Endogenous sulfur dioxide (SO₂) used to be perceived as a notorious, toxic pollutant of the atmosphere. However, recently several studies revealed that in vivo generated mainly from sulfur-containing amino acids, SO₂ serves as an essential novel gasotransmitter involved in the regulation of extensive biological activities. Several studies indicate that endogenous SO₂ protects against inflammation by inhibiting the production of inflammatory mediators via different molecular pathways. The present review, therefore, summarized the anti-inflammatory effect of endogenous SO₂ and its molecular mechanisms.

During assisted mechanical ventilation, the respiratory system is exposed to the positive pressure from the ventilator and the negative pressure generated by the respiratory muscles. Both excessively high and low respiratory drive and effort can injure the respiratory muscles and lungs resulting in worse patient's outcomes. Monitoring respiratory drive and inspiratory effort are key to prevent harm by adjusting sedation and ventilation to meet safe targets of respiratory drive and inspiratory effort. Based on physiological studies and observational data, it is currently recommended to target an intermediate range of drive and effort in most patients, however, these targets need to be validated prospective and adjusted for different patient populations. The gold standard for measuring inspiratory effort requires the insertion of an esophageal catheter and additional equipment. However, recently, several noninvasive techniques using end-expiratory or end-inspiratory occlusions on the ventilator have been validated to estimate respiratory drive and effort allowing clinicians to monitor drive and effort easily at the bedside. In this narrative review, we discuss potential beneficial and deleterious consequences of breathing effort during assisted ventilation, available monitoring techniques, and propose a structured approach for bedside implementation.

This review discusses the clinical beneficial effects of peptide-based enteral nutrition (EN) for critically ill patients, especially those with gastrointestinal (GI) dysfunction. The GI dysfunction is very common in critically ill patients and always leads to intolerance of enteral feeding. Experimental and clinical studies suggest that peptide-based EN can be easily digested and absorbed by the GI tract which improving the feeding intolerance and provide better nutritional effects for critically ill patients. In addition, peptide-based EN may also have anti-inflammation, anti-oxidation, and immune-modulation effects and can facilitate muscle protein synthesis to improve muscle weakness which is commonly seen in critically ill patients. Peptide-based EN may have both nutritional and nonnutritional beneficial effects for critically ill patients. Further, large prospective randomized clinical trials should to be done to make the definite results.

Sepsis is one of the most common severe diseases in clinic. With the progression of the disease, it is very likely to occur acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Despite years of research, the mortality rate from sepsis-associated lung injury remains high. MicroRNAs (miRNAs) are a class of non-coding small RNAs with the function of regulating gene expression. In recent years, miRNAs have become a research hotspot in the field of biomedicine. Therefore, this review summarizes a large body of evidence implicating miRNAs and their target molecules in ALI/ARDS originating largely from studies using animal and cell culture model systems of ALI/ARDS. First, the pathophysiology and potential molecular mechanism of sepsis-associated ALI were briefly discussed at the cellular level, and the regulatory effect of miRNA on sepsis-associated ALI was summarized from the molecular mechanism so as to provide the possibility to find new targets for the treatment of sepsis-associated lung injury. Finally, some promising methods and some shortcomings of existing research are introduced.

Coagulopathy is common in critically ill patients. Under pathogenic factors, the homeostasis of coagulation, anticoagulation, and fibrinolytic system is disrupted, causing a series of cascade reactions that ultimately lead to coagulopathy. The pathophysiology of coagulopathy markedly varies according to the etiology. For sepsis-induced coagulopathy, inflammation interacts with coagulation. This process involves various cells, including endothelial cells, neutrophils, and platelets. Thrombocytopenia, as a common coagulopathy disorder among intensive care unit (ICU) patients, is indicative of poor outcome, and its differential diagnosis is crucial. However, the standardized diagnostic criteria for disseminated intravascular coagulation are yet to be established, and the existing ones have limitations. Therefore, we used PubMed to search literature related to “thrombocytopenia,” “sepsis,” “coagulopathy,” “disseminated intravascular coagulation,” and “coagulation biomarkers” and expected ICU doctors to fully understand knowledgeable of the pathophysiology of Coagulopathy. The traditional coagulation indicators can be combined with novel coagulation-related biomarkers for the accurate diagnosis and treatment of coagulopathy.

Tissue fibrosis is initially an adaptive response to organ injury, but eventually, parenchymal scarring and subsequent cellular dysfunction and organ failure ensue. Few therapies currently exist for fibrosis, especially those that target fibrogenesis. Galectin-3 (Gal-3) is a member of the lectin family of proteins, is produced predominantly by macrophages, and has essential functions in inflammation and angiogenesis. Gal-3 is activated in fibrotic models and abnormally elevated in fibrotic patients. Gal-3 inhibitors help to ameliorate or prevent fibrosis. For this review, we searched for original articles and reviews published between Jul 1, 2014, and Nov 1, 2019, using the following search terms (or combination of words) in PubMed: “galectin 3”, “fibrosis”, “heart”, “cardiac”, “liver”, “hepatic”, “lung”, “pulmonary”, “kidney”, and “renal”.

Circulatory shock is characterized by a decrease in oxygen delivery to the tissues associated with impairment in oxygen metabolism and tissue hypoxia. Clinical and biological signs of impaired tissue perfusion and tissue hypoxia are used as bedside to detect circulatory failure and trigger resuscitation procedures. The most popular signs of tissue hypoperfusion include mean arterial pressure, capillary refill time and mottling score, central venous oxygen saturation (ScvO₂), veno-arterial difference in PCO₂ (PvaCO₂), microcirculation assessment, and lactate. Both the severity and duration of the alterations in any of these variables are associated with a poor outcome so that it sounds logical to trigger therapy based on these. Using these variables as target for therapy is much more complex. Some of the limits for using some of these variables as targets include an incertitude about the target to reach (should we aim at normalizing or improving the variable, and by how much?) and the time lag between resolution of impaired tissue perfusion/hypoxia and normalization of the variable. The ideal target variable should have a well-defined end point and a rapid response time. Interestingly, hemodynamic resuscitation targeting these variables gave variable results. In this review, we will discuss the interest and limitations of the above-mentioned indices of tissue perfusion and hypoxia as trigger as well as end point of resuscitation in critically ill patients.