A cytokine storm is a hyperinflammatory state secondary to the excessive production of cytokines by a deregulated immune system. It manifests clinically as an influenza-like syndrome, which can be complicated by multi-organ failure and coagulopathy, leading, in the most severe cases, even to death. The term cytokine storm was first used in 1993 to describe the graft-versus-host disease following allogeneic hematopoietic stem cell transplantation. It was then reused to define the adverse syndromes secondary to the administration of immunostimulating agents, such as anti-CD28 antibodies or bioengineered immune cells, i.e., CAR T-cell therapy. Currently, the concept of cytokine storm has been better elucidated and extended to the pathogenesis of many other conditions, such as sepsis, autoinflammatory disease, primary and secondary hemophagocytic lymphohistiocytosis, and multicentric Castleman disease. Moreover, cytokine storm has recently emerged as a key aspect in the novel Coronavirus disease 2019, as affected patients show high levels of several key pro-inflammatory cytokines, such as IL-1, IL-2, IL-6, TNF-α, IFN-γ, IP-10, GM-CSF, MCP-1, and IL-10, some of which also correlate with disease severity. Therefore, since the onset of the pandemic, numerous agents have been tested in the effort to mitigate the cytokine storm in COVID-19 patients, some of which are effective in reducing mortality, especially in critically ill patients, and are now becoming standards of care, such as glucocorticoids or some cytokine inhibitors. However, the challenge is still far from being met, and other therapeutic strategies are being tested in the hope that we can eventually overcome the disease.

The use of non-invasive respiratory strategies (NIRS) is crucial to improve oxygenation in COVID-19 patients with hypoxemia refractory to conventional oxygen therapy. However, the absence of respiratory symptoms may delay the start of NIRS. The aim of this study was to determine whether a simple bedside test such as single-breath counting test (SBCT) can predict the need for NIRS in the 24 h following the access to Emergency Department (ED). We performed a prospective observational study on 120 patients with COVID-19 pneumonia. ROC curves were used to analyze factors which might predict NIRS requirement. We found that 36% of patients had normal respiratory rate and did not experience dyspnea at rest. 65% of study population required NIRS in the 24 h following the access to ED. NIRS-requiring group presented lower PaO2/FiO2 (235.09 vs. 299.02), SpO2/FiO2 ratio (357.83 vs. 431.07), PaCO2 (35.12 vs. 40.08), and SBCT (24.46 vs. 30.36) and showed higher incidence of dyspnea at rest (57.7% vs. 28.6%). Furthermore, SBCT predicted NIRS requirement even in the subgroup of patients without respiratory symptoms (AUC = 0.882, cut-off = 30). SBCT might be a valuable tool for bedside assessment of respiratory function in patients with COVID-19 pneumonia and might be considered as an early clinical sign of impending respiratory deterioration.

Since the end of 2019, the medical-scientific community has been facing a terrible pandemic caused by a new airborne viral agent known as SARS-CoV2. Already in the early stages of the pandemic, following the discovery that the virus uses the ACE2 cell receptor as a molecular target to infect the cells of our body, it was hypothesized that the renin-angiotensin-aldosterone system was involved in the pathogenesis of the disease. Since then, numerous studies have been published on the subject, but the exact role of the renin-angiotensin-aldosterone system in the pathogenesis of COVID-19 is still a matter of debate. RAAS represents an important protagonist in the pathogenesis of COVID-19, providing the virus with the receptor of entry into host cells and determining its organotropism. Furthermore, following infection, the virus is able to cause an increase in plasma ACE2 activity, compromising the normal function of the RAAS. This dysfunction could contribute to the establishment of the thrombo-inflammatory state characteristic of severe forms of COVID-19. Drugs targeting RAAS represent promising therapeutic options for COVID-19 sufferers.

The use of ketamine in patients with TBI has often been argued due to its possible deleterious effects on cerebral circulation and perfusion. Early studies suggested that ketamine could increase intracranial pressure, decreasing cerebral perfusion pressure and thereby reducing oxygen supply to the damaged cerebral cortex. Some recent studies have refuted these conclusions relating to the role of ketamine, especially in patients with TBI, showing that ketamine should be the first-choice drug in this type of patient at induction. Our narrative review collects evidence on ketamine’s use in patients with TBI. Databases were examined for studies in which ketamine had been used in acute traumatic brain injury (TBI). The outcomes considered in this narrative review were: mortality of patients with TBI; impact on intracranial pressure and cerebral perfusion pressure; blood pressure and heart rate values; depolarization rate; and preserved neurological functions. 11 recent studies passed inclusion and exclusion criteria and were included in this review. Despite all the benefits reported in the literature, the use of ketamine in patients with brain injury still appears to be limited. A slight increase in intracranial pressure was found in only two studies, while two smaller studies showed a reduction in intracranial pressure after ketamine administration. There was no evidence of harm from the ketamine’s use in patients with TBI.

Background: The digestive tract represents an interface between the external environment and the body where the interaction of a complex polymicrobial ecology has an important influence on health and disease. The physiological mechanisms that are altered during the hospitalization and in the intensive care unit (ICU) contribute to the pathobiota’s growth. Intestinal dysbiosis occurs within hours of being admitted to ICU. This may be due to different factors, such as alterations of normal intestinal transit, administration of variuos medications or alterations in the intestinal wall which causes a cascade of events that will lead to the increase of nitrates and decrease of oxygen concentration, liberation of free radicals. Objective: This work aims to report the latest updates on the microbiota’s contribution to developing sepsis in patients in the ICU department. In this short review were reviewed the latest scientific findings on the mechanisms of intestinal immune defenses performed both locally and systemically. In addition, we considered it necessary to review the literature to report the current best treatment strategies to prevent the infection spread which can bring systemic infections in patients admitted to ICU. Material and Methods: This review has been written to answer at three main questions: what are the main intestinal flora’s defense mechanisms that help us to prevent the risk of developing systemic diseases on a day-to-day basis? What are the main dysbiosis’ systemic abnormalities? What are the modern strategies that are used in the ICU patients to prevent the infection spread? Using the combination of following keywords: microbiota and ICU, ICU and gut, microbiota and critical illness, microbiota and critical care, microbiota and sepsis, microbiota and infection, gastrointestinal immunity,in the Cochrane Controlled Trials Register, the Cochrane Library, medline and pubmed, google scholar, ovid/wiley. Finally, we reviewed and selected 72 articles. We also consulted the site ClinicalTrials.com to find out studies that are recently conducted or ongoing. Results: The critical illness can alter intestinal bacterial flora leading to homeostasis disequilibrium. Despite numerous mechanisms, such as epithelial cells with calciform cells that together build a mechanical barrier for pathogenic bacteria, the presence of mucous associated lymphoid tissue (MALT) which stimulates an immune response through the production of interferon-gamma (IFN-y) and THN-a or by stimulating lymphocytes T helper-2 produces anti-inflammatory cytokines. But these defenses can be altered following a hospitalization in ICU and lead to serious complications such as acute respiratory distress syndrome (ARDS), health care associated pneumonia (HAP) and ventilator associated pneumonia (VAP), Systemic infection and multiple organ failure (MOF), but also in the development of coronary artery disease (CAD). In addition, the microbiota has a significant impact on the development of intestinal complications and the severity of the SARS-COVID-19 patients. Conclusion: The microbiota is recognized as one of the important factors that can worsen the clinical conditions of patients who are already very frailty in intensive care unit. At the same time, the microbiota also plays a crucial role in the prevention of ICU associated complications. By using the resources, we have available, such as probiotics, symbiotics or fecal microbiota transplantation (FMT), we can preserve the integrity of the microbiota and the GUT, which will later help maintain homeostasis in ICU patients.

Background: During general anesthesia, mechanical ventilation can cause pulmonary damage through mechanism of ventilator-induced lung injury which is a major cause of postoperative pulmonary complications, which varies between 5 and 33% and increases significantly the 30-day mortality of the surgical patient. Objective: The aim of this review is to analyze different variables which played key role in safe application of mechanical ventilation in the operating room and emergency setting. Method: Also, we wanted to analyze different types of population that underwent intraoperative mechanical ventilation like obese patients, pediatric and adult population and different strategies such as one lung ventilation and ventilation in trendelemburg position. The peer-reviewed articles analyzed were selected according to PRISMA (Preferred Reporting Items for Systematic reviews and Meta-Analyses) from Pubmed/Medline, Ovid/Wiley and Cochrane Library, combining key terms such as: “pulmonary post-operative complications”, “protective ventilation”, “alveolar recruitment maneuvers”, “respiratory compliance”, “intraoperative paediatric ventilation”, “best peep”, “types of ventilation”. Among the 230 papers identified, 150 articles were selected, after title - abstract examination and removing the duplicates, resulting in 94 articles related to mechanical ventilation in operating room and emergency setting that were analyzed. Results: Careful preoperative patient’s evaluation and protective ventilation (i.e. use of low tidal volumes, adequate PEEP and alveolar recruitment maneuvers) has been shown to be effective not only in limiting alveolar de-recruitment, alveolar overdistension and lung damage, but also in reducing the onset of pulmonary post-operative complications (PPCs). Conclusion: Mechanical ventilation is like “Janus Bi-front” because it is essential for surgical procedures, for the care of critical care patients and in life-threatening conditions but it can be harmful to the patient if continued for a long time and where an excessive dose of oxygen is administered into the lungs. Low tidal volume is associated with minor rate of PPCs and other complications and every complication can increase length of Stay, adding cost to NHS between 1580 € and 1650 € per day in Europe and currently the prevention of PPCS is only weapon that we possess.

Background: Cerebral vasospasm is one of the frequent complications that can occur following subarachnoid hemorrhage (SAH). With new protocols in the management of SAH, the combined risk of death and long-term disability has been reduced by about 10% compared with the past. Objective: This work aims to report the latest updates on the vasospasm developing after the SAH in patients in the ICU department. In this short review, we reviewed the latest scientific findings on the mechanisms of vasospasm, and, in addition, we considered it necessary to review the literature to report the tools for early diagnosis of vasospasm and the best treatment strategies to prevent the negative outcome in patients admitted to ICU. Scope: The aim of this narrative review is to report the main characteristics of vasospasm, new diagnostic methods and, especially, more effective treatment of vasospasm. Materials and methods: The peer-reviewed articles analyzed were selected from PubMed, google scholar, Embase, Scopus databases in the previous 20 years and using the keywords words "vasospam", "vasospasm diagnosis", "vasospasm and SAH", "vasospasm treatment", non-traumatic brain injury. Among the 78 papers identified, 43 articles were selected; after title - abstract examination and removing the duplicates, only 31 articles were examined. Results: Vasospasm can be classified according to clinical (asymptomatic vs symptomatic) and diagnostic (angiographic vs ultrasound) methods. Various procedures such as TCD and CT perfusion are used for early diagnosis and close monitoring of this condition. The treatment of vasospasm consists of both prevention (nimodipine, statitis, magnesium sulphate) and active treatment (mainly endovascular). Conclusion: As the review shows, vasospasm is a complication of SAH, a complication that is difficult to recognise early and treat with the best outcome. However, with the equipment we have, it has been possible to improve the outcome, even if it is still not ideal, of patients who develop vasospasm. Several studies are in the final stages to improve the outcome of this unfortunately frequent condition.

External ventricular drainage is often considered a life-saving treatment in acute hydrocephalus. Given the large number of discussion points, the ideal management of EVD has not been completely clarified. The objective of this study was to review the most relevant scientific evidence about the management of EVD in its main clinical scenarios. We reviewed the most recent and relevant articles about indications, timing, management, and complications of EVD in neurocritical care, with particular interest in patients with subarachnoid hemorrhage (SAH), severe traumatic brain injury (TBI), and intraventricular hemorrhage (IVH) using the following keywords alone or matching with one another: intracranial pressure, subarachnoid hemorrhage, traumatic brain injury, intraventricular hemorrhage, external ventricular drainage, cerebrospinal shunt, intracranial pressure monitoring, and ventriculoperitoneal shunt. In the management of EVD in SAH, the intermittent drainage strategy is burdened with an elevated risk of complications (e.g., clogged catheter, hemorrhage, and need for replacement). There seems to be more ventriculoperitoneal shunt dependency in rapid weaning approach-managed patients than in those treated with the gradual weaning approach. Although there is no evidence in favor of either strategy, it is conventionally accepted to adopt a continuous drainage approach in TBI patients. Less scientific evidence is available in the literature regarding the management of EVD in patients with severe TBI and intraparenchymal/intraventricular hemorrhage. EVD placement is a necessary treatment in several clinical scenarios. However, further randomized clinical trials are needed to clarify precisely how EVD should be managed in different clinical scenarios.