The critical care involved in solid-organ transplantation (SOT) is complex. Pre-, intra- and post-transplant care can significantly impact both – patients’ ability to undergo SOT and their peri-operative morbidity and mortality. Much of the care necessary for medical optimization of end-stage organ failure (ESOF) patients to qualify and then successfully undergo SOT, and the management of peri-operative and/or long-term complications thereafter occurs in an intensive care unit (ICU) setting. The current literature specific to critical care in abdominal SOT patients was reviewed. This paper provides a contemporary perspective on the potential multifactorial advantages of sub-specialized transplant critical care units in providing efficient, comprehensive, and collaborative multidisciplinary care.
Ventilator-associated pneumonia (VAP) is a common and serious nosocomial infection in mechanically ventilated patients and results in high mortality, prolonged intensive care unit- (ICU) and hospital-length of stay and increased costs. In order to reduce its incidence, it is imperative to better understand the involved mechanisms and to identify the source of infection. The role of the endotracheal tube (ET) in VAP pathogenesis became more prominent over the last decades, along with extensive research dedicated to medical device-related infections and biofilms. ET biofilm formation is an early and constant process in intubated patients. New data regarding its temporal dynamics, composition, germ identification and consequences enhance knowledge about VAP occurrence, microbiology, treatment response and recurrence.
This paper presents a structured analysis of the medical literature to date, in order to outline the role of ET biofilm in VAP pathogenesis and to review recommended methods to identify ET biofilm microorganisms and to prevent or decrease VAP incidence.
A comprehensive analysis of published cases of Takotsubo cardiomyopathy, occurred in liver transplant recipients in the perioperative period, has been attempted in this review. Predisposing factors, precipitating events, potential physiological mechanisms, acute and post-event management have been discussed.
Use of transcranial Doppler has undergone much development since its introduction in 1982, making the technique suitable for general use in intensive care units. The main application in intensive care units is to assess intracranial pressure, confirm the lack of cerebral circulation in brain death, detect vasospasm in subarachnoid haemorrhage, and monitor the blood flow parameters during thrombolysis and carotid endarterectomy, as well as measuring stenosis of the main intracranial arteries in sickle cell disease in children.
This review summarises the use of transcranial Doppler in intensive care units.
Sepsis represents a severe pathology that requires both rapid and precise positive and differential diagnosis to identify patients who need immediate antimicrobial therapy. Monitoring septic patients’ outcome leads to prolonged hospitalisation and antibacterial therapy, often accompanied by substantial side effects, complications and a high mortality risk.
Septic patients present with complex pathophysiological and immunological disorders and with a predominance of pro-inflammatory or anti-inflammatory mediators which are heterogeneous with respect to the infectious focus, the aetiology of sepsis or patients’ immune status or comorbidities. Previous studies performed have analysed inflammatory biomarkers, but a test or combinations of tests that can quickly and precisely establish a diagnosis or prognosis of septic patients has yet to be discovered. Recent research has focused on re-analysing older accessible parameters found in the complete blood count to determine the sensitivity, specificity, positive and negative predictive values for the diagnosis and prognosis of sepsis.
The neutrophil/lymphocyte count ratio (NLCR), mean platelet volume (MPV) and red blood cells distribution width (RDW) are haemogram indicators which have been evaluated and which are of proven use in septic patients’ management.
Lactic acidosis (LA) in end-stage liver disease (ESLD) patients has been recognized as one of the most complicated clinical problems and is associated with increased morbidity and mortality. Multiple-organ failure, associated with advanced stages of cirrhosis, exacerbates dysfunction of numerous parts of lactate metabolism cycle, which manifests as increased lactate production and impaired clearance, leading to severe LA-induced acidemia. These problems become especially prominent in ESLD patients, that undergo partial hepatectomy and, particularly, liver transplantation. Perioperative management of LA and associated severe acidemia is an inseparable part of anesthesia, post-operative and critical care for this category of patients, presenting a wide variety of challenges. In this review, lactic acidosis applied pathophysiology, clinical implications for ESLD patients, diagnosis, role of intraoperative factors, such as anesthesia- and surgery-related, vasoactive agents impact, and also current treatment options and modalities have been discussed.
Sepsis associated coagulopathy is due to the inflammation-induced activation of coagulation pathways concomitant with dysfunction of anticoagulant and fibrinolytic systems, leading to different degrees of haemostasis dysregulation. This response is initially beneficial, contributing to antimicrobial defence, but when control is lost coagulation activation leads to widespread microvascular thrombosis and subsequent organ failure. Large clinical trials of sepsis-related anticoagulant therapies failed to show survival benefits, but posthoc analysis of databases and several smaller studies showed beneficial effects of anticoagulants in subgroups of patients with early sepsis-induced disseminated intravascular coagulation. A reasonable explanation could be the difference in timing of anticoagulant therapy and patient heterogeneity associated with large trials. Proper selection of patients and adequate timing are required for treatment to be successful. The time when coagulation activation changes from advantageous to detrimental represents the right moment for the administration of coagulation-targeted therapy. In this way, the defence function of the haemostatic system is preserved, and the harmful effects of overwhelming coagulation activation are avoided.
Sepsis is an injurious systemic host response to infection, which can often lead to septic shock and death. Recently, the immune-pathogenesis and genomics of sepsis have become a research topic focusing on the establishment of diagnostic and prognostic biomarkers. As yet, none have been identified as having the necessary specificity to be used independently of other factors in this respect. However the accumulation of current evidence regarding genetic variations, especially the single nucleotide polymorphisms (SNPs) of cytokines and other innate immunity determinants, partially explains the susceptibility and individual differences of patients with regard to the evolution of sepsis. This article outlines the role of genetic variation of some serum proteins which have the potential to be used as biomarker values in evaluating sepsis susceptibility and the progression of the condition.
This review summarizes the most recent developments in providing advanced supportive measures for cardiopulmonary resuscitation, and the results obtained using these new therapies in patients with cardiac arrest caused by acute myocardial infarction (AMI). Also detailed are new approaches such as extracorporeal cardiopulmonary resuscitation (ECPR), intra-arrest percutaneous coronary intervention, or the regional models for systems of care aiming to reduce the critical times from cardiac arrest to initiation of ECPR and coronary revascularization.
Systemic inflammatory activation in sepsis often leads to coagulation activation, but the relationship is bilateral, as coagulation also modulates the inflammatory response. This close associate has significant consequences for the pathogenesis of microvascular thrombosis and organ dysfunction in sepsis. While coagulation activation can be beneficial for immune defense, it can also be detrimental once it becomes widespread and uncontrolled. The knowledge of the pathophysiologic mechanisms involved in the interaction between infection and coagulation may lead to the better timing for the administration of targeted antithrombotic therapies in septic patients. This brief review highlights the pathophysiologic pathways leading to the prothrombotic state in sepsis and the mechanisms that play a role in the interaction between infection and coagulation.