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FROM THE AMERICAN ACADEMY OF PEDIATRICS:
Nancy D. Kellogg and the Committee on Child Abuse and Neglect
Evaluation of Suspected Child Physical Abuse
Pediatrics 2007; 119: 1232-1241 [Abstract] [Full text] [PDF]
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[Read P3R] Eye findings and Allegations of Shaking and Non-Accidental Injury
John G Galaznik   (8 August 2007)

Eye findings and Allegations of Shaking and Non-Accidental Injury 8 August 2007
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John G Galaznik,
Pediatrician
University of Alabama School of Medicine at Tuscaloosa

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Re: Eye findings and Allegations of Shaking and Non-Accidental Injury

jgalaznik1{at}aol.com John G Galaznik

Letter to the Editor

RE: Evaluation of Suspected Child Physical Abuse

Editor,

I read with interest the recent Clinical Report from Dr. Nancy D. Kellogg and the AAP Committee on Child Abuse and Neglect (1). However, I was very concerned by the authors’ handling of the issue of eye findings and the implication that they are speaking for the Academy in this Clinical Report. Given the role that eye findings presently play in the evaluation of physical abuse of infants, I feel that the authors owe us a clearer justification for their assertions in this article.

First, Kellogg (2007) relied exclusively on the Morad (2002) article for valid information in this area (1). The Morad article relied on data collected between 1993 and 1999 at one hospital and by one examiner (2). In that article, the presence of any abnormal findings on neuroimaging plus any findings of ocular injury was all that was required for the diagnosis of “apparent nonaccidental head injury consistent with SBS” (2). At that time, the potential for short distance falls and accidental injuries to result in retinal hemorrhages, schisis, and perimacular retinal folds had not been published and caregivers giving such histories were assumed to be lying and hiding the fact that they had shaken their wards. At that time, the documentation of the appearance and progression of retinal findings in the presence of markedly increased intracranial pressure (ICP) had not been reported. In my case load alone, I have two cases where the in-hospital documented appearance of schisis and perimacular folds clearly occurred >24 hours post ALTE presentation. It should also be pointed out that in the Morad data, 100% of the infants included had abnormal neuroimaging and 85% had retinal findings, and when retinal hemorrhages were present, greater than 83% were extensive in at least one eye (2). Morad gave no indication of timing between eye exam, neuroimaging, and state of the anterior fontanelle, or data on the measured ICPs when obtained; further, it gave no data on autopsy retinal findings as compared to findings at clinical exam in life, that might have documented the appearance and progression of eye findings under post-event conditions of markedly increased ICP, compromised cerebral profusion pressure induced hypoxia/ischemia, and disseminated intravascular coagulation/coagulopathy. The evaluation of data from a series of patients, attempting to determine the potential cause of a finding has to be suspect, when the finding under scrutiny is essentially universally present in the patient pool and not correlated with secondary issues. Given the experimental and clinical data published since 2001, the Morad article would now appear to be obsolete and certainly not appropriate for exclusive citing in the American Academy of Pediatric’s current position in this area. Even in the final two paragraphs of the Morad article itself, where the vitreous traction hypothesis is discussed, it is not asserted as fact, but only as theory that needs further laboratory and clinical studies (2).

Second, the acceleration-deceleration traction hypothesis, to my knowledge, is the only proposed mechanism of eye injury that would be specific for abuse. If eye findings are to be used as indicators of abuse, this mechanism must be shown to be both valid and uniquely able to cause primary eye findings that cannot be explained by secondary factors common to brain injury from a variety of causes. Kellogg et al. should be required to prove both before making their statement, “Location, depth, and extent of retinal hemorrhages may distinguish between abusive and nonabusive causes of head trauma. Retinal hemorrhages occur in approximately 85% of infant and children who are subjected to abusive, repetitive acceleration-deceleration (shaking) forces with or without impact,” (1) while citing only Morad (2002) as their proof.

Data from Plunkett (2001) indicated that retinal hemorrhages were present in 2/3 of the fatal accidental head injuries when eye exams were recorded (3). Gilles (2003) reported the appearance and progression of eye findings in the presence of a markedly increased intracranial pressure after head injury (4). Lantz (2004), reported on that finding of perimacular folds in a case of crush injury to an infant’s head (5). Goldsmith (2004) reported on a videotaped fatal short distance fall with “extensive” bilateral retinal hemorrhages (6). In the February 2007 issue of the Journal of the American Association of Pediatric Ophthalmology and Strabismus, three abstracts relevant to this issue were published and were subsequently presented at the national meeting of the American Association of Pediatric Ophthalmology and Strabismus in Seattle in April. Obi (2007) reported on two cases where similar retinal hemorrhages, schisis, and folds were found in two patients—one injured accidentally in a witnessed short distance fall and one presumed to have been abused (7). Brown/Levin (2007) reported on the experimental observation of two kittens and a rabbit, which were killed by observed vigorous shaking by a large dog. These animals were found to have no eye findings on autopsy (8). The most provocative is the laboratory experiments by Binenbaum (2007) utilizing an appropriate animal model (3-5 day-old piglets) (9) and the well-published technique of Raghupathi (2002, 2004) (10,11). When subjected to impulse loaded acceleration-deceleration through 110 degrees of rotation over 15 msec., achieving measured accelerations > 55,000 rad/sec2, these researchers could produce no eye findings of retinal hemorrhages, schisis, folds, or intradural optic nerve sheath hemorrhages in the piglets (9). This represents >20 times the rotational acceleration-deceleration that Prange (2003) predicted could even be achievable with a horizontal abusive shaking of a 10 pound infant (12); and still, Binenbaum (2007) could produce no primary eye findings (9). In view of this recent literature, the assertion of any unique ability of repetitive acceleration- deceleration to cause “highly characteristic” eye findings cannot be sustained. Furthermore, these recent publications create a real question as to the validity of the acceleration-deceleration mechanism for the formation of any primary eye findings in the cases of alleged abuse that we presently encounter.

In view of the current published experimental and clinical information available since the Morad article, the AAP Committee on Child Abuse and Neglect has a duty to the Academy, to children and their parents, and to the legal system: 1) to address and deal with current challenges to the acceleration-deceleration vitreous traction hypothesis (shaking); 2) to come forth with real experimental data proving its validity before even implying that it has a role in the genesis of eye findings in head injury; and 3) to justify their implying a role for eye findings to even enter the picture in efforts to distinguish accidental from non-accidental injury in infants.

It should also be noted that since the publication of recent articles in the JAAPOS in February 2007, the American Academy of Ophthalmology has taken down its website on Shaken Baby Syndrome and shaking injury. Pediatricans who continue to assert a role for eye findings in the evaluation of NAI can no longer rely on the American Academy of Ophthalmology for support.

REFERENCES

1. Kellogg ND, and Committee on Child Abuse and Neglect. Evaluation of Suspected Child Physical Abuse. Pediatrics. 2007;119:1232-41. 2. Morad Y, Kim YM, Armstrong DC, Huyer D, Mian M, Levin AV. Correlation Between Retinal Abnormalities and Intracranial Abnormalities in the Shaken Baby Syndrome. Am J Ophthalmol. 2002;134:354-359. 3. Plunkett J. Fatal Pediatric Head Injuries Caused by Short-Distance Falls. Am J Forensic Med Pathol. 2001;22:1-12. 4. Gilles EE, McGregor ML, Levy-Clarke G. Retinal Hemorrhage Asymmetry in Inflicted Head Injury: A Clue to Pathogenesis? J Pediatr. 2003:143:494-9. 5. Lantz PE, Sinal SH, Staton CA, Weaver Jr RG. Evidence based case report: Perimacular retinal folds from childhood head trauma. BMJ. 2004;328:754-756. 6. Goldsmith W, Plunkett J. Biomechanical analysis of the causes of traumatic brain injury in infants and children. Am J Forensic Med Pathol. 2004;25:89-100. 7. Obi E, Watts P. Are there any pathognomonic signs in shake baby syndrome? J AAPOS. 2007;11:99-100. 8. Brown S, Levin AV, Ramsey D, Serbanescu I. Natural animal shaking: A model for inflicted neurotrauma in children? J AAPOS. 2007;11:85-86. 9. Binenaum G, Forbes BJ, Raghupathi R, Judkins A, Rorke L, Marguiles SS. An animal model to study retinal hemorrhages in nonimpact brain injury. J AAPOS. 2007;11:84-85. 10. Raghupathi R, Margulies SS. Traumatic axonal injury after closed head injury in the neonatal pig. J Neurotrauma. 2002;19:843-845. 11. Raghupathi R, Mehr MF, Helfaer MA, Margulies SS. Traumatic axonal injury is exacerbated following repetitive closed head injury in the neonatal pig. J Neurotrauma. 2004;21:307-316. 12. Prange MT, Coats B, Duhaime AC, Margulies SS. Anthropomorphic simulations of falls, shakes, and inflicted impacts in infants. J Neurosurg. 2003;99:143-150.

John Gilbert Galaznik, M.D. (Pediatrician) Student Health Center University of Alabama School of Medicine, Tuscaloosa Campus Box 870360 Tuscaloosa, Alabama 35487-0360 (205) 348-6262

Disclosure: I am a medical consultant on cases involving allegations of physical abuse to infants and small children. I have testified in both civil and criminal cases.

Conflict of Interest:

None declared