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Introduction: The majority of patients with severe COVID-19 suffer from delirium as the main sign of encephalopathy associated with this viral infection. The aim of this study was to identify early markers of the development of this condition. Materials: The prospective cohort-based study included patients with community-acquired pneumonia and confirmed pulmonary tissue infiltration based on CT data, with a lesion consisting of at least 25% of one lung. The main group included patients who have developed acute encephalopathy (10 patients, 3 (30%) women; average age, 47.9 ± 7.3 years). The control group included patients who at discharge did not have acute encephalopathy (20 patients, 11 (55%) women; average age, 51.0 ± 10.5 years). The study collected clinical examination data, comprehensive laboratory data, neurophysiological data, pulse oximetry and CT data to identify the predictors of acute encephalopathy (study ClinicalTrials.gov identifier NCT04405544). Results: Data analysis showed a significant relationship between encephalopathy with the degree of lung tissue damage, arterial hypertension, and type 2 diabetes mellitus, as well as with D-dimer, LDH, and lymphopenia. Conclusions: The development of encephalopathy is secondary to the severity of the patient’s condition since a more severe course of the coronavirus infection leads to hypoxic brain damage.

Ischemic stroke is caused by atherosclerotic lesions in extra- and intracranial arteries in about 25% of cases. Revascularization surgery has been long and widely used for secondary prevention of ischemic stroke in patients with atherosclerotic lesions of the carotid arteries. However, currently the changes in cerebral perfusion in patients with atherosclerotic lesions of brachiocephalic arteries, who underwent surgical revascularization, are still not fully understood. This article highlights the issues of changes of cerebral hemodynamics in patients undergoing surgery on the carotid arteries.

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from 1.01.14.-1.07.14. Information was collected about the use of medication and CHA 2 DS 2-VASc score was calculated before the onset of stroke. Discharged patients or theyre relatives were interviewed by phone after 180 days. Standardized questions were asked about the use of secondary prevention medication, 4 patients groups (according to prescribed medication) were compared accordingly. Results: CHA 2 DS 2-VASc score before the onset of stroke was calculated using non-parametric tests. Calculated median = 4, mode = 4. Of 247 patients before the onset of stroke 51.4% didn't use any antithrombotic medication, 40.1% were using antiplatelet agents, 8.1% warfarin, 0.4% TSOACs. On discharge 5.5% patients were not prescribed antithrombotic medication, 25.6% patients were discharged on antiplatelet agents, 36.1% on warfarin and remaining 22.8% on TSOACs. 180 days after discharge 111 stroke survuivors were contacted-4.5% were not using any antithrombotic medication, 24.3% patients were using antiplatelet agents, 48.6% on warfarin and 22.5% TSOACs. Conclusion: In Latvia cardioembolic stroke primary and secondary prevention is inusfficient. Stroke severity and incompliance of patients limit the use of oral anticoagulants after stroke. Use of oral anticoagulants is a cornerstone of primary and secondary stroke prevention.

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