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
eLetters: ![[Read eLetters]](/icons/misc/sectionDOWN.gif){kind=icon}
