Although cerebrospinal fluid (CSF) shunt placement is the most common procedure performed by pediatric neurosurgeons, shunts remain among the most failure-prone life-sustaining medical devices implanted in modern medical practice. This article provides an overview of the mechanisms of CSF shunt failure for the 3 most commonly employed definitive CSF shunts in the practice of pediatric neurosurgery: ventriculoperitoneal, ventriculopleural, and ventriculoatrial. The text has been partitioned into the broad modes of shunt failure: obstruction, infection, mechanical shunt failure, overdrainage, and distal catheter site-specific failures. Clinical management strategies for the various modes of shunt failure are discussed as are research efforts directed towards reducing shunt complication rates. As it is unlikely that CSF shunting will become an obsolete procedure in the foreseeable future, it is incumbent on the pediatric neurosurgery community to maintain focused efforts to improve our understanding of and management strategies for shunt failure and shunt-related morbidity.
The treatment of hydrocephalus by cerebrospinal fluid shunting is plagued by ventricular catheter obstruction. Shunts can become obstructed by cells originating from tissue normal to the brain or by pathological cells in the cerebrospinal fluid for a variety of reasons. In this review, the authors examine ventricular catheter obstruction and identify some of the modifications to the ventricular catheter that may alter the mechanical and chemical cues involved in obstruction, including alterations to the surgical strategy, modifications to the chemical surface of the catheter, and changes to the catheter architecture. It is likely a combination of catheter modifications that will improve the treatment of hydrocephalus by prolonging the life of ventricular catheters to improve patient outcome.
The central nervous system's (CNS) complicated design is a double-edged sword. On the one hand, the complexity is what gives rise to higher order thinking; but on the other hand, damage to the CNS evokes its unforgiving nature. The cerebrospinal fluid (CSF) circulation system is an intricate system embedded in and around the CNS that has been the topic of debate since it was first described in the 18th century. It is underscored by the choroid plexus's distinct vascular network which has conventionally been seen as the most prominent structure in CSF production through a variety of active transporters and channels. Despite the ubiquity of this circulation system in vertebrates, some aspects remain understudied. Recent advances in scientific methodology and experimentation have proven to be effective tools for elucidating the mechanisms of the CSF circulation system and the pathological conditions associated with its malfunction. In this review, we capitulate the classical understanding of CSF physiology as well as a new, emerging theory on CSF production.
This study suggests that macrophage and astrocyte adhesion generally decreases with increasing hole diameter under flow conditions and underscores the necessity for future work to examine how hole diameter impacts inflammatory-based shunt obstruction.
These results indicate that a reactive astrocytic response continues to rise dramatically in chronic hydrocephalus, suggesting ongoing gliosis and potential damage. Shunting partially ameliorates the continuation of astrogliosis, but does not completely reverse this inflammatory reaction even after a long recovery.
BackgroundShunt obstruction in the treatment of hydrocephalus is poorly understood, is multi-factorial, and in many cases is modeled ineffectively. Several mechanisms may be responsible, one of which involves shunt infiltration by reactive cells from the brain parenchyma. This has not been modeled in culture and cannot be consistently examined in vivo without a large sample size.MethodsWe have developed and tested a three-dimensional in vitro model of astrocyte migration and proliferation around clinical grade ventricular catheters and into catheter holes that mimics the development of cellular outgrowth from the parenchyma that may contribute to shunt obstruction.ResultsCell attachment and growth was observed on shunt catheters for as long as 80 days with at least 77 % viability until 51 days. The model can be used to study cellular attachment to ventricular catheters under both static and pulsatile flow conditions, which better mimic physiological cerebrospinal fluid dynamics and shunt system flow rates (0.25 mL/min, 100 pulses/min). Pulsatile flow through the ventricular catheter decreased cell attachment/growth by 63 % after 18 h. Under both conditions it was possible to observe cells accumulating around and in shunt catheter holes.ConclusionsAlone or in combination with previously-published culture models of shunt obstruction, this model serves as a relevant test bed to analyze mechanisms of shunt failure and to test catheter modifications that will prevent cell attachment and growth.
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