Many patients suffer from multiple organ dysfunction syndrome (MODS), which represents a dominant cause of death in the intensive care unit. Current theories about the mechanisms of MODS include inflammation, dysregulated immune response, reduced cellular oxygen utilization, cytopathic hypoxia, and apoptosis. Moreover, an increasing number of studies have shown that endoplasmic reticulum stress (ERS) is related to organ dysfunction. The endoplasmic reticulum is an organelle that is responsible for secretion and membrane protein synthesis and assembly as well as some other physiological activities. Under certain conditions, the homeostasis of ER can be lost, causing the accumulation of unfolded or misfolded protein, which is termed as ERS. During ERS, unfolded protein response (UPR) is activated. Once UPR fails to rebuilt cellular homeostasis, cell function will be impaired and apoptosis will be induced. To better understand the relationship between ERS and severe diseases, we summarize the current research in the context of ERS and UPR signaling associated with various organ dysfunction and severe diseases, including acute lung injury, hepatic injury, heart failure, hemorrhagic shock with multiple organ dysfunction, sepsis, and some other diseases. We also discuss ERS or UPR as a novel therapeutic target and their future directions.

Liver injury is one of the most common critical clinical illnesses and is one of the manifestations of multiple organ dysfunction induced by sepsis. The liver plays a central role in the development of sepsis. The role of the liver in removing bacteria and regulating immune inflammation is crucial, and the liver is the target of sepsis-related injuries. However, the mechanism of liver injury in sepsis is still not clear. This review discusses the pathophysiology, clinical manifestations, and treatment of sepsis-related liver injury. Liver injury, pathophysiological mechanism, sepsis, sepsis-related liver injury

Neurotoxicity has been an adverse effect described for almost all B-lactams; since its launch in 1994, there are numerous reports of patients treated with cefepime, covering a wide spectrum of clinical manifestations ranging from delirium to a nonconvulsive status epilepticus (NCSE), being the most of them reported in patients with decreased renal function, but also in patients with preserved renal function. We attempted to illustrate the clinical spectrum of cefepime neurotoxicity in relation to neurocritical care. We identified 13 publications describing neurotoxicity following cefepime administration from PubMed using search terms were cefepime, neurotoxicity, seizures, delirium, encephalopathy, NCSE, myoclonus, confusion, aphasia, agitation, coma, disability, and death. Two reviewers independently assessed identified articles for eligibility and used for this review writing. Most reports occur in elderly patients, although cases have been described in children and newborns. In general, patients recover soon after stopping beta-lactams or after reducing the dose or replacing them with another antibiotic; however, there is a likelihood of recurrence of symptoms after reintroducing Cefepime again at a dose low.

Severely ill neurosurgical patients are those who present with pathologies of the nervous system associated with either a high mortality or that which leaves significant sequelae in those who survive. Desmopressin is a synthetic analog of the antidiuretic hormone that is stored in neurohypophysis. Its function is to decrease urinary volume by increasing reabsorption of water in the convoluted tubules and nephron collectors, additionally increasing the expression of coagulation factor VII and the von Willebrand factor. For this reason, its usefulness in the management of various pathologies has been tested, from coagulopathies to posttraumatic and postsurgical diabetes insipidus. It contributes in improving hyponatremia and in maintaining the balance of fluids and electrolytes in traumatic brain injury and subarachnoid hemorrhage (SAH) patients. It has been additionally studied for its role in the risk of rebleeding in SAH patients and in those with coagulopathies, where its implicated mechanism of action is through platelet anti-aggregation.

The mucosal immune system plays a central role in the pathophysiology of health and disease. As the home to the largest population of lymphocytes in the body, the mucosal immune system closely communicates within other elements of the intestine, with constant cross talk with the gut microbiome and epithelial layer. Further, the gut's immune system plays a central role in communicating with remote organs. The mucosal immune system is critical in preventing autoimmunity, while simultaneously retaining the capacity to respond vigorously to mucosal invaders. This results in a state where the mucosal immune system not only can help restore homeostasis in critical illness but can also worsen inflammation and organ injury in sepsis. The purpose of this minireview is to provide an overview of mucosal immunity in health and in sepsis, with a focus on intraepithelial lymphocytes. Understanding the role of the mucosal immune system in both controlling and propagating sepsis is vital for future efforts designed to target it for therapeutic gain in the intensive care unit.

Fluid overload is one of the main complications associated with intravenous fluid therapy. Weight-based fluid accumulation is often calculated for fluid balance status in most researches. Fluid overload was defined as more than a 10% increase in body weight relative to baseline. There are many evidences that fluid overload is associated with an increased risk of acute kidney injury (AKI) and mortality. This review focuses on the pathophysiological link between fluid overload and AKI. Disruption of endothelial glycocalyx induced by fluid overload plays an important role in AKI. In addition, the compositions of the fluids (some colloids and chloride-rich fluids) may also contribute to kidney injury. On the other side, fluid overload is more obvious and the outcome in patients with AKI or with more critical illness. Therefore, the relationship between fluid overload and AKI should be fully understood and carefully managed.

Cerebrovascular disease (CVD) has been studied for many years, representing a cause of high morbidity and mortality; it has a great impact at a social, economic, and psychological level in the young adult population. There are different etiological factors that we do not find in the adult population, for that it is important to know how to differentiate them. There is no definitive etiological factor in this population given that the epidemiologic profile fluctuates considerably throughout regions and provinces, even if the same country is considered to make comparisons. CVD in young adults is caused by many etiological factors, predominantly the rare ones, such as cardioembolic, small vessel disease, due to thrombophilias, and undetermined cause. Despite being the main cause, the undetermined etiology is overestimated because it deserves for a detailed investigation in search of one of the rare causes, also, because of the lack of more complex studies in centers worldwide. No atherosclerotic large vessels diseases, such as cervicocephalic artery dissection, moyamoya disease, systemic vasculitis, and other rare syndromes should be considered to make an accurate diagnosis approach.

Acute kidney injury (AKI) is a common complication of acute illness and carries a significant risk of mortality and morbidity, resulting in high health-care-associated costs. The incidence of AKI appears to be rising, making it ever more important to understand its acute and chronic consequences. In this review, we explore the evolving epidemiology of AKI, describe the impact of AKI on other organs, and discuss the short- and long-term effects of AKI on mortality and morbidity and its economic burden.

Following the initial introduction of clinical decision support systems (CDSS) into the clinical practice in the 1970s, the complexity and performance quality of CDSSs have increased. The current literature on the efficacy and effectiveness of such systems shows conflicting results. While some studies show a clear benefit in quality-of-care improvement, others fail to replicate these outcomes. Heterogeneity of studies and the complexity of CDSS characteristics drive these conflicting conclusions. The lower cost and the easier implementation of pragmatic clinical trials provide an excellent platform to prove the effectiveness of CDSS in the real-world scenarios. To achieve better results, a series of explanatory trials are needed to identify the most effective CDSS in controlled settings. Therefore, utilization of both explanatory and pragmatic trial designs is necessary to evaluate the safety and efficacy of CDSS on the care of patients with acute kidney injury (AKI) in the acute setting. In this review, the authors provide an overview of the literature on critical care-related CDSS, its characteristics and dimensions, differences between pragmatic and explanatory trials, and potential proposals for both trial designs for AKI.

Malignant middle cerebral artery infarction is a devastating subtype of ischemic stroke, which carries a significant mortality rate (up to 80%) despite of conservative treatment. On the other hand, surgical decompressive procedure is the only established therapy to rescue the adverse effects of malignant edema and thus improve outcome. Accordingly, the early recognition of a possible malignant course as well as prediction of outcome is crucial for clinical decision-making. Numerous neuromonitoring techniques have been applied to address this issue. In theory, these techniques have the potential to present the information needed to guide targeted and timely intervention before irreversible damage takes place. However, the results were heterogeneous yet conflicting. We examined and summarized the recent evidence in this review, which may shed light on current trends.

Despite decades of efforts, severe traumatic brain injury (TBI) is still the leading cause for mortality and immobility of children and young adults worldwide and is a great burden to the health-care system. After injury, the oxygen supply is conventionally considered the monitoring parameter in a neurosurgical Intensive Care Unit. However, the overall mortality rate has only slightly improved since the late twentieth century. Evolving evidence suggests that dysfunction of oxygen utilization might be the underlying pathophysiology of secondary brain injury, which should also be a key parameter for multimodal monitoring and management after severe TBI. In this review, we summarize the current and advanced understanding of multimodal monitoring for severe TBI along with novel noninvasive technologies in this field. By continuously monitoring patients with severe TBI, the use of multimodal monitoring technologies including (but not limited to) computed tomography, cerebral microdialysis, near-infrared spectroscopy, magnetic resonance spectroscopy, high-performance liquid chromatography, and magnetic induction phase shift method will be crucial for observing disease changes such as intracranial pressure and brain tissue oxygen partial pressure as well as developing potential therapeutic strategies after severe TBI.

Interest in the use of angiotensin (AT) (particularly in the context of shock) had been rekindled by recent randomized trial data (notably the AT II for the Treatment of High-Output Shock-3 study). This review article outlines the renin–AT system in health and during sepsis as well as the proposed clinical uses of AT II. The potential for wider application within critical care is also considered.