Compliance with venous thromboembolism chemoprophylaxis guidelines in non-operative traumatic brain injury.

OBJECTIVE: To determine the level of compliance of The American College of Surgeons (ACS) Trauma Quality Improvement Program (TQIP) for initiation of venous thromboembolism (VTE) prophylaxis after non-operative traumatic brain injury (TBI) and the explanation for the deviations. METHODS: A retrospective review from May 2018 to February 2020 in a Level II trauma center for patients with TBI and length of stay of more than 24 h. We performed an analysis of overall and subgroup compliance with guidelines. The ACS TQIP criteria for low and moderate-risk for hemorrhagic progression were used for subgroup classification. RESULTS: Of 393 patients, 239 (60.8%) patients received chemoprophylaxis in a mean of 64 (SD: +/-42) hours since admission. "Compliance" was achieved in 52.2% of patients. In subgroup analysis, 51.4% of patients in "low-risk" and 55.1% in "moderate-risk" were "compliant." The most common rationale for non-compliance in "low-risk" was a stay less than 48 h in 35.9% of patients. However, in "moderate-risk," the most common non-compliance was starting prophylaxis before the recommended 72 h from admission in 37% of cases. CONCLUSIONS: Guidelines streamline clinical practice to optimize outcomes, but there are scenarios in which deviation of the recommendations may be indicated based on clinical judgment. We show that a stay of less than 48 h was the most common rationale for not starting prophylaxis in "low-risk" patients. However, in the "moderate-risk" subgroup, the most common reason was starting chemoprophylaxis before the recommended time frame, which we called a "paradoxical" non-compliance.

[Features of the patient management with traumatic brain injury]. / Osobennosti vedeniya patsientov s cherepno-mozgovoi travmoi.

The aim of our study was to consider features of pathogenesis, diagnosis and therapy of traumatic brain injury (TBI) from the viewpoint of neurologist. The mechanisms of emerging injury of the central nervous system, including neuro-inflammation and oxidative stress in patients with TBI, and correlations between clinical manifestations and severity of TBI are discussed. Special attention is paid to the description of certain TBI consequences, e.g. structural drug-resistant epilepsy and post-traumatic stress disorder. We provide evidence for difficulties and lesser availability of rehabilitation programs to patients with TBI during COVID-19 pandemics. One should mention a need for administration of Mexidol as the antioxidant/antihypoxant drug into complex therapy of TBI in such patients. In the period of COVID-19 pandemics, the role of neurologist in management of TBI patients still increases, especially, at the outpatient treatment stage, and when carrying out therapy and medical rehabilitation programs.

Neuroprotective effects of flavone luteolin in neuroinflammation and neurotrauma.

Neuroinflammation leads to neurodegeneration, cognitive defects, and neurodegenerative disorders. Neurotrauma/traumatic brain injury (TBI) can cause activation of glial cells, neurons, and neuroimmune cells in the brain to release neuroinflammatory mediators. Neurotrauma leads to immediate primary brain damage (direct damage), neuroinflammatory responses, neuroinflammation, and late secondary brain damage (indirect) through neuroinflammatory mechanism. Secondary brain damage leads to chronic inflammation and the onset and progression of neurodegenerative diseases. Currently, there are no effective and specific therapeutic options to treat these brain damages or neurodegenerative diseases. Flavone luteolin is an important natural polyphenol present in several plants that show anti-inflammatory, antioxidant, anticancer, cytoprotective, and macrophage polarization effects. In this short review article, we have reviewed the neuroprotective effects of luteolin in neurotrauma and neurodegenerative disorders and pathways involved in this mechanism. We have collected data for this study from publications in the PubMed using the keywords luteolin and mast cells, neuroinflammation, neurodegenerative diseases, and TBI. Recent reports suggest that luteolin suppresses systemic and neuroinflammatory responses in Coronavirus disease 2019 (COVID-19). Studies have shown that luteolin exhibits neuroprotective effects through various mechanisms, including suppressing immune cell activation, such as mast cells, and inflammatory mediators released from these cells. In addition, luteolin can suppress neuroinflammatory response, activation of microglia and astrocytes, oxidative stress, neuroinflammation, and the severity of neuroinflammatory diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and TBI pathogenesis. In conclusion, luteolin can improve cognitive decline and enhance neuroprotection in neurodegenerative diseases, TBI, and stroke.

The Role of NLRP3 Inflammasome in the Pathogenesis of Traumatic Brain Injury.

Traumatic brain injury (TBI) represents an important problem of global health. The damage related to TBI is first due to the direct injury and then to a secondary phase in which neuroinflammation plays a key role. NLRP3 inflammasome is a component of the innate immune response and different diseases, such as neurodegenerative diseases, are characterized by NLRP3 activation. This review aims to describe NLRP3 inflammasome and the consequences related to its activation following TBI. NLRP3, caspase-1, IL-1ß, and IL-18 are significantly upregulated after TBI, therefore, the use of nonspecific, but mostly specific NLRP3 inhibitors is useful to ameliorate the damage post-TBI characterized by neuroinflammation. Moreover, NLRP3 and the molecules associated with its activation may be considered as biomarkers and predictive factors for other neurodegenerative diseases consequent to TBI. Complications such as continuous stimuli or viral infections, such as the SARS-CoV-2 infection, may worsen the prognosis of TBI, altering the immune response and increasing the neuroinflammatory processes related to NLRP3, whose activation occurs both in TBI and in SARS-CoV-2 infection. This review points out the role of NLRP3 in TBI and highlights the hypothesis that NLRP3 may be considered as a potential therapeutic target for the management of neuroinflammation in TBI.