Platelet counts to spleen diameter ratio: A promising noninvasive tool for predicting esophageal varices in cirrhosis patients.

BACKGROUND Liver cirrhosis is the end stage of progressive liver fibrosis as a consequence of chronic liver inflammation, wherein the standard hepatic architecture is replaced by regenerative hepatic nodules, which eventually lead to liver failure. Cirrhosis without any symptoms is referred to as compensated cirrhosis. Complications such as ascites, variceal bleeding, and hepatic encephalopathy indicate the onset of decompensated cirrhosis. Gastroesophageal varices are the hallmark of clinically significant portal hypertension. AIM To determine the accuracy of the platelet count-to-spleen diameter (PC/SD) ratio to evaluate esophageal varices (EV) in patients with cirrhosis. METHODS This retrospective observational study was conducted at Tikur Anbessa Specialized Hospital and Adera Medical Center from January 1, 2019, to December 30, 2023. Data were collected via chart review and direct patient interviews using structured questionnaires. The data were exported to the SPSS software version 26 for analysis and clearance. A receiver operating characteristic curve was plotted for splenic diameter, platelet count, and PC/SD ratio to obtain sensitivity, specificity, positive predictive value, negative predictive value, positive likelihood ratio, and negative likelihood ratio. RESULTS Of the 140 participants, 67% were men. Hepatitis B (38%) was the most common cause of cirrhosis, followed by cryptogenic cirrhosis (28%) and hepatitis C (16%). Approximately 83.6% of the participants had endoscopic evidence of EV, whereas 51.1% had gastric varices. Decompensated cirrhosis and PC were associated with the presence of EV with adjusted odds ratios of 12.63 (95%CI: 3.16-67.58, P = 0.001) and 0.14 (95%CI: 0.037-0.52, P = 0.004), respectively. A PC/SD ratio < 1119 had a sensitivity of 86.32% and specificity of 70% with area under the curve of 0.835 (95%CI: 0.736-0.934, P < 0.001). CONCLUSION A PC/SD ratio < 1119 predicts EV in patients with cirrhosis. It is a valuable, noninvasive tool for EV risk assessment in resource-limited settings.

Introduction: The platelet count/spleen diameter (PC/SD) ratio is a noninvasive method for the diagnosis of esophageal varices (EV) used as an alternative to endoscopy in patients with cirrhosis. Objective: To evaluate the diagnostic performance of the PC/SD ratio (cut-off point <909) to detect EV in patients with cirrhosis treated at a tertiary referral hospital in Bogotá D.C., Colombia. Materials and methods: A prospective diagnostic test accuracy study was conducted in 66 patients with cirrhosis treated at the Hospital Universitario de La Samaritana between July and December 2018. A descriptive analysis of the data was performed. In addition, the diagnostic performance of the PC/SD ratio (cut-off point <909) for the detection of EV was compared with the findings reported in the esophagogastroduodenoscopy (gold standard), calculating its sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), positive likelihood ratio (LR+), and negative likelihood ratio (LR-). A significance level of p<0.05 was considered. Results: The mean age of the participants was 65.5 years, 53.03% were female, and the most common causes of cirrhosis were alcohol consumption (40.90%) and autoimmune hepatitis (22.72%). EV was diagnosed in 48 patients (72.72%). The PC/SC ratio showed sensitivity of 60%, specificity of 78%, PPV of 0.88, NPV of 0.42, LR+ of 2.73, and LR- of 0.51. Conclusion: The low sensitivity, specificity, and NPV found in the present study suggest that the PC/SD ratio (cut-off point <909) may not be a useful diagnostic test for detecting EV in patients with cirrhosis.

Introduction: Cirrhosis management is centered on the treatment of the causes and management of the complications. The AASLD provides clear recommendations for inpatient management of cirrhosis decompensated by ascites, spontaneous bacterial peritonitis (SBP), hepatic encephalopathy (HE), and hepatorenal syndrome (HRS). Methods: We evaluated the current hospital practice for 150 consecutively admitted patients with cirrhosis complications in the period between 2017 and 2021. Decompensated cirrhosis was identified using ICD code K70.30/K70.31 (alcoholic cirrhosis) or K74.69/K74.60 (cirrhosis without alcohol), in addition to R18.8 (ascites), plus/minus any of the following: K65.2 (SBP), K72.91 (HE), and K76.7 (HRS). Results: 21/150 patients had no evidence of clinically decompensated cirrhosis on chart review and thus 129 patients represented the study cohort (decompensated cirrhosis, by at least ascites). The mean age of the cohort was 60±14 years. 83 patients were men, and the majority were White (88 patients, 68%). The most common cause of cirrhosis was alcohol related (72 patients, 56%), most patients had Child Pugh C (64%), and a mean MELD score of 21±7.7 and 20±7.5 on admission and discharge, respectively. Only 49/129 (38%) patients with cirrhotic ascites underwent diagnostic/therapeutic paracentesis. The second most common complication was esophageal varices (52 patients (40%)). SBP was noted in 8 patients, all of whom received appropriate medical treatment. SBP prophylaxis was indicated in 13 patients, and 10 of whom only received prophylaxis on discharge (77%). 41 patients had history of HE, and 21 of whom (51%) were on lactulose treatment. 14 patients developed HRS and were all started on albumin and octreotide therapy. 72 patients (56%) were placed on the appropriate cirrhotic diet, and daily weight was measured in 33/129 patients (26%) undergoing diuresis during the hospital stay. The mean length of stay was 5.9±4.4 days. 54 patients (42%) were re-admitted, and 13 patients (10%) died during the 90-day follow up period. Conclusion: We here demonstrated that further improvement in the medical care provided to hospitalized cirrhotic patients remains necessary. We recommend further education of the medical staff on the current guidelines to improve the care provided as well as adopting an electronic medical record order set (Figure) topromote consistent evidence-based practice, decrease errors of omission, and support provider efficiency.Figure 1.: Cirrhosis complications order set

Screening and Surveillance of Varices in Patients With Cirrhosis

Glue for gastric varices: some sticky issues

We showed racial/ethnic variations in the prevalence of CLD and cirrhosis by underlying etiology; NAFLD was the most common cause of CLD and cirrhosis in the entire cohort, and the high prevalence of NAFLD among Japanese Americans and Native Hawaiians is a novel finding, warranting further studies to elucidate the causes. (Hepatology 2016;64:1969-1977).

Chronic liver disease and decompensated cirrhosis are the major causes of morbidity and mortality in the world. According to current data, deaths due to liver cirrhosis constitute 2.4% of the total deaths worldwide. Cirrhosis is characterized by hepatocellular damage that leads to fibrosis and regenerative nodules in the liver. The most common causes of cirrhosis include alcohol consumption, hepatitis C, hepatitis B, and non-alcoholic fatty liver disease. Dysbiosis and intestinal bacterial overgrowth play a role in the development of complications of cirrhosis through translocation. In liver cirrhosis, ascites, gastrointestinal variceal bleeding, spontaneous bacterial peritonitis infection, hepatic encephalopathy, hepatorenal syndrome, hepatocelluler carcinoma are the most common complications. In addition, there are refractory ascites, hyponatremia, acute on-chronic liver failure, relative adrenal insufficiency, cirrhotic cardiomyopathy, hepatopulmonary syndrome and portopulmonary hypertension. In the primary prophylaxis of variceal bleeding, non-selective beta blockers or endoscopic variceal ligation are recommended for medium and large variceal veins. In current medical treatment, vasoactive agents, antibiotics, blood transfusion, endoscopic band ligation are the standard approach in the treatment of acute variceal bleeding. Sodium-restricted diet, diuretics and large-volume paracentesis are recommended in the management of ascites. In the treatment of hepatic encephalopathy, lactulose, branched chain amino acids, rifaximin and L-ornithine L-aspartate can be used. New therapeutic approaches such as ornithine phenyl acetate spherical carbon and fecal microbiota transplantation have shown beneficial effects on hepatic encephalopathy symptoms. In addition to their antioxidative, anti-proliferative and anti-inflammatory properties, statins have been shown to reduce the risk of decompensation and death by reducing portal pressure in compensated cirrhosis. In the treatment of liver failure, some artificial liver devices such as molecular adsorbent recirculating system, the single albumin dialysis system, fractionated plasma separation and adsorption are used until transplantation or regeneration. The purpose of this chapter is to review the most up-to-date information on liver cirrhosis and to explain the complications assessment, current management and potential treatment strategies in decompensated cirrhosis.

Background: Multi-organ failure and a sharp decline in liver function are hallmarks of acute-on-chronic liver failure (ACLF), carrying high mortality. Objective: To determine the etiology, clinical presentations, and the mortality outcome in patients with acute-on-chronic liver disease. Methods: In this retrospective study, medical records of 109 patients admitted to the Intensive Care Unit (ICU) of Pakistan Kidney and Liver Institute and Research Center, Lahore, Pakistan, from 1st January 2022 to 31st August 2023 with ACLF were included after ethical approval (PKLI-IRB/AP/149). Data regarding demographics, clinical features, comorbidities, Child-Turcotte-Pugh (CTP) score, Chronic Liver Failure Consortium (CLIF-C score), Model for End-stage Liver Disease-Na (MELD-Na), and ACLF grades were recorded, and their outcome in terms of mortality was noted. Results: The mean age was 47.4 ± 10.5. The primary cause of cirrhosis was hepatitis C virus (HCV) infection (52.3%), followed by cryptogenic cirrhosis (14.7%). According to the CTP score, 95.4% of the patients had Child-Pugh class C cirrhosis, and 52.3% were classified as grade 3 ACLF. Out of 109 patients, only 31 survived, with a mortality rate of 71.6%. Acute decompensation was mainly secondary to hepatic encephalopathy precipitated by infections and variceal bleeding. The non-survivors had significantly higher INR=3.4 ± 1.8 vs 2.6 ± 1.1 (p=0.002) and ammonia levels =230.1 ± 241.7 µg/dL vs 125.7 ± 65.7 µg/dL (p=0.002) on ICU admission compared to those who survived. The mean MELD-Na score at hospital admission was 32.9 ± 6.5, and in ICU admission was 34.7 ± 6.7 (p<0.001), but was not significant regarding survival (p=0.195). The CLIF-C score increased from 50.4±10.1 (in ward) to 56.1 ±10.2 (ICU transfer) (p<0.001) and was also higher in non-survivors compared to survivors (p<0.001). It is observed that increasing CLIF-C scores is a sign of poor prognosis. Conclusion: HCV infection was the most common cause of cirrhosis, and hepatic encephalopathy was the common trigger for ACLF. A high INR, hyperammonia, advanced ACLF grade, and an increase in CLIF-C score lead to poor outcomes in terms of survival, while worsening of CLIF-C scores may additionally predict short-term mortality.

Evolving Consensus in Portal Hypertension Report of the Baveno IV Consensus Workshop on methodology of diagnosis and therapy in portal hypertension

Therapies for bleeding gastric varices: is the fog starting to clear?

INTRODUCTION: Non alcoholic Fatty liver disease (NAFLD) is one of the leading cause of chronic liver disease in United States. Combined with diabetes and metabolic syndrome, NAFLD is expected to be the most common cause of liver transplantation. We sought to determine the trend of NAFLD induced cirrhosis in National Population. We also studied the risk of decompensation and in hospital mortality in patients with NAFLD cirrhosis. METHODS: We obtained data from Nationwide Inpatient sample database using International classification of Diseases, the 9th revision, clinical modification codes to identify patients who had diagnosis of Cirrhosis and NAFLD from 2006-2014. We also obtained data on decompensation and patient's mortality in patients who had cirrhosis with history of NAFLD. Decompensated cirrhosis was defined as patients with cirrhosis and having one or more of these conditions: hepatic encephalopathy, hepatorenal syndrome, spontaneous bacterial peritonitis, ascites or variceal bleeding. Data was extrapolated using SPSS statistics software. RESULTS: Total of 4,226,236 patients had diagnosis of cirrhosis, 114,972 had NAFLD diagnosis. Trend of NAFLD is significantly increasing from 2007 (1.2%) to 2014 (3%). 2,313,524 (54.7%) of patients had decompensated cirrhosis. NAFLD was present in 3.2% (74,557) of patients in decompensated cirrhosis as compared to 2.1% (40,415) of patients who had compensated cirrhosis (P < 0.001). In hospital mortality of patients in decompensated cirrhosis with history of NAFLD was 4.3% and without history of NAFLD was 7.9% (P < 0.001). On Univariate analysis, patients with NAFLD were at low risk of in hospital death as compared to patients without NAFLD OR 0.53 (CI: 0.513–0.550). CONCLUSION: There has been significant increasing trend of NAFLD induced cirrhosis in last decade. NAFLD is associated with increased risk of cirrhosis decompensation as compared to other causes of cirrhosis. Interestingly, NAFLD cirrhotic patients have lower in hospital mortality as compared to patients with other causes of cirrhosis.

BackgroundCyanoacrylate alone or in combination with other interventions, can be used to achieve variable rates of success in preventing rebleeding. Our study aims to assess the pooled risk of gastric and esophageal varices rebleeding after an initial treatment with cyanoacrylate alone and/or in combination with other treatments, by a systematic review of the literature and pooled analysis.MethodsPubMed, EMBASE, SCOPUS, and the Cochrane library were searched for studies that reported the risk of rebleeding during the follow-up period after treatment of gastric or esophageal varices with either cyanoacrylate alone or in combination with other treatments. Standard error, upper and lower confidence intervals at 95% confidence interval for the risk were obtained using STATA Version 15 which was also used to generate forest plots for pooled analysis. The random or fixed effect model was applied depending on the heterogeneity (I2).ResultsA total of 39 studies were found to report treatment of either gastric or esophageal varices with either cyanoacrylate alone or in combination with other treatments. When gastric varices are treated with cyanoacrylate alone, the risk of rebleeding during the follow-up period is 0.15(Confidence Interval: 0.11–0.18). When combined with lipiodol; polidocanol or sclerotherapy the rebleeding risks are 0.13 (CI:0.03–0.22), 0.10(CI:0.02–0.19), and 0.10(CI:0.05–0.18), respectively. When combined with percutaneous transhepatic variceal embolization; percutaneous transhepatic variceal embolization; endoscopic ultrasound guided coils; or with ethanolamine, the rebleeding risk are 0.10(CI:0.03–0.17), 0.10(CI:0.03–0.17), 0.07(CI:0.03–0.11) and 0.08(CI:0.02–0.14), respectively.When esophageal varices are treated with cyanoacrylate alone, the risk of rebleeding is 0.29(CI:0.11–0.47). When combined with percutaneous transhepatic variceal embolization; sclerotherapy; or band ligation, the risks of rebleeding are 0.16(CI:0.10–0.22), 0.12(CI:0.04–0.20) and 0.10(CI:0.04–0.24), respectively. When combined with a transjugular intrahepatic portosystemic shunt; or ethanolamine, the risks of rebleeding are 0.06(CI: − 0.01-0.12) and 0.02 (CI: − 0.02-0.05), respectively.ConclusionIn treating both gastric and esophageal varices, cyanoacrylate produces better results in terms of lower risk of rebleeding when combined with other treatments than when used alone. The combination of cyanoacrylate with ethanolamine or with endoscopic ultrasound guided coils produces the lowest risk of rebleeding in esophageal and gastric varices, respectively. We call upon randomized trials to test these hypotheses.

Experiencia del programa de aplicación de cianoacrilato en pacientes con varices gástricas del Hospital General de México

Etiology of cirrhosis in the young

Background:The advantages of spleen stiffness in prediction of high-risk varices (HRV) in cirrhosis patients have been confirmed. Recently, a new device utilizing a 100 Hz probe dedicated to spleen stiffness measurement (SSM) was developed.Objectives:To validate the clinical applicability of SSM@100 Hz in predicting HRV by comparing it with other non-invasive tests (NITs).Design:A prospective cohort study.Methods:A total of 171 cirrhosis patients who underwent esophagogastroduodenoscopy (EGD) examination were included in this study. SSM using a 100 Hz probe and liver stiffness measurement using a 50 Hz probe were performed. Additionally, 22 healthy controls underwent spleen stiffness evaluation using the 100 Hz probe.Results:The failure rates of spleen stiffness examination in patients with cirrhosis and in healthy controls were 2.9% and 4.5%, respectively. The means of SSM values were 56.4 ± 21.6 and 13.8 ± 6.7 kPa in cirrhosis and controls. SSM increased proportionally with the severity of esophageal varices. The area under receiver operating characteristic (ROC) for spleen stiffness in predicting HRV was 0.881 (95% confidence interval 0.829–0.934), with a cutoff value of 43.4 kPa. The accuracy, false negative rate and EGD spare rate were 86.5%, 2.5% and 24.3%, respectively. For HRV prediction, SSM was comparable to expanded Baveno VI and VII and superior to other NITs. As to viral versus non-viral cirrhosis and compensated versus decompensated cirrhosis, the cut-off and performance of SSM were different.Conclusion:SSM@100 Hz demonstrates high accuracy in predicting HRV with a low missed HRV rate. Our findings suggest that SSM@100 Hz can be used independently due to its simplicity and effectiveness. However, further studies are needed to determine appropriate cutoff values based on the cause of cirrhosis and liver function.Trail Registration:ChiCTR2300070270.