Man Claims He Was Wrongfully Accused Following Smith’s Testimony
2008/10/01 | CityNews.ca Staff
In light of Justice Stephen Goudge’s scathing review of Ontario’s child forensic pathology system, up to 140 cases involving the deaths of children will be reviewed. That includes the case of Dinesh Kumar, who was accused of shaking his young son to death in 1992.
He’s one of a slew of people who claim they were wrongfully accused of a crime they didn’t commit.
His 5-week-old son died suddenly and inexplicably 16 years ago. Disgraced pathologist, Dr. Charles Smith, concluded at the time that the child died from shaken baby syndrome and Kumar was charged.
It’s a charge he adamantly denies, and now that Smith’s incompetence has been revealed, he’s hoping to be fully exonerated.
“It’s very hard to explain…when you suffer these type of situations,” Kumar said Wednesday. “Those pains, nobody can explain it.”
Despite his vehement claim that he had nothing to do with the death, Kumar still pleaded guilty to criminal negligence causing death rather than face Smith’s testimony — which at the time was considered infallible.
He served just three months in jail but has had to live with the stigma of being called a baby killer.
“It was very painful for me…especially when they charged me, I was totally destroyed.”
Now he’s determined to clear his name.
He’s being represented by attorney for the wrongfully accused, James Lockyer, who has filed a formal notice of appeal. They hope that once the Crown has a closer look at the evidence, he’ll be exonerated without having to go through a full trial.
The child with unexplained fractures
By Dr Colin R Paterson, Department of Medicine, University of Dundee
Unexplained fractures may be the hallmark of all forms of brittle bone disease, explains Dr Colin Paterson
A recently reported judgment¹ has drawn attention to the frequent difficulty attending the diagnosis of the child with unexplained fractures. To many observers the failure of parents to come up with an explanation for fractures found radiologically is ipso facto evidence for non-accidental injury; the lack of explanation must represent a failure to tell the truth about their own or their partners’ actions. However, unexplained fractures in childhood are also the hallmark of all forms of brittle bone disease and immense harm can be done to families by the inaccurate diagnosis of non-accidental injury.
Much of our research over the last 25 years has related to the clinical aspects of the brittle bone diseases and we hold a database with details of over 1,300 patients. The best known of these is osteogenesis imperfecta which has a prevalence of about one in 10,000 in the United Kingdom. It is caused by abnormalities in collagen, the fibrous protein essential for the mechanical strength of bone. In turn, in most cases, this is now known to be caused by defects in the genes responsible for collagen formation. Since collagen is abnormal in tissues other than bone, patients with osteogenesis imperfecta now have detectable features in addition fractures. These include blue or grey coloration of the sclerae (whites of the eyes), discoloration and fragility of teeth, laxity of joints and an increased tendency to bruising or pinpoint bruises known as petechiae. The bruising thought to reflect abnormalities in the collagen of small blood vessels. X-rays may show obvious abnormalities but in a majority of patients the appearances are normal at the time of the first few fractures; many of the abnormalities seen later reflect the fractures and the immobilisation used in their treatment. In some cases osteogenesis imperfecta is passed down from a parent to a child, but many cases are “sporadic” with no known family history.
In most patients with osteogenesis imperfecta the diagnosis is made without undue difficulty on the basis of the clinical signs, the fracture history or the family history. In a retrospective survey of 802 known cases of osteogenesis imperfecta in the United Kingdom² we found that in 691 the diagnosis had been made confidently at birth or at the time of the first fracture. In 96 cases the parents were accused of non-accidental injury on at least one occasion. In 15 cases they had had to contend with case conferences, care proceedings or criminal proceedings.
Over the last 12 years we have identified a distinctive pattern in a minority of patients initially thought to have osteogenesis imperfecta. In this variant, known as temporary brittle bone disease³, the fractures are limited to the first year of life and, to a large extent, the first six months of life. The fracture pattern is often distinctive with rib fractures and fractures at the ends of long bones (metaphyseal fractures) being frequent. These patients may have other features such as vomiting [often projectile) and anaemia. While there s usually no family history of fractures, there is a family history of joint laxity in about two thirds of cases. The cause of the disorder is not yet known but it appears o be more common in twins and infants born before full term.
It is not surprising that both osteogenesis imperfecta and temporary brittle bone disease are often considered in cases in which a child is found to have unexplained fractures. This article summarises a personal experience of cases in which the author prepared a report on the causes of fractures and the likelihood of an underlying bone disease. Since these cases have been studied over some 21 years it has been possible to follow up most of the children concerned for substantial periods.
A database was prepared to include details of each child with information on the mode of referral, the diagnosis reached personally, the legal outcome and the details of follow-up. Additional clinical information was recorded in each case. The current report is restricted to 128 patients living in the United Kingdom, in whom the major problem was the fractures.
Table I shows the source of the referrals. Table II shows the diagnosis made by the author in each case. While patients with temporary brittle bone disease were not recognised as such before 1985, it was clear in retrospect that some patients seen earlier had this disorder. Two infants with an initial diagnosis of temporary brittle bone disease were later re-classified as osteogenesis imperfecta in the light of subsequent fractures.
Of the 105 patients thought to have bone disorders the author provided evidence for care proceedings in 102. Of these infants the eventual outcome was that 78 were returned to their parents (56 initially with conditions), three went to other family members and 21 were removed permanently from their families. In three of these the parents had given up before formal proceedings. In seven families the parents separated; in three because one parent was blamed.
Of the 33 children thought to have osteogenesis imperfecta 25 were returned to their parents. One died later with bronchopneumonia and multiple unexplained gastrointestinal problems. The remaining patients have been followed up for between one and 18 years (total 136 patient-years, mean 5.6 years). There was no evidence of non-accidental injury in this period.
Of the 65 children thought to have temporary brittle bone disease, 48 were returned to their parents. Two died later; one with a cot death and one with late sequelae of birth injury; in neither was non-accidental injury postulated. In 43 of the remaining patients follow-up information was available for between 1 and 11 years (total 248 patient years, mean 5.8 years). There was no evidence of non-accidental injury during this period.
Source of medico-legal referrals 1974-96
Parents' representatives 102
Guardians ad litem 8
Local authority 6
Senior hospital staff 8
General practitioners 3
Diagnosis in 128 patients referred for the diagnosis of unexplained fractures
Osteogenesis imperfecta 33
Temporary brittle bone disease 65
Vitamin D deficiency rickets 5
Scurvy (vitamin C deficiency) 1
Accidental injury 9
Unresolved/non-accidental injury 14
* Hypophosphatasia is an uncommon heritable disorder of bone
In the whole group of 105 children thought to have bone disease the evidence was rejected judicially in 29 cases and formally accepted in 23. In the remaining cases there was no formal finding for a variety of reasons, most commonly because rehabilitation of the child with the family was agreed without a hearing. Among the 65 patients thought to have temporary brittle bone disease this evidence was rejected in 18 and accepted in 11; in the remaining 36 patients there was no judicial finding. An analysis of the clinical findings in these three groups did not demonstrate any differences in relation to a wide range of clinical features.
Over the last 20 years there has been some reduction in the number of new cases referred in which the diagnosis was osteogenesis imperfecta. Increased familiarity with the clinical features of this disorder has led to more frequent early diagnosis. In the past some of the cases referred to the courts had classical features such as abnormal sclerae or teeth, or had a clearly positive family history which had not been sought.2
However, retrospective study of confirmed cases of osteogenesis imperfecta continues to demonstrate that in a minority of patients the diagnosis was extremely difficult at the time of the earlier fractures. Since there may be long fracture-free periods in known cases it is possible to be misled by the lack of subsequent fractures. In one particularly unfortunate family, in which the author was not involved legally, a child was taken into care at the age of 18 months after two fractures.
A subsequent fracture did not occur for a further 18 months and the diagnosis of osteogenesis imperfecta was only made at the age of five years when she was returned to her mother. Retrospective study of the medical records and x-rays in this case revealed little evidence that would have helped to make the correct diagnosis at the time.
While such difficult cases are uncommon they occur too frequently in the United Kingdom as a whole to allow for complacency. Our experience in the current series indicates that where a diagnosis of osteogenesis imperfecta is made and the child is returned to the parents no evidence of subsequent non-accidental injury has been observed in 136 patient-years of follow up. In most cases subsequent fractures occurred but mainly at ages at which the child was able to give a clear account of the events.
In recent years it has become possible to identify abnormalities in collagen formation by cells grown in culture from excised samples of skin. With one approach it was claimed that such abnormalities could be demonstrated in over 80 per cent of cases of osteogenesis, imperfecta4. Such assays are time-consuming and labour-intensive; they are not widely available.
In the past some reports have relied on such methods even in cases in which there was already ample clinical evidence of osteogenesis imperfecta. It is important that the limitations of such tests are recognised.
Temporary brittle bone disease is a much more controversial subject 5, 6, 7. Some of its features as reported by us are those that have been conventionally regarded as typical of non-accidental injury for the last thirty years8 9. However, the evidence that these features, including rib fractures, and metaphyseal fractures are linked to non-accidental injury, is limited. In addition these fractures occur in a wide range of known bone disorders. For example, rib fractures occur spontaneously in known cases of ordinary osteogenesis imperfecta and may occur in utero. Metaphyseal fractures occur not only in osteogenesis imperfecta but also in at least five other bone disorders in the first year of life.
There are four principal types of evidence that support the view that temporary brittle bone disease exists and does not represent misdiagnosed non-accidental injury. First the patients all show striking similarities in their clinical features, the types of fractures, the ages at which they occur, the other symptoms such as vomiting, the other signs such as enlarged fontanelles, and the family history observations. Were these infants not thought to have sustained non-accidental injury they would readily have been recognised as having a distinctive syndrome.
Second, as with ordinary osteogenesis imperfecta, there is often a striking discrepancy between the fractures and other evidence of injury. In typical non-accidental injury bruises greatly outnumber fractures. In this disorder there may be over twenty fractures but reliable evidence that no superficial sign of injury was present at the time when the fractures occurred.
Third, the same syndrome occurs in infants in whom non-accidental injury can be excluded with confidence, generally because the fractures occurred while the child was in hospital.
Fourth, the evidence provided in this report emphasises that when these patients were returned to their parents no subsequent evidence of non-accidental injury has been identified in 248 patient-years of follow up. The premise underlying care proceedings is that abusive parents remain abusive and that there is substantial risk of further non-accidental injury if an abused child is returned. The follow up findings in this report support the view that in this small distinctive group of infants with unexplained fractures the diagnosis was not non-accidental injury.
Dr Colin R Paterson, Department of Medicine, University of Dundee
¹ Wall ] Re AB (child abuse: expert evidence) (1995)1 FLR 181.
² Paterson CR, McAllion SJ (1989) Osteogenesis imperfecta in the differential diagnosis of child abuse. BM] 299:1451.
³ Paterson CR, Burns ], McAllion S] (1993) Osteogenesis imperfecta: the distinction from child abuse and the recognition of a variant form. Amer J Med Genet 45:187.
4 Steiner RD, Pepin M, Byers PH (1996) Studies of collagen synthesis and structure in the differentiation of child abuse from osteogenesis imperfecta. J Pediatr 128: 542.
5 Smith R, Wynne JM, Hobbs C], Carty H (1995) Osteogenesis imperfecta, non-accidental injury and temporary brittle bone disease Arch Dis Childh 72:269.
6 Shaw DC, Hall CM, Carty H (1995) Osteogenesis imperfecta: the distinction from child abuse and the recognition of a variant form Amer J Med Genet 56:116.
7 Paterson CR Burns }, McAllion S] (1995) Osteogenesis imperfecta variant v child abuse: reply Amer J Med Genet 56: 117.
8 Carty HML (1993) Fractures caused by child abuse J Bone Joint Surg 75-B: 849.
9 Chapman S (1993) Recent advances in the radiology of child abuse Baill Clin Paediatr 1: 222.
I am indebted to Mrs E A Monk for preparing the databases used in this work, to Dr SL] McAllion and Ms ] Hoyal for advice on this article in draft and to the Cunningham Trustees for their support for our work on osteogenesis imperfecta.
Shaken Or Not: That Is The Question
On Dec. 3, The Royal Gazette newspaper in Bermuda published an article by Elizabeth Roberts entitled “Expert witness undisciplined.” Apparently the country’s Court of Appeal “quashed” a young father’s earlier murder conviction and mandatory life sentence for killing his six-month-old daughter and criticized the way a pediatrician testified at the original trial, describing his performance as “unduly theatrical and undisciplined.” The court then convicted the young father of manslaughter and sentenced him to 10 years in prison. According to the report, the pediatrician apparently shook a plastic doll violently “before smacking its head down on the witness box, and is said to have then turned the doll over and done the same to the other side of its head.”
The higher court decreed that “Anyone who used the degree of violence … against a six-month-old child could only have intended to cause at least really serious harm. It no doubt formed the basis of the jury’s decision to convict of murder rather than manslaughter.” The judges added that the expert witness “was wrong to act as he did. It was his duty to give evidence in the least emotive way possible, particularly in a case such as this where feelings were likely to run high. His performance was, to say the least, unduly theatrical and undisciplined.” They addedthat the “evidence was out of line with evidence received by the Court of Appeal in England, which has accepted that a much lesser degree of force than that illustrated by him is all that is required to produce a non-accidental head injury to a child.”
The Bermuda case will not be discussed in full as its details are not available, but general aspects of shaken baby syndrome (SBS) will be explored.
Dolls in Court
Dolls have been used extensively by pediatricians and psychologists to question children and demonstrate how injuries occur. Their use in sexual abuse cases is well known; so is the fact that the technique has been both misused and abused.
Many will recall court scenes where large men, prosecutors or their medical experts, are holding a rubber doll the size of a two-month old baby around the upper torso and shaking it back and forth vigorously to demonstrate to the judge and jury how the accused must have shaken the injured or deceased infant.
The proponents of the SBS (and shaking — impacting baby syndrome) describe the injuries and how they occur usually as follows. “When someone forcefully shakes a baby, the child’s head rotates about uncontrollably because infants’ neck muscles aren’t well-developed and provide little support for their heads. The violent movement pitches the infant’s brain back and forth within the skull, rupturing blood vessels and nerves throughout the brain and tearing the brain tissue.
“The damage is even greater when the shaking ends with an impact — hitting a wall or a crib mattress, for example — because of the strong forces of acceleration and deceleration associated with an impact. After the shaking, swelling in the brain can cause enormous pressure within the skull,compressing blood vessels and increasing overall injury to its delicate structure.” (1)
Since the 1970s, hundreds (maybe thousands) of adults have been jailed because they were believed to have injured their babies or killed them by shaking. Some of these convicted child abusers may themselves have been beaten in prison, even murdered, because everyone, including criminals, hates a child abuser.
There is obviously no doubt that some parents, babysitters and guardians have tortured and killed innocent infants and children. They should be severely punished if they are sane, and receive expert psychiatric therapy if they are deranged.
There is also no doubt that many innocent young parents and caregivers are in jail because they were unjustly accused of shaking or shaking-impacting their children. At trial, the prosecution with its might and resources usually parades expensive medical experts who swear — with authority — that a big man can, indeed, cause subdural and retinal hemorrhages in a small baby and even kill him or her without visible external bruises and injuries, and with no prior history of abuse. In most cases, the only crime the adult committed was to be alone with the child when he or she stopped breathing, a “sinister game of musical chairs” — as one of our Australian colleagues calls the situation.
In September, renowned neuropathologist J.E. Leestma published an important review of the shaken baby syndrome in the American Journal of Forensic Medicine and Pathology, the official publication of the National Association of Medical Examiners. (2)
He stated in the abstract: “The English-language medical case literature was searched for cases of apparent or alleged child abuse between the years 1969 and 2001. Three hundred and twenty-four cases that contained detailed individual case information were analyzed yielding 54 cases in which someone was recorded as having admitted, in some fashion, to have shaken the injured baby. Individual case findings were tabulated and analyzed with respect to shaking as being the cause for the injuries reported. For all 54 admittedly shaken-infant cases, the provided details regarding the shaking incidents and other events are reported. Data in the case reports varied widely with respect to important details. Only 11 cases of admittedly shaken babies showed no signof cranial impact (apparently free-shaken). This small number of cases does not permit valid statistical analysis or support for many of the commonly stated aspects of the so-called shaken baby syndrome.”
In other words, there were only 11 confirmed reports of infants or children who had injuries that could be attributed to shaking and only shaking in the complete English-language medical literature.
According to the Centers for Disease Control and Prevention (CDC) and the National Center on Shaken Baby Syndrome (2005), “Shaken baby syndrome (SBS) is a form of child abuse affecting between 1,200 and 1,600 children every year. SBS is a collection of signs and symptoms resulting from violently shaking an infant or child.” (3)
Some areas of the country seem to report more cases of SBS than others and in certain states, medical centers with organized child abuse teams somehow diagnose more cases than rural and community hospitals.
The “Preventing Child Abuse” web site of The Children’s Hospital Medical Center in Denver, Colorado, features the following information under “Babies are Fragile.” “Shaken Baby Syndrome is the leading cause of death among child abuse cases in the United States. The syndrome results from injuries received when someone vigorously shakes an infant — usually from 5 to 20 seconds. This can cause severe brain injury and even death. In 2004, The Children’s Hospital saw an average of one child a week with signs of Shaken Baby Syndrome — the youngest just 2 weeks old.” (4)
In 2004, the population of Colorado was estimated at 4,301,261 — or 1.5 percent of the entire population of the United States. The state is 380 miles east to west and 280 miles north to south. It has high mountains and snow in the winter. Even if every case of SBS in Colorado was seen at Denver Children’s Hospital, 52 cases of Shaken Baby Syndrome in one year would translate to a national incidence of 3,467 cases, almost three times the CDC figures.
According to a 2004 publication, a study conducted by the University of North Carolina at Chapel Hill found that an estimated 50,000 cases of shaken baby syndrome occur each year in the United States. Of that number, 300 children die. (5)
It is obviously unlikely that the good people of Colorado and North Carolina shake their children more frequently than in the rest of the country or that the CDC and the National Center on Shaken Baby Syndrome are underestimating the national number of cases of SBS.
Shaking and neck injury
Werner Goldsmith, PhD, former chair of the head injury model committee at the National Institutes of Health and a professor at the University of California, Berkeley and its 2001 Distinguished Engineering Alumnus Award recipient, has stated unequivocally: “I am absolutely convinced that in order to do serious or fatal damage to an infant by shaking you have to have soft tissue neck damage.” Goldsmith has calculated that a fall backward from three feet onto a hard surface, like concrete, can produce nearly 180 Gs of acceleration — 180 times the force of Earth’s gravity — enough to cause a subdural hematoma. Shaking a child once a second through a range of one foot produces only 11 Gs, at the most. “There is an order of magnitude difference between shaking and falling,” he says, “From the point of view of the brain, shaking is a much, much milder form of braking than a fall.” To complicate matters, between five and 10 percent of children are born with undiagnosed subdural hematomas, and 30 percent are born with retinal bleeding. “If you get a rebleed, you may get something that looks like shaken baby syndrome…. You should be able to show neck damage to prove shaken baby syndrome.” (6)
In most of the cases I have reviewed, an MRI of the neck had been ordered and every time, it was normal. Yet, in every one of those cases, accusations were still made and charges were still filed. There is no doubt that the ordering physicians would have considered positive cervical findings as uncontestable proof of SBS and yet, not one of those physicians has ever accepted a totally normal MRI of the neck as proof of innocence and against shaking as demonstrated by Goldsmith. It seems strange to send an infant near death into a tube halfway across the hospital to get an expensive MRI and then to ignore the results of that study.
Obviously everyone knows that a passenger in a stopped car (whether a child or an adult) who is rear-ended by another car or truck going at least 40 miles an hour is likely to suffer a severe whiplash injury to the neck without brain damage, retinal bleeding and/or a brain hemorrhage.
A rush to judgment
As a rule, regardless of the history — past and present — the symptoms and the laboratory findings, if an infant or a child is discovered to have retinal hemorrhages and intracranial bleeding (subdural hemorrhages or subarachnoid hemorrhages), the case is immediately labeled ”shaken baby syndrome” and other diagnoses are not even considered. Social Service is consulted and the Child Abuse Team promptly endorses the notion that the infant must have been shaken and the adult, who happened to be there at the time, must be the perpetrator — even when objective evidence of other causes is glaring. From that moment on, the unfortunate parent is considered guilty, till proven otherwise, which is not easy if he or she is poor and uninformed.
John Plunkett, a renowned forensic pathologist at Regina Medical Center in Hastings, Minnesota, wrote in a 1998 letter to the American Journal of Forensic Medicine and Pathology: “Too many of my colleagues (and most other physicians and almost the entire general public) think our profession is the “whodunit” discipline. It is not. Forensic pathology is the “what happened” specialty. When our focus is on the “who,” we forget the “what” or may consider it unimportant. Worse, we may alter our explanation/interpretation of the “what” to make it conform to our opinion of the “who.” The need to consider alternative explanations ceases, doors to further inquiry close: Do not go beyond, you will find nothing there. Objectivity fails because we are forced to defend an advocacy role, be it for the state or for the defendant. We must not forget that our only responsibility is to bear witness within the limits of science.”
The most tragic thing about our present obsession with SBS is not only that an innocent adult ends up in jail, but that often valuable time is lost, appropriate investigations of the real causes are not undertaken, the correct diagnosis is not even considered, and important and urgent treatment is not provided to the infant who is certainly innocent. Most often, trying to “nail the guilty party,” instead of focusing on helping the baby in the hospital, further injures the infant and compromises recovery.
In March 2004, Plunkett co-authored a landmark editorial in The British Medical Journal with British neuropathologist J. F. Geddes titled “The evidence base for shaken baby syndrome.” (7) I suggest that interested Red Flags readers review that editorial because it is certain to become a major reference on SBS.
In the cases that I have reviewed, important events and findings during the pregnancy and delivery have rarely if ever been considered by the admitting staff. A thorough examination and analysis of every detail is essential to discover the truth and arrive at a scientific and not an impulsive diagnosis.
Radiological examinations should be judicious and carefully ordered. Exposing the infant to an inordinate amount of irradiation and sending him or her from the close observation of the intensive care unit to the x-ray department repeatedly trying to prove that a distal hair line fracture exists is immoral and borders on malpractice. Such investigations can be done more appropriately when the child improves and, by then, the presence or absence of a callus will clarify the diagnosis.
Laboratory examinations must include bleeding/clotting studies and liver function tests in addition to the routine admission orders. Sometimes, extensive testing may be required to assess nutritional status, enzyme levels and liver, gut and kidney function. The results should then be interpreted properly and the tests repeated to demonstrate a trend — if needed. The diagnosis of SBS should not be made till all the results are considered.
On admission, blood should be drawn for a PIVKA -II test to rule out late-onset hemorrhagic disease (8) and for a blood histamine and serum vitamin C levels to rule out subclinical scurvy and histaminemia. (9)
In addition to details of the recent past history including illnesses, antibiotic use, exposures, feeding problems, etc., it is essential to list and date vaccinations given in the 21 days preceding admission. (10)
The following statement by Australian pathologist-hematologist and SBS expert Michael Innis summarizes his beliefs and is shared by many of us now: “They will have successfully demolished my explanation if they can document a single case of shaken baby syndrome or “inflicted shaking/impact injury” (as they prefer to call it), which occurred outside the 21-day period and in which a disorder of haemostasis, nutrition or liver disease was convincingly excluded. I repeat, the diagnosis of shaken baby syndrome or inflicted shaking/impact injury is a proven figment of the imagination of some in the medical profession and should be relegated to the scrap heap of history before it causes any more shame to the profession and disaster to innocent families.” (10)
For more than 30 years, it has been assumed that the presence of retinal hemorrhages in an unconscious child is “evidence” of shaking or shaking impacting. The unquestionable scientific fact is that although retinal hemorrhages with or without intracranial bleeding can occur after abuse, they are not seen only in cases of SBS.
In 1997, Rohrbach stated: “Intraretinal hemorrhages alone are typical, though not pathognomonic for the battered-child syndrome.”
Renowned neurosurgeon Ronald Uscinski recently wrote in the British Journal of Neurosurgery (12) “prior to 1972, the presence of retinal hemorrhages was a diagnostic aid in detecting the presence of chronic subdural hematoma in children, and has long been known among neurosurgeons to reflect an abrupt increase in retinal venous pressure.”
There are three important statements about retinal hemorrhages:
- The actual mechanism of retinal hemorrhages is unknown. (Riffenburgh 1991)
- There have been no controlled studies supporting a purely mechanical etiology for retinal bleeding.
- There is no agreement on what specific pattern or appearance of retinal hemorrhages absolutely suggests inflicted trauma by shaking.
Retinal hemorrhages have been associated with asphyxia, hypoxia, increased venous pressure and cerebral venous spasm. Studies by Jacobi (1986) have shown that increasing intracranial pressure and subarachnoid hemorrhage lead to retinal hemorrhages. In 1998, Jayawant reported an 80 percent association between subdural hemorrhages and retinal hemorrhages and postulated that retinal hemorrhages are not independent risk predictors, but simply markers of the extensiveness and severity of intracranial bleeding.
Retinal hemorrhages can occur with increased intracranial pressure and following subarachnoid and other intracranial hemorrhages (Terson Syndrome). A number of studies (Giangiacomo 1985, Weingeist 1986, Jacobi 1986, Keithahn 1993, Poepel 1994) point out the similarities between Terson’s syndrome and the retinopathy of SBS. Retinal hemorrhages have been reported following accidents, with infections, with coagulopathies and bleeding disorders, in cases of vitamin C and K deficiency, following a third of normal vaginal deliveries (Kaur), and after vigorous cardiopulmonary resuscitation (Goetting).
It is now almost always assumed that subdural hemorrhages in the absence of a witnessed fall or injury are also an indication of child abuse and the result of acceleration-deceleration by shaking or shaking impacting.
This is not true.
Subdural hemorrhages are not exclusively the result of intentional trauma and can be caused by a multitude of biomedical disorders.
Because of their open fontanels, young infants with a subdural bleed may remain neurologically asymptomatic for some time. Babies with subdural hemorrhages often have seemingly unrelated symptoms such as crankiness, restless sleep, poor feeding, vomiting, and failure to thrive.
In a 1998 British retrospective study, Jayawant reported that 60 percent of the children with subdural hemorrhages, which he reviewed, exhibited signs of other trauma (bruising, fractures, etc.). Duhaime (1987), Alexander (1990) and Lancon (1998) reported that in cases of severe cerebral damage and death, overt signs of trauma and abuse were reported even more frequently.
Scientific documentation exists that subdural hemorrhage can and does complicate many medical — non-traumatic — disease entities including non-specific coagulopathies, coagulopathies secondary to bacterial endotoxemia, certain enzyme defects, liver, blood and connective tissue disorders.
Sometimes, the identification of a chronic, as well as an acute, subdural hemorrhage makes the well-paid “prosecution experts” jump to the conclusion that this finding must mean recurrent abuse, when, in fact, the opposite conclusion may be more appropriate. The simple fact that the baby was well-cared for and had no visible external injuries when seen repeatedly for routine pediatric care, while having a subdural hemorrhage, is strong evidence against inflicted trauma.
When such cases are later reviewed with an open mind, other more plausible non-traumatic causes are easily discovered and become the basis for successful appeals.
The infant may have spontaneous and separate acute and chronic subdural hemorrhages or may have a re-bleed in a chronic subdural hemorrhage. The appearance of acute and chronic subdural hemorrhages is different on CT-scans.
In 1977, Bergstrom et al reported: “The histories reveal no new traumas in association with onset of symptoms. Spontaneous rebleeding may well explain the onset of symptoms as well as the attenuation values being so much higher than those of CSF and serum.” (12)
Ommaya, Goldsmith and Thibault in a comprehensive review (22 pages, 126 references) published in 2002 in the British Journal of Neurosurgery wrote: “The five categories of CT imaging were as follows: Layering type SDH hyperfibrinolytically active with a highest tendency to rebleed. The mixed density type has also a high tendency to rebleed but with lower hyperfibrinolytic activity.”(13)
Also in 2002, Uscinskiwrote: “Rebleeding in subdural hematomas may occur, with minimal or no trauma, owing to the nature of the membranes and the process of resorption…. Common sense would seem to indicate that not all the subdural hemorrhages in children are inflicted injuries and prior to 1972 the presence of retinal hemorrhages was a diagnostic aid in detecting the presence of chronic subdural hematoma in children and has long been known among neurosurgeons to reflect an abrupt increase in intracranial pressure. Lastly, a simple point of consideration: When an adult presents with a chronic subdural hematoma, abuse is rarely a diagnostic consideration. Given the similar pathology of the subdural hematoma in adults and children, why, logically, should the opposite be true in a child? (11)
Shaken or not: That certainly is the question.
“Injustice anywhere is a threat to justice everywhere” —— Martin Luther King Jr.
- Leestma, JE. Case analysis of brain-injured admittedly shaken infants: 54 cases, 1969-2001. Am J Forensic Med Pathol. 2005 Sep; 26(3):199-212. PMID: 16121073
- BMJ 2004;328:719-720 (March 27), doi:10.1136/bmj.328.7442.719 http://bmj.bmjjournals.com/cgi/content/full/328/7442/719
- Yazbak, F.E. K comes after C and H in SBS. http://bmj.bmjjournals.com/cgi/eletters/328/7442/719#64501
- Clemetson, C.A.B. “Shaken Baby” or Barlow’s Disease Variant? http://bmj.bmjjournals.com/cgi/eletters/328/7442/719#63250
- Uscinski, R. Shaken Baby Syndrome: fundamental questions.
Br J Neurosurg. 2002 Jun;16(3):217-9. PMID: 12201392
- Bergstrom, M., Ericson, K., Levander, B., Svendsen, P. Computed tomography of cranial subdural and epidural hematomas: variation of attenuation related to time and clinical events such as rebleeding. J Comput Assist Tomogr. 1977 Oct; 1(4):449-55.
- Ommaya AK, Goldsmith W, Thibault L. Biomechanics and neuropathology of adult and paediatric head injury. Br J Neurosurg. 2002 Jun;16(3):220-42. PMID: 12201393
Imwinkelreid on Shaken Baby Syndrome Experts
- The national campaign against child abuse has changed the face of American evidence law during the past 30 years. The campaign has led to the relaxation of witness competency standards for alleged child victims, the recognition of new procedures for presenting child testimony such as the use of support persons, the creation of new hearsay exceptions, and the development of novel species of expert testimony. One of the most controversial new types of expert testimony is shaken baby syndrome. The proponents of the syndrome claim that the violent shaking of an infant by an adult can generate enough force to inflict fatal brain injuries on the infant even without impact. Many pediatricians and pathologists subscribe to this theory. However, many biolmechanical experts dispute the theory. To date, the vast majority of courts have admitted testimony based on the syndrome. The purpose of this article is to critically evaluate the available empirical data relevant to the question of the validity of the syndrome. The article concludes that this is one of the rare situations in which both sides’ expert claims pass muster under Federal Rule of Evidence 702 and the Supreme Court’s leading decisions, Daubert and Kumho. Once a decision-maker posits the validation standard enunciated in Daubert, it is possible to have genuine battles of the experts. In this case, the syndrome opponents can point to relatively well designed experiments finding that even violent shaking by an adult cannot generate enough force to cause fatal injuries to the infant brain. However, syndrome opponents note that in a large number of cases in which infants suffered such fatal brain injuries, the infant’s custodian admitted shaking without impact. It may be tempting to conclude that classical experimentation should always trump more anecdotal expert reasoning. However, that conclusion is indefensible as a matter of both statutory construction and epistemology.
By Elizabeth Roberts
The Court of Appeal judges who quashed the murder conviction of a man who killed his baby daughter, heavily criticised the way a Florida paediatrician gave evidence in an �unduly theatrical and undisciplined� manner.
Karim Salahuddin was convicted in October 2004 of murdering his six-month-old daughter Cassidy after a jury found that he had shaken her violently on May 5 2003, causing her to suffer a brain injury.
The 21-year-old defendant, of Serpentine Road, Pembroke, appealed against that conviction, having maintained at his trial that he had slipped and fallen, dropping his daughter by accident. Last month at the appeal, his defence team asked for leave to present fresh evidence which contradicted the conventional view of �shaken baby syndrome�.
They criticised the trial judge, Chief Justice Richard Ground, for the way that he directed the jury and handled witnesses, and also criticised the way evidence was given by paediatrician Dr. Randall Alexander, a witness for the crown.
The three judges who heard the appeal, Justices Sir Anthony Evans, Austin Ward and Sir Charles Mantell quashed the murder conviction and mandatory sentence of life imprisonment that had previously been handed to Salahuddin, and replaced this with a ten-year sentence.
Giving their reasons for this in a written judgement released yesterday, they rejected the criticism put forward by the defence of the way the Chief Justice acted during the trial.
But they did accept the defence argument in relation to the behaviour of Dr. Randall Alexander, and cited this as their reason for reducing the murder conviction to one of manslaughter.
Dr. Alexander had, while in the witness box, used a plastic doll to illustrate his evidence. He shook the doll violently, before smacking its head down on the witness box, and is said to have then turned the doll over and done the same to the other side of its head.
The judges said that the manner in which this �highly disturbing� evidence was presented �came as a complete surprise to the Chief Justice�.
They said that it had been of critical importance in the trial as it went directly to the question of whether Salahuddin intended to kill his daughter or not.
�Anyone who used the degree of violence demonstrated by Dr. Alexander against a six-month-old child could only have intended to cause at least really serious harm. It no doubt formed the basis of the jury�s decision to convict of murder rather than manslaughter,� said the judges.
�We think that Dr. Alexander was wrong to act as he did. It was his duty to give evidence in the least emotive way possible, particularly in a case such as this where feelings were likely to run high. His performance was, to say the least, unduly theatrical and undisciplined.�
The judges also found that Dr. Alexander�s evidence was out of line with evidence received by the Court of Appeal in England which has accepted that a much lesser degree of force than that illustrated by him is all that is required to produce a non-accidental head injury to a child.
However, they rejected an application from the defence to call fresh evidence challenging the conventional diagnosis of �shaken baby syndrome� as they said this would not have made any difference to their manslaughter ruling.