, rejects many of the previous beliefs regarding the pathobiology of traumatic brain injury.

In other words; trauma does not always result in an immediate shearing effect, as claimed by the prosecution. This also leads one to suspect that the so-called 'acceleration/deceleration' mechanism, described by many is not necessarily correct—as far as diffuse axonal injury is concerned.

The foregoing articles demonstrate some vital issues:

• Anoxia can cause axonal injury
• Once the cascade of abnormal biochemical events is initiated it is virtually impossible to reverse the process
• The extreme complexity of the issue
• Reoxygenation ('reperfusion'), which occurs when the circulation is reestablished, often accelerates the cascade instead of stopping it.
• Iron hemostasis (here meaning 'chemical control') when deregulated, that is when iron, which is normally carefully controlled, gets loose, there is an addition to the cascade of abnormal biochemical processes.

It is extraordinary, when the seriousness of charges laid, are considered, that factors such as those just considered are not raised during shaken baby trials. To understand the issue more fully it is necessary to consider what are called 'free radical reactions', the control of these by 'antioxidants' (particularly vitamin C), the role of bacterially produced toxins (endotoxins and exotoxins), the manner by which these toxins damage the endothelium (lining of blood vessels) and utilize reserves of vitamin C.

Francine's prenatal records show that she was treated with antibiotics for a chronic E.coli infection, and she tested positive for E.coli six months postpartum. So it is necessary to describe some of the mechanisms involved in these infections, and the role played by what is known as 'endotoxin'. Endotoxin is formed by so-called 'Gram-negative' bacteria: the best known is E.coli. This organism normally inhabits the gut. It plays an essential role in digestive processes and produces some compounds that are necessary for life. However, under certain conditions it can become invasive and cause illness or death either directly or indirectly through a variety of mechanisms.

Endotoxin is usually stored in the bacterial wall, and only small amounts are released into the environment. It is essential for bacterial reproduction of Gram-negative bacteria and, normally, under strictly controlled conditions, plays an important role in the development of host immune responses. It is released when the bacterial cell wall breaks down so an abnormal amount of Gram-negative bacterial death can result in the release of excessive amounts of endotoxin. Mechanisms involved are complex.

Factors involved in excessive amounts of endotoxin being produced in infants include:

• Failure to exclusively breast-feed
• The administration of antibiotics
• Infections, bacterial and viral
• The administration of vaccines
• Immune disturbances resulting in the 'overgrowth' of 'abnormal' intestinal bacteria.
• The oral administration of excessive amounts of iron
• Events following what is known as 'reperfusion injury'. When body tissue or organs are temporarily deprived of oxygen and nutrients (for example, when a tourniquet is applied for a period to a limb and then released, or the brain is temporarily deprived when respiration ceases for a period). The circulation is reestablished and products, formed in the tissues during the period of anoxia, are released. These products are carried in the blood stream to the gut, where excessive amounts of endotoxin are quickly produced and absorbed into the blood stream. A cascade of abnormal biochemical processes is initiated and a rapid destruction of some body tissues, including parts of the brain, can result.
The problem does not stop there. Endotoxin can:

• Disturb coagulation/bleeding factors
• Damage the endothelial linings of blood vessels and cause hemorrhages
• Utilize vast quantities of vitamin C (vitamin C 'detoxifies' endotoxin.)
• Precipitate any of a multitude of forms of scurvy, which in turn may result in hemorrhage in a variety of organs or tissues
• Specifically 'target' the brain.
• Disturb liver functions

There are several important issues that must be documented first:
Endotoxin can occur in the absence of bacteremia

Danner et al. Critical Care Medicine Department, Warren G. Magnuson Critical Center, National Institutes of Health, Bethesda, Md 20892. Chest 1991 Jan:99(1):169-75. state:

Detectable endotoxin occurred in 43 of 100 patients with septic shock, but only one of ten patients with shock due to nonseptic causes. During septic shock, endotoxemia frequently occurred in the absence of Gram-negative bacteremia.

Endotoxins have a very fast action

Aleo et al, Inhibition of ascorbic acid uptake by endotoxin: evidence of mediation by serum factor(s), Proc Soc Exp Biol Med 1998 May;179(1):128-31. states:

The effect of endotoxin appears to be instantaneous since the inhibition seen in the cells without any preexposure was similar to the cells preexposed to endotoxin for up to 6 hours.

Endotoxin 'inhibits' the uptake of vitamin C

Aleo, in the article just documented states:
Endotoxin inhibited ascorbic acid uptake by fibroblasts in a dose dependent manner

The inhibition of the ascorbic acid transport by endotoxin

Garcia et al, Department of Biochemistry and Molecular Biology 1, Faculty of Chemistry, Universidad Complutense, Madrid, Proc Soc Biol Med 1990 Apr;193(4):280-284, state:

Lipopolysaccharide (endotoxin) of E.coli modifies the ascorbic acid uptake in a calcium-dependent manner. At low calcium concentrations, lipopolysacharide exerts a stimulating effect on ascorbic acid transport and at high concentrations lipopolysaccharide produces a dose-dependent inhibitory effect. This inhibition of the ascorbic acid transport by the endotoxin can alter the ascorbic acid accumulation in the adrenal gland.

Activation of blood coagulation system during endotoxemia

Luscher, Activation of blood coagulation system during endotoxemia. Fortschr Med 1975 Aug 14;93(22-23):1072-6, states:

Endothelial cells are in fact severely affected by endotoxin and may even be removed from the vascular wall, thus making accessible the subendothelial activating factor X11. Thrombin in turn affects the vascular endothelium therefore, once initiated, the process of intravascular activation of coagulation will perpetuate, this the more as platelets in turn will be stimulated into activity.

The microcirculation during endotoxemia

McCusky et al, Department of Cell Biology and Anatomy, College of Medicine, University of Artizona, Tucson 85724-5044, USA, Cardiovasc Res 1996 Oct;32(4):752-63, state:

The initial responses to endotoxemia are detectable in the microcirculation as microvascular inflammatory responses characterized by activation of the endothelium stimulating these cells from their normal anticoagulant state to a procoagulant state with increased adhesiveness for leucocytes and platelets. Concomitantly, arteriolar tone is lost and reactivity to a variety of agonists is modified. Tissue damage subsequently results not only from reduced perfusion of the exchange vessels, but also from injurious substances released from activated, sequestered leucocytes as well as activated endothelial cells, macrophages, and platelets. This is the result of endotoxins inducing activation and interaction of a number of effector cells, cascades, and acute-phase responses, such as the complement, coagulation, bradykinin/kinin, and hematopoietic systems accompanied by the release of a myriad of mediators. These include eicosanoids, cyctokines, adhesion molecules, reactive free radicals, platelet-activating factor, and nitric oxide.

Free radical reactions and endotoxins
(Note at this stage the association discussed in the above article.)

Ascorbic acid reduces endotoxin-induced lung injury

Dwenger et al, Institut fur Klinische Biochemie, Medizinische Hochshule Hannover, Germany, Eur J Clin Invest 1994 Apr,24(4):229-35, state
Paired experiments were performed on eight sheep in which they received either endotoxin alone (ET group) or in combination with ascorbic acid (Et plus Asc group). As a result, for the ET=ASC group a general and most significant improvement in the early hypertensive phase and the late permeability phase of cardiorespiratory function was observed in comparison with the ET group.

Endotoxin affects the permeability of the blood-brain barrier and causes activation of the microglia

Mayer, Department of Pharmacology, Chicago College of Osteopathic Medicine, Midwestern University, Downers Grove, Illinois; Medicina (B Aires) 1998;58(4):377-85, states:

Lipopolysaccharide (endotoxin) affects the permeability of the blood-brain barrier and causes activation of brain microglia (cells that are between the neurons).

Brain injury induced by continuous infusion of endotoxin

Tamada, Department of Pathology, National Defense Medical College, Saitama, Japan; No To Shinkei 1993 Jan:45(1):49-56, states:

Hemorrhagic intracerebral lesions, analogous to multiple punctate hemorrhagic necrosis seen in the brain of human disseminated intravascular coagulation (DIC) can be induced in rats by continuous infusion of E.coli endotoxin.

Coagulation disturbances after endotoxin administration

Wyshock et al, Sol Sherry Thrombosis Research Center, Temple University School of Medicine, Philadelphia; Thromb Res 1995 Dec 1;80((5):377-89, state:
Low doses of endotoxin administered to human volunteers stimulate activation of fibrinolytic, contact and coagulation systems.

Activation of clotting factor XI in experimental human endotoxemia

Minnema et al, Centre for Hemostasis, Thrombosis, Atherosclerosis and Inflammation Research, Amsterdam; Blood, 1998 Nov 1;92(9):329-301, state:

These data provide the first evidence for Factor XI activation in low-grade endotoxemia and suggest that FXI is activated independently of FXII.

Endotoxin affects platelets

Stohlawetz et al, Clinic of Blood Group Serology and Transfusion medicine, Transfusion Medicine, Vienna University of Medicine; Thromb Haemost 1999 Apr;81(4):613-7, state:

Low grade endotoxemia induces a rapid fall of platelet counts, which is followed by an early increase in reticulated platelets and plasma thrombpoietin levels but not of glcocalicin levels, Finally, peripheral platelet counts increase several days after endotoxin infusion.

Sheu et al, Graduate Institute of Medical Svciences, Taipei Medical College, Tawain; Eur J Haematol 1999 May;62(5):317-26, state:
Therefore, endotoxin-mediated alteration of platelet function may contribute to bleeding diathesis in endotoxemic patients.

Ascorbic acid modulates in vitro the function of macrophages from mice with endotoxemic shock, and helps to control free radical reactions

Victor et al, Department of Sanimal Physiology, Faculty of Biological Sciences, Complutense University, Madrid; Immunopharmacology 2000 Jan;46(1):89-101, state:

The toxic effects of oxygen radicals (free radicals) produced by immune cells can be controlled to certain degree by endogenous antioxidants because of their scavenger action (a chemical reaction). Antioxidants, such as ascorbic acid, are free radical scavengers and improve the immune response. In the pathogenesis of endotoxic shock the reactive oxygen species produced by phagocytes have been implicated. These data suggest that ascorbic acid can regulate the phagocytic process in endotoxin shock, principally decreasing free radical production and thus it could reduce endotoxic shock severity.

Antibiotics release endotoxin

Holzheimer, Klinik fur Allgemeichirurgie, Martin-Luther-Universitat-Wittenberg, Germany; Infection 1998 Mar-Apr;26(2):77-84, states:

There is clinical evidence for antibiotic-induced endotoxin release.

Rotimi, et al, Department of Microbiology, Faculty of Medicine, Kuwait University; J Chemother 2000 Feb;12(1):40-7,state:

Endotoxin liberation was detected in the filtered broth cultures after exposing the organisms to four different concentrations of the antibiotics. All seven gram-negative bacteria investigated liberated induced cell-free endotoxin.

Ischemia-reperfusion injury causes endotoxemia but not bacterial translocation

Yassin et al, Department of Surgery, Queen's University of Belfast; Br J Surg 1998 Jun;85(6):785-0, state:

It has been suggested that reperfusion of the acutely ischaemic limb alters gut permeability. The effect of lower limb ischaemia-reperfusion on systemic endotoxin and antiendotoxin antibody concentrations and the incidence of bacterial translocations was investigated. These results demonstrate that a remote and isolated ischaemic-reperfusion injury to the lower limb, in the absence of infection or bacterial translocation, causes endotoxaemia.

Yang et al, Burn Center, Postgraduate Medical College, Hospital, Beijing; Chin Med J (Eng) 1997 Feb;110(2):118-124, state:

Tissue reperfusion might induce the production of oxygen free radicals, resulting in lipid peroxidation injury, especially to intestinal mucosa, and resulting in disruption of mucosal barrier function followed by endotoxemia.

Endotoxin targets the brain within specific cellular populations

Lacroix et al, Laboratory of Molecular Endocrinology, CHUL Research Center and Laval University, Quebec; Brain Pathol 1998 Oct;8(4):625-40, state:
These results provide the very first evidence of a direct role of endotoxin on specific cell populations of the central nervous system, which is likely to be responsible for the transcription of proinflammatory cytokines, first within accessible structures from the blood vessels and thereafter through scattered cells.

Endotoxin causes focal necrosis in the brain

Gilles et al, Ann Neurol 1997 Jul;2(1):49-56, state:
Telencephalic white matter of the neonatal kitten frequently contained astrogliosis or focal necrosis (sometimes including the thalamus and the caudate) following a single injection of endotoxin. No evidence for a disseminated intravascular coagulopathy was found. Large hemispheric cavity lesions are not accompanied by neurological deficits in the kitten.

This last reference shows what has been observed in human neonates—that sometimes quite extensive brain trauma is not accompanied by abnormalities in clinical states detected by ordinary neurological examinations.

Vitamin C and E prevent endotoxin induced cell death in human endothelial cells

Haendler et al, department of Internal medicine1V. Johann Wolfgang Goethe University, Frankfurt; Eur J Pharmacol, Dec 19;317(2-3):407-11, state:
The reduction of endotoxin-induced apoptosis (cell death) by vitamin C and E was paralleled by an increase in Bel-2 and a decrease in Bax protein levels. Thus vitamin C and E seem to interfere with the Bel-2 family of apoptosis regulators in human umbilical venous endothelial cells.

Immunological imbalance produces susceptibility to endotoxin

Chedid, Institut Pasteur and Center National de la Recherche Scientifique, Paris; Journal of Infectious Diseases, Vol128, supplement, July 1973, pages S112-S117, states:

It is now well established that, in many cases, immunological imbalance produces susceptibility to endotoxins.

Increased sensitivity to endotoxin can develop suddenly—and be fatal

Braude, Bacterial Endotoxins, Scientific American ?date, states:

Giuseppi Sanarelli of the University of Rome and Gregory Ahwartzman of Mount Sinai Hospital in New York independently found that if they injected a somewhat less than fatal dose of endotoxin into a rabbit and followed this with another 12 to 24 hours later, the second dose led to massive destruction of the kidney tissues. Other investigators - Rene Dubos and Russell Schaedler of the Rockefeller Institute and Herndon F. Douglas and I found that exposure to endotoxin can increase the lethal effect of the toxin, with the result that a smaller dose will kill the animal.

Bacteria in the gut of normal breast-fed infants, bottle-fed infants and infants that are fed in both ways

Iseki, Department of Pediatrics, Fukagawa General Hospital, Hokkaido Igaku Zasshi, 1987 Dec,62(6):895-906, states:

The development of faecal bacterial flora was studied to determine the differences between various types of feeding. Enterobacteria first colonized predominately in neonatal intestine. In the breast-fed group enterobacteria decreased gradually. Bifidobacteria began to increase after 2 or 3 days of life and outnumbered other bacteria. In the bottle-fed group, enterobacteria maintained their high counts despite the increase of bifidobacteria. At 1 and 3 months of age, bifidobacteria were the most prevalent organisms in all feeding groups. However, the numbers of other bacteria such as enterobacteria were significantly greater in the bottle-fed infants. In the breast-fed formula supplemented group, bacterial colonization of the intestine was in the middle range. In addition to the microbiological study, physiochemical properties of faeces and milk (i.e, pH and buffering capacity) were examined to explore their effects on the faecal bacterial flora. Faeces from breast-fed infants had a lower pH. Low buffering capacity of human milk seems to produce an acidic environment in the intestine, which is favourable for the growth of bifidobacteria and unfavourable for the growth of potential pathogenic bacteria. These results suggest that breast feeding is beneficial for protection against intestinal and/or systemic infection.

Golding et al, Unit of Pediatrics and Perinatal Epidemiology, University of Bristol, U.K., Early Hum Dev 1997 Oct 29;949 Suppl:S131-S142, state:
The major health advantage of breast feeding that has been clearly demonstrated remains in the protection of the infant from certain infections in early life.

Failure to exclusively breast feed may set the stage for gastrointestinal disturbances, and/or gastrointestinal or systemic infections, and set the stage for excessive endotoxin production. Francine did not exclusively breast feed.


Neonatal deaths after vaccine administration
The older form of pertussis vaccine contained a variable and uncontrollable amount of endotoxin and many of the serious adverse side effects were attributed directly to this. The acellular vaccine, recently introduced, is safer but not entirely free from problems. Hepatitis B vaccine has its share of problems.

Pertussis toxin by itself (without endotoxin) can cause encephalopathy

Steinman et al, Proc NatlAcad Sci USA 1985 Dec;82(24):8733-6, state:
A mouse model for encephalopathy induced by pertussis immunization has been described; it has features that closely resemble some of the severe reactions, including seizures and shock-like state leading to death, occasionally seen after administration of Bordetella pertussis (whooping cough) vaccine. Two lines of evidence implicate pertussis toxin as the active bacterial component. Purified pertussis toxin plus bovine serum albumin was tested and found to induce the lethal encephalopathy, demonstrating that the toxin was the critical constituent of B. pertussis responsible for encephalopathy.

However one interprets these results the fact is that either or both—pertussis toxin and endotoxin—can cause fatal encephalopathy.

Manette et al, Neonatal deaths After Hepatitis Vaccine, The Vaccine Adverse Reporting System, 1991-1998; Arch Pediatr Adolesc MED/VOL 153. Dec1999, states:

The causes of death reported by the medical examiner at autopsy were SIDS, infections, bronchopneumonia (no causative organisms noted)—and one case of intracerebral hemorrhage.

Slack et al, Department of Paediatrics Royal Hampshire County Hospital, Winchester, Hampshire, U.K; Arch Dis Child Fetal Neonatal Ed, 1999 Jul;81, state:

Four premature infants developed apnoeas severe enough to warrant resuscitation after immunization with diphtheria, pertussis, and tetanus (DPT), and Haemophilis influenza B (Hib). Although apnoeas after immunizations are recognised, they are not well documented. It is time to further research to elucidate the best time to immunize such infants.

Endotoxin can be identified and its concentration measured, after death

Crawley et al, Department of Microbiology, Withington Hospital, West Didsbury, Manchester, U/K; FEMS Immunol Med Microbiol 1999 Aug 1;25(1-2):131-5, state:

Following the development of an animal model which confirmed that endotoxaemia could be detected after death, we studied endotoxin levels in blood and tissue taken at autopsy.

There is a synergistic effect when two toxins are administered at the same time

Drucker et al, Department of Cell and Structural Biology, University of Manchestser; J Clin Pathol 1992 Sept;45(9):799-801, states:

Straphylococcus aureus toxin preparations showed high lethality when tested alone. E.coli toxin preparations showed high lethality except in high dilution. When the same toxin preparations were tested simultaneously in combination, lethality rose to 14 out of 15. Similar findings were observed over a range of toxin dilutions.

This could be an important issue when an infant has an infection (of any sort), because endotoxin could be produced. If a vaccine is administered at that time more endotoxins can be injected. It must be remembered that the older form of pertussis vaccine contains an uncontrollable amount of endotoxin. Even with the so-called 'acellular' pertussis vaccine toxins are present.

Controversy surrounding this vitamin has escalated during the past 40 years and reached a level that often prevents logical discussion. Several facts need to be considered:

• We cannot live without vitamin C
• Requirements vary enormously from one individual to another
• Requirements can vary from day to day according to a host of factors including environmental conditions and the development of infectious diseases.
• Scurvy, although accepted as a 'specific' disease, is found to be, in clinical practice, a combination of several diseases. The mode of presentation can vary enormously and the presenting picture can be complicated by the multitude of precipitating factors, many of which can overwhelm the situation before there is time for the development of classical signs of scurvy.
• Dietary deficiency of vitamin C is one cause.
• Excessive utilization is another cause.
• Precipitating factors can often be identified when suspected cases of scurvy (in one of its many forms) are investigated
• Reasons for excessive utilization are responsible for many of the atypical presentations.
• The brain, because of its extreme dependence on vitamin C can be specifically targeted by problems involving vitamin C utilization when cerebral circulation is disturbed for any reason—including anoxia, or endotoxin damage.
• Free radical reactions, particularly in the brain, initiated by anoxia (that can be universal throughout the body—as seen after a cardiac arrest—or localized in the brain (or a part of the brain) when parts of the cerebral circulation is disrupted, can trigger these reactions.
• Endotoxin can trigger free radical reactions by damaging the endothelium (blood vessel linings) of cerebral blood vessels, then entering the brain tissue where the cascade of reactions accelerates violently
• At the same time the endotoxin-initiated damage utilizes available stores of brain vitamin C, the disruption of the cerebral circulation prevents supplies of vitamin C entering the damaged brain areas, and the cascade of free radical reactions accelerates further. At the same time, vital supplies of oxygen, glucose and other nutrients are prevented from entering the damaged brain tissue and aiding brain tissue recovery. That is one reason for the rapid development of total brain circulation failure, cerebral edema and brain death.
• At the same time brain, retinal, and other intracranial hemorrhages can occur.
• In 'pure' cases of scurvy, vitamin C deficiency can damage the connective tissue of blood vessels and this can result in hemorrhages
• Vitamin C deficiency (excessive utilization has the same effect) can disturb clotting factors.
• The extreme complexity of so-called 'scurvy' is apparent to anyone who seriously studies the disease. The old 'gold standard' where a response to the administration of vitamin C was used as proof for a diagnosis, no longer applies, because many conditions that are obviously not scurvy (such as acute alcoholism) respond to the intravenous administration of large doses of vitamin C. These conditions do, however, demonstrate the complex role that vitamin C plays in human biochemistry.

Vitamin C utilization and requirements

Sherry Lewin, Department of Postgraduate Molecular Biology, North-East London Polytechnic, London, in a book, Vitamin C: Its Molecular Biology and Medical Potential, 1976, Academic Press, ISBN:0 12 446 3509, on page 137, states:
The daily dose of ascorbate intake is dictated by the need to maintain an ascorbate reservoir in the body at a level which can readily meet the demands made upon it The demands under 'normal' conditions and those when the body is exposed to attack differ considerably.

On pages 182-183) Lewin states:

It follows that the variation in vitamin C requirements by different individuals allowing for the various parameters noted, is of the order of a hundred to a thousand-fold. If the 'minimal' ideal antiscurvy-based requirement of ascorbate are in the region of 5 to 20 mg daily, the probable range for the needs of ascorbate extended by a hundred-fold to a thousand-fold is between 0.5 and 20 g. However, if the probability of oxidation and delactonization prior to absorption into the blood is eliminated, the range is likely to lie between very approximate limits of 0.2 to 10 g daily.

These figures do not allow for problems in specific organs or tissues when the blood supply is temporarily restricted, and these figures will be not accepted by most medical authorities. However, they match closely what I have observed clinically over nearly 33 years. It is the increased need for vitamin C, in some circumstances, that initiated my interest in the subject and enabled me to deal successfully with a range of previously fatal conditions. It is not, in the case being considered (Alan Yurko), of critical importance, because there are many aspects of the case for the defense that can be logically argued without it. However, it does help when attempts are made to make some sense of the complex issues involved.

Most authorities state that a figure of between 5 to 60 mg of vitamin C daily (for an adult) is sufficient. No attempt is made, in individuals, to examine biochemical pathways that are dependent on vitamin C. A true scientist would not just assume that all was well. Tests would show if, in some organs, vitamin C was not present in sufficient amounts to allow normal biochemical pathways to function normally or to maximum ability when necessary. This simple and logical approach, for reasons that are difficult to understand, is not followed when vitamin C needs and utilization are considered. It is certainly not good science to state that a particular intake of vitamin C will prevent scurvy and, therefore, that is all that is required.

Levene et al, Laboratory of Cell Biology and Genetics, National Institute of Diabetes, Digestive, and Kidney Diseases, National Institute of Health, Bethesda; Am J Clin Nutr, 1991 Dec;54(6 Suppl):1157S-1162S, state:

Ascorbic acid requirements are based on preventing the deficiency disease scurvy and on urinary excretion of vitamin C. We proposed the first quantitative approach to determining optimal requirements for ascorbic acid and other vitamins, called in situ kinetics. In situ kinetics biochemically is based on the application of Michaelis-Menten reaction kinetics to ascorbic acid-dependent reactions in situ.

Scurvy, despite being supplemented with vitamin C

Hess, page 229,states:
In spite of the fact that it (an infant) had been receiving an antiscorbutic for almost this entire period, it developed scurvy.

A more recent reference is as follows:

Presse Med. 2004 Feb 14;33(3):170-1 states:
Scurvy can occur in hospitalized patients despite vitamin supplementation...A 63-year-old patient who had spent several weeks in intensive care developed an unexplained anemia and ecchymoses [extravasation of blood into the subcutaneous tissues]. Despite daily administration of 130 mg/day of vitamin C since his admission, his ascorbic acid blood levels had collapsed. Administration of 1g/day relieved his symptoms within four weeks.

I would assume that the cause was excessive utilization of Vitamin C, and administration by injection would have resulted in a more rapid response.

Some infants and adults are susceptible to scurvy

Hess, page 229, (a continuation of the previous reference) states:
It was evident that this baby was peculiarly susceptible to scurvy.

Scurvy can be precipitated by infections (through increased utilization)

Hess, page 229, (a continuation of the previous reference) states;

It may be added that the second attack was complicated by nasal diphtheria.
Hess, page 219, states:

This is an instance where latent scurvy was prematurely changed to acute scurvy by an intercurrent infection; an epidemic of grippe precipitated a pseudo-epidemic of scurvy.

Hemorrhage in any part of the body is a striking manifestation of scurvy. This includes the brain, the meninges, spinal cord, and retina.

Hess, page 84, states:

Hemorrhage is such a striking manifestation of scurvy that it is not surprising to find it was regarded by older writers as the pathognomonic sign of scurvy.
Hess, page 92, states:

Hemorrhage may occur into the brain substance, into the cord or the membranes surrounding them. Petechial hemorrhages may or may not occur in cases of scurvy.
Hess, pages 192-193, states:

The skin, mucous membranes and subcutaneous tissues are frequently the sites of hemorrhage. There is a difference of opinion as to how frequently petechial hemorrhages occur in scurvy, particularly as to whether they are encountered early in the disorder. Great variations in this regard may be noted in individuals and in groups of cases occurring at different times. The idiosyncrasy of the individual has to be considered.

This raises, again, the important issue of the variation in the presentation of scurvy—atypical presentations being, more or less, the norm.

Hess, page 105, states:
Retinal hemorrhages were found by Jacobsthal, and by Kitamura.

Miura et al, Rinsho Ketsueki, 1982 Aug;23(8):1235-1240, states:
A case of scurvy with subdural hematoma.

Clemetson, Volume 111, page 223, states:
In a treatise on scurvy, the famous English physician, Willis (1668) mentioned the occurrence of intracranial hemorrhage in the course of the disease. Likewise. Heym (1871) describing his findings at autopsy in eight patients who died of scurvy during the siege of Paris, mentioned one case of hemorrhagic pachymeningitis.

Sutherland (1894) described the findings of recent and old subdural hemorrhages, respectively in two young children who died at 24 and 14 months of age. Both had classical signs of scurvy, with subcutaneous petechiae, ecchymoses, and subperiosteal hemorrhages, but not the spongy bleeding gums which are said to be rare in infancy and early childhood. Another report on 379 cases of infantile scurvy by the American Pediatric Society (1898) ascribed 3 out of 29 deaths to cerebral hemorrhage.

Spinal cord changes are found in some scurvy cases

Hess, page 104, states:
In an infant a 'focal degeneration' of the cord has been described.

Scurvy is not always 'typical'.

Hess, page 183, states:
This is the syndrome which the medical student is taught to carry away to guide him in his every-day practice. It is the acute, florid type, and presents a striking picture, but must not be regarded as the common form of the disorder. If we are to diagnose infantile scurvy early and not overlook its more subtle manifestations, the classical textbook description must be augmented by portrayals of types of the disorder which are less crude and more difficult to recognize.

Coagulation is disturbed in scurvy.

Hess, pages 211-212 states:
A consideration of factors concerned in the coagulability of the blood (Hess's own italics) is of interest. In an investigation (Hess and Fish) it was found that the oxylated plasma (of blood directly from a vain) showed a slightly delayed coagulation time—eight to fourteen minutes. The ' bleeding time' carried out according to the simple method of Duke was slightly increased. Holt reports a case where a child bled to death following incision into an epiphyseal swelling at the lower end of the femur. The number of blood platelets is increased, running parallel, as is usually the case, with the number of red cells.This increase in the blood platelets, recently confirmed by Tobler and by Brandt, is a very exceptional phenomenon, and was not anticipated in connection with a disorder characterized by hemorrhage. The antithrombin content of the plasma is normal.

Note that the platelet counts were significantly raised when baby Alan was admitted after the acute collapse. This is an important issue will be discussed later under the heading of 'coagulation/bleeding disorders'.

Hindriks et al, Department of Haematology, University Hospital Utrecht, The Netherlands, Thromb Haemost 1991 Oct 1;66(4):505-509, states:

We conclude that ascorbic acid feeding had a significant effect on endogenous deposited matrix of smooth muscle calls and fibroblasts, and that the changed composition had profound effects on platelet interaction with these matrices.

Sushkevich et al, Vopr Pitan 1969 Sep-Oct 28:5 23-7, state:

The significance of changes in the functional properties of blood platelets, factor XIII activity and fibrin clot quality in the pathogenesis of hemorrhagic diathesis secondary to experimental vitamin C deficiency.

There will be further discussion of this in the section dealing with coagulation/bleeding disorders. Infantile scurvy has changed in its presentation, and to an extent, in its nature since Hess wrote his book, because of several reasons:

• The use of antibiotics - that release endotoxin
• The widespread use of vaccines that act, in some infants, like infections, increasing the need for vitamin C and precipitating scurvy
• Pollution of the environment, which increases the need for vitamin C that plays an essential role in detoxification systems.

I have been informed by Francine Yurko that all the baby bottles of milk were heated in a microwave. I researched the possible effects of this on the Vitamin C content and found that this did not substantially affect the levels. However, 'hot spots' can be formed in the milk, and these can scald the mouth, gullet, and stomach. Francine was not given this information.

If a nightmare of complexities ever existed in medicine, its cause was the extreme complexity and variability of coagulation/bleeding factors. That is; the causes of spontaneous hemorrhages. Coagulation/bleeding factors are:

• Complex in the extreme
• Poorly understood, despite availability of an enormous array of knowledge.
• Interact with one another in an extremely complex manner
• The clinical history of the patient is of equal importance, and sometimes of greater importance, than the array of special tests available.

Rock et al, New Concepts In Coagulation, Crit Rev Lab Sci 1997 Oct;34(5):475-501, state:

The process of blood coagulation is a complex and incompletely understood process. Now the challenge of the future is to better elucidate the interactions of these components.

Sallah et al, Division of Hematology and Oncology, East Carolina University School of Medicine, Greenville, North Carolina, Postgrad Med 1998 Apr; 103(4):209-210, state:

A single optimal screening laboratory test for hemostasis would evaluate vascular, platelet, coagulation and fibrinolytic functions. Unfortunately, such a test does not exist. The key factor in determining the presence of a bleeding diathesis is obtaining a detailed patient history.

Dr. Jean McPherson, Senior Lecturer in Medicine, University of Newcastle (Australia) Visiting Hematologist, John Hunter Hospital, in a paper supported by the Australian Commonwealth of Health (ISSN 1036-9630), states:

The practice of routine coagulation tests (APTT, PT) without a bleeding time, prior to invasive diagnostic procedures or surgery is often justified as 'covering oneself' in case the patient bleeds. On this basis, tests with a low sensitivity and specificity are done at the expense of a simple clinical assessment.

In the case of Alan Yurko a number of useful tests were done but the principle expressed in the above references still applies. Furthermore, there is a problem when one attempts to interrupt the test results.

Factor XIII - a coagulation/bleeding factor

Problems involving this factor need to be considered in every so-called 'shaken baby' case. Already considered under 'endotoxin' is the relationship between coagulation/bleeding abnormalities, Factor XIII, platelet properties, fibrin quality and vitamin C deficiency. This illustrates clearly how complex the issue is.

Dr. Kovar, Chelsea & Westminister Hospital, London, in a report filed for the 'Australian nanny' (Louise Sullivan) case in London 1998, states:

Factor XIII consists of two subunits: Subunits A and B. Only the subunit A is enzymatically active and acts on ? and ?-chains of fibrin by crosslinking the ?-chains to so-called ?-dimere and the ?-chain to ?-chain polymerisation respectively. This reaction is dependent on the activity of FXIII, which ranges in the normal human beings between 70 and 130%.

Reduced activity of FXIII occurs congenitally and is acquired (in several disorders by reduced synthesis or increased consumption). Acquired FXIII deficiency occurs more often than generally expected in patients suffering from infectious disorders including some virus infections.

Professor Samuel J. Machin, in a report filed in the 'Australian Nanny' (Louise Sullivan, case in London (Dec. 1998), States:

Similarly as Factor XIII is synthesized mainly in the liver (there is also evidence that the a subunit may be synthesized in platelets and the placenta) one also has to consider if the patient has any degree of liver pathology, which could cause deficient synthesis of the protein involved. Therefore when assessing a specific abnormality in coagulation mechanism it is also standard practice to perform liver function tests at the same time. Similarly if a child had any form of acute viral or bacterial illness with associated pyrexia, such an acute illness may have caused increased consumption of Factor XIII activity and may also be due to the generalized effect of such a septicaemic illness to have potentially increased the risks of a child developing a bleeding episode.

On the plasma sent to my laboratory on 20th April 1998 the first test which we performed was an immunological laurall rocket assay which uses specific antibodies against the subunit a and the subunit s. This test showed a partial deficiency. Further tests at that time were not performed as we were not provided with sufficient plasma. A further plasma sample was sent, and an overall functional Factor XIII activity assay was performed by photometric determination. The test on this sample confirmed that the patient had overall deficiency of Factor XIII.

Problems with Factor XIII are not a critical issue in the defense of the Yurko case. However, existence of a problem here cannot be ruled out. Note the abnormal liver function tests which could reflect endotoxin damage. The problem in this case is that specific tests for Factor XIII were not complete so there is no way of knowing if a temporary (acquired) problem existed.

D-dimer and 'consumptive coagulopathy.

D-dimer is a fibrin degradation product and is used as a 'marker' for ongoing fibrinolysis, the activation of fibrinolysis and the severity of the hypercoagulable state. There are, however, some problems in measurement.

Matsuo et al, Hyogo Prefectural Awaji Hospital, Sumoto, Japan, Semin Thromb Hemost 2000;26(1):101-7, state:
The reactivity to cross-linked fibrin degradation products produced during fibrin degradation differs depending on the kind of antibody used against D-dimer. In patients with disseminated intravascular coagulation or earthquake-induced mental and physical stress and in patients with percutaneous transluminal coronary angioplasty, all of which are associated with acute fibrin formation and degradation, some discrepancies between two methods of D-dimer detection, automated latex agglutination assay (LPIA) and enzyme-linked immunosorbent assay (Stago), were found.

No discrepancies in persistent fibrin formation and degradation were found among the healthy elderly, patients with lacunar stroke, and patients with coronary artery disease, almost all of whom had levels under 5.0 microg/mL, as determined by both methods. Although the clinical utility of D-dimer can be achieved by their detection with specific antibodies, measurement of D-dimer as high molecular-weight fragments may be useful to determine whether patients will undergo further fibrin degradation. When intermediate products of the degradation need to be assessed, D-dimer level measurement by LPISA may serve as a suitable marker for ongoing fibrinolysis.

There is a difference in hemostatic/coagulation factors between trauma and sepsis.

Boldt et al, Departmant of Anesthesiology and Intensive Care Medicine Klinikum der Stadt Ludwigshafen, Germany, Crit Care Med 2000 Feb;28(2):445-50, state:
Fifteen patients with severe trauma, 15 sepsis patients secondary to major surgery, and 15 neurosurgery patients (cancer surgery) were studied. Standard coagulation data and molecular markers of coagulation activation and finrinolytic activity (soluble thrombomodulin, protein C, free protein S, thrombin/antithrombin III complex, plasmin=alpha 2-antiplasmin complex, tissue plasmogen activator, platelet factor 4, beta-thromboglobulin) were measured from arterial blood on the day of admission to the intensive care unit (trauma/neurosurgery patients) or on the day of diagnosis of sepsis (baseline value) and serially during the next five days.

Antithrombin III, fibrinogen, and platelet counts were highest in neurosurgery patients but without significant differences between sepsis and trauma patients. Thrombin/antithrombin III complexes increased in sepsis patients but decrease in trauma and neurosurgery p[atients. Tissue plasminogen activator increased in sepsis patients and remained almost unchanged in the other two groups. Soluble thrombomodulin plasma concentration increased significantly in the sepsis group, while it remained elevated in the trauma and was almost normal in the neurosurgery patients. Protein C and free protein S remained decreased only in the sepsis group.

CONCLUSIONS: Alterations of the hemoistatic network were seen in all three groups of critically ill patients. Hemostasis normalized in the neurosurgery patients and post traumatic hypercoagulability recovered within the study period. By contrast, monitoring of molecular markers of the coagulation process demonstrated abnormal hemostasis in the sepsis patients during the entire study period indicating ongoing coagulation disorders in fibrinolysis in these patients.

It is reasonable to assume that sepsis includes endotoxemia. This study demonstrates:

• The complexity of the issue
• That the so-called 'standard' coagulation profiles do not provide sufficient information (as already discussed).
• The lack of information (about these complex coagulation disorders) when so-called 'shaken baby cases are investigated.
• This lack of information denies the defense a potentially powerful weapon, which makes the trial very undemocratic.

I am uncertain reading the Yurko case notes what method was used to determine the D-dimer level, so I cannot assess the full significance of the result, except to state that it was raised >8.00. Normal range quoted is ?0.4) and represents a state of coagulopathy. It is unfortunate that the level of D-dimer did not reveal how far it was above 8.00. In SIDS cases (and there is no need to become involved here in a debate about the significance of this, except to state that there is some evidence that endotoxin is involved in the genesis of SIDS) levels have been found to be extraordinarily high.

Goldwater, et al, The Medical Journal of Australia, Vol 153 July 2, 1990, state:
To our knowledge there have been no published investigations into why babies who have died of SIDS have liquid blood. Cross-linked fibrin degradation products (XLFOPs) were measured using the D-Di test which utilizes a monoclonal antibody directed against the fibrin degradation product, D-dimer molecule.The mean XLFOP level for SIDS sera was 1792 mg/l and for control sera was 56.6. The high levels seen in sera from SIDS cases most probably reflect a massive consumptive coagulopathy.

The pathogenetic mechanism underlying this is uncertain, but it is possible that in some cases it may be related to bacterial toxaemia. This would concur with our finding that toxigenic E.coli are isolated from the intestinal contents more often than from age-matched controls who have died from established causes or from live age and contemporaneously matched babies' faecal samples. Furthermore, intravascular coagulation is known to occur in other conditions caused by E.coli verotoxins, including the haemolytic uraemic syndrome, the pathogenesis of which involves platelet aggregation in vitro, and endothelial damage could contribute to the common pathological findings in SIDS.

Note, obviously, the extraordinarily high levels of D-dimer found. If such levels existed (and they may have existed) in the Yurko case, at least some evidence assisting the defense would have been forthcoming.

Liver function abnormalities and endotoxin.

My interest in this began more than forty years ago when I observed, in some infants, that sudden unexpected death was associated, before death, with liver tenderness. In severe cases, there was obvious liver pain. Autopsies sometimes revealed yellowish patches on the surface and in the body of the livers, surrounded sometimes by red areas. Reports on liver sections were non-specific—a degree of fatty change and some cellular swelling. The changes were not considered to be the cause of death. Years later I was able to associate these liver changes to endotoxin.

In severe cases the liver pain was sufficient to create acute discomfort. Breathing, typically, would be 'grunting' an observation that I have made many times. How did I know that the grunting (in these cases) was due to liver pain? When I administered Vitamin C by injection the grunting ceased quickly and liver tenderness disappeared.
Liver function tests with Alan Yurko were distinctly abnormal. It is certainly possible, indeed probable, that this was due to endotoxin. Other causes, such as viral hepatitis, were not looked for.

Lund et al, Ugeskr Laeger 1998 Nov;160(46):6632-7, state:
Shaken baby. A combination of subdural haematomas and retinal haemorrhages with minimal or no trauma and no coagulopathy is almost pathognomonic of the syndrome.

Note that they state that 'no coagulopathy' is a factor. This, in most cases is never considered.

The earliest suggestion that a coagulopathy may have existed can be found in the Florida Hospital, Emergency Department, notes, dated 11/2/98:
Presenting complaint: Constipation, dry blood in nose (mother) noticed streaks of dried blood - nose and spit (?'spat') up streaks of bright red blood.

This could, of course, be interpreted in various ways. However, the existence of a coagulopathy cannot be excluded. Taken in conjunction with the history, since birth, what is known about coagulopathys/endotoxin/vitamin C utilization, this is highly significant. Certainly, it cannot be ignored. At the very least it is a powerful piece of evidence supporting the defense—a positive detail that clearly fits the 'hypothesis' I have generated.

Next, there is the presence of many of the factors that are known to 'trigger' coagulation/bleeding disorders. These revolve around endotoxin formation.

• Infection, following birth and later
• Antibiotics administered after birth and again later
• Failure to exclusively breast-feed
• The administration of vaccines

Next, there is the 'detail' of the rib and acromion 'pathology', wrongly reported as 'fractures'. At the very least, a differential diagnosis should have been considered in the radiologist's report; and that differential diagnosis should have included 'infantile scurvy'. Had the report been worded in such a fashion, other signs of infantile scurvy and its causes may have been investigated. Obviously, this was not done, and, once again, a critical piece of evidence for the defense was not made available. This is a characteristic feature of most 'shaken baby' trials. For reasons I cannot understand, this feature, instead of aiding the defense, is used as a weapon by the prosecution—indirectly of course—but it has tremendous influence on the outcome.

Next, there are the results of coagulation tests that were performed. In scurvy, the bleeding time may be normal or increased. It is necessary to comment further on this phenomenon. The complexity of the issue is extreme. Variables, including the presence or absence of endotoxin, can render the interpretation of results difficult. And, what is found on clinical examination and with the aid of special investigations may vary, from time to time, in a particular patient.

Capillary fragility can in some cases be demonstrated in cases of scurvy.

Hess, page 212-213, states:
To this end the 'capillary resistance test' was devised. A blood-pressure band, or torniquet, is placed about the arm, and the pressure increased until the forearm becomes cyanosed and the radial pulse is almost obliterated. The pressure is then maintained at this level for 3 minutes. The principle of this test consists in subjecting the capillaries and venules to increased pressure to observe whether this strain results in the escape of blood. In infants the pressure was raised to 90 mm; in some cases it had to be raised higher in order to entirely obstruct the return flow of blood.

The test is considered to be 'positive' when the forearm shows many petechial spots. In normal infants petechiae were almost always absent, or there were few to be seen. This is not a specific test for scurvy, but demonstrates a weakness of the vessel walls, whatever may be the cause. It is found to be positive in the majority of cases of scurvy.

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.


Dianne Jacobs Thompson  Est. 2007
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