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Acute kidney injury (AKI) has been reported in up to 25% of critically-ill patients with SARS-CoV-2 infection, especially in those with underlying comorbidities. AKI is associated with high mortality rates in this setting, especially when renal replacement therapy is required. Several studies have highlighted changes in urinary sediment, including proteinuria and hematuria, and evidence of urinary SARS-CoV-2 excretion, suggesting the presence of a renal reservoir for the virus. The pathophysiology of COVID-19 associated AKI could be related to unspecific mechanisms but also to COVID-specific mechanisms such as direct cellular injury resulting from viral entry through the receptor (ACE2) which is highly expressed in the kidney, an imbalanced renin–angotensin–aldosteron system, pro-inflammatory cytokines elicited by the viral infection and thrombotic events. Non-specific mechanisms include haemodynamic alterations, right heart failure, high levels of PEEP in patients requiring mechanical ventilation, hypovolemia, administration of nephrotoxic drugs and nosocomial sepsis. To date, there is no specific treatment for COVID-19 induced AKI. A number of investigational agents are being explored for antiviral/immunomodulatory treatment of COVID-19 and their impact on AKI is still unknown. Indications, timing and modalities of renal replacement therapy currently rely on non-specific data focusing on patients with sepsis. Further studies focusing on AKI in COVID-19 patients are urgently warranted in order to predict the risk of AKI, to identify the exact mechanisms of renal injury and to suggest targeted interventions.

In severe SARS-CoV-2 infections, emerging data including recent histopathological studies have emphasized the crucial role of endothelial cells (ECs) in vascular dysfunction, immunothrombosis, and inflammation. Histopathological studies have evidenced direct viral infection of ECs, endotheliitis with diffuse endothelial inflammation, and micro- and macrovascular thrombosis both in the venous and arterial circulations. Venous thrombotic events, particularly pulmonary embolism, with elevated D-dimer and coagulation activation are highly prevalent in COVID-19 patients. The pro-inflammatory cytokine storm, with elevated levels of interleukin-6 (IL-6), IL-2 receptor, and tumor necrosis factor-α, could also participate in endothelial dysfunction and leukocyte recruitment in the microvasculature. COVID-19-induced endotheliitis may explain the systemic impaired microcirculatory function in different organs in COVID-19 patients. Ongoing trials directly and indirectly target COVID-19-related endothelial dysfunctions: i.e., a virus-cell entry using recombinant angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS-2) blockade, coagulation activation, and immunomodulatory therapies, such as anti-IL-6 strategies. Studies focusing on endothelial dysfunction in COVID-19 patients are warranted as to decipher their precise role in severe SARS-CoV-2 infection and organ dysfunction and to identify targets for further interventions.

An increasing number of critically ill patients are immunocompromised. Acute hypoxemic respiratory failure (ARF), chiefly due to pulmonary infection, is the leading reason for ICU admission. Identifying the cause of ARF increases the chances of survival, but may be extremely challenging, as the underlying disease, treatments, and infection combine to create complex clinical pictures. In addition, there may be more than one infectious agent, and the pulmonary manifestations may be related to both infectious and non-infectious insults. Clinically or microbiologically documented bacterial pneumonia accounts for one-third of cases of ARF in immunocompromised patients. Early antibiotic therapy is recommended but decreases the chances of identifying the causative organism(s) to about 50%. Viruses are the second most common cause of severe respiratory infections. Positive tests for a virus in respiratory samples do not necessarily indicate a role for the virus in the current acute illness. Invasive fungal infections (Aspergillus, Mucorales, and Pneumocystis jirovecii) account for about 15% of severe respiratory infections, whereas parasites rarely cause severe acute infections in immunocompromised patients. This review focuses on the diagnosis of severe respiratory infections in immunocompromised patients. Special attention is given to newly validated diagnostic tests designed to be used on non-invasive samples or bronchoalveolar lavage fluid and capable of increasing the likelihood of an early etiological diagnosis.

Coronavirus disease 19 (COVID-19) has posed unprecedented healthcare system challenges, some of which will lead to transformative change. It is obvious to healthcare workers and policymakers alike that an effective critical care surge response must be nested within the overall care delivery model. The COVID-19 pandemic has highlighted key elements of emergency preparedness. These include having national or regional strategic reserves of personal protective equipment, intensive care unit (ICU) devices, consumables and pharmaceuticals, as well as effective supply chains and efficient utilization protocols. ICUs must also be prepared to accommodate surges of patients and ICU staffing models should allow for fluctuations in demand. Pre-existing ICU triage and end-of-life care principles should be established, implemented and updated. Daily workflow processes should be restructured to include remote connection with multidisciplinary healthcare workers and frequent communication with relatives. The pandemic has also demonstrated the benefits of digital transformation and the value of remote monitoring technologies, such as wireless monitoring. Finally, the pandemic has highlighted the value of pre-existing epidemiological registries and agile randomized controlled platform trials in generating fast, reliable data. The COVID-19 pandemic is a reminder that besides our duty to care, we are committed to improve. By meeting these challenges today, we will be able to provide better care to future patients.

Chimeric antigen receptor (CAR) T-cell therapy is an effective adoptive cell treatment that constitutes a powerful new class of therapeutic agents to treat patients with B‐cell leukemia and lymphoma [1]. It uses patient’s T lymphocytes harvested through cytapheresis and manipulated ex vivo to express specifc antigens before infusion back to the patient. Although the clinical responses are beyond expectations, CAR T-cells also frequently produce life-threatening acute toxicities [2], chiefy the cytokine-release syndrome (CRS) and neurotoxicity (Fig. 1). Tumor lysis syndrome that has been reported in up to 5% of the patients in the frst trials, is not discussed in this short article. Obviously, in these high risk immunocompromised patients with altered B cell and T cell response and frequent neutropenia, sepsis should be ruled out and treated empirically. In this what’s new paper, we have listed the top ten tips to manage critically ill CAR T-cell recipients.

Given the rapidly changing nature of COVID-19, clinicians and policy makers require urgent review and summary of the literature, and synthesis of evidence-based guidelines to inform practice. The WHO advocates for rapid reviews in these circumstances. The purpose of this rapid guideline is to provide recommendations on the organizational management of intensive care units caring for patients with COVID-19 including: planning a crisis surge response; crisis surge response strategies; triage, supporting families, and staff.

Every day, people leave their country, families, and belongings because of war, persecution, or poverty. According to United Nations (UN) last estimate, there were 272 million international migrants in 2019, a 51 million increase compared to 2010 [1]. This number includes economic migrants, political refugees, and asylum seekers (the word “migrants” is used hereafter to encompass all these categories). Among them, 65 million (23.9%) say they were forcibly displaced from their hometown [1]. Asia, Latin America, Africa, and East Europe are among the primary points of departure, while Asia, Europe, and North America are the preferred destinations [2]. Migrants are often young energetic individuals and are, therefore, healthier than average at the early stages of displacement [3, 4]. However, exposure to violence and war, grueling travel conditions, and extreme poverty often coupled with appalling levels of exploitation in the countries, they cross take a heavy toll on their mental and physical health.

Intensive Care organization varies across Europe where the number of intensive care unit (ICU) beds is 11.5/100,000 people but varies from 4.2/100,000 (Portugal) to nearly 30/100,000 (Germany). This variation also applies to nurse ratio: from one to three patients/nurse according to countries [2]. The need for ICU beds is growing continuously, not only in response to a pandemic but also to our aging societies’ needs. Recent medical progress (complex surgical operations, cell therapy with CAR-T cells, etc.) required more ICU beds. During the pandemic, critical care outreach has allowed opening more beds in the wards, where noninvasive respiratory support has been provided [3]. Expanding ICU’s beds automatically requires increasing the number of competent, skilled ICU specialists, nurses and other allied professionals. Failure to do so will mean ICU beds’ shortage across Europe.