Ventriculoatrial shunts are the most common second-line procedure for cases in which ventriculoperitoneal shunts are unsuitable. Shunting-associated thrombosis is a potentially life-threatening complication after ventriculoatrial shunt insertion. The overall prevalence of this complication is still controversial because of substantial differences in the numbers found in studies using clinical data and in those analyzing postmortem findings. The etiology of thrombosis may be multifactorial, including shunt catheter itself, contents of cerebrospinal fluid, shunt infection, and genetic disorder. The clinical presentation can vary widely, ranging from asymptomatic to a life-threatening condition. Timely recognition of thromboembolic lesions is critical for treatment. However, early diagnosis and management is still challenging because of a relatively long asymptomatic latency and lack of clear guideline recommendations. The purpose of this review is to provide an overview of ventriculoatrial shunt thrombosis, especially to focus on its etiopathogenesis, diagnosis, treatment, and prevention.
Background: Acquired hydrocephalus (AH) is a common complication in patients with severe brain injury. Brain tissue injury has been proposed to induce a neuroinflammatory reaction reflected by cytokines release, particularly interleukin-6 (IL-6), which associates with early brain damage. The present study measured IL-6 in the cerebrospinal fluid (CSF) of AH patients and determined its relationship to functional outcome following shunt operation.Methods: The study included a total of 32 patients with a shunt operation due to hydrocephalus. CSF samples from 26 AH subjects and 6 iNPH patients were collected via lumbar puncture before surgery. IL-6 level was measured using the micro ELISA immunoassay method. AH subjects were dichotomized into good versus poor outcomes based on modified Rankin Scale (mRS) at 3 months after shunting.Results: CSF analysis demonstrated that IL-6 was significantly elevated in the CSF of the AH group compared to controls (p = 0.023). Within the AH group, eighteen (69.2%) had a good outcome while eight (30.8%) patients had a poor outcome. Mean IL-6 level in the good outcome group was approximately four-times higher than the poor outcome group (p = 0.004). Glasgow Coma Scale (GCS) on admission was significantly different between the two groups (p = 0.014). IL-6 level and admission GCS were significantly correlated with improvement of mRS score (r = 0.473, p = 0.015 and r = 0.691, p<0.0001, respectively). Receiver operating characteristic curve analysis showed that both factors can accurately differentiate between patients with good versus poor functional outcome (AUC = 0.861, p = 0.0039 and AUC = 0.823, p = 0.0098, respectively). Conclusions: The CSF level of IL-6 is elevated in AH patients and higher levels correlate with improvement of post-shunt functional outcome. Therefore, IL-6 CSF level might serve as a complementary surrogate parameter for operative indication. A possible IL-6 threshold in clinical routine might be a 6.98-pg/ml cutoff value to rule out unresponsive and poor outcome AH patients that are under the 6.98-pg/ml threshold.
We reported a case of ischaemic stroke with moyamoya disease with simultaneous occurrence of patent foramen ovale. The patient underwent percutaneous closure of patent foramen ovale and was scheduled for follow-up.
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