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A traumatic brain injury (TBI) initiates an inflammatory response with molecular cascades triggered by the presence of necrotic debris, including damaged myelin, hemorrhages and injured neuronal cells. Molecular cascades prominent in TBI-induced inflammation include the release of an excess of proinflammatory cytokines and angiogenic factors, the degradation of tight junctions (TJs), cytoskeletal rearrangements and leukocyte and protein extravasation promoted by increased expression of adhesion molecules. The brain-gut axis consists of a complex network involving neuroendocrine and immunological signaling pathways and bi-directional neural mechanisms. Importantly, modifying the gut microbiome alters this axis, and in turn may influence brain injury and neuroinflammatory processes. In recent years it has been demonstrated that the activity and composition of the gastrointestinal (GI) microbiome population influences the brain through all of above-mentioned pathways affecting homeostasis of the central nervous system (CNS). The GI microbiome is involved in the modulation of cellular and molecular processes which are fundamental to the progression of TBI-induced pathologies, including neuroinflammation, abnormal blood brain barrier (BBB) permeability, immune system responses, microglial activation, and mitochondrial dysfunction. It has been postulated that interaction between the brain and gut microbiome occurs mainly via the enteric nervous system and the vagus nerve through neuroactive compounds including serotonin or dopamine and activation by bacterial metabolites including endotoxin, neurotransmitters, neurotrophic factors, and cytokines. In recent years the multifactorial impact of selected immunomodulatory drugs on immune processes occurring in the CNS and involving the brain-gut axis has been under intensive investigation.

Background:Traumatic brain injury (TBI) is often associated with cardiac dysfunction, which is a consequence of the brain–heart cross talk. The subendocardial viability ratio (SEVR) is an estimate of myocardial perfusion. The aim of this study was to analyze changes in the SEVR in patients with severe TBI without previous cardiac diseases.Methods:Adult patients treated for severe TBI with a Glasgow coma score <8 were studied. Pressure waveforms were obtained by a high-fidelity tonometer in the radial artery for SEVR calculation at five time points: immediately after admission to the intensive care unit and 24, 48, 72, and 96 h after admission. SEVRs and other clinically important parameters were analyzed in patients who survived and did not survive after 28 days of treatment, as well as in patients who underwent decompressive craniectomy (DC).Results:A total of 64 patients (16 females and 48 males) aged 18–64 years were included. Fifty patients survived and 14 died. DC was performed in 23 patients. SEVRs decreased 24 h after admission in nonsurvivors (p< 0.05) and after 48 h in survivors (p< 0.01) and its values were significantly lower in nonsurvivors than in survivors at 24, 72, and 96 h from admission (p< 0.05). The SEVR increased following DC (p< 0.05).Conclusions:A decreased SEVR is observed in TBI patients. Surgical decompression increases the SEVR, indicating improvement in coronary microvascular perfusion. The results of our study seem to confirm that brain injury affects myocardium function.

To investigate age-related differences in outcomes of critically ill patients with sepsis around the world.

Several initiatives have recently focused on raising awareness about limitations of treatment in Poland. We aimed to assess if the propensity to limit LST among elderly patients in 2018-2019 increased compared to 2016-2017.

The occurrence of cardiovascular diseases in the group of patients undergoing vascular surgery because of abdominal aorta aneurysm is very high. Endovascular procedures are regarded as hemodynamically safer for the patients. The aim of this study was to compare the changes in electrophysiological, hemodynamic, and metabolic parameters depending on the type of operation, using invasive hemodynamic monitoring and Holter electrocardiography recording.