Traumatic Brain Injury as a Result of Cranial Bone Defects Following Fronto-Orbital Advancement
Shareef Jandali, MD, Mirko Gilardino, MD, MSc, FRCSC, Scott P. Bartlett, MD, Linton A. Whitaker, MD.
University of Pennsylvania Health System, Philadelphia, PA, USA.
BACKGROUND: Fronto-orbital advancement (FOA) is a surgical technique used in the repair of craniosynostosis which involves wide exposure of the skull, craniotomy and repositioning of the supraorbital and frontal bone. This procedure often results in a cranial defect posterior to the advanced skull segments. In spite of its frequent use, no data exists regarding the risk of traumatic brain injury secondary to the bony defect prior to its reossification, a process that takes anywhere from 6 to 24 months. In addition, an average of 20% of these patients fail to reossify these defects altogether, thus requiring a cranioplasty for closure. It is our impression that despite the cranial defect and potential for brain injury, the actual rate of traumatic brain injury is extremely low.
METHODS: A retrospective analysis of the 416 patients who underwent FOA for craniosynostosis at the Children’s Hospital of Philadelphia between 1997 and 2007 was performed. Patients with less than two years of follow-up were excluded, yielding a total of 396 patients. The incidence of traumatic brain injury as a result of cranial defects was determined from office charts and ER visit records. In addition, records were reviewed for patients who had failed to reossify their FOA defects (CT-documented) to determine the risk of traumatic brain injury in active, growing children with cranial defects.
RESULTS: No traumatic brain injuries as a consequence of the temporary cranial defects created from the FOA were encountered in the 396 identified. During the same period, a total of seven patients with persistent CT-documented cranial defects ranging in size from 3 cm2 to 80 cm2 as a result of FOA were identified. Although all of these patients eventually underwent cranioplasty to address these defects later in life, they had a combined brain injury-free survival time of 77 years and 7 months prior to defect closure. Cranioplasty was performed using either bone paste or autologous bone graft. There were no complications in seven cranioplasty patients, except for partial resorption of bone grafts in 2 of 7 patients, and significant intra-operative blood loss in 2 of 7 patients.
CONCLUSIONS: Despite the production of significant skull defects following FOA for the treatment of craniosynostosis in children, the risk of traumatic brain injury to the brain prior to reossification of these defects is extremely low. In addition, although cranioplasty is often deemed necessary for patients who have persistent cranial defects, our experience is that the risk of brain injury in these patients is also exceptionally low, and the decision to proceed with cranioplasty should be weighed against the risk of known complications (hemorrhage, failure, infection, etc.) from this procedure for each individual patient.