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Hepatic encephalopathy (HE) is a neuropsychiatric syndrome of both acute and chronic liver disease. As a metabolic disorder, HE is considered to be reversible and therefore is expected to resolve following the replacement of the diseased liver with a healthy liver. However, persisting neurological complications are observed in up to 47% of transplanted patients. Several retrospective studies have shown that patients with a history of HE, particularly overt-HE, had persistent neurological complications even after liver transplantation (LT). These enduring neurological conditions significantly affect patient's quality of life and continue to add to the economic burden of chronic liver disease on health care systems. This review discusses the journey of the brain through the progression of liver disease, entering the invasive surgical procedure of LT and the conditions associated with the post-transplant period. In particular, it will discuss the vulnerability of the HE brain to peri-operative factors and post-LT conditions which may explain non-resolved neurological impairment following LT. In addition, the review will provide evidence; (i) supporting overt-HE impacts on neurological complications post-LT; (ii) that overt-HE leads to permanent neuronal injury and (iii) the pathophysiological role of ammonia toxicity on astrocyte and neuronal injury/damage. Together, these findings will provide new insights on the underlying mechanisms leading to neurological complications post-LT.

BackgroundOvert hepatic encephalopathy (OHE) is a serious complication of liver dysfunction, which is associated with severe morbidity/mortality and healthcare resource utilization. OHE can be medically refractory due to spontaneous portosystemic shunts (SPSSs) and therefore a new treatment option for these SPSSs is critical.MethodsThis is a retrospective study of 43 patients with medically refractory OHE, who underwent CARTO (Coil-Assisted Retrograde Transvenous Obliteration) procedures between June 2012 and October 2016. The patient demographic characteristics, technical and clinical outcomes with an emphasis on HE improvement, and complications are reviewed and analyzed.ResultsThe overall clinical success rate was 91% with a significant HE improvement. Eighty-one percent of patients had clinically significant improvement from OHE and 67% of patients had complete resolution of their HE symptoms during our follow-up period of 893 ± 585 days (range 36–1881 days, median 755.0 days). The median WH score improved from 3 (range 2–4) pre-CARTO to 1 (range 0–4) post-CARTO (p < 0.001). The median ammonia level significantly decreased from 134.5 pre-CARTO to 70.0 post-CARTO (p < 0.001) in 3 days. The overall mean survival was 1465.5 days (95% CI of 1243.0 and 1688.0 days). Only three patients had recurrent HE symptoms. There were 39.6% minor complication rate including new or worsened ascites and esophageal varices, and only 2.3% major complication rate requiring additional treatment (one patient with bleeding esophageal varices requiring treatment). No procedure-related death is noted.ConclusionsCARTO appears to be a safe and effective treatment option for refractory overt hepatic encephalopathy (OHE) due to spontaneous portosystemic shunts. CARTO could be an excellent addition to currently available treatment options for these patients.

Transjugular intrahepatic portosystemic shunt (TIPS) creation using the Viatorr stent remains relatively uncommon in underdeveloped and high-burden disease regions in Asia–Pacific, and there is a lack of comparative studies regarding its prognostic effects compared with the generic stent-graft/bare stent combination. The purpose of this retrospective study is to compare the prognostic endpoints of these two treatments in patients who underwent TIPS creation. Clinical data from 145 patients were collected, including 82 in the combination group and 63 in the Viatorr group. Differences in prognostic endpoints (shunt dysfunction, death, overt hepatic encephalopathy [OHE], rebleeding) between the two groups were analyzed using Kaplan–Meier curves. The Cox proportional hazards model was used to identify independent risk factors for post-TIPS shunt dysfunction. The TIPS procedure was successful in all patients. After TIPS creation, both groups showed a significant decrease in porto-caval pressure gradient compared to that before TIPS creation. The stent patency rates at 6, 12, and 18 months were high in both the combination and Viatorr groups (93.7%, 88.5%, and 88.5% vs. 96.7%, 93.4%, and 93.4%, respectively). The stent patency rates was higher in the combination group than in the Viatorr group, although not statistically significant (HR = 2.105, 95% CI 0.640–6.922, Log-rank P  = 0.259). There were no significant differences in other prognostic endpoints (death, OHE, rebleeding) between the two groups. The Cox model identified portal vein diameter (HR = 0.807, 95% CI 0.658–0.990, P  = 0.040) and portal vein thrombosis (HR = 13.617, 95% CI 1.475–125.678, P  = 0.021) as independent risk factors for post-TIPS shunt dysfunction. The shunt patency rates between the Viatorr stent and the generic stent-graft/bare stent combination showed no significant difference and the generic stent-graft/bare stent combination may be a viable alternative in areas where the Viatorr stent is not yet available.

The effect Helicobacter pylori (Hp) infection and small intestinal bacterial over growth (SIBO) in minimal hepatic encephalopathy (MHE) is not well understood. The aim of the study was to determine the effect of eradication of Hp infection and SIBO treatment on MHE in patients with cirrhosis. Patients with cirrhosis were enrolled and MHE was determined by psychometric tests and critical flicker frequency analysis. Hp infection and SIBO were assessed by urea breath and Hydrogen breath tests respectively in patients with cirrhosis and in healthy volunteers. Patients with Hp infection and SIBO were given appropriate treatment. At six weeks follow-up, presence of Hp infection, SIBO and MHE status was reassessed. Ninety patients with cirrhosis and equal number of healthy controls were included. 55 (61.1%) patients in the cirrhotic group were diagnosed to have underlying MHE. Among cirrhotic group, Hp infection was present in 28 with MHE (50.9%) vs. in 15 without MHE (42.8%) (p = 0.45). Similarly, SIBO was present in 17 (30.9%) vs. 11 (31.4%) (p = 0.95) in patients with and without MHE respectively. In comparison with healthy controls, patients with cirrhosis were more frequently harboring Hp and SIBO (47.7% vs. 17.7% (p < 0.001) and 31.1% vs. 4.4% (p < 0.001) respectively. On follow-up, all patients showed evidence of eradication of Hp and SIBO infection. Treatment of SIBO significantly improved the state of MHE in cirrhotics, however eradication of Hp infection did not improve MHE significantly. Additionally, patients with low Model for End-Stage Liver Disease (MELD) score and belonging to Child class B had significantly better improvement in MHE. A large number of patients with cirrhosis had either active Hp infection or SIBO with or without MHE, compared to healthy controls. Treatment of SIBO significantly improved MHE in patients with cirrhosis, whereas eradication of Hp did not affect the outcome of MHE in these patients.

The KPS scores were divided into three groups: 0–40% (requirement of hospital care, or deteriorating or dead), 50–70% (able to live at home and requires varying assistance), and 80–100% (able to carry on normal activity or work and no assistance required). The univariate analyses [Supplementary Table 4, http://links.lww.com/CM9/B922] and multivariate analyses for the first post-LT 6-month mortalities in ACLF with grade 3–4 HE were done, which were independently associated with EAD (Hazard ratio [HR]: 3.29, 95% confidence interval [CI]: 1.28–8.43, P = 0.011), XDR isolates–related bacteremia (HR: 4.50, 95% CI: 2.24–9.05, P <0.001), XDR isolates–related pneumonia (HR: 13.11, 95% CI: 2.70–63.57, P = 0.002), and abdominal MDR bacterial infections (HR: 3.57, 95% CI: 1.48–8.62, P <0.001). LT is considered a rescue treatment for ACLF patients who cannot get well by conservative treatment alone. [...]we suggest that LT for ACLF with grade 3–4 HE should be done in time when conditions permit. [8] The in-hospital mortality rate in solid organ transplant patients with bacteremia caused by MDR or XDR non-lactose-fermenting GNB is over 50%, whereas in patients with septic shock, the rate sharply increases to 95%.

Introduction Liver transplant (LT) recipients are at significant risk for the development of neurological complications, such as altered mental status and seizures, in the postoperative period. Identifying accurate predictors of these events may allow optimal selection and preparation of candidates, and minimize risk after transplantation. Methods One hundred and one consecutive adult LT recipients were evaluated retrospectively for neurological morbidity occurring in the first 30 days postoperatively. These events were analyzed in relation to specific predictive variables including preoperative complications of liver failure, such as hepatic encephalopathy (HE). Results Median age was 50 years, 63% were male and hepatitis C was the most common indication for LT ( n  = 36). Median Child-Pugh score was 9 with 45% being Class C. Over half ( n  = 52) had experienced clinical HE prior to LT, while one quarter ( n  = 26) were encephalopathic at the time of LT. Neurological complications occurred in 31 patients in the postoperative period, with encephalopathy occurring in 28 and seizures occurring in 4; drug toxicity was responsible for neurological morbidity in 12 patients (39%). Length of hospital stay was significantly prolonged (median 19 vs. 12 days, P  = 0.005) and all mortality ( n  = 3) occurred in those with neurological complications. There was no association between etiology of liver failure and complications; logistic regression identified active preoperative HE as the strongest predictor of postoperative morbidity (OR 10.7 95% CI 3.8–29.9). Conclusion Neurological events, manifesting most often as encephalopathy, occurred in almost one-third of patients after LT. Those suffering from HE at the time of LT may be more vulnerable to the metabolic stresses of surgery and the neurotoxicity of the drugs used, and were at highest risk for such complications.

Background. Post-TIPS hepatic encephalopathy (PSE) is a complex process involving numerous risk factors; the root cause is unclear, but an elevation of blood ammonia due to portosystemic shunt and metabolic disorders in hepatocytes has been proposed as an important risk factor. Aims. The aim of this study was to investigate the impact of pathological features of mitochondrial ultrastructure on PSE via transjugular liver biopsy at TIPS implantation. Methods. We evaluated the pathological damage of mitochondrial ultrastructure on recruited patients by the Flameng classification system. A score ≤2 (no or low damage) was defined as group A, and a score >2 (high damage level) was defined as group B; routine follow-up was required at 1 and 2 years; the incidence of PSE and multiple clinical data were recorded. Results. A total of 78 cases in group A and 42 in group B completed the study. The incidence of PSE after 1 and 2 years in group B (35.7% and 45.2%, respectively) was significantly higher than that in group A (16.7% and 24.4%, respectively); the 1- and 2-year OR (95% CI) were 2.778 (1.166-6.615) and 2.565 (1.155-5.696), respectively, for groups A and B. Importantly, group B had worse incidence of PSE than group A [P=0.014, hazard ratio (95%CI): 2.172 (1.190-4.678)]. Conclusion. Aggressive damage to mitochondrial ultrastructure in liver shunt predicts susceptibility to PSE. The registration number is NCT02540382.

A clinical toxicologist was consulted and amatoxin poisoning was diagnosed; NAC, penicillin G, vitamin K, and silibinin were commenced. According to the King's College Criteria for acute liver failure, liver transplantation was indicated and transplant workup started. [...]the ‘acute liver failure phase' sets in, with drastic surges in liver enzymes, renal failure, encephalopathy, hepatorenal syndrome,10 and multi-organ failure. N-acetylcysteine, silibinin, penicillin G, multiple-dose activated charcoal, and enhanced elimination methods constitute the mainstay of medical treatment.4 5 6 7 9N-acetylcysteine protects the liver by being an oxygen free radical scavenger, while silibinin works by inhibiting the organic anion transmembrane transporter responsible for the uptake of amatoxins by hepatocytes and the enterohepatic recycling of these toxins.4 The role of penicillin G in treating amatoxin poisoning is controversial.

Hypermanganesemia is commonly recognized in human patients with hepatic insufficiency and portosystemic shunting. Since manganese is neurotoxic, increases in brain manganese concentrations have been implicated in the development of hepatic encephalopathy although a direct causative role has yet to be demonstrated. Evaluate manganese concentrations in dogs with a naturally occurring congenital shunt before and after attenuation as well as longitudinally following the changes in hepatic encephalopathy grade. Our study demonstrated that attenuation of the shunt resolved encephalopathy, significantly reduced postprandial bile acids, yet a hypermanganasemic state persisted. This study demonstrates that resolution of hepatic encephalopathy can occur without the correction of hypermanganesemia, indicating that increased manganese concentrations alone do not play a causative role in encephalopathy. Our study further demonstrates the value of the canine congenital portosystemic shunt as a naturally occurring spontaneous model of human hepatic encephalopathy.

Hepatic encephalopathy (HE) is a common complication after implantation of a transjugular intrahepatic portosystemic shunt (TIPS). Neuroimaging offers a variety of techniques for non-invasive evaluation of alterations in metabolism, as well as structural and functional changes of the brain in patients after TIPS implantation. In this article, we review the epidemiology and pathophysiology of post-TIPS HE. The potential of neuroimaging including positron emission tomography and multimodality magnetic resonance imaging to investigate the pathophysiology of post-TIPS HE is presented. We also give a perspective on the role of neuroimaging in this field.