Acute-on-chronic liver failure(ACLF),which was first described in 2013,is a severe form of acutely decompensated cirrhosis characterized by the existence of organ system failure(s)and a high risk of short-term mortality.ACLF is caused by an excessive systemic inflammatory response triggered by precipitants that are clinically apparent(e.g.,confirmed microbial infection with sepsis,severe alcohol-related hepatitis)or not.Since the description of ACLF,some important studies have suggested that patients with ACLF may benefit from liver transplantation and should therefore be urgently stabilized for transplantation by receiving appropriate etiological treatment and comprehensive management,including support of organ systems in the intensive care unit(ICU).The goal of the present clinical practice guidelines is to provide the most reliable evidence available to assist the clinical decision-making process in the management of patients with ACLF,to make triage decisions(ICU vs.no ICU),to identify and manage acute precipitants,to identify organ systems that require support or replacement,to define potential criteria for futility of intensive care,and it also provides suggestions for identifying potential indications for liver transplantation.

Liver diseases in pregnancy comprise both gestational liver disorders and acute and chronic hepatic disorders occurring coincidentally in pregnancy.Whether pregnancy-related or not,liver diseases in pregnancy are associated with a significant risk of maternal and fetal morbidity and mortality.Thus,the European Association for the Study of the Liver invited a panel of experts to develop clinical practice guidelines aimed at providing recommendations,based on the best available evidence,for the management of liver diseases in pregnancy for hepatologists,gastroenter-ologists,obstetric physicians,general physicians,training specialists and other healthcare professionals who provide care for this patient population.

This Practice Guidance intends to coalesce best practice recommendations for the identification of portal hypertension （PH）， for prevention of initial hepatic decompensation， for the management of acute variceal hemorrhage （AVH）， and for reduction of the risk of recurrent variceal hemorrhage in chronic liver disease. The most significant changes in the current Guidance relate to recognition of the concept of compensated advanced chronic liver disease， codification of methodology to use noninvasive assessments to identify clinically significant PH （CSPH）， and endorsement of a change in paradigm with the recommendation of early utilization of nonselective beta-blocker therapy when CSPH is identified. The updated guidance further explores potential future pharmacotherapy options for PH， clarifies the role of preemptive transjugular intrahepatic portosystemic shunt in AVH， discusses more recent data related to the management of cardiofundal varices， and addresses new topics such as portal hypertensive gastropathy and endoscopy prior to transesophageal echocardiography and antineoplastic therapy.

Acute-on-chronic liver failure (ACLF), which was first described in 2013, is a severe form of acutely decompensated cirrhosis characterised by the existence of organ system failure(s) and a high risk of short-term mortality. ACLF is caused by an excessive systemic inflammatory response triggered by precipitants that are clinically apparent (e.g., comfirmed microbial infection with sepsis, severe alcohol-related hepatitis) or not. Since the description of ACLF, some important studies have suggested that patients with ACLF may benefit from liver transplantation and should therefore be urgently stabilized for transplantation by receiving appropriate etiological treatment and comprehesive management, including support of organ systems in the intensive care unit (ICU). The goal of the present clinical practice guidelines is to provide the most reliable evidence available to assist the clinical decision-making process in the management of patients with ACLF, to make triage decisions (ICU vs. no ICU), to identify and manage acute precipitants, to identify organ systems that require support or replacement, to define potential criteria for futility of intensive care, and it also provides suggestions for identifying potential indications for liver transplantation.

Liver diseases in pregnancy comprise both gestational liver disorders and acute and chronic hepatic disorders occurring coincidentally in pregnancy. Whether pregnancy-related or not, liver diseases in pregnancy are associated with a significant risk of maternal and fetal morbidity and mortality. Thus, the European Association for the Study of Liver invited a panel of experts to develop clinical practice guidelines aimed at providing recommendations, based on the best available evidence, for the management of liver disease in pregnancy for hepatologists, gastroenterologists, obstetric physicians, general physicians, obstetricians, training specialists and other healthcare professionals who provide care for this patient population.

Hemorrhage and thrombosis prevention and treatment in patients with cirrhosis faces certain clinical difficulties. Therefore, this guideline is formulated to provide practical guidance on controversial topics, such as the current perspectives on hemostasis in liver disease, whether invasive procedures need to correct thrombocytopenia and coagulation abnormalities, and the necessity of thromboprophylaxis in hospitalized patients with abnormal coagulation. Many of the recommendations in the guidelines are not useful measures; however, they were stem under the oversight of an expert panel, and are widely used in clinical practice. Here, we compile and summarize the recommendations on the above topics in order to share them with readers.

Objective:To explore the mechanism of early pancreatic exocrine function changes in severely scalded rats.Methods:The experimental research methods was used. Eighty male Sprague-Dawley rats aged 7-8 weeks were divided into simple sham injury group ( n=8), sham injury+cholecystokinin octapeptide (CCK8) group ( n=8), severe scald+CCK8 group ( n=32), and extremely severe scald+CCK8 group ( n=32) by the random number table, which were treated accordingly. Immediately after injury of rats in the 2 sham injury groups and 1, 2, 3, and 7 days after injury of rats in the 2 scald groups, the improved methods including pancreatic duct puncture and catheterization were used to dynamically collect the pancreatic-bile juice (PBJ) of rats. The PBJ secretory volume within 1 h was recorded, and the content of pancreatic lipase, α-amylase, and trypsin in PBJ was detected by enzyme-linked immunosorbent assay (ELISA), and the number of samples was 8. The femoral venous blood was collected, and the concentrations of pancreatic lipase and α-amylase in serum were detected by standard colorimetry to reflect their activity ( n=8). The pancreatic tissue was extracted, and the levels of interleukin-1β (IL-1β) and IL-6 in pancreatic tissue were detected by ELISA ( n=8), the expression of hypoxia-inducible factor 1α (HIF-1α) in pancreatic tissue was detected by immunofluorescence method, and the histopathological changes in pancreatic tissue were observed by hematoxylin-eosin staining, the severity of pancreatic tissue injury in the 2 scald groups was evaluated by modified Schmidt method ( n=6), and the ultrastructure of acinar cells in pancreatic tissue was observed by transmission electron microscopy. Data were statistically analyzed with analysis of variance for factorial design, Tukey test, independent sample t test, and least significant difference test. Results:Compared with the PBJ secretory volume (0.740±0.030) mL in the pancreatic tissue of rats in simple sham injury group within 1 h immediately after injury, the (0.823±0.033) mL in sham injury+CCK8 group was significantly increased ( t=4.92, P<0.05). Compared with that of rats in sham injury+CCK8 group immediately after injury, the PBJ secretory volume of rats within 1 h in severe scald+CCK8 group ((0.681±0.024), (0.608±0.056), (0.525±0.025), and (0.720±0.044) mL) and extremely severe scald+CCK8 group ((0.540±0.025), (0.406±0.021), (0.475±0.036), and (0.690±0.018) mL) was significantly decreased on 1, 2, 3, and 7 days after injury ( P<0.05). Compared with that in severe scald+CCK8 group, the PBJ secretory volume of rats within 1 h in extremely severe scald+CCK8 group was significantly decreased on 1 and 2 days after injury ( P<0.05). Compared with that of rats in simple sham injury group immediately after injury, the content of pancreatic lipase, α-amylase, and trypsin in PBJ of rats in sham injury+CCK8 group immediately after injury was significantly increased (with t values of 4.56, 3.30, and 4.99, respectively, P<0.05). Compared with that of rats in sham injury+CCK8 group immediately after injury, the content of pancreatic lipase and α-amylase in PBJ of rats in severe scald+CCK8 group and extremely severe scald+CCK8 group was significantly decreased on 1, 2, 3, and 7 days after injury ( P<0.05), the trypsin content in PBJ of rats in extremely severe scald+CCK8 group was significantly decreased on 2 days after injury ( P<0.05). Compared with that in severe scald+CCK8 group, the content of pancreatic lipase in PBJ of rats in extremely severe scald+CCK8 group was significantly decreased on 1, 2, and 3 days after injury ( P<0.05), and the content of α-amylase and trypsin in PBJ was significantly decreased on 1 and 2 days after injury ( P<0.05). There were no statistically significant differences in the activities of pancreatic lipase and α-amylase in serum of rats among the 4 groups at various time points after injury ( P>0.05). Compared with that of rats in sham injury+CCK8 group immediately after injury, the levels of IL-1β in pancreatic tissue of rats in severe scald+CCK8 group on 1, 2, and 3 days after injury and in extremely severe scald+CCK8 group on 1, 2, 3, and 7 days after injury were significantly increased ( P<0.05), and the levels of IL-6 in pancreatic tissue of rats in severe scald+CCK8 group and extremely severe scald+CCK8 group were significantly increased on 1, 2, 3, and 7 days after injury ( P<0.05). Compared with that in severe scald+CCK8 group, the IL-1β level in pancreatic tissue of rats in extremely severe scald+CCK8 group was significantly increased on 2 and 3 days after injury ( P<0.05), and IL-6 level in pancreatic tissue was significantly increased on 2 days after injury ( P<0.05). The expression levels of HIF-1α in pancreatic tissue of rats in simple sham injury group and sham injury+CCK8 group immediately after injury were lower; and compared with that in sham injury+CCK8 group immediately after injury, the expression levels of HIF-1α in pancreatic tissue of rats in the 2 scald groups increased to a certain extent at different time points after injury, and the expression position was transited from the edge of the pancreatic tissue to the whole pancreas, the expression levels of HIF-1α in pancreatic tissue of rats in the 2 scald groups tended to be normal on 7 days after injury. Compared with that in simple sham injury group immediately after injury, the proportion of acinar cell cytoplasm in pancreatic tissue of rats in sham injury+CCK8 group was increased; and with the increase of time after injury, edema, hemorrhage, necrosis, and inflammatory infiltration appeared in pancreatic tissue of rats in the 2 scald groups. Compared with that in severe scald+CCK8 group, the scores of edema, inflammatory cell infiltration, bleeding, and necrosis in pancreatic tissue of rats in extremely severe scald+CCK8 group were increased to varying degrees at various time points after injury, and the scores of pancreatic tissue of rats in the 2 scald groups basically recovered to normal on 7 days after injury. Compared with that in simple sham injury group immediately after injury, the number of enzyme granules in acinar cells of pancreatic tissue of rats in sham injury+CCK8 group was increased, and with the increase of time after injury, the enzyme granules in acinar cells of rats in the 2 scald groups were gradually reduced basically. Conclusions:The exocrine functions of pancreas, such as synthesis and secretion of pancreatic enzymes, are decreased in the early stage in severely scalded rats. And the greater the scalded area, the more significant the decline of pancreatic exocrine function. This change may be related to hypoxic injury and inflammation in pancreatic tissue after severe scald.

Objective:To explore the predictive factors for adverse clinical outcomes in critically ill adult patients with autoimmune encephalitis by analyzing their clinical characteristics and prognosis.Methods:Clinical data of patients diagnosed with " confirmed" or " possible" autoimmune encephalitis who were hospitalized in the intensive care unit (ICU) of the Department of Neurology at the Second Xiangya Hospital of Central South University from January 2015 to December 2023 were retrospectively collected. The neurological function of patients at 3, 6, and 12 months of onset was followed up, and the modified Rankin Scale (mRS) at 12 months was used as an evaluation index for clinical prognosis; Further analysis was conducted on the relationship between clinical features, auxiliary examinations, and prognosis.Results:The 12-month survival rate of critically ill adult patients with autoimmune encephalitis in our center was 90.7%(117/129), and the 6-month poor prognosis rate was 28.7%(37/129). Univariate logistic regression analysis found that age of onset ( P<0.01), presence of tumors ( P<0.01), mechanical ventilation ( P<0.01), Glasgow Coma Scale (GCS) at ICU admission ( P<0.01), Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score ( P<0.01), cerebrospinal fluid glucose ( P<0.01), cerebrospinal fluid protein level ( P=0.02), epileptic waves in electroencephalography (EEG) ( P=0.03), use of glucocorticoids ( P=0.04), and time interval between initiation of intravenous immunoglobulin (IVIG) and onset ( P=0.04) were associated with prognosis. The results of multiple logistic regression analysis showed that mechanical ventilation [ P=0.01, area under the curve (AUC)=0.72)], APACHE Ⅱ score ( P=0.04, AUC=0.68), cerebrospinal fluid protein content ( P=0.04, AUC=0.65), and the time interval between initiation of IVIG and onset ( P=0.02, AUC=0.64) were independent predictive factors for the prognosis of adult critical autoimmune encephalitis. The prognostic prediction model for adult critical autoimmune encephalitis established by combining these four indicators has a higher AUC (0.85). Conclusions:Mechanical ventilation, APACHE Ⅱ score, cerebrospinal fluid protein level, and the time interval between initiation of IVIG and onset are predictive factors for poor clinical outcomes in critically ill autoimmune encephalitis in adults; The prognostic prediction model for adult critical autoimmune encephalitis established by combining these four indicators can identify patients with poor prognosis early, which is beneficial for early comprehensive management and intervention treatment to improve patient prognosis.

Objective:To investigate the influencing factors for splenomegaly secondary to acute pancreatitis (AP) and construction of a nomogram prediction model.Methods:The retrospective case-control study was conducted. The clinicopathological data of 180 patients with AP who were admitted to Xuanwu Hospital of Capital Medical University from December 2017 to December 2021 were collected. There were 124 males and 56 females, aged (49±15) years. Among them, 60 AP patients who developed secondary splenomegaly were taken as the case group, including 48 males and 12 females, aged (47±13)years, and the rest of 120 cases of AP without secondary splenomegaly were taken as the control group, including 76 males and 44 females, aged (50±16)years. Observation indicators: (1) occurrence and clinical characteristics of splenomegaly secondary to AP; (2) influencing factors for splenomegaly secondary to AP; (3) construction and evaluation of a nomogram prediction model for splenomegaly secondary to AP. Measurement data with normal distribution were represented as Mean± SD, and comparison between groups was analyzed using the t test. Measurement data with skewed distribution were represented as M( Q1, Q3), and comparison between groups was analyzed using the rank sum test. Count data were represented as absolute numbers, and comparison between groups was analyzed using the chi-square test or Fisher exact probability. The univariate analysis was performed using statistical methods appropriate to the data type. The optimal cut-off value was determined by the receiver operating characteristic curves. Multivariate analysis was conducted using the Logistic regression model with forward method. Based on the results of the multivariate analysis, a nomogram prediction model was constructed. The receiver operating characteristic curve was drawn, and the discrimination was evaluated using the area under curve. The consistency of the nomogram prediction model was evaluated using calibration curve, and its clinical benefit was evaluated using decision curve. Results:(1) Occurrence and clinical characteristics of splenomegaly secondary to AP. The first detection time of 60 patients with splenomegaly secondary to AP was 60(30,120)days after the onset of AP. Cases with persistent respiratory dysfunction, multiple organ failure, severity of illness as mild or moderately severe/severe, pancreatic and/or peripancreatic infection, surgery were 19, 17, 4, 56, 37, 32 for 60 patients with splenomegaly secondary to AP, versus 16, 19, 43, 77, 39, 29 for 120 patients without splenomegaly secondary to AP, respectively, showing significant differences in the above indicators between the two groups ( χ2=8.58, 3.91, 17.64, 13.95, 15.19, P<0.05). (2) Influencing factors for splenomegaly secondary to AP. Resuts of multivariate analysis showed that white blood cell count <5.775×10?/L within 24 hours of AP onset, revised computed tomography (CT) severity index >7 in 3-7 days after onset and the presence of local complications were independent risk factors influencing the splenomegaly secondary to AP ( odds ratio=3.85, 2.86, 6.40, 95% confidence interval as 1.68-8.85, 1.18-6.95, 1.56-26.35, P<0.05). (4) Construction and evaluation of a nomogram prediction model for splenomegaly secondary to AP. The nomogram prediction model was constructed based on white blood cell count within 24 hours of AP onset, revised CT severity index in 3-7 days after onset and local complications. The area under the receiver operating characteristic curve of the nomogram prediction model was 0.76 (95% confidence interval as 0.69-0.83, P<0.05), with a sensitivity of 0.87 and a specificity of 0.55. The calibration curve demonstrated consistency between the predicted rate from the nomogram prediction model and the actually observed rate. The decision curve analysis indicated that the nomogram prediction model had favorable clinical practicability. Conclusions:Patients with AP who develop secondary splenomegaly tend to have a higher severity of illness than those develop no secondary splenomegaly. White blood cell count <5.775×10?/L within 24 hours of AP onset, revised CT severity index >7 in 3-7 days after onset and presence of local complications are independent risk factors influencing splenomegaly secondary to AP, and its nomogram prediction model can predict incidence rate of splenomegaly secondary to AP.