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Published on: July 5, 2021
Childhood optic pathway tumors associated with ascites following ventriculoperitoneal shunt placement
G A West1, M S Berger, J R Geyer
1Department of Neurological Surgery, University of Washington and Children's Hospital and Medical Center, Seattle.
Insights
Elevated cerebrospinal fluid protein in children with optic pathway gliomas may cause ascites after ventriculoperitoneal shunt placement. Converting to a ventriculoatrial shunt resolved ascites in these cases.
Area of Science:
- Neuro-oncology
- Pediatric Neurosurgery
- Gastroenterology
Background:
- Ventriculoperitoneal (VP) shunts are used to treat hydrocephalus.
- Ascites is an uncommon complication following VP shunt placement.
- Optic pathway gliomas can lead to elevated cerebrospinal fluid (CSF) protein levels.
Observation:
- Three children with optic pathway gliomas developed ascites post-VP shunt placement.
- All patients had elevated CSF protein before initial shunt insertion.
- No infection or tumor seeding was found in the peritoneal cavity.
Findings:
- Ascites resolved completely after converting to a ventriculoatrial (VA) shunt.
- Elevated CSF protein, potentially from the glioma, may impair peritoneal CSF absorption.
- This suggests a link between high CSF protein and VP shunt-associated ascites.
Implications:
- Consider CSF protein levels in optic glioma patients undergoing CSF diversion.
- VA shunts may be a viable alternative for managing ascites in such cases.
- This highlights a specific risk factor for VP shunt complications in pediatric neuro-oncology.
Abstract:
Three children with optic pathway gliomas who developed ascites following ventriculoperitoneal shunt placement are presented. In all 3 cases there was an elevated cerebrospinal fluid (CSF) protein level at the time of initial shunt placement. At the time of developing ascites following placement of the ventriculoperitoneal shunt, none of the patients had evidence of infection or tumor seeding in the peritoneal cavity. The ascites completely resolved in each instance after converting the shunt to a ventriculoatrial system. Ascites following ventriculoperitoneal shunt insertion is an uncommon complication. A review of the literature and discussion of the possible etiologic factors in the development of ascites after ventriculoperitoneal shunt placement are presented. For patients diagnosed with optic gliomas, it is suggested that because the tumor is widely exposed to the CSF space, protein exuded by the mass into the subarachnoid space will cause an elevated CSF protein concentration. The elevated CSF protein may then lead to ascites as a result of poor absorption of CSF in the peritoneal cavity after placement of a ventriculoperitoneal shunt. Although ascites following ventriculoperitoneal shunt placement is not typical in patients with optic gliomas, attention should be given to CSF protein levels documented at the time of CSF diversion for hydrocephalus, recognizing that ascites may occur as a result of poor CSF absorption in the periotoneum, subsequently requiring a ventriculoatrial shunt in patients who develop hydrocephalus.
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