Initial Clinical Experience and Biomechanical Analysis of a Novel Gravity Unit–Assisted Valve (M.blue) in Pediatric Patients With Hydrocephalus

Neurosurgery 93:555–562, 2023

Overdrainage is a widely reported complication representing common indication for shunt revision. Despite recent advances in valve design, repeated shunt revisions represent burden on healthcare systems.

OBJECTIVE: To investigate the efficiency of a novel gravity unit–assisted programmable valve “M.blue” in pediatric hydrocephalus using clinical and biomechanical analyses.

METHODS: This retrospective single-center study included pediatric patients who received M.blue valve between April 2019 and 2021. Several clinical and biomechanical parameters were documented including complications and revision rates. Flow rate, functional assessment in vertical and horizontal positions, and extent of depositions inside valve were analyzed in explanted valves.

RESULTS: Thirty-seven M.blue valves in 34 pediatric patients with hydrocephalus (mean age 2.82 ± 3.91 years) were included. Twelve valves (32.4%) were explanted during a follow-up period of 27.3 ± 7.9 months. One-year survival rate of 89% and overall survival rate of 67.6% with a valve survival average of 23.8 ± 9.7 months were observed. Patients with explanted valves (n = 12) were significantly younger, with 0.91 ± 0.54 years of age in average (P= .004), and showed significantly more adjustments difficulties (P= .009). 58.3% of explanted valves showed deposits in more than 75% of the valve surface despite normal cerebrospinal fluid findings and were associated with dysfunctional flow rate in vertical, horizontal, or both positions.

CONCLUSION: The novel M.blue valve with integrated gravity unit is efficient in pediatric hydrocephalus with comparable survival rate. Deposits inside valves could affect its flow rate in different body positions and might lead to dysfunction or difficulties in valve adjustments.

Pathophysiology of shunt dysfunction in shunt treated hydrocephalus

Pathophysiology of shunt dysfunction in shunt

Acta Neurochir (2013) 155:1763–1772

We hypothesized that shunt dysfunction in the ventricular catheter and the shunt valve is caused by different cellular responses. We also hypothesized that the cellular responses depend on different pathophysiological mechanisms.

Methods Removed shunt material was collected. Macroscopic tissue in the catheters was paraffin-embedded and HE-stained. Valves were incubated with trypsin-EDTA in order to detach macroscopically invisible biomaterial, which was then cytospinned and HE-stained. Associated aetiological and surgical data were collected by reviewing patient files, and ventricular catheter position was examined using preoperative radiology (CT scans).

Results We examined eleven ventricular catheters and ten shunt valves. Catheters: 6/11 catheters contained intraluminal tissue consisting of vascularised glial tissue and inflammatory cells (macrophages/giant cells and a few eosinophils). Catheter adherence correlated with the presence of intraluminal tissue, and all tissue containing catheters had some degree of ventricle wall contact. All obstructed catheters contained intraluminal tissue, except one catheter that was dysfunctional because of lost ventricular contact. Valves: Regardless of intraoperative confirmation of valve obstruction, all ten valves contained an almost uniform cellular response of glial cells (most likely ependymal cells), macrophages/giant cells, and lymphomonocytic cells. Some degree of ventricle wall catheter contact was present in all examined valves with available radiology (9/10).

Conclusions The same cellular responses (i.e., glial cells and inflammatory cells) cause both catheter obstruction and valve obstruction. We propose two synergistic pathophysiological mechanisms. (1) Ventricle wall/parenchymal contact by the catheter causesmechanical irritation of the parenchyma including ependymal exfoliation. (2) The shunt material provokes an inflammatory reaction, either nonspecific or specific. In combination, these mechanisms cause obstructive tissue ingrowth (glial and inflammatory) in the catheter and clogging of the valve by exfoliated glial cells and reactive inflammatory cells.