Intraoperative hemorrhage is a life-threatening complication during neurosurgery, especially in posterior fossa surgery, where critical vasculature and brain structures are present. Adenosine has been used in neurovascular surgery, particularly in the management of intraoperative aneurysm rupture and hemorrhage for its ability to produce transient flow arrest. This case report describes a novel application for adenosine, in which adenosine-induced flow arrest was used to facilitate control of a vascular injury sustained during meningioma surgery.

A 46-year-old female diagnosed with a petroclival meningioma after presenting with a several-month history of headache, dizziness, and loss of balance underwent craniotomy and excision of the meningioma. The patient received general endotracheal anesthesia, and was maintained on remifentanil, propofol, and low-dose sevoflurane. During posterior excision of the meningioma, the basilar artery was inadvertently lacerated, resulting in significant blood loss. Adenosine was given through a subclavian catheter, and produced severe bradycardia, hypotension, then asystole for approximately 50 seconds. Adenosine-induced flow arrest allowed for initial control of the vascular injury through coagulation, while further hemostasis was achieved through hemostatic agents and muscle tamponade.

This case report demonstrates the usefulness of adenosine-induced flow arrest in the management of intraoperative hemorrhage from an intracranial vascular injury. Adenosine-induced flow arrest has documented safety and efficacy in other neurosurgical applications. As the management of intraoperative hemorrhage is an essential component of neuroanesthesia, this technique may be considered in similar circumstances of major vascular injury to facilitate hemostasis.

BACKGROUND AND OBJECTIVE

Meningiomas represent the most prevalent benign intracranial tumors, comprising 13- 26% of primary intracranial neoplasms. These tumors derive their blood supply from both extracranial and intracranial circulation. Over recent decades, pre-operative embolization (POE) has emerged as a potential adjunctive therapy to surgery, aiming to reduce tumor vascularity. Our study seeks to explore the potential correlation between the extent of devascularization following POE of meningiomas and intraoperative blood loss.

This cross-sectional study involved nine meningioma patients at a tertiary hospital, involving chart review of patients across four years. These patients were referred for POE due to angiographic evidence of a hypervascular mass between January 2018 and January 2022. We collected demographic data, tumor characteristics (including location, size, and vascular supply), and intraoperative variables such as total operative time and blood loss. Statistical analyses aimed to uncover correlations between vascularization degree and various factors.

Our population consists predominantly of females (53.68%), with a mean age of 45.85 ± 13.65 years. Only one mortality was recorded (7.7%). Pre-operative embolization achieved devascularization in the majority (69.2%) of cases, with approximately two-thirds (66.7%) experiencing complete devascularization. Mean total operative time stood at 336.11 ± 301.88 minutes, with a mean post-operative blood loss of 985.56 ± 1013.72 milliliters. Additionally, for those with recorded recovery times, the mean recovery time was 14.32 ± 13.51 hours.

Mortality rates showed no association with sex, devascularization status, or number of feeding vessel zones. Furthermore, the extent of devascularization did not correlate with age, sex, number of feeding vessel zones, postoperative blood loss, total operative time, or recovery time (p >0.05).

In summary, this study represents a significant endeavor to elucidate factors influencing meningioma outcomes following pre-operative embolization. Despite limitations regarding patient numbers, our study offers valuable insights into operative parameters and embolization considerations for future analyses in our tertiary center.

BACKGROUND: Lead is a persistent inorganic environmental pollutant with global implication for human health. Among the diseases associated with lead exposure, the damage to the central nervous system has received considerable attention. It has been reported that long-term lead exposure increases the risk of meningioma; however, the underlying mechanism remains poorly understood. Clinical studies have indicated that loss-of-function and mutations in the neurofibromin-2 (NF2) gene play a crucial role in promoting meningioma formation. METHODS: The effect of Pb on meningioma were tested in-vitro and in-vivo. Two human meningioma cell lines were used in this study, including NF2-wildtype IOMM-Lee cell and NF2-null CH157-MN cell. Cell viability, cell cycle and cell size were examined after Pb exposure. The expression of Merlin, mammalian sterile 20-like kinases 1 and 2 (MST1/2) and Yes-associated protein (YAP) from these two meningioma cells were analyzed by Western blot. A xenograft mouse model was constructed by subcutaneous injection of IOMM-Lee meningioma cells. RESULTS: This study demonstrated that treatment with lead induce dose-dependent proliferation in IOMM-Lee cell (with an EC₅₀ value of 19.6 µM). Moreover, IOMM-Lee cell exhibited augmented cell size in conjunction with elevated levels of phosphorylated histone H3, indicative of altered cell cycle progression resulting from lead exposure. However, no significant change was observed in the CH157-MN cell. Additionally, the Merlin-Hippo signaling pathway was inactivated with decreased Merlin and phosphorylation levels of MST1/2 and YAP, leading to increased YAP nuclear translocation in IOMM-Lee cells. However, there was no change in the Merlin-Hippo signaling pathway in CH157-MN cells after lead treatment. The administration of Pb resulted in an acceleration of the subcutaneous IOMM-Lee meningioma xenograft growth in mice. CONCLUSIONS Overall, the current study elucidates the potential mechanism by which lead exposure promotes the proliferation of meningioma with NF2 expression for the first time.
Meningioma/genetics* ; Neurofibromin 2/genetics* ; Humans ; Cell Proliferation/drug effects* ; Animals ; Signal Transduction/drug effects* ; Mice ; Hippo Signaling Pathway ; Lead/adverse effects* ; Cell Line, Tumor ; Protein Serine-Threonine Kinases/genetics* ; Meningeal Neoplasms ; Environmental Pollutants/adverse effects* ; Female

Humans ; Meningioma/surgery* ; Tomography, X-Ray Computed ; Meningeal Neoplasms/surgery*

Background and Objective: Meningiomas represent the most prevalent benign intracranial tumors, comprising 13- 26% of primary intracranial neoplasms. These tumors derive their blood supply from both extracranial and intracranial circulation. Over recent decades, pre-operative embolization (POE) has emerged as a potential adjunctive therapy to surgery, aiming to reduce tumor vascularity. Our study seeks to explore the potential correlation between the extent of devascularization following POE of meningiomas and intraoperative blood loss. Methods: This cross-sectional study involved nine meningioma patients at a tertiary hospital, involving chart review of patients across four years. These patients were referred for POE due to angiographic evidence of a hypervascular mass between January 2018 and January 2022. We collected demographic data, tumor characteristics (including location, size, and vascular supply), and intraoperative variables such as total operative time and blood loss. Statistical analyses aimed to uncover correlations between vascularization degree and various factors. Results: Our population consists predominantly of females (53.68%), with a mean age of 45.85 ± 13.65 years. Only one mortality was recorded (7.7%). Pre-operative embolization achieved devascularization in the majority (69.2%) of cases, with approximately two-thirds (66.7%) experiencing complete devascularization. Mean total operative time stood at 336.11 ± 301.88 minutes, with a mean post-operative blood loss of 985.56 ± 1013.72 milliliters. Additionally, for those with recorded recovery times, the mean recovery time was 14.32 ± 13.51 hours. : Mortality rates showed no association with sex, devascularization status, or number of feeding vessel zones. Furthermore, the extent of devascularization did not correlate with age, sex, number of feeding vessel zones, postoperative blood loss, total operative time, or recovery time (p >0.05). Conclusion In summary, this study represents a significant endeavor to elucidate factors influencing meningioma outcomes following pre-operative embolization. Despite limitations regarding patient numbers, our study offers valuable insights into operative parameters and embolization considerations for future analyses in our tertiary center.
Meningioma ; Radiology, Interventional

Humans ; Meningioma/pathology* ; Central Nervous System/pathology* ; Meningeal Neoplasms/pathology* ; World Health Organization ; Central Nervous System Neoplasms/pathology*

Humans ; Meningioma/pathology* ; Prognosis ; Meningeal Neoplasms/pathology*

Humans ; Stroke Volume ; Incidence ; Goals ; Meningioma/complications* ; Postoperative Complications/epidemiology* ; Fluid Therapy/adverse effects* ; Meningeal Neoplasms/complications*

Humans ; Meningeal Neoplasms/diagnosis* ; Meningioma/diagnosis* ; Staining and Labeling

ABSTRACT: Meningiomas are the most common primary intracranial neoplasm with diverse pathological types and complicated clinical manifestations. The fifth edition of the WHO Classification of Tumors of the Central Nervous System (WHO CNS5), published in 2021, introduces major changes that advance the role of molecular diagnostics in meningiomas. To follow the revision of WHO CNS5, this expert consensus statement was formed jointly by the Group of Neuro-Oncology, Society of Neurosurgery, Chinese Medical Association together with neuropathologists and evidence-based experts. The consensus provides reference points to integrate key biomarkers into stratification and clinical decision making for meningioma patients. REGISTRATION Practice guideline REgistration for transPAREncy (PREPARE), IPGRP-2022CN234.
Humans ; Meningioma/pathology* ; Consensus ; Neurosurgical Procedures ; Meningeal Neoplasms/pathology*