Intraventricular hemorrhage following removal of external ventricular drains: Report of 2 pediatric cases

Risk of intraventricular bleeding following External Ventricular Drains (EVDs) placement is well recognized. On the contrary, hemorrhage following removal of EVD is considered highly unlikely. We report two cases of massive, symptomatic intraventricular hemorrhage that occurred soon after removal of EVD, in two pediatric patients, one affected by posterior fossa tumor, and the other by acute post-traumatic hydrocephalus. This complication significantly affected outcome: in both cases EVD should be replaced, hospitalization was prolonged and further surgery was required for persisting hydrocephalus. The first patient also presented neurological deficits and delay in starting oncological therapies. There are currently no articles that specifically address hemorrhagic risk in EVDs removal. Only one paper that evaluates EVD associated hemorrhage also discuss about hemorrhages caused by removal of the catheter in children. Such risk appears to be not negligible, with hemorrhagic rate of 21.9%. More often, these hemorrhages have few clinical significance, but severe sequelae, may also occur. This should be considered in decision making, and in discussing the risks with a patient's family. Keywords: Hydrocephalus, Pediatric, Complication, Shuntin

Subgroup-specific structural variation across 1,000 medulloblastoma genomes.

Medulloblastoma, the most common malignant paediatric brain tumour, is currently treated with nonspecific cytotoxic therapies including surgery, whole-brain radiation, and aggressive chemotherapy. As medulloblastoma exhibits marked intertumoural heterogeneity, with at least four distinct molecular variants, previous attempts to identify targets for therapy have been underpowered because of small samples sizes. Here we report somatic copy number aberrations (SCNAs) in 1,087 unique medulloblastomas. SCNAs are common in medulloblastoma, and are predominantly subgroup-enriched. The most common region of focal copy number gain is a tandem duplication of SNCAIP, a gene associated with Parkinson's disease, which is exquisitely restricted to Group 4α. Recurrent translocations of PVT1, including PVT1-MYC and PVT1-NDRG1, that arise through chromothripsis are restricted to Group 3. Numerous targetable SCNAs, including recurrent events targeting TGF-β signalling in Group 3, and NF-κB signalling in Group 4, suggest future avenues for rational, targeted therapy