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Managing cirrhosis complications is an important measure for improving patients' clinical outcomes. Therefore, in order to provide a complete disease assessment and comprehensive treatment, improve quality of life, and improve the prognosis for patients with cirrhosis, it is necessary to pay attention to complications such as thrombocytopenia and portal vein thrombosis in addition to common or severe complications such as ascites, esophagogastric variceal bleeding, hepatic encephalopathy, and hepatorenal syndrome. The relevant concept that an effective albumin concentration is more helpful in predicting the cirrhosis outcome is gradually being accepted; however, the detection method still needs further standardization and commercialization.

In order to standardize the diagnosis, treatment and management of esophagogastric variceal bleeding (EVB) in cirrhotic portal hypertension, the Chinese Society of Hepatology, Chinese Society of Gastroenterology, and Chinese Society of Digestive Endoscopology of Chinese Medical Association organized relevant experts, reviewed domestic and international latest progress in clinical research on EVB in cirrhotic portal hypertension, and followed the evidence of evidence-based medicine to update the Guidelines on the Management of EVB in Cirrhotic Portal Hypertension. The guideline provides recommendations for the diagnosis, treatment and management of EVB in cirrhotic portal hypertension and aims to improve the level of clinical treatment of EVB in cirrhotic portal hypertension.

Objective: To verify Baveno VI criteria, Expanded-Baveno VI criteria, liver stiffness×spleen diameter-to-platelet ratio risk score (LSPS), and platelet count/spleen diameter ratio (PSR) in evaluating the severity value of esophageal varices (EV) in patients with non-cirrhotic portal hypertension (NCPH). Methods: 111 cases of NCPH and 204 cases of hepatitis B cirrhosis who met the diagnostic criteria were included in the study. NCPH included 70 cases of idiopathic non-cirrhotic portal hypertension (INCPH) and 41 cases of nontumoral portal vein thrombosis (PVT). According to the severity of EV on endoscopy, they were divided into the low-bleeding-risk group (no/mild EV) and the high-bleeding-risk group (moderate/severe EV). The diagnostic value of Baveno VI and Expanded-Baveno VI criteria was verified to evaluate the value of LSPS and PSR for EV bleeding risk severity in NCPH patients. The t-test or Mann-Whitney U test was used to compare the measurement data between groups. Comparisons between counting data groups were performed using either the χ 2 test or the Fisher exact probability method. Results: Considering endoscopy was the gold standard for diagnosis, the missed diagnosis rates of low/high bleeding risk EVs in INCPH/PVT patients with Baveno VI and Expanded-Baveno VI criteria were 50.0%/30.0% and 53.8%/50.0%, respectively. There were no statistically significant differences in platelet count (PLT), spleen diameter, liver stiffness (LSM), LSPS, and PSR between low-bleeding-risk and high-bleeding-risk groups in INCPH patients, and the area under the receiver operating characteristic curve (AUC) of LSPS and PSR was 0.564 and 0.592, respectively ( P =0.372 and 0.202, respectively). There were statistically significant differences in PLT, spleen diameter, LSPS, and PSR between the low and high-bleeding risk groups in PVT patients, and the AUCs of LSPS and PSR were 0.796 and 0.833 ( P =0.003 and 0.001, respectively). In patients with hepatitis B cirrhosis, the Baveno VI and Expanded-Baveno VI criteria were used to verify the low bleeding risk EV, and the missed diagnosis rates were 0 and 5.4%, respectively. There were statistically significant differences in PLT, spleen diameter, LSM, LSPS and PSR between the low-bleeding-risk and high-bleeding-risk groups ( P <0.001). LSPS and PSR AUC were 0.867 and 0.789, respectively ( P <0.05). Conclusion: Baveno VI and Expanded-Baveno VI criteria have a high missed diagnosis rate for EVs with low bleeding risk in patients with INPCH and PVT, while LSPS and PSR have certain value in evaluating EV bleeding risk in PVT patients, which requires further clinical research.

In order to standardize the diagnosis, treatment and management of esophagogastric variceal bleeding (EVB) in cirrhotic portal hypertension, the Chinese Society of Hepatology, Chinese Society of Gastroenterology, and Chinese Society of Digestive Endoscopology of Chinese Medical Association organized relevant experts, reviewed domestic and international latest progress in clinical research on EVB in cirrhotic portal hypertension, and followed the evidence of evidence-based medicine to update the Guidelines on the Management of EVB in Cirrhotic Portal Hypertension. The guideline provides recommendations for the diagnosis, treatment and management of EVB in cirrhotic portal hypertension and aims to improve the level of clinical treatment of EVB in cirrhotic portal hypertension.

In this article, the author proposes the concept of pre-cirrhotic portal hypertension syndrome (PcPH), aiming to optimize the clinical management of patients with cirrhosis. PcPH is a certain stage of the progression of cirrhosis: starting from the presence of clinically significant portal hypertension, and ending with the occurrence of high-risk varices or any decompensated events (including ascites, variceal hemorrhage, hepatic encephalopathy). Defining PcPH is conducive to the early screening, early diagnosis and early treatment of cirrhosis and homogeneous management, conducive to patients with chronic liver disease to pay more attention to the hazards of cirrhosis and portal hypertension and popularization of science and education, and conducive to the sinking of high-quality hepatic medical resources and the construction of a hierarchical diagnosis and treatment system.

Idiopathic non-cirrhotic portal hypertension is a rare group of clinical syndromes characterized by clinical manifestations of portal hypertension in the absence of histological manifestations of liver cirrhosis, and with the exclusion of known intrahepatic and extrahepatic causes of portal hypertension. Importantly, its etiology and pathogenesis are unclear, but it has been determined to be related to the development of intrahepatic vascular disease. It is currently believed that possible pathogenic mechanisms include immune disorders, chronic infections, drug-related poisoning or injury, microthrombosis, genetic abnormalities, etc. The most common clinical manifestations are esophagogastric varices and splenomegaly. Ascites and hepatic encephalopathy are the least common. Laboratory test demonstrates anemia, leukopenia, and thrombocytopenia due to hypersplenism, and normal or mild liver function abnormality. In addition, in the preclinical stage, despite the presence of abnormal portal vein during liver biopsy, no signs of portal hypertension can be detected in some patients. Therefore, the diagnosis is based on the diagnosis of exclusion and mandatory liver biopsy. The overall prognosis of idiopathic non-cirrhotic portal hypertension is better than that of patients with liver cirrhosis, but symptomatic treatment (controlling gastroesophageal varices bleeding and preventing thrombosis) is still the main treatment.

Portal hypertension is a clinical syndrome which is a consequence of a pathological increase in portal vein pressure due to various causes, among which, cirrhosis being the most common cause. The most basic pathophysiological features of portal hypertension in cirrhosis are increased portal vein pressure due to blocked portal vein blood flow and open collateral circulation. Among the clinical manifestations of portal hypertension in cirrhosis, esophageal and gastric fundus varicose bleeding is the most urgent and the mortality rate is the highest. In order to standardize the diagnosis and treatment plan of esophagogastric variceal bleeding in cirrhotic portal hypertension, the Chinese Society of Spleen and Portal Hypertension Surgery, Chinese Society of Surgery, have renewed and revised this consensus on diagnosis and treatment of esophagogastric variceal bleeding in cirrhotic portal hypertension (2015 edition) hope to provide references for the clinical practices.

Objective: To explore the noninvasive indicators for predicting the occurrence of esophageal varices (EV) in patients with liver cirrhosis., Methods: A total of 202 patients with liver cirrhosis caused by hepatitis B or C or alcoholic hepatic disease were enrolled in this study. EV and high risk esophageal varices (HREV) were confirmed in these patients by gastroscopy. The hematological, serum biochemical and ultrasonic parameters of the patients were analyzed, and a model for predicting EV was established by stepwise logistic regression analysis., Results: The areas under receiver operating characteristics curve (AUROC) of splenic thickness (SPT) for detecting EV and HREV were 0.827 and 0.766, respectively. The combined index USWA (SPT, US, WBC and albumin [ALB]) showed an AUROC of 0.873 for detecting EV, and the index SPA (combining SPT and ALB) showed an AUROC of 0.777 for detecting HREV. The direct combination of SPT with USWA or with platelet/splenic thickness ratio (PSA) was capable of completely excluding a definite diagnosis of EV, while the sequential combination of SPT with USWA or with platelet was capable of a diagnosis of EV and clarifying the condition of EV in approximately half of the cirrhotic patients in the absence of gastroscopic findings. The combination of SPT and SPA allowed for a definite diagnosis of the condition of HREV in 10% of the cirrhotic patients., Conclusion: SPT combined with SPT derived indexes or platelet status allows for a definite diagnosis of EV in patients with liver cirrhosis to offer a noninvasive option for diagnosis.

Objective: To investigate reliability of FibroScan (FS) in diagnosing size of oesophageal varices (OV) in patients with liver cirrhosis., Methods: A total of 260 patients with liver cirrhosis were enrolled in the study. All patients underwent endoscopy to assess OV stage and FS to measure liver stiffness. Receiver operating characteristic (ROC) curves were generated to evaluate the diagnostic reliability of FS., Results: The FS values according to OV stage were 20.9 ± 10.3 kPa for patients without OV, 32.2 ± 13.5 kPa for patients with mild OV, 45.6 ± 18.3 kPa for patients with moderate OV, and 55.1 ± 15.6 kPa for patients with severe OV. Significant differences were found among the groups (P < 0.001) as well as between any two groups (t=6.574, 10.533, 13.247, 4.719, 7.072 and 2.171, P less than 0.05 respectively). ROC curves of FS for the diagnoses of patients with various OV stages showed the following:with vs. without OV, 0.824 (95% CI:77.5% to 87.4%); less than moderate vs. more than moderate OV, 0.849 (95% CI:79.6% to 90.2%); and less than severe vs. severe OV, 0.871 (95% CI:81.1% to 93.0%); the corresponding FS cut-off values were 22.8 kPa, 30.6 kPa, and 34.6 kPa., Conclusion: Liver stiffness measurement by FibroScan allows prediction of the oesophageal varices stage in patients with liver cirrhosis.

Objective: To study ability of FibroScan (FS) in diagnosing the size of oesophageal varices (OV) in patients with HBV-related cirrhosis., Methods: A total of 158 patients with HBV-related liver cirrhosis were enrolled in the study. The relation between the presence of OV assessed by endoscopy, and liver stiffness measurement by Fibroscan was studied, and ROC curves were drawn to assess the diagnostic ability of FS value., Results: For the patients without OV, mild OV, moderate OV, and severe OV, their corresponding FS values were (21.7 +/- 9.9) kPa, (32.1 +/- 13.6) kPa, (42.3 +/- 20.0) kPa and (54.5 +/- 16.2) kPa, respectively. Significant difference was found among the groups (P < 0.001) and also between any two groups (P < 0.05). ROC curve for the diagnosis of with vs. without OV, moderate OV, and < severe vs. severe OV were 0.798 (95% CI: 73.1%-86.5%), 0.823 (95% CI: 74.5%-90.0%) and 0.879 (95% CI: 80.8%-95.0%), respectively, with corresponding FS cut-off value of 23.3 kPa, 31.5 kPa and 34.6 kPa., Conclusion: Liver stiffness measurement allows to predict the sizes of oesophageal varices in patients with HBV-related cirrhosis.

Objective: To evaluate the value of multi-detector row CT (MDCT) in the diagnosis and hemodynamic studies of gastric varices (GV) in portal hypertension by comparison with endoscopy and DSA direct portography., Methods: Thirty-six consecutive cirrhotic patients with GV confirmed by endoscopy underwent tri-phase contrast-enhanced CT scans and CT portography (CTP) within 2 weeks after endoscopy examination. Three independent experienced radiologists, who were blinded to the patients' clinical data, analyzed the CT images, including the size and location of GV as well as afferent and efferent veins of GV, separately. Interobserver agreement among the 3 radiologists with regard to the diagnosis of submucosal and perigastric GV was determined by Kappa (k) values. The findings of endoscopy were used as standards., Results: Sub mucosal GV was diagnosed in 34 of the 36 patients (94.4%) and perigastric GV in all 36 patients (100%) by the observation of the 3 radiologists. MDCT showed an excellent interobserver reliability with regard to the diagnosis of submucosal GV (kappa = 0.85) and perigastric GV (kappa = 1.0). Agreement between MDCT and endoscopy with regard to the opacification of variceal size and location were 86.1% and 88.9% respectively. The sensitivity, specificity, accuracy, and positive predictive value of CTP in the opacification of afferent and efferent veins of GV were all more than 80%. The frequencies of participation of posterior gastric vein and short gastric vein in blood supply to gastric fundal varices in the isolated gastric varices and gastroesophageal varices type 2 (GEV2) were 94.1% and 70.6% respectively, both significantly higher than those in the gastroesophageal varices type 1 (GEV1, 52.6% and 31.6%, respectively, both P < 0.05). The main blood drainage route of GEV1 was via azygous system into the super vena cava (100%), whereas in the gastric fundal varices the main blood drainage route was via the gastrorenal shunts into the inferior vena cava (82.4%)., Conclusion: MDCT can be used as an important tool for detecting submucosal and perigastric GV, and can clearly reveal the size, location, and hemodynamics of GV.