RESUMO
Background: Gross total resection (GTR) of intracranial meningiomas is curative in most cases. However, perioperative blood transfusions may be necessary for complex skull bases and/or high-grade meningiomas. Guidelines for blood transfusions during intracranial meningioma surgery remain unclear. This scoping review aims to delineate the main characteristics of patients who underwent intracranial meningioma surgery, the prevalence of the selected patients who required blood transfusions, and common causes for transfusion. Methods: A scoping review was conducted following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses-Extension for Scoping Reviews guidelines to include studies reporting eligibility, protocols, and potential complications related to blood transfusion within the perioperative management of intracranial meningiomas. Results: A total of 33 articles encompassing 3009 meningioma patients were included in the study. The most common symptom was headache (18%), and the most frequent type of meningioma was World Health Organization grade-1 meningothelial (50.4%). The lateral supraorbital approach was the most common surgical corridor (59.1%) in skull base meningiomas, and most patients underwent GTR (69%). Blood transfusion was required for 20% of patients, with a mean estimated intraoperative blood loss of 703 mL (ranging from 200 mL to 2000 mL). The main indications for blood transfusion in meningioma surgery were intraoperative blood loss (86%) and preoperative anemia (7.3%). Conclusion: This scoping found that 20% of the included patients required blood transfusion. It also points out that several factors could influence the necessity for a transfusion, encompassing surgical blood loss, pre-existing anemia, and the surgery's length. This scoping review may provide surgeons with a potential guide to inform their decision-making process regarding blood transfusions during meningioma surgeries.
RESUMO
Traumatic brain injury (TBI) is one of the foremost causes of disability and mortality globally. While the scientific and medical emphasis is to save lives and avoid disability during acute period of injury, a severe health problem can manifest years after injury. For instance, TBI increases the risk of cognitive impairment in the elderly. Remote TBI history was reported to be a cause of the accelerated clinical trajectory of Alzheimer's disease-related dementia (ADRD) resulting in earlier onset of cognitive impairment and increased AD-associated pathological markers like greater amyloid deposition and cortical thinning. It is not well understood whether a single TBI event may increase the risk of dementia. Moreover, the cellular signaling pathways remain elusive for the chronic effects of TBI on cognition. We have hypothesized that a single TBI induces sustained neuroinflammation and disrupts cellular communication in a way that results later in ADRD pathology. To test this, we induced TBI in young adult CD1 mice and assessed the behavioral outcomes after 11 months followed by pathological, histological, transcriptomic, and MRI assessment. On MRI scans, these mice showed significant loss of tissue, reduced CBF, and higher white matter injury compared to sham mice. We found these brains showed progressive atrophy, markers of ADRD, sustained astrogliosis, loss of neuronal plasticity, and growth factors even after 1-year post-TBI. Because of progressive neurodegeneration, these mice had motor deficits, showed cognitive impairments, and wandered randomly in open field. We, therefore, conclude that progressive pathology after adulthood TBI leads to neurodegenerative conditions such as ADRD and impairs neuronal functions.