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Introduction: severe acute liver injury (SALI) formerly known as severe acute hepatitis is an acute inflammation of the liver with markers of liver injury (elevated transaminases) and signs of hepatocellular failure (jaundice and INR greater than 1.5) according to the latest definition of the European Association for the Study of the Liver (EASL). An important prognostic factor in SALI is the development of hepatic encephalopathy (HE) and thus its progression to acute liver failure (ALF), formerly known as acute severe hepatitis. The purpose of this study is to investigate factors predicting the development of hepatic encephalopathy during SALI. Methods: we conducted a retrospective study of patients treated for SALI between January 2000 and December 2019. We divided patients into two groups depending on whether hepatic encephalopathy occurred. We performed an analytical study comparing the two groups according to their epidemiological, biological and evolutionary data. Results: data from the medical records of fifty-nine patients were collected. A virus was the most frequent cause (63%). Hepatic encephalopathy occurred in 15 patients (25.4%). Factors predicting the development of HE in univariate analysis were a delay in consultation of more than 9 days, an INR level of more than 2.45, a bilirubin level of more than 230 µmol/l, creatinine greater than 60.5 µmol/l, urea greater than 5.5 mmol/l and MELD score greater than 26.5 (p=0.023, p=0.017, p=0.0001, p=0.049, p=0.0001, p=0.0001 respectively). Autoimmune hepatitis and an undetermined cause were associated with the development of HE (p=0,003 and p=0,044, respectively). In multivariate analysis, autoimmune aetiology and a urea level above 5.5 mmol/l were significantly associated with the occurrence of HE. No statistically significant differences were found between the two groups with regard to age, sex and diabetes. Conclusion: SALI is a rare disease, mainly due to a virus in our country. Predictive factors of HE are important for early identification of patients at risk of adverse outcomes. [ABSTRACT FROM AUTHOR]

Résumé Les encéphalopathies métaboliques (EMtb) sont des causes fréquentes de recours au système de soins, via les urgences, l'hospitalisation et même la réanimation. Elles pourraient représenter jusqu'à 10 à 20 % des causes de coma en réanimation et compromettre le pronostic vital, notamment chez le sujet âgé. L'EMtb correspond à une altération du fonctionnement cérébral due à un déficit en une substance indispensable au métabolisme normal ou à l'accumulation d'une substance toxique que celle-ci soit endogène ou exogène. Elle survient préférentiellement chez des patients présentant des comorbidités, complexifiant ainsi son diagnostic et sa prise en charge. Son diagnostic clinique repose sur la survenue subaiguë de troubles des fonctions supérieures et de mouvements anormaux, myoclonies principalement, en l'absence de signe de localisation neurologique. Indispensables pour éliminer les diagnostics différentiels, certains examens complémentaires sont parfois en mesure d'apporter des arguments positifs en faveur du diagnostic. C'est le cas pour certains dosages biologiques, et l'électroencéphalogramme. Une fois les mesures symptomatiques simples mises en œuvre à l'évocation du diagnostic, le traitement repose souvent sur le traitement de la cause. Seules certaines encéphalopathies métaboliques dont l'encéphalopathie hépatique bénéficient de prises en charge spécifiques. Nous décrirons successivement les principaux mécanismes physiopathologiques et les étiologies les plus fréquentes d'EMtb, les circonstances favorisantes, la présentation clinique, les diagnostics différentiels à éliminer, et les examens complémentaires utiles au diagnostic. Nous proposerons enfin une stratégie de prise en charge de l'EMtb. Abstract Metabolic encephalopathies (ME) are a common cause of admission to emergency rooms, to hospitalization wards or to intensive care units. They could account for 10 to 20% of causes of comatose states in ICU and could be associated to a poor outcome especially in older patients. Nevertheless, they are often reversible and are associated with a favorable outcome when diagnosed and rapidly treated. They correspond to an altered brain functioning secondary to the deficiency of a substance that is mandatory for the normal brain functioning or to the accumulation of a substance that can be either endogenous or exogenous. It preferably occurs in co-morbid patients, complicating its diagnosis and its management. Altered brain functioning, going from mild neuropsychological impairment to coma, movement disorders especially myoclonus and the absence of any obvious differential diagnosis are highly suggestive of the diagnosis. Whereas some biological samplings and brain MRI are essential to rule out differential diagnosis, some others, such as electroencephalogram, may be able to propose important clues in favor of the diagnosis. Once simple symptomatic measures are introduced, the treatment consists mainly in the correction of the cause. Specific treatment options are only seldom available for ME; this is the case for hepatic encephalopathy and some drug-induced encephalopathies. We will successively describe in this review the main pathophysiological mechanisms, the main causes, favoring circumstances of ME, the differential diagnosis to rule out and the etiological work-up for the diagnosis. Finally, a diagnostic and therapeutic strategy for the care of patients with ME will be proposed. [ABSTRACT FROM AUTHOR]

In patient with cirrhosis, minimal hepatic encephalopathy (MHE) is defined by the presence of neuropsychological abnormalities detectable by psychometric or neuropsychological tests without any clinical sign of hepatic encephalopathy. Its frequency is high, affecting between 20 and 60% of hospitalized cirrhotic patients. MHE is predictive of the occurrence of clinical hepatic encephalopathy, is a factor of poor prognosis and is associated with higher mortality. MHE also impacts everyday life by increasing traffic and household accidents. Diagnostic methods are complex, require time and a trained practitioner which explains the low screening rate despite the existence of effective therapies. [ABSTRACT FROM AUTHOR]

TIPS correspond in a prothetic and calibrated anastomosis between portal and hepatic veinous network. Efficiency of TIPS is now well known to prevent portal hypertension complications and, more recently, to improve transplant free survival in cirrhotic patients. However, patients may develop complications and a full workup is required to be sure that there is no contraindication before TIPS creation. A better patient selection, an improvement of technique and TIPS's long term patency should give to TIPS, in the coming years, a more important and earlier place in the therapeutic regimen for cirrhotic patients with severe complications of portal hypertension. [ABSTRACT FROM AUTHOR]

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome that ultimately occurs as a complication of acute or chronic liver failure; accompanied by hyperammonemia. This study aimed to evaluate the potential of biopropolis as a hepato- and neuro-protective agent using thioacetamide (TAA)-induced acute HE in rats as a model. Sixty Wistar rats were divided into 5 groups: Group 1 (normal control) received only saline and paraffin oil. Group 2 (hepatotoxic control) received TAA (300 mg/kg, once). Groups 3, 4, and 5 received TAA followed by vitamin E (100 mg/kg) and biopropolis (100 and 200 mg/kg), respectively, daily for 30 days. Evidences of HE were clearly detected in TAA-hepatotoxic group including significant elevation in the serum level of ammonia, liver functions, increased oxidative stress in liver and brain, apoptotic DNA fragmentation and overexpression of iNOS gene in brain tissue. The findings for groups administered biopropolis, highlighted its efficacy as a hepato- and neuro-protectant through improving the liver functions, oxidative status and DNA fragmentation as well as suppressing the brain expression of iNOS gene. In conclusion, biopropolis, at a dose of 200 mg/kg per day protected against TAA-induced HE through its antioxidant and antiapoptotic influence; therefore, it can be used as a protective natural product. [ABSTRACT FROM AUTHOR]

Recent studies suggest endogenous opioids and nitric oxide (NO) are involved in the pathophysiology of hepatic encephalopathy (HE). In this study, the interaction between the opioid receptor antagonist and NO was investigated on lipopolysaccharide (LPS)-induced HE in cirrhotic rats. Male rats were divided in the sham- and bile duct ligation (BDL)-operated groups. Animals were treated with saline; naltrexone (10 mg/kg, i.p.); or L-NAME (3 mg/kg, i.p.), alone or in combination with naltrexone. To induce HE, LPS (1 mg/kg, i.p.) was injected 1 h after the final drug treatment. HE scoring, hepatic histology, and plasma NO metabolites levels and mortality rate were recorded. Deteriorated level of consciousness and mortality after LPS administration significantly ameliorated following both acute and chronic treatment with naltrexone in cirrhotic rats. However, acute and chronic administration of L-NAME did not change HE scores in cirrhotic rats. The effects of acute but not chronic treatment of naltrexone on HE parameters were reversed by L-NAME. Plasma NOx concentrations elevated in BDL rats, which were decreased after acute and chronic treatment by naltrexone or L-NAME, significantly. We suggest both acute and chronic treatment with naltrexone improved LPS-induced HE. But, only acute treatment with naltrexone may affect through NO pathway. [ABSTRACT FROM AUTHOR]

Background: Diagnosis of Armillifer armillatus infestation is usually incidental, commonly via autopsy or radiography. Affected individual are usually asymptomatic. The case presented here, however, had severe thoracic and abdominal involvement with clinical manifestations. Aim: To report a case of heavy A. armillatus infestation in an adult female Nigerian rural dweller complicated by hepatic parenchyma damage. Setting: Case report from semi-urban southern Nigeria, using clinical records and imaging findings. Materials and Methods: Clinical case records, including laboratory results and radiographic /computed tomography images. Conclusion: Parenchymal damage with organ dysfunction can be seen with severe A. armillatus infestation. Thus, there is a need for regular health education regarding the risk of A. armillatus infestation for individuals who consume snake meat. [ABSTRACT FROM AUTHOR]

Summary: Objective: To compare electroencephalographic spectral analysis obtained by periodogram (calculated by means of Fast Fourier Transform) and autoregressive (AR) modelling for the assessment of hepatic encephalopathy. Methods: The mean dominant frequency (MDF) and the relative power of delta, theta, alpha, and beta bands were computed by both techniques from the electroencephalograms (EEG) of 201 cirrhotics and were evaluated in the clinical and prognostic assessment of the patients. Results: The values of all the five indexes computed by periodogram and AR modelling matched each other, but the latter provided stable values after the analysis of fewer epochs. Independently of the technique, the relative power of theta and alpha bands fitted the clinical data and had prognostic value. The relative power of beta and delta bands computed by AR modelling fitted more closely with clinical data fitted the clinical data more closely. Conclusions: The electroencephalographic spectral indexes obtained by periodogram and AR modelling were found to be, on average, undistinguishable, but the latter appeared less sensitive to noise and provided a more reliable assessment of low-power bands. [Copyright &y& Elsevier]

Summary: Study aim: To provide a consensus of European leading authorities about the optimal use of clinical neurophysiological (CN) tests (electroencephalogram [EEG]; evoked potentials [EP]; electroneuromyography [ENMG]) in the intensive care unit (ICU) and, particularly, about the way to make these tests clinically useful for the management of individual patients. Methods: This study gathered together several European clinical neurophysiologists and neurointensivists whose leading contributions in the adult or paediatric ICU and in continuous neuromonitoring had been peer-acknowledged. It was based on both a literature review and each participant''s own experience. Given the methodological impossibility to gather studies fulfilling criteria of evidence-based medicine, this article essentially relies on expert opinions that were gained after several rounds, in which each expert was invited to communicate his own contribution to all other experts. A complete consensus has been reached when submitting the manuscript. Results: What the group considered as the best classification systems for EEG and EP abnormalities in the ICU is first presented. CN tests are useful for diagnosis (epilepsy, brain death, and neuromuscular disorders), prognosis (anoxic ischemic encephalopathy, head trauma, and neurologic disturbances of metabolic and toxic origin), and follow-up, in the adult, paediatric, and neonatal ICU. Regarding prognosis, a clear distinction is made between these tests whose abnormalities are indicative of an ominous prognosis and those whose relative normalcy is indicative of a good prognosis. The prognostic significance of any test may vary as a function of coma etiology. Conclusion: CN provides quantitative functional assessment of the nervous system. It can be used in sedated or curarized patients. Therefore, it should play a major role in the individual assessment of ICU patients. [Copyright &y& Elsevier]

Abstract: Objective: To assess mortality and to identify variables that could predict it in cirrhotic patients hospitalized to the medical intensive care unit (MICU) for hepatic encephalopathy (HE). Study design: Retrospective cohort study. Patients and methods: From January 1995 to December 2004, the cirrhotic patients admitted consecutively in MICU were screened and those with altered level of consciousness were included. The MICU mortality rate was assessed. Nearly 80 variables were analyzed and compared between survivors and non-survivors. Statistical analysis: t test, χ2 or Fisher exact tests, Kaplan-Meier and log rank, Cox regression analysis. Results: A total of 180 patients (42 women - 138 men, mean age: 59±10 years) were admitted (incidence: 2.6%). The SAPS II was 30.1±11, Acute Physiology Age and Chronic Health Evaluation II (APACHE II): 16.5±5.3, Child-Pugh score: 9.1±1.9 and GCS: 11±2.8. The causes of liver cirrhosis was identified in 41.2% of cases (viral: 35.6%, alcohol: 5.6%). Nearly 18% of patients had an antecedent of HE. The causes of HE were: infection (65.6%), upper gastrointestinal bleeding (32.2%), drugs (5%) and metabolic cause (5%). MICU mortality rate was 33.3% and seemed higher in gastrointestinal bleeding. Eighteen variables were significantly associated with poor prognosis in univariate analysis. Only three variables remained significant in multivariate analysis: systolic blood pressure<90 mmHg (RR=4; IC95%=2–8.1), total WBC>12000 n/mm3 (RR=3.1; IC95%=1.8–5.3) and use of mechanical ventilation (RR=3.1; IC95%=1.7–5.6). Conclusion: The MICU mortality of cirrhotic patients with HE was high and significantly associated with haemodynamic instability, hyperleucocytosis and mechanical ventilation. [Copyright &y& Elsevier]

Abstract: [1] Done under the auspices of the CIRMAN MEC, University of Padova, Italy. Aim of the study. – To provide an objective EEG assessment of hepatic encephalopathy (HE), we set up and tested an entirely automatic procedure based on an artificial neural network-expert system software (ANNESS). Patients and methods. – A training set sample of 50 EEG (group A) and a test sample of 50 EEG (group B) of 100 cirrhotic patients were considered. The EEGs had been visually classified by an expert electroencephalographer, using a modified five-degree Parsons-Simith classification of HE. The efficiency of the ANNESS, trained in group A, was tested in group B. Results. – Both the ANNESS and the visually-based classifications were found to be correlated to liver insufficiency, as assessed by the Child–Pugh score (Spearman''s coefficient ρ =0.485, P <0.0001; ρ =0.489, P <0.0001, respectively) and by the biochemical indexes of hepatic function (bilirubin: ρ =0.31 vs. 0.27; albumin: ρ =–0.13 vs. –0.18; prothrombin time ρ =–0.35 vs. –0.52). The classifications were found to be correlated to each other (ρ =0.84 P <0.0001, Cohen''s kappa=0.55). However, the ANNESS overestimated grade 2 EEG alterations. Conclusion. – An ANNESS-based classification of EEG in HE provided data comparable with a visually-based classification, except for mild alterations (class 2) that tended to be overestimated. Further optimization of automatic EEG staging of HE is desirable, as well as a prospective clinical evaluation. [Copyright &y& Elsevier]

Brain oedema leading to intracranial hypertension occurs in a significant proportion of patients with acute liver failure in whom it is a leading cause of death. Although precise pathogenic mechanisms associated to this severe complication remain incompletely understood, increasing evidence points to gut-derived neurotoxins including ammonia as key mediators in cerebral osmotic and perfusion disturbances. The management of brain oedema and intracranial hypertension requires a multidisciplinar approach in a center where liver transplantation is available, as this option is the only treatment modality that provides improvement in outcome. This article reviews the most common causes of acute liver failure and the standard of supportive care management, and describes future potential therapeutic aspects of brain oedema and intracranial hypertension. [Copyright &y& Elsevier]

Introduction L’encéphalopathie hépatique est une complication grave de la cirrhose hépatique et représente ainsi un enjeu thérapeutique et socioéconomique important. Sa survenue chez des patients non cirrhotique présentant une thrombose des veines extra-hépatiques est rare. Observation Nous rapportons le cas d’un homme âgé de 46 ans, sans antécédents pathologiques particuliers qui consulte pour désorientation temporospatiale. Son histoire de la maladie remonte à 1 mois avant son admission par la survenue d’un état d’agitation nocturne sans mouvements toniques ni cloniques d’une durée 30 min à 12 heures qui récidivent avec une fréquence quotidienne. L’examen neurologique ne montre pas de signes de localisation. L’évolution était marquée par la persistance de ces épisodes associés à une régression cognitive (MMSE : 20/30), des fausses reconnaissances, un ralentissement psychomoteur marqué et des troubles dysexécutifs qui retentissent sur sa vie quotidienne. L’imagerie par résonance magnétique a montré des anomalies de signal des noyaux bipallidales en hypersignal T1 et en isosignal T2 et Flair. L’électroencéphalogramme (EEG) a montré des complexes triphasiques : des ondes lentes triphasiques à prédominance antérieur avec une activité de fond ralentie et réactive à l’ouverture des yeux. Le diagnostic d’une encéphalopathie métabolique était suspecté. Le contrôle du bilan hépatique qui était initialement strictement normal, a montré une diminution du Taux de prothrombine à 50 % et le dosage de l’amoniémie était élevé à un taux de 267,7 UI/L. Le diagnostic d’encéphalopathie hépatique était confirmé. L’échographie abdominale a montré des signes d’hypertension portale avec un cavernome porte. Le patient était mis sous lactulose avec une nette amélioration. Conclusion Il faut toujours penser à l’encéphalopathie hépatique devant tout tableau de démence rapidement progressive et pratiquer un EEG même chez des patients non connus cirrhotiques. [ABSTRACT FROM AUTHOR]