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PATHOLOGY OF PERIMACULAR FOLDS DUE TO VITREORETINAL TRACTION IN ABUSIVE HEAD TRAUMA

Abed Alnabi, Waleed, MD*; Tang, Garland J., MD; Eagle, Ralph C. Jr, MD; Gulino, Sam, MD§; Thau, Avrey, BS; Levin, Alex V., MD, MHSc*,†

doi: 10.1097/IAE.0000000000002273
Original Study: PDF Only

Purpose: To demonstrate vitreoretinal traction as a mechanism for perimacular folds in abusive head trauma.

Methods: We performed gross and histopathologic examination of eyes of children with suspected abusive head trauma and identified those with typical perimacular folds. Information was collected regarding the incident that led to the child's death and systemic manifestations noted at autopsy. Eyes were prepared in a fashion that allowed for demonstration of the vitreoretinal interface.

Results: Ten eyes of five patients (2–13 months) were examined. All patients had systemic manifestations of abusive trauma including intracranial injury. All cases provided evidence of vitreoretinal traction producing perimacular folds. Condensed vitreous was seen attached to the apices of the retinal folds, and the detached internal limiting membrane comprising the inner surfaces of the schisis cavity. Four cases showed severe bilateral multilayered symmetric retinal hemorrhages extending to the ora serrata. All cases showed optic nerve sheath subdural hemorrhage and subarachnoid hemorrhage. Orbital hemorrhage was unilateral in two cases and bilateral in three cases. Four cases showed orbital fat hemorrhage. One case showed extraocular muscle sheath and cranial nerve sheath hemorrhage. Two cases showed juxtapapillary intrascleral hemorrhage.

Conclusion: Vitreoretinal traction is the likely mechanism of perimacular folds in abusive head trauma.

Gross and histopathologic examination was performed on eyes of patients with suspected abusive head trauma who demonstrated typical perimacular folds. The results suggest vitreoretinal traction as the mechanism. These findings have critical forensic implication when perimacular folds and retinoschisis are seen clinically.

*Pediatric Ophthalmology and Ocular Genetics, Wills Eye Hospital, Philadelphia, Pennsylvania;

Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania;

Department of Pathology, Wills Eye Hospital, Philadelphia, Pennsylvania; and

§Philadelphia Department of Public Health, Medical Examiner's Office, Philadelphia, Pennsylvania.

Reprint requests: Alex V. Levin, MD, MHSc, Pediatric Ophthalmology and Ocular Genetics, Wills Eye Hospital, Suite 1210, 840 Walnut Street, Philadelphia, PA 19107; e-mail: alevin@willseye.org

Supported in part by the Foerderer Fund (A.V.L.) and the Robison D. Harley, MD Endowed Chair in Pediatric Ophthalmology and Ocular Genetics (A.V.L.) and the Joseph F. Bradway Endowed Research Fellow (A.T.).

None of the authors has any financial/conflicting interests to disclose.

A. V. Levin has testified for both the defense and prosecution in civil and criminal cases related to child abuse.

© 2018 by Ophthalmic Communications Society, Inc.