Acute kidney injury (AKI) is a common presentation in patients with advanced cirrhosis hospitalized with acute decompensation. A new revised classification now divides AKI in cirrhotic patients into two broad subgroups: hepatorenal syndrome AKI (HRS AKI) and non−hepatorenal syndrome AKI (non-HRS AKI). HRS AKI represents the end-stage complication of decompensated cirrhosis with severe portal hypertension and is characterized by worsening of renal function in the absence of prerenal azotemia, nephrotoxicity, and intrinsic renal disease. Non-HRS AKI may be caused by prerenal hypoperfusion, bile acid nephropathy, nephrotoxicity, or acute parenchymal insult. There have been several mechanisms proposed to explain the pathophysiology of HRS AKI and non-HRS AKI, and a number of biomarkers have been suggested to aid in differentiation between these types of AKI and to act as prognostic indicators. The standard of care clinical management for patients with HRS AKI is to exclude other etiologies of AKI, followed by volume expansion with human albumin solution and then the introduction of vasopressors. However, some 40% of patients treated for HRS AKI fail to respond. In this review, we discuss the current and recent data about classification, pathophysiology, and management of AKI in general, with specific insight about the treatment of HRS AKI.
Grant support and Acknowledgements: This work has been supported by funding from EU H2020 Research & Innovation programme, No. 731875 (LIVERHOPE).We acknowledge Nicola Van Berckel for her administrative support and her valuable collaboration with the development of the Liverhope Project.
Acute-on-chronic liver failure (ACLF) is a recently described entity in chronic liver disease defined by acute hepatic decompensation, organ failure and a high risk of short-term mortality (usually less than 4 weeks). This condition is distinct from acute liver failure and stable progression of cirrhosis in numerous ways, including triggering precipitant factors, systemic inflammation, rapid progression and a potential for recovery. While a clear definition of ACLF has been forwarded from a large European Consortium study, some heterogeneity remains in how patients present and the types of organ failure, depending on whether they are described in Asian or European studies. Active alcoholism, acute alcoholic hepatitis and infections are the most frequent precipitants for ACLF. Underpinning the pathophysiology of ACLF is a state of persistent inflammation and immune dysfunction, collectively driving a systematic inflammatory response syndrome and an increased propensity to sepsis. Prevention and early treatment of organ failure are key in influencing survival. Given increasing organ shortage and more marginal grafts, liver transplantation is a limited resource and emphasises the need for new therapies to improve ACLF outcomes. Recent data indicate that liver transplantation has encouraging outcomes even in patients with advanced ACLF if patients are carefully selected during the permissive window of clinical presentation. ACLF remains a significant challenge in the field of hepatology, with considerable research and resource being channelled to improve upon the definition, prognostication, treatment and unravelling of mechanistic drivers. This Review discusses updates in ACLF definition, prognosis and management.
Acute liver failure (ALF) is a life-threatening illness precipitated by an acute liver injury in patients with no pre-existing liver disease. Acute viral hepatitis and drug-induced liver injury account for the majority of cases, the clinical course characterised by the development of coagulopathy and hepatic encephalopathy (HE), often progressing to multi-organ disease which is associated with high fatality rates. The outcomes have improved significantly over time with improving standards of organ system support and access to liver transplantation for the very sick. The King's College Hospital criteria (KCH) is the most commonly used tool for determination of prognosis and consideration for transplantation. Prompt diagnosis, immediate initiation of supportive care and aetiology-specific treatment, where applicable, and early discussions and transfer to transplant centre are keys to successful outcome. KEYWORDS Acute liver failure, fulminant hepatitis, critical care, hepatic encephalopathy, multi-organ failure, intensive care, liver transplantation. DEFINITION AND CLASSIFICATION Acute liver failure (ALF) is a rare, life-threatening illness, triggered by a de novo liver injury to a previously healthy liver, frequently progressing within hours and weeks to multisystem involvement and failure. Coagulation abnormalities of liver origin (elevated prothrombin time (PT) or International Normalised Ratio (INR) above 1.5) and mental alterations due to hepatic encephalopathy (HE) are the key defining clinical criteria required to make a diagnosis. ALF is a specific clinical entity in terms of the clinical phenotype, disease course, prognosis, and eligibility for emergency liver transplantation. This must be distinguished from secondary liver injury in sepsis or congestive cardiac disease or failure following major liver resection, none of which would qualify as ALF and would not be indications for emergency liver transplantation. Conversely, acute presentations of Wilson's disease, acute Budd-Chiari syndrome and some cases of autoimmune hepatitis may have undiagnosed chronic liver involvement but are treated as ALF because of the poor prognosis without transplantation in these conditions and clinical features consisting predominantly of coagulopathy and HE.
Background and Aim: Serum bilirubin is an established marker of liver disease. Reliable tools for non-invasive assessment of jaundice in cirrhosis patients, at risk of clinical decompensation, are highly desirable. While smartphone-based imaging has been described in neonatal jaundice, it has not been investigated in advanced cirrhosis patients. Methods: We included 46 hospitalized patients with acute cirrhosis decompensation and jaundice. Scleral images using an Android smartphone were taken to derive "Scleral Color Values (SCV)," which were matched with same day serum bilirubin measurements. In 29 patients, repeat SCV and bilirubin measurements were performed over time. We analyzed the relationship of SCV and its dynamics with serum bilirubin, clinical scores, and patient outcomes. Results: Of 46 patients, 26 (57%) had alcoholic hepatitis as the decompensation precipitant. Seven patients died during admission; a further 12 following hospital discharge. SCV had an excellent linear correlation with serum bilirubin (rho = 0.90, P < 0.001); changes in SCV and serum bilirubin across different time points, were also closely associated (rho = 0.77, P < 0.001). SCV correlated significantly with CLIF Consortium Acute Decompensation score (rho = 0.38, P < 0.001) and grade of Acute-on-Chronic Liver Failure (rho = 0.42, P = 0.039). SCV was higher in patients who died, however, not significantly ], P = 0.22). The associations of SCV with clinical parameters mirrored those of serum bilirubin. Conclusion: Smartphone-based assessment of jaundice shows excellent concordance with serum bilirubin and is associated with clinical parameters in acute cirrhosis decompensation. This approach offers promise for remote assessment of cirrhosis patients at-risk of decompensation, post hospital discharge.
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