EASL Clinical Practical Guidelines on the management of acute (fulminant) liver failure

Wendon, Julia; Córdoba, Juan; Dhawan, Anil; Larsen, Fin Stolze; Manns, Michael P.; Nevens, Frederik; Samuel, Didier; Simpson, Kenneth J.; Ilan, Yaron; Bernardi, Mauro

doi:10.1016/j.jhep.2016.12.003

Cited by 640 publications

(494 citation statements)

References 352 publications

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“…No patient received invasive ICP monitoring during the study period. This practice is divergent from previous literature and in accordance with modern recommendations . Mortality of patients with severe hepatic encephalopathy has been reported between 23% and 50% .…”

Section: Discussioncontrasting

confidence: 69%

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Outcome of Acetaminophen‐Induced Acute Liver Failure Managed Without Intracranial Pressure Monitoring or Transplantation

Porteous¹,

Cioccari

Ancona³

et al. 2019

Liver Transpl

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Acetaminophen‐induced acute liver failure (ALF) may require emergency liver transplantation (LT) in the presence of specific criteria, and its management may also include intracranial pressure (ICP) monitoring in selected patients at high risk of cerebral edema. We aimed to test the hypothesis that management of such patients without ICP monitoring or LT would yield outcomes similar to those reported with conventional management. We interrogated a database of all patients treated in an intensive care unit for acetaminophen‐induced ALF between November 2010 and October 2016 and obtained relevant information from electronic medical records. We studied 64 patients (58 females) with a median age of 38 years. Such patients had a high prevalence of depression, substance abuse, or other psychiatric disorders and had ingested a median acetaminophen dose of 25 g. No patient received ICP monitoring or LT. Overall, 51 (79.7%) patients survived. Of the 42 patients who met King’s College Hospital (KCH) criteria, 29 (69.0%) survived without transplantation. There were 45 patients who developed severe hepatic encephalopathy, and 32 (71.1%) of these survived. Finally, compared with the KCH criteria, the current UK Registration Criteria for Super‐Urgent Liver Transplantation (UKRC) for super‐urgent LT had better sensitivity (92.3%) and specificity (80.4%) for hospital mortality. In conclusion, in a center applying a no ICP monitoring and no LT approach to the management of acetaminophen‐induced ALF, during a 6‐year period, overall survival was 79.7%, and for patients fulfilling KCH criteria, it was 69.0%, which were both higher than for equivalent patients treated with conventional management as reported in the literature. Finally, the current UKRC may be a better predictor of hospital mortality in this patient population.

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Section: Discussioncontrasting

confidence: 69%

“…Moreover, the use of ICP monitoring in ALF is controversial and should only be considered in a highly selected subgroup of patients because this practice is challenging in patients with clotting abnormalities and may not improve survival …”

mentioning

confidence: 99%

Outcome of Acetaminophen‐Induced Acute Liver Failure Managed Without Intracranial Pressure Monitoring or Transplantation

Porteous¹,

Cioccari

Ancona³

et al. 2019

Liver Transpl

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“…While some liver injury outcomes may fall into established definitions such as acute liver failure (5, 6) or acute on chronic liver failure (7, 8), other outcomes are more nebulous to define. Even resolution can be open to debate.…”

Section: Definitionsmentioning

confidence: 99%

Long-Term Outcomes After Drug-Induced Liver Injury

Hayashi

Bjõrnsson

2018

Curr Hepatology Rep

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Purpose of the review: This review serves to update the reader on emerging data regarding a spectrum of drug-induced liver injury (DILI) outcomes that lie between complete resolution and acute liver failure. Such outcomes can range from mild chronic injury to late liver failure and mortality. Recent findings: Several large registries are maturing with large numbers of DILI cases thus shedding light on outcomes including chronic injury and late fatality. We cover definitions commonly used to describe resolution versus chronic injury and mortality due to DILI. We look at rates of occurrence for these different outcomes in major registries. Three specific types of chronic DILI that are illustrative but also easily missed by clinicians are also described. Summary: A small but important proportion of DILI cases do not resolve, going on to develop chronic injury and even liver failure. Defining and recognizing these cases is a challenge because DILI is rare, and chronic injury rarer still. Large registries are beginning to define these previously overlooked long term outcomes.

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“…The pathogenesis of ICH development on the background of liver failure is not fully understood and is considered as multifactorial. Unfortunately, despite certain successes in intensive care AHE which developed on the background of acute liver failure to date can most effectively be cured only by liver transplantation, which would neutralize the initiating factor of hepatogenic neurointoxication [12].…”

Section: Introductionmentioning

confidence: 99%

“…In sectional investigations the subject of research is CHE on the background of the final stages of liver cirrhosis, as AHE on the background of ALF to date is a more rare disease and is due to fulminant forms of viral hepatitis A, B, D, E (which have the highest incidence in Africa and Asia), acute poisoning by hepatotoxic poisons and suicide or accidental poisoning by drugs -mostly acetaminophen (paracetamol, N-acetyl-p-aminophenol [APAP]), -which are responsible for 50 % of all cases of AHE in the US and UK [16]. Reliable data on the incidence of HE in the European Union and Eurasia in the literature are not given in the absence of such studies [12]. In the US, approximately 5 million cases of chronic liver insufficiency are diagnosed each year [17].…”

Section: Introductionmentioning

confidence: 99%

Modern view on hepatic encephalopathy: basic terms and concepts of pathogenesis

Shulyatnikova

Shavrin

2017

Patologìâ

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Background. The problem of acute and chronic forms of hepatic encephalopathy (HE) is not clearly identified among modern problems of hepatology and neuroscience in Ukraine. Despite the significant contribution to the development of lethal complications in patients with liver pathology and long history of the study of this issue, there is still no unified opinion on the links of HE pathogenesis.The aim of this review is to conduct a comprehensive analysis of current data on the spreading and mechanisms of development of HE.HE is a complex of potentially reversible neurocognitive disorders in patients with chronic or acute hepatic failure (ALF). HE is more often a complication of liver cirrhosis and is the second most frequent cause of hospitalization of such patients after ascites. When decompensating liver failure in acute or chronic hepatic pathology in patients severe forms of HE develop, accompanied by a progressive increase in intracranial pressure and the development of coma, which often ends lethal due to poor corrigibility of intracranial hypertension while maintaining hepatogenic neurointoxication. HE is considered as the end result of the accumulation of a number of neurotoxic substances in the brain, among which are ammonia, mercaptans, short chain fatty acids, false neurotransmitters, gamma-aminobutyric acid, manganese. The most popular among the reasons for the development of HE is the neurotoxic theory of ammonia. Ammonia is subjected to detoxification in the liver, turning into urea, a smaller fraction with the participation of glutamine synthetase is used in the synthesis of glutamine in muscles, liver and astrocytes of brain. In case of hepatic dysfunction and/or portosystemic shunting, the concentration of ammonia in blood increases up to 10 times and the main load for its detoxification is shifted to myocytes and astroglia. In ALF glutamine overload of astrocytes occurs with a change in intracellular osmolarity and subsequent edema of astroglia, which is accompanied by the development of cytotoxic edema of the brain. In this case, in astrocytes damaging of mitochondrial respiratory chain occurs and mitochondrial insufficiency develops, as well as processes of nitrosative-oxidative stress and oxidation of astrocytic and neuronal RNA, disruption of gene expression, synthesis of neuro-and gliotransmitters and synaptic plasticity. The increased influx of aromatic amino acids into brain leads to the synthesis of false neurotransmitters, which worsens serotoninergic, GABA-ergic, dopaminergic and glutamatergic neurotransmission. Damage to the components of the blood-brain barrier leads to aggravation of the water imbalance, penetration of hematogenous cytokines, endotoxins and other products of systemic inflammatory reaction into the cerebral parenchyma and development of neuroinflammation, which makes an important contribution to the further progression of cerebral edema.Conclusions: despite a comprehensive study of the problem, many open questions remain in the pathogenesis of HE. Special attention ...

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EASL Clinical Practical Guidelines on the management of acute (fulminant) liver failure

Cited by 640 publications

References 352 publications

Outcome of Acetaminophen‐Induced Acute Liver Failure Managed Without Intracranial Pressure Monitoring or Transplantation

Outcome of Acetaminophen‐Induced Acute Liver Failure Managed Without Intracranial Pressure Monitoring or Transplantation

Long-Term Outcomes After Drug-Induced Liver Injury

Modern view on hepatic encephalopathy: basic terms and concepts of pathogenesis

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