Background: Little is known about the incidence and risk of intensive care unit (ICU)‐acquired bloodstream infections (BSI) in critically ill patients with coronavirus disease 2019 (COVID‐19).Materials and methods: This retrospective, single‐centre study was conducted in Northern Italy. The primary study objectives were as follows: (a) to assess the incidence rate of ICU‐acquired BSI and (b) to assess the cumulative risk of developing ICU‐acquired BSI.Results: Overall, 78 critically ill patients with COVID‐19 were included in the study. Forty‐five episodes of ICU‐acquired BSI were registered in 31 patients, with an incidence rate of 47 episodes (95% confidence interval [CI] 35‐63) per 1000 patient‐days at risk. The estimated cumulative risk of developing at least one BSI episode was of almost 25% after 15 days at risk and possibly surpassing 50% after 30 days at risk. In multivariable analysis, anti‐inflammatory treatment was independently associated with the development of BSI (cause‐specific hazard ratio [csHR] 1.07 with 95% CI 0.38‐3.04 for tocilizumab, csHR 3.95 with 95% CI 1.20‐13.03 for methylprednisolone and csHR 10.69 with 95% CI 2.71‐42.17 for methylprednisolone plus tocilizumab, with no anti‐inflammatory treatment as the reference group; overall P for the dummy variable = 0.003).Conclusions: The incidence rate of BSI was high, and the cumulative risk of developing BSI increased with ICU stay. Further study will clarify if the increased risk of BSI we detected in COVID‐19 patients treated with anti‐inflammatory drugs is outweighed by the benefits of reducing any possible pro‐inflammatory dysregulation induced by SARS‐CoV‐2.

(2020). Multiple organ dysfunction in SARS-CoV-2: MODS-CoV-2. Expert Review of Respiratory Medicine. Ahead of Print.

Severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) causes a wide spectrum of clinical manifestations, with progression to multiorgan failure in the most severe cases. Several biomarkers can be altered in coronavirus disease 2019 (COVID-19), and they can be associated with diagnosis, prognosis, and outcomes. The most used biomarkers in COVID-19 include several proinflammatory cytokines, neuron-specific enolase (NSE), lactate dehydrogenase (LDH), aspartate transaminase (AST), neutrophil count, neutrophils-to-lymphocytes ratio, troponins, creatine kinase (MB), myoglobin, D-dimer, brain natriuretic peptide (BNP), and its N-terminal pro-hormone (NT-proBNP). Some of these biomarkers can be readily used to predict disease severity, hospitalization, intensive care unit (ICU) admission, and mortality, while others, such as metabolomic and proteomic analysis, have not yet translated to clinical practice. This narrative review aims to identify laboratory biomarkers that have shown significant diagnostic and prognostic value for risk stratification in COVID-19 and discuss the possible clinical application of novel analytic strategies, like metabolomics and proteomics. Future research should focus on identifying a limited but essential number of laboratory biomarkers to easily predict prognosis and outcome in severe COVID-19.

Early detection of cardiovascular dysfunctions directly caused by acute ischemic stroke (AIS) has become paramount. Researchers now generally agree on the existence of a bidirectional interaction between the brain and the heart. In support of this theory, AIS patients are extremely vulnerable to severe cardiac complications. Sympathetic hyperactivity, hypothalamic–pituitary–adrenal axis, the immune and inflammatory responses, and gut dysbiosis have been identified as the main pathological mechanisms involved in brain–heart axis dysregulation after AIS. Moreover, evidence has confirmed that the main causes of mortality after AIS include heart attack, congestive heart failure, hemodynamic instability, left ventricular systolic dysfunction, diastolic dysfunction, arrhythmias, electrocardiographic anomalies, and cardiac arrest, all of which are more or less associated with poor outcomes and death. Therefore, intensive care unit admission with continuous hemodynamic monitoring has been proposed as the standard of care for AIS patients at high risk for developing cardiovascular complications. Recent trials have also investigated possible therapies to prevent secondary cardiovascular accidents after AIS. Labetalol, nicardipine, and nitroprusside have been recommended for the control of hypertension during AIS, while beta blockers have been suggested both for preventing chronic remodeling and for treating arrhythmias. Additionally, electrolytic imbalances should be considered, and abnormal rhythms must be treated. Nevertheless, therapeutic targets remain challenging, and further investigations might be essential to complete this complex multi-disciplinary puzzle. This review aims to highlight the pathophysiological mechanisms implicated in the interaction between the brain and the heart and their clinical consequences in AIS patients, as well as to provide specific recommendations for cardiovascular management after AIS.