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

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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.


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