Chapter 3

Shaken Baby Syndrome: Where Are We Now?

4515 W Dravus St Seattle, WA 98199 tel: (206) 286-9138 fax: (206) 378-6963 hkirkwood2@comcast.net

Heather Kirkwood

Heather Kirkwood
Heather Kirkwood works pro bono on actual innocence cases involving alleged child abuse, including shaken baby syndrome. On her own or in conjunction with innocence clinics at the University of Michigan and University of Washington law schools, she reviews cases and/ or represents parents or caretakers unjustly convicted or accused of child abuse. Ms. Kirkwood graduated with honors from Harvard Law School in 1973, practiced as a senior attorney at the Federal Trade Commission, and has successfully represented plaintiffs and defendants in major civil litigation.

Table of Contents
• Outline ...............................................................................................3–1 I. History and Recent Developments ..................................................3–1 II. How to Analyze a Shaken Baby/Abusive Head Trauma Case ...........3–5 III. Practical Issues ...............................................................................3–7 IV. Meet the People: If you do all this, what are you likely to find? ......3–7 • September 2010 Letter Excerpt (with slight modifications) ...................3–8 I. Research Basis for Shaken Baby Syndrome ......................................3–8 II. Resistance to Change ....................................................................3–22

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I. History and Recent Developments A. SBS widely accepted as cause of the triad – subdural hemorrhage (SDH), retinal hemorrhage (RH) and edema/brain swelling 1. Very simple theory: torn bridging veins (BV), torn retinal veins, torn axons – tearing is traumatic by definition and must cause immediate effects But usually no signs of abuse/trauma: shaking hypothesized as traumatic cause that would not leave external marks (Guthkelch, Caffey, 1971-1974) Hypothesized force equivalent to major motor vehicle accident or fall from multistory building (3-10 stories) Basic terms you need to know - subdural hemorrhage: bridging veins, dura, intradural bleed - retinal hemorrhage and variants - cerebral edema/brain swelling: brain parenchyma, grey/white differentiation, infarcts - mass effect/midline shift - hypoxia/ischemia (lack of oxygen) B. Very little challenge through 1998 – Louise Woodward “au pair” case 1. 2. C. Jury convicted, lengthy sentence; judge reduced to time served Publicity spurred questioning within the medical profession

2.

3.

4.

Medical developments/erosion of shaking mechanism 1. 1987: shaking doesn’t generate sufficient force; even mild impact generates much greater force than shaking; resulted in “shaken/slammed” hypothesis (Duhaime) 1998: 24 hour (up to 72 hour) “lucid interval” between shaking/impact trauma and serious symptoms (Gilliland) 1999: BECC as risk factor for SDH; can result from minor trauma (Piatt)

2. 3.

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4.

2001: American Academy of Pediatrics (AAP) & National Association of Medical Examiners (NAME) position papers endorse SBS theory (NAME paper rejected by peer reviewers) • brain swellling hypoxic (lack of oxygen) rather than traumatic (tearing); SDH in infants generally thin film; findings virtually identical in natural death; scant evidence for traumatic cause for triad (Geddes) • collection of short falls resulting in some/all of triad (Plunkett) • shaking model improbable; would damage soft tissues of neck; short fall has much greater forces than shaking; can have spontaneous rebleeds from chronic SDH (Ommaya)

5.

2002: Aprica dummy; violent shaking plus slamming onto sofa created less than half force of accidental short fall from chest level (Jenny) • SDH can occur in accidental & natural settings, including pregnancy related conditions, birth trauma, metabolic or genetic disease, clotting disorders; old SDH can rebleed (Hymel) • lack of support for SBS under evidence-based medicine; need to recognize mimics (Barnes) • birth subdurals with rebleeds v. shaking (Uscinski)

• The debate over shaken baby syndrome continues to rage in our country. Because there is very little scientific, experimental or descriptive work, the pathophysiology remains obscure and the relationship to mechanics even cloudier. The evidence that does exist has not been subjected to evidence based scrutiny in a multidisciplinary scientific forum. (NIH) 6. 2003: evidence on SBS inadequate to support diagnostic assessment; evidence analogous to an inverted pyramid with a small data base (mostly poor quality original research, retrospective in nature and without appropriate control group); repeated opinions based on poor quality data cannot improve the quality of evidence. (Donohoe) • infant death study indicated SDH might be intradural (IDH), possibly hypoxia-related or cascade of events rather than traumatic BV rupture (Geddes)

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• case report on 72 hr interval between accidental short fall and collapse (Denton) 7. 2004: 81 perpetrator admissions to inflicted traumatic injury; 91% had immediate symptoms, 5 cases within 24 hrs; source material unavailable (Starling) • retinal findings (perimacular retinal folds, RH, optic nerve sheath hemorrhage, retinoschisis) found in TV tip-over; association of ocular findings with abuse is problematic (Lantz) • reaffirmed biomechanical shortcomings of SBS theory; RH likely related to retinal occlusion, may be related to edema rather than trauma (Goldsmith) 8. 2005: levels of force suggested by SBS theorists excludes tolerance of neck; force of manual shaking on same order as 3 ft. fall (Bandak) • documented confessions in medical literature did not permit valid statistical analysis or support for many commonly stated aspects of SBS (Leestma) • triad strong pointer to non-accidental injury but declined invitation to find triad was fact, not hypothesis; all factors to be taken into account; cause to be left to judges/juries (English Court of Appeals) 9. 2006: child abuse text recognized many mimics of abusive head trauma, including pregnancy related conditions, birth trauma, stroke, genetic & metabolic disorders, hematological diseases, infectious disease, toxins, etc. (Frasier) • paroxysmal coughing can raise intracranial pressure sufficient to damage veins, causing SDH & RH (coughing, vomiting, choking) (Geddes) • RH in 17% of 425 deaths and in wide variety of natural and accidental deaths; of RH in 19 children, only 4 related to abuse (Lantz) • NAME withdraws 2001 position paper; conference presentations include “Where’s the Shaking? Dragons, Elves, the Shaking Baby Syndrome and Other Mythical Entities.” (2006 NAME conference) 10. 2007: review of controversies & non-traumatic causes of findings; radiologists urged to familiarize themselves with literature in

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providing differential diagnosis for radiological findings previously associated with abuse (Barnes) • review of lack of evidence base for SBS; experts need to examine details & adopt rigorous and questioning approach (Squier) 11. 2008: 46% of asymptomatic newborns have SDH; resolved within 3 mos (Rooks) • so-called SDHs were IDH; found in natural deaths; unlikely to result from BV tears; associated with hypoxia/ischemia (Cohen) • post-conviction relief granted in Edmunds based on new learning; significant & legitimate doubt has developed over shaking alone as mechanism, lucid interval and mimics (Wisconsin Court of Appeals) • major inquiry found systemic misdiagnoses in pediatric head injury cases; recommended review of all shaken baby cases (Goudge Report, Ontario, Canada; review currently ongoing) 12. 2009: SDH in infants often traumatic, ruptured BV thought to be source but non-traumatic conditions also associated with SDH in infants; traumatic BV rupture unlikely to be cause of thin film bleeds; IDH more likely, susceptible to rebleed (Mack) • association between hypoxia/ischemia & SDH; hemorrhage related to degree of hypoxia, appears to be leakage in dural border cell layer (Cohen) • AAP modified position paper; advances in understanding compel modification, terminology changed to abusive head trauma; continued to endorse shaking as mechanism of injury but recognized overlap with accidental injury & mimics (AAP) • editorial acknowledged that BV rupture theory may be incorrect; however, inflicted head trauma (Slovis) • major law review article “The Next Innocence Project: Shaken Baby Syndrome and the Criminal Courts” concluded that science of SBS can no longer support a finding of proof beyond a reasonable doubt in triad only cases (Tuerkheimer) 13. 2010: eye evaluations of limited value in child death investigations; RH found in natural death, accidental death and homicides; severe RH linked to edema and life support rather than trauma (Matshes)

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• extensive RH of type previously viewed as diagnostic of shaking or abuse found in deaths from strep pneumonia meningitis (Lopez) 14. 2011: major clinical review of radiology in abuse cases and mimics concluded that literature fails to establish evidence base for reliably distinguishing non-accidental injury from accidental injury or the mimics; need to consider differential diagnosis & other findings (Barnes) • New York Times Magazine cover asks “Has a Flawed Diagnosis Put Innocent People in Prison? A Re-Examination of Shaken-Baby Syndrome; article reviews three shaken baby cases http://www.nytimes.com/2011/02/06/magazine/06babyt.html?pagewanted=1&_r=2&ref=magazine II. How to analyze a Shaken Baby/Abusive Head Trauma case A. Is it possible to get a fair trial in a child abuse case? Pre-trial publicity is not the big difficulty. It is generic prejudice. I do not think that you can get a fair child abuse trial before a jury anywhere in the country. I really don’t. . . I do not care how sophisticated or law smart jurors are, when they hear that a child has been abused, a piece of their mind closes up, and this goes for the judge, the juror, and all of us. Abner Mivka, U.S. Court of Appeals, D.C. Circuit, 1990. B. Attorney’s job is to gather the facts, understand the evolving medical literature, and overcome generic prejudice. 1. Get all medical records and organize for experts, e.g., a) Medical records (1) (2) (3) (4) Autopsy report (if death) 911 call EMT records (any other transport records) Hospital records (by category; separately for each hospital) • admission records • discharge records • • labs • consults (surgery if applicable) • doctor orders • nursing records

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(5) (6) (7) (8) b) Other (1) (2) (3) 2.

• medications • charts (by section) • organ donation (if applicable) Prenatal records Birth records (mother and child) Pediatric records Sibling records/family

police records (including interviews) attorney/investigator interviews – interview everyone who has seen child (get affidavits) (“shaking baby syndrome”) CPS or family court records

Create a timeline based on medical records and reports – this will often tell you what happened, or at least get you started. Work with your client and interview, interview, interview. Use informal sources – your own doctor, google, friends, attorneys who have handled similar cases . . . Choosing experts: very case-specific. Know the categories – • • • • • • • • • • • forensic pathologists (autopsy; cause & manner of death) neuropathologists (brain/CNS) neurosurgeons radiologists and neuroradiologists neurologists pediatric intensivists pediatricians biomechanical engineers coagulation experts other specialties, depending on case (genetics, heart, lungs, bones, etc.)

3.

4.

It is essential to retain appropriate medical experts and to work with them. Begin this process immediately! Remember, if your client isn’t guilty, you are responsible for explaining the medical findings and/or death. Always work with the family because they know the child best. Interview prosecution witnesses – and don’t let prosecutors turn witnesses against each other based on mistaken diagnosis of abuse.

5.

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Make sure family court rulings are not based on inadequate information or representation. III. Practical issues A. B. C. D. E. F. IV. Confessions Plea bargains Translation problems: language/medical/word meaning Daubert/Frye Evidentiary issues for trial: how to use the literature Other medical issues: fractures, bruises, sexual assault

Meet the people: if you do all this, what are you likely to find? • • • • • • • • The Finnegans: The Felixes: Julie Baumer: The Kinnards: Ernie Lopez: Zamora: Liebich: Rieken: warfarin overdose traumatic lumbar puncture venous sinus thrombosis (childhood stroke) neurofibromatosis I & metabolic bone disease pneumonia and underlying coagulopathy birth trauma with rebleeds pancreatitis/abdominal injury previous fall on stairs

Fuller explanation of history and complete citations are provided in the handout. February 2011

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HEATHER KIRKWOOD
Member: Washington and Texas State Bars ATTORNEY 4515 WEST DRAVUS STREET SEATTLE, WA 98199 Phone (206) 286-9138 Fax (206) 378-6963 hkirkwood2@comcast.net

Excerpted with slight modifications from September 2010 letter: I. Research Basis for Shaken Baby Syndrome It is not possible to understand shaken baby/abusive head trauma cases without understanding the history of “shaken baby syndrome.” “Shaken baby syndrome” was advanced and popularized in the early 1970s as a hypothesis to explain three medical findings: (1) subdural hemorrhage (i.e., bleeding between the dura and the brain); (2) retinal hemorrhage and other eye findings; and (3) cerebral edema (brainswelling).1 Together, these features are commonly known as the “triad.” Although the SBS hypothesis initially included signs of trauma (broken ribs, bruises, etc.), it was soon applied to children who had no signs of trauma. The SBS hypothesis was simple: under this hypothesis, subdural hemorrhages were caused by the traumatic tearing of bridging veins (i.e., the veins that drain blood from the brain and enter into the dural sinus); retinal hemorrhages were caused by traumatic traction or tearing within the eye; and cerebral edema was caused by traumatically torn axons in the brain. Under this theory, the “triad” proved the existence of trauma in three different ways. Since it was assumed that the child would collapse immediately following such an injury, the perpetrator also could be easily identified. Since there were rarely specific signs of trauma (bruises, fractures and the like), “shaking” was proposed as the only traumatic injury that would explain the findings. This led to courtroom testimony that the “triad” – or even one or two of its components – was pathognomonic of shaking, i.e., could have no other reasonable cause. The first serious challenge to shaken baby theory arose in 1987, when Dr. Duhaime, a neurosurgery resident, worked with biomechanical engineers at the University of Pennsylvania to compare the forces of violent shaking to established injury thresholds.2 Although the purpose of the experiment was to validate shaken baby theory, the experiments showed that the force from shaking fell far below established injury thresholds and was approximately 1/50 the force from impact. This study indicated that shaking was a biomechanically improbable cause of subdural hemorrhage and gave rise to shaking/impact theory (the notion that shaking is combined with impact). In this
1

This theory is generally credited to Dr. Caffey and Dr. Guthkelch. See Caffey J, The Whiplash Shaken Infant Syndrome: Manual Shaking by the Extremities With Whiplash-Induced Intracranial and Intraocular Bleedings, Linked With Residual Permanent Brain Damage and Mental Retardation, Pediatrics 1974; 54(4):396-403; Guthkelch A, Infantile Subdural Haematoma and its Relationship to Whiplash Injuries, Br Med J 1971; 2:430-431. 2 Duhaime A, Gennarelli T, Thibault L et al., J Neurosurg 1987; 66:409-415.

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study, Dr. Duhaime noted that the subdural hemorrhages in shaken baby syndrome are small, and that the real problem is brainswelling. It has taken more than two decades for the medical community to recognize the implications of these observations. The issue of whether shaking could cause the triad was not seriously revisited until the 1997 trial of Louise Woodward, an English nanny who was charged with shaking the child of an American ophthalmologist and her husband.3 The prosecution experts testified that, based on the triad, the child had been violently shaken immediately prior to his fatal collapse. However, several defense experts testified that the subdural hemorrhage attributed to violent shaking resulted from a chronic (old) subdural, accompanied by re-bleed. Although Ms. Woodward was convicted of second degree murder and sentenced to life imprisonment by a jury, the judge concluded that while she may have treated the child roughly, the evidence did not support the type of violence portrayed by the prosecutors. He therefore reduced the verdict to involuntary manslaughter and the sentence to time served. At the time, the notion of a chronic subdural with rebleed was viewed as a heretical courtroom diagnosis, and its proponents were attacked by proponents of shaken baby syndrome.4 Today, however, chronic subdurals with rebleeds are accepted by the “mainstream.”5 Since the Woodward trial, the research and literature reviews have continued to systematically undermine the theoretical basis for shaken baby syndrome and to identify alternative diagnoses. For example: 1998. In 1998, a study by Dr. Gilliland, a supporter of shaken baby theory, found that in approximately 25% of alleged abuse cases (shaking, shaking/impact or impact), there was an interval of more than 24 hours (and sometimes more than 72 hours) between the alleged abuse and the onset of severe symptoms.6 This study contradicted the “mainstream” belief that the severity of the injuries caused by shaking, shaking/impact or impact was inconsistent with a “lucid interval” and that the last person with the child was therefore the perpetrator. In the same year, an editorial in The Lancet noted that “[i]f 26 years after Caffey’s description, doctors are still undecided about the “shaken-baby syndrome,” the difficulties faced by experts in presenting medical evidence in court, and by the judge and jury in making sense of it, are readily imaginable.”7 The editorial warned that increased
3 4

See Commonwealth v. Woodward, 694 N.E.2d 1277 (1998). See, e.g., Chadwick D et al., Shaken Baby Syndrome—a Forensic Pediatric Response, Pediatrics 1998; 101(2):321-323 (72 signatories); Amaya M et al., Shaken Baby Syndrome and the Death of Matthew Eappen, http://silcon.com/-ptave/shaken.htm (Nov. 11, 1997; accessed Nov. 2, 2000) (51 signatories). 5 See, e.g., Frasier L et al., Abusive Head Trauma in Infants and Children, A Medical, Legal, and Forensic Reference (G.W. Publishing 2006) at 81 (septations or membranes that develop within chronic hematomas may predispose infants to repeated episodes of bleeding within these collections; rebleeding can occur with little or no trauma). The shift in the mainstream can be seen by the fact that two of the editors of this book (Dr. Frasier and Dr. Alexander) also signed the Chadwick letter, supra. 6 Interval Between Injury and Severe Symptoms in Nonaccidental Head Trauma in Infants and Young Children, J For Sci.1998; 43(3):723-725. 7 Shaken Babies, The Lancet 1998; 352:335.

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awareness of “shaken-baby syndrome” should be “tempered with caution against overdiagnosis” and that the “lessons of Cleveland, UK, in the late 1980s, must stay welllearned,” a reference to the misdiagnosis of sexual abuse by pediatricians based on small physical signs that proved unreliable. 1999. In 1999, Dr. Piatt identified external hydrocephalus (large heads due to CSF collections) as a risk factor for subdural and retinal hemorrhages from minor trauma, such as a bump on the head.8 Other articles have similarly recognized that children with external hydrocephalus (also known as benign extracerebral collections of infancy) may develop small subdural hemorrhages spontaneously or from minor trauma.9 2001. In 2001 – a year that may be viewed as both the peak of shaken baby theory and the beginning of its unraveling – the American Academy of Pediatrics (AAP) and the National Association of Medical Examiners (NAME) issued policy statements on shaken baby syndrome. The AAP position paper endorsed shaken baby syndrome and suggested that child abuse be presumed whenever a child younger than 1 year suffers intracranial injuries.10 The NAME paper, which was published despite failing peer review, also endorsed shaken baby theory, stating that inflicted head injuries in children under the age of 4 or 5 usually create shearing injuries of the brain and blood vessels, resulting in diffuse axonal injury and subdural, subarachnoid and retinal hemorrhages.11 In recent years, both papers have been modified or withdrawn.12 In the same year, Dr. Jennian Geddes published the first careful neuropathological studies of infants who were allegedly the victims of nonaccidental head injury, including shaking. In the first paper (“Geddes I”), Dr. Geddes found that, unlike the findings in older children, the subdural hemorrhages in infants were typically “trivial” in terms of quantity and almost invariably described as “thin film,” and that the brainswelling (edema) in infants was hypoxic (i.e., due to lack of oxygen) rather than traumatic in nature.13 Some infants also showed evidence of localized axonal injury to the craniocervical junction or cervical cord. In a companion paper (“Geddes II”), Dr. Geddes found that the scientific evidence for the proposition that the triad is traumatic in origin is “scanty” and that the subdural hemorrhage and brain findings in infants who died natural

8

Piatt J, A Pitfall in the Diagnosis of Child Abuse: External Hydrocephalus, Subdural Hematoma, and Retinal Hemorrhages, Neurosurg Focus 1999; 7(4). 9 See, e.g., McNeely P et al., Subdural Hematomas in Infants with Benign Enlargement of the Subarachnoid Spaces Are Not Pathognomonic for Child Abuse, Am J Neuroradiol 2006; 27:1725-28; Amodio J et al., Spontaneous development of bilateral subdural hematomas in an infant with benign infantile hydrocephalus: color Dopper assessment of vessels traversing extra-axial spaces, Pediatr Radiol (2005) 35:1113-1117. 10 Kairys S, Alexander R and the Committee on Child Abuse and Neglect, Shaken Baby Syndrome: Rotational Cranial Injuries-Technical Report, Pediatrics 2001; 108(1):206-210 (citations omitted). 11 Case M et al., Position Paper on Fatal Abusive Head Injuries in Infants and Young Children, Am J For Med & Path 2001; 22(2):112-122; e-mail from Dr. DiMaio, Editor, to the NAME listserve at Emory University (Feb. 7, 2002) (position paper was rejected by 4 of the 5 peer reviewers). 12 As addressed below, the NAME paper was rescinded in 2006; the AAP paper was modified in 2009. 13 ., Neuropathy of Inflicted Head Injury in Children: I. Pattern of Brain Damage, Brain 2001; 124(7):1290-1298 (often referred to as “Geddes I”).

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deaths were virtually indistinguishable from the findings in allegedly abused infants.14 An accompanying editorial described this research as “meticulous” and noted that, given the findings of hypoxia, the vascular complications of hypoxia and/or raised intracranial pressure should be considered.15 Although Dr. Geddes and her findings were initially vilified by shaken baby advocates, Geddes I and II are now part of the mainstream. In 2001, Dr. Plunkett, a forensic pathologist, addressed the common courtroom testimony that the triad could not be caused by falls unless the falls were from multiple stories (anywhere from 3-10 stories, depending on the witness). In an article published in NAME, the leading journal for forensic pathologists, Dr. Plunkett described multiple witnessed short falls that resulted in some or all of the triad.16 Of these, the most compelling was a videotaped fatal fall of a 23 month old toddler from a plastic gym set (28 inches high) in the carpet-covered garage of her home. The child cried and talked after the fall but vomited and became stuporous approximately five minutes later. The hospital findings included subdural hemorrhage, edema and bilateral retinal hemorrhage. This videotape established dispositively that short falls can be fatal and can cause the triad. For years, shaken baby advocates claimed that the videotape was fabricated or altered; now, however, it is an accepted part of the mainstream. 2002. In 2002, a review of the biomechanical literature in the British Journal of Neurosurgery concluded that the assumptions made in the shaking model were unvalidated, ambiguous and/or incorrect and that it was improbable that manual shaking could produce the triad.17 The review further concluded that severe shaking would damage the soft tissues of the neck before producing intracranial injuries; that a three foot fall produced forces approximately ten times greater than shaking; that spontaneous rebleeds may explain the onset of symptoms in children with chronic subdural hemorrhage; and that the levels of force required for shaking to produce retinal bleeding or damage the eye were biomechanically improbable. In the same time period, Professor Carole Jenny, a leading proponent of shaken baby syndrome, was working with Aprica, a Japanese baby products company, to validate shaken baby syndrome using a more biofidelic dummy.18 Their initial findings, which were presented at a workshop on injury biomechanics in 2002, did not validate shaken baby syndrome. Instead, these studies confirmed that violent shaking produced a maximum linear acceleration less than 1/3 the maximum linear acceleration produced by rolling off a sofa and less than 1/10 the maximum linear acceleration produced by a fall from chest level when the carrier stumbled when walking. Violent shaking followed by
14

Geddes J et al., Neuropathy of Inflicted Head Injury in Children: II. Microscopic Brain Drain Injury in Infants, Brain 2001; 124(7):1299-1306 (often referred to as “Geddes II”). 15 Graham D, Paediatric Head Injury, Brain 2001; 124(7):1261-1261. 16 Plunkett J, Fatal Pediatric Head Injuries Caused by Short-Distance Falls, Am J For Med & Path 2001; 22(1):1-12. 17 Ommaya A, Goldsmith W, Thibault L, Biomechanics and Neuropathology of Adult and Paediatric Head Injury, Brit J Neurosug 2002; 16(3):220-242. 18 Jenny C et al., Development of a Biofidelic 2.5kg Infant Dummy and Its Application to Assessing Infant Head Trauma During Violent Shaking, Injury Biomechanics Research, Thirtieth Int’l Workshop, sponsored by the National Highway Traffic Safety Administration, Ponte Vedra Beach, Fla. (Nov. 10, 2002).

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slamming onto a sofa (shaking/impact) produced a maximum linear acceleration less than half that of the accidental short fall from chest level, while violent shaking followed by slamming onto a thin carpet over a wood floor produced a maximum linear acceleration of approximately the same magnitude as the accidental fall from chest level. Slamming onto a mat without shaking produced a maximum linear acceleration approximately 50% greater than the accidental fall from chest level. This work – which takes the shaking out of shaken baby and shaken/impact syndrome – has not been published in the peerreviewed literature. At the same time, Dr. Jenny and other supporters of shaken baby syndrome published an article that recognized that subdural hemorrhages in children also occurred in accidental and natural settings.19 The article described two minor accidental injuries that resulted in intracranial hemorrhage, both of which were witnessed by medical personnel. It also identified many nontraumatic etiologies for subdural hemorrhages, including prenatal, perinatal and pregnancy-related conditions; birth trauma; metabolic diseases; congenital malformations; genetic diseases; oncologic diseases; autoimmune disorders; clotting disorders; infectious diseases; the effects of poisons, toxins or drugs; and other miscellaneous conditions. The article recognized that older subdural collections can rebleed spontaneously or as a consequence of minor cranial impact, and that no comparative studies had measured the frequency or consequences of rebleeding in young children with chronic subdural collections. In 2002, Professor Patrick Barnes, Professor of Radiology at Stanford University and currently Chief of Pediatric Neuroradiology at Lucile Salter Packard Children’s Hospital, published an article revisiting the evidence base for shaken baby syndrome in view of the new evidence, including the Geddes research.20 In this article, Professor Barnes – who had been a lead prosecution witness in the Woodward case – addressed the lack of a scientific evidence base for shaken baby syndrome and pointed out that “[f]rom an evidence-based medicine perspective, quality of evidence ratings for diagnostic criteria regarding the literature on SBS reveal that few published reports merit a rating above class IV . . . Such quality of evidence ratings hardly earn a diagnostic criteria recommendation level of ‘optional,’ much less as a ‘guideline or a ‘standard.’” Professor Barnes emphasized that radiologists must be aware of conditions that may mimic abuse, including accidental injury, certain coagulopathies, vascular diseases, infectious or postinfectious conditions (e.g., postvaccinal), metabolic disorders, neoplastic diseases, certain therapies, and some congenital and dysplastic disorders. In addition to ruling out these conditions, the physician must consider the possibility of combined mechanisms with synergistic effects. In the same year, Dr. Uscinski, a neurosurgeon, published an article in the British Journal of Neurosurgery concluding that the research raised considerable questions on “whether the intracranial injuries hitherto ascribed to shaking are really the result of
19

Hymel K, Jenny C, Block R, Intracranial Hemorrhage and Rebleeding in Suspected Victims of Abusive Head Trauma: Addressing the Forensic Controversies, Child Maltreatment 2002; 7(4); 329-348. 20 Barnes P, Ethical Issues in Imaging Nonaccidental Injury: Child Abuse, Top Mag Res Imaging 2002; 13(2):85-93.

such.”21 Dr. Uscinski specifically addressed birth subdurals and the possibility of rebleeds with minimal or no trauma, consistent with the nature of the membranes and the process of resorption. Given the increasing controversies over shaking as a mechanism of injury, the National Institutes of Health held a conference in October 2002.22 An editorial preface to the papers presented at the conference states, “[t]he debate over “shaken baby syndrome” continues to rage in our country. Because there is very little scientific experimental or descriptive work, the pathophysiology remains obscure, and the relationship to mechanics even cloudier. The evidence that does exist has not been subjected to evidence-based scrutiny in a multidisciplinary scientific forum.” While most conference presenters supported shaken baby theory, the presentations acknowledged the limitations of current knowledge, the alternative diagnoses, and the need for additional research. 2003. In 2003, an article by Dr. Mark Donohoe in the NAME journal reviewed the evidence base for shaken baby syndrome from 1966-1998 using the criteria of evidence-based medicine.23 Dr. Donohoe found that there was no evidence on SBS that exceeded QER III-2, which meant that the data in the medical literature was inadequate to support diagnostic assessment. Instead, the evidence for SBS “appears analogous to an inverted pyramid, with a small database (most of it poor-quality original research, retrospective in nature, and without appropriate control groups) spreading to a broad body of somewhat divergent opinions. One may need reminding that repeated opinions based on poor-quality data cannot improve the quality of evidence.” Dr. Donohoe concluded that without published and replicated studies, the commonly held opinion that the finding of subdural and retinal hemorrhage in an infant was strong evidence of SBS was unsustainable, at least from the medical literature. In 2003, Dr. Geddes published Dural hemorrhage in non-traumatic infant deaths: does it explain the bleeding in ‘shaken baby syndrome’? (often referred to as Geddes III).24 This article reported on 50 nontraumatic infant deaths (intrauterine to 5 months), with causes of death including infection, hypoxia and sudden infant death syndrome (SIDS). It also included three “shaken baby” deaths. Since most of the natural deaths and all three SBS deaths showed intradural bleeding, i.e., bleeding within rather than below the dura, Dr. Geddes suggested that the mechanism for the bleeding may be hypoxiarelated leakage from veins within the dura, rather than traumatic rupture of bridging veins. This paper suggested that intradural bleeding might result from a cascade of events including raised intracranial pressure, central venous and systemic arterial hypertension, combined with immaturity and hypoxia-related vascular fragility.

21 22

Uscinski R, Shaken Baby Syndrome: fundamental questions, Br J Neurosurg 2002; 16(3):217-219. Reece M and Nicholson C, Inflicted Childhood Neurotrauma, Proceedings of a Conference Sponsored by HHS, NIH, NICHD, ORD and NCMMR, October 10 and 11, 2002, Bethesda, MD. The conference papers were published in book format by the American Academy of Pediatrics in 2003. 23 Donohoe M, Evidence-Based Medicine and Shaken Baby Syndrome: 61998, Am J For Med & Pathol 2003; 24:239-242. 24 Geddes J et al., Dural Haemorrhage in Non-Traumatic Infant Deaths: Does it Explain The Bleeding in ‘Shaken Baby Syndrome’?, Neuropath and Applied Neurobio 2003; 29:14-22 (“Geddes III”).

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In 2003, a case fatality report in the NAME journal documented a 72 hour asymptomatic delay between an accidental short fall and collapse.25 This case involved a skull fracture, subdural and subgaleal hemorrhage, cerebral edema, and focal axonal injury, with no retinal hemorrhage. 2004. In 2004, an article by Dr. Starling analyzed 81 perpetrator admissions to inflicted traumatic brain injury in children.26 In 91% of the cases, the symptoms appeared immediately after the abuse; in 5 cases, the timing was less clear but occurred within 24 hours. This study is often used to support SBS theory based on the asserted admissions by perpetrators. Since the source material is unavailable, the findings have not been validated. In the same year, Dr. Lantz published a case report finding perimacular retinal folds, retinal and optic nerve sheath hemorrhage and retinochisis – which had previously been considered to be diagnostic of abuse – in an accidental television tipover.27 Based on a literature review, Dr. Lantz concluded that the association of ocular findings with abuse had the same problems identified by Donohoe in 2003 for shaken baby syndrome, i.e., selection bias, inappropriate controls, lack of precise criteria, a fallacy of assumption, unsystematic reviews, and consensus statements that mingled opinion with facts. In 2004, Professor Goldsmith, a biomechanical engineer at the University of California at Berkeley, and Dr. Plunkett published another article addressing the biomechanical shortcomings of shaken baby theory.28 The article concluded that the experimental biomechanical data indicated that the mechanism for retinal hemorrhage is functional or mechanical venous occlusion and suggested that this might be related to cerebral edema, rather than trauma. 2005. A 2005 article by Dr. Bandak, a biomechanical engineer, confirmed that the levels of force suggested by proponents of shaken baby theory would exceed the tolerance of the neck, causing total neck failure, and that the force from manual shaking is of the same order as a fall from approximately three feet.29 While some of his calculations are disputed, Dr. Bandak’s conclusions are consistent with the other biomechanical studies. In the same year, an article by Dr. Jan Leestma, a neuropathologist, found that the documented confessions in the medical literature (11 cases involving shaking only) did not permit valid statistical analysis or support for many commonly stated aspects of shaken baby syndrome.30
25

Denton S and Mileusnic D, Delayed Sudden Death in an Infant Following an Accidental Fall, A Case Report with Review of the Literature, Am J For Med & Path 2003; 24(4):371-376. 26 Starling S et al., Analysis of Perpetrator Admissions to Inflicted Traumatic Brain Injury in Children, Arch Pediatr Adolesc Med 2004; 158:454-458. 27 Lantz P et al., Evidence based case report, Perimacular retinal folds from childhood head trauma, Br Med J 2004; 328:754-756. 28 Goldsmith W and Plunkett J, A Biomechanical Analysis of the Causes of Traumatic Brain Injury in Infants and Children , Am J For Med & Path 2004; 25(2):89-100. 29 Bandak F, Shaken Baby Syndrome: A Biomechanics Analysis of Injury Mechanisms 2005; 151:71-79. 30 Leestma J, Case Analysis of Brain2001, Am J For Med & Path 2005; 26(3):199-212.

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In the midst of this new learning, the English Court of Appeals addressed four appeals in child death cases in R v Harris, Rock, Cherry and Faulder.31 In its opinion, the Court recognized that “there remains a body of medical opinion which does not accept that the triad is an infallible tool for diagnosis. This body of opinion, whilst recognizing that the triad is consistent with NAHI [nonaccidental head injury], cautions us against its use as a certain diagnosis in the absence of other evidence.” Harris ¶ 69. The Court also held that Geddes III could no longer be regarded as a credible or alternative cause of the triad of injuries – a somewhat puzzling finding since Geddes III was never presented as anything other than a hypothesis – but declined the prosecution’s invitation “to find that the triad was proved as a fact and not just a hypothesis,” stating: “On the evidence before us we do not think it possible for us to do so. Whilst a strong pointer to NAHI on its own we do not think it possible to find that it must automatically and necessarily lead to a diagnosis of NAHI. All the circumstances, including the clinical picture, must be taken into account.” The Court further declined the prosecutor’s invitation to find that Dr. Squier’s evidence that bleeding previously identified as subdural might be intradural in nature could not be accepted, contenting itself “with the observation that even on the interpretation of objective evidence there can be two views expressed by highly experienced and distinguished medical experts.” Harris ¶ 73. The Court also declined to make any findings on the significance of retinal hemorrhages and on the issue of “how much force” is required to cause all three elements of the triad. Harris ¶ 100. Instead, the Court left these issues to judges and juries. Harris ¶ 70. 2006. In 2006, a textbook by leading supporters of shaken baby syndrome recognized that many medical disorders “mimic” shaken baby syndrome/abusive head trauma.32 These include prenatal, perinatal and pregnancy related conditions; birth trauma; congenital malformations; various forms of childhood stroke; accidental injury; genetic and metabolic disorders; hematological diseases and disorders of coagulation and clotting; infectious diseases; autoimmune and vasculitis conditions; oncological processes; toxins, poisons and nutritional deficiencies; and medical and surgical complications. While some of these conditions can be confirmed or ruled out through diagnostic testing, others are indistinguishable from abusive head trauma or can only be ruled out by tests conducted while the child is living. In 2006, Dr. Geddes and Dr. Talbert, an engineer, used old medical records on pertussis (whooping cough) to model paroxysmal coughing.33 Using a computer model used for diagnostic purposes, they found that paroxysmal coughing could raise intracranial pressure sufficiently to damage veins and impede venous return, causing subdural and retinal hemorrhage. This suggested that coughing, vomiting, choking and various Valsalva maneuvers might explain retinal and subdural bleeding in some instances.
31 32

R v. Harris, Rock, Cherry and Faulder [2005] EWCA Crim 1980. Sirotnak A, Medical Disorders that Mimic Abusive Head Trauma, Ch. 14 in Frasier L et al., Abusive Head Trauma in Infants and Children: A Medical, Legal, and Forensic Reference (G.W. Publishing 2006). 33 Geddes J and Talbert D, Paroxysmal Coughing, Subdural and Retinal Bleeding: a computed modeling ed Neurobio 2006; 1-10.

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In the same year, Dr. Lantz presented a study of retinal hemorrhages in 425 deaths (birth to age 96).34 In this study, retinal hemorrhages were found in 17% of all deaths and in a wide variety of natural and accidental deaths, including deaths from SIDS (sudden infant death syndrome), meningitis, trauma, aneurysms, strokes, cancer, high blood pressure, bleeding disorders, diabetes and gunshot wounds. Of the retinal hemorrhages found in 19 children, only 4 were related to abuse. In October 2006, the NAME Board of Directors officially withdrew the 2001 position paper, which it had previously extended.35 By then, the NAME annual meeting included presentations with titles such as “Where’s the Shaking?: Dragons, Elves, the Shaking Baby Syndrome and Other Mythical Entities” and “The Use of the Triad of Scant Subdural Hemorrhage, Brain Swelling, and Retinal Hemorrhages to Diagnose NonAccidental Injury is Not Scientifically Valid.”36 2007. In a 2007 article, Professor Barnes addressed the forensic controversies from an evidence-based perspective and urged radiologists to thoroughly familiarize themselves with the imaging, clinical, surgical, pathological, biomechanical and forensic literature and the principles of evidence-based medicine in providing a differential diagnosis for radiological findings previously associated with shaking or abuse.37 He provided a five page summary of known nontraumatic causes for these findings, including the by-now-familiar list of accidental trauma, birth trauma, hypoxia-ischemia, cardiopulmonary resuscitation, infectious or postinfectious conditions (e.g., sepsis, meningoencephalitis, postvaccinal), vascular diseases, coagulopathies, venous thrombosis, metabolic disorders, neoplastic processes, certain therapies, extracorporeal membrane oxygenation, and other conditions. He pointed out that subdural hemorrhage may occur spontaneously or as a result of minor trauma in children with benign extraaxial collections of childhood (i.e., prominent subarachnoid spaces) or chronic subdural hematomas, and that the pathophysiology seems to be some combination or sequence of factors, including increased intracranial pressure, increased venous pressure, systemic hypotension or hypertension, vascular fragility, hematologic derangement and/or collagenopathy superimposed on the immature CNS and other systems. In the same year, Dr. Squier published “Shaken baby syndrome: the quest for evidence.”38 In this article, Dr. Squier reviewed the lack of an evidence base for shaken

34

Lantz P and Stanton A, Postmortem Detection and Evaluation of Retinal Hemorrhages, American Academy of Forensic Sciences 2006:271. Like Drs. Squier and Mack, Dr. Lantz has presented his research at meetings conducted by those on both sides of the “shaken baby” debate and in neutral settings, such as the American Academy of Forensic Sciences. 35 Personal communication with Dr. DiMaio, NAME Bd. of Directors (Annual Meeting, Oct. 2006); confirmatory e-mail from Davis G, NAME Bd. of Directors to Plunkett J and Wright R (Oct. 17, 2006). 36 Scientific Program, 40th Annual Meeting, National Association of Medical Examiners, San Antonio, TX (Oct. 13-18, 2006). 37 Barnes P and Krasnokutsky M, Imaging of the Central Nervous System in Suspected or Alleged Nonaccidental Injury, Including the Mimics, Top Magn Reson Imaging 2007; 18(1):53-74. 38 Squier W, Shaken baby syndrome: the quest for evidence, Dev’l Med and Child Neurol 2007 (49):1-4.

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baby syndrome and other theories, including the Geddes III hypothesis. In this article, she made clear her own views on expert testimony in shaken baby-type cases: Giving evidence is in itself daunting and many clinicians are reluctant to become involved. But clear, thoughtful, and balanced input is essential if we are to assist in the promotion of justice. Our responsibility is to examine all the details in every case of unexplained infant collapse and to adopt a rigorous and questioning approach. If we are intellectually honest we will sometimes be forced to admit that we simply do not know the cause. Dr. Squier further recognized that the stakes are high, for “[c]hildren must be protected from harm, and parents and families must be protected from hasty and wrongful accusation, which itself can wreak dreadful and lasting damage.” 2008. A 2008 study by Rooks found that 46% of asymptomatic newborns have subdural hemorrhage on MRIs taken within 72 hours of birth.39 Of those who had follow-up visits, all hemorrhages resolved within three months. While the percentage of subdural hemorrhages was higher than in previous studies, these findings were generally consistent with earlier studies. In May 2008, Dr. Cohen presented a paper at the 3rd Intercontinental Congress of Pathology in Barcelona, Spain entitled “Myths and facts of the subdural haemorrhage in the perinatal period.”40 In this paper, Dr. Cohen, a histopathologist, reviewed the anatomy of the infant brain, identifying several “myths” that had been adopted by the medical and legal professions but that did not comport with the anatomy and histopathology of the infant brain. Dr. Cohen’s research confirmed that, in young infants, the bleeding often referred to as “subdural” was in fact intradural in nature; that it is also found in natural deaths, including perinatal in-hospital deaths, pneumonia and sudden infant death syndrome; and that it is unlikely in many cases to result from tears in bridging veins. Instead, the common strand in these cases was often hypoxia/ischemia, or lack of oxygen to the brain, from any source, including natural disease processes. By 2008, the legal system was beginning to recognize the “new learning” on pediatric head injury. In 2008, the Wisconsin Court of Appeals reversed a 1996 firstdegree reckless homicide conviction against Audrey Edmunds based on shaking or shaking/impact, holding that “a significant and legitimate debate in the medical community has developed in the past ten years over whether infants can be fatally injured through shaking alone, whether an infant may suffer head trauma and yet experience a significant lucid interval prior to death, and whether other causes may mimic the symptoms traditionally viewed as indicating shaken or shaken impact syndrome.”41 The Court further recognized that “the debate between the defense and State experts reveals a
39

Rooks V et al., Prevalence and Evolution of Intracranial Hemorrhage in Asymptomatic Term Infants, Am J Neuroradiol 2008. 40 Cohen, M., Myths and facts of the subdural haemorrhage in the perinatal period, 3rd Int’l Congress of Pathology, Barcelona, Spain (May 17-22, 2008). 41 State v. Edmunds, 746 N.W.2d 590 (Ct. App. Wisc. 2008).

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fierce disagreement between forensic pathologists, who now question whether the symptoms Natalie displayed indicate intentional head trauma, and pediatricians, who largely adhere to the science as presented at Edmunds’s trial.” The Court held that this legitimate and significant dispute within the medical community required a new trial. Ultimately, all charges were dismissed. In October 2008, Commissioner Goudge issued his report on the Inquiry into Pediatric Forensic Pathology in Ontario, Canada.42 While many of his findings focused on the misdiagnoses by a single pediatric pathologist, Commissioner Goudge concluded that the problem was systemic and “there is one set of cases in which a further review is justified. Simply put, the changes in pathology knowledge concerning shaken baby syndrome and pediatric head injuries over the last two decades provide cogent reason for a carefully constructed review of the cases” since some convictions may have been based on pediatric pathology that today would be seen as unreasonable. This review is ongoing. 2009. In 2009, Dr. Mack, Dr. Squier and Dr. Eastman published an article on the anatomy and development of the meninges in infants, particularly the dura.43 In this article, they note that subdural hemorrhage in infants is often traumatic and that ruptured bridging veins are thought to be the source of subdural blood in such cases. However, nontraumatic conditions are also associated with subdural hemorrhage in infants. Since the bridging veins are relatively large caliber vessels that would produce larger, more localized bleeds, traumatic bridging vein rupture is a particularly unlikely source of the small thin film bleeding identified in the shaken baby/abusive head trauma literature. To explain these bleeds, this article goes back to the anatomical literature, which confirms that the infant dura contains an inner vascular plexus that is much larger than in adults. Given the size and location of the thin film hemorrhages, the authors conclude that the extensive capillary and venous plexuses of the dura are the most likely candidates for the source of hemorrhage in nontraumatic conditions, particularly in the first year of life. In the same year, Dr. Squier and Dr. Mack published an article on the neuropathology of infant subdural hemorrhage in which they concluded that it is unlikely that the widespread bilateral thin film subdural hemorrhage seen in infants has the same causality as the thick, space-occupying and often unilateral clot seen in older children and adults after trauma.44 Since biomechanical studies had concluded that the forces required to cause bridging vein rupture would likely exceed the strength of the infant neck, alternate mechanisms should be considered. Based on the anatomical literature, they concluded that the unique anatomy of the infant dura suggests a dural (rather than bridging vein) origin for the thin film subdural seen in infants, including nearly 50% of newborns. While most birth subdurals resolve rapidly, some may develop into chronic
42

The Honorable Stephen T. Goudge, Report on Inquiry into Pediatric Forensic Pathology in Ontario (4 volumes), Executive Summary at 48-49. Commissioner Goudge references an earlier review in England following the 2005 Harris decision, which found only a few cases that it regarded as potentially unsafe. Since the law often lags behind the science by 5-10 years, it is unclear whether a review that considered more recent developments would reach the same conclusion. 43 Mack J, Squier W and Eastman J, Anatomy and development of the meninges: implications for subdural collections and CSF circulation, Ped Radiology 2009; 39:200-210. 44 Squier W, Mack J, The neuropathology of infant subdural haemorrhage, For Sci. Int’l 2009; 187:6-13.

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fluid collections that are susceptible to rebleed, either spontaneously or after an otherwise innocuous event. In February and June 2009, Dr. Squier and Dr. Mack presented their findings at two conferences, one on each side of the “shaken baby” debate.45 In the second conference, which was sponsored by a leading supporter of shaken baby syndrome, Dr. Mack, a keynote speaker, presented “The Dural Venous Plexus: Implications of Subdural Collections.”46 A complementary presentation by Dr. Squier was entitled “Does Immaturity of Infant Dural Physiology Confer Vulnerability to Dural Bleeding?” These presentations received little criticism at either conference, and “intradural bleeding” is rapidly becoming part of the mainstream. If correct, there is no longer any basis for the violently ruptured bridging vein theory that formed the underpinnings of SBS theory. In the meantime, Dr. Cohen and Dr. Scheimberg had published the results of a two year study conducted by Sheffield Children’s Hospital (NHS Foundation Trust) and Barts (London NHS Trust).47 This study confirmed the association between hypoxic ischemic encephalopathy (a hypoxic brain) and intradural/subdural hemorrhage in fetuses and neonates first identified in Geddes I and II, and further found that the degree of the hemorrhage was closely related to the degree of hypoxia. Specifically, mild or early hypoxic ischemic encephalopathy was more frequently associated with small intradural hemorrhages with no subdural hemorrhage, while moderate or severe hypoxic ischemic encephalopathy was more frequently associated with diffuse intradural hemorrhage and accompanying subdural hemorrhage. Based on earlier research, Cohen and Scheimberg suggested that subdural hemorrhages in infants were likely due to leakage in the dural border cell layer, rather than burst bridging veins.48 In May 2009, the Committee on Child Abuse and Neglect of the American Academy of Pediatrics updated its policy statement on Abusive Head Trauma in Infants and Children, stating that the “advances in the understanding of the mechanisms and clinical spectrum of injury associated with abusive head trauma compel us to modify our terminology to keep pace with our understanding of pathologic mechanisms.”49 The AAP recommended that physicians use a less mechanistic term, “abusive head trauma,” reserving the term shaken baby syndrome for the “popular vernacular.” Based on confession evidence, the Committee continued to endorse shaking or shaking/impact as a mechanism of injury but acknowledged that the “mechanisms and resultant injuries of
45 46

See note 3, supra. Dr Cohen also presented at the first conference. See note 4, supra. Second Int’l Conference on Pediatric Abusive Head Trauma: Medical, Forensic, and Scientific Advances & Prevention, Penn State College of Medicine, Jackson Hole, Wyo. (June 25-26, 2009). 47 Cohen M and Scheimberg I, Evidence of Occurrence of Intradural and Subdural Hemorrhage in the Perinatal and Neonatal Period in the Context of Hypoxic Ischemic Encephalopathy: An Observational Study from Two Referral Institutions in the United Kingdom, Ped and Dev’l Path 2009; 12:169-176. 48 – including Dr. Squier (a British neuropathologist), Dr. Mack (an American neuroradiologist) and Dr. Cohen (an Argentinian/British histopathologist) – were reaching the same conclusions, albeit from very different perspectives and geographic locations. 49 Christian C, Block R and the Committee on Child Abuse and Neglect, Abusive Head Trauma in Infants and Children, Pediatrics 2009; 123:1409-1411.

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accidental and abusive head injury overlap” and that medical diseases can also “mimic” the presentation of abusive head trauma. The following month, an editorial in Pediatric Radiology by leading supporters of shaken baby theory (now renamed abusive head trauma) acknowledged that “[m]aybe our current understanding of the actual pathogenesis of subdural bleeding (tearing of bridging veins) is incorrect.”50 This conclusion was based on the research of Geddes, Mack, Squier and Eastman, and Cohen and Scheimberg.51 While Dr. Slovis, the editor of Pediatric Radiology, and Dr. Thomas, of the Radiology Department at Birmingham Children’s Hospital, continued to support the view that inflicted head trauma is “a real entity” – a proposition with which no one would disagree – their recognition that the torn bridging veins that formed a key element of shaken baby syndrome might not exist was yet another major blow to shaken baby theory. In September 2009, the “new learning” was reflected in a law review article entitled “The Next Innocence Project: Shaken Baby Syndrome and the Criminal Courts.”52 After reviewing the literature, Professor Tuerkheimer, a former child abuse prosecutor, concluded that “As a categorical matter, the science of SBS can no longer support a finding of proof beyond a reasonable doubt in triad-only cases – cases which represent a significant number of SBS prosecutions . . . Despite its lingering presence in the popular imagination, the scientific underpinnings of SBS have crumbled over the past decade as the medical establishment has deliberately discarded a diagnosis defined by shaking. Although no single nomenclature has emerged in its place, doctors are now in widespread agreement that SBS is an unhelpful characterization, and the presence of retinal hemorrhages and subdural hematoma cannot conclusively prove that injury was inflicted.” Professor Tuerkheimer noted that the polarization of the issue has tended to obscure the fact that there is significant consensus on the invalidity of previously accepted dogma and that even doctors who continue to defend the legitimacy of SBS “are willing to concede that the science has evolved – and that even mainstream thinking has changed in a number of areas.” 2010. By 2010, there was considerable agreement that brainswelling reflected hypoxia rather than trauma (Geddes I and II), that there are many causes of subdural hemorrhage (Jenny, Barnes, Frasier and others), and that the thin subdurals seen in infants were unlikely to have been caused by burst bridging veins (Squier, Mack, Cohen and others). Since two elements of the “triad” had been seriously undermined, shaken baby syndrome theory increasingly relied on retinal hemorrhages to diagnose shaking or abuse. While the literature recognized many causes for retinal hemorrhages, the
50

Chapman S and Slovis T, Response to Galaznik, Cohen & Scheimberg and Rorke-Adams & Christian, Pediatr Radiol 2009; 39:770-77. 51 Drs. Chapman and Slovis took issue with some implications of the Sheffield/Barts study but did not criticize the quality of the research, the correlation between the hypoxia seen in the brain and the size of the intradural/subdural hemorrhages, or the conclusion that bridging vein theory was not supported by the anatomy of the infant dura. Drs. Chapman and Slovis further emphasized that subdural hemorrhages have many etiologies that should be thoroughly investigated. 52 Tuerkheimer D, The Next Innocence Project: Shaken Baby Syndrome and the Criminal Courts, Wash. Univ. Law Rev. 1 (Fall 2009) (“Tuerkheimer”).

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supporters of shaken baby theory (now renamed abusive head trauma) claimed that shaking or other forms of abuse could be reliably diagnosed based on particular eye findings, such as optic nerve sheath and/or bilateral multi-layered retinal hemorrhages extending to the ora serrata. This hypothesis was severely undermined in February 2010. On February 24, 2010, Dr. Evan Matshes reported that a retrospective review of retinal hemorrhages at the Dallas Medical Examiner’s Office, a major metropolitan center that routinely removed the eyes for evaluation by consultant ophthalmologic pathologists, found that eye evaluations are of “limited value” in child death investigations.53 Dr. Matshes noted that “[f]or many years, the dogma of pediatric forensic pathology was ‘retinal and optic nerve sheath hemorrhages are pathognomonic of abusive head injury,’ including shaken baby syndrome. Growing controversy surrounding the existence of SBS led to questioning of that dogma.” The review confirmed that retinal hemorrhages are found in natural and accidental deaths as well as homicides, and identified a statistically significant relationship between retinal and optic nerve sheath hemorrhage and restitution of a perfusing cardiac rhythm following advanced cardiac life support with short term survival and cerebral edema regardless of etiology. Retinal hemorrhages were slightly more severe in children whose deaths were ruled homicides; however, these children were also more likely to have brain swelling and more lengthy post-injury survival periods. These empirical findings indicate that severe retinal hemorrhages are linked to resuscitation and life support rather than trauma. In the same month, an article published in the Journal of the American Association for Pediatric Ophthalmology and Strabismus reported retinal hemorrhages of the type previously viewed as diagnostic of shaking or abusive head trauma in two children who died from Streptococcus pneumoniae meningitis, a common communityacquired pneumonia in children.54 These findings are the first reports of retinal hemorrhages in deaths from natural causes identical to the retinal hemorrhages previously viewed as diagnostic of shaking or abuse.55 Conclusion. As this brief survey of the literature indicates, the underpinnings of shaken baby syndrome have been seriously undermined over the past decade. The implications are obvious: if the “new learning” is correct, parents and caretakers have been convicted of harming – often murdering – their children for nearly 40 years based on theories that were unproven and have increasingly been shown to be wrong. As a result of these and other research findings, Innocence Projects are beginning to seek postconviction relief for those convicted on medical evidence that is no longer viewed as [t]he trajectory of SBS in the criminal courts reveals fundamental limitations of our system’s ability to absorb forensic advances
53

Matshes E, Southwestern Institute of Forensic Sciences, Retinal and Optic Nerve Sheath Hemorrhages Are Not Pathognomonic of Abusive Head Injury, American Academy of Forensic Sciences, Seattle WA (Feb. 24, 2010). 54 Lopez J et al., Severe retinal hemorrhages in infants with aggressive, fatal Streptococcus pneumoniae meningitis, J Am Ass Ped Ophthal Strab (1):97-98 (Feb. 2010). 55 A reference in Henderson to a report on the presence of severe retinal hemorrhages in a child with leukemia suggests that this is just the beginning of such findings.

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in a manner consistent with the administration of justice. The law may ultimately align itself with the latest scientific thinking, but it is doing so slowly, arbitrarily, and in a wholly unreasoned (and unstudied) fashion. In the interim, we are witnessing patterned injustice.”56 Inevitably, the incorporation of the “new learning” involves attacks on those whose research undermines established dogma – attacks that are now playing themselves out in the media and the courts. At the same time, many of the concepts viewed as “heretical” just a few years ago are now accepted even by the staunchest shaken baby advocates. At the same time, doctors, lawyers and courts are wrestling – largely on a case by case basis – with the underlying question: if these children were not murdered by their parents or caretakers, why did they die? There is, however, no single answer to this question. Instead, infants die from many causes, some known and some unknown. Sometimes specific causes can be identified; often, however, the correct answer is “we don’t know.” Sometimes this is enough; other times, judges and juries demand that an alternative cause of death be proven – a burden that is not placed on the prosecution witnesses, many of whom continue to advance unproven or even disproven hypotheses. As this suggests, the end of the story is still unwritten. II. Resistance to change Since much of the “new learning” is “old news,” the second question is why it is taking so long for these conclusions to be incorporated into “mainstream” medical and legal analysis, and why the attacks are often so vicious. Factors that influence the resistance of the medical and legal professions to the “new learning” on shaking baby syndrome include: (1) the natural human reaction to child abuse; (2) the nature of medical/legal versus scientific decision making; (3) the role of clinicians; (4) a misunderstanding of the scientific method; (5) the lack of institutional safeguards and/or corrective mechanisms; (6) the reluctance to accept new ideas and desire for certainty; (7) Sherlock Holmes reasoning; and (8) peer pressure and advocacy groups. Child abuse 90 symposium on pretrial publicity, Judge Abner Mivka, a highly respected member of the U.S. Court of Appeals for the District of Columbia, made the following comment: Pre-trial publicity is not the big difficulty. It is generic prejudice. I do not think that you can get a fair child abuse trial before a jury anywhere in the country. I really don’t . . . I do not care how sophisticated or law smart jurors are, when they hear that a child has been abused, a piece of their mind closes up and this goes for the judge, the juror, and all of us.57

56

Tuerkheimer D, Criminal Justice at a Crossroads: Science-Dependent Prosecution and the Problem of Epistemic Contingency, 62 Ala. L.W. __ (forthcoming 2010), electronic copy ssrn.com/abstract-1579394. 57 Vidmar N, Generic Prejudice and the Presumption of Guilt in Sex Abuse Trials, Law and Human Behavior 1997; 21(1):5-25 at 5 (emphasis added).

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Judge Mivka’s comments apply equally to law enforcement, social workers and the medical profession. When child abuse is alleged, even the most sensible people often jump on the bandwagon, even when the wagon has no wheels. Medical/legal decisionmaking. Unlike engineering and the hard sciences, medical and legal thinking are not scientific in nature and are often based on limited information. In law, we have learned from DNA analysis that our judgments about people and past events are often wrong. In How Doctors Think, Dr. Jerome Groopman, Recanati Professor of Medicine at Harvard Medical School, describes the tendency of doctors to reach early decisions, the psychological commitment to distorted conclusions, and the powerful temptation to provide simple answers to complicated problems.58 This problem is magnified when incorrect and/or unverified medical theories are incorporated into legal precedent, which is then often viewed as sacrosanct. Reliance on clinicians. Like most professions, the medical profession consists of academics and researchers, on the one hand, and clinicians, on the other. In general, clinicians attempt to determine the cause for the patient’s symptoms by synthesizing the clinical history, the medical tests and their own experiences with the medical literature. The clinical history, i.e., the description of symptoms and events provided by the patient (or, in pediatric cases, the patient’s parents or caretakers) is the cornerstone of the diagnosis. In shaken baby and similar cases, this process has broken down. Instead of relying on the clinical history provided by the parents or caretakers, clinicians have been told to reject the clinical history and to instead treat the parents and caretakers as suspects. Clinicians cannot, moreover, rely on their own experiences, for to my knowledge no clinician has witnessed a case of violent shaking. In shaken baby and similar cases, therefore, clinicians are often reduced to reciting what they have been told, i.e., that the triad is caused by shaking or (sometimes) shaking/impact. Often, moreover, the clinicians who testify at trial are not the child’s pediatrician or even the hospital clinicians who treated the child; instead, they are consultants who may be deeply wedded to particular theories. The scientific method. Despite the belief of many judges and jurors that medical evidence is “scientific” in nature, it rarely follows the scientific method that most of us learned in high school. The scientific method consists of four steps: (1) the observation and description of phenomena; (2) the formulation of a hypothesis to explain the phenomena; (3) the use of the hypothesis to predict other phenomena or the results of the performance of experiments to test these predictions by several independent experimenters conducting properly designed and properly performed experiments. If a sufficient number of experiments bear out the hypothesis, the hypothesis may be elevated to a theory. Even so, new observations or experiments may disprove the theory, leading to a shift in the paradigm. Under this methodology, shaken baby syndrome is at best a hypothesis that has never been validated and whose basic tenets have been undermined (or in some instances disproven) by research, analysis and biomechanical experiments. The mistaken belief that shaken baby syndrome has been scientifically “proven” has led to profound misunderstandings by the public, the police,
58

Groopman J, How Doctors Think, Houghton Mifflin (2nd ed. 2009).

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the prosecutors, the medical community and the courts, resulting in a shift in the burden of proof from “innocent until proven guilty” to “guilty until proven innocent” – a task that is often impossible given the current state of scientific knowledge. Institutional safeguards/corrective mechanisms. In science, theories are validated and mistakes corrected through experimentation and testing. In other areas, we rely on market forces, government regulation, the legal system and/or self-regulation. These mechanisms are, however, often slow and imperfect. In the financial arena, market corrections may take decades and exact high interim costs, as we have learned from the savings and loan and subprime mortgage crises. In areas that are essentially selfregulating – such as religion, medicine and the legal system – there are even fewer safeguards, for the natural inclination of most institutions is to protect themselves. When medicine and the legal system become entwined, the only protection against unsupported or incorrect theories may be the “marketplace of ideas,” which depends on a free and open debate between those with opposing views. When this debate is stifled, even egregious errors may go uncorrected. Reluctance to accept new ideas and desire for certainty. There is a wellestablished human tendency to reject new ideas. In psychology, this is known as cognitive dissonance: we tend to accept findings that confirm our beliefs, and reject those that don’t. This tendency often goes hand in hand with a preference for certainty over uncertainty. In this context, it is not surprising that many members of the medical and legal communities prefer the “simple answers to complicated problems” provided by shaken baby theory to the “new learning,” which often describes complicated issues, fraught with uncertainty, with no simple answers in sight. As Professor Tuerkheimer recognized, a fundamental aspect of the shaken baby controversy is that “scientific developments have cast new doubt without yet creating certainty in its place.”59 Sherlock Holmes reasoning. In a classic article, Professor Alan Moritz, founder of the Department of Legal Medicine at Harvard Medical School, described one of the common mistakes in forensic pathology as follows: This brings me to one of the most dangerous mistakes in forensic pathology, and one that is particularly prevalent among experienced forensic pathologists who, for one reason or another, acquire a propensity for what might be called “categorical intuitive deduction.” This Sherlock Holmes type of expert may see certain bruises and conclude without doubt that they were produced by the thumb and forefinger of the right hand of the stranger . . . He ignores the essential component for proof of the correctness of any such scientific deduction, namely, the nonoccurrence of such lesions or changes in control cases. . . He may be highly esteemed by the police and by the prosecuting attorney because he is an emphatic and impressive witness. His prestige, together with his exclusive access to the original evidence, places him in an
59

Tuerkheimer at 58.

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exceedingly powerful position in the courtroom. Rarely can the defense attorneys find anyone with comparable experience to evaluate the postmortem findings. On the other hand, if they do, it seems obvious to the jury 1) that the outside expert was hired to say something that would help the accused, and 2) that the outside expert, unlike the state’s witness, was handicapped by the fact that he did not see the evidence with his own eyes. It is difficult to estimate how much harm is done by these people. I know of a man who was hanged largely on the weight of such uncritical evidence. The ordinary hospital pathologist is not accustomed to being so continuously unchallenged as to permit him to acquire a full-blown God complex of the kind that I am discussing . . . It is only the full-time forensic pathologist who is likely to become accustomed to having his opinions go virtually unchallenged. The stakes are too high to play hunches in forensic pathology.60 In the shaken baby area, many experts – not just forensic pathologists – employ “Sherlock Holmes” reasoning, and they have become accustomed to having their opinions go virtually unchallenged by their peers and the legal community. They hold sway in their institutions, they form groups where their ideas will not be questioned, and they are powerful witnesses in court, for the evidence that they present is simple and persuasive. There is only one problem: their conclusions are often dead wrong, and it is difficult to estimate the harm that they have done. Peer pressure and advocacy groups. In shaken baby circles, the difficulty of the issues is exacerbated by peer pressure and well-financed advocacy groups. On a local level, it is not uncommon for treating physicians to disagree with child abuse diagnoses but to refuse to testify, in part because they are uncertain of their diagnoses and in part for fear of retaliation by their peers, their institutions and the legal system. Often these fears are justified. On a national and international level, the polarization is exacerbated by a well-organized training apparatus. As Professor Tuerkheimer points out, training materials provided by The National Center on Shaken Baby Syndrome, an advocacy group dedicated in part to training prosecutors and law enforcement officers, ignore significant challenges to the conventional wisdom, fail to acknowledge the shifting of the center, and present “a view of the science refracted through an advocate’s lens.”61 This problem is further exacerbated by the legal system, which tends to solidify its own conclusions: Finally, prosecutorial thinking about these cases is pervaded by an echo of the methodological fallacy of the early SBS literature. If, across the country over the years, defendants have been proven guilty of shaking
60

Moritz, A., Classical mistakes in forensic pathology, Am J Clin Path 26 at 1383 (1956), reprinted Am J For Med Path 1981; 2(4):299-308. 61 Tuerkheimer at 28. This group’s International Advisory Board includes the strongest supporters of shaken baby theory in the U.S. and the U.K.

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babies to death based on the presence of retinal hemorrhages, subdural hematomas and cerebral edemas, then the presence of these symptoms must mean that someone is guilty of shaking a baby to death. All that remains is to identify the last person with the conscious child. That person becomes the suspect, who can then be confidently pursued. In this manner, the triad-based crime constructed by the medical establishment has been reified – its existence affirmed – by the systematic conviction of its apparent perpetrators.62 Professor Tuerkheimer describes the suggestion that this scientific dispute be decided in the courts as “untenable.”63 Today, judges and juries are being asked to decide questions that have not been answered by the medical profession. They are expected to do so, moreover, in the context of highly contentious debates between well credentialed experts, with extraordinarily high stakes for parents, children and families. The defense bar has an important role to play in this process, as do prosecutors and innocence clinics. At present, we all need to do our best in addressing cases on a case-by-case basis. At the same time, we need to be looking for broader solutions to a system that is, at the moment, seriously flawed.

62 63

Tuerkheimer at 32. Tuerkheimer at 57.

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