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Anterior ischemic optic neuropathy complicating cranial vault reconstruction for sagittal synostosis in a child
Jonathan Lee1, Mark W Crawford, James Drake
1Department of Anesthesia, The Hospital for Sick Children, Toronto, Ontario, Canada.
Insights
Pediatric cranial vault reconstruction can lead to vision loss due to ischemic optic nerve injury. Prolonged prone positioning and blood loss are potential risk factors for this serious complication.
Area of Science:
- Neurosurgery
- Ophthalmology
- Pediatric Surgery
Background:
- Cranial vault reconstruction is a complex surgical procedure.
- Nonsyndromic sagittal synostosis requires surgical correction in pediatric patients.
- Maintaining hemodynamic stability during surgery is crucial.
Observation:
- A 5-year-old boy developed bilateral blindness post-cranial vault reconstruction.
- Edematous eyelids and nonreactive pupils were noted postoperatively.
- Optic disc pallor and edema were observed, with normal imaging studies.
Findings:
- The patient experienced bilateral blindness, presumed to be anterior optic nerve infarction.
- Prolonged prone positioning (6 hours) and controlled hypotension were employed.
- Significant intraoperative blood loss (hematocrit 23-31%) occurred.
Implications:
- Pediatric patients undergoing cranial vault reconstruction face risks of ischemic optic nerve injury.
- Surgeons should consider patient positioning and blood loss as potential risk factors.
- Early recognition and intervention may improve visual outcomes, as seen in this case with partial recovery.
Abstract:
The authors report a case of postoperative visual loss in a pediatric patient who underwent an uneventful cranial vault reconstruction. A 5-year-old boy underwent total cranial vault reconstruction for nonsyndromic sagittal synostosis. He was positioned prone for 6 hours and then supine for the final 2 hours of surgery. Controlled hypotension was used to maintain the systolic arterial pressure at 80 mmHg to 90 mmHg. The intraoperative hematocrit was 23% to 31%. In the immediate postoperative period, both pupils were noted to be reactive to light. After an uneventful night in the intensive care unit, he was transferred to the ward. The eyelids were edematous on postoperative day 1, and visual examination was no longer possible. He was discharged home on postoperative day 4, and readmitted 2 days later with bilateral blindness. The pupils were nonreactive, and the optic discs were pale and edematous. Computed tomography and magnetic resonance imaging of the head revealed no abnormality. Intravenous steroid therapy was initiated, and the patient was taken to the operating room for re-exploration; the intracranial pressure was found to be normal. The presumed diagnosis was bilateral infarctions of the anterior optic nerves. Visual acuity 14 months after surgery was less than 3/200 in the right eye and 20/20-2 in the left, indicating significant recovery. Pediatric patients undergoing cranial vault reconstruction are at risk for postoperative visual loss because of ischemic optic nerve injury. Prolonged duration in the prone position and significant blood loss may be risk factors.
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