Sepsis-associated brain dysfunction (SABD) may be the most common type of encephalopathy in critically ill patients. SABD develops in up to 70% of septic patients and represents the most frequent organ insufficiency associated with sepsis. It presents with a plethora of acute neurological features and may have several serious long-term psychiatric consequences. SABD might cause various pathological changes in the brain through numerous mechanisms. Clinical neurological examination is the basic screening method for SABD, although it may be challenging in subjects receiving with opioids and sedative agents. As electrographic seizures and periodic discharges might be present in 20% of septic patients, screening with electroencephalography (EEG) might be useful. Several imaging techniques have been suggested for non-invasive assessment of structure and function of the brain in SABD patients; however, their usefulness is rather limited. Although several experimental therapies have been postulated, at the moment, no specific treatment exists. Clinicians should focus on preventive measures and optimal management of sepsis. This review discusses epidemiology, clinical presentation, pathology, pathophysiology, diagnosis, management, and prevention of SABD.

Background: Medical nutrition therapy may be associated with clinical outcomes in critically ill patients with prolonged intensive care unit (ICU) stay. We wanted to assess nutrition practices in European intensive care units (ICU) and their importance for clinical outcomes. Methods: Prospective multinational cohort study in patients staying in ICU ≥ 5 days with outcome recorded until day 90. Macronutrient intake from enteral and parenteral nutrition and non-nutritional sources during the first 15 days after ICU admission was compared with targets recommended by ESPEN guidelines. We modeled associations between three categories of daily calorie and protein intake (low: < 10 kcal/kg, < 0.8 g/kg; moderate: 10–20 kcal/kg, 0.8–1.2 g/kg, high: > 20 kcal/kg; > 1.2 g/kg) and the time-varying hazard rates of 90-day mortality or successful weaning from invasive mechanical ventilation (IMV). Results: A total of 1172 patients with median [Q1;Q3] APACHE II score of 18.5 [13.0;26.0] were included, and 24% died within 90 days. Median length of ICU stay was 10.0 [7.0;16.0] days, and 74% of patients could be weaned from invasive mechanical ventilation. Patients reached on average 83% [59;107] and 65% [41;91] of ESPEN calorie and protein recommended targets, respectively. Whereas specific reasons for ICU admission (especially respiratory diseases requiring IMV) were associated with higher intakes (estimate 2.43 [95% CI: 1.60;3.25] for calorie intake, 0.14 [0.09;0.20] for protein intake), a lack of nutrition on the preceding day was associated with lower calorie and protein intakes (− 2.74 [− 3.28; − 2.21] and − 0.12 [− 0.15; − 0.09], respectively). Compared to a lower intake, a daily moderate intake was associated with higher probability of successful weaning (for calories: maximum HR 4.59 [95% CI: 1.5;14.09] on day 12; for protein: maximum HR 2.60 [1.09;6.23] on day 12), and with a lower hazard of death (for calories only: minimum HR 0.15, [0.05;0.39] on day 19). There was no evidence that a high calorie or protein intake was associated with further outcome improvements. Conclusions: Calorie intake was mainly provided according to the targets recommended by the active ESPEN guideline, but protein intake was lower. In patients staying in ICU ≥ 5 days, early moderate daily calorie and protein intakes were associated with improved clinical outcomes. Trial registrationNCT04143503, registered on October 25, 2019. Graphical

Background: The purpose of this review was to summarize the up-to-date knowledge on clinical presentation and management of neurocardiogenic injury and to deliver the evidence of common pathophysiology of this broad spectrum of disorders. Methods: Medline and EmBase databases were searched to obtain original research articles and review papers using the following key words: neurocardiogenic injury, stress cardiomyopathy,tako-tsubo, subarachnoid hemorrhage, ECG abnormalities, catecholamine toxicity, neuropulmonary edema. Results: Various forms of cerebral pathology, most importantly subarachnoid hemorrhage (SAH), are accompanied by transient cardiac dysfunction with ST-segment elevation and QT interval prolongation and T wave inversion with simultaneous release of cardiac troponin. In the past 20 years a great deal of data emerged concerning stress cardiomyopathy (‘tako-tsubo’) presenting as a rare transient apical ballooning syndrome following stressful life events with symptoms and signs resembling acute myocardial infarction (AMI), yet without significant coronary artery stenosis. Both forms of cardiac dysfunction are mediated by catecholamine toxicity, triggered by physical and psychological distress, leading to a specific type of neurogenic myocardial stunning reflected by histopathological image of contraction band necrosis. Conclusions: Neurocardiogenic injury should be carefully differentiated from AMI. Cardiac dysfunction in SAH heralds increased mortality. The criteria for the diagnosis of stress cardiomyopathy should be revised to comprise the diversity of its clinical symptomatology and to include cardiac dysfunction accompanying cerebral pathology. Background: The purpose of this review was to summarize the up-to-date knowledge on clinical presentation and management of neurocardiogenic injury and to deliver the evidence of common pathophysiology of this broad spectrum of disorders. Methods: Medline and EmBase databases were searched to obtain original research articles and review papers using the following key words: neurocardiogenic injury, stress cardiomyopathy,tako-tsubo, subarachnoid hemorrhage, ECG abnormalities, catecholamine toxicity, neuropulmonary edema. Results: Various forms of cerebral pathology, most importantly subarachnoid hemorrhage (SAH), are accompanied by transient cardiac dysfunction with ST-segment elevation and QT interval prolongation and T wave inversion with simultaneous release of cardiac troponin. In the past 20 years a great deal of data emerged concerning stress cardiomyopathy (‘tako-tsubo’) presenting as a rare transient apical ballooning syndrome following stressful life events with symptoms and signs resembling acute myocardial infarction (AMI), yet without significant coronary artery stenosis. Both forms of cardiac dysfunction are mediated by catecholamine toxicity, triggered by physical and psychological distress, leading to a specific type of neurogenic myocardial stunning reflected by histopathological image of contraction band necrosis. Conclusions: Neurocardiogenic injury should be carefully differentiated from AMI. Cardiac dysfunction in SAH heralds increased mortality. The criteria for the diagnosis of stress cardiomyopathy should be revised to comprise the diversity of its clinical symptomatology and to include cardiac dysfunction accompanying cerebral pathology.